Status epilepticus: quick reference for emergency treatment

Definition and aims of treatment

Convulsive status epilepticus in adults is present with:

• an ongoing generalised tonic-clonic seizure lasting at least 5 minutes, or
• repeated generalised tonic-clonic seizures without the patient regaining consciousness between them.

Five minutes is the practical threshold for treatment, known as t1. After about 30 minutes of continuous convulsive activity, t2, the risk of permanent neuronal injury increases. Treatment must therefore start at 5 minutes and be escalated without unnecessary pauses [1].

The aims are, simultaneously, to:

1. terminate clinical and electrographic seizure activity,
2. secure oxygenation, ventilation and the circulation,
3. identify and treat the precipitating cause,
4. prevent recurrence and secondary brain injury.

The doses in the treatment ladder below follow the Swedish local sequence given in the original article. International guidelines and studies support the same principles, but local choices of drug, formulations and infusion rates may differ. Always follow the current hospital protocol and check the strength and the maximum infusion rate.

Rapid overview

Benzodiazepines are the established first-line treatment. Intravenous lorazepam and diazepam are effective, and intramuscular midazolam is particularly useful where there is no intravenous access [2,3]. Respiratory complications occur, but untreated convulsive status itself carries a considerable risk of hypoxia and respiratory failure. In placebo-controlled trials, respiratory depression was no more common — and sometimes less common — after a benzodiazepine than with continued untreated status [3,4].

In parallel with the drug treatment

Resuscitation, investigation and drug treatment must proceed simultaneously. Do not wait for laboratory results, CT or EEG before the first dose of benzodiazepine is given.

Airway, breathing and circulation

• Perform an ABCDE assessment and document the time of seizure onset, or the time the patient was last known to be well.
• Protect the patient from injury. Do not restrain the limbs and do not put anything in the mouth.
• Suction the mouth as needed and place the patient in the recovery position when this is practicable.
• Give oxygen if hypoxaemic. Use a bag and mask if ventilation is inadequate.
• Monitor the saturation, respiratory rate, blood pressure, heart rate and a continuous ECG.
• Establish two intravenous cannulae where possible. Use intraosseous access if intravenous access cannot be obtained quickly and parenteral treatment is needed.
• Prepare airway equipment and contact anaesthesia early with a prolonged seizure, repeated doses of benzodiazepine, aspiration, hypoventilation, circulatory failure or an anticipated need for anaesthesia.
• Consider a 12-lead ECG when the acute situation allows, particularly before fosphenytoin, or where poisoning, arrhythmia or cardiac involvement is suspected.

Transient apnoea, hypoxaemia, a rising lactate, acidosis, hypertension and tachycardia are common during a generalised seizure. In prolonged status the initial sympathetic response can give way to hypotension, hypoxia, hypoglycaemia and circulatory failure [5].

Plasma glucose immediately

• Check the capillary or venous glucose immediately.
• Treat hypoglycaemia at once according to the local emergency protocol.
• Give parenteral thiamine to patients with alcohol dependence, prolonged malnutrition or another clear risk of thiamine deficiency.
• Treatment of hypoglycaemia with glucose must not be delayed while awaiting thiamine. Thiamine can be given before or at the same time where this is practicable.

Correct other acute metabolic causes as well, for example severe hyponatraemia, hypocalcaemia or hypomagnesaemia. Symptomatic severe hyponatraemia requires specific emergency treatment according to a separate protocol and careful control of the rate of correction.

Initial investigations

Take samples without delaying seizure treatment:

• full blood count,
• sodium, potassium, calcium and magnesium,
• glucose,
• creatinine and urea,
• liver function tests,
• a blood gas including lactate,
• creatine kinase,
• CRP and other infection markers according to the clinical picture,
• concentrations of the relevant antiseizure drugs, where the assay is available,
• toxicology and ethanol where suspected,
• a pregnancy test where the result would affect management,
• blood cultures where infection is suspected.

