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Organophosphorus Poisoning with Homicidal Intention in a Neonate |
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Laxman Basany, Roja Aepalapala 1. Neonatologist, Department of Neonatology, Dolphin Kids Hospital, Hanamkonda, Telangana, India. 2. Consultant, Department of Paediatrics, Dolphin Kids Hospital, Hanamkonda, Telangana, India. |
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Correspondence Address : Laxman Basany, Flat 301 B, Legend Galaxy, Kothapet, Hyderabad, Telangana, India. E-mail: laxmanbasani@yahoo.co.in |
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| ABSTRACT |  | ||||||||||||||||||||||||||||||||||
: Organophosphorus Compounds (OPC) are widely used as pesticides, and poisoning due to OPC is very rare in neonates. A 12-day-old female neonate was admitted with gasping respiration, excessive oral secretions and cold extremities. She had frothing from mouth and nose with an offensive odour, and was hypothermic, hypotonic, cyanosed and in mild stupor. Pupils were pin pointed, capillary refill time was 4-5 sec and had bilateral crepitations of lungs on auscultation. The baby was intubated, given 0.1 mg of atropine followed by 0.9% saline bolus and gastric lavage. She was treated with empirical antibiotics, atropine, Pralidoxime (PAM) and respiratory support. The baby responded well to treatment and was discharged on 10th day of admission. This could be the second case of Organophosphorus (OP) poisoning with homicidal intention reported in neonates. | |||||||||||||||||||||||||||||||||||
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| Keywords : Atropine, Newborn, Organophosphate, Pralidoxime | |||||||||||||||||||||||||||||||||||
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DOI and Others :
DOI: 10.7860/IJNMR/2022/58467.2358
Date of Submission: Jun 15, 2022 Date of Peer Review: Jul 28, 2022 Date of Acceptance: Sep 16, 2022 Date of Publishing: Dec 31, 2022 AUTHOR DECLARATION: • Financial or Other Competing Interests: None • Was informed consent obtained from the subjects involved in the study? Yes • For any images presented appropriate consent has been obtained from the subjects. Yes PLAGIARISM CHECKING METHODS: • Plagiarism X-checker: Jun 25, 2022 • Manual Googling: Sep 09, 2022 • iThenticate Software: Sep 20, 2022 (20%) Etymology: Author Origin |
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| Case Report |
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A 12-day-old female neonate was referred to the Neonatal Intensive Care Unit (NICU), with a history of OP poisoning. The baby was born to a 23-year-old primigravida mother, who had regular antenatal check-ups and normal antenatal period. The baby was born by normal vaginal delivery with birth weight of 2450 grams. She cried immediately after birth and was breastfed. However, 3 hours prior to admission, she had poor feeding, lethargy, jerky respiration and excessive secretions. She was exclusively breastfed and weighed 2520 grams. The baby had profuse secretions from the mouth, with irregular respiration and bradycardia with heart rate of 72/min. She had non reactive pupils, hypotonia and was in mild stupor (Table/Fig 1). Questioning the mother and relatives revealed that the baby was deliberately fed monocrotophos (an organophosphate insecticide) mixed with milk by the maternal aunt, 4 hours prior to admission. Emergency airway management comprised of immediate oropharyngeal suction, endotracheal intubation and assisted ventilation. In view of signs of cholinergic overactivity, 0.1 mg of atropine was administered. Following administration of atropine, heart rate increased from 72/min to 120/min after 10 min. A presumptive diagnosis of OP poisoning was made based on history, clinical features and prompt response to atropine (1),(2). Gastric lavage and skin decontamination was done. After administration of 2 doses each of 0.1 mg atropine 15 minutes apart, atropine infusion was started at 0.02 mg/kg/hour. The dose was increased to a maximum of 0.08 mg/kg/hour for complete atropinisation as assessed from bronchial secretions, heart rate and pupil size. Atropine infusion was continued for 2 days, after which it was tapered over a 24 hour period and stopped. Loading dose of Pralidoxime (PAM) at 25 mg/kg was given over 30 min followed by infusion at 8 mg/kg/hour for 48 hours (3). Laboratory investigations showed leukocytosis (White Blood Cell count 18600/cumm) and normal blood levels of glucose, urea, creatinine and electrolytes. Arterial blood gas showed pH of 7.32, Partial Pressure of Oxygen (PaO2) was 62 mmHg, Partial Pressure of Carbon Dioxide (PCO2) was 52 mmHg and Bicarbonate (HCO3) of 17.1 mEq/1. Prothrombin time (PT) and Activated Thromboplastin Time (APTT) were normal. Septic screen was negative. Serum cholinesterase level was low at 1.66 kU/L (reference value 4.62-11.5 kU/L) which confirmed the diagnosis of exposure to OPC. In view of gasping respiration at admission, the baby was put on mechanical ventilation. As respiratory efforts improved and secretions decreased, ventilator settings were weaned and baby was extubated after 72 hours of conventional ventilation. Feeds were started on day 4 of admission and baby tolerated feeds well. Baby was discharged after 10 days of hospital stay with no obvious neurologic or pulmonary sequelae. Parents and relatives were counselled by social worker prior to discharge. Baby had normal growth and development on follow-up visit at 4 months of age. | |||||||||||||||||||||||||||||||||||
