Monday, January 30, 2006


Tuesday January 31, 2006
IPV - adjuvant therapy in COPD exacerbations ?

Interesting study of 33 patients, published from france last year on acute exacerbation of COPD. Inclusion and exclusion criteria were established (see reference # 1). Patients were randomly assigned to receive either standard treatment (control group) or standard treatment plus Intrapulmonary percussive ventilation (IPV group). The IPV group underwent two daily sessions of 30 minutes performed by a chest physiotherapist through a full face mask. Thirty minutes of IPV led to a significant decrease in respiratory rate, an increase in PaO2 and a decrease in PaCO2. Exacerbation worsened in 6 out of 17 patients in the control group versus 0 out of 16 in the IPV group. Therapy was tagged successful when both worsening of the exacerbation and a decrease in pH to under 7.35, which would have required non-invasive ventilation, were avoided. Also, the hospital stay was significantly shorter in the IPV group.

IPV is essentially a very effective technique to assist patients to clear retained endobronchial secretions and the resolution of diffuse patchy atelectasis. Please see full manual of IPV therapy from Dr. Bird's website here.

References / suggested readings: Click to get article/abstract
Intrapulmonary percussive ventilation in acute exacerbations of COPD patients with mild respiratory acidosis: a randomized controlled trial - Crit Care. 2005; 9(4): R382–R389
Effect of Intrapulmonary Percussive Ventilation on Mucus Clearance. in Duchenne Muscular Dystrophy Patients: A Preliminary Report - Respir Care 2003;48(10):940–947
A Comparison of Intrapulmonary Percussive Ventilation and Conventional Chest Physiotherapy for the Treatment of Atelectasis in the Pediatric Patient - Respir Care 2002:47(10):1162-1167
Airway Clearance in the ICU - - The Journal of Respiratory Care Practitioners, March 2005

Sunday, January 29, 2006


Monday January 30, 2006
Should we abandon Aprotinin ?

The majority of patients undergoing cardiovascular surgery routinely receive antifibrinolytic therapy - aminocaproic acid, tranexamic acid or aprotinin during and after procedure to control bleeding. Very important and large study of 4374 patients published this week in New England Journal of Medicine from Ischemia Research and Education Foundation, comparing these three agents in cardiac surgery. Study found that the use of aprotinin was associated with a dose-dependent doubling to tripling in the risk of renal failure requiring dialysis among patients undergoing primary or complex coronary-artery surgery. Probable reason of this difference is aprotinin's high affinity for the kidneys. Also, for the majority of patients undergoing primary surgery, evidence of multiorgan damage involving the heart (myocardial infarction or heart failure) and the brain (encephalopathy) in addition to the kidneys found, suggesting a generalized pattern of ischemic injury. It has been suggested in article that the replacement of aprotinin with aminocaproic acid would prevent renal failure requiring dialysis in 11,050 patients per year globally, yielding an savings of more than $1 billion per year. Also to note, Aprotinin is way more expensive than other 2 agents.

Bonus Pearl:
Action of captopril may get block with concurrent use of Aprotinin.

References / suggested readings: Click to get article/abstract
The Risk Associated with Aprotinin in Cardiac Surgery - NEJM Jan. 26, 2006 Volume 354:353-365
Is Aminocaproic Acid as Effective as Aprotinin in Reducing Bleeding With Cardiac Surgery? - Circulation. 1999;99:81-89
Hemostatic effects of aprotinin, tranexamic acid and aminocaproic acid in primary cardiac surgery - Ann Thorac Surg 1999;68:2252-2256
Tranexamic acid compared with high-dose aprotinin in primary elective heart operations: Effects on perioperative bleeding and allogeneic transfusions - J Thorac Cardiovasc Surg 2000;120:520-527
A Study of a Weight-Adjusted Aprotinin Dosing Schedule During Cardiac Surgery - Anesth Analg 2002;94:283-289

Saturday, January 28, 2006


Sunday January 29, 2006
What is Lazarus Syndrome

Lazarus Syndrome is a generic term use in hospitals when patient shows sign of life after clinically declared dead, like a patient that develops vital signs after cessation of resusitative efforts or organ-donation team arrives to find a live person. The syndome is named after bible story in which Jesus brought back to life a dead person named Lazarus from his tomb. Term became very popular after publication of book "The Lazarus syndrome: Burial alive and other horrors of the undead" (Rodney Davies - 1978). In recent years, 'Lazarus Syndrome' has also been use for HIV/AIDS patients who feel having new chance of living with new HIV medications.

Xenical and Coumadin

Saturday January 28, 2006
Xenical and Coumadin

Last week FDA advisory panel voted to recommend that the regulatory agency approve the nonprescription form of weight reducing agent, Xenical (orlistat), which Glaxo would market as Alli. It may be of importance to know its possible effect with warfarin (coumadin), cyclosporin and amiodarone. Orlistat is a reversible inhibitor of lipases. It forms a covalent bond with gastric and pancreatic lipases. The inactivated enzymes are thus unavailable to hydrolyze dietary fat in the form of triglycerides into absorbable free fatty acids and monoglycerides. As a side effect deficiency of fat-soluble vitamins like Vitamin A, D, E and K may occur. Recommendation is to take a multi-vitamin two hours before Xenical. Patients on coumadin (warfarin) may have potential of bleed due to increase INR (as absorption of Vitamin K is decrease). We cannot find any mention in literature describing any such real case but frequent INR check is recommended for safety. Also to remember, Xenical can decrease the amount of cyclosporine and 25-30% reduction in systemic exposure to Amiodarone. Also, there may be some concern of electrolyte imbalance with associated diarrhea. But again, we didn't find any evidence-base literature against Xenical in our search but as xenical expects to do well as over-the-counter medicine, intensivists should be ready for any potential adverse arrival in hospital.

