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Status Epilepticus

Updated 4/12/2016 by Tom Heaton

Short Notes

​Status epilepticus means persistent seizure activity.
The exact definition involves:
  • Persistent seizure activity for over 5 minutes, or
  • 2 or more seizures without an intervening period of neurological recovery
5 mins is used rather than previous definitions of 30 mins as:
  • Seizures going beyond this duration are less likely to self-terminate
The harms of persistent seizing probably start to occur before this time
​The focus of management is:
  1. Maintaining body function status (cardiorespiratory adequacy)
  2. Terminating the seizure
  3. Treating complications
  4. Identifying the cause
Benzodiazepines are the first line anticonvulsant of choice.
Lorazepam IV (0.1mg/kg) or Midazolam IM 10mg are well established choices

Long Notes

​Status epilepticus means persistent seizure activity.
The exact definition involves:
  • Persistent seizure activity for over 5 minutes, or
  • 2 or more seizures without an intervening period of neurological recovery
Previous definitions used a time frame of 30 mins to define status, but it is recognised that the harms (as discussed below) occur well before this time, and thus treatment must start earlier. There is also that recognition that once seizures have persisted more than 5 mins they are less likely to self-terminate.
This takes into account that many ‘benign’ seizures will terminate spontaneously before this time, and if they haven’t by 5 minutes, they are likely to need treatment.
This primarily looks at tonic-clonic status epilepticus, but the other seizure types may also exist in prolonged forms.

​Pathophysiology

​As with ‘normal’ seizures, status epilepticus represents an imbalance of the excitatory and inhibitory components of the neurotransmitters.
Glutamate is the primary excitatory neurotransmitter whilst GABA is the primary inhibitory neurotransmitter.  
The exact reason why this imbalance persists in the case of status epilepticus is unclear. 
The consequences of prolonged seizure activity are significant and indeed the primary reason for wanting to rapidly halt seizure activity is due to the significant harm that such activity causes.
These can be broken down into:
Neurological
  • Excitotoxic neuronal injury – probably from excess calcium
  • Intracranial hypertension
  • Receptor alteration – this may explain reduced responsiveness to benozodiazepines with ongoing seizure
  • There may be secondary injury from the cardiorespiratory consequences.
Respiratory
  • Impaired ventilation – hypoxia and hypercapnia
  • Pulmonary oedema (neurogenic)
  • Risk of aspiration
Cardiovascular:
There is a significant catecholamine surge which is probably partly responsible for these effects:
  • Hypertension initially, BP may drop as seizure persists
  • tachycardia,
  • cardiac arrhythmias
Metabolic
  • Hyperthermia – secondary to heat created by muscle activity
  • Acidosis – metabolic and respiratory component. Is anti-convulsant in its effect and shouldn’t be treated. There is a notably raised lactate
  • Leukocytosis – both in blood and CSF
  • Rhabdomyolysis
  • Hyperglycaemia – though may drop with persisting activity

Assessment

​Assessment is identical to that described for seizures. However, the primary focus will be the cessation of the seizures and prevention of harm, as described below.
As such an ABCDE approach will be employed to rapidly assess and correct life threatening problems.

Management

The focus of management is:
  1. Maintaining body function status (cardiorespiratory adequacy)
  2. Terminating the seizure
  3. Treating complications
  4. Identifying the cause (and treat)
A step wise approach is advised, and there are several guidelines on the approach.
Step 1 – Stabilisation (0-5 mins)
  • Maintain an airway (consider need for a secure airway)
  • Apply oxygen
  • Asses cardiovascular status (instigate treatment as needed)
  • Secure IV access
  • Measure capillary blood glucose (CBG)
    • Treat hypoglycaemia
  • Consider administering IV thiamine with glucose if suspicion of alcohol excess or malnutrition
  • Consider non-epileptic seizure
Step 2 – Emergency treatment (0-20 mins)
  • Start emergency AED treatment (below)
  • Perform emergency investigations
    • Bloods: ABG, U&Es, FBC, LFTs, Bone profile, Mg2+, AED levels
    • Consider head imaging and LP if clinically indicated
  • Instigate regular monitoring: NIBP, ECG, SpO2, temp
Step 3 – Established status (0-60 mins)
  • Establish aetiology
  • Identify and treat complications
  • Inform ICU +/- anaesthesia
  • Continue emergency AED drugs
Step 4 – Refractory Status (30-60 mins)
  • ICU to take over care – may need transfer to ICU
  • Instigate critical care and EEG monitoring
  • Instigate ICP monitoring where appropriate
  • Initiate long term AED therapy

