II. Background
- This page refers to Spontaneous Intracerebral Hemorrhage
- Contrast with Subarachnoid Hemorrhage (due to Cerebral Aneurysm, Cerebral AVM or Trauma)
- Trauma also causes Intracerebral Hemorrhage (in addition to Epidural Hematoma, Subdural Hematoma, SAH)
III. Epidemiology
- Spontaneous Intracerebral Hemorrhage is responsible for up to 9% of CVAs in U.S. (40,000 to 67,000 per year)
IV. Pathophysiology
- Intraparenchymal Hemorrhage is associated with small vessel Cerebrovascular Disease (penetrating arteries, arterioles)
- Most commonly affects the Basal Ganglia and Thalamus (but may affect Cerebrum, Cerebellum or Brain Stem)
-
Neuronal injury mechanisms
- Poor perfusion from ruptured vessel
- Swelling from bleeding and inflammatory response further decreases perfusion
V. Causes: Primary Intraparenchymal Hemorrhage
- Background
- Primary Intraparenchymal Hemorrhage Accounts for 90% of cases
- Results from damaged small blood vessels due to Hypertension or Cerebral amyloid angiopathy (CAA)
- Damaged vessels are more prone to rupture which results in Intraparenchymal Hemorrhage
-
Hypertension
- Most common cause in adults with Spontaneous Intracerebral Hemorrhage
- Hypertension results in degenerative changes in small perforating arteries, weakening their walls
- Typically affects Basal Ganglia, Thalamus, Brainstem, Cerebellum
- Cerebral amyloid angiopathy (CAA)
- Most common cause of non-Traumatic lobar Intracerebral Hemorrhage in older patients
- Beta amyloid accumulates in cortical blood vessels resulting in vascular weakening, microaneurysms
- Typically affects lobar regions
- Risk factors include advanced age, male, asian, Diabetes Mellitus, daily Alcohol. Anticoagulants, Sympathomimetics
- Matsukawa (2012) Acta Neurol Scand 126(2):116-21 +PMID: 22067041 [PubMed]
VI. Causes: Secondary Intraparenchymal Hemorrhage
-
Cerebral Arteriovenous Malformation (AVM)
- Most common cause of Intracerebral Hemorrhage in children
- Hemorrhagic conversion of Ischemic Stroke
- Septic cerebral embolism
- Intracranial Mass
- Anticoagulants or Thrombolytics
- Coagulopathy
- Cerebral Venous Thrombosis
- Encephalitis (e.g. HSV Encephalitis)
- Stimulant Drugs of Abuse (e.g. Cocaine, Methamphetamine)
- Moyamoya Disease
- Mycotic aneurysm rupture
- Vasculitis
VII. Risk Factors:
- Tobacco Smoking
- Strenuous activity
- Oral Anticoagulants (especially Warfarin)
- Hypertension
- Heavy Alcohol use (>30 drinks/month or binge drinking)
- Increasing age
- Risk doubles every 10 years after age 35 years
VIII. Symptoms
- Severe Headache
- Vomiting
-
Decreased Level of Consciousness
- Glasgow Coma Scale (GCS) <=12 in 60% of presentations
- Deterioration occurs in transport or with emergency department in 50% of patients
IX. Signs
- Focal and gradually progressive presentation of neurologic deficits developing over minutes to hours
- Hemiplegia
- Aphasia
- Cushing Triad
- Reflex response to reincreased ICP with large volume intraparenchymal Hemorrhage
- Hypertension
- Bradycardia
- Slow, irregular respirations
X. Labs
- Fingerstick Blood Sugar
- Complete Blood Count with Platelet Count
- Prothrombin Time (PT) or INR
- Partial Thromboplastin Time
- Troponin
- Electrocardiogram
XI. Imaging
-
CT Head
- Obtain at presentation
- Identifies Hemorrhage location, ventricular extension and degree of surrounding edema
- Identifies mass effect, including midline shift and Cerebral Herniation
- Repeat Head CT (consult neurosurgery for recommendations)
- Consider repeat at 6 hours after first CT Head
- Consider repeat at 24 hours (esp. if Anticoagulant use)
- Repeat Head CT for any significant change in neurologic status
- CTA Head and Neck (CT Angiography)
- Spot Sign (extravasation of contrast in an expanding Hematoma)
- Identifies vascular cause of Hemorrhage in up to 15% of cases
- May also identify active, continued Hemorrhage
- Indications
- Lobar Hemorrhage in age <70 years old