References: Click to see abstract/article

Mechanism of Action - Orlistat -
Important Patient Information Patient Information about XENICAL -

Friday, January 27, 2006

Friday January 27, 2006
Amiodarone Neurotoxicity !!

Amiodarone neurotoxicity has been reported in up to 40% and may easily get miss or misdiagnose when an elderly patient presents with multiple symptoms. Major manifestation are peripheral neuropathy causing proximal motor weakness, ataxia and fine resting tremor. It may also present as neuromyopathy. A case has been described with autonomic dysfunction presented as incapacitating orthostatic hypotension. Cases has been reported with Amiodarone-Induced Delirium . Most neurotoxicities are dose related and resolved with discontinuation of Amiodarone. Being an intensivist it may be important to keep this very common dose related toxicity in mind while evaluating patient with neurologic symptoms.

Related: our pearl on Amiodarone pulmonary toxicity.

References: Click to see abstract/article
1. Amiodarone-Induced Neuromyopathy: Three Cases and a Review of the Literature - Journal of Clinical Neuromuscular Disease. 3(3):97-105, March 2002.
Severe Ataxia Caused by Amiodarone - Volume 96, Issue 10, Pages 1463-1464 (15 November 2005) - Am J of Card
Amiodarone toxicity presenting as pulmonary mass and peripheral neuropathy: the continuing diagnostic challenge - Postgraduate Medical Journal 2006;82:73-75
Amiodarone: Guidelines for Use and Monitoring - - Vol 68, No. 11, Dec., 2003
Atypical pulmonary and neurologic complications of amiodarone in the same patient. Report of a case and review of the literature - Vol. 147 No. 10, October 1, 1987 - Archive of Int Med.
Amiodarone-Induced Delirium - Am J Psychiatry 156:1119, July 1999

Thursday, January 26, 2006

Thursday January 26, 2006
Pearls of Hand Hygiene - Yaap !! - So Basic !! .

Following are the national standard guideline for Hand Hygiene from Healthcare Infection Control Practices Advisory Committee. Are we doing it right way?.

1. Wet hands first with water, apply an amount of product as recommended by the manufacturer, and rub hands together vigorously for at least 15 seconds, covering all surfaces of the hands and fingers.

2. Rinse hands with water and dry thoroughly with a disposable towel.

3. Use towel to turn off the faucet.

4. Avoid using hot water (may increase the risk of dermatitis).

5. If bar soap is used, soap racks that facilitate drainage and small bars of soap should be used .

6. Multiple-use cloth towels of the hanging or roll type are not recommended for use in health-care settings.

7. The cost of hand-hygiene products should not be the primary factor influencing product selection.

8. Do not add soap to a partially empty soap dispenser. This practice of "topping off" dispensers can lead to bacterial contamination of soap.

9. Do not wear artificial fingernails or extenders when having direct contact with patients at high risk (e.g., those in ICUs or ORs).

10. Keep natural nails tips less than 1/4-inch long.

11. Wash hands with soap and water if exposure to spores like Bacillus anthracis or C.diff. is suspected. The physical action of washing and rinsing hands under such circumstances is recommended because alcohols, chlorhexidine, iodophors, and other antiseptic agents have poor activity against spores.

12. If hands are not visibly soiled, an alcohol-based hand rub may be use for routinely decontaminating hands.

13. Decontaminate hands also before inserting indwelling urinary catheters.

(Wearing rings is an unresolved issue but studies have shown increase bacterial growth beneath rings but no evidence yet on increase transmission).

Read full Guideline for Hand Hygiene in Health-Care Settings .

Tuesday, January 24, 2006

Wednesday January 25, 2006
Statins – Adjuvant Therapy for Sepsis

Statins are powerful hypolipemic drugs with pleiotropic effects and have been shown to improve survival in the primary and secondary prevention of atherosclerosis in numerous large randomized clinical trials. Interestingly, in many of these trials, their beneficial clinical impact included noncoronary events. Several cellular and animal models demonstrate the pleiotropic activity of statins, including anti-inflammatory and anti-oxidative properties, immunomodulatory effects, improvement in endothelial function, reduction in blood thrombogenicity, and increased nitric oxide (NO) bioavailability. Some or all of these effects may account for a substantial potential impact of statins on the complex pro- and anti-inflammatory sequence of events occurring during sepsis. A few clinical studies have been published recently in support of this hypothesis.

Almog et al. conducted a prospective observational cohort study to determine the impact of statin pretreatment on the occurrence of severe sepsis in infected patients. Of 361 patients with confirmed acute bacterial infection, 82 (23%) had been receiving statins for at least 4 weeks prior to their admission. The crude mortality rate was low and did not differ significantly between the two groups (3.7% vs. 8.6%, P=0.21), but severe sepsis developed in 2.4% and 19% of patients, respectively, in the statin and no-statin group (risk ratio 0.13; 95% CI, 0.03–0.52), and the ICU admission rate was 12.2% for the no-statin group compared with only 3.7% of the statin group (P=0.025).

In another retrospective review of 388 patients with bacteremia, Liappis et al reported a significant reduction in both overall (6% vs. 28%, P=0.002) and attributable (3% vs. 20%, P=0.010) mortality among patients taking statins at the time of admission compared with patients not taking statins. The survival benefit persisted after adjustment for prognostic factors in a multivariate analysis (odds ratio 7.6; 95% CI, 1.01–57.5).

