Chapter 54 urine and kidney disease

Kidney surgery

A patient may undergo surgery to remove obstructions that affect the kidney (tumors or calculi), to insert a tube for draining the kidney (nephrostomy, ureterostomy), or to remove the kidney involved in unilateral kidney disease, renal carcinoma, or kidney transplantation. Management of Patients Undergoing Kidney Surgery Preoperative Considerations Surgery is performed only after a thorough evaluation of renal function. Patient preparation to ensure that optimal renal function is maintained is essential. Fluids are encouraged to promote increased excretion of waste products before surgery unless contraindicated because of pre-existing renal or cardiac dysfunction. If kidney infection is present preoperatively, broad-spectrum antimicrobial agents may be prescribed to prevent bacteremia. Antibiotic agents must be given with extreme care because many are toxic to the kidneys. Coagulation studies (prothrombin time, partial thromboplastin time, platelet count) may be indicated if the patient has a history of bruising and bleeding. The preoperative preparation is similar to that described in Chapter 17. Because many patients facing kidney surgery are apprehensive, the nurse encourages the patient to recognize and verbalize concerns. Confidence is reinforced by establishing a relationship of trust and by providing expert care. Patients faced with the prospect of losing a kidney may think that they will have to depend on dialysis for the rest of their lives. The nurse reassures the patient and family that normal function may be maintained by a single healthy kidney. Perioperative Concerns Kidney surgery requires various patient positions to expose the surgical site adequately. Three surgical approaches are common: flank, lumbar, and thoracoabdominal (see Fig. 54-9). During surgery, plans are carried out for managing altered urinary drainage. These may include inserting a nephrostomy or other drainage tube. Postoperative Management Because the kidney is a highly vascular organ, hemorrhage and shock are the chief potential complications of kidney surgery. Fluid and blood component replacement is frequently necessary in the immediate postoperative period to treat intraoperative blood loss. Abdominal distention and paralytic ileus are fairly common after renal and ureteral surgery and are thought to be due to a reflex paralysis of intestinal peristalsis and manipulation of the colon or duodenum during surgery. Abdominal distention is relieved by decompression through a nasogastric tube. See Chapter 48 for treatment of paralytic ileus. Oral fluids are permitted when the passage of flatus is noted. Figure 54-9 • Patient positioning and incisional approaches—flank (A), lumbar (B), thoracoabdominal (C)—for kidney surgery are associated with significant postoperative discomfort. If infection occurs, antibiotics are prescribed after a culture reveals the causative organism. The toxic effects that antibiotic agents have on the kidneys (nephrotoxicity) must be kept in mind when assessing the patient. Low-dose heparin therapy may be initiated postoperatively to prevent thromboembolism in patients who have had any type of urologic surgery. Nursing Management In addition to those interventions listed in this section, Chart 54-12 provides a plan of nursing care for the patient undergoing kidney surgery. (Hinkle 1602-1603) Hinkle, Janice L., Kerry Cheever. Lippincott's CoursePoint for Hinkle & Cheever: Brunner & Suddarth's Textbook of Medical-Surgical Nursing, 14th Edition. CoursePoint, 10/2017. VitalBook file. Providing Immediate Postoperative Care Immediate postoperative care of the patient who has undergone surgery of the kidney includes assessment of all body systems. Respiratory and circulatory status, pain level, fluid and electrolyte status, and patency and adequacy of urinary drainage systems are assessed. Respiratory Status As with any surgery, the use of anesthesia increases the risk of respiratory complications. Noting the location of the surgical incision assists the nurse in anticipating respiratory problems and pain. Respiratory status is assessed by monitoring the rate, depth, and pattern of respirations. The location of the incision frequently causes pain on inspiration and coughing; therefore, the patient tends to splint the chest wall and take shallow respirations. Auscultation is performed to assess normal and adventitious breath sounds. Circulatory Status and Blood Loss The patient's vital signs and arterial or central venous pressure are monitored. Skin color and temperature and urine output provide information about circulatory status. The surgical incision and drainage tubes are observed frequently to help detect unexpected blood loss and hemorrhage. Pain Postoperative pain is a major problem for the patient because of the location of the surgical incision and patient's position on the operating table to permit access to the kidney. The location and severity of pain are assessed before and after analgesic medications are given. Abdominal distention, which increases discomfort, is also noted. Urinary Drainage Urine output and drainage from tubes inserted during surgery are monitored for amount, color, and type or characteristics. Decreased or absent drainage is promptly reported to the primary provider because it may indicate obstruction that could cause pain, infection, and disruption of the suture lines. Monitoring and Managing Potential Complications Bleeding is a major complication of kidney surgery. If undetected and untreated, it can result in hypovolemia and hemorrhagic shock. The nurse's role is to observe for these complications, to report their signs and symptoms, and to administer prescribed parenteral fluids and blood and blood components. Monitoring of vital signs, skin condition, the urinary drainage system, the surgical incision, and the level of consciousness is necessary to detect evidence of bleeding, decreased circulating blood, and fluid volume and cardiac output. Frequent monitoring of vital signs (initially monitored at least at hourly intervals) and urinary output is necessary for early detection of these complications. If bleeding goes undetected or is not detected promptly, the patient may lose significant amounts of blood and may experience hypoxemia. In addition to hypovolemic shock due to hemorrhage, this type of blood loss may precipitate a myocardial infarction or transient ischemic attack. Bleeding may be suspected when the patient experiences fatigue and when urine output is less than 0.5 mL/kg/hr. As bleeding persists, late signs of hypovolemia occur, such as cool skin, flat neck veins, and change in level of consciousness or responsiveness. Transfusions of blood components are indicated, along with surgical repair of the bleeding vessel. Pneumonia may be prevented through the use of an incentive spirometer, adequate pain control, and early ambulation. Early signs of pneumonia include fever, increased heart and respiratory rates, and adventitious breath sounds. Preventing infection involves using asepsis when changing dressings and handling and preparing catheters, other drainage tubes, central venous catheters, and IV catheters for administration of fluids. Insertion sites are monitored closely for signs and symptoms of inflammation: redness, drainage, heat, and pain. Special care must be taken to prevent UTI, which is associated with the use of indwelling urinary catheters. Catheters and other invasive tubes are removed as soon as they are no longer needed. Antibiotics are commonly given postoperatively to prevent infection. If antibiotic agents are prescribed, serum creatinine and BUN values must be monitored closely because many antibiotic agents are toxic to the kidney or can accumulate to toxic levels if renal function is decreased. Preventing fluid imbalance is critical when caring for a patient undergoing kidney surgery, because both fluid loss and fluid excess are possible adverse effects of the surgery. Fluid loss may occur during surgery as a result of excessive urinary drainage when the obstruction is removed, or it may occur if diuretic agents are used. Such loss may also occur with GI losses, with diarrhea resulting from antibiotic use, or with nasogastric drainage. When postoperative IV therapy is inadequate to match the output or fluids lost, a fluid deficit results. Fluid excess, or overload, may result from cardiac effects of anesthesia, administration of excessive amounts of fluids, or the patient's inability to excrete fluid because of changes in renal function. Decreased urine output may be an indication of fluid excess. Astute assessment skills are needed to detect early signs of fluid excess (such as weight gain, pedal edema, urine output below 0.5 mL/kg/hr, and slightly elevated pulmonary artery wedge pressure if available) before they become severe (appearance of adventitious breath sounds, shortness of breath). Fluid excess may be treated with fluid restriction and administration of furosemide (Lasix) or other diuretic agents. If renal insufficiency is present, these medications may prove ineffective; therefore, dialysis may be necessary to prevent heart failure and pulmonary edema. Deep vein thrombosis (DVT) may occur postoperatively because of surgical manipulation of the iliac vessels during surgery or prolonged immobility. Antiembolism stockings are applied, and the patient is monitored closely for signs and symptoms of thrombosis and encouraged to exercise the legs. Heparin may be given postoperatively to reduce the risk of thrombosis. Promoting Home, Community-Based, and Transitional Care Educating Patients About Self-Care If the patient has a drainage system in place, measures are taken to ensure that both the patient and family understand the importance of maintaining the system correctly at home and preventing infection. Verbal and written instructions and guidelines are provided to the patient and family at the time of hospital discharge. The patient may be asked to demonstrate management of the drainage system to ensure understanding. The importance of strategies to prevent postoperative complications (urinary tract obstruction and infection, DVT, atelectasis, and pneumonia) is stressed to the patient and family. The nurse reviews the signs, symptoms, problems, and questions that should be referred to the physician or other primary provider with the patient and family. Continuing and Transitional Care The need for postoperative assessment and care after kidney surgery continues regardless of the setting: the home, subacute care unit, outpatient clinic or office, or rehabilitation facility. Referral for home care is indicated for the patient going home with a urinary drainage system in place. During the home visit, the home care nurse reviews the instructions and guidelines given to the patient at hospital discharge. The nurse assesses the patient's ability to carry out the instructions in the home and answers questions that the patient or family has about management of the drainage system and the surgical incision. In addition, the home care nurse obtains vital signs and assesses the patient for signs and symptoms of urinary tract obstruction and infection. The nurse also ensures that pain is adequately controlled and that the patient is complying with recommendations. The home care nurse encourages adequate fluid intake and increased levels of activity. Together, the nurse, patient, and family review the signs, symptoms, problems, and questions that should be referred to the primary provider. If the patient has a drainage tube in place, the nurse assesses the site and the patency of the system and monitors the patient for complications, such as DVT, bleeding, or pneumonia. Because it is easy for the patient, family, and health care team to focus on the patient's immediate disorder to the exclusion of other health issues, the nurse reminds the patient and family about the importance of participating in health promotion activities, including appropriate health screenings. (Hinkle 1606-1607) Hinkle, Janice L., Kerry Cheever. Lippincott's CoursePoint for Hinkle & Cheever: Brunner & Suddarth's Textbook of Medical-Surgical Nursing, 14th Edition. CoursePoint, 10/2017. VitalBook file.

