Sunday March 23, 2008
Dilantin in Torsade
Q: Which anti-seizure drug can be use in the treatment of Torsade de pointes if conventional therapy fails?
A: Phenytoin (Dilantin).
References:
1. Torsades de pointes therapy with phenytoin - Ann Emerg Med.1991 Feb;20(2):198-200.
2. Few case reports from literature: remarkablemedicine.com
Sunday, March 23, 2008
Saturday, March 22, 2008
Saturday March 22, 2008
Q: Once patient receive Digoxin Fragmented Antibody (DIGIFAB or Digibind), how frequent digoxin level should be measured ?
A: Digoxin level after giving Digibind will rise and will remain distorted for about 7 days. This is due to ability of Digibind to pull all of the digoxin into blood stream. These are inactive fragments and not toxic. There is no need to follow Dig level after administration of Digibind as it will be erroneously high and misleading.
Q: Once patient receive Digoxin Fragmented Antibody (DIGIFAB or Digibind), how frequent digoxin level should be measured ?
A: Digoxin level after giving Digibind will rise and will remain distorted for about 7 days. This is due to ability of Digibind to pull all of the digoxin into blood stream. These are inactive fragments and not toxic. There is no need to follow Dig level after administration of Digibind as it will be erroneously high and misleading.
Friday, March 21, 2008
Friday March 21, 2008
"Locked-in" Syndrome (coma vigilante)
"patient is a silent and unresponsive witness to everything that is happening" - from story of Nick Chisholm 1
Patient with Locked-in syndrome is a fully conscious person, but all the voluntary muscles of the body are completely paralyzed, other than those that control eye movement. Term was first introduced about 25 years ago by Plum and Posner with complete occlusion of the basilar artery. 3
Any catastrophy involving ventral pons can cause this syndrome like massive stroke, traumatic head injury, ruptured aneurysm, pontine infarction after prolonged vertebrobasilar ischaemia, haemorrhage, tumor, central pontine myelinolysis, pontine abscess or postinfective polyneuropathy. As all of the nerve tracts responsible for voluntary movement pass through the ventral pons but fortunately or unfortunately, consciousness are above the level of the ventral pons. 2
Only supportive rehabilitation is the answer. Being an intensivist, it is extremely important to educate staff and to protect patient from any physical or psychological harm (like procedure without adequate analgesia), with upmost understanding that it is an "imprisoned mind buried alive in a dead body’’ (as said for character with paralysis like locked-in syndrome in Thérèse Raquin by Emile Zola - 1868).
References: Click to get articles/abstract
1. The patient's journey: Living with locked-in syndrome - BMJ 2005;331:94-97 (9 July)
2. Locked-in Syndrome - enotes.com
3. Plum F, Posner JB. The diagnosis of stupor and coma. Philadelphia: FA Davis, 1982; 377
4. Locked-in syndrome: a catastrophic complication after surgery - British Journal of Anaesthesia, 2004, Vol. 92, No. 2 286-288
"Locked-in" Syndrome (coma vigilante)
"patient is a silent and unresponsive witness to everything that is happening" - from story of Nick Chisholm 1
Patient with Locked-in syndrome is a fully conscious person, but all the voluntary muscles of the body are completely paralyzed, other than those that control eye movement. Term was first introduced about 25 years ago by Plum and Posner with complete occlusion of the basilar artery. 3
Any catastrophy involving ventral pons can cause this syndrome like massive stroke, traumatic head injury, ruptured aneurysm, pontine infarction after prolonged vertebrobasilar ischaemia, haemorrhage, tumor, central pontine myelinolysis, pontine abscess or postinfective polyneuropathy. As all of the nerve tracts responsible for voluntary movement pass through the ventral pons but fortunately or unfortunately, consciousness are above the level of the ventral pons. 2
Only supportive rehabilitation is the answer. Being an intensivist, it is extremely important to educate staff and to protect patient from any physical or psychological harm (like procedure without adequate analgesia), with upmost understanding that it is an "imprisoned mind buried alive in a dead body’’ (as said for character with paralysis like locked-in syndrome in Thérèse Raquin by Emile Zola - 1868).
