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Competencies: ABI/TBI

Prepared By: Corbin Lippert RN BScN CNN(c)

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Understands the pathophysiology related to TBI/ABI Primary vs Secondary injury

Initial injury may involve a contusion/laceration/hemorrhage as a primary injury but over time, edema, herniation etc may cause secondary damage

Diffuse vs Focal Damage may be isolated to one lesion, vascular distribution,

intracerebral compartment etc. Or, it may be spread generally throughout the brain in typical or atypical distribution patterns (ie. Watershed, gray/white matter junctions, etc)

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Concussion: transient, temporary neurologic dysfunction caused by mechanical force to the brain

Can vary in severity and duration

Moderate to severe involve a loss of consciousness

May include loss of reflexes, respiratory arrest, retrograde or antegrade amnesia, headache, dizziness, photophobia, gait disturbances, irritability, giddiness and confusion

Post-concussion syndrome with a broad range of symptoms can persist up to one year

Diffuse Axonal Injury: aka Shear Injury. Caused in high spped acceleration/deceleration injuries (MVC). Wide spread lesions throughout cerebral white matter, focal lesions at the corpus callosum and midbrain at the level of the pons and superior cerebellar peduncles.

Poor prognosis for recovery

Pathology not only related to axonal tearing but to release of cytotoxins which lead to axon destruction

Not always picked up on CT unless associated hemorrhage is seen

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Hypoxic brain injury: deprivation of oxygen to brain tissue though traumatic and non-traumatic mechanisms results in cell death

Damage is commonly seen in the areas between major arterial known as “watershed” areas

The hippocampus is particularly vulnerable and paired with generalized encephalopathy and cerebral atrophy account for the severe persistent memory impairments that are seen in survivors

Ischemic Brain Injury

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Focal Injuries

Cerebral contusions: bruising of brain tissue Caused by rupture of capillary blood vessels

Common sites: under depressed skull fractures

Frontal poles, Temporal pole, frontotemporal junction, Orbito frontal related to sphenoid bone and shape of basal skull

Contusions can result in mass effect from local edema and increased ICP and may lead to herniation syndromes

Produce signs and symptoms related to the area of the cortex involved

Terms coup and contra-coup refer to the direction of the force applied to the head and the location of the resulting injury

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Cerebral Laceration: Tearing of the cortical surface of the brain

Creates hematoma and contusion formation

Signs also relate to the the area damaged

Brain Stem Injury: Immediate unconsciousness (deep coma)

Decerebration, autonomic dysfunction, non-reactive pupils (small-midpoint).

Often accompanied by DAI (seldom see in isolation)

Intracranial Hemorrhage: results from bleeding beneath a fracture or as a result of accel/decel forces resulting in shearing of bridging veins or a cortical artery

Allows blood to enter the epidural, subdural, subarachnoid or intraventricular space

The effect of the bleed may not be immediate, symptoms may start off minor and then deteriorate later

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Epidural Hemorrhage: bleed occurs between the periosteum and the dura (potential space).

Most commonly (85%) associated with a skull fracture, particularly in the squamous portion of the temporal bone where the middle meningeal artery runs.

Can be venous or arterial and this will change the rapidity of decline in LOC

Initially a person may become unconscious, wake and function for a period of a few minutes to 2 days and then rapidly deteriorate in LOC to coma

Must be treated surgically and urgently

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Subdural Hematoma: bleeding between the dura and the arachnoid layer Caused by: rupture of subdural bridging veins, small arterial

branches, from contused or lacerated areas and extension from an intracerebral hematoma

Occurs in 10-15% of head injuries

Acute: within 48 hours

Subacute: 2-14 days

Chronic: 2 weeks-months

Acute Subdural Hematoma: Symptoms: Headache, drowsiness, slow thinking, confusion worsening

over time. Ipsilateral pupil becomes fixed an dilated.

Subacute Subdural Hematoma: Failure of a patient to regain consciousness may be an indication that a

SDH has been slowly developing and had been missed previously

Chronic Subdural Hematoma: Develop very slowly over time and may become encased in a

membrane and eventually produces symptoms of a space occupying lesion: headache, decreased mentition, confusion, and seizure.

Common in elderly due to cerebral atrophy with puts a strain on bridging vessels and the increased space allows more room for hematoma formation.

Treatment: medical management, burr hole drainage, craniotomy

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Intracerebral Hematoma: Bleeding into the brain parenchyma accounts for 2-3% of TBI

Primarily related to contusions, often found in frontal and temporal lobes

Can be related to shearing strain on deep vessels

Signs: Headache, deteriorating LOC to coma, contralateral hemiplegia, ipsilateral dilated pupil, increase ICP

Surgery not always beneficial d/t widespread contusion and swelling

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Subarachnoid and Intraventricular Hemorrhage: Rare event in traumatic injuries

Non-Traumatic Acquired Brain Injury

Aneurysm Rupture: Causes bleeding into the Subarachnoid area(SAH), Intraparenchymal

tissue (Hemorrhagic stroke) and ventricles (IVH) Common sites:

