Diagnostic imaging of the pediatric liver

Imaging modalities: from ultrasound to MRI

Ultrasound (US) remains the first-line method. However, magnetic resonance imaging (MRI) is used for detailed characterization of masses. The standard protocol includes T1-weighted gradient echo with intravenous contrast. This allows detection of typical centripetal enhancement in infantile hemangiomas or rapid washout (washout), characteristic of malignant neoplasms.

Non-contrast MR angiography (balanced steady-state techniques) is promising for evaluating the portal vasculature. Hepatospecific contrast agents are still used off-label in pediatrics, but perform exceptionally well in detecting small lesions and assessing functional bile flow — for example, when hepatoblastoma recurrence is suspected.

Computed tomography (CT) in children is strictly limited. Infants have sparse adipose tissue, which makes tissue planes difficult to differentiate, and radiation exposure requires minimizing scans. If CT is inevitable, non-contrast series are omitted — only scans with intravenous contrast are performed. Angiography is used extremely rarely, usually as a preparatory step before endovascular intervention.

Age-related features of imaging anatomy

The anatomy of a child's liver changes dynamically. In newborns, the parenchyma is hypoechoic relative to the kidneys, but in infancy this relationship reverses. Normal liver dimensions vary widely, so uncritical use of reference values is not recommended — it is better to rely on age-adjusted percentile charts.

An important marker is the status of fetal shunts. The umbilical vein and ductus venosus (ductus venosus) are patent in newborns during the first hours of life. In most children, they close by the end of the first week. Persistence of blood flow in them after 2–3 weeks of life is considered pathological.

The diameter of the portal vein must be measured while fasting in the supine position. Normally, in infants under one year of age, it is 3.0–6.4 mm, and by 10 years of age it can reach 10.8 mm.

Chronic disorders: cirrhosis and fibrosis

Progressive fibrosis leads to anatomical restructuring of the organ, hepatocyte dysfunction, and portal hypertension. The main causes of cirrhosis in children are cholestasis (including biliary atresia), cystic fibrosis, prolonged parenteral nutrition, and in older children, the proportion of non-alcoholic fatty liver disease (NAFLD) is increasing.

The typical ultrasound picture of cirrhosis includes a heterogeneous or multinodular hyperechoic parenchyma and a nodular contour. Atrophy of the right lobe against the background of compensatory hypertrophy of the left and caudate lobes is frequently observed. Doppler evaluation of the portal system is mandatory.

For hepatocellular carcinoma (HCC) screening in the setting of cirrhosis, ultrasound is insufficient. MRI reliably differentiates nodules:

• Regenerative nodules: appear as normal parenchyma.
• Steatotic nodules: show high signal that drops on opposed-phase images.
• Dysplastic nodules and HCC: demonstrate high signal on T2-WI and typical rapid contrast washout following a bright arterial phase.

Vascular pathology and portal hypertension

Portal hypertension in children is frequently caused by extrahepatic portal vein occlusion (a consequence of omphalitis, umbilical vein catheterization, trauma, or infections). The liver parenchyma is usually unaffected in these cases. The main imaging sign in such cases is cavernous transformation at the porta hepatis.

General ultrasound signs of portal hypertension include slowed blood flow (less than 15–18 cm/s), disappearance of respiratory pulsations, appearance of hepatofugal (reverse) blood flow, and visualization of dilated collateral varices. Against the background of decreased portal inflow, arterial blood flow in the liver increases compensatorily.

A highly specific finding is gas in the portal vein. On ultrasound, it appears as mobile hyperechoic foci within the vessel lumen. Unlike gas in the biliary tract, portal gas extends to the peripheral capsule. In newborns, this is a ominous sign of necrotizing enterocolitis, in which gas from the affected bowel wall is forced into the mesenteric vasculature.

Focal and infectious processes

The spectrum of inflammatory lesions is broad: from congenital infections (rubella, cytomegalovirus) causing hepatosplenomegaly and small calcifications, to large abscesses. Pyogenic abscesses in children are most often (in 80% of cases) caused by Staphylococcus aureus. Immunocompromised patients frequently present with fungal multifocal lesions with simultaneous splenic involvement.

In chronic granulomatous disease, children are predisposed to catalase-positive infections. Instead of typical fluid abscesses, granulomas are formed — heterogeneous solid masses that enhance with contrast and leave behind calcifications.

Important: in febrile neutropenia, clinical and laboratory diagnosis is difficult due to a weak immune response. Thorough ultrasound examination using a high-frequency linear transducer is mandatory for such patients.

Briefly: answers to topical questions

What else to study on this topic

• Congenital portosystemic shunts: classification and hepatopulmonary syndrome
• Differential diagnosis of neonatal hepatitis and biliary atresia
• Fibropolycystic liver disease and Caroli syndrome
• Ultrasound and MR elastography of the liver in pediatrics
• Budd-Chiari syndrome and veno-occlusive disease in children

Other Topics in "Pediatric Diagnostic Radiology"

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