Birth Injuries Series #1

Subdural and Primary
Subarachnoid Hemorrhages:
A Case Study
Stacie Barker, RN, MSN, NNP

I

ntracranial h e morrhag e ( I C H )  can b e  lif e
the skull are the meninges, which consist of three layers
t­ hreatening to an infant and emotionally devastating to
(Figure 1): the dura mater, the arachnoid mater, and the pia
the family. It is important for the neonatal nurse to recognize mater. There are three spaces that lie within the meninges:
the infant at risk for ICH to help prevent serious neurologic
the epidural space, the subdural space (a potential space), and
sequelae.
the subarachnoid space.3
There are five major types of
The dura mater, the tough,
Abstract
ICH in the newborn: subdural
inf lex ible outer men ingea l
Subdural hemorrhage (SDH) and primary subarachnoid
(SDH), primary subarachnoid
covering, is a double-layered
hemorrhage (SAH) are two forms of intracranial bleeding
(SAH), intracerebellar, intramembrane: the outer periosteal
that can be encountered in infants. These events can be
ventricular, and intraparenlayer, which is separated by the
life threatening to the infant and devastating to his family.
chymal or bleeding in multiple
epidural space, and the inner
Neonatal nurses need to have an understanding of these
sites. This article focuses on
meningeal layer (see Figure 1).
unfortunate, yet not uncommon, types of intracranial
SDH and SAH (Table 1), briefly
The main arterial blood supply
hemorrhage. This article explains the etiology, the
reviews normal cranial anatomy
to the dura mater is the middle
diagnosis, and the treatment of SDH and SAH, concluding
and circulatory physiology, and
m e n i ng e a l a r t e r y, w h i c h
with a case study.
addresses the etiology, pathobranches off from the external
physiology, clinical features,
carotid artery. 3 Between the
diagnosis, treatment, managelayers of the dura mater lie the
ment, and prognosis of SDH and SAH in infants.
venous sinuses.4 Created by the two dural layers, the venous
SDH and SAH, which can be encountered in both term
sinuses drain the blood from the brain and empty it into the
and preterm infants, often occur after trauma to the head
jugular veins.3 The superior sagittal sinus and the inferior
during delivery, usually with vacuum or forceps assistance.
sagittal sinus are depicted in Figure 1. The cerebral bridging
They are also common complications of head injuries in the
veins serve as connections between the brain and the venous
older infant population.1 SDH is the least common type of
sinuses in the dura mater, and ruptures in them can cause
ICH in the newborn, and SAH is the most common.2 This
subdural bleeding.3
article focuses on a case study of a neonate who had SDH
The dura mater extends vertically and inward to form parand SAH.
titions within the cranium. The sheet of dura mater that lies
vertically into the longitudinal fissure is called the cerebral
Normal Cranial Anatomy and
falx (see Figure 1), which separates the cerebral hemispheres
of the brain. Another segment of the dura layer, the tentoCirculatory Physiology
The outermost layer covering the bony skull is made up
rium, separates the cerebellum from the occipital lobe of the
of the skin, subcutaneous tissue, and periosteum. Beneath cerebrum.4
Accepted for publication February 2006. Revised March 2006.

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Table 1 n Major Types of Neonatal Intracranial Hemorrhage
Type of
Hemorrhage

Maturation
of Infant

Relative
Frequency

Usual
Clinical
Gravity

Subdural

Full-term>Premature

Uncommon

Serious

Primary
subarachnoid

Premature>full-term

Common

Benign

Intracerebellar

Premature>full-term

Uncommon

Serious

Intraventricular

Premature>full-term

Common

Serious

Uncommon

Variable

Miscellaneous:
Full-term>premature
Intraparenchymal,
multiple sites

Figure 2 n Flow

Please refer to the print edition of Neonatal Network

From: Volpe, J. (2001). Intracranial hemorrhage: Subdural, primary subarachnoid, intracerebellar, intraventricular (term infant), and miscellaneous. In Neurology of the newborn (4th ed., p. 398). Philadelphia:
WB Saunders. Reprinted by permission.

