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Trench Foot

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Other Names

  • Peripheral vasoneuropathy
  • Nonfreezing Cold Injury (NFCI)
  • Acute trench foot
  • Chronic trench foot
  • Immersion foot
  • Sea boot foot
  • Bridge foot

Background

  • This page refers to Trench Foot, a nonfreezing cold injury (NFCI) combined with moisture and infection results in a peripheral vasoneuropathy
    • The term nonfreezing cold injury (NFCI) can be used synonymously with Trench Foot

History

  • First described by Dr Dominique Jean Larrey in 1812, a French surgeon, as Napoleon's army retreated from Russia[1]
  • The term 'trench foot' was first introduced during World War I[2]
    • Estimated to have contributed to the death of 75,000 British Soldiers in WWI[3]
    • US Armed Forces sustained 11,000 cases in the European theatre in 1944[4]
    • In the 1982 Falkland's conflict, one UK Brigade had a 76% Incidence[4]

Epidemiology

  • There is no clear epidemiological data
  • Incidence and prevalence appear to be decreasing
    • May be due to advances in clothing and better prevention of NFCIs
    • Better conditions during war time (little or no trench warfare in modern conflicts)
    • There is also no standard for diagnosing NFCI

Pathophysiology

  • General
    • Trench foot is a type of non freezing cold injury; moisture is required to produce a NFCI
    • It is typically accompanied by moisture, sometimes infection, resulting in a peripheral vasoneuropathy
    • NFCI is affects the nerves, microvasculature, and soft tissue of the distal limbs, most often the feet
    • Overall, the pathophysiology is poorly understood and described
  • Acute trench foot
    • Thrombi form, causing vascular occlusion and tissue death, nerve fiber inflammation[5]
  • Chronic trench foot
    • Partial recanalization of vessels may occur, but residual symptoms persist
    • Chronicity tends to follow repeated episodes of acute trench foot, resulting in 'chronic trench foot'
    • This leads to increasing severity, necrosis and potentially cellulitis, sepsis
  • Natural history
    • Most cases described with cold, wet extremities for at least one to three days
    • but NFCI can develop after 14 to 22 hours of exposure to sea water at 0 to 8 °C
    • Typically occurs in wet, cold conditions in patients who are unable to remove their shoes or boots whilst they are relatively immobile.
    • Patients are also usually fatigued and calorie-depleted.

Etiology

  • Nonfreezing cold injury (NFCI)
    • Exposure to cold temperatures just above freezing
    • Predominant manifestations are dysfunction of circulatory control and injury to the microcirculation
    • If sufficient duration and severity results in neurovascular changes, leading to peripheral vasoneuropathy[6]
    • Combined with moisture and pressure, drives a reactive hyperemia with subsequent edema and destruction of capillaries
    • This impairs tissue perfusion, leading to the destruction of nerves and tissue necrosis[7]
    • Blood flow is reduced in the toes due to a reduction in arterial diameter
    • Reduced blood flow leads to ischemia and subsequently reperfusion injury, which can result in long-term tissue damage
  • Nerve conduction
    • Among UK servicemen, nerve conduction was normal, however intra-epidermal nerve fiber density was markedly reduced in 91% of patients[8]
    • Animal models show a reduction in nerve conduction, distal degeneration of nerve fibers after cold exposure[9]
    • Cold exposure primarily affects sensory fibers, with 95% of patients with NFCI experiencing neuropathic pain

Associated Conditions


Risk Factors

  • Occupations (with risk of cold, wet feet)
    • Military
    • Fish processers
    • Harbor workers
  • Sports/ Recretional
    • Diving[10]
    • Hiking
    • Mountaineering
    • Festival attendees
  • Military Training[11]
    • Winter training exercises
    • Younger, unseasoned soldiers
    • Afro-Caribbean troops
  • Socioeconomic/ Other
    • Homelessness
    • Alcoholism
    • Inability to dry socks, boots
    • Immobility
    • Wet clothing or footwear
    • Poor caloric intake

