Temporary left ventricular dysfunction in mushroom poisoning: report of three cases

Abstract

Mushroom poisoning can result in acute kidney injury and fulminant hepatic failure as well as gastrointestinal and neurological disorders. The effects of mushroom poisoning on cardiac functions have not been known well. Only a few case reports have been published to date (1–3). We report 3 patients out of 45 patients who were followed due to acute kidney injury and hepatic injury secondary to naturally growing mushroom ingestion between 2009 and 2012. These three cases suffered from transient impairment in cardiac systolic function in addition to other manifestations of mushroom poisoning.

• Amanita phalloides
• cardiac dysfunction
• mushroom
• poisoning
• toxicity

Case 1

A 27-year-old female with no known medical illness was admitted with dizziness, nausea, and vomiting to a local hospital twenty-four hours after ingestion of naturally growing mushroom. Initial laboratory studies revealed normal kidney and liver functions. The patient presented to our hospital with complaints of diminished urine output and continuing of previous symptoms two days after initial hospitalization. Vital signs were normal at first evaluation; blood pressure 110/70 mmHg, pulse rate 90/min, body temperature 36.7 °C. Physical examination was normal except a mild tenderness in the epigastric region. Laboratory values on admission were as follows: BUN: 101 mg/dL, creatinine 6.16 mg/dL, AST 72 U/L, ALT 484 U/L, potassium 4.1 mEq/L, and sodium 134 mEq/L. The patient underwent 4-hour hemoperfusion with a charcoal cartridge (Adsorba 300 C Gambro, Sweden). She was administered penicillin G infusion along with normal saline hydration. Sibilin was not applied due to unavailability at that time. Hemodialysis was performed as needed. Volume status of the patient was assessed with central venous pressure measurements. On the fourth day of admission, she developed severe dyspnea which was more prominent with physical activity, orthopnea and sinus tachycardia. The pulse rate was rhythmic and 140/min, and blood pressure was 90/60 mmHg. There was no fever. Physical exam revealed S3 Gallop and inspiratory crackles at both lung bases. ECG showed sinus tachycardia as well as antero-septal T wave negativity, which was not present at admission. Transthoracic echocardiography showed diffuse hypokinesia in left ventricle, third degree mitral insufficiency, left ventricular relaxation impairment and an ejection fraction (EF) of 35%. Some biochemical values were as follows, Troponin I 0.4 ng/mL (0–0.2 ng/mL), creatine kinase 59 U/L, CK–MB 23 U/L, AST 24 U/L, ALT 187 U/L, and LDH 960 U/L. Dobutamine infusion along with iv furosemide was started. Urine output improved on the fifth day of hospitalization. Dyspnea and orthopnea disappeared and heart rate returned to normal on the seventh day. The patient was discharged on the 13th day of hospitalization with normal cardiac (normal left ventricular systolic and diastolic function, EF: 60%), liver and kidney function (serum creatinine 0.79 mg/dL).

Case 2

A 46-year-old female had presented to another hospital with complaints of nausea, vomiting, diarrhea and diminished urine output after 3 days of ingestion of naturally growing mushroom. She had undergone three sessions of hemodialysis due to anuria and uremia. She had been referred to our hospital on the sixth day of hospitalization because of deterioration of her general health status. On admission her blood pressure was 120/70 mmHg, pulse rate 72/min. Physical exam revealed prolonged emporium with rare expiratory crackles with no pretibial edema. Initial lab values were as follows; BUN 91 mg/dL, creatinine 7.07 mg/dL, albumin 2.7 g/dL, AST 31 U/L, ALT 48 U/L and serum amanitin level 6.19 ng/mL (BÜHLMANN LABORATORIES AG, Schönenbuch, Switzerland, Elisa kit). The patient underwent 4-hour hemoperfusion with a charcoal cartridge in addition to rehydration with normal saline. Since she experienced newly developed dyspnea, tachycardia on the second day of hospitalization along with finding of inspiratory coracles at both lung bases, fluid infusion was stopped and furosemide IV was commenced. Hemodialysis was continued until urine output was adequate. Transthoracic echocardiography revealed hypokinesia in left ventricular wall, second degree mitral insufficiency, and second degree tricuspid valve insufficiency with an EF of 32%. Biochemistry studies during this time were serum Troponin 1.59 ng/mL, CK: 200 U/L, LDH: 968 U/L, AST: 39 U/L, and ALT: 45 U/L. On the 8th day of hospitalization daily urine output was 1500 cc. Dyspnea and tachycardia disappeared. On the 10th day, BUN 43 mg/dL, creatinine 1.6 mg/dL, AST 8 U/L, ALT 11 U/L, Troponin 0.08 ng/mL, CK 52 U/L, and LDH 340 U/L. Control echocardiography showed improved left ventricular function, first degree mitral insufficiency with an EF of 50%.

