Friday, July 21, 2006

Friday July 21, 2006
Prohibiting cell phones in ICUs - Are we over-reacting !

Truely speaking, there have been no studies to determine the harm or benefit of mobile/cell phones in ICUs. Generally, cell phones are prohibited in hospitals, particularly in ICUs and telemetry floors due to concern of EMI* with pacemakers, ventilators, infusion pumps and other electronic units. It became pretty standard with a report published about 12 years ago

* EMI = electromagnetic interference

At the 2003 meeting of the ASA (American Society of Anesthesiologists), 7878 five-questions survey, regarding modes of communication in the ORs/ICUs, were distributed. 4018 responses were received

  • 65% of surveyed reported using pagers as their primary mode of communications,
  • 17.5% of surveyed reported using cell-phones as their primary mode of communications and
  • 17.5% used overhead paging (or did not respond to this question)


  • Among the 2607 respondents using pagers, 1179 (45%) reported experiencing significant delays in communication and 407 indicated that these delays led to medical error or patient injury.
  • 31% of cell-phone users reported delays in communications.
  • Only 2.4% of the respondents indicated that they had ever experienced interference between a cell phone and a medical device.

It has been suggested that through proper policy controls, hospitals can provide a more safe environment taking advantage of this 2-way communication technology, with a reduction in the risk of medical error or injury resulting from delay !!.

It has been recommended that as far as cell phones be kept at least 1 meter away from medical equipment, they seems safe 3.

Similar theme was echoed in an editorial in BMJ about 3 years ago: Mobile phones in hospitals (BMJ 2003;326:460-461 - 1 March)

Related previous pearl:
Noise level in ICUs

References: click to get abstract/article
Mobile telephones interfere with medical electrical equipment - Australas Phys Eng Sci Med.1994 Mar;17(1):23-7.
Communication in Critical Care Environments: Mobile Telephones Improve Patient Care - Anesth Analg 2006;102:535-541
Modern Wireless Telecommunication Technologies and Their Electromagnetic Compatibility with Life-Supporting Equipment - Anesth Analg 2005;101:1393-1400

Thursday July 20, 2006

Q: what is "cryo reduced plasma"?

A; Yesterday we learned that: one unit of cryoprecipitate is derived from one unit of fresh frozen plasma (FFP). Left over FFP, after removal of cryoprecipitate is called supernatant plasma or CRYO-REDUCED PLASMA.

Clinical Significance:
Cryo-reduced plasma is used as a treatment in plasmapheresis for TTP, not responding to regular plasma exchange with FFP. Some physicians even use it as first line for plasmapheresis/Therapeutic Plasma Exchange (TPE) for a patient with Thrombotic Thrombocytopenic Purpura (TTP).

Wednesday, July 19, 2006

Wednesday July 19, 2006

Q: Why we call it cryoprecipitate?

A: The name explains everthing. cryoprecipitate means "cold precipitate". When FFP is thawed slowly at 4 degree C, a white precipitate forms at the bottom of the bag, which can then be separated from the supernatant plasma. This precipitate is rich in fibrinogen, factor VIII, von Willebrand factor, factor XIII, and fibronectin - and call crayoprecipitate. One unit of cryoprecipitate is derived from fresh frozen plasma (FFP) prepared from a unit of whole blood and as it is only a little precipitate at the bottom of the bag, 1 unit of cryoprecipitate comprised only a volume of 10-20 mL.


  • 80-100 units of factor VIII, which consists of both the procoagulant activity and the von Willebrand factor,
  • 150-250 mg of fibrinogen,
  • 50-100 units of factor XIII, and
  • 50-60 mg of fibronectin.

Half life is about one year if stored at -18 degree C. When ordered (generally given as 6 units at a time), cryoprecipitate is thawed back to 37 degree C. Once thawed it must be kept at room temperature and has an expiration time of 4 to 6 hours.

Previous related pearls:
How much FFP? and Some facts about FFP

Monday, July 17, 2006

Tuesday July 18, 2006

Q: How IV (intravenous) DDAVP (desmopressin) should be given?

A: DDAVP, short name of 1-deamino-8-D-arginine vasopressin and also known as desmopressin is use for varity of reasons in ICUs including uremic bleeding diasthesis, some platelet disorders, to boost the plasma level of factor VIII and von Willebrand factor (VWF) and in diabetes insipidus. It may be given as nasal spray or subcutaneous injection but in ICUs mostly get administrated via IV route.