| Discussion |
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Organophosphates (OP) are widely used as pesticides. Accidental OP poisoning is reported all over the world but is extremely rare in neonates. These compounds phosphorylate the esteric site of the enzyme acetylcholinesterase in the peripheral and central nervous system causing accumulation of acetylcholine at the cholinergic receptor sites leading to cholinergic toxicity (1). Literature search of PubMed, EMBASE, MEDLINE and Google scholar done from 1970 till June 2022 using the words: neonate, poisoning, organophosphorus, atropine and PAM showed only 8 cases of OP poisoning in neonates including one case of homicidal poisoning in a 15-day-old neonate (Table/Fig 2) (2). The index case of 12-day-old female neonate was brought with gasping respiration, excessive oral secretions and cold extremities. The baby was hypothermic, hypotonic, cyanosed, and was in mild stupor. Pupils were pin pointed and capillary refill time was 4-5 sec with bilateral crepitations of lungs. The diagnosis of OP poisoning was based on the history of exposure and characteristic signs of cholinergic toxicity (1). History of exposure may not be evident, unless revealed by relatives as in the present case. Presence of features suggestive of cholinergic toxicity warrants a therapeutic trial with atropine even when there is no history of exposure to OPC. Unlike adults, infants and children usually manifest with neurological signs such as stupor, coma, and weakness of muscles. Miosis, excessive salivation and respiratory distress are seen in almost all cases of OP poisoning in infants (3). The Salivation, Lacrimation, Urination and Diarrhoea (SLUD) complex is characteristic of OP poisoning in adults, but is unreliable in infants and children. Only 15-20% of children present with bradycardia, which was present in the current case at admission. The baby did not have any fasciculations or seizures, which are seen in 25% of patients (3). OP poisoning is rare, mimics sepsis and needs high index of suspicion to diagnose. Zweiner RJ and Ginsburg MC, observed that diagnosis was made in only 20% of cases prior to transfer to higher centre (4). These cases are usually diagnosed based on history of exposure or contact and the characteristic clinical picture especially presence of pin point pupils, excessive secretions and the offensive odour of the patient’s breath and secretions that characterise these compounds. The differential diagnosis includes sepsis, bronchopneumonia, opiate overdosage, diabetic ketoacidosis and carbamate poisoning (5). The onset of symptoms of OP poisoning varies from minutes to several days depending on the dose ingested, route of exposure, lipid solubility and potency of the compound (6). Most patients become symptomatic within 24 hours of exposure. Most deaths occur due to cardiorespiratory failure, obstruction due to bronchial secretions and delay in diagnosis and initiation of treatment (6). The hallmark of diagnosis of OP poisoning is reduction in serum and Red Blood Cell (RBC) cholinesterase activity. RBC cholinesterase activity is considered to be more sensitive and specific for OP poisoning, and it correlates well with serum cholinesterase activity in 80% of cases (7). In clinical practice, both serum and RBC cholinesterase levels may be used to confirm the diagnosis of OP poisoning. Decrease in cholinesterase activity by ≥50% confirms the diagnosis of OP poisoning (7). Therapy is aimed at antagonising cholinergic effects and providing respiratory support as respiratory failure is the usual cause of death (3). Decontamination prevents further absorption of OPC from the skin and contamination of medical personnel. Atropine antagonises muscarinic and central effects, but has little effect on nicotinic receptors. The recommended dose is 0.02-0.05 mg/kg Intravenous (i.v.) given every 5-10 minutes or as continuous infusion at 0.02-0.08 mg/kg/hour to maintain a steady state (8). The response to atropine is judged by the resolution of cholinergic signs. However, atropine may be required for days to weeks depending on the fat solubility of the OP preparation (3),(9). Pralidoxime (PAM) is a cholinesterase reactivator which restores the enzyme activity at neuromuscular junction causing reversal of respiratory muscle paralysis. PAM should be administered within 24 hours of OP poisoning at a dose of 25-50 mg/kg as an infusion over 20 minutes. The dose may be repeated after 1-2 hour and then at intervals of 10-12 hours, if cholinergic signs recur or as a continuous infusion to maintain a steady state (10). Recently, a quaternary ammonium compound glycopyrrolate was found to be as effective as atropine with fewer adverse effects and is being used as an antidote to OP poisoning (9). After recovery, the patient should be monitored for next 24-48 hours to identify recurrence of effects as the action of antidote wears off. Late effects of poisoning include ventricular tachycardia, pulmonary oedema and demyelinating polyneuropathy (11). | |||||||||||||||||||||||||||||||||||
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Case report
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