References: Click to get articles/abstract
1. The patient's journey: Living with locked-in syndrome - BMJ 2005;331:94-97 (9 July)
2. Locked-in Syndrome - enotes.com
3. Plum F, Posner JB. The diagnosis of stupor and coma. Philadelphia: FA Davis, 1982; 377
4. Locked-in syndrome: a catastrophic complication after surgery - British Journal of Anaesthesia, 2004, Vol. 92, No. 2 286-288
Thursday, March 20, 2008
Thursday March 20, 2008
MINI MENTAL STATUS EXAM (MMSE)
Although older adults are at higher risk than the rest of the population, changes in cognitive function often call for prompt and aggressive action, particularly in hospital / ICU setting. The Mini Mental State Examination (MMSE) is a tool that can be used systematically. It is an 11-question measure that tests five areas of cognitive function:
The maximum score is 30. A score of 23 or lower is indicative of cognitive impairment. The MMSE takes only 5-10 minutes to administer and has been validated in clinical practice.
MINI MENTAL STATUS EXAM (MMSE)
Although older adults are at higher risk than the rest of the population, changes in cognitive function often call for prompt and aggressive action, particularly in hospital / ICU setting. The Mini Mental State Examination (MMSE) is a tool that can be used systematically. It is an 11-question measure that tests five areas of cognitive function:
- orientation,
- registration,
- attention and calculation,
- recall, and
- language
The maximum score is 30. A score of 23 or lower is indicative of cognitive impairment. The MMSE takes only 5-10 minutes to administer and has been validated in clinical practice.
Wednesday, March 19, 2008
Wednesday March 19, 2008
Case: You inserted central line. While you were on your way to check CXR to confirm line placement, nurse request you to check KUB also to confirm enteral feeding tube placement (DHT). Interestingly, KUB shot this morning had IVC filter which is no more present there ?
Answer: Guide wire during central line procedure probably travelled into inferior vena cava and dislodged IVC filter !!!
Reference: click to get abstract / article
1. Guidewire Dislodgment of Inferior Vena Cava Filters During Insertion of Central Venous Catheters, Vascular and Endovascular Surgery, Vol. 31, No. 5, 587-593 (1997)
2. Direct measurement of the distance from subclavian and internal jugular vein access sites to the superior vena cava-atrial junction during central venous catheter placement. Crit Care Med 2000; 28: 138–42
3. Greenfield Inferior Vena Cava Filter Dislodged During Central Venous Catheter placement, Chest 1994;106;957-959
Case: You inserted central line. While you were on your way to check CXR to confirm line placement, nurse request you to check KUB also to confirm enteral feeding tube placement (DHT). Interestingly, KUB shot this morning had IVC filter which is no more present there ?
Answer: Guide wire during central line procedure probably travelled into inferior vena cava and dislodged IVC filter !!!
Related previous pearls:
Reference: click to get abstract / article
1. Guidewire Dislodgment of Inferior Vena Cava Filters During Insertion of Central Venous Catheters, Vascular and Endovascular Surgery, Vol. 31, No. 5, 587-593 (1997)
2. Direct measurement of the distance from subclavian and internal jugular vein access sites to the superior vena cava-atrial junction during central venous catheter placement. Crit Care Med 2000; 28: 138–42
3. Greenfield Inferior Vena Cava Filter Dislodged During Central Venous Catheter placement, Chest 1994;106;957-959
Tuesday, March 18, 2008
Tuesday March 18, 2008
Case: 57 year old female, newly hemodialysis patient, transferred from floor to ICU after she developed seizure at the end of her dialysis session. No significant risk factor could be find otherwise. Nurse reports patient appear irritable and restless before episode and complain of headache, nausea and blurred vision. While resident was called to evaluate as patient also noticed to have muscular twitching and confusion, symptoms progressed and seizure was witnessed.
Answer: Dialysis disequilibrium syndrome.
