HYPER- & HYPOTHYROIDISM

WHAT YOU NEED TO KNOW

Raymond C. Roy, Ph.D., M.D.

Professor & Chair of Anesthesiology
Wake Forest University Baptist Medical Center
Winston-Salem, North Carolina 27157-1009
rroy@wfubmc.edu
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 -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
 -ADRENERGIC RECEPTOR NUMBERS AND
SENSITIVITY MARKEDLY INCREASED
– THUS -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 g iv (because poor GI absorption)
– Hydrocortisone hemisuccinate 100 mg iv
OVERT HYPOTHYROIDISM – 1
Easy 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 – 2
Easy 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 -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 STORM
 TREATMENT OF THYROTOXICOSIS

• INHIBITION OF T4 SYNTHESIS
– Propylthiouracil (PTU) or methimazole
• INHIBITION OF T4 SECRETION
– Iodide, sodium iopanoate
• BLOCK CONVERSION OF T4 TO T3
 -blockers, PTU, amiodarone
• BLOCK PERIPHERAL ACTIONS OF T3
 -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 -blockers or
with -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
 CASE PRESENTATION - 2
• 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
 CASE PRESENTATION - 3
• Readmitted <1 month later
– non-compliant (common if severe)
– emotionally labile (concern re storm)
– HR 142 bpm (sinus tachycardia)
– scheduled for surgery
 CASE PRESENTATION - 4
• Pharmacologic preparation for surgery
– PTU & propranolol as before
– dexamethasone
– SSKI
• supersaturated solution of potassium iodide
 CASE PRESENTATION - 5
• 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!
 CASE PRESENTATION - 6
• 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 -blockers? Yes
 CASE PRESENTATION - 7
• Prior to incision
– Thiopental 1 gm
– Fentanyl 500 mcg
– Lidocaine 100 mg
– Rocuronium 50 mg
– Propanolol 18 mg
– Desflurane
– BP 105/68, HR 103
 CASE PRESENTATION - 8
• Incision BP 130/78, HR 128
– Esmolol infusion
• 320 mg over 10 min (very aggressive!)
• HR 116
• SBP 60-70 mmHg
 CASE PRESENTATION - 9
• 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
 CASE PRESENTATION - 10
• 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
 CASE PRESENTATION - 11
• PACU
– Admission
• HR 100, BP 105/78
• Sleepy but arousable to obey commands
– 40 min later
• HR 148
• Acting like a “zombie”
• Thyroid storm
 CASE PRESENTATION - 12
• Thyroid storm
 -blockers (propanolol, “ran out”, then
metoprolol)
– Nasogastric tube
• PTU 400 mg down NG
• Considered but did not give SSKI (no gland)
– Did not give amiodarone (to block conversion
of T4 to T3
– Storm broke 30-45 min after the PTU
 SUMMARY PEARLS
• AGGRESSIVE USE OF -BLOCKERS
NECESSARY BUT NOT SUFFICIENT
• PTU
• PTU, double usual dose before surgery
• PTU, redose if more than 3 hrs after last
dose before surgery
• PTU, in PACU if “jittery”