Toxcard: Shellfish Poisoning

Authors: Shane Ali, MD (EM Resident Physician, Atrium Health’s Carolinas Medical Center); Christine Murphy, MD (EM Attending Physician / Medical Toxicologist, Atrium Health’s Carolinas Medical Center) // Reviewed by: Cynthia Santos, MD (@CynthiaSantosMD); Alex Koyfman, MD (@EMHighAK); and Brit Long, MD (@long_brit)

Case:

A 27-year-old male presents to your ED with paresthesias, nausea, vomiting, non-bloody diarrhea, and ataxia that began about an hour prior to arrival. He states that “a few hours ago”, he had harvested mussels on a beach near his hotel and ingested them about 2 hours ago. On examination, the patient has dysarthria, subjective dyspnea, and paresthesias around his lips.


Question:

What is your suspected diagnosis and management of the patient?


Background:

Shellfish are exoskeleton-bearing aquatic invertebrates that can be univalve (one shell) organisms, bivalve (two shell) organisms, and crustaceans. They include clams, oysters, scallops, and mussels. These organisms are known as filter feeders that feed on suspended matter and food particles in water. However, dinoflagellates produce toxins which can be accumulated in shellfish. In the above clinical vignette, the patient is suffering from a form of shellfish poisoning. There are four classic shellfish poisoning which we will be discussing: paralytic shellfish poisoning (PSP), diarrhetic shellfish poisoning (DSP), amnesic shellfish poisoning (ASP), and neurologic shellfish poisoning (NSP).


Paralytic Shellfish Poisoning Pearls

Background

  • Since 1970, there have been 900 cases of paralytic shellfish poisoning (PSP) reported in North America and Europe.
  • While PSP is typically associated with consumption of shellfish like clams and mussels, cases of PSP following ingestion of crustacea and gastropods have been reported in Japan and Malaysia. [1]

Toxin

  • Saxitoxin, a very potent neurotoxin is responsible for PSP. [2]
  • The LD50 of ingested saxitoxin is 5.7 mcg/kg. To put that in perspective, the LD50 of cyanide is 1.5 mg/kg. [2][3]
  • Saxitoxin blocks voltage gated fast sodium channels and inhibits signal propagation in neuronal tissue. [2][4]
  • Exposure occurs through ingestion of shellfish contaminated with toxic algae, especially dinoflagellates, that produce saxitoxin. Shellfish are exposed to dinoflagellates during harmful algal blooms that can cause red tides or occur in clear water. [2]
  • Saxitoxin is concentrated in the flesh of filter feeders like clams, oysters, mussels, and mollusks [2]. It is heat and acid stable, so not eliminated by normal cooking methods.
  • Individuals affected are customers of local distributors or those collecting shellfish at the beach. Commercially harvested shellfish are routinely tested for saxitoxin, and seafood harvesting bans occur when levels > 80 ug/100g tissue of saxitoxin.

Clinical features

  • Patients manifest symptoms within minutes to hours.
  • Neurologic symptoms are the most prominent and include ataxia, dizziness and paresthesias.
  • Paresthesias progress from the lips, to the face, then to the extremities.
  • A flaccid paralysis can occur which can lead to respiratory failure.
  • In severe cases, patients can develop hypertension, seizures, and myocardial injury.
  • GI symptoms such as nausea, vomiting and diarrhea are less common.
  • Recovery occurs within 24-48 hours, but patients can have fatigue for several days after.

Management

  • Supportive care is the mainstay of management.
  • Negative inspiratory force measurements can be used to monitor a patient’s respiratory status, and patients require early intubation for signs of impending respiratory failure.
  • Treat seizures with benzodiazepines.
  • Attempt GI decontamination with activated charcoal for patients who present within 4 hours of ingestion.
  • Obtain an EKG to assess for arrhythmias or abnormalities that may predispose the patient to arrhythmias, and monitor the patient’s electrolytes to avoid exacerbation of any arrhythmias.
  • Antibodies against saxitoxin have shown some efficacy in reversing respiratory failure in animals; however, there is currently no antidote available for humans.

