Frostbite 150 150 Endeavour Medical



What is Frostbite?

Frostbite is a preventable injury which occurs when fluid in the cells and interstitial space freezes following tissue exposure to temperatures below their freezing point (typically -0.55°C) [1]. This occurs in environmental conditions below -10 °C [2,3], but may occur earlier than this. The peripheries are most prone to frostbite, with the feet and hands accounting for 90% of frostbite injuries reported [4]. Other areas commonly affected include the nose, cheeks, chin, ears, lips and penis, though any poorly-perfused peripheral site is at risk.

Records of frostbite date back thousands of years [5]. Until relatively recently, frostbite has been a disease largely confined to certain geographical locations or those exposed to the harshest elements, such as the military or winter mountaineers.

The prevalence of frostbite is now increasing in other populations [1]. This is likely due to several factors including ease of international travel; increased participation in winter and high-altitude sports; an ageing, multi-morbid population with pre-existing risk-factors; and increases in homelessness [6].


Cutaneous circulation plays a significant role in peripheral thermal regulation, allowing heat to escape the body in the form of radiation heat loss in warm environments, whilst swiftly shunting blood away from the peripheries to preserve core body temperature in colder settings. This adaptation is more effective at ‘dumping’ rather than retaining heat, in keeping with our greater adaptation to warm-weather environments.

For frostbite to occur, temperatures have to be low enough for the skin to freeze. At skin temperatures of 15 °C maximal vasoconstriction is reached. At 10 °C neuropraxia occurs with loss of cutaneous sensation. Below 0 °C cutaneous blood flow is low enough for the skin to freeze [2]. The local microvasculature, followed by the venous system are next to be affected. This cascade is characterised by four stages [1,3]:

  1. Pre-freeze phase: The affected area cools, with associated vasoconstriction, increased blood viscosity, and subsequent ischaemia without ice crystal formation.
  2. Freeze-thaw phase: Ice crystals form either intracellularly (in rapid-onset freezing injury) or, more commonly, extracellularly (during slower-onset freezing injuries), causing electrolyte shifts, cellular dehydration, cell membrane destabilisation, and cell death. The thawing process may further exacerbate ischaemia, induce reperfusion injury, and an inflammatory response.
  3. Vascular stasis phase: Alternate vasoconstriction and vasodilation causes sludgy blood flow, coagulation cascade activation, and thrombus formation as well as leakage from the vessels.
  4. Late ischaemia phase: The prior ischaemic events, subsequent inflammatory response and ongoing vascular stasis culminate in a final phase of cell death.

Risk Factors:

Cooler temperatures (averaging below -10 °C) and prolonged exposure both predispose to more severe frostbite, though amputation of injured parts correlates more closely with the duration of cold exposure [7].

In large scale analyses, behaviours which cause intoxication or impair judgement have been identified as increasing risk of sustaining frostbite [7]. Ethnicity has also been studied, with those of Afro-Caribbean descent four times more likely to sustain cold weather injuries than Caucasians in one cross-sectional study [8].

Risk-factors include [9]:
Extremely cold weather, changing weather patterns, wet weather, high-winds, high-altitude.

Alcohol or drug intoxication, smoking, poor nutritional/fluid intake, inadequate layering, poor understanding of the environment and/or the risks of frostbite.

Age*, ethnicity.

Trauma (particularly if it inhibits distal perfusion), diabetes, Raynaud’s disease, peripheral vascular disease, psychiatric illness, neuropathies, dementia, previous frostbite.

Sedatives, beta-blockers.

*Age is an interesting risk-factor. Whilst extremes of age predispose to frostbite (secondary to increased surface area in children and reduced mobility with a more labile autonomic nervous system in the elderly), frostbite is more commonly sustained by adults between the ages of 30 and 49 years [4]. This is likely secondary to behavioural patterns, including increased exposure to colder temperatures and increased risk-taking [4].


Frostbite occurs in environments where hypothermia is a significant risk [3]. Consider hypothermia as a differential or co-existing condition in all frostbitten patients.

Cold-injuries are either freezing (i.e. frostbite) or non-freezing (i.e. frostnip, trench foot, chilblains). 

Non-freezing cold injuries more commonly affect the feet than the hands [10].

Trench foot occurs in cold, wet environments. Prolonged exposure produces peripheral neurovascular damage which is reversible if identified early.

Pernio (chilblains) is caused by repeated exposures to damp, non-freezing conditions. It is associated with localised swelling, erythema and vesicles and is more common in young women.

Frostnip is a superficial injury associated with ice crystal formation on the skin surface secondary to peripheral vasoconstriction. Crystals do not form within the tissue. Any numbness and pallor swiftly resolve, however frostnip heralds conditions favourable for frostbite [3].

Signs and symptoms of frostbite:

The affected area may initially feel cold and painful. This progresses to paraesthesia, numbness, and anaesthesia as the frostbite progresses. This may be elicited on testing fine and gross motor dexterity, with the affected area exhibiting clumsiness and loss of function.

It is very difficult to identify the severity of the frostbite on examination. Typically, tissues blanch before becoming mottled, waxy, or bruised in appearance. Blisters usually form on re-warming.

Classification of frostbite:

Frostbite is difficult to classify acutely, particularly in a pre-hospital setting. Classification tools can be divided into those which prioritise classifying the severity of the injured site and those which try to quantify the amount of injured tissue.

Frostbite can be classified into four stages, similar in nature to that followed by thermal burns. However, classification into these four tiers is based on physical findings as well as advanced imagery after re-warming, making it an incomplete tool pre-hospitally.

The Wilderness Medicine Society thus suggested a two-tier score in their practice guidelines [3], with scoring taking place following re-warming efforts but prior to imaging. ‘Superficial’ frostbite equates to first- or second-degree, with ‘no or minimal anticipated tissue loss’. ‘Deep’ is associated with ‘anticipated tissue loss’ and equates to third- and fourth-degree frostbite.

Above: Frostbite scoring tools based on appearance and severity of the affected site. Table from Hallam M, Cubison T, Dheansa B, Imray C. Managing frostbite. BMJ 2010;341(7783):1151-1156.

Above: Table outlining the Cauchy classification of frostbite, detailing the severity and risk of amputation.

Two tools which attempt to classify topographical extent of the frostbite are the Hennepin score [11] and Cauchy classification [12]. The Hennepin score maps body surface area affected, and applies this to assess effectiveness of treatment. The Cauchy classification measures the extent of the frostbite anatomically. This often proves more useful for assessing how debilitating an injury will be to the patient long-term.

Cauchy E, M.D., Davis CB, M.D., Pasquier M, M.D., Meyer EF, M.D., Hackett PH, M.D. A New Proposal for Management of Severe Frostbite in the Austere Environment. Wilderness Environ Med 2016;27(1):92-99.

Management of frostbite in the field:

Initial assessment of the patient should be undertaken in a systematic manner. The usual ABCDE approach should be followed. Concurrent conditions such as hypothermia and significant trauma must be managed prior to focusing on isolated freezing injuries.

When approaching the frostbitten patient consider their risk-factors, duration and severity of exposure, evacuation options, and how to prevent further heat-loss.

When treating frostbite [1,3,9]:

  1. Prevent further heat loss:
  • Find shelter out of the wind and elements.
  • Replace wet clothes with dry loose clothing (be careful of removing boots, as if the feet swell, they may not fit back in).
  • Remove constrictive items including rings, watches, etc.
  • Rehydrate.
  • Give ibuprofen 400mg BD (also consider other analgesics).

NSAID’s block the production of harmful prostaglandins and thromboxanes whose release leads to vasoconstriction and resultant tissue damage.

