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Flashcards in Spinal injuries Deck (28):

Components on brain CT to identify/consider

1. Soft tissues 2. Bones 3. Sulcal pattern 4. Brain parenchyma 5. Ventricular system 6. Vessels 7. Symmetrical 8. Expected density 9. Age appropriate


Coup vs counter coup

1. Coup= injury site 2. Counter-coup= non contact site


How does contusion happen and swelling response

1. Vascular tensile stress as skull shock wave recoils with overshoot outwards 2. Early and delayed swelling->ICP monitoring required


Extradural hematoma: cause, S&S, imaging, management

1. Tearing of middle meningeal artery, fractures temporal / parietal bone commonly 2. Deteriorating consciousness after injury, no LOC/improvement, w/ lucid interval. Then +ICP->seizures, vomiting, headache, brisk reflexes, upgoing plantars, dilated ipsilater pupil, deep/irregular breathing, weakness 3. CT->lens shaped hematoma 4. management Stabilise Transfer urgently for clot evacuation + ligation of bleed ABC + mannitol + ventilation/intubation


Subdural: presentation, signs, imaging, management

1. Fluctuating consciousness/evolving stroke, bleeding of bridging vessels->hematoma between dura and arachnoid 2. Insidious signs, cognitiv slowing, sleepiness, HA, personality changes 3. +ICP 4. CT/MRI->shifting midline w/ clot, crescent shaped over 1 hemisphere 5. Irrigation/evacuation->operation to remove ASHD and remove bone flap, burr hole craniotomy, ICP monitoring


Difference on imaging between an acute SDH and chronic

1. Acute->hyperdense (darker) 2. Chronic->hypodense (lighter)


Etiology, CADAS of intracerebral hemorrhage

Primary vascular injury within parenchyma 1. Hypertension 2. Cerebral amyloid angiopathy: deposition of amyloid on medium-small arteries->weakens- hemorrhage 3. Coag disorder, neoplasm, vasculitis, aneurysm, vascular abnormality

4. CADASIL= cerebral autosomal dominant arteriopathy w subcortical infarcts and leukoencephalopathy->recurrent ischemic strokes->deposits lead to concentric thickening of media and adventitia->stroke and dementia


Mechanism of diffuse axonal injury, imaging

1. Cortex accelerates and decelerates at different speeds to underlying white matter

2. Axons stretch

3. Rupture, loss of granules, loss of gradients, influx of calcium, swelling->necrosis

4. CT may not show, MRI required.

5. Scattered petechial hemorrhages


Diffuse axonal injury grading

1. Grade 1: hemispheric WM

2. Grade 2: Hemispheric WM + corpus callosum

3. Grade 3: Hemispheric WM + CC + Basal granglia


Primary injury mechanisms cellular trauma and delayed consequences

1. Mechanoporation- transient traumatic defects in cell membrane: lipid bilayer transiently seperated from stiffer protein inclusions

2. Ion influxe->depolarisation->excito-toxicity

3. DAI->shearing of white matter tracts


4. Na/Ca into cells->cell death

5. K rapid out

6. Genomic response-> c fos, c jun, jun B= NGF + B-APP + apoptosis


Relate genetic predisposition in apoE4 for dementia pugilistica

1. Worse outcomes in head injury with ApoE4 genotype->cerebral amyloid B deposition after head injury= dementia pegulistica


Secondary injury

1. Secondary injury superimposed on primary

2. Ischemic and metabolic effects


4. ABC problems

5. Seizures

6. Mass effect

7. Commonest= compound fracture, swelling, hydrocephalus, hyponatremia, clot


Herniation syndromes

1. Uncal (transtentorial): Ipsilateral CN 3 palsy + contra-hemiplegia/posturing, contraL HH

2. Central transtorial: coma + bi/l small pupils->decprticate->decerebrate + rostral->caudal loss brainstem reflexes->diffuse cerebral edema->displacement on diencephalon