The available evidence today suggests that the potential for statins as adjuvant therapy for sepsis should be further tested. Given their pleiotropic effects related to many pathophysiologic determinants of sepsis, statin therapy could well be the next step in the search for adjuvant therapy.

References: click to get article/abstract
1. Almog Y, Shefer A, Novack V, Maimon N, Barski L, Eizinger M, Friger M, Zeller L, Danon A (2004)
Prior statin therapy is associated with a decreased rate of severe sepsis. Circulation 110:880–885
2. Liappis AP, Kan VL, Rochester CG, Simon GL (2001)
The effect of statins on mortality in patients with bacteremia. Clin Infect Dis 33:1352–1357 -

Monday, January 23, 2006

Tuesday January 24, 2006

Conventional mechanical ventilation is provided at a rate < 2 Hz (1 Hz = 60 breaths/min). With high frequency ventilation (HFV), rates are provided at 2 – 15 Hz. The frequency range is determined by the specific technique and the size of the patient. Regardless of the technique, adults are generally ventilated at the low end of the rate spectrum and neonates at the high end of the spectrum. There are three techniques that have been classified as high frequency ventilation:

High frequency positive pressure ventilation (HFPPV)
High frequency Oscillation (HFO)
High frequency jet ventilation (HFJV)

conventional ventilators are used to provide rates at the low end of the HFV spectrum.

HFO has both an active inspiratory and expiratory phase. Oscillators establish gas flow by the movement of a diaphragm or piston, perpendicular to a bias flow that moves across the airway. With HFO, rates across the whole frequency spectrum are possible but in general 10 to 15 Hz range are most common with neonates and 3 to 8 Hz range are used with adults. The two conceptual advantages to HFO are lower peak airway pressures and the fact that non bulk-flow mechanisms may improve V/Q matching. Inadequate humidification is a well-known complication when using high gas flows and delivered minute volumes and may result in necrotizing tracheobronchitis. HFO may also cause direct physical airway damage.

During HFJV, gas under high pressure is injected into the airway with a secondary gas source entrained to provide tidal volume. With the HFJV, both a jet ventilator and conventional ventilator may be needed to establish gas delivery in the low to middle part of the HFV rate spectrum. This form of ventilation is mostly used in the operating room where a surgeon is working in the airway (laser Rx of papilloma on vocal cords) and an ETT cannot be placed or as an emergency airway. It is also used in the treatment of a disrupted airway or massive bronchopleural fistula as the non-bulk flow of gas decreases the amount of gas escaping out of the fistula. HFJV has been approved by the FDA for ventilating patients in whom a large and persistent bronchopleural fistula has developed.

See nice Review article
HIGH FREQUENCY OSCILLATORY VENTILATION: Clinical Management from VIASYS. (more details/tools at site). has no connection with VIASYS and info here is solely for educational purpose.

References: Click to get abstract/article
1. Schuster, DP, Klain, M, Snyder, JV.
Comparison of high frequency jet ventilation to conventional ventilation during severe acute respiratory failure in humans. Crit Care Med 1982 Oct;10(10):625-30.
2. Holzapfel, L, Robert, D, Perrin, F, et al.
Comparison of high-frequency jet ventilation to conventional ventilation in adults with respiratory distress syndrome. Intensive Care Med 1987; 13:100.
3. Fort, PF, Farmer, C, Westerman, J, et al.
High-frequency oscillatory ventilation for adult respiratory distress syndrome. Crit Care Med 1997; 25:937.
4. Mehta, S, Granton, J, MacDonald, RJ, et al.
High-frequency oscillatory ventilation in adults: the Toronto experience. Chest 2004; 126:518.

Sunday, January 22, 2006

Monnday January 23, 2006
Suture at central venous catheter site - a risk?

Interesting article published in Managing Infection Control, december 2002 issue by Dr. Bierman
1 suggesting that sutures at central venous catheter site may also play part in CRBSI's (catheter related bloodstream infection). One study from Hospital of the University of Pennsylvania randomized 170 patients requiring PICCs, to suture (n = 85) or Sutureless Securement Device (n = 85). 3

Beside other advantages, a significant difference noted in the number of systemic infections (10 suture vs. 2 Sutureless Securement Device group; P = .0032). And, the difference in confirmed CRBSIs was (8 suture vs 1 Sutureless Securement Device; P = .04).

August 2002 Guidelines for Prevention of Intravascular Catheter-Related Infections from CDC (Center for Disease Control) acknowledged that “suture-free securement devices can be advantageous over suture in CRBSIs".

Only commercially available Sutureless Securement Device in USA is
Statlock. ( has no connection with company and name given here is only for information purpose).

References: click to get abstrat/article
1. Suture: An Unlikely Culprit in Infections and Accidental Needlesticks - Managing Infection Control, dec. 2002
Guidelines for the Prevention of Intravascular Catheter-Related Infections (MMWR 2002)
Sutureless Securement Device Reduces Complications of Peripherally Inserted Central Venous Catheters - Journal of Vascular and Interventional Radiology 13:77-81 (2002)
OSHA Fact Sheet: Securing Medical Catheters - from STATLOCK site.
Sunday January 22, 2006
Arterial pressure-based continuous cardiac output (APCO)

In our quest of finding less and less invasive techniques for our patients, it would be interesting to evaluate arterial pressure based continuous cardiac output (APCO). The whole concept is based on measuring cardiac output simply on arterial pulsatility. Advantages are:

1. It does not require any calibration.
2. Connects to an existing peripheral arterial catheter.
3. No injection of dilutional medium required.

here to see video on commercially available device from Edwards Lifesciences.