The arachnoid mater is an avascular, weblike structure
below the dura mater. The pia mater is a vascular membrane,
supplied by the internal carotid and vertebral arteries, that
adheres to the outer surface of the brain and conforms to
the gyri and sulci. The subarachnoid space lies between the
arachnoid mater and the pia mater (Figure 1) and communicates with the ventricles of the brain.4 Cerebrospinal fluid
(CSF) fills the entire subarachnoid space (Figure 2) as well
as the ventricles, surrounding the brain and spinal cord and

From: Hickey, J. V. (2003). The clinical practice of neurological and neurosurgical nursing (5th ed., p. 57). Philadelphia: Lippincott Williams &
Wilkins. Reprinted by permission.

Figure 1 n Layers of the scalp, cranium, and meninges.
This figure shows the layers that protect the brain from the outermost to the innermost: skin, dura mater, arachnoid mater, and pia mater. Also shown
in this figure are the superior sagittal sinus, the cerebral falx, and the cerebral artery in the subarachnoid space.

From: Netter, F. H. (2006). Atlas of human anatomy (4th ed., p. 102). Philadelphia: Saunders. Reprinted by permission.

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Table 2 n Pathogenesis of Neonatal Subdural Hemorrhage
At Risk

Predisposing Factors

Mother

Primiparous
Older multiparous
Small birth canal

Infant

Large, full term
Premature

Labor

Prolonged
Precipitous

Delivery

Breech extraction
Foot, face, brow presentation
Difficult forceps or vacuum extraction
Difficult rotation

Figure 3 n Mechanism of tentorial hemorrhage after vacuum

Please refer to the print edition of Neonatal Network

From: Volpe, J. (2001). Intracranial hemorrhage: Subdural, primary subarachnoid, intracerebellar, intraventricular (term infant), and miscellaneous. In Neurology of the newborn (4th ed., p. 401). Philadelphia:
WB Saunders. Reprinted by permission.

acting as a shielding cushion for the brain tissue. The subarachnoid space is supplied with arterial and venous blood
by the main blood supply from the two internal carotid
arteries. The cerebral artery (see Figure 1) also supplies the
subarachnoid space.4

Etiology and Pathophysiology
of SDH and SAH
Subdural Hemorrhage

SDH is uncommon, usually occurring in full-term infants
with serious delivery complications.2,5,6 Table 2 summarizes
the predisposing factors for neonatal SDH. These factors
can result in conditions that cause trauma to the head of the
newborn before or during delivery. This most likely occurs
during labor under circumstances when anterior-posterior
compression of the head is associated with excessive vertical
molding and frontal occipital elongation of the cranium
(Figure 3). 2,7 SDH may occur in utero before delivery.8 It
may also occur without known trauma.5
Figure 4 depicts an SDH that resulted from tearing of a
cerebral vein as it enters the superior sagittal sinus. As this
case illustrates, SDH occurs when the blood vessels that
bridge the subdural space are stretched. Rupturing can then
cause venous blood to escape and spread thinly because of
the limitation from the falx and tentorium, which serve as
dural barriers. The subdural space is small in infants, and
a hemorrhage can increase the intracranial pressure significantly.9 Figure 5 illustrates an SDH causing compression on
the brain, displacement of the cerebral falx and ventricles,
and tentorial herniation.

