1. J.J.M MEDICAL COLLEGE, DAVANGEREDEPT OF ANAESTHESIA CHAIR PERSONPRESENTED BY Dr. RavishankarM.D, D.A Dr. Pritam Professor Postgraduate Date – 18/02/2011 1

2. INTRODUCTION Thyrotoxicosis is defined as the state of thyroid hormone excess. Hyperthyroidism is the result of excessive thyroid function. The most common cause of hyperthyroidism being – Grave`s Disease. 2

3. CAUSES 3

4. GRAVES' DISEASE Epidemiology Its an hyper-metabolic state Accounts for 60–80% of thyrotoxicosis. Occurs in up to 2% of women but is 1/10 as frequent in men. Typically occurs between 20-50 years of age, but it also occurs in the elderly. 4

6. Duration of disease,

7. Individual susceptibility to excess thyroid hormone and

8. Patient's age. In the elderly, features of thyrotoxicosis may be subtle or masked, and patients may present mainly with fatigue and weight loss, a condition known as apathetic thyrotoxicosis. 5

9. Central nervous system manifestations Hyperactivity, nervousness & irritability  easy fatigability Insomnia & impaired concentration. Fine tremor. Hyperreflexia, muscle wasting & proximal myopathy without fasciculation. Chorea rare feature. Hypokalemicperiodic paralysis 6

10. Cardiovascular Manifestation: 7

11. Sinus tachycardia/supraventricular tachycardia palpitations The high cardiac output bounding pulse Systolic hypertension widened pulse pressure. Aortic systolic murmur Worsening of angina or heart failure Atrialfibrillation is more common in patients >50 years. 8

12. Skin & Nail Manifestations Warm and moist Sweating & Heat intolerance Palmar erythema, onycholysis, pruritus, urticaria & diffuse hyperpigmentation Hair texture fine Diffuse alopecia occurs in up to 40% of patients. 9

13. Thyroid dermopathyoccurs in <5%. Most frequent over the anterior & lateral aspects of the lower leg (hence the term pretibialmyxedema). Typical lesion noninflamed, indurated plaque with a deep pink or purple color and an "orange-skin" appearance. 10

14. Thyroid Acropachy a form of clubbing found in <1% of patients with Graves' disease. 11

15. Gastrointestinal System Transit time is decreased  increased stool frequency diarrhea/steatorrhea. Weight loss inspite of increased appetite 12

16. Reproductive system Frequent oligomenorrhea or amenorrhea; Pregnancy  low birth weight babies & pre-eclampsia. In men  impaired sexual function & rarely gynecomastia. 13

17. Skeletal System Osteopeniain long-standing cases. Mild hypercalcemia occurs in up to 20% of patients, but hypercalciuria is more common. Small increase in fracture rate. 14

18. Thyroid Usually diffusely enlarged to >2–3 times its normal size. The consistency is firm. Thrill or bruit increased vascularity of the gland and the hyperdynamic circulation. 15

19. Eye signs & symptoms Lid retraction staring appearance  sympathetic overactivity. Associated with specific eye signs that comprise Graves' ophthalmopathy. This condition is also called thyroid-associated ophthalmopathy. 16

20. The earliest manifestations of ophthalmopathy are usually a sensation of grittiness, eye discomfort & excess tearing. About 1/3 pts have proptosis, 17

21. Periorbital edema, scleral injection, & chemosis are also frequent. In 5–10% of patients, the muscle swelling is so severe that diplopia results. Most serious manifestation  compression of the optic nerve at the apex of the orbit, leading to papilledema, peripheral field defects, & if left untreated, permanent loss of vision. 18

22. The "NO SPECS" scheme is an acronym derived from the following eye changes: 0 = No signs or symptoms 1 = Only signs (lid retraction or lag), no symptoms 2 = Soft tissue involvement (periorbital edema) 3 = Proptosis (>22 mm) 4 = Extraocular muscle involvement (diplopia) 5 = Corneal involvement 6 = Sight loss 19

23. Toxic MultinodularGoiter Etiology and Pathogenesis MNG occurs in up to 12% of adults. More common in women than men and increases in prevalence with age. It is more common in iodine-deficient regions 20

