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Anatomy > Epidural haemorrhage > Flashcards

Epidural haemorrhage Flashcards

1
Q

What is a common cause of epidural haemorrhage?

A

Trauma to the temporal region
- contains the pterion- junction of parietal, temporal, frontal, zygoma and sphenoid bone where the middle meningeal artery runs -> most vulnerable area of the skull -> rupture results in extradural haemorrhage

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2
Q

What are signs of a raised ICP?

A

• Thunderclap headache- stretch of pain receptors in dura and BVs
• Similar episodes in past month- leak warning of impending rupture (50% cases)
• Decreased GCS- compression of brainstem reticular formation
• Cognitive deterioration
• Irritability
• Nausea/vomiting- stimulation of brain stem vomiting centre
• Papilloedema- raised ICP compresses veins -> blood back flow -> engorged retinal veins -> bilateral, swollen optic discs, surrounding retinal haemorrhages
• Mydriasis (unilateral pupil dilation)- CN3 parasympathetic fibers compressed
• Seizures
• Focal neurological signs
• Cushing’s reflex
- HTN- compensatory response to raised ICP (CPP = MAP – ICP)
- Bradycardia- compensatory parasympathetic up-regulation to increased BP
- Irregular breathing- brainstem compression
• Herniation syndromes
• Cessation of cardiorespiratory drive (death)- tonsillar herniation

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3
Q

What are the differing CT findings for epidural and subdural haemorrhages?

A

Epidural haemorrhage: haematoma does NOT follow suture margins (as it is contained within the dura) -> lens-shaped

Subdural haemorrhage: cross suture lines (but cannot cross dural margins) -> appear crescent shaped

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4
Q

Describe the pathology and causes of an epidural haemorrhage?

A

Path: Bleed into potential space between skull and dura
• Tearing of middle meningeal artery (closely adheres to pterion, entering skull via foramen spongiosum) -> haemorrhage over cerebral convexity of middle cranial fossa
External carotid -> maxillary a -> middle meningeal a
• If anterior meningeal artery (occasional) -> haemorrhage in anterior cranial fossa

Causes: traumatic head injuries (pterion- temporal or occipital regions of skull)

Epi: most common in younger pts (dural less tightly adhered to skull, risky activity)

Clinical:
• Initial, temporary improvement in condition post-TBI (“lucid interval”) -> then deteriorates (20-50% cases)
• Headache, decreased LOC, nausea/vomiting, head contusion

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5
Q

Describe the pathology and causes of a subdural haemorrhage?

A

Path: bleeding into space between dura and arachnoid mata

  • > Tearing of bridging veins draining brain surface to dural sinuses
  • > Rising ICP -> self-limits venous bleeding

Cause: trauma, Berry aneurysm

Risk: elderly and ETOH (cerebral atrophy stretches bridging veins), also smoking, HTN, FMHx

Clinical: thunderclap headache, vomiting, reduced LOC, seizures, meningism

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6
Q

What are the herniation syndromes?

A
  1. Subfalcine- crosses midline, compresses ACA
  2. Central- supratentorial brain tissue displaces into infratentorial compartment (including thalamus and hypothalamus. Compresses CN3, pituitary stalk, pontine a tearing, rostral interstitial nucleus of MILF
  3. Uncal- temporal lobe displaces into infratentorial compartment. Compresses CN3, reticular formation, cerebral peducle
    - Clinical: CN3 palsy (down and out gaze), decreased LOC, contralateral haemiparesis
  4. Tonsilar- cerebellar tonsils displace into foramen magnum.
    - Compresses cardiorespiratory centres in medullar oblongata -> death
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7
Q

Describe the pathogenesis of an uncal herniation?

A

⇒ Progressive haemorrhage -> growing haematoma
⇒ Overcomes cranial cavity capacity to compensate for SOL
⇒ Raised ICP
⇒ Inner part of temporal lobe (uncus) moves tentorium (dura mater extension separating cerebrum from cerebellum) to put pressure on brainstem
⇒ Uncal (transtentorial) herniation
⇒ Displaces medial lobe over edge of tentorium cerebelli
⇒ CN3 entrapped and midbrain compressed

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8
Q

Describe the clinical presentation of an uncal herniation?

