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Consequences of captivity: Health effects of far East imprisonment in World

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Q J Med 2009; 102:87–96
doi:10.1093/qjmed/hcn137 Advance Access publication 14 October 2008

Review

Consequences of captivity: health effects of far

East imprisonment in World War II
D. ROBSON, E. WELCH, N.J. BEECHING and G.V. GILL
Liverpool School of Tropical Medicine, Pembroke Place, Liverpool, L3 5QA, UK

Summary

Downloaded from http://qjmed.oxfordjournals.org/ by guest on June 11, 2013

Though medical consequences of war attract
attention, the health consequences of the prisoner-
of-war (POW) experience are poorly researched and
appreciated. The imprisonment of Allied military
personnel by the Japanese during the World War II
provides an especially dramatic POW scenario in
terms of deprivation, malnutrition and exposure
to tropical diseases. Though predominantly British,
these POWs also included troops from Australia,
Holland and North America. Imprisonment took
place in various locations in Southeast Asia and the
Far East for a 3.5-year period between 1942 and
1945. Nutritional deficiency syndromes, dysentery,
malaria, tropical ulcers and cholera were major
health problems; and supplies of drugs and medical
equipment were scarce. There have been limited
mortality studies on ex-Far East prisoners (FEPOWs)
since repatriation, but these suggest an early (up to
10 years post-release) excess mortality due to tuber-
culosis, suicides and cirrhosis (probably related to
hepatitis B exposure during imprisonment). In terms
of morbidity, the commonest has been a psychiatric
syndrome which would now be recognized as post-
traumatic stress disorder—present in at least one-
third of FEPOWs and frequently presenting decades
later. Peptic ulceration, osteoarthritis and hearing
impairment also appear to occur more frequently. In
addition, certain tropical diseases have persisted in
these survivors—notably infections with the nema-
tode worm Strongyloides stercoralis. Studies 30 years
or more after release have shown overall infection
rates of 15%. Chronic strongyloidiasis of this type
frequently causes a linear urticarial ‘larva currens’
rash, but can potentially lead to fatal hyperinfection if
immunity is suppressed. Finally, about 5% of FEPOW
survivors have chronic nutritional neuropathic
syndromes—usually optic atrophy or sensory per-
ipheral neuropathy (often painful). The World War II
FEPOW experience was a unique, though often
tragic, accidental experiment into the longer term
effects of under nutrition and untreated exotic
disease. Investigation of the survivors has provided
unique insights into the medical outcome of depriva-
tion in tropical environments.

Introduction
Medical consequences of war are attracting increas-
ing attention. Obvious problems are those of
trauma, both physical and psychological. For
example post-traumatic stress disorder (PTSD) is
now well documented in veterans from the Vietnam
conflict1,2 and more recently, obscurer disorders
such as ‘Gulf War Syndrome’ have been described.3
Many more recent conflicts have occurred in
tropical areas (e.g. Africa and the Middle East),
and conditions including various worm infestations4
and cutaneous leishmaniasis have been described5
in military personnel from such areas.
The medical consequences of war captivity are
less well reported. PTSD and depression has been

Address correspondence to Prof. G. V. Gill, Liverpool School of Tropical Medicine, Pembroke Place, Liverpool,
L3 5QA, UK. email: g.gill@liv.ac.uk
! The Author 2008. Published by Oxford University Press on behalf of the Association of Physicians.
All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org
88 D. Robson et al.
recorded in concentration camp survivors.6 Health
problems of American (US) veterans who were
imprisoned in the Far East theatre of war in World
War II, or on the Korean conflict have been
reviewed.7 However, the majority of prisoners of
war (POWs) in Southeast Asia and the Far East
during the World War II were British, and the health
effects of their ordeal has not been systematically
recorded. At the Liverpool School of Tropical
Medicine, UK, we have assessed in detail over
2000 ex-Far East POWs (FEPOWs), and have noted
a number of ongoing tropical8 and non-tropical
disorders.9 In this article we describe conditions and
health in captivity, and the experience of ourselves
and others on long-term clinical sequelae of the
FEPOW experience.
