Injury in medicine ,any stress upon a part or the whole of an organism that disrupts its structure or function or both,to such a degree as to result in a pathologic process.
Brain injury may be of traumatic or non traumatic origin (2)
Traumatic brain injury may be due to the trauma associated with accident or personal violence.
Alternatively the trauma may accompanying a variety of operative procedure including retraction,shear forces,direct tissue destruction,hemorrhage,vessels disruption with subsequent infarction.(2)
Traumatic brain injury can be devided into primary and secondary injury(5).
Primary injury is the injury occuring during the traumatic event therefore can not be minimized.
Secondary injury on the otherhand occuring after traumatic event as a result of hypoxia,hypercarbia and ischaemia induced by hypotension,vasospasm or increased intracranial pressure (ICP).
The most common contributors to secondary injury are hypoxaemia and hypovolemia with hypotension.(5,6)
At the tissue level hypoxia can be defined as a reduction in O2 availability to a level insufficient for tissue demands.
This hypoxia can be caused by either hypoxaemia (Low PaO2) or ishaemia(low cerebral blood flow)(CBF).
When the blood supply to the brain is decreased below a critical level,ischemic damage is occur.
Ischaemic can be global or focal,complete or incomplete.
Incomplete ishaemia differs from complete ischaemia in that there is a continuing supply of glucose sustain anaerobic metabolism increasing the brain lactic acid level.
Mechanical injury,haemorrhage,edema and ischaemia are the most important causes of brain damage in patient with head injury, particularly edema and ishaemia that are concern to the anesthesiologist (5,6).
BASIC MECHANISM OF INJURY:(2,5,6)
The pathophysiology associated with this process may reflect simple patho physiological consequence of ischaemia arising from pressure effects to underlying and distant brain regions. Shift of vital structures and axonal disruption reduction of CBF,hydrocephalus and herniation.
Ischaemia may not just be due to local microcirculatory compression but also the consequence of vasoactive substance released from the hematoma.
The extravasated subarachnoid blood can cause vasospam both locally and distant sites with aggravation of ischemia.
Systemic physiolological insult may occur as a consequence of primary injury include (hypoxia,hypotension,hypercarbia,
hyperthermia,anaemia and electrolyte disturbances) can contribute worsening neural injury.
Hypoxia may be the result of airway obstruction,aspiration,
thoracic injury,primary hypoventilation, or pulmonary shunting.
Hypotension has been found to occur in 32-35% in emergen
cy department which may be due to systemic causes.
This cause a decrease in cerebral perfusion pressure(CPP) which may aggravated by a high ICP;disruption cerebral vascular autoregulation,vasospasm and change in cerebral blood flow pattern.
Cerebral perfusion pressure(CPP) is the driving force for substrate (O2 and glucose)delivery to the brain.
Hyperthermia may be due to infection,thrombophlebitis,
drug reaction,or defect in the thermoregulatory center.
This results in excessive excitotoxic neurotransmitter,
altered protein kinase activity and augmented pathophy
siological effects of ischaemia.
Hypercarbia causes vasodilation of cerebral blood vessels with increased ICP and exacerbation of any mass or edema effects and cerebral acidosis.
Imbalance between cerebral oxygen delivery and demand arise a consequence of systemic and local secondary insults may result in focal or global ischaemia. Ischaemia is defined as severe reduction of bloodflow such the energy production is compromised. The reduced energy production is due to the limited availability of both oxygen and glucose.
The reduced blood flow also leads to impairment of the removal of metabolites such as CO2 and lactic acid.
INITIAL ASSESSMENT (1,3,4,6)
A patient who initially presents unconscious with focal neurologic deficits or with deteriorating neurologic signs should be assumed to have on going brain injury.
Any evidence of trauma should raise the suspicion of associated occult injured involving the spinalcord,thorax or abdomen.
Data regarding physical trauma,pre existing cardiovascular
pulmonary,renal and hepatic disease as well evidence of drug abuse should be found.
The patient level conciousness is the single most important clinical sign in the assessment of the severity of head injury and this should be noted at the scene immediately following
the accident.
Based on GCS,head trauma patient is classified into mild (13-15),mode rate(8-12) and severe head injury (0-7).
Other variables such as pupillary activity,brain stem function,vital signs,age,Ht and type of injury can be used as a basic for predicting outcome.
