PSGS MASTERCLASS NEUROSURGERY REVIEW RHOBY U. ORATA, MD, MMHOA FAFN,FPCS journey of aNeurosurgery * Content Area- Surgical Specialties (Neurosurgery) Topic- Head/Spine Trauma Expected Questions- Problem/solving analytical type etc ON Soe NOMUN CN 1A) aaa Ve ele Le OPTIONS Surgical Cases, DETECTION AND MANAGEMENT OF COMPLICATIONS and OVER ALL CARE of the patients. (oo) Natural history, clinical course and basic pathology/pathopysiology OVERVIEW Neurologic and surgical emergencies Glasgow coma scale Traumatic brain injury Spinal cord injury Case based discussionNeurologic and Neurosurgical emergencies a ereecd (es = ICP is normally 4 and 14 mmHg. = levels above 20 mmHg can injure the brain « The Vionro-Ke) ie cocirne states that the Colg= Tale |INYce1 0] [ot n= 1a | therefore, the total volume of the contents determines ICP. PRAM Colma ean Rereya CNM OLE UL MCLE AVELU 1h brain tissue, blood, and CSF = The brain’s contents can expand due to swelling from traumatic brain injury (TBI), stroke, tumors or reactive edema.Le Monro-Kellie doctrine - hydrocephalus ae eo ey) fer Tare 4 = Increased ICP can injure the brain in several ways.TENTORIAL HERNIATIONAlateral): FUNIRTEELEXDanding masetauses SUBFALCINE ‘MIDLINE’ SHIFT: occurs early tentorial{(uncal) Herniation as, "7 With UNTTSCEPET SHBCE-OCCUYIng lesions. the mediaedge of the temporal Seldom produces any clinical effect, ‘~~. although ipsilateral anterior cere: bral artery occlusion has been recorded. lobe herniates through the tentorial hiatus. As the intracranial pressure continues to rise, ‘central’ herniation follows. |. TONSILLAR HERNIATION: a ‘BOBYERtOTIAN expanding mass causes herniation of the cerebellar tonsils through the foramgn.magnum. A degree of upward parniation / | through te tentorial hiatus may also occur. Clinical -NTORIAL HERNIATION "~ ke Sie effects are difficult to distinguish from effects of swelling of te earetral direct brainstem/midbrain hemispheres results in a compression. vertical displacement of the midbrain and diencephalon through the tentorial hiatus. Damage to these structures occurs either from mechanical distortion or from ischaemia secondary to stretching of the perforating vessels. Brain Herniation Patterns ese) eor a Mett Laced a) Sa TSSTLE RoR MU Cm eects oe Dares Rien c ei Pe Meee + The uncus (medial temporal lobe gyrus) shifts medially and compresses the Re eae sc ICME 3. Central transtentorial herniation. Re ee en eee Nae AR eu ST) Bilaterally small Pam)Uncal herniation. + The uncus (medial temporal lobe gyrus) shifts medially and compresses the midbrain and cerebral peduncle. * PCA- occipital infarct . Central transtentorial herniation. + The diencephalon and midbrain shift caudally through the tentorial incisura. Cet eveole-| arcane gore) om 00) + Respiratory irregularities Sa lanlor-Ugro eon raro ao)ee YY ead) Cardiorespiratory impairment Systemic hypertension Cheyne stokes respiration Neurogenic ventilation Impaired consciousness a ereecd (es = often will present with headache, nausea, vomiting, and progressive mental status decline. B is the classic presentation of hypertension. = should undergovy Initial management of intracranial hypertension 1. Airway protection and adequate AUT iCoda) 2. Bolus of up to 1 g/kg -free water diuresis, -increased serum osmolality, and -extraction of water from the brain. (effect is delayed by about 20 minutes and has a transient benefit) . Ventriculostomy and/or craniectomy - Definitive decompression a eeu Compression oT can cause mass effect that can rapidly kill the patient in two ways . can lead to acute obstructive = mass effect can lead to = brain stem compression:«A patient came in with head trauma «What are you going to do? a to assess your patient » Prehospital medical personnel should provide = critical parts of the history PMU On- SEU RRO AD [UB See ae NCU Una ue o (ROS) Sa Cue Se UMC Aan verbalization, and movement of