UNIT: Internal Medicine REG NO.: BMS/2014/72732 DATE: 30/7/2021 ASSIGNMENT: Status Epilepticus
UNIT: Internal Medicine REG NO.: BMS/2014/72732 DATE: 30/7/2021 ASSIGNMENT: Status Epilepticus
UNIT: Internal Medicine REG NO.: BMS/2014/72732 DATE: 30/7/2021 ASSIGNMENT: Status Epilepticus
DATE: 30/7/2021
STATUS EPILEPTICUS
Introduction
In 1993 the American Epilepsy Society Working Group had put forward an operational
definition of status epilepticus as a continuous seizure lasting more than 30minutes or two or
more seizures without full recovery of consciousness in between them, the rationale for
stipulating this duration was the observation from experimental models that any seizure that
persist for more than 30 minutes accompanied by serious metabolic decompensation and
permanent neuronal damage.
Currently it is recommended that seizures lasting more than 5 minutes should be managed as
status epilepticus.
Cardiac dysrhyrthmias,
metabolic derangements
Autonomic dysfunction
Neurogenic pulmonary edema
Hyperthermia
Rhabdomyolysis
Pulmonary aspiration
Classification
Near continuous generalized electrical seizures activity lasting for at least 30 minutes but
without physical convulsions.
Most cases of ASE are actual cases of CSPE that have generalizaed.ASE is easier to treat and
is not associated with neuronal damage.
Epidemiology
Etiology
Pathophysiology
Intensity and duration n of stimulation has direct influence to the transition to maintenance
phase.
Hypothesis-Within the limbic system the dentate gyrus acts as a gate keeper and prevents
excitatory stimulation from spreading through the hippocampus until a point of maximum
dentate activation is reached. Once this point is exceeded excitatory inputs can spread
through the hippocampus and may propagate to involve widespread cortical areas. Ineffective
recruitment of inhibitory neurons, together with excessive neuronal excitation plays a role in
initiation and propagation of electrical disturbance in status epilepticus.
GABA is a key inhibitory neuro- transmitter in the brain .GABA receptor mediated
inhibition may be responsible for termination of seizures. The activation of the NMDA
receptor by excitatory neurotransmitter results in increased levels of intracellular calcium
seen in patients with nerve cell injury seen in patients with status epilepticus.
Diagnosis
Non-convulsive status epilepticus may be difficult in patients with subtle writhing and in-
phase limb movement and unresponsive behaviour.
Investigation
CSF studies
Toxicology studies
Metabolic studies for in-born errors of metabolism
Neuro-imaging studies after stabilization
DIFERRENTIAL DIAGNOSIS
TREATMENT
Principles of management
ONGOING
When seizures continue after 30minutes
IV infusion with cardiac monitoring with endotracheal intubation is required together
with nasogastric tube insertion to ensure the stomach is empty thus preventing
aspiration.
Phonation 15mg/kg at 50mg/min; The main action of phonation is to block voltage
sensitive use dependent sodium channels
Fosphenytoin 15mg/kg at 100mmg/min:
Cardaic monitor and pulse oximetry moitor neurologic condition,blood
pressure,respiration check blood gases
Primary end-point for therapy suppression of encephalographic spikes when EEG monitoring
is done or ceasation of clinical manifestation of status epilepticus.
Complications
PROGNOSIS
REFERENCES