Hypothyroidism is caused by insufficient thyroid hormone secretion or loss of thyroid function. Treatment with levothyroxine sodium replacement therapy is nearly always successful and allows patients to live normal lives. Approximately 5% of the global population has hypothyroidism. Hypothyroidism treatment aims to replace thyroid hormones and maintain euthyroidism by monitoring TSH levels and adjusting levothyroxine doses accordingly. Congenital hypothyroidism requires early diagnosis and treatment to prevent intellectual disability and developmental delays.

1. Hypothyroidism
Updated Management
Dr Shahjada Selim
Associate Professor
Department of Endocrinology, BSMMU
&
Organizing Secretary, BES

2. THYROID DISORDERS

3. Category Primary Secondary
Functional Hormone
Excess
Graves’ Disease Pituitary TSHoma
MNG
Adenoma
SAT
Hormone
Deficiency
Hashimoto’s Thyroiditis Hypopituitarism
Atrophic Hypothyroidism
Structural/ Non-
functional
Goitre Diffuse
STN
MNG- Nontoxic
MNG- Toxic
Tumours Disseminated Carcinoma
Medullary Carcinoma
Lymphoma
Thyroiditis Acute
Subacute
Chronic
Overview of Thyroid Disorders

4. HYPOTHYROIDISM

5. Hypothyroidism is caused by insufficient
secretion of thyroid hormones by the thyroid
gland or by the complete loss of its function.
Hypothyroidism is usually progressive and
irreversible.
Treatment, however, is nearly always
completely successful and allows a patient to
live a fully normal life.

6. Globally, approximately 200 million people have
thyroid disorders of various types, with more than
50% remaining undiagnosed.
About 5% of the global population has
hypothyroidism, and about 2% has hyperthyroidism.
Thyroiditis has been seen in as many as 12.5% of
populations in various countries.
Global prevalence of thyroid disorders
Taylor, P., Albrecht, D., Scholz, A. et al. Global epidemiology of hyperthyroidism and hypothyroidism. Nat Rev Endocrinol 14, 301–316 (2018).

7. 1. Taylor, P., Albrecht, D., Scholz, A. et al. Global epidemiology of hyperthyroidism and hypothyroidism. Nat Rev Endocrinol 14, 301–316 (2018).
https://doi.org/10.1038/nrendo.2018.18
2. Vanderpump, M. P. The epidemiology of thyroid disease. Br. Med. Bull. 99, 39–51 (2011).
…Global prevalence of hypothyroidism
Incidence of Hashimoto’s thyroiditis increases with
aging and affects about 5% of the global population,
usually between ages 30 and 60.1
In iodine-sufficient countries, the prevalence of
hypothyroidism ranges from 1% to 2%, rising to 7%
in individuals aged between 85 and 89 years.2
Hypothyroidism is 8-15 times more prevalent in
women than men.2

8. 1. Unnikrishnan, A. G. et al. Prevalence of hypothyroidism in adults: an epidemiological studyin eight cities of India. Indian J. Endocrinol. Metab. 17, 647–652 (2013).
Regional variations were reported in India, with
higher rates of hypothyroidism in inland than in
coastal regions.1
Among all cities, Kolkata recorded the highest
prevalence of hypothyroidism (21.67%). Cities
located in the inland regions of India (Delhi,
Ahmedabad, Kolkata, Bangalore and Hyderabad)
reported a significantly higher prevalence of
hypothyroidism (11.73%) than those in the coastal
areas (Mumbai, Chennai and Goa) (9.45%; P =
0.01).1

9. Classification of Hypothyroidism
A. Primary
1. Enlarged Thyroid
- Hashimoto’s (65%)
- Iodine Deficiency (25%)
- Drug-induced (Lithium)
- Dysharmonogenesis
- Infiltrative Diseases
2. Normal Thyroid
- Spontaneous Atrophic
- Post thyroidectomy
3. Post Ablative
- Permanent
- Transient
- Sub-clinical
4. Congenital
www.drsarma.in 9
B. Secondary / Central
Pituitary/ hypothalamic

10. Signs and Symptoms of Hypothyroidisms

11. Progression of Thyroid Disease
Ayala AR, et al. Endocrinologist. 1997;7:44-50.
Years
Normal
Range
TSH
Overt
Hypothyroidism
Subclinical
HypothyroidismEuthyroid
T3
T4

