Tuesday September 30, 2008
Q: Why its not a good idea to give "amp. of bicarb" via same line from where LR (Lactate Ringer) is infusing?
A: Reason, its not a good idea to mix "bicarb" with LR (Lactated Ringer) as LR contains calcium which will bind bicarbonate and will make the whole management ineffective.
Related previous pearls: LR and NS
Tuesday, September 30, 2008
Sunday, September 28, 2008
Sunday September 28, 2008
CURB-65 Score
Lim and colleagues have designed a score called CURB-65 to rate mortality in community acquired pneumonia (CAP) - based on information available at initial hospital assessment. Give one point each for following values
C = Confusion
U = Urea (BUN) if more than 20 mg/dl (7 mmol/l)
R = Respiratory rate if more than / = 30/min,
B = BP if SBP less than 90 or DBP less than/= 60,
65 = If age more than / = 65 years
With score 0 expected mortality is 0.7%,
With score 1 expected mortality is 3.2%,
With score 2 expected mortality is 13%,
With score 3 expected mortality is 17%,
With score 4 expected mortality is 41.5% and
With score 5 expected mortality is 57%
Reference: click to get abstract
1.Defining community acquired pneumonia severity on presentation to hospital: an international derivation and validation study - W S Lim, M M van der Eerden, R Laing, W G Boersma, N Karalus, G I Town, S A Lewis and J T Macfarlane - Thorax 2003;58:377-382
CURB-65 Score
Lim and colleagues have designed a score called CURB-65 to rate mortality in community acquired pneumonia (CAP) - based on information available at initial hospital assessment. Give one point each for following values
C = Confusion
U = Urea (BUN) if more than 20 mg/dl (7 mmol/l)
R = Respiratory rate if more than / = 30/min,
B = BP if SBP less than 90 or DBP less than/= 60,
65 = If age more than / = 65 years
With score 0 expected mortality is 0.7%,
With score 1 expected mortality is 3.2%,
With score 2 expected mortality is 13%,
With score 3 expected mortality is 17%,
With score 4 expected mortality is 41.5% and
With score 5 expected mortality is 57%
Reference: click to get abstract
1.Defining community acquired pneumonia severity on presentation to hospital: an international derivation and validation study - W S Lim, M M van der Eerden, R Laing, W G Boersma, N Karalus, G I Town, S A Lewis and J T Macfarlane - Thorax 2003;58:377-382
Saturday, September 27, 2008
Saturday September 27, 2008
An important score card to remember !
An important score card to remember !
TIMI RISK SCORE FOR STEMI
Category = Points
Age more than 75 yrs = 3
Age 65-74 yrs = 2
DM or HTN or Angina = 1
SBP less than 100 mm hg = 3
HR more than 100 bpm = 2
Killip II-IV = 2
Weight less than 67 kg (150 lbs) = 1
Anterior STE or LBBB = 1
Time to treatment more than 4hrs = 1
Total points (0-14)
TIMI RISK SCORE AND 30 DAY MORTALITY
Risk Score = 30 day mortality
0 = 0.8
1 = 1.6
2 = 2.2
3 = 4.4
4 = 7.3
5 = 12
6 = 16
7 = 23
8 = 27
more than 8 = 36
Morrow et al. , TIMI Risk Score for ST-Elevation Myocardial Infarction: A Convenient, Bedside, Clinical Score for Risk Assessment at Presentation, Circulation 2000; 102:2031-2037
Friday, September 26, 2008
Friday September 26, 2008
KILLIP Classification
The Killip classification (designed about 40 years ago) is a system used in individuals with an acute myocardial infarction (heart attack), in order to risk stratify them. Individuals with a low Killip class are less likely to die within the first 30 days after their myocardial infarction than individuals with a high Killip class.
Patients were ranked by Killip class in the following way:
Killip class I includes individuals with no clinical signs of heart failure
Killip class II includes individuals with rales or crackles in the lungs an S3 gallop, and elevated jugular venous pressure.
Killip class III describes individuals with frank acute pulmonary edema.
Killip class IV describes individuals in cardiogenic shock or hypotension (measured as SBP lower than 90 mmHg), and evidence of peripheral vasoconstriction (oliguria, cyanosisor sweating).
Mortality rate based on Killip classification
Killip class I: 81/250 patients; 32% (27 to 38%). Mortality rate was found to be at 6%.
Killip class II: 96/250 patients; 38% (32 to 44%). Mortality rate was found to be at 17%.
Killip class III: 26/250 patients; 10% (6.6 to 14%). Mortality rate was found to be at 38%.
Killip class IV: 47/250 patients; 19% (14 to 24%). Mortality rate was found to be at 81%.
Killip T, Kimball JT. Treatment of myocardial infarction in a coronary care unit: a two year experience of 250 patients. Am J Cardiol 1967; 20: 457-464.
KILLIP Classification
The Killip classification (designed about 40 years ago) is a system used in individuals with an acute myocardial infarction (heart attack), in order to risk stratify them. Individuals with a low Killip class are less likely to die within the first 30 days after their myocardial infarction than individuals with a high Killip class.
Patients were ranked by Killip class in the following way:
Killip class I includes individuals with no clinical signs of heart failure
Killip class II includes individuals with rales or crackles in the lungs an S3 gallop, and elevated jugular venous pressure.
Killip class III describes individuals with frank acute pulmonary edema.
Killip class IV describes individuals in cardiogenic shock or hypotension (measured as SBP lower than 90 mmHg), and evidence of peripheral vasoconstriction (oliguria, cyanosisor sweating).
Mortality rate based on Killip classification
Killip class I: 81/250 patients; 32% (27 to 38%). Mortality rate was found to be at 6%.
Killip class II: 96/250 patients; 38% (32 to 44%). Mortality rate was found to be at 17%.
Killip class III: 26/250 patients; 10% (6.6 to 14%). Mortality rate was found to be at 38%.
Killip class IV: 47/250 patients; 19% (14 to 24%). Mortality rate was found to be at 81%.
Killip T, Kimball JT. Treatment of myocardial infarction in a coronary care unit: a two year experience of 250 patients. Am J Cardiol 1967; 20: 457-464.
Thursday, September 25, 2008
Thursday September 25, 2008
Q: Does Phenytoin (Dilantin) get cleared by hemodialysis or hemoperfusion?
A; No (clinically insignificant removal)
Clinical significance:
1. In Phenytoin toxicity/overdose, Hemodialysis or hemoperfusion are ineffective for enhancing elimination.
2. Hemodialysis patients do not require extra dosing post dialysis though require frequent monitoring due to lower albumin level.
Q: Does Phenytoin (Dilantin) get cleared by hemodialysis or hemoperfusion?
A; No (clinically insignificant removal)
Clinical significance:
1. In Phenytoin toxicity/overdose, Hemodialysis or hemoperfusion are ineffective for enhancing elimination.
2. Hemodialysis patients do not require extra dosing post dialysis though require frequent monitoring due to lower albumin level.