DDAVP should be diluted in 100 ml of normal saline and given by slow intravenous infusion over 30 minutes. The usual dose is 0.3 mcg/kg. Rapid infusion may result in tachycardia, flushing, tremor and abdominal discomfort. Also thrombosis and even myocardial infarction after an infusion of DDAVP has been reported and should be used with caution in patients with signs of arterial disease.
Monday July 17, 2006
Intensivists' compensation

We looked into recent surveys' from different sources and found the following:

* All compensations in US dollar annually
* K = 1000

Average base salary compensation for intensivist has been ranged from annual 195K (new graduate) to 240K (3/5 years experienced). Highly experienced intensivist (15-20 years) should have compensation around 255K - 263K annual.

Latest market: all these surveys were published atleast a year ago and in last 12 months advertisements for intensivists' opportunities continue to show rising trend of salaries even upto 225-250K for new graduates.

Academic factor: Intensivist at a university setting make less but have better life style due to house staff availability and protected time for research (average 168 K), while critical care staff physicians employed by a non-university-affiliated hospital gets higher compensation (avaerage 240K) but more burn out.

Total clinical time in university setting is around 26-34 weeks per year but in private groups it all depends on local needs with 40-47 weeks (with 4 weeks vacation and one week for CME). Many groups prefer to work in block scheduling (like '7 days on 7 days off' to wear off burn out).

VA factor: VA system intensivits have good benefits and life style (like their university based colleagues) but salary remained low around 130-140K 3. Recently, there are strong indications that salaries would go up.

eICU factor: Recently eICU physicians have been offered higher than average compensation with heavy investments in this sector from major health systems but still very few intensivists have been found to take it as a full time employment.

Subspeciality factor: Overall critical care anesthesiologists and critical care non-trauma surgeons were under-compensated per one survey 1. Out of all PEDIATRIC intensivists found to be in highest demand due to lowest supply.

Geographical: Region wise east coast (particularly north east) has about 5-10% less compensation in all fields as compared to other regions.

Benefits: Benefits and bonuses upto 15% on top of base salary is a norm. In benfits - continuing medical education (CME) allowance range from 1000 - 5000 per year with average of 3000 US annual. 401 K (retirement), ADD, life insurance are usually part of the package but 3 essential benefits should include

  1. Malpractice with tail coverage
  2. Health/dental benefits for self and family
  3. CME

Mal-practice coverage: As a standard, malpractice with tail should be covered. New graduates often fail to ask for tail coverage and later found themselves in hot water with a condition call 'locked by the tail'. If candidate fail to negotiate but in later years want to relocate or leave the group, tail buying costs around 30K to 80K, depending on region. Tail buying is 200% of annual malpractice premiums.

Non-compete clause: Ideally, there should not be any non-compete or restrictive covenant clause as intensivists are unlikely to carry their own patient base but when private group is contracted or busy in one ICU its natural to have restrictive covenant and should be accepted as standard business practice.


Compensation for Physicians in Critical Care - Compensation of Critical Care Professionals 2005 - Society of Critical Care Medicine
The 2005 AMGA (American Medical Group Association) Medical Group Compensation and Financial Survey -
Testimony of Dr. Stephen P. Rosenthal President National Association of VA Physicians and Dentists
4. Intensive care unit physician staffing: Financial modeling of the Leapfrog standard - Critical Care Medicine. Interface of Public Policy and Critical Care Medicine. 34(3) Suppl:S18-S24, March 2006.

Sunday, July 16, 2006

Sunday July 16, 2006
Optimum patients' load for intensivist

ICUs in united stated range anywhere from 6 to 24 beds or may be more. At this point, it is not clear at what point intensivist's efficiency plateau out and effects the overall outcome.

Drs. Saqib Dara, MD and Bekele Afessa, MD from Division of Pulmonary and Critical Care Medicine, Mayo Clinic College of Medicine, Rochester, MN looked into the issue with regression analyses of about 25,00 patients. They divided intensivits' patients load into 4 groups:

  • 1:7.5,
  • 1:9.5,
  • 1:12, and
  • 1:15

They found that the ICU period with one intensivist for 15 beds had a longer adjusted ICU LOS (length of stay). Although the ICU period with an intensivist-to-bed ratio of 1:7.5 had the shortest ICU LOS ratio, the difference was not statistically significant compared to the periods with intensivist-to-ICU bed ratios of 1:9.5 or 1:12.

