dr a. badrek-amoudi frcs pancreatic diseases dr a. badrek-amoudi frcs

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Pancreatic Diseases Dr A. Badrek-Amoudi Dr A. Badrek-Amoudi FRCS FRCS

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Page 1: Dr A. Badrek-Amoudi FRCS Pancreatic Diseases Dr A. Badrek-Amoudi FRCS

Pancreatic DiseasesDr A. Badrek-Amoudi Dr A. Badrek-Amoudi FRCSFRCS

Page 2: Dr A. Badrek-Amoudi FRCS Pancreatic Diseases Dr A. Badrek-Amoudi FRCS

Anatomy & Physiology I

Page 3: Dr A. Badrek-Amoudi FRCS Pancreatic Diseases Dr A. Badrek-Amoudi FRCS

Anatomy & Physiology II

Page 4: Dr A. Badrek-Amoudi FRCS Pancreatic Diseases Dr A. Badrek-Amoudi FRCS

Anatomy & Physiology III

1-2 L alkaline, clear, isoosmolar enzyme rich fluid Na & K at plasma levels (165mmol/L) 20 enzymes are secreted Secretion is regulated by: Secretin, CCK, Vagus

and low Ph Proteolytic enzymes (Tryp, Chemotryp, elastase …

etc Lipolytic (lipase, colipase, phospholipase..etc) amyloytic Endocrine function: insulin, glucagon,

somatostatin..etc)

Page 5: Dr A. Badrek-Amoudi FRCS Pancreatic Diseases Dr A. Badrek-Amoudi FRCS

Pancreatitis II

Oedametous pancreatitisOedametous pancreatitis

Necrotizin PancreatitisNecrotizin Pancreatitis

Infected Necrosis/ Hemorrhagic necrosisInfected Necrosis/ Hemorrhagic necrosis

AutodigestionActivation of neutrophils and macrophagesRelease of cytokinesEndocrine and exocrine function is usually preserved

Page 6: Dr A. Badrek-Amoudi FRCS Pancreatic Diseases Dr A. Badrek-Amoudi FRCS

Pancreatitis Pathogenesis

1.1. Obstruction- SecretionObstruction- Secretion

2.2. Common Channel theoryCommon Channel theory

3.3. Duodenal refluxDuodenal reflux

4.4. Increased permeability of pancreatic Increased permeability of pancreatic ductduct

5.5. Enzyme Auto-activationEnzyme Auto-activation

Page 7: Dr A. Badrek-Amoudi FRCS Pancreatic Diseases Dr A. Badrek-Amoudi FRCS

PancreatitisAetiology I1.1. Gall stoneGall stone

1. 90% of acute pancreatitis . 2. Life risk of 3-5% 3. Age 40’s . 4. F>m5. Transient obstruction

2.2. Alcohol 75% of chronic pancreatitisAlcohol 75% of chronic pancreatitis1. Spasm of the sphinctor of Oddi2. Increases the concentration of enzymes3. Structural damage caused by the precipitation of

calcium4. Transient reduction of blood flow

3.3. DrugsDrugs1. Steroids, AZT2. Sulphonomids, Tetracyclin3. Oestrogen

Page 8: Dr A. Badrek-Amoudi FRCS Pancreatic Diseases Dr A. Badrek-Amoudi FRCS

Pancreatitis Aetiology II

1.1. Trauma & Post op Trauma & Post op 5%5%2.2. Post ERCP Post ERCP 1-40%1-40%3.3. HyperparathyroidismHyperparathyroidism

