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Chapter 3
Intracerebral Hemorrhage (ICH)
Approach: Bedside Practical Review
ThomasJ.Cusack andWendyZiai
Key Points
1. Recognize intracerebral hemorrhage (ICH) and stabilize the patient’s airway and
circulation. Recognize intracranial hemorrhage as soon as possible utilizing
computed tomography (CT) and computed tomography angiography (CTA).
Unstable patients (those with rapidly declining Glasgow Coma Scale or anyone
with a Glasgow Coma Scale less than 8) should undergo emergent intubation to
secure their airway and be sedated after a thorough neurologic exam has been
obtained. The ICH score and Functional Outcome in Patients with Primary
Intracerebral Hemorrhage (FUNC) scores should be assessed.
2. Systolic blood pressure should be rapidly controlled to a range of 140–180mmHg
in small hemorrhages without intracranial hypertension using beta blockers or
calcium channel blockers. Target the goals of normothermia, normoglycemia,
and normonatremia.
3. Elevate the head of the bed to 30° and treat elevated intracranial pressure if pres-
ent with appropriate surgical and medical measures. Patients should be assessed
for the need for surgical intervention for control of elevated intracranial pressure; using an external ventricular drain or, in appropriately selected patients,
decompressive craniotomy. Also, consideration of evacuation may be appropriate in a select subset of ICH patients. Not all patients benet from surgical
intervention.
4. Correct any coagulopathy if present. Reverse anticoagulation in patients with
ICH who are on anticoagulant or antiplatelet drugs.
5. Once stabilized, patients should be reassessed with CT imaging and have ongo-
ing management of blood pressure, cerebral edema, intracranial pressure, and
seizures as they arise.
T. J. Cusack · W. Ziai (*)
Division of Neurosciences Critical Care, Departments of Neurology, Neurosurgery, and
Critical Care Medicine, The Johns Hopkins Hospital, Baltimore, MD, USA
e-mail: tcusack1@jhmi.edu; weziai@jhmi.edu
C. N. Rodríguez et al. (eds.), Neurosonology in Critical Care,
https://doi.org/10.1007/978-3-030-81419-9_3
47© Springer Nature Switzerland AG 2022
48
T. J. Cusack and W. Ziai
3.1 Introduction
The delivery of neurocritical care is not so much the performance of one large lifesaving act but rather the careful execution and minding of hundreds of smaller
things that taken together can add up to saving a life that might otherwise be lost and
hopefully improving a life that otherwise would be greatly limited. This is particularly true in the care of intracerebral hemorrhage (ICH), a challenging entity faced
around the world by neurosurgeons, neurologists, and emergency care providers of
all stripes. The past 40years have seen marked improvement in the mortality of ICH
from around 47% to 29% for those cases that make it to the hospital [1], but while
a great deal of research has demonstrated the safety of a number of approaches that
will be discussed in this chapter, very little research has been denitively shown to
improve outcomes or mortality. Only 10–20% of patients who survive hospitalization currently regain functional independence [2]. It is not possible to point to any
one intervention or approach that has improved outcomes, so obtaining the best
possible outcomes for your patient will involve minding both the specic issues surrounding management of ICH as well as the general principles of good quality critical care. In this sense the problem space for ICH is limited by the solutions available
to the caregiver at the time. In this chapter, we will review the approach to ICH from
the practical perspective of the bedside practitioner, distilling the approach the
authors take at the bedside, and showing the evidence from which that approach is
derived. At the end of the chapter an algorithm for care is presented, but please
understand that the care of ICH is far from standardized as the range of patients and
pathology that falls under this category is exceedingly broad.
3.2 Intracerebral Hemorrhage (ICH)
Intracerebral hemorrhage is a type of intracranial bleed that occurs specically
within the tissue of the brain or ventricles. In the eld, the sudden onset of neurologic decits should immediately raise concern for a stroke. Rapid recognition of
neurologic decits by bystanders or trained emergency medical responders is essential and rapid transport to a hospital capable of rapid imaging with a CT scan of the
head and brain is the essential rst step in appropriate diagnosis and treatment.
