Low-dose oral propranolol for treatment of thyrotoxic periodic paralysis with hypokalaemia in the emergency department: A case report.

WHAT IS KNOWN AND OBJECTIVE: Thyrotoxic periodic paralysis (TPP) with hypokalaemia is a rare acute phenomenon. Reports of the use of high-dose non-selective ß-blockers describe symptom resolution, but often administration does not occur promptly enough in the treatment course and patients may experience overcorrection and hyperkalaemia. CASE DESCRIPTION: A 37-year-old Hispanic male developed TPP. Patient was successfully treated with low-dose oral propranolol and potassium supplementation with no overcorrection. WHAT IS NEW AND CONCLUSION: Delay in the administration of non-selective ß-blockers may lead to overcorrection of potassium with exogenous supplementation. Low-dose propranolol administered in the Emergency Department was successful in preventing overcorrection of potassium.

Parálisis periódica hipopotasémica tirotóxica: a propósito de un caso / Thyrotoxic hypokalemic periodic paralysis. A case report

La parálisis periódica hipopotasémica tirotóxica (PPT) es una rara complicación de la tirotoxicosis caracterizada por la aparición de episodios de debilidad muscular asociados a hipopotasemia en pacientes con hipertiroidismo, más frecuentemente con enfermedad de Graves-Basedow. El tratamiento con antitiroideos y suplementos de potasio revierte la sintomatología de debilidad muscular y evita la reaparición de estos síntomas (AU)

Thyrotoxic hypokalemic periodic paralysis is an uncommon complication of thyrotoxicosis, characterized by attacks of generalized muscular weakness associated with hypokalemia in patients with hyperthyroidism, most frequently with Graves-Basedow disease. Treatment with antithyroid drugs and potassium supplements reversed the symptoms and the episodes of acute muscular weakness did not reappear (AU)

Heparin-induced hyperkalemia in a patient diagnosed with thyroid storm.

OBJECTIVE: To describe a case of heparin-induced hyperkalemia and the role for transtubular potassium gradient (TTKG) to guide fludrocortisone therapy. CASE SUMMARY: A 52-year-old white male developed hyperkalemia after receiving intravenous unfractionated heparin (UFH) for atrial fibrillation during thyroid storm. Admission laboratory results were noteworthy for normal potassium levels, undetectable thyroid-stimulating hormone, and mild transaminitis. Treatment for thyroid storm was initiated but UFH was stopped because the international normalized ratio was subsequently found to be elevated. Rising potassium levels developed just 24 hours after UFH discontinuation, without exogenous potassium supplementation, renal dysfunction, or acidosis. A TTKG was low, reflecting a hypoaldosterone state. In addition, the Naranjo probability scale indicated probable medication-associated hyperkalemia. Heparin-induced hyperkalemia (HIH) was suspected and oral fludrocortisone 0.2 mg was given daily alongside serial TTKG measurements. TTKG and hyperkalemia normalized with 2 days of treatment. DISCUSSION: UFH is commonly used; therefore, clinicians must be cautious of hyperkalemia. Although HIH usually resolves after discontinuation of heparin, it may persist despite discontinuation of the drug, as highlighted by this case. In this setting, a TTKG should be determined, which can be used to guide fludrocortisone therapy. CONCLUSIONS: HIH can occur despite discontinuation of heparin, and TTKG can be helpful in guiding fludrocortisone treatment in this circumstance.

Two cases of thyroid storm-associated cholestatic jaundice.

OBJECTIVE: To describe the association of the rare and serious complication of jaundice with severe thyrotoxicosis, a potentially lethal endocrine disorder. METHODS: We report the clinical, laboratory, and pathologic findings of 2 cases of severe jaundice (total bilirubin levels: 35.2 mg/dL in case 1 and 42 mg/dL in case 2) associated with thyroid storm in the absence of a history of liver disease, thionamide exposure, or congestive heart failure. We also present other relevant reports available in the literature. RESULTS: Case 1 was a 38-year-old woman who presented with nausea, vomiting, fatigue, pruritus, and frequent nonbloody diarrhea. She was transferred to our institution because of worsening hyperbilirubinemia. Case 2 was a 35-year-old woman admitted to a community hospital with thyroid storm and jaundice. Upon transfer to our institution, the patient was unconscious, mechanically ventilated, and in atrial fibrillation. In case 2, liver biopsy results revealed diffuse hepatocellular ballooning with intrahepatic cholestasis with mild portal lymphocytic infiltration. Both patients presented with severe cholestatic jaundice in the absence of congestive heart failure; underlying liver disease (infectious or autoimmune); or previous exposure to thionamides, other hepatotoxic agents, or complementary and alternative medications. In both cases, jaundice responded to therapy with antithyroid medications. Both patients eventually underwent thyroidectomy with complete resolution of the jaundice. CONCLUSION: The data strongly suggest that in these patients, the hepatic dysfunction was primarily due to hyperthyroidism. These cases indicate that the mere presence of hyperbilirubinemia during severe thyrotoxicosis should not per se delay the use of potentially life-saving thionamides once a thorough evaluation for other causes of liver disease has been completed.

Effects of potassium supplementation on the recovery of thyrotoxic periodic paralysis.

