Wednesday May 31, 2006
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 the patient safely.
Tuesday, May 30, 2006
Capnography in CPR
Tuesday May 30, 2006
Use of Capnography in Assessment of CPR Adequacy
Myocardial blood flow is determined by the difference between aortic diastolic and right atrial pressures. Because both aorta and atrium experience the same intrathoracic pressure change during cardiopulmonary resuscitation (CPR), myocardial blood flow is very poor during cardiac resuscitation. Even high compression forces that may generate acceptable systemic and pulmonary artery pressures yield only small coronary perfusion pressures.
The arterial blood gas values during CPR manifest complex abnormalities. The reduction in cardiac output, and thus tissue perfusion, promotes anaerobic metabolism and lactic acidosis. However, arterial blood samples reflect either a normal or low PCO2 during CPR, while venous blood gases manifest both a respiratory and metabolic acidosis.
When perfusion is absent in the presence of ventilation, the primary influence on arterial acid-base status is alveolar ventilation. Venous acidosis develops as tissue beds drain CO2 and lactate is produced by anaerobic metabolism. The PCO2 in pulmonary veins increases due to reduced pulmonary blood flow and a resulting decrease in CO2 excretion.
With effective CPR or return of spontaneous circulation, pulmonary blood flow is improved and arterial pH decreases as more of the venous acid load (CO2 and lactate) reaches the arterial side. Aerobic and anaerobic metabolism produce carbon dioxide that is transported in venous blood to the lung and eliminated from the lung by minute ventilation. End-tidal CO2 is a measure of the partial pressure of carbon dioxide at the airway opening at the end of expiration.
During cardiac arrest, the abrupt decrease in cardiac output results in reduction of carbon dioxide transport from the tissues to lung and, hence, decreased carbon dioxide. More recently, capnography has been used to determine the adequacy of cardiopulmonary resuscitation.
There are 2 good sources to understand capnography:
1. capnography.com , educational site on subject from Bhavani-Shankar Kodali MD, Department of Anesthesia, Brigham and Women's Hospital, Harvard Medical School, Boston, USA
2. See concise INTERPRETATION OF CAPNOGRAPHIC WAVEFORM
(from biotel.ws website)
Use of Capnography in Assessment of CPR Adequacy
Myocardial blood flow is determined by the difference between aortic diastolic and right atrial pressures. Because both aorta and atrium experience the same intrathoracic pressure change during cardiopulmonary resuscitation (CPR), myocardial blood flow is very poor during cardiac resuscitation. Even high compression forces that may generate acceptable systemic and pulmonary artery pressures yield only small coronary perfusion pressures.
The arterial blood gas values during CPR manifest complex abnormalities. The reduction in cardiac output, and thus tissue perfusion, promotes anaerobic metabolism and lactic acidosis. However, arterial blood samples reflect either a normal or low PCO2 during CPR, while venous blood gases manifest both a respiratory and metabolic acidosis.
When perfusion is absent in the presence of ventilation, the primary influence on arterial acid-base status is alveolar ventilation. Venous acidosis develops as tissue beds drain CO2 and lactate is produced by anaerobic metabolism. The PCO2 in pulmonary veins increases due to reduced pulmonary blood flow and a resulting decrease in CO2 excretion.
With effective CPR or return of spontaneous circulation, pulmonary blood flow is improved and arterial pH decreases as more of the venous acid load (CO2 and lactate) reaches the arterial side. Aerobic and anaerobic metabolism produce carbon dioxide that is transported in venous blood to the lung and eliminated from the lung by minute ventilation. End-tidal CO2 is a measure of the partial pressure of carbon dioxide at the airway opening at the end of expiration.
During cardiac arrest, the abrupt decrease in cardiac output results in reduction of carbon dioxide transport from the tissues to lung and, hence, decreased carbon dioxide. More recently, capnography has been used to determine the adequacy of cardiopulmonary resuscitation.
There are 2 good sources to understand capnography:
1. capnography.com , educational site on subject from Bhavani-Shankar Kodali MD, Department of Anesthesia, Brigham and Women's Hospital, Harvard Medical School, Boston, USA
2. See concise INTERPRETATION OF CAPNOGRAPHIC WAVEFORM
(from biotel.ws website)
Monday, May 29, 2006
Blumberg's sign
Monday May 29, 2006
Blumberg's sign
Q: You received call from an old fashioned experienced ER physician to consult a patient with hypotension and positive Blumberg's sign ?
Do you know what is Blumberg's sign ?
A; Sudden release of steadily applied pressure on a suspected area of the abdomen cause sudden stab of pain - an indication of peritonitis. Yes its another name of rebound tenderness. Ideal technique requires to watch patient's face to assess severity of pain while doing above maneuver (there is an innocent tendency to watch abdomen).
Historically this maneuver was described to assess peritoneal inflammation as an early sign of appendicitis by pressing hands over McBurney's point *. Sign was first described by a german surgeon and gynaecologist, Jacob Moritz Blumberg (1873 -1955).
* McBurney's point is located one third of the distance along a line from the front of the right pelvic bone and the belly button (click to see image).
Blumberg's sign
Q: You received call from an old fashioned experienced ER physician to consult a patient with hypotension and positive Blumberg's sign ?
Do you know what is Blumberg's sign ?
A; Sudden release of steadily applied pressure on a suspected area of the abdomen cause sudden stab of pain - an indication of peritonitis. Yes its another name of rebound tenderness. Ideal technique requires to watch patient's face to assess severity of pain while doing above maneuver (there is an innocent tendency to watch abdomen).
Historically this maneuver was described to assess peritoneal inflammation as an early sign of appendicitis by pressing hands over McBurney's point *. Sign was first described by a german surgeon and gynaecologist, Jacob Moritz Blumberg (1873 -1955).
* McBurney's point is located one third of the distance along a line from the front of the right pelvic bone and the belly button (click to see image).
Sunday, May 28, 2006
MEDiC Bill
Sunday May 28, 2006
MEDiC bill
Senators Hillary Rodham Clinton and Barack Obama have coauthored the proposed MEDiC bill. (National Medical Error Disclosure and Compensation Bill).
Main ideas of the bill:
1. This legislation would create an Office of Patient Safety and Health Care Quality within the Department of Health and Human Services. The director of this office will be responsible for establishing a National Patient Safety Database, conducting data analyses to inform policy and practice recommendations, establishing and administering the National Medical Error Disclosure and Compensation (MEDiC) program, and supporting studies related to MEDiC and the medical liability system.
2. The MEDiC program would provide federal grant support and technical assistance for doctors, hospitals, and health systems that disclose medical errors and problems with patient safety and offer fair compensation for injuries or harm. Participants would submit a safety plan and designate a patient-safety officer, to whom these disclosures and notices of related legal action would be reported.
3. If a patient was injured or harmed as a result of medical error or a failure to adhere to the standard of care, the participant would disclose the matter to the patient and offer to enter into negotiations for fair compensation. The terms of negotiation for compensation ensure confidentiality, protection for any disclosure made by a health care provider to the patient in the confines of the MEDiC program, and a patient's right to seek legal counsel; they also allow for the use of a neutral third-party mediator to facilitate the negotiation.
4. Any apology offered by a health care provider during negotiations shall be kept confidential and could not be used in any subsequent legal proceedings as an admission of guilt if those negotiations ended without mutually acceptable compensation.
Is it a fantasy land OR another bureaucratic hurdle ?. OR a real geniune workable idea as argued by senators by citing experiences and studies from University of Michigan Health System and Veterans Affairs (VA) Hospital in Lexington, Kentucky ?. Read by yourself the full article (available free by clicking link below) published by senators in The New England Journal of Medicine, Volume 354:2205-2208, Number 21. May 25, 2006
Making Patient Safety the Centerpiece of Medical Liability Reform
MEDiC bill
Senators Hillary Rodham Clinton and Barack Obama have coauthored the proposed MEDiC bill. (National Medical Error Disclosure and Compensation Bill).
Main ideas of the bill:
1. This legislation would create an Office of Patient Safety and Health Care Quality within the Department of Health and Human Services. The director of this office will be responsible for establishing a National Patient Safety Database, conducting data analyses to inform policy and practice recommendations, establishing and administering the National Medical Error Disclosure and Compensation (MEDiC) program, and supporting studies related to MEDiC and the medical liability system.
2. The MEDiC program would provide federal grant support and technical assistance for doctors, hospitals, and health systems that disclose medical errors and problems with patient safety and offer fair compensation for injuries or harm. Participants would submit a safety plan and designate a patient-safety officer, to whom these disclosures and notices of related legal action would be reported.
