頭部創傷(Head Injury) 陳俊逸 高雄榮民總醫院 神經外科

Glasgow Coma Scale level of consciousness 分 eye opening, verbal response and motor response.

Classifications of Severity Mild head injury (GCS= 14-15) Moderate head injury (GCS=9-13) Severe head injury (GCS≦ 8)

Immediate Management of Head Injury General principles: Not a single disorder. Tailored therapeutic plans for the specific lesion and individual patient from time to time. No stable hemodynamics, no accurate GCS score. 56-60% of severe head injured patients have one or more other organ system injured. There is a 4-5% incidence of associated spine fractures with significant head injury.

Begin at the trauma scene Airway with cervical spine control Breathing Circulation with hemorrhage control Stabilizing the cervical and thoracolumbar spine (Disability) ==> C-spine, CXR, pelvis Identifying and stabilizing Extracranial injuries Mini-neurologic Examination. 記ABCDEE 記ABCDEE: A: airway, B: breathing, C: circulation, D: disability-spine board, E: extracranial injuries, E: examination

Mini-neurological Examination Level of consciousness (E4V5M1???) Pupillary function (unilateral? L/R? Doll eye sign?) Lateralized extremity weakness 測意識,看瞳孔,比較左右.

Risk Factors (5H-CSI) Hypotension  double mortality rate Hypoxia  add hypotension  75% mortality Intracranial Hypertension (IICP) Hyperthermia Electrolyte disturbance (H) Coagulopathy Seizure Infection 記5H-CSI

Mild Head Injury (GCS 14-15) Brain concussion (initial loss of consciousness) All head-injured patients should have a CT scan, except the true asymptomatic patients. If CT scan is not available  admission and observation for 1-2 days. 2-3% serious intracranial insult. Abnormal CT scan: 18%  5% need op Mild traumatic head injury is one of the most common neurological disorders. Mild to moderate head injury: causes of mortality are extracranial injuries; Severe multi-trauma: head injury is a major determinant. Brain concussion: brief loss of consciousness as a result of non penetrating traumatic injury to the brain with no gross or microscopic parenchymal abnormalities. (duration: a few seconds to up to 6 hours)

Mild Head Injury Risk factors of neurological deterioration: Older age and anticoagulant therapy CPR Alcohol or drug abuse Presence of subdural effusion or hematoma at the initial CT scan Epilepsy Previous neurosurgical treatment. 記: 開過腦的老人喝酒吃藥跌個硬膜下出血,結果癲癇又急救. 記:開腦的老人喝酒吃藥跌個硬膜下出血,結果癲癇又急救.

Mild Head Injury Admission criteria: (至少建議於ER留觀一晚) Penetrating head injuries Abnormal CT scan or skull fracture Loss of consciousness or amnesia Moderate to severe headache or vomiting Worsening in GCS score Pneumocephalus or CSF leakage Associated extracranial injuries Alcohol or drug abuse, coagulopathy and other risk factors for deterioration No reliable assistance at home

Mild Head Injury While being discharged, give a warning sheet (頭部外傷須知) Within 1-2 weeks, OPD F/U.

Moderate Head Injury (GCS 9-13) CT scan should be done in all cases of moderate head injury. (abnormal CT: 40%) Admission criteria In non-severe head injury, causes of mortality are inadequate observation and extracranial injuries. Higher risk of deterioration: Older An initial abnormal CT scan Lower GCS motor score

Moderate Head Injury NS OPD F/U within one week after discharge.

Severe Head Injury (GCS <=8) First priority (before calling NS Drs) Securing airway, breathing, and circulation (ABC). Emergent intubation !! Avoid hypoxia (PaO2<60mmHg) Avoid hypotension (SBP<90mmHg) Avoid electrolyte imbalance: Na, K, Glu, Mg Other system injury (life threatening): check chest and abdomen Nasotracheal intubation and NG tube are contraindicated in patients with possible anterior cranial base or midface fractures. Hypoxia: apnea, cyanosis, PaO2 < 60 mmHg, SaO2 < 90%. Hypotension: hemorrhagic shock or spinal shock  N/S vs N/S + vasopressor agents. A reliable basic NE during the primary survey and before sedating or para;yzing the patient. An accurate NE is useless until the patient is hemodynamically stable. Hyperglycemia is thought to worsen ischemic cell damage; hyponatremia lowers the seizure threshold and can exacerbate cerebral edema. Hypomagnesemia also lowers the seizure threshold. Other system injury: life-threatening extracranial lesions such as cardiac tamponade, tension pneumothorax, or major vascular injuries with hypovolemic shock may require immediate operative intervention before the neurological injury can be addressed.