Lactate and metabolic acidosis can be marked after a generalised tonic-clonic seizure and often normalise gradually once the seizure has stopped. A normal lactate does not, however, exclude an epileptic seizure, particularly if the sample is taken late.

Look for and treat the cause

Common or clinically important causes are:

• missed doses, a dose reduction, or withdrawal of an antiseizure drug,
• alcohol withdrawal or abrupt withdrawal of sedative drugs,
• poisoning or a drug-induced seizure,
• acute ischaemic stroke,
• intracerebral or subarachnoid haemorrhage,
• cerebral venous thrombosis,
• traumatic brain injury,
• a tumour or other space-occupying lesion,
• meningitis or encephalitis,
• hypoxic-ischaemic brain injury,
• hypoglycaemia or another metabolic disturbance,
• eclampsia,
• autoimmune encephalitis,
• new-onset refractory status without a clear cause.

In older people, stroke, hypoxic brain injury and metabolic disturbances are particularly important causes. Older patients can also have a prolonged postictal reduction in consciousness, but this must not automatically be assumed to be the explanation before continuing non-convulsive status has been considered [6].

Imaging and lumbar puncture

An urgent CT of the brain must be performed once the patient is stable enough, particularly in:

• new-onset status,
• focal neurological signs,
• trauma,
• anticoagulant treatment,
• suspected stroke or haemorrhage,
• malignancy,
• immunosuppression,
• a persisting reduction in consciousness without a clear explanation.

MRI of the brain is more sensitive for, for example, encephalitis, small infarcts, tumour, cortical lesions and peri-ictal changes. MRI should be considered when the CT does not explain the condition, or when the status is refractory [7].

Perform a lumbar puncture where meningitis, encephalitis or inflammatory disease is suspected and it is safe to do so. Antimicrobial treatment, including aciclovir for suspected herpes encephalitis, must not be delayed while awaiting the lumbar puncture or complete imaging.

Step 1: early convulsive status epilepticus

Give a benzodiazepine at 5 minutes of ongoing generalised convulsive activity. Early and correctly dosed treatment matters more than the choice between equivalent benzodiazepines. Underdosing and splitting the dose into several small increments is common and reduces the likelihood of rapid seizure termination [8].

With intravenous access

Give an adequate treatment dose, not repeated small test doses. If the seizure stops during a slow intravenous injection, further administration must be weighed against the risk of sedation and respiratory depression, but the patient must not be left with an insufficient total dose because of unjustified fear of benzodiazepines.

The dose can be repeated once after about 5 minutes if the seizure persists. At the same time, check which benzodiazepines and doses have already been given prehospitally. Several repeated doses of benzodiazepine after two adequate doses increase the risk of respiratory failure and delay effective step 2 treatment.

Intravenous lorazepam and diazepam have not shown any definite clinically decisive difference in efficacy when correctly dosed. Lorazepam has a longer antiseizure effect, while diazepam is redistributed more quickly out of the central nervous system [2,3,4].

Without intravenous access

Do not spend several minutes trying to establish intravenous access before treatment is given if intramuscular midazolam is available. In the prehospital RAMPART trial, 10 mg of intramuscular midazolam was at least as effective as 4 mg of intravenous lorazepam. Freedom from seizures on arrival at the emergency department was achieved more often in the midazolam group, chiefly because treatment could be started sooner [9]. A systematic review of adult studies reached the same conclusion [2].

The evidence for buccal and intranasal midazolam in adults with convulsive status is less extensive than for the intramuscular route. In children, non-intravenous routes are better studied [10]. The choice of formulation and dose must therefore follow the local adult protocol.

Start preparing step 2 straight away

Order and prepare the drug for step 2 as soon as the first dose of benzodiazepine is given. Do not wait until two doses of benzodiazepine have failed before the drug is fetched, the dilution checked and the infusion pump made ready.

Even if the visible convulsion stops after the benzodiazepine, a longer-acting intravenous antiseizure drug should as a rule be considered to prevent recurrence, particularly when no rapidly reversible cause has been corrected [5].

