Monday, November 12, 2007

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

Sunday November 11, 2007
amurthy.com

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

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

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

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

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.

RESULTS:



  • 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.



CONCLUSIONS:
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

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
  • Nutrition
  • 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

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:


  1. Patient population was not as selected to produce same results. Many eligible patients were excluded.
  2. 72 hours has been allowed to start stress dose steroid in contrast to early start (24 hours) as in 2002 study.
  3. 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

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

Saturday November 3, 2007
Hypothermia portal




Following site is an excellent portal of hypothermia from University of Pennsylvania.




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

Friday November 2, 2007
Vasoconstrictor extravasation


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

Thursday November 1, 2007
criticalcarenutrition.com



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