Subarachnoid Hemorrhage

Primary SAH is more common in the premature infant
(see Table 1) than in the term infant and usually does not
result in significant clinical compromise when compared to

From: Holland E. (1922). Cranial stress in the foetus during labor and
on the effects of extensive stress on the intracranial contents: with an
analysis of eighty-one cases of torn tentorium cerebelli and subdural
cerebral haemorrhage. Journal of Obstetrics and Gynaecology of the
British Commonwealth. 29, 553. Reprinted by permission.

other forms of ICH. 2 SAH may occur as an isolated event
(primary SAH) or secondary to an ICH that causes blood to
leak into the subarachnoid space (secondary SAH), such as
in an intraventricular hemorrhage. The etiology of primary
SAH is not understood entirely, but it is thought to be caused
by trauma or by circulatory events related to prematurity. 2
Traumatic injury to the head occurs during or around delivery by the same mechanisms as described for SDH, resulting in stretching, tearing, and laceration of the blood vessels
flowing within the subarachnoid space (Figure 6). When
blood enters the subarachnoid space and mixes with the CSF,
it circulates over the brain and spinal cord, which can cause
irritation of the meninges.10
The primary concern following SAH is hydrocephalus. 2
This is caused by blood in the villi-lined subarachnoid space
that can impair CSF production, f low, or reabsorption. 3
However, this occurs rarely.

Clinical Features of SDH and SAH
Subdural Hemorrhage

There is wide variability in the symptoms associated with
SDH in the infant, ranging from an absence of symptoms to
death. The symptoms depend on the extent of the hemorrhage
(Table 3). In an effort to determine the frequency of SDH in
asymptomatic infants, Whitby and colleagues prospectively
evaluated 111 newborns with magnetic resonance imaging
(MR I) scans. Only 9 of the 111 infants (8 percent) had

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Figure 4 n Subdural hematoma.
This figure depicts a subdural hematoma, which usually results from a tearing of the cerebral vein due to
trauma in vacuum- or forceps-assisted delivery.

SDHs detected with MRI scans that were clinically silent throughout the
course of the study. All SDHs were small.11 Chamnanvanakij and coworkers evaluated 26 near term and term non­asphyxiated infants with SDH.
Fifty-eight percent presented with respiratory symptoms, such as apnea
and dusky episodes, and 39 percent presented with neurologic symptoms,
such as seizures, hypotonia, lethargy, and full anterior fontanel.5 When
seizure activity occurs, it will usually do so on day of life (DOL) 2 or 3.
Signs of focal cerebral disturbance may also occur, including focal seizures, hemiparesis, and eye deviations.2

Subarachnoid Hemorrhage

From: Moore, K. L., & Agur, A. (1995). Essential clinical
anatomy. (p. 356). Baltimore: Lippincott Williams &
Wilkins. Reprinted by permission.

Most often, infants with SAH are asymptomatic with no clinical
signs.2,12 When clinical signs and symptoms of SAH do occur, they are
nonspecific and depend on the extent of the hemorrhage.3 The infant may
develop seizure activities beginning on DOL 2, but will generally look
healthy between seizures. Infants with seizures may display posturing in
which the head, neck, and spine are arched backward. They may have
recurrent apnea; this is usually more common in preterm infants. Rarely,
an infant can have a massive SAH with a catastrophic deterioration and a
rapid, fatal course.2 An infant may present with an SDH or SAH later as a
result of increasing head size, rebleeding into a “chronic SDH,” or blood that
is still present several weeks after the acute hemorrhage.13
Hyperthermia often accompanies cerebral dysfunction such as SDH or
SAH; the hemorrhage causes irritation to the cerebral area, leading to an
increase in temperature. In these cases, it is important to implement measures to reduce the infant’s temperature to help prevent brain damage.
Hyperthermia can increase the infant’s metabolic demands, thus resulting in
an inadequate oxygen supply.3

Diagnosis of SDH and SAH

Figure 5 n Subdural hematoma.
Note compression of brain tissue with shifting of ventricles and tentorial herniation.

From: Bryant, R. (2005). The child with cerebral dysfuction. In M. J. Hockenberry & W. Winkelstein (Eds.),
Wong’s essentials of pediatric nursing (7th ed, p. 1027).
St. Louis: Elsevier Mosby. Reprinted by permission.

