Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

General surgery > Spinal injuries > Flashcards

Spinal injuries Flashcards

1
Q

Components on brain CT to identify/consider

A
  1. Soft tissues 2. Bones 3. Sulcal pattern 4. Brain parenchyma 5. Ventricular system 6. Vessels 7. Symmetrical 8. Expected density 9. Age appropriate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Coup vs counter coup

A
  1. Coup= injury site 2. Counter-coup= non contact site
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How does contusion happen and swelling response

A
  1. Vascular tensile stress as skull shock wave recoils with overshoot outwards 2. Early and delayed swelling->ICP monitoring required
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

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

A
  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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Subdural: presentation, signs, imaging, management

A
  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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Difference on imaging between an acute SDH and chronic

A
  1. Acute->hyperdense (darker) 2. Chronic->hypodense (lighter)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Etiology, CADAS of intracerebral hemorrhage

A

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

  1. 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Mechanism of diffuse axonal injury, imaging

A
  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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Diffuse axonal injury grading

A
  1. Grade 1: hemispheric WM
  2. Grade 2: Hemispheric WM + corpus callosum
  3. Grade 3: Hemispheric WM + CC + Basal granglia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Primary injury mechanisms cellular trauma and delayed consequences

A
  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

Delayed

  1. Na/Ca into cells->cell death
  2. K rapid out
  3. Genomic response-> c fos, c jun, jun B= NGF + B-APP + apoptosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Relate genetic predisposition in apoE4 for dementia pugilistica

A
  1. Worse outcomes in head injury with ApoE4 genotype->cerebral amyloid B deposition after head injury= dementia pegulistica
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Secondary injury

A
  1. Secondary injury superimposed on primary
  2. Ischemic and metabolic effects
  3. CPP= MAP - ICP
  4. ABC problems
  5. Seizures
  6. Mass effect
  7. Commonest= compound fracture, swelling, hydrocephalus, hyponatremia, clot
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Herniation syndromes

A
  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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Immediate Mx plan head injury

A
  1. ABC, GCS
  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

  1. Neurological exam
  2. History: when, where, how, fit, lucid, alcohol
  3. Evaluate laceration of face/scalp, check for fractures
  4. Check for CSF leak, rhinorrhea, ear, blood behind ear drum
  5. If ?fracture->CT, tetanus, contact neurosurgeons
  6. Palpate neck posterior for tenderness/deformity
  7. Radiology
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Risk of developing ICH hematoma following head injury and GCS

A
  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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Inidications for CT/neurosurgical referral

A
  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?
17
Q

What is Kernohans notch

A
  1. When kinking of CL cerebral peduncle at tentorial edge causes an ipsilateral motor weakness
18
Q

Should you operate based on side of hemiplegia in head injury

A
  1. No->false localising signs
  2. Remember Kernohans notch
19
Q

Why is a abducens palsy a false localising

A
  1. Due to long intracranial tract can be compromised by wide variety of SOL emanating from either side
20
Q

Describe PTA

A
  1. Confusion
  2. Agitation
  3. Amnesia

NB alcohol/drug/psychiatric history

NB opiate/AED prescriptions

21
Q

Brain stem death requirements

A
  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
22
Q
A
  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
23
Q

Concept of neuroprotection in primary head injury

A
  1. An attempt to prevent primary injury
  2. Hypothermia
  3. Antioxidants
  4. Steroids
  5. Hormones->insulin, estrogens, GF, erythropoietin
24
Q

Targets for ICP and PCO2 in secondary HI

A
  1. ICP <25mmHg
  2. PCO2 35mmHg
25
Q

What role does mannitol have

A
  1. Not a treatment specifically
  2. Osmotic diuresis->holds swelling until definitive
  3. Risk of hypotension
  4. Hypertonic saline can do same job
26
Q

Outback craniotomy

A
  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)
27
Q

Complications

A
  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
28
Q

OPD follow up

A
  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

General surgery (36 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions