Abstract
In this chapter, we consider spontaneous hemorrhage into the brain parenchyma and ventricles (intracerebral hemorrhage, ICH). Non-traumatic bleeding into the subarachnoid space (subarachnoid hemorrhage, SAH) is covered in Chapter 13. Traumatic subdural and epidural hemorrhages are not covered in this book.
Intracerebral hemorrhage is associated with very high morbidity and mortality. It is important to realize that, as with acute ischemic strokes, time is of the essence in ICH. The reason for this is that the blood accumulates rapidly, and the volume of the hematoma is the most important determinant of outcome.
In this chapter, we consider spontaneous hemorrhage into the brain parenchyma and ventricles (intracerebral hemorrhage, ICH). Non-traumatic bleeding into the subarachnoid space (subarachnoid hemorrhage, SAH) is covered in Chapter 13. Traumatic subdural and epidural hemorrhages are not covered in this book.
Intracerebral hemorrhage is associated with very high morbidity and mortality. It is important to realize that, as with acute ischemic strokes, time is of the essence in ICH. The reason for this is that the blood accumulates rapidly, and the volume of the hematoma is the most important determinant of outcome.1 As a result of bleeding, there can be rapid development of intracranial hypertension as a result of mass effect from the blood, and occasional hydrocephalus in cases of intraventricular hemorrhage (IVH). Therefore, anything that can be done in the first few minutes after the onset of ICH to limit bleeding will reduce morbidity. In the last decade, progress has been made in the pharmacological reversal of coagulopathy and “optimal” blood-pressure management after ICH. These are discussed extensively later in the chapter. In the days to weeks following the ictus, vasogenic edema develops around the hematoma and can contribute to significant (and sometimes life-threatening) mass effect, especially in large ICH or those associated with an inflammatory or vascular etiology (e.g., tumors, vascular malformations). We address medical and surgical management to combat brain swelling and its consequences in Chapter 7.
Definition
Intracerebral hemorrhage is spontaneous bleeding into the brain parenchyma or ventricles from a ruptured artery, vein, or other vascular structure (Figure 12.1). It is important to distinguish primary ICH, which is the topic of this chapter, from hemorrhagic transformation of an ischemic infarct, covered in Chapter 7. In primary ICH, the initial event is vascular rupture, while in hemorrhagic transformation the initial event is vascular occlusion. This is obviously an important distinction, since the etiologies and treatments are completely different. The term “hemorrhagic stroke” is used loosely and imprecisely and is often applied to either of these conditions. We prefer the more precise distinction.
Figure 12.1 Location of hemorrhages: (A) penetrating cortical branches of the anterior, middle, or posterior cerebral arteries; (B) basal ganglia, originating from ascending lenticulostriate branches of the middle cerebral artery; (C) the thalamus, originating from ascending thalamogeniculate branches of the posterior cerebral artery; (D) the pons, originating from paramedian branches of the basilar artery; and (E) the cerebellum, originating from penetrating branches of the posterior inferior, anterior inferior, or superior cerebellar arteries.
Etiology
(most common) – classic locations for hypertensive intracerebral hemorrhage:
Basal ganglia (putamen most common)
Thalamus
Pons
Cerebellum
2. Cerebral amyloid angiopathy
Results from beta-amyloid protein deposition in the walls of small and mid-sized arteries, compromising vessel wall integrity.
More often cortical in location than hypertensive hemorrhages.
Older patients (> 65 years) or positive family history.
Frequently associated with cognitive impairment or dementia.
Microbleeds in cortical locations seen as hypointense/black lesions (due to hemosiderin deposition) on gradient-echo (GRE) or susceptibility-weighted imaging (SWI) sequences on MRI.
3. Other angiopathies – moyamoya, vasculitides, RCVS
4. Drugs
Iatrogenic, e.g., heparin or warfarin
Drugs of abuse, especially cocaine
5. Vascular malformation – aneurysm, AVM, cavernous malformation
6. Cerebral vein thrombosis (see Chapter 11)
Caused by bleeding from congested vein feeding into an occluded cortical vein or venous sinus thrombosis.
