Liver: abscess, hydatid cyst, tumours and portal hypertension

Overview

Liver surgery questions in PGET cluster around infections common in Pakistan (amoebic abscess, hydatid cyst), the solid liver lump (benign vs malignant) and portal hypertension with bleeding varices. Knowing the segmental anatomy explains how resections are planned.

Surgical anatomy

• Couinaud divided the liver into eight functional segments, each with its own portal pedicle (portal vein, hepatic artery, bile duct) and hepatic vein drainage.
• Cantlie's line (gallbladder fossa to IVC, along the middle hepatic vein) divides the functional right liver (V-VIII) from the left liver (II-IV). Segment I (caudate lobe) drains straight into the IVC, so it is spared in Budd-Chiari syndrome and enlarges.
• Blood supply: mostly from the portal vein, the rest from the hepatic artery, which is the main supply of the bile ducts.
• Pringle manoeuvre: clamping the hepatoduodenal ligament (portal vein and hepatic artery) through the epiploic foramen to control bleeding. Bleeding that continues points to hepatic vein or IVC injury.
• Anatomical variants: a replaced right hepatic artery from the SMA, and an extra left hepatic branch arising from the left gastric, are each common.

Liver abscess

Clinical features (both): fever with rigors, right upper quadrant pain, tender enlarged liver, intercostal tenderness, sometimes right shoulder pain, cough and a right basal effusion; jaundice is uncommon in amoebic abscess.

Investigations:

• Ultrasound is the first and best initial test; CT for multiple or complex abscesses.
• Raised white cell count, ALP; chest X-ray shows a raised right hemidiaphragm and effusion.

When to aspirate an amoebic abscess:

• No improvement after a few days of metronidazole.
• Large abscess at risk of rupture, or left lobe abscess (risk of rupture into the pericardium).
• Diagnosis in doubt (to exclude pyogenic abscess).

Complications: rupture into the pleura (empyema), lung (anchovy sauce sputum, hepatobronchial fistula), peritoneum, or pericardium (left lobe); secondary infection.

Hydatid disease of the liver

• Caused by the larval stage of Echinococcus granulosus. Dogs are the definitive host; sheep are the usual intermediate host; humans are accidental intermediate hosts after swallowing eggs.
• Common in sheep-rearing areas, including parts of Pakistan (Balochistan, northern areas).
• The liver (mostly right lobe) is the commonest site, then the lung.

Cyst structure: outer pericyst (host fibrous layer), the parasite's laminated ectocyst, and the inner germinal layer (endocyst) that buds daughter cysts and scolices ("hydatid sand").

Clinical features: often found by chance; RUQ mass or discomfort. Complications:

• Rupture into bile ducts: obstructive jaundice, cholangitis, biliary colic (daughter cysts block the duct).
• Rupture into the peritoneum (after minor trauma): anaphylaxis and spread of daughter cysts.
• Rupture through the diaphragm into the pleura or bronchus; secondary infection (abscess).

Investigations:

• Ultrasound and CT: cyst with daughter cysts, wall calcification, and a detached floating membrane ("water lily sign").
• Serology (ELISA) supports the diagnosis; eosinophilia in some.
• Do not do a diagnostic aspiration outside a planned PAIR procedure (anaphylaxis, spillage).

Treatment:

• Albendazole (or mebendazole): alone for small or inoperable cysts, and as cover before and after any procedure.
• PAIR: Puncture, Aspiration, Injection of a scolicidal agent (20% hypertonic saline), Re-aspiration, under ultrasound guidance with albendazole cover. Not used if the cyst communicates with the biliary tree (risk of sclerosing cholangitis).
• Surgery: deroofing and evacuation of the cyst (conservative) or pericystectomy/liver resection (radical). Pack the field with hypertonic saline-soaked swabs, inject scolicide before opening, look for and suture bile leaks, and fill the cavity with omentum (omentoplasty).
• Daughter cysts in the bile duct are cleared by ERCP.
• Calcified cysts are often dead and can be watched.

Liver cysts

• Simple cysts: common, usually solitary, women; leave alone unless symptomatic; laparoscopic deroofing.
• Polycystic liver disease: autosomal dominant; about half also have polycystic kidneys.
• Caroli disease: congenital dilatation of the intrahepatic ducts with stones, cholangitis and a risk of cholangiocarcinoma.

Benign liver tumours

Malignant liver tumours

Metastases

Secondary tumours are the commonest malignant liver tumours, mainly from the colon and rectum, stomach, pancreas, breast and lung.

• Liver metastases from bowel (colon and rectal) cancer can be cured by resection in selected patients when all disease can be removed with a clear (R0) margin and enough healthy liver is left (a future liver remnant of at least about 25% in a normal liver).
• Perioperative chemotherapy is usual and can convert some unresectable cases to resectable.
• Ablation (radiofrequency or microwave) for small lesions or unfit patients.