Wednesday, September 24, 2008
Wednesday September 24, 2008
Is there any change in criteria for identifying exudative pleural effusion
Heffner and Steven Sahn did the study to determine multilevel likelihood ratios for pleural fluid tests that are commonly used to discriminate between exudative and transudative pleural effusions. Studies were identified by searching MEDLINE and related bibliographies. Data were obtained for 1,448 patients from seven primary investigators led to modified Light criteria. These incorporate the test combination of the value of LDH of pleural fluid to serum ratio, PF/serum protein ratio, PF/serum LDH ratio, LDH of pleural fluid alone. If any of these being positive that indicates exudative effusion.
Pleural fluid Test/ Metaanalysis cut Points
Pleural fluid protein = more than 2.9 g/dl
PF/serum protein ratio = more than .5
Pleural fluid LDH = more than 0.45 upper limit of normal
PF/serum LDH ratio = more than 0.6
Pleural fluid cholesterol = more than 45 mg/dl
Conclusion: Multilevel likelihood ratios combined with a clinician’s estimation of the pretest probability of an exudative effusion improve the diagnostic accuracy of discriminating between exudative and transudative pleural effusions. Likelihood ratios avoid the use of confusing terms, such as “pseudoexudates,” that derive from the use of single cutoff points for pleural fluid tests.
Reference: click to get abstract
Heffner JE, Sahn SA, Brown LK. Multilevel Likelihood Ratios for Identifying Exudative Pleural Effusions. CHEST 2002; 121:1916–1920
Is there any change in criteria for identifying exudative pleural effusion
Heffner and Steven Sahn did the study to determine multilevel likelihood ratios for pleural fluid tests that are commonly used to discriminate between exudative and transudative pleural effusions. Studies were identified by searching MEDLINE and related bibliographies. Data were obtained for 1,448 patients from seven primary investigators led to modified Light criteria. These incorporate the test combination of the value of LDH of pleural fluid to serum ratio, PF/serum protein ratio, PF/serum LDH ratio, LDH of pleural fluid alone. If any of these being positive that indicates exudative effusion.
Pleural fluid Test/ Metaanalysis cut Points
Pleural fluid protein = more than 2.9 g/dl
PF/serum protein ratio = more than .5
Pleural fluid LDH = more than 0.45 upper limit of normal
PF/serum LDH ratio = more than 0.6
Pleural fluid cholesterol = more than 45 mg/dl
Conclusion: Multilevel likelihood ratios combined with a clinician’s estimation of the pretest probability of an exudative effusion improve the diagnostic accuracy of discriminating between exudative and transudative pleural effusions. Likelihood ratios avoid the use of confusing terms, such as “pseudoexudates,” that derive from the use of single cutoff points for pleural fluid tests.
Reference: click to get abstract
Heffner JE, Sahn SA, Brown LK. Multilevel Likelihood Ratios for Identifying Exudative Pleural Effusions. CHEST 2002; 121:1916–1920
Tuesday, September 23, 2008
Tuesday September 23, 2008
Mortality in Acute Lung Injury due to Pulmonary vs. Nonpulmonary Sepsis
Janothan Sevransky from John Hopkins studied 288 patients with sepsis induced ALI and prospectively classified as having pulmonary vs. non pulmonary sources of sepsis.
Result: Unadjusted analysis revealed, lower in hospital mortality for pulmonary sepsis vs. nonpulmonary sepsis (42% vs. 66%, p less than 0.0001).
Conclusion: Although lower mortality was observed for ALI patients with a pulmonary vs. non pulmonary source of sepsis, this finding was due to lower severity of illness in those with pulmonary sepsis.
Reference: click to get abstract
Sevransky JE, Martin GS, Mendez-Tellez P, Shanholtz C, Brower R, Pronovost PJ, Needham DM. pulmonary vs nonpulmonary sepsis and mortality in acute lung injury. Chest 2008; 134: 534-538
Mortality in Acute Lung Injury due to Pulmonary vs. Nonpulmonary Sepsis
Janothan Sevransky from John Hopkins studied 288 patients with sepsis induced ALI and prospectively classified as having pulmonary vs. non pulmonary sources of sepsis.
Result: Unadjusted analysis revealed, lower in hospital mortality for pulmonary sepsis vs. nonpulmonary sepsis (42% vs. 66%, p less than 0.0001).
Adjusted analysis several factors predicted the mortality:
- Age: OR 1.03
- Charlson co morbidity index: OR 1.15
- ICU length of stay prior to ALI diagnosis: OR 1.19
- APACHE II score: OR 1.07
- Lung injury score: OR 1.64
- SOFA score: OR 1.15
- Cumulative fluid balance in first 7 days after ALI diagnosis: OR 1.06
Conclusion: Although lower mortality was observed for ALI patients with a pulmonary vs. non pulmonary source of sepsis, this finding was due to lower severity of illness in those with pulmonary sepsis.
Reference: click to get abstract
Sevransky JE, Martin GS, Mendez-Tellez P, Shanholtz C, Brower R, Pronovost PJ, Needham DM. pulmonary vs nonpulmonary sepsis and mortality in acute lung injury. Chest 2008; 134: 534-538
Monday, September 22, 2008
Monday September 22, 2008
Preventing sympathetic surge during head injured patient's intubation
Orotracheal intubation cause sympathetic surges resulting in increase ICP (intracranial pressure). Despite no definite answer, endeavours continue to minimize iatrogenic expansion of hematoma. 3 drugs have shown some neuroprotective benefit during intubation of spontaneous or traumatic brain injury although they remained controversial and their benefit never get purely established.
1. Lidocaine: One study 25 years ago (but later studies were negative) showed that about 100 mg of Lidocaine (1.5 mg/kg), blunt ICP by approximately 15 mm Hg with tracheal suctioning 1. Mechanism of action is not entirely clear but probably lidocaine decreases cough reflex and dysrhythmias. No studies document any harmful effects of prophylactic lidocaine 2.
2. Fentanyl: Idea is to achieve sympatholysis and block hypertension and tachycardia. Dose of 2.5-3 μg/kg has been found to be without risk of hypotension.
3. Esmolol: Here again, goal is to achieve sympatholysis. Esmolol with dose of 100-200 mg has effect said to be superior to fentanyl and markedly superior to lidocaine 3, 4.
Combinations of above drugs have been described to have synergestic and better effect than using them alone, either esmolol and fentanyl or fentanyl and lidociane.
Related previous pearl: ICP (Intracranial pressure) wave forms
Related Link: Airway Management of the Critically Ill Patient (Chest.
2005;127:1397-1412)
References: click to get abstract
1. Intravenously administered lidocaine prevents intracranial hypertension during endotracheal suctioning. Anesthesiology 1980;52:516-8
2. Prophylactic lidocaine use preintubation: a review - J Emerg Med. 1994 Jul-Aug;12(4):499-506.
3. Attenuation of hemodynamic responses to rapid sequence induction and intubation in healthy patients with a single bolus of esmolol. J Clin Anesth 1990;2:343-52.
