Neuro and NSx Flashcards
What is the Canadian CT head injury rule and some exclusion criteria
Rule out tool for intracranial injuries that would require neurosurgical intervention
100% sensitivity for injuries that require NSx and 87-100% for ‘clinically important’ injuries that don’t
Most consistent, validated and effective rule for minor head injuries
70% sensitive for ‘clinically important’ brain injury in ETOH intoxicated pts
CAN ONLY BE APPLIED
GCS 13-15 +
- LOC
- Amnesia to event
- Witnessed disorientation
EXCLUSION
Age<16
Blood thinners
Seizure after injury
HIGH RISK CRITERIA - rules out NSx intervention
GCS<15 2hrs post injury
Suspected open or depressed skull fracture
Signs of basilar skull fracture
>/=2 episodes of vomiting
Age>/=65
MEDIUM RISK - For clinically important brain injury that may require admission
Retrograde amnesia >30minutes from event
Dangerous mechanism (Pedestrian MVA, Ejected from car, fall>3 feet or 5 stairs
What is the NEXUS Head CT rule
Rule out tool to avoid unnecessary CTs in pts of ANY age with blunt head injury within 24hrs
Evidence of skull fracture - basilar or depressed
Scalp hematoma
Neurological deficits
Altered LOC - GCS<15, delayed or inappropriate responses
Abnormal behavior - Agitation, inconsolability etc
Coagulopathy
Presistent vomiting - >1 episode of projectile or forceful emesis
Age>/=65
What is the PECARN head injury algori
PREDICT
What are the modifiable and non-modifiable risk factors for SAH?
Modifiable
- HTN (mild risk increase)
- Smoking (3-10 times risk)
- Alcohol abuse
- Sympathomimetic drugs (cocaine)
Non-modifiable
- Gender (Female 1.6 x men)
- Known aneurysm (either previous rupture or unruptured is greatest risk factor)
- Fatal second degree relative with SAH (4 times risk)
- AVMs
- Associated genetic condition such as Autosomal PCKD, connective tissue disorders (Ehlers Danlos, Marfan), Coarctation of the aorta, hereditary hemorrhagic telangiectasia
Where do aneurysms commonly occur?
85% in carotid system
- 30% AComA
- 25% PComA
- 20% MCA
- 10% other
15% posterior circ
- 10% in Basilar and at bifucation most common
- 5% on vertebral artery, PICA junction most common
25% have multiple
What is the Ottawa SAH Rule for Headache evalutation
Scoring system recommended by the American College of Emergency Physicians to potentially avoid unnecessary scanning.
Has 100% Sensitivity but ~15% specificity so cannot be used to diagnose, only determine need for further imaging.
CAN NOT be used in
- Pts <15 yrs old
- GCS <15
- head trauma or fall within 7 days
- New deficits
- known aneurysms or brain tumors
- Chronic recurrent headaches (>/= 3 headaches of the same character and intensity for >6 months)
IF
Age >/= 40
Neck pain or stiffness
Witnessed LOC
Onset during exercise
Thunderclap headache
Limited neck flexion on exam
Then SAH can NOT be ruled out
What are some causes of a false negative non con CTB for SAH
Time, most sensitive in first few hours (<6hrs)
Anemia
Low volume SAH
Technically poor scan
What is the Modified Fisher Scale (also known as Claasen grading sytem)
Radiological grading system to determine risk of cerebral vasospasm
Grade 0 - Normal CT
Grade 1 - ‘Thin’ focal or diffuse SAH with no Intraventricular hemorrhage (24% incidence DCI)
Grade 2 - ‘Thin’ focal or diffuse SAH WITH IVH (33% DCI)
Grade 3 - ‘Thick’ focal or diffuse SAH with NO IVH (33% DCI)
Grade 4 - ‘Thick’ focal or diffuse SAH WITH IVH (49% DCI)
What is the WFNS scale (World Federation of Neurosurgical Societies)
Clinical grading system based on GCS and neurological deficits. Should be used AFTER Neurological resus (EVD or clot evacuation) and best correlation with outcomes is 12hr post surgery
WFNS 1 - GCS 15 with no deficit
WFNS 2 - GCS 13-14 and NO deficit
WFNS 3 - GCS 13-14 WITH focal deficit
WFNS 4 - GCS 7-12
WFNS 5 - GCS <7
What are the pros and cons of the SAH grading systems?
WFNS Pros
- Fast and easy to calculate
- Does not require imaging
- High interobserver reliability
- Step wise increase in likelihood of poor outcome with increasing grades
WFNS Cons
- Relies on accurate examination
- Significant increase in likelihood for poor outcome in between steps 2 and 3
- Groups wide range of pts in grade 4 (GCS 7-12 +/- deficit) so possible to have widely differing outcomes
MFS Pro
- Very high inter-reliability
-Validates prognostic tool for radiological vasospasm
- Risk of vasospasm increased with each grade (previously peaked at 3 and then decreased slightly at 4)
MFS Cons
- Doesnt prognostic overall outcome, only radiological vasospasm
- Clot density in not a feature of the system
What is the Hunt and Hess grading system?