Brain CT and careful history and neurologic exam can serve to help delineate an
ischemic stroke from an intracranial bleed. Intracranial bleeds can occur within the
parenchyma of the brain or in the meninges and associated potential spaces including the epidural space, subdural space, and subarachnoid space. Bleeds in these
areas are covered in detail in other chapters. Intracerebral hemorrhage is a subtype
of intracranial bleed that is intraparenchymal with or without extension into the
ventricles and can occur anywhere in the brain. It is broadly categorized as either
“deep” or “lobar.” “Deep ICH” describes ICH within the basal ganglia and internal
3 Intracerebral Hemorrhage (ICH) Approach: Bedside Practical Review
49
capsule (35–70% of cases), brain stem (5–10% of cases), or cerebellum (5–10% of
cases). “Lobar ICH” describes the other 15–30% of cases where it is seen in cortical
and subcortical areas [3].
3.3 ICH: Presenting Symptoms
The presenting symptoms of ICH are as varied as the regions of the brain that can
be affected. Headache and vomiting are seen in approximately one half of patients
with ICH [4]. While there can be sudden onset during marked physical exertion or
emotional moments, most occur during routine activity. Unlike ischemic embolism
or subarachnoid hemorrhage, the neurologic symptoms of ICH are often not abrupt
or maximal at the time of onset but rather the symptoms usually worsen over a
period of minutes to hours. Symptoms can be absent in small hemorrhages, which
clinically are indistinguishable from a gradually progressing stroke until imaging
can be obtained. ICH is rarely a clinical diagnosis alone, but exam and history can
help. If a headache is present, it can be due to elevated intracranial pressure or blood
in the cerebral spinal uid irritating the meninges. Most headaches occur with lobar
or cerebellar hemorrhages. Patients may also have stiff neck or meningismus if
there is intraventricular blood.
If the putamen is involved, the white matter tracts will be affected with hemisensory loss, hemiplegia, possible homonymous hemianopsia, and possible gaze palsy.
A cerebellar hemorrhage will often have extension into the fourth ventricle and
often originate in the dentate nucleus. There is often a sudden loss of balance with
consequent inability to ambulate, notably without any hemiparesis, as well as vomiting, headache (sometimes with referred pain to the back of head or shoulders), and
neck stiffness, and in patients with extension into the pontine tegmentum gaze,
palsy and facial weakness can be observed. A hemorrhage in the thalamus can cause
hemiparesis, hemisensory loss, and aphasia if the bleed is in the dominant hemisphere and hemineglect if it is in the nondominant hemisphere. Most lobar hemorrhages occur in the parietal and occipital lobes. Lobar hemorrhages have a higher
incidence of seizures as seizure is a cortical symptom. Occipital hemorrhages often
present with dense contralateral homonymous hemianopsia. Frontal hemorrhages
often cause a contralateral paresis of the leg with relative sparing of the upper
extremity. The most neurologically severe location for an ICH is the pons, which
often causes a deep coma and total paralysis with pinpoint pupils and absent horizontal eye movements. Facial palsy, deafness, dysarthria, and ocular bobbing may
be observed if the patient is awake. Seizures will occur in the rst 72h after ICH in
4–29% of patients [5], again most commonly in those with lobar hemorrhages. In
larger bleeds, decreased level of consciousness is commonly seen. Stupor or coma
is an ominous sign in ICH.
