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GOITER PHILIPPINE THYROID ASSOCIATION Philippine Thyroid Association, Inc. 2/F, Development Office Clinical Division, University of Santo Tomas, Espana, Manila Telephone Nos.: 731-4548; 731-3001 loc 2473 Fax No.: 731-4548 Officers and Board of Directors President Vice President Secretary Treasurer P.R.O. Teofilo San Luis, Jr., M.D. Benigno L. Ong, M.D. Leilani Mercado-Asis, M.D., Ph.D. Consolacion O. Obmerga, M.D. Roy J. Cuison, M.D. Board of Directors Lourdes S. Paulino, M.D. Rogel H. Kalalo, M.D. Susan Yu-Gan, M.D. Ruben V. Ogbac, M.D. Vincent C. Santos, M.D. Luis Roy P. Colendrino, M.D. Immediate Past President Luis Roy P. Colendrino, M.D. 123 GOITER cpm 4TH eDITION A General Approach to Patients Presenting with Goiter 1 Patient with goiter 2 History & PE (A) 4 3 Obstructive symptoms? (B) Y Surgical consult N 5 6 Are there signs of thyro- Y T3, T4, TSH toxicosis? (D) (C) 7 8 N Toxicity confirmed? (E) Y 10 12 Nodule palpated? (F) 13 Y N Diffuse toxic goiter (see Figure 3) 11 Nodular non- toxic goiter (see Figure 4) N Diffuse nontoxic goiter (see Figure 5) Figure 1 124 Nodule palpated? (E) N 9 Y Nodular toxic goiter (see Figure 2) CPM 4TH EDITION GOITER Algorithm for Patients with a Nodular Toxic Goiter 1 Nodular toxic goiter (G) 3 2 Solitary nodule? Radionuclide scan (H) 4 5 N Y Hot nodule? 6 N Warm nodule 7 Compensated autonomous adenoma 9 Anti-thyroid drugs + β-blockers (J) 8 Y Multiple nodules (I) Responsive? (K) 12 11 10 N Y Monitor thyroid function; adjust dose (L) Refer for RAI or surgery (M) Figure 2 125 GOITER cpm 4TH eDITION Algorithm for Patients with a Diffuse Toxic Goiter 1 Diffuse toxic goiter 4 3 2 Eye signs? (N) Graves' disease (O) Ophtha consult; possible steroid therapy (P) 5 N Y Thyroid antibodies if available 6 Antithyroid drugs + β- blockers (J) 8 7 Responsive? (K) 9 N Refer for RAI or surgery (M) Figure 3 126 Y Monitor thyroid function; adjust dose (L) CPM 4TH EDITION GOITER Algorithm for Patients with a Nodular Non-Toxic Goiter 1 Nodular nontoxic goiter (Q) 3 2 Solitary nodules? Thyroid ultrasound 4 5 N Y Liquid? N Aspiration & Cytology (R) 8 Solid or complex (S) 10 N Suspicious or definitely malignant N Refer to surgery Hormone Supression 11 12 Recurrence? 14 13 Thyroid Y See Figure 4B Benign? See Figure 4A 9 Multiple nodules 7 6 Y N Persistence? 16 Y Reaspirate; surgical consult (T) 15 Y Surgical consult N Observe Figure 4 127 GOITER cpm 4TH eDITION Algorithm for Patients with a Nodular Non-Toxic Goiter (Multiple) 1 Multinodular non-toxic goiter (U) 2 Radionuclide scan 4 3 5 Refer for Y Is RAI uptake possible RAI Y increased? 6 Predominantly warm nodules? N N Thyroid Hormone Supression (W) 8 7 Regression? Predominantly cold nodules 10 9 N Refer for possible surgery Figure 4A 128 therapy (V) Y Continue therapy and follow-up CPM 4TH EDITION GOITER Algorithm for Patients with a Nodular Non-Toxic Goiter (Complex or Solid) From Fig. 4 2 1 Complex nodule? Radionuclide scan hormone supression N 8 Suspicious or definitely malignant Hot nodule 13 Y Thyroid hormone suppression 14 Regression? 17 Y Continue therapy & follow-up N Surgical consult 15 N Go to # 2 Y 9 Regression? 11 N Warm nodule? 16 Y 7 Thyroid Y N Cold nodule? 12 6 Benign? N Solid nodule? 10 4 3 5 Y Fine needle aspiration biopsy Y Continue therapy & follow-up N Refer for possible RAI therapy Figure 4B 129 GOITER cpm 4TH eDITION Algorithm for Patients with a Diffuse Non-Toxic Goiter 1 Diffuse non-toxic goiter (X) Normal TSH & normal T4? 4 3 2 Y Euthyroid goiter Thyroid hormone supression (Y) 5 6 N Regression? 7 N Refer for possible surgery 9 8 High TSH & normal T4? 10 N High TSH & low T4? 