Far East Captivity 1942–1945
In late 1941 and early 1942 the Japanese rapidly
over-ran Southeast Asia and the Oceanic islands.
The single major loss to the Allies was the fall of
Singapore, where over 100 000 mainly British troops
were captured. Other smaller groups were captured
in Burma, Hong Kong, Java, Sumatra and elsewhere.
For the next 3.5 years, these men were held in
prison camps, also with considerable movement of
some FEPOWs—notably in the crammed holds of
‘hell ships’ particularly en route from Singapore and
Java to Japan.10,11
Over half of the captured Singapore garrison were
transported later in 1942 to Siam (now Thailand).
The journey was a hellish 3 days, packed in cattle
trucks with little food or water, and widespread
dysentery frequently breaking out. In Thailand
they were used, along with an occupying force
of 290 000 local (‘coolie’) labourers, to construct
the infamous Thai-Burma Railway (also known as
the ‘Burma Railway’ or ‘Death Railway’).12 This was
a 400 km track from Boon Pong in Thailand to
Thanbyuzayat in Burma; over inaccessible moun-
tainous jungle country. The plan (which was never
fulfilled) was to provide a supply line to mount
an invasion of India. Overwork, malnutrition and
indigenous tropical diseases (which could rarely be
effectively treated), led to an overall mortality
amongst Allied POWs on the railway of 25%
(though in some of the more remote jungle camps
it was 50% or more). With no structured organiza-
tion or medical facilities, the total ‘coolie’ death rate
was 50%.
Elsewhere in Southeast Asia and the Far East,
POWs fared only slightly better. A shorter but
more remote railway was built across Sumatra,
POWs were used for mine work in Formorsa,
airfield construction in the Maluccon Islands, and
in factories and docks in Japan. Everywhere under-
nutrition and lack of medical facilities were major
problems. The ordeal did not end until Japanese
surrender in September 1945 (after the atom
bombing of Hiroshima and Nagasaki).
Illness in captivity
The major factors leading to the increased illness
rates and mortality can be summarized as follows:
 inadequate diet—both quantity and quality;
 hazardous and excessive labour;
 exposure to tropical infections;
 shortage of drugs and medical supplies.
Several first-hand accounts are available describing
the condition and illnesses encountered during
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captivity, and the resourcefulness and ingenuity
of the POW medical officers in supplementing
the meagre supplies of drugs and equipment given
by the Imperial Japanese Army.13–15 Indeed, sig-
nificant supplies of drugs were often only obtained
by smuggling in items bought or donated by local
traders. The major illness is captivity can be broadly
divided into nutritional and infective.
Nutritional disease
Weight loss was severe and universal, as energy
output greatly exceeded caloric intake. The diet was
entirely rice-based, with very small amounts of
vegetables and occasionally meat or fish. The rice
was polished and of poor quality, and vitamin B
deficiency became rapidly a major problem. As
well as classical syndromes such as beriberi, due
to thiamine deficiency, a variety of more obscure
neurological and dermatological syndromes were
seen summarized in Table 1.16–27 Painful lower leg
neuropathy was especially common20,22 with symp-
toms worse at night. It became known as ‘electric’ or
(more ironically) ‘happy feet’. Cranial second and
eighth nerve damage was less common but hugely
debilitating.23,24 Autonomic and myelopathic syn-
dromes were also seen—usually clinically mani-
fested as bladder dysfunction and spastic diplegia.21
Apart from night blindness (due to vitamin A
deficiency) and classical thiamine-deficient beriberi;
these syndromes were probably related to riboflavin
and/or nicotinamide deficiency. They became parti-
cularly common after dysentery outbreaks, and
generally responded to, or improved with vitamin
B supplementation. Vitamin tablets were generally
in short supply, and ‘marmite’ was sometimes used
with good effect. Also, ingenious extracts of grass
and other local plants were used.13,14 Of the
 Consequences of captivity
Table 1 Nutritional syndromes seen in FEPOW camps
(from ref.16–27)
Nutritional Symptoms
syndromes
Cardiac Wet beriberi (high output heart
failure)
Neurological Peripheral paraesthesia (dry beriberi)
Painful dysaesthetic neuropathy
(‘electric feet’, ‘happy feet’)
Amblyopia (‘camp eyes’)
Deafness and/or vertigo (‘camp ears’
or ‘camp deafness’) Night blindness
Myelopathy
Bladder dysfunction Dysphonia
(recurrent laryngeal neuropathy)
Dermatological Xeroderma
Angular stomatitis
Blepharitis Pellagra
Glossitis Scrotal dermatitis
(‘strawberry balls’)
nutritional skin syndromes (Table 1), perhaps the
most unusual and distressing was scrotal dermatitis.
