Acute Kidney Injury Chapter 47.

Acute Kidney Injury Chapter 47

Acute kidney injury (AKI), previously known as acute kidney failure, is the term used to encompass the entire range of the syndrome, including a very slight deterioration in kidney function to severe impairment. AKI is characterized by a rapid loss of kidney function. This loss is accompanied by a rise in serum creatinine level and/or a reduction in urine output. The severity of dysfunction can range from a small increase in serum creatinine or reduction in urine output to the development of azotemia (an accumulation of nitrogenous waste products [urea nitrogen, creatinine] in the blood). AKI can develop over hours or days with progressive elevations of blood urea nitrogen (BUN), creatinine, and potassium, with or without a reduction in urine output.

Acute Kidney Injury Etiology and Pathophysiology
Prerenal Causes are factors external to the kidneys that reduce renal blood flow Severe dehydration, heart failure, ↓ CO Decreases glomerular filtration rate Causes oliguria Autoregulatory mechanisms attempt to preserve blood flow The oliguria is caused by a decrease in circulating blood volume (e.g., severe dehydration, heart failure, decreased cardiac output) and is readily reversible with appropriate treatment. It is important to distinguish prerenal oliguria from the oliguria of intrarenal AKI. In prerenal oliguria there is no damage to the kidney tissue (parenchyma). With a decrease in circulating blood volume, autoregulatory mechanisms that increase angiotensin II, aldosterone, norepinephrine, and antidiuretic hormone attempt to preserve blood flow to essential organs. Prerenal azotemia results in a reduction in the excretion of sodium (less than 20 mEq/L), increased salt and water retention, and decreased urine output. Prerenal conditions can lead to intrarenal disease if renal ischemia is prolonged. If decreased perfusion persists for an extended period of time, the kidneys lose their ability to compensate and damage to kidney parenchyma occurs (intrarenal damage). Refer to Table 47-2 for common causes of acute kidney injury as we discuss prerenal, intrarenal, and postrenal causes.

Intrarenal Causes include conditions that cause direct damage to kidney tissue Results from Prolonged ischemia Nephrotoxins Hemoglobin released from hemolyzed RBCs 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. Diseases of the kidney such as acute glomerulonephritis and systemic lupus erythematosus may also cause AKI.

Intrarenal Acute tubular necrosis (ATN) Results from ischemia, nephrotoxins, or sepsis Severe ischemia causes disruption in basement membrane Nephrotoxic agents cause necrosis of tubular epithelial cells Potentially reversible Acute tubular necrosis (ATN) is the most common cause of intrarenal AKI and is primarily the result of ischemia, nephrotoxins, or sepsis (Fig. 47-1). Ischemic and nephrotoxic ATN are responsible for 90% of cases of intrarenal AKI. Severe kidney ischemia causes a disruption in the basement membrane and patchy destruction of the tubular epithelium. Nephrotoxic agents cause necrosis of tubular epithelial cells, which slough off and plug the tubules. ATN is potentially reversible if the basement membrane is not destroyed and the tubular epithelium regenerates.

Acute Kidney Injury

Postrenal Causes include Benign prostatic hyperplasia Prostate cancer Calculi Trauma Extrarenal tumors Postrenal causes of AKI involve mechanical obstruction in the outflow of urine. As the flow of urine is obstructed, urine refluxes into the renal pelvis, impairing kidney function. Bilateral ureteral obstruction leads to hydronephrosis (kidney dilation), increase in hydrostatic pressure, and tubular blockage that results in a progressive decline in kidney function. If bilateral obstruction is relieved within 48 hours of onset, complete recovery is likely. If it is not relieved after 12 weeks, recovery is unlikely.

Case Study iStockphoto/Thinkstock J.K. is a 37-year-old man who fell off the roof of a house he was constructing. He sustained severe lacerations of his face and left leg, with substantial blood loss. We will now walk through a case study of a patient with acute kidney injury.

