SEMINAR

ON
ACUTE PANCREATITIS

SUBMITTED TO:
Dr. Premila Lee,
Professor & HOD,
Surgical Nursing,
CON, CMC, Vellore

SUBMITTED BY:
Ms. Joice Das,
M.Sc. Nursing,
Medical-Surgical Nursing-II,
CON, CMC, Vellore
College of Nursing, Christian Medical College, Vellore
Medical-Surgical Nursing Speciality –II
Master plan on Acute Pancreatitis

FACULTY GUIDE: Dr. Premila Lee, Professor & HOD, Medical- Surgical Nursing-II

STUDENT: Ms. Joice Das, M.Sc. Nursing, Medical-Surgical Nursing-II

 Introduction

 Review of anatomy and physiology of pancreas

 Definition- Pancreatitis is an inflammatory process in which pancreatic

enzymes auto digest the gland. The gland sometimes heals without any
impairment of function or any morphologic changes; this process is known
as acute pancreatitis.

 Incidence- Global, National, Tamil Nadu

 Etiology
- Long standing alcohol consumption and biliary stone disease cause of
acute pancreatitis.
- Unknown: 10-30%
- Idiopathic pancreatitis: 70%
- Biliary tract disease
- Alcohol
- Endoscopic Retrograde cholangiopancreatography
- Trauma
-Drug
- Less common causes: Infection, Hereditary pancreatitis, Hypercalcemia,
Developmental abnormalities of pancreas, Hypertriglyceridemia, Tumors,
 Toxins, Surgical procedures, Vascular abnormalities, Autoimmune
pancreatitis.

 Pathophysiology
- Normal pancreatic function
- Pathogenesis of acute pancreatitis

 Clinical presentation
- History:
- Dull, boring and steady pain, sudden in onset and gradually intensifies in
severity until reaching a constant ache, located in the upper abdomen,
usually in the epigastric region.
- Nausea and vomiting (bile stained)
- Diarrhea
- Anorexia

-Physical Examination:
- Fever
- Tachycardia
- Hypotension
- Abdominal tenderness and muscular guarding ( Ominous sign)
- Jaundice
- Dyspnea due to irritation of the diaphragm
- In severe cases, hemodynamic instability
- Cullen’s sign and Grey- turner sign
- Erythematous skin nodule
- Purtscher retinopathy

 Prognosis
- Overall mortality is 10-15%
- Higher in biliary pancreatitis than alcoholic pancreatitis
- Type-II Diabetes mellitus ha higher mortality

 Criteria for predicting severity of pancreatitis

 - Criteria on admission to hospital
- Criteria within 48 hours of hospital admission

 Diagnostic studies
- Laboratory studies
- Abdominal radiography
- Ultrasonography : Abdominal ultrasonography, Endoscopic
ultrasonography, Computer Tomography scanning, Magnetic resonance
cholangiopancreatography, Endoscopic Retrograde
Cholangiopancreatography, Image- guided aspiration and drainage,
Genetic testing, Histologic findings

 Medical Management
- Pain management
- Respiratory care
- Fluid resuscitation
- Nutritional support
- Antibiotic therapy
- Biliary drain

 Guidelines
- ACG guidelines
- AGA guidelines
- WSES guidelines

 Surgical Intervention
- Diagnostic laparotomy

 Post-acute management

 Nursing management
- Relieving pain and discomfort
- Improving breathing pattern
 - Improving nutritional status
- Maintaining skin integrity
- Monitoring and managing potential complications
- Promoting home and community based care

 Complications
 Differential diagnosis
 Complementary and alternative medicine for pancreatitis

REFERENCE

Book
1. Hinkle, J. L., Cheever, K. H (2014). Assessment and Management of Patients
with Biliary Disorders. Brunner & Suddarth’s textbook of Medical-Surgical
Nursing (Volume-2). 13th Edition. Wolters Kluver publication

E-book
1. Tang, J. C. F (2021). Acute Pancreatitis. Medscape.
https://emedicine.medscape.com/article/181364-overview

2. https://pancreasfoundation.org/patient-information/acute-pancreatitis/
complementary-pancreatitis-therapies/

Journal
1. Tenner, S., Baillie, J., DeWitt, J., Vege, S. S.(2013). American College of
Gastroenterology guideline: management of acute pancreatitis. Am J
Gastroenterol.108(9):1400-15; 1416.

