askep pankreatitis
TRANSCRIPT
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Pancreatitis
Konsep Medis Dan
Asuhan Keperawatan
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Suatu proses peradangan akut pada pankreas. Derajat peradangan bervariasi dari sedang-
edema-nekrosis.
Acute PancreatitisDefinition
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Kebanyakan terjadi pada usia pertengahan. Derajat keperahan penyakit tergantung pada
seberapa besar kerusakan pankreas. Bisa Mengancam Nyawa.
Acute PancreatitisEtiology and
Pathophysiology
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Primary etiologic factors are
Biliary tract disease Most common: Gallbladder disease
Alcoholism
Acute PancreatitisEtiology and
Pathophysiology
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Less common causes
Trauma (postsurgical, abdominal) Viral infections (mumps, coxsackievirus HIV) Penetrating duodenal ulcer Cysts Idiopathic
Acute PancreatitisEtiology and
Pathophysiology
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Less common causes (cont’d)
Abscesses Cystic fibrosis Kaposi’s sarcoma Metabolic disorders Vascular diseases Postop GI surgery
Acute PancreatitisEtiology and
Pathophysiology
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Less common causes (cont’d)
Drugs Corticosteroids Thiazide diuretics Oral contraceptives Sulfonamides NSAIDs
Acute PancreatitisEtiology and
Pathophysiology
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Caused by autodigestion of pancreas Etiologic factors
Injury to pancreatic cells Activate pancreatic enzymes
Acute PancreatitisEtiology and
Pathophysiology
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Acute Pancreatitis
Fig. 44-14
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Trypsinogen
Activated to trypsin by enterokinase Inhibitors usually inactivate trypsin Enzyme can digest the pancreas and can
activate other proteolytic enzymes
Acute PancreatitisEtiology and
Pathophysiology
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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
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Phospholipase A
Plays a major role in autodigestion Activated by trypsin and bile acids Causes fat necrosis
Acute PancreatitisEtiology and
Pathophysiology
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Acute PancreatitisEtiology and
PathophysiologyTrypsin Edema, necrosis,
hemorrhageElastase Hemorrhage
Phospholipase A Fat necrosis
Kallikrein Edema, vascular permeability, smooth muscle contraction, shock
Lipase Fat necrosis
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Alcohol
May stimulate production of digestive enzymes Increases sensitivity to hormone
cholecystokinin Stimulates production of pancreatic enzymes
Acute Pancreatitis Etiology and
Pathophysiology
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Edematous pancreatitis
Mild and self-limiting Necrotizing pancreatitis
Degree of necrosis correlates with severity of manifestations
Acute PancreatitisEtiology and
Pathophysiology
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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
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Abdominal pain (cont’d)
Sudden onset Severe, deep, piercing, steady Aggravated by eating Not relieved by vomiting
Acute PancreatitisClinical Manifestations
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Flushing Cyanosis Dyspnea Edema Nausea/vomiting Bowel sounds decreased or absent
Acute PancreatitisClinical Manifestations
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Low-grade fever Leukocytosis Hypotension Tachycardia Jaundice Abdominal tenderness
Acute PancreatitisClinical Manifestations
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Abdominal distention Abnormal lung sounds
Crackles Discoloration of abdominal wall
Acute PancreatitisClinical
Manifestations
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Two significant local complications
Pseudocyst Abscess
Acute PancreatitisComplications
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Pseudocyst
Cavity surrounding outside of pancreas filled with necrotic products and liquid secretions
Abdominal pain Palpable epigastric mass
Acute PancreatitisComplications
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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
Acute PancreatitisComplications
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Pancreatic abscess
A large fluid-containing cavity within pancreas Results from extensive necrosis in the pancreas Upper abdominal pain Abdominal mass
Acute Pancreatitis Complications
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Pancreatic abscess (cont’d)
High fever Leukocytosis Requires surgical drainage
Acute Pancreatitis Complications
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Main systemic complications
Pulmonary Pleural effusion Atelectasis Pneumonia
Acute PancreatitisComplications
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Systemic complications (cont’d)
Cardiovascular Hypotension
Tetany (caused by hypocalcemia)
Acute PancreatitisComplications
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History and physical examination Laboratory tests
Serum amylase Serum lipase 2-hour urinary amylase and renal amylase
clearance
Acute PancreatitisDiagnostic Studies
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Laboratory tests (cont’d) Blood glucose Serum calcium Triglycerides
Acute PancreatitisDiagnostic Studies
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Flat plate of abdomen Abdominal/endoscopic ultrasound Endoscopic retrograde
cholangiopancreatography (ERCP) Chest x-ray
Acute PancreatitisDiagnostic Studies
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are needed to see this picture.
