Pediatric Seizures (2025)

by Neema Francis, Faiz Ahmad, Thiagarajan Jaiganesh

You Have A New Patient!

A 5-year-old female was brought into the ED as her parents noticed that she was not very responsive. She was diagnosed with otitis media 3 days ago and has been taking oral amoxicillin for it. This morning, she became irritable and was less active than usual. On arrival at the ED triage, the patient was tachypneic (40 bpm), tachycardic (145 bpm), and had a temperature of 39.4°C.

The image was produced by using ideogram 2.0.

The child did not respond to vocal stimuli but was opening her eyes spontaneously. She had a sluggish pupillary response to light, and she seemed unaware of her surroundings. Suddenly, the patient began seizing, with her eyes up-rolled and her hands clenched and stretched downwards.

What Do You Need To Know?

Importance

Pediatric seizures are a significant health concern due to their high incidence, diagnostic complexity, diverse causes, and potential for severe consequences. Seizures are among the most common neurological disorders in children, with approximately 4–10% experiencing at least one seizure by age 16 [1,2]. The incidence is highest in the first year of life and remains substantial throughout childhood, particularly in children under three years old [3]. Seizures can result from various causes, including fever, infections, genetic disorders, head injuries, metabolic disturbances, and structural CNS abnormalities, which often complicates diagnosis and treatment [3,4]. Prolonged seizures, such as status epilepticus lasting five minutes or more, can lead to lactic acidosis, neuronal injury, network alterations, or even neuronal death, particularly when lasting beyond 30 minutes [3]. These severe outcomes impact development, quality of life, and increase the risk of comorbidities such as intellectual disability, depression, and anxiety. Children with epilepsy face a 5–10 times higher mortality risk compared to their peers and are prone to medical complications and long-term educational and social challenges [3,5]. The condition places a significant burden on healthcare systems and induces considerable psychological stress on children and their families [6,7]. 

Epidemiology

Seizures affect up to 10% of children, with incidence rates ranging from 33.3 to 82 cases per 100,000 annually, peaking in the first year of life and declining during adolescence [6,8]. Most (94%) of children presenting to the emergency department (ED) with a first seizure are under 6 years of age [4]. Febrile seizures, the most common type in young children, affect 3–4% of all children, primarily those under five years old [5,6]. Neonatal seizures, with distinct characteristics due to brain immaturity, are a common neurological condition in newborns [9]. Key risk factors include a family history of seizures, fever, CNS infections (e.g., meningitis, viral infections), head injuries, pre-existing neurological conditions, and maternal factors such as alcohol use, smoking, and prenatal exposures [3,7].

Seizures can be symptomatic or idiopathic. Acute symptomatic seizures arise from recent events, while remote symptomatic seizures result from chronic conditions. Generalized tonic-clonic seizures are the most frequent type [4], while status epilepticus (SE), a critical condition, is often triggered by fever or CNS infections in children [3]. Genetic factors, metabolic disorders, electrolyte imbalances, and structural brain abnormalities are recognized as key causes [6]. Mortality in pediatric epilepsy is 2–4 times higher than the general population and significantly elevated in children with neurological comorbidities, with sudden unexpected death in epilepsy (SUDEP) as a leading cause [3]. Febrile seizures are often benign, but complex febrile seizures may increase the risk of future epilepsy [2,6]. 

Pathophysiology

The pathophysiology of pediatric seizures involves complex interactions of neuronal excitation and inhibition in the brain, influenced by age, developmental stage, and underlying conditions [9]. Seizures arise from abnormal, excessive, and synchronous neuronal activity, leading to transient signs and symptoms such as involuntary muscle activity [3,9]. This activity stems from an imbalance between excitatory and inhibitory neurotransmission.

Basic Mechanisms of Seizures

The primary mechanism behind seizures involves either a deficit in neuronal inhibition or an excess of excitatory stimuli. The inhibitory neurotransmitter gamma-aminobutyric acid (GABA) plays a crucial role. In mature brains, GABA inhibits neuronal firing, maintaining balance in the central nervous system [3]. However, in neonatal brains, the immature GABA system can paradoxically cause excitation, making neonates more susceptible to seizures [9]. Additionally, alterations in GABA function, such as receptor dysfunction, can lead to prolonged and high-intensity neuronal stimulation, further increasing excitability. Voltage-gated ion channels and excitatory neurotransmitters like glutamate also contribute to seizure generation. Glutamate receptors, such as NMDA and AMPA, are primary excitatory receptors in the CNS and are involved in seizure propagation.

Age-Related Factors and Neuronal Imbalance

The immature state of the neonatal brain predisposes it to seizures due to developmental differences. In early life, the formation of excitatory synapses occurs before the development of inhibitory synapses, contributing to an imbalance in neuronal activity [7,9]. Additionally, the GABA receptor in neonates can cause depolarization rather than hyperpolarization, further enhancing neuronal excitability. Ion channel imbalances, especially the premature maturation of channels involved in depolarization, exacerbate this vulnerability [7].

Specific Factors Contributing to Seizures

Several specific factors influence seizure pathophysiology:

  1. Genetic Factors: Mutations in genes regulating synapse development, ion transport, protein phosphorylation, and gene transcription can disrupt neuronal activity [7].
  2. Metabolic Disturbances: Conditions like hypoglycemia, hypocalcemia, hyponatremia, and other metabolic imbalances impair neuronal function, triggering seizures [2,3].
  3. Hypoxic Conditions: Perinatal asphyxia and hypoxic-ischemic encephalopathy damage brain cells, increasing seizure risk [2,6,7].
  4. Infections: CNS infections such as meningitis and encephalitis disrupt normal brain function, leading to seizures [2,4,10].
  5. Structural Abnormalities: Malformations of cortical development and acquired lesions alter neuronal networks, predisposing to seizures [2,9].
  6. Fever: Although the exact mechanism is unclear, fever lowers the seizure threshold in some children, particularly those prone to febrile seizures [2]. In febrile seizures, inflammatory mediators such as IL-1 have been shown to increase neuronal stimulation. Animal models and preliminary studies suggest that these mediators play a role in seizure pathophysiology, although the clinical significance remains under investigation.

Medical History

A detailed history is crucial for accurately diagnosing and managing seizures in children. The history should focus on the events immediately preceding the seizure, the seizure itself, and the period following the seizure. It is important to obtain information from the child (when possible) and any witnesses [2]. When taking a medical history for pediatric seizures in the emergency department, it is important to gather information about the following key features [2,3,7-9,11,12]:

1. History of Present Illness:

  • Onset and duration of seizures: This information helps determine the type and underlying cause of the seizure. Note how the event began, including any preceding aura. An aura is a subjective sensation or experience that may precede a seizure [2,9].
  • Precipitating factors: Certain triggers, such as sleep deprivation, fever, trauma, or stress, can increase the likelihood of seizures in some children [2,4,7].
  • Description of the seizure: A detailed description of the seizure (e.g., focal or generalized) is crucial, including the child’s behavior, movements, and any changes in consciousness. Any evidence of partial (focal) onset, such as twitching or jerking on one side of the body, should also be noted [2]. It is also important to note if the child experienced incontinence during the seizure. It’s important to gather information about the postictal period including the length of the period, and any focal neurologic deficits, such as weakness or confusion, that may be present after the seizure. Also important is whether the child was able to easily fall back asleep after the seizure.
  • Current symptoms and vital signs: Assess the child’s current symptoms, vital signs, and whether they have recovered from the seizure or not.

2. Past Medical History:

  • Developmental and medical history: Information about the child’s developmental milestones and any previous medical conditions or treatments is important in identifying potential causes of seizures [6].
  • Immunization status: Some seizures are related to diseases that are preventable by vaccination, so it’s important to inquire about the child’s immunization history.
  • Previous seizures: This may indicate an underlying neurological condition or epilepsy. 
  • Previous treatment for seizures: Determine whether the child has received prior treatment for seizures, including medications, and if these treatments were effective [2].

3. Medication History:

  • Assess whether the child is taking any medications that can lower the seizure threshold or exacerbate seizures.

4. Family History:

  • A family history of seizures or other neurological disorders may suggest a genetic predisposition.

It is important to note that seizures may sometimes occur without a clear cause. The emergency department’s priority is stabilizing the patient and preventing further seizures or complications.

Several risk factors for pediatric seizures should be considered during medical history-taking. There may be a higher likelihood of seizures occurring in children who have a familial history of seizures or epilepsy. Children born prematurely or with a low birth weight may be at an increased risk of seizures because they are more likely to have brain injuries or developmental problems. Children with neurological disorders, such as cerebral palsy, or brain injuries, such as traumatic brain injury, may also be at an increased risk of seizures because these conditions can cause abnormal electrical activity in the brain. Metabolic disorders, such as hypoglycemia or hyponatremia, are also known risk factors. Certain infections, such as meningitis or encephalitis, can cause inflammation in the brain and are thus predisposing factors for pediatric seizures. Developmental disorders, such as autism or intellectual disability, have also been identified as risk factors for pediatric seizures. Having one or more of these risk factors does not necessarily mean that a child will develop seizures, but it is essential to be aware of them to detect seizures early and initiate appropriate treatment.

As with all medical emergencies, it is important to look out for red flags. Concerns should be raised if the seizure was delayed or related to a head injury. Developmental delay or regression should be ruled out. Bleeding disorders or anticoagulation therapy are important considerations during history-taking in cases of pediatric seizures. It is also critical to rule out CNS infections as a possible cause of the seizure. Red flags in the history may include fever, headache, photophobia, vomiting, bulging fontanelles, neck stiffness, decreased consciousness, and focal neurologic symptoms.

Physical Examination

A thorough physical examination is essential when evaluating a child with a suspected seizure. It aids in identifying underlying causes, associated conditions, and guiding further diagnostic and treatment decisions. The examination should be performed in conjunction with a detailed history and adapted to the child’s clinical condition and developmental stage [7,12]. Children with seizures may have developmental delays or regression, which can indicate an underlying problem.

Initial Assessment

  1. Stabilization: If the child is actively seizing, focus on stabilizing the airway, breathing, and circulation (ABC) and stopping the seizure [2,10,12].
  2. Vital Signs [2,5,7]:
    • Temperature: Identify fever (above 38°C/100.4°F), the most common cause of seizures in children.
    • Heart Rate and Blood Pressure: Monitor for abnormalities that may indicate underlying conditions or complications.
    • Oxygen Saturation: Ensure adequate oxygenation.

General Appearance

  1. Level of Consciousness: Assess alertness and orientation. Note any altered mental status, which may suggest ongoing issues like status epilepticus or other underlying conditions [4,10].
  2. Activity Level and Responsiveness: Observe for irritability, excessive sleepiness, or signs of distress. Are they irritable? Are they playful? Are they well-kept? Look for signs of neglect or child abuse.
  3. Dysmorphic Features: Look for unusual physical features that may suggest a genetic or developmental syndrome [2].

Head and Neck Examination

  1. Head Circumference: Measure head size, especially in infants, as microcephaly can indicate an underlying condition [2,6].
  2. Signs of Trauma: Check for bruising or swelling that may suggest head injury.
  3. Fontanelles: In infants, examine the anterior fontanelle for bulging, which may indicate increased intracranial pressure.
  4. VP Shunt: Assess for ventriculoperitoneal (VP) shunt placement and any signs of malfunction or infection [2].
  5. Meningeal Signs: Look for nuchal rigidity or other signs of meningeal irritation, suggesting CNS infection [12].
  6. Eye and ear examination: Changes in pupils, papilledema, and retinal hemorrhages, or abnormal movements of the eyes that can indicate brain injury. Bulging tympanic membranes can indicate otitis media.

Skin Examination

  1. Bruising: Identify unexplained bruising, which may point to bleeding disorders or child abuse.
  2. Skin Rashes: Look for signs such as café au lait spots (indicative of neurofibromatosis), adenoma sebaceum or ash leaf spots (associated with tuberous sclerosis) [6], and port wine stains (typical of Sturge-Weber syndrome).
  3. Neurocutaneous Markers: Use a Woods lamp to detect signs of neurocutaneous syndromes.

Cardiovascular and Abdominal Examination

  1. Heart Sounds: Listen for abnormalities that may indicate a cardiac issue. Heart murmurs or arrhythmias that may be related to seizures.
  2. Abdomen: Palpate for masses or organomegaly, which may suggest a metabolic disorder. Children with metabolic disorders, such as liver or kidney disease, may have an enlarged liver or spleen, which can contribute to seizures.

Neurological Examination [2,4,12]

  1. Mental Status: Evaluate consciousness, orientation, and behavior.
  2. Cranial Nerves: Check pupillary responses, eye movements, and facial symmetry.
  3. Motor Function: Assess muscle strength, tone, symmetry, and any abnormal movements. Look for Todd’s paresis or focal weakness post-seizure.
  4. Reflexes: Evaluate deep tendon reflexes, noting asymmetry.
  5. Meningeal signs: Brudzinski’s or Kernig’s sign. Neck stiffness should also be assessed.
  6. Sensory Function: Test sensory responses, noting any deficits.
  7. Gait and Coordination: Observe gait, coordination, and balance in age-appropriate children.

Postictal Examination [6]

  1. Neurological Status: Note persistent confusion, weakness, or other deficits during the postictal phase, which may help localize the seizure origin.
  2. Symmetry: Pay close attention to symmetrical muscle tone, reflexes, and movements to identify potential focal brain issues.

Important Considerations

  1. Age-Appropriate Assessment: Adjust the neurological exam based on the child’s developmental stage, as young children may not fully cooperate [6].
  2. Clinical Context: Always interpret findings within the context of the child’s history and other clinical information [12].

Alternative Diagnoses

It is important to distinguish between true seizures and seizure mimics in the pediatric population, as the causes, treatment options, and outcomes can be quite different [14,15]. Examples of seizure mimics include vasovagal syncope, breath-holding spells, reflex anoxic seizures, arrhythmias, and non-epileptic paroxysmal events. It is helpful to look for clues in the history to rule out such mimics. A vagal reflex can be precipitated by a sudden fright or minor trauma. Temper tantrums should prompt consideration of breath-holding spells, which can lead to hypoxia and, in turn, a short tonic-clonic event with a quick recovery time. Visual and auditory changes paired with lightheadedness are suggestive of a vasovagal attack. A history of palpitations or strenuous exercise just before the event could indicate arrhythmias.