Any infant born following a traumatic or instrument-assisted delivery
should be closely examined and observed for signs and symptoms of SDH
and SAH. If there is any suspicion, a lumbar puncture should be obtained
to evaluate for blood in the CSF. Imaging studies should be also be completed by cranial ultrasound (CUS), computerized tomography (CT), or
MRI. Emphasis should be placed not on a single, isolated abnormality,
but on a combination of findings, which could include abnormal CT scan,
abnormal CSF, seizure activity, and apnea and/or bradycardia.2
The gold standard for a diagnosis of SDH and SAH is a CT scan.14,15
Small amounts of subdural blood may be undetectable on CUS, and blood
can be difficult to differentiate from CSF in the subarachnoid space.15
CT scanning is more complicated than CUS because the infant has to be
transported to the site of the scanner. Nonetheless, the scan should be
performed promptly if the infant’s condition allows. A CT scan provides
more global information than a CUS, particularly at the periphery of the
brain. The CT scan is used to diagnose SDH and SAH as well as cerebral
edema or infarction. The CT scan should also be used to evaluate for an
aneurysm or an arteriovenous malformation.
CUS diagnosis of SAH is still in its beginning phases, and increased
awareness of the normal appearance of subarachnoid regions may expand
the diagnostic capability of CUS in the future to include reliable detection of
SAH and its complications.16 CUS is performed to rule out intraventricular
hemorrhage and to grade the size of the ventricles. It is simple and accessible and does not require contrast or sedation. However, at the present,
CUS should not be relied upon as an exclusive way to identify or rule out

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either SDH or SAH.2,15 It does not yet demonstrate the necessary sensitivity and specificity.
MR I is a noninvasive technique that is
superior to CT scan for imaging the brainstem,
spinal cord, and soft tissue. It can help visualize
blood in positions that are not well seen on CT
scan.15 As a technique for mapping blood flow
within the cranial vault, MRI can help accurately diagnosis SDH in infants. However, acute
SDH can be difficult to detect by MRI, and it
is possible for some SDH to be missed when
using MRI alone.11 The advantages of MRI are
the absence of ionizing radiation and the ability
to visualize vascular anatomy without contrast.
The disadvantages are that it may be difficult to
do with critically ill infants requiring ventilatory
support, it takes longer than a CT scan, and it
may require sedation.
There are several laboratory tests that the
clinician should consider when SDH or SAH
is suspected, including an arterial blood gas
(ABG), serum electrolytes, complete blood
count with differential, blood glucose, and
blood culture. The following findings after a
nontraumatic lumbar puncture add to the diagnostic picture: elevated red blood cell (RBC)
count, decreased CSF glucose level, and elevated protein content in the CSF.2,17 CSF findings are considered positive for SAH if the CSF
is xanthochromic and there are as many RBCs
found in the last specimen tube of CSF as in the
first.17,18 Prothrombin time, partial thromboplastin time, platelet count, and other clotting
factor levels may also be indicated to rule out a
coagulopathy. A meconium drug screen should
also be done to rule out an ICH secondary to
maternal use of cocaine, street drugs, or other
neurotoxic drugs.

Treatment and Management

The management of SDH and SAH depends
on the etiology of the hemorrhage and the
clinical symptoms present. If the hemorrhage is
linked to a coagulopathy or inherited bleeding
disorder, a hematologist may be consulted for
treatment. Treatment should be explained to
the parents and arrangements made for genetic
counseling if the cause is an inherited disorder.
Generally, the treatment requirements for
SDH and SAH correlate with the severity of the
hemorrhage. Respiratory support in the form of
oxygen administration and mechanical ventilation may be necessary. Antiseizure medication,
antibiotics, and other medications may be called
for. Subdural taps are a common treatment, and

a ventriculoperitoneal (VP)
shunt or subdural peritoneal shunt can be inserted.
Head circumference will
be monitored and charted
daily because these infants
can have rapid head growth
immediately after the perinatal period.13

Figure 6 n Subarachnoid hemorrhage.
This is a coronal section of the brain illustrating subarachnoid hemorrhage secondary to a ruptured
artery, with hemorrhage into the subarachnoid
space.

