Status epilepticus is a life-threatening condition defined as a seizure lasting more than 5 minutes or recurrent seizures without regaining consciousness. It can be caused by changes in medication, infection, stroke, or other medical conditions. Symptoms include muscle spasms, confusion, and impaired consciousness. Diagnosis involves examination and electroencephalography. Treatment goals are resuscitation, terminating seizures, decreasing cerebral metabolism, and treating underlying causes. First-line treatments are benzodiazepines while refractory cases may require barbiturates, propofol, or midazolam infusion. Prognosis depends on duration and cause, with prolonged seizures carrying higher mortality and worse outcomes.

1. Management of
Ahmed Essam Elsayed Farrag
3rd Year Medical Student
Mansoura Faculty Of Medicine - Egypt

2. Status epilepticus (SE) is a common,
life-threatening neurologic disorder
that is essentially an acute, prolonged
epileptic crisis ..
epileptic seizure lasting more than five minutes* or two or more
seizures within a five-minute period without the person returning to
normal between them ..
* Years ago, a seizure needed to last longer than 30 minutes to be considered status epilepticus ..

5. SE can represent an exacerbation of a
preexisting seizure disorder, the initial
manifestation of a seizure disorder, or
an insult other than a seizure disorder ..
In patients with known epilepsy, the most
common cause is a change in medication ..
Most seizures terminate spontaneously ..

6. Focal status epilepticus. Electroencephalograph (EEG) in a patient
with epilepsia partialis continua caused by Rasmussen encephalitis
before hemispherectomy. The patient had long-standing, intractable
partial epilepsy since the first decade of life. Seizures included
complex partial with occasional secondary generalization and
repetitive myoclonus involving the left side of the body. Note the
frequent epileptiform discharges at 1-2 Hz involving the right
frontocentral channels. These were evident on many of the patient's
routine EEGs. Clinical myoclonus is often correlated with high-
voltage bursts of such activity.

7. Status epilepticus can be divided into two categories:
convulsive and nonconvulsive (NCSE) ..

8. Status epilepticus with convulsions may be more
likely to lead to long-term injury. Convulsions may
involve jerking motions, grunting sounds, drooling,
and rapid eye movements.
Convulsivestatusepilepticus

9. People with this type may appear confused or look
like they're daydreaming. They may be unable to
speak and may be behaving in an irrational way.
Nonconvulsive status epilepticus

10. What causes status epilepticus?
Inchildren,themain cause of status epilepticus
isan infectionwitha fever.
Inadults, thecommoncauses include:
• Stroke
• Imbalance of substances inthe blood,such as
lowblood sugar
• Drinkingtoomuch alcoholor havingalcohol
withdrawalafter previousheavyalcoholuse

11. Who is at risk for status epilepticus?
There are manyrisk factors for status epilepticus including:
• Poorly controlled epilepsy
• Low blood sugar
• Stroke
• Kidneyfailure
• Liver failure
• Encephalitis (swelling or inflammationof the brain)
• HIV
• Alcohol or drug abuse
• Genetic diseases such as Fragile X syndrome andAngelmansyndrome
• Headinjuries

12. What are the symptoms of status epilepticus?
These are possible symptoms of status epilepticus:
• Muscle spasms
• Falling
• Confusion
• Unusualnoises
• Lossof bowel or bladder control
• Clenched teeth
• Irregular breathing
• Unusualbehavior
• Difficulty speaking
• A "daydreaming" look

13. How is status epilepticus diagnosed?
Definitions vary, but currently it is defined as one continuous,
unremitting seizure lasting longer than five minutes, or recurrent
seizures without regaining consciousness between seizures for greater
than five minutes..
Previous definitions used a 30-minute time limit.
Diagnosis of NCSE can be challenging. It may not be considered in
patients who present in altered sensorium or coma following a
convulsion. All comatose patients should therefore be carefully
examined for evidence of minor twitching, which may involve the face,
hands, or feet or may present as nystagmoid jerking of the eyes ..
Continuous EEG monitoring can be helpful in such instances

14. How is status epilepticus diagnosed?
Examination for status epilepticus includes the following:
• Generalized convulsive status epilepticus: Typical rhythmic tonic-clonic activity,
impaired consciousness; rarely, may present as persistent tonic seizure
• Status epilepticus due to the use of illicit, or street, drugs: needle-track marks
• Status epilepticus due to possible mass lesion or brain infection: Papilledema,
lateralized neurologic features
• Subtle or transformed status epilepticus: Any patient without improving level of
consciousness within 20-30 minutes of cessation of generalized seizure activity
• Associated injuries in patients with seizures: May include tongue lacerations
(typically lateral), shoulder dislocations, head trauma, facial trauma

