The risk of development of AKI in critically ill patients has been classified by a multinational group of nephrologists.10 The classification uses the acronym RIFLE (risk, injury, failure, loss, and end-stage kidney disease [ESKD]).¹¹ The RIFLE system classifies AKI into three categories of increasing severity (R, I, F) and two outcome criteria (L, E) based on GFR status reflected by the change in urine output or loss of kidney function¹¹ (Table 20-1). If AKI is superimposed on a kidney that is already compromised, the term chronic is added to the RIFLE criteria to denote the cause as acute-on-chronic kidney failure.¹¹

The Acute Kidney Injury Network (AKIN) criteria are listed in Box 20-1. These criteria are similar to those proposed by the RIFLE group, and both groups intend to make the point that in the acutely ill patient, small changes in the serum creatinine level and urine output may signal important declines in the GFR and kidney function. A conceptual model that combines the features of the RIFLE criteria and AKIN criteria are shown in Figure 20-1.¹¹

Any condition that decreases blood flow, blood pressure (BP), or kidney perfusion before arterial blood in the renal artery enters the kidney may be anatomically described as prerenal AKI. When arterial hypoperfusion due to low cardiac output, hemorrhage, vasodilation, thrombosis, or other cause reduces the blood flow to the kidney, glomerular filtration and, consequently, urine output decrease (see Box 20-2). This is a major reason that the critical care nurse monitors the urine output on an hourly basis. Initially, in prerenal states, the integrity of the kidney’s nephron structure and function may be preserved. If normal perfusion and cardiac output are restored quickly, the kidney will not suffer permanent injury. However, if the prerenal insult is not corrected, the GFR will decline, the blood urea nitrogen (BUN) concentration will rise (prerenal azotemia),⁹ oliguria will develop, and the patient will be at risk for significant kidney damage. Oliguria (urine output <400 mL/day) is a classic finding in AKI.⁵ Prerenal AKI is seen frequently in the critically ill. In a study of hospitalized older patients with kidney failure, prerenal AKI occurred in 58%.⁵ This compares with rates of 34% for intrarenal AKI and 8% for postrenal AKI in the same study.⁵

Any condition that produces an ischemic or toxic insult directly at the site of the nephron places the patient at risk for development of intrarenal AKI (see Box 20-2).

Ischemic damage to the kidney can also damage internal structures from prolonged hypotension or low cardiac output. In the multicenter study of critical care patients with AKI by Mehta and colleagues,⁴ 50% of the patients had ischemic injury, which was largely precipitated by hypotension (20%) and sepsis (19%).

Toxins that damage kidney tubular endothelium include medications that are administered to treat a coexisting condition¹² as well as radiopaque (contrast) dye administered during an interventional or diagnostic radiological study. Complications from the contrast dye cause AKI in 9% to 14% of patients.⁴ In affected patients, the serum creatinine levels typically begin to rise 48 to 72 hours after the study, peak at 3 to 5 days, and return to baseline within another 3 to 5 days.¹³ Kidney dysfunction can persist up to 3 weeks after the procedure. Although patients with normal kidney function are not considered to be at risk, those with elevated serum creatinine levels, diabetes, or microvascular disease are highly vulnerable.¹³

The term azotemia is used to describe an acute rise in the BUN level.9 Uremia is another term used to describe an elevated BUN value.

The oliguric or anuric phase, the second phase of AKI, lasts 5 to 8 days in the nonoliguric patient and 10 to 16 days in the oliguric patient.14 The accumulation of necrotic cellular debris in the tubular space blocks the flow of urine and causes damage to the tubular wall and basement membranes. Backleak occurs because damage in the tubular wall causes the glomerular filtrate to flow passively into the kidney tissue rather than to be passed out as urine through the ureters and bladder. Oliguria is encountered more often in ischemic damage and is a sign that the damage is extensive and severe. During the oliguric or anuric phase, the GFR is greatly reduced, leading to increased levels of BUN (azotemia), elevated serum creatinine values, electrolyte abnormalities (hyperkalemia, hyperphosphatemia, hypocalcemia), and metabolic acidosis.

