6. Primary Injury
• Occurs in conjuction with
mechanical forces that cause
disruption to the brain tissue.
• It occurs immediately (minutes
to hours after the impact) and is
not amenable to medical
intervention
• Contusions
• Diffuse axonal injury
Contusions
• Bruising of cortical tissue
• coup- contrecoup injuries
7. Primary Injury
• Occurs in conjuction with
mechanical forces that cause
disruption to the brain tissue.
• It occurs immediately (minutes
to hours after the impact) and is
not amenable to medical
intervention
• Contusions
• Diffuse axonal injury
Diffuse Axonal Injury
• Immediate disruption of the axons
due to acceleration–deceleration and
rotational forces that cause shearing
upon impact.
8. Secondary Injury
• develops over the hours and
days after the initial impact
• associated with disruption of
cerebral blood flow and
metabolism, massive release of
neurochemicals, cerebral
edema, and disruption of ion
homeostasis
Excitotoxicity
• neuronal damage occurs as a result of
a massive surge in neurotransmitters
9. Secondary Injury
• develops over the hours and
days after the initial impact
• associated with disruption of
cerebral blood flow and
metabolism, massive release of
neurochemicals, cerebral
edema, and disruption of ion
homeostasis
Brain swelling
• Increase in cerebral blood volume
results to elevated intracranial
pressure
• Results to decreased cerebral
perfusion pressure
• May lead to herniation
10. Secondary Injury
• develops over the hours and
days after the initial impact
• associated with disruption of
cerebral blood flow and
metabolism, massive release of
neurochemicals, cerebral
edema, and disruption of ion
homeostasis
Brain edema
• Occurs later after head injury
• Vasogenic edema
• Due to outpouring of protein rich fluid
through damaged vessels
• Cytogenic Edema
• Hypoxic and ischemic brain
damage
11. Focal Hemorrhages
Epidural Hematoma
• Seen in skull fracture of temporal
bone
• Hematoma expansion is slowed by
the tight adherence of the
dura to the skull
• Clinically presents with a lucid
interval (50%) prior to rapid
deterioration.
12. Focal Hemorrhages
Subdural Hematoma
• 30% of severe head trauma
• Usually in the elderly
• Result from shearing of bridging
veins between pia-arachnoid
and the dura
13. Focal Hemorrhages
Subarachnoid Hemorrhage
• Closely associated with ruptured
cerebral aneurysms and AVM
• CT findings: demonstrate blood
within the cisterns and the
subarachnoid space within 24
hours
15. Mild TBI (Concussion)
• Key criterias:
• Confusion, disorientation, LOC of less
than 30 min
• PTA for less than 24 hours
• Transient focal neurologic abnormalities
• GCS 13-15
• Usually unremarkable CT scan findings
• Symptoms usually resolve over time
• A subset of patients will have
persistent symptoms classified
as postconcussion syndrome
17. Coma
• Lack of wakefulness as
evidenced by the lack of sleep
wake cycles on
electroencephalography (EEG)
• Eyes remain closed
• No spontaneous purposeful
movement or ability to discretely
localize noxious stimuli.
• Results damage to RAS
18. Vegetative State
• Characterized by the resumption of the sleep–wake cycle on EEG
• No awareness of self or environment
• No perceivable evidence of purposeful behavior
• Presence of a verbal or auditory startle but no localization or tracking
• Related to diffuse cortical injury
• Persistent vegetative state: if VS is persistent for more than 1 month
after initial brain injury
19. Minimally Conscious State
• Able to exhibit environmental awareness
• Shows evidence of inconsistent but purposeful behaviors
• Patient may also show:
• Visual fixation
• Smooth pursuit tracking
• Emotional or motor behaviors
• Often difficult to differentiate with VS
• Better prognosis than VS
21. CT scan
• Current standard neuroimaging modality for initial evaluation
• Allow for rapid, noninvasive three-dimensional imaging, which
accurately detects facial and skull fractures, as well as acute
hemorrhaging and mass effect
• Allows for optimal medical management of trauma patients who
may require immediate surgical intervention
• May be done serially to evaluate recovery or monitor complications
22. When to request CT scan?
• In mild TBI cases, less than 10%
have positive CT scan findings
• CTs should be obtained in cases
of mild head trauma, if specific
additional criteria suggesting the
possibility of more severe or
evolving neurologic injury are
met
23. Magnetic Resonance Imaging
• Second method of structural
neuroimaging that has demonstrated
clinical use in TBI
• Does have superior resolution vs CT
scan and provides much higher details
of soft tissue
• Important in:
• Evaluating frontal area and brainstem
• Detecting small hemorrhages
• Detecting non-hemorrhagic white matter
injury
• Not ideal for acute imaging
Useful MRI sequences
• T1 weighted
• Attain anatomic maps of the brain
• T2 sequences
• Sensitive to changes in water (edema)
and iron content (blood)
• FLAIR
• Improved visualization of cortical and
periventricular lesions
• Visualize non-hemorrhagic shear injury
associated with DAI
• GRE
• Additional sensitivity to blood breakdown
products useful in DAI
25. Post-traumatic Amnesia
• One of the most commonly used predictors of outcome
• Longer PTA leads to worse outcome
• Severe disability is unlikely when PTA lasts <2 months
• Good recovery is unlikely when PTA lasts >3 months
• PTA correlates strongly with the length of coma in patients with
DAI but poorly in patients with the primarily focal brain injuries (contusions).
• Galveston Orientation and Amnesia Test (GOAT)
• Standard technique for assessing PTA
• End of PTA: score of 75 or higher in GOAT for 2 consecutive days
29. Ranchos Level of Cognitive Functioning Scale
• Eight-level global scale that
focuses on cognitive recovery
and behavior after TBI
• Represents recovery as a
progression through 8 typical
stages
31. • Focus is to assist each patient in improving functional independence
• Multidisciplinary
• Physical therapist
• Occupational therapist
• Speech language pathologist
• Psychologist
• Medical issues and complications may occur
32. Post-traumatic Seizure
• Significant complication arising from TBI
• 86% of patients with one seizure after TBI will have a second within 2
years of injury
• Risk Factors: genetic, biparietal contusions, dural penetration
with bone and metal fragments, multiple intracranial operations,
cortical contusions, subdural hematoma, significant midline shift,
early PTS, and skull fractures
• Phenytoin is used as early prophylaxis
33. Heterotrophic Ossification
• Incidence: 11-28%
• Risk factors: TBI secondary to blast
injuries, more severe TBI,
dysautonomia
• HO is considered as a risk factor for
poorer outcomes and decreased
home discharge rates
• Bone scan is sensitive identifying
HO in early stages
• Management:
• Prophylaxis:NSAIDS, indomethacin,
Calcium binding chelating agents
• Treatment: Surgical excision
34. Other complications
Deep venous thrombosis
• 40% chance of having pulmonary
embolism
• Use of heparin or low molecular weight
heparin
• Risk factors:
• advanced
age
• severe injury
• prolonged immobilization
• significant
fractures
• presence of clotting disorder
Swallowing and Nutrition
• Increased caloric requirements
• Early institution of enteral nutritional
support may decrease morbidity and
mortality
• Clinical nutritionist is an integral part of
the team
• Assessment: bedside swallowing
assessment, video fluoroscopy
• Use of gastrostomy or jejunostomy tube
35. Other complications
• Bowel and bladder dysfunctions
• Spasticity
• Endocrine dysfunctions
• Post-traumatic headaches
37. Cognitive Deficits
• Among the most debilitating and complex aspects of TBI to manage
and treat
• Spans domains
• Arousal
• Attention
• Memory
• Executive control
38. Agitation
• Common in acute phase of TBI
• Prevalence: 11-42%
• “An excess of one or more
behaviors that occurs during an
altered state of consciousness.”
