Acute Pancreatitis

Dr Tayyeb

PANCREAS

Core Contents

Definition Introduction Causes Pathophysiology Clinical Features Differential diagnosis Investigations Severity assessment

Core Contents
Management Prognosis Complications Role of antibiotics Role of nutrition Role of surgery Role of ERCP

Definition

Acute condition presenting with abdominal pain and is usually associated with raised pancreatic enzymes levels in the blood as a result of inflammatory diseases of the pancreas

Introduction
Accounts for about 3% of all cases of abdominal pain patients admitted to hospital May occur at any age with a peak in young men and older women. 80% are mild to moderate 20 % are severe cases

Causes

The Big Three:

Gall

Stones

(40%) (35%) (20%)

Alcohol Idiopathic

CAUSES

Trauma (pancreatic duct injury)

Post-ERCP Drugs (rare)

30 meds identified Azothioprine Valproic acid Didanosine Mesalamine

CAUSES
Organ

transplant, major surgery

Hypertryglycerides

(rare) Greater than 1000 mg/dL

Pregnancy
Third

trimester until 6 weeks post partum

CAUSES
HIV
35

to 800 times greater risk of AP c/w general pop.

Hypercalcemia
Most

often secondary to hyperparathyroidism spider, and Gila Monster lizard

Scorpion,

bites

Pathophysiology

Gall stones: Bile reflux, Pancreatic duct obstruction, Reflux of infected fluid, Activation of pancreatic enzymes, Autodigestion of pancreas and surrounding tissues, Activation of cytokines

Pathophysiology

Alcohol: Direct toxicity, Hypersecretion Ducts obstruction Hyperlipidemia Malnutrition

Pathophysiology
Ischemia: Hypoxaemia Free radicals production Vascular endothelial injury Drug induced: Direct injury Altered secretion

MORPHOLOGY
EDEMA
FAT

NECROSIS ACUTE INFLAMMATORY INFILTRATE PANCREAS AUTODIGESTION BLOOD VESSEL DESTRUCTION SAPONIFICATION

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Clinical Features

No pathognomonic symptoms and signs PAIN is the cardinal symptom Develops quickly, reach maximmum intensity and persist for hours and days Refractory to usual analgesics doses Classically upper abdominal pain radiating to back Nausea, vomiting and retching

Clinical Features
On examination: Findings depends on severity Ranges from a well patient to a gravely ill with shock, toxicity and confusion Tachycardia, tachypnea, hypotension Mild icterus

Clinical Features
Abdomen: Distended, tender, guarding, absent gut sounds Acute peritonitis picture Grey Turner and Cullen sign may be there Chest findings

Differential diagnosis
All causes of acute abdomen like, perforated duodenal ulcer, acute cholecystitis, gut ischemia ruptured aortic aneurysm etc MI Pneumonia

Investigations
Serum Enzymes: Amylase and Lipase Ultrasound X-Rays CT Scan Investigations for assessing the severity Investigations for diagnosis the cause of pancreatitis

Serum Amylase level

Raised early and come to normal early

Sensitive but not specific May be raised in other conditions as well like gut ischemia, parotitis, ruptured ectopic pregnancy.

Serum Lipase level

More specific Persist longer than amylase

X-Ray
Sentinel loop (localized ileus) Colon cut-off sign Renal halo Pleural effusion Calcified gall stone All are nonspecific

Ultrasound
Swollen pancreas in 30-50 % cases Gall stones Dialated CBD CBD stones Ascites

Ct Scan
>95 % sensitivity and specificity for detecting Pancreatitis Will exclude other cause of acute abdomen Detect pancreatic necrosis Can grade severity (Balthazar Scoring system) Costly and not easily available

Investigations

MOST important lab test is.?????

AMYLASE !!!!!!!

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SEVERITY

Early identification of severity and appropriate ICU care has significantly reduced mortality over the last 20 yrs Bedside eval (compared to severity scoring) missed over 50% of severe cases

Severity

Assessment

SEVERITY
When do you do early transfer to ICU? When do you consult critical care team? When do you start antibiotics? When do you get a CT scan? They say people crash fast who are these people? What is aggressive fluid resuscitation?

SEVERITY

APACHE II
Best

test

Can be done at 24 hrs, can be repeated Needs to be done at 24 and 48 hrs

Ransons Criteria (1974!)

Balthazars (CT scan criteria) Glasgow Single Markers of Severity

Ransons Criteria
3 is severe

SINGLE MARKERS

Management

Depends on the severity

Either manage the patient on the ward, HDU or ICU depends on the severity of the attack

Management

Symptomatic Supportive

Specific

Symptomatic

Analgesia
Antemetics N/G tube for decompression Antipyretics

Supportive

OXYGENATE
Give

O2 Liberal intubation /ventilation to treat ARDS

Intake and out put monitoring Vitals monitoring

TREATMENT

Vigorous intravenous hydration alone is the best available option in the prevention of pancreatic necrosis.

