Spontaneous Intracerebral Hemorrhage (ICH)

Primary Category

Neurocritical Care

P-Category

Secondary Category

S-Category

Authors:

Talha Nazir MD,
Hafiz Muhammad Waqas Siddique MD,
Junaid Kalia MD

Introduction

Spontaneous intracerebral hemorrhage is defined as focal bleeding from the blood vessel into parenchyma of the brain in the absence of trauma or surgery.

One of the three main types of stroke, the other two being ischemic stroke and subarachnoid hemorrhage (SAH).

ICH is a medical emergency requiring immediate treatment. Less common than ischemic stroke but is more serious.

Epidemiology

Stroke can lead to disability as well as the fifth leading cause of mortality in the United States, out of which 8-13% (10%) stroke cases are due to ICH.

ICH is twice as common as SAH.

The incidence of ICH per 100,000 person-years during the years 2002-2008 was 51.8 in Asians, 19.6 in Hispanics and 22.9 in Blacks.

The incidence of ICH in American Blacks is more than the White Population.

12-15 per 100,000 individuals are affected by ICH annually; 350 per 100,000 elderly patients have hypertensive hemorrhages in the US. Asian countries have a greater incidence.

Carries a 40% risk of mortality. ICH is associated with more mortality or major morbidity as compared to ischemic stroke or SAH.

More than 20,000 patients die of ICH in the US, with a 30-day death rate of 44%.

Pontine and brainstem intracerebral hemorrhages are associated with a 24-hour death rate of 75%.

Associated with long-term deficits post-ICH at a rate of about 70%.

One-third of ICH cases result in IVH

Etiology and Risk Factors

Most important risk factors include an advancing age and hypertension, while the commonest causes of ICH include hypertension and AV (arteriovenous) malformations. (Table 1)

Table 1: Etiology and Risk Factors

Pathophysiology

Development of Charcot-Bouchard aneurysm, fibrinoid necrosis and lipohyalinosis as a result of chronic hypertension cause the thin-walled arteries of the brain – namely, the thalamoperforators, lenticulostriates, superior and anterior inferior cerebellar arteries, as well as paramedian branches– to rupture, blood builds up, clots and increases pressure within the rigid skull, causing the brain to crush against the bone or resulting in its herniation.

Blood from the ICH first collects as mass then dissects through as well as compresses adjacent tissues of the brain resulting in dysfunction of the neuronal system.

Toxins released due to hypoxia cause further damage to the brain cell.

ICH may also be as a result of auto-regulatory dysfunction with extreme cerebral flow of blood, as in reperfusion injuries, hemorrhagic alteration, or exposure to cold

Table 2: Sites of Intracerebral Hemorrhage

Table 3: Presentation

Intracerebral hemorrhage Score (Table 4)

ICH score is a common measurement used to predict the mortality of patients

Table 4: Intracerebral hemorrhage Score

Differential diagnosis

Ischemic stroke due to hemorrhage

Subarachnoid Hemorrhage

Vascular Malformation such as arteriovenous malformation

Other causes of acute neurological dysfunction, such as seizures or hypoglycemia

Investigations/Workup

Begin with a general physical examination (GPE). Level of Blood glucose must be checked immediately at the bedside of the patient, post-presentation. Look for:

Cardiac arrhythmias
Fever
Retinal hemorrhages
Hypertension
Nuchal rigidity
ASOC
Anisocoria
Cranial bruits (suggestive of an AVM)
Focal neurological deficits

Following the GPE, important investigations include:

Computed Tomography (CT) Scan

Non-invasive.
Reviews anatomical structures within the brain to detect bleeds.
Can detect AVMs >1 cm in diameter. Confirm with MRI.
Shows acute hemorrhages as hyperdense signal intensities. Multifocal hemorrhages are suggestive of trauma.
Can also appreciate perihematomal edema as well as tissue displacement with the herniation.
Tumors and vascular malformations require an iodinated contrast to increase yield.

Radiological Sign of Hematoma Expansion

CT angiography may show a ‘spot sign’, whereby the contrast extravasation into the hematoma indicates that the bleed is ongoing and is suggestive of the hematoma expanding, meaning poor outcome.

Calculation of ICH volume

Calculate hematoma volume in cm3 by an altered ellipsoid calculation: (A x B x C)/2, in which A, B, and C denote the extended linear dimensions of the hematoma in cm in every orthogonal plane.

