Pancreatitis

Acute Pancreatitis
An acute inflammatory process of the pancreas Varies from mild edema to
severe necrosis
Most common in middle-aged persons and African Americans
Definition
It is defined as acute nonbacterial inflammatory condition caused by
activation ,interstitial liberation, and autodigestion of pancreas presenting as
acute abdominal pain.
Acute Pancreatitis :
Etiology
Alcohol abuse ( 40 to 50% )
Major cause in India
Alcohol stimulates pancreatic secretions rich in protein, forms protein plugs and
results in obstruction of the pancreatic duct.
Alcohol stimulates trypsinogen.
It causes spasm of sphincter of Oddi.
It also has a direct toxic effect on the pancreas.
Tobacco smoking contributes to its effects.
Biliary tract disease
Stones in the biliary tract . 40% in western world .
In India 20 to 30 %
Collagen vascular disorders. Autoimmune disorders such as polyarteritis nodosa
Drugs: Corticosteroids, Tetracyclines, Oestrogens, Azathioprine, Valproic Acid,
And Diuretics.
Endoscopic procedures : Sphincterotomy, cannulation of CBD or pancreatic
duct, or basketing of stones from CBD, cause duct disruption and extravasation.
Familial or genetic factors. Hereditary pancreatitis may be due to mutation of
cationic trypsinogen gene. Symptoms begin in early childhood.
Hyperparathyroidism causing hypercalcemia may stimulate pancreatic juices. It
also facilitates precipitation of Ca in the ducts.
Hyperlipidemia ( > 1000mg per dl of triglycerides) .
Hypothermia and hypotension : can cause ischemia to the pancreas resulting in
acute pancreatitis.
Injury to the pancreas either postoperative or followingpenetrating injury.
Infection : Virus- Mumps, Coxsackie . Scorpion sting can also cause pancreatitis.
Ductal: 20%. Some of them are due to pancreatic divisum seen during ERCP. The
opening of the minor papillae is inadequate for drainageof pancreatic juice.
Idiopathic : 15 %.

Quick reference to common causes of pancreatitis

Pancreatitis in teens: suspect hereditary or APBDJ( Abnormal PancreaticoBiliary
Duct Junction ).
Pancreatitis in women : suspect gall stones
Pancreatitis in males: alcoholic pancreatitis
Pancreatitis with fleeting joint pain: autoimmune pancreatitis Pancreatitis
with bony lesions/cysts: hyperparathyroidism.
Pancreatitis with fever: viral .

