Symptomatic treatment poisoning

Full Fanconi syndrome has been reported to be present in some children with lead encephalopathy (Chisolm 1968 Chisolm et al. 1955). According to the National Academy of Sciences (NAS 1972), the Fanconi syndrome is estimated to occur in approximately one out of three children with encephalopathy and PbB levels of approximately 150 pg/dL. Aminoaciduria occurs at PbB levels >80 pg/dL in children with acute symptomatic lead poisoning (Chisolm 1962). The aminoaciduria and symptoms of lead toxicity disappeared after treatment with chelating agents (Chisolm 1962). 

A report from a poisons unit in Israel included 13 patients who had used the juice of the squirting cucumber, either orally or topically, for unreported reasons (6). They subsequently had edema of the pharynx, dyspnea, drooling, dysphagia, vomiting, and conjunctivitis. With symptomatic treatment they recovered within a few days. 

In a retrospective study of 199 cases of accidental or intentional acute poisoning with eprazinone, eprozinol, and zipeprol, collected at the Poison Control Center in Paris from 1975 to 1982, there were seven cases of seizures, aU after ingestion of eight times the therapeutic dose. They resolved rapidly and without recurrence with symptomatic treatment (1). 

Five patients with acute accidental poisoning with V. album rapidly developed nausea, vomiting, abdominal pain, hypotension, and bradycardia (26). In four cases the electrocardiogram showed sinus bradycardia and in one there was complete atrioventricular block with an ectopic atrial bradycardia and an intermittent idioventricular rhythm. Symptomatic treatment and/or atropine led to recovery within a few hours. 

Only symptomatic treatment is available. Adequate measures should be taken to maintain fluid and electrolyte balance and keep the body temperature within tolerable limits. Measures should be taken to remove the poison from the body through gastric lavage and saline cathartic. Gastrointestinal absorption may be... 

Exposure to dinoseb requires symptomatic treatment. Blood glucose, liver function, and renal function tests should be monitored in symptomatic patients. Adequate ventilation and oxygenation should be provided with close monitoring of arterial blood gases. The fluid and electrolyte balances should be maintained. The body temperature should be kept within tolerable limits. Antipyretic drugs are, however, not effective because dinoseb poisoning involves peripheral metabolism, not central nervous system control of temperature. Diazepam is administered to... 

Symptomatic treatment is recommended as there is no specific antidote available for poisoning by these... 

Pyrethroid compounds formulated with the insect repellant DEBT were responsible for numerous deaths in cats and dogs in the past decade. Pyrethroids interfere with sodium channels in nerves causing them to fire repetitively. Clinical signs of pyrethroid poisoning in small animals include ataxia, excitement, and muscle fasciculations and tremors. There is no antidote for pyrethrin poisoning, but symptomatic treatment, such as decontamination procedures and sedation, usually results in full recovery. 

Another area that would be of direct benefit to the medical personnel responsible for treating pesticide exposure in humans is the development of antidotal and symptomatic treatment for the various classes of pesticides. Although we have more specific antidotes available to treat pesticide poisoning than for any other single class of acute poisons, the number of antidotes is small for non-insecticidal pesticides and these cases must be treated symptomatically. The current acute toxicity protocols do not currently provide the kind of clinical information that is needed in such cases. 

Edetate calcium disodium, a metal-chelating agent, is indicated in the treatment of symptomatic lead poisoning without encephalopathy and blood lead concentrations less than 100 mcg/dL, or in the treatment of severe lead poisoning with symptoms of encephalopathy and/or blood lead concentrations greater than 100 mcg/dL. 

Table 7-2 shows the oral doses of atropine causing undesirable responses or symptoms of overdosage. Measures to limit intestinal absorption should be initiated without delay if the poison has been taken orally (see Chapter 64). For symptomatic treatment, intravenous physostigmine rapidly abolishes the delirium and coma caused by large doses of atropine, but carries some risk of overdose in mild atropine intoxication. Since physostigmine is metabolized rapidly, the patient may again lapse into coma within 1-2 hours, and repeated doses may be needed (see Chapter 8). 

A. Symptomatic cyanide poisoning (see p 177). Nitrites are not usually used for empiric treatment unless cyanide is very strongly suspected, and they are not recommended for smoke inhalation victims. 

