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Practice Guidelines for Thyroid Disorders
The Malaysian Consensus 2000
CPG 1/2000
FOREWORD
Thyroid disorders together with diabetes mellitus are the most common and prevalent
endocrine and metabolic diseases in this country. Thus, having completed a guideline on
the management of type 2 diabetes mellitus, the Malaysian Endocrine and Metabolic
Society (MEMS) took the task to prepare the Malaysian Consensus for Practice
Guidelines for Thyroid Disorders. These guidelines hopefully will be of use to assist
practising doctors in the management of patients with thyroid disorders.
The draft for the guidelines was drawn up by members of the Malaysian Endocrine and
Metabolic Society during the two meetings in February and May 1998. Following this,
three consensus development workshops were held to discuss the draft and to agree on
this Malaysian Consensus for Practice Guidelines for Thyroid Disorders. On behalf of
MEMS, I would like to thank the Academy of Medicine and Ministry of Health for their
collaboration and support in preparation of this consensus. I would also like to express
the Society’s appreciation and gratitude for the participation of representatives of the
Ministry of health, College of Physicians, College of Surgeons, Malaysian Medical
Association and Malaysian Paediatric Association in developing this consensus. Finally,
my personal word of thanks to YBhg Professor Dato’ Khalid Abdul Kadir and Associate
Professor Ng Mee Lian, who have generously contributed their time and energy to make
this consensus a realisation.
Professor Dato’ Mustaffa Embong
President
Malaysian Endocrine and Metabolic Society (MEMS)
CONTENTS
FOREWORD
1
TASKFORCE AND CONTRIBUTORS
4
LIST OF ABBREVIATIONS
8
1. THYROTOXICOSIS
1.1 Clinical Features
1.2 Laboratory Investigations
1.3 Management
1.3.1 Medical Treatment
1.3.2 Surgery
1.3.3 Radioiodine Therapy
1.4 Management of Complications
1.4.1 Thyrocardiac complications
1.4.2 Hypokalaemic periodic paralysis
1.4.3 Ophthalmopathy
1.4.4 Dermopathy
2. THYROID CRISIS
2.1 Clinical Features
2.2 Management
9
10
11
13
13
14
14
14
15
16
16
3. HYPOTHYROIDISM
3.1 Clinical Features
3.2 Laboratory Investigations
3.3 Management
3.3.1 Overt Hypothyroidism
3.3.2 Subclinical Hypothyroidism
3.3.3 In pregnancy
3.4 Monitoring
18
18
19
19
20
20
4. MYXOEDEMA COMA
4.1 Management
21
2
5. CONGENITAL HYPOTHYROIDISM
5.1 Clinical Features
5.2 Laboratory Investigations
5.3 Management
5.4 Monitoring
22
22
23
23
6. THYROIDITIS
6.1 Clinical Features
6.1.1 Hashimoto’s thyroiditis
6.1.2 Riedel’s thyroiditis
6.1.3 Subacute (De Quervain’s) thyroiditis
6.1.4 Postpartum thyroiditis
6.1.5 Painless thyroiditis
6.1.6 Acute pyogenic thyroiditis
6.2 Laboratory Investigations
6.3 Management
24
24
24
25
25
25
25
25
26
7. SINGLE THYROID NODULE
7.1 Diagnosis
7.2 Laboratory Investigations
7.2.1 Fine-needle aspiration cytology (FNAC)
7.2.2 Ultrasound scan
7.2.3 Thyroid scintiscan
7.2.4 Other scans
7.2.5 Thyroid function tests
7.3 Management
27
28
28
28
28
28
28
28
8. MULTINODULAR GOITRE
8.1 Clinical Features
8.2 Laboratory Investigations
8.3 Management
30
30
31
STATEMENT OF INTENT
32
REFERENCES
33
3
TASKFORCE
AND
CONTRIBUTORS
Malaysian Endocrine and Metabolic Society
1. Professor Dato Dr Mustaffa Embong
Department of Medicine, School of Medical Sciences,
University Science Malaysia (USM)
2. Assoc Prof Dr Mafauzy Mohamed
Dean, School of Medical Sciences ,USM
3. Assoc Prof Dr Wan Mohamad Wan Bebakar
Head, Department of Medicine, School of Medical Sciences, USM
4. Dr Fuziah Md Zain
Department of Paediatrics, School of Medical Sciences,USM
3. Professor Dato Dr Anuar Zaini Mohd Zain
Dean, Faculty of Medicine, University of Malaya (UM)
6. Professor Dr Amir S Khir
Deputy Dean, Faculty of Medicine, UM
7. Assoc Prof Dr Chan Siew Pheng
Department of Medicine, Faculty of Medicine, UM
8. Assoc Prof Dr Ikram Shah Ismail
Department of Medicine, Faculty of Medicine, UM
9. Assoc Prof Dr Fatimah Harun
Department of Paediatrics, Faculty of Medicine, UM
10. Dr Rokiah Pendek
