Chris Thompson
Thyroid disease and Anaesthesia
Embryology
Endodermal invagination of epithelium from base of tongue, descends along Thyroglossal duct. By 10 weeks
can concentrate and organify Iodine.
Anatomy
15 -25 grams in weight; 2 lobes; pretracheal; isthmus at tracheal rings 2,3,4.
Close relationship with rec. laryngeal nerve.
Bloodflow very high at 5 ml/min/gm (2x kidney!) from superior (1st branch of External Carotid) and inferior
thyroid arteries
Sup. mid. and inf. veins. Lymph follows arteries.
Function
Regulation of metabolic rate by T3 and T4 ex thyroid follicular cells.
Modification of Ca2+ metabolism by Calcinonin ex Parafollicular cells.
Iodine Metabolism
Dietary intake 300-500 ug/day (if < 200 μg /day → goitre); 95% absorbed, only 10-20 μg lost in faeces.
Total body store 5,000-8,000 μg.
80 μg/day I- actively pumped (against electrical and concentration gradients) into colloid; the same amount
leaves the gland as T3 or T4.
Non-utilised I-, and I- from metabolism of T3 and T4, is excreted in the urine.
Follicle cell functions: Iodine trapping, thyroglobulin synth, T3,T4 release.
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Thyroxine Synthesis
1) Iodine oxidation: Peroxidase on colloid membrane. Essential for uptake. Blocked by high serum Iodine
levels (Wolff-Chaikoff effect), also inhibited by Perchlorate, Pertechnetate, Tc, CN-, SCN, Azides.
2) Organic Binding: MIT, DIT (Mono and di-iodotyramine). Blocked by Thiouracil, Carbimazole.
3) Oxidative coupling:
2 DIT → T4 (3,5,3',5', tetra-iodothyramine)
DIT + MIT → T3 (3,5,3',tri-iodothyramine)
4) Storage: colloid contains 23% MIT, 33% DIT, 35% T4, 7% T3 bound to thyroglobulin.
5) Release: Endocytosis of colloid, destruction of thyroglobulin and release of T3 20 μg/day and T4 80 μg/day.
6) Metabolism: Hepatic deiodination, decarboxylation, conjugation.
Control of thyroxine release
HYPOTHALAMUS
→ TRF (↑ by Cold, Emotions; ↓ by Heat, Stress)
ANTERIOR PITUITARY (Basophil cells)
→ TSH (TSH: 211 AA's, glycoprotein, t½ 60 min) (diurnal, mw 60,000)
THYROID GLAND (Adrenaline, vasopressin may act directly)
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Effects of thyroxines
20μg/day T4 is converted to T3 in cell cytoplasm - T4 is a precursor ( ↓ in severe illness, usually associated with ↑
reverse T3, which is inactive).
Throxines act by binding to specific m-RNA causing protein synthesis with the following effects:
1) CALORIGENIC effects: ↑ 02 consumption up to 2 times; ↑ C.O., ↑ BMR, basal body temp.
2) METABOLIC effects:
↑ COH absorbtion and glucose metabolism
↑ Protein and lipid metabolism; vit. deficiency
↓ serum Cholesterol
3) CNS: Irritability, agitation, insomnia.
4) CVS: Enhanced effect of catecholamines, ↑ C.O.,↑ HR, ↑ B.P.; ↑ SVR, etc.
5) Genitourinary: ↑ Menstrual flow.
6) Essential for growth and development.
Hormone assays and blood levels
In view of high protein binding, assays of total T3 or T4 are greatly affected by pregnancy, serum protein levels,
etc. High T3 strongly suggests hyperthyroidism.
Hormone Blood level Protein binding
T4 50-200 μg/l (70-270 nM/l) 99.97 % - TBG, Pre-albumin
T3 1-3 μg/l (2-5 nM/l) 99.5 % - TBG, Albumin
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T3RU: Add blood sample to resin, then add labelled T3; measure amount of labelled T3 that binds to resin. High
T3RU = few empty binding sites, suggesting hyperthyroidism or reduced protein sites. Newer tests measure T3
Plasma Uptake and are the oppposite of the old test.
FTI = T4 x T3RU(% of control) and has many subtle problems in interpretation, but looking at T4 and thinking about
protein binding is the simplest early test.
Free T3 and T4: very useful. Free T4 (10-30 pM/l) may be low in the sick euthyroid patient; T3 toxicosis will show
normal T4 in a toxic patient. FT3(3-12 pM/l).
I131 uptake: ↑ in thyotoxicosis. ↓ in hypothyroidism, T3 replacement, after iodine containing radiographic tests,
amiodarone.