12 Y Subclinical hypothyroidism (Z) 11 Y Overt hypo- thyroidism N Other combinations of TSH & T4 13 Refer Figure 5 130 Y Continue therapy & follow-up CPM 4TH EDITION GOITER Algorithm for Patients with Hypothyroidism 1 Hypothyroidism (AA) 3 2 Congenital? (BB) 4 Y 5 N Acquired Refer to pediatric Diet origin (goitrogens, I deficiency, I excess)? (CC) 7 Y Discontinue Y May need thyroid hormone if persistent N 13 N Less common causes N Y PostY inflammatory? 15 9 N Post-RAI? 12 Dietary corrections 8 Post-thyroidectomy? 11 Y N Antithyroid drug intake? 10 6 Thyroid hormone replacement 14 Monitor TSH 16 Refer Figure 5A 131 GOITER cpm 4TH eDITION Guidelines for the Management of Goiter Footnotes A. Thyroid gland enlargement may be graded according to the WHO GOITER GRADING SYSTEM Stage O - No goiter Stage IA - Goiter detectable only by palpation and not visible even when the neck is fully extended Stage IB - Goiter palpable but visible when the neck is fully extended Stage II - Goiter visible with the neck in normal position; palpation is not needed for diagnosis Stage III - Very large goiter that can be recognized at a considerable distance B. OBSTRUCTION refers to the significant difficulty in swallowing or breathing due to thyromegaly with or without nodules. Interpretation of Total Score <1 - Probable Hypothyroid 1-10 - Probable Euthyroid >11 - Probable Hyperthyroid D. In general, T3, T4 and TSH determination should suffice to screen for hyperthyroidism. However, the use of FT4 and FT3 is indicated in conditions which can cause alteration in TBG saturation, as in pregnancy, kidney or liver disease, or use of birth control pills, steroid, salicylates, androgens, etc. E. Toxic goiter is confirmed by an increased T4, increased T3, decreased TSH, increased FT3 or increased FT4. These laboratory findings must always be correlated with the clinical signs and symptoms as described in footnote C. In some situations, an increased T4 does NOT necessarily indicate hyperthyroidism. These include thyroiditis, thyrotoxicosis factitia, increased TBG (congenital, estrogen, birth control pills), autoantibodies against T4, peripheral resistance to thyroid hormones, decreased peripheral deiodination of T4 to T3, non-thyroidal illness (acute psychiatric disease), and use of x-ray contrast media. Similarly, not all elevated T3 indicates T3 toxicosis. These exceptions include states of increased TBG (as in footnote (D), iodine deficiency, T3 administration (e.g. Cytomel), autoantibodies against T3, and mild primary hypothyroidism. Finally, some patients consult with results indicating increased radioactive iodine uptake (RAIU). This also does not always indicate hyperthyroidism, and may be seen in patients with iodine deficiency, prior antithyroid treatment, preceding subtotal thyroidectomy, or congenital disturbance of hormone synthesis. C. Signs and symptoms of thyrotoxicosis may be evaluated according to a UST - formulated clinical scoring index modified from Wayne's criteria. Hyperthyroid SYMPTOMS Weight Loss +4 Weight Gain Nervousness +4 Easy Tiredness +2 Palpitations +1 Increased Sweating +1 Dyspnea on Effort +1 Irritability +1 Weakness +1 Increased Appetite +1 Decreased Appetite Intolerance of Heat +1 Constipation SIGNS Warm, Moist Skin +4 Rough, Dry Skin Thyroid Enlargement Diffuse +2 Nodular Exophthalmos +4 Fine Finger Tremor +3 Pulse Rate Above 110 +2 100-110 +1 70-100 0 Below 70 Hyperkinetic Movement +1 Sluggish Movement 132 Hypothyroid -2 -2 -2 -3 -1 -1 -4 F. The palpatory finding of a nodule(s) changes the complexion of the disease process at hand. Extra effort must therefore be exerted to rule in or rule out nodular changes. The number, size, and consistency of the nodule(s) must also be noted. G. A high proportion of patients with nodular thyroid gland develop thyrotoxicosis. This often comes about insidiously, with the patient unaware of symptoms, infiltrative ophthalmopathy is absent. H. Radionuclide scan using I131 or Tc99 classifies a toxic nodule into hot or cold. A “hot” nodule is one that is very active and so avid that the radionuclide is removed from the extranodular