Tuesday February 28, 2006
Hypertonic Solution (3% NS) in cerebral edema and intracranial hypertension
Q: What is the level of Sodium (Na), you will target if hypertonic solution (3% NS) has been choose as management plan in cerebral edema and intracranial hypertension.
A: 145-155 Meq/L.
Although mannitol with close monitoring of serum osmolality remains mainstay of treatment, no major clinical trial has yet established the use of Hypertonic Solution (3% NS) as standard of treatment in cerebral edema and intracranial hypertension but literature has growingly show its comparable and sustained effect on lowering ICP (Intra-cranial pressure).
Related: Read concise review article here on Spontaneous intracerebral hemorrhage from Dr. Matthew E. Fewel and coll., Department of Neurosurgery, University of Michigan Health System, Ann Arbor, Michigan (Neurosurg. Focus / Volume 15 / October, 2003)
References: Click to get abstract/article (second popup overrides first popup).
1. Use of hypertonic saline solutions in treatment of cerebral edema and intracranial hypertension. Critical Care Medicine. 28(9):3301-3313, September 2000.
2. Treatment of elevated intracranial pressure in experimental intracerebral hemorrhage: Comparison between mannitol and hypertonic saline. Qureshi AI, Wilson DA, Traystman RJ: Neurosurgery 1999; 44: 1055-1064 -via pubmed
3. Hypertonic saline for cerebral edema and elevated intracranial pressure - Cleve Clin J Med. 2004 Jan;71 Suppl 1:S9-13.
4. Introducing Hypertonic Saline for Cerebral Edema: An Academic Center Experience - Neurocritical Care Winter 2004, Volume 1, Issue 4, pps. 435-440
5. Treatment of intracerebral haemorrhage - Lancet Neurology 2005; 4:662-672
Tuesday, February 28, 2006
Monday, February 27, 2006
iido
Monday February 27, 2006
Introducing icudelirium.org
Delirium is one of the most hidden and deadly enemy in ICU. It increases mortality, it cost money and its hard to recognise. In this regard an organised effort is underway in the form of website charged by Dr. E.Wesley Ely of Vanderbilt University Medical Center.
www.icudelirium.org
It contains numerous tools and information for Critical Care staff, particularly this slide show (Dr. Ely) is worth browsing.
Just to have a flavor, see this simple mnemonics from the site.
D Drugs, Drugs, Drugs
E Eyes, ears 1
L Low 02 (MI, ARDS, PE, CHF, COPD)2
I Infection
R Retention (of urine or stool), Restraints
I Ictal
U Underhydration/Undernutrition
M Metabolic
(S) Subdural, Sleep deprivation
1 Poor vision and hearing are considered more risk factors than true causes, but should be "fixed" or improved if possible. Cerumen is common cause of hearing impairment.
2 "Low 02 states" does NOT necessarily mean hypoxia, rather it is a reminder that patients with a hypoxic insult (e.g. Ml, stroke, PE) may present with mental status changes with or without other typical symptoms/signs of these diagnoses.
Introducing icudelirium.org
Delirium is one of the most hidden and deadly enemy in ICU. It increases mortality, it cost money and its hard to recognise. In this regard an organised effort is underway in the form of website charged by Dr. E.Wesley Ely of Vanderbilt University Medical Center.
www.icudelirium.org
It contains numerous tools and information for Critical Care staff, particularly this slide show (Dr. Ely) is worth browsing.
Just to have a flavor, see this simple mnemonics from the site.
D Drugs, Drugs, Drugs
E Eyes, ears 1
L Low 02 (MI, ARDS, PE, CHF, COPD)2
I Infection
R Retention (of urine or stool), Restraints
I Ictal
U Underhydration/Undernutrition
M Metabolic
(S) Subdural, Sleep deprivation
1 Poor vision and hearing are considered more risk factors than true causes, but should be "fixed" or improved if possible. Cerumen is common cause of hearing impairment.
2 "Low 02 states" does NOT necessarily mean hypoxia, rather it is a reminder that patients with a hypoxic insult (e.g. Ml, stroke, PE) may present with mental status changes with or without other typical symptoms/signs of these diagnoses.
Sunday, February 26, 2006
haimi
Sunday February 26, 2006
Hypomagnesemia and IV Magnesium (Mg) infusion
Hypomagnesemia has been reported in upto 60% of ICU patients and sometimes can be clinically very significant like in recovery phase of DKA (diabetic ketoacidosis). Symptoms of severe hypomagnesemia (less than 1 mEq/L) include respiratory failure, hyperactive deep-tendon reflexes, muscular fibrillations, mental status changes, tetany, seizures, positive Chvostek and Trousseau signs. EKG manifestations are prolong PR interval, widened QRS complex, ST depression, altered T waves and last but not the least is loss of voltage. About 33% of serum magnesium is protein-bound but unfortunately wide-spread test for free or active (ionized) magnesium is not available. It is a common practice to write IV Mg orders in grams or mls.
1 gram of IV Mg contains 8.12 meq of Mg and 1 meq of Mg provides 12 mg of elemental Mg.
One ml MgSO4 50% Solution = 4 meq Magnesium
One ml MgSO4 10% Solution = 8 meq Magnesium
Rapid IV administration can induce life threatening cardiac dysrhythmias, hypotension, flushing, sweating, sensation of warmth and hypocalcemia. In non-emergent cases, general rule of thumb is to infuse 1 gram per 1 hour. In risky situations, like impending arrhythmia, 2 grams of IV Magnesium sulfate may be given over 20 minutes. In extremely emergent cases 2 grams (16 mEq) of IV MgSO4 may be administered over 5 minutes and actually may be given as IV push if there is no permission of time.
In Preeclampsia, load IV 4-6 grams of MgSO4 in 100 ml of D5W over 20-30 minutes and maintenance is 2-3 grams/hour with close monitoring of target level (goal of 4-7 mEq/L) and clinical manifestations like decrease deep tendon reflexes. It is not a bad idea to keep IV calcium at bedside during massive IV magnesium infusion as in preeclampsia. IV calcium is an antidote for magnesium overdose.
In kidney dysfunction, IV magnesium dose should be reduced by about 50%.
Hypomagnesemia and IV Magnesium (Mg) infusion
Hypomagnesemia has been reported in upto 60% of ICU patients and sometimes can be clinically very significant like in recovery phase of DKA (diabetic ketoacidosis). Symptoms of severe hypomagnesemia (less than 1 mEq/L) include respiratory failure, hyperactive deep-tendon reflexes, muscular fibrillations, mental status changes, tetany, seizures, positive Chvostek and Trousseau signs. EKG manifestations are prolong PR interval, widened QRS complex, ST depression, altered T waves and last but not the least is loss of voltage. About 33% of serum magnesium is protein-bound but unfortunately wide-spread test for free or active (ionized) magnesium is not available. It is a common practice to write IV Mg orders in grams or mls.
1 gram of IV Mg contains 8.12 meq of Mg and 1 meq of Mg provides 12 mg of elemental Mg.
One ml MgSO4 50% Solution = 4 meq Magnesium
One ml MgSO4 10% Solution = 8 meq Magnesium
Rapid IV administration can induce life threatening cardiac dysrhythmias, hypotension, flushing, sweating, sensation of warmth and hypocalcemia. In non-emergent cases, general rule of thumb is to infuse 1 gram per 1 hour. In risky situations, like impending arrhythmia, 2 grams of IV Magnesium sulfate may be given over 20 minutes. In extremely emergent cases 2 grams (16 mEq) of IV MgSO4 may be administered over 5 minutes and actually may be given as IV push if there is no permission of time.
In Preeclampsia, load IV 4-6 grams of MgSO4 in 100 ml of D5W over 20-30 minutes and maintenance is 2-3 grams/hour with close monitoring of target level (goal of 4-7 mEq/L) and clinical manifestations like decrease deep tendon reflexes. It is not a bad idea to keep IV calcium at bedside during massive IV magnesium infusion as in preeclampsia. IV calcium is an antidote for magnesium overdose.
In kidney dysfunction, IV magnesium dose should be reduced by about 50%.
Friday, February 24, 2006
Intraabdominal compartment syndrome
Friday February 24, 2006
Grading of Intra-abdominal Hypertension (intra-abdominal compartment syndrome)
Burch and co. defined a grading system of IAH :
Grade I (10-15 cmH2O),
grade II (15-25 cmH2O),
grade III (25-35 cmH2O) and
grade IV (>35 cmH2O).
With massive fluid resuscitation as part of critical care management, intensivists need to be constantly cautious of this complication. End-organ damage has been described with bladder pressure as low as 10 cm H2O. Intra-abdominal Hypertension is defined as sustained or repeated pressure more than/= 12 and Intra-abdominal compartment syndrome as sustained or repeated pressure more than/= 20.
Although bladder pressure is not the accurate method of diagnosing IAH but so far has been used as standard due to its bedside ease. Dr. Cheatham has proposed APP (Abdominal Perfusion Pressure) as better indicator with formula
APP = MAP- IAP (like CPP = MAP - ICP).
where MAP is mean arterial pressure and IAP is intra-abdominal pressure.
Intra-abdominal Hypertension is defined as sustained or repeated APP less than or = 60
See good review here with details of how to measure bladder pressure to diagnose Intra-abdominal Hypertension from euroanesthesia.org (Dr. MALBRAIN - Hôpital Sainte Elisabeth, Bruxelles, Belgium).
Another review article here from emedicine.com (Dr. Paula Richard).
Referencss: Click to get abstract /article
1. The abdominal compartment syndrome. - Burch JM, Moore EE, Moore FA, Franciose R Surg Clin North Am. 1996 Aug;76(4):833-42.
2. Abdominal Perfusion Pressure: A Superior Parameter in the Assessment of Intra-abdominal Hypertension Journal of Trauma-Injury Infection & Critical Care. 49(4):621-627, October 2000.