Prognosis

  • The mortality of untreated patients is up to 12% and usually results from respiratory failure, often within 12 hours of symptom onset.

Diarrhetic Shellfish Poisoning Pearls

Background

  • Outbreaks are limited to cold and warm temperate areas in Atlantic and Pacific oceans.
  • Dinophysis and Prorocentrum species are the causative organisms. [5]

Toxin

  • The associated toxins include okadaic acid, as well as dinophysistoxins, pectenotoxins, and yessotoxins. [5]
  • Toxins can inhibit phosphatase 1 and 2A, which alters the permeability of intestinal cell membranes. Intestinal cells are stimulated to excrete sodium, which results in GI fluid accumulations and symptoms including abdominal cramping along with secretory diarrhea. [5]
  • Toxins usually accumulate in the digestive gland.
  • Metabolic processes in marine animals such as bivalves can alter toxins thus leading to toxic derivatives. [5]
    • In case of scallops, removal of the gland and eating only the adductor muscle or the fleshy parts make it safe to eat.

Clinical Features

  • Symptoms can begin within 30 minutes to 15 hours.
  • Acute GI symptoms predominate including nausea, vomiting, watery diarrhea, abdominal pain.
    • Symptoms last up to 3 days. [5]

Management

  • Supportive
    • Resuscitate with IV fluids.
    • Treat nausea and vomiting with antiemetics.
    • Treat abdominal pain with analgesics.
  • Workup
    • CBC, electrolytes to monitor for electrolyte abnormalities.
    • Rule out other causes of diarrheal illness with stool sample studies including gram stain, C & S, ova & parasite studies.

Prognosis

  • No known chronic complications from ingestion.

Amnesic Shellfish Poisoning Pearls

Background

  • Cases of amnesic shellfish poisoning with domoic acid have been found in the US along the pacific coast, northeast coast, and western coast of Florida. [6, 7]
  • First reported human poisoning occurred in Canada in 1987 when 143 people became ill and 3 died from eating domoic acid contaminated mussels. [8]

Toxin

  • Domoic acid is structurally similar to glutamate, which leads to excessive excitation and neuronal damage.
  • This toxin inhibits glutamate reuptake by astrocytes, decreasing neuronal concentration and diminishing conversion to GABA.
  • May lead to neuronal necrosis in the hippocampus and amygdala. [6, 7]

Clinical features

  • Symptoms can begin within minutes of ingestion and fully develop within 24 hours of ingestion of toxin.
  • Symptoms include nausea, vomiting, diarrhea, anterograde amnesia, seizures, motor and sensory neuropathies.
  • Severe cases can cause hypotension, bronchorrhea, arrhythmias, ophthalmoplegia, coma, and even death. [6, 7]

Management

  • Supportive
    • Fluid resuscitation.
    • Treat nausea and vomiting with antiemetics.
    • Treat seizures with benzodiazepines.
    • Monitor patient’s airway for respiratory compromise.
  • Work up
    • Basic lab work to monitor shifts in electrolytes – consider CBC and electrolyte panel.
    • Stool sample testing to assess for other etiologies.
    • ECG to assess for arrhythmias.
    • EEG if patient develops seizures.

Prognosis

  • Can involve severe anterograde short-term memory deficits.
  • Some patients have had severe retrograde amnesia extending years prior to ingestion of the shellfish.
  • Based on animal studies, the placental barrier is unable to prevent fetal exposure to domoic acid. Due to this risk, pregnant women are encouraged to avoid consumption of high-risk shellfish.[6, 7]

Neurologic Shellfish Poisoning Pearls:

Background

  • Poisoning is typically seen from consumption of shellfish from Gulf of Mexico and mid-Atlantic waters that are contaminated with brevetoxins. [5]

Toxin

  • Brevetoxins are a group of more than ten natural neurotoxins produced by the marine dinoflagellate Karenia brevis.
  • Brevetoxin can become aerosolized by surf and produce an allergic response which involves rhinorrhea, conjunctivitis, bronchospasm, and cough among individuals by the shore.
  • This toxin affects voltage-gated sodium channel and induces sodium ion influx resulting in neuro-excitation from nerve membrane depolarization and spontaneous firing [9]
    • In some cases, only nerves are depolarized; in other cases, nerve and muscle depolarization occurs. [9]
  • Brevetoxin is rapidly absorbed by the body and is lipid soluble; thus it can readily cross the blood-brain barrier. It is metabolized by the liver and primarily excreted in bile within first 48 hours.

