5 - Hepatobiliary Flashcards
What is a splenic infarct?
Occlusion of the splenic artery or one of its branches resulting in tissue necrosis
Often not complete necrosis due to collateral supply from splenic artery and short gastric (left gastroepiploic)
What is the aetiology of a splenic infarct?
- Haemotological Disease: Lymphoma, Myelofibrosis, Sickle cell, CML, Polycythemia Vera, Hypercoagulable states
- Thromboembolism: endocarditis, AF, post MI mural thrombus,
- Rare causes: trauma, vasculitis, liver surgery, panreatectomy
How do haemtological diseases cause splenic infarction?
Congestion of the splenic artery with abnormal cells
What are the clinical features of a splenic infarct?
- Often asymptomatic
- LUQ pain/tenderness that radiates to the left shoulder (Kehr’s sign)
- Fever
- N+V
- Pleuritic chest pain
What differential diagnoses can be considered when a patient presents with symptoms of a splenic infarct?
- Peptic ulcer disease
- Pyelonephritis
- Ureteric colic
- Left sided basal pneumonia
What investigations should be done if you suspect a splenic infarct and what will the findings be?
- Gold standard: CT abdomen with IV contrast
Will show segmental wedge shaped infarct towards hilum of the spleen. Whole spleen hypoattentuated if splenic artery occluded not a branch
- Routine bloods: FBC, LFTs, U+E’s, coagulation screen
What is the immediate and long term management for a patient with a splenic infarct?
Immediate:
- Analgesia
- IV fluids
- Manage underlying condition
- Consider long term anticoagulation
- Avoid splenectomy due to OPSI
Long-term:
- Vaccination against encapsulated bacteria NHS
- Prophylatic low dose abx (Penicillin V)
What are the complications of a splenic infarct?
- Splenic rupture: do splenectomy
- Splenic abscess: when cause of infarct was non-sterile embolus e.g infective endocarditis. May be seen on CT scan but confirmed with explorative surgery
- Pseudocyst formation
- Autosplenectomy: causes asplenism. Repeated splenic infarcts leads to progressive fibrosis and atrophy of the spleen. Common in sickle cell as when crises there is splenic artery occlusion. Leaves patient susceptible to infection
What are some of the causes of splenic rupture?
- Blunt trauma: seatbelt injuries, falls onto the left side
- Iatrogenic
- Splenomegaly: EBV, haemtological malignancy. Cause capsule to stretch and thin so susceptible to rupture
What are the clinical features of splenic rupture?
- Abdominal pain
- Hypovolemic shock
- LUQ tenderness/Peritonism
- Kehr’s sign due to diaphragm irritation
What investigations do you do for a suspected splenic rupture?
Haemodynamically unstable with peritonism: immediate laparotomy
Haemodynamically stable: urgent CT chest-abdomen-pelvis with IV contrast
How do you grade splenic injuries?
- American Association for the Surgery of trauma.
- Used to help guide which patients should have conservative maagement and which should have surgical
How should we manage patients with splenic rupture?
All: assessed and resuscitate with ATLS protocol
Haeodynamically unstable/Grade 5: Urgent laparotomy
Haemodynamically stable/Grade 1-3: Conservative. Move to high dependency area on strict bed rest and regular abdominal exams for deterioration. CT repeated 1/52 post injury. Increasing tenderness or peritonitis re-image/laparotomy/embolisation. Prophylatic vaccinations on discharge
What are the main complications of conservative treatment and embolisation treatment for splenic rupture?
- Ongoing bleeding
- Splenic necrosis
- Splenic abscess or cyst formation
- Thrombocytosis (give aspirin if platelet count rises)
- OPSI so give prophylatic Penicillin V and vaccinations to prevent sepsis
What is bile made from?
Stored in the gallbladder until released to duodenum:
- Cholesterol
- Phospholipids
- Bile pigments from Hb metabolism
What are the three main types of gallstones?
- Cholesterol: linked to poor diet and obesity
- Pigment : due to excess bille pigment production, seen in haemolytic anaemias
- Mixed: both cholesterol and bile pigments
What are the risk factors for gallstones?
