ANATOMY AND PHYSIOLOGY Anatomy The name pancreas is derived from the Greek pan all and kreas flesh the pancreas is situated in the retroperitoneum It is divided into a head which occupies 30 of the gland by mass and a body and tail which together constitute 70 ID: 1036174
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1. PancreasPART 1by Dr. Ali Adil
2. ANATOMY AND PHYSIOLOGYAnatomyThe name ‘pancreas’ is derived from the Greek ‘pan’ (all) and‘kreas’ (flesh), the pancreas is situated in the retroperitoneum. It is divided into a head, which occupies 30% of the gland by mass, and a body and tail, which together constitute 70%.Structures should be known around the pancreas:the duodenum encircle the head of pancreasL2 and IVC behind the head of pancreasThe aorta and the superior mesenteric vessels lie behind the neck of the gland.The superior mesenteric vein joins the splenic vein behind the neck of the gland to form the portal vein.
3. The pancreas weighs approximately 80 g. Of this, 80–90%:Is composed of exocrine acinar tissue, which is organised into lobules.The main pancreatic duct branches into interlobular and intralobular ducts, ductules and, finally, acini.Clusters of endocrine cells, known as islets of Langerhans, are distributed throughout the pancreas.Islets consist of different cell types: 75% are B cells (producing insulin); 20% are A cells (producing glucagon); and the remainder are D cells (producing somatostatin) and a small number of pancreatic polypeptide cells, these constitute the endocrine function of the pancreas.
4. FIGURE 1: pancreas and its relations.
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6. Malrotation of the ventral bud in the fifth week results in an annular pancreas. The mode of ductule fusion in the seventh week produces the various possible ductular patterns. Between the 12th and 40th weeks of fetal life, the pancreas differentiates into exocrine and endocrine parts.
7. Anomalies of the pancreas●● Aplasia●● Hypoplasia●● Hyperplasia●● Hypertrophy●● Dysplasia●● Variations and anomalies of the ductsa Pancreas divisum●● Rotational anomalies Annular pancreasa●● Pancreatic gall bladder●● Polycystic diseasea●● Congenital pancreatic cysts Cystic fibrosisa von Hippel–Lindau syndrome
8. ●● Ectopic pancreatic tissue, accessory pancreasa●● Vascular anomalies●● Choledochal cystsa●● Horseshoe pancreasa The more frequent anomalies encountered in surgical practice
9. Figure 2 Variations in the pancreatic ducts. (a) Normal. (b–d) Progressive suppression of the accessory duct (30%). (e–g) Progressive suppression of the main duct (10%). (f, g) Pancreas divisum.
10. Figure 3: Variations in the relation of the common bile duct and main pancreatic duct at the main duodenal papilla. In (a), there is a common channel with no sphincter mechanism protecting flow between the ducts. In (b), there is a partial common channel, while in(c), there is separation of the two channels. Gallstone pancreatitis is more likely with (a) and (b).
11. PhysiologyIn response to a meal, the pancreas secretes:Digestive enzymes (by the CCK) in an alkaline (pH 8.4) bicarbonate-rich fluid by (the hormone secretin).Vagal stimulation increases the volume of secretion.The proteolytic enzymes are in an inactive form, the maintenance of which is important in preventing pancreatitis.
12. Measurement of serum amylase is the most widely used test of pancreatic damage (serum lipase is more sensitive and specific, but is not widely available)A markedly elevated serum level is highly suspicious but not diagnostic of acute pancreatitis.INVESTIGATIONSEstimation of pancreatic enzymes in body fluidsWhen the pancreas is damaged, enzymes such as amylase, lipase, trypsin, elastase and chymotrypsin are released into the serum.
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14. Pancreatic function testsLundh test: assessment of pancreatic exocrine function by directly measuring pancreatic secretion in response to test meal.NBT–PABA testStool elastase: Measurement of the enzyme elastase in stool is simple, specific and now used widely. A low level of faecal elastase indicates exocrine insufficiency.