Acute treatment for severe head injury ABCDE E 解決5H-CSI. 5H-CSI

To control ICP should be started empirically even before a CT scan is obtained. Comatose patients Decline in GCS Pupillary asymmetry Hemiparesis Any signs of presence of a traumatic mass lesion. Intubation Mild hyperventilation IV bolus of mannitol Prophylactic phenytoin Sedation CT room

頭部外傷的進步 二次大戰以來，在頭部外傷的治療上有兩項主要的改變： 一、是加護照護觀念的興起，這包括了呼吸道及呼吸器的使用， 癲癇的控制，感染和體溫的調控。 二、是電腦斷層的普及(since 1973)，這使得早期手術成為可能。

神經加護照顧及腦部監測 主要面對的是腦部的二度傷害(secondary injury )，如顱內出血、腦水腫、血氧不足及缺血(常因顱內壓升高或休克)等。因此需要有良好腦部監測系統才能及時找出問題，以避免二度腦傷害的發生，或是使它的傷害減到最少的程度。 Primary injury: cortical contusion, laceration, bone fragmentation, diffuse axonal injury, brainstem contusion, Secondary injury: intracranial hematomas, edema, hypoxemia, and ischemia ( due to elevated ICP and/or shock)

神經加護照顧及腦部監測 神經學檢查及生理監測(neurological examination monitoring) 顱內壓監測((ICP monitor) 穿顱都卜勒超音波(Transcranial Doppler, TCD) 頸靜脈竇氧氣飽和度(jugular bulb oxygen saturation , SjvO2) 腦部氧飽和度(brain oxygen saturation monitoring) 神經電生理監測(neurophysiology monitoring):主要包括腦波(EEG)及誘發電位(evoked potential, EP) 神經代謝監測(neurometabolic monitoring) 腦內氧氣分壓(PaO2)、二氧化分壓(PaCO2)、及酸鹼值(pH)的監測

神經學檢查及生理監測 昏迷指數(GCS)、瞳孔及各種反射等神經學檢查在神經加護病房是最基本的監測。 連續性的生理監測，如血壓、血氧飽和度(SaO2)、心電圖(ECG)、中心靜脈壓(CVP)、體溫及潮氣末二氧化碳(End tidal CO2)等也是現代神經加護病房所不可或缺的。 連續性顯示的中心靜脈壓、體溫及潮氣末二氧化碳常被忽略，這三項唯有連續性的監測才能對顱內壓與腦灌流壓以及腦部代謝做即時的調控。 系統性的問題也會造成二度傷害，尤其是低血壓(hypotension)和缺氧(hypoxia)。

為什麼要測量顱內壓? 許多的腦病變所引起腦部的死亡都和顱內高壓有密切的相關。 以嚴重頭部外傷為例，早期文獻均報告當顱內壓持續大於二十五毫米汞柱時，則預後不好。 死後的解剖研究發現，缺血是腦死的主要原因。

什麼是顱內壓? Monro-Kellie假說: 在人體密閉的顱腔內， 腦實質、血液容積及腦脊液三者的體積總和為定數，成年人約為1500-1900西西。 在這密閉的容器中一定體積產生均佈的壓力稱之為顱內壓(intracranial pressure, ICP)

Intraventricular space Monro-Kellie假說 Total 1700ml 腦脊液 CSF 150ml 血液容積 Blood 150ml 腦實質 Parenchyma 1400ml 排擠效應 腦室內 Intraventricular space 50ml 蜘蛛網膜下腔 Subarachnoid space 100ml

