Introduction

Obesity is a complex entity involving the interaction of multiple environmental, genetic and neuroendocrine factors. In recent years there has been an alarming increase in average body size, measured by the body mass index or BMI, in a number of countries, that has been referred to as an “obesity epidemic” [24]. Specifically, review of adult body weights from 199 countries over the three decades between 1980 and 2008 showed that the mean body mass index (BMI) had risen by 0.4 kg/m2/decade, with countries such as the United States, Australia and New Zealand having the most significant increases [5]. BMI is measured as the weight in kilograms divided by the height in meters squared: a normal BMI falls in the range 18.5–24.9, with obesity ≥30, and morbid obesity ≥40 [6]. An estimated two thirds of the American population is now either overweight or obese, resulting in 300,000 deaths per year and a reduction in life span of 5–20 years [7]. Globally there are now more than 1 billion overweight individuals, with 300 million classified as obese [8].

There has been an awareness in forensic pathology of an increasing number of overweight bodies presenting to medicolegal facilities for autopsy. For example, a study in South Australia showed that the percentage of obese and morbidly obese cases had risen from 1.3 to 4.8 and 14.8 to 27.2%, respectively between 1986 and 2006 [6]. The focus in the forensic literature has tended to be on the technical difficulties that these cases present [6, 9]. Obesity is, however, associated with a much wider range of other issues that may directly impact on forensic practice (Table 1). In addition to directly causing disease, obesity may act as a risk modifier, causing a worse outcome in certain conditions. The following review details the spectrum of conditions and situations that may now be encountered more frequently due to their association with high BMIs. Given the increasing incidence of obesity it is important to be aware at the time of autopsy of the diverse manifestations that may be found in multiple organ systems.

Table 1 Issues and findings at autopsy in obesity

Problems with mortuary handling

Practical difficulties with the handling of bodies in the mortuary have been previously reported [6, 9]. Large bodies are difficult to both remove from death scenes and transport to mortuaries. On occasion special vehicles have to be utilized. At the mortuary lifting devices have to be capable of coping with weights of over 300 kg, and trolleys reinforced, and/or increased in size, to cope with abnormally large corpses. Autopsies may have to be performed on floors, or ladders may have to be utilized to appropriately position dissectors to enable them to make standard incisions and to adequately examine body cavities. Mortuary staff may require assistance to lift skin flaps to enable suturing to be performed during reconstruction procedures.

Increased rates of decomposition

Increased amounts of subcutaneous and abdominal fat slow the rate of cooling, a feature seen in females who cool more slowly than males of identical weight due to their higher fat content [10]. This means that the process of decomposition, including both autolysis and putrefaction, is enhanced in the obese, as higher core temperatures are maintained for longer periods of time. This may be exacerbated in morbidly obese individuals who have been bedridden for some time, as bed coverings further increase insulation and thus the amount of retained heat. Given that putrefaction results in skin slippage with blistering, this means that very large bodies become even more difficult to handle as they are often wet and slippery, sometimes with extensive insect infestation [6]. Break down of excessive amounts of adipose tissue also results in large amounts of putrefactive fluid which may make mortuary floors slippery and dangerous to walk on. Thus, dissections that were already made difficult by the size of the decedent often have these added complications. While accuracy of diagnosis may not necessarily be compromised by decomposition [11], these changes further complicate the autopsy examination.

External and internal examinations

An essential part of every forensic autopsy is a full external examination of the body, however, morbidly obese bodies make this process difficult. Rolling of a body to inspect the back is not easy, and genital and perineal inspection may be obscured by large folds of subcutaneous upper thigh adipose tissue, and covering of the area by an extensive lower abdominal fatty apron. Intertrigenous rashes and reddening within skin folds and creases around the anogenital region may mimic injury.

Normal dissection is also challenging as access, particularly to intra-abdominal organs, is impeded by many centimeters of overlying adipose tissue, resulting in examinations being performed in the depths of body cavities. Once located at autopsy, internal organs may be embedded in layers of surrounding fat which may also be putrefying.

Special dissections

Pelvic exenteration is a technique that is required in cases of suspected sexual assault. It involves dissecting out the intact pelvic organs, perineum and rectum so that careful examination can be made of mucosal and skin surfaces for evidence of trauma. This dissection may be made difficult if there is a significantly increased depth of subcutaneous adipose tissues around the perineum and if the area is obscured by “overflow” of inner thigh and lower abdominal fat.

