Mushroom ingestion

CASE CONFERENCE ingestion, mushroom; mushroom poisoning; poisoning, pediatric, mushroom

Mushroom Ingestion ]Bivins HG, Knopp R, Lammers R, McMicken DB, Wolowodiuk O: Case conference: Mushroom ingestion. Ann Emerg Med November 1985;14: 1099-1104.] INTRODUCTION Herbert G Bivins, MD: The case for today's discussion is that of a 3-yearold girl who presented to our ED 24 hours after the ingestion of a mushroom. The case will be presented by Oleh Wolowodiuk, MD, a resident in emergency medicine, and will be discussed by members of the faculty.

CASE PRESENTATION Oleh Wolowodiuk, MD: A 3-year-old girl presented to the ED approximately 24 hours after ingesting a mushroom that her mother had gathered in a field. Eight hours after ingestion, she experienced the sudden onset of severe abdominal pain followed by five episodes of vomiting and six episodes of diarrhea. Despite these symptoms, no medical attention was sought until the following day when the child's mother became worried about her persistent abdominal pain and increasing lethargy. The patient had been in good health with no prior medical problems, and she was not taking any medications. There was no history of viral illnesses. No aspirin or acetaminophen had been given to the child. There was no history of blood transfusions, foreign travel, or known exposure to hepatitis. On presentation the patient was lethargic but responded appropriately to questions. Vital signs were as follows: supine blood pressure, 98/68 m m Fig; pulse, 160 and regular; respirations, 36; and oral temperature, 36.5 C. Physical examination revealed right upper quadrant abdominal tenderness without rebound or guarding. The liver was approximately 2.5 cm below the right costal margin. The remainder of the physical examination was normal. Neurologically the patient was lethargic but easily arousable. There were no focal or pathological neurologic findings. She did not appear jaundiced. Laboratory evaluation revealed a WBC cotmt of 9,600 m m 3 with 68 segments, 22 lymphocytes, four monocytes and six bands; hemoglobin was 14.3 g/dL, and hematocrit was 40%. The metabolic panel was as follows: sodium, 131 mEq/L; potassium, 4.7 mEq/L; chloride, 100 mEq/L; CO2, 19 mEq/L; glucose, 252 mg/dL; and BUN, 36 mg/dL. Platelets appeared adequate on peripheral smear. The prothrombin time (PT) was 15.6 seconds, with a control of 11.3 seconds. The partial thromboplastin time (PTT) was 28.4 seconds (range, 20 to 36 seconds). SGOT was 548 U/L and SGPT was 419 U/L. Serum ammonia was 63 ~g/dL (range, 18.7 to 59.5 mg/mL). The patient was given 20 g charcoal orally and an IV of DsW V4 normal saline in the ED and was admitted to the pediatric intensive care unit with the diagnosis of toxic mushroom ingestion. In the intensive care unit, charcoal was administered every four hours in the hope of binding any residual toxin left in the gastrointestinal tract. Liver function tests, liver enzymes, electrolytes, BUN, and glucose were monitored closely. The patient's clinical condition deteriorated rapidly and by the following morning she was more lethargic. She responded to painful, but not verbal, stimuli. Repeat liver studies revealed an SGOT of 5,148 U/L and an SGPT of 3,744 U/L. Serum ammonia was 122 ~g/dL. The coagulation profile revealed

14:11 November 1985

Annals of Emergency Medicine

Herbert G Bivins, MD Robert Knopp, MD Richard Lammers, MD David B McMicken, MD Oleh Wolowodiuk, MD Fresno, California From the Emergency Medicine Residency Program, Valley Medical Center, Fresno, California. Received for publication December 10, 1984. Revision received June 7, 1985. Accepted for publication July 2, 1985. Address for reprints: Herbert G Bivins, MD, Department of Emergency Medicine, Valley Medical Center, 445 South Cedar Avenue, Fresno, California 93702.