Subdural Hemorrhage

If the infant is showing
any signs of SDH, then
serial CUS and CT scans
can be obtained. 2 If the
infant has a hemorrhage
of the falx and tentorium,
then emergency surgery
to relieve the pressure and
attempt to stop the bleeding is necessary.12,19 SDH
may be ma naged w it h
Moore, K. L., & Agur, A. (1995). Essential
subdural taps or surgery, From:
clinical anatomy. (p. 356). Baltimore: Lippincott
depending on the size of
Williams & Wilkins. Reprinted by permission.
the hematoma. Subdural
tapping is performed for
chronic SDH that has not been spontaneously
reabsorbed. If the infant does not respond after
two taps, a shunt is placed to drain the fluid from
the subdural space into the peritoneal cavity.19
SDH requires surgical intervention in 30–50
percent of cases.2,8 It can be difficult to predict
which SDH will become chronic.

Subarachnoid Hemorrhage

The medical management of SAH generally involves monitoring for and preventing
posthemorrhagic hydrocephalus. 2 Whether
hydrocephalus will develop after SAH depends
directly on the amount of hemorrhaging
into the subarachnoid space.2 According
to Gomella and associates, resolution of Table 3 n Symptoms of SDH
the hydrocephalus usually occurs without
Fever
treatment.12 There may be a need for a VP
Cyanosis
shunt to be surgically placed, depending
Apnea
on the amount of hydrocephalus after
Shrill cry
the SAH. The shunt will shift blood or
Oxygen desaturation
CSF from the subarachnoid space to the
Hypertonicity
peritoneal cavity to relieve pressure.
Hypotonia

Prognosis
Subdural Hemorrhage

The prognosis for the infant with
SDH is relatively favorable. With early
diagnosis and suitable treatment, from

Lethargy
Full anterior fontanel
Seizures
Hemiparesis
Eye deviations
Death

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50 to 90 percent of affected infants are well on follow-up.19
However, prognosis for SDH also depends on the area of brain
hemorrhage, the severity of the hemorrhage, and the underlying cause.8 If a tear or rupture of the tentorium and falx is
large or if the condition worsens with delayed or missed diagnosis, severe neurologic morbidity or even death can occur.2,19
Severe neurologic morbidity could include cerebral palsy,
severe mental retardation, or even paralysis. Occasionally, an
infant with SDH will develop hydrocephalus.2

Subarachnoid Hemorrhage

The prognosis for infants with SAH without serious
traumatic or hypoxic injury is excellent.2 In a study of term
infants, the follow-up on those who presented with seizures
as the primary manifestation of hemorrhage was normal in
approximately 90 percent of cases. 20 Rarely, infants with
massive SAH of unknown origin suffer from serious neurologic morbidity or mortality. 2 After SAH, there may be
an eventual need for a VP shunt.16 This sometimes occurs a
month after diagnosis.

Case Study

Baby A was a 3,220 gm, appropriate for gestational age
male infant born at 38 weeks gestation by unassisted vertex
vaginal delivery after ten hours of labor. The mother was a
26-year-old, gravida 1, para 0, woman with an uncomplicated pregnancy. The maternal Group B streptococcus screen
was negative, and the other prenatal laboratory results were
unremarkable. The mother’s blood type was A+, and her
medication during pregnancy included prenatal vitamins.
The labor was complicated by fetal heart rate decelerations.
A single nuchal cord was found at delivery. The infant was
vigorous at birth, with Apgar scores of 8 and 9 at one and five
minutes, respectively, and no resuscitation was required. The
infant was transferred to the newborn nursery for routine
care and monitoring.
In the newborn nursery, Baby A was placed under a radiant
warmer and given routine newborn care, which included
administration of vitamin K. His vital signs were normal, and
the physical assessment was unremarkable, with no observable lesions or injuries to the head. He began ad lib nipple
feedings on demand shortly after birth. He tolerated feedings
well and was voiding and stooling normally throughout his
first day of life.
On DOL 1 at approximately 12 hours of age, the infant
had two episodes of diffuse cyanosis, approximately 10–15
minutes apart, with possible apnea. Each episode lasted about
2 minutes, and required repositioning and tactile stimulation
for resolution. After the second episode, Baby A was placed
on a cardiorespiratory monitor and a pulse oximeter (PO)
until the pediatrician arrived to examine him. Baby A had
a small amount of emesis after each episode, but within 2
minutes, he was no longer dusky and the oxygen (O2) saturation was noted to be 100 percent on room air. An 8 French
catheter nasogastric tube was passed through both nares to

