Progressive atrophy in a deformed liver as a contributor to sigmoid volvulus.

The effect of a prior defect on secondary liver atrophy is unknown. We describe a case of sigmoid volvulus that was facilitated by progressive atrophy in a deformed liver. A 75-year-old man with abdominal pain and fullness was referred to our hospital. Computed tomography (CT) revealed reduced left hepatic lobe volume and a whirl sign, characteristic of sigmoid volvulus. The sigmoid volvulus was successfully detorted with endoscopy. Retrospective evaluation of liver morphology on CT and magnetic resonance imaging showed that the portal vein at the liver hilum was denuded due to a parenchymal defect of the medial segment, with compression by the crossing artery. As pulse Doppler ultrasonography demonstrated reduced portal blood flow in the region where liver atrophy developed, compression of the denuded portal vein presumably facilitated secondary atrophy and contributed to sigmoid volvulus. The present case shows that a deformed liver itself can be a cause of secondary atrophy. Therefore, continued monitoring of liver morphology and evaluation of portal blood flow to predict liver atrophy may be required, when an individual with a partial liver defect is encountered.

Spontaneous Celiac and Splenic Artery Dissection.

Dissection of the splanchnic artery unrelated to an aortic lesion is extremely rare. We describe a patient with dissection of the celiac and splenic arteries causing splenic circulatory impairment. A 55-year-old Japanese man was referred to our hospital for left back pain that suddenly occurred 3 days previously and spread to the left flank. He had complicated sleep apnea syndrome well controlled with continuous positive airway pressure, and had been prophylactically taking aspirin (100 mg/day) because of asymptomatic cerebral lacunar infarcts. Contrast-enhanced computed tomography (CT) in the arterial phase revealed dissection from the celiac root extending to the entire splenic artery, the caliber of which was irregularly narrowed, causing malperfusion in the spleen. Because of hemodynamic stability and lack of impending sequelae, the patient was carefully observed with rest, strict blood pressure control, and aspirin administration. One month later, CT revealed restoration of the caliber of the dissected arteries and regression of the organizing false lumen, which confirmed the patient's recovery. Despite the extreme rarity or nonspecific symptoms, splanchnic artery dissection should be considered a potentially life-threatening emergency. This case supports the possible benefit of starting antithrombotic treatment early to prevent thrombotic sequelae such as organ infarction and aneurysmal formation.