3. If a patient was injured or harmed as a result of medical error or a failure to adhere to the standard of care, the participant would disclose the matter to the patient and offer to enter into negotiations for fair compensation. The terms of negotiation for compensation ensure confidentiality, protection for any disclosure made by a health care provider to the patient in the confines of the MEDiC program, and a patient's right to seek legal counsel; they also allow for the use of a neutral third-party mediator to facilitate the negotiation.
4. Any apology offered by a health care provider during negotiations shall be kept confidential and could not be used in any subsequent legal proceedings as an admission of guilt if those negotiations ended without mutually acceptable compensation.
Is it a fantasy land OR another bureaucratic hurdle ?. OR a real geniune workable idea as argued by senators by citing experiences and studies from University of Michigan Health System and Veterans Affairs (VA) Hospital in Lexington, Kentucky ?. Read by yourself the full article (available free by clicking link below) published by senators in The New England Journal of Medicine, Volume 354:2205-2208, Number 21. May 25, 2006
Making Patient Safety the Centerpiece of Medical Liability Reform
Saturday, May 27, 2006
RT or Iced Saline
Saturday May 27, 2006
Room temperature or Iced Saline ?
Critical Care literature is not clear, actually controversial, regarding the suitable temperature of the solution use as injectable to measure cardiac output via thermodilution. Let see what is the major pro & con of iced saline.
Advantage: Iced injectate gives a higher signal/noise ratio and more reliability in the measured cardiac output. Signal-to-noise ratio is an engineering term for the power ratio between a signal (meaningful information) and the background noise.
Disadvantage: Iced injectate may affect heart rate and cardiodynamics 5.
But practically does it matter ?. Also, iced solution may not be as cold as we think after it passes through the operator's hand and long port.
Overall literature favours room temperature or atleast does not show any major advantage of using iced saline 1-4.
Related: Thermodilution Cardiac Output Measurement Protocol
(sample from Univ. of Carolina Hospitals)
References:
1. Cardiac output measured by thermal dilution of room temperature injectate. - Evonuk E, Imig CJ, Greenfield W, et al: J Appl Physiol 1961; 16:271-275
2. Cardiac output by thermodilution technique. Effect of injectate's volume and temperature on accuracy and reproducibility in the critically Ill patient - Chest, Vol 84, 418-422, 1983
3. Effect of injectate volume and temperature on thermodilution cardiac output determination - Anesthesiology.1986 Jun;64(6):798-801.
4. Iced versus room temperature injectate for assessment of cardiac output, intrathoracic blood volume, and extravascular lung water by single transpulmonary thermodilution - J Crit Care. 2004 Jun;19(2):103-7.
5. The slowing of sinus rhythm during thermodilution cardiac output determination and the effect of altering injectate temperature. Anesthesiology 1985; 63:540-541
Room temperature or Iced Saline ?
Critical Care literature is not clear, actually controversial, regarding the suitable temperature of the solution use as injectable to measure cardiac output via thermodilution. Let see what is the major pro & con of iced saline.
Advantage: Iced injectate gives a higher signal/noise ratio and more reliability in the measured cardiac output. Signal-to-noise ratio is an engineering term for the power ratio between a signal (meaningful information) and the background noise.
Disadvantage: Iced injectate may affect heart rate and cardiodynamics 5.
But practically does it matter ?. Also, iced solution may not be as cold as we think after it passes through the operator's hand and long port.
Overall literature favours room temperature or atleast does not show any major advantage of using iced saline 1-4.
Related: Thermodilution Cardiac Output Measurement Protocol
(sample from Univ. of Carolina Hospitals)
References:
1. Cardiac output measured by thermal dilution of room temperature injectate. - Evonuk E, Imig CJ, Greenfield W, et al: J Appl Physiol 1961; 16:271-275
2. Cardiac output by thermodilution technique. Effect of injectate's volume and temperature on accuracy and reproducibility in the critically Ill patient - Chest, Vol 84, 418-422, 1983
3. Effect of injectate volume and temperature on thermodilution cardiac output determination - Anesthesiology.1986 Jun;64(6):798-801.
4. Iced versus room temperature injectate for assessment of cardiac output, intrathoracic blood volume, and extravascular lung water by single transpulmonary thermodilution - J Crit Care. 2004 Jun;19(2):103-7.
5. The slowing of sinus rhythm during thermodilution cardiac output determination and the effect of altering injectate temperature. Anesthesiology 1985; 63:540-541
Friday, May 26, 2006
CO Pitfalls
Friday May 26, 2006
Cardiac Output Pitfalls
Determination of cardiac output by thermodilution has several technical pitfalls. Any deviation in technique can produce inaccurate and inconsistent results.
Basis of thermodilutional cardiac output: The method relies on an injection of a known volume of fluid (5-10 mL) into the right atrium. This fluid, either normal saline or D5W is at room (or iced at known *) temperature and therefore cooler than blood. The cooler injectate mixes with blood, thus lowering its temperature. The cooled blood is ejected into the pulmonary artery and flows past a thermistor located in the distal end of the PA catheter. The thermistor generates a change in temperature to time curve. The area under this curve is calculated by integration and is inversely proportional to the flow past the thermistor. In other words, the longer it takes for this change in temperature to “wash out,” the slower the flow past the thermistor. The converse is also true. The greater the flow, the faster the temperature “wash out,” and therefore the smaller the area under the curve. Anything that can disrupt the “washout” of this temperature change can affect the accuracy of this measurement.
* iced saline has been said to provides a better "signal-to-noise" ratio but controversy continues in literature regarding iced vs room temperature solution.
Clinical pitfalls:
1. Severe tricuspid regurgitation causes the injectate to recycle back and forth across the valve falsely lowering cardiac output.
2. An injectate volume that is too large will also falsely lower cardiac output.
3. Intracardiac shunts can falsely elevate cardiac output. In a right-to-left shunt, part of the injectate escapes through the shunt and decreases the amount of time required for washout of the temperature change. An injectate volume that is too small will cause an abbreviated washout and therefore falsely elevate the cardiac output.
Also see Pulmonary Artery Catheter Primer from American Thoracic Society (About 100 MCQ questions covering almost all aspects of PAC).
Related previous pearl: Arterial pressure-based continuous cardiac output
Cardiac Output Pitfalls
Determination of cardiac output by thermodilution has several technical pitfalls. Any deviation in technique can produce inaccurate and inconsistent results.
Basis of thermodilutional cardiac output: The method relies on an injection of a known volume of fluid (5-10 mL) into the right atrium. This fluid, either normal saline or D5W is at room (or iced at known *) temperature and therefore cooler than blood. The cooler injectate mixes with blood, thus lowering its temperature. The cooled blood is ejected into the pulmonary artery and flows past a thermistor located in the distal end of the PA catheter. The thermistor generates a change in temperature to time curve. The area under this curve is calculated by integration and is inversely proportional to the flow past the thermistor. In other words, the longer it takes for this change in temperature to “wash out,” the slower the flow past the thermistor. The converse is also true. The greater the flow, the faster the temperature “wash out,” and therefore the smaller the area under the curve. Anything that can disrupt the “washout” of this temperature change can affect the accuracy of this measurement.
* iced saline has been said to provides a better "signal-to-noise" ratio but controversy continues in literature regarding iced vs room temperature solution.
Clinical pitfalls:
1. Severe tricuspid regurgitation causes the injectate to recycle back and forth across the valve falsely lowering cardiac output.
2. An injectate volume that is too large will also falsely lower cardiac output.
3. Intracardiac shunts can falsely elevate cardiac output. In a right-to-left shunt, part of the injectate escapes through the shunt and decreases the amount of time required for washout of the temperature change. An injectate volume that is too small will cause an abbreviated washout and therefore falsely elevate the cardiac output.
Also see Pulmonary Artery Catheter Primer from American Thoracic Society (About 100 MCQ questions covering almost all aspects of PAC).
Related previous pearl: Arterial pressure-based continuous cardiac output
Thursday, May 25, 2006
open abdomen
Thursday May 25, 2006
Q; What is the antibiotic of choice for prophylaxis in "abdomen left open"?
A; The open abdomen (or abdomen left open after damage control) does not require antibiotic prophylaxis (unless there is an evidence of infection).
Keep as reference, nice bedside management review article:
Role of ICU in the management of the acute abdomen.
Kapadia F. Indian J Surg 2004;66:203-208
Reference:
Management of the patient with an open abdomen: techniques in temporary and definitive closure. Curr Probl Surg. 2004;41:815-876.
Q; What is the antibiotic of choice for prophylaxis in "abdomen left open"?
A; The open abdomen (or abdomen left open after damage control) does not require antibiotic prophylaxis (unless there is an evidence of infection).
Keep as reference, nice bedside management review article:
Role of ICU in the management of the acute abdomen.
Kapadia F. Indian J Surg 2004;66:203-208
Reference:
Management of the patient with an open abdomen: techniques in temporary and definitive closure. Curr Probl Surg. 2004;41:815-876.
