Pancreas PART 1 by Dr Ali Adil ANATOMY

Pancreas PART 1 by Dr. Ali Adil

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%. Structures should be known around the pancreas: • the duodenum encircle the head of pancreas • L 2 and IVC behind the head of pancreas • The 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.

• 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.

FIGURE 1: pancreas and its relations.

• 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 12 th and 40 th weeks of fetal life, the pancreas differentiates into exocrine and endocrine parts.

Anomalies of the pancreas ●● Aplasia ●● Hypoplasia ●● 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

●● Ectopic pancreatic tissue, accessory pancreasa ●● Vascular anomalies ●● Choledochal cystsa ●● Horseshoe pancreas a The more frequent anomalies encountered in surgical practice

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.

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).

Physiology In response to a meal, the pancreas secretes: • Digestive enzymes (by the CCK) in an alkaline (p. H 8. 4) bicarbonaterich 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.

INVESTIGATIONS Estimation of pancreatic enzymes in body fluids • When the pancreas is damaged, enzymes such as amylase, lipase, trypsin, elastase and chymotrypsin are released into the serum. • 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.

Pancreatic function tests • Lundh test: assessment of pancreatic exocrine function by directly measuring pancreatic secretion in response to test meal. • NBT–PABA test • Stool elastase: Measurement of the enzyme elastase in stool is simple, specific and now used widely. A low level of faecal elastase indicates exocrine insufficiency.

Imaging investigations Ultrasonography • Ultrasonography 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.

Computed tomography/CT scan • It’s the investigation of choice that diagnose most significant pathologies within the pancreas. • A specific pancreatic protocol should be followed: ØAn initial unenhanced CT scan is essential to determine the presence of calcification within the pancreas and gall bladder. ØThen, following rapid injection of intravenous contrast, scanning is performed in the arterial and venous phases. • Pancreatic diseases or pathologies diagnosed by CT scan: • Calcifications • Pancreatic carcinomas of even 1– 2 cm in size. • Pancreatic necrosis • Pancreatic pseudocysts or collection • It can be therapeutic: CT-guided drainage is helpful in the treatment of pancreatic collections, cysts and pseudocysts.

Unenhanced CT contrast CT a) Unenhanced computed tomography scan of a man with chronic pancreatitis, showing a focus of calcification (marked by an arrow) in the head of the pancreas and a cyst adjacent to that. Oral contrast has been administered. (b) The same area after injection of intravenous contrast.

carcinoma of the pancreatic head

insulinoma

Magnetic resonance imaging • MRI 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 a patient with obstructive jaundice. A dilated common bile duct was seen on ultrasound, but no pancreatic mass lesion was visible on computed tomography. The bile duct and the main pancreatic duct are seen very well, with a stone visible in the lower part of the bile duct and another in the neck of the gall bladder.

Endoscopic retrograde cholangiopancreatography ERCP is performed using a side-viewing fibreoptic duodenoscope. The ampulla of Vater is intubated, and contrast is injected into the biliary and pancreatic ducts to display the anatomy radiologically.

Figure Endoscopic retrograde cholangiopancreatography. (a) Normal pancreatic duct with filling of the duct of Santorini from the duct of Wirsung. (b) Diagrammatic outline of (a).

Figure : Endoscopic retrograde cholangiopancreatography: pancreatic carcinoma. Irregular stricture of the main pancreatic duct (arrow) with dilatation distal to the obstruction.

Diagnostic uses: • Visualization of bile and pancreatic ducts and their abnormalities such stricture or dilatation. • Diagnosis of bile leak. • Brush cytology Therapeutic uses: • Placement of stents • Dilatation of strictures • Extraction of obstructing lesions such as stones.

Figure : (a) Endoscopic retrograde cholangiopancreatography: relapsing acute pancreatitis. Normal biliary tree. Pancreatogram shows stricture of the main duct in the body with distal dilatation and cyst formation. (b) Diagrammatic outline of (a). CBD, common bile duct; PD, pancreatic duct.

Figure (a) Endoscopic retrograde cholangiopancreatography: chronic pancreatitis. Long stricture of the pancreatic duct in the head; distal pancreatic duct shows sacculation with intervening short strictures, ‘chain of lakes’. (b) Diagrammatic outline of (a).

Endoscopic ultrasound (EUS) is performed using a special endoscope that has a high-frequency ultrasonic transducer at its tip. Diagnostic uses: 1. Assessment of the pancreas and its surrounding vasculature and lymph nodes 2. 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 duct 5. Distinguish cystic tumours from pseudocysts. 6. FNA or Trucut biopsy.

CONGENITAL ABNORMALITIES Cystic fibrosis • This 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 sweat • Most of the organ damage is due to blockage of narrow passages by thickened secretions. • May cause meconium ileus at birth

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 characteristics • signs of portal hypertension • Infertility is common, due to the absence of the vas deferens in men and thick cervical mucus in women.

Diagnosis: • Genetic testing • Sweat 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 disease • Pulmonary 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.

Pancreas divisum • Pancreas 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: • MRCP • EUS • ERCP

Treatment: • Endoscopic sphincterotomy and stenting of the minor papilla • Surgical intervention can take the form of sphincteroplasty, pancreatojejunostomy or even resection of the pancreatic head.

Annular pancreas • This 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 (duodenostomy). • 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.