1. Ca deposition2. Increases the activation of enzymes

4.4. MalnutritionMalnutrition : : Results in paranchymal fibrosis

5.5. HyperlipidaemiaHyperlipidaemiaMay interfere with the levels of amylase

Page 9: Dr A. Badrek-Amoudi FRCS Pancreatic Diseases Dr A. Badrek-Amoudi FRCS

Pancreatitis Aetiology III

1.1. Pancreatic DividismPancreatic Dividism

2.2. Duodenal obstructionDuodenal obstruction

3.3. InfectionInfectionViral : Mumps, Coxacki, Herpes

4.4. IschamiaIschamia

5.5. HereditaryHereditary Mutation in Trypsin formation

6.6. Scorapian VenomScorapian Venom

Page 10: Dr A. Badrek-Amoudi FRCS Pancreatic Diseases Dr A. Badrek-Amoudi FRCS

Acute Pancreatitis Clinical Presentation Abdominal Pain

• Constant, quick onset, variable in severity• Epigastric • Radiating to the back in 50% of patients• Associated with nausea, vomiting & retching • Relieved by lying on to the L side, legs-up

Other precipitating factors Fever in 70% Jaundice in 30% Shock +/_ in 10% Hematemasis & malena in 5%

Page 11: Dr A. Badrek-Amoudi FRCS Pancreatic Diseases Dr A. Badrek-Amoudi FRCS

Acute Pancreatitis Clinical Presentation II Dyspnoea in 10% Tender Abdomen: Mild to

severe Peritonitis,could be diffuse BS: hypoactive Abdominal Mass:

• Phlegmon

• Pseudocyst,

• Abcess Ascitis Cullen’s Gray-turner signs Erythametous skin lesions

Page 12: Dr A. Badrek-Amoudi FRCS Pancreatic Diseases Dr A. Badrek-Amoudi FRCS

Differential diagnosis Perforated DU Perforated GB Emphsymatous cholecystitis Mesenteric infarction AAA Others

Page 13: Dr A. Badrek-Amoudi FRCS Pancreatic Diseases Dr A. Badrek-Amoudi FRCS

Acute Pancreatitis Investigation Diagnostic Amylase: >1000 is diagnostic

• High levels do not correlate with the severity of pancreatitis

• False Low: 1. Rapid clearance by the kidney 2. Hyperlipidaemia. 3. Chronic pancreatitis

• False High: Salivary, Ovarian, Liver tumor Lipase

Page 14: Dr A. Badrek-Amoudi FRCS Pancreatic Diseases Dr A. Badrek-Amoudi FRCS

Acute Pancreatitis Investigation II

High amylase may be caused by:1. Perforated DU2. Cholecystitis3. Small bowel obstruction4. Perforated Small bowel5. Ectopic pregnancy

Page 15: Dr A. Badrek-Amoudi FRCS Pancreatic Diseases Dr A. Badrek-Amoudi FRCS

Acute Pancreatitis Investigation III Radiological:

• Plain X- rays: • AXR: calcification, sentinle

loop SB,colonic spasm• CXR: pleural effusion &

differntial• USS: GB stones, pancreatic

peripancreatic info• CT: Diagnosis, prognosis, F/U• Endoscopic USS• MRCP• ERCP

Others:

• FBC: Hct, WBC, Plat.• U&E, LFT, Ca, glucose.• ABG

Page 16: Dr A. Badrek-Amoudi FRCS Pancreatic Diseases Dr A. Badrek-Amoudi FRCS

Acute Pancreatitis Prognostic Indicators

Biochemical Markers: Sensitivity/ Specificity

1. Ranson’s / Emeri’s 75%

2. CRP 70% Physiological parameters

• Appache II Scoring 80% Radiological

• Spiral CT 87% Peritoneal Lavage

Page 17: Dr A. Badrek-Amoudi FRCS Pancreatic Diseases Dr A. Badrek-Amoudi FRCS

Ranson’s CriteriaRanson’s Criteria

0-2= 2%, 3-4=15%, 5-6= 40%, 7-8=100% Mortality rates

On admissionOn admission Age>55 WBC> 16 Glucose> 200 LDH>350 SGOT>250

11stst 48 Hours 48 Hours HCT Fall> 10% Ca< 8 PO2<60 Base def<4 Estimate

sequestration>600 ml

Only applies to the first 24 hoursMakes no distinction between derangements due to alcoholic disease

