Abstract

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 tuberculosis, 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 nematode 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 peripheral 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 deprivation in tropical environments.

Introduction

Medical consequences of war are attracting increasing 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 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 mountainous 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 organization 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 undernutrition 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: Several first-hand accounts are available describing the condition and illnesses encountered during 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, significant 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.

  • inadequate diet—both quantity and quality;

  • hazardous and excessive labour;

  • exposure to tropical infections;

  • shortage of drugs and medical supplies.

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 symptoms 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 syndromes were also seen—usually clinically manifested 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 particularly 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 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 constructing aircraft runways, was painful blepharospasm and blepharitis, lacrimation and photophobia. Probably analogous to snow blindness, it became known as ‘coral blindness’.

Table 1

Nutritional syndromes seen in FEPOW camps (from ref.16–27)

Nutritional syndromes Symptoms 

 
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 syndromes Symptoms 

 
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’) 

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 sparingly in less severe attacks. Dysentery also became a part of everyday life—particularly the bacillary form, but additionally the more chronic and debilitating amoebic type was seen. The prototype sulphonamide drug ‘M&B’ was only occasionally 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 defunctioning ileostomies—apparently with some success.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 (without 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 needed—usually carried out under spinal anaesthetic. The Canadian POW surgeon ‘Marko’ Markowitz recorded a remarkable series of 100 such amputations 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.

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  
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  

Other tropical illnesses are listed in Table 2; and additionally, conditions such as pneumonia, bronchitis 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.

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 sometimes 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 overall 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 excessive for all ages. The mortality increases were offset by a significant reduction in IHD deaths (hence the overall equivalent mortality with the general population). 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 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 consistent 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, particularly 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 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 eruption’. 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 strongyloidiasis in British ex-FEPOWs appeared in 194943,44—both emphasizing the ‘creeping eruption’. 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 numbers, 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 autoinfection, 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).

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.

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.

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. Transmission 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, 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 multiplication 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 polymyositis (reported in 1985),56 and the second was an Australian FEPOW with a bronchogenic carcinoma (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 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 peripheral sensory neuropathy, spinal cord syndromes, optic atrophy or nerve deafness. A detailed neurological 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 abnormalities.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).

Table 3

Persisting nutritional neuropathy amongst UK ex-FEPOWs, followed upto 36 years post-release (from ref.64).

Nutritional neuropathy Number (percentage) 

 
Symptomatic patients (POWs—58 conditions) 49/898 (5.5%) 
Peripheral neuropathy 24 (41%) 
Optic atrophy 19 (33%) 
Sensorineural deafness 13 (22%) 
Myelopathy 2 (4%) 
Asymptomatic patients (POWs—42 abnormalities) 38/898 (4.2%) 
Absent tendon reflexes 21 (50%) 
Sensory loss 13 (31%) 
Optic atrophy 5 (12%) 
Fasciculation 1 (2%) 
Wasting and weakness 1 (2%) 
Spastic monoparesis 1 (2%) 
Combined data (A + B) (POWs—100 abnormalities) 88/898 (9.7%) 
Peripheral neuropathy 60% 
Optic atrophy 24% 
Sensorineural deafness 13% 
Myelopathy 3% 
Nutritional neuropathy Number (percentage) 

 
Symptomatic patients (POWs—58 conditions) 49/898 (5.5%) 
Peripheral neuropathy 24 (41%) 
Optic atrophy 19 (33%) 
Sensorineural deafness 13 (22%) 
Myelopathy 2 (4%) 
Asymptomatic patients (POWs—42 abnormalities) 38/898 (4.2%) 
Absent tendon reflexes 21 (50%) 
Sensory loss 13 (31%) 
Optic atrophy 5 (12%) 
Fasciculation 1 (2%) 
Wasting and weakness 1 (2%) 
Spastic monoparesis 1 (2%) 
Combined data (A + B) (POWs—100 abnormalities) 88/898 (9.7%) 
Peripheral neuropathy 60% 
Optic atrophy 24% 
Sensorineural deafness 13% 
Myelopathy 3% 

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 pensionable nutritional neurological syndrome (four amblyopia and one neuropathy). They undertook CT brain scanning, psychometric evaluation, auditory and visual evoked ptotentials, and nerve conduction studies. As well as the known neurological conditions two had extrapyramidal syndromes, one myelopathy, one dementia, one cortical atrophy and two had psychometric evidence of non-dominant hemisphere dysfunction. The authors concluded that the abnormalities represented widespread sub-clinical damage to the nervous system induced by past malnutrition.

Other tropical conditions

Tropical ulcer

Though most tropical ulcers either healed or required amputation, some continued after repatriation—either chronically or undergoing cycles of healing and breaking down. Of a group of 602 FEPOWs seen in Liverpool upto 1980,8 there were 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 asymptomatic but one had suffered bouts of intermittent diarrhoea for over 30 years. Treatment with metronidazole and diloxanide completely and permanently cured this patient.

Malaria

As most malarial attacks during POW life were benign forms (mainly Plasmodium vivax), recurrences 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 malnutrition 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

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 surprisingly 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, retardation, 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 treatment 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 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; including 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.

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 population, 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 osteoarthritis. 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 longstanding. 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 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 mortality,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 experiences. 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 examinations, 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 treatment. Finally, and perhaps most sadly, over a third of these men were to suffer classical PTSD prior to the syndrome being described. Without understanding 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 remarkable medical lessons for the current generation of doctors.

Conflict of interest: None declared.

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