• Salicylates is the broad term used for Acetylsalicylic acid (ASA), salicylic acid, and their derivatives

• Acetylsalicylic acid (ASA) is the active ingredient of aspirin

  • Irreversible cyclooxygenase-1 inhibitor that is used as an analgesic, antipyretic, anti-inflammatory, and antiplatelet drug

• ASA is a common medication used by many ED patients for the management of cardiovascular events (e.g., acute MI, angina) and for primary/secondary prophylaxis of cardiovascular disease

History

• The earliest evidence of salicylate use comes from Sumerian clay tablets, where willow bark was noted for its pain-relieving properties

• In 1828, a German chemist named Johann Andreas Buchner isolated a yellow substance from willow bark and named it salicin, after the Latin name for white willow (Salix alba)

• By the late 1800s, large-scale production of salicylic acid began for pain and fever treatment

• Bayer marketed it under the brand name Aspirin in 1899, revolutionizing pain management

Pathophysiology of Toxicity

• Directly stimulate the respiratory center of the brain causing hyperventilation and CO2 washout leading to a primary respiratory alkalosis

• Mitochondrial toxin that uncouple the electrons from ATPase in the electron chain transport resulting in cessation of oxidative phosphorylation

• Organic products such as lactate, keto acids and pyruvate that are generated as a result of uncoupling of the electron chain transport drive a metabolic acidosis

• As a result, you have a “mixed picture” acid-base disturbance with a primary respiratory alkalosis followed by metabolic acidosis

Clinical Features

• Early symptoms: tinnitus, nausea, vomiting, tachypnea, hyperpnea

• Late symptoms: hyperthermia, agitation, delirium, seizures, noncardiogenic pulmonary edema

• Also known to be an imitator of sepsis (hyperthermia, hypotensive, lactate, altered, respiratory distress)

• Common offenders: Aspirin (often intentional overdose), bismuth subsalicylate, oil of wintergreen (methyl salicylate), and excessive use of pain relief creams i.e. Aspercreme, BenGay.

• Perspective: 1 tablespoon of oil of wintergreen = equivalent of 7g of aspirin

Labs/Workup

• Initial labs should include VBG, salicylate level and CMP

• Therapeutic salicylate range = 10-15 mg/dL

• Toxicity is a concern with ingestion of 150 mg/kg or more

• Toxicity in adults starts around 30 mg/dl and at 20 mg/dl in kids

• Because salicylate levels may be falsely low within 4 hours of ingestion and do not necessarily correlate with clinical presentation, a high index of suspicion should be maintained when caring for a patient with symptoms of salicylate poisoning

Treatment

Alkalinize then Dialyze

• The definitive treatment is dialysis

• Treatment should be based on the clinical picture, but if approaching 90 mg/dL (inn acute toxicity), then it may be worth empirically dialyzing

• Until dialysis can be initiated, the goal is to treat the acidosis

  • At a physiologic serum pH, salicylic acid exists in an ionized state as a weak acid; in toxicity (acidic environment), it is converted to an un-ionized (highly permeable) state

  • First step is to initiate IV sodium bicarbonate bolus (1-2 mEq/kg) and infusion (150 mEq (3 amps) in 1 L of 5% dextrose in water (D5W) at 1.5-2 times maintenance)

  • Goal serum pH = 7.45-7.55

  • Bicarbonate infusion creates a higher pH which Ion traps salicylates in the urine

• As with most metabolic acidosis, you want to avoid intubation as much as possible as patients are able to compensate more effectively from a respiratory standpoint than the ventilator.

  • If necessary, these patients make good candidates for awake/delayed intubation.

  • Will require larger tidal volumes and respiratory rate to compensate for metabolic acidosis

• Ongoing care

  • Patients requiring frequent blood gasses, sodium bicarbonate infusions, or emergent dialysis will require ICU level care

  • Consider psychiatric consultation for acutely suicidal patients

• Discharge may be considered after 6 hours if the patient has down trending levels less than 30, is asymptomatic and maintains a normal pH.

AUTHORED BY: JAKE PERINO, MD, PGY3

FACULTY EDITING BY: LAUREN PORTER, DO

References

1. American College of Medical Toxicology. Guidance document: management priorities in salicylate toxicity. J Med Toxicol. 2015;11(1):149-152.

2. Katz K, Koons A. Salicylate poisoning. In: Johnson W, Nordt S, Mattu A, Swadron S, eds. CorePendium. Burbank, CA: CorePendium LLC; updated May 5, 2021. Accessed March 14, 2024. https://www.emrap.org/corependium/chapter/recdUAKgBNpqpYseX/Salicylate-Poisoning

3. Dargan PI. An evidence-based flowchart to guide the management of acute salicylate (aspirin) overdose. Emerg Med J. 2002;19(3):206-209.

4. Ciejka M, Nguyen K, Bluth MH, Dubey E. Drug toxicities of common analgesic medications in the emergency department. Clin Lab Med. 2016;36(4):761-776.

5. Gummin DD, Mowry JB, Spyker DA, et al. 2018 annual report of the American Association of Poison Control Centers’ National Poison Data System (NPDS): 36th annual report. Clin Toxicol (Phila). 2019;57(12):1220-1413.

6. ResearchGate. Chemical structures of salicylic acid and its synthetic and natural derivatives. Accessed March 14, 2024. https://www.researchgate.net/figure/Chemical-structures-of-salicylic-acid-and-its-synthetic-and-natural-derivatives_fig1_284693818

7. Farkas J. Salicylate intoxication. EMCrit Project. Published February 12, 2023. Accessed March 14, 2024. https://emcrit.org/ibcc/salicylates/

8. Salicylate toxicity. Rosh Review. Published February 8, 2023. Accessed March 14, 2024. https://www.roshreview.com/

Kratom

• Herbal product

• Derived from Mitragyna speciosa tree of Southeast Asia

• Contains 40 bioactive alkaloids

• Growing use in the United States with increasing presentations to emergency departments (ED) for toxicity and withdrawal.

History and Epidemiology

• Used in SE Asia for over a century (2)

  • Leaves were chewed or brewed into tea

• Therapeutic uses

  • Analgesic

  • Antidiarrheal

  • Antispasmodic

  • Antipyretic

• Functional uses

  • Stimulant to increase endurance and productivity among manual laborers

• Popularity in US has increased

• Legal at Federal level; regulated in 24 states and DC

  • Variability in potency, preparation and alkaloid content (3)

• Marketed online and in gas stations and head shops

• “natural remedy” for pain, anxiety, fatigue and opioid withdrawal

  • Appeal is particularly strong among patients with opioid use disorder who seek alternatives to methadone or buprenorphine (1)

• Historical accounts describe its use for withdrawal management in Thailand and Malaysia dating back to the 1800s (2)

  
  

Ohio-Specific Laws & Regulations

• Currently legal in Ohio but can only be sold in natural, dried leaf or powdered form

  • August 2025, Governor DeWine called to classify all forms as scheduled I controlled substances

  • Proposed bans/regulation are introduced in the House and Senate

  • FDA is recommending 7-hydroxymitragynine (7-OH) as Schedule I

• Regulation vs legalization

  • Risks and benefits to both

    
    

Pharmacology & Mechanism of Action

• 40 Bioactive alkaloids - 4 primary agents identified (5)

• Mitragynine

  • Most abundant

  • Active at mu, delta and kappa opioid receptors

  • Interacts with adrenergic and serotonergic systems

• 7-hydroxymitragynine

  • Metabolite of mitragynine (hepatic)

  • Significantly more potent

  • 13x higher affinity for opioid receptors compared to morphine (7)

  • 46x more potent than mitragynine (7)

• Dual actions à dual effects

  • CNS stimulant effects at low doses & opioid-like sedative effects at higher doses

    
    

Clinical Presentations in the ED

• Acute toxicity

  • Common effects

    • Agitation, tachycardia, drowsiness, vomiting, confusion

  • Severe effects

    • Seizures, hallucinations, respiratory depression, coma, cardiac and respiratory arrest

• Withdrawal

  • Similar to opioid withdrawal and is treated the same;

  • Symptoms

    • Piloerection, rhinorrhea, abdominal cramping, diarrhea, lacrimation, mydriasis, insomnia, irritability (1)

  • Onset

    • 12-24 hours after last use (2)

  • Duration

    • 3-7 days, severity correlating to chronicity and dose (2)

Management in the ED

• Acute toxicity

  • ABCs remain the cornerstone

  • Naloxone (3,4)

• Withdrawal

  • Buprenorphine and methadone

  • Dosing the same as with OUD

• Symptomatic therapy

  • Clonidine for autonomic hyperactivity

  • Dicyclomine for abdominal pain

  • Ondansetron for nausea and vomiting

    
    

Take Home Points

• Kratom is an unregulated herbal product increasingly seen in US emergency departments

• Contains multiple alkaloids with mixed opioid, adrenergic and serotonergic activity

• Clinical effects are dose-dependent

• Stimulant at lower doses and opioid-like sedation

• Presentations include nausea, tachycardia and agitation but severe toxicity is possible

• Naloxone may be effective in reversing kratom-induced respiratory depression

• Withdrawal resembles opioid withdrawal and should be managed in similar fashion

AUTHORED BY: ABBY WISSMAN, DO, PGY3

FACULTY EDITING BY: LAUREN PORTER, DO

References

1. Eggleston W, Stoppacher R, Suen K, Marraffa JM, Nelson LS. Kratom use and toxicities in the United States. Pharmacotherapy. 39.7 (2019): 775-777.

2. Kerrigan, Sarah, and Stephanie Basiliere. "Kratom: A systematic review of toxicological issues." Wiley Interdisciplinary Reviews: Forensic Science 4.1 (2022): e1420.

3. Overbeek DL, Abraham J, Munzer BW. Kratom (Mitragynine) Ingestion Requiring Naloxone Reversal. Clin Pract Cases Emerg Med. 2019 Jan 4;3(1):24-26.

4. Ahmed S, Tran QV, McLean M. The Great Imitator: A Case of Accidental Kratom Overdose. Cureus. 2023 Aug 8;15(8):e43144.

5. Henningfield JE, Chawarski MC, Garcia-Romeu A, Grundmann O, et al. Kratom withdrawal: Discussions and conclusions of a scientific expert forum. Drug Alcohol Depend Rep. 2023 Mar 15;7:100142.

6. Arhin M, Mobley J, Hamad H, Remick P. Successful Management of Kratom Use Disorder With Buprenorphine and Naloxone. Cureus. 2023 Jun 29;15(6):e41146.

7. Sokup B, Pippin MM. Kratom. [Updated 2023 Aug 28]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK585120/

8. https://www.poison.org/articles/kratom

9. https://www.vcuhealth.org/news/is-kratom-safe-rising-health-concerns-explained/

83-year-old male with a history of chronic obstructive pulmonary disease (COPD) presented to the emergency department (ED) for pleuritic chest pain and shortness of breath that started after a coughing fit. He reported two weeks of flu-like symptoms prior to this. He arrived to the ED on a non-rebreather, slightly tachypneic but satting well and otherwise well-appearing.

Lung ultrasound was performed and showed the following:

POCUS Findings: Lung ultrasound demonstrated a lung point, representing the interface between normal pleural sliding and absent sliding, consistent with pneumothorax and helpful for localizing its extent. In addition, M-mode (not shown here) demonstrated a transition from seashore sign to barcode sign, corresponding to normal lung sliding and absent lung sliding, respectively — see representative example below.

Case Conclusion: The patient underwent chest tube placement in the ED with imaging guidance to optimize insertion site selection, and he tolerated the procedure well. He experienced symptomatic improvement and was admitted to the hospital, where he was successfully weaned off supplemental oxygen and had an uncomplicated course.

Pneumothorax

Overview

A pneumothorax is the presence of air within the pleural space, external to the lung parenchyma, which can lead to partial or complete lung collapse. Pneumothoraces are classified as simple, tension, or open. A simple pneumothorax does not cause mediastinal shift, whereas a tension pneumothorax results in progressive intrathoracic pressure with mediastinal displacement and hemodynamic compromise. An open pneumothorax, commonly referred to as a “sucking” chest wound, occurs when air freely enters the pleural space through a chest wall defect, communicating with the external environment (1).

Epidemiology

Primary spontaneous pneumothorax (PSP) most commonly occurs in individuals aged 20-30 years, with an annual incidence of approximately 7 per 100,000 men and 1 per 100,000 women in the United States (2). Recurrence is common, occurring in 25-50% of patients, with the highest risk within the first year, and particularly early after the initial event (1-3).

Secondary spontaneous pneumothorax (SSP) typically occurs in older adults (60–65 years) and is associated with underlying lung disease (1,3). The incidence is approximately 6.3 per 100,000 men and 2 per 100,000 women, with a male-to-female ratio of approximately 3:1 (3). Chronic obstructive pulmonary disease (COPD) is a major risk factor for SSP (1). Heavy tobacco use markedly increases pneumothorax risk, with rates reported to be substantially higher than in non-smokers (1,3).

Diagnostic Imaging

Computed tomography (CT) is considered the gold standard for diagnosing pneumothorax (1). However, when performed by experienced operators, lung ultrasound is often more sensitive than chest radiography, allows for rapid bedside diagnosis and avoids ionizing radiation, making it particularly valuable in acute and resuscitative settings (4-6).

Lung Ultrasound

Lung ultrasound is one of the most commonly used applications of point-of-care ultrasound (POCUS) in the ED and has gained widespread adoption over the past decade. It can be utilized to evaluate a wide range of pathologies, including pneumothorax, pleural effusion, pulmonary edema, pneumonia, and atelectasis (7,8). While lung ultrasound should not delay definitive management, such as emergent operative intervention or other life-saving measures, it is a low-risk examination with no significant contraindications (7).

Image Acquisition

A comprehensive lung ultrasound examination involves assessment of each hemithorax across the anterior, lateral, and posterior lung zones, in both transverse and longitudinal orientations (7,8), see Figure 1. In emergency settings, a focused, clinical question–driven approach is often sufficient and should be tailored to the clinical context and patient positioning (7). Curvilinear probes (5–9 MHz) are well-suited for general lung assessment, while high-frequency linear probes (7–12 MHz) provide superior resolution of superficial structures and are particularly useful in pediatric patients and when assessing for pneumothorax (7,8). Switching to a linear probe can be especially helpful when findings are subtle, improving visualization of lung sliding or a suspected lung point.

Because lung ultrasound is largely artifact-based, the probe should be held perpendicular to the skin to optimize artifact generation and interpretation (8). Larger body habitus may limit visualization of the pleural line and deeper structures.

Assessing for Pneumothorax

Assessment for pneumothorax on lung ultrasound centers on evaluation of pleural motion rather than direct visualization of intrapleural air (7,8). After identifying the pleural line, first assesses for pleural sliding (Figure 2), which reflects normal apposition of the visceral and parietal pleura; its presence effectively rules out pneumothorax at that location (5,7). Because air preferentially accumulates in the least dependent regions of the lung, focusing the initial assessment in these areas provides the highest diagnostic yield.

When pleural sliding is absent (figure 3), pneumothorax should be considered; however, this finding alone is not diagnostic, as absent sliding may also be seen in apnea, mainstem intubation, pleurodesis, or severe underlying lung disease. In this setting, additional features — such as B-lines or a lung pulse (pulse-like pleural movement synchronous with cardiac activity, see figure 4) — indicate apposition of the visceral and parietal pleura, arguing against pneumothorax and prompting consideration of alternative explanations for absent pleural sliding (7,9).

When findings that argue against pneumothorax are absent, or when the clinical context remains concerning, the probe should be moved laterally and posteriorly to search for the lung point, which is highly specific for pneumothorax (10,11).

Key Diagnostic Finding: The Lung Point

The lung point represents the interface between normally aerated lung and pneumothorax, with pleural sliding present on one side and absent on the other (10), see figure 5. The lung point has a reported sensitivity of approximately 66% and a specificity approaching 100% for pneumothorax (11).

M-mode can help confirm a lung point by demonstrating a transition from the barcode sign to the seashore sign as the pleural interface alternates between absent and normal sliding (figure 6).

Estimating Pneumothorax Size

Because larger pneumothoraces are more likely to require thoracostomy, identifying the location of the lung point can help estimate pneumothorax size. If lung sliding is absent anteriorly, the probe can be moved laterally and posteriorly to identify the lung point. The more lateral or posterior the lung point, the larger the pneumothorax; conversely, an anterior lung point indicates a smaller pneumothorax (10,11).

Lung Point Mimics

Several entities may mimic a true lung point and should be interpreted within clinical context. A physiologic lung point may occur near the mediastinal border, where cardiac motion simulates pleural movement (12). In patients with bullous lung disease, a lung-point-like appearance may be seen at the interface between a bulla and aerated lung. This occurs only when subpleural lung tissue is completely absent beneath the pleura; even a thin preserved layer prevents this artifact. Differentiation requires integration of ultrasound findings with the clinical picture (9,13).

Take-Home Points

• Lung ultrasound is a rapid, low-risk bedside tool for pneumothorax detection

• A complete exam includes multiple zones and probe orientations, though focused exams are often sufficient

• The lung point is highly specific for pneumothorax

• Lung point location helps estimate pneumothorax size and guide chest tube decision-making

• Ultrasound findings must always be interpreted in clinical context, particularly in bullous lung disease

AUTHORED BY: JORDAN DEANGELIS, DO

FACULTY EDITING BY: LAUREN MCCAFFERTY, MD

References

1. McKnight CL, Burns B. Pneumothorax. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025.
   https://www.ncbi.nlm.nih.gov/books/NBK441885/

2. Melton LJ, Hepper NG, Offord KP. Incidence of spontaneous pneumothorax in Olmsted County, Minnesota: 1950-1974. Am Rev Respir Dis. 1979;120(6):1379-1382.

3. Gupta D, Hansell A, Nichols T, Duong T, Ayres JG, Strachan D. Epidemiology of pneumothorax in England. Thorax. 2000;55(8):666-671.

4. Goel A, Carroll D, Fortin F, et al. Pneumothorax (ultrasound). Radiopaedia.org.
   https://radiopaedia.org/articles/pneumothorax-ultrasound-1

5. Chan SS. Emergency bedside ultrasound to detect pneumothorax. Acad Emerg Med. 2003;10(1):91-94.

6. Volpicelli G, Elbarbary M, Blaivas M, et al. International evidence-based recommendations for point-of-care lung ultrasound. Intensive Care Med. 2012;38(4):577–591.

7. Taylor A, Anjum F, O’Rourke MC. Thoracic and lung ultrasound. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025.
   https://www.ncbi.nlm.nih.gov/books/NBK500013/

8. Marini TJ, Rubens DJ, Zhao YT, Weis J, O’Connor TP, Novak WH, Kaproth-Joslin KA. Lung ultrasound: technique, findings, and clinical applications. Radiol Cardiothorac Imaging. 2021;3(2):e200564.

9. Skulec R, Pařízek T, David M, Matoušek V, Černý V. Lung point sign in ultrasound diagnostics of pneumothorax: imitations and variants. Emerg Med Int. 2021;2021:6654272.

10. Emory University Department of Emergency Medicine. Lung Point.
    https://med.emory.edu/departments/emergency-medicine/sections/ultrasound/case-of-the-month/lung/lung-point.html

11. Husain LF, Hagopian L, Wayman D, Baker WE, Carmody KA. Sonographic diagnosis of pneumothorax. J Emerg Trauma Shock. 2012;5(1):76-81.

12. Zhang Z, Chen L. A physiological sign that mimics lung point in critical care ultrasonography. Crit Care. 2015;19(1):155.

13. Matoušek V, Zemanová P, Stach Z. Pneumothorax, which was not a pneumothorax. J Anesth Intensive Care Med. 2021;32(1):48-51.

Introduction

Point of Care Ultrasound (POCUS) has become established as an essential diagnostic modality for both the ED and ICU, allowing clinicians real time insight into patient physiology and guiding technique for procedures including central venous catheter insertion. The addition of agitated saline (AS) to the POCUS tool kit offers expanded capabilities for faster, more informed patient care at the bedside including confirmation of central line placement, assessment of right heart function and detecting right to left cardiac shunting.

Background

The images created by ultrasound are the result of sound waves transmitted by the ultrasound probe scattering as they interact with different media; some scattered waves return to the probe and are detected by the probe’s piezoelectric crystal array. The degree to which a structure is visible to ultrasound is a function of how much scatter and reflection of sound waves it causes (Figure 1). Higher density substances (muscle) create significantly more sound wave reflection and scatter and therefore brighter images while lower density substances (blood or lung) produce a darker image because sound waves are transmitted or refracted rather than scattering. Because of this ultrasound is highly effective in highlighting interfaces between solid, liquid, and gaseous phases in the body such as identifying blood vessels within soft tissue or the junction between the pleural border the chest wall (1,2).

Microbubbles enhance ultrasound imaging by increasing the echogenicity of the vasculature as they create numerous micro-interfaces between the surrounding medium (blood) and the air or other gas contained in the bubble. Since initial trials of agitated saline (AS) showed improvement the quality of echocardiography in 1968, ultrasound enhancing agents (UEAs) have become a widely accepted supplement to cardiovascular imaging (3).  Per the guidelines by the American society of Echocardiography (ASE) in 2018 a wide array of UEAs with a variety of shells and gaseous components have demonstrated safety and efficacy for detecting cardiac pathology including agents such as activated perfluorocarbon, sulfur hexafluoride microbubbles in a phospholipid shell and activated nanoparticles (see Figure 2) (1,3–5). Significant advances in UEAs notwithstanding, AS is still favored in the acute setting due to its widespread availability, low cost, and relative simplicity of use.

Technique

Note: Although relevant to all of the applications of AS described here, these methods were reported for use of AS to detect PFO and right to left cardiac shunt.

Unlike many commercially available UEAs whose external capsules are disrupted by passage through an IV catheter AS, which has no capsule and may be injected through relatively small-bore peripheral IVs. Other than central venous access, a 20g or larger IV catheter at or proximal to the antecubital fossa is the most studied administration technique although hand IVs have also been reported (1).  

In the set up described for evaluation of right to left shunting, a syringe containing 9 – 9.5 mL of normal saline and a syringe containing 1.0 – 1.5 mL of room air are connected to the three-way stopcock (see Figure 3). Adequate agitation can be achieved by vigorously mixing the contents of the two syringes back and forth with the stopcock closed to the J-loop and venous access. Luer Locks on the syringes were recommended to avoid accidental leakage during mixing. Once unform bubbles form and no large air pockets are visible, the mixture should be injected rapidly into venous access followed by a normal saline flush to facilitate rapid travel of AS to desired location while bubbles are intact (1).

Variations exist on AS additives on composition and other UEAs; evidence exists for improved bubble stability by including 1 mL of aspirated blood from the patient (see Table 1).

Table 1: Various ultrasound enhancing agents and their recommended dosages(1,3).

When examining the right heart as well as confirming central line placement, authors recommend that injection be performed by an assistant while another clinician or sonographer maintained the desired view with the ultrasound probe to capture real time bubble-enhanced images (1,6)

Applications:

1. Confirming central line placement.

Central venous access is foundational to resuscitation care provision of lifesaving vasoactive medications and large volumes of fluids. POCUS has long been used to guide central venous catheter (CVC) insertion which has contributed to improved safety (7). However, for supradiaphragmatic CVCs acute mechanical complications of line placement are still relatively common including misplaced catheter tip (5% - 9% reported incidence), pneumothorax (reported incidence up to 3.3%) and arterial puncture (reported incidence of 8.4%) (6–8).

Currently the standard for ensuring correct placement is portable chest X-ray (CXR). Even in resource rich settings, X-ray is rarely immediately available in both the ED and ICU, contributing to delays in CVC use for vital patient care.  One study found an average delay of 65 minutes between CVC placement and CXR confirmation (6,9). Additionally, there is currently debate on the clinical necessity of classically taught placement of the CVC tip in the lower portion of the SCV. Several studies indicate that alternative placement within venous system including the right atrium, brachiocephalic veins, and subclavian veins are tolerated without additional complications (6,10). The exception to these findings is inadvertent canulation of the contralateral internal jugular vein on a subclavian approach resulting in the catheter tip pointing cephalad. This is problematic due to possible disruption of cranial venous drainage.  

Since 2015 multiple studies show that AS in combination with the ultrasound techniques already widely used in the ED can be used to confirm CVC placement in the venous system. Similarly, ultrasound can be used to rule out complications including pneumothorax and cephalad IJ cannulation (6,9,11,12). In these studies, CVC placement was confirmed by detection of hyper-echogenicity from rapid saline flushing through the CVC on apical 4 chamber and subcostal views (see Figure 4). Ultrasound was also used to assess lung sliding in order to rule out pneumothorax, and to visualize the contralateral IJ, pericardium and right atrium to locate the catheter tip and rule out IJ canulation and pericardial effusion.

When compared to CXR imaging, several studies showed high levels of concordance in tip location with comparable specificity and sensitivity for complications (6,9,11). In terms of expediting patient care, one study indicated that the total ultrasound time was 23.1 minutes faster than CXR acquisition without a radiology read which was significantly longer. While promising, it is worth noting that all of these studies were used small sample sizes and larger scale trial would be helpful to validate these findings as complications are rare enough that few were captured in these trials.  

2.      Assessing RV function

Right ventricular dysfunction presents an important clinical challenge in resuscitation and significantly changes both management and prognosis. Echocardiography has long been the standard for diagnosing RV dysfunction. A formal echo may not possible in the acutely ill patient or unstable and conversely POCUS alone is inconsistent as for a reliable assessment of RV function as it is significantly affected provider skill level (13,14).  

A 2024 study in Annals of Emergency Medicine indicates that the addition of agitated saline to the diagnostic toolbox in the ED setting allows for rapid, more objective measure of RV function. Cohen et al. measured “bubble time” or the interval between agitated saline injection and appearance of bubble hyperechoic artifact in the RV. This was done in an ED convenience sample of patients for whom a comprehensive echocardiogram had already been ordered by their treating physician. Their findings indicate that a bubble time greater than or equal to 40 seconds is 97% sensitive and 87% specific for RV dysfunction when compared to formal echocardiography (see Table 2 summarizing Cohen et al’s test characteristics).

Table 2: From Cohen et al., summary of test characteristics for bubble time greater than 40 seconds (14).

Though it demonstrated exciting potential for objective, timely diagnostic information on the RV, this study was limited by small sample size with only 196 patients. Additionally, all measurements and ultrasounds were performed by a trained sonographer rather than an ED physician which may decrease the transferability of these results between institutions given variable degrees of confidence with ultrasound. Lastly, there was no ability to blind ultrasonographers to patient appearance and presentation during measurement of bubble time which may have introduced a degree of bias.

Overall, agitated saline may offer useful, more objective measure of RV function at the bedside, and more study in the area to test its usefulness in other institutions and patient populations is certainly warranted.

3.      Detecting PFO and other intracardiac defects.

Severe sequelae including embolic stroke and refractory hypoxemia can result from patent foramen ovale, atrial septal defects, pulmonary arterio-venous anomalies, and other cardiac or pulmonary anomalies which allow for right to left shunting. Although complications are rare, patent foramen ovale (PFO) can be found in 20-25% of healthy individuals and poses a risk for thromboembolic complications. Inappropriate treatment of acutely ill patients with shunt physiology can result in precipitous decompensation (1,3).

Transesophageal echocardiography (TEE) is currently the gold standard for detecting right to left shunts, and “bubble” studies have been used in the context of formal imaging studies for decades. In both the ICU and ED, an abbreviated version of the bubble study has the potential to rapidly detect of clinically significant intracardiac shunting and expedite appropriate care.

Because the microbubbles in agitated saline are too large to pass through pulmonary circulation, they provide a simple but powerful tool for detecting shunt physiology, as the passage of intact bubbles from the right to left heart most likely indicates a circulatory anomaly bypassing the pulmonary vasculature. In oriented patients, shunt enhancing maneuvers like Valsalva may be used to increase right atrial pressure and briefly exacerbate an existing shunt to improve sensitivity (see Figure 5). In obtunded patients, lung recruiting maneuvers such as briefly applying positive pressure ventilation may function similarly to Valsalva.

Although agitated saline may be clinically useful for detecting shunts in the acute setting, there are also several limitations to this technique. Several mechanisms may lead to false positive or false negative interpretations of bubble studies (See Tables 3 and 4 for common inaccuracies and proposed solutions).

Table 3: Summary of false positive mechanisms for POCUS assessment of various right to left shunts and proposed solutions. Table from Montreif et al (1)

Table 4: Summary of false negatives mechanisms for POCUS assessment of various right to left shunts and proposed solutions. Table from Montreif et al (1)

Given the need for detailed classification of right to left shunts and cardiac anatomy for definitive care, formal echocardiography and buble studies will remain an essential element of diagnosis. However, agitated saline may allow for a rapid assessment of the shunt clinically significant physiology saline in the acute setting.

AUTHORED BY: GRACE VAN HARE, MS4

FACULTY EDITING BY: COLIN MCCLOSKEY, MD

References

1. Montrief T, Alerhand S, Denault A, Scott J. Point-of-care echocardiography for the evaluation of right-to-left cardiopulmonary shunts: a narrative review. Can J Anaesth. 2020;67(12):1824-1838.

2. Au AK, Zwank MD. Sonoguide: Physics and Technical Facts for the Beginner. American College of Emergency Physicians; 2020.

3. Soliman OI, Geleijnse ML, Meijboom FJ, Nemes A, Kamp O, Nihoyannopoulos P, et al. The use of contrast echocardiography for the detection of cardiac shunts. Eur J Echocardiogr. 2007;8(3 suppl):S2-S12.

4. Porter TR, Mulvagh SL, Abdelmoneim SS, Becher H, Belcik JT, Bierig M, et al. Clinical applications of ultrasonic enhancing agents in echocardiography: 2018 American Society of Echocardiography guidelines update. J Am Soc Echocardiogr. 2018;31(3):241-274.

5. Kothapalli S. Ultrasound contrast agents loaded with magnetic nanoparticles: acoustic and mechanical characterization. Thesis. Washington University School of Medicine; 2013.

6. Duran-Gehring PE, Guirgis FW, McKee KC, Goggans S, Tran H, Kalynych CJ, et al. The bubble study: ultrasound confirmation of central venous catheter placement. Am J Emerg Med. 2015;33(3):315-319.

7. Nayeemuddin M, Pherwani AD, Asquith JR. Imaging and management of complications of central venous catheters. Clin Radiol. 2013;68(5):529-544.

8. Kornbau C, Lee KC, Hughes GD, Firstenberg MS. Central line complications. Int J Crit Illn Inj Sci. 2015;5(3):170-178.

9. Zanobetti M, Coppa A, Bulletti F, Piazza S, Nazerian P, Conti A, et al. Verification of correct central venous catheter placement in the emergency department: comparison between ultrasonography and chest radiography. Intern Emerg Med. 2013;8(2):173-180.

10. Montrief TMM. Trick of the trade: bubble study for confirmation of central line placement. Academic Life in Emergency Medicine. Published 2019.

11. Oliveira L, Pilz L, Tognolo CM, Bischoff C, Becker KA, Oliveira GG, et al. Comparison between ultrasonography and X-ray as evaluation methods of central venous catheter positioning and their complications in pediatrics. Pediatr Surg Int. 2020;36(5):563-568.

12. Liu YT, Bahl A. Evaluation of proper above-the-diaphragm central venous catheter placement: the saline flush test. Am J Emerg Med. 2011;29(7):842.e1-842.e3.

13. Hockstein MA, Haycock K, Wiepking M, Lentz S, Dugar S, Siuba M. Transthoracic right heart echocardiography for the intensivist. J Intensive Care Med. 2021;36(9):1098-1109.

14. Cohen A, Li T, Bielawa N, Nello A, Gold A, Gorlin M, et al. Right ventricular “bubble time” to identify patients with right ventricular dysfunction. Ann Emerg Med. 2024;84(2):182-194.

Clinical Presentation & Diagnosis:

Patients with SCAPE will experience tachypnea and dyspnea that onset rapidly within a few hours and are accompanied by severe hypoxemia1. Patients will also have vital sign abnormalities including hypertension, often SBP > 160 and / or DBP > 120, and tachycardia due to the sympathetic drive1. They often have diffuse rales on pulmonary exam and may have frothy sputum2.

POCUS is an incredible diagnostic tool for making the diagnosis of SCAPE. Lung POCUS will demonstrate B-lines throughout the chest in SCAPE1,2. If there are no diffuse B-lines, SCAPE can be confidently excluded as the cause of dyspnea2. Cardiac POCUS may demonstrate findings consistent with heart failure such as decreased EF or ventricular hypertrophy2. Finally, patients with SCAPE can have variable volume status— they can be hypovolemic, euvolemic, or hypervolemic 1,2. Therefore, the patient may not have signs of gross volume overload that might otherwise be associated with a heart failure exacerbation such as a distended IVC or peripheral edema. Chest x-rays may be useful, demonstrating interstitial edema and sometimes pleural effusions. However, some patients with SCAPE can have a normal x-ray1, making POCUS the best diagnostic tool in this case.

Patients with SCAPE may have troponinemia and ECG should be obtained to ensure that there is no underlying acute coronary syndrome1. However, troponinemia is most likely to be related to a Type 2 MI from demand ischemia1.

Differential Diagnosis

The differential diagnoses for patients presenting with hypertension, tachypnea, and dyspnea is broad and the management strategies for each vary considerably. Listed below are a few notable mimics.

Asthma exacerbation:

• Patients with an asthma exacerbation may present with dyspnea and vital sign abnormalities such as hypoxemia, hypertension, and tachycardia— just like in SCAPE.

• However, the physical exam is critical as patients with an asthma exacerbation will not have diffuse rales or B-lines on ultrasound.

• Utilize POCUS quickly to assess for pulmonary edema.

• Importantly, while patients with an acute asthma exacerbation should be administered epinephrine, patients with SCAPE will get worse with epinephrine due to the increased sympathetic drive.

ARDS

• ARDS is respiratory failure characterized by non-cardiogenic pulmonary edema and hypoxemia3. ARDS is driven by an inflammatory process rather than by sympathetic activation as is the case with SCAPE.

• ARDS is not associated with hypertension, but patients with ARDS can still be hypertensive.

• Patients with SCAPE should respond very rapidly to interventions, which will be discussed below. If patients do not respond to interventions, reconsider ARDS2.

Fluid Overload with Subacute Pulmonary Edema

• Patients with subacute pulmonary edema may present with dyspnea and vital sign abnormalities, but their symptoms onset more gradually and the patient is not often critically ill1.

• Patients with subacute pulmonary edema can still develop SCAPE2. 

• Patients usually do not need positive airway pressure with subacute pulmonary edema but are typically hypervolemic and the key intervention for therapy is diuresis2.

Management of SCAPE

Patients with SCAPE should immediately be provided respiratory support with CPAP or BiPAP starting at a low pressure and escalating rapidly as tolerated if the patient remains distressed, to a maximum of 20 cm H2O1,2. If the patient resists ventilation, consider haloperidol, ketamine, or fentanyl for comfort1,2. If the patient continues to decompensate, progress to intubation.

The other mainstay of treatment in patients with SCAPE is high-dose nitroglycerin. The appropriate dosage of nitroglycerin is debated in the literature, though it is generally accepted that high-dose nitroglycerin is safe and superior to low-dose nitroglycerin1,2,4,5. A recent randomized controlled trial in India, performed in 2023, has supported this theory. The trial included 54 patients randomized to either high-dose nitroglycerin (600-1000 microgram boluses followed by a 100 microgram per minute infusion) or low-dose nitroglycerin (20-40 micrograms per minute without bolus) and the high-dose group had significantly improved outcomes including shorter hospital stays, fewer cardiovascular events, and lower intubation rates4. Other studies have found that even larger doses of nitroglycerin can be safe1,4-7.  

A comprehensive review by Long et al. published in 2025 recommends:

• A bolus of 500-1000 micrograms over 2 minutes followed by an infusion of 100-200 micrograms per minute.

• If the patient is not responsive to these doses or SBP does not decrease to less than 160 mmHg, nitroglycerin can be up titrated further to 800 mcg/min, or bolus dosing can be repeated.

• If still not responsive to therapy, re-assess possible differential diagnoses and / or consider other medications such as calcium channel blockers.

Volume removal with either loop diuretics or dialysis may be appropriate if the patient appears hypervolemic once SBP is controlled1.

AUTHORED BY: MEGAN CALLAGHAN, MS4

FACULTY EDITING BY: COLIN MCCLOSKEY, MD

 References

1. Long B, Brady WJ, Gottlieb M. Emergency medicine updates: Sympathetic crashing acute pulmonary edema. Am J Emerg Med. Published online January 5, 2025. doi: 10.1016/j.ajem.2024.12.061. Available on PubMed: https://pubmed.ncbi.nlm.nih.gov/39799613/

2. Farkas, J. Sympathetic crashing acute pulmonary edema (SCAPE). EMCrit. Published August 30, 2021. Accessed January 29, 2025. https://emcrit.org/ibcc/scape/

3. Matthay MA, Zemans RL, Zimmerman GA, et al. acute respiratory distress syndrome. Nat Rev Dis Primers. 2019;5(1):18. Published 2019 Mar 14. doi:10.1038/s41572-019-0069-0. Available on PubMed: https://pubmed.ncbi.nlm.nih.gov/30872586/

4. Siddiqua N, Mathew R, Sahu AK, et al. High-dose versus low-dose intravenous nitroglycerine for sympathetic crashing acute pulmonary edema: a randomised controlled trial. Emerg Med J. 2024; 41:96-102. doi:10.1136/emermed-2023-123456. Available on PubMed: https://pubmed.ncbi.nlm.nih.gov/38050078/

5. Houseman BS, Martinelli AN, Oliver WD, Devabhakthuni S, Mattu A. High-dose nitroglycerin infusion: description of safety and efficacy in sympathetic crashing acute pulmonary edema: The HI-DOSE SCAPE study. Am J Emerg Med.2023; 63:74-78. doi: 10.1016/j.ajem.2022.10.018. Available on PubMed:  https://pubmed.ncbi.nlm.nih.gov/36327753/

6. Wang K, Samai K. Role of high-dose intravenous nitrates in hypertensive acute heart failure. Am J Emerg Med. 2020;38(1):132-137. doi: 10.1016/j.ajem.2019.06.046. Available on PubMed: https://pubmed.ncbi.nlm.nih.gov/31327485/

7. Stemple K, DeWitt KM, Porter BA, Sheeser M, Blohm E, Bisanzo M. High-dose nitroglycerin infusion for the management of sympathetic crashing acute pulmonary edema (SCAPE): A case series. Am J Emerg Med. 2021; 44:262-266. doi: 10.1016/j.ajem.2020.03.062. Available on PubMed: https://pubmed.ncbi.nlm.nih.gov/32278569/

70-year-old male with past medical history including severe ureteral stenosis requiring bilateral nephrostomy tubes and ureteral stents who presented to the emergency department for fatigue, chills, and decreased oral intake. He reported that he still urinates spontaneously, though his recent output has decreased. His vital signs were stable, and he was alert and mentating appropriately. On exam, he did not have any abdominal or costovertebral angle tenderness. His nephrostomy tubes were in place and draining non-bloody urine.

Given his complex urologic history, a broad workup was initiated, including labs, urinalysis, and CT abdomen/pelvis. While waiting for results, a renal point-of-care ultrasound (POCUS) was performed to quickly assess for any evidence of hydronephrosis.

POCUS findings:

Dilated renal pelvis with multiple coalescing, anechoic calyces and parenchymal thinning, consistent with severe hydronephrosis bilaterally — new on the left, with more cortical thinning noted on the right. The bladder (not shown here) was fully decompressed.

A Review of Renal POCUS

Key Clinical Questions: Is hydronephrosis present? Is there urinary retention?

Anatomy of the kidney

Understanding normal renal anatomy is essential before interpreting pathology on ultrasound. A normal kidney typically demonstrates: a hyperechoic renal sinus (central area), hypoechoic or isoechoic renal cortex, and well-defined corticomedullary differentiation [1].

How to Perform the Exam

Patient Positioning: Supine.

Transducer: Curvilinear probe (2–5 MHz) is ideal.

Right Kidney

• Longitudinal: Place the probe in the right mid-axillary line between the 10th-11th intercostal space, with the indicator toward the patient’s head. Rotate slightly counterclockwise to try to avoid rib shadows.

• Transverse: Rotate the probe 90° counterclockwise from the longitudinal view so the indicator points posteriorly.

 Left Kidney

• Longitudinal: Place the probe in the left posterior axillary line between the 8th-10th intercostal space. Because the left kidney lies more superior/posterior, your knuckles should be touching the bed.

• Transverse: Rotate 90° counterclockwise from longitudinal so the indicator points anteriorly [1,2].

Bladder

• Always include a bladder view for a complete renal ultrasound exam. Place the probe in a the suprapubic region in sagittal and transverse planes (indicator toward the patient’s head and right, respectively), and fan through the entire structure [3,4]. This allows assessment for urinary retention (i.e. large post-void volume) and identification of causes of hydronephrosis, such as bladder outlet obstruction, stones, clot burden, or mass effect [3].

Hydronephrosis

Definition: Hydronephrosis is dilation of the renal pelvis and calyces due to more distal obstruction of urine outflow [3].

Pathophysiology: Obstruction → increased hydrostatic pressure in the collecting system → increased intraglomerular pressure → decreased GFR [3].

Causes: Ureteral or bladder stones, benign prostatic hyperplasia (BPH), neoplasm (bladder, renal, pelvic), aneurysms (e.g., AAA), pregnancy (especially with a full bladder) [3].

Hydronephrosis Grading:

• Grade 1: Dilatation of the renal pelvis only

• Grade 2: Dilatation of the renal pelvis and major calyces

• Grade 3:  Dilatation of the renal pelvis, major and minor calyces

• Grade 4: Dilatation of the entire collecting system (i.e. renal pelvis, major and minor calyces), with thinning of the renal parenchyma [3].

**Both of this patient’s kidneys appear to have grade 4 or severe hydronephrosis based on ultrasound.

Hydronephrosis mimics:

Extrarenal pelvis: Anechoic area adjacent to the renal sinus without calyceal dilatation or cortical thinning (which are seen with hydronephrosis) [5].

Parapelvic cysts: Cystic masses in the renal sinus. They are non-communicating unlike hydronephrosis where calyces communicate [6].

Prominent renal vasculature: Anechoic central regions may mimic hydronephrosis. Apply color doppler to differentiate — vessels will show flow [6].

Clinical Significance of Renal POCUS

Renal POCUS is a great rapid bedside tool for evaluating urinary tract pathology, especially hydronephrosis and urinary retention [7,8]. It can reduce CT utilization, limiting contrast and radiation exposure [7].

A meta-analysis found that in acute kidney injury, POCUS had a sensitivity of 85% (CI 71-94%) and specificity of 78% (CI 68-87%) for diagnosing hydronephrosis [9]. 

While outside the scope of the emergency department, POCUS can also guide procedures such as renal biopsies or percutaneous drainage, enhancing safety and minimizing radiation exposure [10].

Case Conclusion

Labs revealed acute kidney injury. CT confirmed severe bilateral hydroureteronephrosis with displacement of the left ureteral stent. Urology and Interventional Radiology were consulted, and the patient was admitted to medicine for further management.

Take Home Points

• POCUS is a rapid, safe, and effective first-line imaging tool for evaluating for hydronephrosis.

• POCUS can reliably detect hydronephrosis (as well as urinary retention), differentiate it from mimics, and expedite care.

• Accurate interpretation requires proper scanning technique and knowledge of renal anatomy.

• Hydronephrosis appears as an anechoic area within the renal collecting system, starting centrally and expanding outward with increasing severity.

• Always include a bladder view: a full bladder suggests outlet obstruction, while a decompressed bladder points to an upstream cause.

AUTHORED BY: NICOLE MINNERATH, DO

FACULTY CO-AUTHOR/EDITOR: LAUREN MCCAFFERTY, MD

References

1. Deschamps J, Dinh V. Renal Ultrasound Made Easy: Step-by-Step Guide. POCUS 101. Published 2023. Accessed September 24, 2024. Available from: https://www.pocus101.com/renal-ultrasound-made-easy-step-by-step-guide/.

2. Noble VE, Nelson BP. Manual of Emergency and Critical Care Ultrasound. 2nd ed. Cambridge, UK: Cambridge University Press; 2011.

3. Soni N, Hariri R. Ultrasound of the Kidneys and Urinary Tract. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023. Available from: https://www.ncbi.nlm.nih.gov/books/NBK563217/.

4. University of Chicago Medicine. Renal ultrasound. Vimeo. Published 2013. Accessed September 24, 2024. Available from: https://vimeo.com/69556457.

5. García-Pérez A, Romero-Fresnedo M, Morales-Ruiz M, et al. The Role of Ultrasound in the Evaluation of Renal Pathology: An Overview. J Clin Med. 2017;6(10):87. doi:10.3390/jcm6100087. Available from:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5628238/.

6. Renal Fellow. The Ultrasound Mimics of Hydronephrosis. Renal Fellow Network. May 10, 2019. Accessed September 24, 2024. https://www.renalfellow.org/2019/05/10/the-ultrasound-mimics-of-hydronephrosis/

7. Harris B, Lentz K, Bell E, et al. Ultrasound in the Diagnosis of Kidney Disease: A Review. Am J Kidney Dis. 2020;76(6):857-867.

8. Moore CL, Daniels B, Singh D, et al. Prevalence and clinical importance of non-diagnostic point-of-care renal ultrasound. Acad Emerg Med. 2016;23(4):468-476.

9. Zarifian A, Tabrizi R, Arshadi H, et al. The role of point-of-care ultrasound in detecting hydronephrosis: A systematic review and meta-analysis. Ultrasound. 2023;11(1):1-11.

10. Rao R, Gubbi S, Shivakumar V, et al. Role of Point-of-Care Ultrasound in Evaluating Acute Renal Failure: A Systematic Review. Ultrasound Q. 2021;37(3):237-245. Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8377938/.

A 30-year-old male with a history of tricuspid valve endocarditis status post tricuspid valve replacement and prior IV drug use presented to the emergency department for fever and concern for abscess. He reported nearly a week of fevers, chills, nausea, painful swollen areas on his arm, and chest pain. He stated he has been abstinent from drugs for the past year but noted multiple prior abscesses requiring drainage.

He was mildly tachycardic with otherwise stable vitals. On exam, he had two raised, fluctuant areas. One lesion had an overlying eschar with mild surrounding erythema. No crepitus or drainage appreciated.

Point-of-care ultrasound (POCUS) was used to evaluate the lesions for abscess.

POCUS Findings

There is a well-circumscribed fluid collection with echogenic debris, consistent with an abscess. Surrounding cobblestoning was also present, supporting concurrent cellulitis in this clinical context. The second lesion demonstrated similar findings of a fluid collection with surrounding cellulitic changes.

Case Conclusion

The patient underwent bedside incision and drainage (I&D) and was started on broad-spectrum antibiotics given his history. He was admitted to the hospital for further management, and cultures ultimately grew methicillin-resistant Staphylococcus aureus (MRSA).

Abscess Formation

Overview

Skin and soft tissue infections (SSTIs) account for approximately 3% of all emergency department (ED) visits, representing more than three million visits per year [1]. An abscess is a localized collection of pus within the tissue, most often the result of a bacterial infection. Patients typically present with pain, tenderness, warmth, and swelling at the affected site, though deeper abscesses can also cause systemic symptoms such as fever, anorexia, and fatigue.

The process of abscess formation begins in compromised tissue where leukocytes accumulate. As neutrophils infiltrate the area, pus forms and necrosis of surrounding cells causes the cavity to expand. Risk factors for abscess formation include impaired host defenses, presence of foreign bodies, obstruction of normal drainage, and tissue ischemia or necrosis. If left untreated, abscesses can lead to complications such as bacteremic spread, rupture into adjacent structures, bleeding from erosion of nearby vessels, or impaired function of vital organs [2].

Microbiology

Most SSTIs are caused by Gram-positive organisms, most notably Staphylococcus aureus and Streptococcus pyogenes. S. aureus is particularly important given its ability to form abscesses and its variable resistance patterns, including methicillin-resistant strains (MRSA). In certain patient populations — such as those with recurrent infections, immunocompromise, or prior healthcare exposure — other pathogens may be implicated. These include enterococci, Gram-negative bacilli such as E. coli, and Pseudomonas aeruginosa, which may be associated with higher morbidity and mortality [3]. Recurrent abscesses should raise suspicion for MRSA, and empiric antibiotic coverage should reflect both common organisms and individual patient risk factors [4].

Diagnostics

Superficial abscesses can often be identified on physical exam by the presence of fluctuance, tenderness, and erythema. However, deeper collections may be more difficult to detect and often require imaging, such as CT or ultrasonography, for confirmation. POCUS can quickly identify a fluid collection, delineate its size and extent, and detect internal characteristics such as echogenic debris or loculations [5].

Another advantage of ultrasound is its ability to differentiate an abscess from cellulitis. Cellulitis typically demonstrates a cobblestone pattern of hyperechoic fat lobules separated by hypoechoic fluid, while abscesses appear as discrete fluid collections with well-defined borders. Ultrasound can also identify nearby vasculature with the use of color Doppler, reducing the risk of complications I&D. In some cases, POCUS has been shown to change management in nearly half of patients initially thought to have cellulitis [6].

Management

When to drain?

The primary treatment for most abscesses is I&D, which can usually be performed safely at the bedside. Smaller abscesses (< 1cm) may resolve with warm compresses and close follow-up, while larger or deeper collections sometimes require image-guided aspiration or surgical consultation [3].

When are antibiotics indicated?

Antibiotics are not always required after drainage, but they are indicated for patients with multiple or recurrent abscesses, significant cellulitis, systemic illness, immunocompromise, or abscesses greater than 2 cm [4]. Empiric therapy should target the most likely pathogens: first-generation cephalosporins or anti-staphylococcal penicillins are appropriate for many community-acquired infections. Outpatient options with MRSA coverage include trimethoprim-sulfamethoxazole, doxycycline, or clindamycin, while cephalexin or dicloxacillin remain appropriate for non-purulent cellulitis. Severe or complicated infections may require treatment with vancomycin or other advanced agents, with broader regimens such as vancomycin plus piperacillin-tazobactam for high-risk or polymicrobial cases [7].

Importantly, recurrent abscesses should raise suspicion for MRSA, and cultures should be obtained whenever possible to guide therapy [4].

Ultrasound Technique for Identifying Abscess

• Probe selection: Use a linear transducer for most soft tissue abscesses; switch to a curvilinear probe if the collection is large or deep.

• Establish normal: Begin scanning away from the affected area to appreciate normal soft tissue appearance, see Figure 1.

• Assess the affected area: Slide or fan the probe across the area (from one end to the other), then rotate 90° to obtain orthogonal views and define its full extent.

• Color Doppler: If a fluid collection is visualized, apply color doppler to identify nearby vasculature and differentiate abscess from pseudoaneurysm [8].

• Correlate anatomy: Place a fingertip on the area of maximal fluctuance, then slide the probe to the fingertip to align surface anatomy with the ultrasound image.

• Guidance for drainage: Consider real-time ultrasound guidance during I&D, regardless of size or depth, to improve accuracy and safety.

• Post-procedure check: Repeat ultrasound after drainage to assess for residual fluid [9].

Ultrasound Findings

Abscess

• Well-circumscribed, anechoic or hypoechoic fluid collection.

• Often contains hyperechoic debris from pus or necrotic material.

• Walls are usually distinct and hyperechoic.

• Probe compression may produce swirling of fluid, known as the “squish sign” (see Figure 2) [8].

Cellulitis

• Early: thickened skin and increased echogenicity with loss of distinct soft tissue layers (see Figure 3).

• Advanced: hypoechoic fluid tracking between fat lobules, producing the classic cobblestone appearance, as seen in Figure 4 [5].

• May occur with or without an associated abscess.

