Traumatic Intracranial Hemorrhage

Aaron C. Sigler, DO, MS Neurosurgery

Tulane NeurosciencesNor

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Disclosures

■ None

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Outline

■ Overview ■ Anatomy ■ Epidural hematoma ■ Subdural hematoma ■ Cerebral contusions

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Traumatic ICH Overview■ Hemorrhage within cranium from traumatic injury

– Epidural – Subdural – Cerebral contusions:

▪ Subarachnoid ▪ Intraparenchymal ▪ Intraventricular

http://www.cohyperbarics.com/tbi-therapy/

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Cerebral Vascular Anatomy■ Common Carotid – Anterior Circulation

– ECA (External) – ICA (Internal)

▪ C1 – cervical segment ▪ C2 – Petrous segment

– Caroticotympanic, Vidian artery ▪ C3 – Lacerum segment ▪ C4 – Cavernous segment

– Meningohyposeal trunk, Capsular branches, Inferolateral trunk ▪ C5 – Clinoid segment ▪ C6 – Ophthalmic segment

– Ophthalmic artery, superior hypophyseal artery ▪ C7 – Communicating segment

– Posterior communicating artery (PCOMM), anterior choroidal artery – Terminal branches: Anterior Cerebral Artery (ACA), Middle Cerebral

Artery (MCA)North

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Vascular Anatomy

■ Posterior circulation – Vertebral arteries ▪ Posterior inferior cerebellar artery (PICA) ▪ Basilar artery

– Anterior inferior cerebellar artery (AICA) – Pontine branches – Superior cerebellar artery (SCA) – Terminal branches: Posterior Cerebral Artery (PCA)

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Vascular Anatomy

https://sites.google.com/a/wisc.edu/neuroradiology/anatomy/under-spin/vascular-anatomy

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https://sites.google.com/a/wisc.edu/neuroradiology/anatomy/under-spin/vascular-anatomy

Vascular territories

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Epidural Hematoma (EDH)

■ Epidural space ■ Arterial ■ Direct head trauma ■ Neurosurgical Emergency! ■ “Lucid Period” ■ Iatrogenic (post surgery) – not usually an

emergencyhttps://www.mypacs.net/cases/70817609.html

Let’s play, Where’s the Lesion??

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Lucid Period

■ Patient sustains injury ■ Brief LOC ■ Regains consciousness ■ later lapses into unconsciousness ■ “talked and died” ■ Arterial injury, rapid build up of ICP, brain

compression, potential herniationNor

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Exam Findings

■ AMS ■ Focal weakness ■ Focal numbness/tingling ■ GCS lowered ■ Cushing’s Triad

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Glasgow Coma Scale■ Maximum 15, Minimum 3 ■ 3 Parts:

– Eyes (4) ▪ 4 spontaneous, 3 to speech, 2 to pain, 1 none

– Verbal (5) ▪ 5 oriented, 4 confused, 3 inappropriate, 2

incomprehensible, 1 none – Motor (6) ▪ 6 commands, 5 localizing to pain, 4 withdrawals, 3

flexor posturing, 2 Extensor posturing, 1 none

Teasdale G, Jennett B: Assessment of coma and impaired consciousness: A practical scale. Lancet 2:81-4, 1974.

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“Cushing’s Triad”

■ Brain compression causes: – HYPERTENSION – REFLEX BRADYCARDIA – RESPIRATORY INSTABILITY

■ Terminal sign of lethal intracranial pressure ■ Herniation imminent or in process

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Imaging

■ CT head without contrast: – Hyperdense lens-shaped lesion with smooth

inner margin underlying skull not crossing sutures (generally)

■ CT C-spine without ■ MRI

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Management

■ ABCs stabilization ■ Cervical collar until cleared ■ GCS ≤8 INTUBATE ■ Correction of underlying coagulopathy ■ Correction of underlying thrombocytopenia ■ ICP control: Mannitol, etc

■ SURGERY!!! ■ Postop: ICP monitoring, seizure prevention, DVT/PE

prevention, stress ulcer prevention, PT/OTNor

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Subdural Hematoma (SDH)

■ Subdural space ■ Venous ■ Traumatic, spontaneous, iatrogenic ■ Acute versus Chronic ■ Typically collateral intracerebral injuries

(contusions/concussions) ■ Predisposing factors: age, ataxia,

coagulopathy, and anti-coagulationNor

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Acute SDH

Where’s the lesion?