15. How is status epilepticus diagnosed?

16. • Excitation of a group of nerves.
This is causedby inward currents of Na, Ca and involvement of excitatory
neurotransmitters like Glutamate andAspartate.
• Too little inhibition.
• Epileptogenesis andhyperexcitability and hypersynchronization of neuronsthat
facilitates spread.
There has to be abnormal synchronization – aproperty of a population of neurons to
discharge together independently. Alone, a hyperexcitable neuron cannot generate a
seizure.
Mechanism of seizure formation
Pathogenesis

19. Pathophysiological Effects
Neurological
• excitotoxic neuronal injury
• secondary injuryfrom systemic complications (hypotension,hypoxia, hyperthermia)
• excessive intracellularcalcium influx -> intracellularneurochemical medicated cell damage/death.
• intracranialhypertension
• increased cerebrospinal fluidprotein
Respiratory
• hypoxia
• respiratory acidosis
• neurogenic pulmonaryoedema
• aspiration pneumonitis
Cardiovascular
• hypertension -> hypotension
• tachycardia
• dysrhythmias
Metabolic
• lactic acidosis
• hyperpyrexia
• hypoglycaemia

20. Management Goals :
1. Resuscitationto prevent secondary brain injuryandmaintaincerebral perfusion pressure
2. Terminateseizure
3. Decreasecerebral metabolicrate
4. Diagnoseand treatcause
5. Treatcomplications

21. Resuscitation
• Attend to ABCS andaddresslife threats
• Manage airway with recovery position, airway adjunctsandintubation if required
• Optimize oxygenation andprovide ventilatory support as needed (prone to hypercapnia)
• EarlyIV orIOaccess, optimizecerebralperfusionpressure
• Treat hypoglycaemia andlife-threatening electrolyte disturbance if present
• Maintainnormothermia
• Give relevant antidote if due to toxic agent (e.g. pyridoxine for isoniazid)

22. Terminate seizure
Firstline therapies:
• Bolus dose benzodiazepines
• Midazolam 0.1mg/kg IV – also buccal or IM (IM not inferior to IV lorazepam)
• Lorazepam 0.1mg/kg IV (onsetin 3-5 minutes and lasthours; preferredfor longeractingeffects)
• Diazepam 5mg IV/PR (avoid IM as painful)(onset in~1 minute but lasts only about ~20 minfor antiseizureactivity)
• Clonazepam

23. Terminate seizure
 Second linetherapies(typicallyrequiresintubation and mechanical ventilation)
• Phenytoin15-20 mg/kg IV over 30 minutes or longer
should be used to terminateseizures as a sole agent, always with benzodiazepines
some regard phenytoin as a first line therapy, however not all seizures require therapy in
addition to terminationwith benzodiazepines
avoid if usually on phenytoin
avoidrapid push to risk of cardiovascular toxicity from the propylene glycol diluent
• Valproic acid 40mg/kg IV over10 min (may giveadditional20mg/kgover 5 min ifstillseizing)

24. Terminate seizure
Third line therapies
(forrefractory status epilepticus;typicallyrequireintubation and ventilation and cEEG monitoring)
• propofol 2-3mg/kg IV then <4mg/kg/hr
• midazolam IV infusion
• Barbiturates
• Phenobarbitone infusion 10mg/kg IV boluses -> 0.2-0.4mg/kg/min
• Thiopentone 4mg/kg IV (then repeat boluses or infusion targeting burst suppression)
• Clonzepam IV infusion

25. Treat underlying cause
 bacterial infection –Antibiotics
 viral infection – Antivirals
 Abscess – surgery
 Increased ICP – neurosurgical decompression
 Eclampsia – Mg2+ and BP management (early delivery of baby andplacenta)
 Isoniazid OD or pyridoxine-dependent seizures (e.g. neonates) – pyridoxine
 Cholinergic syndrome – atropine,( palidoxime if organophosphate poisoning)
 Sodium channel blocker overdose –sodium bicarbonate, intralipid

26. Restore
Ensure patientreceivesnormaltherapeuticprophylaxis
Checklevels
Consider adding anew generationin difficultcases

28. prognosis
prolonged seizures have higher mortality and worse outcomes
mortality of statusepilepticus ranges
from ~ 10-30% in different studies,
depending on the definition used