Acute Pancreatitis 🐼🐧 + Chronic Pancreatitis Flashcards
(35 cards)
Acute pancreatitis definition
- Reversible acute inflammation of pancreatic parenchyma & or peripancreatic tissues
or
- Inflammation associated with pancreatic parenchymal necrosisand/orperipancreatic necrosis.
Incidence of acute pancreatitis
- 5 – 80/100000
- M > F
- 80% mild disease, 20% severe disease
- 5% mortality (1.5% mild 20% in severe pancreatitis)
Etiology of Acute Pancreatitis
- Idiopathic 10 - 20% : Microlithiasis (calculi < 3mm or sludge) or hypertensive sphincter
- Gallstone 45%
- Ethanol 35%
- Tumor : Pancreas, Ampulla, Cholangiocarcinoma
- Surgery
- Trauma
- Infection: Viral (HIV, Mumps, Varicella-zoster virus (VZV)), TB, Leptospirosis, Parasite (Ascariasis)
- Autoimmune: SLE, PAN, Crohn’s
- Biliary stricture, Choledochal cyst
- Hyper Triglycerides, Hypercalcemia 1 – 4%
- Post ERCP 1 – 3%
- Drugs: Diuretic, ACEi, Azathioprine, ASA, NSAID, Steroids
Pathophysiological of acute pancreatitis
Common Channel Theory - Passing of gallstone/parasite through ampulla → blockage of common channel → leads to reflux of bile into pancreatic duct → pancreatitis
- Momentarily incompetent sphincter → reflux of duodenal juice → enzyme activation
- Chemical Insult → release of lysosome & enzyme → acinar cell injury
-
Alcohol →
- ↑ ductal permeability → improperly activated enzyme in duct leak into surrounding tissue → pancreatitis
- ↑ secretion of enzyme → enzyme precipitate in duct by calcium → duct obstruction → pressure build up → pancreatitis.
Phases of acute pancreaetitis
Phase 1 (Vasoactive/SIRS) – Management - Supportive care
Phase 2 (Septic) – Management - Treatment of local & systemic complications
Classification of acute pancreatitis
What is interstitial Edematous Pancreatitis
Inflammation of pancreatic parenchyma and peripancreatic tissue, but without obvious tissue necrosis. 80%–90% of patients presenting with acute pancreatitis.
CECT Criteria
- Enhancement of the pancreatic parenchyma by contrast agent
- No evidence of peripancreatic necrosis
Can divided into:
- Acute peripancreatic fluid collection (APFC)
- Pancreatic pseudocyst
Types of Interstitial edematous pancreatitis
APFC (acute peripancreatic fluid collection): Peripancreatic fluid seen within first 4 weeks after onset of interstitial edematous pancreatitis and no peripancreatic necrosis.
CECT Criteria
- Homogeneous collection with fluid density adjacent to pancreas confined by normal
peripancreatic fascial planes. - No recognizable wall encapsulating the collection
Pancreatic pseudocyst: Encapsulated fluid collection occurring > 4 weeks after onset of interstitial edematous pancreatitis, with minimal or no necrosis and with a well-defined inflammatory wall usually outside the pancreas.
CECT Criteria
- Round or oval well circumscribed, homogeneous fluid collection
- No non liquid component
- Well-defined wall
- Occurs after interstitial edematous pancreatitis
Types of Necrotizing Pancreatitis
Inflammation with pancreatic parenchymal necrosis and/or peripancreatic necrosis.
CECT Criteria
- Areas of pancreatic parenchymal lacking by intravenous contrast agent and/or
- Findings of peripancreatic necrosis (see below—ANC and WON)
ANC (acute necrotic collection): A collection of both fluid and necrosis associated with necrotizing pancreatitis involving pancreatic parenchyma and/or the peripancreatic tissues.
CECT Criteria
- Heterogeneous, nonliquid density of varying degrees
- No definable encapsulating wall
- Location: intrapancreatic and/or extrapancreatic
- Occurs in setting of acute necrotizing pancreatitis
WON (walled-off necrosis): A mature, encapsulated collection of pancreatic and/or peripancreatic necrosis with a well-defined inflammatory wall occurring > 4 weeks after onset of necrotizing pancreatitis.
