Surgery - HPB Flashcards
1
Q
How are gallstones made, what are they made of, what is bile made of?
What are some risk factors for gallstones?
A
- Bile = c_holesterol, phospholipids, bile pigments_
- Bile is stored in the gallbladder then passes into duodenum
- Gallstones form when bile is supersaturated
- Cholesterol stones = purely cholesterol
- Pigment stones = purely bile pigments
- Mixed stones = cholesterol +bile pigments
Risk factors = Fat, Female, Fertile (pregnancy), Forty, Fhx
And Oral contraceptives, haemolytic anaemia, malabsorption (crohns)
2
Q
What are the 2 presentations associated with gallstones?
A
Presentations are biliary colic or acute cholecystitis
3
Q
How does biliary colic present?
A
- When gallbladder neck is impacted by a gallstone
- No inflammatory response but the contraction of the occluded gallbladder neck causes pain
- Presentation
-
Dull sudden colicky pain in RUQ
- can radiate to epigastrium and back
- precipitated by eating fatty foods (fatty acids stimulate Cholecystokinin release which causes contraction of gallbladder)
- nausea and vomiting
4
Q
How does acute cholecystitis present?
A
- constant pain in RUQ or epigastrium
- signs of inflammation eg. fever, lethargy
- tender in RUQ and +ve Murphys sign
- Murphys sign = press RUQ and get pt to breathe in. +ve when there is a halt in inspiration due to pain (shows inflamed gallbladder)
- guarding can indicate gallbladder perf
5
Q
How would you investigate gallstones?
A
- Routine bloods (crp is raised in cholecystitis)
- Lfts (raised alp showing occlusion, but normal alt and bilirubin)
- Amylase to rule out pancreatitis
- Urinalysis and pregnancy test
-
1st line = Trans abdo US
- Presence of gallstones
- Thick gallbladder wall = inflammation
- Bile duct dilation = possible stone
- If US inconclusive, do Magnetic Resonance Cholangiopancreatography (MRCP)
6
Q
How would you manage gallstones?
A
Biliary Colic
- Analgesia
- Lifestyle = low fat diet, weight loss, exercise
- Elective laparoscopic cholecystectomy within 6 weeks due to high risk of recurrence
Acute Cholecystitis
- IV antibiotics (coamoxi + metronidazole)
- Analgesia and antiemetics
-
Laparoscopic cholecystectomy within 1 week
- If readmitted post chole with RUQ pain, do an US abdo or MRCP to rule out retained CBD stone
- If not fit for surgery or unresponsive to antibiotics do a percutaneous cholecystostomy
7
Q
What are some complications of gallstones?
A
Mirizzi syndrome
- a stone in hartmanns pouch or in cystic duct can compress the adjacent common hepatic duct = obstructive jaundice even with no stone in common hepatic or cbd
- Confirm with mrcp
- Manage with lap chole
Gallbladder empyema
- Gallbladder fills with pus
- Similar to acute chole but more septic
- Diagnose with US or CT and treat with lap chole
Chronic cholecystitis
- Hx of recurrent or untreated cholecystitis resulting in persistent inflammation of gallbladder
- Ongoing RUQ or epigastric pain + N/V
- Diagnose with CT and manage with elective chole
Cholecystoduodenal fistula
- Fistula between gallbladder wall and small bowel due to recurrent inflammation of gallbladder
- Lets gallstones pass into small bowel and cause bowel obstruction eg. gallstone ileus (terminal ileum) or bouverets syndrome (prox duodenum)
8
Q
What is acute cholangitis?
How does it happen?
A
Infection of biliary tract
- Due to biliary outflow obstruction + biliary infection (bacterial colonisation due to fluid stasis)
- In a pt without outflow obstruction, bacterial colonisation would probably not cause cholangitis. It is this combo that is pathological
Causes of obstruction = gallstones, ercp, cholangiocarcinoma, pancreatitis, PSC, etc
Causes of infection = EColi, Klebsiella, Enterococcus
9
Q
How does acute cholangitis present?
A
- Charcots Triad = RUQ pain, fever, jaundice
- Reynolds Pentad = RUQ pain, fever, jaundice, hypotension, confusion
- Pruritus due to bile accumulation
- Pale stool and dark urine (obstructive jaundice)
- Mhx of gallstones or recent ercp or prev cholangitis
- Dhx of oral contraceptives and fibrates increase risk
- Hx of Lipid rich diet could suggest gallstones
10
Q
How would you investigate and manage acute cholangitis?