2. Crockett, S. D., Wani, S., Gardner, T. B., Falck-Ytter, Y., Barkun, A. N(2018).
American Gastroenterological Association Institute Guideline on Initial
Management of Acute Pancreatitis. Gastroenterology. 154(4):1096-101.
3. Leppäniemi, A., Tolonen, M., Tarasconi, A. et al.(2019). WSES guidelines for
the management of severe acute pancreatitis. World J Emerg Surg.14(27)
https://doi.org/10.1186/s13017-019-0247-0

INTRODUCTION

 Patients with severe acute pancreatitis need to be recognized and treated

as soon as possible to achieving optimal outcomes.

 Management depends largely on severity. Medical treatment of mild

acute pancreatitis is relatively straightforward and involves intensive care.

 The Dutch anatomist- Dr. Nicholas Tulp in 1652 first described about the
pathogenesis and characteristics of acute pancreatitis.

DEFINITION

 Pancreatitis is an inflammatory process in which the pancreatic enzymes

auto digest the gland. The gland sometimes heals without any
impairment of
function or any morphologic changes.

EPIDEMIOLOGY

GLOBAL
• Incidence of acute pancreatitis ranges between 5 and 80 per 100,000
population.
• Highest incidence recorded in the United States and Finland.
• The incidence is 17.5 cases per 100,000 people.
• In Finland, the incidence is 73.4 cases per 100,00 people.

INDIA
• Prevalence rate for Pancreatitis in India is 7.9 per 100,000.
 • Men- 8.6 per 100,000 population.
• Women- 8.0 per 100,000 population.

SOUTH INDIA
• Southern states - Highest incidences- 114-200/100,000 population.

ETIOLOGY
 Chronic alcohol consumption and biliary stone disease cause most cases
of acute pancreatitis.

 In 10%-30% of cases, the cause is unknown, though studies have

suggested that as many as 70% of cases of idiopathic pancreatitis are
secondary to biliary microlithiasis.

Biliary tract disease

 One of the most common causes of acute pancreatitis in most developed

countries (accounting for approximately 40% of cases) is gallstones
passing into the bile duct and temporarily lodging at the sphincter of
Oddi. The risk of a stone causing pancreatitis is inversely proportional to
its size.

 It causes acinar cell injury secondary to increasing pancreatic duct

pressures caused by obstructive biliary stones at the ampulla of Vater.

Alcohol

 Alcohol use is a major cause of acute pancreatitis (accounting for at least

35% of cases.

 At the cellular level, ethanol leads to intracellular accumulation of

digestive enzymes and their premature activation and release.
  At the ductal level, it increases the permeability of ductules, allowing
enzymes to reach the parenchyma and cause pancreatic damage.
exacerbation of chronic pancreatitis.

Endoscopic retrograde cholangiopancreatography

 Pancreatitis occurring after endoscopic retrograde

cholangiopancreatography (ERCP) is probably the third most common
type (accounting for approximately 4% of cases).

 The risk of post-ERCP acute pancreatitis is increased if the endoscopist is

inexperienced, if the patient is thought to have sphincter of Oddi
dysfunction, or if manometry is performed on the sphincter of Oddi.

 Aggressive preintervention intravenous (IV) hydration has been durably

shown to prevent post-ERCP pancreatitis in randomized studies.

Trauma

 Abdominal trauma (approximately 1.5%) causes an elevation of amylase

and lipase levels in 17% of cases and clinical pancreatitis in 5% of cases.

 Pancreatic injury occurs more often in penetrating injuries (eg, from

knives, bullets) than in blunt abdominal trauma (eg, from steering wheels,
horses, bicycles).

