Neurogenic pulmonary edema due to delayed radiation necrosis
نویسندگان
چکیده
منابع مشابه
Mechanisms of neurogenic pulmonary edema.
The pulmonary edema that develops quickly after a variety of cerebral insults, such as head injury, epileptic seizures, intracranial hypertension, and subarachnoid hemorrhage, is often accompanied by rapid flooding of airways with a protein-rich edema fluid (Weisman, 1939; MacKay, 1950; Richards, 1963; Simmons et al., 1968; Ciongoli and Posner, 1972; Theodore and Robin, 1976; Fisher and AboulNa...
متن کاملNeurogenic pulmonary edema due to traumatic brain injury: evidence of cardiac dysfunction.
BACKGROUND Acute neurogenic pulmonary edema, a common and underdiagnosed clinical entity, can occur after virtually any form of injury of the central nervous system and is a potential early contributor to pulmonary dysfunction in patients with head injuries. OBJECTIVE To explore myocardial function in patients with evident neurogenic pulmonary edema after traumatic head injury. METHODS Duri...
متن کاملNeurogenic pulmonary edema: a current literature review.
Neurogenic pulmonary edema in the setting of critically ill neurologic patients is a condition that is not fully understood, and it is a relatively rare condition. Severe brain damage, such as cerebral and subarachnoid hemorrhage, head injuries and seizures, represents a risk factor for developing neurogenic pulmonary edema. Misdiagnosis and inappropriate management may worsen cerebral damage b...
متن کاملMechanisms of neurogenic pulmonary edema development.
Neurogenic pulmonary edema is a life-threatening complication, known for almost 100 years, but its etiopathogenesis is still not completely understood. This review summarizes current knowledge about the etiology and pathophysiology of neurogenic pulmonary edema. The roles of systemic sympathetic discharge, central nervous system trigger zones, intracranial pressure, inflammation and anesthesia ...
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ژورنال
عنوان ژورنال: Indian Journal of Critical Care Medicine
سال: 2005
ISSN: 0972-5229,1998-359X
DOI: 10.4103/0972-5229.16266