Page 18: Dr A. Badrek-Amoudi FRCS Pancreatic Diseases Dr A. Badrek-Amoudi FRCS

Acute Pancreatitis Complications I

Local and regionalLocal and regional Pseudocysts:

• Infection, Hemorrhage, Rupture, obstruction

Pancreatic Necrosis• Sterile/ Infected

Pancreatic Abscess Colonic infarction Pancreatic Fistula Chronic Pancreatitis

Vascular: • portal vein thrombosis• Aorto-pancreatic fistula

Page 19: Dr A. Badrek-Amoudi FRCS Pancreatic Diseases Dr A. Badrek-Amoudi FRCS
Page 20: Dr A. Badrek-Amoudi FRCS Pancreatic Diseases Dr A. Badrek-Amoudi FRCS

Acute Pancreatitis Complications IIComplications II

SystemicSystemicI. Metabolic

• Hypokalaemia, Hypochloraemia & Metabolic alkalosis

• Hypocalcaemia• Hypomagnesemia• Hypoxemia

Page 21: Dr A. Badrek-Amoudi FRCS Pancreatic Diseases Dr A. Badrek-Amoudi FRCS

Acute Pancreatitis Complications IIIComplications III

II. Respiratory• Respiratory insufficiency• Atelactesis• ARDS

III. Renal Failure

IV. Depressed myocardial contractility

V. Multiple organ Failure

Page 22: Dr A. Badrek-Amoudi FRCS Pancreatic Diseases Dr A. Badrek-Amoudi FRCS

Acute Pancreatitis TreatmentI. Conservative

( Admit in ICU VS Common Surgical Ward) • NBM vs Early nutrition• ? NGT• Analgesia: narcotic• Adequate fluid replacement ( Initial crystalloid then

colloid)• Antibiotics (organisms & penetration)• ??Anticholinergics, somatostatin have no proven

benifitII. Minimally invasive

• Early ERCP & sphinctorotmy for impacted stones• CT-guided drainage of Psedocusysts

Page 23: Dr A. Badrek-Amoudi FRCS Pancreatic Diseases Dr A. Badrek-Amoudi FRCS
Page 24: Dr A. Badrek-Amoudi FRCS Pancreatic Diseases Dr A. Badrek-Amoudi FRCS
Page 25: Dr A. Badrek-Amoudi FRCS Pancreatic Diseases Dr A. Badrek-Amoudi FRCS

Treatment II

The indications for surgical intervention areThe indications for surgical intervention are:1. Uncertain diagnosis2. Early cholecystectomy3. CBD stone extraction4. Debridement of necrotic pancreatic tissue5. Pancreatic abcess (Infected Necrosis)6. Complicated Pseudocysts

Surgery is contraindicated in uncomplicated attacks.

Page 26: Dr A. Badrek-Amoudi FRCS Pancreatic Diseases Dr A. Badrek-Amoudi FRCS

Chronic Pancreatitis Recurrent prolonged attacks of pancreatitis Associated with endocrine and exocrine

insufficiency, weight loss and abnormal glucose tolerance test

75% is caused by alcoholism, 20% stones Normal architecture is replaced by dense fibrous

tissue, dilated pancreatic duct with areas of narrowing, Cysts & Psuedocysts are common.

Amylase may remain normal with the acute attack.

Page 27: Dr A. Badrek-Amoudi FRCS Pancreatic Diseases Dr A. Badrek-Amoudi FRCS

Chronic PancreatitisComplications

1. Narcotic addiction

2. Loco-Regional

1. Pseudocyst, fistula formation.

2. Pseudoaneurysm, vascular thrombosis

3. Bile duct stenosis

3. Diabetes with associated neuropathies & myopathies

4. Malabsobtion

Page 28: Dr A. Badrek-Amoudi FRCS Pancreatic Diseases Dr A. Badrek-Amoudi FRCS

Chronic PancreatitisDiagnosis: Lab AXR: calcification in 20-50% CT Image of choice ERCP shows duct anomalies:

• Dilatation• Strictures• Stones• Cysts

FNAC: Occasionally difficult to

distinguish from cancer.