5 F’s:
- Fat
- Female
- Fertile
- FHx
- Forty
Also: pregnancy, COCP (oestrogen causing more cholesterol in bile), haemolytic anaemia, malabsorption (e.g Crohn’s)
What are the clinical features of biliary colic?
- Sudden, dull, colicky pain in RUQ that may radiate to back or epigastrium
- Precipitated by eating fatty foods due to release of CCK causing gallbladder contraction
- Can be N+V
- Settles with pain relief and no inflammatory response
What are the clinical features of acute cholecystitis?
- Constant pain and tenderness in RUQ/epigastrium
- Signs of inflammation e.g fever or lethargy
- Murphy Sign +
- Guarding may suspect peritonitis/sepsis
What investigations should you do if someone presents with RUQ pain that you suspect to be gallbladder related?
- Lab tests (see image):
- FBC, CRP, LFTs, Amylase, Pregnancy
- Imaging:
- Transabdominal US 1st line
- MRCP Gold standard if US inconclusive
What would you see on ultrasound with gallstone pathology?
- Gallstones or sludge
- Thickened gallbladder wall if inflamed
- Bile duct dilatation (stone in the distal bile ducts)
How is biliary colic managed?
- Analgesia
- Lifestyle advice (weight loss, low fat diet, exercise)
- Elective laparoscopic cholecystectomy within 6 weeks due to high risk of recurrence/complications
How is acute cholecystitis managed?
- IV Abx (Co-amoxiclav +/- Metronidazole)
- Analgesics
- Antiemetics
- IV fluids
- Laparoscopic cholecystectomy within a week, better within 72 hours of presentation
- Percutaneous cholecystostomy if not fit for surgery/not responsive to abx. Drains infection
What is the difference between MRCP and ERCP?
MRCP - Identifies any biliary obstruction
ERCP - Identifies any biliary obstruction and allows for intervention
If a patient presents with RUQ post-cholecystectomy, what is the likely pathology and what should you do?
- Retained CBD stone
- Use US abdomen but if unremarkable do MRCP
What are some complications of gallstones?
- Mirizzi Syndrome
- Gallbladder empyema
- Chronic cholecystitis
- Bouveret’s Syndrome
- Gallstone ileus
What is Mirizzi Syndrome and how is it managed?
- Stone located in Hartmann’s pouch or the cystic duct, that compresses the common hepatic duct
- Causes obstructive jaundice
- Confirmed with MRCP and manage by laparoscopic cholecystectomy
What is gallbladder empyema and how is it managed?
- Gallbladder filled with pus
- Patient unwell and often septic, same clinical picture as acute cholecystitis
- Diagnose with US or CT
- Manage with laparoscopic (often switches to open) cholecystectomy or percutaneous cholecystotomy
What is chronic cholecystitis, what are the complications of this and how is it managed?
- History of recurrent or untreated cholecystitis
- Ongoing RUQ or epigastric pain w/wo N+V
- Complications: gallblader carcinoma, biliary enteric fistula
- Diagnose with CT or often histologically post-cholecystectomy.
- Treat with elective cholecystectomy
What is Bouveret’s Syndrome and Gallstone Ileus?
Inflammation of gallbladder can form cholecystoduodenal fistula allowing gallstones into small bowel, resulting in bowel obstruction
- Bouveret’s Syndrome – stone impacts proximal duodenum, causing a gastric outlet obstruction
- Gallstone Ileus – stone impacts terminal ileum (narrowest part of small bowel), causing a small bowel obstruction
What is cholangitis and what are some of the causes of this?
Infection of the biliary tract due to biliary outflow obstruction. Obstruction causes stasis of fluid and increased intraluminal pressure that allows bacteria to colonise the billiary tree
Common Causes: Gallstones, ERCP/Iatrogenic, Cholangiocarcinoma
Rare causes: Pancreatitis, Primary Sclerosing Cholangitis, Ischaemic Cholangiopathy, and parasitic infections
What are the most common infective organisms in cholangitis?
- Escherichia Coli
- Klebsiella species
- Enterococcus
What are the clinical features of cholangitis?
- Charcot’s Triad
- Reynold’s Pentad
- Pruitis
- Pale stool/Dark urine
- Tachycardia
- History of gallstones, ERCP, meds like COCP and fibrates
What investigations should you do when you suspect cholangitis to find the underlying cause and what will the findings be?
