Clinical Presentation of Intraventricular Hemorrhage in Infants
C H A P T E R
93
Clinical Aspects of Intraventricular
Hemorrhage
B. Daou1, D. Hasan2, P. Jabbour1
1Thomas Jefferson University and Jefferson Hospital for Neuroscience, Philadelphia, PA, United States; 2University of
Iowa Hospital and Clinics, Iowa City, IA, United States
INTRODUCTION
Intraventricular hemorrhage (IVH) is the presence
of blood within the ventricular system including the
lateral, third and fourth ventricles. Primary IVH refers
to bleeding directly into the ventricular system within
the brain, from an intraventricular source or a lesion
contiguous to the ventricles. Primary IVH is uncom-
mon. Secondary IVH occurs more frequently (70% of
IVH patients) and refers to bleeding extending from the
parenchyma or subarachnoid space into the ventricular
chambers. Once blood is inside the ventricles, it mixes
with the cerebrospinal fluid (CSF) and circulates toward
the subarachnoid space, which may result in obstruc-
tive hydrocephalus and increased intracranial pressure
(ICP) that may be associated with significant morbidity
or mortality.
ETIOLOGY OF INTRAVENTRICULAR
HEMORRHAGE IN INFANTS
Premature infants, especially those born before
32 weeks of gestation and neonates with low birth
weight (<1500 g) are at an increased risk of developing
IVH compared to full-term infants. The reported rate
of IVH is about 20–45% in infant with birth weight less
than 1500 g [1–3]. In premature infants, bleeding occurs
in small blood vessels in the subependymal or germinal
matrix [4]. The pathogenesis of neonatal germinal matrix
IVH is thought to result from hemodynamic changes
and alterations in cerebral blood flow coupled with
impaired autoregulation resulting in disturbance of per-
fusion to the delicate cellular structures of the germinal
Primer on Cerebrovascular Diseases, Second Edition
http://dx.doi.org/10.1016/B978-0-12-803058-5.00093-X
457
matrix located periventricularly and injury of the fragile
blood vessels of the germinal matrix [5]. These changes
lead to potential hypoxic ischemic encephalopathy, cell
death, and subsequent hemorrhage within this injured
brain tissue.
IVH in term infants, toddlers, or children is more
frequently associated with trauma. It can also be asso-
ciated with inherited coagulopathies and vascular
malformations.
Several additional risk factors may contribute to an
increased risk of IVH including: maternal hyperten-
sion during pregnancy, maternal chorioamnionitis, pre-
eclampsia, breech presentation, intrapartum asphyxia,
malformed or weak blood vessels in the brain, respi-
ratory distress, mechanical ventilation, blood-clotting
abnormalities, shaken baby syndrome, and head injury.
CLINICAL PRESENTATION OF
INTRAVENTRICULAR HEMORRHAGE
IN INFANTS
Neonatal IVH usually occurs in the first 72 h after
birth. There are several nonspecific signs and symp-
toms that suggest IVH in infants, full-term infants, tod-
dlers, or children including lethargy and excessive sleep,
decreased feeding, nausea, vomiting, weak suckling,
apnea, abnormal eye movement, abnormal and persis-
tent crying, hypotonia, and decreased reflexes. More
severe presentations may include seizures, cranial nerve
abnormalities, bulging fontanelles, hemodynamic insta-
bility, and decreased blood count. On the other hand,
IVH in infants can be clinically silent, detected only on
routine screening.
© 2017 Elsevier Inc. All rights reserved.
458 93. Clinical Aspects of Intraventricular Hemorrhage
TABLE 93.1 Grading of IVH in Premature Infants [6]
Grade I Bleeding occurs just in the germinal matrix
Grade II Bleeding also occurs inside the ventricles without
significant enlargement
Grade III Ventricles are enlarged by the accumulated blood
Grade IV Bleeding extends into the adjacent/periventricular
brain tissue
GRADING OF INTRAVENTRICULAR
HEMORRHAGE IN INFANTS
In the preterm infants, IVH is often classified into four
grades depending on whether the bleeding is confined
