Persistent headache associated with scombroid poisoning: resolution with oral cimetidine

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1 Journal of Wilderness Medicine 1, (1990) Persistent headache associated with scombroid poisoning: resolution with oral cimetidine P.S. AUERBACH Departments ofsurgery and Medicine, 1367 Emergency, Vanderbilt University Medical Center, Nashville, Tennessee 37232, USA This case report describes a classical case of scombroid fish poisoning, following which the victim suffered persistent headache, abdominal cramps and diarrhea. The sequelea of the intoxication were refractory to symptomatic therapy. An oral histamine-2 antagonist, cimetidine, successfully relieved the victim of her symptoms. This is the first description of an effective therapy for the clinical residua following a bout of scombrotoxism. Key words: scombroid, headache, marine poisoning, cimetidine Introduction Scombroid poisoning is a well-recognized entity that follows ingestion of certain types of improperly preserved fish. The clinical management of victims has been described for the acute setting of pseudo-allergy, but has not addressed some of the lingering manifestations of an intoxication, such as headache and persistent dyspepsia, which may range in severity from nuisance to debilitating. This report describes the dramatic effect of oral cimetidine upon a patient after four days of unsuccessful traditional therapy for severe headache associated with a classical case of scombroid poisoning. Case report A 40-year-old white female was admitted to the Emergency Department at Vanderbilt University Hospital complaining of severe headache. The patient reported that approximately 90 min prior to admission, she had eaten a luncheon meal of 'blackened' (spiced and fried) tuna, which was also ordered by a male companion. After an interval of approximately 60 min, she suddenly developed a 'bright red flushed face', 'racing heart', overwhelming sensation of warmth, severe frontal headache, nausea and one episode of explosive, watery diarrhea. Her distress became marked in a public area, so an ambulance was summoned, which transported the victim to the hospital. The male companion was similarly stricken, but to a lesser degree, and did not seek medical attention. On initial examination, the patient was an anxious young woman in moderate distress. Vital signs were temperature, 98.4 P; pulse, 80 beats min- 1 and regular; blood pressure, 118/22 mm Hg; and respirations, 24 per min. The remainder of the physical survey was unremarkable with the exception of a fading, nonpalpable and erythematous rash over the chin, neck, chest and upper abdomen, more marked on the ventral surfaces. The victim complained of intermittent and moderate abdominal cramping. Bowel sounds /90 $ Chapman and Hall Ltd.

2 280 Auerbach were hyperactive, but the abdomen was nontender to palpation without masses or organomegaly. Because the victim was no longer nauseated, she was administered diphenhydramine 50 mg by mouth and observed. Over the next hour, the skin appearance returned to normal and the victim remarked that her headache was somewhat relieved. After two additional watery bowel movements, the abdominal cramping subsided. The patient was discharged with a presumptive diagnosis of scombroid poisoning and instructions to continue intermittent oral diphenhydramine for 24 h. The restaurant that had served the fish was notified and promptly removed the fish from the kitchen. The supplier to the restaurant was notified and reported that it had received other telephone calls reporting illness after eating portions of a single large tuna, which was the culprit. Other persons had eaten meals prepared from flesh carved from a different part of the fish without ill effect. The remainder of the fish was destroyed. Four days after her initial visit to the Emergency Department, the victim reported persistent severe headache unrelieved by acetaminophen or diphenhydramine, and continuing episodes of belching and lower abdominal cramping followed by loose bowel movements. Based upon a previous report which documented the efficacy of intravenous cimetidine in managing acute scombroid poisoning, oral cimetidine 300 mg every 6 h for 72 h was prescribed. The woman reported that within 2 h following the first dose, the headache ceased, and that her abdominal discomfort was markedly relieved. All symptoms resolved within 48 h and did not recur after cimetidine was discontinued. Discussion Fish of the families Scombridae and Scomberesocidae (suborder Scombroidei) include the albacore, bluefin and yellowfin tuna, mackerel, saury, needlefish, wahoo, skipjack, and bonito. Nonscombroid fish which produce scombroid (mackerel-like) poisoning include mahi-mahi (dolphin), kahawai, sardine, black marlin, pilchard, anchovy, herring, amberjack (yellowtail or kahala), and the Australian ocean salmon [1-3]. In Hawaii, the most commonly implicated fish is the dolphin Coryphaena hippurus [4]. In the northeastern United States, bluefish (Pomatomus saltratix) has been linked to scombrotoxism [5,6]. Scombroid poisoning accounts for 5% of foodborne outbreaks reported to the Centers for Disease Control in Atlanta, Georgia [7]. Because greater numbers of nonscombroid fish are now recognized as 'scombrotoxic', Prescott has suggested that the syndrome be more appropriately entitled 'pseudo-allergic fish poisoning' [5]. During conditions of inadequate preservation or refrigeration (optimal temperatures for bacterial growth of C), the musculature of these dark-fleshed fish undergoes bacterial decomposition [8-12]. Piscine surface bacteria Proteus morganii, Klebsiella pneumonia, Aerobacter aerogenes, Escherichia coli, Alcaligenes metalcaligenes and others have been implicated in the putrefactive process, which includes decarboxylation of the amino acid L-histidine to histamine and saurine (histamine P0 4 and histamine HCI) [4,13-16]. The term 'saurine' originated because of the association of scombrotoxism with saury, a Japanese dried fish delicacy [17]. Histamine levels of greater than mg 100 gm- I (mg%) are noted in toxic fish. It is not unusual to record levels in excess of 400 mg% in scombrotoxic fish, while normal fresh fish contains less than 1 mg% of histamine [2]. The toxin is heat stable and not destroyed by domestic or commercial cooking [11]. Affected fish typically have a sharply metallic or pepperytaste;

