Wednesday October 7, 2009
Vasoconstrictor extravasation
Antidote for vasoconstrictor extravasation in skin and tissues (dopamine, epinephrine, or norepinephrine) is PHENTOLAMINE. Infiltrate 5-15 mg of PHENTOLAMINE in 10 ml of normal saline into the area of extravasation as soon as possible. Treatment may be applied and effective up to 12 hours post extravasation of vasoconstrictor. Keep yourself ready for fluid bolus post treatment.
Mechanism of action: Phentolamine is a nonspecific alpha-adrenergic blocking agent which inhibits vasoconstriction and allow improved blood circulation through the affected area.
References: Click to get abstract or article
1. Treating Extravasation Injuries - extravasation.org
2. The use of phentolamine in the prevention of dopamine-induced tissue extravasation - J Crit Care 1998 Mar;13(1):13-20
Wednesday, October 7, 2009
Tuesday, October 6, 2009
Tuesday October 6, 2009
Sympathetic Storming
Sympathetic storming after traumatic brain injury remains one of the most dramatic clinical scene particularly in neurological units. It occurs due to uncontrolled sympathetic surge with a diminish or unmatch parasympathetic response. Acording to Baguley criteria 5 out of the 7 clinical features should be present -
tachycardia,
tachypnea,
hyperthermia,
hypertension,
dystonia,
posturing, and
diaphoresis
Various agents have been used for treatment (see review article below) but haloperidol may worsen the symptoms.Dr. Blackman and coll. coined the term "PAID" - paroxysmal autonomic instability with dystonia- in Archives of Neurology March 2004.
References: click to get abstract/article
1. Dysautonomia after traumatic brain injury: a forgotten syndrome? - J Neurol Neurosurg Psychiatry 1999;67:39-43 ( July )
2. Paroxysmal autonomic instability with dystonia (PAID) - Arch Neurol. October 2004;61:1625.
3. Paroxysmal Autonomic Instability with Dystonia After Brain Injury - Arch. Neurol. March 2004;61:321-328
Sympathetic Storming
Sympathetic storming after traumatic brain injury remains one of the most dramatic clinical scene particularly in neurological units. It occurs due to uncontrolled sympathetic surge with a diminish or unmatch parasympathetic response. Acording to Baguley criteria 5 out of the 7 clinical features should be present -
tachycardia,
tachypnea,
hyperthermia,
hypertension,
dystonia,
posturing, and
diaphoresis
Various agents have been used for treatment (see review article below) but haloperidol may worsen the symptoms.Dr. Blackman and coll. coined the term "PAID" - paroxysmal autonomic instability with dystonia- in Archives of Neurology March 2004.
References: click to get abstract/article
1. Dysautonomia after traumatic brain injury: a forgotten syndrome? - J Neurol Neurosurg Psychiatry 1999;67:39-43 ( July )
2. Paroxysmal autonomic instability with dystonia (PAID) - Arch Neurol. October 2004;61:1625.
3. Paroxysmal Autonomic Instability with Dystonia After Brain Injury - Arch. Neurol. March 2004;61:321-328
Monday, October 5, 2009
Monday October 5, 2009
Patients who code while on pressors have low chance of survival
Following pearl contributed by:
Tony Halat, MD
Clinical Instructor in Medicine Department of Medicine,
The Methodist Hospital
Weill Medical College, Cornell University
A small retrospective study looked at the outcome of patients who code in the ICU, including those who were on pressors prior to the code.
In this group of patients only 17% of all those who coded survived to discharge and only 4% of those already on vasopressors at the time of code survived. Interestingly the patients comprising the 4% all had underlying conditions amenable to intervention (myocardial infarction, aortic dissection).
The study concluded that the administration of vasopressors prior to the code strongly predicted non survival.
Reference: click to get article
Outcomes of cardiopulmonary resuscitation for patients on vasopressors or inotropes: A pilot study - Journa of Critical Care - Volume 24, Issue 3, Pages 415-418 (September 2009),
Patients who code while on pressors have low chance of survival
Following pearl contributed by:
Tony Halat, MD
Clinical Instructor in Medicine Department of Medicine,
The Methodist Hospital
Weill Medical College, Cornell University
A small retrospective study looked at the outcome of patients who code in the ICU, including those who were on pressors prior to the code.
In this group of patients only 17% of all those who coded survived to discharge and only 4% of those already on vasopressors at the time of code survived. Interestingly the patients comprising the 4% all had underlying conditions amenable to intervention (myocardial infarction, aortic dissection).
The study concluded that the administration of vasopressors prior to the code strongly predicted non survival.