Step 2: established status epilepticus

Established status is present when the convulsions persist or recur despite adequate benzodiazepine treatment. Give a full intravenous loading dose without further delay.

ESETT was a randomised, blinded trial of benzodiazepine-refractory convulsive status in children and adults. Seizure termination with improved alertness within 60 minutes was achieved in 47 per cent with levetiracetam, 46 per cent with valproate and 45 per cent with fosphenytoin. No clinically relevant difference in efficacy or in serious adverse effects could be demonstrated [11]. Later reviews and a meta-analysis of randomised trials have likewise not shown levetiracetam to be superior to valproate [12,13].

There is therefore no support for the view that any one of these three drugs is generally more effective. Choose on the basis of contraindications, comorbidity, interactions, the risk in pregnancy, previous treatment and local availability.

Sodium valproate

Advantages:

• a broad-spectrum agent,
• a low risk of acute hypotension or arrhythmia,
• it can be given rapidly,
• few sedative effects compared with phenobarbital.

Avoid it, or use it only after specialist assessment, in:

• known severe liver disease,
• suspected mitochondrial disease, particularly POLG-related disease,
• a known urea cycle defect,
• marked thrombocytopenia or a significant coagulation disorder,
• acute pancreatitis,
• pregnancy or the possibility of pregnancy, where a suitable alternative exists.

The claim that valproate is always absolutely contraindicated in all women of childbearing potential is too categorical in an immediately life-threatening situation. Valproate carries substantial fetal and reproductive risks and should as a rule be avoided when an equivalent alternative can be given. With ongoing refractory status, however, the acute benefit and the available alternatives must be weighed. Swedish product information and local restrictions must be followed.

Monitor liver function, the platelet count and the ammonia with continued treatment or with an unexplained reduction in consciousness. Hyperammonaemic encephalopathy can occur even without marked hepatic impairment.

Levetiracetam

Advantages:

• few drug interactions,
• a low risk of hypotension and arrhythmia,
• no significant hepatic metabolism,
• rapid and practical to administer.

The loading dose in status must not normally be reduced merely on account of old age, low body weight or impaired renal function. The loading dose is determined by the volume of distribution and by the need to reach an effective concentration quickly. The subsequent maintenance dose and dosing interval must, however, be adapted to renal function. In older patients the creatinine clearance needs to be assessed, since the serum creatinine can underestimate the degree of renal impairment [6].

Be alert for agitation, irritability or other psychiatric adverse effects during continued treatment, but these must not delay the acute loading dose in convulsive status.

Fosphenytoin

Fosphenytoin is an effective alternative and had equivalent efficacy to levetiracetam and valproate in ESETT [11]. It has taken a more marginal place in some Swedish local recommendations because of availability, cost and practical handling.

Bear in mind:

• continuous ECG and repeated blood pressure measurement,
• caution in bradycardia, conduction disturbance, hypotension or severe cardiac disease,
• several clinically significant drug interactions,
• that the dose is given in phenytoin equivalents,
• checking the total and, where needed, the free phenytoin concentration with continued treatment, particularly in hypoalbuminaemia, renal failure or concurrent valproate treatment.

In ESETT there were numerically more episodes of hypotension and intubation with fosphenytoin, but the differences were not statistically significant [11].

Other options

Phenobarbital can be effective, particularly in alcohol withdrawal or abrupt barbiturate withdrawal, but it carries a greater risk of prolonged sedation, hypotension and respiratory depression. Internationally, 15 to 20 mg/kg intravenously is often used, but the dose and infusion rate must follow the local intensive care protocol [13,14].

Lacosamide is sometimes used as an add-on, particularly in focal status, but the evidence in generalised convulsive status is weaker. It can prolong the PR interval and requires caution in conduction disturbance or with concurrent treatment with other drugs affecting conduction [13].

Trying several step 2 drugs in succession may be reasonable in selected cases where intubation and anaesthesia are judged to carry a very high risk. With continuing generalised convulsive activity, this must not delay the treatment of refractory status.

