ACUTE PANCREATITIS. ANATOMY ACUTE PANCREATITIS -Acute pancreatitis (AP) are characterized by...

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ACUTE PANCREATITIS

Transcript of ACUTE PANCREATITIS. ANATOMY ACUTE PANCREATITIS -Acute pancreatitis (AP) are characterized by...

Page 1: ACUTE PANCREATITIS. ANATOMY ACUTE PANCREATITIS -Acute pancreatitis (AP) are characterized by edematous lesions, eventually necrosis and bleeding inside.

ACUTE PANCREATITIS

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ANATOMY

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ACUTE PANCREATITIS

-Acute pancreatitis (AP) are characterized by edematous lesions, eventually necrosis and bleeding inside and in peripancreatic area.

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A. Pathology: - 2 types of AP

• 1. Edematous AP• congestion and edema of the pancreas. • swelling • normal/mild inflammation of the retroperitoneum

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• 2. Necrotic pancreatitis

• Severe +++.• Important swelling of the pancreas, bleeding multiples areas

and hematomas till the complete distruction of the gland. • Involvement of all retroperitoneum, fatty necrosis- white

spots• Plasmal escape – peripancreatic and retroperitoneal spaces + ascites

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ETIOLOGY: 2 MAIN CAUSES1. GALLSTONES2. ALCOHOL

1. GALLSTONES

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• 2. ALCOHOL

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• 3. Rare etiology• Less than 10%

• Postoperative and postraumatic AP– Billiary ,pancreatic, gastric surgery– Kidney transplantation– Post- ERCP

• Pancreatic tumors• Infections

– Leptospirosis– Ascaridiosis

• Metabolical factors– Hypercalcemia– Hypertriglyceridemia

• Drug induced– Corticotherapy– Chlorothiazide, Isothiazide– Immunosupressors– Oral Contraceptives

• Auto-immune AP• Idiopathic factors

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• C. PATHOPHYSIOLOGY

3 mechanisms STOP the autodigestion of the pancreas

1.enzymes - preserved as zymogenes separates from other proteins2.enzymes sont secreted – inactive forms3.inhibitors of proteolitic enzymes in the pancreatic tissu and pancreatic juice

• AP= enzimatic autodigestion of the pancreas--- trypsinogen activation in trypsine in the pancreatic cells .

• Trypsine --- cascade activation of proenzymes from zymogens granules – pancreatic acinar cell distruction

• SIRS --- proinflammatory cytokines(Il-1, TNF) in the pancreatic tissu and other organs (kidney, liver, lung) SEVERE SYSTEMIC EVENTS

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PATHOPHYSIOLOGY

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D. CLINICAL SIGNS• ABDOMINAL PAIN Describe it!!!• Nausea and vomiting• Abdominal distension- paralitic ileus • +/ tachycardia, low/ high temperature, hypotension, tachypnea-

severe forms• Oliguria• Jaundice• Ascites

!! Pain intensity vs poverty of clinical signs

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• 50 %- symptoms are not specific Differential dg:• Acute cholecystitis• Mesenteric infarction• Bowel obstruction• Ruptured abdominal aortic aneurism • Respiratory distress• Oligo-anuria • Peritonitis

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E. DIAGNOSTIC

• 1. Blood tests• HIGH levels of amylase and lipase (≥ 3 N) ESSENTIAL BUT NOT SPECIFIC!!• CRP > 15 mg/100 ml – SEVERE AP.

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2. IMAGING DG • Plain abdominal X- Ray- localised ileus- sentinel loop, free

air, calcifications• Abdominal US- swelling , diffuse hypoechogenity - Eventually the cause - gallstones

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CT SCAN

• SEVERITY EVALUATION criteria

• Balthasar score- severity and extent of necrosis, peripancreatic fluid collection

• Correlation with morbidity and mortality

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MRCP

• Non-invasive• Safer• Faster THAN ERCP but less sensitive

WHEN Suspicion of bile ductobstruction

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MRI - severity of AP - no iodine contrast - bile obstruction

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• F. COMPLICATIONS• PANCREATIC NECROSIS• PSEUDOCYST• PANCREATIC ABCESS

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PSEUDOCYST- necrosis organising - Wirsung disruption - after aprox 4 w evolution of AP

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PANCREATIC ABCESS- pseudocyst infection/ infection of necrotic areas

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OTHER COMPLICATIONS

Venous thrombosis ( splenic, portal, SMV ) Pleural effusion Ascites Fatty necrosis- cutaneus

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• G. PROGNOSIS• Good – Edematous AP – mortality< 2%• Bad – Necrotic forms of AP- high mortality Severity prediction RANSON scale- if > 3 crt- AP severe if > 7- 100% mortality AP induced by alcohol

RANSON scale

Admission After 48 H

Age > 55 yearsLeucocytes/mm³ > 16.000Glycemia > 200 mg%LDH > 1.5 NSGOT > 6 N

Hematocrit reduced with 10%Urea raised with 5 mg %Calcemia < 8 mg%PaO2 < 60 mm HgBase deficit > 4 mEq/lLiquid sechestration > 6 l

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!!! Admission: High levels of CPR – bad prognosisOther severity scales- Glasgow, Apache III

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TREATMENT

• MEDICAL- NPO- NGT ?- IVF- PPI - PAIN CONTROL- ANTIBIOTICS- ????

• SURGICAL- Indications !!!WHEN WE HAVE THEPROOF OF INFECTIONChoosing of the moment!!

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• ERCP with sphyncterotomyINDICATIONS- gallstones in bile duct

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SURGICAL TREATMENT

• Surgical infected necrose debridement

• Drainage• +/- Laparostomy

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SURGICAL TREATMENT- PSEUDOCYSTS

INDICATIONS:• IF > 7 cm• Rapidly growing• Bleeding• Compression • Disruption• Pain• Infection

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PSEUDOCYST TREATMENT- TRANSPAPILLARY

DRAINAGE; IF COMMUNICATING- STENT

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PSEUD0CYST TREATMENT-EXTERNAL DRAINAGE

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SURGICAL TREATMENT – if proximal duct disrupted- WHIPPLE