Reversible bradycardia secondary to myxedema coma: case-report.

Myxedema coma occurs mostly in patients with long-standing untreated or undertreated hypothyroidism. Bradycardia is a well-known cardiac manifestation for myxedema coma; however, not all bradycardia with hypothyroidism are sinus bradycardia. Sick sinus syndrome is a group of arrhythmias caused by the malfunction of the natural pacemaker of the heart. Tachy-Brady syndrome is considered to be a type of sick sinus syndrome, where the heart alternates between tachycardia and bradycardia, and it is usually treated with pacemaker implantation along with rate slowing medical therapy. Here we report a case of an 83-year-old female who presented with myxedema coma and atrial fibrillation with tachycardia and intermittent slow ventricular response. We attempt to review the relationship between these two diseases and conclude that appropriate diagnosis of myxedema coma, may be beneficial in reducing the need for pacemaker implantation.

[Myxedema coma]. / Coma mixedematoso.

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.

[Graves' dermopathy on the big toe]. / Dermopathie basedowienne localisée aux hallux.

BACKGROUND: Localized myxoedema is a rare dermopathy in patients with Graves' disease. The pretibial area is the most commonly affected region but herein we present a case of myxoedema of the big toe. PATIENTS AND METHODS: A 44-year-old male with Graves' disease ongoing for seven years presented bilateral ophthalmopathy and myxoedema of the big toes. The myxoedema was treated successfully with intralesional steroids. DISCUSSION: The physiopathology of myxoedema involves fibroblast activation and glycosaminoglycan production. This activation could result from stimulation of TSH receptors at their surface by TSH receptor antibodies (TRAK) or from an inflammatory process. The pretibial topography may be related to the high frequency in this area of microtrauma, with modulation of the cytokine microenvironment. CONCLUSION: The atypical localization seems to correlate with a Koebner phenomenon. Treatment of Graves' disease is generally insufficient to resolve the cutaneous problems. Topical corticosteroid therapy generally results in rapid improvement of recent lesions.

Heart failure presenting as myxedema coma: case report and review article.

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.

Homeostasis 3: nurses as external agents of control in hypothyroidism.

The role of healthcare practitioners in reversing homeostatic imbalances essentially makes them external agents of homeostatic control-they are replacing the usual assessment, controlling and effector aspects that operate intrinsically in health (homeostasis) but have failed in ill-health (homeostatic imbalances). This article examines the homeostatic imbalance of hypothyroidism, using a case study to draw analogies between the components of homeostatic theory and those of the nursing process. After reading this article, nurses should be able to explain: how the components of homeostasis are associated with health, and how failure of one or more of these components of homeostasis is associated with illness; that illness arises from a cellular, and therefore chemical, homeostatic imbalance; that hypothyroidism is a cellular imbalance of low levels of thyroid hormone, which is identified by signs and symptoms (i.e. other homeostatic imbalances) related to these low levels; and understand how primary care nurses looking after people with hypothyroidism are acting as external agents of homeostatic control.

[Etiology and pathogenesis of secondary edema of the lower extremities in patients with limited pretibialnoy myxedema on the background of hyperthyroidism].

UNLABELLED: Results of the examination of patients with secondary lymphedema in the period 2006-2010. Revealed that the most frequent concomitant diseases in 150 (57,6%) patients with secondary lymphostasis lower extremities is hyperthyroidism. CLINICAL MANIFESTATIONS: an increase in thyroid size, infiltrative endocrine ophthalmopathy; balanced, solid consistency swelling of the lower extremities to the level of the upper third of the leg; hyperkeratosis; paresthesias. The results of functional studies of the condition of peripheral lymph in patients with different stages of secondary lymphostasis lower extremities against a background of hyperthyroidism showed a direct relationship between the severity of the disease, the degree of decompensation of peripheral lymph and the state of thyroid function.

When to consider thyroid dysfunction in the neurology clinic.

There are many neurological manifestations of thyroid disease, and thyroid function has taken its place in the "routine bloods" of neurology practice. However, although conditions such as carpal tunnel syndrome prompt thyroid testing despite any clear evidence for this approach, other symptoms of potential significance in terms of thyroid disease may be overlooked in the busy general neurology clinic, or abnormal thyroid tests may be assumed to be incidental. Psychiatric disorders, loss of consciousness, movement disorders and weakness may all be manifestations of primary thyroid disease. This is a symptom-based review where we will consider the evidence (or lack of it) for the association of various neurological problems with thyroid dysfunction, and also the pitfalls in interpretation of the biochemical tests.

Postoperative myxedema coma in patients undergoing major surgery: Case series.

