ASKEP PANKREATITIS

Copyright © 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved.

Pancreatitis

Konsep Medis Dan

Asuhan Keperawatan


Suatu proses peradangan akut pada pankreas. Derajat peradangan bervariasi dari sedang-

edema-nekrosis.

Acute PancreatitisDefinition


Kebanyakan terjadi pada usia pertengahan. Derajat keperahan penyakit tergantung pada

seberapa besar kerusakan pankreas. Bisa Mengancam Nyawa.

Acute PancreatitisEtiology and

Pathophysiology


Primary etiologic factors are

Biliary tract disease Most common: Gallbladder disease

Alcoholism


Pathophysiology


Less common causes

Trauma (postsurgical, abdominal) Viral infections (mumps, coxsackievirus HIV) Penetrating duodenal ulcer Cysts Idiopathic


Pathophysiology


Less common causes (cont’d)

Abscesses Cystic fibrosis Kaposi’s sarcoma Metabolic disorders Vascular diseases Postop GI surgery


Pathophysiology


Less common causes (cont’d)

Drugs Corticosteroids Thiazide diuretics Oral contraceptives Sulfonamides NSAIDs


Pathophysiology


Caused by autodigestion of pancreas Etiologic factors

Injury to pancreatic cells Activate pancreatic enzymes


Pathophysiology


Acute Pancreatitis

Fig. 44-14


Trypsinogen

Activated to trypsin by enterokinase Inhibitors usually inactivate trypsin Enzyme can digest the pancreas and can

activate other proteolytic enzymes


Pathophysiology


Elastase

Activated by trypsin Plays a major role in autodigestion Causes hemorrhage by producing dissolution of

the elastic fibers of blood vessels

PancreatitisEtiology and

Pathophysiology


Phospholipase A

Plays a major role in autodigestion Activated by trypsin and bile acids Causes fat necrosis


Pathophysiology



PathophysiologyTrypsin Edema, necrosis,

hemorrhageElastase Hemorrhage

Phospholipase A Fat necrosis

Kallikrein Edema, vascular permeability, smooth muscle contraction, shock

Lipase Fat necrosis


Alcohol

May stimulate production of digestive enzymes Increases sensitivity to hormone

cholecystokinin Stimulates production of pancreatic enzymes

Acute Pancreatitis Etiology and

Pathophysiology


Edematous pancreatitis

Mild and self-limiting Necrotizing pancreatitis

Degree of necrosis correlates with severity of manifestations


Pathophysiology


Abdominal pain is predominant symptom

Pain located in the left upper quadrant Pain may be in the midepigastrium Commonly radiates to the back

Acute PancreatitisClinical Manifestations


Abdominal pain (cont’d)

Sudden onset Severe, deep, piercing, steady Aggravated by eating Not relieved by vomiting



Flushing Cyanosis Dyspnea Edema Nausea/vomiting Bowel sounds decreased or absent



Low-grade fever Leukocytosis Hypotension Tachycardia Jaundice Abdominal tenderness



Abdominal distention Abnormal lung sounds

Crackles Discoloration of abdominal wall

Acute PancreatitisClinical

Manifestations


Two significant local complications

Pseudocyst Abscess

Acute PancreatitisComplications


Pseudocyst

Cavity surrounding outside of pancreas filled with necrotic products and liquid secretions

Abdominal pain Palpable epigastric mass



Pseudocyst (cont’d)

Nausea, vomiting, and anorexia Elevated serum amylase May resolve spontaneously within a few weeks

or may perforate, causing peritonitis Treatment: Internal drainage procedure



Pancreatic abscess

A large fluid-containing cavity within pancreas Results from extensive necrosis in the pancreas Upper abdominal pain Abdominal mass

Acute Pancreatitis Complications


Pancreatic abscess (cont’d)

High fever Leukocytosis Requires surgical drainage

Acute Pancreatitis Complications


Main systemic complications

Pulmonary Pleural effusion Atelectasis Pneumonia



Systemic complications (cont’d)

Cardiovascular Hypotension

Tetany (caused by hypocalcemia)



History and physical examination Laboratory tests

Serum amylase Serum lipase 2-hour urinary amylase and renal amylase

clearance

Acute PancreatitisDiagnostic Studies


Laboratory tests (cont’d) Blood glucose Serum calcium Triglycerides



Flat plate of abdomen Abdominal/endoscopic ultrasound Endoscopic retrograde

cholangiopancreatography (ERCP) Chest x-ray



QuickTime™ and aYUV420 codec decompressor

are needed to see this picture.