Some small initial studies have so far shown comparable results with intermittent bolus thermodilution cardiac output (ICO) and continuous thermodilution cardiac output (CCO).
1,2,3 But before accepting this modality as a standard we need a good well controlled clinical trial as we don't know the effect of age, gender, vessel's disease state, vessel's compliance with distending pressure, body positioning etc. 4

References: click to get abstrat/article

1. Continuous Cardiac Output Measured by Arterial Pressure Analysis in Surgical Patients - Anesthesiology 2005; 103: A834
Pressure recording analytical method (PRAM) for measurement of cardiac output during various haemodynamic states - British Journal of Anaesthesia 2005 95(2):159-165
Continuous cardiac output by pulse contour analysis? - British Journal of Anaesthesia, 2001, Vol. 86, No. 4 467-468

Friday, January 20, 2006

Saturday January 21, 2006
Noise level in ICU !!

Unnecessary noise in ICU can mask vital alarms, verbal communications and may be an unseen added cause of mental stress for staff itself. There are 2 kinds of noise in ICU - one you can't control like "ventilator and IV pump alarms" and other you can modify like "conversations and TV".

One interesting and landmark work was done by Kahn and coll. which showed that:

1. "Talking" and "TV" contribute to 49% of noise in ICU.

2. EPA (Enviromental Protection Agency) recommends noise level not to exceed beyond 45 dBA in hospitals but mean peak sound level in study (medical ICU) was 80 dBA !! (which showed mark decrease with behavior modification).

Do you know beepers contribute 1% to ICU noise pollution with 84 dBA - why not to turn it to vibrate mode !!. Click
here to see various measures which can decrease noise pollution in ICU: (

References: click to get abstrat/article

1. Identification and modification of environmental noise in an ICU setting - Chest, Vol 114, 535-540 - full article available as pdf
Contribution of the Intensive Care Unit Environment to Sleep Disruption in Mechanically Ventilated Patients and Healthy Subjects - American Journal of Respiratory and Critical Care Medicine Vol 167. pp. 708-715, (2003)
Noise in the postanaesthesia care unit - British Journal of Anaesthesia, 2002, Vol. 88, No. 3 369-373
Friday January 20, 2006
Cryptococcosis meningitis !!

5 tips to differential diagnose cryptococcosis meningitis.

1. Neck stiffness is uncommon rather non-specific signs may be present ranging anything from headache to coma including personality change.

2. CT scan or MRI should be performed prior to Lumbar punture (LP) and may present with specific findings of leptomeningeal enhancement and enlarged Virchow-Robin spaces. CT scan and MRI may be normal but if scan shows mass lesion (cryptococcomas), avoid LP and consult a neurosurgeon.

See images
here, Radiological findings in CNS cryptococcus, from Journal of the chinese medical association 2003;66: 19-26

3. High opening pressure on LP (greater than 200 mm H2O) is common and may have trio of low glucose, high protein and more lymphocytes but CSF may be normal !!. The cryptococcal organism is surrounded by a polysaccharide capsule, which may protect it from the host inflammatory response.

4. Make sure to send CSF for india ink.

5. Eye exam is essential to r/o optic neuritis, endophthalmitis or compressive optic neuropathy from high intracranial pressure. Quick treatment can salvage patient vision and emergent opthalmology and neurosurgical consults are indicated. (see healthy discussion at ref. # 3).

References: click to get abstrat/article

1. Overwhelming CNS cryptococcus in AIDS - Neurology 2001 57: 1560
Central Nervous System Cryptococcal Invasion -
Cryptococcal Meningitis Resulting in Irreversible Visual Impairment in AIDS Patients - A Report of Two Cases - SINGAPORE MEDICAL JOURNAL
Cryptococcosis -
CNS Infections Laboratory -

Thursday, January 19, 2006

Thursday January 19, 2006
Angel dust !!

Phencycladine is probably one of the most dangerous available street drug and as with widest variety of symptoms. 7 Pearls regarding Phencyclidine (PCP) toxicity.
1. PCP can also get absorb percutaneously.

2. Patient may exhibit waxing and waning symptoms of PCP due to its reabsorbtion in duodenum.

3. It has 5 properties of sympathomimetic, serotoninergic, cholinergic, anticholinergic, and narcotic effects and so can present with wide variety of symptoms including hypersalivation and bronchorrhea.

4. Nystagmus is a common presentation but hyperthermia or status epilepticus may be a presenting symptom.

5. Muscle rigidity can present as dystonia, opisthotonos or torticollis, and may cause life-threatening rhabdomyalysis.

6. Postive urine screen is usually diagnostic.

7. Dialysis does not help and treatment is supportive.

References: click to get abstrat/article
1. PCP -
PCP (Phencyclidine) - The National Institute on Drug Abuse (NIDA)
Toxicity, Phencyclidine -

Wednesday, January 18, 2006

Wednesday January 18, 2006
"Locked-in" Syndrome (coma vigilante)

"patient is a silent and unresponsive witness to everything that is happening" from story of Nick Chisholm

Patient with Locked-in syndrome is a fully conscious person, but all the voluntary muscles of the body are completely paralyzed, other than those that control eye movement. Term was first introduced about 25 years ago by Plum and Posner with complete occlusion of the basilar artery. 3

Any catastrophy involving ventral pons can cause this syndrome like massive stroke, traumatic head injury, ruptured aneurysm, pontine infarction after prolonged vertebrobasilar ischaemia, haemorrhage, tumor, central pontine myelinolysis, pontine abscess or postinfective polyneuropathy. As all of the nerve tracts responsible for voluntary movement pass through the ventral pons but fortunately or unfortunately, consciousness are above the level of the ventral pons.

Only supportive rehabilitation is the answer.

