Traumatic brain injury (TBI), causes substantial disability and mortality.
It occurs when a sudden trauma damages the brain and disrupts normal brain function.
TBI may have profound physical, psychological, cognitive, emotional, and social effects.

TBI may be divided into primary injury and secondary injury .
Primary injury is induced by mechanical force and occurs at the moment of injury.
Secondary injury is not mechanically induced. It may be delayed from the moment of impact, and it may superimpose injury on a brain already affected by a mechanical injury.

The 2 main mechanisms that cause primary injury are:
Contact (as an object striking the head or the brain striking the inside of the skull)
Acceleration-deceleration.

Primary injury due to contact may result in; injury to the scalp , fracture to the skull and surface contusions.
Contusions are distinct areas of swollen brain tissue,typically found on the poles of the frontal lobes, the inferior aspects of the frontal lobes, the cortex above and below the operculum of the sylvian fissures, and the lateral and inferior aspects of the temporal lobes.

Primary injury due to accelerationdeceleration results from unrestricted movement of the head and leads to shear, tensile, and compressive strains.
These forces can cause intracranial haematoma or diffuse axonal injury
(injury to cranial nerves and the pituitary stalk.

Intracranial haematoma is the most common cause of death and clinical deterioration after TBI.
Haematomas may be:
Epidural haematomas caused by fracture of the temporal bone and rupture of the middle meningeal artery, clotted blood collects between the bone and the dura.It can grow quickly creating pressure against the brain tissue.
Subdural haematomas are usually caused by rupture of the bridging veins in the subdural space.
They can grow large enough to act as mass lesions, and they are associated with high morbidity and mortality rates.
Subarachnoid haematomas result from damage to blood vessels in the posterior fossa stalk.

Diffuse axonal injury (DAI) is one of the most common and important pathologic feature of TBI.
It constitutes mostly microscopic damage, and it is often not visible on imaging studies.
The main mechanical force that causes DAI is rotational acceleration of the brain, resulting in unrestricted head movement.
Rotational acceleration produces shearing and tensile forces, and axons can be pulled apart at the microscopic level.
Microscopic evaluation of the brain tissue often shows numerous swollen and disconnected axons.
Rapid stretching of axons is thought to damage the axonal cytoskeleton and, therefore, disrupt normal neuron function.

Secondary injury:
It may occur hours or even days after the inciting traumatic event.
Injury may result from impairment or local declines in CBF after TBI as a result of local edema, haemorrhage or increased ICP.
As a result of inadequate perfusion, cellular ion pumps may fail, causing a cascade involving intracellular calcium and sodium which may contribute to cellular destruction.

Excessive release of excitatory amino acids, such as glutamate and aspartate, exacerbates failure of the ion pumps.
As the cascade continues, cells die, causing free radical formation, proteolysis, and lipid peroxidation.
These factors can ultimately cause neuronal death.

To summarize causes of secondary brain injury:
Hypotension
Hypoxaemia
Hypercarbia
Hyperthermia
Hyperglycaemia
Hypoglycaemia
Hyponatraemia
Seizures
Infection

Head injuries can be classified into mild, moderate, and severe.
The Glascow Coma Scale (GCS),is the most commonly used system for classifying
TBI severity;
TBI with a GCS of 13 or above is mild, 9 –
12 is moderate, and 8 or below is severe.
Other classification systems are also used to help determine severity; duration of posttraumatic amnesia (PTA), and loss of consciousness (LOC).

Mild
GCS PTA LOC
13-15
Moderate 9-12
Severe 3-8
Less than 1 day
0-30 min.
1-7 days 30min.-
24hrs.
More than 7 days
More than
24hrs.

Symptoms are dependent on the injury's severity:
• With mild TBI, the patient may remain conscious or may lose consciousness for a few seconds or minutes.
• Other symptoms of mild TBI include; headache, vomiting, nausea, lack of motor coordination, dizziness, difficulty balancing, lightheadedness, blurred vision or tired eyes, ringing in the ears, bad taste in the mouth, fatigue or lethargy, and changes in sleep patterns.
• Cognitive and emotional symptoms include; behavioral or mood changes, confusion, and trouble with memory, concentration, attention, or thinking.

A person with a moderate or severe TBI may have a headache that does not go away, repeated vomiting or nausea, convulsions, an inability to awaken,dilation of one or both pupils,slurred speech, aphasia , dysarthria, weakness or numbness in the limbs, loss of coordination, confusion, restlessness, or agitation.
Common long-term symptoms of moderate to severe TBI are changes in appropriate social behaviour, deficits in social judgment, and cognitive changes, especially problems with sustained attention, processing speed, and executive functioning.

