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N u t r i t i o n a l Su p p o r t i n A c u t e an d C h ro n i c P a n c re a t i t i s

John P. Grant,
KEYWORDS  Pancreatitis  Nutrition  Nutritional support


About 300 per 1 million individuals develop acute pancreatitis each year. The clinical spectrum ranges from a mild, self-limited, edematous form, in which patients often do not seek medical attention; to an acute, necrotizing, or hemorrhagic pancreatitis in which mortality may be as great as 80%. In some patients, the disease develops into a chronic relapsing variant. The clinical diagnosis of acute pancreatitis is based on characteristic nausea and abdominal pain localized to the upper abdomen that typically penetrates through to the back. Patients are often found sitting with their arms folded over in front, bending over at the waist. The diagnosis is confirmed by an increase of the serum concentrations of amylase and lipase, an increased white blood count (WBC), and fever. Causes of pancreatitis include gallstone disease, abdominal trauma, hyperlipidemia, general anesthesia, viral infections, alcohol, trauma, and some medications (azathioprine, thiazides, and estrogens). Pancreatitis is now recognized as a complex inflammatory condition similar to inflammatory bowel disease. Patients with mutations in genes linked to cationic and anionic trypsinogen, serine protease inhibitor Kazal 1, cystic fibrosis transmembrane conductance regulator, chymotrypsinogen C, and calcium-sensing receptor have been shown to be at increased risk of pancreatitis when exposed to these causes.1 Obesity seems to increase risks for progression to severe pancreatitis.2

Based on the Atlanta criteria,3 approximately 75% of patients experience mild disease, with a mortality of less than 1%.4 Mortality increases up to 20% if the disease progresses to its severe necrotizing form,5–10 and, in the most severe cases, mortality can increase to 30% to 40%.9,10 In some patients, the inflammation may lead to

The author has nothing to disclose. Duke University Medical Center, Durham, NC, USA E-mail address: Surg Clin N Am 91 (2011) 805–820 doi:10.1016/j.suc.2011.04.005 0039-6109/11/$ – see front matter Ó 2011 Published by Elsevier Inc.

In their experience. and the presence of pleural effusions. Roses DF. age greater than 60 years.12 ACUTE PHYSIOLOGY AND CHRONIC HEALTH EVALUATION II SCORE Studies suggest that the Acute Physiology and Chronic Health Evaluation (APACHE) II score is accurate in predicting It is recommended that APACHE II scores be generated during the first 3 days of hospitalization and thereafter as needed to help identify and follow high-risk patients. The presence of 3 or more factors represents a high risk for morbidity and mortality. and abscess. Although cumbersome to calculate. Surg Gynecol Obstet 1974.139:69–81. Several scoring indices have been developed and are used as early predictors of severity and survival. Ranson and colleagues11 identified 5 criteria related to the severity of pancreatitis (Box 1). fistula. impaired mental status. Rifkind KM.html).000/mm3  Lactate dehydrogenase greater than 700 IU/L  Aspartate aminotransferase greater than 250 U/L  Signs within first 48 hours  Hematocrit decrease greater than 10%  Calcium less than 8. it can be fully calculated at the time of admission.sfar.0 mg/dL  Base deficit greater than 4 mEq/L  Blood urea nitrogen increase greater than 5 mg/dL  Fluid sequestration greater than 6 L  Partial pressure of arterial oxygen (PaO2) less than 60 mm Hg Data from Ranson JH. presence of the systemic inflammatory response syndrome. . more than 60% of patients subsequently expired of the disease during that hospitalization. Prognostic signs and the role of operative management in acute pancreatitis. Internet sites are available to aid in calculations (http://www. et al.806 Grant complications such as pseudocyst. Six other clinical criteria had a significant impact on outcome if they developed in the first 48 hours after admission. if 3 or more of these criteria were present at the time of admission. BEDSIDE INDEX FOR SEVERITY IN ACUTE PANCREATITIS SCORE The Bedside Index for Severity in Acute Pancreatitis (BISAP) score can be derived on admission based on the following risk factors: blood urea nitrogen (BUN) greater than 25 mg/dL.12 A score greater than or equal to 8 is associated with a poor prognosis. Box 1 Ranson criteria  Signs within first 24 hours  Age greater than 55 years  Blood glucose greater than 200 mg/dL  WBC greater than 16. RANSON SCORE In 1974.

