Thyrotoxic periodic paralysis after urethral dilatation

Abstract

Thyrotoxic periodic paralysis (TPP) is a rare and serious manifestation of thyrotoxicosis that causes flaccid paralysis. In severe cases, it can be life-threatening due to respiratory failure and cardiac arrhythmias. TPP is due to increased sodium/potassium ATPase activity during thyrotoxic states, which is due to mutations encoding potassium channels. It is precipitated by situations that cause a surge in catecholamines, insulin, or both. It can be treated with potassium supplementation and nonselective beta blockers, and it can be prevented by establishing euthyroid state. With the increasing numbers of outpatient procedures performed nowadays and the stress related to these procedures, patients with TPP may develop paralysis after these procedures, so clinicians should be aware of this condition and the importance of identifying it in patients presenting with flaccid paralysis.

Early to recognize and Early to recover: A case series on Thyrotoxic periodic paralysis

“…Likewise, hyperthyroidism increases tissue responsiveness to beta-adrenergic stimulation, which is linked to enhanced Na-K ATPase activity [5]. In addition to catecholamine surge during the early morning, another feature contributing to periodic paralysis is potassium influx into skeletal muscles at night followed by exercise-induced potassium efflux during day time [11].…”

Intravenous Iodinated Contrast Induced Thyrotoxic Periodic Paralysis: A Case Report

“…Other causes include toxic multinodular goiter, thyroiditis, or iodine-induced thyrotoxicosis [ 4 ]. It is more common in people of Asian descent and following a carbohydrate-rich meal, which results in an increase in the insulin level [ 5 , 6 ]. Patients tend to present during early morning hours, as a catecholamine peak occurs during this time [ 3 ].…”

“…The cardinal finding is hypokalemia and the culprit in this case is thought to be a rise in thyroid hormone levels [ 7 , 8 ]. The severity of the weakness correlates with the degree of hypokalemia [ 5 , 7 ]. During thyrotoxicosis, there is an increase in transcription of Na/K ATPase pumps as well as increased activity through two mechanisms: directly by thyroid hormones and via the resulting increased B2-adrenergic receptor sensitivity [ 4 , 7 , 9 ].…”

“…No reported transient paralysis was noted in the patient's family history. In addition, hypomagnesemia and hypophosphatemia tend to occur in TPP only due to intracellular shift from a catecholamine increase [ 4 , 5 ]. The initial laboratory findings for our patient did not include magnesium test but his phosphate was low.…”

“…The initial laboratory findings for our patient did not include magnesium test but his phosphate was low. Patients with TPP also tend to have a preserved acid-base balance as well as low creatinine [ 5 , 7 ]. In our patient, the anion gap was elevated while the bicarbonate level was normal.…”