Algunos elementos de interés acerca del diagnóstico y tratamiento de la tormenta tirotóxica / Some elements of interest about the diagnosis and treatment of thyrotoxic storm

Introducción: La tormenta tirotóxica se produce por la liberación repentina y rápida de hormonas tiroideas al torrente sanguíneo. Constituye la complicación más peligrosa de la tirotoxicosis. Objetivo: Describir los principales elementos de interés acerca del diagnóstico y del tratamiento de la tormenta tirotóxica. Métodos: Se utilizaron como motores de búsqueda los correspondientes a las bases de datos Google Académico, Pubmed y SciELO. Las palabras clave utilizadas fueron: tormenta tirotóxica, tormenta tiroidea, tirotoxicosis, hipertiroidismo, diagnóstico y tratamiento. Se evaluaron y se incluyeron los trabajos de revisión, de investigación y las páginas web que tuvieran menos de 10 años de publicados y que por el título trataban el tema de estudio. Fueron excluidos los artículos que no estuvieran en idioma español, portugués o inglés. En total 34 artículos fueran referenciados. Conclusiones: El diagnóstico es eminentemente clínico y se realiza por la detección de factores desencadenantes. Se suma la exacerbación del cuadro clínico de tirotoxicosis previamente existente, el cual afecta a varios sistemas del organismo como consecuencia del aumento de las hormonas tiroideas circulantes. Lo ideal es prevenir la tormenta tirotóxica, aunque ya establecido el tratamiento no se debe retrasar la terapia de la causa desencadenante y de la causa específica. Deberá estar encaminada a reducir la síntesis y la secreción de las hormonas tiroideas y a minimizar las acciones periféricas de estas. Deberán emplearse diferentes fármacos y otras medidas terapéuticas para tratar las complicaciones sistémicas para complementar el tratamiento(AU)

Introduction: Thyrotoxic storm is caused by the sudden and rapid release of thyroid hormones into the bloodstream. It is the most dangerous complication of thyrotoxicosis. Objective: Describe some elements of interest about the diagnosis and treatment of thyrotoxic storm. Methods: Search engines corresponding to Google Scholar, Pubmed and SciELO databases were used. The keywords used were: thyrotoxic storm; thyroid storm; thyrotoxicosis; hyperthyroidism; diagnosis and treatment. The review papers, research papers and web pages, which in general, had less than 10 years of publication and that by the title dealt with the subject of study were evaluated and included. Articles that were not in Spanish, Portuguese or English were excluded. A total of 34 articles were referenced. Conclusions: The diagnosis is eminently clinical and is made by the detection of triggers, to which is added the exacerbation of the clinical picture of thyrotoxicosis previously existing, which affects several systems of the body as a result of the circulating thyroid hormones increase. The ideal is to prevent the thyrotoxic storm; although if the treatment is already established, the therapy of the triggering cause and the specific cause should not be delayed. It should be aimed at reducing the synthesis and secretion of thyroid hormones and minimizing their peripheral actions. Different drugs and other therapeutic measures should be used to treat systemic complications to complement treatment(AU)

Hipertiroidismo en personas mayores de 65 años: serie de casos de un hospital universitario / Thyrotoxicosis in the elderly: case series report from a university hospital