Investigative efforts to suppress or avoid the cytokine response are showing some early promise. enlarged body and tail of pancreas with fluid collection in peripancreatic spaces. enlarged pancreas with haziness and increased density of peripancreatic fat. extensive fluid collections in lesser sac and anterior pararenal space. However. The severity numbers for edema and necrosis are added together to estimate the severity of the disease (Table 1). it has been standard practice to initiate immediate bowel rest. 2. grade B. Vriens and colleagues14 evaluated application of the Balthazar CT Severity Index within 48 hours of admission and found it to be an excellent prognostic tool for complications and mortality. grade E. Of recent interest is the role that the intestine likely plays in disease progression. To minimize pancreatic stimulation. however. from 31% to 50% necrosis. normal. and more than 50%. or inflammation. oxygen free radicals. based on current research. platelet aggregating factor. Patients with a score of 0 to 3 could safely be discharged from the intensive care unit (ICU) and managed in a regular hospital bed. up to 30%. grade D. elastase. all leading to development of the systemic inflammatory response syndrome (SIRS). these efforts have not yet achieved clinical use. The degree of pancreatic necrosis is estimated from enhanced CT of the pancreas. with no necrosis assigned a severity number of 0. whereas all others were best kept in the ICU. diffuse enlargement of the pancreas without peripancreatic inflammatory changes. Because the full extent of pancreatic necrosis does not usually develop until 72 to 96 hours after the onset of the disease. producing even more injury. Each grade is assigned a severity number from grade A 5 0 to grade E 5 4. The amount of pancreatic edema is estimated from an unenhanced CT of the pancreas: grade A. with possibly glutamine Table 1 Balthazar CT severity index Mild 0–3 Percent Morbidity/Mortality 3/10 35/6 92/17 Moderate 4–6 Severe 7–10 . although not proven and likely to change somewhat. it might be argued that CT scanning should only be performed in selected patients after 4 to 5 days following admission. grade C. Pancreatitis is initiated by release of inappropriately activated zymogen digestive enzymes within the acinar cell. and the amount of necrosis of the pancreas on computed tomography (CT). Any oral intake during the first 24 hours can stimulate the injured pancreas to produce more secretions. with conversion of trypsinogen to trypsin and subsequent autodigestion. The expanding pancreatic injury results in the release of cytokines (mainly interleukin 1 and tumor necrosis factor) that cause release of nitric oxide. coupled with lysosomal hydrolase cathepsin-B. the reduction in luminal nutrients. is the most favored. However. 6. 4.Acute and Chronic Pancreatitis 807 COMPUTED TOMOGRAPHY SEVERITY INDEX Balthazar and colleagues13 identified 2 radiographic factors useful in predicting those patients who will develop severe pancreatitis: the amount of edema. and multiple other interleukin products. MECHANISMS LEADING TO SEVERE ACUTE PANCREATITIS The following scenario for the progression of mild to severe acute pancreatitis.

