Patients w/ renal Disorders (chapter. 27)
CLASSIFICATIONS OF AKI Postrenal: result of obstructed outflow of urine This may result from ureteral blockage, such as from bilateral renal calculi, benign prostatic hyperplasia (BPH), strictures, tumors, or congenital defects (Dirkes, 2015). Any sudden or complete cessation of urine output with an indwelling catheter should alert the nurse to possible obstruction. The catheter should be inspected and kinks removed or the catheter irrigated or changed to reestablish urine flow.
FOUR CLINICAL PHASES OF ARF: Initiation or onset, oliguric (FVE), diuretic (FVD), and recovery The onset phase begins with the triggering event and ends when cellular injury and oliguria develop. Common events include significant fluid or blood loss, burns, or diabetes insipidus (Dirkes, 2015). A small number of patients develop nonoliguric renal failure, usually associated with nephrotoxic agents; it may also occur with burns, traumatic injury, and the use of halogenated anesthetic agents.
CHRONIC GLOMERULONEPRHITIS MANIFESTATIONS As kidney failure progresses and the GFR falls, 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 and reabsorb 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 its decreased renal excretion Decreased serum calcium level (calcium and phosphorus exist in an inverse ratio in the body) and decreased vitamin D activation Mental status changes due to buildup of nitrogenous wastes Impaired nerve conduction due to electrolyte abnormalities and uremia
DIAGNOSTICS Chest x-rays may show cardiac enlargement and pulmonary edema. The electrocardiogram (ECG) may be normal or may indicate left ventricular hypertrophy (LVH) associated with hypertension. Signs of electrolyte disturbances, such as tall, tented T waves associated with hyperkalemia or dysrhythmia may appear. Computed tomography (CT) and magnetic resonance imaging (MRI) scans reveal a decrease in the size of the renal cortex.
Preventing Acute Kidney Injury; HEALTH PROMOTION Provide adequate hydration to patients at risk of dehydration: Perioperative patients Patients on fluid restriction Patients undergoing diagnostic studies with or requiring contrast agents (e.g., barium enema, intravenous pyelograms, angiography), especially elderly patients who may have marginal renal reserve Patients with neoplastic disorders and those receiving chemotherapy Patients with metabolic disorders, such as gout, glycosuria Prevent and treat hypotension or shock promptly with blood and fluid replacement
Preventing Acute Kidney Injury; HEALTH PROMOTION Monitor hourly urine output of patients who are critically ill to detect the onset of kidney failure as early as possible. When available, monitor central venous and arterial pressures Continually assess renal laboratory values Properly identify patients to prevent transfusion reactions, which can precipitate myoglobinuria Prevent and treat infections promptly. Infections can lead to sepsis and renal damage Intervene promptly with wounds, burns, and other precursors of sepsis To prevent infections from ascending in the urinary tract, give meticulous care to patients with indwelling catheters. Remove catheters as soon as possible To prevent toxic drug effects, closely monitor dosage, duration of use, and blood levels of all medications metabolized or excreted by the kidneys
ACUTE GLOMERULONEPHRITIS MANIFESTATIONS varying degrees of severity, kidneys become large, edematous and congested; hematuria microscopic or macroscopic (visible to the eye), proteinuria (over 3 to 5 g/day) with hypoalbuminemia, RBC casts (may indicate kidney bleeding), azotemia (excessive nitrogenous wastes in blood), edema and hypertension The urine with myoglobin (myoglobinuria) is dark and may be described as brown in color. Cola-colored or coffee colored urine develops when the released myoglobin from skeletal muscle is quickly cleared from the serum into the urine. Glomerulonephritis may be mild, and the hematuria may be discovered incidentally through a routine microscopic urinalysis, or the disease may be severe, with AKI, oliguria (less than 400 mL), and shortness of breath.
ACUTE GLOMERULONEPHRITIS MANIFESTATIONS Assessing for pharyngitis, impetigo, or a heart murmur (endocarditis) edema and hypertension is present in most patients. BUN and serum creatinine levels may increase as urine output decreases. In addition, anemia may be present. headache, malaise, and flank pain (pain on sides below ribs and above the pelvis). Elderly patients may experience circulatory overload with dyspnea, engorged neck veins, cardiomegaly, and pulmonary edema. Atypical symptoms include confusion, somnolence, and seizures, which often are confused with the symptoms of a primary neurologic disorder.
