**5. Prevention and management**

#### **5.1. GM-IVH in preterm infants**

**4.2. Intracranial hemorrhage (ICH) in term newborns**

6 Intracerebral Hemorrhage

subdural hemorrhage and the two may co-exist. [3]

or in association with infarction may also occur.[3]

for months and may be associated with rebleeding.[3]

hemoglobin.[30]

Subarachnoid hemorrhage (SAH) is the most common type of hemorrhage among the symptomatic term newborns.[6] On FLAIR (fluid attenuated inversion recovery) sequence of MRI, SAH is detected as hyperattenuating fluid in the basal subarachnoid spaces or along the cerebral sulci. Extensive subarachnoid hemorrhage may be difficult to distinguish from

Subdural hemorrhage (SDH) is the most frequent hemorrhage among asymptomatic term newborns.[5] SDH is usually infratentorial, may result from rupture of the vein of Galen, straight or transverse sinus. On imaging, SDH can be seen as a crescent-shaped hyperattenu‐ ating region conforming to the adjacent brain. Small posterior fossa SDHs are common in infants and are usually of no clinical significance; however, when large, may result in com‐ pression of the brain stem and death. Infratentorial SDH may be difficult to distinguish from transverse sinus thrombosis. The two may co-exist or a SDH may compress the sinus predis‐ posing to thrombosis. Convexity SDH are less common than posterior fossa hemorrhage and the two may co-exist. Rupture of superficial cortical veins gives rise to convexity SDH, which may be accompanied by SAH. Convexity SDH is mainly unilateral. Large convexity hemor‐ rhage may be associated with infarction of the brain either from arterial occlusion or impaired venous drainage. Associated parenchymal hemorrhage either due to hemorrhagic tendency

Large SDH may result in impairment of CSF flow and associated ventricular dilatation or widening of the extracerebral space (external hydrocephalus). The evolution of SDH may result in the formation of a subdural effusion which may remain at the site of a previous SDH

Parenchymal hemorrhagic lesions may co-exist with hemorrhage elsewhere in the cranium. Parenchymal hemorrhage may be focal or multifocal and of any size. Multifocal small hemorrhages may be found in term infants presenting with convulsions during the first few days of life. Thalamic hemorrhage is usually unilateral and associated with IVH. Primary thalamic hemorrhage needs to be distinguished from the bilateral thalamic abnormalities seen in HIE. The thalamic lesions in HIE are focal, usually involving the lateral thalamic nuclei and sometimes the medial nuclei, these lesion have high signal intensity on T1-weighted images and low signal intensity on T2-weighted images due to capillary proliferation in region of infarction (not due to hemorrhage). However, infants with HIE may develop large intracranial hemorrhage. Basal ganglia hemorrhage may occur as an isolated event in term newborn, sometimes it is difficult to differentiate it from a hemorrhagic infarction involving a deep branch of middle cerebral artery. Cerebellar hemorrhage may be primary, secondary to venous infarction or may complicate massive intraventricular or subarachnoid hemorrhage. The MR appearance of parenchymal hemorrhage varies with time depending on the oxidation state of Modern practice should emphasize on (i) prevention of GM-IVH, (ii) halting its progression, and (iii) reducing its complications. Important preventive measures include (i) special obstetric care for high-risk pregnancies, (ii) treatment of bacterial vaginosis for reducing premature delivery, (iii) prevention of imminent premature labor using tocolytic agents, cesarean section delivery in selected cases, and (iv) maternal administration of magnesium sulfate. In addition, optimal ventilation and strict hemodynamic control of the premature infant are the corner‐ stones of preventing GM-IVH and its progression. Several postnatal pharmacological agents for prevention of GM-IVH are still under trial.[25,31,32]

PHH, a complication of GM-IVH has a very unpredictable course. 60% of the infants may undergo spontaneous resolution while 40% may require a ventriculoperitoneal shunt, the definitive treatment of progressive PHH.[25] Repeated lumbar puncture may temporarily arrest the progression of PHH, but the long-term benefit of this approach remains unknown.[3]

#### **5.2. ICH in term newborns**

The single most important primary prevention is successful accomplishment of a vaginal delivery with or without obstetric instrument. However, forceful vaginal delivery should not be attempted if either vacuum extraction or forceps delivery has failed.[33]