• Significant impact on patient’s
ability to actively participate in
therapies
• Generally lasts only 2-3 weeks
Management
• Pharmacologic: beta-blockers,
atypical antipsychotics,
benzodiazepenes
• Cognitive-behavioral techniques
• Medications should be chosen
carefully and used in conjunction
with other behavior management
techniques
for maximum effect
• Use of restraints
39. When a patient must be restrained
• Use of enclosure beds are
preferable to belts or other
restraints
• Rear-fastening wheelchair
seatblets
• Soft hand mitts
40. Sleep Disturbance
• Alterations in circadian rhythms,
sleep patterns, sleep quality
• Result of diffuse cerebral
dysfunction associated with
primary and secondary injury
• Sleep pattern: decreased REM
and slow wave sleep
• Total sleep time and sleep
efficiency are disturbed
Management
• Pharmacologic: SSRI (Trazodone)
• Cognitive behavioral therapies
• Sleep restriction
• Stimulus control
• Sleep hygiene
41. Psychological Complications
Depression
• Most common psychological
problem after TBI
• Prevalence: 6-77%
• Highest within 1st year after injury
• May result from biomechanical
changes following injury
• may
• Posttraumatic Stress Disorder
• More likely to occur in mild TBI
without amnesia or LOC
• Likely to be able to recall traumatic
event
• Express unconscious fear response
for the event
• May form a triad of
• TBI
• PTSD
• Chronic pain syndrome
“an alteration in brain function, or other evidence of brain pathology, caused by an external force.”375 These types of injuries result from a jolt or blow to the head or are caused by an object penetrating the skull and injuring the brain. Examples include motor vehicle accidents, falls, assaults, or gunshot wounds. A TBI can be further defined as either open or closed. An open, or penetrating, TBI occurs when the head is hit by an object that breaks the skull and enters the brain. A closed TBI occurs when the brain is injured but the skull remains intact.
The Glasgow Coma Scale (GCS) is the gold standard for primary initial assessment of severity of injury based on level of consciousness.
The score is obtained by rating the best visual, verbal, and motor responses. The total score is simply a sum of these ratings, with scores ranging from 3 to 15. Generally accepted guidelines identify three levels of severity based on GCS scores: mild (GCS = 13 to 15), moderate (GCS = 9 to 12), and severe (GCS = 3 to 8). Severity of injury is also defined by the duration of loss of consciousness/coma and the severity of symptoms.
The two age groups most at risk for sustaining a TBI are 0- to 4-year-olds and 15- to 19-yearolds.316 Motor vehicle accidents result in the greatest number of TBI injuries for people age 15 to 19.316 Another group at risk for TBI is adults over the age of 75. Fall-related injuries are highest among adults over the age of 75
The pathophysiologic processes associated with TBI are complex and consist of (1) a primary injury that disrupts brain tissue and function at moment of impact; (2) secondary injury through multiple biochemical cascades that propagate cellular dysfunction and lead to cell death; and (3) a chronic degeneration, repair, and regeneration process that occurs over the long term after the injury has occurred
Direct disruption of the brain parenchyma from the shear forces of the impact. It occurs immediately (minutes to hours after the impact) and is not amenable to medical intervention. Primary injury includes the following: Contusions, DAI Inertial forces associated with translational acceleration result in a head movement that is in line with the brain’s center of gravity. The resulting differential movement of the brain relative to the skull causes focal injuries such as contusions. Contusions may occur under the impact site (coup injury) and result from a rapid change in skull distortion during impact.189
Contusions remote from the injury site and opposite of the impact are contrecoup injuries and occur because of negative pressure generated from the impact associated with translational acceleration.
Inertial forces associated with angular acceleration result in diffuse axonal injury (DAI), a process that causes tensile strains resulting in microscopic disruption of axons, cerebral edema, and neuron disconnection.
The severity of DAI depends on the duration, magnitude, direction of the angular acceleration, and associated impact.189 In severe cases of DAI, more than just superficial axons are affected and injuries affect deeper white matter structures. The gray-white matter junction is also particularly vulnerable to DAI. Midline brain structures, such as the corpus callosum, are often affected by DAI, which is also associated with loss of consciousness and coma. Recovery from DAI is gradual and can be linked to the duration of coma
Brain swelling
occurs early on after acute head injury (within 24 hours) due to an increase in cerebral blood volume (intravascular blood).