Case Study Which type of kidney injury is J.K. at risk for?
iStockphoto/Thinkstock Which type of kidney injury is J.K. at risk for? What are the contributing factors for this? What signs and symptoms of renal involvement would you assess for? Which type of kidney injury is J.K. at risk for? Prerenal What are the contributing factors for this? Fluid volume loss from blood loss Leads to decreased cardiac output and decreased renal perfusion What signs and symptoms of renal involvement would you assess for? {See next slides.}

Acute Kidney Injury Clinical Manifestations
RIFLE classification Risk (R) Injury (I) Failure (F) Loss (L) End-stage kidney disease (E) Clinically, AKI may progress through phases: oliguric, diuretic, and recovery. When a patient does not recover from AKI, then CKD may develop. The RIFLE classification is used to describe the stages of AKI (Table 47-3). RIFLE standardizes the diagnosis of acute kidney injury. Risk (R) is the first stage of AKI, followed by injury (I), which is the second stage, and then increases in severity to the final or third stage of failure (F). The two outcome variables are loss (L) and end-stage kidney disease (E).

Oliguric phase Urinary changes Urinary output less than 400 mL/day Occurs within 1 to 7 days after injury Lasts 10 to 14 days Urinalysis may show casts, RBCs, WBCs Urinary changes: Oliguria is a reduction in urine output to less than 400 mL/day. Oliguria usually occurs within 1 to 7 days of the injury to the kidneys. If the cause is ischemia, oliguria will often occur within 24 hours. The duration of the oliguric phase lasts on average about 10 to 14 days but can last months in some cases. The longer the oliguric phase lasts, the poorer the prognosis for complete recovery of kidney function. A urinalysis may show casts, RBCs, and white blood cells (WBCs). The casts are formed from mucoprotein impressions of the necrotic renal tubular epithelial cells, which detach or slough into the tubules.

Oliguric phase Fluid volume Hypovolemia may exacerbate AKI With decreased urine output, fluid retention occurs Neck veins distended Bounding pulse Edema Hypertension Fluid overload can lead to heart failure, pulmonary edema, and pericardial and pleural effusions Fluid volume: Hypovolemia (volume depletion) has the potential to exacerbate all forms of AKI. The reversal of hypovolemia with fluid replacement is often sufficient to treat many forms of AKI, especially those with prerenal causes. When urinary output decreases, fluid retention occurs. The severity of the symptoms depends on the extent of the fluid overload. In the case of reduced urine output (anuria and oliguria), the neck veins may become distended with a bounding pulse. Edema and hypertension may develop. Fluid overload can eventually lead to heart failure, pulmonary edema, and pericardial and pleural effusions.

Oliguric phase Metabolic acidosis Serum bicarbonate level decreases Severe acidosis develops Kussmaul respirations Sodium balance Increased excretion of sodium Hyponatremia can lead to cerebral edema Potassium excess Usually asymptomatic ECG changes Metabolic acidosis: In kidney failure, the kidneys cannot synthesize ammonia (needed for hydrogen ion excretion) or excrete acid products of metabolism. The serum bicarbonate level decreases because bicarbonate is depleted in buffering hydrogen ions. In addition, defective reabsorption and regeneration of bicarbonate occurs. With development of severe acidosis, the patient may develop Kussmaul respirations (rapid, deep respirations) in an effort to compensate by increasing the exhalation of carbon dioxide. Sodium balance: Damaged tubules cannot conserve sodium. Consequently, the urinary excretion of sodium may increase, resulting in normal or below-normal levels of serum sodium. Excessive intake of sodium should be avoided because it can lead to volume expansion, hypertension, and heart failure. Uncontrolled hyponatremia or water excess can lead to cerebral edema. Potassium excess: The kidneys normally excrete 80% to 90% of the body’s potassium. In AKI, the serum potassium level increases because the kidney’s normal ability to excrete potassium is impaired. Patients with hyperkalemia usually have no symptoms. Acute and/or rapid development of hyperkalemia may result in clinical signs that are apparent on electrocardiogram (ECG). These changes include peaked T waves, widening of the QRS complex, and ST segment depression.

