The Chamber Was the Fifth Thing They Tried After the Snakebite

Editorial still life on a dark slate bench: five amber antivenom vials standing in a steel rack at the left, and a brass hyperbaric chamber pressure gauge at the right with its red needle pointing into the green treatment band

The patient was a man in his fifties, bitten on the plantar surface of the midfoot by what the wound service at the University of Texas at San Antonio believed was a cottonmouth. He received ten vials of Crotalidae immune F(ab’)2, the equine antivenom fragment used across North America, during his first admission. Five days later the foot was in trouble again: severe swelling, pain that kept escalating, pins and needles, pallor, a capillary refill too slow to trust, and pedal pulses that could no longer be felt through the tissue.

That is the moment hyperbaric oxygen tends to enter these stories. In this case, published in the October issue of the Journal of the American Podiatric Medical Association, it came in fifth, behind the antivenom, behind the decision to operate, behind the drainage that found purulent fluid under pressure and tissue already dead, and alongside a set of acellular fish-skin grafts and, eventually, a split-thickness skin graft. The authors do not claim the chamber saved the limb. They report the sequence, note that compartment pressures were never actually measured — the concern was clinical — and let the reconstruction speak for itself.

From a Texas midfoot to a Lisbon finger

The Texas case is not the only 2026 report in which a hyperbaric chamber turned up at the edge of a snakebite. In June, clinicians in Lisbon described a 39-year-old man bitten on the fourth finger by a horned viper (Vipera latastei), a species endemic to the Iberian Peninsula. His first dose of antivenom arrived ten hours after the bite, and two more were needed because his coagulation would not settle. Alongside those, the team added two things: a transdermal nitroglycerin patch and ten sessions of hyperbaric oxygen, both described in Acta Médica Portuguesa as measures “to optimize local perfusion” whose use and benefit “are still discussed in the medical community.” The finger survived with full function.

What makes these two papers worth reading together is what they do not do. Neither proposes that oxygen treats venom. Neither offers a mechanism by which pressure reverses a metalloprotease. Both treat the chamber as one instrument among many in the salvage of tissue that is dying for reasons — oedema, ischaemia, infection — that happen to overlap with indications hyperbaric medicine already owns.

That framing is old, and it is the strongest argument the field has. In 2010 the Undersea and Hyperbaric Medicine journal published a case from Graz in which a 26-year-old Austrian man, bitten by a puff adder he had been keeping illegally at home, developed incipient compartment syndrome on the second day and was put in a chamber until the eleventh, recovering completely. The same issue carried a brief report from Martinique, where five patients among more than 250 bites recorded between 1988 and 2009 received hyperbaric oxygen for local complications — necrotising soft-tissue infection, compartment syndrome, abscess — despite prompt wound care and antivenom. Four did well; one was left with a functional defect of the hand. The Martinique authors wrote the sentence that has been the specialty’s position ever since: snake bites are not a recommended indication, but the local complications are approved uses, and would benefit from prospective study. The journal also ran a two-page commentary beside the Graz case, a pairing that suggests the editors were not entirely persuaded.

A decade later, in Toyama, Japan, a 23-year-old man bitten by another illegally kept puff adder could not be given antivenom at all because none was in stock. He received recombinant thrombomodulin for his coagulopathy and hyperbaric oxygen “to reduce local swelling,” and recovered. His physicians ended their report with the standard request: further studies are needed to prove safety and efficacy.

The only randomised trial in this corner of medicine was run in dogs

The request has been made repeatedly for thirty years. What has been delivered, instead, is a veterinary trial.

Between 2017 and 2021, researchers at the University of Tennessee and several collaborating practices enrolled 36 client-owned dogs that presented within 24 hours of a confirmed or suspected Crotalinae bite. It was prospective, randomised, controlled and blinded. Nineteen dogs received two hyperbaric sessions — compression over 15 minutes, 30 minutes at 2 ATA, decompression over 15 minutes — and sixteen received two hours at 1 ATA as a control, all on top of standard care. Swelling, a wound severity score and a pain score were measured at admission, around each intervention and at discharge.

There was no significant difference in any of the three. Swelling gave a p of 0.414, severity 1.000, pain 0.689. Pain fell significantly over time in both groups, which is what pain does when a snakebite is treated properly and then left alone. The authors, writing in the Journal of Veterinary Emergency and Critical Care in 2024, added the caveat that the study may have been underpowered — a fair point, and also the point: this is the closest thing to a controlled human-equivalent experiment that exists in crotaline envenomation, and it is 36 dogs at a single pressure for half an hour.

The older laboratory record is not more encouraging. Three controlled animal trials of hyperbaric oxygen in brown recluse spider envenomation appeared in the mid-1990s. The Denver group, testing oxygen against dapsone and cyproheptadine in rabbits with adequate power to detect a meaningful difference, found none and declined to recommend any of the three. A swine study at Scott & White reached the same verdict. Only the Duke rabbit work found a signal — smaller lesions at ten days at 2.5 ATA twice daily — and even there the authors noted the effect was not explained by improved blood flow between treatments.

Positive results do exist, but they sit at the mechanistic level. A 2024 mouse study from Zunyi Medical University found that hyperbaric oxygen added to antivenom improved 24-hour survival and reduced venom-induced lung injury in Deinagkistrodon acutus poisoning, with shifts in the Th17/Treg balance. It is careful work in 96 mice, and not a reason to put a person in a chamber.

