JC38 (Medicine) - Thyrotoxicosis and Hypothyroidism Flashcards
Describe the physiological process of thyroid hormone synthesis
(1) Thyroglobulin biosynthesis
• Thyroglobulin is synthesized in ribosomes of follicle cells
• Stimulated by thyroid-stimulating hormone (TSH) and cAMP
• Thyroglobulin in follicular cells is incorporated into exocytotic vesicles and extruded into colloid in lumen of follicle
(2) Thyroid hormone biosynthesis
• Iodide trapping: Dietary iodide is taken up actively by Na-I symporter
• Oxidation: Iodide is oxidize to iodine by thyroidal peroxidase
• Iodination / Organification: Tyrosine residue in thyroglobulin is iodinated and form monoiodotyrosine (MIT) and diiodotyrosine (DIT)
• Coupling: MIT and DIT are coupled together to form T3 and T4
(3) Secretion of thyroid hormones
• Stimulation of thyroid gland leads to endocytosis of colloid
• Endocytic vesicles fuse with lysosomes inside the follicular cells
• T3 and T4 are cleaved from the thyroglobulin and released into circulation
Forms of thyroid hormone transport in blood
o Thyroxine-binding globulin (TBG) (70%)
o Pre-albumin (15%)
o Albumin (15%)
o Free in circulation (< 1%)
Describe activation and deactivation of thyroid hormone
Deiodination reactions in the peripheral tissues activate and inactivate TH
• Deiodinase Type 1 / 2 /3 to catalyse the reaction
• Deiodination of T4 into T3 (active) or reverse T3 (inactive)
Effect of thyroid hormone on target cells
Thyroid hormones receptors (TRs)
• Located in the nuclei of target cells
• Bound to thyroid hormone response elements in DNA
Mechanism of action
• Cells receive free thyroid hormones (TH) from blood
• T4 is deiodinated to T3 once inside cell
• T3 then enters nucleus and binds to thyroid hormone receptors (TRs)
• T3 triggers the dissociation of co-repressor from TRs and binding of co-activator
• TRs and T3 forms a complex with nuclear receptor- retinoid X receptor (RxR) to initiate gene transcription
• Results in mRNA and protein production
Compare T3 and T4
- Mode of transport in blood
- Pool size
- Source
- Location
- Activity
- Onset of action
- Half-life
Compare T3 and T4
- Mode of transport in blood
- Pool size
- Source
- Location
- Activity
- Onset of action
- Half-life
Effect of thyroid hormone on target end-organs
- Increase Basal metabolic rate: Increase O2 consumption and ATP production
- Growth: permissive effect on growth hormone, protein synthesis, bone remodeling, coordinate PTH and Calcitonin
- Biphasic control of carbohydrate and lipid synthesis/ breakdown: Increase glucose and lipid metabolism, remove LDL and cholesterol
- CVS: increase contractility, permissive effect on catecholamines, vasodilation
- CNS: development and behavior
- Temperature: heat production
Differentiate hyperthyroidism and thyrotoxicosis
Thyrotoxicosis is defined as the state of thyroid hormone excess
Hyperthyroidism is the result of excess thyroid function
Causes of primary hyperthyroidism
Grave’s diseases
Toxic multinodular goitre
Toxic adenoma
Metastatic thyroid cancer
Mutation of TSH receptor
Mutation of Gsa (McCune-Albright syndrome)
Causes of secondary hyperthyroidism
TSH-secreting pituitary adenoma
Chorionic gonadotropin-secreting tumour
Gestational thyrotoxicosis
Causes of thyrotoxicosis without hyperthyroidism
(Very similar to transient hypothyroidism)
Subacute (De Quervain’s) thyroiditis
Silent thyroiditis
Destructive thyroiditis
• Amiodarone/ Irradiation
• Release of TH into blood
Levothyroxine (T4) overdose
Causes of primary hypothyroidism
Iodine deficiency
Autoimmune hypothyroidism
• Hashimoto’s thyroiditis
• Atrophic thyroiditis
Congenital hypothyroidism
• Congenital absence or ectopic thyroid gland
• Thyroid gland dysgenesis (80 – 85%)
• Dyshormonogenesis (10 – 15%)
• TSH-R antibody-mediated (5%)
Infiltrative hypothyroidism
• Sarcoidosis
• Amyloidosis
• Scleroderma
• Riedel’s thyroiditis
Drug-induced hypothyroidism
• Amiodarone
• Lithium
Iatrogenic hypothyroidism
• 131I treatment
• Subtotal or total thyroidectomy
• External irradiation of neck
Causes of secondary hypothyroidism
Hypothalamic disease
• Hypothalamic tumours
• Trauma/ Infiltrative disorders
Hypopituitarism
• Pituitary tumour
• Pituitary surgery or irradiation
• Sheehan’s syndrome
• Trauma/ Infiltrative disorders
Causes of transient hypothyroidism
Subacute (De Quervain’s) thyroiditis
Silent thyroiditis (including post-partum thyroiditis)
Withdrawal of supraphysiologic T4 treatment
Post-131I treatment
Post-subtotal or total thyroidectomy
Tests for thyroid function
Which marker screens for thyroid dysfunction?
