Chapter 10. Intracranial Hemorrhage: Subdural, Primary Subarachnoid, Cerebellar, Intraventricular (Term Infant), and Miscellaneous

484



UNIT IV



TABLE 10-1



INTRACRANIAL HEMORRHAGE



Major Types of Neonatal Intracranial Hemorrhage



Type of Hemorrhage



Maturation of Infant



Relative Frequency



Usual Clinical Gravity



Subdural

Primary subarachnoid

Cerebellar

Intraventricular

Miscellaneous: intraparenchymal, multiple sites



Full term > premature

Premature > full term

Premature > full term

Premature > full term

Full term > premature



Uncommon

Common

Uncommon

Common

Uncommon



Serious

Benign

Serious

Serious

Variable



hemorrhage (see later). Thus, I do not recommend

lumbar puncture as a routine diagnostic procedure

for hemorrhage.

Cerebrospinal Fluid in the Recognition

of Intracranial Hemorrhage

‘‘Traumatic’’ Lumbar Puncture. The finding of

bloody CSF in a newborn often is attributed to ‘‘traumatic’’ lumbar puncture. This conclusion primarily

relates to the relative difficulty of performing the puncture in the newborn but also to the relative frequency of

finding bloody CSF in infants without overt neurological signs. I believe that traumatic lumbar puncture in

the newborn is much less common than is generally

thought. For example, in a study in which we performed lumbar punctures on the third postnatal day

in all infants of less than 2000 g in our neonatal intensive care unit, the 76 infants who had grossly bloody

CSF with elevated protein content were evaluated

by CT scan (Table 10-2). Only 6 (8%) had no increased attenuation consistent with blood observable.

Subarachnoid blood was detectable in 22 (29%), and

intraventricular hemorrhage was noted in 48 (63%).

Although I believe that the finding of bloody CSF in an

infant is an indication for a definitive search for a locus of

intracranial hemorrhage (see subsequent discussion),

certain indirect techniques have been used to determine

whether the finding is ‘‘real’’ or related to a ‘‘traumatic’’

lumbar puncture. These approaches include determination of the ratio of fetal to adult hemoglobin in both

circulating blood and the blood in CSF, determination

of the penetration into CSF of systemically administered

fluorescein dye during the collection of CSF, highintensity transillumination of the frontal subarachnoid

space by a fiberoptic device applied to the overlying scalp,

determination of CSF glutamine levels, and detection of

D-dimers of fibrinogen.1-5 None of these approaches is

in wide use.

TABLE 10-2



Computed Tomography Scan

Correlates of Bloody Cerebrospinal

Fluid in 76 Infants Weighing Less

than 2000 g



Blood on Scan

None

Subarachnoid

Germinal matrix–

intraventricular



No. of

Patients



Percentage of

Total Group



6

22



8%

29%



48



63%



Cerebrospinal Fluid Findings of Intracranial

Hemorrhage. CSF findings that indicate intracranial

hemorrhage are, primarily, xanthochromia of the centrifuged fluid and elevations of the number of red

blood cells (RBCs) and the protein content. Particular

emphasis should be placed on the occurrence of combinations of findings rather than on a single, isolated

abnormality.

Xanthochromia of the CSF develops within several

hours after hemorrhage in older children and adults.

(In one particularly large study of adults with subarachnoid hemorrhage, nearly 90% exhibited xanthochromia

within 12 hours of the ictus.6) The evolution of xanthochromia in newborns has not been studied systematically, although I have the impression that it occurs more

slowly than in older patients. This slower evolution may

relate to a delay in the induction of the enzyme, heme

oxygenase, which is located in the arachnoid and is

responsible for the conversion of heme to bilirubin,

the major pigment accounting for xanthochromia of

the CSF.7 In adult rats, the activity of heme oxygenase

reaches peak values 6 to 12 hours after injection of heme

into the subarachnoid space.7 These data are closely

comparable to the clinical observations with adult

patients cited. Determination of the significance of xanthochromia in newborns is occasionally difficult in the

presence of elevated serum bilirubin levels. Although

this difficulty is rarely a major consideration, demonstration of spectrophotometric differences between

CSF bilirubin pigments derived from the systemic circulation and those derived from the hemorrhage could

be used in the evaluation.8 When xanthochromia is

evaluated in the context of the total CSF profile, difficulties in assessing significance are very unusual.

The number of RBCs that should be considered significant is difficult to state conclusively, in part because

of the remarkably wide range of values considered

normal (see Chapter 4).9-16 For example, some observers

consider as normal a few hundred RBCs/mm3. In studies

of infants in neonatal intensive care facilities, median

values of 100 to 200 RBCs/mm3 have been observed. In

the only report with ultrasonographic correlates, among

43 infants of less than 1500 g birth weight, the median

value was 112, but the mean value was 785, and 20% of

CSF samples had more than 1000 RBCs/mm3.16 These

infants did not exhibit ultrasonographic evidence of intracranial hemorrhage. However, exclusion of minor

subarachnoid hemorrhage by cranial ultrasonography

is not reliable. Thus, the data indicate that findings of

more than 100 RBCs/mm3 in the newborn are common,

and in the very-low-birth-weight infants, values greater



Chapter 10



Intracranial Hemorrhage: Subdural, Primary Subarachnoid, Cerebellar, Intraventricular, and Miscellaneous



than 1000 occur in a substantial minority in the absence

of apparently clinically significant intracranial hemorrhage. Again, the combination of findings is important in

the evaluation.

Values for CSF protein are higher in newborns in an

intensive care nursery than in older children. In the

series of Sarff and co-workers,15 an average protein

content in CSF of 90 mg/dL was observed for term

infants, and a content of 115 mg/dL was observed for

preterm infants. We obtained similar data.14 In general,

values for CSF protein are higher in the most premature infants; in one series, the mean value at 26 to

28 weeks of postconceptional age was 177 mg/dL,

and at 35 to 37 weeks, it was 109 mg/dL.16 Values in

intracranial hemorrhage are usually severalfold or

higher than these.

