Acute Kidney Injury Critical Care, Summaries of Nursing

Download Acute Kidney Injury Critical Care and more Summaries Nursing in PDF only on Docsity! Acute kidney injury In the event of AKI in the patient with impending or actual TLS, a nephrology consult should be placed. The goals are to minimize delays in anticancer therapy and optimize renal function. The tenets of AKI management include managing volume status, correcting electr abnormalities,avoidingnephrotoxins,and adjusting medications for renal function (Abu- Alfa and Younes, 2010). The development of AKI may exacerbate preexisting electrolyte abnormalities, particularly hyperkalemia and hyperuricemia (Benoit and Hoste, 2010). Hemodialysis or renal replacement therapy may be considered in patients with large tumor burden, elevated WBC count, chronic kidney disease, end-stage renal disease, or AKI at the time of presentation, or congestive heart failure. Other authors have suggested that renal replacement therapy be employed when hyperphosphatemia continues for more than 6 h after the initiation of vigorous hydration (Darmon, Roumier, and Azoulay, 2009). The use of hemodialysis in this setting is not well studied and cannot be routinely recommended. Suggested criteria for hemodialysis include the following parameters unresponsive to other measures (Mughal et al., 2010; Varon and Acosta, 2010): Potassium ≥ 6 mEq/l Uric acid ≥ 10 mg/dl Phosphorous ≥ 10 mg/dl Fluid volume overload unresponsive to diuretics Symptomatic hypocalcemia Severe acidosis Uremic symptoms such as mental status changes Evidence-based treatment guidelines In 2008, evidence-based guidelines for the prevention and treatment of TLS in adults and children were published (Coiffer et al., 2008). The guidelines are the first to outline specific roles for both allopurinol and rasburicase (Mughal et al., 2010). An algorithm based on TLS risk was developed. For low-risk patients, no interventions for prevention are recommended. For intermediate-risk patients, hydration and allopurinol are recommended as initial therapy to prevent hyperuricemia. Allopurinol should start 12 h prior to anticancer the most common primary tumor type that involves the pericardium and is a difficult disease to treat. Other primary tumors of the heart include malignant fibrous histiocytoma, rhambdomyosarcoma, and angiosarcoma (Turner Story, 2006). Most effusions develop from lung or breast cancer; other causes include melanoma, leukemia, or lymphoma (Higdon and Higdon, 2006). Tumor obstruction of mediastinal lymph nodes can interfere with lymph drainage from the pericardium, leading to fluid accumulation. This is the most common cause of pericardial effusion in malignancy. Malignant effusions progress to tamponade more often than nonmalignant effusions because the presence of tumor cells stimulates the pericardium to produce excessive fluid (Turner Story, 2006). Tumors may also cause bleeding in the pericardial space, allowing rapid accumulation of fluid and increasing the risk for tamponade (Flounders, 2003). Many patients have metastatic disease in other sites at the time of presentation with pericardial effusion; the mean interval from diagnosis to development of tamponade is 17.4 months (Cozzi et al., 2010). Radiation therapy with doses of 4000 cGy or more to the chest is associated with the development of pericardial effusions. The majority of cases occur in the first year after radiation therapy (Miaskowski, 1999). Chemotherapy and biotherapy agents can also cause pericardial effusions. Other conditions that may increase risk include underlying heart disease, systemic lupus erythematosus, rheumatoid arthritis, scleroderma, myxedema, tuberculosis, bacterial endocarditis, and pericarditis (Turner Story, 2006). Pericardial effusions are classified by fluid type. Transudative fluids are low in protein and are the result of abnormal capillary permeability caused by benign mechanical factors such as cirrhosis. Transudative fluid is defined as having LDH levels less than 200 IU/l and protein levels less than 35 g/dl. Exudative effusions are protein-rich and are caused by leaking blood vessels due to increased capillary permeability. Exudative fluid has LDH levels greater than 200 IU/l and protein levels greater than 35 g/dl. Most malignant pericardial effusions are exudates.