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ANESTHESIA MANAGEMENT OF PATIENTS WITH COEXISTING AND ENDOCRINE DISEASES

It is a course which can help readers( anesthetists) to manage patients with coexisting and endocrine problems.

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ANESTHESIA MANAGEMENT OF PATIENTS WITH COEXISTING AND ENDOCRINE DISEASES

  1. 1. DEPARTMENT OF ANESTHESIOLOGY ANESTHESIA MANAGEMENT OF PATIENTS WITH ENDOCRINE & CO-EXISTING DISEASES By Nurhussien (BSc) in Anesthsiology
  2. 2. Course objectives • At the end of this course students will be able to: -Describe the normal physiology of thyroid, parathyroid, pancreas and adrenal glands. -Assess the sign and symptoms of thyroid, parathyroid, pancreatic and adrenal glands malfunctioning -Determine the surgical complications, treatment and anaesthesia considerations -Describe the Pathophysiology of MH, MG,Parkinsonism, Phaeochromocytoma, and ARDS. -Finally determine the anaesthesia consideration and peri opertive management of the above pathologies.
  3. 3. ANESTHESIA FOR PATIENTS WITH THYROID GLAND DISORDERS
  4. 4. Brain storming What are the hormones secreted from the anterior part of the pituitary gland?
  5. 5. • TSH: Controlls synthesis and secretion of thyroid hormones • FSH: Sperm cell maturation and follicular dev’t & estrogens synthesis in ovaries • LH: Stimulates testosterone synthesis in testis and stimulates ovulation • Growth hormone: Stimulates protein synthesis and overall body growth
  6. 6. Cont. • Prolactin: Stimulates milk production and secretion in breasts • ACTH: Stimulates synthesis and secretion of cortisol, androgens and aldosterone. • MSH: Stimulates melanin synthesis
  7. 7. The thyroid gland • Anatomy:  The thyroid gland is formed by two lateral lobes connected by the thyroid isthmus at about the second tracheal ring.  It is situated anterior to the trachea.  Is the first endocrine gland to appear during embryonic dev’t.  Weight 15-25 gms in adults  It is supplied by the superior and inferior thyroid arteries.  Venous drainage is through superior, middle and inferior thyroid veins
  8. 8. cont’d……  It is a highly vascularised endocrine gland  Attached to the trachea by a loose connective tissues  Covered by: -Anteriorly by skin and paltysma muscle -Antero laterally by @ Sternocleidomastoid muscle @Sternothyroid muscle @Sternohyoid bone -Posteriorly parathyroid glands are located on both sides
  9. 9. • Thyroid gland contains two separate hormone producing cells. 1.Follicular cells: they synthesize, store and release thyroid hormones(T4 and T3) • They also trap iodide from the circulation • The iodide is then oxidized to iodine which is catalysed by thyroid peroxidase (organification) takes place on the apical membrane of the follicular cells
  10. 10. Cont. • They synthesize and secrete thyroglobulin a substance containing tyrosine. • This tyrosine is then iodinated by the oxidized iodine to form monoiodotyrosine(MIT) and diiodotyrosine
  11. 11. Cont’d…….. • MIT+DIT=T3 • DIT+DIT=T4 • This iodinated thyroglobulin is the storage form of thyroid hormones which is kept inside the follicle
  12. 12. 3,5,3´-triiodothyronine (T3)
  13. 13. Thyroxine (T4) 3,5,3´,5´-tetraiodothyronine
  14. 14.  Iodide transport-trap iodide moving it into the thyroid follicle and then oxidizes it  Organification- iodine is combined with tyrosine to form MIT & DIT  Coupling- two DIT combine to make thyroxin (T4) or one MIT combines with one DIT to form triiodotyronine (T3)  Storage- hormones migrate to the colloid space in the centre of the thyroid follicular cells  Secretion- release of hormones by reversing process of storage reversal of migration through cell membranes.
  15. 15. cont’d…… • TSH- it is one of the hormones produced in the anterior part of the pituitary gland • It controls the function of follicular cells and secretion of thyroid hormones(T3 & T4). • it stimulates the thyroid to release T3 & T4 • It also increases thyroglobulin synthesis & iodine uptake • It’s secretion is regulated by TRH produced from the hypothalamus • Excess T3 & T4 suppress the release of TSH (-ve feedback mechanism).
  16. 16. Brain(hypothalamus) TRH Anterior pituitary TSH Thyroid Thyroid hormones Body tissues
  17. 17. cont’d………  Negative feedback mechanism  Low blood levels of hormones stimulate hypothalamus  Hypothalamus stimulates pituitary to release TSH  TSH stimulates the thyroid to raise the amount of hormones in the blood
  18. 18. cont’d…… NB: the over all result of any type of negative feedback in the endocrine system is : -inhibition when the level of the hormone in the periphery is high -stimulation when there is low amount of hormones in the periphery
  19. 19. 2. Para follicular cells:  They secrete calcitonin which has a minor role in maintaining calcium homeostasis.  Two main effects of calcitonin are : 1. It enhances excretion of calcium into urine 2. Inhibition of bone resorption of calcium, which would minimize fluxes of calcium from bone to blood.
  20. 20. SPECIFIC ACTIONS OF THYROID HORMONE: METABOLIC • Regulation of Basal Metabolic Rate (BMR). • Increases oxygen consumption in most target tissues. • Permissive actions: TH increases sensitivity of target tissues to catecholamines, thereby elevating lipolysis, glycogenolysis, and gluconeogenesis. • The high sensitivity of target tissues to cathecolamines also causes tachycardia, palpitations and high cardiac out put.
