Hemorrhagic stroke


Sensory Homonculus - courtesy AnatomyZone.com
  • Also known as "spontaneous intracerebral hemorrhage" and sometimes generally as "cerebral hemorrhage"
  • ~10% of all acute strokes
  • Warfarin use is significant risk factor
    • Accounts for 5-15% of all cases
    • Risk of ICH doubles for each 0.5 increase in INR above 4.5

Hemorrhagic stroke causes (13%)

Clinical Features

Often clinically indistinguishable from SAH and ischemic stroke

  • Signs and symptoms suggestive of hemorrhagic stroke
  • Headache and nausea and vomiting often precede the neurologic deficit
  • Findings dictated by location of bleed (in order of most common)
    • Putamen
    • Thalamus
    • Pons
    • Cerebellum
  • The ICH score can predict mortality

Anterior Circulation

  • Blood supply via internal carotid system
  • Includes ACA and MCA

Internal Carotid Artery

  • Tonic gaze deviation towards lesion
  • Global aphasia, dysgraphia, dyslexia, dyscalculia, disorientation (dominant lesion)
  • Spatial or visual neglect (non-dominant lesion)

Anterior Cerebral Artery (ACA)

Signs and Symptoms:

  • Contralateral sensory and motor symptoms in the lower extremity (sparing hands/face)
  • Urinary and bowel incontinence
  • Left sided lesion: akinetic mutism, transcortical motor aphasia
  • Right sided lesion: Confusion, motor hemineglect
  • Presence of primitive grasp and suck reflexes
  • May manifest gait apraxia

Middle Cerebral Artery (MCA)

Patient with stroke (forehead sparing).

Signs and Symptoms:

  • Hemiparesis, facial plegia, sensory loss contralateral to affected cortex
  • Motor deficits found more commonly in face and upper extremity than lower extremity
  • Dominant hemisphere involved: aphasia
    • Wernicke's aphasia (receptive aphasia) -> patient unable to process sensory input and does not understand verbal communication
    • Broca's aphasia (expressive aphasia) -> patient unable to communicate verbally, even though understanding may be intact
  • Nondominant hemisphere involved: dysarthria (motor deficit of the mouth and speech muscles; understanding intact) w/o aphasia, inattention and neglect side opposite to infarct
  • Contralateral homonymous hemianopsia
  • Gaze preference toward side of infarct
  • Agnosia (inability to recognize previously known subjects)

Posterior circulation

Signs and Symptoms:

Basilar artery

Signs and Symptoms:

  • Quadriplegia, coma, locked-in syndrome
  • "Crossed signs" in which a patient has unilateral cranial nerve deficits but contralateral hemiparesis and hemisensory loss suggest brainstem infarction
    • Millard-Gubler syndrome (ventral pontine syndrome) -- ipsilateral CN VI and VII palsy with contralateral hemiplegia of extremities
  • Sparing of vertical eye movements (CN III exits brainstem just above lesion)
    • Thus, may also have miosis b/l
  • One and a half syndrome (seen in a variety of brainstem infarctions)
    • "Half" - INO (internuclear ophthalmoplegia) in one direction
    • "One" - inability for conjugate gaze in other direction
    • Convergence and vertical EOM intact
  • Medial inferior pontine syndrome (paramedian basilar artery branch)
    • Ipsilateral conjugate gaze towards lesion (PPRF), nystagmus (CN VIII), ataxia, diplopia on lateral gaze (CN VI)
    • Contralateral face/arm/leg paralysis and decreased proprioception
  • Medial midpontine syndrome (paramedian midbasilar artery branch)
    • Ipsilateral ataxia
    • Contralateral face/arm/leg paralysis and decreased proprioception
  • Medial superior pontine syndrome (paramedian upper basilar artery branches)
    • Ipsilateral ataxia, INO, myoclonus of pharynx/vocal cords/face
    • Contralateral face/arm/leg paralysis and decreased proprioception

Superior Cerebellar Artery (SCA)

Posterior Cerebral Artery (PCA)

Signs and Symptoms:

  • Common after CPR, as occipital cortex is a watershed area
  • Unilateral headache (most common presenting complaint)
  • Visual field defects (contralateral homonymous hemianopsia, unilateral blindness)
  • Visual agnosia - can't recognize objects
  • Possible macular sparing if MCA unaffected
  • Motor function is typically minimally affected
  • Lateral midbrain syndrome (penetrating arteries from PCA)
    • Ipsilateral CN III - eye down and out, pupil dilated
    • Contralateral hemiataxia, tremor, hyperkinesis (red nucleus)
  • Medial midbrain syndrome (upper basilar and proximal PCA)
    • Ipsilateral CN III - eye down and out, pupil dilated
    • Contralateral paralysis of face, arm, leg (corticospinal)

Anterior Inferior Cerebellar Artery (AICA)

Posterior Inferior Cerebellar Artery (PICA)

Signs and Symptoms:

  • Lateral medullary/Wallenberg syndrome
  • Ipsilateral cerebellar signs, ipsilateral loss of pain/temperature of face, ipsilateral Horner syndrome, ipsilateral dysphagia and hoarseness, dysarthria, vertigo/nystagmus
  • Contralateral loss of pain/temp over body
  • Also caused by vertebral artery occlusion (most cases)

Internal Capsule and Lacunar Infarcts

  • May present with either lacunar c/l pure motor or c/l pure sensory (of face and body)[4]
    • Pure c/l motor - posterior limb of internal capsule infarct
    • Pure c/l sensory - thalamic infarct (Dejerine and Roussy syndrome)
  • C/l motor plus sensory if large enough
  • Clinically to cortical large ACA + MCA stroke - the following signs suggest cortical rather than internal capsule[5]:
    • Gaze preference
    • Visual field defects
    • Aphasia (dominant lesion, MCA)
    • Spatial neglect (non-dominant lesion)
  • Others
    • Ipsilateral ataxic hemiparesis, with legs worse than arms - posterior limb of internal capsule infarct
    • Dysarthria/Clumsy Hand Syndrome - basilar pons or anterior limb of internal capsule infarct

Anterior Spinal Artery (ASA)

Superior ASA

  • Medial medullary syndrome - displays alternating pattern of sidedness of symptoms below
  • Contralateral arm/leg weakness and proprioception/vibration
  • Tongue deviation towards lesion

Inferior ASA

  • ASA syndrome
  • Watershed area of hypoperfusion in T4-T8
  • Bilateral pain/temp loss in trunk and extremities (spinothalamic)
  • Bilateral weakness in trunk and extremities (corticospinal)
  • Preservation of dorsal columns

Differential Diagnosis

Intracranial Hemorrhage Types


Hemorrhagic stroke (i.e. spontaneous intracranial hemorrhage).
Hemorrhagic stroke in the posterior fossa.
12-lead ECG of a patient with acute stroke, showing large deeply inverted T-waves.

Stroke Work-Up

  • Labs
    • POC glucose
    • CBC
    • Chemistry
    • Coags
    • Troponin
    • T&S
  • ECG
    • In large ICH or stroke, may see deep TWI and prolong QT, occ ST changes
  • Head CT (non-contrast)
    • In ischemia stroke CT has sensitivity 42%, specificity 91%[6]
    • In acute ICH the sensitivity is 95-100%[7]
    • The goal of CTH is to identify stroke mimics (ICH, mass lesions, etc .)[8]
  • Also consider:
    • CTA brain and neck
      • To check for large vessel occlusion for potential thrombectomy
      • Determine if there is carotid stenosis that warrants endarterectomy urgently
    • Pregnancy test
    • CXR (if infection suspected)
    • UA (if infection suspected)
    • Utox (if ingestion suspected)

MR Imaging (for Rule-Out CVA or TIA)

  • MRI Brain with DWI, ADC (without contrast) AND
  • Cervical vascular imaging (ACEP Level B in patients with high short-term risk for stroke):[9]
    • MRA brain (without contrast) AND
    • MRA neck (without contrast)
      • May instead use Carotid CTA or US (Carotid US slightly less sensitive than MRA)[10] (ACEP Level C)


Elevating head of bed

  • 30 degree elevation will help decrease ICP by increasing venous outflow[11]