Differential Diagnosis


Clinical Features

Example of stage 1 appearance of trench foot[12]
  • History
    • Diagnosis is clinical
    • History of exposure to wet cold for at least several hours in temperatures near freezing
      • Or an exposure for days with higher temperatures, as high as about 15 °C
    • History of losing feeling for at least 30 min and having pain or abnormal sensation on rewarming
    • Most commonly occurs in the feet, but can occur elsewhere in the body, including hands
  • Physical Exam: Physical Exam Foot
    • Red, edematous hands or feet
    • Demarcations are not sharp between diseased and non-diseased tissue (unlike frostbite)
  • Special Tests

Evaluation

  • The diagnosis of NFCI is made clinically
  • Imaging and laboratory testing are not helpful in most cases

Classification

  • Stages of Trench Foot[13]
    • Length varies widely
    • Some stages may be very short, easy to miss
    • Transition times vary
  • Stage 1 (cold exposure)
    • Characterized by complete loss of sensation
    • Patients report numbness, hands or feet feel like blocks of wood
    • May have trouble walking due to loss of sensation
    • Limbs may appear bright red, then become pale or white due to vasoconstriction
    • Stage is painless
  • Stage 2 (pre-hyperemic or post-exposure)
    • Starts when the victim is rescued from cold, placed in warm environment
    • Takes place during and following rewarming
    • Duration is extremely variable (hours to days)
    • Light skin: appears mottled and pale blue, indicating mild return of circulation
    • Dark skin: difficult to see color changes
    • Pulse is weak, but may become strong later, slow capillary refill
    • Limb is cold and insensate, with or without swelling
  • Stage 3 (hyperemic)
    • Starts suddenly then persists for days or weeks
    • Limb is bright red, swollen with strong pulses
    • Capillary refill remains delayed due to injury to the microcirculation
    • Hyperalgesia replaces numbness, although some distal areas may still be diminished or insensate
    • There is usually no tissue damage
    • Blisters may arise in injured areas that have suffered pressure injury or infection.
    • Blistering or discoloration may signify incipient necrosis.
  • Stage 4 (post-hyperemic)
    • Last for weeks to years or be permanent
    • Appearance is normal except in rare cases where tissue has been lost
    • Limbs are cool and are usually exquisitely cold-sensitive, vasoconstrict when exposed
    • Limbs may stay cold for hours, even after very brief cold exposure
    • Chronic pain in response to cold is common
    • Hyperhidrosis: often complain of excessive sweating
    • Victims may develop symptoms that resemble complex regional pain syndrome (CRPS)
    • Amputation is rare, but can occur with tissue necrosis

Management

Prevention

  • Primary treatment is prevention
    • Not well studied or published
  • General
    • Avoid wet-cold environments
    • Some recommendations are from warm water immersion injuries
    • Clothing should be warm, even when wet
    • Material: Synthetic materials are preferred over wool, avoid cotton as it gets very cold when wet
    • Remain active to encourage circulation
    • Elevate feet when possible
    • Education and training for cold to prevent, minimize stress and risk
    • Rotate personal in and out of cold environments
  • Dry feet
    • Air dry feet >8 hours a day is effective in preventing warm water immersion foot
    • Recommend to dry feet for a day after every 2 days of immersion[14]
  • Soldiers guide from WWI[15][3]
    • Paired with battle buddy, responsible to check each others feet
    • Increase rations, provide dry socks in waterproof bags
    • Change socks regularly, keep warm, avoid friction blisters
    • Inspect for blisters, signs of gangrene
    • Raise feet to prevent venous edema
    • Rotation schedules to avoid prolonged periods in wet, muddy trenches
    • Wraps around the calf and ankle above boots
    • Remain as active as possible to prevent vasoconstriction
    • Gum boots with foot powder instead of using oils (which probably increaser risk)

