The Spectrum of Histologic Findings in Hepatic Outflow Obstruction

Abstract

Context: -Cardiac hepatopathy and Budd-Chiari syndrome are 2 forms of hepatic venous outflow obstruction with different pathophysiology but overlapping histologic findings, including sinusoidal dilation and centrilobular necrosis.

Objective: -To determine whether a constellation of morphologic findings could help distinguish between the 2 and could suggest the diagnoses in previously undiagnosed patients.

Design: -We identified 26 specimens with a diagnosis of cardiac hepatopathy and 23 with a diagnosis of Budd-Chiari syndrome. Slides stained with hematoxylin and eosin and with trichrome were evaluated for several distinctive histologic findings.

Results: -Features common to both forms of hepatic outflow obstruction included sinusoidal dilation and portal tract changes of fibrosis, chronic inflammation, and bile ductular reaction. Histologic findings significantly more common in cardiac hepatopathy included pericellular/sinusoidal fibrosis and fibrosis around the central vein. Only centrilobular hepatocyte dropout/necrosis was significantly more common in Budd-Chiari, regardless of duration.

Conclusions: -The finding of pericellular/sinusoidal fibrosis in cardiac hepatopathy compared with Budd-Chiari is not unexpected, given the chronic nature of most cardiac hepatopathy. Portal tract changes are common in both forms of hepatic outflow obstruction and should not deter one from making the diagnosis of hepatic outflow obstruction. Fibrosis along sinusoids and around the central vein may be suggestive of cardiac hepatopathy in biopsies from patients without a prior diagnosis.

Figure 1.

Low-power view of a liver biopsy from a patient with cardiac (congestive) hepatopathy. The most striking finding is centrilobular sinusoidal dilation. This is commonly seen in hepatic outflow obstruction and can also be observed in patients with Budd-Chiari syndrome (hematoxylin-eosin, original magnification ×40).

Figure 2.

Fibrosis along the central vein and sinusoids (highlighted by Masson trichrome stain) were the main findings significantly more common in cardiac hepatopathy than in Budd-Chiari syndrome (original magnification ×200).

Figure 3.

Centrilobular inflammation, including neutrophils, was more commonly seen in the liver in cardiac hepatopathy than in Budd-Chiari syndrome (hematoxylin-eosin, original magnification ×200).

Figure 4.

Low-power view of a case of Budd-Chiari syndrome, with prominent centrilobular dropout/necrosis, which was significantly more often present in this condition (hematoxylin-eosin, original magnification ×40).

Figure 5.

High-power view of the case in Figure 4. Red blood cells can be seen in the space of Disse (hematoxylin-eosin, original magnification ×200).

Figure 6.

Masson trichrome stain highlighting the centrilobular dropout (light blue, upper right), compared with mild portal fibrosis in the same biopsy (darker blue, bottom left) (original magnification ×200).

Figure 7.

End-stage liver in a patient with Budd-Chiari syndrome. There is patchy, haphazard fibrosis extending between central veins, without well-defined nodule formation as would be seen in classic cirrhosis. This pattern is more commonly seen in patients with cardiac hepatopathy, where it is termed cardiac cirrhosis or cardiac sclerosis (hematoxylin-eosin, original magnification ×40).