Neonatal Venous Cerebral Hemorrhage: Report of Two Cases

Sanjay N. Misra, M.D.; Ashish K. Misra, M.D.

Disclosures

Neurosurg Focus. 2003;15(4) 

In This Article

Abstract and Introduction

Intracranial pathological changes can occur as a result of impaired craniocervical venous return. Thrombosis of central venous access catheters was demonstrated in two neonates born at 38 and 27 weeks' gestation. Neither infant developed hemorrhage of prematurity as confirmed on cranial ultrasonography. Clinical evidence of vena cava thrombosis and associated spontaneous intraventricular hemorrhage developed on Day 24 and 36, respectively, and these findings were confirmed on imaging studies. In one infant the hemorrhage was accompanied by communicating hydrocephalus.

The cause of the intracranial disease was attributable to the retrograde cerebral venous congestion. This, together with the primitive venous bed developing in the periventricular region, was associated with the spontaneous hemorrhage in the region of the foramen of Monro.

To the authors' knowledge, this is the first report in the English-language literature of spontaneous neonatal intracerebral hemorrhage, due to thrombosis of the superior or inferior vena cava.

The natural history of this condition is resolution without sequelae after appropriate therapeutic intervention for the vena cava thrombosis.

Spontaneous intracerebral hemorrhage and secondary communicating hydrocephalus are well described in preterm infants, and result from germinal matrix immaturity compounded by extravascular factors.[3,7,8,14,15,23] Central venous access catheters are often required in neonates admitted to the neonatal ICU. Venous thrombosis due to the placement of central venous access catheters is a recognized complication.[9,16,19,20]

As a result of long-term venous access, an intraluminal foreign body and altered flow in the vessel are present, both predisposing to thrombosis. The incidence of catheter line–related thrombosis is as high as 28%.[9,16,20] Infants and neonates may be more prone to this complication because the major venous structures are smaller in diameter than those in adults, and they are also comparatively polycythemic.[18] The role of cerebral venous obstruction as a cause of various intracranial lesions is well described.[5,11,12,21,22] Superior vena cava and collateral inferior cava cardiac return are both significant cerebral outflow tracts in normal neonates.[17] We propose that interference with either of these functions by venous thrombosis will result in pathological cerebral venous congestion. Associated with this pathological state is the predisposition for spontaneous intracerebral hemorrhage in neonates beyond the usual period of the hemorrhage of prematurity.

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