Acute

Pancreatitis : Pathophysiology
Caused by autodigestion of pancreas
Injury to pancreatic cells
Activation of pancreatic enzymes
Activation of trypsinogen to trypsin . It acts and stimulates ……
Lipase :
Lipase splits the fat into fatty acids and glycerol.
Fatty acids combine with Ca to form Ca soap. This is represented as fat necrosis
seen in the omentum , subsynovial pockets of knee joint, etc.
This also explains hypocalcemia and tetany in acute pancreatitis.
Elastase
It digest the elastic fibers of blood vessels resulting in rupture and hemorrhage
into the peritoneal cavity.
Lysolecithinase
This is derived from the bile. It produces extensive tissue necrosis resulting in
destruction of pancreas.
Prostaglandins, bradykinins, kallikrein etc.
These are the inflammatory mediators.
They produce profound hypotension, shock and collapse due to loss of
fluid in the retroperitoneum.
Extensive necrosis of the pancreas.
It produces MDF ( Myocardial depressant factor) which depresses ventricular
contraction resulting in cardiac failure.
Ultimate result is the development of multi organ failure.
Mild pancreatitis
Edematous or interstitial
Severe pancreatitis
Necrotizing
Endocrine and exocrine dysfunction
Necrosis, organ failure, sepsis
Rate of mortality: 25%
Acute Pancreatitis: Clinical Manifestations
Abdominal pain predominant
Left upper quadrant or midepigastrium ,Radiates to the back
Sudden onset, increases over a period of hours.
Deep, piercing, continuous or steady ,Aggravated by eating/ alcohol.
Starts when recumbent
Not relieved with vomiting
Low grade fever.
Hematemesis and Malena can occur due to necrosis of duodenum.
It is a poor prognostic sign.
Signs
Febrile, tachypnoeic patient in agony
Cyanosis: improper perfusion of lungs
Faint jaundice due to oedema of the head of the pancreas.
Features of shock: feeble pulse, tachycardia , hypotension , cold extremities.
Abdominal findings
Tenderness in epigastrium
Upper abdominal guarding and rigidity
Distension of the abdomen
Mass in epigastrium
Muscle guarding
Abdominal distension due to either accumulation of blood or fluid in the
peritoneal cavity or due to paralytic ileus.
Cullen’s sign.
Bluish ecchymotic discolouration seen around umbilicus.
Grey Turner’s sign
Bluish discoloration in the flanks.
Both these signs are due to peri pancreatic and retroperitoneal hemorrhage
and seepage of blood along facial planes, into the anterior abdominal wall and
spread through falciform ligament.
Evidence of respiratory signs
Tachypnoea
Dullness
Effusion
Crepetations
Rhonchi- PULMONARY OEDEMA, ARDS.
Acute Pancreatitis: Complications
Pseudocyst
Fluid, enzyme, debris, and exudates surrounded by wall
Abdominal pain, palpable mass, nausea/vomiting, anorexia
Detected with imaging
Resolves spontaneously or may perforate and cause peritonitis
Surgical or endoscopic drainage
Pancreatic abscess
Collection of pus
Results from extensive necrosis
May perforate
Upper abdominal pain, mass, high fever, leukocytosis
Surgical drainage
Systemic complications
Pleural effusion
Atelectasis
Pneumonia
ARDS
Hypotension
Hypocalcemia: tetany
Diagnosis
Hb: low due to hemorrhagic pancreatitis
TC raised due to inflammation
BU, S.Cr. To rule out RF
S.Amylase:
Normal level 40 to 80 Somogyi Units.
Values around 400 are suggestive and > 1000 diagnostic of acute pancreatitis
It is increased in first 24 to 48 hrs and returns to normal within 3 to 4 days.
Persistent high level of amylase in acute pancreatitis indicates ………
Unresolving inflammation
Recurrent attacks of pancreatitis
Complications: pseudocyst, pancreatic abscess.
S.Lipase level – more specific, but difficult to measure .
Blood and urine sugar estimation: glycosuria is present in almost 100 %.
Lipase level tend to be higher in alcoholic pancreatitis and amylase levels are
higher in gallstone pancreatitis .
S. Ca : hypocalcemia due to hypoalbuminemia or fat necrosis.
Total protein usually low especially albumin
Plain X ray abdomen
Calcification suggests chronic pancreatitis.
Sentinal loop sign. : one dilated jejunal loop of intestine which is seen in the
region of pancreas.
USG ABDOMEN
Oedematous abdomen
Fluid in the abdomen or biliary tract disease.
Contrast enhanced CT Scan
Contrast enhanced CT Scan of abdomen is done after 3 to 5 days inpatients
who fail to respond to conservative treatment .
If CT Scan demonstrates infective necrosis an urgent CT guided FNAC is done
and Gram stain is sent.
If Gram Stain is positive , it has to be treated urgently.
Endoscopic ultrasonography (EUS)
Magnetic resonance cholangiopancreatography (MRCP)
Angiography
Chest x-ray