OBJECTIVE: Myxedema coma is a serious complication of hypothyroidism that can be precipitated by major surgery. It is extremely rare, with only a few reports in the literature. This study aims to present a relatively large case series of post-surgical myxedema coma and to analyze medical and surgical risk factors. METHODS: Analysis of the patients' surgical records and medical charts. RESULTS: Four patients developed postoperative myxedema coma and were evaluated for risk factors. Three had known hypothyroidism. Two had undergone large head and neck composite resections necessitating a free flap repair for malignant disease. One had undergone coronary artery bypass graft for ischemic heart disease, and another had undergone endoscopic cholecystectomy for complicated cholecystitis. All four patients required prolonged hospitalization, including treatment in the intensive care unit. One patient had undergone full cardiopulmonary resuscitation directly related to the myxedema coma state. CONCLUSION: We present a series of four patients who developed myxedema coma following major surgery. We recommend that patients with known hypothyroidism who are scheduled for major surgery should be tested for thyroid function status and assessed for postoperative risk of hypothyroidism. Those who develop complications following major surgery, should be immediately tested for thyroid function to rule out myxedema coma.

Myxedema Heart Disease: A Rare Disease Entity: Case Report and Brief Review of the Literature.

BACKGROUND: Myxedema heart disease is an extremely rare disease entity and should be suspected in patients with unexplained heart failure refractory to conventional treatment. Myxedema coma with co- existent heart disease is not well known and very few cases have been reported. CONCLUSION: Here, we present an interesting case of myxedema coma with severe valvular cardiomyopathy followed by a concise review of the literature with special emphasis on epidemiology, pathophysiology, diagnosis and therapeutic modalities.

Myxedema coma precipitated by diabetic ketoacidosis after total thyroidectomy: a case report.

BACKGROUND: Myxedema coma is profound decompensated hypothyroidism usually precipitated by stressors, and its occurrence in association with total thyroidectomy or metabolic disorders, such as diabetic ketoacidosis, is unusual. CASE PRESENTATION: A 43-year-old Asian man with history of total thyroidectomy who was scheduled for a second radioactive iodine therapy presented to our hospital with decreased mental status and hyperglycemia. He had a history of thyroid cancer but did not have diabetes mellitus. He was in a hypothermic state and had a Glasgow Coma Scale score of 10 out of 15 at presentation; arterial blood gas analysis revealed a state of metabolic acidosis and laboratory findings suggested hyperglycemia with glycosuria, ketoacidosis, and severe hypothyroidism. A thyroid function test showed thyroid-stimulating hormone of 34.126 uIU/mL, free thyroxine of 1.02 ng/dL, and triiodothyronine of 1.04 ng/mL. The glycated hemoglobin of this patient was checked due to hyperglycemia and the value of glycated hemoglobin was 16.5% which met the criteria for a diagnosis of diabetes. After treatment for myxedema with liothyronine 5 mcg two times per day and levothyroxine 175 mcg once daily via a nasogastric tube and diabetic ketoacidosis with intravenously administered fluid and insulin, his clinical condition rapidly improved including mental status, hyperglycemia, and acidosis. During the hospitalization, a workup for diabetes mellitus was performed and the results suggested that a diagnosis of type 2 diabetes mellitus would be appropriate. CONCLUSIONS: This case demonstrated that diabetic ketoacidosis not only could be a potential contributor to myxedema coma but also mask typical clinical features, making diagnosis more difficult. Considering the possibility of an increasing number of potential patients with hypothyroidism developed after thyroidectomy, constant vigilance is required for a better clinical outcome, including early recognition and management in critical care in advance for unusual diabetic ketoacidosis which could precipitate decompensated hypothyroidism.

Predictors of outcome in myxoedema coma.

Myxoedema coma is a rare and life-threatening illness the outcome of which has not been robustly studied in large numbers, partly due to its low incidence. Dutta and colleagues have explored outcome predictors in a developing country where access to thyroid function tests is more limited than in the Western world. Cardiovascular instability, reduced consciousness, persistent hypothermia, and sepsis all contributed to a poorer outcome, as has been demonstrated before, but a generic outcome predictor model was shown to be useful in this group of patients. Unfortunately, this observational study was unable to show differences in outcome based on replacement treatment methods and the mortality remains at 40%.

[A man who was unable to open his eyes]. / De man die zijn ogen niet goed kon openen.

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.

Effect of alterations in the thyroid state on the intrinsic contractile properties of isolated rat skeletal muscle.

