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emDOCs Podcast – Episode 132: Benzodiazepine-Refractory Status Epilepticus

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Today on the emDOCs cast, Jess Pelletier and Brit Long cover benzodiazepine-refractory status epilepticus.

Episode 132: Benzodiazepine-Refractory Status Epilepticus

 

Background: 

  • Seizures are a common chief complaint in the ED, accounting for 1% of ED visits per year in the U.S.1
  • Among patients with seizures, 22% have SE.2
  • SE refers to a seizure lasting 5 or more minutes, or back-to-back seizures without a return to neurologic baseline in between.3
  • SE is a self-sustaining condition.4 Risk of long-term neurologic damage becomes more likely once SE reaches the 30-minute mark.5
  • Up to 40% of SE cases are actually refractory to benzodiazepines.6
  • There can be SE with motor symptoms (convulsive SE is a subtype of that), or without motor symptoms (i.e., non-convulsive SE, NCSE) (Table 1).

Table 1. Differences in timing to note for subtypes of SE.5

Type of SE Duration of Seizure Needed to Call it SE (in minutes) Duration of Seizure Suspected to Cause Long-Term Neurologic Damage (in minutes)
Convulsive 5 30
Focal/partial, with impaired LOC 10 >60
Absence 10-15 Unknown

 

Table 2. SE subtypes.5  

Motor Symptoms Present? (yes/no) Subtypes
Yes (i.e., CSE) Convulsive Focal onset → secondary generalization

Generalized

Unknown whether either of the above
Myoclonic With or without coma
Focal motor Adversive status

EPC

Ictal paresis

Oculoclonic status

Repeated motor
Tonic
Hyperkinetic
No (i.e., NCSE) With coma
Without coma Generalized Atypical absence

Myoclonic absence

Typical absence
Focal Aphasic

With impaired consciousness

Without impaired consciousness

CSE = convulsive SE, EPC = epilepsia partialis continua, NCSE = non-convulsive SE, SE = status epilepticus.

  • Up to 11% of SE cases have new neurologic disabilities; higher risk of in kids.7
  • Mortality ranges between 15%-33% .8 Unfortunately, these numbers have not improved over time.9

 

Differential Diagnosis:

  • Significant differential of potential underlying causes for benzodiazepine-refractory SE (Table 3).10

Table 3. Potential causes of benzodiazepine-refractory SE.10

Body System Underlying Cause
Endocrine or Metabolic Cerebral edema from DKA

Electrolyte derangements – hypocalcemia, hypomagnesemia, hypo-/hypernatremia, hypophosphatemia

HHS

Uremia
Infectious or Immune Cerebral malaria

Encephalitis

Meningitis

Neurocysticercosis

Sepsis

Tuberculous meningitis/tuberculoma
Neurologic Brain mass or abscess

CVST 

Epilepsy 

ICH 

Ischemic stroke 

PRES
Obstetric Eclampsia
Toxicologic Carbon monoxide poisoning

Drug intoxication or withdrawal

Alcohol withdrawal 

Benzodiazepine/barbiturate withdrawal 

Cathinone intoxication 

Cocaine/methamphetamine intoxication 

GHB intoxication 

MDMA intoxication 

Opioid overdose (especially fentanyl, tramadol) 

Synthetic cannabinoid intoxication

Isoniazid

Seizure threshold-lowering medications

Amphetamines

Antibiotics (cephalosporins, PCN, fluoroquinolones)

Antipsychotics 

Bupropion 

Carbamazepine 

Phenytoin 

SSRI/SNRI 

TCA
Traumatic TBI

CVST = cerebral venous sinus thrombosis, DKA = diabetic ketoacidosis, GHB = gamma-hydroxybutyrate, HHS = hyperosmolar hyperglycemic state, ICH = intracranial hemorrhage, MDMA = 3,4-Methylenedioxymethamphetamine, PCN = penicillin, PRES = posterior reversible encephalopathy syndrome, SSRI = selective serotonin reuptake inhibitor, SNRI = selective norepinephrine reuptake inhibitor, TBI = traumatic brain injury, TCA = tricyclic antidepressant.

