ACUTE PANCREATITIS

Presented by: Dr. Okoronkwo Emmanuel

Emenike
House Officer
Gastroenterology Unit
Department of Internal Medicine
FMC Yenagoa
21/3/2025
 OVERVIEW

• Introduction
• Anatomy
• Aetiology
• Epidemiology
• Pathophysiology
• Clinical Presentation
• Investigation
• Assessment of Severity
• Management Modalities
 INTRODUCTION

The name ‘pancreas’ is derived from the Greek ‘pan’ (all) and ‘kreas’
(flesh)
The average gland weighs between 75 and 125gm. and measures 10
to 20 cm
 Retroperitoneal organ that lies in an oblique position, sloping upward
from the C-loop of the duodenum to the splenic hilum
Due to its retroperitoneal location, pain associated with pancreatitis
often is characterized as penetrating through the back.
 ANATOMY

 Anatomically divided into 4 parts -

① Head
② neck
③ Body
④ Tail
 Head occupies 30% of the gland by
mass, whereas body and tail comprises
70% of the whole organ
 Coming off the side of the pancreatic head and passing to the left and
behind the superior mesenteric vein is the Uncinate process of the
pancreas
 ANATOMY

 80-90% is composed of exocrine acinar tissue, which is

organized into lobules which synthesize, store and
secretes digestive enzymes into the duodenum

 The main duct(duct of Wirsung) is lined by columnar

epithelium, which becomes cuboidal in the ductules
carries pancreatic juice

 The endocrine cells arrange in clusters, known as Islets

of Langerhans, are distributed throughout the pancreas,
which consists of ‘B’ cells (producing insulin), ‘A’ cells
Source: Schwartz
 DEFINITION

 Pancreatitis is inflammation of the gland parenchyma

of the pancreas

 Acute pancreatitis is defined as an acute condition

presenting with abdominal pain and associated with
raised pancreatic enzymes levels in the blood or urine
as a result of pancreatic inflammation
• Acute pancreatitis may be categorized into..

 Mild acute pancreatitis

- characterized by interstitial edema of the gland and minimal organ
dysfunction.
- Self limited and subsides spontaneously within 3-7 days after treatment
has been instituted.
- Low fat solid diet is a reasonable choice after recovering.
- mortality is around 1%.

 Severe acute pancreatitis

- characterized by pancreatic necrosis, a severe systemic inflammatory
response and often multi-organ failure
- mortality varies from 20-50%
- death occurs in the early phase from multi-organ failure, while deaths
occurring after 1st week of onset are due to septic complication.
 AETIOLOGY

1) Biliary or gallstone pancreatitis (40-60%)

2) Alcohol induced injury (35%)
3) Post ERCP(Endoscopic Retrograde Cholangiopancreatography)
4) Anatomic obstruction (ampullary tumor, pancreas divisum)
5) Drug induced (corticosteroids, azathioprine, asparaginase,
valproate, thiazides, estrogens)
6) Metabolic factors (hypertriglyceridemia, hypercalcemia)
7) Abdominal trauma
8) Following biliary, upper GI and cardiothoracic surgery
9) Autoimmune pancreatitis
10)Viral infections (mumps, coxsackie B)
11)Scorpion bite
12)Idiopathic
 EPIDEMIOLOGY

• Recent U.S. estimates from the National Inpatient Sample report that AP is the most
common inpatient principal gastrointestinal diagnosis.
• The incidence vary in different countries and depends on cause.
• The annual incidence ranges from 13-45/100,000 persons.
• Hospitalization rates increases with Age, 88% higher among blacks and higher
among males than females.
• A study conducted by Jos University Teaching Hospital showed AP is not a common
disease in sub-Sahara Africa.
• In Nigeria, AP is not common however its incidence is increasing, with gallstones
and alcohol use being the most frequent cause.
 PATHOPHYSIOLOGY

 Exact mechanism of AP not completely known

 Most researchers believe that AP begins with the

activation of zymogens inside acinar cells, which causes
acinar cell injury

 Severity of AP may be determined by the events that

occur subsequent to acinar cell injury, which include
release of cytokines and other chemical mediators of
inflammation
 PATHOPHYSIOLOGY

• Events of pathogenesis of Acute Pancreatitis include:

