Stupor & Coma Flashcards
Lethargy
sleepy but easily aroused
Hypersomnia
-excessively sleepy but normal cognition when awakened
Obtundation
mental blunting, dec. alertness
Stupor
eyes open only briefly after vigorous stimulation before returning to deep sleep
-cognition impaired
Coma
eyes remain closed after vigorous stimulation
Delirium
- disoriented, misperception of sensory stimuli, hallucinations
- vacillates b/w quite, sleepy periods & hyper-vigilance/agitation
Abulia
- awake but apathetic, no spontaneity
- with vigorous stimulation, cognitive function may be normal (bilateral frontal lobe disease, lobotomized)
Akinetic Mutism
- silent, alert-appearing immobility
- no mental activity with vigorous stimulation (disease of frontal lobes & hypothalamus)
Minimally Conscious State
-fragments of awareness
Vegetative State
-awake, no awareness or meaningful interaction with the environment
Consciousness
- Arousal: sleep-wake cycles
- ascending arousal system of the rostral brainstem
- disease causes stupor & coma - Content: awareness of: oneself, environment
- Corrtical circuits - cognition, purposeful interaction with world
- Disease causes dementia
Cataplexy
-sudden involentary loss of muscle tone during emotional excitement
Primary Lesions that Cause Coma
- extensive, acute bihemispheric disease
- lesions of diencephalon (thalamus & hypothalamus)
- Lesions of midbrain peri-aqueductal grey
- Involvement of upper 1/3 of pontine tegmentum
Causes of Coma
- Structural Cause: supratentorial mass lesions, acute obstructive hydrocephalus, infratentorilal mass lesion
- Metabolic (non-structural): reversible injury (sedative overdose), irreversible injury (hypoxia in cardiac arrest)
**always rule out psychogenic coma
Oculomotor nerve is near the?
tentorium
Central Herniation
- Rostral-Caudal deterioration
- Diencephalon (thalamus & hypothalamus) to midbrain failure
- reduced consciousness
- small reactive pupils (1-3mm)
- decorticate postruing
- Cheyne-Stokes respirations
- Midbrain failure follows (fixed mid-postiion pupils, decerebration)
Infratentorial Lesions
- Intrinsic brainstem lesions:
- top of basilar artery ischemic stroke
- pontine hemorrhage - Extrinsic lesions compress & distory the brainstem
- cerebellar hemorrhage
- cerebellar infarction
- cerebellar brian tumor
Primary Brainstem Lesions cause:
- Segmental cranial nerve deficits
- ascending (spinothalamic) tract dysfunction
- descending (corticospinal, central sympathetic) tract dysfunction
- early cerebellar signs
Pontine Hemorrhage Clinical Syndrome
- coma abrupt
- pupils are pinpoint
- decerebrate rigidity or flacid quadriplegia
- horizontal gaze paresis
- ocular bobbing
Metabolic Encephalopathy (toxic-metabolic coma)
- Non-cerebral disease may interfere w/metabolism of the cerebral cortex & rostral brainstem AAS
- Endogenous toxins in uremia & hepatic failure
- Exogenous toxins in drug overdose, poisons, & sepsis
- Hypoxia, hypoglycemia, hypo & hyper-osmolality
- Electrolyte & acid-base imbalances
- Metabolic insult to brain is global, diffuse, symmetric
- Neuro-exam is “non-focal”
- Head CT is neg.
- Pupils stay reactive even as other reflexes are lost
- Asterixes, multifocal myoclonus & tremor
- Stupor & coma are reversible with metabolic correction & ICU support
Causes of Metabolic Encephalopathy
- hypoxia, CO2 narosis, Hypoglycemia, Hyperglycemia, Hyperosmolar, Hyponatremia, Dehydration, Uremia, Liver failure, Hyperthermia, Hypotheria, Acidosis
- Drug intox, toxins, sepsis, Wernicke’s, Post-ictal state, DIC, TTP, Sever anemia, Lupus
Coma: Immediate Management
- Stablilize vital signs (ABC’s first): secure ariway, cardiac monitor, IV access & blood drawing
- Stabilize neck (trauma)
- Determine the circumstances in which coma occurred
- Rapidly examine patient
- Empirical D50, thiamine, naloxone (opiate OD)
- tasks performed simulaneously by ED team
Respiratory Patterns in Coma
-Cheyne Stokes respirations can be an early sign of herniation, both central & transtentorial
Noxious stimuli to arouse patients who do not respond to voice command?
- supraorbital pressure
- nailbed pinch
- sternal rub
Glasgow coma scale
-prognosis in head trauma
-highest 15
12 or better is excellent prognosis
-scores of 7 or below: nursing home care
-3 means death
Flexor response to Pain
(decorticate posturing)
-due to loss of cortical control of brainstem
Extensor response
(decerebrate posturing)
-arises with loss of red nucleus & rubrospinal tract in the midbrain
Coma: Diagnostic Testing
-STAT Head CT (or MRI if available)
-CXR
-Tests: EEG (status epilepticus, brain death)
Spinal tap (CNS infection, subarachnoid hemorrhage)
Cervical Spine X-ray (trauma)
Stat toxicology: cocaine, opiates, phencyclidine, barbiturates, anticonvulsants, & sedatives, ethanol, methanol, ethylene glycol, acetaminophen, salixylates, tricyclics
Treatment of Coma
- Ensure Oxgenation
- Maintain circulation
- Control glucose
- Lower Intracranial pressure
- Stop Seizures
- Treat Infection
- Restore acid-base balance & electrolytes
- Adjust body temperature
- Give thiamine
- Consider specific antidotes (naloxone, flumazenil)
- Control agitation
Coma Prognosis
- Non-traumatic coma: absence of pupillary light & comeal reflex of 3 days carries poor prognosis
- In hypoxic coma, absence of purposeful motor movements at 3 days also carries a poor prognosis
