Thyroid DisordersT₃: Triiodothyronine

T₄: Thyroxine

I. Hyperthyroidism (Thyrotoxicosis)

• Characterized by hypermetabolism of all body systems & increased serum levels of free thyroid hormones.

• More common in women.• Rare in children• Less common than hypothyroidism

• Thyroid Storm:• Exaggerated form of hypertoxicosis.• Medical emergency Prompt treatment• May be precipitated by : -Infection

-Trauma - Surgery -Embolism -Diabetic ketoacidosis -Others…

• Subclinical Hyperthyroidism:• Suppressed TSH level w/ NL thyroid hormone

levels.• Symptoms are NOT always present esp. in

elderly.

• Pathophysiology: See p. 987-990

• Treatment Goals of Hyperthyroidism:

1) Reverse S/S, normalize thyroid hormone levels, min. deleterious S/Es of T₄ on organ systems, prevent thyroid storm, & improve overall functional capacity.

2) Reverse hyperthyroid complaints.3) Reverse hyperthyroid physical findings.4) Normalize free T₄, T₃, & TSH levels.5) Reduce goiter size.

6) Improve cardiac function & prevent systemic embolism.7) Preserve bone density& prevent osteoporosis.8) Improve emotional well being& quality of life.9) Support placenta development & maintenance of pregnancy.10) Promote normal growth, & physical & mental development.

• Causes of Hyperthyroidism: (table38.3 p.993)1) Graves disease: -Autoimmune

-May occur w/ other autoimmune disorders. -Most common cause -Charact. by hyperthyroid. &

one or more of the following: * Goiter

* Exophthalmos * Dermopathy

2) Toxic Nodules: -Single & multinodular -Autonomous: independent

of TSH control. -May be caused by:

*Iodine deficiency*Genetic abnormality*Immune System

3) Subacute Thyroiditis:- Inflammatory thyroiditis,

i.e.Postpartum(PPT), viral (i.e. de Quervain).

- Hyperthyroid. from leakage of thyroid hormones into circulation due to inflamed gland & NOT increased synthesis.

-Hypothyroidism may follow.

4) Drug Induced: -Iodides (Jod-Basedow), Amiodarone, Lithium,

Cytokines5) Neonatal thyrotoxicosis (Graves):

-Transplacental passage of TRab causing the infant to be extremely ill w/in delivery hrs.

-Self-limiting.

6) Hashitoxicosis: -Hyperthyroid phase of Hashimoto thyroiditis

7) T₃ toxicosis: -Preferential secretion of T₃, often precedes T₄ toxicosis.

8) Tumors:-Secretion of thyroid stimulating substances.

9) Factitious:-Self-administration of levothyroxine

• Clinical Presentation & Diagnosis:

- Characteristics of Graves Dz. p.997 Table 38.6

-SxS of Hyperthyroidism & Hypothyroidism p.995 Table 38.4

- Thyroid Function Tests (TFTs) p.987-988

• Diagnosis of Hyperthyroidism :1) Confirmed w/ abnormally high levels of FT₄

or TT₃ & undetectable TSH.2) +Antibodies, opthalmopathy, or dermopathy

confirms the diagnosis of Graves.3) RAIU in Graves but is NOT cost-effective4) TT₃ & + TRab are essential for atypical

presentation, i.e. in elderly.

5) Subacute Thyroiditis (PPT,…), Diagnosis is confirmed by:*Low or undetectable RAIU.* TH levels.*Suppressed or undetectable TSH level.* ESR* No Thyroid Ab.* Leukocytosis, gland tenderness, & S/S of hyper or hypothyroidism.

• Therapeutic Plan: (table 38.7, p.998-999)• Major Modalities for Management of

Hyperthyroidism, include:1) Thioamides2) RAI3) Surgery

** Treatment must be individualized, each has advantages & limitations **Effective Treatment Selection p.1000, Fig.38.3

• Treatment Adjuncts:• Iodides• Iodinated Contrast Media• K Perchlorate• Adrenergic Antagonists• Corticosteroids• Cholestyramine• Rarely Li

• In U.S., RAI is most commonly used except in younger pts. for whom Thioamides are used.

• In Europe & Japan, Thioamides are the TOC.

