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.