Finally, determination of the CSF glucose level may be

helpful in the diagnosis. In term and preterm infants

evaluated in a neonatal intensive care unit and free of

intracranial infection, the ratios of CSF to blood glucose

levels are relatively high (i.e., 0.81 and 0.74, respectively).15 As with CSF protein levels, values for CSF glucose tend to be higher in the most premature infants; in

one series, the mean value at 26 to 28 weeks was 85 mg/

dL, and at 38 to 40 weeks, it was 44 mg/dL.16 After neonatal intracranial hemorrhage, the CSF glucose level is

frequently low (Table 10-3).17-21 Indeed, in one study in

which serial lumbar punctures were performed (for

therapeutic purposes) on 13 infants with intraventricular hemorrhage, the CSF glucose concentration

decreased on subsequent measurements in all the

infants.21 Eleven of the 13 infants had CSF glucose

values lower than 30 mg/dL at some point subsequent

to the hemorrhage, and values of 10 mg/dL or less were

common. The low values occurred as early as 1 day after

the hemorrhage but usually became apparent between

approximately 5 and 15 days after the hemorrhage. (The

hypoglycorrhachia observed after subarachnoid hemorrhage in adults reaches lowest values after a similar time

interval.22,23) The depressed CSF glucose values persist

for weeks and have been noted as long as 3 months after

the hemorrhage.18,19

The basis of hypoglycorrhachia is probably related to an

impairment of the mechanisms of glucose transport

into CSF. This impairment may occur at the level of

the plasma membrane glucose transporter.23 Other

proposed pathogeneses have included glucose use by

RBCs or by contiguous brain. The former is ruled out

by the lack of correlation between RBC number and



TABLE 10-3



Major Features of Hypoglycorrhachia

after Neonatal Intracranial

Hemorrhage



Nearly uniform occurrence after major hemorrhage

Onset usually 5 to 15 days after hemorrhage

Duration of weeks to months

Accompanied by concomitant decrease in cerebrospinal

fluid lactate level

Mechanism not proved but probably related to impaired glucose transport



485



CSF glucose level and by the negligible rates of glucose

consumption observed when the cellular CSF is incubated in vitro. The possibility of excessive anaerobic

use of glucose by contiguous brain rendered hypoxicischemic by hemorrhage, ventricular dilation, or other

insult24 appears unlikely in view of simultaneous, serial

determinations of CSF glucose and lactate.21 Thus, in

13 infants described with CSF hypoglycorrhachia, CSF

glucose and lactate concentrations decreased pari

passu; if anaerobic use of glucose had been operative,

a concomitant increase in CSF lactate would have been

expected. These observations favor the notion of a

defect in glucose transport mechanisms.

An important practical problem arises when the low CSF

glucose level is accompanied by pleocytosis and elevated protein

content. This not uncommon occurrence is related presumably to meningeal inflammation from blood products and raises the question of bacterial meningitis.

Although appropriate cultures are always indicated,

and even initiation of antimicrobial therapy may be

necessary (until results of cultures are known), the

CSF formula of pleocytosis, depressed glucose, and elevated protein content is not infrequent after neonatal

intracranial hemorrhage.

The optimal imaging procedure for diagnosis becomes

apparent in the following discussions of the respective

lesions, and the relative value of cranial ultrasonography, CT, and MRI in diagnosis is reviewed in Chapter

4. Suffice it to say here that cranial ultrasonography is

often used as a screening procedure, CT is a more

definitive approach, and MRI is the most effective

methodology. The sometimes confusing features of

MRI signal change after neonatal parenchymal hemorrhage are reviewed in Table 10-4. (On the first day after

the hemorrhage, CT is perhaps more sensitive for

detection of hemorrhage than is MRI.) The MRI

changes relate primarily to changes in hemoglobin

state, which proceed from predominately intracellular

deoxyhemoglobin, to intracellular methemoglobin, to

extracellular methemoglobin, and finally hemosiderin.

SUBDURAL HEMORRHAGE

Subdural hemorrhage is the least common of the

major varieties of neonatal intracranial hemorrhage.

Recognition of the disorder is important because in



TABLE 10-4



Predominant Magnetic Resonance

Imaging Signal Changes after

Parenchymal Hemorrhage

SIGNAL CHANGES



Age of Hemorrhage



T1 Weighted



T2 Weighted



1–3 days

3–10 days

10–21 days

3–6 wk

6 wk–10 mo



Isointense

High

High

High

Isointense



Low

Low

High

High

Low



Adapted from Rutherford M: MRI of the Neonatal brain, Philadelphia:

2002, WB Saunders, and from personal experience.



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INTRACRANIAL HEMORRHAGE



patients with large hemorrhages, therapeutic intervention can be lifesaving.



TABLE 10-5



Neuropathology of Subdural

Hemorrhage



Source of Bleeding

Tentorial Laceration

Straight sinus, vein of

Galen, transverse sinus,

and infratentorial veins



Anatomy of Major Veins and Sinuses

The neuropathology of neonatal subdural hemorrhage

is readily understood after a brief review of the major

anatomical features of the veins and sinuses involved in

the production of such hemorrhage (Fig. 10-1). The

deep venous drainage of the cerebrum empties into

the great cerebral vein of Galen at the junction of the

tentorium and falx. The confluence of the vein of Galen

and the inferior sagittal sinus, the latter located in the

inferior margin of the falx, forms the straight sinus.

This sinus proceeds directly posteriorly and joins the

superior sagittal sinus, located in the superior margin

of the falx, to form the transverse sinus. Blood in the

transverse sinuses, located in the lateral margins of the

tentorium, proceeds eventually to the jugular vein.

