DRHEM

The Lion's Roar

2011-09-14T06:19:00.000-07:00

“Roooaaarrrrrrrrr!”

“What was that?” I said to the nurse sitting next to me.

“It sounded like it came from the patient behind you,” said the nurse.

I spin around in my chair. My eyes make contact with an elderly man lying in bed. His hair is white and reminds me of Albert Einstein, the way it sticks up from his head. He is covered in a white blanket. I walk over to find out more.

I check his chart. “Mr. Altman, what brings you to the hospital today?” I ask.

He responds after a 5-second delay. “My head. It is pounding. Right here,” Mr. Altman said as he pointed to a small spot on the right side of his forehead about 3 inches above his eyebrow. “I've never had pain like this before; never a migraine, not even a headache. I don't know what is wrong but I just don't feel well,” he says.

“What was that roar I heard before?” I asked.

“What roar?” he replies.

I decide not to pursue the issue.

I look at the man standing next to Mr. Altman. “Hi, I am Steve, Mr. Altman's son.”

“Hi, Steve. Can you tell me more about your father's headache?”

“Well, I noticed my father was not acting like himself this evening. He seemed confused. He forgot my name and didn't know the date. This is unusual. He never complains either. You know, he survived the Holocaust.”

I performed a quick physical exam on Mr. Altman, focusing on the neurological aspects. I asked him to smile, raise his eyebrows, puff out his cheeks, and stick out his tongue—looking for the slightest imperfection to signal a neurologic dysfunction. He performed all of these functions perfectly. Then I tested his motor skills. I asked him to push, pull, and raise various parts of his body against resistance. Again, all was normal. I cannot isolate a neurologic abnormality and therefore decide to order a head CT scan and alert the stroke team of a possible stroke.

I wheeled Mr. Altman across the hall to the CT scanner. The radiology technician positioned the stretcher next to the CT table. We slid Mr. Altman onto the table and strapped him in. We placed folded sheets on each side of his head so it does not move—careful to avoid streak artifact and degrade the quality of the scan. We double check to make sure everything is in place and leave the room.

The tech entered the orders into the computer and told Mr. Altman to hold still. “Don't move even an inch,” the tech says over the loudspeaker. The large mouth of the CT scanner swallows Mr. Altman. We all watch as the images appear slice by slice.

“Oh boy,” I say to myself. “That does not look good!”

Mr. Altman's brain was being compressed by an epidural hematoma. The blood is located exactly where Mr. Altman pointed to when we spoke just minutes ago. If this condition is not corrected, Mr. Altman's brain will start to herniate through the foramen magnum, leading to rapid decompensation and likely death. We don't have much time.

The tech walks over to open the door. I see him struggling with it so I ask what is happening. He says he cannot open the door. It is jammed. “What do you mean?” I ask. I push past him, and wiggled the handle and thrust my shoulder against the door. It doesn't budge. It's clear the door is not jammed, but locked.

“Who has the key?” I ask the tech.

“What key?” he replies, dead serious. “I never lock this door. I have never even seen a key ever used in this door.”

I peered into the room through the glass window and saw Mr. Altman lying on his back on the CT scanner table. He doesn't know we can't get him out.

“Call security,” I said. “Maybe they have a key.”

Security arrives minutes later with a ring of keys.

“Are you going to save the day?” I ask the guard. “Please tell me that one of those keys will open this door!” Five minutes and at least 20 keys later, I asked the clerk to call the fire department. “We need this door open now.”

While we waited for the fire department, we kept checking on Mr. Altman. We told him over the speaker not to worry, we are going to get him out soon. He doesn't respond. We can barely see his face because he is lying on his back inside the CT scanner. I started thinking about his brain filling with blood, pressure quickly building, causing his breathing to gradually slow and eventually stop. This man survived the Holocaust, I say to myself; he can hold out a few more minutes. I tried to see his chest rising but he is covered with so many sheets. I kept watching and waiting.

I decided not to wait any longer.

A security guard and I rammed our bodies into the door. It didn't budge. We took a few steps back to get some momentum, and then both of us hit the door at the same time. Nothing. I peer into the room and see Mr. Altman's face. His eyes are closed and I still can't tell if he is breathing. I look at the security guard and tell him we have to get this door opened. We raised our legs and kicked the door as hard as possible. I heard a crack. We kicked it again and again. Finally the door swung open. I rushed over to Mr. Altman's side. As I pulled down the blanket that partially covered his face all I hear is “Rooooaaaarrrrr,” coming from the mouth of Mr. Altman. Again, I am not sure what this is. I check his vital signs, which are unchanged.

We returned to the emergency department and called the neurosurgeons so that they could operate on Mr. Altman's hematoma. I explained the diagnosis to Mr. Altman's son and briefly discussed the next steps. I shook the son's hand and wished him luck. Just as I am about to walk away to see my next patient, I stopped and turned around. “Have you ever heard your father roar before?” I ask.

“Oh, his yawn,” the son said. “He's been doing that his whole life. He kind of sounds like a lion, doesn't he?”

I nod. He sure does.

[Ann Emerg Med. 2009;54:625-626.]

MH#4

2011-09-05T17:58:00.000-07:00

Half of what you learn in medical school would prove to be wrong in ten years

-Dr Sydney Burwell, Dean Harvard Medical School

Intern Report Case Presentation 4.3

2011-06-06T10:48:00.000-07:00

Case Presentation by Dr. Dan Helzer

HPI

36 year old AA female presents to the emergency department complaining of “passing out.” Pt states that she was sitting down watching TV when she stood up, became very dizzy and lightheaded but no vertigo and fell to the ground. She stated that she remembers almost everything but could not stay standing up for some reason. Family members stated that she was not arousable for a few seconds and then came too. She felt uneasy as family members helped her up and needed assistance getting into the car to be brought to the ED. She has felt a little weak over the last few days but has experienced nothing like this recently. Pt also states that she has had heavy vaginal bleeding for the last 10 days, it began with her normal menses but never stopped. Her last normal menstruation was a month and a half ago. Typically she has heavy menses but it only lasts 3-4 days. She says that currently she is passing large clots and goes through multiple pads daily. She denies headaches, abdominal pain, chest pain, palpitations, and SOB. She denies ever being told that she has an abnormal heart beat or problems with her heart. Her family denies any bladder or bowel incontinence during the event.

Past medical history is significant for anemia and fibroid uterus. Pt is G3P3 and is sexually active. Her medications include Fe pills.

Past surgical history positive for C-section x 2.

Social Hx includes a 30 pack/year smoking history.

Vitals: 108/55, HR 104, RR 16, Pulse Ox 99 % on RA, Temp 37.7

General: Pt is in no acute respiratory distress, appears pale.

HEENT: Normocephalic/atraumatic, PERRLA, EOMI, no nystagmus, conjunctiva pale and non-icteric, mucous membranes moist and pale. Fundoscopy demonstrated no pappiledema.

Neck: No lymphadenopathy, no JVD, no masses

Respiratory and Lungs: Equal excursion bilaterally, CTAB, no wheezes, rales, rhonchi, or stridor.

Cardiovascular and Heart: Tachycardic rate and rhythm, S1/S2 auscultated, no murmurs, gallops, rubs, or thrills. Pulses palpated in all 4 extremities.

Gastrointestinal and Abdomen: BS +, Abdomen soft, non-tender, non-distended. No masses. No CVA tenderness.

Neurological: Patient is alert and oriented to person place and time, CN II-XII intact, sensation to pinprick intact in all 4 extremities, strength 5/5 in all extremities. No pronator drift was present. Reflexes are 2+. Heal to shin was normal. Upon standing pt became lightheaded and dizzy and felt the need to sit back down, therefore gait and Romberg were not properly evaluated. Dix-Hallpike test was normal.

Genitourinary: External genitalia were normal. Examination of the pelvis and vagina revealed active bleeding from the closed cervical os with pooling of blood and blood clots in the vaginal vault, no tissue like material was present. The uterus was not enlarged. CMT was absent. The adnexa were non-tender and no masses were palpated.

Orthostatic Vital Signs:

-Supine BP 109/60, HR 103

-Sitting BP 100/59, HR 111

-Standing BP 88/52, HR 127

Lab Results:

Urine pregnancy negative

WBC 11.3, Hemoglobin 2.9, Hematocrit 11.7, Platelets 35

Electrolytes all WNL

Diagnostic Studies:

12 Lead ECG: Sinus Tachycardia at 107 BPM.

Ultrasound showed?

Version:1.0 StartHTML:0000000175 EndHTML:0000014694 StartFragment:0000003558 EndFragment:0000014658 SourceURL:file://localhost/Users/adamrosh/Desktop/Syncope%20Case.doc

Pelvic US with Duplex:

Findings suspicious for adenomyosis.

Nabothian cyst in the cervix largest measuring 0.7 x 0.5 x 0.8 cm

Paraovarian cyst adjacent to left ovary.

Questions:

1. What is the most common cause of syncope in adults aged 18-65 who present to the ED?

A. Postmicturation

B. Orthostatic

C. Psychogenic

D. Unknown or Idiopathic

E. Cardiac

2. The same pt is brought in by family members who tell you that when she fell down after standing up her whole body started shaking for at least one minute and she was completely unresponsive during this time. They said it looked just like a seizure that the patient’s cousin with epilepsy has all the time. Which clue in the HPI can often be the only distinguishing feature between syncope and seizure?

A. The patient has never had a seizure before

B. The patient remembers everything

C. The patient has an abrupt and complete recovery to baseline

D. The patient has generalized tonic/clonic movements during the episode.

E. The patient ate 10 tacos from taco bell and drank a liter of cola earlier in the afternoon.

3. Of the following, which pt with syncope should be discharged from the ED with follow up by PCP and not be admitted.

A. A 17 year old male with exertional syncope and crushing chest pain.

B. A previously healthy 37 year old male with 5 seconds of asystole on carotid sinus massage.

C. Our patient with a hematocrit of 11 and orthostatic hypotension

D. A 90 year old female with an EF of 22% and enlarged heart borders on CXR

E. A 52 year old male with SOB on initial presentation.

Please submit your answers as a comment. Your submission will not immediately post. Answers with a case discussion will post on Friday. If you have any difficulty, please contact the site administrator at arosh@med.wayne.edu. Thank you for participating in Receiving’s: Intern Report

Intern Report Case Discussion 4.2

2011-06-06T10:40:00.000-07:00

Case Presentation by Dr. Deepa Japra

Case Presentation

Answers: 1) c, 2) c, 3) c

Discussion:

The patient in this case is suffering from Pelvic inflammatory disease (PID) caused by Neisseria gonorrhoeae infection. PID includes a spectrum of diseases of the female upper genital tract including endometritis, salpingitis, pelvic peritonitis, and tubo-ovarian abscess. It is an ascending infection most commonly caused by N. gonorrhoeae and Chlamydia trachomatis where the bacteria spread from the cervix and vagina to the upper portions of the female genital tract. PID is responsible for approximately 30% of female infertility and 50% of ectopic pregnancies.

Risk factors for PID include multiple sexual partners, STD status of the sexual partner(s), age, and history of previous PID. Numerous studies have shown that having multiple sexual partners resulted in increased risk of PID ranging from 4.6 to 20 fold. (Question 1c). In one study which compared 712 women hospitalized for PID to 2,719 controls, the risk of PID was increased 3.4 times in patients with four or more sexual partners during the previous six months, and 3.2 times in patients who had intercourse with one partner six or more times per week. Having a partner with symptomatic gonococcal infection including dysuria and urethral discharge also increases a woman’s risk of PID (Question 1e). PID is more common in the 15 to 25 year old age group, with the incidence in women greater than 35 years old being only one-seventh of that in younger women. (Question 1a). Women with previous PID have increased risk of subsequent episodes, with one study citing an increase by a factor of 2.3. (Question 1d). However, caution should be used in diagnosing a woman who presents with abdominal pain in the ED with PID based on a previous diagnosis of PID. IUD usage (Question 1b) causes minimal risk of PID, and risk is usually limited to the first 3 weeks after IUD insertion. There is no evidence indicating that an IUD should be removed in a patient with acute PID.

