EVALUASI

PREOPERATIVE DAN
PENATALAKSANAAN
POST OPERATIVE
Dr. R. SUTANTRI EDI PRABOWO, SpAn
RSUD ARIFIN ACHMAD / FK UNRI

INTRODUCTION

The incidences of head injury in the United State reached 500.000 cases yearly. Ten percents
or them died before reach the hospital. The victims who reached the hospital 80% are
classified as mild head injury, 10% moderate head injury and 10% severe head injury1. The
management of head injury has to be started at the place of accident (prehospital) to prevent
secondary brain damage (secondary injury).
The results of head injury, primary injury is caused by direct damage both of the neurons or
blood vessels by collision. Secondary injury taking place for several minutes, hours even days
after primary injury and resulting further neurons damage.
The secondary injury can be caused by systemic disorder or intracranial. The systemic
disorders are hypoxemia, hypercapnia, arterial hypotension, anemia, hypovolemia, and
hyponatremia imbalance of osmotic pressure, hyperthermia, sepsis, coagulopathies, and
hypertension. While intracranial caused by epidural/ subdural hematomes, contusion cerebral,
intracranial infection and post trauma epilepsy.
Secondary injury can be considered as a complication from early injury. Several substances
like enzyme proteolytics, biogenic amine (serotonin and histamine), neurotransmitter
(glutamate), unsaturated lipids (aracidonic acid and its metabolic), free radical and kalikreinkinin, showed as reversible and irreversible physiology mediator of secondary injury. This
mechanism including vasogenic edema caused by the circulation disorder, cytotoxic edema
and cells nectrosis.
The important of secondary injury to the outcome has been showed in patients while right after
a trauma or a few moments after trauma still conscious and talking, them getting worse and
died. At these patients the death can be mentioned by effect of secondary injury.

Because of secondary injury might developed during patient

therapy in the hospital, require active intervention in the
management of the patient. The important contribution in
secondary injury is hypoxemia and hypovolemia with hypotension,
which have to be actively found and corrected immediately.
In order to deal with head injury patients, there are several
considerations according to physiology disorders after injury. The
goal of these considerations is to administered anesthesia, which
do not disturb cerebral perfusion pressure (CPP). It has been
known that brain function and cell neuron depend on adequacy of
brain blood vessels. The brain blood vessels affect the brain
perfusion pressure. In normal individual, the auto regulation will
maintain constant blood flow at certain pressure (MAP 50- 150
mmHg). Head injury causes defect in auto regulation. The
increase of ICP by head injury or decrease of MAP caused by
bleeding in other place can risked the brain perfusion.

PREOPERATIVE EVALUATION

The history of accident has to be known, The mechanism of injury will help to determine
the prognosis. For example, pasient with falling accident, has for times greater possibility
for intra cerebral hematoma than vehicle accident. The condition of patient immediately
after injury is a base for reevaluation especially regarding level of consciousness, Also
patients condition before injury can help to evaluate the patient.
Physical Examination
Vital signs evaluated immediately for hypotension, which caused by injuries in other
place. Hypertension especially accompanied by bradycardia showed elevation of ICP,
which caused by mass lesion (Cushings Syndrome) that need the surgery.
The evaluation is primary and secondery.. Primary evaluation correlated with patients
life saving are:
a. Airway control with C-spine protection
b. Breathing
c. Circulation & Hemorrhage
d. Disability/ disorder of CNS
e. Exposure the whole body

Secondary evaluation is physical examination from head to toe and diagnostic

procedures (X-ray, CT-scan, MRI, ect.).
Several uncooperative patients for CT-scan have to be intubated to control the
ventilation. In trauma capitis patient sedation must be given carefully for CT-scan
evaluation because of hypoventilation can occurred. Study estimated approximately 517% incidence of cervical fracture in trauma capitis. If spine radiography includes C7
cannot be done properly, better be assumed there is cervical fracture, cause a simple
lateral radiography can not excluded for cervical fracture and serial cervical radiography
are needed.
If there are indications for intubation have used standard fast induction with thiopental,
succinylcholine and cricoid pressure. Collar can be removed if disturb the intubation and
put it back after intubation. To avoid the sliding of posterior cervical when cricoid
pressure applied, one of the helper has to put both palms beside the neck (remember
inline C position).
Laboratory evaluations have to be done prior to surgery like Hgb, Hct, chemical blood,
arterial blood gas, thrombocyte, bleeding time and clothing time.7,9 Hgb < 10 g% is one
of the important factor for worsen condition of head injurys patient. Several trials
showed that hematocryte of 30% still optimal to deliver oxygen in cerebral ischemic,
however hematocryte less than 30% worsen the condition, consider to give blood earlier
in multiple trauma to prevent worse condition.