- Serum free thyroid hormone fT3, fT4: unbound thyroid hormone
- Serum TSH
- Serum total T4: T4 bound to plasma-binding proteins
Serum TSH screens for thyroid dysfunction
MOST sensitive indicator of thyroid function due to short t1/2
Symptoms of hyperthyroidism
Hyperactivity/ Irritability/ Dysphoria
Heat intolerance and increased sweating
Palpitations
Fatigue and weakness
Weight loss with increased appetite
Hair loss
Diarrhea
Polyuria
Oligomenorrhea and amenorrhea
Loss of libido
Signs of hyperthyroidism
Tachycardia and AF
Tremor
Goitre
Warm and moist skin
Muscle weakness and proximal myopathy
Lid lag and lid retraction
• Permissive effect on catecholamine leading to sympathetic overactivity
• Sustained contraction of superior tarsal muscles
Thyroid eye signs
Pretibial Myxoedema
Gynecomastia
List all thyroid eye signs
Periorbital edema
Lid lag and lid retraction
Exophthalmos (proptosis)
Ophthalmoplegia (extra-ocular muscle involvement)
Corneal involvement (exposure keratitis)
Vision loss
Symptoms of hypothyroidism
General:
Fatigue and weakness
Cold intolerance
Weight gain with decreased appetite
Hair loss, Dry skin
Neuro:
Difficulty concentrating and poor memory
Impaired hearing
Paraesthesia
GI:
Constipation
Respi:
Dyspnea
Hoarseness
Gyn:
Menorrhagia (later oligomenorrhea or amenorrhea)
Signs of hypothyroidism
Skin:
Dry and cold skin
Alopecia
Puffiness of face, hands and feet/ Myxedema
Cardiovascular:
Bradycardia
Peripheral non-pitting edema
Neuro:
Hyporeflexia
Delayed tendon reflex relaxation
Carpal tunnel syndrome
Grading of Grave’s ophthalmopathy
Pathophysiology of periorbital edema and proptosis
T-cells and autoantibodies are reactive to extraocular muscles and retro-orbital tissues
Inflammation leads to deposition of collagen and glycosaminoglycan in muscles
Swelling of extraocular muscle and periorbital edema
Pathophysiology of Proptosis due to thyrotoxicosis
ONLY occurs in Grave’s disease
Protrusion of eyeball from orbit
Sclera is not covered by the lower eyelid
Eyes are anterior to the superior orbital margin when viewed from the back
How to examine for proptosis
ONLY occurs in Grave’s disease
Protrusion of eyeball from orbit
Sclera is not covered by the lower eyelid
Eyes are anterior to the superior orbital margin when viewed from the back
Complications of proptosis due to thyrotoxicosis
Opthalmoplegia/ Diplopia
Corneal ulceration
Chemosis
Conjunctivitis
Optic atrophy
Thyrotoxicosis hand signs
Fine tremor* - Due to sympathetic overactivity
Sweating, warm and moist skin* - Due to sympathetic overactivity
Onycholysis - Separation of nail from bed
Palmar erythema - Signs of Grave’s disease
Finger clubbing
Thyroid acropachy - Soft-tissue swelling of hands and finger clubbing
Abnormal pulse
Sinus tachycardia (Sympathetic overactivity)
Atrial fibrillation (Shortened refractory period of atrial cells related to sympathetic drive)
Bounding pulse and wide pulse pressure (High cardiac output associated with AS murmur)
Signs of thyrotoxicosis on arms and legs
Arms
- *- Proximal myopathy**
- *- Hyperreflexia**
Legs
- Proximal myopathy: Ask patient to stand up from squatting position
- Pretibial myxedema
Occurs in Grave’s disease and rarely Hashimoto’s thyroiditis
Localized non-pitting edema of skin
Bilateral firm, elevated dermal nodules and plaques
Can be pink, brown or skin-colored
Hyaluronic acid accumulates in dermis and subcutis
Hypothyroidism hand signs
Peripheral cyanosis - Reduced cardiac output
Palmar crease pallor
Anemia due to
• Anemia of chronic disease
• Iron deficiency (menorrhagia)
• Folate deficiency (bacterial overgrowth)