Certain symptoms can indicate a genuine seizure [14,15], including but not limited to:

  • Biting of the tongue on one side (high specificity).
  • Swift blinking of the eyes.
  • Fixed gaze with dilated pupils.
  • Repetitive lip movements.
  • Elevated heart rate and blood pressure during the episode.
  • A post-seizure phase.

Fevers are the most common cause of seizures in children [16]. Febrile convulsions can be further categorized into simple or complex febrile seizures:

  • Simple febrile seizures are generalized, last less than 15 minutes, and occur only once within a 24-hour timeframe. They are typically not associated with neurological deficits or other significant findings.
  • Complex febrile seizures last longer than 15 minutes, are focal (involving only one part of the body), or occur multiple times within a 24-hour period. While both types of febrile seizures are generally benign, complex febrile seizures require further investigation to rule out organic causes and carry a slightly higher risk of developing into epilepsy or other neurological disorders later in life.

In an afebrile child presenting with seizures, the differential diagnoses are extensive. Possible causes include:

  • Structural abnormalities in the brain, such as tumors, cysts, or malformations [16].
  • Metabolic disturbances, such as hypoglycemia, electrolyte imbalances, or trauma.

Status epilepticus is a medical emergency, defined as a seizure lasting longer than 5 minutes or recurrent seizures without regaining consciousness in between [16]. It can occur in both children and neonates and is associated with significant morbidity and mortality. Non-convulsive status epilepticus should be considered in any child with an altered mental status; it is ill-defined and remains a diagnosis of exclusion.

Neonatal seizures can be caused by a variety of factors, including hypoxic-ischemic encephalopathy, metabolic disturbances, infections, and intracranial hemorrhage [16]. Neonatal seizures can have serious consequences if left untreated, including brain damage and developmental delays.

Acing Diagnostic Testing

A bedside blood glucose level should be obtained as soon as possible to rule out hypoglycemia [4,15,17]. Venous blood gas, magnesium, and phosphorus levels are also valuable investigations to assess other electrolyte imbalances [12]. When there is concern for metabolic or respiratory disturbance, an arterial blood gas test may be considered [10]. Basic laboratory tests, including CBC, CRP, urine and blood cultures, are indicated when there is suspicion of underlying infections [2,4]. Beta HCG levels may be measured in pediatric seizures because a rare cause of seizures in children is a brain tumor called a germinoma, which secretes beta HCG. Beta HCG can be detected in blood or cerebrospinal fluid (CSF) to help confirm the diagnosis. Ammonia, Lactate, Pyruvate, if an inborn error of metabolism is suspected, these tests may be performed [2]. Antiepileptic drug  levels should be measured in children with known seizure disorders to ensure they are receiving an appropriate dose. Under-dosing can result in continued seizures, while overdosing can lead to side effects such as drowsiness, nausea, or confusion. A toxicology screen may be ordered if there is a concern for drug or alcohol use [12].

Imaging studies such as CT or MRI should be considered for children with focal seizures, persistent seizures despite acute management, or seizures in children under six months of age [4,6]. Signs of elevated intracranial pressure (ICP) also warrant imaging, especially in the context of a history of bleeding disorders or anticoagulant use. Although MRI provides superior anatomic detail, it often requires sedation, which can interfere with the patient’s assessment, making CT the preferred initial imaging study.

Lumbar puncture is recommended for infants aged 6 to 12 months who have not received adequate vaccination against H. influenzae or Streptococcus pneumoniae, or whose vaccination status is unknown, as these bacteria are common causes of bacterial meningitis in this age group [6]. Additionally, lumbar puncture should be considered in infants receiving active antibiotic therapy, as antibiotics can mask meningeal signs. Infants with focal or prolonged seizures, abnormal neurological examinations, or toxic appearance are high-risk groups in which lumbar puncture is strongly advised.

 

An electroencephalogram (EEG) is a non-invasive test that measures electrical activity in the brain and is crucial for identifying seizure activity and epileptiform discharges [5,6,18]. It aids in classifying seizure disorders, such as generalized or partial seizures, and can detect specific patterns associated with particular epilepsy syndromes [18]. Ideally, an EEG should be performed within 24 hours of the seizure to maximize its diagnostic utility [6].

Risk Stratification

The range of potential causes for non-febrile seizures in pediatric patients is broad, including metabolic imbalances, mass lesions, and non-accidental trauma. One specific diagnosis that is relatively common in children under 6 months of age and easily detectable to prevent extensive invasive testing is hyponatremia caused by formula over-dilution. In the emergency department, 3 ml/kg of 3% hypertonic saline is the mainstay of therapy.

A first febrile seizure is concerning and requires prompt evaluation and management [16]. It may be a sign of an underlying medical condition. Some factors increase the risk of bacterial infection, such as age less than 6 months or more than 60 months with the first febrile seizure, or age less than 12 months with incomplete or unknown immunization history. In addition, a first febrile seizure in a clinically unwell child with symptoms of infection, meningeal signs, or dehydration may indicate a more serious underlying condition and requires urgent medical attention.

Febrile status epilepticus, which is a prolonged seizure lasting more than 30 minutes or a series of seizures without full recovery between them, is another potential complication that can occur in the context of a febrile illness. It is important to recognize the signs and symptoms of febrile status epilepticus, such as a fever, stiff neck, or convulsions, and seek immediate medical attention to prevent serious neurological damage.

Management

The management of pediatric seizures in the emergency department primarily focuses on stabilizing the patient, treating the underlying cause, and preventing further seizures or complications [16,19]. The initial management of an actively seizing child includes ensuring that the child’s airway is protected and providing adequate oxygen and circulatory support. Oxygen can be supplied via a nasal cannula or simple face mask, and preparations for endotracheal intubation should be made if airway management requires escalation. The next step is to assess vital signs and check blood glucose levels to rule out hypoglycemia. Intravenous (IV) or intraosseous (IO) access should be established promptly, and the patient should be connected to a monitor by this stage. In febrile seizures, antipyretic therapy is the mainstay of treatment to relieve symptoms and is usually sufficient. Seizures lasting 15 minutes or longer should be managed in accordance with status epilepticus protocols, with the goal of rapidly stopping the seizure using antiepileptic medications to prevent permanent neuronal injury.

A seizure lasting 5 minutes is highly likely to be prolonged; thus, most protocols use a 5-minute definition. Initial management includes maintaining airway, breathing, and circulation (ABCs), administering oxygen, and preparing for intubation if required [16,19]. Hypoglycemia, defined as a capillary blood glucose (CBG) level of less than 60 mg%, should be corrected with a bolus of IV 10% dextrose at 5 mL/kg; this can be repeated to normalize serum glucose levels. IV or IO access should be secured, and blood samples should be sent for investigations. Benzodiazepines are the first-line antiepileptic agents. Options include intramuscular (IM) Midazolam (10 mg for patients >40 kg; 5 mg for patients 13–40 kg), IV Lorazepam (0.1 mg/kg/dose, maximum 4 mg/dose; can be repeated once), or IV Diazepam (0.15–0.2 mg/kg/dose, maximum 10 mg/dose; can be repeated once). If these are not feasible, IV Phenobarbital (15 mg/kg/dose as a single dose), rectal Diazepam (0.2–0.5 mg/kg, maximum 10 mg/dose; can be repeated once), or intranasal/buccal Midazolam may be used.

If first-line therapy is unsuccessful, second-line agents should be administered. Options include IV Fosphenytoin (20 mg PE/kg, maximum 1,500 mg PE/dose as a single dose), IV Valproic Acid (40 mg/kg, maximum 3,000 mg/dose as a single dose), or IV Levetiracetam (60 mg/kg, maximum 4,500 mg/dose as a single dose). IV Phenobarbital (15 mg/kg as a single dose) is another option if other agents are not appropriate. If first- and second-line therapies fail, anesthetic doses of Thiopental, Midazolam, Phenobarbital, or Propofol can be administered. This requires continuous EEG monitoring.

If the patient responds to any of these agents and returns to baseline, symptomatic medical therapy should be initiated. Management of non-convulsive status epilepticus follows a similar approach to that of convulsive status epilepticus. (Figure 1) [20]

Figure 1 - Interventions and management of SE in the ED and inpatient setting [2]. (SEHA pediatric seizure algorithm. Permission granted by Dr. Thiagarajan Jaiganesh)

In neonates, the same stabilization principles apply, including maintaining ABCs, collecting blood samples, and checking and correcting electrolytes [16]. IV Phenobarbitone (20 mg/kg) is administered as the first-line antiepileptic; this can be repeated in 5 mg/kg boluses every 15 minutes (maximum dose of 40 mg/kg) until the seizure is aborted. If the seizure persists, IV Phenytoin (15–20 mg/kg), diluted in equal parts with normal saline, should be administered at a maximum rate of 1 mg/kg/min over 35–40 minutes.

If the seizure remains unresolved, IV Lorazepam (0.05–0.1 mg/kg) or Diazepam (0.25 mg/kg bolus or 0.5 mg/kg rectal) may be used. Alternatively, IV Midazolam can be administered as a continuous infusion; this involves an initial IV bolus of 0.15 mg/kg followed by a continuous infusion starting at 1 μg/kg/min, increasing by 0.5–1 μg/kg/min every 2 minutes (maximum 18 μg/kg/min). Lastly, if all else fails, 100 mg IV or oral Pyridoxine may be administered. This is particularly useful for treating Pyridoxine-dependent neonatal seizures or seizures caused by Isoniazid (INH) toxicity. (Figure 2) [21].

Figure 2 - Neonatal seizure algorithm [21] - Open access https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8857130/figure/Fig2/

When To Admit This Patient

In most cases, hospitalization is not necessary after a first unprovoked seizure, provided that a neurological examination is normal and prompt follow-up evaluation can be arranged [13]. Consultation with a neurologist and electroencephalography (EEG) can typically be performed on an outpatient basis. However, children who have experienced a prolonged seizure or who do not return to their baseline state within a few hours should be admitted to the hospital.

Hospitalization should also be considered in cases of extreme parental anxiety or if adequate follow-up evaluation cannot be arranged. It is essential to counsel parents about the increased likelihood of recurrence, which is approximately 33% overall. The risk of recurrence is higher in children under 18 months of age, when the temperature during the first convulsion is below 40°C, when the first seizure occurs within an hour of the onset of fever, or if there is a family history of febrile seizures.

Revisiting Your Patient

The image was produced by using ideogram 2.0.

Our patient was immediately moved to the resuscitation unit, placed on a simple face mask, and connected to monitors. She was administered rectal Diazepam; however, the seizure did not resolve. By this time, intraosseous (IO) access was established, and 0.1 mg/kg of Lorazepam (same as the IV dose) was given. This successfully aborted the seizure.

At this point, her vitals were as follows: temperature (T) 40°C, heart rate (HR) 93, respiratory rate (RR) 29, and blood pressure (BP) 118/90. She was lethargic and responsive only to painful stimuli. Other notable findings on examination included a full and tense anterior fontanelle, questionable neck rigidity, red and bulging tympanic membranes, reactive but unfocused pupils, a normal heart, lungs, and abdomen, good color and perfusion, and no petechiae or rashes. The patient displayed weak movement in all limbs and hyperactive deep tendon reflexes.

Pediatrics was consulted, and a presumptive diagnosis of meningitis was made. A complete blood count (CBC), C-reactive protein (CRP), blood culture, and chemistry panel were drawn. IV access was established at this point. Since increased intracranial pressure (ICP) was suspected, a lumbar puncture (LP) was initially deferred, and she was immediately given 500 mg of IV Ceftriaxone. A stat CT scan of the brain was normal, so an LP was performed, revealing visibly turbid cerebrospinal fluid (CSF).

The CSF analysis showed a white blood cell (WBC) count greater than 1000 cells/μL, with 95% neutrophils and 5% monocytes, a total protein level of 75 mg/dL, and a glucose level of 25 mg/dL. A Gram stain of the CSF revealed numerous WBCs and a few gram-positive cocci. She was admitted to the pediatric intensive care unit (PICU) for further management.

Authors

Picture of Neema Francis

Neema Francis

Dr. Neema Francis was born and raised in Dubai, UAE. She is currently a fourth-year emergency medicine resident at Tawam Hospital. She graduated with an MBBS from Gulf Medical University in 2020 and completed her internship at Sheikh Shakbout Medical City in 2021. Dr. Francis has a passion for volunteering and has been involved in various healthcare initiatives. She is also a competent researcher with publications to her name and a keen interest in emergency medicine and pediatric emergency medicine.

Picture of Faiz Ahmad

Faiz Ahmad

Picture of Thiagarajan Jaiganesh

Thiagarajan Jaiganesh

Dr. Jaiganesh is a Chairman and Consultant in Adult and Pediatric Emergency Medicine and serves as an Adjunct Assistant Professor at UAE University. As the former Director of the Emergency Medicine Residency Program at Tawam Hospital in Al Ain, UAE, Dr. Jaiganesh is dedicated to training the next generation of emergency medicine professionals. With a strong academic and professional background, Dr. Jaiganesh has published numerous peer-reviewed articles on emergency medicine and contributes as a Section Editor and Chapter Author for notable medical texts, including the Oxford Handbook for Medical School. A sought-after speaker, Dr. Jaiganesh has been invited to present at numerous national and international conferences and serves as an instructor in various life support courses. Additionally, Dr. Jaiganesh is an expert in medico-legal and clinical negligence matters, providing valuable insights into complex legal and ethical cases in healthcare.

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  20. Al-Hashaykeh NO, et al. Pediatric Status Epilepticus Clinical Practice Guideline. SEHA Pediatric Critical Care Council; 2023.
  21. Vegda H, Krishnan V, Variane G, Bagayi V, Ivain P, Pressler RM. Neonatal seizures—perspective in low-and middle-income countries. Indian J Pediatr. 2022;89(3):245-253. doi:10.1007/s12098-021-04039-2.

Reviewed and Edited By

Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

Arif Alper Cevik, MD, FEMAT, FIFEM

Prof Cevik is an Emergency Medicine academician at United Arab Emirates University, interested in international emergency medicine, emergency medicine education, medical education, point of care ultrasound and trauma. He is the founder and director of the International Emergency Medicine Education Project – iem-student.org, chair of the International Federation for Emergency Medicine (IFEM) core curriculum and education committee and board member of the Asian Society for Emergency Medicine and Emirati Board of Emergency Medicine.

