Abstract
Chronic high‐frequency gastric electrical stimulation (GES) has been shown to improve gastroparetic symptoms and quality of life (QOL) in up to 70% of patients with refractory gastroparesis (Gastroenterology 2003; 125:421–8). Little is known about factors associated with treatment failure. Clinical and gastric function data (gastric emptying test, GET; electrogastrogram, EGG) were extracted from a retrospective analysis of 87 gastroparetic patients (48 diabetic, 20 idiopathic and 19 postsurgical) who completed GES therapy (Enterra™ System, Medtronic) for at least 1 year. Total symptom score (TSS) (sum of severity of nausea, vomiting, early satiety, bloating, postprandial fullness, epigastric pain and burning using a 5‐point scale, 0 = non, 4 = extremely severe), quality of life (SF‐36 Health Status Survey questionnaire including physical composite score (PCS) and mental composite score (MCS)) and GET (4‐hour scintigraphy of a low‐fat meal) were examined at baseline and 1 year follow‐up. A non‐responder had <25% reduction in TSS and a responder was defined as having a ≥ 50% reduction in TSS after 1 year of GES therapy.Results: Overall the non‐responder rate was 23% (10% in diabetic vs. 16% in postsurgical vs. 35% in idiopathic subgroup). Non‐responder rates were similar for men (22%) and women (23%) and age was not a factor. Compared to responders of GES therapy, non‐responders had similar mean baseline vomiting (2.6 vs. 3.2) and nausea scores (3.3 vs. 3.6) but a lower TSS (17.6 vs. 20.1, P < 0.05). Also non‐responders had less improvements in mean gastric retention both at 2 hours (+5.4 vs. 8.7%) and at 4 hours (+4.0 vs. 10.5%), less improvement in mean PCS (+2.0 vs. +12.4, P < 0.05) and gained less weight (0.4 kg vs. +3.7 kg) than responders. 67% of non‐responders had an abnormal EGG (dysrhythmia >30% or decrease in postprandial EGG power) vs. 33% in responders. Non‐responders had more baseline mean tachygastria both in the fasting state vs. responders (26% vs. 11%, P < 0.05) and in the fed state (24% vs. 11%, P < 0.05) and less increase in postprandial EGG power (1.3 dB vs. 1.6 dB, P < 0.05). Conclusions: The best symptom improvement achieved by high‐frequency GES therapy in refractory gastroparesis is in diabetics (10% treatment failure rate) and postsurgical (16% failure) while the worst results are in idiopathics (35% non‐responder rate). Baseline EGG abnormalities are predictors of poor symptomatic response to GES therapy and may be useful in developing a patient profile to optimize selection and expectations for GES therapy.
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