 Many

head injury patients accompany with multi system

trauma and signs of hypovolemic. Maintain adequate
intravascular circulation to avoid hypotension and
maintain CPP volume is very important. Intravascular
volume has to be maintained and replaced with free
glucose isotonic crystalloid solution (Saline Normal
0.9%), albumin (5%) or blood product.
Adult patient hematocryte concentration has to be
maintained around 30% to optimize oxygen transport.
Fluid restriction to decrease cerebral fluid volume and
prevent cerebral edema assumed have not applicable
anymore. Then, the inotropic and vasopressor might
needed to increase blood pressure.

olloid vs Crystalloid: Shifting of fluid and solution from

intravascular space to interstitial and intracellular affected by
hydrostatic pressure, osmotic pressure and oncotic pressure.
Cerebral capillary endothels are bound tightly, except if Blood
Brain Barrier (BBB) damaged, electrolyte cannot enter extra
cellular brain. Although colloid (Albumin and Hetastarch) have
higher oncotic pressure and theoretically can reduce edema
cerebral, oncotic pressure, as pusher energy is smaller than
osmotic. Therefore the experimental studies in reducing
osmolalitas without reducing osmotic always accompanied by
edema cerebral, while reducing oncotic pressure without changing
osmotic pressure do not have affect to ICP and cerebral fluid
volume. Therefore maintain osmotic pressure is more important
than maintaining oncotic pressure.so that, the usage of colloid
versus crystalloid in head injury still controversial, even though the
usage of crystalloid still acceptable practice.

ANESTHESIA MANAGEMENT

Anesthesia management of head injury, principally same with others patient with
increase of ICP.
1. Optimize cerebral perfusion
2. Avoid cerebral ischemia
3. Avoid the usage of drugs/ technique that caused increase intracranial pressure.
Premedication
In head injury premedication is unnecessary for sedation. The effect of increase PaO2 is
undesirable and the requirement of control ventilation when respiratory depressant
drugs have been given. It is enough to give anti cholinergic to prevent hyper salivation,
glycopyrolate is drug of choice for anti secretion by its lesser effect to the heart. But if
there are medulla spinalis injury with tendency to bradycardia, administration of sulfas
atropine is recommended 0.02 mg/kg body weight, IV when heart rate is below 70.
Metoclopropamide (10 mg, IV) reduce gastrointestinal motility.
Generally narcotic drug, barbiturate, tranquilizer are not recommended can bother
neurologic evaluation and depress the ventilation.
Induction

Once general anesthesia chosen, an ideal induction are to avoid hypotension, increase either
blood pressure or ICP. Therefore has to determine weather blood volume is enough and stabile,
when CVP is not attached can be done a simple test (tilt test).
Although blood pressure is already normal do not mean the circulation volume is enough because
induction in hypovolemia caused immediately shock. Avoid condition that can caused pain which
can increase blood pressure and ICP like application infuse, suction of secretion, manipulation at
trauma area, ect.
Not all authors agree, but majority are indicated that head elevation 15- 30 degree will reduce
increase of ICP without influencing CPP or cerebral oxygenation. Elevation >30 degree earn
influence increase ICP in some patients through auto regulation process by vasodilatation, better
head elevation 20 degree can prevent neck vein obstruction in supine position. When patient has to
be in lateral or prone position, chest and abdomen have to be freed from pressure.
When larygoscopy and intubation prevent cough and strain which can caused increase of blood
pressure, ICP, edema, and brain herniation. This can be reached by usage of fentanyl 50-100 g, IV
prior to induction, both Sufentanyl and Alfentanyl caused increase ICP.6
Penthotal is an ideal induction agent when there are no contra indication because its ability to
reduce CBF and ICP. When penthotal is contra indication, propofol is an alternative because its
effect to reduce CBF and intra cerebral pressure without disturbing cerebral perfusion pressure.
Norcuron is a choice for relaxant because its cardiovascular stability and effect to ICP is minimal.
Succinylcholine caused increase CBF and ICP, possibility of hyperkalemia, Roccuronium 0.6 mg/kg
body weight is an alternative with 60 seconds intubations can be done with duration of action for
30- 40 minutes.

