Subarachnoid Hemorrhage in Children:
A Nursing Perspective

Christina Stewart-Amidei, RN, MSN, CNRN, CCRN
Lynn Louise Hill, RN, BSN

ABSTRACT: Spontaneous subarachnoid hemorrhage occurs less frequently in children than in
adults. Overall incidence is estimated at less than 5%. Lesions implicated in children are similar to
those in adults but have unique aspects. Lesions seen include arteriovenous malformations and
aneurysms, although other causes exist. Examination of four different causes of spontaneous
subarachnoid hemorrhage in children through case studies highlights similarities and differences
in presentation, diagnosis, treatment, nursing problems, and outcome

Subarachnoid hemorrhage (SAH), a catastrophic
event, occurs in all age groups but presents a unique
challenge in the age group 18 years of age or younger.
SAH in this population is rare, with less than 5% of
all SAH occurring before adulthood.

Asubarachnoid hemorrhage is the accumulation of
blood (usually arterial) below the arachnoid on the
surface of the brain. The hemorrhage typically occurs
as a sudden burst rather than a slow accumulation.
As blood moves into the subarachnoid space, it mixes
with cerebrospinal fluid and circulates over the con-
vexity of the brain and spinal cord, which accounts for
many of the symptoms associated with SAH.

Classification of SAH is based on the origin of the
hemorrhage. SAH may be traumatic (hemorrhage
occurs when arteries on the surface of the brain are
stretched or lacerated during a traumatic event) or
spontaneous (occurring without traumatic origin,
usually from an abnormality in the brain paren-
chyma or from an abnormal vessel). Traumatic SAH
is more common in children. SAH may originate from
an arterial bleed on the surface of the brain (primary
SAH) or from a deeper bleed; blood dissects through
brain parenchyma into the ventricular system or
subarachnoid space (secondary SAH). Spontaneous
hemorrhage tends to be secondary, while traumatic
hemorrhage tends to be primary. For purposes of this
paper, only primary or secondary spontaneous SAH,
occurring in the population 18 years of age or under,
will be discussed.

Questions or comments regarding this article may be directed to
Christina Stewart-Amidei at: Loyola University Medical Center,
Department of Neurosurgery, 2160 S First Ave, Maywood, Illinois
60153. She is neuroscience clinical nurse specialist and Lynn
Louise Hill is coordinator of the Cerebral Blood Flow Laboratory.

Copyright © The American Association of Neuroscience Nurses
0047-2603/86/1802/0063$01.25

63

Causes of SAH

Arteriovenous malformations (AVMs) are by far
the most common cause of SAH in children, account-
ing for about 51% of SAH in this age group. An-
eurysms in children are much less common than
AVMs, but are much more prone to rupture, account-
ing for 25% of all SAH in children. Hypertensive
cerebral vascular disease, brain tumors, or other ab-
normalities in the brain account for 9% of SAH in
children. Systemic disease, particularly hematologic
disorders such as hemophilia, sickle cell disease, or
leukemia, account for 5% of SAH in children. In-
terestingly, 10% of SAH in children cannot be traced
to an identifiable cause.

Comparison of causes of SAH in children vs adults
reveals that in adults, aneurysms predominate (Ta-
ble 1). AVMs account for only 6% of all SAH in the
adult population. Hypertensive cerebrovascular dis-
ease is more common in adulthood, accounting in part
for the higher percentage of other neurologic disease
causing SAH in adults. Lastly, SAH in adulthood is
less likely to be associated with a specific cause than
in childhood.

Arteriovenous Malformation

The primary cause of SAH in children is AVM,
with slightly more than half (51%) of all SAH at-
tributable to this cause. There is thought to be a
greater tendency in the childhood population toward
hemorrhage; in contrast, adults most commonly pre-
sent with seizures from AVM rather than hemor-
rhage. Although AVMs are often anatomically small-
er in children, they are more prone to early second
hemorrhage, leading to a greater mortality rate from
AVM in children than in adults. AVMs are also more
frequently subtentorial in children; 10% to 20% of
AVMs in children are subtentorial, compared with
less than 5% in adults. The older child is more prone

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JOURNAL OF NEUROSCIENCE NURSING, APRIL, 1986, VOL 18, NO 2

to develop symptoms from AVM; 85% of AVMs in
children are diagnosed in the 7 to 13 years of age
group.”

