	Acute Kidney Injury	Chronic Kidney Disease
Onset	Sudden	Gradual, often over many years
Most common cause	Acute tubular necrosis	Diabetic nephropathy
Diagnostic criteria	Acute reduction in urine output and/or Elevation in serum creatinine	GFR <60 mL/min/1.73m² for >3 mo and/or Kidney damage >3 mo
Reversibility	Potentially	Progressive and irreversible
Primary cause of death	Infection	Cardiovascular disease

GFR, Glomerular filtration rate.

eNursing Care Plan 47-1 Patient With Chronic Kidney Disease

Nursing Diagnosis* Excess fluid volume related to impaired kidney function as evidenced by edema, hypertension, bounding pulse, weight gain, shortness of breath, pulmonary edema
Patient Goal Maintains an acceptable body weight and fluid balance with dietary modifications and/or with peritoneal dialysis or hemodialysis treatments
Outcomes (NOC)	Interventions (NIC) and Rationales
Fluid Overload Severity • Periorbital edema _____ • Sacral edema _____ • Ankle edema _____ • Ascites _____ • Generalized edema _____ • Rales _____ • Malaise _____ • Increased blood pressure _____ • Weight gain _____ • Decreased urine output _____ • Confusion _____ Measurement Scale 1 = Severe 2 = Substantial 3 = Moderate 4 = Mild 5 = None	Hypervolemia Management • Monitor respiratory pattern for symptoms of respiratory difficulty (e.g., dyspnea, tachypnea, shortness of breath) that are indicators of fluid excess. • Weigh patient daily and monitor trends to evaluate interventions. • Monitor intake and output to determine effect of treatment on kidney function. • Provide appropriate diet to help control edema and hypertension. • Instruct patient and/or caregivers on measures instituted to treat the hypervolemia (e.g., daily weights, fluid restrictions) to help monitor and control fluid overload and related hypertension. Hemodialysis Therapy/Peritoneal Dialysis Therapy • Draw blood sample and review blood chemistries (e.g., BUN, creatinine, sodium, potassium, phosphate levels) before treatment to evaluate response. • Record baseline vital signs: weight, temperature, pulse, respirations, and blood pressure to evaluate response to therapy. • Institute and discontinue dialysis according to protocol. • Adjust filtration pressure to remove an appropriate amount of fluid. • Work collaboratively with patient to adjust length of dialysis, diet regulations, fluid limitations, and medications to regulate fluid and electrolyte shifts between treatments.
Nursing Diagnosis Risk for electrolyte imbalance related to impaired kidney function resulting in hyperkalemia, hypocalcemia, hyperphosphatemia, and altered vitamin D metabolism
Patient Goals 1. Maintains electrolyte levels within normal ranges 2. Does not experience effects of electrolyte imbalances
Outcomes (NOC)	Interventions (NIC) and Rationales
Kidney Function • 24-hour intake and output balance _____ • Blood urea nitrogen _____ • Serum creatinine _____ • Urine specific gravity _____ • Urine electrolytes _____ Measurement Scale 1 = Severely compromised 2 = Substantially compromised 3 = Moderately compromised 4 = Mildly compromised 5 = Not compromised Electrolyte and Acid-Base Balance • Serum potassium _____ • Serum calcium _____ • Serum magnesium_____ • Serum pH _____ • Serum bicarbonate _____ Measurement Scale 1 = Severe deviation from normal range 2 = Substantial deviation from normal range 3 = Moderate deviation from normal range 4 = Mild deviation from normal range 5 = No deviation from normal range	Electrolyte Management: Hyperkalemia • Monitor renal function (e.g., BUN and Cr levels) as a cause of increasing serum potassium levels. • Monitor cardiac manifestations of hyperkalemia (e.g., decreased cardiac output, peaked T waves, fibrillation, asystole) to initiate ACLS if needed. • Encourage adherence to dietary regimens (e.g., avoiding high-potassium foods, meeting dietary needs with salt substitutes and low-potassium foods) to control serum potassium