Friday, November 30, 2007
Q: What is the maximum length of guide-wire to be advanced to avoid guide-wire lost and embolism during subclavian or internal jugular venous catheterization?
A: About 18 cm (may be little less in right IJ)Beside not to loose control of guide-wire, it is appropriate to know the markings on guidewire of CVC kit used in your unit / hospital. Patient height is less reliable in predicting a safe wire length. 18 cm should be considered the upper limit of guidewire introduced during central catheter placement in adults 1.
Related Previous Pearl: Peres Nomogram to calculate appropriate length of central line depth
Reference: click to get abstract
How much guidewire is too much? Direct measurement of the distance from subclavian and internal jugular vein access sites to the superior vena cava-atrial junction during central venous catheter placement - Critical Care Medicine. 28(1):138-142, January 2000.
Thursday, November 29, 2007
Calcium in Dig 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
Wednesday, November 28, 2007
Tuesday, November 27, 2007
Revisiting Pulmonary Artery Diastolic-Pulmonary Wedge Pressure Gradient
We don't see floatation of pulmonary artery catheter (PAC) as much as we used to see. Lets revisit one important but forgotten value obtained via PAC.
Most of the literature in regards to this value is 15-30 years old but proven to be very easy to calculate but very vital to follow 1, 3.
Once this gradient starts to exceeds by 6 mm Hg or more, the patient has shown to have a much poorer prognosis particularly in septic patients. Probable explanation is pulmonary venous vasoconstriction induced by endotoxemia in sepsis or postcapillary lekocyte aggregation in development of ARDS 2, 4.
One study suggests that although an initial PAD-PWP gradient in patients with sepsis is associated with a high mortality, a much more sensitive indicator is to follow the trend. There was a 91% mortality in patients with persisting or increasing gradients 2.
References: click to get abstract/artice
1. Pulmonary hypertension in sepsis: Measurement by the pulmonary arterial Diastolic-pulmonary wedge pressure gradient and the influence of passive and active factors. Chest 1978; 73:583-91
2. Significance of the pulmonary artery diastolic-pulmonary wedge pressure gradient in sepsis. Crit Care Med 1982; 10:658-61
3. Pulmonary artery diastolic and wedge pressure relationships in critically and injured patients. Arch Surg 1988; 123:933-6
4. Increased Pulmonary Venous Resistance Contributes to Increased Pulmonary Artery Diastolic-Pulmonary Wedge Pressure Gradient in Acute Respiratory Distress Syndrome - Anesthesiology: Volume 102(3) March 2005 pp 574-580
Monday, November 26, 2007
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
Sunday, November 25, 2007
What's the right length of endotracheal tube (ETT) for oral intubation?
As a gold standard the only way to make sure that tip of ETT is atleast 2 cm away from carina (or at appropriate place) is via chest X-ray. But there are many bedside quick tricks/formulae described in literature. One such formula 1 which also found to have good clinical correlation, is
ETT length (incisors to midpoint of trachea, cm) = patient's height (cm)/10+5
Like, if patient's height is 170 cm, ETT should be taped at
170/10 + 5 = 22 cm
Another trick is to have ETT's cuff palpable at sternal notch, a technique described about 40 years ago ! 2 .
Related previous pearl:
Movement of endotracheal tube (ETT) with neck
1. Anaesthesia Intensive Care 1992; 20:156;
2. Anesthesiology 1964; 25:169
Saturday, November 24, 2007
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 .
Q; Which antibiotic may give false positive urine drug screen for opiates ?
A; Gatifloxacin (Tequin) and other fluoroquinolones.
Fluoroquinolones as a class are among compounds that have a propensity to cross-react with enzyme immunoassay urine drug screens for opiates. The exact mechanism is unknown.False-positive results could have negative effects on patient care so analysis with another assay method should be done to verify the urine drug screen.