4. A comparison of lidocaine, fentanyl, and esmolol for attenuation of cardiovascular response to laryngoscopy and tracheal intubation. Acta Anaesthesiol Sin 1996;34(2):61-7.
Preventing sympathetic surge during head injured patient's intubation
Orotracheal intubation cause sympathetic surges resulting in increase ICP (intracranial pressure). Despite no definite answer, endeavours continue to minimize iatrogenic expansion of hematoma. 3 drugs have shown some neuroprotective benefit during intubation of spontaneous or traumatic brain injury although they remained controversial and their benefit never get purely established.
1. Lidocaine: One study 25 years ago (but later studies were negative) showed that about 100 mg of Lidocaine (1.5 mg/kg), blunt ICP by approximately 15 mm Hg with tracheal suctioning 1. Mechanism of action is not entirely clear but probably lidocaine decreases cough reflex and dysrhythmias. No studies document any harmful effects of prophylactic lidocaine 2.
2. Fentanyl: Idea is to achieve sympatholysis and block hypertension and tachycardia. Dose of 2.5-3 μg/kg has been found to be without risk of hypotension.
3. Esmolol: Here again, goal is to achieve sympatholysis. Esmolol with dose of 100-200 mg has effect said to be superior to fentanyl and markedly superior to lidocaine 3, 4.
Combinations of above drugs have been described to have synergestic and better effect than using them alone, either esmolol and fentanyl or fentanyl and lidociane.
Related previous pearl: ICP (Intracranial pressure) wave forms
Related Link: Airway Management of the Critically Ill Patient (Chest.
2005;127:1397-1412)
References: click to get abstract
1. Intravenously administered lidocaine prevents intracranial hypertension during endotracheal suctioning. Anesthesiology 1980;52:516-8
2. Prophylactic lidocaine use preintubation: a review - J Emerg Med. 1994 Jul-Aug;12(4):499-506.
3. Attenuation of hemodynamic responses to rapid sequence induction and intubation in healthy patients with a single bolus of esmolol. J Clin Anesth 1990;2:343-52.
4. A comparison of lidocaine, fentanyl, and esmolol for attenuation of cardiovascular response to laryngoscopy and tracheal intubation. Acta Anaesthesiol Sin 1996;34(2):61-7.
Sunday, September 21, 2008
Sunday September 21, 2008
What's the right length of endotracheal tube (ETT) for oral intubation?
As a gold standard the only way to make sure that tip of ETT is atleast 2 cm away from carina (or at appropriate place) is via chest X-ray. But there are many bedside quick tricks/formulae described in literature. One such formula 1 which also found to have good clinical correlation, is
ETT length (incisors to midpoint of trachea, cm) = patient's height (cm)/10+5
Like, if patient's height is 170 cm, ETT should be taped at
170/10 + 5 = 22 cm
Another trick is to have ETT's cuff palpable at sternal notch, a technique described about 40 years ago ! 2 .
Reference:
1. Anaesthesia Intensive Care 1992; 20:156;
2. Anesthesiology 1964; 25:169
What's the right length of endotracheal tube (ETT) for oral intubation?
As a gold standard the only way to make sure that tip of ETT is atleast 2 cm away from carina (or at appropriate place) is via chest X-ray. But there are many bedside quick tricks/formulae described in literature. One such formula 1 which also found to have good clinical correlation, is
ETT length (incisors to midpoint of trachea, cm) = patient's height (cm)/10+5
Like, if patient's height is 170 cm, ETT should be taped at
170/10 + 5 = 22 cm
Another trick is to have ETT's cuff palpable at sternal notch, a technique described about 40 years ago ! 2 .
Reference:
1. Anaesthesia Intensive Care 1992; 20:156;
2. Anesthesiology 1964; 25:169
Saturday, September 20, 2008
Saturday September 20, 2008
Diagnostic criteria of Delirium
Q: What are 4 basic criteria to label patient as having Delirium?
A: Per American Psychiatric Association's Diagnostic and Statistical Manual of Mental Disorders. 4th ed. (DSM-IV), Patient is having delirium if
1. Disturbance of consciousness (eg, reduced clarity of awareness of the environment) with reduced ability to focus, sustain, or shift attention.
2. A change in cognition such as memory deficit, disorientation, language disturbance (or the development of a perceptual disturbance that is not better accounted for by a preexisting, established, or evolving dementia).
3. The disturbance develops over a short period of time (usually hours) and tends to fluctuate during the course of the day.
4. Disturbance caused by a general medical condition or substance intoxication or medication use.
References: click to get abstract/article
1. An Empirical Study of Different Diagnostic Criteria for Delirium Among Elderly Medical Inpatients - J Neuropsychiatry Clin Neurosci 15:200-207, May 2003
2. Delirium in Elderly Patients - Focus 3:320-332 (2005)
3. Delirium in Older Persons - N. Engl. J. Med., March 16, 2006; 354(11): 1157 - 1165
4. Delirium - emedicine.com
5. Delirium - American Family Physician® Vol. 67/No. 5 (March 1, 2003)
Diagnostic criteria of Delirium
Q: What are 4 basic criteria to label patient as having Delirium?
A: Per American Psychiatric Association's Diagnostic and Statistical Manual of Mental Disorders. 4th ed. (DSM-IV), Patient is having delirium if
1. Disturbance of consciousness (eg, reduced clarity of awareness of the environment) with reduced ability to focus, sustain, or shift attention.
2. A change in cognition such as memory deficit, disorientation, language disturbance (or the development of a perceptual disturbance that is not better accounted for by a preexisting, established, or evolving dementia).
3. The disturbance develops over a short period of time (usually hours) and tends to fluctuate during the course of the day.
4. Disturbance caused by a general medical condition or substance intoxication or medication use.
References: click to get abstract/article
1. An Empirical Study of Different Diagnostic Criteria for Delirium Among Elderly Medical Inpatients - J Neuropsychiatry Clin Neurosci 15:200-207, May 2003
2. Delirium in Elderly Patients - Focus 3:320-332 (2005)
3. Delirium in Older Persons - N. Engl. J. Med., March 16, 2006; 354(11): 1157 - 1165
4. Delirium - emedicine.com
5. Delirium - American Family Physician® Vol. 67/No. 5 (March 1, 2003)
Friday, September 19, 2008
Friday September 19, 2008
Case: 52 year old male is back from cardiac angioplasty with abciximab (ReoPro) infusion. Pre-cath labs were normal. CBC was send per protocol after 4 hours of abciximab infusion and lab call with critical platelet level of 62. Abciximab was stopped and hematology consulted. Hematology advised to restart abciximab !!
