Stupor And Coma

Question 1

Consciousness

Answer 1

State of alert cognition in which
individual is aware of self and environment

Question 2

Depressed

Answer 2

lethargic and less responsive to
environment, but capable of normal responses

Question 3

Obtunded

Answer 3

capable of responding to stimulation,
but responses blunted

Question 4

Stupor

Answer 4

somnolent at rest; rousable only with
vigorous tactile or noxious stimulation

Question 5

Comatose

Answer 5

unconscious and unresponsive to any
applied stimulus; reflexes may be present

Question 6

Brain dead

Answer 6

comatose, comprised brainstem
reflexes and vital functions requiring life support
– +/- abnormal electrophysiologic or provocative tests of brain function
– Electrophysiologic and provocative tests must corroborate clinical exam

Question 7

Anatomy of consciousness

Answer 7

ARAS received incoming info - synapses in thalamus and send info to appropriate locations
Cerebral cortex - ultimate measure of consciousness

Question 8

Bilateral/diffuse cerebrocortical disease

Answer 8

Traumatic cerebral edema
Toxic and metabolic encephalopathies
Inborn errors of metabolism

Question 9

Damage to RAS in brainstem

Answer 9

Compressive
Infiltration or destruction of parenchyma

Question 10

Intracranial pressure physiology

Answer 10

Pressure inside the calvarium
Generated by resident tissue volumes
- brain parenchyma 80%
- blood 10%
- CSF 10%
Inelastic calvarium
Normal ICP - 5-10 mmHg

Question 11

Monro-kellie hypothesis

Answer 11

Compensatory responses to ICP elevation
Two methods to decrease pressure
– remove CSF to spinal Spinal subarachnoid space
– decrease CSF production
Last resort - decrease Cerebral blood flow (CBF)

Question 12

Intracranial hypertension

Answer 12

Increase due to abnormal tissue, brain edema, obstructive hydrocephalus
Ultimately decreases cerebral blood flow
As CBF ^ —> mean arterial blood pressure ^ = increased intracranial pressure
CBF = mABP - ICP

Question 13

Decreased CBF

Answer 13

Decreased cerebral perfusion

Question 14

Reversible injury

Answer 14

Hypoxia/ischemia
Excitotoxic injury cascade

Question 15

Cell death

Answer 15

Selective vulnerability of brain tissues
Neurons
Glia
Endothelium

Question 16

Caudal transterntorial herniation

Answer 16

Midbrain compression
Stupor to coma
Mydriasis no PLR
Decerebrate posture
+/- Ventrolateral strabismus

Question 17

Rostral transtentorial herniation

Answer 17

Cerebellar and midbrain compression
Decerebellate posture

Question 18

Foramen magnum herniation
Acute

Answer 18

Stupor to come
Respiratory arrest; hypoventilation
CN IX-XII deficits
Death

Question 19

Subfalcine herniation

Answer 19

Common on one side of the cerebrum
Easy to ID in images
Clinical signs represent location
• right forebrain

Question 20

Transcalvarial herniation

Answer 20

herniation through a defect in the skull - common by trauma or after surgery

Question 21

Clinically detrimental ICP value

Answer 21

Absolut value unknown
- 20-25 mmHg too high
- 30 mmHg will decrease CBF
Rate of change is more important
Measuring ICP
- indirect Doppler
- direct - fiber optic probes

Question 22

Evaluation of altered consciousness patients

Answer 22

Postural abnormalities and motor function
Brainstem reflexes
Level of consciousness
Composite scoring system
- small animal coma scale (SACS)
- modified Glasgow coma scale

Question 23

Pupils and prognosis

Question 24

Brainstem reflex - oculovestibular

Question 25

SACS

Question 26

Traumatic brain injury

Answer 26

Open - defect in skull, open in skull Closed - skull intact but brain is injured

Question 27

Primary brain injury

Answer 27

Tissue deformation produced at moment of injury Contusion, concussion, laceration, diffuse axonal injury (spinning), vascular disruption (hemorrhage) - these injuries have already happened and are beyond our control - cascade into secondary injury

Question 28

secondary brain injury

Answer 28

Initiation by primary injury Complex Inflammation, excitotoxicity (free radicals), ischemia, lactic acidosis Pathways are primary targets of medical treatment Primary and secondary injury contribute to ICH

Question 29

Imaging for TBI

Answer 29

Cross sectional modalities preferred (3D imaging) Consider if surgery is end goal

Question 30

Imaging considerations for closed injury

Answer 30

Closed injury - focal problem - deteriorating SACs score - indication of other injury

Question 31

Imaging considerations for open injury

Answer 31

Open injury - penetrating missile - depressed skull fracture - contaminated wounds

Question 32

When would you not consider 3D imaging?

Answer 32

In animal has history or potential for bullet fragments which can disrupt the CT or MRI images - radiograph is ideal for those patients

Question 33

Prognosis for TBI

Answer 33

Forebrain & cerebellar injury = Better prognosis SACS of 8 = 50% probability they’ll survive 48 hours Post traumatic epilepsy can develop m-y after injury

Question 34

Managing altered consciousness patient

Answer 34

emergency ABC Commonly poly systemic injury - get BP *** Check for axial, intrathoracic, abdominal, appendicular, cutaneous injury

Question 35

Goal 1 for altered conscious management

Answer 35

Restore vital parameters Fluids - colloids or crystaloids are ideal Correcting shock can greatly improve prognosis

Question 36

goal 2 for managing ICH

Answer 36

Reduce Intracranial pressure Physical non invasive - head elevation - induce hypothermia Avoid jugular compression, Invasive Decompressive craniectomy & durotomy CSF diversion - REFER

Question 37

Pharmacological methods to decrease ICP

Answer 37

Diuretics Mannitol - osmotic diuretic, positive theological agent, free radical scavenger Furosemide - synergistic w mannitol, prevents rebound ICP

Question 38

when should diuretics be admin for intracranial hypertension?

Answer 38

1. Vital parameters restored/stable 2. SACS score deteriorating despite therapy • ICP spikes commonly associated with clinical decline 3. Brain edema identified on imaging study

Question 39

Drug induced coma

Answer 39

Barbituates and NMDA antagonists – Neuroprotective • Disadvantages – Hypoventilation – Hypotension – Complicates clinical assessment of SACS

Question 40

Goal 3 for altered patient management

Answer 40

Supportive systemic care Analgesics • Nursing/Hygiene • Nutritional support • Physical therapy

Question 41

Daily monitoring

Answer 41

Serial or continual MaBP ECG Blood glucose PCV/TS Urine output SACS Body weight 24 hour care is necessary