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THYROID COMPLICATING
PREGNANCY
THYROID GLAND
MATERNAL THYROID PHYSIOLOGY
During pregnancy, maternal thyroid function is
modulated by three factors
• An increase in HCG concentrations that stimulate
the thyroid glands,
• Significant increases in urinary iodide excretion,
resulting in a fall in plasma iodine concentrations,
• An increase in thyroxine-binding globulin (TBG)
during the first trimester, resulting in increased
binding of thyroxine
THYROID IN PREGNANCY
• Thyroid hormone concentrations in blood are
increased in pregnancy, partly due to the high
levels of oestrogen and due to the weak
thyroid stimulating effects of human chorionic
gonadotropin(hCG) that acts like TSH.
• Thyroxine (T4) levels rise from about 6–12
weeks, and peak by mid-gestation; reverse
changes are seen with TSH
AUTOIMMUNE THYROID DISEASE
 There are mainly two types of thyroid antibodies: Those that are
directed towards cytoplasmic antigen(thyroid peroxidise(TPOAb) and
thyroglobulin (TgAb) antibodies) and those directed to the TSH
receptor(TSHRAb).
 The thyroid autoimmunity,with normal thyroid function ,has been
associated with increased miscarriage rate which may be due to:
 Subtle maternal thyroid dysfunction
 An underlying autoimmune imbalance reflected by the presence of
thyroid antibodies which result in rejection of the fetus.
 Thyroid antibodies which crosses the placenta and directly affecting
the developing fetal thyroid gland ,increase early loss
 Increased maternal age of women with thyroid autoimmunity
 Definition: It is defined by excessive thyroid
hormone production due to an overactive gland.
 Incidence: Hyperthyroidism occurs in about 2
per 1000 pregnancies
 Types: Based on biochemical test
 Subclinical:- suppressed TSH ,normal T4 and T3
 Overt:- suppressed TSH and elevated T4 and /or
T3
Causes :
• Intrinsic thyroid disease :
• Autoimmune
hyperthyroidism(Grave’s
disease) due to thyroid
stimulating antibody
• Nodular thyroid disease –
single or multiple –nodule >3
cm
• Sub – acute thyroiditis –
generalised thyroid tenderness
• Excessive ,exogenous thyroid
hormone
• Factitious
• Therapeutic
• Gestational thyrotoxicosis:
• Hyperemesis gravidarum
• Placenta mediated
• Hydatidiform mole
• Multiple gestation
• hydrops
• Trophoblastic diseases
 Restlessness
 Fatigue
 Weakness
 Weight loss
 Diarrhoea
 Heat intolerance
 Nervousness
 Tachycardia/palpitations
 Increased frequency of bowel habits
 Skin/hair/nail changes
 Skin is soft and moist
 Onycholysis (separation of distal nail from its
bed)
 Hair becomes soft,fine and may thin
 Eye signs
 Lid lag
 Lid retraction and stare
Specific to grave’s disease:
 Grave’s orbitopathy
 Chemosis
 Proptosis
 Dysconjugate gaze
 Pretibial myxedema
 Thyroid bruit
 Clubbing
On examination, patient may exhibit
 Tachycardia
 Tremor
 Goitre
 Muscle weakness
 Lid retraction or lag
 TSH decreased and T4 elevates
 Patients with grave’s disease may have antibodies
to thyroid peroxidise or TSH receptor.
 Clinical diagnosis of hyperthyroidism is
always be confirmed by measuring free T4
and T4 levels along with TSH
 Suggestive complaints include nervousness,
heat intolerance, palpitations, thyromegaly or
goitre, failure to gain weight or loss weight,
exophthalmos.
 Women with gestational thyrotoxicosis are
rarely symptomatic,have minimal thyroid
enlargement and are TSHRAb negative
 Antithyroglobulin antimicrosomal antibodies
and thyroid stimulating immunoglobulin
should be measured
 Radioactive iodine uptake and scans should
not be done during pregnancy as it cross the
placenta and damage the fetal thyroid gland
permanently
 The goal of management of thyrotoxicosis is
primarily to normalize ,but not to suppress
thyroid hormone levels and to secondarily
treat bothersome adrenergic symptoms of
hyperthyroidism
 Treatment of hyperthyroidism in pregnancy
focuses on stopping release of T4 and
inhibiting conversion of T4 to T3
 Treatment options for nonpregnant women
include treatment for 12 – 24 months with
antithyroid drugs, radioactive iodine to
partially ablate the thyroid gland and near
total thyroidectomy.
