Hepatobiliary Surgery JC064: A Large Liver: Liver Cancer Flashcards

1
Q

***Hepatomegaly DDx

A

Malignant:
Primary
1. **HCC (most common)
2. **
Cholangiocarcinoma
3. Others (e.g. Lymphoma)

***Secondary
1. GI tract
2. Other primary (Breast, Lung)

***Haematological
1. Lymphoma
2. Leukaemia
3. Myeloproliferative disease

Benign:
Benign tumours
1. **Haemangioma
2. **
Adenoma
3. Focal nodular hyperplasia

Cyst
1. Simple cyst
2. ***Polycystic disease

Others
1. **Alcoholic cirrhosis
2. **
Liver abscess

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2
Q

History taking of Hepatomegaly

A
  1. ***Pain (site, onset, duration)
  2. ***Tea-colour urine (Jaundice)
  3. N+V
  4. Bowel changes
  5. Systemic review: any symptoms suggestive of other primary malignancy
  6. Constitutional symptoms: LOW, LOA, malaise
  7. ***Past history of HBsAg carrier, Hep C, Liver disease
  8. Social history: ***Alcohol
  9. Family history of malignancy
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3
Q

Physical examination of Hepatomegaly

A

General:
1. Pallor
2. **Jaundice
3. **
Lymphadenopathy
4. ***Stigmata of chronic liver disease
5. Cachexia

Abdomen:
1. Hepatomegaly
- **size (cm below costal margin)
- tenderness
- **
consistency (hard, firm, soft)
- **surface (nodular)
—> Smooth: Fatty liver, alcoholic cirrhosis, primary biliary cholangitis
—> Nodular: Polycystic kidney and liver disease
—> Large nodules: HCC
- edge
- **
bruit (suggest vascular tumour e.g. HCC)
—> Vascular tumour (e.g. HCC) —> heard all over
—> Alcoholic hepatitis —> heard all over
—> Compression of aorta —> turn patient to right side and bruit less prominent

  1. Other organomegaly
    - Splenomegaly: **Portal hypertension, **Haematological malignancy
  2. Mass
  3. ***Ascites
  4. PR exam

Other systems

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4
Q

***Characteristics of Hepatomegaly

A

Diffuse smooth firm Hepatomegaly:
- Alcoholic liver disease
- Haematological malignancies (∵ diffuse infiltrative process)

Irregular hard Hepatomegaly (likely to be solid tumours):
- HCC
- Cholangiocarcinoma
- Secondary malignancies

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5
Q

***Investigations of Hepatomegaly

A

Blood tests
1. CBC
- e.g. **thrombocytopenia: ∵ hypersplenism in cirrhosis
- **
abnormal WBC: haematological malignancies

  1. Coagulation profile
    - e.g. ***prolonged INR in cirrhosis
  2. LFT
    - clue to chronic hepatitis / cirrhosis
  3. Viral hepatitis serology
    - **HBsAg
    - **
    Anti-HCV Ab
  4. Tumour markers
    - **AFP: HCC, Embryonal carcinoma, Yolk sac tumour
    - **
    CEA: Cholangiocarcinoma, CRC
    - **CA 19.9: Cholangiocarcinoma, GI malignancies (e.g. **Pancreatic CA)
    —> Help but NOT diagnostic
    —> NOT all patients have ↑ tumour markers, mildly ↑ tumour markers can occur in benign conditions

Imaging
1. CXR (primary lung cancer, cannon ball lesions)

  1. USG (**1st line)
    - whether a mass
    - confirm whether hepatomegaly
    - cirrhosis
    - **
    splenomegaly
    - tumours in pancreas
  2. CT (***Contrast)
  3. MRI
    - more phases, accuracies generally higher than CT
  4. PET-CT
    - confirm primary tumour + detect metastasis in other organs

Endoscopy (for suspected primary GI malignancy)
1. Upper endoscopy
2. Colonoscopy