Being an intensivist, it is extremely important to educate staff and to protect patient from any physical or psychological harm (like procedure without adequate analgesia), with upmost understanding that it is an "imprisoned mind buried alive in a dead body’’ (as said for character with paralysis like locked-in syndrome in
Thérèse Raquin by Emile Zola - 1868).

References: Click to get articles/abstract
1. The patient's journey: Living with locked-in syndrome - BMJ 2005;331:94-97 (9 July)
Locked-in Syndrome -
3. Plum F, Posner JB. The diagnosis of stupor and coma. Philadelphia: FA Davis, 1982; 377
Locked-in syndrome: a catastrophic complication after surgery - British Journal of Anaesthesia, 2004, Vol. 92, No. 2 286-288
Thérèse Raquin

Tuesday, January 17, 2006

Tuesday January 17, 2006
Recovery of Critical illness polyneuropathy (CIP) and prevention with tight insulin therapy

Critical illness polyneuropathy (CIP) remains a major problem in ICU particularly in post-disease phase. Very little literature is available regarding recovery from CIP. A rather small but worth looking study done in france with 2-year clinical follow-up of 19 patients who suffered from CIP. Three parameters were significantly correlated with poor recovery:

1. longer length of stay in the critical care unit,
2. longer duration of sepsis and
3. greater body weight loss.

On prevention side, its worth recalling Dr. Van den Berghe famous 2001 NEJM article re. Intensive Insulin Therapy in Critically Ill Patients which showed intensive insulin therapy also reduced critical-illness polyneuropathy by 44 percent, and 49% in another followup study by same author.

Here is a good review article on CIP with free registration at
Clinical Outcomes of Critical Illness Polyneuropathy - Pharmacotherapy 22(3):373-379, 2002

References: Click to get articles/abstract
1. Critical Illness PolyneuropathyA 2-Year Follow-Up Study in 19 Severe Cases - European Neurology 2000;43:61-69
Intensive Insulin Therapy in Critically Ill Patients NEJM Nov. 2001, Volume 345:1359-1367
Paresis Acquired in the Intensive Care Unit JAMA. 2002;288:2859-2867 (full article available with free registration).
Insulin therapy protects the central and peripheral nervous system of intensive care patients - NEUROLOGY 2005;64:1348-1353

Monday, January 16, 2006

lovenox and protamin

Monday January 16, 2006
LMWH and Antidot (protamine)

If protamine is given within 4 hours of the enoxaparin (Low Molecular Weight Heparins - LMWH), then a neutralizing dose is: 1 mg of protamine per 1 mg of enoxaparin. The IV protamine should be administered slowly atleast over 10 minutes as rapid infusion may cause anaphylactoid type reaction. May repeat half of earlier dose of protamine after 6 hours with postulation that half life of enoxaparin is longer than protamine.

It appears that that the LMWH anti-Xa reversal is not related to protamine-LMWH binding or LMWH size, but rather to the density of sulfate residues in the particular LMWH. Another available variety of LMWH, dalteparin (Fragmin) has higher degree of sulfonation and appear to be more responsive to protamine reversal.

2 clinical pearls

1. Protamine does not help in reversing bleeding from Fondaparinux (Arixtra). Only supportive treatment should be given with mean half-life of fondaparinux of 17-21 hours in mind.

2. Fresh frozen plasma is ineffective in reversal of LMWH to achieve hemostasis and should not be use in these situations.

References: Click to get article/abstract
Accidental overdosage following administration of Lovenox -
2. Incomplete Reversal of Enoxaparin Toxicity by Protamine: Implications of Renal Insufficiency, Obesity, and Low Molecular Weight Heparin Sulfate Content - Obesity Surgery, Volume 14, Number 5, 1 May 2004, pp. 695-698(4)

Sunday, January 15, 2006

Sunday January 15, 2006
“MEL GIBSON” in ICU / ICU Daily Goals Worksheet

Dr. Vincent, Jean-Louis proposed "Fast Hug" mnemonic (Feeding, Analgesia, Sedation, Thromboembolic prophylaxis, Head-of-bed elevation, stress Ulcer prevention, and Glucose control) to make sure we cover key aspects of day to day care of ICU. 1 Here is another mnemonic "MEL GIBSON" everyday in ICU.

M Medication list reviewed.

E Extremities covered. (DVT prophylaxis). Also “E” for exercise (change of position, Out of bed).

L Labs and Radiological studies reviewed.

G Glucose control.

I Infection control measures taken, including elevation of bed to 30 degrees, lines reviewed etc.

B Breathing. Did we allow our patient to have sponteneous breathing everyday. This include sedation break everyday to patient.

S Swan /Hemodynamics/volume status reviewed.

O Oxygen supply status, including review of Oxygen Extraction ratio, if applicable.

N Nutrition/GI prophylaxis.

Related: Please click
here to read about ICU Daily Goals Worksheet from IHI.

References: Click to get articles/abstract
1. Give your patient a fast hug (at least) once a day - Critical Care Medicine. 33(6):1225-1229, June 2005

Friday, January 13, 2006

Friday January 13, 2006
RIFLE Criteria for Acute Renal Dysfunction

Acute Dialysis Quality Initiative (ADQI) Group has proposed the escalating RIFLE system using either glomerular filtration rate-GFR or urine output-UO to classify Acute Renal Failure (ARF):

R = Risk of renal failure - if increase in Scr is x 1.5 or decrease in GFR is > 25% or decrease in UO is < .5 ml/kg/hr x 6 hours.

I = Injury to the kidney - if increase in Scr is x 2 or decrease in GFR is > 50% or decrease in UO is < .5 ml/kg/hr x 12 hours.

