Abstract
Editor:
Diabetes mellitus (DM) is the primary cause of endstage renal disease (ESRD) in approximately 45% of new patients. Another major complication of DM is gastroparesis secondary to autonomic neuropathy, since gastrointestinal motor function requires precise coordination of sympathetic and parasympathetic nervous systems. Gastroparesis leads to nausea, vomiting, bloating, early satiety, abdominal pain, weight loss, and failure to thrive (1,2). The prevalence of diabetic gastroparesis, as diagnosed by gastric emptying studies, in the general diabetic population is 40%. However, symptoms are evident in only 10% of the patients. Despite a variety of treatment modalities [e.g., metoclopramide, cisapride, prochlorperazine, ondansetron (3,4), intravenous erythromycin], the management of DM gastroparesis remains a challenge for clinicians.
We report here a 32-year-old white female with type I DM and ESRD, on continuous cycling peritoneal dialysis (CCPD) for 1 year, who was seen in our peritoneal dialysis (PD) clinic for chronic nausea, vomiting, abdominal pain, and weight loss. Her medical history also includes hypothyroidism, migraine headaches, depression, and hypertension. She had been evaluated on multiple occasions for her complaints but her symptoms persisted. Initial adjustment of her PD prescription (reducing fill volumes from 3 L to 2 L) had not improved her symptoms. She continued with nighttime CCPD and a midday exchange: a total volume of 16 L per 24 hours. She had undergone multiple imaging studies for evaluation of her gastrointestinal symptoms. Initial obstructive series, upper gastrointestinal series, ultrasound, and computed tomography scan of her abdomen and pelvis did not reveal any pathology. A hepatobiliary nuclear scan was also normal. Esophagogastroduodenoscopy showed evidence of gastritis and retained food in the fundus (after several hours), indicating gastroparesis. Colonoscopy was unremarkable except for a small rectal ulcer.
The patient was prescribed ondansetron by mouth but she was unable to tolerate it secondary to vomiting. Oral ondansetron was changed to intramuscular (IM) injections (5); however, she continued having the symptoms. The dose of ondansetron was increased from 4 mg IM every 4 – 6 hours to 8 mg IM every 4 hours. She did have some improvement in nausea and vomiting but the injection volume and the unavailability of personnel at home to administer the drug were the limiting factors in continuation of this therapy. Thus, ondansetron at a dose of 16 mg was added to the last fill bag and the midday exchange. She had marked improvement in her symptoms, with resolution of nausea and vomiting. There were no side effects associated with this mode of therapy. There was no visible precipitation upon addition of 16 mg of ondansetron to 2-L Dianeal bags (Baxter Health Care Corporation, Deerfield, Illinois, USA) of either 1.5% or 2.5% dextose concentration. She was seen in the PD clinic on a frequent basis, with no reports of symptoms related to her DM gastroparesis. She continues with this regimen to date and remains asymptomatic.
There are no reports in the literature, or pharmaceutical data, on intraperitoneal administration of this drug for the management of severe DM gastroparesis. Our experience suggests that ondansetron may be safely administered intraperitoneally to PD patients for the management of severe diabetic gastroparesis.