Acute intoxication

One of the worries about many previous investigations of the effects of solvent abuse has been that, because objective measures to detect current intoxication have rarely been included, it has not been possible to reject the hypothesis that the cases were intoxicated, or at least still subject to the acute effects of solvents, at the time the psychological tests were administered. In order to ensure that the present study was concerned with the long-term effects of solvent abuse rather than the immediate effects of intoxication, it was necessary to be able to detect and, if necessary, exclude those children who were under the acute influence of solvents (or alcohol) at the time of testing. This was done by analyzing breath samples om each child 

Subcutaneous injections of cadmium salts in animals result in capillary stasis, edema, and hemorrtiages in the testis These events are followed by regressive changes of the seminiferous epithelium 4-6 h after injection and total necrosis within 24-48 h. The vascular lesions are morphologically similar to those in peripheral sensory ganglia.  

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Aromatic Hydrocarbons. These are the most toxic of the hydrocarbons and inhalation of the vapor can cause acute intoxication. Benzene is particularly toxic and long-term exposure can cause anemia and leukopenia, even with concentrations too low for detection by odor or simple instmments. The currendy acceptable average vapor concentration for benzene is no more than 1 ppm. PolycycHc aromatics are not sufftcientiy volatile to present a threat by inhalation (except from pyrolysis of tobacco), but it is known that certain industrial products, such as coal tar, are rich in polycycHc aromatics and continued exposure of human skin to these products results in cancer. 

Acute intoxication with DHBs occurs mainly by the oral route symptoms are close to those induced by phenol poisoning including nausea, vomiting, diarrhea, tachypnea, pulmonary edema, and CNS excitation with possibiUty of seizures followed by CNS depression. Convulsions are more frequent with catechol as well as hypotension due to peripheral vasoconstriction. Hypotension and hepatitis seem more frequent with hydroquinone and resorcinol. Methemoglobinemia and hepatic injury may be noted within a few days after intoxication by DHBs. 

Necrotic changes were characteristic of acute intoxication in mice, especially after single doses of 1, 2 and 2. Porphyrogenic effects appeared after repeated exposure to all studied compounds, mostly following dibromobenzenes and 5. 

The active drug and metabolites can be detected from the urine by thin-layer chromatography, gas-liquid chromatography, or gas chromatography-mass spectrometry. However, assays are available only at specialized centers. Treatment of acute intoxication with mescaline is virtually identical to the treatment outlined for LSD intoxication. DOM-induced vasospasm responds well to intra-arterial tolazohne or sodium nitroprusside. Major life-threatening complications of hallucinogenic amphetamine derivatives include hyperthermia, hypertension, convulsions, cardiovascular collapse, and self-inflicted trauma. 

Inexperienced users or individuals who are exposed to the drug unexpectedly (e.g., who unknowingly consume PCP-adulterated cannabis) may develop severe anxiety and panic because of the intensity and variety of symptoms. Perceptual distortions have sometimes led to extremely violent behavior, accidents, or self-damaging acts. An especially high risk of violent behavior has been reported in acutely intoxicated PCP users who have a history of psychiatric problems. Intoxication with doses in excess of 150 mg may lead to convulsions, coma, and death from respiratory arrest. Other complications include hypertensive crisis, intracerebral hemorrhage, and renal failure (Table 6-5). 

Cardiovascular Effects. Eesions in the heart and blood vessels have been reported in humans acutely intoxicated with methyl parathion (Wofatox) (Fazekas 1971) and are discussed in Section 3.2.2.2. However, many of these lesions may be secondary to the effects of methyl parathion on the conduction system of the heart, to other components ingested, or to therapeutic regimens that some of these patients received. 

Hepatic Effects. Liver lesions have been reported in humans acutely intoxicated by methyl parathion formulation (Wolfatox) (Fazekas 1971 Fazekas and Rengei 1964). These studies are discussed in detail in Section 3.2.2.1. Liver lesions were hepatocellular swelling, degeneration, and fatty change. 