Acute Kidney Injury (AKI)

Acute kidney injury (AKI) is a rapid loss of renal function due to damage to the kidneys. Depending on the duration and severity of AKI, a wide range of potentially life-threatening metabolic complications can occur, including metabolic acidosis as well as fluid and electrolyte imbalances (Vritis, 2013). Treatment is aimed at replacing renal function temporarily to minimize potentially lethal complications and reduce potential causes of increased kidney injury with the goal of minimizing long-term loss of renal function. AKI is a problem seen in patients who are hospitalized and those in outpatient settings. A widely accepted criterion for AKI is a 50% or greater increase in serum creatinine above baseline (normal creatinine is less than 1 mg/dL) (Vritis, 2013). Urine volume may be normal, or changes may occur. Possible changes include nonoliguria (greater than 800 mL/day), oliguria (less than 0.5 mL/kg/hr), or anuria (less than 50 mL/day) (Vritis, 2013). Pathophysiology Although the pathogenesis of AKI and oliguria is not always known, many times there is a specific underlying cause. Some of the factors may be reversible if identified and treated promptly, before kidney function is impaired. This is true of the following conditions that reduce blood flow to the kidney and impair kidney function: (1) hypovolemia; (2) hypotension; (3) reduced cardiac output and heart failure; (4) obstruction of the kidney or lower urinary tract by tumor, blood clot, or kidney stone; and (5) bilateral obstruction of the renal arteries or veins. If these conditions are treated and corrected before the kidneys are permanently damaged, the increased BUN and creatinine levels, oliguria, and other signs may be reversed. Although renal stones are not a common cause of AKI, some types may increase the risk of AKI. Some hereditary stone diseases (see Chapter 55), primary struvite stones, and infection-related urolithiasis associated with anatomic and functional urinary tract anomalies and spinal cord injury may cause recurrent bouts of obstruction as well as crystal-specific damage to tubular epithelial cells and interstitial renal cells. Classifications of Acute Kidney Injury The term acute kidney injury has replaced the term acute renal failure because it better describes this syndrome in patients, not only simply those who require renal replacement therapies but also those patients who experience minor changes in renal function. Classification criteria for AKI include assessment of three grades of severity and two outcome-level classifications. This 5-point system is known as the RIFLE classification system (Davies & Leslie, 2012). RIFLE stands for risk, injury, failure, loss, and ESKD (Vrtis, 2013). Risk, injury, and failure are considered grades of AKI severity, whereas loss and ESKD are considered outcomes of loss that require some form of renal replacement therapy, at least temporarily (Dring & Hipkiss, 2015). Table 54-2 lists the classification criteria for the RIFLE system for AKI (Vritis, 2013). This classification system is used by health care professionals to identify kidney injury and improve patient outcomes. (Hinkle 1576-1577) Categories of Acute Kidney Injury The major categories of AKI are prerenal (hypoperfusion of kidney), intrarenal (actual damage to kidney tissue), and postrenal (obstruction to urine flow). Prerenal AKI, which occurs in 60% to 70% of cases, is the result of impaired blood flow that leads to hypoperfusion of the kidney commonly caused by volume depletion (burns, hemorrhage, GI losses), hypotension (sepsis, shock), and renal artery stenosis, ultimately leading to a decrease in the GFR (Vritis, 2013). Intrarenal AKI is the result of actual parenchymal damage to the glomeruli or kidney tubules. Acute tubular necrosis (ATN), or AKI in which there is damage to the kidney tubules, is the most common type of intrinsic AKI. Characteristics of ATN are intratubular obstruction, tubular back leak (abnormal reabsorption of filtrate and decreased urine flow through the tubule), vasoconstriction, and changes in glomerular permeability. These processes result in a decrease of GFR, progressive azotemia, and fluid and electrolyte imbalances. CKD, diabetes, heart failure, hypertension, and cirrhosis can lead to ATN. Postrenal AKI usually results from obstruction distal to the kidney by conditions such as renal calculi, strictures, blood clots, benign prostatic hypertrophy, malignancies, and pregnancy. Pressure rises in the kidney tubules, and eventually the GFR decreases. Common causes of each type of AKI are further summarized in Chart 54-4. (Hinkle 1577) Phases of Acute Kidney Injury There are four phases of AKI: initiation, oliguria, diuresis, and recovery. The initiation period begins with the initial insult and ends when oliguria develops. The oliguria period is accompanied by an increase in the serum concentration of substances usually excreted by the kidneys (urea, creatinine, uric acid, organic acids, and the intracellular cations [potassium and magnesium]). The minimum amount of urine needed to rid the body of normal metabolic waste products is 400 mL in 24 hours or 0.5 mL/kg/hr. In this phase, uremic symptoms first appear and life-threatening conditions such as hyperkalemia develop. The diuresis period is marked by a gradual increase in urine output, which signals that glomerular filtration has started to recover. Laboratory values stabilize and eventually decrease. Although the volume of urinary output may reach normal or elevated levels, renal function may still be markedly abnormal. Because uremic symptoms may still be present, the need for expert medical and nursing management continues. The patient must be observed closely for dehydration during this phase; if dehydration occurs, the uremic symptoms are likely to increase. The recovery period signals the improvement of renal function and may take 3 to 12 months. Laboratory values return to the patient's normal level. Although a permanent 1% to 3% reduction in the GFR may occur, it is not clinically significant. Some patients have decreased renal function with increasing nitrogen retention but actually excrete normal amounts of urine (1 to 2 L/day). This is the nonoliguric form of kidney injury and occurs predominantly after exposure of the patient to nephrotoxic agents (any substance, medication, or action that destroys kidney tissue), burns, traumatic injury, and the use of halogenated anesthetic agents. Clinical Manifestations Almost every system of the body is affected with failure of the normal renal regulatory mechanisms. The patient may appear critically ill and lethargic. The skin and mucous membranes are dry from dehydration. Central nervous system signs and symptoms include drowsiness, headache, muscle twitching, and seizures. Table 54-3 summarizes common clinical characteristics in all three categories of AKI. Assessment and Diagnostic Findings Assessment of the patient with AKI includes evaluation for changes in the urine, diagnostic tests that evaluate the kidney contour, and a variety of laboratory values. See Chapter 53 for information about the normal characteristics of urine, diagnostic findings, and laboratory values in the renal system. In AKI, urine output varies from scanty to a normal volume, hematuria may be present, and the urine has a low specific gravity (compared with a normal value of 1.010 to 1.025). One of the earliest manifestations of tubular damage is the inability to concentrate the urine (Vritis, 2013). Patients with prerenal azotemia have a decreased amount of sodium in the urine (less than 20 mEq/L) and normal urinary sediment. Patients with intrarenal azotemia usually have urinary sodium levels greater than 40 mEq/L with urinary casts and other cellular debris. Ultrasonography is a critical component of the evaluation of patients with kidney disease. A renal sonogram or a CT or MRI scan may show evidence of anatomic changes. The BUN level increases steadily at a rate that depends on the degree of catabolism (breakdown of protein), renal perfusion, and protein intake. Serum creatinine levels are useful in monitoring kidney function and disease progression and increase with glomerular damage. With a decline in the GFR, oliguria, and anuria, patients are at high risk for hyperkalemia. Protein catabolism results in the release of cellular potassium into the body fluids, causing severe hyperkalemia (high serum potassium levels). Hyperkalemia may lead to dysrhythmias, such as ventricular tachycardia and cardiac arrest. Sources of potassium include normal tissue catabolism, dietary intake, blood in the GI tract, or blood transfusion and other sources (e.g., IV infusions, potassium penicillin, and extracellular shift in response to metabolic acidosis). Progressive metabolic acidosis occurs in kidney disease because patients cannot eliminate the daily metabolic load of acid-type substances produced by the normal metabolic processes. In addition, normal renal buffering mechanisms fail. This is reflected by decreased serum carbon dioxide (CO2) and pH levels. Blood phosphate concentrations may increase; calcium levels may be low due to decreased absorption of calcium from the intestine and as a compensatory mechanism for the elevated blood phosphate levels. Anemia is another common laboratory finding in AKI, as a result of reduced erythropoietin production, uremic GI lesions, reduced RBC lifespan, and blood loss from the GI tract. (Hinkle 1577-1578) Prevention AKI has a high mortality rate that ranges from 40% to 90%. Factors that influence mortality include increased age, comorbid conditions, and pre-existing kidney and vascular diseases and respiratory failure (Vritis, 2013). Therefore, prevention of AKI is essential (see Chart 54-5). A careful history is obtained to identify exposure to nephrotoxic agents or environmental toxins. The kidneys are susceptible to the adverse effects of medications because the metabolic by-products of most medications are excreted by the kidneys. Patients taking nephrotoxic medications (e.g., aminoglycosides, gentamicin [Garamycin], tobramycin, colistimethate [Coly-Mycin], polymyxin B, amphotericin B, vancomycin, amikacin [Amikin], cyclosporine [Neoral]) should be monitored closely for changes in renal function. Kidney function needs to be monitored prior to initiation of these medications and during therapy (Prentice, 2013). Any agent that reduces renal blood flow (e.g., long-term analgesic use) may cause renal insufficiency. Chronic use of analgesic agents, particularly nonsteroidal anti-inflammatory drugs (NSAIDs), may cause interstitial nephritis (inflammation within the renal tissue) and papillary necrosis. Patients with heart failure or cirrhosis with ascites are at particular risk for NSAID-induced kidney disease. Increased age, pre-existing kidney disease, and the simultaneous administration of several nephrotoxic agents increase the risk of kidney damage. Radiocontrast-induced nephropathy (CIN) is a major cause of hospital-acquired AKI. Patients undergo more than 1 million radiocontrast studies in the United States annually; of these, approximately 150,000 patients will experience CIN, and at least 1% of them will require dialysis and experience a prolonged length of hospital stay (Kane-Gill et al., 2015). This is a potentially preventable condition. Baseline levels of creatinine greater than 2 mg/dL identify patients at high risk. Limiting the patient's exposure to contrast agents and nephrotoxic medications will reduce the risk of CIN (Rank, 2013). Administration of N-acetylcysteine and sodium bicarbonate before and during procedures reduces risk, but prehydration with saline is considered the most effective method to prevent CIN (Rank, 2013). Gerontologic Considerations About half of all patients who develop AKI during hospitalization are older than 60 years. The etiology of AKI in older adults includes prerenal causes such as dehydration, intrarenal causes such as nephrotoxic agents (e.g., medications, contrast agents), and complications of major surgery (Elliott, 2012). Suppression of thirst, enforced bed rest, lack of access to drinking water, and confusion all contribute to the older patient's failure to consume adequate fluids and may lead to dehydration, further compromising already decreased renal function. AKI in older adults is also often seen in the community setting. Nurses in the ambulatory setting need to be aware of the risk. All medications need to be monitored for potential side effects that could result in damage to the kidney either through reduced circulation or