  21. 21. SPECIFIC ACTIONS OF THYROID HORMONE: DEVELOPMENT • TH is critical for normal development of the skeletal system and musculature. • TH is also essential for normal brain development and regulates synaptogenesis, neuronal integration, myelination and cell migration. • Cretinism is the term for the constellation of defects resulting from untreated neonatal hypothyroidism.
  22. 22. DISEASES OF THE THYROID GLAND
  23. 23. HYPERTHYROIDISM • It is a syndrome caused by excessive secretion of TH when there is over active thyroid gland. • This can be due to over functioning of the entire gland or due to the presence single or multiple adenomas of the gland. • Its clinical manifestation is thyrotoxicosis a syndrome caused when the body tissues are stimulated by a high level of TH.
  24. 24. • Causes : • The most common cause is graves disease(w/c is a diffuse enlargement of the gland) • Thyroid adenoma • Thyroid carcinoma • TSH pituitary adenomas • Iatrogenic
  25. 25. Pathophysiology : • B/c the action of thyroid hormones on the body is stimulatory, hyperthyroidism results in sympathetic over activity. • The excessive amount of TH stimulates the cardiac system and increases the number and sensitivity of beta adrenergic receptors -tachycardia -increased CO and stroke volume -increased adrenergic responsiveness -increased peripheral blood flow
  26. 26. cont’d  Increased metabolism leads to:  Negative nitrogen balance  Lipid depletion  Stage of nutritional deficiency  Increased oxygen consumption  TH and catecholamine work together in metabolic acceleration  Increased oxygen consumption, BMR, and heat production  Positive inotropic and chromo tropic effect by increasing calcium-ATPase & beta receptors.
  27. 27. cont’d…..  There is also increased GI motility.  Increased bone and protein turn over, glycogenolysis, hepatic gluconeogenesis, intestinal glucose absorption, cholesterol synthesis and degradation.  High BMR => high body temperature =>peripheral vessel dilatation=>increased CO=> high out put failure.  Prolonged period of hyperthyroidism leads to bone destruction, and hunger damage due to increased catabolism of cellular proteins and fat.
  28. 28.  Symptoms and signs:  Symptoms: Nervousness Increased sweating ( warm and moist skin ) Heat intolerance Palpitation Fatigue and weakness Weight loss Increased appetite Hyperdefication
  29. 29.  Signs: Thyroid enlargement Tachycardia Atrial fibrillation Systolic hypertension ( wide pulse pressure) Eye signs (exophthalmus )
  30. 30. TESTS NORMAL VALUES INCREASED DECREASED T4 60-120 nmole/L -Hyperthyroidism -Thyroditis -Early hepatitis -Pregnancy -Oestrogen therapy -Exogenous T4 -Hypothyroidism -Androgens -Salicylates -Sulphonamides T3 0.92-3 nmole/L Hyperthyroidism -Hypothyroidism -Cirrhosis -Uraemia -Malnutrition TSH 0.25-8micIU/L Primary hypothyroidism Hyperthyroidism
  31. 31. TREATMENT • Anti thyroid drugs: o PTU, methimazole and carbimazole- these drug inhibits the synthesis of TH by blocking the action of peroxidise enzyme (an enzyme that converts I- to I+ ) o PTU also inhibits the peripheral conversion of T4 to T3.
  32. 32. CONT. o Potassium or Sodium iodide prevent the release of TH to the tissues o Dosage : PTU 100-150 mg PO TID, Methimazole 15-60 mg PO BID, Carbimazole 20-40 mg PO TID for at least 6-8 weeks and potassium or sodium iodide 100 mg PO QID for7-10 days prior to surgery.
  33. 33. Beta blockers: o Propranolol 40-80 mg PO QID. This drug blocks the high responsiveness of beta adrenergic receptors to catecholamine there by reducing pulse rate. o Beta blockers also have little effect on preventing peripheral conversion of T4 to T3
  34. 34. • Although blockage of hormone synthesis is rapid, clinical improvement occurs after months. • This is b/c a large pool of stored TH continues to be released from the gland. • Most patients become euthyroid 2-3 months after the beginning of anti-thyroid therapy.
  35. 35. • After clinical improvements, dosage should be tapered to the minimum to maintain an euthyroid state. • The drug should continue up to one year. • A free T4 level should be checked after one month of therapy and then every 2-3 months
  36. 36. • Indications for surgery  Large goitre not amendable to RAI  Compressive symptoms  Children and young patients  Patients with cancer or suspicious nodule  Allergy to anti-thyroid drugs  Pregnant and those with a desire to conceive soon  Moderate to severe opthalmopathy  Cosmetic desire of the patient
  37. 37. ANESTHESIA MANAGEMENT Preoperative preparation: – Careful assessment of upper airway & tracheal deviation – Thoracic inlet X-ray, CT scan – Patient must be rendered EUTHYROID – Use anti-thyroid drugs and B - blockers – Resting pulse rate 85-90 bpm
  38. 38. – Lugol’s iodine 3-5 drops BID for 10 days to decrease vascularity of the gland – Benzodiazepines premedication – Continue the morning dose of anti thyroid and beta blocking drugs.