顱內壓之病理生理變化 顱內壓力上升 代償機轉 當顱內成份增加，例如腦瘤、顱內出血 腦脊髓液循環障礙：水腦症 腦水腫 血液成份增加：腦充血，靜脈回流受阻 代償機轉 血液容積及腦脊液再分佈

腦循環的流體力學 腦血流與腦灌流壓(cerebral perfusion pressure，CPP)成正比。 CBF=CPP/CVR 腦灌流壓又等於平均動脈壓(mean arterial pressure，MAP)減顱內壓。 CPP=MAP-ICP 在腦血管自動調節下，腦血流維持恒定。

正常的顱內壓值 正常的顱內壓值隨年紀而異: 正常成人的腦灌流壓: 60-80mmHg 成年人的正常值為10-15mmHg

顱內高壓 多數學者認為,當顱內壓大於二十至二十五毫米汞柱即稱為顱內高壓(intracranial hypertension)。 An ICP higher than 20 mm Hg that lasts for more than 5 minutes should be treated.

顱內高壓之症狀及病徵 顱內壓上升可能沒有症狀，須要隨時提高警覺。 頭痛。 噁心及嘔吐。 視乳頭水腫(papilledema) 。 意識障礙--顱內壓升高之晚期。 腦疝脫(herniation)。 頭痛(headaches)--大多在早晨或睡眠中痛醒，整個頭都痛。有時是血管性痛(throbbing)或鈍痛。 噁心及嘔吐--噴射性嘔吐(projectile vomiting):典型但少見，較晚期才發生，小孩較易發生。 視乳頭水腫(papilledema)-- 須要使用眼底鏡檢查。有時有視力變化。久之可能有視神經萎縮。

顱內高壓之症狀及病徵 Cushing triad: 庫欣氏三徵象 心跳緩慢、高血壓、呼吸不規則。 為晚期徵象，表示橋腦或延腦已經受到壓迫或損傷。

顱內壓監測適應症 Severe head injury with an abnormal admission CT scan. Severe head injury with a normal CT scan if two or more of the following features are noted at admission: Age over 40 years, unilateral or bilateral motor posturing Systolic blood pressure < 90mmHg. Not routinely indicated in patients with mild or moderate head injury. An abnormal CT scan of the head is one that reveals hematomas, contusions, edema, or compressed basal cisterns. 一般並不建議昏迷指數介於9-13分頭部外傷病患使用顱內壓監測，但是如果電腦斷層顯示顱內有可能需要手術的血塊存在時也應該考慮使用顱內壓監測。

ICP monitor techniques The gold standard technique for ICP monitoring is by means of an intra-ventricular catheter. (ventriculostomy, EVD: external ventricular drainage 腦室外引流) Alternative techniques: Parenchymal, subdural, or epidural catheter. Complication: parenchymal injury, infection, hemorrhage, malfunction, or malposition. Up to one week and providing prophylactic antibiotics. The most accurate, low-cost, and reliable technique, and also allows for CSF drainage and analysis.

顱內高壓的監測與治療 Focus on CPP!! 傳統顱內高壓的控制: 維持適當腦灌流壓： 限水(fluid restriction) 高滲透壓利尿劑(例如mannito1、glycerol) 過度通氣(hyper-ventilation) 降低體溫(hypothermia)以降低代謝率等方式 維持適當腦灌流壓： 「將含氧的血擠入腫脹的腦中(squeezing the oxygenated blood through a swollen brain)」 CPP = MAP - ICP Focus on CPP!!

避免顱內壓升高的基本原則 在考慮降低顱內壓之前,應先懂得避免顱內壓升高: 頭部抬高30度(比平躺顱內壓低5~6mmHg) 病人疼痛躁動不安 吐氣末正壓(PEEP) 腹壓上升(Valsalva maneuvers) 例行之護理工作(如抽痰、翻身拍背、擦澡)均會使得顱內壓上升 高血壓或低血壓 發燒或發抖 貧血或缺血 血中二氧化碳過高(大於45mmHg)或氧氣太低 癲癇

維持穩定的血液循環 保持腦灌流壓大於70mmHg。 體液至少為正常容積狀態。 (normovolemia) 中心靜脈壓應保持在6-15cmH2O 肺動脈楔壓12-15mmHg。 體液的維持以等張晶狀液(isotonic crystalloid)或膠狀液(colloid)為主；避免使用低張溶液。 Cerebral ischemia may occur below a CPP of 50 mmHg. A CPP below 60 mm Hg generally is associated with poorer outcomes. A CPP that is too high also may have a deleterious effect: a CPP higher than 140 mm Hg may cause blood-brain barrier damage or brain edema and lead to an increase in ICP.

