Relevant past medical history and interventions of a 14-year-old Saudi boy whose medical history was irrelevant.
| Dates | Summaries from Initial and Follow-up Visits | Diagnostic Testing (including dates) | Interventions |
|---|---|---|---|
| Intial at presentation | Presented to the emergency room with sudden-onset paralysis. The patient had gone to bed at 11 p.m. with no weakness and woke up at 6 a.m. unable to move his lower extremities. This was associated with mild pain but no paresthesia; however, during the day, his upper extremities were involved. The weakness was bilateral and involved both the proximal and distal muscles of both the upper and lower limbs. | potassium level, 1.3 mmol/L (reference range: 3.5–5.5 mml/L); sodium, blood urea nitrogen, creatinine, and creatine phosphokinase were all within normal laboratory ranges. Complete blood count, coagulation profile, and liver enzyme tests showed normal findings. ECG= classical finding of low K, normal CT brain | Received Intravenous potassium |
| Intial at presentation | Follow-up visits: - After IV potassoium, patient’s neurologic symptoms had completely resolved once serum potassium level normalized | Follow-up studies were performed to determine the etiology of hypokalemia. Urine electrolytes, serum electrolytes, serum aldosterone, and renin levels were measured to rule out adrenal involvement; the results were normal. Thyroid panel results were also normal. Whole exome sequencing revealed a heterozygous pathologic variant in the CACNA1S gene | -Parental fluid therapy and electrolytes without dextrose, which resulted in the improvement of his symptoms. Oral acetazolamide was administered, and he was discharged |
| 2 months later | - The patient was readmitted 2 months after his discharge from the emergency room with the same signs and symptoms | ||
| Few months later | Final outcome for this episode of care. He was examined during two subsequent follow-up visits and did not report new episodes of paralysis |