Critical Care Medicine

NIPAH VIRUS INFECTION

2018-05-21T10:43:00.000+05:30

A newly emerging zoonosis
RNA virus of the family Paramyxoviridae, genus Henipavirus, and closely related to Hendra virus.
Gets its name from the village in Malaysia where the person from whom the virus was first isolated succumbed to the disease.

Spread-

Natural host - fruit bats of the Pteropodidae Family, Pteropus genus. (Grey-headed flying foxes - Pteropus poliocephalus)
The virus is present in bat urine and potentially, bat faeces, saliva, and birthing fluids.
Transmission may be due to fomites – or carrying the virus on clothing, equipment, boots, vehicles.

Outbreaks-

First outbreak - in Kampung Sungai Nipah, Malaysia, 1998. Intermediate hosts- Pigs.
In 2004, Bangladesh - humans became infected with NiV as a result of consuming date palm sap that had been contaminated by infected fruit bats.
Human-to-human transmission - documented.
Can cause disease in pigs and other domestic animals

Clinical features-

incubation period of 5 to 14 days
Presenting symptoms - 3-14 days of fever and headache, followed by drowsiness, disorientation and mental confusion.
Can progress to coma within 24-48 hours.
Ranges from asymptomatic infection to acute respiratory syndrome and fatal encephalitis.
Some patients have a respiratory illness during the early part of their infections, and half of the patients showing severe neurological signs showed also pulmonary signs.
Long-term sequelae noted -persistent convulsions and personality changes.
Latent infections with subsequent reactivation of Nipah virus and death have also been reported months and even years after exposure.

Treatment -

No specific treatment
Intensive supportive care
No vaccine

Ref -

WHO

CDC

Burkholderia

2018-05-18T07:06:00.000+05:30

Historically, considered Pseudomonas species - previously known as Pseudomonas multivorans and Pseudomonas kingie.

Aerobic gram-negative bacteria
Acquire motility via multitrichous polar flagella.
Do not ferment glucose
Many clinical isolates give a weak oxidase reaction.
Slow-growing morphotypes, may go undetected in routine cultures
Free-livingorganisms present in most aquatic and humid environment, including hospital drinking water.
nine genomovars grouped under “B. cepacia complex” (BCC)
Burkholderia cenocepacia and Burkholderia multivorans are the prominent bacterial strains isolated from patients with cysticfibrosis.

Infection-

Lung -

B. cepacia gained notoriety as the cause of a rapidly fatal syndrome of respiratory distress and septicemia (the “cepacia syndrome”) in CF patients.
B. cepacia regarded as important multi-drug resistant gram-negative bacteria in the immunosuppressed cancer and transplant populations.
Nebulizer-associated BCC pneumonia outbreaks have occurred in patients with lymphoid and myeloid neoplasms receiving aerosolized antimicrobial prophylaxis
The risk for nosocomial BCC pneumonia includes patients in a critical care unit for longer than 1 week, those requiring assisted ventilation, and those on broad-spectrum antimicrobial therapy.
Hospital fomites and ventilator humidification system may be potential sources

2. Skin, Skin Structure, and Joint Infection -

Risk factors - patients receiving care in burn units and those in critical care units exposed to contaminated disinfectants or unsterilized skin moisturizing products.
Hematogenous B. cepacia dissemination may present as ecthyma gangrenosum–like skin lesions, particularly in patients with underlying cancer or other immunosuppression.
B. cepacia septic arthritis via hematogenous seeding is serious, although a rare complication.

3. Genitourinary Tract Infection -

Iatrogenic infection from manipulation of the genitourinary tract such as with transrectal prostate biopsy and a cystoscopy-related intramural bladder wall B. cepacia abscess have been rarely observed.
In critical care units, nosocomial B. cepacia genitourinary tract infection arises from prior colonization of a urinary catheter.

Diagnosis-

Antibiotic-containing media can be used to promote selective growth (e.g., Pseudomonas cepacia agar, oxidation-fermentation polymyxin bacitracin lactose agar, and B. cepacia selective agar). These culture media containing gentamicin, polymyxin B, and vancomycin can be used to isolate over 90% of BCC within 48 to 72 hours.
Upto 36% of Burkholderia speciesmay be misidentified by automated systems as other nonfermentativebbacteria,such as Achromobacter or Ralstonia.

Resistance patterns -

Drug-resistance pathways include efflux pumps (including adenosine triphosphate–binding cassette transporters), antimicrobial degradation and/or modifying enzymes, and altered membrane function.

Rx-

Monotherapy not recommended as high chances of failure and infection relapse
Carbapenems, TMP/SMX, chloramphenicol, and tetracycline
Susceptible to minocycline(38%), meropenem(26%), and ceftazidime(23%).
Ceftazidime, tobramycin, and ciprofloxacin retain antimicrobial activity against planktonic and biofilm-embedded organisms.
Tigecycline is less effective compared with minocycline, and overexpression of efflux pumps may result in development of de novo drug resistance.
Combination therapy for serious pulmonary infection (e.g., in CF) is suggested when multidrug-resistant strains are implicated.
The combination of meropenem and TMP-SMX may be antagonistic, however.

Ref-

Mandell - Principles and practice of Infectious Diseases , 8th edition

Harrison’s Principles of Internal Medicine, 19th edition

Mixed venous oxygen saturation (SvO2) - Pathophysiologic basis

2011-06-26T23:26:00.009+05:30

Ref: Functional Hemodynamic monitoring by M.R. Pinsky, D. Payen

As DO2 (Oxygen delivery) is reduced - in critical illness by hypoxemia (hypoxic hypoxia), anemia ( anemic hypoxia), decreased cardiac output (stagnant hypoxia), or any combination thereof - oxygen consumption (VO2) is maintained by virtue of peripheral tissues taking up a greater fraction of the oxygen delivered.

At a sufficiently low level of delivery, approximately 7 ml/kg/min in this example - VO2 becomes dependent on DO2 and further reductions in DO2 are associated with a fall in VO2. This delivery-dependent limb of the VO2-DO2 relationship is characterized by lactic acidosis, organ dysfunction, physiologic instability and death.

As shown in the figure above, SvO2 falls as DO2 is diminished, reflecting tissue uptake being maintained, extraction fraction (VO2/DO2) rising, and arterio-venous content difference widening. SvO2 decreases because oxygen extraction increases. Thus, SvO2 can provide an early signal to determine the adequacy of delivery.

Oxygen extraction fraction (VO2/DO2) is not maximal at the critical delivery point - it continues to increase as DO2 falls below the critical point. However the increase in extraction fraction is not sufficient to maintain VO2, which becomes DO2 supply-dependent.