Editors' note: Tequin has been taken off USA market last year but as mentioned in JAMA's article (reference # 2), 13 quinolones were tested and 11 of the 13 quinolones caused some opiate activity by at least 1 assay system. So be careful with all quinolones. Actually, JAMA report mentioned Levaquin as one of the top 3 !
Thursday, November 22, 2007
Nasogastric tube syndrome
Q; 65 year old female admitted to ICU 9 days ago with small bowel obstruction. Pt. is now stable and actually is about to get transferred out of unit. Patient suddenly start complaining of choking sensation with two hands on neck. Monitor shows oxygen desaturation. Patient intubated emergently. No laryngeal or vocal edema seen on laryngoscope but vocal cord paralysis noted.
A; Nasogastric tube syndrome : Nasogastric tube syndrome was described about 25 years ago by Sofferman and coll. It is a life-threatening complication of an indwelling (more than a week) nasogastric tube. The syndrome may present as complete vocal cord abductor paralysis. The syndrome is thought to result from perforation of the NG tube-induced esophageal ulcer and infection of the posterior cricoid region (postcricoid chondritis) with subsequent dysfunction of vocal cord abduction. Unilateral paralysis of cord is also described. Treatment is protection of airway, removal of NG tube and antibiotics. Some advocates antireflux therapy too. Another variant is described with no esophageal ulcer but possibly because of ischemia of the laryngeal abductor muscle secondary to physical compression of the postcricoid blood vessels by NG tube.
References: Please click to get abstract
1. The nasogastric tube syndrome: two case reports and review of the literature. Head Neck. 2001 Jan;23(1):59-63.
2. A variant form of nasogastric tube syndrome. Intern Med. 2005 Dec;44(12):1286-90.
3. Case Report - Nasogastric Tube Syndrome: The Unilateral Variant - Medical Principles and Practice Vol. 12, No. 1, 2003
4. Sofferman, R.A. and Hubbell, R.N., "Laryngeal Complications of Nasogastric Tubes," ANNALS OTOLOGY, RHINOLOGY, AND LARYNGOLOGY, 90:465-468, 1981.
Wednesday, November 21, 2007
Difference between Lactate Ringer's and Normal Saline solutions
Lactated Ringer's Solution was invented about 125 years ago by a British physiologist Sydney Ringer. It is a different intravenous solution from normal saline.
Normal Saline is the solution of 0.9% NaCl. It has a slightly higher degree of osmolality compared to blood. One litre of Normal Saline contains
154 mEq/L of Na+ and
154 mEq/L of Cl−
One liter of Lactated Ringer's Solution contains:
130 mEq/L of Na+ but total cations of 137 mEq/L , so still is isotonic.
109 mEq/L of Cl−28 mEq/L of lactate
4 mEq/L of potassium
3 mEq/L of calcium.
Lactate converts to bicarbonate in liver.
Tuesday, November 20, 2007
Q: Propofol causes deficiency of which essential element ?
A: Zinc Though propofol cause greater urinary losses of zinc and lower serum zinc concentrations, the actual clinical implication is not established .
Related previous Pearl: Essential trace elements
1.Trace element homeostasis during continuous sedation with propofol containing EDTA versus other sedatives in critically ill patients - Intensive care medicine. Supplement (Intensive care med., Suppl.) , 2000, vol. 26, n 4, pp. S 413-S421
Monday, November 19, 2007
Scleroderma Renal Crisis (SRC)
Scleroderma Renal Crisis is one of the few rheumatological emergency where early diagnosis and treatment can make big difference in outcome. Wrong diagnosis may lead to wrong management pathway and eventually to very high mortality.
SRC is heralded with hypertensive crisis associated with acute renal failure but the pearl is to avoid IV Labetolol or nitroprusside and gradually decrease blood pressure with PO angiotensin-converting enzyme (ACE) inhibitors. (yes! its a renal crisis but require ACE-I). calcium channel blockers may help. Renal dialysis is a last resort.
Another important differential diagnosis is from SLE (renal). 5 It has been suggested that use of steroids is associated with onset of scleroderma renal crisis.
