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A 47-years-old man presented with the complaint that he could not open his eyes in the morning. Facial myxedema caused by hypothyroidism was evident. Pictures taken after treatment for six months with levothyroxine showed complete recovery. Myxedema is caused by accumulation of glycosaminoglycans in the dermis.

Thyroid emergencies are rare life-threatening endocrine conditions resulting from either decompensated thyrotoxicosis (thyroid storm) or severe thyroid hormone deficiency (myxedema coma). Both conditions develop out of a long-standing undiagnosed or untreated hyper- or hypothyroidism, respectively, precipitated by an acute stress-associated event, such as infection, trauma, or surgery. Cardinal features of thyroid storm are myasthenia, cardiovascular symptoms, in particular tachycardia, as well as hyperthermia and central nervous system dysfunction. The diagnosis is made based on clinical criteria only as thyroid hormone measurements do not differentiate between thyroid storm and uncomplicated hyperthyroidism. In addition to critical care measures therapy focusses on inhibition of thyroid hormone synthesis and secretion (antithyroid drugs, perchlorate, Lugol's solution, cholestyramine, thyroidectomy) as well as inhibition of thyroid hormone effects in the periphery (β-blocker, glucocorticoids).Cardinal symptoms of myxedema coma are hypothermia, decreased mental status, and hypoventilation with risk of pneumonia and hyponatremia. The diagnosis is also purely based on clinical criteria as measurements of thyroid hormone levels do not differ between uncomplicated severe hypothyroidism and myxedema coma. In addition to substitution of thyroid hormones and glucocorticoids, therapy focusses on critical care measures to treat hypoventilation and hypercapnia, correction of hyponatremia and hypothermia.Survival of both thyroid emergencies can only be optimized by early diagnosis based on clinical criteria and prompt initiation of multimodal therapy including supportive measures and treatment of the precipitating event.

Thyroid emergencies are major life-threatening endocrine conditions associated with life-threatening disorders resulting from either severe deficiency or excess of thyroid hormones. Deficiency of thyroid hormones may present as myxedema coma whereas excessive hormone production can present as life threatening thyrotoxic storm. The diagnosis of both requires a high index of clinical suspicion. Thyroid storm, in spite of accurate diagnosis, continues to have high fatality, whereas myxedema management has markedly improved with advancement in intensive care facility. The key to successful management of these emergencies is timely diagnosis and management by experienced physician in an intensive care setting. This article discusses the basic differences of both entities with an attempt to appropriate recognition and awareness of clinical signs and symptoms, highlight the salient diagnostic points and delineate the rational approach, which can lead to appropriate treatment at the earliest and reduce mortality., (© Journal of the Association of Physicians of India 2011.)

Raionale: Myxedema coma (MC) is extremely rare but lethal in pediatric patients with hypothyroidism leading to altered mental status and hypothermia. But there is no clinical guideline for such cases., Patient Concerns: A 6-year-old Chinese girl presented with coma and hypothermia preceded by pneumonia. Her lab results were: free thyroxin (T4) 4.18 pmol/L and thyroid-stimulating hormone (TSH) > 150 μIU/mL with extremely elevated anti-thyroid peroxidase (TPO-Ab) and anti-thyroglobulin. Pneumonia, mild pleural, and pericardial effusion were seen on computed tomographic (CT) scan., Diagnoses: MC, autoimmune hypothyroidism, pneumonia and sepsis were diagnosed., Intervention: Gastric levothyroxine, intravenous dexamethasone and antibiotics were administered., Outcome: Her consciousness was restored and temperature returned to normal 2 days after starting levothyroxine. She was discharged two weeks later., Conclusion: MC is rare but may be the initial presentation in pediatric patients with prolonged untreated hypothyroidism. Autoimmune thyroiditis could cause hypothyroidism in children. MC should be suspected in pediatric patients with altered mental status, hypothermia and cardiovascular instability. Treatment with 100 mg/m of gastric levothyroxine is an option for pediatric patients with MC.

