Altered Mental StatusComa SedationParalysis

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Altered Mental Status/Coma/Sedation/Paralysis
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Altered Mental Status

• AKA reduced consciousness
• Associated with disorientation, emotional
  lability, hallucinations, and memory
  losscomplication of many illnesses
• Commonly associated with metabolic encephalopathy
  and seizures

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Altered Mental Status

• Causes
• Metabolic disorders
• Respiratory
• Hypoxia (PaO2 lt45)
• Hypercapnia (PaCO2 gt 60)
• Renal/hepatic
• Na lt120 or gt155
• Glucose lt3 or gt 30 mmol/liter
• Ca lt 1.7 or gt 3.0
• Elevated urea/ammonia
• Endocrine thyrotoxicosis, myxedema
• Hypothermia/hyperthermia
• Acute sepsis
• Drug/toxin ingestion (alcohol, LSD)
• Vitamin deficiency (Wernickes encephalopathy)
• Seizures
• Structural (tumor/trauma/edema) or increased ICP
• Inadequate cerebral perfusion

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Coma

• A state of unconsciousness from which the person
  can not be aroused
• Glasgow Coma Score lt8
• May be preceded by altered mental
  status/progressive loss of consciousness
• Extent of impairment depends on age, mental
  status, CV status, underlying dx, rate of
  progression
• Pathophysiological causes
• Metabolic/toxic encephalopathy
• Generalized seizures
• Cerebral compression from structural lesions
• Elevated ICP
• Inadequate cerebral perfusion

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Coma

• Potentially reversible causes
• Hypotension/hypoperfusion
• Hypoxemia/hypercapnia
• Hypoglycemia
• Hypertension
• Status epilepticus
• Myxedema
• CO poisoning
• Hypercalcemia
• Poisoning
• CNS infection/hemorrhage
• Wernickes encephalopathy

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Coma

• Assessment
• History helps determine causesudden onset
  suggests a sz/vascular eventslow onset suggests
  a metabolic cause
• Physical exam
• State of consciousness alert, lethargic
• Pupillary response normal suggests a metabolic
  cause or lesion above the midbrain
• Eye movement ice water in the ear should cause
  eyes to deviate to that sideif not, pons is
  non-functional
• Respiratory pattern ataxic breathing severe
  brainstem dysfunction
• Motor function spontaneous movement, no
  response to painpontine compression causes
  decerebrate posturinglesions above the pons
  cause decorticate

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Coma

• Management
• Investigations
• Depends on the cause
• May include toxicology, ABG, CT, EEG, lumbar
  puncture
• Treatment
• Secure the airway
• ID if a reversible cause exists and fix it
• Prognosis
• Can only be determined after drug and metabolic
  defects have been corrected/excluded
• Deteriorates with duration of coma
• Signs of poor prognosis comagt3 days,
  decerebrate posturing, absent pupillary reflexes

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Sedation

• Indications
• Relieve pain and anxiety
• Control seizures
• Reduce ICP
• Patient paralyzed

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Sedation

• Opioids
• Morphine
• Potent analgesic/anxiolytic
• Reduces respiratory drive
• May cause N/V
• Reduces GI motility
• Causes histamine release
• Fentanyl
• Accumulates in fat with subsequent slow release,
  which can prolong the effect
• Alfentanil is shorter acting and doesnt
  accumulate
• Remifentanil is also short acting
• Reverse with naloxone (Narcan)

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Sedation

• Paracetamol
• A mild analgesic and antipyretic
• Cant be given IV
• NSAIDs
• Inhibit cyclooxygenase
• Have analgesic properties
• Cause GI bleed/renal toxicity
• Most cant be given IV

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Sedation

• Benzodiazepines
• Sedative, anxiolytic, amnesiac
• No analgesia
• Midazolam
• Rapid onset
• Accumlates in fat tissue so withdrawal is
  prolonged
• Metabolized in liver
• Patients with liver enzyme induction (alcoholics,
  epileptics) may require large doses for effect
• Lorazepam
• No hepatic metabolism or active metabolites
• Flumazenil
• Benzodiazepine antagonist
• Reveres benzodiazepine effects quickly

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Sedation

• Propofol
• No analgesiaonly sedative
• Short duration of action with rapid withdrawal
• May cause hypotension
• Mixed in an egg/soybean emulsion which can cause
  allergic rx and which supports bacterial growth
• Other sedatives
• Haloperidol a benzodiazepine
• Barbiturates and phenothiazines are sedative but
  cause lots of side effects

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Paralytic agents

• Depolarizing neuromuscular blockers
• Resemble acetylcholine
• Cause depolarization
• Are not metabolized by acetylcholinesterase
• Depolarization continues until the blocker
  diffuses out of the neuromuscular junction
• Succinylcholine is the only one
• Rapid onset/short duration of action (lt10 min)
• Causes potassium release

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Paralytic agents

• Non-depolarizing
• Block acetylcholine receptors preventing
  depolarization
• Have a slower onset but last longer (up to an
  hour)
• Prolonged use of paralytics (especially if using
  steroids at same time) can cause severe myopathy
• Some cause histamine release