Toxicon 55 (2010) 630–632

Contents lists available at ScienceDirect

Toxicon
journal homepage: www.elsevier.com/locate/toxicon

A case report of an unusual complication of Amanita phalloides poisoning:

Development of cardiogenic shock and its successful treatment with
intra-aortic balloon counterpulsation
Nazif Aygul*, Mehmet Akif Duzenli, Kurtulus Ozdemir, Bulent Behlul Altunkeser
Selcuk University, Meram Faculty of Medicine, Cardiology Department, Konya, Turkey

a r t i c l e i n f o a b s t r a c t

Article history: Amanita phalloides is responsible for the majority of the fatalities caused by mushroom
Received 21 May 2009 poisoning. It causes damage in liver, kidneys and rarely pancreas, causing encephalopathic
Received in revised form coma, disseminated intravascular coagulation, hemorrhage and hypovolemic shock.
30 September 2009
However, its effect on cardiac functions has not been established yet. In this case report, we
Accepted 15 October 2009
aimed to present a female patient poisoned by A. phalloides mushroom complicated with
Available online 21 October 2009
multi-organ failure and cardiogenic shock due to advanced left ventricular systolic
dysfunction. This case report was the first to show a successful treatment of cardiogenic
Keywords:
Amanita phalloides shock due to mushroom poisoning with intra-aortic balloon counterpulsation, whereas
Cardiogenic shock she did not respond to other therapies.
Intra-aortic balloon counterpulsation Ó 2009 Elsevier Ltd. All rights reserved.
Mushroom poisoning

1. Introduction 2. Case report

Amanita phalloides (A. phalloides) is responsible for the
majority of the fatalities caused by mushroom poisoning
(Escudié et al., 2007; Klein et al., 1989). It causes damage in
liver, kidneys and rarely pancreas, causing encephalopathic
coma, disseminated intravascular coagulation, hemor-
rhage, hypovolemic shock and death (Karlson-Stiber and
Persson, 2003). However, its effect on cardiac functions has
not been established yet.
In this case report, we aimed to present a female patient
poisoned by mushroom complicated with multi-organ
failure and cardiogenic shock due to advanced left ventric-
ular (LV) systolic dysfunction. The patient was treated
successfully with intra-aortic balloon counterpulsation.
* Corresponding author. Selcuk Universitesi, Meram Tip Fakultesi,
Kardiyoloji AD, 42080 Meram, Konya, Turkey. Tel.: þ90 533 653 1042; fax:
þ90 332 241 2151.
E-mail addresses: nazifaygul@yahoo.com, nazif.aygul@tkd.org.tr
(N. Aygul).
A 24-year-old female had admitted to a local hospital
with complaints of abdominal pain, nausea, emesis and
weakness. She had consumed mushroom 6 h before she
admitted to local hospital. Her initial management had
included placement of a nasogastric tube for aspiration and
administration of 60 g charcoal every 4 h. Simultaneously,
fluid and electrolyte resuscitation to treat the copious
emesis were given in the course of intoxication. She had
multi-organ failure in spite of supportive treatment such as
intravenous inotropic therapy and 4 times hemodialysis
were performed between day 1 and day 4. Not with
standing all supportive treatment, her condition deterio-
rated. The patient was transferred to our center with the
diagnosis of mushroom poisoning at 4th day of mushroom
digestion because of multi-organ failure including liver,
renal, and cardiac failure. When the patient was transferred
to our center, she was orthopneic, cyanotic and somnolent.
She had a regular pulse with a tachycardia of 130 beats/
min. Blood pressure was 70/50 mmHg. On auscultation,
bilateral crepitations to upper zones in lung fields were