17 The loss of gut integrity also promotes luminal bacterial interaction with the gutassociated lymphoid tissue and upregulates systemic immunity. development of vital organ failure in spite of adequate support.808 Grant depletion or cytokine effect. Prophylactic antibiotic administration remains controversial. Although not suspected at that time. and shock. and most survived. Whenever possible. early initiation of nutritional support seems to have a significant impact on eventual outcome. thereby minimizing pancreatic ischemia and subsequent reperfusion injury. and reduced mortality. allowing healing . further aggravating SIRS. Only the animals given full support beginning 2 hours after the burn had a minimal metabolic response. Subsequent surgical exploration is indicated by the need for continued pressor support. The amount of fluid required is often underestimated. Continued starvation of the patient leads to a reduction in antiinflammatory Th2 lymphocytes and secretory IgA-producing immunocytes. and some other surgical catastrophe might be present. The inciting factor should be addressed.22–24 The possible role of nutrition in modulating the cytokine response was first reported by Mochizuki and colleagues25 in 1984. especially when provided enterally and especially when given to a patient with moderate to severe acute pancreatitis. Broad-spectrum antibiotics are best given to treat specific infections. lead to vascular leakage. or when the diagnosis is not clear. in turn.16. All other animals showed a marked hypermetabolic response. Use of H2 blocker agents remains of unproven value. or at 115% support beginning after 72 hours. with some studies showing reduced need for surgery. even after adequate volume replacement. and avoidance of any toxins such as alcohol or medications. They subjected the pigs to a 30% body surface burn and began gastric tube feedings at full support 2 hours or 72 hours later. can lead to loss of gut integrity with increased permeability and release of more cytokines and their products. Pulmonary support with oxygen or intubation should be provided as indicated. They reported on the impact of gastric feeding on survival in a guinea pig burn model. control of hypertriglyceridemia. and commonly totals more than 6 L. the probable explanation for the observed impact of early enteral feeding was that these feedings preserved gut integrity and aborted the early cytokine response. general deterioration of the medical status. and most expired. Activation of macrophages and stimulation and proliferation of Th1 CD4 helper lymphocytes results in a proinflammatory process. The adequacy of volume replacement can in part be monitored by normalization of the BUN and serum sodium. such as removal of a common bile duct gallstone by endoscopic retrograde cholangiopancreatography (ERCP). acute respiratory distress syndrome.21 Narcotics are required to control pain. a feeding jejunostomy should be placed during any intra-abdominal procedure. decreased incidence of major organ failures.15 These products. hypovolemia. and eventually to a toxin-producing pathogenic bacterial overgrowth of the intestine. NUTRITIONAL SUPPORT In addition to the clinical interventions mentioned earlier. proven or suspected pancreatic abscess. CLINICAL MANAGEMENT Clinical management of patients with acute severe pancreatitis must concentrate initially on the restoration of blood volume and electrolyte balance.18–20 whereas others do not. Replacement of fluid lost or fluid sequestered into third spaces is critical to maintain microcirculation.

hypertonic solutions given into the jejunum. but especially early enteral nutrition. Infusion of any hypertonic solution into the jejunum decreases pancreatic exocrine secretion. OPTIMAL FEEDING FORMULATIONS Provision of nutrition should minimally stimulate exocrine pancreatic secretions and. Most studies suggest that there is a narrow window of about 72 hours within which this effect can be obtained.23 and 1.28–31 Although each study was small. Inadequate data are available to evaluate effectiveness of special formulas such as glutamine-enriched. the best method for determination of energy requirements in acute pancreatitis remains performance of indirect calorimetry whenever it is available. Intravenous lipid emulsions and oral medium-chain fatty acids (MCFA) do not seem to stimulate pancreatic secretion. Other studies. Ideal feeding solutions for patients with acute pancreatitis. consistent again with the known onset of the cytokine response. Intravenous infusions of amino acids and hypertonic glucose have been shown not to stimulate exocrine secretion. water and bicarbonate pancreatic exocrine secretion is stimulated by acid and by meat extracts in the duodenum. and by the process of eating as well as antral distention. reduce complications and improve survival. . ESTIMATING AND MEETING METABOLIC NEEDS Caloric Experience has shown that metabolic expenditure during acute pancreatitis seldom exceeds what might be expected with other stressful events. multifiber. and by antral distention. Owing to patient variability. suppress secretions. compared with delayed enteral feedings (mean resting energy expenditure was 139% of normal in early enterally fed patients and 160% of normal in delayed enterally fed patients).27 However. calcium. which might be expected to decrease exocrine function are discussed later. perhaps.Acute and Chronic Pancreatitis 809 and recovery. Wang and colleagues26 confirmed a similar benefit of early enteral feeding in patients with burns. Four older studies have evaluated the metabolic expenditure of patients with acute pancreatitis (Table 2). Standard formulas will likely be less well tolerated. protein. Energy expenditure varies with time and with clinical conditions and that these estimates only represent averages. or probiotic supplemented products. low LCFA (MCFA enriched). Enteral Enteral feeding includes peptide-based formula. confirm that early enteral and parenteral nutrition in pancreatitis. Parenteral Parenteral feeding includes crystalline amino acids and hypertonic glucose (intravenous fat in sufficient dosage to meet essential fatty acid requirements). and magnesium in the duodenum. reviewed later.49 times that predicted from the Harris-Benedict equation. They found that the resting energy expenditure decreased by an average of 27% in the first 14 postburn days when early enteral feeding was given. Enzyme secretion is stimulated by long-chain fatty acids (LCFA). it seems that a patient’s energy expenditure is somewhere between 1. but may be satisfactory in some patients. Subsequently.

