Myasthenic crisis-like syndrome due to Cleistanthus collinus poisoning.

Poisoning with Cleistanthus collinus frequently causes cardiac manifestations such as rhythm disturbances and also results in other manifestations such as metabolic acidosis and hypokalemia. We present the case of a patient who presented with a rare myasthenic crisis-like syndrome requiring assisted ventilation due to Cleistanthus collinus poisoning, which responded to treatment with neostigmine.

Cleistanthus collinus poisoning.

Cleistanthus collinus is an extremely toxic plant poison. Cleistanthin A and B, the toxins of Cleistanthus collinus, are diphyllin glycosides which produce cardiac arrhythmias, urinary potassium wasting, hypoxia, metabolic acidosis and hypotension. We report ARDS, distal renal tubular acidosis and distributive shock secondary to inappropriate vasodilatation in a case following ingestion of its leaves.

Cleistanthus collinus poisoning: case reports and review of the literature.

We report the cases of two previously healthy young patients who ingested the liquid extracted from the crushed leaves of Cleistanthus collinus (Family: Euphorbiaceae) in an attempt to commit suicide. Both patients developed life threatening complications such as hypokalemia, hypotension, cardiac arrhythmias, neuromuscular weakness, respiratory failure, and renal failure following a transient quiescent period of up to 4 days. Other significant findings noted include leucocytosis, coagulopathy, elevated liver enzymes, hyperchloremic metabolic acidosis, and an alkaline urinary pH. Both patients received supportive care as no specific antidote was available, and ultimately died. We have reviewed the published literature on C. collinus poisoning.

A clinical and laboratory profile of Cleistanthus collinus poisoning.

AIMS: 1. To study the clinical features in patients with Cleistanthus collinus poisoning, 2. To study in them the effect of Cleistanthus collinus poisoning on the various organ systems and metabolic parameters using standard laboratory investigations. METHODS: All patients admitted to the hospital between September 1998 and April 2000 were studied. Statistical analysis of the results was done using chi-square test, Fisher's exact test and Student's 't' test. RESULTS: Forty six cases were studied, 15 (32%) of whom died. Eighty percent of the patients were in the second to third decade. The female:male ratio was 3:2. Ingestion of the poison as a decoction prepared from the leaves and ingestion of a large number of leaves otherwise were associated with a poor outcome. While survivors remained relatively asymptomatic, fatally poisoned patients presented with significant clinical signs and symptoms, however, laboratory abnormalities such as hypokalaemia, hyponatremia, an elevated AST/LDH/CPK/CPK-MB, nonspecific ST-T changes and QTc prolongation on ECG, metabolic acidosis and hypoxia with widened alveolar-arterial oxygen difference (A-aDO2) were seen in both groups. CONCLUSION: It is a poisoning seen in the young with significant mortality. Cause of death appears to be mainly due to its cardiac and respiratory effects. Metabolic disturbances especially hypokalaemia was a prominent feature. Most deaths occurred on the 3rd day and all within a week. No specific antidote is available.