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INTRODUCTION Epidemiology young: 50% MVA, 25% falls, etc elderly: 62% falls, 27% MVA 50% involve alcohol (must document) Leading cause of death in trauma pt < 25 yo Second peak at age 65 yo Classification open versus closed; blunt versus penetrating Mild: GCS 14 - 15 Moderate: 9 - 13 (Using BEST motor response) Severe: < 8 Glascow Coma Scale localization means that the patient removes from a painful stimulus and MUST cross the midline withdrawl does not cross the midline do not confuse withdrawl w/ reflex Coma the inability to obey commands, utter words, open eyes basically, coma is defined as GCS < 8 Factors and Outcome Age: < 18 is good, 18 - 60 is mod, > 60 is poor GCS Bilateral unreactive pupils Intracranial mass lesion Multiple system injuries EtOH Unilateral nonreactive pupil pupilary inequality ** Overall mortality is 50% (increases w/ age and decreasing GCS)** ** Elderly more likely to have mass lesion b/c of brain shrinkage ** ** Young more likely to have diffuse injury and systemic injuries ** ANATOMY/PHYSIOLOGY (Rosen p. 417 - 420) Scalp and Cranium Brain and CSF Cerebral Hemodynamics Biomechanics of head trauma

BRAIN CELLULAR DAMAGE AND DEATH Primary Head Injury (occur at time of injury w/i seconds - minutes)

Primary Impact HI at time of impact, usu NOT progressive, can be due to shear axonal injury (shaking), laceration, hemorrhages or contusion Diffuse Axonal Injury Can present with concussion or death, always greater in hemispheres than in brainstem, pts w/ a brain mass lesion always have diffuse axonal injury which determines the outcome Secondary Head Injury (evolves subsequent to impact; preventable; treatable; imp) Intracranial increased ICP and herniations SDH/EDH/SAH/ICH stroke hydrocephalus meningitis brain edema (vasogenic, cytotoxic) Extracranial BP changes hypoxia lytes, fluids (DI, SIADH)

CLINICAL PATHOPHYSIOLOGY Increased ICP Post - Traumatic brain swelling and cerebral edema Congestive Brain Swelling Cerebral Edema Alteration in consciousness Cushing Reflex Herniation Uncal Central Transtentorial Cerebellotonsillar Upward transtentorial


CONCUSSION See Denver Scale (below) DIFFUSE AXONAL INJURY Definition = widespread traumatic brain damage not presenting as localized injury, herniation, or perfusion failure Epidemiology

40% of severe head injury Accounts for 1/3 of deaths MCC neuro disability Pathophysiology Probably related to tearing or shearing of nerve fibers at the time of impact which results in functional or physiological abnormalities rather than grossly demonstrable anatomic lesions Necrosis/hemorrhage in corpus callosum is most commonly seen lesion (microscopic), rostral pontine hemorrhagic necrosis is second most common finding, axonal swelling secondary to shearing is 3rd most common finding Presentation Prolonged traumatic coma not caused by mass lesion is due to DAI No specific focal abnormality on CT MC finding after severe head truama: 44% of all comatose head injure pts Mild diffuse axonal injury Coma for 6 - 24 hrs 1/3 will have posturing Moratality 15% but those who recover don't have permanent deficits usually Moderate DAI Coma for > 24hrs Most common severity of DAI Transient posturing in most 25% die of complications of coma Severe DAI Prolonged traumatic coma Persistent posturing and autonomic dysfunction (Htn, hyperpyrexia) Most die, some remain in PVS, some awake but all have severe permanent disability


SKULL FRACTURES Linear Skull Fractures Single fracture that goes through the entire thickness of the skull Clinically important if the cross the middle meningeal groove or major venous drual sinuses (worry about EDHs); most others are clinically unimportant How can you tell fracture vs sutures: fractures are more lucent, sutures are < 3mm, fractures are > 3mm Healing in 3mo peds or up to 3yrs adults Sutural diastasis: traumatic disruption of suture Combined skull fractures Cysts can form DO CT to look for associated HI