The clinical features of PID can vary widely, with lower abdominal or pelvic pain being the most common presenting symptom to the ED. Patients may also present with dyspareunia, abnormal bleeding, and/or vaginal/cervical discharge. Physical examination can demonstrate lower abdominal tenderness, cervical motion tenderness, unilateral or bilateral adnexal tenderness on bimanual exam, and/or fever (>38 C). Though clinical examination has a low sensitivity for the diagnosis of PID, current recommendations by the CDC recommend empirical treatment based on clinical exam due to the long term sequelae, which include risk of ectopic pregnancy and infertility.

The CDC criteria for empirical treatment of PID include a minimum of cervical motion tenderness or adnexal/uterine tenderness in the presence of lower abdominal or pelvic pain (Question 2c). Additional criteria which are used to support a clinical diagnosis of PID includes oral temperature > 38.3 C (Question 2e), abnormal cervical or vaginal mucopurulent discharge (Question 2a), the presence of numerous WBCs on microscopy of a vaginal sample (Question 2d), elevated erythrocyte sedimentation rate (ESR), and elevated C-reactive protein (CRP). These additional criteria, however, are not necessary for empirical treatment. A history of gonorrhea/Chlamydia infection in the past (Question 2b) is not part of the CDC criteria indicating empirical treatment for acute PID.

Findings which confirm a diagnosis of PID in a patient that presents with clinical signs and symptoms suggesting PID include endometritis or acute salpingitis on histological evaluation of a biopsy, demonstration of N. gonorrhoeae in the genital tract (Question 3c), gross salpingitis seen during laparoscopy/laparotomy, isolation of pathogenic bacteria from a clean specimen in the upper genital tract, or inflammatory/purulent pelvic peritoneal fluid without another source of infection. A confirmed diagnosis of N. gonorrhoeae infection in the past does not confirm acute PID (Question 3a). Though a patient with a positive pregnancy test and clinical symptoms of PID is at increased risk for ectopic pregnancy, a positive pregnancy test or a vaginal ultrasound demonstrating an ectopic pregnancy does not confirm PID (Question 3e and 3b). An elevated serum WBC count may suggest acute inflammation/infection, but is not in the diagnostic criteria to confirm PID (Question 3d).

As discussed above, empiric treatment of acute PID in the ED should be initiated in patients with lower abdominal pain and cervical motion tenderness, uterine tenderness, or adnexal tenderness due to the potential adverse consequences of untreated PID, which include infertility and ectopic pregnancy. Currently, CDC outpatient recommendations include ceftriaxone 250mg IM PLUS doxycycline 100mg BID for 14 days, with or without metronidazole 500mg BID for 14 days. An alternative regimen includes: cefoxitin 2g IM AND probenecid 1g oral PLUS doxycycline 100 mg BID for 14 days with or without metronidazole 500mg BID for 14 days. Metronidazole should be administered in patients with pelvic abscess, proven or suspected infection with Trichomonas vaginalis or bacterial vaginosis, or history of gynecological instrumentation in preceding 2-3 weeks.

Approximately 10 to 25% of women with PID require hospitalization. CDC recommendations for hospitalization include pregnancy, failure to respond to outpatient treatment, inability to tolerate oral medications, nonadherence to outpatient therapy, presence of pelvic abscess, or severe clinical illness including elevated fever, nausea/vomiting, and severe abdominal pain. Inpatient treatment options include cefoxitin 2g IV q6h OR cefotetan 2g IV q12h PLUS doxycycline 100mg q12h. An alternative regimen is Clindamycin 900mg IV q8h PLUS gentamicin (2mg/kg) loading dose with maintenance dose of 1.5mg/kg q8h.

Clinical Pearls:

- Pelvic Inflammatory Disease includes a spectrum of diseases of the female upper genital tract including endometritis, salpingitis, pelvic peritonitis, and tubo-ovarian abscess

- Empiric treatment of acute PID in the ED should be initiated in patients with lower abdominal pain and cervical motion tenderness, uterine tenderness, or adnexal tenderness due to the potential adverse consequences of untreated PID, which include infertility and ectopic pregnancy

- Male sexual partners of women with PID should be treated if they have had sexual contact with the patient during the 2 months prior to patient’s onset of symptoms

- Patients with PID should be tested for other sexually transmitted diseases, including HIV

Intern Report Case Presentation 4.2

2011-06-06T10:37:00.000-07:00

Case Presentation by Dr. Deepa Japra

A 25-year-old woman presents to the emergency department with persistent nausea and vomiting for 6 days. She complains of pain in the lower chest and upper abdomen that she rates as a 6/10. She describes the pain "like a heart beating real hard”, which is constant and throbbing in character. She is unable to tolerate a regular diet and states she vomits everything she eats. The vomitus is described as white and yellowish without hematemesis. The patient had a small bowel movement today, which was soft with no gross blood. She denies any genitourinary symptoms including no polyuria, dysuria, or hematuria. She does describe a vaginal discharge X 6 days. She is sexually active with one partner, and does not use protection. Her LMP ended 9 days ago. She has also had subjective fevers and chills, and lightheadedness, but without any syncopal episodes.

Past medical history is significant for genital herpes infection.

VS: BP: 122/75, P: 59, R:18, T: 36.5, O₂ saturation 100% on RA

GENERAL: Pt is conscious, alert, and cooperative

HEENT: Conjunctivae are pink without pallor, sclera anicteric. Mouth without intraoral lesions. Pharyngeal soft tissues are normal.

NECK: Supple. Trachea midline. No thyromegaly or lymphadenopathy.

RESPIRATORY: Clear symmetric breath sounds. Good air exchange in all lung fields. No accessory muscle use.

CARDIOVASCULAR: Normal S₁ and S₂. No S₃ or S₄ gallops. No murmurs or rubs. CHEST WALL: Nontender.

ABDOMEN: Soft, nondistended, bowel sounds present. mild discomfort to palpation in the epigastric and suprapubic areas, but there is no guarding, masses or rebound tenderness.

BACK: No spinal or paraspinal tenderness. No CVA tenderness.

MUSCULOSKELETAL: FROM, symmetrical strength, no acutely inflamed joints. SKIN: No rashes or lesions.

NEUROLOGIC: No gross focal motor or sensory deficits.

PELVIC EXAM: External genitalia are normal. Slight discharge in vaginal vault, cervical os is closed. Positive cervical motion tenderness. Mild uterine and adnexal tenderness, no masses.

Laboratory Studies are as follows:

CBC: Hb 15.5, Hct 43.1, WBC 9.2, Pl 234

Electrolytes: Na 139, K 3.7, Cl 101, HCO3 26, BUN 21, Cr 1.0, Glu 90, Ca 9.5

Lipase 294

ALT 30, AST 19, Alk Phos 77, TBili .8, DBili .2,

Urine Pregnancy negative

UA: trace glucose, 3+ ketones, 1+ blood, 1+ protein, Positive nitrite, 1+ leukocyte esterase, RBC 2-5, WBC 5-10, 1+ mucus, 1+ bacteria

Rapid HIV negative

Gonorrhea PCR positive, Chlamydia PCR negative

Questions:

Question 1

Which of the following is the greatest risk factor for development of pelvic inflammatory disease?

a. age

b. intrauterine device usage

c. multiple sexual partners

d. previous PID

e. sexually transmitted disease status of sexual partner

Question 2:

According to CDC guidelines, which of the following is essential in the diagnostic criteria for empirical treatment of PID?

a. abnormal cervical or vaginal mucopurulent discharge

b. history of Gonorrhea/Chlamydia infection

c. lower abdominal or pelvic pain with cervical motion tenderness or uterine/adnexal tenderness

d. numerous WBCs on microscopy of vaginal secretions

e. oral temperature > 38.3 C

Question 3:

In addition to clinical symptoms and physical exam findings, which of the following criteria suggests a confirmed case of PID?

a. confirmed N. gonorrhea infection in the past

b. confirmation of ectopic pregnancy on vaginal ultrasound

c. demonstration of N. gonorrhea in the genital tract

d. elevated serum WBC count

e. positive Pregnancy test

Intern Report Case Discussion 4.1

2011-06-06T10:26:00.000-07:00

Case Presentation by Dr. Sarah Hyatt

Case Presentation

Answers: 1. D, 2. B, 3. E

Discussion:

This patient has a Valsava retinopathy. Immediately following a Valsava maneuver, a sudden rise in intraocular pressure causes retinal capillaries to spontaneously rupture. The prognosis for Valsava retinopathy is generally good.

Unilateral manifestations are most commonly seen, but bilateral findings have been reported. Sudden decreased vision occurs in the affected eyes, ranging from complaints of floating spots to complete loss of central vision. Vision often improves over weeks to months, depending on the severity of the retinal findings.

Risk factors for Valsava retinopathy are a history of vascular disease, diabetes, hypertension, sickle cell disease, anemia, idiopathic thrombocytopenic purpura.

Ocular findings are usually described as preretinal hemorrhages. Valsava retinopathy has a predilection for the macula. The ruptured vessels in the perifoveal capillaries usually cause a sudden and painless loss of central vision.

Causes: coughing, weight lifting, vomiting, bungee jumping, aerobic exercise, sexual activity, end-stage labor, colonoscopy procedures, constipation, and blowing musical instruments.

Medical care: patients should be advised to avoid anticoagulants and strenuous activities to prevent a rebleed. Patients should be instructed to sleep in a sitting position to promote blood settling, which may improve visual acuity, stool softeners may need to be considered for those with constipation. A diet rich in fiber is advisable. Physical activity should be limited until the retina has sufficiently healed. The patient should always try to limit activities that cause sudden increases in intrathoracic pressure against a closed glottis. Consultation to ophthalmology is recommended and needed for follow up.

Vision usually returns to normal over a short time period from weeks to months.

Key points:

When testing visual acuity use a Snellen chart at a distance of 20 feet or a Rosenbaum chart at a distance of 14 inches. If the patient is unable to do this test visual acuity by testing ability to count fingers (CF), if unable to do this test ability to perceive hand motion (HM), if unable to do this test ability to perceive light (LP). The result may be recorded as “patient able to count fingers at 5 feet”

Acute angle-closure glaucoma: Pt has a narrow anterior chamber angle; folds of the peripheral iris can block the angle, which prevents aqueous humor outflow. The rapid elevation of intraocular pressure causes optic atrophy if not treated promptly. Patient often complains of nausea, vomiting, and pain. Emergent ophthalmologic consultation is indicated. Acute glaucoma is treated with IV mannitol or glycerol to decrease intraocular pressure by osmotic dieresis, topical miotics (i.e., 2% pilocarpine or 0.5% timolol) to decrease pupil size and increase aqueous outflow, and acetazolamide IV to decrease aqueous production

Vitreous hemorrhage: Suspect if sudden painless monocular loss of vision, more common in diabetics with an obscured red reflex and retinal details. Patients often report seeing flashing lights. Patients also complain of seeing dark floating spots or floaters, which reflect benign vitreous separations

Central retinal artery and vein occlusion: both occur in middle-aged atherosclerotic patients or elderly hypertensive patients and present as sudden painless loss of vision. Occlusion of the retinal artery or its branches results in a dilated nonreactive pupil with an APD on the affected side. The retina is pale with a cherry-red spot on the macula. Occasionally amaurosis fugax precedes central retinal artery occlusion.

The fundoscopic examination of a central retinal vein occlusion is described as a “blood and thunder fundus” because of the presence of multiple large hemorrhages. Prognosis for both CRAO and CRVO is poor.

