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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A high mortality rate still exists for the patient with ARDS 20 years after the severe syndrome was first formally defined. Hypoxia and hypercarbia remain major clinical challenges requiring mechanical ventilation. The pulmonary vascular bed has been identified as a prime site of injury. The major working hypothesis is that cellular injury is caused by oxyradicals produced by activated neutrophils. There is no present pharmacologic therapy based on this hypothesis. Steroids have no demonstrable effect on outcome. Major advances have been made in the use of extracorporeal membrane lungs to relieve hypercarbia and hypoxia while minimizing pulmonary oxygen toxicity and barotrauma. The most promising current technique is extracorporeal CO2 removal during venovenous perfusion. Further advances must await definition of the early stages of the ARDS.
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PMID:Adult respiratory distress syndrome in the trauma patient. 240 41

Cerebellar masses are a heterogenous group of conditions that can cause compression of the aqueduct or fourth ventricle, resulting in obstructive hydrocephalus, brainstem compression, and upward/downward herniation as a direct result of mass effect. Untreated lesions can be fatal in a few hours, but prompt and appropriate treatment of the mass effect can produce very good outcomes. These patients should be closely followed in a critical care setting that has rapid access to neurosurgical expertise. Medical measures to decrease brain edema should be taken, including elevation of the head of the bed and avoidance of hypo-osmolar solutions, hypercarbia, or hyperthermia. Osmotic diuretics should be initiated promptly in patients with clinical worsening and radiographic evidence of edema resulting in mass effect. However, medical measures should not delay surgical intervention, which should proceed as rapidly as possible when indicated. Cerebellar hemorrhages more than 3 cm in diameter and cerebellar hemispheric strokes involving more than one third of the hemisphere should be considered for early suboccipital craniotomy with decompression. Regardless of lesion size, neurologic deterioration and radiologic signs of obstructive hydrocephalus should call for emergency decompressive surgery with resection of hematoma or necrotic brain tissue. Ventriculostomy should be considered as a bridge to surgical decompression, given the theoretical concern of upward herniation mediated by supratentorial drainage in the face of an underlying posterior fossa mass lesion. Steroids are not indicated for cerebrovascular disease but should be used to treat vasogenic edema induced by tumor. Anticoagulation is reserved for cerebellar venous and dural sinus thrombosis. Specific treatments targeting the underlying pathology should be used aggressively: thrombolysis and endovascular interventions for eligible stroke patients, antibiotic therapy for abscesses, and radiotherapy, chemotherapy, or both for tumors.
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PMID:Treatment of cerebellar masses. 1833 36