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 of an undetermined cause. An ICH in preterm infants is periventricular or intraventricular in location but originating from vascular rupture within the subependymal germinal matrix. Preterm infants may have periventricular hemorrhagic infarctions of white matter that follow germinal matrix-intraventricular hemorrhages.
Definition. SDH involves tears of veins or venous sinuses traversing the subdural space. 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 or reside as a hematoma that slowly evolves as a chronic subdural hematoma with increasing fluid accumulation and increasing intracranial pressure.
Incidence. SDH is uncommon in term and preterm infants. When it occurs, it usually follows a traumatic delivery of a late preterm or term infant. Among 111 asymptomatic term infants studied prospectively by MRI, 9 had SDH (8.0%), 3 after spontaneous vaginal deliveries and 6 after instrumented deliveries. None required treatment, and all were free of hematoma by 4 weeks of age. Moreover, all infants were normal at 2 years. Although SDH is the least common of all ICH and often self-resolving, it can be a serious to catastrophic event clinically.
Pathophysiology. SDH is typically related to traumatic events surrounding the delivery and birth. 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, 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. As noted, clinical signs may be minimal to none with the SDH self-resolving; however, 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.
Risk factors include precipitous delivery, instrumented deliveries using midforceps or vacuum assist (extraction), or circumstances involving a large for gestational age infant and cephalopelvic disproportion.
Clinical presentation. 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. Signs of increasing intracranial pressure may include a bulging fontanel, deviations of eye movements, and increasing occipital-frontal head circumference. Other observations are decreased feeding, intermittent vomiting, and failure to thrive, which are more often related to late post-SDH neuropathic events.
Hematocrit. Unexplained anemia.
Total serum bilirubin. Persistent ...
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