A 43-year-old indigenous Guatemalan woman with achondroplasia presented to our clinic with chronic fatigue and generalised oedema. She had limited contact with the formal healthcare system. However, 1 year prior, she had sought medical evaluation from a private physician. Her symptoms had been attributed to a combination of heart failure and physical disability due to the musculoskeletal complications of her achondroplasia. She was lost to follow-up due to inability to pay for further testing or treatment. On initial laboratory evaluation in our clinic, she was found to have a thyrotropin level greater than assay. With initiation of oral levothyroxine supplementation, her dyspnoea and oedema completely resolved. The case illustrates how indigenous patients in rural Guatemala experience many barriers to accessing high-quality medical care. As a result, presentations of common illnesses are often very advanced and definitive diagnoses and treatments are frequently delayed., (2017 BMJ Publishing Group Ltd.)

Myxoedema coma is a rare life-threatening disease, and it is essential that it is managed appropriately to reduce the associated high mortality. However, in the setting where efficient healthcare delivery is hampered by inadequacies, the management of such cases may pose a significant challenge. We present the case of a middle-aged woman diagnosed with myxoedema coma and severe hyponatremia. The case report highlights some of the challenges that may be encountered during the management of myxoedema coma in similar settings and outlines the management strategies undertaken to overcome them in the absence of national guidelines. It also brings to the fore the need for clinicians to look out for clinical features suggestive of hypothyroidism particularly among high risk individuals for early diagnosis and treatment., Funding: None declared., Competing Interests: Conflict of interest: None declared

Background: Myxedema coma is a life-threatening and emergency presentation of hypothyroidism. However, the clinical features and outcomes of this condition have been poorly defined because of its rarity., Methods: We conducted a retrospective observational study of patients diagnosed with myxedema coma from July 2010 through March 2013 using a national inpatient database in Japan. We investigated characteristics, comorbidities, treatments, and in-hospital mortality of patients with myxedema coma., Results: We identified 149 patients diagnosed with myxedema coma out of approximately 19 million inpatients in the database. The mean (standard deviation) age was 77 (12) years, and two-thirds of the patients were female. The overall proportion of in-hospital mortality among cases was 29.5%. The number of patients was highest in the winter season. Patients treated with steroids, catecholamines, or mechanical ventilation showed higher in-hospital mortality than those without. Variations in type and dosage of thyroid hormone replacement were not associated with in-hospital mortality. The most common comorbidity was cardiovascular diseases (40.3%). The estimated incidence of myxedema coma was 1.08 per million people per year in Japan. Multivariable logistic regression analysis revealed that higher age and use of catecholamines (with or without steroids) were significantly associated with higher in-hospital mortality., Conclusions: The present study identified the clinical characteristics and outcomes of patients with myxedema coma using a large-scale database. Myxedema coma mortality was independently associated with age and severe conditions requiring treatment with catecholamines., (Copyright © 2016 The Authors. Production and hosting by Elsevier B.V. All rights reserved.)

Hypothyroidism is a frequently diagnosed and simply treated disease. If not recognised, however, in time it may develop into the most severe manifestation of hypothyroidism known as myxedema coma. The term "myxedema coma" is generally seen as misleading since most patients do not initially present in a coma. The typical progression is lethargy evolving into stupor and, eventually, into coma with respiratory failure and hypothermia. It mainly affects elderly women, often occurring in winter and is relatively rare. It can be considered a form of decompensated hypothyroidism often triggered by a variety of non-thyroid conditions or diseases provoking an extremely severe condition of multiple system failure with lethal consequences unless an early diagnosis is made and an aggressive treatment is administered.

Myxedema coma and thyroid storm are thyroid emergencies associated with increased mortality. Prompt recognition of these states-which represent the severe, life-threatening conditions of extremely reduced or elevated circulating thyroid hormone concentrations, respectively-is necessary to initiate treatment. Management of myxedema coma and thyroid storm requires both medical and supportive therapies and should be treated in an intensive care unit setting.