Dialysis disequilibrium syndrome is common during hemodialysis particularly patient’s first few dialysis sessions. It is characterized by neurologic symptoms of varying severity and actually may lead to herniation and death. The rapid reduction in BUN lowers the plasma osmolality, creating a transient osmotic gradient that promotes water movement into the cells, causing cerebral edema and consequently acute neurologic dysfunction. With better understanding of the process and newer dialysis techniques, severe form of syndrome is now not commonly seen. This not only explains that why our nephrology colleagues start with gentle but frequent sessions but also explains one of the several benefits of mannitol during dialysis.
Read interesting article from University of Calgary, Alberta, Canada : Dialysis Disequilibrium Syndrome: Brain death following hemodialysis for metabolic acidosis and acute renal failure - A case report followed with discussion and different management modalities (Ref.: BMC Nephrol. 2004; 5: 9.)
Case: 57 year old female, newly hemodialysis patient, transferred from floor to ICU after she developed seizure at the end of her dialysis session. No significant risk factor could be find otherwise. Nurse reports patient appear irritable and restless before episode and complain of headache, nausea and blurred vision. While resident was called to evaluate as patient also noticed to have muscular twitching and confusion, symptoms progressed and seizure was witnessed.
Answer: Dialysis disequilibrium syndrome.
Dialysis disequilibrium syndrome is common during hemodialysis particularly patient’s first few dialysis sessions. It is characterized by neurologic symptoms of varying severity and actually may lead to herniation and death. The rapid reduction in BUN lowers the plasma osmolality, creating a transient osmotic gradient that promotes water movement into the cells, causing cerebral edema and consequently acute neurologic dysfunction. With better understanding of the process and newer dialysis techniques, severe form of syndrome is now not commonly seen. This not only explains that why our nephrology colleagues start with gentle but frequent sessions but also explains one of the several benefits of mannitol during dialysis.
Read interesting article from University of Calgary, Alberta, Canada : Dialysis Disequilibrium Syndrome: Brain death following hemodialysis for metabolic acidosis and acute renal failure - A case report followed with discussion and different management modalities (Ref.: BMC Nephrol. 2004; 5: 9.)
Monday, March 17, 2008
Monday March 17, 2008
DVT prophylaxis - our poor record card !!
Dr. Alpesh Amin and coll. from School of Medicine, University of California, Irvine, looked into thromboprophylaxis rates in US medical centers: and guess what? We failed miserably !
Methods: Patients included were
- 40 years old or more,
- with a length of hospital stay of 6 days or more, and
- had no contraindications for anticoagulation
A total of 196,104 discharges from 227 hospitals met the inclusion criteria.
Results:
- The overall VTE thromboprophylaxis rate was 61.8%, although the appropriate thromboprophylaxis rate was only 33.9%.
- Of the 66.1% discharged patients who did not receive appropriate thromboprophylaxis, 38.4% received no prophylaxis,
- 4.7% received mechanical prophylaxis only,
- 6.3% received an inappropriate dosage, and
- 16.7% received an inappropriate prophylaxis duration
(based on ACCP recommendations)
Conclusions: This study highlights the low rates of appropriate thromboprophylaxis in US acute-care hospitals, with two-thirds of discharged patients not receiving prophylaxis in accordance with the 6th ACCP guidelines. More effort is required to improve the use of appropriate thromboprophylaxis in accordance with the ACCP recommendations.
Reference: click to get article / abstract
Thromboprophylaxis rates in US medical centers: success or failure? - Journal of Thrombosis and Haemostasis, Volume 5 Issue 8 Page 1610-1616, August 2007
Sunday, March 16, 2008
Sunday March 16, 2008
Propofol lipidic infusion promotes resistance to antifungals !
See this interesting study explaining why sometime antifungals do not work ! and why there are discrepancies between in vitro and in vivo susceptibility to antifungals.
During study, Candida and Aspergillus were studied regarding the ability to grow and its susceptibility profile to antifungals in the presence of propofol infusion and its lipidic vehicle.
