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Biomedical subjects

A R Colohan

Publications and source records attributed to A R Colohan.

24 records · Page 2Linked to original sources
PubMed1985

Intravenous fluid loading as prophylaxis for paradoxical air embolism.

Paradoxical cerebral air embolism has been described in neurosurgical operations performed on patients in the seated position. This problem is thought to result most often from a probe-patent foramen ovale. It has been postulated that right atrial pressure exceeds left atrial pressure when paradoxical air embolism occurs. A study is described in which intravenous fluid loading is compared with routine fluid management in 20 patients undergoing neurosurgical operations in the seated position. In order to investigate if intravenous fluid loading would decrease the risk of paradoxical air embolism during neurosurgical operations on seated patients, 20 patients were assigned randomly to two groups: 10 patients received normal intravenous fluid replacement (1220 +/- 102 ml), and 10 received augmented fluid replacement (2800 +/- 400 ml). Right atrial and pulmonary capillary pressures were monitored for evidence of an interatrial pressure gradient that would force air emboli from the right atrium into the left atrium via a probe-patent foramen ovale. Four of 10 patients receiving routine fluid administration developed right atrial pressure greater than pulmonary capillary wedge pressure (and hence, indirectly, greater than left atrial pressure), whereas none of the 10 patients with augmented fluid loading developed this condition (p = 0.04). The authors conclude that augmented intravenous fluid loading may be effective in preventing systemic air embolism during neurosurgical operations performed on patients in the seated position.

Adolescent↗
PubMed1985

Frontal sinus approach to the orbit. Technical note.

The authors have previously advocated a supraorbital approach to tumors of the orbit. In this paper, they describe a technique in which they take advantage of a large frontal sinus as a means of entering the orbit without the necessity of intracranial exposure, as required by the more conventional supraorbital approach. This is achieved without frontal burr holes, allowing for a superior cosmetic result. The anterior wall of the frontal sinus is removed, and with it the roof of the orbit as a single bone flap. A case in which this technique was used is described.

Female↗
PubMedDate not supplied

Cerebral vasospasm following aneurysmal subarachnoid hemorrhage.

Cerebral vasospasm following aneurysmal subarachnoid hemorrhage is one of the most important causes of cerebral ischemia, and is the leading cause of death and disability after aneurysm rupture. There are two definitions of cerebral vasospasm: angiographic and clinical. Care must be exercised to be certain that it is clear which entity is being addressed. The diagnosis of the clinical syndrome is one of exclusion and can rarely be made with absolute certainty. The pathogenesis of cerebral vasospasm is poorly understood. Most current theories focus on the release of factors from the subarachnoid clot. More attention must be given to the role of endothelial damage and alterations in the blood-arterial wall barrier. The application of modern techniques for studying vascular smooth muscle which have been developed as a result of research in the areas of hypertension and atherosclerosis must be applied to the problem of cerebral vasospasm. A stress test to select patients with angiographic arterial narrowing who have adequate cerebral vascular reserve to undergo surgery should be developed. The optimal treatment of vasospasm awaits development of agents for blocking or inactivating spasmogenic substances or blocking arterial smooth muscle contraction. Rheological or hemodynamic manipulations to prevent or reverse ischemic consequences of vasospasm are relatively effective, but complicated and hazardous, and should be viewed principally as interim measures awaiting development of more specific therapies for the arterial narrowing.

Anti-Inflammatory Agents↗
PubMedDate not supplied

The effect of dichloroacetate on brain lactate levels following incomplete ischemia in the hyperglycemic rat.

Dichloroacetate (DCA) is known to prevent the phosphorylation of the pyruvate dehydrogenase complex (PDHC) by blocking the action of PDH kinase. This action allows the active PDHC to exert its effect on the metabolism of glucose, lactate and alanine to acetyl CoA. DCA has been shown to reduce serum lactate levels in humans and animals in such conditions as diabetes, phenformin-induced hepatic failure, exercise, and endotoxin-induced shock. Lactic acidosis in the brain has often been postulated as a cause of neuronal damage following ischemia and hypoxia. Therefore, we examined the effect of intravenously administered DCA (100 mg/kg) in rats that were rendered hyperglycemic by intravenous glucose (2 g/kg), and then made to undergo 15 minutes of incomplete cerebral ischemia by bilateral carotid ligation and systemic hypotension (mean arterial pressure of 50 mm Hg). DCA significantly reduced serum lactate levels pre-ischemia, but had no effect on serum lactate levels after ischemia induction. Brain levels of lactate, ATP and PCr after 15 minutes of incomplete ischemia were unaffected by DCA. We conclude that in this in-vivo model the control of PDHC activity in the brain may be different than that in the periphery, and that DCA was not effective in reducing brain tissue lactate levels.

Acetates↗