颅脑损伤（英文版）

“Boy, do I have an Excedrin headache!” managing the head injured patient,Leaugeay Webre BS, CCEMT-P, NREMT-P,Scenario,While descending Mt Hood in Oregon, Bob tumbled head over heels, and came to a stop dangling off a precipice by his Telemark ski at 11,000 ft. On arrival the ski patrol paramedics Bobs breathing was sonorous and shallow, and he had a GCS of 3-4. The only obvious injuries were to his head. His BP was 87/55, HR 100 and RR 16,How should the paramedics treat this patient? Should he be intubated? Should he be fluid resuscitated?,Common major trauma 4 million people experience head trauma annually Severe head injury is most frequent cause of trauma death GSW to cranium: 75-80% mortality At Risk population Males 15-24 Infants Young Children Elderly,Introduction to Head, Facial, & Neck Injuries,TIME IS CRITICAL Intracranial Hemorrhage Progressing Edema Increased ICP Cerebral Hypoxia Permanent Damage Severity is difficult to recognize Subtle signs Improve differential diagnosis Improves survivability,Introduction to Head, Facial, & Neck Injuries,Scalp Strong Flexible mass of Skin Fascia Muscular Tissue Highly Vascular Hair provides Insulation Structures Beneath Galea Aponeurotica Between scalp and skull Fibrous connective sheath Subaponeurotica (Areolar) Tissue Permits venous blood flow from the dural sinuses to the venous vessels of scalp Emissary Veins: Potential route for Infection,Anatomy & Physiology of the Head,Parietal,Suture Line,Frontal,Temporal,Orbits,Maxillae,Mandible,Temporal Mandibular Joint,Occiptal,Nasal Bones,Zygomatic Arch,Sphenoid,Foramen Magnum (Hole in Base),Cranium,Brain Occupies 80% of cranium Comprised of 3 Major Structures Cerebrum Cerebellum Brainstem High metabolic rate Receives 15% of cardiac output Consumes 20% of bodys oxygen Requires constant circulation IF Blood supply stops Unconscious within 10 seconds Death in 4-6 minutes,Anatomy & Physiology of the Head,Cerebral Perfusion Pressure Pressure within cranium (ICP) resists blood flow and good perfusion to the CNS Pressure usually less than 10 mmHg Mean Arterial Pressure (MAP) Must be at least 50 mmHg to ensure adequate perfusion MAP = DBP + 1/3 Pulse Pressure Cerebral Perfusion Pressure (CPP) Pressure moving blood through the cranium CPP = MAP - ICP,Anatomy & Physiology of the Head,Calculating MAP (mean arterial pressure) DBP + 1/3 PP PP (pulse pressure) = SBP - DBP SBP + 2(DBP) 3 Calculating CPP (cerebral perfusion pressure) MAP ICP ICP normally 10,Anatomy & Physiology of the Head,Cerebral Perfusion Pressure Autoregulation Changes in ICP result in compensation Increased ICP = Increased BP This causes ICP to rise higher and BP to rise Brain injury and death become imminent Expanding mass inside cranial vault Displaces CSF If pressure increases, brain tissue is displaced,Anatomy & Physiology of the Head,Types of Trauma,Soft tissue Skull fracture Primary brain injuries Secondary brain injuries,The patient presented to the emergency department with the golf cub in his head, which was removed in the operating room,Lateral skull x-ray of a patient who presented with a severe intracranial injury produced by a golf club,Scalp Injury,Contusions Lacerations Avulsions Significant Hemorrhage ALWAYS Reconsider MOI for severe underlying problems,Brain Injury,As defined by the National Head Injury Foundation “a traumatic insult to the brain capable of producing physical, intellectual, emotional, social and vocational changes.” Classification Direct Primary injury caused by forces of trauma Indirect Secondary injury caused by factors resulting from the primary injury,Direct Brain Injury Types,Coup Injury at site of impact Contrecoup Injury on opposite side from impact,Intracranial Perfusion,Review Cranial volume fixed 80% = Cerebrum, cerebellum & brainstem 12% = Blood vessels & blood 8% = CSF Increase in size of one component diminishes size of another Inability to adjust = increased ICP,Intracranial Perfusion,Compensating for Pressure Compress venous blood vessels Reduction in free CSF Pushed into spinal cord Decompensating for Pressure Increase in ICP Rise in systemic BP to perfuse brain Further increase of ICP Dangerous cycle,ICP,BP,Intracranial Pressure,Role of Carbon Dioxide Increase of CO2 in CSF Cerebral Vasodilation Encourage blood flow Reduce hypercarbia Reduce hypoxia Contributes to ICP Causes classic Hyperventilation & Hypertension Reduced levels of CO2 in CSF Cerebral vasoconstriction Results in cerebral anoxia,Factors