Stupor And Coma Flashcards
Consciousness
State of alert cognition in which
individual is aware of self and environment
Depressed
lethargic and less responsive to
environment, but capable of normal responses
Obtunded
capable of responding to stimulation,
but responses blunted
Stupor
somnolent at rest; rousable only with
vigorous tactile or noxious stimulation
Comatose
unconscious and unresponsive to any
applied stimulus; reflexes may be present
Brain dead
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
Anatomy of consciousness
ARAS received incoming info - synapses in thalamus and send info to appropriate locations
Cerebral cortex - ultimate measure of consciousness
Bilateral/diffuse cerebrocortical disease
Traumatic cerebral edema
Toxic and metabolic encephalopathies
Inborn errors of metabolism
Damage to RAS in brainstem
Compressive
Infiltration or destruction of parenchyma
Intracranial pressure physiology
Pressure inside the calvarium
Generated by resident tissue volumes
- brain parenchyma 80%
- blood 10%
- CSF 10%
Inelastic calvarium
Normal ICP - 5-10 mmHg
Monro-kellie hypothesis
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)
Intracranial hypertension
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
Decreased CBF
Decreased cerebral perfusion
Reversible injury
Hypoxia/ischemia
Excitotoxic injury cascade
Cell death
Selective vulnerability of brain tissues
Neurons
Glia
Endothelium
Caudal transterntorial herniation
Midbrain compression
Stupor to coma
Mydriasis no PLR
Decerebrate posture
+/- Ventrolateral strabismus
Rostral transtentorial herniation
Cerebellar and midbrain compression
Decerebellate posture
Foramen magnum herniation
Acute
Stupor to come
Respiratory arrest; hypoventilation
CN IX-XII deficits
Death
Subfalcine herniation
Common on one side of the cerebrum
Easy to ID in images
Clinical signs represent location
• right forebrain
Transcalvarial herniation
herniation through a defect in the skull - common by trauma or after surgery
Clinically detrimental ICP value
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
Evaluation of altered consciousness patients
Postural abnormalities and motor function
Brainstem reflexes
Level of consciousness
Composite scoring system
- small animal coma scale (SACS)
- modified Glasgow coma scale
Pupils and prognosis
Brainstem reflex - oculovestibular
SACS
Traumatic brain injury
Open - defect in skull, open in skull
Closed - skull intact but brain is injured
Primary brain injury
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
secondary brain injury
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
Imaging for TBI
Cross sectional modalities preferred (3D imaging)
Consider if surgery is end goal
Imaging considerations for closed injury
Closed injury
- focal problem
- deteriorating SACs score
- indication of other injury
Imaging considerations for open injury
Open injury
- penetrating missile
- depressed skull fracture
- contaminated wounds
When would you not consider 3D imaging?
In animal has history or potential for bullet fragments which can disrupt the CT or MRI images - radiograph is ideal for those patients
Prognosis for TBI
Forebrain & cerebellar injury = Better prognosis
SACS of 8 = 50% probability they’ll survive 48 hours
Post traumatic epilepsy can develop m-y after injury
Managing altered consciousness patient
emergency ABC
Commonly poly systemic injury
- get BP ***
Check for axial, intrathoracic, abdominal, appendicular, cutaneous injury
Goal 1 for altered conscious management
Restore vital parameters
Fluids - colloids or crystaloids are ideal
Correcting shock can greatly improve prognosis
goal 2 for managing ICH
Reduce Intracranial pressure
Physical non invasive
- head elevation
- induce hypothermia
Avoid jugular compression,
Invasive
Decompressive craniectomy & durotomy
CSF diversion - REFER
Pharmacological methods to decrease ICP
Diuretics
Mannitol - osmotic diuretic, positive theological agent, free radical scavenger
Furosemide - synergistic w mannitol, prevents rebound ICP
when should diuretics be admin for intracranial hypertension?
- Vital parameters restored/stable 2. SACS score deteriorating despite therapy
• ICP spikes commonly associated with clinical decline - Brain edema identified on imaging study
Drug induced coma
Barbituates and NMDA
antagonists
– Neuroprotective • Disadvantages
– Hypoventilation
– Hypotension
– Complicates clinical
assessment of SACS
Goal 3 for altered patient management
Supportive systemic care
Analgesics • Nursing/Hygiene • Nutritional support • Physical therapy
Daily monitoring
Serial or continual
MaBP
ECG
Blood glucose
PCV/TS
Urine output
SACS
Body weight
24 hour care is necessary