Biopsy
1. USG-guided percutaneous **FNAC
2. **
Trucut core biopsy
- 1-2% bleeding risk
- 1-2% chance percutaneous needle tract seeding
—> **NOT advocate biopsy for all patients if well-established cancer + resectable (will do surgical resection + pathology instead)
—> only useful in patients with **
advanced malignancy beyond surgery (chemotherapy + histopathology to establish nature)

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6
Q

Management of Hepatomegaly

A

Depends on underlying pathology
- Surgical / Non-surgical

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7
Q

Hepatocellular Carcinoma (HCC)

A

Causes:
1. ***HBV (80% of HCC)
2. HCV (common in japan, western)
3. Cirrhosis (Alcoholic and other types)
4. Alflatoxin (fungal derivatives, ↑ chance of HCC esp. in HBV carrier, in peanuts not probably stored, contaminated by mould)

3 pathological / macroscopic types:
1. Massive (i.e. big mass)
2. Diffuse (i.e. infiltrative)
3. Nodular (i.e. multiple small nodules)
4. Fibrolamellar HCC (very rare histological variant, in young females, in western mainly, good prognosis)

Pathology:
- **Rapid tumour growth (double size in 3-4 months)
- **
Venous invasion tendency (portal vein / hepatic vein)
- **Intrahepatic metastasis to rest of liver (via **portal venous circulation)
- **Lung metastasis (via hepatic vein dissemination)
- **
Peritoneal metastasis
- frequency association with cirrhosis (80% in HK)

Incidence:
- 1800 new cases per year
- commonest primary liver cancer
- 2rd commonest cancer deaths
- 5th commonest cancer incidence
- ***M:F = 4:1
- mostly >50 yo (but can occur in young patient)

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8
Q

***Clinical features of HCC

A
  1. Subclinical
    - liver relatively insensitive organ, large tumour can be asymptomatic, usually in HBV carrier who perform regular imaging surveillance —> incidental findings
    - screening with **AFP, **USG in HBsAg carrier / cirrhotic patients
  2. RUQ / Epigastric pain
    - can be mistaken as peptic disease
  3. Hepatomegaly
    - abnormal mass felt in upper abdomen
  4. LOA, LOW, malaise
  5. ***Decompensation of cirrhosis
    - Child-Pugh A suddenly develop ascites, variceal bleeding, hepatic encephalopathy
    - NB: HCC may also occur in patients without cirrhosis!
  6. ***Tumour rupture
    - rare, intraperitoneal haemorrhage, acute abdominal pain, shock
  7. Paraneoplastic features
    - rare, e.g. **polycythaemia, refractory diarrhoea, **fever of unknown origin, **hypercalcaemia, **hypoglycaemia
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9
Q

***Diagnosis of HCC

A

One of cancers that no need histological diagnosis
1. ↑ AFP ***>400 ng/mL (quite specific)
- AFP normal (<20) in 30% HCC
- can be ↑ in chronic hepatitis / cirrhosis esp. with active viral replications (high HBV DNA in blood)

  1. Imaging
    - USG
  • CT scan (typical appearance)
    —> Non-contrast phase: hypodense
    —> Arterial phase / Contrast phase (1st 30 seconds, contrast still in arterial system): **
    hyperdense (tumour takes up blood mainly from hepatic artery instead of portal vein, on CT scan: compare with aorta (
    hyperdense aorta —> arterial phase))
    —> Portal venous phase: **
    hypodense (washout) (compared to parenchyma ∵ surrounding liver has more blood supply from portal vein)
    (NB: other cancers e.g. Cholangiocarcinoma / Secondary malignancy: arterial phase: ***hypodense instead (exact reverse))
  • Post-Lipiodol CT (lipiodol injected via arteriography, repeat CT in 2 weeks for uptake by tumour, for uncertain cases after CT + Hepatic arteriography)
  • MRI (alternative to CT, may also be useful in uncertain cases after CT)
  • Hepatic arteriography (past, typical neovascularisation, for uncertain cases after CT)
  • **PET scan (2 phases: **FDG + ***C-11 acetate) (FDG alone can miss HCC up to 50%)
  1. Biopsy (only for inoperable cases / very uncertain imaging results)
    - FNAC
    - Trucut biopsy
  2. Indocyanine (ICG) clearance test
    - a special dye excreted solely by liver
    - best test for ***liver function reserve if planning for surgical resection
    - ICG retention at 15 mins of <14% —> Adequate liver function
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10
Q

