Mrs. D. is the robust, upstanding matriarch of her large and thriving family, which spans four generations. Now 84 years old, she’s the wife of Dr. J.D., a retired general surgeon and pillar of the local medical community.
Mrs. D. has enjoyed remarkably good health throughout her life and, other than a spinal fusion of L4/L5 20 years earlier for intractable back pain, she has not required much in the way of medical services.
Six months ago, however, our patient presented to my office with epigastric pain associated with heartburn. The pain was intermittent but when it did occur, it was constant and was rated a 4 out of 10 in intensity. There was no nausea or vomiting, no fever, no change in bowel habit, and no melena. It almost invariably occurred at night.
I diagnosed the patient with gastroesophageal reflux disease and started her on a course of pantoprazole, which seemed to alleviate her symptoms. After a few short weeks, though, Mrs. D. returned to my office with on-going complaints. On examination, there was tenderness to palpation of the epigastrium but no organomegaly or masses. I ordered some lab tests and an upper GI series.
The tests, which included a CBC, LFT’s, creatinine, electrolytes, amylase, and stool for occult blood, were all normal, other than a normocytic anemia of 108. The upper GI series was normal too. Mrs. D., meanwhile, was getting steadily worse, with increasing pain both in frequency and severity, along with a 4½ kilo weight loss. I ordered an abdominal ultrasound and arranged for the patient to be seen by a gastroenterologist. This specialist performed an endoscopy, which showed mild gastritis, and a colonoscopy, which was unremarkable. The abdominal ultrasound was normal. Mrs. D. was given a prescription for more pantoprazole by the specialist, but she continued to decline.
What would you do next?
I still felt that we were missing something in Mrs. D.’s abdomen, so I ordered a CT scan. This showed “tiny hypodensities within the liver, too small to characterize.” I was just deciding how to proceed with this new information when Mrs. D. became acutely worse.
Six months after she first developed symptoms, our patient presented to the Emergency Department in severe abdominal distress. Her white blood cell count was 22. A surgeon was summoned and Mrs. D. underwent a laparotomy for an acute abdomen. What do you think was discovered?
Much to everyone’s surprise, Mrs. D. had a gangrenous gall bladder, but there were no stones found inside. This condition is known as “acalculous cholecystitis,” or “necrotizing cholecystitis,” and accounts for 10-15% of all cases of cholecystitis. Because of the frequent delay in diagnosis and treatment, it’s associated with a much higher rate of mortality than the calculous variety, so the astute clinician must have a high index of suspicion for the disease.
The etiology of acalculous cholecystitis is not known but is felt to be multifactorial. One important contributing factor though, appears to be localized microvascular disease. Acalculous cholecystitis is most commonly seen in elderly patients with comorbid illnesses. Had we thought of it, the test that would probably have given us the correct diagnosis would have been radionuclide hepatobiliary imaging.
Mrs. D. had a protracted post-operative course, complicated by the development of multiple liver abscesses. But eventually, after weeks of intravenous antibiotics and care in our ICU, she made it back home. In hindsight, even the great Dr. D. confided to me, “Damn, I should have thought of that!”
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