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J Am Board Fam Pract: first published as 10.3122/jabfm.8.5.376 on 1 September 1995. Downloaded from In The Elderly

(vnthia G. Olsen, M[)

Background: in the elderly, although uncommon, is frequently overlooked and has a high mortality rate. are many and are often insidious. Nearly every organ system is involved. Prompt recognition and treatment are mandatory for a successful outcome. Methods: A case study is presented. Using the key words "myxedema" with the word "aged," MEDLINE files were searched from 1989 to present. Articles dating before 1989 were accessed from the reference lists of the more recent articles. Results and Conclusions: This review describes the signs and symptoms of myxedema coma in the elderly. Epidemiology and histopathology of the disorder are discussed. Prompt recognition and emergency medical treatment are essential for a successful outcome. Prevention requires of elderly patients at risk for and assuring replacement therapy. (J Am Board Fam Pract 1995; 8:376-83.)

Myxedema coma, the extreme expression of sodium depletion. A history of for hypothyroidism, is a medical emergency re­ goiter in the remote past was discovered, and the quiring a high degree of clinical suspicion. The patient had not received thyroid hormone re­ term myxedema was proposed by Ord in 1878 placement therapy. A family history was notable to describe the peculiar nonpitting swelling in that her son had a thyroid goiter. of in the hypothyroid adult and has been During the physical examination the woman used interchangeably with hypothyroidism in was obtunded and unable to communicate with the medical literature. 1 Although the actual inci­ the examiner. She weighed 72.7 kg, her tempera­ dence is unknown, myxedema coma is uncom­ ture was 36.3° C, her pulse was ret,Tular at 80 beats mon; only 200 cases were reported between 1953 per minute, respirations were 24/min, and her and 1986.2 The mortality rate in these patients is blood pressure was 178/94 mmHg. On appear­ 50 percent or greater even with immediate thy­ ance her face was swollen, especially about the roid hormone replacement therapy and support­ eyes. Her mucous membranes were dry and the ive measures. Early recognition and intervention tongue was thickened. Neck masses were not can be lifesaving. found. Her skin was cool and doughy in consis­ tency, and there was marked pitting of the http://www.jabfm.org/ Illustrative Case lower extremities up to the knees. Lung examina­ A 90-year-old woman who had been residing in a tion demonstrated bilateral pulmonary edema nursing home for several years was brought in for with pleural effusions. The heart had a regular cOllSultation. The nursing staff and family re­ rate and rhythm with a grade IIM systolic ejec­ ported gradually increasing lethargy, , tion murmur. Neurologically the patient was

and diminished mental alertness. semicomatose. Deep tendon reflexes were dimin­ on 24 September 2021 by guest. Protected copyright. She had a history of cerebrovascular accidents, ished with a slowed response. Rectal examination which precipitated her nursing home admission. found a . The medical chart reflected persistent chronic La bora tory studies discl osed the following unresponsive to fluid restriction. values: sodium 127 mEq/L, potassium 3.9 mEqlL, The patient had increasing pulmonary and pe­ chloride 93 mEqlL, and carbon dioxide 25 mEqlL. ripheral edema as a result of congestive heart fail­ Blood urea nitrogen (BUN) and serum creati­ ure. '[reatment with had worsened her nine were 17 mg/dL and 0.6 mg/dL, respectively. Serum osmolality was 250 mOsm/kg. Her fast­ ing blood glucose was 128 mg/dL. The serum

Submittl'd, ITviSl'd, ~ May 1')');. total protein was 5.8 g/dL, and serum albumin From thl' Department of Family rvkdicillc, V\rright State Uni­ was 3.l g/dL. A complete blood count showed a versity School of Medicine, Dayton, Ohio. Address rl'print re­ mild microcytic, normochromic . A urin­ quests to Cynthia G Olsen, MD, Department of Family Ml'di­ cinc, School of ,Vlcdicine, \Vright St'ltc University, (,27 Edwin alysis was positive for pyuria and bacteriuria. C. .'vloses Boulcvard, Dayton, 011 .:tHOll. Thyroid function studies showed a depressed