Grading of Intra-abdominal Hypertension (intra-abdominal compartment syndrome)
Burch and co. defined a grading system of IAH :
Grade I (10-15 cmH2O),
grade II (15-25 cmH2O),
grade III (25-35 cmH2O) and
grade IV (>35 cmH2O).
With massive fluid resuscitation as part of critical care management, intensivists need to be constantly cautious of this complication. End-organ damage has been described with bladder pressure as low as 10 cm H2O. Intra-abdominal Hypertension is defined as sustained or repeated pressure more than/= 12 and Intra-abdominal compartment syndrome as sustained or repeated pressure more than/= 20.
Although bladder pressure is not the accurate method of diagnosing IAH but so far has been used as standard due to its bedside ease. Dr. Cheatham has proposed APP (Abdominal Perfusion Pressure) as better indicator with formula
APP = MAP- IAP (like CPP = MAP - ICP).
where MAP is mean arterial pressure and IAP is intra-abdominal pressure.
Intra-abdominal Hypertension is defined as sustained or repeated APP less than or = 60
See good review here with details of how to measure bladder pressure to diagnose Intra-abdominal Hypertension from euroanesthesia.org (Dr. MALBRAIN - Hôpital Sainte Elisabeth, Bruxelles, Belgium).
Another review article here from emedicine.com (Dr. Paula Richard).
Referencss: Click to get abstract /article
1. The abdominal compartment syndrome. - Burch JM, Moore EE, Moore FA, Franciose R Surg Clin North Am. 1996 Aug;76(4):833-42.
2. Abdominal Perfusion Pressure: A Superior Parameter in the Assessment of Intra-abdominal Hypertension Journal of Trauma-Injury Infection & Critical Care. 49(4):621-627, October 2000.
Thursday, February 23, 2006
caabp
Thursday February 23, 2006
Community-Acquired Acinetobacter baumannii Pneumonia !
As we are seeing more and more nosocomial infections moving out in community, recently chest has reported the largest series of CAP-AB (community-acquired pneumonia - Acinetobacter baumannii ) - and comparing its severity to HAP-AB (hospital-acquired pneumonia -Acinetobacter baumannii). 19 cases of CAP-AB has been compared to 74 cases of HAP-AB. Risk factors for CAP-AB were ever-smokers and COPD patients. It was characterized by more positive blood cultures (31.6% vs 0%), a higher frequency of ARDS (84.2% vs 17.6%), and DIC (57.9% vs 8.1%). The median survival time was only 8 days in the CAP-AB group vs 103 days in the HAP-AB group (p = 0.003). CAP-AB described to have a fulminant course, with an acute onset of dyspnea, cough, and fever that rapidly progresses to respiratory failure and shock. As discussed further in article, it may be important to consider empirical coverage for CAP-AB with presence of risk factors.
Earlier series of 13 patients were studied and read this interesting conclusion: "A baumannii should be considered as a possible etiologic agent in community-acquired lobar pneumonia when (1) patients with a fulminant course present during the warmer and more humid months of the year, and (2) patients are younger alcoholics".
Referencss: Click to get abstract/article (second popup overrides first popup)
1. Fulminant Community-Acquired Acinetobacter baumannii Pneumonia as a Distinct Clinical Syndrome - Chest. 2006;129:102-109
2. Severe Community-Acquired Pneumonia due to Acinetobacter baumannii Chest. 2001;120:1072-1077
Community-Acquired Acinetobacter baumannii Pneumonia !
As we are seeing more and more nosocomial infections moving out in community, recently chest has reported the largest series of CAP-AB (community-acquired pneumonia - Acinetobacter baumannii ) - and comparing its severity to HAP-AB (hospital-acquired pneumonia -Acinetobacter baumannii). 19 cases of CAP-AB has been compared to 74 cases of HAP-AB. Risk factors for CAP-AB were ever-smokers and COPD patients. It was characterized by more positive blood cultures (31.6% vs 0%), a higher frequency of ARDS (84.2% vs 17.6%), and DIC (57.9% vs 8.1%). The median survival time was only 8 days in the CAP-AB group vs 103 days in the HAP-AB group (p = 0.003). CAP-AB described to have a fulminant course, with an acute onset of dyspnea, cough, and fever that rapidly progresses to respiratory failure and shock. As discussed further in article, it may be important to consider empirical coverage for CAP-AB with presence of risk factors.
Earlier series of 13 patients were studied and read this interesting conclusion: "A baumannii should be considered as a possible etiologic agent in community-acquired lobar pneumonia when (1) patients with a fulminant course present during the warmer and more humid months of the year, and (2) patients are younger alcoholics".
Referencss: Click to get abstract/article (second popup overrides first popup)
1. Fulminant Community-Acquired Acinetobacter baumannii Pneumonia as a Distinct Clinical Syndrome - Chest. 2006;129:102-109
2. Severe Community-Acquired Pneumonia due to Acinetobacter baumannii Chest. 2001;120:1072-1077
Wednesday, February 22, 2006
cnucofks
Wednesday February 22, 2006
Colonic Necrosis - unusual complication of Kayexalate-Sorbitol
We are using sodium polystyrene sulfonate (SPS or Kayexalate) since last 45 years with great confidence. It is a common practice to add sorbitol to dissolve Kayexalate mainly to avoid fecal impaction or possible bowel obstruction. (Kayexalate binds intraluminal calcium and may cause constipation, fecal impaction or bowel obstruction). One of the relatively unknown complication of Kayexalate-sorbitol combination is colonic necrosis, although has been reported in literature earlier. The exact reason for colonic necrosis is not clear but the diagnosis can be made by the pathologic examination of post-operative specimen or material from endoscopic biopsy and may require specialized expertise and special stains. Sorbitol part is taught to be responsible for complication.
Intensivist need to be wary of possible complication of acute abdomen after administration of kayexalate-sorbitol in 1% of cases, particularly in first 24-36 hours.
See interesting review (full text and references) here from medscape.com with free registration. Originally, published at Southern Medical Journal , 93(5): page numbers 511-513, 2000.
Colonic Necrosis - unusual complication of Kayexalate-Sorbitol
We are using sodium polystyrene sulfonate (SPS or Kayexalate) since last 45 years with great confidence. It is a common practice to add sorbitol to dissolve Kayexalate mainly to avoid fecal impaction or possible bowel obstruction. (Kayexalate binds intraluminal calcium and may cause constipation, fecal impaction or bowel obstruction). One of the relatively unknown complication of Kayexalate-sorbitol combination is colonic necrosis, although has been reported in literature earlier. The exact reason for colonic necrosis is not clear but the diagnosis can be made by the pathologic examination of post-operative specimen or material from endoscopic biopsy and may require specialized expertise and special stains. Sorbitol part is taught to be responsible for complication.
Intensivist need to be wary of possible complication of acute abdomen after administration of kayexalate-sorbitol in 1% of cases, particularly in first 24-36 hours.
See interesting review (full text and references) here from medscape.com with free registration. Originally, published at Southern Medical Journal , 93(5): page numbers 511-513, 2000.
Tuesday, February 21, 2006
sasb
Tuesday February 21, 2006
Shock alert - Shock bed
In nontraumatic shock, timing is everything as proved again by this organized hospital approach from Dr. Sebat and coll.
As a first step of program - 2.5 years of planning and 1 month of intensive education done for early recognition and treatment of shock. Prehospital personnel, nurses, and physicians were empowered to mobilize a Shock Alert depending on screening criteria. Shock bed was made available in ICU all the time. (please see article below for full inclusion, exclusion criteria and protocol details). In second phase, 86 and 103 patients were randomized to the control and protocol groups. The protocol group had significant reductions in the median times to interventions, as follows:
intensivist arrival time - decreased from 120 minutes to 50 minutes
ICU admission - decreased from 167 minutes to 90 minutes
2 L fluid infused - decreased from 232 minutes to 105 minutes
Pulmonary artery catheter placement - decreased from 230 minutes to 130 minutes
Result: The hospital mortality rate was 40.7% in the control group and 28.2% in the protocol group (p = 0.035).
Reference: Click to get abstract/article
A Multidisciplinary Community Hospital Program for Early and Rapid Resuscitation of Shock in Nontrauma Patients - Chest. 2005;127:1729-1743
Shock alert - Shock bed
In nontraumatic shock, timing is everything as proved again by this organized hospital approach from Dr. Sebat and coll.
As a first step of program - 2.5 years of planning and 1 month of intensive education done for early recognition and treatment of shock. Prehospital personnel, nurses, and physicians were empowered to mobilize a Shock Alert depending on screening criteria. Shock bed was made available in ICU all the time. (please see article below for full inclusion, exclusion criteria and protocol details). In second phase, 86 and 103 patients were randomized to the control and protocol groups. The protocol group had significant reductions in the median times to interventions, as follows:
intensivist arrival time - decreased from 120 minutes to 50 minutes
ICU admission - decreased from 167 minutes to 90 minutes
2 L fluid infused - decreased from 232 minutes to 105 minutes
Pulmonary artery catheter placement - decreased from 230 minutes to 130 minutes
Result: The hospital mortality rate was 40.7% in the control group and 28.2% in the protocol group (p = 0.035).
Reference: Click to get abstract/article
A Multidisciplinary Community Hospital Program for Early and Rapid Resuscitation of Shock in Nontrauma Patients - Chest. 2005;127:1729-1743
Monday, February 20, 2006
crusade
Monday February 20, 2006
CRUSADE: Can Rapid Risk Stratification of Unstable Angina Patients Suppress Adverse Outcomes with Early Implementation of the ACC/AHA Guidelines.
CRUSADE: Can Rapid Risk Stratification of Unstable Angina Patients Suppress Adverse Outcomes with Early Implementation of the ACC/AHA Guidelines.
