1. Altered Consciousness
(3% of referrals to ER)
Definitions
Differential diagnosis
Assessment - evaluation
Management

2. Unconsciousness: Loss of wakefulness other than sleep
Bi-hemispheral dysfunction (awareness* + wakefulness) or
RAS dysfunction (wakefulness)
Injury and recovery
patterns:
Injury
Fore>mid>hindbrain
Recovery
Hind>mid>forebrain
Reticular Activating
System
Motor Response
Sensorium
*Awareness: cortical cognitive function

3. Clinical Assessment of Unconsciousness
Definitions and Commonly Used Jargon
Full Consciousness
Wakefulness
Awareness
Somnolence – drowsiness
Altered consciousness
(Encephalopathy)
Stupor
Semi-coma
Coma
Altered intellectual
functioning and behavior
Confusional state
Delirium [acute cognitive
dysfunction]
Agitation
Psychosis
Syncope
Short, transient loss of consciousness
with loss of postural tone
Near-syncope- premonition of syncope
without loss of consciousness
Vegetative state
+ Wakefulness
- Awareness

4. Syncope
Short, transient loss of consciousness with loss of postural tone
Causes
Transient reduction in CBF
Vaso-vagal syncope: carotid, valsalva, micturation, tussive
Neuro-cardiogentic syncope: prolonged standing, fright (tilt-test +)
Orthostatic hypotension
Dehydration, drugs, neuropathy, etc.
Arrhythmia
Tachy-arrhythmia (VF, VT, torsad, SVT in patients with pre-excitation)
Brady-arrhythmia (Adams Stocks – AVB)
Valvular disease (Aortic stenosis, HOCM) PE
TIA – transient ischemic attack
Seizures* (epilepsy)
* Short clonus & loss of urinary sphincter control do not indicate epilepsy

5. Evaluation in ER and on follow up
Syncope
Evaluation in ER and on follow up
Medical history:
True syncope vs. “faintness”, dizziness, blurred vision, etc.
Routine: previous episodes, precipitating factor(s), other illness,
Medications
Eye witness: setup, sequence of events, pallor, cyanosis, sweating
seizure, initial vital signs (pulse), gaze direction
PE:
Routine, particularly cardiovascular and neurological, orthostatism
evidence for trauma, tongue, loss of sphincter control
Other important factors in likelihood assessment: age, gender
Family history of SD
Further evaluation:
ECG >>> monitoring >>>holter 24h>>>holter 72h>>>loop recorder
Cardiac echo
EEG
Carotid sensitivity, tilt test

6. Glasgow Coma Scale
Assessing the Degree of Unconsciousness

7. Glasgow Coma Scale Eyes Opening Motor Response Verbal Response
Maximum – 15
Minimum – 3
7> Coma
Used by Trauma and Neurosurgery
disciplines to assess prognosis…
… but is meaningless in that respect
in non-trauma causes
Eyes Opening
4 - spontaneous, to speech
3 - to loud noise
2 - to pain
1 - none
Motor Response
6 – obeys orders
5 – directed to pain
4 – not directed to pain
3 – decortication response to pain
2 – decerabration response to pain
1 - none
Verbal Response
5 – spontaneous, relevant
4 – confusional, disoriented
3 – clear but meaningless
2 – non articulated sounds
1 - none

9. Altered Consciousness Differential Diagnosis
Anatomical vs. metabolic causes
Mixed / combined
head trauma during driving “under the influence”
One leads to the other
metabolic encephalopathy >> brain edema>>altered CBF

10. Altered Consciousness
Causes (1)
Altered anatomy
Trauma (concussion/comotio cerebri<<lacerations<<hemorrhage)
CVA: affecting RAS
affecting both hemispheres (rare, obliteration of unilateral functioning ICA)
affecting one hemisphere (with a contralateral already injured hemisphere)

