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Nursing:
doi: 10.1097/01.NURSE.0000394078.60229.0a
Feature: CE Connection

Limiting the damage from Acute kidney injury

Ali, Becky MSN, ARNP; Gray-Vickrey, Peg DNS, RN

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Author Information

Becky Ali is an instructor II in the School of Nursing at Florida Gulf Coast University, and Peg Gray-Vickrey is professor and associate vice president at Florida Gulf Coast University, Fort Myers, Fla.

The authors have discolosed that they have no financial relationships pertaining to this article.

MR. P, 79, WAS ADMITTED with a diagnosis of colon cancer. He underwent a colon resection yesterday and has been stable for 24 hours.

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Mr. P has a history of osteoarthritis, heart failure (HF), and benign prostatic hyperplasia (BPH). Because he had difficulty urinating due to his BPH, an indwelling urinary catheter was inserted. Assessing him at the beginning of your shift, you find that his hourly urine output has fallen below 0.5 mL/kg/hour during the previous shift. As you complete a focused physical assessment, you note bibasilar pulmonary crackles, an S3, and 1+ pitting edema in his feet and ankles.

Although Mr. P's vital signs remain stable, you're concerned and contact his surgeon.

Good call. Based on your assessment findings, the surgeon orders additional diagnostic studies, which reveal that Mr. P has acute kidney injury (AKI).

This article will discuss your role in early detection and management of AKI with an emphasis on care for older adults. You'll learn the pathophysiology of this complex condition, the particular risks facing older adults, and the collaborative management required to return patients to optimal functioning.

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What's AKI?

By definition, AKI is an abrupt decrease (within 48 hours) in kidney function that includes an increase in serum creatinine (either an absolute increase of greater than 0.3 mg/dL or a percentage increase of 50%) or a decrease in urine output (less than 0.5 mL/kg/hour for more than 6 hours).1 The term AKI is replacing the earlier term acute renal failure (ARF) to better reflect the spectrum of injury to the kidneys that arises from multiple factors and that can result in various conditions ranging from mild elevations in serum creatinine to ARF.2 You'll still see the term ARF used to refer to patients whose kidney injury results in the need for renal replacement therapy (RRT), including traditional intermittent hemodialysis and newer continuous renal replacement therapies.3

AKI is seen in 1% to 5% of all hospitalized patients and up to 25% of patients in the ICU.4–6 Approximately 70% of patients who develop AKI are age 70 or older.4

Because kidney function usually returns to baseline if AKI is identified early and appropriately treated, all nurses need to be alert for risk factors for AKI, able to recognize the early signs and symptoms, and prepared to implement nursing interventions and treatment prescribed by the healthcare provider. The following brief physiology review will help you put clinical findings and interventions in context.

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How the kidneys work

The kidneys are highly complex organs with numerous functions and regulatory processes. They primarily function to excrete metabolic wastes, maintain fluid and electrolyte balance, and regulate acid-base balance.7 But they also have endocrine functions, secreting the hormones renin and erythropoietin and 25-hydroxyvitamin D3-1-hydroxylase, the enzyme that converts vitamin D to the active form.8

The functional units of the kidneys are the nephrons. Each kidney contains approximately 1.2 million nephrons.7 See Anatomy of a nephron for a closer look at these vital structures.

Each kidney is supplied with blood by a renal artery. This divides into smaller vessels to the level of the nephron, where an afferent arteriole delivers blood to the glomerulus. Beyond the glomerulus, the capillaries combine to become an efferent arteriole, which then divides again to form another capillary network that surrounds the tubular system. Eventually the blood returns to the venous circulation.8 (See Efferent and afferent arterioles of the glomerulus.)

The afferent and efferent arterioles directly control blood flow to the glomerulus.7 From 20% to 25% of all cardiac output (1,200 mL/minute) is delivered to the kidneys each minute.8 The glomerulus has a porous membrane that allows about 125 mL/minute of filtrate to pass through to Bowman capsule. The glomerular filtration rate (GFR) is the volume of plasma filtered at the glomerulus per unit of time. Normal GFR is 90 to 120 mL/minute/1.73 m.2,7

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In the tubular system, all but about 1 mL/minute is reabsorbed through the peritubular capillary network and becomes urine.8

Although the glomerulus allows for so much fluid to be filtered, it doesn't allow larger proteins, such as blood cells and platelets, to be filtered under normal conditions. However, renal disorders may disrupt this process, allowing protein or blood cells to pass into the urine.