Compartment syndrome is the hook the chamber gets hung on

If there is one clinical situation where the hyperbaric argument becomes plausible, it is venom-induced compartment syndrome — and 2026 produced the best map of that territory to date. A scoping review in PLoS Neglected Tropical Diseases, led from Groningen and the Liverpool School of Tropical Medicine with co-authors from Kano, Kumasi and the Rocky Mountain Poison and Drug Center, pooled 115 published cases. Viperids caused 73 per cent. Upper limbs were affected in 63 per cent. Europe contributed 40 per cent of the cases, South-East Asia 13 per cent and Africa 6 per cent — an inversion that says more about publishing than about snakes. Compartment pressure was actually measured in only 38 per cent of patients. Coagulopathy was present on admission in 40 per cent.

Two findings matter for anyone tempted to reach for oxygen. First, antivenom is the first-line treatment for venom-induced compartment syndrome, supported by eight animal studies and seventeen human observational studies. Second, analysis of those observational studies suggests the condition is overdiagnosed when clinicians rely on symptoms alone — pain, tenseness, paraesthesia — which is exactly the picture that makes a surgeon open a leg. Among the 12 per cent of patients managed without surgery, none developed ischaemic contracture and none required amputation. The review’s own conclusion is that better diagnostics, possibly ultrasound, are needed before fasciotomy decisions can be made well, and that the timing of surgery as a rescue therapy remains unresolved.

A Turkish cohort published in September in the Journal of Clinical Medicine shows how that uncertainty plays out at the bedside. Of 50 patients with extremity snakebite treated at a single centre between 2023 and 2025, six underwent fasciotomy. Those six had higher composite clinical scores — median 6 out of 6 versus 1 — and presented later, a median of 4.5 hours versus 2. The authors concede their retrospective score has no established diagnostic validity, and that the association does not prove the operations were necessary.

Now consider the Texas foot, where pressures were never obtained, where imaging showed nothing, and where an operation was indicated independently by necrosis and suspected infection after the patient had been walking in contaminated floodwater. In that grey zone — a limb that looks compartment-syndromic, an antivenom already given, a surgeon already committed — hyperbaric oxygen is neither absurd nor proven. It is an adjunct borrowed from adjacent indications: crush injury, compromised grafts and flaps, progressive necrotising infection. In the Martinique series, that borrowing was stated openly. It is the most defensible version of the practice, and it is still an inference.

None of this is a cleared indication

The regulatory picture has not moved. Snake envenomation appears nowhere on the Undersea and Hyperbaric Medical Society’s list of accepted indications, now in its fifteenth edition, whose entries run from air or gas embolism to avascular necrosis of bone. It appears nowhere in Medicare’s National Coverage Determination 20.29, which limits payment to a named list that includes crush injuries and suturing of severed limbs, progressive necrotising infections, compromised skin grafts and qualifying diabetic lower-extremity wounds.

A centre that treats a bite victim therefore has to decide which of those boxes the patient actually fits. “Crush injuries” is the box most often implied, and a bite is not a crush. “Progressive necrotising infection” is defensible when there is one, and both 2026 cases had tissue that had died. The diabetic-wound category comes with a thirty-day standard-therapy precondition, and continued treatment is not covered if measurable healing has not appeared within any thirty-day window. None of these categories was written with venom in mind.

The device side carries its own warning. In August 2025 the Food and Drug Administration wrote to health care providers about fires involving hyperbaric oxygen therapy devices that “resulted in serious injuries and deaths,” with the root cause not yet known, and listed the precautions it expects: the manufacturer’s instructions for use, fire prevention measures, proper grounding, staff training, monitoring the patient for the duration of treatment, cleaning and maintenance intervals, no prohibited electrical or static devices inside the chamber, and clothing made of hyperbaric-compatible materials such as cotton rather than wool or synthetics. Nothing in that letter carves out an exemption for unproven indications, lower pressures or a patient whose alternative is amputation. Barotrauma and oxygen toxicity do not become hypothetical because the cause is sympathetic.

Where the bites actually are

The World Health Organization’s fact sheet puts the global burden at roughly 5.4 million bites a year, of which 1.8 to 2.7 million involve envenoming, causing between 81,410 and 137,880 deaths and about three times as many amputations and permanent disabilities. Its road map aims to halve mortality and disability from snakebite by 2030. The organisation is blunt that the decisive intervention already exists: high-quality antivenoms, which sit on the WHO List of Essential Medicines and should be part of any primary care package in an affected region.

That geography is the quiet problem with the hyperbaric hypothesis. The burden sits in rural Africa and Asia, in district hospitals that struggle to stock antivenom, let alone run a chamber with trained attendants, medical gas and fire protocols. Hyperbaric oxygen is concentrated in wealthy coastal cities and in countries where snakebite is a rare occupational curiosity. Whatever the biological plausibility of pressurised oxygen in venom-injured tissue, a therapy that cannot reach the patients with the most to gain is not going to move the 2030 numbers. Ten vials of antivenom, given early, will.

Which returns the argument to where it should sit: a testable question rather than a belief. The scoping review effectively wrote the protocol. Take patients with pressure-confirmed venom-induced compartment syndrome, standardise the antivenom, randomise the chamber against sham pressurisation, and measure hard outcomes — contracture, amputation, function at ninety days — rather than swelling on day two. Until someone runs it, the honest description of hyperbaric oxygen in snakebite is what the Lisbon authors wrote: an adjunct whose benefits remain under discussion, used in the hope that a limb does better, reported afterwards in case reports that cannot tell us whether it helped.

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