• Surgery is the last choice unless there is:*Obstructive symptoms

or* Malignancy

• Treatment is individualized a/c to:1. Etiology2. Pt. age3. Goiter size4. Thyroid & Medical complications5. Social & Economic issues

1. Graves: All 3 methods are effective but pt. or Dr. may prefer meds. over RAI or surgery.

2. TMG: RAI or surgery > effective than meds., but factors as medical condition or pt. or Dr. may prefer RAI use over surgery.

3.Transient Treatment : may be used when the disease is self-limited, i.e.:

* Subacute Thyroiditis (PPT,…)*Neonatal Graves*Drug-Induced Hyperthroidism

• In Uncomplicated Graves esp. in children, Thioamides are preferred until remission.

• Thioamides: - Do NOT destroy the gland - Control the disease - Chronic thyroid replacement may not be necessary (not like w/ RAI or Surg.), however, hypothyroid. may still developeventually.

• If RAI or Surgery is selected, most older pts. & all severely ill thyrotoxic pts. should be pretreated w/ Thioamides.

• Pretreatment: 1) Depletes gland of stored hormones.2) Hypermetabolic rate.3) Prevents leakage of hormone from gland after

RAI or during surgery preventing thyroid storm.

• Optimal Tx of hyperthyroidism in Graves opthalmopathy is unresolved.

• Some prefer RAI or surgery (<desirable) to remove the antigen source (gland) & > effective than thioamides to prevent progressive opthalmopathy.

• Prophylactic systemic corticosteroid (e.g., Prednisone 30-40mg daily starting within a few days of RAI & cont. for ~2-3 wks. to prevent further progression of opthalmopathy in pts. w/ re-existing cases.

• Hypothyroidism can aggravate preexisting eye complaints.• Hyperthyroidism control & hypothyroidism prevention are

essential to prevent progression of opthalmopathy.

• Single or Toxic multinodular Dz.: • Best managed with definitive Tx, i.e. RAI or

surgery, because spontaneous remission is unlikely.

• Hyperthyroid Children:The usual Tx choices are Thioamides & subtotal thyroidectomy, although all 3 methods have been used.

• In Pregnancy:• Hyperthyroidism is difficult to manage. • Spontaneous remission may occur because of

the decrease in TRab.• Antithyroid meds. are often NOT necessary.• If untreated, complications may occur.• RAI & Iodides are Contraindicated in pregnancy.• Surgery in 2nd trimester is an option.

• Neonatal Graves:• Infants extremely ill w/in delivery hrs.• Supportive measures, i.e. *sedation

*O₂*Fluids/Electrolytes

• Short-term (temporary) thioamides, iodides, or beta blockers since it is self-limiting.

• Symptoms disappear in 1-2 months, therefore, withdraw antithyroids at this time.

• Subacute Thyroiditis:• Self-limiting (common spontaneous recovery).• Symptomatic treatment: *Heat

*Rest*NSAIDs *Beta-blockers

* Thioamides are NOT effective since it is due to thyroid hormone leakage & NOT increase in TH synthesis.

• Cont. Subacute Thyroiditis:• Corticosteroids are indicated for severe

inflammation if NSAIDs are ineffective.

• In Hypothyroid phase: Transient thyroid replacement is used to suppress further TSH stimulation to damaged gland & treat hypothyroid symptoms.

• Treatment: Fig.38.3 p.1000• Pharmacotherapy:1) Thioamides:*Long-term 1⁰ therapy for Graves esp. in children & adolescents.

*Transiently used to reduce TH levels before definitive therapy w/ RAI or surgery.

*TOC for small goiters & mild dz. For whom a high remission rate is likely.

• Advantages:• Potential for remission without gland damage.• Limitations:1.Non-adherence2.Strict parental & physician supervision in kids.3.Low success rates.4. Risk of ADRs.

• Thioamides:1. Methimazole2. Propylthiouracil (PTU)a. They prevent TH synthesis.b. PTU (Not Methimazole) inhibits peripheral

deiodination of T₄ to T₃.c. They suppress TSH receptor Ab level by

unknown immunosuppressive MOA.

• Thioamides Selection:• Pharmacologic Differences:** Methimazole is preferred over PTU, because:

1. Single daily dose ( PTU Q6-8H)2. More potent than PTU3. Less toxic than PTU @ low doses.

4. Less costly.** Both are equally effective @ equipotent doses.

• PTU is preferred over methimazole in pts. w/ **Thyroid Storm Or **Severe HyperthyroidismBecause:1. PTU blocks the conversion of T₄ to T₃ peripherally.2. PTU may have faster OA.*PTU is preferred in pregnancy because methimazole may be associated w/ congenital skin defect ( NOT sufficiently supported & has been used in pregnancy without deleterious effects).*Both can be used safely in pregnancy*PTU is preferred in lactation because insignificant amounts are secreted in the breast milk. *Generally, Methimazole is the thioamide of choice EXCEPT in the situations mentioned above where PTU is preferred , or if the patient cannot tolerate methimazole.