Drugs

 Accounts for approximately 2% of cases and is probably related to an

unknown predisposition. Fortunately, drug-induced pancreatitis is usually
mild.
  Drugs definitely associated with acute pancreatitis include the following:
 Azathioprine, Sulfonamides, Sulindac, Tetracycline, Valproic
acid,Furosemide

Less common causes

The following causes each account for less than 1% of cases of pancreatitis.

Infection

 Viral causes include mumps virus, coxsackievirus, cytomegalovirus (CMV),

hepatitis virus, Epstein-Barr virus (EBV), echovirus, varicella-zoster virus
(VZV), measles virus, and rubella virus.

 Bacterial causes include Mycoplasma pneumoniae, Salmonella,

Campylobacter, and Mycobacterium tuberculosis. Worldwide, Ascaris is a
recognized cause of pancreatitis resulting from the migration of worms in
and out of the duodenal papillae.

 Pancreatitis has been associated with AIDS; however, this may be the
result of opportunistic infections, neoplasms, lipodystrophy, or drug
therapies.

Hereditary pancreatitis

 Hereditary pancreatitis is an autosomal dominant gain-of-function

disorder related to mutations of the cationic trypsinogen gene (PRSS1),
which has an 80% penetrance.

 Mutations in this gene cause premature activation of trypsinogen to

trypsin.
  Activated mutant cationic trypsin can then trigger the entire zymogen
activation cascade.

PATHOPHYSIOLOGY

SIGNS AND SYMPTOMS

  ABDOMINAL PAIN

SEVERITY - Mild discomfort to severe incapacitating distress

ONSET - Sudden in onset
CHARACTER - Dull, boring and steady
RADIATING - Radiates to the flank
RELIEVING FACTOR - Sitting with trunk flexed and knees draws up
ASSOCIATED FACTORS - Nausea,vomiting,anorexia
EXACERBATING FACTORS - Fatty food and ethanol intake
SITE - Periumbilical and epigastric

 Nausea and vomiting are often present, along with accompanying

anorexia.
 Diarrhea can also occur.
 Fever (76%) and tachycardia (65%)
 Hypotension

PHYSICAL EXAMINATION

 Abdominal tenderness, muscular guarding (68%), and distention (65%)

 Diminished or absent bowel sounds
 Jaundice (28%)
 Dyspnea (10%); tachypnea; basilar rales- left lung.
 Hemodynamic instability (10%)
 Hematemesis or melena (5%)
 Pale
 Diaphoretic, and listless appearance
 Occasionally, extremity muscular spasms secondary to hypocalcemia
 The Cullen sign is a bluish discoloration around the umbilicus resulting
from hemoperitoneum
 The Grey-Turner sign is a reddish-brown discoloration along the flanks
resulting from retroperitoneal blood dissecting along tissue planes.
  Erythematous skin nodules may result from focal subcutaneous fat
necrosis.

PROGNOSIS

 Overall mortality rate is 10-15%.

 Higher in biliary pancreatitis than alcoholic pancreatitis.
 Type-II Diabetes mellitus ha higher mortality.

RANSON’S CRITERIA FOR ACUTE PANCREATITIS

LABORATORY FINDINGS
Serum amylase —
• Serum amylase rises within 6 to 12 hours of the onset.
• Returns to normal within three to five days.
Serum lipase —
• Has a sensitivity- 82 to 100%
• Rises within 4-8 hours of the onset of symptoms, peaks at 24 hours, and
returns to normal within 8 to 14 days

Trypsinogen activation peptide (TAP) (5-amino acid peptide)—

• Cleaved from trypsinogen to produce active trypsin
• Early event in the pathogenesis of acute pancreatitis

Trypsin, phospholipase, carboxypeptidase, carboxylester lipase, colipase, and

pancreatic isoamylase.

