Review article CED

Clinical and Experimental Dermatology

CPD

A review of trench foot: a disease of the past in the present

K. Mistry,1 C. Ondhia2 and N. J. Levell1,2
1
Norwich Medical School, University of East Anglia, Norwich, UK; and 2Department of Dermatology, Norfolk and Norwich University Hospital, Norwich, UK

doi:10.1111/ced.14031

Summary From the French Invasion of Russia in 1812, to Glastonbury festival in 2007, trench
foot has been reported, yet the exact nature of the condition remains unclear. This
review explores the pathogenesis and treatment of trench foot. Trench foot is consid-
ered to be a nonfreezing cold injury often complicated by infection, in which expo-
sure to cold temperatures just above freezing, combined with moisture, results in a
peripheral vasoneuropathy. The presence of physical trauma, bacterial or fungal
infections, malnutrition, venous hypertension and lymphoedema mean that some
individuals are at greater risk of trench foot. Trench foot may be prevented by
warming the feet, changing socks, staying active, rubbing the skin with oil and reg-
ularly inspecting the feet. Avoiding risk factors may help prevent the condition. The
management of trench foot is less clear. Vasodilators such as iloprost and nicotinyl
tartrate or sympathectomy may help. Trench foot may lead to necrosis, cellulitis,
sepsis and amputation. It remains a poorly understood condition.

History of trench foot
In the brutal Russian winter of 1812, as Napoleon’s
Grande Armee retreated to France, trench foot was
described for the first time by Dr Dominique Jean Lar-
rey, a French surgeon.1,2 In World War I, it was esti-
mated that trench foot contributed to the deaths of
approximately 75 000 British soldiers. Soldiers living
ankle-deep in muddy and wet conditions wearing
tight, cold and wet boots noticed their feet became
cold, pale, sweaty, swollen and painful.3 Over time,
the soldiers observed skin changes such as mottling
and hyperkeratosis with accompanied muscle stiffness
and low grade fever.4,5 Worse cases, where tissue per-
fusion was severely compromised, led to the absence
of foot pulses and development of paraesthesia (numb-
ness, tingling, itching) followed by erythema, xerosis
and warmth upon hyperaemia. Complicated cases
Correspondence: Mr Khaylen Mistry, University of East Anglia Faculty of
Medicine and Health Sciences, Norwich Medical School, Norwich, NR4
7TJ, UK
E-mail: khaylen.mistry@uea.ac.uk
Conflict of interest: the authors declare that they have no conflicts of
interest.
Accepted for publication 18 June 2019
resulted in a black and blistered gangrenous foot that
required amputation.4
Trench foot is not a disease limited to the past.
Recent cases have been described in homeless individ-
uals, and in 1998 and 2007 in over 270 revellers at
the large, multiday Glastonbury festival in the UK,
where there were sustained cold, wet and muddy con-
ditions.6 Immersion foot is the pseudonym for trench
foot seen in sailors following prolonged exposure to
cold water, with a similar pathogenesis and clinical
course.5 Understanding the true nature of trench foot
is a challenge, which this review aims to address.
Pathogenesis of trench foot: frostbite or
cellulitis?
Many theories exist around the pathogenesis of trench
foot, ranging from venous hypertension and stasis to
tinea infections and physical trauma.
The most established theory regarding the patho-
genesis of trench foot is that of nonfreezing cold injury
(NFCI), first suggested in 1942. This described trench
foot as a cold immersion syndrome: exposure to cold
temperatures just above freezing with sufficient dura-
tion and severity results in neurovascular changes

ª 2019 British Association of Dermatologists Clinical and Experimental Dermatology 1