Oliguric phase Hematologic disorders Leukocytosis Waste product accumulation Elevated BUN and serum creatinine levels Neurologic disorders Fatigue and difficulty concentrating Seizures, stupor, coma Hematologic disorders: Hospital-acquired AKI often occurs in patients who have multiorgan failure. Leukocytosis is often present with AKI. The most common cause of death in AKI is infection. The most common sites of infection are the urinary and respiratory systems. Waste product accumulation: The kidneys are the primary excretory organs for urea (an end product of protein metabolism) and creatinine (an end product of endogenous muscle metabolism). BUN and serum creatinine levels are elevated in kidney failure. Neurologic disorders: Neurologic changes can occur as the nitrogenous waste products accumulate in the brain and other nervous tissue. The manifestations can be as mild as fatigue and difficulty concentrating and then escalate to seizures, stupor, and coma.

Case Study iStockphoto/Thinkstock J.K.’s injuries have been repaired, but his urine output has dropped below 350 mL/day. J.K.’s laboratory results reveal BUN 53 mg/dL and serum creatinine 2.7 mg/dL. He complains of fatigue. His BP has risen to 178/98. J.K. is in the oliguric stage of prerenal AKI.

Case Study What other manifestations should you observe for?
iStockphoto/Thinkstock What other manifestations should you observe for? What other laboratory results should you monitor? J.K.’s urine output suddenly increases to 2 L overnight. Is this a positive sign? J.K. is in the oliguric stage of prerenal AKI. What other symptoms should you observe for? What other laboratory results should you monitor? J.K.’s urine output suddenly increases to 2 L overnight. Is this a positive sign? {See next slides.}

Diuretic phase Daily urine output is 1 to 3 L May reach 5 L or more Monitor for hyponatremia, hypokalemia, and dehydration Recovery phase May take up to 12 months for kidney function to stabilize Diuretic phase: During the diuretic phase of AKI, daily urine output usually is approximately 1 to 3 L but may reach 5 L or more. The high urine volume is caused by osmotic diuresis from the high urea concentration in the glomerular filtrate and the inability of the tubules to concentrate the urine. The kidneys have recovered their ability to excrete wastes but not to concentrate urine. Because of the large losses of fluid and electrolytes, the patient must be monitored for hyponatremia, hypokalemia, and dehydration. The diuretic phase may last 1 to 3 weeks. Near the end of this phase, the patient’s acid-base, electrolyte, and waste product (BUN, creatinine) values begin to normalize. Recovery phase: The recovery phase begins when the GFR increases, allowing the BUN and serum creatinine levels to plateau and then decrease. Although the major improvements occur in the first 1 to 2 weeks of this phase, kidney function may take up to 12 months to stabilize. The outcome of AKI is influenced by the patient’s overall health, the severity of kidney failure, and the number and type of complications.

Audience Response Question
Which assessment would indicate to the nurse that a patient has oliguria related to an intrarenal acute kidney injury? Urinary sodium levels are low. The serum creatinine level is normal. Oliguria is relieved after fluid replacement. Urine testing reveals a specific gravity of Answer: d Rationale: The urine specific gravity in oliguria of intrarenal acute kidney injury will be fixed at This value reflects tubular damage with loss of concentrating ability by the kidneys. The serum creatinine level is above normal in oliguria of intrarenal acute kidney injury. Urinary secretion of sodium increases with oliguria of intrarenal acute kidney injury. Prerenal oliguria related to hypovolemia will usually respond to fluid replacement.

Acute Kidney Injury Diagnostic studies Thorough history
Serum creatinine Urinalysis Kidney ultrasonography Renal scan Computed tomography (CT) scan Renal biopsy A thorough history is essential for diagnosing the etiology of AKI. Consider prerenal causes when there is a history of dehydration, blood loss, or severe heart disease. An increase in serum creatinine may not be evident until there is a loss of more than 50% of kidney function. Urinalysis is an important diagnostic test. The urine osmolality, sodium content, and specific gravity are measured, and urine sediment, hematuria, pyuria, and crystals may be seen. Kidney ultrasonography is often the first test done because it provides imaging without exposure to potentially nephrotoxic contrast agents. A renal scan can help assess abnormalities in kidney blood flow, tubular function, and the collecting system. A computed tomographic (CT) scan can identify lesions and masses, as well as obstructions and vascular anomalies. Renal biopsy is considered the best method for confirming intrarenal causes of AKI.