There is no effective treatment of the poisoning. One case of toxic psychosis was treated with electroshock therapy (Boyd et at 1957). Symptomatic treatment with barbiturates has been recommended (Raz-SUDOV 1976). No effect is obtained by BAL, EDTA, or penicillamine which are used in the management of poisoning with inorganic lead (Boyd et at 1957, Cremer 1959, Kitzmiller et at 1954). 

The management of OP poisoning has been reviewed. Management of OP poisoning involves symptomatic treatment and the use of antidotes, especially atropine. Hypoxia, hypotension, cardiac arrhythmias and fluid balance and electrolytes may require attention. 

Treatment for chronic benzene poisoning is supportive and symptomatic, with chemotherapy and bone marrow transplants as therapeutic agents for leukemia and aplastic anemia (127). 

Treatment of chloroform poisoning is symptomatic no specific antidote is known. Adrenalin should not be given to a person suffering from chloroform poisoning. 

In most situations, adequate, usuaHy forced, ventilation is necessary to prevent excessive exposure. Persons who drink alcohol excessively or have Hver, kidney, or heart diseases should be excluded from any exposure to carbon tetrachloride. AH individuals regularly exposed to carbon tetrachloride should receive periodic examinations by a physician acquainted with the occupational hazard involved. These examinations should include special attention to the kidneys and the Hver. There is no known specific antidote for carbon tetrachloride poisoning. Treatment is symptomatic and supportive. Alcohol, oHs, fats, and epinephrine should not be given to any person who has been exposed to carbon tetrachloride. FoHowing exposure, the individual should be kept under observation long enough to permit the physician to determine whether Hver or kidney injury has occurred. Artificial dialysis may be necessary in cases of severe renal faHure. 

The pharmacist will, from time to time, be called upon to examine an eruption or condition and make recommendation for treatment. If and only if the condition is unmistakable in origin, delimited in area, and of modest intensity should the pharmacist recommend an over-the-counter remedy for its symptomatic relief. Physicians neither need nor want to see inconsequential cuts, abrasions, or mosquito bites or unremarkable cases of chapped skin, sunburn, or poison ivy eruption, and so on. However, if infection is present and at all deep-seated or if expansive areas of the body are involved, otherwise minor problems can pose a serious threat and physician referral is mandatory. Patients should also be directed to counsel with a physician whenever the origins of a skin problem are in question. 

There is no specific treatment for ingestion of ibotenic acid or muscimol rather, treatment is symptomatic and supportive. Anxiety, hysteria, or convulsions can be treated with sedatives, such as diazepam. This should be done cautiously, however, and with the lowest effective dose because animal studies revealed that respiratory arrest may occur. In severe cases, with prolonged nausea, vomiting, or diarrhea, monitoring of fluid and electrolyte status may be required. Recent cases of muscarine poisonings were reported by Benjamin (1992), and Tupalska-Wilczynska et al. (1997). 

Management of methanol and ethylene glycol poisoning is similar. Symptomatic support of respiration and circulation is augmented by correction of metabolic acidosis with intravenous bicarbonate infusion, and control of seizures with diazepam. Ethanol inhibits the metabolism of methanol and ethylene glycol to the toxic metabolites, and can give time for further treatment. The goal is to maintain blood ethanol concentrations between 100 and 150 mg per decilitre, sufficient to saturate alcohol... 

The uflinily of mercury for sulfhvdrvl groups provides the basis lor treatment of mercury poisoning using chelaling agents Iqvl such as dimcrcaprol (for high level exposures or symptomatic patients), or penicillamine llor low level exposure or asymptomatic patients). 

This toxic protein is contained in caster seeds but does not pass into the oil. Similar phytotoxins occur in croton seeds (Crotin) jequirity seeds (Abrin) the bark of the locust tree, Robinia pseudo-acacia (Robin) and in the seeds of some leguminous plants (Phasin). The last is but weakly toxic. Ricin is responsible for the toxic effects on eating castor seeds 5 or 6 of these are fatal to a child, 20 to adults, and 3 or 4 seeds may cause violent gastroenteritis with nausea, headache, persistent vomiting, colic, sometimes bloody diarrhea, thirst, emaciation, and great debility. The symptoms usually do not set in until after several days. More severe intoxications cause small frequent pulse, cold sweat, icterus, and convulsions. Death occurs in 6 to 8 d, from the convulsions or from exhaustion. The fatality rate is about 6%. This low fatality rate is due to the destruction of the poison in the alimentary canal. The treatment would be evacuant and symptomatic. Usually, 3 to 10 d are required to complete recovery. 

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