Our patient exhibited lower motor neuron quadriparesis with no bladder or bowel problems. Flaccid quadriparesis can be caused by Guillain-Barre Syndrome, transverse myelitis, myasthenia gravis, tick paralysis, or botulism. There was no sensory impairment or bladder/bowel involvement, therefore transverse myelitis was ruled out clinically. In myasthenia gravis, there was no diurnal fluctuation, facial weakness, or eyelid drooping. 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 family history or previous such occurrence. Familial periodic paralysis, spontaneous periodic paralysis, and thyrotoxicosis periodic paralysis are the differential diagnosis. The diagnosis of thyrotoxicosis periodic paralysis was confirmed by elevated free T3 and T4 levels and a very low TSH value.
Hypokalemic periodic paralysis is a rare and possibly fatal illness that can be caused by a primary (familial) or secondary (environmental) cause. 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 (6).To exclude the primary causes, we couldn’t do a genetic test as it's not available in our country. TPP is widespread in Asian men, including Chinese, Japanese, Vietnamese, Filipinos, and Koreans, and Graves' disease is the most common cause of hyperthyroidism linked to TPP (7). TPP is less common, 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. (8). This illness primarily affects Asian men. Many persons with hyperthyroidism have no evident symptoms or indicators. Because the illness is uncommon in Caucasians, it is commonly misdiagnosed when it manifests(2).
A high-carbohydrate, high-salt diet, alcohol consumption, trauma, menses, infections, certain medications (e.g., steroids, diuretics, epinephrine, acetazolamide, and insulin), and strenuous exercise are all potential precipitating factors for hypokalemia and paralysis in patients with underlying thyrotoxicosis. Viral gastrointestinal infection and the usage of oral prednisone were discovered as plausible causes of our patient's paralysis episodes (9). Our patient ate a high carbohydrate meal before he slept.
Deaths from respiratory paralysis and heart failure have been reported, even though the condition is rarely life-threatening and rarely involves the cranial nerves. The paralysis normally goes away in 3–36 hours, in the reverse sequence in which it appeared. Serious morbidity, such as dysrhythmias, ventilator failure, and death, is uncommon (4).
TPP's pathophysiology is unclear. Membrane excitability and muscle contraction are controlled by sodium, chloride, calcium, and potassium channels on cell membranes. Any of these cellular transport mechanisms, particularly the potassium ion channel, can be disrupted, resulting in aberrant muscle contractility and paralysis. The main flaw 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 improve the activation of pump-action by b2-adrenergic agonists by increasing intracellular cAMP synthesis. Hyperinsulinemia is also seen in acute TPP attacks, and insulin release in response to oral glucose challenge is increased in TPP patients, implying that insulin plays a role in the pathophysiology of hypokalemia in TPP (10).
Aside from potassium supplements, acute TPP is treated by immediately reducing thyroid hormone levels. It's vital to remember that during the recovery period, the release of K and phosphate from the cells can contribute to rebound hyperkalemia. Intravenous K therapy for hypokalemia causes a faster response than oral supplements. Prophylactic potassium dosage between attacks has not been proved to be useful. Non-specific beta-blockers have been shown to reduce the frequency and severity of episodes. Hyperthyroidism can be controlled and even reversed to prevent attacks and muscle weakness. (11).