Reference: click to get article
Outcomes of cardiopulmonary resuscitation for patients on vasopressors or inotropes: A pilot study - Journa of Critical Care - Volume 24, Issue 3, Pages 415-418 (September 2009),
Sunday, October 4, 2009
Sunday October 4, 2009
Call for dialysis in Lithium overdose
Call for dialysis in Lithium overdose
Call for Hemodialysis in Lithium toxicity is "clinical" depending on symptoms particularly neurological symptoms such as myoclonus, seizure, confusion or coma. There is no laboratory cutoff value as patient with chronic exposure to lithium may show clinical signs at much lower value. Also some recent data favors CVVHD (or HD followed by CVVHD) as it showed to prevent rebound of lithium serum concentration.
To dialyse or not to dialyse… - pwr point presentation - S. Gosselin, MD
Reference:
HD followed by continuous hemofiltration..: Am J Kidney Dis. 2001 May;37(5):1044-7
Reference:
HD followed by continuous hemofiltration..: Am J Kidney Dis. 2001 May;37(5):1044-7
Saturday, October 3, 2009
Friday, October 2, 2009
Friday October 2, 2009
Following pearl contributed by:
Tony Halat, MD
Clinical Instructor in Medicine
Department of Medicine, The Methodist Hospital
A study looked at the outcome of limited codes in which certain treatments were intentionally not provided versus full ACLS protocol codes. These limited codes had a much lower survival rate than those run with no such limitations (29.4% vs 58.6% p=0.023)
The authors concluded that limited codes have lower rates of survival and this information should be conveyed to patients and families when making decisions about code status.
Reference: click to get abstract
Analysis of limited resuscitations in patients suffering in-hospital cardiac arrest - Resuscitation. 2009 Sep;80(9):985-9. Epub 2009 Jul 5
Following pearl contributed by:
Tony Halat, MD
Clinical Instructor in Medicine
Department of Medicine, The Methodist Hospital
Weill Medical College, Cornell University
Limited codes do not work
There is no such thing as soft code
There is no such thing as soft code
A study looked at the outcome of limited codes in which certain treatments were intentionally not provided versus full ACLS protocol codes. These limited codes had a much lower survival rate than those run with no such limitations (29.4% vs 58.6% p=0.023)
The authors concluded that limited codes have lower rates of survival and this information should be conveyed to patients and families when making decisions about code status.
Analysis of limited resuscitations in patients suffering in-hospital cardiac arrest - Resuscitation. 2009 Sep;80(9):985-9. Epub 2009 Jul 5
Thursday, October 1, 2009
Thursday October 1, 2009
Clonidine and Bradycardia!
Clonidine is a alpha adrenergic agonist with sympatholytic activity and has been used for various clinical indications beside blood pressure control including treatment for migraines, menopausal complaints, narcotic and alcohol withdrawal symptoms, spasticity after spinal cord injury, attention-deficit hyperactivity disorder as well as rate control for atrial fibrillation.
Mechanism of action: Symptomatic bradycardia is a side effect of clonidine which many times go ignored. Clonidine's central effect results in decreased sympathetic outflow and enhanced vagal tone, lowering blood pressure and heart rate. This also cause side effects of drowsiness, lethargy and dry mouth. Clonidine acts peripherally within the heart to inhibit norepinephrine release, contributing to further reductions in heart rate.
Risk factors: Patients at higher risk for clonidine-induced bradycardia seem to be those with an already-diseased conduction system, renal failure, high doses of clonidine, concomitant therapy with medications known to cause bradycardia or heart block, (eg, beta-blockers, verapamil, diltiazem, digoxin).
Treatment: For severe, symptomatic bradycardia, atropine can be used. For refractory symptomatic cases, isoproterenol, epinephrine, dopamine, and pacing may be required.
Clonidine and Bradycardia!
Clonidine is a alpha adrenergic agonist with sympatholytic activity and has been used for various clinical indications beside blood pressure control including treatment for migraines, menopausal complaints, narcotic and alcohol withdrawal symptoms, spasticity after spinal cord injury, attention-deficit hyperactivity disorder as well as rate control for atrial fibrillation.
Mechanism of action: Symptomatic bradycardia is a side effect of clonidine which many times go ignored. Clonidine's central effect results in decreased sympathetic outflow and enhanced vagal tone, lowering blood pressure and heart rate. This also cause side effects of drowsiness, lethargy and dry mouth. Clonidine acts peripherally within the heart to inhibit norepinephrine release, contributing to further reductions in heart rate.
Risk factors: Patients at higher risk for clonidine-induced bradycardia seem to be those with an already-diseased conduction system, renal failure, high doses of clonidine, concomitant therapy with medications known to cause bradycardia or heart block, (eg, beta-blockers, verapamil, diltiazem, digoxin).
Treatment: For severe, symptomatic bradycardia, atropine can be used. For refractory symptomatic cases, isoproterenol, epinephrine, dopamine, and pacing may be required.
Subscribe to:
Posts (Atom)