Upper GI surgeon Anatomy 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: 915426
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Slide1
The pancreas
Dr. Ali Jaffer Upper GI surgeon
Slide2Anatomy
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%.The head lies within the curve of the duodenum, overlying the body of the second lumbar vertebra and the vena cava.The aorta and the superior mesenteric vessels lie behind the neck of the gland
.
Coming off the side of the pancreatic
head and passing to the left and behind the superior mesenteric vein is the uncinate process of the pancreas.Behind the neck of the pancreas, near its upper border, the superior mesenteric vein joins the splenic vein to form the portal vein.The tip of the pancreatic tail extends up to the splenic hilum.
Slide3Anatomy
VasculatureArteries:Splenic a., superior
pancreaticoduodenal
a
, inferior pancreaticoduodenal a
.
Veins:
Splenic vein, superior mesenteric veinLympahatics:The pancreas is drained by lymphatic vessels that follow the arterial supply. They empty into the pancreaticosplenal nodes and the pyloric nodes, which in turn drain into the superior mesenteric and coeliac lymph nodes.
Slide4INVESTIGATIONS
Estimation of pancreatic enzymes in body fluidsserum amylase, lipasePancreatic function testsThe nitroblue
tetrazolium–
para-aminobenzoic acid (NBT–PABA)The pancreolauryl testFaecal elastase
Imaging investigations
Ultrasonography
Ultrasonography is the initial investigation of choice in patients with jaundice to determine whether or not the bile duct is dilated, the coexistence of gallstones or gross disease within the liver such as metastases. It may also define the presence or absence of a mass in the pancreas . However, obesity and overlying bowel gas often make interpretation of the pancreas itself unsatisfactory.b. Computed tomography Most significant pathologies within the pancreas can be diagnosed on high-quality CT scans.c. Magnetic resonance imaging Magnetic resonance cholangiography and pancreatography (MRCP) may well replace diagnostic endoscopic cholangiography and pancreatography (ERCP) as it is non-invasive and less expensive
Slide5Invstigation
d. 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. Diagnostic and theraputice. Endoscopic ultrasound This is particularly useful in identifying small tumours that may not show up well on CT or MRI, and in demonstrating the relationship of a pancreatic tumour to major vessels nearby. Transduodenal or transgastric fine needle aspiration (FNA) or Trucut biopsy performed under EUS guidance avoids spillage of tumour cells into the peritoneal cavity.
Slide6CONGENITAL ABNORMALITIES
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 5% to10% .Pancreas divisum found incidentally in an asymptomatic person does not warrant any intervention. The incidence of pancreas
divisum
ranges from 25–50% in patients with recurrent acute pancreatitis, chronic pancreatitis and pancreatic pain. The minor papilla is substantially smaller than the major papilla (and many of these patients probably have papillary
stenosis). A large volume of secretions flowing through a narrow papilla probably leads to incomplete drainage, which may then cause obstructive pain or pancreatitis. Idiopathic recurrent pancreatitis, pancreas divisum should be excluded. The diagnosis can be arrived at by MRCP, EUS or ERCP, augmented by injection of secretin if necessary. Endoscopic sphincterotomy and stenting of the minor papilla may relieve the symptoms. Surgical intervention can take the form of sphincteroplasty, pancreatojejunostomy or even resection of the pancreatic head.
Slide7CONGENITAL ABNORMALITIES
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.It is most often seen in association with congenital duodenal stenosis
or
atresia
and is therefore more prevalent in children with Down syndrome. The usual treatment is bypass (duodenoduodenostomy). The disease may occur in later life as one of the causes of pancreatitis.
Ectopic pancreas
Islands of ectopic pancreatic tissue can be found in the
submucosa in parts of the stomach, duodenum or small intestine (including Meckel’s diverticulum), the gall bladder, adjoining the pancreas, in the hilum of the spleen and within the liver.Ectopic pancreas may also be found in the wall of an alimentary tract duplication cyst.