nephrotoxicity. Outpatient procedures that require fasting or a bowel preparation may cause dehydration and therefore require careful monitoring. Medical Management The kidneys have a remarkable ability to recover from insult. The objectives of treatment for AKI are to restore normal chemical balance and prevent complications until repair of renal tissue and restoration of renal function can occur. Management includes eliminating the underlying cause; maintaining fluid balance; avoiding fluid excesses; and, when indicated, providing renal replacement therapy. Prerenal azotemia is treated by optimizing renal perfusion, whereas postrenal failure is treated by relieving the obstruction. Intrarenal azotemia is treated with supportive therapy, with removal of causative agents, aggressive management of prerenal and postrenal failure, and avoidance of associated risk factors. Shock and infection, if present, are treated promptly (see Chapter 14). The presence of myoglobin in the urine (i.e., myoglobinuria) in the patient who has had a crush injury, compartment syndrome, or heat-induced illness is treated for rhabdomyolysis (see Chapter 72). Maintenance of fluid balance is based on daily body weight, serial measurements of central venous pressure, serum and urine concentrations, fluid losses, blood pressure, and the clinical status of the patient. The parenteral and oral intake and the output of urine, gastric drainage, stools, wound drainage, and perspiration are calculated and are used as the basis for fluid replacement. The insensible fluid produced through the normal metabolic processes and lost through the skin and lungs is also considered in fluid management. Fluid excesses can be detected by the clinical findings of dyspnea, tachycardia, and distended neck veins. The patient's lungs are auscultated for moist crackles. Because pulmonary edema may be caused by excessive administration of parenteral fluids, extreme caution must be used to prevent fluid overload. The development of generalized edema is assessed by examining the presacral and pretibial areas several times daily. Mannitol (Osmitrol), furosemide (Lasix), or ethacrynic acid (Edecrin) may be prescribed to initiate diuresis (Walton, 2015). Adequate renal blood flow in patients with prerenal causes of AKI may be restored by IV fluids or transfusions of blood products. If AKI is caused by hypovolemia secondary to hypoproteinemia, an infusion of albumin may be prescribed. Dialysis may be initiated to prevent complications of AKI, such as hyperkalemia, metabolic acidosis, pericarditis, and pulmonary edema. Dialysis corrects many biochemical abnormalities; allows for liberalization of fluid, protein, and sodium intake; diminishes bleeding tendencies; and promotes wound healing. Hemodialysis (a procedure that circulates the patient's blood through an artificial kidney [dialyzer] to remove waste products and excess fluid), peritoneal dialysis (PD; a procedure that uses the patient's peritoneal membrane [the lining of the peritoneal cavity] as the semipermeable membrane to exchange fluid and solutes), or a variety of continuous renal replacement therapies (CRRTs) (methods used to replace normal kidney function by circulating the patient's blood through a hemofilter) may be performed (Dirkes, 2014). These and other treatment modalities for patients with renal dysfunction are discussed later in this chapter. Pharmacologic Therapy Hyperkalemia is the most life threatening of the fluid and electrolyte changes that occur in patients with kidney disorders. Therefore, the patient is monitored for hyperkalemia through serial serum electrolyte levels (potassium value greater than 5.0 mEq/L [5 mmol/L]), ECG changes (tall, tented, or peaked T waves), and changes in clinical status (see Chapter 13). Other symptoms of hyperkalemia include irritability, abdominal cramping, diarrhea, paresthesia, and generalized muscle weakness. Muscle weakness may present as slurred speech, difficulty breathing, paresthesia, and paralysis. As the potassium level increases, both cardiac and other muscular function declines, making this a medical emergency. The elevated potassium levels may be reduced by administering cation-exchange resins (sodium polystyrene sulfonate [Kayexalate]) orally or by retention enema. Kayexalate works by exchanging sodium ions for potassium ions in the intestinal tract. Sorbitol may be given in combination with Kayexalate to induce a diarrhea-type effect (it induces water loss in the GI tract). If a Kayexalate retention enema is given (the colon is the major site of potassium exchange), a rectal catheter with a balloon may be used to facilitate retention if necessary. The patient should retain the Kayexalate for at least 30 to 60 minutes (preferable 6 to 10 hours) to promote potassium removal (Comerford, 2015). Afterward, a cleansing enema may be prescribed to remove remaining medication as a precaution against fecal impaction. If the patient is hemodynamically unstable (low blood pressure, changes in mental status, dysrhythmia), IV dextrose 50%, insulin, and calcium replacement may be given to shift potassium back into the cells. The shift of potassium into the intracellular space is temporary, so arrangements for dialysis need to be made on an emergent basis. Many medications are eliminated through the kidneys; therefore, dosages must be reduced when a patient has AKI. Examples of commonly used agents that require adjustment are antibiotic medications (especially aminoglycosides), digoxin (Lanoxin), phenytoin (Dilantin), ACE inhibitors, and magnesium-containing agents. In addition, many medications have been used in patients with AKI in an attempt to improve patient outcomes. Diuretic agents are often used to control fluid volume, but they have not been shown to improve recovery from AKI (Prentice, 2013). In patients with severe acidosis, the arterial blood gases and serum bicarbonate levels (CO2) must be monitored because the patient may require sodium bicarbonate therapy or dialysis. If respiratory problems develop, appropriate ventilatory measures must be instituted. The elevated serum phosphate level may be controlled with phosphate-binding agents (e.g., calcium or lanthanum carbonate) that help prevent a continuing rise in serum phosphate levels by decreasing the absorption of phosphate from the intestinal tract. Nutritional Therapy AKI causes severe nutritional imbalances (because nausea and vomiting contribute to inadequate dietary intake), impaired glucose use and protein synthesis, and increased tissue catabolism. The patient is weighed daily and loses 0.2 to 0.5 kg (0.5 to 1 lb) daily if the nitrogen balance is negative (i.e., caloric intake falls below caloric requirements). If the patient gains or does not lose weight or develops hypertension, fluid retention should be suspected. Nutritional support is based on the underlying cause of AKI, the catabolic response, the type and frequency of renal replacement therapy, comorbidities, and nutritional status. Replacement of dietary proteins is individualized to provide the maximum benefit and minimize uremic symptoms. Caloric requirements are met with high-carbohydrate meals, because carbohydrates have a protein-sparing effect (i.e., in a high-carbohydrate diet, protein is not used for meeting energy requirements but is "spared" for growth and tissue healing). Foods and fluids containing potassium or phosphorus (e.g., bananas, citrus fruits and juices, coffee) are restricted. The oliguric phase of AKI may last 10 to 14 days and is followed by the diuretic phase, at which time urine output begins to increase, signaling the patient is in the recovery phase (Prentice, 2013). Results of blood chemistry tests are used to determine the amounts of sodium, potassium, and water needed for replacement, along with assessment for over- or underhydration. Following the diuretic phase, the patient is placed on a high-protein, high-calorie diet and is encouraged to resume activities gradually. Nursing Management The nurse has an important role in caring for the patient with AKI. The nurse monitors for complications, participates in emergency treatment of fluid and electrolyte imbalances, assesses the patient's progress and response to treatment, and provides physical and emotional support. In addition, the nurse keeps family members informed about the patient's condition, helps them understand the treatments, and provides psychological support. Although the development of AKI may be the most serious problem, the nurse continues to provide nursing care indicated for the primary disorder (e.g., burns, shock, trauma, obstruction of the urinary tract). p. 1580 p. 1581 Monitoring Fluid and Electrolyte Balance Because of the serious fluid and electrolyte imbalances that can occur with AKI, the nurse monitors the patient's serum electrolyte levels and physical indicators of these complications during all phases of the disorder. IV solutions must be carefully selected based on the patient's fluid and electrolyte status. The patient's cardiac function and musculoskeletal status are monitored closely for signs of hyperkalemia. Quality and Safety Nursing Alert Hyperkalemia is the most immediate life-threatening imbalance seen in AKI. Parenteral fluids, all oral intake, and all medications are screened carefully to ensure that sources of potassium are not inadvertently given or consumed. The nurse monitors fluid status by paying careful attention to fluid intake (IV medications should be given in the smallest volume possible), urine output, apparent edema, distention of the jugular veins, alterations in heart sounds and breath sounds, and increasing difficulty in breathing. Accurate daily weights, as well as I&O records, are essential. Indicators of deteriorating fluid and electrolyte status are reported immediately to the primary provider, and preparation is made for emergency treatment. Severe fluid and electrolyte disturbances may be treated with hemodialysis, PD, or CRRT. Reducing Metabolic Rate The nurse takes steps to reduce the patient's metabolic rate. Bed rest may be indicated to reduce exertion and the metabolic rate during the most acute stage of the disorder. Fever and infection, both of which increase the metabolic rate and catabolism, are prevented or treated promptly. Promoting Pulmonary Function Attention is given to pulmonary function, and the patient is assisted to turn, cough, and take deep breaths frequently to prevent atelectasis and respiratory tract infection. Drowsiness and lethargy may prevent the patient from moving and turning without encouragement and assistance. Preventing Infection Asepsis is essential with invasive lines and catheters to minimize the risk of infection and increased metabolism. An indwelling urinary catheter is avoided whenever possible due to the high risk of UTI associated with its use but may be required to provide ongoing data required to accurately monitor fluid I&O. Providing Skin Care The skin may be dry or susceptible to breakdown as a result of edema; therefore, meticulous skin care is important. In addition, excoriation and itching of the skin may result from the deposit of irritating toxins in the patient's tissues. Bathing the patient with cool water, frequent turning, and keeping the skin clean and well moisturized and the fingernails trimmed to avoid excoriation are often comforting and prevent skin breakdown. Providing Psychosocial Support The patient with AKI may require treatment with hemodialysis, PD, or CRRT. The length of time that these treatments are necessary varies with the cause and extent of damage to the kidneys. The patient and family need assistance, explanation, and support during this period. The purpose of the treatment is explained to the patient and family by the primary provider. However, high levels of anxiety and fear may necessitate repeated explanation and clarification by the nurse. The family members may initially be afraid to touch and talk to the patient during these procedures but should be encouraged and assisted to do so. In an intensive care setting, many of the nurse's functions are devoted to the technical aspects of patient care; however, it is essential that the psychological needs and other concerns of the patient and family be addressed. Continued assessment of the patient for complications of AKI and precipitating causes is essential (Davies & Leslie, 2012). (Hinkle 1579-1581) Hinkle, Janice L., Kerry Cheever. Lippincott's CoursePoint for Hinkle & Cheever: Brunner & Suddarth's Textbook of Medical-Surgical Nursing, 14th Edition. CoursePoint, 10/2017. VitalBook file.

