neurovascular injuries and closed head injuries Flashcards
head trauma statistics: what gender, age group, mcc, common findings, complications
-Men>Women
-Trimodal: Ages 0-4, 15-24, >75 yo
-MC MOI: FALLS, MOTOR VEHICLE ACCIDENT,
pedestrian/bike, projectiles, assaults, sports, abuse
-Common findings: Loss of consciousness, scalp hematoma, vomiting (13%), headache (46%)
-Complications: Post-traumatic seizure (1%), skull fractures , bleeds, concussions
key history questions for head trauma
-Was it a High risk MOI: falling >3-5 feet, motor vehicle collision, penetrating trauma
-was there loss of consciousness?
-Confusion
-Seizure
-Severe or worsening headache
-Vomiting
-does pt have known arteriovenous malformation or bleeding disorder?
-Child: Acting normally?
traumatic brain injury: definition and severity scale
Definition:
-brain function impairment as a result of external force
-Clinical manifestations are broad: brief confusion, coma, disability, to death
Measure severity using GCS:
- Mild (80% TBIs): GCS 13-15; possible CT using scoring tools
- Moderate: GCS 9-12; head CT
- Severe: GCS < 9; immediate head CT; mortality = 40%
TBI: GCS scoring in relation to what imaging they need -> Canadian head CT rules inclusion and exclusion criteria
If GCS under 13: NEED head CT; this is for GCS 13-15 with at least one of the following:
- loss of consciousness
- amnesia to the head injury event
- witnessed disorientation
Exclusion criteria:
- under 16
- pt on blood thinners
- seizures after injury or anticoagulation use
Note:
-HIGH sensitivity 83-100% for clinically important brain injuries
-HIGH sensitivity 100% for injury requiring neurosurgery
-No false negatives for serious injury: serious brain injuries are reliably detected
what is the canadian CT head rule
If GCS under 13: NEED head CT; this is for GCS 13-15 with at least one of the following:
- loss of consciousness
- amnesia to the head injury event
- witnessed disorientation
NEED CT if they have anything from below:
High-Risk Criteria (for Neurological Intervention):
- GCS score < 15 at 2 hours post-injury
- Suspected open or depressed skull fracture.
- Signs of basal skull fracture (ex: hemotympanum, raccoon eyes, Battle’s sign, CSF leakage from ears or nose)
- Vomiting 2+ episodes
- Age 65+
Medium-Risk Criteria (for Brain Injury on CT):
If any of the following apply, the patient should
- Amnesia for events before impact lasting 30+ min
- Dangerous mechanism of injury (pedestrian struck by vehicle, occupant ejected from vehicle, fall from a height of >3-5 ft)
TBI: phases
Primary phase: at the time of impact
- Due to BLEEDING or DIRECT TRAUMA
-Includes:
-Hematoma (EDH/SDH)
-SAH
-Contusion
-Diffuse axonal injury
Secondary phase: hours/days later
- due to IMPAIRED CEREBRAL BLOOD FLOW -> often the cause of cognitive difficulties
-Causes:
-Edema / ↑ ICP
-Small vessel bleed
-Inflammation
-Physiologic dysfunction
-Often the cause cognitive difficulties
PECARN: pediatric head CT rules
Determines which patients DO NOT NEED a CT scan
-PECARN screening tool for pediatric patients: split into under 2 and 2-16 yrs
Note: If GCS<15, AMS, palpable skull fracture/signs of basillar skull fracture they require CT **
- CT in children does cause RISK of BRAIN CANCER
Possible CT:
- LOC
- severe vomiting
- severe headache
- severe mechanism
Severe mechanism definition:
-motor vehicle collision WITH -> Ejection, rollover, vs. pedestrian, death at scene
-High impact object
-Fall >3ft (<2yo) or >5ft (>2yo)
concerning findings in kids
Basilar skull fracture:
- HEMOTYMPANUM (1st sign -> do ear exam!!!)
- raccoon eyes (tarsal plate sparing)
- halo sign: indicates CSF mixed with blood; place csf on gauze
- postauricular ecchymosis
orbital fracture:
occipital scalp hematoma (non frontal)
Depressed skull fracture
Mild TBI (mTBI) vs concussion
Mild: 13-15 ± brief LOC (<30min)
-Trauma induced alteration in mental status : GCS 13-15 ± brief LOC (<30min)
-mTBI may lead to significant, debilitating short- and long-term sequelae.