rule out choanal atresia, and then the stomach was suctioned,
with large amounts of air noted.
A third dusky episode occurred approximately 35 minutes
later. During this episode, the infant’s O2 saturation level
fell to 65 percent, and he appeared grayish blue in color.
The episode lasted 1 minute, and then the infant returned
to a pink color, with O2 saturations at 95–100 percent on
room air. Baby A was then placed on blow-by oxygen, with
O2 saturations remaining at 100 percent. When the oxygen
blow-by was taken away, he had a fourth dusky and apneic
episode, with O2 saturations dropping to 50 percent. During
this episode, the infant’s heart rate remained within normal
limits.
The dusky spells were not related to feedings or choking.
At this time, no seizure activity was noted. After the fourth
episode, the infant was transferred to the intensive care
nursery (ICN) without incident.
Upon Baby A’s admission to the ICN, his physical exam
was normal, including the examination of the head and neurologic status. During the examination, the infant was quiet
but alert, had good tone and strength, and moved all extremities well. There was no evidence of seizure activity, and there
were no areas of bruising, ecchymosis, or abnormal bleeding
from needle punctures.
Between 16 and 19 hours of age, Baby A had a total of five
more dusky episodes without bradycardia that lasted between
20 and 30 seconds and required blow-by oxygen. One of the
episodes was severe, with apnea lasting approximately two
minutes, and required tactile stimulation, repositioning, and
oxygen with bag and mask ventilation. The only change in
Baby A’s neurologic status was a shrill cry after the episodes.
Diagnostic tests and exams were done after admission to
the ICN to evaluate for sepsis/meningitis, seizures, ICH,
apnea of infancy, gastrointestinal ref lux, metabolic diseases, and pneumonia and other respiratory pathology. An
ABG, serum electrolytes, complete blood count with differential, blood glucose, and blood culture were obtained,
and all values were within normal limits: ABG on room air
and crying: pH 7.38; partial pressure of carbon dioxide 37
mmHg; partial pressure of oxygen 49 mmHg; bicarbonate 22 mmol/liter, and base excess –3 mmol/liter; glucose
70 mg/dl (3.9 nmol/liter); sodium 140 mmol/liter; potassium 4.3 mmol/liter; blood ionized calcium 1.17 mmol/liter;
hematocrit 51 percent; platelet count 273,000/mm3 ; white
blood cell count 13.6/µl; 69 percent segmented neutrophils, 8 percent basophils, 16 percent lymphocytes, 7 percent
monocytes, nucleated RBC count 1/100. A meconium drug
screen was done because the mother had a history of marijuana use in high school; the results were negative.
A chest x-ray demonstrated normal lung fields and cardiac
size. An echocardiogram was done to rule out congenital
heart disease and to check for persistent pulmonary hypertension; the results were normal.
Upon the infant’s admission to the ICN, a peripheral intravenous (IV) line was started with 10 percent dextrose with

