Traumatic Brain InjuryThe First Affiliated Hospital, Medical College, Zhejiang UniversityNeurosurgical DepartmentYing Tong

EpidemiologyTraumatic brain injury (TBI) continues to be an enormous public health problem. 500,000 to well over 1 million cases of head injury every year. mild(80%), moderate(10%) and severe(10%) injuries. Head injury results in half of the 150,000 trauma deaths. 5.3 million people are living with brain injuryrelated disabilities.

PathophysiologyPrimary injury occurs at the moment of impact. Primary injury includes bone fracture, concussion, contusion, hematoma, traumatic subarachnoid hemorrhage, and diffuse axonal injury. Secondary injury to the brain occurs as a result of decreased oxygen delivery to the brain, which in turn sets off a cascade of events that causes even more damage than the initial injury.

PathophysiologyPrimary injury Concussion ContusionIntracranial hemorrhage: epidural, subdural, subarachnoid, and intraparenchymal or intracerebral traumatic subarachnoid hemorrhage

PathophysiologyPrimary injury Diffuse axonal injury(DAI) is a rotational acceleration-deceleration injury to the white-matter pathways of the brain resulting in a functional or anatomic disruption of these pathways and is cited as the cause of loss of consciousness in patients without mass lesions.

PathophysiologySecondary injury : Effects of hypotension, hypoxia, and herniation with elevated ICP due to mass effect, as a result of decreased oxygen delivery to the brain, which in turn sets off a cascade of events(mediators of inflammation, excitotoxicity, calcium influx, and Na+,K+-ATPase dysfunction ) leads to neuronal cell dysfunction and death.

PathophysiologySecondary intracranial insults to the brain HemorrhageIschemiaEdemaRaised intracranial pressure (ICP)VasospasmInfectionEpilepsyHydrocephalus

PathophysiologySecondary systemic insults to the brain HypoxiaHypercapniaHyperglycemiaHypotensionSevere hypocapniaFeverAnemiaHyponatremia

Mechanisms of brain injury Physical mechanisms of brain injury Impact loading - Collision of the head with a solid object at a tangible speedImpulsive loading - Sudden motion without significant physical contact Static or quasistatic loading - Loading in which the effect of speed of occurrence may not be significant

Mechanisms of brain injury Basic types of tissue deformation Compressive - Tissue compressionTensile - Tissue stretching Shear - Tissue distortion produced when tissue slides over other tissue

Mechanisms of brain injury Coup injuries are caused by direct transmission of impact energy through the skull into the underlying brain and occur directly below the site of injury because of the creation of negative pressure when the skull, distorted at the site of impact, return to its normal shape.

Mechanisms of brain injuryContrecoup injuries are similar to coup contusions but are located opposite the site of direct impact. Contrecoup injuries are caused by rotational shear and other indirect forces that occur contralateral to the primary injury. Rotational force causes the basal frontal and temporal cortices to impact or sweep across rigid aspects of the skull, the sphenoid wing, and petrous ridges. They are commonly seen in the frontal and temporal lobes.

Classification By mechanism Closed: High velocity (auto accidents); Low velocity (falls, assault)Penetrating: Gunshot wounds; Other open injuriesBy severityMild: GCS 13-15; Moderate: GCS 9-12; Severe: GCS 8 or less, comatose

ClassificationBy morphologySkull fractures: Vault ---Linear or stellate ---Depressed or nondepressed Basilar ---With/without CSF leak --- With/without nerve VII palsyIntracranial lesions Focal --- Epidural --- Subdural --- Intracerebral Diffuse --- Mild concussion --- Classic concussion --- Diffuse axonal injury

Prehospital and Emergency Department Management Cardiopulmonary stabilization :ABCs ; avoid hypotension and hypoxia; systolic blood pressure> 90 mm Hg , PaO2 > 60 mm Hg. Medical history: AMPLEGeneral examinationNeurologic examination: The Glasgow Coma Scale (GCS)and the pupils.