Affecting ICP,Vasculature Constriction Cerebral Edema Systolic Blood Pressure Low BP = Poor Cerebral Perfusion High BP = Increased ICP Carbon Dioxide Reduced respiratory efficiency,Increased pressure Compresses brain tissue Against & around Falx Cerebri Tentorium Cerebelli Herniates brainstem Compromises blood supply Signs & Symptoms Upper Brainstem Vomiting Altered mental status Pupillary dilation Medulla Oblongata Respiratory Cardiovascular Blood Pressure disturbances,Pressure & Structural Displacement,Altered Mental Status Altered orientation Alteration in personality Amnesia Retrograde Antegrade Cushings Reflex Increased BP Bradycardia Erratic respirations,Signs & Symptoms of Brain Injury,Vomiting Without nausea Projectile Body temperature changes Changes in pupil reactivity Decorticate posturing,Pathophysiology of Changes Frontal Lobe Injury Alterations in personality Occipital Lobe Injury Visual disturbances Cortical Disruption Reduce mental status or Amnesia Retrograde Unable to recall events before injury Antegrade Unable to recall events after trauma “Repetitive Questioning” Focal Deficits Hemiplegia, Weakness or Seizures,Signs & Symptoms of Brain Injury,Upper Brainstem Compression Increasing blood pressure Reflex bradycardia Vagus nerve stimulation Cheyne-Stokes respirations Pupils become small and reactive Decorticate posturing Neural pathway disruption,Signs & Symptoms of Brain Injury Physiological Changes,Middle Brainstem Compression Widening pulse pressure Increasing bradycardia CNS Hyperventilation Deep and Rapid Bilateral pupil sluggishness or inactivity Decerebrate posturing,Signs & Symptoms of Brain Injury Physiological Changes,Lower Brainstem Injury Pupils dilated and unreactive Ataxic respirations Erratic with no pattern Irregular and erratic pulse rate ECG Changes Hypotension Loss of response to painful stimuli,Signs & Symptoms of Brain Injury Physiological Changes,Different pathology than older patients Skull can distort due to anterior and posterior fontanelles Bulging Slows progression of increasing ICP Intracranial hemorrhage contributes to hypovolemia Decreased blood volume in peds General Management Avoid hyperextension of head Tongue pushes soft pallet closed Ventilate through mouth and nose,Signs & Symptoms of Brain Injury Pediatric Head Trauma,Signs & Symptoms of Brain Injury Glasgow Coma Scale,Physiological Issues Indicate pressure on CN-II, CN-III, CN-IV, & CN-VI CN-III (Oculomotor Nerve) Pressure on nerve causes eyes to be sluggish, then dilated, and finally fixed Reduced peripheral blood flow Pupil Size & Reactivity Reduced Pupillary Responsiveness Depressant drugs or Cerebral Hypoxia Fixed & Dilated Extreme Hypoxia,Signs & Symptoms of Brain Injury Eye Signs,Skull Fractures,The skull will not fracture without extreme force Closed/ open linear depressed comminuted basilar impaled object,Cranial Injury,Trauma must be extreme to fracture Linear Depressed Open Impaled Object Basal Skull Unprotected Spaces weaken structure Relatively easier to fracture,Cranial Injury,Basal Skull Fracture Signs Battles Signs Retroauricular Ecchymosis Associated with fracture of auditory canal and lower areas of skull Raccoon Eyes Bilateral Periorbital Ecchymosis Associated with orbital fractures,Cranial Injury,Basilar Skull Fracture May tear dura Permit CSF to drain through an external passageway May mediate rise of ICP Evaluate for “Target” or “Halo” sign,Basilar Skull Fracture,Cribiform plate fracture Battles sign Periorbital ecchymosis CSF leakage,Primary Brain Injury,Results from direct trauma Focal Diffuse,Direct Brain Injury Categories,Focal Occur at a specific location in brain Differentials Cerebral Contusion Intracranial Hemorrhage Epidural hematoma Subdural hematoma Intracerebral Hemorrhage Subarachnoid Hemorrhage Diffuse Concussion Moderate Diffuse Axonal Injury Severe Diffuse Axonal Injury,Focal,Contusions Intracerebral hematoma Subdural hematoma Subarachnoid hematoma Epidural hematoma,Contusions,LOC with resultant cellular damage “bruising” Temporal injury often presents with repetitive questioning,A young male arrived in the emergency department after experiencing a gunshot wound to the brain. The entrance was on the left occipital region. A CT scan shows the skull fracture and a large underlying cerebral contusion. The patient was taken to the operating room for debridement of the wound and skull fracture, with repair of the dura mater,Focal Brain Injury,Cerebral Contusion Blunt trauma