  • Evaluate evacuation options including time to secondary care, time to adequate shelter, treatment options in the area, and transport options available.

2. Consider the risk of re-freezing injury:

  • If there is a high risk that the frostbitten area could re-freeze following re-warming efforts e.g., if there is a protracted evacuation, then do not re-warm the affected area.

Re-freezing injuries exacerbate the cycle of vasoconstriction, platelet aggregation, thrombosis and cell death sustained with prostaglandin and thromboxane release and worsen initial injuries.

3. If there is a HIGH risk of re-freezing, then prioritise evacuation to a site where the frostbitten area can be re-warmed with a low risk of re-freezing:

  • If possible, minimise movement and contact with the affected area during this time with splinting, padding, etc. Pragmatic decisions may need to be made at this time to facilitate timely evacuation.

4. If there is a LOW risk of re-freezing injury, then start re-warming efforts:

  • Re-warming is painful, so give analgesia early.
  • The ideal method of re-warming is rapidly in a warm water bath between 37 – 39 °C for 30 – 60 minutes. Use the casualty’s uninjured limb to check the water temperature is acceptable if a thermometer isn’t available.

Rapid re-warming has been found to result in better outcomes than slow re-warming [13]. The water should be agitated and changed regularly to ensure it stays warm. Whilst there isn’t an evidence base for adding antiseptic solutions such as chlorhexidine or iodine to the water, it has a theoretical benefit and is an accepted standard of care [3].

  • Passive re-warming is acceptable if there aren’t resources for water immersion.
  • Do not allow affected areas to come into contact with intense heat such as from hot rocks, the sides of a water bath, radiators, chemical heat pads, etc. The numb area will likely suffer burns as a result.
  • The area is deemed sufficiently re-warmed when it is a red/purple colour, pliable to touch, and soft. Let the area air dry or blot it dry. Do not rub the frostbitten area.

5. Adjunct treatments:

  • Hydrate the patient.
  • Blisters should be left alone, unless they’re tense and at risk of rupture. In this instance, aspirate with a needle and cover with dry gauze. Haemorrhagic blisters should be left alone.
  • Topical aloe vera has evidence to support its use through reduction in prostaglandin and thromboxane formation [14]. However, as it is a topical agent, it is unlikely to be of benefit in deeper injuries. 
  • After covering with aloe vera, bulky dressings should be applied to protect the thawed region. Significant oedema is likely, so circumferential dressings should be loosely applied.
  • Elevate the affected region to minimise oedema. Avoid using the affected region as much as possible. This may have to be pragmatically applied in the case of evacuation or transport.

Management of frostbite in secondary care facilities:

Secondary care of frostbite is a specialist area. The key intervention above all else is time

In the absence of a surgical emergency such as sepsis or compartment syndrome, complete demarcation of tissue necrosis may take one to three months [3].

Good wound care, prophylactic treatment, and medications (outlined below) give time for what is seemingly necrotic tissue to revascularise. 

This can be stressful and difficult for patients who may feel that little progress is being made in their care during this time. It is important to make sure they are actively involved in their care and understand that this time is allowing for revascularisation to occur and will lead to better outcomes long-term. Reassurance as well as open and ongoing communication is essential for this to succeed.

Wound care:

  • As described above, regular application of aloe vera and bulky gauze dressings are recommended, with the affected area being elevated as much as possible.
  • Given the amount of time the patient may be living with the frostbitten area, awaiting revascularisation, rehabilitation aides including crutches, orthotics, splints, etc need to be considered early on.
  • Strongly advise the patient to stop smoking and manage their other risk-factors for poor wound healing such as diabetes.

Prophylactic treatment:

  • Tetanus prophylaxis is standard practice.
  • Systemic antibiotics may be considered, though they’re often unnecessary.

Medical treatments:

  • Ibuprofen is recommended at a dose of 12mg/kg divided twice daily for four to six weeks. Co-prescribe gastric protection when possible.
  • Thrombolytic therapy is considered if it can be administered within 24 hours of thawing. Best outcomes occur with earlier treatment: Hennepin County found each hour of delay in therapy reduced salvage rate by 28% [15]. The goal of thrombolysis is to lyse microvascular thromboses. 

Whilst it reduced digital amputation rates from 41% to 10% in one retrospective study [16], thrombolysis has a high-risk profile, requiring facilities familiar in its use, angiography on site for repeated scans to evaluate responsiveness, and capacity for higher-level monitoring. It is thus only recommended for grade three and four frostbite, where there is a significant risk of morbidity.

  • Iloprost is a prostacyclin analogue which inhibits platelet clumping and is an effective vasodilator [3]. Treatment can be started up to 72 hours post-thawing [17] and its lower risk-profile makes it suitable for infusion in locations where the use of thrombolytics is too high-risk. It is recommended in grade three and four frostbite. There are multiple studies which attest to the efficacy of iloprost [18].

Iloprost is typically run for six hours per day for five to eight days. Unlike thrombolysis, it doesn’t require radiological intervention during administration, can be managed on a surgical ward not requiring a critical care bed, and can be given in cases with a history of recent trauma.

 It is not licenced for use in the USA.


  • Hydrotherapy is an area of research. There is no significant body of evidence supporting its use at present, but the drawbacks are seemingly few.
  • Hyperbaric oxygen therapy is beneficial in wound healing [19]. Whether this can be extrapolated to frostbite, which is a wound with significantly reduced blood supply to peripheral tissues is unclear. The expense and availability of hyperbaric oxygen chambers is also a limiting factor.


  • Should the patient develop complications such as wet gangrene, compartment syndrome or sepsis, timely operative management is crucial.
  • Barring emergent management, surgery is to be delayed until the demarcation of dead tissue is absolutely clear. This can be ascertained clinically and with the aid of imaging, such as technetium-99 bone scan, MRI, and angiography


Prevention largely lies in addressing the potential risk-factors for contracting frostbite [20].

    • Environmental exposure is to be controlled as much as is possible. This is largely dependent on the location and goals of the group, however weather windows and poor weather patterns can still be interpreted and acted upon even in the harshest of environments.
  • Individuals should be thoroughly briefed on the risks and early warning signs of frostbite. They must have adequate layering for the environment they are working in and multiple spares, with particular focus placed on the extremities.  Co-morbidities must be addressed and managed, preferably prior to environmental exposure.
  • Boots and clothing must not be tight and restrictive. Chemical warmers can help maintain warmth but must not impede peripheral blood flow.
  • Maintain adequate nutrition and hydration. 
  • Avoid alcohol, illicit substances, and smoking.
  • Those with previous freezing injuries must be especially careful, as they are more prone to further freezing injuries to previously affected sites.

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(1) Hallam M, Cubison T, Dheansa B, Imray C. Managing frostbite. BMJ 2010;341(7783):1151-1156.

(2) Danielsson U. Windchill and the risk of tissue freezing. Journal of applied physiology (1985); J Appl Physiol (1985) 1996;81(6):2666-2673.

(3) McIntosh SE, Freer L, Grissom CK, Auerbach PS, Rodway GW, Cochran A, et al. Wilderness Medical Society Clinical Practice Guidelines for the Prevention and Treatment of Frostbite: 2019 Update. Wilderness Environ Med 2019;30(4):S19-S32.

(4) Reamy BV. Frostbite: Review and Current Concepts. Journal of the American Board of Family Medicine 1998;11(1):34-40.

(5) Post PW, Donner DD. Frostbite in a pre-Columbian mummy. Am J Phys Anthropol 1972;37(2):187-191.