acute nephritic syndrome

Acute nephritic syndrome is a type of kidney disease with glomerular inflammation (Grossman & Porth, 2014). Glomerulonephritis is an inflammation of the glomerular capillaries that can occur in acute and chronic forms. Pathophysiology Primary glomerular diseases include postinfectious glomerulonephritis, rapidly progressive glomerulonephritis, membrane proliferative glomerulonephritis, and membranous glomerulonephritis. Postinfectious causes are group A beta-hemolytic streptococcal infection of the throat that precedes the onset of glomerulonephritis by 2 to 3 weeks (see Fig. 54-1). It may also follow impetigo (infection of the skin) and acute viral infections (upper respiratory tract infections, mumps, varicella zoster virus, Epstein-Barr virus, hepatitis B, and human immune deficiency virus [HIV] infection). In some patients, antigens outside the body (e.g., medications, foreign serum) initiate the process, resulting in antigen-antibody complexes being deposited in the glomeruli. In other patients, the kidney tissue itself serves as the inciting antigen. Clinical Manifestations The primary presenting features of an acute glomerular inflammation are hematuria, edema, azotemia (an abnormal concentration of nitrogenous wastes in the blood), and proteinuria (excess protein in the urine) (Grossman & Porth, 2014). The hematuria may be microscopic (identifiable only through microscopic examination) or macroscopic (visible to the eye). The urine may appear cola colored because of red blood cells (RBCs) and protein plugs or casts; RBC casts indicate glomerular injury. Glomerulonephritis may be mild and the hematuria discovered incidentally through a routine urinalysis, or the disease may be severe, with AKI and oliguria. Figure 54-1 • Sequence of events in acute nephritic syndrome. Some degree of edema and hypertension is present in most patients. Marked proteinuria due to the increased permeability of the glomerular membrane may also occur, with associated pitting edema, hypoalbuminemia, hyperlipidemia, and fatty casts in the urine. Blood urea nitrogen (BUN) and serum creatinine levels may increase as urine output decreases. In addition, anemia may be present. In the more severe form of the disease, patients also complain of headache, malaise, and flank pain. Older patients may experience circulatory overload with dyspnea, engorged neck veins, cardiomegaly, and pulmonary edema. Atypical symptoms include confusion, somnolence, and seizures, which are often confused with the symptoms of a primary neurologic disorder. Assessment and Diagnostic Findings In acute nephritic syndrome, the kidneys become large, edematous, and congested. All renal tissues, including the glomeruli, tubules, and blood vessels, are affected to varying degrees. Patients with an immunoglobulin A (IgA) nephropathy have an elevated serum IgA and low to normal complement levels. Electron microscopy and immunofluorescent analysis help identify the nature of the lesion; however, a kidney biopsy may be needed for definitive diagnosis. See Chapter 53 for discussion of kidney biopsy. If the patient improves, the amount of urine increases and the urinary protein and sediment diminish. The percentage of adults who recover is unknown. Some patients develop severe uremia (an excess of urea and other nitrogenous wastes in the blood) within weeks and require dialysis for survival. Others, after a period of apparent recovery, insidiously develop chronic glomerulonephritis. Complications Complications of acute glomerulonephritis include hypertensive encephalopathy, heart failure, and pulmonary edema. Hypertensive encephalopathy is a medical emergency, and therapy is directed toward reducing the blood pressure without impairing renal function. This can occur in acute nephritic syndrome or preeclampsia with chronic hypertension of greater than 140/90 mmHg. Rapidly progressive glomerulonephritis is characterized by a rapid decline in renal function. Without treatment, ESKD develops in a matter of weeks or months. Signs and symptoms are similar to those of acute glomerulonephritis (hematuria and proteinuria), but the course of the disease is more severe and rapid. Crescent-shaped cells accumulate in Bowman space, disrupting the filtering surface. Plasma exchange (plasmapheresis) and treatment with high-dose corticosteroids and cytotoxic agents have been used to reduce the inflammatory response. Dialysis is initiated in acute glomerulonephritis if signs and symptoms of uremia are severe. The prognosis for patients with acute nephritic syndrome is excellent and rarely causes CKD (Grossman & Porth 2014). Medical Management Management consists primarily of treating symptoms, attempting to preserve kidney function, and treating complications promptly. Treatment may include prescribing corticosteroids, managing hypertension, and controlling proteinuria. Pharmacologic therapy depends on the cause of acute glomerulonephritis. If residual streptococcal infection is suspected, penicillin is the agent of choice; however, other antibiotic agents may be prescribed. Dietary protein is restricted when renal insufficiency and nitrogen retention (elevated BUN) develop. Sodium is restricted when the patient has hypertension, edema, and heart failure. Nursing Management Although most patients with acute uncomplicated glomerulonephritis are cared for as outpatients, nursing care is important in every setting. Providing Care in the Hospital In a hospital setting, carbohydrates are given liberally to provide energy and reduce the catabolism of protein. I&O is carefully measured and recorded. Fluids are given based on the patient's fluid losses and daily body weight. Insensible fluid loss through the lungs (300 mL) and skin (500 mL) is considered when estimating fluid loss (see Chapter 13; Table 13-2). If treatment is effective, diuresis will begin, resulting in decreased edema and blood pressure. Proteinuria and microscopic hematuria may persist for many months; in fact, 20% of patients have some degree of persistent proteinuria or decreased GFR 1 year after presentation (Grossman & Porth, 2014). Other nursing interventions focus on patient education about the disease process, explanations of laboratory and other diagnostic tests, and preparation for safe and effective self-care at home. Promoting Home, Community-Based, and Transitional Care Educating Patients About Self-Care Patient education is directed toward managing symptoms and monitoring for complications. Fluid and diet restrictions must be reviewed with the patient to avoid worsening of edema and hypertension. The patient is instructed verbally and in writing to notify the primary provider if symptoms of kidney disease occur (e.g., fatigue, nausea, vomiting, diminishing urine output) or at the first sign of any infection. Continuing and Transitional Care The importance of follow-up evaluations of blood pressure, urinalysis for protein, and BUN and serum creatinine levels to determine if the disease has progressed is stressed to the patient. A referral for transitional, home, or community-based care may be indicated. A home visit from a nurse provides an opportunity for careful assessment of the patient's progress and detection of early signs and symptoms of renal insufficiency. If corticosteroids, immunosuppressant agents, or antibiotic medications are prescribed, the nurse uses the opportunity to review the dosage, desired actions, and adverse effects of medications and the precautions to be taken. (Hinkle 1570-1572) Hinkle, Janice L., Kerry Cheever. Lippincott's CoursePoint for Hinkle & Cheever: Brunner & Suddarth's Textbook of Medical-Surgical Nursing, 14th Edition. CoursePoint, 10/2017. VitalBook file.

Nephrotic syndrome

Nephrotic Syndrome Nephrotic syndrome is a type of kidney disease characterized by increased glomerular permeability and is manifested by massive proteinuria (Grossman & Porth, 2014). Clinical findings include a marked increase in protein (particularly albumin) in the urine (proteinuria), a decrease in albumin in the blood (hypoalbuminemia), diffuse edema, high serum cholesterol, and low-density lipoproteins (hyperlipidemia). The syndrome is apparent in any condition that seriously damages the glomerular capillary membrane and results in increased glomerular permeability to plasma proteins. Although the liver is capable of increasing the production of albumin, it cannot keep up with the daily loss of albumin through the kidneys. Thus, hypoalbuminemia results (see Fig. 54-2). Pathophysiology Nephrotic syndrome occurs with many intrinsic kidney diseases and systemic diseases that cause glomerular damage. It is not a specific glomerular disease but a constellation of clinical findings that result from the glomerular damage. Clinical Manifestations The major manifestation of nephrotic syndrome is edema. It is usually soft and pitting and commonly occurs around the eyes (periorbital), in dependent areas (sacrum, ankles, and hands), and in the abdomen (ascites). Patients may also exhibit irritability, headache, and malaise. Figure 54-2 • Sequence of events in nephrotic syndrome. Reprinted with permission from Grossman, S. C., & Porth, C. M. (2014). Pathophysiology: Concepts of altered health states (9th ed.). Philadelphia, PA: Lippincott Williams & Wilkins. Assessment and Diagnostic Findings Proteinuria (predominately albumin) exceeding 3.5 g/day is the hallmark of the diagnosis of nephrotic syndrome. Protein electrophoresis and immunoelectrophoresis may be performed on the urine to categorize the type of proteinuria. The urine may also contain increased white blood cells (WBCs) as well as granular and epithelial casts. A needle biopsy of the kidney may be performed for histologic examination of renal tissue to confirm the diagnosis. Complications Complications of nephrotic syndrome include infection (due to a deficient immune response), thromboembolism (especially of the renal vein), pulmonary embolism, AKI (due to hypovolemia), and accelerated atherosclerosis (due to hyperlipidemia). Medical Management Treatment is focused on addressing the underlying disease state causing proteinuria, slowing progression of CKD, and relieving symptoms. Typical treatment includes diuretic agents for edema, ACE inhibitors to reduce proteinuria, and lipid-lowering agents for hyperlipidemia. Nursing Management In the early stages of nephrotic syndrome, nursing management is similar to that of the patient with acute glomerulonephritis, but as the condition worsens, management is similar to that of the patient with ESKD (see the following section). Patients with nephrotic syndrome need adequate instruction about the importance of following all (Hinkle 1573-1574) Hinkle, Janice L., Kerry Cheever. Lippincott's CoursePoint for Hinkle & Cheever: Brunner & Suddarth's Textbook of Medical-Surgical Nursing, 14th Edition. CoursePoint, 10/2017. VitalBook file.