7 to 6. . or improved whole body protein synthesis. measured energy expenditure.86 MEE 2080 2525 26 kcal/kg 1687 Average ratio MEE/Harris-Benedict EE 5 1. and carbohydrate infusion should be reduced instead. The process of fat synthesis is associated with increased carbon dioxide production. and infusions at a higher rate were associated with no further increase in protein synthesis. pyruvate. energy is consumed in production of an unnecessary substrate: fat. an energy consuming process.8 mg/kg/min glucose infusion. So instead of benefits from high insulin infusion. although not clinically confirmed. 1. When in doubt.81 0. Insulin strongly stimulates uptake of amino acids by the skeletal muscle. builds up in tissues. Attempts at improving glucose use using high-dose insulin have successfully shown depression of blood sugar concentrations. Burke.5 g/kg/d protein are required. Another more pertinent side effect of insulin loading is its inhibition of pyruvate dehydrogenase. MEE. Nitrogen In general. which may stress the respiratory system. administration of more than 60 units of insulin daily should be avoided.35 As glucose infusion is increased. and colleagues32 showed that the conversion of intravenously administered labeled glucose to labeled carbon dioxide was maximal at a rate of 6 mg/kg/min. especially if significant chronic obstructive pulmonary disease is present. Glucose Providing glucose in excess of maximal glucose use is of no clinical value and may be of some harm.23 mg/kg/min in stressed patients.0 to 1. It is therefore recommended that stressed patients receive a maximum of 5 to 6 mg/kg/min glucose as a caloric substrate. Black and colleagues33 studied maximal glucose uptake and use in patients in intensive care compared with nonstressed patients and found a marked decrease in glucose disposal from 9. the critical enzyme for entry of glucose intermediates into the Krebs cycle for oxidative metabolism. could provide a source of energy for skeletal muscle in the presence of severe glucose intolerance. In 1979. RQ. depending on the degree of stress.78 0. improved nitrogen balance. theoretically.810 Grant Table 2 Caloric expenditure in acute pancreatitis Author Van Gossum et al28 Bouffard et al29 Dickerson et al30 Velasco et al31 No. In general. of Patients 4 6 5 23 RQ 0. energy expenditure.34 but no study has shown improved glucose oxidation.87 0.24 Abbreviations: EE. the anaerobic end product of glucose metabolism. a 24-hour nitrogen balance study can be helpful if renal function is normal. respiratory quotient.46 mg/kg/min in normal subjects to only 6. There are some potential adverse side effects of insulin loading that militate against its routine use. A relative block of pyruvate dehydrogenase by increasing concentrations of insulin favors diversion of pyruvate to fat synthesis. They further showed that a maximal benefit of glucose loading during stress with respect to whole body protein synthesis occurred with 4. may alter or deplete the amino acid pool sufficiently to interfere with normal protein synthesis. Use of branched-chain enriched amino acid solutions has not been studied specifically in acute pancreatitis but. which. Infusions at lower rates resulted in a reduced protein synthesis.

