anesthesia for Adrenal gland disorder.pptx

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1. Anesthesia consideration for patients with adrenal gland disorders Hawassa university School of medicine Department of anesthesia Belete Alemu 1

2. Outline General objective Anesthesia consideration for adrenal disease. 2

3. General objective At the end of this presentation you will be able to describe: Anesthesia consideration for adrenal disease. 3

4. Anesthesia consideration for patients with adrenal gland disorder The Adrenal Gland Pheochromocytoma Cushing syndrome Conn’s syndrome Addison’s disease Hypoaldosteronism 4

5. The Adrenal Gland Physiology The adrenal gland is divided into the cortex and medulla. The adrenal cortex secretes: Androgens Mineralocorticoids (eg, aldosterone) and Glucocorticoids (eg, cortisol). 5

6. Conti. The adrenal medulla secretes, Catecholamines Primarily epinephrine, Small amounts of norepinephrine and dopamine ) 6

7. Adrenal gland 7

8. Conti. 8

9. Conti. 9

10. Pheochromocytoma Is a catecholamine-secreting tumor. Accounts for 0.1% of hypertension. The tumor is usually localized in a single adrenal gland, 10% to 15% are bilateral or extra adrenal. 10

11. Cardinal manifestations of pheochromocytoma Paroxysmal hypertension ,headache, sweating, and palpitations. 11

12. Conti. Unexpected intraoperative hypertension and tachycardia during manipulation of abdominal structures may occasionally be the first indications of an undiagnosed pheochromocytoma.. 12

13. Anesthetic Considerations Preoperative assessment should focus o n : The adequacy of α-adrenergic blockade and Volume replacement. 13

14. Conti. Specifically the following should be evaluated. Resting arterial blood pressure Orthostatic blood pressure and heart rate Ventricular ectopy and Electrocardiographic evidence of ischemia 14

15. Conti. A decrease in plasma volume and red cell mass contributes to the severe chronic hypovolemia. The hematocrit may be normal or elevated, depending on the relative contribution of hypovolemia and anemia. 15

16. Conti. Preoperative α-adrenergic blockade with phenoxybenzamine helps correct the volume deficit in addition to correcting hypertension. 16

17. Conti. β Blockade Should not be initiated prior to α blockade. But may be added if there is a need to control HR and to reduce arrhythmias. 17

18. Conti. A decline in hematocrit should accompany the expansion of circulatory volume. An underlying anemia may be unmasked by volume expansion. 18

19. Invasive arterial pressure monitoring. Potentially life-threatening variations in BP. particularly during induction and manipulation of the tumor. 19

20. Central venous line Indicated for Patients with evidence of cardiac disease. 20

21. Intubation Deep level of general anesthesia should be established before attempt to intubate. . 21

22. Intraoperative hypertension Can be treated with Phentolamine Nitroprusside Nicardipine, or clevidipine 22

23. Conti. Drugs or techniques that indirectly stimulate or promote the release of catecholamines are best avoided. E.g. Ephedrine Hypoventilation Large bolus doses of ketamine. 23

24. Conti. Drugs that potentiate the arrhythmic effects of catecholamines (halothane), or consistently release histamine (eg, large doses of atracurium or morphine sulfate) are best avoided. 24

25. Conti. After ligation of the tumor’s venous supply , the primary problem frequently becomes hypotension . From hypovolemia Persistent adrenergic blockade Tolerance to the increased concentrations of endogenous catecholamines, that have been abruptly withdrawn. 25

26. Conti. Appropriate fluid resuscitation should reflect surgical bleeding and other sources of fluid loss . Assessment of intravascular volume guided by Echocardiographic assessment of left ventricular filling or Noninvasive measures of cardiac output and stroke volume. 26

27. Conti. Infusions of adrenergic agonists, such as phenylephrine or norepinephrine , often prove necessary. Postoperative hypertension is rare and may indicate the presence of unresected occult tumors. 27

28. Cushing syndrome (Glucocorticoid Excess) Is caused by either overproduction of cortisol by; The adrenal cortex or Exogenous glucocorticoid therapy 28

