WEBVTT

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Snow,

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cold rain,

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mud,

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these conditions lead to trench foot

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especially when men
are immobilized or crouched

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in wet cold foxholes for hours.

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Constricting clothing and tight shoes
contribute.

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Trench foot ranked high
in military importance.

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When there was
considerable combat activity

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on the Fifth's Army front
in the winter of 1944,

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the ratio
of trench foot to battle casualties

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was one to three and a half.

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These feet illustrate
the ischemic phase of trench foot.

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The peripheral vessels are constricted.

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Oxygen deficiency in the capillaries leads

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to increase permeability, exudation,
and edema.

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Tight clothing,

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direct injury to the skin due to cold,

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and trauma
from walking on damaged feet,

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probably accentuated the mechanism.

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When the affected feet
were exposed to warmth,

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the hyperemic phase developed.

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The vessels in these feet are dilated.

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Excessive vasodilatation is not controlled
because the nerves have been injured.

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There's absorption of catabolites
from tissues damaged by cold

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or indirectly
by prolonged vasoconstriction.

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Permanently damaged capillaries

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allow extensive outpouring of plasma
into tissue interspaces.

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The pressure of this interstitial fluid
on nerves

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gives pain, paresthesia, anesthesia,
and sudomotor disturbances.

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Numbness of the feet
and clumsiness in walking

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are the most prominent symptoms
of trench foot during onset.

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Many men do not realize
that anything is wrong

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until they remove shoes and socks.

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Such was the history of this case,

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a foot soldier stationed above [?] Italy.

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Clinical manifestations are variable,

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but a mild case like this
is commonly characterized

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by erythema,

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slight sensory changes,

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and little or no pitting edema.

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It was a month
before this man returned to active duty.

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Trench foot can put a man out of action
as effectively as a bullet wound

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and may disable him
for a much longer time,

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occasionally forever.

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A moderate case shows
the same manifestations as a mild one,

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plus blebs, discoloration,
and pitting edema.

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This case shows typical clinical signs
of trench foot during the hyperemic phase.

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Feet become red, dry, and hot.

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Peripheral pulses, full and bounding.

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Initial anesthesia and hyperesthesia

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are replaced by an intense burning pain
over the surface of the entire foot,

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relieved by cold and aggravated by heat.

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As healing progresses,
pain subsides and recedes distally.

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Edema usually reaches its height
by the fifth day

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and gradually recedes
followed by a fine wrinkling of the skin.

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The red color slowly fades

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and may turn into a waxy pallor
at about 10 days.

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For injuries not too grave,

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normal skin color returns
after some exfoliation.

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In a cross-section of skin at this stage,

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we note superficial scaling,

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disappearance of rete pegs,
and skin appendages,

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and increased and partly [?]
collagen of the corium.

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In a severe trench foot condition,

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we see
all previously mentioned manifestations

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more pronounced,

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with evidence
of massive extravasations of blood

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and incipient or actual gangrene.

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These are the feet of a sergeant,

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also hospitalized from the Italian front
and eventually evacuated to the State.

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A well-marked line of demarcation
developed in time,

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and at Walter Reed General Hospital
five months after leaving the front lines,

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this articulation of the toes
was accomplished without incident.

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The patient is sent to the hospital
as a litter case

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as soon as symptoms appear.

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His body kept warm by blankets,

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and his involved extremities
exposed to cool air

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with only a loose clean covering over them
for aseptic purposes.

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The injured parts are handled
as gently as possible.

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In the early stages,
they must not be rubbed or massaged.

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They may be washed carefully
with mild white soap and water

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and dried.

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Affected parts are protected
against pressure necrosis,

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particularly at the heel.

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They are maintained at a horizontal level

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and elevated to slightly above heart level

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only if there is no evidence
of inadequate circulation

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indicating incipient gangrene.

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In the early ischemic stage

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when spasm of vessels is evident
and persists for longer than six hours,

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1-ounce doses of whiskey may be given
for its vasodilating effect.

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For the same purpose,

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sympathetic blocks
using 1% procaine hydrochloride solution

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may be used.

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Both block and whiskey

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are not indicated
after the hyperemic stage begins

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and should be discontinued.

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Maintenance of minimal tissue
metabolism in the affected parts

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is especially
important during the hyperemic phase.

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Where the room temperature
is not above 70°F,

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simple exposure of the parts
may be sufficient.

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If not,

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increased cooling
is accomplished with a fan.

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Cooling could be still further increased
by spraying cold water through the fan.

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Measures to prevent secondary infection,

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including administration
of tetanus toxoid,

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are always instituted.

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Strict asepsis
must be observed constantly.

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Sulfadiazine by mouth is used
in cases with threatened infections.

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Ordinarily, blisters are not disturbed.

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If opening becomes necessary,
it is done aseptically.

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Heavy dressings
and all antiseptic solutions

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are avoided.

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Areas of necrosis and ulceration,
which may develop,

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are treated conservatively.

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In cases of gangrene,

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amputation is delayed as long as possible

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and is done early

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only in the presence
of superimposed infections.

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A nutritious diet should be supplied,
one high in proteins and vitamins.

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Physical therapy

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including diathermy,

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warm baths,

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exercises,

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and massage

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is of value in the late stages
and should be used.

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Sympathectomy is indicated

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only in cases showing objective evidence
of circulatory insufficiency,

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or in which manifestations
resembling Raynaud's phenomenon

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develop and persist months or years
after the acute phase of the disease

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and can be shown to be relieved
by test sympathetic blocks.

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In milder trench foot cases,
recovery is apparently complete.

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In more severe cases,

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sequelae have been observed
for months or years after exposure.

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There may be recurrence
of pain, tingling, and swelling,

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especially on walking,
or prolonged standing,

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or exposure to cold.

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In some cases,

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deep-seated aching pain persists

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and may be associated
with tenderness in the joints,

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usually worse at night.

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In others, there may be
limitation of motion in the joints,

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muscle weakness,
and difficulty in walking.

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Some cases complain
of excessive perspiration of the feet.

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Anesthesia and paresthesia
in the tips of the toes

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are not uncommon.

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The leg pains, the paresthesia,
and rigidity of the parts

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may be due to compression of nerve endings

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and infiltration of muscle bundles
with scar tissue.

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In this tissue section, for example,

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we see much fibrosis
and some atrophy of muscle fiber.

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In this one, the nerve,
still somewhat [?],

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is being pressed upon

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by increased fibrous tissues
surrounding it.

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When such preventive measures
are followed,

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if in cases
where trench foot has already developed,

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further injury is avoided
by proper first aid,

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and if infection and added fibrosis

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from careless
or ill-advised preliminary treatment

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are prevented or reduced.

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If all these things are done,
needless casualties can be avoided.

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The greatest of these ifs is prevention.

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The time to eliminate trench foot
is before it happens.

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Unit commanders should be cognizant
of trench foot factors

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and back medical discipline
with military discipline

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in the prevention and cure
of this important injury.

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Trench foot causes can be minimized,
and its effects can be reduced.

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It takes intelligent cooperation

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among medical staff, combat units,
and each individual fighting man.

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This is medicine in action.

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