12. Subclinical Hypothyroidism-
This is a biochemical diagnosis and describes
the finding of elevated serum TSH with normal
free thyroid hormones.
Symptoms may be present or absent
1. Cooper DS. N Engl J Med. 2001;345:260-265.
2. Vanderpump MP, Tunbridge WM, French JM, et al. The incidence of thyroid disorders in the community:
a twenty-year follow-up of the Whickham Survey. Clin Endocrinol (Oxf) 1995; 43: 55e68.
 Subclinical hypothyroidism is found in 5e10% of the
population, being more common in women and
increasing with age.
 It can progress to overt hypothyroidism, particularly
if patients have elevated concentrations of thyroid
antibodies. The most common etiology is chronic
autoimmune thyroiditis.2

13. Subclinical Hypothyroidism-
An isolated elevated TSH level in the
setting of normal T3 and T4 levels
Symptoms may be present or absent
1. Cooper DS. N Engl J Med. 2001;345:260-265.
Definition1

14. Potential benefits from treatment1
Prevent progression to overt hypothyroidism
Improve serum lipid profile, which may reduce the
cardiovascular disease risks
Reduce symptoms, including psychiatric and
cognitive abnormalities
Better fertility outcome
Improves menses irregularities
1.Cooper DS. N Engl J Med. 2001;345:260-264.
Rationale for Treating Subclinical
Hypothyroidism

15. Hypothyroidism
Work up
Thyroxine
Replacement
Therapy
ATA 2017

16. HYPOTHYROIDISM TREATMENT GOAL:
EUTHYROIDISM
The goal of hypothyroidism therapy is to
replace thyroxine to mimic normal,
physiologic levels and alleviate signs,
symptoms, and biochemical abnormalities.1
Braverman LE, et al. Werner & Ingbar’s The Thyroid. A
Fundamental and Clinical Text. 8th ed. 2018.

17. THERAPY INITIATION AND TITRATION
Endocr Pract. 2019;8:457-469.Singer PA, et al. JAMA. 1995;273:808-812.
Therapy requires individualized patient dosing
Careful titration: use a formulation with consistent
doses
Clinical evaluation: symptoms resolve more slowly
than TSH response
Laboratory monitoring: need consistent, sensitive
TSH measurements (preferably 3rd gen assay)
Individualized patient dosing is influenced by
Age and weight
Cardiovascular health
Severity and duration of hypothyroidism
Concomitant disease states and treatment

18. Hypothyroidism Treatment
Levothyroxine sodium is the treatment
of choice for the routine management of
hypothyroidism
Adults: about 1.7 g/kg of body weight/d
Children up to 4.0 g/kg of body weight/d
Elderly <1.0 g/kg of body weight/d
Singer PA, et al. JAMA. 2019;273:808-812.Endocr Pract. 2002;8:457-469.

19. Hypothyroidism Treatment
Clinical and biochemical evaluations at 6- to
8 week intervals until the serum TSH
concentration is normalized
Given the narrow and precise treatment
range for levothyroxine therapy, it is preferable
to maintain the patient on the same brand
throughout treatment
Singer PA, et al. JAMA. 2019;273:808-812.Endocr Pract. 2002;8:457-469.

20. Primary Hypothyroidism Treatment and Follow-Up
Algorithm1,2
TSH >3.0 IU/mL TSH <0.5 IU/mL
Initial Levothyroxine Dose
Increase
Levothyroxine
Dose by
12.5 to 25 g/d
Repeat TSH Test
6-8 Weeks
TSH 0.5- 2.0 IU/mL
Symptoms Resolved
Measure TSH at 6 Months,
Then Annually or
When Symptomatic
Continue Dose Decrease
Levothyroxine
Dose by
12.5 to 25 g/d
1, Singer PA, et al. JAMA. 1995;273:808-812.
2. Demers LM, Spencer CA, eds. The National Academy of Clinical Biochemistry Web site.
Available at: http://www.nacb.org/lmpg/thyroid_lmpg.stm. Accessed July 1, 2003.

22. Caution in Patients with Underlying
Cardiac Disease
Using LT4 in those with ischemic heart disease
increases the risk of MI, aggravation of angina, or
cardiac arrhythmias
For patients <50 years of age with underlying cardiac
disease, initiate LT4 at 25-50 g/d with gradual dose
increments at 6- to 8-week intervals
For elderly patients with cardiac disease, start LT4 at
12.5-25 g/d, with gradual dose increments at 4- to
6-week intervals
The LT4 dose is generally adjusted in 12.5-25 g
increments
Braverman LE, et al. Werner & Ingbar’s The Thyroid. A Fundamental and Clinical Text. 8th ed. 2000.
Kohno A, et al. Endocr J. 2001;48:565-572.
Synthroid® [package insert]. Abbott Laboratories; 2003.

