Traumatic Brain Injury Epidemiology, Pathology, and Clincial Considerations

Why study brain injury

}Serious and debilitating injury that permanently affects individual’s lives.

}Affects the lives of family members and can cause patients and their families to experience daily changes in emotion

}grief, guilt, anger, blame, denial and hopefully acceptance/hope.

}Discrete therapies (PT, OT, SLP) often spend more time with patient than any discipline, aside from nursing

}Therapies play important role throughout continuum of care

Acquired brain injury

uThis “basket” term describes any trauma that occurs to the brain after birth.

uAlthough traumatic injury is one form of acquired brain injury, acquired brain injury also encompasses damage from disease processes including: tumors, stroke, infection, or substance disease.  

uAcquired brain damage can also occur from anoxia – or lack of blood supply to deliver needed oxygen the brain.

Causes of (non-traumatic) ABI

uMalignancy

uBenign mass

uAnoxia/Hypoxia

uCommonly from allergic response, asphyxiation, secondary result of TBI

uInfections

uMeningitis

uEncephalitis

uCerebral Vascular Accidents

uHemorrhage

uAneurysm

Ingestion of toxins

Traumatic brain injury

uAn injury that affects how the brain works. It may be caused by a:

uBump, blow, or jolt to the head

uPenetrating injury (such as from a gunshot) to the head

Consequences of brain inury

uMotor Impairments

uSensory Impairments

uAutonomic Impairments

uCognitive Impairments

uPersonality and Behavioral Changes

uLifestyle Consequences

Motor impairments of BI

Orthopedic complications, decreases in strength, impaired functional mobility, poor coordination, balance impairments, problems with fine motor and hand function, impairments in speech, etc.

Sensory impairments of BI

Taste, touch, hearing, vision, smell

Autonomic impairments of BI

Arousal, awareness, sleep disturbances

Cognitive impairments of BI

Memory, attention, difficulty learning, problem solving, planning, judgment and safety awareness

Personality and behvioral changes of BI

Social and coping skills, frustration, anger, denial, reduced insight, disinhibition, impulsivity, apathy, anxiety, depression

Lifestyle consequences of BI

• Loss of independence

• Unemployment and financial hardship

• Lack of transportation

• Lack of leisure and recreation opportunities

• Difficulty with interpersonal relationships

• Loss of roles

Epidemiology

u1.4-1.7 million new TBIs each year in US

uHistorically 75-80% mTBI

u15-30% with residual symptoms

uFrequency of moderate TBI increasing (19% in 1992, 37% 2002)

uTBI is a contributing factor to a third (30.5%) of all injury-related deaths in the United States

u52,000 deaths per year, 70-90,000 with residual deficits

u6-12% prevalence in adult population

u426 of 7288 subjects found to have TBI (5.8%)

u3,044 of 25,134 subjects found to have TBI (12.1%)

Risk factors and at-risk demographics

uThe very young (0-4 years old)

uThe very old

uAdolescent males

uLow health literacy

uLow SES

uAlcohol abuse + drug abuse

Estimated number of TBI hospitalizations by age

Risk factors and at-risk demographics

Etiology

u0-4 years: Up to 66% non-accidental trauma

u0-14 years: Up to 50% falls

u16-25 years: Up to 67% MVA

•26-35 years: Up to 50% MVA

•65+: Up to 60% falls

•85+: Up to 90% falls

TBI Cost

u2000 Census data

• Direct costs of TBI: $9.22 billion/yr

• Indirect costs (lost wages, productivity): $51.21 billion/yr

u2010 Census data

• Combined direct/indirect costs: $76.5 billion

uSevere TBI accounts for nearly 90% of total TBI related costs

Primary injury

• Closed head injury

• Open head injury

  • Depressed skull fx

  • Compound skull fx

  • Basilar skull fx

• Coup-Contrecoup injury

• Intracranial pressure/elevated ICP

• Brain herniations

• Subarachnoid hemorrhage

• Epidural hematoma

• Subdural hematoma

• Intraparenchymal hemorrhage

• Diffuse axonal injury

Closed head injury

• A closed head injury occurs when a person receives a traumatic blow to the head without a facture or displacement to the skull.

• Closed head injuries are quite dangerous because secondary swelling occurs within the brain, either from edema or bleeding.  Resulting compression causes further injury (secondary injuries).

  • Brain swelling may manifest by liquid or brain tissue swelling through any available openings, including the eye sockets.

    • This affects the cranial nerves controlling the eye muscles with resultant eye muscle impairment. 