***Surgical treatment of HCC

A
  1. Hepatic resection
    - 20% HCC resectable
    —> **Unilobar
    —> **
    Absence of main portal vein invasion
    —> **Absence of distant metastasis
    —> **
    Adequate liver function (ICG retention at 15 mins of <14%)
    - 5 year survival rate >50%
    - operative mortality rate 1-5%
    - recurrence **50% (mainly in liver remnant due to **intrahepatic metastasis via portal vein / multicentric tumours, need regular 3-monthly surveillance with AFP, CT, early detection of recurrence —> re-resection / TOCE / ethanol injection)
  2. Liver transplantation (one of few solid tumours that can be treated by transplantation)
    - HCC **<5-6.5cm (i.e. **Early HCC) (5cm: Milan criteria, 6.5cm: UCSF criteria)
    - **no macroscopic venous invasion / distant metastasis
    - **
    Child B/C cirrhosis (∵ may not be good candidate for surgery due to poor LFT)
    - 5-year survival rate 70-80%
    - immunosuppressants may ↑ recurrence chance, ∴ not for advanced cancers
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11
Q

***Locoregional treatment of HCC

A

Embolisation
1. Transarterial oily chemoembolisation (TACE / TOCE) / Radioembolisation
- Local Chemotherapy + Embolisation
—> **Lipiodol (selectively taken up by HCC, unknown reasons)
+
—> **
Cisplatin / Doxorubicin
+
—> **Gelfoam (block arterial supply of tumour —> slow down growth)
- bilobar / unilobar **
unresectable tumours, reasonable liver function (bilirubin **<50), absence of main **portal vein thrombosis / distant metastasis
- **1st choice if **ruptured HCC (if still uncontrolled bleeding —> laparotomy)
- response rate: 30-40%
- continue once every 2-3 months

Ablation treatment (chemical / energy)
2. Percutaneous ethanol injection
- USG-guided for **<=3 tumours of **<=3-5 cm

  1. Cryotherapy
  2. Microwave / Radiofrequency thermoablation (**RFA)
    - for tumours **
    <5 cm, ***<4 nodules
    - outcome ~ surgical resection
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12
Q

Non-surgical Palliative treatment

A
  • for Metastasis to other organs
  • Overall response rate: only 15-25%
  1. Chemotherapy (e.g. doxorubicin), Tamoxifen, IFN
    - not proven to be effective (∵ HCC is a ***chemo-resistant cancer + poor LFT cannot tolerate chemo well)
  2. External radiotherapy
    - stereotactic body radiation therapy (SBRT)
    - benefit limited for large tumours
  3. Targeted therapy (***Sorafenib, Lenvatinib)
    - prolong survival by 3-4 months
  4. ***Anti-PD1 immunotherapy (Nivolumab)
    - modulate immune cells to kill cancer cells
    - response ~20%
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13
Q

Distribution of treatment in HCC

A

100 HCC patient:
- 20 Surgery
- 15 RFA
- <5 Liver transplantation (∵ only suitable for ***early HCC + scarce supply of organs)
- 20 TACE
- 35 Systemic treatment

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14
Q

Long-term survival rate of HCC

A

5-year survival rate
- **Partial hepatectomy: 60%
- **
Transplantation: 75%
- ***RFA: 50%
- TACE: 15%
- Systemic therapy: <5%

Advanced HCC with supportive treatment: 2-4 months

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15
Q

Cholangiocarcinoma

A
  • 5-20% of primary liver cancer
  • ***Adenocarcinoma of bile duct
  • > 50 yo