  39. 39. Intraoperatively - Anesthetic options: A- No difficulty anticipated: - usual iv induction & intubation (fentanyl, non-depolarizing muscle relaxant B- possible difficulty in intubation: - iv induction, test ventilation when pt is unconscious, intubation +- suxamethonium C- definite intubation problem / evidence of airway obstruction  awake fibreoptic intubation  inhalational induction  choice of ETT- armoured ETT (< risk of kinking)  The size of ETT to be used should be 0.5 mm ID smaller than the normal calculated size
  40. 40. cont’d……..  Intra operatively:  Allow safe induction and awakening  Maintain adequate level of anaesthesia (avoid exaggerated sympathetic response to surgical stimulus) Drugs of choice • Etomidate, propofol and barbiturates for induction • Atracurium, vecuronium for muscle relaxation • Isofulrane choice of inhalational.
  41. 41. cont’d………….. Avoid drugs like: oAtropine oPancuronium oHalothane oketamine
  42. 42.  Positioning and skin preparation: o Put an iv bag between scapulas o Protect eyes o ETT is strapped firmly in position o Gentle traction the arms along the side body o Put patient in a head up position 15-20 degrees to facilitate venous drainage o Surgeon stands on the opposite to the lobe to be removed o Skin prepared and draped o IV line on opposite
  43. 43. • If a hyperthyroid patient with clinically apparent disease requires an emergency surgery: Propranolol 0.5 mg/kg iv is given Or esmolol infusion 50-150 micg/kg/minute If the site allows regional technique is preferred but adrenalin containing LA should be avoided. It is also important to avoid all the causes of sympathetic stimulations
  44. 44. C) POSTOPERATIVE Possible problems 1.Thyroid storm /crisis An acute exacerbation of hyperthyroidism with excessive release of thyroid hormone Onset – intraoperative or 6-24 hours after surgery Sign and symptom:- hyperpyrexia, tachycardia or atrial fibrillation, hypotension, vomiting, dehydration, tachypnoea, acute abdominal pain simulating an acute abdomen, agitation, psychosis Dx: primarily clinical DDx: MH,Pheochromocytoma or light anesthesia
  45. 45. Management: A) Supportive and medical management.  Investigate for precipitants – FBC, , blood glucose, FT4, FT3 If the cause is Hyperthyroidism mange as follows: 1) Inhibition of thyroid hormone formation  PTU 900-1200mg/day orally / NG in 3-4 divided doses OR  Carbimazole 60-120mg/day 3-4 divided doses orally / NG
  46. 46. Precipitants - infection, surgery, poorly prepared thyroid surgery, diabetic ketosis, radioiodine therapy in a poorly prepared pt, MI
  47. 47. 2) Inhibition of thyroid hormone release: - sodium iodide IV 1gm/24hr – slow infusion or - oral potassium iodide 100mg 6hrly - Given 1hr after 1st dose PTU/carbimazole 3) Steroids - iv dexamethasone 2mg 6hrly - inhibits thyroid hormone release & peripheral conversion
  48. 48. 4) Receptor blockade ( in the absence of HF) - Iv propranolol 1-2mg slowly 4-6hrly / oral propranolol 40-80mg 6hrly 5) Cardiac failure - diuretics, digoxin, O2 +-propranolol if d/t uncontrolled AF with good LV function 5) Hyperpyrexia - fans, tepid sponge, PCM 6) Dehydration - IV fluid replacement
  49. 49. 2) Airway obstruction Possible causes: - neck hematoma with tracheal compression - tracheomalacia - incomplete reversal of NDMR - CNS depression
  50. 50. 3) Tetany - clinical manifestations: circumoral tingling, paraesthesia, laryngeal spasm, (+) ve Chvostek & Trousseau signs - May result from respiratory alkalosis - over-ventilation in immediate postoperative period - hypocalcemia from hypoparathyroidism Mx - calcium replacement - Slow injection of 10% calcium gluconate 10 mls IV
  51. 51. 4) RLN injury Manifestations: 1) Unilateral  Asymptomatic unless larygoscopic examination is done  Weak and horse voice chocking and coughing during drinking and aspiration 2) Bilateral  Usually manifests immediately after extubation  Laryngeal stridor, acute respiratory distress, phonation lost and desaturation
  52. 52. • Management  Unilateral  Re intubation & observe for 6-12 minutes  If normal function of cords is not returned with in 6- 12 minutes Teflon injection  Speech therapy  Medialization and re -innervation  Other than the above measures there is no definitive Rx until 6 months
  53. 53. Cont’d….  Bilateral  temporarily: = re intubation muscle paralysis = hydrocortisone 100 mg TID = if extubation fails after 48 hrs Tracheostomy is mandatory
  54. 54. ANESTHESIA MANAGEMENT OF HYPOTHYROIDISM • Definition o It is a condition when the body tissues are exposed to decreased circulating concentration of thyroid hormones.
  55. 55. • Causes 1. Primary- b/c of destruction of thyroid gland  Thyroid gland can be destructed by  Chronic thyroiditis( Hash Moto's disease)  Previous STT  Previous RAI therapy  Irradiation of the neck
  56. 56. • Hashimoto’s thyroiditis is an autoimmune destruction of the thyroid gland in which antibodies may either frankly destroy the gland or block TH synthesis. • And this remains the most common cause of primary hypothyroidism
  57. 57. Cont’d…. Thyroid hormone deficiency secondary to:  Anti thyroid drugs  Excessive iodine ( inhibits TH release)  Dietary iodine deficiency
  58. 58. Cont’d…. 2. Secondary – b/c of CNS dysfunction Hypothalamic dysfunction which causes TRH deficiency Anterior pituitary dysfunction which causes TSH deficiency
  59. 59. • NB:  Depending on the cause, the level of TSH may be increased or decreased.  If the defect is in the thyroid gland (e.g. thyroiditis) TSH level will be increased by a negative feedback mechanism as the low circulating level of TH will stimulate the pituitary to secrete more TSH  If the defect is in the hypothalamus or in the pituitary the level of TSH will be decreased.