CRUSADE is a national quality improvement initiative that is designed to increase the practice of evidence-based medicine for patients diagnosed with non-ST segment elevation acute coronary syndromes (unstable angina or NSTE myocardial infarction). It has now over 400 participating sites in the US.
Being an intensivist, beside guidelines and other resources available at site following tools (click to get) may be very helpful.
1. QI Clearinghouse is an extensive collection of tools like
Standing Orders for the Management of Non-ST-segment Elevation (NSTE) ACS
GPIIb-IIIa Dosing Charts
2. The Performance Indicators Record - Acute Care
3. The Reference Guidelines Flipchart,
Sunday, February 19, 2006
robtl
Sunday February 19, 2006
Ratio of Bumex (Bumetanide) to Lasix (Furesmide)
What is the conversion equivalence of Bumex to Lasix?
1 mg of Bumex is equal to 40 mg of Lasix.
Ratio of Bumex (Bumetanide) to Lasix (Furesmide)
What is the conversion equivalence of Bumex to Lasix?
1 mg of Bumex is equal to 40 mg of Lasix.
Saturday, February 18, 2006
dd
Saturday February 18, 2006
Delphi definition - new clinical definition of acute respiratory distress syndrome (ARDS)
Beside 2 definitions of ARDS used commonly - the American-European consensus conference definition and the lung injury score, a relatively new definiation - Delphi definition- developed and published last year in Journal of Critical Care and appears to have better specificity.
According to Delphi definition, ARDS is diagnosed if 1- 4 of below present with 5a and/or 5b:
1. PaO2/FiO2 ratio is less than or = 200 on PEEP more than or= 10.
2. Bilateral airspace disease on CXR.
3. Onset is within 72 hours.
4. No clinical evidence/subjective finding of CHF.
5a. Objective finding of non-cardiogenic edema (PWP less than or=18 or LVEF more than or=40%)
5b. Presence of risk factor for ARDS.
In one of the recent study where autopsy results were matched with clinical diagnoses to determine and compare the diagnostic accuracy of all three clinical definitions of ARDS, the specificity of the most commonly use, the American-European definition, was low.
References: Click to get article/abstract
1. Development of a clinical definition for acute respiratory distress syndrome using the Delphi technique. Volume 20, Issue 2, Pages 147-154 (June 2005) - caution of slow internet download
2. Acute respiratory distress syndrome: Underrecognition by clinicians and diagnostic accuracy of three clinical definitions. Critical Care Medicine: Volume 33(10) October 2005 pp 2228-2234
Delphi definition - new clinical definition of acute respiratory distress syndrome (ARDS)
Beside 2 definitions of ARDS used commonly - the American-European consensus conference definition and the lung injury score, a relatively new definiation - Delphi definition- developed and published last year in Journal of Critical Care and appears to have better specificity.
According to Delphi definition, ARDS is diagnosed if 1- 4 of below present with 5a and/or 5b:
1. PaO2/FiO2 ratio is less than or = 200 on PEEP more than or= 10.
2. Bilateral airspace disease on CXR.
3. Onset is within 72 hours.
4. No clinical evidence/subjective finding of CHF.
5a. Objective finding of non-cardiogenic edema (PWP less than or=18 or LVEF more than or=40%)
5b. Presence of risk factor for ARDS.
In one of the recent study where autopsy results were matched with clinical diagnoses to determine and compare the diagnostic accuracy of all three clinical definitions of ARDS, the specificity of the most commonly use, the American-European definition, was low.
References: Click to get article/abstract
1. Development of a clinical definition for acute respiratory distress syndrome using the Delphi technique. Volume 20, Issue 2, Pages 147-154 (June 2005) - caution of slow internet download
2. Acute respiratory distress syndrome: Underrecognition by clinicians and diagnostic accuracy of three clinical definitions. Critical Care Medicine: Volume 33(10) October 2005 pp 2228-2234
Friday, February 17, 2006
me
Friday February 17, 2006
38,000 medication errors in 4 years - only in ICUs !!
The United States Pharmacopeia (USP)* announced the largest national data set of Intensive Care Unit (ICU) medication errors. These causes are identified in the 6th annual MEDMARX® Data Report. MEDMARX, operated by USP, is an anonymous, internet-accessible program used by hospitals and related institutions nationwide to report, track, and analyze medication errors. Since its inception in 1998, MEDMARX has received more than one million reports of medication errors from more than 850 healthcare facilities across the U.S. From 2000-2004, the number of reported errors that occurred in ICUs was 38,371. Reasons include orders that were incomplete or incorrect, illegible handwriting, using abbreviations that were misinterpreted, improper use of IV pumps and a lack of familiarity with some drug information. The big 3 culprits are:
1. 24.4% errors originated during the prescribing.
2. 24% during transcribing of the order.
3. 11% are due to incorrect programming of IV pumps.
It is reported that mix-ups in the IV tubing during pump set-up or mix-ups in programming the infusion rates for each drug have resulted in serious harm.
* USP is a self-sustaining nonprofit, independent, science-based public health organization. USP is the official public standards-setting authority for all prescription and over-the-counter medicines, dietary supplements, and other healthcare products manufactured and sold in the United States.
Reference: Click to get abstract/article
1. USP news center
38,000 medication errors in 4 years - only in ICUs !!
The United States Pharmacopeia (USP)* announced the largest national data set of Intensive Care Unit (ICU) medication errors. These causes are identified in the 6th annual MEDMARX® Data Report. MEDMARX, operated by USP, is an anonymous, internet-accessible program used by hospitals and related institutions nationwide to report, track, and analyze medication errors. Since its inception in 1998, MEDMARX has received more than one million reports of medication errors from more than 850 healthcare facilities across the U.S. From 2000-2004, the number of reported errors that occurred in ICUs was 38,371. Reasons include orders that were incomplete or incorrect, illegible handwriting, using abbreviations that were misinterpreted, improper use of IV pumps and a lack of familiarity with some drug information. The big 3 culprits are:
1. 24.4% errors originated during the prescribing.
2. 24% during transcribing of the order.
3. 11% are due to incorrect programming of IV pumps.
It is reported that mix-ups in the IV tubing during pump set-up or mix-ups in programming the infusion rates for each drug have resulted in serious harm.
* USP is a self-sustaining nonprofit, independent, science-based public health organization. USP is the official public standards-setting authority for all prescription and over-the-counter medicines, dietary supplements, and other healthcare products manufactured and sold in the United States.
Reference: Click to get abstract/article
1. USP news center
Thursday, February 16, 2006
pms
Thursday February 16, 2006
PAC-MAN study !
Benefits of pulmonary artery catheter (PAC) are debatable in Critical Care. Last year ESCAPE trial 2 failed to show any benefit. Untill we get results of FACTT trial (ARDSnet), lets have a look on PAC-MAN study. (Assessment of the clinical effectiveness of pulmonary artery catheters in management of patients in intensive care) published in Lancet, last year (august 2005 issue). 1 This is one of the largest study of 1013 patients in this regard. Patients were compared to management with (n = 506) or without (n = 507) a PAC with primary end-point of hospital mortality. No difference in hospital mortality between subjects managed with or without a PAC was noted - 68% vs 66%. Complications associated with insertion of a PAC were noted in 46 of 486 patients but none were considered fatal.
In subsets analysis, of patients randomized to receive either a PAC or no monitor of cardiac output, mortality was 71% [75 of 105] vs. 66% [71 of 107] and of patients randomized in ICUs allowing the possibility of an alternative monitor of cardiac output, mortality was 68% [271 of 401] vs. 66% [262 of 400].
In conclusion, there was no clear evidence of benefit or harm in managing critically ill patients with a PAC.
Related previous pearl: ESCAPE Trial - setback to swan lovers?
References: Click to get abstract/article (secondpopup override first popup)
1. Assessment of the clinical effectiveness of pulmonary artery catheters in management of patients in intensive care (PAC-Man): a randomised controlled trial - Harvey S, Harrison DA, Singer M, Ashcroft J, Jones CM, Elbourne D, Brampton W, Williams D, Young D, Rowan K, The Lancet - Vol. 366, Issue 9484, 06 August 2005, Pages 472-477 - (abstract-review printed at cleveland clinic journal of medicine, november 2005 page 1048)
2. Evaluation Study of Congestive Heart Failure and Pulmonary Artery Catheterization Effectiveness - JAMA. 2005;294:1625-1633.
3. Impact of the Pulmonary Artery Catheter in Critically Ill Patients -JAMA. 2005;294:1664-1670.
PAC-MAN study !
Benefits of pulmonary artery catheter (PAC) are debatable in Critical Care. Last year ESCAPE trial 2 failed to show any benefit. Untill we get results of FACTT trial (ARDSnet), lets have a look on PAC-MAN study. (Assessment of the clinical effectiveness of pulmonary artery catheters in management of patients in intensive care) published in Lancet, last year (august 2005 issue). 1 This is one of the largest study of 1013 patients in this regard. Patients were compared to management with (n = 506) or without (n = 507) a PAC with primary end-point of hospital mortality. No difference in hospital mortality between subjects managed with or without a PAC was noted - 68% vs 66%. Complications associated with insertion of a PAC were noted in 46 of 486 patients but none were considered fatal.
In subsets analysis, of patients randomized to receive either a PAC or no monitor of cardiac output, mortality was 71% [75 of 105] vs. 66% [71 of 107] and of patients randomized in ICUs allowing the possibility of an alternative monitor of cardiac output, mortality was 68% [271 of 401] vs. 66% [262 of 400].
In conclusion, there was no clear evidence of benefit or harm in managing critically ill patients with a PAC.
Related previous pearl: ESCAPE Trial - setback to swan lovers?
