BRAIN SPECT SCANNING

experience with a patient who was found to have retained a large number of nifedipine GITS shells. An 88-year-old nondemented patient with a history of hypertension, atrial fibrillation, and strokes was referred to our geriatric unit because of diarrhea and recent abdominal distention. Except during the last months, there was no history of gastrointestinal complaints and/or disease, Four months earlier she had been hospitalized for 16 days for bronchitis. Her medication included: nitrendipine (10 mgld), furosemide (40 mgld), digoxin (0.1 mgld), aspirin (100 mg/d), nadroparine (0.3 mud), and fluoxetine (20 mg/ d). She was treated by amoxy-clav (3 x 500 mg/d), acetylcysteine (3 x 200 mg/d), methylprednisolone (40 mg/d initially, 4 mg on discharge), and aerosols (ipratropium bromide and salbutamol). On the second day of hospitalization, nitrendipine was replaced by nifedipine GITS 30 mglday. A few days later, the patient developed diarrhea and hypokaliemia (K+ = 2.7 mmoyL). The patient was discharged and nifedipine GITS therapy was pursued at home. One week later, anorexia was observed. Five weeks later, she developed severe crampy abdominal pain. The following weeks watery diarrhea persisted (stool cultures were negative). A few weeks later, soon after the administration of two laxative tablets (because of abdominal distention), she developed nausea and vomiting, and two tablets of nifedipine GITS were identified in the vomit. Ten days before admission in our unit because of hypokalemia (K+ = 2.6 mmol/L), furosemide was discontinued and a matrix form containing kalium chloride was given. The serum digoxin was 0.9 p a . Despite kalium supplementation (39 mmoYd), hypokaliemia persisted. On admission, physical examination revealed a major abdominal distention, peristalsis was weak, blood pressure was 160/80 mm Hg, and the diarrhea (without blood or mucus) persisted. Serum K+ was between 1.7 and 2.3 mmol/L, serum Na+ 137 mmol/L, serum glucose 5.0 mmoyL, urea 3.6 mmoYL, serum creatinine 45 pmoyL, and digoxin 1.7 pgL; bacterial stool cultures were negative. Abdominal radiographs showed dilated small bowel loops, important colonic dilation, and air fluid levels. The pseudoobstruction syndrome was treated effectively by gastrografin enema and rectal cannula. Abdominal films during this radiologic procedure showed two filling defects whose size and shape were similar to the nifedipine GITS tablet. Dehydration and hypokaliemia were corrected by intravenous fluids supplemented with potassium chloride. A dozen nifedipine shells were found in the stools. On the sixth day of hospitalization, the nifedipine GITS tablets were withheld, During the following 2-week period, diarrhea persisted and 63 pill shells identified as nifedipine GITS were found in the stools. Most often 5 to 12 shells were excreted simultaneously (51 shells were excreted between Day 15 and Day 19). During the weeks following the excretion of the 63 nifedipine shells, a moderate increase in consistency of stools was noted, but abdominal distention persisted. Abdominal X-rays showed thumbprinting repeatedly (indicating ischemic colitis). Esophagoduodenoscopy was normal. The patient was discharged on Day 27. The following weeks, the serum K+ level was between 3.0 and 4.8 mmoVL. One month later abdominal distention still persisted. Abdominal films revealed colonic dilation with a large distended sigmoid loop. Dilation and atonia of the colon were confirmed by a gastrografin enema. The patient died the day after this procedure (cardiorespiratory arrest, ventricular fibrillation, and inhalation). The retention of more than 60 shells of nifedipine GITS we observed in this patient can be explained ( 1 ) by the physical (density, size, adhesiveness, hardness) and pharmacological (especially a direct relaxing effect on smooth muscle) properties of nifedipine GITS and (2) by the fact that advanced age, concurrent medication (ipratropium bromide), and serious coexistent disease are risk factors for bezoar formation.’ Except for chronic diarrhea (the causes of which remain uncertain), the gastrointestinal symptoms observed in our patient were similar to those described in patients with symptomatic nifedipine GITS be~oar.~-* We hypothesized that the retention of the nifedipine tablets could have contributed to some gastrointestinal symptoms observed in our patient, but some symptoms could also have been caused by underlying disease (especially colonic ischemia). Given the increasing popularity of extended release delivery systems, the retention phenomenon (leading to pharmacobezoar formation) may become an increasingly recognized entity. Clinicians should be aware of this complication, which occurs especially in vulnerable patients.