histopathology 2014-64-200

Postmortem examination in the morbidly obese

Eve Fryer,1 Ian S D Roberts,1 Mary N Sheppard2 & Clare Verrill1,31Department of Cellular Pathology, John Radcliffe Hospital, Oxford, 2Department of Cellular Histopathology, Royal

Brompton Hospital, London, and 3Oxford Biomedical Research Centre, John Radcliffe Hospital, Oxford, UK

Date of submission 10 May 2013Accepted for publication 4 July 2013Published online Article Accepted 8 July 2013

Fryer E, Roberts I S D, Sheppard M N & Verrill C

(2014) Histopathology 64, 200210

Postmortem examination in the morbidly obese

Aims: The incidence of obesity is rising, and morbidobesity is associated with increased mortality rates.Pathologists will therefore encounter increasingnumbers of postmortems in the morbidly obese. It isessential that pathologists recognize morbid obesityand can identify its consequences at postmortem. Theaims of this study were to assess how often obesity isincluded in the cause of death of morbidly obeseindividuals, and whether obesity-related causes ofdeath are being missed.Methods and results: The postmortem database of theJohn Radcliffe Hospital was searched to identify allmedicolegal postmortems performed on morbidlyobese individuals between January 2007 and Septem-

ber 2012. Of 4742 coronial postmortems performed,3911 (82%) reports contained a record of height andweight, allowing body mass index calculation. Twohundred and two (5.2%) were performed on morbidlyobese individuals. Death resulted from natural causesin 189 (93.6%), of which obesity was included in themedical certificate of cause of death in 41 (22%).Conclusions: Postmortems in the morbidly obese rep-resent a significant percentage of the total performed,but recognition of the contribution of obesity to deathand of obesity-associated conditions is poor. Postmor-tems performed on the morbidly obese represent adistinct group with specific causes of death, andshould be approached as such.

Keywords: body mass index, obesity, postmortems

Introduction

In 2010, over one-quarter of the population in Eng-land was classed as obese; 26.2% of the male popula-tion and 26.1% of the female population.1 Obesity isdefined by the WHO as a body mass index (BMI) of30 kg/m2,2 and morbid obesity refers to a BMI of40 kg/m2. The prevalence of morbid obesity in Eng-land increased from 0.8% in 1993 to 2.0% in 2008,3

and is predicted to rise further.4 In 2004, a House ofCommons select committee estimated that 34 100deaths were attributable to obesity (6.8% of all deathsin England) and ~9000 of these were prematuredeaths (occurring before state retirement age).1

Mortality increases with BMI,5 and increased num-bers of postmortems are being performed on the mor-

bidly obese.6,7 In view of the clear association ofobesity with many medical conditions, one wouldpredict that obesity would frequently feature in thecause of death issued by pathologists following post-mortem. This, however, is not the case. In the 2006National Confidential Enquiry into Patient Outcomeand Death (NCEPOD) report into the quality of coro-nial postmortems, of 15 cases where postmortemswere carried out on morbidly obese individuals, onlyfour included obesity in the cause of death,8 and inonly 52% of all reports were both body height andweight recorded, enabling BMI to be calculated.9 Thereason for this lack of inclusion is uncertain; it mayreflect a lack of knowledge among pathologistsregarding obesity-related causes of death, but alsopathologists may feel reluctant to include obesity onthe death certificate for fear of offending or upsettingthe family of the deceased.Postmortem examination of the morbidly obese pre-

sents a challenge to pathologists, and not just in terms

Address for correspondence: Dr E Fryer, Department of Cellular

Pathology, Level One, John Radcliffe Hospital, Headley Way,

Headington, Oxford OX3 9DU, UK. e-mail: [email protected]

2013 John Wiley & Sons Ltd.

Histopathology 2014, 64, 200210. DOI: 10.1111/his.12224

of the practicalities of handling and dissecting largerbodies. There are a number of potentially fatal condi-tions that almost exclusively occur in the obese, suchas obstructive sleep apnoea (OSA), obesityhypoventi-lation syndrome (OHS; Pickwickian Syndrome),10 andobesity cardiomyopathy (OCM). These conditions aregenerally poorly understood by pathologists, withdeaths potentially being misattributed to other causes.In addition, there are a number of medical conditionsfor which obesity is a strong risk factor, such as venousthromboembolic disease (VTED).11

