HYPERTHYROIDISM A Practical Approach to Dx. and Rx.

HYPERTHYROIDISM A Practical Approach to Dx. and Rx.
PROF. BIKHA RAM DEVRAJANI MB,FCPS,FACP,FRCP LUMHS JAMSHORO

A 27 years unmarried lady presented with the history of weight loss increased appetite , sweating and palpitation Q what is D/D ?

THYROID GLAND

Clinical Exam. of Thyroid
Have patient seated on a stool / chair Inspect neck before & after swallowing Examine with neck in relaxed position Palpate from behind the patient Remember the rule of finger tips Use the tips of fingers for palpation Palpate firmly down to trachea Pemberton’s sign for RSG

Where to look for Thyroid ?

Clinical Anatomy of Thyroid

Clinical Exam of Thyroid

Thyromegaly

Hyperthyroidism A hyper metabolic biochemical state
It is a multi system disease with Elevated levels of FT4 or FT3 or both What is thyrotoxicosis ? What is hyperthyroidism ? What are the various causes ? How to differentiate the causes ? What is the appropriate treatment ?

Causes of Hyperthyroidism
Graves Disease – Diffuse Toxic Goiter Plummer’s Disease – Toxic MNG Toxic phase of Sub Acute Thyroiditis - SAT Toxic Single Adenoma – STA Pituitary Tumours – excess TSH Molar pregnancy & Choriocarcinoma (↑↑ βHCG) Metastatic thyroid cancers (functioning) Struma Ovarii (Dermoid and Ovarian tumours) Thyrotoxicosis Factitia ; INF, Amiodarone, SSRIs

Graves Disease The most common cause of thyrotoxicosis (50-60%).
Organ specific auto-immune disease The most important autoantibody is Thyroid Stimulating Immunoglobulin (TSI) or TSA TSI acts as proxy to TSH and stimulates T4 and T3 Anti thyro peroxidase (anti-TPO) antibodies Anti thyro globulin (anti-TG) Anti Microsomal and other Autoimmune diseases - Pernicious Anemia, T1DM RA, Myasthenia Gravis, Vitiligo, Adrenal insufficiency.

I 123 or TC 99m Normal v/s Graves
Graves Disease I 123 or TC 99m Normal v/s Graves

Graves Disease

Toxic Multinodular Goiter (TMG)
TMG is the next most common hyperthyroidism - 20% More common in elderly individuals – long standing goiter Lumpy bumpy thyroid gland Milder manifestations (apathetic hyperthyroidism) Mild elevation of FT4 and FT3 Progresses slowly over time Clinically multiple firm nodules (called Plummer’s disease) Scintigraphy shows - hot and normal areas

Toxic Multinodular Goiter (TMG)

Sub Acute Thyroiditis (SAT)
SAT is the next most common hyperthyroidism – 15% T4 and T3 are extremely elevated in this condition Immune destruction of thyroid due to viral infection Destructive release of preformed thyroid hormone Thyroid gland is painful and tender on palpation Nuclear Scintigraphy scan - no RIU in the gland Treatment is NSAIDs and Corticosteroids

Toxic Single Adenoma (TSA)
TSA is a single hyper functioning follicular thyroid adenoma. Benign monoclonal tumor that usually is larger than 2.5 cm It is the cause in 5% of patients who are thyrotoxic Nuclear Scintigraphy scan shows only a single hot nodule TSH is suppressed by excess of thyroxines So the rest of the thyroid gland is suppressed

Toxic Single Adenoma (TSA)
Nucleotide Scintigraphy

Age and Sex Age Graves disease 20 to 40 Toxic MNG > 50 yrs
Toxic Single Adenoma 35 to 50 Sub Acute Thyroiditis Any age Sex M : F ratio Graves Disease 1: 5 to 1:10 Toxic MNG 1: 2 to 1: 4

