TOPIC PRESENTATION

ACUTE PANCREATITIS

NOUMAN MEMONRESIDENT 1,

SURGICAL UNIT 4CHK

EPIDEMIOLOGY

17 per 100,0002-3% overall mortality from acute pancreatitisMale: female ratio is 1:3- in those with

gallstones and 6:1 in those with alcoholismThe median age at onset depends on the

etiology AIDS-related - 31 yearsVasculitis-related - 36 yearsAlcohol-related - 39 yearsDrug-induced etiology - 42 yearsERCP-related - 58 yearsTrauma-related - 66 years Biliary tract–related - 69 years

CAUSES Obstructive(75%)

Gall Bladder stone Tumor

Traumatic (5%) Operative trauma Blunt/penetrating

trauma Lab test(ERCP /

angiography)

Drugs 6-mercaptopurine Azathioprine DDI (2 ′ 3 ′

dideoxyinosine) Estrogens Thiazides• Sulfa drugs etc

• Metabolic TG ~ 4% > 1000

mg/dl PTH < 0.5%

Toxins Alcohol Scorpion bites Tityus trinitatis & T. serrulatus Insecticides

• Infection• Viral• HIV/EBV/Coxsackie/Mumps• CMV/Varicella/Hep A&C

• Parasitic• Ascariasis, clonorchiasis

• Bacterial• Mycoplasma, C. jejuni, TB• MAI, Leptospirosis,

Legionella

• Vascular• Ischemia• Embolic• Vasculitis

• MISC• Hereditary• Cystic Fibrosis• Idiopathic: 10 to 30%• microlithiasis• P. divisum• Annular pancreas• SOD• Crohn’s Dz• Post Perf DU

Idiopathic Acute PancreatitisThe etiology of acute pancreatitis should be

determined in at least 80% of cases and no more than 20% should be classified as idiopathic

Gall stone disease represents approximately half the cases of acute pancreatitis, and 20–25% are related to alcohol abuse

The correct diagnosis of acute pancreatitis should be made in all patients within 48 hours of admission.

The diagnosis of idiopathic pancreatitis should not be accepted in the absence of a vigorous search for gall stones as a minimum, it is necessary to obtain at least two good quality ultrasound examinations.

Clinical Presentation Pain (95%)

◦ Acute onset ◦ Mid-abdominal or mid-epigastric ◦ Radiates to the back (50%)◦ Peak intensity in 30 minutes◦ Lasts for several hours

Nausea and vomiting (80%) Fever Shock Abdominal distension (75%) Abdominal guarding and tenderness (50%) Restlessness and agitation

Grey-Turner's sign (hemorrhagic discoloration of the flanks) Cullen's sign (hemorrhagic discoloration of the umbilicus)

Cullen's sign

Grey-Turner's sign

Laboratory Diagnosis

BASELINE INVESTIGATION LFT’S Increased amylase and/or lipase >3 times

◦ Amylase levels rise w/in 2-12h Peak w/in first 48hr Remain elevated 3-5days before return to

baseline ◦ Lipase much more specific Height of elevation does not correlate with severityNo utility in following daily levels after the diagnosis

Serum Ca+ LDH VIRAL ANTIBODY TITERS

OthersU/S ABDOMENCT SCANEUSMRCP

PREDICTION OF SEVERITY

Available prognostic features which predict complications in acute pancreatitis are

clinical impression of severityObesityAPACHE II >8 in the first 24 hoursC reactive protein levels >150 mg/lGlasgow score 3 or morePersisting organ failure after 48 hours

in hospital

APACHE II score (Acute Physiology And Chronic Health Evaluation)

Glasgow coma scale

Signs of Organ FailureCardiovascular

◦ Hypotension◦ Septic physiology

HR, CO and SVR

Respiratory◦ Hypoxemia◦ Pleural effusions

Renal ◦ ATN◦ Oliguria

Hematologic◦ DIC◦ Thrombocytosis

Hepatic◦ Encephalopathy◦ T bili (3 mg/dl)◦ AST/ALT 2X nl

GI◦ Stress ulcer◦ Acalculous cholecystitis

Determining severityClinical assessment,

fluid status vitals UOP pulse oximetry

Clinical criteria◦Ranson criteria◦Atlanta criteria◦POP score

Radiographic criteria◦CT severity index

necrosis may not be evident until 48-72h

Ranson ScoreAt admission age in years > 55 years white blood cell count > 16000 cells/mm3 blood glucose > 11 mmol/L (> 200 mg/dL) serum AST > 250 IU/L serum LDH > 350 IU/L At 48 hours Calcium (serum calcium < 2.0 mmol/L (< 8.0 mg/dL) Hematocrit fall > 10% Oxygen (hypoxemia PO2 < 60 mmHg) BUN increased by 1.8 or more mmol/L (5 or more

mg/dL) after IV fluid hydration Base deficit (negative base excess) > 4 mEq/L Sequestration of fluids > 6 L

Atlanta criteria

Pancreatitis Outcome Prediction Score

When Do I Order A CT?If the patient has…..

