Organophosphate Poisoning Presenting as Acute Respiratory Distress

Abstract

Sir, Organophosphate poisoning [OP] is a potentially fatal but completely treatable condition that is still very prevalent in our country. Early recognition is paramount in preventing fatality. Although rarely reported, it does occur in infants, where history may not be forthcoming and initial presentation often misleading. We report a case of aspiration pneumonia whose evolving symptomatology made us diagnose OP poisoning. A previously healthy baby presented with vomiting whilst breast feeding followed by respiratory distress and altered sensorium. No prior history of fever, respiratory illness, seizures or drug intake. On examination he was a well thriving infant, who was afebrile with severe respiratory distress. He had altered sensorium and was markedly hypotonic with small sluggishly reacting pupils. Emergency management was given and baby was intubated and ventilated. Empirical antibiotics for possible aspiration pneumonia and other supportive treatment was started. Blood counts, chest radiograph and metabolic profile were normal. In the next few hours his sensorium worsened, pupils became pin pointed and unreactive to light. Copious oropharyngeal secretions and diarrhea were also noted. This constellation of symptoms made us suspect cholinergic hyperactivity and a large dose of atropine was given, which did not produce pupil dilatation, suggesting OP poisoning [1]. To confirm cholinesterase [ChE] level [2] was done and was found to be less than 25% reference range. Atropine infusion was immediately instituted at 0.02 mg/kg/hour [5], titrated to drying of secretions. As the nature of OP compound unknown empirical dose of pralidoxime, 25 mg/kg was given to reactivate ChE enzyme [5]. In next 24 h baby showed good improvement in motor tone and power with drying of secretions, and was subsequently extubated. Retrospectively parents revealed that insecticide was sprayed around the house on that day and child most likely got exposed by inhalation. Atropine was continued for 3 days and then weaned over 24 h. Serial monitoring of ChE levels showed a steady rise in titers to normal. The baby was discharged after a week and parents were counseled on the hazards of environmental exposure to OP compounds. OP’s inhibit ChE activity and affect central and peripheral muscarinic and nicotinic receptors [2]. Unlike adults infants mainly present with acute CNS depression and are characterized by the absence of typical muscarinic effects including fasciculation and bradycardia. The pupil examination is the key [3] and pin point pupils with diarrhea at presentation, is described as a triage tool for early recognition in children [4]. As with our infant, periodic pupil examination helped clinch the diagnosis. Therapeutic trial of atropine and serum ChE levels helps to make the diagnosis, however no correlation between the level and severity is noted [2]. Treatment is aimed at decontamination, reversal of muscarinic signs with atropine and enzyme reactivation by oximes. Frequent atropine doses or as continuous infusion titrated to achieve drying of secretions is used. Single dose of pralidoxime, or in severe poisoning a continuous infusion is used. Oximes are continued for 24 h after symptoms resolve or restoration of normal serum ChE levels [5].