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Overdose ethanol

Low antiepileptic drug levels, drug overdose (e.g., cocaine, isoniazid, theophylline, phenothiazine), ethanol-related, and drug withdrawal... [Pg.132]

Chronic ethanol use increases the risk of hepatotoxicity when acetaminophen is used in high doses however, acute ingestion of alcohol along with an acetaminophen overdose decreases the toxicity of acetaminophen. [Pg.534]

Musshoff et al. [35] developed a method for the enantiomeric separation of the synthetic opioid agonist tramadol and its desmethyl metabolite using a Chiralpak AD column containing amylose tris-(3,5-dimethylphenylcarbamate) as chiral selector and a n-hexane/ethanol, 97 3 v/v (5mM TEA) mobile phase nnder isocratic conditions (1 mL/min). After atmospheric pressure chemical ionization (APCI), detection was carried out in positive-ion MS-MS SRM mode. The method allowed the confirmation of diagnosis of overdose or intoxication as well as monitoring of patients compliance. [Pg.666]

Treatment for severe ethanol overdose is generally supportive. Increased intracranial pressure can be relieved by intravenous administration of hypertonic mannitol. Hemodialysis can accelerate the removal of ethanol from the body. Stimulants of ethanol metabolism, such as fructose, are not sufficiently effective, and use of analeptics is not recommended because of the possibility of precipitating convulsions. [Pg.415]

Ethanol is a vasodilator, probably as a result of both CNS effects (depression of the vasomotor center) and direct smooth muscle relaxation caused by its metabolite, acetaldehyde. In cases of severe overdose, hypothermia—caused by vasodilation—may be marked in cold environments. Ethanol also relaxes the uterus and—before the introduction of more effective and safer uterine relaxants (eg, calcium channel antagonists)—was used intravenously for the suppression of premature labor. [Pg.495]

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. [Pg.1260]

Ethanol, also known simply as alcohol, is by far the most widely used depressant. Its structure is shown in Figure 14.34. In the United States, about a third of the population, or about 100 million people, drink alcohol. It is well established that alcohol consumption leads to about 150,000 deaths each year in the United States. The causes of these deaths are overdoses of alcohol alone, overdoses of alcohol combined with other depressants, alcohol-induced violent crime, cirrhosis of the liver, and alcohol-related traffic accidents. [Pg.504]

The concept of clearance is useful in pharmacokinetics because clearance is usually constant over a wide range of concentrations, provided that ehmination processes are not saturated. Saturation of biotransformation and excretory processes may occur in overdose and toxic okinetic effects should be considered. If a constant fraction of drug is eliminated per unit time, the elimination follows first-order kinetics. However, if a constant amount of drug is eliminated per unit time, the elimination is described by zero-order kinetics. Some drugs, for example, ethanol, exhibit zero-order kinetics at normal or non-intoxicating concentrations. However, for any drug that exhibits first-order kinetics at therapeutic or nontoxic concentrations, once the mechanisms for elimination become saturated, the kinetics become zero order and clearance becomes variable.3... [Pg.10]

Toxicity. Methapyrilene has been shown to be carcinogenic in rats and is little used. Fatalities have occurred after ingestion of 7 g or more and toxic effects have been associated with plasma concentrations greater than 30 pg/ml. In 13 fatalities attributed to methapyrilene overdose, reported blood concentrations ranged from 2 to 380 pg/ml (mean 50) (salicylamide and ethanol were also detected in several cases). [Pg.746]

Somnolence was reported in a 27-year-old subject following an overdose of opipramol a maximum serum concentration of 0.115 pg/ml was determined ethanol was also detected (O. L. Pedersen et ai, Eur. J. clin. Pharmac., 1982, 23, 513-521). [Pg.832]

Rothrock JF, Johnson PC, Rothrock SM, Merkley R. Fulminant polyneuritis after overdose of disulfiram and ethanol. Neurology 1984 34(3) 357-9. [Pg.1151]

A 37-year-old man with a history of ethanol abuse presented with hepatic failure and non-cardiogenic pulmonary edema after an overdose of paracetamol, codeine, ibuprofen, and diazepam. He received two... [Pg.3681]

Frequently, diazepam overdoses are adequately managed with clinical observation and supportive care. However, coingestion of ethanol and other CNS depressants which may exacerbate toxicity are common and warrant investigation in the patient history. Flumazenil, a benzodiazepine antagonist, effectively reverses symptoms of CNS toxicity, but is hazardous with the coingestion of other substances such as antidepressants. Therefore, it should not be used routinely. [Pg.784]

The target organ of ether is the CNS. Inhalation of high concentrations may cause CNS effects including headache, dizziness, unconsciousness, and coma. It is, however, rare to And death due to an inhalation exposure. Ingestion poisonings are of rapid onset, short duration and clinically similar to ethanol overdose. Diethyl ether is an irritant to the eye, skin, and mucous membranes. [Pg.844]

The mainstay of medical treatment of patients with ethanol toxicity is supportive care. In general, a conservative approach is recommended for ethanol intoxication. Supportive therapy for overdose may include treatment for respiratory depression, hypotension, and altered glucose or thiamine levels. If the ingestion occurred within one hour of presentation, placing a nasogastric tube and evacuating the stomach contents can prove helpful. In patients with chronic ethanol abuse, therapy may include administration of thiamine to prevent neurologic injury. The administration of medications to cause emesis is not recommended because of the rapid onset of CNS depression as well as aspiration risks. [Pg.1076]

Recommended treatment for acute colloidon ingestions is similar to that recommended for ethanol or ether overdose, including gastric lavage. [Pg.1823]

Benzodiazepines are involved in many intentional overdoses. While these overdoses are rarely fatal when a benzodiazepine is the sole ingestant, they often complicate overdoses with other central nervous system depressants (e.g., ethanol and sedatives) due to their synergistic activity. Flumazenil finds its greatest utility in the reversal of benzodiazepine-induced sedation from minor surgical procedures. The initial flumazenil dose is 0.2 mg and should be administered intravenously over 30 s. If no response occurs after an additional 30 s, a second dose is recommended. Additional incremental doses of 0.5 mg may be administered at 1 min intervals until the desired response is noted or until a total of 3 mg has been administered. Flumazenil should not be administered... [Pg.2044]


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