Thyroid Diseases Emergencies Guide

T H Y R O I D D I S E A S E S &
E M E R G E N C I E S
P R E S E N T E D B Y
N U R U L H I D A Y U B I N T I I B R A H I M
N U R U L H U S N A B I N T I A Z I Z
M U H A M M A D A F F A N S Y A F I Q I

INTRODUCTION
T H Y R O I D D I S E A S E S
 Thyroid diseases are amongst one of the most common endocrine diseases in
Malaysia.
 Through the hormones it produces, the thyroid gland influences almost all the
metabolic process in the body.
 Thyroid diseases can range from a small, harmless goiter that needs no
treatment to life threatening cancer.
 The most common thyroid problems involve abnormal production of
hormones which are hyperthyroidism and hypothyroidism.
 Although the effects can be unpleasant or uncomfortable, most thyroid
problems can be managed well if properly diagnosed and treated.

ANATOMY
T H Y R O I D G L A N D
 The thyroid is a butterfly-shaped gland located in the front of the neck just above
the trachea, weighs approximately 15 to 20 grams in the adult human.
 It consist of two lobes connected by narrow band thyroid tissues called the isthmus.
Four parathyroid glands located posteriorly at each pole of thyroid gland.
 Thyroid gland supplied by:
I. Superior Thyroid Artery – branch of external carotid artery
II. Inferior Thyroid Artery – branch of thyrocervical trunk
III. Thyroid Ima Artery

ANATOMY

ANATOMY
The venous blood is drained via:
 Superior thyroid veins
 Middle thyroid veins
 Inferior thyroid veins – drain into the left and right brachiocephalic veins
drain to the internal jugular vein
Lymphatic drainage:
 Prelaryngeal lymph nodes
 Pretracheal lymph nodes
 Paratracheal lymph nodes
Nerve supply:
 The gland receives sympathetic nerve supply from the superior, middle and inferior
cervical ganglion of the sympathetic trunk.
 The gland receives parasympathetic nerve supply from the superior laryngeal nerve
and the recurrent laryngeal nerve.

ANATOMY
B L O O D S U P P LY O F T H Y R O I D G L A N D

ANATOMY
H O R M O N E S O F T H Y R O I D G L A N D
Hormones secreted by thyroid gland:
 thyroxine (T4)
 triiodothyronine (T3)
The T3 and T4 are created from iodine and
tyrosine
Hormones secreted by parathyroid gland:
 calcitonin
All organ systems are affected by thyroid hormones.
Thyroid hormones increase metabolic rate, heart
rate, and ventricle contractility, as well as muscle
and central nervous system (CNS) excitability.

ANATOMY
H O R M O N E S O F T H Y R O I D G L A N D

PHYSIOLOGY
 The iodide trapped by the thyroid gland is subsequently oxidized to iodine by the
enzyme thyroid peroxidase.
 The iodine then undergoes a series of organic reactions within the thyroid gland to
produce tetraiodothyronine or thyroxine (T4) and triiodothyronine (T3).
 T3 is also produced in other tissues such as the pituitary, liver, and kidney by the
removal of an iodine molecule from T4.
 T4 is considered to be more of a pro-hormone, while T3 is the most potent thyroid
hormone produced.
 T4 and T3are both stored in the thyroglobulin protein of the thyroid gland and
released into the circulation through the action of pituitary derived thyrotropin
(thyroid stimulating hormone or TSH)

PHYSIOLOGY

PHYSIOLOGY
Series of organic
reaction:
1. Iodine trapping
2. Synthesis and
secretion of
thyroglobulin
3. Oxidation of iodine
4. Organification of
thyroglobulin
5. Coupling reaction
6. Storage
7. Secretion

RISK FACTORS
FA C T O R S T H AT A F F E C T T H Y R O I D F U N C T I O N

TYPES
H Y P O T H Y R O I D I S M
H Y P E R T H Y R O I D I S M
 It occurs when the gland produces excessive amounts of thyroid hormones.
 The most common cause is Graves' disease, an autoimmune disorder.
 Hypothyroidism is a state of insufficient thyroid hormone production.
 Worldwide, the most common cause is iodine deficiency.
 Hypothyroidism secondary to iodine deficiency remains the leading cause of
preventable intellectual disability.
 In iodine-sufficient regions, the most common cause of hypothyroidism is
Hashimoto's thyroiditis, also an autoimmune disorder.

