Status Epilepticus

  • Status epilepticus = any seizure lasting longer than 30 minutes or the presence of recurrent seizures (either clinical or electrical) w/o a seizure free period in between
  • Frequently cognitive decline is seen following the incident
  • MOA:  GABA system loses its ability to inhibit seizure activity  (however GABA levels may be elevated during status epilepticus)
    • Can be caused by anticonvulsant level changes (GABA) most commonly or cerebrovascular disease (structural lesions)–2nd most common reason
      • Other causes of status epilepticus:  infection, metabolic, alcohol/drugs, idiopathic
  • Treatment goals:  diagnose seizure type & cause, stabalize ABCs, stop seizures (both clinical & electrical), prevent seizure recurrence
  • GCSE:  tonic-clonic seizures are the most common form of status epilepticus
    • Patient won’t be able to really tell you what happened (persistent post-ictal state)
    • 2 phases
      • 1st phase:  first 30 minutes, body compensates for changes, high levels of NE, EPI, steroids resulting in HTN, tachycardia, potentially fatal arrhythmias
      • 2nd phase:  continuous muscular contractions, lactic acidosis, hypotension/shock, airway obstruction, aspiration
  • Treatment of GCSE:
    • Check blood gases, treat metabolic acidosis (pH < 7.2; NaBicarb), admin glucose w/ thiamine (b/c pt will progress to hypoglycemic state & thiamine will help to prevent Wernicke’s encephalopathy)
    • Also need to control the seizures:  admin injectable benzo for immediate seizure control & anticonvulsant for LT control
      • Lorazepam is preferred b/c it binds to tighter to receptor, is less lipophilic & in the blood longer (elicits effects for ~12 hours) than diazepam
        • Diazepam (more lipophilic & thus shorter DOA) & midazolam (aka versed; used for refractory seizures only) are both also used
        • Rapid acting med must be continued until the EEG is clear of evidence of seizures (after 24 hours up to half of pts still show electrical seizure activity w/o outwardly recognizable signs)
      • Phenytoin (aka dilantin) & fosphenytoin are both admin’d for long term seizure control
        • Need to admin phenytoin in perservative free saline
        • Paresthesias & pruritis are both common admin issues with fosphenytoin
      • Other meds used for long term control & in pts w/ refractory seizures:  phenobarb, levetiracetam (aka keppra), propofol, valproate, lidocaine
  • Complications of GCSE  (aka tonic clonic seizures)
    • Metabolic:  lactic acidosis, hypoglycemia, hypercapnia, hyperkalemia, hyponatremia, leukocytosis
    • Autonomic:  hyperpyrexia, cerebral dysregulation, vomiting, incontinence
    • CV/respiratory:  hypoxia, arrhythmia, high output failure, pneumonia
    • Renal:  ARF, myoglobinuria
  • Non-convulsive status epilepticus (NCSE)
    • More difficult to diagnose clinically (need an EEG, pt may have non-specific alterations in consciousness)
    • Symptoms are variable but may include:  mental clouding, unresponsive despite eyes being open, twitching, language disturbances, inappropriate behavior, mildly obtunded
    • Absence seizures:  aren’t life-threatening but should be treated with benzos or rectal valproic acid
    • Myoclonic seizures:  aren’t life threatening but should be treated with valproic acid
  • Complex-partial seizures:  can be life threatening & require aggressive treatment in order to prevent permanent damage.  Treat complex partial seizures in the same way as GCSE (clonic-tonic seizures)

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