See this precise review article on SRC here from Department of Rheumatology and Internal Diseases, Medical University in Białystok, Poland. (2005)
References: Click to get articles/abstract
1. What Is Scleroderma Renal Crisis and How Is it Managed? via medscape.com with free registration
2. Systemic Sclerosis With Renal Crisis and Pulmonary Hypertension - stanford.edu
3. Long-Term Outcomes of Scleroderma Renal Crisis - 17 October 2000 Volume 133 Issue 8 Pages 600-603 - annals
4. Scleroderma Renal Crisis: The Sword of Damocles. - JCR: J. of Clinical Rheum. 10(5):234-235, October 2004.
5. Rheumatologic Renal Disease: SLE vs. Scleroderma - ucsf.edu
Sunday, November 18, 2007
Clonidine in alcohol withdrawal
Relatively unknown but clonidine is a very viable option beside benzodiazepines in ETOH withdrawal symptoms.
Clonidine reverses central adrenergic discharge, relieving tachycardia, hypertension, tachypnea, tremor, and possibly some craving for alcohol. Also in patch form, it provides a part of sedation.
Oral dose of clonidine is 0.1- 0.2 mg tid. It can also be use in IV drip form but with caution (not available in USA as IV).
Please note, though clonidine is very effective in the treatment of alcohol, opiate, nicotine withdrawal syndromes, attention-deficit/hyperactivity disorder (ADHD) and Tourette's syndrome -but does not help if symptoms progress to seizures and hallucinations-delirium tremens.
2 major cautions for ICU physicians:
1. Clonidine itself can cause withdrawal symptoms if discontinued abruptly. It should be slowly decreased over several days to avoid withdrawal symptoms. Withdrawal can cause hypertension, irritability, nervousness, insomnia, and headache.
2. Clonidine dose should be reduced and should be use with caution in patients with chronic renal failure and coronary artery disease.
Trivia: Clonidine was first introduced in 1960s as a nasal decongestant.
Reference: Click to get abstract
1. Clonidine and alcohol withdrawal - Adv Alcohol Subst Abuse. 1987;7(1):17-28
2. Pharmacological management of alcohol withdrawal. A meta-analysis and evidence-based practice guideline. American Society of Addiction Medicine Working Group on Pharmacological Management of Alcohol Withdrawal - JAMA, Vol. 278 No. 2, July 9, 1997
3. CLONIDINE IN THE TREATMENT OF ALCOHOL WITHDRAWAL IN THE INTENSIVE CARE UNIT- British Journal of Anaesthesia, 1992, Vol. 68, No. 1 106-108
4. Intrathecal and Oral Clonidine as Prophylaxis for Postoperative Alcohol withdrawal Syndrome: A Randomized Double-Blinded Study - Anesth. Analg., March 1, 2004; 98(3): 738 - 744.
Saturday, November 17, 2007
Hemodynamic monitoring video
Watch and keep in file this excellent presentation on Pulmonary Artery Catheter and Arterial waveforms. Total presentation is about 36 minutes. It has 3 modules
Module 1: Interpretation Requirements, Central Venous Pressure, Right Ventricular Wave, Pulmonary Artery Wave, Wedge Pressures, PAOP Interpretation.
Module 2: Effect of Respiratory Artifact, Abnormal Waveforms, Common Abnormal Waves, Avoiding Errors
Module 3: Accurate Waveforms,Technical Requirements, Zeroing and Leveling, Arterial Line Accuracy, Using a Square Wave Test
Presented by: Tom Ahrens DNS RN CCRN CS Barnes-Jewish Hospital St. Louis, Mo
To view this content you need Microsoft's newest version of Windows Media Player. Click the Windows Media Player 9 Series button to install, which you can download free here
Friday, November 16, 2007
Intensivists do make difference
Here is another study endorsing the positive effect of intensivists on ICU mortality. This study was performed to examine the association of closed vs open models with patient mortality with ALI (acute lung injury).