15. Imaging investigationsUltrasonographyUltrasonography is the initial investigation of choice in patients with jaundice to determine the presence of gallstones or liver metastasis.It may define the presence or absence of a mass in the pancreas.Obesity and overlying bowel gas often make interpretation of the pancreas itself unsatisfactory.
16. Computed tomography/CT scanIt’s the investigation of choice that diagnose most significant pathologies within the pancreas.A specific pancreatic protocol should be followed:An initial unenhanced CT scan is essential to determine the presence of calcification within the pancreas and gall bladder.Then, following rapid injection of intravenous contrast, scanning is performed in the arterial and venous phases.Pancreatic diseases or pathologies diagnosed by CT scan:CalcificationsPancreatic carcinomas of even 1–2 cm in size.Pancreatic necrosisPancreatic pseudocysts or collectionIt can be therapeutic: CT-guided drainage is helpful in the treatment of pancreatic collections, cysts and pseudocysts.
17. Unenhanced CT contrast CTa) Unenhanced computed tomography scan of a manwith chronic pancreatitis, showing a focus of calcification (marked byan arrow) in the head of the pancreas and a cyst adjacent to that. Oralcontrast has been administered. (b) The same area after injection ofintravenous contrast.
18. carcinoma of the pancreatic head
19. insulinoma
20. Magnetic resonance imagingMRI and MRCP can clearly visualize the pancreas, pancreatic and bile ducts.MRCP may well replace diagnostic endoscopic cholangiography and pancreatography (ERCP) as it is non-invasive and less expensive.Figure : Magnetic resonance cholangiopancreatography in apatient with obstructive jaundice. A dilated common bile duct wasseen on ultrasound, but no pancreatic mass lesion was visible oncomputed tomography. The bile duct and the main pancreatic ductare seen very well, with a stone visible in the lower part of the bile ductand another in the neck of the gall bladder.
21. Endoscopic retrograde cholangiopancreatographyERCP is performed using a side-viewing fibreoptic duodenoscope. The ampulla of Vater is intubated, and contrast is injectedinto the biliary and pancreatic ducts to display the anatomy radiologically.
22. Figure Endoscopic retrograde cholangiopancreatography.(a) Normal pancreatic duct with filling of the duct of Santorini fromthe duct of Wirsung. (b) Diagrammatic outline of (a).
23. Figure : Endoscopic retrograde cholangiopancreatography:pancreatic carcinoma. Irregular stricture of the main pancreatic duct(arrow) with dilatation distal to the obstruction.
24. Diagnostic uses:Visualization of bile and pancreatic ducts and their abnormalities such stricture or dilatation.Diagnosis of bile leak.Brush cytologyTherapeutic uses:Placement of stentsDilatation of stricturesExtraction of obstructing lesions such as stones.
25. Figure : (a) Endoscopic retrograde cholangiopancreatography:relapsing acute pancreatitis. Normal biliary tree. Pancreatogramshows stricture of the main duct in the body with distal dilatation andcyst formation. (b) Diagrammatic outline of (a). CBD, common bileduct; PD, pancreatic duct.
26. Figure (a) Endoscopic retrograde cholangiopancreatography:chronic pancreatitis. Long stricture of the pancreatic duct in thehead; distal pancreatic duct shows sacculation with intervening shortstrictures, ‘chain of lakes’. (b) Diagrammatic outline of (a).
27. Endoscopic ultrasoundEndoscopic ultrasound (EUS) is performed using a special endoscope that has a high-frequency ultrasonic transducer at its tip. Diagnostic uses:Assessment of the pancreas and its surrounding vasculature and lymph nodes2. Identifying small tumours that may not show up well on CT or MRI.3. Demonstrating the relationship of a pancreatic tumour to major vessels nearby.4. clarify the relationship of a neuroendocrine tumour to the main pancreatic duct5. Distinguish cystic tumours from pseudocysts.6. FNA or Trucut biopsy.