The intensity of fluorescence after staining with FUN1, in the presence and absence of propofol infusion, was determined by flow cytometry. Radioactivity assays were also performed in order to quantify the input of [3H]- itraconazole into the fungal cell in the presence of propofol. Assays were repeated after addition of sodium azide, in order to block efflux pumps.
Results
Conclusion
Propofol infusion, due to its lipidic vehicle, increased the fungal germination and promoted resistance to antifungals. This effect seems to be related to the reduced access and/or permeabilization to fungal cells by antifungals.
Reference: click to get article / abstract
Propofol lipidic infusion promotes resistance to antifungals by reducing drug input into the fungal cell - BMC Microbiol. 2008; 8: 9. - pdf non-pdf version is available here
Propofol lipidic infusion promotes resistance to antifungals !
See this interesting study explaining why sometime antifungals do not work ! and why there are discrepancies between in vitro and in vivo susceptibility to antifungals.
During study, Candida and Aspergillus were studied regarding the ability to grow and its susceptibility profile to antifungals in the presence of propofol infusion and its lipidic vehicle.
The intensity of fluorescence after staining with FUN1, in the presence and absence of propofol infusion, was determined by flow cytometry. Radioactivity assays were also performed in order to quantify the input of [3H]- itraconazole into the fungal cell in the presence of propofol. Assays were repeated after addition of sodium azide, in order to block efflux pumps.
Results
- Propofol infusion promoted budding of Candida and the germination of Aspergillus, latter forming a lipid layer around the hypha.
- An increase of minimal fungicidal concentrations regarding both Candida and Aspergillus strains was found for all antifungals when incubated simultaneously with propofol infusion.
- A decrease of the intensity of fluorescence of Candida cells was systematically observed, as well as a significant reduced intracellular uptake of [3H] itraconazole in cells treated with propofol infusion, even after the blockade of efflux pumps.
Conclusion
Propofol infusion, due to its lipidic vehicle, increased the fungal germination and promoted resistance to antifungals. This effect seems to be related to the reduced access and/or permeabilization to fungal cells by antifungals.
Reference: click to get article / abstract
Propofol lipidic infusion promotes resistance to antifungals by reducing drug input into the fungal cell - BMC Microbiol. 2008; 8: 9. - pdf non-pdf version is available here
Saturday, March 15, 2008
Friday, March 14, 2008
Friday March 14, 2008
Four generations of Quinolones
The classification of the fluoroquinolones on the basis of generations (imitating from cephalosporins) is not officially standardized, but it is now commonly use to classify them by their spectrum of action.
1st generation - Gram negative coverage but not pseudomonas (example: Nalidixic acid)
2nd generation - Gram negative coverage with pseudomonas and some gram postive coverage including s.aureus but not strep pneumoniae. (example: Ciprofloxacin, Ofloxacin, Norfloxacin)
3rd generation - Gram negative coverage with pseudomonas. More gram postive coverage including penicillin sensitive and resistant s. pneumoniae. (example: Levofloxacin, Sparfloxacin, Gatifloxacin (tequin), Moxifloxacin (avalox)). Avalox has been said to be the most effective in this generation.
4th generation - Same as 3rd generation but with anaerobic coverage (example: Trovafloxacin (Trovan) ).
Read comprehensive review on Quinolones (Source: Am Fam Physician 2002;65:455-64, authors: CATHERINE M. OLIPHANT, PHARM.D., University of Wyoming School of Pharmacy and GARY M. GREEN, M.D., Kaiser Permanente, California)
Four generations of Quinolones
The classification of the fluoroquinolones on the basis of generations (imitating from cephalosporins) is not officially standardized, but it is now commonly use to classify them by their spectrum of action.
1st generation - Gram negative coverage but not pseudomonas (example: Nalidixic acid)
2nd generation - Gram negative coverage with pseudomonas and some gram postive coverage including s.aureus but not strep pneumoniae. (example: Ciprofloxacin, Ofloxacin, Norfloxacin)
3rd generation - Gram negative coverage with pseudomonas. More gram postive coverage including penicillin sensitive and resistant s. pneumoniae. (example: Levofloxacin, Sparfloxacin, Gatifloxacin (tequin), Moxifloxacin (avalox)). Avalox has been said to be the most effective in this generation.
