Jakarta, 29 May 2010

Fluid and Nutrition Management in Acute Pancreatitis

Fluid and Nutrition Management  in Acute Pancreatitis

Introduction

Adequate fluid and nutrition therapy is still a major medical problem  in patients with acute pancreatitis.

Acute pancreatitis occurs when there is activation of pancreatic enzymes within the pancreas with subsequent autodigestion. An initiating event causes the extrusion of zymogen granules from acinar cells, into the interstitium and activates trypsinogen into trypsin. This activation leads to various pathophysiological changes from mild inflammation to necrosis (frequently haemorrhagic) and development of peripancreatic infiltration. The pathological findings, which correlate with clinical severity, range from mild oedema to pancreatic necrosis. Secondary infection and splanchnic hypoperfusion can lead to the development of septic complications and subsequent multiorgan failure.

The two most common causes of acute pancreatitis are alcohol over consumption and gallstones, although etiology includes other factors (hypertriglyceridemia, drugs, iatrogenic ERCP, trauma, idiopathic, etc). Together, they represent more than 80% of cases ^_(1,2)

Clinical Presentation

Mid epigastric pain which  radiates to the back associated with nausea and vomiting. Patients often appear very ill. Findings that suggest severe pancreatitis include hypotension and tacypnea with decreased basilar breath sounds. Flank ecchymoses (Grey Turner’s sign) or periumbilical ecchymoses (Cullen’s sign) indicate hemorrhagic pancreatitis.^₍₂₎

Lab findings:

• Leucocytosis, hemoconcentration and hyperglycemia are common.
• Dehydration, pre-renal azotemia
• Elevated amylase level often confirms the clinical diagnosis
• Serum lipase is a more reliable diagnostic marker of AP than serum amylase. Urinary strip tests for trypsinogen activation peptide (TAP) and trypsinogen-2 provide a reliable early diagnosis of AP (3)
• Radiology : CT scan may reveal necrosis, psedocyst and abscess

1. NPO (nothing per oral)
2. IV fluid resuscitation (isotonic crystalloids such as Asering, Lactated Ringer) in severe cases with hypovolemia and hypotension. Severe acute pancreatitis is associated with microcirculatory impairment, increased gut permeability and metabolic changes
3. Nutrition
4. Pain control
5. Antibiotics, octreotide etc.

• Aggressive nutritional support is not required for mild to moderate forms of acute pancreatitis. In this regard, Aminofluid ® 1-2 L   is suitable to proivide water, electrolytes and microminerals as well as maintenance requirement of glucose and amino acids. . Nutritional therapy has to be considered earlier if restoration of oral feeding is delayed. In severe pancreatitis nutritional support isessential.

• The route of nutrient delivery (parenteral/enteral) should be determined by patient tolerance. Enteral should be attempted in all patients. The clinician should monitor intakes carefully to ensure adequate nutritional support as well as avoiding nutrient excess. Many patients will require a combination of enteral and parenteral nutrition.

• Patients with severe disease, complications or the need forsurgery require early nutritional support to prevent the adverse effects of nutrient deprivation (enteral and/or parenteral nutrition is possible according to the patient condition).

• Some authorities recommend early jejunal feeding with an elemental diet and others parenteral nutrition with concomitant  enteral given to tolerance;

• When side effects occur or the caloric goal cannot be achieved,enteral nutrition should be combined with parenteral  nutrition.

• The combined approach allows the achievement of nutritional goals most of the time.

• The use of intravenous lipids as part of parenteral nutrition is safe only  when severe hypertriglyceridaemia (<10 mmol/L) is avoided. However, the concentration of plasma triglycerides should be <3–4 mmol/L, due to metabolic problems connected with hypertriglyceridaemia

• When nutritional support is necessary, start with enteral feeding by jejunal feeding tube (when the caloric goal cannot  be reached, give additional parenteral support).

– When enteral nutrition is not possible (e.g. prolonged paralytic ileus), combine parenteral nutrition with a small content of immuno-enhancing diet  eg Neomune® (10–30 ml/hr ). (4)

Conclusion

Treatment  of  severe acute pancreatitis including initial fluid resuscitation, a moderate and hypocaloric parental nutrition as the preferred route for nutritional support and a non-strict glucose control should be encouraged. (5)

In SAP, oral intake is inhibited by cytokine induced anorexia,ileus, duodenal compression and consequent nausea and vomiting. Traditionally patients were kept ‘nil by mouth’ to minimise pancreatic stimulation as this was thought to exacerbate inflammation of the pancreas. The importance of nutrition became clear when reduced mortality and complications were reported in patients supported with parenteral nutrition (PN) as compared with no nutritional support. Thereafter parenteral nutrition became standard care in SAP.

However disuse of the gut leads to a degree of intestinal ischaemia and consequent decrease in gut mucosal barrier
function. Bacterial translocation results with infected pancreatic necrosis and sepsis. Absorption of bacterial products such as endotoxins further stimulates a generalised inflammatory response. It has been suggested that enteral nutrition (EN )may help preserve mucosal function and limit the stimulus to the inflammatory response pathways; thus attenuating disease severity, improving therapeutic results. However, intra-gastric nutrition increases pancreatic exocrine secretions, which may aggravate pancreatitis. This led to investigation of post-pyloric naso–jejunal enteral nutrition. ^₍₆₎


Note: Neomune® Each 48 g/ sachet, contains :Energy 200 kcal Protein 12.5 g (Casein 8.76 g Arginine 2.50 g Glutamine 1.25 g)Carbohydrate 25.01 g,Fat 5.79 g,Vitamins, Minerals   

References:

1. B. W. M. Spanier et al Epidemiology, aetiology and outcome of acute and chronic pancreatitis: An update. Best Practice & Research Clinical Gastroenterology Vol. 22, No. 1, pp. 45–63, 2008
2. Brenner M, Safani M. Critical Care Medicine. Current Clinical Strategy Publishing 2002-2003. Pp 101-104
3. Ahmed Z. Al-Bahrani, Basil J. Ammori Clinical laboratory assessment of acute pancreatitis Clinica Chimica Acta 362 (2005) 26–48
4. Meier RF ,Sobotka L.  Basics in Clinical Nutrition: Nutritional support in acute and chronic pancreatitis e-SPEN, the European e-Journal of Clinical Nutrition and Metabolism, Volume 5, Issue 1, February 2010, Pages e58-e62
5. Gunilla Eckerwall, Hanna Olin, Bodil Andersson, Roland Andersson Fluid resuscitation and nutritional support during severe acute pancreatitis in the past: What have we learned and how can we do better? Clinical Nutrition (2006) 25, 497–504
6. Ahmad Al Samaraee et al. Nutritional strategies in severe acute pancreatitis: A systematic review of the evidence. the surgeon 8          ( 2010 ) 105 – 110

Iyan Darmawan, MD
Medical Director
iyan@ho.otsuka.co.id

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