Trench foot: a disease of the past in the present  K. Mistry et al.
leading to a peripheral vasoneuropathy.7 The cold
environment, combined with moisture and pressure,
drives a reactive hyperaemia with subsequent oedema
and destruction of capillaries, thus impairing perfusion
to tissues and ultimately leading to the destruction of
nerves (particularly large myelinated fibres8) and to
tissue necrosis.9 Following acute trench foot, blood
flow is reduced in the toes due to a reduction in arte-
rial diameter.10 This reduced blood flow leads to
ischaemia, and subsequent reperfusion injury follow-
ing the ischaemia may result in long-term tissue dam-
age.
Nerve conduction studies on 42 UK armed service
members with NFCI were normal; however, in the
same study skin histology showed intraepidermal
nerve fibre density to be markedly reduced in 91% of
the participants.11 Conversely, animal experiments
showed a reduction in nerve conduction and distal
degeneration of nerve fibres after cold exposure.12
Cold exposure primarily affects sensory fibres, with
95% of patients with NFCI experiencing neuropathic
pain.11
Cold injuries can be classified into freezing cold
injury (frostbite) and NFCI (Fig. 1). The pathogenesis
of frostbite differs from that of NFCI. At temperatures
below 0 °C, extracellular ice crystals form, which
directly damage the cell membrane and osmotic gradi-
ent across it, resulting in intracellular dehydration.13
Ice crystals may expand, causing mechanical destruc-
tion of cells.14 The body responds by alternating cycles
Figure 1 Classification of cold injuries and risk factors for nonfreezing cold injury and secondary infection.
2 Clinical and Experimental Dermatology
of vasoconstriction and vasodilation, known as the
‘the hunting reaction’.15 Vasodilation results in
increased perfusion and hence thawing, which is fol-
lowed by refreezing upon vasoconstriction.16 This con-
tinuous cycle of thawing and refreezing drives a
thrombotic inflammatory response mediated by prosta-
glandins and thromboxanes.17,18 The end result is ves-
sel occlusion, dermal ischaemia and tissue death.19
The presence of various risk factors may increase an
individual’s susceptibility to NFCI (Fig. 1).
There may be a difference between the pathogenesis
of acute trench foot (developed over a weekend in
Glastonbury) and the chronic form (developed over
weeks on sentry duty). With acute disease, thrombi
form, causing vascular occlusion and tissue death.13
This is accompanied by inflammation of nerve fibres.20
Chronically, partial recanalization of vessels may
occur, but residual symptoms persist.20 These chronic
sequelae follow repeat episodes of acute trench foot
resulting in ‘chronic trench foot’. Increasing severity,
leading to necrosis, can then be complicated by celluli-
tis and sepsis. This may have been the cause of the
high mortality, in the pre-antibiotic era, in exhausted
and malnourished soldiers.
Management of trench foot: vasodilators to
avoid amputation?
The approach to managing trench foot has evolved
with time, but the most important factor has always
ª 2019 British Association of Dermatologists