Closed ICUs are defined as units that required patient transfer to or mandatory patient comanagement by an intensivist. Open ICUs as those relying on other organizational models.
13 ICUs were designated closed and 11 open.
- Closed ICUs had reduced hospital mortality (adjusted odds ratio, 0.68; 95% confidence interval, 0.53, 0.89; P = 0.004).
- Consultation by a pulmonologist in open ICUs was not associated with improved mortality (adjusted odds ratio, 0.94; 95% confidence interval, 0.74, 1.20; P = 0.62).
- The use of low tidal volume in patients with ALI was different between closed and open ICUs. In open ICUs had triple the risk of receiving injurious (>12 ml/kg PBW) tidal volumes, whereas patients in closed ICUs were almost three times more likely to receive lung-protective tidal volumes (6.5 ml/kg PBW) on Day 3 of mechanical ventilation after ALI onset.
Conclusions: Patients with ALI cared for in a closed-model ICU have reduced mortality. These data support recommendations to implement structured intensive care in the United States.
Reference: click to get abstract/article
1. Effect of Intensive Care Unit Organizational Model and Structure on Outcomes in Patients with Acute Lung Injury - American Journal of Respiratory and Critical Care Medicine Vol 176. pp. 685-690, (2007)
Thursday, November 15, 2007
Sympathetic storming after traumatic brain injury remains one of the most dramatic clinical scene particularly in neurological units. It occurs due to uncontrolled sympathetic surge with a diminish or unmatch parasympathetic response. Acording to Baguley criteria 5 out of the 7 clinical features should be present -
- posturing and
Various agents have been used for treatment (see review article below) but haloperidol may worsen the symptoms.Dr. Blackman and coll. coined the term "PAID" - paroxysmal autonomic instability with dystonia- in Archives of Neurology March 2004.
See great review articlehere on Sympathetic Storming from Denise M. Lemke, published in J Neurosci Nurs 36(1):4-9, 2004. © 2004
References: click to get abstract/article
1. Dysautonomia after traumatic brain injury: a forgotten syndrome? - J Neurol Neurosurg Psychiatry 1999;67:39-43 ( July )
2. Paroxysmal autonomic instability with dystonia (PAID) - Arch Neurol. October 2004;61:1625.
3. Paroxysmal Autonomic Instability with Dystonia After Brain Injury - Arch. Neurol. March 2004;61:321-328
Wednesday, November 14, 2007
Venous Air Embolism - VAE - immediate maneuvers
If Venous Air Embolism is suspected during line procedure with symptoms of sudden occurrence of cardiopulmonary dysfunction like hypotension, hypoxia or churning murmur over left sternal border ( "millwheel murmur" ) - following 7 steps are essential:
1. Clamp the line (do not withdraw) - to prevent further air.
2. Rotate patient to left lateral decubitus position - to decrease air leaving through RV outflow tract.
3. Place patient in Trendelenburg position - to help air trap in the apex of the ventricle.
4. Increase oxygen to 100% - Supplemental oxygen reduces the size of embolus. (Avoid High PEEP as it may increase the risk of paradoxical emboli).
5. Advance the catheter little, unclamp the line and aspirate from the 'distal port' to attempt to remove air. (PA-catheter is not as effective as triple lumen catheter in aspirating air).
6. If hypotension occurs - start IVF wide open and add pressor if needed (catecholamines are prefered).
7. Continue supportive treatment till air is absorbed or further management for complications like paradoxical emboli or hyperbaric oxygen therapy is planned.
Refrences: Click to get abstract/article.
1. Venous Air Embolism - emedicine.com
2. Gas Embolism - NEJM, feb. 2000, Volume 342:476-482
3. Venous air embolism: a review. J Clin Anesth 1997;9:251-257
Tuesday, November 13, 2007
Propofol and colorful urine (and hair !)