and phosphorus. the median APACHE II score was 18 (range 4–40). Of 69 patients with acute severe pancreatitis. and the overall hospital mortality was 39%. enteral nutrition was superior in decreasing infectious morbidity. Other In addition to provision of adequate nutrients. Gastric Residuals Residual volumes have been used by physicians. but a product with decreased LCFA and increased MCFA is preferred. Twenty-three did not have any nutritional support during their ICU stay. The mortality was higher among patients who received TPN alone compared with those who had at least some enteral nutrition (60% vs 24%). a clear perception of intolerance must be understood. Recently. Calcium must also be monitored and supplemented as needed.42 In 2000. high-volume small bowel fistula). essential fatty acids must be given in required doses. and colleagues43 evaluated patients with acute severe pancreatitis who were admitted to the ICU and received either nasogastric or jejunostomy enteral nutrition. and resulting in faster resolution of the SIRS. The sixth study randomized patients after 4 full days of hospitalization. These electrolytes are potassium. studies have raised considerable doubt as to the value of declaring any arbitrary residual volume as unacceptable and have pointed out how rigid rules related to . because dramatic consumption can occur with onset of anabolism. but care must be taken to ensure that the fat is cleared from the blood if it is used as a caloric source. adequate supplementation of the anabolic electrolytes is critical. Patients were only given total parenteral nutrition (TPN) when enteral nutrition was persistently inadequate or when this route was contraindicated (eg. Similar data are accumulating in the management of acute pancreatitis. There are 4 clinical responses to be managed. Other studies have documented that early enteral feeding reduces the incidence of gastric stasis and intestinal ileus. reducing overall complications. ENTERAL FEEDING In many critical care disease states. Of 6 prospective randomized controlled trials of enteral versus parenteral nutrition. and nurses for many years as objective measures to judge tolerance or intolerance to enteral tube feedings. Seventeen patients were managed with enteral feedings alone.44–46 To administer enteral feeding successfully. although benefits were observed in both feeding groups. shortening hospital length of stay. magnesium. 5 showed significant positive effects on clinical outcome if feedings were started within 48 hours of admission. and no significant impact of feeding was observed. Consideration should be given to providing oral pancreatic enzymes when an oral diet is resumed. 10 with TPN alone. Standard enteral feeding formulas containing fat are often well tolerated.Acute and Chronic Pancreatitis 811 Fat At a minimum.36–41 In these 5 studies. Ample B-complex vitamins (especially thiamin in an alcoholic patient) and maintenance amounts of fat-soluble vitamins should be given. The efficiency of fat use as an energy source diminishes as the level of stress increases. rendering fat a poor caloric source in severe pancreatitis. Intravenous lipid emulsions seem to be well tolerated. dietitians. during which initiation of nutritional support may change the clinical outcome. and 19 with a combination of both. Schneider. studies support the concept of an early window of opportunity after admission (36 hours).

49. especially with transition to an oral diet. and 81% had improved nutritional indices following therapy.2 Ranson criteria) to receive either standard intravenous fluids or TPN.50 Nearly All Patients Show an Increase in Trypsin.5%). There was no difference between the groups with respect to total hospital days. Sitzmann and colleagues55 administered TPN to 73 patients with moderate to severe pancreatitis (average 2. or days to oral intake. Amylase. Catheter-related sepsis occurred more frequently in the TPN group than in other patients receiving TPN (10. Sax and colleagues53 randomized 54 patients with mild pancreatitis (1. In spite of improved nutritional care.5 Ranson criteria). Goodgame and Fisher56 reported on treatment of 46 patients with severe acute pancreatitis using TPN. number of complications of pancreatitis. evaluation of the volume of gastric contents is an unreliable method for monitoring feeding tolerance. CLINICAL EXPERIENCE: PARENTERAL NUTRITION DURING ACUTE PANCREATITIS Parenteral nutrition should only be attempted on failure of enteral feedings.1 Æ 0. and Lipase Although these indicators nearly always increase as enteral feedings are started.2). and only 3 episodes of catheter-related sepsis occurred. Computer models have shown that. and these patients should be transitioned to parenteral feedings. Overall mortality was only 4%. gastric emptying. these increases are rarely associated with clinical symptoms or any adverse clinical effects. Fifty-five percent of patients required insulin (average 69 U/d). the serologic changes should be ignored. Robin and colleagues54 reported on the administration of TPN to 70 patients with mild to moderate pancreatitis (average Ranson criteria 1. and gastric capacity. because of the complex relationship between infusion volume. They found minimal technical and metabolic complications and reported that nutritional requirements were easily met. Mortality was 10 times greater if a positive nitrogen balance was not achieved. this will not improve with interruption of the feedings.66) and 86 with moderate to severe pancreatitis (average Ranson criteria 2.47.52 Only about 4% of patients truly worsen when enteral feedings are begun.51 Exacerbation of Abdominal Pain Up to 21% of patients may experience an uncomplicated exacerbation of abdominal pain.  The amount of residual volume is often greatest during the first several hours after feeding is begun. The TPN was well tolerated and nutritional status was improved. Sixty percent of patients required insulin for hyperglycemia (average of 35 U/d).48  The amount of gastric residual volume is dependent on the infusion rate. and the feeding solution should be continued. the residual volume tends to plateau and then decrease.  Abdominal distention can be caused by gas-filled loops of bowel from aerophagia and may not be caused by increased gastric residual volume. little effect was observed on the course of . Returning to enteral feedings usually quickly resolves the symptoms. The following are suggestions to improve clinical practice:  Whenever residual volumes are measured.5% vs 1. With continued feeding.812 Grant residual volumes have at times rendered enteral nutritional support of limited value. they should be interpreted along with the appearance of the patient’s abdomen and any complaints of fullness or discomfort. and 79% of the patients developed pancreatitis caused by alcohol intake. Average age was 39 years. If symptoms are absent.

