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Trauma > Head / Neuro trauma > Flashcards

Head / Neuro trauma Flashcards

1
Q

What are the layers of the scalp and cranium?

A

SCALP MAP

  • Skin - dermis
  • sub-Cutaneous tissue + blood supply
  • Aponeurosis - Galea
  • Loose areolar tissue - where sub-galeal haematomas form
  • Pericranium -> firmly attached to the skull
  • Meningeal dura mater
  • Arachnoid mater
  • Pia mater
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2
Q

What tissue produces CSF?

Where is it located?

A

The choroid plexus is located in the lateral ventricles.

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3
Q

What is the pathway of flow of CSF?

A

Lateral ventricles -> foramen of Munro -> third ventricle -> aqueduct of Sylvius -> fourth ventricle -> foramina of Magendie and Luschka -> subarachnoid space over brain and spinal cord -> reabsorbed into venous sinus blood via arachnoid granulations.

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4
Q

What are the functions of CSF?

A
  1. Protection
  2. Transport of nutrients and hormones
  3. Removal of waste
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5
Q

What are the functions of the Blood Brain Barrier?

A

Barrier to pathogens and hormones - NB also prohibits passage of some drugs and antibiotics

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6
Q

What is the effect of cerebral oedema on the BBB?

A

The permeability of the BBB increases - it becomes leaky.

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7
Q

List the seven secondary insults that pertain to brain injury.

A
  1. Hypotension - SBP < 90mmHg
    1. Ischaemia
    2. Infarct
  2. Hypoxia - paO2 < 60mmHg
    1. Apnoea
    2. Obstruction
    3. Poor ventilation
    4. Pulmonary injury
    5. Poor airway mgt/intubation
      1. -> anaerobic celluar metabolism
  3. Anaemia
    1. Reduced O2 carrying capacity
  4. Hyperpyrexia (T >38.5)
    1. Inc’d metabolic demands
  5. Hypercarbia
    1. Inc’d CO2 -> inc’d IC blood flow -> inc’d ICP
  6. Coagulopathy
    1. Inc’d IC haemorrhage
  7. Seizures
    1. Inc’d metabolic demands and toxic metabolites
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8
Q

What is the normal level of CSF ICP?

A

6-20cm H2O

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9
Q

List three methods of acutely decreasing ICP.

A
  1. Hyperventilation -> dec’d pCO2 -> dec’d IC blood flow -> dec’d ICP
  2. Osmotic and diuretic agents (hypertonic saline or mannitol) -> fluid shifts -> dec’d ICP
  3. Facilitate CSF drainage (ventricular or lumbar drain)
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10
Q

What is Cushing’s reflex?

Why does it occur?

A
  1. Hypertension
  2. Bradycardia
  3. Irregular breathing
  4. Inc’d ICP approaches and surpasses IC MABP -> reduced IC perfusion -> sympathetic activation -> peripheral vasoconstriction and inc’d HR -> inc’d BP to restore IC perfusion
  5. Aortic arch baroceptors sense inc’d BP and inc vagal tone -> bradycardia
  6. Inc’g ICP -> pressure on brainstem (medulla oblongata) -> irregular breathing
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11
Q

List the 7 causes of ALOC.

A
  1. Hypotension
  2. Hypoglycaemia
  3. Hypoxia
  4. Post-ictal (think stunned neurons)
  5. Post-intoxicating drugs
  6. Brain or brainstem compression due swelling or a mass
  7. Bleeding
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12
Q

What are the drugs and doses of diruetic agents that can be used to treat inc’d ICP?

A
  • Mannitol 0.25-1g/kg IV bolus
  • Hypertonic 3% normal saline - 0.1-1ml/kg/hr
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13
Q

How is the severity of head injuries classified?

What is the mortality rate for each?

A
  • Mild TBI - GCS 14-15 - <0.1% mortality
  • Moderate TBI - GCS 8-13 - <20%
  • Severe TBI - GCS 3-8 - ~40%
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14
Q

Describe the age and sex distribution of head injuries.

A
  • Age - tri-modal
    • Infants 0-4y
    • Adolscents 15-24y
    • Elderly - >75y
  • Sex M:F = 2:1
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15
Q

What is the target MAP for the head injured patient?

Why is this the case?

A
  • Aim for MAP >= 80mm Hg
  • Needs to be higher due to diminished ability to auto-regulate in the injured brain
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16
Q

What are the two types of brain oedema?

A
  • Cytotoxic oedema -> caused by cellular damage -> ion shifts, cell membrane damage, release of free radicals etc
  • Extracellular oedema -> caused by damage to the BBB
17
Q

What are the indications for seizure prophylaxis?

A
  • GCS <10
  • Abnormal CT head
  • Already seized
18
Q

List ten clinical signs of raised ICP.

A

Think:

  • Head injury signs
  • Cushing’s reflex
  • Herniation
  1. Severe headache
  2. N+V
  3. Focal neurological findings
  4. Visual disturbances
  5. Dec’d LOC/GCS
  6. Pupillary dilatation (or constriction)
  7. Hypertension
  8. Bradycardia
  9. Seizures
  10. Coma
  11. Agonal respirations
19
Q

Which skull fractures require prophylactic IV Ab treatment?