11. CVA types Ischemic – arterial thrombosis
Atherosclerosis, atheroembolic
Thrombembolic (RHD, A. Fib, paradoxical)
Vasculitis
Thrombophyllia (anticardiolipin, hyperhomocysteinemia, etc.)
Hyperviscosity (leukemia, thrombocythemia, PP, etc.)
Air embolus, decompression injury
Venous thrombosis
Thrombophilia, vasculitis, hyperviscosity etc.
Hemorrhagic CVA
Intra-parenchymal hemorrhage (primary / transformation)
Subarachnoid hemorrhage
Other intracranial hemorrhage
Epidural hemorrhage
Subdural hemorrhage

12. Subarachnoid Hemorrhage
Bleeding Berry aneurism
Within circle of Willis
Association with PCKD etc.
Trauma brain lacerations
Hemorrhagic CVA complicated by intraventricular hemorrhage
Subarachnoid hemorrhage leads to
cerebral vascular vasoconstriction !!
>>>subsequent hypoxic damage!!
Headache
Meningeal irritation

13. Epidural Hematoma
herniation
Arterial bleeding (from MMA), often associated with fracture of parietal bone
Commotio cerebri>>
short lucid interval>>
rapid and dramatic evolution

14. Subdural Hematoma
Venous bleeding from veins in subdural space, near attachment to sinuses
caused during “minor” head concussion, particularly in babies and elder patients
Slow insidious presentation
(Particularly in the aged: unnoticed trauma, extra-space)

15. Altered Consciousness
Causes (1)
Altered anatomy
Trauma:
CVA:
Tumor: Primary / metastatic
Loss of BBB and edema
Brain edema (increased ICP, altered CBF, herniation)
“closed box phenomenon”

16. Glioblastoma Mass effect Herniation Altered consciousness Vasogenic
edema
Mass effect
Herniation
Roramen magnum
Trans-tentorial etc.
Altered consciousness
tumor

17. Brain Edema Final Common Pathway
↑ICP
↓CBF →herniation
Drugs, toxins
hypoxia-induced
Brain damage
Trauma
Hemorrhage
Severe HTN
Infection
(meningitis, encephalitis
Abscess, Rey)
Altered CSF drainage
Acute hyponatremia
High internal osmolytes
Tumor
Primary/metastatic

18. Altered Consciousness
Causes (2)
Altered Blood Supply
Syncope
Severe shock
Lethal arrhythmia
CVA
Increased ICP (elder patients tolerate it better d/t brain atrophy)
Altered brain oxygenation
Altered blood supply
Hypoxia
CO intoxication
Methemoglobinemia
Cyanide poisoning
(mitochondrial Anoxia)

19. Altered Consciousness
Causes (3)
CNS Infection
Meningitis
Enchephalitis
Brain abscess
Meningococcemia

21. Measles

22. AIDS

23. Altered Consciousness
Causes (3)
Electrical disorder (seizure)
Primary (epilepsy: primary vs. secondary)
Secondary to any other acute CNS disorder

24. Altered Consciousness
Causes (4)
Metabolic causes
Hypoxia
Hypercarbia (acidosis, brain edema, hypoxia)
Hyperglycemia
Hypoglycemia
Altered osmolality:
↑↓ Na
Other electrolyte disorders
↑↓ Ca, Mg
↑ K
↓ P
Acid-base anomalies
Severe metabolic & respiratory acidosis
Severe metabolic & respiratory alkalosis

26. Altered Consciousness
Causes (5)
Metabolic causes (cont.)
Hepatic failure (hepatic encephalopathy)
Renal failure (uremic encephalopathy)
Endocrinopathy
Hypothyroidism (myxedema coma)
Addison crisis
Pan-hypopituitarism
Altered core temperature
Hypothermia
Hyperthermia
Sepsis (multifactorial)
Deficiency states
thiamine, B6 and others
Acute intermittent porphyria