Prehospital

  • Patient moved to warm environment quickly
  • Patient may need to be carried
  • Wrapped in vapor barrier with insulation, over wet clothing as needed
    • Can remove wet clothing in warm environment

Emergency Department/ Acute Management

  • Correct hypothermia, if present
    • Use core temperature to identify
  • Rewarming limbs
    • If frostbite is present, rewarm affected limbs in water at 37-39 °C
    • If frostbite is absent, limbs do not need to be rewarmed
    • Rewarm gradually with rest, elevation, gentle pat drying
    • Rapid rewarming can cause severe pain, increased oedema, and increased tissue ischemia
  • Hydrate to address fluid losses
    • Recommend warming to ~42 °C
  • Avoid
    • Rubbing affected limb due to damaged skin
  • Tetanus Booster should be administered
  • Antibiotics are not routinely needed
  • Pain control
  • Consider prophylaxis for Venous Thromboembolism

Hospital Management/ Acute Management

  • Limb care
    • Elevate above level of heart
    • Dressings, if necessary, should be loose to protect circulation
  • Stage 3/ hyperemic
    • Sensation returns, limb becomes hyperalgesic
    • Recommend cool limbs using a fan at room temperature to 15-18 °C
    • Analgesics are generally ineffective including opioids
  • Amitriptyline
    • Initiate at the onset of pain[16]
    • 50 to 100 mg orally at bedtime
    • Higher doses for breakthrough pain
  • Gabapentin
    • Can be added or substituted if Amitriptyline is insufficient
  • Mild fever in the first 12 to 36 hours is common and usually transient
  • If cellulitis is present, antibiotics to cover staphylococci, streptococci, and pseudomonas
  • Surgical consultation if there are signs of tissue necrosis (hemorrhagic blisters)
  • Not helpful
    • Vasodilators including Nifedipine

Long Term Care

  • Pain management
    • Neuropathic pain, CRPS are common
    • Often require pain management specialist
  • Occupation
    • Outdoor work only if minor symptoms without numbness
    • Some soldiers can return to full duty if normal response to cold
  • Peripheral neuropathy
    • Should see neurologist for further investigation
  • Prostaglandin Analogue
    • Iloprost (a synthetic prostaglandin I2 analogue), temporarily reduced pain, increased mobility in a case report[17]
  • Nicotinyl tartrate
    • Demonstrated improved symptoms in 16 (44%) of 36 patients, with particular improvement in pain, paraesthesia and exercise capacity.[18]
  • Ineffective drugs
    • Aminophylline
    • Papaverine
  • Future research
    • Thromboxane and prostaglandin inhibitors have shown increased tissue survival in frostbite[19]
  • Tinea Pedis
    • If present, should be treated with systemic or topical antifungals

Operative

  • Indications
    • Unclear
    • Recommend surgical consult if evidence of significant necrosis
  • Technique
    • Lumbar Sympathectomy (obsolete, not recommended)

Rehab and Return to Play

Rehabilitation

  • Needs to be updated

Return to Play/ Work

  • There are no clear guidelines
    • Athlete/ worker needs to be able to progress through increasingly cold environments without pain

Complications and Prognosis

Prognosis

  • More severe injuries correlate with more severe sequelae/ complications
    • Typically permanent unless the injury was mild

Complications

  • Acute tissue necrosis
  • Infection
  • Difficulty ambulating
    • Patients may have a ‘slapping, flat-footed, springless gait' which often resolves in about 1 week[20]
  • Cold feet
    • Limbs often feel cold with persistent vasoconstriction, especially after cold expsure
    • This can cause pain, even when walking
  • CRPS/ Chronic Pain/ Hyperalgesia
    • Occurs frequently
  • Nail pathology
    • Intermittent nail loss
  • Severe arthropathy of major joints
  • Hyperhydrosis
  • Raynauds Syndrome
  • Chronic fungal infections
  • Psychiatric/ behavioral
    • Including Depression, suicidal thoughts
    • Substance and alcohol abuse
  • Occupation
    • Inability to work outdoors
    • Soldiers may be unable to redeploy
      • In one study, NFCI was career ending for 25/42 soldiers and career altering for the remaining 17[8]