- Routine bloods: FBC (raised WBC) and LFTs (raised ALT, gamma GT and bilirubin)
- Blood cultures: take before broad spectrum abx
- US of biliary tract: bile duct dilatation >6mm
- ERCP: gold standard diagnostic and therapeutic. May do MRCP before
How is cholangitis managed?
- Sepsis 6 with IV broad spectrum abx (Co-amoxiclav)
- Endoscopic biliary decompression with ERCP or percutaneous transhepatic cholangiograpy (PTC) 2nd line
- Elective cholecystectomy if the cause was gallstones
What are the complications of ERCP?
- Repeated cholangitis
- Pancreatitis
- Bleeding (more common when sphincterotomy performed)
- Perforation
What is the prognosis for cholangitis and what factors increase mortality?
- 5-10% for those given early abx therapy
- Increased mortality: delayed diagnosis, liver failure, cirrhosis, CKD, hypotension, female, over 50
What is a cholangiocarcinoma and what is the common histology and location of these?
- Cancer in the biliary system but usually extrahepatic
- Common location: bifurcation of right and left hepatic ducts (Klatskin tumour).
Slow growing that invades locally and metastases to lymph nodes then peritoneal cavity, liver, lung
- Histology: 95% adenocarcinoma, SCC, lymphoma, sarcomas, small cell cancers
What are the main risk factors for cholangiocarcinomas?
- Primary sclerosing cholangitis
- Ulcerative colitis
- Infective (Liver flukes, HIV, hepatitis virus)
- Toxins (Chemicals in rubber and aircraft industry)
- Congenital (Caroli’s disease, choledochal cyst)
- Alcohol excess
- Diabetes mellitus
What are the clinical features of cholangiocarcinomas?
- Usually asymptomatic until later disease
- Post hepatic jaundice
- Pruitis
- Pale stools/dark urine
- Cachexia
- Sometimes: RUQ pain, malaise, early satetity, weight loss
What is Courvoisier’s Law?
In the presence of painless jaundice and an enlarged gallbladder/RUQ mass, there is likely an obstructing pancreatic or gallbladder malignancy not gallstones
Sign only present if tumour obstructing distal to cystic duct
What are some differentials for cholangiocarcinoma?
Think of other causes of post-hepatic jaundice:
- obstructive choledocholithiasis
- bile duct strictures
- external compression from extra-biliary tumour
- benign biliary tumours
- pancreatic tumours
- primary biliary cirrhosis
- primary sclerosing cholangitis.
What investigations need to be done when you suspect a cholangiocarcinoma and what do you expect to find?
Bloods
- Raised ALP, Gamma GT, Bilirubin
- Tumour markers CEA/CA19-9
Imaging
- US
- MRCP GOLD STANDARD will show strictures in biliary tree
- ERCP (can take biopsies)
- CT for staging as can look for distant metastases
- Angiography for pre-op planning of hepatic arteries
The only cure for cholangiocarcinomas is complete surgical resection, what are some of the procedures used?
Intrahepatic or Klatskin tumour: partial hepatectomy and reconstruction of the biliary tree
- Distal common duct tumour: pancreaticoduodenectomy (termed a Whipple’s procedure).
- Radiotherapy as neo/adjuvant therapy
Most patients with cholangiocarcinoma will require palliative treatment. What are some of the options for this?
Stenting: with ERCP to relieve obstructing symptoms but may need to be replaced every few months as prone to occlusion
Surgical bypass: if obstruction not relieved by stenting
Palliative radiotherapy and chemotherapy to slow tumour growth e.g cisplatin
What are some of the complications with cholangiocarcinomas?
- Increased risk of biliary tract sepsis due to obstruction
- Secondary biliary cirrhosis
- Prognosis 12-18 months to live after diagnosis
- Distal tumours better prognosis than proximal
What are simple liver cysts and some of the clinical features of these?
Fluid-filled epithelial-lined sacs within the liver, most commonly occurring in the right lobe
Though to be congenitally malformed bile duct cells, failing to connect to the extrahepatic ducts
Symptoms: mostly asymptomatic and found on imaging, some have ab pain, nausea and early sateity due to mass effect
How are simple liver cysts investigated?