Although enteral nutrition is preferred. enteral nutrition should be initiated. 13 of whom had severe pancreatitis. The fat emulsion was well tolerated. their most striking finding was a 23. and resting energy expenditure during parenteral nutrition in 15 patients with acute pancreatitis.5 g/kg/d protein. Twelve patients developed complications of a pseudocyst or pancreatic fistula. Nutritional status improved in all patients. via a nasogastric tube. or the Balthazar CT Severity Index is 4 to 6. and 85% of patients developed pancreatitis caused by gallstones. trace elements. and if intestinal motility is not adequate. Perhaps the most interesting report has been that of Kalfarentzos and colleagues57 in 1991. They administered TPN to 67 patients with severe pancreatitis (>3 Ranson criteria). If no recovery of motility is observed. body protein stores were significantly increased. minerals. There was an increased incidence of catheter-related sepsis (8. If Balthazar CT Severity Index is 4 to 6. and contrast-enhanced CT should be considered to identify fluid collections. The feeding formula should be peptide based and low in LCFA. They provided Harris-Benedict recommendation for calories.6% complication rate and a 38% mortality if started later. giving insulin as required. Moderate Pancreatitis If symptoms are more significant. and if intestinal motility is adequate. or other complications that may require intervention. and none require surgical intervention. In 2005. SUMMARY SUGGESTIONS FOR NUTRITIONAL MANAGEMENT DURING ACUTE PANCREATITIS Mild Pancreatitis If admission severity scores are low. If motility recovers. If symptoms worsen or persist beyond 5 days. and 300 mL of a 10% lipid emulsion twice a week. compared with a 95. Jejunal feedings may also be well tolerated by patients who have undergone exploratory laparotomy. if not achievable. pancreatic necrosis. Using neutron activation analysis and tritium dilution studies. preferably via a nasojejunal tube. then a nasogastric tube) should be initiated within 48 hours of admission. there is an apparent beneficial role for parenteral nutrition when enteral feedings are not tolerated. they found that body composition was preserved during 14 days of parenteral nutrition. However. Extra vitamins. it should be given intravenously or as MCFA.6% complication rate and 13% mortality if TPN were started within 72 hours of onset of symptoms. at which time an oral diet can be resumed. Average age was 58 years. observation is indicated. enteral nutrition via a nasojejunal feeding tube (if not feasible.9% vs 2. consideration should be given to initiating intravenous nutrition within 48 hours. Chandrasegaram and colleagues58 reported on changes in body composition.9% in other patients receiving TPN). . Care must be taken to avoid complications of glucose intolerance. at which time a feeding jejunostomy should be placed. Hyperglycemia occurred in 88% of patients and required an average of 46 U/d insulin. Their findings again emphasize the possible role of early nutrition in reduction of the cytokine response. plasma proteins.5 to 2. enteral feedings should be started. 1. and electrolytes may be needed based on the clinical course.Acute and Chronic Pancreatitis 813 the acute pancreatitis. Of concern was a high incidence of catheter-related sepsis (17% occurring primarily during the first 14 days of therapy). all of which resolved while continuing to receive TPN. patients may initially be followed. In patients without sepsis or recent surgery. but. If additional fat is necessary. Patients should be placed nil per os until blood chemistries and symptoms nearly resolve.