F = Failure of kidney function - if increase in Scr is x 3 or decrease in GFR is > 75% or Scr > 4 mg/dl or decrease in UO is < .3 ml/kg/hr x 24 hours or Anuria x 12 hours.

L = Loss of kidney function - Persistent ARF > 4 weeks, and

E = End-stage renal failure - Persistent ARF > 3 months.

here to see the proposed Cone Diagram of RIFLE system for ARF.

References: Click here to see abstract/article:
Acute renal failure – definition, outcome measures, animal models, fluid therapy and information technology needs: the Second International Consensus Conference of the Acute Dialysis Quality Initiative (ADQI) Group - Critical Care 2004, 8:R204-R212
The Outcome of Acute Renal Failure in the Intensive Care Unit According to RIFLE: Model Application, Sensitivity, and Predictability - AJKD - Volume 46, Issue 6, Pages 1038-1048 (December 2005)
Practice patterns in the management of acute renal failure in the critically ill patient: an international survey - Advance Access published online on December 2, 2005, Nephrology Dialysis Transplantation

Wednesday, January 11, 2006

Thursday January 12, 2006

Linezolid (Zyvox) being a reversible, nonselective monoamine oxidase inhibitors (MAOIs) can cause a serious serotonin syndrome if use concomittently with antidepressents citalopram (Celexa) 2, sertraline (Zoloft), fluoxetine (Prozac), and paroxetine (Paxil) . Case has been reported with use of linezolid 18 days after the discontinuation of fluoxetine. Norfluoxetine (fluoxetine’s active metabolite) is thought to be the culprit. 1

Being an intensivist it is a very important drug interaction need to be aware of as most patients admitted to ICU from long term care may be on antidepressents and may require Zyvox for MRSA treatment. Related: See brief review on Serotonin syndrome here from McGill University, Montreal. CMAJ • May 27, 2003; 168 (11) followed with letter Serotonin syndrome: not a benign toxidrome CMAJ • September 16, 2003; 169 (6). It was discussed in detail in our related pearl on Dec. 31, 2005

References: Click to get abstract or article
1. Serotonin Syndrome Associated With Linezolid Treatment After Discontinuation of Fluoxetine - Psychosomatics 46:274-275, June 2005
Serotonin Syndrome after Concomitant Treatment with Linezolid and Citalopram - Clinical Infectious Diseases, volume 36 (2003), page 1197 - pdf file
3. Serotonin Syndrome and Linezolid - Clinical Infectious Diseases, volume 34 (2002), pages 1651–1652 - pdf file
4. The Serotonin Syndrome - NEJM, March 2005 Volume 352:1112-1120

Tuesday, January 10, 2006


Wednesday January 11, 2006
Dopamine-S and Dopamine-R patients ?

Interesting article published in October 2005 issue of Critical Care Medicine which concluded that "Dopamine sensitivity is associated with decreased mortality rate".

In 110 patients after failure of vascular loading, Dopamine infusion started with 5 μg/kg/min and infusion rate was increased by 5 μg/kg/min every 10 mins up to a maximum dose of 20 μg/kg/min to target mean arterial pressure ≥ 70 mm Hg. (So total time needed to reach the highest dose of 20 μg/kg/min was 30 mins). Dopamine resistance was defined by a mean arterial pressure <70.>In the Dopa-S group, the 28-day mortality rate was 16% (seven of 44 patients) compared with 78% (52 of 66 patients) in the Dopa-R group (p = .0006). The capacity of dopamine resistance to predict death was associated with a sensitivity of 84% and a specificity of 74%.

Do we need to qualify our patients as Dopamin-S or Dopamin-R to execute different management strategy?

References: click to get article/abstract
1. Cardiovascular response to dopamine and early prediction of outcome in septic shock: A prospective multiple-center study. - Critical Care Medicine. 33(10):2172-2177, October 2005
Tuesday January 10, 2006
Doxy or Mino ! - trick in the pocket for MRSA

Second generation tetracyclines has been used for MRSA (methicillin-resistant Staphylococcus aureus) for long time but with very few real data available. One study from 1984 showed cure rate of 76%.

Recently Ruhe and coll. look into the issue. Though its a small study of only 24 patients but showed cure rate of 83% with "serious" MRSA icluding skin/skin structure, septic arthritis, Bacteremia/sepsis, osteomyelitis, UTI. 13 patients were treated with Doxycycline and 11 were treated with Minocycline (5 patients in minocycline group were treated in combination with rifampin +/- bactrim). Patients were treated with 100 mg PO bid dose with median total treatment time of 19 days. Also, interestingly, no patient in minocycline group complaint of vertigo.

If intravenous access is an issue in a patient with serious MRSA, except for ZYVOX (linezolid) all mainstream drugs are available only in parenteral form. If Zyvox is contraindicated or not available - you have trick available in your pocket. Plus added advantage of cost-effectiveness.

References: Click to get abstract or article
1. Clumeck and coll. - Treatment of severe staph. infections with rifampin-minocyclin association - J of antimicrob chemother 1984;13 suppl. :C17-C22
Use of Long-Acting Tetracyclines for Methicillin-Resistant Staphylococcus aureus Infections: Case Series and Review of the Literature - Clin Infect Dis 40:1429-1434 electronically published 6 April 2005. - Caution: we found this link not working all the time but atleast refence is checked and available in hard print.

Monday, January 09, 2006

Monday January 9, 2006
Sedatives and sexual dreams - a legal liability?

In 1847, after a year of ether anesthesia introduction, a dentist was convicted to 6 years of jail for sexually assaulting two girls under the influence of anaesthesia. There are well documented cases where physicians and dentists have lost their licenses for similar allegation. Anaesthetics particularly propofol (widely use in ICU) has been reported to be associated with vivid dreams and sexual fantasies though a fairly good study failed to show any association.