AVMs are thought to develop primarily on a con-
genital basis and are sometimes associated with
other congenital anomalies. AVMs develop em-
bryologically when the normal cerebral vasculature
is developing. The capillary system fails to differen-
tiate, and there is direct shunting of blood from ar-
teries to veins, bypassing the capillary network.!®
(The AVM is an embryonic vasculature that lacks a
capillary network.) Without a normal capillary net-
work, the function of tissue perfusion is bypassed.
Inadequate tissue oxygenation results in cerebral is-
chemia. Because blood is shunted directly from ar-
teries to veins, a state of altered cerebral vascular
resistance occurs.'® The AVM offers the blood a
pathway of less resistance than does a normal capil-
lary network. Hence, arteries dilate to bring more
blood to the lesion, and veins dilate to carry the excess
blood away. Collateral vessels develop and add to the
evolving mass. Cerebral blood flow (CBF) through
the lesion may be increased 50% to 100% above nor-
mal. Adjacent brain tissue is robbed of its normal
flow, a phenomenon known as “intracerebral steal.”
Blood is diverted from the normal area of the brain to
the vascular abnormality, an area of lower vascular
resistance.2? AVMs may become symptomatic as a
result of this phenomenon or from SAH. The AVM
may hemorrhage because its vessels are thin walled
and under a great deal of pressure.

If the AVM becomes large, local and systemic in-
volvement can occur. Local involvement is signaled
not only by intracerebral steal but also by the pres-
ence of the AVM acting as a space-occupying lesion.
Systemic involvement occurs with dilation of the
arterial trunk of the AVM moving toward the heart.
As the circulatory demand of the AVM increases,
cardiac output must increase, potentially precipitat-
ing heart failure.'*

Aneurysms in Children

Aneurysm as a cause of SAH in children is rare;
aneurysms in childhood account for 1.3% of aneu-
rysms for all ages. Specific incidence of aneurysm by
age is 0 to 10 years, 15%; 11 to 14 years, 30%; 15 to 20
years, 55%. Aneurysms in children are predominant
in males; female incidence predominates for all ages.
As in adults, childhood aneurysmal symptoms most
commonly are attributed to SAH; rarely do childhood
aneurysms present as space-occupying lesion. The
anatomic location of childhood aneurysms is unique
in that over 20% of cases occur at the carotid bifurca-
tion, whereas in adults, the percentage is about 8% in
this location.

Interestingly, a number of cases have been re-
ported in the literature describing children with

Table 1
Causes of SAH-Child vs Adult
Child Adult
Arteriovenous malformation 51% 6%
Aneurysm 25% 51%
Other neurologic disease % 15%
Systemic disease 5% T%
No identifiable cause 10% 22%

aneurysms having an associated unrepaired coarcta-
tion of the aorta. Children with cyanotic heart dis-
ease and subacute bacterial endocarditis (SBE) are
prone to bacterial embolization as a cause of aneu-
rysm. Also, morbidity and mortality rates associated
with SAH from aneurysm in children are more favor-
able than in adults in spite of the tendency toward an
early second hemorrhage."!

Other Causes of SAH

While AVM and aneurysm are the primary causes
of SAH, other causes have been identified. Vascular
malformations of the spinal cord may result in SAH.
Spinal cord malformations are usually located in
the mid- to lower-thoracic and upper-lumbar regions
of the cord. They often become symptomatic during
childhood, and the onset of hemorrhage may be pre-
cipitated by trauma or exercise. Involvement of as-
cending and descending pathways of the spinal cord
leads to motor weakness and sphincter disturbances.
There is usually no change in the level of conscious-
ness.”

Brain tumor (particularly pituitary adenoma,
hemangioblastoma, and intraventricular tumors)
and abscess can also cause SAH, but both have a more
gradual onset of neurological involvement. Often,
prior to the hemorrhage, the patient experiences
headache and vomiting in addition to other signs of
increased intracranial pressure. Arteriosclerotic ves-
sels have also been identified as a source of SAH.?°
Systemic diseases, especially those affecting coagula-
tion, may precipitate SAH in the child or adult. In
children, hemophilia, idiopathic thrombocytopenia,
purpura, disseminated intravascular coagulation,
and sickle cell disease have all been associated with
SAH as complications.? Central nervous system
leukemia in children may also cause SAH.

