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Nutrition in Pancreatitis

How does Acute pancreatitis or Chronic pancreatitis lead to malabsorption?

  • Pancreatitis (chronic) and pancreatic resection leads to decreased production of digestive enzymes and pancreatic juice, due to loss of acinar and ductal cells respectively
  • Malabsorption due to impaired ability to break down macronutrients ingested
  • At least 90% of pancreatic secretory function must be lost for clinically significant malabsorption

What are the symptoms?

  • Weight loss
  • Steatorrhoea or loose, bulky, buoyant stools
  • Lipase largely produced by pancreas, whereas other digestive enzymes are also secreted elsewhere

How is it assessed?

  • Most commonly used in clinical practice are faecal elastase-1 and the 13C-triolein breath test

What is the recommended treatment?

  • Pancreatic enzyme replacement therapy (PERT) and gastric acid suppression with (PPI)
  • Provided the dose of PERT is adequate, no other dietary supplements or restrictions are necessary

Management of Nutrition in Severe Necrotic Pancreatitis and Pancreatic Abscess

  • Source: Arvanitakis M, Eckenga J, Bezmarevic M, Gianotti L, Kznaric Z, Lobo D, et al. ESPEN guideline on clinical nutrition in acute and chronic pancreatitis. Clinical Nutrition.

General Points

  • Hyperlipidaemia is the third most common cause of acute pancreatitis – accounts for 4-10% of cases

Key Questions and Answers

Which pts with acute pancreatitis are considered at nutritional risk?

  • All pts with AP should be considered at moderate to high nutritional risk because of the catabolic nature of the disease and because of the impact of the nutritional status for disease development
  • Recommendations: All pts with predicted mild to moderate acute pancreatitis should be screened using validated screening methods, such as the Nutritional Risk Screening – 2002. However, the pt with predicted severe acute pancreatitis should always be considered at nutritional risk.

Is early oral feeding feasible in pts with predicted mild acute pancreatitis?

  • Oral feeding shall be offered as soon as clinically tolerated and independent of serum lipase concentrations
  • Low fat, soft oral diet shall be used when reinitiating oral feeding

If required, what type of medical nutrition (enteral or parenteral) is preferable in pts with acute pancreatitis?

  • In AP pts who cannot feed orally, enteral nutrition shall be preferred
  • Enteral feeding – preserves integrity of gut mucosa, stimulates intestinal motility, prevents bacterial overgrowth and increase the splanchnic blood flow

What is the optimal timing for initiating enteral nutrition in pts with acute pancreatitis?

  • EN should be started early, within 24-72 hrs of admission in case of intolerance to oral feeding

What type of enteral nutrition is indicated?

  • A standard polymeric diet shall be used

What route should be used for enteral nutrition in pts with acute pancreatitis?

  • If EN is required in pts with acute pancreatitis, it should be administered via a NG tube
  • Administration via a NJ tube should be preferred in case of digestive intolerance

In pts with acute pancreatitis, when should TPN be initiated?

  • Administered in pts who do not tolerate enteral nutrition or who are unable to tolerated targeted nutritional requirements or if contraindications for EN exist (e.g. bowel obstruction, abdominal compartment syndrome, prolonged paralytic ileus, and mesenteric ischaemia)

How should medical nutrition be provided in case of necrosectomy (endoscopically or by minimally invasive surgery) in patients with severe acute pancreatitis?

  • Oral food intake in pts undergoing minimally invasive necrosectomy is safe and feasible, and should be initiated in the first 24 hrs after the procedure, if the clinical state (haemodynamic stability, septic parameters, gastric emptying) of the pt allows it
  • In pts undergoing minimally invasive necrosectomy who are unable to be fed orally, enteral nutrition is indicated via nasojejunal as preferred route
  • PN is indicated in pts undergoing minimally invasive necrosectomy who do not tolerate EN or who are unable to tolerate targeted nutritional requirements, or if there exist contraindications for EN.

How should medical nutrition (EN and PN) be provided in critically ill pts with severe acute pancreatitis (IAH, ACS) with need for open abdomen?

  • In pts with severe AP and intra-abdo pressure < 15 mmHg, early EN shall be initiated via nasojejunal as the preferred route, or NG tube
  • IAP and the clinical condition of pts during EN shall be monitored continuously
  • In pts with severe AP and IAP > 15 mmHg, EN should be initiated via NJ route starting at 20 ml/hr, increasing the rate according to the tolerance.
  • Temporary reduction or discontinuation of EN should be considered when IAP values further increase under EN
  • In pts with severe AP and IAP > 20 mmHg or in the presence of ACS, EN should be (temporarily) stopped and PN should be initiated
  • In pts with severe AP and open abdomen EN should be administered, at least in a small amount If required for achievement of nutritional requirements, supplementary or total PN should be added

Is there any role for immunonutrition (glutamine, antioxidants) in severe acute pancreatitis?