Medical interventions should be implemented on the very first clinical suspension of ICH. The goal of medical therapy is to provide adequate ventilation, prevent metabolic acidosis, to keep vital organs well perfused and to control seizure activity. Sick newborns with ICH are managed in the intensive care unit. Any treatable etiological factor (e.g. sepsis, dehydration, thrombo‐ cytopenia, vitamin K deficiency or coagulopathy) should be identified and treated promptly. Most symptomatic newborns with intracranial hemorrhage do not require neurosurgical intervention. Neurosurgical intervention could, however, be lifesaving in a situation in which there is a sudden clinical deterioration primarily due to rise in intracranial pressure as a result of massive ICH and PHH.[34] The secondary prevention is to limit the extent of parenchymal injury to the brain due to neurosurgery or hematoma.[35]

#### **6. Summary**

GM-IVH and its complications have potential impact on morbidity, mortality and long-term neurodevelopmental outcome. The mechanism of GM-IVH is multifactorial and involves a combination of vascular anatomic immaturity and complex hemodynamic factors. Goals are prevention of GM-IVH, halting its progression and reducing its complications.

A strong association between traumatic deliveries especially vacuum extraction/forceps delivery and hemorrhagic lesions has been well established in term newborns. Hemorrhage is often present at more than one site. MRI can be used to time the onset of lesions. Hemorrhage may be primary or secondary and occur within an arterial or venous infarct. Neurodevelop‐ mental outcome varies with the site of hemorrhage and the underlying cause. In the majority of term newborns with ICH, medical therapy is the primary mode of treatment; rarely, surgical intervention may be needed in selected cases.

[7] Sandberg DI, Lamberti-Pasculli M, Drake JM, Humphreys RP, Rutka JT. Spontane‐ ous intraparenchymal hemorrhage in full-term neonates. Neurosurgery

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[8] Hayden CK Jr. Shattuck KE, Richardson CJ, Ahrendt DK, House R, Swischuk LE. Subependymal hemorrhage in full-term neonates. Pediatrics 1985;75:714-8.

[9] Volpe JJ. Intracranial hemorrhage: subdural, primary subarachnoid, intracerebellar, intraventricular (term infant), and miscellaneous. In: Neurology of the newborn. 4th

[10] Jhawar BS, Ranger A, Steven D, Del Maestro RF. Risk factors for intracranial hemor‐ rhage among full-term infants: a case-control study. Neurosurgery 2003;52:581-90.

[11] Baun J. Neonatal intracranial hemorrhage. Journal of Diagnostic Medical Sonography

[12] Quinn M, Ando Y, Levene M. Cerebral arterial and venous flow-velocity measure‐ ments in post-hemorrhagic ventricular dilation and hydrocephalus. Dev Med Child

[13] Maalouf EF, Duggan PJ, Counsell SJ, et al. Comparison of findings on cranial ultra‐ sound and magnetic resonance imaging in preterm infants. Pediatrics

[14] Papile LA, Burstein J, Burstein R, et al. Incidence and evolution of subependymal and intraventricular hemorrhage: a study of infants with birth weights less than 1,500

[15] Volpe JJ. Intracranial hemorrhage: germinal matrix-intraventricular hemorrhage of the premature infant. In: Neurology of the newborn. Philadelphia: W.B. Saunders;

[16] Kuban KC, Allred EN, O'Shea TM, et al. Cranial ultrasound lesions in the NICU pre‐ dict cerebral palsy at age 2 years in children born at extremely low gestational age. J

[17] Laptook AR, O'Shea TM, Shankaran S, et al. Adverse neurodevelopmental outcomes among extremely low birth weight infants with a normal head ultrasound: preva‐

[18] Bassan H, Limperopoulos C, Visconti K, et al. Neurodevelopmental outcome in sur‐ vivors of periventricular hemorrhagic infarction. Pediatrics 2007;120:785-92.

[19] Broitman E, Ambalavanan N, Higgins RD, et al. Clinical data predict neurodevelop‐ mental outcome better than head ultrasound in extremely low birth weight infants. J

[20] Counsell SJ, Maalouf EF, Rutherford MA, et al. Periventricular haemorrhagic infarct

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