34 Nursing2016 L Volume 46, Number 8 Copyright 2016 .

Transcription

34 l Nursing2016 l Volume 46, Number 8Copyright 2016 Wolters Kluwer Health, Inc. All rights reserved.www.Nursing2016.com

2.0ANCCCONTACT HOURSUnderstandingacutepancreatitisJOHN BAVOSI /S CIENCE S OURCEBy Maureen E. Krenzer, MS, RN, ACNS-BCMR. W, 56, ENTERS THE ED reporting severeabdominal pain that started suddenly after hisevening meal. He describes it as constant andradiating to his back. He rates his pain as an 8on a 0-to-10 pain intensity rating scale. He tellsthe ED nurse who takes his history that he’s“probably been drinking too much” since helost his job a year ago.Lab tests reveal elevated levels of serum amylase and lipase. He’s N.P.O. and receiving I.V.fluids at 150 mL/hour. An abdominal ultrasound is negative for gallstones, but a computed tomography (CT) scan of the abdomenshows pancreatic inflammation. The patient isadmitted and the facility’s protocol for acutealcohol withdrawal is put into effect.Mr. W has classic signs and symptoms ofacute pancreatitis. The onset is usually abrupt,often occurring after a large meal or excessivealcohol use. Patients typically have severe,constant pain in the midepigastric region thatradiates to the back and flanks.Although common, acute pancreatitis ispotentially life-threatening, especially if complications occur. This article discusses the latestclinical information about pancreatitis and describes appropriate nursing interventions andpatient teaching.August l Nursing2016 l 35www.Nursing2016.comCopyright 2016 Wolters Kluwer Health, Inc. All rights reserved.

leads to micro- and macrovascularfailure as the activated digestive enzymes autodigest the pancreas andperipancreatic tissues. In the last stage, extrapancreatic orsystemic inflammation and injurymay occur.In mild pancreatitis, the stages areless severe and self-limiting.Gallstones and chronic alcoholabuse account for 90% of acute pancreatitis cases.2 When a gallstonelodges in the common bile duct, theobstruction raises pancreatic ductalpressure and leads to inflammationand rupture of the small pancreaticducts, resulting in premature activation of pancreatic enzymes. Alcoholincreases the tendency for production of pancreatic secretions and formation of protein plugs within thepancreatic ducts. The multifactorialeffect of alcohol on the acinar cellsmay obstruct the flow of pancreaticsecretions and lead to inflammationand pancreatic damage. Spasms ofPathogenesis of acute pancreatitisthe sphincter of Oddi may also leadto inflammation, although these results have been controversial.1Acute pancreatitis in pregnancy isa rare event but can lead to pretermlabor and delivery.3 (See What cantrigger acute pancreatitis? for morepotential causes).Classifying typesof pancreatitisThe most common type of pancreatitis is mild acute pancreatitis, alsocalled interstitial or edematous pancreatitis. Areas of fat necrosis andinterstitial edema develop in andaround the pancreas (the peripancreatic tissues). Mild acute pancreatitis is usually self-limiting withoutorgan failure or local or systemiccomplications.Severe acute pancreatitis, alsoknown as necrotizing pancreatitis, isa life-threatening disorder associatedwith local and systemic complications including intra-abdominal infections, pancreatic necrosis, andorgan failure.4 An additional type,moderately severe acute pancreatitis, isdescribed as transient organ failureor local or systemic complications.(See Severity of pancreatitis for abreakdown of levels.)Key assessment findingsThe most common symptom ofacute pancreatitis is a sudden onsetof sharp, twisting, deep, upper abdominal pain. It frequently radiatesto the back and is associated withnausea and vomiting. Localized paincommonly reflects mild acute pancreatitis, while more diffuse painmay be associated with severe ornecrotizing pancreatitis. The degreeof pain may or may not reflect theseverity of the disease process.Other common signs and symptoms of acute pancreatitis are anorexia, hypoactive bowel sounds,upper abdominal tenderness withoutrigidity, abdominal distension, anddiarrhea. In more severe cases, the36 l Nursing2016 l Volume 46, Number 8Copyright 2016 Wolters Kluwer Health, Inc. All rights reserved.www.Nursing2016.comIMAGE FROM RUBIN E MD AND FARBER JL MD. PATHOLOGY, 3RD EDITION. P HILADELPHIA:L IPPINCOTT WILLIAMS & WILKINS, 1999.Inflammation triggersautodigestionBesides producing insulin, the pancreas secretes digestive enzymes.Acute pancreatitis is characterized bypancreatic inflammation resulting inautodigestion, or the breakdown ofpancreatic tissue by its own activatedenzymes. (See Pathogenesis of acutepancreatitis.)Normally, pancreatic enzymesdon’t become active until they leavethe pancreas. During pancreatitis,however, inflammation delays releaseof activated enzymes, giving themtime to attack pancreatic cells andleak into surrounding tissues. Thisprocess causes more inflammation.The damage in acute pancreatitisoccurs in stages:1 Premature activation of trypsin,amylase, lipase, and other enzymesoccurs inside the pancreas. Intrapancreatic inflammationthrough the release of cytokines andother proinflammatory mediators