Decompensated hypothyroidism is a rare endocrine emergency but a differential that should be considered in patients presenting critically unwell with systemic illness. We report a case of myxoedema coma in a woman presenting with respiratory failure, hypotension, hypothermia and a reduced level of consciousness, all of which are poor prognostic features in decompensated hypothyroidism. The patient was admitted to critical care for mechanical ventilation and cardiovascular support and treated with a combination of insulin, liothyronine and levothyroxine, making a good recovery. We wanted to highlight this case of myxoedema coma occurring in the context of a hyperglycaemic hyperosmolar state (HHS), as the former condition is normally associated with hypoglycaemia, hyponatraemia and hypo-osmolality. Decompensated hypothyroidism should be considered in presentations of HHS as well as with other metabolic derangements, as delays in thyroid hormone replacement are associated with poorer outcomes. It has multisystem effects challenging its recognition and we discuss potential complications and their management., (2016 BMJ Publishing Group Ltd.)

Myxedema coma, a rare entity, with a reported 25%-65% mortality had no objective criteria for making the diagnosis when we began our study. We developed an objective screening tool for myxedema coma to more easily identify patients and examine the best treatment method in future prospective studies to reduce the mortality of this entity. We conducted a retrospective chart review to find all patients aged ≥18 years admitted with myxedema coma from January 1, 2005 through June 13, 2010 at Indiana University Health Methodist Hospital. On the basis of both our retrospective chart review and on literature accounts, we identified 6 criteria to diagnose myxedema coma. We identified 10 patients initially diagnosed with myxedema coma and established a control group consisting of 13 patients identified with altered mental status and increased thyroid-stimulating hormone (TSH) levels. The 6 variables we created for the screening tool were heart rate, temperature, Glasgow coma scale, TSH, free thyroxine, and precipitating factors. The screening tool has a sensitivity and specificity of about 80%. We ran a logistic regression model using the 10 study patients and 13 controls with the 6 variables. No variables alone significantly contributed to the model. However, the overall model was highly significant (P = 0.012), providing strong support for a scoring system that uses these variables simultaneously. This screening tool enables physicians to rapidly diagnose myxedema coma to expedite treatment. A more refined diagnostic tool may be used in future clinical studies designed to determine the optimal treatment., (Copyright © 2015 Elsevier Inc. All rights reserved.)

Ureteral myxedema is exceptionally rare. We describe computed tomography and magnetic resonance imaging findings in a case of ureteral myxedema. The demonstration of water-like hyperintensity around the ureteral lumen on heavily T2-weighted sequences should be considered a strongly suggestive sign for ureteral myxedema., (Copyright © 2015 Elsevier Inc. All rights reserved.)

We report a case of life-threatening myxoedema presenting with hypothermia, hypotension, bradycardia, pericardial effusion and deep coma. The condition was complicated by prolonged status epilepticus. The optimal treatment strategy has been debated over the years and the literature is briefly reviewed. Treatment with l-thyroxine (LT4) monotherapy without initial loading dose and with no l-triiodothyronine (LT3) treatment was successful with full recovery after hospitalisation for more than a month. Myxoedema coma is a rare, reversible condition with a high mortality and should be considered as a differential diagnosis in medical emergencies., (2015 BMJ Publishing Group Ltd.)

History and Admission Findings: A 51-year-old man presented with progressive tiredness, proximal muscle weakness, hair loss and weight gain for months. The patient showed mild pretibial myxedema and dry skin. Laboratory findings revealed strongly elevated cardiac enzymes as well as marked hypothyroidism., Investigations: The electrocardiogram, echocardiography, abdominal sonography and chest X-ray were unremarkable. Thyroid ultrasound demonstrated features of Hashimoto thyroiditis., Treatment and Course: The findings supported the diagnosis of an overt hypothyroidism with myxedema and rhabdomyolysis. After starting levothyroxine and volume substitution laboratory parameters and clinical condition slowly normalized., Conclusion: Severe overt hypothyroidism may rarely present primarily as myopathy with myositis and cardiac involvement., (© Georg Thieme Verlag KG Stuttgart · New York.)