Pseudothrombocytopenia
Pseudothrombocytopenia is a common phenomenon with patients on abciximab (ReoPro). It is a benign condition and is not a real thrombocytopenia as platelets actually clump in collecting tubes containg EDTA. It is an important diagnosis to make as it may leave patient without an appropriate treatment. Diagnosis can be made by reviewing peripheral blood film or drawing blood in citrated or heparinized tube. It is not clear why abciximab cause more EDTA-induced platelet clumping.* EDTA (Ethylenediaminetetraacetic acid) is a commonly used anticoagulant in sampling tubes for blood counts.
References: click to get abstract/article
1. Occurrence and clinical significance of pseudothrombocytopenia during abciximab therapy J Am Coll Cardiol. 2000 Jul;36(1):75-83.
2. Abciximab-Associated Pseudothrombocytopenia - Circulation. 2000;101:938
3. EDTA dependent pseudothrombocytopenia caused by antibodies against the cytoadhesive receptor of platelet gpIIB-IIIA - Journal of Clinical Pathology 1994;47:625-630
4. Pseudothrombocytopenia Volume 329:1467 Nov. 11, 1993
Case: 52 year old male is back from cardiac angioplasty with abciximab (ReoPro) infusion. Pre-cath labs were normal. CBC was send per protocol after 4 hours of abciximab infusion and lab call with critical platelet level of 62. Abciximab was stopped and hematology consulted. Hematology advised to restart abciximab !!
Pseudothrombocytopenia
Pseudothrombocytopenia is a common phenomenon with patients on abciximab (ReoPro). It is a benign condition and is not a real thrombocytopenia as platelets actually clump in collecting tubes containg EDTA. It is an important diagnosis to make as it may leave patient without an appropriate treatment. Diagnosis can be made by reviewing peripheral blood film or drawing blood in citrated or heparinized tube. It is not clear why abciximab cause more EDTA-induced platelet clumping.* EDTA (Ethylenediaminetetraacetic acid) is a commonly used anticoagulant in sampling tubes for blood counts.
References: click to get abstract/article
1. Occurrence and clinical significance of pseudothrombocytopenia during abciximab therapy J Am Coll Cardiol. 2000 Jul;36(1):75-83.
2. Abciximab-Associated Pseudothrombocytopenia - Circulation. 2000;101:938
3. EDTA dependent pseudothrombocytopenia caused by antibodies against the cytoadhesive receptor of platelet gpIIB-IIIA - Journal of Clinical Pathology 1994;47:625-630
4. Pseudothrombocytopenia Volume 329:1467 Nov. 11, 1993
Thursday, September 18, 2008
Thursday September 18, 2008
Increased mortality of ventilated patients with endotracheal Pseudomonas aeruginosa without clinical signs of infection
The patients who have Pseudomonas aeruginosa colonization do worse compared to patients who have ventilator associated pneumonia, according to this prospective study in Journal of CCM 1.
Objective: To investigate the frequency and outcomes of ventilated patients with newly acquired large burdens of Pseudomonas aeruginosa and to test the hypothesis that large quantities of bacteria are associated with adverse patient outcomes. It was a prospective, single-center, observational, cohort study in a medical-surgical intensive care units in a tertiary care university hospital.
Patients: All adult patients requiring more than/ =48 hrs of mechanical ventilation and identified as having newly acquired P. aeruginosa in their lower respiratory tracts.
Results:
Furthermore, more patients with high P. aeruginosa burdens secreted the type III secretion facilitator protein, PcrV (p = 0.01).
Conclusions: A group of patients with large burdens of P. aeruginosa who did not meet clinical criteria for ventilator-associated pneumonia had an increased risk of death when compared with patients who had high P. aeruginosa burdens and met ventilator-associated pneumonia criteria. Patients with high P. aeruginosa burden seemed to possess more virulent strains.
Trivia: Do you know that P. aeruginosa is capable of growth in Diesel and Jet fuel where it is known as a hydrocarbon utilizing microorganism ("HUM bug") and also has the ability to grow at 42 degree Celsius?
References: Please click to get abstract
1. Increased mortality of ventilated patients with endotracheal Pseudomonas aeruginosa without clinical signs of infection - Critical Care Medicine. 36(9):2495-2503, September 2008
Increased mortality of ventilated patients with endotracheal Pseudomonas aeruginosa without clinical signs of infection
The patients who have Pseudomonas aeruginosa colonization do worse compared to patients who have ventilator associated pneumonia, according to this prospective study in Journal of CCM 1.
Objective: To investigate the frequency and outcomes of ventilated patients with newly acquired large burdens of Pseudomonas aeruginosa and to test the hypothesis that large quantities of bacteria are associated with adverse patient outcomes. It was a prospective, single-center, observational, cohort study in a medical-surgical intensive care units in a tertiary care university hospital.
Patients: All adult patients requiring more than/ =48 hrs of mechanical ventilation and identified as having newly acquired P. aeruginosa in their lower respiratory tracts.
Results:
- Of 45 patients with high P. aeruginosa burdens ( more than/=1,000,000 cfu/mL in endotracheal aspirates; more than/=10,000 cfu/mL in bronchoalveolar-lavage), 17 (37.8%) patients did not meet clinical criteria for ventilator-associated pneumonia and had a statistically significant higher risk of death (p = 0.002) when compared with the patients who had P. aeruginosa ventilator-associated pneumonia.
- When excluding the ten patients who had ventilator-associated pneumonia attributed to bacteria other than P. aeruginosa or attributed to multiple bacteria including P. aeruginosa, the risk of death remained statistically significant (p = 0.006).
Furthermore, more patients with high P. aeruginosa burdens secreted the type III secretion facilitator protein, PcrV (p = 0.01).
Conclusions: A group of patients with large burdens of P. aeruginosa who did not meet clinical criteria for ventilator-associated pneumonia had an increased risk of death when compared with patients who had high P. aeruginosa burdens and met ventilator-associated pneumonia criteria. Patients with high P. aeruginosa burden seemed to possess more virulent strains.
Trivia: Do you know that P. aeruginosa is capable of growth in Diesel and Jet fuel where it is known as a hydrocarbon utilizing microorganism ("HUM bug") and also has the ability to grow at 42 degree Celsius?
References: Please click to get abstract
1. Increased mortality of ventilated patients with endotracheal Pseudomonas aeruginosa without clinical signs of infection - Critical Care Medicine. 36(9):2495-2503, September 2008
Wednesday, September 17, 2008
Wednesday September 17, 2008
Q; 65 year old female admitted to ICU 9 days ago with small bowel obstruction. Pt. is now stable and actually is about to get transferred out of unit. Patient suddenly start complaining of choking sensation with two hands on neck. Monitor shows oxygen desaturation. Patient intubated emergently. No laryngeal or vocal edema seen on laryngoscope but vocal cord paralysis noted.
A; Nasogastric tube syndrome : Nasogastric tube syndrome was described about 25 years ago by Sofferman and coll. It is a life-threatening complication of an indwelling (more than a week) nasogastric tube. The syndrome may present as complete vocal cord abductor paralysis. The syndrome is thought to result from perforation of the NG tube-induced esophageal ulcer and infection of the posterior cricoid region (postcricoid chondritis) with subsequent dysfunction of vocal cord abduction. Unilateral paralysis of cord is also described. Treatment is protection of airway, removal of NG tube and antibiotics. Some advocates antireflux therapy too. Another variant is described with no esophageal ulcer but possibly because of ischemia of the laryngeal abductor muscle secondary to physical compression of the postcricoid blood vessels by NG tube.