Blood in the posterior fossa in part drains into the occipital sinus, which empties into the torcular. The

superficial portion of the cerebrum is drained by the

superficial, bridging cerebral veins, which empty into

the superior sagittal sinus. Tears of these several veins

or venous sinuses, occurring secondary to forces to be

described and often accompanying laceration of the

dura, result in subdural hemorrhage.

Major Varieties of Subdural Hemorrhage

The major varieties of neonatal subdural hemorrhage

include the following (Table 10-5): tentorial laceration

with rupture principally of the straight sinus, transverse

sinus, vein of Galen, or smaller infratentorial veins;



Infratentorial (posterior

fossa), supratentorial



Occipital Osteodiastasis

Occipital sinus



Infratentorial (posterior

fossa)



Falx Laceration

Inferior sagittal sinus



Longitudinal cerebral

fissure



Superficial Cerebral Veins



Neuropathology



Location of Hematoma



Surface of cerebral

convexity



occipital osteodiastasis with rupture of the occipital

sinus; falx laceration with rupture of the inferior sagittal sinus; and rupture of bridging, superficial cerebral

veins.

Tentorial Laceration. With major, lethal tears of

the tentorium, hemorrhage is most often infratentorial.25-31 This finding is the case particularly with

rupture of the vein of Galen or straight sinus or with

severe involvement of the transverse sinus. The clots

extend into the posterior fossa and, when large, very

rapidly result in lethal compression of the brain

stem.25,26,28,32-35 (Massive infratentorial hemorrhage

from a rupture of the vein of Galen also may occur

without visible tear of the tentorium.)

Lesser degrees of tentorial injury, with the advent

of modern brain imaging techniques, are recognized



Superior sagittal sinus



Inferior sagittal sinus

Vein of Galen

Cavernous sinus

Figure 10-1 Major cranial veins and dural sinuses.

The ventricular system is also outlined. The superior

sagittal sinus runs in the superior border of the falx;

the inferior sagittal and straight sinuses run in the

inferior border; and the transverse sinus runs

in the outer border of the tentorium. The occipital

sinus (shown but not labeled) runs in the midline of

the posterior fossa and empties into the torcular.



Straight sinus



Transverse sinus

Pterygoid plexus



Anterior facial vein



Internal jugular vein



Chapter 10

TABLE 10-6



Intracranial Hemorrhage: Subdural, Primary Subarachnoid, Cerebellar, Intraventricular, and Miscellaneous



Spectrum of Tentorial HemorrhageÃ



Anterior Extension

Excrescence (on free edge of tentorium)

Velum interpositum

Intraventricular

Subarachnoid

Superior Extension

Supratentorial subdural

Cerebral parenchymal hemorrhage{

Inferior Extension

Infratentorial (posterior fossa) subdural

Cerebellar parenchymal hemorrhage{

Ã

{



See text for references.

Often associated hemorrhage rather than true extension.



now to be more common than the major lethal lacerations just described and probably are much more

common than previously suspected. Thus, several

series (with a cumulative total of >200 newborns)

documented a spectrum of intracranial hemorrhage,

primarily subdural, associated with apparent or presumed tentorial injury.25,27-31,36-44a This spectrum,

summarized in Table 10-6, includes both infratentorial

(usually retrocerebellar) subdural hemorrhage, secondary to inferior extension, and supratentorial subdural hemorrhage, secondary to superior extension

(Fig. 10-2). (The infratentorial, posterior fossa subdural

hemorrhages may relate also to tear of cerebellar bridging veins, with or without accompanying overt tears of

the tentorium.) In addition to infratentorial or supratentorial extension, the hemorrhage of a tentorial tear

may remain confined to the free edge of the tentorium, most

often near the junction of the tentorium and falx, or it

may extend anteriorly further into the subarachnoid

space, velum interpositum, or ventricular system

(see Table 10-6). Very minor varieties of this spectrum

may account for the relatively high RBC counts in CSF

in ‘‘normal’’ newborns (see earlier discussion).

Occipital Osteodiastasis. A prominent traumatic

lesion in some infants who die after breech delivery is

occipital diastasis with posterior fossa subdural hemorrhage and laceration of the cerebellum (see Table 10-5

and Chapter 22).41,45,46 The diastasis lesion consists of

traumatic separation of the cartilaginous joint between



487



the squamous and lateral portions of the occipital bone.45,47 In its most severe form, the dura and occipital sinuses are torn, resulting in massive subdural

hemorrhage in the posterior fossa and cerebellar laceration. The bony lesion may be more common than

has generally been recognized because it is missed

easily at postmortem examination.

Falx Laceration. Laceration of the falx alone is distinctly less common than laceration of the tentorium

and usually occurs at a point near the junction of the

falx with the tentorium. The source of bleeding is usually the inferior sagittal sinus, and the clot is located in

the longitudinal cerebral fissure over the corpus callosum (see Table 10-5).

Superficial Cerebral Vein Rupture. Rupture of the

bridging, superficial cerebral veins results in hemorrhage over the cerebral convexity, the well-known convexity subdural hematoma (see Table 10-5). The

hematoma is usually more extensive over the lateral

aspect of the convexity than near the superior sagittal

sinus. Although convexity subdural hemorrhage is

usually unilateral, bilateral lesions are not uncommon.39,40,43,48-50 Subarachnoid blood is a typical

accompaniment. Convexity subdural hemorrhage is

not a rare event, and, indeed, in small amounts, it is a

frequent incidental finding at autopsy of the term

infant.35 The trauma that leads to the hemorrhage

may result also in cerebral contusion, which, in fact,

may dominate the clinical picture.