Common causes of nontraumatic loss of vision

Transient monocular

Amaurosis fugax

Temporal arteritis

Migraine

Persistent monocular

Central retinal artery occlusion

Central retinal vein occlusion

Retinal detachment or hemorrhage

Vitreous or macular hemorrhage

Optic or retrobulbar neuritis

Internal carotid occlusion

Acute binocular

Migraine

Vertebral basilar insufficiency

Cerebrovascular disease

Toxins (methanol, salicylates, quinine, ergot)

Optic or retrobulbar neuritis

Hysteria

Malingering

Sudden painless loss of vision

Central retinal artery occlusion

Central retinal vein occlusion

Vitreous hemorrhage

Retinal detachment

Ischemic optic neuropathy

Nonarteritic ischemic optic neuropathy

Valsava retinopathy

Functional visual loss, hysterical conversion or malingering

References:

1.Retinopathy, Valsalva, eMedicine http:emedicine.medscape.com/article/1228106

2.Emergency Medicine Secrets, fourth edition, 2006, pages 117-121, Markovchick

3.Rosen’s Emergency Medicine, seventh edition, 2010, pages 870-873, Marx

4.Uptodate, Approach to the adult with acute persistent vision loss, 2010, Leaveque

5.http://www.virginiaretina.org/pix/vitreous_hemorrhage.jpg, Virginia Retina Foundation

Intern Report Case Presentation 4.1

2011-06-06T10:18:00.000-07:00

Case Presentation by Dr. Sarah Hyatt

Case

Chief complaint: “I can’t see”

28 year old female comes to the ER for loss of vision for 2 days, patient states that this happened suddenly after she was vomiting. Patient is 6.5 months pregnant and has hyperemesis gravidarum that has persisted through her entire pregnancy. She denies any eye pain and the vision has not improved. She says she is unable to see anything from the left eye. Previous to this she has not had any trouble with her vision, other than wearing reading glasses. She decided to come to the ER because her vision still has not improved. She has history of hypertension but no longer requires medication. Denies any headache, fever, chills, chest pain, palpitations, shortness of breath, abdominal pain diarrhea, constipation, dysuria, vaginal bleeding or discharge, no recent travel, no sick contacts.

ROS: negative except as noted per HPI.

PMH: Hx of Hypertension no longer on medication

Surg hx: none

Gyn: G1P0, good prenatal care

Meds: Prenatal vitamins

Allergies: Vicodin causes “throat to close”

FH: Hypertension and diabetes run in the family

SH: No tobacco/alcohol/drugs

PE: vitals: T 98.7, HR 76, BP 110/56, RR 18, pulse ox 100% RA, weight 231, 5’5’’

General: 28 year old, African American female, sitting converses without difficulty

Skin: No rashes or scars

Head: normocephalic, atraumatic

Eyes: EOMI, PERRLA constricting from 6 to 3 mm bilaterally with light, no afferent pupillary defects, Pt has 20/20 VA in right eye, left eye able to finger count correctly at 5 ft. In her left eye her vision is more clear in her peripheral fields than centrally, intraocular pressure R eye 12, L eye 13, peripheral fields are intact by confrontation, on fundoscopy there were no distinct optic discs visualized, no pallor, no icterus

Nose: symmetric, no discharge

Mouth, throat: No erythema or exudates

Neck: No tracheal deviation or masses

Heart: RRR, S1, S2 heard no murmurs rubs or gallops

Respiratory: CTA BIL

Abd: gravid uterus above the umbilicus consistent with 26 week gestation, soft NT ND,

CNS: Alert and oriented x 3, cranial nerves: II, III, IV, and VI see eye exam above, good eyelid opening bilaterally; V, corneal reflex intact bilaterally facial sensation intact bilaterally in V1,V2, V3, good jaw opening, and bite strength; VII, eyebrow raise, eyelid close, smile, frown, pucker, and taste all intact and equal bilaterally; VIII equal auditory acuity to finger rub bilaterally; IX good swallow reflex, positive gag reflex; XI good lateral head rotation, neck flexion, shoulder shrug bilaterally; XII midline tongue protrusion and equal strength on lateral deviation bilaterally. Equal strength in the upper and lower extremities bilaterally, speech and gait are normal.

Extremities: no peripheral edema, all peripheral pulses are felt, good range of motion, no weakness

Labs: 136 101 5 Glucose 82, Ca 9.1, ALT 13, AST 21, total protein 7.1, albumin 3.4, uric acid 4.2 4.0 23 0.7 Alkaline phosphatase 166, negative UDS and UA

10.2

13.5 451 MCV 81.7 Fetal heart tone 150’s

32.6

Questions

1. After you dilate the pupil this is your fundoscopic exam. Your diagnosis is?

A. acute glaucoma

B. vitreous hemorrhage

C. central retinal vascular occlusion

D. valsava retinopathy

E. central retinal vein occlusion

2. The patient should be advised which of the following?

A. use aspirin

B. sleep in a sitting position

C. decrease fiber intake

D. resume normal physical activity

E . all of the above

3.Which of the following are risk factors for the above diagnosis?

A.diabetes

B.hypertension

C.anemia

D. idiopathic thrombocytopenic purpura

E. all of the above

Intern Report Case Discussion 4.0

2011-06-06T09:48:00.000-07:00

Case Presentation by Dr. Stephanie Wise

Case Presentation

Answers

1) A. The most common inherited hypercoagulable state is Factor V Leiden. This is characterized by the production of a “rogue clotter” protein, which is also resistant to proteolysis by protein C. It is inherited in an autosomal recessive fashion, and is most common in people of northern European descent. Von Willebrand disease is the most common genetic cause of excessive bleeding. The other options are other inherited hypercoagulable disorders.

2) B. Of the options provided, the correct statement is that T wave inversions are the most specific finding (81%) in the presence of pulmonary embolism. This has been the most common finding in some studies (68%).

S1Q3T3 is an indicator of cor pulmonale, which makes it less specific of a finding, and it is also not considered sensitive as it is only present in approximately 50% of cases.

Typically an ECG of a PE patient is abnormal; the difficulty is that the abnormalities are non-specific. The value of the ECG is more in ruling out other causes of the patient’s symptoms, especially myocardial infarction.

Sinus tachycardia is a common finding, but again, very non-specific.

3) C. Pulmonary angiography is the gold standard for diagnosis of pulmonary embolism. Doppler imaging can indicate a source of PE, but up to 60% of ambulatory patients (the people we’ll be seeing in the ED) do not have DVT.

In the presence of pulmonary embolism, the chest x-ray typically has some abnormality, but the abnormalities are usually both non-sensitive and non-specific. The findings more specific to PE (Hampton’s hump, Westermark sign and Fleischner’s lines) are rare. If you see them, however, you should be able to recognize them. Also, if you suspect PE, you should at least be aware of these findings so that you can identify them when present.

The value of D-dimer in diagnosis of PE is to rule it out. If clinical suspicion is low and the D-dimer is normal, PE is rare (2% or less). Thus, the value is in its negative predictive value.

4) C. Half of patients who present to the ED with a pulmonary embolism will have no identifiable clinical risk factors. Work-up will ultimately try to identify previously unidentied risk factors, but for the ED physician, a high index of suspicion needs to be present even if there is not a “convenient” history like what our patient in this case provided. Otherwise cases will be missed, which could be detrimental to our patients.

Intern Report Case Presentation 4.0

2011-06-06T09:46:00.000-07:00

Case Presentation by Dr. Stephanie Wise

A 42-year-old man presents to the Emergency Department with a 2-day history of coughing up blood. His symptoms started about 5 days after he returned from a week-long business trip in South Africa. He has not had any fevers or weight loss. He does have chest pain, however, on the left antero-lateral side. He describes this pain as sharp, worse with a deep breath. He denies any shortness of breath. No nausea or vomiting or diarrhea. Appetite has been normal.

PMH: Asthma
Medications: albuterol HFA PRN
Allergies: None
Surgeries: Appendectomy, age 19
FH: HTN, "blood problem" in two uncles
SH: Smokes 1/2 pack daily for 12 years; occasional alcohol, denies ilicit drugs

Physical exam:

BP 134/85, HR 108, RR 21, Temp 37.1
General: Well-developed overweight male, sitting up on stretcher, mild distress
HEENT: PERRL, EOMI; trachea midline, no LAD
CV: Regular rhythm, tachycardic, no murmurs
Resp: Breath sounds decreased at the left base with mild crackles; otherwise clear to auscultation, no wheezing
ABD: soft, non-tender, non-distended; normal active bowel sounds
Extremities: pulses equal, no deformities seen
Neuro: AOx3, normal strength and sensation in all extremities; no facial droop or other focal deficits; gait normal; reflexes 2+ in all extremities

Labs:
143 105 12
4.1 21 0.9 Glucose 88
WBC 9.9
Hb 14.2
Platelets 248
EKG shows sinus tachycardia, rate of 112, no ST elevations or depressions
CXR:

________________________________________
Questions:

1. What is the most common inherited hypercoagulable state?
a. Factor V Leiden
b. Protein C deficiency
c. Anti-thrombin III deficiency
d. von Willebrand disease
e. Sticky platelet syndrome

2. In the presence of acute pulmonary embolism, what is true of ECG findings:
a. "S1Q3T3" is the most sensitive finding
b. Anterior T wave inversions are the most specific finding
c. Typically no abnormality is seen on ECG
d. Sinus tachycardia is an uncommon finding

3. Which statement is correct about the diagnosis of pulmonary embolism?
a. Lower extremity Doppler studies that are positive for DVT are present in 70% of PE patients
b. The chest x-ray is typically normal
c. Pulmonary angiography is the gold standard
d. A D-dimer's value is in its positive predictive value

4. What percentage of ambulatory patients who present with PE have no identifiable clinical risk factors?
a. 10%
b. 30%
c. 50%
d.80%

Please submit your answers as a comment. Your submission will not immediately post. Answers with a case discussion will post on Friday. If you have any difficulty, please contact the site administrator at arosh@med.wayne.edu. Thank you for participating in Receiving’s: Intern Report

Intern Report Case Discussion 3.9

2011-06-06T09:40:00.000-07:00

Case Presentation by Dr. Deshon Moore

1. (C) Hydrochlorothiazide-induced hyponatremia. In the elderly, diuretic use has been associated with hyponatremia and usually occurs within 1 to 2 weeks of starting the drug. Diuretics can cause volume depletion and stimulate the release of antidiuretic hormone (ADH), which acts on the collecting duct to cause water reabsorption. However, this movement of water depends on a medullary concentration gradient. Loop diuretics like furosemide impair this gradient, and therefore water reabsorption is diminished even with adequate ADH levels. Thiazide
diuretics have no effect on the medullary gradient and water reabsorption is sustained. Diuretics
can also cause a heightened thirst response leading to increased fluid intake and further elevations of plasma free water. Older women in particular have been found to be most susceptible to thiazide related hyponatremia (reference below by Clark). Although thyroid disease and adrenal insufficiency can be associated with hyponatremia, there is nothing in the patient’s history to support these conditions as the reason for an acute presentation. A high urine sodium level may be caused by SIADH, but in this case, the elevated urinary sodium level is due to diuretic use. SIADH is characterized by an inappropriately concentrated urine (urine osmolality > serum osmolality), which
is not the case here.

2. (A) Give IV normal saline (0.9%). This woman has chronic hypovolemic hyponatremia as a result of diuretic use, and the hyponatremia must be corrected slowly. In cases in which hyponatremia is not life-threatening (sodium > 120 mEq/L), the goal is to replace about a 3rd of the sodium deficit over the first 12 to 24 hours (not to exceed 12mEq/ day) and the remainder over the next 2 to 3 days. IV normal saline can correct hyponatremia because the stimulus for ADH release in this case (volume depletion) is inhibited. This patient’s total sodium deficit is 450 mEq/L (Weight kg x 0.5 x (desired NA- current NA)), which equals approximately 3 L of normal saline (154 mEq/L). One liter of normal saline should be given over the first 8 to 12 hours (at 125ml/hr) with a subsequent infusion rate reduction. Using hypotonic saline at a slow rate is not indicated in severe hypovolemic hyponatremia. Although restriction of free water may have initially prevented the development of hyponatremia, it will not play a role in its correction or in raising blood pressure. Salt tablets, which can play a role in treatment of SIADH, would not be used for immediate treatment in this case.