They reported an incidence of recurring pain following refeeding. and mineral supplementation. with Gram staining and culturing of the aspirate. patients should have a nasojejunal tube passed under fluoroscopy. SPECIAL CONSIDERATIONS Pancreatic Necrosis/Abscess Pancreatic necrosis occurs as diffuse or focal areas of nonviable pancreatic tissue. no clear demarcation is evident between viable and nonviable tissue. When refeeding is begun. As the severity of acute pancreatitis resolves and gastrointestinal function returns. the patient should be converted to enteral nutrition via nasojejunal feeding. A balanced amino acid solution should be administered intravenously using hypertonic dextrose and appropriate electrolyte.814 Grant Severe Pancreatitis When the APACHE II score is greater than or equal to 10 or the Balthazar CT Severity Index is greater than 6. the diet need not be limited to clear liquids. fineneedle aspiration should be performed.60 Supplementation with pancreatic enzymes and insulin may be necessary. low-fat. in the early stages. antibiotics alone cannot resolve the infection. heralded by a decrease in temperature. and with serum lipase concentrations greater than 3 times normal just before refeeding. Observation is indicated. Within 48 hours of admission. reduction in serum amylase and lipase. with open debridement . with injection of contrast material to evaluate intestinal motility. solid diet as tolerated. Furthermore. and after fluid resuscitation. normalization of the WBC. The risk of beginning an oral diet too soon is stimulation of the pancreas with reactivation of pain and acute pancreatitis. Delaying pancreatic debridement for at least 2 weeks is recommended. but each patient should be closely monitored to assure that the lipid is cleared from the blood (serum lipid levels should be monitored and ideally kept within normal limits). guided by either CT or ultrasonography. Administration of 3-in-1 solutions seems to be safe. vitamin. requiring cessation of feeding in 21% of patients studied. If satisfactory antegrade motility is present. enteral nutrition was considerably more effective in preventing pancreatic necrosis during severe pancreatitis than intravenous nutrition (23% vs 72%). conversion to an oral diet should be attempted. It usually develops during the first few days of pancreatitis secondary to hypoperfusion. Levy and colleagues59 studied this problem to determine factors that might predict patients at risk for starting an oral diet. Pain relapse occurred mainly in those patients with a long period of pain. necrotic acute pancreatitis (Balthazar score of !3). Close observation for glucose intolerance and catheter-related infections must be maintained to ensure patient safety. and decrease in abdominal pain. because surgery within the first few days of onset of severe acute pancreatitis is associated with rates of death up to 65%. The diagnosis of a pancreatic abscess mandates immediate intervention. jejunal tube feedings should be begun using a peptide-based.61 If infection of the necrotic material is suspected based on leukocytosis and fever. fluid resuscitation should be initiated immediately. intravenous nutrition should be begun within 48 hours of admission. but are required in the perioperative period. In a recent study. high-calorie. consideration can be given to beginning an oral diet. Surgery remains the treatment of choice. or if an ileus is present. Resolving Pancreatitis As the severity of acute pancreatitis resolves. If retrograde motility is observed. In no event should drainage be delayed for nutritional support. low LCFA feeding formula. With further improvement. but can be initiated with a lowfat soft diet and advancement to high-protein.

63 Increased serum amylase concentration is the hallmark of a developing pseudocyst and does not necessarily indicate a worsening of the pancreatic inflammation. or surgical intervention may be needed. then medical. If no leak is identified on ERCP. bowel rest. various percutaneous drainage approaches have been proposed. internal drainage to an intestinal segment should be considered. Malabsorption. The reduced dietary intake is mostly a consequence of chronic pain. malabsorption. along with provision of pancreatic enzyme supplementation. A peritoneal aspirate of the ascitic fluid will contain high levels of amylase if the ascites originates from pancreatitis. If leakage is found in the tail or body of the pancreas. or an empirical distal pancreatectomy can be performed. and recurrent infections. If the ascites persists after 2 weeks. In general. cause pain. If the pseudocyst decreases in size in 2 to 3 weeks. internal surgical drainage should be performed after 6 weeks. it is recommended that TPN. or compress adjacent organs. either TPN can be continued for another 2 to 4 weeks with a repeat study. Twenty-four hours after drainage has been accomplished. a distal pancreatectomy is curative. when the pseudocyst wall usually matures satisfactorily to hold a suture. Onset and progression of a fever and an increased WBC suggest development of an infected pseudocyst and mandates immediate evaluation and probable drainage. ERCP should be performed to evaluate possible disruption of the pancreatic duct. surgery should be delayed. Suggested Clinical Management The first effort should consist of manipulation of an oral diet.Acute and Chronic Pancreatitis 815 and wide drainage of the peripancreatic area. Unpalatable dietary restrictions for pancreatitis-related diabetes mellitus can also reduce intake. and medical care be provided for at least 2 weeks. is caused by pancreatic insufficiency and characterized by steatorrhea. nutritional support (preferably enteral) should be initiated or resumed. however. There seems to be no aggravation of pseudocysts secondary to instillation of enteral feedings into the jejunum. Although little has been published on the treatment of pancreatic ascites. their results have not been compared prospectively with open surgery. CHRONIC PANCREATITIS Malnutrition of Chronic Pancreatitis Patients with chronic pancreatitis often suffer progressive malnutrition caused by decreased dietary intake. These collections are usually managed conservatively and resolve spontaneously. when present. Recently. If a leak is seen from a pseudocyst or from the duct in the head of the pancreas. Pancreatic Ascites Ascites in alcoholic patients with pancreatitis must be differentiated from cirrhotic ascites. Carefully designed dietary modifications. If the fluid collections continue to enlarge. with reduced dietary fat. If the pseudocyst is unaltered or enlarged. and bowel rest with or without TPN has not been shown to be of any added benefit in their treatment. commonly aggravated by oral intake. endoscopic. surgical and diagnostic procedures.62 Planned reoperations may be required to remove all necrotic material.64 . Pancreatic Pseudocyst Up to 57% of patients have at least 1 fluid collection evident on CT. anticipating spontaneous resolution. it seems that some cases resolve spontaneously. can be effective in restoring and maintaining nutritional status in up to 80% of patients.

