Acute Pancreatitis

Acute Pancreatitis

Acute Pancreatitis is an acute inflammatory process of the pancreas caused by premature activation of pancreatic digestive enzymes leading to autodigestion, inflammation, edema, necrosis, and systemic inflammatory response.

It ranges from:

  • Mild self-limiting interstitial edema
    to
  • Severe necrotizing pancreatitis with multiorgan failure.

Diagnostic Criteria (Revised Atlanta Classification)

Diagnosis requires 2 of 3 criteria:

Criteria

Details

1. Typical abdominal pain

Acute severe epigastric pain radiating to back

2. Elevated pancreatic enzymes

Lipase or amylase >3× upper limit

3. Imaging findings

CT/MRI/USG compatible with pancreatitis

Differential Diagnosis

Condition

Key Difference

Perforated ulcer

Free air

Acute cholecystitis

RUQ dominant

Mesenteric ischemia

Severe pain/lactate

MI

ECG/troponin

Aortic dissection

Tearing pain

Etiology

Remember:“I GET SMASHED”

Most common causes:

  1. Gallstones
  2. Alcohol

Cause

Examples

I

Idiopathic

G

Gallstones

E

Ethanol

T

Trauma

S

Steroids

M

Mumps/malignancy

A

Autoimmune

S

Scorpion sting

H

Hypertriglyceridemia/hypercalcemia

E

ERCP

D

Drugs

Common Causes

1. Gallstone Pancreatitis

Most common overall cause.

Mechanism:

  • Transient obstruction of ampulla
  • Bile reflux
  • Pancreatic duct obstruction

Suggestive features:

  • Female
  • Obesity
  • RUQ pain
  • Elevated ALT (>150 IU/L strongly suggests biliary cause)

2. Alcoholic Pancreatitis

Mechanisms:

  • Direct acinar toxicity
  • Protein plug formation
  • Oxidative stress

Typically occurs after years of drinking.

 

3. Hypertriglyceridemia

Usually TG >500 mg/dL
High risk >1000 mg/dL

Mechanism:Toxic free fatty acid release

Clues:

  • Lactescent serum
  • Diabetes
  • Obesity

4. Drug-Induced Pancreatitis

  • Azathioprine
  • Valproate
  • Didanosine
  • Thiazides
  • Furosemide
  • GLP-1 agonists
  • DPP4 inhibitors
  • Estrogens

5. Post-ERCP Pancreatitis

Risk factors:

  • Difficult cannulation
  • Sphincterotomy
  • Female sex
  • Sphincter of Oddi dysfunction

Prevention:

  • Rectal NSAIDs
  • Pancreatic duct stent

6. Hypercalcemia

Causes:Hyperparathyroidism,Malignancy

Mechanism:Intrapancreatic trypsin activation

 

7. Autoimmune Pancreatitis

Associated with:IgG4 disease

Features:

  • Painless jaundice
  • Diffuse enlargement
  • Steroid responsive

Pathophysiology

Central Event:

Premature activation of trypsinogen → trypsin inside pancreas.

Trypsin activates:Elastase/Phospholipase/Lipase

Result:Fat necrosis/Vascular injury/Hemorrhage/Cytokine storm

 

Systemic Pathophysiology

Massive cytokine release:TNF-α/IL-1/IL-6

Leads to:SIRS/Capillary leakARDS/ShockAKI/MODS

 

TYPES

1. Interstitial Edematous Pancreatitis

  • Most common
  • Mild inflammation
  • Good prognosis

2. Necrotizing Pancreatitis

  • Pancreatic necrosis
  • Peripancreatic necrosis
  • Infected necrosis possible

Clinical Features

Pain

Classic:

  • Sudden severe epigastric pain
  • Radiates to back
  • Worse supine
  • Better leaning forward

Associated Symptoms

  • Nausea
  • Vomiting
  • Fever
  • Abdominal distension
  • Ileus

Examination Findings

Finding

Significance

Tachycardia

Hypovolemia/SIRS

Fever

Inflammation/infection

Hypotension

Severe disease

Epigastric tenderness

Common

Guarding

Severe inflammation

Jaundice

Gallstones

Reduced bowel sounds

Ileus

Hemorrhagic Signs

Rare but severe.

