# 09 - 439 Intracerebral Hemorrhage

### 439 Intracerebral Hemorrhage

or symptomatic stenosis. The 30-day risk of stroke was 4.1% in the 
stent group and 2.3% in the surgical group, but the 30-day risk of MI 
was 1.1% in the stent group and 2.3% in the surgery group, suggest­
ing relative equivalence of risk between the procedures. At median 
follow-up of 2.5 years, the combined endpoint of stroke, MI, and 
death was the same (7.2% stent vs 6.8% surgery) and remained so at 
10-year follow-up. The rate of restenosis at 2 years was also similar 
in both groups. The International Carotid Stenting Study (ICSS) 
randomized symptomatic patients to stents versus endarterectomy 
and found a different result: at 120 days, the incidence of stroke, 
MI, or death was 8.5% in the stenting group versus 5.2% in the 
endarterectomy group (p = .006). At median follow-up of 5 years, 
these differences were no longer significant except a small increase 
in nondisabling stroke in the stenting group but no change in the 
average disability. In meta-analysis, carotid endarterectomy (CEA) 
is less morbid in older patients (aged ≥70) than is stenting. Recently, 
transcarotid artery revascularization (TCAR), which involves the 
reversal of blood flow during an angioplasty and stenting proce­
dure, has been offered as an alternative to transfemoral carotid 
artery stenting or when CEA presents high risks. Investigation is 
ongoing in asymptomatic patients to compare medical therapy to 
stenting and CEA. This will likely answer how well medical patients 
do with more modern medical therapy (statins, close blood pres­
sure control, and lifestyle modification).
BYPASS SURGERY
Extracranial-to-intracranial (EC-IC) bypass surgery has been 
proven ineffective for atherosclerotic stenoses that are inaccessible 
to conventional CEA. In patients with recent stroke, an associated 
carotid occlusion, and evidence of inadequate perfusion of the brain 
as measured with positron emission tomography, no benefit from 
EC-IC bypass was found in a trial stopped for futility.
PATENT FORAMEN OVALE
In patients with PFO and/or atrial septal aneurysm with an embolic 
stroke and no other cause identified, three randomized trials using 
various endovascular closure devices individually and in metaanalysis reported a significant (1% per year) reduction in second 
stroke compared to antiplatelet agents. If the neurologic opinion is 
that no other source of stroke is identified and consultation with a 
cardiologist knowledgeable about PFO closure supports interven­
tion, we recommend endovascular PFO closure.
INTRACRANIAL ATHEROSCLEROSIS
The WASID trial randomized patients with symptomatic stenosis 
(50–99%) of a major intracranial vessel to either high-dose aspirin 
(1300 mg/d) or warfarin (target INR, 2.0–3.0), with a combined 
primary endpoint of ischemic stroke, brain hemorrhage, or death 
from vascular cause other than stroke. The trial was terminated 
early because of an increased risk of adverse events related to 
warfarin anticoagulation. With a mean follow-up of 1.8 years, the 
primary endpoint was seen in 22.1% of patients in the aspirin group 
and 21.8% of the warfarin group. Death from any cause was seen in 
4.3% of the aspirin group and 9.7% of the warfarin group; 3.2% of 
patients on aspirin experienced major hemorrhage, compared to 
8.3% of patients taking warfarin.

PART 13
Neurologic Disorders
Intracranial stenting of intracranial atherosclerosis was found to 
be dramatically harmful compared to aspirin in the Stenting and 
Aggressive Medical Management for Preventing Recurrent Stroke 
in Intracranial Stenosis (SAMMPRIS) trial. This trial enrolled newly 
symptomatic TIA or minor stroke patients with associated 70–99% 
intracranial stenosis to primary stenting with a self-expanding stent 
or to medical management. Both groups received clopidogrel, aspi­
rin, statin, and aggressive control of blood pressure. The endpoint 
of stroke or death occurred in 14.7% of the stented group and 5.8% 
of the medically treated groups (p = .002). This low rate of second 
stroke was significantly lower than in the WASID trial and suggests 
that aggressive medical management had a marked influence on 
secondary stroke risk. A concomitant study of balloon-expandable 
stenting was halted early at 125 patients because of the negative 