The rationale for a low SvO2 signalling inadequate DO2 is less clear in pathophysiologic processes associated with high output hypotension - sepsis, liver failure, pancreatitis, and other conditions marked by a systemic inflammatory response syndrome. In these conditions, once fluid resuscitation has taken place, the circulation is characterised by high flow, low systemic arterial pressure, and a high SvO2 despite an elevated oxygen consumption. It is also arguable that tissue hypoxia does not exist under these conditions, or at least is not the primary determinant of lactic acidosis.

Nonetheless, it has been argued that while a high SvO2 may not guarantee absence of lactic acidosis or a risk for progression of organ failures, a low SvO2 signals inadequate resuscitation and has in fact been used as an endpoint for outcome studies assessing benefit from specific algorithms titrating therapy to this endpoint.

WHO Guidelines for the Management of Malaria

2010-09-01T00:38:00.001+05:30

Recommendations for Parasitological diagnosis:

Recommendation	Level of Evidence
In areas of low to moderate transmission, prompt parasitological confirmation of the diagnosis is recommended before treatment is started.	E
In areas of high stable malaria transmission, children under 5 years should be treated on the basis of clinical diagnosis. In older children and adults including pregnant females, a parasitological diagnosis is recommended before treatment is started	E
In all suspected cases of severe malaria, a parasitological confirmation of the diagnosis of malaria is recommended. In absence or delay in diagnosis, patients should be treated on clinical grounds.	E

Treatment of Uncomplicated P. Falciparum Malaria:

To counter the threat of resistance of P. Falciparum to monotherapies, and to improve treatment outcome, combination of antimalarials are now recommended.

Recommendation	Level of evidence
The treatment of choice for uncomplicated falciparum malaria is a combination of two or more antimalarials with different mechanisms of action	S, T, O
Artemisinin-based combination therapies (ACTs) are the recommended treatments for uncomplicated falciparum malaria	S
The following ACTs are currently recommended: Artemether+Lumefantrine, Artesunate+Amodiaquine, Artesunate+Mefloquine, Artesunate+Sulfadoxine-pyrimethamine	S, T, O
The choice of ACT in a country or region will be based on the level of resistance of the partner medicine in the combination: - in areas of multidrug resistance (SouthEast Asia), Artesunate+Mefloquine or Artemether+Lumefantrine - in Africa, Artemether+Lumefantrine, Artesunate+Amodiaquine,	E S
The artemisinin derivative components of the combination must be given for at least 3 days for an optimum effect	S
Artemether+Lumefantrine ahould be used with a 6-dose regimen	T, E
Amodiaquine+Sulfadoxine-Pyrimethamine may be considered as an interim option where ACTs cannot be made available	E

If malaria is suspected and the decision to treat is made, then a full effective treatment is required, whether or not the diagnosis is confirmed by a test.

Recommendations on treatment approaches that should be avoided:

Recommendation	Level of evidence
Partial treatment should not be given even when the patients are considered to be semi-immune or the diagnosis is uncertain.	E
The Artemisinin and the partner medicines of ACTs should not be available as monotherapies	E

Recommendation for Treatment Failure Management:

Failure within 14 days:

- Must be confirmed Parasitologically

- Should be treated with second line drugs

Failure after 14 days:

- Can be treated with the first line ACTs, except when initially treated with Mefloquine.

- Parasitological confirmation is desirable, but not a pre-condition.

Recommended Second-line antimalarial treatments:

- Alternative ACT known to be effective in the region

- Artesunate + Doxycycline/ Tetracycline/ Clindamycin

- Quinine + Doxycycline/ Tetracycline/ Clindamycin

Solution to Quiz 6:

2010-06-23T12:18:00.001+05:30

Answer: This patient was diagnosed to have a Descending thoracic Aortic aneurysm, just distal to the origin of Subclavian Artery.

On enquiry, he gave a history of upper back pain since last 6 months which he kept ignoring as muscular back pain.

As the aneurysm kept increasing in size he started getting compression of surrounding structures and hence the symptoms of Hoarseness of voice and Dysphagia.

The giddiness that he had was possibly due to increase in dissection and hypotension associated.

I’ll be discussing more about this case including the management principles in my new blog ‘Interesting Cases’ http://icucases.blogspot.com/

QUIZ 6:

2010-06-16T16:21:00.003+05:30

A 54 year old male patient,

known Hypertensive, Ischaemic heart disease, had undergone CAG – PTCA to LAD about 8 mnths back.

Now presents with

H/o Fever – low grade, on and off for last 6 mnths, being treated on out patient basis with multiple antibiotics;

H/o 1 episode of giddiness/ black-out about 2 months back;

H/o hoarseness of voice since last 3 weeks, IDL done: suggestive of Left vocal cord palsy; followed by

H/o dysphagia, to both solids and liquids, sudden in onset, since today morning.

What is your diagnosis?

FAST HUGS BID (updated….)

2009-11-28T16:12:00.001+05:30

Everyone on a Ventilator deserves a…..

F………… Feeding

A……….. Analgesia

S……….. Sedation

T……….. Thromboprophylaxis

H……….. Head-of-bed elevation

U……….. Ulcer prophylaxis

G……….. Glycemic control

S……….. Spontaneous breathing trial

B………… Bowel care

I…………. Indewelling catheter removal

D………… De-escalation of antibiotics

Trauma scores:

2009-10-20T16:00:00.001+05:30

Glasgow Coma Score:

Trauma Score:

Revised Trauma Score:

The CRAMS scale:

Other major Trauma Scoring Systems:

Severity-of-illness Scoring Systems in ICU:

2009-10-20T15:52:00.001+05:30

The scoring systems most commonly used in critically ill
adults are APACHE II, APACHE III, MPM II, SAPS II, and SOFA.

Calculation of Acute Physiology and Chronic Health Evaluation II (Apache II)

The Acute Physiology and Chronic Health Evaluation II
(APACHE II) system is the most commonly used clinical
severity-of-illness scoring system in North America. APACHE II is a disease-specific scoring system. It uses age, type of admission, chronic health evaluation, and 12 physiologic
variables (acute physiology score or APS) to predict hospital mortality. The 12 physiologic variables are defined as the most abnormal values during the 24 hours after ICU admission.

Acute Physiology Score:

APACHE III:

APACHE III is a disease-specific score that was developed
from 17,440 admissions in 40 U.S. hospitals. Eighteen
variables were included, and their respective weights were derived by logistic regression modeling.

The final APACHEIII score can vary between 0 and 300.
Risk estimate equations for hospital mortality are calculated
from the weighted sum of disease category (78 diagnostic categories are included), a coefficient related to prior treatment
location, and the APACHE III score. In the original derivation
sample, estimates of mortality for the first day in the ICU
had an area under the ROC curve of 0.90, and the correct
classification at 50% mortality risk level was 88%. Although
APACHEIII scores can be calculated from published information, weights to convert the score to probability of death are proprietary, therefore the APACHE III system has not been
widely accepted or used.