*Note: Cobblestoning and well-circumscribed fluid collections are not specific for infection and may also be seen in non-infectious processes such as hematomas or sterile fluid collections.

Complicated infections

• Ultrasound may reveal fluid along fascial planes or subcutaneous air (Figures 5 and 6, respectively), raising concern for necrotizing fasciitis [9].

Utility of POCUS for Abscess

POCUS improves patient care by helping clinicians distinguish cellulitis from abscess and determine the extent. This ensures that patients with drainable fluid collection receive timely I&D, while those without abscess avoid unnecessary procedures [5].

Evidence suggests that ultrasound frequently changes management decisions in suspected cellulitis. In one prospective study, it altered management in 39 of 82 patients (48%): 33 went on to receive drainage, while 6 were directed toward further diagnostics or consultation. Among those in whom drainage was originally believed to be needed, ultrasound changed management in 32 of 44 patients (73%) — eliminating drainage in 16 and prompting additional diagnostics in 16 others [6]. In a randomized controlled trial, patients who underwent I&D with POCUS had significantly lower treatment failure rates (defined as the need for repeat drainage or ongoing infection) compared with those managed by physical exam alone [10].

POCUS can also detect concerning findings such as fluid tracking along fascial planes or subcutaneous emphysema, which should raise immediate concern for necrotizing fasciitis, a surgical emergency requiring prompt recognition and intervention [9].

Take-Home Points

• SSTIs are common in the ED, and ultrasound is a powerful adjunct for evaluation.

• POCUS can differentiate cellulitis from abscess and guide safe drainage.

• Dynamic ultrasound guidance with color Doppler improves safety and helps confirm adequate drainage.

• Recurrent abscesses should raise suspicion for MRSA, and cultures are essential for guiding therapy.

• Ultrasound frequently changes management decisions and improves patient outcomes.

AUTHORED BY: TIANA SARSOUR, MD

FACULTY CO-AUTHOR/EDITOR: LAUREN MCCAFFERTY, MD

References

1. Yusuf S, Hagan JL, Adekunle-Ojo AO. Managing Skin and Soft Tissue Infections in the Emergency Department Observation Unit. Pediatr Emerg Care. 2019;35(3):204-208.

2. Bush LM. Abscesses – Infectious Diseases. Merck Manuals Professional Edition. December 8, 2023. Accessed January 30, 2024. https://www.merckmanuals.com/professional/infectious-diseases/biology-of-infectious-disease/abscesses

3. Ioannou P, et al. Gram-Negative Bacteria as Emerging Pathogens Affecting Mortality in Skin and Soft Tissue Infections. Hippokratia. 2018;22(4):153-161. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6528699/

4. Stevens DL, Bisno AL, Chambers HF, et al. Practice Guidelines for the Diagnosis and Management of Skin and Soft Tissue Infections: 2014 Update by the Infectious Diseases Society of America. Clin Infect Dis. 2014;59(2):e10-e52.

5. O’Rourke K, et al. Ultrasound for the Evaluation of Skin and Soft Tissue Infections. Mo Med. 2015;112(3):202-205. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6170135/

6. Tayal VS, et al. The Effect of Soft Tissue Ultrasound on the Management of Cellulitis in the Emergency Department. Acad Emerg Med. 2006;13(4):384-388.

7. Fung HB, et al. A Practical Guide to the Treatment of Complicated Skin and Soft Tissue Infections. Drugs. 2003;63(14):1459-1480.

8. American College of Emergency Physicians. Abscess Evaluation. ACEP Sonoguide. Accessed January 30, 2024. https://www.acep.org/sonoguide/procedures/abscess-evaluation

9. Menegas S, et al. Abscess Management: An Evidence-Based Review for Emergency Medicine Clinicians. J Emerg Med. 2020;59(6):817-828.

10. Gaspari RJ, Sanseverino A, Gleeson T. Abscess Incision and Drainage With or Without Ultrasonography: A Randomized Controlled Trial. Ann Emerg Med. 2019 Jan;73(1):1-7.

70-year-old male with a history of hypertension, hyperlipidemia, and age-related cataracts presented for acute vision loss in his left eye that started while sitting in a car, approximately eight hours prior to arrival.  When closing this eye, he reported painless “splotchy” vision with some areas where light was able to shine through. He spoke with his ophthalmologist who sent him to the ED for an emergent ophthalmologic evaluation. He denied numbness, weakness, tingling, headaches, temporal pain, or changes in the vision in his right eye. He reported no recent illnesses, trauma, or head strike.

Ophthalmology was consulted, and while awaiting their evaluation, an ocular ultrasound was performed.

POCUS Findings: Ocular ultrasound revealed a small hyperechoic focus over the distal optic nerve in the retrobulbar space, raising concern for central retinal artery occlusion (CRAO) in the setting of painless monocular vision loss. Color doppler demonstrated diminished arterial flow in his region, further supporting the diagnosis.

Case Conclusion: Ophthalmology performed a dilated fundoscopic exam, which revealed a cherry-red spot over the left macula, confirming the diagnosis of CRAO. The patient was admitted for further management and workup.

Central Retinal Artery Occlusion

Central retinal artery occlusion (CRAO) is a relatively rare ocular emergency, with an incidence of approximately 1.0 per 100,000 person-years in the United States. It primarily affects male patients, with a mean age of 60 to 65 years (1). CRAO presents with sudden, painless monocular vision loss. Often referred to as the ocular equivalent of a cerebral stroke, its visual prognosis is usually poor — approximately 61% of patients retain vision no better than counting fingers (2).

In 2013, the American Heart Association and American Stroke Association updated their stroke classifications to include CRAO and branch retinal artery occlusion (BRAO). Like cerebral ischemic strokes, retinal artery occlusions result from thromboembolic events that cause vascular occlusion and lead to end-organ ischemia. In CRAO, the occlusion occurs within the central retinal artery, a branch of the ophthalmic artery that supplies the retina (see Figure 1) (2). The most common site of occlusion is the narrowest portion of the artery, where it passes through the dural sheath of the optic nerve (3). Dilated fundoscopic examination is the gold standard for diagnosis, typically revealing a pale retina with a characteristic “cherry-red spot.” However, this exam is often impractical in the emergency department, where ophthalmology consultation may not be readily available. Point-of-care ultrasound (POCUS) may be a valuable adjunct to support a timely diagnosis. CRAO that is not reversed within four hours results in severe retinal ischemia, and recovery of vision is rarely possible after that window (4).

Ocular Ultrasound

While ocular ultrasound is not routinely part of the standard diagnostic workup for CRAO specifically, it is a valuable and effective tool for evaluating other causes of painless vision loss, such as retinal detachment, vitreous detachment, and vitreous hemorrhage (5). The exam should be avoided if globe rupture is suspected, as this is one of the few absolute contraindications to ocular ultrasound.

Image Acquisition

Begin by placing a tegaderm over the closed eyelid to prevent ultrasound gel from getting into the eye. When performing ocular ultrasound, it is essential to minimize pressure on the globe. To achieve this, use an abundance of gel to allow for minimal to no applied pressure. To help stabilize your hand and avoid applying too much force, rest your fifth digit on the patient’s nose or temple while scanning.

Use a high-frequency linear probe to scan in both transverse (demonstrated in Figure 2) and sagittal planes. Adjust the depth so the globe is centered in the image and the optic nerve sheath is visible posterior to the globe. This appears as a hypoechoic structure extending from the posterior aspect of the vitreous body (see Figure 3). Increasing the gain may help identify subtle findings within the vitreous body.

Be sure to include a dynamic (kinetic) exam by asking the patient to move their eyes during scanning. In the transverse plane, ask them to look left and right; in the sagittal plane, ask them to look up and down. This technique improves visualization and helps differentiate mobile versus fixed pathology (6).

“Retrobulbar Spot Sign”

A hyperechoic focus over the distal optic nerve — referred to as the retrobulbar spot sign — has been observed on ocular ultrasound in cases of CRAO and may help differentiate it from other causes of painless monocular vision loss (7,8). Illustrated in Figures 4-6, this finding is considered highly specific for embolic CRAO and, when present, is associated with a significantly lower likelihood of temporal arteritis (9). However, its true prevalence remains unclear, and most studies evaluating its diagnostic accuracy have been small. In one study, the retrobulbar spot sign demonstrated a sensitivity of 83% and specificity of 100% for CRAO (9).

If a hyperechoic spot is identified, consider using color Doppler to assess for diminished or absent arterial flow distal to the focus (see Figure 6). Keep in mind that Doppler signal is angle-dependent, and poor probe positioning may limit its reliability.

Given the limited evidence, a dilated fundoscopic examination remains the gold standard for diagnosing CRAO. However, POCUS can still serve as a valuable adjunct in the emergency setting — aiding in earlier diagnosis, expediting stroke workup, and facilitating timely management, especially when ophthalmologic evaluation is delayed or unavailable.

Potential Mimicker: Optic Nerve Drusen

Optic nerve drusen can mimic the retrobulbar spot sign seen in CRAO, as both appear as hyperechoic foci overlying the distal optic nerve. However, drusen are typically larger, are often more irregular in shape, and are located at the very distal portion of the optic nerve, near the retinal surface — sometimes even protruding into the vitreous (see Figure 7). In contrast, the hyperechoic foci associated with CRAO are usually smaller, more discrete, and located slightly deeper in the retrobulbar space (6, 10).

More Common Pathology

While ocular ultrasound can support the evaluation of CRAO, it is most commonly used to assess for retinal detachment and vitreous pathology, such as vitreous hemorrhage or detachment — which are more frequent causes of acute painless monocular vision loss. For a deeper dive into their sonographic features, check out any of our related posts, such as Retinal Detachment, Vitreous Hemorrhage.

Take-Home Points

• CRAO presents as painless monocular vision loss and is a true ocular emergency.

• Dilated fundoscopic exam remains the gold standard, but POCUS can aid early diagnosis when an ophthalmology evaluation is delayed or unavailable.

• A retrobulbar spot sign is not always present—but when it is, it strongly supports embolic CRAO in the appropriate clinical context.

• Scan both eyes for comparison, and consider using color Doppler to strengthen your findings.

• For any ocular ultrasound exam, always include a dynamic (kinetic) exam to help identify subtle or mobile pathology within the vitreous body.

• Optic nerve drusen may mimic the spot sign but are typically larger and located more distally near the retinal surface.

AUTHORED BY: HANNAH HENDRIX, MD, PGY2

FACULTY CO-AUTHOR/EDITOR: LAUREN MCCAFFERTY, MD

References

1. Sim S, Ting DSW. Diagnosis and management of central retinal artery occlusion. American Academy of Ophthalmology. August 1, 2017.  Available from: https://www.aao.org/eyenet/article/diagnosis-and-management-of-crao.

2. Chen C, Singh, G, Madike R, and Cugati S. Central retinal artery occlusion: A stroke of the eye. Eye. 2024. Available from https://www.nature.com/articles/s41433-024-03029-w.

3. Kang D, Jung, K, Yang W, et al. Presence of embolic source and outcome in central retinal artery occlusion. Neurology. 2023;101(13): e1364-e1369.

4. Hayreh SS. Acute retinal arterial occlusive disorders. Prog Retin Eye Res. 2011 Sep;30(5):359-94.

5. Lahham S, Shniter I, Thompson M, et al. Point-of-care ultrasonography in the diagnosis of retinal detachment, vitreous hemorrhage, and vitreous detachment in the emergency department. JAMA Netw Open. 2019;2(4):e192162.

6. Situ-LaCasse E, Adhikari SR. Ocular Emergencies. ACEP Sonoguide. August 18, 2020. Retrieved from https://www.acep.org/sonoguide/advanced/ocular-emergencies.

7. Usheva E, Williams D, Musgrave H, Zhou S. Sonographic retrobulbar spot sign in diagnosis of central retinal artery occlusion: A case report. JETem. 2023. 8(4):V5-8.

8. Caja KR, Griffith KM, Roth KR, et al. Detection of central retinal artery occlusion by point-of-care ultrasound in the emergency department: A case series. Cureus. 2021;13(7):e16142.

9. Ertl M, Altmann M, Torka E, et al. The retrobulbar "spot sign" as a discriminator between vasculitic and thrombo-embolic affections of the retinal blood supply. Ultraschall Med. 2012 Dec;33(7):E263-E267.

10. Core Ultrasound. CRAO. https://coreultrasound.com/crao/

Pericardiocentesis is a procedure performed to remove excess fluid from the pericardial sac surrounding the heart. It is most often indicated when cardiac tamponade develops, an emergent and potentially fatal condition. In this setting, pericardial fluid exerts extrinsic pressure on the heart, impairing venous return. On echocardiography, tamponade manifests as right atrial systolic collapse followed by right ventricular diastolic collapse, ultimately leading to reduced cardiac output [1]. Clinically, cardiac tamponade is classically suggested by Beck's triad: hypotension, jugular venous distention, and distant heart sounds.

Indications and contraindications

Indications

The primary indication for pericardiocentesis is a pericardial effusion causing tamponade. Emergent pericardiocentesis is required when tamponade causes hemodynamic instability or impending arrest, whereas non-emergent pericardiocentesis may be performed for symptomatic effusions, large effusions at risk of tamponade, or for diagnostic purposes [2].

Absolute contraindications

While pericardiocentesis can be a life-saving procedure, certain conditions, such as ventricular free wall rupture and aortic dissection, are absolute contraindications. In these cases, pericardiocentesis is generally avoided but may still be considered as a temporizing measure until definitive surgical interventions are available. Relative contraindications include anticoagulation therapy, uncorrected coagulopathy, and thrombocytopenia (platelets <50,000), as these increase bleeding risk. In such cases, the risks and benefits should be carefully weighed, but tamponade with instability remains an indication to proceed [2,3].

Supplies

• 18-20 gauge pericardiocentesis (or spinal) needle

• 30 cc syringe (or larger)

• Ultrasound machine

• Chlorhexidine swab*

• Sterile gloves*

• Sterile probe cover*

• Sterile drape*

  *in ideal circumstances, depending on the urgency of the procedure

Technique

Pericardiocentesis may be performed from the subxiphoid, parasternal, or apical approaches. The optimal window will depend on the patient’s body habitus and anatomy. The optimal needle entry site is where ultrasound demonstrates the largest and most superficial pocket without close proximity to vital structures [3].

General Steps

1. Identify the effusion and select the safest window with phased-array probe.

2. Optimize your image: decrease the depth so the effusion and proximal cardiac structures are centered on the screen — this improves resolution.

3. Consider switching to a linear probe after localization for better needle visualization.

4. Prep the skin with chlorhexidine; apply sterile drape and probe cover, if time permits.

5. Introduce a 20-gauge (or larger) needle under real-time ultrasound guidance at ~45° using an in-plane approach, carefully advancing toward the pericardial space.

6. Aspirate continuously until pericardial fluid is obtained [4,5].

*The following cardiac views describe probe orientation based on a cardiac preset, with the indicator on the right side of the screen.

Subxiphoid Approach

• Probe Placement: Transverse on the left costal margin, adjacent to the xiphoid.

• Probe Orientation: Indicator directed toward the patient’s left shoulder.

• Anatomy: Liver borders the right ventricle.

• Needle: Insert at 45° relative to the skin, directed toward the left scapula.

• Pros/Cons: Traditional landmark-based site. With ultrasound, visualization may be limited due to a deeper trajectory, and there is greater risk of liver or peritoneal injury compared with parasternal or apical approaches [4-5].

Parasternal Approach

• Probe Placement: Left parasternal region, usually 4th intercostal space.

• Probe Orientation: Indicator toward the patient's left shoulder.

• Needle: Insert in-plane at ~45°, directed toward the effusion.

• Pros/Cons: Often preferred due to closer proximity of effusion to the chest wall and distance from lung/liver. The needle trajectory aligns well with cardiac structures, improving needle visualization [4-5].

Apical

• Probe Placement: 4th-5th intercostal space, under the left breast or inframammary fold, near mid-axillary line.

• Probe Orientation: Indicator toward left axilla.

• Needle: Insert in-plane at ~45°, advancing toward the pericardial space.

• Pros/Cons: Similar to parasternal approach in advantages; the short distance from chest wall allows improved visualization and safety [4,5].

Complications

The overall complication rate for ultrasound-guided pericardiocentesis is low, with major complications in 0.3 to 3.9% and minor complications in 0.4 to 20% of cases [2,6]. Major complications include injury to cardiac chambers, coronary artery or intercostal vessel lacerations, pneumothorax, injury to abdominal viscera, ventricular arrhythmias, pericardial decompression syndrome, pneumopericardium, and death. Minor complications include dry taps, transient vasovagal hypotension, supraventricular arrhythmias, and pneumothorax not requiring a chest tube [7-8].

Take Home Points

• Emergent pericardiocentesis is indicated for tamponade with hemodynamic instability or arrest.

• Absolute contraindications include free wall rupture or aortic dissection, though drainage may be considered as a temporizing measure until surgery is available.

• Ultrasound guidance improves safety; parasternal and apical approaches often provide better visualization, but the best window is the one that shows the effusion most clearly.

• Major complications are uncommon but can be life-threatening.

AUTHORED BY: THOMAS EVANS, MD,

FACULTY CO-AUTHOR/EDITOR: LAUREN MCCAFFERTY, MD

References

1. Alerhand S, Adrian RJ, Long B, Avila J. Pericardial tamponade: A comprehensive emergency medicine and echocardiography review. Am J Emerg Med. 2022; 58:159-174.

2. De Carlini CC, Maggiolini S. Pericardiocentesis in cardiac tamponade: indications and practical aspects. CardioPractice. 2017; 15(19).

3. Loukas M, Walters A, Boon JM, Welch TP, Meiring JH, Abrahams PH. Pericardiocentesis: a clinical anatomy review. Clin Anat. 2012;25(7):872-81.

4. Mirza M, Bryczkowski C. Pericardiocentesis. Sonoguide. Published November 17, 2021. Accessed June 2024. https://www.acep.org/sonoguide/procedures/pericardiocentesis.

5. Swaminathan A. Core EM: Ultrasound-guided pericardiocentesis. emDOCs.net. Published September 9, 2015. Accessed June 2024. https://www.emdocs.net/core-em-ultrasound-guided-pericardiocentesis/

6. Tsang TS, Enriquez-Sarano M, Freeman WK, et al. Consecutive 1127 therapeutic echocardiographically guided pericardiocenteses: clinical profile, practice patterns, and outcomes spanning 21 years. Mayo Clin Proc. 2002;77(5):429-36.

7. Maggiolini S, Gentile G, Farina A, et al. Safety, Efficacy and Complications of Pericardiocentesis by Real-Time Echo-Monitored Procedure. Am J Cardiol. 2016; 117 (8): 1369-74.

8. Akyuz S, Zengin A, Arugaslan E, et al. Echo-guided pericardiocentesis in patients with clinically significant pericardial effusion. Outcomes over a 10-year period. Herz. 2015; 40(2): 153-159.

Epidemiology

• 39.4% of Medicaid insured and 27.7% of privately insured women of reproductive age (15-44 years) filled an outpatient prescription for an opioid each year (2008-2012) (1)

  Proportion of pregnant women admitted to substance abuse treatment facilities that reported a history of prescription opioid abuse increased from 2% to 28% between 1992-2012 (2)

• By 2012, one infant was born, on average, every 30 minutes in the United States having drug withdrawal (NAS), accounting for an estimated $1.5 billion in healthcare expenditures (3)

Medical-Assisted vs Non-Assisted Withdrawal

• Previously thought medically assisted withdrawal was associated with adverse fetal outcomes such as stillbirth, fetal stress, which has since been disproven (4, 5)

  • Systematic reviews have reported that fetal loss and preterm birth rates were similar among patients who did and did not undergo medically assisted withdrawal (6)

• Medication for opioid use disorder is now preferred, methadone or buprenorphine.

  • Prevents withdrawal symptoms, reduces or eliminates cravings.

Methadone

• Daily visits to federally certified opioid treatment program

• Greater risk of sedation compared to partial agonists

• 50% exposed neonates treated for NAS

  • Monitor for 4-7 days after delivery (7)

  • Longer NAS duration compared to buprenorphine

• Safe for breastfeeding (8)

Buprenorphine

• Can be prescribed in office setting with weekly to bi-weekly dispensing

  • Meta-analysis did not detect any statistically significant differences when comparing the groups of women using buprenorphine-naloxone with the groups of women prescribed with other medications as part of the medication-assisted treatment (9)

• Milder risk of sedations effects compared to methadone (full mu opioid agonists)

• Decreased risk severity of neonatal withdrawal for patients with OUD (10)

• Lower risk of preterm birth, higher birth weight, larger head circumference compared to methadone (11)

• 50% of neonates are treated for NAS

  • May be milder compared to full mu opioid agonists

  • Monitor neonates 4-7 days after delivery (12)

  • Shorter NAS duration compared to methadone

• Safe for breastfeeding (13)

Neonatal Abstinence Syndrome

• Symptoms:

  • Sleep & wake cycle disturbances: fragmented sleep, difficulty staying awake

  • Changes in tone: hypertonicity, tremors, jitteriness

  • Autonomic dysfunction: sweating, sneezing, mottling, fever, yawning

  • Easy over-stimulation, sensitivity, hyperarousal: irritability, crying

  • Difficulties with feeding: poor weight gain, tachypnea, GI symptoms

  • Low birth weight 2/2 intrauterine growth restriction

Prenatal Buprenorphine vs Methadone Exposures & Neonatal Outcomes: Systematic Review & Meta-Analysis

• Systematic review, meta-analysis from Jan 2000 to Oct 2013 for total of 515 BMT-exposed and 855 MMT-exposed neonates

• Risk ratio of NAS treatment was 0.90 (95% confidence interval (CI): 0.81, 0.98) in BMT-exposed versus MMT-exposed neonates

• Average hospital stay was shorter (−7.23 days, 95% CI: −10.64, −3.83) for BMT

• Length of treatment (−8.46 days, 95% CI: −14.48, −2.44) and the total amount of morphine used (−3.60 mg, 95% CI: −7.26, 0.07) were lower in BMT-exposed versus MMT-exposed neonates

• Mean differences in gestational age at birth (0.89 weeks, 95% CI: 0.50, 1.29), birth weight (243.63 g, 95% CI: 154.36, 332.91), body length (1.34 cm, 95% CI: 0.69, 1.99), and head circumference (0.87 cm, 95% CI: 0.45, 1.29) were higher in BMT-exposed versus MMT-exposed neonates

• No difference in the risk of preterm birth (<37 vs. ≥37 weeks’ gestation) by exposure (risk ratio = 0.82, 95% CI: 0.46, 1.45) (14)

Conclusions

• Medication-assisted withdrawal is preferred

• Can use buprenorphine or methadone, no change in fetal or maternal outcomes

• May reduce hospital duration or treatment of NAS for buprenorphine compared to methadone

• Monitor for NAS and treat as needed

AUTHORED BY: AUBREY STICKLAND, MS4

FACULTY EDITING BY: LAUREN PORTER, DO

References

1. Ailes EC, Dawson AL, Lind JN, Gilboa SM, Frey MT, Broussard CS, Honein MA. Opioid Prescription Claims Among Women of Reproductive Age - United States, 2008-2012. MMWR Morb Mortal Wkly Rep. 2015;64(2):1–41.

2. Martin CE, Longinaker N, Terplan M. Recent trends in treatment admissions for prescription opioid abuse during pregnancy. J of Subst Abuse Treat. 2015;48(1):37–42.

3. Patrick SW, Davis MM, Lehmann CU, Cooper WO. Increasing incidence and geographic distribution of neonatal abstinence syndrome: United States 2009 to 2012. J Perinatol. 2015;35(8):650–655.

4. Rementeriá JL, Nunag NN. Narcotic withdrawal in pregnancy: stillbirth incidence with a case report. Am J Obstet Gynecol. 1973 Aug 15;116(8):1152-6.

5. Zuspan FP, Gumpel JA, Mejia-Zelaya A, Madden J, Davis R. Fetal stress from methadone withdrawal. Am J Obstet Gynecol. 1975 May 1;122(1):43-6. doi: 10.1016/0002-9378(75)90613-4. PMID: 1130446. Zuspan FP, Gumpel JA, Mejia-Zelaya A, Madden J, Davis R. Fetal stress from methadone withdrawal. Am J Obstet Gynecol. 1975 May 1;122(1):43-6.

6. Terplan M, Laird HJ, Hand DJ, Wright TE, Premkumar A, Martin CE, Meyer MC, Jones HE, Krans EE. Opioid Detoxification During Pregnancy: A Systematic Review. Obstet Gynecol. 2018 May;131(5):803-814.

7. Hudak ML, Tan RC, American Academy of Pediatrics (AAP) Committee on Drugs, AAP Committee on Fetus and Newborn. Neonatal drug withdrawal. Pediatrics 2012; 129:e540.

8. Reece-Stremtan S, Marinelli KA. AMB clinical protocol #21: Guidelines for breastfeeding and substance use disorder, revised 2015. Breastfeed Med 2015; 10:135.

9. Link HM, Jones H, Miller L, Kaltenbach K, Seligman N. Buprenorphine-naloxone use in pregnancy: a systematic review and metaanalysis. Am J Obstet Gynecol MFM. 2020 Aug;2(3):100179.

10. Nanda S, Brant R, Regier M, Yossuck P. Buprenorphine: a new player in neonatal withdrawal syndrome. W V Med J. 2015 Jan-Feb;111(1):16-21. PMID: 25665273.

11. Zedler BK, Mann AL, Kim MM, Amick HR, Joyce AR, Murrelle EL, Jones HE. Buprenorphine compared with methadone to treat pregnant women with opioid use disorder: a systematic review and meta-analysis of safety in the mother, fetus and child. Addiction. 2016 Dec;111(12):2115-2128.

12. Hudak ML, Tan RC, American Academy of Pediatrics (AAP) Committee on Drugs, AAP Committee on Fetus and Newborn. Neonatal drug withdrawal. Pediatrics 2012; 129:e540.

13. Reece-Stremtan S, Marinelli KA. AMB clinical protocol #21: Guidelines for breastfeeding and substance use disorder, revised 2015. Breastfeed Med 2015; 10:135.

14. Brogly, S. B., Saia, K. A., Walley, A. Y., Du, H. M., & Sebastiani, P. (2014). Prenatal buprenorphine versus methadone exposure and neonatal outcomes: Systematic review and metaanalysis.American Journal of Epidemiology, 180(7), 673–686.

• Most common and most severe form of shellfish poisoning

• Globally, there are 2,000 cases reported per year

• Ingestion of shellfish contaminated with saxitoxins and other “paralytic shellfish poisons”

  • Saxitoxins - neurotoxins formed by dinoflagellates of Alexandrium genus

• PSPs are 1,000 times more potent than cyanide (used in some WWII suicide pills)

How Do You Get Exposed?

• Certain shellfish:

  • Bivalve mollusks

    • Highest risk with salt-water bivalve mollusks (mussels, clams)

  • Gastropod mollusks

  • Crustaceans

  • Pufferfish

  • Zooplanktivorous fish

• Certain places/events:

  • Algal blooms (red tides)

  • Temperate climates

    • Can also be in tropical waters

  • In the United States:

    • Seafood in Northeast, Pacific Northwest, Alaskan waters

  • Non-commercial shellfish (esp. Alaska)

• NOTE:

  • Toxin cannot be destroyed by heat, marinating, or freezing

  • Contaminated seafood smells, tastes, and appears normal

Pathophysiology

• Saxitoxins from dinoflagellates → taken up by shellfish vectors (do not become ill) → eaten by humans → block voltage-gated Na ion channels → blocks propagation of action potentials in nerve axons and skeletal muscle fibers

Symptoms

• Neurologic symptoms - can be mild or severe

  • Perioral tingling

  • Ataxia

  • Difficulty swallowing

  • Dizziness

  • Paresthesias

  • Weakness

  • Paralysis

  • Brainstem dysfunction

  • Respiratory failure

  • Other symptoms: diarrhea, vomiting, headache, nausea

Timeline

• Onset: a few minutes to ~4 hours

• Symptoms tend to improve gradually after 12 hours

• Resolve completely within a few days

• Death may occur within 2-12 hours of ingestion

Making the Diagnosis

• Working dx: Hx of consumption → onset of neurologic symptoms

  • Often can identify a cluster of cases with ingestion of noncommercial harvest

• Confirmed dx: saxitoxin detected in urine (or samples of seafood)

  • Contact health department to assist with lab confirmation

• Side note: ruling out others on differential: Tetrodotoxin pufferfish poisoning, Botulism, Ciguatera fish poisoning

Management

• Treatment is primarily supportive

  • May need to mechanically ventilate if severe

• Mortality: fatality rate as high as 12% in untreated patients

  • Can be particularly high in children

• Prevention with health authority monitoring of shellfish beds and notification of public with identifying contaminated shellfish

In Today’s News

• In May/June 2024, US FDA identified and issued an advisory about elevated levels of saxitoxins in shellfish in Oregon and Washington state

  • Were distributed to restaurants/retailers in several states in USA

  • At least 31 people sick in Oregon

• Outbreak was attributed to an algal bloom along the coast

• Such high levels of the toxin have not been detected in Oregon in decades.

AUTHORED BY: JANINE CORLEY, MS4

FACULTY EDITING BY: LAUREN PORTER, DO

References

• UpToDate

• CDC

• EMRA

• Algal Toxins in Seafood and Drinking Water

• USA Today

• US News

Indications for ECMO During Pregnancy:

1. Respiratory failure: refractory ARDS, status asthmaticus, aspiration, bridge to lung transplant, sepsis, and hypertensive disorders of pregnancy

2. Cardiogenic shock: cardiac failure, peripartum cardiomyopathy, malignant arrhythmias, myocardial infarction, pulmonary hypertension, amniotic fluid embolism, pulmonary embolism, and intoxications

3. Cardiac arrest

Physiological Changes During Pregnancy:

There are various physiological adaptations that occur during pregnancy that affect cardiopulmonary function. Elevated serum progesterone leads to increased respiratory drive along with increased tidal volume and minute ventilation. As the pregnancy progresses, second trimester patients develop respiratory alkalosis with compensatory metabolic acidosis, correlating to decreased PaCO2 and bicarbonate compared to non-pregnant patients. This is physiologically helpful during pregnancy because of the advantageous pressure gradient for fetal gas exchange. The presence of a fetus additionally leads to increased oxygen requirements, as the body requires 20% more oxygen to adequately perfuse both mother and fetus.

Cardiac function is also altered during pregnancy, with these patients often having elevated stroke volume, heart rate, cardiac contractility, and cardiac output (up by 30-40%) from baseline. Cardiac output peaks immediately after delivery, with up to a 150% increase in cardiac output from baseline in the setting of strain from labor and delivery. Additionally, elevated progesterone promotes smooth muscle relaxation, leading to decreased systemic and pulmonary vascular resistance (Naoum et al. 2024) (Wong et al. 2022) (Wong et al. 2024) (Yeomans and Gilstrap 2005).

ECMO Parameters and Goals During Pregnancy

To date, there is no robust clinical trial data for optimal ECMO settings during pregnancy, but several review articles have offered current best practices (Naoum et al. 2024) (Wong et al. 2022) (Wong et al. 2024).

Flow Rate: To accommodate increased cardiac output, ECMO flow rates of 100 to 120 mL/kg/min (5–6 L/m2/min) should be initiated in pregnant populations compared to the standard 60 to 80 mL/kg/min (3–4 L/m2/min) in non-pregnant patients.

Oxygenation Goal: Since pregnancy corresponds with increased oxygen demand, usual SaO2 goals of >80% are not viable for pregnant patients, and the ideal minimum maternal SaO2 should be >90%. According to one review, in clinical practice, ECMO levels are often titrated to SaO2 >95%, with constant monitoring for fetal decelerations or other abnormalities to indicate switching to a higher ECMO flow rate (Wong et al. 2024). This translates to PaO2 targets of >70mmHg.

Blood Gas Goals: PaCO2 ideally should match a target of 28-32 mmHg since deviations from this goal can be associated with fetal hypoxemia and acidosis. Pregnant patients should also have a goal pH of greater than 7.4 given that maternal acidosis is poorly tolerated by the fetus. Bicarbonate levels are reduced during pregnancy secondary to chronic respiratory alkalosis and patients on ECMO should fall between 18-21 mmol/L.

Positioning: Left lateral tilt of 15 to 30 degrees that promotes left uterine displacement is ideal to mitigate the effects of aortocaval compression on the venous drainage cannula.

Conclusion

ECMO is a useful tool for the cardiopulmonary support of antepartum and postpartum patients and shows promising rates of maternal and fetal survival. In one systematic review from JAHA, the 30‐day survival rate after use of ECMO during the peripartum or postpartum period was found to be 75.4% for mothers and 64.7% for fetuses (Naoum et al. 2020). However, current evidence for ECMO in obstetric patients is primarily derived from case reports and retrospective reviews, which prove difficult in guiding standardized protocols. More clinical trial data is imperative to identify safe and effective parameters in this special population.

AUTHORED BY: SAILAKSHMI KUMAR, MS4, CWRU SOM

FACULTY EDITING BY: COLIN MCCLOSKEY, MD

References

1. Ong, J., et al. "Extracorporeal membrane oxygenation in pregnancy and the postpartum period: a systematic review of case reports." International Journal of Obstetric Anesthesia 43 (2020): 106-113.

2. Naoum, Emily E., et al. "Extracorporeal Life Support in Pregnancy: A Systematic Review." Journal of the American Heart Association 9.13 (2020).

3. Naoum, Emily E., Erika R. O’Neil, and Amir A. Shamshirsaz. "Extracorporeal membrane oxygenation (ECMO) in pregnancy and peripartum: a focused review." International Journal of Obstetric Anesthesia 60 (2024).

4. Wong, Michael J., et al. "Extracorporeal membrane oxygenation for pregnant and postpartum patients." Anesthesia & Analgesia 135.2 (2022): 277-289.

5. Wong, M. J., B. S. Kodali, and S. Rex. "Extracorporeal Membrane Oxygenation and Pregnancy." Best Practice & Research Clinical Anaesthesiology (2024).

6. Yeomans, Edward R., and Larry C. Gilstrap III. "Physiologic changes in pregnancy and their impact on critical care." Critical care medicine 33.10 (2005): S256-S258.

A 16-year-old female presents to the emergency department for an intentional overdose of iron pills after a fight with her boyfriend. She notes that she has taken 40 pills of her mom’s iron tablets. Should you be concerned?

Well it depends…

Iron Toxicity

To better discern whether our patient has a potentially lethal ingestion of iron, we need a little more information.

• Iron supplements come in a variety of forms, all of which have different concentrations of elemental iron.

• This information is vital for us to ascertain, as it can guide our expected clinical course for the patient.

• There are three forms of supplemental iron: Iron Fumarate, Iron Sulfate, and Iron Gluconate.

  • I use the following mnemonic to remember the concentration of elemental iron in each (shoutout to our friends at OHSU Tox for this one)

• A 357 Magnum is a Fast Shooting Gun

  • Iron Fumarate: 1/3 elemental iron

  • Iron Sulfate: 1/5 elemental iron

  • Iron Gluconate 1/7 elemental iron

Our Patient

• When talking with our patient’s mother, she is able to show us her medication list and demonstrate that she is taking Iron Gluconate 300 mg once daily.

• Based on this information, we can calculate out to see that the patient has taken about 1.7 grams of elemental iron.

• A 357 Magnum is a Fast Shooting Gun

  • Iron Fumarate: 1/3 elemental iron

  • Iron Sulfate: 1/5 elemental iron

  • Iron Gluconate 1/7 elemental iron

• (300 mg iron gluconate) x (1/7) x (40 tablets) = 1.7 grams

Stages of Toxicity

Emergency Evaluation

• The usuals

  • EKG, metabolic panel, CBC, coagulation screen, liver function testing, and acetaminophen/salicylate levels.

• The extras

  • With an unclear story a KUB can be useful to evaluate for radio-opaque tablets in the stomach

    • It however does not rule out or rule in ingestions reliably on its own

  • Serum Iron level between 4-6 hours post ingestion

    • When serum concentrations will be the highest

• If you don’t have the information for weight-based ingestion, this level can help guide your expected course as well:

Treatment

• Symptomatic management.

  • Utilize antiemetics (keeping in mind QTc based on possible co-ingestions

  • Resuscitate with IV fluids despite our current shortage

• Antidote therapy

  • Deferoxamine for chelation therapy

• Additional therapies

  • WBI

  • FFP/Vitamin K

  • Hemodialysis

    
    
    
    

Deferoxamine

• When to use your antidote?

  • If a patient develops hypotension or metabolic acidosis, just give it.

  • If they have a confirmed severe ingestion… just give it.

  • If they have severe toxicity based on blood iron levels, you can use this as well.

• Side effects

  • It can worsen a vasodilatory state & hypotension---why it’s started at 15mg/kg/hr and increased as tolerated to 45mg/kg/hr

    • Supplement with IVF/Vasopressors as needed

  • Pulmonary edema

  • Yersinia infections

• Dosing

  • Maximum of 8 grams in the first 24-hour period.

  • This should be stopped after 24 hours or 8 grams (whichever comes first).

    
    
    
    

Disposition

• 3 decision points to consider

  • Asymptomatic at 6 hours

    • Medically clear for DC vs psychiatry evaluation

  • Submassive ingestions with isolated GI symptoms

    • Regular nursing floor

  • Requiring antidote or adjunctive therapies

    • ICU level of care due to high risk of decompensation.

• For our patient, her ingestion resulted in moderate GI symptoms requiring 24 hours of regular nursing floor care for IV fluids and antiemetic therapy.

• She was able to be discharged home after psychiatry evaluation.

AUTHORED BY: MATTHEW MULLINS, MD

FACULTY EDITING BY: LAUREN PORTER, DO

References

• Yuen HW, Becker W. Iron Toxicity. [Updated 2023 Jun 26]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK459224/

• Baranwal AK, Singhi SC. Acute iron poisoning: management guidelines. Indian Pediatr. 2003 Jun;40(6):534-40.

• Singhi SC, Baranwal AK, M J. Acute iron poisoning: clinical picture, intensive care needs and outcome. Indian Pediatr. 2003 Dec;40(12):1177-82.

• Nickson DC. Iron Overdose • LITFL • CCC Toxicology. Life in the Fast Lane • LITFL • Medical Blog. Published January 4, 2019. https://litfl.com/iron-overdose/

  OHSU Tox. OHSU Tox Shorts: Iron Toxicity. YouTube. Published January 22, 2016. Accessed November 14, 2024. https://www.youtube.com/watch?v=mAEKdZFoAjk

A 60-year-old female with a past medical history of metastatic breast cancer currently receiving chemotherapy presented to the emergency department for dyspnea on exertion and generalized fatigue. She was only able to take a few steps prior to becoming significantly short of breath but denied any associated chest pain. She reported some occasional palpitations and chronic generalized pain, unchanged from baseline.

Vital signs were notable for tachycardia, tachypnea, and hypoxia, but she had a stable blood pressure and was afebrile. She was in mild respiratory distress and had diminished breath sounds throughout.  Cardiac exam was remarkable for tachycardia with mild jugular venous distention present. There was 2+ pitting edema in the bilateral lower extremities and the patient was mentating appropriately with an otherwise non-focal neurologic exam. She was placed on 2 liters of oxygen via nasal cannula and her hypoxia was corrected.

The initial concern was for pulmonary embolism (PE) in the setting of active cancer and chemotherapy and a CT angiogram of the chest was obtained, but a pericardial effusion was also the differential. An EKG was obtained and showed tachycardia without evidence of ischemia but did show subtle electrical alternans.

A cardiac point-of-care ultrasound (POCUS) was performed with the following images obtained:

POCUS Findings: There is a large circumferential pericardial effusion with right ventricular systolic collapse and left atrial systolic collapse, indicating tamponade physiology. The left ventricular function appears preserved and there is no right-sided chamber enlargement.

Cardiac Tamponade

Epidemiology

Cardiac tamponade is an uncommon diagnosis, occurring in five out of every 10,000 medical admissions (1).  The most common causes of cardiac tamponade include complications from percutaneous interventions (33%), postpericardiotomy syndrome (15%), neoplasm (15%), inflammatory processes such as pericarditis (12.5%), uremia (2%), and acute myocardial infarction (1.5%) (2).

Pathophysiology

Cardiac tamponade occurs when fluid accumulates within the pericardial sac, leading to an increase in pressure that exceeds the pressure required for the right heart to fill during diastole. This results in decreased compliance of the right ventricle, impairing its ability to adequately receive blood during diastole and reducing preload to the left heart. Consequently, this leads to a decrease in cardiac output, which worsens as the pressure in the pericardial sac rises. If left untreated, cardiac output can decrease to a level where myocardial perfusion is inadequate, potentially resulting in cardiac arrest (3,4).

The volume of pericardial fluid required to overcome the diastolic filling pressure depends on the chronicity of the effusion. In a healthy state, the pericardial sac generally contains 15-50 mL of plasma ultrafiltrate (3). If fluid accumulates suddenly - such as from traumatic aortic or cardiac rupture, aortic dissection, or coronary vessel rupture - the diastolic filling pressure can be easily overcome with as little as an additional 50 mL of fluid. Conversely, if fluid builds up gradually, cardiac tamponade may not occur until up to 2 liters are present. Common causes of subacute cardiac tamponade include viral syndromes, uremia, or neoplasms (4,5). Recognizing the factors influencing the onset of cardiac tamponade is crucial for timely intervention and improved patient outcomes.

Clinical Presentation

The typical clinical presentation of cardiac tamponade is highly dependent on the chronicity of the pericardial effusion. Patients with chronic effusions, i.e. those developing over greater than three months, are often asymptomatic, especially earlier in its course. Subacute effusions, which develop over several days to weeks, may present with a variety of symptoms, including dyspnea, generalized fatigue, peripheral edema, and chest pain. As the pericardial pressure surpasses the diastolic filling pressure, leading to cardiac tamponade, patients often experience lightheadedness, fatigue, anorexia, syncope, and may even progress to cardiac arrest (4,6). Acutely developing pericardial effusions can result in hemodynamic instability due to the rapid increase in pericardial pressure, leading to a faster onset of symptoms. Similar to late presentations of subacute tamponade, patients with acute cardiac tamponade typically present with lightheadedness, chest pain, syncope, rapidly declining mental status, and/or cardiac arrest (4,6,7).

Physical Exam

In addition to the clinical symptoms, specific physical examination findings can be critical for diagnosing cardiac tamponade. Common presentations include hypotension characterized by a narrow pulse pressure and reflexive tachycardia. A decrease in systolic blood pressure during inspiration of greater than 10 mmHg, referred to as pulsus paradoxus, may also be observed. Patient often exhibit marked jugular venous distention (JVD) and peripheral edema. Extremities may be cool and cyanotic, consistent with signs of cardiogenic shock. Heart sounds are frequently muffled or even absent, depending on the size of the effusion (4,6,7). Beck’s triad —consisting of hypotension, JVD, and muffled heart sounds—is particularly indicative of cardiac tamponade and should be assessed during the physical exam (8). Although not commonly used in emergency medicine, the central venous pressure waveform may show the absence of the Y-descent, a sign that can indicate tamponade physiology (9).

Diagnosis

The diagnosis of cardiac tamponade is often considered when a patient presents with the signs and symptoms of Beck’s triad. Unfortunately, this triad does not occur in the majority of patients, which limits its diagnostic utility (9). Imaging studies, such as computed tomography (CT) or cardiovascular magnetic resonance (CMR), can provide evidence of a pericardial effusion as well as associated chest abnormalities. An echocardiogram is a dynamic study that identifies pericardial effusions and specific signs suggesting cardiac tamponade (which will be discussed below); it is the recommended initial test in patients with suspected tamponade to evaluate the size, location, and degree of hemodynamic impact, with a Class IC Recommendation from the European Society of Cardiology Working Group on Myocardial and Pericardial Diseases (6). The diagnosis is further confirmed when there is improvement of hemodynamic abnormalities after pericardiocentesis, alongside clinical and imaging findings. Cardiac tamponade can also be confirmed with cardiac catheterization, though this is not commonly used in practice (6).

Management

Management of cardiac tamponade requires early identification of the diagnosis and removal of the pericardial fluid via pericardiocentesis. If tamponade is identified on point-of-care ultrasound (POCUS) and the patient is hemodynamically stable, the case should be discussed with interventional cardiology, if available, as the procedure is ideally performed in a catheterization lab where additional resources are available. If the patient is hemodynamically unstable or in cardiac arrest, emergent pericardiocentesis should be performed at the bedside. While traditionally a landmark-based procedure, ultrasound-guidance has several advantages; this technique will be discussed below in the POCUS section. Patients with acute cardiac tamponade due to traumatic cardiac injury or aortic dissection will require surgical intervention to address the underlying cause. In contrast, patients with subacute cardiac tamponade, particularly neoplastic effusions, are at higher risk for recurrence and may need a cardiac window procedure (6).

Administration of intravenous fluids in the acute setting, whether the patient is hemodynamically stable or unstable, has shown improved outcomes since this process is preload-dependent (10). Positive pressure ventilation should ideally be avoided in patients with cardiac tamponade, as it can decrease venous return to the heart and worsen the tamponade (7).

Point-Of-Care Ultrasound & Pericardial Effusions

For patients presenting to the emergency department with signs and symptoms concerning for cardiopulmonary pathology, POCUS is an invaluable diagnostic tool that enables clinicians to quickly gather critical information. When cardiac tamponade is part of the differential diagnosis, the initial step is to evaluate for the presence of a pericardial effusion, which is one of the primary clinical questions that cardiac POCUS aims to address. An effusion can be identified in any of the four standard cardiac windows, but it is most commonly visualized is in the parasternal long axis or subxiphoid views, as fluid typically accumulates in the most dependent portions of the pericardial sac. The phased array probe is generally used for identifying effusions in medical patients during cardiac examinations, while the curvilinear probe is commonly utilized in trauma settings during the FAST exam.

A pericardial effusion appears as an anechoic (black) stripe of fluid surrounding the heart’s borders, separating the hyperechoic (bright white) pericardium from the more neutrally-echogenic myocardium. The size of the effusions can be graded based on where the anechoic stripe is visible. Small effusions are usually only seen in the dependent posterior/inferior (far field) regions of the pericardium, while moderate and large effusions extend toward and into the anterior (near field) regions, eventually becoming circumferential.

A common pitfall when identifying effusions with POCUS is misinterpreting a pleural effusion as a pericardial effusion. The parasternal long-axis view is particularly useful for distinguishing between the two. A pericardial effusion appears as an anechoic stripe between the cardiac border and the descending aorta, as shown in Figure 1. In contrast, a pleural effusion tapers toward the descending aorta and does not cross over it, as the pleura attaches to the aorta, confining the fluid to the inferior/posterior region (11).

Another common pitfall is mistaking a pericardial effusion with an epicardial or pericardial fat pad. A fat pad may appear hypoechoic, similar to an effusion, or may contain echoes, but it moves with the myocardium and tends to be localized to the anterior aspect of the heart, unlike an effusion which usually involves the posterior, more dependent areas of the heart (11-12).

Sonographic Signs of Tamponade

-Chamber Collapse-

After identifying a pericardial effusion, the next step is to assess for sonographic evidence of cardiac tamponade. The earliest and most sensitive sign of tamponade is right atrial systolic collapse. Although this finding may be challenging to identify, it is best evaluated in an apical four-chamber or subxiphoid view, as these provide the most direct visualization of the right atrium. To accurately assess for atrial systolic collapse, observe the collapse of the right atrial free wall (or “scalloping”) when the tricuspid and mitral valves are closed, indicating ventricular systole (11). This is shown in Figure 2 below.

Right ventricular diastolic collapse is the classic and more specific, yet less sensitive, indicator of cardiac tamponade. The parasternal long-axis view is particularly useful for assessing this, as it provides a clear visualization of the right ventricle, aortic valve, and mitral valve. To optimally identify right ventricular diastolic collapse, it is important to capture an image that includes all three structures, as shown in Figure 3. Additionally, M-mode can assist in detecting cardiac tamponade by focusing on measurements through the right ventricular wall and the mitral valve. During ventricular diastole, the mitral valve opens between the E and A waves, corresponding to a dip in the right ventricular wall signal in the near field of the M-mode tracing, as illustrated in Figure 4 (12, 14).

A highly specific but less common finding, seen in only approximately 25% of patients, is left atrial systolic collapse (4). This may occur with extensive circumferential effusions, localized left-sided effusions or in patients with severe pulmonary hypertension where left-sided pressures are lower than those on the right (6, 11, 12). This can be seen in an apical, subxiphoid, or even parasternal view (demonstrated in this case - see Figure 5) where the collapsing left atrial free wall can be visualized with the closed mitral and tricuspid valves, thus confirming systole, can be seen. This is illustrated in Figures 5 and 6.

-Plethoric Inferior Vena Cava (IVC)-

A useful adjunct to the cardiac views is assessment of IVC. A dilated or plethoric IVC (greater than 2cm in diameter, measured within centimeters as it approaches the right atrium) with little to no respiratory variation (less than 50% collapsibility with inspiration) indicates increased right-sided pressures, seen in a variety of conditions including tamponade. This is present in the majority of cases of tamponade but is not specific (17).

-Respirophasic Variation in Mitral and Tricuspid Inflow Velocities-

To further support the diagnosis of cardiac tamponade, measuring mitral and tricuspid inflow velocities can be beneficial. Flow through these valves varies with the respiratory cycle, and this variation is often exaggerated in the setting of tamponade; this is echocardiographic surrogate for pulsus paradoxus. Using pulse wave doppler in the apical four-chamber view, place the doppler gate just beyond the tips of the valve leaflets. The resulting waveform illustrates blood velocity over time, with variations in peak height reflecting changes in blood flow throughout the respiratory cycle. When examining the highest and lowest peaks, a variation of greater than 25% for the mitral valve and greater than 40% for the tricuspid valve inflow velocities supports the presence of tamponade physiology (18). This is commonly seen in tamponade but is not specific (17).

Pericardiocentesis

Definitive management of cardiac tamponade is achieved through pericardiocentesis, which is ideally performed under ultrasound guidance. Several techniques can be employed, including subxiphoid, parasternal, and apical approaches (11). Regardless of the approach, the needle must be aligned in-plane with the probe marker to ensure direct visualization of the needle tip as it enters the pericardial sac, minimizing the risk of myocardial puncture, as illustrated in Figure 8. The various ultrasound-guided techniques, probe orientation relative to the needle, and potential complications are depicted in Figure 9. This will be discussed further in a future blog post.

Case Continued

The patient continued to remain hemodynamically stable throughout her time in the emergency department. The ultrasound findings above were discussed with the on-call interventional cardiologist, who agreed with the interpretation of sonographic tamponade. Given her stability, she was transported to the cardiac catheterization lab where she had an emergent pericardiocentesis performed leading to the drainage of 750 mL of maroon-colored fluid. The patient’s symptoms significantly improved after completion of the pericardiocentesis and she was admitted to the cardiology service for further management. The pericardial fluid was analyzed and was positive for malignant cells.

AUTHORED BY: RYAN STARKMAN, MD, PGY1

FACULTY CO-AUTHOR/EDITOR: LAUREN MCCAFFERTY, MD

References

1. Al-Ogaili, A, Ayoub, A, Fugar, S. et al. Cardiac Tamponade Incidence, Demographics and In-Hospital Outcomes: Analysis of the National Inpatient Sample Database. JACC. 2018 Mar. 71(11):A1155.

2. Adamczyk M, Wasilewski J, Niedziela JT, Zembala MO, Gąsior M. Baseline characteristics, management and long-term outcomes of different etiologies of cardiac tamponade evaluated in a cohort of 340 patients. Kardiochir Torakochirurgia Pol. 2021 Dec;18(4):216-220.

3. Sharma NK, Waymack JR. Acute Cardiac Tamponade. [Updated 2023 Jul 31]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK534806/.