Sampling difficulties

Femoral punctures may be performed prior to formal autopsy to enable screening for infectious agents or drugs. This involves inserting a needle through the skin and subcutaneous tissues of the groin into the femoral vessels, which may be exceedingly difficult if the vessels are buried deeply beneath a thick layer of adipose tissue. A similar problem with venesection occurs in hospitals.

Obtaining uncontaminated vaginal swabs in cases of suspected sexual assault may also not be possible if the area is occupied by upper thigh skin folds.

Alternative diagnostic modalities

While computed tomographic (CT) scanning is an extremely useful technique to augment standard autopsy dissections, problems also arise in trying to adequately image the morbidly obese as large bodies may simply not fit into standard scanners due to their weight and/or girth.

Increased incidence of specific diseases/conditions

Obesity is associated with an increased incidence of a number of quite diverse conditions. In a 14-year prospective study in the United States of over a million individuals the relative risk of death from all causes was between 2.00 and 2.58 in those with BMIs of 35 or higher [12]. However it should be recognized that abdominal obesity, which has also increased markedly in certain populations possibly even more than BMI, may be a better marker for increased risk of cardiovascular disease, diabetes mellitus and the metabolic syndrome. Abdominal obesity is defined as a waist circumference of 103 cm (40 inches) or more in men, or 88 cm (35 inches) or more in women [7].

Cardiovascular conditions

The “obesity paradox” refers to the higher survival rates that have been demonstrated in some studies amongst obese individuals who had suffered a previous cardiac event [7, 13]. The reasons for this finding are unclear, but may relate to earlier ages of onset of the first cardiovascular event, or to better tolerance of the catabolic effects of myocardial ischemia in the obese. It is also possible that the results have been skewed by a higher representation of chronically ill, cachexic individuals in the lower weight categories who have reduced survival [7, 13].

Ischemic heart disease

There is a definite association between obesity and an increased risk of death from coronary artery atherosclerosis and myocardial ischemia. This was shown in the Framingham Heart Study, with more recent studies demonstrating a 2% increased relative risk of a cardiovascular event for every 1 cm increase in waist circumference [14]. Obesity may mediate coronary artery disease due to concomitant hypercholesterolemia and hypertension, but will also accelerate already established arterial disease. Obesity is associated with a younger age of the first episode, often with a worse outcome [7]. It has been suggested that obesity may amplify other risk factors through synergistic mechanisms [15] and that endothelial dysfunction from oxidative stress or the actions of pro-inflammatory cytokines may cause accelerated atherogenesis [16].

Cardiac failure

Obesity is an independent risk factor for cardiac failure with a twofold risk for cardiac failure in those with BMIs above 30 (2.12 for women and 1.90 for men). In a review of 5,881 participants in the Framingham Heart Study obesity was the sole cause of cardiac failure in 11% of the men and 14% of the women [17]. The mechanism of this relationship is not clear, however left ventricular hypertrophy and dilation occur with a high BMI, most likely due to increased hemodynamic load, oxidative stress and neurohormonal activation. The changes in hemodynamic load involve increases in blood and stroke volume, filling pressures and cardiac output [7, 17]. It has also been proposed that adipocytes may have a direct toxic effect on the myocardium inducing a non-ischemic, dilated cardiomyopathy (see below) [18].

Systemic hypertension

The Framingham Heart Study showed obesity to be an independent risk factor for hypertension in both sexes, with markedly obese women in their fourth decade having seven times the risk of having an elevated blood pressure [19]. It has been proposed that 50% of cases of hypertension are related to obesity [15], with 40.8% of the obese population being hypertensive [20].

The etiology of hypertension in obesity is complex involving hemodynamic factors such as increased preload, stroke volume and blood volume which result in left ventricular hypertrophy and on occasion sudden death [7]. In addition there is sympathetic stimulation with activation of the renin-angiotensin-aldosterone system, and secretion of leptin [21]. These factors may cause chronic renal damage which can be detected at autopsy and which may have initiated a vicious circle of changes [7]. Leptin has also been shown to stimulate endothelin ET1, generating reactive oxygen species and stimulating cardiac myocyte hypertrophy [20].

