INTRACRANIAL HEMORRHAGE IN

NEWBORNS

OVERVIEW Incidence varies from 2% to >30% in

newborns

depends on the gestational age (GA) at birth and the type of ICH

Diagnosis typically depends on clinical suspicion

The presence and severity of parenchymal injury is the best predictor of outcome

SUBDURAL HEMORRHAGE (SDH)

Rupture of the draining veins and sinuses of the brain

molding, fronto-occipital elongation, and torsional forces acting on the head during delivery

provoke laceration of dural leaflets of tentorium cerebelli or falx cerebri

Often results from trauma in the full-term infant

SDH in the supratentorial space results from rupture of the bridging veins

ETIOLOGY large head size, rigid pelvis (e.g., in a primiparous or

older multiparous mother), nonvertex presentation (breech, face,

etc.), very rapid or prolonged labor or

delivery, difficult instrumental delivery, or rarely, a bleeding diathesis

CLINICAL PRESENTATION Large collection especially in

infratentorial SDH results in rapid deterioration.

Systemic signs like hypovolemia and anemia

Seizures may occur in up to half of neonates with SDH, particularly with SDH over the cerebral convexity

DIAGNOSIS suspected on the basis of history and

clinical signs and confirmed with a computed tomography (CT) scan.

ultrasonic imaging subdural space is inadequate

MRI- timing of the lesion and for detecting other lesions

Lumbar puncture after CT

MANAGEMENT Most infants with do not require

surgical intervention

prompt stabilization with volume replacement

Open surgical evacuation of the clot in case of large SDH

The outcome for infants with nonsurgical SDH is usually good

SUBARACHNOID HEMORRHAGE (SAH)

Primary SAH is probably frequent but clinically insignificant.

normal “trauma” associated with the birth process.

source of bleeding is usually ruptured bridging veins of the subarachnoid space or ruptured small leptomeningeal vessels

Usual scenario is a well appearing term infant

developing SAH on day 2 or 3 of life

Clinical presentation is similar to other forms of ICH

The diagnosis is best established with a CT scan or MRI, or by LP to confirm or diagnose small SAH

Ultrasonography is not sensitive for the detection of small SAH

Management of SAH usually requires only symptomatic therapy, such as anticonvulsant therapy for seizures

INTRAPARENCHYMAL HEMORRHAGE (IPH) Rare

Intracerebral or intracerebellar variety

More commonly a secondary event

Hypoxic ischemic brain injury, venous infarction or thrombosis, ECMO therapy, large ICH in another compartment

Presentation and management similar to SDH

MRI – extent and age of hemorrhage and other associated parenchymal lesions

LP to rule out meningitis

Symptomatic management

Treat any coexisting pathology or predisposing factors

Monitoring for hydrocephalus

INTRAVENTRICULAR HEMORRHAGE 15-20% at <32 weeks gestation

Venous (or sinus)thrombosis and thalamic infarction in term infants

Related to birth trauma or perinatal asphyxia

No identifiable risk factors in 25%

PRETERM IVH PATHOGENESIS

Intravascular factors

(Pressure passive circulation)

• Ischemia/Reperfusion• Fluctuating or increase

CBF• Increase in cerebral

venous pressure• Platelet dysfunction• Coagulation

disturbances

Vascular factors • Fragile, involuting capillaries with large diameter lumen

Extravascular factors • Deficient vascular support

• Excess fibrinolytic activity

CLINICAL PRESENTATION Usually a clinically silent syndrome in

preterms

Term newborns – seizures, apnea, irritability, lethargy, vomiting, full fontanelle

Catastrophic presentation less likely

Complications

DIAGNOSIS Routine CUS in all infants born at <32

weeks and in older infants at risk for IVH

Days 3,7,30 and 60 days

Monitoring for complications

Grading of GMH/IVH is important for determining management and prognosis

Grading Severity Description

Papile (CT)

IIIIIIIV

Isolated GMH (no IVH)IVH without ventricular dilatationIVH with ventricular dilatationIVH with parenchymal hemorrhage

Volpe (CUS)

I

II

III

Separate notation

GMH with no or minimal IVH (<10% ventricular volume)IVH occupying 10-50% of ventricular area on parasagittal viewIVH occupying >50% of ventricular area, usually distending lateral ventricle

Periventricular echodensity

PREVENTION OF IVH Antenatal steroids

Slow infusion of colloid or hyperosmolar solutions

Avoid rapid fluctuations in CBF and hypotension

Sedative or paralytic medication in ventilated babies

IVH IN PRETERM BABIES Supportive care and watch for

complications

Maintaining Normal BP, electrolytes and blood gases

Transfusions as necessary

Correct thrombocytopenia and coagulation disturbances

IVH IN TERM INFANTS Supportive care and treatment of

seizures

Serial LPs and eventual VP shunts

Prognosis relates to factors other than IVH alone

Monitor OFC and fontanelle daily, Serial CUS q2-7 days to assess ventricle size, shape and RI

No PVD Slowly Progressive Ventricular dilation (over weeks)

Rapidly progressive ventricular dilatation(over days)

No further treatment Close surveillance for 2-4 wk

Dilatation stops Continued dilatation

No therapy, close observation for 1 yr

Serial LP Every 1-3 d, depending on rate of ventricular dilatation

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