Probably due to riboflavin deficiency, this led to
inflammation, exudation and swelling of the scrotal
skin, and was intensely uncomfortable. In Changi
Gaol, Singapore, it was known as ‘Changi Balls’;
and on the Thai/Burma Railway it was referred to as
‘Strawberry Balls’.19 A final problem localized to the
coral beaches of some of the Southeast Asian
beaches, where POWs were set to work construct-
ing aircraft runways, was painful blepharospasm
and blepharitis, lacrimation and photophobia.
Probably analogous to snow blindness, it became
known as ‘coral blindness’.
Infective disease
With no previous exposure to tropical infections,
and immunity lowered by malnutrition, all FEPOWs
succumbed to multiple infective illnesses, the major
ones of which are summarized in Table 2. Malaria
and dysentery were especially common, with most
POWs experiencing several attacks each year of
captivity. The jungle areas of Burma and Thailand
are hyper-endemic for malaria. Plasmodium vivax
was most common, but P. falciparum infections
also occurred with deaths not uncommonly from
cerebral malaria or blackwater fever.28 Quinine was
variably available, and often had to be used spar-
ingly in less severe attacks. Dysentery also became
a part of everyday life—particularly the bacillary
form, but additionally the more chronic and debili-
tating amoebic type was seen. The prototype
89
Table 2 Infective tropical diseases encountered in
FEPOW camps
Diseases Types
Malaria Mainly P. vivax, but also P. falciparum,
P. malariae and P. ovale
Dysentery Bacillary and amoebic
Tropical ulcer
Cholera
Typhoid
Diptheria Faucal and cutaneous
Dengue
Typhus
Smallpox
Tuberculosis
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sulphonamide drug ‘M&B’ was only occasion-
ally available for bacillary dysentery. Also in short
supply was emetine for amoebic dysentery. This
drug was not highly effective, and occasionally
severe and chronic cases were treated by defunc-
tioning ileostomies—apparently with some suc-
cess.29,30 The strange syndrome of tropical ulcer
was very common on the Thai/Burma Railway.
A small cut or abrasion on the ankle would rapidly
ulcerate and become infected, and not infrequently
would extend to involve the bones below. Curretage
of slough was done using sharpened spoons (with-
out anaesthetic), and innovative treatments such as
maggots or ever river fish were used (for the latter
treatment, men would immerse their legs in a river,
where small fish would eat the slough, helping
to clean the wound). Amputation was often neede-
d—usually carried out under spinal anaesthetic.
The Canadian POW surgeon ‘Marko’ Markowitz
recorded a remarkable series of 100 such amputa-
tions after the war.31 Cholera came in terrifying
epidemics, particularly when the monsoon season
hit the more remote jungle camps. Attempts were
made at oral and even makeshift intravenous fluid
therapy, but the mortality rate was high.32 The dead
were burned in hideous funeral pyres on the
outskirts of camps.
Other tropical illnesses are listed in Table 2; and
additionally, conditions such as pneumonia, bron-
chitis and meningitis were encountered. The effects
of trauma were also common—beatings by the
Imperial Japanese Army guards were frequent and
sometimes severe enough to cause fractured limbs
or ribs. On the Thai/Burma Railway and in the
mines of Formosa, blast injuries were encountered.
Towards the end of the war there were also
casualties from Allied bombing raids.