A
Investigations
- Routine bloods
- leucocytosis typically found
- also raised alp and ggt
- raised bilirubin
- Blood cultures
- US of biliary tract shows bile duct dilation (CBD dilation is >6mm) and any underlying cause like gallstones
- ERCP is gold standard** as it is also therapeutic (most do **MRCP first)
Management
- Sepsis 6 if necessary
- Endoscopic biliary decompression to remove obstruction
-
1st line = ERCP
- Ercp complications = pancreatitis, bleeding, perf, repeated cholangitis
- 2nd line = percutaneous transhepatic cholangiography
-
1st line = ERCP
- Long term = elective cholecystectomy if gallstones are the cause
11
Q
What is a cholangiocarcinoma?
What are some risk factors?
A
- Cancer of the biliary system
- Most commonly at bifurcation of right and left hepatic ducts
- 95% are adenocarcinomas, others are squamous cell etc
- Risks = psc, uc, infection like hiv or hepatitis, toxins in rubber and aircrafts, congenital, alcohol, diabetes mellitus
12
Q
How does a cholangiocarcinoma present?
A
- Asymptomatic until late stage
- Post hepatic jaundice, pruritus, pale stools, dark urine
- Jaundice and cachexia o/e
- Less commonly RUQ pain, early satiety, weight loss, malaise
Courvoisiers law = Jaundice + Enlarged Gallbladder is unlikely to be gallstones. so think malignancy of biliary tree or pancreas
13
Q
How would you investigate and manage a cholangiocarcinoma?
A
Investigations
- Routine bloods (obstructive jaundice = high bili, alp, ggt)
- Tumour markers CEA and CA19-9 can be elevated
- US to confirm obstruction
- MRCP is gold standard for diagnosis
- CT CAP for staging and mets
Management
-
Radiotherapy as neoadjunct or adjunct to surgery
- Cure is complete surgical resection but majority are inoperable at presentation
- Partial hepatectomy and reconstruction of biliary tree for intrahepatic or klatskin tumours
- Pancreaticoduodenectomy for distal common duct tumours
- Palliative for majority
- Stenting via ERCP to relieve obstructive symptoms
- Surgical bypass procedures if stenting doesn’t work
- Palliative radiotherapy
14
Q
What is a simple liver cyst?
A
Simple cysts = fluid filled epithelial lined sacs in the liver (commonly Right lobe)
- Generally asymptomatic
- Otherwise abdo pain, nausea, early satiety due to mass effect
Investigations =
- raised ggt, raised cea and ca19-9
- US is gold standard imaging
Management =
- For cysts >4cm do follow up US at 3,6,12 months to check for growth.
- For symptomatic cysts do US guided aspiration or laparoscopic deroofing.
15
Q
What is polycystic liver disease?
A
Polycystic liver disease = >=20 cysts within liver parenchyma, each >= 1cm
- Due to…
- autosomal dominant polycystic kidney disease (PKD1 and PKD2 mutations)
- Or autosomal dominant polycystic liver disease (PRKCSH and SEC63 mutations)
- Asymptomatic otherwise abdo pain and cysts grow
- Hepatomegaly
- US shows multiple cysts
- Asymptomatic = monitor and leave it
- Symptomatic or query malignancy then do surgery
- US guided aspiration
- Laparoscopic deroofing of cysts
16
Q
What is a hydatid cyst?
A
due to tapeworm infection
17
Q
What is a liver abscess?
How would it present?
A
- Due to polymicrobial bacterial infection typically spread from biliary or gi tract (eg cholecystitis, cholangitis, diverticulitis, appendicitis)
- Commonly EColi, K pneumonia, S constellatus
- Presentation
- Fever, rigors, abdo pain
- Bloating, nausea, anorexia, weight loss, fatigue, jaundice
- O/E RUQ tenderness and hepatomegaly
18
Q
How would you investigate and manage a liver abscess?
A
Investigations
- Routine bloods (leucocytosis, raised alp, deranged alt and bili)
- Peripheral blood and fluid cultures for microscopy
- US = poorly defined lesions with hypo and hyperechoic areas
- CT imaging with contrast can also be used
Management
- A-e, fluid resus etc
- Antibiotic therapy
- Us or ct guided aspiration of abscess
- Be aware of amoebic abscesses that spread to liver via portal system
19
Q
What is liver cancer and what are some risk factors?