to the germinal matrix region or if it extends into the
ventricles or brain parenchyma (Table 93.1) [6]. Grades
I (mild) and II (moderate) are the most common and are
often associated with minimal clinical complications.
Grades III and IV IVH have a higher-risk morbidity and
mortality, including long-term brain injury and neurode-
velopmental impairment [6]. One of the main sequelae
of grade III or IV IVH is obstructive hydrocephalus
requiring intervention.
DIAGNOSIS OF INTRAVENTRICULAR
HEMORRHAGE IN INFANTS
Cranial ultrasound is the method of choice for screen-
ing, diagnosis, and follow-up of IVH in infants. These
infants require repeated imaging to monitor the progres-
sion of IVH and potential hydrocephalus.
In older children, noncontrast head CT is used more
frequently to diagnose IVH because of the marked limi-
tation of cranial ultrasounds to give detailed imaging of
the brain due to closure of skull sutures and thickening
of the skull.
TREATMENT OF INTRAVENTRICULAR
HEMORRHAGE IN INFANTS
Several methods have been shown to help in pre-
venting the development of neonatal IVH in preterm
infants including antenatal corticosteroids [7], delayed
clamping of the umbilical cord [8], and prompt resus-
citation to avoid hemodynamic instability and meta-
bolic abnormalities that may impair cerebrovascular
autoregulation.
Interventions that could decrease the morbidity
and mortality of obstructive hydrocephalus associ-
ated with IVH include diuretic therapy [9], repeated
lumbar or intraventricular puncture [10], injection of
intraventricular thrombolytics [11], or a combination
VI. CLINICAL ASPECTS: MEDICAL AND SURGICAL
of interventions including drainage using external
ventricular drain (EVD), irrigation, and fibrinolytic
therapy (DRIFT) [12].
In premature babies with low birth weight (<1500 g),
repeated lumbar or mainly ventricular punctures can be
employed to decrease the effects of increased ICP second-
ary to obstructive hydrocephalus. Ventriculoperitoneal
shunting is the permanent solution for persistent hydro-
cephalus secondary to IVH. Shunting can be performed
when the infant reaches a reasonable weight (>1.5 kg) [13].
ETIOLOGY OF INTRAVENTRICULAR
HEMORRHAGE IN ADULTS
Spontaneous Primary Intraventricular
Hemorrhage
Primary IVH confined to the ventricular system
accounts for about 30% of all IVH cases [14], and only
about 3% of all spontaneous intracerebral hemor-
rhages (ICHs) [15]. Primary IVH is typically caused by
intraventricular aneurysm rupture, small ependymal,
subependymal, or choroid plexus vascular malfor-
mations (Figs. 93.1 and 93.2) or intra/periventricular
neoplasms (Table 93.2).
Intraventricular Hemorrhage Secondary to
Intracerebral Hemorrhage
IVH secondary to ICH results from expansion of an
existing intraparenchymal hemorrhage into the ventric-
ular system. This is most commonly due to hypertensive
hemorrhage, especially basal ganglia hemorrhage and
lobar hemorrhage [14]. Deep, subcortical structures tend
to be most at risk for IVH, including caudate, putamen,
thalamus, pons, and cerebellum locations [16].
Arteriovenous malformations (AVM) (Fig. 93.3) and
dural arteriovenous fistulas (dAVFs) (Fig. 93.4) of any
size and location with deep cerebral venous drainage
can rupture into both adjacent parenchyma and ventric-
ular systems. Less commonly, periventricular AVMs that
reach the ventricular wall can rupture primarily into the
ventricle. Extension of ICH into the ventricles has been
consistently demonstrated as an independent predictor
of poor outcome [17].
Intraventricular Hemorrhage Secondary to
Aneurysmal Subarachnoid Hemorrhage
In patients with aneurysmal subarachnoid hemor-
rhage (SAH), the frequency of IVH is reported to be
between 28% and 50%, especially with Hunt and Hess
grades 3–5 (Fig. 93.5) [18]. IVH is an independent pre-
dictor of death and poor outcome after aneurysmal
 Etiology of Intraventricular Hemorrhage in Adults 459