A 48-year-old man was admitted to department of emergency medicine at a tertiary referral hospital due to dizziness and fatigue. Clinical features on admission were non-pitting oedema, dry skin, very sparse hair, a hoarse voice, hypothermia (rectal temperature 28.7°C), macroglossia, sinus bradycardia and slow cerebration. Blood tests revealed severe hypothyroidism. During admission, the patient developed respiratory failure, renal failure, bleeding symptoms and diffuse colitis. The patient was treated with hydrocortisone and levothyroxine and he survived miraculously. This case describes a patient with myxoedema coma with severe hypothermia and cardiac involvement with development of multiorgan dysfunction all linked to the severe depletion of triiodothyronine.

The case report describes an 88-year-old patient who presented with new-onset ascites. After excluding frequent causes of ascites, he was diagnosed with myxoedema ascites. Myxoedema ascites is rare. Analysis of ascitic fluid shows a high serum-ascites albumin gradient and a high protein level. Myxoedema ascites resolves completely after starting thyroid hormone replacement therapy.

Woltman's sign of myxoedema, named after Henry Woltman in 1956, is the delayed relaxation phase of the muscle stretch reflex in patients with myxoedema. Although a change in these reflexes was mentioned as being clinically evident possibly as early as the 1870s, no formal description was published until 1924 when William Calvert Chaney objectively quantified the change. Woltman was involved in training Chaney, and it has been proposed that he guided Chaney's study of these reflexes. Despite the attachment of Woltman's name to the eponym, little evidence exists that directly links him to the first objective study of the muscle stretch reflex in myxoedema performed by Chaney., (Copyright © 2013 Elsevier Ltd. All rights reserved.)

Although thyroid dysfunction will develop in more than 12% of the US population during their lifetimes, true thyroid emergencies are rare. Thyroid storm and myxedema coma are endocrine emergencies resulting from thyroid hormone dysregulation, usually coupled with an acute illness as a precipitant. Careful assessment of risk and rapid action, once danger is identified, are essential for limiting morbidity and mortality related to thyroid storm and myxedema coma. This article reviews which patients are at risk, explains thyroid storm and myxedema coma, and describes pharmacological treatment and supportive cares.

Hypothyroidism is a common medical problem easily treated when diagnosed but requiring regular follow-up and patient medication compliance. At times, this diagnosis can go untreated resulting in the development of severe consequences such as Myxedema Coma. Of all the clinical symptoms, cardiovascular manifestations tend to be especially severe and often life threatening.

Localized or pretibial myxedema is one of the signs of Graves disease (along with goiter, exophthalmus, thyroid acropathy, and high circulating levels of long-acting thyroid-stimulating hormone) and usually tends to occur at a later stage of the disease or even after the patient becomes euthyroid post treatment. Very rarely has it been reported in euthyroid patients. We report a euthyroid man presenting with localized myxedema on the extensor surface of his forearm with clinical and histopathological features consistent with pretibial myxedema. He responded partially to topical clobetasol propionate cream and tacrolimus ointment 0.1 percent for about 7 months. To the best of our knowledge, this is the first case of preradial myxedema in a euthyroid patient in the English international dermatological literature.

Myxedema coma is defined as severe hypothyroidism leading to decreased mental status, hypothermia, and other symptoms related to dysfunction in multiple organs. It is very rare disease with high mortality rate. Early recognition and therapy of myxedema coma are essential, and treatment should be begun on the basis of clinical suspection. However, regimen of myxedema is not well established even now, especially about thyroid hormone supplementation. Japan Thyroid Association is drawing up "The diagnostic criteria of myxedema coma (3rd draft) and preliminary guide to treatment of it". According to this criteria and preliminary guide, the clinical presentation, diagnosis, and treatment of myxedema coma will be reviewed here.