  60. 60. Cont’d…… • Diagnosis  Is based on clinical signs and symptoms plus TFT
  61. 61.  Signs and symptoms  Generalized decrement in metabolic activity  Cold intolerance  Lethargy  Decreased COP ( up to 40% ) and BV  Prolonged circulation time and narrow pulse pressure  PVR to decrease heat loss
  62. 62. Treatment • Slow initiation • Patients with; -severe hypothyroidism -older patient and - patients CVS disease may have increased sensitivity to TH and are at risk of acute CVS and other complications if hypothyroidism is corrected quickly.
  63. 63. Cont’d….. • Therefore , these patients should be given a very small dose of TH initially -25 micgm of levo thyroxine which will gradually be increased to a full maintenance dose every 2-4 weeks for about 6-12 weeks period
  64. 64. • Rapid initiation • Younger patients, and patients with less severe hypothyroidism may be given a slightly higher dose of TH ( 50 micgm levo thyroxine) & can be advanced to a full replacement dose quickly • For example the dose may be raised to 100 micgn in 2 weeks & 125-150 micgm in the next 2 weeks
  65. 65. • Maintenance • Most patients need 75-100 micgm of levo thyroxine daily
  66. 66. Anesthetic management • Elective surgeries should be differed in poorly controlled hypothyroidism due to the high risk of CVS complications • But there are no controlled studies about sensitivity of such patients to IAA & opioids
  67. 67. Cont’d….• Myxedema • It is a severe form of hypothyroidism characterized by Stupor Coma Hypoventilation Hypotension Hypothermia and hypernatremia It is a medical emergency with a mortality rate of 25-50%
  68. 68. Cont’d… • Management • ETTI and ventilation is needed • Sodium levo thyroxine 200-300micgm iv over 10 minutes initially and maintenance 200 micgm iv daily • Hydrocortisone 100mg iv then 25 mg iv QID to prevent coexisting adrenal gland suppression. • Fluid and electrolyte supplementation • Avoid hypothermia
  69. 69. Cont’d…. • Preoperative  Patients with uncorrected severe hypothyroidism or with myxedema coma should not undergo elective surgery and should be treated with TH prior to emergency surgery.
  70. 70. • Although an euthyroid state is ideal, mild to moderate hypothyroidism are not absolute CI to surgery • Hypothyroid patients usually do not require much more preoperative sedation and are very prone to respiratory depression • They fail to respond to hypoxia by increasing minute ventilation
  71. 71. • Since patients have delayed gastric emptying time Premedicating with metoclopramide and H2 blockers is important • The normal dose of TH should be continued in the morning of surgery • It should however be known that half life of most TH drug preparations is long • For example half life of T4 is about 8 days.
  72. 72.  Due to their depressant effect avoid opioids  Cortisol supplementation is considered if there is coexisting adrenal gland suppression.  If possible give the premedication in OR
  73. 73. Cont’d….. • Induction of anesthesia  Ketamine is a preferable induction agent  If no severe CVS depression, thiopental can be used  When using relaxants keep in mind that there is a coexisted skeletal muscle weakness
  74. 74. Cont’d… • Maintenance of anesthesia N2O, +- short acting opioids , BZD or ketamine is best Volatiles CI in overtly hypothyroid situation Reduce MAC if body temperature is <37degree Celsius CIPPV is indicated Pancuronium is best relaxant
  75. 75. Cont’d…. • Regional anesthesia  Preferable than GA  Maintain IVFV adequately  PNB- drug dose should be reduced
  76. 76. Cont’d….. • No special consideration about the use of reversals • IV fluids should contain Na+ • Delay extubation until patient responds appropriately with an accepted body temperature • Monitor variables repeatedly
  77. 77. Cont’d… • Recovery  Emergence is delayed from GA due to hypothermia, respiratory depression and slow drug biotransformation
  78. 78.  Prolonged post operative somnolence(sleep)  Inability to wean earlier => need mechanical ventilation  Avoid post operative hypothermia  Give adequate anti pain  Opioids drugs have depressant effects we should use non opioid analgesics like ketorolac.
  79. 79. 100 Q
  80. 80. THE PARATHYROID GLANDS • ANATOMY o Four bean shaped glands are located behind the upper and lower poles of the thyroid gland. o Inferior glands are located ventral(to the front) to RLN. o Superior glands usually dorsal( to the back) to the RLN at level of cricoid cartilage
  81. 81. Cont’d….. • They get most of their blood supply from branches of inferior thyroid artery, although branches from superior thyroid supply at least 20% of upper glands. • They drain their venous blood through superior, middle, and inferior thyroid veins
  82. 82. • PHYSIOLOGY • The main physiologic role of the parathyroid glands is production of a polypeptide hormone called parathyroid hormone. • Maintenance of calcium, phosphate and magnesium homeostasis is under the influence of two polypeptide hormones; parathyroid hormone(PTH), and calcitonin
  83. 83. Cont’d.. • These hormones regulate the flow of minerals in and out of the extracellular fluid compartments through their actions on intestine, kidneys, and bones. • The PTH acts directly on the bones and kidneys and indirectly on the intestine through its effect on the synthesis of 1,25 (OH)2D3. Its production is regulated by the concentration of serum ionized calcium.