TSH:
↑ in Primary hypothyroidism or inadequate replacement
↓ in Thyroid hyperfunction or pituitary hypothyroidism
Anaesthesia for Hyperthyroidism
1) Assesment:
Should be clinically euthyroid, using:
Anti-thyroid drugs orally ( takes 6 weeks)
Lugols Iodine (5% KI ) for 1-2 weeks preop or Na Iodide 500 mg IV q12h
Beta-blockers to control sympathetic nervous system
Occasionally may need alpha-blockers, steroids, sedatives, lithium, etc.
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Airway assessment should include:
ENT check of laryngeal nerves ( hoarseness, poor high pitch)
Asessment of postop airway adequacy; tomograms, CT, thoracic inlet XRays; exclusion of tracheomalacia
Selection of ETT type / size (north rae / reinforced flexible are common choices)
Hypertension, tachycardia, tremor, anxiety, fever, heat intolerance, weight loss, exophthalmos, myopathy, atrial
fibrillation, all suggest poor preoperative control.
2) Premedication:
Anxiolytic, narcotic; reassurance.
3) Choice of Anaesthesia.
Usually intubation and IPPV is used to provide airway control, decreased requirements for volatile agents, still
patient with little chance of coughing or straining.
Avoid agents which increase catecholamines like cyclo, ketamine. Halothane is relatively contraindicated if the
surgeon uses adrenaline, and also because of tendency for postop hepatic dysfunction in thyrotoxic patients.
4) Monitoring:
Detection of disconnection or cyanosis essential and difficult as patient is completely covered in drapes.
Ventilator alarm, precordial stethoscope, ETCO2, oximetry, etc should be considered.
IV, BP, ECG essential. Consider arterial line if poorly controlled.
Temperature monitoring and provision for cooling.
5) Induction:
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Aim for safe induction with potentially difficult airway - consider fibreoptic, inhalational, or awake intubation in
extreme cases. Test ventilate prior to nondepolarising relaxant or use sux+preoxygenation.
Choices for ETT - Latex/armoured/PVC/oral/nasal.
Control over cardiovascular refexes at all times - adequate depth of anaesthesia required.
6) Posture:
Head-down slightly, protect eyes and nerves, extend neck.
7) Extubation:
Check cord movements. IV lignocaine / Volatile agent + 100% O2.
Complications
1) Thyroid Storm
Classically 6-18 hours postoperatively. Signs:
Pyrexia, sweating, dehydration, hypoglycaemia, ketosis
Tachycardia, arrythmias, cardiac failure; occ. hypotension
Nausea, vomiting, diarrhoea, abdo pain
Restlessness, confusion, delerium.
Rx:
O2, cooling, IV fluids (dextrose), electrolytes, CVS monitoring + support.
Sedation, respiratory support as required.
Beta-Blockers, steroids, Na iodide (1-2 g IV/day), antithyroid drugs via NGT.
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2) Nerve Damage
a) Recurrent laryngeal.
Loss causes cord adduction, sensory loss below cords.
Unilateral: Hoarseness
Bilateral: Inspiratorystridor + airway obstruction + hoarseness
b) Superior Laryngeal.
Loss causes cricothyroid paresis + sensory defect above cords.
c) Other nerves.
Phrenic / Symp chain rarely damaged.
3) Hypocalcaemia
Usually from parathyroid damage ( direct or vascular compromise); may be transient; commonly 24-48 hours
postop. May cause stridor early.
4) Airway obstruction
Many possible causes, including:
Oedema ( laryngeal, glottic, supraglottic)
Haematoma causing external compression (usually acts via oedema )
RLN damage
Hypocalcaemia
Tracheal collapse
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Manage as for any patient with compromised upper airway.
5) Others
Tracheal laceration, pneumothorax, tracheo-oesophageal fistula.
Anaesthesia for hypothyroidism
1) Assessment
Should be Euthyroid from Thyroxine replacement titrated to clinical state (100 -200 ug/day). Look for Anaemia,
neuropathy, associated pituitary or adrenal hypofunction, cardiac failure.
Airway assessment as before - macroglosssia commmon.
Bradycardia, mental dullness, hypothermia, slow reflexes and TSH elevation suggest inadequate replacement.
Slow drug metabolism, exaggerated responses to anaesthetic agents, decreased ventilatory responses likely.
2) Premedication
? Reduced dose.
3) Choice of anaesthetic
Intubation for same reasons as before. Avoid excessive myocardial depression.
4) Monitoring
As above. Temperature monitoring important. Use warming blanket, space blanket, humidifier. CVP if cardiac
failure.
5) Posture
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Care to avoid nerve compression.
Myxoedema Coma
Rx:
Slow warming, IV dextrose, fluids, steroids, inotropic support if required.
IV T3 100 ug/litre by slow infusion ( NB 40 μg/day secreted normally; give about 10 μg hourly to a max of
about 80 μg - expect slow onset of effect)
Last updated Tuesday, April 13, 2010
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