Epilepsy and Status Epilepticus (2024)

by Rand Redwan Al Sari & Imad Khojah

You have a new patient!

A 22-year-old woman is brought to the ER because of violent, jerky movements of her limbs that started 30 minutes ago. Her husband reports that the patient has a history of epilepsy. She is unresponsive. Her examination reveals tonic-clonic episodes and blood in her mouth. How would you manage this case? What are the initial steps you would take? What actions are needed to stop the seizure?

a-photo-of-a-22-year-old-female-patient-with-seizure (the image was produced by using ideogram 2.0)

What do you need to know?

Epidemiology and Importance

Epilepsy is one of the most common neurological diseases that can present to the emergency department [1]. It affects about 50 million people around the world, with an incidence of approximately 50.4 to 81.7 per 100,000 per year [1]. Epilepsy refers to having a lower seizure threshold than normal due to genetic, pathological, or unknown causes [2]. It is characterized by recurrent unprovoked seizures that present with motor, sensory, autonomic, or cognitive function alterations [2]. Previously diagnosed patients can present to the ED with breakthrough seizures due to factors like changes in the anti-seizure regimen or noncompliance with medication [2]. Other factors like sleep deprivation, stress, and flashing lights can also precipitate breakthrough seizures [2].

Prolonged or repetitive uncontrollable seizures are termed status epilepticus [2,3]. This emergency requires prompt treatment to prevent neuronal injury, severe disability, coma, or death [3]. The overall case fatality rates can reach up to 15% [2].

Pathophysiology

Neurons are normally stabilized by a balance between excitatory and inhibitory neurotransmitters [2]. A disruption of this balance leads to abnormal electrical discharge [2]. This discharge can propagate to nearby areas in the brain, which is evident clinically by the stepwise spread of the seizure (known as Jacksonian March) [2, 4]. Loss of consciousness in some cases is explained by the widespread involvement of large areas of the brain [2]. Many drugs used to restore this balance work by enhancing inhibitory activity through targeting GABAA subtype receptors [2]. Prolongation of the seizure leads to sequestration of GABAA receptors and upregulation of excitatory receptors; therefore, patients become unresponsive to medication [2, 5]. This explains the importance of timely treatment through early seizure control to prevent morbidity and mortality in patients with status epilepticus [2,3].

Medical History

A common scenario presenting to the ER is a patient complaining of a seizure-like episode with a sudden loss of consciousness and motor activity involvement [6]. However, various other presentations of seizures and other differential diagnoses with similar complaints should not be neglected. If the patient presents with status epilepticus, timely management, depending on the seizure type, is urgently needed (see management) [2].

Through history and examination, distinguishing a seizure from other acute medical conditions is important. An accurate diagnosis has crucial, direct consequences for activity restriction and therapy planning. Paying attention to features, especially at the onset, can help in identifying the seizure type for therapeutic implications and facilitate communication between physicians. Semiology at onset is important to classify seizures as focal, focal with impaired awareness (complex seizures), generalized, or unknown [7]. Further classification divides motor and non-motor seizures based on the descriptive assessment of the first symptom, which can vary widely according to the area of the brain affected [2].

The main aim of history-taking is to identify seizures from other similar conditions, classify them, identify triggers of new seizures, and detect a cause for a decreased seizure threshold in a patient previously diagnosed with epilepsy [8].

It is important for any patient with seizures to consider critical causes such as eclampsia, toxic ingestion, hypoglycemia, electrolyte imbalance, and increased intracranial pressure [9]. Emergent diagnoses, such as infection, acute brain injury, and serious mimics of seizure activity, must be identified and treated as soon as possible [2].

Initial history approach to a patient with suspected seizure [2] is a systematic evaluation, starting with the assessment of whether the event is likely to be a seizure, followed by differentiation of first-time versus recurrent seizures, and identifying factors that may trigger or reduce seizure thresholds [10].

Algorithmic Approach in Seizure History [2]

Determining Likelihood of a Seizure

The process begins by evaluating whether the event could be a seizure. Key indicators include:

  • Aura: A subjective sensation preceding the seizure.
  • Abrupt onset: Sudden occurrence of the event.
  • Non-suppressible limb shaking: Movements that are not voluntary or suppressible.
  • Postictal state: A transient neurological state after the event, characterized by confusion or fatigue.
  • History of epilepsy: Previous diagnosis or known history can strongly support the likelihood.

If these features are absent, the clinician is prompted to consider alternative diagnoses, such as:

  • Syncope (fainting),
  • Stroke,
  • Complex migraine, or
  • Non-epileptic spells, which may mimic seizures but lack neurological underpinnings.

Differentiating First-Time Seizures

If the event is determined to likely be a seizure, the next step is assessing whether it is the patient’s first seizure. For first-time events, the focus shifts to identifying potential triggers, including:

  • Medications: Use of or withdrawal from drugs that may lower the seizure threshold.
  • Exposures: Environmental or toxicological factors.
  • Immunosuppression: Conditions that may predispose to infections affecting the brain.
  • History of head trauma: A common precipitant for seizures.
  • Pregnancy: Associated risks like eclampsia.

Characterization of the Seizure

If it is not a first-time seizure, further characterization of the event is essential. Key aspects include:

  • Onset: Understanding preceding events to identify immediate triggers and auras.
  • Duration: Length of the seizure episode.
  • Awareness: Assessing the patient’s level of consciousness during the seizure.
  • Automatisms: Involuntary, purposeless movements that occur during the seizure and can be observed by others.
  • Postictal state: The presence of transient neurological deficits following the seizure (absent in some types, such as absence seizures).

The clinician also verifies whether the current event is consistent with the patient’s previous seizure patterns.

Exploring Factors Reducing the Seizure Threshold

For patients with recurrent seizures, it is crucial to evaluate factors that might decrease the seizure threshold, including:

  • Non-compliance or changes to anti-seizure drug (ASD) regimens.
  • Illness or trauma: Physical or psychological stressors.
  • Drug or alcohol use: Acute intoxication or withdrawal.
  • Catamenial exacerbations: Hormonal influences in menstruating individuals.
  • Pregnancy: Increased risk of seizures due to physiological changes or complications.
  • Sleep deprivation: A well-documented precipitant of seizures.

This step ensures that modifiable triggers or exacerbating factors are identified and addressed.

Physical Examination

Physical examination is crucial for identifying etiologies and directing the management plan. During an active seizure, pay close attention to posture, motor activity, eye deviation, and nystagmus, observing asymmetries and focal findings [11]. Check if the clonic activity is suppressible by applying gentle pressure. Unlike insuppressible seizures, suppression suggests a different diagnosis, such as nonepileptic spells or movement disorders. Check for mydriasis in the eyes, which is commonly found during seizures, but its persistence afterward can indicate toxic exposure [2].

Vital signs should be measured after seizure activity has ceased. They are of high importance and may direct the physician to possible causes (e.g., fever suggests meningoencephalitis, tachycardia and hypertension suggest toxic sympathomimetic exposure, while hypertension and bradycardia can indicate herniation syndromes) [2].

Moreover, a general examination should aim to search for both findings and sequelae of the seizures. Physical findings such as nuchal rigidity, stigmata of substance abuse, and lymphadenopathy may be present. Potential sequelae of seizures should also be assessed [12]. Evaluation of soft tissue and skeletal trauma is important, as injuries are common. Check for head trauma, tongue injury, shoulder dislocation, bone fractures, or aspiration [2].

Finally, a complete neurological examination should be performed. Immediately following the seizure, hyperreflexia, focal motor deficit (Todd’s paralysis), and extensor plantar response (positive Babinski) can occur and are expected to generally resolve within an hour [13]. If Todd’s paralysis does not resolve quickly, it raises the suspicion of a focal structural deficit that caused the seizure (e.g., stroke). The persistence of altered consciousness or signs of ongoing subtle seizures, such as automatisms, abnormal eye movements, and facial myoclonus, suggests the persistence of the seizure and must not be missed (nonconvulsive seizures and status epilepticus) [2].

Alternative Diagnoses

Although no single clinical finding or diagnostic modality is 100% confirmatory of the diagnosis of seizures [14, 15], understanding the circumstances of the event and the factors surrounding it can help rule out or confirm diagnoses with similar presentations [2].

Findings that make the diagnosis of seizures more probable include postictal disorientation and amnesia, cyanosis during the event, lateral tongue biting, non-suppressible limb shaking, and dystonic posturing [2, 15].

If the patient experienced diaphoresis, palpitations, nausea, and vomiting before the seizure, it may suggest transient cerebral ischemia due to arrhythmias [2].

The presence of motor activity, commonly including a tonic extension of the trunk or myoclonic jerks of the extremities associated with bradycardia, raises the suspicion of convulsive syncope [16]. Once cerebral perfusion is restored, convulsions stop without any postictal period [2].

The diagnosis of migraine can sometimes be misleading due to the presence of a preceding aura that might be confused with nonconvulsive seizures (e.g., the positive visual phenomenon in occipital seizures) [17]. Unlike occipital seizures, migraines have a peak preceded by gradual evolution and followed by gradual resolution. Moreover, patients typically have a positive history of migraines with a similar presentation [2].

Nonepileptic spells or psychogenic seizures mimic status epilepticus in their presentation [18]. Due to the prolonged duration of the spells (five minutes or more, and sometimes exceeding 20 minutes), patients commonly receive high doses of benzodiazepines and need to be monitored for any respiratory compromise. Findings consistent with this diagnosis include a stop-and-go pattern of the convulsions, horizontal head shaking, forward pelvic thrusting, asynchronous bilateral convulsions with eyes closed, a short postictal period despite the long duration of spells, avoidance of noxious stimuli, and preserved recollection of events. Furthermore, laboratory testing lacks reactive leukocytosis and lactic acidosis, which are present in nearly all cases of prolonged generalized convulsive seizures or status epilepticus [2, 19].

Acing Diagnostic Testing

Due to the challenges of diagnosing a seizure, seeking diagnostic testing is of high value. Laboratory studies, radiology, and other special procedures frequently provide important elements in patient assessment [20]. Although some cases require extensive metabolic testing, it is not indicated for cases with an unremarkable history and normal examination findings. Serum glucose levels should be measured in all cases, as hypoglycemia is a common cause of provoked seizures [21]. It is also important to note that hypoglycemia could result from prolonged seizures. If correcting the glucose level does not stop a seizure, an alternate diagnosis should be evaluated. Lactic acid and creatinine kinase should also be measured in cases of prolonged seizures to assess for acute metabolic acidosis and rhabdomyolysis, respectively [22]. A low level of lactic acid during a prolonged convulsive episode makes a seizure less likely (nonepileptic convulsions) [2].

On the other hand, the presence of advanced age, comorbidities, abnormal examination findings, or an ill appearance demands comprehensive metabolic testing. Such testing includes serum glucose, creatinine kinase, lactic acid, electrolytes, complete blood count, urea nitrogen, creatinine, AST, ALT, anti-seizure drug levels, pregnancy tests, and drug-of-abuse screening. Checking for electrolyte derangements is important, as these can trigger seizures (e.g., hyponatremia, hypocalcemia, and hypomagnesemia) [23]. Patients with a low bicarbonate level should undergo blood gas analysis. An anion gap metabolic acidosis resulting from lactic acidosis is expected to decline within the first hour after the convulsive seizure stops unless another cause is present. Liver enzymes are tested to check for liver-mediated metabolic abnormalities that can impact therapeutic decisions [2].

Furthermore, patients on antiseizure medication should have their levels checked to confirm compliance. Some drugs are known to be epileptogenic, and it may be necessary to test their levels as well. Drug-of-abuse screening can also be considered in patients presenting with first-time seizures, despite the fact that such testing cannot prove causation or change outcomes [2, 24].

Urgent neuroimaging is indicated for most cases of a first-time seizure, whereas patients with epilepsy who have returned to baseline do not require one. Prompt neuroimaging and CT consideration in the ER is indicated for patients with coma, focal neurological deficits, immunocompromised states, advanced age, anticoagulation use, malignancy, previous intracranial hemorrhage, severe thunderclap headache, status epilepticus, neurocutaneous syndromes, or suspected trauma [25]. Computed tomography (CT) is widely available, but MRI and CT perfusion can provide additional information. If an infection is suspected, lumbar puncture is indicated [2].

Electroencephalography (EEG) is useful for diagnosing nonconvulsive seizures, epilepsy, nonepileptic spells, and status epilepticus [26]. EEG can guide therapy and monitor the treatment of refractory cases. Although it is not cost-effective, it is a high-yield modality for cases with an unclear diagnosis [2].

Lastly, ECG monitoring might benefit patients with preceding or ongoing cardiac symptoms. It can provide early clues in cases of drug toxicity and help understand the etiology of the seizure [2, 27].

Risk Stratification

The presentation and findings of a seizure case can provide clues as to whether this case has any red flags that demand urgent care. History and examination findings such as immunocompromisation, the presence of a thunderclap headache, sudden neurological deficit, status epilepticus presentation, head trauma, persistent altered consciousness, and concurrent infection can indicate a worse outcome [10]. Such patients require extensive investigations and prompt treatment to minimize morbidity and mortality due to the cause of the seizure or as a consequence of the seizures themselves [28]. Critical care for these patient groups is essential to reduce complications such as infection-related issues, irreversible intracranial structural disease, refractory status epilepticus, hemodynamic compromise, and death [2].

The risks of experiencing a secondary seizure following the current presentation may change the management plan to include secondary seizure prophylaxis. Risk stratification, weighing the chances of recurrence (higher in patients with previous brain insult, abnormal EEG, brain imaging abnormalities, and the presence of nocturnal seizures) against the risks of adverse effects from antiseizure medication, should be conducted in collaboration with a consulting neurologist [2].

Management

The initial priorities in managing unstable patients are to recognize and treat hypoxia, hypotension, and hypoglycemia, and to initiate pharmacologic treatment when needed [2, 28, 29].