SAMMPRIS results and due to harm. Therefore, routine use of 
intracranial stenting is harmful, and medical therapy is superior for 
intracranial atherosclerosis.
Dural Sinus Thrombosis  Limited evidence exists to support shortterm use of anticoagulants, regardless of the presence of intracranial 
hemorrhage, for venous infarction following sinus thrombosis. The 
long-term outcome for most patients, even those with intracerebral 
hemorrhage, is excellent.
Acknowledgment
The authors acknowledge the contributions of S. Claiborne Johnston to 
earlier editions of this chapter.
■
■FURTHER READING
Goyal M et al: Endovascular thrombectomy after large-vessel isch­
aemic stroke: A meta-analysis of individual patient data from five 
randomised trials. Lancet 387:1723, 2016.
Grotta JC et al: Prospective, multicenter, controlled trial of mobile 
stroke units. N Engl J Med 385:971, 2021.
Jiang H et al: An updated meta-analysis on the clinical outcomes of 
percutaneous left atrial appendage closure versus direct oral anti­
coagulation in patients with atrial fibrillation. J Am Coll Cardiol 
200:135, 2023.
Joglar JA et al: 2023 ACC/AHA/ACCP/HRS guideline for the diag­
nosis and management of atrial fibrillation: A report of the American 
College of Cardiology/American Heart Association Joint Committee 
on Clinical Practice Guidelines. Circulation 149:e1, 2024.
Powers WJ et al: Guidelines for the early management of patients with 
acute ischemic stroke: 2019 update to the 2018 guidelines for the early 
management of acute ischemic stroke: A guideline for healthcare 
professionals from the American Heart Association/American Stroke 
Association. Stroke 50:e344, 2019.
Saver JL et al: Time to treatment with endovascular thrombec­
tomy and outcomes from ischemic stroke: A meta-analysis. JAMA 
316:1279, 2016.
Sprint Research Group et al: A randomized trial of intensive versus 
standard blood-pressure control. N Engl J Med 373:2103, 2015.
Torbey MT et al: Evidence-based guidelines for the management of 
large hemispheric infarction: A statement for health care profes­
sionals from the Neurocritical Care Society and the German Society 
for Neuro-intensive Care and Emergency Medicine. Neurocrit Care 
22:146, 2015.
J. Claude Hemphill, III, 

Edilberto Amorim, Wade S. Smith

Intracerebral Hemorrhage
Intracerebral hemorrhage (ICH) is a form of stroke (see Chap. 437). 
Compared to ischemic stroke, patients with ICH are more likely to 
present with headache; however, brain imaging is required to distin­
guish these entities. CT imaging of the head is highly sensitive and 
specific for intracranial hemorrhage and determines the location(s) of 
bleeding. Hemorrhages are classified by their location and the under­
lying vascular pathology. ICH is defined as spontaneous hemorrhage 
directly into the brain parenchyma and will be considered here along 
with intracranial vascular anomalies such as arteriovenous malforma­
tions (AVMs) of the brain. Other categories of intracranial hemorrhage 
include bleeding into subarachnoid, subdural, or epidural spaces, usu­
ally caused by trauma (Chap. 454), and subarachnoid hemorrhage due 
to trauma or the rupture of an intracranial aneurysm (Chap. 440).

FIGURE 439-1  Hypertensive intracerebral hemorrhage. Transaxial noncontrast 
computed tomography scan through the region of the basal ganglia reveals a 
hematoma involving the left putamen in a patient with rapidly progressive onset of 
right hemiparesis.
■
■DIAGNOSIS
Intracranial hemorrhage is often identified on noncontrast computed 
tomography (CT) imaging of the head during the acute evaluation of 
stroke. Because CT is more widely available and may be logistically 
easier to perform than magnetic resonance imaging (MRI), CT imag­
ing is generally the preferred method for acute stroke evaluation 
(Fig. 439-1). The location of the hemorrhage narrows the differential 
diagnosis to a few entities. Table 439-1 lists the causes and anatomic 
spaces involved in intracranial hemorrhages.
■
■EMERGENCY MANAGEMENT
Close attention should be paid to airway management because deterio­
ration in the level of consciousness is common and often progressive. 
The initial blood pressure should be maintained until the results of the 
CT scan are reviewed and demonstrate ICH. A higher blood pressure 
may promote hematoma expansion, but it remains unclear if lower­
ing of blood pressure reduces hematoma growth. Recent clinical trials 
have shown that systolic blood pressure (SBP) can be safely lowered 
acutely and rapidly to <140 mmHg in patients with spontaneous ICH 
whose initial SBP was 150–220 mmHg. The INTERACT2 trial was a 
large phase 3 clinical trial to address the effect of acute blood pres­
sure lowering on ICH functional outcome. INTERACT2 randomized 
patients with spontaneous ICH within 6 h of onset and a baseline SBP of 
150–220 mmHg to two different SBP targets (<140 and <180 mmHg). 
In those with the target SBP <140 mmHg, 52% had an outcome of 
death or major disability at 90 days compared with 55.6% of those 
with a target SBP <180 mmHg (p = .06). There was a significant shift 
to improved outcomes in the lower blood pressure arm, whereas both 
groups had a similar mortality. ATACH2 was a similarly designed clini­
cal trial that assessed the same blood pressure targets but demonstrated 
no difference in outcome between groups; however, aggressive blood 
pressure lowering did increase renal adverse events. Current U.S. and 
European guidelines emphasize that blood pressure lowering to a target 
SBP is likely safe and possibly beneficial. While the specific optimal 
target remains a point of debate, the most recent American Heart Asso­
ciation/American Stroke Association guidelines for the management of 
spontaneous ICH endorse achieving and maintaining a target SBP of 
130–150 mmHg in these patients to avoid unintended hypoperfusion. 
It is unclear whether these clinical trial results apply to patients who 
have higher SBP on presentation or who are deeply comatose with 
possible elevated intracranial pressure (ICP). In patients who have ICP 
monitors in place, maintaining the cerebral perfusion pressure (mean 
arterial pressure [MAP] minus ICP) of 60 to ≥70 mmHg is reasonable, 