Contractile properties of soleus muscles isolated from 31 euthyroid (EU), 20 hyperthyroid (HT), and 18 myxedematous (MY) rats were studied in a myograph. At 100 stimuli/sec maximum isometric tension was essentially identical in EU (17.2 +/-0.5 g/mm(2)) and HT (17.7 +/-0.5 g/mm(2)) muscles, but was significantly depressed in MY muscles (11.5 +/-0.7 g/mm(2)). The rate of tension development was increased in HT (103 +/-4.5 g/sec per mm(2)) as compared to both EU (86.2 +/-4.6 g/sec per mm(2)) and MY (38.4 +/-2.2 g/sec per mm(2)) muscles, while the duration of the active state was shortened in HT (77.1 +/-2.3 msec) as compared to EU (105.1 +/-1.1 msec) muscles and was prolonged in MY muscles (153.3 +/-6.0 msec). The mean rate of isometric relaxation was 26.5 +/-4.9 g/mm(2) per sec in EU muscles, more rapid in HT muscles (33.1 +/-1.3 g/sec per mm(2)), and slower in MY muscles (16.0 +/- g/mm(2) per sec). The fusion frequency was greater in HT muscles, averaging 68.5 +/-3.6 stimuli/sec compared to EU muscles (38.1 +/-1.2 stimuli/sec) and to MY muscles (33.3 +/-4.0 stimuli/sec). At 40 stimuli/sec tension averaged 16.4 +/-0.8 g/mm(2) in EU muscles while at the same frequency tension was reduced in HT muscle, averaging 14.2 +/-0.5 g/mm(2). All differences were significant (P < 0.01). In conclusion, HT and MY result in profound alterations in the intrinsic contractile properties of skeletal muscle. While tension in HT muscles is maintained in vitro at a stimulus frequency of 100 stimuli/sec, the reduction in duration of active state may lower tension in vivo by preventing complete fusion of contractile events. In MY tension is reduced as a consequence of the lowered intensity of the active state. These changes explain, at least in part, the weakness of muscle activity in both HT and MY.

Thyroid Emergencies.

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.

Hypothyroidism: mimicker of common complaints.

Hypothyroidism is a common condition presenting a challenge to emergency physicians in diagnosing the underlying etiology of vague complaints. Making the diagnosis of a critically ill patient in myxedema coma allows early treatment with appropriate thyroid hormone replacement and avoids higher patient mortality. To do this, the emergency physician must maintain a high degree of clinical suspicion for thyroid disease.

Complete recovery after severe myxoedema coma complicated by status epilepticus.

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.

Serum markers of type I collagen formation and degradation in metabolic bone disease: correlation with bone histomorphometry.

Type I collagen makes up more than 90% of bone matrix. Therefore, analysis of antigens related to collagen formation and degradation in bone should provide good and specific estimates of both bone resorption and bone formation rates. In this study we measured serum levels of the pyridinoline cross-linked telopeptide domain of type I collagen (ICTP) as a marker of bone resorption and serum carboxy-terminal propeptide of type I procollagen (PICP) as a marker of bone formation. Serum levels of the two antigens were correlated to histomorphometric indices of bone resorption and bone formation calculated from iliac crest bone biopsies in a group of 18 individuals with high- and low-turnover bone disease (myxedema, primary hyperparathyroidism, and thyrotoxicosis). After logarithmic transformation the regression of S-ICTP on volume-referent resorption rate (BRs/R/BV) was significant (r = 0.61, p < 0.01, SEM/Y = 56%). S-ICTP also showed a significant regression on the volume-referent cancellous bone balance (r = -0.45, p < 0.05, SEM/Y = 412%). S-PICP was significantly correlated to the mineral appositional rate (r = 0.53, p < 0.05) and volume-referent bone formation rate (r = 0.61, p < 0.01, SEM/Y = 48%). The correlation to bone turnover as expressed in the activation frequency was also highly significant (r = 0.61, p < 0.01, SEM/Y = 51%). No significant correlation with wall thickness or bone balance was demonstrable per remodeling cycle. Thus, assays employing antigens that reflect collagen formation and degradation are useful instruments for the evaluation of rates of bone remodeling in metabolic bone disease.

Arginine vasopressin secretion in thyroidectomized sheep..

Indwelling, exteriorized, jugular vein catheters were placed in five thyroidectomized ewes at a time when myxedema was manifested clinically and chemically and three euthyroid sheep were used as controls. Post-operatively, tracer doses of [125I]-iodovasopressin were injected and serial blood specimens were obtained for determination of volume of distribution, plasma disappearance, and blood production rates. Serum vasopressin was measured by radioimmunoassay. The mean volumes of distribution for vasopressin in the hypothyroid and euthyroid sheep, respectively, were 8.15 and 5.90 liters, mean t1/2 of vasopressin 9.5 and 19.3 min, mean serum vasopressin concentrations 5.1 and 1.2 muU/ml, and mean blood production rates 2.84 and 0.23 mU/kg/h. Renal and organ biologic effectiveness of the elevated vasopressin levels was suggested by the lowered serum osmolalities in the hypothyroid sheep over controls (272 vs. 301 mosmol/kg). These results suggest an augmented secretion of vasopressin in the myxedematous state.