Nucleotide Scintigraphy

Clinical Features Those that occur with any type of thyrotoxicosis
Those that are specific to Graves disease Non specific changes of hyper metabolism

Common Symptoms Nervousness Anxiety Increased perspiration
Heat intolerance Tremor Hyperactivity Palpitations Weight loss despite increased appetite Reduction in menstrual flow or oligo-menorrhea

Common Signs Hyperactivity, Hyper kinesis
Sinus tachycardia or atrial arrhythmia, AF, CHF Systolic hypertension, wide pulse pressure Warm, moist, soft and smooth skin- warm handshake Excessive perspiration, palmar erythema, Onycholysis Lid lag and stare (sympathetic over activity) Fine tremor of out stretched hands – format's sign Large muscle weakness, Diarrhea, Gynecomastia

Specific to Graves Disease
Diffuse painless and firm enlargement of thyroid gland Thyroid bruit is audible with the bell of stethoscope Ophthalmopathy – Eye manifestations – 50% of cases Sand in eyes, periorbital edema, conjunctival edema (chemosis), poor lid closure, extraocular muscle dysfunction, diplopia, pain on eye movements and proptosis. Dermoacropathy – Skin/limb manifestations – 20% of cases Deposition of glycosamino glycans in the dermis of the lower leg – non pitting edema, associated with erythema and thickening of the skin, without pain or pruritus - called (pre tibial myxedema)

Clinical Presentations

Diffuse Graves Thyroid
MNG and Graves Huge Toxic MNG Diffuse Graves Thyroid

Higher grades of Goiter
Toxic MNG (Diffuse) Graves

Grade IV Toxic MNG Huge Toxic MNG Huge Toxic MNG

Thyroid Ophthalmopathy
Proptosis Lid lag

Ophthalmopathy in Graves
Periorbital edema and chemosis

Ophthalmopathy in Graves
Occular muscle palsy Laka Laka Laka

Severe Exophthalmia

Pink and skin coloured papules, plaques on the shin
Thyroid Dermopathy Pink and skin coloured papules, plaques on the shin

Graves with Acropathy Graves Goiter Acropathy

Thyroid Acropathy Clubbing and Osteoarthropathy

Onycholysis

Non specific changes Hyperglycemia, Glycosuria
Osteoporosis and hypercalcemia ↓ LDL and Total Cholesterols Atrial fibrillation, LVH, ↑ LV EF Hyper dynamic circulatory state High output heart failure H/o excess Iodine, amiodarone, contrast dyes

THYROID STIMULATING HORMONE - TSH
Nine Square Approach PRIMARY HYPERTHYROID FREE THYROXINE or FT4 LOW NORMAL HIGH LOW NORMAL HIGH THYROID STIMULATING HORMONE - TSH

THYROID STIMULATING HORMONE - TSH
Nine Square Approach SUB CLINICAL HYPERTHYROID FREE THYROXINE or FT4 LOW NORMAL HIGH LOW NORMAL HIGH THYROID STIMULATING HORMONE - TSH

Diagnosis Typical clinical presentation
Markedly suppressed TSH (<0.05 µIU/mL) Elevated FT4 and FT3 (Markedly in Graves) Thyroid antibodies – by Elisa – anti-TPO, TSI ECG to demonstrate cardiac manifestations Nuclear Scintigraphy to differentiate the causes

Primary (T4) Thyrotoxicosis Sub Acute Thyroiditis, I2, ↑ Thyroxine
Algorithm for Hyperthyroidism Measure TSH and FT4  TSH,  FT4  TSH, FT4 N  TSH,  FT4 N TSH, FT4 N Primary (T4) Thyrotoxicosis Pituitary Adenoma FNAC, N Scan Measure FT3 High T3 Toxicosis Features of Grave’s Normal Sub-clinical Hyper Yes No  RAIU Low RAIU F/u in 6-12 wks Rx. Grave’s Single Adenoma, MNG Sub Acute Thyroiditis, I2, ↑ Thyroxine