3. (A) Serum osmolality. This is a case of pseudohyponatremia Secondary to high triglycerides. With high triglycerides, plasma gets expanded. When this happens, the assays we use that employ plasma dilution while measuring serum sodium levels may report an abnormally low value. However, these lipids and proteins do not contribute to serum osmolality (2 × plasma Na + [glucose/18] + [blood urea nitrogen/2.8]). Therefore, pseudohyponatremia is diagnosed when serum osmolality is normal. Pseudohyponatremia can also be seen with multiple myeloma and the production of paraproteins. Urine osmolality, urine sodium, and serum uric acid can vary and have no role in diagnosing pseudohyponatremia.

4. (B) Initiate IV short-acting insulin therapy. Because glucose is an effective osmole, hyperglycemia leads
to hyponatremia by causing an osmotically driven shift of water from cells into the extracellular compartment,
resulting in dilution of serum sodium. This osmotic shift can be estimated by a correction
factor that predicts a 1.6 mEq/L decrease in sodium for every 100 mg/dL rise in glucose above 100 mg/dL.
Thus, in this patient, the corrected sodium would be 135 mEq/ based on the correction factor : Na+ (0.016 x (Glu-100)). In patients with intact renal function, the osmotic shift in water to the extracellular compartment caused by glucose is somewhat balanced by an osmotic diuresis also driven by glucose. These pts usually have a mild decrease
in serum sodium. A patient on dialysis cannot respond with diuresis, and therefore hyponatremia tends to be more pronounced. In this case, the treatment is to remove the osmotic driving force, which will require immediate IV insulin. Subcutaneous insulin is not recommended for managing critical hyperglycemia. Free water intake will likely worsen the underlying hyponatremia. Although the patient missed his hemodialysis, hyponatremia is not a primary indication for urgent dialysis; correction of hyperglycemia is the first line of treatment. In addition, this patient has no other indications for receiving immediate hemodialysis, such as critical hyperkalemia or volume overload.

5. This is for you to realize your water intake. Stay hydrated, but remember that too much of a good thing can actually be bad! For my purposes I’m just referring to water…

REFERENCES
1. Rosen’s Emergency Medicine. Electrolyte Disturbance. Ch 123 p 1615
2.Clark BA, Shannon RP, Rosa RM, Epstein FH. Increased
susceptibility to thiazide-induced hyponatremia in the
elderly. J Am Soc Nephrol 1994;5:1106–11.
3. Douglas I. Hyponatremia: why it matters, how it presents,
and how we can manage it. Clev Clin J Med 2006;73
4. Hillier TA, Abbott RD, Barnett EJ. Hyponatremia: evaluating
the correction factor for hyperglycemia. Am J Med
1999;106:399–403.

Intern Report Case Presentation 3.9

2011-04-22T12:33:00.000-07:00

Case Presentation by Dr. Deshon Moore

A 67-year-old man with a significant medical history of COPD, CAD requiring many interventions, CHF, sustained ventricular tachycardia, and diverticulosis came to the emergency department with a 2-week history of generalized abdominal pain non positional and not related to food. He also complained of general weakness over the past several months. No c/o weight loss, no changes in urination volume.

Physical exam showed no pertinent findings.

Initial laboratory values were drawn and showed a serum sodium concentration of 117 mEq/L (normal 135-145 mEq/L). The patient's medical records indicated that almost 3 months earlier his serum sodium concentration was 134 mEq/L. Three weeks after that visit, his serum sodium concentration was 126 mEq/L.

On presentation the patient stated he was on amiodarone, Aspirin, Metoprolol, Nitroglycerin, lisinopril, furosemide, spironolactone, and simvastatin. The majority of his meds were started 3 mos ago.

Further Labs:

Serum osmolality 264 mOsm/kg,

U osm-730 mOsm/kg

Glu 120 mg/dl,

BUN 11 mg/dl,

Cr 1.0 mg/dl,

K- 4.4 mEq/L

Complete blood count and thyroid-stimulating hormone and thyroxine levels were normal; corticotropin stimulation test result was negative; chest radiograph showed no infiltrates or masses; and thoracic CT revealed no evidence of malignancy. An abdominal CT scan was normal.

Despite fluid restriction (< 1000 ml/day), serum sodium concentrations were 118-120 mEq/L over the next 2 days after admission.

Amiodarone was discontinued based on a publications suggesting that this drug can cause SIADH-induced hyponatremia.The patient's serum sodium concentration began to rise within 3 days of discontinuation and was 129 mEq/L at discharge the next day. At an internal medicine follow-up visit the patient's serum sodium concentration was within normal limits at 136 mEq/L. Symptoms of abdominal pain and general weakness improved as serum sodium levels increased.

Questions:

An 80-year-old woman who presented to the emergency department with weakness and dizziness had labs reveal a serum osmolality of 260 mOsm/kg, serum sodium of 125 mEq/L (normal 135–154 mEq/L), Urine sodium level of 50 mEq/L (normal, 0–300 mEq/L) and urine osmolality of 200 mOsm/kg. She takes furosemide for peripheral edema. Her PCP prescribed HCTZ for htn 1 week ago. The patient denies fevers, chills, nausea, or vomiting. She claims to be more thirsty than usual and has been drinking apple juice in response. BP is 100/60 mm Hg lying down and 84/40 mm Hg sitting. She weighs 60 kg.

1. Which of the following is this patient’s most likely diagnosis?

(A) Adrenal insufficiency

(B) Furosemide-induced hyponatremia

(D) Syndrome of inappropriate antidiuretic hormone

(SIADH)

(E) Thyroid disease

2. How should this patient be managed?

(A) Give intravenous (IV) normal saline (0.9%) at

125 mL/hr

(B) Give IV 5% dextrose in half-strength normal

saline at 50 mL/hr

(D) Provide salt tablets orally

3. 50-year-old man admitted to the CCU with a MI has a sodium level of 124 mEq/L. There are no other laboratory abnormalities; however, the sample is lipemic. The patient is resting comfortably and denies any symptoms. Which of the following is most likely to establish the diagnosis?

(A) Serum osmolality

(B) Serum uric acid

(D) Urine sodium

4. You have a type 2 diabetic with ESRD on HD who presents with weakness. He missed dialysis and ran out of his long-acting insulin 2 days ago. No other complaints. Physical Examination is unremarkable, including a normal neurologic examination. CXR negative. 12 lead ECG-NSR w no T wave abnormality

Labs: Sodium-125 mEq/L, K-5.2 mEq/L, Serum Glu- 700 mg/dL, Serum Osm 310 mOsm/kg

Which of the following is the most appropriate

next step in this patient’s management?

(A) Immediate hemodialysis

(B) Initiate IV short-acting insulin therapy

at home

(D) Restrict free water to correct hyponatremia

5. How many oz of water do you drink a day?

(A) <16 oz/ day

(B) 16-32 oz/day

(D) >54 oz/day

(E) Only coffee

2011-04-22T12:09:00.000-07:00

Case Discussion by Dr. Dan Paling

Discussion

Abdominal Aortic Aneurysm (AAA) is a potentially life-threatening condition that is frequently diagnosed incidentally when working up various abdominal complaints, and is often undiagnosed until the time of rupture. It is important for EM physicians to know that elderly white males are at the highest risk of having an AAA. High risk patients complaining of abdominal or back pain should receive a bedside ultrasound to screen for the possibility of AAA as the cause of their clinical presentation.

Managing patients with an AAA in the emergency department is primarily focused on heart rate and blood pressure control as well as appropriate surgical consultation. Once an AAA is diagnosed (normally with u/s), a CT angiogram should be performed to determine the AAA’s location and potential involvement with other vessels including the SMA, IMA, renal and iliac arteries. Patients with asymptomatic AAAs less than 5.5 cm can be watched and followed by a vascular surgeon. The patient should undergo abdominal ultrasonography every 6 to 12 months to assess the extent of further dilation if the aneurysm is less than 5.5 cm, is completely infrarenal, and only involves the aorta.

A CT angiogram should be performed every 6 to 12 months in patients with SMA, renal and/or iliac artery involvement.

Symptomatic patients may present with vague or sharp abdominal pain, low back pain, and/or the sensation of an abdominal pulsation. Patients with AAA not complaining of pain may present with syncope, nausea, vomiting, or early satiety. Patients with AAA that complain of abdominal tenderness (usually epigastric) are likely to have an expanding or infected AAA. These patients should receive an immediate surgical consultation as rupture can be spontaneous and imminent. Blood pressure control is the goal in these patients. Intravenous beta blockers are the drug of choice for acutely reducing blood pressure and heart rate. Goals of treatment include a heart rate of 55 to 65 bpm and a systolic blood pressure of 100 to 120mmHg or a MAP of 60 to 65 mmHg. If this SBP range is not achieved with a beta blocker alone and the patient has good mentation, nitroprusside can be added at 0.5mcg/kg/min until the blood pressure is controlled.

A ruptured AAA can present similarly to a myocardial infarction with syncope, hypotension, epigastric pain, nausea, vomiting, and diaphoresis. As many as 30% of AAAs are misdiagnosed on presentation, therefore ED physicians should have a high level of suspicion in patients with h/o AAA or that fall into the high risk categories (ie., white males of advanced age, patients with MCTD (spell out), or smokers with PVD). Rapid diagnosis, resuscitation and surgical consultation are required for treating these patients.

Answers to Questions

“(e) tobacco smoking” is the correct answer. There are several risk factors, both unmodifiable and modifiable, for developing an AAA. Smoking is the leading modifiable risk factor. It is hypothesized to increase a patient’s risk by 8-fold over a nonsmoker of similar age and comorbidities. (c) stress and (d) insomnia are not risk factors for the development of an AAA. (a) alcohol abuse and (b) diabetes mellitus are modifiable risk factors for the development of many other disorders including cardiovascular disease, but have not been linked to an increased incidence of AAA.

“(b) AAA that has enlarged from 4.7 to 5.0cm in the past 6 months” is the correct answer. Many AAAs are medically managed while being monitored by a vascular surgeon. Asymptomatic AAAs that are less than 5.5cm in diameter are managed medically until they become (a) symptomatic (regardless of size), (b) rapidly expanding (>0.5 cm in a 6 month period), (c) larger than 5.5 cm in diameter, or (e) ruptured, at which time surgical intervention is necessary.

“(b) aneurysm diameter” is the correct answer. The three main predictors of AAA rupture are size (aneurysm diameter), (c) rapid expansion (>0.5cm in 6 month period), and (e) female gender (18 vs 12% in males with aneurysms > 5.5cm), but the most important predictor for AAA rupture is aneurysm diameter. (d) Family history of AAA rupture and (a) advanced age are risk factors for AAA development, not rupture.

Clinical Pearls

AAA rupture is misdiagnosed in nearly 30% of patients upon presentation. Have a high level of clinical suspicion for the high risk groups!
Heart rate (<65 bpm) and systolic blood pressure (100 to 120 mmHg) control are the keys to managing symptomatic / acutely expanding AAAs. Intravenous beta blockers are the drug of choice for HR and BP control.
Patients should be counseled on smoking cessation and proper follow-up once an AAA is diagnosed.

Intern Report Case Presentation 3.8

2011-04-18T21:54:00.001-07:00

Case Presentation by Dr. Dan Paling

History and Physical

61-year-old obese male was sent to the local Emergency Department by his primary care physician with a complaint of low back pain. He reported a history of intermittent, worsening low back pain over the past 2 months. The patient experienced pain with movement of his low back. The pain was characterized as dull, aching, and rated 6-7/10 in intensity located at the level of L3-L5. He patient denied any radiation of the pain down his legs, but admitted that sitting and standing for long periods aggravated his pain. He denied recent or remote falls and/or trauma to this region of his back. The patient denied urinary or fecal incontinence. He stated that he had similar pain about one year ago and was treated for a lumbar muscular strain. The patient felt that he has had fevers intermittently over the past 3 months for which he took acetaminophen. He denied any complaint of chest pain or shortness of breath. He also reported having occasional epigastric abdominal pain with nausea, but no vomiting. He attributed this to a history of heartburn.

Past Medical History: hypertension and peripheral artery disease. No surgical history

Medications: hydrochlorothiazide and metoprolol, but has been noncompliant.