  84. 84. Cont’d.. • Lowering of the serum calcium levels will induce an increased rate of parathyroid hormone secretion • Calcitonin is released by the “C” cells (Para follicular cells in the thyroid gland) in response to small increases in plasma ionic calcium. It acts on the kidney and bones to restore the level of calcium to just below a normal set point which in turn inhibits secretion of the hormone
  85. 85. Cont’d… • Calcitonin is therefore the physiological antagonist of PTH. The two hormones act in concert to maintain normal concentration of calcium ion in the extracellular fluid. • The total calcium concentration in the blood is 10mg/dl • Of this 40% is bound to plasma proteins mainly albumin
  86. 86. • The remaining 60% is found in two different forms • The first is complexed with anions ( sulfate, phosphate and citrate) which accounts about 10% • About 50% is found as free ionized calcium and this is the only form of calcium which is biologically active.
  87. 87. • This free Ca++ is important for o Skeletal muscle contraction o coagulation, o neurotransmitter release, o endocrine function, other intracellular functions
  88. 88. Actions of major calcium regulating hormonesHORMONE BONE KIDNEY INTESTINE PTH Increase resorption of calcium and phosphate  Incr. reabsorption of calcium  Decr. reabsorption of phosphate  Incr. conversion of 25OHD3  to 1,25(OH) 2 D3 No direct effect Calcitonin Decr. Resorption of calcium & phosphate Decr. Reabsorption of calcium & phosphate No direct effect VtD Maintains calcium transport system Decr. Reabsorption of calcium Incr. reabsorption of calcium & phosphate
  89. 89. DISORDERS OF THE PARATHYROID GLAND
  90. 90. PRIMARY HPT • Primary HPT is due to excessive production of PTH by one or more of hyper functioning parathyroid glands. • This leads to Hypercalcemia and hypo phosphatemia • It affects patients older than 40 years • Female to male ratio is 3:1
  91. 91. • 85% caused by isolated adenoma, 14% by diffuse hyperplasia, 1% by parathyroid CA
  92. 92. HPT CONT’D…. • C/M • Clinical manifestations are mostly due to Hypercalcemia. • CVS: HTN, arrhythmias, short QT, prolonged PR • Renal: impaired renal concentration, metabolic acidosis ,polyuria, dehydration, polydipsia, renal stones (nephrolithiasis), renal failure • GI: ileus, nausea & vomiting, pancreatitis,
  93. 93. Cont’d… • Musculoskeletal: weakness, osteoporosis(a fragile bone) & pathological fractures • CNS: mental status changes(delirium, psychosis and coma) • Eyes- calcification, conjunctivitis
  94. 94. SECONDARY HPT • An increase in PTH secretion which is adaptive and unrelated to intrinsic disease of the parathyroid glands is called secondary hyperparathyroidism. • This is due to chronic stimulation of the parathyroid glands by a chronic decrease in the ionic calcium level in the blood
  95. 95. SECONDARY HPT CONT’D.. • Is a compensatory hyper functioning of the parathyroid glands caused by hypocalcemia or peripheral resistance to PTH • Treating the underlying cause can reverse secondary HPT • It is commonly seen in a patient with an end organ failure e.g. in chronic renal insufficiency
  96. 96. TERITIARY HPT • It occurs in previous secondary HPT • In such conditions the glandular hyper functioning continues despite correction of the underlying problem. • Most of the c/m of secondary & tertiary HPT are the same as that of primary HPT as they are caused by Hypercalcemia
  97. 97. • DIAGNOSIS • The presence of established Hypercalcemia in more than one serum measurement accompanied by elevated immunoreactive PTH is characteristic feature of HPT o Marked increase in Ca++ usually b/o cancer o Serum Ca++>2.8mmol/L; (NR=2.13-2.55) o Ionized Ca++>1.25mmol/L (NR=1.1-1.25)
  98. 98. Cont’d… • Less commonly caused by  calcium malabsorption  VtD. Deficiency or deranged VtD metabolism
  99. 99. MEDICAL MG’T & ANESTHESIA CONSIDERATIONS o Medical mg’t o Saline infusion & loop diuretics o Biphosphonates(cause binding &inhibit bone resorption) that may be administered IV when levels are life threatening o Calcitonin produces transient results
  100. 100. • In acute severe forms the main stay of therapy is adequate hydration with saline and forced diuresis by diuretics to increase the urinary excretion of calcium rapidly along with sodium and prevent its reabsorption by the renal tubules
  101. 101. Cont’d… o Hem dialysis o SURGERY. Resection of the parathyroid lesion is curative with recurrences observed mainly in the multiple glandular disease.
  102. 102. CONT’D….. • Anesthesia mg’t Pre operative evaluation should include ass’t of volume status to avoid hypotension during induction. • Hydration with normal saline and diuresis with furosemide usually decreases serum calcium to acceptable levels. • Check labs • Evaluate status of co morbidities • Any issues with bone fragility?
