ACUTE PANCREATITIS

Dr. Mihai CIOCRLAN

Chapters
1) 2) 3) 4) 5) 6) Definition and incidence Positive diagnosis Severity assessment Etiological diagnosis Differential diagnosis Principles of therapy
Clinical Biological Imaging

1) Definition and incidence

Definition = acute inflammation of the pancreas due to various causes Incidence = 5 50 /100.000 habitants

2) Positive diagnosis
Clinical
PAIN (90%)
Tipical = epig./hcd/horisontal posterior irad. /whole abd., chien de fusil

VOMITING (50%) ILEUS (30%) SHOCK (10%), Mt. > 40% DISPNOEA (15%), Mt. > 30% OLIGO/ANURIA (10-15%), Mt. 30-50% NEUROLOGICAL (5%), Mt. 30% INFECTIOUS (4%), Mt. 15% HAEMORRHAGE (3%), Mt. 20%

Independent on the severity of the AP

2) Positive diagnosis
Clinical
Atypical forms, only moderate, transitory PAIN

2) Positive diagnosis
Biological
Lipase > 3xN Amylase, not to be used

AP = (typical abdominal pain) + (lipase > 3 x N)

2) Positive diagnosis
Imaging
If the diagnosis is clear, straightforward, no imaging test is necessary In doubt? An abdomen-pelvis CT scan is required
Without iv contrast if renan failure With iv contrast if normal renal function (creatinine)

Other imaging tests

No plain abdominal X-ray No abdominal ultrasound (but rapid, can be done for etiology)

3) Severity assessment
Clinical
oedematous AP, ~ benign
PAIN, VOMITING, ILEUS (typical) Only moderate PAIN (atypical)

necrotic AP, ~ severe

Same as oedematous AP, typical/atypical + MODS - Shock, ARDS, Renal failure Infectious complications Other complications (digestive, coagulation, neuropsihical, cutaneous)

3) Severity assessment
Clinical
Severe AP - imediate = SIRS (cytokines):
Circulatory: shock Respiratory: ARDS dispnoea (pleural effusion also) Renal: Functional renal failure (75%) / organic (25%)

Severe AP late = through infectious complications

4% of AP,0% benign AP, 30% of severe AP When? At the end of week 1 to week 4 (W1-W4) How? Infection of the pancreatic necrois by bacterial translocation
Clinical (&biological) worsening, imaging air bubbles in pancreatic necrosis CT/EUS guided necrosis aspiration + cultures

Other infections also: pulmonary, urinary, etc;

3) Severity assessment
Clinical
Severe AP late = through other complications
Digestive: duodenal ulcers +/- bleeding, ischemic colitis, internal duodeal/gastric/colic fistulas Coagulation: DIC Haemorrhage: peritoneal, in pseudocyst (arterial erosion by necrosis) Neuropsyhic: encefalopathy Cutaneous: systemic cytosteatonecrosis (ChristianWeber): Cullen, Grey-Turner

3) Severity assessment
Clinical
Other complications
Pseudocysts
10-50% of AP When? W1-W6 asymptomatic / abdominal pain / symptoms by compression 50% spontaneous resolution 50% haemorrhage, rupture, compression local organs (bile ducts, duodenal) Dg + US/CT/ EUS

3) Severity assessment
Biological
(Severe PA, imediate or late) CRP > 150mg/dl at 48h, then // with evolution Scores (clinical and research)
Ranson, specific to AP (etanol) Modified Glasgow (Imrie), specific AP APACHE II nonspecific AP, for ICU mainly
Score > 3 pt. = severe AP

3) Severity assessment

*Ranson et al. Prognostic signs and the role of operative management in acute pancreatitis. Gynecol Obstetr 1974; 139: 69 81.

3) Severity assessment

*Blamey SL, Imrie CW, O'Neill J, Gilmour WH, Carter DC. Prognostic factors in acute pancreatitis. Gut. 1984 Dec;25(12):1340-6

3) Severity assessment
Imaging
CT scan +/- contrast > 48h (lesions are visible) Baltasar score

3) Severity assessment

Mortalitaty 3%(<3 pt.), 6% (4-6 pt.), 17% (7-10 pt.)

*Baltazar. Acute pancreatitis: Value of CT in establishing prognosis. Radiology 1990; 174: 331 336.