Table 2
Assessment of Patients with SAH

Grade 1 Conscious with signs of subarachnoid blood

Grade 2. Drowsy without significant deficit

Grade 3 Drowsy with a neurological deficit

Grade 4 Deteriorating with major neurological deficit

Grade 5 Moribund with extensor rigidity and failing vital signs

From Botterell EH et al: Hypothermia and interruption of circu-
lation in the surgical management of intracranial aneurysms. J
Neurosurg 1956; 13:1-42.

JOURNAL OF NEUROSCIENCE NURSING, APRIL, 1986, VOL 18, NO 2

65

Table 3
Assessment of Patients with SAH

Grade I Asymptomatic, or minimal headache and slight nu-
chal rigidity.

Grade II Moderate to severe headache, nuchal rigidity. No
neurological deficit other than cranial nerve palsy.

Grade III_ Drowsiness, confusion, or mild focal deficit.

Grade IV Stupor, moderate to severe hemiparesis, possibly
early decerebrate rigidity and vegetative distur-
bances.

Grade V Deep coma, decerebrate rigidity, moribund appear-
ance.

From Hunt W, Hess R: Surgical risk as related to time of inter-
vention in the repair of intracranial aneurysms.J Neurosurg 1968;
28:14-20.

Symptomatology

Overall symptomatology associated with SAH is
consistent among all age groups, with individual
variations depending on the site and extent of hemor-
rhage. Premonitory symptoms, such as localized
headache with nausea and vomiting or even visual
disturbances, occur from days to weeks prior to the
hemorrhage in almost 60% of cases of SAH.!? Classi-
cally, the child with SAH presents with an acute
onset of excruciating headache, followed by neck pain
and stiffness and/or back pain and stiffness. Vomit-
ing with or without nausea, photophobia, restless-
ness, and irritability are common. Changes in vital
signs can occur, including mild elevations in blood
pressure and temperature as well as a decrease in
heart rate. Focal signs of neurological dysfunction
(ie, weakness, paralysis, cranial nerve palsy, etc) or
decreased consciousness may or may not be present.
Bleeding into the ventricular system often presents
with progressive stupor. Severity of the hemorrhage
may be evaluated using the Botterell system (Table
2) or the scale by Hunt and Hess (Table 3).*° Partial
or generalized seizures signaling SAH are not com-
mon in children but may occur. In addition, symp-
tomatology may be seen in the absence of SAH as a
result of cerebral ischemia (in AVMs, due to intra-
cerebral steal) or the presence of a space-occupying
lesion.

Evaluation and Management

The child presenting with symptoms indicative of
SAH requires a comprehensive diagnostic evalua-
tion. A CT (computed tomography) scan (with and
without contrast) is necessary to document the pres-
ence and location of SAH. Source of the hemorrhage
(ie, aneurysm or AVM) may be identifiable on the
contrast scan. Angiography is essential to more
clearly identify the source of hemorrhage and to out-
line the extent of vascular abnormality present.
Vasospasm may also be documented via angiog-
raphy. Lumbar puncture is not used except where
symptoms of SAH exist without identification of the

Table 4
Clinical Guidelines for Hypervolemic Hemodilution

Initial Patient Evalution

¢ Establish baseline motor and speech function for subsequent
comparisons during therapy.

© Detect altered level of consciousness, which may indicate in-
creased ICP and thereby preclude use of hypervolemic
hemodilution.

e Examine cranial CT scan for evidence of acute structural cereb-
ral damage (hypodensity, enhancement, hemorrhage, and/or
mass effect), etiology of present insult, and presence of previous
cerebral infarctions.

e Examine cerebral angiogram for etiology of present insult and
degree of collateralization.

© Determine baseline hematocrit, central venous pressure and, in
cases of elderly or cardiac patients, pulmonary wedge pressure
or cardiac output.

Infusion Technique

© Intravenously infuse 250 mL of 5% albumin over 30 minutes.

e Adjust infusion rate to maintain reduced hematocrit at about 33
(usually requires 250 mL of 5% albumin every four hours).