23. Special conditions

24. Congenital Hypothyroidism
Congenital hypothyroidism (CH) is
defined as thyroid hormone
deficiency present at birth
It can occur because of an anatomic
defect in the gland, an inborn error of
thyroid metabolism, or iodine
deficiency.
Diseases may manifest from birth
or later

25. Epidemiology
Incidence increased to about 1 in 2,000 due to
more stringent screening strategies.
Incidence in Bangladesh 1: 1,300, According to
the research paper of 'Institute of Nuclear
Medicine, Dhaka, Bangladesh'.
Male: Female = 1:2
1: 4000

26. Neonatal Physiology
Surge in
TSH
30 mins
after
delivery
peak at
6 hours
rapid decline
over 24hrs.
T3 and
T4 levels
increase sharply
within 24 hours slow decline
Preterm infant-TSH
surge is less
marked
T4 and T3 responses are blunted.

27. Etiology of Congenital Hypothyroidism
Primary CH
Thyroid
dysgenesis: 85% -
agenesis,
hypoplasia, ectopia
dyshormonogenes
is- 15%
Resistance to TSH
binding
Secondary
(central) CH
 TSH
deficiencies
Congenital
hypopituitarism
(multiple pituitary
hormone
deficiencies)
Peripheral CH
Thyroid
hormone
-transport defect
-metabolism
defect
-Thyroid
hormone
resistance

28. Clinical Manifestations..
95% -asymptomatic at birth
Some infants escape newborn screening, and
laboratory errors occur, so pediatricians must still
be alert for symptoms and signs of
hypothyroidism if they develop.

29. Clinical Manifestations…..
 Early
Prolong gestation
LGA
Large poterior fontanelle
Hypotonia.
Feeding / respiratory difficulty
Delayed passage of meconeum
Constipation
Umbilical hernia
Prolonged neonatal jaundice
Hypotharmia
• Late
Coarse/puffy face
Coarse hair
Large Tongue
Myxedema, Hoarse cry
Hearing Impairment
Speech delay

30. Newborn Screening
Screening Technique
 Specimen is blood spot in filter paper
 Obtained by heel prick
 and Cord blood

31. Newborn at High Risk..
Preterm and low birth weight infants
Infants with trisomy 21 or cardiac defects have an
increased risk of congenital hypothyroidism.
Monozygotic twins , if they are monochorionic,
fetal hypothyroidism in the affected twin may get
compensated by the normal twin through their
shared fetal circulation.

32.  A cord blood TSH value of >20 mIU/L can be used for
the purpose of screening for congenital hypothyroidism.
 For logistic angles, a higher cutoff of >30 mIU/L can be
used.

33. Thyroid Ultrasonography- helpful to
separate a structural defect from normal or
enlarged gland. But may miss some ectopic
glands.
Thyroid Scan (Scintigraphy)- most
accurate diagnostic modality to detect
dysplastic or ectopic thyroid tissue Iodide 123
or sodium pertechnetate (tc99m) is preferred.
Diagnostic studies to determine
underlying etiology

34. Serum thyroglobulin
Anti thyroid antibody (TBG-AB)- In case of maternal
autoimmune disease
CBC with PBF- anemia (normo, micro and macro)
CXR- Cardiomegaly
ECG- bradycardia and low voltage ECG
CT Scan and MRI
Other relevant Investigation

35. TSH > 20 MIU/L
High TSH
Low T4
Transient Hypothyroidism or
permanent Hypothyroidism
Start treatment soon,
Further investigation to identify the cause
High TSH
Normal T4
FT4, TSH again
TSH > 20mIU/L
TSH 6 -20 mIU/L:
Repeat FT4, TSH weekly until normal,
≥10 mIU/L Persistently consider Rx
When to Start Treatment?
New born screening

36. Treatment
The aim of therapy is to ensure normal growth
and development by maintaining :
- serum TSH in the reference (optimally 0.5–2.0
mU/L) and
- FT4 in the upper half of the reference range for
age.
 Treatment preferably within the 2nd wk of
life is essential to prevent irreversible brain
damage

37.  Levothyroxine
 The recommended dose of L -T4 is 10-15
μg/kg/day given orally
 Rapid normalization of thyroid function (ideally
within 2 wk) is important in achieving optimal neuro-
developmental outcome.
LT4 must be ingested in the empty stomach, avoid
soya, calcium and iron containing diet
Treatment..

38. FOLLOW-UP
Clinical Follow-up
Clinical assessment of growth and development,
should be performed every few months during
the first 3 years of life.