(6) Maekinen TM, Jokelainen J, Naeyhae S, Laatikainen T, Jousilahti P, Hassi J. Occurrence of Frostbite in the General population-work-related and Individual Factors. Scand J Work Environ Health 2009;35(5):384-393.

(7) Valnicek SM, Chasmar LR, Clapson JB. Frostbite in the prairies: a 12-year review. Plast Reconstr Surg 1993;92(4):633-641.

(8) Degroot DW, Castellani JW, Williams JO, Amoroso PJ. Epidemiology of U.S. Army Cold weather injuries, 1980-1999. Aviat Space Environ Med 2003;74(5):564-570.

(9) Handford C, Buxton P, Russell K, Imray CE, McIntosh SE, Freer L, et al. Frostbite: a practical approach to hospital management. Extreme physiology & medicine; Extrem Physiol Med 2014;3(1):7.

(10) Sumner DS, Criblez TL, Doolittle WH. Host Factors in Human Frostbite. Mil Med 1974;139(6):454-461.

(11) Nygaard RM, Whitley AB, Fey RM, Wagner AL. The Hennepin Score: Quantification of Frostbite Management Efficacy. Journal of burn care & research; J Burn Care Res 2016;37(4):e317-e322.

(12) Cauchy E, M.D., Davis CB, M.D., Pasquier M, M.D., Meyer EF, M.D., Hackett PH, M.D. A New Proposal for Management of Severe Frostbite in the Austere Environment. Wilderness Environ Med 2016;27(1):92-99.

(13) Frostbite. A method of management including rapid thawing. Northwest Med 1966;65(2):119-125.

(14) McCauley RL, Hing DN, Robson MC, Heggers JP. Frostbite Injuries: A Rational Approach Based on the Pathophysiology. J Trauma 1983;23(2):143-147.

(15) Nygaard RM, Lacey AM, Lemere A, Dole M, Gayken JR, Lambert Wagner A,L., et al. Time Matters in Severe Frostbite: Assessment of Limb/Digit Salvage on the Individual Patient Level. Journal of burn care & research; J Burn Care Res 2017;38(1):53-59.

(16) Bruen KJ. Reduction of the Incidence of Amputation in Frostbite Injury With Thrombolytic Therapy. Archives of surgery (Chicago.1960) 2007;142(6):546.

(17) Pandey P, Vadlamudi R, Pradhan R, Pandey KR, Kumar A, Hackett P. Case Report: Severe Frostbite in Extreme Altitude Climbers—The Kathmandu Iloprost Experience. Wilderness Environ Med 2018;29(3):366-374.

(18) Kaller M. BET 2: Treatment of frostbite with iloprost. Emerg Med J 2017;34(10):689-690.

(19) Thom SR. Hyperbaric oxygen: its mechanisms and efficacy. Plast Reconstr Surg 2011;127 Suppl 1(1):131S-141S.

(20) Imray C, Grieve A, Dhillon S. Cold damage to the extremities: frostbite and non-freezing cold injuries. Postgrad Med J 2009;85(1007):481-488.

Marine Life Injuries : what you need to know 150 150 Endeavour Medical

Marine Life Injuries : what you need to know


Introduction to marine life injuries

A vast array of flora and fauna inhabits the waterways, lakes, rivers and oceans which crisscross and surround Earth’s continents. The World Register of Marine Species has formally identified approximately 250,000 species with many more not yet formally reported. [1]

Whereas the majority of marine species are harmless to humans, there are a significant minority of marine creatures which are capable of causing harm. This harm falls across a broad spectrum from the mildly irritating to the severe and life-threatening. This risk of marine life injuries varies greatly depending on region, environment and human activities being undertaken in the area. 

Before engaging in an environment where injuries from marine life could pose a significant risk, healthcare practitioners must consider:

  • What dangerous species may be present in the area of travel?
  • What preventative measures can be taken to minimise the risk these species pose to the patient population, including system measures (e.g., choice of location) and individual measures (e.g., education).
  • How likely is an incident leading to marine creature injuries to occur, and if an incident should occur, what are the injuries / pathology likely to be suffered by the patient? What medical equipment may be required to manage these? 
  • What additional support may be required to deal with marine like injuries and how can it be accessed? (e.g., secondary-care for further treatment and monitoring, national centres for consideration of anti-venoms).

Due to the gamut of potentially dangerous marine species and leading to marine life injuries, this article is a non-exhaustive list covering some of the more well known dangerous marine species which the medic may have to familiarise themselves with in certain environments.

Marine Life injuries : identifying the species and potential dangers

Sharks : understanding the actual risks

Unfortunately, sharks have been unfairly maligned. They are largely harmless to humans and only four (great white, tiger, bull and whitetip) of over four hundred species have been involved in unprovoked attacks on humans. These attacks were most likely because the victims were mistaken for the shark’s typical prey. There are an average of 70 shark attacks,both provoked and unprovoked worldwide every year [2].

Sharks are found in all of the world’s oceans, typically preferring coastal regions between the tropics. Bull sharks exist in both seawater and freshwater.

Marine life injuries from sharks are likely to be bites or puncture wounds, with the extent of the injury varying from minor to extensive. Treatment depends on the extent of tissue disruption and underlying structures which might have been damaged. Consider antibiotics to prevent secondary infection. Any penetrating or significant injuries necessitate secondary-care involvement.

To minimise your risk [3]:

  • Avoid areas where sharks are known to be present! This can include sewage outlets and fishing boats.
  • Stay in groups when swimming.
  • Avoid the water between dusk and dawn when sharks are most active.
  • Sharks have excellent olfaction: don’t enter the water if bleeding. Extra caution is advised if menstruating.
  • Don’t wear bright colours or jewellery: reflected light imitates the sheen of fish scales.
  • Don’t splash excessively: it imitates struggling prey. If you see a shark and are able to, then swim smoothly away.
marine life injuries : tiger shark

Tiger shark

Illustration by Mark Dando, image from the Shark Research Institute.

Taken from: https://www.sharks.org/tiger-shark-galeocerdo-cuvier

Crocodiles and alligators : understanding the native habitats and risks

Alligators are only native to the USA, Mexico and China and are generally considered less aggressive than crocodiles. Species of crocodile can be found throughout Central America, Africa, India, Southeast Asia and Australia. Crocodile attacks on humans are not uncommon. The Nile crocodile and saltwater crocodile are the most prolific, attacking humans which they view as prey in East / Sub-Saharan Africa and Southeast Asia / Australia respectively.

Crocodiles are ambush predators that can move surprisingly quickly and cause harm by biting down and clamping onto their prey with their jaws as they try to drag them into the water. A crocodile can exert almost 1000 kg of force with their bite [4].

Should someone survive the initial ambush from a crocodile – when the principal risks are drowning and major trauma – then there is likely to be extensive, significant disruption to soft tissue and skeletal structures with injuries both penetrating and blunt-force. Fractures, bleeding and nerve injury are all to be considered. Extremities are most commonly affected (as a target of convenience which the crocodile latches onto). Wounds are considered heavily contaminated and require surgical debridement. Secondary care is required.

Marine life injuries, such as those caused by crocodile attacks, often present logistical challenges.: whereas shark bites typically happen near well-populated and easily accessible coastal areas, crocodile attacks most often occur in remote, difficult-to-reach areas.

Preventative measures include [4]:

  • Avoid areas where crocodiles are known to be present! Clarify this with local services if necessary.
  • Don’t camp near the water’s edge if crocodiles inhabit the area.
  • Don’t leave food scraps out or near water. Don’t collect water from the same site on multiple occasions.
  • Don’t swim or wade in water which has any risk of crocodile infestation.
marine life injuries : crocodile

Nile crocodile

Image sourced from Wikipedia: Nile Crocodile article.