Pathogenesis

Subdural hemorrhage in the neonatal period is most

commonly a traumatic lesion, when the lesion is

large.25-31,33,38-41,49,51 Most cases have involved fullterm infants. However, as the incidence of grossly traumatic deliveries and of subdural hemorrhages has

decreased, the relative proportion of premature infants

with subdural hemorrhage has increased. Indeed, in

some surveys, the proportion of cases in premature

and full-term infants has been approximately similar.45,52 However, most modern reports still indicate a

predominance of full-term infants, especially with cerebral convexity subdural hemorrhages.27-31,38,40,41,53,54



Figure 10-2 Tentorial subdural hemorrhage at the

junction of the falx and tentorium. A, Computed tomography (CT) scan along the free margin of tentorium, demonstrating blood accumulated in the

quadrigeminal areas and at the free edge of the tentorium (arrowhead). B, Coronal CT scan, reconstruction view, disclosing the hemorrhage located at the

falcotentorial junction. (From Huang CC, Shen EY:

Tentorial subdural hemorrhage in term newborns:

Ultrasonographic diagnosis and clinical correlates,

Pediatr Neurol 7:171-177, 1991.)



A



B



488



UNIT IV



TABLE 10-7



INTRACRANIAL HEMORRHAGE



Pathogenesis of Neonatal Subdural

Hemorrhage



At Risk



Predisposing Factors



Mother



Primiparous

Older multiparous

Small birth canal

Large full term

Premature

Precipitous

Prolonged

Breech extraction

Foot, face, brow presentation

Difficult forceps or vacuum extraction

Difficult rotation



Infant

Labor

Delivery



The pathogenesis of major neonatal subdural hemorrhage is best considered in terms of predisposing

factors referable to the mother, the infant, the duration

and progression of labor, and the manner of delivery

(Table 10-7). Thus, large subdural hemorrhage is most

likely to occur under the following circumstances

(1) when the infant is relatively large and the birth

canal is relatively small; (2) when the skull is unusually

compliant, as in a premature infant; (3) when the pelvic

structures are unusually rigid, as in a primiparous or an

older multiparous mother; (4) when the duration of

labor is either unusually brief, not allowing enough

time for dilation of the pelvic structures, or unusually

long, subjecting the head to prolonged compression

and molding; (5) when the head must pass through

a birth canal not gradually adapted to it, as in foot or

breech presentation; (6) when the head is subjected to

unusual deforming stresses, such as in face or brow

presentation; or (7) when the delivery requires difficult

vacuum extraction or challenging forceps or rotational

maneuvers.

Under the circumstances just described, excessive

vertical molding and frontal-occipital elongation or



oblique expansion of the head occur (Fig. 10-3).

These effects result in stretching of both the falx and

one or both leaves of the tentorium, with a tendency for

tearing of the tentorium, particularly near its junction

with the falx, or, less commonly, tearing of the falx

itself. Even if a laceration does not occur, the sinuses

into which the vein of Galen drains are stretched, and

the result may be a tear of the vein of Galen or its

immediate tributaries. Similarly, rupture of cerebellar

bridging veins may occur in this context. Tear of the

falx occurs particularly with extreme frontal-occipital

elongation, especially that associated with face or

brow presentation. Extreme vertical molding appears

to underlie many tears of superficial cerebral veins

and the formation of convexity subdural hematoma.

In the special case of occipital osteodiastasis with

breech delivery, the injury results from suboccipital

pressure, which most commonly occurs if the fetus is

forcibly hyperextended with the head trapped beneath

the symphysis.41,45 The lower edge of the squamous

portion of the occipital bone is displaced in a forward

direction, thus lacerating dura, occipital sinus, or cerebellum. (A roughly analogous situation in the supratentorial compartment probably occurs with difficult

forceps extractions, which may result in skull fracture,

convexity subdural hemorrhage, and cerebral contusion by direct compressive effects.)

Fortunately, many of the aforementioned pathogenetic factors have been eliminated by vastly improved

obstetrical practices in most medical centers. Indeed,

subdural hemorrhage is by no means invariably a traumatic lesion. For example, coagulation disturbances

(e.g., maternal aspirin ingestion, early vitamin K deficiency secondary to maternal phenobarbital administration) may play at least a contributing role in some

infants.40,41,55,56 Moreover, with the advent of intrauterine brain imaging, subdural hematoma has been

identified in the fetus before intrapartum events could

be responsible.56-60 In one report, maternal abuse



Figure 10-3 The likely mechanism of tentorial

hemorrhage after vacuum extraction. A, The

vein of Galen joins the straight sinus and tributaries from the deep venous system at the tentorial notch. B, Traction in the occipital-frontal

direction produces stress on the vertical axis of

the falx and tentorium with kinking of the deep

venous system. Engorgement and venous rupture lead to hemorrhage into the surrounding

subdural space. (From Hanigan WC, Morgan

AM, Stahlberg LK, Hiller JL: Tentorial hemorrhage

associated with vacuum extraction, Pediatrics

85:534-539, 1990.)



A



B



Chapter 10



Intracranial Hemorrhage: Subdural, Primary Subarachnoid, Cerebellar, Intraventricular, and Miscellaneous



with blunt abdominal trauma was documented in an

infant with bilateral subdural hematomas identified

in the first day of life.49 In other intrauterine cases,

other forms of external abdominal pressure or coagulopathy have been important.56 Moreover, in the

largest single series of neonatal subdural hemorrhage

(n = 48), 31% of cases had ‘‘simple spontaneous’’

vaginal delivery.29 Indeed, in one prospective MRI

study of 111 asymptomatic term infants, 9 (8%)

infants had subdural hemorrhage, and only 5 of

these had a complicated vaginal delivery (failed

vacuum extraction followed by forceps delivery).44

In a later study, utilizing 3.0 T-MRI, 15 of 65

(23%) vaginally delivered asymptomatic term infants

exhibited small posterior fossa subdural hemorrhages.44a At any rate, on modern obstetrical services,

subdural hemorrhage of any sort is a very uncommon

occurrence. Indeed, considered together, subdural

hemorrhages are by far the least common of the

major varieties of neonatal intracranial hemorrhages.