It is becoming increasingly recognized that beingobese does not just mean being bigger than normal,but rather that obesity is a condition that has specificpathophysiological effects. Adipose tissue has anendocrine role, and secretes adipocytokines that cre-ate a proinflammatory state, which has implicationsfor the development of conditions including cancer,atherosclerosis, and thrombosis.Postmortem studies have shown that missed diagno-

ses are more common in the obese, suggesting that alarger body habitus impedes the clinical diagnostic pro-cess.12 Postmortems in the obese need specific consider-ation, and guidelines akin to those published by theRoyal College of Pathologists on, for example, deaths inanaphylaxis are required, but are conspicuously absent.In this study, we retrospectively audited postmor-

tem reports in the morbidly obese over a 5-year,9-month period in a UK teaching hospital to determinepostmortem findings, the frequency of obesity-specificconditions, and the accuracy of cause of death, withthe aim of providing guidance on how to approachthese challenging deaths.

Materials and methods

The postmortem database of the John Radcliffe Hospi-tal, Oxford was searched to identify medicolegal post-mortems performed on the morbidly obese in theperiod January 2007 to September 2012. Morbidobesity was defined by a BMI of 40 kg/m2. BMI wascalculated as weight (kilogrammes) divided by thesquare of height (metres). Cases in which BMI couldnot be calculated were excluded. Data including thecircumstances of death, position of the body, cause ofdeath and heart weight were recorded.The Davies category for each cardiac death was

determined. The Davies categories constitute a well-recognized system for estimating the likelihood of car-diac pathology present at postmortem causing death(Table 1).13 Davies category 3, 4 and 5 deaths, i.e.those where a cardiac cause is less certain, werereviewed to assess the evidence for the stated causesof death, with the aim of identifying deaths that werelikely to have been caused by OSA, OHS or OCM butwere mistakenly attributed to another cause. The his-tology sections from cases that were suspected tohave been caused by OCM were reviewed by a spe-cialist cardiac pathologist (M.S.), if there was consentto use of the tissue for research.In Oxford, it is standard practice to include the entire

clinical history provided by the Coroners Officer in theautopsy report. In most cases, if pathologists obtainadditional information from the medical notes, this isalso included in the report, and therefore all of theinformation should be available in the report for any-one undertaking a retrospective review.

Table 1. A description of the Davies criteria, which assess the probability of the cardiac pathology present at postmortemhaving caused death13

Davies criteria Description

1 Coronary atheroma and clear evidence of coronary thrombosis and/or acute myocardial infarction very high probability of causing sudden death

2 Coronary atheroma with at least one coronary artery

Results

During the period January 2007 to September 2012,4742 coronial postmortems were performed, of which3911 (82%) contained a record of height and weight,allowing BMI to be calculated. Of these, 202 (5.2%)were performed on morbidly obese individuals. Deathresulted from natural causes in 189 (93.6%). Thebreakdown of cases by year is shown in Table 2.Of the 202 morbidly obese individuals, 120 were

female and 82 were male. The mean age was63 years (range 1888 years). The median BMI was44.1 kg/m2 (range 4094.1 kg/m2). The heartweights for cases where death was due to naturalcauses were as follows: female, range 142892 g

(mean 527 g, median 510 g); and male, range 3521699 g (mean 640 g, median 609 g). The heartweights for the six female unnatural deaths were260, 312, 386, 438, 485, and 500 g (mean 397 g,median 412 g). The heart weights for the seven maleunnatural deaths were 333, 405, 573, 624, 627,648, and 652 g (mean 552 g, median 624 g).

C A U S E O F D E A T H

The stated causes of death for the 202 morbidly obeseindividuals are shown in Table 3, and the respiratoryand cardiac deaths are further subdivided in Tables 4and 5. Table 6 shows the subdivision of the cardiacdeaths into Davies categories.