MPM II:

The Mortality Probability Model(MPMII)20 was developed from 19,124 ICU admissions in 12 countries. MPM II is not disease specific. MPM-0 is the only severity-of-illness scoring system that was derived at ICU admission and can therefore be used at ICU admission. MPM II does not yield a score, but rather a direct probability of survival. Burn, coronary care, and cardiac surgery patients are excluded. MPM-0 includes three physiologic variables, three chronic diagnoses, five acute diagnoses, and three other variables: cardiopulmonary resuscitation prior to admission, mechanical ventilation, and medical or unscheduled surgery admission. Each variable is scored as absent or present and is allocated a coefficient. The sum of these coefficients constitutes the logit that is used to calculate the probability of hospital mortality.

The MPM-24 was designed to be calculated for patients who remained in the ICU for 24 hours or longer. MPM-24 includes 13 variables, 5 of which are used in the MPM-0.

SAPS II:

The most recent version of the Simplified Acute Physiology Score II (SAPS II) was developed from a sample of 13,152 admissions from 12 countries, based on a European/North American multicenter database. SAPS II is not disease specific.
SAPS II uses 17 variables that were selected by logistic regression: 12 physiology variables, age, type of admission (scheduled surgical, unscheduled surgical, or medical), and three underlying disease variables (acquired immunodeficiency syndrome, metastatic cancer, and hematologic malignancy). The probability of hospital mortality is calculated from the score

Type of Admission

Scheduled surgery

Unscheduled surgery

Medical

Chronic diseases

None

Metastatic Carcinoma

Hematological malignancy

AIDS

Age

<40

40-59

60-69

70-74

75-79

≥ 80

Temperature

<39

>39

Heart Rate

<40

40-69

70-119

120-159

≥160

Systolic Blood Pressure, mmHg

<70

70-99

100-199

≥200

Urine output, cc/24 hrs

<500

500-999

>1000

Glasgow Coma score

6-8

9-10

11-13

14-15

Serum Urea or BUN

<10

10-29.9

≥30

Serum sodium, mEq/L

>146

125-144

<125

Serum Potassium, mEq/L

3-4.9

WBC, per cubic mm

<1000

1000-19000

>20000

Bicarbonate, mEq/L

<15

15-19

>20

Serum Bilirubin, mg/dl

4-5.9

PaO₂/FiO_2,(if ventilated or CPAP)

<100

100-199

>200

SOFA Score:

The Sequential Organ Failure Assessment (SOFA) was originally developed as a descriptor of a continuum of organ dysfunction in critically ill patients over the course of their ICU
stay.The SOFA score is composed of scores from six organ systems, graded from 0 to 4 according to the degree of dysfunction/failure. The score was primarily designed to describe morbidity; however, a retrospective analysis of the relationship between the SOFA score and mortality was developed using the European/North American Study of Severity System database. Subsequently, SOFA was evaluated as a predictor of outcome in a prospective Belgium study. SOFA score on admission was not a good predictor of mortality; however, mean SOFA score and highest SOFA score had better discrimination. Independent of the initial value, an increase in the SOFA score during the first 48 hours of ICU admission predicts a mortality rate of at least 50%.

MCQ1: FNBE- 2008,2009: Toxicology

2009-10-06T15:18:00.005+05:30

All the following drugs are dialysable except
1. Salicylate
2. Sertaline
3. Ethylene Glycol
4. Methanol

(This question appeared both in 2008 and 2009 FNB Enterance)

Answer: Sertaline

Toxins removable by Hemodialysis:
- Salicylates
- Lithium
- Methanol
- Ethylene Glycol
- Isopropanol

Toxins removable by Hemoperfusion
- Barbiturates
- Carbamazepine
- Theophylline
- Valproic Acid

TRALI – Prevention

2009-09-15T02:16:00.002+05:30

Prevention Strategies:

1. The best way to prevent TRALI is by limiting the amount of transfused products and rethinking the need for and efficacy thereof of transfusion.

Triggers for transfusion of blood and blood products should be raised. SHOT strongly advises against unnecessary blood product transfusion.

2. Screening blood products for white cell antibodies.

The prevalence of HLA antibodies in the donor pool ranges from 8% to 22%, but the prevalence of neutrophil-specific antibodies is not known. If these antibodies are found in the donor, it is still debated whether these donors should be deferred from donation, their blood should only be used for low plasma volume products, or no intervention taken.

3. Debate on the prevention of TRALI often centers on the female donor, especially the multiparous donor. Parity is especially associated with increased antibody prevalence, and the majority of donors associated with TRALI are multiparous
females.

In late 2006, the American Association of Blood Banks (AABB),made several recommendations to reduce the frequency
of TRALI, including moving toward the use of high plasma volume containing products that are donated only by men.

4. Leukoreduction; it is currently employed by several Western countries. However, the various methods of leukoreduction have drawbacks. For example, although washing may also reduce biologically active substances, it decreases blood product quantity and shelf-life.

5. As aging RBCs accumulate both lipid mediators and leukocyte-derived substances, an argument can also be made for using fresher RBCs, when possible, to minimize the immune consequences of transfusion.

6. Finally, with regards to the management of a donor involved in a TRALI reaction, the AABB provides a series of guidelines, including deferring the donor from all donations, deferral of donation from high plasma volume containing products only, washing donor RBCs, and plasma fractionation.

Ref : Journal of Intensive Care Medicine / Vol. 23, No. 2, March/April 2008

Click here to read about 'Definition' of TRALI

Click here to read about Pathophysiology of TRALI

Click here to read about Clinical Presentation of TRALI

Click here to read about Treatment of TRALI

What to read for FNB enterance???

2009-09-15T01:49:00.001+05:30

This is the most confusing question….because critical care is a really vast topic….

FNB Enterance has 2 steps… Total 115 marks

1. Theory: 100 multiple choice questions for 100 marks

Books to read:

- Paul Marino

- Washington Manual Of Critical Care

- Hemodynamic Monitoring from Miller

- Antibiotics from any good Pharmacology book

Weightage for DNB Qualification: 5 marks

2. Aptitude Test: 10 marks

- Read about latest Guidelines and Studies and Review Articles

Venous Oximetry – The concept of SvO2 and ScvO2

2009-08-10T16:20:00.001+05:30

Abbreviations:

SvO2 - True mixed venous oxygen saturation
ScvO2 - Central venous oxygen saturation
VO2 – Consumption of oxygen
DO2 – Delivery of oxygen

Determining the adequacy of tissue oxygenation in critically ill patients is central to ascertain the health of the patient. Unfortunately, normal values in blood pressure, central venous pressure, heart rate, and blood gases do not rule out tissue hypoxia or imbalances between whole-body oxygen supply and demand. This discrepancy has led to increased interest in more direct indicators of adequacy of tissue oxygenation such as mixed and central venous oxygen saturations.