See Also


References

  1. Gajic V. Forgotten great men of medicine – Baron Dominique Jean Larrey (1766–1842). Med Pregl 2011; 64: 97–100.
  2. Smith, J.L.; Ritchie, J.; Dawson, J. On the pathology of trench-frostbite. Lancet 1915, 2, 595–598.
  3. 3.0 3.1 Haller JS. Trench foot – a study in military-medical responsiveness in the Great War, 1914–18. West J Med 990; 152: 729–33.
  4. 4.0 4.1 Whayne, T.F.; DeBakey, M.E. Cold Injury, Ground Type; Office of the Surgeon General Department of the Army: Washington, DC, USA, 1958.
  5. Redisch W, Brandman O, Rainone S. Chronic trench foot: a study of 100 cases. Ann Intern Med 1951; 34: 1163–8.
  6. Ungley CC, Blackwood W. Peripheral vasoneuropathy after chilling. Lancet 1942; 2: 447–51.
  7. Friedman NB. The reactions of tissue to cold; the pathology of frostbite, high altitude frostbite, trench foot and immersion foot. Am J Clin Pathol 1946; 16: 634–9.
  8. 8.0 8.1 Vale TA, Symmonds M, Polydefkis M et al. Chronic nonfreezing cold injury results in neuropathic pain due to a sensory neuropathy. Brain 2017; 140: 2557–69.
  9. Kennett RP, Gilliatt RW. Nerve conduction studies in experimental non-freezing cold injury: II. Generalized nerve cooling by limb immersion. Muscle Nerve 1991; 14: 960–7.
  10. Laden, G.D.; Purdy, G.; O’Rielly, G. Cold injury to a diver’s hand after a 90-min dive in 6 degrees C water. Aviat. Space Environ. Med. 2007, 78, 523–525.
  11. Kuht, J.A.;Woods, D.; Hollis, S. Case series of non-freezing cold injury: Epidemiology and risk factors. J. R. Army Med. Corps 2019, 165, 400–404.
  12. Zafren, Ken. "Nonfreezing Cold Injury (Trench Foot)." International Journal of Environmental Research and Public Health 18.19 (2021): 10482.
  13. Thomas, J.R.; Oakley, H.N. Nonfreezing cold injury. In Medical Aspects of Harsh Environments; Pandolf, K.B., Burr, R.E., Eds.; Borden Institute: Washington, DC, USA, 2001; pp. 467–490.
  14. Taplin, D.; Zaias, N.; Blank, H. The role of temperature in tropical immersion foot syndrome. JAMA 1967, 202, 546–549.
  15. Hughes B. The causes and prevention of trench foot. Br Med J 1916; 1: 712–14.
  16. McGreevy, K.; Bottros, M.M.; Raja, S.N. Preventing Chronic Pain following Acute Pain: Risk Factors, Preventive Strategies, and their Efficacy. Eur. J. Pain Suppl. 2011, 5, 365–372.
  17. Ionescu AM, Hutchinson S, Ahmad M, Imray C. Potential new treatment for non-freezing cold injury: is Iloprost the way forward? J R Army Med Corps 2017; 163: 361–3.
  18. Redisch W, Brandman O. The use of vasodilator drugs in chronic trench foot. Angiology 1950; 1: 312–16.
  19. Raine TJ, London MD, Goluch L. Antiprostaglandins and antithromboxanes for treatment of frostbite. Surg Forum 1980; 31: 557–9.
  20. Webster, D.R.;Woolhouse, F.M.; Johnston, J.L. Immersion foot. J. Bone Jt. Surg. Am. 1942, 24, 785–794.
Created by:
John Kiel on 30 June 2019 22:55:53
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Last edited:
24 March 2022 11:23:36
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