  • When EN is not feasible or contraindicated and PN is indicated, parenteral glutamine should be supplemented at 0.20g/kg per day of L-glutamine. Otherwise, there is no role for immunnutrition in severe acute pancreatitis

Is there any role for probiotic use in severe acute pancreatitis?

  • Probiotics cannot be recommended

Is there any role for the use of oral enzyme supplementation in acute pancreatitis?

  • Pancreatic enzymes should not be supplemented generally except in pts with obvious pancreas exocrine insufficiency

What are the causes of malnutrition in patients with chronic pancreatitis?

  • Pancreatic insufficiency, abdominal pain, alcohol abuse, lower food intake, diabetes mellitus, and smoking are the main causes

What diagnostic tests are preferred to assess nutritional status in pts with chronic pancreatitis?

  • Nutritional status should be assessed according to symptoms, organic functions, anthropometry, and biochemical values.
  • Solely BMI should not be used, because it does not register sarcopenia in the obese pt with chronic pancreatitis
  • Nutritional Assessment in the pt with chronic pancreatitis:
    • Anthropometric
      • Change in body weight
  • Functional assessment: hand-grip strength dynamometry, 6 min walk test, sit to stand tests
  • Skin fold thickness, waist circumference, and mid arm muscle circumference
  • Presence of ascites/oedema
    • Biochemical assessment
      • Fat soluble vitamins
      • Bone health (PTH)
      • Trace elements – Mg, Selenium, Zinc
      • Anaemia screen (Fe studies, B12, Folate, Ferritin, and CRP)
      • Glycaemic control: HbA1c, and random glucose
    • Symptom assessment
      • Change in dietary intake
      • Appetite
  • Presence of symptoms that impact on oral intake (nausea/pain/indigestion/early satiety)
  • Presence of exocrine/endocrine dysfunction
    • Body composition
      • CT/US imaging of muscle stores (muscle mass)
      • DXA scanning (bone mineral density)

What is the frequency of screening for micro- and macro-nutrient deficiencies in pts with chronic pancreatitis?

  • Patients should undergo screening for micro and macro-nutrient deficiencies at least every 12 months
  • May need to occur more frequently in those with severe disease or uncontrolled malabsorption

What recommendations regarding diet and intake of fat, carbohydrates and proteins should be given in pts with chronic pancreatitis?

  • Do not need to follow a restrictive diet
  • If normal nutritional status, then should adhere to well-balanced diet
  • Malnourished pts should be advised to consume high protein, high energy food in five to six small meals per day
  • Avoid high fibre
  • No need for dietary fat restriction unless symptoms of steatorrhea cannot be controlled

Are oral supplements with or without medium chain triglycerides indicated in pts with chronic pancreatitis?

  • Oral nutritional supplements should be prescribed to undernourished patients only if oral nutrition is insufficient for reaching the calorie and protein goals
  • If inadequate enzyme supplementation and exclusion of bacterial overgrowth has not led to relief of malabsorption and its accompanying symptoms, ONS and MCT can be administered

When is micronutrient supplementation indicated in pts with CP (not included osteoporosis prevention)?

  • Fat soluble and water soluble vitamins as well as minerals such as magnesium, iron, selenium, and zinc should be monitored and administered if low concentrations are detected or if clinical signs of deficiency occur.
  • Supplementation should be proposed to pts with known malabsorption

When is EN indicated in pts with CP and how should it be administered?

  • EN should be administered in pts with malnutrition who are not responding to oral nutritional support
  • EN should be administered via the NJ route in pts with pain, delayed gastric emptying, persistent nausea or vomiting and gastric outlet syndrome
  • Long-term jejunostomy access (perc endoscopic gastrostomy with jejunal extension (PEG-J) or direct percutaneous endoscopic jejunostomy (DPEJ) or surgical jejunostomy) can be used in those requiring EN for more than 30 days
  • Semi-elemental formulas with medium chain triglycerides can be used if standard formulas are not tolerated
  • Pancreatic enzymes should be supplemented in pts requiring EN, if signs of exocrine failure

When is PN indicated in pts with CP and how should it be administered?

  • PN may be indicated in pts with gastric outlet obstruction and in those with complex fistulating disease, or in case of intolerance of EN
  • For PN, the preferable route is central venous access

What are the indicators for starting pancreatic enzyme replacement (PERT) in pts with CP?