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TABLE. Mushroom toxins, effects, and treatments Specific Treatment and Symptoms Expected Recovery Sweating, salivation, Atropine sulfate, 1 to 2 mg lacrimation, blurred IV for severe poisonings; vision, abdominal symptoms subside in cramps, watery diar- 6 to 24 hrs rhea, hypotension, and bradycardia 30 min after alco- Disulfiram-like ef- Flushing, paresthesias, Avoid alcohol; recovery Coprine metallic taste, tachy- usually 2 to 4 hr hol consumption; fect, autonomic cardia, hypotension, as long as 5 symptoms nausea, vomiting, days after eating and sweating mushrooms Dizziness, incoordina- Avoid sedatives; avoid atroIbotenic 30 min to 2 hr Affects CNS tion, ataxia, muscular pine sulfate unless severe acid and jerking, hyperkinetic cholinergic symptoms; other isoxrecovery 4 to 24 hr activity, stupor, and azoles hallucinations Reassurance; benAffects CNS Mood elevation, apPsilocybin 30 min to 1 hr prehension, hyperzodiazepine for severe and other symptoms; recovery within kinetic activity, indoles 6 hr muscle weakness, drowsiness, and hallucinations Hydration, support; recov30 min to 2 hr Affects GI tract Nausea, vomiting, Diverse, abdominal cramps, ery several hours to days mostly and diarrhea unknown Pyridoxine, hydrochloride* Monome- 6 to 12 hr Cellular destruction Nausea, vomiting, 25 mg/kg IV for neurologwatery or bloody dithylhyical symptoms; titrate dose arrhea, abdominal drazine to symptoms, up to 15 to pain, muscle cramps, loss of coor- 20 g/day; intensive support; recovery in days; dination; convulsion, death in 5 to 7 days in coma, and death in severe poisonings severe cases Nausea, vomiting, ab- Thioctic acid, 75 mg IV Cyclo6 to 24 hr Cellular destrucdominal pain, proevery 6 hr, titrated to peptides tion; hepatic, reamanitin hal, and GI fuse diarrhea; short symptoms and transremission, then jaun- aminase level;* penicillin G necrosis dice, liver and renal sodium, 250 mg/kg/day IV, failure, convulsions, vitamin B complex, vitamin coma, and death K, 40 mg daily; ? highdose corticosteroids; ? plasma exchange, charcoal hemoperfusion; intensive monitoring; recovery, days to weeks; death in 4 to 7 days in severe poisonings *No controlled studies documenting efficacy.

Incubation Toxin Period Muscarine 30 min to 2 hr and muscarinic compounds

Mechanism of Action Affects autonomic nervous system

a PT of 54.1 (control, 10.9 seconds) and a PTT of 54.6 (control, 20 to 36 seconds). The patient was given Vitamin K 5 mg IV and fresh frozen plasma, and her maintenance fluids were changed to Dlo with Hepatamine ®. Because of her rapidly deteriorating clinical course and her hepatic failure, she was transferred to another hospital and a liver transplant was performed the following day. Question: What is the differential diagnosis of a mushroom ingestion? 102/1100

Principal Mushrooms

Cfitocybe dealbata, Clitocybe cerussata, Clitocybe illudens, (Omphalotus olearius), Inocybe species Coprinus atramentarius, Clitocybe clavipes

Amanita muscaria, Amanita pantherina

Psilocybe cubensis, Psilocybe baeocystis, and other

Many different genera and species

Gyromitra esculenta and other species

Amanita phalloides, Amanita bisporigera, Amanita ocreata, Amanita verna, Amanita virosa, Galerina autum natis, Galerina marginata, Galerina venenata, Lepiota species

Dr Bivins: Ideally the patient who ingests a toxic mushroom presents to the ED giving that history and providing a sample of the mushroom. The emergency physician then can either identify the mushroom or contact consultants. Without the history of m u s h r o o m ingestion it is extremely difficult to confirm the diagnosis based on presenting symptoms. Mushroom ingestion should be considered in patients who present with an u n k n o w n ingestion, or with symptoms of nausea, vomiting, diarrhea, dizziness, ataxia, liver or renal failure, anticholinergic or cholinergic syndrome, seizures, hallucinations, altered mental status, coma, or a

