Acute pancreatitis Department of Surgery ,Medicine , IIUM

Sariu Ali 0616253IIUM

Anatomy

Physiology

Exocrine pancreas

•85% •1-2 L of alkaline enzyme rich juice/ day• trypsin-key proteolytic enzyme•Amylase/lipase/elastase

Endocrine pancreas

•2%•Islets of langerhans •A cells – glucagon•B cells – insulin•D cells – somatostatin•PP cells – pancreatic polypeptite

Autoprotection of the pancreas

Autodigestion of the pancreas is prevented by the packaging of protease in precursor form

Protease inhibitors Pacreatic secretory trypsin inhibitor (PSTI) Serine protease inhibitor- kazal type 1 (SPINK1)

These protese inhibitors are found in the acinar cells, pancreatic secretions, plasma.

In addition, low calcium concentration within the pancreas decreases trypsin activity

Loss of any of these protective mechanisms leads to zymogen activation and , autodigestion, and acute pancretitis

Acute pancreatitis

Sudden onset of diffuse inflammation of pancreas.

Results from premature activation of pancreatic exocrine enzymes (trypsin, phospholipase A, and elastase)

Acute interstitial/edemato

us pancreatitisAcute

hemorrhaging/necrotizing pancreatitis

Epidemiology

In developed countries annual incidence 1:2000

Mortality 2% 15% severe pancreatitis Women > Men Men: Recurrent Attacks Peak age : 50- 60 years

Aetiology

Non Traumatic (75%)

Traumatic (5%)

Idiopathic (20%)

Biliary Tract Disease ( 50%)Alcohol (20 -30%) viral infections (mumps)Drugs (Steroids )HyperlipidemiaHypercalcemiaPancreatic cancerScorpion bites

Operative trauma Blunt or penetrating injury Investigation (ERCP)

I GET SMASHED

Idiopathic

GallstonesEthanolTrauma

SteroidsMumps (& other viruses: CMV, EBV)

Autoimmune (SLE, polyarteritis nodosa)

Scorpion sting(Tityus Trinitatis)

Hyper Ca, TG ERCP (5-10% of pts undergoing procedure)

Drugs (thiazides, sulfonamides, ACE-I, NSAIDS, azathioprine)

Pathogenesis

Acute pancreatitis

Intracellular pancreatic enzymes activation

Increased capillary permeability

Tissue response: inflammation

Cytokines release

Fluid, protein, electrolytes loss (3rd space loss)

Hypovolaemic shock

Acinar cell injury

Multiorgan failure

Pancreatic duct obstruction

haemorrhage

ARDS

ARFDIVC

infection

sepsis

Pancreatic necrosis

+

Gallstone pancreatitis

• Transient blockage of common duct

• Reflux of bile in to pancreatic duct and/or impair flow of normal pancreatic juice

• Trigger premature activation of pancreatic enzymes within duct system

Microlithiasis

Treatment of microlithiasis (by cholecystectomy, endoscopic sphincterotomy) results in a significant reduction in the frequency of attacks of acute pancreatitis.

Recent studies have shown that a significant number of patients with idiopathic acute pancreatitis will have microlithiasis. This may be diagnosed either as gallbladder sludge on ultrasound (ultrasound of gallbladder sludge) or as crystals on microscopic examination of bile 

Alcohol-associated Pancreatitis

Long standing alcohol intake for at least 2 years or single session of heavy drinking.

Direct toxic effect of alcohol in genetically predisposed individuals.

Alcohol cause secretion of viscid juice with the formation of protein plugs and impairment of flow.

Clinical Features

Abdominal pain: pain vary from mild tolerable discomfort to severe

constant incapacitating characteristically in the epigastrium , radiate through

to the back, relieved by leaning forward.

May cause shoulder tip pain if diaphragmatic peritoneum inflamed

+/- Fever +/- Hypotension or shock

Nausea, vomiting and abdominal distension due to gastric and intestinal hypo motility and chemical peritonitis are also frequent complaints

Physical Examination

Distressed and anxious pt Low grade fever /Tachycardia /Tachypnea/Hypotension Shock Mild jaundice

Abdominal tenderness, distension, guarding, and rigidity Diminished or absent bowel sounds Mass palpable in epigastrium (pseudocyst)

Occasionally, in the extremities, muscular spasm may be noted secondary to hypocalcaemia.

Pleural Effusion (Left Side )

Cullen’s sign - periumbilical discoloration (rare)

Grey Turner sign - flank discoloration due to retroperitoneal bleed in pt. with pancreatic necrosis (rare)

Clinical classificationAssessment of Severity/prognosis

Assess on admission and next 48 hours of admission. Ranson Criteria

- a clinical prediction rule for predicting the severity of acute pancreatitis. It was introduced in 1974.

Glasgow Criteria-uses the data collected during the first 48 hours following an admission for pancreatitis.

APACHE II (Acute Physiology and Chronic Health Evaluation II)

is a severity of disease classification system (Knaus et al., 1985), one of several ICU scoring systems.