This is the only study of its kind from single institution but it appears that optimum number of patients,
intensivist should carry to produce maximum outcome is around 12 or less.

It is all good work of intensivists' that observed ICU mortality did not differ significantly in any group despite progressive increase of load of work.

Reference: click to get article/abstract
Intensivist-to-Bed Ratio - Association With Outcomes in the Medical ICU - chest. 2005;128:567-572.

Saturday, July 15, 2006

Saturday July 15, 2006

Case: 32 year old male with history of HIV presented to ED with complaint of upper quadrant pain. Initial lab shows elevated LFT and severe acidosis with bicarb of 8 in initial chemistry. You quickly start working through your mnemonic of increased anion gap acidosis - "CAT MUD PILES" !! *. Lactic acid level reported 9.4 mg/dl. CT scan of abdomen done to rule out ischemic colitis but showed only hepatic steatosis. Patient clinically does not appears toxic or septic though you started him on IV fluid and prophylactic antibiotics. Pt. is ruled out for DKA and other causes of acidosis also. What is the probable source of his severe lactic acidosis ?

Answer: Cause is patient's HIV medicines (HAART - Highly Active Anti-Retroviral Therapy), mostly likely the nucleoside reverse-transcriptase inhibitors (NRTIs), - stavudine. NRTIs can cause hyperlactatemia by disrupting the function of the mitochondria. This is known as mitochondrial toxicity. NRTIs also cause fatty liver (hepatic steatosis), may be acute liver failure, and inefficient liver cannot metabolize lactic acid quickly resulting in severe hyperlactatemia.

This week The New England Journal of Medicine has posted a free article
Intensive Care of Patients with HIV Infection (N Engl J Med 2006; 355:173-181, Jul 13, 2006).

* The mnemonic "CAT MUD PILES" is a easy way to remember the differential for an increased anion gap acidosis

Carbon monoxide, Cyanide,

Alcoholic ketoacidosis,

Diabetic ketoacidosis,

Paraldehyde, Phenformin,
Iron, Isoniazid,
Lactic acidosis,
Ethylene glycol,

Friday, July 14, 2006


Friday July 14, 2006
If SC central line ends up in IJ vein ?

It is always a possibility that central venous catheter placed in subclavian (SC) vein may take path upward and travel in internal jugular (IJ) vein. Incidence is about 5.4% and does not vary with side of insertion or with the head position during the procedure

First 2 preventive measures,

1) One study clearly showed that if you direct 'tip of J-wire' caudally, the relative risk for cannulating the ipsilateral internal jugular vein is low 2.


2) After cannulating subclavian vein, apply little pressure at ipsilateral IJ vein while passing wire. If wire stop threading or resistance felt, it means you need to pull back wire for few centimeters (making sure you don't loose vein cannulation) and thread again.

Alternatively, after you place subclavian catheter, before applying sutures there are 2 ways to make sure you are not in IJ vein.

1) Hook central line to central venous pressure (CVP) measurement. Apply firm pressure over the ipsilateral IJ vein in the supraclavicular region for approximately 10 seconds. Quick change in transducer pressure and waveform, like CVP increased by 5 mm Hg (fictitious rise in CVP) or flattening of waveforms indicates jugular misplacement of the catheter tip. Its called Internal Jugular Vein Occlusion Test


2) Flush about 3 -5 cc of saline and put your sthethoscope or even finger on ipsilateral IJ vein to hear or feel the bruit/flow.

In case, you don't do above maneuvers while inserting SC central line and CXR shows IJ placement, pull central venous cather back upto 4-5 cm from punture point and try above maneuvers. Another trick you can apply in case you have to pull back catheter and pass over J-wire again - thread J-wire only partially till you are sure you are in vein, pull back catheter completely (preferably use new catheter to avoid risk of infection) , slightly curve the tip of catheter downwards (like S tip PA-catheters) and pass with little twist.