The tubular system functions to reabsorb all glucose, most amino acids and small proteins, many of the electrolytes, bicarbonate (HCO3-), and most of the fluid. This is accomplished by both active and passive transport and is regulated by parathyroid hormone (calcium [Ca2+] and phosphate [PO42-] balance), aldosterone (sodium [Na+], water, and potassium [K+] balance), and antidiuretic hormone (fluid reabsorption) as well as other hormones. The tubules also secrete hydrogen (H+) ions, K+ ions, creatinine, and ammonia.8

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What AKI means to your patient

AKI refers to an abrupt decrease in kidney function.6 As kidney function declines, serum creatinine and blood urea nitrogen (BUN) increase, and oliguria (urine output less than 0.5 mL/kg/hour) usually occurs, although in some cases urine output is initially normal or even increased.9 Additionally, fluid, electrolyte, and acid-base balance can all become impaired.6,10

AKI is categorized as prerenal, intrarenal (intrinsic), and postrenal:9

* Prerenal AKI refers to conditions that decrease renal perfusion, such as hypovolemia, decreased cardiac output, fluid shifts, and impaired renal blood flow.10,11

* Intrarenal (intrinsic) AKI results from direct injury to the kidneys. Possible causes include ischemia (prolonged drop in renal perfusion), nephrotoxins, infections, and primary renal disease.

* Postrenal AKI results from obstruction of urine outflow by tumors, calculi, or prostate gland enlargement.11 The obstruction causes urine to back up into kidney structures, causing increased pressure, decreased GFR, and kidney injury. Although postrenal AKI is less common in the general population, aging increases the risk.

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Advancing age alters kidney function

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As a person ages, the kidney undergoes structural and functional changes. Renal blood flow is decreased by 1% per year after age 30.12 Renal function may decline by 50% or more by age 70.13 Functional changes in the renal system include decreased ability to excrete a sodium load, decreased ability to conserve water when the person is experiencing dehydration, and decreased GFR.13,14 These renal changes associated with aging, combined with other pathophysiologic challenges, can make the development of AKI more likely.12

Many of the causes of AKI are related to underlying medical conditions. Older patients are more likely to have one or more chronic diseases that increase the risk of AKI, such as coronary artery disease, HF, or diabetes mellitus. Infection such as H1N1 influenza or septic shock also increases the risk of AKI in vulnerable older adults.9,15,16 Other causes are iatrogenic—that is, resulting from the patient's medical or surgical treatment. In your older patients, AKI usually has several causes and may develop from even mild insults to the kidney.12

Many medications are associated with AKI. Some of the most common culprits are nonsteroidal anti-inflammatory drugs (NSAIDs); antimicrobials such as aminoglycosides, amphotericin B, and acyclovir; cardiovascular drugs such as angiotensin-converting enzyme (ACE) inhibitors and angiotensin-receptor blockers (ARBs); diuretics; antidepressants; and intravascular contrast media.17

NSAIDs, ACE inhibitors, and ARBs affect blood flow to the kidneys, causing prerenal AKI. Many of the others damage the kidneys directly, which classifies them as intrarenal causes of AKI.4,17 The risk of nephrotoxicity increases when these medications are given over a long period or at high doses, and when more than one nephrotoxic medication is administered.17

Vancomycin is an antimicrobial commonly prescribed for hospitalized patients with severe infections. Historically, it hasn't been identified as a nephrotoxic drug. However, recent guidelines for management of severe infection now recommend higher trough levels of the medication; as a result, healthcare providers are prescribing vancomycin in higher dosages. Several cases of AKI associated with high-dose vancomycin have been reported in patients with no other risk factors for AKI.18,19

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Tracking the clinical course of AKI

AKI usually follows a predictable clinical course, although the severity of the injury, complexity of the kidney dysfunction, development of complications, and length of time to recovery can vary considerably. The clinical course generally follows these four phases:11

* Initial phase. This is the time between the kidney injury and the reduction in kidney function. By recognizing the risk of AKI, you can help reduce any injury. During this time you can identify hypotensive episodes, nephrotoxic medications, and other risks and help to prevent or minimize kidney injury.

