Pleural Effusion Caused by Ventriculopleural Shunt: A Case Report

Abstract

Pleural effusion of extra-vascular origin (PEEVO) refers to a pleural effusion that does not originate from the pleural vasculature, but rather migrates from an extrapleural space. Our case describes one such cause, malfunctioning of ventriculopleural shunts, causing a pleural effusion due to imbalance between the production and absorption of cerebrospinal fluid. Case: A 38-year-old Caucasian female with a past medical history of Chiari malformation and syringomyelia status post ventriculopleural shunt was admitted for chest tightness, exacerbated by lying down, for the past three weeks. The patient previously had a ventriculoperitoneal shunt status post several revisions, which was then converted to a ventriculopleural shunt two years ago (Figure 1. A). CT of the chest revealed a large, right-sided, loculated pleural effusion at the shunt insertion site (Figure 1. B). Patient was observed for signs of infection or increased hypoxia, but remained stable for 24 hours. As the collection was anterior and not amenable to easy drainage, a shared decision was made with the patient, pulmonary and neurosurgery teams to continue serial monitoring of the effusion outpatient. The patient was discharged with appropriate follow up. Discussion: PEEVO is an unusual entity, which requires a high level of suspicion for diagnosis. Causes for PEEVO can be broadly divided into transudates (associated with peritoneal dialysis or ventriculopleural shunts) and exudates (secondary to perforated esophagus or misplaced enteral feeding tubes). Our case demonstrates symptomatic pleural effusion secondary to a malfunctioning ventriculopleural shunt. Various extracranial shunts have been used to manage hydrocephalus, most commonly ventriculoperitoneal (VP) and ventriculoatrial shunts. Ventriculopleural shunts may be used in the management of patients without other viable options, and many centers are adopting it as the second-line of treatment after VP shunts. Although generally well tolerated, they can rarely cause symptomatic pleural effusions. There are currently no guidelines for management, however, case series have noted that for asymptomatic or mildly symptomatic effusions, patients can be managed with close observation. For symptomatic or large effusions, thoracentesis may be a temporizing measure before definitive management by shunt revision. In cases like ours, the risks and benefits of replacing the shunt must be considered with collaboration with pulmonary medicine and neurosurgery teams. These unusual causes of a very commonplace entity (pleural effusion) are to be considered in the appropriate clinical setting, and knowledge of these entities will help in avoiding delays in diagnosis and management.