Thursday April 8, 2010
Factor-7 in GI bleed
Case; 67 year old male admitted with acute GI bleed seconday to coumadin (warfarin) overdose with INR more than 7. You ordered, pRBC, FFP (fresh frozen plasma) and IV vitamin K. But you are afraid that patient may not survive before all the infusions are available. What could be your choice in such desperation?
A; recombinant FVIIa (Novo seven)
In many anecdotal reports (see references), novoseven has showed very quick reversal of PT / INR.
References:
1. Recombinant factor VIIa corrects prothrombin time in cirrhotic patients: A preliminary study: Gastroenterology 113:1930-1937, 1997
2. Recombinant factor VIIa (rFVIIa) successfully and rapidly corrects the excessively high international normalized ratios (INR) and prothrombin times induced by warfarin. Blood 96 (11 Part 1): 638a, 2000
3. Reversal of Warfarin-Induced Excessive Anticoagulation with Recombinant Human Factor VIIa Concentrate. Ann Inter Med. 137:884-888, 2002
4. Hemorrhagic complication of thrombocytopenia and oral anticoagulant: Is there a role for recombinant activated factor VII ?. Intensive Care Med 28 (Suppl 2):S228, 2002
Thursday, April 8, 2010
Wednesday, April 7, 2010
Wednesday April 7, 2009
Scenario: 48 year old male, hemodialysis dependent, admitted with gastro-intestinal bleed. Last dialysis was 3 days ago. Patient received 4 units of pRBC and now hemodynamically stable. Nurse calls you as she felt that rhythm looks different on monitor. Patient is asymptomatic. Walking towards patient's bed what would be your top diagnosis ?
Answer: Hyperkalemia
Transfusion-associated hyperkalemia is a potential life threatening condition in patients with renal failure who have not been dialysed recently or with already elevated/borderline potassium level and should be followed closely.
Scenario: 48 year old male, hemodialysis dependent, admitted with gastro-intestinal bleed. Last dialysis was 3 days ago. Patient received 4 units of pRBC and now hemodynamically stable. Nurse calls you as she felt that rhythm looks different on monitor. Patient is asymptomatic. Walking towards patient's bed what would be your top diagnosis ?
Answer: Hyperkalemia
Transfusion-associated hyperkalemia is a potential life threatening condition in patients with renal failure who have not been dialysed recently or with already elevated/borderline potassium level and should be followed closely.
Tuesday, April 6, 2010
Tuesday April 6, 2010
Precedex (dexmedetomidine) for Cocaine overdose?
Objectives: The aim of this study was to determine whether cocaine’s sympathomimetic actions can be reversed by a potent centrally acting 2 adrenergic receptor (AR) agonist (dexmedetomidine).
Background: We recently showed that cocaine stimulates the human cardiovascular system primarily by acting in the brain to increase sympathetic nerve activity (SNA), the neural stimulus to norepinephrine release. Thus, SNA constitutes a putative new drug target to block cocaine’s adverse cardiovascular effects at their origin.
Methods: In 22 healthy cocaine-naïve humans, we measured skin SNA (microneurography) and skin blood flow (laser Doppler velocimetry) as well as heart rate and blood pressure before and after intranasal cocaine (2 mg/kg) alone and in combination with dexmedetomidine or saline.
Results: During intranasal cocaine alone, SNA increased by 2-fold and skin vascular resistance increased from 13.2 ± 2.3 to 20.1 ± 2.2 resistance units while mean arterial pressure increased by 14 ± 3 mm Hg and heart rate by 18 ± 3 beats/min (p less than 0.01). Dexmedetomidine abolished these increases, whereas intravenous saline was without effect. Dexmedetomidine was effective in blocking these sympathomimetic actions of cocaine even in all 7 subjects who were homozygous for the Del322-325 polymorphism in the 2C AR, a loss-of-function mutation that is highly enriched in blacks.
Conclusions: The data advance the novel hypothesis that central sympatholysis with dexmedetomidine constitutes a highly effective countermeasure for cocaine’s sympathomimetic actions on the human cardiovascular system, even in individuals carrying the 2CDel322-325 polymorphism.
Central Sympatholysis as a Novel Countermeasure for Cocaine-Induced Sympathetic Activation and Vasoconstriction in Humans - J Am Coll Cardiol, 2007; 50:626-633
Precedex (dexmedetomidine) for Cocaine overdose?
Objectives: The aim of this study was to determine whether cocaine’s sympathomimetic actions can be reversed by a potent centrally acting 2 adrenergic receptor (AR) agonist (dexmedetomidine).
Background: We recently showed that cocaine stimulates the human cardiovascular system primarily by acting in the brain to increase sympathetic nerve activity (SNA), the neural stimulus to norepinephrine release. Thus, SNA constitutes a putative new drug target to block cocaine’s adverse cardiovascular effects at their origin.
