Anterior Neck Mass
Sabalvaro Dyan, Salac Carmina, Salazar Janelle , Salazar Riccel,
Salcedo Von, Saldana Emmanuel, Sales Stephanie, Salonga Cryscel
65 year old female with anterior neck mass
History of Present Illness
5 years
PTC
4 years
PTC
• Noted presence of 2x2 cm anterior neck mass
• No accompanying symptoms
• Progressive increase in size and felt a “lump in the throat” which prompted consult
• Prescribed L thyroxine 100 ug/tab 1 tab TID which she took for one month until she noted
easy fatigability, palpitations, and weight loss.
• She consulted again and the physician requested for serum T3 ,T4, and TSH
• after which she was advised to discontinue taking the medication.
• Due to persistence of the mass, she sought consult at your clinic.
Consult
Physical Examination
BP=120/80 PR=85/min
RR=28/min
Neck: 8 X 6 cm firm
anterior neck mass
with well‐defined
borders and moves
with deglutition
Pink palpebral
conjunctive, anicteric
sclerae
No palpable cervical
adenopathies
Heart/Chest/Abdomen
unremarkable
Salient Features
65 y/o Female
 2 X 2 cm anterior neck
mass
 Progressive increase in size
– “lump in throat
 Prescribed L thyroxine 100
ug/tab 1 tab TID

◦ took for one month until she
noted easy fatigability,
palpitations, and weight loss

Discontinued medication as
advised by physician
Physical Examination
 VS: BP=120/80 PR=85/min
RR=28/min
 Pink palpebral conjunctive,
anicteric sclerae
 Neck: 8 X 6 cm firm
anterior neck mass with
well‐defined borders and
moves with deglutition; no
palpable cervical
adenopathies
 Heart/Chest/Abdomen –
unremarkable
1. If you were the physician who initially saw
the patient one year ago, what would you have
done?
2.What do you think were the serum T3 ,T4, and
TSH levels in the previous consult? What do you
call this condition?
◦
◦
Low circulating levels of T4 and T3
Primary Thyroid Failure

◦
Raised TSH levels
Secondary Hypothyroidism

Low TSH levels that do not increase following
TRH stimulation
HYPOTHYROIDISM

Deficiency in the circulating levels of
thyroid hormone leads to hypothyroidism,
and, in neonates, to cretinism, which is
characterized by neurologic impairment
and mental retardation.
◦ Hypothyroidism may also be associated with
deafness (Pendred's syndrome)4 and Turner's
syndrome.
•
In adults, symptoms in general are nonspecific:
– Tiredness, weight gain, cold intolerance,
constipation, and menorrhagia
– Patients with severe hypothyroidism or myxedema
• Facial and periorbital puffiness
– Characteristic facial features as a consequence of the deposition of
glycosaminoglycans in the subcutaneous tissues
• The skin becomes rough and dry and often develops a
yellowish hue from reduced conversion of carotene to
vitamin A.
• Hair becomes dry and brittle, and severe hair loss may
occur
• Loss of the outer two-thirds of the eyebrows.
– An enlarged tongue may impair speech, which is
already slowed, in keeping with the impairment of
mental processes.
– Myxedema madness
• Untreated dementia
– Nonspecific abdominal pain accompanied by distention
and constipation.
– Libido and fertility are impaired in both sexes.
– Cardiovascular changes in hypothyroidism include:
• Bradycardia, cardiomegaly, pericardial effusion, reduced cardiac
output, and pulmonary effusions
• Cardiac failure is uncommon
• When hypothyroidism occurs as a result of pituitary failure,
features of hypopituitarism such as pale, waxy skin, loss of body
hair, and atrophic genitalia may be present
LABORATORY FINDINGS
Hypothyroidism is characterized by low circulating levels of
T4 and T3.
• Raised TSH levels are found in primary thyroid failure, whereas
secondary hypothyroidism is characterized by low TSH levels
that do not increase following TRH stimulation.
• Thyroid autoantibodies are present and are highest in
patients with autoimmune disease (Hashimoto's thyroiditis,
Graves' disease), although they are also elevated in patients
with nodular goiter and thyroid neoplasms.
• Other findings include anemia, hypercholesterolemia, and
decreased voltage with flattening or inversion of T waves on
electrocardiogram. Comatose patients with myxedema also
have hyponatremia and CO2 retention.
•
TREATMENT
•
•
THYROXINE
Treatment of choice
– 50 to 200 mcg per day, depending upon patient's size
and condition.
– Starting doses of 100 mcg of thyroxine daily are well
tolerated
– Elderly patients and those with coexisting heart
disease and profound hypothyroidism should be
started on a considerably lower dose such as 25 to 50
mcg daily because of associated
hypercholesterolemia and atherosclerosis.
– The dose can be slowly increased over weeks to
months to attain a euthyroid state.
A baseline ECG should always be obtained in patients
with severe hypothyroidism prior to treatment.
• Patients are instructed to take tablets in the morning,
usually without other medications, or at mealtime to
assure good absorption.
• Thyroxine dosage is titrated against clinical response
and TSH levels, which should return to normal.
• Patients who present with myxedema coma, in
contrast to the patients with mild to moderate
hypothyroidism, require an initial emergency treatment
with large doses of intravenous thyroxine (300 to 400
g), and careful monitoring in an ICU setting.
•
3.What is your diagnosis? Other
considerations? Explain.
Diagnosis
◦
Hyperthyroidism secondary to over
dosage to L thyroxine
Other Considerations
Differential Diagnoses
Nodular Non-toxic Goiter
 Graves’ Disease
 Toxic Multinodular Goiter
 Toxic Adenoma
 Solitary Thyroid Nodule