References: Click to get abstract/article (secondpopup override first popup)
1. Assessment of the clinical effectiveness of pulmonary artery catheters in management of patients in intensive care (PAC-Man): a randomised controlled trial - Harvey S, Harrison DA, Singer M, Ashcroft J, Jones CM, Elbourne D, Brampton W, Williams D, Young D, Rowan K, The Lancet - Vol. 366, Issue 9484, 06 August 2005, Pages 472-477 - (abstract-review printed at cleveland clinic journal of medicine, november 2005 page 1048)
2. Evaluation Study of Congestive Heart Failure and Pulmonary Artery Catheterization Effectiveness - JAMA. 2005;294:1625-1633.
3. Impact of the Pulmonary Artery Catheter in Critically Ill Patients -JAMA. 2005;294:1664-1670.
Wednesday, February 15, 2006
lre
Wednesday February 15, 2006
Linezolid-resistant enterococcus (LRE!)
This study was presented at Infectious Disease Society of America meeting 2005 from Dr. Devasia. Fifteen patients in a 500-bed teaching hospital were diagnosed with Linezolid(Zyvox)-resistant enterococcus during 13 months of study. In a comparison of these patients with 60 control patients with Linezolid-sensitive enterococcus, the resistant cases had a significantly higher mortality rate - 40% vs 7%. Interestingly, 8 LRE patients were vancomycin sensitive enterococcus but what make it thought-provoking, 8 cases out of 15 had no prior exposure to Linezolid. As expected, length of stay was way higher (35 days vs 11 days) but scary part is - median age of patients was only 54 years (vs 65 years for control).
Are younger patients more prone to LRE even without prior exposure? Are we up for another battle against microbes?. Atleast one thing is sure, its time for very judicious use of Linezolid.
To note, similar related report was published about 4 years ago in NEJM.
References: Click to get abstract/article (secondpopup override first popup)
1. Abstracts Infectious Disease Society of America Meeting 2005 - Scroll down to page 238 (abstract # 1079) - may take little time to download due to big pdf file.
2. Nosocomial Spread of Linezolid-Resistant, Vancomycin-Resistant Enterococcus faecium - NEJM, March 14, 2002 Volume 346:867-869
Linezolid-resistant enterococcus (LRE!)
This study was presented at Infectious Disease Society of America meeting 2005 from Dr. Devasia. Fifteen patients in a 500-bed teaching hospital were diagnosed with Linezolid(Zyvox)-resistant enterococcus during 13 months of study. In a comparison of these patients with 60 control patients with Linezolid-sensitive enterococcus, the resistant cases had a significantly higher mortality rate - 40% vs 7%. Interestingly, 8 LRE patients were vancomycin sensitive enterococcus but what make it thought-provoking, 8 cases out of 15 had no prior exposure to Linezolid. As expected, length of stay was way higher (35 days vs 11 days) but scary part is - median age of patients was only 54 years (vs 65 years for control).
Are younger patients more prone to LRE even without prior exposure? Are we up for another battle against microbes?. Atleast one thing is sure, its time for very judicious use of Linezolid.
To note, similar related report was published about 4 years ago in NEJM.
References: Click to get abstract/article (secondpopup override first popup)
1. Abstracts Infectious Disease Society of America Meeting 2005 - Scroll down to page 238 (abstract # 1079) - may take little time to download due to big pdf file.
2. Nosocomial Spread of Linezolid-Resistant, Vancomycin-Resistant Enterococcus faecium - NEJM, March 14, 2002 Volume 346:867-869
Tuesday, February 14, 2006
Lasa
Tuesday February 14, 2006
What are LASA drugs
Many studies have shown so far that errors in administration of drugs remain high and actually twice in ICUs. In this regard, its important to know the term LASA medications. LASA are "look-alike sound-alike" medications and are responsible for 12.5 percent of the medication errors reported to the FDA. Other factors making it worse include illegible handwriting, look alike packaging, unclear verbal directions, similar pronunciation etc etc. We all went through the experiences of confusion between dopamine and dobutamine, phenylephrine and norepinehrine, heparin and hespan, primacor and primaxin, diflucan and diprivan and so on. Institutions are taking initiatives like computer based drug entry, verbal read backs, automated alerts, advise to prescribers to write both the brand and generic name on problematic drugs or to include the intended purpose of the medication. Make sure your institution is working on this issue as JCAHO has now made LASA drugs part of its National Patient Safety Goals and institutions are expected to prepare organisational list of LASA drugs.
Click here to read position paper on critical care pharmacy services from Society of Critical Care Medicine and American College of Clinical Pharmacy Task Force on Critical Care Pharmacy Services.
Related previous Pearls:
1. ICU satellite pharmacy
2. Preventing intra-venous (IV) drip errors
3. "Five Rights"
Reference:
Preventable adverse drug events in hospitalized patients: A comparative study of intensive care and general care units Critical Care Medicine. 25(8):1289-1297, August 1997.
What are LASA drugs
Many studies have shown so far that errors in administration of drugs remain high and actually twice in ICUs. In this regard, its important to know the term LASA medications. LASA are "look-alike sound-alike" medications and are responsible for 12.5 percent of the medication errors reported to the FDA. Other factors making it worse include illegible handwriting, look alike packaging, unclear verbal directions, similar pronunciation etc etc. We all went through the experiences of confusion between dopamine and dobutamine, phenylephrine and norepinehrine, heparin and hespan, primacor and primaxin, diflucan and diprivan and so on. Institutions are taking initiatives like computer based drug entry, verbal read backs, automated alerts, advise to prescribers to write both the brand and generic name on problematic drugs or to include the intended purpose of the medication. Make sure your institution is working on this issue as JCAHO has now made LASA drugs part of its National Patient Safety Goals and institutions are expected to prepare organisational list of LASA drugs.
Click here to read position paper on critical care pharmacy services from Society of Critical Care Medicine and American College of Clinical Pharmacy Task Force on Critical Care Pharmacy Services.
Related previous Pearls:
1. ICU satellite pharmacy
2. Preventing intra-venous (IV) drip errors
3. "Five Rights"
Reference:
Preventable adverse drug events in hospitalized patients: A comparative study of intensive care and general care units Critical Care Medicine. 25(8):1289-1297, August 1997.
Monday, February 13, 2006
rdf
Monday February 13, 2006
Renal dose Fenoldopam ?
We are done with renal dose dopamine but than we heard about renal dose norepinephrine1 and now renal dose fenoldopam? Look at this study of 300 septic patients with baseline serum creatinine concentrations less than 150 umol/L (2 mg/dL)*.
150 patients with a continuous infusion of fenoldopam at 0.09 μg·kg-1·min-1 (nonhemodynamic dose) has been compared with 150 placebo patients. The primary outcome measure was the incidence of acute renal failure, defined as a serum creatinine concentration increase to >150 μmol/L (>2 mg/dL), during study drug infusion. The incidence of acute renal failure was significantly lower in the fenoldopam group compared with the control group (29 vs. 51 patients; p = .006). Also, the length of ICU stay in surviving patients was significantly lower in the fenoldopam group compared with the control group (10.64 vs. 13.4; p < .001). Its not clear why fenoldopam which is also a dopaminergic agonist like low-dose dopamine, has protective effect on kidney but dopamine does not. We need a large multiple-center trial to have more answers.
* 1 mg/dL = 88.4 mol/L of serum Cr.
References:Click to get article/abstract (second popup overwrites first popup)
1. Renal Dose Norepinephrine! - Chest. 2004;126:335-337
2. Prophylactic fenoldopam for renal protection in sepsis: A randomized, double-blind, placebo-controlled pilot trial - Critical Care Medicine: Volume 33(11) November 2005 pp 2451-2456
Renal dose Fenoldopam ?
We are done with renal dose dopamine but than we heard about renal dose norepinephrine1 and now renal dose fenoldopam? Look at this study of 300 septic patients with baseline serum creatinine concentrations less than 150 umol/L (2 mg/dL)*.
150 patients with a continuous infusion of fenoldopam at 0.09 μg·kg-1·min-1 (nonhemodynamic dose) has been compared with 150 placebo patients. The primary outcome measure was the incidence of acute renal failure, defined as a serum creatinine concentration increase to >150 μmol/L (>2 mg/dL), during study drug infusion. The incidence of acute renal failure was significantly lower in the fenoldopam group compared with the control group (29 vs. 51 patients; p = .006). Also, the length of ICU stay in surviving patients was significantly lower in the fenoldopam group compared with the control group (10.64 vs. 13.4; p < .001). Its not clear why fenoldopam which is also a dopaminergic agonist like low-dose dopamine, has protective effect on kidney but dopamine does not. We need a large multiple-center trial to have more answers.
* 1 mg/dL = 88.4 mol/L of serum Cr.
References:Click to get article/abstract (second popup overwrites first popup)
1. Renal Dose Norepinephrine! - Chest. 2004;126:335-337
2. Prophylactic fenoldopam for renal protection in sepsis: A randomized, double-blind, placebo-controlled pilot trial - Critical Care Medicine: Volume 33(11) November 2005 pp 2451-2456
Sunday, February 12, 2006
coaii
Sunday February 12, 2006
Cycling of Antibiotics in ICU
Concept of antibiotics cycling to reduce antibiotics resistance remains debatable in medical literature. 2 recent papers earlier showed it may not work.1,2 But a new study of 346 patients from spain (comparing mixing in one ICU vs cycling in another ICU) published this month in Critical Care Medicine points that this may actually have some potential.
Patients, who according to the physician's judgment required an anti-Pseudomonas drug, were assigned to receive 1) cefepime/ceftazidime 2) ciprofloxacin 3) a carbapenem or 4) piperacillin-tazobactam in this order. Cycling was accomplished by prescribing one of these antibiotics during 1 month each. 2 cycles were given of 4 months each. Mixing was accomplished by using the same order of antibiotic administration on consecutive patients. The main outcome variable was the proportion of patients acquiring enteric or nonfermentative Gram-negative bacilli resistant to the antibiotics under intervention.
