Synonyms: Isolated germinal matrix hemorrhage, subependymal hemorrhage.

Prevalence: Less than 20 cases of intracranial hemorrhage have been diagnosed prenatally.

Definitions: Grade I periventricular hemorrhage remains confined to one or both germinal matrices. Grade II and III denote rupture into the ventricles. In grade III, ventricular dilation is observed, and grade IV represents extension of the hemorrhage into the adjacent white matter¹ (fig. 3).

Etiology: The etiology of prenatal periventricular hemorrhage is not clear, but trauma, infections, asphyxia and blood dyscrasias should be considered^2-4. In the neonate, possible causes are: prematurity, increased or decreased blood supply to subependymal matrix due to impaired autoregulation, capillary endothelial injury and/or increased fibrinolitic activity due to sepsis⁵.

Pathogenesis: Vasodilatation and vascular damage of the delicate germinal matrix vasculature.

Differential diagnosis: Periventricular leukomalacia (PVL).

Prognosis: Only a small minority of children affected with Grade I periventricular hemorrhage develop neurologic deficits.

Recurrence risk: Not known to be increased.

Management: Trials on the prophylactic use of Phenobarbital and steroids are being conducted. After delivery, avoid the development of hypercapnea and acidosis.

MESH Cerebral-Hemorrhage-diagnosis ICD9 767.0 CDC 767.000

Address correspondence to: Haim Zakut, DVM, MD, Dept. of Obstetrics and Gynecology, The Edith Wolfson Medical Center, P.O. Box 5, Holon 58100, Israel. Ph: 972-3-502-8712; Fax: 972-3-501-4111.

Introduction

The occurrence of prenatal brain damage, particularly in the form of white matter necrosis, has been reported in neuropathological and clinical studies. Although more common in the neonate, periventricular hemorrhage rarely occurs in the prenatal period^6,7. However, several cases of intracranial and intraventricular hemorrhages have been diagnosed in utero^5,6, and were reviewed by Fogarty et al⁴. Two new cases were published since then (Table 1).

We report one case of periventricular hemorrhage (grade I) in a 32-week fetus diagnosed by transvaginal sonography and confirmed after delivery by neonatal ultrasound.

Case report

A 22-year-old woman was admitted at 32 weeks of gestation because of excessive weight gain and edema. Her past history was negative, and she denied the use of any medication during pregnancy, including specific questions of the use of aspirin-like drugs. The course of this pregnancy was uneventful and trauma, seizures, hypertension, diabetes mellitus or any other disease during pregnancy were excluded.

On physical examination the fundal height was 320 mm, no contractions or increased uterine tone were observed. The cervix was closed and uneffaced, the fetus was in cephalic presentation and the head was not engaged. The blood count was normal without thrombocytopenia.

Fetal cardiotocography showed an isolated prolonged bradycardia after a spontaneous uterine contraction. Abdominal ultrasound at this time was considered normal, and the fetal weight estimation was 2000g.

Transvaginal sonography was performed in the context of a study being conducted on the normal fetal anatomy of the brain and showed the presence of a small hyperechogenic area at the level of the left caudate nucleus consistent with subependymal hemorrhage (fig.1).

Fig. 1: Fetal brain at 32 weeks. A small echogenic area to the left of the lateral ventricle. Left: coronal scan, Right: parasagital scan.

Oxitocin challenge test was negative, but later on the same day the pattern of prolonged bradycardia developed again several times. Cesarean section resulted in a 1970g female fetus with an Apgar score of 5 and 8 at 1 and 5 minutes, respectively.

Ultrasound examination 14 hours after the delivery confirmed the presence of the described hemorrhage (fig. 2).

Fig. 2: Coronal section at the same plane as in fig. 1, obtained 14 hours after delivery.

On day 4, a new ultrasound examination was performed because of the development of hypotonus; at this time, a grade III intraventricular hemorrhage and dilation of the left ventricle was observed. Follow-up at 28 days of age showed the development of small cysts consistent with subependymal cysts.

The development of the child at 12 months of age was normal, without any neurological handicaps.

Discussion

The diagnosis of intracranial hemorrhage in the newborn has profound clinical and medicolegal implications. Fifty to ninety percent of all intracranial hemorrhages are evident by the 12^th postnatal hour^7-10. Leviton et al¹¹ found that 33% of all germinal matrix hemorrhages were present by the 12^th postnatal hour.

Increasing amount of evidence is being provided on the prenatal occurrence of at least some of these hemorrhages. Ellis et al⁶ found that from 89 infants who died at 7 days or less, 22 (25%) had neuropathological evidence of prenatal brain damage; in only 4 infants the lesions were consistent with prenatal intracranial hemorrhage (deposits of considerable amounts of hemosiderin).