Bloods: LFTs normal but may have raised gamma GT and tumour markers CEA/CA19-9
US: imaging modality of choice. well defined, thin walled, spherical lesions with no septation and strong posterior wall acoustic enhancement
How are simple liver cysts managed?
- <4cm asymptomatic: no intervention
- >4cm asymptomatic: follow up US scans at 3,6,12 months to check for growth. If size of cyst remains unchanged for 2-3 years no intervention unless becomes asymptomatic
- Symptomatic: ultrasound-guided aspiration or laparoscopic de-roofing (lower rates of recurrence)
What is polycystic liver disease and what is it caused by?
Presence of ≥20 cysts in liver parenchyma, each of which are ≥1cm in size.
Caused by ADPCKD or ADPLD
Structures are not connected to intrahepatic bile ducts so do not drain and lead to dilatation and cyst formation filled with bile fluid
What are the clinical features of polycystic liver disease?
- Asymptomatic
- Abdominal pain and hepatomegaly as increases in size
- May have urinary symptoms if kidneys involved
- Eventual liver cirrhosis and portal hypertension
What are the investigations and management for cystic neoplasms?
- Bloods: normal LFTs but may have mildly raised CEA, ALP, CA19-9
- US: can tell the different between simple and complicated cysts
- CT imaging with contrast: to diangose and look for metastases
- Management: liver lobe resection whether adenoma or adenocarcinoma and histological diagnosis
What are hyatid cysts?
Liver cysts formed by infection by the tapeworm Echinococcus granulosus.
Eggs are passed faeco-orally (dogs) and pass into the hepatic portal system where they form cysts
High prevalence in South America, North Africa, Central Asia
What are some clinical features of hyatid cysts and what investigations can be done to diagnose this?
- Asymptomatic for years as slow growing
- Vague abdominal pain due to mass effect or rupture
- May cause jaundice, cholangitis, vomiting, dyspepsia
- Bloods: LFTs normal, eosinophillia, positive antibody titre
- US: calcified, spherical lesion with multiple septations. Anechoic with snowflake inclusions
- CT Imaging with contrast
How are hyatid cysts managed?
- If asymptomatic can monitor
- Surgical cyst deroofing
- Antiparasitics e.g albendazole, mebendazole and/or praziquantel
- DO NOT ASPIRATE AS RUPTURE CAN CAUSE ANAPHYLAXIS
What is the pathophysiology of a liver abscess?
Polymicrobial bacterial infection spreading from the biliary or gastrointestinal tract, either via contiguous spread or seeding from portal and hepatic veins
Common organsims: E. Coli, K. pneumoniae, and S. constellatus, Fungal in immunocompromised
Causes: cholecystitis, cholangitis, diverticulitis, appendicitis, or septicaemia
What are the clinical features of a liver abscess?
- Fever, rigors, abdominal pain
- Bloating, nausea, anorexia, weight loss, fatigue and jaundice
- On examination will have RUQ pain with hepatomegaly
- If ruptures may have signs of sepsis
What investigations should you do if you suspect a liver abscess, and what will they show?
- Bloods: raised WBC, raised ALP
- Blood and fluid cultures: should be sent off
- US: poor defined lesions with hypo- and hyper-echoic areas, with gas bubbles and septations
- CT with contrast: similar findings to US with surrounding oedema
How are liver abscesses managed?
DEPENDS ON SIZE
- Fluid resuscitation
- Antibiotics
- US/CT guided aspiration w or w/o catheter drainage
- Cyst deroofing
- Surgery if ruptures
TREAT ANY UNDERLYING CAUSE TOO
What is an amoebic abscess?
Most common extra-intestinal manifestation of Entomoeba Histiolytica (from spread via portal system)
Spreads faeco-oral and once in colon invades mucosa to get to portal system. Common in developing world e.g South America, India
What are the clinical features of an amoebic abscess?
- Vague symptoms of abdominal pain, nausea, fever or rigors, weight loss, and bloating
- May have prodrome of abdominal pain and diarrhoea
- History of recent travel (<6 months) to an endemic area
How are amoebic abscesses investigated and managed?