Social History: 40-pack-year tobacco, currently smoking 4 to 5 cigarettes a day.

Physical Examination: BP is 184/112, HR 78, RR 15, Temp 38.2 (oral), O₂ Sat 95% on RA.

General appearance: mild distress secondary to pain.

HEENT: AT/NC, PERRL, EOMI

CV: RRR, S1 S2, no m/r/g

Resp: CTAB/L, equal breath sounds, no wheezes or ronchi appreciated

ABD: obese, soft, diffuse tenderness to palpation worse in the umbilical region, no rebound or guarding, no CVA tenderness

Extremities: 2+ distal pulses present in all extremities, no cyanosis, clubbing, or edema

Rectal exam: guaiac negative, normal tone, no masses

Neuro: strength 5/5 bilaterally in all extremities, no sensory or motor deficits, straight leg test positive bilaterally at 60 degrees of hip flexion, reflexes 2+ b/l

Musculoskeletal: point tenderness over spinous processes of L3, L4, and L5, no soft tissue pain

Laboratory Results

WBC 21, Hb 13.6, Platelets 426, Na 134, K 4.5, Cl 102, CO₂ content 23, BUN 28, Cr 1.1

ALT 35, AST 38, Alk Phos 98, Lipase 23, Lactate 0.8

Diagnostic Studies

EKG:

Acute abdominal Series is unremarkable. No free air. No evidence of obstruction

MRI Lumbar Spine: as shown…

Interpretation: Osteomyelitis of L3 and L4 vertebral bodies. Inflammation extends into adjacent structures including the abdominal aorta. Marked dilation of the abdominal aorta at approximately 4 cm in diameter showing inflammatory changes of the vessel wall.

Questions

1. Which of the following is a modifiable risk factor for developing an abdominal aortic aneurysm?

alcohol abuse
diabetes mellitus
stress
insomnia
tobacco smoking

2. Which of the following cases requires medical management ONLY?

AAA that has enlarged from 3.0 to 3.7cm over the past 6 months
AAA that has enlarged from 4.7 to 5.0cm in the past 6 months
55 YOM with newly diagnosed symptomatic 4.5cm infrarenal AAA
65 YOM with asymptomatic 5.7cm infrarenal AAA
71 YOM with ruptured 5.0cm AAA exhibiting good mentation and stable vital signs

3. Which is the most important predictor of AAA rupture?

advanced age
aneurysm diameter
expanding AAA
family history of AAA rupture
female gender

Intern Report Case Discussion 3.7

2011-04-18T21:53:00.000-07:00

Case Presentation by Dr. Cameron Kyle-Sidell

Case Presentation

Discussion:

1. Answer: a

The common pathway leading to all forms of renal failure is decreased renal blood flow. Patients can be oliguric or non-oliguric. Decreased urine output, if present, is a result of decreased GFR. Rising BUN and creatine is the hallmark of ARF and encompassed in the definition of it, but is a result of, not a cause of renal failure. The cause, regardless of the type of renal failure, is decreased renal perfusion. In prerenal, failure, this is due to decreased blood flow to vessels supplying the kidneys. In intrinsic renal failure, various disease state are associated with release of renal afferent vasoconstrictors and or/ direct ischemic renal injury. In post-obstructive renal failure, the increase in tubular pressure decreases the filtration driving force. As the pressure gradient equalizes, the maintenance of a depressed GFR is dependent upon renal efferent arteriole vasoconstriction, again leading to ischemia of the distal arterioles supplying the renal parenchyma.

2: Answer: b

In prerenal failure, the diminished renal perfusion causes activates the renin-angiotensin-aldosterone system, stimulated the increased absorption of sodium from the proximal tubules of the kidney. In pre-renal failure, the parenchyma of the kidney is not damaged and so the concentrating capacity of the kidney remains intact. Prerenal kidney will therefore lead to increased sodium reabsorption (and the resulting fluid reabsorption) and concentrating of the urine. One can therefore expect to see a FENa <1 and urine sodium concentration < 20 mEq/dl (body retaining sodium), and increased specific gravity (concentrated urine). Because BUN, as opposed to creatinine, can be freely filtered and absorbed by the kidneys, when the concentrating ability of the kidney’s remain intact, one can expect BUN levels to rise faster than creatinine (BUN absorbed while creatinine is not), leading to a BUN/Cr ratio greater than 10:1.

3: Answer: d

A single creatinine measurement cannot be used to determine between either the kinds of acute renal failure, or to distinguish between acute and chronic renal failure. Rising creatinine is a result of decreased GFR, and does not indicate whether or not injury to the kidney parenchyma has occurred. This is especially important to note when dealing with prerenal and intrinsic azotemia, as at some point, prolonged prerenal azotemia, or diminished renal perfusion, will lead to ischemic injury of the renal parenchyma. As Emergency physicians, we currently have no way now of knowing “when that line has been crossed,” and so we can only hope that our early intervention will be performed before such insult has occurred. It is important to note that if, when after rehydrating the patient, we do not witness sufficient increased urine output, we should be careful in further hydration, since we may be “too late,” (ie. the patient is now oliguric due to intrarenal damage) and further hydration can lead to complications from volume overload. There are some researches currently trying to develop assays that will can accurately and quickly determine the extent of active intraparenchymal renal damage (ie would be like looking forward elevated kidney “troponins.”)

BONUS QUESTION:

Answer: d

Patient was admitted to hospital, where after three days of rehydration w/ careful observation of urine output, patient creatinine levels gradually decreased from 6.4 to 2.2. Three months later at an outpatient visit, patient creatinine had reduced further to her baseline of 1.3.

Intern Report Case Presentation 3.7

2011-04-13T05:21:00.001-07:00

Case Presentation by Dr. Cameron Kyle-Sidell

CHIEF COMPLAINT(S): "My mother keeps throwing up"
HISTORY OF PRESENT ILLNESS: This is an 84-year-old woman who was brought in by her daughter and granddaughter. They report that she's been throwing up constantly for 3 days, approx 10 times per day. Unable to tolerate food or water. Reports having some lightheadedness when she walks. No fevers, cough, rashes, or sick contacts. No abdominal pain. No recent trauma. She did fall several weeks ago hurting her elbow and her left, but came to the emergency room and got a CT of the head which showed no bleed. Patient medical history includes only hypertension treated with lisinopril. Previous cesarean section.
VITAL SIGNS: Systolic blood pressure 105, heart rate 71, oral temperature 35.1. Pulse oximetry is 98% on room air.

PE: No pertinent findings

Course in the ED:
CBC, electrolytes, lipase, and ALP ordered. IV established and patient received 1 L NS. Abd X-ray ordered. First thing to come back were the electrolytes. Patient’s creatinine is 6.4. Per CIS, patient’s baseline creatinine was 1.3 on November 28, 2010, two months previous. BUN is 108. All other labs WNL. Patient currently awaiting abdominal x-ray.

1. Regardless of the type, what is the final common pathway leading to all ARF?

Reduced renal blood flow
Decreased urine output
Rising BUN and creatinine
Increased urine output

2. Prerenal Failure is characterized by all except:

BUN/Cr ratio greater than 10:1
Decreased specific gravity
Urine sodium concentration less than 20 mEq/dl
FENa less than 1%

3. Our patient’s extremely elevated creatinine level of 6.4 tells us that she is experiencing:

Prerenal azotemia only
Intrinsic azotemia only
Prerenal and intrinsic azotemia
Impossible to tell

AND THE BONUS MILLION DOLLAR QUESTION:
After treatment, the patient’s creatinine…?:

who cares, we lost the patient
remained super high, like, because, the patient is on dialysis
came down to, like, 2-something
returned to baseline

Intern Report Case Discussion 3.6

2011-04-13T05:01:00.000-07:00

Case Presentation by Dr. John Wilburn

Case Presentation (click to see the case)

Answers: 1.b 2.a 3.d 4.a

Discussion:

This patient is suffering from gallstone pancreatitis. Gallstones are the major cause of acute pancreatitis accounting for 40% of cases. Other causes of pancreatitis include alcohol, ERCP induced, medications, metabolic, and idiopathic. Gallstone pancreatitis takes place when a stone impacts and obstructs the ampulla of vater or the pancreatic duct resulting in early activation of exocrine enzymes and auto digestion of the pancreas. Prognosis is generally good if pancreatitis is mild and appropriately treated. Mortality of mild to moderate gallstone pancreatitis is around 10% which is a decrease in 10-15% over the past 30 years.

Severe pancreatitis is defined by local complications (pseudocyst, hemorrhage, and infection), or signs of organ damage (hypoxia, ARF, DIC, hypocalcemia <7.5). The overall mortality of severe pancreatitis is 30% which has not changed over the past 30 years.

Risk factors for gallstone pancreatitis include: female, advanced age, obesity, multiparous women, high cholesterol, alcoholism, and smoking.

Most patients have the cardinal symptom of abdominal pain in the epigastric region, but can be in the left or right upper quadrants. Patients usually describe the pain as rapid in onset, constant steady, or boring pain increasing in intensity till it reaches a maximum. When the pain reaches pinnacle with no relief most patients seek medical attention. Patients can present with tachycardia, febrile, and elevation or depression of blood pressure. This pain can be associated with nausea and emesis and anorexia. Patients can appear jaundiced as obstruction of the ducts causes back up in the biliary system. Most patients on physical exam are tender in the epigastric region and may have a positive Murphy sign.

Pancreatitis should always be in the differential for any patient with upper abdominal pain. The work up for pancreatitis includes cbc, metabolic panel, LFT, and lipase. There is no gold standard diagnosis of pancreatitis most experts agree that lipase is just as sensitive as amylase and has more specificity at 3x normal values. Recently experts in the United Kingdom recommend that lipase should be used for the diagnosis of pancreatitis. Amylase can still be used to diagnose pancreatitis; however it is not as specific at 3x the normal values. ALT above the level of 150IU/L is the most sensitive and specific liver enzyme for gallstone pancreatitis. If pancreatitis is diagnosed ultrasound should be conducted within the first 24 hours to either confirm or rule out gallstones as the cause. CT may also be indicated in severe pancreatitis to rule out peripancreatic complications such as pseudocyst, hemorrhage, and necrosis of pancreas.

Medical management:

Medical management of pancreatitis is usually supportive and tailored to the cause of pancreatitis with emphasis on avoiding complications. Patients should be admitted to the hospital for intravenous fluids, pain control, antiemetic, and made NPO in the initial phase. There should be a consult to general surgery for management, ERCP, and cholecystectomy the same hospital admission. Intravenous fluids are the most important intervention in the initial setting, some patients may require up to 6L of fluid as the inflammation leads to sequestration of fluid out of the intravascular space. Give 2-3L bolus of .9ns initially and reassess, if sufficient; place the patient on infusion at 250ml/hr normal saline. Pain control with morphine, no evidence has shown clinical difference or outcome when compared to meperidine. Nasogastric tube is only indicated in patients with intractable emesis, severe abdominal distention and ileus. Routine use has shown no clinical benefit and has increased the number of days hospitalized. ERCP with sphincterotomy and stone extraction is indicated after the initial pain has subsided and patient clinically improves. This is usually 24-48 hours after admission; early ERCP is only indicated in severe episodes of pancreatitis not responding to conservative management or cholangitis. ERCP may actually induce pancreatitis 5% of the time and is not the definitive treatment for gallstone pancreatitis. Studies have shown a 30-50% recurrence of gallstone pancreatitis with ERCP alone. Cholecystectomy is the definitive treatment and should be performed on the same hospital admission. Patients with severe pancreatitis require ICU admission.

There are cardiopulmonary, renal, metabolic, infectious, and hematologic complications of pancreatitis. All complications are caused by the inflammatory reaction of pancreatitis. Usually cardiopulmonary collapse due to hypotension or ARDS is the cause of death within the first week. Patients who develop ARDS have a mortality of 50-60% which is the highest of the complications in pancreatitis.

