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Thyrotoxicosis and myxedema-Anesthetic implications

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Thyrotoxicosis and Myxedema - Clinical features, Diagnosis, Treatment , Anesthetic MAnagement, Complications.

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Thyrotoxicosis and myxedema-Anesthetic implications

  1. 1. Thyrotoxicosis and Myxedema -Preoperative preparation and Intraoperative complications and Management R.Srihari
  2. 2. Topics for Discussion • Thyrotoxicosis: – Etiology – Signs and Symptoms – Diagnosis – Treatment – Management of Anesthesia – Thyroid Storm • Myxedema: – Etiology – Signs and Symptoms – Diagnosis – Treatment – Management of Anesthesia – Myxedema Coma
  3. 3. Thyrotoxicosis • Introduction – Thyrotoxicosis: • State of thyroid hormone excess – Hyperthyroidism: • State of excessive thyroid function • Major etiologies of thyrotoxicosis are hyperthyroidism caused by primary and secondary causes
  4. 4. Etiology • Thyotoxicosis caused by hyperthyroidism: – Graves Disease – Toxic MNG – Toxic adenoma – Struma ovari – TSH secreting pituitary adenoma – Chorionic gonadotropin secreting tumours – Iodine overdose • Thyrotoxicosis caused by hypothyroidism: – Drug induced thyroiditis – Subacute thyroiditis
  5. 5. Clinical Manifestations • Symptoms: – Hyperactivtity and Irritability – Palpitations – Fatigue and Weakness – Weight loss with increased appetite – Diarrhoea – Polyuria – Oligomenorrhoea with loss of libido • Signs: – Tachycardia – Atrial Fibrillation – Tremors – Goitre – Warm, moist skin – Muscle weakness – Proximal myopathy – Lid retraction – Cardiomyopathy (severe)
  6. 6. • Graves’ Disease: – Associated with Graves’ ophthalmopathy and dermopathy – Graves’ Ophthalmopathy: • Dalrymple sign • Von Grafe sign • Joffroy sign • Moebius sign
  7. 7. • NO SPECS scheme – acronym derived from following eye changes: – N – no changes – O – only signs, no symptoms (lid retraction/lag) – S – Soft tissue involvement (Periorbital edema) – P – Proptosis (>22m) – E – Extraocular muscle involvement (diplopia) – C – Corneal involvement – S – Slight loss
  8. 8. – Thyroid dermopathy: • Almost always seen with Graves ophthalmopathy • Overall incidence < 5% • Although most frequent over anterior and lateral aspects of lower leg( aka pretibial myxedema) Skin changes can occur at any site esp. after trauma • Typical lesion – non inflamed, indurated plaque with deep purple/pink color and orange skin appearance – Thyroid acropachy: • Clubbing seen in Thyrotoxicosis pt (<1%) – strongly a/w Thyroid dermopathy
  9. 9. • Investigations: – CBC Microcytic anemia with thrombocytopenia – ECHO/Ecg if cardiac symptoms + – S. Creatinine (if patient more 60 yrs) – IDL  to r/o pre-existing vocal cord palsy – CT scan of neck – Flow volume loop – Thyroid function tests
  10. 10. Treatment • Hyperthyroidism of Graves’ Disease is treated by decreasing thyroid hormone synthesis – Using antithyroid drugs OR – Reducing the amount of thyroid tissue OR – Thyroidectomy
  11. 11. • Antithyroid drugs: – Main drugs  Thionamides PTU/Carbimazole/Methimazole Act by inhibiting TPO  decreasing oxidation and organification Decreasing Antithyroid antibody levels PTU also inhibits T4T3
  12. 12. • Carbimazole/ Methimazole : – 10-20 mg Q8h-Q12h initially  once euthyroid 10-20mg OD  Duration of action- 6 hours • PTU: – 100-200mg Q6h-Q8h dose decreased as thyrotoxicosis improves • TFTs and clinical manifestation are reviewed 3-4 weeks after starting treatment • Euthyroid state seen 6-8 weeks following therapy • Remission rates seen after 18-24 months following therapy
  13. 13. • Common side effects of anti-thyroid drugs: – Rash – Urtacaria  May resolve spontaneously – Fever or substituting with alternatives – Arthralgia • Rare but major side effects: – Hepatitis – SLE like vasculitis – Agranulocytosis  confirmed with complete blood count
  14. 14. • Propanolol: – 20-40 mg Q6h – Helps to control adrenergic symptoms especially in early stages brfore antithyroid drugs take effect – Alternatives: atenolol • Sodium ipodate/ iopanoic acid: – 500mg- 3g OD – Mainly used in adequate response to treatment/relapse – Progressive destruction of thyroid cells and can be used as initial treatment or for relapses after a trial of antithyroid drugs – Pregnancy: Contraindicated
