salicylates and Brain-Edema

Cerebral edema is a potentially life-threatening complication shared by diseases of different etiology, such as diabetic ketoacidosis, acute liver failure, high altitude exposure, dialysis disequilibrium syndrome, and salicylate intoxication. Pulmonary edema is also habitually present in these disorders, indicating that the microcirculatory disturbance causing edema is not confined to the brain. Both cerebral and pulmonary subclinical edema may be detected before it becomes clinically evident. Available evidence suggests that tissue hypoxia or intracellular acidosis is a commonality occurring in all of these disorders. Tissue ischemia induces physiological compensatory mechanisms to ensure cell oxygenation and carbon dioxide removal from tissues, including hyperventilation, elevation of red blood cell 2,3-bisphosphoglycerate content, and capillary vasodilatation. Clinical, laboratory, and necropsy findings in these diseases confirm the occurrence of low plasma carbon dioxide partial pressure, increased erythrocyte 2,3-bisphosphoglycerate concentration, and capillary vasodilatation with increased vascular permeability in all of them. Baseline tissue hypoxia or intracellular acidosis induced by the disease may further deteriorate when tissue oxygen requirement is no longer matched to oxygen delivery resulting in massive capillary vasodilatation with increased vascular permeability and plasma fluid leakage into the interstitial compartment leading to edema affecting the brain, lung, and other organs. Causative factors involved in the progression from physiological adaptation to devastating clinical edema are not well known and may include uncontrolled disease, malfunctioning adaptive responses, or unknown factors. The role of carbon monoxide and local nitric oxide production influencing tissue oxygenation is unclear.

Topics: Altitude Sickness; Animals; Brain Edema; Capillaries; Diabetic Ketoacidosis; Humans; Ischemia; Liver Failure, Acute; Renal Dialysis; Salicylates

Topics: Antidepressive Agents, Tricyclic; Arrhythmias, Cardiac; Brain Diseases; Brain Edema; Diazepam; Gastric Lavage; Humans; Hypotension; Myocardial Infarction; Pacemaker, Artificial; Physostigmine; Pyridostigmine Bromide; Respiration, Artificial; Salicylates

Topics: Acute Kidney Injury; Barbiturates; Brain Edema; Humans; Hyperkalemia; Methanol; Methods; Osmolar Concentration; Osmotic Pressure; Peritoneal Dialysis; Poisoning; Pulmonary Edema; Salicylates; Time Factors; Uremia

The course of 177 consecutive patients with severe salicylate self-poisoning treated in an intensive care unit (ICU) during a period of 15 years is presented. On admission, cerebral depression was observed in 61% respiratory failure was present in 47%, acidosis in 36% and cardiovascular function was impaired in 14%. A mortality rate of 15% was observed, which was proportionally higher in patients more than 40 years old and in patients with delayed diagnosis. Twenty-seven patients died and an autopsy was performed on 26 patients. The main autopsy diagnosis was ulcers of the gastrointestinal tract in 46%, pulmonary oedema in 46%, cerebral oedema in 31% and cerebral haemorrhage in 23%.

Topics: Acute Disease; Adolescent; Adult; Aged; Aged, 80 and over; Brain Edema; Cerebral Hemorrhage; Child; Child, Preschool; Duodenal Ulcer; Female; Humans; Infant; Intensive Care Units; Male; Middle Aged; Pulmonary Edema; Respiratory Distress Syndrome; Retrospective Studies; Salicylates; Salicylic Acid; Stomach Ulcer; Suicide, Attempted

Histology or necropsy records of 13 children with accidental or therapeutically induced salicylate intoxication were examined for the presence of hepatic and cerebral pathology findings characteristic of Reye's syndrome. Liver sections stained with haematoxylin and eosin showed intrahepatocytic microvesiculation (10 of 12 children) and absence of significant inflammation or necrosis (10 of 12 children). All 6 specimens of liver tissue stained with oil red O showed intrahepatocytic microvesicular fat with central hepatocytic nuclei distributed either diffusely throughout the lobule or more prominently in the lobular periphery. Liver tissue stained with the periodic-acid/Schiff method showed complete absence of stainable glycogen in 5 of 6 children. 9 of 12 children for whom information was available had cerebral oedema. It is concluded that the light-microscopy hepatic findings and the gross cerebral findings for the majority of these children with salicylate intoxication are the same as those for children with Reye's syndrome.

Topics: Accidents, Home; Acute Disease; Adolescent; Brain; Brain Edema; Child; Child, Preschool; Female; Humans; Infant; Liver; Liver Glycogen; Male; Reye Syndrome; Salicylates; Staining and Labeling

Topics: Aspirin; Brain Edema; Child, Preschool; Coma; Female; Humans; Infant; Mannitol; Salicylates; Time Factors

Topics: Adolescent; Brain Edema; Electroencephalography; Female; Humans; Rheumatic Fever; Salicylates