24. Hyperfunctioning Solitary Nodule A solitary, autonomously functioning thyroid nodule  Toxic Adenoma. Thyrotoxicosis is usually mild. Suggested by the presence of the palpable thyroid nodule & by the absence of clinical features suggestive of Graves' disease or other causes of thyrotoxicosis. 21

25. Differences 22

26. Laboratory Evaluation Normal thyroid function tests 23

27. TSH Assay single best test of Thyroid Hormone action at cellular level. Normal level  0.4-5.0 mU/L. Subclinical hyperthyroidism  TSH level is 0.1-0.4mU/L with normal FT3 & FT4. Overt hyperthyroidism  TSH level is <0.03mU/L with increased T3 & T4. Thyroid Storm  TSH level is <0.01mU/L. Free T4 (FT4) approx 0.02% of total T4. Elevated in 90% of patients with hyperthyroidism. Decreased in 85% of patients with hypothyroidism. 24

28. T3 resin uptake test (RT3U)  Indirect measure of unbound fraction of T4. It quantitates the degree of saturation of TBG sites by T3 & T4. It is directly proportional to FT4 & inversely proportional to TBG sites. FT4 index = T4 x RT3U. Normal value- 1.4-4.9 In 2–5% of patients, only T3 is increased (T3 toxicosis). The converse state of T4 toxicosis hyperthyroidism is induced by excess iodine. 25

29. Radioactive iodine uptake  I123, I131 & Tc99 Varies directly with functional state of thyroid. 24 hr thyroid uptake is measured. Normal value range – 10-25% Used to confirm Hyperthyroidism. 26

30. TRH stimulation test  used to test pituitary function. Measurement of TPO antibodies is useful in differential diagnosis. Measurement of TBII or TSI will confirm the diagnosis but is not needed routinely. 27

31. Other tests Serum Antimicrosomal Antibodies. Antithyroglobulin antibodies. Long acting thyroid stimulators (LATS). Thyroglobulin 28

32. Ultrasonography to differentiate between cystic, mixed or solid lesion in gland. Thyroid scan using I123 or Tc99 evaluate nodules as Warm/ Normal Hot/ Hyperfunctioning. Cold/ Hypofunctioning. 29

33. In Toxic Multinodular Goiter The TSH level is low. The T4 level may be normal or minimally increased; T3 is often elevated to a greater degree than T4. Thyroid scan shows heterogeneous uptake with multiple regions of increased and decreased uptake; 24-h uptake of radioiodine may not be increased 30

34. In Toxic Adenoma A thyroid scan provides a definitive diagnostic test. Focal uptake in the hyperfunctioning nodule and diminished uptake in the remainder of the gland, as activity of the normal thyroid is suppressed. 31

35. 32

36. Diagnosis of Hyperthyroidism: Wayne’s diagnostic index 33

37. Index : < 11: Non toxic Between 11 – 19: Equivocal > 19 : Toxic 34

38. TREATMENT OF THYROTOXICOSIS Includes : Antithyroid drugs -adrenergic blockers and other antihypertensive drugs Radioactive iodine Surgery 35

39. Antithyroid drugs Indications : In children In young adults with mild thyrotoxicosis Conjugation with radioactive iodine to hasten recovery, while awaiting the effects of radiation. In pregnant women 36

40. Surgical Treatment Reserved for MNG with Severe hyperthyroidism in children Pregnant women who can’t tolerate ATD Large goiters with severe Ophthalmopathy Large MNGs with pressure symptoms Who require quick normalization of thyroid function 37

41. Radioiodine Therapy Indications Primary Thyrotoxicosis after 45yrs of age In autonomous toxic nodule In recurrent thyrotoxicosis. 38

42. Preoperative Evaluation 39

43. History History of onset, duration, rate of growth History suggestive of primary or secondary thyroid toxicity History of pain History of palpitation, precordial pain, exhaustion History of pressure effects- like dyspnoea, dysphagia, hoarseness of voice. Past history/family history. Personal history-diet, menstrual, mental attitude, sleep 40

44. General Physical Examination Built, nourishment Fullness of thyroid region, pallor, icterus, cyanosis, clubbing, oedema Temperature, Sleeping pulse rate, blood pressure Skin- hot and moist palm Tremors Mental status-anxiety, nervousness. Airway assessment 41

