IntroductionGastroparesis symptoms can be severe and debilitating. Many patients do not respond to currently available treatments. Mirtazapine has been shown in case reports to reduce symptoms in gastroparesis.AimTo assess the efficacy and safety of mirtazapine in gastroparetic patients.MethodsAdults with gastroparesis and poorly controlled symptoms were eligible. Participants were prescribed mirtazapine 15 mg PO qhs. Questionnaires containing the gastrointestinal cardinal symptom index (GCSI) and the clinical patient grading assessment scale (CPGAS) were completed by patients’ pretreatment, at 2 weeks, and at 4 weeks. Primary end point was nausea and vomiting response to mirtazapine using the GCSI. Secondary end point was nausea and vomiting severity assessment using the CPGAS. P-values were calculated using the paired two-tailed Student’s t-test. Intention to treat analysis was used.ResultsA total of 30 patients aged 19–86 years were enrolled. Of those, 24 patients (80%) completed 4 weeks of therapy. There were statistically significant improvements in nausea, vomiting, retching, and perceived loss of appetite at 2 and 4 weeks (all P-values <0.05) compared with pretreatment. There was a statistically significant improvement in the CPGAS score at week 2 (P=0.003) and week 4 (P<0.001). Of the total patients, 14 (46.7%) experienced adverse effects from mirtazapine and due to this, 6 patients stopped therapy.ConclusionMirtazapine significantly improved both nausea and vomiting in gastroparetics after 2 and 4 weeks of treatment. Side effects led to treatment self-cessation in a fifth of patients. From these data, we conclude that mirtazapine improves nausea and vomiting, among other symptoms, in patients with gastroparesis and might be useful in select patients.

BackgroundFor severe, complicated Clostridium difficile infection (CDI), concomitant treatment with IV metronidazole and oral vancomycin is usually prescribed. Sometimes vancomycin per rectum (VPR) is added to increase colonic drug delivery. Our purpose was to examine clinical outcomes of patients with CDI treated with VPR and compare results to a matched control group.MethodsThis was a retrospective case-control study in a setting of tertiary-care ICU on diarrhea patients with a positive toxin test for C. difficile. We identified all ICU patients prescribed VPR from January 2003 to December 2013. The dose of VPR mixed in 100 cc of tap water ranged from 125 to 250 mg Q 6 - 8 hours. All patients had diarrhea and a positive test for C. difficile toxin. Included patients received ≥ 4 doses of VPR. The primary outcome was the combined endpoint of colon surgery or death. We matched VPR cases 1:2 with CDI controls that had identical APACHE II scores.ResultsWe identified 24 CDI patients who received VPR and met inclusion criteria: 11 male, mean age 61.8 ± 15.9 years. All patients received concomitant CDI therapy. Four patients (16.7%) required colectomy, and overall mortality was 45.8%. For the 48 controls, need for surgery was identical (16.7%; P = 1.00). The mortality rate also did not differ (41.7%; P = 0.74). For the combined outcome of surgery or death, the rate was 45.8% for the controls and 50.0% for the VPR group (P = 0.73).ConclusionIn a case-control study, the use of VPR was not demonstrated to reduce the need for colectomy or decrease mortality. Based on our modest sample size and failure to show efficacy, we cannot strongly advocate for the use of VPR.

The numerous motor functions and neural inputs that control gastric motility are complex and not fully understood. Our lack of understanding of its pathophysiology has led to treatment options which are empirical, palliative and often ineffective. Newly intensified interest in the cellular pathophysiology behind gastroparesis provides promise for a new era of treatments. Identification of common cellular changes in gastroparesis has provided targets for treatment that may allow us to one day better treat the symptoms of gastroparesis related to its underlying pathophysiology. This is the future of gastroparesis therapy.

A 24-year-old man with sickle cell anemia presented with fatigue, dark stool, and coffee ground emesis. He was found to have large esophageal varices and experienced massive variceal hemorrhage in the hospital. The varices were caused by diffuse splanchnic venous thrombosis, and his only risk factor for hypercoagulability was sickle cell anemia. Splanchnic venous thrombosis due to sickle cell anemia is exceedingly rare.

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