Nursing management of Acute Kidney Injury Today’s topic is Nursing Management for clients with a acute kidney injury-previously known as acute renal failure.

Acute Kidney Injury (AKI) Definition: A sudden loss of kidney function caused by failure of renal circulation or damage to tubules or glomeruli Usually reversible Ischemia is primary cause Pre-renal Intra-renal Post-renal The definition of acute kidney injury is a sudden loss of kidney function caused by failure of renal circulation or damage to tubules or glomeruli. AKI is characterized by a rapid loss of kidney function demonstrated by an increase in serum creatinine and/or reduction in urine output. AKI is potentially reversible, it has a high mortality rate. The primary cause of death among clients with AKI is infection. AKI develops over hours to days with trends in blood urea nitrogen, creatinine, and potassium with or without reduction in UO. AKI is usually reversible with early recognition, aggressive treatment, monitoring progression and responses to the interventions. AKI is a sign of lack of perfusion to the kidneys. The goal is focused on adequate renal perfusion. The causes can be classified as prerenal, intrarenal, and postrenal

Common Causes of AKI PRERENAL INTRARENAL POSTRENAL Hypovolemia Dehydration hemorrhage diarrhea/vomiting Burns Nephrotoxic Injury Drugs Contrast dye Crush injury Benign Prostrate Hypertrophy (BPH) Decreased cardiac output Heart failure, MI Interstitial Nephritis Allergies (antibiotics) Infections (bacterial) Bladder cancer Decreased peripheral vascular resistance Anaphylaxis Septic shock Acute glomerularnephritis Malignant hypertension Calculi formation (kidney stones) Decreased renovascular blood flow Bilateral renal vein thrombosis Thrombotic disorders Spinal cord disease There are 3 categories of pathophysiologic states of azotemia: prerenal, intrarenal, and postrenal causes. Prerenal causes of AKI are factors external to the kidneys. These factors reduce systemic circulation causing reduction in renal blood flow, and lead to decreased glomerular perfusion and filtration. Prerenal causes include, hypovolemia as in dehydration, hemorrhage, diarrhea and vomiting and burns. Decreased cardiac output as seen in heart failure and myocardial infarction. Decreased peripheral vascular resistance as seen in anaphylaxis and septic shock. And lastly, a prerenal cause is decreased renovascualr blood flow events like bilateral renal vein thrombosis. Prerenal conditions can lead to intrarenal disease if the lack of oxygenated tissue in the kidneys is prolonged. Intrarenal causes of AKI include conditions that cause direct damage to the kidney tissue resulting in impaired nephron function. The damage causes usually results from prolonged ischemia, nephrotoxins, hemoglobin released from hemolyzed RBCs or myoglobin released from necrotic muscle cells. Nephrotoxins can cause obstruction of intrarenal structures by crystallization or by causing damage to the epithelial cells of the tubules. Hemoglobin and myoglobin can block the tubules and cause renal vasoconstriction. Nephrotoxic injury are caused by events such as overuse or misuse of medications, contrast dye, crush injuries, interstial nephritis, acute glomerularnephritis, malignant hypertension, and thromboitic disorders. Acute tubular necrosis (ATN) is the most common cause of intrarenal AKI. Postrenal causes involve mechanical obstruction in the outflow of urine. As the flow of urine is obstructed, urine refluxes or backs up into the renal pelvis, impairing kidney function. Common postrenal causes are BPH, bladder cancer, kidney stones, and spinal cord disease.

Here is a pathophysiologic map of how kidney failure occurs and the complications associated with the damage.