- Deep or Posterior Fossa Hemorrhage in age <45 years (or <70 if no Hypertension history)
- Isolated Intraventricular Hemorrhage
- Any vascular etiology Hemorrhage
- Other imaging
- Consider CT Venogram
- Consider MRI in stable patients
XII. Grading
XIII. Precautions
- Cerebellar bleeding can rapidly deteriorate
XIV. Management: General
- Similar overall management as for Subarachnoid Hemorrhage (SAH)
- Exceptions include aneurysm specific management and Blood Pressure targets
-
ABC Management
- Endotracheal Intubation is frequently needed due to decreased GCS, aspiration risk
- Correct coagulation deficits and reverse Anticoagulants
-
Blood Pressure Management
- Opioid Analgesics for Headache may help to control Blood Pressure
- Blood Pressure target
- BP Target range is per local neurosurgical Consultation recommendations
- As of 2022 (AHA/ASA), if SBP 150-220 mmHg, then target SBP 140 mmHg (range 130 to 150 mmHg)
- For large spontaneous ICH or pending emergent surgical intervention, targets vary, but keep <180 mmHg
- Avoid dropping systolic Blood Pressure <130 mmHg
- If presenting systolic Blood Pressure >220 mmHg
- Avoid decreasing Blood Pressure by >20%
- Target continuous smooth and sustained Blood Pressure control (avoid wide fluctuations, infusions are preferred)
- Control Blood Pressure while still maintaining Cerebral Perfusion Pressure
- Initiate Blood Pressure management within 2 hours of diagnosis
- Goal BP range at target within one hour of starting control (do not delay for ICU transfer)
- Labetalol, Clevidipine and Nicardipine are most often used to control Blood Pressure (Esmolol may also be used)
- Avoid venous vasodilators (e.g. Nitroglycerin, Nitroprusside)
- Qureshi (2016) N Engl J Med 375(11):1033-43 [PubMed]
- Manage Seizures
- See Status Epilepticus
- More common in first 72 hours with large lobar intraparenchymal Hemorrhage with ventricular extension
- When used, Seizure Prophylaxis is most common with Levetiracetam (or Valproic Acid)
- Use Benzodiazepines as first-line initial agents in active Seizures (see Status Epilepticus)
- Phenytoin and Fosphenytoin are generally avoided (narrow therapeutic range, Drug Interactions)
- Seizure Prophylaxis indications (not recommended unless Seizures occur)
- Witnessed Seizure
- Seizure activity on EEG with Altered Level of Consciousness
- Early Neurosurgery Consultation
- Ventricular drainage indications
- Surgical drainage indications
- Hydrocephalus
- Increasing intraparenchymal Hemorrhage
- Clinical worsening
- Craniectomy indications
- Coma
- Large intracerebral Hematoma with midline shift
- Refractory high Intracranial Pressure
- Secondary lesion indications for neurosurgical intervention
- Hemorrhagic Brain Tumor
- Arteriovenous Malformation or fistula
- Cavernous malformation
- Distal or Mycotic aneurysm
- Moyamoya
- Disposition
- Admit to Intensive Care unit or dedicated stroke unit
XV. Management: Traumatic intraparenchymal Hemorrhage
- Expect Traumatic intraparenchymal Hemorrhage to stabilize within first 48 hours
- Neurosurgical decompression indications
- Neurologic deterioration or GCS <8
- Contusion volume >50 ml
- Frontal or temporal Contusion >20 ml
- Midline shift >5 mm
- Loss of subarachnoid space (basal cistern effacement)
- Bullock (2006) Neurosurgery 58(3 Suppl): S25-46 [PubMed]
XVI. Prognosis
- See Intracerebral Hemorrhage Score
- Higher mortality with decreasing alertness on presentation
- One year survival: 40%
XVII. References
- Chiara and Flint (2024) Crit Dec Emerg Med 38(12): 25-31
- Dreis (2020) Crit Dec Emerg Med 34(7):3-21
- Burgess and Stowens (2014) Crit Dec Emerg Med 28(5): 2-13
- Kreutzer and Maldonado (2022) Crit Dec Emerg Med 36(7): 16-7
- Marcolini and Swaminathan in Swadron (2023) EM:Rap 23(3): 3-6
- Rordorf and McDonald in Kasner (2014) Spontaneous Intracerebral Hemorrhage, Uptodate, accessed 5/8/2014
- Greenberg (2022) Stroke 53(7):e282-361 +PMID: 35579034 [PubMed]
- Gross (2019) JAMA 321(13): 1295-303 [PubMed]