4. Spodick DH. Acute cardiac tamponade. N Engl J Med. 2003 Aug 14;349(7):684-90.

5. Reddy PS, Curtiss EI, O'Toole JD, Shaver JA. Cardiac tamponade: hemodynamic observations in man. Circulation. 1978 Aug;58(2):265-72.

6. Adler Y, Charron P, Imazio M, et al. 2015 ESC Guidelines for the diagnosis and management of pericardial diseases: The Task Force for the Diagnosis and Management of Pericardial Diseases of the European Society of Cardiology (ESC) Endorsed by: The European Association for Cardio-Thoracic Surgery (EACTS). Eur Heart J. 2015 Nov 7;36(42):2921-2964.

7. Reddy PS, Curtiss EI, Uretsky BF. Spectrum of hemodynamic changes in cardiac tamponade. Am J Cardiol. 1990 Dec 15;66(20):1487-91.

8. Sternbach G. Claude Beck: cardiac compression triads. J Emerg Med. 1988 Sep-Oct;6(5):417-9.

9. Ranganathan N, Sivaciyan V. Jugular Venous Pulse Descent Patterns: Recognition and Clinical Relevance. CJC Open. 2022 Nov 25;5(3):200-207.

10. Sagristà-Sauleda J, Angel J, Sambola A, Permanyer-Miralda G. Hemodynamic effects of volume expansion in patients with cardiac tamponade. Circulation. 2008 Mar 25;117(12):1545-9.

11. Noble VE, Nelson B. Manual of Emergency and Critical Care Ultrasound. Cambridge, UK: Cambridge University Press; 2014

12. Ma OJ, Mateer JR. Emergency Ultrasound, 2nd ed., McGraw-Hill Education, 2011.

13. Gibbons R. Pericardial vs pleural effusion. Temple Point-of-Care Ultrasound. February 8, 2018. Accessed July 2024. Available from: www.templepocus.com/tips-tricks/2018/2/3/pericardial-vs-pleural-effusion.

14. Smith B. UOTW #11 Answer - Core ultrasound. Core Ultrasound. July 28, 2014. Accessed July 2024. Available from: coreultrasound.com/uotw-11-answer/.

15. Royster K, McCafferty L. Intern ultrasound of the month: pericardial effusion and cardiac tamponade in COVID-19 pericarditis. University Hospitals Emergency Medicine Residency. Published January 31, 2022. Accessed July 2024. Available from: www.thelandofem.com/blog/2022/1/30/iusotm-tamponade.

16. Welch TD, Oh JK. Pericardial effusion, tamponade, and constrictive pericarditis. In: Nihoyannopoulos P, Kisslo J, eds. Echocardiography. Cham, Switzerland: Springer; 2018. Accessed July 2024.

17. Eke OF, Selame L, Gullikson J, et al. Timing of pericardiocentesis and clinical outcomes: Is earlier pericardiocentesis better? Am J Emerg Med. 2022;54:202-207.

18. Alerhand SA, Adrian RJ, Long B, Avila J. Pericardial tamponade: A comprehensive emergency medicine and echocardiography review. Am J Emerg Med. 2022; 58:159-174.

19. Echocardiography. TPA. Accessed July 2024. Available from: www.thepocusatlas.com/echocardiography-2.

20. Foamcast. Episode 54: The Pericardium. Accessed July 2024. Available from: foamcast.org/2016/08/08/episode-54-the-pericardium/.

A 90-year-old male with past medical history significant for chronic urinary retention requiring an indwelling Foley catheter complicated by urinary tract infections (resulting in a hospitalization for septic shock approximately one month prior to this), benign prostatic hyperplasia, pulmonary embolus (on apixaban), and severe aortic stenosis presented to the emergency department for urinary retention. The patient stated that after he recovered from urosepsis during his last admission, he was discharged from the hospital with a Foley catheter, which was most recently changed five days ago at his nursing facility. According to the patient and his wife, since the new foley was placed, it had not been draining, with little to no urine output. He denied any additional symptoms, including fevers, chills, nausea, abdominal pain, diarrhea, nausea, vomiting.

On exam, there was approximately 5 cc of straw colored urine in the foley bag. He had suprapubic fullness with moderate tenderness to palpation. There were no other masses, organomegaly, or overlying skin changes present. The rest of his physical exam was normal, including +2 dorsalis pedis pulses bilaterally, and no costovertebral angle (CVA) tenderness. 

To evaluate placement of his foley and to estimate bladder volume, point-of-care ultrasound was performed. 

POCUS Findings: 

There is urinary retention with a bladder volume of approximately 450 ml of urine with the foley balloon faintly visualized. Deep to the bladder is an incidental well-circumscribed hypoechoic structure measuring just over 5cm; when color doppler is applied, there is pulsatile flow, raising concern for an aneurysm.

Iliac aneurysms

Aneurysm of the abdominal aorta is a relatively common disease in patients over fifty years of age, and rupture of an abdominal aortic aneurysm (AAA) has high mortality (1). As well-described in a previous blog post by Dr. Thai, AAA can be diagnosed when the AP diameter of the aorta exceeds 3.0 cm. The risk of rupture increases dramatically when the diameter of the aorta exceeds 5.0 cm (1). Clinicians with less ultrasound experience may focus solely on the aorta and end their exam once they determine it is less than 3cm… But what about the iliac arteries?

A complete aortic ultrasound exam includes obtaining a longitudinal axis view and a short axis/transverse view of the proximal, mid, and distal portions of the aorta, as well as extending down to the aortic bifurcation. This requires continuing to slide your probe caudally until you visualize the aorta bifurcating into the left and right common iliac arteries, which is usually around the level of the umbilicus (2-3).

Iliac artery aneurysms are present in up to 20% of AAAs, but are found in the absence of AAA in 2-7% of cases. The normal diameter of the iliac arteries is approximately 1 cm. A diameter that exceeds 1.5 cm is considered an aneurysm, and elective repair is generally considered once it reaches 3.5 cm (4).

Recap of the components for a complete aortic ultrasound:

1. Transverse view of the proximal aorta

2. Transverse view of the mid aorta

3. Transverse view of the distal aorta

4. Transverse view of the aortic bifurcation into the right and left common iliac arteries

5. Longitudinal view of the aorta

…with the focused clinical questions:

1. Is the abdominal aorta > 3 cm in diameter?

2. Are the iliac arteries > 1.5 cm in diameter?

**Measure outer wall to outer wall to ensure an accurate determination of size (2). This is especially important when an intraluminal thrombus is present, as the diameter of only the patent part of the lumen may underestimate the true aortic size.

Point-of-care ultrasound (POCUS) can help quickly aid in the diagnosis of an aneurysm with high sensitivity and specificity (5-6). Ultrasound has been found to be comparable to CT in identifying aneurysms, especially when the size exceeds 5.5 cm (7). While POCUS cannot rule out rupture, the presence of the following findings raise concern for rupture: aneurysmal deformation, intraluminal thrombus +/- interruption, retroperitoneal hematoma, and hemoperitoneum (8). Optimal definitive management is largely dependent on several factors including the aneurysm size, presence of rupture, and patient comorbidities/risk factors (9).

Evaluation of foley placement

In patients with indwelling urinary catheters who have flank or abdominal pain, POCUS is useful for evaluating proper placement and functioning of the catheter. A functioning catheter will appear as a spherical object (the saline filled bulb) and a decompressed bladder (10), as shown in Figure 4.

In an obstructed foley, which can occur from a variety of reasons, the bladder will be distended since the outflow tract is impeded, as seen in Figure 5. Common causes of catheter malfunction include stagnant clots that occlude the tip of the catheter’s intake as well as tip occlusion when pressed against bladder wall (10), illustrated in Figures 6 and 7, respectively.

Another potential reason for foley malfunction is inappropriate placement. In our patient’s case, there was initial concern that the foley balloon was inflated outside of the bladder wall. There is a case report from 2022 where a foley catheter was placed through a bladder diverticulum in an outpatient setting 5 days prior, see Figure 8; the chief complaint on presentation was lower abdominal pain (11). Another common location for foley misplacement is within the prostatic urethra, see Figure 9 (12). This, too, is often painful.

Bladder volumes

There is much utility in estimating bladder volume with POCUS, with or without the presence of a foley. From this quick exam, you can directly visualize the amount of urine within the bladder rather than relying on a bladder scanner to correctly distinguish the bladder from other fluid. This can indicate if there is clinical utility in decompressing a full bladder while also potentially identifying causes of post-renal obstruction. For simplicity, the shape of the bladder in calculating volume is approximated to an ellipsoid or cylinder. There are many calculations to use and varying machines will often provide their own calculations with measurement inputs. If stuck with nothing but a probe and a calculator, the quickest and easiest calculation is 0.75 x width x length x height (2). For these measurements, you will need to obtain a transverse, longitudinal, and depth measurement, which will look like a “Plus” sign on your transverse view, and a “minus” sign on your sagittal view, see Figure 10. Post void residual volume of <50 ml is considered normal for most people, but <100 ml may be acceptable for people over 65 years old (13).

Clinical application / discussion

As with everything we do in emergency medicine, ambiguous ultrasound (or other imaging) findings require clinical reasoning. Here, we had an anechoic spherical structure outside of the bladder wall following recent replacement of a foley catheter. The differential of this finding included foley catheter misplacement, free fluid in the pelvis, fluid filled bowel, abscess, and iliac aneurysm. Due to the defined circular structure of the object, this made free fluid in the pelvis unlikely. The patient was lying supine, and free fluid would most likely appear as anechoic fluid in the rectosigmoid space without its own distinct shape. A vascularized structure was distinguished from fluid-filled bowel, a foley bulb, or abscess/cyst by applying color doppler, which showed the structure to be pulsatile. This quickly narrowed the possibilities of our finding to an aneurysm versus pseudoaneurysm; since the entire vessel could be visualized without a focal outpouching or jet of color flow, we suspected this was more likely a true iliac aneurysm. Additionally, the foley balloon was deflated under ultrasound visualization and this hypoechoic structure persisted, making the foley balloon an unlikely explanation for this finding.

With these simple steps and using our clinical knowledge, our undifferentiated incidental ultrasound finding was identified in a matter of seconds.

Case Conclusion:

Following the identification of this patient’s iliac aneurysm, urgent CT angiography was obtained. Further chart investigation found that the patient had been diagnosed with this in the past but was lost to follow up with vascular surgery; at the time, they felt that he was not a good surgical candidate due to his multiple comorbidities. When comparing our POCUS images to comprehensive studies years prior to this, the aneurysm appeared to be slightly increased in size. Vascular surgery was consulted during this visit, and based on overall stability of the aneurysm on CT, they felt that outpatient follow up with frequent monitoring was appropriate. The patient’s foley catheter was exchanged with subsequent good return of urine and relief of the obstruction. He was discharged home in stable condition.

AUTHORED BY: JAKE PERINO, MD (PGY1)

FACULTY CO-AUTHOR/EDITOR: LAUREN MCCAFFERTY, MD

References

1. US Preventive Services Task Force. Screening for Abdominal Aortic Aneurysm: US Preventive Services Task Force Recommendation Statement. JAMA. 2019;322(22):2211–2218.

2. Noble V, Nelson B. Manual of Emergency Medicine and Critical Care Ultrasound, 2nd ed. Cambridge: Cambridge UP, 2011.

3. Risler Z, Dean AJ, Ku BS. Abdominal aortic aneurysm (AAA). American College of Emergency Physicians Sonoguide. August 2020. Accessed January 2024. https://www.acep.org/sonoguide/basic/aorta.

4. Lewiss RE, Egan DJ, Shreves A. Vascular abdominal emergencies. Emerg Med Clin North Am. 2011;29(2):253-72, viii.

5. Costantino TG, Bruno EC, Handly N, Dean AJ. Accuracy of emergency medicine ultrasound in the evaluation of abdominal aortic aneurysm. J Emerg Med. 2005;29(4):455-60.

6. Rubano E, Mehta N, Caputo W, Paladino L, Sinert R. Systematic review: emergency department bedside ultrasonography for diagnosing suspected abdominal aortic aneurysm. Acad Emerg Med. 2013;20(2):128-38.

7. Foo FJ, Hammond CJ, Goldstone AR, et al. Agreement between Computed Tomography and Ultrasound on Abdominal Aortic Aneurysm and Implications on Clinical Decisions. Eur J Vasc Endovasc Surg. 2011; 42, 608-614.

8. Catalano O, Siani A. Ruptured abdominal aortic aneurysm. Categorization of sonographic findings and report of 3 new signs. J Ultrasound Med. 2005;24(8):1077–1083.

9. Chaikof EL, Dalman RL, Eskandari MK, et al. The Society for Vascular Surgery practice guidelines on the care of patients with an abdominal aortic aneurysm. J Vasc Surg. 2018;67(1):2-77.e2.

10. Koratala A, Bhattacharya D, Kazory A. Point of care renal ultrasonography for the busy nephrologist: A pictorial review. World J Nephrol. 2019;28;8(3):44-5

11. Pettet D, Smilios C, Nelson M. Where did that catheter go? A case report of Foley catheter placement in bladder diverticulum with point-of-care ultrasound. JEM Reports. 2022 Dec 1;1:100001.

12. Misplaced Foley in the prostatic urethra. Nephro POCUS. Available from: https://nephropocus.com/2020/02/07/misplaced-foley-in-the-prostatic-urethra/

13. Woods A. POCUS for Bladder Assessment and Volume: Technique, Tips, and Role in System-Wide Use [Internet]. [cited 2024 Jul 28]. Available from: https://www.acep.org/emultrasound/newsroom/may-2022/pocus-for-bladder-assessment-and-volume-technique-tips-and-role-in-system-wide-use

A 45-year-old woman with a past medical history of diabetic neuropathy, hypertension, and migraines presented to the emergency department with one day of left eye blurriness and vision change. The patient also reported a headache with photophobia and phonophobia, similar to past migraines.

Physical exam was notable for visual acuity of 20/200 in the left (affected) eye and 20/40 in the right eye with no pain with extraocular movements and no relative afferent pupillary defect.

Ocular point-of-care ultrasound (POCUS) was performed and showed the following:

POCUS Findings: There is a hyperechoic linear membrane within the vitreous attached posteriorly at the lateral aspect of the optic nerve that does not cross the midline, which indicates a retinal detachment. Additionally, there is a small amount of mobile echogenic matter floating in the posterior chamber, consistent with a vitreous hemorrhage.

How to Do an Ocular POCUS

Equipment Needed:

• Ultrasound machine with a high-frequency linear transducer (10-15 MHz)

• Gel

• Tegaderm

  
  
  

Patient Preparation:

• Position the patient comfortably, either lying supine or in a reclined position.

• Explain the procedure to the patient to alleviate anxiety.

• Apply a tegaderm directly over the closed eye, avoiding air trapping under the plastic film as it can create artifacts that will limit your exam.

• Apply a copious amount of gel over the Tegaderm to help ensure the probe does not contact the eye directly and to facilitate sound wave transmission. This also reduces the amount of pressure you need to apply to the eye to get good visualization of structures.

  
  
  

Equipment Preparation:

• Ensure the ultrasound machine is set to the appropriate settings for ocular imaging (ocular or superficial preset is best).

• Select the high-frequency linear transducer (10-15 MHz).

  
  
  

Scanning Technique:

• Rest your hand lightly on the bridge of the patient’s nose or face to stabilize the transducer and control the amount of pressure you apply.

• Obtain a transverse view (probe marker pointing toward the patient’s right) with the transducer perpendicular to the eye and fan through the entire eye.

  • Visualize the following anatomic structures (anterior to posterior): eyelid, anterior chamber, lens, iris, vitreous body, retina, optic nerve

  • Then, perform a dynamic/kinetic exam by asking your patient to look left and right.

• Obtain a sagittal view by rotating the transducer 90 degrees so that the indicator points superiorly (toward patient’s head). Visualize similar structures as you did in the transverse view and ask the patient to look up and down (superior and inferior).

• When evaluating the vitreous body for pathology, be sure to increase the gain to help detect subtle intraocular pathology that may be missed with normal gain settings (1).

POCUS Indications & Potential Associated Pathology:

Painless Vision Changes/Loss

• Retinal and Vitreous Detachment, Vitreous Hemorrhage

  • Presents as flashers/floaters and may have partial/complete vision loss. See below for more details.

• Central Retinal Artery Occlusion

  • Patient typically have sudden painless monocular vision loss. Ultrasound findings may include a lack of arterial flow of the central retinal artery with color doppler as well as a retrobulbar hyperechoic spot (1,2).

Headache

• Increased Intracranial Pressure and Papilledema

  • Since the optic nerve communicates with the subarachnoid space, an increase in intracranial pressure (ICP) leads to optic nerve sheath expansion as well as optic disc bulging into the vitreous chamber. Studies have shown a correlation between increased ICP and optic nerve sheath diameter (ONSD) greater than 5 mm (measured 3 mm posterior to the retina) or optic disc elevation greater than 6mm. The evidence for ONSD is somewhat poor, and optic disc elevation may be a more promising indicator (3-5).

Trauma

• Lens Dislocation

  • The lens can be seen as a bi-convex hyperechoic structure in the vitreous chamber outside of its normal position behind the iris.

• Retrobulbar Hematoma

  • This is an accumulation of blood in the retrobulbar space that can lead to pain, increased intraocular pressure, ischemia, and ultimately necrosis of the optic nerve and is considered an ocular emergency. The increased retro-bulbar pressure distorts the globe into a cone-like shape.

• Periorbital Edema — Consensual pupillary response & extraocular movement

  • Ultrasound can help visualize consensual pupillary response and extraocular movement when significant periorbital soft tissue swelling prevents an adequate exam (including direct pupillary reflex or extraocular movement) of the affected eye.

• Foreign Body

  • These will appear echogenic (including wood) and can be seen within or around the globe. Metallic objects will often have reverberation artifact. Visualization of a foreign body should raise concern for globe rupture.

• Globe Rupture

  • Ultrasound is NOT recommended if you have a high suspicion of globe rupture. If visualized sonographically, there is usually a loss of the spherical shape of the globe, buckling of the sclera, compression/flattening of the anterior chamber, and may appear as a heterogeneous collection of hematoma, blood, and vitreous humor in the posterior chamber (1-2).

Retinal Detachment

Ocular complaints represent 2-3% of all emergency department visits with 40% being emergent conditions (6-7). A retinal detachment is considered an ocular emergency and requires prompt ophthalmology evaluation. Patients often present with painless vision changes, including flashes, floaters, or a curtain coming down over their eye. In addition to a fundoscopic exam, retinal detachments can be diagnosed with ultrasound. In a meta-analysis study, detection of a retinal detachment on POCUS performed by emergency physicians had both a sensitivity and specificity of 94% (8).

Sonographic findings:

1. Retinal Separation — Ultrasound can detect the separation of the neurosensory retina from the retinal pigment epithelium. This separation is often seen as a hypoechoic space between the two layers with the detached retina within the vitreous body.

2. Echogenicity/key features — The detached retina typically appears as a thick hyperechoic undulating membrane that is tethered posteriorly to the optic nerve and may be saddle-shaped or V-shaped. Its attachment points are on the same side of the globe and the membrane generally does not cross midline. It has a snake-like movement with a kinetic exam and tends to be less mobile than vitreous detachment/hemorrhage.

3. Retinal tear — A retinal tear or break may be visualized as a focal discontinuity in the retina on ultrasound, though this is often not well-visualized.

4. Location and extent — Ultrasound can help determine the location and extent of the detachment, which is crucial for surgical planning. It may helpful in distinguishing the type of detachment, i.e. rhegmatogenous (caused by retinal tears) vs non-rhegmatogenous (caused by other factors), but simply identifying the retinal detachment, not the type, is not the focus of ocular ultrasound (1).

Vitreous Hemorrhage

While this is not considered an ocular emergency, vitreous hemorrhage can also be readily detected with POCUS. In a study by Propst et al, POCUS performed by emergency physicians had a sensitivity and specificity of 81.9% and 82.3%, respectively (9).

Sonographic findings:

1. Echogenicity/key features — Vitreous hemorrhage may appear as dense, variably echogenic material within the vitreous body that is often best seen with increased gain. It is generally highly mobile and readily swirls with dynamic movement, giving it a ‘washing machine’ appearance.

2. Location — The blood may be dispersed throughout the vitreous chamber but often layers in the more posterior, dependent portion.

*A potential mimicker of vitreous hemorrhage is asteroid hyalosis, which is reviewed in this previous blog post by Dr. Eni Gros (10).

Vitreous Detachment

A posterior vitreous detachment (PVD) often presents with similar symptoms as a retinal detachment but is not considered an ocular emergency.

Sonographic findings: Thinner hyperechoic membrane that is NOT tethered to the optic nerve. It often crosses midline and moves more freely compared to a retinal detachment, giving it a ‘swaying seaweed’ appearance (1-2).

Case Conclusion

Ophthalmology concluded that the patient had a tractional retinal detachment (i.e. separation due to tractional forces) without breaks, as well as dense vitreous hemorrhage. The patient underwent a pars plana vitrectomy, membrane peel, and endolaser. Post-operatively, optical coherence tomography (below) showed with an intact retina and no detachment seen.

Take Home Points

• POCUS has good diagnostic utility for several ocular pathologies, including retinal detachment, which is an ocular emergency, as well as vitreous detachment/hemorrhage, among others.

• A retinal detachment appears as a thick echogenic membranes within the vitreous that attaches posteriorly at/near the optic nerve, does not cross midline, and has a serpentine-like motion with a dynamic exam. In contrast, a posterior vitreous detachment or vitreous hemorrhage have no relation to the optic nerve, can cross midline, and are more mobile or free floating.

• Have a systemic approach to ocular ultrasound, making sure you visualize anatomic structures, increase gain when evaluating within the vitreous body, and perform a dynamic exam.

AUTHORED BY: YANINA GUEVARA, MD

FACULTY CO-AUTHOR/EDITOR: LAUREN MCCAFFERTY, MD

References

1. Ahn, Jessica. “Ocular Ultrasound Made Easy: Step-By-Step Guide.” POCUS 101. September 5th, 2023. https://www.pocus101.com/ocular-ultrasound-made-easy-step-by-step-guide/

2. Bates A, Goett HJ. Ocular Ultrasound. [Updated 2023 Jul 24]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK459120/

3. Ohle R, McIsaac SM, Woo MY, Perry JJ. Sonography of the Optic Nerve Sheath Diameter for Detection of Raised Intracranial Pressure Compared to Computed Tomography: A Systematic Review and Meta-analysis. J Ultrasound Med. 2015 Jul;34(7):1285-94.

4. Agrawal D, Raghavendran K, Zhao L, Rajajee V. A Prospective Study of Optic Nerve Ultrasound for the Detection of Elevated Intracranial Pressure in Severe Traumatic Brain Injury. Crit Care Med. 2020 Dec;48(12):e1278-e1285.

5. Teismann N, Lenaghan P, Nolan R, Stein J, Green A. Point-of-care ocular ultrasound to detect optic disc swelling. Acad Emerg Med. 2013 Sep;20(9):920-5.

6. Walker RA, Adhikari S. Eye emergencies. In: Tintinalli JE, Stapczynski S, Ma OJ, Yealy DM, Meckler JD, Cline DM, eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. Chicago, IL: McGraw-Hill Medical; 2011: 236:1517-1549.

7. Channa R, Zafar SN, Canner JK, Haring RS, Schneider EB, Friedman DS. Epidemiology of eye-related emergency department visits. JAMA Ophthalmol. 2016; 134(3):312-319.

8. Propst SL, Kirschner JM, Strachan CC, Roumpf SK, Menard LM, Sarmiento EJ, Hunter BR. Ocular Point-of-Care Ultrasonography to Diagnose Posterior Chamber Abnormalities: A Systematic Review and Meta-analysis. JAMA Netw Open. 2020; 3(2):e1921460.

9. Lahham S, Shniter I, Thompson M, et al. Point-of-Care Ultrasonography in the Diagnosis of Retinal Detachment, Vitreous Hemorrhage, and Vitreous Detachment in the Emergency Department. JAMA Netw Open. 2019; 2(4):e192162.

10. Gros E, McCafferty L. A Mimicker of Vitreous Hemorrhage: Asteriod Hyalosis. The Land of EM POCUS Blog. April 11, 2022. Accessed September 5th, 2023.

A 30-year-old male presents to the emergency department after an accident at work. He works as a logger, and while cutting down a tree, he accidentally cut along his knee with a chainsaw. The patient is hemodynamically stable, bleeding is controlled, and he denies other trauma. He has an 8cm linear laceration extending horizontally across the knee. He has limited range of motion secondary to pain.

What are the next best steps in approaching the workup of this patient?

Traumatic Arthrotomy (TA): Background

Definition

TA occurs when there is violation of a joint space from an overlying soft tissue injury. Violation of the sterile joint capsule exposes the joint space to microbes which predisposes to deep infection and significant morbidity with potential mortality if left untreated.

Epidemiology

• Occurs most commonly in mid-twenty to early thirty-year-old men

• Common mechanisms: MVA, GSW

• Knee is the most commonly affected joint (53 to 91% of all TA presentations)

• Can occur at any joint including the shoulder, elbow, wrist, hip, ankle, hands, and feet

• TA increases the risk of septic arthritis and is considered an emergent surgical condition

• Incidence of concurrent fracture: 24% to 55%; infection rate: 0% to 11.8% [1]

Clinical Signs

• Peri-articular laceration

• Limited ROM

• Synvoial fluid extravasation

• Open fracture

• Severe: Neurovascular deficit, hemodynamic instability

Morbidity

• Prior to antibiotics, septic arthritis occurred in up to 100% of traumatic arthrotomies

• Since development of novel diagnostic techniques and appropriate treatment, the rate of septic arthritis after a traumatic arthrotomy is less than 5% [1]

• Septic arthritis carries 15% mortality even when appropriately diagnosed and treated in the hospital

• Irreversible decrease in joint function rate between 25 and 50%

• Delayed debridement leads to worse pain, limp, range of motion, and joint instability [2]

Diagnostic Approach

For decades, the gold standard for the emergency department diagnosis of TA involved the Saline Load Test (SLT). While this approach (with or without the addition of methylene blue) has been more extensively studied, and generally carries favorable testing characteristics, more recent studies suggest that a CT scan may have a higher diagnostic yield, is less operator-dependent, and may be more tolerable for patients.

SLT Technique

The SLT involves injecting sterile saline into a joint where a penetrating articular injury is suspected. The site of injection is judiciously chosen to avoid the periarticular wound. Extravasation of saline from the joint represents a positive test. Failure of extravasation is defined as a negative SLT and classically implies an intact joint capsule [3].

No single study has comprehensively assessed the SLT's efficacy in detecting open wounds across various joints. Existing literature predominantly concentrates on the knee joint, leaving other joints inadequately explored.

Additionally, there is no consensus regarding the optimal amount of saline to inject to yield a reliable result. The most comprehensive data suggests that within the knee joint volumes ranging from 155 to 194 mL can provide a sensitivity of 95%,[4,5], while a volume of 175 mL has been shown to provide a sensitivity of 99% [4]. A proposed explanation of the wide range of reliable volumes is the heterogeneous sizes of lacerations included in the studies [3].

Regarding other joints, a study involving ankle SLT found a sensitivity ranging from 95% to 99% using 30 mL of saline [6]. A study of elbow SLT demonstrated a 95% sensitivity of SLTs employing 40 mL of saline combined with methylene blue dye [7].

Notably, SLT can lead to iatrogenic injury from increased joint pressure leading to decreased blood flow, injury of surrounding structures if the needle is improperly placed, and disturbance of an intact joint [8,9].  Further, it can lead to increased pain for patients [8].

Methylene Blue

Only one study to date has compared whether the addition of methylene blue improves the reliability of SLT. While it is intuitive to anticipate that its addition would increase diagnostic yield, the study found no statistically significant difference between SLT regardless of the addition of methylene blue [10]. Notably, however, many providers still prefer its addition as it has not been shown to cause harm [7, 11].

CT Scan

While SLT is still considered a relatively reliable diagnostic modality for TA, recent research suggests that CT scans have several advantages. For instance, a study compared the accuracy of SLT and CT scans and found CT outperformed SLT with a sensitivity and specificity of 100% (compared to a sensitivity of 92%) [12].

The inter-operator reliability, lack of potential for iatrogenic injury, and the patient satisfaction impact of obtaining a CT scan compared to SLT to assess for TA has already led to a change of practice for many providers. Further research is necessary to ensure this data is reliable and safe to employ as standard of care.

Clinical Practice Guideline

While the literature on the diagnostic approach to TA is heterogeneous and largely inconclusive, I have proposed a Clinical Practice Guideline that attempts to address these inadequacies while applying the best available data.

Case Continued

Our patient’s exam was concerning for a penetrating joint injury. We first obtained an XR’s of the knee which did not show a fracture and was inconclusive regarding joint penetration. A CT of the knee was then obtained (below) showing air along the joint space, prompting an orthopedic consult, IV antibiotics, and the patient was made NPO. He was taken the next morning for washout without any functional deficits at 6 months.

Take Home Points

• Suspect TA with peri-articular lacerations

• Most commonly occurs in knee joints of young adult men

• Carries significant morbidity and potential mortality if unaddressed

• CT appears adequately sensitive and specific enough to identify the majority of TA

• If CT is negative, and there is still a concern for TA, it is reasonable to perform a SLT

AUTHORED BY: NICK DIMEO, MD, PGY3

FACULTY EDITING BY: NIK SEKOULOPOULOS, MD

References

1. Colmer HG 4th, Pirotte M, Koyfman A, Long B. High risk and low prevalence diseases: Traumatic arthrotomy. Am J Emerg Med. 2022 Apr;54:41-45.

2. Kaandorp CJ, Krijnen P, Moens HJ, Habbema JD, van Schaardenburg D. The outcome of bacterial arthritis: a prospective community-based study. Arthritis Rheum. 1997 May;40(5):884-92.

3. Browning BB, Ventimiglia AV, Dixit A, Illical E, Urban WP, Jauregui JJ. Does the saline load test still have a role in the orthopaedic world? A systematic review of the literature. Acta Orthop Traumatol Turc. 2016 Dec;50(6):597-600.

4. Nord RM, Quach T, Walsh M, Pereira D, Tejwani NC. Detection of traumatic arthrotomy of the knee using the saline solution load test. J Bone Joint Surg Am. 2009 Jan;91(1):66-70.

5. Keese GR, Boody AR, Wongworawat MD, Jobe CM. The accuracy of the saline load test in the diagnosis of traumatic knee arthrotomies. J Orthop Trauma. 2007 Aug;21(7):442-3.

6. Bariteau JT, Blankenhorn BD, Digiovanni CW. Evaluation of saline load test for simulated traumatic arthrotomies of the ankle. Injury. 2013 Nov;44(11):1498-501.

7. Feathers T, Stinner D, Kirk K, et al. Effectiveness of the saline load test in diagnosis of traumatic elbow arthrotomies. J Trauma. 2011 Nov;71(5):E110-3.

8. Goddard NJ, Gosling PT. Intra-articular fluid pressure and pain in osteoarthritis of the hip. J Bone Joint Surg Br. 1988 Jan;70(1):52-5.

9. Beck M, Siebenrock KA, Affolter B, Nötzli H, Parvizi J, Ganz R. Increased intraarticular pressure reduces blood flow to the femoral head. Clin Orthop Relat Res. 2004 Jul;(424):149-52.

10. Metzger P, Carney J, Kuhn K, Booher K, Mazurek M. Sensitivity of the saline load test with and without methylene blue dye in the diagnosis of artificial traumatic knee arthrotomies. J Orthop Trauma. 2012 Jun;26(6):347-9.

11. Raskind JR, Marder RA. Arthroscopic versus open debridement of penetrating knee joint injuries. Iowa Orthop J. 1993;13:121-3.

12. Konda SR, Davidovitch RI, Egol KA. Computed tomography scan to detect traumatic arthrotomies and identify periarticular wounds not requiring surgical intervention: an improvement over the saline load test. J Orthop Trauma. 2013 Sep;27(9):498-504.

13. Ladeira Craveiro V, Henderson S, Boateng H, Garner MR. The role of computed tomography in the detection of traumatic arthrotomies of the elbow: a cadaveric study. OTA Int. 2023 Jun 19;6(3):e275.

14. Jackowski JR, Wellings EP, Cancio-Bello A, Nieboer MJ, Barlow JD, Hidden KA, Yuan BJ. Computed tomography provides effective detection of traumatic arthrotomy of the elbow. J Shoulder Elbow Surg. 2023 Jun;32(6):1280-1284.

15. Shultz CL, Schrader SN, Garbrecht EL, DeCoster TA, Veitch AJ. Operative Versus Nonoperative Management Of Traumatic Arthrotomies from Civilian Gunshot Wounds. Iowa Orthop J. 2019;39(1):173-177.

16. Kermani P. Herndon A. (April 25, 2022). Traumatic Arthrotomy. NUEM Blog. Expert Commentary by Levine M. Retrieved from: http://www.nuemblog.com/blog/traumatic-arthrotomy.

17. Pirotte M, Pirotte A (Nov 17, 2017). How To Confidently Rule Out Traumatic Arthrotomy of the Knee. EP Monthly. Retrieved from: https://epmonthly.com/article/confidently-rule-traumatic-arthrotomy-knee/.

18. Long B (June 21, 2023). emDOCs Podcast – Episode 80: Traumatic Arthrotomy. emDOCs Podcast. Retrieved from: https://www.emdocs.net/emdocs-podcast-episode-80-traumatic-arthrotomy/.

19. Strong JM (April 13, 2020). Saline Load or CT: What’s the Best Test for Traumatic Arthrotomy? ACEPNow. Retrieved from: https://www.acepnow.com/article/saline-load-or-ct-whats-the-best-test-for-traumatic-sarthrotomy/.

1. To understand the prevalence and morbidity associated with deep venous thrombosis (DVT) and pulmonary embolism (PE)

2. To develop a framework for selecting individuals most appropriate for outpatient management of VTE

3. To describe outpatient options for VTE

Definitions

Pulmonary embolism (PE): blood clot formation within a branch of the pulmonary arterial system

Deep venous thrombosis (DVT): blood clot formation in a deep vein, most commonly within the lower leg, thigh, or pelvis

Venous thromboembolism (VTE): a collective term referring to both DVT and PE

Epidemiology

• Approximately 900,000 diagnoses of DVT or PE in the US per year (1)

• Estimated incidence of 1 per 1000 adults, although limited by underdiagnosis (2)

• About two-thirds manifest as DVT, and one-third as PE (2)

• 30-day mortality in Medicare beneficiaries is 5.1 and 9.1 percent for DVT and PE respectively (3)

• PE is responsible for about 100,000 deaths per year (1) 

Who is sent home?

A 2016 study by Singer et al. found that 90% of PE and 52% of DVT patients presenting through the emergency department were hospitalized for initiation of anticoagulation and monitoring. Fifty-one percent of patient with PE in that study were considered low-risk based on sPESI score, many of whom would have been appropriate for discharge with outpatient initiation of anticoagulation (4). Several clinical decision tools exist to help clinicians risk-stratify patients, as discussed below. When utilized appropriately, these tools can be used to reduce hospitalization of otherwise low-risk patients with VTE (4-6).

5 steps to manage DVT and PE as outpatient

Adapted from: A clinical decision framework to guide the outpatient treatment of emergency department patients diagnosed with acute pulmonary embolism or deep vein thrombosis: Results from a multidisciplinary consensus panel (6):

1. Make the diagnosis of DVT or PE

2. Stratify your patient’s risk of clinical decompensation

3. Stratify your patient’s risk of bleeding on anticoagulation

4. Select and start an appropriate anticoagulant

5. Ensure your patient has access to medications with timely follow-up and discussion of appropriate return precautions

General inclusion and exclusion criteria

Inclusion criteria:

• Age 18 to 80

• BMI < 40*

• Able to follow-up with PCP within 7 days

• Able to comply with home medication regimen

• Adequate home support

Exclusion criteria:

• Known coagulopathy or currently on anticoagulation

• New or active* malignancy

• Renal dysfunction (CrCl < 30)

• Currently on dual antiplatelet therapy

• Active use of strong CYP450 3A4 agents

*relative contraindication

Step 1: Diagnosis of DVT or PE

Diagnosis of DVT

• Venous duplex ultrasound

Diagnosis of PE

• CT pulmonary angiography (CT-PA or CTPE)

• VQ scan

• Although not necessary, point-of-care or comprehensive echocardiography can be useful to identify other high-risk features discussed below

   

Step 2: Stratify your patient’s risk of clinical decompensation

Hemodynamic instability

• SBP < 100

• HR > 100 to 110

• Tachypnea or hypoxia

• During prehospital or ED course

• INCLUDES pre-syncope and syncope (indicative of transient period of hypotension)

Clinical decision rules

• Apply simplified PESI or Hestia clinical decision rule

• Hestia clinical decision rule is more specific for identifying patients appropriate for outpatient management, and includes not only physiologic considerations, but social considerations as well (7)

• When compared to simplified PESI, Hestia criteria has similar rates of home treatment and adverse effects, but requires less frequent over-ruling by clinician judgment (7)

High-risk imaging findings

• Radiographic evidence of right heart strain on CT-PA or bedside echocardiogram

• Thrombus located in the main pulmonary artery branches or “saddle” physiology

• Clot in transit (visualized within the right heart) on CT or echocardiogram

High-risk lab findings

• Troponin level elevation

• BNP elevation

Associated high-risk DVT

• Includes iliofemoral clots, extensive clot burden, and clots with associated skin changes (further discussed below)

High-risk EKG findings

• New right heart strain pattern

• New RBBB

• Deep T-wave inversions

• S1Q3T3 pattern

• New-onset arrythmia (e.g. atrial fibrillation or atrial flutter)

Risk stratification of DVT

In the absence of associated PE, risk stratification of DVT is relatively simple, and involves assessing for only a few high-risk features.

Iliofemoral DVT or extensive clot burden

• Associated with greater morbidity and mortality (8)

• Includes those patients appropriate for mechanical thrombolysis

Phlegmasia cerulea dolens or phlegmasia alba dolens

• Reddish or milky-white discoloration of the affected extremity indicative of severe venous outflow obstruction and congestion

• Often associated with severe pain and extensive clot burden 

Step 3: Stratify your patient’s risk of bleeding on anticoagulation

Stratifying bleeding involves consideration of multiple risk factors listed below. Although frequently used, scores such as VTE-BLEED or HAS-BLED have limited utility in the emergency department, as they are designed to quantify the risk of continued long-term anticoagulation, and not to direct the initiation of anticoagulation in acute VTE.

Risk factors:

• Active bleeding or recent (< 1 month) major bleeding*

• Thrombocytopenia (< 100×10^3 / µL)

• Recent major surgery, trauma, or stroke

• Recent epidural, neurosurgical, or cerebrospinal procedure

• Active malignancy of critical site intolerant of bleeding

  • Intracranial, spinal, ocular, oropharyngeal, or retroperitoneal

• Cirrhosis or severe liver dysfunction

• Severe renal dysfunction (CrCl < 30) or ESRD on dialysis

*clinician judgment

Step 4: Select and start an appropriate anticoagulant

DOACs are the preferred agent for most patients seen in the emergency department. Pregnant patients should be started on low-molecular-weight heparin after discussion with OB/GYN or maternal-fetal medicine. Patients requiring anticoagulation with warfarin due to co-morbid conditions are not appropriate for discharge from the emergency department, as they are considered high-risk due to their co-morbidities. These patients should be started on heparin and admitted for observation and bridge to warfarin.

DOACs (e.g. apixaban and rivaroxaban)

• Preferred agent for most patients

• Ask about timing of other medications and ease of taking medications

  • Apixaban is twice daily dosing, but has lowest rate of adverse bleeding

  • Rivaroxaban is once daily dosing, but has higher rates of bleeding, especially GI bleeds (9)

Low molecular weight heparin (e.g. lovenox)

• Preferred in pregnancy (10)

• Consult OB or MFM prior to discharging a patient with VTE

Warfarin (coumadin)

• Preferred in patients with severe liver dysfunction, prosthetic valves, antiphospholipid syndrome, or high-risk of bleeding requiring reversal (7, 11)

• These patients should be admitted for initiation of anticoagulation with heparin bridge therapy

Step 5: Ensure your patient has access to medications with timely follow-up and discussion of appropriate return precautions

• Give the first dose of anticoagulant in the emergency department, and instruct patients to return to the emergency department if they are unable to fill their prescription

• Ensure patients have short-term follow-up with primary care, ideally within 7 to 10 days

• Discuss signs of adverse bleeding and worsening thromboembolic disease requiring prompt return to the emergency department

AUTHORED BY : BEJAN KANGA, MD

FACULTY EDITING BY: NIK SEKOULOPOULOS, MD

References

1. Data and Statistics on Venous Thromboembolism. Centers for Disease Control and Prevention. Updated May 15, 2024. Retrieved from: https://www.cdc.gov/blood-clots/data-research/facts-stats/index.html.

2. Cushman M. Epidemiology and risk factors for venous thrombosis. Semin Hematol. 2007 Apr; 44(2):62-9.

3. Lutsey PL, Zakai NA. Epidemiology and prevention of venous thromboembolism. Nat Rev Cardiol. 2023 Apr; 20(4):248-262.

4. Singer AJ, Thode HC Jr, Peacock WF 4th. Admission rates for emergency department patients with venous thromboembolism and estimation of the proportion of low risk pulmonary embolism patients: a US perspective. Clin Exp Emerg Med. 2016 Sep; 3(3):126-131.

5. Bledsoe JR, Woller SC, Stevens SM, et al. Management of Low-Risk Pulmonary Embolism Patients Without Hospitalization: The Low-Risk Pulmonary Embolism Prospective Management Study. Chest. 2018 Aug; 154(2):249-256.

6. Kabrhel C, Vinson DR, Mitchell AM, et al. A clinical decision framework to guide the outpatient treatment of emergency department patients diagnosed with acute pulmonary embolism or deep vein thrombosis: Results from a multidisciplinary consensus panel. J Am Coll Emerg Physicians Open. 2021 Dec; 2(6):e12588.

7. Roy PM, Penaloza A, Hugli O, et al. Triaging acute pulmonary embolism for home treatment by Hestia or simplified PESI criteria: the HOME-PE randomized trial. Eur Heart J. 2021 Aug; 42(33):3146-3157.

8. Jiménez D, Aujesky D, Díaz G, et al. Prognostic significance of deep vein thrombosis in patients presenting with acute symptomatic pulmonary embolism. Am J Respir Crit Care Med. 2010 May; 181(9):983-91.

9. Adeboyeje G, Sylwestrzak G, Barron JJ, ET AL. Major Bleeding Risk During Anticoagulation with Warfarin, Dabigatran, Apixaban, or Rivaroxaban in Patients with Nonvalvular Atrial Fibrillation. J Manag Care Spec Pharm. 2017 Sep; 23(9):968-978.

10. Bates SM, Rajasekhar A, Middeldorp S, et al. American Society of Hematology 2018 guidelines for management of venous thromboembolism: venous thromboembolism in the context of pregnancy. Blood Adv. 2018 Nov 27; 2(22):3317-3359.

11. Pengo V, Denas G, Zoppellaro G, et al. Rivaroxaban vs warfarin in high-risk patients with antiphospholipid syndrome. Blood. 2018 Sep; 132(13):1365-1371.

90-year-old male with past medical history including dementia presented to the ED after multiple unwitnessed falls at his skilled nursing facility. He was having difficulty ambulating due to pain in his left hip and thigh. He was only oriented to self so additional history was limited. His exam did not show obvious deformity or ecchymosis but he was tender to palpation along his left hip. His vitals were stable and he was neurovascularly intact without any other notable exam findings.

Plain films of his chest, hip, and femur were obtained, along with CT head and C-spine, all of which were negative for acute pathology. A CT abdomen/pelvis was also ordered to evaluate for occult hip fracture as well as intra-abdominal pathology given his falls and limited history. Labs were unremarkable aside from his urinalysis which was suggestive of a urinary tract infection and a large amount of blood. He did have frank hematuria as well.

While awaiting CT, point-of-care ultrasound of the kidneys and FAST exam was performed…

POCUS findings: In the right upper quadrant, a large complex cystic structure was seen extending from the superior pole of the right kidney. It has mixed echogenicity with hypoechoic areas suggestive of fluid. It appears contained and no free fluid is seen. Color doppler shows no evidence of internal flow. His other kidney was normal-appearing and his bladder was decompressed.

Case Continued: CT was read as a large (9 x 9 x 8 cm) complex, mostly cystic mass in the right kidney with thickened walls with nodularity and internal debris with infiltration into the perinephric fat along with fluid. This was concerning for a complex mass versus hematoma in the setting of trauma. Ultimately, radiology and urology felt that this was most likely a rare cystic renal cell carcinoma. He was admitted for pain control, physical and occupational therapy, and facilitation of further workup.

Renal POCUS

Image Acquisition (1)

Right kidney: The right kidney may be found by placing the probe in the mid-axillary line with the indicator pointing toward the patient's head, then sliding inferior to the liver until a characteristic “bean” shape is found. The kidney is typically seen around the 10th-11th intercostal space. You may need to rotate your probe to slide in between rib spaces and better visualize the kidney. In this view, you should be able to visualize the renal cortex, parenchyma, renal pelvis, renal sinus, major and minor calyces. Once you have an adequate view of structures, fan anteriorly and posteriorly through the entire kidney to help ensure you do not miss any major abnormalities. While maintaining this view, you may then rotate your probe 90 degrees to obtain a transverse view and fan through once again. In addition, color doppler should be applied to help differentiate prominent vasculature from hydronephrosis or other abnormalities such as cysts.

Left kidney: The major difference when moving to the left kidney is the initial placement of the probe, as the left kidney is more superior and posterior compared to the right kidney. The probe should be placed around the level of ribs 8-10 and in the posterior axillary line, which often requires your knuckles to touch the bed. Fan through the entire kidney in a longitudinal orientation then rotate the probe 90 degrees for a transverse view. Also remember to apply Color Doppler.

Bladder: It is important to evaluate the bladder as part of a renal ultrasound to assess for urinary retention and potentially identify a cause for renal pathology.

Hydronephrosis

Evaluation for hydronephrosis is the most common application for renal POCUS. Hydronephrosis is an abnormal dilation of the kidney resulting from obstructive uropathy, caused by kidney/ureteral/bladder stones, masses, prostate enlargement, dysfunctional bladder, among others. It appears as a hypoechoic area in the kidney starting centrally and extending peripherally with greater degrees of severity (2), see Figure 3. As mentioned above, applying Color Doppler can help differentiate hydronephrosis from prominent renal vasculature (1). While less sensitive than CT, POCUS is a great initial diagnostic test with comparable diagnostic accuracy to radiology-performed ultrasound and shorter length-of-stay (4).

While evaluating for the presence of hydronephrosis is the primary focus of POCUS studies, it is important to recognize other pathology that may be easily visualized. When you see abnormal findings, take a closer look and correlate with the clinical context.

Renal Cysts

Renal cysts are a relatively common and often benign pathology among hypoechoic kidney lesions. It is estimated that about 50% of people over the age of 50 have some form of cystic renal disease (5). A simple cyst is defined by ultrasound as a distinct circular mass of homogeneous anechoic content with smooth, well-defined margins with a barely detectable submillimeter wall, see Figure 5. In addition, the interface between the cyst and surrounding structures must be simple without a wall-off appearance. If these criteria are not met, then the lesion cannot be considered simple and instead moves into the atypical or complex category. Complex cysts often have internal septations, thickened irregular walls, or nodularity. Ultrasound can detect these findings with high sensitivity, sometimes outperforming CT (6). However, these atypical lesions are often incidentally identified and characterized by CT.

The Bosniak classification, developed in 1986 (7), is a well-validated and widely-used diagnostic system for renal cysts based on a CT protocol. A more recent update providing further clarification was proposed in 2019 (8). This classification system categorizes renal cystic lesions based on number and characteristics of septa, wall thickness, and enhancement along with nodularity (7-8). See Figures 6 and 7 to see key features. This helps inform providers of malignant potential which can guide follow-up recommendations (9-10)

Renal Masses

Renal masses have a wide range of appearance but are often heterogeneous without well-defined walls. The most common renal malignancy is renal cell carcinoma (RCC) followed by transitional cell carcinoma, squamous cell carcinoma, adenocarcinoma, lymphoma and possible metastasis from other locations. Lesions can be multifocal and have cystic elements due to necrosis or calcifications. More than 50% of patients with RCC are asymptomatic and diagnosed during unrelated imaging (11). Signs of advanced disease can include hematuria, flank pain, and a palpable abdominal mass; however this triad is only seen in 10% of cases (5). Lower extremity edema may develop if the tumor has caused compression of the IVC (11).

Cystic renal cell carcinoma (CRCC), a rare form of RCC as seen in this case, often appears sonographically as a hypoechoic mass with hyperechoic septa, thick capsule walls, and possible nodules attached to the septa. It is rare but not impossible for CRCC to have a unilocular appearance, potentially causing diagnostic delay as it can mimic benign simple cysts. Nephrectomy is the treatment of choice for CRCC with most data supporting nephron-sparing surgery (5). The prognosis is reassuring, with the 10-year survival rate and non-recurrence rates of 97.3% and 90.3% (12). 

Renal Abscess
A renal abscess is often a complication of pyelonephritis. Predisposing factors include diabetes, renal calculi, and urinary obstruction. A renal abscess develops within the parenchyma and is typically well-defined and hypoechoic (see Figure 9), which does share overlapping features with a renal cyst. Clinical clues such as flank pain, fever, dysuria and signs of infection on urinalysis may help differentiate. CT is currently the test of choice where the thickness and irregularity of the abscess wall can be clearly seen. The kidney may also look more hypoechoic if the kidney is affected by pyelonephritis. Treatment consists of antibiotics and drainage via ultrasound or CT-guidance (13). 

Perinephric Abscess

While a renal abscess is a walled-off space within the kidney, a perinephric abscess is more diffuse and involves the renal capsule and Gerota’s fascia and potentially extending into surrounding areas. They are typically hypoechoic or have mixed echogenicity. It is another complication of pyelonephritis and less commonly results from a renal abscess that ruptures into the perirenal space. It may also be caused from a non-renal contiguous infection (15). Like renal abscesses, these are typically treated under percutaneous drainage and antibiotics (16). 

Subcapsular Renal Hematoma

Subcapsular renal hematomas develop from hemorrhage that accumulates within the capsule of the kidney. They can be caused by trauma, procedures, or spontaneously from underlying pathology, such as a tumor or abscess, anticoagulation use, among others. These lesions are best confirmed by CT but can and have been promptly diagnosed with POCUS (18). While these are generally asymptomatic initially, as time progresses the capsule will become more fibrous, which will restrict further outward hematoma expansion. This may cause compression of the underlying structures, leading to hematuria, hypertension, decreased urine output, impaired renal function, and adrenal insufficiency/failure. Not only can color doppler be used to evaluate for extravasation but can also help identify underlying ischemia and compression of the renal parenchyma. Treatment is largely dependent on hemodynamic status, renal function, and etiology. Patients with reassuring clinical findings may be sent home with close follow up. More aggressive action can be taken if renal function is compromised or if the contralateral kidney is not functioning well; this may include removing the capsule, percutaneous drainage, or possible partial or total nephrectomy (18-19).

General Takeaway

While POCUS is typically used to evaluate for hydronephrosis, there are many other renal lesions that may be found incidentally, such as abscess, hematoma, cystic lesions, and masses. It is important to keep our differential broad, correlate ultrasound findings with the clinical picture, and adjust further workup and management within the appropriate context.

AUTHORED BY: ABBY WISSMAN, DO, PGY1

FACULTY CO-AUTHOR/EDITOR: LAUREN MCCAFFERTY, MD

References

1. Deschamps J, Dinh V, Ahn, et al. Renal Ultrasound made easy: Step-By-Step Guide. POCUS 101. (n.d.). Accessed May 2024.

2. Koratala A, Bhattacharya D, Kazory A. Point of care renal ultrasonography for the busy nephrologist: A pictorial review. World J Nephrol 2019; 8(3): 44-58.

