TRAUMATIC BRAIN INJURY

Ketut Widyastuti

AIMS : Able to understand of traumatic brain injury

LEARNING OUTCOME :

1. Able to describe pathobiology of Traumatic Brain Injury

2. Able to describe how to implement a neurological assessment for patient with
traumatic brain injury
3. Able to describe management of patient with Traumatic Brain Injury
4. Able to describe the prognosis patient with Traumatic Brain Injury

ABSTRACT

Traumatic Brain Injury (TBI) also known as acquired brain injury, head injury or brain injury
causes substantial disability and mortality. It occurs when a sudden trauma damages the brain
and disrupts normal brain function.

Pathophysiology of TBI: Classified as primary and secondary or focal and diffuse injury.

a.The Primary Mechanism

The two main mechanism that cause primary injury are contact and acceleration-
deceleration. As primary mechanisms of injury; in rapid acceleration/deceleration forces,
brain contusions most commonly occurs in the frontal and temporal poles and the inferior
surfaces of the frontal and temporal lobes, where bony protuberances at the skull base serve
as a less than friendly cushion for the brain moving the cranium.

b.The Secondary Mechanism

Injury may result from impairment or local declines in cerebral blood flow (CBF) after a TBI.
Decreases in CBF are result of local edema, hemorrhage, or increased intracranial pressure
(ICP). As a result of inadequate perfusion, cellular ion pumps may fail, causing a cascade
involving intracellular calcium and sodium. The metabolic cascades involves molecular and
cellular events that have multiple consequences. These include breakdown of the blood-brain
barrier and cerebral autoregulation, edema formation, impairment of energy metabolism,
changes in cerebral perfusion, disruption of ionic homeostasis, activation of autodestructive
neurochemicals, generation of free radicals and genomic changes, which all are considered
secondary mechanism of neural dysfunction and cell death. Clinical conditions associated with
the risk of a decreased CBF are arterial hypotension, hypoxemia, intracranial hemorrhage and
malignant brain edema and hyperthermia.

Prognosis of head injury depend on :

1. The anatomical area involved
The outcome and complications of frontal , lateral and occipital impacts are to some
extent dictated by the local anatomy, e. g. precense of air sinuses, large blood
vessels, etc.
2. The type of injury
Injury forces applied to particular anatomical areas produce a patetern of injury for
the individual, e. g.
 - Acceleration/ Deceleration : - applied to entire head, evident as disordered
consciousness from the time of impact resulting from concussion, often with
diffuse axonal injury and /or cerebral contusions [coup or contrecoup].
- Local impact : - coup injuries to scalp, skull, meninges, brain.
- Penetrating : - pathway of injury velocity and nature of projectile
- Crush injury : - scalp, skull, and cranial nerve injuries.
3. The pathology of injury
Primary :
Scalp : - contusion, abrasion, laceration
Skull fracture : open, close, linear, depressed, comminuted
Meningeal injury : - contusion, laceration
Brain injury: concussion, diffuse axonal, focal contusion, laceration and penetration
Secondary: Intracranial haemorrhage, Cerebral swelling, Cerebral hypoxia, C.S.F.
leakage and pneumocephalus, Metabolic disorders, Infection, Epilepsy
4. The evolution of the injury
The rate of deterioration will influence the time available for specific treatment..
Cognitive impairments after TBI include difficulty concentrating, difficulty remembering,
forgetting recent events, confusion, answering slowly and amnesia. Duration of post traumatic
amnesia (PTA) can also provide of injury severity ranging from very mild (<5 minutes) to
extremely severe (>4 weeks). Retrograde amnesia involving minutes or more rarely days,
immediately preceding the accident frequently accompanies PTA.

The TBI severity spectrum ranges from mild impact with no behavioral syndromes, resulting
in no lasting structural injury and producing only transient and temporary changes in
neurologic function to patients in prolonged coma/ vegetative state from catastrophic brain
injury. Cognitive impairments after a concussion can include difficulty concentrating, difficulty
remembering, feeling slowed down, forgetting recent events, confusion, repeating question,
answering slowly and amnesia.

Retrograde Amnesia is characterized by memory loss for events before brain trauma. This
likely results from inability to retrieve those memories from our memory storage with related
to an inability appropriate cues for memory retrieval.

Anterograde Amnesia is an inability to form a new memories or new information following brain
trauma, likely as a result of damage to the temporal or frontal lobes and the white matter
connecting them.

SCENARIO

A 23-year-old woman was taken to the hospital with a decrease in consciousness after a head
hit due to falling from a motorbike during a traffic accident. Head CT was performed and a
cerebral frontotemporal hemorrhage and cerebral edema were found. Decompression
craniectomy was performed in patients by neurosurgeons. On the third day postoperatively,
the patient was well aware of the weakness in the left side of the body. Patients do not
remember chronologically when the event took place.

Learning Task:
1. What kind of history points are needed in the case?
2. How to diagnose this patient?
3. Please explain physical assessment and plan of care in this patient! I
4. Please explain the prognosis in this patient