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Comprehensive case study: acute kidney injury.

In the United States, renal disease has continued to be a prevalent problem. Current data suggest 1% of patients admitted to the hospital are diagnosed initially with acute kidney injury (AKI), while about 2%-5% of hospitalized patients develop AKI secondarily (Workeneh, 2013). An estimated 1%-25% of patients in intensive care settings are affected by AKI with a mortality rate of 15%-60% (Singbartl & Kellum, 2012). Dirkes (2011) suggested the mortality rate is closer to 40%-90%. The cost of treatments required for AKI is astonishing; hemodialysis is approximated to cost $32 million annually (Jorgensen, 2013). In fact, nearly 95% of nephrologist consults are related directly to AKI (Workeneh, 2013).

Acute kidney injury is "a sudden decline in kidney function, causing disturbances in fluid balance, electrolyte shifts, acid base imbalance, and a loss in kidney function that causes a decline in the glomerular filtration rate" (Dirkes, 2013, p. 125). Acute kidney injury, previously known as acute renal failure, can be caused by three different injury pathways: prerenal, intrarenal, and postrenal. Prerenal causes are the most common as they are related directly to lack of blood flow to the kidneys; examples would include sepsis, severe hypotension, renal artery stenosis, and hypovolemia from severe blood loss (Kache & Trinkus, n.d.). Intrarenal injury occurs inside the kidney, such as acute tubular necrosis or contrast-induced nephropathy. Postrenal injury is caused by an obstruction below the kidneys; examples include calculi, blood clot, enlarged prostate, and strictures (Yaklin, 2011).

The outcome for an affected patient will depend on the cause of AKI and the glomerular filtration rate (GFR) (Dirkes, 2011). Acute kidney injury can be reversible, although recovery does take a significant amount of time (Russell, 2009). In many cases, however, AKI can result in chronic kidney injury, "a gradual and progressive reduction of functioning kidney mass" (Russell, 2009, p. 328), or death. As nephrons do not regenerate, early identification and treatment are essential to reverse AKI. Goldberg and Dennen (2008) found 12.5% of patients who survived AKI became dependent on long-term dialysis.

Case Study

Mr. Benning, age 57, presented to the emergency department with altered mental status, oliguria, hypertension, and nausea. In triage, his vital signs were as follows: temperature 97.0[degrees], pulse 123 beats/minute, respirations 10 breaths/minute, blood pressure 240/118 mm Hg, and oxygen saturation 87% on room air. The patient was admitted immediately to investigate the extent of his illness.

Past Medical History

Gastroesophageal reflux disease, hypertension, and diabetes mellitus type 1. Mr. Benning had not been seen by his physician in the past year, as he continually missed his scheduled appointments.

Home Medications

Omeprazole (Prilosec[R]) 10 mg daily, insulin glargine (Lantus[R]) 45 units daily in the morning, insulin aspart (Novolog[R]) 10 units before meals, lisinopril (Prinivil[R]) 10 mg daily, furosemide (Lasix[R]) 40 mg twice daily, potassium chloride 10 mEq daily, metoprolol tartrate (Lopressor[R]) 50 mg twice daily, diltiazem (Cardizem LA[R]) 240 mg daily (U.S. Department of Health and Human Services [DHHS], 2003)

Laboratory Results

Potassium 6.9 mEq/L, blood urea nitrogen (BUN) 70 mg/dl, creatinine 7.2 mg/dl, phosphorus 7.0 mg/dl, calcium 6.2 mg/dl, hemoglobin 7.0 g/dl, hematocrit 28%, white blood count 4.5/mcL, hemoglobin A1C 11.5

Assessment in the Emergency Department

The patient was found to have altered mental status, tachycardia, crackles, malignant hypertension, and EKG changes, including peaked-T waves. Mr. Benning was diagnosed with acute kidney injury and underwent insertion of a temporary dialysis access catheter. He was admitted to the medical unit, where his first hemodialysis treatment was begun.

Nursing Considerations

1. What underlying causes in Mr. Benning's medical history may have put him at increased risk for AKI? The two leading causes of kidney disease in the United States are hypertension and diabetes mellitus (National Kidney Foundation, 2013). The risk of developing kidney disease increases when these two conditions are not well controlled. Over time, this lack of control leads to damage to the renal microvasculature. Mr. Benning has a history of both disorders, increasing his risk for renal disease (Russell, 2009). In addition, Mr. Benning was taking an angiotensin-converting enzyme inhibitor which can lead to renal disease (DHHS, 2003).

