Brain cerebral edema

Amino groups released by deamination reactions form ammonium ion (NH " ), which must not escape into the peripheral blood. An elevated concentration of ammonium ion in the blood, hyperammonemia, has toxic effects in the brain (cerebral edema, convulsions, coma, and death). Most tissues add excess nitrogen to the blood as glutamine. Muscle sends nitrogen to the liver as alanine and smaller quantities of other amino acids, in addition to glutamine. Figure I-17-1 summarizes the flow of nitrogen from tissues to either the liver or kidney for excretion. The reactions catalyzed by four major enzymes or classes of enzymes involved in this process are summarized in Table T17-1. 

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... 

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... 

Magnetic resonance imaging (MRI) or computed tomography (CT) is used to measure changes in brain size and volume and rule out stroke, brain tumor, or a cerebral edema. 

The goals of treatment of brain metastases are to manage symptoms by reducing cerebral edema, treat the underlying malignancy both locally and systemically, and improve survival. 

In 1954, a proprietary formulation, Stalinon , was marketed in France for oral administration of boils. The formulation was primarily linoleic acid but was contaminated with triethyltin (TET)iodide (LD50 in rats, ca 0.7 mg/kg1) and may have contained the mono-, di- and tetraethyltin compounds. The formulation led to the death of 102 people and the intoxication of more than 200 others. The TET caused altopic cerebral edema of the white matter of the brain. Since the Stalinon Affair , a great deal of control has been exerted in the manufacture and marketing of organotins and few deaths have occurred11. The accidental exposure of six industrial workers to TMT led to one death and to two seriously... 

Patients with acute stroke should be monitored intensely for the development of neurologic worsening, complications, and adverse effects from treatments. The most common reasons for clinical deterioration in stroke patients are (1) extension of the original lesion in the brain (2) development of cerebral edema and raised intracranial pressure (3) hypertensive emergency (4) infection (e.g., urinary and respiratory tract) (5) venous thromboembolism (6) electrolyte abnormalities and rhythm disturbances and (7) recurrent stroke. The approach to monitoring stroke patients is summarized in Table 13-3. 

Dexamethasone Testing of adrenal cortical hyperfunction cerebral edema associated with primary or metastatic brain tumor, craniotomy, or head injury. Tnamc/no/one Treatment of pulmonary emphysema where bronchospasm or bronchial edema plays a significant role, and diffuse interstitial pulmonary fibrosis (Hamman-Rich syndrome) in conjunction with diuretic agents to induce a diuresis in refractory CHF and in cirrhosis of the liver with refractory ascites and for postoperative dental inflammatory reactions. 

Cerebral edema In adults, administer an initial IV dose of 10 mg, followed by 4 mg IM every 6 hours until maximum response has been noted. Response is usually noted within 12 to 24 hours. Dosage may be reduced after 2 to 4 days and gradually discontinued over 5 to 7 days. For palliative management of patients with recurrent or inoperable brain tumors, maintenance therapy with either the injection or tablets in a dosage of 2 mg 2 or 3 times daily may be effective. 

Thyroid 1 uptake may be decreased. False-negative results with the nitroblue-tetrazolium test for bacterial infection. Dexamethasone, given for cerebral edema, may alter the results of a brain scan (decreased uptake of radioactive material). 

MRI is the diagnostic modality of choice. Tumor localization as well as alterations of the blood brain barrier can be characterized for most tumors. However, the differentiation of tumor tissue and cerebral edema is difficult. 

Weakness, dizziness, insomnia, headache, and nausea can occur in mountain travelers who rapidly ascend above 3000 m. The symptoms are usually mild and last for a few days. In more serious cases, rapidly progressing pulmonary or cerebral edema can be life-threatening. By decreasing cerebrospinal fluid formation and by decreasing the pH of the cerebrospinal fluid and brain, acetazolamide can increase ventilation and diminish symptoms of mountain sickness. 

Neurologic disorders Cerebral edema (large doses of dexamethasone are given to patients following brain surgery to minimize cerebral edema in the postoperative period), multiple sclerosis... 

TThe catabolic production of ammonia poses a serious biochemical problem, because ammonia is very toxic. The molecular basis for this toxicity is not entirely understood. The terminal stages of ammonia intoxication in humans are characterized by onset of a comatose state accompanied by cerebral edema (an increase in the brain s water content) and increased cranial pressure, so research and speculation on ammonia toxicity have focused on this tissue. Speculation centers on a potential depletion of ATP in brain cells. 

The use of acetazolamide in the presence of unrecognized cerebral edema due to fat embolism, with sudden normalization of brain C02, as occurred in this patient when her previous state of hypocapnia was no longer sustained by ventilatory effort, resulted in cerebral acidosis, vasodilatation, and a further increase in intracranial pressure. This proved catastrophic and led to brainstem herniation and brain death. Acetazolamide should be avoided if at all possible in patients with bony and traumatic brain injuries, particularly during weaning from mechanical ventilation, since it can precipitate coning in patients with raised intracranial pressure. 

Other than in sensitive individuals, the aromatic nitro compounds are only moderately irritating to the skin, but very toxic to the liver, kidneys and nervous system. The basic mechanism of toxicity is stimulation of oxidative metabolism in cell mitochondria through interference with the normal coupling of carbohydrate oxidation to phosphorylation (ADP to AT ). The increased oxidative metabolism leads to pyrexia, tachycardia, dehydration and the ultimate depletion of fat stores. The most severe toxicity occurs when workers are concurrently exposed to hot, humid environments. Pyrexia and direct action on the brain cause cerebral edema, clinically evidenced by toxic psychosis and, at times, convulsions. Degenerative changes occur in the liver parenchyma, and renal tubules, and clinical signs of renal injury appear (albuminuria, hematuria, pyuria, increased BUN). 

The only information regarding neurological effects in humans after oral exposure to chromium(VI) is the report of an enlarged brain and cerebral edema upon autopsy of a 14-year-old boy who died after ingesting 7.5 mg chromium(VI)/kg as potassium dichromate (Table 2-2 and Figure 2-2). These effects may be the result of accompanying renal failure (Kaufman et al. 1970). 

Brain enlargement and cerebral edema were observed upon autopsy of a boy who died after ingesting potassium dichromate (Kaufman et al. 1970). However, more chronic lower exposures to chromium(III) did not result in any somatopsychic changes in patients on total parenteral nutrition (TPN) solutions (Lovrincevic et al. 1996). In this study, the TPN patients were examined for somatopsychic responses. 

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