Ranson criteria

Present on admission:

1. Age greater than 55 y/o (non gall stone Pancreatitis) or 70 years (gallstone pancreatitis )

2. WBC greater than 16,000/uL

3. Blood glucose greater than 10mmol/L (non diabetic)

4. Serum LDH greater than 350 IU/L

5. SGOT (AST) greater than 100 U/L

During the next 48 Hours:

6. Hematocrit fall greater than 10%

7. serum urea increase greater than 8 mg/dL despite adequate IV therapy

8. Hypocalcemia (corrected serum ca <2.0mmol/L)

9. Arterial oxygen saturation less than 60 mm Hg

10. Metabolic acidosis (Base deficit greater than 4 mEq/L)

11. Estimated fluid sequestration greater than 6L

0-2 = minimal mortality3-5 = 10-20% mortality> 5 = > 50% mortality

Imrie (Glasgow scoring system)

Mnemonic letter

Criterion Positive when

P PaO2 < 60mmHg

A Age > 55 y/o

N Neutrophil count > 15 x 109/L

C Calcium (blood) < 2 mmol/L

R Raised plasma urea > 16 mmol/L

E Enzyme (serum LDH) > 600 iu/L

A Albumin (plasma) < 32 g/L

S Sugar (plasma glucose) > 10 mmol/L0-2 = mild pancreatitis> 2 = severe pancreatitis

APACHE II score

A: assessment of clinical parameters, e.g vital signs, electrolytes, arterial blood gases, etc.

B: points allocated in accordance with age

C: points added for co- morbid disease or chronic health of patient

A+B+C > 9 : severe acute pancreatitis

Mild acute pancreatitis

Common Patient looks generally well with

minimal systemic features Considerable pain Abdomen usually distended &

diffusely tender with little guarding Patient maybe jaundiced due to

periampullary edema

Severe acute haemorrhagic pancreatitis

Pt looks apathetic, pale and shocked Generalised peritonitis sx – extreme

tenderness, guarding & rigidity Can be complicated with ARDS

Differential Diagnosis

For mild Acute Pancreatitis Acute cholecystitis. Peptic ulcer (PU). Inferior myocardial infarction Lower lobe pneumonia Acute appendicitis

For severe Acute Pancreatitis Fecal peritonitis due to perforated colon Ruptures abdominal aortic aneurysm Ruptured ectopic pregnancy Massive bowel infarction

Investigations

Serum Amylase : >1000 diagnostic , can be lower in alcoholic pancreatitis , (also rise in cholecystitis, PU etc..)

Serum lipase ( more specific ) ALT raised /LFT Serum calcium level (low ) Lipid profile RBS ABG Full Blood Count (leukocytosis)

Investigations

Imaging Erect CXR (look for air under

diaphragm), supine AXR (‘ground glass’ appearance for peritoneal exudate)

HBS US – TRO gallstone pancreatitis CT scan Axial CT image of the

same patient (done a few hrs later) shows extensive inflammation and necrosis of the pancreas (arrows) with free fluid in the abdomen (stars).

Gall stone pancreatitis by ERCP

Management

Mild attackFluid resuscitation – pt may loose about

4-12 LAnalgesia No evidence to support use of antibiotic Nil by mouth (to “rest” the pancreas)Treat underlying causes○ Cholecystectomy for gallstone 2-4 weeks

after recovery○ Endoscopic removal of ductal stone○ Discouraged alcohol intake

No specific treatment , conservative management

Mx of Severe attack

Oxygen support Insert large bore branulasFluid resuscitation (crystalloid , plasma/dextran )Monitor CVP , urine output, Blood pressure, pulse, respiratory

rate Pain Relief (pethidine)Nasogastric tube to aspirate stomach contentEnteral NG/naso-jejunal feeding to decrease morbidityConsider TPN in pt who is not tolerating to enteral feeding

because of ileusProphylactic IV antibiotic – minimize infection to necrotic

pancreatitisAdmit ICU for close monitoring and vigorous RX of CVS,

pulmonary, renal and septic CxOthers

PPI to prevent stress ulcers DVT prophylaxis

Recommended frequent Ix in severe AP

TWBC ABG Blood sugarSerum amylase – to see the disease progressCRP ○ Better indicator for systemic inflammation○ If CRP > 100 on D5 → pancreatic infection, abscess

or pseudocystLiver function – see evidence biliary

obstructionRenal function – TRO ARF

Endoscopy & surgery for severe AP

All patients with suspected or proven gallstone etiology

Urgent ERCP within 72 hours of onset of pain

Sphincterectomy of sphincter of Oddi whether +/- stone

Biliary stent if stones seen or cholangitis or jaundice present

Endoscopic Biliary sphinterectomy with stone removal

Indications for Surgery

When the diagnosis is uncertain.

When patient fails to improve with conservative management or deteriorates.

If general condition and other indices (APACHE II score , CRP level )deotriatrating pancreatic or peripancreatic necrosis must be suspected.

When gall stones are present : surgery once the acute attack resolved

When complications develop.

Complications

Local

Necrosis & infection

Pancreatic fluid collections

Pancreatic pseudocyst

Pancreatic abscess

Systemic

Hypovolaemia and shock

Coagulopathy

Respiratory failure (ARDS)

Renal failure

Hyperglycaemia (late Cx lead to DM)

Hypocalcaemia

References

1. Bailey & Love’s short practice of surgery 24th ed2. Essential surgery 4th ed3. Pathophysiology of disease Lange, 5th ed4. Acute pancreatitis in north-eastern peninsular Malaysia: an

unusual demographic and aetiological pattern, Raj SM et al Singapore Med J 1995 Aug; 36(4): 371-4

5. Characteristics of acute pancreatitis in University Kebangsaan Malaysia.Nadesan S. et al Med J Malaysia. 1999 Jun;54(2):235-41.

Thank you