Thursday September 17, 2009

Q: What is the maximum length of guide-wire is recommended to insert (advance) 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 in CVC kit. 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

Wednesday September 16, 2009
Warning: Ceftriaxone (Rocephin®)—Calcium Interaction

The FDA has warning about Ceftriaxone—Calcium interactions due to potential precipitate/crystalline formation in the IV tubing or vasculature when the two agents are combined. These reactions are potentially lethal. This includes all calcium-containing infusions (e.g. Lactated Ringers, Total Parenteral Nutrition).

Data is not available on interactions between ceftriaxone and oral calcium products or intramuscular ceftriaxone and calcium containing products.

Cases of fatal reactions with calcium-ceftriaxone precipitates in the lungs and kidneys have been reported in both term and premature neonates. Some of these cases occurred even when ceftriaxone and the calcium-containing products were administered by different routes at different times. The use of ceftriaxone with calcium products is now contraindicated in all age groups.

Ceftriaxone and Calcium containing solutions should not be administered at different times via different infusion lines or within 48 hours of each other in any patient of any age.



http://www.fda.gov/safety/medwatch

Tuesday September 15, 2009
Tracheostomy

Monday September 14, 2009
Malignant Hyperthermia: Agent of choice…Dantrolene

Malignant Hyperthermia is a rare, but potentially lethal musculoskeletal disorder associated with exposure to halogenated anesthetic gases or succinylcholine. Some signs/symptoms include tachycardia, hyperthermia, supraventricular and ventricular arrhythmias, and even cardiac arrest.

The mainstay of treatment is Dantrolene. It is a direct-acting skeletal muscle relaxant that blocks calcium release from intracellular stores in the sarcoplasmic reticulum. Dantrolene is dosed 1mg/kg to a maximum cumulative dose of 10 mg/kg. Infuse over approximately 1 hour. Doses may be repeated until signs of malignant hyperthermia are reversed.

It is highly lipophilic, thus poorly soluble in water. Dantrolene is currently available for intravenous use in vials containing 20mg lyophilized dantrolene sodium added to 3 gm mannitol to improve water solubility. The contents in the vial are to be dissolved in 60 mL water, yielding a final concentration of 0.33 mg/mL. The vials are to be protected from light and should be used within 6 hours once reconstituted. Due to the high irritability, it is recommended that dantrolene be infused into a large vein. Dantrolene peaks in 6 hours, and has a half life of 12 hours. It is metabolized by liver microsomes and are excreted mainly via urine and bile.


Reference:

Krause T, et al. Anaesthesia 2004;59:364
Rosenbaum HK, et al. Anesthesiology Clin N Am 2002;20:623

Sunday September 13, 2009

Q: What is the dosing adjustment of Primaxin (Imipenem/Cilastatin) in Hemdialysis and CVVHD (CRRT)?


Answer: Primaxin (Imipenem/Cilastatin) need to be adjusted in Hemodialysis and CVVHD (CRRT) patients.

DOSING IN HEMODIALYSIS:
250 mg IV q12h with 250 mg post dialysis on dialysis day.

DOSING IN HEMOFILTRATION:
1. CVVHD with dialysis flow rate less than 1.5L/hr: 500 mg IV q12h;
2. CVVHD with dialysis flow rate 2L/hr: 500 mg IV q 8h.

Saturday September 12, 2009


Q: Kayexalate (Sodium Polystyrene) is a cation exchange resin that enhance potassium clearance across the GI tract. What is the exchange ratio of Na and K?

Answer: For each mEq of potassium removed, 2-3 mEq of sodium is added. So it is important to watch for hypernatremia.

Lasix can be given to enhance removing both sodium and potassium via diuresis.

Friday September 11, 2009 (pediatric pearl)
Neuron Specific Enolase (NSE) and S-100 as markers of outcomes in pediatric cardiac arrest

NSE is a dimeric glycoprotein found in neurons and neuroectodermal cells. S-100B is a calcium binding protein found primarily in the astroglial and Schwann cells. At nanomolar concentrations it promotes astroglial proliferation and neuronal differentiation, but at micromolar concentrations it induces astroglial and neuronal cell death.

The timing, intensity, and duration of serum NSE and S-100B biomarker concentration patterns are associated with neurologic and survival outcomes following in or out-of-hospital cardiac arrest pediatric cardiac arrest.