Sign

Description

Cullen sign

Periumbilical ecchymosis

Grey-Turner sign

Flank ecchymosis

Fox sign

Groin ecchymosis

Suggest hemorrhagic pancreatitis.

 

Laboratory Diagnosis

Serum Amylase

Serum Lipase

Less specific for pancreatitis

More specific for pancreatitis

Rises within 6–12 hours

Rises within 4–8 hours

Peaks at 24–30 hours

Peaks at about 24 hours

Returns to normal in 3–5 days

Remains elevated for 8–14 days

Can be normal in hypertriglyceridemia-induced pancreatitis

More reliable in hypertriglyceridemia

May rise in intestinal ischemia, perforation, ectopic pregnancy, renal failure

May rise in renal failure, bowel ischemia, cholecystitis

Macroamylasemia can falsely elevate level

No macro-lipasemia equivalent commonly significant

Macroamylasemia and Macrolipasemia

These are benign biochemical conditions in which pancreatic enzymes bind to large molecules (usually immunoglobulins), forming high-molecular-weight complexes that cannot be easily filtered by the kidneys.

This leads to:

  • Persistently elevated serum enzyme levels
  • Reduced urinary excretion
  • No true pancreatic injury

Other Labs

Test

Importance

CBC

Hemoconcentration/leukocytosis

LFTs

Gallstone cause

ALT >150

Strong biliary predictor

Calcium

Hypocalcemia severity

Triglycerides

HyperTG pancreatitis

CRP

Severity marker

ABG

Hypoxemia/metabolic acidosis

Lactate

Shock severity

Imaging

1. Ultrasound

First imaging in all patients.

Purpose:Detect gallstones/CBD dilation

Limitation:Pancreas poorly visualized due to gas

 

2. Contrast CT Abdomen

Best for:Necrosis/Complications/Severity assessment

Not needed routinely at admission.

Ideal timing:After 72 hours if severe/not improving.

 

CT-Based Severity Assessment in Acute Pancreatitis

Feature

Balthazar Grading

CT Severity Index (CTSI)

Modified CT Severity Index (MCTSI)

Purpose

Describes morphologic severity on CT

Combines Balthazar grade + necrosis

Simplified and clinically superior modification

Main Components

Pancreatic inflammation and collections

Inflammation + necrosis

Inflammation + necrosis + extrapancreatic complications

Necrosis Included?

No

Yes

Yes

Extrapancreatic Complications Included?

No

No

Yes

Maximum Score

Grade A–E

10 points

10 points

Best Use

Morphologic description

Severity prediction

Modern preferred CT severity scoring

 

Balthazar Grading

Grade

CT Findings

Points in CTSI

A

Normal pancreas

0

B

Focal/diffuse enlargement

1

C

Peripancreatic inflammation

2

D

Single peripancreatic fluid collection

3

E

≥2 fluid collections OR gas in pancreas/retroperitoneum

4

 

Pancreatic Necrosis Scoring (Used in CTSI)

Extent of Necrosis

CTSI Points

None

0

<30%

2

30–50%

4

>50%

6

 

CT Severity Index (CTSI) Formula=Balthazar Score+Necrosis Score

CTSI Score

Severity

Mortality/Complications

0–3

Mild

Low

4–6

Moderate

Intermediate

7–10

Severe

High

 

Modified CT Severity Index (MCTSI)

Components

Parameter

Score

Pancreatic inflammation

0–4

Pancreatic necrosis

0–4

Extrapancreatic complications

2

 

