The Case: Suspected Amanita spp Mushroom Poisoning

A 12-week-old, 10-pound, intact male springer spaniel was presented to its primary veterinarian for severe lethargy, minimal responsiveness, and vomiting. He had eaten white mushrooms under a tree in the owner’s yard 36 hours prior to presentation. There was no past pertinent history. The puppy had not yet completed the puppy vaccination series.

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Diagnostics

• Complete Blood Count

• White blood cells: 20.9 × 103/μL (range, 4.0–15.5)

• Absolute neutrophils: 17,138/μL (range, 2060–10,600)

• Absolute monocytes:  2090/μL (range, 0–840)

• Red blood cells: 5.28 ×106/μL (range, 4.8–9.3)

• Hematocrit: 36.2% (range, 36–60)

• Hemoglobin: 12.0 g/dL (range, 12.1–20.3)

• Serum Chemistry Panel

• Glucose: 31 mg/dL (range, 70–138)

• Blood urea nitrogen: 9 mg/dL (range, 6–31)

• Creatinine: 0.1 mg/dL (range, 0.5–1.6)

• Total protein: 4.6 g/dL (range, 5.0–7.4)

• Albumin: 2.5 (range, 2.7–4.4)

• Globulin: 1.5 g/dL(range, 1.6–3.6)

• Alanine aminotransferase: >1000 IU/L (range, 8–75)

• Alkaline phosphatase: 304 IU/L (range, 5-131)

• Gamma-glutamyl transferase: 13 IU/L (range, 1-12)

• Total bilirubin: 0.6 mg/dL (range, 0.1–0.3)

• Sodium: 148 mEq/L (range, 139–154)

• Potassium: 3.2 mEq/L (range, 3.6–5.5)

• Chloride: 108 mEq/L (range, 102–120)

Treatment

• Intravenous and oral dextrose

• Broad-spectrum antibiotics—type unknown

• Antiemetic––type unknown

• Intravenous crystalloids––type unknown

The patient was referred for further treatment after stabilization.

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Physical examination (~40 hr after mushroom ingestion) When examined at the referral clinic, the dog was depressed but responsive, with sinus tachycardia (180–220 bpm), 5% dehydration, and pale pink mucous membranes. The remainder of the physical examination was unremarkable.

• The patient was admitted for supportive care and monitoring with a suspected diagnosis of Amanita mushroom toxicity. While hospitalized, the dog remained hypotensive (blood pressure ranged from 108/63 [81] to 80/33 [60] via indirect oscillometric sphygmomanometry) and tachycardic despite intravenous crystalloid and hetastarch boluses. He continued to vomit and developed mucoid diarrhea.

Diagnostics

Outcome

Patient continued to decline clinically. Tachycardia and hypotension progressed despite treatment.  Attempted sampling catheter placement on Day 2 was unsuccessful. The patient hemorrhaged when a bandage was removed at the site of venous access 2 hours after  puncture.

More aggressive treatments and diagnostics including monitoring coagulation and a probable plasma transfusion were recommended at this time. The owner declined further treatment/diagnostics and elected euthanasia.

The Generalist’s Opinion

Barak Benaryeh, DVM, DABVP

Treatment for this dog was fitting for acute liver failure, and it is more than likely that the tragic outcome of this case could not have been prevented. There are some specific areas of treatment that we can examine.

Identify the Mushroom if Possible

Mushroom poisoning in dogs is extremely serious and potentially fatal. The diagnosis in this case was presumptive but certainly seems fitting with the history and clinical signs. If possible, it would have been ideal to try to find the mushrooms the dog had eaten. If attempting to identify a mushroom species, it is important to store the sample correctly: do not place the mushroom in a plastic bag; instead, wrap the sample in a moist paper towel or wax paper, or place in a paper bag.¹

Milk Thistle

Milk thistle or silymarin has been shown to be of benefit in cases of mushroom poisoning. It has a synergistic effect with vitamin E.² Together they have antioxidant, antiinflammatory, antifibrotic, and hepatoprotective properties and can increase survival in cases of Amanita spp poisoning.^2,3 In any case of liver disease, some form of hepatoprotective agent is recommended.

