Exposure , hypothermia caused

Attempts to diminish the overall metabolism of trichloroethylene might be useful (e.g., hypothermia, mixed-function oxidase inhibitors, competitive inhibitors of trichloroethylene metabolism [i.e., P-450 substrates]), if instituted soon enough after trichloroethylene exposure. Catecholamines (especially beta agonists) act in concert with trichloroethylene, increasing the risk of cardiac arrhythmias. Hence, catecholamines should be administered to patients only in the lowest efficacious doses and for certain limited presentations of trichloroethylene poisoning. Ethanol should also be avoided because concurrent exposure to trichloroethylene and ethanol can cause vasodilation and malaise and may potentiate central nervous system depression at high dosage levels of either compound. 

Thermal burns result from the radiant heat emitted by a hydrogen fire and absorbed by a person, which is directly proportional to many factors including exposure time, burning rate, heat of combustion, size of the burning surface, and atmospheric conditions (mainly wind and humidity). For instance, thermal radiation flux exposure level of 0.95 W/cm2 may cause skin burns in 30 s. Cryogenic burns may result from contact with cold fluids or cold vessel surfaces. Exposure to large liquefied hydrogen spills could result in hypothermia, if proper precautions are not taken [17]. 

Systemic effects of nickel exposure include hyperglycemia, increased levels of plasma glucagon, damage to the pancreatic islet cells, decreased body weight, reduced food and water intake, and hypothermia (NAS 1975 USEPA 1980 USPHS 1993). Acute administration of nickel salts caused prompt hyperglucagonemia and subsequent hyperinsulinemia in rats, rabbits, and guinea pigs (WHO... 

Rabbits exposed to 190 ppm for 6 hours/day for 50 days showed slight liver and kidney injury. At 3 09 ppm there was slight conjunctival irritation, and at 1414ppm lethargy was observed. At 3082 ppm effects were incoordination, salivation, labored breathing, narcosis, and some deaths. Five of six rats survived exposure to 2 000 ppm for 4 hours, but 4000 ppm caused coma and death of all six. Narcosis, hypothermia, and decreased respiration were observed in guinea pigs exposed to 4000 ppm for 6 hours. Recovery from narcosis was slow, and 3 of 10 animals died within 4 days of exposure. 

Patients with ethanol or sedative-hypnotic overdose may be euphoric and rowdy ("drunk") or in a state of stupor or coma ("dead drunk"). Comatose patients often have depressed respiratory drive. Depression of protective airway reflexes may result in aspiration of gastric contents. Hypothermia may be present because of environmental exposure and depressed shivering. Ethanol blood levels greater than 300 mg/dL usually cause deep coma, but regular users are often tolerant to the effects of ethanol and may be ambulatory despite even higher levels. Patients with GHB overdose are often deeply comatose for 3-4 hours and then awaken fully in a matter of minutes. 

In the two last cases, the most common causes of hypothermia, such as hypothyroidism, infection, and cold exposure, were ruled out. 

Psychiatric nurses and psychiatrists are particularly well suited as members of the medical team, as they can also be alert to organic mental disorders caused by conditions such as head injuries, toxic exposures, preexisting illnesses, dehydration, or hyper-/hypothermia. Because nurses have a tradition of practice in homes, in schools, and other natural settings, they tend to be readily accepted by members of the community. Agencies and staff that will be activated for counseling and... 

Acute oral administration of amitraz causes central nervous system (CNS) depression. The toxic effects of amitraz are possibly from a2-adrenoreceptor agonist action. Chronic exposure of amitraz results in CNS depression, increases blood glucose levels, and produces hypothermia. 

With chronic exposure, side effects may include rash, thrombocytopenia, leukopenia, and a lupus-like disorder. Chronic therapy is likely to result in tolerance, and withdrawal symptoms if primidone therapy is abruptly stopped. Doses in excess of 1500 mg (twice the maximum recommended daily dose) should be considered toxic. Less common side effects are hypotension, hypothermia, and dermal bullae. Encephalopathy has been observed in an epileptic patient with high plasma levels and poor renal function. With plasma concentrations exceeding 80pgml primidone may precipitate and cause crystalluria. Plasma levels >10 rgpml are associated with toxic effects. The therapeutic range is reportedly 5-10pgml , but clinical effects correlate more closely with phenobarbital blood levels. 

Aerobiologists at the U.S. Army Medical Research Institute of Infectious Diseases (Fort Detrick, MD) have developed a reproducible, head-only ricin aerosol exposure model for laboratory nonhuman primates (NHP) that yielded acute LCtso values for African green monkeys or rhesus monkeys corresponding to approximately 6-10 or 15 pg/kg, respectively (Wilhelmsen and Pitt, 1996). Exposure of NHP to aerosolized ricin (particle size 1-2 pm) caused a dose-dependent toxicity that is delayed from 8 to 24 h early anorexia and lethargy were frequently observed, followed by gastric distress, hypothermia, hypotension, acute respiratory distress, and death. Rhesus monkeys exposed to the equivalent of approximately 20-40 pg/kg ricin by aerosol died from acute respiratory distress about 36-48 h after exposure necropsy revealed fibrinopurulent pneumonia, acute inflammation of the trachea and airways, and massive pulmonary alveolar flooding (Wilhelmsen and Pitt, 1996). 

SEB and ricin can cause similar systemic symptoms, however, neither of them produce eye or skin symptoms. If the eyes are exposed, eye pain, tearing, redness, foreign-body sensation, and blurred vision may result. Irrespective of the route of exposure, when the toxin reaches the rest of the body s systems, it may cause weakness, prostration, dizziness, ataxia, and loss of coordination. When victims have been exposed to lethal doses, tachycardia, hypothermia, and hypotension follow. Death may occur in minutes, hours, or days. No antidotes are known for mycotoxins. Treatment is supportive and symptomatic. 

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