* Oliguric phase. During this phase, urine output decreases. In AKI, this phase usually occurs 1 to 7 days after the kidney injury and lasts 10 to 14 days. However, in some cases the oliguric phase lasts for weeks or months.11

Some patients with AKI don't develop oliguria (nonoliguric AKI) and maintain adequate urine output. No consensus exists as to whether patients with nonoliguric AKI have a poorer outcome than those with oliguric AKI. Although some sources state that patients with nonoliguric AKI have better outcomes, others dispute this and say that, in some instances, it may result in a delay of aggressive treatment, increasing mortality.4,11

If your patient develops oliguria, likely findings include fluid volume overload, hyponatremia (impaired renal reabsorption of sodium and dilutional hyponatremia), hyperkalemia, metabolic acidosis, and elevations of BUN and creatinine, reflecting nitrogenous waste accumulation.11 If this phase continues for a significant period, you may also see hypocalcemia, hyperphosphatemia, anemia, platelet abnormalities and bleeding, immune system dysfunction, and various neurologic changes ranging from fatigue to seizures and coma.6,11

Oliguria can also be caused by hypovolemia, which must be recognized and corrected to prevent AKI. To differentiate between oliguria from hypovolemia and oliguria from AKI, assess urine specific gravity and urine sodium levels. Specific gravity reflects the ability of the kidneys to concentrate or dilute urine and is normally between 1.010 and 1.025 in adults.20 (Reference values may differ slightly from one lab to another.) Urine of a patient with oliguria related to hypovolemia will have a high specific gravity and low urine sodium level (normal is 40 to 220 mEq/24 hours in adults).20 The urine of a patient with oliguria from AKI will have a specific gravity that's fixed at 1.010 and a high urine sodium level.11

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* Diuretic phase. In this phase, urine production increases because the nephrons have regained the ability to secrete urea, which draws the fluid across the glomerular membrane (osmotic diuresis). However, they don't have the ability to concentrate that filtrate. Urine output is usually 1 to 3 L/day, but can be as high as 5 L/day.11 Because of fluid loss, your patient experiences hypovolemia, hypotension, continuing hyponatremia (due to sodium loss in the filtrate), and hypokalemia.

As this phase continues, you'll start to see normalization of acid-base and electrolyte imbalance, and improvements in the BUN and creatinine.11 This phase can last for 1 to 3 weeks.

* Recovery phase. The recovery phase occurs when the kidneys regain the ability to manage metabolic waste, and BUN and creatinine return to baseline. This process usually takes several weeks, but in some cases, it continues for up to a year.11 In some patients, the kidneys never fully recover and mild elevations in BUN and creatinine may remain. Other patients will progress to chronic kidney disease (CKD) and need lifelong treatment.

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Assessing an at-risk patient

Obtain a very detailed history for any patient at risk for AKI. You want to determine whether this patient might possibly have CKD rather than AKI. With CKD your patient will be more likely to have chronic normocytic anemia, hypocalcemia, hyperphosphatemia, and a grayish cast to skin color, in addition to elevated BUN and creatinine.6

Ask about any recent infections because some kidney injuries can be associated with infections. Acute poststreptococcal glomerulonephritis, Escherichia coli gastrointestinal infection, and H1N1 influenza are some examples.6,15,16 Assess for the possibility of rhabdomyolysis; this results from large amounts of myoglobin, which is nephrotoxic, being released from injured skeletal muscle. This can develop from trauma, muscle overexertion, drug overdose, or other types of skeletal muscle injury.6 Muscle compression can also trigger myoglobin release and cause problems in patients with crush injuries and in those who've been immobile for a prolonged period. An example of this would be a patient who suffered a stroke at home, was unable to move, and wasn't discovered for hours or days.

Also determine whether the patient has any history of cardiovascular disease. This provides background information about the likelihood of your patient experiencing impaired renal perfusion.

Perform medication reconciliation and assess for potentially nephrotoxic drugs. Besides prescription drugs, specifically ask about over-the-counter medications, herbal remedies, or dietary supplements the patient takes because many people don't think of these as medications.