extremities. = Clinically important features of the neurologic Claire = mental status and GCS aT eos emcee AURIS SUM amie acto) = motor, sensory, and brainstem function PeaNut ee tte Cems recur Feros4 Classification of Head Injury = GCS( Glasgow Coma Scale)- universal grading for severity of head injuries. Clinical tool for rapid, reproducible assessment/detection of neurologic deterioration = Head Injury Severity Scale vy Glasgow coma scale = Dr Jennet and Dr Teasdale , 1974 = Institute of Neurological Science of Glasgow » Reliable, universal and objective test for the level of consciousness of head trauma patients = Initial and subsequent monitoring can be done = 3 components:BE eee OC Rn Se eye opening sao) Yel ay a= LotR Ce) (Gennaio pre er to pressure on the patient's fingernail bed if this does not elicit a response, supraorbital and sternal pressure lata loney mete) Seton ace (Not to be confused with an awaking of a sleeping person; such patients receive a score of 4, not 3.) a Vone)—alaled Nene eS sounds. (Moaning but no words.) b (Random or exclamatory articulated speech, but no conversational exchange) ‘ Wai clemag cee Reka ens Sansa ata usa EG contusion) a (ie Wiop SRS Tole Reo ML NAN! Fro elgol SENN MMe Moco AU eg eh uated or caiet ar tals and age, where they are and why, the year, month, etc.)ironetelao to pain (. of arm, external Ronee cnel ite ene acon ames onnod Rata response ) I to pain ( rua Mca hexeukom nelle cn euon ciao ane moo) a (flexion of elbow, supination of forearm, flexion of wrist when supra-orbital pressure applied ; pulls part of body away when nailbed pinched) to pain. (Purposeful movements denenas painful stimuli; e.g., hand crosses mid-line and gets above clavicle when supra-orbital pressure applied.) (The patient does simple tal HEMEL 16 years of age presenting to emergency department within 24 hours of injury, with admission GCS score of 14 or 15 and no multisystem trauma (ACEP/CDC joint practice guidelines?) Loss of consciousness or posttraumatic amnesia? Subacute or chronic TBI with persistent symptoms or neurological deficits: + MRI may be preferable to CT for detection and characterization of nonsurgical lesions in the subacute or chronic stage*” Role of advanced neuroimaging: + DTI, (MRI, PET, SPECT, perfusion CTIMRI, MR spectroscopy may have utility in better understanding selected patients but are not yet considered routine in clinical management of TBI? Yes No Noncontrast head CT indicated Noncontrast head CT should be for’ considered for + Headache * Focal neurological deficit * Vomiting * Severe headache * >65 years of age * Physical signs of basilar skull fracture * GCS score <15, jeagulopathy * Dangerous mechanism of injury (ejection from motor vehicle, pedestrian struck by motor vehicle, fall from >3 feet or >5 stairs) + Voriting © >60 years of age ‘© Drug or alcohol intoxication ‘* Deficits in short-term memory ‘* Physical evidence of trauma above clavicle Posttraumatic seizure * GCS score <15, + Focal neurological deficit * Coagulopathyq en 1. Low risk for intracranial injury — asymptomatic Beare (let me 24) — scalp hematoma, laceration, contusion, or abrasion — no history of loss of consciousness + In this group, there is an (ICI) (incidence of ICI: <8.5 in 10,000 cases with 95% Cl) r Category 1. Low risk for intracranial injury = Management recommendations i ed CLS oM- KM O ME -TeOLMNTENTA Le =70| = Linear non-displaced skull fractures in this group require no treatment, although in-hospital observation (at least overnight) may be considered.LZ ategory 2. Moderate risk for intracranial injury Table 54.7 Findings with moderate risk of ICI history of change or loss of consciousness on or after injury progressive H/A HOH or drug intoxication posttraumatic seizure unreliable or inadequate history (unless trivial injury) posttraumatic amnesia signs of basilar skull fracture multiple trauma serious facial injury . possible