Taken from: https://en.wikipedia.org/wiki/Nile_crocodile

Sea-snakes : understanding the threat

Marine life injuries are not limited to encounters with large aquatic predators but also include incidents with smaller, yet equally dangerous creatures like sea snakes. They are almost all elapids, a family of snakes endemic to tropical and subtropical regions, commonly venomous, most often neurotoxic in nature. Sea snakes, despite their name and excellent adaptation to the water, sea animal injuries involving sea snakes are not uncommon as these creatures commonly prefer shallow, sheltered waters and regularly swim up rivers.

Despite being extremely venomous [5], sea snakes are not known for their aggression and often only bite when handled, making these interactions a major cause of sea animal injuries. When they do bite, their venom has nephrotoxic, myotoxic and neurotoxic properties (dependent on species) [5]. Breakdown of skeletal muscle causes myalgia and rhabdomyolysis with classic Coca-Cola coloured urine. This is compounded by tubular necrosis as the venom targets the kidneys directly. Finally, envenomation also causes a progressive paralysis of muscles including those involved in swallowing and breathing. Onset is gradual and the bite itself may be painless.

If a bite occurs try to reassure and calm the patient. Many snakes bite without injecting venom (‘dry bites’). Try to identify the snake if possible but DO NOT approach it or try to kill it: even a dead snake can envenomate you. Leave the bite alone. Give analgesia (not NSAIDs which worsen the effects of haemotoxic venoms), remove tight clothing and jewellery from affected extremities. Immobilise the person and, most specifically, the affected site entirely. Use a pressure dressing over the affected site but make sure distal sensation and pulses are intact. [6]

The above measures slow the spread of the venom. Ultimately, evacuation is necessary, preferably to a site that you have already reviewed during the planning stage and you know stocks antivenom. A patient may simply need observation for a period of time in secondary care:this time is variable dependent on bite-burden and the suspected species. However if they develop complications of envenomation, which may include rhabdomyolysis, paralysis, shock or incoagulable blood, then antivenom may need to be administered. 

Antivenom is not ubiquitous: it is a product which varies between regions dependent on the local venomous snake species. It is either monovalent (i.e., specific to a certain venom) or polyvalent (i.e., an antidote to several venoms). Administration of antivenom, particularly polyvalent preparations, has a high incidence of anaphylaxis  and therefore needs to be administered in a high-dependency setting with close monitoring and adrenaline available. [6] [7]

Preventative measures include:

  • Avoiding sites known to have high populations of sea snakes!
  • Wear a high-quality wetsuit and boots (difficult for sea snakes to pierce these).
  • Don’t touch / try to get close to a sea snake should you spot one. It’s also worth noting that it’s often hard to tell a sea snake’s head from its tail.
marine life injuries : sea snake

Black-banded sea krait

Image sourced from Ocean Fauna.

Taken from: https://oceanfauna.com/black-banded-sea-krait/?utm_content=cmp-true

Jellyfish : understanding and treating jellyfish stings

Jellyfish are organisms with a bell which provides propulsion and tentacles which have stinging cells called nematocysts. The bell alone can range in size from a few millimetres to nearly two metres in length. The tentacles can extend a jellyfish’s length to over 30m in some instances. Jellyfish often do well in oxygen-poor waters or regions where other marine life is limited due to human factors such as overfishing and excess land runoff. Here they form ‘blooms’ – large populations of jellyfish which can migrate en masse. There are many types of jellyfish and their stings are similarly broad in the symptoms they can cause in humans, often resulting in marine life injuries. Two types of jellyfish which are more commonly encountered include the Portuguese Man o’ War and Box Jellyfish.

The Portuguese Man o’ War is found in the Atlantic, Indian and Pacific Oceans. The name comes from its similarity in appearance to a sixteenth century Portuguese warship at full-sail. Its tentacles leave raised welts on exposed skin and cause pain lasting three to four hours. Death is rare but has been recorded following Portuguese Man o’ War stings. This is likely secondary to an increased sting burden, causing significant pain and breathing issues or due to an anaphylactoid reaction. [8] [9]

There are many species of Box Jellyfish, named after the cube shape of their bell. They are found in most tropical and subtropical oceans and typically reside close to shore. The most dangerous species of Box Jellyfish are mainly found in the Indian and Pacific oceans. One notorious species of Box Jellyfish is the Irukandji, found off the coasts of northern Australia. Irukandji are small, translucent and extremely venomous, capable of causing sea animal injuries like ‘Irukandji syndrome’ in humans. This syndrome includes severe myalgia, anxiety, tremor, headache, hypertension, tachycardia, pulmonary oedema and even death. [6] [9]

Treatment for jellyfish stings focuses on pain management and monitoring the patient’s breathing in particular. Remove any nematocysts from the skin to prevent further envenomation, a crucial step in dealing with marine creature injuries. Depending on the species, this is best achieved with seawater or vinegar (as is the case with Irukandji) to neutralise them, followed by scraping them away with a razor, credit card or using a gloved hand. There has been some recent controversy about the use of vinegar in Boxfish stings, however it is still currently recommended by the Australian Resuscitation Council [9] [10]. Removal of the nematocysts relieves pain and reduces venom burden. Further analgesia is advised and should the patient develop systemic compromise then a full primary assessment should be re-visited. There are now antivenoms available for certain jellyfish stings.

Prevention includes:

  • Paying attention to local guidelines regarding where and when to swim.
  • Swim in netted areas (which mostly keep jellyfish out) in at-risk areas.
  • Wear protective clothing in the water e.g., wetsuits.
  • Don’t approach even dead jellyfish or tentacles no longer attached to the body: both are still very much capable of stinging.
  • Take care when surfacing if diving underwater and remember to check above you.
marine life injuries : jellyfish

Box jellyfish

Image sourced from Encyclopedia Britannica.

Taken from: https://www.britannica.com/animal/box-jellyfish

Stonefish : dealing with the most venomous fish

Stonefish, more properly called Synanceia, are found in the Indian and Pacific Oceans and are the most venomous fish known to science [11]. They derive their name from their camouflaged appearance which makes them appear similar to rocks. Their camouflage unfortunately is what makes them dangerous to humans: swimmers often don’t notice the stonefish and thus step on them, causing the stonefish to sting the swimmer.

The venom is a neurotoxin which initially causes intense pain on envenomation, a typical marine animal injury. Subsequent symptoms can include respiratory weakness, cardiovascular compromise, paralysis and death. Treatment includes hot water (to denature the venom) and, in severe cases, antivenom. Spines often break off in the wound, so will need to be removed, when possible, to avoid further complications from these sea creature injuries. [6]

Prevention includes:

  • Be aware of local distributions of stonefish (some areas are more heavily affected than others).
  • Wearing footwear in the water.
  • Entering the water slowly with a shuffling gait: this gives the fish plenty of time to move away from you and reduces the risk of stepping directly onto one.
  • Disturb the water ahead of you e.g., with a stick: again, this gives the fish plenty of warning.
marine life injuries : stone fish


Image sourced from Encyclopedia Britannica

Taken from: https://www.britannica.com/animal/stonefish-Synanceiidae-family

Blue-ringed Octopus : a small but significant contributor of marine life injuries

Small, cute, deadly. Blue-ringed octopus are found in the Pacific and Indian Oceans and, as their name suggests, have beautiful iridescent colouring which makes them irresistible to the unwary, curious human. They are typically less than 20cm in size and will try to retreat if they feel threatened. If retreat doesn’t work, then they employ their powerful toxin, tetrodotoxin, leading to severe marine life injuries.