Management: NO surgical intervention if closed; open require irrigation, debridement (bone removal rare) Depressed skull Fractures Definition: the outer table of one or more of fracture edges lies below the normal anatomic level of the inner table of the surrounding skull Presentation: depressed skull segment but this may be difficult to feel b/c of swelling or mobility of the scalp (scalp laceration may not be overlying fracture ­> normal skull under laceration does not r/o depressed fracture) Predisposed to significant underlying HI and complications May penetrate dura and brain CT head bony windows best for dx; also look for other HI Tangential views can help visualize the depressed segment Management Elevation of depressed fragment usually does NOT change focal neuro deficits (due to underlying brain injury) :. rationale for surgery is (i) decrease infection (ii) repair underlying brain injury (iii) cosmesis Closed: elective elevation within days if no associated HI needing OR Open: emergent (<12hr) elevation/repair b/c of risk of infection; remove contaminants, debride damaged tissue, watertight dural closure (essential), cosmetic repair Open skull fracture Scalp laceration overlying a fracture Disruption of paranasal sinus and middle ear also considered open Requires careful I & D for above reasons Basillar Skull Fractures Linear fractures at the base of the skull MC lesion is in the petrous portion of temporal bone Longitudinal #s are much more common (90%) Transverse #s are much less common (10%) High risk for infection: the skull base has no scalp barrier to infection, dura is torn easily and the subarachnoid space is in direct communication with the paranasal sinuses, mastoid air cells, middle ear -----> routes of infection Diagnosis with head CT: about 80% sensitive; suspect clinically Look for: bruising: battle signs orracoon eyes hemotympanum: temporal bone bleeding into middle ear CSF leak: otorrhea, rhinorrhea (ring test: put discharge on filter paper, CSF will form a large transparent ring around the blood b/c it migrates farther on the filter paper). Beta 2 - transfeerrin ? specific marker for CSF leak vascular complications: ICA occlusion, cavernous fistulae, traumatic aneurysms cranial nerve abnormalities(CN pass through the basil foramina) I anosmia, ant fossa # (most common) II #s involving the optic canal

III/IV/VIless common VIII common (50% with transverse petrous) VII common (50% with transv, 25% long) Management NO CSF leak: observe, repeat checks for CSF leak, no px abx CSF leak: observe, may require Sx if doesn't stop spontaneously (most do)

SCALP WOUNDS Can cause significant hemorrhage including exsanguination in severe wounds Hemostasis: direct pressure, lidocaine + epinephrine, staples, sutures, plastic Raney clips Need thorough irrigation, exploration, and debridement Use antibiotic ointment to "plaster" hair out of the way; do not remove hair Must close galea if disrupted Staples can be used if galea not involved

EPIDURAL HEMATOMA Blood collection b/w inner skull and the dura Relatively uncommon May rapidly expand into fatal lesion Pathophysiology Arterial bleeding: 80% are associated w/ a skull # which tears a meningeal artery (middle meningeal is most common), usually detectable within one hour Venous bleeding: 20% are associated with tearing of a dural venous sinus, diploic veins, or middle meningeal vein, bleeding slower and may not be detectable for several hours/day Underlying brain injury is seldom severe Usually unilateral; 40% have other intracranial lesions usually SDHs Note: most common traumatic lesion of posterior fossa (CB findings on physical exam only in 50%) Rare in elderly (b/c of close attachment of dura to periosteum of inner table) and children < 2yo Presentation (30%) Classic: loss of consciousness at time of injury then lucid intervals w/i hours then progression to obtundation, herniation signs ("lucid interval" and "talk and die" syndromes. NOTE: lucid interval not pathognomonic for EDH Symptoms: severe H/A, sleepiness, dizziness, nausea, vomiting ---> coma CT: cresentic, lens shaped hyperdensity underneath skull Prognosis EDH present in 0.5% of all HI pts and 1% of those who present in coma Presents in coma, EDH, mortality 20% Presents not in coma, EDH, mortality nearly 0 %

