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
How does acute pancreatitis present?
* 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
How would you investigate and manage acute pancreatitis?
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
What is chronic pancreatitis?
* 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
How would chronic pancreatitis present?
* 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
How would you investigate and manage chronic pancreatitis?
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
What is pancreatic cancer?
What are some risk factors?
* **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
How would you investigate and manage pancreatic cancer?
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
What are the endocrine tumours of the pancreas?
* 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
How would you investigate and manage endocrine tumours of the pancreas?
* 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
What is a pancreatic cyst?
What are high and low risk?
* 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
How would pancreatic cysts present?
* 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
How would you investigate and manage pancreatic cysts?
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
What is a splenic infarct?
What are some causes?
* 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
How would a splenic infarct present?
* LUQ abdo pain which radiates to left shoulder
* Fever, nausea, vomiting, pleuritic chest pain
39
How would you investigate and manage a splenic infarct?
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
What are some complications of a splenic infarct?
* 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
When would splenic rupture happen?
* 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
How would splenic rupture present?
* 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
How would you investigate and manage splenic rupture?
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
What is overwhelming post splenectomy infection?
* 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