been prevention. In World War I, soldiers were paired
up and made responsible for their partner’s feet. Sol-
diers were advised to change their socks regularly to
keep their feet warm and avoid friction blisters, to
inspect their feet for blisters or other signs of gan-
grene, to keep their feet raised to prevent venous
hypertension/oedema, and to rub whale oil to promote
circulation and avoid venous eczema.21 Rotation
schedules were also set up to avoid prolonged periods
in the wet, muddy trenches, thus restricting cold and
wet exposure.21 More recently, an educational manual
(designed by army experts) on the prevention and
treatment of trench foot highlighted many of the
above points. The manual was shown to be an effec-
tive educational instrument for preventing and treat-
ing trench foot.22
In one report, iloprost (a synthetic prostaglandin I2
analogue) was used in a patient with persistent pain
secondary to NFCI; it reduced pain and increased
mobility initially, but symptoms worsened after a sec-
ond infusion.23 In an open study, nicotinyl tartrate
showed improved symptoms in 16 (44%) of 36
patients, with particular improvement in pain, paraes-
thesia and exercise capacity.24 Other studies on
vasodilators, including aminophylline and papaverine,
have been ineffective.24 Thromboxane and prostaglan-
din inhibitors have shown increased tissue survival in
frostbite25 and thus offer a potential area for future
clinical research in NFCI by targeting the vascular
component of the disease.
Sympathectomy had varied results in a case ser-
ies.26 Some patients had useful improvement (particu-
larly those with gangrenous limbs secondary to
vasospasm) but most had partial or no symptom relief.
Patients should always be checked for tinea pedis,
which should be treated with topical or systemic anti-
fungals.27 Secondary cellulitis should be treated early
with oral or intravenous penicillin V or flucloxacillin,
or with clarithromycin if penicillin-sensitive. Once-
daily intravenous cephalosporins are effective in cel-
lulitis treated in an outpatient setting.28 If anaerobes
are suspected, for example in the presence of necrosis,
then metronidazole may be added. When trench foot
leads to necrosis, surgical debridement or amputation
may be required.
Conclusion
There is uncertainty regarding the pathogenesis of
trench foot. All the factors shown in Fig. 1 may con-
tribute to a ‘trench foot syndrome’. A combination of
risk factors may combine with cold exposure so that
ª 2019 British Association of Dermatologists
Trench foot: a disease of the past in the present  K. Mistry et al.
vasoneuropathy occurs. Some risk factors, for example
physical trauma, damage the skin barrier, increasing
vulnerability to cold water. Other factors such as
venous hypertension, lymphoedema and dietary inade-
quacy reduce the ability to cope with cold exposure.
Addressing these risk factors may help to prevent
trench foot.
The basis of treatment of trench foot is prevention
or removal of exacerbating factors. The role of
vasodilators is unclear, other than a possible benefit
from iloprost, with no published evidence on calcium
antagonists or other more modern agents. There may
be a role for drugs such as amitriptyline, gabapentin
and pregabalin for neuropathic pain.
Trench foot remains a condition that is not well-de-
fined and is under-researched, with cases in the litera-
ture probably comprising a group of infection and
cold-related acute and chronic lower limb disorders.
Learning points
• Trench foot is not a disease limited to the past,
and continues to be reported in certain groups of
individuals including revellers at festivals and
homeless individuals.
• Trench foot is an NFCI; exposure to cold tem-
peratures combined with a moist environment
leads to peripheral vasoneuropathy and tissue
damage.
• Tinea infection, lymphoedema, venous hyper-
tension, physical trauma, dietary inadequacy and
fatigue may increase an individual’s susceptibility
to trench foot.
• Trench foot may lead to cellulitis/sepsis, which
can be fatal without prompt medical interven-
tion.
• Trench foot may be prevented by regularly
changing socks, keeping the feet warm, staying
mobile, rubbing oil on the feet and keeping the
feet raised.
• Vasodilators such as iloprost or nicotinyl tar-
trate and treatment with sympathectomy may
help trench foot; however, the management of
trench foot remains under-researched.
References
1 Anderson AF. A chance encounter with William
Sturgeon. Electron Power 1986; 32: 129–31.
Clinical and Experimental Dermatology 3
Trench foot: a disease of the past in the present  K. Mistry et al.
2 Gajic V. Forgotten great men of medicine – Baron
Dominique Jean Larrey (1766–1842). Med Pregl 2011;
64: 97–100.
3 Haller JS. Trench foot – a study in military-medical
responsiveness in the Great War, 1914–18. West J Med
1990; 152: 729–33.
4 Abramson DI, Lerner D, Shumacker HB et al. Clinical
picture and treatment of the later stage of trench foot.
Am Heart J 1946; 32: 52–71.
5 Friedman NB. The pathology of trench foot. Am J Pathol
1945; 21: 387–433.
6 Wrenn K. Immersion foot: A problem of the homeless in
the 1990s. Arch Intern Med 1991; 151: 785–8.
7 Ungley CC, Blackwood W. Peripheral vasoneuropathy
after chilling. Lancet 1942; 2: 447–51.
8 Irwin MS. Nature and mechanism of peripheral nerve
damage in an experimental model of non-freezing cold
injury. Ann R Coll Surg Engl 1996; 78: 372–9.
9 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.
10 Mendlowitz M, Abel HA. Quantitative blood flow
measured calorimetrically in the human toe in normal
subjects and in patients with residual of trench foot and
frostbite. Am Heart J 1950; 39: 92–8.
11 Vale TA, Symmonds M, Polydefkis M et al. Chronic non-
freezing cold injury results in neuropathic pain due to a
sensory neuropathy. Brain 2017; 140: 2557–69.
12 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.
13 Bracker MD. Environmental and thermal injury. Clin
Sports Med 1992; 11: 419–36.
14 Heggers JP, Robson MC, Manavalen K et al. Experimental
and clinical observations on frostbite. Ann Emerg Med
1987; 16: 1056–62.
CPD questions
Question 1
When was trench foot first described?
(a) In 1812, as Napoleon’s Grande Armee retreated to
France.
(b) In 1939–45, in the German army during World
War II.
(c) In 1982, in the British army during the Falklands
war.
(d) In 2007, in revellers during Glastonbury Festival.
(e) Trench foot has never actually been documented.
4 Clinical and Experimental Dermatology
15 Britt LD, Dascombe WH, Rodriguez A. New horizons in
management of hypothermia and frostbite injury. Surg
Clin North Am 1991; 71: 345–70.
16 Mazur P. Causes of injury in frozen and thawed cells.
Fed Proc 1985; 24: 14–15.
17 Merryman HT. Mechanisms of freezing in living cells and
tissues. Science 1956; 124: 515–18.
18 Robson MC, Heggers JP. Evaluation of hand frostbite
blister fluids as a clue to pathogenesis. J Hand Surg Am
1981; 6: 43–7.
19 Zawacki BE. The natural history of reversible burn
injury. Surg Gynecol Obstet 1974; 139: 867–72.
20 Redisch W, Brandman O, Rainone S. Chronic trench foot:
a study of 100 cases. Ann Intern Med 1951; 34: 1163–8.
21 Hughes B. The causes and prevention of trench foot. Br
Med J 1916; 1: 712–14.
22 Mendes B, Salome GM, Pinheiro FAM et al. Preventing
and treating trench foot: validation of an educational
manual for military personnel. J Wound Care 2018; 27
(Suppl): S33–8.
23 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.
24 Redisch W, Brandman O. The use of vasodilator drugs in
chronic trench foot. Angiology 1950; 1: 312–16.
25 Raine TJ, London MD, Goluch L. Antiprostaglandins and
antithromboxanes for treatment of frostbite. Surg Forum
1980; 31: 557–9.
26 Shumacker HB, Abramson DI. Sympathectomy in trench
foot. Ann Surg 1947; 125: 203–15.
27 Mistry K, Sutherland M, Levell NJ. Lower limb cellulitis:
low diagnostic accuracy and underdiagnosis of risk
factors. Clin Exp Dermatol 2019; 44: e193–5.
28 Levell NJ, Wingfield CG, Garioch JJ. Severe lower limb
cellulitis is best diagnosed by dermatologists and
managed with shared care between primary and
secondary care. Br J Dermatol 2011; 164: 1326–8.
Question 2
Which of the following are implicated in the pathogen-
esis of trench foot?
(a) Exposure to cold temperatures just above freezing
combined with moisture results in a peripheral
vasoneuropathy.
(b) Autoimmune dysfunction.
(c) Hyperproliferation of abnormal cells.
(d) Infection.
(e) Exposure to freezing temperatures below zero
results in a peripheral vasoneuropathy.
ª 2019 British Association of Dermatologists
 Trench foot: a disease of the past in the present  K. Mistry et al.

