Case Study: Susan Summers and Cushing Syndrome

This is an essay in which a study is done of a patient known to have type two diabetes mellitus and also presented to the hospital with symptoms and signs of Cushing syndrome. She was admitted to hospital where she underwent laparoscopic adrenalectomy surgery to correct the Cushing's syndrome. The patient however developed a complication postoperatively. The essay seeks to create a proper understanding of the patient's presenting complaint and the deterioration that occurred after the patient was taken to the ward for recovery. The causes and pathological changes that occur in a patient suffering from Cushing syndrome will be discussed. In this essay, the pathological changes underlying the deterioration of the patient after the surgery will also be outlined and explained. This will be followed by an outline of the plan of nursing management for the patient in the ward to ensure that the situation is alleviated. At the end of the essay, a discussion will be presented to other healthcare providers who would be contacted to assist in the management of the patent before she is discharged.

The patient presented to the hospital with Cushing syndrome, which is a disease that occurs as a result of prolonged exposure to high levels of glucocorticoids (Guyton et al. 2006). These glucocorticoids may be endogenous or exogenous. The specific glucocorticoid hormone implicated in this disease is Cortisol. The hormone is produced in zona fasiculata of the adrenal cortex (McMinn, 2013). Hormone production is regulated by the pituitary gland which produces adrenocorticotropic hormone (ACTH) that stimulates its secretion. The pituitary gland is in turn controlled by the hypothalamus which secretes corticotropin-releasing hormone (CRH). The primary role of cortisol in the boy is in the regulation of blood glucose. The hormone stimulates utilization of blood glucose thus lowers its blood levels (Barret et al. 2010)

The etiology of Cushing syndrome is divided into two depending on the source of the elevated levels of glucocorticoids. It may be from outside the body; exogenous or from inside the body; endogenous. Exogenous Cushing syndrome is mostly caused by intake of glucocorticoids, especially when it is administered as medication for some diseases exemplified by inflammatory bowel disease amongst others (Hopkins, 2008). Endogenous Cushing is divided further into two based on the role of ACTH in the development f disease

ACTH Dependent Cushing Syndrome

This type comes about when the pituitary gland produces excessive amounts of ACTH due to the presence of a tumor known as a pituitary adenoma. The high ACTH thus causes the production of glucocorticoids from the adrenal gland which results in the syndrome. The ACTH may also be produced from an ectopic site such as lung cancer cells and other carcinoid tumors (Nguyen, 2017). When there is increased secretion of CRH for any reasons, for example, ectopic production, this ultimately leads to increased secretion of glucocorticoids and development of the disease. (Barret, et al. 2010)

ACTH Independent Cushing Syndrome

This type of disease may be caused by lesions in the adrenal glands that stimulate increased production of the hormones. Such a lesion may be adrenal adenoma, carcinoma or hyperplasia. Besides these neoplastic changes, some patients suffer from conditions that lead to adrenal gland hyperfunction and excessive hormone production. One such example is McCune- Albright syndrome (Nguyen, 2017). The increased levels of glucocorticoids may also be as a result of extra hormone secretion from an ectopic site. Such ectopic sites are best exemplified by ovarian carcinoma which is the commonest source of ectopic cortisol. Some rare cases of ACTH independent Cushing syndrome have been reported where the adrenocortical cells express abnormal receptors for gastric inhibitory polypeptide, vasopressin and other hormones, which impairs regulation of the secretion of cortisol (Barret, et.al. 2010)

When a patient has the increased levels of cortisol in their blood, some pathological changes occur which lead to the eventual manifestation of the disease. The patients have low protein levels, therefore they have thin skin and subcutaneous tissue. They also have poorly developed muscles which leads to the thin limbs. They heal poorly, and their hair is thin and scraggly due to the low protein levels. Most patients experience increase in body hair and acne. This is attributed to increased secretion of androgens which usually accompanies an increase in the secretion of glucocorticoids. The patients also have a classical pattern of distribution of body fat. It collects in the face, abdominal wall and upper back while the extremities remain thin (Nguyen, 2017). This may have been the case in Susan summers who was reported to have had a body mass index of35kg/m2. As the thin skin over the abdominal wall is stretched for at to be deposited underneath, the sub-dermal tissues rupture, forming prominent purple striae. The amino acids released from catabolism of proteins are mostly converted to glucose in the liver, which may lead to development of type two diabetes mellitus in a susceptible individual (Barret, et. al. 2010). This may also have been the cause for the diabetes that was diagnosed in Susan. The high levels of glucocorticoids in Cushing syndrome may exert some mineralocorticoid activity in the kidneys leading to salt retention and development of hypertension. Most patients with this syndrome also have collapsed vertebral bodies and increased frequency o bone fractures as a result of increased bone resorption and reduced deposition precipitated by the high levels of glucocorticoids. The high hormone levels also lead to mental aberrations that are seen in some of the patients (Barret, et.al. 2010)

