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12 February 2024: Articles  USA

An Unusual Presentation of Severe Ciguatera Poisoning: Case Report

Unusual clinical course, Challenging differential diagnosis, Management of emergency care, Educational Purpose (only if useful for a systematic review or synthesis)

Moshe Bengio ORCID logo1AEFG*, Glenn Goodwin1DEF, Katherine L. O'Neil1A, Laura E. Tortora1AEF

DOI: 10.12659/AJCR.943149

Am J Case Rep 2024; 25:e943149




BACKGROUND: Ciguatera poisoning is presently estimated to afflict approximately 16 000 people in the United States each year. Ciguatera toxicity is due to the ingestion of warm-water reef fish that are known to consume dinoflagellates that contain ciguatoxins (CTXs). Historically, the diagnosis of ciguatera poisoning is confirmed in the emergency department when this ingestion is followed by manifestations of neurologic and gastrointestinal organ symptoms. Some individuals also manifest cardiac symptoms. These symptoms can vary within each organ system in type and duration.

CASE REPORT: In this report, 2 patients (husband and wife) are presented that consumed the same barracuda, resulting in severe ciguatera poisoning diagnosed in the emergency department. One had the complete triad of symptoms of gastrointestinal (GI), neurologic, and cardiac involvement. The other patient lacked neurological symptoms but did experience severe gastrointestinal and cardiac symptoms. It was assumed by the inpatient team, the consulted infectious disease specialist, and, initially, the in-house toxicologist that the lack of neurologic symptoms excluded the diagnosis of ciguatera.

CONCLUSIONS: If these patients had presented separately, only the former would have been considered to have ciguatera poisoning. These 2 cases demonstrate the misunderstanding among healthcare practitioners of the literature on the diagnostic criteria. Therefore, this article aims to analyze ciguatera diagnosis in the emergency department, which will ultimately guide prognostics and management, particularly for severe cardiac symptoms.

Keywords: Ciguatera Poisoning, Emergency Medicine, Toxicology


Ciguatera poisoning is estimated to afflict approximately 16 000 people per year in the United States, although this number is likely underestimated, given that reporting is not required in every state [1,2]. Globally, ciguatera underreporting is estimated at approximately 80% of actual cases [3]. South Florida, particularly Miami-Dade County, which has the highest incidence in the U.S. at 42 cases per population of ~2.9 million in 2019, is still estimated to underreport by a factor of 55–87, despite required state reporting [2,4]. This underestimation is due to the difficulty of diagnosing ciguatera caused by its dynamic range of symptoms [5]. Ciguatera poisoning is due to the ingestion of warm-water reef fish and marine invertebrates that contain ciguatoxins (CTXs) [6]. Similar to anaphylaxis, which requires 2 organ systems for clinical diagnosis, ciguatera is classically diagnosed with the combination of any variety of involvement of both gastrointestinal (GI) and neurological systems in a person that consumed high-risk fish [7]. The additional involvement of cardiac symptoms often constitutes severe symptomatology of bradycardia and/or hypotension, which can rarely be fatal [3,7,8]. Following this, the emergency medicine (EM) textbook definition of ciguatera reports GI and neurologic symptoms with possible cardiac symptoms [9]. Many practitioners, as was the case in the present case report, could follow the textbook definition and deduce that the lack of neurologic or GI symptoms effectively rules out ciguatera. This error could lead to multiple problems in the emergent setting, such as not anticipating severe cardiac manifestations, or if cardiac symptoms are present, physicians may instead turn to more costly inpatient investigations for cardiac disease.

Case Reports

A man (60s) with past medical history of hypertension and right bundle branch block (RBBB) presented with his wife to a South Florida emergency department (ED) in the fall season with diffuse abdominal pain, nausea, severe vomiting, diarrhea, and lightheadedness occurring 2.5 h after consuming a barracuda that he caught earlier in the day and ate 4 h before presenting at the ED. He denied neurological symptoms, including sensory and motor abnormalities, paresthesia, pruritus, cold dysesthesia, changes in taste, headache, excessive sweating, salivation, and lachrymation. Anaphylactic-/histamine-related symptoms common to Scombroid poisoning symptoms such as facial flushing, swelling, itching, or respiratory distress were also not present. His initial vital signs were temperature of 36.4°C, blood pressure (BP) 73/48 mmHg, and new sinus bradycardia of 37 beats per minute (BPM) as seen in the EKGs in Figures 1 and 2. The neurologic exam did not reveal any abnormalities or focal neurological deficits. Additionally, the thoracic exam revealed clear lung sounds and no heart murmurs. Serum laboratory findings were significant for hemoglobin 12.8 g/dL and potassium 3.4 mEq/L, but otherwise were within normal limits, including normal troponin level. At 2 h after arrival at the ED, after 2 L of normal saline boluses, Trendelenburg positioning, and 2 mg of atropine, repeat vitals were 110/56 mmHg and 77 BPM (Figures 3, 4).