90 D. Robson et al.
Post-captivity mortality
Studies of mortality in FEPOWs post-release are
available, but have selection and interpretation
difficulties. Firstly, due to the high mortality in
captivity there is a significant ‘survivor effect’ i.e.
the POW experience itself selected out fitter
men, making interpretation of subsequent mortality
data difficult. Secondly, good mortality studies
are available only for certain nationalities of
FEPOW—mostly US veterans. This is because of
enumeration difficulties in many countries, notably
in the UK where FEPOWs were returned home after
release with little or no debriefing or tracking. The
US Veterans Administration system of healthcare
greatly facilitated subsequent POW mortality
studies. There are three major reports from the
USA,33–35 which despite the shortcomings
described above, provide useful information.
In 1955, Cohen and Cooper showed an excess of
mortality from tuberculosis (TB) and accidents in
US FEPOWs compared with ex-POWs from other
theatres of war.33 The accidents tended to be
contributed by motor vehicles, alcohol and some-
times psychiatric disorders (perhaps retrospectively
PTSD). Nefzger studied US FEPOW mortality rates
up to 1965, using Korean ex-POWs as controls.34
There was increased FEPOW mortality in the earlier
study years, but by the 1950s the two groups
showed similar mortality rates. Finally, Keehn
extended US FEPOW mortality surveillance to
30 years post-release. There was an excess of
death due to cirrhosis upto the mid-1950s, but over-
all death rates were comparable with controls.35
Studies from Canada compared FEPOW mortality
upto 1964 with that of the general population, and
showed a slight increase in FEPOW mortality due to
accidents, TB and ischaemic heart disease (IHD).36
In Australia, Freed and Stringer compared the
mortality of 14 000 FEPOWs from 1946 to 1963,
using general population figures as controls,37
similar to the Canadian study of Richardson.36 The
overall mortality was similar, but as in other studies
there was an excess of motor accident deaths
in the early post-war years, and an increase in
cirrhosis and TB mortality for the period between
1951 and 1963. Suicides were significantly exces-
sive for all ages. The mortality increases were offset
by a significant reduction in IHD deaths (hence the
overall equivalent mortality with the general popu-
lation). A further Australian study by Dent and
colleagues compared a cohort of 908 ex-Japanese
POWs with 797 other non-imprisoned veterans of
the same theatre of war.38 A mortality excess from
5 to 14 years post-release amongst the POWs
was demonstrated, but could not be significantly
attributed to any particular cause of death.
A structured review of relevant Australian studies
found no significant excess of mortality amongst
Japanese POWs (or veterans of the Vietnam conflict)
compared to the general population.39 These
workers did, however, point out the problem of
the ‘healthy conscript’ effect, i.e. that selection of
particularly healthy individuals for military service
may conceal a future increase in morbidity and/or
mortality.
In the UK, a small death certificate and autopsy
survey suggested a younger age of death, more
malignancies and less IHD as causes of death
compared to the general population.40 The study
was, however, limited by small sample size. A much
larger cohort in Britain was traced from the War
Pensions Agency, involving 11 134 ex-FEPOWs.41
Deaths from 1952 to 1997 were recorded, and
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compared with the general population. An
increased mortality from chronic liver disease and
cirrhosis was found, but strangely, overall mortality
was lower than expected—standardized mortality
rate 0.85. This included reductions in IHD and
malignancy-related mortality. Problems of this study
may be the lack of a true control group, and the fact
that early post-war mortality (1945–1952) was not
recorded.
Summarizing this data, there has been a consis-
tent increase in suicide and traffic accidents in the
early years after release—presumably related to
the psychological effects of imprisonment. Excess
deaths due to TB are also understandable, as
infection was common during imprisonment. The
increase in cirrhosis deaths was probably related to
hepatitis B, an infection unknown during and for
some time after the war. This will be discussed later,
as will be the interesting question of whether the
FEPOW experience may have actually conferred
some degree of later mortality protection, partic-
ularly from coronary artery disease.
