The study of complications of vivax malaria in comparison with falciparum malaria in Mumbai.

INTRODUCTION: Severe malaria due to P. vivax infection is increasingly observed now a days. Organ failure in vivax malaria is caused by mechanisms of inflammation as well as sequestration. In this study we have compared the complications in vivax malaria with those in falciparum or mixed malaria. AIMS AND OBJECTIVES: 1) To study various complications in adult inpatients of vivax malaria. 2) To compare the incidence of complications in vivax, falciparum and mixed malaria. MATERIALS AND METHODS: This was a retrospective observational study done at a tertiary care hospital in Mumbai over 3 months period. All adult indoor patients positive for malarial infection based on peripheral smear or malarial antigen (LDH) spot test were included in the study. Their demographic profile, complications, course in ward till discharge or death was noted. Data was analysed using appropriate statistical tests. RESULTS: 680 cases of malaria were included in the study. 338 were infected with P. vivax, 206 with P. falciparum, 136 with mixed infection. Severe disease was present in 162 (23.82%) cases of malaria of which 50 (31%) had vivax infection, 64 (39%) had falciparum infection and 48 (30%) had mixed infection. The complications seen in vivax malaria were: thrombocytopenia (68%), leukopenia (19%), ARDS (3%), high bilirubin (5%), acute renal failure (3.5%), anemia (3%), mucosal bleeding (8%), cerebral malaria (3.5%), hypotension (5%), metabolic acidosis (4%) and death (1.77%). CONCLUSIONS: 31% cases of severe malaria had vivax monoinfection. Thrombocytopenia, leukopenia, acute respiratory distress syndrome, hypotension, mucosal bleeding were seen as frequently as in falciparum and mixed malaria. Acute renal failure, cerebral malaria, high bilirubin, anaemia, metabolic acidosis and death were also found in vivax malaria but less frequently than in falciparum and mixed malaria.

Effect of inhaled terbutaline on platelet activity in bronchial asthma.

Thirty five young subjects with long standing bronchial asthma were studied for the effects of terbutaline misthaler (500 micrograms) during acute asthma. Bronchodilators were omitted for a day before the test. Ten matched controls were also studied. In all subjects, basal IgE level (ELISA), pulmonary parameters (FVC, FEV, PEFR, FEF 25-75 and FEF 75-85) and platelet activity, (platelet clumping/150 WBC on smear, platelet adhesiveness, blood recalcification time and kaolin clotting time for platelet factor3) were compared. During acute asthma, the subjects displayed IgE levels > or = 500 IU/ml (n = 33), activation of clotting (n = 30) and eosinophilia > or = 450/cmm (n = 28). These changes were not seen in normal controls. Terbutaline resulted in a reversal of airway obstruction, mainly of small airways, while the platelet hyperactivity and blood hypercoagulability were rectified (P < 0.001). It is concluded that platelet activity increases in acute asthma and is corrected by inhaled terbutaline concomittant with the relief of bronchospasm.

Intensive respiratory care service. Organisation, orientation, system and future. Our experience of management of 288 cases.

Between Jan. 1983 and Dec. 1986, 288 patients with acute respiratory failure of varied aetiologies were admitted to tetanus and respiratory care ward. One hundred and twenty patients (41.66%) had primary respiratory diseases, 107 (37.15%) of poisoning, 24 (8.3%) had neuromuscular diseases and 37 (12.48%) had miscellaneous disorders. Ventilatory support was given for more than 6 hours to 118 patients. The overall survival was 61.81% and on ventilator 38.13%. The mortality was high with ARDS (100%), miscellaneous (100%) pneumonia with septicaemia (75%) and COAD (54.28%). Patient with COAD had high mortality with acidosis (pH less than 7.1, P less than 0.01), hypotension (systolic BP less than 90 mm of Hg, p less than 0.05) and oliguria (urine out put less than 400 ml/24 hours, p less than 0.05). Organophosphorus compound was the commonest poison (89.75%) and patients who had moderate to severe hypoxia (pO2 less than 60 mm of Hg), hypotension and an interval of more than 4 hours between the consumption of poison and admission (all P less than 0.05) expired; 68.18% expired within the first 72 hours. All the patients with primary neuromuscular paralysis and bronchial asthma survived. Hospital acquired infections (160 patients), retained secretions (108 patients) and hypotension (64 patients) were the commonest complications seen in the 288 patients. Staphylococcus aureus (32.14%) was the commonest organism isolated. Financial constraints, drug shortages and frequent failure of machines were other major problems in the intensive respiratory care unit.

Six month follow-up of fourteen victims with short-term exposure to chlorine gas.

Fourteen cases, 5 with pre-existing COAD, exposed to up to 30 p.p.m. chlorine gas in an accidental leakage, were followed up clinically, radiologically and by spirometry at 2 weeks, 4 weeks, 8 weeks and 6 months. All the patients were asymptomatic by 2 weeks and did not reveal any radiological abnormality. The FVC, FEV1 and FVC observed/predicted improved at 4 weeks (p less than 0.05, p less than 0.05, p less than 0.01) and the improvement in FEF0.25-0.75 reached statistical significance (p less than 0.05) at 6 months. The mean improvement in FVC was 0.84 l and FEV1 was 0.6 l at 4 weeks. The 5 patients with pre-existing COAD did not show any evidence of additional lung damage. The observations have been consistent with acute tracheobronchitis with trends towards complete recovery.