2017 - CIRTA

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2- Nutrition Management and Total Parenteral Nutrition

18.8 - 21st century malnutrition: When bariatric surgery precipitates decompensated liver disease and intestinal failure

Presenter: Brooke, Chapman, Heidelberg, Australia
Authors: Brooke Chapman, Kate Hamilton, Peter De Cruz, Graham Starkey, Adam Testro

21st century malnutrition: When bariatric surgery precipitates decompensated liver disease and intestinal failure

Brooke Chapman1, Kate Hamilton1, Peter De Cruz2, Graham Starkey2, Adam Testro2.

1Department of Nutrition & Dietetics, Austin Health, Melbourne, Australia; 2Liver & Intestinal Transplant Unit, Austin Health, Melbourne, Australia

Introduction: Bariatric surgery (BS) using restrictive and malabsorptive techniques remains the most effective treatment option for morbid obesity. Intestinal failure (IF) and decompensated chronic liver disease (CLD) are rare post-operative complications of BS. We reviewed a cluster of 3 post-bariatric surgery cases presenting to our centre with IF and decompensated CLD to identify perioperative factors that may be associated with these life-threatening complications.

Methods: A retrospective review of referrals to our IF unit in 2016 was performed to identify patients with a history of BS. Patient demographics, nutritional indices, liver function and investigations, nutritional management and outcomes were reviewed.

Results: Cases: Three of 10 patients who commenced HPN at our institute in 2016 presented with IF and decompensated CLD following BS. All patients were female (49-60 years) with co-existing liver failure (2 NASH, 1 HCV). All operative procedures were malabsorptive: jejunoileal bypass (n=2) and biliopancreatic diversion (n=1); mean BMI at surgery 44kg/m2. Mean time between BS and liver disease diagnosis was 9.6 years; development of decompensated CLD occurred on average 2.3 years later, and; referral to our service with rapid weight loss and IF arose on average 2.4 years thereafter. At presentation, patients exhibited severe malnutrition, poor muscle strength and micronutrient deficiencies. Parenteral nutrition and vitamin/mineral supplementation was implemented in each case. All patients underwent diet modification and medical therapy to enhance enteral absorption, and 2 of 3 patients remain HPN dependent.

Postulated mechanisms for decompensated CLD and IF: (i) Malabsorption from BS resulted in rapid weight loss and progression to cirrhosis in patients already suffering NASH/HCV related liver fibrosis. (ii) The increased energy demands of liver disease precipitated liver decompensation due to malabsorption, and; (iii) IF developed as patients were unable to meet their CLD driven energy demands.

Conclusion: IF and decompensated CLD are rare but life-threatening complications of malabsorptive BS. The risk of these complications likely relates to the degree of pre-operative fibrosis. Such patients should be monitored closely post-operatively as CLD and IF can occur many years after surgery. Management options should be tailored to the severity of CLD and degree of malnutrition. Early diagnosis may avert liver disease progression via "prophylactic" reversal surgery alone in well patients. In malnourished patients with advanced liver disease, TPN followed by reversal surgery may be required. Liver transplant and reversal should only be reserved for those with irreversible liver disease.

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