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disulfiram-type reaction. Obviously this is a broad spectrum of complaints. The liver damage produced by some mushrooms may provide a more manageable differential diagnosis, but other causes of hepatitis still must be considered. Hepatitis A and B; together w i t h Epstein-Barr virus, h e r p e s v i r u s , and cyt0megalovims, account for most cases of acute hepatitis. Less common causes of'an acute hepatitis-like illness include toxoplasmosis, rickettsia, leptospirosis, syphilis, and Wilson's diseaseA, 2 Fulminant hepatic necrosis is rare in the pediatric population; its incidence is less than one in !,000 patients who are icteric due to presumed viral hepatitis. 2 In the ED, clinical clues suggesting an atypical course of hepatitis include relapse of initial symptoms, persistent or increasing jaundice, a low BUN, SGOT of more than 3,000, bilirubin of more than 20 mg/dL, ascites, hypoglycemia, leukocytosis and thrombocytopenia, appearance of a respiratory alkalosis, and neuropsychiatric changes.Z, ~ In neonates and infants, the most common causes of acute hepatic failure are viral. Severe forms of congenital heart disease and inborn errors of metabolism also may result in acute hepatic failure. Fulminant hepatic necrosis in older children is of viral etiology 10% to 30% of the time. Other infectious agents causing fulminant hepatic failure include leptospirosis, yellow fever, Q fever, and hepatic abscesses from bacteria or ameba. Specific serologic markers and appropriate cultures usually will identify the responsible agent. Wilson's disease (a rare inherited disorder of copper metabolism) presenting as acute hepatic failure is difficult to distinguish from idiopathic forms of acute liver failure. The diagnosis is suggested by extremely high bilirubin levels, mild increases in the transaminases, low hemoglobin, and an elevated serum copper. Kayser-Fleischer rings {green or golden deposits of copper in Descemet's membrane of. the comea}, when present, are the most helpful physical findings. 4 Reyes syndrome rarely may present as acute fulminant liver failure. Typically, however, the child appears to be recovering from a viral illness and t h e n relapses. The liver disease is manifested by elevation of the transaminases with the SGOT at two to three times normal levels; the bilimbin is normal or mildly elevated and the child is not jaundiced. The serum ammonia usually is elevated and the PT usually is greater than two standard deviations above the mean.2, s I n a child who is well prior to presenting with acute liver failure, the possibility of exposure to a toxic substance should be considered. Ingestions and inhalations of a wide variety of chemical substances may result in fulminant hepatic failure. Acetaminophen, aspirin, isoniazid, valproic acid, hal0thane, carbon tetrachloride, phosphorus, and the cyclic peptides of certain species of Amanita and Galerina may result in acute fialminant liver failure.2, 3 Clinical features of toxic liver disease are nonspecific. Unless the hepatic injury occurs in the postsinusoidal hepatic venous system, neither hepatomegaly nor liver tenderness are present. Frequently extrahepatic symptoms predominate, and unless the physician maintains a high degree of awareness and obtains the history of exposure to a hepatotoxin, the diagnosis of toxic liver disease will be missed. 2 Once the history of a mushroom ingestion is obtained, it is possible to develop a reasonable differential diagnosis of 14:11 November 1985

the type of mushroom ingested. The common mushroom toxins can be grouped by the clinical presentation, organ system involvement, and the time from ingestion to onset of symptoms [Table).6-8 For prognostic purposes the time of onset of symptoms is important. Mushroom ingestion with symptoms beginning within two hours of the ingestion usually are not fatal; those that have delayed(six hours or more) manifestation of symptoms should be considered as potentially fatal ingestions.6-s Certain species of Amanita are responsible for most fatalities in the United States; Amanita phalloides is the prototype. Symptoms typically begin approximately six to 12 hours after ingestion and include nausea, vomiting, and diarthea. Symptoms often remit during the next 24 to 36 hours and the patient appears to be recovering. This latent phase may last as long as three to five days and probably explains the delay in seeking medical attention. After the latent period, lix,er failure may develop, and this may be accompanied by renal failure, coma, and cardiovascular collapse~9 Delayed onset of symptoms also is seen with some species of the Gyromitra group, which are less Common in the United States. Patients usually present within six to eight hours of ingestion, but symptoms may occur a s soon as two hours after ingestion. Clinical symptoms may assist the clinician in d i s t i n g u i s h i n g b e t w e e n Gyromitra and Amanita. The patient who ingests Gyromitra typically presents with headache and emesis in the absence of diarrhea. Patients w h o ingest Amanita usually have nausea, vomiting, and diarrhea without headaches. It is very easy to distinguish visually between the two: Amanita mushrooms have gills, and Gyromitra do notA o In this cash a previously well child presented with delayed onset of symptoms after ingesting a wild mushroom. A potentially fatal ingestion, possibly secondary to a species of Amanita, should be considered and treated accordingly. The child's mother subsequently identified a picture of Amanita pha21oides as the species ingested. Every effort should be made to obtain a sample of the mushroom ingested so that positive identification may be made. Even when a Specimen is available, positive identification often is difficuk. There are thousands of species of mushrooms, many of which, both poisonous and nonpoisonous, resemble one another (personal communication, R Winter, MD, March 1985).6;7,9,11 Identification is even more difficult when t h e sample has been akered by Cooking, eating, gathering, or storage. Numerous field guides aid in the identification of wild mushrooms, and the Poisindex has pictures of the most common toxic mushrooms. Mycologists from local colleges, universities, or mycological societies should be c o n s u l t e d p r i o r to the emergency so that a list of mycologists who are interested in identifying mushrooms may be developed. It is important to remember that mukiple species with both slow- and fast-acting toxins may be ingested. Unless all species are identified, the potentially lethal ingestion may be missed. Patients with symptoms that are serious enough to require therapy should have renal and liver function monitored for at least 48 hours regardless of the time at which symptoms present. 6 Question: What are the pathophysiology and toxicology