​Emergency drug therapy

​This will be a step wise approach and (initially) dependent on the environment.
Prehospital
Diazepam 10-20mg rectally – can repeat after 15 mins if persisting, or
Midazolam 10mg buccal
Hospital
1st line

Lorazepam 0.1mg/kg (usually max 4mg bolus) – repeat at 15 min
Or
Midazolam 10mg IM (5mg if 13-40kg) – this may be more effective, especially if no IV access
Diazepam 0.15mg/kg IV (10mg max bolus)
2nd Line (Established Status)
Phenytoin 15-18mg/kg – at a rate of 50mg/min (to minimise SEs)
Or
Fosphenytoin 15 -20mg/kg phenytoin equivalent (PE) dose - 50-100mg PE dose/min (this is better tolerated and probably preferred when available)
Phenobarbital 10-15mg/kg – 100mg/min
Valproic Acid 40mg/kg – 10 mins
3rd Line (refractory status)
General anaesthesia
Choice of agent includes: propofol, thiopentone, midazolam.
Further options (Ongoing refractory)
Volatile anaesthetic agent
Ketamine
Magnesium
​Lidocaine

​Underlying Cause

​Certain causes may need instigation of parallel treatment
Eclampsia – Mg2+, BP control and delivery
Infection – antibiotics
Cholinergic syndrome – atropine
Sodium channel blocker overdose – intralipid, sodium bicarbonate

Practice Notes

Muscle relaxation for intubation should be with suxamethonium to allow easier monitoring of ongoing seizure activity.
LP is relatively contraindicated immediately post ictal – a raised leucocytes count is possible in the absence of infection.
Hypotension is the most common adverse event associated with treatment (approx. 30% of patients). Hypoventilation is also common (approx. 10%), but is actually less than placebo treatment, indicating it is actually a significant complication of status epilepticus itself.

​Prognosis

​The mortality of convulsive status epilepticus is relatively high; 9-21% at hospital discharge.
For refractory status epilepticus this is even higher at 23-61%.
Severe neurological sequalae occurs in 11-16% of cases.
The age of the patient and the aetiology of the seizure have the biggest impact on prognosis - wihdrawal of AEDs and alcohol have better prognosis, with intracerebral bleeds and anoxic brain injury having worse.

​References

  1. C Nickson. Status epilepticus. LITFL. 2016. (Accessed 30/12/2016, available at http://lifeinthefastlane.com/ccc/status-epilepticus/)
  2. J Roth. Status epilepticus. Medscape. 2016. (Accessed 30/12/2016. Available at http://emedicine.medscape.com/article/1164462-overview#a1)
  3. NICE. Epilepsies; diagnosis and management. CG137. 2016. (accessed 24.11.16, available at https://www.nice.org.uk/guidance/cg137/)
  4. T Glauser et al. Evidence- based guideline: treatment of convulsive status epilepticus in children and adults: Report of the guideline committee of the American Epilepsy Society. Epilepsy Currents. 2016. 16(1); 48-61. (Available at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4749120/)
  5. G Brophy et al. Guidelines for the evaluation and management of status epilepticus. Neurocrit Care. 2012. 17; 3-23
  6. O Flower. Status epilepticus - when the seizure doesn't stop. SMACC. 2016. (Accessed 7.12.16, available at http://www.smacc.net.au/2014/11/status-epilepticus-when-the-seizure-doesnt-stop-oli-flower/) 
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