Table 2. Coronial postmortems performed by year

2007 2008 2009 2010 2011 2012* Total

Total no. of cases 731 742 778 913 771 807 4742

Reports including height and weight 708 642 645 709 690 517 3911

Morbidly obese individuals 42 24 31 30 43 32 202

Death due to natural causes 40 23 29 28 40 29 189

*Nine months only assessed.

Table 3. Summary of stated causes of death, which are also further subdivided into BMI categories 40.044.9, 45.049.9,and 50.0 kg/m2 [no. (%)]

40.044.9 kg/m2 45.049.9 kg/m2 50.0 kg/m2 Total

Cardiac disease (for subdivision, see Table 5) 41 (38.3) 29 (62) 16 (33.3) 86 (42.6)

Respiratory disease (for subdivision, see Table 4) 22 (20.6) 7 (14.9) 11 (22.9) 40 (19.8)

Pulmonary embolism 12 (11.2) 4 (8.5) 12 (25.0) 28 (13.9)

Diseases of blood vessels 6 (5.6) 2 (4.3) 2 (4.2) 10 (5.0)

Complications of surgery 6 (5.6) 2 (4.3) 1 (2.1) 9 (4.5)

Diseases of the gastrointestinal tract 3 (2.8) 1 (2.1) 3 (6.3) 7 (3.5)

Accident 4 (3.7) 1 (2.1) 1 (2.1) 6 (3.0)

Drug toxicity/hanging 4 (3.7) 1 (2.1) 1 (2.1) 6 (3.0)

Malignancy 3 (2.8) 0 0 3 (1.5)

Diseases of the liver, pancreas, and biliary tree 3 (2.8) 0 0 3 (1.5)

Intracranial pathology 3 (2.8) 0 0 3 (1.5)

Diseases of the kidneys 0 0 1 (2.1) 1 (0.5)

Total 107 47 48 202

2013 John Wiley & Sons Ltd, Histopathology, 64, 200210.

202 E Fryer et al.

O B E S I T Y I N T H E M E D I C A L C E R T I F I C A T E O F C A U S E

O F D E A T H

Of the 189 deaths resulting from natural causes,obesity was included in the Medical Certificate ofCause of Death (MCCD) in 41 (22%).Obesity was most commonly included in the MCCD

in deaths resulting from ischaemic heart disease (9/61), venous thromboembolic disease (14/28), respira-tory disease (4/31), and other cardiac causes (7/21).

O B S T R U C T I V E S L E E P A P N O E A

There were two deaths recorded as resulting fromOSA. The position of the body was recorded in onlyone of these cases, the deceased being found on theirback. There was a further death that had beenrecorded as congestive cardiac failure resulting fromischaemic heart disease, but, on review by theauthors, was felt to have been caused by OSA, asthere was a history of OSA and there had been aproblem with a continuous positive airway pressure(CPAP) mask around the time of death. A summaryof the three OSA deaths is shown in Table 7.The supine position of the body is pivotal to diag-

nosing OSA at postmortem. Forty of the 202 caseswere found dead in bed, and in only nine of 40 wasthe position of the body provided to the pathologist.

O B E S I T Y H Y P O V E N T I L A T I O N S Y N D R O M E

Three cases of OHS were identified (Table 8). In twocases, OHS was given explicitly as the cause of death

in the MCCD; in the other case, the cause of deathwas given as hypertensive heart disease and obesity,but the possibility of OHS was discussed in the com-ments. In all three cases the deceased had a historyof shortness of breath; one had a history of obesity-related hypoventilation and one had a history ofOSA. One patient died during exertion, one wasfound dead in bed, and one was found dead on thebedroom floor. In all three cases, obesity was includedin the MCCD.