ACUTE GLOMERULONEPHRITIS: Inflammation of the glomerular capillaries. CHRONIC GLOMERULONEPHRITIS Repeated episodes of glomerular injury that result in renal destruction, decreased size, scarring and fibrous tissue. NEPHROTIC SYNDROME Intrinsic renal or systemic disease that affects the glomerulus causing structural changes.
ACUTE GLOMERULONEPHRITIS: In acute glomerulonephritis, the kidneys become large, edematous, and congested. Box 27-2 depicts the pathophysiology of glomerulonephritis. Acute GN may occur after infections of the pharynx or skin (i.e., impetigo) caused by certain strains of group A beta-hemolytic streptococcal infections; this is referred to as PSGN. Systemic lupus erythematosus (SLE), vascular injury, disseminated intravascular coagulation (DIC), or diabetes may be additional causes
Gerontologic Considerations [box 27-1] Kidney Dysfunction Because alterations in renal perfusion, glomerular filtration, and renal clearance increase the risk for medication-associated changes in renal function or toxicities, precautions and surveillance are warranted. When elderly patients undergo diagnostic testing 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 kidney failure. With aging, the kidney is less able to respond to acute fluid and electrolyte changes. Elderly patients may develop atypical and nonspecific signs and symptoms of disturbed renal function as well as fluid and electrolyte imbalances. Recognition of these problems is hampered further by their association with pre-existing disorders and the misconception that they are normal changes of aging
ACUTE GLOMERULONEPHRITIS: RISK FACTORS include a family history of glomerulonephritis; a pre-existing history of known diseases, such as a streptococcal infection (27.9%) of the upper respiratory tract; other infections with organisms (Parmar & Batuman, 2015) and viral infectious diseases, such as hepatitis, mumps, and varicella zoster. Additionally, other diseases, such as Goodpasture syndrome, Wegener granulomatosis, SLE, subacute bacterial endocarditis, and sepsis, have been implicated as risk factors.
COMPLICATIONS infection, atherosclerosis, VTE, PE myeloma, and renal vein thrombosis may be seen. Body image may be altered due to anasarca and edema, causing a change in appearance.
ACUTE RENAL FAILURE ; PATHO reversible; abrupt loss of kidney function and GFR over a period of hours to days. ; Reversible if treated before permanent renal impairment, causes (etiology) Box 27-3 major risk factor for the development of chronic kidney disease (CKD).
MANIFESTATIONS [table 27-2] critically ill and lethargic oliguria (less than 400 mlc day) anuria with resulting azotemia (increased serum creatinine, phosphate BUN, and other nitrogenous waste products). Hematuria Patients with AKI have decreased urine sodium levels and urinary casts, and other cellular debris may be present. dyspnea, crackles, tachycardia, hypertension, and distended neck veins, as well as generalized edema Acidemia, fluid volume excess, alterations in calcium and phosphorus balance and BP alterations develop rapidly. Erythropoiesis fails with resulting anemia. Nausea, vomiting, lethargy, headache, muscle twitching, and seizures may occur. oliguria and anuria (less than 50 mL/day) are at high risk for hyperkalemia
ASSESSMENT AKI The ECG may reveal changes, including tall, tented, or peaked T waves, absent P wave, widened QRS, or bradydysrhythmia. The nurse should be aware of exogenous sources of potassium, such as IV infusions, or medications, such as potassium penicillin, as well as dietary sources (avocado, brussels sprouts, okra, spinach (green leafy vegetables), potatoes, pumpkin, spinach, sweet potatoes, tomatoes, yams, apricots, bananas, nectarines, orange juice, prune juice
CHRONIC GLOMERULONEPRHITIS MANIFESTATIONS As chronic glomerulonephritis progresses, signs and symptoms of chronic kidney failure may develop. patient appears poorly nourished, with a yellow-gray pigmentation of the skin due to uremia. Periorbital and peripheral (dependent) edema with a normal or severely elevated BP may be noted. Mucous membranes are pale due to anemia. Cardiomegaly, a gallop rhythm, distended neck veins, and other signs and symptoms of heart failure may be present. Crackles can be heard in the lungs.