Causes:
- no exact known cause
- associated with
—> **HBV carrier
—> **
RPC (common in chinese)
—> ***PSC
—> Ulcerative colitis (rare in chinese)

2 types:
- Intrahepatic Cholangiocarcinoma (~ HCC, present as a mass)
- Extrahepatic Cholangiocarcinoma (present as strictures —> **Jaundice)
—> **
different presentation

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16
Q

Clinical features of Cholangiocarcinoma

A
  1. RUQ pain
  2. ***Hepatomegaly
  3. ***Jaundice (depend on location, e.g. near liver hilum)
  4. LOA, LOW, fever
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17
Q

Diagnosis of Cholangiocarcinoma

A

Tumour markers (may be ↑):
1. CEA (carcinoembryonic antigen)
2. CA 19.9

Imaging:
1. USG
2. CT
- hypodense in arterial phase (can be difficult to differentiate from secondary metastasis, must also do other imaging e.g. PET)
3. MRI
4. FDG-PET (no need dual tracer)
5. ***ERCP (can do stenting)

Biopsy (only for unresectable cases):
1. FNAC
2. Trucut

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18
Q

Treatment of Cholangiocarcinoma

A
  1. Surgical resection
    - treatment of choice
    - resectability 20%
    - **Bile duct excision + **Hepatectomy + ***Hilar LN clearance (important for staging) + Bile duct reconstruction
  2. Palliative systemic chemotherapy (Cholangiocarcinoma ***more sensitive to chemo than HCC) + RT (for unresectable cases)
    - targeted therapy little role
19
Q

Metastatic cancer to Liver

A
  • ***more common than primary liver cancer
  • 2nd most common site of metastasis (lung most common)
  • commonest site of metastasis for ***GI primary (∵ all blood supply from abdominal visceral organs go through portal vein through liver first)

Commonest site of Primary:
1. **Colon
2. **
Stomach
3. **Pancreas
4. **
Biliary tree

Other common sites of Primary:
1. Lung
2. Kidney
3. Breast
4. Gynaecological tract

20
Q

Clinical features of Metastatic cancer to Liver

A
  1. Known primary with Hepatomegaly
  2. Hepatomegaly / RUQ pain without symptoms referable to primary
  3. Constitutional symptoms: LOA, LOW, cachexia
  4. Ascites (suggest peritoneal seedling from GI / gynaecological primary)
21
Q

Diagnosis of Metastatic cancer to Liver

A

Tumour markers
1. CEA
2. CA 19.9

Imaging
1. USG
2. CT
3. MRI
4. PET

Biopsy (only for unresectable cases)
1. FNAC
2. Trucut
—> differentiate primary from secondary using ***immunostaining —> can tell origin

***Investigations for Primary
1. CXR (lung)
2. CT thorax (lung, breast)
3. Endoscopy (GI primary)

22
Q

Surgical treatment of Metastatic cancer to Liver

A

Hepatic resection
- **can be curative + prolong survival in patients with resectable **colorectal metastasis
- solitary / <=4 metastasis all within 1 lobe
—> 5-year survival 40%
—> 5-year disease-free survival 30%
—> 1/3 recurrence in liver remnant

  • may be useful for palliation of symptoms from **carcinoid / **neuroendocrine tumours (∵ prolong survival + stop secretion of vasoactive peptides —> prevent symptoms e.g. flushing, diarrhoea)
  • other metastasis suitable: **breast, **kidney, ***ovarian
  • generally NOT indicated in metastasis from **pancreas, **lungs, ***stomach (∵ usually are widespread metastasis, very poor prognosis —> systemic chemotherapy instead)
23
Q

Non-surgical treatment of Metastatic cancer to Liver

A
  1. Local ablative therapy e.g. ***RFA, SBRT
  2. Chemotherapy
    - depends on response of type of tumour
    - systemic / transarterial with colorectal metastasis (response 20-30%)
  3. Transarterial embolisation
    - generally not used for metastatic cancer except for ***neuroendocrine tumours which have good respond to TACE (for palliation)
24
Q