Seizure Prophylaxis and Treatment

  • Prophylactic antiepileptics not recommended[12]
  • Continuous EEG monitoring probably indicated in ICH patients with depressed mental status that is out of proportion fo degree of brain injury[13]
  • Antiepileptics indicated for clinical seizures or seizures on EEG in patients with altered mental status[14]

Blood Pressure

  • Rapid SBP lowering <140 has been advocated with early research showing improved functional outcome[15], but more recent work has found no difference between SBP <140 and <180[16]
  • SBP >200 or MAP >150
    • Consider aggressive reduction w/ continuous IV infusion
  • SBP >180 or MAP >130 and evidence or suspicion of elevated ICP
    • Consider reducing BP using intermittent or continuous IV meds to keep CPP >60-80
  • SBP >180 or MAP >130 and NO evidence or suspicion of elevated ICP
    • Consider modest reduction of BP (e.g. MAP of 110 or target BP of 160/90)

  • Nicardipine in ICH: Start at 5mg/hr, increase 2.5mg q5min until the target blood pressure is achieved and then immediately titrate down to maintenance infusion of 3mg/hr.
  • Labetalol in ICH: 20mg bolus over 1-2 minutes, repeat q3-5 mins until target blood pressure is achieved and then start an infusion of 1-8mg/min.

Reverse coagulopathy

Antiplatelet Reversal

Includes aspirin, prasugrel, clopidogrel

  • Consider desmopressin (0.3mcg/kg)
  • Platelet transfusion
    • No known thrombocytopenia: increases mortality; do NOT give[18]
    • Known or diagnosed thrombocytopenia: consider if platelets <50,000
      • Some hematologists and neurosurgeons recommend for <100,000, despite lack of evidence for improved outcomes


  • Consider neuroprotective intubation
  • Ensure patient is pain-free for post-intubation sedation
    • Propofol with fentanyl
    • Try to prioritize pain control with fentanyl

AHA Spontaneous ICH BP Guidelines 2015[20]

  1. If SBP is 150-220mmHg without contraindication to BP lowering, it is safe to acutely lower BP to 140mmHg and can be effective for improving functional outcome. (Class I Level A)
  2. For ICH patients presenting with SBP >220 mm Hg, it may be reasonable to consider aggressive reduction of BP with a continuous intravenous infusion and frequent BP monitoring (Class IIb; Level of Evidence C)

AHA ICH Coagulopathy Guidelines 2015[21]

  1. Patients with a severe coagulation factor deficiency or severe thrombocytopenia should receive appropriate factor replacement therapy or platelets, respectively (Class I; Level of Evidence C). (Unchanged from the previous guideline)
  2. Patients with ICH whose INR is elevated because of VKA should have their VKA withheld, receive therapy to replace vitamin K–dependent factors and correct the INR, and receive intravenous vitamin K (Class I; Level of Evidence C). PCCs may have fewer complications and correct the INR more rapidly than FFP and might be considered over FFP (Class IIb; Level of Evidence B). rFVIIa does not replace all clotting factors, and although the INR may be lowered, clotting may not be restored in vivo; therefore, rFVIIa is not recommended for VKA reversal in ICH (Class III; Level of Evidence C). (Revised from the previous guideline)
  3. For patients with ICH who are taking dabigatran, rivaroxaban, or apixaban, treatment with FEIBA, other PCCs, or rFVIIa might be considered on an individual basis. Activated charcoal might be used if the most recent dose of dabigatran, apixaban, or rivaroxaban was taken <2 hours earlier. Hemodialysis might be considered for dabigatran (Class IIb; Level of Evidence C). (New recommendation)
  4. Protamine sulfate may be considered to reverse heparin in patients with acute ICH (Class IIb; Level of Evidence C). (New recommendation)
  5. The usefulness of platelet transfusions in ICH patients with a history of antiplatelet use is uncertain (Class IIb; Level of Evidence C). (Revised from the previous guideline)
  6. Although rFVIIa can limit the extent of hematoma expansion in noncoagulopathic ICH patients, there is an increase in thromboembolic risk with rFVIIa and no clear clinical benefit in unselected patients. Thus, rFVIIa is not recommended (Class III; Level of Evidence A). (Unchanged from the previous guideline)

BP Goals in Acute Stroke[22]