TABLE 439-1  Causes of Intracerebral Hemorrhage (ICH)
CAUSE
LOCATION
COMMENTS
Primary ICH
 
 
Cerebral amyloid 
angiopathy
Lobar
Degenerative disease of 
intracranial vessels; associated 
with dementia, rare in patients 
<60 years
Coagulopathy
Any
Risk for hematoma expansion
Drug
Any, lobar, subarachnoid
Cocaine, amphetamine
Hypertension
Putamen, globus pallidus, 
thalamus, cerebellar 
hemisphere, pons
Chronic hypertension 
produces hemorrhage from 
small (~30–100 μm) vessels in 
these regions
Secondary ICH
 
 
Aneurysm
Subarachnoid, 
intraparenchymal, rarely 
subdural
Mycotic and nonmycotic forms of 
aneurysms
CHAPTER 439
Arteriovenous 
malformation
Lobar, intraventricular, 
subarachnoid
Risk is ~2–4% per year for 
bleeding if previously unruptured
Capillary 
telangiectasias
Usually brainstem
Rare cause of hemorrhage
Intracerebral Hemorrhage
Cavernous 
angioma
Intraparenchymal
Multiple cavernous angiomas 
linked to mutations in KRIT1, 
CCM2, and PDCD10 genes
Dural 
arteriovenous 
fistula
Lobar, subarachnoid
Produces bleeding from venous 
hypertension
Dural sinus 
thrombosis
Along sagittal sinus, 
posterior temporal/
inferior parietal
Sagittal sinus thrombosis can 
cause hemispheric parasagittal 
hemorrhage with edema; vein of 
Labbé occlusion from transverse 
sinus occlusion produces 
posterior temporal and/or inferior 
parietal hemorrhage
Metastatic or 
primary brain 
tumors
Lobar
Lung, choriocarcinoma, 
melanoma, renal cell carcinoma, 
thyroid, hepatocellular 
carcinoma, and pilocytic 
astrocytoma are more commonly 
associated with bleeding 
complications
Transformation 
of prior ischemic 
infarction
Basal ganglion, 
subcortical regions, lobar
Occurs in a significant proportion 
of ischemic strokes, more 
commonly in large hemispheric 
infarctions; is symptomatic in 
3–9% of patients undergoing 
acute intervention
depending on the individual patient’s cerebral autoregulation status 
(Chap. 318). Blood pressure should be lowered using IV drugs with 
less cerebral vasodilating action such as nicardipine, clevidipine, labet­
alol, or esmolol. Patients with radiographic evidence of hydrocephalus 
or cerebellar ICH with depressed mental status should undergo urgent 
neurosurgical evaluation; these patients require close monitoring 
because they can deteriorate rapidly. Based on the clinical examination 
and CT findings, further imaging studies may be necessary, includ­
ing MRI or conventional x-ray angiography. Stuporous or comatose 
patients with clinical and imaging signs of herniation can be presump­
tively treated for elevated ICP with tracheal intubation and sedation, 
administration of osmotic diuretics such as mannitol or hypertonic 
saline, and elevation of the head of the bed while surgical consultation 
is obtained (Chap. 318). Rapid reversal of coagulopathy ideally within 
1 h of presentation and consideration of surgical evacuation of the 
hematoma (detailed below) are two other principal aspects of initial 
emergency management.
■
■INTRACEREBRAL HEMORRHAGE
ICH accounts for ~10% of all strokes, and ~35–45% of patients die 
within the first month. Incidence rates are particularly high in Asian and 
Black patient groups. Hypertension, coagulopathy, sympathomimetic

drugs (cocaine, methamphetamine), and cerebral amyloid angiopathy 
(CAA) cause most of these hemorrhages. Advanced age, heavy alcohol, 
and low-dose aspirin use in those without symptomatic cardiovascular 
disease increase ICH risk, and cocaine or methamphetamine use is one 
of the most important causes in the young.

Hypertensive ICH 
• 
PATHOPHYSIOLOGY  Hypertensive ICH 
usually results from spontaneous rupture of a small penetrating artery 
deep in the brain. The most common sites are the basal ganglia (espe­
cially the putamen), thalamus, cerebellum, and pons. The small arter­
ies in these areas seem most prone to hypertension-induced vascular 
injury. When hemorrhages occur in other brain areas or in nonhyper­
tensive patients, greater consideration should be given to other causes 
such as hemorrhagic disorders, neoplasms, vascular malformations, 
vasculitis, and CAA. The hemorrhage may be small, or a large clot 
may form and compress adjacent tissue, causing herniation and death. 
Blood may also dissect into the ventricular space, which substantially 
increases morbidity and may cause hydrocephalus.
PART 13
Neurologic Disorders
Most hypertensive ICHs initially develop over 30–90 min, whereas 
those associated with anticoagulant therapy may evolve for as long 
as 24–48 h. It is now recognized that about a third of patients even 
with no coagulopathy may have significant hematoma expansion 
within the first day. Within 48 h, macrophages begin to phagocytize 
the hemorrhage at its outer surface. After 1–6 months, the hemor­
rhage is generally resolved to a slitlike cavity lined with a glial scar and 
hemosiderin-laden macrophages.
CLINICAL MANIFESTATIONS  ICH generally presents as the abrupt 
onset of a focal neurologic deficit. Seizures are uncommon on pre­
sentation but may occur in 6–15% of patients within the first 3 days. 
Although clinical symptoms may be maximal at onset, more com­
monly, the focal deficit worsens over 30–90 min and is associated with 
a diminishing level of consciousness and signs of increased ICP such 
as headache and vomiting.
The putamen is the most common site for hypertensive hemorrhage, 
and the adjacent internal capsule is usually damaged (Fig. 439-1). 
Contralateral hemiparesis is therefore the sentinel sign. When mild, 
the face sags on one side over 5–30 min, speech becomes slurred, the 
arm and leg gradually weaken, and the eyes deviate away from the side 
of the hemiparesis. The paralysis may worsen until the affected limbs 
become flaccid or extend rigidly. When hemorrhages are large, drowsi­
ness gives way to stupor as signs of upper brainstem compression 
appear. Coma ensues, accompanied by deep, irregular, or intermittent 
respiration, a dilated and fixed ipsilateral pupil, and decerebrate rigid­
ity. Edema in adjacent brain tissue may cause progressive deterioration 
over 24–96 h.
Thalamic hemorrhages may also produce a contralateral hemiple­
gia or hemiparesis from pressure on, or dissection into, the adjacent 
internal capsule. A prominent sensory deficit involving all modalities 
is usually present. Aphasia, often with preserved verbal repetition, may 
occur after hemorrhage into the dominant thalamus, and construc­
tional apraxia or mutism occurs in some cases of nondominant hemor­
rhage. There may also be a homonymous visual field defect. Thalamic 
hemorrhages cause several typical ocular disturbances by extension 
inferiorly into the upper midbrain. These include deviation of the eyes 
downward and inward so that they appear to be looking at the nose, 
unequal pupils with absence of light reaction, skew deviation with the 
eye opposite the hemorrhage displaced downward and medially, ipsi­
lateral Horner’s syndrome, absence of convergence, paralysis of vertical 
gaze, and retraction nystagmus. Patients may later develop a chronic, 
contralateral pain syndrome (Déjérine-Roussy syndrome).
In pontine hemorrhages, deep coma with quadriplegia often occurs 
over a few minutes. Typically, there is prominent decerebrate rigidity 
and “pinpoint” (1 mm) pupils that react to light. There is impairment 
of reflex horizontal eye movements evoked by head turning (doll’shead or oculocephalic maneuver) or by irrigation of the ears with ice 
water (Chap. 30). Hyperpnea, severe hypertension, and hyperhidrosis 
are common. Most patients with deep coma from pontine hemorrhage 
ultimately die or develop a locked-in state, but small hemorrhages are 
compatible with survival and significant recovery.

Cerebellar hemorrhages usually develop over several hours and are 
characterized by occipital headache, repeated vomiting, and ataxia of 
gait. In mild cases, there may be no other neurologic signs except for 
gait ataxia. Dizziness or vertigo may be prominent. There is often pare­
sis of conjugate lateral gaze toward the side of the hemorrhage, forced 
deviation of the eyes to the opposite side, or an ipsilateral sixth nerve 
palsy. Less frequent ocular signs include blepharospasm, involuntary 
closure of one eye, ocular bobbing, and skew deviation. Dysarthria and 
dysphagia may occur. As the hours pass, the patient often becomes stu­
porous and then comatose from brainstem compression or obstructive 
hydrocephalus; immediate surgical evacuation before severe brainstem 
compression occurs may be lifesaving. Hydrocephalus from fourth 
ventricle compression can be relieved by external ventricular drainage; 
however, in this situation, definitive hematoma evacuation is recom­
mended rather than treatment with ventricular drainage alone. If the 
deep cerebellar nuclei are spared, full recovery is common.
Lobar hemorrhages usually present with symptoms related to the 
specific site of origin. The major neurologic deficit with an occipital 
hemorrhage is hemianopsia; with a left temporal hemorrhage, aphasia 
and confusion; with a parietal hemorrhage, hemisensory loss; and with 
frontal hemorrhage, arm weakness. Large hemorrhages may be associ­
ated with stupor or coma if they compress the thalamus or midbrain. 
Most patients with lobar hemorrhages have focal headaches, and more 
than one-half vomit or are drowsy. Seizures may occur.
Other Causes of ICH and Intracranial Hemorrhage 
CAA is 
a disease of the elderly in which arteriolar degeneration occurs and 
amyloid is deposited in the walls of the cerebral arteries. Amyloid 
angiopathy causes both single and recurrent lobar hemorrhages and is 
probably the most common cause of lobar hemorrhage in the elderly. 
It accounts for some intracranial hemorrhages associated with IV 
thrombolysis given for myocardial infarction. This disorder can be 
suspected in patients who present with multiple hemorrhages (and 
infarcts) over several months or years or in patients with “microbleeds” 
in the cortex, seen on brain MRI sequences sensitive for hemosiderin 
(susceptibility weighted imaging), but it is definitively diagnosed by 
pathologic demonstration of Congo red staining of amyloid in cerebral 
vessels. The ε2 and ε4 allelic variations of the apolipoprotein E gene are 
associated with increased risk of recurrent lobar hemorrhage and may 
therefore be markers of amyloid angiopathy. Positron emission tomog­
raphy imaging can image amyloid-beta deposits in CAA using specific 
antibody labels and may be helpful in diagnosing CAA noninvasively. 
Although cerebral biopsy is the most definitive method of diagnosis, 
evidence of inflammation on lumbar puncture should prompt con­
sideration of CAA-associated vasculitis as an underlying cause, and 
oral glucocorticoids may be beneficial. Noninflammatory CAA has no 
specific treatment. Oral anticoagulants are typically avoided.
Cocaine and methamphetamine are frequent causes of stroke in 
young (age <45 years) patients. ICH, ischemic stroke, and subarach­
noid hemorrhage (SAH) are all associated with stimulant use. Angio­
graphic findings vary from completely normal arteries to large-vessel 
occlusion or stenosis, vasospasm, or changes consistent with vasculop­
athy. The mechanism of sympathomimetic-related stroke is not known, 
but cocaine enhances sympathetic activity causing acute, sometimes 
severe, hypertension, and this may lead to hemorrhage. Slightly more 
than one-half of stimulant-related intracranial hemorrhages are intra­
cerebral and the rest are subarachnoid. In cases of SAH, a saccular 
aneurysm is usually identified. Presumably, acute hypertension causes 
aneurysmal rupture.
Head injury often causes intracranial hemorrhage. The common 
sites are intraparenchymal (especially temporal and inferior frontal 
lobes) and into the subarachnoid, subdural, and epidural spaces. 
Trauma must be considered in any patient with an unexplained acute 
neurologic deficit (hemiparesis, stupor, or confusion), particularly if 
the deficit occurred in the context of a fall (Chap. 454).
Intracranial hemorrhages associated with anticoagulant therapy can 
occur at any location; they are often lobar or subdural. Anticoagulantrelated ICHs may continue to evolve over 24–48 h, especially if coagu­
lopathy is insufficiently reversed. Coagulopathy and thrombocytopenia