 Use of antithyroid drugs (carbimazole,
methimazole, propylthiouracil)
 Thyroid function should be assessed every 4-
6 weeks.
 Subtotal thyroidectomy is an option for
patients who are noncompliant or refractory
to medications.Surgery is best undertaken in
the second trimester.Radioiodine treatment is
contraindicated in pregnancy.
 Thyrotoxicosis or thyroid storm is treated
with large dose of PTU,600mg loading dose
,followed by 200 – 300mg every 6 hrs should
be administered
 Pregnancy outcomes
 Thio – amide drugs
 Radio – ablative therapy
ANTENATAL MANAGEMENT:
 The goal of the treatment during pregnancy is to maintain free T4
in the upper normal range with lowest dose of thio amides.
 Treatment with beta blockers for the symptomatic relief of severe
adrenergic symptoms until freeT4 levels are normalised
 Women on thio –amide prior to pregnancy or newly diagnosed
toxic nodules or Grave’s disease should be continued or started
on thio amide during pregnancy.
 The usual starting dose of PTU is 50 – 100 mg 3 times a day and
methiomezole 5 – 20 mg twice daily.
 Thyroid studies should be repeated every 4 weeks and the
dosage should be based on T4 level and not on TSH level .
Dosage should be reduced when the T4 level reaches the normal.
FETAL MONITORING:
 Foetuses of women taking antithyroid drug during the
third trimester or those with a persistent TSHRAb
have an increased risk for developing goiter.
 Because of the placental transfer of thyroid
stimulating immunoglobulins fetal grave’s disease
may develop that results in nonimmune hydrops or
fetal demise.
 Documentation of fetal heart rate at each visit and
USG every 2- 4 weeks in the third trimester
 If any fetal abnormlity present routine fetal blood
sampling for thyroid indices are recommended
Labor and delivery:
 Treatment of symptomatic women with
hyperthyroidism in labor include antithyroid
medication , beta – blockers if necessary and
supportive care.
 If thyrotoxicosis is suspected in labor
appropriate management include –elective
caesarean delivery may be suitable to avoid
dystocia from an extremely large fetal goitre
and for the management of fetal airway.
 The ex utero intrapartum treatment(EXIT)
was developed to to manage airway
obstruction with large neck masses.
 There may be relapse of Grave’s disease
usually within the first 3 months after
delivery
 Antithyroid therapy needs to be
reintroduced.
 Perform TSH and free T4 approximately 6
weeks post partum.
 Methimazole cause thyroid dysfunction in
breast feeding infants .In low dose (10 – 20
mg/day) does not pose a major risk to
nursing infants.
 Miscarriage
 Pre-term delivery
 Pre-eclampsia
 CCF
 Placental abruption
 Thyroid storm
 Infection
 IUGR
 Prematurity
 Stillbirth
 Hyperthyroidism
 Hypothyroidism
 Increased perinatal mortality and morbidity
HYPOTHYROIDISM
• Definition: It is defined as inadequate thyroid
production despite pituitary gland
stimulation(primary) or insufficient stimulation
of the thyroid by the pituitary or hypothalamus.
(central hypothyroidism)
• Incidence: 1-3 per 1000 pregnancy
• Types:
• Subclinical:- elevated TSH and normal free T4
• Overt:- elevated TSH and low free T4
HYPOTHYROIDISM
Causes:
• Autoimmune distruction of thyroid
gland(hashimoto’s thyroiditis) –most common
• Iodine deficiency – leading cause
• Radio ablation of the thyroid for Grave’s disease
or thyroid nodule
• Thyroidectomy – partial or near complete for
treatment of benign or malignant
neoplasm,Grave’disease)
• Medications – Lithium,amioderone
HYPOTHYROIDISM
Signs and symptoms:
• vague ,nonspecific signs and symptoms that are
insidious in onset
• fatigue
• constipation
• cold intolerance
• weight gain
• carpel tunnel syndrome
• hair loss
• voice changes
• reduced memory
• muscle cramps
• dry skin
 Diagnosis during pregnancy is very
difficult
 serum TSH is more sensitive than free T4 for
detecting hypothyroidism.If TSH is
abnormal , then elevation of free T4 is
recommended.