Stoke Type Target BP
(mm Hg)
Acute ischemic stroke
IV tPA eligble <185/110
During/after tPA <180/105 Monitor BP every 15 min for 2 hr, then every 30 minfor 6 hr, then hourly until 24 hr.
No tPA <220/120
Mechanical thrombectomy ≤180/105 Maintain during and for 24 h after procedure
Aneurysmal subarachnoid hemorrhage
Unsecured SBP <140-160 Controversy regarding exact number; others recommend <100 MAP
Secured Unclear May depend on ppremorbid BP and presence of vasospasm
Intraparenchymal hemorrhage
Initial SPB 150-220 SBP <140
Initial SPB >220 SBP 140-160


  • Admission for acute or subacute

See Also

External Links


  1. Itoh Y, Yamada M, Hayakawa M, Otomo E, Miyatake T. Cerebral amyloid angiopathy: a significant cause of cerebellar as well as lobar cerebral hemorrhage in the elderly. J Neurol Sci. 1993 Jun;116(2):135-41.
  2. Macdonell RA, Kalnins RM, Donnan GA. Cerebellar infarction: natural history, prognosis, and pathology. Stroke. 18 (5): 849-55.
  3. Lee H, Kim HA. Nystagmus in SCA territory cerebellar infarction: pattern and a possible mechanism. J Neurol Neurosurg Psychiatry. 2013 Apr;84(4):446-51.
  4. Rezaee A and Jones J et al. Lacunar stroke syndrome. Radiopaedia. http://radiopaedia.org/articles/lacunar-stroke-syndrome.
  5. Internal Capsule Stroke. Stanford Medicine Guide. http://stanfordmedicine25.stanford.edu/the25/ics.html
  6. Mullins ME, Schaefer PW, Sorensen AG, Halpern EF, Ay H, He J, Koroshetz WJ, Gonzalez RG. CT and conventional and diffusion-weighted MR imaging in acute stroke: study in 691 patients at presentation to the emergency department. Radiology. 2002 Aug;224(2):353-60.
  7. Suarez JI, Tarr RW, Selman WR. Aneurysmal subarachnoid hemorrhage. N Engl J Med. 2006; 354(4):387–396.
  8. Douglas VC, Johnston CM, Elkins J, et al. Head computed tomography findings predict short-term stroke risk after transient ischemic attack. Stroke. 2003;34:2894-2899.
  9. ACEP Clinical Policy: Suspected Transient Ischemic Attack full text
  10. Nederkoorn PJ, Mali WP, Eikelboom BC, et al. Preoperative diagnosis of carotid artery stenosis. Accuracy of noninvasive testing. Stroke. 2002;33:2003-2008.
  11. http://stroke.ahajournals.org/content/38/6/2001.full
  12. AHA/ASA Guidelines for the Management of Spontaneous Intracerebral Hemorrhage 2015
  13. AHA/ASA Guidelines for the Management of Spontaneous Intracerebral Hemorrhage 2015
  14. AHA/ASA Guidelines for the Management of Spontaneous Intracerebral Hemorrhage 2015
  15. Anderson CS, Heeley E, Huang Y, et al. Rapid blood-pressure lowering in patients with acute intracerebral hemorrhage. N Engl J Med. 2013; 368:2355-2365.
  16. Qureshi AI, Palesch YY, Barsan WG, et al. Intensive Blood-Pressure Lowering in Patients with Acute Cerebral Hemorrhage. N Engl J Med. 2016; 1-11. [Epub ahead of print].
  17. Crash-3 Trial
  18. (PATCH trial)
  19. Bucher J and Koyfman A. Intubation of the neurologically injured patient. J Emerg Med. 2016; 49:920-927.
  20. Hemphill JC, et al. AHA/ASA Guideline: Guidelines for the Management of Spontaneous Intracerebral Hemorrhage: A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association. Stroke 2015.
  21. Hemphill JC, et al. AHA/ASA Guideline: Guidelines for the Management of Spontaneous Intracerebral Hemorrhage: A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association. Stroke 2015.
  22. Cocchi MN, Edlow JA. Managing Hypertention in Patients with Acute Stroke. 2020. Annals of EM 75(6):767771