Methods: In 22 healthy cocaine-naïve humans, we measured skin SNA (microneurography) and skin blood flow (laser Doppler velocimetry) as well as heart rate and blood pressure before and after intranasal cocaine (2 mg/kg) alone and in combination with dexmedetomidine or saline.
Results: During intranasal cocaine alone, SNA increased by 2-fold and skin vascular resistance increased from 13.2 ± 2.3 to 20.1 ± 2.2 resistance units while mean arterial pressure increased by 14 ± 3 mm Hg and heart rate by 18 ± 3 beats/min (p less than 0.01). Dexmedetomidine abolished these increases, whereas intravenous saline was without effect. Dexmedetomidine was effective in blocking these sympathomimetic actions of cocaine even in all 7 subjects who were homozygous for the Del322-325 polymorphism in the 2C AR, a loss-of-function mutation that is highly enriched in blacks.
Conclusions: The data advance the novel hypothesis that central sympatholysis with dexmedetomidine constitutes a highly effective countermeasure for cocaine’s sympathomimetic actions on the human cardiovascular system, even in individuals carrying the 2CDel322-325 polymorphism.
Central Sympatholysis as a Novel Countermeasure for Cocaine-Induced Sympathetic Activation and Vasoconstriction in Humans - J Am Coll Cardiol, 2007; 50:626-633
Monday, April 5, 2010
Monday April 5, 2010
Case: 54 year old female is admitted to ICU with pulmonary embolism. Patient is started on heparin and has been switched to coumadin (warfarin). Patient platelet count remained low and further workup confirmed HIT (Heparin induced thrombocytopenia). What should be administrated to patient along with initiation of either argatroban or lepirudin?
Answer: Vitamin K (10 mg po or 5 to 10 mg IV)
Warfarin should be postponed until substantial platelet recovery. If warfarin has already been started, vitamin K should be given to reverse the effect of warfarin. Warfarin should be avoided in acute HIT. Warfarin has been associated with worsening venous thrombosis, venous limb gangrene, and/or skin necrosis when used alone or in combination with ancrod in acute HIT. However, warfarin is appropriate for longer term anticoagulation in patients with HIT and thrombosis. Warfarin should be delayed until there is substantial resolution of the thrombocytopenia.
Treatment and Prevention of Heparin-Induced Thrombocytopenia - American College of Chest Physicians Evidence-Based Clinical Practice Guidelines (8th Edition) - CHEST June 2008 vol. 133 no. 6 suppl 340S-380S
Case: 54 year old female is admitted to ICU with pulmonary embolism. Patient is started on heparin and has been switched to coumadin (warfarin). Patient platelet count remained low and further workup confirmed HIT (Heparin induced thrombocytopenia). What should be administrated to patient along with initiation of either argatroban or lepirudin?
Answer: Vitamin K (10 mg po or 5 to 10 mg IV)
Warfarin should be postponed until substantial platelet recovery. If warfarin has already been started, vitamin K should be given to reverse the effect of warfarin. Warfarin should be avoided in acute HIT. Warfarin has been associated with worsening venous thrombosis, venous limb gangrene, and/or skin necrosis when used alone or in combination with ancrod in acute HIT. However, warfarin is appropriate for longer term anticoagulation in patients with HIT and thrombosis. Warfarin should be delayed until there is substantial resolution of the thrombocytopenia.
Treatment and Prevention of Heparin-Induced Thrombocytopenia - American College of Chest Physicians Evidence-Based Clinical Practice Guidelines (8th Edition) - CHEST June 2008 vol. 133 no. 6 suppl 340S-380S
Sunday, April 4, 2010
Sunday April 4, 2010
On heparin resistance and antithrombin deficiency
Case: 64 year old male is admitted to ICU with atrial fibrillation associated with RVR (rapid ventricular response). Patient has previous history of stroke. With rate control management patient is started on heparin for anticoagulation purpose. Heparin drip is now at 2400 units/hour but PTT is still not therapeutic, You suspect Anti-Thombin deficiency and indeed its level is low. Unfortunately pharmacist reports to you that there is an Anti-Thrombin shortage and will not be available. What is your other option?
Answer: Heparin principally exerts its anticoagulant effect by activating Antithromin (AT); the heparin-antithrombin (H-AT) complex then inactivates thrombin, activated factor X (fXa) and other activated clotting factors.
Heparin resistance is defined as the need for more than 35 000 Units in 24 h to prolong the activated partial thromboplastin time (APTT) into the therapeutic range. In contrast, during cardiac bypass procedures, the definition of heparin resistance is based on the activated clotting time (ACT), with at least one ACT less than 400 s after heparinization and/or the need for exogenous antithrombin administration. Heparin therapy produces a decrease in circulating antithrombin that is independent of the initial dose, is detectable after 1 day, and peaks after 2–4 days.