O B E S I T Y C A R D I O M Y O P A T H Y

Six possible cases of OCM were identified by reviewingthe Davies criteria 3, 4 and 5 deaths, and these aresummarized in Table 9. One case had been recordedas OCM, three as dilated cardiomyopathy, and oneas biventricular hypertrophy; a sixth case had the

Table 4. The 40 stated respiratory causes of death in mor-bidly obese patients

Cause of death Number of cases

Pneumonia 20

Asthma 5

Mechanical airway obstruction 3

Obesityhypoventilation syndrome 2

Obstructive sleep apnoea 2

Pulmonary fibrosis 2

Mesothelioma 2

Adult respiratory distress syndrome 2

Chronic obstructive pulmonary disease 1

Pneumothorax 1

Table 5. The 86 stated cardiac causes of death in morbidlyobese patients

Cause of death Number of cases

Ischaemic heart disease (no evidence ofacute myocardial infarction)

28

Myocardial infarction 18

Ischaemic and hypertensive heart disease 13

Hypertensive heart disease 8

Dilated cardiomyopathy 3

Valvular disease 3

Congestive cardiac failure, nototherwise specified (NOS)

2

Ischaemic heart disease andvalvular disease

2

Left ventricular hypertrophy, NOS 2

Biventricular hypertrophy, NOS 1

Cor pulmonale 1

Hypertensive heart diseaseand cor pulmonale

1

Cardiac amyloidosis 1

Obesity cardiomyopathy 1

Pericarditis 1

Infective endocarditis 1

Sudden adult death syndrome 0


Postmortems in the obese 203

immediate cause of death recorded as aortic dissec-tion, but with dilated cardiomyopathy as a contribu-tory factor (in part 2 of the MCCD). Two of the sixcases (cases 2 and 4) had no histology for review; allfour cases available for review were felt to representOCM after specialist cardiac pathology review.

Case 1This was a case of sudden death at home after gastricbypass surgery. The cause of death had been recordedas OCM, and this was confirmed on review. The heart

weighed 497 g, but it was difficult to be certainabout hypertrophy because of decomposition. Therewas extensive fat infiltration in the right ventricle onhistology.

Case 3This patient collapsed and died in the street. Thecause of death had been originally recorded as dilatedcardiomyopathy. There was a slightly heavy heart, at520 g (the normal adult male heart weighs up to500 g), with left ventricular concentric hypertrophy

Table 6. The numbers of cardiac deaths in each Davies category

Davies category 2007 2008 2009 2010 2011 2012 Total %

1 7 1 2 1 0 4 15 18

2 3 5 4 4 7 2 25 30

3 2 2 2 4 4 4 18 21

4 4 3 6 4 3 5 25 30

5 0 0 0 0 0 0 0 0

Uncategorizable 0 0 0 1 0 0 1 1

Table 7. A summary of the three deaths resulting from obstructive sleep apnoea (OSA)

BMI ToxicologyHeartweight (g)

Right ventricularhypertrophy

History of sleepapnoea priorto death Position of body

Cause of deathgiven as OSA

45.8 Not done 555 Yes Yes In bed, exactposition not given

No

40.3 Negative 635 Yes No In bed on back Yes

42.3 Ethanol level unknown,morphine 124 lg/l,nordiazepam

600 Not stated inpostmortemreport

Yes Not given Yes

Table 8. A summary of the main features of the three deaths in which obesityhypoventilation syndrome (OHS) was diag-nosed

BMI ToxicologyHeartweight (g)

Right ventricularhypertrophy

History of OHSprior to death Position of body Stated COD

51.7 Not done 684 Yes No Collapse in street Acute bronchitis, and OHS andpulmonary hypertension

43.8 Not done 628 Not known No Dead in bed Hypertensive heart disease andobesity

43.9 Not done 568 Yes No Floor of bedroom OHS with pulmonary hypertensionand cor pulmonale


204 E Fryer et al.

with biventricular dilatation. There was only mild ath-eroma (

awareness of the role of obesity in the cause of deathin many of these cases needs to be addressed witheducation, perhaps best achieved by a Royal Collegeof Pathologists dataset and a national audit of thesedeaths. There is a balance to be struck when consid-ering inclusion of obesity in the MCCD, as it is impor-tant to remember that many deaths in the morbidlyobese will be unrelated to obesity, and not to over-state the issue. Obesity should be included in thecause of death when it has a strong association;either it directly causes the condition (part 1 of theMCCD) or it is a well-recognized risk factor for thecondition (part 2 of the MCCD). It should be includedin cases of OSA where it is a direct cause of this con-dition, and placed in part 1 of the death certificate. Inthis study, in the three cases of OSA, obesity wasincluded in the cause of death (in part 2) in one caseonly. In OCM and OHS, obesity is present in thename of the condition, and is therefore automaticallyincluded in part 1 of the MCCD. Obesity should beincluded in part 2 of the MCCD in cases such as pul-monary embolism where obesity is a risk factor. Obes-ity is an independent risk factor for coronary heartdisease, and therefore should be included in part 2,along with conditions such as hypertension and dia-betes mellitus, although, in actual practice, this maynot happen in every case.This study evaluated the MCCD only in cases

