PANCREATITIS

DEFINITION OF PANCREATITIS:

Pancreatitis is an inflammation of the pancreas resulting in autodigestion of the pancreas by

its own enzymes, is fairly Common.

However, it is potentially lethal inflammatory process associated with edema, various

amounts of autodigestion, fat necrosis and sometimes hemorrhage.

-Brunner & suddarth’s

TYPES:

There are two types:

1. Acute pancreatitis
2. chronic pancreatitis.

ACUTE PANCREATITIS:

Acute pancreatitis is an acute inflammation of the pancreas. The degree of inflammation

varies from mild edema to severe hemorrhagic necrosis. Acute pancreatitis is common in
middle aged men and women.

The main two types of acute Pancreatitis (mild and severe) are classified as

1. Intestinal edematous pancreatitis.

2. Necrotizing pancreatitis

-Brunner and suddarth’s

INTESTINAL EDEMATOUS PANCREATITIS:

 It affects the majority of patients.

 It is characterized by a lack of Pancreatic (or) peripancreatic parenchymal neurons
with diffuse enlargement of the gland due to inflammatory edema.
  The edema and inflammation in intestinal Pancreatitis is confined to the pancreas
itself.
 Minimal organ dysfunction is present and return to normal function usually occurs
within 6 months.

NECROTIZINGY PANCREATITIS:

 There is presence of tissue necrosis in either the pancreatic parenchyma or in the

tissue surrounding the gland.
 A more widespread and complete enzymatic digestion of the gland characterizes
necrotizing pancreatitis.

CAUSES:

Alcohol abuse (40 to 50%):

 It is the major cause of acute pancreatitis in our Country and is seen in about 50%. of
the cases.
 Alcohol stimulates pancreatic secretions rich in protein, forms protein plugs and
results in obstruction to the pancreatic duct. Alcohol stimulates trypsinogen.

Biliary Tract disease:

 Stone in the biliary tree [gall stone pancreatitis is the major cause of acute pancreatitis
in the western world (40%)
 In our country, it may be responsible for pancreatitis is about 20-30% of patients.

Collagen Vascular disorders:

Autoimmune disease such as Polyarteritis nodosa can be a causative factor in acute

pancreatitis.

Drugs:

Corticosteroids, tetracycline, estrogens, azathioprine, Valproic acid and diuretics

can cause pancreatitis.
Obstruction:

It is obvious that some sort of obstruction pancreatic ducts is required to produce acute
pancreatitis.

Metabolic factors:

 Hyperlipidemia has got some relation with acute pancreatitis.

 Hypercalcemia and pancreatitis are often associated with.
 Haemochromatosis has been thought to produce pancreatic fibrosis and atrophy due to
irritating properly of deposited iron in pancreas.

Vascular factors:

 Pancreatitis may be induced by injection of microspheres of various sizes into the

Pancreaticoduodenal arteries.
 These particles occlude the terminal arterial supply and produce local ischemia.
 Sometimes can older patients who have widespread Vascular obstruction from
atherosclerosis and patient who have undergone cardiopulmonary bypass are
sometimes seen with severe hemorrhagic pancreatitis.

POSTOPERATIVE PANCREATITIS:

 Following certain intra abdominal operations pancreatitis may occur.

 These operations are mainly on the stomach or on the biliary tract.
 During gastrectomy when the region of the head of the pancreas is being dissected
injury will cause pancreatitis.
 After splenectomy pancreatitis may result following operative injury to the tail of the
pancreas.

Other causes:

Viral infections e.g.: mumps, echovirus, coxsackie viruses have been cause pancreatitis.

 Trauma.
 Scorpion sting.
 Vasculitis.
  Porphyria.
 Abscesses
 cystic fibrosis
 penetrating duodenal ulcer cysts.
 Renal failure.
 Kaposi Sarcoma
 Certain investigation procedure like ERCP.
 Idiopathic.

PATHOPHYSIOLOGY:

Etiological Factors

[Alcohol, gallstone, Trauma, Idiopathic etc],

Activation of pancreatic enzymes.

[Amylase, protease, Lipase, insulin, glucagon, polypeptides somatostatin].

Trypsinogen converts Trypsin.

Activates protease which cause autodigestion of Pancreas and Activation of other proteolytic
enzymes.

Elastase ⇒ haemorrhage.

[It digests the elastic fibers of the food vessels resulting in rupture and haemorrhage into
peritoneal cavity]

Excessive tissue necrosis resulting in destruction of pancreas.

Inflammation of pancreas.

[Pancreatitis].

CLINICAL FEATURES:

Severe abdominal (upper) epigastric pain radiating to the back increases over a period of hour
–illimitable agony is a characteristic feature.
Abdominal findings:

o Tenderness in epigastric
o upper abdominal guarding and rigidity
o Distension of the abdomen
o Mass in epigastrium.
o Muscle guarding.
o Abdominal distension due to either accumulation of blood (or) fluid in the peritoneal
Cavity (or) due to paralytic ileus.

Cullen’s sign:

Bluish ecchymoses discoloration seen around umbilicus.

Grey Turner's sign:

o Bluish discoloration in the flanks.

o Both these signs are due to peri-pancreatic and retroperitoneal hemorrhage and
seepage of blood along fascial planes, into the anterior abdominal wall and spread
through falciform ligament.

Vomiting:

o Varies in severity but is usually protacted

o Worsened by ingestion of food or fluid.
o Does not relieve the pain.
o Usually accompanied by Nausea.

Abdominal pain:

o Steady and severe excruciating.

o Located in the left upper quadrant or in the mid epigastrium may radiate to the back.
o Worsened by lying supine maybe lessened by flexed knee, curved back positioning.
Fever:

Rarely exceed 102°F.