A
  • unilateral fixed pupil dilation: CN3 squeezed -> contained parasympathetic fibres surrounding motor fibres first affected, unopposed sympathetic fibres -> dilation
  • down and out gaze: CN3 palsy -> loss of ocular muscle innervation, except LR and SO
  • contralateral homonymuos hemianopia (partial visual field loss): ipsilateral PCA compression causes ischaemia of primary visual cortex
  • ipsilateral hemiparesis: contralateral cerebral curs (part of cerebral peduncle in midbrain, containing descending corticospinal and corticobulbar tracts), contralateral hemiparesis also seen
  • Duret haemorrhage: brainstem distortion (downward displacement) -> rupture of pontine arteries -> midbrain and upper pons (brainstem) bleeding (duret haemorrhages)
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9
Q

Outline the pathogenesis of an epidural haemorrhage with transient lucid interval followed by unconsciousness?

A

⇒ TBI -> skull # (pterion, weak junction of 5 bones)
⇒ fractured bone edges lacerate middle meningeal artery (adheres to pterion)
⇒ Initial LOC: disrupted reticular activating system (controls transition between conscious states) -> initial LOC from concussive force
⇒ Bleeding into extradural space
⇒ Brief lucid interval: transient neuronal recovery from concussive force -> haematoma not accumulated enough to raise ICP (cranial cavity still able to buffer pressure with venous blood and CSF movements)
⇒ Raised ICP (beyond compensatory capacity) -> headache, vomiting, contusion
⇒ Cushing’s reflex (HTN, bradycardia, irregular breathing)
⇒ Focal neurological symptoms
⇒ Herniation -> compression of midbrain -> LOC

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10
Q

What are the causes and consequences of a CSF leak post-TBI?

A

CSF leak post-TBI causes: indicates base of skull fracture, with underlying dural/meningeal laceration
- cribiform plate: otorrhoea CSF elak
- petrous temporal bone: rhinorrhoea CSF leak
Complications: risk CNS infection (meningitis, abscess), cranial nerve defects

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11
Q

What are signs of a base of skull fracture?

A
  • CSF leak
  • Battle sign- subcut bleeding over mastoid process
  • Racoon eyes- subcut bleeding around orbit (base of skull # confines bleed to orbit/contained in fascia, black eyes are not)
  • Cranial nerve deficits
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12
Q

Describe the innervation of the ocular muscles?

A

Mneumonic: LR6SO4O3

  • Lateral rectus (LR)- CN6 (abducens)
  • Superior oblique (SO)- CN4 (trochlear)
  • Others (O)- CN3 (oculomotor)
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13
Q

Describe the clinical presentation of an oculomotor nerve compression?

A

Impaired medial rectus (MR), superior rectus (SR), inferior rectus (IR), inferior oblique (IO)
-> eyes rest down and out

Also, compression of parasympathetic activity -> unopposed sympathetic activity -> unilateral pupil dilation

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14
Q

Describe the clinical presentation of a trochlear nerve compression?

A

Impaired superior oblique (SO) movement

-> inability to move affected eye down and out

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15
Q

Describe the clinical presentation of an abducens nerve compression?

A
  • impaired innervation of lateral rectus (LR) muscle -> inability to move eye outwards laterally
  • convergent strabismus (cross-eyed)
  • side-by-side diploplia
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16
Q

What is the criteria for a C-spine injury?

A

Nexus criteria (C-spine # cannot be excluded if any criterion present):
NSAID mnemonic
N- neurological deficit (focal)
S- spinal tenderness (midline cervical)
A- altered mental status (GCS <15)
I- intoxication
D- distracting injury (any injury w sufficient pain to distract pt from C-spine injury, e.g. long bone #, visceral injury, large laceration, extensive burns)

17
Q

What are the consequences of a vertebral injury at C2?

A

C2: loss of phrenic nerve (C3, 4, 5 keeps us alive) -> loss of diaphragm movement -> respiratory muscle weakness/paralysis-> death

18
Q

What are the consequences of a vertebral injury at C6?

A

C6:

  • sensory loss below C6
  • loss of arm medial rotation and adduction
  • loss of elbow extension
19
Q

What are the consequences of a vertebral injury at T2?