Step 3: refractory status epilepticus

Refractory status epilepticus is present when the seizure activity persists after an adequate dose of a benzodiazepine and an appropriately loaded intravenous antiseizure drug. No additional minimum seizure duration is required [15].

The condition requires:

• immediate contact with anaesthesia and neurology,
• intensive care or neurointensive care,
• intubation and controlled ventilation in most cases,
• continuous EEG as soon as possible,
• simultaneous investigation and treatment of the cause,
• optimised maintenance treatment with longer-acting antiseizure drugs.

There are no randomised trials that reliably show whether propofol, midazolam or a barbiturate is best. The choice must be based on the haemodynamics, the comorbidity, the suspected cause, the risk of adverse effects and local experience [15,16].

Common anaesthetic options

The doses are a guide. The haemodynamics, the EEG and the local intensive care protocol govern further titration.

Propofol

Propofol has a rapid onset and a relatively rapid offset. The risk of propofol infusion syndrome increases with a high dose and with treatment for longer than about 48 hours. The syndrome can include:

• severe metabolic acidosis,
• rhabdomyolysis,
• hyperkalaemia,
• renal failure,
• bradyarrhythmia and circulatory collapse,
• hepatic involvement and hyperlipidaemia.

Check the blood gas, lactate, creatine kinase, electrolytes, creatinine, liver function tests and triglycerides regularly. The risk is particularly important with concurrent catecholamine or steroid treatment, severe critical illness and suspected mitochondrial disease [15,17].

Midazolam

Midazolam is often used internationally as the first continuous anaesthetic treatment. Give a loading dose before the infusion is started. Simply increasing the infusion rate produces a slower rise in concentration and can delay seizure termination. With a prolonged infusion, tachyphylaxis and accumulation can occur, particularly in renal or hepatic failure [16,18].

Thiopental

Thiopental can be effective when propofol or midazolam are not enough. Barbiturates carry, however, a greater risk of hypotension, prolonged mechanical ventilation, infection, ileus and protracted impairment of consciousness. Accumulation in fat means that waking can be considerably delayed after the infusion is stopped [16,18].

Ketamine

Ketamine blocks NMDA receptors and can be particularly relevant late in the course of status, when glutamatergic excitation has increased and GABA-mediated drugs have become less effective. Ketamine generally causes less hypotension than propofol and barbiturates. The evidence rests chiefly on observational studies and case series, and the drug is therefore used as an adjunct or alternative under neurointensive care supervision [13,15].

EEG targets and weaning

Continuous EEG is central, since motor seizure activity can disappear after sedation or neuromuscular blockade while electrographic seizures continue.

Treatment targets

The primary aim is:

• cessation of clinical seizures,
• cessation of electrographic seizures.

A routine requirement for burst suppression has no strong evidential basis. Deeper EEG suppression can reduce breakthrough seizures but increases the risk of hypotension and other intensive care complications. It is therefore reasonable to aim initially for freedom from seizures on the EEG. Burst suppression can be considered with continuing or recurrent electrographic seizures despite an adequate depth of anaesthesia [16,18].

Duration of treatment

Once freedom from seizures has been achieved, 24 to 48 hours of clinical and electrographic seizure freedom is generally recommended before gradual weaning. The evidence is chiefly observational data and expert consensus, not randomised trials [15,19].

Before weaning:

• the precipitating cause must be treated as far as possible,
• longer-acting antiseizure drugs must be loaded and prescribed as maintenance,
• electrolytes, glucose, temperature and oxygenation must be corrected,
• continuous EEG must be available throughout the weaning.

Continue the EEG throughout the weaning of the anaesthetic and for at least 24 hours after electrographic seizures have stopped. In comatose patients, at least 48 hours of recording may be needed to detect late seizures [8,19].

If status recurs during weaning, anaesthetic treatment must generally be resumed, often with a new bolus and a reassessment of the choice of drug, the maintenance treatment and the underlying cause.