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0.2 percent saline infusing at 80 ml/kg/day. The mother
was allowed to continue breast feeding ad lib amounts every
three to four hours. After the blood culture was completed,
Baby A was started on ampicillin and cefotaxime to cover for
sepsis. A lumbar puncture was performed after the antibiotics were started; bloody fluid was obtained that never cleared
or thinned out, and so it was not sent to the lab. The bloody
fluid was thought to be a sign of hemorrhage not related to a
traumatic procedure.
After the bloody CSF was obtained, a CT scan was done
to rule out ICH. The CT scan, at 20 hours of age (Figure 7),
revealed multiple areas of ICH, including the subarachnoid
space (SAH), a small hemorrhage in the subdural space
(SDH) along the falx posteriorly on the right, and possibly
some extent of hemorrhage into the parenchyma in the right
posterior parietal occipital region. The extent of intracranial
bleeding was unexpected given that the delivery had been
nontraumatic and unassisted.
Coagulation studies were obtained to rule out a coagulopathy as the etiology for the extensive ICH detected on
CT scan. A normal prothrombin time (15.5 seconds) and
partial thromboplastin time (31 seconds) were obtained.
A repeat complete blood count revealed that the platelet
count was 254,000/mm3. The hematocrit level was stable at
51 percent. Family medical history was checked at this time
for the presence of clotting/bleeding disorders, but did not
reveal any concerns. The infant was started on prophylactic
IV phenobarbital for seizure control, with a loading dose of
20 mg/kg.

DOL 3

At approximately 35 hours of age, Baby A experienced a
45-second apneic episode that was associated with O2 desaturation and probable seizure activity: lip smacking, a fixed
gaze, and increased tone and pointing of the left foot and
leg. He did not respond to tactile stimulation, and an additional 10 mg/kg dose of phenobarbital was given at this
time. Throughout DOL 3, Baby A had four additional apneic
episodes associated with occasional clonic jerks. An electroencephalogram (EEG) revealed at least one well-established
seizure associated with apnea.
At this time a CUS was done, revealing stable extra-axial
and parenchymal hemorrhage in the right posterior fossa
and posterior parietal lobe with intraventricular extension.
This result was considered unchanged from the CT scan
performed on DOL 2. The total bilirubin was 8.9 mg/dl
(152 µmol/liter) in the morning of DOL 3 and had increased
to 10 mg/dl (171 µmol/liter) by the afternoon. The phenobarbital level was 19.1 µg/ml. This result indicated adequate
blood levels for seizure control, but Baby A was still having
seizures.
An antithrombin 3 (AT3) level was drawn at this time to
evaluate factor VIII and factor IX levels and help rule out
hemophilia. The AT3 level was low at 44 µg/ml (normal
range is 88–126 µg/ml). A hematologist consulted at this

time did not think that this was low enough to cause a
coagulopathy.

DOL 4

On DOL 4, a second CUS was completed to evaluate the
hemorrhages. This study revealed hemorrhage into the posterior fossa, with what appeared to be hemorrhage extending
into the occipital horn of the right lateral ventricle and with
evidence for extra-axial hemorrhage about the tentorium.
This hemorrhage appeared to be increased in prominence
compared with the previous day’s CUS. The parenchymal
hemorrhage had not changed.
Baby A had one dusky episode on DOL 4 accompanied by
a shrill cry and increased tone that appeared to be a seizure.
Ampicillin and cefotaxime were discontinued after 48 hours
of administration because of negative blood and CSF cultures
and negative history for sepsis/meningitis. The phenobarbital dosage was changed to oral administration of 12 mg once
per day. The total bilirubin level increased to 11.8 mg/dl
(202 µmol/liter) and peaked at 12.6 mg/dl (215 µmol/liter)
on DOL 5, and Baby A never required phototherapy. The
peripheral IV was discontinued, and Baby A continued to
nipple feed without difficulty every three to four hours, either
breast milk or formula, until discharge.

DOL 5–9

Over the next four days, Baby A exhibited intermittent
elevations in axillary temperature, with the highest reading

Figure 7 n CT scan of Baby A.
A CT scan showing the subdural and subarachnoid hemorrhage of Baby
A at the posterior aspect of his occiput.