Renal trauma

The kidneys are protected by the rib cage and musculature of the back posteriorly and by a cushion of abdominal wall and viscera anteriorly. They are highly mobile and are fixed only at the renal pedicle (stem of renal blood vessels and the ureter). With traumatic injury, the kidneys can be thrust against the lower ribs, resulting in contusion and rupture. Rib fractures or fractures of the transverse process of the upper lumbar vertebrae may be associated with renal contusion or laceration. Failure to wear seat belts contributes to the incidence of renal trauma in motor vehicle crashes. Up to 80% of patients with renal trauma have associated injuries of other internal organs. Injuries may be blunt (automobile and motorcycle crashes, falls, athletic injuries, assaults) or penetrating (gunshot wounds, stabbings). Blunt renal trauma accounts for 80% to 90% of all renal injuries; penetrating renal trauma accounts for the remaining 10% to 20% (Counts, 2015; USRDS, 2015). Figure 54-11 • Types and pathophysiologic effects of kidney injuries: contusions, lacerations, rupture, and pedicle injury. Blunt renal trauma is classified into one of four groups, as follows: Contusion: Bruises or hemorrhages under the renal capsule; capsule and collecting system intact Minor laceration: Superficial disruption of the cortex; renal medulla and collecting system are not involved Major laceration: Parenchymal disruption extending into cortex and medulla, possibly involving the collecting system Vascular injury: Tears of renal artery or vein The most common renal injuries are contusions, lacerations, ruptures, and renal pedicle injuries or small internal lacerations of the kidney (see Fig. 54-11). The kidneys receive half of the blood flow from the abdominal aorta; therefore, even a fairly small renal laceration can produce massive bleeding. The majority of patients are in shock when admitted to the hospitals. In some cases, there is an isolated renal artery thrombosis. Clinical manifestations include pain, renal colic (due to blood clots or fragments obstructing the collecting system), hematuria, mass or swelling in the flank, ecchymoses, and lacerations or wounds of the lateral abdomen and flank. Hematuria is the most common manifestation of renal trauma; its presence after trauma suggests kidney injury. There is no relationship between the degree of hematuria and the degree of injury. Hematuria may not occur, or it may be detectable only on microscopic examination. Signs and symptoms of hypovolemia and shock (see Chapter 14) are likely with significant hemorrhage. p. 1612 p. 1613 Medical Management The goals of management in patients with renal trauma are to control hemorrhage, pain, and infection as well as to preserve and restore renal function. All urine is saved and sent to the laboratory for analysis to detect RBCs and to evaluate the course of bleeding. Hematocrit and hemoglobin levels are monitored closely; decreasing values indicate hemorrhage. The patient is monitored for oliguria and signs of hemorrhagic shock, because a pedicle injury or shattered kidney can lead to rapid exsanguination (lethal blood loss). An expanding hematoma may cause rupture of the kidney capsule. To detect hematoma, the area around the lower ribs, upper lumbar vertebrae, flank, and abdomen is palpated for tenderness. A palpable flank or abdominal mass with local tenderness, swelling, and ecchymosis suggests renal hemorrhage. The area of the original mass can be outlined with a marking pen so that the examiner can evaluate the area for change. Renal trauma is often associated with other injuries to the abdominal organs (liver, colon, small intestines); therefore, the patient is assessed for skin abrasions, lacerations, and entry and exit wounds of the upper abdomen and lower thorax, because these may be associated with kidney injury. With a contusion of the kidney, healing may take place with conservative measures. If the patient has microscopic hematuria and a normal IV urogram, outpatient management is possible. If gross hematuria or a minor laceration is present, the patient is hospitalized and kept on bed rest until the hematuria clears. Antimicrobial medications may be prescribed to prevent infection from perirenal hematoma or urinoma (a cyst containing urine). Patients with retroperitoneal hematomas may develop low-grade fever as absorption of the clot takes place. Surgical Management In renal trauma, any sudden change in the patient's condition suggests hemorrhage and requires rapid surgical intervention. Depending on the patient's condition and the nature of the injury, major lacerations may be treated through surgical intervention or conservatively (bed rest, no surgery). Vascular injuries require immediate exploratory surgery because of the high incidence of involvement of other organ systems and the serious complications that may result if these injuries are untreated. The patient is often in shock and requires aggressive fluid resuscitation. The damaged kidney may have to be removed (nephrectomy). Early postoperative complications (within 6 months) include rebleeding, perinephritic abscess formation, sepsis, urine extravasation, and fistula formation. Other complications include stone formation, infection, cysts, vascular aneurysms, and loss of renal function. Hypertension can be a complication of any surgery but usually is a late complication of kidney injury. Nursing Management The patient with renal trauma must be assessed frequently during the first few days after injury to detect flank and abdominal pain, muscle spasm, and swelling over the flank. During this time, the patient who has undergone surgery is educated about care of the incision and the importance of an adequate fluid intake. In addition, instructions about changes that should be reported to the physician, such as fever, hematuria, flank pain, or any signs and symptoms of decreasing kidney function, are provided. Guidelines for gradually increasing activity, lifting, and driving are also provided in accordance with the physician's prescription. Follow-up nursing care includes monitoring the blood pressure to detect hypertension and advising the patient to restrict activities for about 1 month after trauma to minimize the incidence of delayed or secondary bleeding. The patient should be advised to schedule periodic follow-up assessments of renal function (creatinine clearance, BUN, and serum creatinine analyses). If a nephrectomy was necessary, the patient is advised to wear medical identification. (Hinkle 1612-1613) Hinkle, Janice L., Kerry Cheever. Lippincott's CoursePoint for Hinkle & Cheever: Brunner & Suddarth's Textbook of Medical-Surgical Nursing, 14th Edition. CoursePoint, 10/2017. VitalBook file.

end-stage kidney disease (ESKD)

When a patient has sustained enough kidney damage to require renal replacement therapy on a permanent basis, the patient has moved into the fifth or final stage of CKD, also referred to as ESKD. Pathophysiology As renal function declines, the end products of protein metabolism (normally excreted in urine) accumulate in the blood. Uremia develops and adversely affects every system in the body. The greater the buildup of waste products, the more pronounced the symptoms. The rate of decline in renal function and progression of ESKD is related to the underlying disorder, the urinary excretion of protein, and the presence of hypertension. The disease tends to progress more rapidly in patients who excrete significant amounts of protein or have elevated blood pressure than in those without these conditions. Clinical Manifestations Because virtually every body system is affected in ESKD, patients exhibit a number of signs and symptoms. The severity of these signs and symptoms depends in part on the degree of renal impairment, other underlying conditions, and the patient's age. Cardiovascular disease is the predominant cause of death in patients with ESKD (Walton, 2015). Peripheral neuropathy, a disorder of the peripheral nervous system, is present in some patients. Patients complain of severe pain and discomfort. Restless leg syndrome and burning feet can occur in the early stage of uremic peripheral neuropathy. The precise mechanisms for many of these systemic signs and symptoms have not been identified. However, it is generally thought that the accumulation of uremic waste products is the probable cause. Chart 54-6 summarizes the systemic signs and symptoms. Assessment and Diagnostic Findings Glomerular Filtration Rate As the GFR decreases (due to nonfunctioning glomeruli), the creatinine clearance decreases, whereas the serum creatinine and BUN levels increase. Serum creatinine is a more sensitive indicator of renal function than BUN. The BUN is affected not only by kidney disease but also by protein intake in the diet, catabolism (tissue and RBC breakdown), parenteral nutrition, and medications such as corticosteroids. (Hinkle 1581-1582) Hinkle, Janice L., Kerry Cheever. Lippincott's CoursePoint for Hinkle & Cheever: Brunner & Suddarth's Textbook of Medical-Surgical Nursing, 14th Edition. CoursePoint, 10/2017. VitalBook file. Sodium and Water Retention The kidney cannot concentrate or dilute the urine normally in ESKD. Appropriate responses by the kidney to changes in the daily intake of water and electrolytes, therefore, do not occur. Some patients retain sodium and water, increasing the risk for edema, heart failure, and hypertension. Hypertension may also result from activation of the renin-angiotensin-aldosterone axis and the concomitant increased aldosterone secretion. Other patients have a tendency to lose sodium and run the risk of developing hypotension and hypovolemia. Vomiting and diarrhea may cause sodium and water depletion, which worsens the uremic state. Acidosis Metabolic acidosis occurs in ESKD because the kidneys are unable to excrete increased loads of acid. Decreased acid secretion results from the inability of the kidney tubules to excrete ammonia (NH3−) and to reabsorb sodium bicarbonate (HCO3−). There is also decreased excretion of phosphates and other organic acids. Anemia Anemia develops as a result of inadequate erythropoietin production, the shortened lifespan of RBCs, nutritional deficiencies, and the patient's tendency to bleed, particularly from the GI tract. Erythropoietin, a substance normally produced by the kidneys, stimulates bone marrow to produce RBCs. In ESKD, erythropoietin production decreases and profound anemia results, producing fatigue, angina, and shortness of breath. Calcium and Phosphorus Imbalance Another abnormality seen in ESKD is a disorder in calcium and phosphorus metabolism. Serum calcium and phosphate levels have a reciprocal relationship in the body: As one increases, the other decreases. With a decrease in filtration through the glomerulus of the kidney, there is an increase in the serum phosphate level and a reciprocal or corresponding decrease in the serum calcium level. The decreased serum calcium level causes increased secretion of parathormone from the parathyroid glands. However, in kidney disease, the body does not respond normally to the increased secretion of parathormone; as a result, calcium leaves the bone, often producing bone changes and bone disease as well as calcification of major blood vessels in the body. In addition, the active metabolite of vitamin D (1,25-dihydroxycholecalciferol) normally manufactured by the kidney decreases as kidney disease progresses (Counts, 2015). Uremic bone disease, often called renal osteodystrophy, develops from the complex changes in calcium, phosphate, and parathormone balance. There is also evidence of calcification of blood vessels. Complications There are a number of potential complications of ESKD that necessitate a collaborative approach to care. These include the following: Anemia due to decreased erythropoietin production, decreased RBC lifespan, bleeding in the GI tract from irritating toxins and ulcer formation, and blood loss during hemodialysis Bone disease and metastatic and vascular calcifications due to retention of phosphorus, low serum calcium levels, abnormal vitamin D metabolism, and elevated aluminum levels Hyperkalemia due to decreased excretion, metabolic acidosis, catabolism, and excessive intake (diet, medications, fluids) Hypertension due to sodium and water retention and malfunction of the renin-angiotensin-aldosterone system Pericarditis, pericardial effusion, and pericardial tamponade due to retention of uremic waste products and inadequate dialysis Medical Management The goal of management is to maintain kidney function and homeostasis for as long as possible. All factors that contribute to ESKD and all factors that are reversible (e.g., obstruction) are identified and treated. Management is accomplished primarily with medications and diet therapy, although dialysis may also be needed to decrease the level of uremic waste products in the blood and to control electrolyte balance. Pharmacologic Therapy Complications can be prevented or delayed by administering prescribed phosphate-binding agents, calcium supplements, antihypertensive and cardiac medications, anticonvulsant medications, and recombinant human erythropoietin (epoetin alfa [Epogen]). Calcium and Phosphorus Binders Hyperphosphatemia and hypocalcemia are treated with medications that bind dietary phosphorus in the GI tract. Binders such as calcium carbonate (Os-Cal) or calcium acetate (PhosLo) are prescribed, but there is a risk of hypercalcemia. If calcium is high or the calcium-phosphorus product exceeds 55 mg/dL, a polymeric phosphate binder such as sevelamer hydrochloride (Renagel) may be prescribed (Walton, 2015). This medication binds dietary phosphorus in the intestinal tract; one to four tablets are given with food to be effective. Magnesium-based antacid agents are avoided to prevent magnesium toxicity. Antihypertensive and Cardiovascular Agents Hypertension is managed by intravascular volume control and a variety of antihypertensive agents (Weiner, Brunelli, Hunt, et al., 2014). Heart failure and pulmonary edema may also require treatment with fluid restriction, low-sodium diets, diuretic agents, inotropic agents such as digoxin or dobutamine (Dobutrex), and dialysis. The metabolic acidosis of ESKD usually produces no symptoms and requires no treatment; however, sodium bicarbonate supplements or dialysis may be needed to correct the acidosis if it causes symptoms. Anticonvulsant Agents Neurologic abnormalities may occur, so the patient must be observed for early evidence of slight twitching, headache, delirium, or seizure activity. If seizures occur, the onset of the seizure is recorded along with the type, duration, and general effect on the patient. The primary provider is notified immediately. IV diazepam (Valium) or phenytoin is usually given to control seizures. The side rails of the bed should be raised and padded to protect the patient. See Chapter 66 for discussion of nursing management for the patient with seizures. Erythropoietin Anemia associated with ESKD is treated with erythrocyte-stimulating agents (recombinant human erythropoietin). Patients with anemia (hematocrit less than 30%) present with nonspecific symptoms, such as malaise, general fatigability, and decreased activity tolerance. Erythrocyte stimulation therapy is initiated to achieve a hematocrit of 33% to 38% and a target hemoglobin of 12 g/dL, which generally alleviates the symptoms of anemia. Epoetin alfa is administered IV or subcutaneously three times a week in ESKD. It may take 2 to 6 weeks for the hematocrit to increase; therefore, the medication is not indicated for patients who need immediate correction of severe anemia. Adverse effects seen with erythropoietin therapy include hypertension (especially during early stages of treatment), increased clotting of vascular access sites, seizures, and depletion of body iron stores (Arslanian, 2015). Management involves adjustment of heparin to prevent clotting of the lines during hemodialysis treatments, frequent monitoring of hemoglobin and hematocrit, and periodic assessment of serum iron and transferrin levels. Because adequate stores of iron are necessary for an adequate response to epoetin alfa, supplementary iron may be prescribed. Common iron supplements include iron sucrose (Venofer), iron dextran (INFeD or Dexferrum), and ferric gluconate (Ferrlecit). In addition, the patient's blood pressure and serum potassium level are monitored to detect hypertension and increasing serum potassium levels, which may occur with therapy and the increasing RBC mass. The occurrence of hypertension requires initiation or adjustment of the patient's antihypertensive therapy. Hypertension that cannot be controlled is a contraindication to recombinant erythropoietin therapy. Patients who have received erythropoietin therapy have reported decreased levels of fatigue, increased feelings of well-being, better tolerance of dialysis, higher-energy levels, and improved exercise tolerance. In addition, this therapy has decreased the need for transfusion and its associated risks, including bloodborne infectious disease, antibody formation, and iron overload. Nutritional Therapy Dietary intervention is necessary with deterioration of renal function and includes careful regulation of protein intake, fluid intake to balance fluid losses, sodium intake to balance sodium losses, and some restriction of potassium. At the same time, adequate caloric intake and vitamin supplementation must be ensured. Protein is restricted because urea, uric acid, and organic acids—the breakdown products of dietary and tissue proteins—accumulate rapidly in the blood when there is impaired renal clearance. The allowed protein must be of high biologic value (dairy products, eggs, meats). High-biologic-value proteins are those that are complete proteins and supply the essential amino acids necessary for growth and cell repair. Usually, the fluid allowance per day is 500 to 600 mL more than the previous day's 24-hour urine output. Calories are supplied by carbohydrates and fat to prevent wasting. Vitamin supplementation is necessary because a protein-restricted diet does not provide the necessary complement of vitamins. In addition, the patient on dialysis may lose water-soluble vitamins during the dialysis treatment. Hyperkalemia is usually prevented by ensuring adequate dialysis treatments with potassium removal and careful monitoring of diet, medications, and fluids for their potassium content. Sodium polystyrene sulfonate (Kayexalate), a cation-exchange resin, may be needed for acute hyperkalemia. Dialysis The patient with increasing symptoms of kidney disease is referred to a dialysis and transplantation center early in the course of progressive kidney disease. Dialysis is usually initiated when the patient cannot maintain a reasonable lifestyle with conservative treatment. Nursing Management The patient with ESKD requires astute nursing care to avoid the complications of reduced renal function and the stresses and anxieties of dealing with a life-threatening illness. Nursing care is directed toward assessing fluid status and identifying potential sources of imbalance, implementing a dietary program to ensure proper nutritional intake within the limits of the treatment regimen, and promoting positive feelings by encouraging increased self-care and greater independence. It is extremely important to provide explanations and information to the patient and family concerning ESKD, treatment options, and potential complications. A great deal of emotional support is needed by the patient and family because of the numerous changes experienced. Specific interventions, along with rationale and evaluation criteria, are presented in more detail in the plan of nursing care for the patient with ESKD (see Chart 54-7). Promoting Home, Community-Based, and Transitional Care Educating Patients About Self-Care The nurse plays an important role in educating the patient with ESKD. Because of the extensive education needed, the home care nurse, dialysis nurse, and nurses in the hospital and outpatient settings all provide ongoing education and reinforcement while monitoring the patient's progress and compliance with the treatment regimen. A referral to a nutritionist is made because of the dietary changes required. The patient is instructed to check the vascular access device for patency and to use appropriate precautions, such as avoiding venipuncture and blood pressure measurements on the arm with the access device. In addition, the patient and family need to know what problems to report to the primary provider. These include the following: Worsening signs and symptoms of kidney disease (nausea, vomiting, change in usual urine output [if any], ammonia odor on breath) Signs and symptoms of hyperkalemia (muscle weakness, diarrhea, abdominal cramps) Signs and symptoms of access problems (clotted fistula or graft, infection) These signs and symptoms of decreasing renal function, in addition to increasing BUN and serum creatinine levels, may indicate a need to alter the dialysis prescription. The dialysis nurses also provide ongoing education and support at each treatment visit. Continuing and Transitional Care The importance of follow-up examinations and treatment is stressed with the patient and family because of changing physical status, renal function, and dialysis requirements. Referral for home care provides the home care nurse with the opportunity to assess the patient's environment, emotional status, and the coping strategies used by the patient and family to deal with the changes in family roles often associated with chronic illness. The home care nurse also assesses the patient for further deterioration of renal function and signs and symptoms of complications resulting from the primary kidney disorder, the resulting kidney disease, and effects of treatment strategies (e.g., dialysis, medications, dietary restrictions) (Hain, 2015). Patients need education and reinforcement of the dietary restrictions required, including fluid, sodium, potassium, and protein restriction. Reminders about the need for health promotion activities and health screening are an important part of nursing care for the patient with kidney disease. Gerontologic Considerations Diabetes, hypertension, chronic glomerulonephritis, interstitial nephritis, and urinary tract obstruction are among the causes for ESKD in older adults. The signs and symptoms of kidney disease in older adults are often nonspecific. The occurrence of symptoms of other disorders (heart failure, dementia) can mask the symptoms of kidney disease and delay or prevent diagnosis and treatment. Hemodialysis and PD are used effectively in treating older patients with ESKD. Initiation of dialysis among older patients has dramatically increased in the past decade. Implementation of palliative care has also increased among patients who choose not to start dialysis or who decide to stop dialysis. Although there is no specific age limitation for kidney transplantation, concomitant disorders (e.g., coronary artery disease, peripheral vascular disease) have made it a less common treatment for older adults. However, the outcome is comparable to that in younger patients. Some older patients elect not to undergo dialysis or transplantation. Conservative management and palliative care, including nutritional therapy, fluid control, and medications such as phosphate binders, may be considered in patients who are not suitable for or elect not to have dialysis or transplantation (Prentice, 2013). Palliative care for the patient with ESKD focuses on relieving suffering, promoting health-related quality of life, and facilitating dignity at the end of life (see Chapter 16). (Hinkle 1582-1584) Hinkle, Janice L., Kerry Cheever. Lippincott's CoursePoint for Hinkle & Cheever: Brunner & Suddarth's Textbook of Medical-Surgical Nursing, 14th Edition. CoursePoint, 10/2017. VitalBook file.