Department of Medicine, Faculty of Medicine, UM
4
11. Dr Hew Fen Lee
Department of Medicine, Faculty of Medicine, UM
12. Professor Dato Dr Khalid Abdul Kadir
Director, Hospital Universiti Kebangsaan Malaysia (HUKM)
13. Professor Dr Ibrahim Sheriff
Department of Medicine, Faculty of Medicine, HUKM
14. Professor Dr Wu Loo Ling
Department of Paediatrics, Faculty of Medicine, HUKM
15. Assoc Prof Dr Nabishah Mohamad
Department of Physiology, Faculty of Medicine,UKM
16. Assoc Prof Dr Ng Mee Lian
Department of Biochemistry, Faculty of Medicine,UKM
17. Dr Faridah Ismail
Department of Medicine, Faculty of Medicine, HUKM
18. Dr Rahmah Rasat
Department of Paediatrics, Faculty of Medicine, HUKM
19. Dr Hapizah Mohd Nawawi
Department of Pathology, Faculty of Medicine, HUKM
20. Ms Khalidah Mazlan
Department of Pathology, Faculty of Medicine, HUKM
21. Dr Wan Nazaimoon Wan Mohamud
Head, Endocrinology Division, Institute for Medical Research (IMR)
22. Dr GR Letchuman
Department of Medicine, Hospital Ipoh (HIpoh)
5
23. Dr Jamilah Baharom
Chemical Pathology Division, Hospital Kuala Lumpur (HKL)
24. Dr Arlene Ngan
Consultant Physician & Endocrinologist, Subang Jaya Medical Centre (SJMC)
25. Dr Yap Piang Kian
Consultant Physician & Endocrinologist, Subang Jaya Medical Centre (SJMC)
26. Dr Sakinah Othman
Consultant Physician & Endocrinologist, Hospital Ampang Putri
Ministry of Health
1. Dato Dr A Thayaparan
Consultant Physician, Hospital Seremban (HS’ban)
2. Dr M Ramanathan
Consultant Physician, Hospital Taiping (HTaiping)
3. Dr Norshinah Dato Kamaruddin
Consultant Physician & Endocrinologist, Hospital Kuala Lumpur (HKL)
4. Miss Particia Gomez
Consultant Surgeon, Hospital Kuala Lumpur (HKL)
5. Miss Nor Aina Emran
Consultant Surgeon, Hospital Kuala Lumpur (HKL)
College of Surgeons
1. Dr Ng Chuan Wai
Consultant Surgeon, Gleneagles Intan Medical Centre
2. Dr Chang Keng Wee
Consultant Surgeon, Gleneagles Intan Medical Centre
6
3. Dr Hisham Abdullah
Consultant Surgeon, Hospital Kuala Lumpur (HKL)
College of Physicians
1. Dato Dr (Mrs) ST Kew
Consultant Physician, Hospital Kuala Lumpur (HKL)
2. Dr Liew Yin Mei
Consultant Physician, Hospital Kuala Lumpur (HKL)
3. Dr Wong Wing Keen
Consultant Physician, Pantai Medical Centre
Malaysian Paediatric Association
1. Assoc Prof Dr Wan Ariffin Abdullah
Department of Paediatrics, Faculty of Medicine, UM
2. Dr Tang Swee Fong
Department of Paediatrics, Faculty of Medicine, HUKM
Malaysian Medical Association
1. Dr Sahathevalingam
2. Dr Radhakrishna
7
LIST
OF
ABBREVIATIONS
AF
CMZ
CNS
CT
ESR
FNAC
fT4
fT3
IHD
K+
MEN
MNG
MRI
MTC
NSAID
PTU
SSKI
TSH
TRH
T4
T3
Atrial fibrillation
Carbimazole
Central Nervous System
Computerised Tomography
Erythrocyte Sedimentation Rate
Fine-Needle Aspiration Cytology
Free T4
Free T3
Ischaemic Heart Disease
Potassium ion
Multiple Endocrine Neoplasia
Multinodular Goitre
Magnetic Resonance Imaging
Medullary Thyroid Carcinoma
Non-Steroidal Anti-inflammatory Drug
Propylthiouracil
Saturated Solution of Potassium Iodide
Thyroid-stimulating Hormone, Thyrotropin
Thyrotropin-releasing Hormone
Thyroxine
Tri-iodothyronine
8
1. THYROTOXICOSIS
Thyrotoxicosis is a clinical state due to excess thyroid hormones. Two hormones
tri-iodothyronine (T3) and thyroxine (T4) are produced by the thyroid gland of which
T3 is the active hormone. The causes include:
*
*
*
*
Graves' disease (most common)
Toxic multinodular goitre
Toxic adenoma
Others - thyroiditis
- factitious intake of thyroxine
- ovarian causes (struma ovarii, molar pregnancy)
1.1 Clinical Features
These include:
History:
weight loss despite good appetite
excessive sweating especially at night, in cold weather
excitability, irritability, tremulousness
palpitations
Physical examination:
goitre (usually with/without bruit) in Graves’ disease
proximal muscle weakness, hyperreflexia
warm, sweaty palms
fine finger tremors
lid retraction, lid lag
resting tachycardia
One or more of these signs and symptoms may be absent or modified by
duration of illness, severity of thyrotoxicosis, patient’s age and presence of
concurrent illnesses.