2. Why was Mr. Benning experiencing altered mental status and nausea? First, his kidneys were unable to excrete waste products, leading to accumulation of urea and creatinine in the bloodstream. This also caused nausea, vomiting, decreased appetite, and altered mental status (Russell, 2009). Second, the insufficient hemoglobin caused a reduction in oxygen delivery to the brain and contributed to altered mental status. Without sufficient hemoglobin to carry oxygen to vital organs, those areas have a decrease in oxygen delivery. In this case, the decreased oxygen delivery to the brain resulted in altered mental status (Olson, 2009). Because the kidneys produce erythropoietin, which in turn causes the bone marrow to replenish red blood cells, renal patients often require blood transfusions to maintain homeostasis (Russell, 2009). Mr. Benning's nausea is a result of the excess urea in the bloodstream and stomach. Because the body is trying to eliminate this waste product, it will likely cause him to vomit (Russell, 2009).

3. What vital signs changes need to be addressed immediately?

* Blood pressure--Mr. Benning's blood pressure is elevated for several reasons. First, the kidneys regulate blood pressure by releasing hormones (renin and angiotensin) in response to water and sodium content in the body or as a reaction to hypoperfusion. The kidneys are not functioning normally to react appropriately. Assessment identified crackles; Mr. Benning likely has fluid overload because he cannot excrete the excess fluid via the kidneys (Russell, 2009). The increase in volume has increased Mr. Benning's blood pressure, which will improve with hemodialysis (Yaklin, 2011).

* Oxygen saturation--Mr. Benning is hypoxic due to pulmonary edema from fluid overload; his alveoli cannot perform the proper gas exchange at the capillary level. Administering oxygen will improve his oxygen saturation level and possibly the tachycardia (Burton, 2009).

* Heart rate--Tachycardia is often a compensatory response. The underlying problem must be addressed in order to reduce Mr. Benning's heart rate. In this situation, fluid overload, hypoxia, and electrolyte imbalances may be contributing factors. Hyperkalemia can result in a variety of cardiac signs and symptoms including tachycardia (McIntyre, Femenia, Arce, Perez-Riera, & Baranchuk, 2011). Therefore, hemodialysis would be indicated to reduce his serum potassium, thus alleviating Mr. Benning's tachycardia (Russell, 2009).

* The EKG changes with the peaked T-wave are a result of Mr. Benning's high serum potassium. Ultimately, he will need hemodialysis to reduce this value to prevent dysrhythmias or cardiac arrest (Russell, 2009).

4. What is the significance of the different laboratory results? Why is the hemoglobin A1C a concern? Patients with AKI have an elevated serum potassium, BUN, and creatinine as a direct result of the inability to excrete the excess waste via the urine. Critically high potassium can result in cardiac arrhythmias and even death. Calcium and phosphorus values tend to occur in opposition to each other; when one is high, the other is low. High phosphorus in turn leads to low calcium, which can cause cardiac arrhythmias and long-term bone loss. The hemoglobin A1C demonstrates poor glycemic control for the last 3 months, most likely contributing to the acute kidney injury (Quinn, 2009). Arterial blood gases should be drawn to assess Mr. Benning's acid base balance. Patients diagnosed with AKI are more likely to be in a metabolic acidotic state (Yaklin, 2011).

5. The patient received hemodialysis immediately to alleviate the emergent concerns and issues. What other treatments are expected for his long-term care? Mr. Benning either will recover slowly or have irreversible damage leading to chronic renal failure. The nephrologist will continue hemodialysis and monitor his serum creatinine as the best indicator of kidney function (not urine output). Based on past medical history and laboratory results, Mr. Benning may not recover fully from this event. In this situation, he would be expected to maintain a schedule of routine hemodialysis in the outpatient setting approximately 3 days a week. In addition, close monitoring by a nephrologist would be optimal (Rahman, Shad, & Smith, 2012).

6. What specific nursing care should be provided? Strict intake and output measurements, daily weights, and venous thromboembolism (VTE) prophylaxis are key in patients with AKI. They are highly susceptible to VTE and infection. Meticulous catheter care is of utmost importance. In addition, laboratory results suggest a risk for cardiac arrhythmias. This patient should be transferred to a unit where cardiac monitoring is performed continuously (Russell, 2009).