Clinical Features

In contrast to the considerable amount of medical writings relative to the neuropathological and radiological

aspects of subdural hemorrhage, surprisingly few clinical neurological data are available. However, some

important conclusions can be drawn from our own

observations and from those recorded by other investigators.25-32,37,39-41,43,46,54,61-74

Tentorial Laceration, Occipital Diastasis, and

Syndromes Associated with Posterior Fossa

Subdural Hematoma

Rapidly Lethal Syndromes. Tentorial laceration with

massive infratentorial hemorrhage is associated with

neurological disturbance from the time of birth.

The majority of the most severely affected infants

weigh more than 4000 g at birth.27,33 Initially, the

baby demonstrates signs of midbrain-upper pons

compression (i.e., stupor or coma, skew deviation of

eyes with lateral deviation that is not altered by doll’s

eyes maneuver, and unequal pupils, with some disturbance of response to light). With such infratentorial

hemorrhage, nuchal rigidity with retrocollis or opisthotonos may also be a helpful early sign.28,61 When

these features are associated with bradycardia,25 a large

infratentorial clot with brain stem compression should

be suspected. Over minutes to hours, as the clot

becomes larger, stupor progresses to coma, pupils

may become fixed and dilated, and signs of lower

brain stem compression appear. Ocular bobbing and

ataxic respirations may occur, and finally, respiratory

arrest ensues.

The severe clinical syndrome associated with occipital

osteodiastasis resembles that described for major tentorial laceration. With occipital osteodiastasis, delivery

is characteristically breech. A depressed Apgar score

at 1 minute is common, and the course is one of

rapid deterioration. In the six infants described by

Wigglesworth and Husemeyer,45 the age at the time

of death ranged from 7 to 45 hours.



489



Less Malignant Syndromes Associated with Posterior

Fossa Subdural Hematoma. Less severe clinical syndromes accompany most examples of posterior fossa subdural hematoma currently encountered on obstetrical

and neonatal services.27-30,37,40,41,43,54,74 These syndromes appear to result from smaller tears of the tentorium than those just noted, from rupture of bridging

veins from superior cerebellum without tentorial tear,

or, perhaps, from lesser degrees of occipital diastasis.

The clinical syndrome consists of three phases. First,

no neurological signs are apparent for a period that

varies from several hours after birth (usually a difficult

vacuum, forceps, or breech extraction or both) to as

much as 3 or 4 days of age. Most commonly, the interval is less than 24 hours. Presumably, this period is

associated with slow enlargement of the hematoma.

Second, various signs develop referable to increased

intracranial pressure (e.g., full fontanelle, irritability,

‘‘lethargy’’). Most of these signs appear to relate to

the evolution of hydrocephalus secondary to a block

of CSF flow in the posterior fossa. Third, signs referable to disturbance of brain stem develop, including

respiratory abnormalities, apnea, bradycardia, oculomotor abnormalities, skew deviation of eyes, and

facial paresis. These deficits relate to direct compressive

effects of the posterior fossa hematoma. In addition to

brain stem signs, seizures occur in the majority of

infants, perhaps because of accompanying subarachnoid blood. In infants who clearly worsen over hours

or a day or more, as do approximately one half, lethal

brain stem compression may develop.

In more recent years, particularly small posterior fossa

subdural hemorrhages have been identified by CT or

MRI. In one carefully studied series of 26 small subdural hemorrhages detected by CT, 19 were infratentorial,

and the leading clinical features were respiratory

abnormalities (apnea, ‘‘dusky episodes’’) in approximately 60% and neurological features (subtle seizures,

hypotonia) in approximately 40%.43 None of the

infants developed progressive neurological signs.

Falx Laceration

No careful description of the clinical course of falx tears

with major subdural hemorrhage is available. However,

it is likely that initially bilateral cerebral signs will

appear, in view of the locus of the hematoma. However, striking neurological findings probably do not

develop until the clot has extended infratentorially,

and the resulting syndrome is then similar to that

described for tentorial laceration and posterior fossa

subdural hematoma.

Cerebral Convexity Subdural Hemorrhage

Subdural hemorrhage over the cerebral convexities is

associated with at least three neurological syndromes

(Table 10-8). First, and probably most commonly,

minor degrees of hemorrhage occur, and minimal or

no clinical signs are apparent. Irritability, a ‘‘hyperalert’’

appearance, unexplained apneic episodes, or no signs

have been noted.25,43,44

Second, signs of focal cerebral disturbance may occur,

with the most common time of onset being the



490



UNIT IV



TABLE 10-8



INTRACRANIAL HEMORRHAGE



Neurological Syndromes Associated

with Cerebral Convexity Subdural

Hemorrhage



Minimal or no clinical signs

Focal cerebral syndrome: hemiparesis, deviation of eyes to

side of lesion, focal seizures, homolateral pupillary abnormality

Chronic subdural effusion



second or third day of life. With this syndrome, seizures, often focal, are common and are frequently

accompanied by other focal cerebral signs (e.g., hemiparesis, deviation of eyes to the side contralateral to

the hemiparesis, although the eyes move by doll’s

eyes maneuver, because this is a cerebral lesion).

These focal cerebral signs are definite, although usually

not striking. The most distinctive neurological sign

with major convexity subdural hemorrhage is dysfunction of the third cranial nerve on the side of the hematoma; this dysfunction is usually manifested by a

nonreactive or poorly reactive, dilated pupil.25,69-72

The latter occurs secondary to compression of the

third nerve by herniation of the temporal lobe through

the tentorial notch. An excellent example of such a

neurological syndrome associated with subdural

hematoma was a newborn with hemophilia whom we

studied.72

A third clinical presentation may be the occurrence

of subdural hemorrhage in the neonatal period with

few clinical signs and then the development over the

next several months of a chronic subdural effusion. It is

certainly well known that many infants presenting in

the first 6 months of life with an enlarging head,

increased transillumination, and chronic subdural

effusions have no known cause for the lesion and

that subdural hemorrhage can evolve into subdural

effusion.75-77



A



B



Diagnosis

The diagnosis of major neonatal subdural hemorrhage

depends principally on recognition of the clinical syndrome, with subsequent definitive demonstration by a

brain imaging study.