Tetrodotoxin is neurotoxic and targets sodium channels. Envenomation is painless and symptoms develop in minutes, starting as nausea and progressing to whole-body paralysis including the diaphragm. Thus, death is secondary to a respiratory arrest. There is no antivenom or cure for tetrodotoxin, therefore respiratory function must be artificially supported until the venom clears the system. [6] [12]

Preventative measures include:

  • Don’t touch cute, bright, innocuous looking creatures!
  • Be careful around rock pools or reefs, where they may be harder to distinguish.
  • Keep your distance: Blue-ringed octopus are shy and prefer to retreat. Give them that option.
marine life injuries : blue-ringed octopus

Blue-ringed octopus

Image sourced from The Natural History Museum

Taken from: https://www.nhm.ac.uk/discover/blue-ringed-octopus-small-vibrant-deadly.html

Marine life injuries : Take home messages

  1. There are many species of marine life dangerous to humans. The nature and severity of the danger varies greatly, and it is important to research the dangerous animals which may inhabit your area of work prior to being confronted by a patient suffering from their ministrations.
  2. Prevention, as always, is better than cure. Once you have identified the potentially hazardous marine life in your area of work, consider how you may be able to minimise that risk. There are likely to be both systemic and individual factors which contribute to this.
  3. A lot of conditions require secondary care, but often for different reasons. Consider your evacuation plans in the event of different issues arising whilst in the field.

Are you interested in learning more about marine creatures and other water related conditions?

If so, why not check out our Marine Medicine course? Whilst you’re there, why don’t you take a look at our other courses too?


[1]. WoRMS Editorial Board (2023). World Register of Marine Species. Available from https://www.marinespecies.org at VLIZ. Accessed 2023-04-11. doi:10.14284/170

[2]. Naylor, G. International Shark Attack File: Yearly Worldwide Shark Attack Summary. [Online]. Available from: https://www.floridamuseum.ufl.edu/shark-attacks/yearly-worldwide-summary/ [Accessed 11 April 2023].

[3]. International shark attack files. Advice to Swimmers. [Online]. Available from: https://www.floridamuseum.ufl.edu/shark-attacks/reduce-risk/swimmers/ [Accessed 11 April 2023]

[4]. Caldicott, D.G.E, Crozer, D, Manolis, C, Webb, G, Britton, A. Crocodile Attack in Australia: An Analysis of Its Incidence and Review of the Pathology and Management of Crocodilian Attacks in General. Wilderness and Environmental Medicine. 2005;16(3): 143-159

[5]. Gopalakrishnakone, P. Sea Snake Toxinology. : NUS Press; 1994

[6]. Warrell, D. Oxford Handbook of Expedition and Wilderness Medicine. (2nd ed.). Oxford: Oxford Medical Handbooks; 2015.2018), https://doi.org/10.1093/med/9780199688418.003.0017

[7]. Isbister GK. Snake bite: a current approach to management. Aust Prescr 2006;29:125-9.https://doi.org/10.18773/austprescr.2006.078 

[8]. Stein, M.R. Fatal portuguese man-o’-war (Physalia physalis) envenomation. Annals of Emergency Medicine. 1989;18(3): 312-315

[9]. Australian resuscitation council. Envenomation – Jellyfish Stings. [Online]. Available from: https://www.revive2survive.com.au/wp-content/uploads/2016/09/guideline-9-4-5july10.pdf [Accessed 11 April 2023]

[10]. Wilcox , C.L, Headlam, J, Doyle, T.K. Assessing the Efficacy of First-Aid Measures in Physalia sp Envenomation, Using Solution- and Blood Agarose-Based Models. Toxins. 2017;9(5)

[11]. Adventure medic. Stonefish Envenomation. [Online]. Available from: https://web.archive.org/web/20120228222240/http:/www.adventuremedicine.net/envenom/marine/94-stonefish [Accessed 11 April 2023]

[12]. Divers alert network. Envenomation. [Online]. Available from: https://dan.org/health-medicine/health-resource/dive-medical-reference-books/hazardous-marine-life/envenomations/#octopus [Accessed 11 April 2023]

Drowning 150 150 Endeavour Medical



Seventy five percent of the world’s surface is covered by water, 95% of which is in our oceans and seas (1). It is a life source, a playground, and may even be a treatment for some illnesses (2). However, it’s also powerful and can be unpredictable; entering the water, intentionally or not, can have serious consequences. In this post, we will look at the body’s response to water immersion and how this can lead to drowning. We will also look at strategies to prevent drowning and how to manage the drowning patient.

What is drowning?

Drowning is defined as the experience of respiratory impairment secondary to submersion or immersion into water (3). Submersion occurs when the upper airway is beneath the surface of the water, whilst immersion refers to the airway remaining above the water. 

Drowning outcomes are categorised as mortality, morbidity, and non-morbidity (3). The Wilderness Medical Society (WMS) does not recommend the use of other terms to categorise drowning including wet, dry, or secondary.  There is also no distinction between salt and freshwater drownings and their management. This is because, regardless of the situation, the pathophysiology is triggered hypoxia, and this is the target of treatment (3,4).

Why is it important?

Drowning causes over 200,000 deaths a year worldwide, making it the third leading cause of death by accidental injury (5). The World Health Organisation recognised it as a major public health issue in 2012, describing it as ‘one of the most preventable, neglected and pressing public health issues’ (5). It kills two thirds of the number that die from malnutrition and half the number that die from malaria, and disproportionately affects low- and middle-income countries, children and males (5). Furthermore, these numbers are likely to significantly underestimate the problem as many data sources don’t include fatalities associated with intentional drowning (suicide or homicide), natural disasters or migrant boat accidents (5). Read the WHO report on the global impact of drowning here: https://www.who.int/publications/i/item/global-report-on-drowning-preventing-a-leading-killer

In the UK, there are around 600 drowning deaths annually (6). These figures do not report non-fatal drownings or rescues that prevent drowning; for example, the Royal National Lifeboat Institution (RNLI) reported over 3000 rescues and many more preventative actions in 2021 (7). These figures highlight the importance of water safety both on and off expedition.

Although there are some cases in which drowning occurs in warm water, these are usually related to hot tubs or exertional hyperthermia in competitive swimmers (8). This article will focus on the physiological phenomena that occur on entering cold water (<20°C) and how this can result in drowning.

Cold Water Immersion

Breath hold time

A person’s ability to hold their breath contributes to their ability to prevent drowning. It allows them to prevent aspiration whilst submerged, under waves or when struggling to keep their head above water. It is determined by oxygen consumption, carbon dioxide production and respiratory drive (8).  

Cold Shock Response 

Immersion into cold water causes sudden cooling of cutaneous thermal receptors. This triggers a dramatic increase in sympathetic activation, causing an involuntary gasp, followed by hyperventilation, and accompanied by peripheral vasoconstriction, tachycardia and hypertension. This is known as the cold shock response (CSR). This reduces breath holding through an increase in oxygen consumption and a high respiratory drive.  It can also result in drowning through aspiration directly, if the gasp occurs while submerged (9). 

The cold shock response can be reduced by habituation, which occurs after just a few short immersions in 15°C water. However, studies have shown that this habituation is likely to be reduced by anxiety (10), potentially moderating its benefits in accidental immersion. 

Diving Response 

The diving response occurs on submersion of the face in cold water and breath holding. It is characterised by a parasympathetically driven bradycardia. It is increased in diving mammals and children and is thought to be a protective mechanism to reduce oxygen consumption, increasing breath hold time and, subsequently, survival underwater (11). 