Ix:
- Bloods: raised WBC, deranged LFTs, E.Histolytica antibodies
- Blood cultures
- Stool samples: for antibodies
- US/CT: poor defined lesions
Mx:
- Antibiotics (Metronidazole or Tinidazole)
- Surgical drainage for large cysts that do not respond to abx
- Luminal agent (Paromycin) to clear colon of amoebiasis
90% of liver cancer is due to metastases. The other 10% of cases is due to Hepatocellular carcinomas. What are some of the causes of HCC?
6th most common cancer due to chronic inflammatory processes:
- Viral hepatitis (most common)
- Chronic alcoholism
- Hereditary haemochromatosis
- PBS
- Aflatoxin (cereals and nuts)
What are some risk factors for developing hepatocellular carcinomas?
- Viral hepatitis (Hep B and C)
- Smoking
- >70
- Aflatoxins
- Family history of liver disease
What are the clinical features of hepatocellular carcinomas and some differentials for this?
- Main symptom: liver cirrhosis
- Irregular enlarged craggy tender liver
- Dull ache in RUQ
- Fatigue, fever, weight loss, lethargy
- Late: ascites and jaundice
Differentials: infectious hepatitis, cardiac failure (smooth liver), benign hepatocellular adenoma, other causes of liver cirrhosis
What are some labatory tests that can be done when diagnosing HCC?
- LFTs: ALP, AST, ALT, Bilirubin all deranged
- Low platelets and prolonged clotting
- Alpha-Fetal Protein (AFP) may be raised and can be used to monitor progression
How is HCC diagnosed with imaging?
- US: inital imaging of choice. Mass >2cm with raised AFP is diagnostic
- MRI liver scanning or percutaneous fine-needle aspiration may be used if US suggestive but not sure. Be careful of seeding
- CT staging scan
What is the staging tool used to stage HCC?
Barcelona Clinic Liver Cancer staging system (BCLC)
Helps to decide which treatment is suitable
What are two risk assessment tools used once a diagnosis of HCC has been made?
Child-Pugh: calculates prognosis of patients with liver cirrhosis.
Looks at serum bilirubin, albumin, INR, degree of ascites, and evidence of encephalopathy
MELD: calculates same prognosis but better and also predicts likelihood of patient tolerating a liver transplant.
Looks at creatinine, bilirubin, INR, sodium, and the use of dialysis (at least twice per week)
Surgery is the only curative treatment for HCC. What is the surgical management for hepatocellular carcinoma?
- Surgical resection: if no cirrhosis and good baseline health. High 5 year recurrence rate
- Transplation: only if fufill the Milan criteria.
One lesion <5cm or three lesions <3cm, no extrahepatic manifestations, no vascular infiltration
What is some non-surgical management used in the treatment of HCC?
- Image guided ablation: if early stage BCLC 0 or A. Put US waves into tumour to cause necrosis
- Alcohol ablation: if small
- Transarterial Chemoembolisation (TACE): BCLC stage B (a large multinodular tumour. High concentrations of chemotherapy are injected directly into hepatic artery and an embolising agent is then added to induce ischaemia.
Radiological techniques used so only embolise branches of arteries supplyin tumour not whole liver
How can you tell the difference between acute and chronic pancreatitis?
Limited damage to the secretory function of the gland, with no gross structural damage developing.
Repeated acute can lead to chronic
What is the aetiology for acute pancreatitis?
(See image)
Most common: Excess alcohol consumption and Gall stones
Cause not found in some patients
What is the pathophysiology of acute pancreatitis?
- Premature and exaggerated activation of digestive enzymes
- Pancreatic inflammatory response (Increasing vascular permeability and fluid shifts, third spacing)
- Pancreatic enzymes in blood stream cause fat autodigestion leading to fat necrosis and hameorraghe into retroperitoneal space
- Free fatty acids react with calcium to form chalky deposits and hypocalcaemia
- End stage is complete necrosis of the pancreas
What are the clinical features of acute pancreatitis?
- Sudden onset severe epigastric pain that can radiate to back
- Nausea and vomiting
- Guarding
- Cullen’s/Grey-Turners if retroperitoneal haemorraghe
- Tetany from hypocalcaemia
- Jaundice if gallstones aetiology
What are some labatory investigations to diagnose acute pancreatitis?