28. CONGENITAL ABNORMALITIESCystic fibrosisThis is inherited as an autosomal recessive condition. It occurs most frequently among Caucasians, in whom it is the most common inherited disorder.There is a mutation in the CFTR gene.CF is a multisystem disorder of exocrine glands that affects the lungs, intestines, pancreas and liver.characterized by elevated sodium and chloride ion concentrations in sweatMost of the organ damage is due to blockage of narrow passages by thickened secretions.May cause meconium ileus at birth
29. Clinical features:Steatorrhoea is usually present from birth, resulting in stools that are bulky, oily and offensive.The earliest clinical signs of CF are poor growth, poor appetite, rancid greasy stools, abdominal distension, chronic respiratory disease and finger clubbing.Delayed secondary sexual characteristicssigns of portal hypertensionInfertility is common, due to the absence of the vas deferens in men and thick cervical mucus in women.
30. Diagnosis:Genetic testingSweat test, Levels of sodium and chloride ions in the sweat above 90 mmol/L confirm the diagnosis.Treatment is aimed at control of the secondary consequences of the diseasePulmonary function is preserved with aggressive physiotherapy and antibiotics.Malabsorption is treated by administration of oral pancreatic enzyme preparations, with low fat diet but contain added salt to replace the high losses in the sweat.
31. Pancreas divisumPancreas divisum occurs when the embryological ventral and dorsal parts of the pancreas fail to fuse.The dorsal pancreatic duct becomes the main pancreatic duct and drains most of the pancreas through the minor or accessory papilla.The incidence of pancreas divisum ranges from 25–50% in patients with recurrent acute pancreatitis, chronic pancreatitis and pancreatic pain.Diagnosis:MRCPEUSERCP
32. Treatment:Endoscopic sphincterotomy and stenting of the minor papillaSurgical intervention can take the form of sphincteroplasty, pancreatojejunostomy or even resection of the pancreatic head.
33. Annular pancreasThis is the result of failure of complete rotation of the ventral pancreatic bud during development, so that a ring of pancreatic tissue surrounds the second or third part of the duodenum.Most often seen in association with congenital duodenal stenosis or atresia and is therefore more prevalent in children with Down syndrome.It presents with duodenal obstruction so treatment is by bypass surgery (duodenoduodenostomy).May occur in later life as one of the causes of pancreatitis, in which case resection of the head of the pancreas is preferable to lesser procedure.
34. Ectopic pancreasIslands of ectopic pancreatic tissue can be found in the submucosa in parts of:the stomach, duodenum small intestine including Meckel’s diverticulumthe gall bladder, adjoining the pancreas, in the hilum of the spleenwithin the liver
35. INJURIES TO THE PANCREASExternal injuryPresentation and managementThe pancreas can be injured by blunt trauma (most common) from direct blow or by steering wheel in RTA, or by penetrating trauma. pancreatic injury usually associated with nearby viscera such as the liver, the spleen and the duodenum.Severity of pancreatic injury:A contusion or laceration of the parenchyma without duct disruption.Major parenchymal destruction with duct disruption.Rarely, massive destruction of the pancreatic head.The most important factor that determines treatment is whether the pancreatic duct has been disrupted.
36. Blunt trauma:Usually presents with epigastric pain, which is mild at first then it become sever.Diagnosis by high serum amylase, CT scan, the duct disruption is best diagnosed by urgent ERCP.Treatment by:IV fluidNil by mouthKeep on conservative treatment unless there is: Pancreatic duct disruptionSigns of peritonitisHaemodynamic instability
37. Penetrating traumaHere there are associated visceral injuries, so, laparotomy is usually indicated.Haemostasis and closed drainage is adequate for minor parenchymal injuriesIf the gland is transected in the body or tail, a distal pancreatectomy should be performed.If damage is purely confined to the head of the pancreas, haemostasis and external drainage is normally effective.In severe injury to the pancreatic head and duodenum, then a pancreatoduodenectomy may be necessary.