  15. 15. – Iodine in high concentration inhibit release of hormones from hyperfunctioning gland  effect occurs immediately but lasts only for several weeks Hence preserved for preserved for • preparing hyperthyroid patients for surgery • Management of patients with thyrocardiac disease – High concentrations of iodide reduce all phases of thyroid synthesis and release  result in decreased gland size and vascularity – Admininistered orally as SSKI  3 drops Q8h  10-14 days
  16. 16. • Surgery: – Indicated only after patient returns to euthyroid state  Anithyroid drugs should be continued – Anticoagulants/ Coumarins: • Used if Atrial fibrillation present
  17. 17. Management of Anesthesia • Preparation : – Extremely important – For elective surgery  all patients should be made euthyroid with course of antithyroid drugs for 6-8 weeks preoperatively • Low TSH levels should not be a contraindication to surgery – TSH levels remain suppressed from prolonged hyperthyroidism in patients who have normalised T3 and T4 levels • SSKI – given 7-14 days prior to Sx • Beta blockers to control heart rate perioperatively
  18. 18. – For emergency surgery: • Antithyroid drug should be administered even though it has limited effect if taken less than 2 weeks • Antithyroid drugs should preceed iodide by 2-3 hours • IV beta blockers (Esmolol -0.5mg/kg  infusion  0.03-0.3mg/kg/min) • Sodium ipodate 500mg BD • Dexamethasone – 2mg q6h • Euthyroid state usually achieved in 5-7 days
  19. 19. • Preoperative Preparation: – Premedication: Barbiturates/BZDs/Narcotics NO ATROPINE – Monitoring: • SpO2, BP, HR,eTCO2 and temperature • IBP  in patients with uncontrolled thyroid condition • Central line  if large amounts of blood loss anticipated
  20. 20. • Induction: – Thiopentone –preferred – Ketamine –avoided – Propofol- large doses to be given • Muscle relaxants: the following can be used safely – SCh – Rocuronium – Vecuronium
  21. 21. • Maintenance of anesthesia: – Should be kept in deeper plane of anesthesia – MAC not affected – Isoflurane and Sevoflurane- ideal with N20 + O2 • Agents to correct hypotension: – IVF – Phenylephrine • Eye protection- very important • Reversal of anesthesia: – Glyco + Neostigmine
  22. 22. • Removal of thyrotoxic gland  does not mean immediate resolution of thyrotoxicosis – T1/2 of T4 7-8 days – Hence beta blocker therapy may be need to be continued post-operative period – Antithyroid drug therapy can be discontinued
  23. 23. Thyroid Storm • Introduction : – Most serious compication of hyperthyroidism with mortality ranging from 10-75% of hospitalised patients – Most common in patients with poorly controlled Graves’ Disease – Clinical diagnosis  acute disruption of the normal steady state of circulating hormones
  24. 24. • Precipitating Factors: – Infection/Sepsis – Withdrawal of anti-thyroid drugs – Surgery/Trauma – Parturition – DKA – Iodinated contrast dyes – Hypoglycemia – Excessive manipulation of thyroid gland – Burns
  25. 25. • Clinical features: – Fever + Tachycardia  Most common – Fever: Most characteristic  >41 C – CVS: • Tachycardia • Atrial fibrillation, Ventricular arrhytmias • Heart failure • Hypertension with wide pulse pressure(early), Hypotension (late)
  26. 26. • Neuromuscular: – Tremors – Encepalopathy – Weakness Can progress to CVA/ Status epilepticus/Thyrotoxic myopathy/Rhabdomyolysis • GI: – Nausea/ Vomiting/ Diarhoea – Jaundice (indicated hepatocellular injury- poor prognosis) • Respiratory – Dyspnea – Increased eTCO2 and O2 consumption  Aggravated with pulmonary oedema/ respiratory muscle weakness and tracheal obstruction from goitre
  27. 27. • Lab testing: – Increased FT3/FT4 – Hyperglycemia – Leucocytosis – Abnormal LFT – Reduced K/Mg ; Increased Ca inc bone resorption
  28. 28. • Management: – Treatment aimed at: • Control and relief of adrenergic symptoms • Control of thyroid function abnormality • Stopping Precipitating factor • Investigation and treatment of underlying thyroid disease • Supportive measures
  29. 29. • Beta blockers: – Mainstay of controlling adrenergic symptoms – IV propanolol – 0.5-1mg increments over 10 minutes while monitoring CV response decreases sympathetic hyperactivity + Inhibits conversion of T4 T3 + Concurrent administration of enteral propanolol with doses of 60-120mg Q4h to Q6h to enhance elimination during thyroid crisis – Esmolol  loading dose -250-500 mcg/kg  infusion  50-100mcg/kg/min  allows titration with minimal side effects