For NSE a cutoff level of 51 µg/L at 48 hrs resulted in a sensitivity of only 50% for poor outcome while achieving a specificity of 100%.With these derived cutoffs the posttest probability of NSE for poor outcome is 99%, which is increased from the pretest probability of poor outcome of 54%. The addition of NSE testing may allow clinicians to increase their prediction of poor outcome in this population.



Reference: Click to get abstract

Neuron-specific enolase and S-100B are associated with neurologic outcome after pediatric cardiac arrest - Pediatric Critical Care Medicine 10(4), July 2009, pp 479-490

Thursday September 10, 2009
Propofol Abuse Growing Problem for Anesthesiologists

"One addict fell asleep at his desk so often that his lolling forehead became a perpetual bruise. Another was so desperate for a fix that he started trolling through sharps bins for discarded needles with traces of drug to inject.

The addicts were two doctors, an anesthesiologist and a family physician. Their drug of choice: propofol.

If that’s surprising, consider this: One in five academic anesthesiology training programs reported at least one case of abuse by physicians or other healthcare workers over the past decade, new research shows. The incidence of propofol abuse has risen fivefold over the last 10 years"



- CLINICAL ANESTHESIOLOGY - ISSUE: MAY 2007 VOLUME: 33:05 -

www.anesthesiologynews.com/

Wednesday September 9, 2009


Case: A patient requires anticoagulation for PE. The patient has a history of HIT (Heparin Induced Thrombocytopenia), an allergy to Argatroban (per documentation), with a creatinine clearance less than 30ml/min. What is the best available agent for anticoagulation?


Answer: Heparin and LMWHs should not be used due to the history of HIT. The Argatroban allergy is questionable, may be considered, but would rather not take the chance. Fondaparinux (Arixtra) is contraindicated in patients with a creatinine clearance less than 30 ml/min.

Bivalirudin (Angiomax) would be the best available choice, even though it’s not FDA approved for HIT. Bivalirudin is a specific and reversible direct thrombin inhibitor, binding to circulating and clot-bound thrombin. The dose range is 0.05 – 0.15 mg/kg/hr , titrating to maintain aPTT 1.5 – 3 x baseline. It is eliminated renally and via enzymatic processes. An initial dose adjustment should be made if CrCl less than 50 ml/hr to 0.05 mg/kg/hr. Bivalirudin peaks in 1-2 hours, with a half life of 10-24 minutes. Unlike heparin, there are no reversal agents available. The advantage of Bivalirudin is that it may be used in multiorgan failure patients, and those on CVVHD.

Monday September 7, 2009


Scenario: 54 year old female is admitted to ICU with pneumonia. Patient is found to be moderately anemic. To be complete in evaluation and to rule out possible GI bleed, you asked resident to do rectal exam for guaiac stool. Resident performed Guaiac stool via rectal exam with latex free glove and surgilube (surgical lubricant). 10 minutes later patient coded with severe anaphylactic reaction. What could be a reason assuming no new medication administered?



Answer: Possible allergic reaction to Chlorhexidine

Surgilubes (surgical lubricants aka KY Jelly) are usually considered innocuous compound but it contains chlorhexidine. Patients with severe allergy to chlorhexidine may react badly particularly if it enters blood circulation as possible with rectal exam.



References: click to get abstract

1. A Case of Anaphylaxis to Chlorhexidine during Digital Rectal Examination - J Korean Med Sci. 2008 June; 23(3): 526–528.

2. Anaphylaxis to the chlorhexidine component of Instillagel®: a case series - Advance Access published online on November 5, 2008, - British Journal of Anaesthesia

3. Chlorhexidine anaphylaxis in Auckland - Br. J. Anaesth., May 1, 2009; 102(5): 722 - 723.

4. Chlorhexidine anaphylaxis: case report and review of the literature - Contact Dermatitis. 2004 Mar;50(3):113-6

Sunday September 6, 2009
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 yourself 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

Treating Extravasation Injuries - extravasation.org
The use of phentolamine in the prevention of dopamine-induced tissue extravasation - J Crit Care 1998 Mar;13(1):13-20

Saturday September 5, 2009
Nosocomial Pneumonia Risk and Stress Ulcer Prophylaxis - Pantoprazole vs Ranitidine


Background: Stress ulcer prophylaxis (SUP) using ranitidine, a histamine H2 receptor antagonist, has been associated with an increased risk of ventilator-associated pneumonia. The proton pump inhibitor (PPI) pantoprazole is also commonly used for SUP. PPI use has been linked to an increased risk of community-acquired pneumonia. The objective of this study was to determine whether SUP with pantoprazole increases pneumonia risk compared with ranitidine in critically ill patients.