Pancuronium is not recommended because its effect of

hypertension and increase CBF & ICP where in head injury
patient auto regulation disorder has occurred. Atracurium has to
be avoided as mush as possible according to its histamine
release effect and metabolite laudanosin, which caused seizure in
animal.
Maintenance of Anesthesia
The usage of drugs for maintaining of anesthesia can effected
CBF, CBV, CMRO2, auto regulation pressure and response to
PaCO2. Anesthesiologist usually uses combination of barbiturate,
benzodiazepine, narcotic, N2O and low MAC of volatile agent.
The usage of Isoflurane and Sevoflurane are based on a good
auto regulation up to 1.5 MAC and its response to CO2 up to 2.8
MAC. The reducing of CMRO2 up to 50% therefore has cerebral
protection. The increase of ICP by Isoflurane 1% is easily against
with hypocapnea and barbiturate.

The usage of Halothane in head injury must be carefully in order to myocardium sensitization to
arrhythmias in acute head injury, catecholamine concentration elevated. Halothane can be used
with caution by hyperventilation and using < 0.5 MAC because cerebral auto regulation diminished
at 1 MAC Halothane and permanently up to postoperative period.
Enflurane is not recommended because its abolished auto regulation at 1 MAC and caused
seizure EEG at moderate dose (1.5 2) MAC where CMRO2 will increase several percent and
increase CBF and ICP for 3 hours after the drug is discontinued.
N2O 60% concentration cause an increase of CBF 100% and CMRO2 20% and avoid its
usage if there any aerocel or risk of air emboli especially accompany by damage of sinus nervosa
or sinus bone contact with air, or there are pneumothorax, abdominal distended as an analgesic
alternative fentanyl can be used.
The usage of muscle relaxant continuously is better than intermittent to prevent patients sudden
movement during the operation which can caused increase ICP dramatically can be used
veccuronium 0.1 mg/kg BW/hour.
Mild hypertension do not need correction, except if MAP > 130 mmHg, low dose of Isoflurane can
be tried when still unresponsive esmolol, propanolol or labetolol. Nitroglycerine or nitroprusside are
not recommended because their cerebral vasodilator effect can increase ICP.
The incidence of intraoperative arrhythmias especially through central hyperadrenergic, lidocaine
bolus (1-1.5) mg/ kgBW IV, and titrated (1-4) mg/ minute, might neutralize it. However every
correction of hypertension and arrhythmia, hypoxia and hypercarbia must be considered.

Intraoperative hypotension must be treated immediately with fluid therapy, when

unresponsive then vasopressor given. The principle of administering fluid is to prevent
hypotension, hypervolume, hypoosmolar and hyperglycemia. NaCl 0.9% is the chosen
fluid where its osmolarity is 300 mOsm/L; while Ringer Lactate is hypoosmolar (273
mOsm/L) therefore its usage must be limited to prevent cerebral edema. To maintain
intravascular colloid is the choice because its ability to absorb water and intravascular
volume expansion.Likely heastart is good enough, relatively cheaper, one liter is able to
expand 750 cc intravascular volume, however must be limited at 20 ml/ kg BW/ day to
avoid coagulation disorder through Factor VIII function.

Manitol is very effective in order to decrease ICP, through its oncotic pressure hence
reduce cerebral edema and cause secondary vasoconstriction to decrease the viscosity.
Its effect started at 10 minutes and reached the peak at 60 minutes. Because the
tendency to repair CBF to prevent cerebral ischemia and has minimal side effects, in
unconsciousness patient manitol advisable to be given immediately at 1.5 gr/ kg BW.
Even though generally is said that manitol given too fast can cause hypotension and it
has to be given slowly for 20 minutes. The other effect from manitol given too fast is
transient hypokalemia (decrease up to 2 mmol/L).