- Measure of perioperative mortality risk based on intensity of meningeal inflammation, severity of neurological deficit, level of arousal and presence of associated disease.
- Uses ambiguous terms in grading system decreasing inter-reliability.
- Predates the GCS by 5 yrs and still one of the most widely recognized scoring systems
H&H 1 - Asymptomatic or minimal headache and slight nuchal rigidity
H&H 2 - Moderate to severe headaches, CN palsies, Nuchal rigidity but no other neurological deficits
H&H 3 - Drowsy and confused or mild focal deficit
H&H 4 - Stupour, moderate to severe hemiparesis, early decerate rigidity and ‘vegetative disturbance’
H&H 5 - Deep coma, decerebrate rigidity, ‘moribund appearance’
What are the CSF findings in SAH
Some RBCs
<5WBC
WBC:RBC ratio 1:700
Xanthochromia
Minimal clearing of RBCs between tubes 1 and 4
If Xanthochromia present, SAH confirmed.
Can be absent early but always present 12hrs after bleed
False positive potential if CSF protein >100mg/dL or bloody taps
What are the common cause of ICH?
Hypertensive Vasculopathy (1/3 of all ICH)
Most commonly in deep structures
- Basal Ganglia (especially putamen)
- Thalamus
- Pons
- Cerebellum
Cerebral amyloid angiopathy (1/5 of all ICH and second most common)
- Risk increase with age and typically peripheral lobar haemorrhages
20% undetermined
Medication related (15%)
- Warfarin, heparin, DOACs, Thrombolysis
Vascular structural lesions
- Tumors, AVM, AVF (dural arteriovenous fistula)
Systemic Disease
Rarer causes
- Moya moya disease (basal ganglia typically)
- Pregnancy and puerperium ( up to 6 weeks post partum and usually with pre/eclampsia
- CN infections (fungal, herpes)
- Vasculitis
- CVS thrombosis
What are some methods of decreasing intracranial pressure in head injury
Ensure head elevation and no tube ties/collars are on the neck
Deep sedation and analgesia with propofol and fentanyl +/- barbiturates
Aim Sats ~95% and paO2 80-120
Hyperventilation aim paCO2 35-38
and avoid unnecessary PEEP
Osmotic agents - Hypertonic saline 3% 3ml/kg or mannitol 0.5-1g/kg
Surgical correction - decompressive craniectomy, burr holes, EVD
Deepening sedation with barbiturates
Theraputic hypothermia
What are the complications of cervical spine immobilisation
- Raised ICP
- Reduced access to the neck
- Pain and discomfort - pressure areas
- Airway compromise added difficulty with airway interventions
- Aspiration risk
- Impaired ventilation
- Impaired head movement
- Potential worsening of spinal cord injury
- Unnecessary distraction from important resuscitation issues
- Unnecessary additional radiology esp in children
- Requirement for log-rolling, increased nursing requirements, staff distraction from other duties
What is the Canadian C Spine Rule and its exclusion criteria?
Well validated rule to avoid unnecessary imaging.
Highly sensitive 99-100%
Can be used on any alert and cooperative pt, despite blood alcohol content
Exclusion criteria
- non trauma pts
- GCS<15
- Unstable vitals
- <16 yrs old
- Acute paralysis
- Known vertebral disease
- Previous C spine surgery
CT indicated if
Age>65, extremity paresthesia or dangerous mechanism
No low risk factors (sitting in ED, ambultory at the time, delayed neck pain, no midline tenderness, simple rearend MVA)
Pt unable to actively rotate neck 45 degrees
What is the nexus rule for C spine imaging and some differences to the CCSR
Well validated rule to help elliminate unnecessary CTs
Highly sensitive but marginally less so then CCSR.
Does not have age limitation so can be used in paediatric population and elderly but needs caution when used over 65 as sensitivity drops to between 66-84%
Also does NOT include mechanism
Unlike CCSR also includes intoxication
types of intracranial herniation
Describe the clinical features of different spontaneous intracerebral hemorrhages (putamen, thalamus, pontine, cerebellum)
Basal ganglia/external capsule most common locations:
- Putamen (most common 1/3) -most commonly along white matter tracts: contralateral hemiplegia, hemisensory loss, homonymous hemianopsia, gaze palsy (eye deviate towards contralateral side). Stupor and coma if large
- Caudate (least common 2%) originate within head of caudate nucleus: acute onset confusion, personality changes, memory impairment, transient contralateral weakness or numbness. Head and drowsiness if extending to intraventricularly space
Pontine (5-12%) from brainstem nuclei and extend to base of pons: Deep coma with few minutes due to disruption of reticular activating system with quadriplegia, pinpoint pupils with loss of horizontal eye movements, decerebrate rigidity. hypertension, hyperhidrosis, hyperpnea.