A
- Hepatocellular carcinoma happens as a result of a chronic inflammatory process affecting the liver
- Most commonly due to viral hepatitis
- also due to chronic alcoholism, hereditary haemochromatosis, PBC etc
- Risks
- Hep b, hep c
- High alcohol
- Smoking
- >70years old
- Aflatoxin exposure
- Fhx of liver disease
20
Q
How would liver cancer present?
A
- Liver cirrhosis
- RUQ dull ache
- o/e irregular enlarged craggy and tender liver
21
Q
How would you investigate and manage liver cancer?
A
Investigations
-
Lfts usually deranged with low platelets or prolonged clotting
- ast:alt ratio>2 likely alcoholic liver disease
- ast:alt around 1 likely viral hepatitis
- alpha fetoprotein usually raised (used to monitor response to treatment)
-
US
- a mass >2cm + raised afp this is pretty diagnostic
- Then do staging CT and CTCAP
- MRI liver scan and contrast ct angio can also be done
- demonstrates a mass with arterial hypervascularisation (characteristic of HCC)
- Barcelona Clinic Liver Cancer staging system
- Child Pugh and MELD score risk assessment tools
- Child pugh to calculate prognosis of cirrhosis pateints
- MELD to predict likelihood of pt tolerating liver transplant
Management
- Mdt, oncologist, radiologist, hepatobiliary surgeons, etc
- Surgical
- Surgical resection
- Transplantation if patients fulfil Milan criteria
- Non surgical
- Ultrasound guided ablation for early disease
- Alcohol ablation for small inoperable cancers
- Transarterial Chemoembolisation for BCLC stage B
22
Q
Bowel (portal circulation), breast, pancreas, stomach, lung commonly mets to liver.
How would you manage mets to the liver?
A
Investigations
- Deranged lfts
- US scan first line
- CT staging
- Biopsy not advised as can lead to seeding of tumour
Management is more complex as disease has already metastasised
- Oncology and palliative services involved
- Transarterial chemoembolization
- Selective internal radiotherapy etc
23
Q
What are some causes of acute pancreatitis?
A
GET SMASHED
- Gallstones
- Ethanol
- Trauma
- Steroids
- Mumps
- Autoimmune (eg SLE)
- Scorpion venom
- Hypercalcaemia
- Endoscopic Retrograde CholangioPancreatography
- Drugs (azathioprine, nsaids, diuretics)
24
Q
What is the pathophysiology of acute pancreatitis?
A
- All these causes cause an exaggerated activation of digestive enzymes in the pancreas
- The resulting pancreatic inflammatory response causes increased vascular permeability and fluid shifts (third spacing)
- Enzymes are released into systemic circulation causing autodigestion of fats (results in fat necrosis) and blood vessels (can result in haemorrhage in retroperitoneal space)
- Fat necrosis can cause free fatty acids to be released and bind with serum calcium to make chalky deposits in fatty tissue = hypocalcaemia
- Severe end stage pancreatitis = necrosis of pancreas
25
Q
How does acute pancreatitis present?
A
- Severe sudden epigastric pain that radiates to back
- Nausea and vomiting
- O/E epigastric tenderness
- Cullens sign (bruising around umbilicus)
- Grey turners sign (bruising in flanks due to retroperitoneal haemorrhage)
- Tetany due to hypocalcaemia
- Underlying cause is Gallstones? Obstructive jaundice
26
Q
How would you investigate and manage acute pancreatitis?
A
Investigations
- Routine bloods
- Serum amylase (3x normal upper limit is diagnostic)
- LFTS (alt >150u/l usually indicates gallstones is the cause)
- Serum lipase remains elevated longer than amylase
- Modified Glasgow Criteria
- Abdo US to identify gallstones too
- AXR shows sentinel loop sign (dilated prox bowel loop adjacent to pancreas due to localised inflammation)
- CT imaging later on to confirm pancreatic necrosis if necessary
- Definitive confirmation = fine needle aspiration of necrosis
Management
- Treat underlying cause
- IV fluids resus
- Ng for vomiting
- Catheterisation and fluid balance chart
- Opioid analgesia
- ITU or HDU admission
- Broad spec antibiotics
- If Gallstones is underlying cause = early laparoscopic cholecystectomy
- If alcohol is underlying cause then refer to appropriate services
27
Q
What is chronic pancreatitis?