9
Less common modes of presentation include:
heart failure/atrial fibrillation in the elderly
hypokalaemic periodic paralysis
unexplained weight loss
diarrhoea
1.2 Laboratory Investigations
To confirm the diagnosis, both serum levels of free T4 and supersensitive TSH
should be assayed.
Results of serum total T4 measurements can be affected by protein binding
abnormalities and may be misleading.
Supersensitive TSH assay is useful for screening but a suppressed TSH level by
itself may not be due to thyrotoxicosis.
A result of normal free T4 (fT4) level may miss a small number of cases of
thyrotoxicosis due to T3 toxicosis.
In patients suspected of T3
toxicosis, serum free T3 (fT3) measurement is indicated.
Isotope uptake scan may be performed in cases suspected of thyroiditis
and toxic adenoma.
1.3 Management
Three forms of therapy are available: antithyroid drugs, surgery and radioiodine.
Treatment may also be necessary for complications e.g. atrial fibrillation,
cardiac failure, ophthalmopathy. The methods used will vary according to the
cause and severity of the disease, the patient’s age and resources available.
Subclinical hyperthyroidism which is characterised by normal fT4 and fT3 and
suppressed TSH levels, is a recognised entity. The need to treat this condition
remains controversial. Close monitoring of clinical and biochemical status is
indicated.
10
1.3.1 Medical Treatment
Thionamides (carbimazole or propylthiouracil) are the commonest forms of
treatment that can be used for most patients with the hope of achieving longterm remission. These drugs may also be used in preparation for surgery and
radioiodine therapy. Permanent remission of Graves’ disease will more likely
occur in the following groups of patients with small goitre and mild disease.
Antithyroid drugs are most useful in:
a) Children – it is effective and more acceptable to patients and parents.
b) Pregnancy - The dose of antithyroid drugs should be kept as low as possible
to reduce the risk of foetal goitre. Propylthiouracil is preferred to
carbimazole in pregnancy and during breast-feeding. Drug therapy may be
continued until term but breast-feeding is generally not advisable for
mothers taking large doses of anti-thyroid drugs (propylthiouracil >100 mg
or carbimazole >10 mg) as these are secreted in breast milk.
c) Patients with contraindications to surgery or who refuse surgery
d) Patients with medical complications - such as thyroid crisis or
heart failure
e) Patients who relapse after thyroidectomy - surgery is more difficult in
those patients who have undergone thyroidectomy.
Although,
radioiodine is the definitive treatment, anti-thyroid drug therapy may be
considered in patients refusing radioiodine
f) Patients in preparation for surgery (thyroidectomy) or while awaiting
radioiodine therapy.
11
Schedule for administration of ant-thyroid drugs in adults
Initial therapy
for 4-6 weeks
Carbimazole
Propylthiouracil
30-45 mg/day
300-450 mg/day
Maintenance therapy
(gradual reduction over
3-6 months from initial dose)
5-10 mg/day
50-100 mg/day
Continue therapy for 1-2 years.
In children, the dose of carbimazole is 0.5-0.7 mg/kg/day (not
exceeding 45 mg/day) the dose for propylthiouracil .is 5-7 mg/
kg/day (not exceeding 450 mg/day)
For maintenance, an alternative form of therapy which is the block and
replace treatment method (antithyroid drugs and thyroxine) may be used.
It is important to explain to patients the need for long term medication and
inform them regarding adverse side effects (due to agranulocytosis which
usually occurs within the first 3 months). Patients with rash or sore throat
are to stop treatment and seek medical advice immediately.
Beta-blockers are useful for symptomatic relief initially, provided there are
no contraindications, e.g. asthma. The usual dose for propranolol is 30-120
mg/day in divided doses or atenolol 25-50 mg/day. In children, the dose for
propanolol is 30-60 mg/day in divided doses.
12
1.3.2 Surgery
Thyroidectomy may be performed in Graves' disease, toxic multinodular
goitre or toxic adenoma.
