Sunday September 16, 2007
Lactate Ringer's and Normal Saline solutions
Lactated Ringer's Solution was invented about 125 years ago by a British physiologist Sydney Ringer and never lost a day in its popularity. Let see its difference from normal saline.
Normal Saline is the solution of 0.9% NaCl. It has a slightly higher degree of osmolality compared to blood. One litre of Normal Saline contains
154 mEq/L of Na+ and
154 mEq/L of Cl−
One liter of Lactated Ringer's Solution contains:
130 mEq/L of Na+ but total cations of 137 mEq/L , so still is isotonic.
109 mEq/L of Cl−
28 mEq/L of lactate
4 mEq/L of potassium
3 mEq/L of calcium.
Sunday, September 16, 2007
Saturday, September 15, 2007

Saturday September 15, 2007
Bedside tip - using bulb to detect proper endotracheal intubation
Esohageal intubation detector bulb is a disposable device used to verify endotracheal tube placement. After endotracheal tube placement, compress the bulb and while holding it in a compressed state, attach the unit to the endotracheal tube. A vacuum is created once the compressed bulb is released. Should the endotracheal tube be in the esophagus, the bulb will not reinflate. however, if the endotracheal tube is properly placed, the bulb will inflate.
If the tube tip is in the esophagus, the tube tip will become occluded with the walls of the esophagus (bulb remain compressed), implying that the endotracheal tube is in the esophagus. By contrast, if the tube tip is in the trachea, the tube tip remains open as the system volume increases and free aspiration of air occurs (bulb re-expand), implying the endotracheal tube is in the trachea.
Bedside tip - using bulb to detect proper endotracheal intubation
Esohageal intubation detector bulb is a disposable device used to verify endotracheal tube placement. After endotracheal tube placement, compress the bulb and while holding it in a compressed state, attach the unit to the endotracheal tube. A vacuum is created once the compressed bulb is released. Should the endotracheal tube be in the esophagus, the bulb will not reinflate. however, if the endotracheal tube is properly placed, the bulb will inflate.
If the tube tip is in the esophagus, the tube tip will become occluded with the walls of the esophagus (bulb remain compressed), implying that the endotracheal tube is in the esophagus. By contrast, if the tube tip is in the trachea, the tube tip remains open as the system volume increases and free aspiration of air occurs (bulb re-expand), implying the endotracheal tube is in the trachea.
Friday, September 14, 2007
Friday September 14, 2007
Regarding cisatracurium and its metabolite !
Cisatracurium is a drug of choice for neuro-muscular blockade in patients with multi-system organ failure.The metabolism of cisatracurium is largely independent of major organs such as liver or kidney. 80% of cisatracurium undergoes Hofmann elimination in plasma which is only a PH and temperature-dependent chemical process and degrade into metabolites.
Dosing: 0.15 to 0.2 mg/kg IV bolus followed by 1 to 3 mcg/kg/min(range: 0.5 to 10.2 mcg/kg/min).
Recently there is a interest in one of the metabolite called Laudanosine. Laudanosine is a metabolite of the cisatracurium with potentially toxic systemic effects. It crosses the blood–brain barrier and may cause excitement and seizure activity. In the cardiovascular system,high plasma concentrations may produce hypotension and bradycardia. In hepatic failure, its elimination half life is prolonged. Also, patients with renal failure have higher plasma concentrations of Laudanosine and a longer mean elimination half-life. Laudanosine crosses the placental barrier.
But all these effects seem theoretical and laudanosine accumulation and related toxicity seem unlikely to be achieved in clinical practice particularly with cisatracurium.
Related previous pearl: Tachyphylaxis Associated With Continuous Cisatracurium (Nimbex)
Reference - click to get abstract / article
1. cisatracurium - rxlist.com
2. Laudanosine, an atracurium and cisatracurium metabolite - European Journal of Anaesthesiology 2002; 19: 466–473
Regarding cisatracurium and its metabolite !
Cisatracurium is a drug of choice for neuro-muscular blockade in patients with multi-system organ failure.The metabolism of cisatracurium is largely independent of major organs such as liver or kidney. 80% of cisatracurium undergoes Hofmann elimination in plasma which is only a PH and temperature-dependent chemical process and degrade into metabolites.