 

Assessment:

History

  • Obtain a thorough history is essential.
  • Speak with EMS, bystanders, or friends/family for collateral information to find out about triggers and seizure features.11–13
  • Clarify type of seizure, duration, whether it has broken at any point, whether the patient had a return to baseline between seizures, and whether they fell during the seizure (sustaining potential injuries).
  • Obtain a travel history is important (malaria 14,15 and tuberculosis16,17 can cause meningitis and encephalitis, leading to seizure activity).
  • For patients with HIV, space-occupying lesions are possible and can lead to seizures (toxoplasmosis and CNS lymphoma).

 

Labs

  • Point-of-care (POC) glucose is vital; hypoglycemia is an easily reversible cause of seizure activity.18
  • Other important labs for patients presenting with SE include:10
    • ASM levels (for patients taking them).19
    • Basic metabolic panel (BMP), calcium, and magnesium – electrolyte derangements that could trigger a seizure.
    • Complete blood count (CBC) – for leukocytosis that might suggest infection, or thrombocytopenia that might raise concern for conditions like thrombotic thrombocytopenic purpura (TTP).
    • Inflammatory markers – CRP and ESR to look for signs of infection
    • Renal and liver function tests (LFTs)11 – derangements of LFTs can occur from ASM use, and acute kidney injury (AKI) can occur secondary to rhabdomyolysis from prolonged seizure activity.
    • Pregnancy testing, where applicable19 – exclude eclampsia as the cause of seizures (since the management differs drastically).
    • Toxicology testing20 – look for potential intoxicants. In patients with alcohol use disorder, a blood alcohol level of 0 may raise concern for alcohol withdrawal seizures. However, patients who chronically “live” at elevated levels may have withdrawal seizures at elevated alcohol levels.
    • Infectious testing, for those having signs and symptoms21
    • Lactate, if questioning whether this was really a seizure22,23
      • This will only really help in the first two hours after a tonic-clonic seizure; it is less helpful in the setting of other seizure types
    • Creatine kinase (CK), if there is concern for rhabdomyolysis (which can happen with prolonged seizures).24

 

Imaging

  • Computed tomography (CT) before lumbar puncture (LP) is important if concerned for meningitis/encephalitis to rule out signs of increased intracranial pressure.
    • If there is a high suspicion of meningitis or encephalitis, start antibiotics and antivirals before LP.
  •  Every SE patient needs a CT in the ED once they are stabilized.12 
  • For patients with known seizure disorders, CT is typically unnecessary- unless they have high-risk features (brain tumor, history of cancer, current treatment with chemotherapy, immune compromise, trauma that might have caused the seizure, if they are on anticoagulation, if the seizure activity is different from prior seizures or if it has a new focal element to it).25
  • CT’s ability to visualize posterior fossa lesions is poor; MRI indicated if this is high on the differential.26–29
  • All SE patients without a clear cause for their seizure need an MRI eventually to look for potential anatomic triggers, but MRI does not need to take place acutely.30–37

 

Other Important Diagnostics

  • Obtain ECG to identify potential causes of syncope: heart blocks, prolonged QTc, Brugada syndrome, etc.
    • Arrhythmias are a common mimic.
  • Emergent EEG for patients actively seizing, if they don’t return to their normal neuro baseline within 30-60 minutes after seizure activity is terminated, or if they have new neuro deficits without a clear structural cause on imaging after their seizing has stopped.37
    • Any seizure patient who ends up getting second- or third-line ASMs should likely undergo EEG.38
    • If EEG is unavailable, transfer patient to a facility where they can see neurology and get an EEG once they are stabilized.