Autonomic Conflict

Rapid submersion in cold water can cause simultaneous stimulation of the diving and cold shock responses. This results in opposing autonomic action on the heart: the diving response increases parasympathetic activity, to cause bradycardia, whilst the cold shock response triggers sympathetic activity, stimulating a tachycardia. This conflicting action within the heart can cause arrhythmias. This is known as autonomic conflict.

A further increase in parasympathetic activity when a breath hold is released increases the incidence of arrhythmias at this time. These arrhythmias are normally benign, but if combined with other predisposing factors, such as QT prolongation, coronary vessel disease or ischaemic heart disease they can be fatal (11).  The true extent of autonomic conflict as a cause of death is not known as arrhythmias are undetectable on autopsy and terminal gasps will likely result in aspiration of water, giving the appearance of drowning (11).

Drowning cause - autonomic conflict

Figure 1: The effects of cold-water immersion resulting in arrhythmias (11).

Swim Failure 

The longer a person is immersed, the risk of swim failure increases, making them unable to hold their head above the water or to self-rescue. This may occur through fatigue or hypothermia. 

Water is thermoneutral at 32°C; below this environmental heat loss exceeds heat production through thermogenesis. Below 25°C, swimming, or treading water to float, becomes detrimental to thermal control, as the increase in thermogenesis is not sufficient to outweigh the increase in conduction as limbs move through cold water (12). As nerves and muscles cool, lack of coordinated muscle contraction can make swimming impossible. In colder water, or longer immersion, reduction in core body temperature can directly cause loss of consciousness through hypothermia. Both can result in submersion and drowning (8). In view of this, the HELP (Heat Escape Lessening Posture) position (3) is recommended for those with a buoyancy aid to maintain body temperature (See figure 2). This involves drawing knees into the chest, crossing ankles and bringing arms in; this reduces heat loss and conserves energy. For more about hypothermia, check out Dr Lucy Longbottom’s post here!

Drowning - the HELP Position

Figure 2: The HELP (Heat Escape Lessening Posture) https://rnli.org/safety

The drowning process

Figure 3 explains the processes that lead to a person being unable to prevent submersion and aspirating or inhaling water, resulting in the respiratory impairment that characterises drowning. 

Tipton and Montgomery described the drowning process in 6 steps (13); the first of which is the struggle to maintain the airway above the water. This begins at the point that ‘swimming becomes struggling’ and is characterised by the ‘Instinctive Drowning Response’; a lack of waving or calling for help, horizontal arm movements and repeated submersion of the airway. It lasts up to a minute, which likely relates to the length of anaerobic activity possible before exhaustion. As a rescuer, it is vital to recognise this response and the urgency of this presentation. 

Following this, a person will become submerged and begin breath holding, causing hypoxaemia and hypercapnia to develop, increasing the respiratory drive, and, eventually, causing resumption of breathing. An adult is not normally able to breath hold to the point of loss of consciousness (13). This resumption of breathing will lead to aspiration. 

Aspirated water enters the lungs and disrupts surfactant function, in turn disturbing membrane integrity and allowing shifts in fluid, plasma and electrolytes. There is also an increase in surface tension and reduction of lung compliance. These combine to result in acute pulmonary oedema, ventilation-perfusion mismatch, and reduced gas exchange. This occurs from around 2.5ml/kg of aspirated water (8). Loss of efficient gas exchange causes further hypoxia and hypercapnia, resulting in loss of consciousness and, eventually, cardiac arrest. 

Submersion into, and aspiration of, ‘icy’ (<6°C) water, may be protective. The entrance of ice-cold water into the lungs causes rapid cooling of blood, and subsequently of the heart, lungs and brain. This rapidly induced hypothermia can dramatically reduce oxygen consumption and extend submersion time without sequelae (8). The most extreme example of this follows a young woman who fell into an icy river while skiing (14). She was submerged for over an hour and had a core temperature of 13.7°C on arrival to hospital and no spontaneous circulation for two hours. Five months after the event she had some residual neurological deficit but had already returned to working, hiking and skiing. It’s thought that the rapid onset of hypothermia reduced her oxygen requirement so much that her body’s oxygen stores were sufficient for survival.

pathophys of drowning

Figure 3: The Physiological Pathways to Drowning. This diagram shows how the above phenomena lead to drowning. Adapted from (13)

Classification of drowning

Figure 4: Classification of the grades of drowning as assessable in the field with associated mortality. (3)

How to manage a drowning situation

The highest predictor of outcome following drowning is submersion time (15). Thus, removing people from the water is vital, but so is keeping yourself safe. The WMS only recommends that rescuers enter the water to rescue a drowning person if they are trained to do so and confident with the environment. The mantra ‘Reach, throw, row, don’t go’ emphasises the use of throwing flotation devices or going by boat, if possible, rather than entering a body of water (3).

Once on land, a full assessment can be made to inform management. Drowning is described by 6 grades of severity: dependent on oxygen saturations, pulmonary auscultation, and signs of shock (9). Figure 4 shows the associated mortality with each of these stages in a way that can be assessed and defined on expedition, while figure 5 summarises the management of these grades.

Grades of drowning

Figure 5: The grades of severity of drowning and management of each, adapted from (15). 

The mainstay of treatment is the reversal of any hypoxia (15). Those who are asymptomatic can be discharged at the scene and continue with activity. Those with added sounds on auscultation should be observed for signs of deterioration for 6 hours, following which they may also continue as normal, if they remain asymptomatic. WMS suggests that, if evacuation from an expedition may be lengthy or difficult, it should be arranged for anyone with abnormal auscultation following submersion and can be stepped down if there is no deterioration throughout the observation period (3). Any respiratory distress, shock or reduction in mental state requires evacuation and further medical treatment. 

Respiratory assistance should be given as required and will range from high flow oxygen to mechanical ventilation in those with respiratory arrest (15). Prior to arrival at a hospital, supplemental oxygen should be given in whatever form is available to reduce hypoxia (3).

Cardiac Arrest 

Cardiac arrest in drowning occurs due to hypoxia and is rarely a shockable cardiac rhythm (9). Consequently, compression-only CPR is not recommended in drowning victims, and 5 ‘rescue breaths’ should be given before the first round of chest compressions (3). Rescuers that are trained to do so can give these peri-rescue prior to extraction from the water (9). Furthermore, WMS recommend that application of AED pads should not be a priority and should not take precedence over chest compressions due to the high likelihood of pulseless electrical activity or asystole (3). Despite this, Brayne et al. found good outcomes from cardiac arrest secondary to drowning with 25% survival from out of hospital cardiac arrest in a study of drowning admissions to hospitals in the southwest (16). 

CPR should continue until the patient is has been in asystole for more than 25 minutes, although WMS highlight awareness of the likelihood of unfavourable outcomes in those that have been submerged more than 30 minutes in >6°C water, or 90 minutes in water below 6°C. Consideration should also be given to the role of concomitant hypothermia, and CPR should continue during attempts at rewarming (3). Read more about the management of hypothermia. WMS also highlights the importance of ceasing resuscitation efforts if, at any point, the rescue team is at risk (3).

Complications of drowning

The major complication arising from drowning is hypoxic brain injury. The risk of severe neurological sequelae and death is almost exclusively determined by length of submersion, with likelihood of survival with good neurological function being almost 0% following submersion of more than 25 minutes (15). Early extraction from the water and administration of supplemental oxygen aids to reduce this. As discussed above, this risk often informs decision making on management in the drowned patient. 