When the pressure within the skull,ICP rises too high, it can be deadly.
Signs of increased ICP include decreasing level of consciousness , paralysis or weakness on one side of the body, and a blown pupil , one that fails to constrict in response to light .
Cushing's triad , a slow heart rate with high blood pressure and respiratory depression is a classic manifestation of significantly raised ICP.
Anisocoria , unequal pupil size, is another sign of serious TBI.
Abnormal posturing , a characteristic positioning of the limbs caused by severe diffuse injury or high
ICP, is an ominous sign.
Small children with moderate to severe TBI may have some of these symptoms.
Other signs seen in young children include persistent crying, inability to be consoled, listlessness, refusal to nurse or eat and irritability.

Neurological examination and assigning a
GCS Score.
Neuroimaging helps in determining the diagnosis and prognosis and proposed treatment.
The preferred radiologic test in the emergency setting is computed tomography (CT) : it is quick, accurate, and widely available.
Followup CT scans may be performed later to determine whether the injury has progressed.

Magnetic resonance imaging (MRI) can show more details than CTas detecting injury characteristics such as diffuse axonal injury. However, MRI is not used in the emergency setting.
X-rays are still used for head injuries that are so mild that they do not need imaging or severe enough to merit the more accurate CT.
Angiography may be used to detect blood vessel pathology.
Electroencephalography and transcranial doppler may also be used.

Posttraumatic seizures ; frequently occur after moderate or severe TBI, they are usually general or partial.
Immediate seizures occur in the first 24 hours.
Early seizures occur in the first 2-7 days.
Late seizures occur after 7 days.
Temkin showed that prophylactic use of phenytoin is effective during the first week after TBI.
He recommended discontinuation after 1 week if no seizures develop because of its lack of effect in preventing late seizures.

Hydrocephalus is characterized as communicating or noncommunicating;
Noncommunicating hydrocephalus occurs secondary to an obstruction in the ventricular system before the point at which CSF exits the fourth ventricle.
Communicating hydrocephalus is the most common form after TBI and occurs when the obstruction is in the subarachnoid space.

Deep vein thrombosis
DVT is common in persons with TBI, with an incidence as high as 54%.
Risk factors for DVT include; immobility, lower extremity fracture, paralysis, and disruption in coagulation and fibrinolysis.
DVT may cause pulmonary embolism, postthrombotic syndrome or recurrence.
DVT best detected by venous Doppler ultrasonography and contrast-enhanced venography.
Prophylaxis for DVT should be started as soon as possible.

Heterotopic ossification is described as ectopic bone formation in the soft tissue surrounding the joints,in TBI, its incidence is 11-76%.
It causes joint pain and decreases range of motion ,it is often associated with low-grade fever, peri-articular swelling, peri-articular warmth, and peri-articular erythema.
The risk of heterotopic ossification is greatest during the first 3-4 months after injury.

Spasticity is defined as velocitydependent increase in tone.
It is found in an estimated 25% of patients with TBI.
First-line treatment for spasticity is correct positioning of the involved body segment and exercises.
Second-line treatment include splinting, casting and other modalities.

GIT and urinary tract complications remain among the most common sequelae in patients with TBI.
Most frequent GIT complications are; stress ulcers, dysphagia, bowel incontinence, and elevated levels of liver function tests.
Urinary tract complications include; urethral strictures, infections, and urinary incontinence.

Posttraumatic agitation is common after
TBI. Furthermore, aggression was consistently associated with depression.
Insomia is common in TBI patients. They may have nighttime awakenings and longer sleep-onset latency.
Posttraumatic headache in 38%.
Posttraumatic depression in 40% after
TBI, it is further associated with cognitive decline, anxiety disorders, substance abuse, dysregulation of emotional expression, and aggressive outbursts.

This is essential in severe TBI.
It includes; ECG, invasive arterial blood pressure, pulse oximetry, central venous pressure, urinary catheter, naso-gastric vs oro-gastric tube (in case of base skull fracture), frequent neurological examination, temperature and capnography.

This is achieved by maintaining MAP above 90mmHg and preventing increases in ICP ,to be between
20-25mmHg .
CPP = MAP – ICP

Maintaining MAP
Treating hypovolaemia by 0.9% NaCl/ colloids/P-RBCs/FFP as indicated.
Avoid glucose containing fluids unless there is hypoglycaemia (blood sugar should be between 4-7 mmols).
Start early enteral feeding as,TBI patients have induced hypermetabolic and hypercatabolic state resulting in increased energy and protein.
Use inotropes (noradrenaline- dopamine), if other causes of hypotension are treated.

Raised ICP leads to secondary brain injury.
It is treated by; osmotherapy , analgesia , sedation , optimal ventilation , surgical and positioning of patient.