¢ Adjust infusion rate to “normalize” intravascular volume (cen-
tral venous pressure less than 12 cm H20).

¢ In elderly or cardiac patients, adjust infusion rate to maintain
stable cardiac output and pulmonary wedge pressure below 20
mm Hg.

¢ Iflevel of consciousness deteriorates, stop infusion and perform
cranial CT scan. If midline shift has increased, give 25 g in-
travenous bolus of mannitol. Maintain infusion for three to four
days, then taper.

© If improved neurological status worsens during infusion taper,
increase rate and reattempt taper in two to three days.

Adapted from Wood J: Hypervolemic hemodilution: Rheologic
therapy for acute cerebral ischemia. J Neurosurg 1982; 10:781.

hemorrhage on CT scan. Other diagnostic testing
may be required, depending on individual situations.

Regional cerebral blood flow measurements
(rCBF) made by xenon inhalation technique can play
an important role in evaluating the functional status
of the cerebral vasculature. In general, rCBF in pa-
tients with SAH has been shown to decrease follow-
ing the hemorrhage; decreases in rCBF contribute to
ischemia and potentially infarction. Decreases in
rCBF are attributed to increased blood viscosity and
elevated hematocrit. Surgical intervention initiated
during the time of decreases in rCBF has been as-
sociated with a higher morbidity and mortality.

In an attempt to improve rCBF following SAH, the
nonsurgical therapy of hypervolemic hemodilution
may be used. (This therapy is thought to be effective
in all age groups.) The goals of this therapy are to
decrease hematocrit and increase intravascular vol-
ume, allowing subsequent improvement of rCBF.!9

These goals may be achieved through the use of
albumin. Albumin is a colloid infusate that remains
within the intravascular compartment after infu-
sion. In contrast, crystalloid infusates such as saline
and dextrose distribute throughout the body with
only 15% remaining in the intravascular compart-
ment. Albumin promotes hemodilution by expanding

JOURNAL OF NEUROSCIENCE NURSING, APRIL, 1986, VOL 18, NO 2

Fig 1. Left thalamic AVM with hemorrhage into left lateral and
third ventricle.

plasma volume, thereby decreasing hematocrit.'® Pa-
tients with SAH grades I through IV may benefit
from this therapy. Prior to initiating the therapy,
baseline hematologic values are reviewed, including
hemoglobin (Hgb), hematocrit, erythrocyte sedimen-
tation rate, and albumin and fibrinogen concentra-
tions. Alert patients with a hematocrit greater than
38 and no evidence of increased intracranial pressure
or midline shift on CT scan should have the therapy
started immediately. Specific guidelines for the
therapy as adapted from Wood are listed in Table 4.19

Problems of fluid overload and pulmonary conges-
tion, which may occur with intravascular volume
expansion, are monitored via CVP or Swan-Ganz
catheter. Infusion rates are adjusted to maintain the
CVP less than 12 cm H20 and pulmonary capillary
wedge pressure less than 20 mm Hg. The hyper-
volemic hemodilution therapy is usually maintained
for three to four days, followed by gradual reduction
of the volume of infusions (weaning). Frequent
neurological exams are necessary during therapy
and tapering of infusions to evaluate any deteriora-
tion in the patient’s neurological status. Deteriora-
tion during weaning may indicate the need to con-
tinue therapy. Alteration in the patient’s neurologi-
cal status during weaning may be corrected by in-
creasing the rate of the infusion.

Case Studies

Case #1:

WB, an 11-year-old girl, complained of sudden
onset of a severe headache while twirling a baton.
This was immediately followed by a decrease in her
level of consciousness and three episodes of vomiting.
On arrival in the emergency room, WB was stuporous
but arousable by vigorous shaking. No seizure activ-
ity was noted. She was unable to speak and was found
to have a right hemiparesis. Nuchal rigidity was