tissues and all CPM 4TH EDITION shifted into the nodule. When the radionuclide still resides in the extranodular tissue in the same avidity as inside the nodule, the nodule is referred to as “warm”. I. Multinodular goiter, especially common among the elderly with no significant distress to patients, can become toxic when exposed to large amounts of iodide in the diet or medications or after use of X-ray contrast materials. J. ATD's are given for months or even years and its dose must be adjusted to the lowest effective dose in order to prevent hypothyroidism. Methimazole (Tapazole) 5 mg, Carbimazole (Neo Mercazole) 5 mg and 20 mg, Thiamazole (Strumazol) 10 mg and 30 mg, and Propylthiouracil 50 mg are the ATD's more commonly used. Beta-blockers have been used as an adjunctive therapy of hyperthyrodism. Although propanolol was the drug originally used for thyrotoxicosis and it is still used most widely, a number of newer agents have a longer duration of action (Atenolol and Metoprolol) or are more cardioselective (Atenolol, Metoprolol and Nadolol). The standard starting dose of Propanolol is in the range of 40-80 mg/day; similar effects are produced by 100-200 mg/day of Atenolol or Metoprolol, or 40-80 mg/day of Nadolol. K. Responsiveness is assessed by subsidence of clinical manifestations and normalization of tests. L. ATD's are given for weeks to a few months in progressively decreasing dose to maintain the optimal clinical status and laboratory parameters. While under medical therapy, thyrotoxicosis is best monitored using TSH. Increasing TSH is a sign of oversuppression, while decrease TSH indicates continuing toxicity. M. RAI therapy is resorted to only when medical therapy with ATD has proven unsuitable. In Graves' disease, there are occasional instances when the ophthalmopathy is worsened by RAI which can really be disconcerting to patients and physicians. Because RAI is a special form of therapy, it should be handled only by physicians licensed to use ionizing radiation. Thyroid surgery, on the other hand, should be attempted only after adequate preoperative management with antithyroid drugs, beta-blockers or short-course inorganic iodide administration. N. The American Thyroid Association Grades Ocular Signs as follows (with mnemonic: NOSPECS) GOITER Class Signs 0 No signs or symptoms 1 Only signs as upper lid retraction with or without lid lag 2 Soft tissue involvement 3 Proptosis 22 mm 4 Extraocular muscle involvement 5 Corneal involvement 6 Sight loss due to optic nerve involvement O. Graves' disease is an autoimmune disease having the manifestation of hypertrophy and hyperplasia of the thyroid (goiter), hyperthyroidism (or thyrotoxicosis), ophthalmopathy, or dermopathy. The thyrotoxicosis of Graves' disease may exist without evidence of thyrotoxicosis. Ophthalmo pathy usually is bilateral but can be unilateral. P. A retroorbital mass lesion may have to be ruled out (e.g., by CT scan). Q. Differential diagnosis of thyroid nodule includes adenoma, cyst, carcinoma, multinodular goiter, Hashimoto's thyroiditis, thyroglossal duct, parathyroid adenoma or cyst, compensatory hypertrophy of thyroidectomy remnants. The discussion will be limited only to the most common diseases. R. Aspiration can be both diagnostic or therapeutic. The typical aspirates can be classified into type 1 (yellow, free-flowing fluid), type 2 (yellow, gelatinous, or viscous fluid), or type 3 (brownish or maroon-colored bloody fluid). Cytology is done on the aspirated specimen. When the aspirate is yellow or brown, it is likely to be benign; type 3 aspirates should be viewed with suspicion. True thyroid cyst, hemorrhagic cyst or cystic degeneration of long-standing goiter (or colloid cyst) can be aspirated as an office procedure with or without local anesthesia. That the nodule is fluid is suggested by the soft to doughy or fluctuant consistency. A rapidly