Case 3

A 33-year-old female had been hospitalized at another hospital with complaints do nausea, vomiting and diarrhea developing 5 years after ingestion of naturally growing mushroom and the patient had undergone hemodialysis. She had been referred to our hospital on the third day of hospitalization due to progressive deterioration on her condition. The vital signs at presentation were as follows: blood pressure 105/70 mmHg, pulse rate 84/min, and body temperature 36.7 °C. Physical examination was unremarkable. ECG showed normal sinus rhythm. Initial lab values on admission showed BUN 117 mg/dL, creatinine 6.13 mg/dL, albumin 3.3 g/dL, AST 89 U/L, ALT 274 U/L, and LDH: 3900 U/L. The patient underwent hemoperfusion and plasmapheresis along with fluid infusion. Since the patient was anuric and hypotensive hemodiafiltration was applied instead of intermittent hemodialysis. On the 7th day of hospitalization she developed dyspnea. There were inspiratory coracles at both lung bases. Transthoracic echocardiography revealed diffuse hypokinesia in left ventricle, second degree mitral insufficiency, minimal pericardial effusion on the lateral wall and 1.3 cm in the posterior of the right atrium along with an ejection fraction of 35%. Urine output started to increase on the 10th day of hospitalization. Serum creatinine value reduced to 1.8 mg/dL. Dyspnea disappeared completely. Control echocardiogram showed normalized left ventricular wall motion, EF of 55% with no pericardial effusion and second degree mitral insufficiency. The patient was discharged on the 15th day of hospitalization with normal renal and cardiac functions.

Discussion

The most common consequences of mushroom poisoning are liver and kidney toxicity. The main ingredient responsible for the systemic toxicity is amatoxin. Due to unavailability of biochemistry kits, we could measure amanitin level of only one patient. Despite considerable amount of reports describing amanita phalloides induced liver and renal injury in the literature, there are few reports about cardiac dysfunction with ingestion of this mushroom.

In our cases, fluid infusion was done according to volume status and CVP measurements of patients; equilibrium of fluid intake and output and vital signs were monitored. On ECHO performed after onset of dyspnea in the absence of volume overload, cardiac systolic dysfunction was evaluated.

Unverir et al.1 reported a 56-year-old patient who had ingested amanita phalloides mushroom with elevated levels of creatine kinase, CK-MB, myoglobin and troponin I in addition to liver and renal dysfunction despite normal echocardiographic and electrocardiographic findings. Aygul and colleagues2 reported a case that developed cardiogenic shock in addition to liver and kidney toxicity due to ingestion of amanita phalloides mushroom in a 24-year-old patient. This case had sinus tachycardia and nonspecific ST-T wave changes in anterior leads in ECG and dilated left ventricular diameter, extensive left ventricular hypokinesia and an EF of 24% in echocardiography. Interestingly cardiac enzymes were within normal levels (ceratin kinase MB fraction 2.14 ng/mL and troponin I 0.01 ng/mL). This patient was managed with application of intraaortic balloon counterpulsation, infusion of inotropic medications and acute peritoneal dialysis and recovered uneventfully. Control echocardiography one month later showed near normal systolic left ventricular functions.

Becanson et al., was reported 2 cases with toxicity due to ingestion of amanita proxima, a white mushroom species.3 In these cases, there were severe left ventricular dysfunction (left ventricular ejection fraction 20% and 35%) in addition to hepatic and renal dysfunction. Troponin level of one of these cases was high, whereas that of the other case was normal.

All of our three cases showed acute reversible left ventricular dysfunction as well as mildly elevated cardiac enzymes. Ferro and Mandli4 reported postoperative systolic dysfunction in three patients who underwent liver transplantation due to fulminant hepatic failure secondary to mushroom poisoning. The authors proposed that cardiac dysfunction observed in their patients might be due to myocardial toxicity of amatoxin. Like in the cases reported by Unverir et al. and Besancon et al.1,3 one of our patients had elevated troponin I level in the acute phase of the toxicity. We also think that amatoxins might have caused myocardial toxicity and ensuing left ventricular dysfunction and/or elevated cardiac enzymes in our patients. On the other hand troponin values may increase due to acute liver failure, uremic myocarditis and secondary to reduced clearance due to acute renal failure.5 Whereas, the case which was reported by Aygul et al.2 did not show troponin elevation despite a significant dysfunction in the myocardium. This discrepancy may be due to variable effects of mushroom toxins manifested either as cell death or temporary dysfunction.

It is indeed interesting to observe the cardiac involvement very rarely in such a relatively common toxicologic setting. One factor may be the underreporting of cardiac involvement among other more severe and tumultuous organ involvements such as liver, gastrointestinal and renal. Another factor responsible for rare reporting of cardiac involvement may be underdiagnosis of cardiac involvement. Physicians might have been attributing hypervolemic symptoms of cardiomyopathy to concurrent acute kidney injury and do not suspect an underlying mushroom associated cardiac disease. One last factor may be the lack of direct cardiac toxicity of amatoxin or development of cardiomyopathy in presence of facilitating factors.

Early administration of hemoperfusion either alone or in combination with hemodialysis and/or plasmapheresis has been reported to decrease mortality associated with mushroom poisonings.6 Hemoperfusion is the perfusion of the blood taken from the patient through a column of cartridge which is made up from an adsorbent materia such as charcoal. The reversibility of the cardiac dysfunction may be as a result of removal of toxins via hemoperfusion.

In conclusion, although rare, mushroom poisoning can lead to myocardial injury and dysfunction as well as more common hepatic and renal injuries. Patients who had mushroom poisoning should also be evaluated in terms of potential cardiac toxicity particularly in the relevant clinical setting. To better elucidate exact mechanism of myocardial injury induced by amatoxins and the prevalence of cardiac dysfunction in mushroom toxicity, experimental and epidemiologic studies are needed.

Declaration of interest

The authors report no conflicts of interest. The authors alone are responsible for the content and writing of this article.