CHRONIC GLOMERULONEPRHITIS MANIFESTATIONS 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 or without a pericardial friction rub A number of laboratory abnormalities occur. Urinalysis reveals a fixed specific gravity of about 1.010, variable proteinuria, and urinary casts, which are proteins secreted by damaged kidney tubules.
CHRONIC GLOMERULONEPHRITIS proteinuria, usually caused by repeated episodes of glomerular injury that results in renal destruction. The kidneys are reduced to as little as one fifth their normal size, consisting largely of fibrous tissue. The glomeruli and their tubules become scarred, and the branches of the renal artery are thickened. RISK FACTORS Acute glomerulonephritis, diabetes, hypertensive nephrosclerosis (sclerosis [hardening] of the small blood vessels in the kidneys), hyperlipidemia, chronic tubulointerstitial injury, or hemodynamically mediated glomerular sclerosis.
CHRONIC GLOMERULONEPRHITIS MANIFESTATIONS The first indication of disease may be a sudden, severe nosebleed, a stroke, or a seizure proteinuria, HTN, vascular changes (routine eye examination when vascular changes or retinal hemorrhages), epistaxis, CVA, seizure, headaches, dizziness and digestive disturbances, nocturia wt loss, irritability oliguria, shortness of breath, weakness, and periorbital and generalized edema (anasarca) slightly swollen (edematous) at night elevated BUN and serum creatinine level Most patients also have general symptoms, such as loss of weight and strength, increasing irritability, and an increased need to urinate at night (nocturia).
CLASSIFICATIONS OF AKI Prerenal: caused by reduced blood flow to the kidney, hypoperfusion clinical situations are volume-depletion states, which include dehydration; hemorrhage or gastrointestinal (GI) losses; decreased cardiac output such as occurs with myocardial infarction, heart failure, or cardiogenic shock; and vasodilated states, such as sepsis or anaphylaxis. mean arterial pressure (MAP) must be 65 mm Hg For patients with a history of hypertension and/or renal vascular diseases, higher pressures may be required to maintain renal perfusion.
CLASSIFICATIONS OF AKI Intrarenal: result of parenchymal damage to nephron or kidney tubules, acute tubular necrosis (ATN) ATN is the most common cause of intrarenal AKI in the patient who is hospitalized. In the early period of renal ischemia, kidney function can be restored completely by improving renal blood flow, typically with IV fluids. If left untreated or when fluid resuscitation is inadequate, ATN will ensue Conditions such as burns, crush injuries, infections, and severe blood transfusion reactions can lead to rhabdomyolysis with myoglobinuria With burns and crush injuries, myoglobin (a protein released from muscle when injury occurs) and hemoglobin are liberated, causing obstruction of renal tubules, renal toxicity, and ischemia. The term rhabdomyolysis, in which breakdown of skeletal muscle is seen, may be used to describe this event.
INTEVERVENTIONS/ PT EDUCATION Fluid restrictions and daily weights Diet restrictions Medication administration Symptoms of renal failure: N,V and decreased U/O Follow-up evaluations for disease progression of BP, urinalysis for protein, and serum BUN and serum creatinine levels The patient is instructed to notify the primary care provider (PCP) if symptoms of kidney failure occur, including fatigue, nausea, vomiting, diminishing urine output, or at the first sign of any infection. Information for patient education should be given verbally and in writing. Nursing Alert Azotemia refers to the accumulation of nitrogen-combining compounds (BUN, creatinine) in the blood. It usually occurs before symptoms are noted. Uremia describes the clinical manifestations of kidney failure (altered fluid, electrolyte, acid-base balance; impaired body function [hypertension, anemia, pruritus, osteodystrophy, etc.]).
COMPLICATIONS hypertensive encephalopathy, pulmonary edema, HF and ESRD Crescent-shaped cells accumulate in Bowman space (the filter within the glomerulus), disrupting the filtering process. 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.
