TRAUMATIC BRAIN INJURY

Definition of TBI

Traumatic brain injury (TBI) is a nondegenerative, noncongenital insult to the brain, possibly leading to permanent or temporary impairments of cognitive, physical, and psychosocial functions with an associated diminished or altered state of consciousness

causes of TBI

1. Skull fractures (e.g., depressed or penetrating)

2. Diffuse axonal injury (e.g., coup/contrecoup injuries, shaken baby syndrome)

3. Hemorrhage (e.g., epidural, subdural, subarachnoid, intracerebral hemorrhage)

4. Anoxia/hypoxia (e.g., post-cardiac arrest, near drowning)

Pathophysiology of TBI

1. Primary brain damage as a result of TBI occurs at the moment of impact.

2. Secondary damage occurs as a result of the subsequent pathologic complications arising from the intracranial and extracranial damage.

Primary brain damage can cause

1. Linear acceleration and deceleration

2. Contusions

3. Haemorrhagic contusion

4. Localized contusion

5. Rotational acceleration

6. Corpus callosum and upper brain stem

Secondary brain damage

1. Late coma

2. Intracranial haematomas

3. Increased ICP

4. Subarachnoid haemorrhage

5. hypoxemia

Classifying severity of TBI based on GSC and Radiographic findings

1. Mild –GCS score of 13-15 at lowest point after resuscitation

   • Uncomplicated-normal brain CT scan

   • Complicated –CT scan evidence of brain injury

2. Moderate–GCS score of 9-12 at lowest point after resuscitation

3. Severe–GCS score of 3-8at lowest point after resuscitation

Neuroimaging of Brain injury

1. CT scanning and MRI are the major neuroimaging modalities.

symptoms of mild TBI

1. head-ache, dizziness, sensory problems, fatigue, change in sleep patterns, and behavioral, mood, and cognitive changes

2. Sensory problems include blurring of vision, tinnitus or a bad taste in the mouth.

3. Cognitive changes include problems with memory, concentration, and attention.

symptoms of moderate or severe TBI

1. persistent and/or worsening headache, nausea and vomiting, seizures, ani-socoria, slurring of speech, ataxia, weakness, numbness in the extremities and altered mental status.

2. Mental status and behavioral changes can range from confusion, restless-ness, and agitation to a vegetative state or coma

Posttraumatic Amnesia PTA

1. PTA occurs in all patients when they emerge from coma.

2. Disorientation to time, place, and person occurs.

3. Patients can have a confused state, diminished memory, and reduced ability to attend and respond to environmental cues.

4. PTA duration has clinical significance and prognostic implications

Complication of TBI

1. Seizures

2. Depression

3. Heterotopic ossification

4. Hydrocephalus

5. Deep venous thrombosis (DVT)

6. Spasticity

7. GI complications: bowel incontinence, stress ulcer

8. GU complications: urinary incontinence, urinary tract infection

9. Endocrine Abnormalities

10. Autonomic Disturbances

11. Respiratory complication

Posttraumatic hydrocephalus

1. Symptoms range from deep coma to the triad of dementia, ataxia and incontinence.

2. Presentation may be atypical, with emotional disturbances, seizures, spasticity or subtle cognitive changes.

3. Diagnosis is based on CT scan in conjunction with clinical assessment.

4. It should be suspected when recovery is slower than expected, progress slows or halt, or function regresses.

5. It can develop anytime after a TBI

Spasticity

Defined as a velocity-dependent increase in muscle tone, resulting from upper motor neurone disease

Hetertopic Ossification (HO)

is ectopic bone formation around joints

Risk factors of Hetertopic Ossification (HO)

coma longer than 2 weeks, spasticity,long bone fractures or decrease in range of motion.

Endocrine Abnormalities

SIADH (Syndrome of Inappropriate ADH secretion) is most frequently seen.

Result in dilutional hyponatremia

Managed with fluid restriction

Diabetes Insipidus is less commonly seen

Autonomic Disturbances

Systemic hypertention

Increased CO and tachycardia are common in acute care setting.

Central fever -uncommon –lesion of anterior hypothalamus

Hypothermia –lesions of posterior hypothalamus

Respiratory complication

Pneumonia is common as bacterial colonization of tracheostomy site

GI complication

Hypermetabolic with high caloric needs

The risk of GI bleeding secondary to stress ulcer is increased and H2 receptor antagonist is frequently prescribed.

Subdural haematoma

Accumulation of blood in the subdural space following rupture of a vein. Follows a head injury, which may be trivial

The interval between injury and symptoms may be days weeks or months.

Headache, drowsiness and confusion are common symptoms.Symptoms are indolent and often fluctuate.

Focal deficits such as hemipresis or sensory loss develop.

Epilepsy occasionally occurs.

Stupor, coma and coning may follow, but there is a tendency for SDH to resolve spontaneously

Extradural haemorrhage

This follows a linear skull valt fracture tearing a branch of the middle meningeal artery.

Blood accumulates rapidly over minutes/hours in the extradural space.

The most characteristic picture is of a head injury with a brief duration of unconsciousness followed by a lucid interval of recovery.

The patient then develops a progressive hemipresis and stupor, and rapid transtentorial coning, with first an ipsilateral dilated pupil, followed by bilateral fixed dilated pupils, tetraplegia and respiratory arrest.

Management of Subdural and extradural haemorrhage

Suspected case needs immediate imaging.

Extradural bleeding requires urgent neurosurgery.

If performed early, the outlook is excellent.

When far from neurosurgical help, surgical drainage through a skull burr-hole has been life saving.

Subdural bleeding may allow more conservative management –even large subdural collections can resolve.

Progress is assessed with serial imaging.

Prognosis and Outcome of TBI

Most patients who remain unconscious 1 mth following brain injury will either recover or die within the first year.

Consciousness is usually regained within 3 months.

20% to 30% of patients who do not regain consciousness will die within the first year.

Paediatric population demonstrates a better outcome than the adult.

Low GCS, impaired movement, pupillary responses, surgical mass lesion and unconsciousness longer than 3 months are with poor prognosis.