FIGURE 93.1 MRI showing a large amount of intraventricular hemorrhage primarily in the right lateral ventricle, within the third ventricle,
fourth ventricle and within the frontal and occipital horns of the left lateral ventricle, with associated subarachnoid hemorrhage (A, B). There is
some enlargement of the ventricular system compatible with hydrocephalus. Head CT shows the IVH (C). A left frontal ventriculostomy catheter
was placed. Angiogram shows a ventricular AVM fed by distal right PCA feeder and draining into the straight sinus (D). Successful embolization
with Onyx was performed (E). Follow-up CT shows that there is improvement in IVH (F).

SAH, with high mortality in these patients [17]. IVH has
been associated with secondary complications including
hydrocephalus, cerebral ischemia, clinical vasospasm,
and poor long-term outcomes [18].
Posterior circulation aneurysms are the most com-
mon aneurysm type that results in concomitant IVH
due to their anatomical proximity to the fourth ventricu-
lar foramina (Fig. 93.6). A large amount of blood in the
fourth ventricle with relatively less blood in the supra-
sellar basal cisterns is especially suggestive of a posterior
circulation saccular aneurysm rupture (e.g., posterior
inferior cerebellar artery aneurysm), whereas rupture of
anterior and posterior communicating artery aneurysms
tends to fill the lateral and third ventricles.
Traumatic Intraventricular Hemorrhage
The prevalence of traumatic IVH among patients with
blunt head trauma is low, between 0.4% and 4% [19]. How-
ever, IVH has been found to occur in 10–35% of moderate
to severe traumatic brain injuries (e.g., penetrating trauma
such as gunshot wound or severe blunt trauma) [20]. Out-
comes of patients with traumatic IVH are poor. In one
study, only 30% of patients made a functional recovery
[19], and in another study less than half the patients were
independent at a 6-month follow-up [21]. Patients with a
lower Glasgow Coma Scale (GCS) score on presentation,
older patients with traumatic IVH, patients with higher
volume of blood and patients with hemorrhage in the third
or fourth ventricles tend to have worse outcomes [19,21].
When blood involves the lateral ventricles only, a better out-
come is expected. Isolated traumatic IVH is rare. Traumatic
IVH usually results from the spread of an adjacent intrace-
rebral hematoma, may be secondary to hypoxia, secondary
to coagulopathy, related to stretch- or shear-related tears of
ependymal vessels or choroid plexus, or related to diffuse
axonal injury along with hemorrhage in the corpus callo-
sum and dorsolateral brain stem [21]. Outcomes in patients
with isolated traumatic IVH are better than patients with
traumatic IVH and associated brain injury. This suggests

VI. CLINICAL ASPECTS: MEDICAL AND SURGICAL

460 93. Clinical Aspects of Intraventricular Hemorrhage

FIGURE 93.2 CT shows diffuse, acute intraventricular hemorrhage within the lateral, third and fourth ventricles and mild hydrocephalus
(A, B, C) and a left thalamic subependymal intracerebral hemorrhage (D). A right frontal ventriculostomy catheter was placed. Angiogram shows
a tuft of vessels in the ventricular surface, consistent with anterior ventral thalamic/intraventricular AVM with deep venous drainage into the
vein of Galen (E). The AVM was embolized using NBCA followed by radiosurgery (F).

TABLE 93.2 Etiology of Intraventricular Hemorrhage
Primary IVH
Intraventricular/periventricular tumors
Choroid plexus tumors
Ependymoma
Intraventricular metastases
Adjacent parenchymal tumors such
as glioblastoma multiforme (GBM) or
metastases
Intraventricular/periventricular vascular
malformations:
Intraventricular aneurysms
Arteriovenous malformations
Dural arteriovenous fistulas
Cavernous malformations especially the
ones with subependymal location
Trauma
Coagulopathy
Moyamoya disease
Fibromuscular dysplasia
Neonatal germinal matrix IVH
Idiopathic
Secondary IVH
Hypertensive intracerebral
hemorrhage
Vascular malformations:
Aneurysms
Arteriovenous malformations
Dural arteriovenous fistulas
Cavernous malformations
Trauma
Tumors
Coagulopathy
Vasculitis
Pituitary apoplexy
Hemorrhagic infarction
that the associated brain injury in these patients is account-
able for the poor outcomes rather than the traumatic ven-
tricular hemorrhage. The hemorrhage usually does not
occur without extensive associated damage, and so the
outcome is rarely good.
SYMPTOMS OF INTRAVENTRICULAR
HEMORRHAGE IN ADULTS
Patients presenting with primary IVH often complain
of a sudden onset of headache, nausea, and vomiting
and occasionally altered mental status and/or level of
consciousness. Occasionally, patients may have progres-
sive or fluctuating symptoms. Focal neurological signs
are either minimal or absent with primary IVH, and
most commonly involve cranial nerve abnormalities
[22,23]. Focal or generalized seizures are not typical but
may occur. As clinical symptoms and signs of primary
IVH are related to a sudden increase in ICP, symptoms
can sometimes be minimal if the ventricles have not
become distended, and there is no increase in ICP [22,23].