where there had been a postmortem examination.Further studies could be undertaken, comparing thesedata with those held by the Office for National Statis-tics (ONS) on MCCD in deaths in the morbidly obesewhich are based on clinical grounds, with no post-mortem taking place.In addition to the conditions described below, obes-

ity is a risk factor for the metabolic syndrome, cere-brovascular accidents, type 2 diabetes mellitus,osteoarthritis, hypertension, some malignancies, sur-gical site infections, nosocomial infections, and skininfections.14

O B S T R U C T I V E S L E E P A P N O E A

In this study, OSA was under-recognized, being statedas the cause of death in two of three cases that weredetermined on review to represent OSA. OSA is acondition characterized by episodes of obstruction ofthe upper airway during sleep, interrupting the flowof air, followed by transient awakening.15 This resultsin chronic alveolar hypoxia, pulmonary artery con-striction, and pulmonary hypertension, and canresult in cor pulmonale.16 It is caused by accumula-tion of fat in the neck region. The condition is sug-

gested by a history including snoring and observedapnoeas, but definitive diagnosis is made by polysom-nography during life, and treatment is by CPAP ven-tilation.Deaths caused by OSA are a challenge at postmor-

tem, because findings are often limited and may berestricted to obesity alone. A history of this conditionduring life is therefore of key importance. An unwarypathologist may mistakenly attribute death toanother condition, such as non-significant ischaemicheart disease. Cases without a history of OSA duringlife present even more of a problem, although thediagnosis may be suggested by the circumstances ofthe death. These deaths will always occur in bed,usually in the supine position,17 and details of theexact position of the body are vital (this was providedfor only nine of 40 cases found dead in bed in thisstudy). OSA should also only be given as a cause ofdeath when all other causes have been excluded,including by histology and toxicology. Toxicology isimportant, because consumption of alcohol or othersedatives exacerbates the condition. Criteria for givingthe cause of death at postmortem as OSA are givenin Table 10 (modified from Robinson et al.17).

O B E S I T Y H Y P O V E N T I L A T I O N S Y N D R O M E

Obesityhypoventilation syndrome is a conditioninvolving obesity, hypoventilation and sleep-disor-dered breathing (usually OSA) with daytime hyper-capnia (which distinguishes it from OSA), in theabsence of other causes of hypoventilation such aschronic obstructive pulmonary disease.18 Like OSA, itrequires a test performed during life for diagnosis(daytime arterial blood gas), making it a difficult diag-nosis to make at postmortem. The chronic hypercap-nia means that OHS is more likely to progress to corpulmonale than is OSA. In OHS, unlike in OSA, deathdoes not typically occur in bed because of respiratoryfailure or ventricular arrhythmia triggered byhypoxia; rather, the mode of death is a fatal cardiacarrhythmia secondary to cor pulmonale. In thisstudy, of the three deceased persons, one was founddead in bed, one was found on the floor of the bed-room, and one collapsed in the street.In the absence of a known history of OHS (one of the

three cases in this study had a history of OHS duringlife, and one had a history of OSA), clues to the diagno-sis from the clinical history include symptoms of sleepapnoea and shortness of breath, and symptoms andsigns of cor pulmonale. As in OSA, deaths that are sus-pected to be secondary to OHS usually require a fullpostmortem with histology and toxicology.


206 E Fryer et al.

Criteria for giving a cause of death as being second-ary to OHS are given in Table 10. Right ventricularhypertrophy is defined by the Fulton technique as anisolated right ventricular weight of greater than 65 gor a reduced left to right ventricular weight ratio (thenormal left: right ventricular weight ratio is 2.33.3).19 OHS is illustrated in Figure 1.

