Forensic Science International 155 (2005) 712 www.elsevier.

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Death due to neurogenic shock following gastric rupture in an anorexia nervosa patient
ttner, G. Mall I. Sinicina*, H. Pankratz, A. Bu
Institute of Legal Medicine, Ludwig-Maximilians-University, Frauenlobstrae 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 difcult to determine the cause of death despite the marked ndings. The death as a consequence of neurogenic shock accounts for all the results of gross examination and histologic analysis. This case is the rst 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 psychopathology, 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 imbalance, dehydration [3], suicide [1], and less commonly, alcoholism [4]. There are two cases of fatal gastric rupture in 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
* Corresponding author. Tel.: +49 89 51605111; fax: +49 89 51605144. E-mail address: inga.sinicina@rechts.med.uni-muenchen.de (I. Sinicina).

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 [6,811]. The patients described in the literature attended a hospital 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

0379-0738/$ see front matter # 2004 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.forsciint.2004.10.021

I. Sinicina et al. / Forensic Science International 155 (2005) 712

Fig. 1. The position of the deceased.

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 hematemesis 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 dilatated stomach, extending from the xyphoid to the pubis, that almost lled 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 attened mucosa. The external anterior surface of the stomach was of a patchy reddish colour. About 5600 ml of yellowish and brownish thick uid were detected in the abdominal cavity and in the stomach (Fig. 3). The gross examination of the serous surface showed no brin formation due to inammation, 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 attening of the gyri, a lling 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

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Fig. 2. Gastric wall with fresh rupture.

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

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I. Sinicina et al. / Forensic Science International 155 (2005) 712

Fig. 4. Gastric wall with thickened gastric submucosa and freshly ruptured blood vessels (EvG, 100).

were found at the margins of the rupture without necrotic areas or inammatory inltration. Some fresh ruptures of intramural blood vessels were observed as well. A marked brous 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 inltration of the bronchial walls was seen. In some small areas of the lungs the alveoli were contained some granulocytes and brin. Toxicologic analysis failed to detect any drugs, 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 be accompanied 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 uid 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 present. Vomiting may cause an acute increase in intragastric

Table 1 Reported cases of gastric rupture due to bulimic attack in anorexia nervosa Number 1 2 3 4 5 6 7 8 Author Evans [9] Lebriquir et al. [5] Saul et al. [6] Abdu et al. [8] Petrin et al. [10] Willeke et al. [16] Nakao et al. [17] Present case Year 1968 1978 1981 1987 1990 1996 2000 2003 Gastric wall Necrosis Necrosis Necrosis Necrosis Necrosis Necrosis Necrosis No Surgical treatment Yes Yes Yes Yes Yes Yes Yes No Outcome Recovery Death (septic shock) Death (septic shock) Recovery Recovery Recovery Recovery Death (neurogenic shock)

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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 obstruction of the venous outow causes infarction and perforation in acute gastric dilatation. In our case, no acute ischemic damage of the mucosa was established by means of histological 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 rst death from 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 treatment. In our case, the autopsy revealed marked signs of sudden death but no hemorrhage, no brin 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, previously healthy 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 brous 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 eating. 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 generalized extensive peripheral vasodilatation and a decrease in blood pressure along with bradycardia. Characteristically, the resulting reduction in blood pressure is severe, sympathetic 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 inuenced the fatal outcome of gastric rupture in our case. Although fatal neurogenic shock is extremely rare and very difcult to prove, forensic pathologists should be aware of such a potential condition.

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I. Sinicina et al. / Forensic Science International 155 (2005) 712 [16] F. Willeke, S. Riedl, A. von Herbay, H. Schmidt, V. Hoffmann, J. Stern, Decompensated acute gastric dilatation caused by a bulimic attack in anorexia nervosa, Dtsch. Med. Wochenschr. 121 (1996) 12201225. [17] A. Nakao, H. Isozaki, H. Iwagaki, T. Kanagawa, N. Takakura, N. Tanaka, Gastric perforation caused by a bulimic attack in an anorexia nervosa patient: report of a case, Surg. Today 30 (2000) 435437.

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