Cardiomyopathy

It has been shown that the weight of the heart increases with body weight. While the cardiac weight as a percentage of body weight is normally 0.043% for males and 0.040% for females, it actually falls to 0.035 and 0.030%, respectively, in the morbidly obese [22]. Deposition of adipose tissue in and around the heart may alter left ventricular function by a variety of processes including physical compression and lipotoxicity. This has been referred to as obesity cardiomyopathy, or adipositas cordis [16].

Pulmonary thromboembolism

The mechanism by which obesity is believed to predispose to deep venous thrombosis and pulmonary thromboembolism is multifactorial, involving reduced mobility, decreased venous return from venous compression, and a probable hypercoagulable state [23, 24]. The latter is thought to be mediated by alterations in proteins involved in both fibrinolysis and coagulation with raised levels of fibrinogen, plasminogen activator inhibitor, factor VII, and factor VIII [25]. In addition, adipocytes may have a direct effect on thrombogenesis by secreting adipsin (complement D), plasminogen activating inhibitor 1, adiponectin and adipocyte complement-related protein (Arcp30) [26]. The risk of pulmonary thromboembolism has been shown to be related directly to the magnitude of the BMI [27].

Some pathologists considerer that adequate dissection of the deep veins of the calf muscles in cases of pulmonary thromboembolism requires a posterior approach with the body being turned prone. Given the difficulties that arise in attempting to turn large bodies on narrow morgue trolleys, a preferable approach is to make a curved incision on the inner aspect of the lower leg with the body supine. In this way adequate access to the deep calf veins can be achieved through a wide skin flap without the significant occupational and health issues of attempting to maneuver massive bodies.

Mesenteric venous thrombosis

In addition to pulmonary thromboembolism, obese individuals may be at increased risk of mesenteric venous thrombosis may also be initiated when increased intra-abdominal pressure from adipose tissue deposition compresses the portomesenteric system causing stasis and thrombosis [28, 29].

Atrial fibrillation

Dilation of the left atrium associated with increased blood volume, left ventricular hypertrophy, sympathetic stimulation, obstructive sleep apnea and diastolic dysfunction have all been demonstrated in obese individuals resulting in an increased incidence of atrial fibrillation with its associated thomboembolic consequences. It has been shown that an increase in BMI by 1 is associated with a 4% increase in the risk of developing atrial fibrillation [30].

Pulmonary hypertension

Microscopic changes of pulmonary hypertension are not uncommonly found in morbidly obese patients, most likely related to sleep apnea and/or obesity hypoventilation syndrome [26]. Pulmonary hypertension has been found in 15–20% of individuals with obstructive sleep apnea [16].

Cerebrovascular accident

It has been shown that an increase in BMI by 1 kg/m2 increases the risk of ischemic stroke by 4% and hemorrhagic stroke by 6%. This most likely relates to the increased incidence of both hypertension and atrial fibrillation, and to the underlying prothrombotic and proinflammatory metabolic alterations that occur in the obese [31]. The risk of stroke is associated not only with increasing BMI but also with increasing waist-to-hip ratio. Compared to males with a BMI < 25, overweight males have an adjusted relative risk for stroke overall of 1.32, for ischemic stroke of 1.35, and for hemorrhagic stroke of 1.25. The corresponding relative risks for obese males are 1.91, 1.87 and 1.91 respectively [16].

Sudden cardiac death

As noted by Hippocrates more than 2,000 years ago [1] obesity carries with it an increased risk of sudden cardiac death. The Framingham Study revealed an increased risk of arrhythmias and sudden death with increasing weight in both sexes, with a 40-times risk of cardiac arrest in the obese compared to those of normal weight [16]. As this may be related to prolonged QT interval there may be no specific findings at autopsy.

Endocrine conditions

A variety of endocrine abnormalities, such as Cushing disease, may cause obesity. Alternatively, endocrine disturbance may be a complication of obesity as adipose tissue acts as an endocrine organ with production of the hormone leptin and the metabolism of steroids. Estrogens cause adipogenesis in subcutaneous tissues and the breast, while androgens stimulate central obesity. Testosterone production may cause hirsutism and male-pattern baldness in obese women [32, 33]. In addition, inflammatory cytokines such as TNFα and IL-6 are produced, as are proteins involved in coagulation, fibrinolysis and the renin-angiortenesin syndrome. All of these have direct impact on the metabolic and cardiovascular effects of obesity [34].