VI. CLINICAL ASPECTS: MEDICAL AND SURGICAL

 Symptoms of Intraventricular Hemorrhage in Adults 461

FIGURE 93.3 A 59-year-old female presented with acute onset of headache, nausea, vomiting, and altered mental status. She was found to
have an intraventricular hemorrhage with casting of the ventricles associated with mild dilatation of ventricular system and large cerebellar
hemorrhage (A, B, C). We placed an emergent ventriculostomy. An angiogram showed an AVM arising from the right posterior inferior cerebel-
lar artery. Patient had a suboccipital craniectomy and resection of the AVM and evacuation of the hemorrhage. The patient had a poor outcome.

FIGURE 93.4 CT showing acute hemorrhage in the deep left cerebellum (A) with intraventricular extension of hemorrhage within the lateral,
third, and fourth ventricles and mild hydrocephalus (B, C). A right frontal ventriculostomy catheter was placed. An angiogram was performed
and showed a left tentorial dural AVF fed by distal branches of the superior cerebellar artery, and the tentorial artery (D). Successful embolization
using Onyx embolic agent was performed. The patient made a tremendous neurological recovery.
462 93. Clinical Aspects of Intraventricular Hemorrhage

FIGURE 93.5 CT shows a posterior fossa hemorrhage including the fourth ventricle, extending into the third and lateral ventricles. There is
hyperdense clot in the fourth ventricle, extending through the cerebral aqueduct into the third ventricle and bilateral lateral ventricles (A, B, C).
We performed an angiogram that showed a distal left PICA aneurysm as the cause of hemorrhage (D). The aneurysm was successfully embolized
using Onyx (E).

In patients with secondary IVH, neurological symptoms
and signs are related to ICH (hemiplegia, hemisensory
loss, visual defects, stupor, and coma) or SAH (worst
headache of life, nausea, vomiting, and meningismus)
and will vary depending upon the location and size of
the hemorrhage. Blood clots may obstruct CSF drainage
resulting in acute obstructive hydrocephalus, especially
with blood in the third or fourth ventricle. Patients may
also develop communicating hydrocephalus [24]. One-
half to two-thirds of patients with IVH have some degree
of hydrocephalus on the initial computerized tomogra-
phy (CT) scan [22–24]. Symptomatic cerebral vasospasm
may occur as well in unusual cases of primary IVH [25].
DIAGNOSIS OF INTRAVENTRICULAR
HEMORRHAGE IN ADULTS
Diagnosis of IVH with or without associated ICH,
SAH, or hydrocephalus can be confirmed by a noncon-
trast head CT scan showing presence of blood inside
the ventricles. On noncontrast head CT, blood appears
hyperdense in the ventricles and tends to pool depend-
ently, best seen in the occipital horns when a small
amount of blood is present within the ventricles. Occa-
sionally, the amount of blood in the ventricles is signifi-
cant with ventricular blood clots resulting in formation
of casts of the entire ventricular chambers.
Magnetic resonance imaging (MRI) further helps in
identifying the etiology of IVH and is more sensitive
than CT in identifying very small amounts of blood in
the ventricles. T2 weighted imaging, fluid-attenuated
inversion recovery (FLAIR) imaging, and susceptibil-
ity weighted imaging (SWI) sequences specifically can
be used to diagnose small amount of IVH. Within 48 h
from IVH onset, blood will appear as hyperintense
relative to the CSF signal on MRI. As time progress,
the signal attenuates and blood become more hypoin-
tense. If no etiology is identified, and there is no obvi-
ous trauma or coagulopathy, catheter angiography
can aid in identifying vascular malformations, dAVFs,
and aneurysms.