OGD: • varicies

Page 29: Dr A. Badrek-Amoudi FRCS Pancreatic Diseases Dr A. Badrek-Amoudi FRCS

Chronic PancreatitisManagementMedicalMedical Manage DM Pain control Exocrine replacement Dietary control

SurgerySurgery Drainage Pain control Pancreatectomy

Page 30: Dr A. Badrek-Amoudi FRCS Pancreatic Diseases Dr A. Badrek-Amoudi FRCS

Pancreatic Cancer Epedemiology

• 5th highest cancer related death• 13: 100000 population• 5 year mortality poor 5%• 20% survive post surgery• Median survival 4-6 months• Genda & race?• 40% are sporadic, 30% related to smoking, 5%

familial, 5% in chronic pancreatitis, 20% dietary and fat intake.

• 95% are exocrine in origin• 75% originate in head & neck of the pancrease

Page 31: Dr A. Badrek-Amoudi FRCS Pancreatic Diseases Dr A. Badrek-Amoudi FRCS

Clinical Manifestation

• Painless obstructive jaundice, • Weight loss, Anorexia.• Deep abdominal/ back pain (75%)• Ascending cholangitis, Pancreatitis (14%)• Onset of Diabetes mellitus• Hepatosplenomegaly, Ascitis• Migratory thrombophlebitis (Trousseaus)• Courvoiser’s sign• Sister Mary Joseph nodule• Evidence of pruritis• Depression

Page 32: Dr A. Badrek-Amoudi FRCS Pancreatic Diseases Dr A. Badrek-Amoudi FRCS

Diagnostic studies

• USS• Endo-USS• CT• ERCP, MRCP • Angiography• FNAC• Endoscopy• Laparoscopy• Tumor markers (CEA & CA 19-9)

Page 33: Dr A. Badrek-Amoudi FRCS Pancreatic Diseases Dr A. Badrek-Amoudi FRCS

Treatment

Palliative• Pain & Depression

• Good analgesia• Sympathetic neurolysis

• Jaundice• Stenting via ERCP• Surgery Dudenal obstruction• Bypass surgery

Curative• (Whipple)

Page 34: Dr A. Badrek-Amoudi FRCS Pancreatic Diseases Dr A. Badrek-Amoudi FRCS
Page 35: Dr A. Badrek-Amoudi FRCS Pancreatic Diseases Dr A. Badrek-Amoudi FRCS

Prognosis

In general poor

Post surgery:• < 3cm • Negative resection

margins• No LN

Page 36: Dr A. Badrek-Amoudi FRCS Pancreatic Diseases Dr A. Badrek-Amoudi FRCS

HistoryA 56 year old patient presented with painless jaundice and weight loss.

• What is your differential diagnosis

• What are the Investigations required

The laboratory results were:

Bili(D) 8mg/100ml, Bili(InD) 2.5mg/100ml, ALP 730 iu/L , AST 60 iu/L, GGT 200 iu/L,

Albumin 4mg/dl, Amylase 200 u/dl, INR 1.9

Page 37: Dr A. Badrek-Amoudi FRCS Pancreatic Diseases Dr A. Badrek-Amoudi FRCS
Page 38: Dr A. Badrek-Amoudi FRCS Pancreatic Diseases Dr A. Badrek-Amoudi FRCS

1.What are the investigations shown in A & B

2. What are the Abnormalities

3. How do you prepare patient for investigation A

Page 39: Dr A. Badrek-Amoudi FRCS Pancreatic Diseases Dr A. Badrek-Amoudi FRCS