Definitions

Grade I periventricular hemorrhage remains confined to one or both germinal matrices. Grade II and III denote rupture into the ventricles. In grade III, ventricular dilation is observed and, grade IV represents extension of the hemorrhage into the adjacent white matter¹ (fig. 3).

Fig. 3: (From left to right) Grade I periventricular hemorrhage remains confined to one or both germinal matrices. Grade II and III denote rupture into the ventricles. In grade III, ventricular dilation is observed, and grade IV represents extension of the hemorrhage into the adjacent white matter¹.

Diagnosis

Germinal matrix hemorrhages are diagnosed by the presence of a zone of increased echogenicity at the level of the head of the caudate nucleus or the caudothalamic notch depicted in coronal and sagittal scans. The transvaginal approach in the vertex presentation is optimal for obtaining those planes.

The echogenic pattern of germinal matrix hemorrhage may be unilateral or bilateral and may compress the floor of the lateral ventricle. Extension into the lateral ventricle will present as a uniform echogenic mass, usually in the occipital horns, the trigone or adherent to the choroid plexus⁵.

Differential diagnosis

The differential diagnosis of periventricular echogenicities includes mainly periventricular hemorrhage and periventricular leukomalacia. Acute periventricular leukomalacia is not always evident at the time of the ultrasound examination or even by CT. When present, they appear as broad bands of increased periventricular echogenicity, frequently bilateral and usually with an associated hematoma in the lateral ventricles. The diagnosis between subtle forms of periventricular leukomalacia and the normal periventricular halo may be difficult, and only the late development of periventricular leukomalacia cysts will confirm the diagnosis.

Prognosis

The extent of the hemorrhage, as defined by Burstein et al¹, is used as a prognostic indicator. Children with grade I and probably also those with grade II periventricular hemorrhage have a prognosis similar to neonates of the same gestational age without brain hemorrhage. In grade III hemorrhages, there is an increased risk for the development of post-hemorrhagic hydrocephalus and associated neurological handicaps.

Grade IV periventricular hemorrhage, although the least common, implies the worst prognosis with a mortality rate of 25-69%¹² and adverse neurologic development in 54% of the survivors⁹.

IUGR: intrauterine growth retardation

At the present time, there is not sufficient experience in the visualization of prenatal intracranial hemorrhages, and the management of each case needs to be individualized. Careful recording and description of the findings are essential because of the medicolegal implications of the diagnosis.

References

1. Burstein J, Papile L, Burstein R: Intraventricular hemorrhage and hydrocephalusin premature newborns: a prospective study with CT. AJR 132:631-365,1979.

2. Becroft DM, Gunn TR: Prenatal intracranial hemorrhages in 47 Pacific Islander infants: is traditional massage the cause? NZ Med J 102:207-10, 1989.

3. Sins ME, Turkel SB, Halterman G et al: Brain injury and intrauterine death. Am J Obst Gynecol 151:721-3, 1985.

4. Fogarty K, Cohen HL, Haller JO: Sonography of fetal intracranial hemorrhage: unusual causes and a review of the literature. J CUltr 17:366-70, 1989.

5. Grant EG: Sonography of the premature brain: intracranial hemorrhage and periventricular leukomalacia. Neuroradiology 28:476-490, 1986.

6. Ellis WG, Goetzman BW, Lindenberg JA: Neuropathological documentation of prenatal brain damage. AJDC 142:858-866, 1988.

7. Bejar R, Wozniak P, Allard M, et al: Antenatal origin of neurologic damage in newborn infants. I. Preterm infants. Am J Obstet Gynecol 159:357-363, 1988.

8. Stoddard RA, Clark SL, Minton SD: In utero ischemic injury: sonographic diagnosis and medicolegal implications. Amer J Obstet Gynecol 159:23-25, 1988.

9. Jennett RS, Duily WJR, Tarby TJ et al: Prenatal diagnosis of intracerebellar hemorrhage: case report. Am J Obst Gynecol 161:1472-5, 1990.

10. Leviton A, Pagano M, Kuban KCK: Etiologic heterogenicity of intracranial hemorrhages in preterm newborns. Pediatr Neurol 4:274-278,1988.

11. Leviton A, Pagano M, Kuban KCK, et al: The epidemiology of germinal martrix hemorrhage during the first day of life. Dev Med Child Neurol 33:138-145, 1991.

12. Sinnar S, Molteni RA, Gammon K et al: Intraventricular hemorrhage in the premature infant. A changing outlook. N Engl J Med 306:1464-1486, 1982.

13. Stewart AL, Thorburn RJ, Hope PL et al: Ultrasound appearance in very preterm infants and neurodevelopmental outcome at 18 months of age Arch Dis Child 58:598-604, 1983.