Monday June 12, 2006

While you are carrying 'code beeper' as an intensivist, you heard 'code blue in cafeteria'. On arrival you found 36 year old female who was in cafeteria after visiting allergy clinic, where according to daughter she received her 'expensive asthma shot'. While you were resuscitating patient from what appears to be anaphylactic shock, you keep wandering about that 'expensive asthma shot'.


Xolair: Omalizumab (xolair) is the subcutaneous injection treatment for allergic asthma that works by blocking immunoglobulin E (IgE). Anaphylaxis is rare but the tricky part is it may cause anaphylaxis even after months of successful and uneventful treatment. There is an indication in atleast one case report that polysorbate present in omalizumab may be responsible for it 1.

Per month cost of treatment is about 500 - 2000 US $.


Reference: Click to get article

1. Late-Onset Anaphylaxis to Omalizumab Reported - from acep.org site

IV to PO conversion

Sunday June 11, 2006
IV to PO conversion - check med list everyday !!


58 year old male admitted with atrial fibrillation with RVR (rapid ventricular rate) and required intravenous (IV) Diltiazem (cardizem). Now patient is stable at 7 mg/hr dose. What would be the equivalent PO dose?


Diltiazem CD 240 mg po qd 1.

Usual IV to PO Cardizem is as follows:

3 mg/h = Diltiazem CD 120 mg po qd
5 mg/h = Diltiazem CD 180 mg po qd
7 mg/h = Diltiazem CD 240 mg po qd
11 mg/h = Diltiazem CD 300 mg po qd
15 mg/h = Diltiazem CD 360 mg po qd


Using this question as an excuse, the objective is to highlight the point that many times PO medications are as effective as IV (See reference # 1). Good intensivist always remain in the quest to simplify the medication list. It always help to have a savy critical care pharmacist in the team !.


Related: Sample INTRAVENOUS TO ORAL/ENTERAL (IV TO PO) MEDICATION SWITCH PROGRAM from American Society of Health-System Pharmacists' site


Reference: click to get abstract/article
1. Intravenous to Oral Conversion Table: source nih.gov

Feeding in ventilated patients

Saturday June 10, 2006
Yes ! Feed Critically Ill Mechanically Ventilated Medical Patients early despite risk of VAP


There is some hesitancy in literature about early feeding for critically ill mechanically ventilated medical patients due to increase risk of ventilator-associated pneumonia (VAP) 1.

Dr. Artinian and coll. from Division of Pulmonary and Critical Care Medicine, Henry Ford Health System, Detroit, MI recently looked into about 4000 patients requiring mechanical ventilation for more than 2 days 2. Those patients who received enteral feeding within 48 hours of mechanical ventilation were labeled as the "early feeding group" otherwise as "late feeding group." Results showed that

• The overall ICU mortality was 18.1% vs 21.4%
• The overall hospital mortality was 28.7% vs 33.5%

In substudy, three separate models were done using APACHE II, simplified acute physiology score II, and mortality prediction model at time 0. In all models, early enteral feeding was associated with

• an approximately 20% decrease in ICU mortality
• a 25% decrease in hospital mortality
• The lower mortality rates in the early feeding group were most evident in the sickest group

The truth was found that in all adjusted analysis, early feeding was found to be independently associated with an increased risk of ventilator-associated pneumonia (VAP).

Study concluded that early feeding significantly reduces ICU and hospital mortality mainly in the sickest patients and should be instituted in medical patients receiving mechanical ventilation especially in patients at high risk of death, despite being associated with an increased risk of VAP developing.

Related previous pearls:
Where is my food dude !! and Is post pyloric feeding absolute ?

Reference: click to get abstract/article
1. Early versus late enteral feeding of mechanically ventilated patients: results of a clinical trial - Journal of Parenteral and Enteral Nutrition, Vol 26, Issue 3, 174-181
2. Effects of Early Enteral Feeding on the Outcome of Critically Ill Mechanically Ventilated Medical Patients - Chest. 2006;129:960-967

Friday June 9, 2006


Case: 76 year old female, admitted 3 days ago to your ICU with possible aspiration pneumonia. Review of report from nursing home also mention of increase diarrhea. You decide to add metronidazole (flagyl) and start the workup. Patient responded well to treatments and appears to be back to her baseline. You decide to keep patient overnight before transferring to floor in AM. Patient complaint of epigastric abdominal pain during night and on-call physician added pancreatic enzymes for AM and lipase is noted to be 1254 (was normal on admission). You could not find any apparent reason of acute pancreatitis. As C.diff came back negative you stopped the Flagyl and pancreatitis resolved.