TYPES
T H Y R O I D I T I S
T H Y R O I D E M E R G E N C I E S
 Thyroid Storm
 Myxedema Coma
 Autoimmune – Hashimoto’s thyroiditis, Post-partum thyroiditis & Atrophic thyroiditis
 Infection – Viral thyroiditis (De Quervain’s thyroiditis)
 Physical – Radiation to the neck
 Idiopathic – Painless thyroiditis, Riedel’s thyroiditis

INTRODUCTION
R I S K FA C TO R S
 Autoimmune thyroiditis
 Previous Graves' disease
 Personal or family history of associated autoimmune disorders (eg, vitiligo,
pernicious anaemia, diabetes mellitus type 1)
 Thyroidectomy or other neck surgery
 Radioactive iodine therapy
 External radiotherapy
 Drugs impairing thyroid function
I. Lithium carbonate
II. Amiodarone
 Hypothalamic disorders
 Pituitary disorders

INTRODUCTION
C L A S S I F I C AT I O N O F H Y P OT H Y R O I D I S M
H Y P OT H Y R O I D I S M
P R I M A R Y
( 9 0 % )
S E C O N D A R Y
( C e n t r a l )
S U B C L I N I C A L T R A N S I E N T
 High TSH
concentration
 Low serum free
thyroxine (T4)
concentration
 Low serum T4
concentration
 Serum TSH
concentration is
not
appropriately
elevated.
 Can be
observed as a
phase of
subacute
thyroiditis
 Normal free T4
concentration
 Elevated TSH
concentration
 Other terms for
this condition
are :
I. Mild
hypothyroidism
II. Early thyroid
failure
III. Preclinical
hypothyroidism

PRIMARY HYPOTYROIDISM
AU TO I M M U N E H Y P OT H Y R O I D I S M
 Autoimmune hypothyroidism may be associated with a goiter (Hashimoto's,
or goitrous thyroiditis) or, at the later stages of the disease, minimal residual
thyroid tissue (atrophic thyroiditis).
 Because the autoimmune process gradually reduces thyroid function, there is
a phase of compensation when normal thyroid hormone levels are
maintained by a rise in TSH. Though some patients may have minor
symptoms, this state is called subclinical hypothyroidism.
 Later, unbound T4 levels fall and TSH levels rise further; symptoms become
more readily apparent at this stage (usually TSH >10 mIU/L), which is referred
to as clinical hypothyroidism or overt hypothyroidism.
 Celebrities who known to has Hashimoto’s thyroiditis are Gigi Hadid & Kim
Cattrall.

PAT H O G E N E S I S
 In Hashimoto's thyroiditis, there is a marked lymphocytic infiltration of the
thyroid with germinal center formation, atrophy of the thyroid follicles
accompanied by absence of colloid, and mild to moderate fibrosis.
 In atrophic thyroiditis, the fibrosis is much more extensive, lymphocyte
infiltration is less pronounced, and thyroid follicles are almost completely
absent. Atrophic thyroiditis likely represents the end stage of Hashimoto's
thyroiditis rather than a distinct disorder.
 Genetic Associations: HLA-DR (3,4,5) & CTLA-4 (Cytotoxic T Lymphocyte
associated antigen 4) polymorphism
 Modifying Environmental Factor : Chronic exposure to high iodine diet

A S S O C I AT E D C O N D I T I O N S
Other Autoimmune disorders:
 Type 1 diabetes mellitus
 Addison's disease
 Pernicious anemia
 Vitiligo
 Alopecia areata
 Celiac disease
 RA, SLE, Sjogren syndrome
 Thyroid associated ophthalmopathy( in 5% of pt)
 Turner syndrome, Down’s syndrome
 Type 1 or 2 polyglandular autoimmune syndrome

SECONDARY HYPOTHYROIDISM
I N T R O D U C T I O N
 Secondary hypothyroidism is usually diagnosed in the context of other
anterior pituitary hormone deficiencies; isolated TSH deficiency is very rare.
 TSH levels may be low, normal, or even slightly increased in secondary
hypothyroidism; the latter is due to secretion of bio inactive forms of TSH.
 The diagnosis is confirmed by detecting a low unbound T4

HYPOTHYROIDISM
C L I N I C A L M A N I F E S TAT I O N
 Patients with Hashimoto's thyroiditis may present with goiter rather than
symptoms of hypothyroidism. It is usually irregular and firm in consistency.
 Hypothyroidism is less prominent clinically and better tolerated when there
is a gradual loss of thyroid function (as in most cases of primary
hypothyroidism) than when it develops acutely after thyroidectomy or abrupt
withdrawal of exogenous thyroid hormone.
 The symptoms of central hypothyroidism are usually milder & less obvious
than in primary hypothyroidism because of concurrent symptoms of
coexisting hormone deficiencies. i.e. hot flashes due to hypogonadism may
mask the cold intolerance of hypothyroidism.