Propofol infusion is noticed to turn color of urine usually green. There are also case reports describing other colors with propofol like pink, white and brown though green urine carries the trademark. Incidence is around 1% and usually associated with propofol infusion longer than 72 hours. It takes about 2-6 hours for urine to resume its natural color after stopping propofol. It is associated with respiratory alkalosis as respiratory alkalosis increases the formation of metabolites responsible for green color.
There is atleast one case report in literature where discoloration of hair secondary to propofol is reported 1.
It is a benign potential side effect of Propofol and does not require any intervention. Recognition of this side effect is important as it averts unnecessary further workup and limits medical expenditures.
1. Propofol and the color green . Anaesthesia 1989;44(1):82.
Monday, November 12, 2007
Scenario; 62 year old male with long history of atrial fibrillation and chronically on Digoxin admitted with dizzyness and found to have 3rd degree AV block. Patient is hemodynamically stable. Patient informed you that about a year ago, he had similar episode and was found to have high digoxin level and was treated with "antidote of digoxin". Later his digoxin dose was decreased by his cardiologist. You assume "Dig toxicity" and indeed Dig. level reported as 3.4 micrograms/ml. You ordered "Digibind". What step you should take in view of history of previously received "digibind" ?
Answer: Skin allergy test for digoxin immune Fab.
Since allergy testing can delay urgently needed therapy, it is not absolutely required before treatment of life-threatening digitalis toxicity with digoxin immune Fab (ovine), but should be considered if situation permits, particularly with previous history.
Skin testing should be considered for high risk individuals with history of multiple allergies, patients who previously treated with digoxin immune Fab. and patients with allergy to papaya extracts. Papain is used to cleave the whole antibody into Fab and Fc fragments, and traces of papain or inactivated papain residues may be present in digoxin immune Fab (ovine).
One should consider the possibility of anaphylactic, hypersensitivity or febrile reactions to digoxin immune Fab (ovine), even with first dose.
How to perform: Diluting 0.1 mL of reconstituted Digibind (9.5 mg/mL) in 9.9 mL sterile isotonic saline (1:100 dilution, 95 µg/mL). Injecting 0.1 mL of the 1:100 dilution (9.5 µg) intradermally and observing for an urticarial wheal surrounded by a zone of erythema. The test should be read at 20 minutes.
If skin testing causes a systemic reaction, a tourniquet should be applied above the site of testing. In case of full blown anaphylactic, hypersensitivity or febrile reactions to digoxin immune Fab (ovine) on test dose or infusion, the drug infusion should be discontinued and appropriate therapy initiated using oxygen, volume expansion, diphenhydramine, corticosteroids and airway management as indicated. Epinephrine should be use very cautiously and only if needed due to higher risk of arrthymias in the setting of digitalis toxicity.
Sunday, November 11, 2007
On sundays, we try to provide links to other Critical Care related endeavours on internet. In this regard, following site provides good synopsis on different topics and could be a quick source for residents' handout.
Recommended reads include
- Heparin induced thrombocytopenia
- ICU Blood Glucose Protocol
- Toxicology Overview
- Myasthenia gravis
- Intensivist burnout
- ICU management of organ donor
- Burn critical care
Saturday, November 10, 2007
7 Pearls of Vitamin K (phytonadione)
1. Oral Vitamin K has similar efficacy as intravenous Vitamin K. 1
2. SQ (subcutaneous) Vitamin K absorption is unreliable.2
3. IM (intramuscular) Vitamin K may promote intramuscular hemorrhage.
4. IV (intravenous) Vitamin K is effective in 6 - 8 hours.
5. IV Vitamin K should be given very slow (preferably .5 mg/min).
6. IV Vitamin K may cause facial flushing, diaphoresis, chest pain, hypotension, dyspnea, anaphylaxis and cerebral thrombosis but pretreatment with antihistamines or corticosteroids is not routinely recommended. 7
7. Although IV Vitamin K has been decribed safe in few studies 3,7, it should be use only in life threatening bleeds from warfarin overdose or due to deficiency of vitamin K as fatality from anaphylactoid reaction could be high 4,5.