37(' JABFP Sept.-Oct.1995 Vol. R No.5 J Am Board Fam Pract: first published as 10.3122/jabfm.8.5.376 on 1 September 1995. Downloaded from thyroxine level of3.0 ,...g/dL and an elevated thy­ Table 1. Precipitating Causes of Myxedema Coma. roid stimulating hormone (TSH) of 53 ,...U/mL. Cause Type An adrenocorticotropic hormone (ACTH) level was normal at 34 pg/mL. A blood gas determina­ tion on 2 L of nasal cannula oxygen revealed aci­ Urinary tract dosis with a pH of 7.24, p02 of 118 mmHg, pC02 of 145 mmHg, and a bicarbonate of 50.4 Drugs mEq/L. A chest radiograph showed marked car­ Sedating Narcotics diomegaly with bilateral pleural effusions. A Phenothiazines two-dimension echo cardiogram showed mild Tranquilizers and aortic stenosis and a dilated left ventricle with Other central nervous preserved function. system depressants The patient was hospitalized for myxedema General coma caused by untreated hypothyroidism with Cardiac drugs f3- Blockers concurrent metabolic derangement, possible , and . She re­ Stressors ceived intravenous hydrocortisone 75 mg every 6 hours. An initial bolus of 400 mg of synthetic Hospitalization thyroxine was followed by 200 mg on day 2 and 100 mg daily thereafter. She received treatment Trauma of her heart failure with diuretics, supplemental Exposure to cold oxygen and potassium, and digoxin. On day 5 she was switched to oral medications of pred­ to the water-binding capacity of the acid gly­ nisone 10 mg, 125 mg, digoxin 25 cosaminoglycans within the papillary and reticu­ mg, and indapamide 2.5 mg. A follow-up chest lar layers.7 Other changes of the skin that contrib­ radiograph showed resolution of the pulmonary ute to edema in myxedema are increased capillary congestion. permeability, lymphatic obstruction, and perivas­ The patient returned to the nursing home on culitis. Acid glycosaminoglycans are also found in supplemental oxygen. During the next few the tissues of the tongue, myocardium, striated months the patient had an improved level of muscle, and intestines.8 Thyroid hormone re­ alertness and was able to recognize family mem­ placement treatment reduces http://www.jabfm.org/ bers. Her cardiac failure improved, and her meta­ concentrations in the skin, whereas the three bolic problems stabilized. other glycosaminoglycans remain unchanged.9 Muscle biopsy in severe myxedema reveals type II Epidemiology muscle fiber loss and atrophy, an increased num­ Myxedema coma occurs almost exclusively during ber of mitochondria, and an accumulation of gly­ or after the 6th decade with 80 percent of the cogen and lipids on the membranes. This effect is on 24 September 2021 by guest. Protected copyright. cases occurring in women.3,4 More than 90 percent also somewhat reversible with treatment. 10 of cases have been reported to have occurred dur­ ing winter months and are frequently associated Clinical Presentations with intercurrent illness or stressors (Table 1). Because the patient is in a coma, the initial diag­ Pneumonia or other infections and sedating drugs nosis is suggested by a history of clinical signs and are common precipitants.4-6 About 50 percent of symptoms of hypothyroidism and a history of myxedema coma patients have lapsed into coma thyroid surgery, high-dose external radiation of after admission to the hospital, probably as the re­ the neck, or discontinuation of thyroid hormone sult of stress caused by diagnostic and therapeutic replacement therapy (Table 2). interventions encountered during hospitalization. In addition to knowing the symptoms preced­ ing the onset of coma, physical findings will also Histopathology aid the physician in making the diagnosis. The The clinical manifestations of myxedema are in- patient typically has periorbital swelling, ptosis, duration and thickening of the skin, attributable and a thickened tongue. Nonpitting edema of the