Initial stabilization of patients with active seizures presenting to the ER includes the following [2, 28, 29]:

  • Assess airway, breathing, and circulation: Do not use nasopharyngeal airway devices during the seizure, as they can cause injury and increase the risk of aspiration.
  • Pulse oximetry.
  • Electrocardiogram (ECG).
  • Finger stick: If the glucose level is less than 60 mg/dL, administer IV dextrose.
  • Aspiration precaution: Place the patient in the lateral decubitus position.
  • Abortive treatment: Administer if the seizure lasts more than 5 minutes or in the case of hemodynamic compromise.

First-line therapy [2, 28, 29]

The first-line pharmacological therapies for managing epilepsy, include three benzodiazepine agents: diazepam, lorazepam, and midazolam. These agents are commonly used for their rapid onset and efficacy in controlling seizures, especially status epilepticus. The table includes critical details on dosing, frequency, maximum permissible dose, pregnancy category, and specific cautions.

  1. Diazepam
  • Dose per kilogram: 0.15-0.2 mg/kg intravenously (IV).
  • Frequency: Administered every 5 minutes as needed.
  • Maximum Dose: Limited to 10 mg per individual dose and a cumulative total of 30 mg across all doses.
  • Pregnancy Category: D (indicating a potential risk to the fetus, but benefits may outweigh risks in life-threatening situations).
  • Cautions/Comments:
    • Continuous monitoring of respiration is essential due to the risk of respiratory depression, a common side effect of benzodiazepines.
  1. Lorazepam
  • Dose per kilogram: 0.1 mg/kg intravenously (IV).
  • Frequency: Administered every 5 minutes as necessary.
  • Maximum Dose: 4 mg per dose, with a cumulative maximum of 12 mg across all doses.
  • Pregnancy Category: D.
  • Cautions/Comments:
    • Similar to diazepam, respiratory monitoring is mandatory.
    • Intramuscular (IM) administration is contraindicated for lorazepam, likely due to inconsistent absorption or slower onset compared to IV administration.
  1. Midazolam
  • Dose per kilogram: 0.2 mg/kg, administered via multiple routes including IV, intramuscular (IM), or intranasal (IN).
  • Frequency: Doses can be repeated every 5 minutes as needed.
  • Maximum Dose: 10 mg per individual dose.
  • Pregnancy Category: D.
  • Cautions/Comments:
    • Respiratory monitoring is critical due to the sedative effects of midazolam.
    • The half-life of midazolam is approximately 7 hours, making it a relatively short-acting agent compared to others, which can influence its clinical use depending on seizure recurrence risk.

All three agents are effective for rapid seizure control but share common risks, including respiratory depression, necessitating vigilant monitoring, particularly in critical care or emergency settings. Their classification in pregnancy category D highlights the need for careful consideration of maternal and fetal risks versus benefits. Midazolam offers more flexibility in administration routes, making it a practical choice in situations where IV access is not readily available.

If the seizure stops, coordinate a disposition plan and consider non-convulsive status epilepticus in patients who do not return to baseline. However, if the seizure does not stop, ensure adequate dosing of first-line therapy, then proceed to second-line therapy, and finally to third-line therapy, one step at a time [2, 28, 29].

Second-line therapy [2, 28, 29]

The second-line treatment options for epilepsy, include on a variety of antiepileptic drugs. These agents are typically used when first-line benzodiazepines are insufficient to control seizures. The table details dosing, frequency, maximum permissible doses, pregnancy categories, and relevant cautions for clinical use.

  1. Levetiracetam
  • Dose per kilogram: 40-60 mg/kg administered intravenously (IV).
  • Frequency: Administered once over a 10-minute period.
  • Maximum Dose: 4500 mg.
  • Pregnancy Category: C (indicating that risks cannot be ruled out, but the drug may be used if benefits outweigh potential risks).
  • Cautions/Comments:
    • Requires renal clearance, so dose adjustments may be necessary in patients with renal impairment.
  1. Fosphenytoin
  • Dose per kilogram: 10-20 mg PE/kg (phenytoin equivalents) given IV or intramuscularly (IM).
  • Frequency: Additional 5 mg PE/kg can be administered after 10 minutes if needed.
  • Maximum Dose: 150 mg PE/kg.
  • Pregnancy Category: D (associated with risk but can be used in life-threatening situations).
  • Cautions/Comments:
    • Can cause hypotension and dysrhythmias, requiring cardiac monitoring during administration.
  1. Lacosamide
  • Dose per kilogram: 200-400 mg IV.
  • Frequency: An additional 5 mg/kg can be administered if necessary.
  • Maximum Dose: 250 mg.
  • Pregnancy Category: C.
  • Cautions/Comments:
    • Can cause arrhythmias.
    • Renal clearance is required, so adjustments are needed for patients with renal insufficiency.
  1. Phenobarbital
  • Dose per kilogram: 15-20 mg/kg IV.
  • Frequency: Additional 5-10 mg/kg can be given as needed.
  • Maximum Dose: Not explicitly mentioned but calculated based on repeated doses.
  • Pregnancy Category: D.
  • Cautions/Comments:
    • Monitor respiration closely due to the sedative and respiratory depressant effects.
    • A strong P450 enzyme inducer, which can affect the metabolism of other drugs.
  1. Phenytoin
  • Dose per kilogram: 15-20 mg/kg IV.
  • Frequency: Additional 5-10 mg/kg can be administered if necessary.
  • Maximum Dose: 30 mg/kg.
  • Pregnancy Category: D.
  • Cautions/Comments:
    • Risk of hypotension and dysrhythmias during administration, necessitating monitoring.
    • A strong P450 enzyme inducer, which impacts the metabolism of other medications.
  1. Valproic Acid
  • Dose per kilogram: 20-40 mg/kg IV.
  • Frequency: Additional doses of 20 mg/kg can be administered if necessary.
  • Maximum Dose: 3000 mg.
  • Pregnancy Category: D.
  • Cautions/Comments:
    • Strong P450 enzyme inducer.
    • May cause hepatotoxicity and platelet dysfunction, warranting caution in patients with liver disease or coagulopathy.

The second-line agents are reserved for scenarios where first-line therapy fails to achieve seizure control. Each agent has specific risks and monitoring requirements. For example:

  • Levetiracetam and lacosamide are generally well-tolerated but require dose adjustments in renal impairment.
  • Phenobarbital, phenytoin, and valproic acid necessitate respiratory and hepatic monitoring due to their systemic side effects.
  • Fosphenytoin and phenytoin require cardiac monitoring due to their potential to induce arrhythmias.

The choice of agent depends on the patient’s clinical status, underlying conditions, and the safety profile of the drug.

Third-line therapy [2, 28, 29]

The third-line therapy agents for managing refractory epilepsy, particularly in patients requiring intubation, mechanical ventilation, and hemodynamic support are administered in critical care settings to control seizures when first- and second-line therapies fail. Each drug is described with its dosing regimen, frequency, maximum dose, pregnancy category, and significant precautions.

  1. Ketamine
  • Dose per kilogram:
    • Loading dose: 1.5 mg/kg intravenously (IV).
    • Maintenance dose: 0.5 mg/kg every 3-5 minutes as needed.
  • Maximum Dose: Not explicitly stated, but administered as required to control seizures.
  • Pregnancy Category: N (Not classified).
  • Cautions/Comments:
    • Ketamine acts as an NMDA antagonist, a unique mechanism among anticonvulsants.
    • Hypotension is a potential side effect, necessitating blood pressure monitoring.
  1. Midazolam
  • Dose per kilogram:
    • Loading dose: 0.2 mg/kg IV.
    • Maintenance dose: 0.2-0.4 mg/kg every 3-5 minutes.
  • Maximum Dose: 2 mg/kg for the loading dose.
  • Pregnancy Category: D (Risk to the fetus exists, but use may be justified in emergencies).
  • Cautions/Comments:
    • Midazolam may cause hypotension and requires continuous hemodynamic monitoring.
  1. Pentobarbital
  • Dose per kilogram:
    • Loading dose: 5-15 mg/kg IV.
    • Additional doses of 5-10 mg/kg may be given if required.
  • Maximum Dose: 25 mg/kg for the loading dose.
  • Pregnancy Category: D.
  • Cautions/Comments:
    • Pentobarbital has a long half-life (22 hours), which makes it effective for sustained seizure control but may prolong sedation.
    • It carries significant risks, including hypotension, ileus, myocardial suppression, immunosuppression, and thrombocytopenia, requiring vigilant monitoring in an intensive care setting.
  1. Propofol Infusion
  • Dose per kilogram:
    • Loading dose: 1-2 mg/kg IV.
    • Maintenance dose: 0.5-2 mg/kg every 3-5 minutes as needed.
  • Maximum Dose: 10 mg/kg for the loading dose.
  • Pregnancy Category: B (Lower risk, but use must be cautious).
  • Cautions/Comments:
    • Propofol has a short half-life (0.6 hours), allowing for rapid onset and recovery.
    • Side effects include hypotension, respiratory depression, hypertriglyceridemia, pancreatitis, and the rare but potentially fatal propofol infusion syndrome. Close monitoring of triglycerides and cardiac function is necessary.

Third-line therapies are used in severe, refractory cases of epilepsy where intubation, ventilation, and hemodynamic support are required. These drugs induce deep sedation or anesthesia to suppress seizure activity effectively. Key considerations for their use include:

  • Ketamine: Offers a unique mechanism (NMDA antagonism), useful in resistant cases.
  • Midazolam and pentobarbital: Provide effective sedation but require careful respiratory and cardiovascular monitoring due to risks of hypotension and prolonged sedation.
  • Propofol: Its short duration of action allows for precise titration, but metabolic side effects and infusion syndrome necessitate caution.

The choice of agent depends on the clinical scenario, patient stability, and institutional protocols. These medications are used alongside comprehensive critical care support to manage complications and optimize outcomes.

Special Patient Groups

Certain notes are important to remember regarding special patient groups. In cases of seizures during pregnancy, considering the diagnosis of eclampsia is a high priority. Magnesium is the drug of choice for acute eclamptic seizures [30]. If a pregnant patient was previously diagnosed with epilepsy, a lower seizure threshold may result due to noncompliance, adjusted regimens, sleep deprivation, nausea and vomiting, or increased drug clearance. When managing status epilepticus, the risks to the fetus from the seizure are higher than the risks from the medication; therefore, manage the patient as you would a nonpregnant individual [31]. In the case of a new, non-eclamptic seizure, a workup is indicated as previously mentioned [2].

When To Admit This Patient

The decision to admit or discharge should be individualized based on the underlying illness, recurrence risk, and need for maintenance pharmacotherapy [32]. Admission for observation alongside neurological consultation should be considered for patients with an uncertain diagnosis, a history of neurological disease or other comorbidities, or in situations where follow-up is unlikely. In contrast, patients can be discharged home with early referral to a neurologist if they have normal examination findings, no significant comorbidities, no known structural brain disease, did not require more than a single dose of benzodiazepines, and are expected to comply with follow-up instructions [2].

Discharge instructions should include guidance on car driving, potentially dangerous activities (e.g., swimming, cycling, climbing ladders), and information regarding any needed follow-up [2, 33].

Revisiting Your Patient

A 22-year-old woman with a previous history of epilepsy was brought to the ER due to generalized tonic-clonic insuppressible movements of her limbs that started 15 minutes ago.

You immediately assessed the airway, breathing, and circulation and placed the patient in the lateral decubitus position to prevent aspiration, as she had a tongue injury. Blood sugar was measured using a finger stick, ruling out hypoglycemia. Lorazepam was then administered as abortive treatment.

You began taking a history from her husband. They were having lunch together when his wife suddenly started seizing, and he was unable to stop it. She had not regained consciousness since then. He mentioned that she had been inconsistent with her antiepileptic medication because she wanted to get pregnant and had read online about potential harms of the medications on a growing baby.

Her lactic acid level was high, her pregnancy test was negative, and the rest of her laboratory findings were within normal limits.

The patient was diagnosed with status epilepticus, a medical emergency requiring urgent management. The ABC approach was performed to ensure the patient’s safety, followed by the administration of benzodiazepines. If first-line therapy fails, second- and third-line therapies should be administered sequentially. Inconsistency with antiepileptic medication highlights the need for patient education and further discussion regarding her concerns and available treatment options.

Authors

Picture of Rand Redwan Al Sari

Rand Redwan Al Sari

Dr Rand Al Sari is a dedicated General Physician practicing in Saudi Arabia. With a strong commitment to patient care, she is also actively engaged in medical research, staying at the forefront of healthcare advancements and integrating this knowledge into her clinical practice. Passionate about medical writing and journaling, Dr Al Sari reflects on her experiences to contribute meaningfully to the medical community, with a focus on evidence-based healthcare and improving patient outcomes.

