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Management of a DKA Patient with Severe Metabolic and Ketoacidosis with Chronic Renal Insufficiency

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Management of a DKA Patient with Severe Metabolic and Ketoacidosis with Chronic Renal Insufficiency Otterbein University Digital Commons @ Otterbein Nursing Student Class Projects (Formerly MSN) Student Research & Creative Work Fall 2014 Management of a DKA Patient with Severe Metabolic and Ketoacidosis with Chronic Renal Insufficiency Brian Albany Otterbein University, [email protected] Follow this and additional works at: https://digitalcommons.otterbein.edu/stu_msn Part of the Endocrine System Diseases Commons, Medical Pathology Commons, and the Nursing Commons Recommended Citation Albany, Brian, "Management of a DKA Patient with Severe Metabolic and Ketoacidosis with Chronic Renal Insufficiency" (2014). Nursing Student Class Projects (Formerly MSN). 6. https://digitalcommons.otterbein.edu/stu_msn/6 This Project is brought to you for free and open access by the Student Research & Creative Work at Digital Commons @ Otterbein. It has been accepted for inclusion in Nursing Student Class Projects (Formerly MSN) by an authorized administrator of Digital Commons @ Otterbein. For more information, please contact [email protected]. Management of a DKA patient with severe metabolic and ketoacidosis with chronic renal insufficiency Brian Albany BSN, CCRN Otterbein University, Westerville, Ohio Introduction Case Study Underlying Significance of Pathophysiology Implications for nursing care References Pathophysiology • Identify if the patient with DKA has [1] Bailey, J. L. (2013). Insulin Resistance and Muscle Metabolism in Chronic Diabetic ketoacidosis (DKA) A 55 year old female patient with a Healthcare providers are able to tailor case-specific treatment through an in- renal insufficiency Kidney Disease. ISRN Endocrinology, 1-14. doi:10.1155/2013/329606 serves as one the leading causes of past medical history of type one depth analysis and dissection on the pathophysiological processes associated with a • Draw serial labs: Chem 7, Beta [2] Brown, C., Watson, W., Morrison, I., & MacLennan, K. (2014). Novel methods of mortality in diabetic patients [14]. diabetes and end-stage renal disease patient in DKA with a comorbidity of chronic kidney disease. The goal of treatment hydroxybutyrate, and ABGs q 6 teaching diabetic ketoacidosis ( DKA) diagnosis and management in a The mortality has decreased over presents to the intensive care unit with for DKA is to reduce serum glucose levels and ketoacidosis through the hours clinical curriculum: Sim- DKA. Practical Diabetes, 31(5), 207-211. the past several decades due to the diabetic ketoacidosis. The patient had administration of parental insulin. This will ultimately result in the improvement of • Consult with physician to obtain doi:10.1002/pdi.1868 rapid recognition of the disease the following lab values: acidosis and will produce a state of acid-base homeostasis. This may not be an order to administer sodium [3] Csaba, K. P. (2013, October 8). Pathogenesis, consequences, and treatment of state and the improvement of effective solution to follow in patients who present with severe metabolic and bicarbonate if pH<6.9 metabolic acidosis in chronic kidney disease (R. H. Sterns & J. P. Forman, management of DKA [14]. Despite a • Glucose-1,107 mg/dL ketoacidosis. • Monitor hourly blood glucose level Ed.). Retrieved October 2, 2014, from UpToDate website: decline in mortality rates over the • Beta hydroxybutyrate-7.6 Insulin resistance is defined as “a clinical condition where there is a reduced • Follow DKA protocol for fluid http://www.uptodate.com past twenty years from 7.96% to mg/dL biological effect for any given blood concentration of insulin,” [8]. It is characterized management strategy [4] Farwell, W., & Taylor, E. (2008). Serum bicarbonate, anion gap and insulin 0.67%, errors in management of the • Anion Gap-36 mEq/l as reduced tissue responses to the action of insulin [1]. One study concluded that • Provide electrolyte resistance in the National Health and Nutrition Examination disease state are associated with • Creatinine-4.54 mg/dL there is a direct relationship between a lower serum bicarbonate and high anion supplementation as blood glucose Survey. Diabetic Medicine, 25(7), 798-804. significant morbidity and mortality • BUN-80 mg/dL gap which are both independently associated with reduced insulin sensitivity [4]. levels normalize [5] Guneysel, O., Guralp, I., & Onur, O. (2008). Bicarbonate therapy in diabetic [2]. Utilization of DKA protocols in • GFR-<5ml/min The data from this study supports the hypothesis that the production of organic • Call physician to transition patient ketoacidosis. Bratislavské Lekárske Listy, 109(10), 453-454. the acute care setting have allowed • Lactate-4.1 mg/dL acid serves as a central feature of