Myxedema Coma 377 J Am Board Fam Pract: first published as 10.3122/jabfm.8.5.376 on 1 September 1995. Downloaded from

Table 2. (;linical Signs and Symptoms of Myxedema atony. This serious condition can lead to visceral (;oma. perforation. The resulting colonic can he in­ distinguishahle from mechanical ohstrllction. H (\rea Si~n or Sy1l1pt' 1111 Barium enem,) shows localized transverse thick­ Constitlltion,d, g·eneral Lethargy ening of the colonic haustration. l ) Myxedema \Veight gain or loss megacolon appearing as pseudomembranolls \\'eakness Sleep disturhance colitis and intestinal ischemia is rare. II) Ilypotonia of the esophagus, stomach, duodenum, gallblad­ I lead and neck llearing imp,]innent Obstructive sleep apnea der, and small intestine can also occur. M,]Croglossia The lowered metabolic state in myxedema Periorbital swellin~ coma patients results in , slowed res­ Lid ptosis piratory rate, , and . 17 I)erm,](ologic I Llir 10" Coarse, dry skin Shivering is diminished or absent. Hypothermia, I'retihiallllyxedellla common in the aging population, can also he Edema found with and occasionally septi­ ( ;,]strointestinal Fecal impaction cemia. IH A core temperature of less than 35 .5°C Megacolon occurs in about HO percent of comatose patients. llrologic Bladder atony In fact, a normal temperature in a myxedema Urinary rdention coma patient should be considered relative hyper­ Musculo'ikelctal Muscle hypertrophy thermia. Underlying infection in these patients is Neurologic and psychiatrie common and might be the precipitating factor Restlessness Delirium leading to coma. Reduced immune defenses often obscure the signs of infection. PsychoJl]otor retardation In the severe, chronic hypothyroid patient, the heart can be dilated and the myocardium atonic. Diminished heart sounds and breath sounds are lower extremities is the hallmark of myxedema; usually found on examination. Infiltrative cardio­ however, 40 percent of patients could have pitting myopathy results in pericardial effusions in 30 to as a result of heart, renal, or liver disease. Most 80 percent of untreated patients. I'! Infrequently hypothyroid patients are within 15 percent of will occur, even months after their ideal body weight; the impression of being thyroid hormone replacement therapy, but even­ http://www.jabfm.org/ might be due to puffiness of the LlCe tually it will respond to treatment."O Pleural effu­ and extremities and the lack of weight loss with sions also occur with or without congestive heart reduced oral intake. In the severely apathetic hypo­ failure. 21 ,11 thyroid patient weight loss will occur. I I Gross is rare. Fine hair texture and nonscarring, Metabolism and Physiology diffuse alopecia can also be present. I2 Diminished Several metabolic derangements occur in myx­ on 24 September 2021 by guest. Protected copyright. eyebrows are a nonspecific finding and might be edema coma and are important diagnostic and found in normal patients. Neck goiter is usually therapeutic considerations. Respiratory acidosis, absent in the elderly hypothyroid patient, al­ , and hypocapnia occur for several reasons though a diffuse or nodular goiter can be present (Table 3). Alveolar is caused in 3.5 percent of patients. I I A neck scar would be by associated muscle weakness, coma, airway ob­ a clue to previous thyroidectomy and would be struction from edellla and secretions, and an in­ very helpful in making the diagnosis. creased sensitivity to sedating drugs."; Further Abdominal findings include , fecal respiratory f~lilure, , and hypoventila­ impaction, abdominal distention, , and a tion result from central nervous system insensitiv­ distended bladder caused by retention and ity to rising arterial blood carbon dioxide (CO,).2"+ atony.II-U Myxedema megacolon is a life-threat­ Obstructive sleep apnea has been reported ~md ening condition. Intestinal mucopolysaccharides complicates this problem.") separate the muscle fibers of the intestine from A reduction in cardiac index also occurs by sev­ the ganglia of the Auerbach plexus with resulting eral mechanisms ([lble 4),23 Infiltrative cardio-