4th generation - Same as 3rd generation but with anaerobic coverage (example: Trovafloxacin (Trovan) ).
Read comprehensive review on Quinolones (Source: Am Fam Physician 2002;65:455-64, authors: CATHERINE M. OLIPHANT, PHARM.D., University of Wyoming School of Pharmacy and GARY M. GREEN, M.D., Kaiser Permanente, California)
Thursday, March 13, 2008
Thursday March 13, 2008
Feeding tube in Brain !
Any procedure, how simple it sounds, may turn into a nightmare. See following images where feeding tube travelled upward in brain.
See important read: VERIFICATION OF FEEDING TUBE PLACEMENT (Ref; American Association of Critical-Care Nurses ) - pdf file
Feeding tube in Brain !
Any procedure, how simple it sounds, may turn into a nightmare. See following images where feeding tube travelled upward in brain.
See important read: VERIFICATION OF FEEDING TUBE PLACEMENT (Ref; American Association of Critical-Care Nurses ) - pdf file
Wednesday, March 12, 2008
Wednesday March 12, 2008
Restless Legs syndrome
Restless legs syndrome is a common condition in non-intubated patients which may get aggravated by ICU enviroment. Major factors associated with Restless Leg Syndrome in ICU are
Various pharmacological agents have been described and used with success including benzodiazepines, carbamazepine and clonidine. In ICU situation, one useful drug in this regard is Ropinirole which is a Dopamine agonist. One of the effect of Ropinirole is heavy sleepiness, which can be use as a bonus benefit in ICU. Dose can be initiated from .25 mg PO QHS upto 4 mg PO QHS.
References: (click to get abstract)
1. Restless Legs Syndrome: Detection and Management in Primary Care - NATIONAL HEART, LUNG, AND BLOOD INSTITUTE WORKING GROUP ON RESTLESS LEGS SYNDROME - Vol. 62/No. 1 (July 1, 2000) - American Family Physician.
2. Ropinirole is effective in the treatment of restless legs syndrome. TREAT RLS 2: a 12-week, double-blind, randomized, parallel-group, placebo-controlled study - Mov Disord. 2004 Dec;19(12):1414-23.
Restless Legs syndrome
Restless legs syndrome is a common condition in non-intubated patients which may get aggravated by ICU enviroment. Major factors associated with Restless Leg Syndrome in ICU are
- Iron-deficiency anemia
- Peripheral neuropathy
- Withdrawal from vasodilator drugs and sedatives
- Cigarette smoking, alcohol and caffeine withdrawal
- Various drugs including phenytoin, antidepressant drugs, H2 blockers, lithium, beta-blockers and antipsychotics
- Hypomagnesemia
- Renal insufficiency (uremia)
Various pharmacological agents have been described and used with success including benzodiazepines, carbamazepine and clonidine. In ICU situation, one useful drug in this regard is Ropinirole which is a Dopamine agonist. One of the effect of Ropinirole is heavy sleepiness, which can be use as a bonus benefit in ICU. Dose can be initiated from .25 mg PO QHS upto 4 mg PO QHS.
References: (click to get abstract)
1. Restless Legs Syndrome: Detection and Management in Primary Care - NATIONAL HEART, LUNG, AND BLOOD INSTITUTE WORKING GROUP ON RESTLESS LEGS SYNDROME - Vol. 62/No. 1 (July 1, 2000) - American Family Physician.
2. Ropinirole is effective in the treatment of restless legs syndrome. TREAT RLS 2: a 12-week, double-blind, randomized, parallel-group, placebo-controlled study - Mov Disord. 2004 Dec;19(12):1414-23.
