Ethanol coma caused

Alcohol is a common cause of coma in all age ranges. Coma depth and length is associated with the amount of alcohol ingested, and this shows wide inter-paiiem variation. Alcoholic coma can be associated with head injuries, hypothermia and the presence of other drugs with which its action may be additive. In most cases, coma caused by ethanol will resolve relatively rapidly, the exception being when there is hepatic insufficiency. In cases where the blood alcohol level exceeds 80 mmol/l. haemodialysis may be required. The fact that alcohol can... 

A. Acute disulfiram overdose (without ethanol) may cause vomiting, ataxia, confusion, lethargy, seizures, and coma. Hypersensitivity hepatitis has occurred, including several deaths resulting from hepatic failure. 

Methanol is also used to "de-nature" ethanol. There s not much difference between synthetic ethyl alcohol and the "real thing" made from rye and other grain. Methanol is added, for political reasons, up to 10%, to the synthetic stuff to keep it from being substituted for the "real" or "natural" ethyl - alcohol. Ethanol "de-natured" in this way is toxic enough to cause headaches, dizziness, vomiting, blindness, and coma, depending on how much is consumed. That s usually a sufficient threat. 

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. 

Liver damage from excessive ethanol consumption occurs in three stages. The first stage is the aforementioned development of fatty liver. In the second stage—alcoholic hepatitis—groups of cells die and inflammation results. This stage can itself be fatal. In stage three—cirrhosis—fibrous structure and scar tissue are produced around the dead cells. Cirrhosis impairs many of the liver s biochemical functions. The cirrhotic liver is unable to convert ammonia into urea, and blood levels of ammonia rise. Ammonia is toxic to the nervous system and can cause coma and death. Cirrhosis of the liver arises in about 25% of alcoholics, and about 75% of all cases of liver cirrhosis are the result of alcoholism. Viral hepatitis is a nonalcoholic cause of liver cirrhosis. 

Sedatives, opioids and ethanol cause signs that may include respiratory depression, miosis, hypo-reflexia, coma, hypotension and hypothermia. 

Ethanol is a central nervous system depressant and ingestion of low to moderate quantities can lead to symptoms of intoxication including muscle incoordination, visual impairment, slurred speech, etc. Ingestion of higher concentrations may cause depression of medullary action, lethargy, amnesia, hypothermia, hypoglycemia, stupor, coma, respiratory depression, and cardiovascular collapse. The lethal human blood-alcohol concentration is generally estimated to be 400-500 mg/ 100 mL. 

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. 

The characteristic signs and symptoms of alcohol intoxication are well known. Nevertheless, an erroneous diagnosis of drunkenness may occur with patients who appear inebriated but who have not ingested ethanol. Diabetic coma, for example, may be mistaken for severe alcoholic intoxication. Drug intoxication, cardiovascular accidents, and skull fractures also may be confused with alcohol intoxication. The odor of the breath of a person who has consumed ethanol is due not to ethanol vapor but to impurities in alcoholic beverages. Breath odor in a case of suspected intoxication can be misleading because there can be other causes of breath odor similar to that after alcohol consumption. BALs are necessary to confirm the presence or absence of alcohol intoxication. 

A. Methanol Methanol (wood alcohol) is sometimes used by alcoholics when they are unable to obtain ethanol and is a constituent of windshield cleaners and canned heat Intoxication from methanol alone may include visual dysfunction, gastrointestinal distress, shortness of breath, loss of consciousness, and coma. Methanol is metabolized to formaldehyde and formic acid, which can cause severe acidosis, retinal damage, and blindness. The formation of formaldehyde is retarded by prompt intravenous administration of ethanol, which acts as a preferred substrate for alcohol dehydrogenase and competitively inhibits the oxidation of methanol (Figure 23-2). 

B. The level sufficient to cause deep coma or respiratory depression is highly variable, depending on the individual s degree of tolerance to ethanol. /M-though levels above 300 mg/dL usually cause coma in novice drinkers, chronic alcoholics may be awake with levels of 500-600 mg/dL or higher. 

DIoxane (dimer of ethylene glycol) May cause coma, liver and kidney damage, The vapor (> 300 ppm) may cause mucous membrane irritation. Dermal exposure to the liquid may have a defatting action. Metabolites unknown. Molecularweight is 88. Role of ethanol and fomepizole is unknown, but they may be effective. 

II. Toxic dose. The toxic dose varies considerably between dmgs, depends largely on individual tolerance, and can be influenced by the presence of other drugs such as ethanol. For most of these dmgs, ingestion of more than 3-5 times the usual therapeutic dose may cause stupor or coma. Death was reported in a 4-year-old who ingested approximately 3500 mg of carisoprodol. 

Reguiatory SARA 311/312 fire hazard, 313 nonreportable Properties BIk. vise, liq. mild odor sol. in acetone, toluene, ethyl ether, CCI, hydrolyzes in water sp.gr. 1.100 vapor pressure < 1.33 hPa (20 C) m.p. < 0 C b.p. > 150 C flash pt. (PMCC) 55 C Toxicology Hydrolyzes in stomach to form ethanol ing. may cause dizziness, drowsiness, euphoria, abdominal discomfort, coma, etc. may cause minor skin irritation, itching, si. local redness TSCA listed Environmental Expected to be resist, to rapid biodegradation may create offensive odor expected to be toxic to fish avoid discharge to sewers and natural waters... 

Properties Colorless liq. sol. in water, 95% ethanol, acetone m.w. 110.54 sp.gr. 1.3219 (20/4 C) b.p. 146 C (18 mm) ref. index 1.4831 (20 C) Toxicology Toxic by ing., inh. can be absorbed thru skin local skin/eye irritant may cause eye/nasal irritation, nausea, vomiting, giddiness, dizziness, incoordination, and coma Precaution Probably combustible Hazardous Decomp. Prods. Heated to decomp., emits toxic fumes... 

Properties Liq. foul, offensive odor probably sol. in ethanol, diethyl ether, acetone, benzene, chloroform probably insol. in water m.w. 102.20 dens. 0.955 (20 C) b.p. 129-131 C (745 mm Hg) flash pt. (CC) 25 C pH very si. acidic Toxicology LD50 (oral, mouse) 2680 mg/kg human poison ing. unlikely, but probably causes CNS depression due to obnoxious odor, detectable before harmful airborne levels are reached inh. may cause CNS depression high cones, may cause convulsions, respiratory paralysis, coma, death may cause mild eye and severe skin irritation TSCA listed Precaution Flamm. liq. 

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