skull penetration or depressed fracture suspected child abuse ificant subgaleal swelling?! vy Category 2. Moderate risk for intracranial injury Management recommendations = 28-46% of patients with minor head injury (MHI) have an intracranial lesion (the most frequent finding was hemorrhagic contusion) unless CTscan not available.vy Category 2. Moderate risk for intracranial injury maybe sent home if: initial GCS= 14 patient is now neurologically intact (amnesia for the event is acceptable) BoM SMe MeeS else] eared SIR ULCS patient patient has reasonable access to return to the hospital SS als -10 Te) no “complicating” circumstances (e.g. no suspicion of domestic violence, including child abuse) le Category 3. High risk for intracranial injury = Criteria = depressed level of consciousness not clearly due to EtOH, drugs, metabolic abnormalities, postictal, etc. focal neurological findings decreasing level of consciousness penetrating skull injury or depressed fracturevy Category 3. High risk for intracranial injury » Management recommendations = 1. admit to hospital =» 2. STAT unenhanced head CT scan = 3. if there are focal findings on neurologic exam racranial Hematomas = Skull fx — most important risk factor in IC hematoma 1) EPIDURAL Pans] oe [0] | 3) Intracerebral= Ina patient with head trauma, the plates revealed a OVATHON eaten el LAM OTe MURR glee tet MM eKel ode TL findings are consistent with a: Pow Nee oR ote Oe MME LOL] B. Subarachnoid hemorrhage Con MUSEO D. Hemorrhagic contusion of the temporal lobe » Fracture » Epidural hematoma » Subdural hematoma » Subarachnoid hemorrhage » Cerebral contusionHematoma between skull and dura fal ta Source of bleeding: ae ela Ali) Sire fel} meningeal artery 2 to pterional fracture( bone) B. bleeding from - diploic bleeding Cc. - superior sagittal, transverse Lentiform/ lens shape/ bi-convex Non contrast CT N SS EALRight Hematoma between dura mater and arachnoid layer Source of bleeding: Tear in RU ees ele Nol MMe n Coal ey Associated with increase ICP OMe CliN ar |m@ale tt 8)Bleed between arachnoid and pia mater ( subarachnoid space) SCOR ETO) 2. ruptured aneurysm- worst headache - diagnostic procedure of choice for aneurysm PMU}primarily in the cortical tissue, especially under the site of impact or in areas of the brain located near Salem iele( MoM UM Ie ROL SF During sudden deceleration of the head causes the brain to impact on bony prominences(frontal, temporal, occipital= Ina patient with head trauma, the at the R Temporal area with slight midline shift. There was cerebral edema. The radiographic findings are consistent with a: Pa RT eee B. Subarachnoid hemorrhage C. Epidural hematoma D. Hemorrhagic contusion of the temporal lobe = AI5 year old boy accepted a dare and dove head first into the sea from pile of rocks. When he did not surface right away, his friends found him unconscious and flaccid all over. When he woke up, he still could not move his extremities. Patient could possibly still be in spinal shock. The end of this condition may be heralded A A. Positive bulbocavernosus reflex Rest VoM er UN Cea sln4 C. Return of motor function D. Return of sensory functionCla Coole Tafa Ae is National Emergency X-Radiography Utilization Study Criteria: Cervical Spine Imaging Unnecessary in Patients Meeting These Five Criteria Absence of midline cervical tenderness Normal level of alertness and consciousness No evidence of intoxication Absence of focal neurologic deficit Absence of painful distracting injury Canadian Cervical Spine Rule for Radiography: Cervical Spine Imaging Unnecessary in Patients Meeting These Three Criteria There are no high-risk factors High-risk factors include: that mandate radiography. Age 65 years or older A dangerous mechanism of injury (fall from a height of >3 ft; an axial loading injury; high-speed motor vehide crash, rollover, or ejection; motorized recreational vehide or bicycle