3 Headache with scombroid 281 however, they may be normal in appearance, color and flavor. Not all pesons who eat a contaminated fish may become ill, possibly due to uneven distribution of toxins [18]. It has been postulated that histamine alone is unlikely to be the sole causative agent of scombrotoxism, as high doses of oral histamine can be administered without ill effect, due to conversion in the bowel to N-acetyl histamine [6,9,14]. Potentiators of histamine toxicity in spoiled fish may include cadaverine or putrescine, which might inhibit intestinal histamine-metabolizing enzymes, such as diamine oxidase or histamine-nmethyltransferase [3]. This would allow the absorption and circulation of histamine. Clinical aspects Symptoms which occur within min of ingestion include flushing (sharply demarcated, exacerbated by ultraviolet exposure, and particularly of the face, neck, and upper trunk), a sensation of warmth without elevated core temperature, conjunctival hyperemia, pruritus, urticaria, angioneurotic edema, bronchospasm, nausea, vomiting, diarrhea, epigastric pain, abdominal cramps, dysphagia, headache, thirst, pharyngitis, burning of the gingiva, palpitations, tachycardia, dizziness and hypotension [4,11,19,20]. Untreated, the symptoms generally resolve within 8-12 h. The reaction may be markedly more severe in a person who is concurrently ingesting isoniazid (isonicotinic acid hydrazide; INH), due to INH blockade of gastrointestinal tract histaminase [21]. Therapy Therapy is directed at reversing the histamine effect. Minor intoxications can be treated with intravenous diphenhydramine or hydroxyzine (also an antiemetic), supported as necessary with subcutaneous epinephrine, inhaled bronchodilators, intravenous steroids, and pressor agents. If large quantities of the tainted fish have been consumed within an hour of presentation of the patient to an emergency facility, it may be of value to empty the stomach and administer activated charcoal with a cathartic (if the patient does not already have diarrhea). The histamine-2 antagonists cimetidine (300 mg IV) or ranitidine (50 mg IV) may be rapidly efficacious in alleviating symptoms in patients who do not respond to diphenhydramine [22]. These should be used cautiously when combined with an H-l blocker to avoid hypotension. Nausea and vomiting are usually controlled by the diphenhydramine, but occasionally require the addition of a specific antiemetic, such as prochlorperazine (2.5 mg IV). If the allergic and gastroenteric components are severe, the cumulative effect may induce hypotension, which mandates administration of intravenous crystalloid solutions and, rarely, pressor agents. The lingering effects of scombroid poisoning may be nearly debilitating. It is not uncommon for the victim to suffer from persistent headache, loss of appetite, intermittent diarrhea and abdominal cramping, nausea, weakness and poor sleep. Prior to this report, drug administration was largely unsatisfactory, and symptoms might persist for up to 10 days. The response of the previously-described victim suggests that headache and gastrointestinal discomfort can be controlled with an oral histamine-2 antagonist in standard doses.