 

Management:

  • Go through ABCs – airway, breathing, and circulation. Seizures can quickly lead to airway and breathing compromise.
  • Log roll the patient onto their side (into the recovery position) to prevent aspiration, use airway maneuvers like head tilt chin lift or jaw thrust to open the airway, and utilize suction to remove vomit or secretions that could result in aspiration.
  • Autonomic dysfunction tends to accompany seizure activity; IV fluids may be necessary.
  • Next address D – disability.
    • Check for hypoglycemia and address any reversible causes if possible. 
  • First-line agents (benzodiazepines) should be administered at appropriate doses (Table 4).
    • Benzodiazepines are underdosed the majority of the time,39 usually due to fears of suppressing respiration.
    • Seizure activity itself is more likely to compromise breathing than benzodiazepines.40 Avoid underdosing.
    • Early dosing of benzo’s at appropriate doses is imperative. 
  •  If seizing after the first dose of benzodiazepines, and known reversible causes have been addressed, administer another dose of benzodiazepines.
  • If 5 minutes have passed since the first dose of benzodiazepines, order second-line agents, with fosphenytoin, levetiracetam, or valproic acid being the agents of choice.3
    • Fosphenytoin (and phenytoin) are not recommended for seizures that are toxicologically-induced; they are unlikely to help and may be harmful.
  • If still seizing after several doses of benzodiazepines and a second-line agent, this is “refractory” SE.
    • Likelihood of permanent neurologic damage or death increases after the 30-minute mark.41,42
    • Consider third-line agents: ketamine, pentobarbital, propofol, or thiopental.
    • Many of these agents will lead to respiratory depression;43 thus, the patient will likely require intubation with propofol infusion at this point, along with EEG.38
  •  *Consider ordering second and third line medications at the same time as the second dose of the benzodiazepine.* If continuing to seize following the second benzo dose, consider giving an agent like ketamine or propofol with preparations for intubation.

 

Figure 1. Suggested algorithm for status epilepticus management.

Suggested algorithm for status epilepticus management

 

Table 4. ASM dosing. 

First-Line Agents38,44,45 Drug Route Dose
Diazepam IV 0.15 mg/kg (max 10 mg per dose, may be repeated once)
Rectal 0.3–0.5 mg/kg (max 20 mg)
Lorazepam IV 0.1 mg/kg (max 4 mg per dose, may be repeated once)
Midazolam Buccal 0.2 mg/kg
IM 10 mg
IN 0.2 mg/kg
IV 0.2 mg/kg
Second-Line Agents Fosphenytoin3 IV 20 mg PE/kg (max 1500 mg PE)
Lacosamide46,47 IV 5–6.5 mg/kg over 15 min
Levetiracetam3 IV 60 mg/kg (maximum, 4500 mg)
Phenobarbital48–50 IV 15–20 mg/kg loading dose, no faster than 1 mg/kg/min; a second dose of 5–10 mg/kg may be given 10 min later
Phenytoin50,51 IV 18 mg/kg (range 15–20)  bolus, no faster than 50 mg/min
Valproic acid3 IV 40 mg/kg (maximum, 3000 mg)
Third-Line Agents Ketamine52–55 IV 1.5–5 mg/kg loading dose → maximum infusion rate of 15 mg/kg/h
Pentobarbital49 IV 5–15 mg/kg, no faster than 1 mg/kg/min
Propofol49,56 IV 1–2 mg/kg → infusion rate of 3–7 mg/kg/h
Thiopental49 IV 2–7 mg/kg, no faster than 1 mg/kg/min

 

 

Take-Home Points: 

  • SE is a high morbidity and mortality presentation in the ED with a vicious cycle – it gets hard to break the longer it goes on.
  • Goal is to stop the seizure as soon as possible, particularly before 30 minutes of seizure. 
  • Go through the ABCs, and don’t forget to reverse hypoglycemia and look for other reversible causes.
  • First-line is a benzo, then another benzo at the right dose. Progress to second- and third-line agents quickly to break the SE cycle.

 

References:

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