Sinusoidal obstruction syndrome pathophysiology

The development of sinusoidal obstruction syndrome begins with the injury to hepatic venous endothelium. It is thought that preexisting liver disease increases the risk of developing sinusoidal obstruction syndrome (SOS) due to impairment of drug metabolism which predisposes to the endothelial injury. The endothelial cells in patients with hepatitis may have abnormal expression of adhesion molecules and pro-coagulant factors. The deposition of fibrinogen and factor VIII within the sinusoids leads to their dilation and congestion by erythrocytes. The progressive occlusion of venules leads to widespread zonal liver disruption and centrilobular hemorrhagic necrosis. Hepatic sinusoidal obstruction syndrome (SOS) is mainly seen in patients of hematopoietic cell transplantation.

• Sinusoidal obstruction syndrome (SOS) occurs due to obstruction of the hepatic venules and sinusoids rather than hepatic vein or inferior vena cava as seen in Budd Chiari syndrome.
• Hepatic sinusoidal obstruction syndrome (SOS) is mainly seen in patients who have undergone hematopoietic stem cell transplantation.
• The development of sinusoidal obstruction syndrome (SOS) begins with the injury to the hepatic venous endothelium. It is thought that preexisting liver disease increases the risk of developing sinusoidal obstruction syndrome (SOS) due to impairment of drug metabolism which predisposes to the endothelial injury.
• The endothelial cells in patients with hepatitis may have abnormal expression of adhesion molecules and pro-coagulant factors.
• The deposition of fibrinogen and factor VIII within the sinusoids leads to their dilation and congestion by erythrocytes. The progressive occlusion of venules leads to widespread zonal liver disruption and centrilobular hemorrhagic necrosis.
• The later changes in sinusoids include deposition of collagen, sclerosis of venular walls, fibrosis of the lumen and ultimately occlusion of hepatic venules.
• The severity of symptoms depends on the number of sinusoids involve and severity of the histologic changes.

• On gross pathology, the liver has diffusely mottled appearance with areas of congestion and normal appearing hepatic parenchyma.^[1]

The most important histopathological characteristics of sinusoidal obstruction syndrome are:^[2][3][4]

• Sinusoidal dilation
• Portal tract changes of fibrosis and bile ductular reaction
• Sclerosis of venular walls
• Sinusoidal endothelial cell detachment from the space of Disse can be seen on electron microscopy

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