3) Severity assessment

3) Severity assessment
In conclusion:
Benign oedematous AP (70 80%)
Medical unit

Severe necrotic AP (20-30%)

ICU unit (medical/surgical/radiological facilities available)

4) Etiological diagnosis
ALCOHOL (40%)
Patient
Typical - man over 40, > 100 g alcohol/day > 10 ani If no other episode of AP and no history of known CP = usually inaugural episode of alcoholic calcifying CP Other stigmata of alcohol consumption: chronic hepatopathy, cardiopathy, Dupuytren, enlargement of parotids, etc

Biological
Stigmata de consum de alcool: GGT, MCV, ASAT/ALAT>1

Imaging
Chronic hepatopathy, cardiopathy, pancreatic calcifications (CP)

4) Etiological diagnosis
BILIARY (40%)
Patient
Tipical overweight woman over 50 (3F fat, female, fifty), multiparitaty, family history of gallstones Gallstones <3mm, more than >3 stones, large cystic duct

Biological
ALAT/ASAT>1, both up to x50N, a rapidly normalised peak within 48h If bilirubin is also elevated = stone impaction in Vaters ampulla

Imaging
Rapid abdominal US so as to diagnose obstrutive gallstones which need desobstruction through ERCP; but low accuracy

4) Etiological diagnosis
RARE CAUSES
Tumours - malignant or benign (IPMN)
> 50 ani (!), CT/MRI/EUS

Postoperative
Biliary or gastric surgery

Post ERCP
5% Young patients, normal pancreas, low experience, high number of Wirsung opacifications with high pression

Trauma
Box, bicycle or automobile accident

4) Etiological diagnosis
EXCEPTIONAL CAUSES
Hiper-trigliceridemia
>1000mg/dl, 30% of cases

Hiper-calcemia (1%)
hiperPTH, 5-10% of cases

Drugs
Azathioprine/6MP, furosemide, estrogens, tetracicline

Infectious
Mumps, CMV + HIV, VHB, enterovirus

Autoimmune
IgG4, Ac. anti lactoferine, Ac. anti carbonica anhidrase pseudotumoral, asociated with other autoimune diseases (Crohn, Sjogren, others)

Canalar (pancreas divisum)

4) Etiological diagnosis
IDIOPATHIC (10%)
Biliary and pancreatic EUS after the PA episode, after oedema dissapearance, generally at 4-6 weeks :
lithiasis = biliary AP Tumors, IPMN

5) Diferential diagnosis
Other causes of acute abdominal pain
Perforated ulcer Mesenteric infarctus Biliary peritonitis Inferior myocardial infarction Abdominal aneurysm rupture

Positive diagnosis

ACUTE PANCREATITIS

Severity assessment

Etiological diagnosis

Therapy

6) Principles of therapy
Monitoring: AP, pulse, SO2, CVP, urine output, ABC - O2, iv coloids & cristaloids ICU circulatory, respiratory, renal

Nil by mouth
IPP IV (omeprazole 40mg/8-12h) or continous iv); Y/N ? NG tube only if vomiting Thrombosis prophilaxy: HBPM (fraxiparine 0.3ml/24 sau ennoxaparine 0.4ml/24h sc) Kinesiterapy, pressure ulcers prevention

6) Principles of therapy
Analgesia
(I) paracetamole (max 4g/24h), no NSAIDs (renal function!) (II) tramadole (max 300mg/24h) (III) morfine (sc/iv)

Nutrition
Parenteral Enteral: better, prevents bacterial translocation (decreases % of infectious complications, decreases hospital stay) Stard alimentation afte5 7 days with no pain and lipase < 3 x N, no vomiting, stools and gas transit; start with low (no) lipid regimen

Antibiotics ?
Prevents necrosis infection?; Y/N? Imipenem for minimum 14 days

6) Principles of therapy
Drainage
Infected necrosis (CT/EUS guided FNA)
Endoscopy : necrosectomy Surgical Usually after > 14 days from the start of the PA

Abscess
Interventional radiology Endoscopy Surgery

6) Principles of therapy
Therapy depending on etiology
Alcoholic AP
Stop alcohol consumption, withdrawal (benzodiazepines DT prevention)

Severe biliary AP
+ angiocholitis (impacted stone), bilirubine >5 mg/dl - ERCP with sphincterotomy and stone extraction in 48h Cholecistectomy before discharge

Autoimmune AP
Corticoterapy ? (yes in CP)

Other AP: treatment hypertrigriceridemia, hypercalcemia, infectious disease Pseudocyst: over 6cm, over 6 weeks, symptomatic = drainage endoscopic/ radiological/ surgical

Take home
AP = acute inflammation +/- important, severity = f(necrosis); potentially lethal ! (Mt total 5%, 20% severe cases) Dg+ = typical pain + lipase > 3 x N; if in doubt CT scan = essential Severity = clinical & biological , CT>48h; if severe or high severity score = ICU

Etiology = longstanding alcohol consumpotion + gallbladder migration

Supportive therapy (pain, nutrition) + complications + etiology