Serum Amylase: 3x upper limit of normal
LFTs: to see if any cholecystic involvement. Raised ALT likely cause is gallstones
Serum Lipase: more accurate than amylase as remains elevated for longer
What are some of the risk tools used to assess the severity of pancreatitis?
- Modified Glasgow Criteria within 48 hours of admission
- Score of 3 or more have severe pancreatitis and a high-dependency care referral is needed
- PANCREAS mneumonic (see image)
Others: APACHE II score, Ranson Criteria, and Balthazar score (CT scoring system)
What imaging is done if you suspect acute pancreatitis and what are the findings?
- US Abdomen: to find cause
- AXR: not routinely done but may have sentinel loop sign. Do CXR to look for pleural effusion or ARDS
- Contrast enhanced CT: done if complications or can’t find underlying cause
if 48 hours after admission there is pancreatic oedema and swelling, or non-enhancing areas suggestive of pancreatic necrosis.
If signs of persistent inflammatory response/organ failure do not CT for severity till 6-10 days after admission
What is the management for acute pancreatitis?
- Manage underlying cause (e.g ERCP and spincterotomy/cholecystectomy for gallstones)
- Supportive treatment (see image OI OI)
- ONLY Broad spectrum abx (Imipenem) IF for prophylaxis against infection in cases with confirmed pancreatic necrosis
- If severe case treat in high dependency unit
What are some systemic complications of acute pancreatitis?
- DIC
- ARDS
- Hypocalcaemia
- Hyperglycaemia as Islets of Langerhan’s destroyed and insulin production halted
What are some local complications of acute pancreatitis and how are they managed?
Pancreatic Necrosis
- Suspect if patient has signs of persistent systemic inflammation for more than 7-10 days after onset
- Necrosis prone to infection so suspect if patient deteriorates and raised inflammatory markers
- Confirm by CT imaging then fine needle aspiration biopsy
- Treat with pancreatic necrosectomy 3-5 weeks after onset so walled off necrosis
Pancreatic Pseudocyst
- Collection of fluid containing pancreatic enzymes, necrotic material and blood. Lack epithelial lining but surrounded by vascular and fibrous that’s why psuedo
- Often in lesser sac blocking gastro-epiploic foramen
- Often found incidentally on image or mass effect e.g biliary or gastric outlet obstruction
- Can haemorraghe, rupture or become infected
- May resolve spontaneously but if still there after 6 weeks surgical debridement or endoscopic drainage
What is chronic pancreatitis and the aetiology of this?
Chronic fibro-inflammatory disease causing progressive and irreversible damage to the pancreatic parenchyma
4x more likely in men and more likely aged >40
Main causes: chronic alcohol abuse or idiopathic
Rare causes: metabolic (hyperlipidaemia, hypercalcaemia), infection (HIV, mumps, coxsackie), hereditary (CF), autoimmune (e.g. AIP or SLE), anatomical (malignancy or stricture formation), or congenital anomalies
What are the clinical features of chronic pancreatitis?
- Chronic Epigastric Pain (radiating to back, eased by leaning forward)
- Exocrine/endocrine insufficiency (see image - Type 3c DM)
- Often pseudocysts present and may have mass effect e.g biliary obstrucution
What imaging is done if you suspect chronic pancreatitis?
CT imaging: may show pancreatic calcification or atrophy and any pseudocysts present. Can show malignancies that can cause chronic pancreatitis
US or MRCP: image biliary tree and pancreas but if normal doesn’t exclude chronic pancreatitis
Secretin Stimulation test or Endoscopic US (EUS) if diagnostic uncertainty
How is chronic pancreatitis managed?
- Treat reversible underlying cause e.g alcohol cessation or statins for hyperlipidaemia
- Analgesics (neuropathic not opiates like acute)
- Exocrine dysfunction give enzyme replacement (like Creon) and fat soluble vitamins
- Endocrine dysfunction may need insulin regimes and annual check of HbA1c
- ERCP for diagnostic and stone removal/sphincterotomy
- Endosonography-guided celiac plexus blockade or thoracoscopic splanchnicectomy for analgesia
- Steroids to reduce symptoms of autoimmune pancreas. High dose prednisolone then low dose maintenance
What is the pathophysiology of pancreatic cancer?
- 90% are ductal carcinoma of the pancreas.