The difficulty with administering milk thistle in this case was that the dog continued to vomit throughout treatment. There is an injectable formulation of silymarin known as silibinin dihydrogen, but it is not available in the United States. We do not know what type(s) of antiemetics were used. If vomiting is protracted and severe, antiemetics such as metoclopramide, maropitant, and ondansetron can be combined for maximal effect.

Enterohepatic Circulation

This is an important concept in many toxicity cases. This dog presented 36 hours after toxin ingestion and was referred to a secondary facility at 40 hours. In theory, recirculation can continue for up to 48 hours.¹ Administering one dose of charcoal, though unlikely to have been of much benefit, may have provided some relief of toxin load. As is the case with any oral agent, controlling vomiting would be important with charcoal administration.

Level of Care

We do not know from this report what was discussed with the clients, what level of care was offered, or the stated prognosis. Dogs can survive Amanita spp poisoning, though exact mortality is hard to predict in any poisoning case as the dose can vary so greatly. This dog’s condition was clearly critical. An aggressive protocol from the outset would have been the ideal approach: multimodal antiemetic therapy, clotting function testing, and possibly additional diagnostics (ultrasound or bile acids) to evaluate the liver could have been included. It is possible the clients would have declined such measures, and it is also possible that there was no saving this dog. In poisoning cases, it is generally a good idea 1) to overtreat initially and then ease up later if the patient is doing well, and 2) to establish an appropriate prognosis and treatment plan and make sure the clients fully understand what is intended. 

Barak Benaryeh, DVM, DABVP, is the owner of Spicewood Springs Animal Hospital. He graduated from University of California–Davis School of Veterinary Medicine in 1997 and completed an internship in Small Animal Medicine, Surgery, and Emergency at University of Pennsylvania. Dr. Benaryeh has also taught practical coursework to first-year veterinary students and was a primary veterinary surgeon for the Helping Hands Program, which trains assistance monkeys for quadriplegic people. Dr. Benaryeh is certified by the American Board of Veterinary Practitioners in Canine and Feline Practice.

The Specialist’s Opinion

Justine A. Lee, DVM, DACVECC, DABT

The most likely cause for hepatopathy in this dog was a toxic mushroom like Amanita spp; however, other hepatotoxicants such as xylitol, blue-green algae, sago palm, and human medications (acetaminophen, NSAIDs, etc) should still be ruled out. Keep in mind that not all mushrooms are toxic, and that there are several toxic classes of mushrooms that cause gastrointestinal, central nervous system, and muscarinic signs (hypersalivation, miotic pupils, vomiting, diarrhea, urination), among others.

When presented with a poisoned patient, it is important to keep in mind that the majority of toxicants lack an antidote. Treatment for the poisoned patient typically is focused on symptomatic and supportive treatment and includes 6 key modalities:

• Decontamination (eg, emesis induction, gastric lavage, administration of activated charcoal, as appropriate)

• Fluid therapy (eg, crystalloids, colloids, transfusions)

• Gastrointestinal support (eg, antiemetics, antacids, prokinetics)

• Cardiovascular support (eg, antiarrhythmics, atropine, beta blockers, blood pressure and electrocardiogram monitoring)

• Neurologic support (eg, anxiolytics, muscle relaxants, anticonvulsants, mannitol)

• Miscellaneous (eg, antidote therapy, vitamin K₁, hepatoprotectants such as n-acetylcysteine or S-adenosylmethionine [SAM-e])

TREATMENT

Decontamination

As this patient presented 36 to 40 hours after exposure, the usefulness of decontamination was limited. Even if the toxicant undergoes enterohepatic recirculation, there is little use of decontamination after 24 hours.^1,2 With more recent ingestion, emesis induction (or gastric lavage) followed by multiple doses of activated charcoal would have been warranted.