increasing nodule (few days duration) especially with or without pain, denotes a hemorrhagic event within the nodule. S. The behavior of a solid nodule indicates its nature. Some clinical criteria suggesting malignancy include rapid increase in size, firm consistency, association with hoarseness, fixed to surrounding structures, presence of cervical lymphadenopathy, male gender or prior history of radiation exposure. T. Reaspiration of the content of the liquid nodule is attempted when there is reaccumulation (suggested 133 GOITER by prominence again of the nodule and firm consistency). If after two or three reaspirations after monthly intervals and the nodule remains prominence, the nodule is better removed. Sclerosing solutions have been attempted by some. U. Multinodular no-toxic goiter is often the result of a long-standing process of stimulation and suppression. It can sometimes attain incredulous sizes which need not be scanned anymore. Since it is not toxic, thyroid function tests are not indicated. V. Nodule which are predominantly warm and having high uptakes may respond beneficially to RAI therapy. The extranodular tissues are relatively spared of the ionizing radiation; thus, the risk for hypothyroidism is relatively lesser compared with the toxic goiters whose cells received the radiation globally. W. Thyroid hormone suppression using levothyroxine is preferred rather than liothyronine, thyroglobulin or desiccated thyroid, because of its longer half-life and more modulated absorption. X. Diffuse non-toxic goiter is the most common thyroid disease usually seen among adolescents, young women (especially when they become pregnant), residents in endemic areas, and patients with familial dispositions, and exposed to goitrogens. Y. Thyroid hormone is given as single daily dose of 0.8-1.0 ug/lb of levothyroxine in an empty stomach at least 30 minutes before breakfast). L-thyroxine (Thyrax, Euthyrox, Eltroxin) at varying appropriate dosage may be given with monitoring of TSH. Z. Patients with subclinical hypothyroidism have no signs and symptoms, with normal T3 and T4 but with elevated TSH (and exaggerated TRH test). AA. TRF test may be useful in further classifying the primary, secondary, and tertiary hypothyroidism. The discussion here will focus particularly on primary hypothyroidism. BB. Congenital or sporadic hypothyroidism refers to the situation due to lack of functionally competent thyroid present before birth or appearing before the first few postnatal months causing physical and mental retardation. When the state of hypothyroidism is complete and prolonged, the term cretin may be used. CC. Iodine deficiency can be expected in endemic 134 cpm 4TH eDITION areas. Iodine excess, on the other hand, can be seen in subjects undergoing contrast studies. Goitrogens can cause goiter if taken in large amounts for sustained periods (cabbage, turnips, cauliflower, cassava, carrots, etc.). GOITER GOITER CPM 4TH EDITION Drugs Mentioned in the Treatment Guideline This index lists drugs/drug classifications mentioned in the treatment guideline. Prescribing Information of these drugs can be found in the Philippine Pharmaceutical Directory (PPD) 8th edition. Opposite the brand name is its page number in the PPD 8th edition. Thyroid Hormones Carbimazole Neo Mercazole Iodine Iodone* Levothyroxine Euthyrox Thyrax Duotab Liothyronine Tertroxin Methimazole Tapazole Potassium iodide Jodid Propylthiouracil Philusa Propylthiouracil Thiamazole Strumazol Thyroxine Eltroxin Q238 Q238 Q238 Q238 Q238 Q238 Q238 Q238 Q238 Q238 Beta-blockers (for adjunctive therapy) Atenolol Nif-Ten* G100 Serten G97 Strada Atenolol G98 Tenoretic* G98 Tenormin G98 UL Atenolol G98 Metoprolol Betaloc G93 Betazide* G93 Betazok G93 Cardiosel G96 Cardiostat G96 Logimax* G100 Propanolol Bedranol G93 Duranol G96 Inderal G96 Phanerol G97 Phoenix Propranolol G97 UL Propranolol G98 135