Management Acute deterioration: intubate (RSI with lidocaine, fentanyl, pentothal, succ - avoid ketamine), elevate head of bed, hyperventilate PaC02 30 - 35 mmHg, mannitol 1 gm/kg bolus, STAT neuro consult for OR, consider Burr Hole if in periphery or unavailability of neurosurgery Immediate craniotomy and evacuation; start with Burr hole in OR for acutely deteriorating Very small EDH: controversial if admission, observation, repeat CT safe

SUBDURAL HEMATOMA Pathophysiology Blood collection b/w dura mater and arachnoid mater usu located over the cerebral convexities Results from tear of bridging veins that extend from the subarachnoid space to the dural venous sinuses; blood then fills the potential space b/w DM and AM More serious than EDH b/c underlying brain damage more severe Common in elderly and alcoholics due to brain atrophy b/c the bridging veins are more easily torn More common than EDH occurring in 30% of severe HI CT: depends on acute, subacute, or chronic Acute SDH Symptomatic w/i 24hrs 50 - 70% have lucid interval followed by declining LOC May or may not have focal findings: anisocoria 50%, hemiparesis 50%, papilledema 16%, CN VI palsy 5% CT: hyperdense, cresentic shaped lesion extending all the way along the hemisphere (usually) Management considerations: size, neurological deficits, increased ICP, overall condition/prognosis of the patient Surgical indications: SDH > 5 mm with mass effect, neurological deficits Observation indications: SDH < 5mm, no mass effect, no neurological deficits Burr holes can be used in periphery with acute deterioration Subacute SDH Symptomatic b/w 24hrs - 2wks Headache, altered mental status, weakness, paralysis CT: isodense lesion Tx: most require evacuation Chronic SDH Symptomatic > 2wks a/f injury Many patients will not recall HI (50%+), especially in alcoholics, thus should be on ddx of altered LOC/weakness etc Head trauma often minor Risks: elderly, alcoholic, epilepsy, coagulopathy Pathology: small bleed, encapsulation, liquifaction, gradual increase or decrease in size CT: hypodense lesion, MRI good 45% will rebleed (hyperdensity on top of hypodensity)

Survival depends on amount of brain damage done by expanding mass; worse in elderly Posterior fossa SDHs rare (1%) and poor survival (5%) Think of child abuse in children 50% will demonstrate unilateral weakness or hemiparesis but the signs may be very subtle decreased LOC 53% hemiparesis 45% papilledema 24% CN III palsy 11% hemianopsia 7% Tx : operative evacuation for symptomatic chronic SDHs (craniotomy, craniostomy, or burr hole) TRAUMATIC SUBARACHNOID HEMORRHAGE Blood w/i subarachnoid space due to tearing of subarachnoid vessels 33% of severe HI Most common CT abnormality seen a/f HI Amount of blood directly correlates with presenting GCS and long term outcome Headache, nausea, photophobia Cerebral vasospasm can cause severe ischemia CT: blood along sulci and in basal cisterns CONTUSION Bruises on the surface of the brain: damage to parenchymal blood vessels Hemorrhage and edema usu occur over crest of gyri with overlying subarachnoid hemorrhage and may be in cout or contracout location MC in frontal & temporal lobes and under depressed skull #s May evolve into intracerebral hematoma Focal neurologic deficits may be present, sz possible Noncontrast CT is best to see CT: small areas of increased density with surrounding edema Mx: observe unless very large shift (removal of contused brain required) INTRAPARENCHYMAL HEMORRAGE/HEMATOMA Parenchymal hemorrhage due to torn blood vessels Most are delayed for days and few are seen on initial CT May cause expanding mass lesion producing herniation 85% are frontal and temporal Mortality if unconscious is about 45% Clinical effects depend on size, location, continued bleeding Intracerebellar Hemorrhage/Hematoma: rare, direct blow to subocciput, very high mortality CT: hyperdensity in the cerebral or cerebellar hemispheres (or deeper) May not be present on CT until few hrs to days after Surgical indications: focal neuro deficits, significant mass effect, decreased LOC, inability to medically control ICP (no surgery if asymptomatic, small, or very deep) SUBDURAL HYGROMA Collection of clear, xanthochromic fluid in subdural space

