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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