After her surgery, Susan was reported to have had an uneventful recovery in the post-anesthetic recovery room. Upon arrival to the ward she was afebrile with a respiratory rate of 30 breaths per minute, systolic blood pressure of 160 mmHg and diastolic pressure of 90mmHg. She also had a pulse rate of 128 beats per minute and reported to have no pain. Her urine output was low, only having passed 5millilitres of urine over an hour. The elevation in both systolic and diastolic blood pressure, respiratory rate and pulse rate in the patient together with the low urine output were symptoms of pre-renal acute renal failure. This was most likely caused by poor perfusion to the kidney that occurred during the surgery. The low supply of blood compromised the kidney function leading to acute renal failure instances such as these have been reported in similar circumstances amongst patients who have had adrenalectomy (Kim, et.al. 2016). The problem comes about when the blood supply to the kidney through the renal artery is compromised. The cause of the compromise of blood supply may be obstruction of the blood vessel. It may also be caused by massive blood loss which reduces the intravascular volume, which causes poor perfusion of the kidneys and acute injury. The blood loss may occur in the setting of a surgical procedure such as the one the patient underwent. (Hope, 2017)

When the blood supply to the kidneys is low, a feedback loop is activated which is designed to increase the blood flow into the kidneys. Notably, this is the renin-angiotensin-aldosterone axis. Renin is produced by the kidneys and it converts angiotensin I to angiotensin II which is the active form. The angiotensin II causes vasoconstriction to increase blood pressure and enhance perfusion into the kidneys. It also stimulates secretion of aldosterone from the adrenal cortex which stimulates retention of sodium ions thus resulting in an increase in blood volume by osmosis and eventually an increase in blood pressure. (Guyton, et. al. 2006). The high blood pressure increases the work of the heart, which leads to an increased heart rate. Poor perfusion of the kidneys leads to retention of materials that are excreted through urine these include hydrogen ions. An accumulation in these ions leads to a drop in the blood pH known as acidosis. The respiratory rate is thus increased in an attempt by the body to lose these ions in the form of carbon (IV) oxide and restore the normal pH value. This explains the fast respiratory rate (Barret, et. al. 2006).

The first step of care for this patient would be to reduce the fluid input for the patient as her output is impaired. She should also be monitored keenly for input and output of fluids to ensure that there is no fluid retention (Adler, 2001). Secondly, the patient should have a physical examination to assess for complications of acute renal failure such as lung edema through auscultation. Assessment of bipedal and facial edema should also be conducted. The cause of the acute kidney failure should be investigated and corrected. This can be done by transfusion if the cause is acute blood loss as is probably the case for this patient. The patient should be put on diuretics to aid in relieving fluid retention during the recovery period before kidney function is maximal again (Adler, 2001).

Other health care providers who would be important in the management of this patient would include a specialist in nephrology because the main affected system is the kidneys. The patient would also require a radiologist since she will need investigations such as a chest X-ray to assess for complications of the renal failure such as lung edema and cardiomegaly. She will also need other investigations such as an abdominal ultrasound to assess the state of the kidneys. The patient would also benefit from having a review from a psychiatrist as acute renal failure frequently leads to an altered mental state.

Conclusion

In conclusion, the patient presented to the hospital with Cushing syndrome, which is caused by elevated glucocorticoids in blood. The patient had symptoms that could have been as a result of the syndrome. After the operation to correct the Cushing, the patient developed acute kidney failure that would have most likely been caused by acute hemorrhage during the surgery. The main goals of nursing care would be to reduce fluid intake so as no to have excessive fluid retention. The underlying cause of the failure should also be corrected and the patient managed with diuretics to prevent fluid retention. The patient would need care from a specialist in nephrology, a radiologist, and psychiatrists as well as primary doctors and nurses.

References

Adler, S.H. (2001). Acute Renal Failure: Pathophysiology and Treatment. Nephrology and Board Review Manual.

Barett, K. Brooks, H. Boitano, S. and Barman, S. (2010). Ganong's Review of Medical Physiology. Twenty Third Edition. Elsevier Saunders Publishers.

Guyton, A.C., and Hall, J.E. (2006). Textbook of Medical Physiology. Eleventh Edition. Elsevier publishers.

Hope, W.W. (2017). Laparoscopic Right Adrenalectomy. Medscape.

Hopkins, R.L., and Leinung, M.C (2008). Exogenous Cushing Syndrome and Glucocorticoid Withdrawal. Division of Endocrinology and Metabolism, Albany Medical College. Elsevier Saunders Publishers.

Kim, D.H. Kwon, J.K. Sang, A.J. Jang, H.R. Jung, S. Kim, J. Kim, J.H. Lee, J.E. Huh, W. Kim, D.J and Oh, H.Y. (2016). Risk Factors For Renal Impairment Revealed After Unilateral Adrenalectomy in Patients with Primary Aldosteronism. National Center for Biotechnology Information.

Kumar, V. Abbas, A.K and Aster, J.C.( 2015). Robins and Cotran Pathologic Basis of Disease. Ninth Edition. Elsevier Publishers.

McMinn, R.M.H. (2013). Last's Anatomy; Regional and Applied. Tenth Edition. Churchill Livingstone Publishers.

Nguyen, H.C.T. (2017). Endogenous Cushing Syndrome. Drugs and Diseases, Endocrinology. Medscape.