Indications:
 Failed medical treatment i.e. relapse after one or more courses of
antithyroid drugs, non-compliance or development of side-effects.
 Those with large goitres, especially with pressure effects.
 Patients who prefer surgery.
 A relative indication is severe progressive ophthalmopathy.
Surgery should preferably be done by a surgeon proficient in thyroid
surgery.
Pre-operative preparation:
 Control thyrotoxic state with medical treatment. Avoid hypothyroidism.
 In the last 1-2 weeks, potassium iodide 5 mg tds or Lugol's iodine
5 -10 drops tds may be added to reduce vascularity of the thyroid gland.
1.3.3 Radioiodine Therapy
Radioiodine therapy is safe and appropriate in nearly all types of hyperthyroidism. It should NOT be used in pregnancy and women who are
breast-feeding. In general, radioiodine therapy is not recommended in
children.
Precautions:
 Patients need to avoid close contact with young children and pregnant
women for a duration of 10 days after radioiodine therapy.
 Women are advised not to become pregnant for at least 4-6 months.
 Severe and complicated hyperthyroidism needs to be adequately
controlled before radioiodine treatment.
There is a need to emphasise on long-term follow-up and early detection of
hypothyroidism
13
1.4 Management of Complications
1.4.1 Thyrocardiac complications
Thyroid cardiomyopathy is a complication of prolonged poorly controlled
thyrotoxicosis and is more frequent in the elderly.
Rapid atrial fibrillation is treated with digoxin (may require higher than
usual dose). A beta-blocker may be added to control the heart rate. If atrial
fibrillation
persists,
anticoagulation
is
recommended
(unless
contraindicated) when there is heart failure, cardiac dilatation, thrombus on
echocardiogram, history of embolization and associated valvular heart
disease.
Cardiac failure is treated with standard regimen. Beta-blockers should be
used with caution in congestive cardiac failure.
1.4.2 Hypokalaemic periodic paralysis
Potassium replacement is required in addition to treatment for
thyrotoxicosis, (potassium chloride 3-6 gm/day or Slow-K 1.8-3.6 gm/day).
Spironolactone 75 mg/day in divided doses may be added to maintain
normal serum K+ levels until euthyroidism is achieved.
1.4.3 Ophthalmopathy
Exophthalmos is a feature of Graves’ disease and may occur in the absence
of thyroid dysfunction. The presence of ophthalmopathy necessitates full
thyroid function assessment. Even though fT4 is normal, TSH may be
suppressed.
CT or MRI scan is indicated in unilateral exophthalmos to exclude tumours.
The degree of proptosis should be serially documented to help in the
decision regarding active treatment.
Combined management with an ophthalmologist is recommended.
14
Mild cases of exophthalmos may only require reassurance.
In patients with moderate eye disease, symptomatic treatment such as
elevation of the head of the bed, taping of eyelids at night, moist chambers,
sunglasses, artificial tears to prevent dryness, are usually adequate.
In severe congestive ophthalmopathy, high dose steroids, immunomodulatory drugs, orbital decompression or irradiation may be necessary.
In active or severe eye disease, radioiodine should be used with caution.
Anti-thyroid therapy should be carefully monitored to avoid
hypothyroidism which can worsen the eye condition. These patients are best
managed in specialised units.
1.4.4 Dermopathy (Pretibial Myxoedema)
This may respond to local steroid application under occlusive dressings.
15
2. THYROID CRISIS
Thyroid crisis is a life threatening exacerbation of the hyperthyroid state with
evidence of decompensation in one or more organ systems. The mortality is 20 - 30 %.
It may be precipitated by stress including concurrent infections, surgery or pregnancy.
2.1 Clinical Features
It is a clinical diagnosis with features of severe thyrotoxicosis, hyperpyrexia
and neuro-psychiatric manifestations such as delirium.
2.2 Management
Rehydration
Treat hyperpyrexia (use fans, tepid sponging and oral paracetamol)
Do NOT use aspirin or NSAIDs
Beta sympathetic blocking agents
Oral propanolol 40 mg qid, or I/V 1-2 mg 4-6 hourly
Iodide
Oral saturated solution of potassium iodide (SSKI) 5 drops 6-hourly
or I/V Sodium Iodide 500 mg 8 hourly
or oral Lugol's iodine 5-10 drops, 6-hourly
Antithyroid Drugs
Carbimazole 15-20 mg 6-hourly
or propylthiouracil 150-200 mg 6-hourly
Corticosteroids
I/V dexamethasone 2 mg 6-hourly
or I/V hydrocortisone 200 mg 6-hourly
16
The above regime should be instituted simultaneously. Once the clinical
situation stabilises (usually after 3 - 4 days), iodide and corticosteroids may be
stopped and the dose of anti-thyroid drugs and beta-blockers may be reduced.