3. Vasculature Mimicking Hydronephrosis on Greyscale-Ultrasound. NephroPOCUS. June 23, 2019. Accessed May 2024. https://nephropocus.com/2019/06/23/vasculature-mimicking-hydronephrosis-on-greyscale-ultrasound/

4. Smith-Bindman R, Aubin C, Bailitz J, et al. Ultrasonography versus computed tomography for suspected nephrolithiasis. N Engl J Med. 2014;371:1100–1110.

5. Zhang J, Liu B, Song N, Hua L, Wang Z, Gu M, Yin C. Diagnosis and treatment of cystic renal cell carcinoma. World J Surg Oncol. 2013 Jul 17;11:158.

6. Hélénon O, Crosnier A, Verkarre V, Merran S, Méjean A, Correas JM. Simple and complex renal cysts in adults: Classification system for renal cystic masses. Diagn Interv Imaging. 2018; 99(4):189–218.

7. Bosniak MA. The current radiologic approach to renal cysts. Radiology. 1986; 158: 1-10.

8. Silverman SG, Pedrosa I, Ellis JH, et al. Bosniak classification of cystic renal masses, version 2019: An update proposal and needs assessment. Radiology. 2019;292:475–488.

9. Nicolau C, Antunes N, Paño B, Sebastia C. Imaging Characterization of Renal Masses. Medicina (Kaunas). 2021;57(1):51.

10. Skalski M. Bosniak classification of renal cysts (illustrations). Case study, Radiopaedia.org. Accessed May 2024. <https://radiopaedia.org/cases/bosniak-classification-of-renal-cysts-illustrations?lang=us>

11. Gray RE, Harris GT. Renal Cell Carcinoma: Diagnosis and Management. Am Fam Physician. 2019;99(3):179-184.

12. Tosaka A, Yoshida K, Kobayashi N, Takeuchi S, Uchijima Y, Saitoh H. A report of two cases of multilocular cystic renal cell carcinoma: review of 51 cases reported and the results of a prognostic survey. Hinyokika Kiyo. 1992;11:1045–1050.

13. Jones J, Sharma R, Niknejad M, et al. Renal abscess. Reference article, Radiopaedia.org. Accessed on May 2024. <https://radiopaedia.org/articles/renal-abscess?lang=us>

14. Yoo EJ, Oh JH, Jung HJ, Lee SJ, Park JE, Pai KS. Primary Subcapsular Reflux as an Etiology of Subcapsular Renal Abscess. Child Kidney Dis. 2021;25(2):133-139.

15. Rai RS, Karan SC, Kayastha A. Renal and Perinephric Abscesses Revisited. Med J Armed Forces India. 2007 Jul;63(3):223-5.

16. Okafor CN, Onyeaso EE. Perinephric Abscess. [Updated 2023 Aug 14]. In: StatPearls [Internet]. Treasure Island(FL): StatPearls Publishing; 2024 Jan-.

17. Patel M, Perinephric abscess. Case study, Radiopaedia.org. Accessed on 31 May 2024. <https://radiopaedia.org/cases/perinephric-abscess?lang=us>

18. Bakardjiev M, Esposito A. FAST exam to diagnose subcapsular renal hematoma. J Educ Train. 2019; 4(4):V32-35.

19. Ayhan O, Mansura DH, Muratb O, Mehmed U, Chafer G. Subcapsular renal hematoma: three case reports and literature reviews. Open Access Emerg Med. 2012; 2:111.

55-year-old male with a past medical history of hypertension and diabetes presented to the emergency department for shortness of breath and dizziness. He reported these symptoms started while he was exerting himself and minimally improved after a period of rest. He reported feeling like he was going to pass out but did not experience loss of consciousness. The patient denied any chest pain, headache, fever, chills, recent illnesses, or nausea/vomiting. He reported similar symptoms in the past without further workup or diagnosis.

His vitals were within normal limits and his examination was unremarkable.

In evaluating his pre-syncopal episode, an EKG was obtained and showed sinus rhythm at a rate of 70 with right axis deviation and T-wave inversions in anteroseptal leads without acute ST elevations, similar to a previous EKG from several months ago.  

While awaiting a chest x-ray and labs, a cardiac point-of-care ultrasound (POCUS) was performed.

Overall impression of POCUS findings:

Right heart enlargement with septal flattening/bowing (“D sign”) in the parasternal short axis view and reduced TAPSE, indicating reduced RV function. The IVC is also plethoric, which further supports this. LV function is preserved and there’s no pericardial effusion.

Case Continued: Labs were significant for a slightly elevated BNP of 300. COVID PCR was negative. Chest x-ray showed mild pulmonary vascular congestion. On review of prior records, the patient had previously been diagnosed with pulmonary hypertension, and a recent echo had similar findings. Given the patient’s overall stability, the ED team held off on additional imaging and admitted him for further evaluation and management.

Right Heart Dysfunction/Failure

Brief Background/Overview

Often overshadowed by the left ventricle (LV), the right ventricle (RV) is a unique chamber of the heart with distinct anatomical and physiologic features. It has a complex shape with longitudinally-oriented muscle fibers whose shortening contributes to much of its contractility (1). Compared to the LV, the RV is thinner and composed of fewer muscle fibers. This is because the pressure in the pulmonary circuit is much lower than that of systemic circulation, allowing the RV to maintain the same stroke volume as the LV but with 75% less stroke work (2). The RV is also more compliant than the LV, which allows the RV to accommodate the large volume fluctuations of venous return without affecting the end-diastolic pressure (2). In contrast, the RV does not withstand an acute pressure load well and is highly sensitive to pressure changes (1). Despite their differences, the RV and LV share the interventricular septum as well as the pericardial space. As a result, they are interdependent, and dysfunction of one often leads to dysfunction of the other (3).

RV function is largely influenced by preload, afterload, and contractility [1]. Dysfunction is defined as abnormal structure or function of the RV, while right heart failure (RHF) refers to a clinical syndrome that can develop from RV dysfunction (4). Potential causes include pulmonary arterial hypertension, massive pulmonary embolism, right-sided myocardial infarction, acute respiratory distress syndrome (ARDS), chronic obstructive pulmonary disease (COPD), chronic lung disease, RV outflow obstruction, myocarditis, and advanced LV failure, to name a few. These pathologies lead to RV dysfunction/failure through pressure overload, volume overload, or decreased contractility of the right heart (1,3,4).

Because RV function is highly sensitive to changes in afterload, even slight increases - especially sudden onset, are poorly tolerated and result in significant changes in stroke volume. Gradual increases in RV afterload may allow the ventricle time to adapt, though it may still eventually lead to RV dysfunction (5). Reduced RV stroke volume leads to RV dilation, which causes tricuspid regurgitation, further exacerbating RV dilation. Due to ventricular interdependence, this leads to impaired LV filling and reduced cardiac output (4).

Clinical Presentation

The clinical presentation of right heart failure largely depends on the underlying cause and severity of the RV dysfunction. Some of the common signs and symptoms include shortness of breath with exertion, peripheral edema, fatigue, jugular venous distention, hepatomegaly, hepatojugular reflux, and ascites (1,3). In advanced cases of RV dysfunction, patients can present with hypotension or shock and signs of hypoperfusion (4).

Diagnosis

The diagnosis of RV dysfunction depends on the patient’s clinical presentation, examination findings, EKG findings, and imaging findings. On EKG, there may be evidence of right axis deviation and right ventricular hypertrophy. If the cause of RV dysfunction is due to a massive PE, there may be the classically-associated “S1Q3T3”, or McGinn-White Sign, due to acute cor pulmonale; this sign is comprised of an S wave in lead I, a Q wave in lead III, and an inverted T wave in lead III (2). X-rays, which are commonly ordered given the clinical presentation, may show signs such as cardiomegaly or pulmonary edema, though findings are not specific to RV dysfunction (4).

Most commonly, RV dysfunction is diagnosed by comprehensive echocardiography. It is a non-invasive study that can assess the size, morphology, and function of the right heart, pulmonary hemodynamics, and associated structures (4,6). While not comprehensive, POCUS allows for a rapid assessment of RV size, global function, the presence of tricuspid regurgitation or pericardial effusion, and inferior vena cava (IVC) size and collapsibility (6).

Cardiac MRI is the gold standard for evaluating for RV abnormalities because it allows for good visualization of anatomy, tissue characterization, calculation of flow, and quantification of function (3). However, MRIs are costly, not always readily available, and may also cause malfunction of implanted devices (such as pacemakers), thus resulting in echocardiography being the initial diagnostic modality of choice (6).

Management

Management of RV dysfunction/failure largely depends on the underlying etiology. Treating the underlying cause and triggering factors is key. The overarching goals of treatment include optimizing RV preload, reducing RV afterload, and increasing RV contractility and perfusion (4,5,7). To optimize preload, assess and carefully support volume status as needed. In the setting of fluid overload, diuretics can be used to decrease venous congestion as well as relieve hypoxia. To reduce RV afterload, first aim to correct hypoxia, acidemia, and hypercapnia, as these can increase pulmonary vascular resistance. In advanced cases, afterload-reducing agents, i.e. prostacycline and other pulmonary vasodilators, may be indicated. Vasopressors can be used to increase systemic arterial blood pressure and improve perfusion. Inotropes, such as Dobutamine or Milrinone, can improve myocardial contractility while also improving afterload; however, these can also reduce systemic vascular resistance so systemic vasoconstrictors may also be needed to counteract this (5,7).

Complications of right heart failure, especially if untreated, include end-organ damage. Primarily affecting the liver and kidneys, this results from increased venous pressure and reduced perfusion from the decreased cardiac output (4).

Evaluating the Right Heart with POCUS

In patients with shortness of breath, hypotension, syncope/near-syncope, JVD, etc, a focused evaluation of the heart with POCUS can provide a lot of information at bedside, which can be especially useful in unstable patients. Specifically when concerned about right heart pathology, POCUS allows us to quickly assess RV size, global function, the presence of a pericardial effusion, gross valvular abnormalities and regurgitation, and IVC size and collapsibility (8,9). Findings are predominantly described qualitatively (normal, mild, severe) or with a yes/no answer, which the clinician can correlate with and apply to the clinical picture. It is important to note that POCUS does have its limitations and should not replace a comprehensive study.

RV Enlargement (RV: LV ratio)

For POCUS, the most basic component to evaluate is RV size, especially relative to the LV. This can be assessed qualitatively in an apical four chamber view. The RV should be smaller than the LV, so if the RV is similar in size or larger than the LV, this indicates enlargement (10). POCUS performed by emergency physicians can accurately identify RV dysfunction with high sensitivity and specificity, outperforming cardiac biomarkers and CT findings (11).

“D Sign”

Seen on a parasternal short axis view, this is characterized by flattening/leftward deviation of the interventricular septum so that the LV has a “D” shape, see Figure 2. This is a result of overload on the RV (10). To determine whether it is pressure or volume overload is causing this RV strain, you can calculate the eccentricity index (EI).

—> Eccentricity Index

• Described by Ryan et al., this consists of measuring the LV diameter parallel and perpendicular to the septum in a parasternal short axis view. Do this in both end-systole and end-diastole and then calculate the ratio for each. See Figure 3.

  • EI = D2/D1 (D2 = LV diameter parallel to the septum, D1 = LV diameter perpendicular to the septum in parasternal short-axis.

• Normal EI ≤ 1 (the LV is circular)

• RV volume overload: EI > 1 during end-diastole but EI ≤ 1 (normal) during end-systole

• RV pressure overload: EI >1 during BOTH end-systole & end-diastole (12).

Tricuspid Annular Plane Systolic Excursion (TAPSE)

Because the majority of the RV muscle fibers contract longitudinally, the vertical motion of the RV roughly indicates RV function (3). The greater the vertical displacement of the tricuspid annulus during systole, the better the function. This can be assessed in an apical four chamber view. Using m-mode, place the bar over the lateral tricuspid annulus. On the waveform produced, measure the distance from the peak to trough, see Figure 4. A measurement less than 17 mm is considered abnormal, indicating reduced RV function. It is important to note that this is angle-dependent so if the view is off-axis or if the m-mode bar is not well-aligned, it can result in an erroneous measurement (13).

RV Wall Thickness

If the thickness of the RV free wall is greater than 5mm, it indicates RV hypertrophy and suggests a chronic process (though it does not exclude a concurrent acute one). This is best measured in parasternal long axis view or subxiphoid view at end-diastole, see Figure 5 (13).

IVC

A quick assessment of the IVC is another adjunct to aforementioned views. A plethoric, or distended, IVC with minimal respiratory variation within roughly 3 cm of the right atrium has been shown to reflect increased right atrial pressure (10).

While not covered in this blog post, there are several additional signs of RV strain that can be evaluated with POCUS. This includes McConnell’s sign (see previous blog post for details) and other quantitative measurements of right ventricular systolic pressure, pulmonary artery pressure and acceleration time, tricuspid regurgitation, among others. See additional resources below to learn more.

Take Home Points

• A patient with right heart failure can present with non-specific symptoms but POCUS can quickly, non-invasively, and effectively help identify and narrow the differential.

• POCUS can identify signs of RV dysfunction, including RV enlargement, a “D” sign, reduced TAPSE.

• To differentiate volume vs pressure overload causing a “D" sign”, calculate the eccentricity index — septal flattening in diastole occurs in both but only in pressure overload states does this also occur in systole.

• The mainstay of treatment is focused on optimizing preload, reducing afterload, and improving contractility and perfusion while addressing the underlying cause.

• Early recognition of RV dysfunction can help initiate and guide appropriate management, monitor progression, and improve morbidity and mortality.  

AUTHORED BY: ISMA DHANANI, MD, PGY1

FACULTY CO-AUTHOR/EDITOR: LAUREN MCCAFFERTY, MD

References

1. Dini FL, Pugliese NR, Ameri P, et al. Heart Failure Study Group of the Italian Society of Cardiology. Right ventricular failure in left heart disease: from pathophysiology to clinical manifestations and prognosis. Heart Fail Rev. 2023; 28(4):757-766.

2. Arrigo M, Huber LC, Winnik S, et al. Right Ventricular Failure: Pathophysiology, Diagnosis and Treatment. Card Fail Rev. 2019;5(3):140-146

3. Ibrahim BS. Right ventricular failure. ESC Escardio.org. 2016; 14(32). https://www.escardio.org/Journals/E-Journal-of-Cardiology-Practice/Volume-14/Right-ventricular-failure.

4. Konstam MA, Kiernan MS, Bernstein D, et al. Evaluation and Management of Right-Sided Heart Failure: A Scientific Statement From the American Heart Association. Circulation. 2018;137(20):e578-e622.

5. Murphy E, Shelley B. Clinical presentation and management of right ventricular dysfunction. BJA Educ. 2019;19(6):183-190.

6. Ro SK, Sato K, Ijuin S, et al. Assessment and diagnosis of right ventricular failure-retrospection and future directions. Front Cardiovasc Med. 2023;10:1030864.

7. Ventetuolo CE, Klinger JR. Management of acute right ventricular failure in the intensive care unit. Ann Am Thorac Soc. 2014;11(5):811-22.

8. Johri AM, Galen B, Kirkpatrick JN, Lanspa M, Mulvagh S, Thamman R. ASE Statement on Point-of-Care Ultrasound during the 2019 Novel Coronavirus Pandemic. J Am Soc Echocardiogr. 2020; 33(6):670-673.

9. Spencer KT, Flachskampf FA. Focused Cardiac Ultrasonography. JACC Cardiovasc Imaging. 2019; 12(7 Pt 1):1243-1253.

10. Reardon RF, Laudenbach A, Joing SA. Cardiac. In OJ Ma, JR Mateer, RF Reardon, SA Joing (eds), Ma and Mateer’s Emergency Ultrasound (3rd ed). 2008. New York, NY: McGraw-Hill Education. pp 93-167. 

11. Weekes AJ, Thacker G, Troha D, Johnson AK, et al. Diagnostic Accuracy of Right Ventricular Dysfunction Markers in Normotensive Emergency Department Patients With Acute Pulmonary Embolism. Ann Emerg Med. 2016;68(3):277-91.

12. Ryan T, Petrovic O, Dillon JC, Feigenbaum H, Conley MJ, Armstrong WF. An echocardiographic index for separation of right ventricular volume and pressure overload. J Am Coll Cardiol. 1985; 5(4):918-27.

13. Rudski LG, Lai WW, Afilalo J, Hua L, Handschumacher MD, Chandrasekaran K, Solomon SD, Louie EK, Schiller NB. Guidelines for the echocardiographic assessment of the right heart in adults: a report from the American Society of Echocardiography endorsed by the European Association of Echocardiography, a registered branch of the European Society of Cardiology, and the Canadian Society of Echocardiography. J Am Soc Echocardiogr. 2010;23(7):685-713.

To learn more, check out these additional resources:

https://www.pocus101.com/the-d-sign-right-heart-strain-from-pressure-vs-volume-overload/

https://coreultrasound.com/right-heart-function/

https://coreultrasound.com/60-60-sign-for-acute-pulmonary-embolism/

77-year-old female with past medical history pertinent for end-stage renal disease, heart failure, and lung cancer who presented to the emergency department (ED) after becoming unresponsive. The patient's family reported that she had been in her usual state of health earlier that day, but while sitting in a chair she suddenly slumped over and stopped responding. EMS arrived, and she was awake and talking en route to the ED. Shortly after arrival, she again became unresponsive. She was found to be pulseless, with pulseless electrical activity (PEA) on the monitor, and ACLS protocol was started. During the resuscitation, a cardiac point-of-care ultrasound was performed to evaluate for potential causes of her PEA arrest. 

POCUS Findings/Interpretation

An apical 4 chamber image series obtained during a brief period of return of spontaneous circulation (ROSC) shows a significantly enlarged right ventricle with free wall hypokinesis and apical sparing, otherwise known as McConnell's Sign. This was concerning for PE.

Case Conclusion:

The patient went into PEA arrest again. Family continued to want to pursue aggressive measures. No other reversible causes were identified. Given her acute onset of symptoms, cancer history, and ultrasound findings, PE was a major concern. Benefits and risks of thrombolytics were considered, and in the setting of recurrent cardiac arrest, the decision to push IV tPA was made. Following tPA administration, ROSC was achieved. Once stabilized, CT was performed which showed a saddle PE. She was transferred to the ICU for further management.

Acute Pulmonary Embolism

Acute pulmonary embolism (PE) is a common clinical entity, with an incidence ranging from 39 to 115 per 100,000 population annually (1). The presentation of patients with PE has an extensive range of clinical implications and severity. PE can be asymptomatic and identified incidentally on imaging studies but, as seen in this case, can traverse the entire spectrum of severity and present as cardiac arrest.

A PE is a disruption or total blockage of flow of blood in the pulmonary arterial tree. These blockages are typically caused by thrombi, most often deep venous thrombosis (DVTs) of the lower extremities (2). PE can also arise in situations where materials other than blood, such as fat, air, or foreign bodies, migrate to the pulmonary arterial system, although this is exceedingly rare when compared with DVT (3).

The classification of PE is based not on the size of the clot or clot burden but the hemodynamic instability that may result as a function of obstructive shock. PEs that cause hemodynamic instability should be referred to and documented as such. This is defined by a systolic blood pressure (SBP) less than 90 mmHg, a drop in SBP by greater than 40mm Hg from baseline, or hypotension requiring vasopressor support; such PEs were previously referred to as 'massive' or 'high-risk'. Hemodynamically stable PEs can range from small, incidentally found, and asymptomatic PE to those which may cause initial hypotension that is fluid-responsive or those causing right ventricular (RV) dysfunction without hemodynamic instability. These are referred to as "low-risk” or ”small” PEs and "sub-massive” or ”intermediate-risk” PEs, respectively (4).

Computed tomography (CT) angiography is the preferred imaging study for PE. While generally not diagnostic of PE, transthoracic echocardiography can detect signs of right heart strain, which can support the diagnosis of PE in the right clinical context (4-7). This can be especially helpful in situations in which patients are too unstable for CT, there is a contraindication to CT, or other confirmatory tests are not readily available.

Given the wide variety of clinical presentation, treatment for PE varies greatly as well. Treatment ranges from anticoagulation only to systemic thrombolytic administration, catheter-directed therapy, or surgical embolectomy (4).

McConnell’s Sign on Point-of-Care Ultrasound

McConnell’s Sign & Its Significance

This ultrasound finding of regional right ventricular dysfunction, with akinesia of the mid free wall and preserved contractility of the apical wall, is known as McConnell's sign (5), see Figure 1. This is a poorly sensitive but highly specific and early indicator for acute PE and has particular diagnostic utility in patients who are too unstable for CT or are being considered for thrombolytic administration (6-7).

McConnell's sign, while highly specific, has occasionally been seen in cases of right ventricular ischemia in the absence of PE (8).  However, the rarity of these "PE-less McConnell's signs" is such that any patient with an identified McConnell's sign on ultrasound should be strongly considered for acute PE. 

McConnell's sign is best appreciated in the apical four chamber view as it allows for visualization of the RV free wall, tricuspid annulus, and apex.

Image Acquisition

Acquiring the apical four chamber view can be difficult, especially in cases such as ours where the patient had an automated CPR device on the chest. Difficulties also arise with body habitus, respiratory distress, and patient positioning. In general, a good first step in your approach to obtaining the desired view is to place the transducer in the 4th or 5th intercostal space often near or lateral to the nipple line with the probe marker facing the 2-3 o’clock position (in cardiac convention), see Figures 2 and 3. If patient condition permits, the left lateral decubitus position can be employed to more readily obtain the desired sonographic windows, as this will bring the heart closer to the chest wall. In an adequate view, all four cardiac chambers are visualized. In addition, the interventricular septum should be vertically oriented on your screen (which often requires rocking the probe toward the axilla), as this will give you the most accurate assessment (9-11); see Figure 4.

Other Sonographic Signs of Right Heart Strain

In addition to McConnell’s sign, other key sonographic signs of right heart strain include:

• Right ventricular (RV) enlargement - Normally, the RV to LV ratio is roughly 0.67. When the RV approaches or exceeds the size of the LV, this is considered pathologically enlarged. This can best evaluated in the apical four chamber view (Figure 5).

• Abnormal septal motion (“D sign”) - When the right ventricle bows towards the left this indicates increased right-sided pressures. This appears as a “D-sign” on a parasternal short axis view, as shown in Figures 6 and 7.

• Tricuspid annular plane systolic excursion (TAPSE) - Briefly, this is a way to estimate RV contractility. Because the RV primarily contracts longitudinally (compared to the LV which contracts concentrically), vertical displacement of the tricuspid annulus correlates with RV contraction. Therefore, decreased TAPSE (i.e. decreased vertical displacement) indicates reduced contractility. TAPSE less than 17 mm is considered abnormal (11-13)

  • How to do it: Obtain an apical four chamber view. Place m-mode cursor over the lateral tricuspid valve annulus. The resulting waveform shows the displacement of tricuspid annulus through the cardiac cycle. Measure the vertical height between peak and trough. See Figure 8.

There are additional, more complex methods to evaluate for right heart strain using ultrasound. See resources below for more details.

AUTHORED BY: GABE ALAGNA, MD (PGY1)

FACULTY CO-AUTHOR/EDITOR: LAUREN MCCAFFERTY, MD

References

1. Wendelboe AM, Raskob GE. Global Burden of Thrombosis: Epidemiologic Aspects. Circ Res. 2016;118(9):1340-7.

2. Turetz M, Sideris AT, Friedman OA, Triphathi N, Horowitz JM. Epidemiology, Pathophysiology, and Natural History of Pulmonary Embolism. Semin Intervent Radiol. 2018;35(2):92-98

3. Khashper A, Discepola F, Kosiuk J, Qanadli SD, Mesurolle B. Nonthrombotic pulmonary embolism. Am J Roentgenol. 2012;198(2):W152-9

4. Vyas V, Goyal A. Acute Pulmonary Embolism. [Updated 2022 Aug 8]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan. Available from: https://www.ncbi.nlm.nih.gov/books/NBK560551/

5. McConnell MV, Solomon SD, Rayan ME, Come PC, Goldhaber SZ, Lee RT. Regional right ventricular dysfunction detected by echocardiography in acute pulmonary embolism. Am J Cardiol. 1996;78:469–473.

6. Patra S, Math RS, Shankarappa RK, Agrawal N. McConnell's sign: an early and specific indicator of acute pulmonary embolism. BMJ Case Rep. 2014;2014:bcr2013200799

7. Fields JM, Davis J, Girson L, Au A, Potts J, Morgan CJ, Vetter I, Riesenberg LA. Transthoracic Echocardiography for Diagnosing Pulmonary Embolism: A Systematic Review and Meta-Analysis. J Am Soc Echocardiogr. 2017;30(7):714-723.e4

8. Rafie N, Foley DA, Ripoll JG, Booth-Kowalczyk ML, Arghami A, Pochettino A, Michelena HI. McConnell's Sign Is Not Always Pulmonary Embolism: The Importance of Right Ventricular Ischemia. JACC Case Rep. 2022;4(13):802-807.

9. Koratala A. Focused Cardiac Ultrasound for the Nephrologist: The apical window. Renal Fellow Network. September 20, 2019. Retrieved from: https://www.renalfellow.org/2019/09/20/focused-cardiac-ultrasound-for-the-nephrologist-the-apical-window.

10. 5 Core Views. IMPoCUS. Retrieved from: https://www.impocus.ca/cardiac-focus---5-core-view---5

11. Prats MI, Bahner DP. Cardiac. Sonoguide. August 18, 2020 Retrieved from: https://www.acep.org/sonoguide/basic/cardiac.

12. Lang RM, Badano LP, Mor-Avi V, et al. Recommendations for cardiac chamber quantification by echocardiography in adults: an update from the American Society of Echocardiography and the European Association of Cardiovascular Imaging. J Am Soc Echocardiogr. 2015;28(1):1-39.e14

13. Alerhand S, Sundaram T, Gottlieb M. What are the echocardiographic findings of acute right ventricular strain that suggest pulmonary embolism? Anaesth Crit Care Pain Med. 2021;40(2):100852

As temperatures fall and w­inter takes hold, the likelihood of seeing a patient presenting to the emergency department with hypothermia climbs. However, depending on the etiology of hypothermia, a hypothermic patient can certainly present to the ED amid a summer heat wave as well. Because there are slight variations in temperature that define hypothermia, accidental hypothermia is defined here as a core temperature less than 35ºC (95ºF) and can be associated with significant morbidity and mortality (1). Accidental hypothermia can be further characterized as primary, due to environmental exposure, or secondary, due to impaired thermoregulation (2).

A complex array of homeostatic interactions occurs to maintain the widely accepted definition of normal body temperature of approximately 37ºC (98.6ºF) (3). The body’s core temperature will fall when the body experiences an amount of heat loss that exceeds heat production. As you may (or may not) recall from your high school and college physics courses, heat loss can occur through a variety of mechanisms including conduction, convection, evaporation, and radiation (Table 2) An elderly patient who had an unwitnessed fall with a prolonged downtime can experience conductive heat loss with the floor. This can be further exacerbated if the patient fell outside on a cool breezy day where they will also lose heat via convection as the wind goes across their skin. Conductive and convective heat loss are the most common mechanisms of accidental hypothermia (4).

Classification

The European Resuscitation Council guidelines classifies hypothermia as mild (core temperature 32-35ºC [90-95ºF]); moderate (core temperature 28-32ºC [82-90ºF]); and severe (core temperature <28ºC [82ºF] (5). Profound hypothermia is classified as a core temperature <24ºC (75ºF) (6). When an accurate temperature measurement is unobtainable such as the prehospital setting, there have been various attempts to create an accurate clinical staging system to estimate the extent of hypothermia. Several studies evaluating the Swiss system developed by the International Commission for Mountain Emergency Medicine revealed a relatively high degree of misclassification of hypothermia severity (7,8). The Swiss system has since been modified to the Revised Swiss System (figure 1) and is more like the Danish system, which has been used by prehospital personnel for several years. Both systems stage hypothermia based on the level of consciousness and the subsequent risk of cardiac arrest rather than core temperature (9).

Pathophysiology

Various central and peripheral thermal receptors monitor the body’s temperature. Through numerous hypothalamic pathways to other organs such as the thyroid and adrenal glands, the body can both produce and conserve heat through behavior modification, peripheral vasoconstriction, increasing metabolic rate, and muscular thermogenesis or shivering (10). When the heat loss exceeds the body’s abilities to produce and conserve heat, the body’s core temperature drops, which leads to a multitude of other physiologic changes including decreased tissue metabolism, central nervous system impairment, myocardial irritability, respiratory impairment, and coagulopathy (2).

Studies have revealed various temperatures that correlate with specific pathologies. The pupils may become fixed and dilated below approximately 29ºC (84.2ºF) and corneal reflexes absent below 23ºC (73.4ºF). As the core temperature falls below 32ºC (89.6ºF), Osborn J waves typically show up on ECG, which are roughly proportional to the degree of hypothermia, and the risk of cardiac arrest increases drastically below 28ºC (82.4ºC) (10). Other ECG changes visible include bradycardia with progressively prolonging intervals (PR, QRS, QTc). When a patient is hypothermic, some ECG findings (T-wave abnormalities associated with hyperkalemia) may be masked, therefore it would be prudent to consider these patients as sick. Given the myocardial irritability and lower threshold to develop dysrhythmia associated with a low core temperature, it is important for patients to be handled especially carefully and kept in a horizontal position. Within the hematological system, when core temperature falls below 34ºC (93.2ºF), activity of clotting factors and platelets can be affected resulting in a hypercoagulable coagulopathy. Hypothermia also results in decreased oxygen consumption by the brain due to decreased metabolic activity and cerebral oxygen requirements are estimated to be around 50% at a core temperature of 28ºC (82.4ºF) and just 11% at 8ºC (46.4ºF) (2).

Clinical Presentation & Evaluation

When patients with suspected hypothermia present to the ED, it is important to not only expedite the time to rewarming, but also obtain vital signs and an accurate core temperature with a low-reading thermometer. If using a pulse oximeter to monitor oxygen, consider using a forehead or earlobe probe due to the delayed response time (11). Because of the extent of vasoconstriction present in hypothermia, peripheral pulses may not be palpable. In these cases, continuous-wave doppler should be used for a full minute to evaluate for a pulse (10). Point-of-care echocardiography can also be utilized to assess for cardiac motion. The various clinical presentations of hypothermia are listed in the table below (table 3).

Core temperature measurements can be done with a rectal thermometer, an esophageal temperature probe in the distal third of the esophagus if they are intubated, and even a temperature-sensing Foley catheter. Because the rectal and bladder temperatures may lag behind the true core temperature, these should be avoided in critical patients and for the purposes of monitoring the rewarming progress.10 When considering laboratory evaluations for patients with hypothermia, one should attempt to identify the presence of lactic acidosis, rhabdomyolysis, and infection. If coagulation studies are ordered, it is important to consider that the study is performed at 37ºC (98.6ºF) and may result as normal despite an obvious coagulopathy in the patient. If resources allow and indicated, thromboelastography (TEG) may provide additional insight to a patient’s coagulopathy for more focused intervention (12). As rewarming is initiated, patients with moderate and severe hypothermia should have labs closely monitored to evaluate for secondary electrolyte derangements due to the rewarming process.

Management

The primary objectives of managing a patient with hypothermia consist of maintaining airway, breathing, and circulation; preventing further heat loss; initiating an appropriate rewarming strategy; and managing complications as needed (10). Management of concomitant injuries and pathologies should accompany the management of hypothermia, however, will not be discussed here. The rewarming strategy selection should be based on the degree of hypothermia; however, all rewarming strategies begin the same. This includes removal of wet clothing, raise patient’s room temperature, and cover with warm blankets. For patients with mild hypothermia, active external warming should be initiated with forced air warming devices such as a Bair Hugger and application of hot packs. In patients with moderate hypothermia, active external warming will be supplemented with administration of warmed IV fluids and warmed humidified oxygen. For patients with severe hypothermia, the above strategies are implemented with the addition of active internal rewarming procedures, which are selected based on the hemodynamic stability of the patient. If the patient is hemodynamically stable, an endovascular temperature catheter can be placed. If the patient is hemodynamically unstable, extracorporeal membrane oxygenation (ECMO) or cardiopulmonary bypass is the preferred approach. Other strategies such as peritoneal or pleural irrigation with warmed fluids should be reserved for situations where ECMO is not available. 

Because of the severe dehydration and fluid shifts that can accompany hypothermia, patients should have two large-bore peripheral IVs. Intraosseous lines can be placed if peripheral IV access is not achieved (10). If the decision is made to place a central line, placement of a temporary femoral venous catheter is preferred to avoid arrhythmia, however it is important to reconsider this femoral placement should ECMO be indicated. When placing central lines superior to the diaphragm, the operator should take special care to minimize guidewire contact with the irritable myocardium. Any fluids administered to the patient to address hypotension should also be warmed as room-temperature fluids can decrease core temperature. The resuscitation of a hypothermic patient may persist for hours because of hypothermia’s neuroprotective effects. One case study out of Italy describes a patient who suffered a hypothermic cardiac arrest and made a full neurologic recovery after approximately 9 hours of cardiopulmonary resuscitation with nearly half of the time being managed with mechanical CPR (13). Withholding resuscitative efforts should only occur if there is a nonsurvivable injury or fatal illness, the body is frozen to the point of inhibiting adequate chest compressions, or if the airway is compromised with snow and ice (5).  

As rewarming progresses, patients should be closely monitored for the development of complications. Clinicians should be cognizant of the development of core temperature afterdrop, which is an adverse effect of active external rewarming. If the patient’s extremities and core are warmed simultaneously, pooled blood in the extremities can return to the core circulation due to vasodilation and ultimately drop the core temperature and pH. Additionally, the arterial vasodilation can result in hypotension. To minimize the risk of core temperature afterdrop, the patient’s core should be rewarmed prior to the extremities (10). 

When active internal rewarming strategies are indicated, endovascular temperature-control catheters demonstrate success in rewarming patients according to case reports (14). However, when ECMO is selected, it is important to consider the additional risks associated with the highly invasive procedure. The ICE-CRASH study is a multi-center study out of Japan that evaluated the 28-day survival of nearly 500 individuals with severe accidental hypothermia. They found that ECMO improved the survival and neurologic outcomes in patients who experienced cardiac arrest, however there was no significant difference in 28-day survival in patients who did not experience cardiac arrest (15). Therefore, ECMO should ideally be reserved for those who experience cardiac arrest, especially if the risks outweigh the potential benefit in patients who do not experience cardiac arrest. While these active internal rewarming procedures can increase the core temperature rapidly, rewarming should not be too rapid. A study of over 600 patients on ECMO for rewarming following accidental hypothermia found that rewarming rates less than 5ºC per hour are associated with improved survival with good neurological outcomes (16). 

Overall, patients who present to the emergency department with hypothermia can require a significant amount of time and resources for resuscitation. It is important to obtain an accurate core temperature early while minimizing the amount of patient movement. While managing the patient, priorities include maintaining airway, breathing, and circulation; preventing further heat loss; initiating appropriate rewarming procedures; and managing complications as necessary. A significant factor that influences the rewarming strategy is the availability of resources. At the very minimum all hypothermia patients should immediately begin active external rewarming with an emphasis of warming the core first, then extremities to minimize the risk of adverse effects such as core temperature afterdrop. If resources allow, ECMO improves 28-day mortality in severe hypothermia patients who experience cardiac arrest. Aim to rewarm the patient at a rate of no more than 5ºC per hour and monitor serial labs for the development of electrolyte derangements.

AUTHORED BY: LUCAS RAPPERT, OMS4

FACULTY EDITING BY: COLIN MCCLOSKEY, MD

References

1. Van der Ploeg GJ, Goslings JC, Walpoth BH, Bierens JJLM. Accidental hypothermia: Rewarming treatments, complications and outcomes from one university medical centre. Resuscitation. 2010;81(11):1550-1555. doi:10.1016/j.resuscitation.2010.05.023

2. Brown DJA. Hypothermia. In: Tintinalli JE, Ma OJ, Yealy DM, et al., eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 9e. McGraw-Hill Education; 2020. accessemergencymedicine.mhmedical.com/content.aspx?aid=1166810571

3. Dinarello CA, Porat R. Pathophysiology and treatment of fever in adults. In: Post T, ed. UpToDate. Wolters Kluwer; 2023.

4. Jolly BT, Ghezzi KT. Accidental hypothermia. Emerg Med Clin North Am. 1992;10(2):311-327.

5. Lott C, Truhlář A, Alfonzo A, et al. European Resuscitation Council Guidelines 2021: Cardiac arrest in special circumstances. Resuscitation. 2021;161:152-219. doi:10.1016/j.resuscitation.2021.02.011

6. Durrer B, Brugger H, Syme D, International Commission for Mountain Emergency Medicine. The medical on-site treatment of hypothermia: ICAR-MEDCOM recommendation. High Alt Med Biol. 2003;4(1):99-103. doi:10.1089/152702903321489031

7. Pasquier M, Zurron N, Weith B, et al. Deep Accidental Hypothermia with Core Temperature Below 24°C Presenting with Vital Signs. High Alt Med Biol. 2014;15(1):58-63. doi:10.1089/ham.2013.1085

8. Pasquier M, Carron PN, Rodrigues A, et al. An evaluation of the Swiss staging model for hypothermia using hospital cases and case reports from the literature. Scand J Trauma Resusc Emerg Med. 2019;27(1):60. doi:10.1186/s13049-019-0636-0

9. Fukuda M, Nozawa M, Okada Y, et al. Clinical relevance of impaired consciousness in accidental hypothermia: a Japanese multicenter retrospective study. Acute medicine & surgery. 2022;9(1):e730. doi:10.1002/ams2.730

10. Zafren K, Mechem CC. Accidental hypothermia in adults. In: Post T, ed. UpToDate. Wolters Kluwer; 2023.

11. MacLeod DB, Cortinez LI, Keifer JC, et al. The desaturation response time of finger pulse oximeters during mild hypothermia. Anaesthesia. 2005;60(1):65-71. doi:10.1111/j.1365-2044.2004.04033.x

12. Martini WZ, Cortez DS, Dubick MA, Park MS, Holcomb JB. Thrombelastography is better than PT, aPTT, and activated clotting time in detecting clinically relevant clotting abnormalities after hypothermia, hemorrhagic shock and resuscitation in pigs. Journal of Trauma - Injury, Infection and Critical Care. 2008;65(3):535-543. doi:10.1097/TA.0b013e31818379a6

13. Forti A, Brugnaro P, Rauch S, et al. Hypothermic Cardiac Arrest With Full Neurologic Recovery After Approximately Nine Hours of Cardiopulmonary Resuscitation: Management and Possible Complications. Ann Emerg Med. 2019;73(1):52-57. doi:10.1016/j.annemergmed.2018.09.018

14. Laniewicz M, Lyn-Kew K, Silbergleit R. Rapid Endovascular Warming for Profound Hypothermia. Ann Emerg Med. 2008;51(2):160-163. doi:10.1016/j.annemergmed.2007.05.020

15. Takauji S, Hayakawa M, Yamada D, et al. Outcome of extracorporeal membrane oxygenation use in severe accidental hypothermia with cardiac arrest and circulatory instability: A multicentre, prospective, observational study in Japan (ICE-CRASH study). Resuscitation. 2023;182:109663. doi:10.1016/j.resuscitation.2022.12.001

16. Saczkowski R, Kuzak N, Grunau B, Schulze C. Extracorporeal life support rewarming rate is associated with survival with good neurological outcome in accidental hypothermia. Eur J Cardiothorac Surg. 2021;59(3):593-600. doi:10.1093/ejcts/ezaa385

80-year-old female with a past medical history significant for hypertension, hyperlipidemia, coronary artery disease status post coronary artery bypass graft, peripheral arterial disease, diverticulitis, PEG tube placement for chronic dysphagia presented to the emergency department for abdominal pain and confusion. The patient’s family reported that she had been complaining of nausea and abdominal pain for the past day. History from the patient was limited by her confusion but no other known symptoms. Prior CT angiography studies showed stable AAA under 5cm, which was being monitored by her physician.

Her physical exam was remarkable for abdominal tenderness in the right and left lower quadrants and suprapubic region. There was no guarding or rebound tenderness. No obvious neurovascular deficits noted.

Point-of-care ultrasound of aorta was performed to evaluate for change in AAA given her presenting symptoms.

POCUS Findings:

An abdominal aortic aneurysm, measuring approximately 5cm in diameter, is visualized in the infrarenal region with an intramural thrombus.

Abdominal Aortic Aneurysm

Overview/Epidemiology

Abdominal aortic aneurysm (AAA) is a potentially life-threatening condition characterized by dilation of the aorta beyond its normal limits. The size of the aorta is influenced by level of the aorta, age, sex, and body size of the patient, resulting in slight variations in baseline diameter (1).

For example, a population study by Wanhainen et al. found the following average diameters:

• Above the celiac artery: Males: 3.0 cm, females: 2.7 cm

• Above the renal arteries: Males: 2.8 cm, females: 2.7 cm

• Just below the renal arteries: Males: 2.4 cm, females: 2.2 cm

• At aortic bifurcation: Males: 2.3 cm, females: 2.0 cm (2)

Despite this variability, a AAA is generally considered present when the anteroposterior (AP) diameter of the aorta exceeds 3.0 cm. Infrarenal aneurysms are most common (1).

Risk factors for AAA include older age, male gender, tobacco use, family history of aneurysm, and cardiovascular disease are associated with increased risk. The risk of rupture is higher once the aneurysm is greater than 5.5 cm or is increasing in size, if the patient has a history of tobacco use or hypertension, is of the female sex, or is symptomatic (1,3).

Clinical Presentation

The clinical presentation is widely variable. Symptoms, if present, often include abdominal, back, flank pain. However, the majority of patients are asymptomatic at the time of diagnosis, as most AAAs are found incidentally on imaging obtained for other indications or with routine screening (1).

Physical exam findings may include a pulsatile mass. While palpation alone cannot reliably diagnose or rule out AAA, the sensitivity of palpation increases with size of the AAA. In a systemic review of 15 studies involving patients not previously known to have an AAA, the sensitivity of abdominal palpation was 29% for AAA 3.0 to 3.9 cm in diameter, 50% for AAA 4.0 to 4.9 cm, and 76% for AAA 5.0 cm or greater (4).  Additionally, patients may present with limb ischemia if associated with thrombus/embolus.

If AAA rupture has occurred, common symptoms include sudden onset back or abdominal pain, associated tenderness, and syncope. Flank ecchymosis (Grey Turner sign) may develop, and hemodynamic instability and hemorrhagic shock may often ensues (1).

Diagnostic Imaging

Ultrasound is the recommended screening modality based on the United States Preventive Services Task Force Recommendation Statement (5), while CT angiography (CTA) is considered a gold standard for diagnosis and perioperative planning (1). When AAA is suspected, the initial diagnostic imaging modality should be dependent on patient stability. If hemodynamically stable, CT is generally the test of choice as it has greater accuracy and is also more comprehensive in evaluating for other causes. However, if the patient is unstable, a focused ultrasound study at the bedside is preferred.

A study by Costantino et al. found point-of-care ultrasound (POCUS) performed by emergency medicine (EM) residents to have a sensitivity of 94% and specificity of 100%. In addition, they found a 4.4 mm difference in ultrasound measurements compared to CT measurements by radiologists (6). Another study by Foo et al. that also compared CT and ultrasound in patients with AAA>5.0 cm found that there was a significantly greater difference in ultrasound measurements between imaging modalities for patients with AAAs 5.0-5.4cm compared to those >5.5 cm. This suggests that the diagnostic utility of ultrasound may be more limited for smaller aneurysms (7). A more recent systematic review, including seven studies and over 650 patients, looking at the diagnostic accuracy of POCUS for AAA showed a pooled sensitivity and specificity of 99 and 98%, respectively (8). Collectively, these studies support that ultrasound is a valuable diagnostic tool for emergency physicians, including residents, to quickly evaluating for AAA size.

Management

Surgical repair is recommended for patients have symptoms attributable to their AAA, regardless of size. For asymptomatic AAA < 5.5 cm, conservative management is indicated. This includes smoking cessation, medication/comorbidity optimization, and surveillance imaging using ultrasound or CT every 6 months for aneurysms 5.0-5.4 cm, every 12 months if 4.0-4.9 cm, and less frequently for smaller aneurysms. Elective repair is most effective for preventing rupture but is not indicated until the risk of rupture outweighs risks of surgery. Once AAA exceeds 5.5 cm, repair is generally indicated due to increased risk of rupture but taking other risk factors into account. Earlier elective repair may be appropriate in certain circumstances including rapidly expanding AAA (>0.5 cm in six months or >1 cm per year), female sex, saccular aneurysm, coexistent aneurysm or peripheral artery disease (1, 9).

Point-of-Care Ultrasound of the Aorta

Key Clinical Question: Is there an aortic aneurysm?

We’ll focus on the abdominal aorta here.

Technique

• Use a low frequency transducer (curvilinear probe is ideal but phased array also works) and use an abdominal preset on your machine

• Place the patient in a supine position

• Place the transducer just below the xiphoid process in a transverse orientation with the indicator pointing toward the patient’s right

• Identify the vertebral body, which appears as a hyperechoic arch with dense shadowing posterior to it. Just anterior to this is the aorta on the patient’s left and the inferior vena cava (IVC) on the patient’s right.

• Evaluate the abdominal aorta in a transverse plane from the level of the celiac trunk down to the bifurcation. Ideally, you can visualize the entirety of the aorta but, at mimimum, should obtain views of the following segments:

  • Proximal aorta: at level of the celiac trunk or liver tip

  • Mid aorta: below the SMA branch point

  • Distal aorta: proximal to the bifurcation

  • Bifurcation to the iliac arteries

• Measure the anterior-posterior (AP) diameter of the aorta from outer wall to outer wall in the transverse view. A normal aorta is less than 3 cm. Normal measurements of the iliac arteries should each be less than 1.5 cm.

• It is also important to include a longitudinal view of the aorta. This can be obtained by rotating the transducer 90 degrees so the probe marker points toward the patient’s head. This helps characterize the type of aneurysm (fusiform vs saccular) and potentially visualize areas that might have been missed in the transverse view (10-11).

Overcoming Bowel Gas: Some Helpful Tips

Bowel gas is often present and can significantly limit visualization of the aorta. Here’s a few ways to try to overcome this:

• Apply gentle, downward pressure with the transducer for up to 1-2 minutes to help displace bowel gas. This is referred to as graded compression.

• Consider repositioning patient in the right decubitus position to help move bowel gas away from the aorta.

• If having difficulty visualizing the distal aorta or bifurcation, you can move the probe below the umbilicus and fan the probe so that it’s directed cephalad.

• Can also try to view the aorta via an oblique angle with the probe placed lateral to the aorta but pointing toward midline (10-11)

Key Pathology, Pearls, Pitfalls

• AAA is diagnosed when the diameter exceeds 3.0 cm. For iliac arteries, an aneurysm is when their diameter is > 1.5cm.

• An intramural thrombus is often present and typically has an echogenic appearance. As a result, the inner rim may be mistaken for the aortic wall, which can lead to a falsely normal measurement if only the patent lumen is measured. This is why measuring outer wall to outer wall is important.

• Some aortas have a tortuous course, so it is important to measure AP diameter to minimize risk of getting an oblique measurement

• Color doppler may show turbulent or bidirectional flow. When a thrombus is present, decreased or absent flow may be seen (10-11).

• Signs of rupture are often not easily seen on POCUS, as it is limited in evaluating the retroperitoneum. Some potential findings may include AAA deformation, hemoperitoneum, para-aortic hemorrhage, retroperitoneal hematoma (12).

——

Case Conclusion:

CT showed similar size and extent of her AAA compared to prior studies. Given her symptoms, vascular surgery was consulted to evaluate the patient in the emergency department. Surgery opted to hold off on emergent intervention but recommended strict blood pressure (BP) and heart rate (HR) control and planned to follow the patient. The patient was started on esmolol and nicardipine with systolic BP goal < 120 mmHg and HR < 70 bpm. She was continued on aspirin 81 mg, Plavix 75 mg, and Rosuvastatin 40 mg daily. Vascular surgery planned to perform endovascular aortic repair (EVAR). However, the patient developed a urinary tract infection, and due to risk of graft infection, outpatient repair was scheduled once her infection improved.

AUTHORED BY: ANNIE THAI, MD, PGY1

FACULTY CO-AUTHOR/EDITOR: LAUREN MCCAFFERTY, MD

References

1. Hirsch AT, Haskal ZJ, Hertzer NR, et al. ACC/AHA 2005 Practice Guidelines for the management of patients with peripheral arterial disease (lower extremity, renal, mesenteric, and abdominal aortic): A Collaborative Report from the American Association for Vascular Surgery/Society for Vascular Surgery, Society for Cardiovascular Angiography and Interventions, Society for Vascular Medicine and Biology, Society of Interventional Radiology, and the ACC/AHA Task Force on Practice Guidelines. Circulation. 2006; 113(11):e463-654

2. Wanhainen A, Themudo R, Ahlström H, Lind L, Johansson L. Thoracic and abdominal aortic dimension in 70-year-old men and women--a population-based whole-body magnetic resonance imaging (MRI) study. J Vasc Surg. 2008; 47(3):504-12.

3. Kent KC , Zwolak RM, Egorova NN, et al. Analysis of risk factors for abdominal aortic aneurysm in a cohort of more than 3 million individuals. J Vasc Surg. 2010; 52 (3): 539-548.

4. Lederle FA, Simel DL. The rational clinical examination. Does this patient have abdominal aortic aneurysm? JAMA. 1999;281(1):77-82).

5. US Preventive Services Task Force. Screening for Abdominal Aortic Aneurysm: US Preventive Services Task Force Recommendation Statement. JAMA. 2019;322(22):2211–2218.

6. Costantino TG, Bruno EC, Handly N, Dean AJ. Accuracy of emergency medicine ultrasound in the evaluation of abdominal aortic aneurysm. J Emerg Med. 2005;29(4):455-60.

7. Foo FJ, Hammond CJ, Goldstone AR, et al. Agreement between Computed Tomography and Ultrasound on Abdominal Aortic Aneurysm and Implications on Clinical Decisions. Eur J Vasc Endovasc Surg. 2011; 42, 608-614.

8. Rubano E, Mehta N, Caputo W, Paladino L, Sinert R. Systematic review: emergency department bedside ultrasonography for diagnosing suspected abdominal aortic aneurysm. Acad Emerg Med. 2013;20(2):128-38

9. Chaikof EL, Dalman RL, Eskandari MK, et al. The Society for Vascular Surgery practice guidelines on the care of patients with an abdominal aortic aneurysm. J Vasc Surg. 2018;67(1):2-77.e2

10. Noble V, Nelson B. Manual of Emergency Medicine and Critical Care Ultrasound, 2nd ed. Cambridge: Cambridge UP, 2011.

11. Risler Z, Dean AJ, Ku BS. Abdominal aortic aneurysm (AAA). American College of Emergency Physicians Sonoguide. August 2020. Accessed January 2024. https://www.acep.org/sonoguide/basic/aorta

12. Catalano O, Siani A. Ruptured abdominal aortic aneurysm. Categorization of sonographic findings and report of 3 new signs. J Ultrasound Med. 2005;24(8):1077–1083

• ‘Whip-its’ (aka Laughing Gas; Cartridges; Hippy Crack; N2O, Nangs) are terms for intentionally inhaled Nitrous Oxide.

• Nitrous oxide is an odorless and colorless gas used in anesthesia and as a propellant (think the last two seconds of a can of whipped cream)

Historical Origins of Recreational Use of Nitrous Oxide

• In 1772 Nitrous Oxide is discovered by English chemist and philosopher Joseph Priestly

• In 1800 British chemist Humphry Davy publishes a book about the properties, psychotropic effects included.  