Initial neurologic examinationGlasgow Coma ScalePupillary response to lightEye movementOculocephalic (dolls eye)Oculovestibular (caloric)Motor powerGross sensory examination

Glasgow Coma Scale (GCS)

Neurologic examination: the pupilsPupillary size and reactivity are also essential components of the initial neurologic examination. The presence of an unresponsive pupil, particularly a dilated pupil, is significantly correlated with a poor outcome and therefore an important part of the examination.

Interpretation of pupillary findings in head injury patients

Diagnostic procedure CT scanning:greater efficacy ; emergency CT scan ; assess the presence or absence of fracture, epidural and subdural hematomas, intracerebral hematomas and contusions, shift of the midline structures, and the appearance of the basal and perimesencephalic cisterns. plain skull films .

CT scan of the head in a patient with a closed head injury. Severe compression of mesencephalic cisterns is seen, indicating midbrain compression (arrowheads).

CT scans of patient with closed head injury. This patient has a right temporal epidural hematoma (arrows). The mesencephalic cisterns are patent in the top left, indicating a lack of brain stem compression despite mass (arrowheads).

CT scans of patient with closed head injury. This patient has suffered an acute left subdural hematoma (arrowheads) with midline shift (arrows).

Intracranial PressureIndication:all patients with a GCS of 8 or less have ICP monitors placed. Types: IVCs and sites other than the ventricles ( brain parenchyma, subarachnoid or subdural or epidural space).

Nonoperative Management Prompt physiologic resuscitation: restoration of blood pressure, oxygenation, and ventilation. Control increased ICP: The goal of treatment is to try to keep the ICP less than 20mm Hg and to maintain cerebral perfusion pressure at or above 70 mm Hg.

Control increased ICPThe head of the bed is elevated to 30 degrees with the head placed in a neutral position. CSF drainage: external ventricular drain, or ventriculostomy.Mannitol and other diuretic agents: Mannitol --- IV bolus of 0.25 to 1 g/kg body weight every 4 to 6 hours. Other diuretics : frusemide .---maintain euvolemia

Control increased ICPHyperventilation: PaCO2 of 30 to 35 mm Hg . lowering PaCO2 ----- vasoconstriction -----decreases intracranial blood volume----- a decrease in ICP Mild hypothermiaSecond-tier therapeutic interventions: hypertonic saline, high-dose barbiturate therapy, decompressive craniectomy.

Other Nonoperative Management nutrition : nonparalyzed patient , 140% of their resting metabolism expenditure; paralyzed patient , 100%;Steroids:not recommend;Anticonvulsants: prevent early post-traumatic seizures .

Operative Management Indication: an intracranial mass lesion and deficits thought to be related to that lesion. [Space-occupying hematomas , the amount of midline shift, the location of the clot and the patients ICP ] In general, any clot or contusion greater than 30 cc is thought to be operable.

OutcomeOutcome has improved since the mid 1970s .Mortality rates have decreased from approximately 50% to less than 30% .

Glasgow Outcome Scale (GOS)

Algorithm for management of mild head injury. *Risk factors include: ambiguous accident history, continued post-traumatic amnesia, retrograde amnesia > 30 min, clinical signs of skull fracture, headache, vomiting, focal neurologic deficit, seizure, age < 2 years and > 60 years, coagulation disorder, or high-energy (speed) accident.

Algorithm for management of moderate head injury.

Initial management of severe head injury

Skull fractures

IntroductionClassification : by pattern (linear, comminuted, depressed), by anatomic location (vault convexity, base), and by skin integrity (open, closed).The pattern of a skull fracture: the force of impact and the ratio of the impact force to the impact area.

Linear skull fractures A linear skull fracture is a single fracture line that goes through the entire thickness of the skull.Diagnosis: CT scan, plain skull radiographs.Management: closed linear fractures require no stabilization or exploration when there is no evidence of epidural hematoma or underlying dural or cortical injury. Open linear fractures are debrided.