Dry and cool skin
Yellow discoloration
Due to hypercarotenemia
Slowing down of hepatic metabolism of carotene
Abnormal pulse
Carpal tunnel syndrome
Sensory loss as carpal tunnel is thickened in myxoedema
Hypothyroidism signs on arms and legs
Arms
- Proximal myopathy
- “Hung-up” biceps reflex
Legs
- Non-pitting edema/ Myxoedema
- “Hung-up” Achilles reflex
Rapid dorsiflexion followed by slow plantar flexion after the tendon is tapped
Signs of hypothyroidism in children/ newborn
Newborn: Cretinism/ Short stature/ Mental retardation/ Puffy face/ Deaf mutism/ Protuberant abdomen/ Umbilical hernia
Children: Retardation of growth, mental retardation
Advantage and limitations of serum TSH test
Advantage:
- MOST sensitive indicator of thyroid function due to short t1/2
- Normal TSH excludes a primary hyperthyroidism
- Does NOT exclude secondary abnormalities (hypothalamic or pituitary)
Limitations:
- Cannot indicate pituitary disease
- High TSH can mean hypothyroidism or secondary hyperthyroidism
- Low TSH can mean hyperthyroidism or secondary hypothyroidism
- Low TSH in 1st trimester pregnancy, high dose corticosteroid or dopamine use
Indication for fT3 and fT4 test
Why is total T4 less useful?
Hypothyroidism: only need fT4 (fT3 normal in 25% patients due to adaptive deiodinase response)
Hyperthyroidism: need both fT3 and fT4 (2-5% have only fT3 elevation in T3 toxicosis)
Total T4 is related to thyroxine-binding globulin with confounding factors:
- High in pregnancy, oral contraceptive, hormonal therapy
- Low in androgen use, hypoalbuminaemia
List 3 thyroid autoantibodies and indications
Thyroid antibodies
• Thyrotropin receptor antibodies (TRA) (Anti-TSH antibodies)
• Anti-thyroid peroxidase (TPO) antibodies
• Anti-thyroglobulin (TG) antibodies
Anti-TSH: Grave’s disease
Anti- TPO: Hashimoto thyroiditis
Anti-TG: Multinodular goiter
Pathophysiology of Grave’s disease
Autoimmune disease: Lymphocytes produce autoantibodies against self-antigen TSH receptor
Thyrotropin-receptor antibody (TRAb) stimulates TSH receptor on thyroid gland:
Stimulate thyroid cell hyperplasia and TH release
Clinical diagnosis of Grave’s disease
- Diffusely enlarged thyroid gland
- High fT3 and fT4, Suppressed TSH
- Diffuse radioactive iodine uptake in scintigraphy scan
- Positive TSH receptor autoantibody in serum
Function of radioisotope thyroid scan
Functional assessment of thyroid
Increased uptake:
- Grave’s disease: diffuse uptake
- TSH-secreting pituitary adenoma: diffuse uptake
- Toxic adenoma: focal area of uptake only
- Multinodular goiter: heterogenous uptake
Decreased uptake:
- Thyroiditis
- T4 overdose
- Iatrogenic: e.g. hemithyroidectomy
Guide FNAC decision
o Hot nodules do NOT require FNAC
o Cold nodules require FNAC
S/S of Grave’s disease
Goiter
S/S hyperthyroidism
Exophthalmos/ Proptosis
Pretibial Myxoedema
S/S of related autoimmune diseases: MG, DM
Complications of hyperthyroidism
Thyroid storm
Thyrotoxic period paralysis (HypoK)
Atrial fibrillation and heart failure
Clinical use of Thyrotropin-receptor antibody (TRAb)
- Prognostic indicator of Antithyroid drug against Grave’s disease: negative TRAb after Tx means better prognosis
- Forecast neonatal Grave’s disease (TRAb passes through placenta)
- Diagnosis of Grave’s disease and monitor response to antithyroid drugs
Outline all treatment options for Grave’s disease
- Antithyroid drugs:
- Thiouracil derivatives: Methimazole, carbimazole, propylthiouracil
- Lithium
- Surgery: thyroidectomy
- RAI therapy
- Ancillary drugs:
Sedatives, B-blocker, Iodine
Compare surgery, Anti-thyroid and RAI therapy
- Relapse risk
- Hypothyroidism risk
