Thyroid Hypo and Hyper[1]

8/9/2019 Thyroid Hypo and Hyper[1]

1/33

HYPER- & HYPOTHYROIDISMWHAT 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 [email protected]


2/33

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 everyconceivable occasion.

A hangover is the wrath of grapes.


3/33

OVERVIEW

Review of thyroid physiology

Definition of thyroid functional states Hypothyroidism - anesthetic concerns

Hyperthyroidism - anesthetic concerns

Case presentation


4/33

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


5/33

NEW INFORMATION

T3 ONLY ACTIVE HORMONE

CONSEQUENCE

ONE KEY TO TREATING THYROID STORMIS TO BLOCK CONVERSION OF T4 TO T3


6/33

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


7/33

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


8/33

CLINICAL EFFECTS OF T3

Increases metabolism & temperature

Sensitizes F-adrenergic receptors,

magnifies the effect of their stimulation Increases contractility, ejection fraction,

heart rate, diastolic relaxation, venous

return, cardiac output.

Decreases afterload


9/33

NEW INFORMATION

SYMPATHETIC NERVOUS SYSTEM IS NOT

REVVED UP IN HYPERTHYROID PATIENTS

SYMPATHETIC NERVE ACTIVITY &

CATECHOLAMINE LEVELS ACTUALLY REDUCED

F-ADRENERGIC RECEPTOR NUMBERS AND

SENSITIVITY MARKEDLY INCREASED

THUS F-BLOCKERS ARE ONE KEY TO

TREATMENT OF HYPERTHYROIDISM


10/33

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


11/33

MEDICAL THERAPY FOR

HYPOTHYROIDISM SUBCLINICAL HYPOTHYROIDISM

TSH 4.5 -10, normal FT4 observe

SUBCLINICAL HYPOTHYROIDISM TSH > 10, normal FT4 (s) 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 500Qg iv (because poor GI absorption)

Hydrocortisone hemisuccinate 100 mg iv


12/33

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


13/33

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


14/33

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


15/33

HYPOTHYROIDISM

ANESTHETIC CONSIDERATIONS

Usually nothing major unless significant

pericardial effusion or severely hypothyroid

(hyporeflexic)

Lower doses of anesthetic agents (?)

Symptomatic therapy - maintain

normothermia


16/33

HYPOTHYROIDISM

ANESTHETIC CONSIDERATIONS

Minimize fluid administration - prone to

CHF Diminished response to F-adrenergic

receptor stimulation used to treat CHF,

bradycardia

Tracheomalacia if large goiter removed

Rare to trigger myxedema coma


17/33

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


18/33

TREATMENT OF THYROTOXICOSIS

INHIBITION OF T4 SYNTHESIS

Propylthiouracil (PTU) or methimazole

INHIBITION OF T4 SECRETION

Iodide, sodium iopanoate

BLOCK CONVERSION OF T4 TO T3 F-blockers, PTU, amiodarone

BLOCK PERIPHERAL ACTIONS OF T3 F-blockers

SUPPORTIVE THERAPY


19/33

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


20/33

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 F-blockers or

withF-blockers & inadequate PTU I COULD FIND NO EVIDENCE THAT THYROIDSTORM HAS BEEN TRIGGERED IN PATIENTSWITH SUBCLINICAL HYPOTHYROIDISM


21/33

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


22/33


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


23/33


Readmitted


24/33


Pharmacologic preparation for surgery

PTU & propranolol as before

dexamethasone SSKI

supersaturated solution of potassium iodide


25/33


Holding area presentation (day 4)

HR 98-115 bpm (sinus tachycardia)

BP11

2/78 jittery

Adequately prepared?

Morning PTU? Yes, but over 4 hrs earlier

Additional PTU? In retrospect, yes!


26/33


27/33


Prior to incision

Thiopental 1 gm

Fentanyl 500

mcg Lidocaine 100 mg

Rocuronium 50 mg

Propanolol 18 mg

Desflurane

BP 105/68, HR 103


28/33


Incision BP 130/78, HR 128

Esmolol infusion

320 mg over10 min (very aggressive!)

HR 116

SBP 60-70 mmHg


29/33


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 cardiacdepression

Epinephrine (to restore BP, counter act esmolol)

Phenylephrine to maintain BP


30/33


Extubate at end of procedure?

Tracheomalacia? No,usually not issue unlesslarge goiter.

Prolonged emergence from increased dose ofagents? No

Reverse with neostigmine but reduced doseof glycopyrrolate? Avoided issue.

T4/T1 = 1, tetanus - no fade No reversal agent given

Extubated uneventfully


31/33


PACU

Admission

HR 100, BP 105/78

Sleepy but arousable to obey commands

40 min later

HR 148

Acting like a zombie Thyroid storm


32/33


Thyroid storm

F-blockers (propanolol, ran out, thenmetoprolol)

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


33/33

SUMMARY PEARLS

AGGRESSIVE USE OF F-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

Documents

Thyroid Hypo and Hyper[1]