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of Amanita phalloides ingestion? David B Mc/Viicken, MD: Poisonous and nonpoisonous Amanita are not easily differentiated (personal communication, R Winter, MD, March 1985). Two principal toxins are involved in Amanita phalloides ingestions. Phallotoxin is a heptapeptide that causes the initial nausea and vomiting. Phallotoxin disrupts hepatic cell membranes and affects the hepatic endoplasmic reticulum. 12 Some authorities believe phallotoxin is an unstable protein that is broken down by cooking or digestive enzymes, producing very few symptoms. 13 This toxin usually acts within six to eight hours. In addition to phallotoxin, there are octapeptides (amatoxins), which are ten to 20 times more toxic and have a delayed onset of 24 to 48 hours. Amatoxin is the principal toxin. The amatoxin binds to RNA polymerase and messenger RNA synthesis is blocked. The half-life of messenger RNA is ten to 12 hours; therefore, cells with a high rate of protein synthesis (eg, hepatocytes and intestinal epithelium) are affected.4,9,14 In some animal studies, up to 60% of the toxin is excreted in the bile, resulting in an enterohepatic circulation. Amatoxin is reabsorbed in the proximal convoluted tubule in the kidney and may cause direct nephrotoxicity. Studies also have shown that the pancreas and blood lymphocytes are affected by the toxin.12,1s There is some variability in symptoms; several members of a family may eat a meal with toxic mushrooms and yet not all wilt develop symptoms. This may be explained by the concentration of toxin, which varies greatly as to the mushrooms , the quantity ingested, or the season and state of maturation of the mushrooms. Usually the ingestion of three mushrooms, or approximately 50 grams, is fatal. 14 Thin-layer chromatography assay is available to detect the presence of phallotoxin or amatoxin from vomitus, intestinal aspirate, stool, or uneaten mushrooms, lz

Question: What is the appropriate initial ED management, as well as definitive and supportive care, of Amanita phalloides ingestion? Richard Lammers, MD: The management of a patient poisoned with an Amanita phalloides mushroom depends on the length of time since the ingestion. If the patient seeks medical attention prior to the development of symptoms, it is very important to minimize absorption of the poison by emptying the patient's stomach. The physician has a choice of two methods, ipecac or gastric lavage. The advantage of the gastric lavage technique is that there is no delay in the administration of charcoal; the charcoal may be delivered through the lavage tube immediately after gastric emptying. The nausea and vomiting induced by ipecac persist for at least an hour after its use. If charcoal is given too soon after the ipecac, the patient usually returns a large portion of the charcoal to the nurse or physician who administered it. On the other hand, the lavage tube may be ineffective in removing large chunks of mushroom. Ipecac is preferable if the patient presents within one to two hours of ingestion. Obviously ff the patient is unconscious, has a progressively decreasing level of consciousness, or is seizing, gastric lavage would be the appropriate method of gastric emptying. If a group of people ate the same type of mushroom and 104/1102

