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An unusual case of inferior acute myocardial
infarction associated with advanced second
grade atrio-ventricular block secondary to
scombroid - sh poisoning.
Central European Journal of Medicine
* E-mail: fsarullo@neomedia.it
Received 10 November 2012; Accepted 15 January 2013
Abstract: Background: Scombroid syndrome (histamine sh poisoning) includes symptoms and signs caused by biogenic amines, mainly
due to histamine-containing food. Methods and results: In this report, we describe a 56 year old female who presented in the clinic
with symptoms of scombroid syndrome after the ingestion of tuna sh, then gradually developed cardiovascular shock and inferior
ST elevation myocardial infarction (STEMI) associated with advanced second grade atrio-ventricular block at the electrocardiogram
(ECG) followed by respiratory arrest. Originally, the patient was treated with intravenous uid infusion, steroids, ranitidine and
chlorpheniramine. Following her cardiovascular shock and respiratory arrest, orotracheal intubation was performed and mechanical
ventilation was started immediately. The patient was treated with dobutamine and uid infusion, which has improved her hemodynamic
conditions. Emergency cardiac catheterization was performed one hour after the onset of symptoms and coronary angiography did
not show a signicant coronary artery disease. The clinical picture has improved during the next days, with complete normalization
of the ECG. Conclusion: Severe symptoms, including myocardial infarction. may occur in cases of scombroid syndrome.
© Versita Sp. z o.o
Keywords: Scombroid syndrome • Tuna sh intoxication • Atrio-ventricular block • ST elevation myocardial infarction •
Cardiac shock
1 Cardiac Rehabilitation Unit, Buccheri La Ferla Fatebenefratelli Hospital, Palermo, Italy.
2 Division of Cardiology “Paolo Borsellino” G.F Ingrassia Hospital, Palermo, Italy.
3 Division of Cardiology, Catholic University of Sacred Heart, Rome, Italy.
Filippo M. Sarullo*1, Antonino Di Franco3, Salvatore Milia1,Ylenia Salerno1,
Pietro Di Pasquale2, Gaetano A. Lanza3
Case Report
1. Introduction
Scombroid syndrome (Histamine Fish Poisoning) com-
prises set of symptoms caused by biogenic amines,
mainly the histamine contained in the food.
This disease state occurs generally upon consump-
tion of tuna and other sh belonging to the Scombridae
and Scomberesocidae families, such as mackerel, bo-
nito and saury that contain high levels of free histidine in
the muscles. However, many clinical cases of scombroid
poisoning have also been reported with non-scombroid
sh, such as bluesh, mahi-mahi, sardine, anchovy,
herring and marlin [1-4]. Histamine and histamine-like
substances are generated from histidine by a decar-
boxylase activity of bacteria such as Proteus, Hafnia
aluei, Morganella morganii, Klebsiella pneumonia, En-
terobacter, Escherichia coli, Serratia, Aerobacter and,
more recently, Photobacterium phosphoreum, which
have been isolated from the sh involved in scombroid
poisoning incidents [5-8]. Some of these liable bacteria
can also be present in the ordinary microbial ora of
the sh; many of them derived from contamination that
might happen during food processing, handling and/or
improper refrigeration [8].
Cent. Eur. J. Med. • 8(5) • 2013 • 586-590
DOI: 10.2478/s11536-013-0169-2
586
FM Sarullo et al.
Histaminosis symptoms occur up to few hours after
the poisoning and resemble an allergic reaction [9].
The main clinical manifestations include the skin rash,
urticaria, edema and localized inammation, the gastro-
intestinal tract symptoms (nausea, vomiting, diarrhea),
the haemodynamic changes (arterial hypotension) and
alterations in neurological function (headache, palpita-
tions, tingling, burning, itching [7]. The most frequent
symptoms reported by Lavon et al., included rash, ush-
ing, gastrointestinal complaints and headaches [10]. In
previous clinical studies, there were similar symptoms
described, although with a widespread incidence of
diarrhea and skin rash [11-13]. While scombroid sh
poisoning represents a mild illness that is usually re-
solved with the administration of antihistamine drugs, in
severe cases serious complications may develop such
as bronchospasm, cardiac and respiratory distress, in
more susceptible individuals [14-18].