Traumatic disruption of arachnoid mater at time of trauma leads to chronic CSF leak Is not the same as a chronic SDH 10% of severe HI; may develop acutely or later CT: hypodense (CSF density), looks like chronic SDH Sx of raised ICP Tx: drainage if symptomatic


EPIDEMIOLOGY GSWs by far the most common 75% are dead at the scene Mortality 70% for those that arrive at ED PATHOPHYSIOLOGY Tangential wounds: impact that occurs at an oblique angle relative to the skull Low energy missiles can travel around the scalp without penetrating the skull Non - skull - penetrating wounds still lead to blunt intracranial injuries Perforating wounds, low energy/velocity: penetrate the skull; usually loose a lot of energy when they go through the skull thus little additional penetration of brain tissue Perforating wounds, high energy/velocity: bounce around in skull, can exit anywhere, massive intracranial damage, extremely high mortality MANAGEMENT Intubate regardless of GCS if there is cranial penetration CT head, skull Xrays IV antibiotics, seizure prophylaxsis

COMPLICATIONS AFTER HEAD INJURY POSTTRAUMATIC SEIZURES Acute = < 24hrs Subacute = 24 - 48hrs Chronic = > 48hrs and persistent Common POSTCONCUSSIVE SYNDROME Headaches, memory loss, poor concentration, behaviour problems in kids, dizziness Normal physical exam No specific Mx POSTTRAUMATIC CNS INFECTIONS Meningitis Typical presentation Especially common with basilar skull #s with CSF leak Early = pneumococcus Late = gram -ves Brain Abcess Most common after penetrating trauma H/A, N/V, increased ICP, focal neuro signs in 50% Cranial Osteomyelitis Pain, tenderness, warmth at site of penetration MEDICAL DIC: tissue thromboplastic activatiors of clotting system Neurogenic pulmonary edema (similar to ARDS) Cardiac dysfunction: arrythmias in 50% with ICH, 70% with SAH


ASSESSMENT OF HEAD INJURY History (Box 31-1) Prehospital personnel Patient condition a/f truama: respiratory effort, duration of LOC, verbalization, mvmt, changes in GCS MOI, time of injury, presence of lucid interval , Drug, alcohol use Pmhx, Meds, allergies Vital Signs Elevated BP may be cushing's relex (HTN and bradycardia) Hypotension rarely due to head injury Can get neurogenic shock from BS lesion (rare) Glascow Coma Scale Level of consciousness is single most important factor Designed for determination at 6 hours GCS has limitations and treatment/prognosis should not be soley based on GCS NEUROLOGICAL EXAMINATION Respiratory Pattern 123-2 Bradypnea (<8/min): EtOH, narcotics, BZD, barbituates Tacchypnea (> 20): many causes Cheyne - Stokes: bilateral cortical or diencephalon, unilateral pons/medulla, CHF, hypoxia, metabolic changes Apneustic Gasp Breathing: usually pontine lesion Ataxic: irreggular rhytm and depth, medullary lesion, impending arrest Posture Decorticate (flexion): spontaneous flexion of wrists, elbows, adduction and internal rotation or the arms, severe bilateral damage above midbrain (de cortex) DecErebrate (Extension): E for Extension; spontaneous extension of the elbows and wrists with adduction of armsdamage in midbrain or diencephalon; can be present regardless of the structural location of the lesion Strict correlation is poor and acute lesions often cause extensor posturing regardles of anatomical lesion Sensory/Motor Abduction avoidance of a limb is a purposeful cortical mediated response