The normal cardiovascular response of increasing VO2 is to increase O2 extraction and cardiac output. Usually VO2 is independent of DO2 since tissues can maintain O2 needs by increasing O2 extraction when DO2 decreases. However, this mechanism has its limits. Below a so-called critical DO2 compensatory increase in O2 extraction is exhausted, and VO2 becomes dependent on DO2. In this case tissue hypoxia occurs, and a rise in serum lactate levels may be observed.

A decrease in SvO2 and ScvO2 represents an increased metabolic stress, either DO2 does not increase in such a way to
cover an increased VO2, or DO2 drops because of decrease in either arterial O2 content, cardiac output, or both. The magnitude of the decrease indicates the extent to which the physiological reserves are stressed.

The cardiocirculatory system may be challenged by two different conditions. Firstly, a drop in DO2 can be induced by anemia, hypoxia, hypovolemia, or heart failure. Secondly, fever, pain, stress etc. may also decrease SvO2 or ScvO2 by increasing whole-body VO2.

Pulmonary artery catheterization allows obtaining true mixed venous oxygen saturation (SvO2) while measuring central venous oxygen saturation (ScvO2) via central venous catheter reflects principally the degree of oxygen extraction from the brain and the upper part of the body. SvO2 reflects the relationship between whole-body O2 consumption and cardiac output. Indeed, it has been shown that the SvO2 is well correlated with the ratio of O2 supply to demand.

The central venous catheter sampling site usually resides in the superior vena cava. Thus central venous blood sampling reflects the venous blood of the upper body but neglects venous blood from the lower body (i.e., intra-abdominal organs). As shown below, venous O2 saturations differ among several organ systems since they extract different amounts of O2. ScvO2 is usually less than SvO2 by about 2–3% because the lower body extracts less O2 than the upper body making inferior vena caval O2 saturation higher. The primary cause of the lower O2 extraction is that many of the vascular circuits that drain into the inferior vena cava use blood flow for nonoxidative phosphorylation needs (e.g., renal blood flow, portal flow, hepatic blood flow). However, SvO2 and ScvO2 change in parallel when the whole body ratio of O2 supply to demand is altered.

The difference between the absolute value of ScvO2 and SvO2 changes under conditions of shock. In septic shock, ScvO2 often exceeds SvO2 by about 8%. During cardiogenic or hypovolemic shock mesenteric and renal blood flow decreases followed by an increase in O2 extraction in these organs. In septic shock, regional O2 consumption of the gastrointestinal tract and hence regional O2 extraction increases despite elevated regional blood flows. On the other hand, cerebral blood flow is maintained over some period in shock. This would cause a delayed drop of ScvO2 in comparison to SvO2, and the
correlation between these two parameters would worsen. Some authors therefore argued that ScvO2 cannot be used as surrogate for SvO2 under conditions of circulatory shock.

Limitations:

Venous oximetry can reflect the adequacy of tissue oxygenation only if the tissue is still capable of extracting O2. In the case of arteriovenous shunting on the microcirculatory level or cell death, SvO2 and ScvO2 may not decrease or even show elevated values despite severe tissue hypoxia. As demonstrated in patients after prolonged cardiac arrest, venous hyperoxia with an ScvO2 higher than 80% is indicative of impaired oxygen use.

Conclusion:

While measurement of SvO2 requires the insertion of a pulmonary artery catheter, measurement of ScvO2 requires only central venous catheterization. ScvO2 directed early goal-directed therapy improves survival in patients with septic shock
who are treated in an emergency department. However, ScvO2 values may differ from SvO2 values, and this difference varies in direction and magnitude with cardiovascular insufficiency. ScvO2 should not be used alone in the assessment of the cardiocirculatory system but combined with other cardio-circulatory parameters and indicators of organ perfusion such as serum lactate concentration and urine output.

Ref: M. R. Pinsky · L. Brochard · J. Mancebo; Applied Physiology in Intensive Care Medicine, Springer-Verlag Berlin Heidelberg 2006

TRALI – Treatment and Outcome

2009-08-08T13:44:00.002+05:30

Treatment:

If the reaction is recognized during transfusion, then the transfusion should be stopped immediately.
The treatment of TRALI is primarily supportive and similar to that for other forms of ALI. Supplemental oxygen is an essential part of treatment. For mild cases, supportive care may suffice.
For more severe cases, intravenous fluids, vasopressor agents, and mechanical ventilation may be necessary. Mechanical ventilatory support may be required in more than 70% of patients. A low tidal volume, lung protective strategy has been advised for these patients.
Generally, administration of diuretics is detrimental and must be avoided, as the pulmonary edema is not because of fluid overload. The only setting where diuretics may possibly be indicated is in the patient with fluid overload who develops TRALI.
The use of steroids remains controversial.
Anecdotally, cardiopulmonary bypass and extracorporeal membrane oxygenation have been successfully used.
Prostaglandin administration and plasmapheresis have only been anecdotally reported and cannot be routinely recommended.

Outcome:

Compared with ARDS, TRALI is a transient phenomenon and has lower mortality; the majority of patients recover within 4 days with supportive care. There does not appear to be late pulmonary fibrosis or parenchymal destruction; long-term lung function in survivors appears to be the same as patients who did not experience TRALI. However, in a minority of cases, (5% to 15%), the disease is fatal .

Ref: Journal of Intensive Care Medicine / Vol. 23, No. 2, March/April 2008

Click here to read about 'Clinical Presentation'

Click here to read about 'Pathophysiology'

Click here to read about 'Definition'

TRALI – Clinical Presentation and Diagnosis

2009-08-02T18:52:00.002+05:30

A high index of suspicion is needed to make the diagnosis of TRALI. The diagnosis of TRALI is primarily clinical and radiographic. As per the Canadian consensus conference, the diagnosis of TRALI is “not dependent on the results of laboratory tests or any proposed pathophysiologic mechanisms”

The symptoms commonly occur within 2 hours after the start of transfusion, with almost all reactions occurring by 6 hours. These symptoms may be rather severe and include dyspnea, hypoxemia, cyanosis, bilateral pulmonary edema, cough, fever, and chills. Both hypertension and hypotension have been reported in the presence of normal cardiac function. The hypotension may be unresponsive to intravenous fluid administration. Production of voluminous frothy secretions and an increase in airway pressures in intubated patients have also been noted. Radiographs of the chest show findings typical of ARDS. The pulmonary edema may be initially localized to the dependent or perihilar areas of the lungs, but more often it becomes generalized relatively rapidly with both alveolar and interstitial infiltrates, without cardiac enlargement or engorged
pulmonary vessels, also noted on radiography are the absence of cardiac enlargement and pulmonary vascular engorgement. Occasionally, a florid radiologic picture exists. This is described as “white out” of the lungs. The radiographic severity of lung injury often contrasts dramatically with the minimal auscultatory findings physical examination.

