Wednesday March 21, 2007
Citrate in CRRT
Q; Why we use citrate (when heparin is not used) to avoid filter clotting in CRRT / CVVHD (continuous renal replacement therapy) ?
A; Citrate combines with calcium and cause extracorporeal chelation of calcium and blocks calcium dependent steps of clotting cascade.
When extracorporeal blood mix with venous blood, the ionized calcium level get resotred and systemic anticoagulation get avoided. Also citrate get metabolized via liver and chelated calcium get release back in circulation which prevents hypocalcemia (though frequent checks required particularly in liver insuff.).
Related: Very nice review article: Acute Renal Failure in ICU (reference: nephrologyrounds.org, december 2006, volume 4, issue 10) - pdf file
Showing posts with label coagulation. Show all posts
Showing posts with label coagulation. Show all posts
Wednesday, March 21, 2007
Monday, March 19, 2007
Monday March 19, 2007
Acute hyperglycemia may lower tPA effect in stroke patients
As benefits of blood sugar control is getting more and more attention, this new study published in stroke 1 from spain is noteworthy which found that "acute" (but not chronic) hyperglycemia may lower tPA effect in stroke patients. As known from before, hyperglycemia has a deleterious effect in stroke patients by accelerating ischemic brain damage. This study showed that antifibrinolytic effect of hyperglycemia may also influence reperfusion.
Glucose level at admission was recorded in 139 consecutive stroke patients who were treated with intravenous tissue-type plasminogen activator (tPA). The existence of previous chronic hypergycemia was determined by glycosylated hemoglobin (HbA1c) and fructosamine.
Results — Patients who recanalized showed lower admission glucose levels but no differences in HbA1c or fructosamine.
Patients with an admission glucose level more than 158 mg/dL had lower recanalization rates (16% vs 36.1%) and a higher NIHSS score at 48 hours (7 vs 14.5). After adjustment for stroke etiology, age, and risk factors, the only independent predictors on admission of no recanalization were
proximal middle cerebral artery occlusion and platelet count less than 219 000/mL
Study concluded that in tPA-treated patients, the acute but not chronic hyperglycemia state may hamper the fibrinolytic process, delaying reperfusion of the ischemic penumbra. Early measures to reduce blood glucose may favor early recanalization.
Reference: Click to get abstract
1. Acute Hyperglycemia State Is Associated With Lower tPA-Induced Recanalization Rates in Stroke Patients -Stroke. 2005;36:1705
Acute hyperglycemia may lower tPA effect in stroke patients
As benefits of blood sugar control is getting more and more attention, this new study published in stroke 1 from spain is noteworthy which found that "acute" (but not chronic) hyperglycemia may lower tPA effect in stroke patients. As known from before, hyperglycemia has a deleterious effect in stroke patients by accelerating ischemic brain damage. This study showed that antifibrinolytic effect of hyperglycemia may also influence reperfusion.
Glucose level at admission was recorded in 139 consecutive stroke patients who were treated with intravenous tissue-type plasminogen activator (tPA). The existence of previous chronic hypergycemia was determined by glycosylated hemoglobin (HbA1c) and fructosamine.
- Transcranial Doppler monitoring assessed complete recanalization 2 hours after tPA bolus.
- National Institutes of Health Stroke Scale (NIHSS) scores were obtained at baseline and 48 hours.
Results — Patients who recanalized showed lower admission glucose levels but no differences in HbA1c or fructosamine.
Patients with an admission glucose level more than 158 mg/dL had lower recanalization rates (16% vs 36.1%) and a higher NIHSS score at 48 hours (7 vs 14.5). After adjustment for stroke etiology, age, and risk factors, the only independent predictors on admission of no recanalization were
Study concluded that in tPA-treated patients, the acute but not chronic hyperglycemia state may hamper the fibrinolytic process, delaying reperfusion of the ischemic penumbra. Early measures to reduce blood glucose may favor early recanalization.
Reference: Click to get abstract
1. Acute Hyperglycemia State Is Associated With Lower tPA-Induced Recanalization Rates in Stroke Patients -Stroke. 2005;36:1705
Wednesday, March 14, 2007
Wednesday March 14, 2007
Heparin Induced HyperKalemia
Hyperkalemia from Heparin is a well know phenomenon and has been detected particularly on geriatric, renal insufficient and diabetic patients. Hyperkalemia can be anywhere from .3 to 1.7 mEq/Litre. It usually occurs around on day 3 with SQ heparin (as for DVT prophylaxis) but can occur early with IV heparin 1,2,3,4. Hyperkalemia has been reported with low- molecular weight heparins too but risk is low 5, 6, 7.
Mechanism of action: Heparin induce hypoaldosteronism and can subsequently lead to hyperkalemia 6.
Treatment: Best thing is to discontinue the culprit but if heparin is absolutely required, fludrocortisone (.1 mg/day) has been reported to be effective in heparin-induced hyperkalemia 8.