Post-release FEPOW health
Persisting tropical disease
Strongyloidiasis
The nematode worm Strongyloides stercoalis is
endemic in wide areas of the tropics and sub-
tropics, including many parts of Southeast Asia. The
parasite has a complex larval life cycle in the soil,
but humans are infected by direct penetration of
the skin (usually of the foot) by filariform larvae.
These larvae migrate to the lungs and then the
bowel where they develop into sexual adults, which
produce rhabditiform larvae, eventually excreted
 Consequences of captivity
with the faeces. Uniquely, however, a process
of ‘autoinfection’ can occur, where larvae penetrate
the rectal mucosa or perianal skin and migrate
through the tissues again to the lungs. This migration
is often characterized clinically by a linear, rapidly-
moving, urticarial wheat in the central trunk
areas—known as ‘larva currens’ or ‘creeping erup-
tion’. The main implication of autoinfection is that
even when an infected individual leaves an
indigenous area for strongyloidiasis, infection can
continue indefinitely.42
Strongyloides infections (with various other
intestinal parasites) where diagnosed at some of
the larger camps (with microscopical facilities) on
the Thai-Burma Railway, but no treatment was
available; and indeed the infection was not thought
to be clinically important. Two reports of strongy-
loidiasis in British ex-FEPOWs appeared in
194943,44—both emphasizing the ‘creeping erup-
tion’. The cases were part of a large cohort of
FEPOWs investigated at Queen Mary’s Hospital,
Roehampton (in south London) from the late
1940s.45 Apart from these brief early reports, no
further publications appeared concerning FEPOW
strongyloidiasis until 1977 when 11 cases from a
FEPOW series of 100 were reported from the
Liverpool School of Tropical Medicine.46 The
Liverpool School had taken over FEPOW screening
from Roehampton, and was assessing large num-
bers, particularly in the 1970s and 1980s. A larger
and more detailed series from Liverpool was
published in 1979—this time describing 88 cases
from a group of 602 (a prevalence of 15%).47 The
larva currens rash was seen in 84%, and only 5%
reported bowel symptoms; in contrast to acute
strongyloidiasis where diarrhoea and/or abdominal
pain predominate and the creeping eruption is
rare.48 It is likely that this is because the chronic
syndrome seen in FEPOWs is reliant on autoinfec-
tion, with a consequent higher load of tissue
larvae.44 An example of the strongyloid rash is
shown in Figure 1. It is classically transient and fast-
moving (hence the diagnosis is often missed), and
occurs on the trunk, shoulders or buttocks (but not
the face or limbs).
Following the Liverpool papers, confirmatory
reports appeared from Australia,49 the USA,50
Holland51 and Canada.52 Similar features of long-
term chronicity and symptomatology were noted.
The risk to FEPOWs of contracting strongyloidiasis
was very much geographically determined. Trans-
mission was low in Hong Kong and Singapore for
example, but very high in Thailand.53 Thus, a final
report from Liverpool recorded 248 cases from
a total FEPOW population of 2072.54 Two-thirds of
cases, had served on the Thai-Burma Railways,
91
Figure 1. The larva currens (‘creeping eruption’) rash
of Strongyloides stercoralis infection in a British
ex-FEPOW—present 35 years after returning to the UK
in 1945.
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which emerged as a major statistical risk factor
for infection. As well as the parasite being common
in this area, the atrocious conditions led to men
having little or no footwear, clearly increasing the
risk of transmission.
Detection and treatment of strongyloidiasis in
ex-FEPOWs is important, as very occasionally the
‘hyperinfection syndrome’ may occur. This happens
when host immunity is reduced—most commonly
by steroid drug treatment.55 Massive larval multi-
plication and migration takes place, including larval
penetration of the bowel wall leading to peritonitis
and Gram-negative septicaemia. Pneumonitis and
meningitis are also frequent, and survival is rare.