The wife (50s) also presented to the ED, with diffuse abdominal pain, watery diarrhea, nausea, and “cold tingling” in her hands and feet, also occurring 2.5 h after the eating the same barracuda. She had no past medical history and reports that it was an average-sized fish that was caught off south Florida’s east coast. She equally shared the entire barracuda with her husband, including all organs, and discarded the inedible parts. Her initial vital signs were temperature of 36.7°C, BP 79/35 mmHg, and sinus bradycardia of 53 BPM, as seen in the EKGs in Figures 5 and 6. Her physical exam showed no focal neurological deficits, clear lung sounds, no cardiac murmurs, and no abdominal rigidity or tenderness. Laboratory testing found a mild leukocytosis of 12.5 (103/mcL) with left shift but was otherwise all within normal limits. Administration of 20 ml/ kg normal saline fluid bolus and 2 doses of atropine 1 mg IV resulted in an improvement of BP to 89/46 mmHg and heart rate to 76 BPM at 2.5 h after arrival at the ER.

The cardiac and GI symptoms of both patients improved within approximately 2 h after arrival at the ER after receiving atropine, normal saline boluses, and ondansetron. The cold tingling in the woman lasted another 8 h after that. The ER team consulted the in-house toxicologist and was initially hesitant to consider ciguatera for the man given the lack of neurologic symptoms. However, the toxicologist later followed up, confirming he had ciguatera, especially considering the classic symptoms in the woman. On admission, the internal medicine team consulted an infectious disease specialist, who ruled that the husband did not have ciguatera given the lack of neurologic symptoms and the diagnosis was changed to gastroenteritis. Both patients were discharged approximately 24 h after admission. The patients were followed up at 30 days and 6 months and reported no recurrent or new symptoms since discharge.



The warm-water, reef-thriving dinoflagellate genera Gambierdiscus and Fukuyoa are responsible for formation of CTXs, which are then ingested by local fish, particularly barracuda, amberjack, moray eel, grouper, parrotfish, red snapper, and less commonly many other fish and marine invertebrates [5,6]. Consumption of these fish that have ingested CTXs lead to development of ciguatera poisoning [5]. Once ingested, CTXs induce voltage-gated Na+ channel activation associated with K+ channel inhibition [5]. The omnipresence of these channels throughout many organ systems leads to a wide array of symptoms that can vary based on fish species and associated toxins, geographical location, fish size, and fish parts consumed [10–12].


There have been more than 175 different non-specific symptoms reported for ciguatera poisoning [6]; 90% of cases have GI symptoms that include abdominal pain, diarrhea, nausea, vomiting [8], and 72% of patients have neurologic symptoms [8]. Caribbean-sourced ciguatera has been reported to cause less neurologic symptoms than Indian Ocean or Pacific cases [13]. Cold allodynia/dysesthesia can manifest as cold sensation felt as painful or burning, reversal of hot and cold sensations, and/or impairment of feeling of hot and cold. Cold allodynia/ dysesthesia is considered pathognomonic for ciguatera poisoning, associated with paresthesia, which occurs first peri-orally then distally [8,12,14,15]. Other typical neurological symptoms include sensory changes, imbalance, visual disturbances, dental pain, pruritus, metallic taste, headache, and facial flushing [8,12,13,15]. It was reported that 22% of patients have cardiac symptoms, including hypotension (<90 mmHg), bradycardia (<60 BPM), palpitations, and various EKG changes [8,12], and 12% had severe cardiac symptoms, defined by the Poison Severity Score as hypotension (<80 mmHg systolic) and/or severe bradycardia (<40 BPM) [8,16]. Figure 7 shows the projected timeline of symptoms from time of ingestion, adapted from a French manuscript, which is based on Lawrence et al [17,18].


