{'fraction_non_alphanumeric': 0.02240325865580448, 'fraction_numerical': 0.005431093007467753, 'mean_word_length': 5.491189427312776, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Liver transplantation in case of acetaminophen poisoning: importance of assessment of the colon if arterial lactate increases despite appropriate care.

Assessment of the Colon if Arterial Lactate Increases Despite Appropriate Care Scarcity of organs justifies efficient transplantation decision making even in toxic acute liver failure (ALF). Modified King’s College Hospital criteria are widely accepted for decision making in emergency liver transplantation (LT) after acetaminophen poisoning: they have good specificity in identifying patients with poor prognosis, but are of low sensitivity in selecting patients who will die of ALF (1). Three of our recent clinical cases illustrate why the LT decision making process should also include careful and early digestive tract assessment. After deliberate acetaminophen poisoning, three young women with no previous medical history were referred for LT in the context of ALF with coma and lactate beyond 14 mmol/L (despite proper 24-hr fluid resuscitation). In these cases, the treatment with N-acetyl cysteine (NAC) had been started beyond 15 hr after acetaminophen intake. In the first patient, the LT proceeded without incident; 48 hr later, clinical worsening and absence of improvement attested in the biological liver tests (i.e., both aspartate aminotransferase and alanine aminotransferase increase and reincrease of arterial lactate) suggested primary liver dysfunction (Table 1). An emergency surgical reintervention disclosed diffuse patches of colon infarction without vascular obstruction, despite the fact that the colon had looked normal at the end of the first LT. Segmental resections were associated to total recovery. While on waiting list for 24 hr, the second patient unexpectedly developed stiffness of the leg with an increase in plasma creatine phosphokinase levels as already reported (2); subsequently, she was withdrawn from the LT list because liver tests no longer worsened. Despite full recovery of her liver tests, the patient developed long-lasting multiple organ failure related to focal colon lesions which resulted in shock requiring multiple segmental colon removal. She ultimately survived without LT. Histological lesions of the colon were similar to those reported previously (3): foci of necrosis and intramucosal hematoma were detected in the right colon. After careful rechecking of the abdominal CT scan taken at admission in connection with long-lasting arterial lactate increase, the presence of signs of mucosa ischemia and of hematoma was confirmed (Fig. 1). The third patient died with uncontrollable lactic academia while on waiting list for 4 days despite normal lactate on admission; the autopsy revealed macroscopic ischemic injury of the entire colon without thrombosis of conductance vessels. Our data further indicate that large doses of acetaminophen taken alone (i.e., without additional drugs or alcohol) trigger multiorgan insults after