First episode of seizure in a 10-year old

A 10-year-old girl, who was previously healthy, presented with her first episode of seizure. The night before, she was assessed in the Emergency Department (ED) for a 1-day history of decreased energy, vomiting, sore throat and tactile temperature and was discharged home in stable condition. Her seizure began at home with focal symptoms of right head and eye deviation, right arm extension, lip smacking and tongue clicking and progressed to generalized tonic-clonic movements that lasted for approximately 30 seconds. She was unresponsive and cyanotic. Her parents attempted chest compressions before paramedics arrived. En route, she received two doses of lorazepam, and became responsive, but was ataxic and confused on arrival in the ED. Her vital signs were as follows: heart rate 130 beats per minute, blood pressure 122/51 mmHg, respiratory rate 24 breaths per minute, oxygen saturation 96% on room air and she appeared well-perfused. In the ED, she subsequently had a second tonic-clonic seizure lasting one minute, during which she was cyanotic but well-perfused, stiff and nonresponsive. This was followed by persistent tongue fasciculations, tachycardia and intermittent desaturations. Her mental status remained altered and she did not respond to pain. She received midazolam, phenytoin and phenobarbital for presumed nonconvulsive status epilepticus and antibiotics for possible meningitis. Her serum glucose, electrolytes and computed tomography (CT) of the brain were normal. She was transferred to the Paediatric Intensive Care Unit, where she remained unresponsive. Twelve hours after the seizure in the ED, she was awake and could follow commands, but her level of consciousness continued to fluctuate and she had persistent agitation, confusion, ataxia and slurred speech. An electroencephalogram (EEG) showed mild, diffuse slowing with no epileptogenic activity. Cerebrospinal fluid (CSF) investigations and a magnetic resonance imaging (MRI) scan of the brain were normal. Serum acetylsalicylic acid (ASA) and acetaminophen, urine culture and blood culture were all negative. She remained tachycardic and hypertensive. Further investigations and history obtained later during the admission revealed the diagnosis. Due to her fluctuating level of consciousness, agitation and confusion, serum thyroid stimulation hormone (TSH), free thyroxine (T4) and triiodothyronine (T3) were done the day after admission and were < 0.02 mIU/L (normal range: 0.46 to 5.80 mIU/L), 73 pmol/L (normal range: 8.0 to 22.0 pmol/L) and 5.31 nmo/L (normal range: 0.9 to 2.9 nmol/L), respectively. Thyroglobulin was elevated at 117.0 pmol/L and antithyroglobulin and antithyroid peroxidase (TPO) antibodies were both negative. She did not have symptoms of hyperthyroidism prior to this presentation. It was discovered that prescription medications were missing from her home, including quetiapine, citalopram and 48 levothyroxine 175 mcg tablets. Presumably, the patient ingested these 2 days prior to her presentation, resulting in a total levothyroxine ingestion of 198 mcg/kg. The etiology of this patient’s seizures and persistent altered level of consciousness was determined to be hyperthyroidism, secondary to intentional ingestion of exogenous levothyroxine. Serotonin syndrome was considered in the context of this multidrug ingestion; however, the delayed symptom onset is unusual for that toxidrome and is most consistent with thyroid storm. Endocrinology recommended treatment with hydrocortisone to slow conversion of T4 to T3 and propranolol 80 mg every 8 hours for symptomatic tachycardia. After 7 days, her vital signs were normal and treatment was discontinued. She was transferred to Psychiatry for management of active suicidal ideation. At the time of discharge, her TSH and T4 were 1.58 mIU/L and 12.9 pmol/L, respectively. She was discharged in stable condition and was followed as an outpatient by her family physician and a community mental health team. Seizure is a known but rare symptom of thyroid storm. It is caused by an excess of T4 or T3 which may be endogenous or exogenous. Common symptoms include tachycardia, hypertension, hyperthermia, diaphoresis and agitation. In case series of paediatric patients who ingested thyroid hormone, the majority presented with only mild symptoms that did not require treatment (1,2). Among these patients, there was a significant range in the amount of thyroid hormone ingested and the serum concentration of T4 and TSH at presentation. A case report described an accidental ingestion of 700 µg/kg with a free T4 level > 100 pmol/L that did not result in seizures (3). Our patient had a smaller ingestion with a lower T4, reinforcing that dose and T4 levels do not correlate with the presence or severity of symptoms (1–4). Symptoms can be delayed for several days after ingestion (1–4). The literature describing seizures associated with thyroid storm in paediatrics addresses primarily endogenous thyrotoxicosis (5) and known, exploratory or unintentional ingestions in young children (4,6). In the adult literature, however, intentional ingestion of thyroid hormone has been reported, in suicide attempts and for weight loss. The patient in our case endorsed suicidality. To our knowledge, this is the first reported case of intentional levothyroxine overdose causing seizure in a paediatric patient. The pathophysiology of the association between thyrotoxicosis and seizure is poorly understood. It is postulated that T4 and T3 may lower the seizure threshold by directly affecting neurons and through increased dopaminergic activity. In addition to medical management of seizures with benzodiazepines and anticonvulsants, treatment with hydrocortisone may be effective because it reduces the peripheral conversion of T4 to T3. Methimazole, although not used in the case, may be helpful in treating underlying hyperthyroidism (5). Propranolol provides symptomatic management of adrenergic effects. Medical management of thyroid hormone ingestion is recommended for symptomatic patients. Conservative management with outpatient observation and follow-up is often appropriate for asymptomatic patients. Families should be counseled that there may be a delay in symptom onset after ingestion, so the patient should have easy access to emergency medical care. 1. Hyperthyroidism is a known cause of seizures, both focal and generalized, and should be considered in the differential of a first presentation of seizure. 2. Neither the amount of levothyroxine ingested nor serum T3, T4 or TSH concentrations correlate with the severity of symptoms, so repeated measurements after diagnosis are not useful. 3. For patients with fluctuating level of consciousness, it is important to consider undisclosed ingestions as a potential cause and to consider all medications and substances the child may have had access to, including those not commonly abused or ingested in excess.

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