closed head injuries Flashcards
head trauma
-Men>Women
-Trimodal: Ages 0-4, 15-24, >75 yo
-MC MOI: !Falls, !MVA, pedestrian/bike, projectiles, assaults, sports, abuse
-Common findings: LOC, scalp hematoma, vomiting (13%), headache (46%)
-Complications: Post-traumatic seizure (1%), skull fractures , bleeds, concussions
-Pertinent historical questions:
-High risk MOI: falling >3-5 feet, MVC, penetrating trauma
-LOC
-Confusion
-Seizure
-Severe or worsening headache
-Vomiting
-AVM or bleeding disorder
-Child: Acting normally?
-Pertinent exam and findings
-GCS
-Neuro exam and MSE
-Hematoma and location
-Scalp fracture: scalp tenderness ± depression
-Basilar skull fracture: Hemotympanum, battle signs, raccoon eyes
-Child: Bulging anterior fontanelle
traumatic brain injury
-brain function impairment as a result of external force
-Clinical manifestations are broad: brief confusion, coma, disability, death
-Measure severity using GCS -> mild, mod, severe
TBI primary and secondary phase
-Primary phase
-Occurs at the time of impact
-Due to bleeding! or direct trauma!
-Includes:
-Hematoma (EDH/SDH)
-SAH
-Contusion
-Diffuse axonal injury
-Secondary phase
-Days/hours laters
-Caused by impaired cerebral blood flow!
-Causes:
-Edema / ↑ ICP
-Small vessel bleed
-Inflammation
-Physiologic dysfunction
-Often the cause cognitive difficulties
GCS
-mild brain injury ≥ 13
-Moderate brain injury 9-12
-Severe brain injury ≤ 8
-8-> intubate
-mild- 13-15 -> utilize scoring tools, ?head CT, 80%
-concussion
-9-12 -> moderate 10%, head CT
-3-8 -> severe, head CT!!
-40% mortality
canadian head CT rules:
-Only applies to patients with a GCS 13-15 and at least one of the following:
-LOC
-Amnesia to the head injury event
-Witnessed disorientation
-Exclusion criteria
-Age <16 years old (not studied in this population)
-Blood thinners
-Seizures after injury, or, anticoagulation use
-CT head rules
-HIGH sensitivity 83-100% for clinically important brain injuries
-HIGH sensitivity 100% for injury requiring neurosurgery
-No false negatives for serious injury!
-if YES to any in pic -> CT head
PECARN: pediatric head CT rules
-PECARN was developed to determine which patientsDO NOTrequire a CT scan
-PECARN screening tool for pediatric patients
-One for children less than 2 years
-One for children 2-16 years old
-If GCS<15 they require CT
-Severe mechanism:
-MVC + -> Ejection, rollover, vs. pedestrian, death at scene
-High impact object
-Fall >3ft (<2yo) or >5ft (>2yo)
-CT in children -> risk of brain cancer
concerning findings in kids
-basilar skull fracture- raccoon eyes (tarsal plate sparing), halo sign, postauricular ecchymosis, hemotympanum (1st sign -> do ear exam!!!)
-orbital fracture
-occipital scalp hematoma (non frontal)
-depressed skull fracture
TBI: mild, moderate, severe
-Mild TBI (mTBI)
-Trauma induced alteration in mental status : GCS 13-15 ± brief LOC (<30min)
-“Mild” is a misnomer
-mTBI may lead to significant, debilitating short- and long-term sequelae.
-Often used interchangeably with “concussion”
-However, by definition, a concussion describes the S&S that occur after a mTBI
-Moderate TBI: GCS 9-12
-Severe TBI: GCS ≤8
concussions
-Functional not structural injury
-Shear forces disrupt neural membranes, allowing potassium efflux into the extracellular space, causing increases of calcium and excitatory amino acids, followed by further potassium efflux and subsequent suppression of neuron activity.