FOUR CLINICAL PHASES OF ARF: The oliguric period is accompanied by fluid overload and an increase in the serum concentration of wastes, such as urea, creatinine, organic acids, and the electrolytes potassium, phosphorous, and magnesium. The average time period for oliguria is 8 to 14 days, but it may last longer (Dirkes, 2015). Because the minimum amount of urine needed to rid the body of fluid and metabolic waste products is 500 mL in 24 hours (Hall, 2016), renal replacement therapy (RRT), such as dialysis, may be needed until kidney function returns. The diuretic phase occurs when the cause of acute renal failure (ARF) is corrected. This phase is marked by a gradual increase in urine output, which signals that glomerular filtration has started to recover.
FOUR CLINICAL PHASES OF ARF: Urine output may be normal, or the patient may excrete large amounts of dilute urine along with electrolytes. The patient should be observed closely for dehydration, which may damage the kidney further, as well as for hypokalemia (Dirkes, 2015). Abnormal laboratory values plateau and begin to decline. The recovery period is signaled by the improvement of kidney function and energy level and may take 6 to 12 months (Grossman & Porth, 2014). If residual damage to the glomerular basement membrane occurs, residual renal impairment may result.
PROVIDING SUPPORT The nurse provides frequent explanations of the purpose and rationale of the treatments, as rising BUN leads to confusion and lethargy. Both the patient and family are included in teaching to allay anxiety and fear. The nurse explains the importance of follow-up with a nephrologist Nursing Alert Muscle mass and GFR can decrease with age; therefore, even small elevations in creatinine may indicate significant renal impairment in the elderly and should be investigated.
GERONTOLOGIC CONSIDERATIONS increased in older patients who are hospitalized due to a decrease in the number of functional nephrons and renal blood flow as well as to atherosclerosis of the renal arteries. diabetes, hypertension, and heart disease Diuretics and NSAIDs increase the risk of AKI threefold, as do ACE inhibitors Nurses need to be aware of the risk of AKI in elderly patients, especially those undergoing diagnostic testing or procedures that can result in dehydration. Suppression of thirst, decreased mobility with lack of access to drinking water, and confusion contribute to the older patient's failure to consume adequate fluids, which may lead to dehydration and further compromise of kidney function.
ACUTE GLOMERULONEPHRITIS: An immune-mediated antigen-antibody reaction and inflammation causes insoluble immune complexes to become trapped in the glomeruli, causing protein and RBCs to enter the urine. Sudden onset of hematuria, proteinuria, and RBC casts in the urine define the disease and cause the smoky or coffee-colored urine typically seen in acute GN. Often this clinical picture is accompanied by hypertension, edema, azotemia (i.e., decreased glomerular filtration rate [GFR], rising blood urea nitrogen [BUN], and creatinine), and retention of renal salt and water.
Gerontologic Considerations [box 27-1] Kidney Dysfunction Ageing increase susceptibility of elderly patients to kidney dysfunction and kidney failure. 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, and nurses in all settings need to be alert for signs and symptoms of renal dysfunction in elderly patients.
PREVENTION Radiocontrast-induced nephropathy is a major cause of hospital-acquired AKI; therefore, those at risk should be identified prior to procedures where contrast media is used creatinine levels greater than 2 mg/dL should receive preprocedure hydration and receive as low a dose of contrast as possible for the study N-acetylcysteine given before and after contrast administration appears to decrease the incidence of contrast nephropath Withhold Metformin prior to procedures requiring IV contrast. While metformin is not nephrotoxic, if AKI occurs after a procedure, the acidosis associated with kidney failure may worsen in the presence of this medication. Promising diagnostic biomarkers allow early detection of AKI.
MEDICAL & NURSING MANAGEMENT Maintaining fluid and electrolyte balance, avoiding fluid excesses, and supporting the patient until repair of renal tissue and restoration of function occur. Dialysis may be used on a temporary basis to restore homeostasis. The underlying cause is identified, treated, and eliminated when possible.
