due to vomiting and bleeding. The mumbling of the patient on day 5 may have
been due to the neurologic eects of cantharidin which have been reported
elsewhere (Harrisberg et al., 1984; Manoguerra and Rumack, 1995). The treatment
given was symptomatic and supportive and was aimed at replacing ¯uids and
electrolytes as well as maintaining urine output and renal function through the
administration of intravenous ¯uids. The treatment given also had the eect of
diluting the excreted cantharidin. This was employed after consultation with the
national Drug and Toxicology Information Service on the day of admission of the
patient to Gweru Hospital. Some authors have suggested alkinasation as a
method of reducing nephrotoxicity (Fisch et al., 1978), but the salts formed
remain biologically active and thus nephrotoxicity would still occur (Presto and
Muecke, 1970). The patient was discharged on nalidixic acid to cover for possible
urinary tract infection secondary to damage of the kidney and bladder due to the
toxin. The length of hospital stay was quite prolonged. This may have been due to
the inadequate treatment given at the rural hospital Ð the attending nursing sta
gave 30 ml of i.v. ¯uids per hour instead of 30 ml/kg bodyweight as speci®ed in
the national standard treatment guidelines for dehydration.