Snow Blindness 150 150 Endeavour Medical

Snow Blindness


What is Snow Blindness?

Snow blindness is a term used to describe a form of photokeratitis: i.e. a burn to the cornea and conjunctiva. 

Photokeratitis occurs when the eyes are exposed to significant ultraviolet (UV) rays. This can be due to artificial exposure e.g. from welding arcs (‘arc eye’ or ‘welder’s eye’), tanning beds, or due to concentrated natural exposure.

Snow blindness occurs after prolonged exposure to  natural UV rays. Snow reflects up to 90% of UV rays [1]. As snow is often encountered in mountainous terrain, this risk is compounded by the increase in UV exposure which occurs at altitude (approximately 4% for every 300m climbed) [2]. These combined factors result in a doubling of UV light exposure at 2000m compared with sea level [3]. It is a well-documented issue, which has dogged many legendary expeditions such as that of Scott’s Terra Nova Antarctic expedition (1910 – 1913) [4].


Whilst the cornea transmits light in the visible spectrum, UV rays are absorbed by the corneal epithelium. This process causes damage to the epithelial layer and results in a delayed sloughing of this superficial layer [5].

Photokeratitis is painful, as when this epithelial layer sheds it leaves the underlying nerve plexus exposed [6]. 

Signs and symptoms:

Symptom onset is usually six to twelve hours following UV exposure; however, this is exposure dependent and symptoms can occur as soon as one-hour post-exposure [7].

Symptoms include:

Bilateral red, painful, gritty eyes with associated photophobia [2].

Patients may be teary, have blurred vision or even suffer temporary blindness in severe cases.

Patients are likely to have surrounding sunburn to the face and eyelids as a diagnostic clue.

Differential diagnosis:

Be mindful not to miss critical ophthalmological diagnoses [2]. 

Signs such as systemic upset, concurrent illness, and unilateral changes should raise suspicion of alternative diagnoses. If there is painless loss of vision then this should be taken extremely seriously.

Similarly, if an individual has taken appropriate precautionary measures to prevent snow blindness, it is important not to develop an anchoring or confirmation bias prior to excluding differentials:

Acute angle closure glaucoma – Acute onset, painful with systemic upset.

Viral conjunctivitis – Can appear similar to snow blindness, however typically starts in one eye.

Contact lens overwear – Based on the history.

Dry eye – Based on the history, contact lens use, response to lubricants.

Foreign body – Based on history and a precipitating event.

High altitude retinopathy – Visual changes, usually painless in nature.

Painless loss of vision – Consider retinal detachment, vitreous haemorrhage, central retinal artery or vein occlusion, cerebral ischaemia, etc. 


Snow blindness will resolve spontaneously in 24 to 48 hours. Care is focused on symptom control and prevention of complications [7].

Patients should rest, avoid light and consider eye dressings to aid comfort. Cooling with cold compresses is a soothing option which is not resource intensive.

Lubricating drops and ointment can be used to manage the dry, gritty sensation.

Oral analgesia should be used, as can cycloplegic drops (e.g. cyclopentolate) to relieve the pain of ciliary spasm.

Adjunct treatments include antibiotic ointment to reduce the rate of secondary infections. 

Local anaesthetic should only be used to aid examination or facilitate evacuation in dangerous settings.


Snow blindness is prevented by minimising corneal exposure to UV rays.

Goggle or sunglasses with protective side pieces are recommended; ideally category 3 or 4 with 100% UV protection. 

Depending on the group size, duration and remoteness of the trip, it would be sensible to consider carrying some spares for the group. Eye protection should also have a hard-case container for storage when not in use and be easily accessible when needed.

In emergencies, sun shields can be made out of most materials by carving a slit into them for the eyes and fixing the material to the head. The small slits minimise refractive UV ray exposure. [2]

Are you interested in learning more about polar medicine?

If so, why not check out our Norway Polar Expedition course? 


  1. Ambach W, Blumthaler M, Schöpf T. Increase of biologically effective ultraviolet radiation with altitude. Journal of wilderness medicine 1993;4(2):189-197.
  2. Morris DS, Mella S, Depla D. Official Standards of the UIAA Medical Commission: Eye Problems on Expeditions. The International Mountaineering and Climbing Federation 2010.
  3. Ellerton JA, Zuljan I, Agazzi G, Boyd JJ. Eye Problems in Mountain and Remote Areas: Prevention and Onsite Treatment—Official Recommendations of the International Commission for Mountain Emergency Medicine ICAR MEDCOM. Wilderness Environ Med 2009;20(2):169-175.
  4. Guly, Henry R.,F.R.C.P., F.C.E.M. Snow Blindness and Other Eye Problems During the Heroic Age of Antarctic Exploration. Wilderness Environ Med 2012;23(1):77-82.
  5. Podskochy A. Protective role of corneal epithelium against ultraviolet radiation damage. Acta Ophthalmol Scand 2004;82(6):714-717.
  6. Bergmanson JPG. Corneal Damage in Photokeratitis???Why Is It So Painful? Optometry Vision Sci 1990;67(6):407-413.
  7. The College of Optometrists. Clinical Management Guidelines: Photokeratitis. 2022; Available at: https://www.college-optometrists.org/clinical-guidance/clinical-management-guidelines/photokeratitis_ultraviolet_uv_burn_arceye_snowblin. Accessed 09/11/, 2023.
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.

Are you interested in learning more about polar medicine?

If so, why not check out our Norway Polar Expedition course? 


(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.

Burnout Prevention in Medical Professionals 150 150 Endeavour Medical

Burnout Prevention in Medical Professionals


Dr Ishani Rao is an NHS GP and emergency medic. After a close encounter with burnout as a junior doctor, she realised the importance of looking after her own mental and physical health, and that of other healthcare professionals.

There are several current buzzwords as we recognise the importance of addressing, managing and preventing mental health issues in medical professionals. ‘Mindfulness’, ‘resilience’, and ‘wellbeing’ are all topics that we read articles about, have training in, and get questioned on by our workplace. However, how has this come about? What is the evidence behind this, and how can we utilise these concepts to reduce burnout and stress in ourselves and our team?

Let’s start with an introduction to burnout, and how we can identify symptoms of this. The term is defined by the International Classification of Diseases as ‘a syndrome conceptualised as resulting from chronic workplace stress that has not been successfully managed’ (1). This term was only added by the World Health Organisation to the 10th revision of the disease manual in 2016. The term was originally coined in the 1970s by a psychologist called Herbert Freudenberger who observed the development of a loss of motivation, emotional instability, and pessimism in mental health workers volunteering at a free clinic for the homeless community and drug offenders in New York City (2). It encompasses a state of physical and emotional exhaustion that may be characterised by multiple non-specific symptoms. These can largely be grouped into emotional symptoms (eg. pessimism, lack of motivation, irritability, helplessness), physical symptoms (eg. pain, headaches, impaired immune system, fatigue, insomnia) and behavioural signs (eg. procrastination, isolation, substance misuse, reduced performance.) It is important to consider the interlink between the mind and the body here. We must also be aware that symptoms may manifest differently in each individual. It must be emphasised that anyone experiencing the aforementioned symptoms should be reviewed by a medical professional to ensure appropriate investigation and consideration of differentials before a diagnosis of burnout is given.