Death Due to Neurogenic Shock Following Gastric

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Death due to neurogenic shock following gastricrupture in an anorexia nervosa patient

I. Sinicina*, H. Pankratz, A. Buttner, G. Mall

Institute of Legal Medicine, Ludwig-Maximilians-University, Frauenlobstraße 7a, D-80337 Munich, Germany

Received 26 March 2004; accepted 26 October 2004

Available online 13 December 2004

Abstract

We report a case of fatal gastric rupture discovered after death, which developed due to a bulimic attack of a 19-year-old

woman suffering from anorexia nervosa. An autopsy revealed an acute gastric dilatation and rupture without commonly

observed ischemic damage of gastric wall structures. However, it may be difficult to determine the cause of death despite the

marked findings. The death as a consequence of neurogenic shock accounts for all the results of gross examination and histologic

analysis. This case is the first reported case of fatal gastric rupture of an anorectic patient discovered after death.

# 2004 Elsevier Ireland Ltd. All rights reserved.

Keywords: Gastric rupture; Anorexia; Binge eating; Fatal

1. Introduction

Anorexia nervosa is a common psychiatric condition of

adolescence in which, apart from the striking psychopathol-

ogy, somatic complications are frequently observed. The

disease has one of the highest death rates of any psychiatric

disorder. The documented crude mortality rates of anorexia

nervosa range from 3.3% in an 8-year follow-up study [1] to

18% in a 33-year outcome study [2]. Causes of death

reported for anorexia nervosa patients include complications

of the eating disorder such as inanition, electrolyte imbal-

ance, dehydration [3], suicide [1], and less commonly,

alcoholism [4]. There are two cases of fatal gastric rupturein anorectic patients reported by Lebriquir et al. [5] and Saul

et al. [6]. The young women treated by the authors died from

septic shock in consequence of surgical treatment. However,

acute gastric dilatation can often be observed in cases of

anorectic patients experiencing episodes of binge eating [7].

Yet only a few case reports exist concerning gastric necrosis

and consequent rupture following acute gastric dilatation

after binge eating [6,8–11].

The patients described in the literature attended a hospi-

tal with a chief complaint of increasing severe abdominal

pain. All patients were surgically treated and all but two

survived. In this paper, we report on a case of a young

anorectic woman who died suddenly and unexpectedly

following an episode of binge eating and we review previous

reports on the subject as well.

2. Case report

A 19-year-old woman was found dead kneeling at

the water-closet in the bathroom of her apartment. Her

left arm loosely hang into the closet, her head bent forward.

On external examination postmortal lividity was present

on the back of the thighs, on the legs below the knees, on

the face and on the forearms of the deceased (Fig. 1). Fully

established postmortem rigidity was observed in all parts

www.elsevier.com/locate/forsciint

Forensic Science International 155 (2005) 7–12

* Corresponding author. Tel.: +49 89 51605111;

fax: +49 89 51605144.

E-mail address: [email protected]

(I. Sinicina).

0379-0738/$ – see front matter # 2004 Elsevier Ireland Ltd. All rights reserved.

doi:10.1016/j.forsciint.2004.10.021



of the body. A faint green discoloration of the skin was

noted at the right abdominal wall. The cornea was slightly

clouded and the pupils showed a circular shape. No petechia

was observed in the palpebral conjunctiva. There were

no signs of any injury to the thoracic or abdominal walls.

The abdomen was remarkably distended. A slight edema

and strong hypostasis of the vaginal and anal entrances were

present, even resembling ‘‘fresh bruises’’. Signs of hema-temesis or vomit around the body or in the closet could not

be found.

The deceased had last been seen the previous evening.

She had been known to suffer from anorexia nervosa for 5

years. Her weight and her height were presently 43 kg and

155 cm, respectively.

Due to the nature of the case any sexual interference

could not be excluded. Photographs were taken and an

autopsy was carried out.

The postmortem examination revealed a massively dila-

tated stomach, extending from the xyphoid to the pubis, that

almost filled the entire abdominal cavity. A single 15 cm

perforation of the anterior wall of the gastric body was

detected (Fig. 2). Fresh hemorrhages surrounded the margin

of the rupture. The gastric wall was extremely thin, with a

flattened mucosa. The external anterior surface of the sto-

mach was of a patchy reddish colour. About 5600 ml of

yellowish and brownish thick fluid were detected in the

abdominal cavity and in the stomach (Fig. 3). The gross

examination of the serous surface showed no fibrin forma-tion due to inflammation, except a slight injection of the

small subserous vessels. The small and large bowel were

both hypostatic. The right lung weighed 180 g, the left lung

155 g. The lungs showed a dry cut surface. The heart

weighed 165 g only, with a small amount of blood within

its cavities. The urinary bladder was empty.

The examination of the brain showed the signs of a slight

cerebral edema with a general flattening of the gyri, a filling

of the sulci and a discrete herniation of the cerebellar tonsils

through the foramen magnum.

The histological examination showed autolysis of the

gastric mucosa. Nevertheless, fresh intramural hemorrhages

I. Sinicina et al. / Forensic Science International 155 (2005) 7–128

Fig. 1. The position of the deceased.



I. Sinicina et al. / Forensic Science International 155 (2005) 7–12 9

Fig. 2. Gastric wall with fresh rupture.

Fig. 3. Gastric content recovered from the stomach and the abdominal cavitiy.



were found at the margins of the rupture without necrotic

areas or inflammatory infiltration. Some fresh ruptures of

intramural blood vessels were observed as well. A markedfibrous thickening of the entire gastric submucosa was

present (Fig. 4).

