Publications by authors named "Manuel M Buitrago Blanco"

Hepatopulmonary syndrome (HPS), defined by the presence of pulmonary vascular dilatations that cause right-to-left transpulmonary shunting of venous blood with a consequential increase in the alveolar-arterial oxygen gradient, is a relatively frequent complication of chronic liver disease. While orthotopic liver transplantation (OLT) is indicated and often curative in HPS patients with end-stage liver disease (ESLD), little is known about the peri- and post-operative-period risks of CVA in OLT recipients with HPS. : We report a case series of five non-consecutive OLT recipients with HPS who developed ischemic and/or hemorrhagic CVAs during or shortly after OLT, raising concern that the risks of neurological complications remain increased even after OLT.

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We have reviewed the English literature published in the last 70 years on Diseases of the Vertebral Basilar Circulation, or Posterior Circulation Disease (PCD). We have found that errors have been made in the conduct and interpretation of these studies that have led to incorrect approaches to the management of PCD. Because of the difficulty in evaluating the PC, the management of PCD has been incorrectly applied from anterior circulation disease (ACD) experience to PCD.

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Background: Isolated acute foot drop due to traumatic brain injury is exceedingly rare and is often misdiagnosed during initial evaluation. Here, we present the case of a patient who presented with left foot drop after falling off a bicycle.

Case Description: The patient is a 55-year-old male who was mountain biking when he fell, hit his head, and lost consciousness.

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This article reviews key concepts of cerebral glucose metabolism, neurologic outcomes in clinical trials, the biology of the neurovascular unit and its involvement in secondary brain injury after traumatic brain insults, and current scientific and clinical data that demonstrate a better understanding of the biology of metabolic dysfunction in the brain, a concept now known as cerebral metabolic energy crisis. The use of neuromonitoring techniques to better understand the pathophysiology of the metabolic crisis is reviewed and a model that summarizes the triphasic view of cerebral metabolic disturbance supported by existing scientific data is outlined. The evidence is summarized and a template for future research provided.

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