Laboratory Diagnosis Serum T3, T4, FT3, FT4 Sensitive TSH assay
Serum TRAb Test of TRH irritation Radioactive iodine uotake: Normal: 3h 5-25%, 24h 20-45%, peak at 24h Thyroid scan: 131I, 99mTc

Diagnosis Symptoms Signs Laboratory examination

Differential diagnosis
Other causes of thyrotoxicosis Anxiety neurosis or mania Some states of hypermetabolism without thyrotoxicosis: severe anemia, leukemia, etc. Cardiac disease: atrial fibrillation, angina Pheochromocytoma Other causes of ophthalmoplegia (myasthenia gravis) and exophthalmos (orbital tumor) Others: COPD, DM, cirrhosis of the liver.

Treatment Options Symptom relief medications Anti Thyroid Drugs – ATD
Methimazole, Carbimazole Propylthiouracil (PTU) Radio Active Iodine treatment – RAI Rx. Thyroidectomy – Subtotal or Total NSAIDs and Corticosteroids – for SAT

Symptom Relief Rehydration is the first step
β – blockers to decrease the sympathetic excess Propranalol, Atenelol, Metoprolol Rate limiting CCBs if β – blockers contraindicated Treatment of CHF, Arrhythmias Calcium supplementation SSKI or Lugol solution for ↓ vascularity of the gland

Anti Thyroid Drugs (ATD)
Imp. considerations Methimazole Propylthiouracil Efficacy Very potent Potent Duration of action Long acting BID/OD Short acting QID/TID In pregnancy Contraindicated Safely can be given Mechanism of action Iodination, Coupling Conversion of T4 to T3 No action Inhibits conversion Adverse reactions Rashes, Neutropenia Rashes, ↑Neutropenia Dosage 20 to 40 mg/ OD PO 100 to 150mg qid PO

How long to give ATD ? Reduction of thyroid hormones takes 2-8 weeks
Check TSH and FT4 every 4 to 6 weeks In Graves, many go into remission after months In such pts ATD may be discontinued and followed up 40% experience recurrence in 1 yr. Re treat for 3 yrs. Treatment is not life long. Graves seldom needs surgery MNG and Toxic Adenoma will not get cured by ATD. For them ATD is not the best. Treat with RAI.

Radio Active Iodine (RAI Rx.)
In women who are not pregnant In cases of Toxic MNG and TSA Graves disease not remitting with ATD RAI Rx is the best treatment of hyperthyroidism in adults The effect is less rapid than ATD or Thyroidectomy It is effective, safe, and does not require hospitalization. Given orally as a single dose in a capsule or liquid form. Very few adverse effects as no other tissue absorbs RAI

Radio Active Iodine (RAI Rx.)
I123 is used for Nuclear Scintigraphy (Dx.) I131 is given for RAI Rx. (6 to 8 milliCuries) Goal is to make the patient hypothyroid No effects such as Thyroid Ca or other malignancies Never given for children and pregnant/ lactating women Not recommended with patients of severe Ophthalmopathy Not advisable in chronic smokers

Surgical Treatment Subtotal Thyroidectomy, Total Thyroidectomy
Hemi Thyroidectomy with contra-lateral subtotal ATD and RAI Rx are very efficacious and easy – so Surgical treatment is reserved for MNG with Severe hyperthyroidism in children Pregnant women who can’t tolerate ATD Large goiters with severe Ophthalmopathy Large MNGs with pressure symptoms Who require quick normalization of thyroid function

Preoperative Preparation
ATD to reduce hyper function before surgery βeta blockers to titrate pulse rate to 80/min SSKI 1 to 2 drops bid for 14 days This will reduce thyroid blood flow And there by reduce per operative bleeding Recurrent laryngeal nerve damage Hypo parathyroidism are complications

Dietary Advice Excess amounts of iodide in some
Avoid Iodized salt, Sea foods Excess amounts of iodide in some Expectorants, x-ray contrast dyes, Seaweed tablets, and health food supplements These should be avoided because The iodide interferes with or complicates the management of both ATD and RAI Rx.