Wednesday, May 24, 2006
Hydrocortisone and Dexamethasone
Wednesday May 24, 2006
Hydrocortisone and Dexamethasone
What are the 3 major differences between Hydrocortisone and Dexamethasone ?
1. Potency of Hydrocortisone and Dexamethasone is 20:1 (precisely 20 : 0.75) - means .75 mg of dexamethasone is equal to 20 mg of hydrocortisone.
2. Mineralocorticoid : Glucocorticoid activity is 1:1 in hydrocotisone but dexamethasone has negligible mineralocorticoid activity as well it does not effect cortisol level.
3. Half life of Hydrocortisone is 8-12 hrs and of dexametasone is 36-54 hrs.
See nice review Relative Adrenal Insufficiency: Case Examples & Review from Bradley J. Phillips, M.D. , Boston Medical Center, Boston Univ. Schl of Med. (ref: The Internet Journal of Endocrinology. 2005. Volume 1 Number 2)
Hydrocortisone and Dexamethasone
What are the 3 major differences between Hydrocortisone and Dexamethasone ?
1. Potency of Hydrocortisone and Dexamethasone is 20:1 (precisely 20 : 0.75) - means .75 mg of dexamethasone is equal to 20 mg of hydrocortisone.
2. Mineralocorticoid : Glucocorticoid activity is 1:1 in hydrocotisone but dexamethasone has negligible mineralocorticoid activity as well it does not effect cortisol level.
3. Half life of Hydrocortisone is 8-12 hrs and of dexametasone is 36-54 hrs.
See nice review Relative Adrenal Insufficiency: Case Examples & Review from Bradley J. Phillips, M.D. , Boston Medical Center, Boston Univ. Schl of Med. (ref: The Internet Journal of Endocrinology. 2005. Volume 1 Number 2)
Monday, May 22, 2006
Acute Liver Failure
Tuesday May 23, 2006
Acute Liver Failure
Q; The chances of survival with medical management in acute liver failure is 26%. How much difference liver transplant can make ?
A; It goes upto 90% !!
Please see / keep in file video lecture
Acute Liver Failure: The Critical Team Approach
Dr. Lorenzo Rossaro, Chief of Gastroenterology and Hepatology and Head of the Liver Transplant Program at University of California Davis Medical Center.
(Total time: 42 minutes). Please click on above link.
You will need Real Player to see the lecture
Acute Liver Failure
Q; The chances of survival with medical management in acute liver failure is 26%. How much difference liver transplant can make ?
A; It goes upto 90% !!
Please see / keep in file video lecture
Acute Liver Failure: The Critical Team Approach
Dr. Lorenzo Rossaro, Chief of Gastroenterology and Hepatology and Head of the Liver Transplant Program at University of California Davis Medical Center.
(Total time: 42 minutes). Please click on above link.
You will need Real Player to see the lecture
PACT
Monday May 22, 2006
PACT - Critical Care distant learning course
The European Society of Intensive Care Medicine (ESICM) has designed a multidisciplinary distance-learning programme PACT, Patient-centred Acute Care Training.
Eventually, the whole programme will have 45 modules divided into 4 major areas -
For USA intensivists, it carries CME via SCCM. See the PACT Newsletter
icuroom.net or its editors have no relationship with PACT and introduction provided here is solely for educational purpose.
PACT - Critical Care distant learning course
The European Society of Intensive Care Medicine (ESICM) has designed a multidisciplinary distance-learning programme PACT, Patient-centred Acute Care Training.
Eventually, the whole programme will have 45 modules divided into 4 major areas -
- CLINICAL PROBLEMS,
- SKILLS AND TECHNIQUES,
- ORGAN SPECIFIC PROBLEM and
- PROFESSIONALISM.
The content of each module is based on real life in the ICU. Each module describes a clinical scenario in which the user is asked to interpret the nature of problems and make management decisions. At the end of each module there are self-assessment multiple-choice questions (MCQs). 12 modules are already available
- ACUTE RENAL FAILURE
- ALTERED CONSCIOUSNESS
- ARRHYTHMIA
- BASIC CLINICAL EXAMINATION
- CLINICAL IMAGING
- COPD and ASTHMA
- HOMEOSTASTIS
- MAJOR INTOXICATION
- NUTRITION
- PYREXIA
- QUALITY ASSURANCE AND COST EFFECTIVENESS
- TRAUMATIC BRAIN INJURY
Click
here to get more info.For USA intensivists, it carries CME via SCCM. See the PACT Newsletter
icuroom.net or its editors have no relationship with PACT and introduction provided here is solely for educational purpose.
Saturday, May 20, 2006
Intrahospital transport and VAP
Sunday May 21, 2006
Intrahospital transport - a risk factor for VAP ?
Interesting study published about 6 months ago in Critical Care Medicine1 from france where 118 ventilated patients who were transported out of the ICU were matched with 118 ventilated patients who did not undergo intrahospital transport. Adjusting all variables, the ventilator-associated pneumonia (VAP) was 26% in transported patients compared with 10% in the matched untransported patients.
Please read full article to see all inclusion criteria, methods and measurements.
The following interventions were recommended by the group to minimize VAP before transportation:
1. a written protocol focusing on the prevention of aspiration during transport of intubated patients.
2. check material and devices necessary for transport for normal working status,
3. aspirate the endotracheal tube,
4. verify endotracheal tube adequate position,
5. check the endotracheal cuff pressure,
6. fit the ventilatory circuit with a filter,
7. stop enteral nutrition,
8. aspirate gastric contents before and sometimes during transport,
9. if possible, transport the patient in semirecumbent position,
10. if necessary, sedation to obtain a Ramsay score less than 4,
11. verify the availability of the area to which the patient has to be transported.
References: click to get abstract/article
1. Intrahospital transport of critically ill ventilated patients: A risk factor for ventilator-associated pneumonia-A matched cohort study Critical Care Medicine. 33(11):2471-2478, November 2005.
Intrahospital transport - a risk factor for VAP ?
Interesting study published about 6 months ago in Critical Care Medicine1 from france where 118 ventilated patients who were transported out of the ICU were matched with 118 ventilated patients who did not undergo intrahospital transport. Adjusting all variables, the ventilator-associated pneumonia (VAP) was 26% in transported patients compared with 10% in the matched untransported patients.
Please read full article to see all inclusion criteria, methods and measurements.
The following interventions were recommended by the group to minimize VAP before transportation:
1. a written protocol focusing on the prevention of aspiration during transport of intubated patients.
2. check material and devices necessary for transport for normal working status,
3. aspirate the endotracheal tube,
4. verify endotracheal tube adequate position,
5. check the endotracheal cuff pressure,
6. fit the ventilatory circuit with a filter,
7. stop enteral nutrition,
8. aspirate gastric contents before and sometimes during transport,
9. if possible, transport the patient in semirecumbent position,
10. if necessary, sedation to obtain a Ramsay score less than 4,
11. verify the availability of the area to which the patient has to be transported.
References: click to get abstract/article
1. Intrahospital transport of critically ill ventilated patients: A risk factor for ventilator-associated pneumonia-A matched cohort study Critical Care Medicine. 33(11):2471-2478, November 2005.
Hypoproteinemia and cosyntropin test
Saturday May 20, 2006
Hypoproteinemia and cosyntropin test
43 year old malnourished patient admitted with septic shock. You started early goal directed therapy protocol. Patient blood pressure remained low despite showing signs of clinical improvement. You suspected adrenal insufficiency and ordered cosyntropin test. Patient failed to respond. You started low dose hydrocortisone. Next day you received call from lab that they also performed 'free cortisol' response to cosyntropin and found it appropriate to label patient as responder ?
Severe hypoproteinemia (as in this malnourished patient) may give false results and responders may get wrongly labelled as non-responders. In blood, about 90 percent of cortisol is bound to protiens (20 percent of cortisol is loosely bound to albumin and 70 percent is tightly bound to cortisol-binding globulin). Only 10 percent cortisol is in the free state. This is a major pittfall and deception to fall in while prescribing steroids in septic and hypoproteinemic patient under presumption of 'nonresponder'.
An important study reported about 2 years ago from Cleveland 1, looked into 66 critically ill patients with 36/66 had hypoproteinemia (albumin 2.5 g/dl or less) and 30/66 had near-normal serum albumin concentrations (above 2.5 g/dl). Baseline and cosyntropin stimulated serum total cortisol level as well as baseline and cosyntropin stimulated serum free cortisol level were measured. Study found that, nearly 40 percent of critically ill patients with hypoproteinemia had subnormal serum total cortisol levels, even though their adrenal function was normal as measured by free cortisol level.
Related previous pearl: Low dose steroid, yes or no ? - responder or non-responder ? - low-dose corticotropin stimulation test or high dose?