Adduction, flexion, or extension may occur as a reflex Triple flexion of the LE is a SC reflex and does not imply intact BS or CRTX Crossing midline indicates cortical function DTRs are SC reflexes Spontaneous mvmt important Brain stem reflexes: yawning and sneezing require some cortical function and intact brainstem Cough, swallow, and hiccup do NOT imply intact brain stem Purposeful movements: shifts in posture, reaching toward face, crossing midline with arm/leg, crossing feet -----> all indicate lighter coma and better prognosis Cranial Nerves Pupil Size and reactivity important Midbrain lesion interrupts parasympathetic fibers in Edinger - Westphal nucleus on CN III thus dilated pupil (mydriasis) Pons lesion or below interrupts sympathetic fibers thus pupils are constricted (miosis) Reactivity is a II - III reflex Remember that the parasympathetic fibers are on the outer part of CN III thus early compression of the nerve may cause dilated pupil w/o ptosis and laterally deviated eye Nearly all metabolic causes have reactive pupils (even though they may be very sluggish) Fundoscopy Signs of increased ICP: Papilledema, absent SVP Papilledema dev'ps slowly and absence is NOT reassuring Layered subhyaline blood with SAH DM, HTN, frank hemorrhage EOM

Most important b/c nuclei are very close to RAS Resting position? Spontaneous mvmt? ADducted: CN VI BS or peripheral lesion ABducted: CN III BS or peripheral lesion Horizontal dysconjugate gaze: drowsiness Vertical dysconjugate gaze (skew deviation): pons or CB Sustained downward conjugate gaze: variety of disorders Sustained upward conujugate gaze: hypoxic encephalopathy

Brainstem Reflexes Pupillary light reflex: II - III Gag: IX - X Corneal: V - VII Occulocephalics: VIII - III, IV, VI Normal BS reflex is to keep eyes midline by turning them away from the direction of head movement; serves to keep eyes midline to protect from approaching objects Abnormal is when eyes follow head mvmt AVOID until C-spine cleared

Terminology confusion when recorded as Doll's eyes present

Occulocalorics Normal BS reflex is COWS: fast phase is cold water opposite and warm water - same Safe to do w/ C-spine injury, check for intact TM Elevate bed 30 degres or Trendelenburg with C-spine injury, irrigate with 10 ml ice water Normal response is fast phase opposite and slow phase towards Absence of quick correction to midline indicates loss of cortex No response at all indicateds loss of pontine function Sustained deviation toward stimulus for 30 - 120 seconds indicates an intact brainstem Cannot voluntarily resist and a normal response in a "comatose" patient should make you think psychogenic

Miscellaneuos look for s/s of basal skull #: battle signs, raccoon eyes, otorrhea, rhinorrhea, hemotympanum, CN I, II, VII, VIII Diagnostic Tests C-spine X rays AP and lateral skull X rays CT head scan (w/ bone windows ------ don't need XR) Skull Xrays: bone windows on CT better Main indications for head CT in the head injured pt persistent decreased level of consciousness clinical neurological deterioration persistent focal deficit or mental status deficit skull #s in vicinity of middle meningeal atery or major venous sinuses Labs: cbc, urea, creatinine, lytes, LFTs, PT, PTT, ABGs, urinalysis, ethanol level, tox screen, type and cross skull , C-spine, CXR, pelvic X rays


INTRODUCTION GCS b/w 3 - 8 or the presence of intracranial contusion, hematoma, laceration 10% of all head injuries that survive to hospital 60% have other associated major trauma :. must look for 40% mortality; only 7% reach good outcome/moderate disability INITIAL ED MANAGEMENT OF SEVERE HEAD INJURY Airway Management Early endotracheal intubation is most important aspect of management Intubate anyone with GCS < 8 or GCS > 8 with other reasons to be intubated Rapid Sequence Induction Pretreatment: pavulon/rocuronium, lidocaine and fentanyl


to blunt the increased ICP response to intubation Induction: pentothal drug of choice if NOT hypotension, etomidate good but not available yet, fentanyl + versed or lower dose pentothal are other options Parlaysis: succinylcholine Note: crash intubation --> only lido + fentanyl for cerebral protection (no induction/paralysis needed)