Recently, Dr. Robert Strickland's report in this regard at the American Society of Anesthesiologists meeting has been widely reported in media and is worth reading. Click on reference # 3.

References: Click to get abstract or article
1. Anesthetics cause sex hallucinations-
2. Dreams, images and emotions associated with propofol anaesthesia -Anaesthesia, Volume 52, Number 8, July 1997, pp. 750-755(6)
3. Anesthesia can give rise to sex illusion - ARIZONA DAILY STAR - 06.21.2005

Sunday, January 08, 2006

Sunday January 8, 2006
Peres Nomogram or rule of thumb

About 15 years ago, Peres developed a nomogram for probable catheter-insertion depth based on patient height in centimeters and still considered to be applicable/reliable.

For right internal jugular vein central venous catheters, "height (cm)/10" would provide the appropriate depth of insertion. For a 160-cm tall person, a catheter would be inserted to 16 cm deep but for a 200-cm tall person, the depth would be 20 cm.

For left internal jugular, central venous catheter placements, "height (cm)/10 + 4" would provide the appropriate depth of insertion. For a 160-cm tall person, a catheter would be inserted to 20 cm. For a 200-cm tall person, the depth would be 24 cm. (originally described for left external jugular insertion). Caution: In left IJ placement, the catheter tip must not lie at a perpendicular angle against the superior vena cava, because of a risk of vascular erosion.

Reference: Peres PW: Positioning central venous catheters: A prospective survey. Anaesth Intensive Care 1990; 18:536-539

Saturday, January 07, 2006

Saturday January 7, 2006
Changing Endotracheal tube and Combitube

Few tips to remember while changing endotracheal tube over catheter.

1. Have resuscitation cart available.

2. Make Laryngeal mask (LMA) and combitube available.

3. Make respiratory and nursing staff informed and available.

4. "Don't rush". Make patient adequately sedated. Paralyse if absolutely necessary.

5. Pre-oxygenate to 100% for atleast 3-5 prior to tube change.

6. Make smaller size tube available at bedside from present one in case edematous airway encountered.

7. Confirm tube placement in regular standard way.

See Full guide to Tracheal Intubation from Update in Anaesthesia and article and video on combitube from Michael Frass, MD (inventor of combitube) in our procedure section. (video is courtesy of

Friday, January 06, 2006

Friday January 6, 2006
Regarding CPR

CPR is probably one of the most ancient procedure (800 BC) recorded in modern history. 2005 CPR guidelines from American Heart Association suggests:

1. 100 compressions per minute.

2. Compression depth of 1 to 2 inches.

3. Allow the chest to recoil completely after each compression (target equal compression and relaxation times)

4. Minimize interruptions in chest compressions. No-flow Fraction* (no-flow fraction of .17)

5. Compression-ventilation ratio of 30:2 (two rescue breaths every 30 chest compressions). Do not deliver more volume or use more force than is needed to produce visible chest rise. Once intubated: ventilate at a rate of 8 to 10 breaths per minute without attempting to synchronize breaths between compressions.

*NFF= No-flow Fraction was defined as the no-flow time (time periods of cardiac arrest without compressions) divided by total cardiac arrest time.

Unfortunately study shows we have not mastered our most ancient procedure yet.3


Click to get articles/abstract
1. History of CPR - Fascinating insight into early attempts to resuscitate people -
2. 2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care - Circulation. 2005;112:IV-19 – IV-34
3. Quality of Cardiopulmonary Resuscitation During In-Hospital Cardiac Arrest - available free with registration - JAMA - Vol. 293 No. 3, January 19, 2005

Wednesday, January 04, 2006

Thursday January 5, 2006
Hemodialysis in Salicylate overdose with normal level

Hemodialysis is recommended in salicylate overdose patients with a level at or above 100 mg/dL (cut it to half if history suggest chronic ingestion). But if there is any sign of neurological manifestation, dialysis is indicated despite normal level.
Salicylate cause "
neuroglycopenia" (lower CNS glucose level) despite normal serum glucose. As patient gets more and more acidotic, salicylate enters CNS and by direct effect cause neuroglycopenia.

7 indications of Hemodialysis in Salicylate poisoning

1. Mental status change
2. Pulmonary edema
3. Cerebral edema
4. Associated or with renal failure
5. Level at or above 100 mg/dL(half if chronic ingestion)
6. If fluid overload prevents alkalinization.
7. Patient continue to deteriorate clinically.

References: Click to get abstract/article
Toxicity, Salicylate - please register free at
2.An evidence based flowchart to guide the management of acute salicylate (aspirin) overdose -Emerg Med J 2002; 19:206-209
Salicylic acid

Tuesday, January 03, 2006

Wednesday January 4, 2006
Low dose steroid, yes or no ? - responder or non-responder ? - low-dose corticotropin stimulation test or high dose?

Role of steroid in sepsis continue to puzzle physicians - "to do or not do" or "when to do" or "how to do" !!

Study of 177 patients published this month from Annane and coll. suggests that " 7-day treatment with low doses of corticosteroids was associated with better outcomes in septic shock-associated early ARDS nonresponders, but not in responders and not in septic shock patients without ARDS (responders or nonresponders)." But study of 41 patients published in Nov. 2005 issue of Critical Care Medicine suggests that "Treatment with low-dose hydrocortisone accelerates shock reversal in early hyperdynamic septic shock...immune effects appeared to be independent of adrenal reserve".