Summary of Hyperthyroidism
Age % Enlarged Pain RAIU Treatment Graves (TSI Ab eye, dermo, bruit) 60% Diffuse None ↑↑ ATD – 18 m Toxic MNG > 50 20% Lumpy Pressure ↑ RAI, Surgery Single Adenoma 5% Single RAI, ATD S Acute Thyroiditis Any age 15% Yes ↓↓ NSAID, Ster. TSH is markedly low, FT4 is elevated

Thyrotoxicosis Factitia
Excessive intake of Thyroxine causing thyrotoxicosis Patients usually deny – it is willful ingestion This primarily psychiatric disorder May lead to wrong diagnosis and wrong treatment They are clinically thyrotoxic without eye signs of Graves High doses of Thyroxine lead to TSH suppression This causes shrinkage of the thyroid Stop Thyroxine and give symptom relief drugs

Case # 1 A patient complains of “sandy” sensation in his eyes,weight loss, and a tremor. His extraocular muscles are inflammed. His thyroid is diffusely enlarged and non tender. The most likely diagnosis is a. Iodine deficiency b. Sub-acute thyroiditis c. Multinodular goiter d. Graves’ disease e. Silent thyroiditis

Case # 2 A 55 year old woman is anxious, irritable, frequent semi solid stools and she reports weight loss of 5 kgs in the past six months. She was having a lumpy bumpy painless swelling in her neck for past 20 years. The most likely diagnosis is a. Iodine deficiency goiter b. Sub-acute thyroiditis c. Multinodular goiter d. Graves’ disease e. Solitary toxic adenoma

Case # 3 A 60 year patient from a mountain region complains of constipation. He has a heart rate of 60, dry thick skin, and a tongue that has scalloped edges from teeth indentation. He has a goiter. The most likely diagnosis is a. Iodine deficiency b. Subacute thyroiditis c. Graves’ disease d. Silent thyroiditis

Case # 5 A 72 year old man complains of tremor and inability to concentrate. On exam, he has a heart rate of 100 beats per minute. He has a large goiter with many nodules. He has a fine tremor. His serum T4 is very high and TSH is very low. Treatments that are likely to improve his symptoms are a. Iodine therapy b. Ethanol injection of his thyroid (PEI) c. 6 weeks of Methimazole d. Radio Active Iodine therapy

Case # 6 In Nuclear Scintigraphy Scan I123 uptake is very high in the thyroid of patients with a. Silent thyroiditis b. Single functional adenoma c. Sub-acute thyroiditis d. Acute ingestion of animal thyroid extract e. Graves’ disease

Hypothyroidism and Myxedeam Coma
PROF.BIKHA RAM DEVRAJANI MB,FCPS,FACP INCHARGE MEDICAL UNIT IV LUMHS JAMSHORO

Normal Thyroid State Synthesis and release of thyroid hormone is controlled by TSH relaesed form the anterior pituitary TSH is controlled by the release of thyroid releasing hormone (TRH) from the hypothalmus and a negative feedback loop to the pituitary Thyroid hormone production s dependent on adequate adequate iodine intake

Normal Thyroid State Thyroid hormone is reversible bound to various proteins including thyronine-binding globulin (TBG) Free unbound portions are biologically active T4 is the predominant circulating hormone T4 is deiodinated to t3 T3 is biologically more active than T4 but has a shorter half-life

Hypothyroidism Occurs when there is insufficient hormone production or secretion Occurs more frequently in women (0.6 to 5.9 %) The most common etiologies are Primary thyroid failure due to autoimmune diseases (Hashimoto thyroiditis is the most common) Idiopathic causes Ablative therapy Iodine deficiency May be transient Pathophysiology is unclear but may be viral in nature