37H JABFP Sept.-Oct. 1995 Vo\. H No.5 J Am Board Fam Pract: first published as 10.3122/jabfm.8.5.376 on 1 September 1995. Downloaded from Table 3. Mechanisms of Respiratory Acidosis in hypothyroid patient. Thyroid-stimulating hor­ Myxedema Coma. mone (TSH) is the most sensitive test in deter­ mining hypothyroidism and is the first laboratory Ventilatory muscle dysfunction abnormality seen in myxedema coma patients. In Myopathy secondary or tertiary hypothyroidism caused by Coma pituitary or hypothalamic dysfunction, respec­ Upper airway obstruction tively, TSH will not be elevated. The newer high­ Secretions Defective cough reflex sensitivity TSH test is helpful in diagnosing Sleep apnea , but levels would also be el­ Diminished central nervous system sensitivity to carbon dioxide evated in cases of hypothyroidism. Sensitivity to sedating drugs The diagnosis of secondary or tertiary hypo­ thyroidism is critical from a mortality and manage­ myopathy and hypothermia depress myocardial ment standpoint. Seeondary hypothyroidism re­ contractility. Bradycardia, increased systemic vas­ sults from pituitary failure. An isolated pituitary cular resistance, and eventual hypovolemia con­ trophic hormone defect is rare, and most cases of tribute to a reduced cardiac index. Because the secondary hypothyroidism result from pituitary tu­ patient's metabolic requirements and oxygen con­ mors or postpartum pituitary necrosis. Tertiary, or sumption are also reduced, a diminished cardiac hypothalamic, hypothyroidism is usually due to index can remain adequate to meet the patient's trauma, tumor, or irradiation. Although idiopathic metabolic needs. cases exist, hypothalamic insufficiency is uncom­ Hyponatremia in the myxedema coma patient mon. In either case of secondary or tertiary hypo­ could be due entirely to hypothyroidism or could thyroidism the TSH and T 4 levels are low, as are be accentuated by systemic illness. Less often the gonadotropins in the postmenopausal woman hyponatremia is due to inappropriate antidiuretic and serum cortisol in both female and male pa­ hormone production or . A tients. A thyroid replacement hormone administra­ decrease in free water clearance attributed to an tion assay would be useful in that no detectable rise increased release of antidiuretic hormone and to in base-line serum TSH would occur. intrarenal abnormalities leading to deceased distal Thyroid microsomal and anti­ tubular delivery of hypotonic filtrate is the princi­ bodies are frequently elevated in cases of primary pal explanation of hyponatremia.26,27 A dimin­ hypothyroidism from autoimmune or idiopathic ished urine output results from a decreased glo­ causes. Knowing the antibody levels can be help­

merular filtration rate and decreased renal blood ful in the diagnosis, because these antibodies fall http://www.jabfm.org/ flow and hypovolemia. dramatically after treatment with thyroid hor­ Hypoglycemia indicates the possibility of adre­ mone replacement therapy. This response might nal insufficiency that occurs in 5 to 10 percent of reflect reduced antigen availability to the immune myxedema coma patients. Adrenal insufficiency is system resulting from a decreased stimulation of due to a sluggish pituitary-adrenal axis and is ex­ thyroid tissue by TSH.30 The degree of abnor­ mality of the thyroid hormone does not correlate acerbated by the increased metabolism of cortisol on 24 September 2021 by guest. Protected copyright. that occurs once thyroid hormone replacement with the level of consciousness in these patients.31 therapy begins. Primary adrenal failure is uncom­ Because myxedema coma has profound effects mon, and when it occurs with Hashimoto thy­ on the cardiovascular system, many cardiac roiditis, it is known as Schmidt syndrome. Serum calcium levels are usually normal or slightly decreased. Occasionally hypercalcemia Table 4. Mechanism of Reduction on Cardiac Index in and result from diminished Myxedema Coma.