A
- Causes progressive and irreversible damage to pancreatic parenchyma
- Main cause is chronic alcohol abuse or idiopathic
- Less common = hyperlipidaemia, hypercalcaemia, infection, hereditary like CF, autoimmune like SLE, anatomical like malignancy or strictures, congenital like pancreas divisum
28
Q
How would chronic pancreatitis present?
A
- Chronic pain and recurring attacks of acute pancreatitis (acute on chronic pancreatitis)
- Pain is epigastric and radiates to back
- Nausea and vomiting
- Damage to pancreatic parenchyma results in endocrine and exocrine insufficiency
- Damage to islets of Langerhans = failure to produce insulin = impaired glucose regulation = eventual DM
- Damage to acinar cells = failure to produce digestive enzymes = malabsorption = weight loss, cachexia, diarrhoea, steatorrhea
- Pseudocysts can be present due to the recurrent acute pancreatitis attacks = mass effect symptoms of biliary obstruction or gastric outlet obstruction
29
Q
How would you investigate and manage chronic pancreatitis?
A
Investigations
- Routine bloods
- Urine dip
- Amylase and Lipase would not usually be raised in chronic disease
- Blood glucose
- Faecal elastase level can be low if there is exocrine insufficiency
- CT shows pancreatic atrophy/calcification and pseudocysts if there are
- US or MRCP for anatomy of pancreas and biliary tree
Management
- Treat any reversible underlying cause eg alcohol cessation
- Analgesia
- Exocrine dysfunction = enzyme replacements like Creon that can be taken with meals
- Also give fat soluble vitamins ADEK
- Pancreatogenic diabetes = insulin regimes and hba1c surveillance
- ERCP sometimes indicated
- Steroids (high dose prednisolone to control, then low dose to maintain) can be used for autoimmune cause
- Those with chronic pancreatitis >20 years are at risk of pancreatic malignancy
30
Q
What is pancreatic cancer?
What are some risk factors?
A
- Ductal carcinoma is most common, then exocrine and endocrine tumours
-
60-70% are in the pancreatic head, then 20% in the body and tail and others only diffusely involve the pancreas
- Head is prognostically better as they will present with obstructive symptoms more early on than body/tail
Risks = smoking, chronic pancreatitis, diet (high meat, low fruit and veg), fhx, late onset DM >50yo
31
Q
How would you investigate and manage pancreatic cancer?
A
Investigations
- Routine bloods (lfts = raised bili, alp, ggt)
- Ca19-9 to assess response to treatment
- Abdo US shows pancreatic mass or dilated biliary tree
- CT is gold standard for diagnosis as it also stages it
- CTCAP for mets
Management
- Surgery = radical resection
- but <20% have a resectable tumour at diagnosis
- SE = pancreatic fistula, delayed gastric emptying, pancreatic insufficiency
- Adjuvant chemotherapy
- Non surgical
- Locally advanced disease = chemotherapy (gemcitabine)
- Metastatic disease = palliative chemo (FOLFIRINOX or gemcitabine for those who cannot tolerate)
- Symptomatic management
- Biliary stent for obstructive jaundice and pruritus
- Exocrine insufficiency = enzyme replacements like creon
32
Q
What are the endocrine tumours of the pancreas?
A
- Usually associated with Multiple Endocrine Neoplasia 1 Syndrome
- Tumours that arise from the endocrine cells
- They are either functional (they secrete hormones) or non functional (present as just their mass effect or malignant spread)
Different tumours
- G cells secrete gastrin (gastrinoma)
- A cells secrete glucagon (glucagonoma)
- B cells secrete insulin (insulinoma)
- δ cells secrete somatostatin (somatostatinoma)
- non islet cells secrete vasoactive intestinal peptide
33
Q
How would you investigate and manage endocrine tumours of the pancreas?
A
- Blood tests to identify specific subtype
- CT imaging, Endoscopic US, MRI
- <1cm are observed otherwise larger need resection
- Somatostatin analogues are used to control effects of hormonal hypersecretion
34
Q
What is a pancreatic cyst?
What are high and low risk?
A
- Collections of fluid in the pancreas, typically incidentally identified on imaging
Examples of high risk cysts (malignant) = intraductal papillary mucinous neoplasm, mucinous cystic neoplasm, etc
Examples of low risk cysts = serous cystic adenoma, simple cyst, mucinous non neoplastic cyst
35
Q
How would pancreatic cysts present?