to local brain tissue Capillary bleeding into brain tissue Common with blunt head trauma Confusion Neurologic deficit Personality changes Vision changes Speech changes Results from Coup-contrecoup injury,Epidural Hematoma,Located between skull and dura mater Usually involves arterial bleeding- middle meningeal artery Sharply defined edges on CT Usually no underlying brain injury Classical presentation is “lucid interval” May quickly evolve into herniation,Lucid Interval,transient LOC followed by a lucid period where patient is neurologically intact followed by a secondary onset of HA and decreasing LOC,Epidural Hematoma Bleeding between dura mater and skull Involves arteries Middle meningeal artery most common Rapid bleeding & reduction of oxygen to tissues Herniates brain toward foramen magnum,Focal Brain Injury Intracranial Hemorrhage,CT scan of an acute left-sided epidural hematoma. Note the typical convex or lens-shaped appearance. The hematoma takes this shape as the dura strips from the undersurface of the cranium, limited by the suture lines. A midline shift of the ventricular system exists.,Subdural Hematoma,Located between the dura mater and pia mater All venous bleeds, usually present with slow onset Indistinct on CT Underlying brain injury May not present with Sx for hours or days,Subdural Hematoma Bleeding within meninges Beneath dura mater & within subarachnoid space Above pia mater Slow bleeding Superior sagital sinus Signs progress over several days Slow deterioration of mentation,Focal Brain Injury Intracranial Hemorrhage,Acute subdural hematoma: note the bright (white) image properties of the blood on this noncontrast cranial CT scan. Note also the midline shift.,Subacute subdural hematoma: the crescent-shaped clot is less white than on CT scan of acute subdural hematoma,Intracerebral Hemorrhage Rupture blood vessel within the brain Presentation similar to stroke symptoms Signs and symptoms worsen over time,Focal Brain Injury Intracranial Hemorrhage,Intracerebral Hematoma,Located in the brain parenchyma Difficult to distinguish from contusion,Intracranial hemorrhage. CT scan of right frontal intracerebral hemorrhage complicating thrombolysis of an ischemic stroke.,Subarachnoid Hemorrhage,May not present with physical findings HA stiff neck nuchal rigidity Blood in CSF,Brain CT scan shows subtle finding of blood at the area of the circle of Willis consistent with acute subarachnoid hemorrhage.,Diffuse Brain Injury,Due to stretching forces placed on axons Pathology distributed throughout brain Types Concussion Moderate Diffuse Axonal Injury Severe Diffuse Axonal Injury,Concussion,Transient LOC Usually complete recovery Mild form of diffuse injury Often presents with a brief period of confusion Pt may exhibit retrograde or posttraumatic amnesia,Diffuse Axonal Injury,Rapid, profound, prolonged unconsciousness Often leads to increased ICP,Mild to moderate form of Diffuse Axonal Injury (DAI) Nerve dysfunction without anatomic damage Transient episode of Confusion, Disorientation, Event amnesia Suspect if patient has a momentary loss of consciousness Management Frequent reassessment of mentation ABCs,Diffuse Brain Injury Concussion,“Classic Concussion” Same mechanism as concussion Additional: Minute bruising of brain tissue Unconsciousness If cerebral cortex and RAS involved May exist with a basilar skull fracture Signs & Symptoms Unconsciousness or Persistent confusion Loss of concentration, disorientation Retrograde & Antegrade amnesia Visual and sensory disturbances Mood or Personality changes,Diffuse Brain Injury Moderate Diffuse Axonal Injury,Brainstem Injury Significant mechanical disruption of axons Cerebral hemispheres and brainstem High mortality rate Signs & Symptoms Prolonged unconsciousness Cushings reflex Decorticate or Decerebrate posturing,Diffuse Brain Injury Severe Diffuse Axonal Injury,Pathway of Deterioration,Cranial insult Tissue edema Increasing ICP Compression of arteries Decreased cerebral blood flow Decreased O2 with cellular death Edema around necrotic tissue,Cont,Increasing ICP with compression of brainstem and respiratory center Accumulation of CO2 resulting in vasodilation Increasing blood volume further increasing ICP Death,Any swelling or bleeding decreases the circulating blood volume and cerebral blood flow Decreased cerebral blood flow results in hypoxia and CO2 rises Hypercarbia dilates cerebral blood vessels causing increasing BP Attempts to perfuse brain resulting