Brain swelling occurs in response to the initial injury and early events involved with secondary injury and results in elevated intracranial pressure (ICP) and decreased cerebral perfusion pressure (CPP). If severe enough, brain swelling can lead to herniation, which has potentially fatal consequences
Brain Edema
occurs later after head injury (in comparison to brain swelling) due to an increase in brain volume secondary to � brain water content Þ extravascular fluid.
Thereare two types of brain edema:
Vasogenic edema
Due to outpouring of protein rich fluid through damaged vessels
Extracellular edema
Related to cerebral contusion
Cytogenic Edema
Found in relation to hypoxic and ischemic brain damage. Due to failing of the cells’ energy supply system leading to increased cell-wall pumping system Þ intracellular edema in the dying cells.
Occurs commonly (90%) with a skull fracture in the temporal bone crossing the vascular territory of the middle meningeal artery (60% to 90%) or veins (middle meningeal vein, diploic veins, or venous sinus; 10% to 40%)
Hematoma expansion is slowed by the tight adherence of the dura to the skull
Clinically presents with a lucid interval (50%) prior to rapid deterioration.
CT Scan: Biconvex acute hemorrhagic mass seen on head CT
Occurs in 30% of severe head trauma. They result from shearing of the bridging veins between the pia-arachnoid and the dura.
They are usually larger in the elderly due to generalized loss of brain parenchyma. CT scan:High density, crescentic, extracerebral masses seen on head CT
These are closely associated with ruptured cerebral aneurysms and arteriovenous malformations (AVMs).
CT findings: demonstrate blood within the cisterns and the subarachnoid space within 24 hours. CT sensitivity decreases to 30% 2 weeks after the initial bleed.
The World Health Organization (WHO) Collaborating Centre Task Force on Mild TBI states that key criteria for identifying persons with a mild TBI include at least one of the following: confusion, disorientation, loss of consciousness for less than 30 minutes, PTA for less than 24 hours, or other transient focal neurologic abnormalities and a GCS score of 13 to 15 after 30 minutes or presentation to a health care facility. Patients with uncomplicated TBI typically do not have associated abnormalities on standard imaging tests like CT.
Concussion severity nomenclature has been developed for the purposes of injury characterization and injury management. Some examples of frequently used grading systems include the Cantu and Colorado concussion scales. For most with mild TBI, symptoms resolve over time. However, a subset of patients will have persistent symptoms classified as postconcussion syndrome and may require outpatient follow-up.
• Lack of wakefulness as evidenced by the lack of sleep wake cycles on electroencephalography (EEG). • Patient’s eyes remain closed.
There is no spontaneous purposeful movement or ability to discretely localize noxious stimuli. • No evidence of language comprehension or expression. • It results from the damage to the RAS in the brainstem or its connections to the thalami or hemispheres. • It can last 2 to 4 weeks for people who do not emerge
Characterized by the resumption of the sleep–wake cycle on EEG. – No awareness of self or environment. – No perceivable evidence of purposeful behavior. – Presence of a verbal or auditory startle but no localization or tracking. – Patient opens eyes (either spontaneously or with noxious stimuli). • Neuropathology of vegetative state – Related to diffuse cortical injury. – Bilateral thalamic lesions are prominent findings in VS. • The term persistent vegetative state (redefined by the Multi-Society Task Force on PVS, 1994) is still currently used in the United States for VS that is present ³1 month after a traumatic or non-traumatic brain injury.
Permanent VS: greater than 3 mos
Patient shows minimal but definite evidence of self or exhibits environmental awareness. • Patient shows evidence of inconsistent but reproducible (or sustained) purposeful behaviors: – Simple command following – Object manipulation – Intelligible verbalization – Gestural or verbal yes/no responses • Patient may also show: – Visual fixation – Smooth pursuit tracking – Emotional or motor behaviors that are contingent upon the presence of specific eliciting stimuli (e.g., patient will cry or get agitated [and behavior is reproducible] only after hearing voices of family members but not with voices of hospital staff). • Often difficult to differentiate from VS. • Several evaluations may be required to differentiate MCS from VS.
MRI becomesincreasingly useful with time from trauma, when patients become more medically stable and additional diagnoses of DAI or other small areas of hemorrhage may be helpful for treatment and prognosis.