levels. • Prepare patient for dialysis (e.g., assist with catheter placement for dialysis) as treatment for imbalanced serum electrolytes. • Monitor patient’s hemodynamic response to dialysis to recognize and treat complications as needed. Electrolyte Management: Hypocalcemia • Monitor trends in bone and mineral indices (e.g., calcium, phosphorus, alkaline phosphatase) to provide early intervention if necessary. • Monitor for electrolyte imbalances associated with hypocalcemia (e.g., hyperphosphatemia, hypomagnesemia, alkalosis) to determine degree of bone demineralization and potential risk for fracture. • Administer appropriate prescribed calcium salt (e.g., calcium carbonate, calcium chloride, calcium gluconate). • Provide adequate intake of vitamin D (e.g., vitamin supplement, organ meats) to facilitate GI absorption of calcium to prevent and/or treat the bone demineralization. • Instruct patient on need for lifestyle changes (dialysis) to control hypocalcemia. Electrolyte Management • Provide a safe environment for the patient with neurologic and/or neuromuscular manifestations of electrolyte balance to prevent injury. • Monitor for manifestations of electrolyte imbalance as all electrolyte levels may be affected in chronic kidney disease.
Nursing Diagnosis Imbalanced nutrition: less than body requirements related to restricted intake of nutrients (especially protein), nausea, vomiting, anorexia, and stomatitis as evidenced by loss of appetite and weight
Patient Goals 1. Maintains an acceptable weight with no more than a 10% weight loss 2. Maintains serum albumin, creatinine, and hemoglobin and hematocrit within normal limits
Outcomes (NOC)	Interventions (NIC) and Rationales
Nutritional Status • Nutrient intake _____ • Food intake _____ • Weight/height ratio _____ • Energy _____ • Muscle tone _____ Measurement Scale 1 = Severe deviation from normal range 2 = Substantial deviation from normal range 3 = Moderate deviation from normal range 4 = Mild deviation from normal range 5 = No deviation from normal range	Nutritional Monitoring • Monitor for nausea and vomiting to intervene as necessary. • Monitor trends in weight loss and gain to detect changes in status. • Monitor albumin, total protein, hemoglobin, and hematocrit levels as indicators of nutritional status and response to treatments. • Monitor caloric and nutrient intake to detect changes. Nutrition Therapy • Provide oral care before meals to prevent stomatitis, remove bad taste, and increase patient’s appetite. • Refer for diet teaching and planning to ensure adequate intake within prescribed diet restrictions. • Provide needed nourishment within limits of prescribed diet to promote adequate nutrition.
Nursing Diagnosis Grieving related to loss of kidney function as evidenced by expression of feelings of sadness, anger, inadequacy, hopelessness
Patient Goals 1. Demonstrates effective coping strategies 2. Reports that life is worth living
Outcomes (NOC)	Interventions (NIC) and Rationales
Acceptance: Health Status • Recognizes reality of health situation _____ • Pursues information about health _____ • Adjusts to change in health status _____ • Makes decisions about health _____ • Reports sense of life being worth living _____ Measurement Scale 1 = Never demonstrated 2 = Rarely demonstrated 3 = Sometimes demonstrated 4 = Often demonstrated 5 = Consistently demonstrated	Grief Work Facilitation • Listen to expressions of grief to convey a caring attitude and foster a relationship and/or to determine how patient is handling the situation. • Identify sources of community support for continued grief work. Coping Enhancement • Assist patient to solve problems in a constructive manner to help facilitate the grieving process. • Encourage family involvement to enable them to assist the patient and foster their support and understanding. • Assist patient to grieve and work through the losses of chronic illness and/or disability.