- Long-term complication risk
- Onset of therapeutic effect
Beta-blocker for hyperthyroidism
- Indication
- Example
- MoA
- S/E
- Indication: Thyrotoxic crisis, before surgery to prevent thyroid storm
- Example: Propanolol
- MoA
Block β1-adrenoreceptors in heart
• Relive palpitations
Block β1-adrenoreceptors in brain
• Relieve anxiety
Block β2-adrenoreceptors in skeletal muscle
• Relieve tremor
- S/E:
Bronchospasm
Hypoglycemia
Heart failure (↓ CO)
Coronary artery spasm
Lugol’s solution
- Indication
- Contraindication
- MoA
- S/E
- Indication: rapid onset, short-term use before thyroidectomy/ thyroid storm
- Contraindication: pregnancy and breast-feeding
- MoA:
High iodine concentration inhibits H2O2 and peroxidase > inhibit iodination of thyroglobulin and production of T3, T4
Decrease size and vascularity of hyperplastic thyroid gland
Decrease bleeding risk during surgery
- S/E: Hypersensitivity (fever, rash, angioedema, conjunctivitis..etc)
Thionamides
- Indication
- Tx course
- Examples
- MoA
- S/E
- Indication: Children/ Pregnancy/ Mild- moderate disease
- Tx course: 12 - 18 months, onset of effects takes 4 weeks
- Examples: Carbimazole/ Methimazole/ Propylthiouracil (PTU)
- MoA:
Carbimazole/ Methimazole: Inhibit the action of peroxidase
• Inhibit iodination (organification) of tyrosine residues of thyroglobulin
• Inhibits coupling of iodotyrosine and production of T3 and T4
• Suppress intra-thyroidal antigen-presenting cells
PTU: Inhibits peripheral conversion of T4 into T3
- S/E:
Skin rash, urticaria and pruritis
Agranulocytosis (first 2 months, fever, sore throat)
Rare: Hepatotoxicity, Acute arthralgia, Cholestatic jaundice, ANCA vasculitis
Describe absorption of thionamide derivatives
Recommendation during pregnancy
Rapid absorption into thyroid in minutes
All transferable into milk
Metimazole/ Carbimazole more teratogenic than PTU
>> Give PTU until second trimester then change to methimazole/ Carbimazole
Predictive patient features associated with higher recurrence of thyroid disease after anti-thyroid drugs
- Larger goiter
- Positive family history
- High initial T3 or T3/T4 ratio
- Shorter course of Tx
- Failure to normalize TSH
- High TSH receptor antibody levels
Surgical treatment options for diffuse toxic goiter
Pre-op preparation
Bilateral subtotal thyroidectomy
Unilateral total and contralateral subtotal lobectomy
Near total thyroidectomy
Pre-op preparation:
- Antithyroid until euthyroid
- Beta-blocker for 2 weeks
- Lugol’s solution 2-3 days before
Indications for surgical treatment of diffuse toxic goiter
- Young age
- Failed medical treatment
- Refuse/ Refractory to anti-thyroid drugs
- Thyroid eye signs
- Pregnancy/ breast-feeding
- Refuse/ Refractory to RAI therapy
- Excessively large goiter +/- compressive symptoms
Complications of thyroid surgery
Hypoparathyroidism
Thyroid storm
Tracheomalacia - trachea cartilage collapse
Vocal cord paralysis: RLN or SLN damage
Wound complications: seroma, hypertrophic scar
Hemorrhage
• Compression and edematous effect compresses on trachea
RAI therapy
- Indication
- Contraindication
- MoA
- S/E
Indications:
- Thyrotoxic heart disease; Refractory to antithyroid drugs; ablation of residual tumor after thyroidectomy; Relapse post-op; C/O surgery
Contraindication:
- Pregnancy/ breast-feeding (transplacental, fetal risks)
MoA:
- Taken up by Na-I symporter and incorporated into thyroglobulin
- Emit B-radiation to cause necrosis of follicular cells, fibrosis and destroy colloid
- Destroy intra-thyroid T-suppression cells, Inhibit release of TSH-receptor antibodies
S/E:
- Hypothyroidism