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reaching 102.9°F. The infant was in an open crib, dressed,
and wrapped in a blanket. The elevated temperature was
thought to be a result of the SAH, which was thought to
have caused subarachnoid irritation. All episodes of fever
responded to acetaminophen, which was given by mouth
every four hours as needed to help decrease temperature. The
vital signs otherwise were stable, and Baby A continued to
nipple feed well.
A repeat CUS done on DOL 5 did not show any change
compared to that obtained on DOL 4. Baby A’s hematocrit
level was stable at 57 percent on DOL 5. The phenobarbital
level on DOL 6 was 34.6 µg/ml, which is in the therapeutic
range for seizure control. No more evidence of seizure activity was noted for the remainder of Baby A’s hospital stay. He
was noted to continue to have a shrill cry and hypertonicity,
his anterior fontanel remained soft and flat. He also continued to have mild lethargy, but was active during caretaking
activities.
On DOL 8, Baby A was transferred to the pediatric floor
to room-in with his mother prior to discharge on DOL 9.
The parents were taught cardiopulmonary resuscitation and
how to properly use a home apnea monitor. They were to
continue to check Baby A’s temperature at home and to
give acetaminophen as needed by mouth. A CUS on DOL
8 revealed stable bilateral intraventricular and right-sided
posterior fossa and parenchymal hemorrhages. A repeat EEG
revealed improvement.
On DOL 9, a repeat CT scan revealed resolving hemorrhages without extension and no evidence of an arterio­venous
malformation or aneurysm. The phenobarbital level on day of
discharge was 27.2 µg/ml, which is therapeutic for seizure
control. Baby A continued without seizure activity.
Baby A was discharged to home on DOL 9 with a home
apnea monitor, phenobarbital by mouth to be given once
per day, and acetaminophen as needed for axillary temperature greater than 100°F. An oto-acoustic emission hearing
screen was passed before discharge. Home nursing visits were
ordered for two times per week for one week, then once a
week for two weeks. Follow-up appointments included visits
to the neurology department in two weeks to follow up the
resolving SDH and SAH and re-evaluate the need for surgery,
to Baby A’s pediatrician for a well baby check in three to four
days, to the pediatric hematology department in three to four
months (although the AT3 was not likely a causative issue),
and to the developmental clinic in three months. This extensive ICH was thought to have been caused by the vaginal
delivery, although there was no use of forceps or vacuum
extraction.

Summary

Earlier diagnosis and more suitable management should
improve survival rates and reduce the incidence of brain
damage in infants with SDH and SAH. 8 Outcomes after
SDH and SAH in infants are dependent on the severity of the
bleeding, the presence of associated intraparenchymal lesions,

the timing of the diagnosis, and the effectiveness of medical
and surgical management. Although in most affected infants
the short-term outcome appears positive, long-term outcomes
remain uncertain, and this condition warrants careful medical
and developmental follow up.5

References

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About the Author

Stacie Barker received her NNP/MSN from the University of
Missouri–Kansas City in May 2006. She received her bachelor of science
in nursing from Deaconess College of Nursing, St. Louis, Missouri, in
1995. Stacie has been a neonatal staff/charge nurse for the past ten
years, with six of those years at Boone Hospital Center in Columbia,
Missouri.
The author would like to thank Bill Barker for his never ending
support and patience during the preparation of this manuscript.
The author would also like to thank the following for their continued
assistance and support with this manuscript: Dr. Laura O’Gorman;Dr.
Tim O’Connor; Lynn Frey, MSN, RN; Dr. Carol Trotter; and Dr.
Lynn Rasmussen.
For further information, please contact:
Stacie Barker, RN, MSN, NNP
Boone Hospital Center, ICN
1600 E. Broadway
Columbia, MO 65201
573-815-3721
E-mail: Staciebarker@centurytel.net

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