patient may have fever, tachycardia,hypotension, weakness, diaphoresis,shock, jaundice, and peritonealsigns, such as guarding and reboundtenderness.5,6 An abdominal massmay be palpable due to the enlargedpancreas.A diagnosis of acute pancreatitisrequires at least two of the following:7 characteristic abdominal pain serum amylase and/or lipase levelat least three times the upper limit ofnormal. These enzymes leak into theblood as pancreatic cells are damaged. (See Serum lab testing for acutepancreatitis.) characteristic findings from abdominal imaging (CT scan, magneticresonance imaging, or ultrasound).What diagnostic tests revealThe healthcare provider may orderthese tests to examine the pancreasand surrounding region. An abdominal ultrasound can helpdetermine the presence of gallstonesquickly, noninvasively, and withoutradiation. An abdominal CT scan is usuallyperformed with contrast to confirman unclear diagnosis and to evaluatethe extent of damage to the pancreasand surrounding region. The nurseshould evaluate the patient’s renalfunction and assess for a history ofadverse reactions to contrast media. Endoscopic retrograde cholangiopancreatography (ERCP), an invasivediagnostic procedure, uses an endoscope to view the ampulla of Vater,pancreas, and bile ducts. ERCP requires contrast medium and fluoroscopy. An advantage of ERCP is that itcan also be used to remove obstructions such as gallstones, performbiopsies, and/or insert a stent topromote drainage. Magnetic resonance cholangiopancreatography (MRCP) is a noninvasiveprocedure that allows visualizationof the biliary tree and pancreaticducts. This doesn’t involve contrastmedia and is less risky for the patientWhat can trigger acute pancreatitis?12,13,16,17 alcohol abuse gallstones, microlithiasis, or biliary sludge obstructing the common bile duct drugs such as acid-suppressing medications, immunomodulators, diuretics,antimicrobials, nonsteroidal anti-inflammatory medications hypercalcemia hypertriglyceridemia ( 1,000 mg/dL) idiopathic; may also develop during pregnancy and postpartum period infections: viral: mumps, coxsackie virus, cytomegalovirus, HAV, HBV, HIV/AIDS;bacterial: mycoplasma, legionella, salmonella; fungal: aspergillus, candida albicans;parasitic: toxoplasma, cryptosporidium inflammatory bowel disease pancreas divisum pancreatic tumors peptic ulcer disease parenteral nutrition scorpion envenomation trauma: blunt or penetrating abdominal trauma; post-ERCP; surgical trauma toxins hypothermia.Severity of pancreatitis15Mild acute pancreatitis No organ failure Lack of local or systemic complicationsModerately severe acute pancreatitis Organ failure that resolves in 48 hours (transient) Local or systemic complications without persistent organ failureSevere acute pancreatitis Persistent single or multiple organ failure ( 48 hours).than ERCP. MRCP may be an alternative for a patient with a history ofadverse reactions to contrast media.The treatment plan after diagnosisdepends on whether pancreatitis ismild or severe. Making this determination can be challenging. Multiplescoring systems exist that may helpto predict outcomes of acute pancreatitis but many of them, such as theRanson criteria, require 48 hours foradditional blood work and completeassessment. The Bedside Index ofSeverity in Acute Pancreatitis (BISAP)and the Harmless Acute PancreatitisScore (HAPS) may be helpful duringinitial assessment for severity in theED.8 BISAP uses vital signs, mentalstatus, age, blood urea nitrogen(BUN), white blood cell count, andpleural effusion detected on imaging;Serum lab testing foracute pancreatitis14In addition to amylase and lipase,additional lab testing may include: complete blood cell count withdifferential electrolytes BUN, creatinine, glucose coagulation studies liver enzymes lactate albumin.all usually completed on presentation to ED.9 HAPS uses absenceof rebound tenderness, creatinine 2 mg/dL, and normal hematocrit topredict mild cases of acute pancreatitis.8 Looking at factors such as age,body mass index, comorbidities, labAugust l Nursing2016 l 37www.Nursing2016.comCopyright 2016 Wolters Kluwer Health, Inc. All rights reserved.