Picture of Imad Khojah

Imad Khojah

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  16. Doležalová I, Brázdil M, Rektor I, Tyrlíková I, Kuba R. Syncope with atypical trunk convulsions in a patient with malignant arrhythmia. Epileptic Disord. 2013;15(2):171-174. doi:10.1684/epd.2013.0564
  17. Schulze-Bonhage A. Visuelle Aura: Differenzialdiagnose zwischen Migräne und Epilepsie [Differential diagnosis of visual aura in migraine and epilepsy]. Klin Monbl Augenheilkd. 2001;218(9):595-602. doi:10.1055/s-2001-17636
  18. Krebs PP. Psychogenic nonepileptic seizures. Am J Electroneurodiagnostic Technol. 2007;47(1):20-28.
  19. van Rooij FJ, Admiraal-van de Pas Y. Lactaatacidose in de postictale fase [Lactic acidosis in the postictal state]. Ned Tijdschr Geneeskd. 2015;159:A9068.
  20. Valeta, Thalia. (2017). Investigations for Epileptic Seizures. 10.1007/978-3-319-61679-7_14.
  21. Nuoffer JM, Mullis PE. Hypoglykämien–Diagnostik und Therapie im Notfall [Hypoglycaemia–diagnosis and therapy in emergencies]. Ther Umsch. 2005;62(8):543-548. doi:10.1024/0040-5930.62.8.543
  22. Nass RD, Sassen R, Elger CE, Surges R. The role of postictal laboratory blood analyses in the diagnosis and prognosis of seizures. Seizure. 2017;47:51-65. doi:10.1016/j.seizure.2017.02.013
  23. Castilla-Guerra L, del Carmen Fernández-Moreno M, López-Chozas JM, Fernández-Bolaños R. Electrolytes disturbances and seizures. Epilepsia. 2006;47(12):1990-1998. doi:10.1111/j.1528-1167.2006.00861.x
  24. Ng SK, Brust JC, Hauser WA, Susser M. Illicit drug use and the risk of new-onset seizures. Am J Epidemiol. 1990;132(1):47-57. doi:10.1093/oxfordjournals.aje.a115642
  25. Rittenberger JC. Early CT imaging of the brain – A guide to therapy. Resuscitation, 2014;85(10):1309-1310. doi: 10.1016/J.RESUSCITATION.2014.06.020
  26. Rosenow F, Klein KM, Hamer HM. Non-invasive EEG evaluation in epilepsy diagnosis. Expert Rev Neurother. 2015;15(4):425-444. doi:10.1586/14737175.2015.1025382
  27. Ufongene C, El Atrache R, Loddenkemper T, Meisel C. Electrocardiographic changes associated with epilepsy beyond heart rate and their utilization in future seizure detection and forecasting methods. Clin Neurophysiol. 2020;131(4):866-879. doi:10.1016/j.clinph.2020.01.007
  28. Bank AM, Bazil CW. Emergency Management of Epilepsy and Seizures. Semin Neurol. 2019;39(1):73-81. doi:10.1055/s-0038-1677008
  29. Huff JS, Morris DL, Kothari RU, Gibbs MA; Emergency Medicine Seizure Study Group. Emergency department management of patients with seizures: a multicenter study. Acad Emerg Med. 2001;8(6):622-628. doi:10.1111/j.1553-2712.2001.tb00175.x
  30. Keepanasseril A, Maurya DK, Manikandan K, Suriya J Y, Habeebullah S, Raghavan SS. Prophylactic magnesium sulphate in prevention of eclampsia in women with severe preeclampsia: randomised controlled trial (PIPES trial). J Obstet Gynaecol. 2018;38(3):305-309. doi:10.1080/01443615.2017.1351931
  31. Thomas SV. Management of epilepsy and pregnancy. J Postgrad Med. 2006;52(1):57-64.
  32. Agarwal P, Xi H, Jette N, et al. A nationally representative study on discharge against medical advice among those living with epilepsy. Seizure. 2021;84:84-90. doi:10.1016/j.seizure.2020.11.018
  33. Engel KG et al. Patient comprehension of emergency department care and instructions: Are patients aware of when they do not understand? Ann Emerg Med2009 Apr; 53:454.

Reviewed and Edited By

Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

Arif Alper Cevik, MD, FEMAT, FIFEM

Prof Cevik is an Emergency Medicine academician at United Arab Emirates University, interested in international emergency medicine, emergency medicine education, medical education, point of care ultrasound and trauma. He is the founder and director of the International Emergency Medicine Education Project – iem-student.org, chair of the International Federation for Emergency Medicine (IFEM) core curriculum and education committee and board member of the Asian Society for Emergency Medicine and Emirati Board of Emergency Medicine.

Seizure (2024)

by Ardi Knobel Mendoza, Danielle Charles-Chauvet, Erik J. Blutinger

Introduction

Seizures are caused by abnormal cortical neuronal activity that manifests as changes in alertness or neurological symptoms. While seizures account for only 1% of all emergency department (ED) visits and 3% of prehospital transports, their potential for significant morbidity undermines the importance of rapid assessment and treatment in emergency settings [1]. The etiology of seizures varies by age group, with the most common causes being fever in infants and metabolic derangements or structural abnormalities in adults over 75. This chapter will explore various seizure presentations, diagnostic assessment tools, and considerations for treatment and disposition decisions in the ED.

You have a new patient!

A 24-year-old female presents to the emergency room after being found on the street. She is minimally responsive, alert, and oriented only to herself. Her heart rate is 87 bpm, blood pressure is 141/94 mmHg, respiratory rate is 14 bpm, and she is afebrile, with oxygen saturation of 99% on room air. She has a gravid uterus with a fundal height of approximately 29 cm (11.4 inches) but is otherwise atraumatic.

a-photo-of-a-24-year-old-female (image was produced by using ideogram 2.0)

What do you need to know?

Seizure Presentation and Classification

It is essential to investigate the cause and categorize the type of seizure after an acute episode to inform the diagnostic and treatment plan. Seizures are often classified as provoked, which occur within 7 days of a neurologic, metabolic, or infectious precipitator, or unprovoked, which has no association with an inciting factor. A history of seizures, febrile illness, malignancy, new medications, recreational drug use, or pregnancy can help to elucidate this. A complete neurological examination, which includes an assessment of mental status, should be performed as an altered postictal state follows most primary seizures. In addition to a change in mental status, the postictal state can present as motor deficits or paresis. Postictal paresis suggests a structural lesion as the cause of the seizure and should prompt cranial imaging [2]. Given that seizures are a manifestation of cortical neuronal activity, the extent of cortical involvement can lead to various symptoms at presentation [3].

Partial seizures involve only some of the cortex. They are classified as either simple, in which the patient is alert throughout, or complex, in which the patient has decreased alertness. Seizures can also begin as partial seizures, involving only some of the cortex, and spread to involve the entire cortex. Seizures involving the entire cortex are termed “generalized” seizures, resulting in decreased alertness. Generalized seizures are further classified based on their physical manifestations:

Absence Seizure: no collapse, automatisms (blinking, staring, lip smacking)

Tonic-clonic Seizure: collapse with stiff non-rhythmic convulsive movements.

Atonic Seizure: collapse without convulsions (similar to syncope) [4].

Febrile seizures typically occur in children 6 months-6 years of age with fevers greater than 38℃ and no neurological infection. 80% of febrile seizures are tonic-clonic in presentation, self-limiting, and do not recur after resolution of the inciting fever [5].

Eclamptic seizures are typically tonic-clonic in presentation and are considered unstable, as they carry significant mortality risk to the mother and fetus. Therefore, any pregnant patient with altered mental status and hypertension, identified as systolic >140 or diastolic >90, should be assessed for eclampsia. In cases with high suspicion of preeclampsia or eclamptic seizures, patients should be treated with magnesium for seizure prophylaxis [6].

Psychogenic seizures present similarly to generalized tonic-clonic seizures but are not associated with cortical neuronal derangements. In the ED, it is difficult to differentiate these seizures from neurogenic seizures, as there is limited access to EEG. However, psychogenic seizures present with more rhythmic and symmetric movements, patients are typically completely aware and conversant throughout, and there is no postictal state.

It is important to consider the duration of a seizure episode in all patients. Most seizures last from 30 seconds to 2 minutes. Seizures lasting longer than 5 minutes meet the criteria for status epilepticus. These patients are considered unstable, as prolonged seizure activity is associated with an increased risk of permanent brain damage. Not all patients with status epilepticus have convulsive seizures, so it is important to assess for subtle symptoms of seizure activity in the unresponsive patient, as they may have non-convulsive status epilepticus—a medical emergency.

Medical History

Thorough history taking in patients with seizure disorders is crucial for accurate diagnosis and effective management. This process involves a structured yet flexible approach to gathering relevant information, ensuring that all aspects of the patient’s condition are considered. Key components of this history include the patient’s medical background, seizure characteristics, and psychosocial factors.

Key Components of History Taking

  • Presenting Complaints: Document the chief complaints, including the nature, frequency, and duration of seizures [7].
  • Seizure Onset and Triggers: Investigate the age of onset, potential triggers (e.g., photosensitivity), and environmental factors that may provoke seizures [8].
  • Medical and Family History: Collect information on past medical history, family history of seizures or neurological disorders, and any relevant social history [7,9].
  • Psychosocial Aspects: Assess the impact of seizures on the patient’s daily life, including emotional and social challenges [8].

A comprehensive history-taking process in seizure patients is crucial for accurate diagnosis and effective management of various seizure types. By gathering essential information regarding seizure semiology, triggers, and patient-specific factors, clinicians can develop tailored treatment strategies to improve outcomes. Seizure semiology, for example, provides valuable insights into the nature of seizures, helping to classify them as either focal or generalized [10]. Detailed accounts of auras and observable signs can further indicate the anatomical origins of seizures, guiding appropriate diagnostic testing [10]. Additionally, identifying seizure triggers, such as environmental factors or specific stimuli, plays a vital role in both diagnosis and management. For instance, patients with photosensitivity may require targeted questions to uncover visual triggers that provoke seizures [8]. Together, these aspects of thorough history-taking form the foundation for effective and personalized seizure management.

When conducting history-taking in patients with seizure disorders, clinicians must be mindful of several common pitfalls that can lead to misdiagnosis or ineffective treatment. These issues often arise from inadequate questioning, overemphasizing certain symptoms, and neglecting the broader context of the patient’s experiences.

Inadequate history-taking, such as missing or incomplete accounts from witnesses, can result in misinterpreting seizure types [11]. Failing to gather detailed descriptions of seizure events, including pre-ictal and post-ictal states, may further obscure the diagnosis [12].

Additionally, an overemphasis on specific symptoms, such as those associated with focal seizures, may mislead clinicians, as these symptoms do not always correlate with the seizure type [13].

Another critical factor is the neglect of contextual elements, such as environmental triggers, which may result in missed diagnoses of reflex seizures, especially in photosensitive patients [8]. Furthermore, ignoring psychosocial aspects and the patient’s overall health can complicate the understanding of seizure disorders [14]. While advancements in technology and neuroimaging provide valuable objective data, the art of listening and thorough history-taking remains an irreplaceable cornerstone in the diagnostic process.

While a comprehensive history is essential, it is also important to recognize that some patients may present atypically, necessitating a tailored approach to history taking that considers individual circumstances and variations in symptom presentation.

Physical Examination

A comprehensive physical examination for patients presenting with seizures in the emergency department is essential for accurate diagnosis and effective management. Key components include a thorough neurological assessment, which involves evaluating consciousness, motor function, and sensory responses to identify any neurological deficits [15]. Monitoring vital signs is equally critical, as instability such as hypotension or tachycardia may indicate underlying issues requiring immediate attention [16]. Additionally, a systematic head-to-toe physical examination can help identify signs of trauma or systemic illness that may contribute to seizure activity [15].

In the emergency department, recognizing physical examination findings indicative of a severe or prolonged seizure episode is critical for timely diagnosis and management, particularly in cases of status epilepticus or non-convulsive seizures. Altered mental status, characterized by confusion, disorientation, or a prolonged postictal state, is a key finding that can suggest non-convulsive status epilepticus (NCSE) [17]. Neurological signs, such as subtle twitching, blinking, or fluctuating sensorium, may also indicate ongoing seizure activity [17]. In cases of generalized tonic-clonic seizures (GTCS), convulsive activity manifests with muscle rigidity and jerking movements, making it a more apparent diagnosis [18]. Additionally, focal seizures can result in specific neurological deficits, which may be misinterpreted as other neurological conditions. While these findings are crucial for identifying severe seizure episodes, it is important to acknowledge that some patients may present with atypical symptoms or lack overt signs of seizure activity, complicating the diagnostic process [17].

While the value of a comprehensive examination cannot be overstated, it is also important to recognize that some patients may present with atypical symptoms or underlying conditions that complicate the diagnosis. This highlights the need for a tailored approach to each case, ensuring that individual factors are carefully considered [16].

Alternative Diagnoses

The diagnosis of seizures primarily relies on the patient’s clinical history, with particular emphasis on accounts provided by witnesses. This is especially important because many seizure types involve impaired consciousness, leaving patients unaware of their episodes. Clinical findings can be supported by interictal electroencephalogram (EEG) abnormalities, although it is essential to note that such abnormalities may also occur in healthy individuals and their absence does not rule out epilepsy. It is equally critical to differentiate seizures from other conditions that may present similarly. These include syncope, such as cardiac arrhythmias or vasovagal episodes; metabolic disturbances like hypoglycemia or hyponatremia; and vascular events such as transient ischemic attacks. Additionally, migraine auras, sleep disorders like narcolepsy or night terrors, movement disorders such as paroxysmal dyskinesia, and gastrointestinal conditions like esophageal reflux in neonates and infants can mimic seizures. Psychiatric conditions, including conversion disorders, panic attacks, malingering, or episodes driven by secondary gain, must also be considered [19].

Acing Diagnostic Testing

When considering diagnostic testing such as labs and imaging, there is a lack of consensus on a set of tests required for all seizing patients. Rather, the diagnostic workup for a patient presenting with a seizure depends on a variety of factors, such as the suspected etiology of the seizure and whether the patient has a known seizure disorder or is presenting with a first-time seizure [20]. In patients with known seizure disorders, it is generally accepted test for levels of the anti-epileptic drug (AED) the patient takes, such as levetiracetam, phenytoin, carbamazepine, phenobarbital, or valproic acid. However, levels can often take hours to days to result or may not be available at a certain facility. In patients without a known seizure disorder, or if there is concern for an etiology for a seizure besides breakthrough from AED treatment, a more extensive workup is warranted. Basic testing should include a finger stick glucose, a urine or serum pregnancy test, and serum chemistry, including calcium and magnesium. Urine/serum toxicologies can also be obtained if there is concern for potential toxic ingestion as a cause. A lactic acid can be obtained, which should be markedly elevated immediately after the seizure and normalize after an hour of seizure onset [21].

A Computed Tomography (CT) Head should be obtained in all first-time seizure patients to assess for a structural lesion such as a mass, a bleed either as the etiology or sequelae of the seizure, or signs of an infection. Seizure sequelae such as significant head trauma can also be assessed with CT imaging to look for a large hematoma or skull fracture in patients who fail to return to baseline mental status after a seizure [22]. Magnetic Resonance Imaging (MRI) can be considered to reveal other diagnoses such as a brain abscess or central vascular event such as infarction; however, this imaging modality is often less available in the emergency setting and may require admission vs. outpatient referral to obtain an image [23]. Electroencephalography (EEG)is when diagnostic testing such as labs and imaging is considered, but there is a lack of consensus on a set of tests required for all seizing patients. Rather, the diagnostic workup for a patient presenting with a seizure depends on a variety of factors, such as the suspected etiology of the seizure and whether the patient has a known seizure disorder or is presenting with a first-time seizure [20]. In patients with known seizure disorders, it is generally accepted test for levels of the anti-epileptic drug (AED) the patient takes, such as levetiracetam, phenytoin, carbamazepine, phenobarbital, or valproic acid. However, levels can often take hours to days to result or may not be available at a certain facility. In patients without a known seizure disorder, or if there is concern for an etiology for a seizure besides breakthrough from AED treatment, a more extensive workup is warranted. Basic testing should include a finger stick glucose, a urine or serum pregnancy test, and a serum chemistry, including calcium and magnesium. Urine/serum toxicologies can also be obtained if there is concern for potential toxic ingestion as a cause. A lactic acid can be obtained, which should be markedly elevated immediately after the seizure and normalize after an hour of seizure onset [21].