urinary excretion of calcium in thyroid-deficient Depressed myocardial contractility patients.28,29 Cardiomyopathy Hypothermia Laboratory Findings Bradycardia Typically a low serum thyroxine ([4) and possibly Increased systemic vascular resistance ([3) are found in the severely Hypovolemia

Myxedema Coma 379

D J Am Board Fam Pract: first published as 10.3122/jabfm.8.5.376 on 1 September 1995. Downloaded from parameters are found to be abnormal. Cardiac roundly ill patient. Carcinoembryonic levels are isoenzyme profiles are elevated, suggesting myo­ elevated and nonspecific, and there can be a mild cardial infarction even in the absence of is­ anemia of the normocytic, normochromic type. chemia. 3! This linding can be misleading, because Microcytosis is rare. The white cell count and the myxedema coma patient is at risk for myocar­ platelets are usually normal. dial compromise and just such a .u.H­ Thrombocytopenia has been reported in hypo­ In addition to elevations in lactic dehydrogenase thermia secondary to the sequestration of plate­ and aspartate aminotransferase, creatinine phos­ lets in the liver and spleen. 'len percent of hypo­ phokinase (CPK) activity is usually increased. thyroid patients also have pernicious anemia, Although CPK myocardial bands can be present, possibly as the result of an immune dysfunction. +0 lllost of the CPK isoenzyme is of muscle origin. There are no electroencephalographic charac­ This abnormality is thought to be due to increases teristics that are pathognomonic of myxedema in membrane permeability in muscle rather than coma. Slowing of the alpha rhythm and diminu­ muscle destruction. IS These enzyme abnormal­ tion of the reaction to light stimulation are ities persist until thyroid hormone replacement present but nonspecific. Hypothermia results in a therapy has occurred. pronounced lowering of the amplitude of back­ Electrocardiographic abnormalities are foune! ground activity. Cerebrospinal fluid in myxedema in myxedema coma with or without pericardial ef­ coma patients has elevated protein levels of 40 to fusions. Common findings include sinus brady­ 90 percent beyond normal and can be greater cardia, small voltage complexes, T wave inver­ than 100 mg/dL. Elevated cerebrospinal fluid anel sions and nonspecific T wave flattening. ~IyPe one serum gamma globulin levels have been reported. atrioventricular (AV) block and prolonged QT in­ The opening pressure upon lumbar puncture is tervals are also seen.!l These findings, with the elevatee!.+l Electromyographic and nerve conduc­ exception of inverted T waves, resolve with treat­ tion abnormalities exist and are consistent with ment, which suggests possible permanent struc­ the commonly found polyneuropathy with a tural changes have occurred.36 Reversible AV demyelinating component.+1 block is rare. 17 ST wave changes are not charac­ teristic in myxedema coma. T wave flattening or Treatment inversion might also be an indication of underly­ Treatment of myxedema coma must be initiated ing coronary disease and cardiac ischemia. upon suspicion of the condition before confirma­

Echocardiographic studies are useful in detect­ tory laboratory findings. Management consists of http://www.jabfm.org/ ing pericardial effusions that might be undetect­ supportive therapy, hormone replacement, and able in a chest radiograph. The incidence of peri­ treatment of underlying and concurrent illness. cardial effusions is 30 to 78 percent in various The myxedema coma patient should be ad­ studies. lli Asymmetric septal hypertrophy or idio­ mitted to an or similar telem­ pathic hypertrophic subaortic stenosis has been etry floor for close and continuous cardiac moni­ reported as being secondary to hypothyroidism. toring. Reestablishment of the airway could be on 24 September 2021 by guest. Protected copyright. These findings can be reversible with thyroid necessary in cases of extreme hypoventilation, hormone replacement therapy. III hypercapnia, and hypoxia. Intubation of the air­ Room air blood gas measurements are neces­ way should be approached with caution. The sary and reflect respiratory acidosis. Electrolyte delicate, swollen laryngeal mucosa is easily disturbance includes hyponatremia, hypokalemia, damaged by traumatic or prolonged intubation. and possibly hypochloremia. Elevated creatinine Hypothyroid patients are more difficult to wean levels are not uncommon. Hypoglycemia sug­ from ventilatory assistance because of carbon gests a pituitary, hypothalamic, or adrenal defect. dioxide retention.+2 Low serum glucose levels can persist several Administration of intravenous fluids is a neces­ weeks after treatment. Elevated C peptide levels sary treatment of hypovolemi,\ and hypotension l can be due to hypometabolism. () Serum lactate is and to correct for electrolyte disturbance. Careful usually normal. Serum and triglycer­ fluid status monitoring is important because of ides are elevated and of little clinical importance, the compromised cardiovascular state, and a though lipid levels can be depressed in the pro- Swan-Ganz catheter can be useful to monitor this