Hypothyroidism Etiologies of Hypothyroidism Primary
Autoimmune etiologies Hashimotos is the most common Idopathic Post ablation (surgical, radioiodine) Post external radiation Thryoiditis (subacute, silent, postpartum) Postpartum thyroiditis occurs within 3-6 months and occurs in % of women Self limited etiologies, often prededed by hyperthroid phase Infiltrative disease (lymphoma, sarcoid, amyloidosis, Tuberculosis Congenital

Hypothyroidism Etiologies of Hypothyroidism Post Partum
Occurs 3-6 months post partum and occurs in 2-16% of women Secondary (pituitary) Neoplasm Infiltrative Dz. Hemorrhage Tertiary (hypothalamic)

Hypothyroidism Etiologies of Hypothyroidism Drugs Amiodarone Lithium
Occurs in 1-32% of patients Most likely due to the large amount of iodine released in the metabolism of the drug which inhibits thyroid hormone synthesis, release, and conversion of T4 to T3 Lithium Acts similarly to iodine and inhibit thyroid hormone release Iodine (in patients with pre-existing autoimmune disease) Antithyroid medication

Hypothyroidism Clinical Features
The typical symptoms of hypothyroidism include fatigue, weakness, cold intolerance, constipation, weight gain, and deepening of voice. Cautaneous signs include dry, scaly, yellow skin, non-pitting, waxy edema of the face and extremities (myxedema): and thinning eyebrows

Hypothyroidism Clinical Features cont.
Cardiac findings include bradycardia, enlarged heart, and low-voltage electrocardiogram Paresthesia, ataxia, are characteristic neurologic findings See table below for more complete list

Hypothyroidism Symptoms and Signs or Hypothyroidism Symptoms Signs
Fatigue Hoarseness Weight Gain Hypothermia Cold intolerance Periobital puffiness Depression Delayed relaxation of ankle jerks Menstrual irregularities Loss of outer third of eyebrow Constipation Cool, rough, dry skin Joint Pain Nonpitting edema Muscle cramps Bracycardia Infertility Peripheral Neuropathy

Hypothyroidism Treatment
Most patient with uncomplicated symptomatic Hypothyroidism may be referred to the primary physician for further evaluation and initiation of treatment If hypothyroidism is due to a secondary etiology initiation of thyroid hormone therapy may exacerbate preexisting adrenal insufficiency

Myxedema Myxedema is a rare life threatening decompensation of hypothyroidism Usually in individuals with long-standing hypothyroidism Most often seen in the winter months More common in elderly women with underdiagnosed or undertreated hypothyroidism

Myxedema Precipitating events include Infection CHF Trauma CVA
Exposure to cold Drugs Sedatives Lithium Amiodarone

Myxedema In addition to the clinical features of hypothyroidism patients may present with Hypothermia Altered metal status Coma, delusions, and psychosis (myxedema maddness) Hyponatremia Dilutional secondary to decreased free-water clearance Hypoglycemia Secondary to impaired gluconeogenesis Hypotension Bradycardia Respiratory Failure Secondary to decreased strength of respiratory muscle Hypercapnia and hypoxia is common

Myxedema Diagnosis Must have high clinical suspicion
Commonly has Hx. Of hypothyroidism Delcine in function is usually insidious in onset

Myxedema Diagnosis cont Laboratory evaluation may reveal Anemia
Hyponatremia Hypoglycemia ↑ Transaminases ↑ CPK ↑ LDH ↓Po2 and ↑PCo2 on ABG’s

Myxedema Diagnosis cont. EKG may reveal Sinus Bradycardia
Prolonged QT interval Low voltage Flattened or inverted T waves