A Computed Tomography (CT) Head should be obtained in all first-time seizure patients to assess for a structural lesion such as a mass, a bleed either as the etiology or sequelae of the seizure, or signs of an infection. Seizure sequelae such as significant head trauma can also be assessed with CT imaging to look for a large hematoma or skull fracture in patients who fail to return to baseline mental status after a seizure [22]. Magnetic Resonance Imaging (MRI) can be considered to reveal other diagnoses such as a brain abscess or central vascular event such as infarction; however, this imaging modality is often less available in the emergency setting and may require admission vs. outpatient referral to obtain an image [23]. Electroencephalography (EEG)is an important study in patients who are continuing to have seizures without clear signs of convulsions, such as in nonconvulsive status epilepticus (NCSE), patients with persistent altered mental status, or intubated patients. EEGs are often unavailable in the emergency setting but have a role in the inpatient or ICU settings with neurology consultants [24]. ECGs should also be considered in patients with new-onset seizures to exclude cardiac conduction disorders that can cause seizure-like activity, such as syncope, Brugada syndrome, or QTc prolongation or shortening.

Risk Stratification

The presence of comorbidities plays a critical role in the risk stratification, prognosis, and management of epilepsy, highlighting the need for a holistic approach to patient care. In the emergency department, recognizing these comorbidities is crucial for tailoring immediate interventions and ensuring acute and comprehensive follow-up care. Studies reveal that 60-70% of adults and 80% of children with epilepsy experience multimorbidity [25]. Among patients with senile epilepsy, 81% have at least one comorbidity, with neurological (61%) and cardiovascular (45%) conditions being the most prevalent [26]. Emergency clinicians must remain vigilant for these conditions, as they may exacerbate seizure episodes or complicate acute management. These comorbidities significantly impact seizure outcomes, as patients with neurological and psychiatric disorders face a higher risk of recurrent seizures and reduced likelihood of achieving seizure freedom [26]. Conditions like depression and anxiety are particularly associated with a more severe course of epilepsy [27], and their identification in the emergency setting can guide referrals for further psychiatric evaluation. Additionally, multimorbidity is linked to lower health-related quality of life and increased healthcare costs due to frequent hospitalizations [25]. Cognitive and psychiatric comorbidities often impair daily functioning more than the seizures themselves [28], necessitating a multidisciplinary approach starting from the emergency department. Addressing these comorbidities, however, has been shown to improve overall health outcomes and enhance the quality of life for patients, emphasizing the importance of comprehensive, patient-centered care [28].

Management

The most important intervention in a patient actively seizing is ensuring adequate brain oxygenation. The airway should be protected via maneuvers that include rolling the patient on their side, jaw thrusts, applying a nasopharyngeal airway, applying supplemental oxygen, and preventing aspiration with suction as needed. Oxygenation status should be monitored with continuous pulse oximetry and capnography when possible.

Providers should also anticipate the impending decompensation of the clinical course and the need for intubation by preparing airway equipment, medications, and IV access, which will be discussed later in the chapter. Along with oxygenation, patients must be protected from injury, e.g., from falling out of bed and preventing trauma.

Most seizures stop on their own within one to two minutes of onset, but the longer the seizure lasts, the less likely it is to stop on its own and can become self-sustaining.

Seizures that are continuous or intermittent, lasting more than 5 minutes without recovery of consciousness, are known as status epilepticus. Medical therapies to terminate a seizure are divided into three stages based on escalation of need and inability to terminate the seizure.

Benzodiazepines are considered first-line agents in terminating seizures, followed by second-line agents such as Levetiracetam, Valproate, Phenytoin, and Fosphenytoin [29]. The third-line medications are infusions of benzodiazepines, propofol, or barbiturates, prepared for likely intubation with paralytics and continued infusions [30].

The following lists these medications by stage, dose, and considerations [31, 32]:

Midazolam (1st Line Agent – Benzodiazepine)

  • Loading Dose:
    • 10 mg IM or 0.1-0.2 mg/kg IV.
  • Maintenance Dose: 0.001 mg/kg/min.
  • Pediatric Dose:
    • IV or IN: 0.2 mg/kg (max 5 mg).
    • IM:
      • <13 kg: 0.2 mg/kg.
      • 13-39 kg: 5 mg.
      • 39 kg: 10 mg.
  • Considerations:
    • IM dosing can be used if no IV is established.
    • Acts faster than Lorazepam but has a shorter duration.
    • May cause respiratory depression and hypotension.

Diazepam (1st Line Agent – Benzodiazepine)

  • Loading Dose: 10 mg over 2 minutes. Repeat every 5-10 minutes to a max of 30 mg.
  • Maintenance Dose: N/A.
  • Pediatric Dose: 0.15 mg/kg IV.
  • Considerations:
    • May cause respiratory depression and hypotension.

Levetiracetam (2nd Line Agent)

  • Loading Dose: 60 mg/kg (up to a max of 4,500 mg), infused over 10 minutes.
  • Maintenance Dose: Same as the loading dose.
  • Pediatric Dose: Same as loading dose.
  • Considerations:
    • If the patient weighs >75 kg, the dose is 4.5 g.
    • If seizures stop, continue to give Levetiracetam to prevent recurrence.

Phenytoin (2nd Line Agent)

  • Loading Dose: 18-20 mg/kg with a max rate of 50 mg/min.
  • Maintenance Dose: N/A.
  • Pediatric Dose: N/A.
  • Considerations:
    • Cardiac monitoring is necessary for QRS complex widening.

Fosphenytoin (2nd Line Agent)

  • Loading Dose: 15-20 mg/kg with a max rate of 150 mg/min.
  • Maintenance Dose: Same as loading dose.
  • Pediatric Dose: N/A.
  • Considerations:
    • Cardiac monitoring is necessary for QRS complex widening.

Valproate (2nd Line Agent)

  • Loading Dose: 20-40 mg/kg over 10 minutes. Repeat if needed.
  • Maintenance Dose: Same as loading dose.
  • Pediatric Dose: Same as loading dose.
  • Considerations: N/A.

Propofol (3rd Line Agent)

  • Loading Dose: 1-2 mg/kg IV over 5 minutes (max load 10 mg/kg).
  • Maintenance Dose: 50-80 mcg/kg/min (3-5 mg/kg/hr) as an infusion.
  • Pediatric Dose: N/A.
  • Considerations:
    • May cause respiratory depression and hypotension.

Phenobarbital (3rd Line Agent)

  • Loading Dose: 10-15 mg/kg bolus up to 60 mg/min.
  • Maintenance Dose: 120-240 mg every 20 minutes.
  • Pediatric Dose: N/A.
  • Considerations: N/A.

Midazolam (for 3rd Line use) (3rd Line Agent)

  • Loading Dose: 0.2 mg/kg IV.
  • Maintenance Dose: 0.1-2 mg/kg/hr.
  • Pediatric Dose: N/A.
  • Considerations:
    • Can be used in patients with hypotension.

Once the provider considers 3rd line medications and starting infusions, they should prepare for intubation as the patient is likely in status epilepticus, requiring continued medication and airway protection. Induction medications for intubation are often the same medications listed above in the 3rd stage of treatment, such as propofol or midazolam, and can be on board before paralytics. Paralytics are used to stop the seizure-like activity and aid in intubation, but it is important to remember that they are not meant to terminate the seizure. Patients can still have seizures despite the lack of tonic-clonic seizure activity such as NCSE. Rocuronium is the preferred paralytic agent as it is not associated with the hyperkalemia seen in succinylcholine, which is a risk for patients seizing for an extended period who could develop rhabdomyolysis. Rocuronium paralysis lasts much longer, which should be a consideration when monitoring for further seizures with EEG.

Finally, other conditions can cause seizures or seizure-like activity that require their own treatment strategies, which are discussed below:

Eclampsia, a life-threatening condition often associated with pregnancy, is treated with magnesium to control seizures, benzodiazepines for acute management, and blood pressure control to address underlying hypertension. For seizures due to isoniazid toxicity, the recommended treatment is pyridoxine (vitamin B6), which counteracts the drug’s neurotoxic effects. In cases of hypoglycemia, seizures can be managed by administering Dextrose 50% in Water (D50W) to restore blood glucose levels rapidly. Hypocalcemia, another potential seizure trigger, requires the administration of calcium gluconate or calcium chloride to normalize calcium levels. For seizures induced by hyponatremia, 3% hypertonic saline is used to increase serum sodium levels safely.

In cases of toxicity from aspirin, tricyclic antidepressants (TCAs), or lithium, hemodialysis is indicated to effectively remove the offending agents from the bloodstream. For seizures caused by meningitis, prompt initiation of appropriate antibiotics is critical to address the underlying infection and prevent further complications.

Special Patient Groups

Pediatrics

Seizures in pediatric patients can present with diverse etiologies ranging from febrile seizures to more serious underlying conditions such as intracranial infections, metabolic disturbances, or congenital disorders. In children under 5, febrile seizures are the most common cause of convulsions and are generally self-limited, though they require careful differentiation from more serious causes like meningitis or encephalitis. Clinical reasoning should prioritize a detailed history, including the onset of the seizure, vaccination status, and any family history of epilepsy or neurodevelopmental disorders. Laboratory tests and imaging may be indicated if there is a high suspicion of an underlying structural or metabolic issue, such as in children with a prolonged postictal state or a first-time seizure without a clear precipitant. In the emergency department (ED), rapid assessment of the child’s airway, breathing, and circulation (ABCs) is paramount, along with ensuring the seizure is appropriately controlled, often with medications like lorazepam or diazepam. Close follow-up is necessary to assess for recurrent seizures or potential neurological sequelae.

Geriatrics

Seizures in elderly patients often present a diagnostic challenge due to the overlap with other common age-related conditions, such as syncope, transient ischemic attacks (TIA), or dementia-related behavioral changes. In this population, new-onset seizures should prompt an urgent evaluation for reversible causes, including cerebrovascular events, metabolic disturbances (such as hyponatremia or hypoglycemia), brain tumors, or infections like meningitis or encephalitis. Seizures in older adults may also be a manifestation of progressive neurodegenerative diseases, including Alzheimer’s or Parkinson’s disease. Emergency management in the ED should focus on stabilizing the patient while considering potential drug interactions, as elderly patients are more likely to be on multiple medications that may lower the seizure threshold (e.g., antipsychotics, antidepressants, or antihypertensives). Antiepileptic drug (AED) therapy initiation, while necessary in recurrent or long-duration seizures, must be approached cautiously due to age-related pharmacokinetic changes and the increased risk of side effects. A thorough evaluation for underlying causes, including neuroimaging and laboratory tests, is critical.

Pregnant Patients

Seizures during pregnancy present unique challenges in both diagnosis and treatment. The differential diagnosis includes pregnancy-specific conditions like eclampsia, in addition to the possibility of preexisting epilepsy or new-onset seizures due to metabolic derangements or intracranial pathology. In a pregnant patient with a seizure, the clinical priority is to ensure both maternal and fetal well-being. Eclampsia, a severe complication of preeclampsia, must be ruled out, as it presents with generalized tonic-clonic seizures and may lead to maternal and fetal morbidity if not promptly treated. Once eclampsia is excluded, consideration should be given to other causes such as hypoglycemia, cerebrovascular accidents, or drug toxicity (e.g., withdrawal from anticonvulsant medications). Emergency management in the ED should prioritize seizure control, typically with benzodiazepines, while avoiding teratogenic medications. Magnesium sulfate is the treatment of choice for eclampsia. Fetal monitoring should be initiated, and careful planning for delivery may be required depending on the severity of the condition and gestational age. The clinical approach should balance the need for immediate seizure control while minimizing risks to both the mother and fetus.

When To Admit This Patient

Few definitive practice guidelines are available to emergency physicians making disposition decisions for seizure episodes. However, all critically ill patients must be admitted to the inpatient setting since overall risk assessment is important for deciding whether to safely discharge patients home. For alternative clinical presentations, the physician should reliably assess whether the patient’s overall presentation warrants further medical interventions in a clinical setting.

For emergency physicians, seizure recurrence, morbidity, and mortality are useful measures to consider for safe discharge. Studies suggest that seizure recurrence most often depends upon EEG findings and the underlying cause—normal EEG and undetectable cause are associated with lower recurrence rates [33]. With positive neuroimaging findings (e.g., structural findings), initiating AED therapy for first-time seizures is recommended given a high 1-year recurrence risk of up to 65% [34].

Any patients with abnormal neurologic signs or symptoms who have not fully recovered from their seizure should not be discharged. Other important clinical benchmarks are the presence of normal vital signs, CT head imaging, EKG, basic lab results (especially renal function and blood counts), and follow-up. As part of the physician’s risk assessment of the patient’s overall condition, social factors must also be taken into account: lack of follow-up care, history of being lost to follow-up, and insufficient assistance available at home should all weigh towards admitting the patient for further monitoring (and possible seizure workup).

Generally, stable patients are those who return to their baseline mental status, do not exhibit any new neurological deficits, have no significant lab result abnormalities, and remain at low risk for recurrent seizure activity in the short term. Coordinating reliable follow-up is important, and all patients should be educated about the “red flag” signs and symptoms that warrant urgent evaluation and treatment.

Revisiting Your Patient

Altered mental status in the gravid, hypertensive patient is concerning for eclampsia. This patient should be started on 2mg of Mg as seizure prophylaxis. Obstetrics should be consulted as urgent delivery via cesarean section is the definitive treatment for this patient’s seizures. After delivery, the patient should be monitored closely for postpartum eclamptic seizures, which can occur up to 6 weeks postpartum.