CT of pancreas Magnetic resonance

cholangiopancreatography (MRCP)



Objectives include

Relief of pain Prevention or alleviation of shock ↓ of pancreatic secretions Fluid/electrolyte balance Removal of the precipitating cause

Acute PancreatitisCollaborative Care


Conservative therapy

Supportive care Aggressive hydration Pain management

IV morphine Combined with antispasmodic agent

Management of metabolic complications Minimizing stimulation



Conservative therapy (cont’d)

Shock Plasma or plasma volume expanders

(dextran or albumin) Fluid/electrolyte imbalance

Lactated Ringer’s solution Ongoing hypotension

Vasoactive drugs: Dopamine (Intropin) ↑ Systemic vascular resistance

Acute Pancreatitis Collaborative Care


Conservative therapy (cont’d)

Suppression of pancreatic enzymes NPO NG suction

Prevent infections Peritoneal lavage or dialysis

Remove kinin and phospholipase A exudate



Surgical therapy indicated if

Presence of gallstones Uncertain diagnosis Unresponsive to conservative therapy Abscess, pseudocyst, or severe peritonitis



Surgical therapy

ERCP Endoscopic sphincterotomy Laparoscopic cholecystectomy



Drug therapy

IV morphine Nitroglycerin or papaverine Antispasmodics Carbonic anhydrase inhibitor Antacids Histamine (H2) receptor



Nutritional therapy NPO status initially to reduce pancreatic secretion IV lipids

Monitor triglycerides Small, frequent feedings High-carbohydrate, low-fat,

high-protein diet Bland diet



Nutritional therapy (cont’d)

Supplemental fat-soluble vitamins Supplemental commercial liquid preparations Parenteral nutrition No caffeine or alcohol



Health history

Biliary tract disease Alcohol use Abdominal trauma Duodenal ulcers Infection Metabolic disorders

Acute PancreatitisNursing Assessment


Medication usage

Thiazides, estrogens, corticosteroids, NSAIDs

Surgical procedures Nausea/vomiting Dyspnea Severe pain



Physical examination findings

Fever Jaundice Discoloration of abdomen/flank Tachycardia Hypotension Abdominal distention/tenderness



Abnormal laboratory findings

↑ Serum amylase/lipase Leukocytosis Hyperglycemia Hyperlipidemia Hypocalcemia Abnormal ultrasound/ CT/ ERCP



Acute pain Deficient fluid volume Imbalanced nutrition: Less than body

requirements Ineffective therapeutic regimen management

Acute PancreatitisNursing Diagnoses


Overall goals

Relief of pain Normal fluid and electrolyte balance Minimal to no complications No recurrent attacks

Acute PancreatitisPlanning


Health promotion

Assessment of predisposing factors Early diagnosis/treatment of cholelithiasis Eliminate alcohol intake

Acute PancreatitisNursing

Implementation


Acute intervention Monitor vital signs IV fluids Observe for side effects of medications Assess respiratory function Pain assessment and management

Frequent position changes Side-lying with HOB elevated 45 degrees Knees up to abdomen


Implementation


Acute intervention (cont’d) Fluid/electrolyte balance

Blood glucose monitoring Monitor for signs of hypocalcemia

Tetany (jerking, irritability, twitching) Numbness around lips/fingers Positive Chvostek or Trousseau sign

Monitor for hypomagnesemia


Implementation


Acute intervention (cont’d)