3HO }ABFP Sept.-Oct. I <)<)5 Vol. H No.5 J Am Board Fam Pract: first published as 10.3122/jabfm.8.5.376 on 1 September 1995. Downloaded from situation. Avoid hemodynamic overcorrection in ing the first 6 months of therapy do not reflect the this low metabolic state. A combination of slow optimal dose of T4 replacement on a long-term infusion and water restriction is the treat­ basis. 47 ment of choice. The lowered metabolic state and possible sec­ Inotropic drugs, such as digoxin, might be ondary or tertiary hypothyroidism complicate needed in the hemodynamically unstable pa­ medical management. All stuporous patients with tient. These drugs must be prescribed with ex­ either hypotension or hyponatremia require treme caution because they are synergistic with stress level replacement. Hydro­ thyroid replacement, and adverse reactions, such cortisone, 200 to 300 mg, should be given in daily as arrhythmias, are common. If a pressor agent is divided doses for 3 to 7 days. In the confirmed ab­ necessary, dopamine is preferred to norepineph­ sence of secondary or tertiary hypothyroidism, rine to maintain coronary, mesenteric, and renal the can be tapered rapidly. Such perfusion. therapy causes no harm to the primary hypothy­ The method of thyroid hormone replacement roid patient and can be lifesaving to the others. therapy in the myxedema coma patient has been a Concurrent illness is frequently present and focus of controversy. Because this condition is acts as a precipitant in the comatose patient. uncommon, controlled studies on the method of Signs of underlying infection, such as fever and replacement therapy do not exist. In early reported leukocytosis, are commonly masked. Pneumonia, cases patients received low-dose thyroid replace­ urinary tract infection, and bacteremia are com­ ment, but the mortality in these cases exceeded 80 mon and should be sought and treated empiri­ percent. In the mid-1960s, Holvey, et al.43 reported cally. Urinalysis, cultures, and chest radiograph several cases successfully treated with high-dose should be obtained early in the workup of the pa­ intravenous thyroxine replacement. L-Thyroxine tient. , congestive heart should be administered intravenously at a dose of failure, and cerebrovascular accident are com­ 250 to 500 mg for a 30- to 60-second period. A mon in such patients and need to be treated dose can be administered 12 hours later if the accordingly. body temperature and sensorium are not im­ proved. The intravenous route results in high Adverse Reactions to Treatment peaks of plasma T 4• Peripheral conversion ofT4 Determinants of fatal outcome in myxedema to T3 allows gradual T] delivery to organ systems coma patients include old age and high serum T3 48 even if only L-thyroxine is used. Although admin­ levels. Treatment of the comatose patient re­ http://www.jabfm.org/ istration ofT3 is more potent, it is associated with sults in immediate cardiovascular changes. In­ greater mortality, whereas T4 is easier to adminis­ creases occur in oxygen consumption, oxygen de­ ter and less stressful to critically ill patients. livery, cardiac output, , and ventricular Once the patient is capable of taking oral medi­ response.49 Overly aggressive treatment of the cations, a maintenance dose can be administered comatose patient precipitates tissue hypoxia and daily. Oral absorption of L-thyroxine is variable, possible myocardial infarction. but a clinical response does occur, even in cases of Actual rewarming equipment is contraindi­ on 24 September 2021 by guest. Protected copyright. myxedema ileus.44 Elderly patients require T4 cated in the hypothermic patient, who will re­ dosing in a range of 100 to 170 mg daily. This spond to thyroid hormone replacement therapy maintenance dose has been found to be lower alone. Active rewarming causes vasodilatation and than that needed for younger patients because the refractory hypotension and can be fatal. Failure to T 4 degradation rate declines with aging.45 ,46 address adrenal insufficiency will likewise result Serum T 4' free thyroxine index, and T 3 can be in cardiovascular collapse. Delayed respiratory transiently elevated early in the course of replace­ failure during treatment of a comatose patient has ment therapy. WIthin the first 6 weeks of replace­ been reported.50 ment therapy, these levels might even be within the thyrotoxic range as a result of the decreased Prevention metabolic clearance rate of the absorbed hor­ Prevention is the greatest treatment for myx­ mone. These levels then stabilize 4 to 8 months edema coma and its complications. Screening eld­ later. As a result the serum T4 and T] levels dur- erly women using a serum TSH measurement has