• No IV preparations of thioamides.• It usually takes 6-8wks before SxS subside & TH

normalize.• Initial dose:

Methimazole 30-40 mg/d orallyor PTU 300-400mg/d in 3-4 divided doses.Tapering down dose only after SxS subside:**Initial dose is reduced gradually by 1/3 each month

until daily M.D. of 5-15mg methimazole or 50-150mg PTU is reached.

• Baseline FT₄ & WBC count w/ differ. should be done before thioamides are started because agranulocytosis can be induced by thioamides & also hyperthyroidism is associated w/ relative reduction of neutrophils.

• FT₄ or FT₄I & TSH should be monitored routinely @ 4-8 wks after starting Tx & after any dose change.

• Once stable thioamide M.D. is reached, TFTs should be monitored Q 2-4 or Q3-6 months.

• Recommended duration of Tx for Graves is emperic: Generally 12-18 months.

• 12 months is the minimum Tx duration recommended to maximize remission potential.

• Longer durations can be used if NO ADRs.• Some pts. remain in remission & others

relapse ????

• Toxic Reactions:1) Pruritic Maculopapular Skin Rash:

Most common & treated w/ antihistamines.2) Hepatatis: *If LFTs normalize w/in 3 months of dose reduction, NO need to discontinue PTU.

*If there is clinical evidence of hepatitis, D/C PTU immediately.

* Routine monitoring of LFTs is required for:1. Pts. w/ liver dz. history.

2. Hepatitis risk factors, i.e. alcoholism

3) Hypoprothrobinemia (w/ PTU):* Rare* Recovery may occur after D/C of PTU, if not start steroids.

4) Agranulocytosis (PMNs<500):*Most serious but rare.* Likely to occur during the 1st 6 wks of Tx.* Complete recovery is seen a few days to 3 wks

after D/C of thioamide. * Granulocyte colony-stimulating factor & corticosteroids may shorten the recovery period.

2) K Perchlorate:MOA: Interferes w/ Iodine binding causing discharge of non-organified iodide from the gland. *Especially useful for the short-term management of drug-induced hyperthyroidism because it is competitive inhibitor of iodide, but its antithyroid effect can be overcome by

iodine administration.*Short-term adm. (2-6wks) is well tolerated.*Limited use of chronic Tx is due to:

1) Irreversible aplastic anemia2) Nephrotic syndrome

3) Iodides:*Clinical use superseded by thioamides & beta blockers.*MOA: 1)Inhibit iodide organification (Wolf-Chaikoff).** 2)Inhibit TH release (Rapid Sx relief in 2-7d) 3)Decrease gland vascularity.*Rapid effect is beneficial for:

1. Thyroid storm2. Pts. awaiting thioamide onset

• Iodides are NOT to be given before RAI because iodides block effective RAI retention by the gland for several wks. after use.

• Iodides are given 10-14days before surgery to:1. Reduce vascularity2. Increase firmness of hyperplastic gland

to facilitate surgical removal.• Preoperatively:

Iodides+ Thioamides Comb. ( Preferred )Iodides + Beta Blockers Comb.All 3 of them could be used.

• Major S/Es of Iodides:1. Hypersensitivity reactions2. Hyperthyroidism ( from failure of Wolff-

Chaikoff block)3. Hypothyroidism ( unable to escape from

Wolf-Chaikoff)4. Chronic adm. in pregnancy

fetal goiter & asphyxation

• Advantages of Iodides:1. Simplicity2. Low cost3. Low toxicity4. No gland destruction• Limitations:1. Escape2. Tx relapse3. Allergy4. Interference w/ subsequent RAI therapy

4) Adrenergic Blockers:**Depletes or blocks the effects of TH on tissue

catecholamines Rapid symptomatic relief before thioamides, RAI, or

surgery.*Do NOT affect underlying dz.*Are NOT used as primary therapy*Propranolol Standard & most widely used (20-40mg TID or QID)

• Severe toxemia may need up to 480mg/day• Symptoms relieved by beta-blockers include:

*palpitations*tachcardia*anxiety*sweating*tremor*diarrhea*Neuromuscular manifestations

• Symptoms NOT affected by beta-blockers include:*circulating TH*Wt. loss*goiter*O₂ consumption*exophthalmos

• Beta-blockers are used as adjunct Tx w/ thioamides or RAI for: *Neonatal thyrotoxicosis*Hyperthyroidism in pregnancy *Thyroid storm*Pre-operatively

• Only used for short term in pregnancy because chronic use in pregnancy esp. 3rd trimester & lactation should be avoided due to fetal complications.