To keep record straight evidence-based guideline from SCCM at this point is: Intravenous corticosteroids (hydrocortisone 200-300 mg/day, for 7 days in three or four divided doses or by continuous infusion) are recommended in patients with septic shock who despite adequate fluid replacement require vasopressor therapy to maintain adequate blood pressure. And to identify "responders" (>9 μg/dL increase in cortisol 30-60 mins post-ACTH administration) and to discontinue therapy in these patients is optional. Clinicians should not wait for ACTH stimulation results to administer corticosteroids.

In this regard another interesting study of 46 patients from Belgium concluded that: low-dose (1 μg) corticotropin stimulation test may identify a subgroup of patients in septic shock that may go missed by the high-dose test (standard 250-μg test) and these patients may also benefit from glucocorticoid replacement therapy.

Corticus study (Corticosteroid Therapy of Septic Shock) will have some definite answer?. Let see.

References: Click on article to get abstract/article
Effect of low doses of corticosteroids in septic shock patients with or without early acute respiratory distress syndrome. Critical Care Medicine. 34(1):22-30, January 2006.
Low-dose hydrocortisone improves shock reversal and reduces cytokine levels in early hyperdynamic septic shock. Critical Care Medicine. 33(11):2457-2464, November 2005.
Use of corticosteroid therapy in patients with sepsis and septic shock: An evidence-based review. Critical Care Medicine. 32(11) Supplement:S527-S523, November 2004.
4. Relative adrenal insufficiency in patients with septic shock: Comparison of low-dose and conventional corticotropin tests. Critical Care Medicine. 33(11):2479-2486, November 2005.

5. Corticosteroid Therapy of Septic Shock – Corticus -
Tuesday January 3, 2006
Procedure Tip - Does that waveform look ‘wedged’?

Many a times, while placing a PA catheter we encounter waveforms that look ‘different’ and we are not sure if it’s the wedged waveform. Of course, you are going to get a CXR but it can only confirm the position and you still may not be sure if the PA catheter is wedged when the balloon is inflated! Here’s a tip.

Take 2 blood samples from the pulmonary artery port: One while the balloon is deflated (mixed venous sample) and the other while the balloon is inflated (wedged sample). If the wedged PaO2 exceeds the mixed venous PaO2, then the catheter is definitely in the wedged position when the balloon is inflated. Also compare the wedged PaO2 with arterial PaO2. If the values are almost identical, the catheter may be too far in. Do you still need the CXR!

PACEP: Pulmonary artery catheter education project.
P. A. Catheterization insertion video (from Edwards Lifesciences).
Invasive HDM Troubleshooting video (from Edwards Lifesciences).
Vigilance Monitor Inservice video (from Edwards Lifesciences).
Videos above need
windows media player

Sunday, January 01, 2006

Neurogenic Cardiac Injury

Monday January 2, 2006
Brain-Heart Connection - Neurogenic Cardiac Injury

Cardiac injury may occur following many types of brain injury, including trauma, ischemic stroke, and intracerebral hemorrhage. Less common etiologies include tumors, electroconvulsive therapy, and central nervous system infections such as meningitis. Although more difficult to prove, tremendous emotional stress typically following natural disasters 2 or during war may lead to augmented sympathetic tone, abnormal electrocardiogram (ECG) changes, and cardiac injury.

Subarachnoid hemorrhage (SAH)-induced cardiac injury provides a robust example of neurocardiogenic injury. Burch et al. first described neurogenic cardiac injury by demonstrating "cerebral T-wave" electrocardiographic abnormalities in humans with SAH. Elevated troponin levels 4 have also been described and provide evidence that myocardial necrosis may occur. The degree of neurologic injury is a strong predictor of myocardial necrosis after SAH. Cardiac injury, specifically left ventricular (LV) systolic dysfunction, has been described after SAH with an approximate incidence of 10% to 28%. 5 Despite recent advances in diagnostic techniques of cardiac disease, the pathophysiology remains unclear. A catecholamine-mediated mechanism of injury has been demonstrated in experimental and clinical studies.

Read interesting article on
Predictors of Neurocardiogenic Injury After Subarachnoid Hemorrhage in stroke (Stroke. 2004;35:548), followed by editorial comment from Dr. Shunichi Homma Myocardial Damage in Patients With Subarachnoid Hemorrhage (Stroke. 2004;35:552.)

References: click to get article/abstract

1. Oppenheimer SM:
The cardiac consequences of stroke. Neurol Clin North Am 1992, 10:167-176. via pubmed
2. Yamabe H, et al.:
Deep negative t waves and abnormal cardiac sympathetic image (123 I-MIBG) after the great Hanshin Earthquake of 1995. Am J Med Sci 1996, 311:221-224. via pubmed
3. Fabinyi G:
Myocardial creatine kinase isoenzyme in serum after subarachnoid haemorrhage. J Neurol Neurosurg Psychiatry 1977, 40:818-820.
4. Horowitz MB: aneurysmal subarachnoid hemorrhage. Acta Neurochir (Wien) 1998, 140:87-93.
The use of cardiac troponin-I (cTnI) to determine the incidence of myocardial ischemia and injury in patients with aneurysmal and presumed Aneurysmal Subarachnoid Hemorrhage
5 Zaroff J, et al.: Frequency and regional distribution of LV systolic dysfunction after subarachnoid hemorrhage: an echocardiographic assessment. J Am Soc Echocardiogr 1998, 11:507.
Sunday January 1, 2006
Happy new Year - ICU Jokes

How do you treat a depressed intensivist?
Give IV fluid bolus.

Nurse: Doctor, what should I do 'wedge' is going up ?
Intensivist: Sell !

What do you call a baby get born in the high tech ICU?

Intensivist: "Well, Mrs. Jones, I'm afraid you're not quite as sick as we'd hoped."