• Initially, use was fairly limited, with artists, scientists, and medical students utilizing the drug

• Increased availability of the drug and popular users such as members of the Grateful Dead, caused a surge in the drugs’ popularity in the 1960’s

User Experience

• Those who use Nitrous Oxide for recreational purposes describe a brief, euphoric disorientation and depersonalization. Experiences range from an experience of giddiness, to hallucinations, to loss of consciousness.

• “Basically, at the beginning of the experience one feels what I would call a 'beer buzz'. You are happy and may giggle or find regular things quite amusing. Next, a stage of confusion begins. If one's eyes are kept open you may hallucinate. I quite vividly saw things that could not have possibly existed.” –Testimonial of Nitrous Oxide recreational use

Mechanism of Action by Effect

• Anesthetic effect- non-competitive NMDA inhibition in the central nervous system.

• Analgesic- Causes the release of endogenous opioids

• Anxiolysis- GABA-A activation via voltage-independent Calcium channels

Adverse Effects

• Respiratory Depression- Nitrous Oxide in isolation seems to have a limited effect, however when used in conjunction with other agents such as sedatives, hypnotics, or opioids, as it often is when used as a drug of abuse/misuse, it potentiates the depressing effects of these agents. Deaths have occurred with this concomitant usage and resulting traumatic injuries

• Diffusion hypoxia: After use, Nitrous Oxide enters the alveolar space faster than Nitrogen leaves, this leads to a dilution of the alveolar gases, specifically oxygen, resulting in hypoxia. In fact, many users describe an ‘air-hunger’ phenomenon immediately after use

• Impairment of DNA synthesis, methylation, and myelin production- Nitrous Oxide irreversibly oxidizes the cobalt ion of cobalamin, rendering cobalamin unusable in its typical role as a co-enzyme in the formation of methionine. This results in a functional deficiency of B12. This can lead to megaloblastic anemia and subacute combined degeneration of the spinal cord, which often presents as paresthesia, ataxia, and flaccid weakness

• Coagulopathy- More recently, chronic usage of Nitrous Oxide has been implicated in STEMI and Venous Thromboembolism through use-associated hyperhomocysteinemiaresulting from the functional B12 deficiency

Management in Toxicity

• Neurologic deficits, while some may be permanent based on the degree of damage, can sometimes be reversible

• Abstinence from Nitrous Oxide is essential to allow for the proper utilization of B12

• Treatment regimens vary based on practice pattern but typically include either IM or PO formulations of Vitamin B12

• Symptomatic management for issues of hypoxia, venous thromboembolism, and other associated complications

Nitrous in the News

AUTHORED BY: GABE ALAGNA, MD, EM PGY1

FACULTY EDITING BY: LAUREN PORTER, DO

References

• Brice, L. (n.d.). Grateful dead lyricist and Electronic Freedom Foundation co-founder... Getty Images. https://www.gettyimages.in/detail/news-photo/grateful-dead-lyricist-and-electronic-freedom-foundation-co-news-photo/915950002

• Davy, H. (1800). Researches chemical and philosophical: Chiefly concerning nitrous oxide or dephlogisticated nitrous air and its respiration / by Humphry Davy. Wellcome Collection. https://wellcomecollection.org/works/wtdr8dvd/items?canvas=7

• Gillman, M. A. (2019). Mini-Review: A brief history of nitrous oxide (N2O) use in Neuropsychiatry. Current drug research reviews. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6637098/

• Gupta, P. K. (1970, January 1). Mechanism of nanotoxicity. SpringerLink. https://link.springer.com/chapter/10.1007/978-3-031-24287-8_3

• James , B. (2005). Nitrous Oxide Revelations of God and Eternity. Nitrous oxide - EROWID exp - “nitrous oxide revelations of god and eternity.” https://www.erowid.org/experiences/exp.php?ID=36803

• Knuf, K. (n.d.). Nitrous oxide - statpearls - NCBI bookshelf. Nitrous Oxide . https://www.ncbi.nlm.nih.gov/books/NBK532922/

• Marcus, E. (2021, January 30). Nitrous Nation. The New York Times. https://www.nytimes.com/2021/01/30/style/nitrous-oxide-whippets-tony-hsieh.html

• Schaffer, D., & Goldfine, C. (2021). Nitrous Oxide Misuse and abuse. ACEP Symbol. https://www.acep.org/toxicology/newsroom/jun2021/nitrous-oxide-misuse-and-abuse

• Shoults, K., & Barbara Mozingo. (2016). case report: Neurological complications of nitrous oxide abuse. BCMJ, vol. 58, no. 4, page(s) 192-194. https://bcmj.org/articles/case-report-neurological-complications-nitrous-oxide-abuse

• TodayShow. (2022, August 30). Why you now need to be 21 to buy canned whipped cream in New York. TODAY.com. https://www.today.com/food/news/why-you-need-id-to-buy-canned-whipped-cream-in-new-york-rcna45419

• U.S. National Library of Medicine. (n.d.). Nitrous oxide. National Center for Biotechnology Information. PubChem Compound Database. https://pubchem.ncbi.nlm.nih.gov/compound/Nitrous-Oxide

Resuscitative Endovascular Balloon Occlusion of the Aorta (REBOA) is a rapidly employed, minimally invasive procedure available for the treatment of life-threatening, non-compressible hemorrhage of the trunk and junctional regions (axilla and groin). Unlike hemorrhage from an injured extremity, which may be staunched with compression and tourniquet use and therefore generally has good outcomes [1], junctional hemorrhage can only be controlled by surgical and endovascular techniques. Due to delays in hemorrhage control, torso injuries account for roughly 90% of exsanguination deaths [2].

Several temporizing measures are available prior to definitive hemorrhage control. The emergent resuscitative thoracotomy (ERT) has been used since at least 1906 for the management of profound hemorrhagic shock due to penetrating thoracic trauma [3]. This procedure involves an incision in the anterior chest extending to the pleural space, and as appropriate clamping of the source of bleeding, pericardiotomy, cross-clamping of the descending aorta, and cardiac massage [3]. Understandably, this extremely invasive procedure is appropriate only for patients in extremis with loss of vital signs, is associated with numerous complications, and typically has poor outcomes [4,5].

REBOA offers a less invasive and potentially more effective alternative to ERT with aortic cross-clamping. This technique uses the percutaneous insertion of a balloon that inflates in the aorta and has been employed in traumas since the Korean War.[6] REBOA has recently gained popularity, although it is still not widely used and has experience in civilian populations is limited.

Method

The steps for performing REBOA are summarized below in Table 1. Briefly, a catheter is advanced to the aorta through access via the common femoral artery (CFA). The balloon may be inflated to partially or completely occlude either the descending thoracic aorta in Zone 1 or the infrarenal abdominal aorta in Zone 3, depending on the suspected location of the hemorrhage (Figure 1) [7]. Occlusion in Zone 1 reduces bleeding within the abdomen, pelvis, and lower extremities, whereas occlusion in Zone 3 preserves perfusion to the abdomen while reducing bleeding from the pelvis and lower extremities [5].

The aortic occlusion time should be monitored and limited, proceeding to definitive hemorrhage control as rapidly as possible, ideally within 15 minutes of REBOA placement in Zone 1 or within 30 minutes of placement in Zone 3 [7]. Although there is insufficient evidence for its efficacy, some centers have protocolized partial occlusion or intermittent occlusion of the aorta with REBOA to minimize complications [8,9].

Potential Benefits of REBOA

REBOA is used in the management of life-threatening hemorrhage from non-compressible sites. It blocks blood loss inferiorly, improving cardiac index and thus maintaining cerebral and myocardial perfusion [2,10]. Some studies suggest that REBOA improves survival in patients with hemorrhagic shock not requiring cardiopulmonary resuscitation when compared to ERT [11]. REBOA has also been proposed for use in hypotensive patients at risk for hemorrhagic shock but who do not meet criteria for ERT [9].

Potential Risks of REBOA

There are significant ischemic risks distal to the REBOA balloon due to the temporary occlusion of the aorta. These effects may result in local ischemia, reperfusion injury causing kidney injury or multisystem organ failure, and systemic metabolic acidosis [12,13]. Complications are possible at the CFA access site, including hematoma, dissection, pseudoaneurysm, thromboembolism, and limb ischemia resulting in amputation [13]. Aortic injury can also occur during catheterization and balloon inflation, causing intimal tears, dissections, and ruptures that may be fatal [13].  

Current & Future Directions

While the idea of temporary aortic occlusion prior to definitive hemorrhage control is conceptually attractive and is well supported by large animal studies [14], the current evidence for REBOA in humans is inadequate and inconsistent [7]. Most reports of REBOA use come from case series and cohort studies and even the three most recent reviews and meta-analyses have arrived at divergent results [2,5,15]. The only randomized clinical trial of REBOA use, published this year, was a small study performed in United Kingdom emergency departments that found that REBOA with standard of care was associated with an increased frequency of mortality due to hemorrhage when compared to standard of care alone [16]. However, this study population was composed predominantly of blunt trauma victims and had a relatively long period time from injury to balloon deployment. These factors may have limited the generalizability of the study results. Despite equipoise in the data, a joint statement by the American College of Surgeons and the American College of Emergency Physicians recommends REBOA for management of hemorrhagic shock resulting from traumatic vascular injury below the diaphragm that is not responsive to resuscitation [7]. Additionally, military guidelines recommend REBOA in certain cases of blunt and penetrating traumatic cardiac arrest [10].

Due to a relatively recent resurgence in interest, insufficient data supporting its clinical use, and resource and training limitations, most trauma centers in the U.S. do not perform REBOA. A minority of large-volume institutions have protocolized REBOA for the management of non-compressible torso and junctional hemorrhage, yet there are no standardized society guidelines regarding its indications or methods to minimize its complications.

Establishing guidelines for REBOA is difficult due to inherent problems in studying its clinical use. Comparing REBOA with ERT or other hemorrhage control measures typically involves selection bias and confounding, as patients receiving ERT are already in cardiac arrest and will therefore reliably have worse outcomes, whereas patients receiving REBOA have already failed resuscitation, thus reliably favoring other hemorrhage control measures [7]. Due to resource constraints, most studies do not examine outcomes after the initial resuscitation and thus fail to measure delayed complications or mortality. Future research should focus on comparing REBOA with ERT or standard of care using randomized controlled trials and should include patients presenting with diverse etiologies of exsanguinating hemorrhage.

AUTHORED BY: MATTHEW MCCABE, MS4 CWRU SOM

FACULTY EDITING BY: COLIN MCCLOSKEY, MD

References

1. Kauvar, D.S., Lefering, R., Wade, C.E. (2006). Impact of Hemorrhage on Trauma Outcome: An Overview of Epidemiology, Clinical Presentations, and Therapeutic Considerations. Journal of Trauma and Acute Care Surgery, 60(6), S3-S11. http://doi.org/10.1097/01.ta.0000199961.02677.19

2. Borger van der Burg, B.L.S., van Dongen, T.T.C.F, Morrison, J.J., Hedeman Joosten, P.P.A, DuBose, J.J., Horer, T.M., & Hoencamp, R. (2018). A Systematic Review and Meta-analysis of the use of Resuscitative Endovascular Balloon Occlusion of the Aorta in the Management of Major Exsanguination. European Journal of Trauma and Emergency Surgery, 44, 535-550. https://doi.org/10.1007/s00068-018-0959-y

3. Pust, G.D., & Namias, N. (2016). Resuscitative thoracotomy. International Journal of Surgery, 33, 202–208. https://doi.org/10.1016/j.ijsu.2016.04.006

4. Morrison, J.J. & Rasmussen, T.E. (2012). Noncompressible Torso Hemorrhage: A Review with Contemporary Definitions and Management Strategies. Surgical Clinics of North America, 92, 843-858. https://doi.org/10.1016/j.suc.2012.05.002

5. Castellini, G., Gianola, S., Biffi, A., et al. (2021). Resuscitative Endovascular Balloon Occlusion of the Aorta (REBOA) in Patients with Major Trauma and Uncontrolled Haemorrhagic Shock: A Systematic Review with Meta-analysis. World Journal of Emergency Surgery, 16(41). https://doi.org/10.1186/s13017-021-00386-9

6. Hughes, C. (1954). Use of an Intra-aortic Balloon Catheter Tamponade for Controlling Intra-abdominal Hemorrhage in Man. Surgery, 36(1), 65. https://doi.org/10.5555/uri:pii:0039606054902664

7. Bulger, E.M., Perina, D.G., Qasim, Z., et al. (2019). Clinical use of Resuscitative Endovascular Balloon Occlusion of the Aorta (REBOA) in Civilian Trauma Systems in the USA, 2019: A Joint Statement From the American College of Surgeons Committee on Trauma, the American College of Emergency Physicians, the National Association of Emergency Medical Services Physicians and the National Association of Emergency Medical Technicians. Trauma Surgery & Acute Care Open, 4, 1-6. https://doi.org/10.1136/tsaco-2019-000376

8. Dubose, J.J. (2017). How I do it: Partial Resuscitative Endovascular Balloon Ccclusion of the Aorta (P-REBOA). Journal of Trauma & Acute Care Surgery, 83,197–199. https://doi.org/10.1097/TA.0000000000001462.

9. Russo, R.M., White, J.M., Baer, D.G. (2021). Partial Resuscitative Endovascular Balloon Occlusion of the Aorta: A Systematic Review of the Preclinical and Clinical Literature. Journal of Surgical Research, 262, 101-114. https://doi.org/https://doi.org/10.1016/j.jss.2020.12.054

10. Glaser, J., Stigall, K., Cannon, J., et al. (2020). Resuscitative Endovascular Balloon Occlusion of the Aorta (REBOA) for Hemorrhagic Shock. Joint Trauma System Clinical Practice Guideline. Accessed: http://prytimemedical.com/wp-content/uploads/2017/07/REBOA_-CPG_FINAL.pdf

11. Brenner, M., Inaba, K., Aiolfi, A., et al. (2018). Resuscitative Endovascular Balloon Occlusion of the Aorta and Resuscitative Thoracotomy in Select Patients with Hemorrhagic Shock: Early Results from the American Association for the Surgery of Trauma's Aortic Occlusion in Resuscitation for Trauma and Acute Care Surgery Registry. Journal of the American College of Surgery, 226(5), 730-740. https://doi.org/10.1016/j.jamcollsurg.2018.01.044

12. Joseph, B., Zeeshan, M., Sakran, J.V., et al. (2019). Nationwide Analysis of Resuscitative Endovascular Balloon Occlusion of the Aorta in Civilian Trauma. JAMA Surgery, 154(6), 500-508. https://doi.org/10.1001/jamasurg.2019.0096

13. Manzano-Nunez, R., Claudia, O., Herrera-Escobar, J., et al. (2018). A Meta-analysis of the Incidence of Complications Associated with Groin Access After the use of Resuscitative Endovascular Balloon Occlusion of the Aorta in Trauma Patients. Journal of Trauma and Acute Care Surgery, 85(3), 626-634. https//doi.org/10.1097/TA.0000000000001978

14. White, J.M., Cannon, J.W., Stannard, A., Markov, N.P., Spencer, J.P., & Rasmussen, T.E. (2011). Endovascular Balloon Occlusion of the Aorta is Superior to Resuscitative Thoracotomy with Aortic Clamping in a Porcine Model of Hemorrhagic Shock. Surgery, 150(3), 400-409. https://doi.org/10.1016/j.surg.2011.06.010

15. Bekdache, O., Paradis, T., Shen, Y.B.H., et al. (2019). Resuscitative Endovascular Balloon Occlusion of the Aorta (REBOA): A Scoping Review Protocol Concerning Indications, Advantages and Challenges of Implementation in Traumatic Non-compressible Torso Hemorrhage. BMJ Open, 9(2), e027572. https://doi.org/10.1136/bmjopen-2018-027572

16. Jansen, J.O., Hudson, J., Cochran, C., et al. (2023). Emergency Department Resuscitative Endovascular Balloon Occlusion of the Aorta in Trauma Patients with Exsanguinating Hemorrhage: The UK-REBOA Randomized Clinical Trial. JAMA, 330(19), 1862-1871. https://doi.org/10.1001/jama.2023.20850

35-year-old male with a history of IV drug use who presented to the ED for left lower extremity pain and swelling. He stated that his leg and foot starting to swell the previous day with associated pain with ambulation. He attempted to go to urgent care but due to long wait times, he eventually left prior to being seen. He noted that the swelling had progressed that morning, ultimately convincing him to return to the ED. The patient denied any trauma to his leg and stated that he thought he may have been bitten by a spider, although he did not remember seeing one. He was noted to have superficial abrasions to his left leg, and he stated that he scraped his left shin two days prior while riding a bike. He denied any significant medical history, including HIV or malignancy, and denied any other systemic symptoms. Additionally, he stated that he had been sober and drug-free for several years.

The patient’s vital signs remained stable in the ED, and he did not appear septic. Physical exam revealed left lower extremity edema, erythema, and induration from below the knee through the foot (see photo to the right) with associated tenderness to palpation. However, no crepitus, bleeding, or purulent drainage was noted. As you can see in the photo, the demarcation line was marked by a skin pen for continued monitoring. There were no signs of a bite found. His dorsalis pedis pulse was 1+.

Point-of-care ultrasound (POCUS) was performed to evaluate for abscess and cellulitis given the exam findings and HPI.

POCUS Findings:

There is extensive cobblestoning in the subcutaneous tissues throughout the affected lower extremity without evidence of any focal fluid collections. This signifies cellulitis without signs of abscess or deeper infection.

Cellulitis

Emergency departments see approximately 6 million patients per year for cellulitis or abscess, with the annual incidence of cellulitis ranging from 22 to 50 per 1000 persons (1). In the United States, there are more than 14 million cases every year (2, 3). It is relatively rare that a patient with cellulitis requires hospitalization, happening in less than 10% of cases with an associated mortality rate of 2.5%. The severity and rate of hospitalization increases for patients over the age of 55 (1,4).

Cellulitis is a form of skin and soft tissue infection. The skin is comprised of three layers; the epidermis, dermis, and hypodermis. Cellulitis is a bacterial infection arising from a cutaneous disruption that primarily affects the middle layer of skin, the dermis, and can extend into underlying tissue. This, in turn, causes a robust inflammatory response with neutrophil infiltration and cytokine production (1-2). An abscess, a collection of pus within the dermis or hypodermis, occurs in a similar fashion but can also include phagocytosis, liquefactive necrosis, and edema due to a portal of entry such as a wound or hair follicle. A fibrous capsule then develops, which is often subsequently surrounded by erythema and induration. Purulent cellulitis is when the erythema and induration spread beyond the margins of the abscess (1).

Staphylococcus and Streptococcus are the two most common bacteria that cause cellulitis. Streptococcus species account for greater than 70% of cases, with Group A streptococcus (Strep. pyogenes) being the most common. Staphylococcus Aureus is the next most common, diagnosed in 14%-27% of cellulitis cases. While a common concern in skin infections, methicillin-resistant Staph. aureus (MRSA) only accounts for approximately 4% of nonpurulent cellulitis. On the other hand, S. Aureus is found as the cause for 60-75% of abscesses, with MRSA accounting for up to 70% of these. Polymicrobial abscesses, which include anaerobic microbes, are common in injection drug users (1,5).

Cellulitis is generally a clinical diagnosis, usually presenting with pain, warmth, edema, tenderness, and poorly demarcated erythema. Oftentimes, it can be challenging to differentiate cellulitis from abscess based on physical exam alone, which has treatment implications since an abscess warrants incision and drainage (I&D) rather than antibiotics alone (1-2). Unfortunately, many common diagnostic tests have poor diagnostic utility. For example, white blood cell count, c-reactive protein, erythrocyte sedimentation rate, and procalcitonin are not always elevated and none are specific (2,6). In addition, blood cultures also do not have high yield, as a meta-analysis showed that patients with cellulitis only had a positive blood culture 7.9% of the time (7). Thus, the Infectious Diseases Society of America (IDSA) does not recommend routine blood cultures unless the patient is systemically ill, immunocompromised, or at risk of atypical infections (5). In cases of abscesses, the IDSA does recommend a culture of the purulent fluid - I&D is the primary treatment - though empiric treatment is reasonable in most cases since the majority of these infections are due to MRSA (5). Plain radiographs are neither sensitive nor specific (1)

POCUS for Soft Tissue Infections

In contrast to labs and plain radiographs, POCUS is a highly useful adjunct to the clinical assessment for cases of suspected cellulitis and abscess, particularly in distinguishing between the two. A systematic review and meta-analysis found POCUS to be 98.7% sensitive and 91% specific in differentiating abscess from cellulitis in adults. They also found that POCUS led to a correct change in management in 10.3% of cases with a number needed to treat of 10 (8). By allowing providers to directly visualize whether or not a fluid collection is present, POCUS can indicate the need for I&D or avoid an unnecessary procedure, while also providing guidance for further imaging or involvement of consultants. POCUS may also identify signs of a more serious infection, such as a necrotizing infection or joint involvement, which can help expedite appropriate management (9-10).

Technique & Findings

The high-frequency linear array transducer is typically the most useful to assess for cellulitis and abscess due to the relatively superficial location of the areas affected. In normal skin and soft tissue, the epidermis and dermis sonographically appear as a relatively hyperechoic structure at the top of the screen. Underlying this is the subcutaneous tissue in which adipose has a hypoechoic (dark gray to almost black) appearance with interspersed fine hyperechoic lines of connective tissue. Deep to this are fascial planes, appearing as distinct hyperechoic membranes, and muscle tissue which has a linear fibrous appearance in long axis. Finally, just below the muscle layer is the highly hyperechoic cortical bone with posterior shadowing due to its highly reflective surface (11-12). Understanding this sonoanatomy is important for soft tissue POCUS evaluations for cellulitis and abscesses; for both, the area of focus is in the more superficial layers.

Scanning for cellulitis is best accomplished by scanning in two planes throughout the affected area, in addition to areas both proximal and distal to this. Cellulitis findings on ultrasound progress through stages based on severity. In early cellulitis, the subcutaneous tissue appears thickened and has increased echogenicity with blurring or delineation of the typical sharp edges of soft tissue planes, see Figure 2. As it progresses, there will be more fat stranding and fluid accumulating in the subcutaneous tissue. Mature cellulitis appears as fluid in the interstitial space between the more hyperechoic fat lobules, described as “cobblestoning” due to its similarity to a cobblestone street (11-12); see Figure 2. It is also important to note that cobblestoning is not specific and can be seen in cases of lymphedema or volume overload (11).

As mentioned previously, discerning an abscess from cellulitis is a key role for POCUS. An abscess appears as a localized collection of fluid typically within the loose connective layer of subcutaneous adipose. It is often largely anechoic or hypoechoic but may contain echogenic debris and often has posterior acoustic enhancement (11-12). It is important to assess the extent of a distinct fluid collection by fanning through the entire structure in two planes. To help verify the presence of an abscess using POCUS, apply intermittent pressure over the area of concern and assess for compressibility. Being a pocket of fluid, an abscess will “squish”, whereas non-localized soft tissue edema or solid structures will not (11). In addition, purulent material can be visualized on ultrasound as echogenic debris that swirls with compression or the presence of loculations, which can help differentiate an abscess from other mimics, such as a simple cyst. It is important to apply color doppler over a fluid collection to ensure it is not a vascularized structure, such as a pseudoaneurysm, and to identify surrounding vasculature and other structures, especially when considering I&D. For both cellulitis and abscess, it is imperative to take into account the clinical context and consider potential mimics on ultrasound, such as non-infectious edema, lymph nodes, vasculature, or even herniated bowel (11-12).

Necrotizing fasciitis is a rapidly progressing, life-threatening soft tissue infection that needs timely surgical intervention. In early stages, the findings can mimic those of cellulitis. However, as the infection progresses, fluid along the fascial plane will develop, see Figure 5. A late, but pathognomonic, finding is the presence of air in the subcutaneous tissues. Sonographically this appears as hyperechoic foci with “dirty shadowing” (10).

Case Conclusion:

An x-ray was performed and was negative for gas, fracture, or foreign body. Lab work revealed a leukocytosis of 13 with a neutrophil predominance and normal lactate. POCUS findings were used in conjunction with the other clinical findings to support a diagnosis of cellulitis. The patient was given broad spectrum antibiotics along with IV fluids. He was then admitted for observation and continued treatment with IV antibiotics. After twenty-four hours, his vitals remained stable, pain was well-controlled with ibuprofen, and there was regression of the infection from the delineated border. Having met those criteria, he was discharged on keflex and ibuprofen with a follow-up appointment with his PCP in one week.

Take Home Message

Cellulitis is a clinical diagnosis but POCUS is a great adjunct to your physical exam, especially when the clinical picture is not obvious. POCUS is especially useful in differentiating cellulitis from abscess, which can guide treatment and indicate need for additional imaging or surgical consultation.

POST BY: DAVID WILLIAMS, DO, PGY1

FACULTY CO-AUTHOR/EDITOR: LAUREN MCCAFFERTY, MD

References

1. Long, B., Gottleib, M. Diagnosis and Management of Cellulitis and Abscess in the Emergency Department Setting: An Evidence-Based Review. J Emerg Med. 2022; 62(1): 16-27.

2. Raff AB, Kroshinsky D. Cellulitis: a review. JAMA. 2016; 316:325–37.

3. Brown BD, Hood Watson KL. Cellulitis. [Updated 2023 Aug 7]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023. Available from: https://www.ncbi.nlm.nih.gov/books/NBK549770/

4. McNamara DR, Tleyjeh IM, Berbari EF, et al. Incidence of lower-extremity cellulitis: a population-based study in Olmsted county, Minnesota. Mayo Clin Proc. 2007; 82:817–21.

5. Stevens DL, Bisno AL, Chambers HF, et al. Practice guidelines for the diagnosis and management of skin and soft tissue infections: 2014 update by the Infectious Diseases Society of America. Clin Infect Dis. 2014;59(2):e10–52.

6. Lazzarini L, Conti E, Tositti G, de Lalla F. Erysipelas and cellulitis: clinical and microbiological spectrum in an Italian tertiary care hospital. J Infect. 2005; 51:383–9.

7. Gunderson  CG, Martinello  RA.  A systematic review of bacteremias in cellulitis and erysipelas.  J Infect. 2012; 64(2):148-155. 

8. Gottlieb M, Avila J, Chottiner M, Peksa GD. Point-of-care ultrasonography for the diagnosis of skin and soft tissue abscesses: a systematic review and meta-analysis. Ann Emerg Med. 2020;76(1):67– 77.

9. Adhikari S, Blaivas M. Utility of bedside sonography to distinguish soft tissue abnormalities from joint effusions in the emergency department. J Ultrasound Med. 2010; 29:519–526.

10. Gan RK, Sanchez Martinez A, Abu Hasan MA, Castro Delgado R, Arcos González P. Point-of-care ultrasonography in diagnosing necrotizing fasciitis-a literature review. J Ultrasound. 2023; 26(2):343-353

11. Burgin C, Morrow D. Utility of POCUS in skin and soft tissue infection. J Urgent Care Med. June 2020; 17-21.

12. Euerle B. “Abscess Evaluation”. American College of Emergency Physicians Sonoguide. Aug 2020. Available from: https://www.acep.org/sonoguide/procedures/abscess-evaluation

While a resuscitative thoracotomy is one of the most extreme and invasive procedures performed in the emergency department, it can be simplified into five major steps: incision, hemorrhage management, pericardiotomy, aortic cross-clamping, cardiac massage, and repair. (3) There are two primary incision options: a left anterolateral thoracotomy in the fifth intercostal space, typically used for patients in extremis or cardiac arrest, and the clamshell incision, which is preferred for patients suspected of having hemorrhage in the right chest cavity. (4) Once the chest is opened, any bleeding from obvious sources should be controlled. Lungs are a potential source of major bleeding, which can be controlled by directly clamping injured lung tissue, clamping the pulmonary hilum, or using the pulmonary hilar twist maneuver. (3) The pericardiotomy is made anterior and parallel to the phrenic nerve, while gently pushing the lung away from the heart in a posterior direction. Cross-clamping of the descending aorta, just above the diaphragm, helps reduce bleeding from intraabdominal or lower extremity injuries and redirects resuscitative circulation to vital organs, particularly the heart, lung, and brain. Cardiac massage involves using both hands to massage the heart at a rate between 80 and 100 compressions per minute. (4)

While the popularity of the resuscitative thoracotomy has fluctuated over the years, it has become a staple intervention for patients in profound refractory shock and those near death due to blunt or penetrating trauma. (5) The history of the resuscitative thoracotomy dates back to the 19th century and has continually evolved since its inception. In 1874, Schiff first described open cardiac massage, and in 1901, Igelsrud reported the first successful resuscitation of a trauma patient in cardiac arrest undergoing a resuscitative thoracotomy and open heart massage. The procedure took on a familiar form in 1906 when Spangaro described the classic left anterolateral thoracotomy incision used for resuscitative thoracotomies. (4) While this highly invasive procedure fell out of favor for less invasive interventions in the 1940s, it regained traction in the 1960s for resuscitating patients with penetrating cardiovascular injuries. (5)

There has been much controversy surrounding the use of resuscitative thoracotomy given the possibilities of severe anoxic brain injury risk to patients and blood-borne pathogen exposure risk to health care providers but has generally been seen as justified in patients in extremis with loss of vital signs with penetrating thoracic trauma and blunt trauma. (5-7) In the latest edition of the trauma textbook, resuscitative thoracotomy should be performed for the following conditions: penetrating trauma outside of the torso with cardiopulmonary resuscitation (CPR) of less than 5 minutes, blunt trauma with CPR of less than 10 minutes, and penetrating torso trauma with CPR of less than 15 minutes. (1)

More specifically, in patients with penetrating thoracic trauma, a resuscitative thoracotomy is considered appropriate for those who are hemodynamically unstable upon arrival in the emergency department, despite appropriate fluid resuscitation. It is also indicated for those who rapidly deteriorate or experience cardiac arrest during initial resuscitation. Additionally, in patients who have been pulseless and receiving cardiopulmonary resuscitation (CPR) for less than 15 minutes, a resuscitative thoracotomy may be warranted. Furthermore, in cases of blunt trauma injuries, a resuscitative thoracotomy is justified for patients who lose vital signs in transit or the emergency department and do not present obvious non-survivable injuries (e.g., massive head trauma or multiple severe injuries). It is also indicated for patients with rapidly diagnosed cardiac tamponade confirmed by ultrasound, provided there are no apparent non-survivable injuries. Chiefly, this intervention should only be performed if appropriate resources including appropriately trained staff are available for continued resuscitation and definitive repair. (3)

In 2021, Aseni et al. conducted a systematic review of medical literature related to emergency department resuscitative thoracotomies and provided three main categories of indications for resuscitative thoracotomies: a) accepted, b) selective, and c) rare. Accepted indications include patients arriving with penetrating cardiac injuries in the area of the cardiac box (the area that is below the sternal notch, between the nipples and above a transverse line halfway between the xiphoid process and the umbilicus) with profound refractory shock who are hemodynamically unstable but have signs of life such as pupillary reactivity, spontaneous ventilation, presence of a carotid pulse, extremity movement, and cardiac electrical activity.

Selective indications pertain to patients who have sustained penetrating thoracic injuries and arrive without a pulse and without signs of life, as long as CPR has been ongoing for less than 15 minutes, and there is potential for a return to cardiac activity. Rare indications encompass patients who arrive with vital signs but experience a witnessed cardiopulmonary arrest, provided that CPR has been ongoing for less than 10 minutes. (7)

Resuscitative thoracotomy is a life-saving procedure in dire situations. It serves multiple critical purposes, including controlling intrathoracic hemorrhage, relieving cardiac tamponade, providing immediate albeit temporary repair of cardiac injuries, enabling open cardiac massage, and facilitating defibrillation to restore cardiac output and circulation. This procedure also aids in controlling both thoracic and abdominal hemorrhage (4, 7). However, there is no consensus on the overall survival rate of resuscitative emergency room thoracotomies. Multiple retrospective studies have reported significant variation in survival rates, ranging from 0% to 56.8%. In cases of penetrating trauma, the survival rate falls between 2.7% and 56.8%, while in instances of blunt trauma, the chances of survival are considerably lower, with rates ranging from 0% to 15.8%. (4)

Eastern Association for the Surgery of Trauma (EAST) evaluated whether emergency department thoracotomy improves outcomes in patients who present to the hospital pulseless after critical injuries by examining survival and neurological intactness rates. EAST used those findings to make corresponding recommendations, see Table 1. They compared patients in six different categories to make these recommendations: Patients presenting pulseless to the emergency department with signs of life after penetrating thoracic injury, without signs of life after penetrating thoracic injury, with signs of life after penetrating extrathoracic injury, without signs of life after penetrating extrathoracic injury, with signs of life after blunt injury, and without signs of life after blunt injury.

It was established that resuscitative thoracotomy significantly enhances both overall survival and the likelihood of achieving neurologically intact survival in patients who arrive pulseless in the emergency department but still exhibit signs of life after experiencing penetrating thoracic injuries. The findings indicated that patients who underwent resuscitative thoracotomy were nearly 7.6 times more likely to survive their hospitalization compared to those who did not receive the procedure (with a survival rate of 21.3% for resuscitative thoracotomy versus 2.8% without it). Furthermore, in terms of neurologically intact survival, patients who received resuscitative thoracotomy were nearly five times more likely to achieve this outcome (with an intact neurologically rate of 11.7% for survivors with resuscitative thoracotomy versus 2.5% for survivors without it).

Resuscitative thoracotomy was found to improve both survival and neurologically intact survival in patients presenting pulseless to the emergency department with absent signs of life after penetrating thoracic injury when resuscitated within 15 minutes of being pulseless. However, both survival and neurologically intact survival are rare after more than 15 minutes of CPR regardless of injury mechanism or anatomic location. Patients presenting pulseless to the emergency department without signs of life after penetrating thoracic injury were 41 times more likely to survive their hospitalization after EDT than without EDT (with a survival rate of 8.3% for resuscitative thoracotomy versus 0.2% without it). In regards to neurologically intactness, patients who underwent a resuscitative thoracotomy were nearly 20 times more likely to survive neurologically intact (with an intact neurologically rate of 3.9% for survivors with resuscitative thoracotomy versus 0.18% for survivors without it).

In the case of patients presenting pulseless to the emergency department with signs of life after penetrating extrathoracic injury, resuscitative thoracotomy was found to improve both hospital survival and neurologically intactness. Patients presenting pulseless to the emergency department with signs of life after penetrating extrathoracic injury were nine times more likely to survive their hospitalization after resuscitative thoracotomy than without (with a survival rate of 15.6% with resuscitative thoracotomy versus 1.7% without). Likewise, patients who underwent a resuscitative thoracotomy were 11 times more likely to survive neurologically intact (with a neurologically intact rate of 16.5% for survivors with resuscitative thoracotomy versus 1.5% for survivors without it).

Regarding patients presenting pulseless to the emergency department without signs of life after penetrating extrathoracic injury, evidence surrounding resuscitative thoracotomy was limited but resuscitative thoracotomy was found to improve both hospital survival and neurologically intactness. For hospital survival there was a 29-fold benefit with resuscitative thoracotomy (with a survival rate of 2.9% with resuscitative thoracotomy versus 0.1% without) and for neurologically intact survival there was a nearly 56-fold benefit (with a neurologically intact rate of 5% for survivors with resuscitative thoracotomy versus 0.09% for survivors without it).

For patients presenting pulseless to the emergency department with signs of life after blunt injury, resuscitative thoracotomy improves hospital survival by nine fold (with a survival rate of 4.6% with resuscitative thoracotomy versus 0.5% without) and neurologically intactness by nearly eight-fold (with a neurologically intact rate of 2.4% for survivors with resuscitative thoracotomy versus 0.3% for survivors without it).

In patients presenting pulseless to the emergency department without signs of life after blunt injury, hospital survival or neurologically intact hospital survival was poor in both groups. Survival in patients with resuscitative thoracotomy was 0.7% compared to 0.001% without. Neurologic outcomes were more grim with only 0.1% of patients surviving with resuscitative thoracotomy compared to an estimated 0.0006% without. (6)

Resuscitative thoracotomies have demonstrated their ability to improve survival and preserve neurological function, especially in cases of penetrating trauma. However, the potential complications associated with this substantial procedure cannot be overlooked in clinical decision-making (6). The complications of resuscitative thoracotomy encompass various issues, including occupational exposure to bloodborne pathogens, accidental ligation of coronary arteries, damage to the phrenic nerve, neurological complications resulting from cerebral hypoperfusion, esophageal damage during aortic cross-clamping, recurrent bleeding from the chest wall or the internal mammary artery, damage to the phrenic nerve, and ischemic damage to distal organs and the spinal cord due to aortic cross-clamping (2), (7). Given the risks to both patients and healthcare providers, coupled with the uncertainty of complication rates, contraindications for resuscitative thoracotomy have been established to minimize potentially futile procedures.

Resuscitative thoracotomy should not be performed when patients have vital signs particularly if the situation appears futile. For instance, where there are no signs of life on scene of injury; asystole as presenting rhythm with no pericardial tamponade; pulseless for greater than 15 minutes; massive, non survivable injuries, pre-hospital penetrating abdominal trauma without cardiac activity, severe head injury, and severe multisystem injury. Because this process is considered to be a temporary stopgap, resuscitative thoracotomy should only be performed when resources to perform the definitive treatment are readily and immediately available. The patient’s age is also taken into consideration, as outcomes for the young and old have been poor. Because of poor outcomes, not performing a resuscitative thoracotomy in patients between ages 0-14 who suffered a blunt thoracic injury and any patient older than 57 years old should be considered (2-3)

POST BY: ERICA FLEMING-HALL, MS4

FACULTY EDITING BY: COLIN MCCLOSKEY, MD

References

1. Burlew C, & Moore E.E. (2020). Resuscitative thoracotomy. Feliciano D.V., & Mattox K.L., & Moore E.E.(Eds.), Trauma, 9e. McGraw Hill. https://accesssurgery.mhmedical.com/content.aspx?bookid=2952&sectionid=249118216

2. Weare S, Gnugnoli DM. Emergency Room Thoracotomy. [Updated 2023 Jul 24]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK560863

3. Eidt JF, Foreman ML. Resuscitative Thoracotomy: Technique. In: UpToDate, Post TW (Ed), UpToDate, Waltham, MA. (Accessed on October 16, 2023.)

4. Pust, G. D., & Namias, N. (2016). Resuscitative thoracotomy. International Journal of Surgery, 33, 202–208. https://doi.org/10.1016/j.ijsu.2016.04.006

5. Burlew, C. C., Moore, E. E., Moore, F. A., Coimbra, R., McIntyre, R. C., Davis, J. W., Sperry, J. L., & Biffl, W. L. (2012). Western Trauma Association Critical Decisions in Trauma. The Journal of Trauma and Acute Care Surgery, 73(6), 1359–1363. https://doi.org/10.1097/ta.0b013e318270d2df

6. Mark J. MD; Haut, Elliott R. MD, PhD; Van Arendonk, Kyle MD; Barbosa, Ronald R. MD; Chiu, William C. MD; Dente, Christopher J. MD; Fox, Nicole MD; Jawa, Randeep S. MD; Khwaja, Kosar MD; Lee, J. Kayle MD; Magnotti, Louis J. MD; Mayglothling, Julie A. MD; McDonald, Amy A. MD; Rowell, Susan MD, MCR; To, Kathleen B. MD; Falck-Ytter, Yngve MD; Rhee, Peter MD, MPH. An evidence-based approach to patient selection for emergency department thoracotomy: A practice management guideline from the Eastern Association for the Surgery of Trauma. Journal of Trauma and Acute Care Surgery 79(1):p 159-173, July 2015. | DOI: 10.1097/TA.0000000000000648

7. Aseni, P., Rizzetto, F., Grande, A. M., Bini, R., Sammartano, F., Vezzulli, F., & Vertemati, M. (2021). Emergency Department Resuscitative Thoracotomy: Indications, surgical procedure and outcome. A narrative review. The American Journal of Surgery, 221(5), 1082–1092. https://doi.org/10.1016/j.amjsurg.2020.09.038

75-year-old male with a past medical history of type 2 diabetes, hypertension, and stroke with residual dysarthria presented to the emergency department for painless vision changes in his right eye. Two hours prior to arrival he experienced sudden loss of vision in his right eye while watching TV. He also reported flashes and floaters since that morning, which were initially intermittent before becoming constant. In addition, he reported a history of dry eyes and wears glasses but denied any history of similar symptoms. Also denied eye pain, trauma, falls, fevers, chills, chest pain, nausea, vomiting, and headache. 

Ocular point-of-care ultrasound was indicated given his painless vision loss to evaluate for retinal detachment, vitreous detachment, and vitreous hemorrhage. 

POCUS Findings:

There is significant vitreous hemorrhage indicated by the mobile echogenic debris in the posterior chamber with no relation to the optic nerve.  These images display the “washing machine sign” with attempts at a kinetic exam, though eye movement was limited due to patient ability. There does not appear to be any evidence of a retinal or vitreous detachment.

Case Conclusion:

The patient was evaluated by ophthalmology, and vitreous hemorrhage was confirmed. Ophthalmology recommended follow-up in their clinic in the morning and he was discharged home with a plan for close monitoring.

Vitreous Hemorrhage: Pathophysiology & Clinical Significance

Vitreous hemorrhage is the extravasation of blood into the vitreous chamber, which occurs secondary to three mechanisms, including abnormal vessels, rupture of vessels, and blood from an adjacent source. Abnormal vessels are typically due to ischemic diseases including diabetes, sickle cell disease, or retinopathy of prematurity. Rupture of vessels can occur with significant trauma overcoming the structural integrity of a vessel. Blood from adjacent sources can occur from retinal macroaneurysms or malignancy [1].

Common symptoms of vitreous hemorrhage include painless floaters, shadows, haziness, or other vision changes [1]. The diagnosis is typically made through a comprehensive ophthalmologic examination, though ultrasound is a useful adjunct that can help expedite the diagnosis [2-3].

Close follow-up with ophthalmology is recommended, as complications of persistent vitreous hemorrhage include glaucoma, retinal damage, and loss of vision. Possible definitive treatment for persistence of vitreous hemorrhage includes vitrectomy [4]. Timing of vitrectomy varies based on the etiology of the vitreous hemorrhage [1].

Ocular Point-of-Care Ultrasound

Materials

• High frequency linear probe

• Tegaderm to cover eye

• Ultrasound gel

Technique for Ocular Ultrasound

Place a Tegaderm over the patient’s eye, being careful to avoid air pockets. Generously apply ultrasound gel to the high frequency linear transducer. Select the superficial preset for the probe. Place the probe gently over the patient’s closed eyelid with the probe marker facing the patient’s right side, using the patient’s nasal bridge or zygoma as a stabilizing point for the hand holding the probe. Ensure the probe is fully contacting the patient’s eye but apply as little pressure as possible to maximize the patient’s comfort [5-7].

Start with a normal gain setting to visualize the anterior chamber and posterior segment of the eye. Fan through the eye in the transverse position, identifying key structures. Significant posterior structures of the eye for a POCUS exam include the vitreous body, retina, and optic nerve. Make sure you have adequate depth to allow for visualization of these structures. If you do not initially see the optic nerve, slowly adjust the probe until it comes in to view. This is important because key pathology, i.e. retinal detachment and vitreous detachment, is differentiated by their relation to the optic nerve.

Slowly increase gain to optimize visualization of abnormalities within the vitreous body, particularly vitreous hemorrhage and detachment [5-7]. A study conducted by Chang et al. noted that high gain settings (75, 100 on scale of 0 to 100) had a higher sensitivity for detecting posterior chamber abnormalities compared to low gain levels [8].

Next, perform a dynamic exam (also known as oculokinetic echography, see Figure 5) where the patient looks left and right (or medial and lateral). This can help distinguish pathology that may not be clearly identifiable with a static image alone [5-7].

In addition to a transverse view, it’s also helpful to assess the globe with the probe in a longitudinal orientation. The process is similar to that of a transverse view, with the exception of asking the patient to look up and down for the kinetic exam [6,7].

Evaluate for Key Pathology: Retinal Detachment, Vitreous Detachment, Vitreous Hemorrhage

Retinal detachment can often be visualized in normal or even low gain settings and appears as a hyperechoic membrane that attaches posteriorly at or near the optic nerve. The membrane moves with eye movement but remains tethered to the optic nerve. Vitreous detachment, on other hand, presents as a (usually thinner) hyperechoic membrane that does NOT attach near the optic disc. It often crosses midline and moves more freely with a dynamic exam, having a “swaying seaweed” appearance (Figure 3). Vitreous hemorrhage appears as diffuse hyperechoic opacities that will appear as a “washing machine” sign on dynamic exam. As mentioned above, increasing the gain will often optimize visualization of vitreous hemorrhage and detachment [5-7].

Utility of Ocular POCUS & Why Incorporate It Into Your Clinical Practice

Ocular chief complaints represent 2-3% of all emergency department visits [9]. Ocular ultrasound has been utilized by ophthalmologists for many years and is recognized as a useful adjunct to a comprehensive ophthalmologic exam [2]. More recently, emergency providers have been using ocular POCUS to promptly detect and differentiate ophthalmologic emergencies (e.g. retinal detachment) from less emergent pathology (e.g. vitreous detachment and hemorrhage). A study published in JAMA by Lanham et al. found that POCUS performed by emergency providers had 97% sensitivity and 88% specificity for retinal detachment, sensitivity and specificity of 82% for vitreous hemorrhage, and 96% specificity and 43% specificity for vitreous detachment [2]. A systematic review and meta-analysis by Propst et al., published in JAMA in 2020, similarly demonstrated high sensitivity and specificity for retinal detachment (both 94%) with slightly higher sensitivity and specificity for vitreous hemorrhage at 90% and 92%, respectively. Vitreous detachment again had poor sensitivity but specificity remained relatively high [3]. Overall, these studies suggest that ocular POCUS is a good diagnostic test for the more imminently vision-threatening retinal detachment and can be a useful diagnostic adjunct for vitreous hemorrhage and vitreous detachment. It can help expedite the diagnosis and determine urgency for ophthalmology evaluation.

Similar to other POCUS applications, focused ocular ultrasound can be completed within minutes at the bedside and is also relatively easy to learn. A study by Lazarow et al. evaluated the ultrasound skills of emergency medicine residents and pediatric emergency medicine fellows before and after a didactic and practical intervention. They found that after only brief instruction and hands-on training, participants showed significant improvement in their subjective and objective ocular ultrasound knowledge as well as in their ability to diagnose ocular pathology with ultrasound [10]. Another study by Kang et al. compared online ocular ultrasound education with hands-on education and found non-inferiority of the latter, offering a potential alternative method for learning [11].

Take Home Points

1. Ocular ultrasound can be performed at the bedside for prompt evaluation of several ocular pathologies, including retinal detachment, vitreous detachment, and vitreous hemorrhage.

2. Vitreous hemorrhage appears sonographically as hyperechoic opacities swirling ( “washing machine” sign) in the vitreous during an oculokinetic exam. 

3. Vitreous detachment presents as a mobile hyperechoic membrane not attached to the optic nerve (and can cross midline) that tends to be more freely mobile during an oculokinetic exam.

4. Retinal detachment is an ophthalmologic emergency that presents as a mobile hyperechoic membrane that remains attached posteriorly to the optic nerve with oculokinetic ultrasonography. Of these three pathologies, the diagnostic utility of POCUS is highest for retinal detachment.

5. Ocular ultrasound does not replace a comprehensive ophthalmologic exam but can help expedite diagnosis, determine the urgency of evaluation by ophthalmology, and can be easily learned in various settings.

POST BY: MATTHEW HOM, MD (PGY2)

FACULTY CO-AUTHOR/EDITOR: LAUREN MCCAFFERTY, MD

References

1. Berdahl J, Mruthyunjaya P. Vitreous hemorrhage: Diagnosis and treatment. American Academy of Ophthalmology. March 2007. Accessed June 25, 2023. <https://www.aao.org/eyenet/article/vitreous-hemorrhage-diagnosis-treatment-2.>

2. Lahham S, Shniter I, Thompson M, et al. Point-of-Care Ultrasonography in the Diagnosis of Retinal Detachment, Vitreous Hemorrhage, and Vitreous Detachment in the Emergency Department. JAMA Netw Open. 2019;2(4):e192162.

3. Propst SL, Kirschner JM, Strachan CC, et al. Ocular Point-of-Care Ultrasonography to Diagnose Posterior Chamber Abnormalities: A Systematic Review and Meta-analysis. JAMA Netw Open. 2020;3(2):e1921460.

4. Spraul CW, Grossniklaus HE. Vitreous Hemorrhage. Surv Ophthalmol. 1997;42(1):3-39.

5. Nagdev A. Ocular Ultrasound: Retinal Detachment and Posterior Vitreous Detachment. ALiEM. March 11, 2014. Accessed June 25, 2023. <https://www.aliem.com/ocular-ultrasound-retinal-detachment-posterior-vitreous-detachment/>

6. Vermeulen M, McDonald L. Floaters: Retinal Detachment, Posterior Vitreous Detachment, or Vitreous Hemorrhage? EM Resident. August 9, 2017. Accessed July 19, 2023. <https://www.emra.org/emresident/article/floaters-retinal-detachment-posterior-vitreous-detachment-or-vitreous-hemorrhage>

7. Dinh V. Ocular Ultrasound made easy: Step-by-step guide. POCUS 101. Accessed July 19, 2023. <https://www.pocus101.com/ocular-ultrasound-made-easy-step-by-step-guide>

8. Chang M, Finney N, Baker J, et al. Optimal Image Gain Intensity of Point-of-care Ultrasound when Screening for Ocular Abnormalities in the Emergency Department. West J Emerg Med. 2023;24(3):622-628.

9. Walker RA, Adhikari S. Eye emergencies In: Tintinalli JE, Stapczynski S, Ma OJ, Yealy DM, Meckler JD, Cline DM, eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. Chicago, IL: McGraw-Hill Medical; 2011:236-

10. Lazarow F, Deal AK, Shaves SC, et al. Evaluation of a point-of-care ultrasound curriculum and ocular phantom in residency training. J Ultrasound. 2022;25(2):259-263.

11. Kang SY, Yoo J, Park S, et al. Online Learning versus Hands-On Learning of Basic Ocular Ultrasound Skills: A Randomized Controlled Non-Inferiority Trial. Medicina (Kaunas). 2022;58(7):960.

Point of care ultrasound (POCUS) is a core tool in the emergency department and is useful in rapidly evaluating critical patients. The use of transthoracic echocardiography (TTE) in cardiac arrests has been shown to be useful in clarifying patient prognosis, identifying reversible pathology, and guiding ongoing resuscitation efforts (1). However, there are challenges associated with TTE that limit its utility and can even lead to suboptimal resuscitation. Limitations of TTE in resuscitation include potential difficulty in acquiring views in the limited time frame of pulse checks as well as challenges associated with obtaining adequate sonographic windows through the chest wall (2). Transesophageal echocardiography (TEE) does not have these constraints, allowing for faster acquisition of images during pulse checks and better visualization of relevant cardiovascular anatomy. As such, it has been increasingly used to overcome some of these limitations and provide additional information to support resuscitation.

Methods

Comprehensive TEE is an advanced imaging modality in cardiology. It involves the capturing of 28 individual views and is outside of the scope of emergency medicine or critical care (3). However, it has been shown that non-cardiologists can be successfully taught to acquire four useful TEE views within the course of a single-day training session (4). This focused TTE exam for critical care includes the mid-esophageal 4 chamber, mid-esophageal long axis, trans-gastric short axis, and bicaval views. Each corresponds to rough TTE view equivalents and can be used to answer specific clinical questions relevant to the resuscitation effort (Table 1). This focused exam, when conducted by trained practitioners, has been shown to have sensitivity, specificity, and accuracy in determining the primary diagnosis in critically ill patients. (5).