References: Click to get abstract/article

1. Misplacement of subclavian venous Catheters: Importance of head position and choice of puncture site. BJA1990; 64: 632-33
Direction of the J-tip of the guidewire, in Seldinger technique, is a significant factor in misplacement of Subclavian vein catheter: A randomized, controlled study - Anesth Analg 2005;100:21-24
Internal Jugular Vein Occlusion Test For Rapid Detection Of Misplaced Subclavian Vein Catheter - The Internet Journal of Anesthesiology. 2005. Volume 9 Number 1

Thursday, July 13, 2006

Thursday July 13, 2006

Case: 54 year old male with history of alcoholic cirrhosis, brought to ED after fall and found to have intracranial bleed. INR noted to be 1.5. Neurology service wrote for FFP (fresh frozen plasma) and IV Vitamin K. Patient admitted to ICU after neurosurgery decided to go conservative route. At admission patient mental status seems appropriate but 2 hours after admission you have been called as patient noted to have seizures by bedside staff. On arrival you noticed patient having generalized muscular contractions but he respond appropriately to your questions.

Probable etiology is: Hypocalcemia induced by citrate present in FFP.

Citrate is usually used in blood products as anticoagulant. It binds to free calcium to form soluble calcium citrate, thereby lowering the free (ionized) but not the total serum calcium concentration. It is important to check the ionized calcium instead of total serum calcium. The slower infusion rate has shown significantly less reduction in ionized calcium than did the higher infusion rates.

Prophylactic calcium infusion is not recommended with each blood product transfusion unless clinically indicated. Citrate is normally rapidly excreted by the liver and transient hypocalcemia is not necessary to treat. However, when a patient receives more than 1 unit of erythrocytes/blood product every 5 minutes or the capacity of the liver to metabolize citrate effectively is exceeded (like in our patient above with cirrhosis), the associated hypocalcemia can cause depressed ventricular contractility and decreased peripheral vascular resistance, causing arrhythmias, hypotension and neurologic symptoms of tetany.

Remember: In addition to calcium, citrate binds to magnesium, which can result in clinically important hypomagnesemia too.

Wednesday, July 12, 2006

Wednesday July 12, 2006

Case: 47 year old morbidly obese female with baseline history of COPD, successfully extubated post-op and admitted to ICU for overnight observation after gastric bypass surgery. Patient appears more lethargic in late evening and ABG was drawn which showed PH of 7.20, PO2 of 59 and PCO2 of 98 (pt's baseline PCO2 is around 55). You ordered nebulizer treatments and applied full face mask's noninvasive positive pressure ventilation (BiPAP) with setting of 10/5 (IPAP of 10 cm H2O and EPAP of 5 cm H20) and ordered ABG after one hour. Followup ABG is PH of 7.24, PO2 of 72 and PCO2 of 86. Patient is still lethargic.Your next step would be:

A) Increase IPAP with followup ABG in 1-2 hours

B) Change to nasal mask with followup ABG in 1-2 hours

C) Intubate patient

D) Continue present settings with followup ABGin 1-2 hours

Answer: C

Noninvasive positive pressure ventilation (BiPAP) should be use with caution in fresh gastric bypass patients and there should be a low threshold to intubate if situation arise. BiPAP pumps air into the small gastric pouch and can lead to complications like breakdown of suture lines, bowel perforation and gastric distension. Though one small study of 27 patients didn't show either any complication or advantage of BiPAP in the first 24 postoperative hours of severely obese patients with comorbid illnesses who have undergone elective gastric bypass 1 but there are case reports in literature showing potential complication and geniune concern for use of of bi-level positive airway pressure after gastric bypass surgery 2.

Reference: click to get abstract/article
The effect of bi-level positive airway pressure on postoperative pulmonary function following gastric surgery for obesity - Respiratory Medicine Volume 96, Issue 9, September 2002, Pages 672-676
A potential complication of bi-level positive airway pressure after gastric bypass surgery - Obes Surg. 2004 Feb;14(2):282-4.

Tuesday, July 11, 2006

Tuesday July 11, 2006
Paracentesis with seldinger technique / with central venous catheter kit

During paracentesis regular single, double or triple lumen central venous catheter may provide some benefits over angiocath (catheter over needle). Using regular central venous catheter kit's needle, advance till you get ascitic fluid. Now pass J-wire through needle upto appropriate length ------->remove the needle ----> advance your catheter over wire -----> remove the wire ----> if you don't see fluid, slowly pull back the catheter till you get flow. Advantages of this technique:

1) This is relatively safe as paracentesis needle in available kits are usually long and may carry risk of trauma if you keep advancing at non-ascitic area. (In commercial kits, usual length of catheter and needle is about 19 cm/ 7.5 inches).