Introducción: En Chile en las últimas décadas ha aumentado la población de personas mayores de 65 años. La tirotoxicosis en este grupo está asociada a complicaciones como fibrilación auricular (FA), insuficiencia cardiaca (ICC), osteoporosis y aumento de la mortalidad. En algunos casos puede presentarse con síntomas no específicos, cuadro conocido como hipertiroidismo apático. Objetivos: Evaluar las características clínicas de la tirotoxicosis en personas mayores. Método: Serie de casos retrospectiva. Se analizaron fichas clínicas de pacientes mayores de 65 años con el diagnóstico de tirotoxicosis controlados en nuestro centro entre enero de 2012 y mayo de 2018. Resultados: En el periodo estudiado 54 pacientes fueron diagnosticados de tirotoxicosis. Se excluyen 4 por datos incompletos. El 80% corresponden a mujeres. La mediana de edad fue 71 años (rango 65-94), sin diferencias por género (p=0,61). La etiología más frecuente fue enfermedad de Graves (EG) en 64%, seguido por bocio multinodular hiperfuncionante en 20%, adenoma tóxico en 10% y asociada a fármacos en 6%. De los pacientes con EG, 28% presentó orbitopatía distiroidea (OD) clínicamente evidente. Un 30% se diagnosticó en contexto de baja de peso, deterioro cognitivo o patología cardiovascular, sin presentar síntomas clásicos de hipertiroidismo. Un 16% presentó FA, 14% ICC y 6% fractura osteoporótica. El 28% fue diagnosticado durante una hospitalización o requirió ser hospitalizado durante los meses siguientes. Los mayores de 75 años presentan una mayor probabilidad de hipertiroidismo apático (OR 5,1, IC95% 1,15-22,7 p=0,01). Además, las complicaciones aumentan en mayores de 75 años, encontrándose en este grupo todos los casos de FA. Conclusiones: La etiología más común de tirotoxicosis fue la EG, a diferencia de lo reportado en otras poblaciones. Un número importante de pacientes debutó sin síntomas clásicos de hipertiroidismo, principalmente mayores de 75 años, por lo que se debe tener una alta sospecha en este grupo etario.

Introduction: Hyperthyroidism in the elderly can produce severe complications such as atrial fibrillation (AF), heart failure (CHF) and osteoporosis. In the elderly, thyrotoxicosis may have only nonspecific symptoms, known as apathetic hyperthyroidism. Objective: To evaluate the clinical characteristics of thyrotoxicosis in the elderly. Methods: Retrospective case series. We reviewed clinical records of patients with thyrotoxicosis older than 65 years, between January 2012 and March 2019. Results: During this period, 54 patients were diagnosed with thyrotoxicosis. Four patients were excluded due to incomplete data. 80% were women. The average age was 73 years (range 65-94), without age difference between gender (p=0,61). The most frequent etiology was Graves' disease in 64%. Hyperfunctioning multinodular goiter was confirmed in 20%, toxic adenoma in 10% and drug-associated in 6%. Twenty eight percent of Graves' disease patients had dysthyroid orbitopathy. Thirty percent presented as apathetic hyperthyroidism. Sixteen percent of the patients presented AF, 14% CHF, and 6% osteoporotic fracture. Twenty-eight percent were diagnosed during hospitalization or required hospitalization in the following months. Those older than 75 years had a greater probability of presenting apathetic hyperthyroidism (OR 5.1, 95% CI 1.15- 22.7 p=0.01). Complications increase in this age group, with all cases of AF. Conclusions: The most common etiology of thyrotoxicosis in this group was GD. This differs from other populations. A significant number of patients presented without classic symptoms of hyperthyroidism, especially in people older than 75 years. Special attention should be paid to atypical symptoms of hyperthyroidism in this group.

La cirugía en el tratamiento de la crisis tirotóxica / Surgery for the Treatment of Thyrotoxic Crisis

RESUMEN La crisis tirotóxica es una complicación de la tirotoxicosis mal tratada y se asocia con una elevada mortalidad. Requiere tratamiento médico urgente en unidades de cuidados intensivos. Mujer de 42 años, con antecedentes personales de hipertensión arterial y nódulo tiroideo hiperfuncionante desde hace 18 años, con abandono del tratamiento médico hace dos años, que acude a urgencias con disnea paroxística nocturna, taquicardia, hipertensión arterial, gran bocio y anasarca. Ingresa en la unidad de cuidados intensivos con diagnóstico de crisis tirotóxica e inicia el tratamiento médico con medidas de soporte precisas, la que incluye intubación orotraqueal. Debido a la dificultad de manejo clínico y respiratorio de la paciente, se decide realizar tratamiento quirúrgico urgente. Se practica una tiroidectomía total de bocio multinodular parcialmente intratorácico y una traqueostomía preventiva. El resultado de anatomía patológica fue: bocio multinodular tóxico. La paciente fue dada de alta con función tiroidea normal, cierre de traqueostomía y buena fonación, tras mes y medio de hospitalización. A pesar de que un tratamiento médico conservador es el adecuado de la tirotoxicosis, los síntomas y signos sistémicos de la crisis tirotóxica y sus manifestaciones órgano-específicas, asociados a una persistente dificultad respiratoria por síntomas compresivos derivados del gran bocio, se consideró que la tiroidectomía urgente en este caso estaba indicada, dato que se corroboró ante la buena evolución posoperatoria. El tratamiento de la tirotoxicosis es fundamentalmente clínico, sin embargo, la cirugía puede ser útil ante la dificultad en el manejo clínico(AU)

Abstract The thyrotoxic crisis is a complication of poorly treated thyrotoxicosis and is associated with high mortality. This condition requires urgent medical treatment in intensive care units. A 42-year-old woman, with a personal history of high blood pressure, hyperfunctioning thyroid nodule for 18 years, and abandonment of medical treatment since two years ago, presented to the emergency department with paroxysmal nocturnal dyspnea, tachycardia, high blood pressure, large goiter, and anasarca. She was admitted into the intensive care unit with a diagnosis of thyrotoxic crisis and started to receive medical treatment under precise support measures, including orotracheal intubation. Due to the patient's difficult clinical and respiratory management, it was decided to perform urgent surgical treatment. She was performed a total thyroidectomy of partial intrathoracic multinodular goiter and a preventive tracheostomy. The result of pathological anatomy was toxic multinodular goiter. The patient was discharged with normal thyroid function, tracheostomy closure, and good phonation, after a month and a half of hospitalization. Despite the fact that conservative medical treatment is the adequate one for thyrotoxicosis, the systemic symptoms and signs of the thyrotoxic crisis, and its organ-specific manifestations, associated with persistent respiratory distress due to compression symptoms derived from large goiter, urgent thyroidectomy needed to be indicated in this case, a fact corroborated after good postoperative evolution. The treatment of thyrotoxicosis is fundamentally clinical; however, surgery can be useful given the difficulty in clinical management(AU)

The multiple effects of thyroid disorders on bone and mineral metabolism / Os múltiplos efeitos das disfunções tireoidianas sobre o metabolismo osteomineral

Differently from most hormones, which commonly are specialized molecules able to influence other cells, tissues and systems, thyroid hormones (TH) are pleiotropic peptides, whose primordial function is difficult to identify. The complex action of TH on human economy can be easily witnessed by examining the diverse consequences of TH excess and deficiency during development and after maturity. In particular, different manifestations in bone modeling and remodeling reflect the circumstantial consequences of thyroid disturbances, which are age dependent. While hyperthyroidism during childhood enhances bone mineralization and accelerates epiphyseal maturation, in adults it induces bone loss by predominant activation of osteoclast activity. Furthermore, the syndrome of TH resistance is a multifaceted condition in which different sites exhibit signs of hormone excess or deficiency depending on the configuration of the TH receptor isoform. The investigation of the impact of TH resistance on the skeleton still remains to be elucidated. We present here a thorough review of the action of TH on bone and of the impact of thyroid disorders, including hyper- and hypothyroidism and the syndrome of TH resistance, on the skeleton.

Diferentemente da maioria dos hormônios, que usualmente são moléculas especializadas capazes de influenciar outras células, tecidos e sistemas, os hormônios da tireoide (HT) são peptídeos pleiotrópicos, cuja função primordial é difícil de identificar. A ação complexa dos HT na fisiologia humana pode ser facilmente reconhecida ao observar as diversas consequências do excesso e da deficiência de HT durante e após o pleno desenvolvimento. Em particular as diferentes manifestações na modelação e remodelação óssea refletem que as consequências esqueléticas das disfunções tireoidianas dependem das circunstâncias e variam com a idade. Enquanto o hipertireoidismo durante a infância aumenta a mineralização óssea e acelera a maturação epifisária, em adultos induz a perda óssea pela ativação predominante da ação osteoclástica. Além disso, a síndrome de resistência ao HT é uma condição multifacetada na qual diferentes tecidos apresentam sinais de excesso ou deficiência hormonal, dependendo da predominância da expressão das diversas isoformas do receptor de HT. O impacto da resistência ao HT sobre o esqueleto ainda é motivo de investigação. Apresentamos aqui uma revisão abrangente sobre as ações ósseas dos HT e o impacto no esqueleto dos distúrbios da tireoide, incluindo hipo e hipertireoidismo e síndrome de resistência ao HT.

