Tuesday July 8, 2008
Corticosteroid and ARDS: Result of meta-analysis

Several articles have been written regarding role of steroids, its advantages or disadvantages in ARDS. Recently John Victor Peter and his group presented their findings in BMJ.

Method: Search of randomized controlled trials from years 1966 to april 2007.

Data extraction: Two investigators independently assessed trials for inclusion and extracted data into standardized forms. Differences were resolved by consensus.

Data synthesis: Nine randomized trials using variable dose and duration of steroids were identified. Preventive steroids (four studies) were associated with a trend to increase both the odds of patient developing ARDS (odds ratio 1.55), and the risk of mortality in those who subsequently developed ARDS (odds ratio 1.52).

• Steroid administration after the onset of ARDS (five studies) was associated with a trend in reduction in mortality (odds ratio .62).
• Steroid increase the number of ventilator free days compared to control (three studies, mean difference 4.05 days, 95% credible interval 0.22 to 8.71).
• Use of steroids was not associated with increase in risk of infection.

Conclusion: Role of use of steroids in ARDS is not clearly established. Preventive use of steroids increase the incidence of ARDS in critically ill patients, whereas use of steroids after the onset of ARDS possibly reduces the mortality and increases the ventilator free days.


Reference: click to get abstract

Peter JV, John P, Graham PL, Moran JL, George IA, Bersten A. Corticosteroids in the prevention and treatment of acute respiratory distress syndrome (ARDS) in adults: meta-analysis. BMJ 2008; 336:1006-1009.

Monday July 7, 2008
Is our ICU nurses sleepier then our floor nurses?

Recent paper published in Journal of Hospital Medicine from Surani and coll. helped to address this issue with their pilot study.

(Dr. S. Surani is co-editor of this website also)

METHODS: Post-night-shift nurses in the ICU and on general floors (medicine and surgery) were assessed using subjective (Epworth Sleepiness Scale [ESS]) and objective (Mean Sleep Latency Test [MSLT]) measures.

RESULTS:

• ESS was abnormal (>8) in 7 of 10 ICU nurses compared with 2 of 10 floor nurses (P < .005), and mean ESS score was also higher (8.7 ± 3.9 vs. 5.6 ± 2.1, respectively; P = 0.042).
• MSLT values for the first nap period were in the pathologic range in the ICU nurses compared with the floor nurses (4.65 ± 5.5 vs. 10.85 ± 7.4 minutes, respectively; P < .05).

CONCLUSIONS: Post-night-shift RNs working in the ICU have a pathologic degree of sleepiness.



Reference: click to get abstract

Surani S, Subramanyan S, Babbar H, Murphy J, Aguillar R. Sleepiness in critical care nurses: Results of a pilot study. Journal of Hospital Medicine 2008; 3(3):200-205

Sunday July 6, 2008

Q: Why we call it cryoprecipitate?

A: The name explains everthing. cryoprecipitate means "cold precipitate". When FFP is thawed slowly at 4 degree C, a white precipitate forms at the bottom of the bag, which can then be separated from the supernatant plasma. This precipitate is rich in fibrinogen, factor VIII, von Willebrand factor, factor XIII, and fibronectin - and call crayoprecipitate. One unit of cryoprecipitate is derived from fresh frozen plasma (FFP) prepared from a unit of whole blood and as it is only a little precipitate at the bottom of the bag, 1 unit of cryoprecipitate comprised only a volume of 10-20 mL. Contents:

• 80-100 units of factor VIII, which consists of both the procoagulant activity and the von Willebrand factor,
• 150-250 mg of fibrinogen,
• 50-100 units of factor XIII, and
• 50-60 mg of fibronectin.

Half life is about one year if stored at minus (-) 18 degree C. When ordered (generally given as 6 units at a time), cryoprecipitate is thawed back to 37 degree C. Once thawed it must be kept at room temperature and has an expiration time of 4 to 6 hours.

Saturday July 5, 2008
"estimated average glucose" (or eAG) instead of HbA1c?


Scenario: You admitted 38 year old female with DKA. Looking at her record, you found that her latest "estimated average glucose" reported is 212. What is her estimated HbA1C?

Answer: 9

The HbA1c measures blood glucose control over the previous 90 days. It is expressed as the percent of hemoglobin molecules that have glucose attached. Recommended goal is less than 7% for people with diabetes.

But a new study (soon to be published) has found a simple mathematical formula that can "translate" HbA1c levels into an eAG level. It almost accurately converted HbA1c levels into average glucose levels.

An "estimated average glucose" or eAG is an accurate and easier way to understand glucose control, and probably will soon become the standard of reporting blood glucose control .

