Symptomatic treatment vomiting

Cholinesterase inhibitors are the only class of drugs currently approved by most Health Authorities and recommended by professional associations (e.g. Doody et al.. 2001) for the symptomatic treatment of AD. However, ChE-Is intervene at a late stage of the pathophysiological cascade leading to AD (Fig. 7.2) furthermore, their efficacy is limited and they may cause a number of side effects, most frequently nausea, vomiting, diarrhea, anorexia and dizziness. For these reasons, major efforts are being made to alter the biological processes... 

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. 

One of the two patients had taken 1500 mg of the lower stem and root of B. officinalis boiled in water in a suicide attempt. She was admitted with vomiting and headache and later developed gastritis, hematuria, and liver damage. Symptomatic treatment resulted in full recovery. 

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. 

A 51-year-old woman with metastatic breast cancer started treatment with capeeitabine 2500 mg/m daily for 14 days every 21 days. Treatment was stopped after 8 days because she developed diarrhoea, vomiting and hand-foot syndrome. She improved with parenteral hydration and symptomatic treatment, but 3 weeks later still had diarrhoea, leg oedema and hand-foot syndrome. She was found to have been taking folic acid 15 mg daily for several weeks before starting capecitabine and had continued to take it during and after capecitabine treatment. The patient s condition improved when the folie acid was stopped, but she then developed diarrhoea and fever followed by necrotic colitis and she died from septic shock and vascular collapse. It is possible that the concurrent use of folic acid enhanced the toxicity of capecitabine. ... 

A 68-year-old woman who had been taking leflunomide 10 mg daily for about 4 months was started on itraconazole 300 mg daily for a fungal infection. About one month later her leflunomide dose was increased to 20 mg daily, and liver function tests were normal. The following month, she developed abdominal pain, vomiting, and weakness. Despite symptomatic treatment and washout with colestyramine, fatal fulminant hepatic failure occurred. The authors of the report attribute the reaction to additive hepatotoxicity between the leflunomide and itraconazole. This interaction serves to highlight the cautions about the use of other hepatotoxic drugs, see (a) and (h). 

Give symptomatic treatment for nausea, vomiting, diarrhoea, pain and sldn symptoms. 

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). 

GI irritants are the most common toxins in Boletes, particularly in red-spored and yellow-spored species. Muscarine is present in a few species, but too low to be significant. Symptoms are nausea, vomiting, and diarrhea. In more severe cases there may be muscle cramps and circulatory disturbance. Treatment is largely symptomatic, and recovery is usually complete one to two days after ingestion. 

Chlorpromazine is the prototype molecule of the series of substituted phenothiazine psychotherapeutic compounds. Chlorpromazine is used for the symptomatic management of schizophrenia and active acute psychoses. The drug is also used for the prevention and treatment of nausea and vomiting, and for the relief of restlessness and apprehension before surgery [1,2]. 

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. 

Basic and advanced life-support measures should be utilized as necessary. Treatment is generally symptomatic and supportive. Gastrointestinal evacuation procedures are generally unnecessary. If the patient is alert and able to swallow, milk or water should be immediately offered, stopping if vomiting occurs during administration. Administration of an acidic substance to neutralize sodium hypochlorite is contraindicated. 

Contact with the skin should be minimized by thoroughly washing affected areas for at least 15 min. Symptoms of dermatitis should be treated if necessary. If ingested, vomiting should not be induced since ether poses an aspiration hazard and chemical pneumonitis may occur. CNS depression may result from ingestion. Treatment should be symptomatic. There are no known antidotes to diethyl ether. 

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