Also assess the course of the patient's hospitalization. For example, determine whether the patient experienced any episodes of hypotension that could have damaged the kidneys. Besides the vital signs logs, also check the perioperative records if the patient underwent surgery.6 (See Assessing risk in surgical patients.) Look for any possibility of sepsis as this can cause profound hypotension. In one recent study, AKI was found in two-thirds of all patients with septic shock.21

Carefully review your patient's cardiovascular status. Any drop in cardiac output will negatively affect renal perfusion, so assess for any record of dysrhythmias or evidence of hemodynamic instability. Determine whether your patient received mechanical ventilation. Some studies have suggested that mechanical ventilation, including the use of positive end expiratory pressure, can alter cardiac output and contribute to the development of AKI.10

Finally, assess the medications prescribed for your patient while hospitalized. Include any intravascular contrast media exposure, which could have been administered for various diagnostic or interventional radiologic procedures, including computed tomography (CT), magnetic resonance imaging (MRI), and cardiac catheterization. Double-check the dosing of prescribed medications as well. In high-risk patients, you can anticipate whether peak and trough levels are to be monitored. Also consider that the dosages of some medications are based on the patient's weight. You need to know whether dosing should be based on ideal or actual body weight. Some medications have been implicated in AKI when dosing is incorrect.22

Assess and closely monitor the patient's fluid status. Start with identifying any recent changes in urination pattern, which may signal hypovolemia or fluid overload. Many patients with hypovolemia experience orthostatic hypotension.23

If the patient is experiencing fluid overload you'll see hypertension, jugular vein distension, acute weight gain, and peripheral edema.6 You may also auscultate a third heart sound. Assess for pulmonary crackles or rhonchi and monitor for dyspnea, orthopnea, and paroxysmal nocturnal dyspnea as well. If fluid overload continues, the patient may also develop ascites and pericardial and/or pleural effusions.11 Prepare the patient for invasive monitoring if the patient is hemodynamically unstable.4

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Monitor lab values closely

As fluid status changes, so does the patient's electrolyte status. Monitor BUN, creatinine, and electrolytes (particularly sodium, potassium, magnesium, calcium, and phosphate).

Many older adults have a decrease in muscle mass and protein intake, which impacts the rate of creatine production. Serum creatinine levels are often within normal limits despite a significant decrease in GFR, so don't rely on serum creatinine to estimate the GFR in your older adult patients.4,12 Serum sodium levels will be low as the damaged tubules prevent sodium reabsorption from the glomerular filtrate.11

Hyperkalemia occurs as the normal excretion of potassium is impaired. Additionally, the potassium levels will increase following tissue trauma, bleeding, or blood transfusions because potassium is released from damaged cells. If the patient is experiencing metabolic acidosis, the potassium levels increase as hydrogen ions enter the cells and force potassium out of the cells.11

Hyperkalemia is particularly worrisome as it can cause cardiac dysrhythmias, so place your patient on a cardiac monitor. Watch for tall, peaked T waves, prolongation of the PR interval, widening QRS complexes, and premature ventricular contractions.6,11 Hyperkalemia may eventually result in ventricular tachycardia, ventricular fibrillation, and cardiac arrest.

Metabolic acidosis is another common sign of AKI. It develops because hydrogen ion secretion is impaired. Arterial blood gas (ABG) analysis shows a low pH and low bicarbonate. Bicarbonate is low because it's used to buffer the elevated hydrogen ions.11

Your patient may also exhibit Kussmaul respirations (rapid, deep breaths), which is the body's attempt to restore the acid-base balance by removing more carbon dioxide from the system.6,11 If this occurs, the patient's PaO2 will be low. Other signs of metabolic acidosis include flushed skin, headache, tachycardia, nausea, and vomiting. As acidosis becomes more severe, the patient may develop hypotension, bradycardia, and alterations in level of consciousness.6

Carefully assess the patient's current and prehospital nutritional status. Protein-calorie malnutrition has been implicated in increased mortality for patients with AKI.6 Studies show that 20% of hospitalized patients are undernourished, and older adults are at particular risk.4,24 The accumulation of metabolic waste products in AKI is associated with nausea, vomiting, and fatigue, which also impair your patient's dietary intake.

To help determine the underlying cause of AKI, the healthcare provider may order diagnostic studies, including:

* urinalysis. Urine will be checked for specific gravity, osmolality, and sodium levels. Protein or cells in the urine may indicate intrarenal damage. Hematuria, pyuria, or urinary crystals may indicate a postrenal cause of the AKI.11

* urine culture and sensitivity if the healthcare provider suspects an infectious cause.

* renal ultrasound, which may show renal tissue damage or urinary tract obstructions.

* renal scan to assess renal blood flow.

* CT scan or MRI to identify masses or obstructions.

Occasionally a renal biopsy is performed to investigate possible intrarenal disorders.