The central principle for diagnosing TRALI is exclusion of hydrostatic (cardiogenic) pulmonary edema. In the setting of blood transfusion, hydrostatic pulmonary edema occurring within 6 hours is referred to as transfusion-associated cardiac overload. The clinical manifestations of transfusion-associated cardiac overload include tachypnea/respiratory distress, cyanosis, tachycardia, and hypertension. Other conditions that are considered in the differential diagnosis of TRALI include allergic/anaphylactic reactions and transfusion of contaminated blood products.

The central venous and wedge pressures are typically low or
normal in TRALI but may be elevated if TRALI occurs in the setting of heart failure. Serum B type natriuretic peptide (BNP) levels may or may not be helpful in excluding cardiogenic edema, as elevated BNP levels have been reported in patients with ALI in the absence of left ventricular dysfunction. Finally, sampling of pulmonary edema fluid, shortly after lung injury, from the endotracheal tube (if present) may help in determining the etiology of the fluid. Pulmonary edema fluid in TRALI, like other causes of pulmonary capillary leak, has an elevated protein content.

Arterial blood gas analysis shows hypoxia, where a PaO2/FiO2 ratio less than 300 is consistent with ALI. Laboratory findings may also include hemoconcentration, leukopenia, neutropenia, hypocomplementemia, and hypoalbuminemia. The leukopenia is transient and thought to result from aggregation of circulating leukocytes in the pulmonary vasculature.

Serologic tests are important in confirming the diagnosis of TRALI. The basic principle is examination of sera from the donor for anti-HLA or anti-HNA antibodies. HLA antibody testing methods include lymphocytotoxicity, leuko-agglutination, and the flow panel reactive antibody assays. This latter method can detect antibodies as well as identify their specificities and is more sensitive than other techniques. Evaluation of neutrophil specific antibodies entails granulocyte agglutination and granulocyte immunofluorescence assays; notably, this latter assay does not necessarily distinguish between HLA I and HNA antibodies. DNA typing of granulocyte antigens may also be done. Although testing for neutrophil-priming activity and for antibodies in the recipient may provide important information about TRALI etiogenesis, they are not considered as part of the routine work-up.

Notification of the blood bank is advised to further evaluate the donor and their blood products for future donation or transfusion. Per the Canadian consensus conference, a donor can be considered as implicated in a TRALI reaction only if they are found to have anti-HLA or anti-HNA antibodies that are specific for antigens on the recipient’s leukocytes or via a positive cross-match.

Ref : Journal of Intensive Care Medicine / Vol. 23, No. 2, March/April 2008

Click here to read about 'Definition' of TRALI

Click here to read about 'TRALI- Pathophysiology'

ACC/AHA/ESC 2006 Guidelines for Management of Atrial Fibrillation – ‘Rate Control’

2009-07-29T23:28:00.001+05:30

In addition to allowing adequate time for ventricular filling and avoiding rate-related ischemia, enhancement of intraventricular conduction with rate reduction may result in improved hemodynamics in atrial fibrillation. It may be useful to evaluate the heart rate response to submaximal or maximal exercise or to monitor the rate over an extended period (e.g., by 24-h Holter recording).

Criteria for rate control vary with patient age but usually involve achieving ventricular rates between 60 and 80 beats per minute at rest and between 90 and 115 beats per minute during moderate exercise.

Hemodynamic and Clinical Consequences of Rapid rate:
Patients who are symptomatic with rapid ventricular rates during AF require prompt medical management, and cardioversion should be considered if symptomatic hypotension, angina, or HF is present. A sustained, uncontrolled tachycardia may lead to deterioration of ventricular function (tachycardia-related cardiomyopathy) and that improves with adequate rate control.

Tachycardia-induced cardiomyopathy tends to resolve within 6 months of rate or rhythm control; when tachycardia recurs, LV ejection fraction declines and HF develops over a shorter period, and this is associated with a relatively poor prognosis.

Pharmacological Rate Control During Atrial Fibrillation
RECOMMENDATIONS:

Class I :

Measurement of the heart rate at rest and control of the rate using pharmacological agents (either a beta blocker or nondihydropyridine calcium channel antagonist, in most cases) are recommended for patients with persistent or permanent AF.
(Level of Evidence: B)
In the absence of preexcitation, intravenous dministration
of beta blockers (esmolol, metoprolol, or propranolol) or nondihydropyridine calcium channel antagonists (verapamil, diltiazem) is recommended to slow the ventricular response to AF in the acute setting, exercising caution in patients with hypotension or HF. (Level of Evidence: B)
Intravenous administration of digoxin or amiodarone is recommended to control the heart rate in patients with AF and HF who do not have an accessory pathway. (Level of Evidence: B)
In patients who experience symptoms related to AF during activity, the adequacy of heart rate control should be assessed during exercise, adjusting pharmacological treatment as necessary to keep the rate in the physiological range. (Level of Evidence: C)
Digoxin is effective following oral administration to control the heart rate at rest in patients with AF and is indicated for patients with HF, LV dysfunction, or for sedentary individuals. (Level of Evidence: C)

Class IIa:

A combination of digoxin and either a beta blocker or nondihydropyridine calcium channel antagonist is reasonable to control the heart rate both at rest and during exercise in patients with AF. The choice of medication should be individualized and the dose modulated to avoid bradycardia. (Level of Evidence:B)
It is reasonable to use ablation of the AV node or accessory pathway to control heart rate when pharmacological therapy is insufficient or associated with side effects. (Level of Evidence: B)
Intravenous amiodarone can be useful to control the heart rate in patients with AF when other measures are unsuccessful or contraindicated. (Level of Evidence: C)
When electrical cardioversion is not necessary in patients with AF and an accessory pathway, intravenous procainamide or ibutilide is a reasonable alternative. (Level of Evidence: C)

Class IIb:

When the ventricular rate cannot be adequately controlled both at rest and during exercise in patients with AF using a beta blocker, nondihydropyridine calcium channel antagonist, or digoxin, alone or in combination, oral amiodarone may be administered to control the heart rate. (Level of Evidence: C)
Intravenous procainamide, disopyramide, ibutilide, or amiodarone may be considered for hemodynamically stable patients with AF involving conduction over an accessory pathway. (Level of Evidence: B)
When the rate cannot be controlled with pharmacological
agents or tachycardia-mediated cardiomyopathy is suspected, catheter-directed ablation of the AV node may be considered in patients with AF to control the heart rate. (Level of Evidence: C)

Class III:

Digitalis should not be used as the sole agent to control the rate of ventricular response in patients with paroxysmal AF. (Level of Evidence: B)
Catheter ablation of the AV node should not be attempted without a prior trial of medication to control the ventricular rate in patients with AF. (Level of Evidence: C)
In patients with decompensated HF and AF, intravenous administration of a nondihydropyridine calcium channel antagonist may exacerbate hemodynamic compromise and is not recommended. (Level of Evidence: C)
Intravenous administration of digitalis glycosides or nondihydropyridine calcium channel antagonists to patients with AF and a preexcitation syndrome may paradoxically accelerate the ventricular response and is not recommended. (Level of Evidence: C)

When rapid control of the ventricular response to AF is required or oral administration of medication is not feasible, medication may be administered intravenously. Otherwise, in hemodynamically stable patients with a rapid ventricular response to AF, negative chronotropic medication may be administered orally. Combinations may be necessary to achieve rate control in both acute and chronic situations, but proper therapy requires careful dose titration. Some patients develop symptomatic bradycardia that requires permanent pacing. Nonpharmacological therapy should be considered when pharmacological measures fail.