Acute Pancreatitis: Collaborative Care

Conservative therapy
Objectives include
Relief of pain
Prevention or alleviation of shock
↓ Pancreatic secretions
Correction of fluid/electrolyte imbalance
Prevention/treatment of infection
Removal of the precipitating cause
 CONSERVATIVE therapy
Supportive care
Aggressive hydration
Pain management
 IV morphine, antispasmodic agent
Management of metabolic complications
 Oxygen, glucose levels
Minimizing pancreatic stimulation
 NPO status, NG suction, decreased acid
secretion, enteral nutrition if needed
Shock
 Plasma or plasma volume expanders (dextran
or albumin)
Fluid/electrolyte imbalance
 Lactated Ringer’s solution
Ongoing hypotension
 Vasoactive drugs: dopamine (Intropin)
Prevent infection
 Enteral nutrition
 Antibiotics
 Endoscopically or CT-guided percutaneous
aspiration
Surgical therapy
For gallstones
 ERCP
  Cholecystectomy
Uncertain diagnosis
Not responding to conservative therapy
Drainage of necrotic fluid collections
Drug therapy
IV morphine
Antispasmodics
Carbonic anhydrase inhibitors
Antacids
Proton pump inhibitors
Nutritional therapy
NPO status initially
Enteral versus parenteral nutrition
Monitor triglycerides if IV lipids given
Small, frequent feedings when able
 High-carbohydrate
No alcohol
Supplemental fat-soluble vitamins
Acute Pancreatitis: Nursing Assessment
Subjective data
 Health history
Biliary tract disease
Alcohol use
Abdominal trauma
Duodenal ulcers
Infection
Metabolic disorders
 Medications
Thiazides
NSAIDs
 Surgery or other treatments
Pancreas, stomach, duodenum, biliary tract
ERCP
 functional health patterns
Alcohol abuse
Fatigue
Nausea, vomiting, anorexia
Dyspnea
Pain
Objective data
Restlessness, anxiety, low-grade fever
Flushing, diaphoresis
Discoloration of abdomen/flank
Cyanosis
Jaundice
Decreased skin turgor
Dry mucous membranes
Tachypnea
Basilar crackles
Tachycardia
Hypotension
Abdominal distention/tenderness
Diminished bowel sounds
 Abnormal laboratory findings
↑ Serum amylase/lipase levels
Leukocytosis
Hyperglycemia
Hypocalcemia
Abnormal findings on ultrasonography/CT scans
Abnormal findings on ERCP
Acute Pancreatitis: Nursing Diagnoses
Acute pain
Deficient fluid volume
Imbalanced nutrition: less than body requirements
Ineffective self-health management
Acute Pancreatitis : Planning
Patient will have
Relief of pain
Normal fluid and electrolyte balance
Minimal to no complications
No recurrent attacks
Nursing Implementation
Health promotion
Assessment and early treatment of predisposing/etiologic factors
Early diagnosis/treatment of biliary tract disease
Elimination of alcohol intake
Acute intervention
Monitoring vital signs
Assess respiratory function
Monitor IV fluids
 Acute intervention
Monitor fluid and electrolyte balance
Chloride, sodium, and potassium
Hypocalcemia
Tetany
Calcium gluconate to treat
Hypomagnesemia
 Acute intervention
Pain assessment and management
Morphine
Position of comfort with frequent position changes
Flex trunk and draw knees to abdomen
Side-lying with head of bed elevated 45 degrees
Frequent oral/nasal care
Proper administration of antacids
 Acute intervention
Observation for signs of infection
TCDB, semi-Fowler’s position
Wound care
Observation for paralytic ileus, renal failure, mental changes
Monitor serum glucose
Post-op wound care
 Ambulatory and home care
Physical therapy
Assessment of narcotic addiction
Counseling regarding abstinence from alcohol and smoking
 Ambulatory and home care
Dietary teaching
Low-fat, high-carbohydrate
No crash diets
Patient/family teaching
Signs of infection, diabetes mellitus, steatorrhea
Medications/diet
Expected outcomes
Have adequate pain control
Maintain adequate fluid volume
Be knowledgeable about treatment regimen
Get help for alcohol dependence ( if appropriate)

Chronic Pancreatitis
Continuous, prolonged inflammatory, and fibrosing process of the pancreas
Etiology
1. Alcohol
2. gallstones, tumor
3. pseudocysts, trauma
4. systemic disease
5. Acute pancreatitis
6. Idiopathic
Chronic Pancreatitis: Pathophysiology
Two major types
Chronic obstructive pancreatitis
Gallstones cause inflammation of sphincter of Oddi
Chronic nonobstructive pancreatitis
Inflammation and sclerosis in head of pancreas and around duct
: Clinical Manifestations
Abdominal pain
Located in the same areas as in acute pancreatitis
Heavy, gnawing feeling; burning and cramplike
Malabsorption with weight loss
Constipation, jaundice, icteric urine, steatorrhea, diabetes mellitus
Complications include
Pseudocyst formation
Bile duct or duodenal obstruction
Pancreatic ascites
Pleural effusion
Splenic vein thrombosis
Pseudoaneurysm
Pancreatic cancer
Chronic Pancreatitis: Diagnostic Studies
Confirming diagnosis can be challenging
Based on signs/symptoms, laboratory studies, and imaging
Laboratory tests
Serum amylase/lipase levels
May be ↑ slightly or not at all
↑ Serum bilirubin level
↑ Alkaline phosphatase level
Mild leukocytosis
↑ Sedimentation rate
ERCP
CT, MRI, MRCP, abdominal and/or endoscopic ultrasonography
Stool samples for fat content
↓ Fat-soluble vitamin and cobalamin levels
Glucose intolerance/diabetes
Secretin stimulation test
Chronic Pancreatitis: Collaborative Care
Analgesics for pain relief (morphine or fentanyl transdermal patch [Duragesic])
Diet
Bland, low-fat
Small, frequent meals No smoking
No alcohol or caffeine
Pancreatic enzyme replacement
Bile salts
Insulin or oral hypoglycemic agents
Acid-neutralizing and acid-inhibiting drugs
Antidepressants
Surgery
Indicated when biliary disease is present or if obstruction or pseudocyst
develops
Diverts bile flow or relieves ductal obstruction
Choledochojejunostomy
Roux-en-Y pancreatojejunostomy
Chronic Pancreatitis: Collaborative Care
Pancreatic drainage
ERCP with spincterotomy and/or stent placement
Chronic Pancreatitis: Nursing Management
Focus is on chronic care and health promotion Patient and family teaching
Dietary control
Pancreatic enzyme with meals/snack
Observe for steatorrhea
Monitor glucose levels
Antacids after meals and at bedtime
No alcohol