Chronic Glomerulonephritis

Chronic Glomerulonephritis Chronic glomerulonephritis may be due to repeated episodes of acute nephritic syndrome, hypertensive nephrosclerosis, hyperlipidemia, chronic tubulointerstitial injury, or hemodynamically mediated glomerular sclerosis. Secondary glomerular diseases that can have systemic effects include systemic lupus erythematosus, Goodpasture syndrome (caused by antibodies to the glomerular basement membrane), diabetic glomerulosclerosis, and amyloidosis. Pathophysiology The kidneys are reduced to as little as one fifth their normal size (consisting largely of fibrous tissue). The cortex layer shrinks to 1 to 2 mm in thickness or less. Bands of scar tissue distort the remaining cortex, making the surface of the kidney rough and irregular. Numerous glomeruli and their tubules become scarred, and the branches of the renal artery are thickened. The resulting severe glomerular damage can progress to stage 5 CKD and require a renal replacement therapy. Clinical Manifestations The symptoms of chronic glomerulonephritis vary. Some patients with severe disease have no symptoms at all for many years. The condition may be discovered when hypertension or elevated BUN and serum creatinine levels are detected. Most patients report general symptoms, such as loss of weight and strength, increasing irritability, and an increased need to urinate at night (nocturia). Headaches, dizziness, and digestive disturbances are also common. As chronic glomerulonephritis progresses, signs and symptoms of CKD may develop. The patient appears poorly nourished, with a yellow-gray pigmentation of the skin and periorbital and peripheral (dependent) edema. Blood pressure may be normal or severely elevated. Retinal findings include hemorrhage, exudate, narrowed tortuous arterioles, and papilledema. Anemia causes pale mucous membranes. Cardiomegaly, a gallop rhythm, distended neck veins, and other signs and symptoms of heart failure may be present. Crackles can be heard in the bases of the lungs. Peripheral neuropathy with diminished deep tendon reflexes and neurosensory changes occur late in the disease. The patient becomes confused and demonstrates a limited attention span. An additional late finding includes evidence of pericarditis with a pericardial friction rub and pulsus paradoxus (difference in blood pressure during inspiration and expiration of greater than 10 mmHg). Assessment and Diagnostic Findings A number of laboratory abnormalities occur. Urinalysis reveals a fixed specific gravity of about 1.010, variable proteinuria, and urinary casts (proteins secreted by damaged kidney tubules). As kidney disease progresses and the GFR falls below 50 mL/min, the following changes occur: Hyperkalemia due to decreased potassium excretion, acidosis, catabolism, and excessive potassium intake from food and medications Metabolic acidosis from decreased acid secretion by the kidney and inability to regenerate bicarbonate Anemia secondary to decreased erythropoiesis (production of RBCs) Hypoalbuminemia with edema secondary to protein loss through the damaged glomerular membrane Increased serum phosphorus level due to decreased renal excretion of phosphorus Decreased serum calcium level (calcium binds to phosphorus to compensate for elevated serum phosphorus levels) Mental status changes Impaired nerve conduction due to electrolyte abnormalities and uremia Chest x-rays may show cardiac enlargement and pulmonary edema. The electrocardiogram (ECG) may be normal or may indicate left ventricular hypertrophy associated with hypertension and signs of electrolyte disturbances, such as tall, tented (or peaked) T waves associated with hyperkalemia. Computed tomography (CT) and magnetic resonance imaging (MRI) scans show a decrease in the size of the renal cortex. Medical Management Management of symptoms guides the treatment. If the patient has hypertension, efforts are made to reduce the blood pressure with sodium and water restriction, antihypertensive agents, or both. Weight is monitored daily, and diuretic medications are prescribed to treat fluid overload. Proteins of high biologic value (dairy products, eggs, meats) are provided to promote good nutritional status. Adequate calories are provided to spare protein for tissue growth and repair. Urinary tract infections (UTIs) must be treated promptly to prevent further kidney damage. Dialysis is initiated early in the course of the disease to keep the patient in optimal physical condition, prevent fluid and electrolyte imbalances, and minimize the risk of complications of kidney disease. The course of dialysis is smoother if treatment begins before the patient develops complications. Nursing Management Whether the patient is hospitalized or cared for in the home, the nurse observes the patient for common fluid and electrolyte disturbances in kidney disease (see Table 54-1). Changes in fluid and electrolyte status and in cardiac and neurologic status are reported promptly to the primary provider. Throughout the course of the disease and treatment, the nurse gives emotional support by providing opportunities for the patient and family to verbalize their concerns, have their questions answered, and explore their options (Ahmad & Al Nazly, 2015). Promoting Home, Community-Based, and Transitional Care Educating Patients About Self-Care The nurse has a major role in educating the patient and family about the prescribed treatment plan and the risks associated with noncompliance. Instructions to the patient include explanations and scheduling for follow-up evaluations: blood pressure, urinalysis for protein and casts, and laboratory studies of BUN and serum creatinine levels. If long-term dialysis is needed, the nurse educates the patient and family about the procedure, how to care for the access site, dietary restrictions, and other necessary lifestyle modifications. These topics are discussed later in this chapter. Periodic hospitalization, visits to the outpatient clinic or office, and home care referrals provide the nurse in each setting with the opportunity for careful assessment of the patient's progress and continued education about changes to report to the primary provider (worsening signs and symptoms of kidney disease, such as nausea, vomiting, and diminished urine output). Specific education may include explanations about recommended diet and fluid modifications and medications (purpose, desired effects, adverse effects, dosage, and administration schedule). Continuing and Transitional Care Periodic laboratory evaluations of creatinine clearance and BUN and serum creatinine levels are carried out to assess residual renal function and the need for dialysis or transplantation. If dialysis is initiated, the patient and family require considerable assistance and support in dealing with therapy and its long-term implications. The patient and family are reminded of the importance of participation in health promotion activities, including health screening. The patient is instructed to inform all health care providers about the diagnosis of glomerulonephritis so that all medical management, including pharmacologic therapy, is based on altered renal function. (Hinkle 1572-1573) Hinkle, Janice L., Kerry Cheever. Lippincott's CoursePoint for Hinkle & Cheever: Brunner & Suddarth's Textbook of Medical-Surgical Nursing, 14th Edition. CoursePoint, 10/2017. VitalBook file.