DIAGNOSTIC Cultures of throat and skin lesions to rule out Streptococcus species may be obtained. Renal Biopsy If the patient improves, the amount of urine increases and the urinary protein and sediment diminish. Some patients develop severe uremia within weeks and require dialysis for survival. Others, after a period of apparent recovery, insidiously develop chronic glomerulonephritis. MEDICAL&NURSING MANAGEMENT Management: fluid and diet (protein and sodium) restrictions antihypertensives/ Diuretics= control hypertension antibiotics if indicated and corticosteroids. Carbohydrates are given liberally to provide energy and reduce the catabolism of protein.
MEDICAL&NURSING MANAGEMENT treating symptoms, attempting to preserve kidney function, and treating complications promptly. When there is no evidence of malnutrition, nitrogen retention (elevated BUN) develop. Bed rest, I/O, Insensible fluid loss of approximately 1 L (lungs and skin) is considered when estimating fluid loss. Diuresis usually begins about 1 week after the onset of symptoms, with a decrease in edema and BP. recovery= takes about 2 weeks. A weight gain of 1 kg is equal to 1,000 mL of retained fluid
MEDICAL AND NURSING MANAGEMENT Treated with medication and modified dietary regimen Reduction in dietary cholesterol and saturated fats helps with lipidemia. Protein intake should be moderate, sufficient to meet protein needs while avoiding excessive intake, which may accelerate renal deterioration and increase urinary protein losses. An intake of 0.7 to 0.8 g/kg/day is suggested with at least half of the protein from high biologic value (HBV) sources, such as meat, fish, poultry, milk, eggs, and soy untreated streptococcal infection may be a risk factor for acute poststreptococcal glomerulonephritis; pathogens in the bloodstream may lead to sepsis with resulting decreased renal perfusion. Diuretics may be prescribed for the patient with severe edema; however, caution must be used because of the risk of reducing the plasma volume to the point of impaired circulation with subsequent prerenal AKI (discussed later in the chapter).
MEDICATIONS angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blocking agents, in combination with diuretics, often reduces the degree of proteinuria corticosteroids, antineoplastic agents (cyclophosphamide [Cytoxan]) or immunosuppressant medications (azathioprine [Imuran], chlorambucil [Leukeran], or cyclosporine [Neoral]). It may be necessary to repeat treatment with corticosteroids if relapse occurs. Patients should be taught to protect themselves from infection and to report any infections promptly due to immunosuppression.
MEDICAL&NURSING MANAGEMENT Assessment priorities include fluid and electrolyte status, cardiac status, and neurologic status. Table 27-1: common fluid and electrolyte disturbances Often anxiety levels are extremely high for both the patient and family. 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 for treatment if the kidneys fail. Specific teaching includes explanations about recommended diet and fluid modifications and medications (purpose, desired effects, adverse effects, dosage, and administration schedule). Major complication is chronic renal failure or end-stage renal disease (ESRD)
NEPHROTIC SYNDROME A cluster of clinical findings that can occur with almost any intrinsic renal disease or systemic disease that affects the glomerulus PATHOPHSYIOLOGY results from damage to the glomerular capillary membrane, increasing capillary permeability, which allows protein to leak out into the urine (proteinuria). The patient may lose as much as 40 g of urinary protein per day, of which 80% is albumin.
NEPHROTIC SYNDROME MANIFESTATIONS Proteinuria, Hypoalbuminemia, hyperlipidemia (results from an increase in hepatic synthesis of lipoproteins and decreased catabolism of circulating lipoproteins) edema (Results from the loss of plasma proteins, primarily in the form of albumin into the urine, resulting in serum hypoalbuminemia.) >> periorbital edema, scrotal swelling, abdominal distention, weight gain, or anasarca. hypoimmunoglobulinemia, HTN, headache, malaise, irritability, fatigue, anorexia , s.o.b, pulmonary. edema. albuminuria >3.5 g/day >>>edema The patient becomes vulnerable to infection and may develop thrombolytic complication related to decreased albumin and loss of antithrombin Figure 27-1 depicts the pathophysiology of nephrotic syndrome.
NEPHROTIC SYNDROME MANIFESTATIONS Urine may contain increased white blood cells (WBCs) as well as granular and epithelial casts. The presence of hypoimmunoglobulinemia places the patient at risk for infections. Hyperlipidemia with increased high-density lipoproteins (HDL) occurs and places the patient at risk for cardiovascular disease. A needle biopsy of the kidney may be performed for histologic examination of renal tissue to confirm the diagnosis.