Dosing: 0.15 to 0.2 mg/kg IV bolus followed by 1 to 3 mcg/kg/min(range: 0.5 to 10.2 mcg/kg/min).
Recently there is a interest in one of the metabolite called Laudanosine. Laudanosine is a metabolite of the cisatracurium with potentially toxic systemic effects. It crosses the blood–brain barrier and may cause excitement and seizure activity. In the cardiovascular system,high plasma concentrations may produce hypotension and bradycardia. In hepatic failure, its elimination half life is prolonged. Also, patients with renal failure have higher plasma concentrations of Laudanosine and a longer mean elimination half-life. Laudanosine crosses the placental barrier.
But all these effects seem theoretical and laudanosine accumulation and related toxicity seem unlikely to be achieved in clinical practice particularly with cisatracurium.
Related previous pearl: Tachyphylaxis Associated With Continuous Cisatracurium (Nimbex)
Reference - click to get abstract / article
1. cisatracurium - rxlist.com
2. Laudanosine, an atracurium and cisatracurium metabolite - European Journal of Anaesthesiology 2002; 19: 466–473
Thursday, September 13, 2007
Thursday September 13, 2007
Effect of oxygen inhalation on heart !
No ! its not good to provide a lot of oxygen to patient. We are well aware of oxygen toxicity in lungs but oxygen also has negative ionotropic effect on heart and may reduce the cardiac output. Its important to wean FiO2 as tolerated to provide 'optimum' oxygenation.
Reference:
1. The effect of normobaric hyperoxia on cardiac index in healthy awake volunteers - Anaesthesia, Volume 58 Issue 9 Page 885-888, September 2003
Effect of oxygen inhalation on heart !
No ! its not good to provide a lot of oxygen to patient. We are well aware of oxygen toxicity in lungs but oxygen also has negative ionotropic effect on heart and may reduce the cardiac output. Its important to wean FiO2 as tolerated to provide 'optimum' oxygenation.
Reference:
1. The effect of normobaric hyperoxia on cardiac index in healthy awake volunteers - Anaesthesia, Volume 58 Issue 9 Page 885-888, September 2003
Wednesday, September 12, 2007
Wednesday September 12, 2007
Diamox (acetazolamide) - an antiepileptic !
Do you know that Diamox was originally introduced as an antiepileptic drug in 1952. It has been used to treat a variety of seizure types, including generalized tonic clonic, absence, and as add-on therapy for partial seizures! Acetazolamide's property of inhibiting carbonic anhydrase appears to retard abnormal, paroxysmal, excessive discharge from central nervous system neurons.
Diamox has been described as an effective drug of choice for catamenial epilepsy (epilepsy related to the menstrual cycle).
Reference:
1. Diamox - rxlist.com
2. Diamox - epilepsyfoundation.org
3. Acetazolamide in Women with Catamenial Epilepsy , Epilepsia, Volume 42, Number 6, June 2001 , pp. 746-749(4)
Diamox (acetazolamide) - an antiepileptic !
Do you know that Diamox was originally introduced as an antiepileptic drug in 1952. It has been used to treat a variety of seizure types, including generalized tonic clonic, absence, and as add-on therapy for partial seizures! Acetazolamide's property of inhibiting carbonic anhydrase appears to retard abnormal, paroxysmal, excessive discharge from central nervous system neurons.
Diamox has been described as an effective drug of choice for catamenial epilepsy (epilepsy related to the menstrual cycle).
Reference:
1. Diamox - rxlist.com
2. Diamox - epilepsyfoundation.org
3. Acetazolamide in Women with Catamenial Epilepsy , Epilepsia, Volume 42, Number 6, June 2001 , pp. 746-749(4)
Tuesday, September 11, 2007
Tuesday September 11, 2007
Correlation of serum glucose concentrations with the severity of the calcium channel blocker intoxication
A very unusual study (n=40 patients) published in this month of "Critical Care Medicine", looking into correlation of serum glucose concentrations with the severity of the calcium channel blocker intoxication 1.
Background: Overdoses of calcium channel blocker agents result in hyperglycemia, primarily due to the blockade of pancreatic L-type calcium channels and insulin resistance on the cellular level. The clinical significance of the hyperglycemia in this setting has not previously been described.