Specail considerations in patients with the Wolff-Parkinson-White (WPW) Syndrome: Intravenous beta blockers, digitalis, adenosine, lidocaine, and nondihydropyridine calcium channel antagonists, all of which slow conduction across the AV node, are contraindicated in patients with the WPW syndrome and tachycardia associated with ventricular preexcitation, because they can facilitate antegrade conduction along the accessory pathway during AF, resulting in acceleration of the ventricular rate, hypotension, or ventricular fibrillation. When the arrhythmia is associated with hemodynamic compromise, however, early direct-current cardioversion is indicated. In hemodynamically stable patients with preexcitation, type I antiarrhythmic agents or amiodarone may be administered intravenously. Beta blockers and calcium channel blockers are reasonable for oral chronic use.

Patients With Both Atrial Fibrillation and Atrial Flutter:
A patient treated with AV nodal blocking drugs whose ventricular rate is well controlled during AF may experience a rise or fall in rate if he or she develops atrial flutter. This is also true when antiarrhythmic agents such as propafenone or flecainide are used to prevent recurrent AF. These compounds may increase the likelihood of 1:1 AV conduction during atrial
flutter, leading to a very rapid ventricular response. Thus, when
these agents are given for prophylaxis against recurrent paroxysmal AF or atrial flutter, AV nodal blocking drugs should be routinely coadministered. An exception may be patients with
paroxysmal AF who have undergone catheter ablation of the
cavotricuspid isthmus to prevent atrial flutter.

Regulation of Atrioventricular Nodal Conduction by Pacing:
Because ventricular pacing prolongs the AV nodal refractory period as a result of concealed retrograde penetration, it eliminates longer ventricular cycles and may reduce the number of short ventricular cycles related to rapid AV conduction during AF. Pacing at approximately the mean ventricular rate during spontaneous AV conduction can regulate
the ventricular rhythm during AF. This may be useful for patients with marked variability in ventricular rates or for those who develop resting bradycardia during treatment with medication.

AV Nodal Ablation:
AV nodal ablation in conjunction with permanent pacemaker
implantation provides highly effective control of the heart rate
and improves symptoms in selected patients with AF. In general, patients most likely to benefit from this strategy
are those with symptoms or tachycardia-mediated cardiomyopathy related to rapid ventricular rate during AF that cannot be controlled adequately with antiarrhythmic or negative chronotropic medications.

Catheter ablation of inferior atrial inputs to the AV node slows the ventricular rate during AF and improves symptoms without
pacemaker implantation. This technique has several limitations, however, including inadvertent complete AV block
and a tendency of ventricular rate to rise over the 6 months following ablation. Ablation of the AV inputs in the atrium may improve the reliability of the junctional escape mechanism.

Complications of AV nodal ablation include those associated with pacemaker implantation, ventricular arrhythmias, thromboembolism associated with interruption of anticoagulation, the rare occurrence of LV dysfunction, and progression from paroxysmal to persistent AF. Limitations include the persistent need for anticoagulation, loss of AV synchrony, and lifelong pacemaker dependency. There is also a finite risk of sudden death due to torsades de pointes or ventricular fibrillation. Patients with abnormalities of diastolic ventricular compliance who depend on AV synchrony to maintain cardiac output, such as those with hypertrophic cardiomyopathy or hypertensive heart disease, may experience persistent symptoms after AV nodal ablation and pacemaker implantation. Hence, patients should be counseled regarding each of these considerations before proceeding with this irreversible measure.

Patients with normal LV function or reversible LV dysfunction
undergoing AV nodal ablation are most likely to benefit from standard AV nodal ablation and pacemaker implantation. For those with impaired LV function not due to tachycardia, a biventricular pacemaker with or without defibrillator capability should be considered. Upgrading to a biventricular device should be considered for patients with heart failure and an RV pacing system who have undergone AV node ablation.

Ref: J. Am. Coll. Cardiol. 2006;48;e149-e246

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Are you preparing for FNB Entrance????

2009-07-28T19:52:00.001+05:30

Hi Friends, while I was preparing for my Fellowship of National Board (FNB) Entrance for Critical Care Medicine; I was totally confused about the kind of questions the Diplomate of National Board (DNB) asks. Cause there is no book, no reference, no site or blog which clearly mentions about them or even gives a few examples.

With the help of my senior, Dr. Suneel Garg, I have managed to collect quite a many of the Multiple Choice Questions (MCQs) that were asked by the DNB for the entrance in the year 2008 and 2009.

So I am starting a new thread “FNB PEARLS” soon, where I will post MCQs asked in the Fellowship of National Board (FNB) Entrance for Critical Care. Not all the MCQs are complete, as it was very difficult to recollect them as they appeared in the exam. But it will definitely give you an idea of the kind of questions asked, the variety, and the topics covered.

I hope it will help all the aspirants preparing for the DNB Fellowship Entrance in Critical Care.

Your queries and suggestions are always welcome. Just post them in the comment box below or you can also write a mail to icucriticalcare@gmail.com.

All the best!!!

The ICU Book - Paul Marino

2009-07-28T19:21:00.001+05:30

Title: ICU Book
Edition Description: Third Edition
Authors: Marino, Paul L.
Dr. Kenneth Sutin contributed to the final 13 chapters of this edition
Publisher: Lippincott Williams & Wilkins
Pub. Date: October 2006
Copyright ©2007 Lippincott Williams & Wilkins

The preface to the 3rd edition states “ This edition continues the original intent to provide a generic textbook that presents fundamental concepts and patient care practices that can be used in any intensive care unit, regardless of the specialty focus of the unit. Highly specialized areas, such as obstetrical emergencies, thermal injury, and neurocritical care, are left to more qualified authors and their specialty textbooks. The ICU Book has been unique in that it reflects the voice of one author. This edition welcomes the voice of another, Dr. Kenneth Sutin, who added his expertise to the final 13 chapters of the book.”

The preface to the first edition states “ The purpose of The ICU Book is to present this common ground in critical care and to focus on the fundamental principles of critical illness rather than the specific interests for each intensive care unit. This text is problem-oriented rather than disease-oriented, and each problem is presented through the eyes of the ICU physician.”