-concussion: the S&S that occur after a mTBI; Trauma-induced brain dysfunction w/o structural injury
-“Mild” is a misnomer -> -Often used interchangeably with “concussion” WRONG
-Moderate TBI: GCS 9-12
-Severe TBI: GCS ≤8
Concussion: MOA
Definition: Sequelae of S/S after a mild TBI = Jolting of the head
MOA: Functional not structural injury*
- Shear forces disrupt neural membranes -> K+ efflux out of neuron to the ECF
- increase of Ca 2+ and excitatory amino acids
- followed by further potassium efflux and subsequent SUPPRESSION of neuron activity
concussion MCC and risk factors
-MC in elderly = Falls
-MC in young = Motor vehicle accident
Risk factors:
-Previous concussions
-Younger age
-High risk sports (football, ice hockey, lacrosse, rugby, womens soccer)
-Female > male
concussion: early vs late symptoms
S/S (Early): within hours
- Confusion and Amnesia = hallmarks!!!!*
-Retrograde amnesia: loss of recall for events immediately before
-Anterograde amnesia: loss of recall for events immediately after
- Headache
- Dizziness
- Nausea/vomitting
- Mental fogging/slowing
- Concentration difficulties
- others: fatigue, lack of awareness of surroundings, unsteadiness
S/S (Late): within hours/days
- Mood or cognitive disturbances
- Sensitivity to light/noise
-Sleep disturbances
Concussion: signs
-Incoordination
-No focal neuro deficits
Neuropsychiatric impairments:
-Emotionality out of proportion**
-Memory deficit *
-Vacant stare
-Delayed verbal expression
-Inability to focus
-Disorientation
-Slurred or incoherent speech
Concussion testing and 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
Step 1: initial rest
-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, aspirin, sleeping pills)
- limit screen time
- don’t drive until cleared by profession
- return to play/sport once cleared by healthcare professional
consider:
-Referral to concussion specialist: Physiatrist, sports medicine, neurologist
-if prolonged symptoms >21 days
-Hx of multiple concussions
-Uncertain diagnosis
concussion: return to play protocol
- any LOC episode -> ER for evaluation
-Suspected Cervical -spine injury -> immobilize, ER
-High impact, high risk -> ER
-Skull fracture findings -> ER
-Seizure post trauma -> ER
-Focal neuro signs (weakness, confusion, or imbalance) -> 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
concussion recovery time
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
1) Post traumatic headaches (25-78%)
2) Post-concussion syndrome
- Similar to concussion except that symptoms last > 3 months (after the brain has healed)
3) Second impact syndrome:
-Fatal brain swelling if a second concussion is sustained before complete recovery from the first concussion
4) Seizures (<5%) – acute symptomatic seizure, not epilepsy
-50% occur within first 24 hours, 25% within first hour
-Increased risk for post traumatic epilepsy
5) Sleep disturbances
6) Chronic traumatic encephalopathy (CTE)
Post-Concussion Syndrome and second impact syndrome
Post concussion syndrome:
- typically starts 4 wks after concussion and sx last > 3 months
- sx: Sleep disturbances*, headache, dizziness, cognitive impairment
Second impact syndrome:
- if you get second concussion before complete recovery from 1st -> FATAL brain swelling
arteriovenous malformations (AVMS): defintion, statistics
Definition: Direct arterial to venous connections without an intervening capillary network
MC:
- Genetic cause: Hereditary Hemorrhagic Telangiectasia; aka osler-weber-rendu syndrome-> autosomal dominant
- MC location: supratentorial region (90%!!)