Acute Kidney Injury Diagnostic studies Contraindicated
Magnetic resonance imaging (MRI) Magnetic resonance angiography (MRA) with gadolinium contrast medium Nephrogenic systemic fibrosis Contrast-induced nephropathy (CIN) Administration of gadolinium has been associated with the development of a devastating and potentially lethal disorder, nephrogenic systemic fibrosis, in patients with kidney failure. In patients with kidney failure, contrast-induced nephropathy (CIN) can occur when contrast medium for diagnostic studies causes nephrotoxic injury.

Case Study iStockphoto/Thinkstock J.K.’s urinalysis reveals slight hematuria and a low specific gravity. Renal ultrasound findings are normal. What is the overall goal in the management of J.K. at this point? What nursing interventions would you implement? What is the plan in regard to J.K.’s management at this point? Manage signs and symptoms and prevent complications. What are the collaborative measures at this stage? What nursing interventions would you implement? {See next slides.}

Acute Kidney Injury Collaborative care Primary goals
Eliminate the cause Manage signs and symptoms Prevent complications Because AKI is potentially reversible, the primary goals of treatment are to eliminate the cause, manage the signs and symptoms, and prevent complications while the kidneys recover (Table 47-4).

Acute Kidney Injury Collaborative care
Ensure adequate intravascular volume and cardiac output Force fluids Loop diuretics (e.g., furosemide [Lasix]) Osmotic diuretics (e.g., mannitol) Closely monitor fluid intake during oliguric phase If AKI is already established, forcing fluids and diuretics will not be effective and may, in fact, be harmful. Closely monitor fluid intake during the oliguric phase of AKI. The general rule for calculating the fluid restriction is to add all losses for the previous 24 hours (e.g., urine, diarrhea, emesis, blood) plus 600 mL for insensible losses (e.g., respiration, diaphoresis).

Acute Kidney Injury Collaborative care Hyperkalemia
Insulin and sodium bicarbonate Calcium carbonate Sodium polystyrene sulfonate (Kayexalate) Hyperkalemia is one of the most serious complications in AKI because it can cause life-threatening cardiac dysrhythmias. The various therapies used to treat elevated potassium levels are listed in Table Both insulin and sodium bicarbonate serve as a temporary measure for treatment of hyperkalemia by promoting a shift of potassium into the cells, but potassium will eventually be released. Calcium gluconate raises the threshold at which dysrhythmias will occur, serving to temporarily stabilize the myocardium. Only sodium polystyrene sulfonate (Kayexalate) and dialysis actually remove potassium from the body. Never give this drug to a patient with a paralytic ileus because bowel necrosis can occur.

Acute Kidney Injury Collaborative care
Indications for renal replacement therapy (RRT) Volume overload Elevated serum potassium level Metabolic acidosis BUN level higher than 120 mg/dL (43 mmol/L) Significant change in mental status Pericarditis, pericardial effusion, or cardiac tamponade The most common indications for RRT in AKI are (1) volume overload, resulting in compromised cardiac and/or pulmonary status; (2) elevated serum potassium level; (3) metabolic acidosis (serum bicarbonate level less than 15 mEq/L [15 mmol/L]); (4) BUN level greater than 120 mg/dL (43 mmol/L); (5) significant change in mental status; and (6) pericarditis, pericardial effusion, or cardiac tamponade.

Acute Kidney Injury Collaborative care Renal replacement therapy (RRT)
Peritoneal dialysis (PD) Intermittent hemodialysis (HD) Continuous renal replacement therapy (CRRT) Cannulation of artery and vein There is no consensus regarding the best approach to renal relacement therapy (RRT). Even though peritoneal dialysis (PD) is considered a viable option for RRT, it is not frequently used. Intermittent hemodialysis (HD) (e.g., at intervals of 4 hours either daily, every other day, or three to four times per week) is the method of choice when rapid changes are required in a short period of time. Continuous renal replacement therapy (CRRT) has been used effectively and involves cannulation of an artery and a vein.