one presents with symptoms, consider the possibility that the others who are not yet symptomatic also may have been poisoned and will require treatment. The techniques of minimizing absorption always are more effective when performed early in the course of the poisoning. Because amatoxins are excreted in breast milk, 16 nursing mothers who have ingested Amanita, asympt0matic or not, should be told to stop nursing until it is determined whether they have been poisoned. The patient usually presents to the ED after the onset of abdominal cramping, vomiting, and diarrhea. In Amanita ingestions this usually implies at least a six-hour delay from the time of ingestion. Because of this delay, and because of the vomiting that already has taken place, most of the mushroom toxins probably will have been absorbed, passed into the duodenum, or removed by vomiting.9, lo Toxins have been found in duodenal aspirates as long as 36 hours after ingestion, however, so delayed gastric emptying may be beneficial. 17 Charcoal may be useful for a much longer time after the ingestion. According to some authors, toxins undergo enterohepatic circulation, making repeated doses of charcoal useful. In addition, charcoal can bind any toxin still in the intestinal contents. Initially the adult patient should be given 50 to 100 g charcoal, and that dose may be repeated every two hours over the next one to one and one-half days. Cathartics usually are not necessary because diarrhea is a prominent feature of the initial Stage of poisoning. 17 Management during the initial stage of poisoning also includes the maintenance of fluid and electrolyte balance. Vomiting and diarrhea can produce severe fluid and electrolyte losses resulting in hypovolemia, hypotension, hypokalemia, and acid-base disturbances. Fluid and electrolyte replacement should be guided by laboratory studies. 17 Volume depletion should be corrected aggressively in order to minimize the severity of renal failure, and the fluid status and urine output should be monitored carefully. Central venous lines, urinary catheters, and frequent vital signs are integral to monitoring fluid status in severely dehydrated patients. Following this initial s y m p t o m a t i c phase~ there is a clinical remission of symptoms, yet hepatocellular damage is occurring. The patient's liver and renal and CNS systems should be monitored during this time. Clotting studies also should be monitoredA 6 Of the commonly used tests, SGOT and SGPT levels are the most sensitive indicators of liver cell damage. Transaminases are among the first laboratory values to rise in the preicteric phase of hepatitis. With liver necrosis large amounts of these enzymes are released from the damaged liver, and levels may increase to ten to 100 times normal. The degree of elevation of these enzymes is of little prognostic value , and abnormalities of these tests are not specific for hepatic disease. SGOT levels may be low in patients with concomitant renal failure. Levels of both enzymes may be low in massive liver necrosis. Nevertheless, the severity of the liver disease in both conditions should be apparent clinically and by other laboratory analyses. Low levels of transaminases in the presence of a high bilirubin level and other signs of liver failur e indicate a poor prognosis. 18,19 Patients sometimes will present to the ED during the third phase of poisoning, when liver and renal failure become clinically evident. If the patient is seizing or is co-

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matose, initial management consists of airway protection, oxygenation, and ventilation as necessary; empiric use of 50% dextrose; and control of seizures with diazepam. Hypoglycemia is a major problem in liver failure. It results from impaired glycogcnolysis and ghiconeogenesis: Serum glucose levels should be monitored hourly at the bedside and confirmed frequently by laboratory analysis. Continous infusion of an IV solution containing 10% dextrose and additional IV boluses of glucose as indicated by the laboratory tests will prevent hypoglycemia.20 Because bradyarrhythmias may occur, these patients require cardiac monitoring during this phase. If liver failure, hypoprothrombinemia and dysfibrinogenemia already are present when the patient presents to the ED, hemorrhage is a concern. 21 Usually the earliest indication of such a c0agulopathy is persistent bleeding from the IV puncture sites. Gastrointestinal hemorrhage can occur, and the patient's stool should be checked for the presence of blood. Coagulation disorders are managed with doses of vitamin K and fresh frozen plasma. 16 If the patient'S renal function is still intact, a urine output of 3 to 6 mL/kg/hr is an optimal range. Whether the use of furosemide, mannitol, and dopamine in impending renal failure presents the oliguric phase of renal failure is not entirely clear. These drugs are used individually or in combination by some physicians. The use of hemodialysis or charcoal hemoperfusion in the management of this type of poisoning is another unsettled issue. Amanita toxin probably is not removed by hemodialysis because of its large molecular size. 12 Dialysis may be useful in the management of significant renal failure. Charcoal hemoperfusion has been shown to be beneficial in the late stages of Amanita poisoning, probably because it removes the metabolites and amino acids that otherwise would cause hepatic encephalopathy.16 Other methods of treating hepatic encephalopathy usually are started once the patient is hospitalized. These indude protein restriction and bowel cleansing. Gram-negative sepsis is a frequent complication of renal failure, and it has been associated with a number of lethal cases of Amanita poisonings. The emergency physician usually will not see patients presenting with this late complication. A number of laboratory studies are helpful once liver failure is apparent. PT is not a sensitive index of liver disease, but it is useful for prognosis and for assessing the danger of bleeding. In viral hepatitis, a prothr0mbin time prolonged more than five to six seconds often (but not invariably) precedes fulminant hepatic necrosisA8, 2o Total serum bilirubin levels may be useful in estimating the patient's prognosis. There are few controlled studies that precisely correlate bilirubin level with prognosis; however, the higher the serum bilirubin concentration in viral hepatitis and acute alcoholic hepatitis, the worse is the prognosis for a protracted course or for death. 18 A single blood ammonia level is not particularly useful in the emergency management of patients in hepatic failure. Ammonia levels usually are not markedly elevated until later in the Course of hepatic failure, and once they are elevated the correlation between blood ammonia and the severity of hepatic encephalopathy is inexact. Arterial ammonia concentrations may be normal in about 10% of patients with grade 4 hepatic encephalopathy. Serial blood ammonia determinations may be of value in that changes 14:11 N0vember 1985