Technically considered transformation of a “venous infarct.”
The clinical presentation of the thrombosis may be dominated by the development of ICH. This is different from arterial occlusion with hemorrhagic transformation, where the initial clinical presentation is almost always the result of the infarct, and the hemorrhage comes hours later.
7. Tumor
Primary tumors (e.g., glioblastoma, pilocytic astrocytoma)
Metastatic tumors (e.g., melanoma, breast carcinoma, papillary carcinoma of thyroid)
8. Trauma
Closed head injury
Penetrating injury
Explosive blast injury
9. Coagulopathy
Presentation
You cannot distinguish ICH from ischemic stroke on the basis of the clinical presentation – they may look exactly alike. This is the reason brain imaging is so critical in initial stroke management, since brain bleeding can be readily detected by CT or MRI immediately after it occurs.
Clinical features that might suggest ICH rather than an infarct include headache, accelerated hypertension, vomiting (always a bad sign in an acute stroke patient, usually indicative of increasing ICP), decreasing level of consciousness, or a dilated and fixed pupil.
Diagnosis and Evaluation
As with ischemic stroke, management in the first few hours may make the difference between a good and bad outcome. We recommend the following initial assessment.
Look for signs of trauma.
Glasgow Coma Scale (GCS) and brainstem reflexes if comatose, NIHSS score if awake.
Consider intubation for airway protection.
Measure blood pressure (see subsequent comment for details on blood-pressure management).
This is the gold-standard test to diagnose an ICH in the hyperacute/acute phase.
Repeat the CT if patient was transferred from outside hospital (the bleed could have extended en route).
▪ Would repeat in 6–24 hours to gauge stability of the bleed.
▪ Repeat STAT in case of neurological deterioration.
Where did the bleed start?
Is there significant mass effect, intraventricular hemorrhage (IVH), or hydrocephalus?
Measure the volume: (diameter A × diameter B × C)/2. (A and B = perpendicular diameters of the hematoma on the CT slice with the largest area of parenchymal hemorrhage, C = number of slices that show hemorrhage × thickness of the slice) (Figure 12.2).
3. Check platelet count, INR, and PTT, and urine drug screen
4. ECG: abnormalities may point to MI or stress cardiomyopathy. In case of abnormality, obtain cardiac enzymes.
5. Consider vascular imaging study
(MRA, CTA, or DSA) to rule out AVM, dural AV fistula, or aneurysm, especially if:
younger patient
or
significant SAH is present
or
ICH is in an atypical lobar or cortical location, or has some other atypical appearance.
To look for multiple old hemorrhages or microbleeds that might suggest amyloid angiopathy. Requires GRE or SWI sequences.
To exclude underlying tumor (this is rather rare and usually requires follow-up imaging in 6–8 weeks after most of the blood has been reabsorbed). Requires gadolinium to look for enhancement indicative of blood–brain barrier disruption.
To check for venous thrombosis, order MR venogram if the suspicion is high: hemorrhage high in convexity, bilateral paramedian in cases of deep venous system thrombosis, substantial perihematomal edema, or temporal lobe hemorrhage without trauma.
7. Consider getting a neurosurgery consult
(see Surgical Intervention, below):
Figure 12.2 Calculating ICH volume on a CT image.
Management
It is important to talk with family and start the process of coming to terms with the often poor prognosis (see Prognosis and Outcome, below). This is a very important management consideration. Discuss “do not resuscitate” (DNR) issues. However, on the first day, don’t be too certain of bad outcome unless herniation has already occurred and the brainstem is significantly compromised. Comatose patients can wake up, especially if the mass effect is decompressed spontaneously into the ventricle, or by surgical intervention. Do not withdraw support in the ED.
Hematoma Enlargement Treatment
Hematoma enlargement occurs in 20–35% of ICH.4
All locations.
Usually in the first few hours after onset of symptoms, but almost always in the first 24 hours.
May occur later in patients with coagulopathy.
Associated with much worse prognosis.
Independent radiographic predictors of hematoma expansion are numerous and include:5
▪ Large initial hematoma volume.
▪ Hematoma heterogeneity – swirl sign, blend sign, island sign, presence of a fluid level.
▪ Active extravasation – spot sign and leak sign. The spot sign is one of the most studied predictor signs of hematoma expansion. While it was thought to be a radiographic sign with good sensitivity and specificity, a preplanned study nested within the multicenter trial ATACH-2 (see below) has more recently shown that the sensitivity and specificity of the spot sign were only 54% and 63% respectively, making it not as accurate a tool for hematoma expansion prediction (Figure 12.3).6
Figure 12.3 Hematoma expansion and CT spot sign. (A) Initial non-contrast head CT showing a left basal ganglia ICH measuring 47 mL. (B) A single spot sign (area of active contrast extravasation, arrow) seen within the ICH on CT angiography. (C) No significant expansion of the ICH (volume 55 mL) on a follow-up CT 7 hours later, attesting to the fact that the accuracy of the spot sign as a radiographic predictor of hematoma expansion may be lower than initially believed. (N.B. This patient had decompressive hemicraniectomy in the interim, but no hematoma evacuation or aspiration.)
1. Aggressive Blood-Pressure Reduction
BP elevation is associated with hematoma expansion, poor functional outcome, and higher mortality.
Lowering SBP to 140 mmHg is safe (no significant perihematomal ischemia) and is recommended in the latest guidelines.7
See below for more detailed information on BP management in acute ICH.
2. Activated Factor VII
In the FAST trial, activated factor VII (NovoSeven) was found to reduce hematoma expansion but did not have any effect on survival or functional outcome at 90 days. Possible explanations are that it was given too late (on average 4 hours after symptom onset) or in patients whose hematomas were already so large that they were in any case doomed to poor outcome.8
Activated factor VII is expensive and can have dose-related occlusive complications such as stroke, myocardial infarction, pulmonary embolism, etc.
Patients with associated arterial occlusive diseases (coronary or cerebral ischemia, peripheral vascular disease, or pulmonary embolism), or who have already herniated, are not considered.
Further study is needed before it is used routinely.
Coagulopathy Reversal
1. Vitamin K Antagonist (VKA)-Related Intracerebral Hemorrhage
Goal: normal INR using prothrombin complex concentrates (PCC) or fresh frozen plasma (FFP) and vitamin K.
Obtain non-contrast CT immediately
a. Labs: INR, PTT, thrombin time, D-dimers, fibrinogen, CBC, type and crossmatch
b. Vitamin K 10 mg IV over 10 minutes (repeat daily for 3 days) should always be given, because it maintains the reversal over time:
▪ Slow onset (2 hours)
▪ Effect peaks at 24 hours if hepatic function not impaired
PCC versus FFP
a. Three different formulations:
▪ Three-factor PCC: II, IX, and X
▪ Four-factor PCC: II, VII, IX, and X
▪ Activated PCC (aPCC): four coagulation factors. Example: FEIBA (Factor Eight Inhibitor Bypassing Activity)
b. Dosing of PCC: 25–50 IU/kg, depending on patient’s weight, INR, and the preparation
c. Advantages of PCC over FFP:
▪ Faster administration (25 minutes versus 30–120 minutes)
▪ No need to thaw
▪ No need for type and crossmatch
▪ Lower risk of infections and transfusion reactions
▪ Much smaller volume than FFP (~250 mL/unit FFP) – important in patients with or at risk for pulmonary edema
d. Advantages of FFP over PCC:
▪ Far less expensive
▪ More widely available
e. The recently published INCH trial compared PCC to FFP in reversing warfarin-induced ICH:9
▪ PCC achieved faster and more complete INR normalization (≤ 1.2 within 3 hours).
▪ PCC was associated with less hematoma growth, but there was no difference in functional outcome or mortality at 90 days.
▪ Other studies of PCC versus FFP in non-brain bleeding have shown lower mortality with PCC.
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