The role of continuous subcutaneous insulin infusion therapy in patients with diabetic gastroparesis

Abstract

Aims/objective To describe the effectiveness of continuous subcutaneous insulin infusion (CSII) in patients with symptomatic diabetic gastroparesis and unstable glycaemic control. Methods Data from 26 patients with symptomatic diabetic gastroparesis and unstable glycaemic control using multiple-dose insulin (MDI) regimens, and subsequently managed with CSII, were analysed. Results Following initiation of CSII, the median length of inpatient bed days associated with hospital admissions related to gastroparesis and glycaemic instability was reduced from 8.5 (range 0-144) days patient −1 year −1 prior to CSII to 0 (range 0-15) days patient −1 year −1 .The median HbA 1c reduction with CSII was 1.8% (22 mmol/mol; p<0.05). The median capillary blood glucose (CBG) with CSII was significantly lower than with MDI: 7.7 mmol/l (range 3.8-15.4 mmol/l) vs 9.8 mmol/l (range 2.3-27 mmol/l), respectively, p<0.001. Glycaemic variability with CSII was significantly reduced compared with MDI: CBG CV 0.37 vs CV 0.53, respectively, p<0.001. Conclusions/interpretation CSII therapy in patients with diabetic gastroparesis results in significant improvement in glycaemic control and reductions in glycaemic variability and number of hospital inpatient bed days.

Severe gastrointestinal autonomic dysfunction in a diabetic boy

“…It has been reported that continuous subcutaneous insulin infusion in diabetic gastroparesis improves the glycemic control, reduces glycemic variability, and the frequency of hypoglycemia, as well as decreases the number of hospitalization days [3]. In our patient, the use of continuous intravenous insulin infusion allows us to obtain glycemic control, and together with prokinetics agents, reverted fastly the severe GI condition.…”

“…However, rarely can be life-threatening and may lead to long periods of debilitating GI symptoms requiring prolonged hospital admissions [2,3]. Gastroparesis is the commonest GI dysautonomia, but constipation, diarrhea, and more rarely megacolon or colonic pseudo-obstruction, stercoral ulcer or viscera perforation may occur [3]. The chronic nonadherence to insulin therapy, with consequent poor glycemic control, predisposed our patient to this severe GI dysautonomia.…”

“…The pathogenesis of GI dysautonomia is multifactorial involving cellular changes, increased oxidative stress, autoimmune and inflammatory factors, impaired hormonal regulation, and genetic predisposition [1]. Acute hyperglycemia has been demonstrated to induce relaxation of the stomach, increased pyloric tone, and suppression of peristalsis [3]. Moreover, acute glycemic fluctuations may adversely affect GI function [3].…”

“…Acute hyperglycemia has been demonstrated to induce relaxation of the stomach, increased pyloric tone, and suppression of peristalsis [3]. Moreover, acute glycemic fluctuations may adversely affect GI function [3]. GI dysmotility may lead to unpleasant GI manifestations, deterioration of nutritional status, or unpredictable oscillations of glycemia due to irregular absorption of food/ medication [1,2].…”

“…GI dysmotility may lead to unpleasant GI manifestations, deterioration of nutritional status, or unpredictable oscillations of glycemia due to irregular absorption of food/ medication [1,2]. However, rarely can be life-threatening and may lead to long periods of debilitating GI symptoms requiring prolonged hospital admissions [2,3]. Gastroparesis is the commonest GI dysautonomia, but constipation, diarrhea, and more rarely megacolon or colonic pseudo-obstruction, stercoral ulcer or viscera perforation may occur [3].…”