  30. 30. – Thionamides: • These drugs block de novo synthesis of thyroid hormones within 1-2 hours of administration  But no effect on release of preformed Glandular store of Thyroid Hormone • PTU- Drug of choice – 200mg Q4h • Methimazole -100mg stat foll by 20mg Q8h – Iodine: • Release of glandular store of thyroid hormone inhibited by administering Iodine/Lithium • Should be given only after Thionamides given after 1 hour or it will exacerbate Storm • SSKI -10 drops Q8h (8mg iodide/iodine per drop)
  31. 31. – Amidarone: • Blocks peripheral conversion of T4  T3 + Decreased concentration of T3 induced adrenoceptors in cardiac myocytes – Bile acid sequesterants: • Thyroid hormone are metabolised in the liver  where they are conjugated with glucoronide and sulfate excreted in bile which are reabsorbed in intestine • Cholestyramine(4g Q6h) interferes the thyroid hormone reabsorption in enterohepatic circulation
  32. 32. • Steroids: – Decrease T4 T3 conversion – Modulate auto-immune process during Thyroid crises – Inj. Hydrocortisone 100mg Q8h or Inj. Dexa 4mg iv Q6h – Supportive therapy: • Fluid management • Nutrition • Drug therapy salicylates and Frusemide AVOIDED • Precipitating factors • Plasmapheresis  LAST RESORT
  33. 33. Myxedema • Etiology: – Primary: • Iodine Deficiency • Hasimoto’s • Iatrogenic- !odine 131 deficiency/ Total thyroidectomy • Drugs: Iodine excess/ Amiodarone/ Antothyroid drugs • Infiltrative disorders: Amyloidosis/ Sarcoidosis – Secondary: • Hypopituitarism • Isolated TSH deficiency
  34. 34. Clinical Manifestations • Symptoms: – Tiredness, weakness – Dry skin – Feeling cold – Difficulty concentrating/poor memory – Constipation – Weight gain with poor appetite – Dypnea – Hoarseness of voice – Menorrhagia – Hearing Loss • Signs: – Dry coarse skin – Cool peripheral extremities – Puffy face,palms – Diffuse alopecia – Peripheral edema – Carpal tunnel syndrome – Delayed tendon reflexes – Myocardial contractility + decreased PR  decreased Stroke volume and bradycardia with increased peripheral vascular resistance
  35. 35. – Non-pitting edema: seen due to accumulation of hydrophilic mucopolysaccharides in dermis and other areas : • Tongue • Vocal cords – hoarseness of voice
  36. 36. Investigations – Findings in Hypothyroidism: • Thyroid function test • Increased CPK • Elevated cholesterol and triglycerides • Macrocytic anemia • Adynamic ileus • ECG: low amplitude P wave and QRS complexes + flattened/ inverted T waves + Sinus bradycardia
  37. 37. Treatment – L-thyroxine- given for treatment of hypothyroidism consistent potency, reliably restores levels of T4 and T3 to normal and has prolonged duration of action – Gradual onset with half life of 7-8 days – If no residual thyroid function, daily replacement dose  1.6mcg/kg (~100-150mcg/day) – In patients who develop hypothyroidism after treatment of Graves’ Disease necessary to replace with 75- 125mcg/day
  38. 38. • Adults <60 years without evidence of heart disease may be started on 50-100 mcg/day daily  Dose is adjusted on basis of TSH levels goal of treatment being normal TSH / less than normal TSH responses are gradual and should be measured at 2 months after instituting therapy or after any subsequent change in levothyroxine dosage
  39. 39. • Clinical effects  after initiation of therapy are slow to appear  Pts may not experience full relief from symptoms 3-6 months after TSH is normal • Adjustments is made in 12.5 to 25 mcg increments if TSH is high • Once full replacement is obtained and TSH stable- follow up – yearly • Important component of therapy Compliance to Rx
  40. 40. • For elderly or those with CAD starting dose of 25 mcg/kg  increasing monthly by 25 mcg till euthyroidism is achieved • Patients with hypothyroid cardiomyopathy improvement in cardiac function in 2-4 months on 100mcg /day of L-thyroxine • Subclinical hypothyroidism treatment started only if – TSH increased persistently for 3 months – TSH>10 mU/l – If TPO Ab+ve
  41. 41. Management of Anesthesia • Preoperative Issues: – Patients with overt hypothyoidism should be treated prior to elective surgery – In emergency , if Surgery can be delayed for 24-48 hours  iv T3 can be given (peak action-24-38 hours) – Because of increased adrenocortical insufficiency + decreased hormone response to stress  hypothyroid patients should receive hydrocortisone cover during periods of increased surgical stress