The precipitating cause should be treated. Subsequently, appropriate treatment
for thyrotoxicosis should be continued.
17
3. HYPOTHYROIDISM
Hypothyroidism is due to deficiency of thyroid hormones resulting in a hypometabolic state. The causes are:
*
*
Primary autoimmune thyroid disease
- thyroid agenesis
- post-thyroidectomy
- post-radioiodine therapy
Secondary hypopituitarism
3.1 Clinical Features
These include:
*
Apathy, fatigue
*
Cold intolerance
*
Slow speech
*
Facial puffiness
*
Weight gain
*
Constipation
*
Coarse features
Less common features are:
*
Menorrhagia
*
Hoarse voice
*
Depression
*
Psychosis
May be asymptomatic.
3.2 Laboratory Investigations
To confirm diagnosis, serum fT4 and TSH should be assayed.
Elevated serum TSH levels are invariably found in primary hypothyroidism.
Serum TSH is useful in assessing adequacy of treatment.
18
To identify autoimmune thyroid disease, thyroid antibodies (anti-thyroid
peroxidase and anti-thyroglobulin) may be assayed.
3.3 Management
The aim is to make the patient clinically and biochemically euthyroid.
Treatment is life long and patient needs to be informed of this to ensure
good compliance. Omission of L-thyroxine for a few days, for example,
in the perioperative period does not result in any deleterious consequences.
3.3.1 Overt Hypothyroidism
The usual starting dose for L-thyroxine is 50 or 100 ug/day increasing
at 1 - 2 weeks interval to a maintenance dose of 100 - 200 ug/day.
Hypothyroidism of recent onset can be given the full replacement dose
immediately.
In patients with ischaemic heart disease (IHD), gross hypothyroidism and in
the elderly, the usual starting dose of L-thyroxine is 25 ug/day. The dosage
should be increased slowly (i.e. every 2-4 weeks) according to the patient’s
response. If angina occurs, reduce to previous dosage or withhold treatment
temporarily, while management of IHD is optimised.
In hypopituitarism, L-thyroxine therapy should be initiated only after
cortisol replacement to avoid possible adrenal crisis.
3.3.2 Subclinical hypothyroidism
In such cases, patients are not overtly hypothyroid and serum fT4 is
normal but TSH is elevated. Treatment with L-thyroxine is recommended
as such patients are more prone to coronary artery disease due to hyperlipidaemia, if left untreated. Treat initially with L-thyroxine 50-100 ug/day
and adjust dosage to maintain normal TSH levels.
19
3.3.3 In pregnancy
There may be a need to increase the dose of L-thyroxine, particularly
during the second and third trimesters.
3.4 Monitoring
The patient should be monitored clinically and biochemically with serum
TSH and fT4 measurements.
Measurements of serum TSH and fT4 should be done 2-3 months after
initiation of therapy to determine the maintenance dose and subsequently
every 6 months to 1 year.
20
4. MYXOEDEMA COMA
Myxoedema
coma
be precipitated by stress, infection, or
drugs
(e.g. CNS suppressants). This is not a common condition but urgent treatment is
required because the mortality is high.
4.1 Management
The treatment consists of:
Gradual rewarming with blankets.
Accurate core temperatures should be recorded with a low reading
Rectal thermometer.
Thyroid hormone replacement with L-thyroxine 300-400 ug given
orally via nasogastric tube or parenterally if available. Alternatively,
doses of tri-iodothyronine 10 ug 8-hourly (IV or orally)
may
be used.
I/V hydrocortisone should be given, 200 mg stat and 100 mg 6-hourly
until patient regains consciousness
Ensure adequate hydration and nutrition;
Use 5-10% dextrose solution to maintain normal blood glucose levels.
Correct electrolyte imbalance (patients tend to be hyponatraemic).
Ensure adequate ventilation.
Patients tend to hypoventilate, resulting in hypercapnoea.
Treat precipitating cause.
Infection may be masked by the hypothyroid state.
21
5. CONGENITAL
HYPOTHYROIDISM
An endocrine disorder resulting from inadequate thyroid hormone for the
metabolic needs of a newborn infant. Incidence is between 1:4000 to 1:5000 in
Malaysia. Most infants with the disease have no obvious clinical manifestations at
birth, therefore neonatal screening of thyroid function should be performed on all
newborns. Intellectual impairment can be prevented by early diagnosis and
treatment. The causes include:
*
*
*
thyroid gland dysgenesis (90% of cases)
dyshormonogenesis
iodine deficiency (endemic goitre)
5.1 Clinical Features
Since most infants are asymptomatic at birth, the presence of prolonged
jaundice, poor feeding, constipation or an unusually quiet baby should alert the
clinician to the possibility of hypothyroidism.