Two cases of Strongyloides hyper-infection in
FEPOWs have been recorded, both related to steroid
treatment. One was a British FEPOW with poly-
myositis (reported in 1985),56 and the second was
an Australian FEPOW with a bronchogenic carci-
noma (reported in 1989).57
Both diagnosis and treatment of strongyloidiasis
has been problematic in the past, but modern
serological ELISA tests have made detection much
easier,58 and treatment regimes with albendazole or
ivermectin are now safe and highly effective.59
Screening and treatment of surviving FEPOWs is
therefore still important, if hyperinfective tragedies
are to be avoided.
Nutritional neuropathy
It was noticed after release that a number of
ex-FEPOWs were suffering nutritional neuropathic
symptoms which had not resolved or improved on
adequate diet and vitamin supplements.60 Persisting
peripheral neuropathy was reported in 1947 in
Canadian FEPOWs released from Hong Kong and
was still present in a re-examination 9 years later.61
92 D. Robson et al.

Table 3 Persisting nutritional neuropathy amongst UK auditory and visual evoked ptotentials, and nerve
ex-FEPOWs, followed upto 36 years post-release (from conduction studies. As well as the known neurolog-
ref.64). ical conditions two had extrapyramidal syndromes,
one myelopathy, one dementia, one cortical atrophy
Nutritional neuropathy Number (percentage) and two had psychometric evidence of non-
dominant hemisphere dysfunction. The authors
Symptomatic patients 49/898 (5.5%)
(POWs—58 conditions) concluded that the abnormalities represented wide-
Peripheral neuropathy 24 (41%) spread sub-clinical damage to the nervous system
Optic atrophy 19 (33%) induced by past malnutrition.
Sensorineural deafness 13 (22%)
Myelopathy 2 (4%)
Asymptomatic patients 38/898 (4.2%) Other tropical conditions
(POWs—42 abnormalities) Tropical ulcer
Absent tendon reflexes 21 (50%)
Sensory loss 13 (31%) Though most tropical ulcers either healed or
Optic atrophy 5 (12%) required amputation, some continued after repatria-
Fasciculation 1 (2%) tion—either chronically or undergoing cycles of
Wasting and weakness 1 (2%) healing and breaking down. Of a group of 602
Spastic monoparesis 1 (2%) FEPOWs seen in Liverpool upto 1980,8 there were

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Combined data (A + B) 88/898 (9.7%)
(POWs—100 abnormalities)
Peripheral neuropathy 60%
Optic atrophy 24%
Sensorineural deafness 13%
Myelopathy 3%
Similar follow-up data was recorded for optic
atrophy (nutritional amblyopia).62,63 In the UK
Roehampton survey,45 there were 679 of 4684
FEPOWs (14.5%), followed up to 1971, with
persisting neurological syndromes—generally per-
ipheral sensory neuropathy, spinal cord syndromes,
optic atrophy or nerve deafness. A detailed neurol-
ogical study from Liverpool of 898 FEPOWs
followed for up to 36 years showed that 49 (5.5%)
had definite symptomatic neurological syndromes,
and a further 38 (4.2%) had asymptomatic abnorm-
alities.64 The details are shown in Table 3. Of the
FEPOWs with long-term nutritional neuropathy,
most (60%) had peripheral neuropathy, 24% had
optic atrophy 13% sensorineural deafness and 3%
myelopathy. Extrapyramidal syndromes did not
feature in the Roehampton45 or Liverpool64 surveys,
but an excess of Parkinsons Disease was reported
in one study65 (though mortality from this condition
does not appear increased among FEPOWs41).
Finally, there is evidence that the overt clinical
syndromes described above may represent only the
‘tip of an iceberg’, with much more widespread
occult underlying neurological damage. In 1985,
Venables et al.66 reported detailed neurological
assessment of five UK FEPOWs with a single pen-
sionable nutritional neurological syndrome (four
amblyopia and one neuropathy). They undertook
CT brain scanning, psychometric evaluation,
three (0.5%) with such persisting tropical ulcers.
Amoebiasis
The same UK series of FEPOWs showed that six
(1%) FEPOWs had stool samples still positive for
Entamoeba histolytica.8 All but one were asympto-
matic but one had suffered bouts of intermittent
diarrhoea for over 30 years. Treatment with metro-
nidazole and diloxanide completely and perma-
nently cured this patient.