Angiogram

Invasive.
Involves insertion of a catheter into an artery. Contrast dye is injected into the blood after its placement followed by X-Rays.
Indicated for patients who are:

Young
Have a lobar hemorrhage
Have no history of hypertension
Surgical candidates with no clear cause of hemorrhage

Magnetic Resonance Imaging (MRI)

Non-invasive.
Uses the magnetic field as well as radiofrequency waves to get a thorough view of the soft tissues of the brain.
MRI appearances of ICH on the T1 and T2 sequences evolve over time due to physical as well as chemical variations in and all over the hematoma.
Several flow voids which are adjacent to hematoma are suggestive of AVMs or cavernous angiomas.
Multilobar hypointense foci provide evidence for cerebral amyloid angiopathies.
Multiple deep foci suggest hypertensive arteriopathies.
Tumors and vascular malformations require a paramagnetic contrast to increase yield.
If it includes injection of a contrast in blood to visualize the brain arteries, then it is known as an MRA (Magnetic Resonance Angiogram)

Other investigations

CBC – look for WBCs and hematocrit plus platelet count.

Coagulation profile – PT/aPTT to rule out bleeding/clotting disorders, fibrinogen and D-dimer to rule out DIC.

Serum chemistries comprising electrolytes as well as osmolarity – to rule out metabolic imbalances.

Toxicology screen in addition to level of serum alcohol to identify exogenous toxins causing ICH.

Electrocardiogram (ECG) – identifies cardiac injury or cerebrum-induced dysrhythmias.

Chest X-Ray (CXR)

Lumbar puncture (LP) followed by cerebrospinal fluid (CSF) analysis

Urinalysis

Screening for hematologic, vasculitic, immunologic, and infectious etiologies, which account for less common causes of ICH.

Table 5: Neurological Features of Intracerebral Hemorrhages

Table 6: Phases of Intracerebral Hemorrhage

Figure 1: Aging of Blood on MRI

From: https://radiopaedia.org/cases/evolution-of-mri-signal-characteristics-of-intracranial-haemorrhage-diagram by Frank Gaillard

Management

Involves both medical and surgical interventions.

Principal treatment strategies include lifesaving measures, supportive measures, symptomatic relief, control of modifiable risk factors, surgical evacuation in some cases, and prevention of complications.

The aim is to halt the blood loss, remove hematoma (blood clot), plus lower the intracranial pressure (ICP).

Better outcomes are associated with prompt management, usually within the first three hours of presentation.

If delayed or ignored the brain will eventually absorb the hematoma in a week or two, nevertheless the damage caused by the ICP and toxins from the dying brain cells may be irreversible.

Indications for Non-Surgical/Medical Management

Small hemorrhages (intracerebral hemorrhage volume of <10 cm3)

Minimal focal neurological deficits

Indications for Surgical Intervention

Large lobar hemorrhages (50 cm3)

Young patients with lobar hemorrhages

Cerebellar hemorrhages (>3 cm3)

Deteriorating patient condition

ICH associated with a structural vascular lesion

Brainstem compression

Hydrocephalus

Medical Management

Pre-hospital Settings

Follow the ABCDE(airway, breathing, circulation, disability and exposure/environment) protocol and transfer the patient to the nearest hospital.

Intubate a patient who has a decreased consciousness level(GCS of 8 or less) as well as poor protection of the airway.

Try to take a detailed history from any witness or a family member.

Informing the ED(emergency department) beforehand reduces the time to get CT done.

Hospital Settings

Reversal of Coagulopathy

The first aim should be to prevent rebleeding in a patient with coagulation abnormalities or a person taking warfarin (vitamin K antagonist), thrombin inhibitor and Factor Xa inhibitor.

Blood Pressure

Manage and monitor blood pressure with the purpose to lessen the hazard of re-bleeding thus provide adequate brain perfusion.

In accordance with the American Heart Association and the American Stroke Association 2015 rules, the target is to lower the BP to 140 mmHg if the systolic BP is between 150 and 220 mmHg, in addition acute antihypertensive management is not contraindicated.

If the systolic BP is greater than 220 mmHg:

Manage aggressively with a continuous IV antihypertensive infusion with frequent monitoring, such as nicardipine hydrochloride, with a primary dose of 2.5 mg/hr IV, which can be augmented by 2.5 mg/hr to extreme of 15 mg/hr as required to lower the systolic BP by 10-15%.An alternative to nicardipine hydrochloride is labetalol.

