Friday November 13, 2009
Central line complication

A 40-year-old man with Crohn's disease underwent an uncomplicated operation involving lysis of adhesions that were causing intestinal obstruction. After surgery, a cardiologist inserted a central venous catheter through the left subclavian vein. No problems with catheterization were noted. Three weeks later, after discharge, mild pain and edema developed in the patient's right lower leg. He was treated with antibiotics for 1 week, and his symptoms diminished. Six months after the operation, the patient presented with posterior cervical pain. A guide wire, presumably lost during the insertion of the central venous catheter, was protruding from the back of his neck (Panel A, arrow). A computed tomographic scan showed the fractured guide wire in the central venous system (Panel B, arrows). The wire protruding from the back of the neck was removed easily; however, it was difficult to remove the part of the wire involving the saphenous vein, and an open procedure with general anesthesia was required. The involved leg vein was thrombosed and occluded. At 1 year of follow-up, the patient was free of symptoms and signs.

Source:

Guo H, Lee JD, Guo M. Guidewire loss: mishap or blunder? Heart 2006;92:602-602

Thursday November 12, 2009


Q: What percentage of patients may experience neurotoxicity from Amiodarone?

Answer: About 3%

Neurologic problems from Amiodarone use include tremor, gait ataxia, peripheral neuropathy, and cognitive impairment. The primary risk factor for amiodarone neurotoxic effects was duration of treatment, not age, drug dose, sex, or indication for therapy. Where this could be assessed, the adverse effects were usually but not always reversible.

Higher estimates of neurotoxic effects in the early amiodarone era may be related to a much higher daily dose.

Reference: click to get abstract

Frequency, Characteristics, and Risk Factors for Amiodarone Neurotoxicity - Arch Neurol. 2009;66(7):865-869

Wednesday November 11, 2009
Sotalol and electrolytes

Calcium: Taking sotalol with a calcium dramatically reduces the absorption of the drug. Consequently, people who take a calcium supplement should take sotalol an hour before or two hours after the calcium.

Magnesium: Sotalol has a side effect of torsades de pointes. This side effect can be prevented by supplemental magnesium.

Potassium: Sotalol with hypokalemia have an increased risk of developing a serious heart arrhythmia. Therefore, special care should be taken when sotalol is prescribed with potassium-depleting diuretics.

Tuesday November 10, 2009
Management of Renal Failure in End Stage Liver Disease

(Total time 44:21)

Monday November 9, 2009

Q: What is the mechanism of action of B-blockers in reducing portal hypertension which ultimately help in reducing variceal bleeding?

Answer: Nonselective beta-blockers like propranolol and nadolol, reduce portal pressure through both local and systemic effects by 9% to 31%.

Local: In the splanchnic circulation, blockade of the vasodilating beta2 adrenoreceptors results in unrestricted alpha-adrenergic activity, splanchnic arteriolar vasoconstriction, and decreased portal inflow.

Systemic: Blockade of the cardiac beta1 receptors decreases the heart rate and cardiac output and secondarily decreases portal inflow.

Sunday November 8, 2009


Q: Which medicine may transiently reverse hepatic encephelopathy?

Answer: flumazenil

GABA is a neuroinhibitory substance produced in the gastrointestinal tract. Of all brain nerve endings, 24-45% may be GABAergic. Increased GABAergic tone is observed in patients with cirrhosis, perhaps because of decreased hepatic metabolism of GABA.

When GABA crosses the extrapermeable blood-brain barrier of patients with cirrhosis, it interacts with supersensitive postsynaptic GABA receptors. The GABA receptor, in conjunction with receptors for benzodiazepines and barbiturates, regulates a chloride ionophore. Binding of GABA to its receptor permits an influx of chloride ions into the postsynaptic neuron, leading to the generation of an inhibitory postsynaptic potential. Administration of benzodiazepines and barbiturates to patients with cirrhosis increases GABAergic tone and predisposes to depressed consciousness.

The GABA hypothesis is supported by the clinical observation that flumazenil, a benzodiazepine antagonist, can transiently reverse hepatic encephalopathy in patients with cirrhosis.

Saturday November 7, 2009
Naloxone for shock

Background: There is pre-clinical evidence, involving several animal species, suggesting that opioid peptides play a role in the physiopathology of shock (endotoxic, hypovolemic, cardiogenic, spinal, anaphylactic). Many case reports have suggested that naloxone (an opiate antagonist) might be an effective treatment for shock in humans, but others have not supported such a point of view. This controversy led us to undertake a meta-analysis of the available evidence on the efficacy of naloxone as a treatment measure for shock in humans.

Objectives: To evaluate the effectiveness and safety of naloxone in human shock and to estimate the methodological quality of the clinical trials.

Search strategy: We searched the Cochrane Injuries Group Specialised Register, CENTRAL (The Cochrane Library), MEDLINE (Ovid SP), PubMed, EMBASE (Ovid SP), ISI Web of Science: Science Citation Index Expanded (SCI-EXPANDED), and ISI Web of Science: Conference Proceedings Citation Index-Science (CPCI-S) (to December 2008). In order to identify further studies the reference lists of all included papers were examined and the primary investigators of eligible studies were contacted.

Selection criteria: Randomized controlled trials evaluating naloxone in human shock, regardless of the patient's age (adult, child, or neonate).

Data collection and analysis: Three independent review authors extracted data on study design, intervention, outcomes, and methodological quality.

Three independent readers reviewed 120 publications and selected six clinical trials. Overall agreement on study selection was perfect (concordance: 100%). The meta-analysis includes six studies involving 126 patients with septic, cardiogenic, hemorrhagic, or spinal shock.

Main results:

• Naloxone therapy was associated with statistically significant hemodynamic improvement (odds ratio 0.24; 95% confidence interval (CI) 0.09 to 0.68).
• The mean arterial pressure was significantly higher in the naloxone groups than in the placebo groups (weighted mean difference +9.33 mm Hg; 95% CI 7.07 to 11.59). No heterogeneity was found for this outcome.
• The death rate was lower in the naloxone group (odds ratio 0.59; 95% CI 0.21 was 1.67) but this was consistent with the play of chance. A significant heterogeneity was detected for the latter outcome (P less than 0.05).

Authors' conclusions: Naloxone improves blood pressure, especially mean arterial blood pressure. However, the clinical usefulness of naloxone to treat shock remains to be determined and additional randomized controlled trials are needed to assess its usefulness.


This is a Cochrane review abstract and plain language summary, prepared and maintained by The Cochrane Collaboration, currently published in The Cochrane Database of Systematic Reviews 2009 Issue 4, Copyright © 2009 The Cochrane Collaboration. Published by John Wiley and Sons, Ltd.. The full text of the review is available in The Cochrane Library.

This record should be cited as: Boeuf B, Poirier V, Gauvin F, Guerguerian AM, Roy C, Farrell C, Lacroix J. Naloxone for shock. Cochrane Database of Systematic Reviews 2003, Issue 3

http://www.cochrane.org/reviews/en/ab004443.html