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Nursing and collaborative care

Patient care includes prompt identification and appropriate management of the underlying cause of AKI, correcting fluid and electrolyte imbalances, maintaining acid-base balance, providing optimal nutrition, and preventing complications.4,6 To provide holistic care, also attend to the patient and family's spiritual, emotional, and educational needs. Reassess the patient frequently to detect subtle changes that may signal the progression of AKI, the development of complications, or the need for RRT.

Monitoring the patient for fluid imbalances is critical. Accurately document intake and output and daily weights. If blood volume or cardiac output is low, this must be corrected as soon as possible to prevent further kidney damage. Fluid replacement usually begins with 0.9% sodium chloride, with colloids and/or blood products added if needed.6 Loop diuretics (usually furosemide) may be prescribed with the fluid. The primary goals of this fluid/diuretic strategy are to maintain renal hemodynamics, cardiac output, and BP, and to decrease pulmonary congestion. Loop diuretics are no longer recommended solely to maintain urine output.4,11

If cardiac output continues to be a problem, the patient may require inotropic medications. However, administering low-dose dopamine (renal dosing), a strategy once thought to benefit patients with AKI by improving renal perfusion, is no longer recommended. Recent studies have shown that using it makes no difference in clinical outcomes. In addition, dopamine can cause cardiac complications and even decrease renal perfusion in patients older than age 55. For these reasons, inotropic medications are indicated only for patients with inadequate cardiac output.4

If your patient has hypervolemia, you may need to restrict fluid intake as prescribed. Generally, patients should receive only 500 to 600 mL above any fluid loss over the previous 24 hours.4,11 In other words, if your patient had 400 mL of urine output yesterday, and no other fluid loss (from vomiting, diarrhea, bleeding, or other causes), he or she may be restricted to a total of 900 to 1,000 mL of total fluid intake for the day.

Monitor the hypervolemic patient closely for signs and symptoms of worsening HF and pulmonary edema. Respiratory deterioration can occur rapidly, so frequently assess for increased work of breathing and decreasing oxygenation. Your patient may need supplemental oxygen or possibly mechanical ventilation.4

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As previously discussed, patients with AKI are at high risk for developing hyperkalemia. If serum potassium is greater than 6.5 mEq/L, I.V. insulin may be prescribed to help drive potassium into the cells.4 In addition, I.V. dextrose may be prescribed to prevent hypoglycemia, depending on the patient's serum glucose level.11 Sodium bicarbonate will also help drive the potassium into the cells and helps correct metabolic acidosis as well.4

The effects of both of these therapies (insulin/glucose and sodium bicarbonate) are only temporary, as the potassium will eventually shift out of the cells again. Carefully monitor lab values as prescribed to evaluate the patient's response to treatment.4,11

Calcium gluconate or calcium chloride may be prescribed to antagonize the toxic effects of hyperkalemia at the myocardial cell membrane and prevent dysrhythmias.4,11 Additional emergency treatments for hyperkalemia include nebulized albuterol and cation-exchange resin (sodium polystyrene sulfonate). If these therapies don't resolve the hyperkalemia, the patient may need to receive RRT.4 Besides ongoing hyperkalemia, indications for RRT include volume overload, compromised oxygenation, metabolic acidosis, cardiac dysrhythmias, pericarditis, pericardial effusion, and impaired or diminishing mental or neurologic status.11

Your thorough assessment will identify any possible nephrotoxic agents; work with the healthcare team to eliminate them from the patient's care plan. If your patient has received intravascular contrast media, note any contrast-induced AKI prophylaxis used. Current recommendations include I.V. fluid hydration with 0.9% sodium chloride solution, which has been shown to be most beneficial when administered before and after the procedure.25 Additional prevention strategies include the use of low-osmolar contrast media and using the lowest dose of contrast media possible.

Be alert to any prescribed medications, or the metabolites of medications, which are excreted by the kidneys. Therapeutic drug level monitoring (peak and trough) may be needed to help determine appropriate dosing. Be aware of specific timing of peak and trough specimen collection, communicate the results to the healthcare team, administer medications on a strict schedule, and adjust doses frequently as prescribed.

Continue to monitor for any signs of infection, the leading cause of death in patients with AKI.6,11 Because your patient has immune system dysfunction,6 implement infection control measures, especially meticulous hand hygiene, and ensure that everyone on the unit does so as well. Educate your patient and family about this, especially hand hygiene.

