Status epilepticus

Dr.V.NAGARJUNA Fellow Critical Care AWARE GLOBAL HOSPITAL

STATUS EPILEPTICUS

STATUS EPILEPTICUS•Medical emergency•Requires prompt intervention to prevent irreversible brain damage

DEFINITIONSeizure activity more than 30 minutes. ORIntermittent seizures with no regaining of consciousness between seizures

ACCEPTED DEFINITION>5 minutes of continuous seizure activity.

or

2 or more discrete seizures with no intervening recovery of consciousnessSeizures persisting beyond this duration are unlikely to cease spontaneously & more likely to cause irreversible brain damage

CLASSIFICATION OF STATUS EPILEPTICUS•Status epilepticus is classified in to two categories

1.Generalized Convulsive Status Epilepticus(GCSE)2.Non Convulsive Status Epilepticus(NCSE)

GCSE•Seizures are primary or secondarily generalised•Patient has generalised tonic &/or clonic convulsive movements with loss of consciousness

NCSEAltered consciousness and EEG evidence of seizures without convulsive movementsMay evolve from GCSE when electrical seizure activity continues with loss of motor manifestations

PATHOPHYSIOLOGY•Imbalance between inhibitory & excitatory mechanisms•GABA(A) receptor mediated inhibition•NMDA receptor mediated excitation

INHIBITORY MECHANISMMajor inhibitory mechanism is GABA acting on GABA(A) receptorCauses:Cl- influxHyperpolarization

EXCITATORY MECHANISM•Major excitatory mechanism is glutamine acting on N-methyl-D-aspartate(NMDA) receptors

Causes:Calcium influxDepolarization

NEURONAL CIRCIUT INJURY•Pathophysiological effects of seizures on the brain are directly due to excito- toxic effect & mitochondrial dysfunction & secondary to systemic complications such as hypoxia , hyperthermia.

ETIOLOGY•Status epilepticus may occur de novo(approximately 60% of presentations) or less commonly in a previously diagnosed epileptic.

CAUSES OF SE IN ADULTS• Low antiepileptic drug levels• Stroke-Ischemic/haemorrhagic• Electrolyte

disturbances(Hyponatraemia,hypocalcemia,hypomagnesemia)• Hypoglycaemia/Hyperglycaemia• Cerebral hypoxia• Alcohol-withdrawal• Head trauma• Organ failure-uraemia/hepatic encephalopathy

CAUES OF SE IN ADULTS•Drug toxicity—cephalosporins,isoniazid,tranexamic acid,cocaine,theophylline)•CNS tumors-primary/secondary•Hypertensive encephalopathy/eclampsia•Immunological disorders-Hashimotos encephalopathy,cerebral lupus

GENERALISED CONVULSIVE STATUS EPILEPTICUSGCSE is the most common & dangerous type accounts for approximately 75%

GCSE CLINICAL PRESENTATION •May range from overt GTCS to subtle convulsive

movements in a profoundly comatose patient.May be tonic or clonicSymmetrical or asymmetrical.Late GCSE may show only small amplitude twitching movements of the face ,hands , or feet and also nystagmoid jerking of the eyes

EEG CHANGESPredictable sequence of EEG changes during untreated GCSE1.Waxing & waning pattern2.Continuous monomorphic discharges3.Increasing periods of electrographic silence4.Periodic epileptiform discharges on a relatively flat background

PHYSIOLOGICAL EFFECTS IN GCSE• Hypoxia• Respiratory acidosis• Lactic acidosis• Hyperpyrexia• Hypertension(early)/Hypotension (late)• Hyperglycemia (Early)• Hypoglycemia (Late)• Tachycardia• Intracranial hypertension• Aspiration pneumonitis• Rhabdomyolysis• Neurogenic pulmonary edema

GCSE Vs PSEDOSEIZURES•Differentiate between true seizures & pseudoseizures•Pseustatus misdiagnosed as true SE is often refractory to initial therapy & can lead to patients receiving GA & MV