- 10% Exocrine (Pancreatic Cystic Carcinoma) or Endocrine (Derived from Islet Cells of Pancreas)
- Direct invasion of local structures typically involves the spleen, transverse colon, and adrenal glands.
- Lymphatic metastasis typically involves regional lymph nodes, liver, lungs, and peritoneum and common at diagnosis
What is the clinical presentation of pancreatic cancer?
Features depend on site of tumour, at tail insidious onset + not symptomatic until late
- *- Obstructive Jaundice**
- *- Abdo Pain** (Secondary to invasion of coeliac plexus)
- *- Weight loss/**Cachetic
- Acute Pancreatitis
- Thrombophlebitis Migrans
- Abdominal mass/enlarged gallbladder
What is Courvoisier’s Law?
What investigations are done when we suspect pancreatic cancer?
Lab
- FBC (anaemia and thrombocytopenia)
- LFTs (raised bilirubin, ALP and gamma GT showing obstructive jaundice)
- CA19-9 not to diagnose but to measure response
Imaging
- Initial USS to look for bile duct dilatation or pancreatic mass
- CT to diagnose followed by chest-abdomen-pelvis CT scan or PET to stage
- Endoscopic US for fine needle aspiration biopsy or ERCP for biopsy
What is the curative treatment for pancreatic cancer?
Surgical resection:
- Whipples Procedure (pancreaticduodenectomy)
or
- Distal Pancreatectomy (if tumour of tail)
CONTRAINDICATED IF METASTASES
Adjuvant chemotherapy:
- Following surgery give 5-fluorouracil
What is a Whipple’s procedure and what are some complications of this procedure?
Removal of the head of the pancreas, the antrum of the stomach, the 1st and 2nd parts of the duodenum, common bile duct, and gallbladder.
All share blood supply of gastroduodenal artery
Tail of the pancreas and the hepatic duct are anastomosed to the jejunum to drain bile and stomach anastomosed too
Complications: pancreatic fistula, delayed gastric emptying, and pancreatic insufficiency
In metastatic disease for pancreatic cancer, what is the chemotherapy regime?
FOLFIRINOX
(folinic acid, 5-fluorouracil, irinotecan, and oxaliplatin)
If not well enough to tolerate this give gemcitabine therapy
Pancreatic cancer has a very poor prognosis as it is a highly metastatic cancer. What are the palliative care options with pancreatic cancer?
Percutaneous or ERCP Biliary stent: to relieve obstructive jaundice and pruitis
Palliative chemotherapy: gemcitabine based. used if good performance status
Enzyme replacements (inc Lipases e.g Creon): for exocrine insufficiency to stop malnourishment and steatorrhea
What are some endocrine tumours of the pancreas?
Functional (symptoms due to secretion) or Non-functional (symptoms due to metastatic spread)
- Gastrinoma (Zollinger-Ellison)
- Insulinoma
- Somatostatinoma
- Glucagonoma
- VIPoma
What are some low risk and high risk pancreatic cysts?
Cysts identified by histology, risk of malignancy and secretions
In general mucinous cysts are high risk and serous cysts are low risk
What are some clinical features of pancreatic cysts?
- Mostly asymptomatic
- Abdominal/back pain (compression), post obstructive jaundice, vomiting
- If turn malignant may have general features of malignancy such as weight loss, loss of appetite, change in bowel habits
How are pancreatic cysts investigated and how do we stratify them as low risk/high risk?
Often picked up on imaging. If found do pancreatic protocol CT scan or magnetic resonance cholangiopancreatography to further assess.
May then do Endoscopic US scan with Fine Needle Aspiration (EUS-FNA) to further assess and work out low risk/high risk
What can cause air in the billiary tree?
- Post ERCP due to sphincterotomy
- Following passage of gallstone
- Scarring from acute pancreatitis
What is gallbladder hydrops?
Gallstone stuck in Hartman’s pouch which in turn chronically blocks the cystic duct. Gallbladder gets enlarged and creates mucus pouch
Abdominal pain with palpable gallbladder without any signs of infection
What are some causes of chronic pancreatitis?
What is the prognostic scoring system used for acute pancreatitis?
Modified Glasgow Score. If >3 suggest HDU/ITU input as severe
P
A
N
C
R
E
A
S