Whilst water entering the lungs can introduce pathogens, most patients do not require antibiotic treatment and empirical therapy has not been shown to improve outcomes (15). Pneumonia is most likely to develop in the days following a drowning event and the risk increases in those who require mechanical ventilation (15). Due to the high prevalence of atypical organisms, sputum and blood cultures should direct antibiotic choice where possible (3). 

Cervical spine injuries and other trauma is uncommon in drowning situations. Unless there is a clear mechanism suggesting that C-spine trauma may have occurred, immobilisation should not take precedence over necessary airway management in a hypoxic drowning patient (3). 

Prevention of drowning

In recognition of the high numbers of deaths from drowning worldwide, the World Health Organisation released a public health prevention guide in 2017 in an attempt to address the ‘preventable and neglected public health issue’ (17). They highlighted important community measures to reduce drowning including raising awareness of the dangers of being around water, erecting barriers around bodies of water and promoting swimming lessons in all children (17).

Closer to home, the RNLI provide a lifeguard service at many of the UK’s beaches. They perform thousands of preventative actions a year (7) to stop people getting into trouble in the water. As well as educating those on the beach, they highlight safer areas for swimming on the beach and alert people that may be straying out of these areas. They also provide rescues for many who get into trouble before they submerge. All these actions prevent thousands of fatal and non-fatal drownings yearly in the UK (7). 

Whilst the above examples are wider, community-based approaches, a lot can be learnt from them when going on expedition. Team members can be educated on safety around water prior to the expedition, including the recommendation to avoid alcohol when around open water; a significant risk factor for drowning (3). For water-based expeditions, WMS suggest that the ability to swim 25m, tread water and hold a floating position is preferable for participation (3). Wearing a lifejacket if taking part in a water-based activity also helps to prevent submersion. During pre-participation screening, those at higher risk of drowning (coronary artery disease, QT prolongation or seizure disorders) should be counselled about this risk and methods of mitigating it (3).

Take home messages

  • Prevention is better than cure – educate team members before departure and wear floatation devices if undertaking water-based activities.
  • If someone does enter the water unexpectedly, or gets into difficulty in the water, extraction from the water as soon as possible is vital. 
  • Rescuer safety is the most important – ‘Reach, Throw, Row, Don’t Go!’
  • Hypoxia is the cause of drowning related mortality and morbidity – give supplemental oxygen as soon as possible. 
  • Consider the effects of hypothermia, especially in individuals who were in the water for a prolonged period. 
  • Give 5 rescue breaths prior to starting CPR if there is no pulse.

Are you interested in learning more about drowning and other water related conditions?

If so, why not check out our Marine Medicine course? Whilst you’re there, why don’t you take a look at our other courses too?

Further reading

We’re very lucky in the UK to have some beautiful coastlines, and a fantastic system of lifeguards, lifeboats, and coastguards for if we do get into trouble. However, as we’ve said before, prevention is always better than cure and staying safe around our coastline is vital. Check out the RNLI website for their tips on keeping yourself and those around you safe: https://rnli.org/safety


  1. Graham S, Parkinson C, Chahine M. The Water Cycle [Internet]. NASA Earth Observatory; 2010 [cited 2023 Mar 6]. Available from: https://earthobservatory.nasa.gov/features/Water/page1.php
  2. Tipton MJ, Collier N, Massey H, Corbett J, Harper M. Cold water immersion: kill or cure?: Cold water immersion: kill or cure? Exp Physiol. 2017 Nov 1;102(11):1335–55. 
  3. Schmidt AC, Sempsrott JR, Hawkins SC, Arastu AS, Cushing TA, Auerbach PS. Wilderness Medical Society Practice Guidelines for the Prevention and Treatment of Drowning. Wilderness & Environmental Medicine. 2016 Jun;27(2):236–51. 
  4. Orlowski JP, Abulleil MM, Phillips JM. The hemodynamic and cardiovascular effects of near-drowning in hypotonic, isotonic, or hypertonic solutions. Annals of Emergency Medicine. 1989 Oct;18(10):1044–9. 
  5. World Health Organization. Global report on drowning: preventing a leading killer [Internet]. Geneva: World Health Organization; 2014 [cited 2023 Mar 6]. 59 p. Available from: https://apps.who.int/iris/handle/10665/143893
  6. Water Incident Database (WAID) 2021 Annual Fatal Incident Report. 2021. 
  7. RNLI Operational Statistic Report 2021 [Internet]. The Royal National Lifeboat Institute; 2021 [cited 2023 Mar 6]. Available from: https://rnli.org/about-us/how-the-rnli-is-run/annual-report-and-accounts
  8. Bierens JJLM, Lunetta P, Tipton M, Warner DS. Physiology Of Drowning: A Review. Physiology. 2016 Mar;31(2):147–66. 
  9. Szpilman D, Bierens JJLM, Handley AJ, Orlowski JP. Drowning. N Engl J Med. 2012 May 31;366(22):2102–10. 
  10. Barwood MJ, Corbett J, Green R, Smith T, Tomlin P, Weir-Blankenstein L, et al. Acute anxiety increases the magnitude of the cold shock response before and after habituation. Eur J Appl Physiol. 2013 Mar;113(3):681–9. 
  11. Shattock MJ, Tipton MJ. ‘Autonomic conflict’: a different way to die during cold water immersion?: Autonomic conflict and cardiac arrhythmias. The Journal of Physiology. 2012 Jul;590(14):3219–30. 
  12. Stocks JM, Taylor NAS, Tipton MJ, Greenleaf JE. Human physiological responses to cold exposure. Aviat Space Environ Med. 2004 May;75(5):444–57. 
  13. Tipton M, Montgomery H. The experience of drowning. Med Leg J. 2022 Mar;90(1):17–26. 
  14. Gilbert M, Busund R, Skagseth A, Nilsen PÅ, Solbø JP. Resuscitation from accidental hypothermia of 13·7°C with circulatory arrest. The Lancet. 2000 Jan;355(9201):375–6. 
  15. Szpilman D, Morgan PJ. Management for the Drowning Patient. Chest. 2021 Apr;159(4):1473–83. 
  16. Brayne AB, Jones W, Lee A, Chatfield-Ball C, Kaye D, Ball M, et al. Critical care drowning admissions in Southwest England 2009–2020, a retrospective study. Journal of the Intensive Care Society. 2023 Feb;24(1):47–52. 
  17. World Health Organization. Preventing drowning: an implementation guide [Internet]. Geneva: World Health Organization; 2017 [cited 2023 Mar 6]. 116 p. Available from: https://apps.who.int/iris/handle/10665/255196
Decompression Illness 150 150 Endeavour Medical

Decompression Illness


When practised safely, scuba diving can be an incredible experience, and is even sometimes a necessary activity in some occupations and for access to certain environments. However, it is a high-risk sport in which a lack of care can result in dangerous consequences. Decompression illness is one of these, and is the most reported diving related incident by the British Sub-Aqua Club (BSAC) (1).

What is a decompression illness ?

Decompression illness (DCI) is split into two conditions: decompression sickness (DCS) and arterial gas embolism (AGE). Decompression sickness or ‘the bends’ is where a rapid reduction in pressure of the patient’s environment results in bubbles of gas that are normally dissolved (usually nitrogen) forming in body tissues and/or blood. This can result in a wide range of non-specific presentations. AGE occurs when this gas enters the arterial circulation. Whilst these are often reported in scuba divers, they can also be seen in flying and space travel, or in caisson or mine workers.

Decompression sickness

Decompression illness (DCI) is caused as a result of ‘evolved’ gas. The basis of this is Henry’s law, where the concentration of gas dissolved in a liquid is directly proportional to the partial pressure of the gas above the solution. As divers descend, pressures increase and each inhaled breath contains a greater concentration of gases. Therefore, the concentration of dissolved gas in the blood increases. This leads to more nitrogen gas being absorbed into tissues than at normal pressures. 