3. Sufalcine: coma + contraL weakness->posturing +leg

4. Cerebellar/tonsillar: Si/Sx of cerebellar + medullary dysfunction->coma and bi/L posturing


Immediate Mx plan head injury


2. 02 100%, intubate/ventilate if necessary

3. Stop blood loss, support circulation. Treat shock if required

4. Treat seizures

5. Rapid examination survey

6. Investigations

UEC, glucose, FBC, blood alcohol, UDS, ABG, clotting

7. Neurological exam

8. History: when, where, how, fit, lucid, alcohol

9. Evaluate laceration of face/scalp, check for fractures

10. Check for CSF leak, rhinorrhea, ear, blood behind ear drum

11. If ?fracture->CT, tetanus, contact neurosurgeons

12. Palpate neck posterior for tenderness/deformity

13. Radiology


Risk of developing ICH hematoma following head injury and GCS

1. GCS 15 1:31 000

2. GCS 9-14 1:180

3. PTA 1:6 000

4. Sk # 1:80

5. Sk # + PTA 1:30


Inidications for CT/neurosurgical referral

1. LOC at impact

2. Skull #

3. PTA or persitent confusion

4. Progressively + HA, N, V

5. Progressively increasing drowsiness

6. Decreased GCS

7. DevelopM of focal neurological signs

8. Predisposing risks->oral anticoagulants

9. Age?


What is Kernohans notch

1. When kinking of CL cerebral peduncle at tentorial edge causes an ipsilateral motor weakness


Should you operate based on side of hemiplegia in head injury

1. No->false localising signs

2. Remember Kernohans notch


Why is a abducens palsy a false localising

1. Due to long intracranial tract can be compromised by wide variety of SOL emanating from either side


Describe PTA

1. Confusion

2. Agitation

3. Amnesia

NB alcohol/drug/psychiatric history

NB opiate/AED prescriptions


Brain stem death requirements

1. Acceptable cause of death (severe brain injuy)

2. No drugs

3. No metabolic factors

4. Sys >90

5. No alcohol

6. No paralysing agents

7. X2 doctors >5 years graduation

8. X2 assessments seperated by an interval


1. Pupil reflex: No pupillomotor agents

2. Corneal reflex:  No paralyzing agents (muscle relaxants)

3. Supra-orbital pain: No facial grimace or limb movement

4. Caloric reflex:  Oculo-vestibular reflex Ice cold water into clear EAM removes input causing eye drift to that side and nystagmus to other

5. Doll's eye reflex Oculo-cephalic reflex NB unstable neck#!

6. Gag reflex ETT stimulation Cough reflex Bronchial suctioning

7. Breathing Disconnect from ventilator 6L O2 down ETT for ~6mins No breaths 2mins after pCO2 > 8kPa (60mmHg) Reconnect to ventilator until certified dead


Concept of neuroprotection in primary head injury

1. An attempt to prevent primary injury

2. Hypothermia

3. Antioxidants

4. Steroids

5. Hormones->insulin, estrogens, GF, erythropoietin


Targets for ICP and PCO2 in secondary HI

1. ICP <25mmHg

2. PCO2 35mmHg


What role does mannitol have

1. Not a treatment specifically

2. Osmotic diuresis->holds swelling until definitive

3. Risk of hypotension

4. Hypertonic saline can do same job


Outback craniotomy

1. Identify major side & site of impact

2. Examine for hemiplegia or side of worst motor response to PS

3. Examine for a fixed & dilated pupil

4. Identify # line upon opening: the source of haemorrhage will lie (somewhere) beneath this (AEDH + ASDH)



1. Epilepsy: early <1 week (AED 7-10 days) and late >1 week, <18 mo (prophylactic AEDs long term, variable driving ban)

2. Base of skull #: otorrhea, rhinorrhea->prophylactic antibiotics not indicated


OPD follow up

1. Seizures

2. Visual field deficits/inattention

3. Persistent neuropsychological disturnabce

4. Driving ban

AEDH-> 6 mo

ASDH-> 1 year

Brain contusions, Compound depressed skull # 6-12 mo

ICH operated 1 year