Stabilize other vital signs rapidly, and call for an emergency CT scan.

Cerebral Perfusion Pressure

Consider raising the head of the patient to 30 degrees, laxatives to avoid straining and hyperventilation if ICP is raised; administer mannitol(0.5-1g/kg) to reduce cerebral edema and blood viscosity for further control. Control and monitor the intracranial pressure (ICP) if GCS score is less than 8 especially if ventricles are filled with blood or the patient needs a large amount of sedatives. Can be done via an ICP monitor positioned directly into ventricles or in the brain.

Place a ventricular catheter (VP shunt) to drain excess cerebrospinal fluid (CSF) to allow the hematoma to expand with no/minimal brain damage.

Alternate strategies to control the ICP include induction of coma with sedatives.

Prefer isotonic fluids over hypotonic for maintenance of euvolemia, so that brain perfusion is maintained without worsening of the edema.

Hypothermia and Seizures control

Avoid hyperthermia by antipyretics such as acetaminophen because hyperthermia worsens neurological injury. It also acts as an analgesic to relieve headache.

Monitor patients with EEG if depression pf mental status is out of proportion to severity of injury. ASA guidelines don't recommend prophylactic use of anti-seizures medications. Administer fosphenytoin or other anticonvulsant for control of seizures induced by the damage of cerebral cortex in lobar hemorrhages especially fronto-temporal seizures.

Other medical treatments include:

Antacids such as famotidine for the prevention of gastric ulcers linked with ICH.

Stool softeners such as lactulose to avoid constipation and straining during bowel movements.

Nutrients and fluids as required – either intravenously (IV) or through a nasogastric/gastrostomy tube especially if the patient has swallowing difficulties.

Following assessment of the patient’s swallowing, initiate the enteral feeding.

Admit patients in a stroke unit or ICU for effective care and close monitoring; or shift to the operation theatre if surgical intervention is required.

Essentials of ICU care include:

Serial Neurologic examination
Ventricular catheterization in case of hydrocephalus.
Avoid both hyper- and hypo-tension (target MAP = 70-130 mmHg).
Minimize cerebral edema by isotonic solutions such as normal saline.
Administer 3 x isotonic saline in case of hyponatremia following cerebral salt wasting.
Avoid hyperthermia.
Manage and prevent seizures.
Prevent venous thrombosis with the intermittent compression stockings with or without subcutaneous low-dose, low-molecular weight or unfractionated heparin.
Manage and prevent gastric ulcer formation.
Physiotherapy.
Psychological support with careful use of tranquilizers if required.
CT scans should be repeated.

Surgical Management

Surgery aims at immediate brain decompression to release pooled blood and relieve pressure, and removing as much of the hematoma as possible in addition to clamping off the source of the bleeding if identifiable (such as a tumor or an AVM). Cerebellar hemisphere hematomas >3 cm in diameter are indications for surgical evacuation because of their strong associations with midline shift or herniation.

Surgical options include:

Craniotomy

When hematoma is adjacent to the brain surface or linked with a tumor or AVM.
Involves drilling a hole into the skull and removing the hematoma.

Craniectomy

Involves partial removal of the skull to allow the swelling brain to expand.

Stereotactic Clot Aspiration

When the hematoma is large and located deep within the brain.
Minimally invasive surgery.
Involves use of a stereotactic frame to guide a hollow cannula directly inside the hematoma after drilling a small burr hole in the skull. The cannula is then attached to a large syringe to extract the liquid portion of the hematoma. This is followed by a smaller catheter for continuous drainage for the subsequent days or weeks.

Others

Superficial AVMs less than 3 cm in diameter are removed by combining the radiosurgery, microsurgery along with endovascular surgery.
Deep AVMs or those which are <3 cm in diameter are removed by endovascular therapy, stereotactic radiosurgery, or coagulation through focused proton beams.

Deep cerebral hematomas seldom require early surgical evacuation because of high surgical mortality and severe neurological deficits post-surgery in case of survival.

Post-acute Management

Keep the patient in the ICU for a period of several weeks for monitoring signs and symptoms of recurrent bleeds, hydrocephalus, and other complications.

Once stable, shift to a regular room.

Bed rest for the initial 24 hours.

Encourage an increase in activity progressively.