Diabetes mellitus

Cases of diabetes mellitus are continually being encountered at autopsy, often in association with cardiovascular disease or metabolic disturbances involving hyperglycemia and ketoacidosis. There is a strong association between diabetes mellitus and obesity with an odds ratio of 7.37 for diabetes in individuals with a BMI of 40 or higher [35]. Nearly 90% of those with type II diabetes are either overweight or obese. Morbidly obese males have five times the risk of developing type II diabetes. This increased to an alarming 29 times in a US study of women who were in the highest quintiles for BMI and waist-to-hip ratios [15]. Accelerated atherogenesis also results from endothelial damage due to hyperglycemia with insulin resistance [7].

Metabolic conditions

Obesity is associated with chronic low grade stimulation of inflammatory responses with high circulating levels of C-reactive protein, tumor necrosis factor-α, interleukin, leptin and plasminogen activator inhibitor-1. It is considered that this may predispose to a systemic inflammatory response with multifocal organ dysfunction. Visceral adipose tissue produces more inflammatory mediators than subcutaneous fat stores [36].

Hyperlipidemia

Hyperlipidemia is a known cause of premature and progressive coronary artery disease [37] and is also related to obesity. Additional compounding factors include type II diabetes mellitus, the metabolic syndrome and high fat and sugar diets. Visceral obesity increases levels of IL-6, free fatty acids and resistin which mediate insulin resistance and accelerate atherogenic dyslipidemia [7]. This involves increased levels of triglycerides and low-density lipoprotein cholesterol and decreased levels of high-density lipoproteins [38].

The metabolic syndrome

Visceral obesity, the increased risk of cardiovascular events, hypertension and metabolic disturbances of dyslipidemia and diabetes mellitus Iink through insulin resistance in what has come to be known as the metabolic syndrome. Definitional criteria involve an increased waist circumference, elevated serum triglycerides and glucose, hypertension and lowered high-density lipoprotein levels [39]. Over 40% of individuals in the United States aged over 60 years have the syndrome, with a 2–3 times risk of a cardiac event or stroke [7].

Dermatological conditions

Dermatological conditions arising from obesity may result from a primary effect of disturbed underlying metabolism or secondarily from excessive and moist skin and fat folds that create an ideal microenvironment for fungal and bacterial overgrowth.

The first lesions that may be observed include acanthosis nigricans, irregular soft brown plaques around the neck and axillae, and skin tags. These occur in as many as 74% of obese individuals and are markers of insulin resistance and hyperinsulinemia (it is hypothesized that high levels of insulin stimulate insulin-like growth factor receptors in the skin prompting skin and fibroblast proliferation) [32]. Other common findings are acne due to increased androgen production and striae distensae, or stretch marks, on the abdomen, buttocks and upper thighs that are caused by dermal scarring. Direct stimulation of pilosebaceous units may also cause furunculosis [32].

Lower limb problems result from varicose ulceration and lymphedema due to venous and lymphatic stasis, both of which may cause recurrent cellulitis with occasional disseminated infection. Intertrigo develops when opposing skin surfaces in excessive fat folds rub together. Infections are then exacerbated, as the obese overheat more easily due to the insulating effect of increased subcutaneous fat causing sweating with increased humidity in anogenital, axillary, umbilical and submammary areas. This fosters the growth of organisms such as Candida albicans within the layers of desquamated and macerated skin debris [32]. Such overgrowth is also promoted by an inability to adequately clean extensive and folded skin surfaces and by concomitant diabetes mellitus [10]. The perineal region in obese women may be particularly prone to the effects of intertrigenous maceration and ulceration as urinary incontinence may be caused by excessive amounts of abdominal fat, raising intra-abdominal pressure and compressing the bladder [32]. In rare instances a rapidly advancing necrotizing infection of the perineal region known as Fournier gangrene may develop. It is usually caused by Eschericia coli that proliferates in the warm and moist environment of the perineum associated with diabetes mellitus and poor hygiene [40].

Gastrointestinal conditions

In addition to the conditions listed below, obese individuals have an increased incidence of cirrhosis, erosive esophagitis, and Barrett esophagus [41].