should be reversed rapidly, as discussed below. ICH associated with 
hematologic disorders (leukemia, aplastic anemia, thrombocytopenic 
purpura) can occur at any site and may present as multiple ICHs. 
Skin and mucous membrane bleeding may be evident and offers a 
diagnostic clue.
Hemorrhage into a brain tumor may be the first manifestation of 
neoplasm. Choriocarcinoma, malignant melanoma, renal cell carci­
noma, and thyroid, lung, and hepatocellular carcinoma are among the 
most common metastatic tumors associated with ICH. Pilocytic astro­
cytoma and glioblastoma multiforme in adults and medulloblastoma in 
children may also have areas of ICH.
Hypertensive encephalopathy is a complication of malignant hyper­
tension. In this acute syndrome, severe hypertension is associated with 
headache, nausea, vomiting, convulsions, confusion, stupor, and coma. 
Focal or lateralizing neurologic signs, either transitory or permanent, 
may occur but are infrequent and therefore suggest some other vas­
cular disease (hemorrhage, embolism, or atherosclerotic thrombosis). 
There may be retinal hemorrhages, exudates, papilledema (hyperten­
sive retinopathy), and evidence of renal and cardiac disease. MRI brain 
imaging shows a pattern of typically posterior (occipital > frontal) 
brain edema. The hypertension may be essential or due to chronic 
renal disease, acute glomerulonephritis, acute toxemia of pregnancy, 
pheochromocytoma, or other causes. Lowering the blood pressure 
reverses the process, but stroke can occur, especially if blood pressure 
is lowered too rapidly. Neuropathologic examination reveals multifocal 
to diffuse cerebral edema and hemorrhages of various sizes from pete­
chial to massive. Microscopically, there is necrosis of arterioles, minute 
cerebral infarcts, and hemorrhages. The terms hypertensive encepha­
lopathy and posterior reversible encephalopathy syndrome (Chap. 318) 
should be reserved for this syndrome and not for chronic recurrent 
headaches, dizziness, recurrent transient ischemic attacks, or small 
strokes that often occur in association with high blood pressure. Dis­
tinguishing hypertensive encephalopathy with ICH from hypertensive 
ICH is important since aggressive lowering of SBP to 130–150 mmHg 
acutely is often considered in hypertensive ICH, but less aggressive 
measures should be used in hypertensive encephalopathy. Having no 
alteration in mental status or other prodrome prior to the ICH favors 
hypertensive ICH as the disease.
Primary intraventricular hemorrhage is rare and should prompt 
investigation for an underlying vascular anomaly. Sometimes bleeding 
begins within the periventricular substance of the brain and dissects 
into the ventricular system without leaving signs of intraparenchymal 
hemorrhage. Alternatively, bleeding can arise from periependymal 
veins. Vasculitis, usually polyarteritis nodosa or lupus erythematosus, 
can produce hemorrhage in any region of the central nervous system; 
most hemorrhages are associated with hypertension, but the arteritis 
itself may cause bleeding by disrupting the vessel wall. Nearly one-half 
of patients with primary intraventricular hemorrhage have identifiable 
bleeding sources seen using conventional angiography.
Venous sinus thrombosis (Chap. 438) causes cortical vein hyperten­
sion, cerebral edema, and venous infarction. This may progress to 
cause intracranial hemorrhage surrounding the region of the occluded 
cerebral venous sinus or within the drainage region of the vein of 
Labbé, producing a posterior temporal or inferior parietal hematoma. 
Despite the presence of hemorrhage, IV anticoagulation is indicated to 
reduce the venous hypertension and limit venous ischemia and further 
bleeding.
Sepsis can cause small petechial hemorrhages throughout the cere­
bral white matter. Moyamoya disease (Chap. 438), mainly an occlusive 
arterial disease that causes ischemic symptoms, may on occasion 
produce ICH. Hemorrhages into the spinal cord are usually the result 
of an AVM, cavernous malformation, or metastatic tumor. Epidural 
spinal hemorrhage produces a rapidly evolving syndrome of spinal cord 
or nerve root compression (Chap. 453). Spinal hemorrhages usually 
present with sudden back pain and some manifestation of myelopathy.
Laboratory and Imaging Evaluation 
Patients should have rou­
tine blood chemistries and hematologic studies. Specific attention to 
the platelet count, prothrombin time, partial thromboplastin time, and 

international normalized ratio is important to identify coagulopathy. 
CT imaging reliably detects acute focal hemorrhages in the supratento­
rial space. Rarely, very small pontine or medullary hemorrhages may 
not be well delineated because of motion and bone-induced artifact 
that obscure structures in the posterior fossa. After the first 2 weeks, 
x-ray attenuation values of clotted blood diminish until they become 
isodense with surrounding brain. Mass effect and edema may remain. 
In some cases, a surrounding rim of contrast enhancement appears 
after 2–4 weeks and may persist for months. MRI, although more sensi­
tive for delineating posterior fossa lesions, is generally not necessary for 
primary diagnosis. MR angiography (MRA), CT angiography (CTA), 
and conventional x-ray angiography are used when the cause of intra­
cranial hemorrhage is uncertain, particularly if the patient is young 
or not hypertensive and the hematoma is not in one of the usual sites 
for hypertensive hemorrhage. CTA or postcontrast CT imaging may 
reveal one or more small areas of enhancement within a hematoma; 
this “spot sign” is thought to represent ongoing bleeding. The presence 
of a spot sign is associated with an increased risk of hematoma expan­
sion, increased mortality, and lower likelihood of favorable functional 
outcome. Because patients typically have focal neurologic signs and 
obtundation and often show signs of increased ICP, a lumbar puncture 
is generally unnecessary and should usually be avoided because it may 
induce cerebral herniation.

