
Psychosomatics 40:130-131, April 1999
© 1999 The Academy of Psychosomatic Medine
Hypoactive Delirium as a Clinical Symptom of Intestinal Perforation
Tatsuya Morita, M.D.,
Junichi Tsunoda, M.D.,
Satoshi Inoue, M.D., and
Satoshi Chihara, M.D.
Received July 17, 1998; revised October 5, 1998; accepted October 19, 1998. From Seirei Hospice, Seirei Mikatabara Hospital, 3453, Mikatabara-cho, Hamamatsu, Shizuoka, 4338105 Japan. Address reprint requests to Dr. Morita at the above address.
Key Words: Delirium Syndromes Secondary to General Medical Disorders Cancer
In terminally ill cancer patients, delirium is frequently observed and associated with multiple causes, such as metabolic failure, medications, and organic brain damage.1 Although complete remission of terminal delirium is difficult in many cases, it is of great significance to recognize delirium and the underlying causes because delirium may indicate poor prognosis.2 The following is a case presentation of hypoactive delirium as a clinical symptom of intestinal perforation.
Case Report
Mr. A., a 62-year-old man, complained about dull abdominal pain and irregular bowel movements, although his appetite was fair. On physical examination, the abdomen was flat and soft with normal bowel sounds, but multiple masses were palpable. Endoscopic, radiographic, and histological examinations revealed Stage IV gastric cancer with multiple peritoneal metastases. Thus, he was admitted to a general medical hospital.
The patient refused chemotherapy and was referred to our palliative care unit on Hospital Day 20. He was able to walk and had no signs of cognitive impairment. Oral slow-released morphine (240 mg/day) and diclofenac sodium (75 mg/day) were administered for abdominal pain with acceptable relief. During the following 1 week, postprandial nausea and vomiting gradually worsened with alternating diarrhea and constipation. The abdominal wall was relaxed with no signs of peritoneal irritation, and bowel sounds were slightly decreased. Plain abdominal roentgenograms showed multiple air-fluid levels. From these findings, the symptoms were ascribed to an incomplete obstruction related to peritoneal metastases. Subcutaneous metoclopramide was started at a dose of 10 mg/day on Hospital Day 28 and increased to 60 mg/day by Day 34, but it produced only minimal improvement. As Mr. A. became unable to take medications orally, analgesics were switched to subcutaneous morphine (120 mg/day) and intravenous flurbiprofen (100 mg/day) along with artificial rehydration.
On Day 38, physical discomfort was essentially unchanged and no new medications were added. However the patient complained about unusual somnolence. The next day he had visual hallucinations and was diagnosed with hypoactive delirium by DSM-IV criteria. Laboratory findings showed normal hepatorenal function and no electrolyte imbalance, while his white blood cell count was 23,900/mm3 and C-reactive protein (CRP) was 22.6. Chest X rays showed intraperitoneal free air beneath the diaphragm. Clinically, he suffered only from occasional postprandial vomiting but complained of no acute severe pain. Also, the abdomen was still soft, and no signs of peritoneal irritation were detected. On Hospital Day 40, he suddenly went into shock, resulting in death within 3 hours despite supportive treatment. A culture of ascites obtained on postmortem revealed Klebsiella Pneumoniae and Candida sp.
Discussion
Terminal delirium has various causes, including intracranial pathology, psychotropic medications, liver and/or renal dysfunction, hypoxia, electrolyte imbalance (e.g., hypercalcemia, hyponatremia), disseminated intravascular coagulation, anemia, dehydration, nutritional deficiencies, and infection.1 Empirical studies have reported that although the etiology of delirium was multifactorial or unestablished in 5496%, infection was determined as a contributing factor in 6.150% of delirious cancer patients.35 Also, delirium can be a clinical symptom of systematic infection in elderly patients without cancer.6,7 But, to our knowledge, there have been no reports of intestinal perforation as a cause of delirium in palliative care settings.
On the other hand, a previous study has revealed that intestinal perforation developed in 5.4% of colorectal neoplasms, and only 42% expressed sudden-onset abdominal pain.8 Terminally ill cancer patients are often administered opioids, NSAIDs, or corticosteroids that could mask the abdominal symptoms related to intestinal perforation.9,10 Therefore, it is of great importance for clinicians to understand unusual clinical symptoms that could lead to the correct diagnosis of perforation.
In this case, we believe that sepsis from intestinal perforation caused hypoactive delirium because laboratory and bacteriological findings strongly suggested intraperitoneal infection and no other factors affecting cognitive capacity were identified. Although mild digestive discomfort preceded somnolence, empirically this symptom was attributed to chronic intestinal obstruction. The patient showed neither acute abdominal pain nor physical findings suggesting intestinal perforation, perhaps because medication (opioids and NSAIDs) and presenting peritonitis cartinomatosa concealed the symptoms. Hypoactive delirium was the only clinical cue prompting further investigations that ultimately disclosed the underlying perforation. Because of his poor general condition, Mr. A.'s death could not have been averted even if the perforation was diagnosed earlier. However, it would be meaningful for the patient and his family members to know the expectable clinical course. This case presentation demonstrates that hypoactive delirium might be a symptom of intestinal perforation in palliative care settings even without typical signs such as acute-onset pain and peritoneal irritation.
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