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Kenny-Joe Wallen The University of Kansas.  Physical  Mental  Emotional  Nutritional  Chemical  Traumatic  Pyscho-spiritual.

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Presentation on theme: "Kenny-Joe Wallen The University of Kansas.  Physical  Mental  Emotional  Nutritional  Chemical  Traumatic  Pyscho-spiritual."— Presentation transcript:

1 Kenny-Joe Wallen The University of Kansas

2  Physical  Mental  Emotional  Nutritional  Chemical  Traumatic  Pyscho-spiritual

3  Stage 1- Alarm  Fight or Flight Response- SNS activation  Hormone release and activation- Adrenalin  HPA axis- Cortisol  Stage 2- Resistances  PSNS activity returns  Glucose, Cortisol, and Adrenalin levels remain elevated in circulation  Stage 3- Exhaustion  If stressor continues beyond body’s capacity, organism exhausts resources and becomes susceptible to disease and death.

4  Hypothalamus  Corticotropin-releasing hormone (CRH)  Pituitary Gland  Adrenocorticotropic (ACTH)  Adrenal gland  Glucocortacoids  Cortisol  Mineralocorticoids  Aldosterone *HPA axis is regulated by a negative feedback mechanism

5  Primary- Destruction of all cortical zones  TB  Autoimmune  Congenital  Infection  AIDS most common cause  Malignancy  Trauma  Secondary  ACTH deficiency secondary to Hypothalamic or Pituitary dysfunction  HPA Suppression due to glucocorticoid therapy **Both forms will require supplemental steroids**

6  1.2% of population > 20 yr (~2,513,259)/ over 20 years  34 million prescriptions/ year  HPA suppression can occur after five daily doses of prednisone ≥ 20 mg and recovery of HPA function occurs gradually and can take up to 12 months  Adrenal gland atrophy and HPA suppression  Unable to respond to the stress of surgery

7  One of the most potent activators of the HPA axis  Endotracheal Intubation  Reversal  Extubation  Negative feedback mechanism fails  ACTH and Cortisol Cortisol  Normal secretion- 20-30 mg/day  During stress- as high as 200-500 mg/day

8  Patients receiving chronic corticosteroid have atrophy of their adrenal gland and subsequent suppression of the HPA axis rendering them incapable of producing an adequate amount of endogenous glucocorticoids to meet the demands of the operative stress. These individuals will present with signs and symptoms of adrenal insufficiency

9  Signs and Symptoms  Hypoglycemia  Hypotension  Tachycardia  Tachypnea  Anorexia, weight loss  Nausea, Vomiting, Abd pain  Hypo NA  Hyper K  Acidosis  Mucosal and Skin pigmentation Δ  Muscle Weakness  Fever

10  Preoperatively  H&P  Disease Process  Medications  How long? Last dose?  Intraoperatively  Avoid Etomidate  Early recognition of S&S of adrenal crisis  Treatment  Rapid IV infusion with saline /c cardiac monitoring  Steroid replacement therapy “Stress dosing”  If hemodynamically unstable consider inotropic support

11 Surgical StressMedical StressGlucocorticoid Dosages Minimal <1° under local anesthesia/ skin biopsy, routine dental work Non-febrile cough/ URI 15-30 mg/ day Minor Hernia repair Colonoscopy Viral Illness Bronchitis UTI 25 mg IV @Induction (40-60 mg/ day PO in divided doses) Moderate Open cholecystectomy Total joint replacement Abdominal hysterectomy Gastroenteritis Pneumonia Pyenephritis 75 mg/ day (25 mg IV q 8°) day of surgery. Taper over next 1-2 days Severe Cardiothoracic surgery Whipple Liver resection Pancreatitis MI Labor 150 mg/ day (50 mg IV q 8°) day of surgery Taper over next 2-3 days Critical/ Intensive Care Major Trauma Life-threatening complication Septic ShockMax 300/ day (50 mg IV q 6° or continuous infusion)

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13 References Finnerty, C. C., Mabvuure, N. T., Ali, A., Kozar, R. A., & Herndon, D. N. (2013). The Surgically Induced Stress Response. Journal of Parental and Enteral Nutrition, 37 (Supplemental 1), 21S-29S. Fournier, D. J., & Galante, M. (1957) Operative and Postoperative Emergency Use of Hydrocortisone Derivatives and Corticotropin. Journal of California Medicine, 86 (6), 374-377. Jung, C., & Inder, W. J. (2008). Management of adrenal insufficiency during the stress of medical illness and surgery. Medical Journal of Australia, 188, 409-413. Karlet, M. C., & Fort, D. N. (2013) The Endocrine System and Anesthesia. In Nagelhout, J. P., & Plaus, K. (5th ed.), Nurse Anesthesia. St. Louis, MO: Saunders/Elsevier. Marik, P. E., & Varon, J. (2008). Requirement of Perioperative Stress Doses of Corticosteroids. Journal of Archive of Surgery, 143 (12), 1222- 1226. Overman, R. A., Yeh, J. & Deal, C. L. (2013). Prevalence of oral glucocorticoid usage in the United States: A general population perspective. Arthritis Care & Research, 15 (3), 5-13. Schwartz, J. J., Akhtar, S., & Rosenbaum, S. H. (2013) Endocrine Function. In Barash, P. G., Cullen, B. F., Stoelting, R. K., Cahalan, M. K., Stock, M. c., & Ortega, R. (6 th ed.), Clinical Anesthesia. Philadelphia, PA: Lippincott Williams & Wolters. Selye, H. (1978) The Stress of Life, revised edition. New York: McGraw-Hill. Tsigos, C. & Chrousos, G. P. (2002). Hypothalamic-pituitary-adrenal axis, neuroendocrine factors and stress. Journal of Psychosomatic Research, 53, 865-871.


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