Ectopic pancreas Islands of ectopic pancreatic tissue can be found in the submucosa in parts of: • the stomach, • duodenum • small intestine including Meckel’s diverticulum • the gall bladder, • adjoining the pancreas, in the hilum of the spleen • within the liver

• INJURIES TO THE PANCREAS • External injury • Presentation and management • The 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: ØA contusion or laceration of the parenchyma without duct disruption. ØMajor parenchymal destruction with duct disruption. ØRarely, massive destruction of the pancreatic head. ØThe most important factor that determines treatment is whether the pancreatic duct has been disrupted.

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: ØIV fluid ØNil by mouth ØKeep on conservative treatment unless there is: 1. Pancreatic duct disruption 2. Signs of peritonitis 3. Haemodynamic instability

Penetrating trauma • Here there associated visceral injuries, so, laparotomy is usually indicated. • Haemostasis and closed drainage is adequate for minor parenchymal injuries • If 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.

Prognosis • The 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 pancreatitis • Pseudocyst is either treated by: ØPercutaneous aspiration (if the duct is intact) ØDistal pancreatectomy (if the duct injured or disrupted) • The possibility of a cystic neoplasm should be considered and excluded

Iatrogenic injury This can occur in several ways: • Injury to the tail of the pancreas during splenectomy, resulting in a pancreatic fistula • Injury 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.

Pancreatic fistula Causes: • As a complication of acute or chronic pancreatitis. • Following operative or external trauma Management: (most of it close spontaneously) • Correction of metabolic and electrolyte disturbances • Adequate drainage of the fistula into a stoma bag with protection of the skin. • Investigation and treatment of the cause of the fistula • Relieve pancreatic duct obstruction with ERCP. • parenteral or nasojejunal nutritional support. • The use of octreotide will also suppress pancreatic secretion.

PANCREATITIS • Pancreatitis 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.

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.

Classification: • Mild (interstitial oedematous pancreatitis) ØInterstitial oedema of the gland minimal organ dysfunction. ØThe majority of patients will have a mild attack of pancreatitis. ØThe mortality from which is around 1%. • Severe (necrotising pancreatitis) Øseen in 5– 10% of patients ØCharacterised by pancreatic necrosis, a severe systemic inflammatory response and often multi-organ failure. ØThe mortality varies from 20 to 50%.

Chronic pancreatitis is defined as a continuing inflammatory disease of the pancreas characterised by irreversible morphological change typically causing pain and/or permanent loss of function.

Acute pancreatitis Incidence • The 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. Aetiology • Biliary 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 diet • malnutrition • direct toxicity of alcohol • concomitant tobacco smoking • Hypersecretion, duct obstruction or reflux. • Hyperlipidaemia

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)

Clinical presentation • Pain ØThe cardinal symptom Ødevelops quickly, reaching maximum intensity within minutes Øpersists for hours or even days Øsevere Øconstant Ørefractory to the usual doses of analgesics ØUsually experienced first in the epigastrium but may be localised to either upper quadrant or felt diffusely throughout the abdomen. Øradiate to the back in about 50% of patients, ØSome 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.

Examination: General: • May be that of a patient who is well with minimal symptoms • Or, at the other extreme: v. One who is gravely ill with profound shock, toxicity and confusion. v. Tachypnoea v. Tachycardia v. Hypotension may present v. The body temperature is often normal or even subnormal, but frequently rises as inflammation develops. v. Mild jaundice v. Subcutaneous fat necrosis may produce small, red, tender nodules on the skin of the legs

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 abdomen • Bluish discolouration of the flanks (Grey Turner’s sign) or umbilicus (Cullen’s sign). Chest: • Pleural effusion is present in 10– 20% of patients. • Pulmonary oedema and pneumonitis

Differential diagnosis: 1. perforated peptic ulcer (The suddenness of onset) 2. Acute cholecystitis (if the pain is maximal in the right upper quadrant). 3. Myocardial infarction, pneumonia or pleuritic pain (radiation to the chest). 4. Acute pancreatitis can mimic most causes of the acute abdomen and should seldom be discounted in differential diagnosis.

Investigations • Clinical presentation • More 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 scan 3 steps should be done in acute pancreatitis: • Is a diagnosis of acute pancreatitis correct? • How severe is the attack? • What is the etiology?

ASSESSMENT OF SEVERITY It 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.

So acute pancreatitis can be stratified into 3 groups: ●● Mild acute pancreatitis: • No organ failure; • No local or systemic complications. ●● Moderately severe acute pancreatitis • organ failure that resolves within 48 hours (transient organ failure); and/or • local or systemic complications without persistent organ failure. ●● Severe acute pancreatitis: • persistent organ failure (>48 hours); • single organ failure; • multiple organ failure

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.

IMAGING 1. plain x-ray, non specific but it can shows: • a generalised or local ileus (sentinel loop) • a colon cut-off sign • Renal halo sign. • calcified gallstones or pancreatic calcification • A chest radiograph may show a • Pleural effusion. • in severe cases, a diffuse alveolar interstitial shadowing may suggest acute respiratory distress syndrome

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 diagnosis • Determine whether the common bile duct is dilated

3. 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: ØIf there is diagnostic uncertainty. ØIn patients with severe acute pancreatitis, to distinguish interstitial from necrotising pancreatitis ØIn patients with organ failure, signs of sepsis or progressive clinical deterioration. ØWhen a localised complication is suspected, such as fluid collection, pseudocyst or a pseudoaneurysm.

Figure Contrast-enhanced computed tomography scan showing acute necrotising pancreatitis. Note the area of reduced enhancement in the pancreas (marked X), the peripancreatic oedema and stranding of the fatty tissues

4. Cross-sectional MRI can yield similar information to that obtained by CT. 5. 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.

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