45. Local examination Inspection : Whether diffuse/ nodular swelling Pizzillo'smethod : in obese and short necked patient hands are placed behind head and patient is asked to push head backwards against her clasped hand. Ask the patient to swallow, thyroid slowly moves upwards on deglutition. Pemberton's sign : Patient is asked to raise both the arm over his head until they touch the ears. This is maintained for a while, congestion of face and distress becomes evident because of obstruction of great veins at thoracic inlet. 42

46. Palpation: Patient should be sit on a stool and neck slightly flexed. Lahey's Method Crile's method Kocher's test Berry's Sign 43

47. Percussion: Over manubriumsterni to exclude presence of a retrosternal goiter. Auscultation: A systolic bruit may be heard over goiter due to increased vascularity in primary toxic goiter. 44

48. Examination for toxic manifestation Exophthalmos: In early stages, may be unilateral but later may become bilateral. Stellwag's sign : Infrequent blinking of eyes with widening of palpabral fissure. Von Graefe`ssign : Upper eye lid lags behind the eye ball as the patient is asked to look downwards. 45

49. Dalrymphe's sign : Upper sclera is visible due to retraction of upper eye lid. Joffroy's sign : Absence wrinkling in the forehead on looking upwards with the face inclined downwards. Moebius sign : Inability or failure to converge the eye balls Gifford's sign: Difficulty in eversion of the upper lid. 46

50. 2. Tachycardia: Resting pulse rate should be recorded at early morning 3am & 3pm. 80-90 bpm -mild thyrotoxicosis 90-110 bpm-moderate thyrotoxicosis > 110 bpm- severe thyrotoxicosis 47

51. 3. Tremors : Finetremors in stretched hands protruded tongue and fingers are seen in primary thyrotoxicosis. 48

52. Systemic examination CVS: Enlarged heart Atrial fibrillation Signs of CCF. Systolic murmurs CNS: Myopathyand tremors Reflexes- hyperreflexia 49

53. Investigation Complete hemogram, BT, CT to rule out anaemia, thrombocytopenia and agranulocytosis. Urine Albumin, Sugar, Microscopy RBS, B. Urea, Serum creatinine Thyroid function tests. ECG- Sinus tachycardia, ST elevation, QT shortening, atrial fibrillation/flutter, ventricular ectopic 50

54. Chest X-ray PA view- position of trachea, deviation, retrosternal goiter, calcification. Lateral view and barium swallow- pressure effects on trachea and oesophagus 51

55. Flow volume loop- best indications of airway obstruction. CT scan and MRI scan-for airway evaluation and extension of thyroid. 52

56. Pre operative preparation Admission Absolute bed rest. Sedation  Diazepam 2mg-5mg-10mg. Β blockers, e.gpropranolol 40mg 1-1-1 Specific drugs, e.gCarbimazole 5mg 1 qid & then slowly reduced to 1 bd. Given for 4-6wks. 53

57. Resting pulse chart. Thyroid function tests should be done every 4wks till thyronormalcy. Thyroid steal Patient must be made euthyroid or near euthyroid at operation. Euthyroid is clinically assessed by- Sleeping pulse rate < 90/min Progressive weight gain 54

58. Disappearance of toxic symptoms like tremors, nervousness, anxiety etc . No requirement of sedation for sleep. Normal pulse pressure, sinus rhythm, disappearance of cardiac murmurs ENT check-up for mobility of cords. The last dose of ATD may be given on the evening before surgery. 55

59. Plan of Anaesthesia General anesthesia, Regional – Cervical Epidural Anesthesia. Local blocks- Cervical plexus block (b/l) 56

60. Premedication : Aim is to suppress sympathetic activity. Psychological : Reassurance to the patient. Pharmacological : T diazepam l0mg PO HS and 5mg PO in the morning or T Lorazepam 2-3mg oral 30 minsbefore operation. 57

61. Inj.Morphine 0.1 to 0.15mg/kg i.m. 30min before operation. Inj. Promethazine 25-50mg iv 30 min before operation. Premedication is avoided if airway problem is anticipated. Anti aspiration prophylaxis Anticholinergic drugs are not recommended. 58