 The range for serum TSH concentration in
nonpregnant individual is 0.45 – 4.5 mU/L
 Strong family history
 Known autoimmune disease
 Presence of goitre
 Previous therapeutic neck irradiation
 Those taking medication known to cause
thyroid disturbance
 TSH testing for hypothyroidism should
ideally be done prior to pregnancy
Management:
Discussion of
 the importance of euthyroidism at the time of
conception
 Risk of hypothyroidism to mother and off
spring
 Anticipation of medication changes during
pregnancy
Management:
Preconceptional councelling:
 The goal of treatment is bringing a euthyroid state
at the time of conception
 TSH should be considered as an indication of
adequate replacement and women should delay
pregnancy until TSH is normal
 Do not take levothyroxine and multivitamins at the
same time since iron and calcium may interfere
with absorption of thyroxine
 All women should have adequate iodine intake
(200microgram/day)
Antenatal management:
 By 16 week of gestation women need an
increase in thyroid hormone by 47 %.
 This begins as early as 5th week of gestation
and those with previous history of
thyroidectomy
 Patients can be told to take a double dose of
their levothyroxine on two days out of seven
 A low normal TSH is the goal during
pregnancy (<2.5mU/ml)
Antenatal management:
 Newly diagnosed women during pregnancy
should be initiated on 1.0 – 2.0 microgram/kg
/day or 100 microgram of levothyroxine daily
 Thyroid stimulating hormone should be
measured in 6 weeks and levothyroxine dose
adjusted in 25 or 50 microgram
 When normalized TSh should be checked
every 6 -8 weeks through out pregnancy
Labor and delivery:
 Known hypothyroid women should be
euthyroid before delivery
 Obstetric complications include increased risk
of still birth , pre term delivery , pre –
eclampsia,and placental abruption,increased
risk of breech and low birth weight
Post partum care:
 After delivery levothyroxine therapy should be
returned to the prepregnant dose and the TSH
should be checked in 6 – 8 weeks
 Breastfeeding is not contraindicated in women
treated for hypothyroidism. Levothyroxine is
excreated into breast milk but levels are too
low to alter thyroid function in infants
 Annual monitoring of serum TSH is
recommended as changing weight and age
may modify thyroid function.
POST PARTUM THYROIDITIS
 Post partum thyroiditis is caused by a rebound in
thyroid autoimmunity after delivery leading to
lymphatic infiltration of the thyroid gland and
transient changes in the thyroid function.
POST PARTUM THYROIDITIS-
Clinical phases:
 Phase 1:- The autoimmune destruction of the gland
first results in release of stored thyroid hormone into
the circulation. This hyperthyroid phase generally
occurs between 1 and 4 months after delivery and is
self limiting to 1 – 2 months. The onset is abrupt ,with
symptoms of fatigue and palpitation . A small painless
goitre may develop. If these symptoms become severe ,
it require treatment with Beta – blockers until
resolution of hyperthyroid phase. Antithyroid
medications are not beneficial.
POST PARTUM THYROIDITIS-
Clinical phases:
 Phase 2:
The loss of functioning thyrocytes from the immune destruction
results in hypothyroid phase between 3 and 8 months
postpartum. The hypothyroid phase usually last longer than
hyperthyroid phase ( 4 – 6 months). This disorder is often
unrecognised because women usually present with nonspecific
symptoms including fatigue , weight gain , loss of concentration
and depression. The hypothyroid phase should be treated in
women who are symptomatic and in those planning a pregnancy
near in future. It is usually recommended to treat women for
approximately for 6 months and withdraw thyroid hormone ,
unless pregnancy is being attempted. A TSH should be
rechecked in 5 – 6 weeks after withdrawal of thyroid hormone.
Nursing care:
 Education of the pregnant women is necessary
to plan treatment.
 Discuss with the women and her family members
about the outcome.