Two major factors associated with severe head injuries are hypoxia and hypovolemia with hypotension.
These complications are most often associated with a bad outcome, and should be initially addressed in field.
Patient with altered states of conciousness have difficulty maintaining and protecting their airway.
Respiratory obstruction is the primary cause of death in 15% of these pa-tients.Spontaneous hyperventilation and mild hypocarbia (PaCO2 30-35 torr) are frequently seen after brain injury.
Central hypoventilation and apnoe are only present with injuries involving the respiratory centers nevertheless in patient in comatose hypoventilation commonly occurs due to upper airway obstruction related to relaxation of the
base of the tongue. Therefore controle airway by endotra
cheal intubation is necessary.But management of airway should begin at the scene with step A for impact coma that is backward tilt of the head and jaw thrust.
And step B for impact apnoe that is mouth to mouth(in tris
mus mouth to nose) ventilation when health professional arrive attempt intubation. Almost 20% of persons killed in vehicular accidents had isolated upper cervical spine injury,usually occur at the C1-2 or C5-6 vertebrae.
All suspect cervical spine injuries should be carefully immobilzed,preventing extension, rotation or flexion of the head until a thorough physical and radiologic examination has occured.
Signs of basilar skull fracture are important to the anesthesiologist. Look for hemotympanum,otorrhoea,
echymosis over the mastoid area (Battle's sign) and echymosis around the eyes without extension beyond the orbit(raccoon eyes).Nasal intubation in these patients is relatively contra indicated because of the significantly increased likelihood of seedling the CSF with bacteria which cause of infection,and because of the risk of inadvertenly placing the tip of endotracheal tube into the cranium.
Possible cause of hypoxaemia include neural induced ventilation/perfusion mismatching,microatelectasis,
increase pulmonary capillary permeability,and unobserved aspiration thus supplemental oxygen is essential in all patients during the initial hours after acute head injury.
Continuous monitoring of oxygen saturation levels by pulse oxymetri is recomended until the patient is clinically stable.
Injuries involving the lower brainstem or spinalcord may result in the loss of autonomic control of blood pressure
however,one should never assume hypotension is secondary a CNS lesion.
As a general rule hypotension is always related to concomittant systemic injury and haemorrhage, pre existing hypovolemia or drug intoxication.
A scalp laceration alone may bleed enough to produce hypovolemia especially in children.
Fear of aggravating cerebral edema should never limit appropriate intravascular volume expansion. Because cerebral hypoperfusion only worsen the initial injury
Vasopressor medications should only be administered transiently during resuscitation to maintain a systolic blood pressure level greater than 90 mmHg (adults).
The optimal choice of fluids for shock resuscitation in brain injury is controversial both isotonic crystalloid or colloid solution are used.
Hypertension occurs commonly after cerebral injury.
In patients with chronic hypertension the limits of autoregulation are shifted upwards improving tolerance for acute elevation in mean arterial pressure (MAP) and
impairing tolerance of lower arterial pressure.
Therefore hypertension and the concomittant increase in CPP may institute an appropriate compensatory response to improve blood flow in ischaemic area of the brain but in the otherhand lowering the blood pressure to normal levels may precipitate a secondary ischaemic insult.
Treatment should be attempted only if the systolic pressure greater than 200 mmHg or MAP greater than 125 to 135 mmHg, Even in that cases an initial lowering of MAP by only 25% is recomended.
Agressive control of blood pressure is allowed with hypertensive encephalophaty and intracranial bleeding.
Cardiac dysrythmia may be related to an elevation of circulating catechol amine and compromise of the CNS centers that modulate sympathetic and parasympathetic outflow.
Ventricular and atrial ectopic as well as supraventricular and ventricular tachycardia all occur with increased frequency especially in patients with intracranial haemor
rhage when arrythmia develop contributing metabolic abnormalities such as hypokalemia,hypocalcaemia and hypomagnesemia should be treated promptly.
Because adrenergic excess contribution to cardiac disturbance beta blocker is the most appropriate therapy for non ventricular tachyarrythmia.
Metabolics abnormalities such as hypogglycaemia,hyponat
remia,hypercalcemia uremia may also cause coma.
Decreasing of conciousness accompanied by fever and leukocytosis suggest meningitis and cerebrospinal fluid(CSF) examination is mandatory.