HYPOTHYROIDISM
C L I N I C A L M A N I F E S TAT I O N
M E C H A N I S M SY M P TO M S S I G N S
Slowing of metabolic processes  Fatigue, weakness
 Cold intolerance
 Dypsnea on exertion
 Weight gain
 Mental retardation (infant)
 Constipation
 Growth Failure
 Slow movement and slow
speech
 Delayed relaxation of tendon
reflexes
 Bradycardia
 Carotenemia
Accumulation of matrix
substances
 Dry skin
 Hoarseness
 Edema
 Coarse skin
 Puffy facies and loss of
eyebrows
 Periorbital edema
 Enlargement of the tongue
Other  Decreased hearing
 Myalgia and paresthesia
 Menorrhagia
 Arthralgia
 Pubertal delay
 Diastolic hypertension
 Pleural and pericardial
effusions
 Ascites
 Galactorrhea

HYPOTHYROIDISM
D E F F E N R I AT I O N B E T W E E N P R I M A R Y A N D S E C O N D A R Y H Y P O T H Y R O I D I S M

HYPOTHYROIDISM
S K I N M A N I F E S TAT I O N
 The skin is cool and pale in patients with hypothyroidism because of
decreased blood flow.
 The epidermis has an atrophied cellular layer and hyperkeratosis that results
in the characteristic dry roughness of the skin.
 Sweating is decreased because of decreases in calorigenesis and acinar gland
secretion.
 A yellowish tinge may be present if the patient has carotenemia, while
hyperpigmentation may be seen when primary hypothyroidism is associated
with primary adrenal failure
 Hair may be coarse, hair loss is common, and the nails become brittle.
 Non-pitting edema (myxedema) occurs in severe hypothyroidism and may be
generalized. It results from infiltration of the skin with glycosaminoglycans
with associated water retention.
 Vitiligo and alopecia areata may be present in patients with hypothyroidism
treatment of Graves‘ hyperthyroidism

HYPOTHYROIDISM
E Y E S M A N I F E S TAT I O N
 Periorbital edema
 Thinning of outer third of eyebrows (Madarosis)
 Graves' ophthalmopathy may persist when hypothyroidism develops after
treatment of Graves' hyperthyroidism
H A E M ATO LO G I C A L M A N I F E S TAT I O N
 Decrease in red blood cell mass
 Normochromic, normocytic hypoproliferative anemia
 Pernicious anemia occurs in 10 percent of patients with hypothyroidism
caused by chronic autoimmune thyroiditis : macrocytic anemia with marrow
megaloblastosis
 Women in the childbearing years may develop iron deficiency anemia,
secondary to menorrhagia.
 In patients with IDA and hypothyroidism, combined therapy with
levothyroxine and oral iron supplements results in correction of the anemia,
which may be refractory to treatment with iron alone

HYPOTHYROIDISM
C A R D I OVA S C U L A R M A N I F E S TAT I O N
 Decrease in cardiac output that is mediated by reductions in heart rate and
contractility
 Thyroid hormone regulation of genes coding for specific myocardial enzymes
involved in myocardial contractility and relaxation is responsible for the
decrease in contractility.
 Reduced cardiac output probably contributes to decreased exercise capacity
and shortness of breath during exercise.
 Hypercholesterolemia, which is caused by a decrease in the rate of cholesterol
metabolism
 Diastolic Hypertension, because of an increase in peripheral vascular
resistance. In normotensive patients, blood pressure increases are small
(<150/100).
 ECG : Low voltage, sinus bradycardia, non-specific ST-T changes

HYPOTHYROIDISM
R E S P I R ATO RY M A N I F E S TAT I O N
 Fatigue, shortness of breath on exertion, rhinitis, and decreased exercise
capacity
 Hypoventilation occurs because of respiratory muscle weakness and reduced
pulmonary responses to hypoxia and hypercapnia
R E S P I R ATO RY M A N I F E S TAT I O N
 Decreased gut motility results in constipation
 Decreased taste sensation.
 Gastric atrophy due to the presence of anti-parietal cell antibodies
 Celiac disease is four times more common in hypothyroid patients
 Modest weight gain (despite poor appetite)due to decreased metabolic rate
and accumulation of fluid

APPROACH
H OW TO A P P R OA C H PAT I E N T ?
H I S TO RY TA K I N G
P H Y S I C A L E X A M I N AT I O N
L A B I N V E S T I G AT I O N S

APPROACH
I N V E S T I G AT I O N S – T H Y R O I D F U N C T I O N T E S T

APPROACH
I N V E S T I G AT I O N S – T H Y R O I D F U N C T I O N T E S T
N O R M A L
T H Y R O I D S T I M U L AT I N G H O R M O N E - T S H
FREETHYROXINEorFT4
NORMAL