Hyperventilation to produces PaC02 of 30 - 35 mmHg Temporarily decreases ICP by promoting cerebral vasoconstriction and reduction of cerebral blood flow Drops ICP by 25% in acute phase; doesn't work a/f acute phase PC02 < 25 may cause profound vasoconstriction and cause ischemia Prophylactic hyperventilation has been shown to have WORSE prognosis at 3 and 6 mo post injury in severe head trauma without signs of increased ICP; thus only do if signs of increased ICP: herniation syndrome, cushing's reflex, papilledema Hypoxia and hypotension are important causes of deterioration General rule: hypotension in the HI patient is due to another cause (note: preterminal head injured can be hypertensive (cushing's) or hypotensive (medullary failure and loss of sympathetic tone) Hypotension can be a terminal finding but must look for associated injuries which occur in 60% Scalp lacerations can bleed a lot and cause hypotension Peds: concealed scalp bleeding can cause hypotension PE unreliable: indication for objective evaluation (CT, DPL, ABUS) Delayed fluid resuscitation does NOT apply to head injured and fluid resuscitation should aim for SBP > 90 mmHg; fluids should not be withheld in fear of increasing ICP - studies show the opposite - pt do worse without fluids; hypotension is the worst scenario for head injured Laparotomy for hypotension takes priority over head CT



GCS: responsive, follow commands, painful stimulus Pupils: size, reactivity, symmetry Extremely important to obtain mini-neurologic examination before sedation or paralyzing agent Secondary survery Look hard for associated injuries More complete neuro assessment Head CT

Should be done ASAP, repeat w/ any change An actual shift of 5mm or greater is generally considered to be significant in pts w/ head trauma and usu indicates Sx is needed

INVESTIGATIONS Laboratory: trauma panel Head CT: indicated in ALL severe head injuries Head MRI: better for ischemic lesions, chronic lesions, BS and posterior fossa lesions Angiography: consider when CT scanning unavailable DISPOSITION Early neurosurgical consultation Transfer all severely head injured patients to site with neurosurgery Must triage other injuries in multitraumatized pt: abdomenal injuries may take precedence over head injuries; may even be too unstable to get CT

INTENSIVE CARE MANAGEMENT OF SEVERE HEAD INJURIES General Minimize secondary insults Determinants of outcome: time to neurosurgical intervention, oxygenation, SBP, time with ICP > 20, arterial vasospasm, episodes of desaturation, level of cerebral perfusion pressure Goals: Euglycemia, Euthermia, Euboxia, Euvolemia, Normotension Hypothermia: may play a role in severe HI management, being studied Monitoring: arterial line, CVP line, ICP monitors ICP monitoring shown to decrease mortality Positioning: 15 - 30 degree elevation of head to decrease ICP Maintain fluid balance Oxygenation Brain VERY sensitive to hypoxemia b/c left shift of oxygen - Hb dissociation curve secondary to respiratory alkalosis thus reduced offloading of oxygen at the tissues Dysregulation of CBF and vasospasm lead to cerebral ischemia/infarction Intubation required with severe head injury to optimize oxygenation Pa02 should be kept > 80 mmHg Ventilation PaC02 target of 30 - 35 mmHg Sedation to allow improved ventilation Effective ventilation decreases atelectasis, decreases work of breathing, decreases pulmonary edema Positive pressure ventilation helps prevent atelectasis and pulmonary edema (secondary to sympathetic excess --> ARDS) PEEP is required for advanced pulmonary insufficiency and pulmonary shunting when Pa02 can't be increased despite high Fi02 PEEP does decrease CO and raises ICP but is safe if < 15 cmH20 Target PaC02 30 - 35: Hyperventilation PaC02 can lead to significant ischemia/infarction