ICA at bifurcation with ACoA ICA and origin of PCoA First bifurcation of MCA Bifurcation of ICA into MCA and ACA Junction of PCoA and PCA Bifurcation of the Basilar Artery Origins of three cerebellar atreries

Various Shapes and Etiologies: Fusiform, Berry Traumatic/Dissecting-due to intima of artery being torn Charcot-Bouchard (hypertensive) Mycotic (septic emboli)

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Cerebral Aneurysm Rupture

Signs & Symptoms: Rupture may be preceded by a prodrome of CNIII palsy (Dilated

pupil, ptosis, diplopia), localized headache (behind and above the eye), Extraocular movement deficits of CN IV of V, neck pain, upper back pain, nausea of vomiting

After rupture: “Thunderclap” or worst headache of your life, Immediate loss of consciousness or decreased LOC, vomitting. Localized effects such as cranial nerve deficits, stroke syndromes and pitutary dysfunction may occur in addition to generalized effects from Increased ICP, edema, meningeal irritation (stiff neck, pain in back and neck, blurred vision, photophobia)

Cerebral Aneurysm Repair

Diagnosis is done by Lumbar Puncture (LP), CT, MRI, cerebral angiography

Grading Systems include: Fisher Scale (Radiographic)

Hunt & Hess (Clinical Observation)

WFNS (GCS + Motor Deficit)

Treatment:Depends on nature of aneuysm: Clipping vs Endovascular

Clipping via Cerebral Angio

Complications include re-bleed, seizure and vasospasm

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Arteriovenous Malformation

Congenital cerebral vascular abnormalities in which there is a direct connection between arteries and veins with no capillary bed between

Hemorrhage is the primary presenting problem (50-70%) with seizure less common at 25%

Surgery, endovascular embolization and radiotherapy are the treatment options and must be weighed against the risk of bleed (lifetime risk (%)=105-pt. age)

1-2/100000/year detection rate but 4% autopsy rate

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Secondary Brain Injury

Hydrocephalus:

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Secondary Brain Injury

Increased Intracranial Pressure:

Secondary Brain Injury

Mass Effect and Herniation Syndromes

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The Glasgow Coma Scale

Created by neurosurgeons Graham Teasdale & Bryan Jennett at the university of Glasgow in Scotland in 1974 to more accurately describe level of consciousness.

It consists of scores applied to: Eye Opening (4), Best Verbal Response (5) and Best Motor Response (6)

Minimum Score is 3 , Max is 15

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Best Eye Opening Response: 4 Opens eyes spontaneously when approached 3 Opens eyes in response to speech (normal or shout) 2 Opens eyes only to painful stimuli (nail bed, not orbital) 1 Does not open eyes to painful stimuli

Best Verbal Response: 5 Oriented to time, place and person 4 Converses, although confused 3 Speaks only in words or phrases that make little or no sense 2 Responds only with incomprehensible sounds (e.g. groans) 1 No verbal response

Best Motor Response: 6 Can obey a simple command (lift hand, 2 fingers) 5 Localizes to painful stimuli and attempts to remove source 4 Purposeless movement in response to pain 3 Flexes elbows and wrists while extending lower legs to pain (decorticate) 2 Extends upper and lower extremities to pain (decerebrate) 1 No motor response to pain on any limb

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Glasgow Coma Scale

An intubated patient may be identified with a T if a tracheostomy/ventilator or endotracheal tube is preventing verbal communication.

Patients with a score of 7 or less are considered to be in “coma”.

GCS is used at the accident scene by paramedics to establish the seriousness of the brain injury and has implications in auto insurance benefits.

Correlative studies have led to the use of GCS as a prognostic indicator for recovery and impairment

Glasgow Coma Scale

In Ontario Insurance terms a GCS of 9 or less signifies a “catastrophic” brain injury

In standard terminology it is like this: Severe less than or equal to 8

Moderate 9-12

Minor 13-15

It can not be used reliably in children -use Pediatric GCS instead

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Rancho Los Amigos Levels of Cognitive Functioning Scale

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Brain Injury Severity

Mild

Moderate

Severe

References

Crimlisk, J., Grande, M., Neurologic Assessment Skills for the Acute Medical Surgical Nurse, Orthopaedic Nursing, January/February 2004, Vol 23, Number 1, p. 3-9

Edwards, P., The Specialty Practice of Rehabilitation Nursing – A Core Curriculum, 4th Edition, 2000

Goldberg, S., Clinical Neuroanatomy Made Ridiculously Simple, MedMaster Inc., 1992

Hendelman, W., Atlas of Functional Neuroanatomy, CRC Press, 2000

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Resources

Diamond, M.C., Scheibel, A.B., Elson, L.M., The Human Coloring Book, HarperPerennial,1985

Pinel, J., A Colorful Introduction to the Anatomy of the Human Brain-a Brain and Psychology Coloring Book, Allyn and Bacon, 1998

Testani-Dufour, Linda, Marano Morrison, C, Brain Attack: Correlative anatomy, Journal of Neuroscience Nursing, august 1997, 29 (4), p. 213-224