50
T. J. Cusack and W. Ziai
3.4 ICH: Who Gets andWhy
Intracerebral hemorrhage is a particularly challenging entity because it can happen
virtually anywhere in the brain with severity ranging from nearly clinically undetectable to the almost invariably fatal. ICH is prevalent throughout the world, with
ICH and subarachnoid hemorrhage (SAH) together accounting for roughly 10–20%
of the world’s strokes, while ischemic stroke accounts for the remaining 80–90%
[6]. There were 5.3 million ICH cases worldwide in 2010 with 3 million deaths of
which 84% were borne by low- and middle-income countries (80% of the cases and
63% of the deaths occurred in Sub-Saharan Africa, Central Asia, and Southeast
Asia) [7]. Between 1990 and 2010, the global incidence of hemorrhagic strokes
(ICH and SAH combined) increased by 47%. In high-income countries, the ageadjusted incidence rate of hemorrhagic stroke reduced by 8% during those two
decades but rose by 22% in the low- and middle-income countries [7]. The incidence of primary ICH in low- and middle-income countries from 2000 to 2008 was
22 per 100,000 person-years, while in high-income countries it was 10 per 1000,000
person-years [6]. The incidence of primary ICH by population closely tracks the
incidence of hypertension in those populations, with a systematic review of 36
population- based epidemiological studies showing the incidence rate of ICH per
100,000 person years to be 51.8 in Asians, 24.2 in Whites, 22.9 in Blacks, and
19.6in Hispanics [2]. Patients who make it to the hospital still face 30-day fatality
risk of up to 45% in some studies [8]. Those who survive have markedly limited
function in activities of daily living, with only 10–20% regaining functional independence [9, 10]. The challenge facing the world in coming decades will be not only
treating the ICH in countries with less developed public health infrastructure but
also preventing it in the rst place, which brings us to our discussion of risk factors.
3.5 Risk Factors forICH
3.5.1 Blood Hypertension
Spontaneous ICH is the product of a complex interplay of risk factors, the most
important of which is hypertension [11, 12]. A meta-analysis of 14 case-control
studies demonstrated an increased relative risk for ICH in hypertensive subjects of
3.68 (95% CI, 2.52–5.38) over normotensive people [11]. Patients with baseline
blood pressure over 160/90 were shown in another meta-analysis to have a ninefold
increased risk of ICH [12]. Even among those with normal blood pressure, increasing blood pressure is related linearly to increasing risk of lobar and nonlobar hemorrhagic stroke [13]. Chronic hypertension is generally associated with ICH in the
basal ganglia, thalamus, brainstem, and cerebellum. Cocaine intoxication and
malignant hypertension should also be considered at the time of presentation.
3 Intracerebral Hemorrhage (ICH) Approach: Bedside Practical Review
51
3.5.2 Other Risk Factors
Smoking carries a 1.5-fold relative risk for ICH [14, 15]. ICH is also more likely in
those with high alcohol intake, low cholesterol levels [16, 17], or diabetics with a
relative risk of 1.6 [18]. Cerebral amyloid angiopathy (CAA) alone accounts for
roughly 50% of all lobar hemorrhages [19]. The ICH seen with CAA is often lobar
and rarely cerebellar. Patients taking aspirin [20], warfarin [21], and direct anticoagulants (DOACs) (dabigatran etexilate, rivaroxaban, and apixaban) have an
increased risk of ICH, although this risk is often far exceeded by the benet provided by the prevention of ischemic strokes [22]. Although no prospective studies
have evaluated the impact of specic modiable risk factor management (e.g., antihypertensive management and smoking cessation on the risk of intraparenchymal
hemorrhage), such lifestyle modications are likely to reduce the risk of ICH signicantly. The job of prevention is largely in the hands of primary care providers
but, after an ICH mitigating, future risk ideally would involve lifestyle modication
and medical treatment for any of the above risk factors.