Metronidazole Induced Pancreatitis: Acute pancreatitis is a potentially serious adverse effect of metronidazole. Any patient while on metronidazole develops nausea, vomitting and epigastric pain should be evaluated for acute pancreatitis. Acute pancreatitis may develop upto 5 weeks after metronidzole exposure and drug intake in previous weeks should be evaluated carefully particularly in long term care facility residents. Diagnosis can be confirmed with rechallenge with metronidazole but obviously it should be avoided. The mechanism of metronidazole-induced pancreatitis is not known but unlike many other antibiotics metronidazole penetrates well into pancreatic tissue and explains atleast part of the problem.


Reference: click to get abstract/article
1. Metronidazole Induced Pancreatitis. A Case Report and Review of Literature - JOP. J Pancreas(Online) 2004; 5(6):516-519
2. Metronidazole-associated pancreatitis - The Annals of Pharmacotherapy: Vol. 34, No. 10, pp. 1152-1155
3. Acute pancreatitis caused by metronidazole - Ned Tijdschr Geneeskd. 1996 Jan 6;140(1):37-8.

Thursday June 8, 2006
What if plasma exchange is not available as treatment of TTP


Q: You just diagnosed a patient with thrombotic thrombocytopenic purpura (TTP) but you were informed by the nursing supervisor that plasma exchange with fresh frozen plasma is not available in hospital due to technical reason and it will take time before patient can be transferred to a facility where the said services are available. What would be your alternate plan to bridge that time?


A; High-dose plasma infusion with rate of 25-30 mL/kg per day. When immediate plasma exchange with fresh frozen plasma is not available, simple plasma infusion can be performed until transfer to a higher care facility is available. There is always a substanial risk of fluid overload with such high plasma infusion and you have to weigh risks and benefits of the clinical decision or to watch patient closely while plasma is infusing.


Reference: click to get abstract/article

High-dose plasma infusion versus plasma exchange as early treatment of thrombotic thrombocytopenic purpura/hemolytic-uremic syndrome - Medicine. 82(1):27-38, January 2003.

acetazolamide for metabolic alkalosis

Wednesday June 7, 2006
Dose of acetazolamide (diamox) for metabolic alkalosis


Many times we use acetazolamide for metabolic alkalosis in mechanically ventilated patients when nothing else is making it better. What dose should we use?. Mazur and coll. from Henry Ford Health System, Detroit, MI looked into 40 mechanically ventilated patients with a metabolic alkalosis (arterial pH more/= 7.48 and serum bicarbonate concentration more/= 26 mEq/L) which were resistant to other therapies such as fluid infusion or potassium therapy.

Study found that a single IV 500-mg dose of acetazolamide is as effective as multiple doses of IV 250 mg of acetazolamide.


Reference: click to get abstract/article

Single versus multiple doses of acetazolamide for metabolic alkalosis in critically ill medical patients: A randomized, double-blind trial. Critical Care Medicine. 27(7):1257-1261, July 1999.

Wells Score of DVT

Tuesday June 6, 2006
Wells Score of DVT

Pulmonary embolism from deep venous thrombosis remains a leading killer. Many times intensivists are faced with the question of proceeding or not with further radiological workup. Although Wells score is not the absolute score to rule out DVT and subsequently the risk of PE (some literature argue against its validity), it still remains a strong quick tool while differential diagnosis with other conditions. It has been said that if the score of low-probability is combined with negative d-dimer, the negative predictive value is 99.5% 1. In other words, you can safely hold on further radiological workup.

3 points if objective signs like localized tenderness, asymmetric calf swelling.
1.5 points if Heart Rate more than 100 beats/min
1.5 points if bedridden for more than 3 days or major surgery within 4 weeks
1.5 points if previous 'documented' diagnosis of DVT or PE
1 point if hemoptysis
1 point if active cancer
3 points if high clinical suspicion of PE (on overall clinical and lab. findings).

• 0 - 2 low probability,
• 2-6 moderate probability,
• 3-6 high probability

Remember,

low-probability + negative d-dimer = -ve predictive value of not having DVT is 99.5%

Related previous pearl: What if even thrombolysis fails in massive PE ?


