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Etiology and Pathophysiology of Cushing's Syndrome

Discuss about the Case Study Cushing Syndrome Temperature management.

A case study of Susan Summers, a forty-year-old female obese patient admitted to the hospital for laparoscopic right adenectomy under general anesthesia due to Cushing’s syndrome. She was obese at 90kg with a BMI of 35kg/m2. She was a diagnosed type 2 diabetic and used nine units of alcohol at night day. She was admitted for removal of a benign tumor of her right adrenal gland. Her immediate post-operative recovery was uneventful. On return to the ward, her vitals become deranged with a respiratory rate of 30 breaths per minute, blood pressure of 160/90 mmHg, pulse rate of 128bpm, and a temperature of 35.00C. She also had a low urine output of 5mls within one hour. She, however, did not have any pain.

The present paper will give a detailed etiology and pathophysiology of Cushing’s syndrome; the patient’s main presenting clinical problem. It will outline the causes, signs, and symptoms of the said condition. It will also describe Susan’s deranged vital signs with reference to the normal vitals and try to link them to her presenting complain and the surgery. A brief outline of the effect of hypothermia on vital signs and reasons for the urine output will also be given. With the problem adequately described, priorities of care will be discussed with emphasis on vital signs and safe care 2 hours postoperative. Appropriate referral MDT team to effectively handle the patient thereafter will be given. Lastly, a summary of the entire work.

Cushing’s syndrome is a syndrome of excess cortisol, a hormone produced by the human adrenal glands. It is a disease mostly seen in women with a male to female ratio of 1:5 (Colledge, Walker & Ralston, 2013). The peak incidence of the disease is between 30-50 years. The adrenal cortex is an endocrine gland that produces cortisol and androgens. It is closely regulated by the hypothalamic-pituitary-adrenal axis through a cascade of hormones and negative feedback. The hypothalamus produces corticotropin-releasing hormone (CRH) which stimulates the pituitary gland to release adrenocorticotrophic hormone (ACTH). ACTH acts on the adrenal cortex to influence the release of glucocorticoids; of note is cortisol. A problem in this axis or in the adrenal cortex that leads to excess cortisol will give rise to Cushing’s syndrome. Exogenous glucocorticoids also give rise to Cushing’s when administered in excess (Colledge, Walker & Ralston, 2013).

Signs and Symptoms of Cushing's Syndrome

The causes of Cushing’s can be broadly divided into primary adrenal disease and secondary adrenal disease. Most primary causes of Cushing’s syndromes are tumors that influence the production of cortisol including adrenal adenomas, adrenal carcinomas, and adrenal cortical hyperplasia. Secondary causes involve ACTH production. Cushing’s disease is an example caused by a pituitary tumor that secretes ACTH which in turn causes overproduction of cortisol. This accounts for the majority of the endogenous causes (80%) (Colledge, Walker & Ralston, 2013). There is also a rare form due to ectopic production of ACTH by tumors that are not pituitary in origin including small cell carcinoma of the lung, medullary carcinoma of the thyroid and carcinoid tumors. Another form termed hypercortisolism or pseudo-Cushing's syndrome is due to major stress including alcohol excess, major depressive illness, and primary obesity.


Cortisol is the body’s main stress hormone and is normally increased during major stress including during illness. It is an adaptive mechanism as it activates gluconeogenesis, glycogenesis, and anti-inflammatory properties. Its effects on metabolism and immunity are what will be deranged in Cushing’s syndrome (Singh, Kotwal & Menon, 2013).

The signs and symptoms of Cushing’s syndrome are widespread (Raff, Sharma, & Nieman, 2014). Weight gain and fat redistribution are the most dramatic symptoms. Otherwise termed cushingoid appearance they include moon facies, weight gain with truncal obesity, buffalo hump, abdominal striae, atrophied thin skin and hyperpigmentation of skin folds (Glynn & Drake, 2014). The patients usually have glucose intolerance and develop diabetes mellitus. Interruption of production of luteinizing hormone and luteinizing hormone-releasing hormone leads to amenorrhea, infertility and decreased libido. In men leads to impotence. Hypertension due to Cushing’s is another important finding due to the mineralocorticoid effects of cortisol and due to activation of the renin-angiotensin-aldosterone system (Singh, Kotwal, & Menon, 2013). Proteolysis is increased in cortisol excess leading to thin skin with easy bruising. Muscle weakness is another cardinal symptom, especially in proximal muscle groups. The patient Susan had Cushing’s syndrome with the expected comorbid conditions of diabetes mellitus and obesity. Her cause was a tumor of the adrenal gland meaning it was an ACTH independent Cushing’s syndrome.