0041-0101/$ – see front matter Ó 2009 Elsevier Ltd. All rights reserved.
doi:10.1016/j.toxicon.2009.10.022
 N. Aygul et al. / Toxicon 55 (2010) 630–632
detected, and saturation of oxygen was 78% in spite of O2
support. There was S3 gallop and 1/6 systolic apical
murmur on cardiac osculation. The admission electrocar-
diogram (ECG) showed sinus tachycardia with non-specific
ST-T wave changes in anterior leads. Laboratory analyses
showed a prolonged prothrombin time (INR 5.19) and
raised liver transaminases (aspartate aminotransferase
2976 u/L, alanine aminotransferase 1869 u/L, and lactate
dehydrogenase 8659 u/L). The patient was anuric, and
creatinine level was considerably high (5.2 mg/dL). A chest
X-ray identified a borderline cardiomegaly with bilateral
totally-congested costophrenic sinuses. Bedside echocar-
diogram revealed a global left ventricular hypokinesia with
LV ejection fraction (EF) of 24%, end-diastolic diameter of
6.2 cm, and systolic pulmonary artery pressure of
50 mmHg. The cardiac enzymes were normal (creatine
kinase MB 2.14 ng/mL and cardiac troponin I 0.01 ng/mL). It
was detected that the mushroom consumed by the patient
was A. phalloides by the mycologists.
An intra-aortic balloon counterpulsation catheter was
placed because of the gradual deterioration of the clinical
status and laboratory parameters of the patient despite the
intravenous positive inotropic supportive treatment with
high dose of dopamine and dobutamine for 24 h. In within
1 h, under hemodynamic support with intra-aortic balloon
counterpulsation, the blood pressure of the patient rose
to 90/70 mmHg, pulmonary crepitations significantly
decreased, and a notable improvement was observed in
clinical status. At the end of the 6th h, 250 cc urine output
was detected. Four units of fresh-frozen plasma were trans-
fused for the correction of prolonged prothrombin time, and
then a peritoneal dialysis catheter was inserted. In the end of
3rd day, under hemodynamic support with intra-aortic
balloon counterpulsation, the clinical status and laboratory
parameters of the patient fully improved. Her urine output
was measured as 3200 cc/day. Repeated echocardiography
showed an obvious increase in EF (42%) and decrease
pulmonary artery systolic pressure (35 mmHg). At the end of
the 5th day of admission, both intra-aortic balloon counter-
pulsation and peritoneal dialysis catheters were removed.
She was discharged after 12 days of admission.
One month later, the clinical and laboratory findings of
the patient were normal. She has no any complaints and
physical examination was normal. In laboratory examina-
tion, ECG showed no ST-T wave deviations; left ventricular
end-diastolic and end-systolic diameters were measured
by echocardiography as 5.3 and 4.1 cm, respectively, LV EF
was 54%, and pulmonary artery systolic pressure was
28 mmHg; blood transaminases and creatinine levels were
also normal. Twelve METS was achieved in exercise stress
test with Bruce Protocol, and the test was considered as
normal. After 1 year of follow-up, the clinical and labora-
tory findings including ECG and echocardiographic
parameters were completely normal.
3. Discussion
Most of the cases of fatal mushroom poisoning in the
world occur after the ingestion of Amanita species, primarily
of A. phalloides, and it is responsible for 90% of the deaths of
mushroom poisoning (Klein et al., 1989). There are 3 main
631
groups of toxins in these mushrooms: amatoxins, phallo-
toxins, and virotoxins (Vetter, 1998). However, the main
responsible toxins from the fatal poisoning are amatoxins.
They are not destroyed by cooking and interact with RNA
polymerase II in the eukaryotic cells, inhibiting transcrip-
tion. This causes a progressive decrease in mRNA, causing
deficient protein synthesis and cell death. Cells with high
rapid turnover and protein synthesis (e.g. those of gastro-
intestinal tract, liver, and kidneys) are particularly sensitive
to injury (Karlson-Stiber and Persson, 2003). In fatal cases,
patients generally die after 6–16 days and death frequently
occurs in consequence of hepatic failure (Diaz, 2005).
In literature, only a few case reports are available about
the effects of A. phalloides poisoning on cardiac functions.
Forró and Mándli (2003) reported that cardiac functions