in the levels correlate with changes in neurologic status. 16,22 The ammonia content of freshly drawn blood increases at the rate of 0.003 mg/mL blood per minute at room temperature. Blood drawn for an ammonia level should be placed in a cold purple-top vacutainer tube or in a heparinized syringe and then placed immediately in ice. The sample may be drawn from an artery or vein. If the laboratory analysis will be delayed for more than about 20 minutes, however, an arterial sample should be drawn and frozen immediately. The only therapy universally accepted as beneficial in Amanita poisoning is that of gastric emptyIng, charcoal, and supportive care. In general, supportive care consists of fluid, electrolyte and glucose replacement, monitoring, and the standard techniques of managing renal and liver failure.

Question: Are any specific antidotes useful in the treatment of Amanita phalloides ingestion? Robert Knopp, MD: Unfortunately the data base on specific antidotes or other specific treatment for mushroom ingestions is very limited. Controlled clinical studies do not exist. Some of the therapeutic modalities recommended in the literature include thioctic acid, penicillin G, pyridoxine, and steroids. None of these regimens has been proven to be beneficial in controlled clinical studies. 9 For several years thioctic acid was recommended for serious Amanita phalloides ingestions to prevent hepatic failure. The exact mechanism of action by which thioctic acid allegedly reduces hepatotoxicity is unclear; several mechanisms were proposed but never proven.8, 9 No controlled studies have been conducted in human beings. Several animal studies have shown no apparent benefit. 9 During the past few years, the use of thioctic acid has become more controversial. Olson and colleagues no longer recommend the use of thioctic acid. 9 The Poisindex recommends that until its value has been disproven or a better treatment is available, thioctic acid should be used in severe ingestions. In this case, toxicologists at two regional poison centers did not recommend the use of thioctic acid. Because of the controversy regarding the use of thioctic acid, treatment decisions should be based on consultation with toxicologists at a regional poison center. Pyridoxine has been recommended for treatment of the neurologic manifestations that accompany the ingestion of some mushrooms. 8 Once again, however, no controlled studies document its effectiveness. This case highlights a new treatment for acute hepatic failure from Amanita ingestion in children - - liver transplantation. Transplantation was performed because of the patient's deteriorating liver function and the known mortality from this complication of Amanita poisoning. The most important point for the emergency physician to consider is that specific treatment recommendations for Amanita phalloides ingestion are based on opinion, not well-controlled studies. In cases of potentially severe ingestions, contact should be made with toxicologists at a regional poison center to determine the current recommendations on m a n a g e m e n t of these patients. Most poison centers affiliated with academic medical centers have toxicologists available on a 24-hour basis. Mushroom identification is best accomplished by contacting a mycologist from the local college or university. If

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no m y c o l o g i s t is available, l o o k to P o i s i n d e x for color photographs of poisonous mushrooms. In conclusion, the crucial actions for the emergency physician are the initial stabilization and initiation of gastric emptying and activated charcoal. If the p a t i e n t is hemodynamically stable and the general treatment for poisonings has been instituted, the regional poison center should be Contacted if a severe ingestion is suspected to determine the most current treatment recommendations.