Chronic kidney disease

Chronic kidney disease is an umbrella term that describes kidney damage or a decrease in the glomerular filtration rate (GFR) lasting for 3 or more months. CKD is associated with decreased quality of life, increased health care expenditures, and premature death. Untreated CKD can result in end-stage kidney disease (ESKD), which is the final stage of CKD ESKD results in retention of uremic waste products and the need for renal replacement therapies, dialysis, or kidney transplantation. Risk factors include cardiovascular disease, diabetes, hypertension, and obesity. Recent research reported that 10% of the U.S. population aged 20 years and older has CKD (Centers for Disease Control and Prevention [CDC], 2014). Diabetes is the primary cause of CKD. More than 35% of the U.S. population aged 20 years and older with diabetes have CKD (CDC, 2014). Diabetes is the leading cause of kidney disease in patients starting renal replacement therapy. The second leading cause is hypertension, followed by glomerulonephritis and pyelonephritis; polycystic, hereditary, or congenital disorders; and renal cancers (U.S. Renal Data System [USRDS], 2015). More than 20% of the U.S. population aged 20 years and older with hypertension have CKD (CDC, 2014). Pathophysiology In the early stages of CKD, there can be significant damage to the kidneys without signs or symptoms. The pathophysiology of CKD is not yet clearly understood, but the damage to the kidneys is thought to be caused by prolonged acute inflammation that is not organ specific and thus has subtle systemic manifestations. Stages of Chronic Kidney Disease CKD has been classified into five stages by the National Kidney Foundation (NKF) (see Chart 54-1). Stage 5 results when the kidneys cannot remove the body's metabolic wastes or perform their regulatory functions; thus, renal replacement therapies are required to sustain life. Screening and early intervention are important, because not all patients progress to stage 5 CKD. Patients with CKD are at increased risk for cardiovascular disease, which is the leading cause of morbidity and mortality (Kane-Gill, Sileanu, Murugan, et al., 2015). Treatment of hypertension, anemia, and hyperglycemia and detection of proteinuria all help to slow disease progression and improve patient outcomes (Lewis, 2013). (Hinkle 1569) Hinkle, Janice L., Kerry Cheever. Lippincott's CoursePoint for Hinkle & Cheever: Brunner & Suddarth's Textbook of Medical-Surgical Nursing, 14th Edition. CoursePoint, 10/2017. VitalBook file. Clinical Manifestations Elevated serum creatinine levels indicate underlying kidney disease; as the creatinine level increases, symptoms of CKD begin. Anemia, due to decreased erythropoietin production by the kidney, metabolic acidosis, and abnormalities in calcium and phosphorus herald the development of CKD (Taal, 2013). Fluid retention, evidenced by both edema and congestive heart failure, develops. As the disease progresses, abnormalities in electrolytes occur, heart failure worsens, and hypertension becomes more difficult to control. Assessment and Diagnostic Findings The glomerular filtration rate (GFR) is the amount of plasma filtered through the glomeruli per unit of time. Creatinine clearance is a measure of the amount of creatinine the kidneys are able to clear in a 24-hour period. Normal values differ in men and women. Calculation of GFR, an important assessment parameter in CKD, is discussed in Chapter 53. Medical Management The management of patients with CKD includes treatment of the underlying causes. Regular clinical and laboratory assessment is important to keep the blood pressure below 130/80 mmHg (Klein-Kauric, 2015). Medical management also includes early referral for initiation of renal replacement therapies as indicated by the patient's renal status. Prevention of complications is accomplished by controlling cardiovascular risk factors; treating hyperglycemia; managing anemia; smoking cessation, weight loss, and exercise programs as needed; and reduction in salt and alcohol intake. Gerontologic Considerations Changes in kidney function with normal aging increase the susceptibility of older patients to kidney dysfunction and kidney disease (Kane-Gill et al., 2015). In addition, the incidence of systemic diseases, such as atherosclerosis, hypertension, heart failure, diabetes, and cancer, increases with advancing age, predisposing older adults to kidney disease associated with these disorders. Therefore, acute problems need to be prevented if possible or recognized and treated quickly to avoid kidney damage. Thus, nurses in all settings need to be alert to signs and symptoms of kidney dysfunction in older patients. Older patients frequently take multiple prescription and over-the-counter medications. Because alterations in renal blood flow, glomerular filtration, and renal clearance increase the risk of medication-associated changes in renal function, precautions are indicated with all medications. When older patients undergo extensive diagnostic tests or when new medications (e.g., diuretic agents) are added, precautions must be taken to prevent dehydration, which can compromise marginal renal function and lead to (Hinkle 1569-1570) Hinkle, Janice L., Kerry Cheever. Lippincott's CoursePoint for Hinkle & Cheever: Brunner & Suddarth's Textbook of Medical-Surgical Nursing, 14th Edition. CoursePoint, 10/2017. VitalBook file.

nephrosclerosis

Nephrosclerosis (hardening of the renal arteries) is most often due to prolonged hypertension and diabetes. Nephrosclerosis is a major cause of CKD and ESKD secondary to many disorders. Pathophysiology There are two forms of nephrosclerosis: malignant (accelerated) and benign. Malignant nephrosclerosis is often associated with significant hypertension (diastolic blood pressure higher than 130 mmHg). It usually occurs in young adults and twice as often in men compared to women (Klein-Kauric, 2015). Damage is caused by decreased blood flow to the kidney resulting in patchy necrosis of the renal parenchyma. Over time, fibrosis occurs and glomeruli are destroyed. The disease process progresses rapidly. Without dialysis, more than half of patients die of uremia (an excess of urea and other nitrogenous waste products in the blood) in a few years. Benign nephrosclerosis can be found in older adults, associated with atherosclerosis and hypertension. Assessment and Diagnostic Findings Symptoms are rare early in the disease, even though the urine usually contains protein and occasional casts. Renal insufficiency and associated signs and symptoms occur late in the disease. Medical Management Treatment of nephrosclerosis is aggressive antihypertensive therapy. An angiotensin-converting enzyme (ACE) inhibitor, alone or in combination with other antihypertensive medications, significantly reduces its incidence. See Chapter 31 for additional information on hypertension. (Hinkle 1570) Hinkle, Janice L., Kerry Cheever. Lippincott's CoursePoint for Hinkle & Cheever: Brunner & Suddarth's Textbook of Medical-Surgical Nursing, 14th Edition. CoursePoint, 10/2017. VitalBook file.

polycistic kidney disease

Pathophysiology Polycystic kidney disease (PKD) is a genetic disorder characterized by the growth of numerous fluid-filled cysts in the kidneys, which destroy the nephrons. PKD cysts can profoundly enlarge the kidneys while replacing much of the normal structure, resulting in reduced kidney function and leading to kidney failure. PKD can also cause cysts in the liver and problems in other areas, such as blood vessels in the brain and heart. The number of cysts and the resulting complications help distinguish PKD from the usually harmless cysts that can form in the kidneys in later years of life. In the United States, PKD and cystic diseases are a leading cause of kidney failure. Two major inherited forms of PKD exist: Autosomal dominant PKD is the most common inherited form. Symptoms usually develop between 30 and 40 years of age, but they can begin earlier, even in childhood. About 90% of all PKD cases are autosomal dominant PKD. Autosomal recessive PKD is a rare inherited form. Symptoms of autosomal recessive PKD begin in the earliest months of life or in utero. When autosomal dominant PKD causes kidneys to fail, which usually happens after many years, the patient requires dialysis or kidney transplantation. Approximately one half of individuals with autosomal dominant PKD progress to stage 5 CKD, requiring renal replacement therapy. Clinical Manifestations Signs and symptoms of PKD result from loss of renal function and the increasing size of the kidneys as the cysts grow. Kidney damage can result in hematuria, polyuria (excessive urine production), hypertension, development of renal calculi and associated UTIs, and proteinuria. The growing cysts are noted with reports of abdominal fullness and flank pain (back and lower sides). Assessment and Diagnostic Findings PKD is a genetic disease; therefore, careful evaluation of family history is necessary. Palpation of the abdomen will often reveal enlarged cystic kidneys. Ultrasound imaging of the kidneys is the preferred technique for diagnosis (Grossman & Porth, 2014). Medical Management PKD has no cure, and treatment is largely supportive and includes blood pressure control, pain control, and antibiotic agents to resolve infections. Once the kidneys fail, renal replacement therapy is indicated (see later discussion in chapter). Genetic linkage studies and counseling may be indicated, particularly when screening family members for potential kidney donation (Grossman & Porth, 2014). (Hinkle 1574) Hinkle, Janice L., Kerry Cheever. Lippincott's CoursePoint for Hinkle & Cheever: Brunner & Suddarth's Textbook of Medical-Surgical Nursing, 14th Edition. CoursePoint, 10/2017. VitalBook file.