If left untreated, overt clinical signs will appear by 3-6 months, namely coarse
facies, dry skin, hoarse cry, umbilical hernia and delayed developmental
milestones.
5.2 Laboratory Investigations
Ideally screening of newborns should be done on heel prick blood 2-5 days after
birth. However, in the local setting, screening of newborn with cord blood TSH
is an acceptable alternative. Those with high cord blood TSH levels should be
recalled for confirmation of diagnosis by measurement of TSH and fT4 using
venous blood at 7-10 days of age.
Interpretation of the above results should take into account the physiological
variations of hormone levels during the neonatal period.
X-ray measurements for bone age may be useful but not diagnostic.
22
5.3 Management
Treatment should commence as soon as the diagnosis is made.
With early adequate thyroid replacement therapy, patients are expected to
have normal intellectual and physical development.
Starting dose of L-thyroxine is 10-12 ug/kg/day.
The aim is to maintain serum TSH levels within the normal range and fT4
at the upper limit of the normal range adjusted for age.
Treatment should be life-long except in children suspected of having
transient hypothyroidism whereby therapy is stopped at 2 years of age for
re-evaluation.
5.4 Monitoring
Patients should be monitored clinically and biochemically at monthly intervals
for the first 6 months then 3-monthly until one year of age; and thereafter
6 monthly.
Checklist for monitoring include growth parameters (weight, height,
head circumference), developmental milestones and bone age progression.
23
6. THYROIDITIS
Thyroiditis is inflammation of the thyroid gland with destruction of the thyroid
tissues to a variable degree. The presentation, functional disturbance and prognosis
depend on the aetiology of the thyroiditis. Presentation may be acute, subacute or
chronic. The causes are:




Autoimmune Infection
Physical
Idiopathic
-
Hashimoto’s thyroiditis
post-partum thyroiditis
atrophic thyroiditis
viral thyroiditis (De Quervain’s thyroiditis)
radiation to the neck
painless thyroiditis
Riedel’s thyroiditis
6.1 Clinical features
The usual presentation is thyroid swelling which is usually diffuse.
Pain or thyroid dysfunction may be present.
Hashimoto’s thyroiditis presents with diffuse firm goitre. Patients are
usually euthyroid but may develop hypothyroidism in the long term. Few patients
may present with thyrotoxicosis due to co-existing Graves’ disease. It is more
common in females in the fourth and fifth decades. There is often a positive
family history of goitre or other autoimmune diseases.
Postpartum thyroiditis is an autoimmune disorder presenting with thyrotoxicosis followed by euthyroid and hypothyroid phases a few months after
delivery. A proportion of patients may present at the hypothyroid phase. Unlike
De Quervain’s, there is no pain in the thyroid which is enlarged in about 50% of
cases. The thyrotoxic phase lasts for about 2 months but the hypothyroid phase
may last for 2-9 months. About 5% of the patients develop permanent
hypothyroidism.
24
Subacute (De Quervain's) thyroiditis usually presents with pain in the
region of thyroid gland which may be mistaken for pharyngitis accompanied in
severe cases by fever. There are also accompanying symptoms and signs of
thyrotoxicosis. On palpation, the gland is slightly to moderately enlarged, firm
and usually exquisitely tender. The disease usually passes through a euthyroid
phase followed by a transient hypothyroid phase prior to full recovery within a
few months in the majority of cases. Rarely, permanent hypothyroidism may
result.
Riedel’s thyroiditis is a rare condition of unknown aetiology presenting
with hypothyroidism and woody hard goitre. The extensive fibrosis may involve
the adjacent structures e.g. trachea and oesophagus and may be associated with
fibrosis elsewhere especially in the retroperitoneal area. Some patients may have
elevated anti-thyroid antibodies but not as high as those of Hashimoto’s
thyroiditis.
Painless thyroiditis is of unknown aetiology and is similar to postpartum
thyroiditis except that this is not associated with pregnancy.
Acute pyogenic thyroiditis is rare and is usually a result of dissemination
from a septic focus elsewhere. It usually presents with fever, pain and signs of
acute inflammation in the thyroid gland. Needle aspiration of the thyroid should
be performed for diagnosis and identification of the organism. Rarely,
tuberculosis or anaplastic carcinoma of the thyroid may present similarly.
6.2 Laboratory Investigations
Thyroid function tests to assess functional status are indicated in all patients
with thyroiditis. since some may have subclinical thyroid dysfunction. Repeat
measurements should be performed as thyroid status may change.
25
Tests to confirm aetiology includes thyroid autoantibodies (anti-thyroid
peroxidase and anti-thyroglobulin), thyroid aspirate (FNAC) for cytological
diagnosis and culture in the case of pyogenic thyroiditis.