Acute Kidney Injury Collaborative care Nutritional therapy
Maintain adequate caloric intake Restrict sodium Increase dietary fat Enteral nutrition The challenge of nutritional management in AKI is to provide adequate calories to prevent catabolism despite the restrictions necessary to prevent electrolyte disorders, fluid disorders, and azotemia. A primary nutritional goal in AKI is to maintain adequate caloric intake (providing 30 to 35 kcal/kg and 0.8 to 1.0 g of protein per kilogram of desired body weight) to prevent the further breakdown of body protein for energy purposes. Adequate energy should be primarily from carbohydrate and fat sources to prevent ketosis from endogenous fat breakdown and gluconeogenesis from muscle protein breakdown. Supplementation of essential amino acids can be given for amino acid replacement. Sodium is restricted as needed to prevent edema, hypertension, and heart failure. Dietary fat intake is increased so that the patient receives at least 30% to 40% of total calories from fat. Fat emulsion IV infusions given as a nutritional supplement provide a good source of nonprotein calories (see Chapter 40). If a patient cannot maintain adequate oral intake, enteral nutrition is the preferred route for nutritional support (see Chapter 40). When the gastrointestinal (GI) tract is not functional, parenteral nutrition is necessary to provide adequate nutrition. The patient treated with parenteral nutrition may need daily HD or CRRT to remove the excess fluid. Concentrated formulas of parenteral nutrition are available to minimize fluid volume.

Case Study iStockphoto/Thinkstock J.K. continues to improve, but he has lost 6 lb since admission. He expresses concern regarding maintaining muscle mass and his ability to perform his job as a construction worker after discharge. Develop a teaching plan related to J.K.’s dietary needs and acute kidney injury.

Nursing Management Acute Kidney Injury
Nursing assessment Measure vital signs Measure fluid intake and output Examine urine Assess general appearance Observe dialysis access site Daily monitoring of a patient’s urine output is essential because this information provides prognostic implications and is crucial in determining therapy and daily fluid volume replacement. Examine the urine for color, specific gravity, glucose, protein, blood, and sediment. Assess the patient’s general appearance, including skin color, edema, neck vein distention, and bruises. If a patient is receiving dialysis, observe the access site for signs of inflammation and exudate.

Nursing assessment Mental status and level of consciousness Oral mucosa Lung sounds Heart rhythm Laboratory values Diagnostic test results Evaluate the patient’s mental status and level of consciousness. Examine the oral mucosa for dryness and inflammation. Auscultate the lungs for crackles and rhonchi or diminished breath sounds. Monitor the heart for the presence of an S3 gallop, murmurs, or a pericardial friction rub. Assess ECG readings for the presence or development of dysrhythmias. Review laboratory values and diagnostic test results.

Nursing diagnoses Excess fluid volume Risk for infection Fatigue Anxiety Potential complication: dysrhythmia Excess fluid volume related to kidney failure and fluid retention Risk for infection related to invasive lines, uremic toxins, and altered immune responses secondary to kidney failure Fatigue related to anemia, metabolic acidosis, and uremic toxins Anxiety related to disease processes, therapeutic interventions, and uncertainty of prognosis Potential complication: dysrhythmias related to electrolyte imbalances

Planning The patient with AKI will Completely recover without any loss of kidney function Maintain normal fluid and electrolyte balance Have decreased anxiety Comply with and understand the need for careful follow-up care

Nursing implementation Health promotion Identify and monitor populations at high risk Control exposure to nephrotoxic drugs and industrial chemicals Prevent prolonged episodes of hypotension and hypovolemia