Hepatocellular carcinoma (HCC)

Risk factors: chronic hepatitis B (more than half of cases worldwide; can cause HCC without cirrhosis), hepatitis C (common in Pakistan), cirrhosis of any cause (alcohol, NAFLD, haemochromatosis), aflatoxin (moulds on stored grain and nuts), obesity and diabetes.

Clinical features: often found on surveillance of cirrhotics; otherwise RUQ pain, weight loss, a hard knobbly liver with a bruit, worsening of liver function, ascites, or bloody ascites after rupture.

Investigations:

• Alpha-fetoprotein (AFP): raised in most; with 6-monthly ultrasound used to screen cirrhotics.
• Triple-phase CT or MRI: arterial phase enhancement with washout in the portal venous phase is diagnostic in a cirrhotic liver, so biopsy is often unnecessary (and risks seeding).
• Fibrolamellar HCC: young patients, no cirrhosis, normal AFP, better prognosis.

Treatment depends on tumour stage and liver function (Barcelona staging):

Cholangiocarcinoma is covered in the bile duct chapter. Other primary tumours (angiosarcoma from vinyl chloride, hepatoblastoma in children) are rare.

Assessing liver function before surgery: Child-Pugh

Class A = 5-6, B = 7-9, C = 10-15. Surgical mortality rises with class, roughly 10% for A, 30% for B and 75-80% for C. The MELD score (bilirubin, INR, creatinine) is used to prioritise transplantation.

Portal hypertension

Definition: a rise in portal venous pressure (hepatic venous pressure gradient above about 10 mmHg is clinically significant), producing portosystemic collaterals.

Causes

Portosystemic collateral sites

Features: splenomegaly with hypersplenism (low platelets and white cells), ascites, variceal bleeding, encephalopathy.

Acute variceal bleeding

1. Resuscitate: two large cannulae, blood transfusion to a cautious target (over-transfusion raises portal pressure), correct clotting (vitamin K, FFP), platelets if very low, protect the airway (intubate if encephalopathic or bleeding heavily).
2. Vasoactive drug: terlipressin (or octreotide/somatostatin) started before endoscopy.
3. Prophylactic antibiotics (for example ceftriaxone or a quinolone): reduce infection, rebleeding and death.
4. Urgent endoscopy once stable: band ligation is preferred over sclerotherapy for oesophageal varices; cyanoacrylate glue for gastric varices. Remember that about half of cirrhotic patients who bleed have a non-variceal source.
5. Uncontrolled bleeding: balloon tamponade (Sengstaken-Blakemore or Minnesota tube) as a short-term bridge, or a covered oesophageal stent.
6. Rescue: TIPSS (transjugular intrahepatic portosystemic stent shunt) between a hepatic vein and the portal vein.
7. Prevent encephalopathy: lactulose.

TIPSS: decompresses the portal system; complications are encephalopathy and shunt stenosis; main contraindication is portal vein occlusion. Also used for refractory ascites and Budd-Chiari syndrome.

Preventing bleeding

• Primary prophylaxis (large varices, never bled): non-selective beta-blocker (propranolol, carvedilol) or band ligation.
• Secondary prophylaxis (after a bleed): beta-blocker plus repeated band ligation until varices are gone; TIPSS for recurrent bleeding.
• Surgery (rare now): portosystemic shunts (non-selective portocaval; selective distal splenorenal (Warren) shunt, less encephalopathy), and devascularisation operations (oesophagogastric devascularisation with splenectomy, Sugiura type) where TIPSS or transplantation is unavailable.
• Liver transplantation treats the underlying cirrhosis.

Budd-Chiari syndrome

• Obstruction of hepatic venous outflow: hepatic vein thrombosis (myeloproliferative disease, thrombophilia, OCP, pregnancy) or IVC webs.
• Acute: abdominal pain, tender hepatomegaly and rapidly developing ascites; caudate lobe enlarges.
• Doppler ultrasound, CT or MRI venography.
• Anticoagulation, angioplasty or stenting, TIPSS, transplantation for failure.

Quick revision

• Amoebic abscess: young man, single, right lobe, anchovy sauce, sterile pus, metronidazole; aspirate if large, left lobe or not settling.
• Pyogenic abscess: elderly diabetic, biliary source, Strep. milleri, E. coli, Klebsiella; antibiotics plus drainage.
• Hydatid: Echinococcus granulosus, dog host; water lily sign; albendazole plus PAIR or surgery; hypertonic saline; avoid spill.
• Haemangioma: commonest, leave. Adenoma: pill, resect over 5 cm. FNH: central scar, leave.
• HCC: HBV, HCV, cirrhosis, aflatoxin; AFP; resection, transplant, ablation, TACE, systemic therapy.
• Child-Pugh: bilirubin, albumin, INR, ascites, encephalopathy; A 5-6, B 7-9, C 10-15.
• Varices: terlipressin, antibiotics, band ligation, Sengstaken bridge, TIPSS; beta-blocker plus banding to prevent rebleeding.

Written by The House Job from standard references (Bailey & Love).

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