Authors

Picture of Ardi Knobel Mendoza

Ardi Knobel Mendoza

Ardi Mendoza, MD is a resident at the Mount Sinai Hospital Emergency Medicine Program. He is interested in Health System and Emergency System Strengthening and local partner/local government-led collaborations. He has prior experiences in the field of Global Surgery while at Rutgers Robert Wood Johnson Medical School, assessing financial risk protection from impoverishing and catastrophic expenditure due to surgical care in the Colombian Healthcare System. He lived in Lima, Peru for a year working with Peruvian researchers at the University Cayetano Heredia as a research coordinator helping to develop a point-of-care diagnostic screening tool for Autism using eye-tracking technology.

Picture of Danielle Charles-Chauvet

Danielle Charles-Chauvet

Danielle Charles-Chauvet, MD is an Emergency Medicine resident at the Mount Sinai Hospital in New York. She is deeply invested in medical education and health disparities and, in affiliation with Harlem Children's Zone, has led several community-based educational initiatives to address these disparities. She designed and taught a course entitled Health and Structures of Oppression at Brown University's medical school. Her dedication to education earned her the 2022 National Outstanding Medical Student Award from the Academic College of Emergency Physicians and the 2021 Medical Education Award from the Society of Academic Emergency Medicine. She is currently working to expand her impact internationally by building Haiti's medical education infrastructure.

Picture of Erik J. Blutinger

Erik J. Blutinger

Erik J. Blutinger, MD, MSc, FACEP is a full-time emergency physician at Mount Sinai Queens Hospital in New York City and Medical Director to the Community Paramedicine program at Mount Sinai Health Partners. He completed his residency training at the University of Pennsylvania, Master's at the London School of Hygiene & Tropical Medicine, and has worked on a variety of health initiatives in quality and patient experience with formal leadership training in Quality Improvement (QI). Erik has worked in multiple national healthcare systems and underserved communities, including townships in South Africa and Guatemala, Bhutan, India, and Austria.

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References

  1. Jagoda, (2010). Seizures: An issue of Emergency Medicine Clinics. Elsevier Saunders.
  2. Werhahn, J. (2010). Weakness and focal sensory deficits in the postictal state. Epilepsy & Behavior, 19(2), 138–139. https://doi.org/10.1016/j.yebeh.2010.06.029
  3. Kim, , Cho, J.-W., Lee, J., Joo, E. Y., Hong, S. C., Hong, S. B., & Seo, D.-W. (2011). Seizure duration determined by subdural electrode recordings in adult patients with intractable focal epilepsy. Journal of Epilepsy Research, 1(2), 57–64. https://doi.org/10.14581/jer.11011
  4. Kumar, , Sharma Maini, K., & Arya, K. (n.d.). Simple partial seizure. National Center for Biotechnology Information. Retrieved April 10, 2023, from https://pubmed.ncbi.nlm.nih.gov/29763181/
  5. Heon, (n.d.). Febrile seizures. Core EM. Retrieved April 10, 2023, from https://coreem.net/core/febrile-seizures/
  6. Wagner, K. (2004, December 15). Diagnosis and management of preeclampsia. American Family Physician. Retrieved April 10, 2023, from https://www.aafp.org/pubs/afp/issues/2004/1215/p2317.html
  7. Hiroshi, S., Hallett, M., ‘History taking’, The Neurologic Examination: Scientific Basis for Clinical Diagnosis, 2 edn (2022; online edn, Oxford Academic, 1 Aug. 2022), https://doi.org/10.1093/med/9780197556306.003.0002, accessed 1 Dec. 2024.
  8. Brinciotti, M., Bouilleret, V, Masnou, P. (2021). Optimizing the Patient’s History: A Modern Approach. 10.1007/978-3-319-05080-5_26.
  9. Dulak SB. A practical guide to a thorough history. RN. 2004;Suppl:14-21.
  10. Wolf P, Benbadis S, Dimova PS, et al. The importance of semiological information based on epileptic seizure history. Epileptic Disord. 2020;22(1):15-31. doi:10.1684/epd.2020.1137
  11. Smith PE. If it’s not epilepsy… J Neurol Neurosurg Psychiatry. 2001;70 Suppl 2(Suppl 2):II9-II14. doi:10.1136/jnnp.70.suppl_2.ii9
  12. Trevathan E. Patient page. The diagnosis of epilepsy and the art of listening. Neurology. 2003;61(12):E13-E14. doi:10.1212/wnl.61.12.e13
  13. Henry JC. Comment: Be careful what you ask when interviewing patients with epilepsy. Neurology. 2015;85(7):594. doi:10.1212/WNL.0000000000001843
  14. Kanner, A. (2008). Common Errors Made in the Diagnosis and Treatment of Epilepsy. Seminars in neurology. 28. 364-78. 10.1055/s-2008-1079341.
  15. Wan, XH & Zeng, R. (2020). Handbook of Clinical Diagnostics. 10.1007/978-981-13-7677-1.
  16. Bank, A & Bazil, C. (2019). Emergency Management of Epilepsy and Seizures. Seminars in Neurology. 39. 073-081. 10.1055/s-0038-1677008.
  17. Hasan, Ahmed. (2016). Non-Convulsive Status Epilepticus in Emergency Department: A Diagnostic Challenge. Journal of Medical Science And clinical Research. 10.18535/jmscr/v4i8.103.
  18. Virani, D., Sangani, S., Patel, C, Patel, V., Saha, J., Kalsariya, R. (2024). 5. Study of Clinical Profile, Management and Outcome of Patients Presented with Seizures in Emergency Medicine Department. BJ Kines: National Journal of Basic & Applied Sciences, doi: 10.56018/bjkines2024065
  19. Ko DY. Epilepsy and Seizures Differential Diagnoses (updated Jul 26, 2002). From https://emedicine.medscape.com/article/1184846-differential?&icd=login_success_email_match_fpf Accessed: Nov 1,
  20. Burgess M, Mitchell R, Mitra B. Diagnostic testing in nontrauma patients presenting to the emergency department with recurrent seizures: A systematic review. Acad Emerg Med. 2022 May;29(5):649-657. doi: 10.1111/acem.14391. Epub 2021 Oct 1. PMID: 34534387.
  21. Teran F, Harper-Kirksey K, Jagoda A. Clinical decision making in seizures and status epilepticus. Emerg Med Pract. 2015 Jan;17(1):1-24.
  22. Harden CL, Huff JS, Schwartz TH, Dubinsky RM, Zimmerman RD, Weinstein S, Foltin JC, Theodore WH; Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology. Reassessment: neuroimaging in the emergency patient presenting with seizure (an evidence-based review): report of the Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology. Neurology. 2007 Oct 30;69(18):1772-80. doi: 10.1212/01.wnl.0000285083.25882.0e. PMID: 17967993.
  23. Gelisse P, Crespel A, Genton P, Jallon P, Kaplan PW. Lateralized Periodic Discharges: Which patterns are interictal, ictal, or peri-ictal? Clin Neurophysiol. 2021 Jul;132(7):1593-1603. doi: 10.1016/j.clinph.2021.04.003. Epub 2021 Apr 27. PMID: 34034086.
  24. Rosenthal Seizures, Status Epilepticus, and Continuous EEG in the Intensive Care Unit. Continuum (Minneap Minn). 2021 Oct 1;27(5):1321-1343. doi: 10.1212/CON.0000000000001012. PMID: 34618762.
  25. Gaitatzis A, Majeed A. Multimorbidity in people with epilepsy. Seizure. 2023;107:136-145. doi:10.1016/j.seizure.2023.03.021
  26. Cao, Z., Li, Y., Liu, S. et al.Clinical characteristics and impact of comorbidities on the prognosis of senile epilepsy in Southwest China: a retrospective cohort study. Acta Epileptologica 6, 11 (2024). https://doi.org/10.1186/s42494-024-00153-8
  27. Kanner, A.M., Ribot, R. and Mazarati, A. (2018), Bidirectional relations among common psychiatric and neurologic comorbidities and epilepsy: Do they have an impact on the course of the seizure disorder?. Epilepsia Open, 3: 210-219. https://doi.org/10.1002/epi4.12278
  28. Mula M, Coleman H, Wilson SJ. Neuropsychiatric and Cognitive Comorbidities in Epilepsy. Continuum (Minneap Minn). 2022;28(2):457-482. doi:10.1212/CON.0000000000001123
  29. Silbergleit R, Durkalski V, Lowenstein D, Conwit R, Pancioli A, Palesch Y, Barsan W; NETT Intramuscular versus intravenous therapy for prehospital status epilepticus. N Engl J Med. 2012 Feb 16;366(7):591-600. doi: 10.1056/NEJMoa1107494. PMID: 22335736; PMCID: PMC3307101.
  30. Falco-Walter JJ, Bleck Treatment of Established Status Epilepticus. J Clin Med. 2016 Apr 25;5(5):49. doi: 10.3390/jcm5050049. PMID: 27120626; PMCID: PMC4882478.
  31. Brophy GM, et : Guidelines for the evaluation and management of status epilepticus. Neurocrit Care 17:3-23, 2012.
  32. Seizure: Emergency Medicine, Second Editor; Adams, James G., MD, 2013, 2008 by Saunders, an imprint of Elsevier Inc. Book Chapter 99
  33. Berg AT, Shinnar The risk of seizure recurrence following a first unprovoked seizure: a quantitative review. Neurology 1991;41:965–72.
  34. Jagoda A; Gupta, K. “The Emergency Department Evaluation of the Adult Patient Who Presents with a First-Time ” Emergency Medicine Clinics of North America, U.S. National Library of Medicine, https://pubmed.ncbi.nlm.nih.gov/21109101/.

Reviewed and Edited By

Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

Arif Alper Cevik, MD, FEMAT, FIFEM

Prof Cevik is an Emergency Medicine academician at United Arab Emirates University, interested in international emergency medicine, emergency medicine education, medical education, point of care ultrasound and trauma. He is the founder and director of the International Emergency Medicine Education Project – iem-student.org, chair of the International Federation for Emergency Medicine (IFEM) core curriculum and education committee and board member of the Asian Society for Emergency Medicine and Emirati Board of Emergency Medicine.

Seizure: Lethal Dissection

Lethal Dissection Seizure

Case Presentation

A 49-year old female without any co-morbidities presented to the emergency department (ED) with seizures. On arrival, she was in a postictal state.

She had recently visited a local hospital with complaints of severe dysmenorrhea and low back pain. The attenders informed us that she was very sleepy and weak at that time, was treated for pain and given tranexamic acid, and sent home. The next day, she had one episode of Generalized Tonic-Clonic Seizure, and she arrived in our ED in a postictal phase. She vomited twice in the ED.

Her vitals were as follows: 

  • Blood pressure (BP): 160/100 mmHg.
  • Heart rate (HR): 22/min
  • Peripheral capillary oxygen saturation (SPO2): 98% on room air
  • General Random Blood Sugar (GRBS): 233 mg/dl
  • Glasgow Coma Scale (GCS): E2V5M6

Her examination was as follows:

  • The patient was drowsy but arousable. 
  • Pupils bilateral reacting to light. No anisocoria.
  • CNS examination could not be completed as the patient was drowsy.
  • A normal pattern of breathing. The respiratory examination was normal.
  • The abdomen was soft, symmetric, and non-tender without distention.

Point-of-care ultrasound (POCUS) showed a flap in the abdominal aorta. (See Figure 1 and 2 for transverse and longitudinal views of the aorta, respectively) Upon this finding, cardiac surgery and neurology consultations were sought.

Transverse section of the abdominal aorta showing a flap.
https://ibb.co/N6VyMD8

Image shows transverse section of the abdominal aorta showing a flap.

Abdominal aorta showing a flap
https://ibb.co/wwkYHJY

Image shows abdominal aorta showing a flap.

The laboratory results were as follows:

  • D-dimer: 1192 ng/ml
  • Haemoglobin (Hb): 10 g/dl
  • The international normalized ratio (INR): 1.25
  • Platelets: 260000 per mcL
  • Total leucocyte count (TLC): 22000 cells/mm3
  • Creatinine :1.6 mg/dl.

Meanwhile, the patient was suffering multiple seizure-like episodes, characterized by staring, deviation of the mouth, and irregular limb movements, but these episodes lasted for few minutes and ended without the postictal phase. The patient was drowsy but obeyed commands and did not have any recollection of those few minutes.

Head computed tomography (CT) showed no infarct or bleeding. It was normal.

CT angiogram and aortogram revealed that the patient had Stanford Type A aortic dissection with the flap extending to the entire left subclavian artery, with severely occluding filling defects and thrombosis of the false lumen into bilateral common carotid arteries (See Figure 3, 4 and 5). On the other end, the dissection extended to the common iliac arteries (See Figure 6).

CT Aortogram showing bilateral common carotid artery filling defects
https://ibb.co/M6TMqpq

Image shows CT Aortogram showing bilateral common carotid artery filling defects

And on the other loose of the string the dissection was extending till the common iliac arteries.
Ascending and descending aortic dissection
https://ibb.co/n8Rbdvm

Image shows ascending and descending aortic dissection

Dissection of the common iliac artery before bifurcation
https://ibb.co/jVjL0qJ

Image shows dissection of the common iliac artery before bifurcation.

 

Management

Initially, the patient was treated symptomatically by anti-epileptics and analgesics. After the cardio-thoracic and vascular surgeon consultations, we decided to airlift the patient to a higher centre as our hospital was tertiary care and there were no grafts for the urgent repair of the extensive aortic dissection. We intubated the patient for secure transportation. However, we learned that the patient expired in the higher centre before reaching the operating room.

Discussion

Before I shed light on the important part of this discussion, I know that the outcome of this case was unfortunately grave. However, I chose this case because of it.

In this case, the patient had low back pain in her previous hospital visit. However, she was sent home with symptomatic management, implying that it could have been addressed more carefully. She visited our ED one day later, and POCUS let us diagnose the dissection in 15 minutes, which was confirmed by a CT aortogram within 40 minutes. After consultations and finding the available facility, we airlifted the patient to a higher centre for urgent repair, but the patient could not make it to the operating room.     