This review presents current knowledge about the thyroid emergencies known as myxedema coma and thyrotoxic storm. Understanding the pathogenesis of these conditions, appropriate recognition of the clinical signs and symptoms, and their prompt and accurate diagnosis and treatment are crucial in optimizing survival., (Copyright © 2012 Elsevier Inc. All rights reserved.)

Although an uncommon location, cutaneous mucinoses may present in the pretibial area in distinct clinical circumstances. The terms pretibial myxedema and pretibial mucinosis often are used interchangeably, but pretibial myxedema should be regarded as a type of pretibial mucinosis. We present a case of cutaneous mucinosis localized to the pretibial area of a patient without Graves disease.

Although pretibial myxedema (PTM) occurs in 4.3% of patients with Graves's disease, the most severe variant, elephantiasis nostras verrucosa, is found in less than 1% of cases. The most frequent location of infiltration is the lower extremities, especially the pretibial areas and on the dorsum of the foot. The authors report one of the most severe cases of elephantiasis nostras verrucosa, following radioactive iodine therapy.

Objective: Pretibial myxedema (PM) is a manifestation of Graves' disease (GD). Currently, its diagnosis depends on physicians' observation and biopsy. No satisfactory, objective, and non-invasive tool is available to record and investigate lesions. Digital infrared thermal imaging (DITI) detects surface temperature, and sonography reflects composition changes in soft tissue. This study was aimed to observe changes in DITI and sonography in PM, and to evaluate their clinical usefulness., Methods: Nineteen GD patients with PM, 22 GD patients with mild diffuse non-pitting edema over lower legs, 46 GD patients with normal appearance of lower legs, and 14 normal volunteers were recruited for observation with DITI; 8, 21, 21, and 11 of them respectively also received soft tissue sonography for investigating the pathogenesis of DITI change., Results: Lower leg temperatures of normal volunteers decreased gradually from proximal to distal parts. In all 19 patients with PM, DITI showed abnormally low focal temperatures over the lesions. In GD patients with mild diffuse non-pitting edema and GD patients with normal appearance of lower legs, DITI showed abnormally low focal temperature in 90.9 and 65.2% of the patients respectively. Areas of clinically visible PM and low focal temperature detected by DITI were sonographically characterized with increased skin thickness, hypoechoic substance deposition in the cutaneous tissue, and blurred boundary lines between dermis and subcutaneous tissue. TSH receptor antibody level correlated positively and significantly with skin thickness change and adjusted temperature difference between the center of temperature defect and the surrounding skin (P=0.046 and 0.033 respectively)., Conclusions: By using DITI and sonography, we detected characteristic changes in PM. These techniques are helpful in recording and may be useful tools to detect early changes of PM.

Myxedema coma (MC) is a rare, but often fatal endocrine emergency. The majority of cases that occur in elderly women with long-standing primary hypothyroidism are caused by particular triggers. Conversely, MC of central origin is extremely rare. Here, we report a case of MC with both central and primary origins. A 56-year-old woman was transferred to our hospital due to loss of consciousness; a chest x-ray demonstrated severe cardiomegaly. Low body temperature, bradycardia, and pericardial effusion suggested the presence of hypothyroidism. Endocrinological examination revealed undetectable levels of serum free thyroxine (T(4)) and free triiodothyronine (T(3)), whereas serum thyroid-stimulating hormone (TSH) levels were not elevated. The woman's serum anti-thyroid peroxidase antibody and anti-thyroglobulin antibody tests were positive, indicating that she had Hashimoto's thyroiditis. Provocative tests to the anterior pituitary revealed that she had TSH and growth hormone (GH) deficiency; however, GH levels were restored after supplementation with levothyroxine for 5 months. This was not only a rare case of MC with TSH deficiency and Hashimoto's thyroiditis; the patient also developed severe osteoporosis and possessed transient elevated levels of serum carcinoembryonic antigen (CEA). This atypical case may suggest the role of anterior pituitary hormone deficiencies, as well as hypothyroidism, in the regulation of bone metabolism.