Thyroid disorder: Causes, Symptoms and Management
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| Thyroid disorder: Hyperthyroidism and Hypothyroidism |
HYPERTHYROIDISM
Major clinical findings in hyperthyroidism are Cardiac findings may be prominent including tachycardia, atrial fibrillation, heart failure, and exacerbation of coronary artery disease. Rarely, severe hyperthyroidism may be associated with fever and delirium, sometimes called "thyroid storm."
Major causes of hyperthyroidism are listed as Graves' disease (which may also cause proptosis) is the most common.
When hyperthyroidism is diagnosed in a critically ill patient, plasma thyroid-stimulating hormone (TSH) and free thyroxine (T4) should be measured. Clinical hyperthyroidism suppresses TSH to <0.1 µU/mL, so a nonsuppressed plasma TSH excludes the diagnosis of hyperthyroidism. Plasma TSH may also be suppressed by severe nonthyroidal illness (about 10% of patients in intensive care units have plasma) TSH <0.1 µU/mL and by therapy with dopamine or high-dose glucocorticoids. Thus, a suppressed plasma TSH alone does not establish the diagnosis.
If plasma TSH is suppressed and plasma free T4 is elevated, the diagnosis of hyperthyroidism is established. If plasma free T4 is not elevated, one of the other causes of suppressed plasma TSH listed earlier is more likely. Heparin therapy may artifactually increase plasma free T4, so in heparin-treated patients, plasma total T4 should be measured instead.
Major Clinical Findings in Hyperthyroidism
Common Findings:
Heat intolerance
Weight loss
Palpitations
Sinus tachycardia
Atrial fibrillation
Brisk tendon reflexes
Fine tremor
Lid lag
Proximal muscle weakness
Seen Primarily in Severe Hyperthyroidism:
Heart failure
Exacerbation of coronary artery disease
Fever and delirium ("thyroid storm")
Major Causes of Hyperthyroidism
Associated with increased radioactive iodine uptake:
Graves' disease
Toxic multinodular goiter
Thyroid adenoma
Associated with decreased radioactive iodine uptake:
Iodine-induced hyperthyroidism (due to amiodarone or iodine-containing contrast media)
Painless thyroiditis
Subacute thyroiditis
Factitious hyperthyroidism (ingestion of thyroid hormone)
Iodine excess can cause both hyper- and hypo-thyroidism depending on the patients' underlying thyroid function and basal iodine consumption.
Treatment
The etiology of hyperthyroidism determines the best long-term therapy, but differential diagnosis can be deferred in the critically ill patient. Emergency therapy is indicated when hyperthyroidism exacerbates heart failure or an acute coronary syndrome, or when thyroid storm is present. It includes rapid inhibition of thyroid hormone synthesis (and conversion of T4 to triiodothyronine [T3]) by the thionamide propylthiouracil (PTU), inhibition of thyroid hormone secretion by iodine, and inhibition of the cardiovascular effects of hyperthyroidism by beta-adrenergic antagonists. Hydrocortisone is usually recommended because it also inhibits T4 conversion to T3.
Some authors have advocated treatment of amiodarone-induced hyperthyroidism with glucocorticoids alone, but the regimen described above has a high success rate in this disorder.
Plasma free T4 should be measured every 3 to 7 days. When free T4 approaches the normal range, the doses of PTU and iodine should be gradually decreased. Iodine can usually be stopped at the time of hospital discharge, and radioactive iodine therapy for Graves' disease or toxic multinodular goiter can be scheduled 2 to 3 weeks later. If long-term thionamide therapy is chosen instead of radioactive iodine PTU should be stopped and methimazole used instead.
Emergency Therapy of Hyperthyroidism
Propylthiouracil (PTU): 300 mg PO Q6h
Iodine (super saturated potassium iodide): 2 drops PO Q12h
Beta-antagonist, with the dose adjusted to control tachycardia; initially:
Propranolol 40 mg PO Q6h, or
Esmolol 500 µg/kg IV followed by 50 µg/kg/min IV
Hydrocortisone: 50 mg IV Q8h
HYPOTHYROIDISM
Major clinical findings in hypothyroidism are listed as: Severe hypothyroidism may contribute to hypothermia, hypoventilation, bradycardia, hypotension, and hyponatremia in the setting of concomitant critical illnesses.
Major causes of hypothyroidism mentioned below. More than 90% of cases are primary hypothyroidism, most often iatrogenic or due to chronic autoimmune thyroiditis. Any pituitary or hypothalamic disorder can cause secondary hypothyroidism, but these disorders are usually clinically apparent because of other manifestations.
When the diagnosis of hypothyroidism is suspected in a critically ill patient, plasma TSH and free T4 should be measured. Even mild primary hypothyroidism causes elevation of plasma TSH, so a normal plasma TSH excludes this diagnosis. Plasma TSH values >20 µU/ml establish the diagnosis of primary hypothyroidism. Milder elevations of plasma TSH are usually due to primary hypothyroidism, but may also occur transiently during recovery from severe nonthyroidal illness.
If plasma free T4 is low and plasma TSH is not elevated, the patient may have secondary hypothyroidism, but in a critically ill patient, this pattern of test results is more likely to be due to functional suppression of TSH and T4 secretion by nonthyroidal illness (the "euthyroid sick syndrome"). If the patient has clinical findings that may be due to hypothyroidism, empiric treatment with T4 should be started.
Major Clinical Findings in Hypothyroidism
Common Findings:
Cold intolerance
Fatigue
Somnolence
Constipation
Weight gain
Slow tendon reflexes
Nonpitting edema (myxedema)
Dry skin
Seen Primarily in Severe Hypothyroidism:
Hypothermia
Bradycardia
Hypoventilation
Hypotension
Hyponatremia
Pericardial or pleural effusion
Major Causes of Primary Hypothyroidism
Chronic lymphocytic thyroiditis (Hashimoto's disease)
Iatrogenic (after radioactive iodine therapy or thyroidectomy)
Drugs:
Iodine excess (e.g., amiodarone, iodine-containing contrast media)
Lithium
Interferon-alpha
Interleukin-2
Iodine deficiency
Iodine excess can cause both hyper- and hypo-thyroidism depending on the patients' underlying thyroid function and basal iodine consumption.
Treatment
Emergency therapy of hypothyroidism is indicated if the patient has clinical signs that could be contributed to by hypothyroidism, such as bradycardia, hypoventilation, hypothermia, or hypotension. Each of these abnormalities should be treated in the standard fashion, since they are rarely due to hypothyroidism alone. Vital signs and cardiac rhythm should be monitored since the treatment can exacerbate underlying heart disease. Hydrocortisone may be given because adrenal failure may be associated with chronic autoimmune thyroiditis.
No clinical trials have determined the optimum method of emergency treatment of hypothyroidism, but this method rapidly alleviates T4 deficiency while minimizing the risk of adverse events. There is no evidence to support treatment of the functional suppression of TSH and T4 by nonthyroidal illness.
The diagnosis should be reassessed after recovery. Otherwise, the patient can be observed with periodic measurement of plasma TSH and free T4 to determine whether the abnormalities resolve with recovery.
Emergency Therapy of Hypothyroidism
Thyroxine 50-100 UR IV Q6-8h for 24 hr. then for 24 hr, then
Thyroxine 75-100 ug IV Q24h until oral intake is possible
Hydrocortisone: 50 mg IV Q8h