References: Please click to get abstract
1. The nasogastric tube syndrome: two case reports and review of the literature. Head Neck. 2001 Jan;23(1):59-63.
2. A variant form of nasogastric tube syndrome. Intern Med. 2005 Dec;44(12):1286-90.
3. Case Report - Nasogastric Tube Syndrome: The Unilateral Variant - Medical Principles and Practice Vol. 12, No. 1, 2003
4. Sofferman, R.A. and Hubbell, R.N., "Laryngeal Complications of Nasogastric Tubes," ANNALS OTOLOGY, RHINOLOGY, AND LARYNGOLOGY, 90:465-468, 1981.
Q; 65 year old female admitted to ICU 9 days ago with small bowel obstruction. Pt. is now stable and actually is about to get transferred out of unit. Patient suddenly start complaining of choking sensation with two hands on neck. Monitor shows oxygen desaturation. Patient intubated emergently. No laryngeal or vocal edema seen on laryngoscope but vocal cord paralysis noted.
A; Nasogastric tube syndrome : Nasogastric tube syndrome was described about 25 years ago by Sofferman and coll. It is a life-threatening complication of an indwelling (more than a week) nasogastric tube. The syndrome may present as complete vocal cord abductor paralysis. The syndrome is thought to result from perforation of the NG tube-induced esophageal ulcer and infection of the posterior cricoid region (postcricoid chondritis) with subsequent dysfunction of vocal cord abduction. Unilateral paralysis of cord is also described. Treatment is protection of airway, removal of NG tube and antibiotics. Some advocates antireflux therapy too. Another variant is described with no esophageal ulcer but possibly because of ischemia of the laryngeal abductor muscle secondary to physical compression of the postcricoid blood vessels by NG tube.
References: Please click to get abstract
1. The nasogastric tube syndrome: two case reports and review of the literature. Head Neck. 2001 Jan;23(1):59-63.
2. A variant form of nasogastric tube syndrome. Intern Med. 2005 Dec;44(12):1286-90.
3. Case Report - Nasogastric Tube Syndrome: The Unilateral Variant - Medical Principles and Practice Vol. 12, No. 1, 2003
4. Sofferman, R.A. and Hubbell, R.N., "Laryngeal Complications of Nasogastric Tubes," ANNALS OTOLOGY, RHINOLOGY, AND LARYNGOLOGY, 90:465-468, 1981.
Tuesday, September 16, 2008
Monday, September 15, 2008
Sunday, September 14, 2008
Sunday September 14, 2008
Digoxin Toxicity
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 may be misleading.
Digoxin Toxicity
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 may be misleading.
Saturday, September 13, 2008
Saturday September 13, 2008
Frog Sign
Q: What is Frog sign?
A: In Paroxysmal Supra-Ventricular Tachycardia (PSVT) a rapid and regular bulging seen in the neck. These are actually prominent jugular venous A waves due to atrial contraction against the closed tricuspid valve, and termed as "frog sign".
References:
1. Brief report: the hemodynamic mechanism of pounding in the neck in atrioventricular nodal reentrant tachycardia - N Engl J Med. 1992 Sep 10;327(11):772-4.
2. Evaluation of Patients with Palpitations - NEJM, May, 1998, Volume 338:1369-1373
Frog Sign
Q: What is Frog sign?
A: In Paroxysmal Supra-Ventricular Tachycardia (PSVT) a rapid and regular bulging seen in the neck. These are actually prominent jugular venous A waves due to atrial contraction against the closed tricuspid valve, and termed as "frog sign".
References:
1. Brief report: the hemodynamic mechanism of pounding in the neck in atrioventricular nodal reentrant tachycardia - N Engl J Med. 1992 Sep 10;327(11):772-4.
2. Evaluation of Patients with Palpitations - NEJM, May, 1998, Volume 338:1369-1373
Friday, September 12, 2008
Friday September 12, 2008
Movement of endotracheal tube (ETT) with neck
Q: Extension of neck (Chin up) will cause ETT to migrate (up or down) ?
Q: Flexion of neck (Chin down) will cause ETT to migrate (up or down) ?
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
Q: Extension of neck (Chin up) will cause ETT to migrate (up or down) ?
Q: Flexion of neck (Chin down) will cause ETT to migrate (up or down) ?
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
Thursday, September 11, 2008
Thursday September 11, 2008
Does Restraint has any influence on unplanned Extubation
Background: Unplanned extubation commonly occurs in ICUs. Various physical restraints have been used to prevent patients from removing their endotracheal tubes. However, physical restraint not only does not consistently prevent injury but also may be a safety hazard to patients
.
Objective:To evaluate the effect of physical restraint on unplanned extubation in adult intensive care patients.
200 age-, sex-, and diagnosis-matched controls
Results:The incidence rate of unplanned extubation was 8.7%. Factors associated with increased risk for unplanned extubation included
Conclusions: An impaired level of consciousness on admission to the intensive care unit and the presence of nosocomial infection intensify the risk for unplanned extubation, even when physical restraints are used.
Reference: click to get abstract/article
Chang LY, Wang KWK, Chao YF. Influence of physical restraint on unplanned extubation of adult intensive care patients: A case-control study. American Journal of critical Care 2008; 17:408-415
Does Restraint has any influence on unplanned Extubation
Background: Unplanned extubation commonly occurs in ICUs. Various physical restraints have been used to prevent patients from removing their endotracheal tubes. However, physical restraint not only does not consistently prevent injury but also may be a safety hazard to patients
.
Objective:To evaluate the effect of physical restraint on unplanned extubation in adult intensive care patients.
Methods:
Results:The incidence rate of unplanned extubation was 8.7%. Factors associated with increased risk for unplanned extubation included
- Physical restraints: 3.11 times
- Nosocomial infection: 2.02 times
- Glasgow coma scale more than 9: 1.98 times
Episodes of unexplained extubation were also associated with increase ICU stay.
Conclusions: An impaired level of consciousness on admission to the intensive care unit and the presence of nosocomial infection intensify the risk for unplanned extubation, even when physical restraints are used.
Reference: click to get abstract/article
Chang LY, Wang KWK, Chao YF. Influence of physical restraint on unplanned extubation of adult intensive care patients: A case-control study. American Journal of critical Care 2008; 17:408-415
Wednesday, September 10, 2008
Wednesday September 10, 2008
Amiodarone Neurotoxicity
Amiodarone neurotoxicity has been reported in up to 40% of patients and may easily get miss or misdiagnosed when an elderly patient presents with multiple symptoms. Major manifestation are peripheral neuropathy causing proximal motor weakness, ataxia and fine resting tremor. It may also present as neuromyopathy. A case has been described with autonomic dysfunction presented as incapacitating orthostatic hypotension. Cases has been reported with Amiodarone-Induced Delirium .
