1. Coma and Depressed Level of Consciousness

2. Epidemiology Up to 3% of ED admissions
85% of coma is caused by metabolic or systemic dysfunction, 15% by structural lesions

3. Alteration of Consciousness
Affects arousal (level)
Cognitive and affective mental function (content)

4. Arousal
Arousal ….. Brainstem and ARAS ….. impaired by toxins, anesthetics, or compression or injury of the brainstem
Small focal lesions within the pons can alter mental status and induce coma, whereas extensive unilateral lesions of the cerebral hemispheres do not blunt consciousness (both cerebral hemispheres must be structural damaged or metabolically depressed to induce coma)

5. Cognition Cognition ….. cerebral cortex
When both cerebral hemispheres are affected, the degree of alteration of consciousness depends on the size of injury and speed with which it progresses. Disorders may be diffuse or focal.
Supratentorial lesions are a more common cause of coma than subtentorial lesions
Associated neurologic findings can assist in distinguishing between diffuse and focal disorders

6. Definitions
Coma : any depression of the level of consciousness (complete failure of the arousal system with no spontaneous eye opening)
Light coma ….. respond to noxious stimuli with a variety of protective reflexes
Deep coma ….. do not respond at all
Vegetative state : complete absence of behavioral evidence for self or environmental awareness

7. Minimally conscious state : altered mental status but are able to follow simple commands, verbalize yes/no responses (regardless of accuracy), or show purposeful behavior
Clouding of consciousness : impaired capacity to think clearly and to perceive, respond to, and remember stimuli
Confusion : alteration in higher cerebral functions, such as memory, awareness, and attention

8. Delirium : disturbed consciousness with motor restlessness, transient hallucinations, disorientation, or delusions
Obtundation : patients are awake but not alert and exhibit psychomotor retardation
Stupor : conscious patients, exhibits little or no spontaneous activity (stuporous patients awaken with stimuli but have little motor or verbal activity when aroused)

9. GCS : Graded scoring methods based on neurologic findings
Coma = GCS of 8 or less
Limitations of the GCS : variable reproducibility, inaccurate measure of level of consciousness, excessive focus on left-sided brain function, and limited clinical relevance
Liege coma scale
APACHE II scale
Swedish reaction level scale

10. The most effective strategy :
patient is alert, awake, or unresponsive and to describe the ocular and motor response to verbal commands and painful stimuli

11. Differential Considerations
The early goals in the emergency department
Provide supportive care
Identify rapidly and treat reversible and Iife-threatening causes
Establish a methodical approach to definitive diagnosis

12. Diagnostic Approach Differential consideration
Diseases that cause no FND, no lateralizing sign, normal brain stem function, normal CT and CSF
Diseases that cause meningeal irritation,
increase WBC or RBC in CSF, no FND,
CT or MRI: no mass lesion
Diseases that cause FND, with or without change in CSF,
abnormal CT or MRI

13. No FND (No Lateralizing Sign, Normal Brain Stem Function, Normal CT and CSF)
Intoxication
Severe infection
Shock
Post-ictal state
Hypertensive encephalopathy
Hypo/ hyperthermia
Concussion
Acute hydrocephalus
Metabolic
Hypoglycemia
Uremia
Hepatic coma
Hypo/ hyperthyroid
Hyperosmolar states
Anoxia
Hypo/ hypernathremia
DKA
Hypercalcemia
Addison

14. History
Environment in which the patient was found and the last time the patient was "normal“
Establish the onset and progression of the altered mental state
The patient's state before the onset of coma
Drug use (prescription, nonprescription, illicit)
Antecedent trauma, fever, headache, and any known prior similar episodes

15. Medical history (especially regarding diabetes, seizures, hypertensive vascular disease, thyroid disease, stroke, malignancy, liver disease, or renal failure)

16. Physical Examination
The initial goal = discriminate between focal structural CNS pathology and global metabolic processes + vital signs stabilization
Signs of trauma
Cervical immobilization
Completely exposed patient
Focused neurologic examination = detailed sensory and motor testing , eye findings, posture, and movement

17. Physical Exam Vital Sign Temperature
Fever:
Systemic infection
Meningitis
Encephalitis
Heat stroke
Anticholinergic drugs
Rarely central
Hypothermia:
Alcohol
Barbiturates
Sedatives
Hypothyroidism
Hypoglycemia
Circulatory failure
Can cause coma only if T<31°c

18. Physical Exam Blood Pressure
Hypertension:
Hypertensive encephalopathy
Increased ICP
Hypotension:
Alcohol
Barbiturate
Internal hemorrhage MI
Sepsis
Profound hypothyroidism
Addison’s crisis