But if the CT scan reveals evidence of a mass effect or massive cerebral edema a lumbar puncture must be postponed because can precipitate a herniation syndrome.
Early therapy for bacterial meningitis before performing imaging study with appropriate antibiotics may be life
saving.
Seizure activity after an acute brain injury increase cerebral oxygen consumption and may increase the ICP if intracranial compliance is reduced, It should be promptly treated with diazepam 0,3-05 mg/kg or lorazepam 0,05-0,1 mg/kg intravenously. Subsequently intravenous loading dose of phenytoin(18-20 mg/kg in non glucose solution,infused no faster than 50mg/min) should be given.If phenytoin is ineffective,intravenous phenobarbital at a rate of 100 mg/min in 5 t0 10 mg/kg boluses to a maximum dose of 20mg/kg usually terminates all seizure activity.
Avoid the use of neuromuscular blocking agents in patients at risk for seizure since seizure activity would be undetec
ted. If neuromuscular blocking agents must be administered
bedside electroencephlography(EEG) monitoring is recom
mended. Rectal diazepam may be administered to children with ongoing seizure who have no intravenous access(dose 0,5 mg/kg).
Midazolam,diazepam or lorazepam can be used in the initial treatment of seizures in children at a dose of 0,1mg/kg iv,with maximum dose of 2 mg.
Phenytoin dosing in children :
Age Loading dose (mg/kg) Maintenance dose(mg/kg)
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<= 3 yrs 16 10
4 - 6 yrs 16 8,8
7 - 9 yrs 14 7,6
10-16 yrs 12 6,6
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GENERAL NEUROLOGIC EXAMINATION :
The preliminary neurologic examination includes vital signs and a funduscopic examination should establish :
-level of conciousness
-intergrity of brainstem function
-presence of purposeful or reflex motor activity.
Cushing's triad(bradycardia,bradypnoe and hypertension) suggest a markedly increased ICP with impending herniation.
Irregular breathing suggest a subcortical lesion.
Fever implies systemic or CNS infection. Funduscopic examination may reveal evidence of hemorrhage,extensive
exudates or papil edema.
Coma or complete unresponsiveness is generally caused by either bilateral hemispheric lesions,or barin stem involving the reticular activating system. Most coma are toxic or metabolic etiology.
Eye examination :
Pupillary size and responsiveness give important informafion
about the function of upper portion of the midbrain.
Preservation of light reflex differentiates metabolic from structural lesion. Small,symmetrical,reactive pupils are seen with bilateral deep cortical lesion and toxic metabolic encephalopathies.
Pontine lesions and narcotic overdose produce pint point pupil with preserved light reflex with midbrain lesions,the pupil are midposition and fixed.
When the third nerve is compressed as in uncal herniation the pupil in the ipsilateral side is dilated and non reactive.
Wide,fixed,non reactive pupils are not uncommon after severe global hypoxia injury.These pupillary changes may be reversible although persistence for >24 hrs implies a poor prognostic.
Eye movement reveal significant information regarding the intergrity of the lower midbrain,pons and medulla.
Spontaneous or roving eye movements indicate normal function. Spontaneous conjugate deviation of the eyes is associated with an ipsilateral frontal hemispheric or contra lateral brainstem lesion.
Conjugate eye movement in the opposite direction of the head movement af-ter moving the head from side to side slowly then briskly indicates normal brainstem function.(Doll's eye or occulocephalic reflex).
After cold caloric test there is no conjugate eye movement toward the side of the ear irrigated with cold solution implies brainstem structural damage.
Unfortunately these reflex eye movements may be abnormal with severe drug intoxication (e.g.phenytoin,
barbiturat and antidepressant) and are therefore not definitive for structural brainstem injury.
Motor movement :
Spontaneous,purposeful movements or movements induced by mild stimulation imply intact corticospinal tracts and minimal injury.
Abduction -avoidance movements with noxious stimulation also indicate relatively mild injury.
Decerebrate posturing(extension and internal rotation of the arms and legs) or decorticate posturing(flexion of the arms with extension of the legs) either spontaneously or with noxious stimulation indicates severe damage to the cerebral hemispheres or midbrain.
In a comatose patient absence of motor response to a noxious stimulation suggest drug overdose or devastating structural injury.
to be continued
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