References: Click here to see abstract/article:
1. Comparison of Oral vs Intravenous Phytonadione (Vitamin K) in Patients With Excessive Anticoagulation - Arch Intern Med. 2003;163:2469-2473. - full article available with free registration.
2. Oral Vitamin K Lowers the International Normalized Ratio More Rapidly Than Subcutaneous Vitamin K in the Treatment of Warfarin-Associated Coagulopathy - Annals - 20 August 2002, Volume 137 Issue 4, Pages 251-254 -pdf file
3. The safety of intravenously administered vitamin K - via pubmed, Vet Hum Toxicol. 2002 Jun;44(3):174-6.
4. Anaphylactoid reactions to vitamin K - via pumed, J Thromb Thrombolysis. 2001 Apr;11(2):175-83.
5. Anaphylaxis after low dose intravenous vitamin K - via pubmed, J Emerg Med. 2003 Feb;24(2):169-72
6. Comparing Different Routes and Doses of Phytonadione for Reversing Excessive Anticoagulation - Arch Intern Med. 1998;158:2136-2140.
7. The incidence of anaphylaxis following intravenous phytonadione (vitamin K1): a 5-year retrospective review - Annals of Allergy, Asthma and Immunology, Volume 89, Number 4, October 2002, pp. 400-406(7)
Friday, November 9, 2007
Fall of Aprotinin !
This week Bayer, maker of aprotinin, has announced that it has elected to temporarily suspend worldwide marketing of Trasylol® (aprotinin injection) until final results from the Canadian BART trial is available 3. The BART study is an independent randomized, controlled trial being conducted in high-risk cardiac surgery patients 4. On October 19, 2007, FDA was notified of the Data Safety Monitoring Board’s (DSMB) recommendation to stop patient enrollment in the aprotinin treatment group arm of the BART study. The preliminary findings suggest that, compared to the antifibrinolytic drugs, epsilon-aminocaproic acid and tranexamic acid, aprotinin increases the risk of death 5.
BART = Blood conservation using antifibrinolytics: A randomized trial in a cardiac surgery population
In last couple of years, use of aprotinin has been questioned following coronary artery bypass grafting, particularly in view of availability of safer and less expensive alternatives (aminocaproic acid and tranexamic acid) . Aprotinin, also known as bovine pancreatic trypsin inhibitor is a protein that is administered by injection to reduce bleeding during complex surgery. Its main effect is the slowing down of fibrinolysis .
One major article published in January 2006 in The New England Journal of Medicine concluded 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. Also, it was suggested that 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 shows a generalized pattern of ischemic injury 1.
Same group of investigators, published an article in February 2007 issue of JAMA, looking into mortality data of 3876 patients from 62 medical centers assessed at 6 weeks, 6 months, and annually for 5 years after CABG surgery 2, comparing aminocaproic acid and tranexamic acid, aprotinin, or no antibleeding agent (control). Study found that Aprotinin treatment was associated with significantly increased long term mortality compared with control, whereas neither aminocaproic acid nor tranexamic acid was associated with increased mortality.
FDA issued a relabeling of aprotinin on December 15, 2006, confining it to use only in high-risk coronary artery bypass graft patients.
References / suggested readings: Click to get article/abstract
1. The Risk Associated with Aprotinin in Cardiac Surgery - NEJM Jan. 26, 2006 Volume 354:353-365
2. Mortality Associated With Aprotinin During 5 Years Following Coronary Artery Bypass Graft Surgery - JAMA. 2007;297:471-479, Vol. 297 No. 5, February 7, 2007
3. Bayer Temporarily Suspends Global Trasylol® Marketing - trasylol.com
4. MAJOR OUTCOMES FOLLOWING HIGH RISK CARDIAC SURGERY Canadian Journal of Anesthesia 53:26231 (2006)
5. FDA Public Health Advisory - fda.gov
Thursday, November 8, 2007
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". 2
Only commercially available Sutureless Securement Device in USA is Statlock. *
* (icuroom.net 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
2. Guidelines for the Prevention of Intravascular Catheter-Related Infections (MMWR 2002)
3. Sutureless Securement Device Reduces Complications of Peripherally Inserted Central Venous Catheters - Journal of Vascular and Interventional Radiology 13:77-81 (2002)
4. OSHA Fact Sheet: Securing Medical Catheters - from STATLOCK site
Wednesday, November 7, 2007
Argatroban anticoagulation in Critically Ill Patients
Since we are diagnosing more and more HIT (Heparin Induced Thrombocytopenia), Argatroban has entered into mainstream ICU care !