HYPOTHYROIDISM
M A N A G E M E N T
 Goal : Normalize TSH level regardless of cause of hypothyroidism
 Treatment of choice is thyroxine
 TSH should be measured at 6 to 8 weeks after any change in L-thyroxine
brand or dose
 Determinants of Thyroxine Requirements:
1. Age
2. Severity and duration of hypothyroidism
3. Weight
4. Malabsorption
5. Pregnancy
6. Presence of cardiac disease
7. Concomitant drug therapy

HYPOTHYROIDISM
M A N A G E M E N T
 Starting dose for healthy patients <50 years should be at 1.6 mg/kg/day
 Starting dose for healthy patients >50 years should be <50 mg/day. Dose
should be increased by 12.5-25 μg/day, if needed, at 6 to 8 weeks intervals.
(Start low and go slow)
 Starting dose for patients with heart disease should be 12.5 to 25 μg/day and
increase by 12.5 to 25 μg/day, if needed, at 6 to 8 weeks intervals

HYPOTHYROIDISM
C O N D I T I O N S T H AT A LT E R L E VOT H Y R OX I N E R EQ U I R E M E N T S

HYPOTHYROIDISM
T R E AT M E N T F O R S U B C L I N I C A L H Y P OT H Y R O I D I S M
 Refers to biochemical evidence of thyroid hormone deficiency in patients
who have few or no apparent clinical features of hypothyroidism.
 Routine treatment not recommended when TSH levels are below 10 mU/L.
 Any elevation of TSH must be sustained over a 3-month period before
treatment is given.
 Treatment is administered by starting with a low dose of levothyroxine (25–50
µg/d) with the goal of normalizing TSH. If thyroxine is not given, thyroid
function should be evaluated annually.
 There is a risk that patients will progress to overt hypothyroidism, particularly
when the TSH level is elevated and TPO antibodies are present.

HYPERTHYROIDISM
Hyperthyroidism is hyperactivity of thyroid gland with sustained increase in
synthesis and release of thyroid hormones.
 Female
 Age more than 60 years old
 Smoking
 Have autoimmune disease
 Family history of thyroid disease or
autoimmune disease
 History of goiter
 Past history of thyroid surgery
 Too much iodine intake through food or
medication
R I S K FA C TO R S

HYPERTHYROIDISM
A E T I O LO G Y
Common causes of hyperthyroidism include :
 Grave disease
 Functioning adenoma and toxic multinodular goiter (TMNG)
 Excessive intake of thyroid hormones
 Abnormal secretion of TSH
 Thyroiditis
 Excessive iodine intake

HYPERTHYROIDISM
PAT H O P H Y S I O LO G Y

HYPERTHYROIDISM
D I S E A S E S I N H Y P E R T H Y R O I D I S M
 Graves’ Disease
 Toxic multinodular Goiter
 Toxic adenoma

HYPERTHYROIDISM
D I S E A S E S I N H Y P E R T H Y R O I D I S M
Toxic multinodular Goiter
 Seen in the elderly and in iodine deficient areas.
 There are nodules that secrete thyroid hormones
 Compression symptoms such dysphagia or dyspnea
 Need surgery for the thyroid that keep on enlarge by removal the nodules
Toxic Adenoma
 There is a solitary nodule producing T3 and T4
 On isotope scan, the nodule is ‘hot’ and the rest of gland is suppressed

GRAVES’ DISEASE
 Also known as toxic diffuse goiter, is an autoimmune disease that affects the
thyroid, presented with enlarged thyroid.
 It is the most common cause of hyperthyroidism.
 Idiopathic causes :
a) Family history of grave disease
b) Genetic factors
c) Triggered by stress, infection
d) Autoimmune disease (type 1 DM, Addison’s disease)
e) Smoking

GRAVES’ DISEASE
 Circulating IgG autoantibodies directed against the thyrotropin receptor
binding to and activating G-protein-coupled thyrotropin receptors, which
cause smooth thyroid enlargement.
 This cause increase hormone production especially T3.
 React with orbital auto-antigens.
 Triggers with stress and infection.

GRAVES’ DISEASE
 Production of thyroid hormones is
regulated by TSH.
 The binding of TSH to a receptor on
thyroid cells activates adenylate
cyclase and stimulates the synthesis of
2 thyroid hormones : T3 & T4
 A person with Grave’s disease makes
auto-antibodies to the receptor for
TSH.
 The binding of these auto-antibodies
to the receptor mimics the normal
action of TSH, without the regulation,
leading to overstimulation of the
gland.
 The auto-antibodies are called long
acting TSH.