62. Monitoring : Pulse oximetry NIBP ECG Temperature monitoring ETCO2 Neuromuscular monitoring CVP line Urine output 59

63. General Anaesthesia Wide bore IV line is secured preferably in lower limb after application of EMLA cream. 1. Pre-oxygenation: With 100% 02 for 3-5 minutes. 2. Induction. Inj. Thipentone sodium 5-7mg/kg i.v is the drug of choice. Inj. Glycopyrolate- 0.0l mg/kg i.v 60

64. Attenuation of sympathetic response to intubation by Inj. Lignocaine 1.5-2mg/kg i.v or Opioid/Esmolol infusion can be used. 3. Relaxation: InjScoline 2mg/kg  if difficult airway anticipated. InjVecuronium 0.08-0.12 mg/kg iv or Inj. Rocuronium 0.5mg/kg iv  if easy airway anticipated 61

65. When airway problem is anticipated Awake/fibreoptic intubation can be done with local anaesthesia. Intubation with gentle laryngoscopy is done with cuffed armored tube/ cuffed ETT/north pole oral tracheal tube or intubating LMA with fiber optic bronchoscopy guidance. 62

66. Patient is positioned with sand bag between the shoulder blades and the head resting on a padded horse shoe or whit lock head rest. Avoid hyperextension. 20°-25° head up tilt to aid venous drainage & to decrease BP. Arms should be secured by the side 63

67. Maintenance of Anaesthesia : Controlled ventilation is used with N20 + 02 + NDMR + inhalation agents + incremental doses of opioids. NDMR : Inj. Vecuronium 0.05 mg/kg or Ini. Atracurium 0.3 - 0.4 mg/kg or Inj. Rocuronium 0.3 - 0.4 mg/kg. 64

68. Already existing myopathy may prolong N-M blockade. Associated myosthenia gravis emphasize the need to reduce initial dose of muscle relaxation. Use of a peripheral nerve stimulator to monitor N-M blockade. Isoflurane is preferred to halothane. 65

69. Reversal and Extubation: With Inj. Neostigmine 0.05 mg/kg + Inj. Glycopyrrolate 0.01 mg/kg Inj. Xylocaine 1-1.5mg/kg IV 60-90 sec. Before extubation. A fibreoptic endoscope may be used to view the vocal cord. When adequate spontaneous respiration and laryngeal reflexes have returned the patient is extubated. 66

70. Complications of Thyroid Surgery 1. Intraoperative: Carotid sinus stimulation - bradycardia + hypotension Tachycardia Thyroid crisis Haemorrhage Air embolism 67

71. contd Tracheal injuries, Pneumothorax, Pneumomediastinum Damage to nerves. Atrial fibrillation 68

72. 2. Post operative 69

73. Thyroid storm Is a life threatening emergency Characterized by sudden appearance of clinical signs of hyperthyroidism due to the abrupt release of T4 and T3 into circulation. Mortality is as high as 25% to 30%. Commonly associated with Grave's disease. 70

74. Predisposing conditions: Medical factors : • Infection • Fever • Uncontrolled toxicity • Irregular drug intake • Pregnancy, toxemia of pregnancy • Radio iodine therapy • DKA. 71

75. Surgical factors: Anxious and nervous patient before surgery, Too much handling of gland just before surgery. This can occur both intraoperative or in the immediate post operative period, but the latter is more common between 6-18 hours post operatively. 72

76. Clinical features : Hyperthermia: rise of 2°C/hr over normal temperature Tachycardia: arrhythmias commonly atrial fibrillation Initially flushing and sweating later leading to dehydration 73

77. CCF - initially high output failure, Later may go for Low output failure. Shock - cardiogenic/hypovolemic Electrolyte imbalance Hypo/hyperglycemia may also be present. Marked anxiety, agitation, psychosis. 74

78. Differential Diagnosis Malignant hyperthermia Neuroleptic Malignant Syndrome. Pheochromocytoma 75

79. Treatment General measures : Stop manipulation Increase the FiO2 to 100%. Cooling measures : surface cooling - sponging, ice packs, decrease OT temperatures. Cold IV fluid Establishment of an indwelling arterial line to follow metabolic derangements and also to aid in diagnosis. Treat the precipitating cause. 76

