Myxoid variant: Loose, basophilic matrix, with thick fibrous septa, and foamy histiocytes
Lipoma-like variant: Univacuolated lipocytes, with only isolated hibernoma cells
Spindle cell variant: Spindle cell lipoma combined with hibernoma

Histochemistry
Oil Red O-positive droplets of cytoplasmic lipid can be seen in most cases

Immunohistochemistry
The neoplastic cells are S100 protein positive (approximately 80%), and show membrane and vacuole CD31 immunoreactivity. Uncoupling protein 1 (UCP1), a unique brown fat mitochondrial protein, is also positive. Cytogenetics
There are structural rearrangements of 11q13-21, which are considered most characteristic. This alteration can be detected by metaphase fluorescent in situ hybridization (FISH). MEN1 gene (11q13.1) is most frequently deleted, while GARP gene (11q13.5) may also be involved. Cytology
The fine needle aspiration smears show small, round, brown fat-like cells, with uniform, small cytoplasmic vacuoles and regular, small, round nuclei. There is usually a rich vascular background of branching capillaries. It is not uncommon to also have mature fat cells. Differential diagnoses
It is important to separate hiberoma from adult rhabdomyoma, a granular cell tumor and a true liposarcoma. Classification
This lesion has been called a fetal lipoma, lipoma of embryonic fat or a lipoma of immature fat. Management
Complete surgical excision is the treatment of choice, associated with an excellent long term clinical outcome. Epidemiology
The tumor is rare, affecting adults in the 4th decade most commonly. Patients are usually younger than those who present with a lipoma. There is a slight male predominance. Hibernoma are most commonly identified in the subcutaneous and muscle tissue of the head and neck region (shoulders, neck, scapular), followed by thigh, back, chest, abdomen, and arms.
Diagnosis
Investigations
The diagnosis of hepatic encephalopathy can only be made in the presence of confirmed liver disease (types A and C) or a portosystemic shunt (type B), as its symptoms are similar to those encountered in other encephalopathies. To make the distinction, abnormal liver function tests and/or ultrasound suggesting liver disease are required, and ideally a liver biopsy. The symptoms of hepatic encephalopathy may also arise from other conditions, such as bleeding in the brain and seizures (both of which are more common in chronic liver disease). A CT scan of the brain may be required to exclude bleeding in the brain, and if seizure activity is suspected an electroencephalograph (EEG) study may be performed. Rarer mimics of encephalopathy are meningitis, encephalitis, Wernickes encephalopathy and Wilsons disease; these may be suspected on clinical grounds and confirmed with investigations.The diagnosis of hepatic encephalopathy is a clinical one, once other causes for confusion or coma have been excluded; no test fully diagnoses or excludes it. Serum ammonia levels are elevated in 90% of people, but not all hyperammonaemia (high ammonia levels in the blood) is associated with encephalopathy. A CT scan of the brain usually shows no abnormality except in stage IV encephalopathy, when brain swelling (cerebral oedema) may be visible. Other neuroimaging modalities, such as magnetic resonance imaging (MRI), are not currently regarded as useful, although they may show abnormalities.