Methods: The cardiothoracic surgery database at our institution was used to identify retrospectively all patients who had received SUP with pantoprazole or ranitidine, without crossover between agents. From January 1, 2004, to March 31, 2007, 887 patients were identified, with 53 patients excluded (pantoprazole, 30 patients; ranitidine, 23 patients). Our analysis compared the incidence of nosocomial pneumonia in 377 patients who received pantoprazole with 457 patients who received ranitidine.

Results:

• Nosocomial pneumonia developed in 35 of the 377 patients (9.3%) who received pantoprazole, compared with 7 of the 457 patients (1.5%) who received ranitidine
• Twenty-three covariates were used to estimate the probability of receiving pantoprazole as measured by propensity score (C-index, 0.77). Using this score, pantoprazole and ranitidine patients were stratified according to their probability of receiving pantoprazole. After propensity adjusted, multivariable logistic regression, pantoprazole treatment was found to be an independent risk factor for nosocomial pneumonia (p = 0.034).
  

Conclusion: The use of pantoprazole for SUP was associated with a higher risk of nosocomial pneumonia compared with ranitidine. This relationship warrants further study in a randomized controlled trial.



Reference

Nosocomial Pneumonia Risk and Stress Ulcer Prophylaxis - A Comparison of Pantoprazole vs Ranitidine in Cardiothoracic Surgery Patients - CHEST August 2009 vol. 136 no. 2 440-447

Friday September 4, 2009 (pediatric pearl)
Poor Nutritional status in children with hypoplastic left heart syndrome

Infants with hypoplastic left heart syndrome (HLHS) experience a high incidence of growth failure in the postoperative period following stage I palliation. The growth failure in these infants may be related to insufficient nutritional intake, gastrointestinal malabsorption, or high energy expenditure. Clinicians are often reluctant to initiate and advance early enteral feedings in this population because of the increased risk of necrotizing enterocolitis and the high incidence of feeding intolerance and gastroesophageal reflux diseaseThe risk of developing necrotizing enterocolitis in infants with HLHS is significantly higher than in neonates with other forms of congenital heart disease (CHD).

This may be related in part to compromised diastolic flow in the mesenteric circulation in infants undergoing Stage 1 palliation with either a Blalock Taussig shunt or an right ventricle to pulmonary artery conduit. Some studies have also found increased permeability of gut mucosal barrier in children with CHD undergoing cardiopulmonary bypass.

The use of an enteral feeding algorithm (Pediatr Crit Care Med 2009; 10:460–466) is a safe and effective means of initiating and advancing enteral nutrition in infants with HLHS following stage I palliation.

Thursday September 3, 2009
Finally relief may be coming from Coumadin


In a study by Connolly they studied the effect of Dabigatran versus Warfarin in Patients with Atrial Fibrillation. Dabigatran is a new oral direct thrombin inhibitor.

In this noninferiority trial, they randomly assigned 18,113 patients who had atrial fibrillation and a risk of stroke to receive, in a blinded fashion, fixed doses of dabigatran — 110 mg or 150 mg twice daily — or, in an unblinded fashion, adjusted-dose warfarin. The median duration of the follow-up period was 2.0 years. The primary outcome was stroke or systemic embolism.

Results:

• Rates of the primary outcome were 1.69% per year in the warfarin group, as compared with 1.53% per year in the group that received 110 mg of dabigatran and 1.11% per year in the group that received 150 mg of dabigatran.
• The rate of hemorrhagic stroke was 0.38% per year in the warfarin group, as compared with 0.12% per year with 110 mg of dabigatran and 0.10% per year with 150 mg of dabigatran.
• The rate of major bleeding was 3.36% per year in the warfarin group, as compared with 2.71% per year in the group receiving 110 mg of dabigatran (P=0.003) and 3.11% per year in the group receiving 150 mg of dabigatran (P=0.31).
• The mortality rate was 4.13% per year in the warfarin group, as compared with 3.75% per year with 110 mg of dabigatran (P=0.13) and 3.64% per year with 150 mg of dabigatran (P=0.051).
  