Tuesday, March 11, 2008
Tuesday March 11, 2008
Efficacy of risperidone for prevention of postoperative delirium in cardiac surgery
Interesting study particularly for folks working in cardio-thoracic ICUs. This randomised, double-blinded, placebo-controlled study was primarily aimed to evaluate the potential of risperidone to prevent postoperative delirium following cardiac surgery with cardiopulmonary bypass. The secondary objective was to explore clinical factors associated with postoperative delirium.
Number: 126 adult patients undergoing elective cardiac surgery with cardiopulmonary bypass were randomly assigned to receive either 1 mg of risperidone or placebo sublingually when they regained consciousness.
The confusion assessment method for intensive care unit was used to assess postoperative delirium.
Results:
Reference:
Efficacy of risperidone for prevention of postoperative delirium in cardiac surgery - Anest. and Intensive care, Volume 35, No. 5, 2007, 714-719
Efficacy of risperidone for prevention of postoperative delirium in cardiac surgery
Interesting study particularly for folks working in cardio-thoracic ICUs. This randomised, double-blinded, placebo-controlled study was primarily aimed to evaluate the potential of risperidone to prevent postoperative delirium following cardiac surgery with cardiopulmonary bypass. The secondary objective was to explore clinical factors associated with postoperative delirium.
Number: 126 adult patients undergoing elective cardiac surgery with cardiopulmonary bypass were randomly assigned to receive either 1 mg of risperidone or placebo sublingually when they regained consciousness.
The confusion assessment method for intensive care unit was used to assess postoperative delirium.
Results:
- The incidence of postoperative delirium in the risperidone group was lower than the placebo group (11.1% vs. 31.7% ).
- Other postoperative outcomes were not statistically different between the groups.
- Many factors were associated with postoperative delirium. However multiple logistic regression analysis showed a lapse of 70 minutes from the time of opening eyes to following commands and postoperative respiratory failure were independent risk factors.
Conclusion: A single dose of risperidone administered soon after cardiac surgery with cardiopulmonary bypass reduces the incidence of postoperative delirium. Multiple factors tended to be associated with postoperative delirium, but only the time from opening eyes to following commands and postoperative respiratory failure were independent risk factors in this study.
Reference:
Efficacy of risperidone for prevention of postoperative delirium in cardiac surgery - Anest. and Intensive care, Volume 35, No. 5, 2007, 714-719
Monday, March 10, 2008
Sunday, March 9, 2008
Sunday March 9, 2008
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
Saturday, March 8, 2008
Saturday March 8, 2008
Response to Warfarin during Initial Anticoagulation is genes dependent !
We all are aware of situations where warfarin (coumadin) takes forever to get upto therapeutic level despite escalating dose. One study of 297 patients who were starting warfarin therapy, is published this week in The New England Journal of Medicine.
2 genotypes were assessed CYP2C9 genotypes VKORC1 haplotypes
Study found that initial variability in the INR response to warfarin was more strongly associated with genetic variability in the pharmacologic target of warfarin, VKORC1, than with CYP2C9.
Reference: click to get abstract/article
1. Genetic Determinants of Response to Warfarin during Initial Anticoagulation - Number 10, Volume 358:999-1008, March 6, 2008, The New England Journal of Medicine
Response to Warfarin during Initial Anticoagulation is genes dependent !
We all are aware of situations where warfarin (coumadin) takes forever to get upto therapeutic level despite escalating dose. One study of 297 patients who were starting warfarin therapy, is published this week in The New England Journal of Medicine.
2 genotypes were assessed CYP2C9 genotypes VKORC1 haplotypes
Study found that initial variability in the INR response to warfarin was more strongly associated with genetic variability in the pharmacologic target of warfarin, VKORC1, than with CYP2C9.
Reference: click to get abstract/article
1. Genetic Determinants of Response to Warfarin during Initial Anticoagulation - Number 10, Volume 358:999-1008, March 6, 2008, The New England Journal of Medicine
Friday, March 7, 2008
Friday March 7, 2008
Ice test - Poor man's test for Myasthenia Gravis
Most of the Myasthenia patients along with other symptoms of weakness usually exhibits ptosis. While at bedside place an ice cube over eye lids for 2 minutes. Cooling improves neuromuscular transmission. Resolution of ptosis with cooling is a positive test for Myasthenia Gravis and reported upto 80% reliable to diagnose ocular myasthenia.