Incidence:
- 1-2% of all strokes,
- 3% of strokes in young adults,
- 9% of spontaneous subarachnoid hemorrhages (SAH)
Presentation: bimodal
- childhood
- 30-50
- M>F
AV malformations: presentation
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)
-Incidental finding (10-20%)
-Headache (non-specific) - <1%
AV malformations: dx and management
Diagnosis
-MRI brain
-CT brain
-+/- CTA or MRA: required for treatment planning and follow up
- suggestive if bruit over eye/mastoid
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 Aneurysm definition and locations
Definition: Thin-walled protrusions from intracranial arteries composed of very thin or absent tunica media
- Develops from HTN or normal hemodynamic stress
Location: Commonly occurs at junction of communicating arteries and cerebral arteries
- 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
Cerebral aneurysms: risk factors and higher risk of formation
RF:
- HTN
- smoking
- Female (2:1)
- ETOH
- Family hx aneurysm
- Coartion of aortic
Conditions with higher risk of formation:
- polycystic kidney disease**
- Ehlers-Danlos
- bicuspid aortic valve
posterior communicating artery aneurysm
-CN3 palsy
-most likely to rupture: Posterior communicating + internal carotid
cerebral aneurysms presentation
INCIDENTAL finding: Asymptomatic until SAH occurs**
-Headache
-Visual Acuity Loss
-Facial Pain
May manifest as compression of CN III Palsy (PCA):
-Diplopia: sudden onset, binocular, horizontal/vertical/oblique
- Ptosis
-Eye pain at onset
Causes of rupture:
- most occur without an identifiable trigger
- strenuous activity (exercise, sex, physical work)
epidural hematoma: def, presentation, dx
Def: ARTERIAL bleed between dura and the skull
- MCC: trauma
- MC: middle meningeal artery from temporal bone fracture
Classic presentation:
- initial trauma injury with brief LOC
- lucid interval for several hours
- neurological sx: AMS, coma
- VOMITTING
- other sx: headache, seizure, confusion, aphasia, hemiparesis
Dx:
- non contrast CT showing football sign (BICONVENX (lens-shaped, lentiform)*
- blood collection that does not cross suture lines of the skull
epidural hematoma tx
management: IMMEDIATE hospitalization to REDUCE ICP**
-Hyperventilation: Goal pCO2 25-30 mmHg (Temporary measure)
-Mannitol: Osmotic diuretic that decreases ICP temporarily
NEUROSURGICAL EVALUATION FOR CRANIOTOMY AND HEMATOMA EVACUATION:
- surgical evacuation indications: volume > 30 mL, acute and in coma (GCS <8), PUPILLARY changes
- if delayed surgical evaluation: BURR HOLE*
Observation:
- mild sx
- volume < 30 mL
- clot thickeness < 15mm
- no midline shift
- no coma
- no focal neuro deficits
Rarely: brain herniation, stroke, seizures occur
subdural hematomas: definition, causes, risk factors
Definition: VENOUS bleed between dura and arachnoid
- most often rupture of BRIDGING veins from surface of brain to dural sinuses
- MC in elderly
Causes:
- BLUNT TRAUMA MC
- “contre-coup”
- shaken baby
- AV malformation spontaneous hematoma
- neurosurgical procedure complication
- non-traumatic causes: ALCOHOLISM, SEIZURES, COAGULOPATHIES
Risk factors:
- cerebral atrophy
- ELDERLY
- TBI
- M > F
subdural hematomas PE and Dx
May have evidence of:
- broken basilar skull
- +/- CSF oto/rhinorrhea
Dx: Non-contrast CT
- head showing a concave (crescent shaped) blood collection that DOES cross suture lines
-note: Initial CT scans can often be normal
subarachnoid hemorrhage: definition and risk factors
Definition: Arterial bleed between arachnoid and pia mater
- MCC: ruptured BERRY aneurysm*, AV malformation
-Can be SPONTANEOUS or from TRAUMATIC event -> rupture and bleeding into subarachnoid space -> blood in CSF -> rapid increased ICP
- high mortality rate: 42% within 30 days
Risk factors:
- age: 40-60
- FEMALES»_space;»»» males
- SMOKING
- HTN
- ETOH, cocaine
- first-degree fam hx SAH
- AA, connective tissue disorders
subarachnoid hemorrhage: dx
Dx:
- non contrast CT: blood within basal cisterns
- if you are highly suspicious with negative CT -> LP*
- LP: gold standard; xanthochromia (yellow CSF from broken down RBCs); increased RBCs in all vials
-CTA/MRA/Digital subtraction cerebral angiography vs. Cerebral angiogram (definitive)
-EKG: Increased QRS, QT intervals, Decreased PR intervals, U waves, dysrhymias
intracerebral hemorrhage (ICH): def, MCC, other causes
Definition: blood accumulation in the intraparenchymal space -> compression of blood vessels and tissue -> HYPOXIA -> hypoxemia
MCC: HTN