Teach a patient at risk for atelectasis how to use an incentive spirometer and to do coughing and deep-breathing exercises. If mobility is impaired, turn and reposition your patient at least every 2 hours to prevent pooling of pulmonary secretions and to prevent skin breakdown. If the patient can be out of bed, explain the importance of early, aggressive ambulation. Inspect the patient's skin daily and implement additional pressure ulcer prevention strategies as indicated.

Prevent urinary tract infections by using an indwelling urinary catheter only if appropriate indications are met and discontinuing it as soon as possible. If your patient needs a urinary catheter, maintain a closed drainage system and unobstructed urine flow. Perform meatal care with soap and water.26

Manage peripheral and central venous access devices, as well as dialysis access catheters with strict sterile technique, following your facility policies. You may need to collect urine, stool, blood, or sputum specimens for culture and sensitivity. Administer prescribed antibiotics strictly on time to prevent any drop in therapeutic drug levels.

The patient with AKI needs adequate calorie intake to prevent catabolism of body protein.11 Administer antiemetic medications as prescribed if your patient is experiencing nausea or vomiting. The patient may also need potassium, sodium, and fluid restrictions. Consult with the dietitian to arrange for appropriate nutritional intake and monitor the patient's protein intake.6 A patient who needs enteral and/or parenteral supplementation may need blood glucose monitoring and RRT to remove the excess fluid.11

Early identification and prevention of dehydration, especially in older patients, is critically important. In older adults, many typical signs and symptoms of dehydration may be vague or absent. Orthostatic hypotension and tachycardia are the most clinically relevant findings. Unless fluid intake is restricted, older adults should have 30 mL of daily fluid intake per kilogram of body weight. For example, a patient who weighs 75 kg should have a fluid intake of 2,250 mL/day. A BUN-to-creatinine ratio greater than or equal to 25 suggests dehydration in the older adult.13

Patients with AKI may experience xerostomia (dry mouth), a metallic taste, and an unusual breath odor from bacterial interaction with urea in the saliva.6,11 Oral lesions may also develop. Assist with frequent oral hygiene and moisturize the oral mucosa and lips every 2 to 4 hours to prevent breakdown and improve comfort.

Decreased mobility and edema can impair tissue perfusion and increase the risk of pressure ulcers.6 Assess the condition of your patient's skin every shift and include strategies for preventing pressure ulcers in the care plan.

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Psychosocial considerations

Your patient and family will experience a range of emotions associated with an AKI diagnosis. For example, the patient may fear developing CKD, needing lifelong dialysis, and all the associated lifestyle changes. Your education about AKI and the course of recovery will be important to helping them maintain a positive outlook.

Hospitalized patients often feel overwhelmed due to the amount of complex information, sensory overload from the environment, unfamiliar caregivers, and interruption of normal routines. A sense of losing control and the possibility of a long illness can cause frustration. Family and work roles are under stress and also impact your patient. Make rounds with the other members of the healthcare team to stay on top of the interdisciplinary care plan so you can advocate for your patient's needs. This will also help you answer questions when the patient asks you to explain what the dietitian or the healthcare provider meant.

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Success story

Mr. P was discharged from your unit 2 weeks after his colon resection. Your early identification of his decreased urine output helped prevent many of the complications of AKI, and he regained kidney function without needing dialysis. His healthcare provider and home healthcare nurse will closely monitor his BUN and creatinine as his recovery progresses.

Kidney damage associated with AKI is often reversible with quick attention, so never underestimate the importance of your role in the assessment, management, and care of a patient with AKI.

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Assessing risk in surgical patients5

From 1% to 5% of all surgery patients and up to 15% of cardiac surgery patients experience AKI as a postoperative complication. For patients scheduled for surgery, assess the AKI risk preoperatively. The surgeon will discuss AKI and other risks during the informed consent process, but your assessment will cue you in to which patients to monitor most closely postoperatively.

Kheterpal et al. have developed a General Surgery AKI Risk Index to increase focus on risk reduction strategies. This AKI Risk Index outlines nine risk factors: Age ≥56, male sex, active congestive heart failure, ascites, hypertension, emergency surgery, intraperitoneal surgery, mild or moderate renal insufficiency (preop serum creatinine >1.2 mg/dL), and diabetes mellitus being treated with either oral antidiabetic medication or insulin therapy. Risk is classified as follows.