Susan’s vital signs were deranged as she was discharged to the wards. Vital signs measured for the monitoring of patients include temperature, blood pressure, pulse rate, respiratory rate and level of consciousness (AVPU). The normal respiratory rate in adults should be 12-20 breaths per minute. The temperature should fall between 36.50C to 37.20C. The blood pressure should be less than 130/85 mmHg and the systolic blood pressure should be more than 90 mmHg with a mean pulse pressure of between 30 -50 mmHg. The pulse rate should range from 60 to 100bpm (Glynn & Drake, 2014).

Deranged Vital Signs of Susan Summers

Susan’s vitals were not in the normal range with hypothermia (350C), a tachycardia of 128bpm, an elevated blood pressure of 160/90 mmHg and a tachypnea of 30 breaths per minute. The post-operative deterioration could be as a complication of the laparoscopic surgery. Complications include bowel perforation, intrabdominal bleeding, venous thrombosis among others (Jean-Francois, Defechereux, Raffaelli, Lubrano, & Gramatica, 2013). The vital signs serve as an indicator of postoperative deterioration. Two hours post-operative in the anesthesia recovery room were uneventful implying it is unlikely to be a complication due to anesthesia medication. Post-operative bleeding is one of the major complications and could explain the vital signs as the patient was slipping into hypovolemic shock. Another cause of hypovolemic shock is dehydration postoperative as fluid losses during and after surgery are not adequately restored. During hypovolemic shock, there is insufficient blood volume leading to a reduced cardiac output, hypoperfusion, and hypoxia. Compensatory mechanisms include the release of catecholamines that try to maintain cardiac output hence the high heart rate and rise in blood pressure. Compensation shunts blood away from non-vital organs like the skin and kidneys to more vital ones like the heart and brain (Colledge, Walker & Ralston, 2013). Renal hypoperfusion and the setting of an acute kidney injury explain the low urine output. A high respiratory rate occurs due to metabolic derangements. Due to hypoxia, the body reverts to anaerobic respiration and lactic acid is produced, accumulates due to poor renal mechanisms and causes a lactic acidosis. Compensation by the respiratory system is by hyperventilation to remove excess acid (Hinkle & Cheever, 2013). The impact of hypothermia on the vital signs is varied. It is caused by both local and general anesthesia. This is mostly due to vasodilatation caused by general anesthesia (Faulds & Meeking, 2013). It could also be caused by the reduced metabolic rate post adrenalectomy. The normal urine output is 0.5- 1.5 ml/kg/hour with the normal fluid intake. The patient should have at least 45ml of urine in the first hour. However, the patient had only produced 5ml of urine. This can be attributed to hypovolemic shock due to inadequate fluid monitoring leading to dehydration or inadequate adrenal response to the surgical stress (Chenitz & Lane-Fall, 2013).


To remedy the deranged vital signs, the cause has to be dealt with. According to the ABCD assessment in the emergency department, circulation has to be prioritized as the patient is displaying signs of circulatory compromise and shock. According to Hinkle & Cheever, (2013), the nursing interventions are geared at rewarming, fluid resuscitation and treatment of the cause of shock. Fluids should be calculated to include losses and titrated effectively. The vitals are to be measured and monitored regularly to note improvement. Patient monitoring should include medical and nursing observations, the operation site, note on complications and changes in management. This should help to stabilize the vital signs as the specific post-operative complication causing the deteriorating condition is sought.