38. PrognosisThe most common cause of death in the immediate period is bleeding, usually from associated injuries.Once the acute phase has passed, the mortality and morbidity related to the pancreatic injury itself are treatable.Complications include:Persistent output drainage (fistula)Duct stricture with recurrent pancreatitisPseudocyst is either treated by:Percutaneous aspiration (if the duct is intact)Distal pancreatectomy (if the duct injured or disrupted)The possibility of a cystic neoplasm should be considered and excluded
39. Iatrogenic injuryThis can occur in several ways:Injury to the tail of the pancreas during splenectomy, resulting in a pancreatic fistulaInjury to the pancreatic head and the accessory pancreatic duct (Santorini), which is the main duct in 7% of patients, during Billroth II gastrectomy.Enucleation of islet cell tumours of the pancreas can result in fistulae.
40. Pancreatic fistulaCauses:As a complication of acute or chronic pancreatitis.Following operative or external traumaManagement: (most of it close spontaneously) Correction of metabolic and electrolyte disturbancesAdequate drainage of the fistula into a stoma bag with protection of the skin.Investigation and treatment of the cause of the fistulaRelieve pancreatic duct obstruction with ERCP.parenteral or nasojejunal nutritional support.The use of octreotide will also suppress pancreatic secretion.
41. PANCREATITISPancreatitis is inflammation of the pancreatic parenchyma.Acute: presents as an emergency.Chronic: prolonged and frequently lifelong disorder resulting from the development of fibrosis within the pancreas.Acute pancreatitis is defined as an acute condition presenting with abdominal pain, a threefold or greater rise in the serum levels of the pancreatic enzymes amylase or lipase, and/ or characteristic findings of pancreatic inflammation on contrast- enhanced CT. Acute pancreatitis may recur.
42. Pathogenesis:The underlying mechanism of injury in pancreatitis is thought to be premature activation of pancreatic enzymes within the pancreas, leading to a process of autodigestion.Inflammatory process triggers the oedema, haemorrhage and necrosis.As inflammatory mediators are released into the circulation, systemic complications can arise.
43. Classification:Mild (interstitial oedematous pancreatitis)Interstitial oedema of the gland and minimal organ dysfunction.The majority of patients will have a mild attack of pancreatitis.The mortality from which is around 1%.Severe (necrotising pancreatitis)seen in 5–10% of patientsCharacterised by pancreatic necrosis, a severe systemic inflammatory response and often multi-organ failure.The mortality varies from 20 to 50%.
44. Chronic pancreatitis is defined as a continuing inflammatory disease of the pancreas characterised by irreversiblemorphological change typically causing pain and/or permanent loss of function.
45. Acute pancreatitisIncidenceThe annual incidence may range from 5 to 50 per 100 000.May occur at any age, with a peak in young men and older women.AetiologyBiliary calculi, which occur in 50–70% of patients. It cause pancreatitis if the CBD and pancreatic duct share the common channel. Alcohol abuse, accounts for 25% of cases. It cause pancreatitis by:the effects of dietmalnutritiondirect toxicity of alcoholconcomitant tobacco smokingHypersecretion, duct obstruction or reflux.Hyperlipidaemia
46. Possible causes of acute pancreatitis●● Gallstones●● Alcoholism●● Post ERCP●● Abdominal trauma●● Following biliary, upper gastrointestinal or cardiothoracic surgery●● Ampullary tumour●● Drugs (corticosteroids, azathioprine, asparaginase, valproic acid, thiazides, oestrogens)●● Hyperparathyroidism●● Hypercalcaemia●● Pancreas divisum●● Autoimmune pancreatitis●● Hereditary pancreatitis●● Viral infections (mumps, coxsackie B)●● Malnutrition●● Scorpion bite●● Idiopathic (20% of cases)
47. Clinical presentationPainThe cardinal symptomdevelops quickly, reaching maximum intensity within minutes persists for hours or even dayssevereconstantrefractory to the usual doses of analgesicsUsually experienced first in the epigastrium but may be localised to either upper quadrant or felt diffusely throughout the abdomen.radiate to the back in about 50% of patients,Some patients may gain relief by sitting or leaning forwards.Nausea, repeated vomiting and retching.Hiccoughs can be troublesome and may be due to gastric distension or irritation of the diaphragm.
