TRAUMATIC BRAIN INJURY

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TRAUMATIC BRAIN INJURY
By Dr.Gihan Seif El Nasr Professor of
Anaesthesia ICU
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• 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.

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Pathophysiology

• 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.

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Primary 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.

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• 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.

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• Primary injury due to acceleration-deceleration
  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.

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• 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.

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• 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.

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• 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.

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• 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.

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

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Severity

• 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, 912 is
  moderate, and 8 or below is severe.
• Other classification systems are also used to
  help determine severity duration of
  post-traumatic amnesia (PTA), and loss of
  consciousness (LOC).

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Severity of traumatic brain injury
GCS PTA LOC
Mild 13-15 Less than 1 day 0-30 min.
Moderate 9-12 1-7 days 30min.- 24hrs.
Severe 3-8 More than 7 days More than 24hrs.
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Signs and symptoms

• Symptoms are dependent on the injury's severity
• With mild TBI, the patient may remain conscious
  or may lose consciousness for few seconds or
  minutes.
• Other symptoms of mild TBI include headache,
  vomiting, nausea, lack of motor coordination,
  dizziness, difficult 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.

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• 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.

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• When the pressure within the skull, ICP, rises
  too high, it can be deadly.
• Signs of increased ICP include decreased 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.
• Young 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.

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Diagnosis

• 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.

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• Magnetic resonance imaging (MRI) can show more
  details than CT as 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.

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Complications

• I- Posttraumatic seizures
  
  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.

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• II- 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.

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• III- 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.

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• IV- Heterotopic ossification
• 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.

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• V- Spasticity
• Velocity-dependent 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.

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• VI- 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.

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

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Management

• Monitoring
• 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.

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• Maintenance of cerebral perfusion pressure(CPP)
• This is achieved by maintaining MAP above 90mmHg
  and preventing increases in ICP,to be between
• 20-25mmHg.
• CPP MAP ICP

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• 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
  requirements.
• Use inotropes (noradrenaline- dopamine), if
  other causes of hypotension are treated.

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

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Osmotherapy

• 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.

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• Mannitol has several limitations
• Hyperosmolality is a common problem, and a serum
  osmolarity gt320 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.

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• 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.

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• If ICP control is still problematic after 34
  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.

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• 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.

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• Analgesia and Sedation
• 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.
• Midazolam should replace propofol for sedation.
  (for fear of propofol infusion syndrome).

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• Mechanical ventilation
• 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.

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• Neuromuscular blockade
• 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.

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

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• Surgical Intervention
• It is decided by neurosurgeon to decrease ICP.
• 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.

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Maintenance of haematological parameters

• 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.

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Control of seizures

• 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.

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Treating hyperpyrexia

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

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Monitoring renal function

• 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 than1005,confirmed by
  serum and urine osmolalities.
• If confirmed , start desmopressin.

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Monitoring increase in ICP

• 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, of pupil size and
  reaction.
• Monitoring ICP if available.

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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 20061021836-1846

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