NM-319
Acute Fulminant Liver Failure Due To Iron Intoxication Requiring Emergent Liver Transplantation
Anwar S, Lei S
New York Presbyterian Columbia, Lindenhurst, New york, United states
INTRODUCTION:
The majority of iron toxicity cases occur in children as a result of accidental ingestion, but can also be due to intentional overdose. Iron toxicity can have damaging effects on the heart, endocrine glands, liver, and other organ systems. Although the initial symptoms are milder, such as abdominal pain, vomiting, and diarrhea, it can quickly progress to hypotension and shock.
CASE REPORT:
A 14-year-old girl with a history of mild asthma was sent from an outside hospital for acute hepatic failure from iron ingestion. The patient had ingested multiple tablets of ferrous sulfate, amoxicillin, and ibuprofen. She was brought to the ED after developing emesis, diarrhea, tonic-clonic movements, and altered mental status. Toxicology screen was negative. Labs were notable for acidosis with pH 7.18, WBC 43.5, lactate 6.7, and the patient was started on empiric antibiotics. Her LFTs were trending up with transaminases to 4000s, elevated bilirubin, and INR of 5.0. She was started on N-acetylcysteine and deferoxamine after discussion with the poison control center for iron toxicity. She was transferred to CUMC PICU, where the course was complicated by altered mental status requiring intubation, and hematemesis and hematochezia with hypotension requiring massive transfusion. She was also started on rifaximin and lactulose for hepatic encephalopathy. She was emergently listed as status 1A for liver transplant and underwent an orthotopic liver transplant on day 6 after ingestion. Intraoperative course was significant for minimal blood loss requiring 2 units of PRBC, 4 units of FFP and 1 unit of cryoprecipitate. She was on low dose epinephrine and vasopressin drips after reperfusion, which were discontinued on arrival to the PICU. Her mental status improved and she was extubated on POD #2. She was discharged on POD #15 to home with prolonged psychiatric support.
DISCUSSION:
Hepatotoxicity from iron poisoning is uncommon, making it low on differential diagnoses. However, when it does occur, it is associated with a high mortality rate. Damage from iron occurs in the periportal regions where cells receive blood with high oxygen and iron, resulting in free radical formation leading to damage. The periportal region is responsible for hepatic regeneration, so hepatic damage due to iron poisoning will carry a much worse prognosis compared to intoxication from other drugs. In the first 6 hours, patients typically present with vomiting, diarrhea, and lethargy. It can progress quickly to hypotension, metabolic acidosis, coagulopathy and shock. Liver failure occurs after a day, although the rate and progression varies case by case. Like our patient, upper and lower GI bleeding can also occur from coagulopathies. The specific treatment for iron poisoning is IV deferoxamine, an iron chelator. However, the only definitive treatment is emergent liver transplantation.
REFERENCES:
1. Daram et al. South Med J. 2005;98(2):241-4.
2. LiverTox. Drug Record: Iron. March 2015.
3. O'Malley et al. Merck Manual Professional Version. May 2015.
4. Shander et al. J Clin Anesth. 2012;24(5):419-25.
5. Steadman et al. Current Opinion in Organ Transplantation.2010: 15(3):368–373
6. Tenenbein et al. Clinical Toxicology. 2001: 39(7): 721-726.
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