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Anatomy of EDH versus SDH

https://www.quora.com/Why-is-it-that-for-an-epidural-hematoma-they-do-not-cross-the-suture-lines

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Exam Findings

■ Focal weakness/numbness/tingling ■ Focal neurologic deficits (speech

difficulties, confusion, visual changes, etc) ■ AMS ■ Seizure activity or GTC ■ GCS decreased ■ Cushing’s Triad

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SDH

■ Kernohan’s notch phenomenon – Unilateral pupillary dilation coupled with

Ipsilateral hemiparesis/hemiplegia – Uncal herniation

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Imaging

■ CT head without contrast: – Sickle shaped area underlying – Acute, subacute, chronic

■ CT C-spine without contrast ■ MRI

– Less useful acutely – Axonal injury – Structural causes

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Where’s the lesion?

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Acute SDH Management■ ABCs stabilization ■ C-collar until cleared ■ GCS ≤ 8 INTUBATE ■ Cautious reversal of anti-coagulation ■ Seizure prophylaxis and/or treatment ■ Control of ICP: mannitol, hyperventilation, etc ■ Surgical indications: Treatment of symptomatic SDH

>1cm at thickest point (>0.5cm in peds) within 4 hrs of injury reduces mortality from 90% to 30% (controversial)

■ Surgical treatment varies ■ Asymptomatic SDH managed expectantlyNor

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Subacute/Chronic SDH Management

■ Factors: – Age, infirmity – Anticoagulants? – Size, location, duration – Symptoms?

■ Surgical treatment – Burr hole(s) versus craniotomy

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What is a Membrane?

■ Forms in late subacute to chronic SDH ■ Primitive cell layer that forms to sequester

SDH in its removal process ■ Primitive and leaky capillaries ■ Pro-lytic chemical milieu creates vicious

cycle that perpetuates SDH

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Cerebral contusions

■ Subarachnoid hemorrhages (SAH) ■ Intraparenchymal hemorrhage (IPH) ■ Intraventricular hemorrhage (IVH) ■ Can have any combination of the above

and include SDH/EDH

https://radiopaedia.org/articles/cerebral-haemorrhagic-contusion

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Subarachnoid Hemorrhage (SAH)

■ Subarachnoid space, bleeding of small vessels (capillaries, small arterioles, etc)

■ Trauma versus spontaneous ■ Spontaneous:

– Ruptured aneurysm (arterial) or AVM – Perimesencephalic hemorrhage (venous)

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Traumatic SAH

■ Main concern: Blossoming ■ Hold anticoagulation ■ Repeat CT head within 6 hours, and again

at 24 hours to confirm stability ■ Conservative management ■ Surgery reserved for expanding life

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Traumatic SAH

https://www.researchgate.net/figure/7426978_fig4_Fig-6-Traumatic-subarachnoid-hemorrhage-Axial-non-enhanced-CT-shows-high-density

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Aneurysmal SAHNor

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Cerebral Angiograms showing various pathology

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Intraparenchymal Hemorrhage (IPH)

■ Bleed within the substance of the brain (capillaries/arterioles)

■ Location highly variable ■ Causes:

– HTN: controlled and uncontrolled – Trauma – Structural lesions

▪ Arteriovenous malformations (AVMs) ▪ Cavernous malformations (cavernomas) ▪ Dural venous sinus thrombosis (venous clot) ▪ Dural arteriovenous fistula (DAVF) ▪ Hemorrhagic tumors (mets, lymphoma, etc) ▪ Amyloid angiopathyNor

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ICH Scoring

Hemphill et al: The ICH score: A simple reliable grading scale for intracerebral hemorrhage. Stroke 32 (4):891-7, 2001

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Diagnostics

■ CT head without contrast: starting point ■ CT C-spine if traumatic ■ CTA with contrast (MRA) ■ CTV with contrast (MRV) ■ MRI brain with and without contrast ■ Diagnostic Cerebral Angiography (DCA)

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Management

■ ABCs ■ C-collar if traumatic/neck pain, until cleared ■ SBP control (<140 rapidly) ■ Anticoagulation reversal* ■ Serial imaging ■ Conservative therapy:

– Transition to PO BP control – Re-assess need for anticoagulation – Anticoagulate?? – Neurology management for hemorrhagic

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Management

■ Surgical intervention – Varies depending upon pathology – Craniotomy for resection

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NICO BrainPath

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Intraventricular hemorrhage

■ Hemorrhage in ventricles ■ Typically associated with other pathology ■ Rarely isolated issue ■ “Casting of the Ventricles” ■ Management:

– Expectant unless obstructive hydrocephalus develops, then EVD in short term possible VP shunt long term

– Intraventricular tPA (tissue plasminogen activator)North

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Questions??

Thank you for your attention!

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