Thursday, October 29, 2009

Thursday October 29, 2009


Q: What could be the supporting finding on lab in (Transfusion-related acute lung injury (TRALI)?



Answer: Laboratory findings may include unexpected haemoconcentration and a sudden fall in serum albumin. As in other causes of acute alveolar capillary leak, the pulmonary exudate in TRALI has a high albumin content. Peripheral blood neutropenia has been reported but neutrophilia is more common.



Reference:

The pathology of transfusion-related acute lung injury. Am J Clin Pathol 1999; 112: 216–21

Wednesday, October 28, 2009

Wednesday October 28, 2009
Reference Standard Change for Heparin

Source: www.fda.gov/Safety/medwatch

Effective October 1, 2009, there is a new reference standard and test method to determine the potency of heparin, as well as, impurities in heparin. This change will result in a 10% reduction in potency of heparin marketed in the United States.

Clinicians should take caution with monitoring and dosing, as more heparin may be needed to achieve and maintain desired level of anticoagulation in patients.

Product with the new “USP unit” potency definition will be available on or after October 8, 2009. Most manufacturers will place an “N” next to the lot number to indicate that the vial is of the new potency.

Tuesday, October 27, 2009

Tuesday October 27, 2009
Sulfonylurea overdose


Anti-diabetic pills overdose remained one of the leading cause of drug overdose worldwide. Among anti-diabetic pills sulfonylureas are the most dangerous and hard to correct. Overdose of metformin rarely causes clinically evident hypoglycemia (It has its own danger of cardiovascular collapse and renal failure, due to severe lactic acidosis).

Unfortunately very few clinicians use the real antidote for sulfonylurea which is Octreotide (Sandostatin) in resistant hypoglycemia. Infusion of glucose to achieve euglycemia in the early phase is an appropriate treatment but there is some literature available which argues that prolong infusion of dextrose in sulfonylurea overdose may make hypoglycemia longer and worse by stimulating insulin release. The dose for Octreotide is 50 mcg SC every 8 hours with adjustment of dose according to blood glucose level. Octreotide is a somatostatin analogue, which activates G-protein K channel and hyperpolarization of the beta cell results in inhibition of Ca influx and insulin release. Another antidote for sulfonylurea overdose beside octreotide is Diazoxide.

Exact mechanism is unknow but probably it increases blood glucose by inhibiting pancreatic insulin release. It is found to be effective within 60 minutes of administration. The usual dose is 5 mg/kg/day intravenously and should be divided every 8 hours. Dose can be increased if needed but still its experience in comparison to octreotide is limited.



References: click to get abstracts/articles

1. Octreotide for sulfonylurea-induced hypoglycemia following overdose - The Annals of Pharmacotherapy: Vol. 36, No. 11, pp. 1727-1732

2. Clinical spectrum of sulfonylurea overdose and experience with diazoxide therapy - Archives of Internal Medicine Vol. 151 No. 9, September 1, 1991

Monday, October 26, 2009

Monday October 26, 2009
Going back to basics


Q: Explain Ejection fraction (Ef)?

Answer: By definition, the volume of blood within a ventricle immediately before a contraction is known as the end-diastolic volume. Similarly, the volume of blood left in a ventricle at the end of contraction is end-systolic volume. The difference between end-diastolic and end-systolic volumes is the stroke volume, the volume of blood ejected with each beat. Ejection fraction (Ef) is the fraction of the end-diastolic volume that is ejected with each beat; that is, it is stroke volume (SV) divided by end-diastolic volume (EDV):


Ef = SV/EDV
OR
Ef = EDV-ESV/EDV


In a healthy 70-kg (154-lb) man, the SV is approximately 70 ml (left ventricular ESV is 50 ml and the left ventricular EDV is 120 ml) giving an ejection fraction of 70/120, or 0.58 (58%)

Sunday, October 25, 2009

Sunday October 25, 2009


Q: What is the basis of treatment for Torsade de Pointes?

Answer: The basis of treatment for Torsade de Pointe is sppression of early afterdepolarizations.

Magnesium is the drug of choice for suppressing EADs and terminating the arrhythmia. This is achieved by decreasing the influx of calcium, thus lowering the amplitude of EADs. Magnesium is effective even in patients with normal magnesium levels.

Some authorities recommend supplemental potassium to increase the potassium concentration to high normal, which increases the efflux of potassium from myocardial cells, thus causing rapid repolarization.

Saturday, October 24, 2009

Saturday October 24, 2009
Medical Trivia


Do you know that -

Coumadin was first approved for medical use in humans in 1954. And a famous early recipient of warfarin was US president Dwight Eisenhower, who was prescribed the drug after having a heart attack in 1955.


Reference: The discovery of dicumarol and its sequels - Circulation. 1959 Jan;19(1):97-107

Friday, October 23, 2009

Friday October 23, 2009
Dexmedetomidine (precedex) reduce total extubation time?


Giving a patient dexmedetomidine prior to removing respiratory ventilation support reduced the total extubation time, according to research presented at the American Society of Anesthesiologists (ASA) 2009 annual meeting held this week in New Orleans. Researchers also found using the sedative resulted in fewer ventilator days and more successful extubation.

“Currently, if a patient cannot be successfully extubated, no viable alternative exists aside from performing additional weaning attempts and, in some cases, a tracheotomy,” said lead author Julin F. Tang, MD, MS, FCCM, clinical professor, Department of Anesthesia and Perioperative Care at San Francisco General Hospital. “This is tremendously hard on the patient. Now, based on the results of this study, dexmedetomidine may be a viable option for patients who have failed previous attempts to remove the respiratory tubes because it appears to inhibit a stress response in the body that can make it difficult to extubate.”

The prospective, randomized, controlled, IRB-approved study, "Dexmedetomidine Facilitates Extubation in Agitated SICU Patients Failing Previous Weaning Attempts," was conducted among 20 critically ill, intensive care patients who had failed previous attempts to remove ventilation support.

Participants not in the control group received dexmedetomidine at 0.5 or 0.7 mcg/kg/hr. Background sedation and analgesia were gradually decreased in the treatment group, and aerosolized lidocaine was initiated prior to weaning. Shortly after dexmedetomidine infusion, pressure support ventilation (PSV) was initiated and patients were weaned and extubated. Researchers measured the medication treatment group’s condition by checking the subjects’ arterial blood gases at three different points throughout the trial.

Following extubation, the amount of time required to take the tube out was distinctly shorter in patients who received dexmedetomidine. Ventilator time was shorter in these patients, and the rate of successful extubation was higher in the treatment group than the control group.

“Although the study size was relatively small, these results suggest that dexmedetomidine infusion during the weaning process may help control those problems that cause weaning attempts to fail such as agitation, tachypnea, tachycardia, and hypertension,” said Tang. “If a patient has these reactions, the medical team must refrain from pulling out the ventilator tube and try again the next day, which adds to the patient’s hospital costs as well as stress level.”


References: Click to get article

1. Study on the Use of Dexmedetomidine to Facilitate Extubation in Surgical Intensive-Care-Unit Patients Who Failed Previous Weaning Attempts - clinicaltrials.gov

2. Use of dexmedetomidine to facilitate extubation in surgical ICU patients who failed previous weaning attempts following prolonged mechanical ventilation: A pilot study - Respir Care 2006;51 (5):492-496.

3. Feasibility of dexmedetomidine in facilitating extubation in the intensive care unit - Journal of Clinical Pharmacy and Therapeutics, Volume 33 Issue 1, Pages 25 - 30, Published Online: 17 Jan 2008