2) While advancing catheter away from needle, it may get kinked. Catheter getting advanced over wire is unlikely to get kinked.

3) Use catheter from original kit as it may provide advantage of bigger diameter but in large fluid removal you may use tripple lumen catheter and leave it lock like regular central line for 4/5 days to drain required fluid everyday.

4) Multiple ports may allow you to drain in 2/3 bags/bottles simultaneously.

Editors' note: Contributor of this peal is a practicing intensivist but request to hold his and institution's name. We often post bedside tips which are fully anecdotal and individual's idea and may not be evidence based. Use it per your discretion.

Monday, July 10, 2006

Monday July 10, 2006

Q; How much intavenous albumin should be given to patient while removing ascitic fluid via paracentesis?

A; Per 2004 guidelines published in
Hepatology 2004 Mar;39(3):841-56, for management of adult patients with ascites due to cirrhosis by Practice Guidelines Committee, American Association for the Study of Liver Diseases (AASLD),

"Post-paracentesis albumin infusion may not be necessary for a single paracentesis of less than 4 to 5 L. For large-volume paracenteses, an albumin infusion of 8 to 10 g per liter of fluid removed can be considered". (Grade II-2 evidence - Cohort or case-control analytic studies).

Read full guidelines

Sunday, July 09, 2006

Sunday July 9, 2006

“NAVEL" is a mnemonic for position of the structures at the inguinal ligament, from lateral to medial. It is always helpful to stand beside patient before attempting femoral central line and say NAVEL and try to feel femoral artery and visualize femoral vein before putting needle. Again!, at the inguinal ligament, from lateral to medial
  • Femoral Nerve
  • Femoral Artery
  • Femoral Vein
  • Empty space
  • Lymphatics

Saturday, July 08, 2006

Saturday July 8, 2006

Q: 21 year old male presented to ER with chest pain. CXR showed small spontaneous pneumothorax with less than 3 cm from apex to cupola. Saturation is 99% on room-air. Management is ?

A) Observation

B) Observation with oxygen

C) Aspiration of the pneumothorax

D) Aspiration of the pneumothorax with application of Heimlich valve or a water seal device

E) Chest tube to suction

Ans. is B (or A)

Clinically stable patient with small primary pneumothorax with less than 3 cm from apex to cupola, should be observed. There is some evidence available that administration of oxygen may speed up resolution of the pneumothorax (exercise caution in patients with COPD).

Read 2 guidelines for management of spontaneous pneumothorax:

An American College of Chest Physicians Delphi Consensus Statement Chest. 2001;119:590-602
BTS guidelines for the management of spontaneous pneumothorax Thorax 2003;58:ii39

Friday, July 07, 2006

Friday July 7, 2006

Q: Which antibiotic interferes with the measurement of serum creatinine and cause "pseudo-acute renal failure" ?

Ans: Cefoxitin: Cefoxitin effects routine measurement of serum creatinine, resulting in falsely elevated levels of renal function. Cefoxitin is a second generation wide spectrum cephalosporin. Other medications which can interfere includes methyldopa and levodopa.

Thursday, July 06, 2006

Thursday, July 6, 2006

Case: 54 year old essentially healthy female admitted to floor with abdominal pain, and found to have only constipation as all major workup reported negative. Primary care physician wrote for fleet enemas till constipation get resolved. You have been called as patient was found in bed having "seizure like symptoms"(which you later diagnosed as tetany). On arrival, you found monitor showing arrhythmias and systolic BP in 70s. You asked for STAT labs, started IVF bolus and pressor. Lab shows phophate level of 12 mg/dl (3.87 mmol/L), magnesium of 0.8 meq/L (0.4 mmol/L) and calcium of 4.5 meq/L (2.25 mmol/L)and Cr of 2.4 mg/dl (pt. had normal kidney function on admission). Patient recovered as electrolytes were replaced and kidney function recovered with hemodynamic support.

Enema induced hyperphosphatemia

The Fleet enema contains 19 g of monobasic sodium phosphate and 7 g of dibasic sodium phosphate per 118 mL of fluid. If series of enemas given, inorganic phosphate salts can readily get absorbed from the gastrointestinal tract and can cause hyperphosphatemia even in patients with normal kidneys. Severe hyperphosphatemia results in acute hypocalcemia and hypomagnesemia. Tetany, seizures, bradycardia prolonged QT interval, dysrhythmias, coma, and cardiac arrest are the possible consequences. Treatment is supportive and replacement of electrolytes. Dialysis may be needed if other measures fail.