 Assist the client to cope with the discomfort and
frustrations due to symptoms.
 Nutritional councelling with a registered dietician
will help in selecting a well balanced diet.

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Thyroid complicating pregnancy

  • 3. MATERNAL THYROID PHYSIOLOGY During pregnancy, maternal thyroid function is modulated by three factors • An increase in HCG concentrations that stimulate the thyroid glands, • Significant increases in urinary iodide excretion, resulting in a fall in plasma iodine concentrations, • An increase in thyroxine-binding globulin (TBG) during the first trimester, resulting in increased binding of thyroxine
  • 4. THYROID IN PREGNANCY • Thyroid hormone concentrations in blood are increased in pregnancy, partly due to the high levels of oestrogen and due to the weak thyroid stimulating effects of human chorionic gonadotropin(hCG) that acts like TSH. • Thyroxine (T4) levels rise from about 6–12 weeks, and peak by mid-gestation; reverse changes are seen with TSH
  • 5.
  • 6. AUTOIMMUNE THYROID DISEASE  There are mainly two types of thyroid antibodies: Those that are directed towards cytoplasmic antigen(thyroid peroxidise(TPOAb) and thyroglobulin (TgAb) antibodies) and those directed to the TSH receptor(TSHRAb).  The thyroid autoimmunity,with normal thyroid function ,has been associated with increased miscarriage rate which may be due to:  Subtle maternal thyroid dysfunction  An underlying autoimmune imbalance reflected by the presence of thyroid antibodies which result in rejection of the fetus.  Thyroid antibodies which crosses the placenta and directly affecting the developing fetal thyroid gland ,increase early loss  Increased maternal age of women with thyroid autoimmunity
  • 7.  Definition: It is defined by excessive thyroid hormone production due to an overactive gland.  Incidence: Hyperthyroidism occurs in about 2 per 1000 pregnancies  Types: Based on biochemical test  Subclinical:- suppressed TSH ,normal T4 and T3  Overt:- suppressed TSH and elevated T4 and /or T3
  • 8. Causes : • Intrinsic thyroid disease : • Autoimmune hyperthyroidism(Grave’s disease) due to thyroid stimulating antibody • Nodular thyroid disease – single or multiple –nodule >3 cm • Sub – acute thyroiditis – generalised thyroid tenderness • Excessive ,exogenous thyroid hormone • Factitious • Therapeutic • Gestational thyrotoxicosis: • Hyperemesis gravidarum • Placenta mediated • Hydatidiform mole • Multiple gestation • hydrops • Trophoblastic diseases
  • 9.  Restlessness  Fatigue  Weakness  Weight loss  Diarrhoea  Heat intolerance  Nervousness  Tachycardia/palpitations  Increased frequency of bowel habits  Skin/hair/nail changes  Skin is soft and moist
  • 10.  Onycholysis (separation of distal nail from its bed)  Hair becomes soft,fine and may thin  Eye signs  Lid lag  Lid retraction and stare
  • 11. Specific to grave’s disease:  Grave’s orbitopathy  Chemosis  Proptosis  Dysconjugate gaze  Pretibial myxedema  Thyroid bruit  Clubbing
  • 12. On examination, patient may exhibit  Tachycardia  Tremor  Goitre  Muscle weakness  Lid retraction or lag  TSH decreased and T4 elevates  Patients with grave’s disease may have antibodies to thyroid peroxidise or TSH receptor.
