Status epilepticus

• Status epilepticus can be classified as:
• Convulsive status epilepticus (which can be further classified according to seizure type e.g. generalised, partial)
• Non-convulsive status epilepticus
• The distinction is partially academic as it does not influence management strategies

• There are EEG findings of uncontrolled seizures without clinically apparent convulsions, e.g. due to:
• Uncontrolled absence or complex partial seizures
• Patient concurrently anaesthetised
• Accounts for up to 25% of status epilepticus

• Initially there are compensatory mechanisms which aim to prevent cerebral damage during the first 30 - 60mins, such as:
• Raised CMRO₂
• Raised CBF
• Raised glucose and lactate concentrations
• Associated sympathetic cardiovascular changes i.e. raised CO, MAP, HR and CVP


• Beyond the initial period, if seizures aren't terminated, the compensatory mechanisms begin to fail
• Cerebral auto-regulation is impaired, leading to cerebral hypoxia, hypoglycaemia, cerebral oedema and raised ICP
• This causes:
• Electrolyte imbalance with hyponatraemia and hyperkalaemia
• Metabolic acidosis
• Eventually DIC, rhabdomyolysis and multi-organ failure


• These changes occur in both convulsive and non-convulsive status epilepticus, though happen more rapidly in the former

• In short, any cause of seizures
• Some patients may develop new-onset refractory status epilepticus ( NORSE ) without a history of prior seizures
• This is associated with high mortality (∽20%) and is often due to unknown causes (50%) or autoimmune disease (36%)

• Prompt treatment is vital, as neuronal GABA receptors undergo altered localisation during seizures making treatment harder and harder the longer the seizure goes on
• Naturally one will perform management and investigatory steps somewhat simultaneously, but the latter is ensconced in a separate section below for clarity

If seizure not self-terminating within a few minutes

• ABCDE approach
• Treat obvious causative factors:
• Hypoglycaemia - IV dextrose
• Hypoglycaemia associated with alcoholism - IV thiamine (Pabrinex) then IV dextrose
• Hyponatraemia - IV hypertonic saline e.g. 3ml/kg 2.7% NaCl if Na⁺ <130mmol/L
• Eclampsia - IV magnesium


• Use the patient's own management plan if they have one
• If not, administer the benzodiazepine du jour:
• Lorazepam 4mg (0.1mg/kg) IV
• Midazolam 10mg buccally
• Diazepam 10 - 20mg (0.2 - 0.3mg/kg) rectally

If seizure not terminated after five minutes

• Give a second dose of benzodiazepine
• Start readying second line agents

If seizure still not terminated after a further five minutes

• Give a second line agent:
• Levetiracetam 40 - 60mg/kg (up to 3g)
• Phenytoin 20mg/kg (up to 2g)
• Sodium valproate 10 - 30mg/kg (according to NICE; unlike the other two the BNF doesn't list status epilepticus as an indication)
• Administer regular doses of chosen anticonvulsant(s) thereafter e.g. 1g keppra BD, phenytoin 100mg TDS
• Call the friendly neighbourhood anaesthetists or intensivist

If seizure still not terminated i.e. refractory status epilepticus

• Induce general anaesthesia e.g. propofol or thiopentone
• Although NMBA should be used for intubation, they shouldn't be continued thereafter

If seizure still not terminated i.e. "super-refractory status epilepticus"

• Further anaesthetic agent infusion(s) titrated to burst-suppression:
• Propofol
• Midazolam
• Thiopentone
• Ketamine (0.4mg/kg/hr then up-titrated)
• Continue infusing said drugs for 12hrs post-cessation of seizure activity


• Other putative pharmacological agents:
• Volatile anaesthetics
• Magnesium
• Lidocaine
• Pyridoxine


• Non-pharmacological therapies a.k.a. kitchen sink:
• Hypothermia; may reduce status duration but with increased adverse events and no 90-day functional outcome difference
• Ketogenic diet
• Deep brain stimulation

• A failure to investigate and treat the underlying cause will contribute to refractory seizures
• Some of these tests can be performed alongside management above; some will have to wait until a modicum of clinical stability is established

• VBG or ABG
• FBC | Urea and creatinine | LFTs | Clotting inc. fibrinogen
• Electrolytes including magnesium, calcium and ammonia
• Glucose
• Toxicology screen
• Anti-epileptic drug levels
• Blood cultures

• Neuroimaging e.g. CT brain, MRI head
• Lumbar puncture - may see pleocytosis as a consequence of status epilepticus
• EEG
• The opinion of a neurologist and/or neurophysiologist

• Excitotoxic CNS injury and hypoxia
• Cerebral oedema
• Cerebral venous thrombosis
• Intracerebral haemorrhage

• <33% of patients with refractory convulsive status epilepticus will return to pre-morbid functional level