The myocardial cells were atrophic and narrow, the

collections of lipofuscin granules were present at the poles

of the nuclei. Areas with atrophic epicardial adipose tissue

were detected.

Occasionally strong granulocytic infiltration of the bron-

chial walls was seen. In some small areas of the lungs the

alveoli were contained some granulocytes and fibrin.

Toxicologic analysis failed to detect anydrugs, alcohol or

unusual substances.Death was attributed to neurogenic

shock in consequence of a gastric rupture.

3. Discussion

Anorexia nervosa is an eating disorder that may beaccompanied by episodes of binge eating. The food intake

during a bulimic attack can be enormous. Under physiologic

conditions the stomach contains up to 3 l fluid and/or food.

During binge eating attacks the stomach may harbour up to

12 l [8]. Gastric emptying and oesophageal motility are

impaired in patients with bulimic episodes. Thus, a bulimic

binge can become life-threatening if the stomach does not

empty spontaneously. The patients who developed an acute

gastric dilatation have a history of progressive abdominal

pain. Other symptoms such as an absent femoral pulses due

to markedly increased intraabdominal pressure can be pre-

sent. Vomiting may cause an acute increase in intragastric


Fig. 4. Gastric wall with thickened gastric submucosa and freshly ruptured blood vessels (EvG, Â100).

Table 1

Reported cases of gastric rupture due to bulimic attack in anorexia nervosa

Number Author Year Gastric wall Surgical treatment Outcome

1 Evans [9] 1968 Necrosis Yes Recovery

2 Lebriquir et al. [5] 1978 Necrosis Yes Death (septic shock)

3 Saul et al. [6] 1981 Necrosis Yes Death (septic shock)

4 Abdu et al. [8] 1987 Necrosis Yes Recovery

5 Petrin et al. [10] 1990 Necrosis Yes Recovery

6 Willeke et al. [16] 1996 Necrosis Yes Recovery

7 Nakao et al. [17] 2000 Necrosis Yes Recovery

8 Present case 2003 No No Death (neurogenic shock)



pressure resulting in rupture, an extreme and relatively rare

complication of anorexia.

We found only six cases of acute gastric dilatation and

rupture (including our case) due to bulimic binging in

anorexia nervosa patients (Table 1). Rupture may be caused

by gastric wall necrosis secondary to ischemia, when the

wall tension exceeds the venous pressure. According to

Wolloch and Dinstman [12] gastric dilatation causes direct

mucosal necrosis. All case reports in Table 1, documented

gastric infarction and rupture and suggested that the obstruc-

tion of the venous outflow causes infarction and perforation

in acute gastric dilatation. In our case, no acute ischemic

damage of the mucosa was established by means of histo-

logical examination.

According to Ishikawa et al. [13], gastric ruptures are

usually located in the lesser curvature of stomach. In our

case, the rupture was located in the anterior wall of

the gastric body. An organic stenosis was found neither in

cardia nor in pylorus. In the English literature, the first deathfrom gastric perforation in a temporarily well-nourished

woman suffering from anorexia was reported by Saul

et al. [6].

In all described cases the patients were admitted to

the hospital with the symptoms of an acute abdomen. All

but two reported patients recovered after a surgical treat-

ment.

In our case, the autopsy revealed marked signs of sudden

death but no hemorrhage, no fibrin or abscess formation nor

peritoneal adhesions, indicating that the gastric rupture was

fatal within an extremely short period of time. Recently,

sudden and unexpected death of a 49-year-old, previouslyhealthy man due to the rupture of the stomach was reported

by Ishikawa et al. [13]. At the autopsy no convincing

morphological explanation of the cause of his death could

be found: no signs of hemorrhage or peritonitis were present.

The cause of death was determined as death from shock

caused by gastric rupture due to overeating. But what type of

shock should be considered?

Extreme gastric distension alone may cause a vaso-vagal

syncope. In our case, the young woman had obviously tried

to induce vomiting. The marked fibrous thickening of gastric

submucosa in our case is consistent with chronic ischemic

damage of the gastric wall. Thus, the deceased was used to

repeatedly occurring gastric distension following binge eat-ing.

Gastric rupture followed by release of approximately

5.6 l of stomach content into the peritoneal cavity leads

to the widespread peritoneal irritation and consequently to

the strong vagal activation. This activation induces general-

ized extensive peripheral vasodilatation and a decrease in

blood pressure along with bradycardia. Characteristically,

the resulting reduction in blood pressure is severe, sympa-

thetic activity is inhibited, plasma norepinephrine levels do

not increase, and the heart rate decreases. Transient sinus

arrest often follows. The defect is not a failure of the heart to

respond effectively to neurogenic or humoral excitatory

drive. Rather, it is a paradoxical interruption of sympathetic

excitation associated with parasympathetic excitation,

which causes profound vasodilatation and bradycardia.

Altogether these reactions result in neurogenic shock, a

distributive shock due to imbalance of sympathetic and

parasympathetic regulation of vascular smooth muscles

and heart rate.

Similar mechanisms are discussed in lethal outcomes

following striking on epigastrium [14,15]. Apart from the

acute gastric rupture, cardiac atrophy and focal pneumonia

were found in our case. A known laxative abuse and

repeatedly induced vomiting suggest at least temporary

hypovolaemia.

The combination of all the above factors with neurogenic

shock likely influenced the fatal outcome of gastric rupture

in our case.

Although fatal neurogenic shock is extremely rare and

very difficult to prove, forensic pathologists should be aware

of such a potential condition.

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Death Due to Neurogenic Shock Following Gastric