27. Hepatic Encephalopathy: Clinical Stages
Personality changes
Flapping tremor
Combative
(“stupor”)
coma

28. Myxedema coma

29. Altered Consciousness
Causes (6)
Intoxications and medications
Toxidromes
Alcohols
Ethanol*, methanol, isopropyl alcohol, ethylene glycol
Odor, determination of levels, osmolar gap,
acid-base status, kidney function, urinary oxalates, optic disc
Sympatholytics
Barbiturates* narcotics, hypnosedatives, benzodiazepines
Flunitrazepam (hypnodorm)
Respiratory depression, bradycardia, myosis, toxic screen
Sympathomimetics
Amphetamines, cocaine
Sympathetic overactivity, tachycardia, hyperthermia,
high BP, mydriasis, convulsions, toxic screen

30. Altered Consciousness
Causes (7)
Intoxications and medications (cont)
Cholinergic
Organic phosphates, carbamate
Muscarinic and nicotinic overactivity: sweating, salivation, tearing, diarrhea,
bronchorrhea & wheezes, myosis, bradycardia,fasciculations, convulsions
Anticholinergics, anti-histamines
Phenothiazines, butirofenons, atropine* containing drugs
and herbal extracts
Dry skin, tachycardia, dysrrhythmias, extrapyramidal disorder, toxic screen
Serotonin syndrome
TCA, SSRI, SNRI, Lithium
Dry skin, hyperthermia, diaphoresis, tachycardia, muscle rigidity, myoclonus,
Hyper-reflexia, seizures, tremor, ataxia, toxic screen

31. Altered Consciousness
Causes (8)
Intoxications and medications (cont)
Hallucinogens
LSD, NMDA (ecstasy), Phencyclidine (PCP), marijuana, mushrooms
Mydriasis (not PCP), nystagmus (PCP),dysrhythmias, seizures, hyperthermia,
Toxic screen
Miscellaneous
Lithium, bromides, salycilates, iron, digitalis, Inhalants (Freon, glue sniffing)
Gamma-hydroxybutirate (GHB)

34. Altered Consciousness
Causes (9)
Withdrawal
Wernicke’s encephalopathy
Psychogenic
Catatonia
Conversion disorder
Butterfly eyes
Evidence for hyperventilation
Limb tonus

35. Epilepsy Focal seizure: any focal type or “Jacksonian March”
Generalized seizure:
Grand mal - Tonus >>>clonus phases
Petit mal
Electrical disorder:
Primary
Secondary: chronic or acute (reflecting major disorders)
i.e. seizure does not imply primary electrical disorder!!
Status Epilepticus:
May induce subsequent anoxic encephalopathy
Neural exitoxicity
Post-ictal state:
Delirium, amnesia
Todd’s paralysis

36. Altered Consciousness
Assessment (1)
Life-threatening condition!
ABC first!
Evaluation in parallel with treatment
Neurological examination – last step of PE
גם כינים וגם פשפשים
Medical History
Eye witness / collateral anamnesis
Patient’s surroundings
Epidemiology (single / multiple cases)
Pre-existing illnesses, medications
Other available medications (used by family members)
Ethylism, Drug abuse
Prior trauma
Preceding headache, fever, convulsions
Description of episode, sequence of events
Look back for evidence at the area of interest

37. Altered Consciousness
Assessment (2)
Physical examination
Vital signs:
HR (may reflect direct cause or secondary effects such as ↑ICP)
BP (may reflect direct cause or secondary effects such as ↑ICP)
Temperature (use of hypothermic thermometer when indicated)
Breathing rate and pattern (Cusmaul, Chain Stocks, cluster, atactic)
Full medical examination:
Look for: trauma signs, needle pricks, purpura, nuchal rigidity
Bracelets/indicators of insulin TX, epilepsy, Immunosupression, anaphylaxis