Wednesday, July 05, 2006

Wednesday, July 5, 2006
SPECT as a 'gold standard' to determine Brain Death ?

Angiography has been considered the gold standard for diagnosis of Brain Death for decades. With arrival of new technologies, we try to move more and more towards non-invasive procedures.

Dr. Munari from Italy looked into 20 clinically brain dead patients. ( 99mTc-HMPAO) SPECT and four-vessel angiography were performed in the same session, with no time delay in between. Then, the results of SPECT and angiography were interpreted separately by a specialist in nuclear medicine and a neuroradiologist, respectively; both of them were blind to the results of the other investigation. Both angiography and SPECT confirmed BD in 19 of 20 patients: angiography showed the absence of filling of intracranial arteries, while SPECT showed a picture of empty skull. For one patient, angiography showed slight and late filling of vessels while SPECT showed faint traces of uptake.For this patient, the tests were repeated 48 hrs later, and both showed the arrest of intracranial circulation, thus confirming brain death.

SPECT = Single Photon Emission Computed Tomography

It was concluded by the authors that: SPECT is a good candidate for the gold standard of diagnosis as:

  • It is noninvasive and, therefore, free from complications and can be repeated for patients who are not brain dead with no harm;
  • It shows a clear-cut picture of empty skull, an image that can be easily understood by physicians and even by patient's relatives;
  • It fully fits the definition of whole Brain death, showing the absence of whole brain perfusion, down to the foramen magnum.

See interesting Power point presentation on

Brain Death: The Neurologist's Perspective from Stephen T. Mernoff, MD, Clinical Assistant Professor of Neurology, Brown Medical School. Also see our neurology section for various related topics as
Brain death determination (Source MGH stroke service)
Pre-Apnea test checklist (sample from
Post-Apnea test checklist (sample from

References: click to get abstract/article

1. Confirmatory tests in the diagnosis of brain death: Comparison between SPECT and contrast angiography - Critical Care Medicine. 33(9):2068-2073, September 2005

Tuesday, July 04, 2006

Happy Birthday America
How many attempts to intubate?

Its hard to give up procedure if you are failing it !!. For intubation, ASA (American Society of Anesthesiologists) recommends to limit laryngoscopic attempts to three. Dr. Thomas C. Mort from Hartford Hospital, CT entered 2833 Critically-ill patients, suffering from cardiovascular, pulmonary, metabolic, neurologic, or trauma-related deterioration into an emergency intubation quality improvement database. Data confirmed that the number of laryngoscopic attempts were directly proportional with the incidence of airway and hemodynamic adverse events (more than 2 attempts).

  • incidence of hypoxemia went from 11.8% to 70%,
  • incidence of regurgitation of gastric contents went from 1.9% to 22%,
  • incidence of aspiration of gastric contents went from 0.8% to 13%,
  • incidence of bradycardia went from 1.6% to 21%, and
  • incidence of cardiac arrest went from 0.7% to 11%

Call for help !! and remember, to limit intubation attempts to 3, unless untill you are trained to deal with 'difficult intubations'.

References: click to get abstract/article

Emergency tracheal intubation: complications associated with repeated laryngoscopic attempts - Anesth Analg 2004;99:607-613

Monday, July 03, 2006

Monday July 3, 2006
Simplify D-dimer

D-dimer has great negative predictive value in excluding pulmonary embolism (PE) or deep vein thrombosis (DVT). So far we had to send blood for laboratory-based quantitative D-dimer.

Simplify D-dimer is a new version of test which can be performed at bedside quickly and can provide instant clue
1. Check
here to see details on test, that can be performed with a drop of blood at bedside.

Recently in chest, Dr. Kline and coll. from Department of Emergency Medicine, Carolinas Medical Center, Charlotte, NC reported that the posttest prevalence of PE among low-risk patients with negative d-dimer results by simplify D-dimer Assay was only 0.7% 2, supplementing the previous famous study on d-dimer by Dr. Wells 3.

Related previous pearls:
Wells Score of DVT ,
What if even thrombolysis fails in massive PE ?

References: click to get abstract/article

1. A new rapid bedside assay for D-dimer measurement (Simplify D-dimer) in the diagnostic work-up for deep vein thrombosis - J Thromb Haemost. 2003 Dec;1(12):2681-3.