CHAPTER 439
Intracerebral Hemorrhage
TREATMENT
Intracerebral Hemorrhage
ACUTE MANAGEMENT
After immediate attention to blood pressure and airway protection 
(see above), focus can switch to medical and surgical management. 
Approximately 40% of patients with a hypertensive ICH die, but 
survivors can have a good to complete recovery. The ICH Score 
(Table 439-2) is a validated clinical grading scale that is useful for 
stratification of mortality risk and clinical outcome. However, a spe­
cific ICH clinical grading scale should not be used to precisely prog­
nosticate outcome because of the concern of creating a self-fulfilling 
prophecy of poor outcome if early aggressive care is withheld. Any 
identified coagulopathy should be corrected as soon as possible. 
For patients taking vitamin K antagonists (VKAs), rapid correction 
of coagulopathy can be achieved by infusing prothrombin complex 
concentrates (PCCs), which can be administered quickly, with 
TABLE 439-2  The Intracerebral Hemorrhage Score
CLINICAL OR IMAGING FACTOR
POINT SCORE
Age
<80 years

≥80 years

Hematoma Volume
<30 cc

≥30 cc

Intraventricular Hemorrhage Present
No

Yes

Infratentorial Origin of Hemorrhage
No

Yes

Glasgow Coma Scale Score
13–15

5–12

3–4

Total Score
0–6 Sum of each category 
above
Source: Reproduced with permission from JC Hemphill 3rd et al: The ICH score: A 
simple, reliable grading scale for intracerebral hemorrhage. Stroke 32:891, 2001.

vitamin K administered concurrently. Fresh frozen plasma (FFP) is 
an alternative, but since it requires larger fluid volumes and longer 
time to achieve adequate reversal than PCC, it is not recommended 
if PCC is available. Idarucizumab is a monoclonal antibody to dabi­
gatran, and the administration of two doses reverses the anticoagula­
tion effect of dabigatran quickly. The oral Xa inhibitors apixaban and 
rivaroxaban can be reversed with andexanet alfa. PCC may partially 
reverse the effects of oral factor Xa inhibitors and are reasonable to 
administer if andexanet alfa is not available. When ICH is associated 
with thrombocytopenia (platelet count <50,000/μL), transfusion of 
fresh platelets is indicated. A clinical trial of platelet transfusions in 
patients with ICH and without thrombocytopenia who were taking 
antiplatelet drugs showed no benefit and possible harm.

Hematomas may expand for several hours following the initial 
hemorrhage, even in patients without coagulopathy. The precise 
mechanism is unclear. A phase 3 trial of treatment with recombi­
nant factor VIIa reduced hematoma expansion; however, clinical 
outcomes were not improved, so use of this drug is not recom­
mended. The administration of tranexamic acid was not found to 
alter outcome in a large randomized trial. Blood pressure lowering 
has been considered due to the theoretical risk of acutely elevated 
blood pressure on hematoma expansion, although clinical trials did 
not find a difference in hematoma expansion between the SBP tar­
gets of 140–180 mmHg. In deep hemorrhages that involve the basal 
ganglia, more intensive blood pressure lowering reduced hematoma 
expansion but had no effect on functional outcome.
PART 13
Neurologic Disorders
Initial clinical trials of evacuation of supratentorial hemato­
mas, primarily via standard craniotomy, did not demonstrate 
clear benefit; however, recent focus on minimally-invasive surgi­
cal techniques holds promise. The International Surgical Trial in 
Intracerebral Haemorrhage (STICH) randomized patients with 
supratentorial ICH to either early surgical evacuation or initial 
medical management. No benefit was found in the early surgery 
arm, although analysis was complicated by the fact that 26% of 
patients in the initial medical management group ultimately had 
surgery for neurologic deterioration. The follow-up study, STICHII, found that craniotomy and hematoma evacuation within 24 h of 
lobar supratentorial hemorrhage did not improve overall outcome 
but might have a role in select severely affected patients. However, 
many centers still consider surgery for patients deemed salvage­
able and who are experiencing progressive neurologic deteriora­
tion due to herniation. Surgical techniques continue to evolve. In 
a clinical trial of minimally invasive hematoma evacuation using 
instillation of the thrombolytic agent alteplase into the clot, mor­
tality was decreased but there was not an improvement in func­
tional outcome. In 2024, the first randomized  trial demonstrating 
improvement in functional outcome after surgical hematoma evac­
uation was published. The Early MiNimally-invasive Removal of 
IntraCerebral Hemorrhage (ENRICH) trial found that surgical 
removal of lobar hematomas within 24 hours of onset in selected 
patients (hematoma volume 30–80 mL; Glasgow Coma Score 5–14 
[Table 454-1]; pre-ICH functionally independent) was beneficial 
compared with medical management alone. Several clinical trials 
testing other minimally invasive surgical hematoma evacuation 
techniques are ongoing.
For cerebellar hemorrhages in patients with decreased level 
of consciousness or obstructive hydrocephalus, a neurosurgeon 
should be consulted immediately to assist with the evaluation. If 
the patient is alert without focal brainstem signs and the hematoma 
is small, surgical removal is usually unnecessary. Patients with 
hematomas >1 cm in diameter require careful observation for signs 
of impaired consciousness, progressive hydrocephalus, and precipi­
tous respiratory failure. Hydrocephalus due to cerebellar hematoma 
generally requires surgical evacuation and should usually not be 
treated solely with ventricular drainage.
Tissue surrounding hematomas is displaced and compressed but 
not necessarily infarcted. Hence, major functional improvement 
often occurs as the hematoma is reabsorbed and the adjacent tis­
sue regains its function over several months following acute injury. 

