Abnormalities of Consciousness Flashcards

1
Q

“Brain-dead”

A

Comatose + compromised brainstem reflexes & vital functions that require life support

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2
Q

What tract is responsible for consciousness?

A

ARAS (Ascending Reticular Activating System)

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3
Q

What etiologies cause altered consciousness

A
  1. Bilateral/diffuse cerebrocortical disease (traumatic cerebral edema, toxins)
  2. Damage to the RAS (compression, damage to parenchyma)
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4
Q

Normal ICP should be what?

A

less than 10mg of mercury (Hg)

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5
Q

What is the Monroe-Kellie Hypothesis?

A

IF ICP increases, body compensates by either first, decreasing CSF volume, and then once this response gets overwhelmed, decreasing cerebral blood flow (latter is BAD after certain point!)

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6
Q

What is Intracranial Hypertension (ICH), and the cycle of ICH & ICP?

A

Elevated ICP // beyond point where physiological function is normal -> -> because ICP is so high, body tries to compensate by decreased cerebral blood flow -> hypotension -> increase CSF & cerebral blood flow -> ICH —> VISCIOUS CYCLE!!

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7
Q

What are detrimental effects of DECREASED CBF?

A

Decreased cerebral perfusion -> hypoxia, ischemia (affects neurons first! then glial cells, then endothelial cells)

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8
Q

Cranial nerve deficits related to midbrain compression?

A

Occipital lobe of cerebrum blood edema-> increased pressure on midbrain (CN III & CN IV)

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9
Q

Caudal Transtentorial Herniation (caused by ICP) increases pressure on what part of the brain?

A

Midbrain

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10
Q

Rostral Transtentorial Herniation (caused by ICP) increases pressure on what part of the brain?

A

Midbrain & Cerebellum

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11
Q

Foramen Magnum Herniation (caused by ICP) increases pressure on what part of the brain?

A

Acute herniation of the midbrain!

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12
Q

Subfalcine Herniation - what is it?

A

Separated cerebrum down midline -> decreased consciousness, hemiparesis, coma

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13
Q

Transcalvarium Herniation - what is it + causes

A

Through defect in skull
-trauma
-iatrogenic (open skull to expose tumor during sx)

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14
Q

What dictates a detrimental ICP?

A

The RATE of change! (absolute value unknown).

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15
Q
A

Right forebrain lesion (head tilt ipsilateral to lesion)

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16
Q
A

Right forebrain lesion (head tilt ipsilateral to lesion) with left thoracic proprioceptive defecits

17
Q

What type of herniation?

A

ROSTRAL transtentorial herniation! - Decerebellate posture

Trunk is twisted and flexed!

18
Q

What type of herniation?

A

CAUDAL transtentorial herniation
- Decerebrate posture (trunk is NOT twisted or flexed!)

19
Q

Small Animal Coma Scale (Lower # = worse clinical presentation). How does this dictate prognosis?

A

Do not base prognosis on single coma scale. Instead, should be based on trends / serial evaluations!

20
Q

Traumatic Brain Injury - 1º vs 2º ?

A

1º = tissue deformation occurs instantaneously to moment of injury, direct damage to parenchyma

2º = initiated by 1º -> self-perpetuating series of events (inflammation, ischemia, free-radical production)

BOTH LEAD TO ICH!!!

21
Q

When not do to cross-sectional imaging of TBI?

A

If pt has gunshot injury (metal in head interferes with CT /MRI magnet)

22
Q

TBI with coma scale of 8 prognosis

A

50% chance of mortality; higher than 8 increases prognosis vitality

23
Q

What increases post-traumatic epilepsy development?

A

The severity of the traumatic brain injury

24
Q

Management of ICH:
Goal 1
Goal 2
Goal 3

A

Goal 1: Restoration of vital parameters!
Goal 2: Reduce ICP (head elevation, induction of hypothermia [reduce cerebral metabolic rate], avoid jugular compression) ; REFERRAL FOR PHYSICAL INTERVENTIONS
Goal 3: Systemic Supportive Care (analgesic, nursing care, physical therapy)

25
Q

Drugs to decrease ICP? Precautions?

A

Diuretics (Mannitol, Furosemide)

Mannitol draws intracellular water out of brain and into bloodstream
- ENSURE VITAL PARAMETERS ARE HEALED/ STORED BEFORE ADMIN!

26
Q

Downsides to using barbiturates and NMDA antagonists for ICH pts

A

hypoventilation, hypotension -> puts pt into pharmacologic-induced coma

27
Q

Describe osmolality & Mannitol’s rheological effects

A

Higher osmolality = lower water concentration, higher solute concentration (e.g., dehydration)

Lower osmolality = higher water concentration, lower solute concentration (e.g., edema)

Fluid flows from areas of LOW osmolality to HIGH osmolality

MANNITOL INCREASES OSMOLALITY of bloodstream -> BLOODSTREAM OSMOLALITY IS HIGHER THAN TISSUE OSMOLALITY –> Fluid from tissue (BRAIN, CSF) flows OUT INTO to the bloodstream