Fig 2. Hemorrhage resolved—left thalamic AVM

present. Prior medical, social, and academic history
was unremarkable, except for a three-month history
of mild headaches. According to family, WB was an
above-average student and a normal eleven year old.
CT scan on admission revealed a left thalamic AVM
with hemorrhage into the left lateral and third ven-
tricles (Fig 1, 2). Angiography identified the thalamic
perforators and lenticulostriate vessels as feeding
vessels; the AVM was drained by thalamic veins (Fig
3). WB’s condition improved over the first 24 hours.
Only a mild right hemiparesis was present, and
speech appeared intact. Although lethargic, WB re-
sponded to verbal stimuli. Her alertness steadily im-
proved over the next seven days. Eight days after
admission, WB was taken to the operating room for
a left temporal-parietal craniotomy and resection of
the AVM. The procedure was tolerated well. Post-
operatively, WB’s right-sided weakness persisted but
was now more pronounced in the lower extremities.
In addition, a right facial droop with deviation of the
tongue to the right was noted. Speech fluency was
again a problem. Over the next several weeks, WB

Fig 3. Left thalamic AVM with thalamic perforators and len-
ticulostriate feeding, draining via thalamic veins.

JOURNAL OF NEUROSCIENCE NURSING, APRIL, 1986, VOL 18, NO 2

67

underwent intense physical therapy rehabilitation.
By the time she was discharged from the hospital,
nine days after surgery, she was able to ambulate and
the right-sided weakness and facial droop had almost
fully resolved. WB was to continue outpatient physi-
cal and speech therapy on a regular basis and was to
be followed up in the outpatient clinic.

Nursing Problems: Although WB's aphasia was
transient, it required nursing intervention. A Broca’s
aphasia was present secondary to the location of her
lesion. Her reading and writing skills remained in-
tact. Nursing interventions were directed toward fos-
tering an environment of effective communication.
Specific nursing interventions included: 1) listening
attentively; 2) anticipating WB’s needs; 3) providing
support and encouragement for the mobility she had
already attained; 4) having only one person at a time
communicating with WB and; 5) providing an at-
mosphere of comfort, calm, and acceptance to help
decrease WB’s anxieties regarding her communica-
tion difficulties. We explained to WB in simple terms
why she was experiencing difficulties and this helped
her to understand and accept her situation.

The right hemiparesis was present both preopera-
tively and postoperatively; spasticity was present as
well. Prior to developing a plan of care, a thorough
assessment of WB’s capabilities was necessary. Ini-
tially, WB had poor strength throughout, especially
in the right arm and right foot. She had fair sitting
balance. Standing balance was poor; proprioception
was decreased, as was kinesthetic awareness. Spe-
cific nursing interventions included the following: 1)
an unhurried approach to assist her with mobility,
transferring, range-of-motion exercises, and ac-
tivities of daily living, with adaptations as necessary;
and 2) assisting WB to recognize and understand her
strengths and weaknesses.

Two months after leaving the hospital, WB re-
turned for a neuropsychological evaluation. By this
time she had resumed almost all of her normal ac-
tivities of daily living. Her speech was fluent, and no
language or vocabulary abnormalities were noted.
Interestingly, it was noted that WB exhibited a right
hemisphere dominance for language, and this was
one of the reasons she experienced only a transient
aphasia preoperatively and postoperatively. Her
neuropsychological evaluation did not suggest any
cognitive dysfunction, and she was given a prognosis
for normal development. WB has resumed all of her
previous activities without limitations.

Case #2:

ST, an 11-year-old boy, presented with complaints
of a severe frontal headache that came on suddenly
while he was swimming. He went home with the
headache and experienced nausea and vomiting for

Fig 4. Anterior communicating artery aneurysm

several hours. Since his symptoms were not relieved
with rest or acetominophen, his mother brought him
to the emergency room. On arrival, ST was found to
have nuchal rigidity, a positive Kernig’s and Brud-
zinski’s sign, and a low-grade fever. Past history was
remarkable for generalized moderate headache
diagnosed as vascular in origin. A lumbar puncture
(LP) was done because of suspicion of meningitis; LP
was grossly bloody, and CSF gram stains were nega-
tive. CT scan done subsequently documented the
SAH. Angiography performed the next day demon-
strated an anterior communicating artery aneurysm
(Fig 4).

ST was placed in a pediatric intensive care unit for
careful observation. Bedrest and sedation were or-
dered to minimize the chance of a rebleed. ST was
kept well hydrated, and the hypervolemic hemodilu-
tion therapy was used. Protocols previously men-
tioned for the therapy were followed. Five days after
admission, ST underwent a left temporal-parietal
craniotomy for clipping of the aneurysm. He toler-
ated the procedure well. Postoperatively, ST had no
neurological deficit nor any complaints. He was dis-
charged home on the fifth postoperative day. His
posthospital period was unremarkable.