-MC in elderly = Falls
-MC in young = MVC
-Risk factors:
-Previous concussions
-Younger age
-High risk sports (football, ice hockey, lacrosse, rugby, womens soccer)
-Female > male
concussions: signs and symptoms
-Symptoms
-Confusion and Amnesia (hallmarks)
-Retrograde amnesia: loss of recall for events immediately before
-Anterograde amnesia: loss of recall for events immediately after
-Repeating same questions
-With or Without Preceding LOC
-Other early symptoms: headache, fatigue, dizziness, lack of awareness or surroundings, nausea/vomiting, unsteadiness, mental fogging/slowing, concentration difficulties
-Can occur up to hours after
-Late symptoms (hours/days): mood or cognitive disturbances, sensitivity to light/noise, sleep disturbances
-signs:
-Incoordination
-Neuropsychiatric impairments
-Vacant stare
-Delayed verbal expression
-Inability to focus
-Disorientation
-Slurred or incoherent speech
-Emotionality! out of proportion
-Memory deficit!
-No focal neuro deficits
concussion dx
-Testing
-Neuro exam
-Mental status exam
-Standardized assessment of concussion (SAC) or Sport concussion assessment tool (SCAT5)
-Consider CT head non-contrast based on Canadian CT head or PECARN criteria
-Diagnosis
-Hx of head injury ± brief LOC
-Neurologic symptoms- Confusion/memory loss
-GCS
concussion/MTIBI tx
-Observation for 24 hours
-Physical and cognitive rest 24-48 hours- Gradual return to activity
-Analgesics for pain
-avoid medications that alter cognition (opioids, tramadol, muscle relaxers, benzos, ETOH, ilicit drugs)
-Referral to concussion specialist
-Physiatrist, sports medicine, neurologist
-Prolonged symptoms >21 days
-Multiple concussion history
-Uncertain diagnosis
-Return to play
-All LOC -> ER for evaluation
-Suspected C-spine injury -> immobilize, ER
-High impact, high risk -> ER
-Skull fracture findings -> ER
-Seizure post trauma -> ER
-Focal neuro signs -> ER
-Suspected concussion should be removed from play immediately
-“When in doubt, sit them out!”
-Re-evaluation in 1-2 days with specialist
-Clearance by licensed health professional usually requires symptom resolution off meds
concussion injury advice
-If you notice any change in behavior, vomiting, worsening headache, double vision or excessive drowsiness, please telephone your doctor or the nearest hospital emergency department immediately.
-!!!!!!!!!Initial rest: Limit physical activity to routine daily activities (avoid exercise, training, sports) and limit activities such as school, work, and screen time to a level that does not worsen symptoms.
-1) Avoid alcohol
-2) Avoid prescription or non-prescription drugs without medical supervision. Specifically:
-a) Avoid sleeping tablets
-b) Do not use aspirin, anti-inflammatory medication or stronger pain medications such as narcotics
-3) Do not drive until cleared by a healthcare professional.
-4) Return to play/sport requires clearance by a healthcare professional
-Recovery
-Symptoms often resolve in 72 hours
-Most sports related concussion resolve in
-2 weeks for adults (85%)
-1-3 months for children (70-80%)
-The most consistent predictor of prolonged recovery = severity of symptoms immediately after injury
graduated return to play protocol
-must be in each stage for 24 hours or longer before you move on
-if you fail a stage -> go back to previous stage
concussion complications
-Second impact syndrome
-Fatal brain swelling if a second concussion is sustained before complete recovery from the first concussion
-Seizures (<5%) – acute symptomatic seizure, not epilepsy
-50% occur within first 24 hours, 25% within first hour
-Increased risk for post traumatic epilepsy
-Post-concussion syndrome- Similar to concussion except that symptoms last > 3 months (after the brain has healed)
-!Post traumatic headaches (25-78%)
-Sleep disturbances
-Chronic traumatic encephalopathy (CTE)
arteriovenous malformations (AVMS)
-Direct arterial to venous connections without an intervening capillary network (pathogenesis not well understood)
-MC genetic cause: hereditary hemorrhagic telangiectasia (HHT; Osler-Weber-Rendu syndrome), autosomal dominant
-MC: supratentorial (90%)
-1-2% of all strokes, 3% strokes in young adults, 9% of SAH
-Presents 10-40 (bimodal: childhood, 30-50)
-M>F
-can bleed easy
arteriovenous malformations (AVMS): symptoms
-Presentations depends on the symptoms produced
-Intracranial Hemorrhage (40-60%): MC intraparenchymal!