If the patient does not wake

Failure to wake after the convulsions have stopped can be due to:

• a postictal reduction in consciousness,
• benzodiazepines or anaesthetic drugs,
• continuing non-convulsive status epilepticus,
• stroke, haemorrhage or encephalitis,
• hypoxic-ischaemic brain injury,
• metabolic or toxic encephalopathy.

After clinically controlled convulsive status, a substantial proportion of patients have continuing electrographic seizure activity. In pooled series, non-convulsive status has been demonstrated in around 14 per cent, and other epileptiform EEG abnormalities in up to almost half of patients [8,19].

Request an urgent EEG therefore if the patient:

• shows no clear improvement in consciousness,
• has a fluctuating level of consciousness,
• has nystagmus, gaze deviation, or subtle rhythmic movements of the face or limbs,
• is pharmacologically sedated after refractory status,
• has an acute brain injury or another high risk of non-convulsive seizures.

The EEG is the principal diagnostic method. The Salzburg criteria and standardised intensive care EEG terminology are used to distinguish definite seizures from rhythmic or periodic patterns on the ictal-interictal continuum. Patterns on the continuum require clinical interpretation and are not automatically equivalent to status [20].

New-onset refractory status without a clear cause

NORSE, new-onset refractory status epilepticus, is a clinical presentation in a person without active epilepsy or relevant previous neurological disease, in whom refractory status arises without a clear acute structural, toxic or metabolic cause being identified immediately. FIRES is a subgroup in which a febrile infection began 24 hours to 2 weeks before the onset of status [21].

Suspect NORSE with:

• new-onset status that rapidly becomes refractory,
• fever or an infectious prodrome,
• new memory disturbance, psychiatric symptoms or a change in behaviour,
• dyskinesias or autonomic instability,
• an inflammatory CSF picture,
• a normal or non-specific initial CT despite severe illness.

The investigation must early on include MRI of the brain with contrast, lumbar puncture, broad microbiological testing, autoimmune and paraneoplastic antibodies in serum and CSF, and a targeted search for malignancy. Save extra serum and CSF where possible [22].

International expert consensus recommends that immunotherapy be considered within 72 hours in persisting NORSE once the common infectious and other causes have been dealt with. A ketogenic diet and second-line immunotherapy can be considered during the first week if the course remains refractory [21,22]. This must take place in neurointensive care in consultation with a neurologist, an infectious diseases physician, an immunologist or another relevant specialist.

Special conditions

Eclampsia

Eclampsia must be treated with magnesium sulfate and emergency obstetric management, not simply according to the ordinary status epilepticus ladder. Contact the obstetrician and anaesthetist immediately. Treat severe hypertension at the same time and plan the obstetric intervention.

A benzodiazepine may be needed for continuing seizures despite magnesium, but magnesium sulfate is the aetiologically directed first-line treatment.

Alcohol withdrawal

Benzodiazepines are the first-line treatment. Give parenteral thiamine where there is a risk of thiamine deficiency, but do not delay glucose in hypoglycaemia. Correct the magnesium, the potassium and other metabolic disturbances. Phenobarbital can be an alternative or an adjunct according to a specific withdrawal protocol and with preparedness for respiratory support.

Isoniazid poisoning

In suspected isoniazid poisoning, the seizures can be very difficult to treat with the usual measures. Pyridoxine is the specific antidote and must be given according to toxicological advice. Contact your national or regional poison control centre immediately.

Stroke

A seizure at the onset of symptoms does not exclude stroke. A persisting focal neurological deficit may be a postictal Todd's paresis but can also be due to acute ischaemic stroke or haemorrhage. Activate the stroke pathway when the clinical picture raises the suspicion, and do not let the seizure alone delay urgent imaging.

Psychogenic non-epileptic seizures

Psychogenic non-epileptic seizures are an important differential diagnosis. In ESETT, around 10 per cent of the patients included were judged in retrospect to have had psychogenic seizures rather than epileptic status [11].

Findings that can support the diagnosis are:

• active eye closure against resistance,
• a prolonged, fluctuating course,
• asynchronous or alternating limb movements,
• side-to-side head movements,
• preserved responsiveness or avoidance movements,
• the absence of an expected postictal phase.