Comminuted fracturesA comminuted fracture occurs when multiple linear fractures radiate from the point of impact. Diagnosis: skull radiographs and CT. Management :1) If skin is closed and no depression of bone fragments greater than the thickness of the skull, management is as for linear skull fractures. 2)With underlying intracranial pathology,surgery. 3)Open and free bone fragments are present, cleansing or debridement.

Depressed skull fracturesIn a depressed skull fracture, the greatest bone depression can occur at the interface of fracture and intact skull or near the center of the fracture if several fragments are displaced inward. Diagnosis: skull radiographs and CT. Physical examination is difficult ( scalp mobility and swelling ).

Depressed skull fracturesManagement: neurologic deficit , epilepsy , cosmetic deformity, infection.The initial surgery is performed within 24 hours and usually within the first 12 hours. Depressed fractures over dural sinuses: 1)fracture carefully elevated, control of the venous sinus as soon as possible, preparing for significant transfusion requirements. 2) scalp debridement alone and massive irrigation( If the fracture site is not grossly contaminated, or will not cause a major cosmetic or functional deformity or not cause intracranial hypertension secondary to sinus occlusion).

Basilar skull fractures Linear fractures in the skull base carry a risk of meningitis. Diagnosis: by clinical findings Anterior skull base fractures: (1)bilateral periorbital ecchymoses (raccoon or panda bear, (2)CSF rhinorrhea (epistaxis), (3)anosmia, visual disturbances. Middle skull base fractures: (1) hemotympanum, blood in the external auditory canal, (2)CSF otorrhea/rhinorrhea, (3) VIIth or VIIIth nerve palsies (facial palsy, deafness, tinnitus). Posterior Fossa Fracture: (1)ecchymosis behind the ear (Battles sign),(2) impaired gag reflex.

Basilar skull fracturesManagement 1)A patient with a basal skull fracture but no leak is observed for 2 to 3 days. Lie on bed. 2) Prophylactic antibiotics are not used on a prolonged basis. 3) Most traumatic CSF leaks resolve spontaneously within the first week. If the leak persists beyond 5 to 7 days, lumbar taps or spinal drainage. 4) CSF leaks refractory to spinal fluid drainage require surgical closure.

Traumatic intracranial hematomas

IntroductionTraumatic intracranial hematomas are localized collections of blood that are directly related to the primary forces (impact, acceleration) and secondary factors that can play a role in head injury, such as coagulopathy, alcohol intake, cocaine abuse, hypotension, rupture of traumatic intracranial aneurysms, and decompression of the brain following removal of the hematoma.

Epidural hematoma (EDH) EDH is a collection of blood between the skull and the dura mater. Etiology: a ruptured artery or vein in the epidural space as a result of a fracture of the skull .The clot enlarges because of the hydrostatic force of the blood from the ruptured vessel stripping the dura from the bone. The most common scenario is a fracture of the temporal bone causing a tear in the middle meningeal artery.

Epidural hematoma (EDH)Clinical manifestations: lucid interval :an initial brief period of loss of consciousness (concussion)-----recovery ----- followed by a progressive deterioration of the level of consciousness.Diagnosis: CT: typical biconvex lens-shaped hematoma adjacent to the skull, displacing the brain. The most common location is the temporoparietal region.

Epidural hematoma (EDH)Treatment:Operative management: Clots larger than 15 mm in thickness, with volume greater than 25 cm3 or with associated compressed basal cisterns and midline shift should be evacuated.Nonoperative Management: a small EDH (ruptured vein ).

Acute subdural hematoma (ASDH) ASDH is characterized by an accumulation of blood between the dura mater and the arachnoid layer within 72 hours of injury. In elderly patients : falls, especially in the face of anticoagulation and alcohol abuse. In young patients : highspeed motor vehicle accidents and assaults. Most often ASDHs are caused by the rupture of bridging veins that traverse the subdural space.

Acute subdural hematoma (ASDH)Clinical manifestations:comatose, ipsilateral pupil dilated, hemiparesis on the contralateral side , extensor posturing,et al. Diagnosis :CT: crescentic hematoma extending over the fronto-temporo-parietal regions, commonly with mass effect, herniation of the uncus, midline shift, associated brain swelling, effacement of basal cisterns and dilatation of the contralateral temporal horn.

