PHILIPPINE THYROID ASSOCIATION - The Filipino Doctor Goiter.pdf · Philippine Thyroid Association,...

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PHILIPPINE THYROID ASSOCIATION

123

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

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.

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.

Luis Roy P. Colendrino, M.D.

Officers and Board of Directors

PresidentVice President

SecretaryTreasurer

P.R.O.

Board of Directors

Immediate Past President

GOITER cpm 4TH EDITION

124

A General Approach to Patients Presenting with Goiter

FIGuRE 1

1

Patient with goiter

2

History & PE (A)

Obstructive symptoms?

(B)

3

Y

N

4

Surgical consult

Are there signs of thyro-

toxicosis? (C)

5

Y

N

6

T3, T4, TSH (D)

Toxicity

confirmed?(E)

7

Y

N

Nodule palpated?

(F)

11

Y

N

12Nodular non-toxic goiter

(see Figure 4)

13Diffuse non-toxic goiter

(see Figure 5)

Nodule palpated?

(E)

8

Y

N

9Nodular toxic

goiter (see Figure 2)

10Diffuse toxic

goiter (see Figure 3)

cpm 4TH EDITION GOITER

125

Algorithm for Patients with a Nodular Toxic Goiter

FIGuRE 2

1Nodular

toxic goiter(G)

Solitary nodule?

2

Y

N

3

Radionuclide scan (H)

Multiple nodules

(I)

Hot nodule?

4

Y

N

5

6

Warm nodule

7

Compensated autonomous

adenoma

9Anti-thyroid

drugs + β-blockers

(J)

Responsive?(K)

10

Y

N

11Monitor thyroid

function; adjust dose

(L)12

Refer for RAI or

surgery (M)

8


126

Algorithm for Patients with a Diffuse Toxic Goiter

1

Diffuse toxic goiter

Eye signs?(N)

2

Y

N

3

Graves' disease

(O)

4

Ophtha consult; possible steroid

therapy (P)

5

Thyroid antibodies if

available

Responsive?(K)

7

Y

8

Monitor thyroid function; adjust

dose (L)

6

Antithyroid drugs + β-

blockers (J)

9

Refer for RAI or

surgery (M)

N

FIGuRE 3


127

Algorithm for Patients with a Nodular Non-Toxic Goiter

1

Nodular non-toxic goiter

(Q)

Solitary nodules?

2

Y

N

3

Thyroid ultrasound

Liquid?

4

Y

N

5

Aspiration & Cytology

(R)

7

Solid or complex

(S)

See Figure4B

6

Multiple nodules

See Figure 4A

Benign?

8

Y

N

9Thyroid

Hormone Supression

10

Suspicious or definitely malignant

N13

Refer to surgery

Recurrence?

11

Y

N

12Reaspirate;

surgical consult (T)

Persistence?

14

Y

N

15

Surgical consult

16

Observe

FIGuRE 4


128

Algorithm for Patients with a Nodular Non-Toxic Goiter (Multiple)

1Multinodular

non-toxic goiter (U)

2

Radionuclide scan

Pre-dominantly

warm nodules?

3

Y

N

Is RAI uptake

increased?

4

Y

N

5Refer for

possible RAI therapy (V)

6Thyroid

Hormone Supression

(W)

Regression?

7

Y

N

8Continue

therapy and follow-up

10Refer for possible surgery

9Predominantly cold nodules

FIGuRE 4A


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Algorithm for Patients with a Nodular Non-Toxic Goiter (Complex or Solid)

From Fig. 4

Complex nodule?

1

Y

6

Radionuclide scan

Cold nodule?

10

Y

N

2Fine needle aspiration

biopsyBenign?

3

Y

N

7Suspicious

or definitely malignant

4Thyroid hormone

supression

Regression?

8

N

Y

9

11

Surgical consult

Warm nodule?

12

Y

16

Hot nodule

13Thyroid hormone

suppressionRegression?

14

Y

17Refer for

possible RAI therapy

N

15

Continue therapy & follow-up

N

FIGuRE 4B

Go to # 2

Solid nodule?

5

Y

N

N



130

Algorithm for Patients with a Diffuse Non-Toxic Goiter

1Diffuse

non-toxic goiter (X)

Normal TSH &

normal T4?

2

Y

N

3

Euthyroid goiter

4Thyroid hormone

supression (Y)

Regression?

5

Y

N

6


7Refer for possible surgery

High TSH & normal T4?

8

Y

N

9Subclinical

hypo-thyroidism

(Z)

High TSH & low T4?

10

Y

N

11

Overt hypo-thyroidism

12Other

combinations of TSH & T4

13

Refer

FIGuRE 5


131

1Hypo-

thyroidism (AA)

Algorithm for Patients with Hypothyroidism

Congenital?(BB)

2

Y

N

3Refer to pediatric

4

Acquired

Diet origin (goitrogens, I- deficiency, I- excess)?

(CC)

5

Y

N

6

Dietary corrections

Anti-thyroid drug

intake?

7

Y

N

8

Discontinue

9May need

thyroid hormone if persistent

Post-thyroid-ectomy?

10

Y

N

Post-RAI?

11

Y

N

Post-inflammatory?

12

Y

N

13Thyroid hormone

replacement

14

Monitor TSH

15Less

common causes

16

Refer

FIGuRE 5A


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Guidelines for the Management of GoiterFOOTNOTEs

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.

C. Signs and symptoms of thyrotoxicosis may be evaluated according to a UST - formulated clinical scoring index modified from Wayne's criteria.

Hyperthyroid HypothyroidSYMPTOMS Weight Loss +4 Weight Gain -2 Nervousness +4 Easy Tiredness +2 Palpitations +1 Increased Sweating +1 Dyspnea on Effort +1 Irritability +1 Weakness +1 Increased Appetite +1 Decreased Appetite -2 Intolerance of Heat +1 Constipation -2SIGNS Warm, Moist Skin +4 Rough, Dry Skin -3 Thyroid Enlargement Diffuse +2 Nodular -1 Exophthalmos +4 Fine Finger Tremor +3 Pulse Rate Above 110 +2 100-110 +1 70-100 0 Below 70 -1 Hyperkinetic Movement +1 Sluggish Movement -4

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.

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


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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)

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 thy-rotoxicosis), 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


134

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

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.).


135

Drugs Mentioned in the Treatment GuidelineThis 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 HormonesCarbimazole Neo Mercazole Q238Iodine Iodone* Q238Levothyroxine Euthyrox Q238

Thyrax Duotab Q238Liothyronine Tertroxin Q238Methimazole Tapazole Q238Potassium iodide Jodid Q238Propylthiouracil Philusa Propylthiouracil Q238Thiamazole Strumazol Q238Thyroxine Eltroxin Q238

Beta-blockers (for adjunctive therapy)

AtenololNif-Ten* G100Serten G97Strada Atenolol G98Tenoretic* G98Tenormin G98UL Atenolol G98

MetoprololBetaloc G93Betazide* G93Betazok G93Cardiosel G96Cardiostat G96Logimax* G100

Propanolol Bedranol G93Duranol G96Inderal G96Phanerol G97Phoenix Propranolol G97UL Propranolol G98

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