References

Rosen’s Emergency Medicine, seventh edition, 2010, pages 1172-1183, Marx

Tintinalli’s Emergency Medicine, sixth edition, 2004, pages 573-577, Tintinalli

Uptodate, Clinical manifestation and diagnosis of acute pancreatitis, 2010, Vege

Pancreatitis, Acute, eMedicine http:emedicine.medscape.com/article/181364

Pancreatitis in Emergency Medicine, eMedicine http://emedicine.medscape.com/article/775867

Dhir, R. et al: Drug-induced pancreatitis: A practical review

Intern Report Case Presentation 3.6

2011-03-30T03:54:00.000-07:00

Case Presentation by Dr. John Wilburn

Pt. E.R. is a 25 Y.O Hispanic female presenting to the emergency Department with a 4 day history of stomach pain in the periumbilical and epigastric area radiating around the right side to the back. Patient describes the pain as Constant 8/10 sharp cramping that is aggravated with food and water. Alleviated by sitting up, patient did take Tylenol but it did not help her pain. She reports nausea and has had four episodes of non bloody emesis the night before after eating some bread, the emesis was described as “yellow with food in it”. She denies any change in the color or consistency of her bowel movements. LMP was 2 week ago and was a normal cycle. Her abdominal pain has been worsening over the past 4 days and it woke her up from her sleep at 4 am, at which time she decided to seek medical attention. She denies any trauma or ever having pain like this before. Denies any recent travel and reports that her kids at have had a cold but no GI illnesses. The patient feeling feverish denies any chest pain, shortness of breath or rashes.

ROS: Negative except as noted per HPI

Past medical history: Denies Diabetes or asthma

Past surgical history: C-section x2

Allergies: Penicillin (rash)

Medication: None

Family history: Father has HTN and Diabetes

Social History: Denies Tobacco, Drinks alcohol socially, denies any illicit drug use. She is currently employed as a waitress and lives at home with her two children ages 3 and 1.

Physical Exam:

VS: 37.5 pulse 106 Bp 128/86 RR 16 99% Room air

General: Laying on her side holding her epigastric area appears uncomfortable but in NAD

HEENT: NC/AT Perrl sclera mildly icteric. EOMI No nasal Discharge no pharyngeal erythema Mucous membranes are dry sublingual has a yellowish color to it.

Neck: Supple No tenderness Trachea is midline. No thyromegaly or Lymphadenopathy

Respiratory: CTAB no W/R/R

Cardiovascular: Tachycardia regular rythm, S1S2 no M/R/G good pulses

Chest: No visible rashes/scars/ no reproducible chest wall tenderness

Abdomen: No lesions or rashes on inspection, Obese, +BS, ST/Tender to Palpation in Epigastric area and RUQ +Murphys sign, No Rebound tenderness, - Rovsings – rigidity. No Guarding.

Extremities: Strength 5/5 b/l upper and Lower ext. Full AROM and PROM palpable radial and dp pulses, SILT and symmetric.

GU: Wnl on inspection no erythema or discharge – No CMT or Adnexal tenderness. Slide shows epithelial cells

Rectal: No Hemorrhoids good tone, no palpable masses. Guaic Negative

Laboratory Results:

Electrolytes: Na 140, K 3.9, Cl 104, HCO3 24, BUN/Cr 14/0.8, Glucose 125, Ca 8.8

CBC: Wbc 10.9, H/H 12.3/39.2, Platelets 427

ALT 193, AST 159, Alk Phos 288, Tbili 2.8, Dbili 1.3, Lipase 8005, Amylase 800

Urine hCG: Negative

U/A: 3+bili, 3+ ketones, Sp Gravity 1.025, trace blood, trace LE, Nitrite negative, rbc 2-5

Wbc 5-10, epithelial cells 5-10, trace bacteria

Ultrasound Demonstrates

Questions

Although there is no gold standard for this diagnosis which of the following is considered by most experts to be the most sensitive and specific test available?

CRP
Lipase
Trypsin
Amylase
ALT

2. Which of the of the following Liver Enzymes is the single best marker for biliary etiology of this diagnosis

a. ALT

b. LDH

c. Total Bilirubin

d. AST

e. Alkaline Phosphatase

3. Which of the following complications of this diagnosis has the highest mortality?

a. Acute Renal Failure

b. Myocardial Infarction

c. Infected Pancreatic Pseudocyst

d. ARDS

e. Splenic Vein Thrombosis

4. Which of the following is the definitive treatment?

a. Cholecystectomy

b. ERCP

c. Lexipafant

d. ERCP with sphincterotomy and stone extraction

e. Conservative management

Intern Report Case Discussion 3.5

2011-03-25T01:00:00.000-07:00

Case Presentation by Dr. Justin Kessler

Case Presentation (click to see the case)

This patient is suffering from an epidural hematoma with possible transtentorial herniation. Epidural hematomas are collections of blood between the skull and dura mater. Epidural hematomas that are large and rapidly expanding are usually caused by arterial bleeding. Classically these are due to damage of the middle meningeal artery or one of its branches sometimes caused by a temporal bone fracture. Without swift diagnosis and intervention, patient with arterial epidural hematomas name rapidly deteriorate and die.

In this patient B.B. underwent initial trauma and was experiencing secondary injury after a "lucid period." Although lucid intervals only account for proximately 20% of all cases of epidural hematoma the history of a head injury minutes to hours before having declining neurological function are classic for epidural hematomas. Patient will often still complain of a progressive headache during these lucid intervals as in the case of patient B.B..

The pathophysiology lies in the increasing arterial bleed causing increased intracranial pressure. Because the craniospinal intradural space nonexpandable, some of the volume of brain, CSF, and blood are factors at which if any volume of these components increases the volume of another must decrease to maintain ICP. This is known as Monroe-Kellie Doctrine. In the case study, CFS may have been displaced from the intracranial vault to the spinal canal office setting increase of blood volume. When this compensatory mechanism is overwhelmed and volumes of blood are still increasing the brain matter may start herniate as it too will continue to swell due to congestive brain swelling as well cerebral edema.

On vital sign examination this patient has to have progressive hypertension associated with bradycardia and diminished respiratory effort. These are specific responses to ICP increase known as the Cushing reflex; usually indicating ICP is that critical levels.

Management ED and this case should include rapid sequence intubation for airway protection since the patient’s GCS is 7. Lidocaine 1.5-2 mg per kilogram IV push may be used to attenuate the cough reflex with intubation since his patient’s gag reflex is still intact.

Hyperventilation may prevent further herniation in the early phases, hyperventilation works by causing cerebral vasoconstriction. Onset is within 30 seconds and peaks at 8 minutes after pCO2 drops to arrange of 30-35 mmHg. However, continued cerebral vasoconstriction also leads to ischemia.

More often hypertonic saline (HTS) is being used to reduce ICP however it is controversial whether it really has an effect. These studies are using the 3% drip however probably not including the 24% bolus that is given by our cavalier neurointensivists.

Further management to prevent herniation and tissue damage would include osmotic agents such as manitol as well as possible barbiturate coma to decrease metabolic demand of the injured brain tissue. Mannitol at 0.25-1g/kg can effectively reduce ICP and prevent further herniation onset 60minutes and lasting for 6-8hrs. However, with such a large bolus of osmolytes you could overwhelm the kidneys. Early seizure prophylaxis of benzodiazepines may also be needed, as up to 12% of patients with traumatic brain injury will develop early posttraumatic seizures. The patient having a depressed skull fracture is indication for acute seizure prophylaxis in his head trauma.

Only after the patient stabilized well CT imaging be required to complete the final diagnosis.

ANSWERS:

#1 Answer: B.) 20% Although Tintinalli's along with was every other study or reference quotes this 20% estimation of the number of the epidural hematomas that will have a heralding lucid interval, if you look back to the original paper below where this estimation came from is actually estimation of 20 up to 50% which has given way to more recent articles stating that the " lucid period" of epidural hematomas is a "classical finding" when doing a workup for epidural hematomas.

However, one must realize that traumatic brain injury that it comes from many different degrees and levels of injury. Therefore, a quantifiable estimation based on a study set of patients must be taken with a grain of salt.

I believe the original author accounted for this wide variation by giving a range in his estimation based on data available. I wrote the question before going to the first source of this statistic sorry.

Liau LM, Bergsneider M, Becker DP. Pathology and pathophysiology of head injury. In: Youmans JR, ed. Neurological Surgery. 4th ed. Philadelphia, Pa: WB Saunders Co; 1996:1549-1594.

#2 Answer: D.) Validated prospective studies have shown that High-risk patients with minor head trauma with any criteria including presence of headache, (mainly a progressive headache), vomiting, age >60, drug or ETOH intoxication, short-term memory deficit, post-traumatic seizures, or evidence of trauma above the clavicals are indicative of increased likelihood of intracranial injuries. Further high risk factors are also considerations for CT scan which include:

Focal neurologic findingsAsymmetrical pupilsSkull fracture on clinical examinationMultiple traumaSerious, painful, distracting injuriesExternal signs of trauma above the claviclesInitial Glasgow Coma Scale score of 14 or 15Loss of consciousnessPost-traumatic confusion/amnesiaProgressively worsening headacheVomitingPost-traumatic seizureHistory of bleeding disorder/anticoagulationRecent ingestion of intoxicantsUnreliable/unknown history of injuryPrevious neurologic diagnosisPrevious epilepsySuspected child abuseAge >60 yr, <2 yr

- For this reason one could argue that choice (E) may be a likely answer since the child is unable to give an accurate history anyway and might be having a progressive worsening headache, or that the Lady in (C) might be trashed from her two glasses of wine. The key rebuttal from the author of this question is “might.”

#3 Answer : C) GCS<8. The factor that is most predictive of posttraumatic head injury seizures is a GCS<8. 38.7 % of patients in the studies below developed seizures compared with 3.8% of patients with GCS> or equal to 8. Patient age, occipital lobe injury, concomitant use of illicit drugs, and generalized brain injury had not been shown to be predictive of posttraumatic seizures. Again, every case is different in traumatic brain injury and every study set of patients in different institutions will also be different. However, this is the data that is available.

Varon J, Marik PE Management of head trauma in children Crit Care Shock 2002;5:133-43.

Varon J, Marik PE Management of head trauma. Chest Aug 2002 vol.122 669-771

#4 Answer: A&D Ken Norton fought Muhammad Ali in the 1970’s however his disability of sounding “punchy” with his speech is due to a TBI from an auto accident.

Intern Report Case Presentation 3.5

2011-03-21T18:39:00.000-07:00

Case Presentation by Dr. Justin Kessler

Patient B.B. a 17–year-old high school football player presenting to the emergency department via EMS after collapsing to the ground unresponsive approximately 3 hours after being struck in the head without a helmet on by another player’s helmet. Initially he was dazed but was able to stand up and joke about what a “hard head he had.” He complained of a headache throughout the rest of practice and vomited once per his coach who thought it was due to the heat. PMHx significant only for acne. Patient takes Tylenol for headaches PRN after football practice. On exam patient is not responsive to name, he makes gurgling mumbles, slowly opens his eyes to painful stimuli, and only has an abnormal flexed posture does not withdraw to pain.

Physical Exam:

Vitals: BP146/92, HR 98 , RR9, Sat87% Room, Temp 37.4

HEENT: HEAD: Slight boney stepoff along the patient's right temporal area. No Scalp Lacerations.
EYES: The pupils are 7mmOD 3mm OS sluggish reactive to light,. fundoscopic exam shows evidence of swelling of optic disk ,hyperma, and loss of physiologic cupping on exam in OD only. Sclera were anicteric, conjunctiva were without palor.
EARS: Pinnae are intact bilaterally, TM are clear,no evidence of hemotympanum Bilaterally.
NOSE: No noticeable deformity, moist mucosa, no erythema, no epistaxis, discharge, no swollen turbinates.
MOUTH AND THROAT: Mucous membranes are moist,no erythema, no tonsillar exudates, no intraoral leisions of the gums, tongue, lips, or palates.
CV: S1 S2 present, regular rhythm and tachycardic rate~ 100bpm, no murmurs
Resp: Slow shallow breaths,
Abd: Soft, nondistended, BS all 4 Qs
Ext: Peripheral pulses present in all 4 limbs, cap refill <2 seconds ROM intact with passive movement of all 4 limbs. Tone increased.
Back: No tenderness to palpation throughout cervical, thoracic, and lumbar spine. No bony deformity, crepitus, or step-offs noted.
Neuro: Pt obtunded, Decorticate posturing, not opening eyes to command or name. Positive gag reflex. Absent ankle jerk bilaterally, Babinski negative bilaterally.

