Saturday November 14, 2009
How Wound V.A.C. Therapy System works

The V.A.C. Therapy System is comprised of three essential components that actively work together to help induce cellular wound healing through promotion of granulation tissue formation.

1. V.A.C. Therapy Unit Provides intermittent and continuous therapy with integrated patient safety features
2. SensaT.R.A.C.™ Technology Regulates pressure at the wound site to provide accurate delivery of prescribed therapy settings
3. V.A.C. GranuFoam™ Dressings Help induce the necessary mechanisms to promote granulation tissue formation

How V.A.C. Therapy Works on the Cellular Level

Under negative pressure, V.A.C. Therapy with V.A.C. GranuFoam Dressings applies both mechanical and biological forces to the wound to create an environment that promotes wound healing. These forces are known as macrostrain and microstrain.

Macrostrain is the visible stretch that occurs when negative pressure contracts the foam. Macrostrain

• Draws wound edges together
• Provides direct and complete wound bed contact
• Evenly distributes negative pressure
• Removes exudate and infectious materials

Microstrain is the microdeformation at the cellular level, which leads to cell stretch. Microstrain:

• Reduces edema
• Promotes perfusion
• Increases cellular proliferation and migration
• Promotes granulation tissue formation
  

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.