CECT Criteria
- Heterogeneous liquid and nonliquid density with varying degrees of loculations
- Well-defined encapsulating wall
- Location: intrapancreatic and/or extra-pancreatic
- Occurs only in setting of necrotizing pancreatitis
Investigation for pancreatitis
- Blood tests (as per diagnostic & severity assessment) - Full Blood Count, Liver Function Test, Amylase, Renal Function test.
- Cut-off value of serum amylase and lipase is normally defined to be three times upper limit.
- CRP ≥ 150 mg/l at third day - prognostic factor for severe acute pancreatitis.
- Hematocrit > 44% - independent risk factor of pancreatic necrosis.
- Urea > 20 mg/dl - independent predictor of mortality.
- Procalcitonin is most sensitive for detection of pancreatic infection, low values strong negative predictors of infected necrosis.
- In absence of gallstones or significant history of alcohol use, serum triglyceride and calcium levels should be measured. Serum triglyceride levels over 11.3 mmol/l (1000 mg/dl) indicate it as the etiology.
- On admission, USG should be performed to determine etiology of acute pancreatitis (biliary).
- When doubt exists, CT provides good evidence of the presence or absence of pancreatitis.
- CT without contrast is an alternative for the first two patient groups, if MRI is not available.
- All patients with severe acute pancreatitis need to be assessed with CE-CT or MRI. Optimal timing for first the CE-CT assessment is 72–96 h after onset of symptoms (overall detection rate of close to 100% sensitivity after 4 days for pancreatic necrosis).
- In severe acute pancreatitis (CT severity index ≥ 3), a follow-up CECT is indicated 7–10 days from initial CT scan, additional CE-CT recommended only if clinical status deteriorates or fails to show continued improvement, or when invasive intervention is considered.
- X- ray Abdomen – nonspecific, signs of bowel ileus.
Accurate Detection of Necrosis: In the initial 72 hours, inflammatory changes and edema can obscure imaging findings, making it challenging to distinguish between edematous and necrotic pancreatic tissue. Delaying CECT allows for clearer visualization and more precise assessment of pancreatic necrosis.
Diagnositic criteria of pancreatitis
2 out of 3 of the following criteria:
- (A) Abdominal pain consistent with acute pancreatitis.
- (B) Serum lipase (or amylase activity) >3 X upper limit of normal
- (C) Characteristic findings of acute pancreatitis on CECT and MRI or transabdominal USG
(A) +ve, & (B) -ve = (C) required to confirm diagnosis.
(A) +ve, & (B) +ve = (C) NOT required to confirm the diagnosis.
Severity Assessment for acute pancreatitis
1) Revised Atlanta Classification
2) Glasgow ( imrie) severity scoring system
3) Modified Marshall Scoring system
Revised Atlanta Classification
Mild Acute Pancreatitis
- No organ failure
- Lack of local or systemic complications
Patients resolve their symptoms rapidly and are discharged usually within first week. Mortality is rare, and pancreatic imaging is often not required.
Moderately Severe Acute Pancreatitis
- Organ failure that resolves within 48 hours (transient organ failure) and/or
- Local or systemic complications (sterile or infected) without persistent organ failure.
Morbidity (longer stay and need for intervention) is increased. Should be admitted to an intensive care unit whenever possible.
Mortality is also increased somewhat (<8%).
Depending on the complications of the acute pancreatitis, patients may be discharged within second or third week or may require prolonged hospitalization because of local or systemic complications.
Severe Acute Pancreatitis
- Persistent single or multiple organ failure (>48 hours)
Should be admitted to an intensive care unit whenever possible.
Patients with severe acute pancreatitis that develops within early phase (first week) are at a 36% to 50% risk of death.
Development of infected necrosis later in course of disease in patients with severe acute pancreatitis also has an extremely high mortality.
Prognostic scoring for pancreatitis
1) Ranson Criteria and prognnosis
2) Bedside index of severity in acute pancreatitis ( BISAP) score
Overview of Pancreatitis Management
Outline of management in Pancreatitis patient
1) ICU admission: Persistent organ dysfunction or organ failure occurrence despite adequate fluid resuscitation is an indication for ICU admission.
