Approach to convulsive status epilepticus: Clinical sciences

Chapters:

Watch video only

Introduction 0:00–0:46

Convulsive status epilepticus is a neurologic emergency that refers to persistent tonic-clonic seizure activity lasting five or more minutes, or multiple seizures without return to baseline in between.
This condition occurs when inhibitory mechanisms responsible for terminating seizures fail to work, or when pathways that lead to prolonged seizures are overactivated.
Some common causes of status epilepticus are medication changes or noncompliance in patients with known epilepsy, substance use, metabolic derangements, and acute brain injury from infectious and non-infectious processes.
Now, if your patient presents with chief concerns suggestive of convulsive status epilepticus, first, perform an ABCDE assessment.

Unstable 0:46–1:19

You should consider all patients with convulsive status epilepticus unstable, so be sure to stabilize their airway, breathing, and circulation.
Sometimes, you might even need to intubate your patient and start mechanical ventilation. Next, obtain IV access and put your patient on continuous vital sign monitoring, including heart rate, blood pressure, and pulse oximetry, as well as cardiac telemetry.
Once you are done with acute management, obtain a focused history and physical exam, and order labs, including fingerstick glucose, CBC, CMP, and a toxicology screen.

H&P 1:19–1:54

Also, don’t forget to check anti-seizure medication levels. History will reveal a tonic-clonic seizure that started 5 or more minutes ago, or multiple seizures without return to baseline in between.
Additionally, the physical exam will demonstrate altered mental status and alternating body stiffening and jerking movements consistent with a tonic-clonic seizure.
At this point, you can diagnose convulsive status epilepticus, so your next step is to proceed with treatment! First, take a look at the fingerstick glucose because hypoglycemia can be an acute symptomatic cause of status epilepticus and seizures in general.

Treatment 1:54–4:44

If the patient’s glucose level is less than 60 milligrams per deciliter, you should give thiamine and dextrose. Be sure to administer thiamine before dextrose to minimize the risk of developing Wernicke encephalopathy, since thiamine is required in the metabolism of glucose.
If fingerstick glucose levels are normal, or if the seizure persists, it’s time to administer the first-line treatment for convulsive status epilepticus, which is a benzodiazepine, such as lorazepam, midazolam, or diazepam.
If the seizure persists after 3 to 5 minutes, you can give a second dose of the same medication. If this doesn’t stop the seizure, move on to a second-line treatment, which is a bolus of an anti-seizure medication, such as fosphenytoin, valproic acid, levetiracetam, or phenobarbital.
If the second-line treatment fails to abort the seizure, proceed with a third-line treatment, which includes giving a second anti-seizure medication or inducing a therapeutic coma with an anesthetic drip using midazolam, propofol, or pentobarbital.
Finally, consider EEG monitoring as a way to guide escalation or de-escalation of your anesthetic drip. You can also use EEG to evaluate for non-convulsive status epilepticus, which is a state where the brain is still seizing, but there are few, if any, physical manifestations of seizure activity.
In this case, your patient might have subtle signs, such as eyelid fluttering or mouth twitching, or they could simply remain altered without any physical indication that a seizure is ongoing.
A high proportion of patients with convulsive status epilepticus can convert to non-convulsive status epilepticus, so this is an important thing to look out for if your patient does not return to their baseline mental status!
Additionally, EEG can help you differentiate epileptic from non-epileptic events, such as psychogenic non-epileptic seizures, which are triggered by psychological factors, such as emotional trauma or stress.
In other words, in this condition, there are no abnormal electrical discharges in the brain, so you will see no EEG findings of epileptic seizures.
Now, here’s a clinical pearl to keep in mind! Hypoglycemia is not the only glucose abnormality that can cause convulsive status epilepticus.
Hyperglycemia can also cause seizures, which is especially common in individuals with type 2 diabetes mellitus who go into a hyperosmolar hyperglycemic state.
Alright, once the seizure has resolved, your next step is to assess the patient’s history of medication or substance use.

Subtherapeutic ASM level 4:44–5:13

If your patient has a known history of epilepsy and is on an anti-seizure medication, they might report missed doses or a change in their medication dose.
Additionally, if the level of their anti-seizure medication is low or undetectable, you can diagnose subtherapeutic anti-seizure medication level as the cause of status epilepticus.
Now, moving on to intoxication and withdrawal as potential causes of seizures! In this case, history might reveal a recent substance use or use of psychiatric medications.

Intoxication/withdrawal 5:13–6:42

Additionally, the patient’s friends and family might report that they found the patient on the floor next to a medication container.
Finally, some individuals might report a history of chronic benzodiazepine or alcohol use! Next, the physical exam may demonstrate evidence of substance use, such as smell, residue, or injection marks on the skin.
The exam could also be consistent with a known toxidrome, such as with certain pupillary changes, depending on the substance.
In this case, you should consider intoxication or withdrawal, which can occur with both prescription and non-prescription substances.
Now, if the toxicology screen reveals substances that can cause seizures, such as cocaine, amphetamines, or phencyclidine; or if you find supratherapeutic levels of prescription medications, including antidepressants, antipsychotics, and anti-seizure medications, diagnose intoxication.
On the other hand, if the toxicology screen is negative for benzodiazepines in a patient with chronic benzodiazepine use, or similarly, if an ethanol level is undetectable in a patient with chronic alcohol use, diagnose withdrawal as the cause of status epilepticus.
Now, let’s go back and take a look at individuals with no history of contributory substance or medication use. In this case, consider metabolic derangement, so be sure to assess the CMP results.

