Coma and Depressed Level of Consciousness

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, nolateralizing 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 ExamVital SignTemperature • 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 ExamBlood Pressure • Hypertension: • Hypertensive encephalopathy • Increased ICP • Hypotension: • Alcohol • Barbiturate • Internal hemorrhage • MI • Sepsis • Profound hypothyroidism • Addison’s crisis

19. Physical ExamRespiratory Rate • Tachypnea: Pneumonia Metabolic acidosis • Bradypneapoisoning ( opiate )

20. PupilReaction 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 ofAltered 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 andnaloxone • Thiamine (chronic alcoholism and malnourishment) …….. 100 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) • Thyroxineand Steroids (myxedematous coma) ...….. 500 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