Methods: This study was a retrospective review of all adult (age, >=15 yrs) patients with a discharge diagnosis of acute verapamil or diltiazem overdose at five university-affiliated teaching hospitals.
The severity of overdose was assessed by determining whether a patient met the composite end points of
Initial and peak serum glucose concentrations were compared with hemodynamic variables between patients who did and did not meet the composite end points.
Result:
Conclusion: Serum glucose concentrations correlate directly with the severity of the calcium channel blocker intoxication. The percentage increase of the peak glucose concentration is a better predictor of severity of illness than hemodynamic derangements. If validated prospectively, serum glucose concentration alone might be an indicator to begin hyperinsulinemia-euglycemia therapy.
Related previous pearl:
Calcium Channel blocker overdose
Regarding Calcium Channel blocker overdose - hyperinsulin/euglycemia therapy
Recommended Reading:
Treatment of Calcium-Channel–Blocker Intoxication with Insulin Infusion - The New England Journal of Medicine , May 31, 2001, Volume 344:1721-1722
High-Dose Insulin Therapy for Calcium-Channel Blocker Overdose - Shepherd and Klein-Schwartz Ann Pharmacother.2005; 39: 923-930
Reference: click to get refrence/article
1. Assessment of hyperglycemia after calcium channel blocker overdoses involving diltiazem or verapamil - Critical Care Medicine. 35(9):2071-2075, September 2007.
Correlation of serum glucose concentrations with the severity of the calcium channel blocker intoxication
A very unusual study (n=40 patients) published in this month of "Critical Care Medicine", looking into correlation of serum glucose concentrations with the severity of the calcium channel blocker intoxication 1.
Background: Overdoses of calcium channel blocker agents result in hyperglycemia, primarily due to the blockade of pancreatic L-type calcium channels and insulin resistance on the cellular level. The clinical significance of the hyperglycemia in this setting has not previously been described.
Methods: This study was a retrospective review of all adult (age, >=15 yrs) patients with a discharge diagnosis of acute verapamil or diltiazem overdose at five university-affiliated teaching hospitals.
The severity of overdose was assessed by determining whether a patient met the composite end points of
- in-hospital mortality,
- the necessity for a temporary pacemaker, or
- the need for vasopressors
Initial and peak serum glucose concentrations were compared with hemodynamic variables between patients who did and did not meet the composite end points.
Result:
- For those patients who did and did not meet the composite end points, the median initial serum glucose concentrations were 188 (range, 143.5-270.5) mg/dL and 129 (98.5-156.5) mg/dL, respectively (p = .0058).
- The median peak serum glucose concentrations for these two groups were 364 (267.5-408.5) mg/dL and 145 (107.5-160.5) mg/dL, respectively (p = .0001).
- The median increase in blood glucose was 71.2% for those who met composite end points vs. 0% for those who did not meet composite end points (p = .0067).
- Neither the change in the median heart rate nor the change in systolic blood pressure was significantly different in any group.
Conclusion: Serum glucose concentrations correlate directly with the severity of the calcium channel blocker intoxication. The percentage increase of the peak glucose concentration is a better predictor of severity of illness than hemodynamic derangements. If validated prospectively, serum glucose concentration alone might be an indicator to begin hyperinsulinemia-euglycemia therapy.
Related previous pearl:
Calcium Channel blocker overdose
Regarding Calcium Channel blocker overdose - hyperinsulin/euglycemia therapy
Recommended Reading:
Treatment of Calcium-Channel–Blocker Intoxication with Insulin Infusion - The New England Journal of Medicine , May 31, 2001, Volume 344:1721-1722
High-Dose Insulin Therapy for Calcium-Channel Blocker Overdose - Shepherd and Klein-Schwartz Ann Pharmacother.2005; 39: 923-930
Reference: click to get refrence/article
1. Assessment of hyperglycemia after calcium channel blocker overdoses involving diltiazem or verapamil - Critical Care Medicine. 35(9):2071-2075, September 2007.