Review:

I have loved this book for its smoothness, liquidity and easy readability. The free flowing language makes it more gripping. It not only provides a general overview and basic information, but also provides enough detailed and specific information to address almost all questions and problems that arise in the ICU. It is a perfect blend of basic fundamentals and applied physiology with the fully updated, problem-based approach. The author clearly, logically and concisely explains all the fundamental principles of intensive care medicine at the physiologic level.

WIth new chapters in this 3rd edition, like hyperthermia and hypothermia syndromes; infection control in the ICU; and severe airflow obstruction, this book is actually ‘A Complete Book’. This book however does not cover trauma and neuro.

‘The ICU book’ is a perfect way to obtain a fairly broad fund of ICU knowledge without having to stop every other paragraph to analyze and digest the words used to express an idea. I find it very useful for residents and ICU fellows, and certainly for new starters. Practitioners at all levels will find something interesting in this book. It is extremely approachable, and the material is presented in a brief and quick-access format which allows for topic and exam review.

If you want to understand ICU, get this book!

Swine flu

2009-07-21T11:51:00.007+05:30

To view a beautiful, informative video show on Swine flu, click below....

Thanks to my friend, Dr Rahul Bahot for contributing this presentation!

Solution to Quiz 5:

2009-07-19T18:53:00.001+05:30

Ans: Purpura fulminans / Warfarin induced skin necrosis.

Explanation: Purpura Fulminans is an acute syndrome of massive purpura caused by widespread vascular necrosis and hemorrhagic infarction of the skin and frequently of the distal limbs and digits. It may occur at birth as a result of congenital thrombophilia (i.e. homozygous deficiency of protein C or protein S), durin DIC, with severe infections such as meningococcemia, or after the administration of warfarin(i.e. warfarin skin necrosis). Rare causes are chronic alcohol abuse, acetaminophen ingestion, antiphospholipid antibodies with or without transient acquired protein S deficiency after varicella infection. The skin necrosis observed with heparin is another thrombotic manifestation of the heparin-dependent platelet autoantibody syndrome, caused by antibodies against heparin complexed with platelet factor-4.

The early clinical appearance of Purpura Fulminans is transient flushing, followed by petechiae, with or without edema. At presentation, however, the appearance is usually of massive raised and indurated bruises. The periphery of the lesions may be hyperemic; the center may be replaced by hemorrhagic bullae and necrosis of the skin, with sparing of the subjacent musclle. Dependent areas are typically involved, but the predilection for the breasts, fatty tissue (i.e. abdominal wall and buttocks), and penis is not understood. Areas of pressure may be involved.

The histopathological findings are thrombosis of the dermal capillaries and venules, with hemorrhagic infarction. Arteries and arterioles are spared. The thrombi are composed of fibrin, platelets, or a mixture of the two. There are few or no associated inflammatory changes.

There is a general agreement that Purpura Fulminans results from an imbalance of pprocoagulants and the vitamin K-dependent anticoagulant protein C and S.

Numerous cases of skin necrosis have been observed after warfarin administration, especially when a large loading dose has been used. Warfarin-induced necrosis is more common in women. It has a prevalence between 0.01 and 0.1 percent and typically presents 3 to 10 days after treatment initiation. Late-onset warfarin necrosis has been reported in a patient who developed palpable purpura with rapid progression to hemorrhagic bullae on her abdomen and thighs 56 days after initiation of warfarin treatment for heart valve replacement.

The incidence is highest during the first 3 days of drug administration because protein C has a short half life (6 to 9 hrs) compared with the other vitamin K-dependent procoagulant factors IX, X and II. Twenty four hrs after initiation of warfarin, the level of protein C may be less than 10% of normal, whereas functional levels of procoagulant vitamin-K dependent factors (other than factor VII) may be still greater than 50%. The problem is accentuated in individuals who are heterozygous for protein C deficiency, which may account for as muchas 2% of the population. Warfarin induced skin necrosis has been reported occasionally in patients who are protein S deficient. In individuals with normal protein c and S levels, anti-phospholipid antibodies may stimulate a deficiency state by interfering with endothelial-dependent protein C activation by thrombomodulin.

Treatment involves prompt cessation of warfarin therapy and occasionally surgical intervention if gangrenous tissue develops. Methicillin-resistant Staphylococcus aureus infection of widely involved areas of warfarin necrosis can lead to fatal septic shock. If protein C or S def is suspected, it is common practice to begin cautious warfarin therapy while the patient is heparinized. However, anecdotal evidence of skin necrosis, even in this setting, has been reported. The most important method of prevention is the use of low initial dose of warfarin. A loading dose has no physiological advantage and is no longer recommended.

Ref: 1. Thrombosis and hemorrhage by Joseph Loscalzo, Andrew I. Schafer, 3rd edition 2. Williams Hematology, 7th edition

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ACC/AHA/ESC 2006 Guidelines for management of Atrial Fibrillation- ‘Theurapeutic Options’

2009-07-15T15:07:00.001+05:30

Pharmacological and Nonpharmacological Therapeutic Options:
Drugs and ablation are effective for both rate and rhythm control, and in special circumstances surgery may be the
preferred option. Regardless of the approach, the need for anticoagulation is based on stroke risk and not on whether sinus rhythm is maintained. For rhythm control, drugs are
typically the first choice and LA ablation is a second-line choice, especially in patients with symptomatic lone AF. In some patients, especially young ones with very symptomatic AF who need sinus rhythm, radiofrequency ablation may be preferred over years of drug therapy. Because the Left Atrial Appendage is the site of over 95% of detected thrombi, this structure should be removed from the circulation when possible during cardiac surgery in patients at risk of developing postoperative AF, although this has not been proved to prevent stroke.

Drugs are the primary treatment for rate control in most patients with AF. While ablation of the AV conduction system and permanent pacing (the “ablate and pace” strategy) is an option that often yields remarkable symptomatic relief, growing concern about the negative effect of long-term RV pacing makes this a fallback rather than a primary treatment strategy. LV pacing, on the other hand, may overcome many of the adverse hemodynamic effects associated with RV pacing.

Heart Rate Control Versus Rhythm Control:

Distinguishing Short-Term and Long-Term Treatment Goals:

For patients with symptomatic AF lasting many weeks, initial therapy may be anticoagulation and rate control, while the long-term goal is to restore sinus rhythm. When cardioversion is contemplated and the duration of AF is unknown or exceeds 48h, patients who do not require long-term anticoagulation may benefit from short-term anticoagulation. If rate control offers inadequate symptomatic relief, restoration of sinus rhythm becomes a clear long-term goal. Early cardioversion may be necessary if AF causes hypotension or worsening HF, making the establishment of sinus rhythm a combined short- and long-term therapeutic goal. In some circumstances, when the initiating pathophysiology of AF is reversible, as for instance in the setting of thyrotoxicosis or after cardiac surgery, no long-term therapy may be necessary.