References: click to get abstract/article
1. Measurements of Serum Free Cortisol in Critically Ill Patients - Volume 350:1629-1638, April 15, 2004, NEJM
2. Septic Shock and Sepsis: A Comparison of Total and Free Plasma Cortisol Levels - The Journal of Clinical Endocrinology & Metabolism Vol. 91, No. 1 105-114
3. Adrenal Insufficiency - Roberto Salvatori, MD JAMA. 2005;294:2481-2488
Hypoproteinemia and cosyntropin test
43 year old malnourished patient admitted with septic shock. You started early goal directed therapy protocol. Patient blood pressure remained low despite showing signs of clinical improvement. You suspected adrenal insufficiency and ordered cosyntropin test. Patient failed to respond. You started low dose hydrocortisone. Next day you received call from lab that they also performed 'free cortisol' response to cosyntropin and found it appropriate to label patient as responder ?
Severe hypoproteinemia (as in this malnourished patient) may give false results and responders may get wrongly labelled as non-responders. In blood, about 90 percent of cortisol is bound to protiens (20 percent of cortisol is loosely bound to albumin and 70 percent is tightly bound to cortisol-binding globulin). Only 10 percent cortisol is in the free state. This is a major pittfall and deception to fall in while prescribing steroids in septic and hypoproteinemic patient under presumption of 'nonresponder'.
An important study reported about 2 years ago from Cleveland 1, looked into 66 critically ill patients with 36/66 had hypoproteinemia (albumin 2.5 g/dl or less) and 30/66 had near-normal serum albumin concentrations (above 2.5 g/dl). Baseline and cosyntropin stimulated serum total cortisol level as well as baseline and cosyntropin stimulated serum free cortisol level were measured. Study found that, nearly 40 percent of critically ill patients with hypoproteinemia had subnormal serum total cortisol levels, even though their adrenal function was normal as measured by free cortisol level.
Related previous pearl: Low dose steroid, yes or no ? - responder or non-responder ? - low-dose corticotropin stimulation test or high dose?
References: click to get abstract/article
1. Measurements of Serum Free Cortisol in Critically Ill Patients - Volume 350:1629-1638, April 15, 2004, NEJM
2. Septic Shock and Sepsis: A Comparison of Total and Free Plasma Cortisol Levels - The Journal of Clinical Endocrinology & Metabolism Vol. 91, No. 1 105-114
3. Adrenal Insufficiency - Roberto Salvatori, MD JAMA. 2005;294:2481-2488
Thursday, May 18, 2006
HIDA, DISIDA and BRIDA scan
Friday May 19, 2006
HIDA, DISIDA and BRIDA scan
Hepatic 2,6-dimethyliminodiacetic acid (HIDA) and Diisopropyl iminodiacetic acid (DISIDA) are nuclear studies to assess the function of the gallbladder and obstruction of the Common Bile Duct (CBD) in cholecystitis, cholangitis, billiary leak and atresia. These tests are ordered when ultrasound is equivocal. When you will order HIDA Scan or DISIDA scan ?
Nuclear Medicine literature is vast in this regard but to be short and simple, HIDA scan is used when serum bilirubin is less than 5-7 mg/dl and DISIDA scan is used when serum bilirubin is more than 7 mg/dl. DISIDA scan is now largely used instead of HIDA scan. The basis of this difference is relatively higher hepatic extraction. HIDA scan can be falsely positive when the gallbladder is not filling despite absence of cholecystitis like in severe liver disease (hyperbilirubinemia), patients on TPN or patient NPO for more than 24 hours, alcohol and opiate abuse. In case, serum bilirubin is extremely high (> 30 mg/dl), you can call for Mebrofenin (BRIDA) scan. Mebrofenin has even higher hepatic extraction than DISIDA scan.
Related Previous pearl: Acute acalculous cholecystitis in ICU
HIDA, DISIDA and BRIDA scan
Hepatic 2,6-dimethyliminodiacetic acid (HIDA) and Diisopropyl iminodiacetic acid (DISIDA) are nuclear studies to assess the function of the gallbladder and obstruction of the Common Bile Duct (CBD) in cholecystitis, cholangitis, billiary leak and atresia. These tests are ordered when ultrasound is equivocal. When you will order HIDA Scan or DISIDA scan ?
Nuclear Medicine literature is vast in this regard but to be short and simple, HIDA scan is used when serum bilirubin is less than 5-7 mg/dl and DISIDA scan is used when serum bilirubin is more than 7 mg/dl. DISIDA scan is now largely used instead of HIDA scan. The basis of this difference is relatively higher hepatic extraction. HIDA scan can be falsely positive when the gallbladder is not filling despite absence of cholecystitis like in severe liver disease (hyperbilirubinemia), patients on TPN or patient NPO for more than 24 hours, alcohol and opiate abuse. In case, serum bilirubin is extremely high (> 30 mg/dl), you can call for Mebrofenin (BRIDA) scan. Mebrofenin has even higher hepatic extraction than DISIDA scan.
Related Previous pearl: Acute acalculous cholecystitis in ICU
RSBI Rate
Thursday May 18, 2006
RSBI Rate - Not only RSBI !
The Rapid Shallow Breathing Index (RSBI) remained an integral part of ventilator weaning parameter. Dr. Segal and coll. from Morristown Memorial Hospital, NJ went one step forward and looked into "RSBI Rate" (rate of change in the RSBI) with the question that as respiratory failure is a dynamic phenomenon - should serial followup of RSBI would be a more accurate predictor of weaning outcome, instead of one RSBI at a given time ?. In a prospective cohort study, patients with following criteria has been included:
Reference:
USE OF THE RATE OF CHANGE OF THE RSBI DURING SPONTANEOUS BREATHING TRIAL AS AN ACCURATE PREDICTOR OF WEANING OUTCOME - Critical Care Medicine: Volume 33(12) Abstract Supplement December 2005 p A20
RSBI Rate - Not only RSBI !
The Rapid Shallow Breathing Index (RSBI) remained an integral part of ventilator weaning parameter. Dr. Segal and coll. from Morristown Memorial Hospital, NJ went one step forward and looked into "RSBI Rate" (rate of change in the RSBI) with the question that as respiratory failure is a dynamic phenomenon - should serial followup of RSBI would be a more accurate predictor of weaning outcome, instead of one RSBI at a given time ?. In a prospective cohort study, patients with following criteria has been included:
- requiring mechanical ventilation for more than 48hrs,
- ET tube size no smaller than 7.5 in the ICU,
- cleared by an intensivist (independent of study investigators) as an appropriate candidate to undergo weaning,
- on hospital respiratory therapist driven weaning protocol.
Spontaneous Breathing Trial (SBT) for up to two hours given and parameters were measured periodically at SBT. The RSBI Rate was calculated by the formula:
RSBI rate: (RSBI2 - RSBI1)/ RSBI1 × 100
Out of 30 patients, 21 were successfully extubated, 3 were re-intubated within 24 hours and six were intolerants to the SBT. The RSBI on the failure plus Intolerance group was 40.2 (SD 14.7) but RSBI rate on every patient that failed or had intolerance to SBT had a RSBI Rate greater that 20%. It was concluded that the RSBI Rate less that 20% has a sensitivity of 90.4% and specificity of 100% in predicting weaning success.Reference:
USE OF THE RATE OF CHANGE OF THE RSBI DURING SPONTANEOUS BREATHING TRIAL AS AN ACCURATE PREDICTOR OF WEANING OUTCOME - Critical Care Medicine: Volume 33(12) Abstract Supplement December 2005 p A20
Wednesday, May 17, 2006
Calcium in Dig toxicity
Wednesday May 17, 2006
Treating Digoxin toxicity
Case: 74 year old male has been found to have arrhythmia with runs of wide complex ventricular tachycardia. Patient so far remained hemodynamically stable. You request crash cart near bed, applied pads to chest and send STAT labs and start reviewing patient's chart. You noticed 4 days ago digoxin level was 1.9 and since then his serum creatinine is steadily rising from 1.6 to 2.8. You suspected "Dig. toxicity" and called lab to run STAT dig. level. Indeed Dig. level is back with 3.4 and accompanying labs showed K+ level of 6.9. You ordered "Digi-bind" (Digoxin Immune Fab). Pharmacy informed you, "it will take time before Digi-bind gets to ICU". Interim you started treating hyperkalemia with IV insulin, D-50, IV bicarb., IV calcium and albuterol neb. treatments.
Where did you go wrong ?
Answer: Calcium has shown to make digoxin toxicity worse. It may be more wise to avoid calcium in management of hyperkalemia from digoxin toxicity. Some literature has shown the similar membrane stabalizing effect from magnesium and may be used instead of calcium.