39. Lab Follow-up
Serum T4 and TSH measurements should be performed
1. 2 and 4 weeks after the initiation of LT4 treatment
2. 4 weeks after any change in LT4 dosage.
3. every 1 to 2 months during the first 6 months of life
4. every 3 to 4 months between 6 months and 3 years
5. every 6 to 12 months until growth is completed; and
6. at more frequent intervals when compliance is questioned, or
abnormal values are obtained.

40. Myxedema denotes uncompensated form of severe
hypothyroidism.
Myxedema coma is a severe and life-threatening form
of decompensated hypothyroidism with an underlying
precipitating factor(s).
The mortality rates may be as high as 25–60% even
with best possible treatment.
Myxedema and
Myxedema Coma
1. Wartofsky, “Myxoedema coma,” Endocrinology Metabolism Clinics of North America, vol. 35, pp. 687–698, 2006.
2.. Rodr´ıguez, E. Fluiters, L. F. Pe´rez-Me´ndez, R. Luna, C. Pa´ramo, and R. V. Garc´ıa-Mayor, “Factors associated with mortality of patients with myxoedema coma: prospective study in 11 cases treated in a single
institution,” Journal of En- docrinology, vol. 180, no. 2, pp. 347–350, 2004.
3. Yamamoto, J. Fukuyama, and A. Fujiyoshi, “Factors associ- ated with mortality of myxedema coma: report of eight cases and literature survey,” Thyroid, vol. 9, no. 12, pp. 1167–1174, 1999.

41. Low intracellular T3 leads to cardiogenic shock, respiratory
depression, hypothermia and coma.
Hypothermia
Infections and septicemia
CVDs
Congestive heart failure
Gastrointestinal bleeding
Trauma and fractures
Drugs—anesthetics, sedatives, tranquilizers, narcotics,
amiodarone, and lithium Withdrawal of thyroid supplements
Precipitating factors of myxedema crisis
Precipitation of Myxedema Coma
Literature reveals that most cases present in winter, and
hypothermia is a common manifestation. Low ambient temperature
may alter thermoregulatory mechanisms and hence will lower the
threshold for encephalopathy.

42. Clinical and laboratory features of myxedema crisis

43. Treatment should be prompt, vigorous and multidimensional
with attention to:
a) intensive care treatment with ventilator support, central
venous pressure monitoring, and pulmonary capillary
wedge pressure if feasible in patients with cardiac disease,
b)Wrap up the pt in a ‘space blanket’ which retains the heat
in a warm room
c) Maintain adequate airway to prevent hypoxemia.
Prevention of hypoxemia is the single important step to
prevent catastrophe.
d) Monitor ABG regularly
Treatment of Myxedema Crisis

44. e) appropriate fluid management and correction of hypotension
and dyselectrolytemia
f) aggressive management of precipitating factors and steroid
supplementation if required
g) Cardiac monitoring
h) Combat hyponatremia:
i) In mild (Na+- 120-140 mEq/L)- fluid restriction
ii) In severe (Na+- 105-10 mEq/L)- 3% NaCl and 40-120mg
frusemide
….Treatment of MyxedemaCrisis

45. i) Combat hypotension:
i) IV NS or 5% to 10% DA
ii) IV or IM 50 to 100mg hydrocortisone 6/8 hourly
iii) Judicious use of dopamine
j) Thyroid hormone therapy:
50-100 µ LT4 by NG tube
+
5µ T3- twice daily
• If IV LT4 is available: 200–300 µ LT4 (4 µ/KBW) + 25µ
T3+ hydrocortisone 5 mg/h

46. This may be followed by IV 100µ LT4 after 24 h +
25µ T3 after 12 h.
This is continued till pt is unconscious. Then LT4
is to be given PO and dose should be determined
by measuring S FT4 and TSH
k) If CCF is present, should be treated as per
standard protocol.

47.  Thyroid hormones are essential for
growth, neuronal development, reproduction
and regulation of energy metabolism.
Hypothyroidism is common, readily
identifiable and easily treatable, but if
undiagnosed or untreated, it can have
profound adverse effects
Carry Home Messages

48.  Iodine nutrition is a key determinant of
thyroid disease risk; however, we are
transforming to ATD era gradually.
 Other factors, such as ageing, smoking
status, genetic susceptibility, ethnicity,
endocrine disruptors and the advent of novel
therapeutics, including immune checkpoint
inhibitors, also influence thyroid disease
epidemiology.
…Carry Home Messages

49.  CH is not uncommon and is a treatable
condition.
 Myxedema is potentially preventable
condition but if occurs, mortality is very high,
even in most advanced centres.
…Carry Home Messages