Thalamic (15-20%) extend transverse to posterior limb of internal capsule, downward to tectum of midbrain or medially to third ventricle: Eyes are down and in, unreactive, ipsilateral horners. Contra lateral hemiplegia with eyes deviated TOWARD weak side
Cerebellar from dentate nucleus and extend into hemisphere and fourth ventricle: Ataxia, vertigo, vomiting, occipital headache. NO HEMIPARESIS but can have gaze/facial palsy. Often deteriorate (high risk of obstructive hydrocephalus or brainstem compression) and need surgery
How is the volume of an intracerebral hematoma calculated and what do they mean
ABC/2
Measurements in cm
A = large axial diameter
B = largest diameter perpendicular to A within axial slice
C = number of axial slices showing hemorrhage multiplied by slice thickness (3-10mm depending on scanner). Slices that show haemorrhage <25% of largest slice are not counted while 25-75% are counted as half and >75% as full
Location is often more important then absolute volume but roughly
<30m is favorable
>30ml correlate to moderate to severe
>70ml uniformly lethal if not undergoing surgical intervention
Risk factors for intracerebral hemorrhage expansion/deterioration and some signs on CT
Most expansion occurs in first 3hrs to 24hrs
RISK
- Shorter time from symptom onset to initial imaging
- Antiplatelet/anticoagulant use
- Contrast extravasation (spot sign is 90% specific and 50% sensitive, leakage sign between initial and delayed phase has 90% sensitivity and specificitiy and associated with poor prognosis)
Non con CT signs:
- Irregular hematoma shape
- Island sign (>3 scattered hematoma separate from main hematoma)
- Swirl sign (unclotted fresh blood has lower attenuation that clotted blood)
- Black hole sign (dark area within hematoma that is not connected to adjacent brain tissue is 94% specific and 32% sensitive)
- Blend sign (hemorrhage that contains hyperdense and hypodense regions)
Intraventricular extension has worse neurological complications and outcomes
Edema takes hours to develop, and extensive or irregular edema suggests underlying
- CVT
- Ischemic stroke with hemorrhagic transformation
- Tumor
How are spontaneous intracerebral hemorrhages managed
Reverse and cease anticoagulants.
BP control
- Presenting SBP 150-220, then aim SBP 140-160 within first hour
- Presenting SBP>220, rapidly to <220 then slowly over next few hours to 140-160
Labetalol 20mg IV with increasing doses 40, 60, 80mg every 10 minutes
Max 300mg OR Infusion 0.5-2mg/min Lasts 2-4hrs
GTN 5-100microg/min lasts 5-10minutes
Nimodipine 1mg/hr for 2hrs
Nicardipine 5-15mg/hr up to 4hrs
Seizure prophylaxis (16% in 1 week)
General methods to avoid increased intracranial pressures
- head up 45 degrees and avoiding neck rotation/IJ lines, compression
- Mild sedation, aim RASS 0 to -2 with benzos
- Avoid hyperthemia
- Avoid hypoxia
- Aim Na >135
Surgical management when indicated
Osmotic therapy, hyperventilation and urgent decompression when concerned regarding raised ICP
Indication for surgery in intracerebral bleeds
Intraventricular hemorrhage with ventricular enlargement and associated neurological decline
Cerebellar Hematoma: Enclosed space that can cause catastrophic direct compression on adjacent brainstem, obstruct fourth ventricular CSF flow or cause herniation. Pts deteriorate rapidly (12-24hrs)
- large volume (>15ml) or >3cm in diameter
- Neurological deterioration
- Brain stem compression
- Hydrocephalus
Supratentorial hematomas: STITCH trials show medical management, but surgery should be considered when there is
- Large hematoma (>30ml) with significant midline shift
- Elevated ICP refractory to medical management
- Hemorrhage secondary to underlying lesions that could benefit from resection
When would a LP without prior CT imaging be safe and what are some contraindication
No need for CT if
- Age<60
- No seizures with past week
- No altered level of consciousness (answer 2 consective questions and follow 2 consecutive commands)
- No focal deficits
- No papilledema
- No hx of CNS disease or suspected metastatic cancer
- Not immunocompromised
CONTRAINDICATIONS
- Decreasing LOC or GCS<8
- Signs of raised ICP like diplopia, decerebrate/decorticate or hypertension/bradycardia
Spinal abscess or cellulitis over site of LP
- Traumatic injury to site of LP
- Bleeding diathesis (plt<50, INR>1.4, hemophilia, von willebrand etc) without correction
Different CSF results
q19
Different menigitis/encephalitis organsims by age and treatements
Stroke management - NHISS, modified RANCO, when to thrombolyse vs clot retrieval
Different stroke syndromes
Wallenberg syndrome - lateral medullar infarction from intracranial vertebral artery occlusion (Vertigo, disequilibrium, ipsilateral horner and ataxia, dissaosciated sensory loss
Brainstem TIA
Cogans
Ataxia causes (adults and children)
What are the differential lists for ascending and descending paralysis
Ascending paralysis
- GBS
- Tick paralysis
- Vitamin B12 or thiamine deficiency
- Heavy metal poisoning (arsenic)
- Hypothyroidism
Descending paralysis
- Myasthenia gravis
- Botulism
- Tetanus
- Tetrodotoxin poisoning
- Snake bite paralysis
What are the causes of GBS and how does it present
Immune mediated polyneuropathy that can affect all myelinated nerves (motor, sensory, cranial, sympathetic) but motor most common.
