thyroid hypo and hyper[1]
TRANSCRIPT
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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]
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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 everyconceivable occasion.
A hangover is the wrath of grapes.
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OVERVIEW
Review of thyroid physiology
Definition of thyroid functional states Hypothyroidism - anesthetic concerns
Hyperthyroidism - anesthetic concerns
Case presentation
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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
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NEW INFORMATION
T3 ONLY ACTIVE HORMONE
CONSEQUENCE
ONE KEY TO TREATING THYROID STORMIS TO BLOCK CONVERSION OF T4 TO T3
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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
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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
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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
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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
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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
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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
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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
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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
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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
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HYPOTHYROIDISM
ANESTHETIC CONSIDERATIONS
Usually nothing major unless significant
pericardial effusion or severely hypothyroid
(hyporeflexic)
Lower doses of anesthetic agents (?)
Symptomatic therapy - maintain
normothermia
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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
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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
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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
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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
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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
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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
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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
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CASE PRESENTATION - 3
Readmitted
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CASE PRESENTATION - 4
Pharmacologic preparation for surgery
PTU & propranolol as before
dexamethasone SSKI
supersaturated solution of potassium iodide
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CASE PRESENTATION - 5
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!
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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
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CASE PRESENTATION - 8
Incision BP 130/78, HR 128
Esmolol infusion
320 mg over10 min (very aggressive!)
HR 116
SBP 60-70 mmHg
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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 cardiacdepression
Epinephrine (to restore BP, counter act esmolol)
Phenylephrine to maintain BP
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CASE PRESENTATION - 10
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
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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
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CASE PRESENTATION - 12
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
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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