A. Precipitating Initial Events

B. Intrapancreatic Events

C. Systemic Events
A. Precipitating Initial Events
 Acinar Cell Events
 When acinar cells are pathologically stimulated, their
Lysosomal(L) & Zymogen(Z) contents colocalize,
consequently trypsinogen is activated to trypsin by
cathespin B
 Increased cytosolic Calcium is required

 Cathespin B and other contents of these colocalized

organelles are released

 Cathespin B activates apoptosis by causing cytochrome c

to be released from mitochondria
 Activation of PKC(Protein Kinase C)
results in a sudden activation of NF
Kappa beta

 Which triggers release of Cytokines

 Cytokines attract inflammatory

response cells which mediate local Schematic
& presentation of the Acinar cell Events
syst inflammation
B. Intrapancreatic Events
 After activation of superoxides (“Respiratory burst”) and release of
proteolytic enzymes (cathespin, elastase and collagenase), activated
neutrophils are attracted to focus of tissue injury

 Macrophages release TNF-alfa, IL-6 & IL-8 which mediate the local and
systemic inflammatory response

 The inflammatory mediators cause increased pancreatic vascular

permeability – leading to edema, hemorrhage & microthrombi

 Failure of pancreatic microcirculation resulting in pancreatic

C. Systemic Events

 Organ failure can develop at any stage of acute pancreatitis, associated with

an overwhelming proinflammatory response early, or secondary to the

development of infected local complications

 The development pancreatic necrosis, the breakdown of the interstitial barrier

and suppression of immune response contribute to the development of

infected pancreatic necrosis

 This may associated with late development of SIRS or MODS

 Organ failure is scored using the Marshall or Sequential Organ Failure

 DIAGNOSIS

A.Clinical presentation

B.Investigation
 CLINICAL PRESENTATION

 The cardinal symptom of AP is epigastric or periumbilical pain that radiates to the back

 Some patients may gain relief by sitting or leaning forward

 Nausea, repeated vomiting and retching are usually marked accompaniments

 Tachypnea, tachycardia and hypotension may be present

 In gallstone pancreatitis mild icterus may be present

 Bleeding into fascial planes can produce bluish discoloration of the flanks (GreyTurner sign)
or umbilicus (Cullen sign)

 Usually muscle guarding in the upper abdomen

 Pleural effusion is present in 10-20% patients

 Source:
Bailey
INVESTIGATIONS
 Cornerstone of diagnosis of AP is the clinical findings plus
elevation of pancreatic enzyme levels in serum
 3 folds or higher elevation of amylase and lipase level
confirms the diagnosis.
 Serum half life of amylase is shorter than that of lipase, thus
lipase level is more sensitive indicator to establish the
diagnosis
 Lipase is more specific marker of AP, because amylase an be
elevated in PUD, mesentric ischemia, salpingitis and
macroamylasemia
 The degree of amylase/lipase elevation does not correlate with
 CBC: Leukocytosis
 Blood sugar: Hyperglycemia in severe cases
 Electrolyte imbalance: Hypokalemia and
hypocalcaemia
 Elevated LDH in biliary disease
 Glycosuria in 10% cases
 CT Scan
 MRI
 EUS(endoscopic ultrasound scan)
 CT scan showing well perfused interstitial edematous acute
pancreatitis of the neck and tail of pancreas with confluent area of
necrosis of the pancreatic body
 DIAGNOSIS

• Any severe acute abdominal pain should suggest the possibility of AP.
• The diagnosis is established by 2 of the following 3 criteria
• 1) Typical abdominal pain in the epigastrium that may radiate to the back.
• 2) Three fold or greater elevation in serum Lipase and/or Amylase.
• 3) Confirmatory Findings of AP on cross-sectional abdominal imaging.
• Patients may also have associated nausea, emesis fever, tachycardia and
abnormal findings on abdominal examination.
• Laboratory findings may reveal leucocytosis, hypocalcaemia and
hyperglycaemia.
• Although not significant for diagnosis, markers of severity may include
 DIFFERENTIAL DIAGNOSIS

• Perforated viscus esp PUD

• Acute Cholecystitis and biliary colic
• Acute Intestinal obstruction.
• Mesenteric vascular occlusion
• Renal colic
• Inferior myocardial infarction
• Dissecting aortic aneurysm.
• Diabetc ketoacidosis
• Connective tissue disorder with vasculitis
• pneumonia
 ASSESSMENT OF SEVERITY OF
DISEASE