During mixing, a significantly higher proportion of patients acquired a strain of Pseudomonas aeruginosa resistant to cefepime (9% vs. 3%, p = .01), and there was a trend toward a more frequent acquisition of resistance to ceftazidime (p = .06), imipenem (p = .06), and meropenem (p = .07).
Read precise review on different point of views in this regard here posted in pulmonaryreviews.com, september 2002 issue. Till we get more data to accept antibiotic cycling as a standard practice, lets concentrate on two basic themes - avoid unnecessary antibiotic use and prevent cross-transmission of pathogens.
References: Click to get article/abstract (second popup overwrites first popup)
1. Ecological theory suggests that antimicrobial cycling will not reduce antimicrobial resistance in hospitals - Proceedings of the National Academy of Sciences of the United States of America - PNAS September 7, 2004 vol. 101 no. 36 13285-13290
2. Antibiotic Rotation and Development of Gram-Negative Antibiotic Resistance - American Journal of Respiratory and Critical Care Medicine Vol 171. pp. 480-487, (2005)
3. Comparison of antimicrobial cycling and mixing strategies in two medical intensive care units. -Critical Care Medicine. 34(2):329-336, February 2006.
4. Antibiotic cycling in intensive care units: The value of organized chaos? - Bonten, Marc J. M. MD; Weinstein, Robert A. MD- Critical Care Medicine: Volume 34(2) February 2006 pp 549-551
Cycling of Antibiotics in ICU
Concept of antibiotics cycling to reduce antibiotics resistance remains debatable in medical literature. 2 recent papers earlier showed it may not work.1,2 But a new study of 346 patients from spain (comparing mixing in one ICU vs cycling in another ICU) published this month in Critical Care Medicine points that this may actually have some potential.
Patients, who according to the physician's judgment required an anti-Pseudomonas drug, were assigned to receive 1) cefepime/ceftazidime 2) ciprofloxacin 3) a carbapenem or 4) piperacillin-tazobactam in this order. Cycling was accomplished by prescribing one of these antibiotics during 1 month each. 2 cycles were given of 4 months each. Mixing was accomplished by using the same order of antibiotic administration on consecutive patients. The main outcome variable was the proportion of patients acquiring enteric or nonfermentative Gram-negative bacilli resistant to the antibiotics under intervention.
During mixing, a significantly higher proportion of patients acquired a strain of Pseudomonas aeruginosa resistant to cefepime (9% vs. 3%, p = .01), and there was a trend toward a more frequent acquisition of resistance to ceftazidime (p = .06), imipenem (p = .06), and meropenem (p = .07).
Read precise review on different point of views in this regard here posted in pulmonaryreviews.com, september 2002 issue. Till we get more data to accept antibiotic cycling as a standard practice, lets concentrate on two basic themes - avoid unnecessary antibiotic use and prevent cross-transmission of pathogens.
References: Click to get article/abstract (second popup overwrites first popup)
1. Ecological theory suggests that antimicrobial cycling will not reduce antimicrobial resistance in hospitals - Proceedings of the National Academy of Sciences of the United States of America - PNAS September 7, 2004 vol. 101 no. 36 13285-13290
2. Antibiotic Rotation and Development of Gram-Negative Antibiotic Resistance - American Journal of Respiratory and Critical Care Medicine Vol 171. pp. 480-487, (2005)
3. Comparison of antimicrobial cycling and mixing strategies in two medical intensive care units. -Critical Care Medicine. 34(2):329-336, February 2006.
4. Antibiotic cycling in intensive care units: The value of organized chaos? - Bonten, Marc J. M. MD; Weinstein, Robert A. MD- Critical Care Medicine: Volume 34(2) February 2006 pp 549-551
Saturday, February 11, 2006
moettwn
Saturday February 11, 2006
Movement of endotracheal tube (ETT) with neck
Extension of neck (Chin up) will cause ETT to migrate (up or down) ?
Ans.: ____________
Flexion of neck (Chin down) will cause ETT to migrate (up or down) ? Ans.: ____________
Answers:
Extension of neck (Chin up) will cause ETT to migrate up.
Flexion of neck (Chin down) will cause ETT to migrate down.
Remember: Chin up - ETT up. Chin down - ETT down.
Movement of endotracheal tube (ETT) with neck
Extension of neck (Chin up) will cause ETT to migrate (up or down) ?
Ans.: ____________
Flexion of neck (Chin down) will cause ETT to migrate (up or down) ? Ans.: ____________
Answers:
Extension of neck (Chin up) will cause ETT to migrate up.
Flexion of neck (Chin down) will cause ETT to migrate down.
Remember: Chin up - ETT up. Chin down - ETT down.
Friday, February 10, 2006
nod
Friday February 10, 2006
Norepinephrine or Dopamine ?
Standard guidelines regarding vasopressor and inotropic support in septic shock states: "Either norepinephrine or dopamine (through a central catheter as soon as possible) is the first-choice vasopressor agent to correct hypotension in septic shock." But overall trend is going towards using norepinephrine as the first-choice vasopressor to correct hypotension in septic shock after fluid resuscitation. In a recent study from Rush University Medical Center, Chicago, IL the safety of Dopamine (DA) versus Norepinephrine (NE) as vasopressor therapy in septic shock has been compared. Sixty-six patients, 35 DA and 31 NE, has been compared. Though there was no significant difference in mortality cardiac dysrhythmias occurred in 31.4% of the DA group compared to only 3.2% for NE (p=0.003). But important aspect of study was, all cardiac dysrhythmias required an intervention.
Related Pearls:
1. Renal Dose Norepinephrine !
2. Dopamine-S and Dopamine-R patients ?
References: Click to get article/abstract: (appears in popup window and second popup overwrites first popup).
1. Vasopressor and inotropic support in septic shock: An evidence-based review Critical Care Medicine: Volume 32(11) Supplement November 2004 pp S455-S465
2. THE SAFETY OF DOPAMINE VERSUS NOREPINEPHRINE AS VASOPRESSOR THERAPY IN SEPTIC SHOCK - chest, 2005
Norepinephrine or Dopamine ?
Standard guidelines regarding vasopressor and inotropic support in septic shock states: "Either norepinephrine or dopamine (through a central catheter as soon as possible) is the first-choice vasopressor agent to correct hypotension in septic shock." But overall trend is going towards using norepinephrine as the first-choice vasopressor to correct hypotension in septic shock after fluid resuscitation. In a recent study from Rush University Medical Center, Chicago, IL the safety of Dopamine (DA) versus Norepinephrine (NE) as vasopressor therapy in septic shock has been compared. Sixty-six patients, 35 DA and 31 NE, has been compared. Though there was no significant difference in mortality cardiac dysrhythmias occurred in 31.4% of the DA group compared to only 3.2% for NE (p=0.003). But important aspect of study was, all cardiac dysrhythmias required an intervention.
Related Pearls:
1. Renal Dose Norepinephrine !
2. Dopamine-S and Dopamine-R patients ?
References: Click to get article/abstract: (appears in popup window and second popup overwrites first popup).
1. Vasopressor and inotropic support in septic shock: An evidence-based review Critical Care Medicine: Volume 32(11) Supplement November 2004 pp S455-S465
2. THE SAFETY OF DOPAMINE VERSUS NOREPINEPHRINE AS VASOPRESSOR THERAPY IN SEPTIC SHOCK - chest, 2005
Thursday, February 09, 2006
JCAHO "DNU" abbreviations
Thursday February 9, 2006
Basic housekeeking - JCAHO mandated "Do Not Use" abbreviations
As intensivists are assuming more and more leadership and role model figure in hospitals, here are the JCAHO (Joint Commission on Accreditation of Healthcare Organizations) mandated "Do Not Use" abbreviations - meeting NPSG (National Patient Safety Goals) Requirement 2B. Please note 3 important points:
1. The minimum expected level of compliance for handwritten documentation and free-text entry is 90 % and for pre-printed forms is 100 %.
2. Clarification of an order prior to implementation and after-the-fact correction of the order by the clinician does not eliminate that occurrence from being counted. (If pharmacy or nurse calls you to clarify the order its an 'occurance').
3. One occurrence equals one per clinician per record and three occurrences equal a Requirement for Improvement.
Here is the JCAHO mandated "Do Not Use" abbreviations
Do not write U or IU - Write "unit" or "international unit".
Do not write Q.D., Q.O.D. - Write "once daily and every other day".
Never write a zero by itself after a decimal point (5 mg instead of 5.0 mg), and always use a zero before a decimal point ( 0.5 mg instead of .5 mg).
Do not write MS or MSO4 - Write "morphine sulfate".
Do not write MgSO4 - Write "magnesium sulfate".
Basic housekeeking - JCAHO mandated "Do Not Use" abbreviations
As intensivists are assuming more and more leadership and role model figure in hospitals, here are the JCAHO (Joint Commission on Accreditation of Healthcare Organizations) mandated "Do Not Use" abbreviations - meeting NPSG (National Patient Safety Goals) Requirement 2B. Please note 3 important points:
1. The minimum expected level of compliance for handwritten documentation and free-text entry is 90 % and for pre-printed forms is 100 %.
2. Clarification of an order prior to implementation and after-the-fact correction of the order by the clinician does not eliminate that occurrence from being counted. (If pharmacy or nurse calls you to clarify the order its an 'occurance').
3. One occurrence equals one per clinician per record and three occurrences equal a Requirement for Improvement.
Here is the JCAHO mandated "Do Not Use" abbreviations
Do not write U or IU - Write "unit" or "international unit".
Do not write Q.D., Q.O.D. - Write "once daily and every other day".
