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INTRODUCTION

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An intracranial hemorrhage (ICH) can occur in term and preterm infants. An ICH occurring in term infants tends to be subdural, subarachnoid, or subtentorial and is most related to birth trauma, hypoxic-ischemic events, coagulopathies (eg, thrombophilias or thrombocytopenia), and undetermined causes. The most common ICH in preterm infants is bleeding from the subependymal germinal matrix and may result in intraventricular or periventricular hemorrhage, either of which can potentially cause hemorrhagic infarctions of the white matter. This chapter reviews the following clinical conditions: subdural hemorrhage (SDH), epidural hemorrhage, subarachnoid hemorrhage (SAH), intracerebral parenchymal hemorrhage, intracerebellar parenchymal hemorrhage (ICPH), and germinal matrix and intraventricular hemorrhage (GM/IVH).

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SUBDURAL HEMORRHAGE

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I. DEFINITION

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A subdural hemorrhage (SDH) is an accumulation of blood between the dura and the arachnoid membrane and involves tears of bridging veins of the subdural compartment. The vascular structures most affected are superficial cerebral veins, infratentorial posterior fossa venous sinuses, the inferior sagittal sinus, and tentorial sinuses and veins (eg, vein of Galen). Blood may accumulate and cause acute symptoms of intracranial pressure (ICP) or reside as a hematoma that slowly evolves as a chronic subdural hematoma with increasing fluid accumulation and increasing ICP.

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II. INCIDENCE

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A SDH is very common after birth: up to 50% of term asymptomatic infants may have SDH. It usually follows a traumatic delivery of a late preterm or term infant. Only on rare occasions does SDH become serious.

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III. PATHOPHYSIOLOGY

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A SDH is typically related to traumatic birth events involving labor and delivery. Undue pressure on the skull and torsion may produce shear forces resulting in rupture of superficial cerebral bridging veins or tears in the dura or dural reflections (eg, either the falx cerebri or tentorium and associated venous sinuses). These events are usually found over the cerebrum or within the posterior fossa. Occasionally skull fractures accompany these findings. Timing of the onset of SDH and clinical findings may be acute or delayed. Clinical signs may be minimal to none with the SDH self-resolving, or subtle findings of slight irritability or a seemingly hyperalert state may foretell an underlying accumulating SDH with delayed onset of more serious neuropathic circumstances. Latent SDH can lead to a subdural hematoma and subdural effusion with increasing intracranial pressure.

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IV. RISK FACTORS

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Include precipitous labor and delivery, instrumented deliveries utilizing forceps or vacuum-assist devices, a large for gestational age infant with cephalopelvic disproportion, and coagulopathies including familial thrombophilias and vitamin K deficiency.

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V. CLINICAL PRESENTATION

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Signs include lethargy alternating with irritability or asymmetric hypotonia of upper and lower extremities on the contralateral side of the SDH. More specific to SDH is impaired third cranial nerve function ipsilateral to the SDH. Focal seizures may present at any time and are much more likely to ...

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