Careful management of the patient during the acute phase of the 
hemorrhage can lead to considerable recovery.
Bundles of care that incorporate multiple interventions may 
provide more value in the management of ICH patients than 
separating out different singular interventions. A hospital in the 
United Kingdom found that an ICH care bundle consisting of 
coagulopathy reversal, blood pressure lowering, and neurosurgical 
referral decreased patient mortality when implemented as a quality 
assurance project. In the INTERACT-3 randomized clinical trial 
performed in low- to middle-income countries, a bundle of care 
that included vitamin K coagulopathy reversal, acute blood pressure 
lowering, glucose control, and temperature control was associated 
with improved functional outcome and fewer adverse events.
Surprisingly, ICP is often normal even with large ICHs. However, 
if the hematoma causes marked midline shift of structures with 
consequent obtundation, coma, or hydrocephalus, osmotic agents 
can be instituted in preparation for placement of a ventriculostomy 
or parenchymal ICP monitor (Chap. 318). Once ICP is recorded, 
CSF drainage (if available), osmotic therapy, and blood pressure 
management can be tailored to maintain cerebral perfusion pres­
sure (MAP minus ICP) of 60 to ≥70 mmHg. For example, if ICP 
is found to be high, CSF can be drained from the ventricular space 
and osmotic therapy continued; persistent or progressive elevation 
in ICP may prompt surgical evacuation of the clot. Alternately, 
if ICP is normal, interventions such as osmotic therapy may be 
tapered. Because hyperventilation may produce ischemia due to 
cerebral vasoconstriction, induced hyperventilation should be lim­
ited to acute resuscitation of the patient with presumptive high 
ICP and eliminated once osmotic therapy or surgical treatments 
have been instituted. Glucocorticoids are not recommended for the 
treatment of intracerebral hemorrhage.
PREVENTION
Hypertension is the leading cause of primary ICH. Prevention is 
aimed at reducing chronic hypertension, eliminating excessive alco­
hol use, and discontinuing use of illicit drugs such as cocaine and 
amphetamines. Oral anticoagulant medications should generally be 
avoided in patients with high-risk features for CAA, but antiplatelet 
agents may be administered if there is an indication based on ath­
erothrombotic vascular disease. Ongoing studies are investigating 
the risk-benefit ratio of reinitiation of anticoagulation in patients 
with recent ICH who have atrial fibrillation.
VASCULAR ANOMALIES
■
■ARTERIOVENOUS MALFORMATIONS
True AVMs are shunts between the arterial and venous systems that 
may present with headache, seizures, and intracranial hemorrhage. 
AVMs consist of a tangle of abnormal vessels across the cortical surface 
or deep within the brain substance. AVMs vary in size from a small 
blemish a few millimeters in diameter to a large mass of tortuous chan­
nels composing an arteriovenous shunt of sufficient magnitude to raise 
cardiac output and precipitate heart failure. Blood vessels forming the 
tangle interposed between arteries and veins are usually abnormally 
thin and histologically resemble both arteries and veins. AVMs occur 
in all parts of the cerebral hemispheres, brainstem, and spinal cord, 
but the largest ones are most frequently located in the posterior half of 
the hemispheres, commonly forming a wedge-shaped lesion extending 
from the cortex to the ventricle. Most AVMs are congenital, but cases 
of acquired lesions have been reported.
Bleeding, headache, and seizures are most common between the ages 
of 10 and 30, occasionally as late as the fifties. AVMs are more frequent 
in men, and rare familial cases have been described. Familial AVM may 
be a part of the autosomal dominant syndrome of hereditary hemor­
rhagic telangiectasia (Osler-Rendu-Weber) syndrome due to mutations 
in either endoglin or activin receptor-like kinase 1, both involved in 
transforming growth factor (TGF) signaling and angiogenesis.
Headache (without bleeding) may be hemicranial and throbbing, 
like migraine, or diffuse. Focal seizures, with or without generalization,