An Interesting Case of Thyrotoxicosis with Choreoathetosis - A Rare Association.

Thyrotoxicosis may present with spectrum of movement disorders. Though tremor is most frequently associated, chorea has also been reported rarely. A rare case of thyrotoxicosis in a young female presenting with choreoathetotic movement is reported here. The choreoathetotic movement in this case was attributed to thyrotoxicosis based on clinical and biochemical criteria after exclusion of other causes.

Icterícia grave e miocardiopatia tireotóxica com trombo atrial / Serious jaundice and thyrotoxic myocardiopathy with atrial thrombus

Icterícia relacionada à tireotoxicose, e não como efeito das drogas antitireoidianas, é uma complicação rara que, em geral, ocorre na presença de insuficiência cardíaca (IC) ou hepatite. Apresentamos o caso de mulher de 54 anos de idade, branca, diagnóstico de hipertireoidismo por doença de Graves com icterícia associada a despeito da suspensão prévia de metimazol. A bilirrubina oscilava em valores elevados entre 30,0 e 52,3 mg/dL, as transaminases eram pouco elevadas com valores de ALT, na admissão, de 46 U/I e AST de 87 U/I; coagulograma e proteínas encontravam-se no limite inferior da normalidade, sendo TAP 68% e albumina = 2,5 g/dL. Sorologias para hepatites foram negativas. Após a primeira dose de radioiodoterapia (RT), a bilirrubina atingiu seu valor máximo, que coincidiu com período de pior exacerbação da IC. A bilirrubina normalizou-se após quatro semanas da segunda dose de RT com a estabilização da IC e a normalização dos hormônios tireoidianos. Discutimos as possíveis etiologias de icterícia severa em pacientes hipertireoideos, assim como a difícil terapia anticoagulante com varfarina.

Jaundice related to thyrotoxicosis and not as an effect of antithyroid drugs is a rare complication that usually occurs in the presence of heart failure (HF) or hepatitis. We report a case of a 54-year-old white woman with hyperthyroidism caused by Graves's disease and jaundice despite methimazole suspension. Bilirubin fluctuated at high values, between 30.0 and 52.3 mg/dL, transaminases were slightly increased, on admission ALT = 46 U/L and AST = 87 U/L; coagulation indices and serum proteins were on the lower limit of the normal range with PT 68% and albumin = 2.5 g/dL. Serology for hepatitis was negative. After the first radioiodine therapy (RT), bilirubin reached its maximum, which coincided with the worst period of HF exacerbation. Bilirubin normalized 4 weeks after the second RT, with the stabilization of HF and normalization of thyroid hormones. We discuss the possible etiologies of severe jaundice in hyperthyroid patients, as well as the difficult anticoagulant therapy with warfarin.

Thyrotoxic myo-neuropathy.

Myopathy is an important complication of thyrotoxicosis. Neuropathy is a less commonly reported complication, and is often subclinical. Here we report a patient of throtoxic myopathy with sub-clinical entrapment neuropathy. This case is reported to emphasise the importance of NCV to look for neuropathy.

Bone disease in thyrotoxicosis.

Thyrotoxicosis, a clinical syndrome characterized by manifestations of excess thyroid hormone, is one of the commonly-recognised conditions of the thyroid gland. Thyrotoxicosis causes acceleration of bone remodelling and though it is one of the known risk factors for osteoporosis, the metabolic effects of thyroxine on bone are not well discussed. Studies show that thyroid hormones have effects on bone, both in vitro and in vivo. Treatment of thyrotoxicosis leads to reversal of bone loss and metabolic alterations, and decreases the fracture risk. There are limited studies in India as to whether these changes are fully reversible. In this review we discuss about the effects of thyrotoxicosis (endogenous and exogenous) on bone and mineral metabolism, effects of subclinical thyrotoxicosis on bone and mineral metabolism and effects of various forms of treatment in improving the bone mineral density in thyrotoxicosis.