Benefits of resuscitative TEE

The primary benefits of intra-arrest TEE over TTE include a reduction in pauses during pulse checks in CPR, ability to monitor the heart in real-time during compressions to improve CPR quality, and increased ability to identify underlying pathology responsible for the arrest. Each is benefit is explored below.

Reducing time required for pulse checks - The strongest evidence in support of the preferential usage of TEE over TTE in resuscitation is the demonstrated difference in time required for pulse checks in CPR. The American Heart Association (AHA) recommends that pauses in compressions last less than 10 seconds for the maintenance of high-quality CPR (6). TTE evaluation during pulse checks has been associated with longer time off the chest and reduced chest compression fractions. A prospective cohort study out of the University of Maryland in 2017 monitoring 123 pulse checks in 23 patients reported a mean duration of checks with POCUS TTE to be 21.0s (95% CI 18-24s), compared with 13.0s (95% CI 12-15s) when conducted without TTE (7). Another prospective cohort study out of Highland Hospital and UCSF in 2018 documented 110 pulse checks in 24 patients and yielded similar results, reporting the median duration of pulse check to be 6.4 seconds (95% CI 2.1-10.8s) longer with POCUS than without (8).  A 2019 prospective cohort study out of University of Utah compared TTE directly to TEE, monitoring 139 pulse checks across 25 cardiac arrest patients at an academic tertiary care facility. Checks with TEE were shown to take significantly less time (mean pause of 9 seconds (95% CI 8-14 seconds) compared to 19 seconds (95% CI 16-22 seconds) with TTE. (9.). This makes sense, as adequate TEE views can be acquired without ceasing compressions, meaning ultrasonic evaluation should not contribute to time off the chest.

Ensuring the effectiveness of CPR - Another unique advantage of using TEE is that it allows for real-time visualization of the heart during CPR, allowing for determination of the area of maximal compression (AMC) and appropriate adjustment as needed. For maximum effectiveness, the AMC should be directly over the left ventricle of the heart. However, anatomical variation and the imprecision of administering compressions over the lower part of the sternum leaves significant room for suboptimal mechanics. This was borne out in a 2009 prospective study of 34 patients with nontraumatic cardiac arrest conducted out of Yonsei University Wonju, which found the AMC was over the aorta in 59% of patients receiving compressions and over the left ventricular outflow tract (LVOT) in another 41% of patients. All patients were found to have significant narrowing of the LVOT with each compression (10). While further study of the effect on hemodynamics and patient outcomes is needed, the ability to observe and modify the positioning of compressions during resuscitation offers a possibility to provide higher-quality CPR with TEE monitoring.

Drawbacks to TEE

The primary drawbacks to resuscitative TEE are increased training requirements over TTE and the potential for complications that arise with a more invasive procedure.

Training - While training and skilled oversight are not available in many centers, focused education such as the program described by Arntfield et al. lowers the barrier to access (4).

Complications - TEE is more invasive and therefore more prone to complications than TTE, but it is generally considered a safe procedure. Complication rates for diagnostic and intraoperative TEE are low, with reports ranging from 0.8%-2.8%. (11). It is noted, however, that there is not published data on complication rates specifically for intra-arrest TEE, and differences in operators and circumstances may affect this.

Conclusions

While significant research including larger multicenter studies, outcome analysis, and specific complication rates is still needed, there is encouraging evidence for possible benefit from the regular use of resuscitative TEE in cardiac arrest. Given the relatively low barrier to training practitioners to proficiency and the low complication rate, academic centers should continue to expand their capabilities with this modality to better understand its potential use.

AUTHORED BY: CHRIS SCHLECHTER, MS4 CWRU SOM

FACULTY EDITING BY: COLIN MCCLOSKEY, MD

References

1. Teran, F., Prats, M. I., Nelson, B. P., Kessler, R., Blaivas, M., Peberdy, M. A., Shillcutt, S. K., Arntfield, R. T., & Bahner, D. (2020). Focused Transesophageal Echocardiography During Cardiac Arrest Resuscitation: JACC Review Topic of the Week. Journal of the American College of Cardiology, 76(6), 745–754. https://doi.org/10.1016/j.jacc.2020.05.074

2. Parker, B. K., Salerno, A., & Euerle, B. D. (2019). The use of transesophageal echocardiography during cardiac arrest resuscitation a literature review. Journal of Ultrasound in Medicine, 38(5), 1141–1151. https://doi.org/10.1002/jum.14794

3. Hahn, R. T., Abraham, T., Adams, M. S., Bruce, C. J., Glas, K. E., Lang, R. M., Reeves, S. T., Shanewise, J. S., Siu, S. C., Stewart, W., & Picard, M. H. (2013). Guidelines for performing a comprehensive transesophageal echocardiographic examination: Recommendations from the american society of echocardiography and the society of cardiovascular anesthesiologists. Journal of the American Society of Echocardiography, 26(9), 921–964. https://doi.org/10.1016/j.echo.2013.07.009

4. Arntfield, R., Pace, J., McLeod, S., Granton, J., Hegazy, A., & Lingard, L. (2015). Focused transesophageal echocardiography for emergency physicians—description and results from simulation training of a structured four-view examination. Critical Ultrasound Journal, 7(1). https://doi.org/10.1186/s13089-015-0027-3

5. Lau, V., Priestap, F., Landry, Y., Ball, I., & Arntfield, R. (2019). Diagnostic Accuracy of Critical Care Transesophageal Echocardiography vs Cardiology-Led Echocardiography in ICU Patients. Chest, 155(3), 491–501. https://doi.org/10.1016/j.chest.2018.11.025

6. Meaney, P. A., Bobrow, B. J., Mancini, M. E., Christenson, J., De Caen, A. R., Bhanji, F., Abella, B. S., Kleinman, M. E., Edelson, D. P., Berg, R. A., Aufderheide, T. P., Menon, V., & Leary, M. (2013). Cardiopulmonary resuscitation quality: Improving cardiac resuscitation outcomes both inside and outside the hospital: A consensus statement from the American heart association. Circulation, 128(4), 417–435. https://doi.org/10.1161/CIR.0b013e31829d8654

7. Huis in ’t Veld, M. A., Allison, M. G., Bostick, D. S., Fisher, K. R., Goloubeva, O. G., Witting, M. D., & Winters, M. E. (2017). Ultrasound use during cardiopulmonary resuscitation is associated with delays in chest compressions. Resuscitation, 119, 95–98. https://doi.org/10.1016/j.resuscitation.2017.07.021

8. Clattenburg, E. J., Wroe, P., Brown, S., Gardner, K., Losonczy, L., Singh, A., & Nagdev, A. (2018). Point-of-care ultrasound use in patients with cardiac arrest is associated prolonged cardiopulmonary resuscitation pauses: A prospective cohort study. Resuscitation, 122, 65–68. https://doi.org/10.1016/j.resuscitation.2017.11.056

9. Fair, J., Mallin, M. P., Adler, A., Ockerse, P., Steenblik, J., Tonna, J., & Youngquist, S. T. (2019). Transesophageal Echocardiography During Cardiopulmonary Resuscitation Is Associated With Shorter Compression Pauses Compared With Transthoracic Echocardiography. Annals of Emergency Medicine, 73(6), 610–616. https://doi.org/10.1016/j.annemergmed.2019.01.018

10. Hwang, S.O., Zhao, P.G., Choi, H.J., Park, K.H., Cha, K.C., Park, S.M., Kim, S.C., Kim, H. and Lee, K.H. (2009), Compression of the Left Ventricular Outflow Tract During Cardiopulmonary Resuscitation. Academic Emergency Medicine, 16: 928-933. https://doi.org/10.1111/j.1553-2712.2009.00497.x

11. Hwang, S. O., Jung, W. J., Roh, Y. Il, & Cha, K. C. (2022). Intra-arrest transesophageal echocardiography during cardiopulmonary resuscitation. Clinical and Experimental Emergency Medicine, 9(4), 271–280. https://doi.org/10.15441/ceem.22.399

A 20-year-old male with no significant past medical history presented to the ED with chief complaint of shortness of breath. The patient presented to urgent care the previous week, was diagnosed with influenza, and sent home with a short course of azithromycin after a benign chest x-ray. Since then, he experienced worsening shortness of breath, fever, and myalgia prompting presentation to ED. Physical exam was notable for tachypnea, increased work of breathing, and diminished lung sounds in the bilateral lower fields.

Lung ultrasound was performed and showed the following:

POCUS findings:

Left thoracic views are significant for a large area of consolidation with dynamic air bronchograms, along with a complex-appearing pleural effusion. Right lower thoracic views are significant for a smaller, more focal area of a consolidation with complex effusion, air bronchograms, and associated focal B-lines posterior to it. Findings were concerning for pneumonia with complex pleural effusion.

Pneumonia on ultrasound

Pneumonia can present in multiple fashions on ultrasound [1]. Findings that raise suspicion are hepatization, lobar or subpleural consolidation, air bronchograms, B-lines, and pleural effusion, the majority of which are seen in this patient and are reviewed briefly below.  Dr. Brallier’s blog post from Dec 2022 also has an excellent review of many of these findings, along with an overview of how to perform lung ultrasound [2].

Consolidation/Hepatization

A prominent feature of this patient’s ultrasound is the area of consolidation in the left lung. When normal areas of lung fill with fluid or cells, it can produce an echogenic appearance similar to the liver or other solid organs and is referred to as “hepatization”. This finding is not specific to pneumonia as it can also be seen in other conditions such as atelectasis and infarct, among others [3]. When concerned about pneumonia, it is important to look for additional features, such as a ragged, irregular borders (“shred sign”) or air bronchograms, as these raises suspicion for an infectious process [1].

Air bronchograms

Air bronchograms are defined by small hyperechoic structures surrounded by relatively hypoechoic tissue (labeled in purple in Figure 3).  Physiologically these represent air-filled bronchi that become visible when the surrounding lung parenchyma becomes consolidated.  The air has high acoustic reflectance and shows up as bright relative to the lower reflectance of consolidated lung tissue. Air bronchograms can be either static, meaning they do not move with respiration, or dynamic, meaning they move with respiration, see Figure 3. Dynamic air bronchograms are highly specific for pneumonia with a specificity of 94% and a positive predictive value of 97% in the appropriate patient. Sensitivity is much lower, implying that lack of dynamic air bronchograms does not rule out pneumonia [4]. The dynamic movement of the hyperechoic areas with respiration indicates the airways in that area are patent, which effectively rules out atelectasis [5]. The ability to distinguish between static and dynamic air bronchograms is one of the major advantages of point-of-care ultrasound as compared with static radiographic studies.

Parapneumonic Effusions - Simple versus Complex Pleural Effusions

In addition to the changes to the lung tissue itself, pneumonia often has associated effusions, as seen in this case. Effusions have a very broad differential but the characteristics of the effusion can help narrow or differentiate this [6].

Simple pleural effusions are hypoechoic or anechoic. The fluid from the effusion readily transmits sound waves which then reflect off the vertebrae back to the transducer. This allows for visualization of the spine above the diaphragm, known as a “positive spine sign”. This is in contrast to a normal lung in which air scatters sound waves and obfuscates the deeper structures, including the spine, preventing visualization above the diaphragm [3]. Simple effusions are commonly caused by a transudative process, see Figure 4. However, infectious or other exudative etiologies can still be on the differential [3,6].

Complex pleural effusions are characterized by more heterogenous and echogenic appearance. This can include pneumonia or less commonly malignancy or clotted blood from a hemothorax (3,6]. Figure 5 shows the area caudal to the consolidation in the left lung field. While this fluid is still relatively hypoechoic, there is some stranding at the edges along with some subtle debris within the fluid, raising suspicion for an exudative process. Another example of a more echogenic complex effusion is seen in Figure 6 where a heterogenous collection of fluid formed in the pleural space in a patient with severe disseminated streptococcus pneumonia infection.

Focal B-lines

Another finding that is nonspecific but can suggest pneumonia in the right clinical context is B-lines.  B-lines are ultrasound artifacts caused by reverberation of the sound wave between two highly reflective surfaces.  The most common source of these reflective surfaces are fluid-filled alveoli, but any fluid or other highly reflective surface can suffice. B lines appear as hyperechoic vertical lines extending from the pleural line to the entire imaging field. In contrast to pulmonary edema where B lines are more diffuse and bilateral, focal or unilateral B lines suggest a more localized process such as pneumonia [1,3]

Case continuation

The patient was started on broad-spectrum antibiotics and admitted to the MICU. Chest x-ray was somewhat equivocal and due to his tenuous status, CT was deferred. He continued to have increasing oxygen requirement and eventually needed intubation due to work of breathing, failure to oxygenate, and anticipated clinical course. Bilateral chest tubes were placed, which drained large amounts of purulent fluid.

CT chest was obtained once the patient was more stable, which confirmed pneumonia, in addition to cavitary lesions, and improved effusions post-drainage. He was subsequently found to have thrombi in his SVC, concerning for Lemierre syndrome, see Figure 8. Cultures grew Fusobacterium. Hospital course was further complicated by decompensation secondary to reaccumulation of the pleural effusions, and he ultimately underwent bilateral VATS procedure. The overall impression by the time of discharge after a month-long hospitalization was post-influenza pneumonia with Fusobacterium superinfection.

Lemierre Syndrome and Post-Influenza Pneumonia

Lemierre syndrome, as seen in this case, is a potentially life-threatening sequelae of usually upper respiratory or oropharyngeal infections [7].  The syndrome is defined by extension of the infection into the pharyngeal spaces with subsequent septic thrombophlebitis when the internal jugular vein and nearby venous system is seeded.  Septic emboli then can migrate into systemic circulation and disseminate to the lung (as seen in this patient) but additionally to joints, bones muscles, spleen, liver or kidney. Lemierre syndrome is defined by the clinical symptoms rather than the pathogen, but the cause in over 70% of cases is Fusobacterium. While this is usually from oral infections, there has been speculation that it may also be secondary to mucosal damage from viral infections, which was suspected in this patient [8]. Postviral bacterial suprainfections that involve distal lung tissue occur far more frequently than Lemierre syndrome and are most commonly from Strep Pneumoniae [9].

POST BY: BRIAN FORT, MD, PhD, PGY1

FACULTY CO-AUTHOR/EDITOR: LAUREN MCCAFFERTY, MD

References

1. Avila J. Pneumonia. 5 Minute Sono. Core Ultrasound. Accessed June 2023. https://www.coreultrasound.com/pneumonia/

2. Brallier I, McCafferty L. Thoracic Ultrasound & Complex Pleural Effusions. The Land of EM POCUS Blog. December 23, 2022. Accessed July 2023.

3. Marini TJ, Rubens DJ, Zhao YT, et al. Lung Ultrasound: The Essentials. Radiol Cardiothorac Imaging. 2021; 3:2

4. Lichtenstein D, Mezière G, Seitz J. The dynamic air bronchogram. A lung ultrasound sign of alveolar consolidation ruling out atelectasis. Chest. 2009;135(6):1421-1425.

5. Shah A, Oliva C, Stem C, Cummings EQ. Application of dynamic air bronchograms on lung ultrasound to diagnose pneumonia in undifferentiated respiratory distress. Respir Med Case Rep. 2022; 30;39:101706.

6. Hassan M, Mercer RM, Rahman NM. Thoracic ultrasound in the modern management of pleural disease. Eur Respir Review. 2020; 29 (156): 1-11.

7. Allen BW, Anjum F, Bentley TP. Lemierre Syndrome. [Updated 2023 Apr 27]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK499846/

8. Yanagi H, Ozawa H. Lemierre's syndrome complicating influenza A virus infection. J Gen Fam Med. 2019 Dec 13;21(2):18-20. doi: 10.1002/jgf2.293. PMID: 32161697; PMCID: PMC7060288.

9. van der Sluijs KF, van der Poll T, Lutter R, Juffermans NP, Schultz MJ. Bench-to-bedside review: bacterial pneumonia with influenza - pathogenesis and clinical implications. Crit Care. 2010;14(2):219.

Thromboelastography (TEG) and Rotational thromboelastography (ROTEM) are the major types of Viscoelastic Tests (VETs, also referred to as a Viscoelastic Hemostatic Assays or VATs). These tests assess the viscoelastic properties (i.e. the ability to initially form and then subsequently breakdown an clot) of whole blood. The single assessment from TEG can provide a synthesized version of information typically gathered from a collection of individual lab tests, including PT, PTT, thrombin time, fibrinogen, and platelet count. With this information, TEG and ROTEM may be used to efficiently assess a patient’s real-time hemostasis and thus change management regarding hemorrhage and resuscitation. (1) (2) (3)

The result from TEG includes measurement of 5 parameters, as well as a coagulation index (CI) which combines several of the individual measurements into a calculation that describes overall coagulation status. For the coagulation index, normal values range from -3.0 to +3.0. A CI of greater than +3.0 corresponds to a hypercoagulable state, while a CI of less than -3.0 indicates coagulopathy. The 5 individual parameters are described below:

The TEG results are also depicted in the form of a thromboelastogram, which is the graphical representation of these parameters:

The combination of the parameter values and the visual thromboelastogram provide significant insight into the patient’s current coagulation status. For instance, if the shape of the thromboelastogram is has a shorter amplitude than normal, but maintains the overall normal length and shape, this would correspond with the decreased alpha angle and decreased MA – which would indicate a problem with platelets (thrombocytopenia and/or platelet dysfunction) and would guide towards therapy with platelets or DDVAP (depending on the diagnosis based on the rest of the clinical scenario). Examples of these variations are below:

TEG has been widely used to guide resuscitative management in cardiopulmonary bypass and cardiac and transplant surgeries. Rapid TEG (rTEG) is a variation of TEG that can provide results within 15 minutes, and therefore may offer an adjunct to clinical decision-making when it comes to resuscitation in the setting of acute trauma and hemorrhage.  

A 2016 study looked at TEG in comparison to common coagulation tests (CCTs) in the setting of trauma-induced coagulopathy (TIC). (4) Approximately 25% of patients admitted to the ED with severe traumatic injuries are found to have coagulopathy. Given that there are multiple theories about the etiology of TIC, involving various aspects of platelet function, tissue factor release, and dysfunctional prothrombotic and fibrinolytic pathways (to name a few of the prevailing theories), there is a need to be able to assess patients for these potential sources of dysfunction to appropriately intervene. This is where TEG may play a unique role. TIC and other coagulopathies are typically diagnosed with CCTs – which includes PT/INR, aPTT, platelet count, and fibrinogen. However, CCTs represent a more static look at hemostasis and are based on the coagulation cascade model of clotting – meaning that they do not fully take into account the complexities of hemostasis (i.e. considering the interplay between cell-based interactions, propagation of clotting, subsequent fibrinolysis, etc.). Alternatively, TEG assesses a sample of whole blood (thus involving most of the “players” in the clotting and breakdown process) and provides a dynamic analysis from initial un-clotted blood sample to formation of a clot to breakdown of the clot. TEG may therefore be able to provide an overall more complete picture of a trauma patient’s hemostasis with the potential for targeted trauma resuscitation and improved outcomes for trauma patients, particularly those who develop TIC.(4)

So, has TEG been shown to be as great as it sounds? A 2012 study in the Annals of Surgery analyzed 1974 major trauma activations at a level I trauma center, with the hypothesis that rTEG would more reliably predict blood component transfusions compared to CCTs. All patients who met the center’s criteria of the highest-level trauma activation were included and had rTEG and CCTs obtained within upon ED admission. They compared rTEG parameters (ACT, R, K, α angle, MA, LY30) to corresponding 5 CCT values (PT, aPTT, INR, platelet count, fibrinogen), and assessed both rTEG and CCT for their correlation with patients’ transfusion requirements. Their results demonstrated that rTEG parameters better predicted transfusion requirements compared to the 5 CCTs, and rTEG was shown to identify patients with increased risk of early RBC, plasma, and platelet transfusions – and rTEG results were faster and of similar or lower cost to patients. Their conclusion was that rTEG can replace admissions CCTs for these severe trauma patients (and they note changing their hospital guidelines to utilize admission rTEG, foregoing the traditional CCTs, based on these results).(5)

TEG seems to be the clear winner here, so why haven’t we all switched over? Well, not every study has shown such a clear-cut benefit. The 2020 ITACTIC study was an RCT which included 411 adult trauma patients across multiple major trauma centers in Europe. ITACTIC similarly compared transfusion strategy augmented by %% (VHA, i.e. TEG and ROTEM) versus CCTs, with primary outcomes of number of patients alive and free of massive transfusion at 24 hours. Their results showed no significant different in the proportion of patients alive and free from massive transfusion at 24 hours in VHA versus CCT (OR1.15, 95% CI 0.76-1.73). They also showed no significant difference in secondary outcomes, or in most sub-group analyses. There was a significantly reduced 28-day mortality in a single sub-group – severe TBI – with VHA vs. CCT (44% vs. 74%, p=0.016); the conclusions remained that VHA (TEG) did not improve overall outcomes when compared to CCT. (6)(7)

So where does that leave us (or in other words, TL;DR): TEG is a valuable tool for assessing real-time coagulation status and guiding management in resuscitation. We still need more evidence to determine whether it has a significant benefit over conventional coagulation tests, particularly in the setting of acute trauma. For now, we can expect TEG to become more frequently discussed and utilized in a variety of clinical settings, including the trauma bay. And when in doubt about what to do when you’re handed a thromboelastogram, here’s a quick visual aid:

POST BY: ALEXANDRIA GERBER, MS4

FACULTY EDITING BY : COLIN MCCLOSKEY, MD

Resources

1. Zehnder, JL. Clinical Use of Coagulation Tests. UpToDate. (Accessed on April 1, 2023). https://www.uptodate.com/contents/clinical-use-of-coagulation-tests?search=viscoelastic%20testing%20of%20hemostasis&source=search_result&selectedTitle=3~80&usage_type=default&display_rank=3#H1279919076

2. Cohen, M and Kutcher, ME. Coagulopathy in Trauma Patients. UpToDate. (Accessed on April 1, 2023.) https://www.uptodate.com/contents/coagulopathy-in-trauma-patients?sectionName=Thromboelastography&search=viscoelastic%20testing%20of%20hemostasis&topicRef=1368&anchor=H3046566855&source=see_link#H3046566855

3. Shaydakov ME, Sigmon DF, Blebea J. Thromboelastography. [Updated 2022 Apr 14]. In: StatPearls [Internet]. StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK537061/#:~:text=Thromboelastography%20(TEG)%20or%20thromboelastometry%20(,adults%20or%20children%20with%20bleeding.

4. K Bader M, et al. Targeted Thromboelastographic (TEG) Blood Component and Pharmacologic Hemostatic Therapy in Traumatic and Acquired Coagulopathy. Current Drug Targets 2016; 17(8) . https://dx.doi.org/10.2174/1389450117666160310153211

5. Holcomb, JB. et al. Admission Rapid Thrombelastography Can Replace Conventional Coagulation Tests in the Emergency Department: Experience With 1974 Consecutive Trauma Patients. Annals of Surgery 256(3):p 476-486, September 2012. https://journals.lww.com/annalsofsurgery/pages/articleviewer.aspx?year=2012&issue=09000&article=00010&type=Fulltext

6. Walker, G. The Bottom Line: ITACTIC. October 2020. https://www.thebottomline.org.uk/summaries/icm/itactic/

7. Baksaas-Aasen, K, et al. Viscoelastic haemostatic assay augmented protocols for major trauma haemorrhage (ITACTIC): a randomized, controlled trial. Intensive Care Med 2020. https://doi:10.1007/s00134-020-06266-1

8. Rezaie, S. Rebel Review #54 Thromboelastogram (TEG). http://rebelem.com/rebel-reviews

• Quick review of the cardiac action potential

• Cardiac medication toxicity

• Non-cardiac medication toxicity

• ECG toxidromes: guessing an agent based on conduction changes

Important Ions

Any perturbation of ion flow, whether through a direct effect of the drug or through indirect mechanisms (e.g. acidosis, etc), can cause conduction abnormalities

Beta Blockers

Mechanism of Toxicity

• Any BB: decrease conduction velocity through AV node

• May exhibit Na+ and/or K+ blocking effects (see below)

• Sotalol: more K+ channel blockade

• Propranolol: more Na+ channel blockade (acts TCA-esque)

EKG Changes

• Decreased conduction velocity à bradycardia, 1st/2nd/3rd degree AV block

• Sotalol: Prolonged QT —> Torsades

• Propranolol: Widened QRS à ventricular arrhythmias

Management

• Hypotension d/t brady: atropine, pressor support

• Glucagon increases Ca2+ influx —> increases chronotropy and inotropy

• QT prolongation: Mg (if c/f TdP)

• QRS widening: sodium bicarb (if VT)

Cardiac Meds: Calcium channel blockers (NDHPs)

Mechanism of Toxicity

• Main effects on the SA and AV node

• Because calcium is a major driver of the action potential at these sites, CCBs decrease chronotropy and increase refraction at the AV node

ECG Changes

• Decreased conduction velocity —> bradycardia, 1st/2nd/3rd degree AV block

• Can also have some QT prolongation

Management

• Like management of severe BB toxicity, focus is on maintaining CO and SVR

• Like BBs, can also use hyperinsulinemic euglycemia to combat many downstream effects of CCB toxicity

Cardiac Meds: Digoxin and other cardiac glycosides

Mechanism of Toxicity

• Inhibition of Na/K exchanger (phase 4) —> increased Ca2+ influx —> increased automaticity

• Increases vagal tone to suppress SA-to-AV conduction

ECG Changes

• Frequent PVCs (including ventricular bigeminy and trigeminy)

• SVT (2/2 increased automaticity) + slow ventricular response (2/2 decreased AV conduction)

Management

• Digibind/Digifab for life-threatening arrhythmias

• If Fab not available, can use antiarrhythmics like atropine/lidocaine

Non-Cardiac Meds: Tricyclic antidepressants

Mechanism of Toxicity

• Inhibition of Na+ channels à prolongs absolute refractory period

• Inhibition of K+ channels à QT prolongation

• Anticholinergic effects: reflex tachycardia (M3 blockade, see later)

ECG Changes

• Na+ blockade: increased QRS duration

• Right side of conduction system more susceptible —> R axis deviation with deep, slurred S wave in lead I and aVL

• K+ blockade: QTc prolongation

• M3 blockade: tachycardia and tachyarrhythmia

Management

• Sodium bicarbonate is the mainstay therapy for life-threatening arrhythmias

Non-Cardiac Meds: Antipsychotics (Haloperidol, quetiapine, chlorpromazine)

Mechanism of Toxicity

• Inhibition of inward K+ rectifier channels —> prolonged cardiac repolarization

• Some Na+ inhibition but less commonly causes issues

• Note: 1st and 2nd gen can all cause increased QTc to varying degrees

ECG Changes

• K+ blockade: QTc prolongation —> TdP

• Na+ blockade: rare QRS widening

Management

• Magnesium sulfate, especially if polymorphic VT begins

• Can also use overdrive pacing or isoproterenol

• Of highest import in preventing TdP: correct electrolytes! (especially K and Mg)

Non-Cardiac Meds: Sedating antihistamines and other anticholinergics

Mechanism of Toxicity

• At large doses: Na+ and K+ channel blockade

• Antimuscarinic effects: increased chronotropy

• Remember that these agents are often mixed with others (e.g. alpha-adrenergic agonists) and, thus, care needs to be taken to consider mechanisms from polypharmacy as well

ECG Changes

• K+ blockade: QTc prolongation—> TdP

• Na+ blockade: QRS widening

Management

• QRS widening and ventricular arrhythmia: sodium bicarbonate

• TdP: correct hypoxia, hypokalemia, hypomagnesemia, hypocalcemia

• Use isoproterenol or overdrive pacing if severe

  
  

  
  

Non-Cardiac Meds: Antidepressants (SSRIs, buproprion)

Mechanism of Toxicity

• Bupropion: blockade of K+ current, Na+ blockade

  • Note: Na+ blockade theorized to be due to gap-junction blockade and not fast Na+ channels and, thus, does not respond to sodium bicarb for wide complex arrhythmias

• Citalopram and escitalopram cause dose-dependent QT prolongation

ECG Changes

• Bupropion: wide complex, ventricular arrhythmias, QT prolongation and risk for TdP

• Citalopram/escitalopram: QT prolongation and risk for TdP

Management

• See note for bupropion

• Can use sodium bicarb for wide complex tachyarrhythmias for due to the other agents

ECG Toxidromes

*Note the extensive overlap between Na+ channel blocking and K+ channel blocking agents! While this presentation goes over just a few of the ECG effects in isolated channel blockade, there will often be a combination of effects and, thus, a difficult to determine ECG. Ultimately, the clinical toxidrome and history will be much more reliable than ECG alone, but ECGs can be used to bolster confidence in the underlying pathophysiology or the identity of an unknown agent!

POST BY: DAVID SWEET, MS4

FACULTY EDITING BY: DR. LAUREN PORTER

References

Nickson C (Feb 5, 2021). EKG in Toxicology. LITFL. Available from: https://litfl.com/ecg-in-toxicology/

Alberter AA, Chambers AJ, Wills BK. Bupropion Toxicity. [Updated 2022 Dec 12]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK580478/

Barrueto FB. Beta blocker poisoning. In: UpToDate. Stolbach A, Grayzel J (Eds). Available from: https://www.uptodate.com/contents/beta-blocker-poisoning

Barrueto FB. Calcium channel blocker poisoning. In: UpToDate. Stolbach A, Grayzel J (Eds). Available from: https://www.uptodate.com/contents/calcium-channel-blocker-poisoning?search=calcium%20channel%20blocker%20overdose&source=search_result&selectedTitle=1~26&usage_type=default&display_rank=1

Chakraborty RK, Hamilton RJ. Calcium Channel Blocker Toxicity. [Updated 2023 Jan 30]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan. https://www.ncbi.nlm.nih.gov/books/NBK537147/

Cummings ED, Swoboda HD. Digoxin Toxicity. [Updated 2022 Jul 4]. In: StatPearls Available from: https://www.ncbi.nlm.nih.gov/books/NBK470568/

Khalid MM, Galuska MA, Hamilton RJ. Beta-Blocker Toxicity. [Updated 2023 Feb 7]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK448097/

Salhanick SD. Tricyclic antidepressant poisoning. In: UpToDate. Hendrickson RG, Ganetsky M (Eds.) Available from: https://www.uptodate.com/contents/tricyclic-antidepressant-poisoning?search=tca%20overdose&sectionRank=2&usage_type=default&anchor=H5&source=machineLearning&selectedTitle=1~62&display_rank=1#H15

Yates and Manini. (2012) Utility of the Electrocardiogram in Drug Overdose and Poisoning: Theoretical Considerations and Clinical Implications. Curr Cardiol Rev. 8(2):137-151

Buprenorphine Best Practice Prescribing FAQ

What is buprenorphine? (brand name = “Subutex;” “Suboxone” if combined with naloxone)

Buprenorphine is a partial agonist of mu-opioid receptors used to treat pain and opioid use disorder.

• While buprenorphine has partial agonism at mu-opioid receptors and can cause some effects commonly associated with standard opioid medications (e.g., analgesia, sedation), it causes less of these effects than traditional full-agonist opioids like morphine, hydromorphone (Dilaudid), oxycodone, hydrocodone, heroin (diacetylmorphine), and the like.

• Because it is a partial agonist, it is also a partial antagonist and can antagonize other opioids. This can block the effects of other opioid pain medicines at traditional doses, and can precipitate opioid withdrawal in patients who are on chronic opioids.

• It will only have antagonist effects in patients actively on opioids, and will cause withdrawal in patients without chronic opioid use or patients who are already withdrawing from opioids (COWS ≥ 8).

• Buprenorphine is most commonly prescribed in the outpatient setting as a sublingual tablet or strip, and can also be given intravenously or subcutaneously. A transdermal formulation is also available for pain. The sublingual formulation is the only form that is approved for management of opioid use disorder; additionally, there are long-acting injectable formulations that are approved for the management of opioid use disorder.

Onset of clinical effects is usually within 30-60 minutes. Duration of action ranges from 6 or more hours of clinical effects up to ~36 hours (biologic half-life).

• Documented allergies and Iintolerances to buprenorphine that include gastrointestinal symptoms such as nausea, vomiting, diarrhea, etc and/or severe headaches, may be are likely signs of precipitated withdrawal OR may be signs of indicate true allergy/intolerance. This may be difficult to tease out.

• Precipitated withdrawal is not a sufficient reason to discontinue or avoid buprenorphine when it is clinically indicated. To mitigate intolerance to the buprenorphine, you may need to order a specific generic formulation, or order brand-name medication, or use mono-buprenorphine.

Indications for prescribing buprenorphine:

Buprenorphine can be prescribed for treatment of pain, treatment of opioid withdrawal, and treatment of opioid use disorder.

• If buprenorphine is being prescribed for treatment of pain, a special DATA-2000 “DEA-X” certification is not needed.

• If buprenorphine is being prescribed for treatment of opioid use disorder, the DATA-2000 “DEA-X” certification IS needed.

Clinical Opioid Withdrawal Score (COWS):

COWS should be calculated on all patients with reported opioid withdrawal, concern for opioid withdrawal or opioid use disorder and risk for opioid withdrawal. Buprenorphine can be given for a score greater than 8 in a patient with recent opioid use.

OARRS & other considerations: See Overdose Risk Score

Patient instructions on how to take buprenorphine:

While buprenorphine comes in different formulations (intravenous, transdermal, and oral) it can be prescribed for opioid withdrawal and opioid use disorder in a daily oral formulation, a buccal film, or as a long-acting subcutaneous abdominal injection

The oral formulation comes as either a dissolving tablet or a film, which is not meant to be swallowed but rather dissolved in the mouth.

Instructions to patients:

• Let Subutex or Suboxone tablets dissolve under your tongue; they are much less effective if swallowed.

• Take no more than two tablets at a time; otherwise you may swallow them by mistake.

• Wetting the mouth before placing the tablets under your tongue can help the tablets dissolve faster.

• Do not smoke for 10 to 15 minutes before you take your medication. Not smoking seems to help the tablets dissolve faster.

Correcting common misconceptions:

• Buprenorphine for opioid use disorder is not “replacing one addiction with another.” It is an evidence-based medical treatment.

• Buprenorphine can be prescribed indefinitely for the treatment of a chronic medical condition, that is, opioid use disorder.

• In comparison to other opioids, buprenorphine has multiple pharmacologic advantages, namely that it is safer than other opioids even in high doses, and it has substantially lower abuse potential than other opioids.

  • Buprenorphine has a more favorable side effect profile than other opioids, most notably with a “ceiling effect” on respiratory depression. Buprenorphine should not significantly depress respiratory status.

  • Additional elements of its favorable side effect profile include lack of cardiac conduction abnormalities, fewer gastrointestinal side effects compared to other opioids (e.g., less constipation, no effect on Sphincter of Oddi), less cognitive impairment, and no known effects on functioning of the immune system, the hypothalamic-pituitary axis, or the reproductive system. No dosing adjustment is necessary in kidney and liver disease.

• While there are reports of buprenorphine-related deaths, the overwhelming majority of these involve other CNS depressant drugs. Furthermore, confirmation of buprenorphine on postmortem or forensic testing is difficult to interpret, given the drug’s extremely long biologic half-life and association with patients at risk for substance use. Historical population-level data confirms that buprenorphine is an unlikely primary or sole cause of death. Buprenorphine even exceeds safety standards for many over-the-counter medications.

• An additional area of concern in regards to increasing buprenorphine availability is the potential for diversion and nonmedical use (aka, misuse) – however, compared to other opioids, buprenorphine has lower rates of nonmedical use.

• Use of other substances (e.g., benzodiazepines, other illicit drugs) is not an absolute contraindication to buprenorphine.

• Pregnant woman can receive buprenorphine-naloxone combination products (“Suboxone”); they are no longer limited to methadone or buprenorphine (“Subutex”) alone.

  From the American College of Obstetricians & Gynecologists:

  • “Buprenorphine is available as a monoproduct or in a combined formulation with naloxone, an opioid antagonist, used to reduce diversion because buprenorphine combined with naloxone causes severe withdrawal symptoms when injected. However, naloxone is not orally active, so withdrawal symptoms do not occur when used sublingually as directed (47).

  • The buprenorphine monoproduct has been recommended during pregnancy to avoid any potential prenatal exposure to naloxone, especially if injected (50). However, recent studies that evaluated the use of the combination product buprenorphine with naloxone found no adverse effects, and outcomes were similar when compared with buprenorphine alone (51, 52).

  • The use of the combination product during pregnancy will likely expand as more safety data are accumulated.” See ACOG’s Opioid Use and Opioid Use Disorder in Pregnancy

CREATED BY: DR. SHAUNA COMBS, PGY2

FACULTY EDITING BY: DRs. LAUREN PORTER, RYAN MARINO, BRYAN ROSS

25-year-old male with past medical history including Down syndrome, remote repair of aortic coarctation, hypertrophic cardiomyopathy presented for a non-productive cough and URI symptoms for the past 2 days. His mother accompanied the patient and provided additional history as the patient is nonverbal at baseline. She stated that he also had a poor appetite and intermittent chest pain, which she attributed to his cough. Otherwise she denied fever, syncope, shortness of breath, leg swelling, GI symptoms, known sick contacts. She believed he been taking his home medications.

His vitals were all within normal limits. Physical exam was unremarkable aside from an occasional cough. He appeared euvolemic and his lungs were clear.

EKG demonstrated normal sinus rhythm, normal rate, left axis deviation, and right bundle branch block that appeared unchanged from prior EKG. Significant lab findings included an elevated high sensitivity troponin of 150 ng/L and positive influenza test.

Though the patient’s presentation was attributed to a viral illness, a point-of-care ultrasound (POCUS) was performed to evaluate for cardiac pathology in the setting of elevated troponin, chest pain, and his prior history.

POCUS Findings

Left ventricular function is relatively normal-appearing without overt evidence of right ventricular enlargement or pericardial effusion. However, the left ventricle is significantly hypertrophic, particularly the interventricular septum (consistent with his history of hypertrophic obstructive cardiomyopathy (HOCM). There were no prior echocardiograms available for comparison.

Case Continued

Given the focused echo findings along with his elevated troponin and cardiac history, cardiology was consulted. They attributed the mildly elevated troponin to his severe left ventricular hypertrophy and associated microvascular disease rather than acute coronary syndrome. In the absence of syncope, they deferred urgent workup or ICD placement. A comprehensive transthoracic echo (TTE) was performed while the patient was in the ED and showed normal left ventricular (LV) systolic function with severe concentric left ventricular hypertrophy with an asymmetrically thickened septum and decreased LV cavity size. Additionally, he was noted to have systolic anterior motion (SAM) of the mitral valve - indicating outflow tract obstruction - along with reduced right ventricular systolic function and evidence of remote surgical repair. The patient remained stable and outpatient evaluation for ICD placement with congenital cardiology was felt to be appropriate. He was advised to continue taking his home beta blocker and calcium channel blocker in the meantime.

Left Ventricular Hypertrophy

Background

Left ventricular hypertrophy (LVH) is a heart condition that results in an increase in the mass of the LV due an increase in wall thickness and/or enlargement of the LV cavity itself. Left ventricular wall thickening occurs in response to pressure overload, while chamber dilation occurs in response to volume overload [1]. LVH is present in approximately 15-20% of the general population and is more prevalent in African Americans, the elderly, and patients with obesity or hypertension. LVH is equally common in women and men [2].

Multiple etiologies can lead to the development of LVH, the most common of which are hypertension and aortic valve disease due to the constant compensation of hemodynamic pressure and volume burden. While LVH may be a compensatory mechanism, it is still abnormal. There is development of an abnormal increase in the LV’s myocardial mass due to a chronically elevated workload on the heart muscle [3]. This pathologic hypertrophy then puts patients at risk of developing heart failure, dysrhythmias and sudden cardiac death. Other common causes of LVH include athletic heart with physiological LVH, ventricular septal defect, coarctation of the aorta, hypertrophic cardiomyopathy, renal artery stenosis and infiltrative cardiac diseases [1].

It should be noted that LVH can be further classified as concentric or eccentric. Concentric LVH is an abnormal increase in left ventricular myocardial mass due to pressure overload from arteriolar vasoconstriction which occurs in chronic hypertension or aortic stenosis. Eccentric LVH, on the other hand, is from increased filling pressure of the left ventricle or diastolic overload. This arises from valvular regurgitation and cases of dilated cardiomyopathy [1].

Clinical Presentation

LVH is difficult to diagnose based off signs and symptoms alone, as the disease process itself reflects a pathophysiologic response over time of the heart to pressure/volume overload. As such, the signs and symptoms are instead related to the underlying pathologic cause of LVH, such as hypertension and abnormal heart sounds, e.g. murmurs, from valvular pathology [4]. Patients may be able to compensate for years with no overt symptoms and nearly normal exercise reserve. Other patients may go on to develop heart failure from diastolic and/or systolic dysfunction [5].

Diagnosis

The diagnosis of LVH is largely dependent on echocardiographic measurements or non-invasive imaging techniques. Analyses from the Framingham Heart Study demonstrated that echocardiographic LVH (17.4%) is more prevalent than LVH detected by electrocardiography (2.4%) [6]. Cine-MRI and ultrafast CT have been used to detect LVH as well, however these current novel imaging studies are limited by a smaller size of study groups and less robust outcome data over time [7]. EKG findings that LVH can produce include: increased QRS duration, increased QRS voltage, left axis deviation, ST-T repolarization changes and left atrial abnormality. However, these findings though relatively specific lack sensitivity [8]. The Framingham Heart Study provided criteria for measurements of LV mass based off a healthy distribution, and thus, the basis to detection of pathological LVH based off adjustments for sex, height and body mass [6]. According to the American Society of Echocardiography and/European Association of Cardiovascular Imaging, LVH is defined as an increased left ventricular mass index (LVMI) to greater than 95 g/m in women and increased LVMI to greater than 115 g/m in men [1].

Management and Potential Complications

The management of LVH is varied and ultimately based on the underlying cause, such as hypertension, with the goal of preventing progression to heart failure and mortality. Overall, treatment is centered around lifestyle changes, medications, surgery and implantable devices. Multiple studies have shown that regression of LVH can occur with appropriate hypertension management. In turn, there is an associated reduction in potential complications such as cardiovascular death, fatal or nonfatal MI and fatal or nonfatal stroke. Additionally, changes in LVH were associated with improved parameters of diastolic function and with decreased recurrent hospitalization for heart failure [9].

POCUS for Evaluation of Left Ventricular Function:

Indications

Bedside echocardiography has invaluable benefits in the emergency department. Focused cardiac ultrasound can quickly evaluate LV function (in addition to pericardial effusion and signs of right heart strain) and help determine etiology of undifferentiated hypotension, chest pain and dyspnea, atrial fibrillation, among others [10-11]. As delineated earlier, not only is the recognition of LVH important on echocardiography, but the consequences on heart remodeling due to LVH may be even more important. Assessment of LV ejection fraction is a hallmark of assessing left ventricular function as a whole and is a valuable tool in the management of patients in the ED [10].

Evaluation and Interpretation of Left Ventricular Systolic Function

LV function is primarily expressed as an ejection fraction (EF) or the fraction of the blood present in the LV during diastole that is ejected. Three methods for LV systolic function estimation used in POCUS are visual assessment, fractional shortening (FS), and E-point septal separation (EPSS) [10-12].

1. Visual assessment:

• The fastest and most practical way to estimate LVEF in the ED

• LVEF is separated into 3 categories:

  • Normal: LVEF > 50% (hyperdynamic function: >70%)

  • Moderate dysfunction: LVEF 30-50%

  • Severe dysfunction: LVEF < 30%

• Subjective visual assessment is made of the degree of contraction between systole and diastole—with the heart evaluated in at least 2 views

• All visualized walls of the ventricle should move symmetrically towards the center of the heart chamber during systole and the walls should thicken as the muscle contracts

2. Fractional Shortening:

• Assessment of the “squeeze” of the left ventricle

• Change in anterior-posterior measurement of the LV at end of systole versus the end of diastole (expressed as a percentage)

• Most reliable in parasternal short and long axis and should be assessed at level of chordae tendinae

• Note that this is not the same as EF; FS is approximately half the EF in most cases

3. E-point Septal Separation (EPSS):

• The mitral valve opens and approaches the septum with every diastole

• EPSS is the distance in millimeters between the anterior leaflet of the mitral valve and the interventricular septum in the parasternal long axis view during the early opening point of the mitral valve in diastole. Images are obtained in M-mode.

  • EPSS ≤ 6mm is seen in normal LVEF

  • EPSS > 7mm is seen with reduced LV function [13]

*Note that this could be falsely normal in the setting of LVH

Pearls and Pitfalls

• Methods of LV assessment are operator-dependent and it is unclear how many studies one must perform to become proficient as estimating LV function

• Asymmetric wall motion abnormalities may be difficult to evaluate and LVEF is not always the best indicator of cardiac output in cases of valvular disease

• Tachycardia with normal EF may mimic a hyperdynamic heart

• Body habitus, hyperinflated lungs, patient positioning may impede good image quality

• Scan in a systematic fashion and consider sonographic findings in the clinical context of the patient [10-11]

A Quick Word on Left Ventricular Hypertrophy

While not one of the common focused clinical questions answered with POCUS, it is important to recognize LV hypertrophy when present. LVH is defined as LV wall thickness measuring >1.5 cm [14], which can be easily assessed with POCUS. When the interventricular septum is involved, the patient is at risk of LV outflow tract obstruction.

Take Home Points

• LVH is a common condition that develops in response to pressure overload and can have potentially life-threatening consequences if not recognized and addressed

• Cardiac POCUS answers focused clinical questions at the bedside, and evaluating for LV function can play an important role in the workup and management of patients in the ED

• Develop a systematic approach to your POCUS assessment and improve your ability to estimate LV function through practice

• Pay attention to LV wall thickness and recognize hypertrophy when present (>1.5cm), especially in patients with concerning clinical findings or historical features

POST BY: DR. SHRUTI AFRICAWALA, PGY1

FACULTY CO-AUTHOR/EDITOR: LAUREN MCCAFFERTY, MD

References

1. Bornstein AB, Rao SS, Marwaha K. Left Ventricular Hypertrophy. [Updated 2022 Aug 8]. In: StatPearls [Internet]. Treasure Island, FL: StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK557534/

2. Cuspidi C, Sala C, Negri F, Mancia G, Morganti A., Italian Society of Hypertension. Prevalence of left-ventricular hypertrophy in hypertension: an updated review of echocardiographic studies. J Hum Hypertens. 2012;26(6):343-9. 

3. Marketou ME, Parthenakis F, Vardas PE. Pathological Left Ventricular Hypertrophy and Stem Cells: Current Evidence and New Perspectives. Stem Cells Int. 2016;2016:5720758.

4. Goldberger AL. Left ventricular hypertrophy: Clinical findings and ECG diagnosis. [Updated 3 November 2022]. Accessed May 2023. <https://medilib.ir/uptodate/show/2112>

5. Gunther S, Grossman W. Determinants of ventricular function in pressure-overload hypertrophy in man. Circulation. 1979; 59:679–688.

6. Levy D, Savage DD, Garrison RJ, et al. Echocardiographic criteria for left ventricular hypertrophy: the Framingham Heart Study. Am J Cardiol.1987; 59:956–960.

7. Lorenz CH, Walker ES, Morgan VL, et al. Normal human right and left ventricular mass, systolic function, and gender differences by cine magnetic resonance imaging. J Cardiov Magn Res.. 1999;1:7–21.

8. Goldberger AL, Goldberger ZD, Shvilkin A. Goldberger's Clinical Electrocardiography: A Simplified Approach, 9th ed, Elsevier/Saunders, Philadelphia 2017.

9. Sayin BY, Oto A. Left Ventricular Hypertrophy: Etiology-Based Therapeutic Options. Cardiol Ther. 2022; 11: 203–230.

10. Siadecki S, Saul T, Lewiss R, Solomon R. Bedside Ultrasound Assessment of Left Ventricular Function. ACEP Now. 3 Feb. 2015. Accessed May 2023. <www.acepnow.com/article/bedside-ultrasound-assessment-left-ventricular-function/?singlepage=1>

11. Woo, Michael. Point-of-Care Echocardiography for the Emergency Physician: A Primer, 1st Edition. Accessed May 2023 <emottawablog.com/wp-content/uploads/2020/07/DEMEchov3.docx-1.pdf>

12. Mallin M, Dawson M. ​Introduction to Bedside Ultrasound: Volume 2​. Apple Books; 2013.

13. Miller T, Salerno A, Slagle D. Advanced Critical Care Ultrasound: E-Point Septal Separation to Estimate Left Ventricular Ejection Fraction. EMRA. 2021; May 2021. Accessed May 2023 <www.emra.org/emresident/article/epss>

14. Cunningham KS, Spears DA, Care M. Evaluation of cardiac hypertrophy in the setting of sudden cardiac death. Forensic Sci Res. 2019; 4(3): 223–240.

A 35-year-old female with a past medical history of recent UTI presented to the ED for two days of left-sided flank pain radiating to her groin. The day prior to presentation she developed urinary urgency, nausea, and vomiting. She denied vaginal bleeding or discharge, fevers, chills, or changes in bowel movement. She endorsed sexual activity but reported using condoms.

Her physical exam revealed a well-appearing and afebrile patient. She had left CVA tenderness and mild suprapubic tenderness with no rebound or guarding.

Renal POCUS was performed to evaluate for hydronephrosis and showed the following:

POCUS findings:

There is hydronephrosis of the left kidney. The right kidney is normal-appearing. Bladder views incidentally revealed a large complex, fluid-containing lesion in the pelvis (color doppler negative).

Case continued: Labs were significant for leukocytosis. Urine pregnancy test was negative and urinalysis did not show evidence of a UTI. CT scan showed a mixed solid and cystic lesion within the left adnexa concerning for a tubo-ovarian abscess and left-sided hydronephrosis likely due to external ureteral compression by the left adnexal mass. Transvaginal ultrasound demonstrated 8 cm tubo-ovarian abscess with dense adhesions between the sigmoid colon and bladder. The patient was started on ceftriaxone, doxycycline, and metronidazole. She was admitted to gynecology and ultimately underwent IR-guided drainage of the abscess.

Tubo-Ovarian Abscess and Pelvic Inflammatory Disease

A Quick Review of Pelvic Inflammatory Disease

Pelvic inflammatory disease (PID) is an ascending infection from the cervix to the upper reproductive tract, usually secondary to polymicrobial infection. The most common pathogens are gonorrhea and chlamydia. However, it can also be caused by H flu, strep pneumonia, group A strep, and staph aureus. It is less common during the second and third trimesters of pregnancy due to obstruction of the cervix with the mucous plug and inability of bacteria to ascend [1].

What is a tubo-ovarian abscess?

A tubo-ovarian abscess (TOA) is a fluid collection involving the ovaries or fallopian tubes that forms as a late-stage complication of PID. It is a potentially life-threatening emergency because it can rupture, leading to severe sepsis. Mortality rates have been reported as high as 5-10% when severe systemic involvement occurs [2].

Clinical Presentation

Common signs and symptoms include adnexal pain, vaginal discharge, leukocytosis, elevated inflammatory markers, or systemic signs of sepsis. Fever may be absent in 35% of patients with TOA [3]. Screening for Neisseria gonorrhea and chlamydia trachomatis are essential to obtain when diagnosing pelvic inflammatory disease or tubo-ovarian abscess but is only positive in 25% of cases [2].

Diagnosis

TOA is commonly diagnosed with transvaginal ultrasound and often appears as complex/cystic mass. A “cogwheel” sign may be seen, which is a thickening of the endosalpingeal folds, see Figure 1. Other imaging such as CT may be useful if concerned about other acute abdominal processes [2].

Management

IV antibiotics are effective in 70% of cases [2,4]. Ceftriaxone, doxycycline, and metronidazole is one of the recommended regimens [1]. Surgical intervention is often indicated when there are signs of TOA rupture like peritonitis or sepsis or for cases refractory to conservative management. Drainage is considered when the abscess is greater than 7 cm (1, 4].

