A Scombroid Poisoning Causing a Life-Threatening

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Patient. Antonio D'Aloia • Enrico Vizzardi • Paolo Della Pina •. Silvia Bugatti • Francesca Del Magro • Riccardo Raddino • ... After few minutes, a supraventricular tachycardia occurred .... Since Scombroid fish poisoning can easily be confused.
Cardiovasc Toxicol DOI 10.1007/s12012-011-9115-1

A Scombroid Poisoning Causing a Life-Threatening Acute Pulmonary Edema and Coronary Syndrome in a Young Healthy Patient Antonio D’Aloia • Enrico Vizzardi • Paolo Della Pina • Silvia Bugatti • Francesca Del Magro • Riccardo Raddino Antonio Curnis • Livio Dei Cas



Ó Springer Science+Business Media, LLC 2011

Introduction Scombroid poisoning, also called histamine fish poisoning, is an allergy-like form of food poisoning that represents one of the major problems in seafood safety. It consists in a clinical syndrome associated with consumption of fish and, less frequently, cheese containing high levels of histamine [1, 2]. Usually certain families of dark meat fish are involved, mainly Scombroidae and Scomberesocidae (e.g., tuna, mackerel, skipjack, Bonito, and Cero). Other nonscombroid fish (e.g., mahi—mahi, herring, anchovies, sardines, Australian salmon, swordfish) was also reported to be associated with scombroid fish poisoning [1–5]. High fish histamine concentrations have been found responsible for this kind of poisoning. Histamine and histamine-like substances are generated from histidine by a decarboxylase activity of bacteria such as Proteus, Klebsiella, Aerobacter, Serratia, Enterobacter, and Escherichia coli [6, 7]. The presence of this bacteria and the massive histamine production detected in the fish is usually secondary to contamination of handlers and improper refrigeration [7]. The clinical presentation is generally characterized by flushing, rash, swelling of face or tongue, sweating, headache, dizziness, abdominal cramps, diarrhea, nausea, vomiting, palpitations, respiratory distress, and hypotension. The onset of symptoms generally occurs few minutes after ingestion of contaminated food. Usually the course is selflimiting and antihistamines can be used to relieve symptoms. We report a rare case of a life-threatening scombroid

A. D’Aloia  E. Vizzardi (&)  P. Della Pina  S. Bugatti  F. Del Magro  R. Raddino  A. Curnis  L. Dei Cas Department of Experimental and Applied Medicine, University of Brescia, Piazzale Spedali civili, 125100 Brescia, Italy e-mail: [email protected]

poisoning with myocardial ischemia and acute pulmonary edema after tuna ingestion.

Case Report A 16-year-old girl without previous history of cardiac or pulmonary abnormalities, allergies, or others relevant diseases, presented to the emergency department after the onset of flushing and palpitations within a short time of eating a grilled tuna. On examination, she had arterial systemic hypotension (90/60 mmHg), tachycardia, and a diffuse skin erythematous rash. She reported nausea and abdominal pain. The first ECG revealed a sinus tachycardia without ventricular repolarization abnormalities (Fig. 1). The patient was initially treated with steroid and chlorpheniramine (Histamine H1 receptor antagonist) intravenous infusion resulting only in cutaneous rash resolution. After few minutes, a supraventricular tachycardia occurred at rate of 160 bpm with diffuse severe ST segment depression (Fig. 2) reversed to sinus rhythm after diltiazem intravenous infusion. Gradually the cardiovascular status worsened with severe hypotension, cardiogenic shock signs, and onset of flush acute pulmonary edema. The patient received norepinephrine, epinephrine, and diuretics in order to stabilize the hemodynamic parameters. Myocardial necrosis markers increased (max Troponin I of 45 ng/ml) and the echocardiogram documented left ventricle (LV) diffuse hypokinesis with severe decrease in ejection fraction (EF) of 30% and severe mitral valve regurgitation. Blood gas analysis showed hypoxemia and lactic acidosis; the urine culture and drug tests were negative. During the next 30 h period, the patient underwent to mechanical ventilator support. In the next days, gradually the hemodynamic, metabolic, and respiratory parameters

Cardiovasc Toxicol

Fig. 1 First ECG recorded at emergency department showing sinus tachycardia

Fig. 2 Second ECG recorded showing supraventricular tachycardia and diffuse severe ST segment depression

Cardiovasc Toxicol Table 1 Time course of main laboratory parameters Laboratory tests

Admission

After 24 h

After 4 days

Discharge

White blood cells (RV: 4.50–10.80 9 10^3/lL)

14500

23100

8800

7160

pH (RV: 7.37–7.45)

7.29

7.50

7.54

7.4

pO2 (RV: 83–108 mHg)

64

173(*)

76

100 40

pCO2 (RV: 32–45 mmHg)

40

41

41

Bicarbonate (RV: 22–29 mmol/L)

19.2

32.0

35

24.0

Lactate (RV: 0.6–2.3 mmol/L)