values, and systemic inflammatoryresponse syndrome (SIRS) to determine those most at risk for developing organ failure is recommended.4(See Understanding SIRS criteria.)After the patient has been diagnosed with acute pancreatitis, thenurse should frequently check vitalsigns and lab values. Likely findingsinclude an increased white blood cell(WBC) count, tachycardia, and feverdue to the inflammatory process.Mild confusion and hypoxemia arealso common, the patient’s pulse oximetry should be monitored andsupplemental oxygen provided ifindicated.Managing the acute episodeTreating an episode of acute pancreatitis includes supportive care andcurative interventions when possible. The first goal is to stabilize thepatient hemodynamically. Administer I.V. crystalloids such as lactatedRinger’s solution or colloids andplasma expanders for more criticallyill patients, as prescribed. Early aggressive I.V. hydration has been associated with less complications andimproved outcomes.4 Monitor vitalsigns, oxygen saturation, pain intensity level, intake and output, hematocrit, and BUN levels to help assesshemodynamic stability. A patientwith severe acute pancreatitis mayneed support with an inotropicdrug such as I.V. dobutamine, hemodynamic monitoring, mechanicalUnderstanding SIRScriteria4SIRS is defined as two or more of thefollowing: temperature, 36 C (96.8 F) or 38 C (100.4 F) respiratory rate 20 breaths/minuteor PaCO2 32 mm Hg pulse 90 beats/minute WBC count 4.0 or 12.0 cells/mm3or 10% immature neutrophils(bands).ventilation, and monitoring of intraabdominal pressure via the bladderfor development of abdominal compartment syndrome.As prescribed, manage pain withan opioid such as fentanyl or hydromorphone. Besides making the patient more comfortable, these drugsdecrease pancreatic enzyme secretion.Consistently assess the patient’s painusing the same pain intensity ratingscale each time to determine changing patterns of pain and evaluate thepatient’s response to treatment.Reducing the stimulation of pancreatic enzyme release as much aspossible reduces inflammation andautodigestion until the pancreasheals. Eating stimulates pancreaticsecretions, so keep the patientN.P.O. until nausea and vomitinghave resolved, serum amylase levelsstart returning to normal, and painsubsides. Although still controversial, the type of diet to resume can beanything from clear liquids to a softlow-fat diet and does not require astepwise approach.7 In mild acutepancreatitis, this may take 3 to 7days. In severe pancreatitis, recoverymay take up to 7 weeks. The patientmay need a nasogastric tube to manage vomiting or paralytic ileus.Severe acute pancreatitis is a hypermetabolic and hypercatabolicevent that requires nutritionalsupport. Enteral feeding via a nasogastric or jejunal tube is safe andrecommended for those requiringnutritional support. Enteral feedingstabilizes gut bacteria, which prevents bacterial translocation andsubsequent infection, and is morephysiologic than parenteral nutrition(PN). PN should be used as a secondline for those who can’t meet nutritional requirements or tolerateenteral feeding.7Treating acute pancreatitis alsoincludes addressing the precipitatingevent. If the patient has mild gallstone pancreatitis, for example, cholecystectomy during this admissionis recommended.10 If the patient hasan obstructing gallstone, the pancreatic inflammation may need moretime to resolve with conservativetreatment, so the patient may bedischarged home with a plan forfollow-up surgery when the acuteinflammatory issues are resolved.If the patient continues to experiencesevere pain, the obstruction may berelieved via ERCP, but many patientshave recurrent episodes and requiresubsequent gallbladder removal.7For patients with acute cholangitis,urgent ERCP and sphincterotomymay be necessary.6Possible systemiccomplicationsPatients with severe acute pancreatitis are at risk for various systemiccomplications. (See On guard forcomplications of severe acute pancreatitis.) For example, most patients withsevere acute pancreatitis experiencehypoxemia or other respiratory issues in the first 2 days.11 Risk factorssuch as obesity, age ( 55), medicalcomorbidities, presence of hypovolemia, SIRS, mental status changes onpresentation, pleural effusion or infiltrates, and multiple or extensivefluid collections outside of the pancreas are associated with development of severe disease.12Routine nursing care should include the following: Monitor patients for early signs andsymptoms of complications, such asincreased abdominal pain and tenderness, fever, and WBC count.Changes in mental status are ea

Treating acute pancreatitis also includes addressing the precipitating event. If the patient has mild gall-stone pancreatitis, for example, cho-lecystectomy during this admission is recommended.10 If the patient has an obstructing gallstone, the pancre-atic inflammation may need more time to resolve with conservative treatment, so the patient may be