Our patient exhibited lower motor neuron quadriparesis with no bladder or bowel problems in association with severe hypokalemia and biochemical thyrotoxicosis, consistent with the diagnosis of THPP. Flaccid quadriparesis can also be caused by Guillain-Barre Syndrome, transverse myelitis, myasthenia gravis, tick paralysis, or botulism. There was no sensory impairment or bladder/bowel involvement in our patient, therefore transverse myelitis was ruled out. Typical clinical features of myasthenia gravis such as diurnal fluctuation of weakness, facial weakness, or eyelid drooping were absent. There were no symptoms of botulism like fever or food poisoning. The patient was first suspected of having Guillain-Barre syndrome, but an arterial blood gas (ABG) showed hypokalemia with a normal pH. The patient denied any personal or family history of such occurrence of paralysis. Familial periodic paralysis, spontaneous periodic paralysis, and THPP are other differential diagnoses in our patient. The diagnosis of THPP was confirmed following thyroid function test showing biochemical thyrotoxicosis in association with severe hypokalaemia and paralysis.

Hypokalemic periodic paralysis is a rare and can be either primary (familial) or secondary (environmental). Hyperthyroidism and a variety of other disorders, such as hyperaldosteronism, diabetic ketoacidosis, nephrotic syndrome, medications, acute tubular necrosis, laxative or diuretic usage, diarrhea, and vomiting, are examples of secondary causes [7]. To exclude the primary causes (familial periodic paralysis), we couldn’t do a genetic test as it is not available in our country. THPP is common in Asian men, including Chinese, Japanese, Vietnamese, Filipinos, and Koreans, and Graves’ disease is the most common cause of hyperthyroidism associated with THPP [8]. THPP is an uncommon condition, so additional diagnoses such as familial hypokalemic periodic paralysis, myasthenia gravis, Guillain-Barre Syndrome, viral and inflammatory myopathies, transverse myelitis, cord compression, and other electrolyte abnormalities should be evaluated. These causes can be ruled out based on the history, physical examination, and other tests [9]. Many patients with THPP have no overt symptoms or signs of thyrotoxicosis. Because the condition is uncommon in non-Asian populations, it is commonly misdiagnosed [2].

A high-carbohydrate, high-salt diet, alcohol consumption, trauma, menstrual cycle, infections (including viral gastroenteritis), certain medications (e.g., steroids, diuretics, epinephrine, acetazolamide, and insulin), and strenuous exercise are potential precipitating factors for THPP in patients with underlying thyrotoxicosis [10]. Our patient had a high carbohydrate meal before he slept.

Deaths from respiratory paralysis and heart failure have been reported in THPP, even though the condition is rarely life-threatening and rarely involves the cranial nerves. The paralysis usually resolves in 3–36 h, in the reverse sequence in which it appeared. Serious morbidity, such as dysrhythmias, ventilator failure, and death, is uncommon [4].

The pathophysiology of THPP remains unclear. Membrane excitability and muscle contraction are controlled by sodium, chloride, calcium, and potassium channels on cell membranes. Disruption of any of these cellular transport mechanisms, particularly the potassium ion channel, can result in aberrant muscle contractility and paralysis. The main defect in THPP is a rapid increase in intracellular potassium. This is related to genetic abnormalities in the Na+/K + ATPase pump in the majority of instances [4]. Thyroid hormone stimulates Na+–K + ATPase in skeletal muscle via genomic mechanisms that work on thyroid hormone-responsive regions to upregulate the transcription of the Na+–K + ATPase gene, as well as nongenomic mechanisms that raise the pump’s intrinsic activity or facilitate membrane insertion. Hyperthyroidism may enhance the activation of pump-action by b2-adrenergic agonists by increasing intracellular cAMP synthesis. Hyperinsulinemia is also seen in acute THPP attacks, and insulin release in response to oral glucose challenge is increased in patients with THPP, implying that insulin plays a role in the pathophysiology of hypokalemia in THPP [1].

Aside from potassium supplements, acute THPP is treated by immediately reducing thyroid hormone levels. It is vital to remember that during the recovery period, the release of potassium and phosphate from the cells can contribute to rebound hyperkalemia. Intravenous potassium therapy for hypokalemia causes a faster response than oral supplements. Prophylactic potassium dosage between attacks has not been proven to be useful. Non-specific beta-blockers have been shown to reduce the frequency and severity of episodes. Hyperthyroidism should be controlled to prevent attacks of muscle weakness [10]. Only a few cases of THPP have been reported from African populations [11].