Nonalcoholic steatohepatitis

It has been suggested that 90% of obese individuals have some degree of fatty liver, ranging from simple steatosis to non-alcoholic steatohepatitis and cirrhosis [42]. Steatohepatitis has been reported in 18.5% of markedly obese patients at autopsy associated with fibrosis in 13.8%, although on occasion this figure may be much higher, approaching 70–80% [26].

Acute pancreatitis

Obesity induces a worse outcome in severe acute pancreatitis with a relative risk of 4.3 for local complications such as abscess, necrosis and pseudocyst formation, 2.0 for systemic complications, and 2.1 for death [36].

Crohns disease

Obese patients with Crohns disease require more aggressive medical therapy and earlier surgery than those of normal weight [43].

Respiratory conditions

On occasion no anatomical cause of death may be found in morbidly obese individuals. In this situation the possibility of respiratory compromise should be considered, as pulmonary dysfunction and sleep apnea in morbid obesity have been demonstrated, even in childhood [44]. Certainly animal studies have shown reduced pulmonary function in immature obese animals, and obesity is known to decrease chest wall compliance, increase fat deposition in pharyngeal tissues and cause upward compression of the diaphragm [45]. As well, reduced pulmonary compliance results from increased pulmonary blood volume, fatty infiltration of the chest wall and extrinsic compression of the thoracic cage by adipose tissue [46]. The etiology of hypoventilation in obese individuals is thus multifactorial involving changes in ventilatory mechanics and also in central control. Inflammatory changes may result in an increased incidence of asthma [47] with a possible link between obesity and asthma being used to explain the dramatic increases in cases of asthma over recent years [48]. It is also possible that obese individuals may have worse outcomes if they develop acute lung injury or acute respiratory distress syndrome [46].

Obstructive sleep apnea

Obstructive sleep apnea, characterized by recurrent episodes of apnea and hypopnea during sleep, has a strong association with central obesity in males [49]. It results in hypersomnolence during the day and has been linked to vehicle crashes as well as being associated with hypertension and increased cardiovascular morbidity and mortality [50]. Approximately 50–60% of individuals with hypertension have obstructive sleep apnea compared to 5–10% of the general population [51]. The reported association of obstructive sleep apnea and sudden cardiac death is unproven [52].

Obstructive hypoventilation syndrome

Also known as Pickwickian syndrome, this syndrome is characterized by obesity, hypoventilation and sleep disordered breathing. Approximately 90% of patients with obstructive hypoventilation syndrome also have sleep apnea. Decreased respiratory drive, reduced response to leptin, and respiratory muscle impairment, all contribute to the syndrome. Obesity markedly increases the work of breathing due to decreased lung compliance with difficulties moving the rib cage and diaphragm such that 15% of daily oxygen consumption is used in breathing compared to 3% in individuals of normal weight [53]. While not diagnosable at autopsy, review of the clinical record may give some assistance in determining whether it may have been involved in the terminal episode.

Problems involving tracheostomies

Although not usually considered in reviews of complications of tracheostomies [54], obesity may result in increased morbidity from this procedure. As the trachea lies deep within cervical adipose tissue a larger incision often has to be made with increased postoperative risks of hemorrhage. In addition, excessive amounts of submental fat may require liposuction or debulking to prevent occlusion of the tracheostomy tube by accessory chins [32].

Sepsis/infection

Studies of infections in obese individuals have often been confounded by the presence of concomitant diabetes mellitus. Controlling for this variable has shown, however, that obesity is associated with an increased incidence of infection, possibly due to the interaction of pro-inflammatory and anti-inflammatory factors with immunosuppressive effects [55]. Obese patients do have an increased rate of nosocomial infections and also of infections after surgical procedures, the later possibly associated with reduced subcutaneous tissue oxygenation. Examples include an increased incidence of mediastinitis following coronary artery bypass grafting and intra-abdominal infection after pancreatic transplantation. The vulnerability of obese patients with influenza virus infection to worse clinical outcomes should be considered in pandemics [56]. Other infections that occur at a higher rate in the obese include periodontal infections (particularly in the young), community acquired respiratory infections, and skin infections (see above). Interestingly, mild to moderate obesity in intravenous drug users with HIV infection may result in a more favorable outcome [57].