  103. 103. Cont’d…. Intraoperatively • Routine monitors • Titration of muscle relaxants(pre existing muscle weakness) • Issues of positioning • If preoperative LOC decrease dose of anesthetic agents • Protect the eyes
  104. 104. cont’d…. • Avoid hypoventilation as acidosis can cause an increase in ionized calcium which in turn causes cardiac dysrhythmias. • Tracheal manipulation during dissection • Proper patient positioning is important b/c osteoporosis predisposes patients to vertebral compression during laryngoscopy and bone fractures during transfer
  105. 105. Cont’d…. Post operatively • • Smooth emergence • Evaluate for recurrent laryngeal n. damage • Pain control
  106. 106. Cont’d….. • Postop complications • Worry about o Neck hematoma o Laryngeal swelling/ glottis edema o Recurrent laryngeal n. damage o Hypocalcemia= tetany o Acute arthritis o Metabolic acidosis with deterioration of renal function (transient)
  107. 107. • PARATHYROID CRISIS: o CA++ >15 mg/dl o Requires hydration (dilutes Ca++) followed by diuresis with loop diuretic (promote Ca++ & H2O excretion) o May also be given,glucocorticoids, calcitonin, dialysis
  108. 108. HYPOPARATHYROIDISM • Most common cause: accidental excision of all glands during thyroidectomy • Also due to: neck trauma, neoplasia • CRF • Hypomagnesaemia • Vt D deficiency
  109. 109. Cont’d….. • Clinical manifestations • CVS: hypotension, CHF, prolonged QT interval • Musculoskeletal system: muscle weakness & cramps
  110. 110. Cont’d…. • Neurologic  Neuro muscular irritability(e.g. laryngeal spasm, inspiratory stridor, tetany and seizures) +Chvosteks sign o Tap facial n at angle of mandible = facial muscle twitch +Trousseau sign o Carpopedal spasm after applying a tourniquet for 3 min  Perioral parasthesia mental status changes (e.g. dementia, depression and psychosis)
  111. 111. • Dx: o Serum Ca++<4.0 mEq/L, ionized fractions <2.0 mEq/L
  112. 112. Cont’d… • RX includes: o Calcium IV in acute conditions until neuromuscular signs are controlled o Correction resp/metabolic alkalosis o Hypoparathyroid without hypocalcemia=oral Ca++ and Vit D o Thiazides tend to increase serum Ca++ concentration
  113. 113. Cont’d.. Treatment of acute episode o Prevent laryngospasm & seizures o Secure airway o IV Calcium slowly o Anticonvulsants
  114. 114. ANESTHESIA CONSIDERATIONS • PREOP EVALUATION o Check Ca++ and Mg levels o Evaluate EKG ; how is the QT? o Replace Ca++ if necessary
  115. 115. Cont’d… • Intraoperatively o Anesthetics that depress the myocardium should be avoided. o Increased sensitivity to Sux o Titrate muscle relaxants slowly and monitor response o Positioning considerations
  116. 116. Cont’d… o Keep them warm b/c hypothermia may impair drug elimination & metabolism o Remember co morbidities o Avoid hyperventilation ( or anything that will change Ca++ level) as alkalosis will further decrease ionized calcium level
  117. 117. • Post operatively o Assess for changes of serum calcium level o Pain control o Close air way follow up
  118. 118. THANK YOU
  119. 119. THE ADRENAL GLANDS
  120. 120. THE ADRENAL GLANDS • ANATOMY • Anatomy was first described in 1563. • Consists of the adrenal cortex and adrenal medulla
  121. 121. Adrenal Histology
  122. 122. CONT’D…. • PHYSIOLOGY  Activities are regulation of fluid volume and stress response • Adrenal Cortex: The cortex synthesizes & secretes 30+ different steroids. o Glucocorticoids o Mineralocorticoids o Androgens
  123. 123. cont’d… o Mineralocorticoids  Aldosterone Function: Regulates electrolyte & fluid homeostasis
  124. 124. Cont’d… o Glucocorticoids  Cortisol  Hydrocortisone Function: Stim. gluconeogenesis & h blood glucose Anti-inflammatory Anti-immunity Anti- allergy
  125. 125. Cont’d… o Androgen • Sex hormones Function: Female= Stim. Sex drive Men = Negligible
  126. 126. • Adrenal Medulla o Epinephrine(Adrenaline) o Function • Prolong & h SNS (sympathetic nervous system) response to stress
  127. 127. • Norepinephrine(noradrenaline) and dopamine. o Function= the same as that of epinephrine
  128. 128. Adrenal Medulla: A Modified Sympathetic Ganglion • Sympathetic stimulation o Catecholamine release to blood • Epinephrine • Norepinephrine o Travel to: • Multiple targets • Distant targets
  129. 129. Review of Efferent Pathways: Motor and Autonomic
  130. 130. Mechanism: Norepinephrine Release and Recycling
  131. 131. Catechalomines: Activity • Stimulate the “fight or flight” reaction • Increase plasma glucose levels • Increase cardiovascular function • Increase metabolic function • Decrease gastrointestinal and genitourinary function
  132. 132. DISORDERS OF THE ADRENAL GLAND 1. Pheochromocytoma( catecholamine excess) 2. Addisons’s disease(adrenal cortex insufficiency) 3. Conn’s syndrome (mineralocorticoid excess) 4. Cushing’s syndrome (glucocorticoid excess)
  133. 133. PHEOCHROMOCYTOMA • History • First recognized by Von Frankel • Pheochromocytoma= dusky colored tumor • Name coined by Pick in 1912 • Successful surgery for excision of tumor- Roux & Mayo ( 1926-27)