Slide8INJURIES TO THE PANCREAS
External injuryPresentation and managementThe pancreas, its somewhat protected location in the retroperitoneum
, is not frequently damaged in
blunt abdominal trauma
. If there is damage to the pancreas, it is often concomitant with injuries to other viscera, especially the liver, the spleen and the duodenum. Pancreatic injuries may range from a contusion or laceration of the parenchyma without duct disruption to major parenchymal destruction
with duct disruption (sometimes complete
transection
) and, rarely, massive destruction of the pancreatic head. Blunt pancreatic trauma usually presents with epigastric Pain with the progressive development of more severe pain due to the sequelae of leakage of pancreatic fluid into the surrounding tissues. A rise in serum amylase occurs in most cases.A CT scan of the pancreas will delineate the damage that has occurred to the pancreas. If there is doubt about duct disruption, an urgent ERCP should be sought. MRCP may also provide the answer.
Slide9INJURIES TO THE PANCREAS
Support with intravenous fluids and a ‘nil by mouth’ regimen should be instituted while these investigations are performed.It is preferable to manage conservatively at first, investigate and, once the extent of the damage has been ascertained, undertake appropriate action. Operation is indicated if there is disruption of the main pancreatic duct; in almost all other cases, the patient will recover with conservative management. Penetrating trauma to the upper abdomen or the back carries a higher chance of pancreatic injury.
In penetrating injuries, especially if other organs are injured and the patient’s condition is unstable, there is a greater need to perform an urgent surgical exploration.
Sequlae
Death, in acute phase as a result of bleeding from associated injuries.Persistent drain output in 1/3 of patientsDuct stricture resulting in recurrent episodes of pancreatitis.Pancreatic pseudocyst.
Slide10INJURIES TO THE PANCREAS
Iatrogenic injuryThis 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.
● Duodenal or
ampullary bleeding following sphincterotomy.Pancreatic fistulaManagement of pancreatic fistulaeTests● Measure amylase level in fluid● Determine the anatomy of the fistula● Check if the main pancreatic duct is blocked or disruptedMeasures● Correct fluid and electrolyte imbalances● Protect the skin● Drain adequately● Parenteral or nasojejunal feeding●
Octreotide
to suppress secretion
● Relieve pancreatic duct obstruction if possible (ERCP
andstent
)
● Treat underlying cause
Slide11Acute pancreatitis
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.Once cellular injury has been initiated, the inflammatory process can lead to pancreatic oedema, haemorrhage and, eventually, necrosis.
As inflammatory mediators are released into the circulation, systemic complications can arise, such as
haemodynamic
instability, bacteraemia (due to translocation of gut flora), acute respiratory distress syndrome and pleural effusions, gastrointestinal haemorrhage, renal failure and disseminated intravascular coagulation (DIC).The majority of patients will have a mild attack of pancreatitis, the mortality from which is around 1%. Severe acute pancreatitis is seen in 5–10% of patients, and is characterised by pancreatic necrosis, a severe systemic inflammatory response and often multi-organ failure.In those who have a severe attack of pancreatitis, the mortality varies from 20 to 50%.Acute pancreatitis has an
early phase that usually lasts a
week. It is characterised by a systemic inflammatory response syndrome (SIRS) which – if severe – can lead to transient or persistent organ failure (deemed persistent if it lasts for over 48 hours).
About one-third of deaths occur in the early phase of the attack, from multiple organ failure. The late phase is seen typically in those who suffer a severe attack, and can run from weeks to months. It is characterised by persistent systemic signs of inflammation, and/or local complications, particularly fluid collections and peripancreatic sepsis. Deaths occurring after the first week of onset are often due to septic complications.
Slide12Acute pancreatitis
Possible causes of acute pancreatitis● Gallstones● Alcoholism 50-70%● Post ERCP 1-3 %● 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
Slide13Acute pancreatitis
Clinical presentationPain characteristically develops quickly, reaching maximum intensity within minutes and persists for hours or even days. The pain is frequently severe, constant and refractory to the usual doses of analgesics. epigastrium but may be localised to either upper quadrant or felt diffusely throughout the abdomen. There is radiation to the back in about 50% of patients, and some patients may gain relief by sitting or leaning forwards.