When methyl parathion was given orally to rats at doses of 1.5 mg/kg and to guinea pigs at 50 mg/kg, plasma, erythrocyte, and brain cholinesterase activity was maximally inhibited within 30 minutes after administration. In rodents of both species that died after acute intoxication, brain cholinesterase levels decreased to 20% of control values and often to 5-7% (Miyamoto et al. 1963b). The species difference in susceptibility to orally administered methyl parathion is noted in Section 3.2.2.1. 

Chromosome aberrations were detected in lymphocytes of individuals acutely intoxicated by methyl parathion by the inhalation route (Van Bao et al. 1974). Blood samples were taken 3-6 days after exposure and again at 30 and 380 days. A temporary but significant (p<0.05) increase was noted in the frequency of stable chromosomal aberrations in the exposed individuals. The study limitations include small sample size, absence of a control group, lack of quantification of exposure levels, and a possible concomitant exposure to other substances via the dermal route. 

Clinical signs and symptoms of toxicity are related to the overstimulation of muscarinic, nicotinic, and central nervous system receptors in the nervous system. Muscarinic receptors are those activated by the alkaloid drug muscarine. These receptors are under the control of the parasympathetic nervous system, and their hyperactivity results in respiratory and gastrointestinal dysfunction, incontinence, salivation, bradycardia, miosis, and sweating. Nicotinic receptors are those activated by nicotine. Hyperactivity of these receptors results in muscle fasciculations even greater stimulation results in blockade and muscle paralysis (Lefkowitz et al. 1996 Tafliri and Roberts 1987). Hyperactivity of central nervous system receptors results in the frank neurological signs of confusion, ataxia, dizziness, incoordination, and slurred speech, which are manifestations of acute intoxication. Muscarine and nicotine are not... 

Blanco-Coronado JL, Repetto M, Ginestal RJ, et al. 1992. Acute intoxication by endosulfan. J Clin Toxicol 30(4) 575-583. 

The safety factor scale takes into account the volatility as well as the toxicity of the substance. It is an acute intoxication factor. As a result, the long term toxicity of benzene, which is carcinogenic, is hardly taken into account. This is a variant of the author s approach. 

Many accidents resulting from dangerous reactions have a history of repeating themselves over the years, without the lessons of history being properly drawn. For example, the accident at Seveso, arising from difficulties in controlling the reaction temperature of sodium hydroxide with 1,2,4,5-tetrachlorobenzene, had already happened three times a few years before. The symptoms due to acute intoxication caused by dioxin were already known. 

Corongiu, F.P., Lai, M. and Milia, A. (1983). Carbon tetrachloride, bromotrichloromethane and ethanol acute intoxication. New chemical evidence for lipid peroxidation in rat tissue microsomes. Biochem. J. 212, 625-631. 

PCP can apparently be inhaled by a person working in a PCP laboratory when the laboratory catches fire. Eight acutely intoxicated people were admitted to the LAC/USC Medical Center prison wards with PCP toxicity and thermal burns incurred during explosions of volatile chemicals in makeshift PCP laboratories (McCarron et al. 1981a). 

Some patients were attracted by the challenge of the risk in using PCP, i.e., not knowing what would happen. Three types of acute intoxication responses were described stimulation, depression, and hallucinogenic. Many patients reported being able to predict... 

It is not uncommon for individuals under the influence of phencyclidine to come to the attention of the criminal justice system. Increasingly, there is a need for forensic experts to advise and testify in cases involving PCP and other psychoactive drugs. With the publication of a paper on acute intoxication and fatalities from PCP use, we began to receive requests from attorneys to evaluate PCP-related cases (Burns et al. 1975). We have now consulted in over 400 civil and criminal cases and have testified in municipal, superior, and Federal courts from Hawaii to Washington, D.C. 

Clinical experience with the infants exposed primarily to PCP pre-natally is remarkably close to Wilson et al. These neonates are difficult to console, have alternating periods of lethargy and irritability, and are unable to control the tremors of their extremities when unswaddled. Vasomotor instability, diarrhea, and voracious sucking movements are infrequently seen in the PCP-exposed infants who were followed. Chasnoff et al. (1983) compared these behaviors in infants exposed prenatally to PCP to those of adults who have acute intoxication. 

