Late complications of ventriculoatrial or ventriculoperitoneal shunts

• Published in: The Lancet (British edition) 2001-11, Vol.358 (9293), p.1569-1570
• Main Authors: Vernet, Olivier, Rilliet, Bénédict
• Format: Article
• Language: English
• Subjects: Child, Preschool; Embolisms; Equipment Failure; Health care; Heart failure; Humans; Hydrocephalus - surgery; Hypertension; Hypertension, Pulmonary - etiology; Infections; Medical diagnosis; Nephritis - etiology; Postoperative Complications; Pulmonary Embolism - etiology; Pulmonary hypertension; Shunts; Staphylococcus epidermidis; Thromboembolism; Thrombosis; Time Factors; Ventriculoperitoneal Shunt - adverse effects
• ISSN: 0140-6736; 1474-547X
• DOI: 10.1016/S0140-6736(01)06670-3

A review in 1998 of published work indicated that in patients with ventriculoatrial shunts pulmonary embolism and pulmonary hypertension were recognised clinically in 0.4% and 0-3%, respectively, whereas, at necropsy the frequency of these complications was 597% and 6.3%, respectively.6 The late occurrence of pulmonary hypertension after insertion of a ventriculoatrial shunt was initially thought to be the result of latent shunt infection. The infection was thought to induce a persistent activation of clotting factors, which in turn leads to recurrent pulmonary embolism. Subsequent studies showed that infection was not a prerequisite for formation of thrombi and pulmonary embolism.6 In 1961, on the basis of necropsy findings in 15 patients with ventriculoatrial shunts, [Emery JL] and Hilton7 suggested that some pulmonary vascular lesions (periarteritis, intimal degeneration) were independent of the presence of thrombi or lung embolism. This proposal could account for the lack of evidence of thromboembolism in the case reported by Caroline Milton and colleagues in today's Lancet. They thought that these histological changes reflected a reaction of the pulmonary endothelium to some proteins in the cerebrospinal fluid.7 In line with such thinking were suggestions by other researchers that pulmonary thrombi were generated by brain thromboplastin that reached the venous circulation via the shunt.8 Although the exact mechanism causing pulmonary hypertension after ventriculoatrial shunting is unclear, there could be a vicious circle of thrombotic components inducing local endothelial damages, which in turn promote platelet aggregation and thus vascular thrombosis. Thus the diffuse eccentric intimal proliferation found in patients with pulmonary hypertension after ventriculoatrial shunting is the result rather than the cause of endothelial damage and leads to in-situ thrombosis and perpetuation of the process even after removal of the embolic source.6 This vicious circle could account for the high mortality rate of 50-100% associated with pulmonary hypertension complicating ventriculoatrial shunting.