  • 13.  Clinical diagnosis of hyperthyroidism is always be confirmed by measuring free T4 and T4 levels along with TSH  Suggestive complaints include nervousness, heat intolerance, palpitations, thyromegaly or goitre, failure to gain weight or loss weight, exophthalmos.  Women with gestational thyrotoxicosis are rarely symptomatic,have minimal thyroid enlargement and are TSHRAb negative
  • 14.  Antithyroglobulin antimicrosomal antibodies and thyroid stimulating immunoglobulin should be measured  Radioactive iodine uptake and scans should not be done during pregnancy as it cross the placenta and damage the fetal thyroid gland permanently
  • 15.  The goal of management of thyrotoxicosis is primarily to normalize ,but not to suppress thyroid hormone levels and to secondarily treat bothersome adrenergic symptoms of hyperthyroidism  Treatment of hyperthyroidism in pregnancy focuses on stopping release of T4 and inhibiting conversion of T4 to T3
  • 16.  Treatment options for nonpregnant women include treatment for 12 – 24 months with antithyroid drugs, radioactive iodine to partially ablate the thyroid gland and near total thyroidectomy.  Use of antithyroid drugs (carbimazole, methimazole, propylthiouracil)
  • 17.  Thyroid function should be assessed every 4- 6 weeks.  Subtotal thyroidectomy is an option for patients who are noncompliant or refractory to medications.Surgery is best undertaken in the second trimester.Radioiodine treatment is contraindicated in pregnancy.  Thyrotoxicosis or thyroid storm is treated with large dose of PTU,600mg loading dose ,followed by 200 – 300mg every 6 hrs should be administered
  • 18.  Pregnancy outcomes  Thio – amide drugs  Radio – ablative therapy
  • 19. ANTENATAL MANAGEMENT:  The goal of the treatment during pregnancy is to maintain free T4 in the upper normal range with lowest dose of thio amides.  Treatment with beta blockers for the symptomatic relief of severe adrenergic symptoms until freeT4 levels are normalised  Women on thio –amide prior to pregnancy or newly diagnosed toxic nodules or Grave’s disease should be continued or started on thio amide during pregnancy.  The usual starting dose of PTU is 50 – 100 mg 3 times a day and methiomezole 5 – 20 mg twice daily.  Thyroid studies should be repeated every 4 weeks and the dosage should be based on T4 level and not on TSH level . Dosage should be reduced when the T4 level reaches the normal.
  • 20. FETAL MONITORING:  Foetuses of women taking antithyroid drug during the third trimester or those with a persistent TSHRAb have an increased risk for developing goiter.  Because of the placental transfer of thyroid stimulating immunoglobulins fetal grave’s disease may develop that results in nonimmune hydrops or fetal demise.  Documentation of fetal heart rate at each visit and USG every 2- 4 weeks in the third trimester  If any fetal abnormlity present routine fetal blood sampling for thyroid indices are recommended
  • 21. Labor and delivery:  Treatment of symptomatic women with hyperthyroidism in labor include antithyroid medication , beta – blockers if necessary and supportive care.  If thyrotoxicosis is suspected in labor appropriate management include –elective caesarean delivery may be suitable to avoid dystocia from an extremely large fetal goitre and for the management of fetal airway.  The ex utero intrapartum treatment(EXIT) was developed to to manage airway obstruction with large neck masses.
  • 22.  There may be relapse of Grave’s disease usually within the first 3 months after delivery  Antithyroid therapy needs to be reintroduced.  Perform TSH and free T4 approximately 6 weeks post partum.  Methimazole cause thyroid dysfunction in breast feeding infants .In low dose (10 – 20 mg/day) does not pose a major risk to nursing infants.