Myxedema Coma 381 J Am Board Fam Pract: first published as 10.3122/jabfm.8.5.376 on 1 September 1995. Downloaded from been proposed.sl Thyroid studies should be ob­ 17. Gupta R, Sinha J, Purohit R. Refractory hypoten­ tained and documented in all symptomatic elderly sion. A clue to myxedema coma. J Assoc Physicians India 1()92; 40(2): I 05. patients and bct()/·c e1cctivc surgcry. Known hy­ 18. Collins K,l, Dore C, Exton-Smith AN, Fox RII, pothyroid p,nients should be questioned about MacDonald Ie, vVoodard PM. Accidental hypother­ compliancc with replaccment therapy, and the ad­ mia and impaired temperature homeostasis in the equacy of their treatment should be periodically elderly. Hr MedJ 1977; 1:353-6. lllonitored. I

II. Watanakunakorn C, Hodges RE, Evans TC. Myx­ thyroid microsomal and thyroglobulin antibodies in on 24 September 2021 by guest. Protected copyright. edema. Arch Intern Med 1%5; 116:IH3-90. idiopathic myxedema and in hypothyroid, but not in 12. Signore RJ, von Weiss J. Alopecia of myxedema: euthyroid Hashimoto's . J Endocrinol In­ clinical response to levothyroxine sodium.] Am Acad vest 1986; 9:299-305. DennatoI199!; 25:<)02-4. 31. Myers L, Hays J Myxedema coma. Crit Care Clin 13. de Castro I'~ Bonacini M, vValden .1 M, Schubert Tl~ 1991; 7:43-56. Myxedema ascites. Report of two cases and review of 32. Hickman PE, Silvester W, Musk M, McLellan GH, the literature . .1 Clin Castroenterol 1991; 13:411-4. Harris A. Cardiac enzyme changes in myxedema 14. Borrie MJ, Cape In~ 'Iroster MM, Fung ST Myx­ coma. Clin Chem 1987; 33:622-4. edema megacolon after external neck irradiation. 33. Nee PA, Scane AC, Lavelle PH, Fellows IW, Hill JAm Ceriatr Soc 1983; 31 :22H-30. PC. Hypothermic myxedema coma erroneously di­ 15. Burrell M, CronanJ, lVlegan D, 'Ii>ftler R. Myxedema agnosed as myocardial infarction because of in­ megacolon. Castrointest Radiol 1980; 5: I 81-6. creased MB. Clin Chem 19H7; 16. Patel R, Hughes RvV ) r. An unusual case of myx­ 36: 1083-4. edema megacolon with features of ischemic and 34. Peter SA. Myxedema mimicking myocardial is­ pseudomembranous colitis. j\hyo Clin Proc 1992; chemia in a young black male. J Nat Med Assoc 67:3(,<)-72. 1991; 83:467-H.

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Myxedema Coma 383