Wednesday, April 18, 2012

Management of Status Epilepticus (PART 1)

DEFINITION:(1,2)
Status epilepticus(SE) is a condition characterized by an epileptic seizure that are so frequently repeated or so prolonged as to produce a fixed and lasting epileptic condition.
Clinically this should be interpreted as any patient who has convulsive activity for more than 30 minutes or who has a 30 minutes of repetitive seizures without rousing to full awareness and clear mental status.
The 30 minutes interval has come from recent animal and human studies that show significant neuronal damage occuring after this time.


Therefore,to prevent brain damage, seizure should be terminated as soon as possible optimally within 30 minutes of onset.
Repeated events associated with impaired conciousness should be considered to represent SE when the recurrence rate does not permit return of conciousness. Non convulsive SE can be considered "electromechanical dissociation" of the CNS where electrographic seizures have no overt clinical manifestation except a diminished mental status.


EPIDEMIOLOGY AND ETIOLOGY:(2,3)
It occurs more frequently in children and in the elderly and in patients with structural cerebral  pathology.The most commonly reported form of SE is tonic-clonic (or convulsive status),which accounts for about 40 to 50% of the total. In the USA alone,convulsive status affects more than 50.000
people each year and in a great proportion of patients the episode of SE represents the initial manifestation of their epilepsy (12 to 18%).


SE occurs relatively frequently during the neonatal period often due to metabolic infectious disorders.It is more common in mentally retarded patients probably because of diffuse cerebral abnormality. The annual incidence of SE in general population is estimated to be about 450 to 650 cases per 1000.000 persons in the USA and SE accounts for
1 to 5% of all hospital admissions for epilepsy.


The frequency of status is greatest in children and most episodes occur before 5 years age.In the first year 75% of episodes of SE were in the context of an acute illness whereas this number falls to 28% in children over 3 year of age.In older children and adults frequent causes of SE
include poor anti epileptic drugs compliance,or drug withdrawal (31%),ethanol related status(28%),drug toxicity or abuse and withdrawal(9%) CNS infections(8%),metabolic disorders(14%),cerebrovascular diseases(10%),cerebral tumor(7%),trauma(10%),fibrile SE(12%),almost exclusively found in children.No etiology is identified in about 20% of events resulting in a diagnosis of idiopathic or cryptogenic SE.


SE can be devided in stages :(1,2)
Premonitory stage    
Usually in patients with established  epilepsy. May last several hours. 


Early status 
This is the stage where(0-30 min)mechanism compensate
for the greatly enhanced metabolic activity(adaptative
or early compensated phase).                                          


Established status
Defines as status that has continued (30-120 min) for 30
minutes in spite of early stage treatment.Physiologic decompensation has begun (maladaptative or late decompensated phase).


Refractory status
Seizures continue after initiation of (>120 min) therapy
Prognosis is worse and there is a high mortality.                    


PATHOPHYSIOLOGY OF SE:(1)
It has been noted that during tonic clonic SE especially motor seizures are frequently restricted in their distribution. In addition focal or lateralized convulsive activity does not necessarily indicate that a localized structural lesion is responsible for the status.
At later stages in the sequence of events,motor activity diminishes or even disappears.Therefore,the end stage may consist of ongoing epileptiform discharges recorded by EEG without motor accompaniment or a form of electromecha-
nical discociation between motor events and brain dischar-
ges.Status epilepticus both convulsive and non convulsive can lead lifethreatening,systemic,metabolic,and physiolo-
gic disturbances.These factors usually account for the poor prognosis associated with this disorder. Status itself,how 
ever,independent of metabolic and physiologic disturbances may lead to lasting brain dysfunction and prolinged status may result in permanent neuronal damages.


Tonic clonic status is often preceded by a premonitoring stage during which seizure activity progressively increases from its habitual levels, resulting in clinical deterioration. 
In patients who have an acute  symptomatic events however,status often starts abruptly.
Physiologic changes in tonic clonic SE are usually divided into two phases with an early compensated phase I, and a late decompensated phase II. The transition from early to late phase occurs often about 30 min, that is why that 30 minutes is the time limit usually defined to represent SE.


During early compensated phase cerebral matabolism is greatly increased due to seizure activity but physiologic mechanism are sufficient to meet the metabolic demands and cerebral tissue is protected from hypoxia or other metabolic damages.The major physiologic changes are related to the increased CBF and metablism(hyperglycae
mia,lacticacidosis), autonomic activity cardiovascular changes(including hypertension, tachycardia,cardiac arrhythmia,hypersecretion and  perspiration,hyperpyrexia vomiting, and incontinence).
Later, if not controlled the status enters a phase of decompensation during which the increased cerebral metabolic demands cannot be fully met,resulting in hypoxia,failure cerebral autoregulation,hypoglycaemia
cerebral edema,resulting in rising ICP;altered systemic metabolic patterns (electrolyte disturbance,metabolic and respiratoric acidosis,multiorgan failure)


THE EEG AND SE (4)
The EEG is important tool in the management of both convulsive or non vulsive SE.While SE is a medical emergency and treatment should not be delayed,if an EEG is not available,clinical examination alone may result
in misdiagnosis of SE for two reasons :
First,psychogenic status,is a common cause of diagnostic confusion.
In one study 20% of patients presenting to an emergency department of a tertiary referral centre with intractable convulsive movements had psychogenic seizures.


Second,non convulsive status is under recognized and patients with non convulsive status are often mislabelled as being confused or postical.


In sedated patients treated with general anesthesia continuous EEG monitoring allows immediate recognition and treatment of seizures.
Seizure activity increases CMRO2 and causes excitotoxic cell damage. Continuous EEG monitoring facilitates adequate seizure control without over treatment in SE and reduces this risk of excitotoxic cell damage.
Mortality in SE increases with the duration of seizures.
It is therefore reasonable to assume that early detection of subclinical seizures in the ICU reduces morbidity and mortality.
Where continuous EEG monitoring is not available it is reasonable to obtain an EEG daily while the patient remains unconcious and to consider performing an EEG before making significant alterations to therapy.
Also continuous EEG monitoring is essential to titrate medications to burst suppression.


to be continued

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