Caution should be taken not to go very aggressive in treating hyperkalemia, or atleast potassium should be followed very closely if DigiFab is planned. With administration of DigiFab (Digibind), potassium shifts back into the cell and life threatening hypokalemia may develop rapidly. Digoxin causes a shift of potassium from inside to outside of the cell and may cause severe hyperkalemia but overall there is a whole body deficit of potassium. With administration of Digi-bind, actual hypokalemia may manifest which could be equally life threatening.
Read related interesting review: Recognising signs of danger: ECG changes resulting from an abnormal serum potassium concentration: A Webster, W Brady and F Morris (reference: Emerg Med J 2002; 19:74-77)
References: click to get abstract/article
1. Calcium for hyperkalaemia in digoxin toxicity - Emerg Med J 2002; 19:183
2. Using calcium salts for hyperkalaemia - Nephrol Dial Transplant (2004) 19: 1333-1334
3. Slow-release potassium overdose: Is there a role for magnesium? Emergency Medicine 1999;11:263–71
Treating Digoxin toxicity
Case: 74 year old male has been found to have arrhythmia with runs of wide complex ventricular tachycardia. Patient so far remained hemodynamically stable. You request crash cart near bed, applied pads to chest and send STAT labs and start reviewing patient's chart. You noticed 4 days ago digoxin level was 1.9 and since then his serum creatinine is steadily rising from 1.6 to 2.8. You suspected "Dig. toxicity" and called lab to run STAT dig. level. Indeed Dig. level is back with 3.4 and accompanying labs showed K+ level of 6.9. You ordered "Digi-bind" (Digoxin Immune Fab). Pharmacy informed you, "it will take time before Digi-bind gets to ICU". Interim you started treating hyperkalemia with IV insulin, D-50, IV bicarb., IV calcium and albuterol neb. treatments.
Where did you go wrong ?
Answer: Calcium has shown to make digoxin toxicity worse. It may be more wise to avoid calcium in management of hyperkalemia from digoxin toxicity. Some literature has shown the similar membrane stabalizing effect from magnesium and may be used instead of calcium.
Caution should be taken not to go very aggressive in treating hyperkalemia, or atleast potassium should be followed very closely if DigiFab is planned. With administration of DigiFab (Digibind), potassium shifts back into the cell and life threatening hypokalemia may develop rapidly. Digoxin causes a shift of potassium from inside to outside of the cell and may cause severe hyperkalemia but overall there is a whole body deficit of potassium. With administration of Digi-bind, actual hypokalemia may manifest which could be equally life threatening.
Read related interesting review: Recognising signs of danger: ECG changes resulting from an abnormal serum potassium concentration: A Webster, W Brady and F Morris (reference: Emerg Med J 2002; 19:74-77)
References: click to get abstract/article
1. Calcium for hyperkalaemia in digoxin toxicity - Emerg Med J 2002; 19:183
2. Using calcium salts for hyperkalaemia - Nephrol Dial Transplant (2004) 19: 1333-1334
3. Slow-release potassium overdose: Is there a role for magnesium? Emergency Medicine 1999;11:263–71
Monday, May 15, 2006
Pseudothrombocytopenia
Monday May 15, 2006
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
Sunday, May 14, 2006
In Hyperkalemia
Sunday May 14, 2006
In Hyperkalemia !!
Q; Nurse call you with K+ level of 7.8 (lab confirmed - no hemolysis). You ordered 10 units of IV insulin with 2 ampules of D-50, 1 ampule of calcium gluconate and 2 ampules of sodium bicarbonate in series. RT was requested to give 2 nebulizer treatments of albuterol. The final order set is followed ultimately by PO Kayexalate/sorbitol.
What is wrong in above orders for the management of hyperkalemia?
A; In the management of hyperkalemia, sodium bicarbonate should be given before calcium. Administrating bicarbonate after calcium will bind calcium and will render it ineffective. This is another reason, we don't prepare "bicarb drip" in LR (Lactated Ringer’s) as it contains calcium which will bind bicarbonate and will make the whole management ineffective.
Related previous pearls:
Difference between Lactate Ringer's and Normal Saline solutions
Colonic Necrosis - unusual complication of Kayexalate-Sorbitol
In Hyperkalemia !!
Q; Nurse call you with K+ level of 7.8 (lab confirmed - no hemolysis). You ordered 10 units of IV insulin with 2 ampules of D-50, 1 ampule of calcium gluconate and 2 ampules of sodium bicarbonate in series. RT was requested to give 2 nebulizer treatments of albuterol. The final order set is followed ultimately by PO Kayexalate/sorbitol.
What is wrong in above orders for the management of hyperkalemia?
A; In the management of hyperkalemia, sodium bicarbonate should be given before calcium. Administrating bicarbonate after calcium will bind calcium and will render it ineffective. This is another reason, we don't prepare "bicarb drip" in LR (Lactated Ringer’s) as it contains calcium which will bind bicarbonate and will make the whole management ineffective.
Related previous pearls:
Difference between Lactate Ringer's and Normal Saline solutions
Colonic Necrosis - unusual complication of Kayexalate-Sorbitol
Friday, May 12, 2006
Hyperbaric oxygen in CO poisoning
Saturday May 13, 2006
Hyperbaric oxygen in CO poisoning
Q; What is the role of hyberbaric oxygen in the management of lethal Carbon-monoxide (CO) poisoning ?
A; It decreases the half life of CO from 5 hours to half hour and so the possible complications. It prevents lipid peroxidation in the brain and preserve ATP levels in tissue exposed to carbon monoxide. It has shown to decrease the cognitive sequelae by 46 % when compared with 'normobaric' group at 6 weeks 2.
Limitations: Hyperbaric oxygen in CO poisoning has its own limitations. It may induce "hyperoxic" seizures (rare) 3. Other adverse effects of hyperbaric oxygen includes reversible myopia, rupture of the middle ear, barotrauma to lungs 4. Hyperbaric oxygen should be reserved for lethal cases of CO poisoning.
Alternate: If hyperbaric oxygen is not available, apply 100% oxygen, high PEEP and if needed high-frequency ventilation. 100% O2 reduces half life of CO effectively to about one and half hour.
Reference: (click to get abstract)
1. Diagnosis and treatment of carbon monoxide poisoning - Respir Care Clin N Am. 1999 Jun;5(2):183-202.
2. Hyperbaric Oxygen for Acute Carbon Monoxide Poisoning - Volume 347:1057-1067, oct. 3, 2002
3. Central nervous system oxygen toxicity during hyperbaric treatment of patients with carbon monoxide poisoning - Hampson NB, Simonson SG, Kramer CC, Piantadosi CA - UNDERSEA & HYPERBARIC MEDICINE 23 (4): 215-219 DEC 1996
4. Hyperbaric-Oxygen Therapy - Volume 334:1642-1648, june 20, 1996
Hyperbaric oxygen in CO poisoning
Q; What is the role of hyberbaric oxygen in the management of lethal Carbon-monoxide (CO) poisoning ?
A; It decreases the half life of CO from 5 hours to half hour and so the possible complications. It prevents lipid peroxidation in the brain and preserve ATP levels in tissue exposed to carbon monoxide. It has shown to decrease the cognitive sequelae by 46 % when compared with 'normobaric' group at 6 weeks 2.
Limitations: Hyperbaric oxygen in CO poisoning has its own limitations. It may induce "hyperoxic" seizures (rare) 3. Other adverse effects of hyperbaric oxygen includes reversible myopia, rupture of the middle ear, barotrauma to lungs 4. Hyperbaric oxygen should be reserved for lethal cases of CO poisoning.
Alternate: If hyperbaric oxygen is not available, apply 100% oxygen, high PEEP and if needed high-frequency ventilation. 100% O2 reduces half life of CO effectively to about one and half hour.
Reference: (click to get abstract)
1. Diagnosis and treatment of carbon monoxide poisoning - Respir Care Clin N Am. 1999 Jun;5(2):183-202.
2. Hyperbaric Oxygen for Acute Carbon Monoxide Poisoning - Volume 347:1057-1067, oct. 3, 2002
3. Central nervous system oxygen toxicity during hyperbaric treatment of patients with carbon monoxide poisoning - Hampson NB, Simonson SG, Kramer CC, Piantadosi CA - UNDERSEA & HYPERBARIC MEDICINE 23 (4): 215-219 DEC 1996
4. Hyperbaric-Oxygen Therapy - Volume 334:1642-1648, june 20, 1996
vasopressin/norepinephrine ratio
Friday May 12, 2006
vasopressin/norepinephrine ratio in septic shock
vasopressin/norepinephrine ratio in septic shock
Role of vasopressin in septic shock seems promising but we don't have enough data yet to support its regular use. Interesting study in Taiwan was done by Lin and co. and published 6 months ago in Am J Emerg Med. 182 patients (consecutive patients visiting the emergency department), who met the inclusive criteria were divided into 3 groups (per standard guidelines):
- septic shock,
- severe sepsis, and
- sepsis.