Malignancy

Obesity has been associated with an increased risk for a wide range of malignancies involving the esophagus, stomach, colon and rectum, gallbladder, pancreas, kidney, thyroid, prostate, breast, liver, uterus, cervix and ovary. In addition, obesity is related to an increased risk of non-Hodgkin lymphoma, leukemia, melanoma and multiple myeloma [41, 58, 59]. It has been estimated that excess body weight accounts for 5% of cancers in Europe (3% for males and 6% for females), representing 27,000 male and 45,000 female cancer victims per year [60]. Certain malignancies may be associated with familial obesity [61].

While the following malignancies may not necessarily all cause sudden and unexpected death they may be associated with side effects such as sepsis, hemorrhage or pulmonary thromboembolism that may lead to a forensic investigation. In addition, the local and distant effects of tumors may play a role in clinical presentation and so the possibility of these lesions should always be considered at autopsy in the obese.

Esophageal adenocarcinoma

A strong association exists between obesity and esophageal adenocarcinoma with a Swedish study showing an odds ratio of 16.2 for individuals with BMI > 30 compared to those with BMI < 22. There was no association with esophageal squamous carcinoma [62].

Gastric adenocarcinoma

Individuals with occult gastric adenocarcinoma may occasionally present with massive and fatal upper gastrointestinal hemorrhage. Risk factors for adenocarcinoma of the gastric cardia include obesity, with a Swedish study demonstrating a 2.3 times increase in this form of malignancy in the heaviest quartile of the population compared to the lightest [63].

Hepatocellular carcinoma

The increased risk of dying from hepatocellular carcinoma in obesity has ranged from approximately 1.6–4.5, with a worse outcome in males [42].

Prostatic adenocarcinoma

It now appears that obesity increases the risk of aggressive prostatic cancer as well as increasing the risk of recurrence following prostatectomy, although it reduces the risk of low-grade prostatic adenocarcinoma [64, 65].

Colorectal adenocarcinoma

A meta-analysis of studies on 70,000 cases of colorectal cancer demonstrated that increasing body weight is directly related to colorectal malignancy. Specifically, those with a BMI ≥ 30 have an approximately 20% greater risk, with a 4% increase in risk for every 2 cm increase in abdominal circumference. There is a gender difference, with males having a 30% higher risk than females. The risk of carcinoma of the colon is higher in the obese than is the risk of carcinoma of the rectum [66].

Endometrial cancer

Obesity is a well-recognized risk factor for endometrial cancer, occurring in both pre and postmenopausal woman, but with a stronger association in older females [67].

Renal cell cancer

The risk of renal cell carcinoma for both sexes increases by 1.07 for every unit increase in BMI, which corresponds to approximately a 3 kg weight increase in an individual of average height [68].

Breast cancer

The mortality rate from breast cancer in postmenopausal women increases with increasing BMI, with a relative risk of 3.08 in those with a BMI ≥ 40 compared to those with a BMI of 18.5–20.49 [69].

Pregnancy

Pregnancy may be more easily missed or concealed in the obese resulting in delayed presentation for medical care, or unexpected birth. Particular problems also arise in mothers with high BMIs as maternal obesity before pregnancy is associated with increased risks of venous thromboembolism, postpartum cardiomyopathy and pregnancy-induced hypertension. Obese mothers are also at higher risk of gestational diabetes with large infants and higher rates of obstructed labor. Infants of obese mothers have more head trauma and also higher rates of intra-uterine death and birth defects such as spina bifida [70]. Cesarian section rates have approached 47.4% in the morbidly obese and 33.8% in the obese, compared to 20.7% in controls. Surgery takes longer in the obese with greater blood loss and more postoperative infections and endometritis, and imaging of fetal anatomy may be suboptimal [70, 71].

A higher maternal death rate occurs in the obese during pregnancy from aspiration of gastric contents associated with hiatus hernia and higher intra-abdominal pressures, and from failed endotracheal intubation. In the morbidly obese the latter has approached 33% of cases [72]. The risk of aspiration may be exacerbated by concomitant diabetes mellitus which delays gastric emptying. Reduced respiratory excursion is an underlying comorbidity that can also prolong recovery from anesthesia. Sudden death has occurred associated with circulatory changes following positional change, and aortocaval compression by the uterus underneath a massive abdominal panniculus can markedly reduce cardiac output and placental perfusion [71].