POST OPERATIVE

When patient is conscious and adequate spontaneous breathing, can be

extubated. Suctioning of secretion and extubation itself can cause patient
cough, straining which potentially increase ICP which worsen the cerebral
edema. Giving Lidocaine 1- 1.5 mg/kg BW IV three minutes prior extubation.
can reduce this event
If GCS < 8 or there are facial fractures, neck trauma and the chest intubation is
advisable maintained for ventilation at ICU & protection of the airway. As long
as transferring the patient from operating room to ICU ventilation, oxygen
saturation and CPP must be observed carefully. Monitoring of blood pressure,
capnograph and pulse oxymetry must be used. If possible monitoring of intra
cranial pressure and cerebral circulation are attached during transport to
ICU.2,3,7 The need of sedation or low dose of narcotic to reduce irritation of
endotracheal tube irritation in the airway. Once emergency condition is
happened like immediately increase blood pressure and intra cranial pressure,
additional dose of sedative, narcotic and labetolol must be given.Trendelenberg
position, hyper flexion of the head, hyperextension or rotation can obstruct
large vein in the neck which cause increase ICP.

Hyperventilation suggested as a priority in management of

increases ICP, however now on its still controversial, because
hyperventilation causes cerebral ischemia even though not
reduce CO2 pressure below 20 mmHg (level of cerebral ischemia
in normal individual). Other problems are its effect only for short
term, because CBF will return to the lowest/ basal in 24 hours.
When blood pressure elevated (MAP > 130 mmHg) has to be
corrected, because its disturbed Blood Brain Barrier, interstitial
edema, increase ICP. Avoid any conditions, which caused
increase in blood pressure like hypoxia, hypercarbia, hypothermia
and fluid overload then giving of anti hypertension. The principle
of fluid administration must be maintained a little restriction to
prevent exacerbation of cerebral edema, but when inadequate
CPP having risk to extent cerebral damage itself, therefore do not
hesitate to give fluids as long as not overhydration.

Many researchers observed the effect of crystalloid on cerebral using Ringer

Lactate or Hartman solution as crystalloid solution and said that this solution is
isotonic. Hartman solution contains 280 mmol soluble ions but incomplete in
particles dissociation, the value is not 280 mmol/ L soluble particle ions. Its
osmolality only 265 osmol/ kg (normal plasma osmolality 285), means is
hypotonic. Normal Salt Solution contains 308 mmol/ L ion with osmolality of 285
and isotonic. Blood glucose concentration maintains below 150 mg% while
more than 200 mg% must be treated with insulin. Hyperglycemia will increase
brain acidosis, which cause brain cells damage where lactate concentration
elevated. Glucose only given when hypoglycemia occurs.
Administration of anticonvulsant should be considered because 10% severe
head injury patients who do not give anticonvulsant develop seizure at the first
weeks ICU care. Consequences of seizure itself are severe increase in CMR,
CBF and CBV, which generate significant increase of ICP that harmful.
Administration of phenytoin loading dose 15 mg/ kg BW slowly to prevent
hypotension.
Avoid hyperthermia where any increase of temperature will lead increase
oxygen consumption. Hypothermia is advisable to reduce oxygen demand and
brain protection but only up to 35 C by regulating room temperature regarding
the complications of shivering, electrolyte disorder, cardiovascular changes and
renal function. Shivering will increase oxygen consumption by 400%.

Bronchial toilet should be done in sedated condition to reduce

airway stimulation, which lead increase intra cranial pressure.
Controlling of seizure can be used phenytoin, (dilantin),
benzodiazepin, barbiturate or lidocaine. This is important to be
done in order with increase intra cranial pressure, hypertension
even cerebral bleeding, and hypoxia and brain cells damage.
Cerebral protection is conducted by maintain oxygen supply,
hemodynamic stability, low intracranial pressure, high O2,
normalize chemical blood results. Lower the temperature, also
administration of drugs that reduce CMRO2 like barbiturate
8,9, can reduce oxygen demand.