collision) The presence of paresthesias in the extremities There are low-risk factors that Low-risk factors include: allow a safe assessment of Simple rear-end motor vehicle crashes range of motion. Patient able to sit up in the ED Patient ambulatory at any time Delayed onset of neck pain Absence of midline cervical tenderness The patient is able to actively Can rotate 45° to the left and to the right rotate his/her neck.CEG iE) EEE indications for Thoracic and Lumbar Imaging after Trauma Mechanism Gunshot High energy Motor vehicle crash with rollover or ejection Fall > 10 ft or 3 Pedestrian hit by car Physical examination Midline back pain Midline focal tenderness Evidence of spinal cord or nerve root deficit Associated injuries Cervical fracture Rib fractures Aortic injuries Hollow viscous injuries vy Spinal Cord Injury » Spinal shock 24-48hrs monitoring anal sphincter contraction in response to squeezing the glans penis or tugging on an indwelling Foley catheter Returns after spinal shock=» Lack of motor and sensory function after the reflex has returned indicates complete SCI. = Absence of this reflex in instances where spinal shock is not suspected could indicate a lesion or injury of the conus medullaris or sacral nerve roots = Injury above T6 autonomic dysreflexia Cole} Ce Ta) (ULNA) injury Brown sequard syndrome Anterior cord syndrome Central cord syndrome Posterior cord syndromeIpsilateral loss of motor function, proprioception, vibration, and light touch. Contralateral loss of pain, temperature, and crude touch sensations motor function, pain sensation, and Alu et RSTO mecie Proprioception and sense of vibration impairment in the arms and hands and, to a lesser extent, in the legs. Loss of proprioception Posterior spinal artery/ damage to posterior columnFEE incomplete spinal Cord Syndromes Syndrome Etiology Symptoms Prognosis* Anterior cord Direct anterior cord Complete paralysis below the Poor compression lesion with loss of pain and Flexion of cervical spine —_ temperature sensation Thrombosis of anterior Preservation of proprioception spinal artery and vibratory function Central cord Hyperextension injuries Quadriparesis—greater in the Good Disruption of blood flow —_ upper extremities than the lower to the spinal cord extremities; some loss of pain Cervical spinal stenosis and temperature sensation, also greater in the upper extremities Brown-Séquard Transverse hemisection of | Ipsilateral spastic paresis, loss of _ Good the spinal cord proprioception and vibratory Unilateral cord ‘sensation, and contralateral compression loss of pain and temperature sensation Cauda equina _Peripheral nerve injury Variable motor and sensory loss Good in the lower extremities, sciatica, bowel/bladder dysfunction, and “saddle anesthesia” *Outcome improves when the effects ‘of secondary injury are prevented or reversed. Incomplete Spinal Cord Syndromes Brown-Sequard Syndrome ‘Typically, this syndrome is the result of penetrating trauma causing hhemi-section of the cord via direct injury. Findings include loss of ipsilateral position and vibratory sense, ipsilateral motor lossand ‘contralateral loss of pain and temperatureone to two levels below the lesion(Figure 11.8). Central Cord Syndrome ‘This injury pattern is most often found in cervical hyperflexion, as may result from motor vehicle collisions. Findings include loss of motor function, typically greater in the upper extremities than the lower, However, complete quadriplegia may result. Typically, the spinothalamic tracts are spared or minimally involved (Figure 11.8). Anterior Cord Syndrome (Often the results of cervical hyperextension, this results in the loss of ‘motor, pain, and temperature function bilaterally below the lesion while vibratory and position sense remain intact. This syndrome may also result from thrombosis of the anterior vertebral artery or direct anterior ‘trauma (Figure 11.8).«Thank you!