Lab Results:
Electrolytes, BUN, creatinine, glucose, and CBC were all within normal limits.
NORMAL ECG
12-lead ECG performed at 1550 is interpreted as revealing tachycardic normal sinus rhythm at a rate of 102 beats per minute. Axis was normal. There were no ST or T wave abnormalities to suggest myocardial ischemia or injury.

Diagnostic Studies: Head CT as Follows:

Questions

1. Following Injury in which there is later radiographic evidence on head CT of an epidural hematoma what is the estimated percentage in which there is a “lucid” period before deterioration?

A. 75%

B. 60%

C. 20%

D. 15%

E. 5%

2. In regards to a Minor Head Trauma which of the following patients would warrant CT scanof head or prolonged emergency department observation?

A. A 23 YO male that bumped his head on a door 2 days ago, currently asymptomatic, no LOC with intact orientation, memory.

B. A 30 YO male with a minor headache after being hit in the head from a falling telephone book(for Kansas City), no vomiting no LOC

C. A 45 YO female with fall to carpeted surface wearing high heels after drinking 2 glasses of wine with no change in consciousness, intact orientation and recall.

D.A 61 YO male who tripped over a shopping cart hit head into a car door with past history of epilepsy, last seizure was >20 years ago.

E. 5 YO female running away from her brother that hit her head on a coffee table complains of headache, witnessed by mother, child consolable on scene.

3.Which of the following factors has the greatest predictive value in the Development of seizures following head trauma?

A Patient Age

B. Occipial Lobe injury

C. Glasgow coma Score <8

D. Concomitant use of illicit drugs

E generalized brain injury.

4.Two of these Famous TBI patients are related other than the fact that they had Traumatic Brain injury which two?

A.Ken Norton

B.Ellen White

C.Natasha Richardson

D.Muhammad Ali

E.Larry Flynt

F.Phineas Gage

Intern Report Case Discussion 3.4

2011-03-21T18:31:00.000-07:00

Case Presentation by Dr. Kevin Sprague

Case Presentation (click to see the case)

The patient is suffering from acute cholecystitis. This is caused by inflammation of the gallbladder, most commonly after a gallstone (cholelithiasis) obstructs the neck of the gallbladder or cystic duct. The obstruction causes mucus layer disruption, irritation and inflammation, which leads to dysmotility and distention. This inflammation occurs in the absence of bacterial infection. The most common type of gallstones in western civilization are cholesterol stones which occur when the cholesterol in the gallbladder exceeds the solubilizing capacity. The cholesterol will then nucleate into monohydrate crystals. These crystals cause gallbladder hypomotility which further accelerates cholesterol stone formation.

Cholesterol stones account for approximately 80% of gallstones in western civilization. The other type are designated pigment stones. These stones are a mixture of abnormal insoluble calcium salts of unconjugated bilirubin along with inorganic calcium salts. The amount of unconjugated bilirubin increases with infection of the biliary tract, and so infection with E. Coli or Ascaris lumbricoides (roundworm) increases the likelihood of pigment stone formation. These stones are radiopaque once the concentration of Ca exceeds 4%.

2-12% of cases are not caused by gallstones and are classified as acalculous. These typically occur in severely ill patients. Common scenarios are: postoperative state after major surgery, severe trauma, severe burns, multisystem organ failure, and sepsis. Diagnosing these patients is much more difficult as the onset is insidious and symptoms are obscured by the previously mentioned scenarios. The incidence of gangrene and perforation are higher in these patients. The mortality rate from acalculous cholecystitis is as high as 41%.

A differential for acute cholecystitis can include hepatitis, hepatic abscess, pyelonephritis, RLL pneumonia/pleurisy, perforated duodenal ulcer, pancreatitis, and appendicitis. Patients may have a mild fever, anorexia, nausea, vomiting, tachycardia, and diaphoresis. They may have had previous episodes of biliary pain. WBC count is normal in 27-40% of patients. Alkaline phosphatase, bilirubin, and serum aminotransferase are often within normal limits, but may be mildly elevated.

Ultrasound imaging is most commonly used in the ED as it is rapid and has good sensitivity. A gallstone or sludge may be visualized as well as gallbladder distention, gallbladder wall thickening, and pericholecystic fluid. A positive sonographic Murphy’s sign has good specificity for cholecystitis.

Treatment includes basic supportive measures, correcting fluid status and electrolyte imbalance. Emesis is managed with antiemetics and nasogastric suction. NG suction may diminish biliary secretion and excretion. Pain control may be achieved with narcotics. Antibiotics should be administered to prevent ascending infection. For uncomplicated cases, a 2nd or 3rd generation cephalosporin is recommended.

Common complications are gangrene, necrosis, and perforation. Emphysematous cholecystitis occurs in 1% of cases. This is the consequence of gas producing organisms (E. Coli, Klebsiella, C. perfringens) invading the mucosa of the gallbladder.

Answers

D. Hepatobiliary Iminodiacetic Acid (HIDA) Scan is the most sensitive at 97% for acute cholecystitis. Ultrasound is a close second at 94% sensitive. According to Rosen’s Emergency Medicine 7th Edition, CT may be 92% sensitive. However, I have also seen it reported as low as 50% sensitive. The bottom line is that CT is a much less preferable imaging modality. X-Ray will pick up 10% of gallstones, or about half of the cases of pigmented stones. I have never seen any information on MRI for acute cholecystitis, but I needed a 5th option.

E. This is sort of a cheap question. Over 90% of cases are caused by mechanical obstruction of the gallbladder neck or cystic duct by a gallstone. Even though the etiology is noninfectious, antibiotic therapy with a 2nd or 3rd generation cephalosporin is recommended. The other 4 choices are the organisms most commonly responsible for ascending cholangitis.

B. Porcelain Gallbladder is caused by calcifications within the gallbladder wall. The gallbladder may be palpable through the skin (Courvoisier’s sign). There is a high incidence of gallbladder carcinoma associated with this radiologic finding. These patients should be referred for a cholecystectomy.

Intern Report Case Presentation 3.4

2011-03-16T19:28:00.000-07:00

Case Presentation by Dr. Kevin Sprague

An otherwise healthy 42 year old female presents to the Emergency Department complaining of 4 hours of constant epigastric pain and vomiting that began 30 minutes after eating lunch. The pain is sharp, constant, radiates to her shoulder blade, and is 8/10 in severity. She has been unable to hold any food or liquid since the vomiting began. She has vomited 3 times She denies hematemesis. She is concerned this is food poisoning. She states she has never had this happen before. However, she has had some episodes of mild abdominal sharp pain after eating that resolved after roughly an hour. After she gives you the history, she vomits yellow liquid in a basin before your eyes.

Physical Exam

Vitals: Temp 38.2, BP 128/62, HR 108, RR 20, Sat 99% on RA

General: Uncomfortable, in no acute respiratory distress

Lungs: CTAB

Cardiac: S1S2, RRR, tachycardic rate, normal rhythm

Abdomen: RUQ tenderness, involuntary guarding, rebound tenderness, normal bowel sounds throughout the abdomen

Otherwise normal physical exam

EKG demonstrates a tachycardic sinus rhythm. Chest X-Ray is negative for any acute process. WBC is mildly elevated at 13.4. The rest of the CBC, electrolytes, U/A, AST/ALT, alk phos, lipase, bilirubin are within normal limits.

You obtain an ultrasound which demonstrates the following.

Questions

1. What is the most sensitive test for cholecystitis?

X-Ray
Ultrasound
CT
HIDA scan
MRI

2. Which infectious agent causes the majority of cholecystitis in the United States?

E. Coli
Klebsiella
Enterococcus
Bacteriodes
No infectious etiology

3. Porcelain Gallbladder is associated with which of the following?

Primary hyperparathyroidism
Carcinoma
Ascending cholangitis
Paget’s disease
Hypercholesterolemia

Intern Report Case Discussion 3.3

2011-03-12T18:24:00.000-08:00

Case Presentation by Dr. Ryan Doss

Case Presentation (click to see the case)

This patient is suffering from acute chest syndrome, a complication of sickle cell disease and currently the leading cause of death in patients with SCD in the United States (with a total mortality in adults of 9%). As we all know, in sickle cell disease the sickling of red blood cells is precipitated by hypoxia. Any condition which results in a relative hypoxia in the pulmonary microvasculature can thus cause an attack localized to the lungs (or of course distributed more diffusely).

ACS is more common but less deadly in the pediatric age group, especially ages 2-4, and the incidence gradually decreases with age. In younger patients an attack of acute chest syndrome is most often brought on by an infection with viruses or bacteria. Fat microembolization from marrow necrosis - itself a complication of a more generalized sickle cell crisis - is more common in adults. Some other causes include asthma, atelectasis from splinting secondary to rib pain, or iatrogenic fluid overload/opiate-induced respiratory depression.

Given his age we can speculate that this patient's ACS is caused by either a fat embolus from his days-long sickle cell crisis or atelectasis from his right lower rib cage infarction. Practically, however, it doesn't really matter what caused his current condition. The management of ACS from any cause involves supportive care, empiric antibiotics, and exchange transfusion.

Aggressive pain control and oxygenation serve to reduce the sickling of the patient's RBCs by decreasing splinting, improving tidal volume, and helping to reduce the localized hypoxemia. Pulse oximetry will probably be inaccurate but can be useful as an approximation. A reading on room air below 92% should be evaluated more fully with an ABG. Calculation of the A-a gradient helps guide the disposition. There are no agreed-upon standards, but in general an elevated A-a gradient or a rapid rise in the gradient should steer the ED physician toward intubation and ICU admission. Inhaled bronchodilator therapy may be helpful, especially if the patient has a history of asthma.

Empiric antibiotics should include coverage for Chlamydia pneumoniae, Mycoplasma pneumoniae, and Streptococcus pneumoniae, the three most commonly encountered bacteria in infectious ACS (with Chlamydia pnemoniae being most common). This would involve a third-generation cephalosporin paired with a macrolide or quinolone.

Simple transfusion of 2-4u PRBCs should be considered early after the diagnosis of ACS. This appears to be as effective as exchange transfusion unless the patient's clinical condition is more severe. It is important to maintain a Hb below 10 mg/dL because higher Hb levels can cause hyperviscosity in the microvasculature in sickle cell patients. This is not normally a concern with simple transfusion due to the sickle cell crisis patient's acute drop in Hb.

Answers

1. As discussed above, calculation of the A-a gradient is an important management tool for the patient with moderate-severe ACS. But nobody wants to do that, including me, because math is hard. Especially when you have a patient in front of you with chest pain struggling to breathe. So let's take this a step at a time. (Or skip ahead to the end of this question if you just want to memorize the equation which is totally cool but cowardly).

First: the A-a gradient is simply the difference between the oxygen in the alveoli and the oxygen in the artery. We know the pressure of oxygen in the artery from the ABG measurement (81). There we're halfway done! (Not really).

The second half involves calculating the pressure of oxygen in the alveoli. Let's start by assuming we're at about sea level and the barometric pressure is 760mmHg. Multiply that by the room air FIO2 (21%, duh) and we have our oxygen pressure (159.6 or 160).

Unfortunately, we can't just use the calculated pressure of oxygen in the surrounding atmosphere. First of all, the pressure of oxygen in the air we inspire changes on its way through our respiratory tract. This is because the atmosphere becomes more humid as the air enters our body. The water vapor pressure (47mmHg) needs to be subtracted from the atmosphere's barometric pressure. Wait...why would we subtract water vapor pressure from barometric pressure? It seems like we should be adding it. BUT the molecular mass of water vapor is actually lower than that of dry air. Ok, crap, rewind and subtract 47 from 760 to get 719. Now 719 x .21 = 150.99 or 151.