References: Click to get abstracts/articles
1. Case report - Heparin-induced hyperkalemia after cardiac surgery - Ann Thorac Surg 2002;74:1698-1700
2. Heparin-induced hyperkalemia -The Annals of Pharmacotherapy: Vol. 24, No. 3, pp. 244-246.
3. Heparin Induced HyperKalemia - Endocrine Abstracts (2002) 4 P26
4. Heparin-Induced Hyperkalemia Confirmed by Drug Rechallenge. American Journal of Physical Medicine & Rehabilitation. 79(1):93-96, January/February 2000.
5. Early onset of hyperkalemia in patients treated with low molecular weight heparin: a prospective study - Pharmacoepidemiol Drug Saf.2004 May;13(5):299-302.
6. Effect of Low-Molecular-Weight Heparin on Potassium Homeostasis - Pathophysiology of Haemostasis and Thrombosis 2002;32:107-110
7. Low Molecular Weight Heparins Can Lead To Hyperkalaemia The Internet Journal of Geriatrics and Gerontology . 2005. Volume 2 Number 2.
8. Fludrocortisone for the treatment of heparin-induced hyperkalemia - The Annals of Pharmacotherapy: Vol. 34, No. 5, pp. 606-610
Heparin Induced HyperKalemia
Hyperkalemia from Heparin is a well know phenomenon and has been detected particularly on geriatric, renal insufficient and diabetic patients. Hyperkalemia can be anywhere from .3 to 1.7 mEq/Litre. It usually occurs around on day 3 with SQ heparin (as for DVT prophylaxis) but can occur early with IV heparin 1,2,3,4. Hyperkalemia has been reported with low- molecular weight heparins too but risk is low 5, 6, 7.
Mechanism of action: Heparin induce hypoaldosteronism and can subsequently lead to hyperkalemia 6.
Treatment: Best thing is to discontinue the culprit but if heparin is absolutely required, fludrocortisone (.1 mg/day) has been reported to be effective in heparin-induced hyperkalemia 8.
References: Click to get abstracts/articles
1. Case report - Heparin-induced hyperkalemia after cardiac surgery - Ann Thorac Surg 2002;74:1698-1700
2. Heparin-induced hyperkalemia -The Annals of Pharmacotherapy: Vol. 24, No. 3, pp. 244-246.
3. Heparin Induced HyperKalemia - Endocrine Abstracts (2002) 4 P26
4. Heparin-Induced Hyperkalemia Confirmed by Drug Rechallenge. American Journal of Physical Medicine & Rehabilitation. 79(1):93-96, January/February 2000.
5. Early onset of hyperkalemia in patients treated with low molecular weight heparin: a prospective study - Pharmacoepidemiol Drug Saf.2004 May;13(5):299-302.
6. Effect of Low-Molecular-Weight Heparin on Potassium Homeostasis - Pathophysiology of Haemostasis and Thrombosis 2002;32:107-110
7. Low Molecular Weight Heparins Can Lead To Hyperkalaemia The Internet Journal of Geriatrics and Gerontology . 2005. Volume 2 Number 2.
8. Fludrocortisone for the treatment of heparin-induced hyperkalemia - The Annals of Pharmacotherapy: Vol. 34, No. 5, pp. 606-610
Tuesday, March 6, 2007
Tuesday March 6, 2007
What if plasma exchange is not available as treatment for TTP
Q: You just diagnosed a patient with thrombotic thrombocytopenic purpura (TTP) but you were informed by the nursing supervisor that plasma exchange with fresh frozen plasma is not available in hospital due to technical reason and it will take time before patient can be transferred to a facility where the said services are available. What would be your alternate plan to bridge that time?
A; High-dose plasma infusion with rate of 25-30 mL/kg per day. When immediate plasma exchange with fresh frozen plasma is not available, simple plasma infusion can be performed until transfer to a higher care facility is available. There is always a substanial risk of fluid overload with such high plasma infusion and you have to weigh risks and benefits of the clinical decision or to watch patient closely while plasma is infusing.
Reference: click to get abstract/article
High-dose plasma infusion versus plasma exchange as early treatment of thrombotic thrombocytopenic purpura/hemolytic-uremic syndrome - Medicine. 82(1):27-38, January 2003.
What if plasma exchange is not available as treatment for TTP
Q: You just diagnosed a patient with thrombotic thrombocytopenic purpura (TTP) but you were informed by the nursing supervisor that plasma exchange with fresh frozen plasma is not available in hospital due to technical reason and it will take time before patient can be transferred to a facility where the said services are available. What would be your alternate plan to bridge that time?
A; High-dose plasma infusion with rate of 25-30 mL/kg per day. When immediate plasma exchange with fresh frozen plasma is not available, simple plasma infusion can be performed until transfer to a higher care facility is available. There is always a substanial risk of fluid overload with such high plasma infusion and you have to weigh risks and benefits of the clinical decision or to watch patient closely while plasma is infusing.
Reference: click to get abstract/article
High-dose plasma infusion versus plasma exchange as early treatment of thrombotic thrombocytopenic purpura/hemolytic-uremic syndrome - Medicine. 82(1):27-38, January 2003.
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