GRAVES’ DISEASE
 History Taking
 Physical Examination
W H AT TO I N C LU D E I N H I S TO RY TA K I N G ?
 Unexplained weight loss even with good appetite
 Excessive sweating especially at night
 Cannot tolerance to heat
 Excitability, irritability, tremulousness
 Palpitations
 Any pressure symptoms such as dysphagia, dyspnea and hoarseness of voice
 Family history of hyperthyroidism
 History of autoimmune disease
 History of goiter and past thyroid surgery
 History of iodine contrast media use
 Smoking or not
 Iodine intake history either medication or diet

GRAVES’ DISEASE
C L I N I C A L F E AT U R E S

GRAVES’ DISEASE
SYMPTOMS
 Palpitation, tremor, heat intolerance, sweating,
increase appetite and unintentional weight loss
 Eye symptoms (30-50%) : exophthalmos,
opthalmoplagia
 Thyroid dermopathy : Pretibial myxedema (7%)
Thickening of the skin, particularly over the lower
tibia due to accumulation of glycosaminoglycan
 Thyroid Acropachy - Clubbing of fingers (rare)

GRAVES’ DISEASE
 History Taking
 Physical Examination
W H AT TO LO O K F O R I N P H Y S I C A L E X A M I N AT I O N ?
 Unilateral neck swelling or
goiter usually with or without
bruit in grave disease
(describe the swelling)
 Proximal muscle weakness
 Hyperreflexia
 Warm and sweaty palms
 Palmar erythema
 Fine finger tremors
 Lid retraction, lid lag,
exophthalmos
 Resting tachycardia

INVESTIGATION
 Full blood count – Hemoglobin (Hb) and Total
White Count (TWC) to rule out sign of infection
 Thyroid function test – TSH, T3 and T4
 Serum thyroid autoantibodies
 Serum calcitonin level
 Serum thyroglobulin level
 Isotopes scan
 Radioactive iodine uptake and scan – to rule out
thyroiditis
 Thyroid ultrasound + Colour flow Doppler
I. Ultrasound
Inhomogeneous diffusely
hypoechoic gland
II. Colour Doppler
Hypervascular – Thyroid inferno

LAB INVESTIGATION
T H Y R O I D F U N C T I O N T E S T

LAB INVESTIGATION
S U M M A RY

GRAVES’ DISEASE
H OW TO M A N A G E T H I S PAT I E N T ?
Three forms of therapy are available:
1. Medical Treatment
Anti-thyroid drug
 Thionamides (carbimazole or propylthiouracil) are the commonest forms of
treatment that can be used for most patients with the hope of achieve long
term remission.
 Also used in preparation for surgery and radioiodine therapy
B- blockers
 For symptoms relief initially
 Propranolol 30-120mg/day

GRAVES’ DISEASE
 Anti-thyroid drug most useful in :
Children  It is effective and more acceptable
to patients
Pregnancy  The doses should lower as possible
to reduce risk of fetal goiter.
 PTU is preferred to carmibazole in
pregnancy and breastfeeding time
Patient with medical complications  Thyroid crisis and heart failure
Patient who contraindicated to surgery
or refuse surgery
Patient who relapse after
thyroidectomy

GRAVES’ DISEASE

GRAVES’ DISEASE
2. Surgery
 Thyroidectomy
 Indication :
I. Failed medical treatment; relapse after one and non compliance to anti
thyroid drug
II. With large goiters and pressure symptoms
3. Radioiodine therapy
 Contraindicated in pregnant and breastfeed mother

INTRODUCTION
 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:
I. Autoimmune – Hashimoto’s thyroiditis, Post-partum thyroiditis &
Atrophic thyroiditis
II. Infection – Viral thyroiditis (De Quervain’s thyroiditis)
III. Physical – Radiation to the neck
IV. Idiopathic – Painless thyroiditis, Riedel’s thyroiditis

THYROIDITIS
T Y P E S
 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.
H A S H I M OTO ’ S T H Y R O I D I T I S

THYROIDITIS
T Y P E S
 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.
P O S T PA R T U M T H Y R O I D I T I S
PA I N L E S S T H Y R O I D I T I S
 Painless thyroiditis is of unknown aetiology and is similar to postpartum
thyroiditis except that this is not associated with pregnancy.

THYROIDITIS
T Y P E S
 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.
 Patient may presented with fatigue, difficulty in swallowing and may also
came with 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.
D E Q U E RVA I N ’ S T H Y R O I D I T I S

THYROIDITIS
T Y P E S
 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.
R I E D E L’ S T H Y R O I D I T I S

THYROIDITIS
T Y P E S
 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.
A C U T E P YO G E N I C T H Y R O I D I T I S

THYROIDITIS
L A B I N V E S T I G AT I O N S
1. 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.
2. Other 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.
3. Isotope uptake scan is useful in differentiating thyrotoxicosis due to
thyroiditis from Graves’ disease.
4. ESR is raised in De Quervain’s thyroiditis and useful in monitoring activity of
the disease.