Never write a zero by itself after a decimal point (5 mg instead of 5.0 mg), and always use a zero before a decimal point ( 0.5 mg instead of .5 mg).
Do not write MS or MSO4 - Write "morphine sulfate".
Do not write MgSO4 - Write "magnesium sulfate".
Wednesday, February 08, 2006
EGDE
Wednesday February 8, 2006
EARLY GOAL-DIRECTED ECHOCARDIOGRAPHY !
Dr. Anthony Manasia and Coll. from Mount Sinai School of Medicine, New York, NY, have introduced this term in one of their paper presented at American College of Chest Physicians (ACCP) meeting last year at Montreal, Canada. Based on their study of 18 patients, they claim that the first echo (done within 5-6 hours of admission) changed the treatment plan in 38.8% (7/18) of the circulatory shock patients when compared to the initial management instituted by the primary ICU team. The treatment plan was changed in 11.7% (2/17) of patients following the second echo exam (done 24 hours later). The echocardiographic exam was performed by an echo-trained intensivist not involved in the patient’s care. But similar kind of retrospective observational study of 100 patients in medical ICU, 2 years back from Mayo Clinic, Rochester, MN failed to show any impressive result but to note time-period of echo was within 48 hours.
Does ultra early echo in shock patients really make difference in 38.8% of patients ?. May be its time for a bigger study.
References: Click to get article/abstract: (appears in popup window and second popup overwrites first popup).
1. CLINICAL IMPACT OF EARLY GOAL-DIRECTED ECHOCARDIOGRAPHY IN SHOCK PATIENTS PERFORMED BY NON-CARDIOLOGIST INTENSIVISTS - chest, 2005
2. Echo in the Medical Intensive Care Unit: Does It Really Impact Patient Management? A Retrospective Observational Study - chest, 2003
EARLY GOAL-DIRECTED ECHOCARDIOGRAPHY !
Dr. Anthony Manasia and Coll. from Mount Sinai School of Medicine, New York, NY, have introduced this term in one of their paper presented at American College of Chest Physicians (ACCP) meeting last year at Montreal, Canada. Based on their study of 18 patients, they claim that the first echo (done within 5-6 hours of admission) changed the treatment plan in 38.8% (7/18) of the circulatory shock patients when compared to the initial management instituted by the primary ICU team. The treatment plan was changed in 11.7% (2/17) of patients following the second echo exam (done 24 hours later). The echocardiographic exam was performed by an echo-trained intensivist not involved in the patient’s care. But similar kind of retrospective observational study of 100 patients in medical ICU, 2 years back from Mayo Clinic, Rochester, MN failed to show any impressive result but to note time-period of echo was within 48 hours.
Does ultra early echo in shock patients really make difference in 38.8% of patients ?. May be its time for a bigger study.
References: Click to get article/abstract: (appears in popup window and second popup overwrites first popup).
1. CLINICAL IMPACT OF EARLY GOAL-DIRECTED ECHOCARDIOGRAPHY IN SHOCK PATIENTS PERFORMED BY NON-CARDIOLOGIST INTENSIVISTS - chest, 2005
2. Echo in the Medical Intensive Care Unit: Does It Really Impact Patient Management? A Retrospective Observational Study - chest, 2003
Tuesday, February 07, 2006
BALTI
Tuesday February 7, 2006
Adrenergic Agonists in Acute Lung Injury - BALTI trial
ß2-Agonists remain the most important inhaled bronchodilators and provide rapid symptom relief for many patients. Short-acting, inhaled, selective ß2-agonists remain the mainstay bronchodilators for asthma, COPD, and airway obstruction of all etiologies. The use of B-adrenergic agonists as a potential therapy for acute lung injury has generated considerable interest. B-agonists have well-recognized antiinflammatory properties and treatment with a B-agonist have shown to enhances the rate of alveolar fluid clearance by increasing intracellular cAMP.
Perkins and colleagues report the results of a clinical trial of 40 patients with acute lung injury in which the effects of B-agonists were examined.1 Salbutamol (albuterol) was administered intravenously at a dose of 15 μg/kg/hour in a double-blind, randomized manner. Extravascular lung water on Day 7, the primary outcome variable, was lower in the salbutamol-treated patients compared with the placebo control subjects (9.2 vs. 13.2 ml/kg, p = 0.04). Post hoc analysis indicated that extravascular lung water was significantly lower in the treated group at earlier time points as well. Plateau airway pressure was also 6 cm H2O lower at Day 7 in the salbutamol-treated group (p = 0.049), and there was a trend toward lower acute lung injury scores in the salbutamol-treated patients.
The results indicate that a multicenter clinical trial may be warranted to test the possible therapeutic benefit of B-agonist therapy for acute lung injury.
References: Click to get article/abstract: (appears in popup window and second popup overwrites first popup).
1. Perkins GD, McAuley DF, Thickett DR, , Gao F The b-agonist lung injury trial (BALTI): a randomized placebo-controlled clinical trial. Am J Respir Crit Care Med 2006;173:281–287
2. Matthay MA, Folkesson HG, Clerici C. Lung epithelial fluid transport and the resolution of pulmonary edema. Physiol Rev 2002;82:569–600.
3. McAuley DF, Frank JA, Fang X, Matthay MA. Clinically relevant concentrations of beta2-adrenergic agonists stimulate maximal cyclic adenosine monophosphate-dependent airspace fluid clearance and decrease pulmonary edema in experimental acid-induced lung injury. Crit Care Med 2004;32:1470–1476.
Adrenergic Agonists in Acute Lung Injury - BALTI trial
ß2-Agonists remain the most important inhaled bronchodilators and provide rapid symptom relief for many patients. Short-acting, inhaled, selective ß2-agonists remain the mainstay bronchodilators for asthma, COPD, and airway obstruction of all etiologies. The use of B-adrenergic agonists as a potential therapy for acute lung injury has generated considerable interest. B-agonists have well-recognized antiinflammatory properties and treatment with a B-agonist have shown to enhances the rate of alveolar fluid clearance by increasing intracellular cAMP.
Perkins and colleagues report the results of a clinical trial of 40 patients with acute lung injury in which the effects of B-agonists were examined.1 Salbutamol (albuterol) was administered intravenously at a dose of 15 μg/kg/hour in a double-blind, randomized manner. Extravascular lung water on Day 7, the primary outcome variable, was lower in the salbutamol-treated patients compared with the placebo control subjects (9.2 vs. 13.2 ml/kg, p = 0.04). Post hoc analysis indicated that extravascular lung water was significantly lower in the treated group at earlier time points as well. Plateau airway pressure was also 6 cm H2O lower at Day 7 in the salbutamol-treated group (p = 0.049), and there was a trend toward lower acute lung injury scores in the salbutamol-treated patients.
The results indicate that a multicenter clinical trial may be warranted to test the possible therapeutic benefit of B-agonist therapy for acute lung injury.
References: Click to get article/abstract: (appears in popup window and second popup overwrites first popup).
1. Perkins GD, McAuley DF, Thickett DR, , Gao F The b-agonist lung injury trial (BALTI): a randomized placebo-controlled clinical trial. Am J Respir Crit Care Med 2006;173:281–287
2. Matthay MA, Folkesson HG, Clerici C. Lung epithelial fluid transport and the resolution of pulmonary edema. Physiol Rev 2002;82:569–600.
3. McAuley DF, Frank JA, Fang X, Matthay MA. Clinically relevant concentrations of beta2-adrenergic agonists stimulate maximal cyclic adenosine monophosphate-dependent airspace fluid clearance and decrease pulmonary edema in experimental acid-induced lung injury. Crit Care Med 2004;32:1470–1476.
Monday, February 06, 2006
tightglycemiccontrolwhereweare
Monday February 6, 2006
Tight glycemic control - where we are ?
This week New England Journal of Medicine has published the second part of Dr. Van den Berghe's Intensive Insulin Therapy. This study was done on 1200 patients in medical ICU. As you may remember, her first study of 1548 patients was done in surgical unit and had shown decrease in morbidity as well as mortality. Her present study from medical ICU, though showed significant reduction in morbidity but failed to show any decrease in mortality. But most surprising part of the study, was the analysis of the subset of patients who stayed in the ICU for less than three days. Mortality was actually greater among those patients with intensive insulin therapy. We don't know yet as this data is reproducible or there are other explanations for this result such as early limitations or withdrawals of care. Also to remember, VISEP study from germany which was designed to randomize 600 subjects with medical or surgical severe sepsis to conventional or intensive insulin therapy, was stopped after recruitment of 488 subjects because of no difference in mortality and frequent hypoglycemia in the intensive insulin therapy arm.
What should we do till reults of other major studies like GLUControl (3000 patients) or NICE - SUGAR (5000 patients) are pending. Here are couple of good advises.
1) As Dr. Atul Malhotra wrote in editorial of same issue of NEJM - "In my opinion, a reasonable approach would be to provide adequate exogenous insulin to achieve target glucose values of less than 150 mg per deciliter (8.3 mmol per liter), at least during the first three days in the ICU. If critical illness persists beyond three days despite the provision of other proven therapies and resuscitation, a goal of normoglycemia (80 to 110 mg per deciliter [4.4 to 6.1 mmol per liter]) could then be considered, to maximize the potential benefits". OR
2). Dr. Angus and Abraham suggested last year: "..it may be valuable to remember that, although the evidence for tight glycemic control does not yet support a grade A recommendation, it does appear to be stronger than that for continuing our existing practice of tolerating hyperglycemia. Thus, we should probably explore ways to introduce some form of tight glucose control during this interim period that seems feasible and safe given local considerations. Once better evidence is available, we can modify our plans accordingly."
References: Click to get article/abstract: (appears in popup window and second popup overwrites first popup).