Question 3 (b) Prophylactic antibiotics.

(c) Using thicker socks.
Which of the following treatments have published evi-
(d) Weight loss.
dence of clinical benefit in trench foot?
(e) Smoking cessation.
(a) Aminophylline.
(b) Papaverine.
(c) Antibiotics. Instructions for answering questions
(d) Nicotinyl tartrate.
This learning activity is freely available online at
(e) Pregabalin.
http://www.wileyhealthlearning.com/ced
Users are encouraged to
Question 4 • Read the article in print or online, paying particular
attention to the learning points and any author
Trench foot has been reported in which of the follow-
conflict of interest disclosures
ing groups of people?
• Reflect on the article
(a) Elderly inpatients. • Register or login online at http://www.wileyhealth
(b) People who stay in the bath for prolonged periods. learning.com/ced and answer the CPD questions
(c) Revellers at Glastonbury Festival. • Complete the required evaluation component of the
(d) Bathers in Hampstead Heath ponds. activity
(e) Marathon athletes.
Once the test is passed, you will receive a certificate
and the learning activity can be added to your RCP
CPD diary as a self-certified entry.
Question 5
This activity will be available for CPD credit for
Which of the following has reported evidence that it 2 years following its publication date. At that time, it
helps prevent trench foot? will be reviewed and potentially updated and extended
for an additional period.
(a) Elevating feet.

ª 2019 British Association of Dermatologists Clinical and Experimental Dermatology 5