VI. CLINICAL ASPECTS: MEDICAL AND SURGICAL

 Grading of Intraventricular Hemorrhage in Adults 463

FIGURE 93.6 CT shows intraventricular hemorrhage in all of the ventricles, with the greatest component in the fourth ventricle (A, B, C).
Additionally there is a thin, hypodense subdural collection along the left aspect of the falx. There is a cisternal subarachnoid hemorrhage. A right
frontal ventriculostomy catheter was placed. Angiogram shows a ruptured distal right anterior inferior cerebellar artery aneurysm (D). The aneu-
rysm was successfully embolized using Onyx (E).

GRADING OF INTRAVENTRICULAR TABLE 93.3 Graeb Score [26]

HEMORRHAGE IN ADULTS
Several scoring systems based on CT scans have been
implemented to estimate the amount and severity of
IVH. The most widely used grading system is the “Graeb
score” that is calculated based on the amount of blood in
each ventricle separately (Table 93.3) [26]. The maximum
Graeb score is 12: grade 1–4 is referred to as mild, 5–8 as
moderate, and 9–12 as severe [26]. The Graeb score can
be used for predicting patient outcomes following IVH.
One study reported that in patients with an ICH volume
greater than 60 cm [3], a Graeb score ≥6 was significantly
associated with acute hydrocephalus, whereas a score ≤5
was associated with a GCS score ≥12 on admission [27].
The expanded or modified Graeb score was devel-
oped to differentiate specific regions of the ventricular
system and give a more accurate measure of change in
IVH volume over time (Table 93.4) [14,28]. It divides
each of the lateral ventricles into compartments: tem-
poral tip, lateral body, and occipital horn in addition
Lateral 1. Point for trace blood
ventricles 2. Points for less than half the ventricle filled with
blood
3. Points for more than half the ventricle filled with
blood
4. Points for ventricle filled with blood and
expanded
Third and 1. Point for blood present with normal size ventricle
fourth 2. Points for ventricle filled with blood and
ventricles expanded
to third and fourth ventricles. It also takes into account
the estimated IVH volume in each compartment. Extra
points are given for expansion of the separate ventricu-
lar compartments, thus the maximum score is 32.
Hallevi et al. proposed another IVH scoring system,
the IVH score (IVHS) that also assigns a number to each
lateral ventricle based on the extent of bleeding (0–3),
then adds one point for the presence of hydrocephalus
(Table 93.5). The third and fourth ventricles each are

VI. CLINICAL ASPECTS: MEDICAL AND SURGICAL

464 93. Clinical Aspects of Intraventricular Hemorrhage

TABLE 93.4 Modified Graeb Score [14]

Score for Each Ventricle

Right Right Lateral Right Occipital Left Temporal Left Lateral Left Occipital Third Fourth
Blood % Temporal Tip Ventricle Horn Tip Ventricle Horn Ventricle Ventricle

None 0 0 0 0 0 0 0 0

≤25 1 1 1 1 1 1 2 2

>25 to ≤50 1 2 1 1 2 1 2 2

>50 to ≤75 2 3 2 2 3 2 4 4

>75 to 100 2 4 2 2 4 2 4 4

Expanded +1 +1 +1 +1 +1 +1 +1 +1

TABLE 93.5 IVH Score [29]