There is no readily-available serum testing; therefore, diagnosis in the ED is made clinically [7]. Another clue may be concurrence of ciguatera symptoms among people who ate the same fish [19]. When considering the neurological, gastrointestinal, and cardiac symptoms, multiple current guidelines, like those of the Food and Drug Administration and Center for Disease Control and Prevention, do not clearly define the minimum diagnostic criteria of ciguatera [20,21], although neurologic and gastrointestinal symptoms appear to be the main features in those guidelines [20,21]. On the other hand, Friedman et al proposed a case definition that may help clinicians with navigating diagnosis [7]. Part of this definition has already been endorsed by the Food and Agriculture Organization of the United Nations (FAO) and the World Health Organization (WHO) [6,7].

The WHO and FAO endorsed some of the criteria reported by Friedman et al, who stated that ciguatera is diagnosed clinically after eating ciguatera-associated species and any post-prandial neurologic symptoms within 48 h. GI symptoms generally precede or follow these symptoms. Cardiac symptoms may or may not be present. Laboratory confirmation of CTXs in the consumed seafood or a ciguatera epidemic are helpful and may be sufficient for diagnosis in the appropriate clinical context, but are not required for a clinical diagnosis. There are 2 exclusion criteria – prior neurologic disease and fever – which are never present in ciguatera poisoning [6,7].

The yet-to-be endorsed part of Friedman et al adds that ciguatera should also be considered when species unknown to cause ciguatera are consumed or with atypical symptoms, like lack of neurologic symptoms [7]. To support this part of Friedman et al, CTXs do not gravitate towards a specific organ system. Instead, ciguatera poisoning in etiology occurs from the effect of CTXs on the voltage-gated Na+ channels that are found in the GI, neurologic, and cardiac systems [12]. Therefore, the myriad of external manifestations of the clinical setting should not distract from the physiology or create compartmentalization of organ systems.


Current recommendations for ciguatera poisoning management are to perform supportive and stabilizing measures [8]. Standard Advanced Cardiovascular Life Support (ACLS) guidelines should be followed, if indicated, such as administering up to three 1-mg doses of atropine in 3–5 min intervals for brady-cardia (<50 BPM), and transcutaneous pacing in refractory or unstable cases [22]. Hypotension should be treated with intravenous (IV) fluid boluses initially and as needed IV vasopressor infusions like norepinephrine. Alternatively, epinephrine can be used, especially with concurrent bradycardia. Ondansetron is a common ED anti-emetic with typical doses starting at 4 mg. For significant dysesthesia, pregabalin may be of benefit [23].

Controversially, mannitol (1 g/kg within the first 48 h of symptom onset for best response) has been proposed as a treatment for the neurological symptoms [7,12,24]. The pharmacological mechanism of mannitol is thought to be 2-fold: the first is its ability to decrease neuronal edema by its osmotic diuresis effect and the other by blocking free radicals caused by CTXs [25,26]. The 1988 study by Palafox et al was the first to document mannitol as a treatment for CTXs after it improved neurologic symptoms in all 24 treated patients [24]. Small case studies indicated much less efficacy, prompting a double-blinded randomized controlled trial by Schnorf et al in 2001 [27], who found no significant difference in the mannitol treatment arm compared to control [27]. However, many studies disagree with the data collection and reporting methods in Schnorf et al, thereby questioning their conclusion [28]. Despite the controversy, no studies demonstrated any adverse effects with mannitol use, making it a reasonable option if typical ED supportive and stabilizing measures are ineffective [28]. However, we do recommend carefully monitoring patients receiving mannitol for dehydration caused by diarrhea and vomiting [7].


We cannot exclude the hypothesis that the treatment administered very early (atropine, normal saline boluses, and ondansetron) could have prevented the development of neurological symptoms, which usually occur later. However, mild or no improvement of neurological symptoms by atropine was previously reported in a case series [29].


Unlike the textbook definition of ciguatera, which may appear to require both GI and neurologic symptoms, the inclusion of any organ system symptom from either the neurologic, cardiac, or GI system associated with high-risk fish consumption creates the suspicion for ciguatera poisoning once the appropriate differential diagnoses are ruled out. For emergency care providers, ciguatera poisoning should be added to the differential for hypotension and bradycardia with a history of marine fish or invertebrate consumption regardless of the presence or lack of other symptoms. In patients that do not yet have cardiac symptoms, providers should monitor these patients for evolvement of severe cardiologic symptoms. Fortunately, mortality is low with the proper interventions.


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American Journal of Case Reports eISSN: 1941-5923
American Journal of Case Reports eISSN: 1941-5923