30 healthy subjects were included as control.
The plasma vasopressin level at baseline was drawn early in course in emergency department. The plasma vasopressin level was significantly lower for those who finally developed septic shock (3.6 +/- 2.5 pg/mL) than severe sepsis (21.8 +/- 4.1 pg/mL) and sepsis group (10.6 +/- 6.5 pg/mL) - kind of bell curve.
Simultaneouly norepinephrine level was measured in the same groups. Norepinephrine level was highest for septic shock group, (3650 +/- 980 pg/mL) in comparion to severe sepsis (3600 +/- 1000 pg/mL) and sepsis group (1720 +/- 320 pg/mL).
The vasopressin/norepinephrine ratio (very early in the course) was significantly lower for the patients with final diagnosis of septic shock (P less than .001).
This study lead us to logical question: Should we use vasopressin early in septic shock instead later ? but probably it is still early to jump on vasopressin, atleast till we get results from evidence based studies such as pending VASST (Vasopressin Vs. Norepinephrine in Septic Shock) study.
*VASST is an ongoing multi-centre triple-blind randomized controlled trial being conducted in Canada and Australia to determine the effectiveness of Vasopressin compared to Norepinephrine (28-day and 90-day survival).
Previous related pearl:
Reference: (click to get abstract)
Low plasma vasopressin/norepinephrine ratio predicts septic shock. Am J Emerg Med. 2005 Oct;23(6):718-24.
Thursday, May 11, 2006
Auto-PEEP
Thursday May 11, 2006
Auto-Peep
M.M. MUGHAL, D.A. CULVER, O.A. MINAI, and A.C. ARROLIGA - CLEVELAND CLINIC JOURNAL OF MEDICINE VOLUME 72 • NUMBER 9 SEPTEMBER 2005
Auto-Peep
Q; What level of extrinsic PEEP should be applied to counter act (intrinsic) auto-PEEP?
A; 75 - 85% of auto-PEEP.
Keeping extrinsic PEEP lower than auto-PEEP not only effectively counter acts auto-PEEP but also any ciruclatory depression or lung hyperinflation is unlikely to occur at extrinsic PEEP slightly lower than intrinsic PEEP value.
Read precise review on auto-peep:
M.M. MUGHAL, D.A. CULVER, O.A. MINAI, and A.C. ARROLIGA - CLEVELAND CLINIC JOURNAL OF MEDICINE VOLUME 72 • NUMBER 9 SEPTEMBER 2005
Wednesday, May 10, 2006
TTKG
Wednesday May 10, 2006
The TransTubular Potassium Gradient - TTKG
TTKG is an index reflecting conservation of potassium by Kidney.
TTKG = (Urine-K / Plasma-K) / (Urine-Osm / Plasma-Osm)
Normal value is 8-9 in normokalemic patient and should be 10-11 in hyperkalemic patient.
Clinical significance:
1. In hyperkalemia if TTKG remains less than 7, most probable cause is hypoaldosteronism. Diagnosis can be confirmed by challenging patient with 0.05 mg of fludrocortisone, which should increase the TTKG. (Mineralcorticoid increases TTKG).
2. In hypokalemia - kidney try to conserve potassium and TTKG should fall to less than 2 (like in GI source). If TTKG remains higher, it suggests renal loss of potassium (like in diuretics).
Limitations:
1. Always check urine sodium simultaneouly. TTKG is unreliable if urine sodium is less than 25 mmol/l.
2. TTKG is unreliable if urine osmolality is less than the serum osmolality.
References: click to get abstracts/articles
1.Potassium excretion indices in the diagnostic approach to hypokalaemia - Q J Med 2000; 93: 318-319
2. Transtubular potassium concentration gradient (TTKG) and urine ammonium in differential diagnosis of hypokalemia - J Nephrol. 2000 Mar =Apr;13(2):120-5
3. Diseases of Potassium metabolism: Atlas of disease of the kidney by Robert W. Schrier, Professor and Chairman, Department of Medicine, University of Colorado School of Medicine, Denver, Colorado
The TransTubular Potassium Gradient - TTKG
TTKG is an index reflecting conservation of potassium by Kidney.
TTKG = (Urine-K / Plasma-K) / (Urine-Osm / Plasma-Osm)
Normal value is 8-9 in normokalemic patient and should be 10-11 in hyperkalemic patient.
Clinical significance:
1. In hyperkalemia if TTKG remains less than 7, most probable cause is hypoaldosteronism. Diagnosis can be confirmed by challenging patient with 0.05 mg of fludrocortisone, which should increase the TTKG. (Mineralcorticoid increases TTKG).
2. In hypokalemia - kidney try to conserve potassium and TTKG should fall to less than 2 (like in GI source). If TTKG remains higher, it suggests renal loss of potassium (like in diuretics).
Limitations:
1. Always check urine sodium simultaneouly. TTKG is unreliable if urine sodium is less than 25 mmol/l.
2. TTKG is unreliable if urine osmolality is less than the serum osmolality.
References: click to get abstracts/articles
1.Potassium excretion indices in the diagnostic approach to hypokalaemia - Q J Med 2000; 93: 318-319
2. Transtubular potassium concentration gradient (TTKG) and urine ammonium in differential diagnosis of hypokalemia - J Nephrol. 2000 Mar =Apr;13(2):120-5
3. Diseases of Potassium metabolism: Atlas of disease of the kidney by Robert W. Schrier, Professor and Chairman, Department of Medicine, University of Colorado School of Medicine, Denver, Colorado
Monday, May 08, 2006
Contrast induced Nephropathy
Tuesday May 09, 2006
Contrast induced Nephropathy
Q: What is the cut off point to suspect Contrast induced Nephropathy ?
A; Unfortunately there is no consensus defination yet to define Contrast Induced Nephropathy but its better to be safer than sorry. The most conservative general rule is to suspect some component of contrast induced nephropathy whenever there is a 25% increase in serum creatinine concentration from the baseline, or an increase of at least 0.3 mg/dL within 48-72 hours, when no other cause could be find.
We found 2 good review articles for further reading :
1. Contrast-Induced Nephropathy, Tadhg G. Gleeson; Sudi Bulugahapitiya, dublin, Ireland. (ref.: Am J Roentgenol 183(6):1673-1689, 2004). This article is available with free registration at medscape.com
2. Radiocontrast-Induced Nephropathy, Resident Grand Rounds by Jeff S. Rose, MD at Wake Forest University School of Medicine, Winston-Salem, NC
Previous related Pearl: Preventing contrast-Induced Nephropathy
Contrast induced Nephropathy
Q: What is the cut off point to suspect Contrast induced Nephropathy ?
A; Unfortunately there is no consensus defination yet to define Contrast Induced Nephropathy but its better to be safer than sorry. The most conservative general rule is to suspect some component of contrast induced nephropathy whenever there is a 25% increase in serum creatinine concentration from the baseline, or an increase of at least 0.3 mg/dL within 48-72 hours, when no other cause could be find.
We found 2 good review articles for further reading :
1. Contrast-Induced Nephropathy, Tadhg G. Gleeson; Sudi Bulugahapitiya, dublin, Ireland. (ref.: Am J Roentgenol 183(6):1673-1689, 2004). This article is available with free registration at medscape.com
2. Radiocontrast-Induced Nephropathy, Resident Grand Rounds by Jeff S. Rose, MD at Wake Forest University School of Medicine, Winston-Salem, NC
Previous related Pearl: Preventing contrast-Induced Nephropathy
Heparin Induced HyperKalemia
Monday May 08, 2006
Heparin Induced HyperKalemia
Hyperkalemia from Heparin is a well know phenomenon and has been detected particularly on geriatric, renal insufficient and diabetic patients. Hyperkalemia can be anywhere from .3 to 1.7 mEq/Litre. It usually occurs around on day 3 with SQ heparin (as for DVT prophylaxis) but can occur early with IV heparin 1,2,3,4. Hyperkalemia has been reported with low- molecular weight heparins too but risk is low 5, 6, 7.
Mechanism of action: Heparin induce hypoaldosteronism and can subsequently lead to hyperkalemia 6.
Treatment: Best thing is to discontinue the culprit but if heparin is absolutely required, fludrocortisone (.1 mg/day) has been reported to be effective in heparin-induced hyperkalemia 8.
References: Click to get abstracts/articles
1. Case report - Heparin-induced hyperkalemia after cardiac surgery - Ann Thorac Surg 2002;74:1698-1700
2. Heparin-induced hyperkalemia -The Annals of Pharmacotherapy: Vol. 24, No. 3, pp. 244-246.
3. Heparin Induced HyperKalemia - Endocrine Abstracts (2002) 4 P26
4. Heparin-Induced Hyperkalemia Confirmed by Drug Rechallenge. American Journal of Physical Medicine & Rehabilitation. 79(1):93-96, January/February 2000.