Most neurotoxicities are dose related and resolved with discontinuation of Amiodarone. Being an intensivist it may be important to keep this very common dose related toxicity in mind while evaluating patient with neurologic symptoms.
Related: Amiodarone pulmonary toxicity.
References: Click to see abstract/article
1. Amiodarone-Induced Neuromyopathy: Three Cases and a Review of the Literature - Journal of Clinical Neuromuscular Disease. 3(3):97-105, March 2002.
2. Severe Ataxia Caused by Amiodarone - Volume 96, Issue 10, Pages 1463-1464 (15 November 2005) - Am J of Card
3. Amiodarone toxicity presenting as pulmonary mass and peripheral neuropathy: the continuing diagnostic challenge - Postgraduate Medical Journal 2006;82:73-75
4. Amiodarone: Guidelines for Use and Monitoring - aafp.org - Vol 68, No. 11, Dec., 2003
5. Atypical pulmonary and neurologic complications of amiodarone in the same patient. Report of a case and review of the literature - Vol. 147 No. 10, October 1, 1987 - Archive of Int Med.
6. Amiodarone-Induced Delirium - Am J Psychiatry 156:1119, July 1999
Amiodarone Neurotoxicity
Amiodarone neurotoxicity has been reported in up to 40% of patients and may easily get miss or misdiagnosed when an elderly patient presents with multiple symptoms. Major manifestation are peripheral neuropathy causing proximal motor weakness, ataxia and fine resting tremor. It may also present as neuromyopathy. A case has been described with autonomic dysfunction presented as incapacitating orthostatic hypotension. Cases has been reported with Amiodarone-Induced Delirium .
Most neurotoxicities are dose related and resolved with discontinuation of Amiodarone. Being an intensivist it may be important to keep this very common dose related toxicity in mind while evaluating patient with neurologic symptoms.
Related: Amiodarone pulmonary toxicity.
References: Click to see abstract/article
1. Amiodarone-Induced Neuromyopathy: Three Cases and a Review of the Literature - Journal of Clinical Neuromuscular Disease. 3(3):97-105, March 2002.
2. Severe Ataxia Caused by Amiodarone - Volume 96, Issue 10, Pages 1463-1464 (15 November 2005) - Am J of Card
3. Amiodarone toxicity presenting as pulmonary mass and peripheral neuropathy: the continuing diagnostic challenge - Postgraduate Medical Journal 2006;82:73-75
4. Amiodarone: Guidelines for Use and Monitoring - aafp.org - Vol 68, No. 11, Dec., 2003
5. Atypical pulmonary and neurologic complications of amiodarone in the same patient. Report of a case and review of the literature - Vol. 147 No. 10, October 1, 1987 - Archive of Int Med.
6. Amiodarone-Induced Delirium - Am J Psychiatry 156:1119, July 1999
Tuesday, September 9, 2008
Tuesday September 9, 2008
Procalcitonin, C-reactive protein and now Chromagranin A in Sepsis. JUST ADD IT ON
Dan Zhang from France studied the link between Chromagranin A (CGA) and systemic inflammatory response syndrome (SIRS). CGA is a stress marker released along with catecholamine by adrenal medulla.
They measured CGA, procalcitonin, and C-reactive protein level in 53 patients and 14 controls. They also assessed Simplified acute physiological score (SAPS).
Results: Serum CGA level was significantly elevated in patients where infection is associated with SIRS with a median value of 138.5mcg/L as compared to controls (p<0.001).
CGA concentration also positively with procalcitonin and C-reactive protein.
Conclusion: Patients with CGA concentration higher then 71 mcg/L have a significantly shorter survival and was independent of SAPS score.
Reference: Click to get abstract/article
Zhang D, Lavaux T, Lavigne T, Castelain V, et al. Serum concentration of chromogranin A at admission: An early biomarker of severity in critically ill patients. Annals of Medicine, 21 August 2008
Procalcitonin, C-reactive protein and now Chromagranin A in Sepsis. JUST ADD IT ON
Dan Zhang from France studied the link between Chromagranin A (CGA) and systemic inflammatory response syndrome (SIRS). CGA is a stress marker released along with catecholamine by adrenal medulla.
They measured CGA, procalcitonin, and C-reactive protein level in 53 patients and 14 controls. They also assessed Simplified acute physiological score (SAPS).
Results: Serum CGA level was significantly elevated in patients where infection is associated with SIRS with a median value of 138.5mcg/L as compared to controls (p<0.001).
CGA concentration also positively with procalcitonin and C-reactive protein.
Conclusion: Patients with CGA concentration higher then 71 mcg/L have a significantly shorter survival and was independent of SAPS score.
Reference: Click to get abstract/article
Zhang D, Lavaux T, Lavigne T, Castelain V, et al. Serum concentration of chromogranin A at admission: An early biomarker of severity in critically ill patients. Annals of Medicine, 21 August 2008
Monday, September 8, 2008
Monday September 8, 2008
And we thought any free fluid in peritoneum is bad
Noriyuki and their colleague studied if peritoneum can be another oxygen storage organ??
They studied the role of peritoneum and its safety by infusing volume of oxygenated RBC and with oxygenated saline in Dogs and followed hemodynamic changes. The controls comprised of dogs that underwent sham operation.
Result: They found that intraperitoneal infusion of less than 1250 ml was hemodynamically safe. Oxygenation levels (PaO2) increased with intraperitoneal infusion of oxygenated RBC.
Conclusion: Peritoneum can potentially serve as an “artificial Lung” in critically ill patients.
Editors' comment: Watch out GI may be now playing as Pulmonalogist in future.
Reference: click to get reference/article
THE PERITONEUM AS A NOVEL OXYGENATION ORGAN: REVITALIZATION OF INTRAPERITONEAL OXYGENATION. Shock. 30(3):250-253, September 2008. Matsutani, Noriyuki; Takase, Bonpei; Nogami, Yashiro ; Ozeki, Yuichi ; Ishihara, Masayuki ; Maehara, Tadaaki
And we thought any free fluid in peritoneum is bad
Noriyuki and their colleague studied if peritoneum can be another oxygen storage organ??
They studied the role of peritoneum and its safety by infusing volume of oxygenated RBC and with oxygenated saline in Dogs and followed hemodynamic changes. The controls comprised of dogs that underwent sham operation.
Result: They found that intraperitoneal infusion of less than 1250 ml was hemodynamically safe. Oxygenation levels (PaO2) increased with intraperitoneal infusion of oxygenated RBC.
Conclusion: Peritoneum can potentially serve as an “artificial Lung” in critically ill patients.
Editors' comment: Watch out GI may be now playing as Pulmonalogist in future.