Prospective Study of the Diagnostic Accuracy of the Simplify D-dimer Assay for Pulmonary Embolism in Emergency Department Patients Chest. 2006;129:1417-1423.)

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 - 17 July 2001 Volume 135 Issue 2 Pages 98-107, Annals

Sunday, July 02, 2006


Sunday July 2, 2006
So what is the cut off of BNP ?

When the landmark article on BNP published in The New England Journal of Medicine in July 2002 1, the cutoff point in establishing or excluding the diagnosis of congestive heart failure in patients with acute dyspnea was given at 100 pg per milliliter. But over time we learned that this level probably carries more negative predictive value and there may be a huge gray zone before a definite high BNP value, atleast in critical care setting. This month in Critical Care Medicine 2, Dr. Rana and coll. from Mayo Clinic College of Medicine, Rochester, MN looked into this gray zone. Their conclusion:

"When measured early after the onset of acute pulmonary edema, a BNP level of less than 250 pg/mL supports the diagnosis of acute lung injury. The high rate of cardiac and renal dysfunction in critically ill patients limits the discriminative role of BNP. No level of BNP could completely exclude cardiac dysfunction".

The median time from the onset of pulmonary edema to BNP testing was 3 hrs.

Other interesting findings in the study:

* The predictive value of BNP in the differentiation between ALI and cardiogenic pulmonary edema was comparable with PAOP (when measured) and superior to troponin and echocardiographic determination of ejection fraction. (Not supported by other studies - see related peal below).

*The accuracy of BNP improved if pts with renal failure were excluded.

* BNP levels of more than 950 pg/dL suggest congestive heart failure and BNP levels of less than 250 suggest ALI, the values in between have no diagnostic value.

Related previous pearls:

References: click to get abstract/article
Rapid Measurement of B-Type Natriuretic Peptide in the Emergency Diagnosis of Heart Failure - July 18, 2002,N Engl J Med 2002; 347:161-167, Jul 18, 2002
B-type natriuretic peptide in the assessment of acute lung injury and cardiogenic pulmonary edema - Critical Care Medicine. 34(7):1941-1946, July 2006.

Saturday, July 01, 2006

Elevation of the head of the bed- 30 or 45 degrees ?

Answer is probably 45 degrees.Elevation of the head of the bed is a must thing in ICU, unless some contra-indication. It is an essential part of VAP (ventilator associated pneumonia) bundle. But there is some debate about the extent of elevation need to be done. Accepted level is atleast 30 degrees but many guidelines wrote for 45 degrees. IHI recommends elevation anywhere from 30 to 45 degrees 3.

Study from The Netherlands 1 compared 109 patients in the supine group to 112 in the semirecumbent group. Target for semirecumbent group was 45 degrees but the targeted backrest elevation of 45° for semirecumbent positioning was not reached, so supine position (10°) was compared with achieved semirecumbent positioning (28°). Elevation of head of bed to 28° did not prevent the development of VAP.

7 years back Drakulovic and coll. published their landmark study in lancet showing 83% decrease of bacteriologically confirmed VAP in a group of patients treated in a semirecumbent position of 45° 2.

So the answer is probably 45 degrees or to be diplomatically right - atleast more than 30 degrees.

But is it easy to do and keep head of bed elevated to 45 degrees in practical world ?. The study group found that despite the presence of dedicated research nurses to control and maintain patient positioning, the semirecumbent treatment position with an aimed backrest elevation of 45° is not feasible for mechanically ventilated patients.

Another interesting question raised in discussion of first study: Is semirecumbent positioning itself a risk for VAP ? !!!, as pooling of colonized oropharyngeal fluids above the inflated cuff of the endotracheal tube is common in mechanically ventilated patients and it is possible that the semirecumbent position (and all movements to keep it) stimulates leakage of oropharyngeal fluid by means of gravity. Whether ETT with continuous aspiration of subglottic secretions (CASS) will be more effective than semirecumbent positioning?

References: Click to get article/abstract
1. Feasibility and effects of the semirecumbent position to prevent ventilator-associated pneumonia: A randomized study - Critical Care Medicine. 34(2):396-402, February 2006.
2. Supine body position as a risk factor for nosocomial pneumonia in mechanically ventilated patients: a randomised trial - Lancet.1999 Nov 27;354(9193):1851-8.
3. Elevation of the Head of the Bed - Institute for Healthcare Improvement