No single clinical sign is diagnostic. A normal lactate, a normal blood gas or a normal prolactin does not exclude an epileptic seizure and must not be used on its own to stop emergency treatment. Video EEG with the recording of a typical event is the reference diagnostic method.

Where there is reasonable uncertainty and ongoing generalised convulsive activity, the patient must initially be treated as convulsive status. If the semiology is strongly atypical and the vital signs are stable, experienced neurological assessment and an urgent EEG should be sought before further sedation, intubation or anaesthetic treatment is given.

Red flags and common pitfalls

Underdosing the benzodiazepine

Small repeated doses give slower and poorer seizure control. Give a full, adequate dose early. Underdosing is common and has been linked to treatment failure and a longer duration of status [8].

Waiting for intravenous access

Give intramuscular midazolam when intravenous access is not immediately available. The faster administration can outweigh the more rapid pharmacological onset of intravenous lorazepam [2,9].

Stopping at the benzodiazepine

A benzodiazepine often terminates the seizure but does not always give sufficiently prolonged protection. Prepare step 2 straight away and give it without further delay if the seizure persists or recurs.

Giving too many doses of benzodiazepine

After two adequate doses, the focus must move to step 2 and, where needed, to treatment of refractory status. Repeated small doses of benzodiazepine delay effective escalation and increase the risk of respiratory failure.

Reducing the loading dose of levetiracetam in renal failure

The acute loading dose must not normally be reduced. Adapt the maintenance dose to renal function.

Regarding valproate as the general first choice

Valproate, levetiracetam and fosphenytoin have equivalent documented efficacy. The choice must be individualised. Valproate must be avoided in, among others, severe liver disease, certain metabolic diseases, and as a rule in pregnancy where a suitable alternative exists.

Missing non-convulsive status

Failure to wake is not automatically postictal or drug-related. Request an urgent EEG.

Using neuromuscular blockade without EEG

Neuromuscular blockade can conceal all motor signs of seizure but does not treat the cerebral seizure activity. Continuous EEG is essential.

Routinely aiming for burst suppression

The primary aim is freedom from seizures on the EEG. Deeper suppression may be needed with recurrence, but it causes more hypotension and more intensive care complications [16,18].

Postponing treatment of the cause

Antibiotics, aciclovir, antidotes, correction of electrolytes, stroke treatment and obstetric intervention must all be started in parallel with the seizure treatment.

Letting thiamine delay glucose

Give thiamine where there is a risk of deficiency, but treat hypoglycaemia immediately.

Drawing an early pessimistic prognosis

The prognosis is governed largely by the aetiology, the age, the level of consciousness, the comorbidity and the duration of status. Prognostic scores can support risk assessment but must not on their own determine the continuing level of care [23]. Tumour-related status and an acute hypoxic or vascular aetiology are examples of conditions with a worse prognosis [24]. Even after prolonged refractory status, meaningful recovery can occur, particularly when no irreversible extensive brain injury has been demonstrated.

After the seizure has stopped

Once status has been terminated, the following must be documented:

• the estimated time of seizure onset and the total duration,
• all drugs given, with doses, times and routes,
• whether the cessation of seizures was clinical or EEG-verified,
• the probable precipitating cause,
• complications such as aspiration, trauma, rhabdomyolysis, renal injury or arrhythmia,
• the plan for maintenance treatment,
• the plan for EEG and neurological follow-up.

Check the creatine kinase, creatinine, potassium, acid–base status and urine output after prolonged convulsions. Assess the risk of aspiration and any signs of infection. Carry out a structured medication review, including adherence, interactions and whether withdrawal or a dose change preceded the seizure.

Patients with known epilepsy at risk of further prolonged seizures should, after recovery, be given a written individual emergency plan with clear instructions on when rescue medication is to be given and when an ambulance is to be called. Such plans can improve the ability of the patient and their relatives to act early [25].

References

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