8.6

1.1

3.1

1.6

C–Reactive protein (RV: ‹5.00 mg/L)

3.2

20

5.86

3.22

Creatine kinase MB (RV: 0.1–4.0 ng/mL)

64.6

228.2

0.6

\ 0.5

Troponine I (RV: C 0.04 ng/mL)

9.60

45

6.64

B0.015

(*)Patient subjected to mechanic ventilator support. RV Reference Values

improved (see Table 1), and ventilatory support and the inotropic therapy were removed. The echocardiogram performed 4 days after the acute event, documented an EF improving from 30 to 52% and mild mitral regurgitation. The blood tests after ten days showed a myocardial enzyme curve normalization (see Table). Subsequent analysis of the tuna ingested by the young girl documented an extremely high histamine level in the flesh fish ([ 1,000 mg/gr), secondary to a prolonged poor conservation.

Discussion Scombroid poisoning is a form of ichthyosarcotoxism causing a clinical syndrome resulting from the ingestion of mishandled fish, mainly of the scombroid family. Histamine and other decomposition products (such as Putrescine and Cadaverine) are generated by the conversion of free histidine, found at high levels in the muscle of several fishes. Inappropriate storage of these fishes can lead to the decarboxylation of histidine in the flesh to histamine by enterobacteria. Although high flesh histamine concentrations are typically demonstrated in the fish implicated in scombroid poisoning (generally levels greater than 50 mg/100 g), the pathogenesis of this syndrome is not totally explained by the only action of histamine. In fact, there is not a clear dose– response relationship between oral administration of histamine and histamine levels in the decomposed fish, with scombrotoxic fish showing higher toxicity than an equivalent oral dose of pure histamine. These observations have leaded to the research of further mechanisms of toxicity. Today the main hypothesis are related to: (1) an inhibition— potentiation of histamine control enzymes; (2) a mast cell degranulators (Scombrotoxin) present in spoiled fish but not individuated yet; (3) the presence of other histamine agonists; (4) histamine intolerance, that could explain the wide variations between individuals in their susceptibility to histamine in decomposed fish.

Diagnosis is generally clinical, based on the history of the patient and the symptoms. Often, the fish poisoning as the cause of illness is detected after the resolution of clinical syndrome. The symptoms of histamine poisoning mimic those of an IgE-mediated food allergy, as well as flushing, headache, diarrhea, and palpitations. However, in some cases, the scombroid poisoning can be characterized by very serious symptoms, as well as cardiovascular compromission. Indeed Scombroid syndrome is often misdiagnosed and therefore under reported. Nevertheless, this condition represents the 38% of all seafood associated outbreaks in United States, and the 32% in England and Wales, with an incidence (in the highest reported outbreak rates) of 2–5 outbreaks/year/million people (Denmark, New Zealand, France, Finland), and the singularly high rate of 31 outbreaks/year/million in Hawaii [6]. About the therapy, there are not data from clinical trials. H1 and H2 antihistamines generally are effective to relieve clinical symptoms. Support therapy with rehydratation and antiemetic could ameliorate the behavior of patient. In some cases is necessary an aggressive therapy like in anaphylactic shock. Our report serves to highlight a really rare case of cardiac presentation of Scombroid syndrome that has triggered a severe acute coronary acute syndrome complicated by cardiogenic shock requiring mechanical respiratory assistance and continuous intravenous inotropics with resolution of symptoms only several days later. Since Scombroid fish poisoning can easily be confused with food allergy or bacterial food poisoning, the physicians should stay alert assessing the previous consumption of fish that must alert to the possibility of this syndrome.

References 1. Taylor, S. L., Stratton, J. E., & Nordlee, J. A. (1989). Histamine poisoning (Scombroid fish poisoning): An allergy-like intoxication. Journal of Toxicology Clinical Toxicology, 27, 225–240.

Cardiovasc Toxicol 2. Dickinson, G. (1982). Scombroid fish poisoning syndrome. Annals of Emergency Medicine, 11, 487–489. 3. Muller, G. J., Lamprecht, J. H., Barns, J. M., et al. (1992). Scombroid poisoning. South African Medicine Journal, 81, 427–430. 4. Morrow, J. D., Margolies, G. R., Rowland, B. S., et al. (1991). Evidence that histamine is the causative toxin of scombroid fish poisoning. New England Journal of Medicine, 324, 716–720. 5. Scoging, A. C. (1991). Illness associated with seafood. CDR (London England: Review), 1(11), 117–122.

6. Lehane, L., & Olley, J. (2000). Histamine fish poisoning revisited. International Journal of Food Microbiology, 58, 1–37. 7. Staruszkiewicz, W. F., Barnett, J. D., Rogers, P. L., et al. (2004). Effects of on-board and dockside handling on the formation of biogenic amines in mahimahi (Coryphaena hippurus), skipjack tuna (Katsuwonus pelamis), and yellowfin tuna (Thunnus albacares). Journal of Food Protection, 67, 134–141.