A. Ranson Prognostic criteria

B. Acute Physiology And Chronic Health Evaluation (APACHE

II)score

C. Computed Tomography Severity Index (CTSI)

D. Atlanta Criteria for Acute Pancreatitis

 Ranson Prognostic Criteria for Non-Gallstone
Pancreatitis
At presentation

 Age > 55 yrs

 Blood glucose level > 200 mg/dl
 White blood cell count > 16,000 cells/ mm3
 Lactate dehydrogenase level > 350 IU/L
 Aspartate Aminotransferase level > 250 IU/L

After 48 hours of admission

 Hematocrit : decrease > 10%

 Serum calcium level < 8mg/dl
 Base deficit > 4 mEq/L
 Blood urea nitrogen level : increase > 5 mg/dl
 Fluid requirement > 6 L
 PaO2 < 60 mm Hg

** Ranson score ≥ 3 defines severe pancreatitis

 Ranson Prognostic Criteria for Gallstone Pancreatitis

At presentation

 Age > 70 yrs

 Blood glucose level > 220 mg/dl
 White blood cell count > 18,000 cells/ mm3
 Lactate dehydrogenase level > 400 IU/L
 Aspartate Aminotransferase level > 250 IU/L

After 48 hours of admission

 Hematocrit : decrease > 10%

 Serum calcium level < 8mg/dl
 Base deficit > 5 mEq/L
 Blood urea nitrogen level : increase > 2 mg/dl
 Fluid requirement > 4 L
 PaO2 : Not available

** Ranson score ≥ 3 defines severe pancreatitis

Acute Physiology and Chronic Health Evaluation
(APACHE II) Score :

 APACHE II provides a general measure of the severity

of the disease
 Based on patient’s age, previous health status and 12
routine physiologic measurements
 The main advantage is that it can be used on
admission and repeated at any time
 APACHE II score of 8 or higher defines severe
pancreatitis
 APACHE II has a positive predictive value of 43% and a
 Computed Tomography Severity Index (CTSI)

FEATURE
POINTS

Pancreatic inflammation
• Normal pancreas
0
• Focal / diffuse pancreatic enlargement 1
• Intrinsic pancreatic alterations with peripancreatic fat 2
inflammatory changes
• Single fluid collection / phlegmon
3
• 2 or more fluid collection or gas, in or adjacent to the 4
Pancreas

Pancreatic necrosis
• None
** CTSI 0-3, mortality03%, morbidity 8%
• ≤ 30%CTSI 4-6, mortality 6%, morbidity 35%
2 17%, morbidity 92%
CTSI 7-10, mortality
• 30% - 50%
 Atlanta Criteria for Acute Pancreatitis

Organ Failure, as Defined by

 Shock (SBP <90mm Hg)
 Pulmonary insufficiency (PaO2 <60 mm Hg)
 Renal failure (creatinine level >2 mg/dl after fluid resuscitation)
 Gastrointestinal bleeding (>500 ml/24 hrs)

Systemic Complication
 DIC ( platelet ≤10,000)
 Fibrinogen <1 g/L
 Fibrin split products >80 mcg/dl
 Metabolic disturbance (calcium level ≤7.5 mg/dl)

Local Complications
 Necrosis
 Abscess
 Pseudocyst
 MANAGEMENT

A. Management of mild acute pancreatitis

B. Management of severe acute pancreatitis
A.Management of mild acute pancreatitis:

 Conservative approach
 Intravenous fluid administration
 Frequent, but non invasive observation
 Brief period of fasting in nauseating patients
 But no justification for prolonged NPM
 Analgesics and antiemetics
 Antibiotics are not indicated
B. Management of severe acute pancreatitis:

 Admission to HDU / ICU

 Analgesia
 Aggressive fluid rehydration
 Oxygenation
 Invasive monitoring of vital signs, CVP, urine output, ABG
 Frequent monitoring of haematological and biomedical parameters (including LFT,
RFT, Clotting, sr. calcium & bl. Glucose)
 Nasogastric drainage
 Antibiotics (imipenem, cefuroxime)
 CT scan essential if sign of organ failure
 ERCP within 72 hrs for severe gallstone pancreatitis / signs of cholangitis
 Supportive therapy for organ failure (inotropes, ventilatory support, hemofiltration
etc.)
 Consider enteral(nasogastric) feeding, if nutritional support is required
1. Resuscitation and monitoring:
 Patients with AP require management strategies specifically
tailored to disease severity
 Aggressive fluid resuscitation is important in order to replenish
extravascular or “third space” fluid losses
 I.V fluid at rates of greater than 200ml/h are often necessary to
restore and maintain intravascular volume
 Fluid resuscitation is important to avoid systemic complications,
particularly acute renal insufficiency
 Inadequate resuscitation pose a significant risk for further
pancreatic injury
 Banks and others have shown that while aggressive fluid
resuscitation does not necessarily prevent the progression of
pancreatic necrosis, patients with inadequate resuscitation have
an increased risk of developing necrosis
 Close monitoring of respiratory, cardiovascular and renal
function is essential
 Close assessment of fluid balance is required including a
Foley catheter
 Patient with severe disease should be admitted to ICU
with capacity for continuous BP and SpO2 monitoring
 Intravenous narcotics are often essential for pain control
 Nasogastric tubes to avoid pancreatic stimulation was a
common practice previously, but no clinical data support
this
 But in paralytic ileus which is quite common in AP,
nasogastric tube should be used to prevent emesis and
2. Nutritional support:

 “Rest the pancreas” by avoiding enteral nutrition is no

longer acceptable
 There are evidences for nutritional support in acute
pancreatitis
 Enteral nutrition should be commenced after initial fluid
resuscitation and within the first 24 hrs of admission
 Can be introduced through NG tube and increased in
stepwise fashion in 2-3 days
 Delay in commencing enteral nutrition may contribute to
the development of intestinal ileus and feeding intolerance
3. The role of ERCP(Endoscopic Retrograde
Cholagiopancreatography):
 ERCP is used as a diagnostic as well as therapeutic modality in
acute pancreatitis
 Randomized trials have demonstrated that early ERCP reduces
complications, but not mortality
 Recent evidences suggested that early ERCP confers no benefit in
the absence of concomitant cholangitis
 ROLE OF URGENT INTERVENTION

• If gallstones are the cause of an attack of predicted or proven

severe pancreatitis, or if the patient has jaundice, cholangitis
or a dilated common bile duct, urgent ERCP should be carried
out within 72 hours of the onset of symptoms
• Sphincterotomy and clearance of the bile duct can reduce the
incidence of infective complications in these patients
• In patients with cholangitis, sphincterotomy should be carried
out or a biliary stent placed to drain the duct
4. Antibiotics:

 Controversy surrounding the use of prophylactic

antibiotics
 Overuse of antibiotics has been associated with
a documented rise in fungal infections and
resistant organisms
 Most recent studies do not support the use of
prophylactic antibiotics
5. Surgical management:

 In majority of AP patients, process is limited to parenchymal

edema without necrosis – they require surgical therapy for
limited indications
 Intervention may be needed to address the etiology or
complications of pancreatitis
 Interventions may be either surgical or endoscopic
 Between 10-30% of patients develop severe illness, with
pancreatic and peripancreatic illness – these patients require
pancreatic debridement as standard of care
 In patients with severe pancreatitis or pancreatic
necrosis, indications for surgical intervention are:

① Diagnostic uncertainty

② Intra-abdominal catastrophe unrelated to necrotizing

pancreatitis such as perforated viscus

③ Severe sterile necrosis

④ Symptomatic organized pancreatic necrosis

 CONCLUSION:

 Acute Pancreatitis is a complex , life

threating disease that requires diligent and
comprehensive medical and nursing care.
 REFERENCES

• Chummy Sinnatamby LAST’S ANATOMY 12th

Edition
• Harrison’s Principles of Internal Medicine 19th
Edition
• Medscape
• Bailey and Love Short Principles of Surgery
 THANK YOU

• My appreciation goes to my consultants Dr. Madubuike

and Dr. Onyia for persistently teaching us esp during ward
round and learning to genuinely want to see patient
improve.
• I also want to thank my senior Registars, Dr, Ugavah and
Dr. Wolo-wolo for the mentorship and coaching and
especially attention to details in patient care.
• I also want to appreciate my Registrar, Dr. Ayerite for
always taking time to explain the lines of management
during call days.
• To my team mates, Dr Obinatu, and Dr Adebayo, I really
love working with you and wouldn’t have asked for a
Thank you