Surgical issues

Surgery may be performed for conditions that are either unrelated to underlying obesity or that may be specifically directed at treating excess weight. The range of surgical treatments for morbid obesity that may be encountered at autopsy include jejunoileal bypass, laparoscopic adjustable gastric banding, biliopancreatic diversion, duodenal switch, vertical band gastroplasty, intragastric balloon, minigastric bypass, open and laparoscopic Roux-en-Y gastric bypass and sleeve gastric resection [73]. Each of these may be associated with particular postoperative problems.

Complications resulting from surgery may be caused by factors related to underlying obesity itself or directly from the process of surgery [26]. Particular difficulties that arise in the morbidly obese that may predispose to unexpected death are their lack of physiological reserve to cope with postoperative problems, and their failure to manifest symptoms and signs such as abdominal pain, fever and leukocytosis [73], thus delaying diagnosis and treatment. The inability to utilize computed tomography in the morbidly obese may also delay diagnoses. Thus at the time of autopsy there may be minimal information in the clinical notes to indicate a likely cause of death.

There is an increased risk of deep venous thrombosis with pulmonary thromboembolism in the obese following surgery for reasons that have already been described. There is also a higher rate of postoperative pneumonia and pulmonary complications resulting from reduced chest expansion and aspiration of gastric contents [74]. Wound infections occur in 1–10% of patients following bariatric surgery [73] associated with difficulties in wound closure, poor wound healing, underlying diabetes mellitus and proximity to areas of infected intertrigenous skin folds. Wound healing is also impaired in the obese due to reduced tissue perfusion which may be exacerbated by tension on wound edges from large amounts of fat in the sutured material [32].

Postoperative hemorrhage may result from injuries to the small intestinal mesentery or spleen that were not recognized at surgery due to the technical difficulties associated with operating in the obese. In addition bleeding may occur from anastomotic sites or trochar injuries [73]. A rare but well-recognized complication of surgery in the morbidly obese is rhabdomyolysis due to compression, particularly of the gluteal muscles, for some time resulting in the development of a compartment syndrome. Muscle ischemia may be exacerbated by hypertension and diabetes mellitus [73]. Assessment of the adequacy of padding of pressure points during surgery may be a required part of the autopsy evaluation.

Specific complications associated with particular bariatric procedures that may have forensic implications include dehiscence with leakage of intestinal and gastric contents, anastomotic stricture formation, and marginal ulceration at gastrojejunostomy and jejunojejunostomy anatomosis sites after Roux-en-Y bypass. Hepatic artery ligation and mesenteric venous thrombosis have also been reported [26]. Intestinal obstruction may occur because of internal herniation, adhesions or kinking of portions of the bypass. Laparoscopic gastric bypass is associated with a lower mortality than an open procedure, but has a higher rate of intestinal obstruction, hemorrhage and stomal stenosis [75]. Erosion of bands into the stomach may follow gastric banding with other problems including obstruction, gastric herniation through the band, and gastroesophageal dilation. Gastric perforation with peritonitis may result from some of these complications [76, 77]. The adjustment port in gastric bands may also leak, detach or become infected [73].

Liposuction may be associated with inadvertent perforation of the peritoneal cavity and intestine and also with the development of fulminant subcutaneous infection leading to necrotizing fasciitis [78, 79]. Fat embolism has also rarely been reported [80] which would necessitate special staining of microscopic slides for fat after autopsy.

A late complication of bariatric surgery that may necessitate further surgery is cholelithiasis, which occurs in up to 70% of individuals who lose weight rapidly [81].

Hospital issues

It has been shown that obese individuals experience longer hospital stays than patients of normal weight [82] and have reduced mobility and greater dependence, with the result that they will have been exposed to the risk of nosocomial infections for greater periods.

While decubitus ulcers, or pressure sores, usually develop over bony prominences in thin debilitated individuals who are unable to regularly move themselves, the situation may be slightly different in the morbidly obese. Necrotic areas may develop within fat folds due to capillary compression with marked tissue destruction that may not be obvious unless careful examination is undertaken. Ulcers may also be found over the hips due to prolonged pressure from bed side rails, bed pans or wheel chairs [32].

