Non-Convulsive Status Epilepticus

Change in consciousness, behaviour, autonomic function, or sensorium with EEG seizure patterns, but no major motor phenomena.

NCSE has a broad spectrum of clinical presentation, and is loosely classified into:

Epidemiology and Risk Factors

Epidemiology:

  • NCSE is present in:
    • Up to 50% of patients with coma
    • 10-30% of post-cardiac arrest patients
    • 10-35% of TBI patients

Risk factors are predominantly conditions which lower seizure threshold:

  • D
    • Known epilepsy
    • Cerebral irritation
      • ICH
      • Encephalitis
      • Stroke
      • TBI
    • Previous cerebral irritation
      • Neurosurgery
      • Previous meningitis
    • Dementia
  • F
    • Electrolyte derangements
  • I
    • Systemic infection
  • Drug
    • Withdrawal
      • Benzodiazepine
      • Alcohol
    • Use
      • Psychotropics

Pathophysiology

Aetiology

Causes include:

  • D
    • Evolution from status epilepticus
  • G
    • Hepatic encephalopathy
  • Trauma
    • CNS trauma

Clinical Manifestations

Seizure manifestations include:

  • Consciousness
    • Level of consciousness
    • Content of consciousness
      • Behavioural changes
      • Delusions
      • Paranoia
      • Speech
  • Autonomic
  • Sensory
  • Motor
    Subtle change sometimes occur:
    • Twitching
    • Automatism
    • Cyclonic jerks
    • Nystagmus
    • Myoclonus

Diagnostic Approach and DDx

NCSE is:

  • Commonly misdiagnosed
  • Requires a high index of suspicion.
  • Difficult to differentiate from non-ictal causes
    • Metabolic encephalopathy
    • Septic encephalopathy
    • Hypoxia

EEG features crossover with other encephalopathies, further confounding diagnosis.

NCSE should be considered in:

  • Altered sensorium with small motor signs
  • Prolonged postictal period following GTCS
  • Unexplained stupor
  • Stroke clinically worse than expected
  • Paradoxical improvement in alertness following anti-epileptic therapy

Differentials include:

  • D
    • Encephalopathies
      • Metabolic
      • Epileptic
    • Encephalitis
    • Migraine
    • Postictal
  • F
    • Hypoglycaemia
  • Drug
    • Intoxication
      • Lithium
      • Baclofen
      • TCA
    • Withdrawal
      • Alcohol
      • Benzodiazepines

Investigations

Bedside:

  • ABG
    Hypoglycaemia, basic electrolytes.

Laboratory:

  • Blood
    • UEC
    • LFTs
  • LP
    • Meningitis
    • Non-infective encephalitis

Other:

  • EEG
    • No pathognomic findings
    • Epileptiform discharges with seizure activity
    • Response to treatment

Management

Resuscitation:

  • A
    • Correct airway compromise
  • D
    • Hypoglycaemia

Specific therapy:

Often unresponsive to initial treatment; 2nd or 3rd line agents are usually required.

  • Pharmacological
    • Seizure termination
    Choice depends on timing, IV access, and drug availability. * Premonitory * 10mg SL or IN midazolam * 10-20mg PR diazepam * Emergent initial therapy (1st line)
    Benzodiazepines Q2-5 minutely: * Lorazepam 0.1mg/kg IV
    Preferred IV option, if available. * Diazepam 0.1mg/kg IV * Midazolam 0.1mg/kg IV/0.2mg/kg IM
    Preferred IM option, if available. * Urgent control therapy (2nd line)
    One of: * Levetiracetam 60mg/kg up to 4.5g * No levels required * Phenytoin 20mg/kg IV load, given at 50mg/min, up to 1.5g
    Always should be combined with a benzodiazepine for seizure termination. * Valproate 40mg/kg IV load up to 3g * Level 2-4 hours following load * Midazolam infusion at 0.05-0.4mg/kg/hr
    Phenobarbital (below) can be used as an alternative. * Refractory therapy (3rd line)
    * Transition to continuous infusions * Duration of therapy usually dictated by EEG * Consideration of: * Anaesthetic agents
    Continue infusions for 12-48 hours before attempting to wean therapy. Options include: * Thiopental 100-250mg IV * Propofol 2mg/kg IV, then infusion at 5-10mg/kg/hr * Phenobarbital 10-15mg/kg IV, given at 100mg/min * Ketogenic diet
    Considered dual 3rd line in some institutions.
    • Maintenance antiepileptic
      All have demonstrated equivalence, but levetiracetam is the most logistically convenient.
      • Levetiracetam
        • 60mg/kg IV load
      • Phenytoin
        • 20mg/kg IV load
        • Wait 2 hours before checking levels following loading dose
        • May precipitate hypotension
        • Avoid if usually on phenytoin
        • Avoid if drug induced seizures
      • Valproate
        • 40mg/kg IV load
        • Non-sedating
        • Levels can be checked immediately

Disposition:

  • ICU admission
    If not responsive to 1st line treatment.

Anaesthetic Considerations

Marginal and Ineffective Therapies

Complications

  • Death
    • 20-50% by hospital discharge
    • Significantly ↑ mortality with diagnosis 24 hours after seizure onset

Prognosis

Features associated with poor outcome:

  • Severe cognitive deficit
    • Longer seizure duration
  • Unknown precipitant

References

  1. Perks A, Cheema S, Mohanraj R. Anaesthesia and epilepsy. Br J Anaesth. 2012 Apr 1;108(4):562–71.
  2. Bersten, A. D., & Handy, J. M. (2018). Oh’s Intensive Care Manual. Elsevier Gezondheidszorg.
  3. Neurocritical Care Society Status Epilepticus Guideline Writing Committee et al. Guidelines for the Evaluation and Management of Status Epilepticus. Neurocritical Care 17, no. 1 (August 2012): 3–23.