JOURNAL OF THE LOUISIANA STATE MEDICAL SOCIETY
the serumCK levels rise to values in the hundreds of thousands. 28
emeticsandcatharticsarecontraindicated. Initialgastrointestinal toxicity may be followed by acute or end-stage renal failure or liver failure and, rarely, pancreatic insufficiency. Any evidence of worsening hepatic or renal function or rhabdomyolysis should alert clinicians to the possibility of potentially fatal toxidromes, and immediate preparations should bemade to transfer patients to the closest facilities equipped and staffed for hemodialysis and kidney and liver transplantation.
Rhabdomyolysis is typically confirmed by significantly elevated creatine kinase (CK) levels with little laboratory evidence of hepatic injury, other than moderate elevations of the serum transaminases. 4 Muscle biopsies usually demonstrate histopathological evidence of acute myopathy. 4 Autopsies may demonstrate myocardial lesions identical to the muscle biopsy lesions and no histopathological evidence of hepatic damage. 4 There are no antidotes for mushroom-induced rhabdomyolysis. Themanagement is entirely supportive with urinary alkalization, correction of electrolyte imbalances, and intravenous fluid loading to support brisk diuresis and with early hemodialysis as indicated for renal insufficiency. The mushroom myotoxins responsible for rhabdomyolysis remain unidentified.
CONCLUSIONS
Although the hepatotoxic amatoxin-containing mushrooms cause most mushroom poisonings and fatalities worldwide, nephrotoxic mushrooms, most commonly Cortinarius species, can cause renal damage and kidney failure. Recently, several new species of nephrotoxic mushrooms have been identified including Amanita proxima and Tricholoma equestre in Europe, Amanita smithiana in the Pacific Northwest of the United States (US) and Canada, Amanita pseudoporphyria in Japan, and Amanita punctata in Korea. Renal replacement therapies including temporary hemodialysis are often indicated in the management of nephrotoxic mushroom poisonings with renal transplantation reserved for extracorporeal treatment failures. Unlike the outcomes of amatoxic mushroom poisonings, which can be fatal without liver transplantation, nephrotoxic mushroom poisonings that are diagnosed early and managed with temporary renal replacement usually have good outcomes with full recoveryof pre-existing renal functionunless irreversible renal failure ensues. Renal transplantation should not be offered too early as partial to complete recovery of pre-existing renal function has ensued even after months of hemodialysis.
Treatment Strategies for Nephrotoxic Mushroom Poisonings
As noted, mushrooms can now be tentatively identified as potentially nephrotoxic in the field using digital telephone images transmitted directly to expert mycologists who often serve as consultants to state of local poison control centers. 16 Any leftover mushroommeals and vomitus should be submitted for toxicological analyses and microscopic spore examination by expert mycologists. The general management of mushroom poisonings should include fluid resuscitation and oral activated charcoal (1g/ kg initially, 0.5g/kg subsequently) which can disrupt the enterohepatic circulation of some mushroom toxins. A baseline laboratory assessment should include complete blood count, peripheral blood smear, serum glucose and electrolytes, including calcium, liver and renal function tests, and serum creatine kinase (CK). Hepatic transaminases, coagulation studies, serum bilirubin, serum glucose, serum creatinine, BUN, and CK will serve as baseline comparative laboratory values over time. Liver and renal function tests should be repeated at least every 12-24 hours following toxic mushroom ingestions and followed periodically in order to exclude late onset hepatotoxicity from cyclopeptide-containing mushroom co-ingestions ( Amanita, Galerina , and Lepiota species) and delayed onset nephrotoxicity fromnephrotoxic Amanitaproxima and A. smithiana mushrooms. Finally, serum CK should be measured every 12-24 hours in the first 5-10 days to every 36 hours for 10-14 days in delayed onset myotoxicity with rhabdomyolysis from Tricholoma or Russula species ingestions. Figure 4 depicts a diagnostic decision algorithm to assist clinicians in the differentiation between the early (≤ 2-4 days) or delayed (>2-14 days) onset of nephrotoxic mushroom poisonings with renal insufficiency and subsequent failure based on the initial clinical manifestations of acute (≤ 6 hours) or delayed (≥ 24-72 hours) and typically mild gastrointestinal symptoms of nausea and vomiting with or without diarrhea.
Since mushroom-poisoned patients often present initially with gastrointestinal findings of nausea, vomiting, and diarrhea,
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