19. Physical Exam Respiratory Rate
Tachypnea:
Pneumonia
Metabolic acidosis
Bradypnea poisoning ( opiate )

20. Pupil Reaction to Light, Size
Reactive and round (mid- size)(2.5-5mm)
Essentially excludes midbrain damage.
Bilateral Fixed: severe mid- brain lesion
Reactive small (Not pinpoint)
Metabolic encephalopathy
Bilateral hemisphere
Hydrocephalus
Thalamic hemorrhage
Pinpoint:
Narcotic
Barbiturate
Pontine hemorrhage

21. Oculocephalic movements (dolls eyes) = normal brainstem pathways originating in the labyrinths and vestibular nuclei and involving the high cervical spinal cord and medulla + integrity of the area of the midbrain and pons surrounding cranial nerves III and VI and an intact medial longitudinal fasciculus
Brainstem dysfunction fixed eyes or movement with the haed
Cerebral problems normal reflex

23. Oculovestibular response (10-30 mL of ice-cold water after elevating the head to 30 degrees above supine or at reverse Trendelenburg position) transient conjugate slow deviation of gaze toward the side of the stimulus (brainstem mediated) followed by a quick beating motion with corrective efforts back to midline alignment (cortically mediated)
COWS
No response = brainstem dysfunction

25. Rapid Assessment/Stabilization
Management of A B C’s must come before investigation of the cause.
but Remember: the prompt reversal of coma
may obviate the need for Advanced airway management

26. Possible Causes!! Not enough oxygen Not enough sugar
Not enough blood flow to deliver O2, sugar
Direct brain injury
Structural (trauma)
Metabolic (toxins, infections, temperature)

27. Mnemonic for Treatable Causes of Altered Mental Status (AEIOU- TIPS)
Alcohol
Epilepsy, Electrolytes, Encephalopathy
Insulin, Intussusception
Opioids/Overdose
Urea (metabolic)
Trauma
Infection
Psychiatric
Shock, Subarachnoid hemorrhage, Snake bite

28. Rapid Assessment and Stabilization
High-flow oxygen
Fully undressed
Assessing responsiveness, pupillary reactivity to light, and movement of extremities,
completes a rapid neurologic screening examination to differentiate diffuse disease from structural causes
Early use of point-of-care blood glucose testing

29. Focal neurologic findings
Thiamine or dextrose administration
Naloxone in patients with opioid ingestion sign and symptoms (e.g., miosis, depressed respirations, "track" marks)
If coma is not rapidly reversible, immediate airway management is indicated to prevent aspiration and ensure adequate ventilation and oxygenation
Evidence of trauma = prompts cervical spine immobilization

30. Excepting glucose disorders metabolic/endocrin causes of coma are generally uncommon
Hyponatremia delirium-like state or bizarre behavior preceded the coma or in patient taking psychotropic medications
Electrolyte = plasma sodium level, acidemia, and anion gap
Psychiatric disorders (conversion disorder)

31. EMPIRIC MANAGEMENT Glucose and naloxone
Thiamine (chronic alcoholism and malnourishment) …… mg IV
Flumazenil (isolated, acute benzodiazepine overdose) ..…… 0.2-mg dose in the first minute followed by 0.2-mg doses every minute until a response is obtained or a total dose of 1 mg
Physostigmine (reverses anticholinergic effects)
Thyroxine and Steroids (myxedematous coma) ...… mg PO or IV T4 on day 1 then 100mg/day
Antibiotics
Activated charcoal (1 g/kg) and Gastric lavage

32. Fever or other significant evidence of CNS infection
(e.g., rash, hypotension, compatible history, immunocompromise)
= antimicrobial (and antiviral, if indicated) agents + imaging and spinal fluid analysis
CNS mass lesions, suggested by focal neurologic findings or evidence or history of trauma or cancer = early computed tomography scanning
Intracranial hemorrhage is suggested by sudden onset of coma or complaint of headache before coma
Toxic causes of CNS depression = supportive care (carbon monoxide, cyclic antidepressants, methanol, and ethylene glycol require specific management)

33. Ancillary Testing Serum or blood glucose level
Serum electrolytes (Na,K,Ca)
Creatinine and blood urea nitrogen levels
Pulse oximetry
Arterial blood gas (CO poisoning)
CBC
Urinalysis (ethylene glycol poisoning)
Blood and urine toxicology screens
Non-contrast-enhanced head CT scan
EEG

34. DISPOSITION
Reversible causes of coma (hypoglycemia or heroin overdose) = discharged after a period of observation and sustained consciousness
Methadone or certain oral hypoglycemics = hospital admission
Alcohol or other CNS depressants = observed in the ER
All other causes of coma = hospital admission