AFFIRM (Atrial Fibrillation Follow-up Investigation of Rhythm Management) found no difference in mortality or stroke rate between patients assigned to one strategy or the other. The RACE (Rate Control vs. Electrical cardioversion for persistent atrial fibrillation) trial found rate control not inferior to rhythm control for prevention of death and morbidity.

The AFFIRM, RACE, PIAF (Pharmacologic Intervention in Atrial Fibrillation), and STAF (Strategies of Treatment of Atrial Fibrillation) studies found no differences in quality of life with rhythm control compared with rate control. Rhythm control in the PIAF and How to Treat Chronic Atrial Fibrillation (HOT CAFÉ) studies resulted in better exercise tolerance than rate control, but this did not translate into improved quality of life.

Ref: J. Am. Coll. Cardiol. 2006;48;e149-e246

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Quiz 5:

2009-07-12T22:28:00.001+05:30

A young male with Rheumatic Heart Disease with Mitral Stenosis, developed Atrial fibrillation. He was started on Tab Warfarin. After 3 days,

he reported to the emergency ward with petechiae and mild edema over his feet, which gradually progressed as shown in the pictures below:

Picture1A----1B-----1C----1D

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TRALI - Pathophysiology

2009-07-10T17:18:00.002+05:30

The lung appears to be the main site for leukocyte activation and bears the majority of tissue damage in TRALI. Possible explanations for this include that the pulmonary microcirculation is the first to encounter transfusion-associated antibodies or immune complexes and that it also contains pulmonary macrophages that can become activated.

The pathogenesis of TRALI depends on the blood product transfused, the underlying mechanism, and “threshold effects” that (may) allow more than 1 mechanism to participate in the lung injury. Nearly all plasma-containing blood products and a variety of blood components have been implicated in TRALI pathogenesis, including whole blood, packed RBC, FFP, platelet concentrates or apheresis, granulocytes, cryoprecipitate, intravenous immunoglobulin, and bone marrow stem cells. Generally, TRALI reactions have not been attributed to washed red cells, albumin, and clotting factor concentrates.

The EHN (European Haemovigilance Network) subtypes TRALI based on underlying mechanism into immune (antibody mediated) or nonimmune TRALI (non-antibody mediated). Others, however, favor a “Two hit” model of TRALI pathogenesis that can apply to both antibody mediated and non-antibody mediated TRALI cases.

Ref: Journal of Intensive Care Medicine / Vol. 23, No. 2, March/April 2008

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ACC/AHA/ESC 2006 Guidelines for the Management of Patients With Atrial Fibrillation- Clinical Evaluation

2009-07-10T13:08:00.006+05:30

AHA 2006 guidelines for management of Atrial Fibrillation

Clinical Evaluation in Patients With AF:

Minimum evaluation:

1. History and physical examination, to define

Presence and nature of symptoms associated with AF

Clinical type of AF (first episode, paroxysmal, persistent, or permanent)

Onset of the first symptomatic attack or date of discovery of AF

Frequency, duration, precipitating factors, and modes of termination of AF

Response to any pharmacological agents that have been administered

Presence of any underlying heart disease or other reversible conditions (e.g., hyperthyroidism or alcohol consumption)

2. Electrocardiogram, to identify

Rhythm (verify AF)

LV hypertrophy

P-wave duration and morphology or fibrillatory waves

Preexcitation

Bundle-branch block

Prior MI

Other atrial arrhythmias

To measure and follow the R-R, QRS, and QT intervals in conjunction with antiarrhythmic drug therapy

3. Transthoracic echocardiogram, to identify

Valvular heart disease

LA and RA size

LV size and function

Peak RV pressure (pulmonary hypertension)

LV hypertrophy

LA thrombus (low sensitivity)

Pericardial disease

4. Blood tests of thyroid, renal, and hepatic function

For a first episode of AF, when the ventricular rate is difficult to control

Additional testing

One or several tests may be necessary.

1. Six-minute walk test

If the adequacy of rate control is in question

2. Exercise testing

If the adequacy of rate control is in question (permanent AF)

To reproduce exercise-induced AF

To exclude ischemia before treatment of selected patients with a type IC antiarrhythmic drug

3. Holter monitoring or event recording

If diagnosis of the type of arrhythmia is in question

As a means of evaluating rate control

4. Transesophageal echocardiography

To identify LA thrombus (in the LA appendage)

To guide cardioversion

5. Electrophysiological study

To clarify the mechanism of wide-QRS-complex tachycardia

To identify a predisposing arrhythmia such as atrial flutter or paroxysmal supraventricular tachycardia

To seek sites for curative ablation or AV conduction block/modification

6. Chest radiograph, to evaluate

Lung parenchyma, when clinical findings suggest an abnormality

Pulmonary vasculature, when clinical findings suggest an abnormality

Management:

Management of patients with AF involves 3 objectives—

1. Rate control,

2. Prevention of thromboembolism, and

3. Correction of the rhythm disturbance, and these are not mutually exclusive.

The initial management decision involves primarily a rate-control or rhythm-control strategy.

Under the rate-control strategy, the ventricular rate is controlled with no commitment to restore or maintain sinus rhythm.

The rhythm-control strategy attempts restoration and/or maintenance of sinus rhythm. The latter strategy also requires attention to rate control. Regardless of whether the rate-control or rhythm-control strategy is pursued, attention must also be directed to antithrombotic therapy for prevention of thromboembolism.

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TRALI - Definition

2009-07-06T14:10:00.006+05:30

Transfusion-related acute lung injury (TRALI)

An international consensus conference on TRALI held in Canada in 2004 advised that TRALI should be recognized as a clinical syndrome and not as a disease with a single etiology.

Definition:

The Canadian consensus conference defined TRALI as having the following criteria:

(a) acute onset,

(b) hypoxemia as defined by a PaO2/FiO2 ≤300 or oxygen saturation by pulse oximetry less than 90% on room air,

(d) no evidence of left atrial hypertension,

(e) occurrence during or within 6 hours of transfusion, and

(f) no preexisting ALI before transfusion or temporal relationship to an alternative ALI risk factor .

Possible TRALI:

In cases of TRALI occurring in the setting of transfusion and an alternative risk factor for ALI, a designation of “possible TRALI” was added. These alternative risk factors included a variety of conditions that may directly or indirectly induce lung injury, such as pneumonia, pulmonary contusion, and sepsis.

Limitations of the definition:

(1) This definition, however, does not acknowledge the effects of positive end expiratory pressure on the PaO2/FiO2 ratio.

(2) An additional important limitation of this definition is that it excludes patients with preexisting ALI, whose lung injury worsens after transfusion.

Ref: Journal of Intensive Care Medicine / Vol. 23, No. 2, March/April 2008

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