MCTSI Detailed Scoring

Finding

Score

Normal pancreas

0

Intrinsic pancreatic abnormalities with/without inflammatory fat changes

2

Pancreatic/peripancreatic fluid collection OR fat necrosis

4

No necrosis

0

≤30% necrosis

2

>30% necrosis

4

Any extrapancreatic complication

2

 

Extrapancreatic Complications in MCTSI

Include:

  • Pleural effusion
  • Ascites
  • Vascular complications
  • GI involvement
  • Parenchymal complications

 

MCTSI Interpretation

MCTSI Score

Severity

0–2

Mild

4–6

Moderate

8–10

Severe

 

 

3. MRI/MRCP

Useful for:

  • Biliary obstruction
  • Duct evaluation
  • Necrosis characterization

Revised Atlanta Classification

Severity Category

Definition / Features

Mild Acute Pancreatitis

• No organ failure 

• No local complications 

• No systemic complications 

• Usually self-limiting with excellent prognosis

Moderately Severe Acute Pancreatitis

• Transient organ failure (<48 hours)  OR

• Local complications (e.g., fluid collection, necrosis, pseudocyst)  OR

• Exacerbation of comorbid disease

Severe Acute Pancreatitis

• Persistent organ failure >48 hours 

• May involve one or multiple organs 

• Respiratory failure 

• Renal failure 

• Shock/cardiovascular failure 

• Associated with high mortality risk

Modified Marshall Scoring System in Acute Pancreatitis

Used in the Revised Atlanta Classification to define organ failure.

  • Score ≥2 in any organ system = organ failure
  • Persistent organ failure (>48 h) defines severe acute pancreatitis

Organ System

0

1

2

3

4

Respiratory (PaO₂/FiO₂)

>400

301–400

201–300

101–200

≤100

Renal (Serum Creatinine mg/dL)

<1.4

1.4–1.8

1.9–3.6

3.6–4.9

>4.9

Cardiovascular (Systolic BP mmHg)

>90

<90, fluid responsive

<90, not fluid responsive

<90, pH <7.3

<90, pH <7.2

Severity Scores

Score

Main Strength

Limitations

Current Role

APACHE II

Most validated ICU severity score; dynamic and repeatable

Complex; many variables

Most accurate overall for predicting severe disease and mortality

BISAP

Simple bedside early score

Slightly less accurate than APACHE II

Most practical early bedside score

Ranson Score

Historically classic

Delayed (48 h), outdated

Mostly exam importance

BISAP Score

Variable

BUN >25

Impaired mental status

SIRS

Age >60

Pleural effusion

Score ≥3:High mortality risk.

 

Initial Management

1.Fluid Resuscitation

Controlled Goal-Directed Fluid Therapy(WATERFALL Trial) – hydration in  first 24 hrs

Preferred Fluid: Lactated Ringer’s (LR)

Advantages over normal saline:

  • Less hyperchloremic acidosis
  • Reduced inflammation
  • Better pH balance
  • Lower SIRS rates

Typical Regimen

  • 5–10 mL/kg/hour OR Initial bolus:10–20 mL/kg if hypovolemic
  • Maintenance:1.5–3 mL/kg/hr

Assessing Fluid Responsiveness

Clinical Parameters

  • HR<120 ,BP≥65 mmHg
  • Capillary refill <3
  • Urine output >0.5ml/kg/hr

Parameter

Goal

MAP

≥65 mmHg

Urine output

>0.5 mL/kg/h

Hematocrit

Avoid rising

BUN

Falling trend

Why Avoid Excessive Fluids? Over-resuscitation causes:

  • Abdominal compartment syndrome
  • Pulmonary edema
  • ARDS
  • Increased mortality

2.Pain Management

Opioids

Commonly used:Fentanyl/Hydromorphone/Morphine

Old concern:“Morphine causes sphincter of Oddi spasm”

Current evidence:Clinically insignificant-Morphine acceptable

 

Multimodal Analgesia

May include:

  • Paracetamol/Ketamine infusion
  • Epidural analgesia (selected ICU patients)

3.Nutrition

Early Enteral Feeding(Within 24–48 hours if possible.)