PaC02 < 30 shown to increase morbidity/mortality Only hyperventilate with signs of increased ICP, NOT indicated for head injury w/o signs of increased ICP

Pulmonary Status Watch for ARDS, neurogenic pulmonary edema, atelectasis, fat embolism Deteriorating resp status: increase Fi02, increase PEEP up to 15 cmH20 (if ICP tolerates) Fat emboli: decreased respiratory function, petechiae on chest/conjunctiva, decreasing neurologic function ----> manage with positive pressure ventilation, volume, steroids, ? heparin Blood Pressure Control hypertension if SBP > 180 (loss of autoregulation) Labetolol, esmolol, nifedipine (sodium nitroprusside contraindicated b/c of cerebral vasodilation and aggravation of increased ICP) Ensure adeuate intravascular volume (CVP monitoring) Steroids NO evidence for benefit, do not reduce edema post trauma, no reduction in morbidity/mortality NOT recommended Seizure Prophylaxis Early post-traumatic seizures in up to 9% (up to 42% in penetrating) Seizure increase ICP and worsen secondary brain injury: disastrous Indications: all severe HI (GCS < 8), depressed skull #, seizure at any time, history of seizures, SDH/EDH/ICH, penetrating trauma Phenytoin load (1000mg): 500 mg bolus (50 mg/min over 10 min), 250 mg over 6hrs, 250 mg over 12hrs Pheytoin maintenance: 100 mg iv q6-8hr Seizure Mx: Ativan (1 - 2 mg iv q 5min up to total 4 mg) first line Antibiotic prophylaxis Indications: penetrating head trauma, open skull #, complicated scalp lac Not indicated for otorrhea/rhinorrhea

INCREASED ICP MANAGEMENT ED managemnt of acute deterioration Intubation, hyperventilation, elevate head of bed, mannitol 1 gm/kg bolus, head CT (may skip), stat neurosurgical consultation for evacuation, burr hole if in periphery or neurosurgery not immediately available ICU management of increased ICP Elevate head of bed, sedation, oxygenate, ventilate, control BP, seizure prophylaxis, metabolic support, ICP monitoring (see chapter on ICP monitors) Consider repeat head CT if difficulty controlling ICP or significant changes Mannitol bolus 0.25 - 1.0 g/Kg iv given over 5 min careful with hypotensive pt b/c it can aggravate hypotension draws fluid into vascular space providing more space osmotic effect w/i minutes, peaks at 1 hour; lasts up to 8 hrs also promotes cerebral blood flow by reducing viscosity,

increases oxygen carrying capacity by reducing rbc deformity, free radical scavenger alters urinary output for monitoring fluid status can induce renal failure can get concentrated in brain with an open BBB and reverse the osmotic effect to drawing fluid into the brain should not be used unless signs of increased ICP exist (shown to increase mortality if used without increased ICP) monitor I/Os, lytes, osmolarity can't use if osmolarity > 320 mOsm/L (risk of renal failure) add lasix 0.5 mg/kg iv if positive fluid balance, high CVP, increased pulmonary capillary wedge pressure increased ICP despite mannitol: ? repeat bolus, ? how often, ? infusion Ventricular Drains intermittent drainage of CSF (can't monitor ICP with continuous drainage) set drainage catheter 15 - 20 cm above foramen of Monroe indications for drainage: ICP > 20 mmHg X 2 min not associated with suction, cough, mvmt, procedure open drain for 5 - 10 min repeat as needed up to several times per hour Barbituates lowers ICP but has significant complications (hypotension) must have art line, swan ganz, and EEG monitoring contraindications: liver or renal failure phenobarbital: 50 - 100mg iv bolus, ? followed by infusion, continue until MAP < 80 (decreases CPP to 60 - 70), d/c after ICP < 20 mmHg X 24 - 48hrs, wean by 50% dose each day Surgery if medical management of increased ICP fails, removal of brain tissue may be required