5. Early onset of hyperkalemia in patients treated with low molecular weight heparin: a prospective study - Pharmacoepidemiol Drug Saf.2004 May;13(5):299-302.
6. Effect of Low-Molecular-Weight Heparin on Potassium Homeostasis - Pathophysiology of Haemostasis and Thrombosis 2002;32:107-110
7. Low Molecular Weight Heparins Can Lead To Hyperkalaemia The Internet Journal of Geriatrics and Gerontology . 2005. Volume 2 Number 2.
8. Fludrocortisone for the treatment of heparin-induced hyperkalemia - The Annals of Pharmacotherapy: Vol. 34, No. 5, pp. 606-610
Heparin Induced HyperKalemia
Hyperkalemia from Heparin is a well know phenomenon and has been detected particularly on geriatric, renal insufficient and diabetic patients. Hyperkalemia can be anywhere from .3 to 1.7 mEq/Litre. It usually occurs around on day 3 with SQ heparin (as for DVT prophylaxis) but can occur early with IV heparin 1,2,3,4. Hyperkalemia has been reported with low- molecular weight heparins too but risk is low 5, 6, 7.
Mechanism of action: Heparin induce hypoaldosteronism and can subsequently lead to hyperkalemia 6.
Treatment: Best thing is to discontinue the culprit but if heparin is absolutely required, fludrocortisone (.1 mg/day) has been reported to be effective in heparin-induced hyperkalemia 8.
References: Click to get abstracts/articles
1. Case report - Heparin-induced hyperkalemia after cardiac surgery - Ann Thorac Surg 2002;74:1698-1700
2. Heparin-induced hyperkalemia -The Annals of Pharmacotherapy: Vol. 24, No. 3, pp. 244-246.
3. Heparin Induced HyperKalemia - Endocrine Abstracts (2002) 4 P26
4. Heparin-Induced Hyperkalemia Confirmed by Drug Rechallenge. American Journal of Physical Medicine & Rehabilitation. 79(1):93-96, January/February 2000.
5. Early onset of hyperkalemia in patients treated with low molecular weight heparin: a prospective study - Pharmacoepidemiol Drug Saf.2004 May;13(5):299-302.
6. Effect of Low-Molecular-Weight Heparin on Potassium Homeostasis - Pathophysiology of Haemostasis and Thrombosis 2002;32:107-110
7. Low Molecular Weight Heparins Can Lead To Hyperkalaemia The Internet Journal of Geriatrics and Gerontology . 2005. Volume 2 Number 2.
8. Fludrocortisone for the treatment of heparin-induced hyperkalemia - The Annals of Pharmacotherapy: Vol. 34, No. 5, pp. 606-610
Saturday, May 06, 2006
Our failures !!!
Sunday May 07, 2006
Our failures !!!
Reference: Click to get abstract
1. Intensive Care and Emergency Medicine - Progress Over the Past 25 Years: Jean-Louis Vincent, MD, PhD; Mitchell P. Fink, MD, FCCP; John J. Marini, MD; Michael R. Pinsky, MD, FCCP; William J. Sibbald, MD, FCCP; Mervyn Singer, MD; Peter M. Suter, MD; Deborah Cook, MD; Paul E. Pepe, MD and Timothy Evans, MD Chest. 2006;129:1061-1067
Our failures !!!
Some big gurus from Critical Care Medicine (all names below in reference) have penned a cumulative article on progress of Intensive Care and Emergency Medicine over the past 25 Years in recent issue of chest 1. The whole article is worth reading but the most interesting part is where authors have pointed out "Our Failures" with following mentions:
- Excessive antibiotic use
- Iatrogenic IV fluid overload
- Excessive administration of inotropic agents
- Ventilation with unnecessarily large tidal volumes
- Excessive, continuous IV sedation
- Unnecessary use of antiarrhythmic agents
- Excessive caloric intake
- Liberal blood transfusions
- Traumatic effects of endotracheal intubation and airway management
- Excessive ventilation in low flow states
Reference: Click to get abstract
1. Intensive Care and Emergency Medicine - Progress Over the Past 25 Years: Jean-Louis Vincent, MD, PhD; Mitchell P. Fink, MD, FCCP; John J. Marini, MD; Michael R. Pinsky, MD, FCCP; William J. Sibbald, MD, FCCP; Mervyn Singer, MD; Peter M. Suter, MD; Deborah Cook, MD; Paul E. Pepe, MD and Timothy Evans, MD Chest. 2006;129:1061-1067
ABCDEF of CXR
Saturday May 06, 2006
ABCDEF of CXR
There are many mnemoics we use in medicine. One mnemonic easy to teach house staff so they don't miss things on chest x-ray is
A (Abnormal) Air and Aqua - (like pneumothorax, pulmonary edema, pleural effusions or even free air below right diaphragm).
B Bone
C Cardia (like pericardial effusion, vena cavae, aortic knob and other cardiac contours)
D Densities (infiltrates, masses and lesions - also include hilar area)
E Elevation of diaphragm (should also take care of atelactasis)
F Foreign bodies (lines, tubes, devices etc).
ABCDEF of CXR
There are many mnemoics we use in medicine. One mnemonic easy to teach house staff so they don't miss things on chest x-ray is
A (Abnormal) Air and Aqua - (like pneumothorax, pulmonary edema, pleural effusions or even free air below right diaphragm).
B Bone
C Cardia (like pericardial effusion, vena cavae, aortic knob and other cardiac contours)
D Densities (infiltrates, masses and lesions - also include hilar area)
E Elevation of diaphragm (should also take care of atelactasis)
F Foreign bodies (lines, tubes, devices etc).
Friday, May 05, 2006
Dialysis disequilibrium syndrome
Friday May 05, 2006
Case: 57 year old female, newly hemodialysis patient, transferred from floor to ICU after she developed seizure at the end of her dialysis session. No significant risk factor could be find otherwise. Nurse reports patient appear irritable and restless before episode and complain of headache, nausea and blurred vision. While resident was called to evaluate as patient also noticed to have muscular twitching and confusion, symptoms progressed and seizure was witnessed.
Answer: Dialysis disequilibrium syndrome.
Dialysis disequilibrium syndrome is common during hemodialysis particularly patient’s first few dialysis sessions. It is characterized by neurologic symptoms of varying severity and actually may lead to herniation and death. The rapid reduction in BUN lowers the plasma osmolality, creating a transient osmotic gradient that promotes water movement into the cells, causing cerebral edema and consequently acute neurologic dysfunction. With better understanding of the process and newer dialysis techniques, severe form of syndrome is now not commonly seen. This not only explains that why our nephrology colleagues start with gentle but frequent sessions but also explains one of the several benefits of mannitol during dialysis. Read interesting article from University of Calgary, Alberta, Canada :
Dialysis Disequilibrium Syndrome: Brain death following hemodialysis for metabolic acidosis and acute renal failure - A case report followed with discussion and different management modalities (Ref.: BMC Nephrol. 2004; 5: 9.)
Case: 57 year old female, newly hemodialysis patient, transferred from floor to ICU after she developed seizure at the end of her dialysis session. No significant risk factor could be find otherwise. Nurse reports patient appear irritable and restless before episode and complain of headache, nausea and blurred vision. While resident was called to evaluate as patient also noticed to have muscular twitching and confusion, symptoms progressed and seizure was witnessed.
Answer: Dialysis disequilibrium syndrome.
Dialysis disequilibrium syndrome is common during hemodialysis particularly patient’s first few dialysis sessions. It is characterized by neurologic symptoms of varying severity and actually may lead to herniation and death. The rapid reduction in BUN lowers the plasma osmolality, creating a transient osmotic gradient that promotes water movement into the cells, causing cerebral edema and consequently acute neurologic dysfunction. With better understanding of the process and newer dialysis techniques, severe form of syndrome is now not commonly seen. This not only explains that why our nephrology colleagues start with gentle but frequent sessions but also explains one of the several benefits of mannitol during dialysis. Read interesting article from University of Calgary, Alberta, Canada :
Dialysis Disequilibrium Syndrome: Brain death following hemodialysis for metabolic acidosis and acute renal failure - A case report followed with discussion and different management modalities (Ref.: BMC Nephrol. 2004; 5: 9.)
Thursday, May 04, 2006
Swan in Amniotic fluid embolism
Thursday May 04, 2006
Pulmonary Artery Catheter in Amniotic fluid embolism !!