7. What educational needs are critical to this patient's long-term success and health? Mr. Benning needs extensive teaching regarding ideal diet, diabetes management, blood pressure control, hemodialysis, infection prevention, and new medications. Involving dieticians, hemodialysis nurses, and diabetic educators is critical. Mr. Benning must understand the importance of taking medication as prescribed so as not to interfere with his hemodialysis. The nurse should advise him never to stop his medications without first discussing with his physician (Russell, 2009).

8. What changes may be necessary to the patient's medications and dietary habits? Mr. Benning needs to change his diabetic and hypertensive regimen regardless of whether his kidney injury is permanent. The nurse should investigate whether he was adherent with his medication regimen and diet. Mr. Benning may need reinforcement and support if he was nonadherent. If he was adherent with his regimen, then an adjustment must be made to his dosages. For chronic kidney disease, the potassium chloride would be discontinued and a phosphorus inhibitor might be added. Additionally, the physician may consider adding erythropoietin (Procrit[R]) to increase red blood cell production. Mr. Benning will need to adhere to a strict renal and American Diabetes Association[R] diet for long-term success (Russell, 2009).

REFERENCES

Burton, J.E. (2009). The respiratory system. In H. Craven (Ed.), Core curriculum for medical-surgical nursing (4th ed.) (pp. 221-250). Pitman, NJ: Academy of Medical-Surgical Nurses.

Dirkes, S. (2011). Acute kidney injury: Not just acute renal failure anymore? Critical Care Nurse, 31(1), 37-50.

Dirkes, S. (2013). Sepsis and inflammation: Impact on acute kidney injury. Nephrology Nursing Journal, 40(2), 125-132.

Goldberg, R., & Dennen, P. (2008). Long-term outcomes of acute kidney injury. Advances in Chronic Kidney Disease, 15(3), 297-307.

Jorgensen, A.L. (2013). Contrast-induced nephropathy: Pathophysiology and preventive strategies. Critical Care Nurse, 33(1), 37-47. Kache, S. & Trinkus, P. (n.d.). Acute renal failure. Retrieved from http://peds.stanford.edu/Rotations/picu/pdfs/21_acute_renal failure.pdf

McIntyre, W.F., Femenia, F., Arce, M., Perez-Riera, A.R., & Baranchuk, A. (2011). Importance of early electrocardiographic recognition and timely management of hyperkalemia in geriatric patients. Experimental & Clinical Cardiology, 16(2), 47-50.

National Kidney Foundation. (2013). Kidney disease: Causes. Retrieved from http://www.kidney.org/atoz/content/kidneydiscauses.cfm

Olson, V.L (2009). The hematologic system. In H. Craven (Ed.), Core curriculum for medical-surgical nursing (4th ed.) (pp. 441-462). Pitman, NJ: Academy of Medical-Surgical Nurses.

Quinn, L. (2009). Diabetes. In H. Craven (Ed.), Core curriculum for medical-surgical nursing (4th ed.) (pp. 293-310). Pitman, NJ: Academy of Medical-Surgical Nurses.

Rahman, M., Shad, F.A., & Smith, M.C. (2012). Acute kidney injury: A guide to diagnosis and management. American Family Physician, 86(7), 631-639.

Russell, S.S. (2009). The renal and urologic systems. In H. Craven (Ed.), Core curriculum for medical-surgical nursing (4th ed.) (pp. 311-338). Pitman, NJ: Academy of Medical-Surgical Nurses.

Singbartl, K., & Kellum, J.A. (2012). AKI in the ICU: Definition, epidemiology, risk stratification and outcomes. Kidney International, 81(9), 819-825. doi:10.1038/ki.2011.339.

U.S. Department of Health and Human Services (DHHS). (2003). JNC 7 express: The seventh report of the joint committee on prevention, detection, evaluation, and treatment of high blood pressure. Retrieved from http://www.nhlbi.nih.gov/guidelines/hypertension/ express.pdf

Workeneh, B.T. (2013). Acute kidney injury. Retrieved from http://emedicine.medscape.com/article/243492-overview#a0156

Yaklin, K.M. (2011). Acute kidney injury: An overview of pathophysiology and treatments. Nephrology Nursing Journal, 38(1), 13-19.

Stephanie Gedeon, BSN, RN, CMSRN, is Clinical Nurse Educator, Henrico Doctors' Hospital, Richmond, VA.
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Title Annotation:Nurses as Educators
Author:Gedeon, Stephanie
Publication:MedSurg Nursing
Article Type:Clinical report
Geographic Code:1USA
Date:Nov 1, 2013
Words:2011
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