INTRODUCTION 10% of all head injured Neurophysiological outcome dependant upon aggressive management to prevent hypoxia and hypotension and further increases in ICP Approach as per severe head injury CLINICAL FEATURES Wide variety of presentations w/ GCS b/w 9 - 13 May or may not have focal neuro findings Amnesia, headache, seizures, facial trauma, and asssociated injuries are imp to think about 40% will have abnormal CT 10% will lapse into a coma Head CT mandatory

DISPOSITION ALL should be admitted for observation, even if CT normal Frequent neuro checks Repeat scan in 48 hrs if not improving COMPLICATIONS Mortality is 20% with isolated moderate HI 3 months: 90% have memory deficits, 70% unable to work, 90% have persistent headaches Permanent deficits in 50% MRI may help in investigation of complications


INTRODUCTION 80% of all head injuries GCS 14 - 15 with isolated HI Variable presentation CLINICAL FEATURES Transient disorientation, confusion, or amnesia Careful physical exam for neuro deficits Decide on high risk vs low risk to determine need for CT Box 31 - 6 High risk: focal neuro findings, skull #, multiple trauma, distracting injury, initial GCS < 13, LOC > 2min, post confusion/amnesia > 20 min, skull fracture, worsening headache, vomiting, sz, bleeding disorder/anticoagulation, intoxicated, unreliable hx, suspected child abuse, age > 60 or < 2 Low risk: no focal findings, no distracting injury, not intoxicated, no LOC or amnesia, trivial mechanism, accurate history, injury > 24hrs ago, reliable home observers Loss of consciousness LOC is not an accurate predictor of severity of HI Overestimated by most Defined different by many Outcomes 3% of minor head injuries deteriorate unexpectedly ("talk and die") <1% have surgically significant lesions Skull Xrays Limited use May be used as screen if CT unavailable Skull #, shift of calcified midline pineal gland, pneumocephalus, fluid in sinuses, foreign bodies Head CT Do all minor head traumas need head CT? NO NOT intoxicated low - risk patient who is fully awake, no neuro focal findings, no major distracting injuries, not multitrauma, no clinical evidence

of skull # ------------------> responsible home observation for 24 hr (no CT) Intoxicated low risk patient ------------> ED observation until sobriety with q1hr neuro vitals, consider head CT early if not improving Intoxicated high risk patient: do CT

DISPOSITION D/C home after normal examination and observation X 4 - 6hr Discuss HI sheet and what to look for and when to return D/C with reliable observation if possible otherwise observe longer in ED Minor HI returns to ED for second visit: look long and hard for complications (do CT??)


INTRODUCTION Concussion = temporary and brief interruption of neurological function after head trauma Mild concussion = confusion +/- amnesia without LOC following blunt head trauma Classic concussion = brief LOC following blunt head trauma Wide range of neurological symptoms: seeing stars, feeling nauseated or dizzy, disorientation, brief LOC for seconds to minutes Time of presentation: GCS 15, headache, dizziness, amnesia for event (length of amnesia generally correlates with severity of event) which usually resolve by 6hrs Children: restlessness, lethargy, vomiting, pale, tachycardic MANAGEMENT Head CT usually not needed but normal if done Manage as per minor head injury CONCUSSION AND SPORTS Sideline evaluation MSE: orientation (months of year in reverse), memory (who playing, president, etc) Neuro: pupils, F/N, gait, rhomberg, tandem Provocative: sprint, push-ups, sit-ups Grading 1 Confusion without amnesia, no LOC Remove from game, examine q5min for amnesia, may return to game if no symptoms present and no amnesia dev'ps in 20 min Grade 2 Confusion with amnesia, no LOC Remove from game and no return, examine frequently and next day, no return to practice until 1 week without symptoms Grade 3 Loss of consciousness Transport to hospital, return to practice until 2 weeks after no symptoms


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