Psicose associada à tireotoxicose: relato de caso / Psychosis associated with thyrotoxicosis: a case report

Pacientes com tireotoxicose podem cursar com alterações psiquiátricas como depressão, mania ou psicose aguda. O objetivo deste trabalho é relatar o caso de paciente com sintomatologia psiquiátrica como manifestação de hipertireoidismo. O diagnóstico correto foi feito após anamnese e exame físico e investigação laboratorial que incluiu a função tireoidiana. Foi realizada breve revisão bibliográfica sobre a ocorrência de alterações psiquiátricas associadas à tireotoxicose. O diagnóstico de doença tireoidiana deve ser considerado sempre diante de alterações classificadas como psiquiátricas agudas.

Patients with thyrotoxicosis may suffer from psychiatric disorders, such as depression, mania or acute psychosis. This paper aims at reporting on the case of a patient with psychiatric symptomatology as manifestation of hyperthyroidism. The correct diagnosis built on physical examination and anamnesis, as well as laboratory examination including thyroid function tests. A brief review of the literature is also reported to gain a better understanding of the occurrence of psychiatric disorders associated to thyrotoxicosis. As this paper shows, diagnosis of thyroid diseases should also account for acute psychiatric disorders.

Thyrotoxic periodic paralysis: a case report and literature review

We describe a 19-year-old girl with a 3-month history of episodic muscular weakness, involving mainly lower limbs. Hypokalemia was documented in one episode and managed with intravenous potassium chloride. Hyperthyroidism was diagnosed 3 months after onset of attacks because of the mild symptoms. The patient was subsequently diagnosed as having thyrotoxic periodic paralysis associated with Graves' disease. Treatment with propranolol and methimazol was initiated and one year later underwent near total thyroidectomy

Autoimmune thyrotoxicosis with achalasia cardia.

We report a case of autoimmune thyrotoxocosis in an 11-year-old boy with achalasia cardia. This case explores autoimmunity as an etiological factor for achalasia based on several autoimmune conditions that have been associated with it.

Thyrotoxic periodic paralysis in a Saudi patient complicated by life threatening arrhythmia

Thyrotoxic periodic paralysis [TPP] is rare in non-Orientals, and sporadic case reports were reported world-wide. Eight cases were reported in Arabs, including 3 Saudis. We present an additional case of TPP in a 38-year-old Saudi man, and review the literature on TPP in Arabs. Our patient presented with complete flaccid quadriplegia, 5 weeks after he was diagnosed with Graves' disease that was treated with carbimazole and propranolol. He was hyperthyroid, and his potassium was extremely low [1.5 mmol/L]. During initial evaluation in the emergency room, he developed transient asystole manifested by syncope. He was resuscitated and his hypokalemia was corrected, and he had a full recovery. This case emphasizes the notion that TPP can occur in patients of any ethnic background. The development of serious cardiac complications in our patient underscores the importance of early and correct diagnosis of this potentially life-threatening complication of hyperthyroidism

A Case of Moyamoya Disease in a Girl with Thyrotoxicosis

Moyamoya disease is a cerebrovascular disorder of unknown cause, characterized by slowly progressive bilateral stenosis or occlusion of the internal carotid arteries and produces collateral vessels. Moyamoya syndrome has rarely been reported in association with Graves' disease, especially in children. Several reports suggest that a cerebral infarction might have occurred in patients with clinical and laboratory evidence of hyperthyroid function. We report a case of Moyamoya disease in a girl with Down syndrome and thyrotoxicosis, and we review the relevant literature. To our best knowledge, this is the first report of Moyamoya disease associated with thyrotoxicosis in a young person in Korea.

Hypokalemic periodic paralysis as a manifestation of thyrotoxicosis.