2. Case Report
A 56-year-old female with a previous history of arterial
systemic hypertension but with no prior cardiac abnor-
malities, allergies, or other relevant diseases, arrived
to the emergency department 30 minutes after eating
cooked tuna sh. Ten minutes after ingestion, she expe-
rienced ushing, headache, nausea, dispnoea, vomiting
and abdominal pain. Physical examination revealed dif-
fuse macular blanching erythema all over the surface of
her body, injected conjunctivae, signs of bronchospasm
to auscultation of the thorax, tachycardia (100 beats
per minute) and arterial systemic hypotension (85/60
mmHg). The rst ECG revealed sinus tachycardia
without ventricular repolarization abnormalities (Figure
1). The cardiovascular examination revealed normal
heart sounds with no murmurs or rub upon auscultation.
Neurological and abdominal examination was normal.
The patient was initially treated with intravenous uids
(crystalloid solutions 1000 ml in 30 minutes followed
by 80 ml/hour infusion), hydrocortisone (1000 mg), ra-
nitidine (50 mg) and histamine H1 receptor antagonist,
chlorpheniramine (10 mg); intravenous infusion result-
ing only in coetaneous rash resolution.
Once admitted to the Emergency Room, arte-
rial blood gas (ABS) showed a pH = 7.098, an arterial
oxygen pressure = 65 mmHg, an arterial carbon dioxide
pressure = 52 mmHg, an oxygen saturation = 86%,
lactate concentration = 3,6 mmol/L, and CHCO3 =–12.3
mmol/L. Gradually the cardiovascular status has wors-
ened, with the emergence of severe arterial hypotension
(70/40 mmHg) and cardiogenic shock signs associated
with an advanced second grade atrio-ventricular block
at the ECG (Figure 2) followed by respiratory arrest.
Endotracheal intubation, mechanical ventilation, and
inotropic therapy (dobutamine: 10 mcg/Kg//min) were
performed. Echocardiogram showed akinesis of the left
ventricular apex and of the inferior wall with an overall
left ventricular systolic function being markedly impaired
with an ejection fraction (EF) of 40%. The patient has
also received intravenous atropine (1 mg) and epineph-
rine (0.5 mg sol. 1:1000), achieving a rapid resolution of
the atrio-ventricular block at the ECG (Figure 3).
Since the clinical picture was consistent with inferior
acute myocardial infarction, the patient was brought to
the Cardiac Catheterization Laboratory, one hour after
the symptom onset, to undergo catheterization. Howev-
er, coronary angiogram showed rather normal coronary
vessels, without atherosclerotic lesions or intravascular
thrombosis.
Blood analysis revealed an increase in the creatine
kinase MB fraction (plasma peak was 38,90 ng/ml; nor-
mal range: 0,1 – 4,5 ng/ml), a signicant positive detec-
tion in troponin T (plasma peak was 278 ng/ml; normal
range: 0,1–14 ng/ml), and a white blood cell count of
25320 per microliter with 88,3% of neutrophilis.
Gradually the hemodynamic, metabolic, and re-
spiratory parameters improved. Within the st day the
ventilatory support was removed and following 26 hours
of admission into the coronary care unit, dobutamine
therapy was gradually reduced until no longer needed.
The ECG revealed normalization of the elevated ST
segment without inversion of T wave in the inferior leads
on the second day (Figure 4). Four days after hospital-
ization, the echocardiogram showed complete normal
left ventricular kinesis, with regression of the akinesis,
previously evidenced, and an EF of 70%. At the fth day
of hospitalization the patient was discharged in good
health.
3. Discussion
Scombroid-sh poisoning is the most common cause
of itchthytoxicosis worldwide [19]. The pathogenesis of
scombroid poisoning has not been clearly elucidated; it
is generally associated with high histamine concentra-
tions in bacterially contaminated sh, because histamine
is heat stable and therefore not destroyed by different
cooking methods [10].
Histamine toxicity is potentiated through inhibition of
metabolizing enzymes , which detoxify histamine, and
through the presence of putrescine and cadaverine [25].