Clinical Syndromes

The clinical syndromes previously reviewed are often

sufficiently distinctive to raise the suspicion of subdural

hemorrhage, as well as the specific variety thereof.

Neurological signs primarily referable to the brain stem

should suggest infratentorial hematoma. Neurological

signs primarily referable to the cerebrum should suggest

convexity subdural hematoma. These signs should provoke more definitive and prompt diagnostic studies

because the clinical course may deteriorate very rapidly.

Lumbar puncture is not a good choice for diagnostic

study in this setting because of the possibility of provoking herniation, either of cerebellar tonsils into the foramen magnum in the presence of a posterior fossa

subdural hematoma or of temporal lobe into the tentorial notch in the presence of a large unilateral convexity

subdural hematoma.

Computed Tomography, Magnetic Resonance

Imaging, and Ultrasound Scans

CT is a safe, definitive means of demonstrating the site

and extent of neonatal subdural hemorrhage. Examples

of the CT demonstration of the varieties of subdural

hemorrhage just discussed are shown in Figures 10-2,

10-4, and 10-5.

MRI is more effective than CT in the delineation

of posterior fossa subdural hemorrhage (Fig. 10-6).31,

40,78-80 This particular superiority of MRI in evaluation

of posterior fossa hemorrhage applies to other types

of lesions in this location (see Chapter 4).

Detection of subdural hematoma by ultrasound scanning (Fig. 10-7), although reported, generally is difficult.28,49,81 Moreover, even when these hematomas



C



Figure 10-4 Subdural hemorrhage, computed tomography scans. A, Convexity subdural hematoma in a newborn with severe hemophilia A. Note

the area of increased attenuation on the right, representing the hematoma, and the shift of ventricles to the left. B, Convexity subdural hematoma

on the left in a 1-day-old infant delivered by forceps for head entrapment. The pupil was dilated on the side of the lesion. Note also deviation of

midline structures to the right, and probable tentorial tear, with associated hemorrhage. C, Probable falx tear in a newborn of 4780 g delivered by a

difficult breech extraction. Note the small circular area of increased attenuation in the midline, representing hemorrhage in the inferior margin of the

falx.



Chapter 10



A



Intracranial Hemorrhage: Subdural, Primary Subarachnoid, Cerebellar, Intraventricular, and Miscellaneous



B



491



C



Figure 10-5 Posterior fossa subdural hemorrhage, computed tomography scans. In the first 24 hours of life, the infant exhibited apnea,

bradycardia, and quadriplegia. A, Axial and, B, coronal scans show the hemorrhage and obstructive hydrocephalus. C, The scan performed 1

year after surgery in the neonatal period shows a small defect in the left cerebellum and normal supratentorial structures. (From Perrin RG, Rutka JT,

Drake JM, Meltzer H, et al: Management and outcomes of posterior fossa subdural hematomas in neonates, Neurosurgery 40:1190-1199, 1997.)



are detected, the extent and distribution of supratentorial lesions are usually demonstrated far better by CT or

MRI and of infratentorial lesions by MRI. The major

difficulty of ultrasound scanning in this setting relates

to acoustical interference by bone at the margins of

the anterior fontanelle and to near-field transducer

artifacts.



Skull Radiographs

Occipital osteodiastasis may be demonstrated by

skull radiographs. The lateral view shows the lesion

(Fig. 10-8).

Prognosis

Infants with major lacerations of the tentorium and falx

and massive degrees of subdural hemorrhage have a

very poor prognosis. Nearly all die; the rare survivor

is left with hydrocephalus secondary to obstruction of

CSF flow at the tentorial notch or over the convexities.

Similarly, severe occipital diastasis and its complications have been associated with a poor outcome.

Nevertheless, it is possible that early diagnosis could

lead to beneficial intervention.

Although they are often serious lesions, moderate

posterior fossa subdural hematomas, recognized frequently

in recent years, primarily by CT and MRI, are



Figure 10-6 Posterior fossa subdural hemorrhage, magnetic resonance imaging (MRI) scan. MRI was performed on the tenth postnatal

day of an infant born after a complicated breech delivery. Note the

increased signal indicative of blood over the cerebellar hemisphere

(arrow). (Courtesy of Dr. Omar Khwaja.)



Figure 10-7 Subdural hemorrhage. Ultrasound scan of a full-term

infant transferred 10 days after traumatic delivery. The coronal scan

shows the subdural hemorrhage on the left (margin outlined by arrowheads), displacing the ventricles to the right. The subdural lesion was

isodense with brain on a computed tomography scan. (Courtesy of Dr.

Gary D. Shackelford.)



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UNIT IV



INTRACRANIAL HEMORRHAGE



A



B



Figure 10-8 Occipital osteodiastasis. Schematic diagram

of the cranium, illustrating, A, the normal state (arrow) and,

B, occipital osteodiastasis, with posterior fossa encroachment (arrow). C, Lateral radiograph of the skull demonstrating

occipital osteodiastasis in an autopsy case (arrow). (From

Pape KE, Wigglesworth JS: Hemorrhage, Ischemia, and the

Perinatal Brain. Philadelphia: 1979, JB Lippincott.)



C

associated with an outcome that is variable but dependent on size, rapidity of diagnosis and, when necessary,

intervention (Table 10-9).28-30,37,40,41,54,74 Thus, of 30

surgically treated infants, 80% either were normal or

exhibited minor neurological deficits on follow-up.

Approximately 15% of surgically treated patients developed communicating hydrocephalus that required

shunt placement. Of 40 nonsurgically treated infants,

nearly 90% had a favorable outcome (see Table 10-9).