Mannitol induces changes in blood rheology and increases cardiac output, leading to improved CPP and cerebral oxygenation.
Improvements in cerebral oxygenation induce cerebral artery vasoconstriction and subsequent reduction in cerebral blood volume and ICP.
Mild dehydration after osmotherapy is desirable and may improve cerebral edema.
Also it decreases CSF production by up to
50%, lead to prolonged ICP decrease.

Mannitol has several limitations;
• Hyperosmolality is a common problem, and a serum osmolarity
>320 mOsmol/L is associated with adverse renal and central nervous system effects.
• Accumulation of mannitol in cerebral tissue may lead to a rebound phenomenon and increased ICP.

The most promising solution investigated as possible substitute for mannitol; is hypertonic saline (HTS).
Serum Na is maintained between 145 and
155 mmol/L in all patients with TBI.
To start osmotherapy,250-mL bolus of 3%
HTS is administered through a central venous cannula.
This dose is repeated until ICP is controlled or a Na level of 155 mmol/L is achieved.
The serum Na is maintained at this level until ICP has stabilized and then gradually allowed to normalize.

If ICP control is still problematic after
3 –4 days of HTS therapy, boluses of furosemide are administered in an effort to mobilize tissue Na.
Serum sodium and potassium concentrations are monitored four hourly on a blood gas analyzer.

The permeability of the BBB to sodium is low.HTS produces an osmotic gradient between the intravascular and intracellular compartments, leading to shrinkage of brain tissue (where BBB is intact) and therefore reducing ICP.
The selectivity of the BBB to NaCl is more than that of mannitol making it potentially a more effective osmotic drug.
HTS augments volume resuscitation and increases circulating BV, MAP, and CPP.
HTS restores the neuronal membrane potential, maintains BBB integrity, and modulates the inflammatory response by reducing adhesion of leukocytes to endothelium.

Morphine or fentanyl can be used for analgesia but with caution for their respiratory depression in case patient is spontaneously breathing.
Remifentanyl can be used in ventilated patients.
Propofol is sedative of choice especially in first 48 hours. It causes cerebral metabolic suppression and has neuroprotective effect. Using propofol in doses more than 5mg/Kg and for longer than
48hrs;
Midazolam should replace propofol for sedation.
(for fear of propofol infusion syndrome).

In TBI patients, hypoxia, hypercarbia / hypocarbia should be prevented.
PaO2 should be above 100mmHg and
SpO2 above 95%.
Mechanical ventilation should be started at
GCS 8.
PaCO2 in first 24hrs should be 34-
38mmHg and mild hyperventilation can be started for PaCO2 to be 32-35mmHg in case of increased ICP.
Monitor end tidal CO2 and perform blood gases 15-20 min. after any change in ventilatory parameters.

May be considersd to facilitate endotracheal intubation.
In cases of difficult ventilation inspite of adequate sedation/analgesia.
Use of neuromuscular blockade may mask seizure activity, increase risk of pneumonia and cause critical illness neuropathy.

Patient head should be in neutral position with head of bed elevated 15-
30 degree.
Neck collar should be applied whenever there is doubt of cervical spine injury.

Whenever decided by neurosurgeon to decrease intracranial hypertension.
Surgery can be performed on mass lesions or to eleminate objects that penetrated the brain.
Mass lesions are like contusions or haematomas causing significant shift of intracranial structures.

Monitor HCT or haemoglobin level as
CBF is influenced by blood viscosity which increases by increase in HCT.
CBF is reduced by HCT levels above
50% and increased by HCT levels below 30%.
HTC of 30-34% is suggested to be best for optimal oxygen delivery to brain tissue.

Seizure activity in TBI patients may cause secondary brain damage as a result of increased metabolic demands, raised ICP and excess neurotransmitter release.
Benzodiazepines should be started together with phenytoin .
Adequate sedation with propofol reduces seizure activity and raises seizure threshold.

Increase in body temperature should be treated agressively; paracetamol, cooling blanket, cool sponging and ice packs.
Hyperthermia increases metabolic demand and aggrevates the condition.

Urine output should be 0.5-
1ml/Kg/min.
Diabetes insipidus should be suspected if urine output is more than
250ml/hr, for more than 3hrs. and specific gravity less than
1005,confirmed by serum and urine osmolalities.
If confirmed , start desmopressin.

CT scan should be done on admission and repeated whenever there is change in symptoms or signs.
Frequent neurological examination is essential.
Hourly recording of GCS, hourly recording of pupil size and reaction.
Monitoring ICP if available.

Figure 1. Suggested algorithm for cerebral resuscitation after traumatic brain injury, adapted from the Brain Trauma Foundation and the European Brain Injury Consortium Guidelines and modified to replace mannitol with hypertonic saline for osmotherapy.
White H et al. Anesth Analg 2006;102:1836-1846