CAUSES
- Campylobacter most common (30%)
- EBV/CMV
- Mycoplasma
- RSV
- HIV
- Lymphoma/SLE
- Uncommon causes include trauma/surgery, immunization or bone marrow transplant
PRESENTATION
GBS manifestations and variants
Acute inflammatory demyelinating polyneuropathy is most common (85-90%) with progressive symmetric weakness and hypo/areflexia
Anti- GQ1b syndromes: optic and oropharyngeal variants
- Miller Fischer syndrome: ophthalmoplegia, ataxia, areflexia
- Bickerstaff brainstem encephalitis: encephalopathy, ophthalmoplegia, ataxia, bulbar symptoms (including pupilar abnormalities) and either normal or hyperreflexia
SCIWORA
What are the differentials for Rim enhancing lesions seen on CT
MAGICAL DR
M - Metastasis (thick and nodular wall and increased edema perfusion)
A - Abscess (thin walled with relatively extensive edema)
G - Glioblastoma (irregular mass with adjacent secondary lesion embedded in same region of edema)
I - Subacute infarct or inflammatory (neurocysticercosis with small thin walled numerous or tuberculoma)
C - Contusion
A - AIDS related toxoplasmosis or cryptococcosis
L - Lymphoma (typically in immunosuppressed)
D - Demyelinating disease (classically incomplete rim or restricted diffusion of enhancing wall)
R - Radiation necrosis or resolving hematoma
Comment on enhancing wall characteristic, surrounding edema, central fluid content and number of lesions
Pseudoseizure vs seizure
PSEUDO
- Asynchronous or purposeful movements
- Side to side head shaking and pelvic thrusting
- Ictal crying and vocalization (stuttering, screaming)
- Eyes closed during seizure onset
- Resisted eye lid opening
- Rapid post ictal reorientation
- Tongue biting on tip
SEIZURE
- Rhythmic, generalized tonic clonic movements
- Eyes open during onset and not resisting opening lid opening during seizure
- Absent pupillary light reflex
- Post ictal period of drowsiness/confusion
- Stertorous breathing postictally
- Tongue biting on side
Delirium vs dementia
DELRIUM
- Abrupt with definite beginning
- Lasts days to weeks and temporary and reversible
- Significant abrupt impairment of attention and orientation
- Symptoms fluctuate frequently throughout the day
- Slow and incoherent
DEMENTIA
- Slow gradual onset
- Persistent, progressive and incurable over period of months to years
- No inattention and alert in early stages, affected much later in severe disease
- Constant symptoms throughout the day
- Word finding difficulty
Compare the presenting signs and symptoms of Guilian Barre and Acute spinal cord compression
Guilian Barre
- Pure motor with sensation typically intact
- Progressive ascending weakness that progresses from limbs to bulbar/respiratory muscles
- Flaccid deep tendon reflexes
- Bladder and bowel function maintains
- Typically preceded by gastroenteritis (2/3 and campylobacter predominate)
Spinal cord compression
- Motor and sensory
- Stable signs below level of injury once established
- Hypo or hyperreflexia
- Bladder and bowel dysfunction
- Hx of malignancy, trauma or back pain. Preceding illness if infective cause (epidural abscess/discitis)
What is autonomic dysreflexia and some causes
Occurs with spinal cord lesions above T6 when there is increased sympathetic discharge below and increased parasympathetic discharge above
SIGNS
>20mmHg rise from baseline (typically 90-100)
Headache
nasal congestion.
CAUSES - stimulation below level of injury
- Urinary retention
- Faecal impaction
- Pressure areas
- Fractures
- Ingrown nails
Horners Syndrome Differentials
Myasthenia Gravis
Myasthenia crisis