Malaria
As most malarial attacks during POW life were
benign forms (mainly Plasmodium vivax), recur-
rences occurred for some years after repatriation
in a number of FEPOWs. These rapidly declined
in frequency, but the Liverpool study revealed
one FEPOW (of the 602) who had genuine
recurrent P. malariae infection8 nearly 30 years
after release.
Cardiac beriberi
Though persisting nutritional neuropathy is well
described—continuing cardiac effects of malnutri-
tion are rare. Some deaths due to cardiac (wet)
beriberi did occur soon after release,67 but the
numbers were small and did not continue.
However, a UK FEPOW died of cardiac failure
31years after release. He had suffered very severe
beriberi as a POW, and at autopsy the coronary
arteries were normal but there was extensive
myocardial fibrosis considered to be due to the
effects of chronic (or previous) severe cardiac
beriberi.68
 Consequences of captivity
Post-release FEPOW health
Non-tropical disease
Psychiatric illness
Retrospectively it is not surprisingly that the 3.5-year
FEPOW experience was to lead to significant
psychiatric and psychological morbidity. As well
as the overwork, inadequate food and illness
burden; the POWs existed in an entirely isolated
environment from which escape was impossible,
and news from home non-existent. They were
reduced to the status of slaves, and frequently
experienced the death of close friends. Studies
from America soon after repatriation found surpris-
ingly good mental health,69 but as the years went
by significant psychiatric disorders appeared.70
The excess suicide mortality amongst Australian
ex-FEPOWs in the early post-release years bares
testimony to this emerging problem.37 The condition
of PTSD did not receive official ICD coding until
1992, and it was subsequently recognized that
war prisoners were clearly susceptible to this
condition.71 Before recognition of PTSD, psychiatric
syndromes were recognized in 41% of the UK
Roehampton series,45 and in 35% of the Liverpool
cohort.9 The features observed included agitation,
depression and mood disorders, flashbacks and
nightmares, sleep disturbance, low esteem, retarda-
tion, memory disturbance and sometimes guilt of
survival. These features were clearly compatible
with PTSD, and it was noted that they often did not
appear until years after release.9
In the late 1980s and early 1990s, PTSD and
depression were demonstrated amongst US
FEPOWs72–75 in several studies, as well as in a
controlled study from Australia.76 There is some
later evidence that the FEPOW PTSD syndrome may
have declined in intensity with time.77 No formal
trials of therapy have been undertaken—at the time
of their release, systems of debriefing, counselling
and cognitive therapy did not exist. It has generally
been assumed that at later stages, definitive treat-
ment would be ineffective. Interestingly, many of
the affected men made no mention of their problems
for many years. During tropical assessments at the
Liverpool School of Tropical Medicine, it was not
unusual for direct questioning to elicit histories of
horrific flashbacks and nightmares (as well as other
features of PTSD), which exPOWs had accepted for
30 years or more as part of their post-war burden.
Liver disease
The increase in cirrhosis deaths in FEPOWs during
the first 10 years after release35 has already been
93
referred to. Abnormal biochemical liver function
tests were common amongst British FEPOWs of the
Roehampton cohort,45 and cases of cirrhosis and
hepotoma were reported. At the time, the liver
damage was often thought to be nutritional in origin.
However, following discovery of the hepatitis B
virus, two studies of ex-FEPOWs in Australia78 and
Britain79 demonstrated high levels of serological
markers of past hepatitis B infection, with rates
particularly high in those who had worked on the
Thai/Burma Railway. In the UK study79 104/209
men (50%) had markers of past hepatitis B; includ-
ing HBsAg 9, anti-HBs 33, anti-HBc 2 and 60 with
anti-HBs and anti-HBc. These rates are, of course,
far higher than in the normal population levels. The
potential modes of transmission in captivity include
blood transfusions and inadequately sterilized
surgical instruments.