A
- 70% are asymptomatic
- Abdo pain or back pain (mass effect)
- Post obstructive jaundice
- Vomiting
- Cysts that are infected have systemic features
- Some become malignant and metastasise (weight loss, appetite loss, etc)
36
Q
How would you investigate and manage pancreatic cysts?
A
Investigations
- Routine bloods
- Ca19-9 to monitor progression
-
Pancreatic protocol CT scan or MRCP is required to fully assess pancreatic cysts = NICE guidelines
- High risk = >3cm diameter, main pancreatic duct dilation >10mm, enhancing solid component, non enhancing mural nodule
- If high risk, complete resection may be warranted or Endoscopic US scan with Fine Needle Aspiration (for a biopsy)
Management
- Majority are benign so just need to be under surveillance every 5 years
- High risk = resection 1st line
- Then MRI follow up scan every 2 years
37
Q
What is a splenic infarct?
What are some causes?
A
- Occurs due to occlusion of the splenic artery or one of its branches = tissue necrosis
- Spleen is supplied by splenic artery and short gastric arteries so infarction is usually not complete (collateral circulation)
Causes
- Haematological disorders eg. lymphoma, myelofibrosis, sickle cell, CML, Polycythaemia vera, hypercoagulable states
- Embolic disorders eg. endocarditis, AF, infected aneurysm grafts
- Rarely Vasculitis, trauma, collagen tissue disease, etc
38
Q
How would a splenic infarct present?
A
- LUQ abdo pain which radiates to left shoulder
- Fever, nausea, vomiting, pleuritic chest pain
39
Q
How would you investigate and manage a splenic infarct?
A
Investigations
- CT abdo with IV contrast = gold standard
- Routine bloods (fbc, u&es, lfts, coagulation)
Management
- Analgesia, iv hydration
- Identify the cause of the infarction = haematologist, ECHO scan, long term anticoagulation
- Long term management
- Avoid splenectomy due to risk of overwhelming post splenectomy infection syndrome (OPSI)
- Vaccine against S pneumonia, N meningitidis, H influenza
- Low dose antibiotics (Pen V) to clear encapsulated bacteria
40
Q
What are some complications of a splenic infarct?
A
- Splenic abscess if cause was eg. non-sterile embolus (eg. infective endocarditis)
- Auto-splenectomy due to repeated splenic infarction and progressive fibrosis and atrophy
- Common cause of auto-splenectomy is sickle cell anaemia
41
Q
When would splenic rupture happen?
A
- The spleen is incredibly vascular so rupture can lead to large intraperitoneal haemorrhage and haemorrhagic shock
- Usually due to blunt abdo trauma eg. seat belt injuries
- Rarely iatrogenic or secondary to underlying splenomegaly in things like infections (like EBV) or haematological malignancies
42
Q
How would splenic rupture present?
A
- Abdo pain following blunt trauma
- Hypovolaemia shock
- O/E LUQ tenderness and peritonism as blood loss increases
- Left shoulder pain (Kehr’s sign) as blood irritates diaphragm
43
Q
How would you investigate and manage splenic rupture?
A
Investigations
- Anyone haemodynamically unstable + peritonism following trauma is Abdo bleeding until proven otherwise
- Do a laparotomy immediately
-
Haemodynamically stable with suspected abdo injury
- Urgent CT CAP with iv contrast
- FAST scans are useful but should not delay CT or laparotomy
- Organ injury scale = American Association for the Surgery of Trauma (AAST) Splenic Injury Scale to grade splenic trauma
Management
- A-e resus
- Haemodynamically unstable or Grade 5 injury = Urgent Laparotomy
- Often With splenectomy
- Some patients may benefit from embolization of splenic vessels if they have vascular abnormalities or higher grade splenic injuries
- This is to reduce the rate of those that need a splenectomy
- Haemodynamically stable (Grade 1-3) = Conservative
- Serial abdo examinations
- Resus
- Strict bed rest
- Repeat ct scan 1 week later
- Prophylactic vaccinations (strep pneumonia, h influenzae B, meningococcus) after discharge
44
Q
What is overwhelming post splenectomy infection?
A
- Spleen plays a role in destroying encapsulated organisms like pneumococcus, meningococcus, h influenzae
- Therefore patients need vaccinations against these organisms and prophylactic Penicillin V
45
Q
A
