Cerebral edema

Human once 260 M (convulsions, cerebral edema, cerebral herniation, sustained epileptic state) Boereboom et al. 1998 Technical... 

Cerebral edema - Cerebral edema and other signs of increased vascular permeability (eg, otitis media, nasal and ear stuffiness) have been seen in patients treated with muromonab-CD3 and may accompany some of the other neurologic manifestations. 

These agents produce marked increases in blood pressure that may precipitate cerebral edema, cerebral hemorrhage, and pulmonary edema. Because of the decrease in vessel diameter, total peripheral resistance is increased, which increases afterload. This increases oxygen demand to the myocardium and may precipitate angina. Prolonged therapy may cause myocardial damage. 

ACUTE HEALTH RISKS irritation of skin, eyes, and respiratory system headache vertigo dizziness giddiness weakness convulsions hallucinations delirium nausea vomiting diarrhea rapid respiration coughing pain and tightness in the chest pulmonary edema cerebral edema diffuse interstitial pneumonitis systemic effects on the brain epigastric pain substemal pain cyanosis leukocytosis (increased blood leukocytes) death. 

Acute benzene poisoning results in CNS depression and is characterized by an initial euphoria followed by staggered gait, stupor, coma, and convulsions. Exposure to approximately 4000 ppm benzene results in complete loss of consciousness. Insomnia, agitation, headache, nausea, and drowsiness may persist for weeks after exposure (126). Continued inhalation of benzene to the point of euphoria has caused irreversible encephalopathy with tremulousness, emotional lability, and diffuse cerebral atrophy (125). In deaths arising from acute exposure, respiratory tract infection, hypo- and hyperplasia of sternal bone marrow, congested kidneys, and cerebral edema have been found at autopsy. 

Untoward effects of both E and NE (usually to a lesser degree) are anxiety, headache, cerebral hemorrhage (from vasopressor effects), cardiac arrhythmias, especially in presence of digitaUs and certain anesthetic agents, and pulmonary edema as a result of pulmonary hypertension. The minimum subcutaneous lethal dose of E is about 4 mg, but recoveries have occurred after accidental overdosage with 16 mg subcutaneously and 30 mg intravenously, followed by immediate supportive treatment. 

Hypervitaminosis A is characterized by hepatomegaly, cerebral edema and bone structure alterations. (3-Carotene... 

Some drains act on the body by changing the cellular environment, either physically or chemically. Physical changes in the cellular environment include changes in osmotic pressures, lubrication, absorption, or the conditions on the surface of the cell membrane An example of a drag that changes osmotic pressure is mannitol, which produces a change in the osmotic pressure in brain cells, causing a reduction in cerebral edema A... 

Mannitol (Osmitrol) is used for the promotion of diuresis in the prevention and treatment of the oliguric phase of acute renal failure as well as for the reduction of IOP and the treatment of cerebral edema Urea (Ureaphil) is useful in reducing cerebral edema and in die reduction of IOE Glycerin (Osmoglyn) and isosorbide (Ismotic) are used in the treatment of acute glaucoma and to reduce IOP before and after eye surgery. 

An estimated oral dose of 260 mg endosulfan/kg caused severe seizures in a 43-year-old man, and brain death from cerebral herniation and massive cerebral edema occurred within 4 days of exposure (Boereboom et al. 1998) there were no signs of myocardial infarction and only slight congestion of the heart, but pulmonary congestion and atelectasis were evident at autopsy. 

Similarly, convulsive seizures and a sustained epileptic state persisted after stomach contents were pumped and activated charcoal and anticonvulsive medication were administered in a 43-year-old man who ingested approximately 260 mg/kg endosulfan (Boereboom et al. 1998). At 4 days after exposure, the man was pronounced brain dead, and autopsy revealed cerebral hernia from massive cerebral edema. Eight additional accidental and/or intentional cases of acute poisoning with endosulfan resulting in adverse neurological effects have been reported in more recent studies, six by Blanco-Coronado et al. (1992), one by Lo et al. (1995), and one by Pradhan et al. (1997) two out of the eight resulted in death. Tonic-clonic convulsions were seen in the Blanco-Coronado et al. (1992) cases, whereas Lo et al. (1995) reported the development of muscle fasciculations and episodes of convulsions in their case. In the case reported by Pradhan et al. (1997), the patient had consumed about 75 mL of hquid endosulfan (35% w/v). In this case, in addition to tonic-clonic seizures and myoclonic jerks, the patient developed... 

Signs of acute endosulfan intoxication similar to those reported in humans have been observed in animals. Also, cerebral congestion and edema is often observed at necropsy in animals that die following acute ingestion of endosulfan (Boyd and Dobos 1969 Boyd et al. 1970 Terziev et al. 1974). The severe... 

Serious adverse effects of epinephrine potentially occur when it is given in an excessive dose, or too rapidly, for example, as an intravenous bolus or a rapid intravenous infusion. These include ventricular dysrhythmias, angina, myocardial infarction, pulmonary edema, sudden sharp increase in blood pressure, and cerebral hemorrhage. The risk of epinephrine adverse effects is also potentially increased in patients with hypertension or ischemic heart disease, and in those using (3-blockers (due to unopposed epinephrine action on vascular Ui-adrenergic receptors), monoamine oxidase inhibitors, tricyclic antidepressants, or cocaine. Even in these patients, there is no absolute contraindication for the use of epinephrine in the treatment of anaphylaxis [1,5,6]. 

Slivka A, Murphy E, Horrocks L. Cerebral edema after temporary and permanent middle cerebral artery occlusion in the rat. Stroke 1995 26 1061-1065. 

Excellent biological arguments exist for a direct impact of fever specifically on neurological outcome. On a local level, fever produces increased levels of excitatory amino acids (e.g., glutamate and dopamine), free radicals, lactic acid, and pyr-uvate. There is an increase in cell depolarizations and BBB breakdown. Enzymatic function is impaired and cytoskeletal stability reduced. These events lead to increased cerebral edema, with a possible reduction in CPP as well as larger volumes of ischemic injury. " ... 

MANAGEMENT OF CEREBRAL EDEMA ASSOCIATED WITH ISCHEMIC STROKE... 

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