38. Spotted fever

39. Altered Consciousness
Assessment (3)
Neurological examination
GCS
Eyes: Gaze: nystagmus, doll’s eye, direction
stroke – towards lesion
seizure – away from lesion
Pupils: equal / unequal, reactive / non-reactive, size
Unequal, structural lesion, herniation, R/O eye drops for glaucoma
Pinpoint: MO, pontine hemorrhage
Small: organic phosphor, barbiturates
Dilated: anticholinergic (including atropine and plants),
antihistamines, antidepressants and other serotoninergic,
anoxic brain damage
Fundus: increased ICP – papiledema, venodilation, loss of venous pulsation

41. Altered Consciousness
Assessment (3)
Neurological examination
GCS
Eyes: Gaze: nystagmus, doll’s eye, direction
stroke – towards lesion
seizure – away from lesion
Pupils: equal / unequal, reactive / non-reactive, size
Unequal, structural lesion, herniation, R/O eye drops for glaucoma
Pinpoint: MO, pontine hemorrhage
Small: organic phosphor, barbiturates
Dilated: anticholinergic (including atropine and plants),
antihistamines, antidepressants and other serotoninergic,
anoxic brain damage
Fundus: increased ICP – papiledema, venodilation, loss of venous pulsation

42. Altered Consciousness
Assessment (4)
Neurological examination (cont)
Posture and muscle tone
Localizing findings:
Cranial motor nerves
Lateralization of motor deficits
Pyramidal signs
Frontal signs
Repeated neurological examination, again and again
Look for dynamics

43. Neurological re-assessment

44. Altered consciousness
Management (1)
Life-threatening condition!
ABC first!
Evaluation in parallel with treatment
Continue ABC
Airway protection (intubation)
Oxygen
Venous excess, glucometer
Blood and urine samplings: CBC, SMAC, blood gases, INR
osmolality, toxicology screen, carboxyhemoglobin, etc.
ECG (hints for cause)
CXR (non-cardiogenic PE, aspiration
and other anomalies)
Eye protection

45. Altered consciousness
Management (2)
Diagnostic / therapeutic interventions
Thiamine 100 mg
Glucose 25-50% 50 ml
Naloxone (narcan) 0.1 >>> 0.8 mg
beware, after tube, go low and slow: acute withdrawal
Flumazenile (anexate) mg
Complementary evaluation
Blood and urine sampling (TSH, porphyrines etc.)
Cultures
Urinalysis CT LP
EEG

46. Altered consciousness
Management (3)
Subsequent measures, related to progress in evaluation
Correction of metabolic abnormalities
Decontamination (NGT, activated charcoal)
Specific treatment for identified disorders
Thrombolysis, surgical TX, medications, dialysis etc.
Monitoring
Supportive care
Repeated assessment
If no cause remains unidentified – repeated evaluation of history
and surroundings, interview of delivering paramedics,
involving the police etc.
Brain Rescue
ICP monitoring, hyperventilation, hypothermia, reducing metabolic activity, Ca++ blockers
EPO, PARPP inhibitors, antioxidants etc. All experimental!!

47. Seizures Management ABC IV line / medications
Benzodiazepines (diazepam, lorazepam, midazolam)
Phenytoin
Carbamazepine
Valproate
Magnesium sulphate
Phenobarbital + (neuromuscular block)
Medical history: if no known epilepsy consider wide
spectrum of conditions, structural, metabolic, intox. etc.
Look for initiating factor
PE:
Lab: If known epilepsy – drug levels. If not – CBC, wide biochemistry,
blood gases, carboxyhemoglobin, tox. screen etc.
Consider: CNS imaging and EEG

48. Take-Home Massages ABC first Collateral anamnesis from eye witnesses
Keep on collecting relevant information – detective work
Don’t jump to haste conclusions. Consider DDs
“CVA” reflects locus minoris resistenti to metabolic derangement
Make sure before labeling HY
“Flees and mites”
encephalopathy + trauma: drivers, alcoholics, metabolic disorders
Hypoxic encephalopathy – final common pathway
GCS is insignificant regarding prognosis in not-trauma cases
In any diabetic patient – treat as hypo
Syncope – recumbent position, raise feet