Nodular Non-toxic Goiter
FAMILIAL
GOITER
Inherited enzyme
defect
Impaired iodine
metabolism
Usually
associated with
hypothyroidism
ENDEMIC
GOITER
SPORADIC
GOITER
Due to iodineNo definite cause
deficient diet
can be established
Mountainous regions
intake of substances
(goitrogens) that
inhibit production of
thyroid hormone—
common goitrogens
include foods such as
cabbage, turnips,
brussel sprouts,
seaweed, and millet
Tx: iodized salt
Enlargement of the thyroid gland
 No toxicity; no cancer
 The following factors increase your
chance of developing nontoxic goiter:

◦ Sex: female (nontoxic goiter is more common
in women than men)
◦ Age: over 40 years
Reference: http://www.mbmc.org/healthgate/GetHGContent.aspx
SYMPTOMS
Nontoxic goiters usually do not have
noticeable symptoms.
 Swelling on the neck
 Breathing difficulties, coughing, or
wheezing with large goiter
 Difficulty swallowing with large goiter
 Feeling of pressure on the neck
 Hoarseness

MANAGEMENT


A goiter only needs to be treated if it is
causing symptoms.
Treatments for an enlarged thyroid include:
◦ Radioactive iodine to shrink the gland, particularly
if the thyroid is producing too much thyroid
hormone
◦ Surgery (thyroidectomy) to remove all or part of
the gland
◦ Small doses of Lugol's iodine or potassium iodine
solution if the goiter is due to iodine deficiency
◦ Treatment with thyroid hormone supplements if
the goiter is due to underactive thyroid
Reference: http://www.nlm.nih.gov/medlineplus/ency/article/001178.htm
INDICATIONS FOR SURGERY
Huge goiter which is cosmetically
unacceptable
 Compression symptoms
 Suspicion of malignancy

GRAVES’ DISEASE
A type of hyperthyroidism, is
caused by a generalized
overactivity of the entire
thyroid gland.
 An autoimmune disease;
thyroid-stimulating antibodies
directed at TSH receptors on
follicular cells.
 It is named for Robert Graves,
an Irish physician, who was the
first to describe this form of
hyperthyroidism about 150
years ago.