Reference: click to get abstract/article
Excluding Pulmonary Embolism at the Bedside without Diagnostic Imaging: Management of Patients with Suspected Pulmonary Embolism Presenting to the Emergency Department by Using a Simple Clinical Model and D-dimer Philip S. Wells and coll.,Ann Intern Med 2001;135:98-107

Four generations of Quinolones

Monday June 5, 2006
Four generations of Quinolones


The classification of the fluoroquinolones on the basis of generations (imitating from cephalosporins) is not officially standardized, but it is now commonly use to classify them by their spectrum of action.


1st generation - Gram negative coverage but not pseudomonas (example: Nalidixic acid)

2nd generation - Gram negative coverage with pseudomonas and some gram postive coverage including s.aureus but not strep pneumoniae. (example: Ciprofloxacin, Ofloxacin, Norfloxacin)

3rd generation - Gram negative coverage with pseudomonas. More gram postive coverage including penicillin sensitive and resistant s. pneumoniae. (example: Levofloxacin, Sparfloxacin, Gatifloxacin (tequin), Moxifloxacin (avalox)). Avalox has been said to be the most effective in this generation.

4th generation - Same as 3rd generation but with anaerobic coverage (example: Trovafloxacin (Trovan) ).



Read comprehensive review on Quinolones (Source: Am Fam Physician 2002;65:455-64, authors: CATHERINE M. OLIPHANT, PHARM.D., University of Wyoming School of Pharmacy and GARY M. GREEN, M.D., Kaiser Permanente, California)

Quinolones in UTI

Sunday June 4, 2006
Quinolones in UTI


Q; Name atleast one quinolone which should not be used for UTI in ICU ?

A: Moxifloxacin (avelox) - as it doesn't reach sufficient level in the urine. On the flip side, the advantage is that you don't need to adjust dose in renal insufficiency unlike other quinolones if use for other reasons. Similarly, Sparfloxacin (Zagam) and trovafloxacin (Trovan - almost off the market due to severe hepatic side effects) should not be used as these 3rd and 4th generation quinolones are more metabolized through liver.

Urinary tract infection (UTI) is a common and many time an isolated or accidental finding in ICU. Rememeber ! Bactrim (TMP/SMX) is still a first line, cost-effective and preferred antibiotic for uncomplicated UTIs. You should jump to quinolone only if your hospital's antibiogram shows local resistance higher than 20% or if patient is allergic to sulfas. Even in this instance nitrofurantoin is a very valid choice. If you decide to use quinolone - ciprofloxacin, ofloxacin, or norfloxacin is a better choice. Levofloxacin is also commonly prescribed but technically it is not really needed for UTI and just contribute to increase resistance in ICU by overuse.


Previous related pearls:

1. Quinolones and errant glycemic reaction

2. Epidemic of new fluoroquinolone induce strain of C. Diff.

Saturday June 3, 2006


Q; Which one electrolyte you will be worried most in patients on TPN (Total Parenteral Nutrition) ?

A; Phosphate. About 33% of patients on TPN develop hypophosphatemia despite supplemented in solution. Patients who require insulin during TPN, or have a history of alcoholism, chronic weight loss, cancer and on diuretic therapy are at increased risk of hypophosphatemia, which also may manifest as "Refeeding syndrome". Serum phophate level below 1.5 mg/dl ( .5 mmol/L), can manifest symptoms of refeeding syndrome.

Read interesting editorial, Refeeding syndrome, Is underdiagnosed and undertreated, but treatable , from BMJ. ( BMJ 2004;328:908-909 )



References: click to get abstract/article

1. Refeeding syndrome: life-threatening, underdiagnosed, but treatable, QJM, April 1, 2005; 98(4): 318 - 319.

4 Ts of HIT

Friday June 2, 2006
4 Ts of HIT

Continuing our theme of Heparin-Induced Thrombocytopenia (HIT) from yesterday, lets talk today about "4 Ts" of HIT.

Thrombocytopenia - more than 50% fall

Timing of platelet count fall - Days 5 to 10, or less than/= 1 day if heparin exposure within past 30 days

Thrombosis or other sequelae - Proven thrombosis, skin necrosis, or, after heparin bolus, acute systemic reaction

Other cause for thrombocytopenia - None

American Society of Hematology has developed a full HIT score which can be seen by clicking here. 1

References: click to get abstract/article

1. When Heparins Promote Thrombosis - Review of Heparin-Induced Thrombocytopenia - Circulation. 2005;111:2671-2683

Thursday June 1, 2006
Argatroban Therapy in Hepatic Dysfunction


Argatroban is a second line anti-coagulation as well as remained one of the drug of choice in patients affected with Heparin-induced thrombocytopenia (HIT). Argatroban improve outcomes in patients with HIT, by reducing new thrombosis 1 . Also reported its safety with no increase risk of bleeding 2 .