Nausea, repeated vomiting and retching. The retching may persist despite the stomach being kept empty by
nasogastric
aspiration. Hiccoughs may be due to gastric distension or irritation of the diaphragm.On examination, the patient may be well or gravely ill.Tachypnoea , tachycardia is usual, and hypotension .The body temperature is often normal or even subnormalMild icterus
can be caused by
biliary
obstruction in gallstone pancreatitis.Bleeding into the fascial planes can produce bluish discolouration of the flanks (Grey Turner’s sign) or umbilicus (Cullen’s sign). Neither sign is pathognomonic of acute pancreatitis; Cullen’s sign was first described in association with rupture of an ectopic pregnancy. Subcutaneous fat necrosis may produce small, red, tender nodules on the skin of the legs.Abdominal examination may reveal distension due to ileus.There is usually muscle guarding in the upper abdomen. A pleural effusion is present in 10–20% of patients. Pulmonary oedema and pneumonitis
Slide14Acute pancreatitis
InvestigationsA serum amylase level three times above normal serum levels lipase contrast- enhanced CT.
ASSESSMENT OF SEVERITY
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 Regardless of the system used, persisting organ failure indicates a severe attack. A serum C-reactive protein level >150 mg/L at 48 hours after the onset of symptoms is also an indicator of severity.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.
Slide15Acute pancreatitis
ASSESSMENT OF SEVERITY
Slide16Acute pancreatitis
Slide17Acute pancreatitis
Slide18Acute pancreatitis
PSEUDOCYSTA pseudocyst is a collection of amylase-rich fluid enclosed in a well-defined wall of fibrous or granulation tissue. Formation of a pseudocyst
requires 4 weeks or more from the onset of acute pancreatitis.
A
pseudocyst is usually identified on ultrasound or a CT scan.EUS and aspiration of the cyst fluid. The fluid should be sent for measurement of carcinoembryonic antigen (CEA) levels, amylase levels and cytology.Fluid from a pseudocyst
typically has a low CEA level, and levels above 400
ng
/mL are suggestive of a mucinous neoplasm.Pseudocyst fluid usually has a high amylase level, but that is not diagnostic, as a tumour that communicates with the duct system may yield similar findings. Cytology typically reveals inflammatory cells in pseudocyst fluid.Pseudocysts will resolve spontaneously in most instances,but complications can develop . Pseudocysts that are thick-walled or large (over 6 cm in diameter), have lasted for a long time (over 12 weeks), or have arisen in the context of chronic pancreatitis are less likely to resolve spontaneously.Therapeutic interventions are advised only if the pseudocyst causes symptoms, if complications develop, or if a distinction has to be made between a pseudocyst
and a tumour.
Slide19Acute pancreatitis
PSEUDOCYSTPercutaneous drainage to the exterior under radiological guidance should be avoided. It carries a very high likelihood of recurrence. Moreover, it is not advisable unless one is absolutely certain that the cyst is not neoplastic and that it has no communication with the pancreatic duct (or else a
pancreaticocutaneous
fistula will develop).
Endoscopic drainage usually involves puncture of the cyst through the stomach or duodenal wall under EUS guidance, and placement of a tube drain with one end in the cyst cavity and the other end in the gastric lumen.Surgical drainage involves internally draining the cyst into the gastric or jejunal lumen
Slide20Acute pancreatitis
STERILE AND INFECTED PANCREATIC NECROSISRefers to a diffuse or focal area of non-viable parenchyma.Acute necrotic collection (ANC). This is typically an intra or extrapancreatic
collection containing fluid and necrotic material, with no definable wall.
Gradually, over a period of over 4 weeks, this may develop a well-defined inflammatory capsule, and evolve into what is termed
walled-off necrosis (WON).Collections associated with necrotising pancreatitis are sterile to begin with but often become subsequently infected, probably due to translocation of gut bacteria.Infected necrosis is associated with a mortality rate of up to 50%.Sterile necrotic material should not be drained or interfered with. But if the patient shows signs of sepsis, then one should determine whether the collection is infected
Dx
: aspiration under Ct scan guidance. (the needle should never pass through hollow viscera)
Rx: if the aspirated is purulent, the patient should be kept on antibiotics according to sensitivity and drain inserted for drainage. The drain should be with larger size when the aspirate is thick content. if sepsis persist this need pancreatic necrosectomy Patients with peripancreatic sepsis are ill for long periods of time, and may require management in an intensive care unit. Nutritional support is essential. The parenteral and nasojejunal approaches are more popular (on the assumption that they rest the pancreas).
