Perioperative Management of Head Injury

PERIOPERATIVE MANAGEMENT OF HEAD INJURY

Written by Monday, 29 May 2006 07:27 - Last Updated Sunday, 13 April 2008 03:39 Muh Ramli Ahmad

Department of Anesthesilogy Anesthesilogy Faculty Faculty of Medicine Medicine Hasanuddin University Makassar RINGKASAN

Di Amerika Serikat kejadian trauma kepala setiap tahunnya diperkirakan mencapai 500.000 kasus, Dari jumlah tersebut 10% meninggal sebelum tiba di rumah sakit.Pengelolaan cedera kepala harus dimulai dari tempat kejadian ( prehospital ) untuk menghindari kerusakan otak sekunder. Kerusakan otak sekunder dapat terjadi karena kelainan sistemik maupun intrakranial, Penyebab sistemik adalah hipoksemia, hiperkapnia, hipotensi, anemia, hipovo;emik, hiponatremia, hipertermi, sepsis, koagulopati. Sedangkan penyebab intrakranial adalah epidural/subdural epidural/subdural hemotoma, kontusio serebri, perdarahan intraserebral, infeksi, epilepsi post trauma. Evaluasi preoperatif meliputi Anamnesis riwayat kecelakaan perlu diketahui, Mekanisme injuri akan menolong dalam menentukan prognosis, Tanda-tanda vital harus segera diperiksa, Hipotensi mungkin disebabkan adanya injuri ditempat lain, Hipertensi terutama bila disertai bradikardi menunjukkan adanya kenaikan ICP akibat lesi massa yang memerlukan pembedahan. Pengelolaan anestesi pada trauma secara prinsip meliputi : Mengoptimalkan perfusi serebri, menghindari iskemia sekunder serta obat/tehnik yang dapat meningkatkan tekanan intra kranial. Premedikasi pada trauma kepala biasanya tidak diperlukan.Bila general anestesi sebagai alternatif maka diperlukan induksi yag ideal adalah menghindari hipotensi , kenaikan tekana darah,dan TIK. Pentotal merupakan obat induksi pilihan bila tidak ada kontraindikasi karena menurunkan CBF dan ICP, bila ada kontraindikasi maka propofol merupakan alternatif. Pemeliharaan anestesi digunakan obat yang kurang mempengaruhi CBF,CBV,CMRO2 dan Autoregulasi, biasanya menggunakan berbagai kombinasi barbiturat, narkotik, N2O ,obat anestesi inhalasi dengani MAC rendah dan relaksasi otot. (J Med Nus. 2004; 25:50-54) SUMMARY

The incidences of head injury in the United State reached 500.000 cases yearly. Ten percents or them died before reach the hospital. Management of head injury has to be started on the spot of the accident (prehospital) in order to avoid secondary brain damage. The secondary brain damage might be caused either by systemic disorder or intracranial. The systemic disorders are hypoxemia, hypercapnia, hypotension, anemia, hypovolemia, hyponatremia, hyperthermia, sepsis, and coagulopathies. Intracranial factors are epidural/ subdural hematoma, cerebral contusion, intracerebral infection, and post-trauma epilepsy. Preoperative evaluations are included: Anamnesis the history of accident and the mechanism of injury, which can help to determine the prognosis. The vital signs have to be examine, hypotension could be caused by injury in others place. Hypertension especially accompanied by bradycardia showed elevated of intracranial pressure by mass lesion that needs surgical procedure. The principal management of head injury are optimize of cerebral perfusion, avoid secondary ischemia and administration of drugs/ techniques which can caused elevation of intracranial pressure. Premedication in head injury usually is unnecessary. However, if general anesthesia is the alternative for ideal induction require maneuver to avoid hypotension, elevation of both blood pressure or intracranial pressure. pressure. Penthotal is an ideal induction agent if there no contraindications where it can reduce the cerebral blood flow (CBF) and intracranial pressure (ICP); while if there any contraindication propofol propofol is the choice. The maintenance maintenance of anesthesia used drugs, drugs, which less affected to the CBF, CBV, CMRO2 and auto regulation, usually using the combination of barbiturate, narcotic, N2O, volatile anesthetic with, low MAC and muscle relaxant.(J Med Nus. 2004; 25:50-54)

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PERIOPERATIVE MANAGEMENT OF HEAD INJURY

Written by Monday, 29 May 2006 07:27 - Last Updated Sunday, 13 April 2008 03:39

{mospagebreak} 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 and 10% severe head head injury1. The management of head injury has to be started at the place of accident (prehospital) to prevent secondary brain damage (secondary injury).1,2 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 t rauma epilepsy.2-4 Secondary injury can be considered as a complication from early injury. Several substances like enzyme proteolytics, biogenic amine (serotonin and histamine), neurotransmitter (glutamate), (glutamate), unsaturated lipids (aracidonic acid and its metabolic), free radical and kalikrein-kinin, 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.2,4 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.4,5 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.4 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.3,4,6 {mospagebreak} PREOPERATIVE EVALUATION

History 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 i njury is a base for reevaluation reevaluation especially regarding regarding level of consciousness, 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

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PERIOPERATIVE MANAGEMENT OF HEAD INJURY

Written by Monday, 29 May 2006 07:27 - Last Updated Sunday, 13 April 2008 03:39

by mass lesion (Cushing’s Syndrome) that need the surgery. The evaluation is primary and secondery.. Primary evaluation correlated with patient’s 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.).7,8 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 5-17% 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. 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).1,5 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 injury’s 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. 3,8 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.5,8,9 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.4,6,7 Then, the inotropic and vasopressor might needed to increase blood pressure.6,7. Colloid vs Crystalloid: Shifting of fluid f luid 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. {mospagebreak}