Features suggestive of pseudoseizures.Lack of sustained convulsions(on-off).Increase in movement if restrained is applied.Abolition of motor movements with reassurance or suggestion.Resistance to eye opening & gaze aversion.Absence of pupillary dilatationNormal tendon reflexes & plantar responses immediately after convulsion.Lack of metabolic consequences

NCSE• Accounts for 25% of SE• Diagnosis of NCSE requires an altered conscious state, no overt

seizure activity and EEG with epileptiform discharges• A response to intravenous antiepileptic drugs(Eg:BZDs) with

clinical improvement & resolution EEG epileptic activity is helpful in confirming the diagnosis• NCSE should be considered in any patient with an unexplained

altered conscious state , particularly those with CNS injury , metabolic disturbance , hepatic encephalopathy or sepsis

DD of NCSE includes•Metabolic encephalopathy•Drug intoxication•Cerebrovascular disease•Psychiatric syndromes(Acute psychosis)•Post-ictal confusion

INVESTIGATIONS IN SE•Initial studies includeglucose,electrolytes Na+,K+,calcium , magnesim),ureaABG analysisAnticonvulsant drug levelsFull blood countUrine analysis

Further investigations after stabilization•LFT•Lactate•Creatine kinase•Toxicology screen•Lumbar puncture•Electroencephalogram•Brain imaging with CT or MRI

OTHER FORMS OF STATUS EPILEPTICUS•Refractory SE:Failure of initial therapy such as BZDs & phenytoin, usually necessitating treatment with agents that induce general anaesthesia•It develops in about 1 in 5 patients with an SE•Associated with a worse prognosis

OTHER FORMS OF SE•SUPER REFRACTORY SE: Continuation or recurrence of SE beyond 24 hours of anaesthetic therapy

MANAGEMENT1.Initial resuscitationAssess A,B,C,sensoriumInitial priority in an ongoing seizure patient is airway protectionThis can be achieved by proper positioning,oral suctioning & oral/nasopharyngeal airway devicesIf necessary, the patient should be intubatedObtain IV access & draw blood for investigationsBlood glucose should be checked

MANAGEMENT•If patient is hypoglycaemic give glucose•Adults: Give thiamine 100mg IV & 100ml of 25% glucose IV

SEIZURE CONTROLA.Give BZDsDiazepam:0.2 mg/kg i.v at 5 mg/min ORLorazepam:0.1 mg/kg i.v at 2mg/min

SEIZURE CONTROL•If seizures persist:Phenytoin:15-20mg/kg at </=50mg/min ORFosphenytoin:15-20mg/kg at </=150mg/min

SEIZURE CONTROL• If seizures persist(refractory SE) intubate & ventilate patientThiopental:Slow bolus 3-5mg/kg i.v followed by infusion 1-5mg/kg per hour ORPropofol:Slow bolus 1-2mg/kg i.v followed by infusion 2-5mg/kg per hourTitrate doses based on clinical & electrographic evidence of seizures, targeting electrographic suppression of seizures.Monitor BP>maintain normo-tension by reducing infusion rates/giving fluids/pressor agents if required

SEIZURE CONTROL.Start reducing propofol or thiopental, approximately 12 hours after resolution of seizures.Continuous EEG monitoring is requiredObserve for further clinical /electrographic seizures.If seizures recur,reinstate the infusion as long as the patients seizures remain refractory

In addition•Look for & treat cause & precipitant•Look for & treat complications like hypotension,hyperthermia & rhabdomyolysis

SURGERY IN REFRACTORY SE•Procedures based on standard epilepsy surgery

Success has been reported with focal resections,subpial transections,corpus callosotomy,hemispherectomy

OUT COME•Depends on age,etiology,degree of impairment of consciousness•Refractory & super refractory>>worse prognosis•No irreversible brain damage>>Good recovery is possible even after weeks of Status epilepticus

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