Slide21Chronic pancreatitis
Chronic pancreatitis is a progressive inflammatory disease in which there is irreversible destruction of pancreatic tissue. Its clinical course is characterised by severe pain and, in the later stages, exocrine and endocrine pancreatic insufficiency.Aetiology and pathology
Alcoholism 60-70%
Duct obstruction due to trauma, acute pancreatitis or pancreatic cancer
Congenital anomalies Hereditary pancreatitisCystic fibrosisHyperlipidemia
Hypercalcemia
Autoimmune pancreatistis (IgG4 phenomena)Idioathic*** At the onset of the disease, the pancreas may appear normal. Later, the pancreas enlarges and becomes hard as a result of fibrosis. The ducts become distorted and dilated with areas of both stricture formation and ectasia. Calcified stones form within the ducts. The ducts may become occluded with a gelatinous proteinaceous fluid and debris, and inflammatory cysts may form. Histologically, the lesions affect the lobules, producing ductular metaplasia and atrophy of acini, hyperplasia of duct epithelium and interlobular fibrosis.
Slide22Chronic pancreatitis
Clinical featuresPain; the site of the pain is depend on the site of the disease. Head of pancreas; the pain felt in the epigastric
and right
subcostal
region, whereas if the disease is limited to the body and tail, the pain felt in the left subcostal region and back.Nausea is common, vomiting may develop.Weight lossThe patient’s lifestyle is gradually destroyed by pain, analgesic dependence, weight loss and inability to work.
Loss of exocrine function leads to
steatorrhoea in more than 30% of patients with chronic pancreatitis.Loss of endocrine function and the development of diabetesInfection
Slide23Chronic pancreatitis
InvestigationsOnly in the early stages of the disease will there be a rise in serum amylase.Tests of pancreatic function merely confirm the presence of pancreatic insufficiency or that more than 70% of the gland has been destroyed.
Pancreatic calcifications may be seen on abdominal X-ray
CT or MRI scan will show the outline of the gland, the main area of damage and the possibilities for surgical correction, An MRCP will identify the presence of
biliary obstruction and the state of the pancreatic ductERCP is the most accurate way of elucidating the anatomy of the ductEUS
Slide24Chronic pancreatitis
Medical treatment of chronic pancreatitisTreat the addiction Help the patient to stop alcohol consumption and tobacco smoking Involve a dependency counsellor or a psychologistAlleviate abdominal pain
Eliminate obstructive factors (duodenum, bile duct, pancreatic duct)
Escalate analgesia in a stepwise fashion
Refer to a pain management specialist For intractable pain, consider CT/EUS-guided coeliac axis blockNutritional and pharmacological measures Diet: low in fat and high in protein and carbohydrates
Pancreatic enzyme supplementation with meals
Correct
malabsorption of the fat-soluble vitamins and vitaminB12 Micronutrient therapy with methionine, vitamins C & E, selenium (may reduce pain and slow disease progression)Steroids (only in autoimmune pancreatitis, for relief of symptoms)Medium-chain triglycerides in patients with severe fat malabsorption (they are directly absorbed by the small intestine without the need for digestion) Reducing gastric secretions may helpTreat diabetes mellitus
Slide25Chronic pancreatitis
Endoscopic, radiological or surgical interventions are indicated mainly to relieve obstruction of the pancreatic duct, bile duct or the duodenum, or in dealing with complications (e.g. pseudocyst, abscess, fistula, ascites or
variceal
haemorrhage).
PrognosisChronic pancreatitis is a difficult condition to manage. Patients often suffer a gradual decline in their professional, social and personal lives. The pain may abate after a surgical or percutaneous intervention, but tends to return over a period of time. In a proportion of patients, the inflammation may gradually burn out over a period of years, with disappearance of the pain, leaving only the exocrine and endocrine insufficiencies.
Development of pancreatic cancer is a risk in those who have had the disease for more than 20 years.
New symptoms or a change in the pattern of symptoms should be investigated and malignancy excluded.
Slide26CARCINOMA OF THE PANCREAS
Risk factors for the development ofpancreatic
cancer
.