Metabolic derangements 6:42–7:33

If you notice severe electrolyte abnormalities, such as severe hypo- or hypernatremia, hypo- or hypercalcemia, or hypomagnesemia, then you should diagnose metabolic derangements as the cause of status epilepticus.
Now, here’s a high-yield fact to keep in mind! Seizures associated with hyponatremia typically occur when the plasma sodium levels rapidly drop below 115 mEq/L.
In this case, management primarily relies on administering hypertonic saline! However, if the CMP reveals no electrolyte abnormalities, you should consider the possibility of a brain injury from infectious and non-infectious causes.

CNS infection 7:33–8:37

First, let’s take a look at CNS infections! In this case, the history will reveal fever, neck stiffness, and light sensitivity, also known as photophobia, and the physical exam may reveal nuchal rigidity.
Lab work might indicate an elevated white blood cell count. With these findings, consider CNS infection, so be sure to perform a lumbar puncture and send a CSF sample for analysis.
Also, consider ordering a brain MRI, especially if you suspect an intracranial mass lesion or increased intracranial pressure!
CSF analysis will likely show an elevated white blood cell count and positive culture or PCR. Additionally, the MRI may show meningeal enhancement or abscess.
These findings suggest that the underlying cause of status epilepticus is a CNS infection. On the flip side, if there is no history of fever, neck stiffness, or light sensitivity; there is no nuchal rigidity, and labs reveal a normal white blood cell count, consider non-infectious intracranial causes.

Non-infectious intracranial process 8:37–9:05

Next, obtain a brain CT or MRI, which is going to help you differentiate between the most common causes, including stroke, hypoxic or anoxic brain injury, trauma, or autoimmune encephalitis.
If your patient has a history of an acute-onset neurologic deficit, the physical exam shows a focal neurologic deficit, and CT or MRI demonstrates infarction or hemorrhage, diagnose a stroke as a cause of status epilepticus.

Stroke 9:05–9:21

Next, let’s take a look at hypoxic or anoxic brain injury. In this case, history typically reveals a known hypoxic or anoxic event, such as drowning, asphyxiation, or cardiac arrest.

Hypoxic/anoxic brain injury 9:21–9:57

Sometimes, history might be unknown but the patient was found down. Next, the physical exam may show loss of brainstem reflexes and flaccid paralysis.
Finally, if the brain CT or MRI shows global loss of gray-white differentiation and signs of cerebral edema such as sulcal effacement, diagnose hypoxic or anoxic brain injury.
Next up are head traumas! These individuals will present with a history of recent head trauma or their history might be unknown but they were found down with signs of physical injury, such as bruising or bleeding.

Trauma 9:57–10:26

If the head CT shows multicompartmental hemorrhages involving the epidural, subdural, intraparenchymal, or subarachnoid spaces, along with skull fractures, diagnose head trauma as a cause of convulsive status epilepticus.
Finally, let’s go over autoimmune encephalitis! Individuals with this condition often have a history of personality or behavioral changes or new-onset psychosis.

Autoimmune encephalitis 10:26–12:04

Additionally, there may have been a preceding infection or a known history of malignancy. Next, the physical exam might reveal a movement disorder, such as dyskinesias, which are abnormal involuntary movements that may include writhing or twisting from sustained muscle contractions.
The brain MRI classically shows an abnormal signal and potential contrast enhancement of the temporal lobes. In this case, you should suspect autoimmune encephalitis and send off serum and CSF autoimmune antibodies.
If those results are positive, you can diagnose autoimmune encephalitis as the cause of status epilepticus. By the way, autoimmune encephalitis due to an immune reaction to cancer cells is also called paraneoplastic encephalitis.
Alright, here’s one more clinical pearl for you! One of the most common forms of autoimmune encephalitis is anti-NMDA-receptor encephalitis.
This condition tends to occur in younger, biologically female patients. Besides behavioral changes and psychosis, your patient may also have orofacial dyskinesias, autonomic dysfunction, and sleep disorders.
If you’re considering NMDA-encephalitis in a biologically female patient, you should order pelvic imaging, such as transvaginal or pelvic ultrasound, because this condition is often associated with ovarian teratomas.
Alright, as a quick recap… Convulsive status epilepticus refers to persistent tonic-clonic seizure activity lasting five or more minutes, or multiple seizures without return to baseline in between.

Review 12:04–13:09

The workup starts with checking the fingerstick glucose levels. If glucose levels are low, you should give thiamine and dextrose.
However, if the fingerstick glucose levels are normal or if the seizure persists, proceed with the first-line treatment, which includes a benzodiazepine, such as lorazepam, midazolam, or diazepam.
If seizures persist, proceed with the second-line treatment, which is a bolus of an anti-seizure medication. If the second-line treatment fails to abort the seizure, proceed with the third-line treatment, which is either giving a second anti-seizure medication or inducing a therapeutic coma with an anesthetic drip.
The most common causes of convulsive status epilepticus include medication changes or noncompliance in patients with known epilepsy, substance use, metabolic derangements, and acute brain injury from infectious