Acute subdural hematoma (ASDH)Treatment:Operative management:low GCS scores and/or evidence of herniation and high intracranial pressure, surgery should be performed as an emergency . decompressive craniectomy Nonoperative Management:GCS of 13 or higher, absence of associated intracerebral hemorrhage, contusions, edema or effacement of basal cisterns, midline shift less than 10 mm, and hematoma volume less than 25 cm3 .

Chronic subdural hematoma (CSDH) CSDH is a subdural hematoma that is older than 3 weeks. Formation : an initial bleeding in the subdural space( usually asymptomatic)----- the acute blood may resolve completely, or enlarge and develop into a subacute SDH causing symptoms, or it may liquefy and continue to enlarge, developing into a CSDH-----expansion of the subdural space , further bleeding as a result of rupture of small bridging veins.

Chronic subdural hematoma (CSDH)Most commonly a CSDH is caused by a minor head trauma or fall. Risk factors are old age, alcohol abuse, seizures, cerebrospinal fluid shunts, anticoagulation, and patients at risk for falls.Clinical manifestations: headaches, nausea, vomiting, hemiparesis, sensory deficits, language disturbances, gait problems, transient-ischemic-attack-like symptoms, and decreased consciousness.

Chronic subdural hematoma (CSDH)Diagnosis: CT:hypo- or isodense fluid collection over the frontoparietal region, often with significant mass effect and midline shift. Treatment: The operative technique for symptomatic patients involves placing burr holes or twist drills. In cases of multiple recurrences, a craniotomy or a craniectomy may be performed with drainage of the clot and membranes.

Cerebral contusion Brain contusion is a common consequence of head injury and is defined as scattered hemorrhages involving the cortex and adjacent white matter. Contusions occur predominantly, in the basal frontal and temporal lobes.The anterior and middle fossa have bony prominences that predispose these lobes to injury. The inertial forces move the brain against these bony indentations and rupture of small cortical and subcortical vessels occurs. Coup contusions occur on the same side as the impact and counter-coup contusions occur on the opposite side.

Cerebral contusionClinical manifestations:variable and in part depends on the nature of the trauma and associated injuries. Image: CT: nonhomogeneous areas of high density, often interspersed with areas of low density (salt and pepper appearance)

Two days later

Cerebral contusionTreatment:Operative management: Obtunded or comatose patients with significant contusions and mass effect or midline shift may benefit from a craniotomy and removal of the contused brain tissue .Nonoperative Management:Patients that are awake and following commands with no significant neurological deficits.

Intraparenchymal hematoma Intraparenchymal hematoma is defined as confluent, homogeneous areas of hemorrhage that occur inside the brain parenchyma. Most commonly in the frontal and temporal regions. 20% of cases are multiple. Round-shaped and occur in the white and gray matter.

Intraparenchymal hematomaMechanism : acceleration-deceleration with "shearing" of perforating vessels for deep located hemorrhages and cortical and subcortical vessels for superficially located ones.

Intraparenchymal hematomaClinical manifestations:variable, depressed level of consciousness .Image: CT: one or more localized and non-contiguous hematoma, quite often deep in location.

Intraparenchymal hematomaTreatment:Operative management: a decreasing level of consciousness and evidence of mass effect or shift from a superficially located clot may benefit from a craniotomy and evacuation .Nonoperative Management.

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Penetrating InjuriesHigh mortality rate : the risk of death in the comatose patient in most studies is approximately 90% .Debridement of the first few centimeters of the tract followed by a watertight dural closure.

Varieties of missile wounds to the head

Intracranial bleeding from gunshot wounds to the head. (A)Subarachnoid hemorrhage. (B)Subdural hematoma. (C)Confluent intracerebral hematoma. (D)Intraventricular hematoma.

ReferenceSabiston Textbook of Surgery (17th and 18th Edition) Rengachary SS, Ellenbogen RG. Principles of Neurosurgery (2nd edition)

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