SpC Interactive tutorial: Advanced liver surgery for HBP malignancy

A

Screening for HCC:
1. HBV / HCV carriers
2. Cirrhosis
3. Family history of HCC

Methods:
1. USG
2. AFP, LFT
- every 6-12 months
- 90% detection rate

(HCC doubling time: 3 months)

25
Evolution of HCC treatment
1. Open to Laparoscopic liver resection —> Early tumours: Minimally invasive approach 2. Improvement in open surgical techniques due to development of living donor liver transplantation —> Advanced tumours: Transplantation techniques, Complement resections
26
Evolution of surgical techniques in liver transplantation
Resection techniques: 1. Anterior approach 2. Use of automatic vascular staplers 3. Use of energy device (Thunderbeat, Harmonic-ace) Living donor liver transplantation techniques: 1. Control of IVC (isolate liver from IVC) 2. Venoplasty techniques (joining 2 veins together) 3. Haemodynamic control under IVC clamping without veno-venous bypass (important role by anaesthetist) 4. Parenchymal transection with patent inflow (living donor hepatectomy) 5. Understanding of small for size graft (i.e. partial graft) for recipient / remnant liver for donor
27
2-stage hepatectomy
ALPPS: Associating Liver Partition and Portal vein Ligation for Staged hepatectomy Indication Major liver resection but ***insufficient future liver remnant (future liver remnant FLR <30%) (i.e. resection >= 3 Couinaud segments) 1. Ligate right portal vein —> allow blood shunted to left liver —> left liver hypertrophy (in 7 days) 2. Remove right liver
28
SpC Interactive tutorial: HCC Etiology of HCC
1. ***Hep B (80% of HCC in HK) 2. Hep C (predominant in Japan) 3. ***Cirrhosis 4. ***Aflatoxin (fungi: misstorage of food) HBV —(10 years if not cleared)—> Chronic hepatitis —(20 years)—> Cirrhosis —(20-30 years (Cirrhotic nodule —> Dysplastic nodule))—> HCC or HBV —> HCC Epidemiology: - Peak age: 50-70 - M>>F
29
Pathology of HCC
Macroscopic appearance: 1. ***Massive type - in ***non-cirrhotic liver - in ***younger age group - ***large tumour with adjoining nodules - variegated cut surface 2. ***Nodular type - multiple greyish white, yellow / brown nodules in cirrhotic liver - follow sequence of regeneration nodules —> dysplastic nodules —> ***cirrhosis 3. Diffuse type - least common - indistinguishable from cirrhosis - more associated with HCV pathway
30
Spread of HCC
1. Local invasion - ***Portal vein (Intrahepatic metastasis: spread to adjacent segment / contralateral lobe —> surgery resection need to resect all downstream liver segments) - ***Hepatic vein - ***Bile duct 2. Lymphatic spread - 1/4 of patients 3. Transperitoneal spread - Rare 4. Haematogenous spread - Lung - Bone
31
Clinical features of HCC
Tumour: 1. Subclinical (majority) 2. ***Vague epigastric distension 3. Abdominal mass (usually 10cm before can be felt (stage T3: >5cm)) 4. ***Paraneoplastic syndrome - Diarrhoea (vasoactive intestinal peptide) - Hypoglycaemia (impaired gluconeogenesis) - Hyperglycaemia (impaired glycogenesis) - Hypercalcaemia (PTH-rP) - Polycythaemia (Erythropoietin) 5. Weight loss Cirrhosis: 6. ***Ascites (∵ decompensated cirrhosis / occlusion of portal vein by tumour thrombus / external tumour compression) 7. ***GI bleeding (variceal bleeding from cirrhosis portal hypertension, stress ulcer formation due to portal vein tumour thrombosis) Complications: 8. ***Secondaries in lung, bone (e.g. cough, bone pain, but usually detected by PET scan) 9. ***Sharp pain due to bleeding (Tumour rupture)
32