◦ Persisting organ failure◦ Signs of sepsis◦ Deterioration in clinical status after 6-10days◦ Diagnostic dilemma◦ Infection suspected

T > 101o F Positive blood cultures

What kind of CT?◦ CT scan with pancreatic protocol

What are you looking for?◦ Necrosis: Lack of enhancement with contrast◦ Fluid Collections◦ Alternate diagnosis

Follow up scan are recommended only if the patient’s clinical status deteriorates or fails to show continued improvement.

CT scan with pancreatic protocol500 ml of oral contrast by mouth

or nasogastric tube. An initial scan without iv contrast show extent of peripancreatic change. A post contrast series is obtained aftr iv inj of 100 ml of nonionic contrast delivered at 3 ml/s Images through the pancreatic bed should be obtained with in 40 sec and before 80 sec.

CT FindingsPancreas

◦ Pancreatic enlargement◦ Decreased density due to edema◦ Intrapancreatic fluid collections◦ Blurring of gland margins due to

inflammationPeripancreatic

◦ Fluid collections and stranding densities◦ Thickening of retroperitoneal fat

* It may take up to 72h for inflammatory changes to become apparent on CT *

CT Findings

Tail Indistinct

Intraperitoneal fluid

PANC

CT FindingsSevere Pancreatitis

NonenhancingNecrosis

Peripancreatic edemaand inflammation

Balthazar ScoringCT grading of severity

POINTSGrade of Acute Pancreatitis A =Normal pancreas 0B =Pancreatic enlargement 1C =Pancreatic/peripancreatic

inflammation 2D =Single peripancreatic fluid collection 3E =Multiple fluid collections 4

Grade E = 50% chance of developing an infection and 15% chance of death

Degree of Necrosis No necrosis 0Necrosis of one third of pancreas 2Necrosis of one half of pancreas 4Necrosis of more than one half 6

CT Severity Index = Grade + Degree of necrosis

When can he eat ?TPN vs. enteral feeding

In patients with severe disease, oral intake is inhibited by nausea; the acute inflammatory response is associated with impaired gut mucosal barrier function.

It has been suggested that nutritional support may help to

limit the stimulus to the inflammatory response. Reduce microbial translocation Enhance gut mucosal blood flow Promote gut mucosal surface immunity

In these circumstances enteral feeding seems to be safer than parenteral feeding, with fewer septic complications.It is also cheaper

Contd…Tube feed if anticipate NPO > 1 week.Nasogastric feeding may be feasible in up to 80% of cases. Caution should be used when administering nasogastric feed to patients with impaired consciousness because of the risk of aspiration of refluxed feed.

In that case nasojeujunal tube can be used.

The use of enteral feeding may be limited by ileus. If this persists for more than five days, and if can’t maintain adequate jejunal access parenteral nutrition will be required.

Possible pathways for pancreatic infection

There are few mechanisms by which bacteria may enter pancreatic and peripancreatic necrosis

The haematogenous route via the circulation.Transmural migration through the colonic

bowel wall either to the pancreas (translocation),or via ascites to the pancreas, or via the lymphatics to the circulation

The biliary duct system from the duodenum via the main pancreatic duct.

Intra abdominal fungal infection can also complicate AP

Bacteriology in severe acute pancreaticEscherichia coli 25%Staphylococcus aureus 17%Pseudomonas spp 15%Klebsiella spp 9%Proteus spp 9%Candida 4%Streptococcus faecalis 3%Enterobacter spp 3%Anaerobes 16%Monomicrobial 76%Polymicrobial 24%

Management All patients with acute pancreatitis should receive adequate

oxygen

Start IV fluids with crystalloid Colloid (blood if Hct <25, albumin if serum alb <2) Rate of fluid replacement should be monitored by frequent

measurement of central venous pressure

Closely follow input output charting 0.5ml/kg /hr in absence of renal failure

Analgseics Opioids

Antiemetics

NGT decompression if frequent emesis or evidence of ileus on plain films

Monitor & correct electrolytes.