If you're still reading at this point, I love you. And I'm sorry because it's about to get a whole lot worse.

Ok so the alveolar pressure of oxygen is 151! Now let's just compare that to the oxygen in the arteries! NO, you FOOL. When we measure the arterial pressure of oxygen we are measuring the oxygen left over in the artery AFTER the tissues take what they need. We don't want to compare the oxygen in the alveoli to the oxygen in the artery AFTER the body uses what it needs. We want to compare the gradient at the exact moment they straddle the air/blood barrier. So we need to add the oxygen the body consumed back into the arterial oxygen reading. OR we need to subtract it from the PIO2. Either way. Whoever wrote down the alveolar gas equation did it the second way since it's less intuitive (hooray...).

The respiratory quotient is a number derived by experimentation (for completely unrelated reasons...namely to calculate BMR based on different types of caloric intake) which equates to (CO2 eliminated/O2 consumed). It is a constant (for our purposes) and this constant is 0.8. So we just need to know CO2 eliminated and we'll know our O2 consumed, which we can then add back into our PaO2. If you think about it we kind of already know our CO2 eliminated, because we measured the CO2 in our artery with the ABG and our body HAS to get rid of all of that or we'll just steadily accumulate CO2 until we die. The PaCO2 in our ABG is 31. Rearrange (R=CO2 eliminated/O2 consumed) and you get (O2 consumed = CO2 eliminated/R or 31/0.8 or 38.75 or 39).

Oh god we're getting so close. Now add our O2 consumed (39) back to our measured PaO2 (81) to get 120. Subtract 120 from our calculated PAO2 (151) to get 31! Normal is less than 10. This guy is screwed.

Or you could memorize (150 – PaCO2/0.8) – PaO2. Whichever you prefer.

Er...P.S. The alveolar gas equation is PAO2 = FIO2(Patm – PH2O) – (PaCO2/R)

Answer: B

2. I don't really have a long-winded explanation for this one. According to Principles of Critical Care, neurologic complications including seizure and stroke are the most common complications of acute chest syndrome. Cardiac, gastrointestinal, and renal complications are infrequent.

Answer: C

3. Again, no big explanation here. This is just experimentally determined as far as I know. If anybody has a hypothetical explanation I'd be very interested in hearing it.

Answer: A

4. So a lot of these would be useful in some way, and arguments could be made for each. I'll skip over A and D and E as they don't involve any treatment (well, not any scientifically proven treatment anyway) and presumably you'd be most interested in treatment.

Answer C could be useful to decrease splinting and increase oxygenation. Plus with a 9% mortality and no REAL effective medical treatment you might as well go out with a smile on your face.

Answer B is a devious misdirection. Phlogisticated (i.e. gaseous) laughing anesthetic is nitrous oxide (N2O). According to Tintinalli's, “Inhaled nitric oxide has shown benefit in the management of acute chest syndrome, apparently due to its vasodilatory effects that improves the coordination between ventilation and perfusion in the damaged lung regions with minimal systemic absorption. In addition nitric oxide reduces adhesion of RBCs and leukocytes to endothelial cells by decreasing the activity of vascular cell adhesion molecule-1.” But of course the chemical formula for nitric oxide is NO and not N2O! HAHAHA you fools! To my knowledge nitrous oxide does not have the useful vasodilatory effects nitric oxide does in the treatment of ACS. While it might be useful in the same sense that heroin would be (anesthesia) you would be decreasing your FIO2 by displacing O2 with another gas. Then again, chugging a bottle of baby heroin would presumably decrease your respiratory drive so I guess you can feel free to pick your poison.

In light of this snap reconsideration, I will accept both B and C.

Intern Report Case 3.3

2011-03-07T19:06:00.000-08:00

Case Presentation by Dr. Ryan Doss

A 28 year old male with a PMH of sickle cell disease presents to the emergency department complaining of a one day history of worsening shortness of breath and a subjective sensation of fever. He states this was preceded by 3 days of intractable “sickle cell crisis” pain unrelieved by his home pain medications. When questioned further about the nature of this pain, he reports lower back and bilateral lower extremity pain which is typical of his previous sickle cell crises. After thinking about it, however, he does report that this time a new right lower chest pain accompanied his usual symptoms. His home medications include morphine and dilaudid po.

Physical Exam:

Vitals: BP 128/62, HR 108, RR 30, Sat 93% on RA, and Temp 38.1C

General:He appears to be anxious and in mild respiratory distress with no accessory muscle use.

HEENT: NC/AT, PERRL, mucous membranes moist

CV: S1 S2 present, regular rhythm and tachycardic rate, no murmurs

Resp: Tachypnea, equal rise and fall, rales auscultated in the RLL

Abd: Soft, nondistended, nontender all 4 Qs

Ext: Peripheral pulses present in all 4 limbs, cap refill <2 seconds, strength 5/5 proximally and distally in all 4 limbs

Back: No tenderness to palpation throughout cervical, thoracic, and lumbar spine. No bony deformity, crepitus, or step-offs noted.

Neuro: A&Ox3, alert, cooperative, no gross focal deficits

An AP and lateral chest radiograph is obtained with the following results:

An ABG is obtained on room air:

7.48/31/81/23/92

Laboratory abnormalities include:

Hb 8.4, WBC 13,000

Questions:

1. Calculate this patient's A-a gradient assuming an FiO2 of 21% (room air) and an Atm pressure of 760 (sea level.)

a) 10

b) 30

c) 5

d) 20

e) 40

2. Of the following, which is the most common complication of acute chest syndrome?

a) Arrythmia

b) Mesenteric ischemia

c) Seizures

d) Acute kidney injury

e) Myocardial infarction

3. Which of the following pathogens is most likely associated with acute chest syndrome?

a) Chlamydia pneumoniae

b) Legionella

c) Streptococcus pneumoniae

d) Staph aureus

e) Neisseria meningitidis

4. Imagine you're lost in the woods, have sickle cell, get dehydrated, and develop an acute chest syndrome. Which of the following devices would you most wish you had brought? Also, it's 1910.

a) Horace P. Winterbottom's Patented Roentogram Generator

b) A tank of phlogisticated laughing anesthetic

c) Bayer Pharmaceutical's “Mother's Relief” Infant Teething Aide with Heroin

d) “Poseidon's Bane” Drowning Resuscitation Tobacco Smoke Enema Kit

e) A hearty sample of mandrake root and a crossroads in which to bury it, post-haste

Intern Report Case Discussion 3.2

2011-03-04T00:01:00.000-08:00

Case Presentation by Dr. Jeanise Butterfield

Case Presentation (click to see the case)

Discussion:

This patient is in adrenal crisis which is likely precipitated by abrupt steroid withdrawal following a long hospitalization for acute COPD exacerbation and pneumonia. Recognition of adrenal crisis and prompt administration of hydrocortisone is critical to patient survival. Adrenal crisis may result from an acute exacerbation of chronic adrenal insufficiency, adrenal hemorrhage, or abrupt withdrawal of steroids in patients with adrenal atrophy. It usually occurs in response to major stressors such as sepsis, myocardial infarction, surgery, major injury or trauma.

The predominant clinical manifestation of adrenal crisis is shock. Symptoms include weakness, abdominal pain, anorexia, confusion, and fever. Patients may be hypotensive and hypoglycemic but other physical findings in patients with adrenal insufficiency may be subtle and nonspecific. Laboratory evaluation may reveal hyponatremia, hyperkalemia, and hypercalcemia.

Glucocorticoids are essential to the management of adrenal crisis and should be administered immediately upon clinical suspicion. The preferred glucocorticoid is hydrocortisone 100 mg IV. Dexamethasone 6-8 mg IV can also be used and has the advantage of not interfering with ACTH stimulation test.

As always, treatment begins with maintenance of airway, breathing and circulation. Should a patient require intubation, etomidate should be avoided as an agent for RSI because it is a steroid synthesis inhibitor and may worsen hemodynamics in shock patients. Aggressive fluid replacement may be required as well as correction of electrolyte abnormalities including hypoglycemia, hyponatremia, hyperkalemia and hypercalcemia. Fluid replacement should be initiated with 0.9% normal saline, but may be changed to D5NS. D50 may be required depending on the extent of hypoglycemia.

It is important to uncover and treat the underlying problem that precipitated the crisis.

Answers

1. D. In the setting of adrenal crisis, glucocorticoids, preferably hydrocortisone 100 mg IV, should be administered immediately. Do not await results of ACTH stimulation testing. CT scan and surgical consult may be indicated after steroid replacement to help diagnose or treat the precipating cause.

2. C. Patients in adrenal crisis may present with several electrolyte abnormalities including hyponatremia, hyperkalemia and hypercalcemia. An early EKG manifestation of hyperkalemia is peaked t waves. U waves are present in hypokalemia.

3. E. Ketoconazole and etomidate impair adrenal hormone synthesis. Phenytoin and rifampin increase steroid metabolism.

Pearls:

Think of adrenal crisis in the setting of hypotension refractory to volume resuscitation and catecholamines.

Patients with history of primary adrenal insufficiency (eg Addison’s Disease) will require increased doses of steroids in the event of increased stress or illness.

The most common iatrogenic cause of adrenal crisis is rapid withdrawal of steroids in the patients with adrenal atrophy secondary to long term steroid administration.

If you suspect adrenal crisis, immediately administer glucocorticoids. Do not wait for ACTH stimulation test or serum cortisol.

Intern Report Case 3.2

2011-02-27T00:01:00.000-08:00

Case Presentation by Dr. Jeanise Butterfield

A 58-year-old woman presents to the emergency department with severe abdominal pain, generalized weakness and subjective fever. She is able to tell you that the pain began yesterday and has been gradually getting worse since onset but she is so weak that she only speaks in short phrases. The pain is constant and cramping in nature, getting worse. She has had 2-3 episodes of emesis per day and decreased appetite. She has been feeling very warm but has not taken her temperature. No diarrhea, last BM yesterday.

She has a history of COPD and hypertension and was recently discharged from an outside hospital after a lengthy stay for COPD exacerbation and pneumonia which required intubation. She was given several prescriptions to fill including inhalers and pills but could not secondary to lack of insurance and financial issues.

PMH: COPD, HTN but noncompliant with medications

Meds: None

Allergies: NKDA

FH: Hypertension

SH: Occasional alcohol use. 25 pack year tobacco history but quit 5 years prior. Denied illicit drug use.

PE: Vital Signs – BP 96/64, heart rate 108, respiratory rate 24, temp 38.2°C, pulse ox 96% on RA

HEENT: Atraumatic, normocephalic; PERRL, EOMI; dry mucus membranes

General – Thin female lying still in fetal position on stretcher

Skin – Diaphoretic, pale, no rashes

Cardiovascular – Tachycardic, regular rhythm, no murmurs

Respiratory – Tachypneic, decreased breath sounds at the right base, slight expiratory wheeze bilaterally, no accessory muscle use

Abdominal – Soft, nondistended, diffusely tender to palpation, + guarding, no rebound, normal bowel sounds,

Musculoskeletal – Full ROM in all 4 extremities, no edema, symmetric pulses bilateral UE & LE

Neuro – A&O x 3, normal speech and hearing, face is symmetric, sensation equal and intact throughout, motor is decreased in all extremities but symmetric, patient not exerting much effort

Pertinent Labs:

Sodium 128 mEq/L, potassium 5.8 mEq/L, glucose 55 mg/dL, cortisol 20 µg/dL.

Questions

1. Immediate management of the patient should include:

a. Surgical consultation

b. Abdominal CT

c. Morphine

d. Hydrocortisone

e. ACTH stimulation test

2. If an EKG was performed on this patient, which abnormality could be expected

a. ST elevation

b. Right bundle branch block

c. Peaked T waves

d. Prolonged QT interval

e. Prominent U waves

3. Which of the following is least likely to precipitate acute adrenal insufficiency:

a. Etomidate

b. Phenytoin

c. Ketoconazole

d. Rifampin

e. Nitroglycerine