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CT of pancreas Magnetic resonance
cholangiopancreatography (MRCP)
Acute PancreatitisDiagnostic Studies
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Objectives include
Relief of pain Prevention or alleviation of shock ↓ of pancreatic secretions Fluid/electrolyte balance Removal of the precipitating cause
Acute PancreatitisCollaborative Care
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Conservative therapy
Supportive care Aggressive hydration Pain management
IV morphine Combined with antispasmodic agent
Management of metabolic complications Minimizing stimulation
Acute PancreatitisCollaborative Care
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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
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Conservative therapy (cont’d)
Suppression of pancreatic enzymes NPO NG suction
Prevent infections Peritoneal lavage or dialysis
Remove kinin and phospholipase A exudate
Acute PancreatitisCollaborative Care
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Surgical therapy indicated if
Presence of gallstones Uncertain diagnosis Unresponsive to conservative therapy Abscess, pseudocyst, or severe peritonitis
Acute PancreatitisCollaborative Care
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Surgical therapy
ERCP Endoscopic sphincterotomy Laparoscopic cholecystectomy
Acute PancreatitisCollaborative Care
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Drug therapy
IV morphine Nitroglycerin or papaverine Antispasmodics Carbonic anhydrase inhibitor Antacids Histamine (H2) receptor
Acute PancreatitisCollaborative Care
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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
Acute PancreatitisCollaborative Care
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Nutritional therapy (cont’d)
Supplemental fat-soluble vitamins Supplemental commercial liquid preparations Parenteral nutrition No caffeine or alcohol
Acute PancreatitisCollaborative Care
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Health history
Biliary tract disease Alcohol use Abdominal trauma Duodenal ulcers Infection Metabolic disorders
Acute PancreatitisNursing Assessment
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Medication usage
Thiazides, estrogens, corticosteroids, NSAIDs
Surgical procedures Nausea/vomiting Dyspnea Severe pain
Acute PancreatitisNursing Assessment
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Physical examination findings
Fever Jaundice Discoloration of abdomen/flank Tachycardia Hypotension Abdominal distention/tenderness
Acute PancreatitisNursing Assessment
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Abnormal laboratory findings
↑ Serum amylase/lipase Leukocytosis Hyperglycemia Hyperlipidemia Hypocalcemia Abnormal ultrasound/ CT/ ERCP
Acute PancreatitisNursing Assessment
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Acute pain Deficient fluid volume Imbalanced nutrition: Less than body
requirements Ineffective therapeutic regimen management
Acute PancreatitisNursing Diagnoses
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Overall goals
Relief of pain Normal fluid and electrolyte balance Minimal to no complications No recurrent attacks
Acute PancreatitisPlanning
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Health promotion
Assessment of predisposing factors Early diagnosis/treatment of cholelithiasis Eliminate alcohol intake
Acute PancreatitisNursing
Implementation
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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
Acute PancreatitisNursing
Implementation
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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
Acute PancreatitisNursing
Implementation
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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
Acute PancreatitisNursing
Implementation
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Ambulatory and home care
Physical therapy Counseling regarding abstinence from alcohol,
caffeine, and smoking Assessment of narcotic addiction
Acute PancreatitisNursing
Implementation
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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
Acute PancreatitisNursing
Implementation
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Expected outcomes
Maintains adequate fluid volume Maintains weight appropriate for height Food and fluid intake adequate to meet
nutritional needs
Acute PancreatitisNursing
Implementation
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Expected outcomes (cont’d)
Describes therapeutic regimen Expresses commitment to lifestyle changes
Acute PancreatitisNursing
Implementation
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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
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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
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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
Chronic PancreatitisEtiology and
Pathophysiology
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Chronic calcifying pancreatitis
Inflammation Sclerosis
Mainly in the head of the pancreas and around the pancreatic duct
Chronic PancreatitisEtiology and
Pathophysiology
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Chronic calcifying pancreatitis
Most common form of chronic pancreatitis May be referred to as alcohol-induced
pancreatitis
Chronic PancreatitisEtiology and
Pathophysiology
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Chronic calcifying pancreatitis
Ducts are obstructed with protein precipitates Precipitates block the pancreatic duct and
eventually calcify
Chronic PancreatitisEtiology and
Pathophysiology
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Chronic calcifying pancreatitis
Calcification is followed by fibrosis and glandular atrophy
Pseudocysts and abscesses commonly develop
Chronic PancreatitisEtiology and
Pathophysiology
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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
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Constipation Mild jaundice with dark urine Steatorrhea Frothy urine/stool Diabetes mellitus
Chronic PancreatitisClinical Manifestations
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Complications include
Pseudocyst formation Bile duct or duodenal obstruction Pancreatic ascites Pleural effusion
Chronic PancreatitisClinical
Manifestations
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Complications (cont’d)
Splenic vein thrombosis Pseudoaneurysms Pancreatic cancer
Chronic PancreatitisClinical
Manifestations
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Confirming diagnosis can be challenging Based on signs/symptoms, laboratory studies,
and imaging
Chronic PancreatitisDiagnostic Studies
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Laboratory tests
Serum amylase/lipase May be ↑ slightly or not at all
↑ Serum bilirubin ↑ Alkaline phosphatase
Chronic PancreatitisDiagnostic Studies
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Laboratory tests (cont’d)
Mild leukocytosis Elevated sedimentation rate
ERCP Visualize pancreatic/common bile duct
Chronic PancreatitisDiagnostic Studies
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CT MRI MRCP Transabdominal ultrasound
Chronic PancreatitisDiagnostic Studies
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Endoscopic ultrasound Secretin stimulation test
Assess degree of pancreatic function Not useful in diagnosis
Chronic PancreatitisDiagnostic Studies
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Prevention of attacks
During acute attack follow acute therapy Relief of pain Control of pancreatic exocrine and endocrine
insufficiency
Chronic PancreatitisCollaborative Care
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Bland low-fat, high-carbohydrate diet Bile salts
Help absorption of fat-soluble vitamins Prevent further fat loss
Control of diabetes No alcohol
Chronic PancreatitisCollaborative Care
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Pancreatic enzyme replacement Acid-neutralizing and acid-inhibiting drugs
Chronic PancreatitisCollaborative Care
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Surgery
Indicated when biliary disease is present or if obstruction or pseudocyst develops
Divert bile flow or relieve ductal obstruction
Chronic PancreatitisCollaborative Care
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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