ETIOLOGY



The trigger for auto-antibody production is
not known.
Genetic predisposition – HLA DR3
Since Graves' disease is an autoimmune
disease which appears suddenly, often quite
late in life, it is thought that a viral or
infection may trigger antibodies which crossreact with the human TSH receptor (a
phenomenon known as antigenic mimicry,
also seen in some cases of Type I diabetes).
◦ Yersinia enterocolitica
Reference: http://en.wikipedia.org/wiki/Graves%27_disease
CLINICAL FEATURES

Triad:

◦ Goiter including the
pyramidal lobe
◦ Thyrotoxicosis
◦ Exophthalmos

Symptoms:
Heat intolerance
 Thirst
 Sweating
 Weight loss despite
adequate caloric intake
 Amenorrhea
 Tachycardia or atrial
fibrillation
 Congestive heart failure

PE:
Weight loss
 Flushing
 Warm and moist skin
 Inappropriate sweating
 Tachycardia
 Widening of pulse pressure
 Fine tremor
 Muscle wasting
 Hyperactive tendon reflexes
 Pretibial myexedema
 Gynecomastia
 Audible bruit over the gland


Laboratory Findings:
Decreased TSH
 Increased circulating T3/T4
levels
 Increased circulating thyroid
autoantibodies

Thyroid stimulating
immunoglobulins (TSI)
Tyhroid stimulating
antibodies (TSAb)

Radioactive iodine scan
shows diffuse uptake
through the gland of 45-90
percent.
MANAGEMENT

Medical:
Propylthiouracil (PTU)
Methimazole (Tapazole)
Carbimazole
Beta-blockers (Propanolol)
Relapse rate in 12-18 months
 Risk for fetal goiter, hypothyroidism
 No morbidity related after surgery
 Treatment of choice for small goiters and
pregnant patients (PTU)
 Euthyroid state is achieved in 4-6 weeks


Radioactive Iodine
◦
◦
◦
◦
Ease of treatment
Highly effective especially in diffuse goiters
No morbidity related to surgery
Treatment of choice for failed surgical
management
◦ The effect is seen in 1.5-4 months
◦ Standard dose = 10 mCl = 8500 cGy

Surgery
◦
◦
◦
◦
◦
◦
Complete and permanent control of toxicity
Rapid control of symptoms
Removal of mass
Treatment of choice for huge goiters
Needs pre-operative preparation
Overall morbidity of 1-2%
Toxic Multinodular Goiter





Usually occur in individuals older than 50 years of
age who often have a prior history of a nontoxic
multinodular goiter
Over several years, enough thyroid nodules
become autonomous to cause hyperthyroidism.
Similar to Graves’ disease, but symptoms and
signs of hyperthyroidism are less severe and
extrathyroidal manifestations are absent.
May present with atrial fibrillation or palpitations,
tachycardia, nervousness, tremor or weight loss.
Low TSH, normal or minimally increased T4,
elevated T3, T3>T4.
Toxic Multinodular Goiter
Thyroid scan – heterogenous uptake with
multiple regions of increased and decreased
uptake.
 24hr uptake of radioiodine may not be increased.
 Management

◦ Antithyroid drugs + beta blockers – normalize thyroid
function and address the clinical features of
thyrotoxicosis, but often stimulates the growth of the
goiter; spontaneous remission does not occur.
◦ Radioiodine – treat areas of autonomy, decrease the
mass of the goiter
◦ A trial of radioiodine should be considered before
subjecting patients to surgery.
Toxic Multinodular Goiter

Surgery
◦ Definitive treatment of underlying
thyrotoxicosis and goiter.
◦ Subtotal thyroidectomy is the standard
procedure.
◦ Patients should be rendered euthyroid using
antithyroid drugs before operation.
Toxic Adenoma
A solitary, autonomously functioning
thyroid nodule
 Typically occurs in younger patients
 (+) thyroid nodule with symptoms of
hyperthyroidism
 Size is at least 3cm before
hyperthyroidism occurs.
 Absent clinical features suggestive of
Graves’ disease or other causes of
thyrotoxicosis

Toxic Adenoma

Thyroid scan –
definitive diagnostic
test
◦ Focal uptake in the
hyperfunctioning
nodules
◦ Diminished uptake in
the remained of the
gland
 Suppression of the activity
of the normal thyroid
Toxic Adenoma