In above case your salvage is in use of a direct antithrombin inhibitor like bivalirudin. An important advantage of using bivalirudin instead of heparin is that there is no need to monitor or supplement ATIII levels for therapeutic effect.
On heparin resistance and antithrombin deficiency
Case: 64 year old male is admitted to ICU with atrial fibrillation associated with RVR (rapid ventricular response). Patient has previous history of stroke. With rate control management patient is started on heparin for anticoagulation purpose. Heparin drip is now at 2400 units/hour but PTT is still not therapeutic, You suspect Anti-Thombin deficiency and indeed its level is low. Unfortunately pharmacist reports to you that there is an Anti-Thrombin shortage and will not be available. What is your other option?
Answer: Heparin principally exerts its anticoagulant effect by activating Antithromin (AT); the heparin-antithrombin (H-AT) complex then inactivates thrombin, activated factor X (fXa) and other activated clotting factors.
Heparin resistance is defined as the need for more than 35 000 Units in 24 h to prolong the activated partial thromboplastin time (APTT) into the therapeutic range. In contrast, during cardiac bypass procedures, the definition of heparin resistance is based on the activated clotting time (ACT), with at least one ACT less than 400 s after heparinization and/or the need for exogenous antithrombin administration. Heparin therapy produces a decrease in circulating antithrombin that is independent of the initial dose, is detectable after 1 day, and peaks after 2–4 days.
In above case your salvage is in use of a direct antithrombin inhibitor like bivalirudin. An important advantage of using bivalirudin instead of heparin is that there is no need to monitor or supplement ATIII levels for therapeutic effect.
Saturday, April 3, 2010
Saturday April 3, 2010
Case: In ACLS, dose for Vasopressin is 40 units IV x1. In desperate situations how quickly you can repeat it?
Answer: Though it is recommended every 20 minutes but in desperate situation you may use in 10 minutes.
Vasopressin is an adrenergic alternative to epinephrine, for promoting the return of spontaneous circulation after cardiac arrest. Vasopressin, a naturally occurring antidiuretic hormone, has powerful vasoconstrictor effects when used at doses much higher than normally found in the body. Its positive effects duplicate those of epinephrine, but with fewer or less-severe adverse effects. Vasopressin is administered intravenously as a one-time dose of 40 units. Compare its 10- to 20-minute half-life with the 3- to 5-minute half-life of epinephrine, and you'll see another reason why vasopressin is now finding favor in resuscitation efforts. However, if the patient doesn't respond to vasopressin, you can use epinephrine.
See this nice review: VASOPRESSIN AND SHOCK (Dr. Paul Forrest)
Case: In ACLS, dose for Vasopressin is 40 units IV x1. In desperate situations how quickly you can repeat it?
Answer: Though it is recommended every 20 minutes but in desperate situation you may use in 10 minutes.
Vasopressin is an adrenergic alternative to epinephrine, for promoting the return of spontaneous circulation after cardiac arrest. Vasopressin, a naturally occurring antidiuretic hormone, has powerful vasoconstrictor effects when used at doses much higher than normally found in the body. Its positive effects duplicate those of epinephrine, but with fewer or less-severe adverse effects. Vasopressin is administered intravenously as a one-time dose of 40 units. Compare its 10- to 20-minute half-life with the 3- to 5-minute half-life of epinephrine, and you'll see another reason why vasopressin is now finding favor in resuscitation efforts. However, if the patient doesn't respond to vasopressin, you can use epinephrine.
See this nice review: VASOPRESSIN AND SHOCK (Dr. Paul Forrest)
Friday, April 2, 2010
Friday April 2, 2010
Case: 43 year old male with previous history of heart transplant found unresponsive and in asystole. Which regularly use 'code medicine' will not work on him?
Answer: Atropine
Patient has a transplanted heart and is denervated so atropine will not work. Immediate transcutaneous pacing (instead of atropine) should be placed.
Case: 43 year old male with previous history of heart transplant found unresponsive and in asystole. Which regularly use 'code medicine' will not work on him?
Answer: Atropine
Patient has a transplanted heart and is denervated so atropine will not work. Immediate transcutaneous pacing (instead of atropine) should be placed.
Thursday, April 1, 2010
Thursday April 1, 2010
CXR diagnosis in Pulmonary Embolism
Looking for Westermark’s and Palla’s Signs together
Answer: Chest radiograph showing
Westermark’s sign - focal oligemia in the right lung (area between white arrowheads) and
Palla’s sign - a prominent right descending pulmonary artery (black arrow).
Westermark’s and Palla’s signs in combination are rare but, when seen, can help confirm diagnosis of pulmonary embolism.
Reference: Westermark’s and Palla’s Signs in Acute Pulmonary Embolism - Circulation. 2007;115:e211.http://circ.ahajournals.org/cgi/content/full/115/8/e211
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