Which drugs should be used?

A
  • Open or depressed skull #s
  • Involvment of a bony sinus
  • Persence of pneumocephalus

Abs:

  • 2g IV ceftriaxone PLUS
  • 1g IV vancomycin
20
Q

List six signs of base of skull #.

A
  1. CSF from nose or TMs
  2. Battle sign
  3. Raccoon eyes
  4. Hearing loss/deafness
  5. Vertigo
  6. Seventh nerve palsy
  7. Headache
21
Q

What abs should be used for base of skull #’s?

A
  • 2g IV ceftriaxone PLUS
  • 1g IV vancomycin

Consult NROS first.

22
Q

What is the most common CT abnormality in patients with mod-severe TBI?

A

SAH

23
Q

A patient suffers a sig’t head injury with short LOC before regaining consciousness and returning to baseline. They then rapidly deteriorate with decreasing GCS in the ED.

What is the likely injury?

A

Sig’t head injury -> lucid interval -> rapid deterioration in GCS = extra-dural

Classic but uncommon.

24
Q

What is the most common region and vessel injured that leads to an extra-dural haemorrhage?

A

Temporal injury -> middle meningeal artery injury

25
Q

Damage to which vessel normally results in SDH?

A

Shearing of the bridging dural veins

26
Q

If an ICH crosses the falx, what type of bleed is it?

A

SDH

27
Q

What are the common CT findings in diffuse axonal injury?

What are two common mechanisms?

A

CT findings

  • Normal CT
  • Punctate haemorrhages at grey/white matter interface and in basal ganglia

Mechanisms

  • Shearing forces
    • MVA
    • Shaken baby syndrome
28
Q

What is second impact syndrome?

A

A second mTBI while the brain is still recovering from the first can lead to:

  • Rapid cerebral oedema
  • Death
29
Q

List two tests that are validated for assessment of mTBI.

A
  • Mini-Cog
  • Quick Confusion Scale
30
Q

What is the method of reversal of wafarin in head-injured patients with ICH?

A
  • FFP, or
  • 4-factor concentrate (II, VII, IX and X PLUS proteins C&S)
31
Q

List three immediate actions to decrease ICP.

A
  • Hyperventilation - transient
  • Osmotic diuretics - mannitol and hypotonic saline
  • CSF drainage - conservative or surgical
32
Q

What are the indications for ICP monitoring?

A
  • Severe TBI - GCS < 9
  • Inability to monitor clinical signs of rising ICP
33
Q

What are the criteria for Head CT according to the Canadian CT Head Rule? Who does this rule apply to?

A

Inclusion criteria:

  • Adults
  • Traumatic cause
  • GCS 13-15
  • LOC, amnesia or confusion
  • Not anti-coagulated
  • Absence of open skull #

High-risk factors for NROS intervention:

  1. Base of skull # signs
  2. Suspected open or depressed skull #
  3. GCS < 15 2h post injury
  4. Vomiting
  5. Age >65y

Medium-risk factors for CT id’d brain injury:

  1. Retrograde amnesia >30mins
  2. Dangerous mechanism
34
Q

Discuss the sens and spec of the Canadian CT Head Rule and the New Orleans CT Head Rule.

List 3 differences in the rules.

A
  • NOCTHR only includes patients with GCS 15
  • BOTH rules 100% sensitive for NROS intervention
  • CCHR more specific for all 3 endpoints, ie:
  1. NROS intervention
  2. Clinically sig’t injury
  3. Any CT Id’d injury
  • NOCTHR identifies more injuries but results in A LOT more scans.
35
Q

What are the indications for acute seizure prophylaxis in head trauma?

A

Think Severity, Seizures, Unable to assess, Type of injury

  • Severity
    • Severe TBI (GCS =<8)
  • Seizures
    • Seizure at time of injury
    • Seizing on presentation
    • Hx of pre-injury seizures
  • Unable to assess:
    • Paralysed, I&V
  • Injury type
    • Any penetrating injury
    • Depressed skull #
    • Acute SDH
    • Acute EDH
    • Any acute ICH
36
Q

List complications of TBI.

A
  • Neuro
    • Seizures
    • CNS infection
      • Meningitis
      • Abscess
      • Cranial osteomyelitis
  • Medical
    • DIC - injured brain releases tissue thromboplastin
    • Cardiac dysfunction
      • Arrhythmias! - SVT ? due catecholamine surge
      • Many ECG changes including
        • STE
        • Long QTc
        • Peaked or inverted T-waves
        • U-waves
    • Neuro-cardiogenic pulm’y oedema
      • Again ? due to catecholamine surge
37
Q

List three CT findings in cerebral oedema.

A
  1. Loss of gray-white differentiation
  2. Compressed sulci
  3. Ventricular effacement
38
Q
A

Trauma (12 decks)

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