Nursing Problems: Altered fluid balance was con-
sidered a problem for ST because he was undergoing
hypervolemic hemodilution therapy. His fluid bal-
ance was monitored with a Swan-Ganz catheter and
frequent monitoring of hematologic values. His vol-
ume status remained within normal physiologic
limits.

The second problem identified was altered psycho-
social status secondary to his illness. ST suffered
many anxieties and fears related to his hospitaliza-
tion and diagnosis. Much of his behavior was
attention-seeking behavior, in which he demanded
much of the nurses’ time. He would continually ask a
nurse to be at his bedside playing with him, talking to

68

JOURNAL OF NEUROSCIENCE NURSING, APRIL, 1986, VOL 18, NO 2

Fig 5. Third and fourth ventricular hemorrhage.

him, or holding his hand. He especially requested
physical comforting. The nursing staff adjusted their
schedules to spend time with him and became adept
at meeting his needs. The support offered helped him
to work through some of his fears and anxieties. One
of ST’s greatest fears was of hair loss. He became
preoccupied with this idea. He was afraid of what he
would look like postoperatively and that his hair
would never grow back. After surgery it was obvious
that ST did not feel good about his body image. ST
was encouraged to express his fears; his value as an
individual was continually emphasized. He was also
encouraged to talk with other children on the unit
who had had similar surgery. ST is back in school,
doing well, and has resumed all of his previous ac-
tivities, including swimming. (His hair is fully
grown.)

Case #3:

MP, a nine-year-old girl, experienced a severe
headache while tumbling in gym class. The headache
was followed a few minutes later by a single episode
of vomiting and an acute loss of consciousness. She
was brought to the emergency room where she was
noted to have spontaneous movement but did not
follow commands (a Glasgow Coma Score [GCS] of 6).
Movemert on the right side was less than on the left;
a positive Babinski was present on the right. A right
facial droop was noted, as well as nuchal rigidity. Her
left pupil was at 8 mm with no reaction, while the
right was reactive at 2 mm. Past history was remark-
able for a two-month history of headaches diagnosed
as possible migrainous headache. She was admitted
to the pediatric ICU.

A CT scan initially showed third and fourth ven-
tricular hemorrhage (Fig 5). Angiography was essen-
tially normal, revealing no vascular abnormality.
Because of the inability to identify a source for the
hemorrhage, magnetic resonance imaging (MRI) was
done—results were compatible with a thalamic le-

Fig 7. Left thalamic infarct

sion (Fig 6). A CT scan repeated about nine days later
showed a thalamic infarct (Fig 7). Treatment con-
sisted solely of supportive care. Dexamethasone and
mannitol were used to treat the mass effect present.
Hydrocephalus developed 24 hours after admission,
requiring external ventricular drainage for five days.
Internalization was not necessary. Because of MP’s
neurological deficits, physical and occupational
therapy were started early.

Nursing Problems: Altered level of consciousness
was a problem because MP initially presented com-
atose. She began to respond consistently on the fourth
day after admission, although her level of conscious-
ness fluctuated. Following discontinuation of the ex-
ternal ventricular drainage, there was concern that
she would develop recurrent hydrocephalus; the pos-
sibility of rebleed also existed. Interventions in-
cluded: 1) frequent assessment of neurological status
with specific observations for trends in conscious-
ness; 2) provision of appropriate sensory stimulation;
and 3) implementation of interventions to protect MP

JOURNAL OF NEUROSCIENCE NURSING, APRIL, 1986, VOL 18, NO 2

69

from hazards of immobility.

Altered mobility was a problem once MP’s con-
sciousness improved. Specific motor deficits included
a spastic right hemiparesis and incoordination. Pro-
prioception was decreased on the right side as well.
Interventions included: 1) gradual implementation of
range of motion activities from passive to active; 2)
gradual ambulation, beginning with transfers from
bed to chair, then several steps at a time; and because
MP tended to be impulsive, 3) supervision for all
motor activities. By discharge, MP was able to ambu-
late 50 feet with only a near assist.

Family coping deficit was the third problem. MP’s
mother verbalized feelings of inadequacy as a
mother, saying she should have recognized MP’s
headaches as a more serious problem. MP’s mother
had recently remarried, and she had thought perhaps
MP’s headaches were adjustments to her marriage.
The nursing staff encouraged MP’s mother to become
involved in her care. Support services for the mother
were identified, and on several occasions she partici-
pated in the parents’ coffee hour on the unit, discuss-
ing her concerns with other mothers.

MP was discharged home three weeks after admis-
sion with a mild right hemiparesis. Physical and oc-
cupational therapy were continued at home for three
months until MP was able to return to school. She
now ambulates independently and rides her bicycle,
although with rapid activity (ie, running) she is noted
to be ataxic. She is doing well in school, although
functioning at a slightly lower level. Recent evalua-
tion by a neuropsychologist revealed a mild Wer-
nicke’s aphasia, which may be related to her change
in grades.

Case #4:

TR, a six-year-old male, woke up in the morning
with complaints of mild headache; his mother noted
that he was irritable. He sat down to breakfast, vom-
ited, and lapsed into a coma. By the time he arrived in
the emergency room, his pupils were at 7 mm and
sluggishly reactive. Decerebration was noted to pain.
Respiratory irregularities were present, requiring
intubation and mechanical ventilation. Past history
was remarkable for an 18-month history of acute
lymphocytic leukemia, which was thought to be in
remission. CT scan showed subarachnoid blood with-
out any specific evidence of intracerebral or in-
traventricular hemorrhage. Lumbar puncture was
done to identify presence of meningeal leukemia.
Opening pressure was 270 mm HzO, and fluid was
grossly bloody. Protein was 80 mg%, and sugar was
40 mg%. Cell count was elevated with the differential
showing 30 mononuclear cells. (Greater than ten
cells is indicative of meningeal leukemia.) Blood
studies showed no evidence of active leukemia al-
though thrombocytopenia was present. Replacement

platelets were given, and intracranial irradiation
was started (a course of 2000 rads over four weeks).
Ten milligrams intrathecal methotrexate was given,
to be repeated every two days. Complete supportive
care was provided.

Nursing Problems: Altered level of consciousness
was a problem—TR’s GCS ranged from 3-4. Family
and staff were encouraged to provide auditory and
tactile stimulation, and his level of consciousness was
assessed hourly. Family involvement in decision
making related to TR’s care was difficult because his
parents were separated and often openly disagreed
about what action to take. Daily meetings were set up
with both parents to give them information; both
parents stayed at the hospital 24 hours a day. The
hospital risk manager was consulted for legal advice.
When the gravity of TR’s situation was apparent,
attempts were made to prepare his family for the
possibility of his death. The dramatic change in his
condition was most difficult for TR’s family to grasp;
blood counts one week earlier showed remission. TR’s
father refused to discuss any of his feelings, but TR’s
mother participated in parents’ group on the unit.
She was referred to the Candlelighter’s—a support
group for parents of children with cancer.

TR showed little response to any of the therapies.
On the fifth day after admission, his condition de-
teriorated to the point where no response was noted.
All extremities were flaccid. Pupils were 9 mm with
no reaction to light. Signs of cranial nerve function
were absent; hypotension and irregular heart rate
were present. With the written consent of both par-
ents, a “do not resuscitate” order was instituted. Two
hours later, five days after admission, TR died. No
autopsy was performed.

Summary

Subarachnoid hemorrhage in children, although
rare, presents challenges in diagnosis and manage-
ment. A comprehensive approach to the unique as-
pects of SAH in children is necessary. Symptomatol-
ogy seen in children is consistent with that observed
in the adult population. Management of the hemor-
rhage focuses on an in-depth diagnostic evaluation of
the source of hemorrhage, institution of hyper-
volemic hemodilution therapy to minimize cerebral
ischemia, and appropriate surgical intervention
where indicated. Nursing problems are unique to the
disease and to the individual child. Outcome of SAH
in children is variable, from little or no deficit, to
substantial deficit or even death.

Acknowledgment

The authors wish to acknowledge Maryann Di-
Prizo for her assistance with the preparation of this
manuscript.

OO LLL

JOURNAL OF NEUROSCIENCE NURSING, APRIL, 1986, VOL 18, NO 2

70
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