Q; Troponins, once secreted, remains elevated for how many days?
Answer: Troponin, once secreted, remains elevated for 7-10 days.
Saturday, August 8, 2009
Friday, August 7, 2009
Friday August 7, 2009 (pediatric pearl)
Uniqueness of Pediatric Lower Airway - Part 2
(see Uniqueness of Pediatric Lower Airway - Part 1 here)
The frequency of acute respiratory failure is higher in infants and young children than in adults for several reasons. This difference can be explained by defining anatomic compartments and their developmental differences in pediatric patients that influence susceptibility to acute respiratory failure.
The intrathoracic airways and lung include the conducting airways and alveoli, the interstitia, the pleura, the lung lymphatics, and the pulmonary circulation. Noteworthy differences among pediatric children include the following:
Uniqueness of Pediatric Lower Airway - Part 2
(see Uniqueness of Pediatric Lower Airway - Part 1 here)
The frequency of acute respiratory failure is higher in infants and young children than in adults for several reasons. This difference can be explained by defining anatomic compartments and their developmental differences in pediatric patients that influence susceptibility to acute respiratory failure.
The intrathoracic airways and lung include the conducting airways and alveoli, the interstitia, the pleura, the lung lymphatics, and the pulmonary circulation. Noteworthy differences among pediatric children include the following:
- Infants and young children have fewer alveoli than do adults. The number dramatically increases during childhood, from approximately 20 million after birth to 300 million by 8 years of age. Therefore, infants and young children have a relatively small area for gas exchange.
- The alveolus is small. Alveolar size increases from 150-180 to 250-300 µm during childhood.
- Collateral ventilation is not fully developed; therefore, atelectasis is more common in children than in adults. During childhood, anatomic channels form to provide collateral ventilation to alveoli. These pathways are between adjacent alveoli (pores of Kohn), bronchiole and alveoli (Lambert channel), and adjacent bronchioles. This important feature allows alveoli to participate in gas exchange even in the presence of an obstructed distal airway.
- Smaller intrathoracic airways are more easily obstructed than larger ones. With age, the airways enlarge in diameter and length.
- Infants and young children have relatively little cartilaginous support of the airways. As cartilaginous support increases, dynamic compression during high expiratory flow rates is prevented.
Thursday, August 6, 2009
Thursday August 6, 2009
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
Wednesday, August 5, 2009
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:
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
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.
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
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:
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.
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
Saturday, August 1, 2009
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