* Class I: 0–2 risk factors

* Class II: 3 risk factors

* Class III: 4 risk factors

* Class IV: 5 risk factors

* Class V: 6 or more risk factors.

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REFERENCES

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7. Huether SE. Structure and function of the renal and urologic systems. In: McCance KL, Huether SE, eds. Pathophysiology: The Biologic Basis for Disease in Adults and Children. 5th ed. St. Louis, MO: Elsevier Mosby; 2006:1279–1300.

8. Johnson VY. Nursing assessment: urinary system. In: Lewis SL, Heitkemper MM, Dirksen SR, O'Brien PG, Bucher L, eds. Medical-Surgical Nursing: Assessment and Management of Clinical Problems. 7th ed. St. Louis, MO: Elsevier Mosby; 2007:1136–1153.

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10. Broden CC. Acute renal failure and mechanical ventilation: reality or myth? Crit Care Nurse. 2009;29(2):62–75.

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12. Rosner MH. Acute kidney injury in the elderly: pathogenesis, diagnosis and therapy. Aging Health. 2009;5(5):635–646.

13. Goldman L, Ausiello D, eds. Cecil Textbook of Medicine. 23rd ed. 2008; Philadelphia PA: Saunders-Elsevier; 2008.

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15. Raina R, Demirgian S, Navneethan S, Schreiber M, Guzman JA. Renal failure in critically ill patients with influenza A (H1N1) infection [abstract]. National Kidney Foundation 2010 Spring Clinical Meetings Abstracts. http://www.kidney.org/news/meetings/clinical/pdf/CM10_abstracts.pdf.

16. Saghir S, Cundiff WB, El-Khatib M, Yadlapalli NG, Thakar C. Acute kidney injury in H1N1/influenza A virus infection related deaths in four adults [abstract]. National Kidney Foundation 2010 Spring Clinical Meetings Abstracts. http://www.kidney.org/news/meetings/clinical/pdf/CM10_abstracts.pdf.

17. Naughton CA. Drug-induced nephrotoxicity. Am Fam Physician. 2008;78(6):743–750.

18. Awua-Larbi S, Ghossein C. Eight cases of acute kidney injury due to vancomycin toxicity [abstract]. National Kidney Foundation 2010 Spring Clinical Meetings Abstracts. http://www.kidney.org/news/meetings/clinical/pdf/CM10_abstracts.pdf.

19. Shah-Khan F, Kanwar Y, Ghossein C. Biopsy proven acute tubular necrosis due to vancomycin toxicity [abstract]. National Kidney Foundation 2010 Spring Clinical Meetings Abstracts. http://www.kidney.org/news/meetings/clinical/pdf/CM10_abstracts.pdf.

20. Fischbach F, Dunning MB. A Manual of Laboratory and Diagnostic Tests. 8th ed. Philadelphia, PA: Wolters Kluwer Health/Lippincott Williams & Wilkins; 2009.

21. Bagshaw SM, Lapinsky S, Dial S, et al. Acute kidney injury in septic shock: clinical outcomes and impact of duration of hypotension prior to initiation of antimicrobial therapy. Intensive Care Med. 2009;35(5):871–881.

22. Hernandez JO, Norstrom J, Wysock G. Acyclovir-induced renal failure in an obese patient. Am J Health Syst Pharm. 2009;66(14):1288–1291.

23. Bradley EG. Nursing management: hypertension. In: Lewis SL, Heitkemper MM, Dirksen SR, O'Brien PG, Bucher L, eds. Medical-Surgical Nursing: Assessment and Management of Clinical Problems. 7th ed. St. Louis, MO: Elsevier Mosby; 2007:761–783.

24. Guigoz Y, Lauque S, Vellas BJ. Identifying the elderly at risk for malnutrition. The mini nutritional assessment. Clin Geriatr Med. 2002;18(4): 737–757.

25. Goldfarb S, McCullough PA, McDermott J, Gay SB. Contrast-induced acute kidney injury: specialty-specific protocols for interventional radiology, diagnostic computed tomography radiology, and interventional cardiology. Mayo Clinic Proceedings. 2009;84(2):170–179.

26. Herter R, Kazer MW. Best practices in urinary catheter care. Home Healthcare Nurse. 2010;28(6):342–349.

© 2011 Lippincott Williams & Wilkins, Inc.

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