In earlier reports, as many as 40% to 50% of infants

who did not undergo operations died, probably



TABLE 10-9



Outcome with Posterior Fossa

Subdural HemorrhageÃ



Management



OUTCOME

Surgical Evacuation

(n = 70)

Yes (30)

No (40)

Ã



because of rapidly progressive lesions, the gravity of

which escaped prompt detection. The small posterior

fossa subdural hemorrhages described in hospitalbased series are associated with no major sequelae or

death.44,82

The prognosis of patients with moderate or large convexity subdural hemorrhage is relatively good; from 50% to

90% of affected infants are well on follow-up.29,3941,71,83 The remainder are left with focal cerebral signs

and, occasionally, hydrocephalus. The deficits appear to

relate to associated parenchymal lesions. The small convexity subdural hemorrhages detected by widespread

imaging in recent years have a generally favorable

outcome.44,82



Good to

Excellent



Major

Sequelae



Deaths



80%

88%



13%

7%



7%

5%



See text for references; also includes personal cases. Lesions have

been of moderate or large size.



Tentorial and Falx Lacerations, Occipital

Osteodiastasis, and Posterior Fossa Subdural

Hematoma

The severity of the initial trauma and the rapid progression to brain stem compromise have rendered effective

treatment nearly impossible in major tears of the



Chapter 10



Intracranial Hemorrhage: Subdural, Primary Subarachnoid, Cerebellar, Intraventricular, and Miscellaneous



tentorium and falx and in overt occipital osteodiastasis

with severe subdural hemorrhage. Theoretically, rapid

surgical evacuation may provide some hope for salvage

of the affected baby. Some support for this suggestion

is obtained by the experience just reviewed with less

severe posterior fossa subdural hematomas (see Table

10-9). Rapid detection and prompt surgical evacuation

in the presence of progression of neurological signs

have been of value in management of these lesions.

However, a normal outcome has been documented in

posterior fossa subdural hematoma without surgical

intervention (see Table 10-9); I have observed several

such cases. Thus, close surveillance alone is appropriate

in the absence of major neurological signs, particularly

brain stem signs, or worsening neurological status.

Surgery should not be delayed if clear neurological

deterioration becomes apparent. With small lesions,

close surveillance is almost always followed by a favorable outcome.

Cerebral Convexity Subdural Hematoma

Effective management of the infant with an acute convexity subdural hematoma requires careful sequential

clinical observation. Surgery is not mandatory if the

infant is stable neurologically.29 The need for surgery

is based on large size of the lesion, signs of increased

intracranial pressure, and neurological deficits, particularly if findings suggest incipient transtentorial

herniation. If a stable subdural hemorrhage evolves to

subdural effusion, subdural taps can be used to reduce

signs of increased intracranial pressure and to prevent

the development of craniocerebral disproportion, the

latter serving only to perpetuate subdural bleeding.76

Repeated subdural taps should not be performed if

the infant is asymptomatic and if the head is not growing rapidly. The development of constricting ‘‘subdural

membranes’’ was overestimated in the past. Surgery is

necessary if subdural taps are not effective in controlling the two complications just discussed. The smaller

convexity subdural hemorrhages detected by imaging

in recent years rarely require intervention.

PRIMARY SUBARACHNOID HEMORRHAGE

Primary subarachnoid hemorrhage refers to hemorrhage

within the subarachnoid space that is not secondary

to extension from subdural, intraventricular, or cerebellar hemorrhage. Moreover, also excluded from this

category are cases in which subarachnoid blood is secondary to extension from intracerebral hematoma, a

structural vascular lesion (e.g., aneurysm or arteriovenous malformation), tumor, hemorrhagic infarction, or

major coagulation disturbance (see later discussion of

miscellaneous causes of intracranial hemorrhage).

Primary subarachnoid hemorrhage, defined in this

way, is a very frequent variety of neonatal intracranial

hemorrhage, mostly because the category includes the

many newborn infants, particularly premature infants,

with a few hundred RBCs per cubic millimeter in the

CSF. The frequency of clinically significant primary

subarachnoid hemorrhage was overestimated in the

past, particularly in the premature infant but also in



493



the full-term infant, mostly because of the lack of

brain imaging data to identify intraventricular hemorrhage. As reviewed in Table 10-2, in our own series of

infants weighing less than 2000 g with grossly bloody

CSF, only 29% exhibited subarachnoid hemorrhage

alone, and 63% exhibited intraventricular hemorrhage

(although with blood also in the subarachnoid space).

Moreover, even many term infants with bloody CSF

who, in the past, would have been considered to have

primary subarachnoid hemorrhage on clinical grounds,

have been shown by ultrasound, CT, or MRI scans to

have intraventricular hemorrhage (see later section).

Finally, a localized variant of subarachnoid hemorrhage, involving the subpial space and superficial cerebral cortex, should also be recognized in this context;

this lesion often occurs with subarachnoid hemorrhage and on brain imaging may be difficult to distinguish from typical primary subarachnoid hemorrhage

(see later).

Neuropathology

Blood is usually located most prominently in the piaarachnoid space over the cerebral convexities, especially posteriorly, and in the posterior fossa.52,84 Small

amounts of subarachnoid blood are found not infrequently at postmortem examinations of newborns not

suspected clinically of having sustained intracranial

hemorrhage.35 Less commonly, large amounts of

blood are observed. The source of the bleeding in primary subarachnoid hemorrhage is presumed to be

small vascular channels derived from the involuting

anastomoses between leptomeningeal arteries present

during brain development.85 Origin from bridging

veins within the subarachnoid space is also possible.46

At any rate, primary subarachnoid hemorrhage in newborn patients is unlike the dramatic large vessel, arterial

hemorrhage in older patients.