Monday, September 10, 2007
Monday September 10, 2007
Norepinephrine plus dobutamine versus epinephrine alone for management of septic shock
Recently a very important randomised trial published in "Lancet" from Annane and coll., (330 patients) comparing Norepinephrine plus Dobutamine versus Epinephrine alone for management of septic shock.
Background: International guidelines for management of septic shock recommend that dopamine or norepinephrine are preferable to epinephrine. However, no large comparative trial has yet been done. Aim of study was compare the efficacy and safety of norepinephrine plus dobutamine (whenever needed) with those of epinephrine alone in septic shock.
Methods: 330 patients were randomized to receive either epinephrine (n=161) or norepinephrine plus dobutamine (n=169), which were titrated to maintain mean blood pressure at 70 mm Hg or more.
The primary outcome was 28-day all-cause mortality.
Result:
Conclusion: There is no evidence for a difference in efficacy and safety between epinephrine alone and norepinephrine plus dobutamine for the management of septic shock.
Norepinephrine plus dobutamine versus epinephrine alone for management of septic shock
Recently a very important randomised trial published in "Lancet" from Annane and coll., (330 patients) comparing Norepinephrine plus Dobutamine versus Epinephrine alone for management of septic shock.
Background: International guidelines for management of septic shock recommend that dopamine or norepinephrine are preferable to epinephrine. However, no large comparative trial has yet been done. Aim of study was compare the efficacy and safety of norepinephrine plus dobutamine (whenever needed) with those of epinephrine alone in septic shock.
Methods: 330 patients were randomized to receive either epinephrine (n=161) or norepinephrine plus dobutamine (n=169), which were titrated to maintain mean blood pressure at 70 mm Hg or more.
The primary outcome was 28-day all-cause mortality.
Result:
- At day 28, there were 64 (40%) deaths in the epinephrine group and 58 (34%) deaths in the norepinephrine plus dobutamine group (p=0·31)
- There was no significant difference between the two groups in mortality rates at discharge from ICU, at hospital and by day 90
- There was no significant difference between the two groups time to haemodynamic success,
- There was no significant difference between the two groups time to vasopressor withdrawal,
- There was no significant difference between the two groups time course of SOFA score
- There was no significant difference between the two groups rates of serious adverse events were also similar
Conclusion: There is no evidence for a difference in efficacy and safety between epinephrine alone and norepinephrine plus dobutamine for the management of septic shock.
Sunday, September 9, 2007
Sunday September 9, 2007
Q; What is the pitfall of converting insulin drip to long acting insuling lantus (insulin glargine [rDNA origin] injection) ?
A; Lantus takes 72 to 120 hours to get effectively on board and provide insulin coverage. Also, it is alleged that pain at LANTUS injected site is higher compared to NPH injection site.
But in case if you decide to use lantus, to convert insulin drip to non-intravenous insulin coverage in ICU, the rule of thumb is to determine the total insulin required in last 24 hours and give half as lantus and the other half as short-acting insulin divided into per 3 meals.
Conversion from NPH to lantus: Determine the total insulin need of NPH in last 24 hours and reduce by 20%. Like, if total requirement is 100 NPH, the lantus dose would be 80 units.
Editors' comment: In ICUs, what is potentially an unstable setting, it is advisable to use long acting insulin with caution.
Q; What is the pitfall of converting insulin drip to long acting insuling lantus (insulin glargine [rDNA origin] injection) ?
A; Lantus takes 72 to 120 hours to get effectively on board and provide insulin coverage. Also, it is alleged that pain at LANTUS injected site is higher compared to NPH injection site.
But in case if you decide to use lantus, to convert insulin drip to non-intravenous insulin coverage in ICU, the rule of thumb is to determine the total insulin required in last 24 hours and give half as lantus and the other half as short-acting insulin divided into per 3 meals.
Conversion from NPH to lantus: Determine the total insulin need of NPH in last 24 hours and reduce by 20%. Like, if total requirement is 100 NPH, the lantus dose would be 80 units.
Editors' comment: In ICUs, what is potentially an unstable setting, it is advisable to use long acting insulin with caution.