Myxedema Treatment No prospective studies on optimal therapy have been done thus treatment recommendations are not uniform Airway stabilization with adequate oxygenation and ventilation or vital Cardiovascular status must be monitored closely Hypothermic patients should be gradually rewarmed with gentle passive external rewarming Hypotension from reversal of hypothermic vasoconstriction should be avoided

Myxedema Treatment cont.
Hyponatremia typically responds to fluid restrictions. Severe cases may require hypertonic saline with lasixs Vasopressors are usually ineffective and should only be used in severe hypotension Lovothyroxine mcg slow IVP followed by mcg daily

Myxedema Treatment cont.
L-triiodothyronine 25 mcg IV or orally q 8 h is a alternative This dose should be halved in patients with cardiovascular disease Hydrocortisone 100 mg IV q 8 hours should be given Send baseline cortisol level to lab if possible Precipitating causes should be sought and treated

Myxedema Treatment of Myxedema Coma Recognition
Supportive therapy including ventilatory support Thyroid replacement Lovothyroxine mcg slow IVP followed by mcg daily or T3 25 mcg IV or PO q 8 hrs Glucocorticoid Hydrocortisone: 100 mg IV q8h Hypothermia Prevent additional loss Passive external rewarming Electrolyte correction Gentle fluid restriction for dilutional hyponatremia Hypertonic saline for severe hyponatremia Hypoglycemia Dextrose-containing IV fluids Monitoring Aggressive treatment of presipitating causes Admit patient to a monitored setting

Myxedema Disposition Admit to appropiately monitored bed

Myxedema Coma

Introduction Myxedema coma still has a high mortality rate (despite intensive treatment).

Clinical Manifestations
Reduced level of consciousness. Seizures. Other features of hypothyroidism. Hypothermia (up to 74oF). There may be a history of treated hypothyroidism with poor compliance, or the patient may be previously undiagnosed.

Clinical Manifestations
Myxedema coma almost always occurs in the elderly and is usually precipitated by factors that impair respiration, such as: Drugs (esp. sedatives, anaesthetics, antidepressants). Pneumonia. Congestive heart failure. Myocardial infarction. Gastrointestinal bleeding. Cerebrovascular accidents. Sepsis. Exposure to cold.

Subclinical hypothyroidism Primary hypothyroidism
Elevated TSH Measure Free T4 Normal Low Subclinical hypothyroidism Primary hypothyroidism TPOAb+ or symptomatic TPOAb–, no symptoms TPOAb+ TPOAb– Autoimmune hypothyroidism Rule out other causes of hypothyroidism T4 treatment Annual follow up T4 treatment

Pituitary disease suspected?
Normal TSH Pituitary disease suspected? No Yes No further testes Measure free T4 Low Normal No further tests Rule out drug effects, sick euthyroid syndrome, then evaluate anterior pituitary function

Pathogenesis Hypoventilation, leading to hypoxia and hypercapnia, plays a major role in pathogenesis. Hypoglycemia and dilutional hyponatremia also contribute to the development of myxedema coma.

Treatment Levothyroxine – single intravenous bolus of 500 g, and usually continued at a dose of 50–100 g. OR Liothyronine (T3) intravenously or via NG tube, dose range from 10 – 25 g every 8 to 12 h. T4  T3 conversion is impaired. Excess dose has the potential to provoke arrhythmias.

Treatment Combine levothyroxine (200 g/d) and liothyronine (25 g) as a single, initial intravenous bolus followed by daily treatment with levothyroxine (50 to 100 g/d) and liothyronine (10 g every 8 h). Supportive therapy should be provided to correct any associated metabolic disturbances. External warming is indicated only if the temperature is <30oC, as it can result in cardiovascular collapse.

Treatment Space blankets should be used to prevent further heat loss.
Parenteral hydrocortisone (50 mg every 6 h), as there is impaired adrenal reserve in profound hypothyroidism. Any precipitating factors should be treated, including the early use of broad-spectrum antibiotics, pending the exclusion of infection.