Isotope uptake scan is useful in differentiating thyrotoxicosis due to thyroiditis
from Graves’ disease.
ESR is raised in De Quervain’s thyroiditis and useful in monitoring activity of
the disease.
6.3 Management
NSAIDs to relieve pain.
In de Quervain’s thyroiditis, if pain persists after 1 week of NSAIDs
treatment, steroid therapy (prednisolone 30 mg/day for 1 week) is
useful.
Antithyroid drugs (e.g. carbimazole) are not indicated.
Beta-blockers may be useful to alleviate symptoms.
L-thyroxine is indicated for hypothyroidism. It may be withdrawn after
6-12 months in postpartum or painless thyroiditis to determine whether
there is recovery of thyroid function.
In Hashimoto’s thyroiditis,
hypothyroidism is likely to be permanent and patients require life-long thyroid
hormone replacement.
Antibiotics are indicated in pyogenic thyroiditis.
Surgical drainage may be required.
26
7. SINGLE THYROID NODULE
The common causes of thyroid nodules are:
*
*
*
*
Colloid goitre and cysts
Adenomatous hyperplasia
Follicular adenoma
Thyroid carcinoma
The incidence of malignancy in solitary nodule may be as high as 10%. The sudden
appearance of a painful thyroid nodule is usually due to bleeding into a colloid cyst;
this resolves spontaneously.
.
7.1 Diagnosis
The history and physical examination are essential in the initial assessment
of thyroid swelling. The suspicion of malignant disease would be high in
the following:








Age groups of <20 years and >50 years have the highest incidence
of thyroid cancer in a palpable nodule
Male gender
History of rapid increase in size and local pressure symptoms
e.g. dysphagia and hoarseness of voice
History of external neck irradiation during childhood or adolescence
A firm/hard irregular and fixed nodule
Ipsilateral cervical lymphadenopathy (probability of malignancy
increases from about 10% to 70%)
Family history is important – Familial medullary thyroid carcinoma has
an autosomal dominant inheritance while papillary thyroid carcinoma is
familial in only 3% of cases
Dominant nodule in a multinodular goitre
27
7.2 Laboratory investigations
7.2.1
Fine-needle aspiration
cytology (FNAC)
by experienced
cytologists is the most effective method in distinguishing benign
from malignant thyroid nodules. It is highly sensitive and
specific.
However, FNAC cannot differentiate follicular adenoma
from carcinoma. Hence, patients with follicular neoplasms need to be
referred for surgery.
7.2.2
Ultrasound scan is able to accurately indicate whether there
are multiple nodules and determine changes in size of the
nodule. It can also confirm whether the nodule is cystic where
risk of malignancy is low, solid with a risk of malignancy of
around 20% or mixed with a 30% risk of malignancy.
7.2.3
Thyroid scintiscan with 99mTc or 123I is useful in differentiating
toxic from cold nodules. The incidence of malignancy in cold
nodules is about 10-20%.
7.2.4
Other scans e.g. CT and MRI scans are not useful
diagnosis of thyroid nodules.
in the
7.2.5
Thyroid function tests (fT4, TSH and if indicated, fT3 )
be done to evaluate a hot nodule.
should
7.3 Management
In colloid cyst, aspiration may be therapeutic.
Surgery should be considered for recurrence.
Toxic adenoma is treated surgically or with radioiodine.
The use of L-thyroxine to reduce the size of thyroid nodules is seldom
effective.
In papillary and follicular carcinoma, total thyroidectomy followed
by ablative radioiodine and L-thyroxine therapy are potentially curative.
28
However, the management and prognosis of thyroid cancer depend on
many factors such as age, histology and TNM classification. Serial
serum
thyroglobulin measurements are useful for monitoring for
recurrence. The patient can also be monitored by whole body iodine
scanning. When serum thyroglobulin level increases, whole body iodine
scanning is indicated.
Anaplastic thyroid carcinoma has a poor prognosis. Treatment is mainly
symptomatic. Palliative measures include surgery, external radiotherapy
and in some cases, chemotherapy.
Medullary thyroid carcinoma can be sporadic, familial or be part of a
multiple endocrine neoplasia (MEN) II syndrome. Phaeochromocytoma
must be excluded, prior to surgery. Screening of family members for MEN
is indicated.
29
8.
MULTINODULAR
GOITRE
Multinodular goitre (MNG) is an enlargement of the thyroid gland due to
multiple nodules. These nodules may be detected clinically or by imaging
techniques. Most MNG are benign. However, it is not possible to differentiate
benign from malignant nodules on clinical grounds alone. The prevalence of
MNG is higher in iodine deficient areas, women and older individuals. In
most cases, the aetiology is unknown. Known causes include:
*
*
*
*
iodine deficiency
goitrogen ingestion
autoimmune disorders
dyshormonogenesis (usually diffuse in the initial stages)
8.1 Clinical features
Most patients present with painless neck swellings and they are usually
euthyroid.