- leads to atherosclerosis of large arteries, subclinical microbleeds, microaneurysms (Charcot-Bouchard aneurysms)
- BASAL GANGLIA, THALAMUS, pons, and cerebellum are most often affected
Other causes:
-Cerebral amyloid angiopathy: Deposition of amyloid into blood vessel walls makes them weak and prone to rupture*
-AVMs*
-Post-traumatic
-Coagulopathies
-Sickle cell disease
intracerebral hemorrhage risk factors
- MALE
- Black, Asian
- Heavy alcohol use
- amphetamines, cocaine
- anti-thrombotic medications
- previous cerebrovascular incident
Very poor prognosis
intracerebral hemorrhage presentation and sx based on location of bleed
Presentation:
-Slow onset, gradually worsening within a few hours, increased ICP
-Fever, AMS, HA, N/V
- anisocoria: UNEQUAL pupil sizes *
Symptoms: depend on location of bleed
-Basal ganglia = Loss of contralateral sensory, motor functions, honomymous hemianopsia
-Thalamus = Contralateral loss of sensory, motor functions, homonymous hemianopsia, aphasia if dominant side / neglect if non-dominant side, small pupils
-Lobar = honomymous hemianopsia, seizures, contralateral leg paresis if frontal
-Pons = coma within few minutes, quadraplegia miosis, deafness, speaking difficulties when awake
-Cerebellum = ataxia, same side face weakness, occipital headache, neck stiffness, loss of face/body sensory functioning
-ACA, MCA = numbness, weakness
-PCA = Impaired vision
-Broca’s area = Slurred speech
-Wernicke’s area = Difficulty understanding speech
signs of increased ICP
- Papilledema (4-9%)*
- Cushing reflex: bradycardia, HTN, irregular breathing **
-CN VI palsy
-Periorbital bruising
-Children more likely to get abnormal gait or poor coordination
-Herniation: Decorticate or decerebrate posturing, Change in GCS
Absent: Hypotension, Hypoxemia, Hypothermia
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 (loss of visibility)
-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
ICP management
resuscitation efforts:
- head of bed at 30 degrees*
- therapeutic hyperventilation: goal of pCO2 of 26-30 mmHg -> induces vasoconstriction and reduce cerebral blood flow
aggressively treat fever: acetaminophen, mechanical cooling
hyperosmolar therapy (in emergencies)
- mannitol: osmotic diuretics
- mechanical ventilation
- AVOID free water solutions that can worsen edema like D5W, half NS; USE ISOTONIC fluids (0.9% NS)**
other tx:
-Furosemide: sometimes given as adjunct therapy to potentiate effects; Can worsen dehydration and hypokalemia
-Decompressive Craniectomy (last line)
uncal herniation
B
-Innermost temporal lobe is compressed and moves towards the brainstem, causing pressure on CN III
-Classic presentation of uncal herniation:
-!Ipsilateral fixed dilated pupil + contralateral hemiplegia + cushing reflex
hydrocephalus definition and two types
Excessive amount of CSF within cerebral ventricles and/or subarachnoid spaces = Ventricular dilation and increased ICP
Two Types:
1) Obstructive (Non-Communicating)
- CSF accumulation due to structural blockage of flow within ventricles
- MCC in children
2) Absorptive (Communicating)
- CSF accumulation due to impaired absorption; rarely excessive CSF production
- normal pressure hydrocephalus
hydrocephalus: risk factors
Low birth weight
prematurity
maternal DM
male sex
low socioeconomic status
race/ethnicity
hydrocephalus: sx and singsn
Symptoms
-HEADACHE: early morning, worse with cough/micturition/defecation/recumbency*
-Irritability, Lethargy , weakness
-Altered mental status / behavioral changes*
-Nausea, vomiting
-Diplopia, abnormal eye movements
Signs:
-Head circumference in children: full anterior fontanelles, frontal bossing, prominent scalp veins
-Developmental delays in children
-Spasticity
-“Setting sun” sign
- papilledema
-Sacral dimpling *
NPH classic triad “wet, whacky, wobbly”
Gait Disturbance
- Magnetic, glued foot gait: small wide based steps
- Difficulty with ambulation: reduced ability to walk
Cognitive Disturbance:
- Dementia that develops over months-years
- early: impaired executive function
-Apathy, depression, psychomotor slowing, decreased attention and concentration
Urinary Incontinence:
- early: Urgency
- Slow gait makes it hard to reach bathroom
- late: lack of concern due to frontal lobe impairment
normal pressure hydrocephalus (NPH): sx and dx
Sx:
-Normally have NO ICP symptoms (other than wet, whacky, wobbly)
-No headache, N/V, vision loss, papilledema
Dx:
-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