Saturday, September 8, 2007
Saturday September 8, 2007
iceinstitute.com
One of the objective of our site is to keep readers posted with quality work going around. Please take time to visit this website:
iceinstitute.com
One of the objective of our site is to keep readers posted with quality work going around. Please take time to visit this website:
Free Archive is available from May 2000 onwards with articles on almost every aspect of infection control. Huge amount of work available on MRSA, VAP, SARS, C. diff., Hand Hygiene, Wound Care, Sharp safety etc.
Paid CME is available along with many free CME hours on Preventing and Controlling Healthcare-Associated Infections (HAIs) - free Webinar series. Click here to go to free CME hours.
Parent site is infectioncontroltoday.com
Friday, September 7, 2007
Friday September 7, 2007
Resident hours !
This week's JAMA (click here to see the index) is dedicated to "Medical education". In this regard, there are two articles published in JAMA related to the ACGME duty hour reform, one showing significant relative improvement in mortality for patients with 4 common medical conditions but the other article showing no change in mortality. Since these changes have significant impact on the way residents work load and working hours and overall impact on the physician staffing especially in the critical care units, it is worth reviewing these publications:
1) Mortality Among Patients in VA Hospitals in the First 2 Years Following ACGME Resident Duty Hour Reform- JAMA. 2007;298:984-992
2) Mortality Among Hospitalized Medicare Beneficiaries in the First 2 Years Following ACGME Resident Duty Hour Reform - JAMA. 2007;298:975-983
3) Evaluating Resident Duty Hour Reforms: More Work to Do - JAMA 2007;298:1055-1057.
It may be of interest to know that one recent small study (by surani and co. at Texas A&M University, TX) found that 'night-float' system may be effective as residents on the night float hours were not found to be sleepier than the normal population 1. Interestingly, control group residents were sleepier as compared to normal population.
Related previous pearl:
Post fellowship shock syndrome
Why we call our housestaff 'residents' in USA ?
Reference: click to get abstract/article
1. TO ASSESS THE SLEEPINESS AMONG MEDICAL RESIDENTS USING MULTIPLE SLEEP LATENCY TEST AS OBJECTIVE ASSESSMENT TOOL, presented as abstract at ACCP meeting, 2006
Resident hours !
This week's JAMA (click here to see the index) is dedicated to "Medical education". In this regard, there are two articles published in JAMA related to the ACGME duty hour reform, one showing significant relative improvement in mortality for patients with 4 common medical conditions but the other article showing no change in mortality. Since these changes have significant impact on the way residents work load and working hours and overall impact on the physician staffing especially in the critical care units, it is worth reviewing these publications:
1) Mortality Among Patients in VA Hospitals in the First 2 Years Following ACGME Resident Duty Hour Reform- JAMA. 2007;298:984-992
2) Mortality Among Hospitalized Medicare Beneficiaries in the First 2 Years Following ACGME Resident Duty Hour Reform - JAMA. 2007;298:975-983
3) Evaluating Resident Duty Hour Reforms: More Work to Do - JAMA 2007;298:1055-1057.
It may be of interest to know that one recent small study (by surani and co. at Texas A&M University, TX) found that 'night-float' system may be effective as residents on the night float hours were not found to be sleepier than the normal population 1. Interestingly, control group residents were sleepier as compared to normal population.
Related previous pearl:
Post fellowship shock syndrome
Why we call our housestaff 'residents' in USA ?
Reference: click to get abstract/article
1. TO ASSESS THE SLEEPINESS AMONG MEDICAL RESIDENTS USING MULTIPLE SLEEP LATENCY TEST AS OBJECTIVE ASSESSMENT TOOL, presented as abstract at ACCP meeting, 2006
Thursday, September 6, 2007
Thursday September 6, 2007
S/F ratio (pulse Ox saturation / FiO2 ratio)
A very interesting study published recently in chest comparing S/F ratio (pulse Ox saturation / FiO2 ratio) with P/F ratio (PO2 / FiO2 ratio).
Study found that S/F ratios correlate with P/F ratios.
S/F ratio of 235 = P/F ratios of 200 and
S/F ratio of 315 = P/F ratio of 300
The correlation formula is
S/F ratio (pulse Ox saturation / FiO2 ratio)
A very interesting study published recently in chest comparing S/F ratio (pulse Ox saturation / FiO2 ratio) with P/F ratio (PO2 / FiO2 ratio).
Study found that S/F ratios correlate with P/F ratios.