Benefits:

  • Preserves gut barrier
  • Reduces infection
  • Reduces bacterial translocation

–Diet-Low-fat solid diet(Fat thought to stimulate pancreas excessively.)

Route

Notes

Oral

If mild and tolerated

NG feeding

Usually adequate(NG feeding generally as effective as NJ feeding)

NJ feeding

If gastric intolerance

TPN only if enteral impossible.

 

4.Antibiotics

NOT routinely indicated

Do NOT give prophylactic antibiotics for sterile necrosis.

 

Indications

Only if:

  • Infected necrosis
  • Cholangitis
  • Extrapancreatic infection(Pneumonia/UTI/CLABSI)

Signs of Infected Necrosis

  • Fever
  • Persistent sepsis
  • Gas in necrosis on CT
  • Positive culture

Antibiotics That Penetrate Pancreas

  • Carbapenems
  • Piperacillin-tazobactam
  • Quinolones
  • Metronidazole

Gallstone Pancreatitis Management

Urgent ERCP if:Cholangitis
OR Persistent biliary obstruction

Not needed routinely in all gallstone pancreatitis.

 

Hypertriglyceridemia Pancreatitis Treatment

  • Insulin infusion
  • Treat DKA if present
  • Fibrates later
  • Plasmapheresis in selected severe cases

Complications

Collection

Timing

Contents

Acute peripancreatic fluid collection

<4 weeks

Fluid only

Pancreatic pseudocyst

>4 weeks

Fluid only

Acute necrotic collection

<4 weeks

Fluid + necrosis

Walled-off necrosis

>4 weeks

Necrosis

Management of Collections

Observation

Most asymptomatic collections require no treatment.

Drainage Indications

  • Infection
  • Gastric outlet obstruction
  • Biliary obstruction
  • Persistent pain
  • Failure to thrive

Infected Pancreatic Necrosis

Major cause of late mortality.

Diagnosis

  • Gas in collection on CT
  • Clinical sepsis
  • FNA rarely needed now

Management: Step-Up Approach

  1. Antibiotics
  2. Percutaneous/endoscopic drainage
  3. Minimally invasive necrosectomy if needed

Timing of Intervention

  • Delay intervention whenever possible
  • Ideally:≥4 weeks after onset
  • Reason:Allows walling-off of necrosis.

Vascular Complications

Complication

Features

Splenic vein thrombosis

Gastric varices

Pseudoaneurysm

Massive bleeding

Hemorrhage

Shock

Pseudoaneurysm often:

  • Splenic artery
  • Gastroduodenal artery

Systemic Complications

System

Complication

Respiratory

ARDS, pleural effusion(left>>right)

Renal

AKI

CV

Shock

Hematologic

DIC

Metabolic

Hypocalcemia

GI

Ileus

ARDS in Pancreatitis

Due to:Cytokine-mediated lung injury/Capillary leak

Major mortality contributor.

 

Abdominal Compartment Syndrome

Causes:Massive fluids/Ileus/Edema

Suspect if:

  • Rising airway pressures
  • Oliguria
  • Tense abdomen

Measure bladder pressure.

 

 AKI in Pancreatitis

AKI in pancreatitis is usually multifactorial.

Major Mechanisms

1. Hypovolemia (Most Important Early Cause)

Acute pancreatitis causes:

  • Massive third spacing
  • Vomiting
  • Reduced oral intake
  • Capillary leak
  • Sweating/tachypnea

This leads to:

  • Reduced renal perfusion
  • Prerenal AKI

2. Systemic Inflammatory Response Syndrome (SIRS)

Result:

  • Renal ischemia
  • Acute tubular injury

3. Persistent Hypotension/Shock

Shock causes:

  • Renal hypoperfusion
  • Ischemic ATN

Septic shock may occur later due to:

  • Infected necrosis
  • Secondary infections

4. Intra-Abdominal Hypertension (IAH)