were depressed during post-operative period in 3 patients
who underwent liver transplantation due to A. phalloides
poisoning, and speculated that amatoxins, and partly
phallotoxins, might have cardiotoxic effects. In a recently
published case report of a patient with A. phalloides
poisoning, an increase was detected in troponin levels even
though ECG and echocardiographic findings were found
normal (Unverir et al., 2007). However, this increase, as the
authors pointed out, might be secondary to renal failure or
pulmonary infection.
Our patient was admitted to our center at 4th day of
poisoning. The patient had respiratory failure and cardio-
genic shock due to severe LV systolic dysfunction in addition
to usual symptoms and signs of mushroom poisoning due to
liver and renal failure. Although our case did not have any
risk factor for atherosclerosis, specific ischemic changes in
ECG, and elevation in cardiac enzymes, severe LV systolic
dysfunction was detected in echocardiographic evaluation.
These findings showed that LV systolic dysfunction was not
resulted from ischemia or myocarditis. LV systolic dysfunc-
tion might be explained by the inhibitory effect of amatoxins
on RNA polymerase II in myocardial muscles resulting in
decreased protein synthesis that regulates cardiac contrac-
tion. The insufficient tissue perfusion resulting from
decreased cardiac output due to severe LV systolic
dysfunction might have contributed to accumulating of
amatoxins in view of incompetent excretion on liver and
kidneys. Likewise, the fundamental principle in A. phalloides
poisoning treatment is to remove toxins from the body
immediately (Karlson-Stiber and Persson, 2003).
An intra-aortic balloon counterpulsation catheter was
inserted, as a final treatment option, to our patient who had
not improved in spite of all previous supportive treatment
and hemodialysis through 5 days. Intra-aortic balloon
counterpulsation is the most common mechanical circula-
tion support device that has been in use for years in
patients with cardiogenic shock due to cardiac pump
failure, especially in acute coronary syndromes. This device
increases coronary blood flow and decreases LV afterload
and LV end-diastolic pressure without increasing oxygen
demand (Topalian et al., 2008). The improvement in the
clinical condition of our patient achieved by intra-aortic
balloon counterpulsation might have been resulted from an
improvement in circulation leading to a better perfusion in
kidneys, which increased renal excretion accelerating the
removal of toxins and metabolites from the body.
632 N. Aygul et al. / Toxicon 55 (2010) 630–632
In conclusion, A. phalloides poisoning might influence
cardiac functions. Intra-aortic balloon counterpulsation
may provide important benefit in the restoration of tissue
perfusion in mushroom poisoning accompanying with
decompensated cardiac situation.
Conflicts of interest
The authors declare that there are no conflicts of
interest.
References
Diaz, J.H., 2005. Evolving global epidemiology, syndromic classification,
general management, and prevention of unknown mushroom
poisonings. Crit. Care Med. 33 (2), 419–426.
Escudié, L., Francoz, C., Vinel, J.P., Moucari, R., Cournot, M., Paradis, V.,
Sauvanet, A., Belghiti, J., Valla, D., Bernuau, J., Durand, F., 2007.
Amanita phalloides poisoning: reassessment of prognostic factors and
indications for emergency liver transplantation. J. Hepatol. 46 (3),
466–473.
Forró, M., Mándli, T., 2003. Liver transplantation after Amanita phalloides
poisoning from the viewpoint of anesthesia and intensive care based
on three cases. Orv. Hetil. 144 (6), 269–273.
Karlson-Stiber, C., Persson, H., 2003. Cytotoxic fungi–an overview. Toxicon
42 (4), 339–449.
Klein, A.S., Hart, J., Brems, J.J., Goldstein, L., Lewin, K., Busuttil, R.W., 1989.
Amanita poisoning: treatment and the role of liver transplantation.
Am. J. Med. 86 (2), 187–193.
Topalian, S., Ginsberg, F., Parrillo, J.E., 2008. Cardiogenic shock. Crit. Care
Med. 36 (1 Suppl), S66–74.
Unverir, P., Soner, B.C., Dedeoglu, E., Karcioglu, O., Boztok, K., Tuncok, Y.,
2007. Renal and hepatic injury with elevated cardiac enzymes in
Amanita phalloides poisoning: a case report. Hum. Exp. Toxicol. 26 (9),
757–761.
Vetter, J., 1998. Toxins of Amanita phalloides. Toxicon 36 (1), 13–24.