Radioiodine ablation – treatment of
choice
◦ 131I is concentrated in the hyperfunctioning
nodule with minimal uptake and damage to
normal thyroid tissue.
◦ Relatively large doses – correct thyrotoxicosis
in about 75% of patients within 3 months.
◦ Hypothyroidism occurs in <10% of patients
over the next 5 years.
Toxic Adenoma

Surgical resection
◦
◦
◦
◦
◦
Limited to enucleation of the adenoma
Lobectomy
Preservation of thyroid function
Low risk of hypoparathyroidism
Low risk of damage to the recurrent laryngeal
nerve
Toxic Adenoma
Medical therapy using antithyroid drugs
and beta blockers – normalize thyroid
function but is not an optimal long term
treatment
 Ethanol injection under ultrasound
guidance

◦ Repeated injections – often >5 sessions
◦ Reduce nodule size
Solitary Thyroid Nodule




Present in approximately 4 percent of
the population
Pain is unusual. When present, it
should raise suspicion for
intrathyroidal hemorrhage in a benign
nodule, thyroiditis, or malignancy.
History of hoarseness - may be
secondary to malignant involvement
of the recurrent laryngeal nerves
Risk factors for malignancy –
exposure to ionizing radiation and
family history of thyroid and other
malignancies associated with thyroid
cancer.
Solitary Thyroid Nodule





Mass moves with swallowing.
Hard, gritty of fixed nodules are more
likely to be malignant.
Most are euthyroid.
If a patient with a nodule is found to
be hyperthyroid, the risk of
malignancy is approximately 1
percent.
FNAB – most important diagnostic
test
◦ Benign – 65% (includes cysts and
colloid nodules)
◦ Suspicious – 20%
◦ Malignant – 5%
◦ Nondiagnostic – 10%
Solitary Thyroid Nodule

Ultrasound
◦ For detecting nonpalpable thyroid nodules
◦ For differentiating solid from cystic
nodules
◦ For diagnosing suspicious nodules with
microcalcifications
◦ For identifying adjacent lymphadenopathy
CT and MRI – unnecessary in except
for large, fixed, or substernal lesions.
 123I or 99mTc – rarely necessary,
unless evaluating patients for “hot” or
autonomous thyroid nodules

Solitary Thyroid Nodule
Malignant tumors – generally treated by total or neartotal thyroidectomy
 Simple thyroid cysts - resolve with aspiration in
approximately 75 percent of cases

 Unilateral thyroid lobectomy - if the cyst persists after three attempts at
aspiration

Lobectomy
◦ For cysts >4 cm in diameter
◦ For complex cysts with solid and cystic components
Solitary Thyroid Nodule

Colloid nodule – should be observed with serial ultrasound
and Tg measurements
◦ Repeat FNAB if nodule enlarges

L-thyroxine – in doses sufficient to maintain a serum TSH
level between 0.1 and 1.0 μU/mL.
◦ 50% decrease in size

Thyroidectomy – if a nodule enlarges on TSH suppression,
causes compressive symptoms, or for cosmetic reasons
◦ Exceptions: Patient who has had previous irradiation of the
thyroid gland or who has a family history of thyroid cancer.
◦ In these patients total or near-total thyroidectomy is
recommended.
 High incidence of thyroid cancer (≥ 40%)
 Decreased reliability of FNA biopsy
4. How would you manage this patient now?

Goal: restoration of clinical and biochemical
euthyroid state by omitting or reducing the
dosage of medications and other measures
as needed depending on clinical status.
 ECG
 Blood test: TSH, T3, T4 levels, monitored regularly

SYMPTOMATIC TREATMENT:
 To control tachycardia, hypertension and atrial
fibrillation: 20 - 40 mg doses of propranolo Q 6hours; d
 If beta blockers are contraindicated: Diazepam and/or
chlorpromazine

RADIOACTIVE IODINE
◦ ingestion of a radioactive iodine tablet (6-12 wks)
which is then taken up by thyroid cells. These
overactive cells are destroyed so that the thyroid can
shrink in size and produce hormone at normal levels.
◦ In patients with underlying heart disease and in
elderly patients, it is desirable to treat with
antithyroid drugs (methimazole) until the patient is
euthyroid. The medication is then stopped for 5-7days
before the appropriate dosage of 131I.
◦ Although it is a safe treatment, most people become
hypothyroid after radioactive iodine therapy and
therefore require lifelong thyroid hormone
replacement therapy.