• Calcium Channel Blockers esp. Diltiazem p.o. 120mg TID or 60mg QIDmay be used as alternative to beta blockers when contraindicated, i.e. asthma or DM1

5) RAI: Radioactive Iodine)*Indicated for:1. Post-adolescent hyperthyroid patients2. Graves opthalmopathy3. Hx of thyroid surgery4. Poor surgical candidates 5. Who fail or experience thioamide toxicity6. TOC for older patients w/ cardiac dz

or those w/ TMGs (Toxic Multinodular Goiter)**I₁₃₁ isotope is the most commonly used**Absolute contraindication in pregnancy: destroys the fetal gland .

• RAI dosage is calculated using a certain formula.• RAI pts. should be pretreated w/: *thioamides to deplete the gland of the stored TH Or*beta blockers or Ca channel blockers before & after RAI to prevent exacerbations of thyrotoxicosis w/in 10-14days after RAI due to leakage of TH after RAI.*Methimazole: *preferred as pretreatment over PTU

*showed > success as preTx. *because PTU is associated w/poorer

RAI retention & higher RAI failure rates

• Resolution of hyperthyroidism is slow:• Sx improvement :by 3-6wks after RAI• Max. effect : 3-4 months after an ablative dose• Other therapies may be needed after RAI due to

delayed onset for symptomatic control.• Major concerns: *Carcinogenesis

* Leukemia * Genetic damage

which are unfounded.

• Advantages of RAI:1) Effective2) Quick3) Painless4) NontoxicMajor Complications:Hypothyroidism : Most common in the 1st year

& increases w/ time.

• Iodinated Contrast Media:(e.g. Ipodate)• Inhibits peripheral deiodination of T₄ to T₃.• Inhibits TH secretion.• Relatively non-toxic.• Useful adjuncts to thioamides in the management of:1. Severe thyrotoxicosis2. Thyroid storm3. Amiodarone-induced thyrotoxicosis4. Alternative for those allergic to thioamides in the preoperative preparation** Chronic use is not indicated because its effectiveness in reducing TH is not sustained for more than 1 month in most cases.

• Non-pharmacological Therapy:• Surgery (Thyroidectomy):• Treatment of Choice for:1. Contraindications of RAI or Thioamides.2. Large goiters causing:*cosmetic disfigurement

* resp. distress * swallowing difficulties

3. Suspected Malignancies.4. Selected children & pregnants.

• Euthyroidism produced by surgery is faster & is assoc. w/ lower relapse rates than w/ RAI or thioamides.

• Poor Surgical Candidates:1. Severe cardiac, resp., or debilitating dz.2. 3rd trimester pregnant (spontaneous labor)**Risk of recurrent thyrotoxicosis is directly proportional to amount of remnant left of the gland.

**Subtotal Thyroidectomy is preferred

• Total thyroidectomy: 1. Increases the risk of hypothyroidism

2. Prevents recurrence of hyperthroidism• Surgery pts. should be adequately prepared

w/standard combination of: 1. Thioamide2. Iodides

or 3. Beta-blockers

• Major Surg. Complication:*Hypothyroidism in the 1st 6mos-3yrsafter surg. or as late as 10yrs. after surgery. Advantages of Surgery:1. Rapid recovery2. Definitive surgical intervention3. Lack of need for the rigid dosing schedule of the thioamides Disadvantages of Surgery:1. Expense2. Need of hospitalization3. Risk of anesthesia4. Postoperative complications5.Fear of surgery

• Special Treatment Issues:1.Subclinical Hyperthyroidism:• Tx is controversial• Tx is considered for high risk pts.:

*>60y.o.*Cardiac dz.*Atrial Fibrillation*Osteoporosis

* Without risk factors: Observe & Do routine TSH monitoring

2. Exophthalmous & Ophthalmologic Complications:*Ocular Tx: symptomatic till euthyroidism occurs*Elevation of bed head for diuresis.*Protective glasses

+ Methylcellulose (lubricant)

+ Hydrocortisone drops*Avoid smoke & dust*Tape eyes during sleep to prevent corneal scarring & drying.*Systemic corticosteroids for progressive inflammatory exophthalmous & reduced visual acuity: Prednisone 60-120mg/d in divided doses X 1-3 wks

then taper when sxs resolve over 2 wks then Discontinue.