  • 23.  Miscarriage  Pre-term delivery  Pre-eclampsia  CCF  Placental abruption  Thyroid storm  Infection
  • 24.  IUGR  Prematurity  Stillbirth  Hyperthyroidism  Hypothyroidism  Increased perinatal mortality and morbidity
  • 25. HYPOTHYROIDISM • Definition: It is defined as inadequate thyroid production despite pituitary gland stimulation(primary) or insufficient stimulation of the thyroid by the pituitary or hypothalamus. (central hypothyroidism) • Incidence: 1-3 per 1000 pregnancy • Types: • Subclinical:- elevated TSH and normal free T4 • Overt:- elevated TSH and low free T4
  • 26. HYPOTHYROIDISM Causes: • Autoimmune distruction of thyroid gland(hashimoto’s thyroiditis) –most common • Iodine deficiency – leading cause • Radio ablation of the thyroid for Grave’s disease or thyroid nodule • Thyroidectomy – partial or near complete for treatment of benign or malignant neoplasm,Grave’disease) • Medications – Lithium,amioderone
  • 27. HYPOTHYROIDISM Signs and symptoms: • vague ,nonspecific signs and symptoms that are insidious in onset • fatigue • constipation • cold intolerance • weight gain • carpel tunnel syndrome • hair loss • voice changes • reduced memory • muscle cramps • dry skin
  • 28.  Diagnosis during pregnancy is very difficult  serum TSH is more sensitive than free T4 for detecting hypothyroidism.If TSH is abnormal , then elevation of free T4 is recommended.  The range for serum TSH concentration in nonpregnant individual is 0.45 – 4.5 mU/L
  • 29.  Strong family history  Known autoimmune disease  Presence of goitre  Previous therapeutic neck irradiation  Those taking medication known to cause thyroid disturbance  TSH testing for hypothyroidism should ideally be done prior to pregnancy
  • 30. Management: Discussion of  the importance of euthyroidism at the time of conception  Risk of hypothyroidism to mother and off spring  Anticipation of medication changes during pregnancy
  • 31. Management: Preconceptional councelling:  The goal of treatment is bringing a euthyroid state at the time of conception  TSH should be considered as an indication of adequate replacement and women should delay pregnancy until TSH is normal  Do not take levothyroxine and multivitamins at the same time since iron and calcium may interfere with absorption of thyroxine  All women should have adequate iodine intake (200microgram/day)
  • 32. Antenatal management:  By 16 week of gestation women need an increase in thyroid hormone by 47 %.  This begins as early as 5th week of gestation and those with previous history of thyroidectomy  Patients can be told to take a double dose of their levothyroxine on two days out of seven  A low normal TSH is the goal during pregnancy (<2.5mU/ml)
  • 33. Antenatal management:  Newly diagnosed women during pregnancy should be initiated on 1.0 – 2.0 microgram/kg /day or 100 microgram of levothyroxine daily  Thyroid stimulating hormone should be measured in 6 weeks and levothyroxine dose adjusted in 25 or 50 microgram  When normalized TSh should be checked every 6 -8 weeks through out pregnancy
  • 34. Labor and delivery:  Known hypothyroid women should be euthyroid before delivery  Obstetric complications include increased risk of still birth , pre term delivery , pre – eclampsia,and placental abruption,increased risk of breech and low birth weight
  • 35. Post partum care:  After delivery levothyroxine therapy should be returned to the prepregnant dose and the TSH should be checked in 6 – 8 weeks  Breastfeeding is not contraindicated in women treated for hypothyroidism. Levothyroxine is excreated into breast milk but levels are too low to alter thyroid function in infants  Annual monitoring of serum TSH is recommended as changing weight and age may modify thyroid function.
  • 36. POST PARTUM THYROIDITIS  Post partum thyroiditis is caused by a rebound in thyroid autoimmunity after delivery leading to lymphatic infiltration of the thyroid gland and transient changes in the thyroid function.
  • 37. POST PARTUM THYROIDITIS- Clinical phases:  Phase 1:- The autoimmune destruction of the gland first results in release of stored thyroid hormone into the circulation. This hyperthyroid phase generally occurs between 1 and 4 months after delivery and is self limiting to 1 – 2 months. The onset is abrupt ,with symptoms of fatigue and palpitation . A small painless goitre may develop. If these symptoms become severe , it require treatment with Beta – blockers until resolution of hyperthyroid phase. Antithyroid medications are not beneficial.
  • 38. POST PARTUM THYROIDITIS- Clinical phases:  Phase 2: The loss of functioning thyrocytes from the immune destruction results in hypothyroid phase between 3 and 8 months postpartum. The hypothyroid phase usually last longer than hyperthyroid phase ( 4 – 6 months). This disorder is often unrecognised because women usually present with nonspecific symptoms including fatigue , weight gain , loss of concentration and depression. The hypothyroid phase should be treated in women who are symptomatic and in those planning a pregnancy near in future. It is usually recommended to treat women for approximately for 6 months and withdraw thyroid hormone , unless pregnancy is being attempted. A TSH should be rechecked in 5 – 6 weeks after withdrawal of thyroid hormone.
  • 39. Nursing care:  Education of the pregnant women is necessary to plan treatment.  Discuss with the women and her family members about the outcome.  Assist the client to cope with the discomfort and frustrations due to symptoms.  Nutritional councelling with a registered dietician will help in selecting a well balanced diet.