When divers begin to ascend, the tissue-based gas begins to move back into the bloodstream. This is known as ‘off-gassing’. Ideally this gas remains dissolved, however if a diver ascends too quickly, resulting in a rapid change in pressure, or if the level of absorbed gas is too high as too long has been spent at too greater depth, bubbles can form in the blood and tissues.

decompression illness - visualization of Henrys law

Figure 1 – Visual representation of Henry’s law (6).

Arterial gas embolism

Bubbles can find themselves in the arterial circulation by one of three processes. 

Pulmonary barotrauma occurs when the volume that an amount of gas occupies increases as pressure decreases; this is known as ‘Boyle’s law’. If divers ascend while holding their breath, or have trapped air in their lungs from pulmonary disease such as COPD, the volume of inhaled gas in their lungs over-expands relative to lung volume, potentially resulting in pneumothorax, pneumomediastinum or alveolar rupture. This can result in an air embolism entering the arterial circulation. 

If the venous gas bubble volume overwhelms the pulmonary filter that usually removes them, some will remain and pass into the arterial circulation. Additionally, having a right to left shunt such as a patent foramen ovale can cause bubbles to pass through this into the arterial circulation.

Bubbles can occlude arteries, resulting in ischaemia wherever the blockage occurs. Even after this resolves, there can be a rebound ischaemia caused by emboli as a result of vessel damage. This often results in neurological symptoms – one study found that 88.5% of divers treated for DCI had some form of neurological symptom at presentation.

decompression illness - visualization of bowles law

Figure 2 – Visual representation of Boyle’s law (7).

Presentation of decompression illness

Decompression Illness (DCI) can occur anytime up to 72 hours post-depressurisation, however, the likelihood that this is the diagnosis increases the earlier after depressurisation that the symptoms occur – 90% of cases present in the first 6 hours after ascent.

Decompression Sickness (DCS) can lead to a wide range of presentations, as bubbles can form almost anywhere in the body, and therefore history and timing of presentation are important in diagnosis. Subclinical venous bubbles are common and cause no symptoms, and are usually filtered out by the pulmonary circulation. 

In type 1 (mild) DCS, bubbles in the muscles, joints and tendons cause an aching pain and inflammation. Symptoms can be vague including malaise, fatigue and headache. An erythematous, mottled rash with areas of pallor (livedo reticularis / cutis marmorata) can develop briefly.  Bubbles in the lymphatic system are rare but can cause localised pain around lymph nodes.

Type 2 DCS is more severe and may have life-threatening consequences affecting the inner ear, cardiorespiratory and neurological systems related to high venous bubble load or AGE. Inner ear symptoms include hearing loss, vertigo, nausea or impaired balance. Bubbles in the lungs can cause ‘the chokes’ – a dry cough and chest pain behind the sternum with associated dyspnoea. Arterial gas emboli may lodge in the coronary vessels causing chest pain and sometimes cardiopulmonary arrest. Sudden stroke-like symptoms (e.g. weakness, paraesthesia, visual changes, facial droop or altered speech), seizures, confusion or sudden loss of consciousness may be caused by a cerebral arterial gas embolus (CAGE). Spinal cord involvement can also lead to weakness and paraesthesia with loss of bowel or bladder control.

Decompression illness - Pulmonary barotrauma resulting in CAGE

Figure 3 – Pulmonary barotrauma resulting in CAGE (5).


Patients should be assessed using an ABCDE format, with particular attention paid to chest examination, looking for signs of pneumothorax and immersion pulmonary oedema. Observations may reveal low oxygen saturations, tachycardia, and tachypnoea. Full neurological examination should also be carried out.

A chest X-ray and/or CT chest can be helpful in determining if any pulmonary barotrauma resulting in pneumothorax is present. If stroke-like symptoms are present, a CT head should be performed. However, decompression illness (DCI) is primarily a clinical diagnosis – a history of recent repressurisation in combination with wide-ranging and otherwise unexplained symptoms.


Prevention is always better than cure. The risk of decompression illness can be reduced by:

  • Making sure that all divers have up to date and appropriate qualifications for the activity they are undertaking.
  • Completing the recommended decompression stops during ascent including a mandatory 3-5 minute safety stop at 5-6 metres depth.
  • Not exceeding the recommended time at depth.
  • Leaving enough time between dives for tissue bubbles to resolve, remembering the added risks of travelling to altitude or flying after diving.

Recommended time at depth and between dives is calculated using a dive planner, prior to commencing the dive.

recreational dive planner

Figure 4 – An example of a recreational dive planner

Primary management of DCI is high-flow oxygen. Given at 15L per minute via a non-rebreather mask, this is the most effective treatment for DCI and will help to relieve any associated pain. Any other pain relief is usually not required. Nitrous oxide (Entonox) in particular is contraindicated for pain relief, as this will increase the quantity of dissolved nitrogen gas in body tissues.

Definitive treatment is via recompression therapy at a dedicated facility. This involves using a hyperbaric chamber to simulate a high pressure environment (2.5 to 3 atmospheres). 100% oxygen is given to the patient for up to 300 minutes at a time to help increase tissue and blood oxygen levels, and decrease gas bubble size and concentrations of nitrogen. Due to the use of 100% oxygen, opiate analgesia should be avoided as this can increase propensity to oxygen toxicity.

It is important to confirm if the patient has a barotrauma-associated pneumothorax prior to recompression therapy, so that a chest drain can be inserted before the patient is moved into the hyperbaric chamber.

Oral and/or IV fluids are recommended to promote increased tissue perfusion.

Differentials to consider

As the symptoms of decompression illness (DCI) can be so varied and vague, it can mimic a wide variety of conditions, from musculoskeletal pain to stroke. As such, it is important to take a detailed history to consider the context of the presentation and the symptoms having occurred in the first 72 hours since depressurisation. 

Diving specific differentials to consider include inner ear barotrauma, middle ear/maxillary sinus over-inflation, contaminated diving gas/oxygen toxicity and immersion pulmonary oedema.

If there is chest pain, an MI or PE should be ruled out. If neurological symptoms such as retention/incontinence occur, spinal cord compression/injury should be considered.

Take home messages

  • Decompression illness is where bubbles of inert gas form in body tissues as a result of rapid environmental pressure change.
  • It comprises decompression sickness and arterial gas embolism.
  • Symptoms are very varied due to the possibility of bubbles forming in almost any body tissue, but pain is the most common symptom.
  • Patients with suspected DCI should be started on high flow oxygen regardless of their oxygen saturations.
  • High flow oxygen usually provides sufficient analgesia. DO NOT give nitrous oxide (Entonox) for pain relief, as this will increase the quantity of dissolved nitrogen gas in body tissues. Avoid opiates as they can increase propensity to oxygen toxicity.
  • Definitive treatment is via recompression therapy through use of a hyperbaric chamber.

Are you interested in learning more about decompression illness and other water related conditions?

If so, why not check out our Marine Medicine course? Whilst you’re there, why don’t you take a look at our other courses too?


  1. BSAC. Annual Diving Incident Report. 2021
  2. J Stephenson, Pathophysiology, treatment and aeromedical retrieval of SCUBA – related DCI, Original Research & Articles, Volume 17 No. 3, Doi No 11.2021-82717932
  3. S Clayton, C Walklett, Decompression Illness, Royal College of Emergency Medicine Learning, published 14/06/2022 https://www.rcemlearning.co.uk/reference/decompression-illness/#1567502925950-0cb9805c-1a89
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