THYROIDITIS
M A N A G E M E N T
 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.

THYROIDITIS
M A N A G E M E N T
 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.

INTRODUCTION
 In the USA, the overall incidence of hyperthyroidism is estimated to be
between 0.05% and 1.3%, with the majority of cases being subclinical in terms
of presentation.
 Among hospitalized thyrotoxicosis patients, the incidence of thyroid storm has
been noted to be <10%.
 The mortality of thyroid storm without treatment ranges between 80% and
100%; with treatment, this figure is between 10% and 50%.
 Multiple organ failure was reported to be the most common cause of death
in thyroid storm.

TYPES
M Y X E D E M A C O M A
T H Y R O I D S T O R M
 Thyroid storm represents the extreme presentation of thyrotoxicosis.
 An extreme complications of hypothyroidism in which patients exhibit multiple
organ abnormalities and progressive mental deterioration.
 Occurs when the body’s compensatory responses to hypothyroidism are
overwhelmed by various precipitating stressors.
 Myxedema coma is used to describe the severe life-threatening manifestations of
hypothyroidism.
 The term myxedema coma itself is a misnomer, as patients do not usually present
with frank coma but more commonly have altered mental status or mental slowing.
 Myxedema actually refers to the non-pitting puffy appearance of the skin and soft
tissues related to hypothyroidism

MYXEDEMA COMA
C O M M O N P R E C I P I TAT I N G FA C TO R S
M Y X E D E M A C O M A
I N F E C T I O N S S T R E S S H Y P O V O L E M I A D R U G S
 Pneumonia
 UTI
 Sedative &
Tranquilizers
 Amiodarone
 Lithium
 Narcotics
 Diuretics
 Anaesthesia
Example : GI
Bleeding, Surgery
 Stroke
 Acute MI
 Trauma

MYXEDEMA COMA

MYXEDEMA COMA
Primarily a clinical diagnosis with features of uncomplicated hypothyroidism but
more exaggerated. Thyroid hormone levels are similar to those found in
uncomplicated hypothyroidism.
 Female at risk
 Elderly
 Positive symptoms and signs of hypothyroidism – Look for thyroidectomy scar
or features of hypopituitarism:
1. Hypothermia
2. Hypotension, bradycardia
3. Hypoventilation
4. Hyporeflexia

MYXEDEMA COMA
The cardinal features of myxedema coma are:
1) Hypothermia, which can be profound
2) Altered mental status – Confusion, Delirium, Psychosis, Fit, Coma
3) Cardiovascular depression
The severely hypothyroid patient essentially becomes poikilothermic due to
disordered thermoregulation. This is the reason many cases occur in the winter
months.
Body temperatures as low as 23.3°C have been reported; thus, rectal
temperatures are essential to making the diagnosis.

MYXEDEMA COMA
D I A G N O S T I C C R I T E R I A – J O H N H O P S K I N

MYXEDEMA COMA
L AB I NV EST I GAT I ONS
1. Full Blood Count –Total White Count and Hb level (Macrocytic Anemia)
2. BUSE – Hyponatremia (usually like SIADH – like picture)
3. Liver Function Test – Elevated transaminases
4. ABG test – Hypercapnia and Hypoxia
5. Lipid profile – Hyperlipidemia
6. Thyroid Function Test
7. Blood C&S – To rule out infections
8. Urine Analysis – microscopic hematuria, leukocytes
9. Urine C&S
B ED SI DE I NV EST I GAT I ONS
 ECG – Abnormal ECG: Prolonged PR, QRS and QT, abnormal T wave and
arrhythmias.
 Random Blood Sugar test – Hypoglycemia
I MAGI NG
Chest Xray – Pericardial effusion ± pleural effusion

MYXEDEMA COMA
MANAGEMENT
1. Treatment should be started on clinical grounds.
 If in genuine doubt, it is worth treating as myxedema coma, as giving L-
tyroxine judiciously is unlikely to be harmful in the short term.
 Ideally patient should be managed in ICU.
2. Thyroid hormone replacement
 Replacement therapy should be gentle if patients are elderly and at risk of
cardiac arrhythmias, heart failure or myocardial ischemia.
 Whether T3 or T4 or both should be given is controversial.
 Reason:
A. T3 is has faster onset of action and is the active hormone. T4 has a much
longer half-life, more gradual onset of action and is converted to T3
endogenously.
B. Use of T4 avoids a sudden rise in active T3, which may have adverse
cardiac effects in patients at risk. However, conversion T4  T3 may be
impaired in critically ill patient.