Table reprinted with permission of the authors. Hanrahan JP, Gordon MA: Mushroom poisoning. JAMA;251:Feb 24, 1984:

REFERENCES 1. Slovis TL, Dubois RS, Roderson DO, et al: The varied manifestation of Wilson's disease. J Pediatr 1971;78:578-584. 2. Silverman A, Claude RC: Pediatric Clinical Gastroenterology, ed 3. St Louis, CV Mosby Co, 1983. 3. Harrison S: Principles of Internal Medicine, ed 9. New York, McGraw Hill, Inc, 1980. 4. Mitchell DH: Amanita mushroom poisoning. Ann Rev Med 1980;31:51-57. 5. McCullough AJ, Fleming CR, Thistle JL, et al: Diagnosis of Wilson's disease presenting a fulminant hepatic failure. Gastroenterology 1983;84:161-167. 6. Mitchell DH, Rumack BH: Symptomatic diagnosis and treatment of mushroom poisoning, in Rumack BH, Salzman E (eds): Mushroom Poisoning: Diagnosis and Treatment. Boca Raton, Florida, CRC Press, Inc, 1978, pp 171-179. 7. Lincoff GA, Mitchell DH, Van Nostrand MD: Toxic and Hallucinogenic Mushroom Poisoning. A Handbook for Physicians and Mushroom Hunters. Reinhold Co, Litton Educational Publishing, Inc, 1977. 8. Hanrahan JP, Mordis GA: Mushroom poisoning, case reports and a review of therapy. JAMA 1984;254:1057-1061.

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9. Olson KR, Pond SM, Seward J, et al: Amanita phall0ides-type mushroom poisoning. West J Med 1982i137:282-289. 10. Lampke KF: Pharmacology and therapy of mushroom intoxications, in Rumack BH, Salzman E {eds): Mushroom Poisoning: Diagnosis And Treatment. Boca Raton, Florida, CRC Press, Inc, 1978, pp 125-154. 11. The Medical Letter. 1984;26:67-60. 12. Becket CE, Tong TG, Boemer U, et al: Diagnosis and treatment of Amanita phalloides-type mushroom poisoning - - use of thioctic acid. West J Med 1976;125:100-109. !3. Arora D: Mushrooms Demystified. Berkeley, Ten Speed Press, 1979. 14. Kisilevsky R: Hepatic and nucleolar changes in Amanita poisoning. Arch Pathol 1974;97:253-258. 15. Plotzker R, Jensen DM, Payne JA: Amanita virosa acute hepati c necrosis: Treatment with thioctic acid. A m J Med Sci 1982;283:79-82. 16. Henry JB (ed): Clinical Diagnosis and Management of Laboratory Methods, ed 17. Philadelphia, WB Saunders Co, 1984. 17. Busi C, Fiume L, Costantino D, et al: Amanita toxins in gastroduodenal fluid of patients poisoned by the mushroom Amanita phalloides (letter). N Engl J Med 1979;300:800. 18. Combes B, Schenker S: Laboratory tests, in Schiff L, Schiff ER (eds): Diseases of the Liver, ed 5. Philadelphia, JB Lippincott Co, 1982, pp 263-283. 19. Zimmerman HJ: Hepatotoxicity: The Adverse Effects of Drugs and Chemicals On the Liver. Appetton-Century~Crofts, New York, 1978, p 84. 20. Saunders SJ, Seggie J, Kvisch RE, et al: Acute liver failure, in Wright R, Alberti KGMM, Kervian S, et al (eds): Liver and Biliary Disease: Pathophysiology, Diagnosis, Management. Philadelphia, WB Saunders Co, 1979, pp 570-575. 21. Wyngaarden JB, Smith LH (eds): Cecil Textbook of Medicine, ed 17. Philadelphia, WB Saunders Co, 1985. 22. Jacobs DS, Kasten BL, Demott WR, et al: Laboratory Test Handbook with DRG Index, St Louis, Mosby Lexi-Comp, 1984.

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