Markers of immune activation —

 Activation of granulocytes and macrophages leads to release of a number
of cytokines and inflammatory mediators.
• Elevations in C-reactive protein (CRP), interleukin (IL)-6, IL-8, IL10, tumor
necrosis factor
• Leukocytosis and an elevated hematocrit from hemoconcentration
• Metabolic abnormalities including elevated blood urea nitrogen (BUN),
hypocalcemia, hyperglycemia, and hypoglycemia may also occur.

Abdominal Radiography
Helps in detecting the inflammatory process that may damage peripancreatic
structures, resulting in a colon cut-off sign, a sentinel loop, or an ileus.

Ultrasonography

Abdominal ultrasonography
  Ultrasonography of the abdomen is the most useful initial test in
determining the etiology of pancreatitis and is the technique of choice
for detecting gallstones.

Endoscopic ultrasonography

 Endoscopic ultrasonography (EUS) is an endoscopic procedure that

allows a high-frequency ultrasound transducer to be inserted into the
gastrointestinal (GI) tract to visualize the pancreas and the biliary tract

 Role in the evaluation of acute pancreatitis is the detection of

microlithiasis and periampullary lesions not easily revealed by other
methods.

COMPUTED TOMOGRAPHY

Abdominal CT scans also provide prognostic information based on the

following grading scale developed by Balthazar and colleagues:

Grade A - Normal pancreas

Grade B - Focal or diffuse gland enlargement

Grade C - Intrinsic gland abnormality recognized by haziness on the scan

Grade D - Single ill-defined collection or phlegmon

Grade E - Two or more ill-defined collections or the presence of gas in or near

the pancreas

MAGNETIC RESONANCE CHOLANGIOPANCREATOGRAPHY

Magnetic resonance cholangiopancreatography (MRCP) has an emerging role
in the diagnosis of suspected biliary and pancreatic duct obstruction in the
setting of pancreatitis.

Heavily T2–weighted images provide a noninvasive image of the biliary and

pancreatic ducts.

MANAGEMENT

INITIAL MANAGEMENT
Initial management of a patient with acute pancreatitis consists of-
• Fluid resuscitation
• Pain control
• Nutritional support

PAIN MANAGEMENT
• Adequate administration of analgesia.
• Parenteral opiods- Morphine, Fentanyl, Hydromorphone.
• Antemetics are prescribed to prevent vomiting.
• Fentanyl can be given as bolus as well as constant infusion.
• Bolus regimen ranges from 20 to 50 micrograms with a 10-minute lock-
out period.
• Meperidine has been favored over morphine for analgesia.
• Meperidine has a short half-life- Metabolite normeperidine

RESPIRATORY CARE
• Moniter arterial blood gases
• Humidified oxygen to intubation and mechanical ventilation
FLUID MANAGEMENT
• Isotonic solution at a rate of 5 to 10 mL/kg per hour of isotonic crystalloid
solution (eg, normal saline or lactated Ringer's solution).

• Severe volume depletion- hypotension and tachycardia- More rapid

repletion with 20 mL/kg of intravenous fluid given over 30 minutes
followed by 3 mL/kg/hour for 8 to 12 hours.

• Adequate fluid replacement can be assessed by an improvement in vital

signs-
• Heart rate <120 beats/minute
• Mean arterial pressure between 65 to 85 mmHg
• Urine output (>0.5 to 1 cc/kg/hour)
• Reduction in hematocrit (goal 35 to 44 percent) and BUN over 24 hours.

Antibiotics
• Drugs of the imipenem class, should be used in any case of pancreatitis
complicated by infected pancreatic necrosis.

• Should not be given routinely for fever, especially early in the disease
course, because this symptom is almost universally secondary to the
inflammatory response and typically does not reflect an infectious
process.

Biliary drainage
• Placement of biliary drains (for external drainage)
• To establish drainage of the pancreas
• Leads to decreased pain and increased weight gain.