***HCC Treatment
Surgical treatment: 1. Partial hepatectomy 2. Liver transplantation (after total hepatectomy) Locoregional treatment: 3. Local ablative therapy (RFA / Microwave) (realisable, predictable, repeatable) (still Curative intent) 4. Transarterial oily chemoembolisation (TACE) (2nd line) 5. Percutaneous intralesional alcohol injection (largely replaced by Local ablative therapy)
33
Pre-op assessment / Investigations of HCC
1. Patient factor: ***General status - Age (not a CI to surgery) - Concomitant medical disease - Hidden medical disease (e.g. CVS disease) —> ***ECG, Spirometry, Astrup (ABG), Glucose, RFT etc. —> Aim to define whether the patient is fit for GA 2. Patient factor: ***Liver function status - Clinical examination (signs of liver decompensation) - Liver biochemistry (Albumin, Bilirubin) - PT - Platelet - ***Child-Pugh classification (anything beyond Child A —> risky for major liver resection) - ***ICG clearance test (>14% remaining after 15 mins —> cannot tolerate major liver resection) —> Aim to define whether liver function is sufficient for the patient to tolerate hepatectomy 3. Disease factor: ***Tumour status - USG (only for screening) - CT (provide better spatial resolution than MRI, ∵ short scanning time —> no need to hold breath) - MRI - +/- Hepatic arteriography (Angiography, obsolete, ∵ invasive, replaced by CT angiogram) - CXR (lung metastasis) - PET scan (FDG + C-11 acetate) —> Aim to define whether tumour still confined to one side of liver / whether technically feasible to resect / classify tumour, study anatomy before planning of surgery 4. Surgeon factor Surgery (Laparoscopy / Laparotomy) can be done if: 1. General condition is good 2. Liver function is satisfactory 3. Tumour is confined to one lobe
34
PET-CT
FDG: - longer t1/2, easier to prepare - good accuracy in CRC but poor sensitivity in HCC (∵ different cell type: well differentiated / moderately differentiated / poorly differentiated HCC —> only poorly differentiated is easily detected by FDG) C-11 acetate: - short t1/2 (~30 mins), harder to prepare - high sensitivity
35
***Staging of HCC
Stage 1: <2cm Stage 2: 2-5cm Stage 3: >5cm Stage 4: Extrahepatic spread
36
1. Partial hepatectomy
Indications: 1. ***Unilobar involvement 2. ***No invasion into IVC / Portal vein 3. Acceptable liver function for major hepatectomy - ***Child A - ***ICG retention 15 min <14% 4. No severe chronic medical illness - Mortality rate 5% - Morbidity rate 30% - Hepatectomy can offer cure and is associated with a 5-year survival of 50%
37
Sites of recurrence of HCC after hepatectomy
1. Liver remnant (80%) 2. Extra-hepatic (50%) 3. Both (5-10%)
38
Laparoscopic liver resection
Now mainstream in small HCC 1. Pneumoperitoneum can compress on surface of hepatic vein —> less bleeding 2. New instruments for liver resection —> Clips and staplers 3. Laparoscopic CUSA 4. High definition monitor Result: - Less bleeding - Comparable survival to open resection
39
2. Liver transplantation
Treat both HCC + Cirrhosis at the same time Indications: 1. Tumour <5cm single / <3cm up to 3 nodules (***Milan criteria) 2. ***Child C cirrhosis
40
3. Local ablative therapy (RFA / Microwave)