Usually a right frontal EVD at the Kocher’s point is pre-
Lateral ventricles 1. Point for blood filling up to one- ferred unless specific contraindications are present. Gen-
third of the ventricle erally, EVD placement is well tolerated, with a relatively
2. Points for blood filling one-third to low incidence of complications [17]. The most frequent
two-thirds of the ventricle
3. Points for blood filling more than
complications are intraparenchymal hemorrhage, cath-
two-thirds of the ventricles eter-related infection, and obstruction requiring reinser-
tion [17,30]. The incidence of ventriculostomy-related
Third and fourth ventricles 0 No blood
infections has been reported to be between 0% and 22%
1 Partial or complete filling with blood [17]. Infection necessitates replacement of the EVD and
Presence of hydrocephalus 0 No may prolong hospital stay, antibiotic-associated cost and
morbidities, and occasionally life-threatening sequelae
1 Yes
[17]. Protocols of prophylactic antibiotic treatment have
Formula to calculate score IVHS = 3 × (RV + LV) + III + IV + 3 × H varied widely, including perioperative use, or continued
Convert to IVH volume [IVH volume (mL) = eIVHS/5] use for the duration of drainage.
EVD is associated with a 0–33% risk of hemorrhagic
III, third ventricle score; IV, fourth ventricle score; H, hydrocephalus; IVHS,
intraventricular hemorrhage score; LV, left lateral ventricle score; RV, right
complication [17,30]. It is usually associated with mul-
lateral ventricle score. tiple passes, use of drill twister, concomitant use of anti-
coagulation and/or antiplatelet therapy, and bleeding
assigned a score of 0 for no blood and 1 for partial or disorders.
complete filling with blood. The IVHS ranges from 0 (no Inadequate placement of the EVD catheter tip is not
IVH) to 23 (all ventricles filled with blood and hydro- infrequent. It could be as high as 12.3% as determined by
cephalus present) [29]. postprocedural CT scans [31]. Several techniques could
minimize complications including the use of the Ghajar
guide, stealth navigating system, and using the appro-
TREATMENT OF INTRAVENTRICULAR priate skull landmarks.
HEMORRHAGE IN ADULTS EVD catheter occlusion secondary to blood clots usually
requires either repeated flushing of the catheter to clear the
Placement of External Ventricular Drain for tubing or EVD replacement using a larger lumen catheter.
Intraventricular Hemorrhage and Obstructive In a prospective case–control study, 59% of IVH with an
EVD required catheter replacement [14,32]. To minimize the
Hydrocephalus
risk of catheter obstruction, a second EVD may be placed in
Acute obstructive hydrocephalus with signs and the contralateral ventricle or the EVD can be placed contra-
symptoms of increased ICP (altered mental status, loss lateral to the ventricle with greatest IVH volume.
of consciousness, nausea, and vomiting) following IVH In the setting of very large IVH (>40 mL) with casting
is a life-threatening condition, and requires immediate and mass effect, a single catheter may be ineffective in
management. Even though ICP can be managed medi- removing substantial hematoma from the contralateral
cally with sedation and osmotic diuretics, medical ther- side, especially if the foramina of Munro is obstructed;
apy is often insufficient necessitating the need for EVD in this case, bilateral simultaneous EVD catheters may
placement for drainage of CSF and ICP monitoring. increase clot resolution [14,33].