THYROIDECTOMY
◦ Now uncommonly performed; the surgeon removes most
or all of the gland
◦ Candidates for surgery: include pregnant hyperthyroid
patients intolerant of anti-thyroid drugs, patients desiring
definitive therapy without the use of radioactive iodine,
children, and patients with very large or
multinodular goiters.
◦ Patients are treated with antithyroid drugs until euthyroid
(about 6wks). In addition, 10-14 days prior to surgery, they
receive saturated solution of potassium iodide 5 drops
BID, to diminish vascularity of the gland and simplify
surgery
◦ However, in cases of total removal of the thyroid gland,
patient must take thyroid replacement pills for the rest of
his or her life
NON-PHARMACOLOGICAL
High calorie diet in order to replace all
the energy burned by the body in
hyperthyroid state
 Drink plenty of water and juices to
replace all the fluid losses. Avoid or limit
caffeinated drinks for such could produce
anxiety.

Journals on Diagnosis and Treatment
of Drug Induced Hyperthyroidism
Diagnosis
“Newly diagnosed thyrotoxicosis in
hospitalized patients: clinical characteristics”
Rotman-Pikielny P et. Al
Background:
Thyrotoxicosis is often diagnosed in an
outpatient setting. Most common
symptoms include irritablility, heat
intolerance ,palpitations and weakness
 The prevalent symptoms in hospitalized
patients with newly diagnosed
thyrotoxicosis have not been fully
characterized

Objective

To determine the clinical characteristics
of patients with thyrotoxicosis newly
diagnosed during hospitalization.
Design

Retrospective computer-based search was
undertaken to detect patients that were
hospitalized in our medical centre during
1999-2006, and discharged with
thyrotoxicosis or thyroiditis primary
diagnosis.
Results
Fifty-eight patients (36F/22M; mean age
52.1 +/- 17.5 years) were identified.
 Weakness, weight loss and palpitations
were the most common manifestations
(50, 40 and 35%, respectively) and were
predominantly present in patients with
hyperthyroidism.
 Sore throat was present in 41% of
patients with thyroiditis.

Sinus tachycardia and atrial fibrillation
occurred in 65.5 and 15.5% of the
patients, more common in those with
hyperthyroidism.
 The diagnoses on discharge were Graves'
disease, subacute thyroiditis and
multinodular goiter in 39.7, 34.5 and 8.9%,
respectively.

Conclusion
Weakness, weight loss and palpitations
were the main symptoms in patients
diagnosed with thyrotoxicosis during
hospitalization.
 Thyrotoxicosis should be included in the
differential diagnosis when patients are
admitted to the hospital with those
symptoms.

Treatment
“Drug induced thyrotoxicosis: the surgical
option”
Lorberboym M., Schacter P.
Background:
Drug induced thyrotoxicosis is not
uncommon, It may worsen life threatening
arrythmias and become refractory to
medical treatment
Summary
The Article talks about a near total
thyroidectomy as valid alternative to
medical therapy
 The article pursues to promote near total
thyroidectomy as an early management of
the disease

Methods
The study included 12 patients 7 men and
5 women aged 63-82 years of age with
drug induced fulminant thyrotoxicosis
 Drugs such as Iodine containing
Amiodarone or IFN a treatment
 Patients has adjunct medical therapy of an
anti thyroid Propylthiouracil 1200 mg and
a Beta receptor antagonist


Thyroid scan was performed in all
patients using Tc-99m pertechnate
Results
4 patients did not respond to 3 months of
medical therapy required surgical
thyroidectomy due to unremitting
thyrotoxicosis.
 Near total thyroidectomy resulted into
rapid correction of thyrotoxicosis
enabling continuation of anti-arrythmic
drugs
 All patients recovered rapidly and
remained well and euthyroid on thyroxine
replacement therapy