    • If Cranial Nerve III is compressed the pupil will appear dilated.

    • Medical personnel can initially assess intracranial pressure through pupil size.

      • ER personnel sometimes term this condition as a “blown pupil” (herniation or cranial compression).

Open head injury

}An open head injury occurs when an individual receives an impact from an outside force severe enough to cause to fracture or displace the skull.

}Positives:  More room for swelling decreases risk of secondary compression injury

}Negatives:  The brain is exposed and vulnerable to infections and/or further injury.

}If the skull is fractured or displaced, bone fragments from the skull can enter the brain and cause further injury.

Types of skull fx in open brain injury

• Depressed skull fx

• Compound skull fx

• Basilar skull fx

Depressed skull fx

• The broken piece of skull bone moves in towards the brain (open or closed head injury)

Compound skull fx

The scalp is cut and the skull is fractured

Basilar skull fx

• The skull fracture is located at the base of the skull (neck area) and may include the opening at the base of the skull.

  • Patients may exhibit Raccoon eyes, or bruising around their eye orbits, or Battle’s sign – bruising behind the ears, or CSF leaking through the eyes and nose.

Why is brain injury so dangerous?

• The brain is closed system with little room for edema uThe brain is a closed vault containing

  ubrain tissue

  ucerebral spinal fluid (CSF)

  ublood supply.

  uAny injury to the skull, brain tissue, arteries, or CSF causes cerebral swelling with accompanying blood pressure increases.  This results in an increase in intracerebral pressure.

Skull landmarks

uThe base of the skull is rough, with many bony protuberances

uThese ridges can result in injury to the temporal and frontal lobes of the brain during rapid deceleration

udefinition: when the head slows or stops suddenly and the brain continues to move

Coup-contrecoup injury

}Any blow to the skull causes damage to the brain at the site of the impact – COUP injury…

}…as well as damage to the brain due to “rebound” when the brain secondarily impacts the opposite side of the skull (CONTRE-COUP injury).

}This phenomenon occurs when the force impacting the head is not only great enough to cause damage at the site of impact, but also is able to move the brain severely enough that damage occurs to the opposite side of the brain as well. 

Intracranial pressure

uNormal: 0 - 15 mmHg.

u>20mmHg usually gets intervention

u>25-30mmHg is fatal if prolonged, except in children, who can tolerate higher pressures for longer times.

uSustained leads to more brain damage

• Be aware that when patients have higher levels of ICP, actions like coughing, agitation, or confusion can further raise their levels. 

• Often patients are placed into a medically induced and “therapeutic coma” to avoid this.

Sx of an elevated CP

uCranial nerve palsies

uHeadache with nausea/vomiting

uMental status changes

uConfusion, agitation, lethargy

uTherapists need to work closely with nurses and doctors in the ICU and notify the nurse in charge with any of these signs occur. 

Fluids of the brain are

uNon-compressible so once pressure begins to build intracerebral pressure (ICP) increases rapidly. This is a life threatening problem!!

uHigher ICP leads to less cerebral perfusion or a lower CPP (cerebral perfusion pressure). This, in turn can cause more damage to brain tissue.

Normally, if the ____ _____ _____ _____, then cerebral vessels will ____, to maintain an even perfusion pressure

• Systemic blood pressure rises

If the ____ _____ ____, then the vessels will _____ to allow better flow, with the same goal in mind

• Systemic pressure falls

• Dilate

uThese mechanisms often fail after brain injury.

uSome compensation occurs through blood & CSF moving from the brain into the spinal column; but too much pressure  can lead to brain tissue herniation or a midline shift.  This causes more brain damage!!

Intervention for elevated ICP

Midline shift and brain herniation

Where does the brain shifts

Subarachnoid hemorrhage

uMost frequent lesion in TBI

uBleeding into subarachnoid space

uBetween dura and pia mater

uTypically diffuse, but can be focal

uMultiple secondary effects with large SAH

Epidural hematoma

u= an accumulation of blood between the skull and the dural membrane.

uSeen in 2-4% of TBI

uBetween dura and skull

uMost commonly middle meningeal artery

uOverall mortality of 10%

• <10% when treated early

Epidural hematoma fun facts

uTypically caused by a focused blow to the head with a blunt object like a baseball, hammer, or baseball bat.

uIn 85-95% of patients, this type of trauma is accompanied by an overlying fracture of the skull.

uBlood vessels in close proximity to the fracture are the sources of the hemorrhage.

uBecause the underlying brain is usually minimally injured, prognosis is excellent if treated quickly and aggressively.

uOutcome from surgical decompression and repair is related directly to patient's preoperative neurologic condition.