Histamine, putrescine and cadaverine are formed post-
mortem in the muscular tissue of sh, through the action
of certain microorganisms. Histamine interacts with
587
Acute inferior STEMI and scombroid poisoning
several receptors and induces a variety of effects like
clinical poisoning (histamine concentration of 20 mg/100
g is considered to be the threshold) or severe poisoning
(histamine levels over 100 mg/100 g) [10,20]. The Food
and Drug Administration allows maximum histamine
levels of 5 mg/100 g of sh [21]. Due to its important role
as a chemical mediator of inammation, vasodilatation,
increased vascular permeability, decreased peripheral
resistance, airway smooth muscles contraction, gastric
acid secretion and induction of pain and itching through
sensory nerves stimulation, histamine levels should be
tightly controlled. Acting at H1 – H2 receptors, histamine
induces the vascular endothelium to release nitric
oxide, leading to vasodilation, erythema, increased
vascular permeability and edema [22]. Vasodilatation
and reduced peripheral resistance may contribute to
a signicant fall in blood pressure [23]. Histamine can
cause, directly or indirectly coronary spasm, which is
proposed as the main underlying mechanism of allergy-
induced coronary syndromes [15-17]. Profound drop in
contractility and disrhythmias such as sinus tachycardia
or idioventricular rhythm during exposure to an allergen,
are in proportion to the amount of released histamine
[24]. The ectopic and sinoatrial node automatism stimu-
lation is H2 receptor dependent, whereas conductance
Figure 1. The ECG revealed a sinus tachycardia without ventricu-
lar re-polarization abnormalities
Figure 2. The ECG revealed a ST elevation in inferior leads with
advanced second grade atrio-ventricular block.
Figure 3. The AV block resolved after atropine and epinephrine
injection.
Figure 4. The ECG revealed normalization of the elevated ST
segment without inversion of T wave in inferior leads on the
second day.
588
FM Sarullo et al.
disturbances are H1 receptor mediated [25]. Histamine
effect on H1 receptor could explain the atrio-ventricular
block that was observed in our case. Just as during the
course of anaphylactic reaction, myocardial ischemia
may result also from the instability in circulatory system
(drop in coronary perfusion pressure) and from the
pathophysiology due to disturbances, shock, or other
etiology [24].
Scombroid poisoning can nevertheless mimic other
conditions. A correct diagnosis is deemed important,
since prompt identication and reporting will assist of-
cials in preventing others from becoming ill. There are
a variety of laboratory methods developed to test the
levels of histamine in sh and sh products. In contrast
to many other more potent seafood toxins, the relatively
high action levels established for histamine in sh, has
allowed for the detection of histamine levels and its use,
involving a variety of different approaches. These range
from simple and inexpensive thin layer chromatography
procedures to labor-intensive and more powerful liquid
chromatography coupled with mass spectrometric
detection methods [26]. Unfortunately, in here reported
case, it was not possible to perform the tests using tuna
sh eaten by the patient.
People who present to an emergency department
with acute symptoms suggestive of allergy should also
be questioned about consumption of dark-eshed sh
in the hours before onset of symptoms. The diagnosis
is based on taking a good food history and ruling out
other causes of the usually dramatic symptoms. How-
ever, measurement of plasma histamine concentration
is not widely available in clinical laboratories. Treatment
is supportive nevertheless and use of antihistamines
and in some case corticosteroids may relieve the symp-
toms, although they may resolve within few hours, even
without specic treatment. Major scombroid poisoning
can induce severe hypotension requiring intravenous
uids and inotropic support with dobutamine and/or
dopamine infusion and intravenous epinephrine [27]. In
severe cases, urticaria and bronchospasm may occur,
but death is unusual [28]. Scombroid poisoning can be
prevented by refrigerating the dark-eshed sh (fresh or
canned sh that has been opened) and by ensuring that
such sh is not consumed if it has been kept opened
for several days. Since the toxins that cause scombroid
poisoning are heat stable [29], cooking of contaminated
sh will not eliminate them nor reduce the risk of illness.
4. Conclusion
Scombroid syndrome may occasionally be very severe
and trigger signicant cardiovascular symptoms. In this
case, the patient required intensive care in order to
hasten a good outcome. Our report serves to highlight a
rare case of one severe scombroid syndrome triggering
acute coronary syndrome complicated by atrio-ventric-
ular block and cardiogenic shock requiring mechanical
respiratory assistance and continuous intravenous
inotropic with clinical resolution only several days later.
Acknowledgments
We thank Edna Sabina Salguero for assisting in English
translation.
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