S/F ratio of 235 = P/F ratios of 200 and
S/F ratio of 315 = P/F ratio of 300
The correlation formula is
S/F = 64 + 0.84 x (P/F)
This is an important study from the clinical bedside pragmatic point of view as A-lines or ABGs may not be instantly available in many casses. Despite the ubiquity of SPO2 due to skin color, oximeter location, disease states like low cardiac output or methemoglobinemia, it may be a quick and instant indicator of underlying lung injury and need for more aggressive attention for early diagnosis and treatment in clinical practice.
Editors' comment: This is a very important read for all intensivists involve in everyday management of respiratory failures due to very simple but high diagnostic value in early recoginition and management of ALI / ARDS.
Reference: click to get abstract/article
1. Comparison of the SpO2/FIO2 Ratio and the PaO2/FIO2 Ratio in Patients With Acute Lung Injury or ARDS - Chest. 2007; 132:410-417
Editors' comment: This is a very important read for all intensivists involve in everyday management of respiratory failures due to very simple but high diagnostic value in early recoginition and management of ALI / ARDS.
Reference: click to get abstract/article
1. Comparison of the SpO2/FIO2 Ratio and the PaO2/FIO2 Ratio in Patients With Acute Lung Injury or ARDS - Chest. 2007; 132:410-417
Wednesday, September 5, 2007
Wednesday September 5, 2007
Q; Metabolic encephalopathy causes .... (choose one)
A) Pupillary constriction (miosis)
OR
B) Pupillary dilatation (mydriasis)
Answers: Pupillary constriction (miosis)If your clinical diagnosis is metabolic encephalopathy but pupils appears dilated, you may need to revisit your diagnosis or may need to consider further radiological workup.In ICU major causes of pupillary constriction are opiates, metabolic encephalopathy, cholinergic toxicity, or pontine lesions.
Tuesday, September 4, 2007
Tuesday September 4, 2007
Saline or Albumin for Fluid Resuscitation in Patients with Traumatic Brain Injury
The Saline versus Albumin Fluid Evaluation (SAFE) study had earlier suggested that patients with traumatic brain injury resuscitated with albumin had a higher mortality rate than those resuscitated with saline. A post hoc follow-up study of patients with traumatic brain injury who were enrolled in the study was published this week in NEJM.
460 patients, of whom 231 (50.2%) received albumin and 229 (49.8%) received saline were followed. The subgroup of patients with GCS scores of 3 to 8 were classified as having severe brain injury (160 [69.3%] in the albumin group and 158 [69.0%] in the saline group).
Conclusions: In this post hoc study of critically ill patients with traumatic brain injury, fluid resuscitation with albumin was associated with higher mortality rates than was resuscitation with saline.
Reference: click to get abstract/article
Saline or Albumin for Fluid Resuscitation in Patients with Traumatic Brain Injury - The SAFE Study Investigators, Volume 357: 874-884 — August 30, 2007 — Number 9
Saline or Albumin for Fluid Resuscitation in Patients with Traumatic Brain Injury
The Saline versus Albumin Fluid Evaluation (SAFE) study had earlier suggested that patients with traumatic brain injury resuscitated with albumin had a higher mortality rate than those resuscitated with saline. A post hoc follow-up study of patients with traumatic brain injury who were enrolled in the study was published this week in NEJM.
460 patients, of whom 231 (50.2%) received albumin and 229 (49.8%) received saline were followed. The subgroup of patients with GCS scores of 3 to 8 were classified as having severe brain injury (160 [69.3%] in the albumin group and 158 [69.0%] in the saline group).
- At 24 months, 71 of 214 patients in the albumin group (33.2%) had died, as compared with 42 of 206 in the saline group (20.4%) (P=0.003)
- Among patients with severe brain injury, 61 of 146 patients in the albumin group (41.8%) died, as compared with 32 of 144 in the saline group (22.2%) (P<0.001)
- Among patients with GCS scores of 9 to 12, death occurred in 8 of 50 patients in the albumin group (16.0%) and 8 of 37 in the saline group (21.6%) (P=0.50).
Conclusions: In this post hoc study of critically ill patients with traumatic brain injury, fluid resuscitation with albumin was associated with higher mortality rates than was resuscitation with saline.