Alternative therapies

The use of alternative therapies for weight loss has on occasion had unanticipated side effects. This occurred in Belgium when the herb Stephania tetranda was replaced by Aristolochia fangchi in a herbal preparation designed to help with weight loss. The herb that was used contained a nephrotoxin, aristolochic acid, that resulted in rapidly progressive interstitial nephritis with terminal renal failure [83].

Predisposition to injury

A factor that is not always considered in traumatic events such as vehicle crashes is the potential effect of larger body mass. While it is likely that obese individuals have a worse outcome following blunt trauma, due to the presence of comorbidities such as ischemic heart disease and the predisposition to postoperative infection, it has been shown that obese individuals also suffer more severe injuries [84]. Those with BMIs greater than 30 are more likely to suffer rib fractures, pulmonary contusion, pelvic and extremity fractures in vehicle crashes (although the incidence of head and liver injuries is lower), and have an increased likelihood and severity of ankle and elbow injuries following falls, [84, 85]. This may be influenced by gender, with some studies showing that obese males have the highest risk of death [86]. As the impact energy of an unrestrained body is directly proportional to mass it is perhaps not surprising that there is an increased risk of lethal and non-lethal injuries in the obese. Given that groups such as motorcycle riders are at increased risk of unrestrained high-speed crashes, increasing BMI’s may intensify the energy of impact and result in significant chest and pelvic injuries [87]. More severe extremity injuries in the obese [88] are associated with a greater need for surgical intervention with associated anesthetic and postoperative complications.

Suicide

It has been reported that increased amounts of intra-abdominal fat are associated with higher rates of depression [89, 90]. Whether this is due to underlying metabolic disturbances is unclear, however it has been proposed that the link may involve the chronic inflammatory state induced by obesity that is associated with increased cytokine and monocyte chemoattractant protein secretion [8]. While the relationship of this to suicide has also not been determined, anecdotally the author has had few cases of suicide in the morbidly obese. Whether this has occurred because common methods of suicide such as hanging or carbon monoxide poisoning are not accessible to those with markedly enlarged body habitus is uncertain.

Problems with attempted resuscitation

Numerous problems may arise during attempted resuscitation of the morbidly obese which may contribute to a negative outcome. Rapid positioning of a body to enable cardiopulmonary resuscitation on a firm surface may not be possible and placing the head and neck into a position to facilitate aeration may not be easy. Endotracheal intubation is more difficult in obese individuals who are at risk of more rapid hypoxemia due to reduction in pulmonary functional residual capacity, decreased compliance, increased airway resistance, and an increase in pulmonary vascular resistance [91].

Problems with dialysis

A higher mortality rate has been reported in obese patients who undergo peritoneal rather than hemodialysis, particularly if they are diabetic. The reasons for this remain unclear [92].

Conclusion

Morbid obesity results in significant derangements of multiple organ systems leading to sudden and unexpected death in some cases, and the exacerbation or initiation of major, although not immediately life-threatening, disease in others [93]. Morbidly obese individuals are a challenge to forensic services in a practical sense from body handling and storage, and also in a theoretical sense given the number of diverse and potentially occult conditions that may only be revealed at autopsy. Given the complex inter-relation and significance of many of the metabolic and disease processes associated with marked obesity, “morbid obesity” should be included in the cause of death in these individuals to reflect the inter-dependence of many of these lethal mechanisms. Despite the technical difficulties involved, autopsy dissection has to be meticulous and wide ranging due to the number of associated diseases and conditions found in those with markedly elevated BMIs.

Key Points

  1. 1.

    Forensic facilities are handling far greater numbers of overweight, obese and morbidly obese bodies than in previous years.

  2. 2.

    Autopsies in morbidly obese individuals are difficult due to problems in moving, positioning, examining and dissecting.

  3. 3.

    Adipose tissue secretes a variety of cytokines and hormones that may predispose to a systemic inflammatory response with multifocal organ dysfunction.

  4. 4.

    Obesity is associated with an increased incidence of sudden death, cardiac failure, arrhythmias, hypertension, coronary artery atherosclerosis and pulmonary thromboembolism.

  5. 5.

    Other conditions with higher rates in the obese include metabolic and endocrine disorders, such as diabetes mellitus, and a wide range of malignancies.

  6. 6.

    Obese individuals have more complications during pregnancy and following surgery.