ACLS, Advanced cardiovascular life support; BUN, blood urea nitrogen; Cr, creatinine.

^*Nursing diagnoses listed in order of priority.

eTABLE 47-1

MANIFESTATIONS OF ACUTE KIDNEY INJURY

Body System	Clinical Manifestations
Urinary	↓ Urinary output Proteinuria Casts ↓ Specific gravity ↓ Osmolality ↑ Urinary sodium
Cardiovascular	Volume overload Heart failure Hypotension (early) Hypertension (after development of fluid overload) Pericarditis Pericardial effusion Dysrhythmias
Respiratory	Pulmonary edema Kussmaul respirations Pleural effusions
Gastrointestinal	Nausea and vomiting Anorexia Stomatitis Bleeding Diarrhea Constipation
Hematologic	Anemia (development within 48 hr) ↑ Susceptibility to infection Leukocytosis Defect in platelet functioning
Neurologic	Lethargy Seizures Asterixis Memory impairment
Metabolic	↑ BUN ↑ Creatinine ↓ Sodium ↑ Potassium ↓ pH ↓ Bicarbonate ↓ Calcium ↑ Phosphate

BUN, Blood urea nitrogen.

eTABLE 47-2

CASE STUDY
Intrarenal Cause of Acute Kidney Injury Following Surgery

Progression of Kidney Injury	RIFLE Staging
• 74-year-old African American female with type 2 diabetes, hypertension, peripheral arterial disease, and chronic kidney disease (CKD) • Diagnosed with triple vessel coronary artery disease and scheduled to undergo emergent coronary artery bypass graft (CABG) • Serum creatinine is 1.8 mg/dL and she weighs 60 kg	*Risk*—increase in serum creatinine in patient with pre-existing CKD Calculated GFR is 35 mL/min /1.73 m² She has stage 3 CKD
• During surgery, she experienced hypotension for a sustained period
• Acute tubular necrosis ensues as a result of ischemia • After surgery: serum creatinine is 3.6 mg/dL, and urine output is reduced to 28 mL/hr	*Injury*
72 hours after surgery and in ICU • She develops ventilator-associated pneumonia and sepsis • Serum creatinine rises to 5.2 mg/dL and urine output drops to 10 mL/hr	*Failure*
• Her blood pressures remain low despite pressor therapy (dopamine up to 10 mcg/kg/min)
• Continuous venovenous hemodialysis is instituted • However, after 4 wk of therapy she has a cardiopulmonary arrest and does not survive	*Loss*

GFR, Glomerular filtration rate.

Acute Kidney Injury

Acute kidney injury (AKI), previously known as acute kidney failure, is the term used to encompass the entire range of the syndrome, ranging from a 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 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).

Although AKI is potentially reversible, it has a high mortality rate.¹ AKI usually affects people with other life-threatening conditions² (Table 47-2). Most commonly, AKI follows severe, prolonged hypotension or hypovolemia or exposure to a nephrotoxic agent.

TABLE 47-2

COMMON CAUSES OF ACUTE KIDNEY INJURY

Prerenal	Intrarenal	Postrenal
Hypovolemia • Dehydration • Hemorrhage • GI losses (diarrhea, vomiting) • Excessive diuresis • Hypoalbuminemia • Burns Decreased Cardiac Output • Cardiac dysrhythmias • Cardiogenic shock • Heart failure • Myocardial infarction Decreased Peripheral Vascular Resistance • Anaphylaxis • Neurologic injury • Septic shock Decreased Renovascular Blood Flow • Bilateral renal vein thrombosis • Embolism • Hepatorenal syndrome • Renal artery thrombosis	Nephrotoxic Injury • Drugs: aminoglycosides (gentamicin, amikacin), amphotericin B • Contrast media • Hemolytic blood transfusion reaction • Severe crush injury • Chemical exposure: ethylene glycol, lead, arsenic, carbon tetrachloride Interstitial Nephritis • Allergies: antibiotics (sulfonamides, rifampin), nonsteroidal antiinflammatory drugs, ACE inhibitors • Infections: bacterial (acute pyelonephritis), viral (CMV), fungal (candidiasis) Other Causes • Prolonged prerenal ischemia • Acute glomerulonephritis • Thrombotic disorders • Toxemia of pregnancy • Malignant hypertension • Systemic lupus erythematosus	• Benign prostatic hyperplasia • Bladder cancer • Calculi formation • Neuromuscular disorders • Prostate cancer • Spinal cord disease • Strictures • Trauma (back, pelvis, perineum)

ACE, Angiotensin-converting enzyme; CMV, cytomegalovirus.

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. Hospitalized patients develop AKI at a high rate (1 in 5) and have a high mortality rate. When AKI develops in patients in intensive care units (ICUs), the mortality rate can be as high as 70% to 80%.3–5

Etiology and Pathophysiology

The causes of AKI, which are multiple and complex, are categorized as prerenal, intrarenal (or intrinsic), and postrenal causes (see Table 47-2).

Prerenal.

Prerenal causes of AKI are factors external to the kidneys. These factors reduce systemic circulation, causing a reduction in renal blood flow. The decrease in blood flow leads to decreased glomerular perfusion and filtration of the kidneys. Although kidney tubular and glomerular function is preserved, glomerular filtration is reduced as a result of decreased perfusion.

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). The oliguria is caused by a decrease in circulating blood volume (e.g., severe dehydration, heart failure [HF], decreased cardiac output) and is readily reversible with appropriate treatment. 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 sodium and water retention, and decreased urine output.

Prerenal conditions can lead to intrarenal disease if renal ischemia is prolonged. Prerenal conditions account for many cases of intrarenal AKI. If decreased perfusion persists for an extended time, the kidneys lose their ability to compensate and damage to kidney parenchyma occurs (intrarenal damage).

Intrarenal.

Intrarenal causes of AKI (see Table 47-2) include conditions that cause direct damage to the kidney tissue, resulting in impaired nephron function. The damage from intrarenal causes usually results from prolonged ischemia, nephrotoxins (e.g., aminoglycoside antibiotics, contrast media), hemoglobin released from hemolyzed red blood cells (RBCs), or myoglobin released from necrotic muscle cells.