Reference: click to get abstract/article
Saline or Albumin for Fluid Resuscitation in Patients with Traumatic Brain Injury - The SAFE Study Investigators, Volume 357: 874-884 — August 30, 2007 — Number 9
Monday, September 3, 2007
Monday September 3, 2007
Q; Name atleast 7 non-septic conditions which can cause low SVR (systemic vascular resistance) ?
1. Hemorrhagic (or necrotizing) Pancreatitis
2. Cirrhosis
3. Adrenal insufficiency
4. Head Injury ( initially increase SVR followed with low SVR)
5. Bactrim (TMP-SMX) in AIDS patient
6. Within 6 hours of postcardiopulmonary bypass (vasoplegic syndrome)
7. Spinal cord Injury above T6 (inhibited vagal tone)
Reference: click to get abstract/article
Low systemic vascular resistance: differential diagnosis and outcome - Critical Care 1999, 3:71-77
Q; Name atleast 7 non-septic conditions which can cause low SVR (systemic vascular resistance) ?
1. Hemorrhagic (or necrotizing) Pancreatitis
2. Cirrhosis
3. Adrenal insufficiency
4. Head Injury ( initially increase SVR followed with low SVR)
5. Bactrim (TMP-SMX) in AIDS patient
6. Within 6 hours of postcardiopulmonary bypass (vasoplegic syndrome)
7. Spinal cord Injury above T6 (inhibited vagal tone)
Reference: click to get abstract/article
Low systemic vascular resistance: differential diagnosis and outcome - Critical Care 1999, 3:71-77
Sunday, September 2, 2007
Sunday September 2, 2007
Uncontrolled diarrhea in C. diff. Colitis - what to do
If Diarrhea persists in C. diff. colitis despite treatment with metronidazole (flagyl) - add Cholestyramine 4 grams PO QID.
Caution: Never add cholestyramine with PO vancomycin. It will render the whole treatment ineffective.Bonus Pearl: Wash hands with soap and water if exposure to C.diff. is suspected. The physical action of washing and rinsing hands under such circumstances is recommended because alcohols, chlorhexidine, iodophors, and other antiseptic agents have poor activity against c. diff spores.
Uncontrolled diarrhea in C. diff. Colitis - what to do
If Diarrhea persists in C. diff. colitis despite treatment with metronidazole (flagyl) - add Cholestyramine 4 grams PO QID.
Caution: Never add cholestyramine with PO vancomycin. It will render the whole treatment ineffective.Bonus Pearl: Wash hands with soap and water if exposure to C.diff. is suspected. The physical action of washing and rinsing hands under such circumstances is recommended because alcohols, chlorhexidine, iodophors, and other antiseptic agents have poor activity against c. diff spores.
Saturday, September 1, 2007
Saturday September 1, 2007
Recalling Winters formula
Just to recall some basics, the easiest way to find the compensation CO2 should have for metabolic acidosis is through winters formula. You need HCO3 level from metabolic profile (BMP or Chem-7) and PCO2 from ABG (arterial blood gas). Winters formula is
PCO2 = HCO3 x 1.5 + 8
example: if your HCO3 level is 12, PCO2 should be
12 x 1.5 + 8 = 18 + 8 = 26 (+/- 2)
If its above 26 +/- 2 means there is a probability of superimposed respiratory acidosis, and if its below 26 +/- 2, means there is a probable compensatory respiratory alkalosis.
Related: ppt presentation onAcid Base Analysis from Don S. Howard M.D. (rcsw.org)
Recalling Winters formula
Just to recall some basics, the easiest way to find the compensation CO2 should have for metabolic acidosis is through winters formula. You need HCO3 level from metabolic profile (BMP or Chem-7) and PCO2 from ABG (arterial blood gas). Winters formula is
PCO2 = HCO3 x 1.5 + 8
example: if your HCO3 level is 12, PCO2 should be
12 x 1.5 + 8 = 18 + 8 = 26 (+/- 2)
If its above 26 +/- 2 means there is a probability of superimposed respiratory acidosis, and if its below 26 +/- 2, means there is a probable compensatory respiratory alkalosis.
Related: ppt presentation on
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