Potassium supplements have been recommended to hasten recovery and prevent cardiopulmonary complications in patients with thyrotoxic periodic paralysis (TPP). However, this recommendation has not yet been proven efficacious. Thirty-two patients with acute attacks of TPP over a 3-year-period were divided into 2 groups. Group A (n = 12) was a control group treated with normal saline infusion 125 mL/hr only. Group B (n = 20) received intravenous KCl administration at a rate of 10 mmol/hr in normal saline 125 mL/hr. During the attack and for 6 hours after muscle recovery, hemodynamics were continuously recorded and muscle strength and plasma K(+) concentration were measured hourly. The sex, age, muscle strength, thyroid function, biochemical values including plasma K(+) levels, as well as the time from attack to therapy (3.6 +/- 1.6 v 3.3 +/- 1.0 hr) were not significant between the 2 groups. However, recovery time was significantly shorter in the KCl group than the control (6.3 +/- 3.8 v 13.5 +/- 7.5 hr, P < .01). Rebound hyperkalemia greater than 5.5 mmol/L occurred in 40% patients receiving KCl. The dose of KCl administered and peak K(+) concentration were positively correlated (r = 0.85, P < .001). In conclusion, KCl therapy proves to help the recovery of paralysis in TPP associated with rebound hyperkalemia. KCl supplementation should be given as small as possible (<10 mmol/hr) to avoid rebound hyperkalemia unless there are cardiopulmonary complications.

Duodenal obstruction in thyroid storm.

A 35-year-old, previously healthy woman, known to be thyrotoxic, was transferred from a community hospital for "acute abdomen." Abdominal pain, distention, and hyperemesis resolved with placement of nasogastric tube (NGT) and return of 2,600 mL of bilious fluid. Continued high NGT output made oral or NGT administration of antithyroid drugs impossible. We gave propylthiouracil (PTU) by retention enemas with therapeutic serum levels and sublingual saturated solution of potassium iodide (SSKI) with 70% absorption based on 24-hour free iodine urinary excretion. The patient's thyroxine (T4) and triiodothyronine (T3) radioimmunoassays were normal on hospital days 10 and 12, respectively. However, free T4 and T3 resin uptake did not normalize until hospital day 31. On hospital day 32, she tolerated removal of NGT without nausea and 4 days later was taking a regular diet. We conclude that our patient's gastrointestinal symptoms were a prominent feature of her thyrotoxicosis and that rectal PTU and sublingual SSKI are effective in administration of antithyroid drugs.

Rectal administration of iodide and propylthiouracil in the treatment of thyroid storm.

We administered potassium iodide and propylthiouracil per rectum, in conjunction with intravenous dexamethasone and propranolol, for emergent treatment of a patient in thyroid storm with small bowel obstruction. Shortly after initiation of this treatment, the patient successfully underwent two emergent surgical procedures for resection of an intestinal volvulus with advanced peritonitis. Serum levels of iodide and propylthiouracil showed substantial absorption of these drugs via the rectal route. Measurement of 24-h urinary-free iodide indicated that the bioavailability of potassium iodide delivered by retention enema was at least 40%. Parenteral iodide preparations have been unavailable in the past, and continue to be difficult to obtain emergently. Rectal administration of inorganic iodide is an effective, readily available and less expensive alternative to parenteral sodium iodide for patients in thyroid storm with upper gastrointestinal tract dysfunction.

[Thyrotoxic crisis after exposure to iodine. A case with fatal outcome]. / Thyreotoxische Krise nach Jodexposition. Ein Fall mit letalem Ausgang.

A 78-year-old woman is presented with a multinodular toxic goiter and euthyroidism under continuous low-dose treatment with antithyroid drugs. A period of hyperthyroidism had been documented 3 years previously. In the preoperative management, prior to resection of a benign ovarian tumour, an intravenous urogram was performed. Perchlorate was given for thyroid protection. One day after surgery the clinical signs of thyroid storm were observed. Immediately, high-dose antithyroid drug therapy was started. Nevertheless, the patient died of acute cardiovascular failure 3 days later. This case report focuses on the risk of thyroid storm following iodine excess in the presence of relevant functional thyroid autonomy without adequate thyroid protection.

Recurrence of 131I-induced thyroid storm after discontinuing glucocorticoid therapy.

A 19-year-old woman with Graves' disease developed thyroid storm 8 days after radioactive iodine therapy. The clinical manifestations of thyroid storm promptly improved after treatment with large doses of propylthiouracil, potassium iodide, propranolol hydrochloride, and dexamethasone. Four days after discontinuing dexamethasone, the syndrome recurred and was corrected by reinstitution of the glucocorticoid. We conclude that dexamethasone was an important adjunct for treating thyroid storm and was effective mainly by reducing peripheral triiodothyronine production.

[Do lithium salts have a place in the treatment of severe hyperthyroidism? (author's transl)]. / Les sels de lithium ont-ils leur place dans le traitement des hyperthyroïdies graves?

In a patient with hyperthyroidism resulting in cachexia, severe cardiac complications and functional renal failure, and a second case of hyperthyroidism refractory to carbimazole as a result of iodine overload, the administration of 1 to 3 g of lithium gluconate every 1 to 3 days, in association with carbimazole, led to persistent clinical and biological improvement in 8 to 16 days. In the first case, the course was complicated by neurological intolerance (blood lithium 0.98 mEq/l) which responded to the temporary interruption of treatment and by a transient escape of thyroid function from the effects of lithium which disappeared after a slight adjustment in the dose. In the second case, the course under treatment was favourable from the outset. Thus in forms of hyperthyroidism in which usual forms of treatment are inadequate and where there is a risk of "acute crises", lithium may be valuable as adjuvant therapy. If the dose is regularly modified in order to obtain a daily blood lithium level of less than 0.60 mEq/l, and on condition of close clinical, electrocardiographic and ionic surveillance, cardiac and renal failure and neuropsychiatric disturbances do not prevent the use of lithium, which the authors feel to be of irreplaceable value.