Treatment Ventilatory support with regular blood gas analysis is usually needed during the first 48 h. Hypertonic saline or intravenous glucose may be needed if there is hyponatremia or hypoglycemia. Hypotonic intravenous fluids should be avoided because they may exacerbate water retention secondary to reduced renal perfusion and inappropriate vasopressin secretion.

Treatment The metabolism of most medications is impaired, and sedatives should be avoided if possible or used in reduced doses. Blood levels should be monitored, when available, to guide medication dosage.

Algorithm for Thyroid Nodule
Low TSH Normal TSH TC 99 Nuclear Scan FNAC or US guided biopsy Hot Nodule Cold Nodule 4% 10% 69% 17% RAI Ablation, Surgery or ATD Non diagnostic – repeat FNAC Malignant Suspicious or follicular Ca Benign Cyst T4 suppression Surgery or Cytology Surgery

Case # 4 A 25 year old woman is three months pregnant. She has a large goiter. Her exam is otherwise normal. Her thyroid tests are normal. You recommend a. Cassava five times weekly b. Fish three times weekly c. Formula milk for the baby when it is born d. A very low salt diet

THYROID DISEASE IN PREGNANCY

Physiologic Changes in Pregnancy
Free thyroxine levels remain within the normal range during pregnancy (though total thyroxine levels are increased secondary to increased TBG.) TSH decreases slightly in first trimester. The thyroid gland increases slightly in size during pregnancy.

Hypothyroidism Untreated patients with hypothyroidism rarely conceive and carry a pregnancy. Treated hypothyroidism usually has no associated pregnancy complications.

Hypothyroidism Some patients will require increased levothyroxine doses during their pregnancies. Monitor thyroid function tests each trimester and at other clinically indicated times. Prenatal vitamins can decrease the absorption of levothyroxine.

Hyperthyroidism 95% of hyperthyroidism in pregnancy is secondary to Graves’ Disease. A good pregnancy outcome can be expected in patients with good control.

Hyperthyroidism Untreated hyperthyroidism is associated with decreased fertility, an increased rate of miscarriage, intrauterine growth retardation (IUGR), premature labor, and perinatal mortality. Poorly controlled thyrotoxicosis is associated with thyroid storm especially at labor and delivery.

Hyperthyroidism Beta Blockers and PTU can be safely used in pregnancy and in nursing mothers. PTU crosses the placenta but does not usually cause fetal hypothyroidism and goiter unless used in high doses. Treatment goals favor mild hyperthyroidism over hypothyroidism.

Hyperthyroidism - Grave’s Disease
Like other immune mediated diseases in pregnancy, Grave’s disease tends to improve in the third trimester. Exacerbations may occur in the first trimester and postpartum.

Hyperthyroidism - Grave’s Disease
Neonatal and fetal thyrotoxicosis may occur because of transplacental passage of thyroid stimulating antibodies.

Postpartum Thyroiditis
Postpartum thyroiditis is a destructive autoimmune thyroiditis that begins with a period of hyperthyroidism followed by a period of hypothyroidism. The gland is often enlarged. There is usually complete recovery but a chance of recurrence in subsequent pregnancies exists.

80-85% of patients will have positive antithyroid antibodies. A radioactive iodine uptake scan can differentiate postpartum thyroiditis from an exacerbation of Graves’ Disease.

Postpartum thyroiditis in an important consideration in women with postpartum depression.

Hyperemesis Gravidarum
Hyperemesis is associated with abnormal thyroid function tests in a significant number of cases. Hyperthyroidism may be the cause of hyperemesis or hyperemesis may be the cause of the hyperthyroidism.

Thyroid Nodules New thyroid nodules should be aggressively investigated during pregnancy because of a high incidence of malignancy.

Thyroid Investigations
Radioactive Iodine is contraindicated in pregnancy. Nursing mothers who have radioactive iodine uptake scans should pump and discard their milk for hours after the test.