Demographic factorsAge (peak incidence 65–75 years)Male genderBlack ethnicity
Environment/lifestyle
Cigarette
smokingGenetic factors /medical conditionsFamily historyGermline BRCA2 mutations in some rare high-risk familiesHereditary pancreatitis (50- to 70-fold increased risk)Chronic pancreatitis (5- to 15-fold increased risk)Lynch syndrome (HNPCC)Ataxia telangiectasiaPeutz–Jeghers syndromeFamilial breast–ovarian cancer syndromeFamilial atypical multiple mole melanomaFamilial adenomatous polyposis – risk of
ampullary
/duodenal carcinoma
Diabetes mellitus
Slide27CARCINOMA OF THE PANCREAS
Pathology of pancreatic tumours
85%
ductal
adenocarcinomaIntense desmoplastic reaction (extensive fibrosis), difficult to differentiate from
ch
pancreatitis
Spread; locally… nerve sheath, blood vessels and lymphatic liver and peritoneal spreadCystic tumours ; serous and mucinousSerous : benign, old female, small and multipleMucinous : potential for malignant transformation it is either Mucinous cystic neoplasm (MCNs) or intraductal papillary mucinous neoplasms
(IPMNs)
Adenomas of
ampulla
of
Vater
; premalignant lesion, may
harbour
invasive
adenocarcinoma
, it is common in patients with FAP, need endoscopic surveillance
Ampullary
adenocarcinoma
Ampullary
neuroendocrine
tumours
Slide28CARCINOMA OF THE PANCREAS
Clinical featuresPainless jaundice, pruritus, dark urine, pale stool,
steatorrhoea
Vague symptoms, weight loss , poor
appitite Recent onset DM over 50 with non specific symptms
Attacks of pancreatitis
Body and tail of pancreas
tumours usually preset late as a big tumour with backacheExamination; jaundice, weight loss, palpable liver and gall bladder, Courvoisier sign, sings of advance disease (acites, supraclavicular LN, pelvic metastasis …etc) Investigation blood test; abnormal liver function test, anemia, tumour markers CA19-9Ultrasound; dilated CBD, pancreatic mass liver metastasis, peritoneal massContrast enhanced CT scan; site of tumour, relation to the arteries vein, duodenum, stomach, bowel, peritoneum
lymphnodes
MRI
ERCP; mainly therapeutic (
stenting
)
EUS, tissue to confirm the
Dx
(
ch
. Pancreatitis,
Mucinous
tumours
)
Diagnostic laparoscopy
Slide29CARCINOMA OF THE PANCREAS
Management85% unrespectable at time of diagnosis palliative treatment Operable surgical resection
1. head of pancreas and
periampullary tumours: pancreaticoduodenectomy – whipple’s
operation ( resection of gastric
antrum
, duodenum, head of pancreas, CBD& gall bladder) or pylorus preserving pancreaticodudenectomy 2. body and tail of pancreas ; distal pancreatectomy and splenectomy 3. total pancreatectomy; a multifocal tumour (e.g. a main duct IPMN), or the body and tail of the gland are too inflamed or too friable to achieve a safe anastomosis with the bowel.
Slide30CARCINOMA OF THE PANCREAS
Palliation of pancreatic cancerRelieve jaundice and treat biliary sepsis Surgical
biliary
bypass
Stent placed at ERCP or percutaneous transhepaticcholangiographyImprove gastric emptying
Surgical
gastroenterostomyDuodenal stentPain relief Stepwise escalation of analgesiaCoeliac plexus blockTransthoracic splanchnicectomySymptom relief and quality of life Encourage normal activitiesEnzyme replacement for steatorrhoea Treat diabetesConsider chemotherapy
Slide31Questions
Which of the following statements are true?A Pancreatic injury is common following blunt abdominal trauma.B Pancreatic injury is often accompanied by damage to the liver, spleen and duodenum
.
C
The serum amylase is raised in most cases of pancreatic injury. D A CECT scan will delineate the damage.E In doubtful cases, urgent ERCP is helpful. BCDEWhich of the following statements is false
?
A
All patients with pancreatic trauma should undergo an exploratory laparotomy.B Pancreatic duct disruption requires surgical exploration.C Severe injury to the duodenum and the head of the pancreas requires pancreatoduodenectomy.D After conservative management for pancreatic injury, duct stricture and pseudocyst may occur as complications.E During splenectomy, iatrogenic injury to the pancreatic tail can occur. A
Slide32Which of the following statements are true
with regard to complications in acute pancreatitis?A Patients with severe acute pancreatitis require a CECT scan to detect pancreatic necrosis.B In severe acute pancreatitis, a laparotomy must be done in all cases of pancreatic
necrosis.
C
Aneurysm of the superior mesenteric artery can occur.D The vast majority of patients with peripancreatic sepsis can be treated conservatively.E Pleural effusion is seen in 10–20 per cent of patients.
ACDE