SURGICAL INTERVENTION
• Performed to assist with diagnosis of pancreatitis
• To establish pancreatic drain
• To resect or debride an infected necrotic pancreas
• Multiple drains and surgical incisions left open for irrigation
POST-ACUTE MANAGEMENT
• Oral feeds- Low in fat and protein are initiated.
• Eliminate alcohol and caffeine.
• Corticosteroids, diuretics and oral contraceptives- Discontinued.
• ERCP- To determine whether pancreatitis is resolved, absence of
pseudocyst and abscesses.

NURSING MANAGEMENT

• Relieving pain and discomfort

• Severe pain- Necessitating the use of analgesics- Assessment
• Proper positioning
• Music therapy, distractions and imagery
• Oral feed with held- Inhibits secretin
• NG suction- Relieve distension, paralytic ileus
• Oral hygiene
• Clouded sensorium- Simple explanation
• Bed rest- To decrease metabolic rate , decrease pancreatic and gastric
enzymes.

IMPROVING BREATHING PATTERN

• Semi-fowler’s position
• Frequent changes to prevent atelectasis and pooling of secretions.
• Pulse oxymetry, ABG
• Coughing and deep breathing.
• Use of incentive spirometry.
• Steam inhalation
• Nebulization

IMPROVING NUTRITIONAL STATUS

• Note down the factors that alters nutritional requirement.
• Moniter serum glucose level every 4-6 hours
• Enteral and parenteral feed
MAINTAINING SKIN INTEGRITY
• Carefully assess the drain site, wound site, pressure points.
• Contact with a wound-ostomy-continence nurse (WOC)
• Position change every 2 hourly.

PROMOTING HOME AND COMMUNITY-BASED CARE

EDUCATING PATIENTS ABOUT SELF CARE

• Prolong period to return to previous level of activity.
• Avoid fatty food, heavy meals, alcohol.
• Signs and symptoms of acute pancreatitis.

CONTINUING CARE
• Referral for home care- Assess the physical and psychological needs
• Adherence to therapeutic regimen
• Fluid and nutrition intake
• Avoidance of alcohol
• Resources and support group to help stop alcohol consumption.

ACG GUIDELINES

In 2013, the American College of Gastroenterology (ACG) issued guidelines for

the management of acute pancreatitis (AP), including the following :

 Contrast-enhanced computed tomography (CT) scanning and/or magnetic

resonance imaging (MRI) of the pancreas should be performed only in the
absence of clinical improvement or to confirm the diagnosis.

 Assessment of the patient’s hemodynamic status should occur

immediately upon presentation, with resuscitative measures initiated as
necessary.
 Patients with systemic inflammatory response syndrome (SIRS) and/or
organ failure should, if possible, be admitted to an intensive care unit
(ICU) or an intermediary care setting.

 All patients should receive aggressive hydration, unless this is precluded

by cardiovascular and/or renal comorbidities; aggressive intravenous (IV)
hydration is most effective within the first 12-24 hours, with possibly little
benefit derived from its administration after this point.

 Within 24 hours of admission, patients with concurrent acute cholangitis

should undergo endoscopic retrograde cholangiopancreatography (ERCP);
in high-risk patients, the risk of severe post-ERCP pancreatitis should be
reduced through the use of postprocedure rectal nonsteroidal anti-
inflammatory drug (NSAID) suppositories and/or pancreatic duct stents.

 The guidelines recommend against routinely using prophylactic

antibiotics in cases of severe acute pancreatitis and/or sterile necrosis;
however, intervention in patients with infected necrosis may be delayed
through the use of antibiotics that do not penetrate the necrotic tissue.

 In mild cases of acute pancreatitis with no nausea and vomiting, oral

feeding can be initiated immediately; enteral nutrition should be used in
severe cases to prevent infectious complications, and parenteral nutrition
should be avoided.

 Regardless of the lesion's size, location, and/or extension, intervention is

not necessary for asymptomatic pancreatic and/or extrapancreatic
necrosis and/or pseudocysts.

 Surgical, radiologic, and/or endoscopic drainage in stable patients with

infected necrosis should be postponed (for 4 weeks if possible) to permit
a wall to develop around the necrosis.