1. Intensive Insulin Therapy in the Medical ICU - NEJM, Feb. 2, 2006, Volume 354:449-461
2. Intensive Insulin Therapy in Critically Ill Patients - N Engl J Med 2001; 345:1359-1367, Nov 8, 2001
3.Intensive insulin therapy in patient with severe sepsis and septic shock is associated with an increased rate of hypoglycemia - results from a randomized multicenter study (VISEP), Infection 2005;33: 19-20.
4. Glucontrol Study: Comparing the Effects of Two Glucose Control Regimens by Insulin in Intensive Care Unit Patients -clinicaltrials.gov
5. Normoglycaemia in Intensive Care Evaluation and Survival Using Glucose Algorithm Regulation (NICE - SUGAR STUDY) - clinicaltrials.gov
6. Intensive Insulin in Intensive Care - Volume 354:516-518, NEJM, feb. 2, 2006
7. Intensive Insulin Therapy in Critical Illness, Angus and Abraham Am. J. Respir. Crit. Care Med..2005; 172: 1358-1359
Tight glycemic control - where we are ?
This week New England Journal of Medicine has published the second part of Dr. Van den Berghe's Intensive Insulin Therapy. This study was done on 1200 patients in medical ICU. As you may remember, her first study of 1548 patients was done in surgical unit and had shown decrease in morbidity as well as mortality. Her present study from medical ICU, though showed significant reduction in morbidity but failed to show any decrease in mortality. But most surprising part of the study, was the analysis of the subset of patients who stayed in the ICU for less than three days. Mortality was actually greater among those patients with intensive insulin therapy. We don't know yet as this data is reproducible or there are other explanations for this result such as early limitations or withdrawals of care. Also to remember, VISEP study from germany which was designed to randomize 600 subjects with medical or surgical severe sepsis to conventional or intensive insulin therapy, was stopped after recruitment of 488 subjects because of no difference in mortality and frequent hypoglycemia in the intensive insulin therapy arm.
What should we do till reults of other major studies like GLUControl (3000 patients) or NICE - SUGAR (5000 patients) are pending. Here are couple of good advises.
1) As Dr. Atul Malhotra wrote in editorial of same issue of NEJM - "In my opinion, a reasonable approach would be to provide adequate exogenous insulin to achieve target glucose values of less than 150 mg per deciliter (8.3 mmol per liter), at least during the first three days in the ICU. If critical illness persists beyond three days despite the provision of other proven therapies and resuscitation, a goal of normoglycemia (80 to 110 mg per deciliter [4.4 to 6.1 mmol per liter]) could then be considered, to maximize the potential benefits". OR
2). Dr. Angus and Abraham suggested last year: "..it may be valuable to remember that, although the evidence for tight glycemic control does not yet support a grade A recommendation, it does appear to be stronger than that for continuing our existing practice of tolerating hyperglycemia. Thus, we should probably explore ways to introduce some form of tight glucose control during this interim period that seems feasible and safe given local considerations. Once better evidence is available, we can modify our plans accordingly."
References: Click to get article/abstract: (appears in popup window and second popup overwrites first popup).
1. Intensive Insulin Therapy in the Medical ICU - NEJM, Feb. 2, 2006, Volume 354:449-461
2. Intensive Insulin Therapy in Critically Ill Patients - N Engl J Med 2001; 345:1359-1367, Nov 8, 2001
3.Intensive insulin therapy in patient with severe sepsis and septic shock is associated with an increased rate of hypoglycemia - results from a randomized multicenter study (VISEP), Infection 2005;33: 19-20.
4. Glucontrol Study: Comparing the Effects of Two Glucose Control Regimens by Insulin in Intensive Care Unit Patients -clinicaltrials.gov
5. Normoglycaemia in Intensive Care Evaluation and Survival Using Glucose Algorithm Regulation (NICE - SUGAR STUDY) - clinicaltrials.gov
6. Intensive Insulin in Intensive Care - Volume 354:516-518, NEJM, feb. 2, 2006
7. Intensive Insulin Therapy in Critical Illness, Angus and Abraham Am. J. Respir. Crit. Care Med..2005; 172: 1358-1359
Sunday, February 05, 2006
metoprololpoivconversion251isamyth
Sunday February 5, 2006
Metoprolol PO:IV conversion - 2.5:1 is a myth ?
IV metoprolol is not FDA-approved for treatment of hypertension but it is in common use and general rule of conversion from PO to IV form is 2.5:1. This comes from a study on 5 healthy volunteers about 30 years ago.
Be aware, this is not the standard by any means. Literature shows coversion effect ranging from 2:1 to 5:1. It may be more safe to disregard any formula and to use initial dosage from 1.25-5 mg and subsequent dosage and frequency depending on the clinical response.
For more detailed discussion and further references, click here to read article from medscape.com (available with free registration) - Am J Health-Syst Pharm 60(2):189-191, 2003
Metoprolol PO:IV conversion - 2.5:1 is a myth ?
IV metoprolol is not FDA-approved for treatment of hypertension but it is in common use and general rule of conversion from PO to IV form is 2.5:1. This comes from a study on 5 healthy volunteers about 30 years ago.
Be aware, this is not the standard by any means. Literature shows coversion effect ranging from 2:1 to 5:1. It may be more safe to disregard any formula and to use initial dosage from 1.25-5 mg and subsequent dosage and frequency depending on the clinical response.
For more detailed discussion and further references, click here to read article from medscape.com (available with free registration) - Am J Health-Syst Pharm 60(2):189-191, 2003
Friday, February 03, 2006
arewedoctorsmostresistanttochange
Saturday February 4, 2006
Are we doctors most resistant to change?
This month's issue of Critical Care Medicine has published an article on physicians lack of embracing of low tidal volume despite clear and proven benefits from Arma trial of ARDSnet. Interestingly, this study (n=88 patients) was done at an ARDSnet participating university hospital. Patients who were ventilated with a tidal volume ≤7.5 mL/kg PBW 2 days after meeting criteria for ALI was only 39% and at day 7 only 56% of patients. During this study, physicians ordered the lung-protective ventilation protocol on only 16% of patients by day 2. In another earlier study to identify the barriers to the implementation of lung-protective ventilation - nursing and respiratory therapy staff at ten ARDSnet centers point finger to physicians' unwillingness to follow a ventilator protocol or recognize the patient as having ALI/ARDS.
Its almost 6 years since ARDSnet study was published and we are still having problem accepting the clear benefit ! Its time to read again famous JAMA article from 1999: " Why don't physicians follow clinical practice guidelines?.." and few major problems were deficits in physician knowledge, attitude difficulties, inertia of previous practice and behavioral issues !!!.
Note: Article from CCM-02'06 also tried to postulate various reasons of this lack of embracing of low tidal volume on available data, which can be found in full content of article and it includes possible fears of side effects from this approach or may be due to the anticipation of rapid recovery by patients with less severe disease.
References: Click to get article/abstract: (appears in popup window and second popup overwrites first popup)
1. Underuse of lung protective ventilation: Analysis of potential factors to explain physician behavior - Critical Care Medicine. 34(2):300-306, February 2006.
2. Prospective, Randomized, Multi-Center Trial of 12ml/kg Tidal Volume Positive Pressure Ventilation for Treatment of Acute Lung Injury and Acute Respiratory Distress Syndrome (ARMA) - ardsnet.org
3. Ventilation with Lower Tidal Volumes as Compared with Traditional Tidal Volumes for Acute Lung Injury and the Acute Respiratory Distress Syndrome - NEJM May 2000, Volume 342:1301-1308
4. Rubenfeld G, Caldwell E, Hudson L: Publication of study results does not increase use of lung protective ventilation in patients with acute lung injury. Am J Respir Crit Care Med 2001; 163:A295
5. Why Don't Physicians Follow Clinical Practice Guidelines?: A Framework for Improvement - JAMA. 1999;282:1458-1465. - full article available with free registration
Are we doctors most resistant to change?
This month's issue of Critical Care Medicine has published an article on physicians lack of embracing of low tidal volume despite clear and proven benefits from Arma trial of ARDSnet. Interestingly, this study (n=88 patients) was done at an ARDSnet participating university hospital. Patients who were ventilated with a tidal volume ≤7.5 mL/kg PBW 2 days after meeting criteria for ALI was only 39% and at day 7 only 56% of patients. During this study, physicians ordered the lung-protective ventilation protocol on only 16% of patients by day 2. In another earlier study to identify the barriers to the implementation of lung-protective ventilation - nursing and respiratory therapy staff at ten ARDSnet centers point finger to physicians' unwillingness to follow a ventilator protocol or recognize the patient as having ALI/ARDS.
Its almost 6 years since ARDSnet study was published and we are still having problem accepting the clear benefit ! Its time to read again famous JAMA article from 1999: " Why don't physicians follow clinical practice guidelines?.." and few major problems were deficits in physician knowledge, attitude difficulties, inertia of previous practice and behavioral issues !!!.
Note: Article from CCM-02'06 also tried to postulate various reasons of this lack of embracing of low tidal volume on available data, which can be found in full content of article and it includes possible fears of side effects from this approach or may be due to the anticipation of rapid recovery by patients with less severe disease.
References: Click to get article/abstract: (appears in popup window and second popup overwrites first popup)
1. Underuse of lung protective ventilation: Analysis of potential factors to explain physician behavior - Critical Care Medicine. 34(2):300-306, February 2006.
