Hannah in Fiji: Poison from fish? Does that mean DON'T eat the sushi...

The title completely gives away what this case is and man, was it depressing for me! I love fish (all seafood really) and being that I am in Fiji, why wouldn't I exploit this? Alas, definitely having second thoughts on the fish curry from yesterday and the grilled snapper from the day before. Fish toxin is pretty common here and off the coast of Austrailia. Stay tuned...

Case: 47 y/o Fijian M with n/v and diarrhea with abdominal cramping also presents with hypotension and bradycardia 40-50 bpm, afebrile. No chest pain. No focality to his abdominal pain. No prior hx of any medical problems. Mental status intact. Sx started yesterday a/w persistent vomiting and mild diarrhea. No melena, hematochezia, or hematemesis. No trauma.

EKG:

DDx: So just hearing his story ACS, hemorrhaging, AAA, severe pancreatitis, other bad abdominal pathology, if he was altered or had some neuro sx maybe intracranial pathology etc. but...

Of note, his family of 3 are also experiencing same sx. His wife also with bradycardia in the 40s. Her abdominal pain is more severe. Being that his wife is having similar sx, toxicology, ingestions and infectious etiologies now immediately jump to the top of the differential.

Further hx indicates they live in a village that commonly consumes fish. They had a large fish dinner the day before and sx presented after. The only toxins I know from consuming fish are ciguatera, scombroid, pufferfish (tetrodotoxin) - more common in Japan.

Final answer: Probable Ciguatera.
Scombroid causes more of a histamine release and while can cause hypotension it is rare.
Pufferfish wasn't the fish he described and that manifests more as a neurotoxin that can induce paralysis.

Ciguatera poisoning is a foodborne illness caused by eating certain types of reef fish whose flesh is contaminated with toxins produced by dinoflagellates. These dinoflagellates typically live in tropical and subtropical waters living on coral, algae, and seaweed. These dinoflagellates are inadvertantly eaten by herbivorous fish that are later eaten by larger fish exacerbating the bioaccumulation.

Ciguatoxin is a lipid soluble, heat stable, acid resistent neurotoxin. Cooking and freezing the fish do not destroy the toxins and the toxins actually have no abnormal taste or smell.

Clinical manifestations:

GI -gastroenteritis including n/v, diarrhea, abdominal cramping which can begin 3-6 hours after eating contaminated fish, but can be delayed for 30 hours
Neurologic - Abnl appear 3-72 hours after the meal, including perioral paresthesias, pruritus without urticauria, temperature related dysesthesias (meaning cold stimuli is perceived as hot). In the South Pacific, paresthesias occur in up to 10% of patients

Note: I researched an article where a New Zealand woman has been suffering from the dysesthesias for 2 years after vacationing in Fiji!

Cardiovascular - CV signs include bradycardia (as per above EKG), heart block and hypotension

Presentations will often differ according to geographic locations due to different local food habits and various toxins. In the Pacific and Indian ocean regions, the more common presentation is early neurologic, GI and CV findings with neurologic findings predominantly. However, in the carribean neuro symptoms often do not present predominantly.

In Fiji, it is not uncommon to see patients present with ciguatera poisoning. (Being that I was so excited to hear about it and the other residents not batting an eye.)

Care for these patients is mainly supportive. Management was done by recurrent doses of atropine and with an atropine drip. The patient responded nicely. However, I was told that if he did not, they would routinely start isoprenaline (a drug I have never used).

Isoprenaline is a nonselective beta adrenergic agonist used for treatment of bradycardia, heart block and sometimes asthma. Good to know.

Another case that was interesting to me, that actually presented in a previous shift and FINALLY now his labs are back to follow up on.

Case: 65 y/o M hx of HTN presenting with high grade fever, nausea, generalized malaise (sound familiar) but with mild chest pain. Pt with mild hypotension, tachycardia 130s, and febrile 41 C. Lung exam and chest XR was negative for acute.

He was a case of possible sepsis r/o dengue, lepto, typhoid etc. However, coronary artery disease is everywhere and increasing more prevalent in the South Pacific, so ACS is something to consider in addition to those other diagnoses.

Initial EKG:

He did have mild chest pain so I did an EKG that had some concerning fx so I would just trend his enzymes and repeat EKG in a few hours. Give him an aspirin. Pt was given IVF x3, empiric antibx (by the way MRSA -methicilin resistant staph aureus is not common here, so empiric antibiotics are cloxacillin and gentamicin...pretty cool.)

His repeat EKG was not dynamic but his mild chest pain still persisted, although he also had diffuse generalized pain. My grievance was I ordered a cardiac panel thinking troponins were included..they were not. I admitted the patient to medicine and told them of the pending troponins and followed up on him today.

Lab:

He was still in our ED today despite being admitted a day before. No further work up was done for ACS. He was just a dengue r/o, he was still hypotensive but more awake and no longer distressed. Medicine admit told me its probably demand ischemia. Is that not really high for demand? Also, I'm a little upset this was not trended. His chest pain had lasted all day and resolved several hours before my shift started. If he had any stemi changes, then he has infarcted already and way beyond any treatment window. At least he is well currently, so enough with that.

Resources: Uptodate, pubmed

Some pictures of the market and Suva port. Also seafood that is probably riddled in ciguatera toxin...