OBJECTIVE: To study the clinical characteristics of patients who suffer from hypokalemic periodic paralysis, as the presenting symptoms of thyrotoxicosis. MATERIAL AND METHOD: A retrospective review of 29 patients who presented with the syndrome of hypokalemic periodic paralysis as the symptom of thyrotoxicosis at Ratchaburi Hospital between January 1,1995 and December 31, 2007. Patients'data, diagnosis, blood chemistry, and thyroid function test were collected from medical records. RESULTS: All patients exhibited muscle weakness for a duration of one to two days, while all patients with hypokalemic periodic paralysis were determined to have high serum thyroid hormone and diagnosed with thyrotoxicosis. Patients with hypokalemic periodic paralysis were the first symptom leading to diagnosis of thyrotoxicosis. The attack of weakness occurred during the night in all patients. The patients, 96.6% being male, showed improvement of their symptoms through potassium replacement and thyrotoxicosis treatment using propylthiouracil and non selective beta adrenergic blocker All patients recovered and did not demonstrate reoccurring hypokalemic periodic paralysis. The degree of muscle weakness was found to correlate significantly (p < 0.05) with level of serum potassium, magnesium, and duration of weakness. CONCLUSION: It is important to determine blood thyroid hormone in all patients with hypokalemic periodic paralysis.

Thyrotoxic periodic paralysis.

A young man of 30 yrs got himself admitted in Bangabandhu Sheikh Mujib Medical University (BSMMU) Hospital, Dhaka, Bangladesh with the complaints of suddenly developed weakness in his all four limbs. He had features of hyperthyroidism and he gave the history of similar attacks of weakness in his all four limbs in the previous months. His potassium was in the lower part of the normal range and his T4 and T3 were elevated but TSH was markedly low. He was diagnosed as a case of thyrotoxic periodic paralysis on the basis of clinical and biochemical findings. After treatment with carbimazole, propranolol and potassium replacement, patient's condition improved dramatically.

Fatal thyrotoxic periodic paralysis with normokalemia.

We present a 10-year-old girl who presented to our emergency services with difficulty in breathing of 2-days duration and progressive weakness of a month's duration. In a previous admission elsewhere, she had not been detected to have hyperthyroidism or electrolyte abnormalities. On admission, the child was in hypercapnic respiratory failure with tachycardia and hepatomegaly. A small goiter as well as signs of thyrotoxicosis were present. Laboratory investigations showed anemia, mildly elevated liver enzymes and serum potassium of 4.8mEq/L. Despite intubation and ventilation and other supportive management including propranolol, the patient could not be saved. Post-mortem biopsy of the thyroid showed diffuse hyperplasia of the follicles and muscles showed evidence of thyroid myopathy.

Subclinical thyrotoxicosis.

Subclinical thyrotoxicosis as a definite entity has been recognised with the development of highly sensitive immunometric TSH assays. The condition is characterised by suppressed TSH in presence of normal T3 and T4. It may be due to exogenous or endogenous causes. The risks may be osteoporosis and atrial fibrillation. Exogenous subclinical thyrotoxicosis must be prevented by optimising laevothyroxine dosage. Endogenous subclinical thyrotoxicosis may or may not be treated depending upon the clinical situation and existing comorbidities.

Irreversible dilated cardiomyopathy due to thyrotoxicosis.

Irreversible dilated cardiomyopathy due to thyrotoxicosis is an unusual clinical entity. We report this case of a young female who presented with congestive cardiac failure and was diagnosed as dilated cardiomyopathy due to thyrotoxicosis. Restoration of euthyroid levels did not revert the cardiomyopathy.

Thyrotoxicosis co-existing with ulcerative colitis.

A 32-year-old lady was admitted with complaints of recurrent episodes of vomiting and loose stools associated with tenesmus and blood and mucus. She also had a neck swelling since 11 years of age, and had features of thyrotoxicosis for five to six months. She responded to balsalazide only after her thyroid status was controlled with carbimazole.

Polyneuropathy from thiamin deficiency associated with thyrotoxicosis.

Polyneuropathy from thiamin deficiency can occur in persons who consume a diet consisting mainly of polished rice with low protein and thiamin content in the setting of excessive physical activity or hypermetabolic states. The authors report here a 17-year-old fisherman who presented with a 3-month history of symptoms and signs consistent with polyneuropathy. There were also clinical features of thyrotoxicosis which was confirmed by thyroid function test. His dietary intake consisted mainly of polished rice and fish both of which contain a small amount of thiamin. This could not cope with his hypermetabolic condition from thyrotoxicosis resulting in thiamin deficiency with polyneuropathy.