- Risk of thyroid eye disease after Tx
- Thyroid storm due to radiation thyroiditis
Advantage of RAI therapy
Low relapse rate
Simple procedure
Economical
No immediate complications
Pathogenesis of Grave’s opthalmopathy
- TSH-receptor antibody stimulate orbital fibroblasts to differentiate into adipocytes/ adipogenesis
- Increase TSH receptor expression on orbital fibroblast after differentiation into adipocytes
- Orbital adipocytes hypertrophy and exerts pressure on eyeball
Histological features of Grave’s ophthalmopathy
- At extra-ocular muscles, retrobulbar fat and optic nerve
Extra-ocular muscles: edema, mononuclear cell infiltration, Mucopolysaccharide deposits, Fibrosis
Retrobulbar fat: Lymphocyte infiltration, fat replaced by fibrous tissue, collagen tissue replaced by hyaluronic acid
Optic nerve: atrophy, replaced by fibrous and fatty connective tissue
Ophthalmopathy must be related to hyperthyroidism
True or False?
False
Can be hyper-, hypo- or euthyroid
80% opthalmopathy first develop eye signs within 18 months of thyrotoxicosis
Treatment of Grave’s opthalmopathy
- Anti-thyroid treatment to achieve euthyroid
- Immunosuppressants against infiltrative ophthalmopathy:
- Steroid - IV or oral methylprednisolone
- Cyclosporin A
- Plasmapharesis for autoantibody
- Immunoglobulin
- TNF-a inhibitor
- IGF-1 receptor inhibitor
- Orbital irradiation
- Orbital decompression/ extra-ocular muscle operation
Thyrotoxic period paralysis
- Pathophysiology
Pathophysiology: hyperthyroidism results in
□ ↑Na+/K+/ATPase activity + ↑insulin release (esp after carbohydrate load) → intracellular shift of K+
□ Consequences: paralysis and hypokalemia
Thyrotoxic Periodic Paralysis (TPP)
Clinical presentation: signs, course, S/S, precipitating events
Always preceded by thyrotoxic S/S (thyrotoxic state essential for pathogenesis)
Attacks of motor paralysis: proximal > distal, LL > UL, seldom respiratory/bulbar muscles
→ Signs: typically hypotonia with hypo/areflexia
→ Course: weekly/monthly attacks lasting mins-days
Precipitants:
- Events a/w ↑adrenaline release: rest after strenuous activity, stress, SABA use
- Events a/w ↑insulin release: namely ↑carbohydrate load
Cardiac arrhythmia due to severe hypoK
Management of Thyrotoxic Periodic Paralysis (TPP)
Mx: usually spontaneous recovery
□ Cardiac monitoring
□ K supplement: use IV K 10-20mmol/h over 2h to accelerate recovery
→ Watch out for rebound hyperkalemia (40-59%) when transcellular shift reverses
→ IV propranolol may be useful to reverse excessive ↑Na+/K+/ATPase activity in refractory cases
□ Manage hyperthyroidism
□ Other prophylactic Tx: low salt diet, moderate carbohydrate intake ± propranolol
4 clinical patterns of hypothyroidism
Cretinism
Juvenile myxedema
Adult myxedema
Myxedema coma
Ddx painless thyroiditis
Autoimmune: Lymphocytic thyroiditis, Atrophic thyroiditis, Hashimoto’s thyroiditis
Silent thyroiditis e.g. Post-partum thyroiditis
Hashimoto’s thyroiditis
- Risk factors
- Pathology
- Histological features
RFs: older female, family history, HLA-DR3, High iodine intake, smoking
Pathology: T-cell mediated autoimmune disease against thyroid tissue
Anti-thyroid antibody after T-cell mediated thyroid injury: Anti-thyroglobulin, Anti-TPO
Histology: profuse lymphocytic infiltration, lymphoid germinal centres and destruction of thyroid follicles ± fibrosis
Clinical presentation of Hashimoto’s thyroiditis
Clinical presentation:
□ Goitre: usually small or moderately sized, diffuse, painless
→ Characteristically firm, rubbery
→ Atrophic variant: predominantly TSHr-blocking Ab → no goiter
□ Hypothyroidism (25%)