S U D D E N C A R D I A C D E A T H I N O B E S I T Y

Obese subjects have an increased risk of arrhythmiasand sudden death, even in the absence of cardiac dys-function.20 The sudden unexplained cardiac mortalityrate is 40 times higher in the obese than in amatched non-obese population.20

In this study, Davies category 4 deaths accountedfor 30% of cases; this is proportionately high whencompared with a previous study of 1292 postmor-tems (616 of which were cardiac causes of death)21

which showed 25% category 1, 27% category 2,19% category 3, 22% category 4, 4% category 5 and3% unclassified deaths.

A prolonged QT interval is seen in a relatively highpercentage of obese subjects,20 but the clinical signifi-cance of this remains speculative. Although no defi-nite cases were found in this study, it seems plausiblethat there is a scenario of sudden death related tocardiac arrhythmia, in morbidly obese patientswithout prominent cardiac hypertrophy or dilatation;and that this is a diagnosis of exclusion, akin to sce-narios such as sudden unexpected death in epilepsy(SUDEP), dead in bed syndrome (type 1 diabetes mell-itus), and sudden unexpected death in alcohol misuse(SUDAM).

C O R O N A R Y H E A R T D I S E A S E

Ischaemic heart disease was the commonest cause ofdeath in this series. Meta-analysis has shown thatabdominal obesity is an independent risk factor forcoronary heart disease.22 Interestingly, there is aninverse relationship between body weight and mortal-ity in patients with known cardiovascular diseaseor post-acute myocardial infarction (the obesity

Table 10. Diagnostic criteria for obstructive sleep apnoea (OSA), obesityhypoventilation syndrome (OHS), and obesity car-diomyopathy (OCM)

Diagnosis Diagnostic criteria

OSA A diagnosis during life of OSA, even in the absence of respiratory failure. Without an establisheddiagnosis, an appropriate history, e.g. snoring

The circumstances of the death, in particular death in bed, during sleep in the supine position,often while not using CPAP

Absence of specific postmortem findings such as an acute cardiac or cerebral event

Evidence of intoxication with alcohol or other sedatives

OHS A history during life of OHS. In the absence of this, a history of OSA or snoring during life. There maybe no prior history

Sudden death in the absence of a clear alternative cause of death such as an acute cardiac or cerebral event

Features of pulmonary hypertension and cor pulmonale such as right ventricular hypertrophy anddilatation (Figure 1)

OCM Increased heart weight (see text)

Left ventricular or biventricular hypertrophy and dilatation of atria and ventricles. Small foci of interstitialfibrosis may be present, but not extensive ischaemic fibrosis

There may be marked fat in the right ventricle, usually subepicardial and extending between blood vessels(in the absence of fibrosis, which suggests arrhythmogenic right ventricular cardiomyopathy), oftenup to the trabeculae. Usually, the anterior and lateral wall is affected to a greater extent than theposterior wall (Figure 2)

Exclusion of significant coronary artery disease, myocarditis, acute infarction, or other clearalternative cause of death



paradox), suggesting that excess body weight actuallyconfers a lower risk for adverse events (includingdeath) in patients with cardiovascular disease, includ-ing those with heart failure.23,24

O B E S I T Y C A R D I O M Y O P A T H Y

Obesity directly causes structural and functionalchanges to the heart,25 and it is difficult to separatethis from coexisting conditions such as hypertensionand OSA/OHS. Obesity produces an increase in totalblood volume and cardiac output, because of the highmetabolic activity of excessive adipose tissue,26 result-ing in biventricular hypertrophy and dilatation. Ifsystemic hypertension is also present, this further

promotes left ventricular dilatation and hypertrophy,their effects being additive, not synergistic.26 Theterm obesity cardiomyopathy is used when the effectsof obesity on the heart have led to congestive cardiacfailure; this typically occurs in those with severeand long-standing obesity, the mode of death beingprogressive congestive cardiac failure or suddenarrhythmia.In this study, OCM was present in four of 202