Critically ill patients with AKI have a high mortality on long-term follow-up.15 Kidney function may return to normal, or near normal, with a GFR that is 70% to 80% of normal within 1 to 2 years.¹⁶ However, if significant kidney parenchymal damage has occurred, BUN and creatinine levels may never return to normal. Of the patients who survive AKI, approximately 62% eventually recover normal kidney function, 33% have residual kidney damage, and at least 5% require long-term hemodialysis.¹⁶

Acidosis (pH <7.35) is one of the trademarks of severe AKI.17 Metabolic acidosis occurs from accumulated metabolic waste products. The acid waste products consist of strong negative ions (anions), elevated serum phosphorus values (hyperphosphatemia), and other normally unmeasured ions (e.g., sulfate, urate, lactate) that decrease the serum pH.¹⁷ A low serum albumin concentration, which often occurs in AKI, has a slight alkalinizing effect, but it is not enough to offset the metabolic acidosis.¹⁷ Even respiratory compensation and mechanical ventilatory support are rarely sufficient to reverse the metabolic acidosis. Information on acidosis and arterial blood gas interpretation is found in Chapter 14. Anion gap measurement is discussed in Chapter 19.

The BUN level is not a reliable indicator of kidney damage.9,18 The BUN concentration is changed by protein intake, blood in the gastrointestinal (GI) tract, and cell catabolism, and it is diluted by fluid administration. An elevated BUN-to-creatinine ratio may signal early AKI. The BUN-to-creatinine ratio is most useful in diagnosing prerenal AKI (often described as prerenal azotemia), in which the BUN value is greatly elevated relative to the serum creatinine value.

Creatinine is a by-product of muscle metabolism that is formed from nonenzymatic dehydration of creatine in the liver18; 98% of creatine is in the muscles,¹⁸ and it is almost totally excreted by the kidney tubules. If the kidneys are not working, the serum creatinine level will increase. When the serum creatinine values doubles (e.g., from 0.75 to 1.5 mg/dL), the increase reflects a decrease of approximately 50% in the GFR.¹⁸ Serum creatinine level is assessed daily to follow the trend of kidney function and to determine whether the kidney function is stable, getting better, or getting worse.¹⁸

Trauma patients have different demographics from those of other critical care populations. They are always emergency admissions, are younger, are more often male, and have fewer coexisting illnesses.29 A 5-year retrospective study of 9449 trauma admissions to critical care units in Australia and New Zealand used the RIFLE criteria to determine incidence of AKI in the first 24 hours after admission; AKI developed in 18% of trauma patients.²⁹ However, if patients were older or had preexisting comorbid illnesses, their risk of AKI rose to 35%.²⁹ Although these AKI numbers are high, they likely underestimate the true incidence because the study did not include patients in whom AKI developed more than 24 hours after admission to the critical care unit.²⁹

Trauma patients with major crush injuries have an elevated risk of kidney failure because of the release of creatine and myoglobin from damaged muscle cells, a condition called rhabdomyolysis.30 Myoglobin in large quantities is toxic to the kidney. Overall survival from rhabdomyolysis is 77%.³⁰

The level of creatine kinase (CK), a marker of systemic muscle damage, increases in patients with rhabdomyolysis. One trauma service reported that of 2083 trauma patients admitted to critical care, 85% had elevated CK values, and acute kidney failure resulting from rhabdomyolysis developed in 10%.³¹ A CK level of 5000 units/L was the lowest abnormal value in patients in whom AKI associated with rhabdomyolysis developed.³¹

Volume resuscitation is the primary treatment for preservation of adequate kidney function and prevention of AKI. In many hospitals, the intravenous (IV) fluids are alkalinized by the addition of sodium bicarbonate, and the urine output is increased by intravenous administration of the diuretic mannitol.³⁰ A bicarbonate and mannitol regimen is instituted to prevent acidosis and hyperkalemia, because both are frequent complications of rhabdomyolysis. Close attention is paid to urine output, CK levels, increases in serum creatinine levels, and any signs of compartment syndrome in all patients admitted with this diagnosis.