in increased ICP,Herniation,Depression of 3rd cranial nerve results in pupillary dilation- aniscoria Lateral paresis Cushings triad Decorticate posturing Decerebrate posturing,Decorticate Posturing,Results from lesions of internal capsules, basal ganglia, thalamus or cerebral hemisphere Interrupts corticospinal pathways Presents with flexed arms and extended lower extremities,Decerebrate Posturing,Results from injury to midbrain and pons Indicative of brainstem dysfunction Presents with extended upper extremities and pronation Extended lower extremities Usually indicative of graver injury,Cushings Reflex,Late sign of increasing ICP Bradycardia Widening pulse pressure/ increasing BP Changes in respiratory patterns,Respiratory Patterns,May be indicative of injury location in the brain Cheyne - Stokes Central Neurogenic hyperventilation Apneustic Cluster breathing Ataxic breathing,Cheyne- Stokes Respirations,Periodic breathing in which depth of each breath increases to peak then decreases to a period of apnea Hyperpneic stage usually lasts longer than apneic phase Bilateral lesions in cerebral hemispheres,Central Neurogenic Respirations,Sustained regular, rapid and deep breathing Midbrain and upper pons injury,Apneustic Respirations,Breathing with a long pause at full inspiration or full expiration Respiratory function present at brainstem level only,Cluster Breathing,Gasping breaths with irregular pauses Lesion high medulla or low pons,Ataxic Breathing,Totally irregular consisting of both deep and shallow breaths associated with irregular pauses Consistent with medulla injury since the inspiratory and expiratory centers are located here,Glascow Coma Scale,Widely used to measure severity of injury in a patient and prognosis Use best possible response Most predictive subsequent to resuscitation,GCS,Eye opening 1- 4 Verbal response 1-5 Motor response 1- 6,Trauma Score,Respiratory rate Blood pressure May be incorporated into the GCS,Secondary Brain Injury,HYPOXIA HYPOTENSION Anemia Hyperglycemia Hypoglycemia Hyperthermia Intracranial mass,Significance,Surviving the initial injury is a small part of the battle for the traumatic brain injured person Secondary injury may have a greater influence over the final outcome than the primary injury Two most common hypoxia and hypotension and may be as devastating as the primary injury,Hypotension,Single most prognostic factor A single episode of decreased BP has been correlated with poorer outcome Brain requires blood flow for perfusion Keep BP 90 systolic CPP= MAP- ICP Most important to keep MAP =/ 70,Hypotension in the face of cerebral edema results in decreased CPP (cerebral perfusion pressure),MAP,(2) DBP + SBP 3 Normal (70- 100),Hypoxia,Defined as SpO2 90% Leads to cell damage and resultant swelling Closely follows hypotension in influence RSI faster and more reliable Less than 8 intubate,Treatment,Provide adequate ventilation Provide adequate fluid resuscitation Continually monitor VS HOB 30 degrees and head midline Consider mannitol and hyperventilation if herniation imminent Prophylactic seizure medication is not indicated,Ventilation,RSI and ventilate at a rate to maintain EtCo2 between 35- 45 mmHg Lidocaine 1mg/ kg prior to any intubation attempt,Hyperventilation,Has become very controversial recently and is no longer automatically recommended May exacerbate brain injury in all but the herniating patient Receptors respond to increased O2 with vasoconstriction Injured tissue is no longer perfused Results in increased edema and necrosis,Fluid Resuscitation,Initiate IV infusion to maintain SBP =/ 90 Preferably Map 70 mm HG Fluid of choice LR or NS Glucose causes fluid to be pulled into cells resulting in cerebral edema,Monitor,Continuously monitor VS for Sx of rising ICP Changes in breathing patterns Increasing BP Decreasing HR Unequal pupils Posturing,Position,Elevated HOB Midline head placement Assists with venous drainage from the head which decreases ICP,Hyperthermia,Causes an increase in ICP and should be regulated Head injured patients often suffer from increased body temperatures and should be monitored Acetaminophen and other cooling techniques may be used Do not induce hypothermia which may lead to shivering which results in increased ICP,Seizures,In the event of seizures treatment should be initiated immediately due to resultant hypoxia and increased ICP Treatment may include the use of Valium and Cerebyx Valium does not terminate abnormal electrical discharge a