(2.0%) deaths after review, having originally beenreported in only one of 202 deaths, again suggestingthat this condition is under-recognized by patholo-gists. Two per cent may be an underestimate, asOCM potentially accounted for death in a further twocases of dilated cardiomyopathy that had no tissueavailable for review. In this study, OCM was misinter-preted as dilated cardiomyopathy and biventricularhypertrophy. In a previous small series of sudden car-diac deaths in 22 morbidly obese patients, dilated car-diomyopathy accounted for death in 10 patients, andmany of these may have had OCM.27

Criteria for giving the cause of death as OCM (mod-ified from Hookana et al.28) are given in Table 10.One of the major difficulties in the obese is determin-ing what is a normal heart weight. Traditionally,this would have been assessed by comparison withan upper limit of normal of, for example, 500 g formales and 400 g for females.29 If this method is used,those in the morbidly obese category will commonlyhave apparent cardiomegaly (even if they have diedof other causes in the unnatural deaths in thisstudy, three of six females and five of seven maleswould have been described as having cardiomegaly).New reference tables for human hearts have beendescribed in which heart weight increases with bodymass index,30 owing to hypertrophy (not fat or fibro-sis). The heart weights of the four OCM cases in thisstudy were 497, 520, 905, and 938 g. The respectivepredicted heart weights (calculated from body weight)were 450, 480, 520 g, and unassessable. In two ofthe assessable cases the heart weight was close tothat predicted for the body weight, but in the other itwas high, as assessed either by comparison with theupper limit of normal or derivation from body weight.The distinction of OCM from DCM is an important

one (a diagnosis of DCM having familial implications),and is not entirely straightforward. One could makethe assumption that, if there is a clear cause for car-diomyopathy, such as alcohol or obesity, this is actu-ally the cause. Alternatively, one could attempt tomake the distinction by using the following features.DCM shows ventricular dilatation with an inadequatedegree of left ventricular (LV) hypertrophy (LV wall

Figure 1. A midventricular slice from the first case of OHS in

Table 8 (BMI 51.7), showing right and left ventricular

hypertrophy.

Figure 2. A case of obesity cardiomyopathy showing extensive fat

within the right ventricular myocardium. Note the absence of

fibrosis.


208 E Fryer et al.

thickness 10 mm)(Figure 2). Microscopically, in DCM there is myocardialfibrosis, but this is less often seen in OCM. Fat may bepresent in the right ventricle, but is not essential fordiagnosis, and can be seen in the right ventricle ofthe non-obese. Fat is not seen in the left ventricle unlessit surrounds blood vessels in the outer wall, which isa normal feature. It is recommended that a sampleof heart and spleen be frozen for genetic studies,to enable the investigation of a possible inheritedcardiomyopathy.Hypertensive heart disease is differentiated from

OCM by the pattern of left ventricular hypertrophy(concentric in hypertension, and eccentric withOCM), and by the presence of little dilatation, non-specific fibrosis, and changes in other organs relatedto hypertension.

O B E S I T Y A N D V E N O U S T H R O M B O E M B O L I C D I S E A S E

In this cohort of morbidly obese patients, VTEDaccounted for 14.8% of deaths attributable to naturalcauses. Obesity is a significant and well-establishedrisk factor for the development of VTED.31,32 How-ever, despite this, obesity was included in the causeof death in only 14 of 28 cases, with a further fourcases having other risk factors recorded (postsurgery,malignancy, and immobility) and 10 having no riskfactors recorded at all. The pathogenesis of increasedVTED risk in the obese is complex, and potentiallyinvolves a number of hormones, cytokines andgrowth factors secreted by adipose tissue.33

Conclusions

In summary, postmortems performed on the morbidlyobese represent a distinct group with specific causesof death, and histology and toxicology are required inmany cases. A history of conditions during life, suchas OSA and OHS, and precise details of the circum-stances of the death and body position should besought. OSA, OHS and OCM are under-recognized,with deaths being misattributed to other causes, andthe role of obesity in deaths resulting from VTED isunder-reported.

Contributions

C. Verrill conceived and planned the study. E. Fryerperformed the data collection. All authors contributedto writing and revising the text.

Acknowledgements

We would like to thank HM Coroner, Oxfordshire, forhis support and helpful comments in the productionof the manuscript.

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