Nephrotoxins can cause obstruction of intrarenal structures by crystallizing 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.

Acute tubular necrosis (ATN) is the most common intrarenal cause of AKI and is primarily the result of ischemia, nephrotoxins, or sepsis (Fig. 47-1). Ischemic and nephrotoxic ATN is responsible for 90% of intrarenal AKI cases.^6,7 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.

FIG. 47-1 Acute tubular necrosis. The kidneys are swollen and pale.

ATN is the most common cause of AKI for hospitalized patients. Risks associated with development of ATN while in the hospital include major surgery, shock, sepsis, blood transfusion reaction, muscle injury from trauma, prolonged hypotension, and nephrotoxic agents (see Table 47-2).

Postrenal.

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. The most common causes are benign prostatic hyperplasia, prostate cancer, calculi, trauma, and extrarenal tumors. Bilateral ureteral obstruction leads to hydronephrosis (kidney dilation), increase in hydrostatic pressure, and tubular blockage, resulting in a progressive decline in kidney function. If bilateral obstruction is relieved within 48 hours of onset, complete recovery is likely. After 12 weeks, recovery is unlikely. Prolonged obstruction can lead to tubular atrophy and irreversible kidney fibrosis. Postrenal causes of AKI account for less than 10% of AKI cases.7,8

Clinical Manifestations

Prerenal and postrenal AKI that has not caused intrarenal damage usually resolves quickly with treatment of the cause. However, when parenchymal damage occurs due to either prerenal or postrenal causes, or when parenchymal damage occurs directly as with intrarenal causes, AKI has a prolonged course. 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). Risk, the first stage of AKI, is followed by Injury, which is the second stage. Then AKI increases in severity to the final or third stage, Failure. The two outcome variables are Loss and End-stage kidney disease. (See eTable 47-2 for a case study showing how RIFLE classification is used.)

TABLE 47-3

RIFLE CLASSIFICATION FOR STAGING ACUTE KIDNEY INJURY

Stage	GFR Criteria	Urine Output Criteria
Risk	Serum creatinine increased × 1.5 OR GFR decreased by 25%	Urine output <0.5 mL/kg/hr for 6 hr
Injury	Serum creatinine increased × 2 OR GFR decreased by 50%	Urine output <0.5 mL/kg/hr for 12 hr
Failure	Serum creatinine increased × 3 OR GFR decreased by 75% OR Serum creatinine >4 mg/dL with acute rise ≥0.5 mg/dL	Urine output <0.3 mL/kg/hr for 24 hr (oliguria) OR Anuria for 12 hr
Loss	Persistent acute kidney failure; complete loss of kidney function >4 wk	—
End-stage kidney disease	Complete loss of kidney function >3 mo	—

GFR, Glomerular filtration rate.

Oliguric Phase.

Manifestations of AKI are presented in eTable 47-1 (available on the website for this chapter). The most common manifestations are discussed in this section.

Urinary Changes.

The most common initial manifestation of AKI is oliguria, a reduction in urine output to less than 400 mL/day. Nonoliguria AKI indicates a urine output greater than 400 mL/day. Oliguria usually occurs within 1 to 7 days of the injury to the kidneys. If the cause is ischemia, oliguria often occurs within 24 hours. In contrast, when nephrotoxic drugs are involved, the onset may be delayed for as long as 1 week. 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.¹

About 50% of patients will not be oliguric, making the initial diagnosis more difficult.⁵ Changes in urine output generally do not correspond to changes in glomerular filtration rate (GFR). However, changes in urine output are often helpful in differentiating the etiology of AKI. For example, anuria is usually seen with urinary tract obstruction, oliguria is commonly seen with prerenal etiologies, and nonoliguric AKI is seen with acute interstitial nephritis and ATN.⁸

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. In addition, a urinalysis may show a specific gravity fixed at around 1.010 and urine osmolality at about 300 mOsm/kg (300 mmol/kg). This is the same specific gravity and osmolality of plasma, thus reflecting tubular damage with a loss of concentrating ability by the kidney. Proteinuria may be present if kidney failure is related to glomerular membrane dysfunction.

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Nov 17, 2016 | Posted by admin in NURSING | Comments Off

Acute Kidney Injury

Etiology and Pathophysiology

Prerenal.

Intrarenal.

Postrenal.

Clinical Manifestations

Oliguric Phase.

Urinary Changes.

Fluid Volume.

Metabolic Acidosis.

Sodium Balance.

Potassium Excess.

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