insulin resistance [4]. The use of alkali therapy in onto subcutaneous insulin when [6] Kobayashi, S., Maesato, K., Moriya, H., Ohtake, T., & Ikeda, T. (2005). Insulin congruency in care and delivery of DKA is controversial because the acidosis should correct itself through the anion gap closes resistance in patients with chronic kidney disease. American Journal Of Kidney effective lifesaving treatment. ABG: administration of insulin and fluids; however, many studies show that insulin Diseases, 45(2), 275-280 Despite advances in standardized • pH-6.85 sensitivity is decreased in uremic patients; therefore, treatment of metabolic [7] Kraut, J., & Madias, N. (2011). Consequences and therapy of the metabolic acidosis DKA protocols, there still remains a • Co2-12 mmHg Figure 1: Pathological process of acidosis through alkali therapy is necessary in achieving a decrease in insulin of chronic kidney disease. Pediatric Nephrology, 26(1), 19-28. gap in how to manage specific • HCO3-1.9 mmol/L DKA [15] resistance with patients that also present with end stage renal disease [1,9,11,13]. doi:10.1007/s00467-010-1564-4 patient populations with end stage • PO2-197 mmHg Data suggests that acidosis should be corrected as soon as possible which will Conclusion [8] Mak, R. H. (2008). Insulin and its role in chronic kidney disease. Pediatric renal disease. Understanding the DKA develops as a result deficient result in increased insulin sensitivity to lower blood glucose levels and decrease Nephrology, 23(3), 355-362. doi:10.1007/s00467-007-0611-2 pathophysiology behind these These lab values indicate the levels of insulin circulating throughout the lipolysis [6]. The exogenous insulin given to treat patients in DKA is insensitive and The current standardized [9] Mak, R. K. (1998). Effect of metabolic acidosis on insulin action and secretion in patient populations will yield better combination of severe ketoacidosis from body causing a triad of hyperglycemia, ineffective without neutralizing the blood pH through bicarbonate therapy in such DKA protocols do not address uremia. Kidney International, 54(2), 603-607. doi:10.1046/j.1523- outcomes with the ultimate goal of DKA and metabolic acidosis related to hyperketonemia, and acidosis [10,14]. extreme circumstances. The American Diabetes Association states how severe patients with renal insufficiency. 1755.1998.00023.x decreasing the mortality rate. chronic renal insufficiency. Counterregulatory hormones consisted of acidosis in hyperglycemic crises can lead to more adverse effects and that adult Treatment for diabetic patients [10] McCance, K. L., & Huether, S. E. (2014). Pathophysiology the biologic basis for The patient arrives to the intensive catecholamines, glucagon, and cortisol are patients with a pH < 6.9 should receive sodium bicarbonate until pH>7.0 is in DKA with chronic kidney disease in adults and children (7th ed.) (V. L. Brashers & N. S. Rote, Eds.). St. care unit with an intact neurological activated in a state of insulin deficiency achieved [5]. disease should revolve around Louis, MO: Elsevier. status, stable vital signs, and on room ultimately causing an increased blood The kidneys play a major role in metabolism of insulin [12]. Approximately correcting extreme metabolic [11] Min-Tser, L., Chih-Chien, S., Kuo-Chin, H., Chia-Chao, W., Lan, L., & Kuo-Cheng, L. air. The nurse titrated the insulin drip glucose level. The glucagon activates 25% of daily insulin production is degraded by the kidneys [12]. Renal metabolism acidosis states (pH<6.9) before (2012). Insulin Resistance in Patients with Chronic Kidney Disease. Journal Of per hospital’s DKA policy. This policy gluconeogenesis in the liver to form more is augmented in diabetic patient’s receiving exogenous insulin because the insulin the administration of parental Biomedicine & Biotechnology, 20121-12. doi:10.1155/2012/691369 states that the nurse is able to double glucose and the body starts to break down bypasses filtration through the liver when injected into the systemic circulation insulin. This approach will [12] Palmer, B. F., & Henrich, W. L. (2013, June 6). Carbohydrate and insulin the insulin infusion rate if the blood adipose tissue through lipolysis which [12]. Since the renal clearance of insulin is 200ml/min, patients with an impaired increase insulin sensitivity and metabolism in chronic kidney disease (J. S. Berns & A. M. Sheridan, Ed.). glucose level has not decreased after yields free fatty acids and a state of GFR will have unfiltered insulin freely circulating in the body [12]. This becomes utilization to decrease blood Retrieved from UpToDate website: http://www.uptodate.com initiating the drip. The patient’s blood hyperketonemia. The circulating ketones significant when treating a DKA patient with renal insufficiency. Administering glucose levels and halt the [13] Siew, E., & Ikizler, T. (2010). Insulin
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