But care should be taken in prescribing Argatroban. See this important study published this year in The Annals of Pharmacotherapy regarding dosing of Argatroban for critically ill patients with multiple organ dysfunction (MODS) and suspected or proven heparin induced thrombocytopenia (HIT).
METHOD: Prospective observation of 24 consecutive patients with suspected HIT who were being anticoagulated with argatroban using 2 µg/kg/min in the first 5 patients and 0.2 µg/kg/min in the subsequent 19 patients.
- Infusion of argatroban 2 µg/kg/min over 4 hours caused bleeding complications in 3 patients as aPTT increased from 51 to 86 secs, and INR increased from 1.4 ± 0.4 to 2.5.
- Infusion of argatroban 0.2 µg/kg/min over 4 hours provided sufficient anticoagulation without bleeding complications. The aPTT in this population increased from 44 ± 9 to 59 ± 13 seconds (p <>
Coagulation variables (aPTT, PT, INR) were significantly different between both dosing regimens after 4 hours of infusion.
In critically ill patients with MODS, argatroban 2 µg/kg/min, as recommended by the manufacturer, resulted in extensive anticoagulation. A tenfold lower starting dose is sufficient and safe for effective anticoagulation in this specific patient population.
References: click to get abstract/article
1. Argatroban Anticoagulation in Critically Ill Patients - The Annals of Pharmacotherapy: Vol. 41, No. 5, pp. 749-754.
Tuesday, November 6, 2007
Intensive care of patients with acute liver failure
This month "Critical Care Medicine" has published a CME article:
Intensive care of patients with acute liver failure:
Recommendations of the U.S. Acute Liver Failure Study Group
This is a very concise review on the said topic dealing with all ICU aspects of Acute Liver Failure including
- Etiology-Specific Treatments like in acetaminophen overdose
- Hepatic Encephalopathy and Hyperammonemia
- Infection Prophylaxis and Surveillance
- Sedation and Analgesia
- Correction of the Bleeding Diathesis
- Assessment of Prognosis and Liver Transplant Listing Criteria
- Seizure Prophylaxis and Surveillance
- Treatment of Circulatory Dysfunction
- Management of Cerebral edema
- Management of Intracranial Hypertension: Specific Recommendations
- Mechanical Ventilation
- Renal Replacement Therapy (RRT); Management of Fluids and Electrolytes
- MANAGEMENT OF ALF DURING AND AFTER OLT
- Intraoperative and Postoperative Monitoring
Its an important article to be aware of. Article is by subscription but reference can be found below.
Related video/lecture: Acute Liver Failure: The Critical Team Approach by Dr. Lorenzo Rossaro, Head of the Liver Transplant Program at UC Davis Med Center (this video requires real player)
References: click to get abstract/article
1. Intensive care of patients with acute liver failure: Recommendations of the U.S. Acute Liver Failure Study Group Critical Care Medicine. 35(11):2498-2508, November 2007.
Monday, November 5, 2007
On stress dose steroid (update from Canada Critical Care Forum meeting)
There was a lot of debate and update particularly in view of results from recent CORTICUS trial. As expected, Dr. Annane, was at center of attraction.
Dr. Annane stand with results of his JAMA 2002 study which showed positive influence of stress dose steroid in septic shock. In his view, CORTICUS trial did not re-produce the same results due to following 3 main reasons:
- Patient population was not as selected to produce same results. Many eligible patients were excluded.