Renal POCUS Review

Indications

• Flank, back, abdominal pain especially if undifferentiated

• Urinary symptoms

• Difficulty voiding

Goal: evaluate for hydronephrosis

Back to Basics: How to perform a renal ultrasound [5-7]

1. Position the patient supine with their arms above their head

2. Use the curvilinear probe

3. Evaluate each kidney followed by the bladder.

4. Right kidney — Obtain a longitudinal view by placing the probe on their midaxillary line on the right around the 10th rib with probe marker pointing toward the patient’s head

5. Identify components of the kidney (see Figure 2).

6. Fan through the kidney in this longitudinal view. Then rotate the probe 90 degrees to obtain the short access view and again fan through.

7. Evaluate primarily for hydronephrosis (and notice other abnormalities if present).

8. Apply color doppler to the kidney, particularly over the renal pelvis, to differentiate vasculature from hydronephrosis.

9. Left kidney — Place the probe on the posterior axillary line near the left flank

10. Similar to the right, evaluate the kidney in both longitudinal and transverse axis view, fan through in both plans, and apply the color doppler.

11. After evaluating both kidneys, it is necessary to obtain a bladder view — obtain a longitudinal view by placing the transducer above the pubic symphysis with the probe marker directed to the patient’s head (sagittal view)

12. Fan through the entire bladder.

13. Turn the transducer 90 degrees so the probe marker is towards the patient’s right and fan through the entire bladder in this transverse view.

14. When obtaining bladder views, the goal is to evaluate for urinary retention and you may find additional information that can indicate a potential cause for hydronephrosis, including a mass, clot, or large prostate.

Troubleshooting tips: if rib shadows are getting in the way, you can rotate the probe slightly (counterclockwise on the right, clockwise on the left) to better fit between the ribs. Can also ask the patient to perform deep inspiratory hold which will help bring the kidney away from rib shadows.

Findings of Hydronephrosis:

Hydronephrosis results from urinary tract obstruction leading to dilation of the renal pelvis +/- ureter depending on the location of the obstruction. Therefore, the differential diagnosis can include any pathology leading to intrinsic or extrinsic obstruction, including but not limited to kidney stones, mass, clot, compression from another organ at any point in or near the genitourinary system. The presence of unilateral versus bilateral hydronephrosis can help narrow the differential, which is why it’s important to always evaluate both kidneys and the bladder, even if the patient only has unilateral symptoms [5,6]

Grading of hydronephrosis:

Hydronephrosis can be graded based on the amount of swelling in the kidney. As the grading increases, the structures in the kidney are more swollen due to the backflow. Grade 1 hydronephrosis is when the pelvis is dilated. As it progresses to grade 2, dilation also involves the major calyces. For grade 3 hydronephrosis, there is also dilation of the minor calyx. Grade 4 is indicated by cortical thinning. Determining the specific grade is less important than identifying hydronephrosis and recognizing that it’s a continuum, starting from more central structures and progressing outward as the severity increases [5].

Pitfalls

Hydronephrosis can commonly be confused with the medullary pyramids of the kidneys, as well as cysts or vascular prominence/malformation. Pyramids and renal cysts are distinct structures and tend to be more peripherally located compared to hydronephrosis which starts centrally. Vasculature can be differentiated from hydronephrosis with color doppler [5-7].

Take Home Points

• POCUS is a useful tool when evaluating flank pain as well as back or abdominal/back pain

• Detecting hydronephrosis can help indicate need for additional imaging

• Hydronephrosis doesn’t just indicate kidney stones; it can also result from ureteral compression, outlet obstruction, dysfunctional bladder

• For renal POCUS, remember to always fan through both kidneys in long and short axis, apply color doppler to differentiate hydro from prominent vasculature, and evaluate the bladder, even if pain is unilateral

• Keep PID/TOA on the differential for young women of reproductive age

POST BY: DR. BROOKE OTT, PGY1

FACULTY CO-AUTHOR/EDITOR: LAUREN MCCAFFERTY, MD

References

1. Vieth J. Gynecologic Infections. EM:RAP CorePendium. 2023 June 1. Accessed June 2023. https://www.emrap.org/corependium/chapter/recMD39dDowygJS9k/Gynecologic-Infections#h.5q7bbzb048j5

2. Munro K, Gharaibeh A, Nagabushanam S, Martin C. Diagnosis and management of tubo-ovarian abscesses. The Obstetrician & Gynecologist. 2018; 20(1): 11-19.

3. Kairys N, Roepke C. Tubo-Ovarian Abscess. In: StatPearls [Internet]. Treasure Island, FL: StatPearls Publishing. 2019. https://www.ncbi.nlm.nih.gov/books/NBK448125/

4. Beigi RH. Management and complications of tuba-ovarian abscess. In: UpToDate. Waltham, MA. Accessed June 2023. https://www.uptodate.com/contents/management-and-complications-of-tubo-ovarian-abscess

5. Dinh V. Renal Ultrasound Made Easy: Step-By-Step Guide. POCUS 101. Accessed June 2023. https://www.pocus101.com/renal-ultrasound-made-easy-step-by-step-guide/

6. Avila J. Hydronephrosis. 5 Minute Sono. Core Ultrasound. Accessed June 2023. https://www.coreultrasound.com/hydronephrosis/

7. Blaivas M. Kidneys. In: Radiology Key. 2016 August 18. Accessed June 2023. https://radiologykey.com/kidneys-6/

History

• Domoic acid (DA/DOM), heat-stable toxin, produced by Pseudo-nitzsche, a single-celled, algae-like organism

• 1958- In a search for new antiparasitic compounds, Japanese scientists discover DA in Chrondria armata, a red algae found in tropical and sub-tropical waters

• 1961- In Capitola, CA, some nonaggressive, fish-eating seabirds exhibit unusual and aggressive behavior such as attacking humans and crashing through glass windows. Residents were quoted as saying the birds “cried like babies”. Alfred Hitchcock used this frightening event as inspiration for his classic 1963 horror film “The Birds”. Marine scientists now largely believe that the Sooty shearwaters in Capitola were suffering from DA poisoning.

• 1987- First documented episode of DA poisoning in humans occurs in Canada. The unusual focus of the clinical symptomology on memory impairment leads to the clinical label of Amnesic Shellfish Poisoning (ASP).

• 1991-1993- First documented episode of DA contamination in the United States occurred on Washington State beaches. During the same period, unusual behavior is noted in seabirds living near Monterey Bay in California.

• 1998- First documentation of large-scale marine mammal killing from DA poisoning. More than 400 sea lion deaths were attributed to DA exposure. Symptoms included weaving and bobbing, seizures, bulging eyes, disorientation, and ataxia.

• 2007-2008- Scientists from the Santa Barbara Museum of Natural History recorded high levels of DA in coastal waters and reported an unusual mortality event involving sea lions, dolphins, and birds.

• Summer of 2015- a massive toxic algal bloom, stretching from central California to the Alaska Peninsula, resulted in a significant impact on coastal resources and marine life.

Mechanism

• The main vectors of algal toxins to humans are filter-feeding bivalve mollusks and herbivorous finfish that ingest toxic algae, such as mussels, clams, scallops, and oysters. Humans are then intoxicated through shellfish consumption.

Domoic Acid

• Domoic acid is structurally related to glutamate and acts as a powerful excitatory neurotransmitter that can cause the death of neurons in the amygdala and hippocampus, which explains the short-term memory loss aspect of the clinical presentation.

• Pharmacokinetic studies have indicated that DA is well distributed in body water and primarily cleared from plasma through the kidneys

Clinical Manifestations

• Non-specific: nausea, vomit, diarrhea, abdominal cramps

• Neurologic symptoms: headache, seizures, hemiparesis, ophthalmoplegia, anterograde amnesia, and abnormalities of arousal ranging from agitation to coma. Affected patients were unable to remember events that occurred after DA intoxication and had difficulty recalling new information.

• Per the original report: “On neuropsychological testing several months later, 12 of the patients had severe anterograde-memory deficits, with relative preservation of other cognitive functions. Eleven patients had clinical and electromyographic evidence of pure motor or sensorimotor neuronopathy or axonopathy. Positron-emission tomography of four patients showed decreased glucose metabolism in the medial temporal lobes. Neuropathological studies in the four patients who died after mussel-induced intoxication demonstrated neuronal necrosis and loss, predominantly in the hippocampus and amygdala”

Episodic Memory & Anterograde Amnesia

• Episodic memory refers to memory for specific experiences, usually associated with a time, place, and emotion.

• For example, recalling a birthday party that you attended, who was there, where it occurred, and your own personal interactions there, reflects your episodic memory of that event.

• In the hippocampus, episodic memories are formed and cataloged to be filed away in long-term storage across other parts of the cerebral cortex.

• Patient H.M. was unable to recall any events from his daily life after his hippocampal resection.

Management

• Amnesic Shellfish Poison toxin isn't destroyed by cooking or freezing.

• There is no antidote for Amnesic Shellfish Poisoning. Medical therapy consists of supportive care.

• Although evidence is lacking, some experts support administration of activated charcoal to bind any non-absorbed food given the potential for poor outcomes, including permanent short-term memory loss, despite appropriate supportive care.

• Most important: After the Canadian outbreak, limits on domoic acid concentration in shellfish were rapidly adopted at 20 micrograms per gram of shellfish flesh. These limits based upon the lowest concentrations in mussels found to cause symptoms (200 micrograms per gram of shellfish flesh) reduced by a factor of 10. Wide adoption of the limits on harvested mussels by developed nations has been associated with no further outbreaks on the scale of the Canadian experience.

• However, the economic hardships can extend beyond fishing-related operations to include other sectors, particularly the hospitality industry, threatening the cultural identities of the affected communities.

Global Warming & Algal Bloom

• Warming water temperature

  • Toxic blue-green algae prefer warmer water.

  • Warmer temperatures prevent water from mixing, allowing algae to grow thicker and faster.

• Changes in salinity

  • Climate change might lead to more droughts, which make freshwater saltier. This can cause marine algae to invade freshwater ecosystems. 

• Higher carbon dioxide levels

  • Algae need carbon dioxide to survive. Higher levels of carbon dioxide in the air and water can lead to rapid growth of algae

• Changes in rainfall

  • Extreme storms followed by periods of drought can lead to more algal blooms

• Sea level rise

  • Scientists predict that sea level could rise up to one meter by the year 2100. This would create more shallow and stable coastal water, conditions that are perfect for the growth of algae.

• Coastal upwelling

  • Coastal upwelling is the process by which winds push surface water offshore and deep water moves towards the coast, bringing nutrients from the ocean floor to the surface. Climate change is expected to alter the timing and intensity of coastal upwelling.

POST BY: RONGYI SUN, MS4

FACULTY EDITING BY: DR. LAUREN PORTER

References

• Amnesic Shellfish Poisoning (ASP) from Domoic Acid. (2022). Washington State Department of Health. https://doh.wa.gov/community-and-environment/shellfish/recreational-shellfish/illnesses/biotoxins/amnesic-shellfish-poisoning

• Climate Change and Harmful Algal Blooms | US EPA. (January 5, 2022). US EPA. https://www.epa.gov/nutrientpollution/climate-change-and-harmful-algal-blooms#:~:text=Warmer%20temperatures%20prevent%20water%20from,warmer%20and%20promoting%20more%20blooms.

• Grant KS, Burbacher TM, Faustman EM, Gratttan L (2010). Domoic acid: neurobehavioral consequences of exposure to a prevalent marine biotoxin. Neurotoxicol teratol. 32(2):132–141.

• James K, Carey B, O’Halloran J, Van Pelt F, Skrabakova Z (2010). Shellfish toxicity: Human health implications of marine algal toxins. Epidemiol Infect. 138(7): 927-940. doi:10.1017/S0950268810000853

• Marcus EN (2021). Overview of shellfish, pufferfish, and other marine toxin poisonings. In: UpToDate, Waltham, MA. (Accessed on March 2023)

• Shellfish poisoning: A neurotoxic consequence of global warming (2022). Open Access Government. https://www.openaccessgovernment.org/shellfish-poisoning-a-neurotoxic-consequence-of-global-warming/137689/

• Pulido OM (2008). Domoic acid toxicologic pathology: a review. Marine drugs. 6(2): 180–219. https://doi.org/10.3390/md20080010

• Saeed AF, Awan SA, Ling S, Wang R, Wang S (2017). Domoic acid: Attributes, exposure risks, innovative detection techniques and therapeutics. Algal Research. 24: 97-110. https://doi.org/10.1016/j.algal.2017.02.007

• Scholin CA, Gulland F, Doucette GJ, et al (2000). Mortality of sea lions along the central California coast linked to a toxic diatom bloom. Nature. 403(6765): 80–84. https://doi.org/10.1038/47481

• Stark S, Stark C (2016). Introduction to Memory. In: Neurobiology of Language. pp841-854.

• Teitelbaum JS, Zatorre RJ, Carpenter S, et al. (1990) Neurologic sequelae of domoic acid intoxication due to the ingestion of contaminated mussels. N Engl J Med. 322(25): 1781–1787. https://doi.org/10.1056/NEJM199006213222505

• The limbic system. The University of Queensland. (Last archived Sept. 29. 2022). https://qbi.uq.edu.au/brain/brain-anatomy/limbic-system

• West Coast Harmful Algal Bloom (May 2, 2016). National Ocean Service. https://oceanservice.noaa.gov/news/sep15/westcoast-habs.html

75-year-old male with past medical history significant for pituitary adenoma (status post resection) who presented with a 24-hour history of acute painless vision loss in his left eye. This started suddenly while riding in a car when he developed a “black hole” in the inferomedial aspect of his left eye. He then felt a “curtain closing down over his eye” with decreased vision in the lower visual fields of that eye. He reported having a history of fuzzy vision in his left eye, occasional floaters, and dry eyes but felt that presenting symptoms were different. He denied any discharge from his eye, periorbital edema, or fevers but did report that his eye felt a little itchy. He also denied any headache, dizziness, or weakness or numbness in the upper or lower extremities.

Ocular point-of-care ultrasound (POCUS) was performed to evaluate for retinal detachment.

POCUS Findings:

There is a large lateral retinal detachment indicated by a distinct hyperechoic linear structure in the posterior chamber that has separated from the choroid and is tethered on temporal side of the vitreous body (screen right). This is further appreciated with the kinetic exam, in which the patient looked left and right. There is also a highly echogenic structure at the base of the optic nerve, most likely drusen, which are calcium deposits that are usually benign.

Case Continued: Ophthalmology was consulted, and through their comprehensive assessment they confirmed retinal detachment with macular involvement (“mac-off”). The patient was discharged with plan to return 8 hours later for laser intervention and reattachment of the detached portion of the retina with a retina specialist.

Retinal Detachment

Pathophysiology of Retinal Detachment

Through the aging process, the vitreous humor shrinks and thins. The vitreous humor moves, without friction, around on the retina. However, if a portion of the vitreous sticks to the retina, it can pull on the attached portion causing a tear allowing fluid to pass through and lift the retina [1]. It is important to remember that the retina is a continuation of the optic nerve. Conditions that increase likelihood of developing a retinal detachment are severe myopia, prior eye surgery (cataract, glaucoma), eye trauma, prior retinal detachments. Common signs and symptoms of retinal detachment are sudden onset of floaters or flashers, shadowing or a “curtain” over the field of vision. [1].

Anywhere from 1.3-3% of emergency department visits are due to eye-related complaints [2-3]. While retinal detachment is not one of the more common pathologies, it is considered an eye emergency for which prompt recognition is important [4].

Review of Imaging Modalities for Retinal Detachment

There are several imaging options, including ultrasound, CT, or MRI, that can be used to evaluate eye conditions. Depending on the pathology, these have varying diagnostic utility [3, 5-7]. While the gold standard for diagnosing retinal detachment is a dilated fundoscopic examination, performed primarily by an ophthalmologist, ultrasound has been used by ophthalmologists for decades. More recently emergency physicians have utilized POCUS to evaluate for retinal detachment and have demonstrated a sensitivity and specificity of 97% -100% and 83% -100%, respectively [3]. Another study among a large heterogeneous group of emergency physicians showed sensitivity of 75% and specificity of 94% [5]. MRI is generally not the preferred imaging modality for evaluating retinal detachment as time to acquire image is lengthy, it is expensive, and may provide a limited assessment. Also, if there is a possibility of metallic foreign body in the globe, MRI would not be favorable. MRI is useful in evaluating for the underlying cause of retinal detachment such as a mass, disease within the globe and orbit, or optic nerve pathology [6]. Given cost, timing, and other logistical barriers associated with MRI, POCUS is a fast and reliable diagnostic modality that should be incorporated into the standard initial workup for retinal detachment, along with ophthalmologist exam, unless there is concern for an open globe injury. It is a particularly useful option when ophthalmology is not immediately available or if a fundoscopic exam cannot be performed [8].

Materials:

• High frequency linear probe

• Tegaderm to cover eye

• Ultrasound gel

Techniques for Ocular Ultrasound

Place a transparent adhesive covering, such as a tegaderm, over the patient’s eye and ensure there are no air pockets. Using a linear transducer (10-5 MHz) offers the highest resolution given the superficial depth of the structures of the eye. The technician should stabilize their hand gently on the patient’s nasal bridge or zygoma to prevent excessive force on the eye with the probe. Probe marker should face the patient’s right side.

With a normal gain setting, adjust depth to allow for visualization of the posterior segment of the eye that includes the retina and optic nerve. Identify (from top to bottom) the cornea, anterior chamber, lens, vitreous chamber, retina, and optic nerve (see Figure 3). Once these structures are identified, reduce gain until the vitreous humor is anechoic. Then using oculokinetic echography, i.e. having the patient look left and right and evaluating the dynamic movement of the eye with ultrasound, examine the vitreous humor for any abnormalities that are not firmly attached to the retina [9-10].

Retinal Detachment

Often visualized in normal or low gain settings, retinal detachment appears as a hyperechoic mobile cord-like structure that is attached to or near the optic nerve in the posterior wall of the eye. If the retinal detachment is large, the flap is often easily visualized where it attaches to the optic nerve sheath. For smaller retinal detachment or those not near the optic nerve, scan through the eye horizontally and vertically and then slow down the image after capture to carefully evaluate for a tethered flap. In addition to its relation to the optic nerve, retinal detachment tends to be less mobile with kinetic movement compared to vitreous detachment or hemorrhage [9-10].

Vitreous Detachment & Hemorrhage

Best visualized with high gain settings, both tend to be more free floating with a “washing machine” appearance with kinetic movement in the posterior chamber of the eye. Posterior vitreous detachment (PVD) often has a thin hyperechoic flap that crosses over the optic nerve and is not tethered to the posterior wall. Vitreous hemorrhage (VH) appears as diffuse echogenic material and may have a “snowglobe” appearance. It is frequently seen in diabetic patients, is easier to distinguish from posterior vitreous detachment and retinal detachment, and is not an ocular emergency [9-10].

Take Home Points

1. Retinal detachments make up a small percentage of atraumatic eye presentations but require emergent evaluation for definitive treatment. Conditions associated with risk of developing RD are severe myopia, prior eye surgery, eye trauma, prior retinal detachments

2. Retinal detachment appears as a hyperechoic flap within the vitreous body that is tethered to the posterior wall at or near the optic nerve. Use oculokinetic echography and slow down image to optimize your evaluation

3. Slowly increase the gain to evaluate for PVD and VH, which are more free floating (washing machine sign) and can cross midline with no relation to the optic nerve.

POST BY: DR. RANJANA RAVIKUMAR, PGY1

FACULTY CO-AUTHOR/EDITOR: LAUREN MCCAFFERTY, MD

References

1. Boyd K. Detached retina. American Academy of Ophthalmology. October 13, 2022. Retrieved May 1, 2023. <https://www.aao.org/eye-health/diseases/detached-torn-retina>

2. Nash EA, Margo CE. Patterns of emergency department visits for disorders of the eye and ocular adnexa. Arch of Ophthalmol. 1998;116(9):1222–1226.

3. Vrablik ME, Snead GR, Minnigan HJ, Kirschner JM, Emmett TW, Seupaul RA. The diagnostic accuracy of bedside ocular ultrasonography for the diagnosis of retinal detachment: A systematic review and meta-analysis. Annals Emerg Med. 2018; 65(2).

4. Channa R. Zafar SN, Canner JK, Haring RS, Schneider EB, Friedman DS. Epidemiology of eye-related emergency department visits. JAMA Ophthalmol. 2016; 134(3):312-9.

5. Kim DJ, Francispragasam M, Docherty G., Silver B., Prager R, Lee D, Maberley D. Test characteristics of point‐of‐care ultrasound for the diagnosis of retinal detachment in the emergency department. Acad Emerg Med. 2019;26(1):16-22.

6. Hallinan JT, Pillay P, Koh LH, Goh KY, Yu WY. Eye Globe Abnormalities on MR and CT in Adults: An Anatomical Approach. Korean J Radiol. 2016 Sep-Oct;17(5):664-73. doi: 10.3348/kjr.2016.17.5.664. Epub 2016 Aug 23. PMID: 27587955; PMCID: PMC5007393.

7. Skidmore C, Saurey T, Ferre RM, Rodriguez-Brizuela R, Spaulding J, Lundgreen Mason N. A narrative review of common uses of ophthalmic ultrasound in emergency medicine. J Emerg Med. 2021; 60(1), 80–89.

8. Botwin A, Engel A, Wasyliw C. The use of ocular ultrasound to diagnose retinal detachment: A case demonstrating the sonographic findings. Emerg Radiol. 2018; 25(4), 445–447.

9. Nagdev A. Ocular ultrasound: Retinal detachment and Posterior Vitreous Detachment. ALiEM. March 11, 2014. Retrieved April 20, 2023. <https://www.aliem.com/ocular-ultrasound-retinal-detachment-posterior-vitreous-detachment/>

10. Dinh V. Ocular Ultrasound made easy: Step-by-step guide. POCUS 101. Accessed May 1, 2023. <https://www.pocus101.com/ocular-ultrasound-made-easy-step-by-step-guide/>

The next alert you get is that your patient in room 21 has a calcium of 14.2. What does this mean? Is this information you place on the back burner or is it something that should play a major role in your decision making during their care?

Physiology

Calcium is regulated through the parathyroid glands and the kidneys. The parathyroid glands detect the calcium level in the blood stream and will secrete PTH to stimulate the kidneys to produce calcitriol. Additionally, vitamin D plays a key factor in aiding this process. This ultimately causes the bones to release calcium and for increased calcium absorption, increasing the serum calcium. Counteractively, when calcium levels are high, the parathyroid stops secreting PTH, downregulating this process. Additionally, the thyroid will secrete calcitonin to promote bones to resorb calcium and promote calcium filtration. See Figure 1.

Pathophysiology of Hypercalcemia

There are various processes that can cause hypercalcemia (see Figure 2 below). For the purposes of this article, we will review the two most common forms. First with hyperparathyroidism and then hypercalcemia of malignancy.

Hyperparathyroidism can be broken down into two forms. Primary hyperparathyroidism, which is hypercalcemia caused by the over secretion of PTH. This is most commonly caused by adenomas or hyperplasia.  These patients will often present with more mild-range calcium levels.

The more feared cause of hypercalcemia would be hypercalcemia of malignancy. This is one of the most common forms of hypercalcemia and can often present with severe ranges of calcium. Of note, these patients can have up to a 50% 30-day mortality rate! The way malignancy causes this is often from a paraneoplastic syndrome, such as a PTHrP secreting tumor, or from osseus destruction from bone metastasis. Some tumors can also hydroxylate vitamin D themselves which leads to the development of hypercalcemia.

Signs and Symptoms

The symptoms are often vague. They can include muscle weakness, confusion, bone pain, perioral numbness, muscle spasms, polyuria and confusion. Some patients may also develop frequent nephrolithiasis. There can be some EKG changes as well. QTc shortening is the most common abnormality noted, but in rare cases AV blocks and bradycardia/asystole can occur as well (see Figure 4).

Interpreting the lab value

The first step to interpreting the lab value is to correct it. Calcium binds to albumin, so in patients who are hypoalbuminemic, the values can be falsely elevated. The formula is as follows:

One caveat to this is that it can often times overestimate calcium. Another option you could do is to order ionized calcium, which is independent of the patient’s albumin.

Once you have an accurate calcium, you can now grade the patient’s hypercalcemia.

Mild: Corrected Ca 10.5-12 mg/dL OR iCa 1.4-2 mmol/L

Moderate: Corrected Ca 12-14 mg/dL OR iCa 2-2.5 mmol/L

Severe: Corrected Ca >14 mg/dL OR iCa >2.5 mmol/L

Managing the hypercalcemia

The grade of the patient’s hypercalcemia has a major impact on how this should be managed. Patients with severe range hypercalcemia is often from a malignant cause, where as mild ranges can be from various other causes, see Figure 5. Hypercalcemia may be the only presenting sign of a patient’s malignancy, so it is key to be aware of this and to work it up appropriately.

Mild range calcium levels often times do not immediate treatment. However, a thorough medical history and medication review should be performed on these patients. They should be aware of these results and be provided with appropriate outpatient follow up. Moderate ranges are based entirely on the patient’s presenting complaint. Again, these patients require a thorough history and medication review. However, if they have signs/symptoms of the hypercalcemia, they should be treated. Severe range hypercalcemia should always be treated.

 The treatment of hypercalcemia includes three parts. The first is with IV fluids. Normal saline is the preferred method, as it has no calcium in it, although lactated ringers is appropriate as well. This will promote diuresis of calcium. These patients want to have a goal urine output of 100-150 cc/hr. Lasix is only indicated if the patient is unable to tolerate fluids or achieve this urine output without it. Next is calcitonin. As we reviewed above, this will promote diuresis of calcium, decreased intestinal absorption, and increased bone deposition. Lastly, bisphosphonates can be used to prevent bone resorption and aid in decreasing calcium levels. However, this will take days-weeks to act. Calcitonin acts within about 1-2 days. Of course, these patients requiring treatment need at a bare minimum telemetry admission. Although, based on comorbidities, an ICU admission or dialysis may be indicated in some circumstances.

POST BY: DR. DAN SAADEH (PGY3)

FACULTY EDITING BY: DR. NIK SEKOULOPOULOS

References

1. Alfaraj DN, Wilson MP, Akeely Y, Vilke GM, Nordstrom K. Psychiatric Emergencies for Clinicians: Emergency Department Management of Hypercalcemia. J Emerg Med. 2018 Nov;55(5):688-692.

2. AlZahrani A, Sinnert R, Gernsheimer J. Acute kidney injury, sodium disorders, and hypercalcemia in the aging kidney: diagnostic and therapeutic management strategies in emergency medicine. Clin Geriatr Med. 2013 Feb;29(1):275-319.

3. Chang WT, Radin B, McCurdy MT. Calcium, magnesium, and phosphate abnormalities in the emergency department. Emerg Med Clin North Am. 2014 May;32(2):349-66.

4. Crowley R, Gittoes N. How to approach hypercalcaemia. Clin Med (Lond). 2013 Jun;13(3):287-90.

5. Dellay B, Groth M. Emergency Management of Malignancy-Associated Hypercalcemia. Adv Emerg Nurs J. 2016 Jan-Mar;38(1):15-25; quiz E1.

6. Lee CT, Yang CC, Lam KK, Kung CT, Tsai CJ, Chen HC. Hypercalcemia in the emergency department. Am J Med Sci. 2006 Mar;331(3):119-23.

7. Lindner G, Felber R, Schwarz C, Marti G, Leichtle AB, Fiedler GM, Zimmermann H, Arampatzis S, Exadaktylos AK. Hypercalcemia in the ED: prevalence, etiology, and outcome. Am J Emerg Med. 2013 Apr;31(4):657-60.

8. Ralston SH, Gallacher SJ, Patel U, et al. Cancer-associated hypercalcemia: Morbidity and mortality. Clinical experience in 126 treated patients. Ann Intern Med. 1990;112:499–504.

9. Sauter TC, Lindner G, Ahmad SS, Leichtle AB, Fiedler GM, Exadaktylos AK, Haider DG. Calcium Disorders in the Emergency Department: Independent Risk Factors for Mortality. PLoS One. 2015 Jul 14;10(7):e0132788.

10. Taylor DM, Date PA, Ugoni A, Smith JL, Spencer WS, de Tonnerre EJ, Yeoh MJ. Risk variables associated with abnormal calcium, magnesium and phosphate levels among emergency department patients. Emerg Med Australas. 2020 Apr;32(2):303-312.

11. Wagner J, Arora S. Oncologic metabolic emergencies. Emerg Med Clin North Am. 2014 Aug;32(3):509-25.

12. Wilson RF, Sibbald WJ. Fluid and electrolyte problems in the emergency department. JACEP. 1976 May;5(5):339-46.

• AKA Fly agaric & Fly amanita

• Description: Red/orange cap with white spots

• Toxins: Ibotenic acid, muscimol, muscarine

• Clinical findings

  • CNS: CNS depression, agitation, hallucinations

  • GI: Nausea, vomiting, diarrhea

  • Symptoms can vary based on amount of each toxin in the mushroom ingested

• Treatment

  • Supportive

  • IVF, antiemetics, benzodiazepines

Amanita pantherina

• AKA Panther cap, false blusher

• Description: Shiny brown or grey brown cap with white spots

• Toxins: Ibotenic acid and mucimol

• Clinical findings:

  • CNS: CNS depression, agitation, hallucinations

  • GI: Nausea, vomiting, diarrhea

  • Symptoms can vary based on amount of each toxin in the mushroom ingested

• Treatment

  • Supportive

  • IVF, antiemetics, benzodiazepines

Amanita Phalloides

• AKA Death cap

• Description: Yellow/green cap, white gills and stem

• Toxin: Amatoxin

• Clinical findings: Onset 6-12 hours

  • GI: nausea, diarrhea; hepatotoxic

• Treatment:

  • NAC

  • Activated charcoal

  • IV Silibinin

  • Transplant

Psilocybin

• AKA Magic mushrooms

• Description: Goldish brown cap, halos, bruises when touched

• Toxin: Psilocybin

• Clinical findings:

  • Onset 30 min

  • Duration 4-12 hours

  • CV: HTN, tachycardia

  • Neuro: Hallucinations, tachycardia

• Treatment: Supportive

Clitocybe dealbata

• AKA iIvory funnel

• Description: White, flat, wavy margin

• Toxin: Muscarine

• Clinical effects:

  • Onset 15-30 min

  • Duration 2-12 hours

  • Symptoms: cholinergic —Increased secretions-GI/respiratory

• Treatment:

  • Atropine

  • Scopolamine

Corprinopsis atramentaria

• AKA Inky cap

• Description: Grey, brown, bell shaped

• Toxin: Coprine

• Clinical effects:

  • Onset 30min-2 hours

  • Duration 2-6 hours

  • Symptoms: Disulfiram like reaction — Flushing, headache, tachycardia, anxiety, chest pain

• Treatment: Supportive

Gyromitra esculenta

• AKA False morel

• Description: Red, brown brain

• Toxin: Gyromitrin

• Clinical effects

  • Onset 4-10 hours

  • Duration 2-5 days

  • Symptoms:

    • GI: Nausea, vomiting, diarrhea

    • Neuro: Refractory seizures

• Treatment:

  • Pyridoxine

  • Benzodiazepines

  • Supportive treatment

Tricholoma equestre

• AKA Yellow knight

• Description: Yellow-brown cap, pale yellow stem and gills

• Clinical effects:

  • Onset 24-72 hours

  • Duration 2-3 weeks

  • Symptoms:

    • Fatigue, nausea, vomiting

    • Myalgias

    • Rhabdomyolysis

• Treatment:

  • IVF

  • Supportive management

POST BY: DR. HALEY WARTMAN, EM PGY3

FACULTY EDITING BY: DR. LAUREN PORTER (Medical Toxicology Faculty)

References

Amanita muscaria: Basic Info. ICEERS. Retrieved March 2023. https://www.iceers.org/amanita-muscaria-basic-info/

Amanita muscaria. North Carolina Extension Gardener Plant Toolbox. Retrieved March 2023. https://plants.ces.ncsu.edu/plants/amanita-muscaria/

Amanita phalloides. First Nature. Retrieved March 2023. https://www.first-nature.com/fungi/amanita-phalloides.php

Bedry R, Baudrimont I, Deffieux G, et al. Wild Mushroom Intoxication as a Cause of Rhabdomyolysis. N Engl J Med. 2001; 345 (11): 798-802.

Fontes K. Tox Cards: Mushrooms. EMdocs.22 Jun 2017. Retrieved March 2023. http://www.emdocs.net/tox-cards-mushrooms/

Gyromitra esculenta, a false morel. BioWeb. Retrieved March 2023. http://bioweb.uwlax.edu/bio203/s2013/hammett-_will/toxicity.htm

Klimaszyk P, Rzymski P. The Yellow Knight Fights Back: Toxicological, Epidemiological, and Survey Studies Defend Edibility of Tricholoma equestre. Toxins (Basel). 2018 10(11): 468.

85-year-old male with past medical history including hypertension and atrial fibrillation (for which he was on Eliquis) presented to the ED for atraumatic right knee pain and swelling. He had been having increasing difficulty walking on the knee for the last few days; however, on the day of presentation, he noticed that any small movements caused severe pain. He denied any recent falls or trauma or previous injury to knee. He had never had these symptoms before and had no history of gout or IV drug use. He denied fevers, chills, nausea, vomiting, or recent dental work.

On arrival to the ED, his vital signs were the following: Temp 98.4, HR 91, RR 18, SpO2 94% on room air, and BP 153/100. Physical exam was notable for a well-appearing male in mild distress secondary to pain. His right knee was swollen and tender to the touch. He had significant pain on passive range of motion that knee and was unable to fully bend the knee due to pain and swelling. No obvious skin changes, rash, or overlying erythema. His distal pulses were intact bilaterally.

In addition to obtaining labs (including inflammatory markers) and x-rays to evaluate for possible etiology, point-of-care ultrasound (POCUS) of the knee was performed to assess for joint effusion prior to performing a diagnostic arthrocentesis to evaluate for septic arthritis.

POCUS Findings:

A moderate volume of hypoechoic synovial fluid with some echogenicity is seen within the right knee joint with the largest area of fluid in the superolateral region. There was no major vasculature present in the area of planned needle entry for arthrocentesis.  

Case continued:

X-ray of the knee showed no acute fracture or malalignment, but there was a moderate nonspecific knee effusion noted. CBC and CMP were unremarkable. He did have an elevated CRP of 2.1 and elevated ESR of 34.

A diagnostic ultrasound-guided arthrocentesis (as described below) was performed without complication. Approximately 35 cc’s of viscous sanguinous fluid was aspirated from the knee joint. Fluid studies including cell count, culture, crystal analysis and gram stain were obtained. Fluid results revealed: WBC 5100, red color, cloudy clarity, RBC 3,375,000, Neutrophils 75, Lymphocyte 10,200. No crystals were seen on microscopy, and no organisms were seen on gram stain. There was no growth aerobically or anaerobically on fluid culture.

Based on these results, the patient was diagnosed with hemarthrosis, thought to be secondary to his anticoagulant use. The joint was wrapped with an ACE bandage and elevated. The patient was comfortable with discharge and was instructed to follow up with his primary care physician.

POCUS in the Evaluation and Management of Joint Effusions

Overview

Historically, joint arthrocentesis has been performed based on physical exam and landmark identification. With the ever-increasing popularity of ultrasound, many providers have started utilizing ultrasound for effusion identification, optimal location for aspiration, and assistance of needle-guidance, which is especially useful for smaller volume effusions. The traditional landmark-based identification method has limitations due to variations in anatomy and effusions. Success rates range from 61-78% depending on the joint involved [1]. Ultrasound offers several advantages, diagnostically and procedurally, by allowing for direct visualization of the effusion. Ultrasound can identify joint effusions as small as 4cc, which are often difficult to palpate on physical exam [2]. It is also useful in differentiating effusions from soft tissue abnormalities, which can reduce unnecessary joint aspirations [3]. Ultrasound guidance for arthrocentesis leads to greater accuracy and lower pain scores both intra- and post-procedurally compared to the traditional landmark-based approach [4]. In novice providers performing arthrocentesis, the use of ultrasound increased first-attempt success over landmark-based techniques, particularly for smaller volume effusions [5]. It has also been shown to result in more fluid aspiration and greater novice provider confidence while not taking any longer than standard palpation alone [6].  

Confirming Joint Effusion

When utilizing ultrasound to assist in the evaluation of a swollen knee joint, use the high-frequency linear probe to obtain longitudinal and transverse views of the knee. For the longitudinal (i.e. sagittal) view, place the probe just above the patella with the probe marker aimed cephalad. The suprapatellar window should include the superior portion of the patella, the quadriceps femoris tendon (long axis), fat pad, and femur. An effusion will be located between the quadriceps tendon and femur, immediately below the fat pad. Depending on the effusion, the fluid will typically appear as hypoechoic, however, it can vary, depending on the type of effusion. To obtain a short axis, or transverse, view, simply rotate the probe 90 degrees [1, 7]. Additional views can be obtained by scanning along the medial and lateral borders of the patella.

Determining Optimal Site for Arthrocentesis & Minimizing Complications

The optimal site for arthrocentesis is generally where the fluid collection is largest and best visualized; this is often the suprapatellar space. Once the best site for needle aspiration is identified, apply color Doppler to the area to ensure there are no vessels within the planned needle trajectory; this is especially important in patients on anticoagulation or with bleeding disorders. To reduce risk of infection, it important to perform this under fully sterile conditions [1].

Static vs Dynamic Ultrasound-Guidance

Once the above steps are taken, providers can choose whether they want to proceed with a static versus dynamic ultrasound-guided technique. With a static technique, ultrasound is used to identify the optimal site for needle entry but the remainder of the procedure is performed without it. Conversely, a dynamic technique involves using ultrasound in realtime to directly guide the needle into the fluid [8]. By allowing the provider to visualize and redirect the needle trajectory to the appropriate joint space, this technique is especially helpful when there is a smaller effusion, a smaller or difficult-to-reach joint space, or the nearby presence of a neurovascular bundle or other important structure(s) to avoid [9]. This technique is demonstrated below.

In-plane vs Out-of-plane Approach

Both in-plane and out-of-plane techniques are described in the literature, though the former is often described as the more preferred technique [1,7]. The in-plane technique refers to inserting the needle at the leading edge of the probe and advancing directly under and parallel to the transducer, thus allowing for visualization of the full length of the needle along its trajectory. The out-of-plane technique refers to inserting the needle perpendicular to and at the center of the transducer, allowing visualization of only a small part of the needle at any given time; ideally, you only visualize the needle tip to help ensure you do not advance the tip beyond the probe [8].

Utility of Ultrasound in Arthrocentesis of Additional Joints

We chose to focus on knee arthrocentesis based on our patient’s presentation. However, ultrasound also provides diagnostic and procedural utility for joint effusions involving the ankle, hip, shoulder, elbow, and wrist, as well as additional smaller joints. Ultrasound is especially advantageous for smaller or less accessible joints given their more limited access and allows for greater accuracy than a palpation-guided approach with increased initial intra-articular success [10]. Similar to the knee, the high frequency linear probe remains the most commonly recommended probe.

The Procedure

Materials

• Sterile US probe cover and gel

• 18g needle attached to 10 cc (or larger) syringe

• Chlorhexidine

• Sterile drape and sterile gloves

• Sterile syringe and needle with lidocaine

Dynamic Ultrasound-Guidance

• Identify the optimal location by evaluating with ultrasound as described above

• Place patient (and yourself) in the optimal position; have patient’s knee slightly flexed to improve fluid visualization

  ***Ensure US machine is positioned in direct line of site if using dynamic guidance

• Clean area and apply sterile field, place US transducer in sterile probe cover and lay on sterile field

• Anesthetize the local subcutaneous tissues using lidocaine

• While multiple techniques can be used, we recommend an in-plane approach to allow for direct visualization of the needle. As previously discussed, the needle should enter the skin at the leading edge of the linear transducer

• Visualize your needle and advance toward the effusion, making small redirections as needed. If you lose site of the needle, realign the probe with the needle to ensure good visualization of the needle shaft before advancing any further

• Apply gentle negative pressure with the syringe until aspiration of synovial fluid is achieved

Pearls and Pitfalls

• Always perform under sterile conditions; this includes using a sterile probe cover when using dynamic ultrasound-guidance to reduce risk of contamination/infection

• Position the patient for increased success, i.e. ensure the knee is slightly bent to open the joint space

• Color Doppler can be used to help identify vascular structures

• Needle-finding skills are user dependent and moving the transducer during procedures can lead to difficult needle visualization

Evaluation of synovial fluid

The evaluation of synovial fluid is the gold standard for excluding septic arthritis in patients with concerning presentation. Arthrocentesis also allows for further determination of the cause of joint effusions. Labs including CBC, CRP, and ESR are often obtained prior to arthrocentesis; however these tests do not sufficiently lower the post-test probability enough to avoid obtaining synovial fluid for analysis [11].

Figure 4 presents a step-wise approach for synovial fluid analysis. Begin by analyzing the gross appearance, including color, clarity and viscosity. Determine if the effusion is hemorrhagic, then evaluate the WBC count to determine if it is inflammatory versus non-inflammatory. Next, evaluate for crystals. Follow-up with gram stain and culture [12].

Typical evaluation includes synovial gram stain, culture, protein, LDH, glucose and lactate [11-13]. There are some variations for cutoff ranges of labs in synovial fluid findings. Synovial fluid WBC count >50 x 10^9/L is concerning for septic arthritis, though this can also be seen in inflammatory arthropathies, including gout, RA, and pseudogout, or in immunocompromised states. Typical guidelines suggest a WBC <200 is normal, 200-2,000 is non-inflammatory, 2,000-50,000 is inflammatory, and > 50,000 is infectious, although upper limit cutoffs in septic arthritis are not clearly established [12-13]. It’s also worth mentioning that synovial WBC counts can be lower than expected in cases of septic arthritis, and any true concern should be treated as assumed positive while further workup is pending. The fluid must also be analyzed for RBC count and crystals. High RBC counts are suggestive of hemarthrosis if remaining labs are otherwise unremarkable. Monosodium urate (needle-shaped) crystals versus calcium pyrophosphate (rhomboid-shaped) crystals will be seen in cases of gout and pseudo-gout, respectively [13]. Cultures of the synovial fluid are considered the most important test and should be obtained for all patients who undergo arthrocentesis. Cultures allow for identification of bacterial organisms, particularly for non-gonococcal septic arthritis [11, 13]. Figure 5 [14] presents a table summarizing findings of different inflammatory versus non-inflammatory arthropathies.

Conclusion

Overall, there are no validated clinical decision tools to help with diagnosing septic arthritis. It’s important to combine the history, physical exam, imaging and lab analysis in order to help decide next steps in care. When considering a septic joint as part of your differential, ALWAYS perform an arthrocentesis.

Take Home Points

• POCUS is a valuable bedside tool for quickly evaluating and managing patients with a swollen joints

• Diagnostically, ultrasound can quickly confirm the presence of a joint effusion and differentiate from other soft tissue pathology

• Synovial fluid analysis is key in diagnosing septic arthritis, so getting comfortable with arthrocentesis and the different techniques is key

• By allowing for direct visualization of the fluid and the needle, ultrasound guidance for arthrocentesis leads to greater accuracy, first-pass success, and provider confidence and reduces complications and pain scores, while not significantly affecting duration of the procedure

AUTHORED BY: DR. KELSIE RHYNE, PGY1

FACULTY CO-AUTHOR/EDITOR: LAUREN MCCAFFERTY, MD

References

1. Puebla DL, Farrow RA. Ultrasound Guided Arthrocentesis. StatPearls. Treasure Island (FL): StatPearls Publishing. 7 Aug 2022. Available from: https://www.ncbi.nlm.nih.gov/books/NBK573084/

2. Hong BY, Lee JI, Kim HW, Cho YR, Lim SH, Ko YJ. Detectable threshold of knee effusion by ultrasonography in osteoarthritis patients. Am J Phys Med Rehabil. 2011; 90(2):112-8. 

3. Adhikari S, Blaivas M. Utility of bedside sonography to distinguish soft tissue abnormalities from joint effusions in the emergency department. J Ultrasound Med. 2010 Apr; 29(4):519-26.

4. Wu T, Dong Y, Song Hx, Fu Y, Li JH. Ultrasound-guided versus landmark in knee arthrocentesis: A systematic review. Semin Arthritis Rheum. 2016; 45(5):627-32. [PubMed]

5. Delesky EM, Gaughan J, Roberts B, Sodhi S. Comparison of knee arthrocentesis first-attempt success between Ultrasound-Guided, Ultrasound-Localised and Landmark-Guided techniques in the novice: A crossover study with random order of events. Australas J Ultrasound Med. 2022; 25(2):74-79.

6. Wiler JL, Costantino TG, Filippone L, Satz W. Comparison of ultrasound-guided and standard landmark techniques for knee arthrocentesis. J Emerg Med. 2010 Jul7; 39(1):76-82.

7. Johnson B, Lovallo E, Mantuani D, et al. How to perform ultrasound-guided knee arthrocentesis. ACEPNow. 2015; 34(8):16-7.

8. Macias M. Ultrasound Leadership Academy: Introduction to procedural ultrasound. EM Curious. 20 December 2014. Retrieved January 20, 2023, from http://www.emcurious.com/blog-1/2014/12/7/ultrasound-leadership-academy-introduction-to-procedural-ultrasound

9. Balint PV, Kane D, Hunter J, et al. Ultrasound guided versus conventional joint and soft tissue fluid aspiration in rheumatology practice: A pilot study. J Rheumatol. 2002;29:2209-2213.

10. Raza K, Lee CY, Pilling D, Heaton S, Situnayake RD, Carruthers DM, et al. Ultrasound guidance allows accurate needle placement and aspiration from small joints in patients with early inflammatory arthritis. Rheumatology (Oxford). 2003; 42(8):976-9.

11. Long B, Koyfman A, Gottlieb M. Evaluation and Management of Septic Arthritis and its Mimics in the Emergency Department. West J Emerg Med. 2019; 20(2):331-341.

12. Sholter, DE, Russell AS. (2022). Synovial Fluid Analysis. UptoDate. Available from: https://www.uptodate.com/contents/synovial-fluid-analysis?search=synovial%20fluid%20analysis&source=search_result&selectedTitle=1~61&usage_type=default&display_rank=1#H1

13. Springer BL, Pennington BM. Joint Arthrocentesis in the Emergency Department. Relias Media. 1 Oct 2017. Retrieved from <https://www.reliasmedia.com/articles/141511-joint-arthrocentesis-in-the-emergency-department>.

14. Nickson C. Synovial fluid analysis. Life in the Fast Lane • LITFL. 2020 November 3. Retrieved January 20, 2023, from https://litfl.com/synovial-fluid-analysis/

A 52-year-old male presented to the emergency department with left heel and lower leg pain. He stated he was running outside the day prior and stepped into a pothole on the trail. There was immediate pain that initially got better with rest; however, it became worse again today. He had dull pain that began a few weeks prior but was manageable with ice and ibuprofen. He has been able to walk but has had limited range of motion at the ankle. He denied any pain or issues with the knee. He is overweight and recently started a running program to lose weight. His medical history was significant for non-insulin dependent diabetes, for which he is on metformin, and obstructive sleep apnea. He quit smoking about 10 years ago and drinks 3-4 beers per week. Six months ago he quit his office job to work in construction renovating homes. 

Physical exam was significant for reduced range of motion in the ankle due to pain and mild tenderness with palpation of the calf, however was otherwise unremarkable. Equivocal Thompson test. There was no point tenderness at the medial or lateral epicondyles. X-rays of the foot, ankle, tibia and fibula were negative for fractures or bony abnormalities. Suspecting an Achilles injury, point-of-care ultrasound was performed to evaluate.

POCUS findings: enlargement of the achilles tendon with near complete disruption of the fibers, retracted and hyperechoic edges, and multiple hypoechoic areas within the tendon. Compare to the unaffected tendon.

Case continued: He was placed in a splint, and Orthopedic surgery was consulted to help facilitate follow up. He was discharged home with crutches, non weight-bearing instructions, and supportive care. Subsequently underwent outpatient surgery without complication.

Achilles Injuries

The Achilles tendon is the strongest tendon in the body, yet, athletes and non-athletes alike often injure it [1]. The common calf muscles, the gastrocnemius and the soleus, meet in the distal leg forming the Achilles tendon before inserting at the posterior calcaneus. These muscles are major players in plantarflexion of the foot. Therefore, when it becomes compromised, there may be a general disruption to the patient’s gait, however ambulation is usually still possible due to accessory muscles, such as the tibialis posterior. The weakest point of the Achilles tendon is 2-6 cm proximal to the insertion at the calcaneus. This is the site of least blood flow to the tendon and is also the site of the greatest tenderness with palpation on exam [2]. It is generally accepted that weakness, inflammation, or a systemic disease usually precipitates Achilles tendon tears, unless one injures it during high energy sports [1]. The Thompson test is a physical exam maneuver that can aide in the diagnosis of an Achilles injury. With the patient laying prone, squeeze the gastrocnemius muscle belly. A lack of plantarflexion with this action is indicative of an Achilles injury. The Thompson test is a well-supported component of the physical exam with a sensitivity of 96% and specificity of 93% [3]. If there is high suspicion of Achilles injury but a negative Thompson test, further imaging should be obtained.

Review of Imaging Modalities

Ultrasound and MRI are the imaging modalities most used to assess muscle, soft tissue and ligamentous injuries. Specifically in the emergency department, ultrasound is a readily used and widely accepted modality to evaluate musculoskeletal complaints [4]. Many studies have recommended ultrasound for the diagnosis of Achilles tendon rupture, specifically over MRI, as it is “cheaper, more dynamic, less time-consuming, [correlates] better with the clinical picture, and showed tendon defects in higher number” [5]. The sensitivity of ultrasound ranged from 80-100% while some studies report a 100% specificity. One study found that performing the Realtime Achilles Ultrasound Thompson (RAUT) test during ultrasound examination is both more sensitive and specific. The RAUT test increased the sensitivity of ultrasound from 76.8% to 87.2% and specificity from 74.8% to 81.1% for novice users [6].

MRI has been shown to have a sensitivity as high as 91% with a specificity of 100% [5]. However, one of the drawbacks of MRI imaging is that it often detects subtle abnormalities that may overestimate the severity of an Achilles injury when compared to the clinical presentation, leading to potentially unwarranted and harmful intervention [7]. Some studies suggest that partial Achilles tears are more difficult to diagnose with ultrasound and recommend MRI for definitive diagnosis [8-Kayser].

Nevertheless, ultrasound may help with patient disposition, especially when MRI is not immediately available, such as in the emergency department. The ease and accessibility of ultrasound is also a good tool to monitor progression of treatment [5]. However, in general, imaging abnormalities outlast functional recovery, so caution should be used with frequent or repetitive monitoring as a benchmark for return to work or sport [7].  

Ultrasound Techniques for Achilles

Point-of-care ultrasound is quick, relatively easy and provides immediate answers. The Achilles tendon is set up well for ultrasound imaging, as it is very superficial and unguarded by bone or other structures [6].

To ultrasound the Achilles tendon, have the patient lay prone on the bed with the feet hanging off the edge of the bed [9]. As with other musculoskeletal scans, use the linear probe in the MSK setting. You’ll want to scan the tendon in both the longitudinal and transverse axis [9-10]. Start by placing the probe in longitudinal axis close to the foot and identify the hyperechoic stripe of the calcaneus [11]. Knowing this is the point of insertion of the Achilles tendon, scan superiorly identifying and following the tendon.

Normal tendon will appear as layered, continuous, linear fibers. Conversely, an Achilles injury appears discontinuous, with hypoechoic disruption of the tendon fibers, often resulting in heterogeneity [11-12]. The tendon will likely have an increased anterior-posterior diameter due to swelling [9, 12]. In a complete Achilles rupture, an anechoic space may separate portions of the tendon [12]. Finally, performing a Thompson test (squeezing the gastrocnemius muscle) while visualizing with ultrasound would show retraction of the superior portion of the tendon [11].