We all know acute aortic dissection is the most common life-threatening disorder affecting the aorta. Over the first several hours, the mortality rate increase up to 1% per hour; therefore, early intervention is critical (1). In our case, the involvement of bilateral carotid arteries caused seizure-like episodes and altered mental status. Also, studies show that patients with similarly located dissections may experience neck pain, transient ischemic attacks (TIA), cerebral ischemia, transient monocular blindness and subarachnoid haemorrhage (SAH) but not seizure(2). In our case, the global hypo-perfusion caused recurrent TIAs, which resembled seizure-like clinical episodes. That’s why emergency physicians should be vigilant about the underlying causes of seizure-like activities, even if altered mental status similar to postictal state is present, especially if the patient does not have a history of seizures and the complaints are unclear. Keep the aortic dissection in mind as a differential. Also, I cannot stress the use of POCUS in the ED enough. It is a game-changer, and in our case, it detected a lethal disease successfully.

Learning Points

  1. Never ignore back pain that does not subside after adequate pain management.
  2. POCUS is always a game-changer. It saves a lot of time and lives, as in my case.
  3. Seizures or not, you must keep a high suspicion for lethal vascular diseases. Remember the basics: If unclear, go back to history.
  4. Once you confirm an aortic dissection, never delay treatment because time = life.
  5. Never ever send a patient back home unless you are completely sure about the cause of the presenting symptom. Over investigating is ok when compared to under investigating, when it might cost a life.

References and Further Reading

  1. Braverman AC. Acute aortic dissection: clinician update. Circulation. 2010;122(2):184-188. doi:10.1161/CIRCULATIONAHA.110.958975
  2. Debette S, Grond-Ginsbach C, Bodenant M, et al. Differential features of carotid and vertebral artery dissections: the CADISP study. Neurology. 2011;77(12):1174-1181. doi:10.1212/WNL.0b013e31822f03fc
[cite]

Question Of The Day #3

question of the day
question of the day 3

Which of the following is the most appropriate next step in management for this patient‘s condition?

Choice A (IV 1,000mL of 0.9% NaCl) is an isotonic crystalloid fluid helpful in a patient with depleted intravascular volume (i.e., dehydration). This patient is clinically dehydrated (dry oral mucosa and mild tachycardia); however, hypertonic 3% NaCl is a more appropriate initial treatment. Choice B (IV 50mL of 25g dextrose solution, or commonly known as “D50”) is an appropriate treatment for a patient with hypoglycemia. Checking a glucose level is a crucial part of the initial assessment of all patients with altered mental status, but this patient has a reported normal glucose level. Choice D (IV 40mg Furosemide) is a diuretic that would worsen this patient’s dehydration and acute kidney injury. This patient has severe hyponatremia along with neurological symptoms (coma and seizure). Hyponatremia plus neurologic symptoms, like vomiting, seizures, reduced consciousness, cardiorespiratory arrest, necessitate rapid correction of sodium with hypertonic (3%) NaCl solution. 3% NaCl solution can be infused 100-150mL over 15-20min and repeated up to 3 doses total. A serum sodium level should be measured after each administration of 3% NaCl in order to limit the increase in the sodium level to no more than 8-12 mEq/L over the first 24hours. This is done to reduce the risk of osmotic demyelination syndrome. Correct Answer: C

Reference

Petrino R, Marino R. Fluids and Electrolytes. “Chapter 17: Fluids and Electrolytes”. In: Tintinalli JE, Ma O, Yealy DM, Meckler GD, Stapczynski J, Cline DM, Thomas SH. eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 9th ed. McGraw-Hill.

[cite]

Triads in Medicine – Rapid Review for Medical Students

triads in medicine

One of the most convenient ways of learning and remembering the main components of disease and identifying a medical condition on an exam are Triads, and medical students/interns/residents swear by them.

Be it a question during rounds, a multiple-choice exam question to be solved, or even in medical practice, the famous triads help physicians recall important characteristics and clinical features of a disease or treatment in an instant.

Since exam season is here, this could serve as a rapid review to recall the most common medical conditions.

While there are a vast number of triads/pentads available online, I have listed the most important (high-yy) ones that every student would be asked about at least once in the duration of their course.

1) Lethal Triad also known as The Trauma Triad of Death
Hypothermia + Coagulopathy + Metabolic Acidosis

2) Beck’s Triad of Cardiac Tamponade
Muffled heart sounds + Distended neck veins + Hypotension

3) Virchow’s Triad – Venous Thrombosis
Hypercoagulability + stasis + endothelial damage

4) Charcot’s Triad – Ascending Cholangitis
Fever with rigors + Right upper quadrant pain + Jaundice

5) Cushing’s Triad – Raised Intracranial Pressure
Bradycardia + Irregular respiration + Hypertension

6) Triad of Ruptured Abdominal Aortic Aneurysm
Severe Abdominal/Back Pain + Hypotension + Pulsatile Abdominal mass

7) Reactive Arthritis
Can’t See (Conjunctivitis) + Can’t Pee (Urethritis) + Can’t Climb a Tree (Arthritis)

8) Triad of Opioid Overdose
Pinpoint pupils + Respiratory Depression + CNS Depression

9) Hakims Triad – Normal Pressure Hydrocephalus
Gait Disturbance + Dementia + Urinary Incontinence

10) Horner’s Syndrome Triad
Ptosis + Miosis + Anydrosis

11) Mackler’s Triad – Oesophageal Perforation (Boerhaave Syndrome)
Vomiting + Lower Thoracic Pain + Subcutaneous Emphysema

12) Pheochromocytoma
Palpitations + Headache + Perspiration (Diaphoresis)

13) Leriche Syndrome
Buttock claudication + Impotence + Symmetrical Atrophy of bilateral lower extremities

14) Rigler’s Triad – Gallstone ileus
Gallstones + Pneumobilia + Small bowel obstruction

15) Whipple’s Triad – Insulinoma
Hypoglycemic attack + Low glucose + Resolving of the attack on glucose administration

16) Meniere’s Disease
Tinnitus + Vertigo + Hearing loss

17) Wernicke’s Encephalopathy- Thiamine Deficiency
Confusion + Ophthalmoplegia + Ataxia

18) Unhappy Triad – Knee Injury
Injury to Anterior Cruciate Ligament + Medial collateral ligament + Medial or Lateral Meniscus

19) Henoch Schonlein Purpura
Purpura + Abdominal pain + Joint pain

20) Meigs Syndrome
Benign ovarian tumor + pleural effusion + ascites

21) Felty’s Syndrome
Rheumatoid Arthritis + Splenomegaly + Neutropenia

22) Cauda Equina Syndrome
Low back pain + Bowel/Bladder Dysfunction + Saddle Anesthesia

23) Meningitis
Fever + Headache + Neck Stiffness

24) Wolf Parkinson White Syndrome
Delta Waves + Short PR Interval + Wide QRS Complex

25) Neurogenic Shock
Bradycardia + Hypotension + Hypothermia

Further Reading

[cite]

Management of Status Epilepticus in ER

References and Further Reading

  1. Glauser T, Shinnar S, Gloss D, 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 Curr. 2016;16(1):48–61. doi:10.5698/1535-7597-16.1.48
  2. Joshua G. Kornegay.  Chapter 171. Seizures. In: Tintinalli JE, ed. Tintinalli’s Emergency Medicine A Comprehensive Study Guide. 8th Edition. McGraw-Hill Education; 2016: 1176-1178
  3. Rabin E, Jagoda AS. Chapter 92. Seizures. In: Walls RM, Hockberger RS, Gausche-Hill  M, eds. Rosen’s Emergency Medicine Concepts and Clinical Practice. 9th Edition. Philadelphia: Elsevier Saunders; 2018: 1256-1264
  4. Sharma AN, Hoffman RJ. Toxin-related seizures. Emerg Med Clin North Am. 2011;29(1):125–139. doi:10.1016/j.emc.2010.08.011

 

[cite]

Febrile Seizures

febrile seizures

A 20 Month-Old Male

It is a busy Wednesday afternoon in your pediatric emergency department. You work at a tertiary center, so you are used to receiving transfers from other hospitals for further evaluation and management. You see a new patient on the board. It is a 20 month-old male who came in as a hospital transfer for evaluation of first-time seizure. You go to bedside to start your evaluation. Parents tell you that he had three episodes of seizures in the past 6 hours. All of them lasted for less than 15 minutes, did not require medication for cessation, one of them was described as partial-focal and two were described as generalized tonic-clonic seizures, and the patient had complete return to baseline behavior a few minutes after each episode. Mom says that the patient had his axillary temperature taken by her at home and by the staff at the outside hospital and he had no fever on these measurements. However, she did notice some runny nose in the past 24 hours. As soon as the mom tells you that information, the nurse looks at you and says that the patient’s rectal temperature is 40.1 C.

Febrile Seizures

The first-step in the management of febrile seizures is to understand its definitions. Following that, we need to appropriately classify the patient’s presentation within one of the two types of febrile seizure.

Definition

  • Age greater than six-months-old and lower than five-years-old
  • Seizure in a patient with a temperature higher than 38 C
  • No inflammation or infection of the central nervous system
  • No metabolic abnormality that may cause seizures
  • No history of afebrile seizures

Two Types of Febrile Seizures

Class Age Number of seizures in 24h Duration Type of seizure Resolution Return to baseline
Simple
6 mo to 5 yo
1
< 15 min
No focal features
No meds required
Yes
Complex
6 mo to 5 yo
> 1
> 15 min
Focal features
Med required
No return to baseline in a reasonable time

You must note that you will be able to easily identify those patients who fit the criteria for simple febrile seizures and those who fit the criteria for complex febrile seizures. However, there will be a group of patients that fill one or two criteria for complex febrile seizure, but are extremely well-appearing. We will talk more about that later on during the discussion.

Workup

Simple Febrile Seizures

The evaluation of a child with a simple febrile seizure should focus on the underlying febrile illness. In the vast majority of the cases the cause for the fever will be a viral infection that does not require further evaluation and treatment other than some acetaminophen (paracetamol), ibuprofen, and oral hydration.

However, as part of your job, you need to think outside of the box and have a broad differential diagnosis for your patient’s presentation. Make sure to rule out signs of CNS infection (altered mental status, nuchal rigidity, petechial rashes, and prolonged, focal or multiple seizures); risk factors, symptoms, and signs of systemic conditions that could be causing a seizure; and, history of afebrile seizures. Special factors that increase the risk for CNS infections and that you should consider in your evaluation are age 6 -12 months with incomplete immunization status (Haemophilus influenzae type b (Hib) or Streptococcus pneumoniae) and pre-treatment with antibiotics for another disorder (which could mask meningitis).

Complex Febrile Seizure in Ill-Appearing Child

The workup in this situation is simple. The patient has meningitis until proven otherwise. You should consider starting antibiotics immediately and obtaining a full sepsis workup including complete blood cell count, urinalysis, urine culture, blood cultures, chest x-ray, and lumbar puncture for cerebrospinal fluid analysis. In addition to the infectious work-up, the differential also includes epileptic seizures, toxic ingestion, metabolic disorders, head trauma, and intracranial hypertension.

Complex Febrile Seizure in Well-Appearing Child

Now we reached the tricky part of the discussion. There are no consensus guidelines for the workup of patients with complex febrile seizures in the well-appearing child. As stated in the simple febrile seizure section, you should consider further workup if any concerns for CNS infection, systemic conditions causing seizures, or history of afebrile seizures. You should decide which workup to perform on a case by case basis. In a perfect scenario, these cases should be evaluated in conjunction with specialist consultation (e.g. with pediatric neurology) for guidance with work-up and treatment.

Case Resolution

After you finish your assessment, you make the diagnosis of complex febrile seizure because the patient had multiple seizures in less than 24 hours and had one episode with focal features. The patient is well-appearing, is fully vaccinated, has not used antibiotics recently, returns to baseline completely soon after an episode, and has no findings concerning for CNS infection on his exam. Therefore, you think that a CNS infection is less likely. Since you are facing a case of complex febrile seizure in a well-appearing child, you consult pediatric neurology for guidance with the workup and treatment. They agree with the low likelihood of CNS infection and recommend symptomatic treatment for the patient’s likely upper respiratory infection with observation during six hours in the ED. The patient has no problems during the period of observation. You re-discuss the case with pediatric neurology and they recommend discharge home with close follow-up on their clinic for further workup of other causes of seizure. A couple days later, you check the patient’s records and find that he had a spot EEG done, which was negative for epileptiform waves, and a brain MRI performed, which was unremarkable. Patient was diagnosed with complex febrile seizure and recommended to keep follow-up with his primary care physician with no need for further follow-up with pediatric neurology.

Take-Home Points

  • Always obtain a temperature from a core source, in the ED the most feasible source is a rectal temperature
  • The differential diagnosis for febrile seizures includes CNS infections, epileptic seizures, toxic ingestion, metabolic disorders, head trauma, and intracranial hypertension
  • There is no consensus about the workup and treatment of the well-appearing patient with a complex febrile seizure

References and Further Reading

  1. Festekjian A. Seizures and Status Epilepticus in Children. In: Cydulka RK, Fitch MT, Joing SA, Wang VJ, Cline DM, Ma O. eds. Tintinalli’s Emergency Medicine Manual, 8e New York, NY: McGraw-Hill; . http://accessemergencymedicine.mhmedical.com/content.aspx?bookid=2158§ionid=162271372. Accessed May 12, 2019.

  2. https://www.emrap.org/episode/kiddos/febrileseizures

  3. https://www.emrap.org/episode/c3seizuresin/seizuresin 

  4. John J Millichap. Clinical features and evaluation of febrile seizures. Mar 25, 2019. https://www.uptodate.com/contents/clinical-features-and-evaluation-of-febrile-seizures?source=history_widget

[cite]

A tongue bite after seizure

771 - new onset seizure - tong bite

A young man presented after a new onset seizure.

The image/video archive reached to 75K views, and we just added 52 new clinical images today. You can search, find the image you want and use them in your exams, presentations freely. Here is the link of the archive.

iEM Education Project Team uploads many clinical picture and videos to the Flickr and YouTube. These images are free to use in education. You can also support this global EM education initiative by providing your resources. Sharing is caring!

ICH

651.1 - ICH

Intracranial Hemorrhage chapter written by Nur-Ain Nadir and Matthew Smetana from USA is just uploaded to the Website!

Approach to Seizure

Seizure chapter written by Feriyde Caliskan Tur from Turkey is just uploaded to the Website!