2. Prospective, Randomized, Multi-Center Trial of 12ml/kg Tidal Volume Positive Pressure Ventilation for Treatment of Acute Lung Injury and Acute Respiratory Distress Syndrome (ARMA) - ardsnet.org
3. Ventilation with Lower Tidal Volumes as Compared with Traditional Tidal Volumes for Acute Lung Injury and the Acute Respiratory Distress Syndrome - NEJM May 2000, Volume 342:1301-1308
4. Rubenfeld G, Caldwell E, Hudson L: Publication of study results does not increase use of lung protective ventilation in patients with acute lung injury. Am J Respir Crit Care Med 2001; 163:A295
5. Why Don't Physicians Follow Clinical Practice Guidelines?: A Framework for Improvement - JAMA. 1999;282:1458-1465. - full article available with free registration
systemiccapillaryleaksyndrome
Friday February 3, 2006
Systemic capillary leak syndrome
Capillary leak syndrome was described first time about 45 years ago. Being an intensivist, it is an important entity to know as episode is often preceded by shock syndromes, low-flow states, infection, ischemia-reperfusion injuries, toxemias, or poisoning and fallout is usually Multiple system organ failure (MSOF). Cause and pathophysiology is still not clear but most cases have been found associated with monoclonal gammopathy, generally an IgG class. Capillary leak syndrome as name says is due to capillary hyperpermeability with massive extravasation of plasma macromolecules and acute phase usually lasts for 1-4 days. Clinical features are abdominal pain, generalized edema, hypotension with possible cardiopulmonary collapse. Acute renal failure is due to hypovolemia and rhabdomyolysis. 6 Now here is the tricky part. Acute phase is followed by recruitment of the initially extravasated fluid causing intravascular overload marked by polyuria and/or pulmonary edema. Edema is usually proportional to earlier fluid resuscitation !. Treatment with Terbullatine and Theophylline has been suggested. 3
References: Click to get article/abstract: (appears in popup window and second popup overwrites first popup)
1. An unusual evolution of the systemic capillary leak syndrome -Nephrol Dial Transplant (2002) 17: 492-494
2. Capillary leak syndrome - orpha.net
3. Treatment of the Systemic Capillary Leak Syndrome with Terbutaline and Theophylline: A Case Series - annals 1 June 1999 Volume 130 Issue 11 Pages 905-909 -full pdf article available with free registration.
4. Systemic Capillary Leak Syndrome - Internal Medicine 41: 953?956, 2002, The Japanese Society of Internal Medicine
5. Lethal capillary leak syndrome after a single administration of interferon beta-1b - Neurology 1999;53:220
6.Idiopathic capillary leak syndrome complicated by massive rhabdomyolysis - Chest, Vol 104, 123-126
7. Lethal systemic capillary leak syndrome associated with severe ventilator-induced lung injury: An experimental study.- Critical Care Medicine. 31(3):885-892, March 2003.
Systemic capillary leak syndrome
Capillary leak syndrome was described first time about 45 years ago. Being an intensivist, it is an important entity to know as episode is often preceded by shock syndromes, low-flow states, infection, ischemia-reperfusion injuries, toxemias, or poisoning and fallout is usually Multiple system organ failure (MSOF). Cause and pathophysiology is still not clear but most cases have been found associated with monoclonal gammopathy, generally an IgG class. Capillary leak syndrome as name says is due to capillary hyperpermeability with massive extravasation of plasma macromolecules and acute phase usually lasts for 1-4 days. Clinical features are abdominal pain, generalized edema, hypotension with possible cardiopulmonary collapse. Acute renal failure is due to hypovolemia and rhabdomyolysis. 6 Now here is the tricky part. Acute phase is followed by recruitment of the initially extravasated fluid causing intravascular overload marked by polyuria and/or pulmonary edema. Edema is usually proportional to earlier fluid resuscitation !. Treatment with Terbullatine and Theophylline has been suggested. 3
References: Click to get article/abstract: (appears in popup window and second popup overwrites first popup)
1. An unusual evolution of the systemic capillary leak syndrome -Nephrol Dial Transplant (2002) 17: 492-494
2. Capillary leak syndrome - orpha.net
3. Treatment of the Systemic Capillary Leak Syndrome with Terbutaline and Theophylline: A Case Series - annals 1 June 1999 Volume 130 Issue 11 Pages 905-909 -full pdf article available with free registration.
4. Systemic Capillary Leak Syndrome - Internal Medicine 41: 953?956, 2002, The Japanese Society of Internal Medicine
5. Lethal capillary leak syndrome after a single administration of interferon beta-1b - Neurology 1999;53:220
6.Idiopathic capillary leak syndrome complicated by massive rhabdomyolysis - Chest, Vol 104, 123-126
7. Lethal systemic capillary leak syndrome associated with severe ventilator-induced lung injury: An experimental study.- Critical Care Medicine. 31(3):885-892, March 2003.
Wednesday, February 01, 2006
cpm
Thursday February 2, 2006
What's new on Central pontine myelinolysis (CPM)
Central pontine myelinolysis, a demyelinating disorder of central pons charaterized by pseudobulbar palsy and spastic quadriplegia, is co-diagnosed by specific MRI findings under know clinical settings or risk factors. Specific MRI findings are increased signal in the central pons on fluid-attenuated inversion recovery images (FLAIR) and hypointense lesions on T1-weighted images. 5 decades ago it was described in chronic alcoholism but over the time it was found in association with malnourished status, renal failure, diabetes mellitus, and post-orthotopic liver transplantation and came to known as hallmark of rapid correction of hyponatremia - but in recent years it has been reported with hypophosphetemia and in DKA (Diabetes Ketoacidosis) despite normal sodium level or no rapid correction of sodium. Treatment is supportive and prognosis thought to be universally fatal. In recent years there are reports of good recovery and long-term survival with proper supportive management.
See nice review article Central Pontine Myelinolysis from emedicine.com
References: Click to get article/abstract: (appears in popup window and second popup overwrites first popup)
1. Central Pontine Myelinolysis Following Hemodialysis - grand round at Depatment of Medicine, Maulana Azad Medical College, New Delhi
2. MR imaging of seven presumed cases of central pontine and. extrapontine myelinolysis. -Acta Neurobiol. Exp. 2001, 61: 141-144.
3. Management and Treatment of Psychotic Manifestations in Older Patients with Alcoholism: Part II - Clinical Geriatrics: 2004;12[5]:33-40
4. Central pontine myelinolysis temporally related to hypophosphataemia - Journal of Neurology Neurosurgery and Psychiatry 2003;74:820
5. Central pontine myelinolysis in a patient with diabetic ketoacidosis - The Journal of Critical Illness - Vol. 20, No. 4 - December 2005
6. Parkinsonism and recovery in central and extrapontine myelinolysis - Neurology India, Vol. 53, No. 2, April-June, 2005, pp. 219-220
What's new on Central pontine myelinolysis (CPM)
Central pontine myelinolysis, a demyelinating disorder of central pons charaterized by pseudobulbar palsy and spastic quadriplegia, is co-diagnosed by specific MRI findings under know clinical settings or risk factors. Specific MRI findings are increased signal in the central pons on fluid-attenuated inversion recovery images (FLAIR) and hypointense lesions on T1-weighted images. 5 decades ago it was described in chronic alcoholism but over the time it was found in association with malnourished status, renal failure, diabetes mellitus, and post-orthotopic liver transplantation and came to known as hallmark of rapid correction of hyponatremia - but in recent years it has been reported with hypophosphetemia and in DKA (Diabetes Ketoacidosis) despite normal sodium level or no rapid correction of sodium. Treatment is supportive and prognosis thought to be universally fatal. In recent years there are reports of good recovery and long-term survival with proper supportive management.
See nice review article Central Pontine Myelinolysis from emedicine.com
References: Click to get article/abstract: (appears in popup window and second popup overwrites first popup)
1. Central Pontine Myelinolysis Following Hemodialysis - grand round at Depatment of Medicine, Maulana Azad Medical College, New Delhi
2. MR imaging of seven presumed cases of central pontine and. extrapontine myelinolysis. -Acta Neurobiol. Exp. 2001, 61: 141-144.
3. Management and Treatment of Psychotic Manifestations in Older Patients with Alcoholism: Part II - Clinical Geriatrics: 2004;12[5]:33-40
4. Central pontine myelinolysis temporally related to hypophosphataemia - Journal of Neurology Neurosurgery and Psychiatry 2003;74:820
5. Central pontine myelinolysis in a patient with diabetic ketoacidosis - The Journal of Critical Illness - Vol. 20, No. 4 - December 2005
6. Parkinsonism and recovery in central and extrapontine myelinolysis - Neurology India, Vol. 53, No. 2, April-June, 2005, pp. 219-220
NMB
Wednesday February 1, 2006
Sedation in Neuro-muscular blockade patients
This month issue of American Journal of Critical Care (see reference # 1) has published interviews of 11 patients to determine and describe the remembered experiences, who were given neuromuscular blocking agents (8=vecuronium 3=cisatracurium) and sedatives and/or analgesics (4=propofol 4=midazolam 3=lorazepam) while they were in ICU. Interview was designed with 4 themes.
1) The first theme was back and forth between reality and the unreal, between life and death; the subtheme was having weird dreams.
2) The second theme was loss of control; the 2 subthemes were fighting or being tied down and being scared.
3) The third theme was almost dying, and
4) The fourth theme was feeling cared for.
It was found that, though patients can have positive recollections of nursing care, they can clearly recall experiences that were frightening and unpleasant, recurrent dreams or nightmares, avoidance of medical care and flashbacks or painful memories possibly leading to PTSD (posttraumatic stress disorder).
Are we doing a good job ?
Related:
Neuromuscular Blockade / Paralytics guidelines (SCCM 2002)
Sedation/Analgesia guidelines 2002 (SCCM)
Also see our previous pearl on Train of Four (TOF) and BIS monitoring
References / suggested readings: Click to get article/abstract
1. Patients’ Recollections of Therapeutic Paralysis in the Intensive Care Unit - American Journal of Critical Care. 2006;15: 86-94
2. Sedation and Neuromuscular Blockade in the ICU -Chest. 2005;128:477-479
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