Fluid and electrolyte disorders

Patients with kidney disorders commonly experience fluid and electrolyte imbalances and require careful assessment and close monitoring for signs of potential problems. The patient whose fluid intake exceeds the ability of the kidneys to excrete fluid is said to have fluid overload. If fluid intake is inadequate, the patient is said to be volume depleted and may show signs and symptoms of fluid volume deficit. The intake and output (I&O) record, a key monitoring tool, is used to document important fluid parameters, including the amount of fluid taken in (orally or parenterally), the volume of urine excreted, and other fluid losses (diarrhea, vomiting, diaphoresis). Patient weight is also important, and documenting trends in weight is a key assessment strategy essential for determining the daily fluid allowance and indicating signs of fluid volume excess or deficit. Quality and Safety Nursing Alert The most accurate indicator of fluid loss or gain in patients who are acutely ill is weight. An accurate daily weight must be obtained and recorded. A 1-kg weight gain is equal to 1000 mL of retained fluid. Clinical Manifestations The signs and symptoms of common fluid and electrolyte disturbances that can occur in patients with kidney disorders and general management strategies are listed in Table 54-1. The nurse continually assesses, monitors, and informs appropriate members of the health care team if the patient exhibits any of these signs. Management strategies for fluid and electrolyte disturbances in kidney disease are discussed in greater depth later in this chapter (see Chapter 13). (Hinkle 1568-1569) Hinkle, Janice L., Kerry Cheever. Lippincott's CoursePoint for Hinkle & Cheever: Brunner & Suddarth's Textbook of Medical-Surgical Nursing, 14th Edition. CoursePoint, 10/2017. VitalBook file. Gerontologic Considerations With aging, the kidney is less able to respond to acute fluid and electrolyte changes. Older adult patients may develop atypical and nonspecific signs and symptoms of altered renal function and fluid and electrolyte imbalances. A fluid balance deficit in older adults can lead to constipation, falls, medication toxicity, urinary tract and respiratory tract infections, delirium, seizures, electrolyte imbalances, hyperthermia, and delayed wound healing. Recognition of acute changes in fluid and electrolytes is further hampered by their association with pre-existing disorders and the misconception that they are normal changes of aging. (Hinkle 1569) Hinkle, Janice L., Kerry Cheever. Lippincott's CoursePoint for Hinkle & Cheever: Brunner & Suddarth's Textbook of Medical-Surgical Nursing, 14th Edition. CoursePoint, 10/2017. VitalBook file.

Kidney transplantation.

Read in book

renal replacement therapy

Read the chapter on this

Renal cancer

Renal cancer accounts for about 5% of all cancers in the United States (American Cancer Society [ACS], 2015), where the incidence of renal cancer at all stages has increased in the past two decades. The incidence of renal cell carcinoma is higher in both men and women with an increased body mass index. Tobacco use continues to be a significant risk factor (see Chart 54-3). American Indians and Alaskans have a higher mortality rate from renal carcinoma compared to other races and population groups. The most common type of renal carcinoma arises from the renal epithelium and accounts for more than 85% of all kidney tumors (ACS, 2015). These tumors may metastasize early to the lungs, bone, liver, brain, and contralateral kidney. One quarter of patients have metastatic disease at the time of diagnosis. Although enhanced imaging techniques account for improved detection of early-stage kidney cancer, it is unknown why the rate of late-stage kidney cancers is high. p. 1574 p. 1575 Chart 54-3 RISK FACTORS Renal Cancer Gender—affects men more than women Obesity Occupational exposure to industrial chemicals, such as petroleum products, heavy metals, and asbestos Polycystic kidney disease Tobacco use Unopposed estrogen therapy Adapted from American Cancer Society (2015). Kidney cancer. Retrieved on 1/10/2015 at: www.cancer.org/cancer/kidneycancer/detailedguide/kidney-cancer-adult-key-statistics Clinical Manifestations Many renal tumors produce no symptoms and are discovered on a routine physical examination as a palpable abdominal mass. Signs and symptoms, which occur in only 10% of patients, include hematuria, pain, and a mass in the flank. The usual sign that first calls attention to the tumor is painless hematuria, which may be either intermittent and microscopic or continuous and gross. There may be a dull pain in the back from the pressure produced by compression of the ureter, extension of the tumor into the perirenal area, or hemorrhage into the kidney tissue. Colicky pains occur if a clot or mass of tumor cells passes down the ureter. Symptoms from metastasis may be the first manifestations of renal tumor and may include unexplained weight loss, increasing weakness, and anemia. Assessment and Diagnostic Findings The diagnosis of a renal tumor may require intravenous (IV) urography, cystoscopic examination, renal angiograms, ultrasonography, or a CT scan (see Chapter 53). These tests may be exhausting for patients already debilitated by the systemic effects of a tumor as well as for older patients and those who are anxious about the diagnosis and outcome. The nurse assists the patient to prepare physically and psychologically for these procedures and monitors carefully for signs and symptoms of dehydration and exhaustion. Medical Management The goal of medical management is to detect the tumor early and to eradicate slow-growing tumors before metastasis occurs. Treatment most often includes a combination of surgery and pharmacologic management. Radiation therapy may be used for palliation in patients who are not candidates for surgery or other treatments. Surgical Management Nephrectomy A radical nephrectomy is the preferred treatment if the tumor can be removed. This includes removal of the kidney (and tumor), adrenal gland, surrounding perinephric fat and Gerota fascia, and lymph nodes. Laparoscopic nephrectomy can be performed for removal of the kidney with a small tumor. This procedure incurs less morbidity and a shorter recovery time. Radiation therapy, hormonal therapy, or chemotherapy may be used along with surgery. Immunotherapy may also be helpful. For patients with bilateral tumors or cancer of a functional single kidney, nephron-sparing surgery (partial nephrectomy) may be considered. Favorable results have been achieved in patients with small local tumors and a normal contralateral kidney. Nephron-sparing surgery is increasingly being used to treat patients with solid renal lesions. The technical success rate of nephron-sparing surgery is excellent, and operative morbidity and mortality are low. Patients with upper tract transitional cell carcinoma may benefit from laparoscopic nephroureterectomy. Although it is a lengthier surgical procedure, it has the same efficacy and is better tolerated by patients than open nephroureterectomy. Renal Artery Embolization In patients with metastatic renal carcinoma, the renal artery may be occluded to impede the blood supply to the tumor and thus kill the tumor cells. After angiographic studies are completed, a catheter is advanced into the renal artery, and embolizing materials (e.g., Gelfoam, autologous blood clot, steel coils) are injected into the artery and carried with the arterial blood flow to occlude the tumor vessels mechanically. This decreases the local blood supply, making removal of the kidney (nephrectomy) easier. It also stimulates an immune response because infarction of the renal cell carcinoma releases tumor-associated antigens that enhance the patient's response to metastatic lesions. The procedure may also reduce the number of tumor cells entering the venous circulation during surgical manipulation. After renal artery embolization and tumor infarction, a characteristic symptom complex called postinfarction syndrome occurs, lasting 2 to 3 days. The patient has pain localized to the flank and abdomen, elevated temperature, and gastrointestinal (GI) symptoms. Pain is treated with parenteral analgesic agents, and acetaminophen (Tylenol) is given to control fever. Antiemetic medications, restriction of oral intake, and IV fluids are used to treat the GI symptoms. Pharmacologic Therapy Depending on the stage of the tumor, percutaneous partial or radical nephrectomy may be followed by treatment with chemotherapeutic agents. Treatment with biologic response modifiers such as interleukin 2 (IL-2) is effective. IL-2, a protein that regulates cell growth, is used alone or in combination with lymphokine-activated killer cells (WBCs that have been stimulated by IL-2 to increase their ability to kill cancer cells). Interferon, another biologic response modifier, appears to have a direct antiproliferative effect on renal tumors. Another promising experimental approach to renal cell carcinoma is a vaccination to stimulate immune response, with autologous tumor cells with IL-2-, granulocyte-macrophage stimulating factor-, and dendritic cell-type vaccines. If patients with renal cancer do not respond to immunotherapy, allogeneic stem cell transplantation may be indicated (see Chapter 15). Nursing Management The patient with a renal tumor usually undergoes extensive diagnostic and therapeutic procedures. Treatment includes surgery, radiation therapy, and medications. After surgery, the patient usually has catheters and drains in place to maintain a patent urinary tract, to remove drainage, and to permit accurate measurement of urine output. Because of the location of the surgical incision, the patient's position during surgery, and the nature of the surgical procedure, pain and muscle soreness are common. Pharmacologic management often includes immunosuppressant agents; therefore, patients are monitored for infection. The patient requires frequent analgesia during the postoperative period and assistance with turning, coughing, the use of incentive spirometry, and deep breathing to prevent atelectasis and other pulmonary complications. The patient and family require assistance and support to cope with the diagnosis and uncertain prognosis. See discussion later in this chapter of postoperative care of the patient undergoing kidney surgery and Chapter 15 for discussion of care of the patient with cancer. Promoting Home, Community-Based, and Transitional Care Educating Patients About Self-Care The nurse educates the patient about how to inspect and care for the incision and to perform other general postoperative care including activity and lifting restrictions, driving, and pain management. Instructions are provided about when to notify the primary provider about problems (e.g., fever, respiratory difficulty, wound drainage, blood in the urine, pain or swelling of the legs). The nurse encourages the patient to eat a healthy diet and to drink adequate liquids to avoid constipation and to maintain an adequate urine volume. Education and emotional support are provided related to the diagnosis, treatment, and continuing care because many patients are concerned about the loss of the other kidney, the possible need for dialysis, or the recurrence of cancer. Continuing and Transitional Care Follow-up care is essential to detect signs of metastases and to reassure the patient and family about the patient's status and well-being. The patient who has had surgery for renal carcinoma should have a yearly physical examination and chest x-ray, because late metastases are not uncommon. All subsequent symptoms should be evaluated with possible metastases in mind. If follow-up chemotherapy is necessary, the patient and family are informed about the treatment plan or chemotherapy protocol, what to expect with each visit, and when to notify the primary provider. Evaluation of remaining renal function (creatinine clearance, BUN, and serum creatinine levels) may also be carried out periodically. A home care nurse may monitor the patient's physical status and psychological well-being and coordinate other indicated services and resources. (Hinkle 1574-1576) Hinkle, Janice L., Kerry Cheever. Lippincott's CoursePoint for Hinkle & Cheever: Brunner & Suddarth's Textbook of Medical-Surgical Nursing, 14th Edition. CoursePoint, 10/2017. VitalBook file.