Routine antibiotic therapy in the management of the local inflammatory swelling in venomous snakebites: results of a placebo-controlled study.

OBJECTIVE: To evaluate the value of routine antibiotic therapy in the management of the local swelling of patients with venomous snakebites. METHODS: A prospective, placebo-controlled study at the General Hospital, Anuradhapura, Sri Lanka where 144 patients with envenoming and local swelling in the leg were allocated to receive either antibiotics (Group A = test group) or placebo (Group B = controls). Benzyl penicillin 2 mega units intravenously 6 hourly and metronidazole 500 mg by intravenous infusion 8 hourly for 5 days from the first day of the bite were given to Group A. Ethical committee approval was obtained from the Committee of General Hospital, Anuradhapura. MAIN OUTCOME MEASURES: Circumference difference between the affected limb and the normal limb, length of the swelling measured in centimetres, and the physical characteristics of the local swelling of both groups were compared. RESULTS: Group A had 69 patients and the Group B 75. The mean circumference difference (MCD) of the leg between the groups showed no significant difference for 4 days (P > 0.05), except at the site of the bite on the third day when the Group B showed a significant improvement (p = 0.02). There was no significant difference in the length of the local swelling or the score of physical characteristics between the two groups (P > 0.05). The proportions of recovery of the local swelling on the fourth and fifth day had no significant difference between the groups (P > 0.05). CONCLUSION: The routine use of antibiotics (penicillin and metronidazole) does not seem to be of value in reducing the local inflammatory swelling in venomous snakebite.

Organophosphorus insecticide poisoning.

Organophosphorus insecticides (OPI) are the commonest cause of poisoning in Sri Lanka. Being inhibitors of esterases, OPI cause an acute cholinergic crisis as the initial phase of neurotoxicity. The intermediate syndrome (IMS) which develops 24 to 96 hours after poisoning, and the delayed polyneuropathy (OPIDP) which manifests several weeks later, suggest a triphasic effect of OP intoxication. OPI may also cause extrapyramidal manifestations. Chronic neurobehavioural effects of longterm exposure to OPI are also a cause for concern. This paper reviews OPI poisoning in man emphasising the clinical, biochemical, and electrophysiological studies done at Peradeniya over the past two decades.

Absence of anti-Purkinje cell antibodies in patients with cerebellar ataxia following falciparum malaria.

Immunological mechanisms have been implicated in the pathogenesis of delayed cerebellar ataxia following falciparum malaria (DCA). We tested serum and CSF samples obtained from 39 Sri Lankan patients with DCA for the presence of antibodies (Ab) directed against cerebellar Purkinje cells by an immunofluorescence (IF) technique and Western blot analysis. For the IF test 7 mu thick frozen sections of histologically normal cerebellum obtained at post mortem were used. Proteins obtained from crude preparations of Purkinje cells isolated from the cerebellum were used for Western blot analysis. Sera obtained from patients known to have antineuronal antibodies associated with cerebellar degenerations and paraneoplastic disorders (anti-Hu and anti-Yo Ab) and sera from normal blood donors served as positive and negative controls, respectively. All serum and CSF samples obtained from patients with DCA were negative for Ab directed against cerebellar Purkinje cells. Humoral mechanisms are, therefore, unlikely to be important in the pathogenesis of this delayed complication of falciparum malaria.

Hypokalaemic periodic paralysis in central Sri Lanka.

We describe 14 Sinhalese male patients with hypokalaemic periodic paralysis (HPP). The age at onset was between 10 and 32 years. Each paralytic episode lasted from 6 to 48 hours (except in one patient who had an attack lasting 5 days). The frequency of attacks varied from 8 to 10 per month in one patient to only 2 attacks over a period of 16 years in another. Four patients (28.6%) had a family history of the disease. Hypokalaemia (serum potassium 1.5 to 3 mmol/l) was documented during an attack in 11 patients. No cause for hypokalaemia was evident in any of them. Investigations including EMG, thyroid hormone level and skeletal muscle histology were within normal limits between episodes. All the patients responded well to treatment with potassium supplementation, alone or with acetazolamide.

Reflex epilepsies: experience in Sri Lanka.

Reflex epilepsy (RE) is characterised by seizures that are regularly elicited by some specific stimulus or event mediated by neural pathways. In a prospective study of 1287 epileptic patients seen at Peradeniya, 223 (17.3%) were found to have RE, eating being the commonest stimulus (191 patients, 85.7%). Photosensitive epilepsy (PSE) was relatively rare. Intermittent photic stimulation on 874 unselected epileptic patients produced a positive photoconvulsive response in 60 (6.9%). None had photosensitive seizures, but 3 had a higher frequency of seizures while watching television. Eating epilepsy (EE) had the highest prevalence at Peradeniya (148/1000 epileptic patients). This group was male predominant, and the onset of epilepsy in most cases was in the second decade. The majority experienced partial complex seizures. Repetitive and chronic stimulation of the amygdala during eating is suggested as the mechanism underlying EE. Twenty-one patients had seizures evoked by calculation, problem solving or spatial tasks. Juvenile myoclonic epilepsy was the commonest form of seizure disorder in them. Although PSE itself is rare, self-induced epilepsy (SIE) was common. There were 8 patients who self-induced seizures. The majority were photosensitive and they induced seizures by gazing at the sun and waving a hand in front of the eyes. In the management of REs, clobazam produced impressive results. As for possible seizure-inhibitory mechanisms, our studies on a "Sathi" mediator showed definite EEG changes during mediation. Can mediation increase the seizure-threshold and abort or prevent the propagation of the epileptic discharge? The answer, apart from its possible therapeutic applications, may provide insight into the mechanisms of seizure generation.

Neurological complications of malaria.

This paper reviews the neurological complications of malaria. Cerebral malaria, the acute encephalopathy which complicates exclusively the infection by Plasmodium falciparum commonly affects children and adolescents in hyperendemic areas. Plugging of cerebral capillaries and venules by clumped, parasitized red blood cells causing blood sludging in the capillary circulation is one hypothesis to explain its pathogenesis. The other is a humoral hypothesis which proposes a nonspecific, immune-mediated, inflammatory response with release of vasoactive substances capable of producing endothelial damage and alterations of permeability. Cerebral malaria has a mortality rate up to 50%, and also a considerable longterm morbidity, particularly in children. Hypoglycemia, largely in patients treated with quinine, may complicate the cerebral symptomatology. Other central nervous manifestations of malaria include intracranial hemorrhage, cerebral arterial occlusion, and transient extrapyramidal and neuropsychiatric manifestations. A self-limiting, isolated cerebellar ataxia, presumably caused by immunological mechanisms, in patients recovering from falciparum malaria has been recognized in Sri Lanka. Malaria is a common cause of febrile seizures in the tropics, and it also contributes to the development of epilepsy in later life. Several reports of spinal cord and peripheral nerve involvement are also available. A transient muscle paralysis resembling periodic paralysis during febrile episodes of malaria has been described in some patients. The pathogenesis of these neurological manifestations in malaria remains unexplored, but offers excellent perspectives for research at clinical as well as experimental level.