  134. 134. Cont’d… • Neuroendocrine tumour of the medulla of the adrenal glands • Originates from the chromaffin cells along the paravertebral sympathetic chain extending from pelvis to base of skull • >95% are abdominal • >90% in adrenal medulla
  135. 135. • Secretes excessive amounts of adrenaline and noradrenaline • 80% occur unilateral
  136. 136. Called “tumor of ten per cent” • 10% extra-adrenal (closer to 15%) • 10% occur in children • 10% familial (closer to 20%) • 10% bilateral or multiple (more if familial) • 10% recur (more if extra-adrenal) • 10% malignant • 10% discovered incidentally
  137. 137.  Tumor Secretion: • Large Pheo: more metabolites (metabolized within tumor before release) • Small Pheo: more catecholamines • Sporadic Pheo: Norepi > Epi • Familial Pheo: Epi > Norepi • Malignant Pheo: Dopamine
  138. 138. • Epidemiology  0.01-0.1% of population with HT  Found in 10% of those screened  M = F  Common between 3rd and 5th decades of life but can occur at any age.  Rare
  139. 139. • Clinical manifestations • The five P’s: • Pressure (HTN) • Pain (Headache) • Perspiration(diaphoresis) • Palpitation • Pallor(there is a decrease in red cell mass)
  140. 140. • The Classical Triad: 1. Pain (Headache) 2. Diaphoresis (excessive sweating) 3. Palpitations
  141. 141. • Cardiac manifestations • Sinus tachy, ventricular ectopic, • Catecholemine induced increased myocardial oxygen consumption, coronary vasospasm o Angina/MI o Cardiomyopathy- hypertrophic Cardiomyopathy- diastolic dysfn- norepi induced o Dilated cardiomyopathy- systolic dysfn- epi induced
  142. 142. • Neurologic manifestations o Hypertensive encephalopathy (altered mental status, focal neurological s/s, seizures) o Stroke – cerebral infarction/ embolus o Intracranial bleeding
  143. 143. Diagnosis 1. Biochemical 2. Localization
  144. 144. 1. Biochemical • 24h Urine Collection Positive results show 2-3 fold elevation from the normal value Normal values: -Dopa=424-2612nmol/d -Epi=10-110nmol/d, -Norepi=12-85.5micg/d -Metanephrine=0-4.9mivmol/d -Normetanephrine=573-933nmol/d
  145. 145. • Test Characteristics: • 24h urinary catechol Sen 83% Spec 88% • 24h U total metanephrine Sen 76% Spec 94% • 24h Ucatechols + Utotal metanephrines Sen 90% Spec 98% • Sensitivity increased if 24h urine collection begun at onset of a paroxysm
  146. 146. • Plasma free metanephrines sensitivity = 99% specificity = 89% • Plasma catecholamine sensitivity 84% and specificity = 81%
  147. 147. 2. Localization: Imaging • CT abdomen • Adrenal pheo sensitivity 93-100% • Extra-adrenal pheo sensitivity 90% • MRI • > sensitive than CT for extra-adrenal pheo • Abdominal U/S and x-ray
  148. 148. ANESTHESIA MANAGEMENT • Prior to 1951, reported mortality rate for excision of pheochromoyctoma was 24 - 50 % due to • HTN crisis, arrhythmia, MI, stroke • Hypotensive shock
  149. 149. Cont’d…. • Currently, mortality: 0 - 2.7 % • The reasons are: • Preoperative preparation, -blockade • New anesthetic techniques • Anesthetic agents • Intraoperative monitoring: arterial line, EKG monitor, CVP line • Presence of experienced & coordinated team: • Endocrinologist, Anesthesiologist and Surgeon
  150. 150. • Preoperative preparation • Preoperative work up - CBC, electrolytes, creatinine - CXR - EKG - Echo (r/o CMY 2º to catechols)
  151. 151. • Preoperative & β blockade • Start at least 10-14d preoperatively • Allow sufficient time for ECF re-expansion • There must also be dose increments with time until there is optimal control of paroxysms
  152. 152. • Adrenergic Receptors • Alpha-Adrenergic Receptors • 1= vasoconstriction, intestinal relaxation, uterine contraction, pupillary dilation • 2=  presynaptic NE (clonidine), platelet aggregation, vasoconstriction,  insulin secretion • Beta-Adrenergic Receptors • 1=  HR/contractility,  lipolysis,  renin secretion • 2= vasodilation, bronchodilation,  glycogenolysis • 3:= lipolysis
  153. 153. Alpha blockade • Phenoxybenzamine (Dibenzyline) a non selective blocker. • Drug of choice • Covalently binds -receptors (1 > 2) • Start 10 mg PO BID  increase by 10-20 mg/d PO BID • Maintenance 40-80 mg/d (some need > 200 mg/d)
  154. 154. • Phenoxybenzamine (cont’d) • Side-effect: orthostasis with dosage required to normalized seated BP, reflex tachycardia • Drawback: periop hypotension/shock unlikely to respond to pressor agents. • Prevents 2 mediated inhibition of catecholamine release • Thus beta blockers needed to be given alongside
  155. 155. • -blockade • Used to control reflex tachycardia and prophylaxis against arrhythmia during surgery • Start only after effective -blockade (may ppt HTN) • If suspect CHF/dilated CMY  start low dose • Propanolol most studied in pheo prep • Start 10 mg PO BID  increase to control HR • Initial dose 80-120 mg/d • IV 1-10 mg
