Conservative Management of a Hepatic CSF Pseudocyst in an Asymptomatic Patient

Abstract

Ventriculoperitoneal (VP) shunting is the most frequently used treatment for hydrocephalus. VP shunt complications are common, with the overall incidence reported at 17 to 33 per cent.1 Abdominal cerebrospinal fluid (CSF) pseudocyst formation is a rare finding in the adult population, occurring in less than 10 per cent of all VP shunts, and the development of a hepatic CSF pseudocyst is an even less common complication of VP shunt placement.2, 3 Herein, we present a case of an intra-axial asymptomatic hepatic pseudocyst. Our patient is a 56-year-old man with an intraaxial hepatic CSF pseudocyst, found incidentally on low-dose lung cancer screening CT of the chest. He initially had a VP shunt placed at an outside institution in 1983 for posttraumatic hydrocephalus after a head injury sustained in an MVC. He has undergone multiple revisions due to shunt malfunctions. After several years with a functioning shunt, a screening CTof the chest was performed, revealing a 4-cm hepatic cyst of the peripheral, superior liver parenchyma closely associated with the VP shunt tip (Figs. 1 and 2). He had no evidence of shunt dysfunction and denied any abdominal pain. Since his presentation, he has remained neurologically stable and asymptomatic. He has since undergone a shunt series that showed no dysfunction. We plan to continue to follow up the patient with serial examinations and imaging. VP shunting is used as the treatment for hydrocephalus secondary to a vast array of underlying etiologies. In patients who develop hepatic CSF pseudocysts, the most common underlying etiologies of hydrocephalus are tumors, meningitis, aqueductal stenosis, congenital hydrocephalus, intraventricular hemorrhage, and, as in our case, trauma.2 Although VP shunts are most common in the pediatric population, the age at diagnosis of hepatic pseudocysts ranges from 3 to 58 years, with a mean age of 24.4 years, and both men and women are equally likely to develop the disease.2 The underlying pathophysiology of hepatic CSF pseudocyst formation is unknown. The prevailing theory is that it is a consequence of an inflammatory process resulting from chronic irritation and focal injury to the liver surface. Local inflammation decreases the capacity for CSF reabsorption on the peritoneal surface of the liver, with subsequent accumulation and cyst formation.2 When the fluid collection is located within the liver parenchyma, as is the case in the patient presented here, it is referred to as intra-axial. Conversely, when no hepatic tissue can be identified in the peripheral wall of the pseudocyst, it is referred to as extra-axial or subcapsular.2 Although reports are limited, extra-axial hepatic CSF pseudocysts are slightly more common than intraaxial hepatic CSF pseudocysts, representing 60 per