  • When PEI is diagnosed through clinical signs and symptoms and/or lab tests of malabsorption,
  • An accurate nutritional assessment is mandatory to detect signs of malabsorption
  • PEI is defined as an insufficient secretion of pancreatic enzymes (acinar function) and/or sodium bicarbonate (ductal function)

What are the enzyme preparations of choice for PERT?

  • pH sensitive, enteric coated microspheres pancreatic enzyme replacement preparations

How should enzyme supplementation be administered?

  • Distributed along with meals and snacks

What is the optimal dosage of enzyme supplementation?

  • The posology aims at individual needs and depends on the severity of the disease and the composition of the meal
  • In practice, a minimum lipase dose of 20,000 – 50,000 PhU (based on the preparation) shall be taken together with main meals, and half that dose with snacks

How should the efficacy of enzyme supplementation be evaluated?

  • Evaluated by the relief of GI symptoms and the improvement of nutritional parameters (anthropometric and biochemical).
  • In pts who do not respond, the evaluation should be extended to pancreatic function tests (faecal fat excretion or 13C-MTG-breath test)

What should be done in cases of unsatisfactory clinical response?

  • PERT dosage should be increased or a PPI should be added
  • If these methods fail, other causes of malabsorption, e.g. small intestinal bacterial overgrowth should be excluded

Does the surgical technique for treating CP affect PERT and nutritional status?

  • Long-term PERT and nutritional status are similarly affected by all surgical procedures
  • Tissue-preserving procedures preferred

What is the risk of developing osteoporosis or osteopenia in pts with chronic pancreatitis?

  • Up to 25% risk for osteoporosis
  • Up to 66% risk for osteopathy, either osteoporosis or osteopenia

What methods should be used to identify pts who are at risk?

  • Dual-energy X-ray absorptiometry (DXA)

What is the recommended management for the prevention and treatment of these conditions?

  • Basic preventative measures should be advised:
    • Adequate calcium/vitamin D intake
    • If indicated, pancreatic enzyme supplementation
    • Regular weight bearing exercise
    • Avoidance of smoking and alcohol
  • Additional pharmacologic treatment should be reserved for pts with osteopathy and, in particular, osteoporosis

Management of Pancreatic Exocrine Insufficiency

Source: Australasian pancreatic club. Australasian guidelines for the management of pancreatic exocrine insufficiency. 2015

Pancreatic exocrine insufficiency and its diagnosis

  • Symptoms of PEI
    • Cluster of symptoms – abdo pain, diarrhoea, weight loss, malnutrition
    • Steatorrhoea and associated symptoms are not evident until duodenal lipase falls below 5-10% of normal post-prandial levels
  • Clinical Consequences
    • Most common: fat maldigestion
    • Consider non-pancreatic causes of steatorrhoea, e.g. Crohn’s disease of ileum
    • Testing for PEI:
      • Pts grouped into: Definite and possible
    • Definite: E.g. Total pancreatectomy, severe calcified pancreatitis, neoplasm of pancreatic head – no diagnostic test for PEI needed
    • Possible: E.g. Moderate structural alteration of pancreas, post-cibal asynchrony, pancreatic sufficient cystic fibrosis
    • Unlikely: E.g. rare cases of IBS, IBD, Coeliac, T2DM
    • Can use same tests as the ‘possible’ group but high chance of being inconclusive
      • Structural imaging: CT with contrast
      • Direct pancreatic function test: Gold standard – secretin-CCK stimulation test
    • Indirect pancreatic function tests: Three-day faecal fat test – gold standard for diagnosing steatorrhoea – but unpopular with pts and lab techs
    • Faecal elastase-1 (FE-1) test more commonly used – appropriate only as a screening test for excluding PEI
    • Blood tests for magnesium, nutritional markers, bone mineral density, and fat-soluble vitamins – important in diagnostic workup

Pancreatic Exocrine Replacement Therapy (PERT)

  • Key Points
    • Pts with PEI should be commenced on the lowest recommended dose of PERT (25,000 – 40,000 units lipase per meal)
    • Titrate dose against presence of malabsorption to lowest effective dose
    • In adults: max recommended dose of PERT: 75,000 to 80,000 units lipase with each meal
    • Trial acid suppressing agents in those pts who continue to experience symptoms of PEI despite high dose PERT