Occasionally, they may present with sudden increase in goitre size,
associated with pain due to haemorrhage.
Large MNGs can extend retrosternally and cause superior vena cava
obstruction or stridor.
Rapidly progressive enlargement and cervical
lymphadenopathy raises the possibility of malignancy.
8.2 Laboratory Investigations
Thyroid ultrasound is a very sensitive method to ascertain the size and
number of nodules as well as differentiating cysts from solid/mixed
nodules. However, ultrasound cannot distinguish benign from malignant
nodules.
Thyroid function tests (fT4 and TSH) should be performed.
30
Thyroid scintiscans are not useful except in cases where toxic (‘hot’)
nodules are suspected.
Fine needle aspiration cytology (FNAC) should be performed when
malignancy is suspected.
8.3 Management
No treatment is required when the goitre is small
symptoms. Reassurance is usually adequate.
and
not
causing
Thyroxine suppression therapy is controversial and contraindicated in
patients with ischaemic heart disease. It may be considered when TSH
levels are not suppressed. Treatment is continued for 1 year in those
whose nodules regress, after which T4 therapy is stopped.
In those
without any regression after 6 months of adequate TSH suppression,
therapy should be stopped and alternative forms of treatment be
considered.
Definitive treatment for toxic MNG is radioiodine therapy or surgery.
Antithyroid drugs can be used to alleviate thyrotoxic symptoms but is
not curative.
Surgery is recommended when goitres are large, causing compressive
symptoms and for cosmetic reasons.
Unless total thyroidectomy is
done, recurrence rate is high and subsequent surgery carries a higher
risk of complications.
Radioiodine therapy is not recommended for large non-toxic goitres
multiple high doses are required and response is poor.
31
as
STATEMENT OF INTENT
“This report is not intended to be construed or to serve as a standard of
medical care.
Standards of medical care are determined on the basis of all
clinical data available for an
individual case and are subject to change as
knowledge and technology advance and patterns evolve.
The ultimate judgment
regarding a particular clinical procedure or treatment plan must be made by
the doctor in the light of the clinical data presented by the patient and the
diagnostic and treatment options available”.
32
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38
PRACTICE GUIDELINES FOR
THYROID DISORDERS
THE MALAYSIAN CONSENSUS 2000
Logo MOH
Logo MEMS
39
Logo Acad Med
Practice Guidelines for Thyroid Disorders
The Malaysian Consensus 2000
CPG 1/2000
All rights reserved. This book may not be reproduced, in whole or in part, in any form or
means, electronic or mechanical, including photocopying, recording, or by any other
information storage and retrieval system now known or hereafter invented, without
written permission from the publisher.
Copyright © Malaysian Endocrine and Metabolic Society
© Academy of Medicine Malaysia
© Ministry of Health Malaysia
Published By
Malaysian Endocrine and Metabolic Society
January 2000
Distributed By
Malaysian Endocrine and Metabolic Society
c/o Department of Medicine, Faculty of Medicine
Hospital Universiti Kebangsaan Malaysia (HUKM)
Jalan Yaakub Latiff, Bandar Tun Razak
56000 Cheras, Kuala Lumpur
40
Practice Guidelines for Thyroid Disorders
The Malaysian Consensus 2000
CPG 1/2000
FOREWORD
Thyroid disorders together with diabetes mellitus are the most common and prevalent
endocrine and metabolic diseases in this country. Thus, having completed a guideline on
the management of type 2 diabetes mellitus, the Malaysian Endocrine and Metabolic
Society (MEMS) took the task to prepare the Malaysian Consensus for Practice
Guidelines for Thyroid Disorders. These guidelines hopefully will be of use to assist
practising doctors in the management of patients with thyroid disorders.
The draft for the guidelines was drawn up by members of the Malaysian Endocrine
and Metabolic Society during the two meetings in February and May 1998.
Following this, three consensus development workshops were held to discuss the
draft and to agree on this Malaysian Consensus for Practice Guidelines for Thyroid
Disorders. On behalf of MEMS, I would like to thank the Academy of Medicine and
Ministry of Health for their collaboration and support in preparation of this
consensus. I would also like to express the Society’s appreciation and gratitude for
the participation of representatives of the Ministry of health, College of Physicians,
College of Surgeons, Malaysian Medical Association and Malaysian Paediatric
Association in developing this consensus. Finally, my personal word of thanks to
YBhg Professor Dato’ Khalid Abdul Kadir and Associate
41