Argatroban is primarily metabolized in the liver and its dosing need to be adjusted in hepatic dysfunction. Dr. Levine and coll. from Texas has reported in this month of chest after retrospectively analysing data of 82 argatroban patients and 34 historical control therapy patients with hepatic impairments (all HIT patients) 5. Their results concluded following points:

1. In hepatic impairment 0.5 µg/kg/min is a reasonable, conservative initial dosage of argatroban.

2. serum bilirubin level appears to be a better indicator than ALT or AST of argatroban dosing requirements and argatroban should be initiated at a dose of 0.5 µg/kg/min if a patient’s serum total bilirubin level is 1.5 mg/dL.

3. Conservatic dose should be the starting point if combined hepatic/renal dysfunction is present.

4. As steady-state anticoagulation will be delayed in many patients with hepatic dysfunction, check the aPTT atleast 4 to 5 h after drug initiation or dose change.

5. Argatroban should be stopped for a more extended period in hepatic dysfuntion if an invasive procedure is planned.


Related: Sample Argatroban Protocol For HIT (from The George Washington University Hospital )


References: click to get abstract/article

1. Argatroban Anticoagulation in Patients With Heparin-Induced Thrombocytopenia - Arch Intern Med. 2003;163:1849-1856
2. Argatroban Anticoagulant Therapy in Patients With Heparin-Induced Thrombocytopenia - Circulation. 2001;103:1838
3. The Pharmacokinetics and Pharmacodynamics of Argatroban: Effects of Age, Gender, and Hepatic or Renal Dysfunction - Pharmacotherapy 2000;20,318-329
4. Argatroban Dosing in Patients with Heparin-Induced Thrombocytopenia The Annals of Pharmacotherapy: Vol. 37, No. 7, pp. 970-975.
5. Argatroban Therapy in Heparin-Induced Thrombocytopenia With Hepatic Dysfunction Chest. 2006;129:1167-1175

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.

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)

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).

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

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

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

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.

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)

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

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 -

• 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

1. ACUTE RENAL FAILURE
2. ALTERED CONSCIOUSNESS
3. ARRHYTHMIA
4. BASIC CLINICAL EXAMINATION
5. CLINICAL IMAGING
6. COPD and ASTHMA
7. HOMEOSTASTIS
8. MAJOR INTOXICATION
9. NUTRITION
10. PYREXIA
11. QUALITY ASSURANCE AND COST EFFECTIVENESS
12. 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.

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.

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

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

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:

• 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

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

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

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

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

vasopressin/norepinephrine ratio

Friday May 12, 2006
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: Vasopressin .07 units/min ?

Reference: (click to get abstract)
Low plasma vasopressin/norepinephrine ratio predicts septic shock. Am J Emerg Med. 2005 Oct;23(6):718-24.

Auto-PEEP

Thursday May 11, 2006
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:

Auto-positive end-expiratory pressure: Mechanisms and treatment
M.M. MUGHAL, D.A. CULVER, O.A. MINAI, and A.C. ARROLIGA - CLEVELAND CLINIC JOURNAL OF MEDICINE VOLUME 72 • NUMBER 9 SEPTEMBER 2005

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

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

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

Our failures !!!

Sunday May 07, 2006
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
• Frequent interruption of chest compressions during CPR

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).

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.)

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.

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.

• 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, Pulmonary Embolism just updated 2 days ago at emedicine.com by Craig Feied M.D.

References: Click to get abstract/article
1. Management of Unsuccessful Thrombolysis in Acute Massive Pulmonary Embolism - Chest. 2006;129:1043-1050

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

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:

1. Type of Fluid.
2. Rate of Fluid Administration.
3. Goal to be Achieved.
4. 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

Post fellowship shock syndrome

Sunday April 30, 2006
Post fellowship shock syndrome

Q; What is Post fellowship shock syndrome ?

A; Post fellowship shock syndrome is a kind of culture shock for young graduates when they transit from big tertiary care academic centers to regular community based medical practice. Transit from high tech, literature oriented, academic based and superior nursing quality to business oriented, "thats how we do things here" practice, no house staff support, no billing experience and wide spectrum of nursing quality - caught unprepared young graduates with mental and culture shock and may leave them frustrated with present situation. Its important to prepare graduating residents and fellows for future practice of medicine.

Read related article The Realities of the First Year of Practice ( NEJM CareerCenter )

(Post fellowship shock syndrome is a term invented by editors of this web-site)