MYXEDEMA COMA
MANAGEMENT
 Reason:
C. Oral T4 has variable oral bioavailability of 40-80%. Avoid co-
administration with antacid, calcium or iron supplement. In contrast oral
T3 has almost 100% oral bioavailability even in hypothyroid patient.
If ischemic heart disease is suspected, dosages of both the above should
be halved.
T4 IV 200 – 500 µg bolus or oral by NG tube followed by
daily dose of 50 – 100 µg until patient can take orally.
(Oral T4 may be given if T3 or IV T4 is not available
but the action is too slow)
T3 IV or oral by NG tube 10 – 20 µg 8 – 12 hourly until T4
can be given orally.

MYXEDEMA COMA
MANAGEMENT
3. Steroids
All patients should be given 100 mg hydrocortisone IV stat and then 50 – 100 mg
6 – 8 hourly until adrenal insufficiency (due to Addison’s disease or
hypothyroidism) has been ruled out.
4. Ventilation
If Pa02 is <60 mmHg with O2 or if PaCO2 is >60 mmHg, assisted ventilation may
be required.
5. Treat accordingly :
Hypothermia
 Passive external rewarming. Do not
warm the patient rapidly as this may
cause cardiovascular collapse.
 Use a lots of blankets and monitor the
rectal temperature.
 Do not correct faster than 1°C/Hour.

MYXEDEMA COMA
MANAGEMENT
Hypothermia
 A low reading thermometer should be
used.
 Give warm humidified oxygen by
facemask.
Hypoglycemia
 Should be corrected
 Exclude concurrent adrenal or pituitary
insufficiency.
Hyponatremia
 Usually resolved with thyroxine
replacement and careful attention to
fluid status.
 If Na <110 mmol/L, hypertonic saline
may be given, with a maximal correction
of serum sodium by not more than 10
mmol/24 hour period.

MYXEDEMA COMA
6. Cardiovascular
 Myxedema patients have:
I. Reduction in total blood volume due to chronic vasoconstriction to preserve
body core temperature
II. Depressed cardiac function and reduced responsiveness to catecholamine.
Hence, they tolerate further volume loss (in GI bleed, diuretic, vasodilation
due to sepsis or rapid rewarming) poorly resulting in hypotension.
 If necessary, plasma expanders or blood products should be given cautiously
guided by CVP.
 Cardiac monitor for supraventricular arrhythmias.
7. Remove or treat precipitating causes. Cover with IV antibiotic if in doubt.
8. Monitor rectal temperature, oxygen saturation, BP, CVP and urine output.
9. On full recovery, doses of replacement thyroxine should be titrated to
maintain an euthyroid state.

THYROID STORM
 Thyroid storm also referred to as
thyrotoxic crisis, is an acute, life
threatening hypermetabolic state
induced by excessive release of
TSH in individuals with
thyrotoxicosis.
 It is a decompensated state of
thyroid hormone - involving
multiple systems and is the most
extreme state of thyrotoxicosis.
 The condition is rare, however,
mortality rates are high and may
approach 10-20%.
PERCI PI TAT I NG FAC TORS
 Infections
 Surgery
 Poorly prepared thyroid surgery
 Diabetic ketoacidosis
 Radioiodine therapy in poorly
prepared patient
 Trauma
 Myocardial Infarction
 Drug : Amiodarone
 Discontinuation of anti-thyroid
drugs
 Labour

THYROID STORM
 The detailed pathophysiology is not fully understood, but it is thought to be
related to increased numbers of beta-adrenergic receptors being exposed to
increased catecholamine levels in states of stress.
U N D E R LY I N G C AU S E S O F T H Y R OTOX I C O S I S T H AT P R E D I S P O S E TO
T H Y R O I D S TO R M
 Graves’ Disease
 Solitory toxic adenoma
 Thyroid carcinoma
 TSH – secreting pituitary adenoma
 Hyadatiform mole
 Iodine exposure (IV radiocontrast dye, amiodarone)

THYROID STORM
Diagnosis is primarily clinical based on high index of suspicion and there are
several factors may precipitate the progression of thyrotoxicosis to thyroid storm.
 Thermoregulatory : High fever, sweating
 CNS dysfunction : Agitation, confusion, acute psychosis, coma
 Cardiovascular : Tachycardia, AF, heart failure
 GIT : Diarrhea and vomiting, acute abdominal pain, jaundice and hepatic
dysfunction.
The combination sign and symptoms makes the diagnosis of thyroid storm, and to
produce scoring systems to improve diagnostic accuracy.
 Burch-Wartofsky point scale
 Japan Thyroid Association categories of thyroid storm 2012
S c o r i n g s y s t e m m u s t n o t b e u s e d a m o n g p a t i e n t s w i t h o u t s e v e r e
t hy r o t ox i c o s i s .