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Other conditions
Dyspepsia occurred frequently in the FEPOW prison
camps, and became known as ‘rice tummy’.21 This
was extremely common, being reported by 70%
of recently released Canadian FEPOWs.60 Of the
Liverpool series of 602 ex-prisoners, examined upto
30 years after release, 7% had previously diagnosed
duodenal ulcers (DU) and 8% had a new diagnosis
of DU on barium meal examination.9 Though
these rates were higher than the general UK popu-
lation, the study was not controlled. However,
Richardson’s study of Canadian FEPOWs from
Hong Kong used their brothers as controls, and a
significant excess of peptic ulcer in general, and DU
in particular was found.36 A similar peptic ulcer
excess has been found in Australian FEPOWs.80,81
Possibly higher rates than normal of chronic
obstructive pulmonary disease in FEPOWs have
been reported,9 but the data was uncontrolled, and
may anyway relate to high rates of smoking both
during and after imprisonment.
The effect of beatings, blows, accidents and
overwork may have led to a higher risk of osteo-
arthritis. Studies in the UK,9 Canada36 and New
Zealand82 suggest such an excess of osteoarthritis
amongst FEPOWs. Head beatings in captivity often
caused tympanic membrane perforations, followed
by infection which sometimes became longstand-
ing. Chronic middle ear disease and conduction
deafness appeared common in studies of UK
FEPOWs.9 Noise-induced deafness was seen in
some men, usually related to POW work in factory
or mine environments. Interestingly, in the early
post-release years US FEPOWs had significantly
increased hospitalization rates for ear diseases
94 D. Robson et al.
compared with ex-POWs from other theatres
of war.33
As discussed previously, there is conflicting
evidence linking the FEPOW experience with
IHD.7 Freed and Stringer’s report on Australian
FEPOWs found significantly reduced IHD mortal-
ity,37 though this was not supported by other
studies.18,20 An intriguing UK report described
a comparison between FEPOWs and Burma
Campaign veterans, 50 years after the end of the
war. The Burma veterans were of similar age and
had fought in the same geographical areas as
the FEPOWs, but of course were not imprisoned.
Rates of IHD were similar in both groups, but lipid
profiles were significantly better in the FEPOWs—in
particular total cholesterol was lower, and HDL
cholesterol higher (compared with the Burma
veterans).83,84 The reasons for this intriguing finding
are uncertain, but may again reflect the beneficial
‘survivor effect’ in FEPOWs.
Conclusions
A year after the war ended, the Royal Army Medical
Corps (RAMC) pathologist Major A. T. H. Marsden,
who had served 3.5 years on the Thai-Burma
Railway, wrote a perceptive paper on his experi-
ences. He noted that he had ‘had the opportunity of
taking part in a large-scale human experiment in
the effects of prolonged malnutrition, conducted by
those experts in malnutrition, the Imperial Japanese
Army’.84 Marsden could perhaps have added
intense exposure to tropical and exotic diseases
with minimal treatment facilities to this ‘human
experiment’. The point is a good one—never before
or since has such a large group been subject
to malnutrition, disease and pestilence on such
a large scale. Though clearly a tragic and regrettable
episode in military history, long-term medical
surveillance of these ex-POWs has significantly
extended medical knowledge. The remarkable
chronicity of Strongyloides stercoralis infections
had not been previously realized. Pictures of the
larva currens rash in a ‘former Far East prisoner’ not
infrequently appear in MRCP and DTM&H exam-
inations, and the UK Chief Medical Officer recently
circulated all British doctors warning them to remain
clinically alert to strongyloiasis in Far East war
veterans.85 The permanent and diffuse nutritional
nervous system damage seen in a number of
FEPOWs has also led to a revision of standard
concepts of ‘dry beriberi’ as a straightforward
sensory neuropathy, amenable to B vitamin treat-
ment. Finally, and perhaps most sadly, over a third
of these men were to suffer classical PTSD prior
to the syndrome being described. Without under-
standing or treatment, they carried this burden
through the years alone.
Relatively few FEPOWs are left alive now, but
they—and their deceased comrades—have left
behind an inspirational insight into survival under
the most desperate of conditions, as well as remark-
able medical lessons for the current generation of
doctors.
Conflict of interest: None declared.
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