  156. 156. • Propranolol ( cont’d) o Side effects- may induce cardiac failure, bronchospasm o Oral bioavailability 25% (extensive 1st pass metabolism) • Atenolol- selective B1 o Dose 50- 100 mg/d PO o Max 300 mg/d o IV 2.5 to 10 mg/d
  157. 157. • Esmolol – selective B1 for rapid intraop BP control o Bolus IV 500 µ/kg/min o Infusion 50 to200 µ/kg/min • Labetolol –mixed ɑ+β o Dose- 50- 100 mg/d PO o IV 0.25 mg/kg o Not used as a sole drug due to unpredictable control of BP
  158. 158. • If BP is still not controlled despite  +  blockade  Add Prazosin to Phenoxybenzamine  Prazosin – competitive, selective 1 blocker o T1/2- 2-3 Hrs. o Dose -1-5 mg PO BD o Side effects- postural hypotension reflex tachycardia o Other selective 1 blockers- terazosin, doxazocin
  159. 159. • Other antihypertensives • CCB- oDiltiazem 60- 120mg/d, max 360mg/d oT1/2- 3 to 5 hrs oSide effects- bradycardia, exacerbates cardiac failure oNifedipine – 30mg/d PO Max. 360mg/d oT1/2-1 to 2 hrs oSide effects- hypotension, peripheral edema • Avoid diuretics as already ECF contracted
  160. 160. • Nicardipine • Started PO 24 Hrs to few weeks preop to control BP and allow ECFV restoration • After intubation  IV Nicardipine (start 2.5 ug/kg/min) • IV Nicardipine adjusted to SBP • Stopped prior to ligation of vein • Tachycardia Rx with concurrent IV esmolol • Advantage: periop hypotension may still respond to pressor agents as opposed to those patients who are completely -blocked
  161. 161. • Evaluation of  adrenergic blockade • Roizen’s criteria o Arterial BP < 160/95 mm Hg in the last 48 hrs prior to surgery. Recommended to measure in stressful environment o Mild orthostatic hypotension indicates optimal  adrenergic blockade but not < 80/45. o ECG- free of ST changes for > 2 wks, o Ventricular ectopic < 1 over 5 min
  162. 162. • Premedication • If patient is anxious give appropriate dose of BDZ in the night prior to the day of surgery
  163. 163. • Monitoring  ECG  CVP  Direct arterial pressure measurements  Capnograph  Temperature  Arterial blood gas analysis  Blood glucose levels
  164. 164. • Anesthetic technique • General anesthesia • Regional anesthesia- mid to low thoracic • Combined regional and general anesthesia • Preferred- combined regional and general anesthesia technique o Here although regional anesthesia protects against stresses of surgery, it cannot prevent catecholamine surges due to tumor manipulation. o In extensive sympathetic blockade, severe hypotension after tumor removal,
  165. 165. • INDUCTION • Essentially important to give induction agents slowly along with close monitoring of HR and arterial pressure • Thiopentone / propofol widely used • Etomidate –causes pain/ involuntary mov’t • Ketamine – should be avoided • Multimodal – BZD+ opioid(avoid pethidine & morphine)+ induction agent
  166. 166. • Attenuate pressor response  Important for laryngoscopy and tracheal intubation  2% lignocaine(with out adrenaline) – 1- 1.5mg/kg one minute before laryngoscopy  Esmolol – 50- 100 µg/kg/min  During laryngoscopy catecholamine levels ↑ o Normally- 200- 2000 pg/ml o During laryngoscopy - 2000- 20,000 pg/ml
  167. 167. • Neuromuscular blockade  NDMR drugs= vecuronium  Suxamethonium- avoided causes fasciculation and rise in intra abdominal pressure  Atracurium/ mivacurium- best avoided due to release of histamine  Cisatracurium/rocuronium- safe cardio stable and least histamine release
  168. 168. • Maintenance • Inhalational agent- isoflurane used extensively b/c it does not sensitize the myocardium to catecholamines • Halothane undesirable due to it’s arrhythmogenic properties • Sevoflurane used successfully (fast onset …..fast offset)
  169. 169. • During surgery • Have ready: IV phentolamine, IV NTP, IV esmolol • Very high uncontrolled BP- tell surgeons to stop manipulation of the gland • Ligation of adrenal vein- care for sudden hypotension • Rx hypotension with crystalloid +/- colloid 1st • may need dopamine/ noradrenaline/ phenylephrine
  170. 170. • Postoperative • Post op ventilation / ICU stay- depends upon the hemodynamic status…. Preferably ICU stay for 24 Hrs • Hypoglycemia post op due to disinhibition of B cell supression….. Increased insulin secretion • Glucose supplementation at end of surgery
  171. 171. • Post op( cont’d) • Most cases can stop all BP meds postop • Postop hypotension: IV crystalloid • HTN free: 5 years 74% 10 years 45% • 24h urine collection 2 week postop • Surveillance: • 24 h urine collections every year for at least 10years • Lifelong follow up • 5 year survival- non malignant pheo- 95% • Malignant- < 50 %
  172. 172.  Conclusion • Long term outlook very good • Managed by an experienced team of anesthesiologist, surgeon, endocrinologist & cardiologist • Principles of anesthetic management o Good adrenergic blockade preop o Vigilant intraop monitoring and treatment of hyper/ hypotension o Post op ICU care • Antihypertensive for a prolonged period
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