2) Fluid administration should be goal directed fluid therapy.
-In the management of acute pancreatitis, fluid resuscitation strategies are critical and can be categorized into two primary regimens: aggressive and moderate. ( for first 48hours to 72 hours)
Aggressive Fluid Resuscitation:
Initial Bolus: Administer 20 mL per kilogram (kg) of body weight of Lactated Ringer’s solution.
Continuous Infusion: Follow with a maintenance rate of 3 mL/kg per hour. (source New England Journal of Medicine)
Moderate Fluid Resuscitation:
- For Hypovolemic Patients:
Initial Bolus: Administer 10 mL/kg of Lactated Ringer’s solution.
Continuous Infusion: Proceed with a maintenance rate of 1.5 mL/kg per hour.
- For Normovolemic Patients:
No Initial Bolus.
Continuous Infusion: Start with a maintenance rate of 1.5 mL/kg per hour..
3) Antibiotics
- No role for routine prophylactic antibiotics
- Indication for antibiotics
- Extra pancreatic infection : Cholecystitis, cholangitis, pneumonia
- Infected pancreatic necrosis: Confirm by CECT or FNA C&S or deterioration after 7-10 days.
- Serum PCT valuable in predicting risk of developing infected pancreatic necrosis.
- Antibiotics that penetrate pancreatic necrosis - Carbapenems, Quinolones, and Metronidazole, high-dose Cephalosporins.
- Antifungal: Only in proven infection.
4) Pain management:
- As per WHO step ladder, NSAIDS should be avoided in AKI
5) Nutrition
- Mild - oral feedings can be started immediately if there is no nausea and vomiting, and after abdominal pain has resolved. Low-fat solid diet - safe as a clear liquid diet.
- TPN if EN route not indicated or tolerated.
⚠️ Clinical Use of ProCalciTonin (PCT)
✅ Helps differentiate bacterial vs viral infections
✅ Aids in deciding antibiotic initiation or discontinuation
✅ Used in sepsis risk stratification
✅ Monitors response to antimicrobial therapy
how Procalcitonin helps to detect infection
⚙️ How PCT Works in Infection:
🔹 In Healthy People
PCT is only produced in thyroid C cells, converted quickly to calcitonin.
🧪 Serum PCT level = very low.
🔥 In Bacterial Infection / Sepsis
- Bacterial toxins (e.g. endotoxins) and cytokines (e.g. IL-1β, TNF-α, IL-6) stimulate PCT production.
- Multiple organs (liver, lungs, kidneys, adipose tissue) begin to produce PCT.
- Unlike thyroid production, this PCT is not converted to calcitonin → it accumulates in blood.
🟠 PCT starts rising within 2–4 hours, peaks at 6–24 hours, and has a half-life of about 24 hours.
❌ In Viral Infections
Interferon-γ (produced in viral infections) inhibits PCT production.
So, PCT remains low → helpful to differentiate bacterial vs viral.
Overview of severe pancreatitis management
Principle of management:
Aims:
- Risk Factor Management
- Local Complication Management (Local & Perivascular)
- Systemic Complication Management
Risk factor management in Severe Pancreatitis
- ERCP in patients with acute gallstone pancreatitis and cholangitis or CBD obstruction is indicated. Sphincterotomy reduces risk of recurrence.
- MRCP or EUS should be considered rather than ERCP to screen for occult common bile duct stones in patients with unknown etiology and when repeat US is negative for pathology suggestive of obstruction.
- Gallstone pancreatitis - Cholecystectomy recommended prior discharge.
- Alcohol induced pancreatitis - Refer psychiatrist for counselling, coping strategy & support group
Local Management of Severe pancreatitis
APFC
- 30 – 50% of severe pancreatitis.
- Non-enzymatic inflammatory fluid, No duct disruption
- 50% settle spontaneously, 50% symptomatic (rupture, infection, pseudocyst, pancreatic ascites)
- Management: Observation for 6 weeks → non resolving – suspect & manage as pseudocyst.