引發反應性血管收縮之良性循環 腦灌流壓提高 顱內壓下降 血管收縮 腦部血容積減少 CBF=CPP/CVR 提高血壓 CPP=MAP-ICP 顱內壓下降 血管收縮 腦部血容積減少 降低血液黏稠度， 過度通氣， 代謝率減少 CSF引流， 顱骨減壓術 PVVP: perfusionvesselsvolumepressure. 頭抬高30度，頸部維持正中 減少病人疼痛，鎮定劑的使用

腦灌流壓降低，引發反應性血管舒張之惡性循環 CBF=CPP/CVR CPP=MAP-ICP 血壓下降， 脫水 腦灌流壓降低 顱內壓上升 血管舒張 腦部血容積增加 血液黏稠度增加， 二氧化碳累積， 代謝率增加 水腦、 腦水腫 PVVP: perfusionvesselsvolumepressure. 靜脈回流受阻，病人躁動 與呼吸器對抗，胸腹壓增加

第一線療法 使用鎮靜劑及神經肌肉阻斷劑 顱內壓監測器，腦脊髓液引流 高張利尿劑(mannitol) 0.25-1gm/kg 血氧飽和度100%、體液為正常容積狀態(euvolemia)、中心靜脈壓維持 在6-15cmH2O 、或者是肺動楔壓12-15mmHg、腦灌流壓大於 70mmHg，及血中二氧化碳分壓35mmHg 使用鎮靜劑及神經肌肉阻斷劑 顱內壓監測器，腦脊髓液引流 HSDOH: hemodynamicsedation drainageosmoticmild hyperventilation (穩定鎮靜引流利尿輕通氣) 高張利尿劑(mannitol) 0.25-1gm/kg 輕微的過度通氣，PaCO2 30-35mmHg 頸靜脈竇氧氣飽和度(SjvO2)的監測 穩定鎮靜引流利尿輕通氣

第二線療法 巴比妥酸昏迷、低溫療法(hypothermia)、高血壓療法、 高度的過度通氣(PaCO2<30mmHg) 減壓開顱術(decompression craniectomy) 1.Pentobarbital come: loading dose-10mg/kg over 1 hour, followed by 5 to 10 mg/kg/hr. the desired blood concentration is 30 to 50 mg/dl, which should produce burst suppression on the EEG with maintenance of MAP over 60 mmHg. Gradual withdrawal of barbiturate therapy can begin after ICP has been controlled for 24 to 48 hours. 2.A mortality rate of 19% vs 58% for decompressive craniectomy vs barbiturate coma. 3.Bone flap re-implantation was done about 12 weeks later. 4.Hyperventilation has been advocated in a targeted way, to control severe intracranial hypertension secondary to hyperemia, cerebral vasodilation, and diffuse brain swelling, commonly seen in children and young adults after severe brain injury. As a general rule, normocapnia should be restored as soon as ICP and CPP are normalized.

鎮靜劑(sedation)及 神經肌肉阻斷劑 (neuromuscular blockade) 一方面使得呼吸器的使用容易控制，另一方面可降低顱內壓。 常用的鎮靜劑如midazolam， propofo1； 神經肌肉阻斷劑如atracurium， pancuronium， vecuronium。 當顱內壓小於20mmHg超過24小時，則可以將藥量逐漸降低。

腦脊髓液引流(CSF drainage) 如果有腦室引流導管(ventriculostomy),腦脊髓液引流是第一個考慮的方法。 每次引流3-5 ml，可達到良好的降壓效果。 一般建議每8小時引流75 ml.屬安全範圍。

