Diffuse Toxic Goiter Treatment & Management

  • Author: Bernard Corenblum, MD, FRCP(C); Chief Editor: George T Griffing, MD   more...
 
Updated: Jul 25, 2011
 

Medical Care

Even though the natural history of diffuse toxic goiter is to possibly spontaneously remit (and perhaps later relapse), or even progress into hypothyroidism, observation without intervention, even in minimally symptomatic people, is not recommended. The risk of bone loss and atrial fibrillation occur, especially in older women and men, even in subclinical cases.

The goals of therapy are to resolve hyperthyroid symptoms and to restore the euthyroid state.

Each therapeutic choice has advantages and disadvantages, so treatment should be individualized. Patient input into the treatment choice is important and must be discussed and considered. The American Thyroid Association and American Association of Clinical Endocrinologists have released guidelines for the management of hyperthyroid and other causes of thyrotoxicosis, including the use of radioactive iodine or surgery to treat toxic multinodular goiter.[1]

Therapy may be by subtotal thyroidectomy, administration of radioiodine, antithyroid drugs, or a combination of these. In North America, radioiodine is the most common treatment and is available for all ages. Adjunctive symptomatic therapy, such as beta-blockers, may help adrenergic symptoms. Nonsurgical therapy occurs in the outpatient setting. Surgical therapy requires first normalization of the hyperthyroid state by medication.

Cardiac decompensation or arrhythmias may require hospitalization.

Thyroid storm is a rare emergency requiring intensive care support and therapy.

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Surgical Care

Subtotal thyroidectomy may be considered if it is the choice of the patient, second trimester of pregnancy, failure (resistance or intolerance) of drug therapy, or poor compliance to drug therapy. Risks are low with experienced surgeons but include anesthetic risks, hemorrhage, hypoparathyroidism, and vocal cord paralysis. Patients should be made euthyroid prior to surgery to minimize anesthetic risks, cardiovascular/hemodynamic complications, and risk of thyroid storm. If normalizing with antithyroid drugs is not possible, then beta-blockers and potassium iodide 4 drops/day for 10 days will decrease vascularity of the thyroid gland.

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Consultations

Oculopathy usually requires ophthalmologic consultation, and dermopathy may require dermatologic consultation.

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Diet

Diet must include caloric intake to meet the energy expenditure of the hypermetabolism. High iodine-containing substances, such as kelp, should be avoided.

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Activity

Physical activity is limited by the presence of symptoms, until recovery occurs. Usually, shortness of breath on exertion, fatigue, and palpitations are the limiting symptoms.

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Contributor Information and Disclosures
Author

Bernard Corenblum, MD, FRCP(C)  Professor of Medicine, Director, Endocrine-Metabolic Testing and Treatment Unit, Ovulation Induction Program, Department of Internal Medicine, Division of Endocrinology, University of Calgary, Canada

Disclosure: Nothing to disclose.

Coauthor(s)

Oluyinka S Adediji, MD  Consulting Staff, Department of Adult and General Medicine, Health Services Incorporated, Montgomery, Alabama

Oluyinka S Adediji, MD is a member of the following medical societies: American College of Physicians and American Medical Association

Disclosure: Nothing to disclose.

Paul Killian, MD  Former Chief of Endocrine Service, Former Associate Professor, Department of Internal Medicine, Harlem Hospital, Harlem Hospital Center

Paul Killian, MD is a member of the following medical societies: American College of Physicians-American Society of Internal Medicine, American Diabetes Association, and Endocrine Society

Disclosure: Nothing to disclose.

Specialty Editor Board

Steven R Gambert, MD  Professor of Medicine, Johns Hopkins University School of Medicine; Director of Geriatric Medicine, University of Maryland Medical Center and R. Adams Cowley Shock Trauma Center

Steven R Gambert, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physician Executives, American College of Physicians, American Geriatrics Society, Association of Professors of Medicine, Endocrine Society, and Gerontological Society of America

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Yoram Shenker, MD  Chief of Endocrinology Section, Veterans Affairs Medical Center of Madison; Interim Chief, Associate Professor, Department of Internal Medicine, Section of Endocrinology, Diabetes and Metabolism, University of Wisconsin at Madison

Yoram Shenker, MD is a member of the following medical societies: American Heart Association, Central Society for Clinical Research, and Endocrine Society

Disclosure: Nothing to disclose.

Mark Cooper, MBBS, PhD, FRACP  Head, Diabetes & Metabolism Division, Baker Heart Research Institute, Professor of Medicine, Monash University

Disclosure: Nothing to disclose.

Chief Editor

George T Griffing, MD  Professor of Medicine, St Louis University School of Medicine

George T Griffing, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Medical Practice Executives, American College of Physician Executives, American College of Physicians, American Diabetes Association, American Federation for Medical Research, American Heart Association, Central Society for Clinical Research, Endocrine Society, International Society for Clinical Densitometry, and Southern Society for Clinical Investigation

Disclosure: Nothing to disclose.

References
  1. Bahn RS, Burch HB, Cooper DS, et al. Hyperthyroidism and other Causes of Thyrotoxicosis: Management Guidelines of the American Thyroid Association and American Association of Clinical Endocrinoloigists. Endocr Pract. May-Jun 2011;17(3):456-520. [Medline].

  2. Nakamura H, Noh JY, Itoh K, Fukata S, Miyauchi A, Hamada N. Comparison of methimazole and propylthiouracil in patients with hyperthyroidism caused by Graves' disease. J Clin Endocrinol Metab. Jun 2007;92(6):2157-62. Epub 2007 Mar 27. [Medline].

  3. FDA MedWatch Safety Alerts for Human Medical Products. Propylthiouracil (PTU). US Food and Drug Administration. Available at http://www.fda.gov/Safety/MedWatch/SafetyInformation/SafetyAlertsforHumanMedicalProducts/ucm164162.htm. Accessed June 3, 2009.

  4. Vanderpump M. Cardiovascular and cancer mortality after radioiodine treatment of hyperthyroidism. J Clin Endocrinol Metab. Jun 2007;92(6):2033-5. [Medline].

  5. Cawood T, Moriarty P, O'Shea D. Recent developments in thyroid eye disease. BMJ. Aug 14 2004;329(7462):385-90. [Medline].

  6. Cooper DS. Antithyroid drugs. N Engl J Med. Mar 3 2005;352(9):905-17. [Medline].

  7. deGroot LJ, Larsen RP, Hennemann G. The Thyroid and Its Diseases. 1996;371-489.

  8. Franklyn JA, Maisonneuve P, Sheppard M, et al. Cancer incidence and mortality after radioiodine treatment for hyperthyroidism: a population-based cohort study. Lancet. Jun 19 1999;353(9170):2111-5. [Medline].

  9. Mestman JH. Hyperthyroidism in pregnancy. Best Pract Res Clin Endocrinol Metab. Jun 2004;18(2):267-88. [Medline].

  10. Sarlis NJ, Gourgiotis L. Thyroid emergencies. Rev Endocr Metab Disord. May 2003;4(2):129-36. [Medline].

  11. Schwartz KM, Fatourechi V, Ahmed DD, Pond GR. Dermopathy of Graves' disease (pretibial myxedema): long-term outcome. J Clin Endocrinol Metab. Feb 2002;87(2):438-46. [Medline].

  12. Weetman AP. Graves' disease. N Engl J Med. Oct 26 2000;343(17):1236-48. [Medline].

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