Reference: click to get reference/article
THE PERITONEUM AS A NOVEL OXYGENATION ORGAN: REVITALIZATION OF INTRAPERITONEAL OXYGENATION. Shock. 30(3):250-253, September 2008. Matsutani, Noriyuki; Takase, Bonpei; Nogami, Yashiro ; Ozeki, Yuichi ; Ishihara, Masayuki ; Maehara, Tadaaki
Sunday, September 7, 2008
Saturday, September 6, 2008
Saturday September 06, 2008
Noise level in ICU !!
Unnecessary noise in ICU can mask vital alarms, verbal communications and may be an unseen added cause of mental stress for staff itself. There are 2 kinds of noise in ICU
One interesting and landmark work was done by Kahn and coll. which showed that:
Do you know beepers contribute 1% to ICU noise pollution with 84 dBA - why not to turn it to vibrate mode !!
Click here to see various measures which can decrease noise pollution in ICU (from nursingspectrum.com)
References: click to get abstrat/article
1. Identification and modification of environmental noise in an ICU setting - Chest, Vol 114, 535-540 - full article available as pdf
2. Contribution of the Intensive Care Unit Environment to Sleep Disruption in Mechanically Ventilated Patients and Healthy Subjects - American Journal of Respiratory and Critical Care Medicine Vol 167. pp. 708-715, (2003)
3. Noise in the postanaesthesia care unit - British Journal of Anaesthesia, 2002, Vol. 88, No. 3 369-373
Noise level in ICU !!
Unnecessary noise in ICU can mask vital alarms, verbal communications and may be an unseen added cause of mental stress for staff itself. There are 2 kinds of noise in ICU
- one you can't control like "ventilator and IV pump alarms"
- and one you can modify like "conversations and TV"
One interesting and landmark work was done by Kahn and coll. which showed that:
- "Talking" and "TV" contribute to 49% of noise in ICU.
- EPA (Enviromental Protection Agency) recommends noise level not to exceed beyond 45 dBA in hospitals but mean peak sound level in study (medical ICU) was 80 dBA !! (which showed mark decrease with behavior modification)
Do you know beepers contribute 1% to ICU noise pollution with 84 dBA - why not to turn it to vibrate mode !!
Click here to see various measures which can decrease noise pollution in ICU (from nursingspectrum.com)
References: click to get abstrat/article
1. Identification and modification of environmental noise in an ICU setting - Chest, Vol 114, 535-540 - full article available as pdf
2. Contribution of the Intensive Care Unit Environment to Sleep Disruption in Mechanically Ventilated Patients and Healthy Subjects - American Journal of Respiratory and Critical Care Medicine Vol 167. pp. 708-715, (2003)
3. Noise in the postanaesthesia care unit - British Journal of Anaesthesia, 2002, Vol. 88, No. 3 369-373
Friday, September 5, 2008
Friday September 05, 2008
Regarding fenoldopam
Case: 39 year old male admitted with hypertensive emergency after he ran out of his prescriptions. "ED Doc" started patient on IV cardene (nicardipine) drip and resumed patient's home med for BP which consist of Toprol (metoprolol) XL - first dose given in ER. On review of CXR you noticed some pulmonary edema and decide to switch to Fenoldopam to get dual effect of lowering BP as well as dopaminergic effect to resolve pulmonary edema. Patient dropped his BP precipitously and coded.
Probable cause: It is not advisable to start fenoldopam on patients with B-blocker or atleast close caution should be maintained. Concomitant use of beta-blockers in conjunction with fenoldopam may cause life threatening hypotension from beta-blocker's inhibition of the sympathetic reflex response to fenoldopam 1.
Related previous pearl: Renal dose Fenoldopam ?
Click to get abstract/article
1. Corlopam - fda.gov
2. Fenoldopam — A Selective Peripheral Dopamine-Receptor Agonist for the Treatment of Severe Hypertension - Volume 345:1548-1557, Number 21, Nov. 22,2001
Regarding fenoldopam
Case: 39 year old male admitted with hypertensive emergency after he ran out of his prescriptions. "ED Doc" started patient on IV cardene (nicardipine) drip and resumed patient's home med for BP which consist of Toprol (metoprolol) XL - first dose given in ER. On review of CXR you noticed some pulmonary edema and decide to switch to Fenoldopam to get dual effect of lowering BP as well as dopaminergic effect to resolve pulmonary edema. Patient dropped his BP precipitously and coded.
Probable cause: It is not advisable to start fenoldopam on patients with B-blocker or atleast close caution should be maintained. Concomitant use of beta-blockers in conjunction with fenoldopam may cause life threatening hypotension from beta-blocker's inhibition of the sympathetic reflex response to fenoldopam 1.
Related previous pearl: Renal dose Fenoldopam ?
Click to get abstract/article
1. Corlopam - fda.gov
2. Fenoldopam — A Selective Peripheral Dopamine-Receptor Agonist for the Treatment of Severe Hypertension - Volume 345:1548-1557, Number 21, Nov. 22,2001
Thursday, September 4, 2008
Thursday September 04, 2008
Bedside tip ! - Tracheal Tube Tolerance
Some intubated patients wake up and cough on the tracheal tube, but may not be ready for extubation and you may be reluctant to re-sedate them. Consider a trial of intravenous Lidocaine. Administer 1 mg/Kg slowly over about two minutes. There is a good chance that the patient will experience immediate and dramatic relief from irritation caused by the tracheal tube (some may even sleep for a while). If the patient has a good response to the bolus, you may even start an intravenous infusion of Lidocaine at 2mg/ min. This can buy you the 1 – 3 hours the patient may need to be able to extubated safely.
Bedside tip ! - Tracheal Tube Tolerance
Some intubated patients wake up and cough on the tracheal tube, but may not be ready for extubation and you may be reluctant to re-sedate them. Consider a trial of intravenous Lidocaine. Administer 1 mg/Kg slowly over about two minutes. There is a good chance that the patient will experience immediate and dramatic relief from irritation caused by the tracheal tube (some may even sleep for a while). If the patient has a good response to the bolus, you may even start an intravenous infusion of Lidocaine at 2mg/ min. This can buy you the 1 – 3 hours the patient may need to be able to extubated safely.
Wednesday, September 3, 2008
Wednesday September 03, 2008
Do we need to start thinking about extracorporeal life support in cardiopulmonary resuscitation?
A study by Chen from national Taiwan University hospital evaluated the role of cardiopulmonary resuscitation with assisted extracorporeal life support versus conventional cardiopulmonary resuscitation in adults with in-hospital cardiac arrest.
Study Design: 3 year prospective observational study with 113 enrolled in the conventional CPR and 59 enrolled in the extracorporeal CPR group out of total 975 patients with in-hospital cardiac arrest.
Results:
Between the propensity matched group, there was a significant difference to survival to discharge hazard ratio (HR=0.51), and a 30 days and one year survival (HR 0.53)
Reference: Click to get abstract/article
Chen Y, Lin J, Yu H, Ko W et al. Cardiopulmonary resuscitation with assisted extracorporeal life support versus conventional cardiopulmonary resuscitation in adults with in-hospital cardiac arrest: an observational study and propensity analysis. Lancet 2008; 372(9638): 554-561
Do we need to start thinking about extracorporeal life support in cardiopulmonary resuscitation?
