Focal Liver Lesions & Liver Abscess

Approach to a focal liver lesion

Context drives the workup. Ask: is the liver cirrhotic, is there a known cancer, and is there infection (fever, RUQ pain, leukocytosis)? In a normal liver, most incidental lesions are benign and can be characterized with multiphase contrast MRI or CT. In cirrhosis, any new nodule is possible hepatocellular carcinoma (HCC). Anechoic, thin-walled simple cysts need no follow-up.

Do not routinely needle a typical hemangioma (bleeding risk, and a biopsy adds nothing), a suspected hydatid cyst outside a PAIR protocol (anaphylaxis, spillage), or a LI-RADS 5 nodule in cirrhosis (imaging is already diagnostic; needle-tract seeding). Biopsy is for a solid lesion that imaging cannot characterize, especially in a noncirrhotic liver.

Benign solid lesions

Hemangioma. The most common benign liver tumor, usually incidental and more frequent in women aged 30–50. Multiphase imaging shows peripheral, nodular, discontinuous enhancement that fills in centripetally on delayed images, and the lesion is very bright on T2 MRI. Typical imaging is the diagnosis: no biopsy and no follow-up.

Focal nodular hyperplasia (FNH). FNH is the second most common benign liver tumor and is seen mainly in young women. It is a hyperplastic response to an anomalous artery, so it shows intense arterial enhancement with a central stellate scar that enhances late. Because it contains Kupffer cells and bile ductules, FNH takes up Tc-99m sulfur colloid and is iso- to hyperintense on hepatobiliary-phase (gadoxetate) MRI; adenomas usually show neither. It has no malignant potential and almost never bleeds, so it needs no treatment or follow-up, and oral contraceptives (OCPs) may continue.

Hepatic adenoma. Adenomas are linked to OCPs (risk rises with dose and duration), to anabolic steroid use in men, and to glycogen storage disease type I. The dangers are hemorrhage or rupture (lesions >5 cm, pregnancy) and transformation to HCC, which is highest in the β-catenin–activated subtype.

Managing an adenoma. Stop OCPs or steroids, encourage weight loss, and repeat MRI in 6–12 months; many adenomas regress. Resect if:

• the lesion stays >5 cm or keeps growing after hormone withdrawal
• the patient is a man, whatever the size, because the malignant risk is several-fold higher
• the lesion carries a β-catenin mutation

A ruptured adenoma with shock is treated with transarterial embolization first, followed by elective resection.

Malignant lesions

HCC in cirrhosis. HCC can be diagnosed on imaging alone. On multiphase CT or MRI, a nodule of at least 1 cm with nonrim arterial-phase hyperenhancement and washout on portal venous or delayed images (with or without an enhancing capsule) is LI-RADS 5, which establishes HCC without a biopsy. AFP supports the diagnosis but is not required.

Fibrolamellar carcinoma. This variant affects young adults without cirrhosis and usually has a normal AFP. Its central scar is often calcified, unlike the scar of FNH.

Metastases. Metastases are the most common malignant liver lesions. They are usually multiple and come from colorectal (via portal drainage), pancreatic, gastric, breast, lung, melanoma, and neuroendocrine primaries. Colorectal metastases confined to the liver can be resected with curative intent.

Pyogenic liver abscess

Sources and organisms. Pyogenic abscess is the most common liver abscess in the US. The biliary tree is the leading source (stones, stricture, malignancy, cholangitis). Next come portal pylephlebitis from diverticulitis or appendicitis, hematogenous seeding (endocarditis, S. aureus), and cryptogenic cases. The flora is often polymicrobial: E. coli, Klebsiella, the Streptococcus anginosus (milleri) group, and anaerobes such as Bacteroides. Hypervirulent K. pneumoniae (K1/K2 capsule) causes a monomicrobial abscess in diabetic and East Asian patients, with metastatic endophthalmitis, meningitis, or lung abscess.

S. anginosus–group organisms in a blood culture should prompt a search for an abscess.

Diagnosis and management. Patients have fever, RUQ pain, leukocytosis, and a raised alkaline phosphatase. CT shows a rim-enhancing, often multiloculated collection. Treat with image-guided aspiration or catheter drainage (culture the pus) plus IV antibiotics covering gram-negatives, streptococci, and anaerobes (ceftriaxone plus metronidazole, or piperacillin-tazobactam), for 4–6 weeks in total. Relieve biliary obstruction with ERCP, and operate if drainage fails. Cryptogenic cases, especially Klebsiella, warrant colonoscopy because of the link with colorectal cancer.

Amebic abscess and hydatid cyst

Amebic abscess. Entamoeba histolytica invades the colon (flask-shaped ulcers) and reaches the liver via the portal vein. The typical patient is a young man seen weeks to months after time in an endemic area such as Mexico, Central America, or India. There is usually a single right-lobe abscess of odorless "anchovy paste" debris, and most patients have no diarrhea. Serology is positive in >90%, whereas stool microscopy is often negative.

Treating amebic abscess. Give metronidazole (or tinidazole) for tissue trophozoites, then paromomycin to clear luminal cysts. The cysts survive metronidazole because the drug is absorbed so completely. Aspirate only for:

• diagnostic doubt
• no response after 3–5 days
• a very large abscess
• a left-lobe abscess, which risks pericardial rupture

Hydatid cyst. Echinococcus granulosus uses dogs as the definitive host and sheep as the intermediate host. Humans swallow eggs from dog feces in sheep-raising regions (Mediterranean, Middle East, South America, Central Asia). About 70% of cysts lodge in the liver; they grow slowly and are often silent. Imaging shows eggshell (rim) calcification, daughter cysts, and a floating "water lily" membrane, and serology confirms the diagnosis.

Treating hydatid disease. Give albendazole around the procedure, plus surgical cystectomy or PAIR (puncture, aspiration, injection of a scolicidal agent such as hypertonic saline, re-aspiration). Small, inactive calcified cysts can be watched. PAIR is avoided if the cyst communicates with the bile ducts, because the scolicidal agent can injure them. E. multilocularis (fox host) causes an infiltrative, tumor-like alveolar disease.

Spilled hydatid fluid (trauma, surgery, careless aspiration) causes anaphylaxis and seeds new cysts; rupture into the bile ducts causes cholangitis and jaundice.