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BACKGROUND: Acute liver failure caused by the ingestion of yellow phosphorus-containing rodenticide has been increasing in incidence over the last decade and is a common indication for emergency liver transplantation in Southern and Western India and other countries. Clear guidelines for its management are necessary, given its unpredictable course, potential for rapid deterioration and variation in clinical practice. METHODS: A modified Delphi approach was used for developing consensus guidelines under the aegis of the Liver Transplantation Society of India. A detailed review of the published literature was performed. Recommendations for three areas of clinical practice, assessment and initial management, intensive care unit (ICU) management and liver transplantation, were developed. RESULTS: The expert panel consisted of 16 clinicians, 3 nonclinical specialists and 5 senior advisory members from 11 centres. Thirty-one recommendations with regard to criteria for hospital admission and discharge, role of medical therapies, ICU management, evidence for extracorporeal therapies such as renal replacement therapy and therapeutic plasma exchange, early predictors of need for liver transplantation and perioperative care were developed based on published evidence and combined clinical experience. CONCLUSION: Development of these guidelines should help standardise care for patients with yellow phosphorus poisoning and identify areas for collaborative research.
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INTRODUCTION: Yellow phosphorus (YP) is a general protoplasmic poison causing hepatic, cardiac, renal, and multiorgan failure. We report an unusual case of fulminant liver failure due to ratol (YP) poisoning complicated by acute pancreatitis postoperatively after liver transplantation. CASE REPORT: A 25-yr-old man presented with alleged consumption of approximately 7 gm of Ratol paste. Serum amylase and lipase levels were 880 and 2423, respectively, and CT imaging of pancreas was normal. He developed fulminant liver failure, fulfilling King's college criteria and an living donor liver transplantation was performed. Intraoperatively fat saponification was seen at the root of mesentery. On postoperative day (POD) 13, he developed incisional wound dehiscence and he underwent laparotomy with extensive slough removal from the lateral aspect of wound. On POD 21, wound showed evidence of burst abdomen. CT abdomen revealed inflamed tail of pancreas with peripancreatic fat stranding and an exploratory laparotomy was performed again. Intraoperatively, walled-off necrotic collection was seen in the tail of the pancreas and necrosectomy was carried out. All the aforementioned re-explorations were carried out under steroid immunosuppression. He was restarted on tacrolimus on POD27. Graft function and cholestatic biochemistry improved progressively, and he was discharged and is on regular follow-up. DISCUSSION: YP is very toxic with rapid absorption and gets accumulated in liver causing acute liver failure. Acute pancreatitis in a patient after liver transplantation for fulminant liver failure owing to Ratol poisoning has not been reported in published English literature. Although clinically relevant pancreatitis is rare in ratol poisoning, despite elevated pancreatic enzymes, it is prudent to meticulously image pancreas before embarking on liver transplantation. In those with pretransplant elevation of pancreatic enzymes, it is desirable to follow up the enzyme values postoperatively.
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Acute liver failure (ALF) is an infrequent, unpredictable, potentially fatal complication of acute liver injury (ALI) consequent to varied etiologies. Etiologies of ALF as reported in the literature have regional differences, which affects the clinical presentation and natural course. In this part of the consensus article designed to reflect the clinical practices in India, disease burden, epidemiology, clinical presentation, monitoring, and prognostication have been discussed. In India, viral hepatitis is the most frequent cause of ALF, with drug-induced hepatitis due to antituberculosis drugs being the second most frequent cause. The clinical presentation of ALF is characterized by jaundice, coagulopathy, and encephalopathy. It is important to differentiate ALF from other causes of liver failure, including acute on chronic liver failure, subacute liver failure, as well as certain tropical infections which can mimic this presentation. The disease often has a fulminant clinical course with high short-term mortality. Death is usually attributable to cerebral complications, infections, and resultant multiorgan failure. Timely liver transplantation (LT) can change the outcome, and hence, it is vital to provide intensive care to patients until LT can be arranged. It is equally important to assess prognosis to select patients who are suitable for LT. Several prognostic scores have been proposed, and their comparisons show that indigenously developed dynamic scores have an edge over scores described from the Western world. Management of ALF will be described in part 2 of this document.