Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This report describes a case of two-yr-old female with severe clinical Reye syndrome (Stage III and over), who was treated with not only conventional therapies but also mild hypothermia therapy. She presented acute episodes of tonic convulsion, hepatic dysfunction and intracranial hypertension. The first treatment consisted of the administration of anticonvulsant and mannitol, which were not effective to control intracranial pressure. Therefore, we induced mild hypothermia to rectal temperature of 33-34 degrees C for ten days to control intracranial hypertension as well as barbiturate therapy and hyperventilation under mechanical ventilation. Although she had hypokalemia, atelectasis of the right upper lung lobe and thrombocytopenia as the side effects during this therapy, we effectively controlled ICP. Glucose fluid therapy is recommended for Reye syndrome. We especially should pay attention to hypokalemia because of hyperventilation, absorption of potassium with insulin and transudation of potassium from the intestine. We determined the initiation and weaning of mild hypothermia therapy by findings of MRI as well as intracranial pressure. MRI findings will contribute to the determination of initiation and weaning of mild hypothermia therapy. Mild hypothermia therapy should be considered in patients with severe clinical Reye syndrome if conventional supportive therapies are not effective.
 ...
PMID:[Successful use of mild hypothermia therapy in a patient with severe clinical Reye syndrome]. 1205 35

A 41-year-old man was admitted to our hospital suffering from generalized convulsion with a high fever and disturbed consciousness one week after exhibiting flu-like symptoms. We made a diagnosis of acute viral encephalitis, based on the clinical features and the evidence of pleocytosis with an increase in protein in the CSF. On admission, MRI was normal and CRP was negative. The levels of transaminase, ammonia, and blood sugar were normal, so that an adult Reye's syndrome could be ruled out. Herpes simplex encephalitis and influenza encephalopathy were also ruled out because of viral examinations, and specific agents could not be determined. Clinical symptoms subsided once after he was treated with dexamethasone, acyclovir, and anti-convulsants, until generalized convulsion accompanied by a high fever again occurred on the 9th day. On the 18th day, the patient showed anisocoria and ataxic respiration due to severe brain edema. Mild hypothermia therapy to rectal temperature 35 degrees C was induced under mechanical ventilation. Cranial CT taken 3 days after the therapy began to show the improvement of the brain edema. After 7 days of the therapy, his clinical symptoms began to recover dramatically. On the 46th day, he was discharged from hospital without showing almost any neurological symptoms. Mild hypothermia therapy should be considered for adult patients as well as non-adult patients suffering from acute encephalitis with severe intracranial hypertension.
 ...
PMID:[Successful use of mild hypothermia therapy in an adult patient of non-herpetic acute encephalitis with severe intracranial hypertension]. 1283 82

Intracranial pressure (ICP) is the pressure exerted by cranial contents on the dural envelope. It comprises the partial pressures of brain, blood and cerebrospinal fluid (CSF). Normal intracranial pressure is somewhere below 10 mmHg; it may increase as a result of traumatic brain injury, stroke, neoplasm, Reye's syndrome, hepatic coma, or other pathologies. When ICP increases above 20 mmHg it may damage neurons and jeopardize cerebral perfusion. If such a condition persists, treatment is indicated. Control of ICP requires measurement, which can only be performed invasively. Standard techniques include direct ventricular manometry or measurement in the parenchyma with electronic or fiberoptic devices. Displaying the time course of pressure (high-resolution ICP tonoscopy) allows assessment of the validity of the signal and identification of specific pathological findings, such as A-, B- and C-waves. When ICP is pathologically elevated--at or above 20-25 mmHg--it needs to be lowered. A range of treatment modalities is available and should be applied with consideration of the underlying cause. When intracranial hypertension is caused by hematoma, contusion, tumor, hygroma, hydrocephalus or pneumatocephalus, surgical treatment is indicated. In the absence of a surgically treatable condition, ICP may be controlled by correcting the patient's position, temperature, ventilation or hemodynamics. If intracranial hypertension persists, drainage of CSF via external drainage is most effective. Other first-tier options include induced hypocapnea (hyperventilation; paCO2 < 35 mmHg), hyperosmolar therapy (mannitol, hypertonic saline) and induced arterial hypertension (CPP concept). When autoregulation of cerebral blood flow is compromised, hyperoncotic treatment aimed at reducing vasogenic edema and intracranial blood volume may be applied. When intracranial hypertension persists, second-tier treatments may be indicated. These include 'forced hyperventilation' (paCO2 < 25 mmHg), barbiturate coma or experimental protocols such as tris buffer, indomethacin or induced hypothermia. The last resort is emergent bilateral decompressive craniectomy; once taken into consideration, it should be performed without undue delay.
 ...
PMID:Prevention and treatment of intracranial hypertension. 1828 35

We present an 11-year-old boy diagnosed as having acute encephalopathy and liver failure with the underlying condition of a metabolic dysfunction. He developed convulsions and severe consciousness disturbance following gastroenteritis after the ingestion of some fried rice. He showed excessive elevation of transaminases, non-ketotic hypoglycemia and hyperammonemia, which were presumed to reflect a metabolic dysfunction of the mitochondrial beta-oxidation, and he exhibited severe brain edema throughout the 5th hospital day. He was subjected to mild hypothermia therapy for encephalopathy, and treated with high-dose methylprednisolone, cyclosporine and continuous hemodiafiltration for liver failure, systemic organ damage and hyperammonemia. The patient recovered with the sequela of just mild intelligence impairment. In this case, Bacillus cereus, producing emetic toxin cereulide, was detected in a gastric fluid specimen, a stool specimen and the fried rice. It was suggested that the cereulide had toxicity to mitochondria and induced a dysfunction of the beta-oxidation process. The patient was considered as having an acute encephalopathy mimicking Reye syndrome due to food poisoning caused by cereulide produced by B. cereus.
 ...
PMID:Acute encephalopathy of Bacillus cereus mimicking Reye syndrome. 1979 86


<< Previous 1 2