VI. CLINICAL ASPECTS: MEDICAL AND SURGICAL

 References
If the patient is responsive, follows commands, and
head CT shows mild hydrocephalus, the patient can be
monitored closely with frequent neurological examina-
tions and head CT to monitor the size of the ventricles
[34]. Occasionally, permanent CSF diversion using ven-
triculoperitoneal shunting is required. It is important to
note that placement of an EVD does not eliminate the
morbidity and mortality of IVH that is related to under-
lying damage from the toxic effects of ventricular blood
on adjacent periventricular brain tissue [17].
Use of Intraventricular Thrombolysis in
Conjunction With External Ventricular Drain
Given the modest effect of EVD on mortality and poor
outcomes associated with IVH, more effective strategies
are required. In preclinical studies using animal mod-
els of IVH, larger volume of blood clot injected into the
ventricles and prolonged exposure of the ventricles to
blood were associated with a higher risk of pathologi-
cal changes including subarachnoid fibrosis, extensive
ependymal cell loss, and subependymal glial prolifera-
tion on the lateral ventricle walls and mortality. These
changes were minimized or reversed when lytic therapy
(urokinase or tissue plasminogen activator (tPA)) was
injected into the ventricles [35–38]. Observational studies
that followed, showed that intraventricular thromboly-
sis was effective in improving IVH clearance, reducing
ICP, and decreasing mortality when used in conjunc-
tion with EVD [39–41]. A systematic review showed that
the fatality rate for conservative treatment in the set-
ting of severe IVH due to SAH or ICH was 78%, 58%
with EVD, and 6% with EVD and fibrinolytic therapy
[42]. Furthermore, the poor outcome rate for conserva-
tive treatment was 90%, 89% with EVD, and 34% with
EVD and fibrinolytic agents [42]. Based on these smaller
case series and animal models [43], the safety and fea-
sibility of intraventricular thrombolysis was tested in
a Phase II prospective randomized clinical trial, which
showed that intraventricular thrombolysis with uroki-
nase demonstrated earlier resolution of intraventricular
blood clots when compared with EVD treatment alone
[44]. However, urokinase was withdrawn from the mar-
ket because of safety concerns, and recombinant tissue
plasminogen activator (rt-PA) became the thrombolytic
of choice for IVH. The Clot Lysis Evaluating Accelerated
Resolution of Intraventricular Hemorrhage (CLEAR-
IVH) trial was a phase 2 randomized clinical trial that
included 48 patients treated with 3 mg rt-PA or placebo
[45]. Patients treated with rt-PA had a more rapid clear-
ance of IVH and improved outcome as compared to
placebo [45]. Blood clot resolution in CSF follows first-
order kinetics, and the injection of thrombolytic agents
into the ventricular space could increase the rate of clot
VI. CLINICAL ASPECTS: MEDICAL AND SURGICAL
465
resolution [44]. The Clot Lysis: Evaluating Accelerated
Resolution of Intraventricular Hemorrhage Phase III
(CLEAR III), a randomized clinical trial testing the ben-
efit of clot removal for IVH with EVD and rt-PA versus
EVD and placebo just closed in 2014 [46]. Preliminary
analyses showed that low doses rt-PA (1.0 mg) is safe
in patients with stable IVH clots and may increase lysis
rates [14].
Open Craniotomy and Surgical Evacuation of
Intraventricular Hemorrhage
There have been mixed results with surgical removal
of IVH using an open craniotomy with direct surgi-
cal evacuation and utilization of minimally invasive
instruments (e.g., neuroendoscope) for drainage of IVH
[14,47,48]. Zhang et al. compared 22 patients with IVH
and less than 30 mL ICH who underwent neuroendo-
scopic aspiration of IVH within 48 h to a control group of
20 patients with IVH treated with EVD and intraventric-
ular urokinase [49]. More patients in the neuroendoscopy
group showed good recovery after 2 months of surgery,
whereas the difference in mortality rate between the two
groups was not statistically significant [49]. The litera-
ture on patients undergoing open craniotomy with direct
surgical evacuation of IVH secondary to SAH is mixed
[50,51]. The use of neuro-endovascular approaches to
extract intraventricular blood has also been described in
some cases [52]. The management strategy in cases with
secondary IVH should include treatment of both the pri-
mary cause of IVH (e.g., aneurysm and AVM) and the
potential secondary effect of obstructive hydrocephalus.
PROGNOSIS
Prognosis of patients who develop IVH is variable,
extending from a good functional recovery to very poor
outcomes and death, depending on the etiology of hem-
orrhage. Secondary IVH, for example, due to a large
hypertensive ICH carries a higher risk of death than
primary IVH (up to 80%) [14]. Advanced age, the extent
of IVH (high Graeb score), GCS score ≤8, development
of obstructive hydrocephalus are also associated with a
higher risk of poor outcomes [23,24].
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C H A P T E R
94
Clinical Aspects of Subdural Hemorrhage
(SDH)
A. Ozpinar, B. Jankowitz
University of Pittsburgh Medical Center, Pittsburgh, PA, United States
ACUTE SUBDURAL HEMATOMA
Epidemiology
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of the tearing of bridging or cortical surface veins, sec-
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accompanied by cortical contusions, parenchymal
hematomas, or global shearing injury such as diffuse
axonal injury (DAI). Approximately 10–20% of all
patients admitted with a traumatic brain injury (TBI)
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have an ASDH. The incidence increases to 60% for
patients with a Glasgow Coma Scale (GCS) score of 8
or less. Approximately 70% of such patients are older
than 45 years and 40% are older than 65 years, with a
male:female ratio of 3:1. As life expectancy rises, the
incidence of ASDH is also expected to rise. The Trau-
matic Coma Data Bank reports that most ASDHs are
caused by motor vehicle accidents (MVAs) and falls.
MVAs are more frequent in the younger population
(15–30 years) and falls are more frequent in the age
group of 45–80 years [1,2].
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