Assessment Clinical manifestations Oliguria phase Oliguria, diuretic, and recovery phase Oliguria phase Urinary changes reduction in urinary output About 50% of clients will not be oliguric, making initial diagnosis difficult UA will show casts, RBCs, WBCs, specific gravity 1.010 Fluid volume volume depletion (fluid retention occurs) Metabolic acidosis lack of excretion of bi-products of metabolism (urea) Sodium balance normal to hyponatremia states Potassium excess Hyperkalemia Hematologic problems Waste product accumulation BUN and serum creatinine are elevated Neurologic problems Due to the nitrogenous waste product accumulation Clinical manifestations follow 3 phases: initiation, maintenance and recovery. The initiation has very few manifestations. The maintenance phase is characterized by oliguria or urine output less than 400 mL/ 24 hours or less than 30 mL/hour. The oliguria phase occurs within 1 to 7 days of the injury to the kidneys. The diuretic phase begins with a gradual increase in daily UO of 1 to 3 L/day but may reach 3 to 5 L/day. Patients in the diuresis process will need to be monitored for electrolyte and volume loss. The diuretic phase lasts about 1 to 3 weeks. The recovery phase begins when the GFR increases, allowing the BUN and serum creatinine levels to plateau and then decrease.

Clinical Manifestations r/t Body Systems Urinary Cerebrovascular Respiratory GI Hematologic Neurologic Metabolic It is important to understand the common clinical manifestations seen throughout the body. The client will have a decrease in urinary output, proteinuria, decreased specific gravity, decreased osmolality, an increase in excretion of sodium. Cardiovascular changes include volume overload, heart failure, hypotension in early phases of AKI and hypertension from fluid volume overload in later stages of AKI, pericarditis, dysrhythmias. Respiratory changes include pulmonary edema, Kussmaul respirations, pleural effusions. Gastrointestinal changes include nausea and vomiting, anorexia, stomatis, bleeding, diarrhea and constipation. Hematologic changes include anemia, increase susceptibility to infection, leukocytosis, defect in platelet functioning. Neurologic changes include lethargy, seizures, Asterixis, memory impairment. Lastly, metabolic changes include an increase in BUN, creatinine, potassium levels, and phosphate levels with a decrease in sodium, pH, bicarbonate, and calcium.

The Client with AKI and CKI

Problem Excess fluid volume Risk for infection Imbalanced nutrition Fatigue (anemia, metabolic acidosis, uremic toxins) Anxiety Potential complication Dysrhythmias (electrolyte imbalances) The overall goals are 1) complete recovery without loss of kidney function 2) maintain normal fluid and electrolyte balance 3) knowledge of management and care post recovery

Dialysis The most common indications for renal replacement therapy in AKI include 1) volume overload resulting in compromised cardiac and/or pulmonary status, 2) elevated potassium levels, 3) metabolic acidosis, 4) BUN level greater than 120 mg/dL 5) significant changes in mental status and 6) pericarditis, pericardial effusion, or cardiac tamponade. Dialysis may be warranted to filter metabolic waste and restore fluid and electrolyte imbalances.

Temporary Dialysis

Treatment Managing electrolyte imbalances Monitoring Intake and Output K+ levels Regular IV insulin Sodium bicarbonate Calcium gluconate IV Dialysis Kayexalate Dietary restrictions Monitoring Intake and Output Volume overload Diuretic therapy Hypovolemia Fluid administration Nutritional support maintain adequate caloric intake to prevent further breakdown of body protein for energy reserves 30-35 kcal/kg and 0.8 to 1.0 gram of protein/kg

Evaluation: Desired Outcomes Regain and maintain normal fluid and electrolyte balance Comply with treatment regimen Experience no untoward complications Have a complete recovery

References Ignatavicius, D. D. & Workman, M. L. (2010). Medical- surgical nursing: patient-centered collaborative care (6th ed.). St. Louis, MO: Saunders Elsevier. Lewis, S. L., Heitkemper, M. M., Dirksen, S. R., & Bucher, L. (2014). Medical-surgical nursing: Assessment & management of client problems (9th ed.). St. Louis, MO: Mosby Hogan, M., Dentlinger, N.C., & Ramdin, V. (2014). Medical-surgical: nursing pearson nursing reviews and rationales (3rd ed.). Boston, MA: Pearson. Lewis, S. L., Heitkemper, M. M., Dirksen, S. R., & Bucher, L. (2014). Medical-surgical nursing: Assessment & management of client problems (9th ed.). St. Louis, MO: Mosby