Abstract

In June, 2009, a 51-year-old woman presented with a 4-day history of abdominal swelling and fever, and a 2-week history of loss of appetite. There was no history of abdominal pain or nausea. She was febrile (38·4°C) and her abdomen was swollen but soft without spontaneous pain or tenderness. She had a history of schizophrenia since the age of 40 years which was well controlled with perospirone 12 mg/day and quetiapine 150 mg/day. At the age of 45 years, she was diagnosed with diabetes mellitus and had achieved good glycaemic control (HbA1c 6·5%) with biphasic insulin aspart 30 (6 U/day). There was no sign of obvious peripheral neuropathy. Laboratory test results showed normocytic anaemia (haemoglobin 95 g/L), leucocytosis (13·3×109/L) with neutrophilia (91·5%), high concentration of C-reactive protein (129 mg/L), and normal liver and kidney function. Urinalysis showed negative protein and no leucocytosis. Chest radiography showed normal lungs with no cardiac enlargement. Abdominal CT showed a large volume of partly encapsulated ascites (fi gure). The peritoneum in her pelvic cavity was thickened, and ascites in the right inferior abdominal cavity contained calcifi cation and air (fi gure). The aspirated ascitic fl uid had an unpleasant smell and was suppurated. Culture of the fl uid was positive for pyogenic agents, including Peptostreptococcus spp and Bacillus subtilis. Blood culture was negative. We diagnosed severe bacterial pan-peritonitis. Surprisingly, her general condition was stable and she did not complain of any abdominal pain. Abdominal drainage was done and antibiotics started (imipenem/ cilastatin 1·5 g/day), but her symptoms did not improve. Therefore, laparotomy was done on the seventh day of admission. On laparotomy, a large amount of yellowish, turbid, gel-like material fi lled the abdominal cavity with retention of pus in the pouch of Douglas. The appendix was necrotic and contained faecolith. The bacterial peritonitis was suspected to be caused by perforation associated with acute appendicitis. Postoperative course was uneventful, and the patient recovered. When last seen in October, 2009, the patient was well. Even though our patient had a purulent pan-peritonitis caused by a perforated appendix, she did not present with abdominal pain, tenderness, or guarding. Diminished pain sensitivity or loss of pain sensation in people with schizophrenia has previously been reported in cases of acute myocardial infarction and perforated gastrointestinal tract. Clinically, diminished pain sensitivity in schizophrenia has been linked to key features of the disorder, such as positive symptoms, aff ective fl attening, or attention defi cits. Disturbances in dopamine, serotonin, glutamate, and opioids have been proposed to account for hypoalgesia in schizophrenia. Hypoalgesia in schizophrenia has been reported throughout the acute phase of illnesses and in medicated stable or drug-free patients; neuroleptic drugs have been suggested to have minor analgesic eff ects. Diabetes occurs in people with schizophrenia two to four times more often than in the general population. Compared with people without diabetes, appendicitis in people with diabetes is more likely to result in perforation or other complications. Decreased pain sensation may result in aggravation of the condition and in a delay of diagnosis and treatment. Our case is an important reminder that people with schizophrenia do not always present with typical clinical features of acute abdominal disease pathology.

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