Related: Click here to read good review article on Myasthenia Gravis ( Dr. Milind J. Kothari The Journal of the American Osteopathic Association.Vol 104 • No 9 • Sept. 2004 • 377-384)
Ice test - Poor man's test for Myasthenia Gravis
Most of the Myasthenia patients along with other symptoms of weakness usually exhibits ptosis. While at bedside place an ice cube over eye lids for 2 minutes. Cooling improves neuromuscular transmission. Resolution of ptosis with cooling is a positive test for Myasthenia Gravis and reported upto 80% reliable to diagnose ocular myasthenia.
Related: Click here to read good review article on Myasthenia Gravis ( Dr. Milind J. Kothari The Journal of the American Osteopathic Association.Vol 104 • No 9 • Sept. 2004 • 377-384)
Thursday, March 6, 2008
Thursday March 6, 2008
Q; While you prescribe 15 mmol of intravenous (IV) potassium phosphate to patient, what amount of potassium is received by patient ?
A; About 20 meq
To be precise, 1 mmol of intravenous phophate delivers 1.46 meq of potassium in "K-phos rider".
To make it in round figure, 7.5 mmol of phosphate is equal to about 10 meq of potassium.
By mouth repletion of phosphate is preferable but if used, intravenous phosphate should be given very slowly. Usual recommended infusion rate is 5 mmol/hour. Rapid phosphate infusion may lead to precipitous fall in serum calcium, hypotension, and acute renal failure. Also, it may lead to hypomagnesemia, metastatic soft tissue calcifications, hypernatremia and volume loss from osmotic diuresis.
Reference: click to get article / abstract
Intravenous phosphate repletion regimen for critically ill patients with moderate hypophosphatemia - Critical Care Medicine. 23(7):1204-1210, July 1995.
Q; While you prescribe 15 mmol of intravenous (IV) potassium phosphate to patient, what amount of potassium is received by patient ?
A; About 20 meq
To be precise, 1 mmol of intravenous phophate delivers 1.46 meq of potassium in "K-phos rider".
To make it in round figure, 7.5 mmol of phosphate is equal to about 10 meq of potassium.
By mouth repletion of phosphate is preferable but if used, intravenous phosphate should be given very slowly. Usual recommended infusion rate is 5 mmol/hour. Rapid phosphate infusion may lead to precipitous fall in serum calcium, hypotension, and acute renal failure. Also, it may lead to hypomagnesemia, metastatic soft tissue calcifications, hypernatremia and volume loss from osmotic diuresis.
Reference: click to get article / abstract
Intravenous phosphate repletion regimen for critically ill patients with moderate hypophosphatemia - Critical Care Medicine. 23(7):1204-1210, July 1995.
Wednesday, March 5, 2008
Wednesday March 5, 2008
Bedside precaution
If patient is recieving Lactate Ringer's solution, than lactate level should not be drawn from same infusion catheter to avoid erroneously high level of lactate. It should be drawn from catheter at any other site of body or peripherally.
Though, once inside circulation lactate ringer does not have any clinically significant effect on serum lactate level.
Reference: click to get abstract / article
1. Effects of crystalloid solutions on circulating lactate concentrations: Part 1. Implications for the proper handling of blood specimens obtained from critically ill patients - Critical Care Medicine. 25(11):1840-1846, November 1997
Bedside precaution
If patient is recieving Lactate Ringer's solution, than lactate level should not be drawn from same infusion catheter to avoid erroneously high level of lactate. It should be drawn from catheter at any other site of body or peripherally.
Though, once inside circulation lactate ringer does not have any clinically significant effect on serum lactate level.
Reference: click to get abstract / article
1. Effects of crystalloid solutions on circulating lactate concentrations: Part 1. Implications for the proper handling of blood specimens obtained from critically ill patients - Critical Care Medicine. 25(11):1840-1846, November 1997
Tuesday, March 4, 2008
Tuesday March 4, 2008
Q; One bag unit of cryoprecipitate is expected to raise fibrinogen by what level?