Manual way to do formula is

28.7 x HbA1c - 46.7 = eAG (in mg/dl)

Or use following graph (HbA1C % is followed with both mg/dl and mmol/L values)

6 % = 126 mg/dl = 7.0 mmol/l
6.5% =140 mg/dl = 7.8 mmol/l
7 % = 154 mg/dl = 8.6 mmol/l
7.5 % = 169 mg/dl = 9.4 mmol/l
8 % = 183 mg/dl = 10.1 mmol/l
8.5% = 197 mg/dl = 10.9 mmol/l
9 % = 212 mg/dl = 11.8 mmol/l
9.5 % = 226 mg/dl = 12.6 mmol/l
10 % = 240 mg/dl = 13.4 mmol/l


Reference: Click to get abstract

Translating the A1C Assay Into Estimated Average Glucose Values - Publish Ahead of Print published online ahead of print June 7, 2008, findings will be printed in the August issue of Diabetes Care

Happy July 4


Patient: Tell me, doctor. Is it serious?
Doctor: Well, I wouldn’t advise you to start watching any serials on TV

Have a Great Bar B Q

Thursday July 3, 2008
Cardiac MRI to determine Myocardium Viability before revascularization

Even severely dysfunctional myocardium in patients with coronary artery disease may show functional improvement after revascularization. Recent literature is showing that Cardiac MRI (CMR) is superior to low-dose dobutamine echocardiography and thallium-SPECT for viability imaging.

The whole concept of viability on Cardiac MRI is based on the fact that all infarcts enhance vividly 10-15 minutes after intravenous contrast administration. Cardiac MRI shows the transmural extent of the infarct very reliably. It tells you that:

"white is dead" (All infarcts irrespective of age enhance)





In areas of hypokinesia, if there is a rim of "black" or non-infarcted myocardium that is not contracting well, it indicates the presence of hibernating myocardium, which is likely to improve after revascularization of the artery supplying that particular territory.

Viability imaging reliably allows identification of areas of hibernation and viable or non-viable myocardium. All infarcts irrespective of age enhance.

The percentage involvement of the myocardial wall thickness by an infarct determines viability. Involvement of the myocardium by more than 50% usually implies that there will be no improvement after revascularization And similarly, less than 25% involvement of the myocardium by infarction usually implies that there is an 80% chance of improvement after revascularization.

Read article CMR in Myocardial Viability (Reference: Bhavin Jankharia: CMR in Myocardial Viability. The Internet Journal of Cardiology. 2004. Volume 2 Number 2.)

Wednesday July 2, 2008

Scenario: You have a patient admitted with confirmed HIT (Heparin-Induced Thrombocytopenia). Patient was started on nonheparin anticoagulant (argatroban). Once platelet count reached a stable plateau and the INR (international normalized ratio) reached the intended target range, for how many days overlap of nonheparin anticoagulation and Coumadin should be continued? - Choose one

A) Switch immediately

B) 2 days

C) 3 days

D) 5 days




Answer: 5 days

According to new (june 2008) American College of Chest Physicians Evidence-Based Clinical Practice Guidelines (8th Edition) on Treatment and Prevention of Heparin-Induced Thrombocytopenia.

"For patients with strongly suspected or confirmed HIT, we recommend against the use of vitamin K antagonist (VKA) [coumarin] therapy until after the platelet count has substantially recovered (usually, to at least 150 x 109/L) over starting VKA therapy at a lower platelet count (Grade 1B); that VKA therapy be started only with low maintenance doses (maximum, 5 mg of warfarin or 6 mg of phenprocoumon) over higher initial doses (Grade 1B); and that the nonheparin anticoagulant (eg, lepirudin, argatroban, danaparoid) be continued until the platelet count has reached a stable plateau, the international normalized ratio (INR) has reached the intended target range, and after a minimum overlap of at least 5 days between nonheparin anticoagulation and VKA therapy rather than a shorter overlap (Grade 1B)".


You can read full guidelines here

Found full range of new ACCP GUIDELINES on ANTITHROMBOTIC AND THROMBOLYTIC THERAPY (8TH ED) here

Tuesday July 1, 2008
THAM

Introduction: In patients with acute respiratory distress syndrome (ARDS), permissive hypercapnia is a strategy to decrease airway pressures to prevent ventilator-induced lung damage by lowering tidal volumes and tolerating higher arterial carbon dioxide tension. A pure respiratory acidosis generally does not require alkali therapy. Alkali therapy is indicated for either a metabolic acidosis or a mixed acidosis. The choice of buffer is based on the type of acidosis, cardiorespiratory status, and lung mechanics.

Problem with NaHCO3: Slow infusions of NaHCO3 can be used to treat non-anion gap metabolic acidosis and some forms of increased anion gap acidosis. But using NaHCO3 to treat type A (hypoxia-related) lactic acidosis can be hazardous, particularly under conditions of hypoxemia, inadequate circulation, and limited alveolar ventilation.

THAM: Under above circumstances, THAM is the preferable buffer because it does not increase PaCO2 and is excreted by the kidneys. Tromethamine (THAM) is a sodium-free alkalinizing agent that acts as a hydrogen ion (proton) acceptor. It is a weak base that combines with hydrogen ions from carbonic acid to form bicarbonate and cationic buffer. Administration of tromethamine decreases hydrogen ion concentration, which results in a decrease in carbon dioxide concentrations and an increase in bicarbonate concentrations. The administration of Tham also increases urine output through osmotic diuresis. Excretion of electrolytes and CO2 is also increased. Urine pH is raised along with the excretion of electrolytes.

Usual Dose:

Dose in ml's of 0.3M THAM = (1.1) (Wt. in Kg) (normal HCO3 – Pt’s HCO3)

OR

Dose in ml’s of 0.3M THAM = body wt in kg X base deficit in MEq/L x 1.1

Total dose should be administered over a period not less than 1 hour via central line. .3M THAM solution is available as premix and is contra-indicated in renal failure, anuria and hyperkalemia. It may cause transient hypoglycemia and respiratory depression.