Clinical Profile:

A 70-year-old man, presented with recurrent episodes of the dizziness and progressive drop in hid hemoglobin levels since five months.

Radiological Investigations:

Ultrasonogram of the abdomen- (fig. 1-3)

Intercostal axial view of the liver shows an approximately 8.6x7.2 cm sized well-defined, heterogeneously hyperechoic lesion in segment VII of the liver. Colour and spectral Doppler of the same lesion shows moderate internal vascularity with RI=0.57. Intercostal axial view of the liver shows perihepatic a 1.6 cm thick haematoma with hemoperitoneum.

Figure 1

Ultrasonogram of liver:

Intercostal axial view of the liver shows an approximately 8.6x7.2 cm sized well-defined heterogeneously hyperechoic lesion in segment VII of the liver.

Figure 2

Colour and Spectral Doppler of the same lesion shows moderate internal vascularity with RI=0.57.

Figure 4

Axial sections of the plain (A), arterial (B) and porto-venous (C & D) phases of the CT abdomen show a well-defined 8.6x7.2x8cm (AP x TRx CC) sized hypodense lesion in the segment VII of the liver that shows progressive heterogenous contrast enhancement with washout in venous phase. There is no calcification.

Radiological Diagnosis:

Hepatocellular carcinoma with subcapsular hematoma and hemoperitoneum.

Pathological diagnosis:

An ultrasound-guided biopsy of the lesion was performed.

Histopathological diagnosis:

Hepatocellular carcinoma.

Course in the hospital:

The patient has a stormy course due to low haematocrit values and other comorbid conditions . She had a cardiac arrest from which she could not be revived.

Timeline:

Discussion:

Hepatocellular adenomas (HCAs) are uncommon and essentially benign tumours in the liver that occur predominantly, but not exclusively, in young women consume oral contraceptives (OCs)(1,2 ) HCAs are caused by benign proliferation of hepatocytes with high glycogen and fat content but lack normal hepatic architecture. They usually present as a solitary nodule that may reach up to 30 cm in diameter.

Clinical manifestations range from asymptomatic presentation or abdominal pain localized to the epigastric region or right upper quadrant to a palpable liver mass or even life-threatening haemorrhage in the case of rupture(3,4). However, these tumours are most often encountered as an incidental finding during imaging for unrelated pathology.

Although the exact pathogenetic mechanism of the development of HCAs remains unknown, an association between formation of HCAs and the use of OCs or androgen-containing anabolic steroids is assumed (5–7). Studies from the past century suggest that long-term use of OCs increases the annual incidence of HCAs from 1 per million to 3 to 4 per 100 000. (1,8). In addition, OCs and androgen-containing steroid anabolics have also been suggested to increase the number and size of these adenomas. Conversely, HCAs may show signs of regression on discontinuance of the use of OC use (9,10). HCAs are further reported to be associated with type I and type III glycogen storage disease (GSD) and, furthermore, are more likely to be multifocal or to become malignant in these patients (11).

The most important complications of HCAs are haemorrhage and malignant transformation into hepatocellular carcinomas (HCCs). Thus, these are the two main reasons for surgical treatment. However, little is known about the true incidence, associated risk factors and the etiology of malignant alteration of HCAs.

Risk factors of malignant transformation of hepatocellular adenomas

1. Size >5cm.

2. A history of androgen or anabolic steroid intake.

3. Patients of male gender

4. Patients with glycogen storage disorder.

5. B-catenin mutation.

Treatment:

Surgical management in the adenoma >5cm. Minimally invasive techniques such as (percutaneous) radiofrequency ablation (RFA) or microwave ablation may alter the treatment of HCA.

Recently, two groups have reported the therapeutic effects of selective arterial embolization to stop haemorrhaging from ruptured adenomas.

References :

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