Wednesday August 5, 2009


Scenario: 25 year old patient presented to the emergency room with complaint of 2 days history of muscular weakness which is symmetric and descending and diplopia. He denies any fever or chills. He does give the history of having injury to the face. He works as marine driller. His symptoms are progressively getting worse. His vitals signs reveal no fever, and bradycardia with the heart rate of 48 and blood pressure of 120/80 mm hg. His Slow vital capacity was 1 liter (33% of predicted). He was admitted in intensive care unit.


Diagnosis: Botulism (110 cases in US per year with 3 percent being wound Botulism)

Differential diagnosis: Mysthenia Gravis, Lambert-Eaton syndrome, Guillain-Barre’s syndrome, poliolmyelitis, Ticks paralysis, heavy metal intoxication.


Botulism has an acute onset with bilateral cranial neuropathies and symmetric descending weakness. Key feature include:

• Patient is afebrile
• Symmetric neurological deficit
• Patient is responsive
• Normal or slow heart rate and normal blood pressure
• No sensory deficit
• Blurred vision
  

Treatment:

• Equine serum botulism antitoxin
• Penicillin G intravenously 3 grams every 4 hours

Tuesday August 4, 2009
Heparin rebound phenomenon

Heparin rebound phenomenon, is considered to be a contributive factor in excessive postoperative bleeding after cardiac surgery. It is due to the reappearance of anticoagulant activity despite adequate neutralization with protamine.This phenomenon is well known since atleast last 45 years 1.

The underlying etiology is due to the fact that a significant amount of heparin remains bound to plasma proteins and escape neutralization by protamine. Later this heparin get released and may contribute to excessive postoperative bleeding after cardiac surgery. Though logically, the treatment is more administration of prtoamine but caution should be taken as high and inappropriate protamine dose may lead to 'acute' pulmonary hypertension 2 and interestingly failed to show decrease in blood product adminstration 3 or any difference in the thrombelastographic profiles or coagulation screen (PT, PTT, ACT and platelets) 2. Also life threatening protamine reactions is another risk need to be considered 5.




Note: This Heparin rebound phenomenon is different from Rebound increase in Thrombin Generation and Activity after cessation of intravenous heparin in patients with acute coronary syndromes which is also often referred as heparin rebound phenomenon 4.





References: click to get abstract/article

1. Heparin rebound phenomenon in extracorporeal circulation - Surg Gynecol Obstet.1962 Aug;115:191-8.

2. Heparin rebound phenomenon--much ado about nothing? - Blood Coagul Fibrinolysis. 1992 Apr;3(2):187-91.

3. Can extra protamine eliminate heparin rebound following cardiopulmonary bypass surgery? - J Thorac Cardiovasc Surg 2004;128:211-219

4. Rebound Increase in Thrombin Generation and Activity After Cessation of Intravenous Heparin in Patients With Acute Coronary Syndromes - Circulation. 1995;91:1929-1935.

5. Life Threatening Protamine Reactions In Cardiac Surgery: Literature Review With A Case Report - The Internet Journal of Thoracic and Cardiovascular Surgery. 2005. Volume 7 Number 1.

Monday August 3, 2009
Atenolol in renal failure

One must use caution while prescribing atenolol to patients with renal insufficiency. The elimination half-life of atenolol is extensively prolonged in patient with renal failure. The normal half life of atenolol is 6 to 7 hours; however, in renal failure patients the half-life may be extended to more than 100 hours 2.

The recommended dosage are following:

• CrCl 35 mL/min or greater - normal dosing
• CrCl 15 - 35 mL/min - MAX. dose 50 mg orally QD
• CrCl less than 15 mL/min - MAX. dose 25 mg orally QD
• Hemodialysis: 25-50 mg orally after each dialysis session.

Treatment of atenolol overdose in a patient with renal failure is recommended with serial hemodialysis and charcoal hemoperfusion 3. On the contrary, metoprolol is extensively metabolized via the hepatic system.



References:

1.Atenolol-DOSAGE AND ADMINISTRATION - rxlist.com

2.Atenolol kinetics in renal failure - Clin Pharmacol Ther. 1980 Sep;28(3):302-9

3. Treatment of atenolol overdose in a patient with renal failure using serial hemodialysis and hemoperfusion and associated echocardiographic findings Vet Hum Toxicol. 2000 Aug;42(4):224-5.

Sunday August 2, 2009
Why Arixtra doesn't cause HIT (Heparin induced thrombocytopenia)






ARIXTRA (Fondaparinux) is not a heparin. ARIXTRA is the first and only pentasaccharide antithrombotic agent inhibiting only factor Xa

Saturday August 1, 2009

Procedure tip - Straight to Cuff Stylet Shaping