High-molecular-weight contrast medium is a potential cause of nephrotoxicity.13,35 Kidney-protection strategies include identification of patients at high risk and use of alternative imaging modalities that do not involve contrast. If radiopaque contrast use is inevitable, smaller contrast volumes should be used for each study, and low-osmolar, or iso-osmolar (iohexol), contrast media that are less nephrotoxic should be selected.^35,36

The best method of prevention is aggressive hydration with intravenous normal saline during and after the procedure.37,38 After some diagnostic intravascular catheterization procedures, the alert patient is asked to drink several liters of water over a 12-hour period to protect the kidney. Avoiding dehydration is vital. In research studies, the addition of sodium bicarbonate or N-acetylcysteine did not confer additional protection to the vulnerable kidney beyond hydration with normal saline only.^37–39

Several medications have been investigated to mitigate the risk of AKI in at-risk patients who undergo diagnostic studies involving radiopaque contrast agents. The agents include oral N-acetylcysteine, intravenous sodium bicarbonate, and an intravenous infusion of fenoldopam.37–40 In randomized, controlled trials, N-acetylcysteine has not lived up to its early promise.^37–40 For sodium bicarbonate, the picture is mixed, with some studies reporting a benefit^39,41 and other studies reporting no effect.^37,38 Because N-acetylcysteine and sodium bicarbonate are inexpensive and have almost no side effects, many physicians prescribe them on an empirical basis, even though the research evidence is not yet conclusive.

In summary, the mainstay measures to protect the kidney from contrast-induced AKI are to use the smallest dose of low- or iso-osmolar contrast media possible, provide vigorous fluid volume expansion, stop all nephrotoxic drugs, and avoid repeat contrast media injections within 48 hours.⁴²

Hemodynamic monitoring includes surveillance of the CVP, pulmonary artery occlusion pressure, cardiac output, and cardiac index.43 A less high-tech method that is also important consists of a daily weight and focused physical assessment.

Physical signs and symptoms are used to assess fluid balance. Signs that suggest extracellular fluid (ECF) depletion include thirst, decreased skin turgor, and lethargy. Signs that imply intravascular fluid volume overload include pulmonary congestion, increasing heart failure, and rising blood pressure. The patient with untreated AKI is edematous. The following factors contribute to this state:

In critical illness, even though there is peripheral edema and the patient may have gained 8 L of fluid over his or her “dry-weight” baseline, the patient may remain “intravascularly dry” and hemodynamically unstable, because the retained fluid is not inside a vascular compartment and cannot contribute to maintenance of hemodynamic stability. The patient with AKI is assessed frequently for pitting edema over bony prominences and in dependent body areas.

Electrolyte levels require frequent observation, especially in the critical phases of AKI (Table 20-4). Potassium may quickly reach levels of 6.0 mEq/L or higher. Specific electrocardiographic changes are associated with hyperkalemia: peaked T waves, a widening of the QRS interval, and ultimately, ventricular tachycardia or fibrillation. If hyperkalemia is identified, all potassium supplements are stopped.⁴⁴ If the patient is producing urine, intravenous diuretics can be administered. Acute hyperkalemia can be treated temporarily by IV administration of insulin and glucose. An infusion of 50 mL of 50% dextrose accompanied by 10 units of regular insulin forces potassium out of the serum and into the cells.

Sodium polystyrene sulfonate (Kayexalate), a cation-exchange resin, is mixed in water and sorbitol and given orally, rectally, or through a nasogastric tube. The resin binds potassium in the bowel, which eliminates it in the feces. Kayexalate and dialysis are the only permanent methods of potassium removal.⁴⁴

Dilutional hyponatremia, associated with kidney failure, is an expected finding in AKI (see Table 20-4). It can be corrected over a few days with fluid restriction. Sodium levels may be raised more rapidly during dialysis by changing the amount of sodium in the dialysate bath.