A

T2:

  • loss of sensation below T2
  • loss of lower limb movements
  • incontinence
20
Q

Why is the C-spine the most vulnerable vertebral region to injury?

A

• Cervical vertebral column shape and facet joint angles -> allow high range of motion on multiple places
• C-spine vulnerable to injury: located in exposed area above torso, carrying weight of skull and brain
• Thoracic and lumbar vertebral columns have greater structural support and more limited range of movement
- Thoracic: ribs articulate with transverse processes and sternum -> fixed rigidly
- Lumbar: anchored by strong paravertebral muscles and internal muscles (e.g. psoas major)

21
Q

Describe how GCS is monitored?

A

Glasgow Coma Scale (GCS): objective recording of conscious state of person
- Documented every 15mins, then hourly
- Give best eye response (4), best verbal response (5), best motor response (6)
Eye- none, pain, verbal stimuli, spontaneous
Verbal- none, incoherent, inappropriate words, confused, oriented
Motor- none, extension to pain or decerebrate (abnormal posture, wrists externally rotated), flexion to pain or decorticate, withdraws from pain, localised pain, obeys commands

Scoring:
o Mild: 14-15
o Moderate: 9-14
o Severe: 3-8
o GCS <8 requires intubation

Prognosis:
o <5 = 85% die, vegetative
o >11 = 85% good chance of recovery, 5-10% die

22
Q

Describe the brainstem control of respiration?

A

• Location: respiratory centre nuclei in both medulla and pons
• Central physiological respiratory control based on chemoreceptors responsive to pH
• pH chemoreceptors located throughout ventrolateral surface of medulla
- Detect pH decreased in CSF
- Stimulated increased RR (hyperventilation) -> blow off CO2 to normalize pH
- Conversely, high pH is controlled with hypoventilation

Medulla has 2 respiratory groups: ventral (expiration) and dorsal (inspiration)
Pons has pneumotaxic centre (rate and depth of breathing_) and apneustic centre (stimulate and limit inspiration)

23
Q

Describe the brainstem control of cardiac function?

A
  • Location: nuclei in medulla and pons
  • HR control
    o Sympathetic supply to SA node- accerlerans nerve (arises from medulla oblongata)
    o Parasympathetic supply to SA node- vagus nerve (arises from medulla oblongata)
  • BV contraction- rostroventral lateral medulla (RVLM)
24
Q

Describe central transtentorial herniation?

A

• Epi: most common
• Path: downward displacement of supratentorial brain tissue into infratentorial compartment
o Thalamus and hypothalamus herniate through tentoria incisura
• Causes: supratentorial mass lesion, diffuse brain swelling, focal oedema, acute hydrocephalus
• Complications:
o CN3 compression -> down and out palsy and fixed, dilated pupil (sympathetic pathways compressed)
o Pituitary stalk compression -> diabetes insipidus (hypothalamus/pituitary damage, lack of antidiuretic hormone)
o Tearing of pontine arteries -> durets haemorrhage (midbrain, upper pons bleed)
o Compression of rostral interstitial nucleus of medial longitudinal fasciculus (riMLF) -> paralysis of upward gaze

25
Q

Describe uncal herniation?

A

• Path: inferior lobe of temporal lobe displaces into infratentorial compartment
• Complications:
o CN3 compression -> down and out gaze and fixed, dilated pupil
o Reticular formation -> decreased LOC
o Cerebral peduncle-> contralateral hemiparesis

26
Q

Describe subfalcian herniation?

A
  • Path: displaced brain tissue across midline, under falx cerebri
  • Complication: ACA compression -> frontal and parietal lobe extensive infarction
27
Q

Describe tonsilar herniation?

A

• Path: downward pressure forces cerebellar tonsils into foramen magnum
-> Compress medulla oblongata and spinal cord
• Complication: compressed medullary cardiac and respiratory centres -> death

28
Q

Describe retro-alar herniation?

A
  • Path: increased frontal lobe pressure causes posterior brain tissue displacement over lesser wing of sphenoid bone
  • Complication: carotid artery compression -> ACA and MCA infarction

Anatomy (21 decks)

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