3.6 ICH: Pathophysiology
ICH occurs after a parenchymal blood vessel in the brain ruptures. Common etiologies include amyloid angiopathy, tumors, ischemic stroke with subsequent hemorrhagic conversion, thrombosis of dural venous sinuses and cortical veins, vasculitis,
and vascular malformations such as cavernous angiomas, arteriovenous stulas,
arteriovenous malformations, venous angiomas, and aneurysms. Most “primary”
cases of spontaneous ICH are thought to be caused by the rupture of Charcot
Bouchard aneurysms in the cerebellum, basal ganglia, pons, and thalamus, where
small penetrating vessels are abundant. Charcot Bouchard aneurysms are presumed
to be the result of chronic hypertension-related lipohyalinosis of small arterioles
which causes defects in the muscular layer making them prone to rupture [23]. The
“primary” etiology is a diagnosis of exclusion based on a thorough investigation for
“secondary” structural causes of ICH. “Secondary” causes of ICH can include arteriovenous malformation (AVM), cerebral venous sinus thrombosis, hemorrhagic
transformation of ischemic stroke, Moyamoya disease, tumor, and aneurysms. If a
patient is younger, and has a lobar ICH or intraventricular blood, this suggests
higher risk of secondary ICH [24].
Advanced age, deep location (basal ganglia, thalami, or posterior fossa), or history of hypertension are often taken to suggest primary ICH, although cerebral angiography studies show that these are not always reliable indicators, and patients with
these features may have coexisting vascular abnormalities [25, 26].
52
T. J. Cusack and W. Ziai
3.7 ICH: Initial Management
The initial triage of a neurological patient should always focus on quickly identifying life-threatening issues and stabilizing the patient before moving on to identify
the cause of neurologic decit with a focus on what is common and what is treatable. The rst step in management should focus on the stabilization of the airway,
breathing, and circulation. The airway should be secured if the patient does not
appear to be able to protect their airway. The need for an accurate neurologic exam,
while of great importance, must be balanced against the risk of airway compromise.
3.7.1 Airway: Intubation
Rapid sequence endotracheal intubation (RSI) may be necessary in the emergent
setting for the rapidly deteriorating patient. Patients undergoing RSI may benet
from pretreatment with lidocaine 1.5mg/kg if they appear to have ICP issues as this
may blunt the rise in intracranial pressure that can be associated with intubation
[27]. Induction with etomidate (0.2mg/kg) may preserve cerebral perfusion pressure. Paralysis can be obtained with succinylcholine (1.5 mg/kg), rocuronium
(1mg/kg), or vecuronium (0.15mg/kg). Propofol 5–80°μg/kg/min may be a good
initial choice as a continuous drip but does carry the risk of propofol infusion syndrome [28]. Elevated creatine kinase, amylase, lipase, or serum triglycerides can
indicate a need to discontinue propofol and initiate another sedative such as midazolam or dexmedetomidine.
3.7.2 Clinical Scoring andExamination
Once stable from a cardiopulmonary perspective, clinical severity should be scored
and documented using the NIH Stroke Scale (NIHSS) and Glasgow Coma Scale
(GCS) [29–31]. Hourly or more frequent neurologic exams should be scheduled
thereafter.
3.7.3 ICH: Imaging
The American Heart Association considers neuroimaging with CT (the gold standard) or MRI mandatory, with the use of contrast-enhanced CT angiography (CTA)
when available to assess for vascular pathology and likelihood of further clot expansion [26]. Vascular abnormalities should be suspected in women, those under the
age of 65, those with lobar ICH, intraventricular hemorrhage (IVH), and patients
without a history of hypertension, smoking, or coagulopathy [32]. Catheter
3 Intracerebral Hemorrhage (ICH) Approach: Bedside Practical Review
angiography can conrm denitively if there is an underlying vascular lesion, but
this is often only available at larger centers [33]. If cerebral venous sinus thrombosis
is suspected based on hematoma location, unusual appearance of cerebral sinuses,
or increased relative edema volume then CT venography or magnetic resonance
venography (MRV) should be performed [34].
The volume of ICH is an important factor in outcomes, with volumes over 30mL
tending to have increased mortality and morbidity [10]. One recent meta-analysis
suggested that for each 1mL increase in hemorrhage volume at hospital admission,
the odds of early neurological deterioration increases by 37% [35]. The volume of
ICH can be accurately assessed using a range of automated computational techniques if the required software is available, but a quick estimate can be garnered by
applying the ABC/2 method to the initial noncontrast CT image. All measurements
should be obtained on axial slices, with A being the largest diameter of hematoma
seen in any slice and B the diameter taken perpendicular to that on the same slice. C
is the slice thickness multiplied by the number of slices. These three values multiplied together and then divided by two give an estimate of the volume of the hematoma assuming a spherical shape. While not as accurate as image analysis software
available commercially, it is an effective method for quickly assessing hematoma
volume [36].
53
3.7.4 ICH: Grading Scales
Intracranial hemorrhage (ICH) grading scales are routinely used to assess baseline
severity, to facilitate communication between providers, and to frame expectations
of family members. They should not be used in isolation, however, as reliance on
grading scales risks producing a self-fullling prophecy in which patients expected
to do poorly will have poor outcomes due to limitations of acute interventions [37,
38]. The ICH score [39] has seen broad clinical adoption as a number of studies
have validated its use. The ICH score includes ve independent risk factors for
30-day mortality which are assigned weights to derive a score from 0 to 6 (Table3.1).
The timing of the GCS is important, with studies showing that the GCS assessed
once the patient has clinically stabilized has the most utility as compared to an initial assessment [40]. Another useful prognostication tool, the FUNC score was
developed to estimate the likelihood of functional independence at 90days and can
help frame expectations for families and caregivers (Table3.1) [41].
3.7.5 Fluid Management
Volume status should be assessed along with routine monitoring of electrolytes. To
avoid exacerbating any brain edema, it is recommended that hyponatremia be
avoided. Hyponatremia has been shown to occur in roughly 15% of ICH patients
54
ICH scoreFUNC score
02
00
91
eD
p1
o1
07
T. J. Cusack and W. Ziai
Table 3.1 The components of the ICH and FUNC scores presented along with their respective
point weights and the mortality and independence implications for each total score, respectively
Component Points Component Points
GCS ICH volume
3–4 2<30 4
5–12 130–6
13–150 >6
Age Age
≥80
<800 70–7
ICH volume
≥30 ml
<30 ml 1Lobar 2
IV hemorrhag
Yes1 Infratentorial 0
No 0 GCS
Infra-tentorial origin
Yes1
No 0 Pre-ICH cognitive impairment
Total ICH score 30-days mortality (%)Yes 0
010N
113 Total FUNC score Independent at 90 days (%)
226 0–4 0
372 5–7 29
4978 48
5–6 100 9–1
1< 70 2
80
0
≥
ICH location
ee
9
≥
≤8
11 95
0
2
0
5
IV intraventricular, FUNC score functional outcome in patients with primary intracerebral hemor-
rhage score, ICH score intracerebral hemorrhage score, ICH intracerebral hemorrhage
and to worsen outcomes in two retrospective case series, with the syndrome of inappropriate antidiuretic hormone being the most common etiology [42, 43].
Normovolemia should be maintained with isotonic uids to avoid exacerbating
brain edema [44]. In patients with elevated ICP from signicant perihematomal
edema or marked mass effect, hyperosmolar therapy with hypertonic saline (either
2% or 3% solution) may be considered. The goal is to target a hypernatremic state
(150–155mEq/L) and a serum hyperosmolarity (300–320mOsm/L). Serum sodium
should never be allowed to decline more than 12mEq/L in a 24-h period as this can
cause rebound cerebral edema and further exacerbate ICP.
3.7.6 Follow-Up Imaging
After initial hemorrhage, the hematoma can expand further in up to one-third of
patients and generally occurs within 24h, although delayed expansion is described
[45]. Expansion is signicantly associated with clinical deterioration and worsened
outcomes, especially when resulting in midline shift or cerebral herniation [10, 46].