When Do I Start Antibiotics?Acute pancreatitis is c/b infection

~ 10% 30-50% of those with necrosis get infection

Prophylactic antibiotics◦ Controversial

No benefit in mild EtOH pancreatitis Selective gut decontamination may be beneficial

General recommendations for use:◦ Biliary pancreatitis with signs of cholangitis◦ > 30% necrosis on CT scan

Antibiotic Efficacy factor

Aminoglycosides• Netilmicin 0.14• Tobramycin 0.12

Acylureidopenicillins• Mezlocillin 0.71• Piperacillin 0.72

Cephalosporins• Cefotiam 0.75• Ceftizoxime 0.76• Cefotaxime 0.78• Ceftriaxone 0.79

Quinolones• Ciprofloxacin 0.86• Ofloxacin 0.87

Carbapenems• Imipenem 0.98

A final word on antibioticsDo not use empirically early in

mild pancreatitis

Fever early in the disease process is almost universally secondary to the inflammatory response and NOT an infectious process

When Do I Consult GI ?Evidence of biliary pancreatitis

◦ Elevated LFTs + pancreatitis No matter what the US shows

Severe pancreatitisRecurrent unexplained pancreatitis

Rule out infected necrosis EUS FNA sampling of fluid collections

Endoscopic treatment of necrosis/abscess

GALL STONE PANCREATITIS AND TREATMENTOF GALL STONES

Q: When should I suspect it ?◦A: Always

Q: How do I evaluate for it ?◦A: (E)US and LFTs

Q: When is ERCP indicated ?

Contd….

Urgent therapeutic ERCP should be performed in patients with acute pancreatitis of gall stone etiology who satisfy the criteria for severe pancreatitis, or when there is cholangitis, jaundice, or a dilated common bile duct.

The procedure is best carried out within the first 72 hrs after the onset of pain.

All patients undergoing early ERCP for severe gall stone pancreatitis require endoscopic sphincterotomy whether or not stones are found in the bile duct. Patients with signs of cholangitis require endoscopic sphincterotomy or duct drainage by stenting to ensure relief of biliary obstruction

Timing of cholecystectomy All patients with biliary pancreatitis

should undergo definitive management of gall stones during the same hospital admission.

For unfit patients, endoscopic sphincterotomy alone is adequate treatment

Complications of APImmediate

Shock DIC ARDS

Late Pancreatic pseudocyst Pancreatic abscess Pancreatic necrosis Progressive jaundice Persistent duodenal ileus GI bleeding Pancreatic ascites

Management of Pancreatic ComplicationsAcute fluid collections

◦ Occur early, seen but not felt◦ No defined wall usually resolve

spontaneously◦ No routine percutaneous or operative

drainage require

Infected pancreatic necrosis

Pancreatic abscess

Pseudocysts

Infected necrosis

All patients with persistent symptoms and greater than 30% pancreatic necrosis, and those with smaller areas of necrosis and clinical suspicion of sepsis, should undergo image guided FNA to obtain material for culture 7–14 days after the onset of the pancreatitis.

Patients with infected necrosis will require intervention to completely debride all cavities containing necrotic material.

Contd…Radiological

percutaneous wide bore drainage

Surgical Debridement of necrotic tissue following this abdomen can be

closed in three ways Closed ovr drain Packed and left open Closed over drain and irrigated

A new approach for surgical debridement of infected necrosis offers the potential to debride necrotic tissue with minimal systemic disturbance, by approaching the cavity along the track of a percutaneously placed drain.The cavity is then debrided piecemeal with an operating nephroscope. Several sessions may be required in order to achieve complete debridement. Postoperatively the cavity is continuously irrigated

PseudocystsCollection of pancreatic fluid

enclosed by non-epithelialized wall of granulation tissue

Complicates 5-10% cases of AP

~ 4 weeks after insult

25-50% resolve spontaneously

Complications of PseudocystInfection - 14%

Rupture - 6.8%

Hemorrhage - 6.5%

Common bile duct obstruction - 6.3%

GI obstruction - 2.6%

Pseudocyst ManagementOld thought

◦Pseudocysts > 5 cm that have been present > 6 weeks must be drained

Current practice◦Asymptomatic pseudocysts,

regardless of size, do not require treatment

Pseudocyst Drainage Techniques

Endoscopic

Surgical

Radiologic

Communicating Non-communicating

Endoscopic Pseudocyst Management

Percutaneous Pseudocyst Drainage

Laparoscopic Cyst Gastrostomy

Open cyst Gastrostomy

Pancreatic abscess

◦CT or EUS guided drainage Walled collection of pus Similar to management of pseudocyst

Closing PointsPatients with severe acute pancreatitis

have an increased risk of death.Patients who die usually have

evidence of organ failure.All patients with severe acute

pancreatitis should be managed in a high dependency unit or intensive therapy unit with full monitoring and systems support

The pancreas is mean organ….respect it