Thyroid Storm A life threatening hypremetabolic state due to hyperthyroidism Mortality rate is high (10-75%) despite treatment Usually occurs as a result of previously unrecognized or poorly treated hyperthyroidism Thyroid hormone levels do not help to differentiate between uncomplicated hyperthyroidism and thyroid storm

Thyroid Storm Preciptatnts of Thyroid Storm (tabel 215-4) Infection
Trauma DKA MI CVA PE Surgery Withdrawal of thyroid med Iodine administration Palpation of thyroid gland Ingestion of thyroid hormone Unknown etiology (20-25%)

Thyroid Storm Clinical features
The most common signs are fever, tachycardia out of proportion to the fever, altered mental status, and diaphoresis Clues include a history of hyperthyroidism, exophthalmoses, widened pulse pressure and a palpable goiter Patients may present with signs of CHF

Thyroid Storm Clinical features cont.
Common GI symptoms include diarrhea and hyperdefication Apathetic thyrotoxicosis is a distinct presentation seen in the elderly Characteristic symptoms include lethargy, slowed mentation, and apathetic facies Goiter, weight loss , and proximal muscle weakness also present

Thyroid Storm Diagnosis
Thyroid storm is a clinical diagnosis based upon suspicion and treated empirically Lab work is non specific and may include Leukocytosis, hyperglycemia, elevated transaminase and elevated bilirubin

Thyroid Storm Treatment
Initial stabilization includes airway protection, oxygenation, fluids and cardiac monitoring Treatment can then be divided into 5 areas: General supportive care Inhibition of thyroid hormone synthesis Retardation of thyroid hormone release Blockade of peripheral thyroid hormone effects Identification and treatment of precipitating events

Thyroid Storm Drug Treatment of Thyroid Storm (table 216-6)
Decrease de novo synthesis: Porpythiouracil mg PO initially, followed by mg q 4 hrs Methimazole 40 mg PO initial dose, then 25 mg PO q6h Prevent relases of hormone (after synthesis blockade intiated) Iodine Iaponoric acid (Telepaque) 1 gm IV q8h for the first 24 h, then 500 mg bid or Potassium iodide (SSKI) 5 drops PO q6h or Lugol solution 8-10 drops PO q6h Lithuim mg PO every day Prevent peripheral effects: B-Blocker Propanolol (IV) titrate 1-2 mg q 5min prn (may need mg PO q day) or Esmolol (IV) 500 mcg/kg IV bolus, then mcg/kg per min maintenance Guanethidine mg PO q 6 h Reserpine mg IM q4-6h Other consideration: Corticosteroids Hydrocortisone 100 mg IV q 8 h or dexamethosone 2 mg IV q 6 hr Antipyretics Cooling blanket acteaminophen 650 mg PO q 4-6h

Thyroid Storm Treatment cont
Propranolol has the additional effects or blocking perpheral conversion of T4-T3 Avoid Salicylates because it may displace T4 from TBG If the patient continues to deteriorate despite appropriate therapy circulating thyroid hormone may be removed by plasma transfusion, plasmapheresis, charchoal plasmaperfusion Remember you must not administer iodine until the synthetic pathway has been blocked

Thyroid Storm Disposition Admit to the ICU

Questions 1. Hyperthyroidism is Characterized by which of the following A. Fatigue B. Palpitations C. Weight Loss D. Heat intolerance E. All the above

2. The most common etiology of hyperthyroidism is
A. Toxic Multinodular B. Graves C. Toxic Nodular D. Amiodarone induces

3. Typical Feature of Hyperthyroidism include
A. Fatigue B. Weakness C. Constipation E. Cold Intolerance F. All the above

4. T or F Hyperthyroidism is more common in women
5. T or F Hypothyroidism is more common in women 6. T or F Mild hyperthyroidism may be treated with B-blockers Answers 1. E 2. B 3. F 4.T 5.T 6.T

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