• External orbital radiation therapy for contraindications to corticosteroids.• After euthyroidism & stable eye Sx Lid or orbital surgery for cosmetic or visual

correction

3. Atrial Fibrillation & CHF:*Hyperthyroidism or subclinical hyperthyroidism can cause or worsen A. Fibrillation & CHF which are

difficult to control until euthyroid.*Hyperthyroid pts. Resistant to Digoxin*Hypothyroid pts. Very sensitive to Digoxin* Warfarin is recommended in pts. w/

hyperthyroidism-related A.Fib, valvular dz.,& CHFdue to high risk of systemic emboli

4. Thyroid Storm:*Treatment:1. Support vital signs w/:

*Sedation*O₂*Fluids/Electrolytes*Antipyretics*Treat infection*Corticosteroids (Hydrocortisone 100-200mg I.V. Q6H)

2. Thioamides & Iodides in large doses:*PTU 200-300mg Q6H or*Methimazole 30-40mg Q6H *Iodides added 1hr after thioamides

3. Lithium used if iodides are contraindicated4. Cholestyramines may also be recommended

• Thyroid Storm cont.:4. Propranolol 20-80mg p.o. Q6H or 0.5-2mg IV or comparable

beta-blocker or Diltiazem 60-120mg p.o. TID or QID to control HR.

5. Eliminating & correcting precipitating factors.6. Removing circulating hormones by:

a. Plasmapheresisb. Exchange transfusionc. Dialysiswhen routine measures fail.

TSH is the most sensitive for diagnosis.

Hypothyroidism

• Hypothyroidism: • Caused by TH deficiency.• Characterized by slowing down of all body systems.

• Myxedema:• Exaggeration of SxS of severe prolonged hypothyroidism

preceding coma

• Myxedema Coma:• End-stage of long-standing uncorrected hypothyroidism.

• Cretinism or Congenital Hypothyroidism;• Hypothyroidism developing in the utero or in neonates

& can lead to mental & growth impairment.

• Subclinical Hypothyroidism:• Increased TSH & Normal TH usually without symptoms of hypothyroidism.

* Primary Hypothyroidism:*Failure of thyroid gland to secrete sufficient TH*Most common type

• Secondary Hypothyroidism:• Rare• Due to pituitary or hypothalamic injury.

• Treatment Goals: p.1007• More common in females• Risk Factors:1.Family hx of thyroid or autoimmune disorder2.Older age, esp. women3.Medically treated thyroid dz.Types of Hypothyroidism by cause:1. Goitrous2. Nongoitrous

1. Goitrous forms include:*Hashimotos thyroiditis: *Most common in U.S.

*Autoimmune*Drug-induced thyroiditis: *Iodides

*Lithium *Cytokines *Thiocyanate

*Dyshormogenesis: *Familial thyroid disorders from abnormalities in synthesis, delivery,

or peripheral action of TH.*Endemic thyroiditis: *Caused by Iodine deficiency during

growth years.*Subacute Thyroiditis*Multinodular Goiters (MNG)

2. Nongoitrous forms include: *Cretinism

*Idiopathic atrophy (uncommon)

*Iatrogenic causes: *2nd most common *by RAI or surgery

*Pituitary causes (uncommon)

• SxS: * Table 38.4 * Atypical in elderly

• SxS from naturally occurring hypothyroidism (Hashimoto): insidious & unnoticed x mos-yrsbefore terminal myxedema state.

• Iatrogenic Hypoth. (by RAI or Surgery):occur rapidly.

• Hypothyroid. pts. : sensitive to meds. i.e.:*Digoxin*Anesthetics*Narcotics*Sedatives-hypnotics

• Medical Tx of concurrent diseases (DM, Hyperlipidemia, Cardiac conditions): Maybe influenced

• Diagnosis: May go unnoticed• Recommended to measure TSH starting @ 35y.o. & every 5

yrs thereafter esp. in women.• Adults:

* Low FT₄I or FT₄ (T₃ may be normal) * Increased TSH• Secondary Hypothyroid:

*Low FT₄*Low TSH*Other features of pituitary or hypothalamic dz.