The first article published using home enteral nutrition in patients with chronic pancreatitis was by Cromer and Grant65 in 2000. following which 19 resumed an oral diet. 26 eventually underwent surgical intervention for debridement (3 deaths). 4 were still receiving enteral support. 6 gallstones. compared with that reported in the literature. peptide-based. A standard enteral diet was tolerated by 86% of patients. because there is usually only minimal stress present. or ductal drainage. from a published level between 58% and 67% to only 14%. They reported a significant reduction in abdominal pain. 3 after ERCP. Nitrogen Requirements Nitrogen requirements are also similar to those in other malnourished patients. and 3 were poorly compliant with administration of feedings). These patients underwent placement of a feeding jejunostomy and were discharged on home enteral feedings. In 2002. They reported on their experience with home enteral nutrition from 1994 to 1999 in 33 patients referred for intravenous nutrition. In 2005. Nonetheless. and subjective global assessment. without aggravation of abdominal pain. resection. Yoder and colleagues66 reported on 33 patients with chronic pancreatitis who were discharged on jejunal feedings using a standard polymeric formula. of 26 initially malnourished patients. and a nasojejunal tube should be placed. All patients were advanced to full enteral support without aggravation of their abdominal pain. they noted a reduction in the need for surgery. beginning slowly and advancing progressively to full support. 2 after surgery. 16 improved. and 6 became worse (3 had pancreatic cancer. consideration can be given to placing a feeding jejunostomy laparoscopically to allow for home enteral nutrition. Of the 33 patients. NUTRITIONAL NEEDS Caloric Requirements Caloric needs are similar to those in other malnourished patients. Comparing nutritional status from beginning to end of therapy with respect to blood proteins and body weight. Causes for the pancreatitis included 8 alcohol. Modifications of the Harris-Benedict formula can be used. and 1 required home intravenous nutrition. and then cycling to nighttime feedings only. and initial nitrogen supplementation should . with 1 patient still on home therapy after 2067 days). Seventy-seven percent of patients achieved nutritional goals with minimal complications. and restoration of nutritional status based on weight gain. nausea. 3 pancreatic cancer. and there were no exacerbations of pancreatitis during home care requiring interruption of feedings. 4 were unchanged. 10 idiopathic. because there is usually only minimal stress present. 27 patients required readmission during their home care for complications unrelated to their feedings. Stanga and colleagues67 established home enteral nutrition using jejunal access in 57 patients. Average duration of home enteral feeding was 127 days (range 11–888. serum albumin. or avoided altogether. and diarrhea. and the caloric source should be divided between glucose and fat in a balanced standard formula. They concluded that use of home enteral nutrition was effective in most patients in maintaining or repleting nutritional status. vomiting. If this regimen is successful. Surgery could either be delayed until nutritional repletion had been accomplished. enteral feeding formula should be given. consideration should next be given to initiating enteral nutrition. decrease in narcotic use from 95% of patients to 27%. A trial of a low-fat. The patient should be hospitalized.816 Grant If dietary modulation does not improve nutrient intake and absorption. In addition. and especially if nutrient intake is complicated by abdominal pain. and 1 hypertriglyceridemia.

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