DIAGNOSTICS FOR NEPHROTIC SYNDROME Urinalysis, blood chemistries including albumin and lipid levels, complete blood count (CBC), coagulation studies, renal function tests, blood glucose to exclude a diagnosis of diabetes, or renal ultrasound to evaluation for structural abnormalities
NEPHROTIC SYNDROME RISK FACTORS Diabetic nephropathy is most common SLE, infections/chronic glomerulonephritis, cancers, preeclampsia, drug addiction, and nephrotoxic drugs. Occasionally, amyloidosis of the kidney, multiple Treated with medication and modified dietary regimen
NUTRITIONAL THERAPY Dietary proteins are restricted and caloric requirements are met with high-carbohydrate meals due to their protein-sparing effect. Dietary restrictions include foods and fluids containing potassium, such as bananas, citrus, tomatoes, or melons. Foods containing phosphorus, including dairy products, beans, nuts, legumes, and carbonated beverages, are restricted as well. Caffeine also is restricted. The patient may require enteral or parenteral nutrition. Suspect fluid retention if the patient develops hypertension, crackles, edema, or weight gain
NUTRITIONAL THERAPY The nurse monitors for complications, participates in emergency treatment of imbalances of fluids and electrolytes, assesses the patient's progress and response to treatment, and provides physical and emotional support. Additionally, the nurse keeps family members informed about the patient's condition, helps them understand the treatments, and provides psychological support. AKI is a serious problem, and the nurse must continue to provide interventions for the underlying disorder (e.g., burns, shock, trauma, obstruction of the urinary tract, etc.).
PREVENTION [box 27-4] Assess changes in diagnostics and laboratory tests: BUN, creatinine, GFR, potassium, phosphate, calcium, metabolic acidosis and anemia Urine output (oliguria), N/V, lethargy, headache, muscle twitching, seizures The nurse assesses for use of potentially nephrotoxic agents and exposure to environmental toxins. Patients taking nephrotoxic medications, such asaminoglycosides (gentamicin, tobramycin, neomycin), amphotericin B, vancomycin, cyclosporine, certain antineoplastics or anesthetics, heavy metals such as cisplatin or bismuth, or radiologic contrast agents, should be monitored closely for changes in kidney function. BUN and serum creatinine levels should be obtained at baseline, during treatment, and after therapy is complete, if indicated.
PREVENTION Chronic use of analgesics, particularly 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 failure. Increased age, pre-existing kidney disease, and the coadministration of nephrotoxic agents increase the risk for kidney damage.
REDUCING 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. Fever increases the insensible water loss by increasing water vapor in the lungs and allowing more water to be lost from the respiratory mucosa
PROMOTING PULMONAAY FUNCTION Attention is given to pulmonary function, and the patient is assisted to turn, cough, and deep breathe frequently to prevent atelectasis and respiratory tract infection. Drowsiness and lethargy may prevent the patient from moving and turning without encouragement and assistance. Maintaining a patent airway through oral or endotracheal suction may be necessary.
PREVENTING INFECTION Asepsis is essential with invasive lines and catheters to minimize the risk of infection and subsequent increased metabolism. Uremia impairs host defenses, particularly leukocyte function, and infection is a significant cause of morbidity and mortality in patients with AKI (Wolfson, 2014, p. 1301). Any fever warrants an assessment and notification of the provider. Sepsis disrupts blood flow, causing cell ischemia and death (Dirkes, 2015). An indwelling urinary catheter is avoided whenever possible because of the high risk of urinary tract infection (UTI) associated with its use.
PROVIDING SKIN CARE The skin may be dry or susceptible to breakdown as a result of edema; therefore, meticulous skin care is important. Additionally, excoriation and itching of the skin may result from the deposit of uremic toxins in the patient's tissues. Turning the patient frequently, bathing the patient with cool water, and keeping the patient's skin clean and well moisturized and the fingernails trimmed to avoid excoriation are comforting and prevent skin breakdown. Nursing Alert The nurse recognizes that edematous tissue is fragile and must assess any edematous area for evidence of erythema to prevent skin breakdown.