• Hashimoto Thyroiditis:*Antibodies present

* Low FT₄I or FT₄ (T₃ may be normal) * Increased TSH

• Therapeutic Plan: Fig. 38.4 p.1011• TH administration provides adequate replacement

therapy for Hypothyroidism & prevents progression to myxedema coma.

• Average Dose=100-150 mcg L-thyroxine QD (parallels normal TH production)

* 100-125 mcg QD in females* 125-150 mcg QD in males

• Dosing requirements depend on: age, weight, severity, cause, cardiac dz.,

hormone absorption.

• Treatment:• Pharmacotherapy:• L-thyroxine: Preparation of choice.

• Other commercial preparations (table 38.9)

• Young-healthy pt. w/ short duration dz.:Administer L-thyroxine 100-150mcg QD(1.6-1.7mcg/kg/d)

• Dose can be adjusted using SxS & lab values@ steady-state (after 6-8 wks of Tx)

• Older pts.= 50-100 mcg QD• Old w. Cardiovascular Dz.= 25 mcg QD

• Lower doses are sufficient for hypothyroidism caused by RAI or surgery than with spontaneous hypothyroidism.

• Pregnancy: Increase the pre-pregnancy dose of L-thyroxine by 20-30% in 1st or 2nd trimester.

*Malabsorption by SBS or coadministration w/ several meds.(tab.38.10)Reduces thyroxine

absorption *Improvement in typical SxS should be seen after 3-4 wks of Tx.*Wt., skin, hair, voice changes: May NOT reverse for months despite normal TFTs. *TSH & FT₄ : Should be evaluated @ SS

(after 2-3 mos. of daily dosing)*Changes in TSH lag behind changes in TH. Therefore, TSH & T₄ should be checked NOT earlier than 4 wks after starting Tx. *Once dose is established: Evaluate Tx @ yearly intervals

• Avoid over-replacement to avoid hyperthyroidism which can increase the risk of: * osteoporosis

* Bone loss* Cardiac arrhythmias

1. L-thyroxine (T₄) whose t⅟₂=7days: The most popular of the 8 commercial preparations because of:1. Potency2. Cost-effectiveness3. Lack of foreign protein antigenicity4. Ease of dosing

2) T₃ (t ⅟₂=1.5d): * May be used for short-term replacement.*NOT recommended for routine Tx due to its:

1. Cardiotoxic effect2. Multiple daily dosing3. Greater difficulty in monitoring therapeutic

& toxic responses.4. High cost

3) T₃+T₄ Combination:• Needs to be further investigated

4) Dessicated Thyroid from Animals: • Considered obsolete although inexpensive

due to allergic reactions & abnormal TFTs.

• Special Treatment Issues:1. Congenital Hypothyroidism:*The earlier the Tx begins, the better the prognosis of mental & growth development.*DOC: L-thyroxine*Infants w/ long standing & severe myxedema: Extremely sensitive to minute doses of TH*Start w/ very small doses (tab.38.11) to prevent toxicity.* TSH should normalize after 3-4months of starting Tx.

2) Subclinical Hypothyroidism:*Treatment: Debatable

*Not all cases progress to hypothyroidism: Higher TSH elevation , greater risk *Risk is greatest w/ TSH > 10mIU/L

*Decision to treat is based on:1. Risk vs. benefit of Tx2. Likelihood of overt hypothyroid (hx RAI or surgery)3. Degree of TSH elevation4. Hx of thyroid dz.

3) Myxedema Coma:a. Hormone replacement +b. Supportive measures

+c. Eliminate or correct precipitating factors

a. Hormone Replacement:• L-thyroxine: Large IV dose (400-600mcg)

then M.D. 50-100 mcg IV QD until p.o. is possible.

• Hydrcortisone: 50-100mg IV Q6H:To prevent adrenal crisis in case of undetectedhypopituitarism exists.

b. Supportive Measures:1. Assisted ventilation2. Glucose infusion for hypoglycemia3. Fluid restriction due to hyponatremia4. Plasma expanders for shock & circulatory

collapse **Heating blankets: NOT recommended because it can aggrevate shock

by vasodilation.c. Eliminate or Correct Precipitating Factors

** If properly treated, Recovery can occur w/in 24 hrs.