CCCF ePoster library. Desai S. Oct 27, 2015; 117372; P123
Sachin Dattatraya Desai
Sachin Dattatraya Desai
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Topic: Case Report


Sachin Desai

Pediatric Critical Care, B C Childrens Hospital, Vancouver, Canada


Yellow phosphorus is an ingredient of fertilizers, fire works, rodenticides and army ammunition. Rodenticide (containing 2-3% phosphorus) is the most common, cheap and easily available form of yellow phosphorus. Yellow phosphorus poisoning can cause fatal systemic disease resulting in liver, cardiovascular, renal toxicity and may result in death. Mortality is variable from 23%-73% depending on involvement of organ systems.

Objectives: To describe variable presentation of three pediatric cases of yellow phosphorus poisoning due to intentional ingestion of rodenticide (rat poison) managed at tertiary care Pediatric ICU in India.

Methods: A report of case series


Case 1. 14 yr old boy consumed rodenticide paste and presented to local community hospital with emesis, abdominal pain. He remained stable for four days with minor gastrointestinal symptoms with elevated liver enzymes. On day four, his liver functions got worst (INR 3.3, APTT 42 sec, total bilirubin 4.2 mg/dL, SGOT 541 IU/L, SGPT 471 IU/L, ammonia 91 μmol/L, lactate 2.6) .On the same day, he developed hypotension with decreased cardiac function (EF 45%) with normal ECG. He required dobutamin for 24 hours and made recovery in next 4 days with liver functions returning to normal. Case 2. 12 year old boy was given food mixed with rodenticide paste by his mother. After few days of emesis, abdominal pain and impaired liver functions, on day 7, he developed fulminant hepatic failure with severe coagulopathy and encephalopathy requiring intubation. His blood results showed (PT>150 sec, INR >16, APTT 180 sec, total bilirubin 13 mg/dL, SGOT 1800 IU/L, SGPT 404 IU/L, ammonia 48 μmol/L, lactate 19.2). CT Brain showed early diffuse edema. Cardiac echo demonstrated good biventricular function. He was managed with supportive therapy (N acetyl cystein, hypertonic saline, prophylactic antibiotics, maintenance of blood glucose, electrolytes and acid base balance, lactulose, rifiximib). He was haemodyanamically stable and renal functions were normal. After two days, he was extubated. Coagulopathy and encephalopathy improved with gradual return of liver functions. Case 3.14 yr old boy had intentional ingestion of rodenticide paste. Initially he remained well and developed acute liver failure on day three (PT>150 sec, INR >16, APTT > 61 sec, total bilirubin 7.2 mg/dL, SGOT 981 IU/L, SGPT 666 IU/L, ammonia 125 μmol/L , lactate 4.5). He developed acute encephalopathy with episode of drowsiness and dilated pupils which responded to hypertonic saline bolus. He did not require intubation. Supportive therapy commenced and he responded well (NAC, antibiotics, 3% saline infusion etc) with return of normal function in next one week. All three patients received gastric lavage at local referring hospital. All patients had Acute Liver Failure and two patients qualified for liver transplant as per King’s College Criteria. All of them received plasma for central line insertion. Although severe coagulopathic, none had bleeding manifestations. All patients responded to timely and aggressive supportive management. All three patients had normal liver function at follow up.

Conclusion: Yellow phosphorus is not so rare cause of drug induced acute liver failure in India. Outcome was better than historically reported cases of yellow phosphorous poisoning in literature. NAC may have played a role in recovery but this needs to be further evaluated.


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