80. Suppression of hormonal activity : Propylthiouracil - 600mg loading dose and 200-300mg every 6th hour given through NGT. OR Carbimazole ->50-100 mg through NGT followed by 20mg 6thhrly. Iodine as sodium iodide 1gm over 24 hours IV or enterally as potassium iodide 100-200mg every 8th hourly X-ray contrast agent sodium ipodate 1gm/day can also be used alternatively. 77

81. Suppression of sympathetic activity : 1) Propranolol1-2mg IV Antagonizes the peripheral effects of thyrotoxicosis and also inhibits peripheral conversion of T4. 2) Esmolol-> 100-300 g/kg/min 78

82. Treatment of shock and CCF : Digoxin Low out failure states. IV fluids should be given with reference to CVP line, otherwise overinfusion may further worsen CCF. IV fluids preferably to crystalloids containing glucose to supply enough energy for increased metabolism. Supplementation of corticosteroids : Hydrocortisone  100- 200mg IV 8thhrly. 79

84. Speed of injection,

85. Pressure in veins,

86. Posture and general conditionsTip of a venous catheter  advanced into the thorax  the negative intrathoracic pressures generated during spontaneous breathing drawing of air into the venous circulation  venous air embolism. 80

87. Clinical Presentation Acute onset of dyspnea during procedure. Hypotension and cardiac arrest can develop rapidly. Air can pass across a patent foramen ovale obstruct cerebral circulation  acute ischemic stroke. A characteristic “mill wheel” murmur can be heard over the right heart, but this murmur may be fleeting. 81

88. Therapeutic Maneuvers A syringe  attached to the hub of the catheter (to prevent any further air entry), & attempt should be made to aspirate air through the indwelling catheter. The patient, placed with the left side down In dire circumstances, a needle inserted through the anterior chest wall  into the right ventricle to aspirate the air. Unfortunately, in severe cases  mortality is high despite any of the suggested therapeutic maneuvers. 82

89. Nerve palsy 3 types of nerve injuries can occur Neuropraxia Axonotemesis Neurotemesis Unilateral Recurrent laryngeal nerve palsy Pt may present with In INCOMPLETE palsy only abductors are paralysed, Vocal cord assumes median position. Voice is unaffected & Pt remains asymptomatic. 83

90. In COMPLETE palsy  both abductors & adductors are paralysed, vocal cord assumes paramedian position, hoarseness of voice present, possibility of voice returning to normal if other cord compensates by crossing midline for closing glottis during phonation 84

91. Treatment Specific treatment for cause. If Asymptomatic no treatment. Hoarseness  Speech therapy Teflon paste Implantation of cartilage Arytenoidopexy Thyroplasty These procedures are attempted if paralysis has persisted for more than 9-12 mts. 85

92. Bilateral Recurrent Laryngeal Palsy Both vocal cords assume median/paramedian position. Severe inspiratory dyspnea with stridor may result if paralysis is sudden in onset 86

93. Treatment Specific treatment for cause. Intubation due to severe inspiratory stridor, replaced by tracheostomy within 2wks prevent laryngeal stenosis. Tracheostomy Arytenoidectomy Nerve –muscle transplantation. 87

94. Hypoparathyroidism Rare cause  0.5% Mainly due to vascular spasm of parathyroid glands & rarely due to accidental removal of parathyroids. Occurs in 2nd -5thpostop day. Presentation  Weakness. Chvostek`s sign +ve. Carpopedal spasm Convulsions 88

95. Treatment Depends on blood calcium level, 10ml of 10% Calcium gluconate/citrate is given 8thhrly. Later supplemented by oral Calcium 500mg 8thhrly. Drug is stopped after 3-6 wks & serum calcium level is repeated. 89

96. REFERENCES Harrisons Principle Of Internal Medicine – 17th ed. Stoeltings anesthesia & co-existing disease – 5th ed. Barash Clinical Anaesthesia - 5th ed. Millers clinical Anaesthesia – 7th ed. Yao & Artusio`s Anesthesiology – 6th ed. 90

97. 91 THANK YOU