Natural Hx: gradual loss in thyroid function over years
Hashimoto’s thyroiditis
Investigations
Management
Ix:
□ TFT: may have ↑TSH + ↓fT4
□ Thyroid Ab: anti-TPO Ab (90-100%), anti-Tg Ab (80-90%), anti-TSHr (10-20%)
Mx:
T4 replacement: treats hypothyroidism + shrinks goiter
List 4 types of subacute thyroiditis
□ Subacute granulomatous (de Quervain’s, giant cell) thyroiditis
□ Subacute lymphocytic thyroiditis
□ Postpartum thyroiditis
□ Palpation thyroiditis
Subacute thyroiditis
Clinical course
S/S
Management
S/S:
□ Pain at thyroid, exacerbate by swallowing or neck movement, only in Quervain’s, not others
□ Goitre: palpable ± tenderness
□ Fluctuating thyroid status > transient hypothyroidism or thyrotoxicosis without hyperthryroidism
□ Systemic symptoms: fever, ↑WBC, ↑ESR
Clinical course:
□ Thyrotoxic phase (4-6w)
→ Due to damage to follicles release of stored T4 until depletion
→ ↓iodine uptake (↓TSH, follicular damage)
□ Hypothyroid phase (4-6mo) due to damage to follicular cells
→ ↓synthesis of thyroid hormones
□ Resolution
Mx: self-limiting → do NOT give antithyroid medications
□ No Mx: spontaneous resolution!
□ NSAIDs/corticosteroids for severe cases → manage systemic upset + pain
□ Temporary β-blocker for hyperthyroid phase (usually mild) → for symptomatic control only
□ Temporary T4 replacement for hypothyroid phase if pronounced or symptomatic
Causes of simple goiter
□ Causes: during ↑requirement (eg. pregnancy, pubertal) or from food (goitrogen, iodine excess/deficiency)
multinodular goiter
Pathology
TFT results
S/S
Pathology: recurrent episodes of hyperplasia and involution
(due to unknown stimulus)
→ hyperplastic nodules growing at varying rates
→ some may secrete thyroid hormone autonomously (toxic MNG, Plummer disease)
TFT findings:
→ 25% with complete suppression of TSH
→ T4/3 can be within reference range (subclinical thyrotoxicosis) or elevated (toxic MNG)
S/S: classically AF + multinodular goitre in elderly
→ Large goiter ± compressive S/S or retrosternal extension
→ Haemorrhage into nodule/cyst → sudden painful swelling
→ Thyrotoxic symptoms/complications, eg. AF
Management of multinodular goiter
Mx:
→ No treatment + annual TFT to screen for toxic MNG in small, non-toxic MNG
- Consider T4 suppression therapy in selected patients → aim low-normal TSH
→ Early definitive treatment for large or toxic MNG (as relapse is invariable after cessation of ATD)49
- Total thyroidectomy for large goitres with compression or cosmetic concerns
- RAI for small toxic goitres
Congenital hypothyroidism
Screening method
Causes
Neonatal cord blood TSH screening: fT4 <12pmol/L, TSH >7mlU/L
Causes:
- Athyroesis
- Dyshormonogenesis
- Ectopic thyroid gland
- Hypothalamic - Pituitary hypothyroidism
- Maternal factors: Anti-thyroid drugs, Iodine deficiency, TSH-autoantibodies, Premature birth
- Associated conditions: Down’s syndrome, Trisomy 18…etc
Cardiac precaution with thyroid disease
- Hypothyroidism - lead to hyperlipidaemia due to decrease lipolysis, increase risk of Coronary atherosclerosis
- Must treat coronary atherosclerosis prior to T4 supplementation: Initiation of thyroxine raises CO and worsens IHD
- Give 4-6 weeks to equilibrate thyroxine
Myxedema coma
- S/S
- Complication
- Tx
General features
• Severe hypothyroidism with hypothermia, respiratory failure with hypoxia and coma, convulsions, confusion
General management
• Treatment of precipitating causes
• Maintenance of body temperature
• Correction of hypoglycemia with D10
• Correction of fluid and electrolytes with NS ± vasopressors
Medical treatment
• Liothyronine (T3)
• Levothyroxine (T4)
