To the Editor:
Urgent liver transplantation is only one treatment modality for individuals who are unable to recover from acute liver failure. Today, contraindication for liver transplantation is very limited. Posttransplantation treatment compliance is essential for a good outcome.
Yellow phosphorus is a highly toxic cellular poison (Fahim, el-Sabbagh, Saleh, & Sallam, 1990; McCarron, Gaddis, & Trotter 1981). Yellow phosphorus is used in the production of fireworks. The mortality of yellow phosphorus intoxication varies from 23% to 73%, and its fatal oral dose is approximately 1 mg/kg. Most reported deaths were attributable to hepatic complications (Fahim et al., 1990; Fernandez & Canizares, 1995; McCarron et al., 1981). Here, we present a case of toxic hepatitis, caused by ingestion of firework crackers containing yellow phosphorus in an uncontrolled paranoid patient with schizophrenia sent for liver transplantation.
A 38-year-old man was referred for probable urgent liver transplantation because of fulminant failure caused by ingestion of fireworks containing yellow phosphorus. After admission, we realized that the patient was psychotic. He was conscious and cooperative but had auditory hallucinations and delusions of persecution. Psychiatric assessment revealed that he was paranoid schizophrenic, and amisulpride (i.e., Solian) was initiated.
Laboratory profile on admission showed elevated serum levels of aspartate aminotransferase 2128 U/L (normal, 0-38), alanine aminotransferase 1304 U/L (normal, 0-41), [gamma]-glutamyl transferase 123 U/L (normal, 8-61), lactate dehydrogenase 2354 U/L (normal, 240-480), total bilirubin 6.51 mg/dL (normal, 0-1.1), direct bilirubin 5.26 mg/dL (normal, 0-0.3), prothrombin time 51 s (normal, 10.2-15.3), international normalized ratio 4.28 (normal, 0.83-1.25), and platelet count 110 / 103/[mu]l (normal, >=150 / 103/[mu]l). Other laboratory tests, including hemoglobin, white blood cell count, alkaline phosphatase, serum urea nitrogen, creatinine, glucose, and electrolytes levels, were within the normal range.
Because of uncontrolled schizophrenia, the patient was followed conservatively and administered supportive treatments. During the follow-up period, prothrombin time peaked up to 79 s (international normalized ratio 6.47) and improved spontaneously in 10 days after admission. The liver enzymes returned to normal on the 26th day of admission. Under amisulpride treatment, the patient's psychiatric findings were clearly improved.
Hepatic encephalopathy can be confused with various neurologic and psychiatric diseases including schizophrenia. In schizophrenia, the content of consciousness is changed but the level of consciousness is generally normal. On the contrary, in hepatic encephalopathy, the level of consciousness is deteriorated. In psychotic patients with liver illness, amisulpride is a safe medication because of renal excretion. Fulminant hepatic failure, which is represented by fulminant hepatitis, is fatal in most cases unless prompt liver transplantation is performed.
Active schizophrenia and recent suicide attempt are absolute and relative contraindications for liver transplantation in the majority of transplantation programs because of poor medication and follow-up compliance (Francoz, Belghiti, & Durand, 2007; Levenson & Olbrisch, 1993; Verdonk, van den Berg, Slooff, Porte, & Haagsma, 2007). The patient had both the contraindications, creating ethical dilemmas for our liver transplant team. Fortunately, he has recovered with supportive therapy.
Gastrointestinal healthcare providers should be aware that all consciousness changes may not mean hepatic encephalopathy in the course of acute liver failure. Hepatic encephalopathy should be distinguished from other acute and chronic causes of altered mental status.
Respectfully,
Abdurrahim Sayilir, MD
Murat Kekilli, MD
Mevlut Kurt, MM
Ibrahim Koral Onal, MD
Yusuf Yesil, MD
Bilge Tunc, MD
Nurgul Sasmaz, MD
Department of Gastroenterology, Turkiye Yuksek Ihtisas Teaching and Research Hospital, Ankara, Turkey
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