The “spot sign” is a hyperdense spot initially dened on CTA source images, which
when seen is predictive of hematoma growth (Fig.3.1) [47]. If a subsequent noncontrast head CT demonstrates extravasation of contrast into the hematoma, this,
along with the spot sign, is signicantly associated with ICH growth and poor
ab
cd
3 Intracerebral Hemorrhage (ICH) Approach: Bedside Practical Review
55
Fig. 3.1 (a) Patient with a spot sign visible in a putaminal ICH. (a) Demonstrates left posterior
putaminal ICH with mild surrounding edema. In (b), an arrow indicated the small focus of contrast
enhancement seen on CTA consistent with the spot sign. (c) Shows the postcontrast CT wherein
the white arrow shows the spot sign has enlarged. (d) Shows an unenhanced CT taken 1 day later
showing the development of IVH and expansion of the ICH (Wada etal. [48])
outcome [47]. Although it is possible to assess for both an “early” (30s postcontrast
injection) and “late” (2–5min postcontrast injection) spot sign on CTA or postcontrast CT, the current utility of this information is not well dened in the absence of
therapies specically targeted to prevent ICH expansion. In the PREDICT study,
patients with the spot sign have signicantly higher mortality at 3months (43.4%)
as compared to patients who were spot sign negative (19.6%) [42].
56
T. J. Cusack and W. Ziai
3.7.7 Blood Pressure Management
A number of trials have tried to arrest the further expansion of ICH by managing
hypertension. INTERACT1 was a feasibility study that demonstrated the safety and
feasibility of intensive blood pressure reduction in acute cerebral hemorrhage. This
led to INTERACT2, an international, multicenter, prospective, randomized, openlabel, blinded end-point trial of patients with hypertension and ICH occurring in the
prior 6h which randomly assigned patients to receive either intensive treatment of
systolic blood pressure (SBP) to less than 140mmHg or guideline recommended
targeting of SBP to less than 180mmHg [49]. This intensive treatment of blood
pressure failed to result in signicant reduction in hematoma volume or improvement in outcomes on the primary outcome. Another large intensive blood pressure
lowering trial was ATACH2 [50]. This randomized, multicenter, open-label trial
looked at patients with ICH volume <60mL and GCS score of 5 or more, randomizing them to either an intensive SBP target of 110–139mmHg or a standard target
of 140–179mmHg using intravenous nicardipine. The primary outcome was death
or disability at 3months, which was equivalent between the two groups. The aggressive treatment of blood pressure in ATACH2 did not improve outcomes. Therefore,
while a goal SBP of 140mmHg seems to be a safe target, it does not represent an
evidence-based target proven to improve outcomes or reduce mortality, and
SBP<140mmHg may cause adverse effects in some patients. Following the evidence, a target range of SBP 140–180mmHg is what is employed at our institution.
Any blood pressure over 180mmHg or MAP over 130mmHg is treated with a
titrated antihypertensive drip, usually nicardipine (5–15mg/h infusion). Oral antihypertensive agents are used to help achieve longer term blood pressure control, but
are not immediate enough in their antihypertensive effects to be used in the acute
setting.
3.7.8 When toUse andNot toUse Hemostatic Therapy?
Patients with abnormalities of platelets, coagulation factors, or who are taking anticoagulants have an increased likelihood of ICH expansion due to their decreased
propensity to form stable clot. Ultra-early hemostatic therapy with replacement of
the decient factors or transfusion with functional platelets is indicated. Patients on
oral anticoagulants account for up to 20% of patients with ICH [51]. Patients on
vitamin K antagonists (VKAs) should have their drug withheld and should receive
vitamin K but as this takes up to 24h to work they benet from prothrombin complex concentrate (PCC), since this corrects the INR more quickly (5.7h vs. 11.8h,
respectively) and has a better safety prole than fresh-frozen plasma (FFP) [52, 53].
If PCC is unavailable, FFP can be administered. Direct oral anticoagulants including direct thrombin inhibitors (DTIs) and factor Xa inhibitors (FXa-Is) are increasingly used due to their apparent advantages over warfarin and increased indications
for anticoagulation. Currently, only dabigatran has a reversal agent (idarucizumab,