Conclusion

Once the diagnosis is made, patients should be referred to either a sports medicine specialist or orthopedic surgeon to review and discuss treatment options. Management of Achilles tendon rupture is debated and includes both operative and conservative measures. Such conservative measures include physical therapy, shockwave therapy, and local injections [13]. Of note, there is no evidence yet to suggest platelet-rich plasma injections improve functional outcomes in patients who are treated conservatively [14]. As with any surgery, there are inherent complications that accompany repair making it less desirable. However, conservative measures may result in incomplete or improper healing which may have functional consequences down the road as well [15].

Take Home Points

• Ultrasound is quick and easily accessible in the emergency department to evaluate musculoskeletal complaints, including Achilles tendon pathology.

• Ultrasound and MRI have similar sensitivity and specificity for diagnosing Achilles tendon tears.

• Look for disruption to tendon fibers, increased tendon diameter, and hypoechogenicity within the tendon or a completely anechoic space within the tendon to diagnose Achilles tendon partial or complete tear.

• Use the Realtime Achilles Ultrasound Thompson (RAUT) test to increase diagnostic accuracy.  

AUTHORED BY: DR. VINCENT MARSHALL (R1)

FACULTY CO-AUTHOR/EDITOR: LAUREN MCCAFFERTY, MD

References

1. Järvinen TA, Kannus P, Paavola M, Järvinen TL, Józsa L, Järvinen M. Achilles tendon injuries. Curr Opin Rheumatol.  2011; 13(2): 150-155.

2. Maughan KL, Boggess BR. Achilles tendinopathy and tendon rupture. In Post TW, Fields K, Grayzel J. (Eds.), UptoDate. 2022. Accessed December 2022.

3. Maffulli N. The clinical diagnosis of subcutaneous tear of the Achilles tendon. A prospective study in 174 patients. Am J Sports Med. 1998;26(2):266

4.  Situ-LaCasse E, Grieger RW, Crabbe S, Waterbrook AL, Friedman L, Adhikari S. Utility of point-of-care musculoskeletal ultrasound in the evaluation of emergency department musculoskeletal pathology. World J Emerg Med. 2018;9(4):262-266.

5. Dams OC, Reininga IHF, Gielen JL, Akker-Scheek IVD, Zwerver J. Imaging modalities in the diagnosis and monitoring of Achilles tendon ruptures: A systematic review. Injury, 2017; 48(11):2383–2399.

6. Griffin MJ, Olson K, Heckmann N, Charlton TP. Realtime Achilles Ultrasound Thompson (RAUT) test for the evaluation and diagnosis of acute Achilles tendon ruptures. Foot Ankle International. 2017; 38(1): 36-40.

7. Khan KM, Forster BB, Robinson J, et al. Are ultrasound and magnetic resonance imaging of value in assessment of Achilles tendon disorders? A two year prospective study. Br J Sports Med. 2003; 37(2):149-153.

8. Kayser R, Mahlfeld K, Heyde CE. Partial rupture of the proximal Achilles tendon: a differential diagnostic problem in ultrasound imaging. Br J Sports Med. 2005;39:838-842.

9. Dong Q, Fessell DP. Achilles tendon ultrasound technique. Am J Roentgenol. 2009; 193(3): W173-W173.

10. Rudy CC, Thompson JA, Bengtzen RR. Ultrasonographic findings of acute Achilles tendon rupture. JETem. 2019; 4(4):V14-16

11. Atta M, Jafari S, Moore K. Analyzing the Use of Ultrasound: Achilles Tendon Rupture. Open J Emerg Med. 2017; 7(3): 41-47.

12. Kälebo P, Allenmark C, Peterson L, Swärd L. Diagnostic value of ultrasonography in partial ruptures of the Achilles tendon.  Am J Sports Med. 1992; 20(4): 378-381.

13. Magnussen RA, Dunn WR, Thomson AB. Nonoperative treatment of midportion Achilles tendinopathy: a systematic review. Clin J Sport Med. 2009; 19(1): 54-64.

14. Keene DJ, Alsousou J, Harrison P, et al.  Platelet rich plasma injection for acute Achilles tendon rupture: PATH-2 randomised, placebo controlled, superiority trial. BMJ. 2019: 367:l6132

15. Maffulli N, Peretti GM. Surgery or conservative management for Achilles tendon rupture?. BMJ. 2019; 364:k5344.

Commotio cordis (CC) is defined as a sudden blow to the precordial chest during ventricular repolarization resulting in ventricular fibrillation (VF) and cardiac arrest in a patient with no predisposed structural cardiac condition and/or no cardiovascular history [1]. The blow is considered “low-energy” as described in a study done in 1998 [2]. In this study, young pigs were used as experimental models while impact to the chest wall was created using a wooden object identical in size and weight of a baseball thrust at 30 mph at specific timings of the cardiac cycle. Ten of the impacts recorded occurred during the ECG upstroke before the peak of the T wave in the cycle and each of these impacts produced VF. Impacts at other instances of the cardiac cycle did not produce VF. Furthermore, the study shows that hits later in the cardiac cycle could result in complete heart block, ST segment elevation, or left bundle branch block, which would all notably be seen on ECG. Figure 1 shows electrocardiogram leads of these impacts causing VF. This study was the first to demonstrate the mechanism of CC and since has been unceasingly referred to as a baseline model of its pathophysiology.

When it comes to those who are at risk for CC and how often this occurs, the national US Commotio Cordis Registry can be consulted, which has been aggregating information since 1997. Less than 30 cases are reported per year with 95% of the cases occurring in boys with a mean age of 15 years [1]. The increased incidence in younger age is due to their thinner chest, allowing more force and energy to be transferred to the myocardium of the heart. CC is second in frequency, behind hypertrophic cardiomyopathy, as a cause of sudden cardiac death in athletes [3,4]. An article published in 2013 by BJ Maron, which is the principle investigator of CC, discusses the risk factors of CC. It mentions that while there seems to be the commonality of young male athletes, there also seems to be a racial component [5]. Survival rate in African Americans is lower due to delayed resuscitation being more common in this population. This same article discussed environment as another risk factor. Specifically, athletes who partake in unorganized, recreational sports had less survivors, presumably due to the lack of a specialized medical team with an AED on standby.

Interestingly enough, we can also take the size and shape of the object itself into consideration when it comes to risk factors causing CC. A study performed by Kalin et al in 2011 evaluated the incidence of VF when projecting flat and smaller diameter spherical objects at a similar swine model as used in the previous study that determined CC pathophysiology [6]. The objects projected were all the same weight, but consisted of a flat object, and 2 round spheres at 42 and 72 mm in diameter to represent a golf ball and base ball, respectively. Velocity and timing of the cardiac cycle were kept constant during projection. The flat object did not produce a single episode of VF. The smaller sphere created more instances of VF than the larger, but the authors state this difference was not statistically significant. It was concluded that smaller diameter objects create a greater rise in left ventricular pressure, providing a favorable setup for VF. Figure 2 shows a graphical representation of this information.

With the vast knowledge and research that has developed over time, with much to owe to BJ Maron and his team of investigators, we have become better equipped at understanding the pathophysiology and epidemiology of CC. Using this, we can be more prepared with plans and resources in place for resuscitation when needed in susceptible populations. The survival rate of CC is based strictly on the immediate recognition of cardiac arrest, followed by quick defibrillation [7]. The primary reason for mortality is a delay in defibrillation and resuscitation. Studies in the 1990’s showed survival rates as low as 10-15%, giving the impression that CC was expected to be fatal. However, due to education on prompt resuscitation and increasing availability and use of AED’s, a study in 2013 has shown a 5 fold increase in survival [8]. Figure 3 below shows a representation of the increasing survival rate over recent years.

CC victims should undergo a complete cardiac work up to rule out any other cause of their ventricular fibrillation and subsequent cardiac arrest, such as a congenital heart condition [9]. This testing could include ECG, echocardiogram, stress testing, ambulatory ECG, or others depending on what the physician deems necessary. Testing for long QT syndromes or Brugada syndrome is also applicable. If the patient has experienced true CC, no other cause will be found, and if the patient has a benign ECG and PE, they will likely have a benign clinical course [9]. Given how many variables it takes for CC to occur, it is unlikely that all of those variables could occur randomly a second time, making repeat instances unlikely. However, patients should be monitored for future dysrhythmias [7].

Prevention of CC has proven difficult with failure of chest protection in preventing fatal dysrhythmias according to studies and data from the national registry [10]. Despite lack of prevention, survival rates are on the rise, now over 50% [1], due to increasingly effective education and availability of medical personnel and AED’s at sporting events. BJ Maron states that these events can be a source of tragedy for the public [5], and with an event recently broadcasted on television, it can be expected that there will be a surge in education and training of recognition and management of cardiac arrest due to  Commotio cordis.

POST BY: SARAH POWELL (MS4)

FACULTY EDITING BY: COLIN MCCLOSKEY, MD

References

1. Tainter CR, Hughes PG. Commotio Cordis. (2022). In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; PMID: 30252270.

2. Link, MS., et al. An Experimental Model of Sudden Death due to Low-Energy Chest-Wall Impact (Commotio Cordis). New Engl J Med. 1998;338: 1805-1811.

3. Westreich R, Haim M, Bereza S, Konstantino Y. Commotio Cordis: Indeed? (2019). JACC Case Rep,1(4):597-601. DOI: 10.1016/j.jaccas.2019.09.010.

4. Semsarian C, Sweeting J, Ackerman MJ. Sudden cardiac death in athletes. BMJ. 2015; 350.

5. Maron BJ. Sudden death in young athletes. New Engl J Med. 2003; 34: 1064-75.

6. Kalin J, Madias C, Alsheikh-Ali AA, Link MS. Reduced diameter spheres increases the risk of chest blow–induced ventricular fibrillation (commotio). Heart Rhythm 2011;8:1578–1581.

7. Bock JS., Benitez, RM. Blunt Cardiac Injury. Cardiology Clinics. 2012; 30: 545-555

8. Maron BJ, et al. Increasing Survival Rate from Commotio Cordis. Heart Rhythm. 2013; 10: 219-223.

9. Link MS, Estes III M, Maron BJ. Eligibility and Disqualification Recommendations for Competitive Athletes With Cardiovascular Abnormalities: Task Force 13: Commotio Cordis. J Am Coll Cardiol. 2015; 66: 2439-43.

10. Doerer JJ, Haas TS, Estes III M, Link MS, Maron BJ. Evaluation of Chest Barriers for Protection Against Sudden Death Due to Commotio Cordis. Am J Cardiol. 2007; 99: 857-859.

Poison is in everything, and nothing is without poison. The dosage makes it either a poison or a remedy. - Paracelsus

Case Presentation

40 y/o M presents to the ED complaining of vomiting, abdominal pain, diarrhea, hematemesis, hematuria.

Arsenic Poisoning

• MOA: Binds sulfhydryl groups of critical enzymes, disrupts oxidative phosphorylation, and blocks cardiac potassium channels.

  • Encephalopathy

  • Peripheral neuropathy, Weakness

  • QT prolongation, Arrythmias

  • Alopecia, Melanosis, Hyperkeratosis, Hyperpigmentation, Mees’ lines

  • Metallic/Garlic taste, N/V/D, ABD pain

  • Hemolysis, Hematemesis, Hematuria

  • Multisystem organ failure

    
    

Evaluation

• Urine arsenic, Whole blood arsenic levels, CBC, CMP, ECG, CXR

Treatment

• Supportive care

• Chelation therapy

  • Dimercaprol

  • DMSA

• Plasmapheresis, HD

Arsenic Facts

• Found naturally throughout the environment, including foods. It's also used in certain common products, including pesticides and pressure-treated wood.

• White arsenic, which is arsenic oxide, is a water-soluble, tasteless solid easily added to drinks.

• Arsenic and its compounds were a popular poison in the Middle Ages because it was easy to obtain and the symptoms of arsenic poisoning resembled cholera.

• In the 1600s it became known as “inheritance powder”.

• In the 1800s arsenic compounds became widely available – as weed-killers, flypapers, rat poisons, etc.

• Arsenic became commonly used in domestic murders and it is estimated to have been used in a third of all criminal cases of poisoning throughout the nineteenth century.

Arsenic History

• Gustaf Adolph Evangelical Church in New Sweden, Maine.

• In April 2003, 16 members of the church in the small farming community became severely ill after consuming coffee brewed in an urn. Walter Reid Morrill, age 78, died from the side effects, and 15 other parishioners were extremely ill.

• Just five days after the incident congregation member Daniel Bondesoncommitted suicide by shooting himself with a rifle. He allegedly left a suicide note that read like a confession to the mass poisoning.

• The contents of Bondeson's note have never been made public, and the case is still considered unsolved.

• Famous people who have died from arsenic poisoning:

  • Napoleon Bonaparte

  • George III of England

  • Simon Bolivar

Case Presentation

37 y/o F presents to the ED with altered mental status, tachycardic, dilated pupils, flushed, dry skin.

Anticholinergic Toxidrome

• MOA: Competitively blocks the effects of acetylcholine at muscarinic cholinergic receptors on smooth muscle, cardiac muscle, secretory gland cells, and in peripheral autonomic ganglia and the central nervous system.

• CNS effects:

  • Most often causes agitated delirium (hallucinations, incoherent speech, carphologia).

  • More severe cases may present with seizure and/or coma.

  • CNS effects may persist after peripheral features have resolved.

  • Pupillary dilation, causing blurry vision and photophobia.

  • Tachycardia

  • Hyperthermia with dry, flushed skin (Toxicology handshake - no sweat in the armpits).

  • Urinary retention

  • Ileus

Mad as a hatter, blind as a bat, red as a beet, hot as a hare, dry as a bone, full as a flask

Evaluation

• POC Glucose, CBC, CMP, CPK, ECG, CXR

Treatment

• Supportive care

• Benzodiazepines

• Physostigmine

• Foley

Atropine Facts

• Atropa belladonna gets its name from the Italian words bella donna for "beautiful lady“

• The plant was a popular cosmetic in the Middle Ages with the juice of the berries being used as a blush and diluting extracts from the plant in water made eye drops to dilate the pupils.

• AKA deadly nightshade bush

• Juice from the plant or its berries was used to tip arrows with poison.

• In small doses this chemical causes hallucinations and was used for this purpose as long ago as ancient Greece.

• In larger doses it was reputed to be one of the favorite poisons of would-be murderers in Medieval Europe and the juice of only a few berries was fatal.

• The symptoms it produces would be easily mistaken for one of the many fevers which afflicted people in those days.

Atropine History

• Legend has it, Macbeth used deadly nightshade to poison Danes invading Scotland in 1040.

• There's evidence that the serial killer Locusta may have used nightshade to kill the Roman emperor Claudius

• It is rumored that the Roman empress Livia Drusilla used the juice of Atropa belladonna berries to murder her husband, the emperor Augustus

• There are few confirmed cases of accidental deaths from deadly nightshade, but there are common plants related to Belladonna that can make you sick.

Case Presentation

35 y/o M presents to the emergency department complaining of headache, N/V, and SOB.

Cyanide Poisoning

• MOA: Poisons the mitochondrial electron transport chain within cells specifically binding to complex IV of cytochrome oxidase and prevents cells from using oxygen.

• People exposed to a small amount of cyanide may have the following signs and symptoms within minutes:

  • Dizziness

  • Headache

  • Nausea and vomiting

  • Tachypnea

  • Tachycardia

  • Restlessness

  • Weakness

  • Exposure to a large amount of cyanide may cause:

  • Convulsions

  • Loss of consciousness

  • Hypotension

  • Respiratory failure leading to death

  • Bradycardia

Evaluation

• CBC, CMP, Lactate, ECG, CXR

Treatment

• Supportive care

• Hydroxocobalamin

• Sodium nitrite

• Sodium thiosulfate

Cyanide Facts

• Cyanide can be distilled from the kernels of certain nuts such as almonds and the leaves of some laurels bushes.

• Cyanide is a rapidly acting, potentially deadly chemical that can exist in various forms.

• Cyanide sometimes is described as having a “bitter almond” smell, but it does not always give off an odor, and not everyone can detect this odor.

• Breathing cyanide gas causes the most harm but swallowing cyanide can be toxic as well.

• Cyanide gas is less dense than air; so, it will rise.

• Cyanide is more harmful to the heart and brain than to other organs because the heart and brain use a lot of oxygen.

• The industrial chemical sodium cyanide is widely used, especially in mining, and has been involved in attempted mass murders.

• Some popular examples of cyanide being used include the mass suicide at Jonestown and Heaven’s gate.

Cyanide History

• It was used to contaminate Tylenol capsules in the US in the 1980s and killed several people in the Chicago area.

• Cyanide can cause death within minutes. It is the fastest acting of all poisons and for this reason it is the poison of suicide pills of the type carried by secret agents.

• Stella Nickell in the early 1980s.

  • In June, 1986, a few years after the infamous unsolved Tylenol poisonings in Chicago, Bruce Nickell arrived at his Auburn, Washington home. He'd left work early with a headache. Four Excedrin later, Bruce collapsed. He died in the hospital. Physicians cited his emphysema. Less than a week later, Susan Snow took some of the same headache medicine and collapsed on her bathroom floor. Examination determined Susan had died from cyanide poisoning. There were fears of another Tylenol-like event but within weeks suspicion turned to Bruce's wife, Stella Nickell.

  • By December of 1987 Nickell was under indictment for product tampering -- police believed she sought the payouts from her husband's life insurance and had orchestrated the product poisoning that ended up killing Susan Snow as a cover-up. Nickell was convicted on all charges against her and sentenced to 90 years in prison.

Case Presentation

25 y/o M presents to the ED complaining of muscle pain, rigidity, fever, and jaw pain.

Strychnine Poisoning

• MOA: Competitive antagonist of the inhibitory neurotransmitter glycine at the ventral horn motor neurons in the spinal cord. Increases motor neuronal excitability leading to increased muscular activity.

• People exposed to low doses may have the following signs and symptoms within the first hour of exposure:

  • Agitation

  • Apprehension or fear

  • Ability to be easily startled

  • Restlessness

  • Painful muscle spasms

  • Uncontrollable arching of the neck and back

  • Rigid arms and legs

  • Jaw tightness

  • Muscle pain and soreness

  • Difficulty breathing

  • Fever

  • Kidney and liver injury

  • Dark urine

• People exposed to high doses may experience the following signs and symptoms within the first 15 minutes of exposure:

  • Respiratory failure

  • Brain death

Evaluation

• CBC, CMP, CPK, Lactate, ECG, CXR

Treatment

• Supportive care

• Benzodiazepines

• Airway control, paralysis if needed

Strychnine Facts

• Strychnine is a white, odorless, bitter crystalline powder.

• Can be extracted from the seeds of the nux vomica tree, which grows in Southeast Asia

• It was reputed to be a tonic and prescribed in small doses by doctors to aid convalescence.

• It was widely used to poison rats and other animals and as such was easily obtained

• Strychnine is a strong poison; only a small amount is needed to produce severe effects in people.

• Jane Stanford

  • In 1905, university co-founder Jane Stanford escaped poisoning when she thought her mineral water tasted off and she immediately vomited it out.

  • Testing found that it had been poisoned with strychnine.

  • One month later in Hawaii, she drank a bicarbonate soda after suffering from an upset stomach. Soon she felt sick and believed she had been poisoned again. The poison caused her to lose control of her body completely and spasm until she died.

  • An autopsy revealed that the cause was strychnine.

  • While a lot of theories have surrounded her death, the killer remains a mystery. 

Case Presentation

63 y/o M presents to the ED complaining of difficulty walking, leg pain, frequent falls, and hair loss.

Thallium Poisoning

• MOA: Interferes with glycolysis, Krebs cycle, and oxidative phosphorylation. Binds sulfhydryl groups on the mitochondrial membrane interrupting the Na/K ATPase. Biochemically like K and is thus treated like potassium in the body.

• Ingestion of toxic amounts of thallium might cause:

  • Abdominal pain

  • Nausea

  • Vomiting

  • Diarrhea

• After a substantial, acute exposure or chronic exposure to limited amounts of thallium symptoms may include:

  • Severely painful ascending neuropathy

  • Ataxia

  • Seizures

  • Alopecia

  • Neurocognitive deficits

Evaluation

• Blood thallium concentration, CBC, CMP, EKG, CXR, ABD XR.

Treatment

• Supportive care

• Consider activated charcoal

• Prussian Blue

Thallium Facts

• Pure thallium is a bluish-white metal that is found in trace amounts in the earth's crust.

• In its pure form, thallium is odorless and tasteless and can also be found combined with other substances such as bromine, chlorine, fluorine, and iodine. When combined it appears colorless-to-white or yellow.

• It has not been produced in the United States since 1984. Currently, all the thallium is obtained from imports and from thallium reserves.

• Thallium is used mostly in manufacturing electronic devices, primarily for the semiconductor industry. It also has limited use in the manufacture of special glass and for certain medical procedures.

• This element was only discovered in the 1860s

• In some countries it has been available as rat poison but has been more widely used as an agent of assassination.

• Thallium sulfate is water-soluble and tasteless, and they take several days for the symptoms to appear and even then, these are generally attributed to other illnesses.

• This poison was used by Saddam Hussein’s secret police and by the Russian KGB.

Thallium History

1995 Beijing, China

• Zhu Ling is the best-known victim of thallium poisoning. Ling, a university student in China, started losing her hair, suffering blurred vision, and having horrible stomach pains before falling into a coma.

• Her friends shared the symptoms on the internet, where the public replied with suspicions of thallium poisoning which was later confirmed by doctors.

• Though she lived, she suffered significant neurological damage.

• The poisoner was never convicted, but her roommate Sun Wei, who comes from a prominent and well-connected family, is still considered the prime suspect. 

POST BY: DR. NATE WILLIAMS (R4)

FACULTY EDITING BY: DR. LAUREN PORTER

References

• EMRA and ACMT Medical Toxicology Guide

• https://truecrimedaily.com/2015/09/23/10-infamous-poisoning-cases-solved-and-unsolved/

• https://www.ranker.com/list/gruesome-poison-cases/lea-rose-emery

• https://www.pbs.org/wnet/secrets/the-five-top-poisons/202/

• https://en.wikipedia.org/wiki/Thallium_poisoning

• http://annerallensbooks.blogspot.com/2017/04/poisoning-people-for-fun-and-profit.html

• https://www.newyorker.com/magazine/2013/10/14/murder-by-poison

• https://emcrit.org/ibcc/anticholinergic/#top

• https://emergency.cdc.gov/agent/strychnine/basics/facts.asp#:~:text=Strychnine%20is%20a%20white%2C%20odorless,produce%20severe%20effects%20in%20people.

• https://emergency.cdc.gov/agent/cyanide/basics/facts.asp

• https://emergency.cdc.gov/agent/arsenic/casedef.asp

• https://emergency.cdc.gov/agent/thallium/index.asp

• https://wwwn.cdc.gov/TSP/ToxFAQs/ToxFAQsDetails.aspx?faqid=308&toxid=49

• https://wwwn.cdc.gov/TSP/ToxFAQs/ToxFAQsDetails.aspx?faqid=19&toxid=3

• https://litfl.com/arsenic-poisoning/

• https://litfl.com/cyanide-toxicity/

• https://litfl.com/strychnine-poisoning/

65-year-old male with a history of heart failure and unspecified arrhythmia presented from home by EMS due to palpitations. While en route, EMS placed him on the monitor and found him to be in ventricular tachycardia (VT) with a pulse. He was hemodynamically stable and otherwise mentating normally, so he received 150 mg of Amiodarone in the field. On arrival, he was transferred to our monitors, and vitals were obtained. He appeared to be in atrial fibrillation with a heart rate ranging from 90-110, normotensive.

The patient reported that over the past few days he felt episodes of his heart “racing,” which improved with rest. To the patient’s fortune, his wife chose to stay home and called 911 when he became diaphoretic. 

His initial EKG showed atrial fibrillation with rate of 90, normal intervals, and no ischemic changes. A cardiac point-of-care ultrasound (POCUS) was performed.

POCUS findings:

In the parasternal long axis image on the left (when the patient had rate-controlled atrial fibrillation), there is decreased LV function without RV dilation or pericardial effusion. The middle and right images capture intermittent episodes of tachycardia (nonsustained VT on the monitor). Note the difference in organized contractility.

Case continued:

The patient was started on an amiodarone drip but continued to have subsequent episodes of NSVT and remained hemodynamically stable. His labs were notable for hypokalemia and hypomagnesemia, which were repleted. Cardiology was consulted and recommended a lidocaine drip, which was initiated, and he was admitted to the cardiac intensive care unit. He went into sustained VT (hemodynamically stable) and ultimately underwent ICD placement.

Ventricular Tachycardia (Overview)

Definition/Classification

Ventricular tachycardia (VT) is a wide complex tachyarrhythmia (QRS > 120 ms) with a heart rate > 100 beats per minute.

Duration is classified as sustained vs nonsustained:

• Sustained VT is defined as the wide complex rhythm lasting > 30 seconds or if hemodynamic instability occurs in less than 30 seconds.

• Nonsustained VT is defined as >3 beats of ventricular origin at rate >100 bpm lasting under 30 seconds in duration [1].

Further classification is based on QRS morphology:

• Monomorphic VT shows a stable QRS from beat to beat.

• Polymorphic VT has changing or variable QRS morphology from beat to beat. Torsade’s de pointes is a common example of polymorphic VT associated with long QT intervals that appears as waxing and waning amplitudes on EKG [1].

A final form of VT is bidirectional in nature, with beat-to-beat alteration. This is commonly associated with digitalis toxicity or catecholaminergic polymorphic VT [1].

Epidemiology

VT is most commonly caused by ischemic heart disease. Other causes include, but are not limited to, congenital heart disease, channelopathies, and electrolyte imbalances [1]. Most cases of sudden cardiac death can be attributed to VT and ventricular fibrillation (VF) with roughly 300,000 deaths annually in the United States, accounting for approximately half of deaths related to cardiac causes [2-3]. Risk factors for ventricular tachycardia are previous myocardial infarction, chronic obstructive pulmonary disease, ST-segment changes at presentation, and hypertension [4]. Even more concerning is VT occurring after 48 hours of hospital presentation as it is associated with increased risk of death compared to VT occurring within the first 48 hours of presentation [5].

Clinical presentation

A strong history and physical exam can help differentiate between VT and supraventricular tachycardia. Patients presenting with a past medical history of myocardial infarction, recently diagnosed angina, or heart failure have a positive predictive value of greater than 9% for VT [4]. Clinical signs and symptoms are highly variable and may include palpitations, altered mental status, diaphoresis, hypotension, pallor, variable-intensity S1, and cannon A waves in the jugular venous waveform (due to atrial contraction against a closed tricuspid valve). EKG findings are the most diagnostic in a patient’s presentation [1,4].

Management

Management is highly dependent on multiple factors including VT classification, hemodynamic stability, and underlying comorbidities and can range from close observation to pharmacologic therapy alone or in combination with cardioversion or defibrillation. For patients who survive, an implantable cardiac defibrillator or ablation is often indicated [1].

While this patient fortunately remained stable, VT can be a fatal arrhythmia so we’ll focus the rest of the discussion below on using POCUS in cardiac arrest as this is more commonly discussed in the literature.

POCUS in Cardiac Arrest

Utility

The use of POCUS in cardiac arrest and resuscitation of critically ill patients is recognized as a core skill by major governing organizations. It can be incredibly useful in differentiating organized cardiac rhythm from ventricular fibrillation, asystole, and pulseless electrical activity (PEA) and in addition to identifying reversible causes of arrest [6]. Gaspari et al. demonstrated that sonographic identification and treatment of a reversible cause of cardiac arrest increases survival. In patients with nonshockable rhythms, POCUS has significant utility in predicting worse survival outcomes in patients with cardiac standstill, i.e. no cardiac activity witnessed with ultrasound [7]. Along with its diagnostic utility, POCUS also has a vital role in procedural guidance prior to and after return of spontaneous circulation (ROSC) [6].

An additional benefit of POCUS in cardiac arrest is determining efficacy of chest compressions by providing direct, real-time visualization of cardiac chambers and surrounding structures. If the left ventricle is not adequately compressed with CPR but other structures are, this can facilitate adjustment of compressor hand placement to a more appropriate position [8].

A Protocolized Approach

Despite its benefits, the use of POCUS in cardiac arrest as been associated with prolonged pulse checks [9]. In 2018, a novel protocol known as the Cardiac Arrest Sonographic Assessment (CASA) was developed to efficiently incorporate POCUS in cardiac arrest while maintaining high-quality cardiopulmonary resuscitation (CPR); see Figure 3. [10]

The CASA exam implements a three-step approach to rapidly evaluate for:

1. Cardiac tamponade

2. Right heart strain secondary to pulmonary embolism

3. Cardiac activity*

The “optimal” view will depend on the patient’s anatomy and is the one(s) that provides the focused answers you need. Only one view should be performed per pulse check and should be accomplished in under ten seconds [10].

By utilizing this stepwise approach, Clattenburg et al. showed significant reduction in pulse check interruptions by over three seconds. They also showed that having the probe on the chest in the desired location prior to pausing compressions can reduce pulse check duration while also improving image acquisition [11]. Other tips to minimize interruptions in compressions include: recording cardiac activity during the pulse check but waiting to review until after compressions have resumed (see Figure 4) and having the correct probe, machine settings (i.e. presets, depth, gain) and a towel to wipe off the gel ready ahead of time [12].  

Adjuncts to the key steps of the CASA exam, which can be performed with ongoing compressions, include a pneumothorax evaluation and focused assessment with sonography in trauma (FAST) exam to help identify non-cardiac causes of arrest [10].

Protocols for repeating POCUS during cardiac arrest have not been well-studied but can be helpful if after an intervention to determine response or after a change in status.

*When evaluating for cardiac activity and none is visualized, m-mode can help confirm the presence or absence of cardiac movement, see Figure 4 [12].

Take Home Points

• Ventricular tachycardia is a potentially fatal arrhythmia most commonly caused by ischemic heart disease.

• POCUS is a safe, reproducible, and cost-effective tool that can quickly provide useful diagnostic information to guide management of critically ill patients, including those in cardiac arrest.

• A protocolized approach, such as the CASA exam, can help optimize integration of POCUS in the resuscitative process maintaining high quality CPR.

• POCUS can rapidly and effectively evaluate for cardiac tamponade, right heart strain (and other reversible causes), and cardiac activity.

• Goal is to avoid interrupting or delaying resuscitation. Tips to minimize pulse check delays include: having the probe in place beforehand, recording a single window during pulse check, and reviewing images after CPR has resumed.

POST BY: DR. POLLY WILTZ (R1)

FACULTY CO-AUTHOR/EDITOR: LAUREN MCCAFFERTY, MD

Resources

1. Foth C, Gangwani MK, Alvey H. Ventricular Tachycardia. [Updated 2022 Aug 8]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan.

2. Tang PT, Shenasa M, Boyle NG. Ventricular Arrhythmias and Sudden Cardiac Death. Card Electrophysiol Clin. 2017;9(4):693-708.

3. McNally B, Robb R, Mehta M, et al. Out-of-hospital cardiac arrest surveillance --- Cardiac Arrest Registry to Enhance Survival (CARES), United States, October 1, 2005--December 31, 2010. MMWR Surveill Summ. 2011;60(8):1-19. 

4. Pellegrini CN, Scheinman MM. Clinical management of ventricular tachycardia. Curr Probl Cardiol. 2010;35(9):453-504. 

5. Volpi A, Cavalli A, Franzosi MG, et al. One-year prognosis of primary ventricular fibrillation complicating acute myocardial infarction. The GISSI (Gruppo Italiano per lo Studio della Streptochinasi nell'Infarto miocardico) investigators. Am J Cardiol. 1989;63(17):1174-8.

6. Labovitz A, Noble V, Bierig M et al. Focused cardiac ultrasound in the emergent setting: a Consensus Statement of the American Society of Echocardiography and American College of Emergency Physicians. J Am Soc Echocardiogr. 2010; 23:1225–1230.

7. Gaspari R, Weekes A, Adhikari S, et al. Emergency department point-of-care ultrasound in out-of-hospital and in-ED cardiac arrest. Resuscitation. 2016; 109:33–39.

8. Ávila-Reyes, D., Acevedo-Cardona, A.O., Gómez-González, J.F. et al. Point-of-care ultrasound in cardiorespiratory arrest (POCUS-CA): narrative review article. Ultrasound J. 2021; 13, 46.

9. Clattenburg EJ, Wroe P, Brown S, et al. Point-of-care ultrasound use in patients with cardiac arrest is associated with prolonged cardiopulmonary resuscitation pauses: A prospective cohort study. Resuscitation. 2017; 122: 65-68.

10. Gardner K, Clattenburg E, Wroe P, et al. The Cardiac Arrest Sonographic Assessment (CASA) exam—a standardized approach to the use of ultrasound in PEA. Am J Emerg Med. 2018; 36:729–731.

11. Clattenburg E, Wroe P, Gardner K, et al. Implementation of the Cardiac Arrest Sonographic Assessment (CASA) protocol for patients with cardiac arrest is associated with shorter CPR pulse checks. Resuscitation. 2018; 131:69–73.

12. Hussein, L., Rehman, M.A., Sajid, R. et al. Bedside ultrasound in cardiac standstill: a clinical review. Ultrasound J. 2019; 11, 35.

13. Neasi E, Kuttab HI. Use of ultrasound in cardiac arrest. ACEP Emergency Ultrasound Newsletter. 2022 Jan 31. <https://www.acep.org/emultrasound/newsroom/january-2022/use-of-ultrasound-in-cardiac-arrest2/>

61-year-old female with no significant PMH presenting with generalized weakness, 80 lb weight loss over 8 months, feeling of impending doom. Endorsed taking Ivermectin to prevent COVID-19 prescribed by her primary care doctor. She endorsed diarrhea and vomiting daily which she treated with Baking Soda.

PMH: None

PSH: Denies

SH: Occasional EtOH, no other drugs, never smoker

Allergies: NKDA

Meds: Ivermectin, Baking soda for 8 months

Findings

Pt was found to have bowel pneumatosis and free air on CT abdomen and pelvis and was admitted to Acute Care Surgery. She underwent exploratory laparotomy, mesenteric lymph node biopsy, EGD, and dobhoff placement

Findings: mesenteric nodules along entire small bowel, large nodule at root of mesentery, hypertrophic pylorus unable to pass endoscope, viable stomach, small bowel, colon, otherwise normal EGD, no succus

Ivermectin

• Anti-parasitic agent that is well tolerated and has a wide therapeutic safety profile

• Also used in veterinary preparations in a variety of concentrations

• MOA in antiparasitics is potentiation of GABA at chloride ion channels in the peripheral nervous system of parasites causing hyperpolarization of cells, paralysis and death

• Humans have GABA only in their CNS and Ivermectin does not penetrate the blood brain barrier well

• Typical dose is 0.15/mg/kg once or for several days to a week

Ivermectin and COVID-19

• Proposed mechanism of action in COVID-19 relates to the inhibition of transport of the viral material into the nucleus by blocking importin.

• Reported initially from an in-vitro study.

• Proposed dosing to treat COVID was 0.2mg/ kg -0.3mg/kg once a day for five days (no toxicity should be expected in these doses)

Multiple Studies have demonstrated no clinical benefit in COVID-19

Summer 2021

it was the season of light

it was the season of darkness

Ivermectin Toxicity

• Ivermectin is limited from crossing the blood brain barrier by the activity of the p glycoprotein pump.

• At high levels of Ivermectin the pump can be overwhelmed

• Toxicity when it does occur CNS effects predominate based on the potentiation of GABA at chloride ion channels

• Factors that may increase toxicity

  • High concentrations

  • Presence of p glycoprotein medications (verapamil)

  • Conditions increasing BBB permeability (ie sepsis)

Presentation

• CNS

  • Dizziness, ataxia

  • Decreased level of consciousness

  • Seizures

• Cardiac

  • Hypotension, bradycardia

Treatment

• Supportive

• Seizures treated with benzodiazepine

• Intubation if needed for CNS depression

• No role for activated charcoal or other GI decontamination

*Typically well tolerated but most common are gastrointestinal upset with nausea, vomiting and diarrhea.

Patient prescription

• 6 tablets 3.0 mg daily for 5 days x 5 days

• Followed by 6 tablets per week

• Per patient after extubation she began taking baking soda due to the stomach upset when she began the Ivermectin

Instructions for use as antacid

• Baking soda misuse can result in serious acid/base and electrolyte imbalance

• Adverse effects were also noted when the recommended doses were administered

• Highest risk for electrolyte derangements include chronic use

Other Complications?

Case reports of spontaneous rupture of the stomach

Case Report Summary

FDA identified 21 cases of stomach rupture in the literature and directly reported to FDA using their reporting system which the amount of sodium bicarbonate was often not known and varied greatly. The symptoms described were acute onset severe abdominal pain shortly after ingestion Injuries that were specifically described are as follows

• 52 year old following ingestion had an exploratory laparotomy that revealed a 6-cm tear in the stomach extending from the gastroesophageal junction down the lesser curvature of the stomach.

• 31 year old male who ingested sodium bicarb to relieve indigestion had acute onset of abdominal pain and exploratory surgery revealed a 5-cm linear tear along the lesser curvature of the stomach.

• 37 year old male who drank sodium bicarb and soda for indigestion was found to have a tear of the stomach just below the gastroesophageal juncture at laparotomy

• 23 year old male who took sodium bicarb following a meal has exploratory laparotomy revealing 6-cm to 7-cm linear tear in the lesser curvature of the stomach.

There was a recorded case of patient with ingestion of baking soda who was subsequently diagnosed with a bowel perforation requiring surgical intervention from California Poison Control but the details of the case were not available

FDA Warning updated based on case reports

Conclusions

• Ivermectin is a well tolerated medication that causes CNS toxicity in large doses its side effect profile includes gastrointestinal upset

• There are no known indications for Ivermectin to treat or prevent COVID-19

• Baking Soda has listed use for antacid

• Sodium bicarbonate can cause metabolic alkalosis, hypernatremia, hypokalemia, hypocalcemia, hypochloremia

• There having numerous case reports of gastric rupture following ingestion of sodium bicarbonate

POST BY: DR. ANNA WILLIAMS (R3)

FACULTY EDITING BY: DRS. RYAN MARINO & LAUREN PORTER

References

68-year-old male with history of metastatic lung cancer for which he was receiving chemotherapy presented to the emergency department for 3 days of shortness of breath and chest pain/tightness. The pain was non-radiating and persisted without alleviation. He also reported a cough productive of white/yellow sputum. These symptoms were similar to his prior hospitalization for a large pleural effusion with lung collapse. He denied any other symptoms including fevers, chills, leg swelling, nausea, vomiting, diarrhea, abdominal pain, numbness, weakness, headache, URI symptoms.

In the ED, his vitals were stable aside from mild hypoxia, for which he required 2L nasal cannula. He was well-appearing and resting comfortably in bed. His breathing was not labored but he had absent breath sounds throughout his left lung. The right lung was clear to auscultation. He appeared euvolemic. The remainder of his exam was unremarkable.

Point-of-care ultrasound (POCUS) of his lungs and heart were performed and showed the following:

POCUS Findings

Lung ultrasound revealed consolidation throughout the majority of the left lung along with a complex-appearing/loculated pleural effusion in the lung base. The right lung was unremarkable.

Cardiac ultrasound was significant for a circumferential pericardial effusion without sonographic signs of tamponade. Left ventricular function was grossly normal and there were no signs of right heart strain. A distended, minimally collapsable IVC was also visualized.

(You can see the abnormal lung findings in the parasternal view)

Case continued

Chest x-ray showed white out of his left lung. CT PE study confirmed a loculated pleural effusion and progression of his extensive tumor burden resulting in occlusion of the left main bronchus and blood supply. He was admitted to the oncology service for further management. Because of his significant tumor burden and lack of perfusion to the associated lung, he was managed conservatively as it was felt that symptomatic relief would not be achieved by thoracentesis or other intervention.

Pleural Effusions, a Review

What is it?

• Pleural effusions are collections of fluid between the parietal and visceral pleura of the lung. They are commonly secondary to underlying medical conditions, such as congestive heart failure, cancer, and pneumonia, though the differential remains broad [1-2].

Classification

• Classification of pleural effusions can be accomplished through content (transudative vs exudative) and appearance (simple vs complex).

• Effusion content is classically defined by Light’s Criteria

  • Sample/serum protein >0.5 or LDH ratio >0.6, or LDH >2/3 the upper limit of normal defines a exudative effusion; if it does not meet any of these criteria, it is classified as transudative [3]

  • Newer systems for classification have gone on to use pro-BNP levels and ratios, particularly for heart failure, as the early use of diuretics can lead to misclassification in 25% of patients [3,4]

• There are several subcategories of exudative effusions (a few described below). In addition to Light’s Criteria, these can often be differentiated through additional characteristics and diagnostic testing.

  • Malignant effusion is associated with malignancy, most commonly lung cancer, breast cancer, or lymphoma, and contains neoplastic cells through contiguous, hematogenous, or lymphatic spread.

  • Empyema is a pus-containing pocket that contains inflammatory cells and/or bacteria that is secondary to infection, occasionally the primary infection, or rarely autoimmune disorders

  • Chylothorax is a collection of lymphatic drainage, most commonly secondary to surgical exploration of the thorax and characterized by white, milky appearance with elevated lipids

  • Hemothorax is a collection of blood or clot that is due to vascular injury, most commonly trauma [2]

• Simple effusions are contiguous, homogeneous collections of fluid within the pleural space, while complex (often referred to as loculated) effusions tend to be septated and contain multiple compartments of fluid in between layers of fibrosis or congealed matter.

• These classifications are vital for diagnostic and therapeutic purposes.

  • Simple effusions may be more easily drained with bedside thoracentesis, while more complex effusions frequently warrant more advanced interventions, such as video assisted thoracoscopy (VATS) or interventional radiology placed thoracostomies [2].

Epidemiology

• Pleural effusions develop in 1.5 million patients per year [1]. Of these, 125,000 are malignant pleural effusions, which carries an 11.6% in-hospital mortality [5]. This can be one of the initial findings in 15% of new or recurrent diagnosis of malignancy [6].
  

Clinical Presentation

• Clinical presentation of pleural effusion depends on the quantity of fluid as well as the underlying cause. Many patients are asymptomatic, especially if the effusion is small. Symptomatic patients commonly present with pleuritic chest pain and dyspnea. If the effusion is massive, respiratory compromise may develop. Patients may also have a wide array of additional symptoms (such as fever, weight changes, orthopnea, leg swelling, nausea) depending on the underlying etiology.

• A history of malignancy, recent surgery or trauma, infection, changes in medications, and underlying health conditions some of the key historical features that may help identify the cause of the effusion and suggest potential concurrent signs and symptoms.

• On physical exam, patients typically have decreased breath sounds with dullness to percussion over the affected lung fields. Additional findings may also be present depending on associated or underlying conditions [2].

Diagnostics

• In addition to obtaining a thorough history and exam, diagnosis of a pleural effusion includes imaging as well as sampling of the fluid to determine underlying cause.

• Common imaging modalities include chest x-ray, CT chest, ultrasound

  • Chest x-ray — findings include blunting of the costophrenic angle if small, basilar opacity or apparent elevation of the hemidiaphragm, and up to complete obscuration of the lung field depending on the quantity of fluid present [2].

    • It is important to note that findings can be ambiguous and may be indistinguishable from pneumonia or other processes. Additionally, x-rays are generally unable to differentiate the type of effusion.

  • CT chest (with contrast) — CT can further characterize the effusion, suggest etiology, and differentiate from solid structures, such as lymph nodes, nodules/masses, or consolidation [2]. CT is frequently indicated if clinical suspicion or surgical planning is necessary [7].

  • Ultrasound — even small pleural effusions can be detected with good accuracy using ultrasonography. Similar to CT, ultrasound can help differentiate fluid vs solid lesions and can suggest transudative vs exudative etiology [2, 8-9]. This assessment is discussed in more detail below.

• Diagnostic evaluation of a pleural fluid is recommended in all new pleural effusions without a known etiology or if there is high suspicion for malignancy based on history and physical

  • Pleural fluid testing should include LDH, protein, cell count, gram stain and culture, triglycerides, and pH [10]

  • Additional serum testing for pro-BNP, CMP, LDH and CBC, as well as calculation of Light’s Criteria, are generally recommended [10,11]

POCUS for Pleural Effusion

Why POCUS?

• POCUS allows for rapid evaluation and further characterization of a pleural effusion among other etiologies (with greater sensitivity compared to chest x-ray), which can help expedite workup and appropriate management [8-9].

• Additionally, if therapeutic or diagnostic thoracentesis is required, use of ultrasound-guidance can reduce the rate of pneumothorax and other complications while improving success rates [12]. A meta-analysis by Gordon et al demonstrated an odds ratio of 0.3 in reducing pneumothorax rates [13].

General Lung Ultrasound Overview

• A number of proposed techniques exist for sonographic evaluation of the thorax with some being more extensive, though time-intensive, than others [14].

• A complete lung assessment generally involves a systematic approach to assessing the superior and inferior aspects of the anterior, lateral and posterior lung fields - see Figure 1. [15]

  • When evaluating for pleural effusions, particular attention should be given to the lung bases, as this is where fluid typically collects first.

• Different probes can be used depending on the area of interest. When assessing for deeper structures, such as pleural effusions, consolidations, or B lines, a lower frequency (curvilinear or phased array) transducer is best as these allow for adequate depth visualization. When focusing more on the pleural line, a high frequency linear probe may be used [15-17].

• Place the probe over the chest with the probe marker pointing toward the patient’s head. This allows you to more clearly identify the pleural line between ribs. You can then rotate the probe to a transverse orientation to better fit between ribs to improve visualization of that particular area [16]

• Regardless of location or orientation, it is best to keep the transducer perpendicular to the chest wall to optimize accuracy of findings [15-16].

Normal Findings

• In a normal air-filled lung, the lung itself is not visualized as air scatters the sound waves, which reflect off the pleura and back to the probe. This creates A lines, which are equally spaced horizontal lines below the pleural line; while they indicate an aerated lung, they can be present in some pathologic conditions [15-16] - see Figure 2.

• At the lung-diaphragm/liver or spleen interface, the air in a normal lung prevents visualization of the spine. As a result, the spine is only visualized below the level of the diaphragm.

B lines

• When the intersitium fills with fluid or thickens, B lines start to appear. These are vertical hyperechoic lines emanating from the pleural surface to the bottom of the image. More than 3 per lung field are considered pathologic and the amount of B lines correlates with severity of disease.

  
  

Consolidation

• As fluid or cells fill the alveoli, areas of consolidation start to replace normal lung. Smaller consolidations may appear as focal hypoechoic areas just below the pleural line, while larger consolidations tend to develop an organ-like appearance (“hepatization”), as seen in the majority of the lung in the case above . Air that gets trapped in the fluid-filled consolidation may be visualized as bright echoes; if they move with respiration, it is a dynamic air bronchogram which is considered pathognomonic for pneumonia. Irregular borders are often seen. [15-16].

Pleural Effusion

• Identification

  • While large effusions may be readily visualized throughout much of the lung fields, smaller effusions require more careful evaluation.

    • At the lung-diaphragm interface, when fluid replaces air, the vertebral bodies can now be visualized above the diaphragm. This is referred to as a spine sign - see Figure 4 [15].

    • A pleural effusion may also appear as anechoic fluid between the pleural line and a relatively parallel, second hyperechoic line below it. [14, 16]

• Sonographic findings can further characterize the effusion and indicate etiology

  • Anechoic effusions can be transudative or exudative

  • Complex effusions are always exudative

    • Echogenicity which may demonstrate a swirling pattern — this is often seen with malignancy-associated effusions

    • Fibrous septations or loculations

    • May also see associated pleural thickening or consolidated tissue [12, 15, 17]

Useful Adjunct: Cardiac Assessment

• Though cardiac POCUS does not directly assess the lungs, it can provide vital evidence for underlying etiology, such as presence or absence of decreased ejection fraction and heart failure.

Take Home Points

• Pleural effusions are fairly common and are secondary to an underlying condition, most commonly heart failure, pneumonia, and cancer.

• Classification of pleural effusions is determined by appearance and fluid characteristics (i.e. Light’s Criteria)

• POCUS is a fast, reliable way to assess for pleural effusions (among other etiologies for dyspnea), is more sensitive than x-ray, and does not involve radiation exposure.

• Ultrasound-guided thoracentesis is recommended to reduce the risks of pneumothorax and other complications.

POST BY: DR. IAN BRALLIER (R1)

FACULTY CO-AUTHOR/EDITOR: LAUREN MCCAFFERTY, MD

References

1. Feller-Kopman, David, and Richard Light. "Pleural disease." N Engl J Med. 2018; 378(8): 740-751.

2. Karkhanis VS, Joshi JM. Pleural effusion: diagnosis, treatment, and management. Open Access Emerg Med. 2012;4:31-52.

3. Light RW. The Light criteria: the beginning and why they are useful 40 years later. Clin Chest Med. 2013;34(1):21-26.

4. Porcel JM, Vives M, Cao G, Esquerda A, Rubio M, Rivas MC, Measurement of pro-brain natriuretic peptide in pleural fluid for the diagnosis of pleural effusions due to heart failure. Am J Med. 2004; 116(6):417-420

5. Taghizadeh N, Fortin M, Tremblay A. US hospitalizations for malignant pleural effusions: data from the 2012 National Inpatient Sample. Chest; 2017;151:845­54.

6. Porcel JM, Gasol A, Bielsa S, Civit C, Light RW, Salud A. Clinical features and survival of lung cancer patients with pleu­ral effusions. Respirology. 2015;20:654­9.

7. Hallifax RJ, Haris M, Corcoran JP, et al. Role of CT in assessing pleural malignancy prior to thoracoscopy. Thorax 2015;70:192-193.

8. Soni NJ, Franco R, Velez MI, et al. Ultrasound in the diagnosis and management of pleural effusions. J Hosp Med. 2015;10(12):811-816.

9. Yang PC, Luh KT, Chang DB, Wu HD, Yu CJ, Kuo SH. Value of sonography in de­termining the nature of pleural effusion: analysis of 320 cases. AJR Am J Roent­ Genol. 1992;159:29­33.

10. Porcel JM, Vives M, Vicente de Vera MC, Cao G, Rubio M, Rivas MC. Useful tests on pleural fluid that distinguish transudates from exudates. Ann Clin Bio­ Chem. 2001;38:671­5.

11. Kolditz M, Halank M, Schiemanck CS, Schmeisser A, Höff ken G. High diagnos­tic accuracy of NT­proBNP for cardiac origin of pleural effusions. Eur Respir J. 2006;28:144­50.

12. Havelock T, Teoh R, Laws D, Gleeson F. Pleural procedures and thoracic ultra­sound: British Thoracic Society Pleural Disease Guideline 2010. Thorax. 2010;65: Suppl 2:ii61­ii76.

13. Gordon CE, Feller-Kopman D, Balk EM, Smetana GW. Pneumothorax following thoracentesis: a systematic review and meta-analysis. Arch Intern Med. 2010;170(4):332-339.

14. Lichtenstein DA. Lung ultrasound in the critically ill. Ann. Intensive Care. 2014; 4(1):1.

15. Marini TJ, Rubens DJ, Zhao YT, et al. Lung Ultrasound: The Essentials. Radiol Cardiothorac Imaging. 2021; 3:2.

16. Rambhia SH, D’Agostino CA, Noor A, et al. Thoracic Ultrasound: Technique, Applications, and Interpretation. Curr Probl Diagn Radiol. 2017; 46(4): 305-316.

17. Hassan M, Mercer RM, Rahman NM. Thoracic ultrasound in the modern management of pleural disease. Eur Respir Review. 2020; 29 (156): 1-11.