48. Examination:General:May be that of a patient who is well with minimal symptoms Or, at the other extreme:One who is gravely ill with profound shock, toxicity and confusion.TachypnoeaTachycardiaHypotension may presentThe body temperature is often normal or even subnormal, but frequently rises as inflammation develops.Mild jaundiceSubcutaneous fat necrosis may produce small, red, tender nodules on the skin of the legs
49. Abdominal:Distension due to ileus or, more rarely, ascites with shifting dullness.A mass can develop in the epigastrium due to inflammation.muscle guarding in the upper abdomenBluish discolouration of the flanks (Grey Turner’s sign) or umbilicus (Cullen’s sign).Chest:Pleural effusion is present in10–20% of patients.Pulmonary oedema and pneumonitis
50. Differential diagnosis:perforated peptic ulcer (The suddenness of onset)Acute cholecystitis (if the pain is maximal in the right upper quadrant).Myocardial infarction, pneumonia or pleuritic pain (radiation to the chest).Acute pancreatitis can mimic most causes of the acute abdomen and should seldom be discounted in differential diagnosis.
51. InvestigationsClinical presentationMore than 3 folds increase in serum amylase (normal amylase doesn’t exclude diagnosis)Serum lipase level can be checked, it provides a slightly more sensitive and specific test than amylase.CT scan3 steps should be done in acute pancreatitis:Is a diagnosis of acute pancreatitis correct?How severe is the attack?What is the etiology?
52. ASSESSMENT OF SEVERITYIt is vital to assess the severity of acute pancreatitis, as those with sever disease have a bad prognosis and need special treatment and nursing in intensive care unit.Severity stratification assessments should be performed in patients at 24 hours, 48 hours and 7 days after admission.The Ranson and Glasgow scoring systems are specific for acute pancreatitis, and a score of 3 or more at 48 hours indicates a severe attack.APACHE is another scoring system that is used in intensive care units.
53. So acute pancreatitis can be stratified into 3 groups:●● Mild acute pancreatitis:No organ failure;No local or systemic complications.●● Moderately severe acute pancreatitisorgan failure that resolves within 48 hours (transientorgan failure); and/orlocal or systemic complications without persistentorgan failure.●● Severe acute pancreatitis:persistent organ failure (>48 hours);single organ failure;multiple organ failure
54. table :The Ranson and Glasgow scoring systems to predict the severity of acute pancreatitis: in both systems, disease is classified as severe when three or more factors are present.
55. IMAGINGplain x-ray, non specific but it can shows:a generalised or local ileus (sentinel loop)a colon cut-off signRenal halo sign.calcified gallstones or pancreatic calcificationA chest radiograph may show aPleural effusion. in severe cases, a diffuse alveolar interstitial shadowing may suggest acute respiratory distress syndrome
56. 2. Ultrasound Ultrasound does not establish a diagnosis of acute pancreatitis. The swollen pancreas may be seen.should be performed within 24 hours in all patients to detect:Gallstones as a potential cause.rule out acute cholecystitis as a differential diagnosisDetermine whether the common bile duct is dilated
57. CT scan is not necessary for all patients, particularly those deemed to have a mild attack, But a contrast-enhanced CT is indicated in the following situations:If there is diagnostic uncertainty.In patients with severe acute pancreatitis, to distinguish interstitial from necrotising pancreatitisIn patients with organ failure, signs of sepsis or progressive clinical deterioration.When a localised complication is suspected, such as fluid collection, pseudocyst or a pseudoaneurysm.
58. Figure Contrast-enhanced computed tomography scanshowing acute necrotising pancreatitis. Note the area of reducedenhancement in the pancreas (marked X), the peripancreatic oedemaand stranding of the fatty tissues
59. 4. Cross-sectional MRI can yield similar information to that obtained by CT.EUS and MRCP can help in detecting stones in the common bile duct and directly assessing the pancreatic parenchyma.In patients with severe acute gallstone pancreatitis and signs of ongoing biliary obstruction and cholangitis, an urgent ERCP should be sought.
60. Thank you