-Seizure (10-30%): focal (simple or complex partial) with secondary generalization
-Focal neurologic deficits (caused by mass effect d/t hemorrhage or post-ictal seizure)
-Headache (non-specific) - <1%
-Incidental finding (10-20%)
AVMs dx and management
-Diagnosis
-MRI brain
-CT brain
-+/- CTA or MRA – required for treatment planning and follow up
-Acute management
-Unruptured, no risk factors: Observe! with possible later treatment
-Unruptured, w/ risk factors (low grade 1-2): Microsurgical excision!
-Small grade 3 lesions (<3cm diameter): Stereotactic radiosurgery!
-Large grade 3 lesions, or grade 4/5/6 (>6cm, high risk surgical morbidity): Conservative medical management !
-Seizure prophylaxis not routinely given
cerebral aneurysms
-Thin-walled protrusions from the intracranial arteries composed of very thin or absent tunica media; absent/fragmented internal elastic lamina
-Develops from normal hemodynamic stress or HTN
-Develops at junction of communicating branch with main cerebral artery
-MC: !Ruptured ”Berry (saccular) aneurysm” (80%)
-!MC location: Anterior Circulation (Circle of Willis) – 85%
-!Anterior Comm. + Anterior Cerebral
-!Posterior Comm. + Internal Carotid Artery (MOST LIKELY TO RUPTURE)
-Bifurcation of Middle Cerebral Artery
-RF: HTN, smoking, female (2:1), ETOH, + family hx aneurysm, CoA
-Higher risk of formation: polycystic kidney disease!, Ehlers-Danlos, bicuspid aortic valve
posterior communicating artery aneurysm
-CN3 palsy
cerebral aneurysms presentation
-Presentation:
-!Incidental finding
-!Asymptomatic until SAH occurs
-Headache
-Visual Acuity Loss
-Facial Pain
-May manifest as compression of CN III (Oculomotor) Palsy
-!Diplopia – sudden onset, binocular, horizontal/vertical/oblique
-!Ptosis
-Eye pain at onset
-Causes of rupture: strenuous activity (exercise, sex, physical work), though most occur without an identifiable trigger
cerebral aneurysms dx
-Diagnostic testing for unruptured aneurysms
-!CTA/MRA can detect ≥5mm aneurysms
-Cons: Invasive d/t contrast injection, radiation
-Cerebral angiography (gold standard)
-XR imaging with injected contrast dye
-Can detect much smaller aneurysms
-Cons: More invasive, higher risk of complications
-!!Not used for screening- no point of it
cerebral aneurysms: management
-Stats: Of patients with rupture there is poor prognosis
-33% die before reaching the hospital
-20% die in the hospital
-30% recover without disability
-Management
-!Observation: If <7mm incident finding without prior SAH
-Monitoring unruptured aneurysms for growth: CTA/MRA annually for 2-3 years, then spread to every 2-5 years, is clinically and radiographically stable
-!Surgical clipping
-!Endovascular coiling (preferred method)
intracranial hemorrhage
-Bleeding within the brain can range in causes from trauma, stroke, aneurysm rupture, vascular malformation bleed, high blood pressure, ilicit drug use, and blood clotting disorders
-Neurologic consequences vary depending on size and location, can vary from headache to death
-We will talk about4 main types
ICP dx
-Non-contrast CT head = initial step
-Look for causes: acute obstructive hydrocephalus, edema, or space-occupying lesions such as intracranial hematoma, masses
-Consider repeat CT if clinical deterioration
-Not everything shows on a CT scan!
-Signs of ↑ ICP on CT scan
-Midline shift
-Effacement of the ventricles, basal cisterns and other CSF spaces
-Brain herniation (uncal, tonsillar)
-Edema: Loss of grey-white matter differentiation
-LP opening pressure of >20cm is indicative of ↑ ICP
-Always image first r/o space occupying lesion… sudden and rapid decrease of ICP from the LP can trigger a brain herniation
interventions to lower ICP
brain herniation
normal pressure hydrocephalus (NPH)
-Normally have NO ICP symptoms (other than previous slide)
-No headache, N/V, vision loss, papilledema
-Lumbar puncture: Normal opening pressure !
-Check labs for other causes of AMS: Include B12, TSH
-MRI brain : Ventriculomegaly !(hallmark) without obstruction
-Diagnosis of exclusion
-Confirmatory tests:
-Remove 30-50mL CSF via LP, then test gait ~60 minutes after, if improvement of gait, would benefit from VP shunt
-Treatment: VP shunt !
