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Thrombotic microangiopathy, which broadly includes thrombotic thrombocytopaenic purpura (TTP) and haemolytic uraemic syndrome (HUS), is a multisystemic disorder that is characterised by thrombocytopaenia, microangiopathic haemolytic anemia and ischaemic manifestations, resulting from platelet agglutination in the arterial microvasculature. Acral necrosis (distal necrosis of fingers and toes) occurs usually as a sequel to severe Raynaud′s phenomenon, a vasculospastic disorder frequently related to endothelial cell dysfunction. We report a case of quinine induced TTP-HUS and acral necrosis, two distinct clinical abnormalities which have not yet been reported together in association with quinine. Both of these conditions in this case resolved promptly to treatment with corticosteroids.

A 38-year-old male with acute myocardial infraction who had received streptokinase presented with acute painless diminution of vision in the left eye. Examination revealed features of central retinal artery occlusion on the left side with vision of perception of light. Treatment in the form of systemic and local intraocular pressure lowering agents, retrobulbar xanthinol nicotinate and systemic injection of B-complex resulted in improvement of vision to counting fingers up to one meter. In this case thrombolytic therapy itself led to embolism into the left central retinal artery resulting in its occlusion and eventually optic atrophy and blindness.

A young girl with nitrobenzene induced methaemoglobinaemia was saved by the timely use of mechanical ventilator, administration of oral methylene blue and parenteral ascorbic acid. Though parenteral methylene blue is the antidote of choice, due to its non-availability, the laboratory preparation of methylene blue have been utilized orally. The rare occurrence of such cases, and the efficacy of oral methylene blue and other supportive measures in evading death due to Nitrobenzene poisoning have been highlighted.

Clinical features and serial cerebrospinal fluid (CSF) samples of 50 patients who underwent myelography with iophendylate were studied. Forty two patients (84%) developed one or more features suggestive of meningism lasting for 2-4 days. There was significant rise in the average (mean) CSF counts from 9.81 in the premyelogram sample to 532.6 at the end of 24 hours (p less than 0.001). Both neutrophil and lymphocyte (p less than 000) count increased. At the end of one week, there was significant decrease of total cells in the CSF to 204 (p less than 0.001). Both, neutrophils and lymphocytes decreased. There was significant rise in total proteins in the 24 hours sample, but the fall at one week was not significant statistically. The sugar and chloride values did not change significantly. All CSF samples were negative for bacterial cultures. In conclusion, a significant proportion of the patients undergoing iophendylate myelography develop clinical features suggestive of meningeal irritation and change in the CSF fractions suggestive of meningitis: however these changes are transient and do not warrant institution of chemotherapy or steroids.