scuba diving and decompression sickness

This patient’s history of scuba diving followed by air travel in the same 24-h period should raise one’s suspicion of decompression sickness (DCS). During scuba diving, the increased barometric pressure saturates tissues with dissolved nitrogen, the amount of which depends on the gas mixture breathed, the depth of the dive, and the duration of time spent at depth. Controlled off-gassing during a slow ascent with appropriate decompression stops allows nitrogen to move from the tissues back into the blood and subsequently into the exhaled gas without coming out of solution. If off-gassing is too rapid, nitrogen bubbles will form in tissues, which leads to symptoms. The risk of DCS is normally very low among recreational divers (approximately 2-4/10,000 dives), but the risk is much higher among commercial divers who typically dive deeper and longer.

In cases of DCS, symptoms usually develop within 3 h of surfacing. However, in the present case, the onset of symptoms was associated with rapid decompression during air travel. Modern commercial aircraft are typically pressurized to the equivalent of 7,500 ft (2,250 m) of elevation or a barometric repressure of approximately 75% of sea level. For this reason, air travel within the same 24-h period of scuba diving is not recommended. Common symptoms of DCS include throbbing articular pain sometimes relieved by bending over, aka “the bends.” Brain or spinal cord involvement may lead to paresthesias, bladder dysfunction, ataxia, confusion, strokelike symptoms, or death. Mottling of the skin and pruritus over the trunk and thighs is seen in some cases (choice B is correct). The treatment for DCS is rapid recompression in a hyperbaric oxygen chamber. 1 2

Ciguatera toxin is a heat-stable neurotoxin found naturally in certain commensal reef algae. The toxin is deposited in the tissues of fish that feed on coral polyps. When successively larger predatory fish eat these smaller reef fish, the toxin is concentrated. Cases have typically been associated with ingestion of larger species of barracuda, snapper, grouper, and amberjack in Florida, the Bahamas, the islands of the Caribbean, and the Yucatán Peninsula. Cooking does not reduce the risk because the toxin is heat stable. Typical symptoms included nausea, vomiting, and crampy abdominal pain. Neurologic symptoms include paradoxical heat sensation. Symptoms may last days to weeks. Physical exertion, alcohol, and caffeine may trigger recurrence. Skin rash, arthralgias, confusion, and paresthesias are not typical features of ciguatera poisoning (choice A is incorrect). 3

The clinical manifestations of scombroid fish poisoning resemble those of an immediate food hypersensitivity; however, in the case of scombroid poisoning, the histamine causing the reaction is produced by bacterial overgrowth on unrefrigerated fish. At temperatures higher than 20 °C, bacterial overgrowth can occur within 2 to 3 h. Besides fish, fermented cheeses and eggs may also contain high levels of histamine. Contaminated food may taste “peppery.” Once produced, histamine cannot be degraded by cooking or freezing. Within 1 h of eating contaminated fish, patients can experience flushing of the face and neck, erythematous or urticarial rash, chest tightness, and shortness of breath. Plasma histamine levels are typically elevated. Treatment is with H1 histamine antagonist. Arthralgias, confusion, and paresthesias are not commonly seen with scombroid poisoning (choice C is incorrect). 4

Tetrodotoxin is a potent neurotoxin that blocks voltage-gated sodium channels in neuronal membranes, thus inhibiting nerve depolarization. The toxin is derived from bacterial species found in puffer fish, porcupine fish, ocean sunfish, triggerfish, and certain octopuses. It can be found in the flesh of affected fish but is especially concentrated within the fish’s liver. Poisoning results from ingestion. Cooking does not inactivate the toxin. The diagnosis is suggested by the rapid onset (10 min to 6 h) of neurologic and gastrointestinal symptoms after an appropriate exposure history. Paresthesias of the lips or extremities, cranial nerve dysfunction, leg and arm weakness, miosis, diaphoresis, hypersalivation, and diarrhea are typical. Dysrhythmias, shock, and fatal neuromuscular respiratory failure can develop. This patient’s exposure history, joint pain, mottling of the skin, and confusion are not typical of tetrodotoxin poisoning (choice D is incorrect).5

Footnotes

  1. SEEK Questionnaires ↩

  2. Mitchell SJ, Bennett MH, Moon RE. Decompression sickness and arterial gas embolism. N Engl J Med. 2022;386(13):1254-1264. PubMed ↩

  3. Friedman MA, Fernandez M, Backer LC, et al. An updated review of ciguatera fish poisoning: clinical, epidemiological, environmental, and public health management. Mar Drugs. 2017;15(3):72. PubMed ↩

  4. Feng C, Teuber S, Gershwin ME. Histamine (scombroid) fish poisoning: a comprehensive review. Clin Rev Allergy Immunol. 2016;50(1):64-69. PubMed ↩

  5. Katikou P, Gokbulut C, Kosker AR, et al. An updated review of tetrodotoxin and its peculiarities. Mar Drugs. 2022;20(1):47. PubMed ↩