NG tube care Frequent oral/nasal care Observe for signs of infection Wound care Observe for paralytic ileus, renal failure, mental

changes


Implementation


Ambulatory and home care

Physical therapy Counseling regarding abstinence from alcohol,

caffeine, and smoking Assessment of narcotic addiction


Implementation


Ambulatory and home care (cont’d)

Dietary teaching High-carbohydrate, low-fat diet

Patient/family teaching Signs of infection, high blood glucose, steatorrhea Medications/diet


Implementation


Expected outcomes

Maintains adequate fluid volume Maintains weight appropriate for height Food and fluid intake adequate to meet

nutritional needs


Implementation


Expected outcomes (cont’d)

Describes therapeutic regimen Expresses commitment to lifestyle changes


Implementation


Continuous, prolonged inflammatory, and

fibrosing process of the pancreas Pancreas becomes destroyed as it is replaced

by fibrotic tissue Strictures and calcifications can also occur

Chronic PancreatitisDefinition


May follow acute pancreatitis May occur in absence of any history of acute

condition Two major types

Chronic obstructive pancreatitis Chronic calcifying pancreatitis

Chronic PancreatitisEtiology and

Pathophysiology


Chronic obstructive pancreatitis Associated with biliary disease

Most common cause Inflammation of the sphincter of Oddi associated with

cholelithiasis

Other causes include Cancer of ampulla of Vater, duodenum, or pancreas


Pathophysiology


Chronic calcifying pancreatitis

Inflammation Sclerosis

Mainly in the head of the pancreas and around the pancreatic duct


Pathophysiology



Most common form of chronic pancreatitis May be referred to as alcohol-induced

pancreatitis


Pathophysiology



Ducts are obstructed with protein precipitates Precipitates block the pancreatic duct and

eventually calcify


Pathophysiology



Calcification is followed by fibrosis and glandular atrophy

Pseudocysts and abscesses commonly develop


Pathophysiology


Abdominal pain

Located in the same areas as in acute pancreatitis

Heavy, gnawing feeling; burning and cramp-like Abdominal tenderness Malabsorption with weight loss

Chronic PancreatitisClinical Manifestations


Constipation Mild jaundice with dark urine Steatorrhea Frothy urine/stool Diabetes mellitus

Chronic PancreatitisClinical Manifestations


Complications include

Pseudocyst formation Bile duct or duodenal obstruction Pancreatic ascites Pleural effusion

Chronic PancreatitisClinical

Manifestations


Complications (cont’d)

Splenic vein thrombosis Pseudoaneurysms Pancreatic cancer

Chronic PancreatitisClinical

Manifestations


Confirming diagnosis can be challenging Based on signs/symptoms, laboratory studies,

and imaging

Chronic PancreatitisDiagnostic Studies


Laboratory tests

Serum amylase/lipase May be ↑ slightly or not at all

↑ Serum bilirubin ↑ Alkaline phosphatase



Laboratory tests (cont’d)

Mild leukocytosis Elevated sedimentation rate

ERCP Visualize pancreatic/common bile duct



CT MRI MRCP Transabdominal ultrasound



Endoscopic ultrasound Secretin stimulation test

Assess degree of pancreatic function Not useful in diagnosis



Prevention of attacks

During acute attack follow acute therapy Relief of pain Control of pancreatic exocrine and endocrine

insufficiency

Chronic PancreatitisCollaborative Care


Bland low-fat, high-carbohydrate diet Bile salts

Help absorption of fat-soluble vitamins Prevent further fat loss

Control of diabetes No alcohol



Pancreatic enzyme replacement Acid-neutralizing and acid-inhibiting drugs



Surgery

Indicated when biliary disease is present or if obstruction or pseudocyst develops

Divert bile flow or relieve ductal obstruction



Focus is on chronic care and health promotion

Dietary control No alcohol

Control of diabetes Taking pancreatic enzymes Patient and family teaching

Chronic PancreatitisNursing Management

Documents

ASKEP PANKREATITIS