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Disturbed sensorium - Coggle Diagram
Disturbed sensorium
Risk factors
· Pulmonary disorders: Cause hypoxia/hypoxemia.
· Drug therapy: Sedation, analgesia, toxicity, interactions.
· Cerebral disorders: Expanding lesions, brain injury.
· Surgical factors: Prolonged anesthesia.
Cardiovascular status: Low cardiac output, low perfusion, arrhythmias.
Age: Incidence increases with age.
Perceptual/Sensory: Sleep deprivation, sensory overload/deprivation.
Metabolic factors: Glucose changes, hyper/hypometabolism.
Fluid/Electrolyte disturbances: Na+/K+ imbalances, hypovolemia.
Continuum
Alert: Responds appropriately.
Confused: Disoriented, impaired judgment.
Lethargic: Drowsy, needs gentle stimulation to respond.
Obtunded: Slow response, needs repeated stimulation.
Stuporous: Minimal response to vigorous/painful stimulation.
Comatose: No observable response to any stimulus.
Iocked in syndrome
· ✓ Wakefulness AND ✓ Awareness AND ✓ Tetraplegia.
Communicate via eye movements/blinking.
Not a Disorder of Consciousness.
· Damage limited to the brainstem; cortex is intact.
· Results in full paralysis; only voluntary movement is eye opening/fluttering.
· Eye movements reflect high-level awareness.
Diagnosis
Perform primary assessment & resuscitation using ABCDE approach.
Perform secondary assessment.
ABCDE Framework
· Drugs (DON'T )
Dextrose
For hypoglycemia
Give after thiamine to prevent Wernicke’s encephalopathy
Oxygen (High flow)
Corrects hypoxia
Protects brain function
Naloxone (0.4–2 mg IV)
Treats opioid overdose
Rapidly restores consciousnes
Thiamine (Vitamin B1)
Administer before glucose
Prevents glucose-induced coma in thiamine deficiency
Secondary Assessment:
History (SAMPLE).
General appearance.
Focused neurological exam.
· Plus head-to-toe examination.
· Focused Neurological Exam:
· Level of Consciousness (GCS vs. FOUR Score).
[· Pupillary
Midbrain damage: pupils slightly dilated, non-reactive to light
Third nerve lesion: fixed, dilated pupil on same side as injury
Metabolic coma: pupillary responses usually preserved
· Mental status / Cognitive function.
· Motor & Sensory function.
· Breathing pattern.
Oculomotor eye movement
Conjugate gaze requires intact CN III, VI, VII connections
Structural lesions → disconjugate gaze
Extraocular movement deficits usually indicate structural causes
Examples
Exotropia: outward deviation of the eye
Esotropia: inward deviation of the eye
CN VI Paralysis: inability to move eye laterally
Ascending RAS
Located in brainstem, near key brainstem reflexes
Pupillary light reflexes: CN II & III
Reflex eye movements: CN III, VI, VIII & medial longitudinal fasciculus (MLF)
Clinical significance:
Preservation of these reflexes → functional ARAS
Absence → possible ARAS or brainstem dysfunction
Coma
Coma: Absent Wakefulness AND Awareness.
Caused by severe bilateral hemisphere, thalamic, or brainstem damage.
No sleep-wake cycles.
Eyes closed.
Usually resolves within 2 weeks, transitioning to Vegetative State (VS) or Minimally Conscious State (MCS).
Vegetative state
Vegetative State (VS): ✓ Wakefulness – ❌ Awareness.
· Spontaneous eye opening.
· No awareness, sporadic gaze, involuntary movements.
No purposeful responses, no language comprehension/expression.
Considered Permanent after >1 year (traumatic) or >3 months (non-traumatic).
Minimally Conscious State (MCS)
Minimally Conscious State (MCS): ✓ Wakefulness AND ✓ Awareness (minimal but definite).
Fragments of meaningful interaction with the environment are preserved.
Patients in MCS may:
· Establish eye contact.
· Purposefully grasp objects.
· Respond to commands.
· Answer with the same word.
Includes eye opening + some language function, command following, visual pursuit, automatic movements.
· Inconsistent but clear signs of self-awareness.
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Emotional responses to family/photos.
· Purposeful movements (e.g., reaching for a glass).
· Considered a transitional state during recovery or decline.
Post-traumatic confusional state
· ✓ Wakefulness – ❌ Awareness (Disoriented, confused).
· Can last for days to years.
· Extended wakefulness but clearly confused.
Can recognize objects and make appropriate movements (e.g., reaching for a glass).
More consistent than MCS in following commands and language.
Ongoing Assessment of Consciousness
Essential to:
Track trends
Evaluate therapy response
Identify new problems or changes from baseline
Enable timely interventions
Mechanism of disturbed sensorium
Consciousness requires intact cerebral hemispheres + functional ascending RAS.
Maintained by continuous impulses from brainstem → cerebral hemispheres.
Causes:
Cerebral hemisphere malfunction
Brain stem malfunction
Facts
Unconsciousness can be Partial (Stupor) or Complete (Coma).
· It can be Reversible (sleep, sedation) or Non-Reversible (some disorders of consciousness).
Sleep involves reduced RAS impulses.
Conscious person: easily arousable, intact protective reflexes.
· Unconscious person: not arousable, loss of protective reflexes.
Consciousness is described as having two parts
Arousal/Wakefulness → function of the RAS (Brainstem).
Awareness/Cognition → function of the Cerebral Hemispheres.
Definitions
Full Consciousness: Aware and responds appropriately to the environment.
Disturbed Sensorium: Disoriented, doesn't follow commands, needs persistent stimulation.
Causes
Structural
Stroke, Cerebral vein thrombosis, Hydrocephalus, Brain tumor, Subdural empyema, Trauma (hemorrhage, swelling).
Metabolic
Anoxia, DKA, Electrolyte abnormalities, Encephalopathy, Hypoglycemia, Temperature extremes, Infection/Sepsis, Meningitis/Encephalitis, Toxins, Uremia, Postictal state.