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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
Function
Iodine Metabolism
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) 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) 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 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.
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
Anaesthesia for Hyperthyroidism 1) Assesment: Should be clinically euthyroid, using:
Airway assessment should include:
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: 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:
Rx:
2) Nerve Damage a) Recurrent laryngeal. Loss causes cord adduction, sensory loss below cords. Unilateral: 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:
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 Care to avoid nerve compression. Myxoedema Coma Rx:
Last updated Tuesday, December 15, 2020 |
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