  42. 42. – Hypothyroid patients may be at increased risk when receiving either general or regional anesthesia: • Airway compromise secondary to swollen oral cavity with large tongue • Edematous vocal cords • Goitrous enlargement • Decreased gastric emptying increasing risk of regurgitation and aspiration
  43. 43. • Hypodynamic cardiovascular system: – Low cardiac output/ Stroke volume/ heart rate/ baroreceptor reflexes and intravascular volume Compromised by surgical stress and cardiac depressant anesthetic agents – Hypothermia occurs quickly and is difficult to prevent and treat
  44. 44. – Hematological and Metabolic abnormalities: • Anemia • Platelet and coagulation factor abnormalities • Hypoglycemia • Hyponatremia – Increased sensitivity to volatiles dec CO – PATIENTS WITH SUBCLINICAL HYPOTHYROIDISM DO NOT PRESENT ANY ANESTHETIC PROBLEM
  45. 45. • If pt is planned for emergency surgery – Increased risk of cardiovascular instability intraoperatively – Myxedema coma postoperatively • Preoperative Sedation: – Contraindicated in hypothyroid patients for elective surgery  increased sensitivity to sedative drugs
  46. 46. • REGIONAL ANESTHESIA IS RECOMMENDED WHERE THERE ARE NO CONTRAINDICATIONS • Monitoring: – Routine – Swan-Ganz  if severe hemodynamic impairment with TEE -> to assess intravascular volume • IVF of choice  DNS
  47. 47. – Induction agents: • Ketamine • Barbiturates and BZDs – in titrated doses – Muscle relaxants: • Sch • Intermediate NDMR: Vecuronium and Rocuronium – Opioids: • Short acting  fentanyl and its derivatives
  48. 48. – Maintenance: • N20:O2 + Volatiles  carefully used esp. in hypovolemia  blunted barorecptor response – Intraop monitoring: • Temperature • Electrolyte and Fluid status • Invasive monitors in patients undergoing major surgery • Peripheral nerve stimulator – Warming: very important
  49. 49. – Exaggerated hypotension: • Common and should be treated with judicious fluid and inotropes and vasopressors – Ephredrine – Dopamine – Epinephrine • NO PURE ALPHA 1 AGONIST • IF unresponsive  steroids should be given
  50. 50. • Ventilation: – Should be controlled – not spontaneous As hypoventilation seen due to increased sensitivity to anesthetic drugs Delayed recovery is common and postoperative ventilation may be required
  51. 51. Myxedema Coma • Introduction: – Myxedema coma extreme manifestation of hypothyroidism  although rare Mortality  30-50% – Term  misnomer – Condition considered in patients presenting with reduced level of consciousness with hypothermia – Most common in elderly women with long standing undiagnosed or undertreated hypothyroidism, in whom an additional significant stress is experienced
  52. 52. – Precipitating Factors: • Infections • Cold environment • Burns • Stroke • Surgery • Trauma • CHF • Co2 retension
  53. 53. – Clinical manifestation: • Decreased mental status • Hypothermia • Clinical features of hypothyroidism – CVS – RS – Airway – GI – Metabolic – Though TBW is increased intravascular volume decreased
  54. 54. • Treatment: – Mainstay of Rx: • Thyroid replacement therapy • Steroid replacement • Supportive measures
  55. 55. – Thyroid Replacement Therapy: • All patients with suspected myxedema coma should receive presumptive treatment with thyroid hormones • Severity of clinical presentation does not correlate with doses of replacement hormone required – Rapid replacement: a/w life threatening myocardial ischemia and arrhythmias – Delayed replacement: exposes prolonged risk of complication from crises
  56. 56. – Loading doses  200-400 mcg iv  saturates binding proteins Followed by 50-100 mcg daily till conversion – Steroid replacement: • Corticosteroids  important part of treatment as relative/ absolute hypoadrenalism may occur concurrent with hypothyroid disease • Inj. Hydrocortisone 100mg iv Q8h (or) Inj. Dexa 4mg iv Q6h  S.Cortisol level should be collected prior to starting therapy (Inj. Hydrocortisone)  if normal ..Rx stopped
  57. 57. – Supportive Treatment: • Hypothermia  warming where possible • Cardiac output monitoring  guide fluid therapy • Hyponatremia  reversible with thyroxine treatment  If severe - fluid restriction + Hypertonic saline • Hypoglycemia 25% Dextrose via central venous line • Precipitating factor should be corrected • DVT prophyllaxis • Ulcer prophyllaxis • Mechanical ventilation
  58. 58. Thank you

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