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SOURCE

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Source: Phelps SJ, Wheless JW. Status epilepticus. In: DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey LM, eds. Pharmacotherapy: A Pathophysiologic Approach. 10th ed. New York, NY: McGraw-Hill; 2017. http://accesspharmacy.mhmedical.com/content.aspx?bookid=1861&sectionid=146063283. Accessed May 10, 2017.

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DEFINITION

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  • Seizure lasting longer than 30 min regardless of whether consciousness is impaired; or recurrent seizures without intervening period of consciousness between seizures.

  • Generalized convulsive status epilepticus (GCSE) is most common and severe form.

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ETIOLOGY

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  • Most episodes in known epileptics occur because of:

    • Acute anticonvulsant withdrawal.

    • Metabolic disorder or concurrent illness.

    • Progression of preexisting neurologic disease.

  • Other common precipitating events in adults:

    • Type I (no structural lesion)

      • Infection.

      • Central nervous system (CNS) infection.

      • Metabolic.

      • Low anticonvulsant serum concentrations.

      • Alcohol.

      • Idiopathic.

    • Type II (structural lesion)

      • Anoxia/hypoxia.

      • CNS tumor.

      • Cerebrovascular accident.

      • Drug overdose.

      • Hemorrhage.

      • Trauma.

      • Congenital malformations.

  • Some prescription, over-the-counter, herbal, and recreational drugs can cause new-onset GCSE.

  • Elevated serum anticonvulsant concentration or rapid anticonvulsant withdrawal can also precipitate GCSE.

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PATHOPHYSIOLOGY

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  • Phase I: Each seizure markedly increases plasma epinephrine, norepinephrine, and steroid concentrations that may cause hypertension, tachycardia, and cardiac arrhythmias. Muscle contractions and hypoxia cause acidosis, hypotension, shock, rhabdomyolysis, and secondary hyperkalemia.

  • Phase II: Begins 30 min into seizure with hypotension, compromised cerebral blood flow, normal or low serum glucose; hyperthermia, respiratory deterioration, hypoxia, and ventilatory failure may develop.

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EPIDEMIOLOGY

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  • US incidence 100,000–152,000 cases/year; worldwide incidence 1.2–5 million cases/year.

  • No predilection for gender or socioeconomic status.

  • Occurs more frequently in nonwhites across all ages.

  • Most episodes occur in individuals with no history of epilepsy, but 5% of adults and 10–25% of children with epilepsy develop GCSE.

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CLINICAL PRESENTATION

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SIGNS AND SYMPTOMS
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  • Impaired consciousness, ranging from lethargy to coma.

  • Disorientation (after GCSE controlled)

  • Pain associated with injuries, for example:

    • Tongue lacerations.

    • Shoulder dislocations.

    • Back pain.

    • Myalgias.

    • Headache.

    • Head trauma.

  • Early signs.

    • Generalized convulsions.

    • Acute injuries or CNS insults that cause extensor or flexor posturing.

    • Hypothermia or fever suggesting intercurrent illnesses (eg, sepsis or meningitis)

    • Incontinence.

    • Normal blood pressure or hypotension.

    • Respiratory compromise.

  • Late signs.

    • Clinical seizures may or may not be apparent.

    • Pulmonary edema with respiratory failure.

    • Cardiac failure (dysrhythmias, arrest, or cardiogenic shock)

    • Hypotension or hypertension.

    • Disseminated intravascular coagulation or multisystem organ failure.

    • Rhabdomyolysis.

    • Hyperpyrexia.

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DIAGNOSIS

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LABORATORY TESTS
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  • Complete blood count (CBC) with differential.

    • Serum chemistry profile.

    • Electrolytes.

    • Calcium.

    • Magnesium.

    • Glucose.

    • Serum creatinine.

    • ALT

    • AST

  • Urine drug/alcohol screen.

  • Blood cultures.

  • Arterial blood gases to assess for metabolic and respiratory acidosis, oxygenation.

  • Serum drug concentrations if previous anticonvulsant use is suspected or known.

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IMAGING
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  • Computed tomography (CT) with and without contrast.

  • Magnetic resonance imaging (MRI)

  • Radiograph if indicated to diagnose fractures.

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DIAGNOSTIC PROCEDURES
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