29. Is a syndrome characterized by; Truncal obesity Hypertension Hyperglycemia Increased intravascular fluid volume 29

30. Conti. Hypokalemia Fatigability Abdominal striae Osteoporosis and Muscle weakness. 30

31. Conti. 31

32. Conti 32

33. Anesthetic Management General consideration and preoperative preparation. Treating hypertension and diabetes Normalizing intravascular fluid volume and electrolyte concentrations. 33

34. Conti. Diuresis with the aldosterone antagonist spironolactone helps mobilize fluid and normalize potassium concentration. Careful positioning of the osteopenic patient is important to avoid fractures. 34

35. Conti. When either unilateral or bilateral adrenalectomy is planned, Glucocorticoid replacement therapy is initiated. Dose equal to full replacement of adrenal output during periods of extreme stress. 35

36. Conti. After bilateral adrenalectomy , most patients require 0.05 to 0.1 mg/day of fludrocortisone Starting around day 5 to provide mineralocorticoid activity . Slightly higher doses may be needed if prednisone is used for glucocorticoid maintenance. Because it has little intrinsic mineralocorticoid activity. 36

37. Conti. The production of glucocorticoids or ACTH by a neoplasm may not be eliminated if the tumor is unresectable. These patients often need continuous medical therapy with; Steroid inhibitors such as metyrapone to control their symptoms. 37

38. Conti. There are no specific recommendations regarding the use of a particular anesthetic technique or medication in patients with hyperadrenocorticism. 38

39. Conti. When significant skeletal muscle weakness is present, A conservative approach to the use of muscle relaxants is warranted. Etomidate has been used for temporizing medical treatment of severe Cushing syndrome, Inhibit steroid synthesis. 39

40. Primary Hyperaldosteronism (Conn’s syndrome) Is the most common cause of aldosterone excess. Bilateral micronodular adrenal hyperplasia (60%) Unilateral adrenal adenoma (40%). Rarely, adrenocortical carcinoma is responsible. 40

41. Clinical features Sodium retention, potassium depletion, Hydrogen depletion with metabolic alkalosis, and Cardiac remodeling. Muscle weakness and cramps occur secondary to hypokalemia. 41

42. Diagnosis Is made by demonstrating an elevated level of plasma aldosterone and low plasma renin. 42

43. Conti. Localization studies include adrenal CT and MRI and adrenal vein sampling. A unilateral adrenal lesion is treated surgically. Bilateral adrenal hyperplasia is managed with spironolactone and eplerenone. 43

44. Anesthetic management Preoperative restoration of intravascular volume, electrolyte levels, renal function, and control of hypertension. Restricting sodium intake and administering spironolactone and potassium are necessary. 44

45. Conti. A preoperative echocardiogram will determine the effects of long-standing hypertension. Excess preoperative diuresis may render the patient hypovolemic. 45

46. Conti. No specific anesthetic technique or medications. Patients have a high incidence of ischemic heart disease. An arterial line should be used. 46

47. Conti. Excision of a solitary adrenal adenoma should not require exogenous cortisol . But bilateral manipulation of the adrenal glands may require supplemental cortisol . If transient hypocortisolism is a consideration. 47

48. Hypoaldosteronism Hyperkalemia in the absence of renal insufficiency suggests the presence of hypoaldosteronism. 48

49. Conti. Heart block secondary to hyperkalemia, orthostatic hypotension, and hyponatremia may also be present. 49

50. Conti. Isolated deficiency of aldosterone secretion may reflect; Congenital deficiency of aldosterone synthetase or hyporeninemia Resulting from defects in the juxtaglomerular apparatus Treatment with ACE inhibitors 50

51. Conti. Hyporeninemic hypoaldosteronism typically occurs in patients older than age 45 with chronic renal disease and/or diabetes mellitus. Treatment of hypoaldosteronism Liberal sodium intake and Daily administration of fludrocortisone 51

52. Addison’s disease (Adrenal Insufficiency) The under secretion of adrenal steroid hormones. May develop as the result of; A primary inability of the adrenal gland to elaborate sufficient quantities of hormone or As the result of a deficiency in the production of ACTH. 52

53. Clinical Presentation The cardinal symptoms of idiopathic Addison disease include chronic fatigue, muscle weakness, anorexia, weight loss, nausea, vomiting, and diarrhea. Hypotension is almost always encountered in the disease process. 53

54. Conti. An acute crisis can present as; Abdominal pain Severe vomiting and diarrhea Hypotension Decreased consciousness and Shock 54