Subdural hematoma

uSeen in 12-29% of TBI

uCollection of blood between dura and arachnoid membrane

uTorn bridging veins

uMay be missed on initial imaging

• Can form later

• Symptoms often delayed

uMortality rate 40-60%

*If a patient develops sudden lethargy, confusion, headache, dizziness…tell medical team

Intraparenchymal hemorrhage

uSevere contusion, laceration or penetrating injury

uFocal

uMay present as coup-contre coup

uSuborbital, anterior temporal lobe

uBlood pools in white matter of brain.

uBrain trauma can cause several severe IPHs, and can result in white matter shear injury—extensive loss of axons w/extensive brain injury.

uThis can cause diffuse axonal injury.

Diffuse axonal injury

uCan accompany any type of brain injury (open or closed), and is caused by the shaking/strong rotation of the head that occurs with impact

uDamage to the brain occurs when the less mobile brain lags behind the movement of the skull, causing brain structures to tear

uOften with extensive tearing of the white matter tracts. 

uSecondary injury occurs with release of white blood cells intended for repair, causing further damage due to effects on both healthy and unhealthy tissue.

uCan lead to temporary, permanent, localized, or widespread brain damage, coma, or death.

uCan only be diagnosed through MRI.

uFunctional impairments  vary depending on where the shearing occurred.

Diffuse axonal injury summary

uFound in 13.9-72% of TBI

uCommon in deceleration injuries

uPrimary injury

uShearing with rotational forces

uSecondary injury

uMechanical stress leads to metabolic cascade and cell death

uLocal ion flux and Ca+ deregulation lead to cytoskeletal dysfunction and reactive axonal swelling

uGrading

I.Scattered, microscopic evidence of axonal damage

II.Includes corpus callosum

III.Involvement of the pons

• The pons is directly involved in maintenance of consciousness

Secondary injury

uFocal

• Hypoxia/Ischemia

• Herniation

uDiffuse

• Hypoperfusion

• Hypotension

• Elevated ICP

• Excitotoxicity

• Apoptosis

u1 or more typically present in >30% severe TBI

uSignificant determinants in prognosis

• Many signs are clinically apparent during therapy

Common medical complications in TBI (secondary)

uHydrocephalus

uSympathetic Storming

uSeizures

uICU Acquired Weakness (ICUAW)

uCIP

uCIM

uHeterotopic Ossification (HO)

Hydrocephalus

•Signs and sx (similar to those of SDH [subdural hemorrhage], elevated ICP)

•Decreased level of consciousness

•Headache

•Nausea

•Vomiting

•Cognitive changes

•Papilledema

•Decreased vision

•Magnetic gait

•Incontinence

Sympathetic storming—Paroxysmal sympathetic hyperactivity

uDysfunction of the autonomic nervous system

u15-33% of severe TBI

•Signs and Symptoms

•Intermittent agitation

•Diaphoresis

•Hyperthermia

•Hypertension

•Tachycardia

•Tachypnea

•Extensor posturing

•Pupillary dilatation

What to do with sympathetic storming/Paroxysmal Sympathetic Hyperactivity

uIdentify, minimize triggers

uMonitor vital sign response to treatment

uReport exaggerated response, symptoms of unchecked autonomic activity

Seizures

•Signs and Symptoms

•Vary depending type and location of seizure

•May include:

•Motor

• Myoclonic jerks

• Sustained contractions

•Autonomic signs or symptoms

•Somatosensory or special sensory symptoms

•Absence seizures

• frequently missed clinically

ICU aquired weakness

• Critical illness polyneuropathy

• Critical illness myopathy

Critical illness polyneuropathy

uAxon-loss neuropathy affecting patients who are significantly medically compromised

uDistal > proximal

uMotor and sensory

uTypically symmetrical

uMay note muscle wasting

• Thenar muscles

• Tib anterior

• Quadriceps

Critical illness myopathy

uDefinition: Acute primary myopathy causing weakness and paralysis in individuals with critical illness

• Proximal > distal muscle weakness

• Sensation spared

• Reflexes diminished

Heterotopic ossification

u“Clinically relevant” H.O. varies between 8-22% in individuals with TBI

uLength of coma and ventilation, surgical fixation of fractures, autonomic dysregulation, spasticity strongly associated with increased H.O. risk.

uMost common location in TBI is hip, followed by shoulders, elbows, knees.

uCan lead to worse outcomes depending on joint