Clinical features

  • Symptoms usually begin between 1-3 hours after exposure and on average resolve within 2-3 days. [4]
  • Symptoms include numbness and tingling in the mouth and legs, loss of coordination, diarrhea, rectal burning, vomiting, sensitivity to hot and cold temperatures, decreased reflexes, mydriasis.
  • Neurologic shellfish poisoning is similar to paralytic shellfish poisoning; however, PSP has a rapid and more severe clinical progression that often involves paralysis, respiratory distress and death if undiagnosed and untreated.

Management

  • Primarily involves supportive care
    • Fluid replacement, observation of respiratory functions, and the administration of sedatives and pain management are the main tasks as there is no current specific antidote available for brevetoxins.
  • Can attempt GI decontamination with activated charcoal within the first 4 hours, but there is no significant evidence of a better clinical outcome. [10]
  • The natural antagonist of brevetoxin is brevenal which is also produced by brevis and may have future therapeutic value but is not currently used for treatment. [11]

Prognosis

  • Symptoms usually resolve within 2-3 days. [5]
  • Brevetoxin may induce DNA damage in human lymphocytes which can impact immune function; however clinical significance is unclear at this time.

Main Points

  • Overall, management is mostly supportive for shellfish poisoning; there is no antidotal therapy available.
  • In the case with paralytic shellfish poisoning, respiratory failure can occur quickly, so be vigilant when addressing patients with rapid paralytic or neurologic symptoms.


References

  1. Chand P (2009) In: Dobbs MRBT-CN (ed) CHAPTER 40 – seafood neurotoxins I: shellfish poisoning and the nervous system. W.B. Saunders, Philadelphia, pp 441–447.
  2. Hurley W, Wolterstorff C, MacDonald R, Schultz D. Paralytic shellfish poisoning: a case series. West J Emerg Med. 2014;15(4):378-381. doi:10.5811/westjem.2014.4.16279.
  3. Schantz EJ, Ghazarossian VE, Schnoes HK, et al. The structure of saxitoxin (letter) J Am Chem Soc. 1975;97(5):1238.
  4. Etheridge SM. Paralytic shellfish poisoning: seafood safety and human health perspectives. Toxicon. 2010;56(2):108–122.
  5. Cetinkaya F, Mus TE. Shellfish poisoning and toxins. Cdc-pdf[PDF – 5 pages]External J Biol Environ Sci. 2012;6:115-19.
  6. Gherezgihier, Bereketabraha, et al. “Detection Shellfish Poisoning, Marine Toxins, Of Food By Hplc:Paralytic Shellfish Poisoning.” International Journal of Advanced Research, vol. 5, no. 10, 2017, pp. 1551–1558., doi:10.21474/ijar01/5671.
  7. Ansdell, VE. Food Poisoning from Marine Toxins. Gary W. Brunette, Editor in Chief. CDC Yellow Book 2018: Health Information for International Travelers. New York: Oxford University Press; May 31, 2017. 77-80.
  8. Lefebvre KA, Robertson A. Domoic acid and human exposure risks: a review.External Toxicon. 2010;56(2):218-30.
  9. Huang JM, Wu CH, Baden DG. Depolarizing action of a red-tide dinoflagellate brevetoxin on axonal membranes. J Pharmacol Exp Ther. 1984 May; 229(2):615-21.
  10. Watkins SM, Reich A, Fleming LE, Hammond R. Neurotoxic shellfish poisoning. Mar Drugs. 2008;6(3):431-455. doi:10.3390/md20080021
  11. Sayer A, Hu Q, Bourdelais AJ, Baden DG, Gibson JE. The effect of brevenal on brevetoxin-induced DNA damage in human lymphocytes. Arch Toxicol. 2005;79(11):683-688. doi:10.1007/s00204-005-0676-2.

Leave a Reply

Your email address will not be published.