- Octreotide - ↓ pancreatic secretions and is used if ductal leak.
- If infection is suspected → CT/US guided FN aspiration → Gram stain & culture
- Antibiotics in infection/sepsis
Necrotizing Pancreatitis
- Diagnosis is by CT scan - 1st CT done after 5 – 7 days since NP occurs early, complete by day 14
- Follow up CT if patient deteriorate clinically
- Pancreas tissue < 50HU, necrosis > 3cm or > 30% gland.
- Pancreatic tissue 50 – 80HU suggest necrosis, edema or fat.
Local Management of severe pancreatitis ( Necrotizing pancreatitis)
1) Sterile Pancreatic / Peripancreatic Necrosis
- CT guided FNA – if sterile, stop antibiotic & conservative management for 6 weeks.
- Intervention indication:
- Mechanical obstruction: GOO, biliary obstruction
- Persistent symptoms: > 6 weeks after pancreatitis
- Disconnected duct syndrome
- Deteriorate even without evidence of infection or despite full intensive therapy
- Persistent organ failure despite maximum ICU Rx
2) Infected Pancreatic Necrosis
- >70% with necrotizing pancreatitis; mortality up to 60%
- Bacteria translocation from small bowel and colon; mainly Gram-negative (E.coli, Enterobacter), Staph aureus, Enterococcus, Candida albicans
- Dx: CT scan/ AXR – gas bubbles. CT/US guided FN aspiration
- All need intervention. Mortality without intervention ~80-90%
- Percutaneous drainage - first line of treatment (step-up approach) delays surgical treatment to a more favorable time or even results in complete resolution of infection in 25–60%.
Overview of Step up Approach in Severe Pancreatitis
Management of pancreatic abscess post pancreatitis
- Limited pancreatic / peripancreatic necrosis → infection, liquefaction → pus formation
- Low-grade infection in a localized acute fluid collection → Infected pseudocyst
- Presence of pus with little or no pancreatic necrosis (differentiate infected pancreatic necrosis)
- Prognosis better than infected necrosis
- Diagnosed by CT Scan
- Drainage as per chart above.
Management of pseudocyst post pancreatitis
- Etiology - Chronic pancreatitis (35%), Acute Pancreatitis (15%), Pancreatic trauma
- Pathophysiology:
- Ductal disruption due to inflammation or trauma,
- Parenchymal injury from pancreatitis or trauma.
- Clinically - Abdominal pain, tender epigastric mass, vomiting ± jaundice. If without history of trauma rule out cystic pancreatic neoplasm.
-
Acute - collection of pancreatic juice enclosed by a wall of fibrous or granulation tissue, lacks an epithelial lining (no well defined wall) → > 4 weeks
- > 80% within or adjacent to the pancreas in lesser sac, also reported in mediastinum, pelvis.
- Chronic - well-defined wall within the pancreatic capsule (intrapancreatic).
- CT, EUS – if suspicious of cystic neoplasm.
- FNA for amylase, CEA, CA 19.9.
- To look for pancreatic fistula - MRCP, ERCP diagnostic & therapeutic.
Complications from pseudocyst, WON or ANC
1) Infection
- May result after endoscopic placement of pancreatic stent
- Rx: antibiotics + removal of stent ± US guided percutaneous drainage
2) Rupture
- <5% rupture spontaneously, can rupture into peritoneal cavity, adjacent viscus (gastric, jejunum, colon), pleural or pericardial cavity
- Features of peritonitis, severe pain
- Rx: Conservative (Octreotide, antibiotics, IVD)
- May need laparotomy, irrigation, biopsy of wall and internal drainage
3) Hemorrhage
- Usually follows erosion of an adjacent artery and formation of a pseudoaneurysm in the cyst wall
- Embolization of bleeding vessel (usually splenic or gastroduodenal artery) → continue bleeding → surgery → suture ligate the bleeding vessel in the cyst wall → internal drainage of cyst
- If possible, excise cyst to avoid recurrent bleeding
4) GOO: vomiting
5) Bile duct obstruction: jaundice, cholangitis