20 years ago it was suggested by Mason that probable diagnosis of Amniotic fluid embolism can be made by analyzing pulmonary artery blood with the logic that amniotic fluid does not ordinarily enter the maternal circulation, and the identification of large numbers of fetal squamous in the postpartum pulmonary microvasculature is of clinical significance. (He applied similar argument for other similar diseases such as fat embolism). Diagnosis becomes more probable if other fetal debris such as mucin or hair is present.
Technique described: Obtain blood from the distal lumen of a pulmonary artery catheter (in wedged position). After discarding the first 10 ml of blood, draw an additional 10 ml, heparinize and analyze utilizing Papanicolaou's method.
Above technique is only suggestive of amniotic fluid embolism and not a gold standard.
References: Click to get abstract/article
1. Pulmonary microvascular cytology. A new diagnostic application of the pulmonary artery catheter - Chest, V. 88, 908-14
2. Amniotic fluid embolism - Masson RG - Clin Chest Med.1992 Dec;13(4):657-65.
Pulmonary Artery Catheter in Amniotic fluid embolism !!
20 years ago it was suggested by Mason that probable diagnosis of Amniotic fluid embolism can be made by analyzing pulmonary artery blood with the logic that amniotic fluid does not ordinarily enter the maternal circulation, and the identification of large numbers of fetal squamous in the postpartum pulmonary microvasculature is of clinical significance. (He applied similar argument for other similar diseases such as fat embolism). Diagnosis becomes more probable if other fetal debris such as mucin or hair is present.
Technique described: Obtain blood from the distal lumen of a pulmonary artery catheter (in wedged position). After discarding the first 10 ml of blood, draw an additional 10 ml, heparinize and analyze utilizing Papanicolaou's method.
Above technique is only suggestive of amniotic fluid embolism and not a gold standard.
References: Click to get abstract/article
1. Pulmonary microvascular cytology. A new diagnostic application of the pulmonary artery catheter - Chest, V. 88, 908-14
2. Amniotic fluid embolism - Masson RG - Clin Chest Med.1992 Dec;13(4):657-65.
Wednesday, May 03, 2006
Massive PE
Wednesday May 03, 2006
What if even thrombolysis fails in massive PE ?
For intensivists massive pulmonary Embolism (PE) is a dreaded situation, especially when even thrombolysis fails. Meneveau and coll. from france have studied such group of 40 patients who did not respond to thrombolysis. Results were published recently in chest.
14/40 patients who were treated by rescue surgical embolectomy were compared with 26/40 patients who were treated by repeat thrombolysis.
References: Click to get abstract/article
1. Management of Unsuccessful Thrombolysis in Acute Massive Pulmonary Embolism - Chest. 2006;129:1043-1050
What if even thrombolysis fails in massive PE ?
For intensivists massive pulmonary Embolism (PE) is a dreaded situation, especially when even thrombolysis fails. Meneveau and coll. from france have studied such group of 40 patients who did not respond to thrombolysis. Results were published recently in chest.
14/40 patients who were treated by rescue surgical embolectomy were compared with 26/40 patients who were treated by repeat thrombolysis.
- There was a trend for higher mortality in the medical group than in the surgical group (10 vs 1 deaths).
- Also, there were significantly more recurrent PEs in the repeat thrombolysis (35% vs 0%).
- While no significant difference was observed in number of major bleed, all bleeding events in the repeat-thrombolysis group were fatal.
Study concluded that rescue surgical embolectomy led to a better in-hospital course when compared with repeat thrombolysis in patients with massive PE who have not responded to thrombolysis.
See comprehensive review,
References: Click to get abstract/article
1. Management of Unsuccessful Thrombolysis in Acute Massive Pulmonary Embolism - Chest. 2006;129:1043-1050
Tuesday, May 02, 2006
Phosphate level in Tylenol toxicity
Tuesday May 02, 2006
Is serum phosphate level better than King’s College Hospital criteria ?
One study of 125 patients published in 'Hepatology' in 2002 looked into relation of serum phosphate level and survival in Acetaminophen-induced hepatotoxicity 1. Study found that Phosphate concentrations were significantly higher in nonsurvivors than in survivors at 48 to 72 hours after overdose as well as at 72 to 96 hours after overdose.
A threshold phosphate concentration of 3.71 mg/dL (1.2 mmol/L) at 48 to 96 hours after overdose had sensitivity of 89%, specificity of 100%, accuracy of 98%, positive predictive value of 100%, and negative predictive value of 98%. The serum phosphate level had higher sensitivity, accuracy, and positive and negative predictive values than the King’s College Hospital criteria, and it identified patients significantly earlier.
References: Click to get abstract/article
1. Serum Phosphate Is an Early Predictor of Outcome in severe Acetaminophen-Induced Hepatotoxicity Hepatology - 2002;36:659-665 -Full article available with free registration
Is serum phosphate level better than King’s College Hospital criteria ?
One study of 125 patients published in 'Hepatology' in 2002 looked into relation of serum phosphate level and survival in Acetaminophen-induced hepatotoxicity 1. Study found that Phosphate concentrations were significantly higher in nonsurvivors than in survivors at 48 to 72 hours after overdose as well as at 72 to 96 hours after overdose.
A threshold phosphate concentration of 3.71 mg/dL (1.2 mmol/L) at 48 to 96 hours after overdose had sensitivity of 89%, specificity of 100%, accuracy of 98%, positive predictive value of 100%, and negative predictive value of 98%. The serum phosphate level had higher sensitivity, accuracy, and positive and negative predictive values than the King’s College Hospital criteria, and it identified patients significantly earlier.
References: Click to get abstract/article
1. Serum Phosphate Is an Early Predictor of Outcome in severe Acetaminophen-Induced Hepatotoxicity Hepatology - 2002;36:659-665 -Full article available with free registration
Monday, May 01, 2006
IVF Bolus
Monday May 01, 2006
How to write order for IVF bolus !!
What we have learnt from guru and professor Jean-Louis Vincent is that the most important thing in Critical care Medicine is to master the 'basic and simple things'. Few months back he taught us the art of everyday rounding in ICUs with simple mnemonic of "Fast Hug" 1. In this month issue of Critical Care Medicine he precisely explains the art of fluid challenge. First he busted 5 myths about fluid bolus. Enjoy !!
* Fluid should be withheld because the CVP is high (myth).
* Fluid should be withheld because there is lung edema on the CXR (myth).
* Fluid should be withheld because the patient has already received a large volume in a short time interval (myth).
* Tachycardia is due to fluid deficit and should prompt fluid(myth).
* I gave fluids to increase the central venous pressure to 12 mm Hg to exclude an underlying hypovolemia (myth).
(Read full article to read details on each).
And now 4 parameters need to be written for IVF bolus order:
Like NS 500 cc over 30 minutes with clinical goal of MAP of 70 mm Hg. Hold if CVP is 15 with assessment every 10 minutes !!
References:
Click to get abstract
1. Give your patient a fast hug (at least) once a day - Critical Care Medicine. 33(6):1225-1229, June 2005. - Vincent, Jean-Louis MD, PhD, FCCM
2. Fluid challenge revisited. Critical Care Medicine. 34(5):1333-1337, May 2006. Vincent, Jean-Louis MD, PhD, FCCM; Weil, Max Harry MD, PhD, ScD (Hon), FCCM
How to write order for IVF bolus !!
What we have learnt from guru and professor Jean-Louis Vincent is that the most important thing in Critical care Medicine is to master the 'basic and simple things'. Few months back he taught us the art of everyday rounding in ICUs with simple mnemonic of "Fast Hug" 1. In this month issue of Critical Care Medicine he precisely explains the art of fluid challenge. First he busted 5 myths about fluid bolus. Enjoy !!
* Fluid should be withheld because the CVP is high (myth).
* Fluid should be withheld because there is lung edema on the CXR (myth).
* Fluid should be withheld because the patient has already received a large volume in a short time interval (myth).
* Tachycardia is due to fluid deficit and should prompt fluid(myth).
* I gave fluids to increase the central venous pressure to 12 mm Hg to exclude an underlying hypovolemia (myth).
(Read full article to read details on each).
And now 4 parameters need to be written for IVF bolus order:
- Type of Fluid.
- Rate of Fluid Administration.
- Goal to be Achieved.
- Safety Limits.
Like NS 500 cc over 30 minutes with clinical goal of MAP of 70 mm Hg. Hold if CVP is 15 with assessment every 10 minutes !!
References:
Click to get abstract
1. Give your patient a fast hug (at least) once a day - Critical Care Medicine. 33(6):1225-1229, June 2005. - Vincent, Jean-Louis MD, PhD, FCCM
2. Fluid challenge revisited. Critical Care Medicine. 34(5):1333-1337, May 2006. Vincent, Jean-Louis MD, PhD, FCCM; Weil, Max Harry MD, PhD, ScD (Hon), FCCM
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