Hypo & hyperthyriodism

HYPER- & HYPOTHYROIDISM WHAT YOU NEED TO KNOW

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BAD PUNS FOR MARDI GRAS

• Practice safe eating – always use condiments.

• Remember that dancing cheek to cheek is really a form of floor play.

• Condoms should be used on every conceivable occasion.

• A hangover is the wrath of grapes.


OVERVIEW

• Review of thyroid physiology

• Definition of thyroid functional states

• Hypothyroidism - anesthetic concerns• Hyperthyroidism - anesthetic concerns

• Case presentation


THYROID HORMONES

• T4 – inactive (prohormone)– 3,5,3’,5’-tetraiodothyronine (thyroxine)

– t1/2 - 6 days

– metabolized by deiodinases to T3 or rT3

• T3 - active– 5’-deiodinase -> 3,5,3’-triiodothryonine

– t1/2 - 0.05 days

• rT3 - inactive– 5-deiodinase -> 3,3’,5’-triiodothyronine


NEW INFORMATION

• T3 ONLY ACTIVE HORMONE

• CONSEQUENCE– ONE KEY TO TREATING THYROID STORM

IS TO BLOCK CONVERSION OF T4 TO T3


HYPOTHALAMIC-PITUITARY- THYROID AXIS

• Hypothalamus– thyrotropin-releasing hormone (TRH)

• Anterior Pituitary– thyroid stimulating hormone (TSH, thyrotropin)

• Thyroid– actively concentrates iodide from blood

– synthesis of T4:T3 = 14:1

• T3 (-) feedback loop


T3 (-) FEEDBACK LOOP

• Source of T3

– 20% from thyroid gland

– 80% from peripheral conversion of T4 to T3

• T3 receptors in cell nuclei

– In hypothalamus, stops release of TRH– In anterior pituitary, stops release of TSH


CLINICAL EFFECTS OF T3

• Increases metabolism & temperature

• Sensitizes β-adrenergic receptors, magnifies the effect of their stimulation

• Increases contractility, ejection fraction, heart rate, diastolic relaxation, venous return, cardiac output.

• Decreases afterload


NEW INFORMATION

• SYMPATHETIC NERVOUS SYSTEM IS NOT “REVVED UP” IN HYPERTHYROID PATIENTS– SYMPATHETIC NERVE ACTIVITY &

CATECHOLAMINE LEVELS ACTUALLY REDUCED

∀ β-ADRENERGIC RECEPTOR NUMBERS AND SENSITIVITY MARKEDLY INCREASED– THUS β-BLOCKERS ARE ONE KEY TO

TREATMENT OF HYPERTHYROIDISM


THYROID FUNCTIONAL STATES

Symptoms TSH (mIU/L) free T4

Overt hypothyroid yes > 10.0 decreased

Subclinical hypothyroid no 4.5-10.0 normal

Euthyroid no 0.45-4.5 normal

Subclinical hyperthyroid no 0.1-0.45 normal

Thyrotoxicosis yes < 0.10 increased


MEDICAL THERAPY FOR HYPOTHYROIDISM

• SUBCLINICAL HYPOTHYROIDISM– TSH 4.5-10, normal FT4 – observe

• SUBCLINICAL HYPOTHYROIDISM– TSH > 10, normal FT4 – (±) thyroxine po

• Thyroxine may trigger angina in patients with CAD

• Untreated 5%/yr progress to overt hypothyroidism

• OVERT HYPOTHYROIDISM– TSH > 10, decreased FT4 – thyroxine po

• MYXEDEMA COMA– Levothyroxine 500 µg iv (because poor GI absorption)

– Hydrocortisone hemisuccinate 100 mg ivwww.freelivedoctor.com

OVERT HYPOTHYROIDISM – 1Easy to overlook diagnosis.

You may be the first to suggest it.

• Carpal tunnel syndrome– Nocturnal paresthesias– Pain in median nerve distribution

• May first manifest postop with fluid retention

• Ataxia and falls– Also consider normal pressure hydrocephalus

• New onset of sleep apnea


OVERT HYPOTHYROIDISM – 2Easy to overlook diagnosis.

You may be the first to suggest it.

• Myopathy– Proximal muscle pain & stiffness

• Increased muscle volume, slowed contraction

– DDx: statin-induced myopathy

• Pericardial effusion– 30-50% of patients with overt hypothyroidism

• Diastolic hypertension– 1% of all patients with are hypothyroid


MYXEDEMA COMA

• Rare syndrome in severe untreated hypothyroid– > 60 yrs old, lethargy, progressive weakness,

hyporeflexia, stupor, hypothermia, bradycardia, cardiovascular collapse, coma

– Hyponatremia, elevated CPK– Mortality untreated is 80%

• Precipitated by– Cold environment, UTI, drugs (opioids, sedatives,

anesthetics), pulmonary infection, CVA, and CHF


HYPOTHYROIDISM – ANESTHETIC CONSIDERATIONS

• Usually nothing major unless significant pericardial effusion or severely hypothyroid (hyporeflexic)

• Lower doses of anesthetic agents (?)