THYROID STORM
D I A G N O S I T I C C R I T E R I A – B U R C H - WA R TO F S K Y P O I N T S C A L E

THYROID STORM
JA PA N T H Y R O I D A S S O C I AT I O N C AT E G O R I E S O F T H Y R O I D S TO R M

THYROID STORM
I N V E S T I G AT I O N S
 Full Blood Count – Total white count, Hemoglobin level
 BUSE – dehydration status
 Blood Glucose - Hypoglycemia
 Liver Function Test
 Thyroid Function Test
 Other additional test to investigate the precipitants
PERCI PI TAT I NG FAC TORS
 Infections
 Diabetic ketoacidosis
 Myocardial Infarction

THYROID STORM
M A N A G E M E N T
 Mortality of untreated storm is high; if the diagnosis is suspected, anti-thyroid
treatment must be started before biochemical confirmation.
 Ideally patient should be managed in ICU.
Hyperthyroidism
A. Inhibition of thyroid hormone formation:
P r o p y l t h i o u ra c i l ( P T U ) C a r b i m a zo l e
Loading dose 600 mg stat and 90-1200
mg/day orally
OR
NG tube in 4-6 divided doses
(e.g 200 mg 4 hourly reduced to 100-200
mg, 6-8 hourly after 24-48 hour)
PTU may be preferable to Carbimazole as
it has the additional action of inhibiting
peripheral conversion of T4 to T3.
60-120 mg/day in 3-4 divided doses
orally or NG tube

THYROID STORM
M A N A G E M E N T

THYROID STORM
M A N A G E M E N T
Hyperthyroidism
B. Inhibition of thyroid hormone release:
S O D I U M I O D I D E
IV 1 g/24 hour by slow infusion
O R A L P OTA S S I U M I O D I D E
100 mg 6 hourly
O R
O R A L LU G O L’ S I O D I N E
10 – 20 drops 8 hourly
O R
Iodine should be given at least one hour after the patient has received the initial
dose of PTU or carbimazole; this is to ensure that the iodine given is not taken up
by the gland for further thyroid hormone synthesis and release.

THYROID STORM
M A N A G E M E N T
Steroids
IV dexamethasone 2 mg 6 hourly. Dexamethasone inhibits both release of
thyroid hormones and peripheral conversion of T4 to T3.
Receptors blockade (in the absence of heart failure)
P R O PA N O LO L
I V P r o p a n o l o l 1 - 2 m g s l o w l y 4 - 6
h o u r l y
O R
O r a l p r o p r a n o l o l 4 0 - 6 0 m g 6
h o u r l y
 Should not be used if there is
pulmonary or peripheral oedema and if
heart failure supervenes, atropine 0.4-1
mg IV should be given.
 Assessment of LV function will help
guide the use of beta-blockers.

THYROID STORM
M A N A G E M E N T
Receptors blockade (in the absence of heart failure)
D i l t i a ze m
6 0 - 1 2 0 m g 6 h o u r l y
 Pulmonery Oedema can be used if beta
blockade is contraindicated e.g bronchial
asthma.
I V E s m o l o l  May be useful in difficult case to allow
rapid titration due to its short half life.
Cardiac Failure
 Usually associated with fast AF
 Diuretics, digoxin, oxygen as appropriate and propranolol if cardiac failure is due to
uncontrolled AF and LV function is good.
 There is relative digoxin resistance with increased renal excretion and decreased action
on AV conduction, so a higher dose of digoxin may be needed.
 Cardioversion of AF is very unlikely to be successful and should wait until patient is
euthyroid and Amiodarone may be useful when given parentally to control acute
arrhythmias.

THYROID STORM
M A N A G E M E N T
Hyperpyrexia
 Fans, tepid sponge, and paracetamol.
Dehydration
 Cautious replacement of fluid. CVP line is helpful.
Anticoagulation
 Give heparin by infusion in patients with AF.
 Other patients should receive SC heparin 5000U 2 times daily or LMWH as
prophylaxis against venous thromboembolism.
Remove or treat precipitating factors
Exchange transfusion of Peritoneal Dialysis/Hemodialysis
 This may be considered in patient who is resistant to the usual
pharmacological measures.

M Y X E D E M A V S T H Y R O I D S TO R M

REFERENCES
1. Harrison’s Principles of internal medicine – 18th Edition
2. Sarawak Handbook of Medical Emergencies 3rd Edition
3. Malaysian CPG 2000
4. UpToDate.com
5. Publications from the American Thyroid Association, American Association of
Clinical Endocrinologists, and the Endocrine Society
6. National Center for Biotechnology Information
[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5667251/]

Thyroid Diseases Emergencies Guide

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