Pitchhumoni et al. Mortality in Acute Pancreatitis, Journal of Clinical Gastroenterology

TREATMENT

AGGRESSIVE FLUID RESUSCITATION

May

require 250-500 cc/hr for first 48 hrs

6 L of fluid is sequestered in abdomen alone Third spacing can consume up to 1/3 of total plasma volume
1/3

of people die in the first phase 50% of these are associated to ARDS

PULMONARY EDEMA CHF

TREATMENT

AGGRESSIVE FLUID RESSUCITATION

You

may create electrolyte imbalances that need to be corrected You may need CVP monitoring (central line) CXRs help (CHF vs ARDS) ABGs help (still hypoxic need more fluids?)
23% 0.5

of SAP pts get ARF 80% mortality

cc/kg/hr urine output is goal (need a Foley)

TREATMENT

How do you know you are resuscitated?

Blood

pressure Heart rate Urine output SPO2/ABGs show good oxygenation and no acidemia

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Specific
Treat/remove the cause Treat the complications Somatostatin, aprotonin etc fail to improve prognosis Magic bullet still awaited

Specific
The

trials with infliximab are an example of the magic bullet approach which has typified anticytokine trials

 Role

of Antibiotics

ANTIOBIOTICS
Controversial Mild to moderate attack NO Abx They DO decrease incidence of infection in necrosis, but do NOT decrease mortality Should cover multiple bugs Should get into pancreas If you see severe attack or necrosis start antibiotics

ANTIOBIOTICS

Imipenem
Cipro + metronidazole

One study showed 24% of pts had fungus

Very

poor prognosis

Role

of NUTRITION

NUTRITION
Normal pancreas secretes up to 2 liters/day of secretions Pancreatic stimulation during AP releases proteolytic enzymes Autodigestion Oral feeding increases release of secretin and cholecystokinin stim pancreas rest the pancreas NPO

NUTRITION

TRADITION:
the pancreas NPO TPN only after 5-7 days (prevent starvation) Ill pts cant be fed (ileus, aspiration)
Rest

NUTRITION

ENTERAL vs TPN Feedings:

If

distal to Ligament of Treitz (nasojejunal tube or J-tube) pancreatic secretion = basal rate Both started after 48 hours
Easier to restart po feedings Average length of nutritional support shorter

7 vs 11 days

Fewer septic complications

NUTRITION

NEW THOUGHTS

Meta-analysis of 15 randomized studies: Compared early vs delayed ENTERAL feedings in 753 critically ill pts Early was 36 hrs! Improved: Wound healing Host immune function Preservation of intestinal mucosal integrity Decreased infections

BUT, no decreased mortality

NUTRITION

Feed to maintain gut integrity Protects against transfer of bacteria

Role

of ERCP

ERCP
If there is a stone or cholangitis (biliary sepsis) or persistent jaundice Need urgent ERCP with sphincterotomy and stone extraction

Otherwise, ERCP not indicated

Role

of Surgery

Role of Surgery

No role for surgery during the initial period of resuscitation and stabilization
Diagnosis at laparotomy indicates poor practice

SURGERY
Used to be very liberal with early surgery Trauma

If

duct damaged

Gallstone etiology and mild

Cholecystectomy

in same admission If no chole 25-69% recurrence rate of pancreatitis within 6-18 wks

Sterile necrosis controversial Infected necrosis yes, but delay

NECROSIS
Starts to occur within 4 days of disease CT with po & IV contrast is gold standard

Necrotic

areas do not enhance You will NOT see it on CT before 48hrs

Once you Dx necrosis mortality jumps

40-60%

get secondary infection Mortality then approaches 80%

SECONDARY INFECTIONS

SYMPTOMS:
N/V,

epigastric pain, distension, fever, elevated WBC needle aspiration

Diagnosis of sterile vs infected necrosis

CT-guided

This is the most devastating complication and marks the second peak in mortality (@ 2 weeks)

SECONDARY INFECTIONS
What bugs? Gram (-) bacteria cross from gut

E.

coli (35%) Klebsiella (24%) Enterococcus (24%) Staph (14%) Pseudomonas, proteus, strep, enterobacter, bacteroides, anaerobes

SECONDARY INFECTIONS

Pathogens colonize gut Intestinal mucosal barrier breaks down

Bacteria crosses through

Complications

Systemic complications
Cardiovascular Pulmonary Renal Haematologica Metabolic Neurological Gastrointestinal

Local complications

Phlegmon Edema Effusion Ascites Infected effusion Pseudocyst Infected necrosis Pancreatic abscess Colonic fistula Spleenic artery aneurysm

Prognosis

MORTALITY

Mild Acute Pancreatitis

<

5%

Severe Acute Pancreatitis

25%

Nearly 20% of all pts with AP develop SAP 25% of SAP pts die

Prognosis
Mortality

reaches up to 50% with infected pancreatic necrosis

DISEASE COURSE
Deaths

occur in 2 phases: PHASE 1 (with in first few days):

SIRS ARDS
PHASE

2 (after second week):

Sterile necrosis Infected necrosis Multiple organ dysfunction

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