Dietary Management of PEI

  • Key Points:
    • Main consequence of PEI: malabsorption of fat and protein and, thus, also of vitamins and trace elements
    • Important to avert development of osteoporosis or osteopenia
    • Monitor weight and anthropometric parameters, fat soluble vitamins, and B12, and iron and calcium levels and treat where necessary
    • Refer pts with PEI to a dietician for nutrition assessment, counselling and support
    • Lipase-deficient chronic pancreatitis pts do not require a fat-restricted diet when adequate enzyme therapy is prescribed
    • Encourage pts to avoid alcohol, consume normal fat diet with sufficient protein and carb foods to achieve adequate nutrition
    • Advise pts to take PERT during the meal or immediately after the meal but not before the meal
    • Oral nutritional supplementation is recommended where additional energy and protein are required and enteral feeding should be initiated when oral intake is inadequate to meet requirements
    • Dietary protein intake should meet 1.0 – 1.5g/kg body weight/day
    • Screen pts with PEI and CP for bone disease using DXA
    • 30% total energy from dietary fat is now considered appropriate

Acute Pancreatitis and PERT

Key points: - Risk of PEI increased with extent of pancreatic necrosis

  • Recommended that all pts recovering from acute pancreatitis should undergo nutritional assessment and those with continuing symptoms suggestive of ongoing malabsorption should be considered for PERT
  • These pts should have pancreatic function testing later in recovery period regardless if they have pancreatic steatorrhoea to assess long term nutritional and enzyme requirements
  • Pts should be monitored for PEI for at least 6-18 months and treated with PERT as indicated
    • Use of PERT in initial stages of acute pancreatitis not recommended
    • Consider PERT in any pt for up to 2 years after severe acute pancreatitis
  • Long-term follow up of pts after severe acute pancreatitis should include monitoring for PEI for up to 6 years

Chronic Pancreatitis

Key Points:

  • One of the most common causes of PEI: chronic pancreatitis
    • Alcohol considered primary cause
  • Presence of steatorrhoea (proven or implied) is the foundation for initiating PERT
  • Required amount of lipase with each meal generally 25,000 – 50,000 lipase units
  • If pts do not respond to therapy, consider bacterial overgrowth

PEI in Cystic Fibrosis

  • Cystic fibrosis (CF) – common, genetic disorder caused by mutations in the gene that encodes the CFTR protein – disruption of the function of water and chloride ion transportation at a cellular level
  • 85% of CF pts are pancreatic-insufficient by early childhood
  • Without treatment – GI losses of fat and nitrogen can be severe ⇒ Growth failure and protein catabolism
  • PERT indicated for those with documented fat malabsorption or PEI as established by pancreatic function test
  • Excessive doses of PERT associated with fibrosing colonopathy – doses should not exceed 10,000 units lipase per kg bodyweight per day or 25,000 units per kg bodyweight per meal
  • Capsules should not be crushed, chewed or sprinkled on foods with a high pH
  • PPIs may have a role in decreasing gastric acidity and improving fat absorption and GI symptoms in CF pts on PERT

PERT after Bowel Surgery

  • PERT should be considered for those with clinical evidence of PEI and its ongoing requirement reviewed regularly because of possible intestinal adaptation
  • Gastric acid suppression therapy should be given with PERT to increase the release of nutrients in the small bowel

PERT after Gastric Surgery

  • After gastric surgery, pts whose wellbeing is not severely affected do not require long term PERT
  • Pts with accelerated gastric emptying should be prescribed PERT granules or capsules can be opened and contents sprinkled on food
  • Consider use of adjunct acid suppressant therapy for pts who have undergone partial gastrectomy
  • Bacterial overgrowth is a common cause of malabsorption after gastric surgery and does not respond to PERT

PERT after Pancreatic Resection

  • Any pt requiring pancreatic resection should be assessed for the presence of PEI post-operatively
  • Any pt with total or subtotal pancreatectomy including pancreatic head resection, require PERT post-op
    • Central pancreatic resection is associated with a lower rate of PEI
    • Pancreatic exocrine function is preserved after distal pancreatectomy
  • Pts who are pancreatic-sufficient in the early period after any pancreatic resection should have routine long-term assessment for the development of PEI
  • PERT is required after pancreatico-gastrostomy because of the effect of acid on endogenous enzymes

PERT in pts with Diabetes

  • Rarely is there a need to use PERT in pts with diabetes. Limited RCT data do not support treating pts with PERT simply on the basis of very low faecal elastase-1 levels

PERT in pts with Coeliac

  • In most CD pts, pancreatic enzyme secretion normalises after intro of gluten free diet
  • In those not responding, testing for PEI is warranted in selected cases.
  • CD may be a risk factor for pancreatic disease, appropriate diagnostic work up is required in CD pts clinically not responding to a gluten-free diet

PERT in IBS pts

  • Pts with diarrhoea predominant irritable bowel syndrome should be investigated for pancreatic exocrine insufficiency

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