Other signs & symptoms:

 Tachycardia and jaundice.

 Hypovolemia as a result of fluid shift
 Shock may be arisen due to hemorrhage
 Toxemia from activated enzymes.
 Pleural effusion.

INVESTIGATIONS:

1. Hemogram (CBC): Hb %may be low due to hemorrhagic pancreatitis.

2. Total count is raised above 15,000 cells/mm³ due to inflammation.
3. Blood for urea, creatinine to rule out renal failure.
4. Serum amylase (widely used test).

Normal levels are 40-80 Somogyi units. Values around 400 are suggestive and values
more than 1000 Somogyi units are diagnostic of acute pancreatitis.

It is increased in the first 24-48 hours and returns to normal within 3-4 days.
5. Serum lipase level - more specific but difficult to measure. Lipase is only secreted by
pancreas. elevated up to 7days.
6. Serum calcium levels: hypocalcaemia is seen, due to hypoalbuminemia (or) fat
necrosis.
7. Total proteins are usually low, especially albumin.
8. Abdominal ultrasound-can demonstrate oedematose pancreas, fluid in the abdomen
(or) biliary Tract (tree) disease.
9. C-reactive protein: possible pancreatic inflammation and necrosis.
10. Liver function Test: AST greater than 250IU/L due to inflammation.
11. Chest X-Ray: small pleural effusion seen in Left Lower lobe and elevated diaphragm
(Left).
12. Abdominal x-Ray (plain): dilated proximal Jejunum gall stones.
13. Stool sample: Fecal fat content.
14. CT and MRI most useful for diagnosis and prognosis.
 15. ERCP: Endoscopic Retrograde cholangiopancreatography.
16. ERCP: Magnetic Resonance cholangiopancreatography.

Both are used if cause is uncertain; assess for duct stones, ampullary tumors and pancreas
divisum.

COLLABORATIVE CARE:

NUTRITIONAL MANAGEMENT:

 It includes moderate high carbohydrate, high proteins and low fat meals and high
calories.
 Avoid Caffeine and alcohol.
 Avoid spices
 Advice small frequent meal.

MEDICAL MANAGEMENT:

 IV Isotonic fluids / IV calcium and magnesium might be needed.

 NPO while acute and to Neutralize the gastric acids.
 Monitor Intake and output.
 Insertion of NG tube in severe Vomiting or biliary obstruction.
 Provide O2 to promote comfort in breathing.
 Monitor the patient weight every day.
 Blood transfusion if Hb% is low, or albumin and amino acids if proteins are low.
 IV morphine (pain medication may be Combine with anti-spasmodic agents].
 Spasmolytics: nitroglycerine (or) papaverine.
 Drugs such as Antacids, PPT, Acetazolamide is administered.
 Enteral nutrition for patient who does not resume oral intake.
 Antibiotic therapy for the patient with acute necrotizing pancreatitis.
 ERCP with sphincterotomy for patients with gallstones or urgent/emergency basis.

SURGICAL MANAGEMENT:

 Laparoscopic surgery for abscess/Pseudocyst and gallstones.

INDICATION FOR SURGICAL MANAGEMENT:

1. Infected necrosis.
2. pancreatic abscess.
3. Diagnoses is in doubt-perforated Viscus cannot be ruled out.
4. cholangitis not responding to treatment.

COMPLICATIONS:

1. Shock for hypovolemia (or) hypoalbuminemia.

2. Hypocalcaemia.
3. Respiratory insufficiency.
4. Pleural effusion, atelectasis, pneumonia.
5. Leukocytosis and anemia.
6. Pancreatic abscess.
7. Pseudocyst of pancreas.
8. Perforation of colon or stomach.
9. Pancreatic necrosis.
10. Hypocalcemia, hyperlipidemia.
11. Pseudo aneurysm resulting in massive upper gastrointestinal (or) lower
gastrointestinal bleeding. Bleeding in pancreatic duct is called hemosuccus
pancreatitis.

NURSING MANAGEMENT OF PANCREATITIS:

1. Fluid and Electrolyte Disturbances:

 Assess fluid and electrolyte status.

 [skin turgor and moistness of mucous).
 Weigh daily.
 Monitor Intake and output and measure abdominal girth.
 Administer in fluids and blood to maintain volume and prevent shock.
 Report decreased BP, Less urine output and low sr. Calcium and Magnesium.
2. Relieving pain and discomfort:

 Administer analgesics as prescribed.

 Pain management is parenteral opioids, including morphine, hydromorphone or
fentanyl via patient-controlled analgesia (or) bolus.
 Frequent assess the intensity and effectiveness of pain.
 use Nasogastric suctioning to remove gastric secretions and relieve abdominal
distension.
 Maintain patient on bed rest to decrease metabolic rate and to reduce secretion of
pancreatic enzymes.

3.Improving Breathing pattern:

 semi-fowler's position to decrease pressure on diaphragm.

 Change position frequently to prevent
 Atlectasis and pooling of secretions.
 Assess respiratory status frequently pulse oximetry, arterial blood gas [ABG).
 Teach the patient techniques of Coughing, deep breathing and the use of incentive
spirometry.

4. Improving Nutritional status:

 Assess nutritional status.

 Monitor laboratory tests result and daily weights.
 Provide enteral Nutrition.
 Monitor serum glucose level every 4 to 6 hours.
 Introduce oral feedings gradually as symptoms subside.
 Avoid heavy meals and alcoholic beverages.

5. Maintaining skin Integrity:

 Assess the wound, drainage sites, and skin carefully for sign of infection.
 Carry out wound care as prescribed and protect intact skin from contact with drainage.
 Turn the patient every 2 hours; use of specialty beds may be indicated to prevent skin
breakdown.