• Symptomatic therapy - maintain normothermia


HYPOTHYROIDISM – ANESTHETIC CONSIDERATIONS

• Minimize fluid administration - prone to CHF

• Diminished response to β-adrenergic receptor stimulation used to treat CHF, bradycardia

• Tracheomalacia if large goiter removed

• Rare to trigger myxedema coma


MEDICAL THERAPY FOR HYPERTHYROIDISM

• SUBCLINICAL HYPERTHYROIDISM– TSH 0.1-0.45, normal FT4

• OBSERVE (YOUNGER) VS TREAT (OLDER)• ATRIAL FIBBRILLATION MORE LIKELY IN OLDER

• SUBCLINICAL HYPERTHYROIDISM– TSH < 0.1, normal FT4 - -BLOCKERS

– Untreated 1%/yr progress to thyrotoxicosis

• THYROTOXICOSIS– TSH < 0.1, elevated FT4 - -BLOCKERS + PTU

• THYROID STORMwww.freelivedoctor.com

TREATMENT OF THYROTOXICOSIS

• INHIBITION OF T4 SYNTHESIS

– Propylthiouracil (PTU) or methimazole• INHIBITION OF T4 SECRETION

– Iodide, sodium iopanoate • BLOCK CONVERSION OF T4 TO T3

�β-blockers, PTU, amiodarone• BLOCK PERIPHERAL ACTIONS OF T3

� β-blockers• SUPPORTIVE THERAPY


THYROID STORM - 1

• EXAGGERATION OF SIGNS OF THYROTOXICOSIS

• NO CHANGE IN SERUM FREE T3 LEVELS

• MANIFESTATIONS– Tachycardia out of proportion to fever

– CNS signs: confusion, apathy, coma• “jittery”, “zombie”, “different”, “on something”


THYROID STORM - 2

• TRIGGERED BY– Palpation of gland during surgery– Emotional stress– Iodine/iodide administration (without prior PTU)

• WHEN & IN WHOM?– Frequently occurs in PACU (DDx: MH)– Occurs in patients treated only with β-blockers or

with β-blockers & inadequate PTU– I COULD FIND NO EVIDENCE THAT THYROID

STORM HAS BEEN TRIGGERED IN PATIENTS WITH SUBCLINICAL HYPOTHYROIDISM


CASE PRESENTATION - 1

• 33-yr-old woman presents to PCP– Headaches, palpitations,

dizziness,diarrhea,severe mood swings– Initial worry was substance abuse– II-III/VI systolic pulmonic flow murmur– ECG:

• 147 bpm (sinus tachycardia), APCs• LVH (voltage criteria)

– TSH < 0.1, markedly elevated free T4 & T3



• Initial Treatment– PTU 200 mg po tid– propanolol 60 mg po tid

– discharged on day 4 when HR < 100 bpm– Plan was to stabilize and give radioactive

iodine



• Readmitted <1 month later– non-compliant (common if severe)– emotionally labile (concern re storm)

– HR 142 bpm (sinus tachycardia)– scheduled for surgery



• Pharmacologic preparation for surgery– PTU & propranolol as before– dexamethasone

– SSKI• supersaturated solution of potassium iodide



• Holding area presentation (day 4)– HR 98-115 bpm (sinus tachycardia)– BP 112/78

– “jittery”– Adequately prepared?

• Morning PTU? Yes, but over 4 hrs earlier• Additional PTU? In retrospect, yes!



• In OR prior to induction– Wt 50 kg– Exophthalmos mild at best

• Lacrilube + “two hands”

– BP 121/81, HR 123 (sinus tachycardia)– Adequately prepared ?

• Cancel? We did not, but…?– Believe I would have if older patient

• Administer β-blockers? Yes



• Prior to incision– Thiopental 1 gm– Fentanyl 500 mcg

– Lidocaine 100 mg– Rocuronium 50 mg– Propanolol 18 mg– Desflurane– BP 105/68, HR 103



• Incision BP 130/78, HR 128– Esmolol infusion

• 320 mg over 10 min (very aggressive!)

• HR 116• SBP 60-70 mmHg



• SBP 60-70 mmHg– Esmolol off– Treat or allow to effect of esmolol to dissipate?

• Pulse oximeter – tracing not as strong as before• ECG – no ectopy• PETCO2 38 -> 21• Treat immediately ( 1 of above abnormal)

– Decreased cardiac output• Air embolism (no change in heart murmur) vs cardiac

depression• Epinephrine (to restore BP, counter act esmolol)• Phenylephrine to maintain BP



• Extubate at end of procedure?– Tracheomalacia? No,usually not issue unless

large goiter.– Prolonged emergence from increased dose of

agents? No– Reverse with neostigmine but reduced dose

of glycopyrrolate? Avoided issue.• T4/T1 = 1, tetanus - no fade• No reversal agent given

– Extubated uneventfully



• PACU– Admission

• HR 100, BP 105/78

• Sleepy but arousable to obey commands

– 40 min later• HR 148• Acting like a “zombie”

• Thyroid storm


Hypo & hyperthyriodism

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