A; A bag of transfused cryoprecipitate is expected to raise the fibrinogen level by a minimum of 30 mg/dL with a half life of 3 to 6 days. Fibrinogen levels of more than 100 mg/dL generally are considered adequate for hemostasis.
Q; One bag unit of cryoprecipitate is expected to raise fibrinogen by what level?
A; A bag of transfused cryoprecipitate is expected to raise the fibrinogen level by a minimum of 30 mg/dL with a half life of 3 to 6 days. Fibrinogen levels of more than 100 mg/dL generally are considered adequate for hemostasis.
Monday, March 3, 2008
Monday March 3, 2008
Q; During lumbar puncture (LP), what is the normal rate of cerebrospinal fluid (CSF) escape via needle into collecting tube ?
A; 1 drop per second
While performing LP, CSF should drop into tube with approximate rate of one drop/sec. A continuous stream of CSF indicates raised intrameningeal pressure.
Sunday, March 2, 2008
Sunday March 2, 2008
Q; 37 year old male admitted to ICU with inability to walk and severe pain in lower extremities. On examination in ER, he was found to have cold feet. No pulses were palpable even in femoral area. Previous record available in hospital computer shows outpatient visits to urology clinic for 'impotency' ?
Answer: Leriche's syndrome
Leriche's syndrome is a triad of
It usually affects males caused by atheromatous involvement or occlusion of the abdominal aorta by a thrombus just above the site of its bifurcation. Onset usually between 30 and 40 years of age. Treatment is surgical.
1. Leriche syndrome. Surgical procedures and early and late results - Angiology. 1997 Jul;48(7):637-42
Q; 37 year old male admitted to ICU with inability to walk and severe pain in lower extremities. On examination in ER, he was found to have cold feet. No pulses were palpable even in femoral area. Previous record available in hospital computer shows outpatient visits to urology clinic for 'impotency' ?
Answer: Leriche's syndrome
Leriche's syndrome is a triad of
- absent or diminished femoral pulses,
- intermittent claudication (pain with walking) and
- penile impotence.
It usually affects males caused by atheromatous involvement or occlusion of the abdominal aorta by a thrombus just above the site of its bifurcation. Onset usually between 30 and 40 years of age. Treatment is surgical.
Leriche Syndrome: Coronal reconstruction from a contrast-enhanced abdominal CT scan shows complete occlusion of the infrarenal aorta (red arrow) by thrombus that extends into both common iliac arteries (yellow arrows). The white arrow points to calcification in the wall of the vessel.
Reference: click to get abstract / article
1. Leriche syndrome. Surgical procedures and early and late results - Angiology. 1997 Jul;48(7):637-42
Saturday, March 1, 2008
Saturday March 1, 2008
Palliative care - Death Rattle
Patients at end of life process, lose their ability to clear oral secretions. As air moves over the secretions, which have pooled in the respiratory tract, the resulting turbulence produces noisy ventilation, call Death rattle.
One easy bedside tip is to use 1% Atropine ophthalmic drops sublingually. Time of onset for action is about 30 minutes. It can be given every 2 hours PRN.
Other treatments are scopolamine patch placed behind the ear once every three days, Benadryl 25-100mg every 4 to 6 hours PRN or Robinul (glycopyrrolate) - 400 mcg SC every 8 hours PRN.
Palliative care - Death Rattle
Patients at end of life process, lose their ability to clear oral secretions. As air moves over the secretions, which have pooled in the respiratory tract, the resulting turbulence produces noisy ventilation, call Death rattle.
One easy bedside tip is to use 1% Atropine ophthalmic drops sublingually. Time of onset for action is about 30 minutes. It can be given every 2 hours PRN.
Other treatments are scopolamine patch placed behind the ear once every three days, Benadryl 25-100mg every 4 to 6 hours PRN or Robinul (glycopyrrolate) - 400 mcg SC every 8 hours PRN.
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