Priorities of Care

Susan’s care needs 2 hours post-operative include pain control, fluid balance, infection control, early mobilization, monitoring for complications and appropriate nutrition (McKinley, 2014). Pain is both a psychological and physiologic hazard and lengthens hospital stay hence pain management post-operative is paramount. Infections following abdominal surgeries are a cause of morbidity and mortality and may complicate the procedure done. Prevention of sepsis and infection through proper surgical site care and the antibiotic cover is necessary. Early mobilization reduces chances of venous thrombosis, pulmonary emboli and pressure sores that further complicate the case (Beretta, Braga, & Casiraghi, 2012).

Safe care practices in nursing are practices aimed at reducing exposure to undesirable outcomes for patients. They include antiseptic barriers to reduce infection, use of antibiotics to reduce postoperative infections, use of pressure relieving bedding to prevent bed sores, appropriate post-operative nutrition among others.


Susan’s care should be multidisciplinary to ensure maximum benefit and quick recovery (Whiteman, Dhesi, & Walker, 2015). Aside from the medical and nursing team, the members of the MDT team that need to be involved in the case include a physiotherapist, a nutritionist, and social worker. The role of the physiotherapist is to help the patient to recover function and help in early mobilization. A nutritionist is important considering the patient is obese, a diabetic and also post-operative. A nutrition plan that will maximize benefit but not cause further harm will be helpful. A social worker will help the patient integrate back into society and deal with social stressors that she was previously dealing with due to a low paying job.

In conclusion, Cushing’s syndrome is an excess of cortisol and is usually comorbid with obesity and diabetes mellitus. Laparoscopic surgery carries several complications chief being bleeding that causes hypovolemic shock explaining the deranged vital signs of the patient two hours postoperative. The nursing care should be aimed at combating the post-operative complication, monitoring for improvement or deterioration while also paying close attention to patient safety. The management of a post-operative patient involves a multidisciplinary team of medical staff, nursing staff, physiotherapists, nutritionist and social workers.

References

Beretta, L., Braga, M., & Casiraghi, U. (2012). The first 24 hours after surgery: how an anesthetist, a surgeon, and a nurse would like to be treated if they were patients. hsr proceedings in Intensive Care and Cardiovascular Anesthesia, 4(3), 149-152.

Chenitz, K., & Lane-Fall, M. (2013). Decreased urine output and acute kidney injury in the PACU. Anesthesiology Clinic. 30(3), 513-526

Colledge, N., Walker, R, & Ralston, S. (2013). Davidson’s Principles and Practice of Medicine. (21st ed). New York, N.Y: ‎Edinburgh.

Faulds, M., & Meeking, T. (2013). Temperature management in critically ill patients. British Journal of Anaesthesia, 13(3), 75-79.

Glynn, M. & Drake, W. (2014). Hutchinson’s Clinical Methods: an integrated approach to clinical practice. London: Elsevier

Hinkle, J.L, Cheever, K.H. (2013). Brunner and Saddarth’s Textbook of Medical and Surgical Nursing, (13th ed) Philadelphia, PA: Wolters Kluwer Health/Lippincott Williams & Wilkins.

Jean-Francois, H., Defechereux, T., Raffaelli, M., Lubrano, D., & Gramatica, L. (2013). Complications of laparoscopic adrenalectomy: results of 169 consecutive procedures. World journal of surgery, 24(11), 1342.

McKinley, M. G. (2014). Introduction to critical care nursing. (10th ed.). Philadelphia: W. B. Saunders

Pivonello, R., De Leo, M., Cozzolino, A., & Colao, A. (2015). The treatment of Cushing’s disease. Endocrine Reviews, 36(4), 385-486.

Raff, H., Sharma, S., & Nieman, L. (2014). Physiologic basis for the etiology, diagnosis, and treatment of adrenal disorders: Cushing’s syndrome, adrenal insufficiency, and congenital adrenal hyperplasia. Comprehensive Physiology, 4(2), 739-769.

Singh, Y., Kotwal, N., & Menon, S. (2013). Endocrine hypertension- Cushing’s syndrome. Indian Journal of Endocrinology and Metabolism, 15(4), 313-316

Whiteman, R., Dhesi, K., & Walker, D. (2015). The high-risk patient: role for a multi-disciplinary team approach. British Journal of Anaesthesia, 116(3), 311-314.

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