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PERIOPERATIVE MANAGEMENT OF HEAD INJURY

Written by Monday, 29 May 2006 07:27 - Last Updated Sunday, 13 April 2008 03:39 ANESTHESIA MANAGEMENT                

Anesthesia management of head injury, principally same with others patient with increase of ICP.,5,6,7,9 1. Optimize cerebral perfusion 2. Avoid cerebral ischemia 3. Avoid the usage of drugs/ technique that caused increase intracranial pressure. 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.7 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).7,8,9 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.9 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.8,9, 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.6,7  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.6,7 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.8,9 Maintenance of Anesthesia

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PERIOPERATIVE MANAGEMENT OF HEAD INJURY

Written by Monday, 29 May 2006 07:27 - Last Updated Sunday, 13 April 2008 03:39

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, 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. {mospagebreak} 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 ³ 1 MAC Halothane and permanently up to postoperative period.2,3,5 Enflurane is not recommended because it’s 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.7,8 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 t here are pneumothorax, abdominal distended as an analgesic alternative fentanyl can be used. The usage of muscle relaxant continuously is better than intermittent to prevent patient’s sudden movement during the operation which can caused increase ICP dramatically can be used veccuronium 0.1 mg/kg BW/hour.7,9 Mild hypertension do not need correction, except if MAP > 130 mmHg, low dose of Isoflurane can be tried when still unresponsive esmolol, propanolol 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.5,9 Intraoperative hypotension must be treated immediately with fluid therapy, t herapy, when unresponsive then vasopressor given. The principle of administering fluid is to prevent hypotension, hypervolume, hypoosmolar 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 i ntravascular volume expansion.5,7 expansion.5,7 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 t o avoid coagulation disorder through Factor VIII function.7,10 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 i n 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).6 POST OPERATIVE

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PERIOPERATIVE MANAGEMENT OF HEAD INJURY

Written by Monday, 29 May 2006 07:27 - Last Updated Sunday, 13 April 2008 03:39

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.7,8,9, 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 it’s 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.6 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.7,8 {mospagebreak} Many researchers observed observed the effect of crystalloid on cerebral using Ringer Lactate or Hartman solution as crystalloid solution and said that this t his 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 It s 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.8,9 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 changes and renal function. Shivering will increase oxygen consumption by 400%.7 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),

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PERIOPERATIVE MANAGEMENT OF HEAD INJURY

Written by Monday, 29 May 2006 07:27 - Last Updated Sunday, 13 April 2008 03:39

benzodiazepin, barbiturate 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.2,5,6 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 barbiturate8,9, can reduce oxygen demand. CONCLUSIONS

The management of head injury is to be able to prevent secondary brain damage (secondary injury). Etiology of secondary injury can be systemic and intracranial. Systemic are hypoxia, hypercarbia, arterial hypotension, anemia, hypovolemia, hyponatremia, osmotic imbalance, hyperthermia, sepsis and coagulopathies. Intracranial are epidural/ subdural hematoma, intracerabral contusion, and intracranial infection, post trauma epilepsy. Anesthesia management of head injury, basically same with any patients with elevation of ICP: Optimize cerebral perfusion, Avoid cerebral ischemia, Avoid drugs/ techniques that cause increase in intracranial pressure. REFERENCES

1. Alexander HR,ProctorJH. Textbook Advanced Trauma life Support course for physicians. Americans College of Surgeons 1 st ed, Chicago; 1993 2. Avellino AM, Lam AM WinnHR. Management of acute head injury . In Albin MS, ed . Textbook of neuroanesthesia with neuroscience perspectives .New York : Mc Grow-Hill; 1997: 1137-75. 3. Lam AM,Maybg TS.Anesthetic management of patient with traumatic head injury, In : Lan AM,ed.Anesthetic management of acute head injury. New York: McGrow Hill inc;1995: 181-221 4. Lian A. Anesthesia for Acute Head Injury. The Indonesian Journal of Anesthesiology and Critical Care .2004; 22 ( 2 ) : 176-181. 5. Sarrafzadeh et al, Secondery Secondery insults in severe head injury injury pasient do worse ?. Critical Critical Care Medicine 2001; 29(6):1116-23. 29(6):1116-23. 6. Prough DS, Perioperative Management of Traumatic Brain Injry,Annual Meeting Refresher Course Lectureres .American Sociaty of Anesthesiologists. San Francisco, California , 2003, 216 – 222, 7. Durieux ML. Anesthesia for head trauma.In:Stome DJ, Sperry RJ,Johnson JO, Spiekermann BF,Yemen TA.eds,. The Neuroanesthesia handbook. St lois: Mosby; 1006: 385-414 8. Gopinath SP, Robertson CS . Management of Severe Head Injury In Anesthesia and Neurosurgery. Neurosurgery. 2001, 661 –684. 9. Lam A, Current Concepsts Concepsts and Controversies Controversies In The Manegement of Head Head Trauma. Anesthesia in the new Millennium , A Selection of Papers Presented at the 11 th Asean Congress of Anaesthesilogists Anaesthesilogists and 3rd Meeting of the Asian Society of Cardiothoracic Cardiothoracic Anaesthesia. Kualalumpur Malaysia 1999, 227 –236.

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