McCarron s paper (this volume) describes the behaviors of 1,000 adults admitted to an inpatient service with acute symptoms of PCP intoxication. She states that some of the patients have appropriate behavior while many have mute and staring episodes, bizarre facial grimacing, localized dystonic reactions, rigidity, tremors, coarse jerky movements, and nystagmus. Thus, there is similarity between the acutely intoxicated adult s behavior and that of the newborn with a positive urine toxic screen for PCP. 

The treatment goals for acute intoxication of ethanol, cocaine/amphetamines, and opioids include (1) management of psychological manifestations of intoxication, such as aggression, hostility, or psychosis, and (2) management of medical manifestations of intoxication such as respiratory depression, hyperthermia, hypertension, cardiac arrhythmias, or stroke. 

The treatment goals for acute intoxication due to ethanol, cocaine/amphetamines, and opioids include (1) management of... 

Patients who are acutely intoxicated with an opioid usually present with miosis, euphoria, slow breathing and slow heart rate, low blood pressure, and constipation. Seizures may occur with certain agents such as meperidine (Demerol ). It is critically important to monitor patients carefully to avoid cardiac/ respiratory depression and death from an excessive dose of opioids. One strategy is to reverse the intoxication by utilizing naloxone (Narcan ) 0.4 to 2 mg IV every 2 to 3 minutes up to 10 mg. Alternatively, the IM/SC route may be used if IV access is not available. Because naloxone is shorter-acting than most abused opioids, it may need to be readministered at periodic intervals otherwise the patient could lapse into cardiopulmonary arrest after a symptom-free interval of reversed... 

Kombian SB, Warenycia MW, Mele FG, et al. 1988. Effects of acute intoxication with hydrogen sulfide on central amino acid transmitter systems. Neurotoxicology 9 587-595. 

The answer is d. (Hardman7 pp 1681-1682. Katzung, pp 392-393J Acute intoxication with methanol is common in chronic alcoholics. Headache, vertigo, vomiting, abdominal pain, dyspnea, blurred vision,... 

Ellenberger, S.A., PC. Baumann, and T.W. May. 1994. Evaluation of effects caused by high copper concentrations in Torch Lake, Michigan, on reproduction of yellow perch. Jour. Great Lakes Res. 20 531-536. Elsenhans, B., W. Forth, and E. Richter. 1991. Increased copper concentrations in rat tissues after acute intoxication with 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin. Arch. Toxicol. 65 429-432. 

Hiromori, T., T. Nakanishi, S. Kawaguchi, H. Sako, T. Suzuki, and J. Miyamoto. 1986. Therapeutic effects of methocarbamol on acute intoxication by pyrethroids in rats. Jour. Pestic. Sci. 11 9-14. 

Ibrahim et al. 1963). Aiken and Braitman (1989) determined that cyanide has a direct effect on neurons not mediated by its inhibition of metabolism. Consistent with the view that cyanide toxicity is due to the inability of tissue to utilize oxygen is a report that in cyanide-intoxicated rats, arterial p02 levels rose, while carbon dioxide levels fell (Brierley et al. 1976). The authors suggested that the low levels of carbon dioxide may have led to vasoconstriction and reduction in brain blood flow therefore, brain damage may have been due to both histotoxic and anoxic effects. Partial remyelination after cessation of exposure has been reported, but it is apparent that this process, unlike that in the peripheral nervous system, is slow and incomplete (Hirano et al. 1968). The topographic selectivity of cyanide-induced encephalopathy may be related to the depth of acute intoxication and distribution of blood flow, which may result in selected regions of vascular insufficiency (Levine 1969). 

Mlingi N, Poulter NH, Rosling H. 1992. An outbreak of acute intoxications from consumption of insufficiently processed cassava in Tanzania. Nutr Res 12(6) 677-687. 

After smoking the first puff, the acute intoxication starts within 6 to 12 minutes, and maximum effects occur at 15 to 30 minutes. Effects typicaiiy iast 2 to 4 hours. TFiC remains in fatty tissues and has a iong haif-iife of 57 hours. The iungs and iiver convert TFiC to the metaboiite 11-OFi-TFiC, which is aiso active. There is a recircuiation of 10-15% of hepatic metaboiites. 11-OFi-TFiC is further converted by the iiver to inactive metaboiites, which are eiiminated by the kidneys. 

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