55. Conti. Diffuse hyperpigmentation occurs in most patients with primary adrenal insufficiency. Secondary to the compensatory increase in ACTH and β-lipotropin . 55

56. Conti. Mineralocorticoid deficiency is characteristically present in primary adrenal disease; There is a reduction in urine sodium conservation. Hyperkalemia may be a cause of life-threatening cardiac dysrhythmias. 56

57. Conti. Adrenal insufficiency secondary to pituitary disease is not associated with: Cutaneous hyperpigmentation or Mineralocorticoid deficiency. 57

58. Conti. Salt and water balance is usually maintained unless severe fluid and electrolyte losses overwhelm the subnormal aldosterone secretory capacity. Organic lesions of pituitary origin require a diligent search for coexisting hormone deficiencies. 58

59. Conti. Acute adrenal insufficiency from inadequate replacement of steroids on chronic steroid therapy: Is rare and Can present as refractory, distributive shock. 59

60. Conti. In critically ill patients , adrenal insufficiency may not present with classic symptoms . The clinical picture may resemble that of sepsis without a source of infection . A high degree of suspicion must be maintained if the patient has cardiovascular instability without a defined cause . 60

61. Diagnosis The patient’s pituitary–adrenal responsiveness should be determined when the diagnosis of primary or secondary adrenal insufficiency is first suspected. 61

62. Conti. Plasma cortisol levels are measured before and 30 and 60 minutes after the IV administration of 250 μg of synthetic ACTH. 62

63. Conti. There are multiple determinants for adequate adrenal reserve; Usually the plasma cortisol rises at least 500 nmol/L 60 minutes after the injection of the synthetic ACTH. Patients with adrenal insufficiency usually demonstrate little or no adrenal response . 63

64. Treatment and Anesthetic Considerations Normal adults secrete about 20 mg of cortisol (hydrocortisone) and 0.1 mg of aldosterone per day. Glucocorticoid therapy is usually given twice daily in sufficient dosage to meet physiologic requirements. 64

65. Conti. Typical regimen in the unstressed patient may consist of; Prednisone, 5 mg in the morning and 2.5 mg in the evening, or Hydrocortisone, 20 mg in the morning and 10 mg in the evening. 65

66. Conti. Secondary adrenal insufficiency often occurs in the presence of multiple hormone deficiencies. A decrease in ACTH production results in; The decreased secretion of cortisol and adrenal androgens, But aldosterone control by more dominant mechanisms remains intact. 66

67. Conti. A liberal salt diet is encouraged. Glucocorticoid substitution follows the same guidelines previously outlined for primary adrenal insufficiency. 67

68. Management of acute adrenal insufficiency 68

69. Steroid replacement during the perioperative period Perioperatively, patients with adrenal insufficiency and those with HPA suppression from chronic steroid use require additional corticosteroids; To mimic the increased output of the normal adrenal gland during stress. 69

70. Conti. The normal adrenal gland can secrete up to 100 mg/m2 of cortisol per day or more during the perioperative period. The pituitary–adrenal axis is usually considered to be intact if a plasma cortisol level higher than 19 μg/dL is measured during acute stress, But there is no precise threshold . 70

71. Conti. The degree of adrenal responsiveness has been correlated with the duration of surgery and the extent of surgical trauma. 71

72. Conti. The mean maximal plasma cortisol level measured during major surgery (colectomy, hip osteotomy) was 47 μ g/dL. Minor surgical procedures (herniorrhaphy) resulted in mean maximal plasma cortisol levels of 28 μ g/dL 72

73. Conti. Adrenal activity may also be affected by the anesthetic technique used. Regional anesthesia is effective in postponing the elevation in cortisol levels during surgery of the lower abdomen and extremities. 73

74. Conti. Deep general anesthesia may also suppress the elevation of stress hormones such as ACTH and cortisol during the surgical procedure. 74

75. Management options for steroid replacement in the perioperative period 75

76. Exogenous glucocorticoid therapy The therapeutic use of supraphysiologic doses of glucocorticoids has Expanded. Dexamethasone, methylprednisolone, and prednisone have less mineralocorticoid effect than cortisone or hydrocortisone. 76

77. References Barash 8 th edition Morgan 7 th edition 77