An 18-year-old ASA-I patient who underwent elective left shoulder arthroscopy developed severe airway obstruction post-extubation due to fluid extravasation from the shoulder joint into the neck and airway tissue. Re-intubation for relief of obstruction resulted in negative-pressure pulmonary oedema. The patient was electively ventilated in the intensive care unit and recovered uneventfully. A high index of suspicion along with monitoring of neck circumference can prevent this kind of complication.
Aluminum phosphide (ALP) is a cheap, easily available agricultural pesticide which causes lethal poisoning by liberation of phosphine and inhibition of cytochrome c oxidase thereby leading to cellular hypoxia. Although there is no known specific antidote, clinical trials are still going on. We present here two cases of ALP poisoning who were successfully managed by treatment with lipid emulsion and intravenous magnesium sulfate.
SummaryImmunofluorescent demonstrations of platelet-free fibrin deposit in the micro and macro-vascular lesions of maturity onset diabetes mellitus and atherosclerosis by earlier workers called for investigations of fibrino-coagulopathy in the two disorders. The present investigation included the determinations of plasma thrombin time (PTCT), fibrinogen concentration (FC), plasma fibrinogen half life (PFT ½) and plasma fibrinogen degradation product (FDP) in (i) the subjects of the two age-onset disorders and their consanguinous family members, and (ii) juvenile diabetes.The assays were carried out by standard methods. 125Iodine labelled human fibrinogen was used for half life studies.In a study of 525 subjects, very highly significant (p <0.001) reduction in PTCT, FC and PFT ½ with a very highly significant (p < 0.001) elevation of FDP were observed in the patients of the two age onset disorders. The results were normal in juvenile diabetes.The study provides convincing evidence of a ‘state of slow consumptive fibrino-coagulopathy’ in the subjects and their siblings with the observed haemostatic defect likely being due to genetically determined Anti-thrombin III deficiency. This observation stimulates a unitary concept of a primary fibrinopathic vascular aetio-pathogenesis, with selective localisation in the macro and microvascular compartment being responsible for the clinical syndromes of ischaemic and metabolic alterations in athersclerosis and maturity onset diabetes mellitus respectively.
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