- 72 hours has been allowed to start stress dose steroid in contrast to early start (24 hours) as in 2002 study.
- Fludrocortisone was not added which could have made a significant difference in outcome.
Also, while answering a question - he recommends not to exceed the dose beyond 200 mg per day in divided doses or preferably in continuous drip (to avoid peak sugar levels).
Despite his stand on use of low / stress dose steroid in septic shock - with performing corticotropin test - he expressed his concern about overuse of steroids in septic shock.
Please note that updated guidelines on sepsis from SCCM / ISF recommends use of hydrocortisone if septic shock is unresponsive to pressors. Fludrocortisone as well as corticotropin test is not recommended.
References: click to get abstract/article
1. Effect of treatment with low doses of hydrocortisone and fludrocortisone on mortality in patients with septic shock. JAMA. 2002;288:862-871.
Sunday, November 4, 2007
Do not treat acidosis aggressively in CO poisoning
Non-invasive Pulse-ox is not reliable in CO poisoing and 100% NRM should be applied ASAP in any suspected CO poisoning irrespective of pulse-ox on monitor. CO has high affinity for Hemoglobin (HB) - forming HbCO and it absorbs light almost identically to that of oxyhemoglobin, making pulse-ox very unreliable. 100% Oxygen delivery displaces CO from Hb and decrease its half life from 4.5 hours to 1 hour.
But the most unknown point in CO poisoning management is to not to treat acidosis very aggressively and PH of even 7.15 is acceptable for 2 reasons:
1. Acidosis is good in CO poisoning ! , as it causes rightward shift in the oxyhemoglobin dissociation curve, increasing tissue oxygen availability (Bohr effect).
2. Simultaneously, acidosis improves progressively by itself with 100% oxygen therapy and over treatment may push patient later into severe alkalosis.
Related previous pearl:
Hyperbaric oxygen in CO poisoning
The Bohr Effect and Permissive Hypercapnia
Saturday, November 3, 2007
It has links to therapeutic hypothermia protocols from 14 major institution around the nation, a long list of references and links to various networks.
Site has ppt. presentation, Hypothermia after cardiac arrest from Benjamin Abella, MD MPhil.
See interesting concept Post-Cardiac Arrest Early Goal Directed Therapy from site.
Friday, November 2, 2007
Antidote for vasoconstrictor extravasation in skin and tissues (dopamine, epinephrine, or norepinephrine) is PHENTOLAMINE. Infiltrate 5-15 mg of PHENTOLAMINE in 10 ml of normal saline into the area of extravasation as soon as possible. Treatment may be applied and effective up to 12 hours post extravasation of vasoconstrictor.
Keep y ourself ready for fluid bolus post treatment. Mechanism of action: Phentolamine is a nonspecific alpha-adrenergic blocking agent which inhibits vasoconstriction and allow improved blood circulation through the affected area.
References: Click to get abstract or article
1. Drug Monographs - Phentolamine - lhsc.on.ca
2. Treating Extravasation Injuries - extravasation.org
3. The use of phentolamine in the prevention of dopamine-induced tissue extravasation - J Crit Care 1998 Mar;13(1):13-20
Thursday, November 1, 2007
Unfortunately nutrition in ICUs does not get due importance. Following website is an important link to know.
Important areas to visit include 'Tools and training kit'
- Enteral Nutrition in The Critically Ill : Practice Guidelines
- Enteral Nutrition: Management of Diarrhea Guideline
- Placement of Small Bowel Feeding Tubes
- Parenteral Nutrition Guidelines
- Daily EN checklist
There are various power point presentations including
- Practical Aspects of Nutrition Support in the ICU
- More Evidence For The Safety and Efficacy of Post Pyloric Feeding in the ICU patient
- Evaluation of Three Different Strategies for Post-Pyloric Placement of Enteral Feeding Tubes