4 282 Auerbach Prevention Scombroid poisoning can be avoided to the greatest extent by proper refrigeration, preservation and preparation of fish. All captured fish should be gutted, chilled and placed on ice immediately [23]. No fish should be consumed if it has been handled improperly or has the odor of ammonia. Fresh fish generally has a sheen or oily rainbow appearance; 'dull' packaged fish should be discarded. Conclusion In this report, a new pharmacologic approach to chronic scombrotoxism is described, utilizing the H-2 antagonist cimetidine. In cases where troublesome clinical effects of scombroid poisoning are refractory to common antihistamics, the victim may benefit from the administration of cimetidine. Reference 1. Foo, L.Y. Scombroid-type poisoning induced by the ingestion of smoked kahawai. NZ Med J 1975; 81, Shaw, J.F.E., Birch, W.E., Hutchesen, R.H. and Staruszkiewicz, W. Restaurant-associated scombroid fish poisoning - Alabama, Tennessee. MMWR 1986; 35, Taylor, S.L., Hui, J.Y. and Lyons, D.E. Toxicology of scombroid poisoning. In: Ragelis, E.P., ed. Seafood toxins. Washington, DC: American Chemical Society, 1984: Kim, R. Flushing syndrome due to mahimahi (scombroid fish) poisoning. Arch Derm 1979; 115, Prescott, B.D. Jr. 'Scombroid poisoning' and bluefish, the Connecticut connection. Connecticut Med 1984; 48, Pugno, P.A, Kaufman, D. and Feder, H.M. Jr. Bluefish: a newly discovered cause of scombroid poisoning. J Fam Prac 1983; 17, Restaurant-associated scombroid fish poisoning. Tenn Comm Dis Bull 1986; 18(2),7. 8. Scombroid fish poisoning - New Mexico. MMWR 1988; 37, Arnold, S.H. and Brown, W.S. Histamine toxicity from fish products. Adv Food Res 1978; 24, Behling, AR. and Taylor, S.H. Bacterial histamine production as a function of temperature and time of incubation. J Food Sci 1982; 47, Merson, M.H., Baine, W.B., Gangarosa, E.J. and Swanson, R.c. Scombroid fish poisoning. Outbreak traced to commercially canned tuna fish. JAMA 1974; 228, Foo, L.Y. Scombroid posioning - recapitulation on the role of histamine. NZ Med J 1977; 85, Foo, L.Y. Scombroid posioning, isolation and identification of 'saurine'. J Sci Food Agric 1976; 27, Geiger, E. Role of histamine in poisoning with spoiled fish. Science 1955; 121, Taylor, S.L. Histamine food poisoning: toxicology and clinical aspects. CRC Crit Rev Toxicol 1986; 17, Kawabata, T., Ishizaka, K. and Miura, T. Studies on the allergy-like food poisoning associated with putrefaction of marine products. Separation of causative substance and some of its chemical characteristics. Jpn J Med Sci Biol1955; 8, Hughes, J.M. and Merson, M.H. Fish and shellfish poisoning. N EnglJ Med 1976; 295, Lerke, P.A Scombroid poisoning - report of an outbreak. West J Med 1978; 129,

5 Headache with scombroid Dickinson, G. Scombroid fish poisoning syndrome. Ann Emerg Med 1982; 11, Etkind, P., Wilson, M.E., Gallagher, K. and Cournoyer, J. Bluefish-associated scombroid poisoning: an example of the expanding spectrum of food poisoning from seafood. JAMA 1987;258, Uragoda, e.g. Histamine poisoning in tuberculous patients after ingestion of tuna fish. Am Rev Resp Dis 1980; 121, Blakesley, M.L. Scombroid poisoning: prompt resolution of symptoms with cimetidine. Ann Emerg Med 1983; 12, Kow-Tong, C. and Malison, M.D. Outbreak of scombroid fish poisoning, Taiwan. Am J Public Health 1987; 77,