高張利尿劑(osmotic diuretics) 最常用的藥物是 mannitol 或 glycerol 降低顱內壓的機轉是增加血管內滲透壓，而使腦部細胞外的水進可入血管，如此能改善腦水腫而降低顱內壓。 另減低血液黏調度、降低血比容，使得血液流速變快,引起反應性的血管收縮,如此能減少腦部血液的體積而降低顱內壓。 在給藥後15分鐘內開始作用。 建議使用方法是單次靜脈快速給藥(bolus, rapid infusion)。

高張利尿劑(osmotic diuretics) 建議使用劑量為0.25-1 g/4-6hrs，必要時可以縮短使用間隔。 應監測血清滲透壓，避免滲透壓大於320 mOsm/L，以免造成腎衰竭。

高張利尿劑(osmotic diuretics) 主要的缺點是會造成低血壓(hypotension)、低容積量(hypovolemia)電解質不平衡及腎衰竭。但是在腦灌流壓的處理流程(CPP protocol)卻很少見到以上的併發症。 利尿劑 lasix 常可和 mannitol 合併使用效果更好。使用劑量:20-40mg/3-4hrs (0.3 to 0.5 mg/kg)，要注意的是液體的補充以免造成低血壓及低容積量而產生腦部缺血。

Steroids Although steroids clearly are useful in reducing the perifocal edema associated with brain tumors, their value in head injury has not been demonstrated.

Anticonvulsants Post-traumatic epilepsy: 15-30% of severe H.I.; 5% of mild H.I. 90% occur within the first 24 hours Indication: GCS ≦10 on admission Acute EDH, SDH, ICH (supratentorial) Open depressed skull fracture with parenchymal injury Cortical contusion on CT scan Seizure within the first 24 hrs after injury Penetrating brain injury History of significant alcohol abuse. If there are no seizures and the follow-up CT scan is satisfactory, we discontinue the treatment. In patients who have had seizures, anticonvulsants are continued for at least 1 year.

D/C of anticonvulsants Taper after 1 week of therapy except in the following: Penetrating brain injury Development of late seizure Prior seizure therapy Patients undergoing craniotomy The above four situations: maintain for 6-12 months.

Indication for Surgery Critical factors: Patient’s neurological status Imaging findings Presence and severity of extracranial lesions. Time is life.

Significant Mass Effect Displacement of midline structures≧ 5mm. Effacement of basal cisterns on CT scan.

EDH (epidural hematoma) Located in the temporal region: tear of the middle meningeal vessel, sinus injury In 50% of patients there is no radiographic evidence of a fracture. Small, stable, asymptomatic  conservative All acute traumatic extraaxial hematoma 1cm or greater in thickness  op Outcome: children better than adult. Because the outcome is invariably better than in adults, surgical evacuation of an epidural hematoma in children always is warranted, unless the patient meets the criteria for brain death.

SDH (subdural hematoma) 30% of severe head injury Bleeding of lacerated brain and cortical vessels avulsed bridging vein No significant mass effect without brain swelling  conservative Larger craniotomy Worsen prognosis than EDH Golden time: 4 hours

Contusional and intracerebral hematomas (ICH) Located in anterior frontal and temporal lobes. Awake and alert conservative >2cm(surface), mass effect, uncontrolled ICP  op Early surgical intervention for temporal and posterior fossa lesions. Adult with GCS of 3, non-reactive & dilated pupil without spontaneous respiration  conservative Over 75 Y/O, GCS of 5 or less  conservative

Skull fracture Non-op: closed, linear, non-depressed skull fracture  heal spontaneously. OP: open fractures or fractures depressed more than the thickness of the skull required surgical elevation or repair. Cosmetic consideration. Near a major dural sinus  non-op, even occluded sinus.

Skull fracture There is no evidence to support the theory that correction of a depressed skull fracture reduces the risk of subsequent seizures.

Growing skull fracture Inspecting the site of injury for a palpable, non-tender swelling. A linear fracture separated more than 3 mm on CT scan suggest an associated dural tear. OP or F/U They rarely occur in children over 18 months of age and rarely show after 6 month from injury. If there is no underlying intraparenchymal injury on CT scan, emergency operative intervention is unnecessary.

Skull Fracture Battle’s sign Raccoon’s eye sign

The End!!