Ask to avoid vigorous activities.

Flowchart 1: Reversal of Coagulopathy

Complications

Neurological

Herniation, pontine or midbrain hemorrhage, intraventricular hemorrhage (IVH), acute hydrocephalus or brainstem dissection are complications that impair consciousness followed by coma and death. Others include:
Paresthesias
Paralysis
Vision loss
Seizures
Cognitive dysfunction
Fever
Fatigue
Compromised language skills
Dysphagia

Psychiatric problems

Personality changes
Spasticity
Neuropathic pain

Infections

Aspiration pneumonia
Urinary complications

Cardiovascular

Deep venous thrombosis (DVT)

Pulmonary embolism

Prognosis and Follow-up

Prognosis depends upon the overall health status of the patient, age, site of ICH, and extent of damage.

Larger hematomas indicate a worse clinical outcome.

Lobar hemorrhages result in better clinical outcomes than deep hemorrhages.

Hydrocephalus or a substantial volume of intraventricular blood are poor prognostic indicators.

Neurologic deficits resulting from an ICH may be short-term or long-term. They may either disappear over time to variable degrees with treatment as the extravasated blood is gradually reabsorbed or remain permanent. The recovery process could take weeks or even months.

Patients may need speech, physical, and occupational therapy to help patients cope with the deficits resulting from brain damage. Speech and physical therapy help improve communication and restore muscle function. Occupational therapy seeks to help redeem certain skills as well as independence by modifying and practicing day-to-day deeds.

Rehabilitation and the extent of rehabilitation possible vary from individual to individual.

Long-term nursing home care is required for a severely paralyzed or comatose patient post-ICH.

Prevention

Maintenance of a healthy lifestyle.

Cessation of smoking.

Timely management of any underlying cardiac disease.

Control of diabetes.

Early diagnosis and aggressive control of hypertension.

Careful use of the anticoagulation as well as antithrombotic medications.

Cautious assortment of patients for the thrombolysis.

Education regarding the hazards of heavy alcoholism and sympathomimetic drug abuse.

Education regarding warning signs of brain trauma, and precautions in the workplace and elsewhere to reduce the incidence of head injuries.

Timely diagnosis and prompt management of obstetric emergencies such as eclampsia.

Bibliography

Brott, M. I., & Aguilar, T. G. (2011). Update in Intracerebral Hemorrhage. Neurohospitalist, 148-159.

Giraldo, E. A. (2017, February). Intracerebral Hemorrhage - Neurologic Disorders - MSD Manual Professional Edition. ((C) 2019 Merck Sharp & Dohme Corp., a subsidiary of Merck & Co., Inc., Kenilworth, NJ, USA) Retrieved October 23, 2019, from MSD Manual Professional Edition: https://www.msdmanuals.com/professional/neurologic-disorders/stroke/intracerebral-hemorrhage

Liebeskind, D. S. (2018, December 7). Intracranial Hemorrhage: Background, Pathophysiology, Epidemiology. (H. L. Lutsep, F. Talavera, H. S. Kirshner, Editors, & Copyright (C) 1994-2019 by WebMD LLC.) Retrieved October 23, 2019, from Medscape: https://emedicine.medscape.com/article/1163977-overview

An, S. J., Kim, T. J., & Yoon, B. W. (2017). Epidemiology, Risk Factors, and Clinical Features of Intracerebral Hemorrhage: An Update. Journal of stroke, 19(1), 3–10. https://doi.org/10.5853/jos.2016.00864

Dastur, C. K., & Yu, W. (2017). Current management of spontaneous intracerebral haemorrhage. Stroke and vascular neurology, 2(1), 21–29. https://doi.org/10.1136/svn-2016-000047

Garcia, D. A., & Crowther, M. (2020, January 22). Management of bleeding in patients receiving direct oral anticoagulants-UpToDate. Retrieved from UpToDate: https://www.uptodate.com/contents/management-of-bleeding-in-patients-receiving-direct-oral-anticoagulants?sectionName=Dabigatran%20reversal&topicRef=1325&anchor=H3105439&source=see_link#H3105467

Rordorf, G., & McDonald, C. (2020, March 16). Spontaneous intracerebral hemorrhage: Treatment and prognosis-UpToDate. Retrieved from UpToDate: https://www.uptodate.com/contents/spontaneous-intracerebral-hemorrhage-treatment-and-prognosis

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