Conclusions: In patients with atrial fibrillation, dabigatran given at a dose of 110 mg was associated with rates of stroke and systemic embolism that were similar to those associated with warfarin, as well as lower rates of major hemorrhage.

Dabigatran administered at a dose of 150 mg, as compared with warfarin, was associated with lower rates of stroke and systemic embolism but similar rates of major hemorrhage.



Editors note: Unlike Warfarin, Dabigatran acts within hours after ingestion and does not require monitoring




Connolly SJ, Esekowitz MD, Yusuf S, et al. Dabigatran versus Warfarin in Patients with Atrial Fibrillation. N Eng J Med 2009; Published at www.nejm.org August 30, 2009

Wednesday September 2, 2009
Role of Procalcitonin as prognostic factors in COPD exacerbation


Rammaert et al studied the effects of Procalcitonin as a prognostic factor in severe acute exacerbation of chronic obstructive pulmonary disease. A prospective observational cohort study was conducted of 116 consecutive patients with severe acute exacerbation of COPD requiring intubation and mechanical ventilation with their mean age being 67 years and mean simplified physiological score was 43.



Results: Sixty-five per cent of patients had chronic respiratory insufficiency.

• Logistic organ dysfunction score (hazard ratio (95% CI) = 1.19 (1.03–1.37), P = 0.013), rapidly fatal underlying disease (3.33 (1.40–7.87), P = 0.003) and procalcitonin level (1.01 (1–1.03), P = 0.018) were independently associated with increased risk for ICU mortality.
• Non-invasive mechanical ventilation use before intubation was independently associated with reduced risk for ICU mortality (0.34 (0.14–0.84), P = 0.020).
  

Conclusions:

In patients with severe acute exacerbation of COPD requiring intubation and mechanical ventilation, logistic organ dysfunction score, rapidly fatal underlying disease and procalcitonin are independently associated with increased risk for ICU mortality.

Non-invasive mechanical ventilation use before intubation was independently associated with reduced risk for ICU mortality.





Reference:

Rammaert B, Verdier N, Cavestri B, Nseir S. Procalcitonin as a prognostic factor in severe acute exacerbation of chronic obstructive pulmonary disease. Respirology 2009; Published online July 30 2009.

Tuesday September 1, 2009
Is Plavix going to be History??

Recent study by wallentin et al looked at the Ticagrelor (Brilinta®) versus Clopidogrel (Plavix) in patients with Acute Coronary Syndromes.

Ticagrelor is an oral, reversible, direct-acting inhibitor of the adenosine diphosphate receptor P2Y12 that has a more rapid onset and more pronounced platelet inhibition than clopidogrel.

They studied 18624 patients in double blind randomized trial ticagrelor (180-mg loading dose, 90 mg twice daily thereafter) and clopidogrel (300-to-600-mg loading dose, 75 mg daily thereafter) in patients admitted to the hospital with an acute coronary syndrome, with or without ST-segment elevation.

Results: At 12 months

• a composite of death from vascular causes, myocardial infarction, or stroke — had occurred in 9.8% of patients receiving ticagrelor as compared with 11.7% of those receiving clopidogrel.
• Secondary end point: Significant differences in the rates of other composite end points, as well as myocardial infarction alone (5.8% in the ticagrelor group vs. 6.9% in the clopidogrel group, P=0.005).
• Death from vascular causes (4.0% vs. 5.1%, P=0.001) but not stroke alone (1.5% vs. 1.3%, P=0.22).
• Death from any cause was also reduced with ticagrelor (4.5%, vs. 5.9% with clopidogre).
• No significant difference in the rates of major bleeding was found between the ticagrelor and clopidogrel groups (11.6% and 11.2%, respectively; P=0.43), but ticagrelor was associated with a higher rate of major bleeding not related to coronary-artery bypass grafting (4.5% vs. 3.8%, P=0.03), including more instances of fatal intracranial bleeding and fewer of fatal bleeding of other types.

Conclusions: In patients who have an acute coronary syndrome with or without ST-segment elevation, treatment with ticagrelor as compared with clopidogrel significantly reduced the rate of death from vascular causes, myocardial infarction, or stroke without an increase in the rate of overall major bleeding but with an increase in the rate of non–procedure-related bleeding.


Reference:

Wallentin L, Becker RC, Budaj A, et al. Ticagrelor versus Clopidogrel in patients with Acute Coronary Syndromes. N Engl J Med 2009; www.nejm.org August 30, 2009