A study by Chen from national Taiwan University hospital evaluated the role of cardiopulmonary resuscitation with assisted extracorporeal life support versus conventional cardiopulmonary resuscitation in adults with in-hospital cardiac arrest.
Study Design: 3 year prospective observational study with 113 enrolled in the conventional CPR and 59 enrolled in the extracorporeal CPR group out of total 975 patients with in-hospital cardiac arrest.
Results:
Conclusion: In patients with in hospital cardiac arrest, extracorporeal CRP had a short and long term benefit over conventional CPR.
Reference: Click to get abstract/article
Chen Y, Lin J, Yu H, Ko W et al. Cardiopulmonary resuscitation with assisted extracorporeal life support versus conventional cardiopulmonary resuscitation in adults with in-hospital cardiac arrest: an observational study and propensity analysis. Lancet 2008; 372(9638): 554-561
Tuesday, September 2, 2008
Tuesday September 02, 2008
Alternatives to Fresh Frozen Plasma in Coagulopathy patients
Coagulopathy is generally treated with fresh frozen plasma in injured patients with coagulopathy. High dose recombinant factor VIIa has been used off label to treat severe coagulopathy following trauma. Deborah Stein from University of Maryland studied the use of Low-dose recombinant factor VIIa for trauma patients with coagulopathy.
Study design: Retrospective with 81 patients receiving 84 doses of low dose factor VIIa. Etiology of the coagulopathy patient in study population included:
- Traumatic brain injury (40%),
- warfarin use (22%)
- Cirrhosis (13%)
Results:
- Mean prothrombin time (PT) fell from 17s (+/-3.2) to 10.6 (+/- 1.4).
- All patients had a good clinical response with no bleeding complications.
- Utilization of packed red blood cells and fresh frozen plasma were significantly less in the 24 h after FVIIa administration as compared to the 24 h prior.
- Subsequent thromboembolic events were observed in 12 of the 81 patients (15%) and included; CVA (6), mesenteric thrombosis (2), myocardial infarction (1), pulmonary embolism/deep venous thrombosis (2), and atrial thrombus (1). Only four of these events were thought to be related to the FVIIa administration, with two of the four contributing to a lethal outcome.
Conclusions: The low dose (1.2mg) Factor VIIa rapidly and effectively treat mild to moderate coagulopathy following injury, and is felt to be cost effective.
Reference: Click to get abstract/article
Stein DM, Dutton RP, Hess JR, Scalea TM. Low-dose recombinant factor VIIa for trauma patients with coagulopathy. Injury 2008; 39 (9):1054-1061
Monday, September 1, 2008
Monday September 01, 2008
Early vs Late Tracheostomy !
It is a common understanding that all prolong ventilated patients eventually require tracheostomy but so far there is no strong evidence-based guidelines for early vs late tracheostomy, and the appropriate timing is still controversial.
Earlier, one study looked into a total of 163 relevant ICU patients and suggests that: "Tracheostomy after 21 days of intubation is associated with a higher rate of failure to wean from mechanical ventilation, longer ICU stay and higher ICU mortality". 1
Another meta-analysis of five studies with 406 patients was published in BMJ and found that "In adult ICU patients, who require prolonged mechanical ventilation, performing an early tracheostomy, may shorten ventilator days and length of stay in ICU but does not alter mortality or the risk of pneumonia". 2
But one very large study failed to show marked benefit. This month a retrospective cohort analysis of about 11,000 patients from 114 acute care hospitals in Ontario, Canada has been published to determine whether earlier tracheostomy is associated with greater long-term survival. 3
Measurements: For crude analyses, tracheostomy timing was classified as early ( less than10 days) vs. late ( more than 10 days) with mortality measured at multiple follow-up intervals.
Results: A total of 10,927 patients received tracheostomy during the study, of which one-third (n = 3758) were early and two-thirds late (n = 7169)
Patients receiving early tracheostomy had little lower unadjusted 90-day (34.8% vs. 36.9%), 1 yr (46.5% vs. 49.8%), and study mortality (63.9% vs. 67.2%)
Conclusions: Physicians performing early tracheostomy should not anticipate a large potential survival benefit. Future research should concentrate on identifying which patients will receive the most benefit.
Refrences: Click to get abstract/article.
1. Timing of Tracheostomy as a Determinant of Weaning Success in Critically Ill Patients: A Retrospective Study - Crit Care. 2005; 9 (1): R46-R52
2. Systematic review and meta-analysis of studies of the timing of tracheostomy in adult patients undergoing artificial ventilation - BMJ 2005;330:1243 (28 May)
3. The effect of tracheostomy timing during critical illness on long-term survival - Critical Care Medicine. 36(9):2547-2557, September 2008
Early vs Late Tracheostomy !
It is a common understanding that all prolong ventilated patients eventually require tracheostomy but so far there is no strong evidence-based guidelines for early vs late tracheostomy, and the appropriate timing is still controversial.
Earlier, one study looked into a total of 163 relevant ICU patients and suggests that: "Tracheostomy after 21 days of intubation is associated with a higher rate of failure to wean from mechanical ventilation, longer ICU stay and higher ICU mortality". 1
Another meta-analysis of five studies with 406 patients was published in BMJ and found that "In adult ICU patients, who require prolonged mechanical ventilation, performing an early tracheostomy, may shorten ventilator days and length of stay in ICU but does not alter mortality or the risk of pneumonia". 2
But one very large study failed to show marked benefit. This month a retrospective cohort analysis of about 11,000 patients from 114 acute care hospitals in Ontario, Canada has been published to determine whether earlier tracheostomy is associated with greater long-term survival. 3
Measurements: For crude analyses, tracheostomy timing was classified as early ( less than10 days) vs. late ( more than 10 days) with mortality measured at multiple follow-up intervals.
Results: A total of 10,927 patients received tracheostomy during the study, of which one-third (n = 3758) were early and two-thirds late (n = 7169)
Patients receiving early tracheostomy had little lower unadjusted 90-day (34.8% vs. 36.9%), 1 yr (46.5% vs. 49.8%), and study mortality (63.9% vs. 67.2%)
Conclusions: Physicians performing early tracheostomy should not anticipate a large potential survival benefit. Future research should concentrate on identifying which patients will receive the most benefit.
Refrences: Click to get abstract/article.
1. Timing of Tracheostomy as a Determinant of Weaning Success in Critically Ill Patients: A Retrospective Study - Crit Care. 2005; 9 (1): R46-R52
2. Systematic review and meta-analysis of studies of the timing of tracheostomy in adult patients undergoing artificial ventilation - BMJ 2005;330:1243 (28 May)
3. The effect of tracheostomy timing during critical illness on long-term survival - Critical Care Medicine. 36(9):2547-2557, September 2008
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