Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085383 (hypocapnia)
 1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the study reported here, rabbits were used to develop an experimental model for inducing pulmonary fat embolism by forced immobilization. The emboli were quantitated by a computerized system. The activity of lipoprotein lipase in post-heparin plasma (PHP-LPL) and concentrations of free fatty acids (FFA) were measured. Also, blood gases were analyzed and pulmonary morphology and ultrastructure were observed. Forced immobilization for 5 hours was found to induce pulmonary embolism. This was accompanied by elevation of PHP-LPL and FFA levels in the blood, hypocapnia, and a tendency for insufficiency of pulmonary surfactant. The results suggest that the disorder of homeostasis caused by immobilization is strong enough to bring about pulmonary embolism without bone fracture.
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PMID:Pulmonary fat embolism in rabbits induced by forced immobilization. 156 12

A 19-year-old woman with multiple fractures and mild brain injury developed severe cerebral fat embolism syndrome after "damage control" orthopaedic surgery. Acetazolamide therapy to manage ocular trauma, in association with hyperchloraemia, caused a profound metabolic acidosis with appropriate compensatory hypocapnia. During ventilator weaning, unexpected brainstem coning followed increased sedation and brief normalisation of arterial carbon dioxide concentration. Autopsy found severe cerebral fat embolism and brain oedema. In patients with multiple trauma, cerebral fat embolism syndrome is difficult to diagnose, and may be more common after delayed fixation of long-bone fractures. Acetazolamide should be used with caution, as sudden restoration of normocapnia during compensated metabolic acidosis in patients with raised intracranial pressure may precipitate coning.
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PMID:Cerebral fat embolism syndrome causing brain death after long-bone fractures and acetazolamide therapy. 1753 90

An active duty male presented to the emergency room with dyspnea for 2 days after undergoing liposuction surgery. Upon presentation, the patient was afebrile, tachycardic, tachypneic, and hypoxemic. The initial chest radiograph demonstrated bilateral patchy opacities and the PaO2/FiO2 ratio was <200. The patient was admitted to the medical intensive care unit for supportive care. He was treated empirically for pneumonia. Blood and sputum cultures were negative. A computed tomography angiogram of the chest was negative for pulmonary embolism but did reveal a bilateral, perihilar air space process. The patient's oxygen requirement improved and the abnormal chest radiographic findings resolved over the next 48 hours. Given his clinical presentation, negative workup, and rapid recovery, the patient was given a presumptive diagnosis of pulmonary fat embolism. Fat embolism occurs when adipocytes and small blood vessels are damaged during the liposuction procedure. Patients may present with low-grade fever, tachycardia, tachypnea, hypoxemia, and hypocapnia. The differential diagnosis includes venous thromboembolism, aspiration pneumonitis, and pneumonia. The mainstay of treatment for pulmonary fat embolism is supportive care. The risk of mortality is 5 to 15%.
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PMID:Acute respiratory distress following liposuction. 1761 55