Indications: 1. ***Tumour <5cm 2. Satisfactory liver function reserve 3. ***CI to Laparoscopic / Open approach for HCC near to viscera - Localised thermal treatment technique (Percutaneous / Open approach) - RFA / Microwave (HIFU) - Replacing Percutaneous intralesional alcohol injection - Heating tumour cells to 45-50oC for >3 mins causes ***protein denaturation + irreversible cell damage - Induces tumour destruction by heating tumour tissue to temp >60oC —> if up to ~70oC —> soot formation —> insulator of heat —> prevent dissipation of heat —> Cool-tip RF system using disposable electrodes (17G) - USG / CT-guidance for introduction of electrodes + monitoring of ablation process HIFU: - ~Magnifying glass - Oscillatory energy at focal point —> Coagulation necrosis - USG energy transmitted through high density medium (e.g. water) —> patient put in waterbath RFA vs HIFU: - Similar effectiveness + survival benefit RFA: - Adhesion in subsequent operation - Needle track - ***CI in patients with ascites - Ablation volume not as precise HIFU: - No adhesion in subsequent operation - No needle track - ***Favourable in patients with ascites - Precise localisation, little collateral damage
41
4. Transarterial oily chemoembolisation (TACE)
Purpose: 1. ***Palliative intention (TACE cannot kill all cancer cells) 2. Augment liver remnant for future hepatectomy Indications: 1. ***Bilobar involvement without distant spread, without complete portal vein obstruction / IVC involvement 2. ***Unilobar involvement but liver function not acceptable for hepatectomy / RFA Puncture femoral artery —> Catheter into hepatic artery —> Cisplatin + Lipiodol emulsion mixture to tumour (cell membrane of tumour absorb Lipiodol —> take in Cisplatin) —> Block feeding vessel by Gelfoam (block blood supply —> ischaemia) Complications (Felix Lai): 1. Post-embolisation syndrome (most common) (60-80%) - Due to hepatocytes + tumour necrosis and ischemic damage to normal liver parenchyma - Fever, N+V, abdominal pain, deranged LFT with ↑ AST/ALT (2:1) transiently for ***1-2 days - Full recovery is typically within 7-10 days - Cover with antibiotics but should perform USG to exclude ***liver abscess if symptoms persist for 1 week 2. ***Liver failure (Hepatic decompensation) (most serious) (20-30%) - Treatment-induced ischemic damage to non-tumour bearing liver is responsible for precipitating or exacerbating liver failure - Usually reversible but it may be irreversible in 2% of cases - Clinically suspected by ↑ ***bilirubin + ↑ ***PT (INR) 3. Ischaemic ulceration (due to disturbed GI blood supply) - Gastritis / Cholecystitis / Pancreatitis - ***Acalculous cholecystitis due to damage to the cholecystic artery
42
5. Percutaneous intralesional alcohol injection
Indications: 1. ***Tumour <3cm 2. ***Tumour number <3 - Need to ***repeat 3-5 times before see effect - Ethanol induce ***dehydration + ***coagulation necrosis of cancer cells —> fibrotic degeneration
43
Systemic therapy
Previously used: 1. Chemotherapy (Doxorubicin) 2. Hormonal therapy (Tamoxifen, Octreotide) 3. Immunotherapy (IFN) - None proven to give survival benefit Current: 1. ***Sorafenib (Molecular targeting drug: RAF kinase + VEGF receptor) - currently only approved drug for HCC - prolong survival for 3 months in clinical trials 2. ***Anti-PD1 / PDL1 - new in 2020
44
Ruptured HCC management
Suspicion of HCC rupture (abdominal pain, pallor, history of Hep B/C, history of HCC, screening USG result) —> Diagnosis of HCC rupture by ***contrast CT —> No ongoing blood loss —> ***Conservative management —> Ongoing blood loss —> Haemodynamically unstable for TACE (TAE?) —> ***Surgical intervention —> Haemodynamically stable for TACE (TAE?) —> ***TACE (TAE?) —> Successful haemostasis —> Work-up for definitive treatment —> Unsuccessful haemostasis —> ***Surgical intervention Surgical intervention: 1. ***Ligation of hepatic artery (associated with risk of liver failure) + Hepatectomy 2. ***RFA in open approach (stop bleeding by coagulation + treat cancer) —> less risky in a shock patient + much better survival