MCQ1: FNBE- 2008,2009: Toxicology

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

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TRALI – Prevention

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

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What to read for FNB enterance???

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

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Venous Oximetry – The concept of SvO2 and ScvO2

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

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