Fluid therapy

Little information was provided regarding how this patient was volume resuscitated. Based on the information provided, it is unclear whether oral dextrose was administered to this critically ill patient. Ideally, when a patient is minimally responsive on presentation as in this case, intravenous access should be established immediately for life-saving drug therapy (eg, 0.5–1.5 mL/kg of 50% dextrose diluted 1:3 with 0.9% saline). Based on the sustained tachycardia and obtundation in this patient and the fact that neonates and juvenile animals have a higher fluid requirement and are quite tolerant of fluid therapy, an aggressive fluid resuscitation rate should have been implemented immediately (eg, 5 mL 50% dextrose diluted with 15–20 mL saline over 1 minute, followed by approximately 30–40 mL/kg of IV fluids). In general, neonates and juvenile animals have a maintenance rate of 80–120 mL/kg/day and require more aggressive fluid therapy as compared with adults. Likewise, potassium supplementation should be initiated in hypokalemic patients.

Also, while the use of colloids is generally considered very safe in veterinary medicine, it is important to note that puppies and kittens have a lower total protein due to lower globulin levels; the total solids of 4.6 g/dL may have been appropriate for this patient and did not necessarily indicate that the patient’s colloid osmotic pressure (COP) was low. That said, use of colloids for volume resuscitation was an excellent choice in this patient.

Gastrointestinal Support

It is unknown what type of antiemetic(s) was used in this dog. Maropitant was likely contraindicated due to the dog’s hepatopathy. As maropitant undergoes hepatic metabolism, another antiemetic (eg, ondansestron, dolasetron) could have been used. If these alternatives are not available, half the normal dose of maropitant (eg, 0.5 mg/kg q24h) can be used.*

As liver failure can result in increased gastrin levels (resulting in increased production of gastric acid and secondary gastrointestinal bleeding), use of an antacid ([eg, an H₂ blocker such as famotidine that utilizes the least p450metabolism], sucralfate, or proton-pump inhibitors [eg, pantoprazole]) would also be warranted in this case.

Miscellaneous Therapy

The use of antibiotics was warranted in this dog, as it was unknown if portal circulation was compromised. Additional treatment should have included more aggressive hepatoprotectant therapy––n-acetylcysteine (a glutathione source) and/or SAM-e (a methyl donor). As both are relatively benign, they should have been started immediately and continued for 2 to 4 weeks, depending on long-term monitoring of liver enzymes.

Conclusion

While the prognosis is grave with hepatotoxicants such as Amanita spp, the use of aggressive decontamination, fluid therapy, hepatic support, and symptomatic and supportive care can be life-saving in these patients. This patient likely needed plasma transfusions and additional diagnostics (prothrombin time, bile acids, ammonia, abdominal ultrasound, liver aspirates, etc). The client may have declined these efforts. However, further focus on therapeutics over diagnostics may have been beneficial. Some alternatives include treating supportively with n-acetylcysteine, SAM-e, and a low-protein diet. Regardless, with acute hepatic necrosis or hepatopathy, the prognosis is generally guarded.

*Personal communication, Dr. David Twedt, NAVC 2014.

JUSTINE A. LEE, DVM, DACVECC, DABT, is CEO and founder of VetGirl (vetgirlontherun.com), a subscription-based podcast and webinar service offering RACE-approved CE for veterinary professionals. She has authored and edited several veterinary texts. She has also authored two humorous pet owner books and numerous journal articles. Dr. Lee completed her DVM at Cornell University, internship at Angell Memorial Hospital in Boston, and an emergency fellowship and residency at University of Pennsylvania. She lectures internationally on emergency, critical care, and toxicology and was the NAVC Conference 2011 Small Animal Speaker of the Year.