Neuropathological complications of neonatal primary

subarachnoid hemorrhage are very unusual. Even in

major degrees of hemorrhage, significantly increased

intracranial pressure with brain stem compression is

rare. The only significant, albeit very uncommon, sequela clearly related to the hemorrhage is hydrocephalus. The latter is secondary either to adhesions around

the outflow of the fourth ventricle or around the tentorial notch, which result in obstruction to CSF flow,

or to adhesions over the cerebral convexities, which

result in impaired CSF flow or absorption.

The variant of subarachnoid hemorrhage noted earlier

involves localized bleeding in the subpial region, with

involvement of the most superficial aspect of cerebral

cortex.74,86,87 Although this hemorrhage often occurs

together with subarachnoid hemorrhage, in subpial

hemorrhage, the blood is found beneath the pia and

is contiguous with bleeding in the most superficial,

largely glial-populated region of cerebral cortex. The

usual location for this type of hemorrhage is in the

region of the anterior temporal lobe, near the pterion,

(a point at the junction of the coronal, squamous

sphenosquamous, and sphenofrontal sutures) or in

localized cerebral regions beneath cranial sutures.



494



UNIT IV



INTRACRANIAL HEMORRHAGE



Pathogenesis

The pathogenesis of neonatal primary subarachnoid

hemorrhage is not entirely understood, but most of

the major hemorrhages appear to relate, on clinical

grounds, to trauma or to circulatory events related to

prematurity. The relationships of trauma to the genesis

of major subarachnoid hemorrhage are similar in many

respects to those described earlier for subdural hemorrhage. The relationships to prematurity are similar to

those described in Chapter 11 for germinal matrix–

intraventricular hemorrhage of the premature infant.

Common to both pathogenetic themes is the substrate

of maturation-dependent involution of leptomeningeal

anastomotic channels.85 The pathogenesis of the

common smaller subarachnoid hemorrhages is unclear,

because most of these hemorrhages occur without any

apparent traumatic or circulatory abnormality.

The interesting subpial hemorrhages may relate to local

trauma with resulting disruption of small veins because

the lesions occur at sites in proximity to cranial sutures

and to likely movement of bone during normal delivery.87 Thus, in one series of seven cases, four occurred

in proximity to the pterion, and the remainder occurred

beneath the coronal or squamosal sutures.87



the normal, slightly increased attenuation in the region

of the falx and major venous sinuses in the newborn may

be difficult. Sometimes, the possibility of primary subarachnoid hemorrhage is raised initially by the findings

of an elevated number of RBCs and an elevated protein

content in the CSF, usually obtained for another purpose (e.g., to rule out meningitis). Exclusion of another

cause of blood in the subarachnoid space (e.g., extension from subdural, cerebellar, or intraventricular

hemorrhage) or from certain unusual sources (e.g.,

tumor, vascular lesions) is made best by CT or MRI.

The localized subpial hemorrhages, often with superficial cortical hemorrhage, are observable both by CT or

MRI (Fig. 10-9).

Ultrasonography is relatively insensitive in detecting

subarachnoid hemorrhage per se because of the normal

increase in echogenicity around the periphery of the

brain.88 A large subarachnoid hemorrhage occasionally

distends the sylvian fissure and thus becomes detectable, but care must be taken not to confuse a sylvian

fissure distended with blood from the wide fissure seen

consistently in premature infants and resulting from

the normal separation of the frontal operculum and

superior temporal region until late in gestation.



Clinical Features



Prognosis



Three major syndromes with primary subarachnoid hemorrhage can be distinguished (Table 10-10). First, and

undoubtedly most commonly, minor degrees of hemorrhage occur, and minimal or no signs develop.

Second, primary subarachnoid hemorrhage can result

in seizures, especially in full-term infants (see Chapter

5). The seizures usually have their onset on the second

postnatal day. In the interictal period, these babies usually appear remarkably well, and the description ‘‘well

baby with seizures’’ often seems appropriate. In the

subpial variant, the seizures often are focal, reflecting

the localized nature of these lesions.

A third and quite rare syndrome is massive subarachnoid hemorrhage with catastrophic deterioration

and a rapidly fatal course. The infants usually have

sustained severe perinatal asphyxia, sometimes with

an element of trauma at the time of birth.25,33 The neurological syndrome is similar to the catastrophic deterioration described in Chapter 11 for some patients

with intraventricular hemorrhage.



In general, the prognosis for infants with primary subarachnoid hemorrhage without serious traumatic or

hypoxic injury is good. The specific outcome correlates

reliably with the neonatal clinical syndrome. Thus, the

many infants with minimal signs in the neonatal period

and documentation of subarachnoid blood do well

virtually uniformly. Those few full-term infants with

seizures as the primary manifestation of the hemorrhage are normal on follow-up in at least 90% of

cases (see Chapter 5). The rare patient with a catastrophic course with massive subarachnoid hemorrhage of unknown origin either suffers serious

neurological residua or dies. The principal sequela,

albeit unusual, after major subarachnoid hemorrhage

is hydrocephalus.



Diagnosis

The diagnosis of primary subarachnoid hemorrhage is

made usually by CT or MRI. On CT, distinction from



TABLE 10-10



Neurological Syndromes Associated

with Primary Subarachnoid Hemorrhage



Minimal or no clinical signs

Seizures in full-term infant; considered ‘‘well’’ during interictal period

Catastrophic deterioration



Management

The management is essentially that of posthemorrhagic

hydrocephalus and is discussed in detail in Chapter 11

in relation to intraventricular hemorrhage of the

premature infant.

CEREBELLAR HEMORRHAGE

Cerebellar hemorrhage has been observed in approximately 5% to 10% of autopsy cases in series of neonatal

intensive care unit populations.84,89 The hemorrhage is

more common among premature than term infants; in

four neuropathological series, the incidence among premature infants less than 32 weeks of gestation or less

than 1500 g birth weight, or both, ranged from 15% to

25%.90-94 In contrast to these neuropathological

reports, some large studies of living premature infants

by CT did not demonstrate cerebellar hemorrhage.95,96