Decisions regarding readiness to transfer a patient from ICU to step-down units and to inpatient rehabilitation are generally based on medical stability and progress, as well as the ability to respond to the environment and to actively participate in therapy. Several behavioral measures are useful in determining the status of a patient’s emergence from coma and progress through the acute phases of recovery from injury.
PTA is one of the most commonly used predictors of outcome. • A longer duration of PTA is associated with worse outcomes. • Resolution of PTA clinically corresponds to the period when incorporation of ongoing daily events occurs in the working memory. Threshold values: – Severe disability is unlikely when PTA lasts <2 months. – Good recovery is unlikely when PTA lasts >3 months. – PTA correlates strongly with the length of coma (and with GOS—see below) in patients with DAI but poorly in patients with the primarily focal brain injuries (contusions).
Galveston Orientation and Amnesia Test (GOAT)—developed by Harvey Levin and colleagues, it is a standard technique for assessing PTA. It is a brief, structured interview that quantifies the patient’s orientation and recall of recent events.
Assesses orientation to person, place, time; recall of the circumstances of the hospitalization; and the last pre-injury and first post-injury memories.
The end of PTA can be defined as the date when the patient scores 75 or higher in the GOAT for two consecutive days. The period of PTA is defined as the number of days beginning at the end of the coma to the time the patient attains the first of two successive GOAT scores ³75
Galveston Orientation and Amnesia Test (GOAT)—developed by Harvey Levin and colleagues, it is a standard technique for assessing PTA. It is a brief, structured interview that quantifies the patient’s orientation and recall of recent events.
Assesses orientation to person, place, time; recall of the circumstances of the hospitalization; and the last pre-injury and first post-injury memories.
Duration of PTA is often used to categorize severity of injury according to the following criteria:
Eight-level global scale that focuses on cognitive recovery and behavior after TBI
Widely accepted to describe the process of cognitive recovery as an individual emerges from coma, then progresses towards emergence from posttraumatic amnesia/delirium, and emerges to near normal cognitive functioning Represents recovery as a progression through 8 typical stages and has been widely adopted to assess patient functioning purposes for rehabilitation planning and treatment and to explain patient progress to families.
Phenytoin is commonly used for early prophylaxis against PTS development and for treatment of PTS The Association of American Neurologists (AAN) still recommends early intervention with phenytoin (intravenously) given as a loading dose as soon as possible followed by a 7-day course in the asymptomatic moderate-to-severely brain-injured population.
DVT
In patients with severe TBI, pulmonary embolus secondary to DVT is an important cause of death, and the estimated incidence of DVT is 40%. Increasing evidence supports the safe use of either heparin or low-molecularweight heparin within 24 to 72 hours after severe TBI or intracranial bleed
Swallowing and Nutrition
Moderate-to-severe TBI is associated with specific nutritional needs. Patients demonstrate increased caloric requirements caused by hypermetabolism, increased energy expenditure, and increased protein loss. Early institution of enteral nutritional support may decrease morbidity and mortality, shorten hospital length of stay, and potentially improve immune function.
“True” clinical agitation occurring during an altered state of consciousness is therefore differentiated from the description of an individual who is “irritable,” “angry,” or “aggressive” when not confused.
Among AAPs, quetiapine is frequently used for post-TBIrelated agitation because of its favorable side effect profile and relatively low actions as a D2 receptor antagonist.
Benzodiazepines are GABA-A receptor agonists that can reduce post-TBI agitation symptoms.
When a patient must be physically restrained, the use of enclosure beds, which allow for patient movement while in a safe environment, are preferable to belts or other restraints while in bed.
When out of bed, rear-fastening wheelchair seatbelts can be used for patients who may attempt to get up without assistance and who have poor safety awareness.
Soft hand mitts are helpful at times to ensure patient safety, especially when patients are at risk for pulling out tracheostomy and/or gastrostomy tubes. It is often preferable to have a one-to-one sitter with the patient if doing so allows for reduction of physical restraints .
Trazodone, a selective 5-HT reuptake inhibitor and 5-HT2 receptor antagonist, is frequently used for its sedating effects in TBI.279 At lower doses its sedative properties likely result from its antagonistic effect of the 5-HT2 receptors.