Nursing implementation Health promotion Monitor intake and output Monitor electrolyte balance Measure daily weight Replace significant fluid losses Provide aggressive diuretic therapy for fluid overload Use nephrotoxic drugs sparingly In the hospital, the factors that increase the risk for developing AKI are the presence of preexisting CKD, older age, massive trauma, major surgical procedures, extensive burns, cardiac failure, sepsis, and obstetric complications. Careful monitoring of intake and output, fluid balance, and electrolyte balance is essential. Assess and record extrarenal losses of fluid from vomiting, diarrhea, hemorrhage, and increased insensible losses. Prompt replacement of significant fluid losses will help prevent ischemic tubular damage associated with trauma, burns, and extensive surgery. Intake and output records and the patient’s weight provide valuable indicators of fluid volume status. Aggressive diuretic therapy for the patient with fluid overload resulting from any cause can lead to a reduction in renal blood flow. Nephrotoxic drugs should be used sparingly in a patient at high risk. When these drugs must be used, they should be given in the smallest effective doses for the shortest possible periods. Angiotensin-converting enzyme (ACE) inhibitors can also decrease perfusion pressure and cause hyperkalemia.

Nursing implementation Acute intervention Accurate intake and output measurements Daily weights Assessment for signs of hypervolemia or hypovolemia Meticulous aseptic technique Careful administration of nephrotoxic drugs Skin care measures Mouth care You have an important role in managing fluid and electrolyte balance during the oliguric and diuretic phases. Observe and record accurate intake and output. Measure daily weights with the same scale at the same time each day to allow for the evaluation and detection of excessive gains or losses of body fluid (1 kg is equivalent to 1000 mL of fluid). Assess for the common signs and symptoms of hypervolemia (in the oliguric phase) or hypovolemia (in the diuretic phase), potassium and sodium disturbances, and other electrolyte imbalances that may occur in AKI (see Chapter 17). Because infection is the leading cause of death in AKI, meticulous aseptic technique is critical. Nephrotoxic drugs (see Table 45-3) should be administered judiciously. Perform skin care, and take measures to prevent pressure ulcers because most patients develop edema, as well as decreased muscle tone. Mouth care is important for preventing stomatitis, which develops when ammonia (produced by bacterial breakdown of urea) in saliva irritates the mucous membranes.

Case Study J.K. progresses well and is preparing for discharge.
iStockphoto/Thinkstock J.K. progresses well and is preparing for discharge. His BUN is 19 mg/dL, serum creatinine is 1.4 mg/dL, and urinalysis is normal. J.K. has gained 2 lb since his nutritional needs were addressed. Have students evaluate the nutrition teaching plan. Discuss teaching fore discharge {see next slides}.

Nursing implementation Ambulatory and home care Regulate protein and potassium intake Follow-up care Teaching Appropriate referrals Recovery from AKI is highly variable and depends on the existence of other organ system failures, the general condition and age of the patient, the length of the oliguric phase, and the severity of nephron damage. Protein and potassium intake should be regulated in accordance with kidney function. Follow-up care and regular evaluation of kidney function are necessary. Teach the patient the signs and symptoms of recurrent kidney disease. Emphasize measures to prevent the recurrence of AKI. The long-term convalescence period of 3 to 12 months may cause psychosocial and financial hardships for both the patient and the family. Make appropriate referrals for counseling as appropriate.

Nursing implementation Evaluation The expected outcomes are that the patient with AKI will Regain and maintain normal fluid and electrolyte balance Comply with the treatment regimen Experience no untoward complications Have complete recovery

Gerontologic Considerations Acute Kidney Injury
More susceptible to AKI Polypharmacy Hypotension Diuretic therapy Aminoglycoside therapy Obstructive disorders Surgery Infection Older adults are at risk for the same causes of AKI as are younger adults. However, they are more susceptible to AKI. Dehydration is associated with polypharmacy (diuretics, laxatives, and drugs that suppress appetite or consciousness), acute febrile illnesses, and being bedridden. Other common causes of AKI in older adults include hypotension, diuretic therapy, aminoglycoside therapy, obstructive disorders (e.g., prostatic hyperplasia), surgery, infection, and contrast media. Impaired function of other organ systems from cardiovascular disease or diabetes mellitus can increase the risk of developing AKI. The aging kidney is less able to compensate for changes in fluid volume, solute load, and cardiac output.

Acute Kidney Injury Chapter 47.

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Acute Kidney Injury Chapter 47.

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