Serum calcium levels are reduced (hypocalcemia) in kidney failure (see Table 20-4). This reduction results from multiple factors, including hyperphosphatemia. Long-term elevations of serum phosphorus (>5.5 to 6.5 mEq/L) are associated with higher mortality rates for patients in kidney failure.^20,45,46 Calcium and phosphorus are regulated in part by parathyroid hormone (PTH). Normally, PTH helps calcium be resorbed back into the bloodstream at the proximal tubule and distal nephron, and it promotes excretion of phosphorus by the kidney to maintain homeostasis. In kidney failure, this mechanism is nonfunctional; the serum phosphorus level rises, and the serum calcium level falls.

Most calcium in the bloodstream is bound to protein. Calcium levels can be measured in two ways: total calcium (tCa) or ionized calcium (iCa).46 Unfortunately, protein-calcium binding confounds the measurement of accurate calcium levels. In the past, calculations were used to estimate the amounts of protein-bound versus unbound calcium, but these calculations have been shown to produce inaccurate results.⁴⁷ The metabolically active, non–protein-bound portion is known as the ionized calcium and is the preferred method of measurement.⁴⁷ Without adequate levels of serum calcium, a compensatory mechanism ‘steals’ calcium from the bones, making the patient with kidney failure more vulnerable to fractures.⁴⁸ Maintaining adequate calcium stores in the body is important and is achieved by administration of calcium supplements, vitamin D preparations, and synthetic calcitriol.⁴⁹

A second method used in tandem with calcium supplements to achieve normal calcium levels is to lower the level of phosphorus in the bloodstream.46 Phosphorus occurs in many foods, and eliminating all phosphorus-containing foods from the diet would make it unpalatable.⁵⁰ Foods that contain particularly high levels of phosphorus include dairy products, processed meats, some carbonated drinks, and nuts.⁵⁰ After these foods are eaten, free phosphorus passes from the GI tract into the bloodstream and raises the serum level. Medications that bind dietary phosphorus in the gastrointestinal tract are administered orally or by nasogastric tube. The binding agent must be taken at the same time as a meal.⁵⁰ After the dietary phosphorus is bound to the binding substance in the bowel, it is eliminated from the intestine with stool. This lowers the serum phosphorus level.

The types of dietary-phosphorus binders used have changed over the years. The original binders were aluminum salts (aluminum hydroxide) that bound dietary phosphorus effectively in the gastrointestinal tract but conferred aluminum toxicity because some of the aluminum metal was also absorbed.⁵⁰ For this reason, aluminum binders have largely been abandoned.⁵⁰

The second generation of dietary phosphorus–binding agents that are most widely prescribed use calcium salts (calcium carbonate; calcium acetate [PhosLo]) to bind dietary phosphorus in the gastrointestinal tract. Calcium-based drugs are safer, but elevated serum calcium values and calcium deposits in other areas of the body (extraosseous calcification) are a problem.⁵⁰ This category of drugs remains in widespread use.

A third generation of dietary phosphorus–binding medications is available. They are not aluminum- or calcium-based. They include sevelamer hydrochloride (RenaGel) and lanthanum carbonate (Fosrenol).⁵⁰

Treatment goals for patients with AKI focus on prevention, compensation for the deterioration of kidney function, and regeneration of the remaining kidney functional capacity. Over the past 4 decades, the mortality rate for AKI has remained at more than 50%.4,5 Key areas that are evaluated include prevention strategies, fluid balance, anemia, medications, and electrolyte imbalance.

The only truly effective remedy for AKI is prevention. Effective prevention requires assessment of the patient’s risk for AKI. Knowledge of the most frequent causes of AKI in the critically ill is essential if prevention strategies are to be enacted. The critical care team collaborates closely with the clinical pharmacist to avoid drugs with nephrotoxic side effects in patients with AKI or CKD.19,20 Nonsteroidal anti-inflammatory drugs (NSAIDs) for pain relief are avoided in patients with elevated creatinine values.² The use of intravascular contrast dye is preferably delayed until the patient is fully rehydrated.⁴²

Prerenal failure is caused by decreased perfusion and flow to the kidney. It is often associated with trauma, hemorrhage, hypotension, and major fluid losses. If contrast dye is used, aggressive fluid resuscitation with normal saline (NaCl) is recommended. Fluid replacement is the only treatment shown to prevent kidney tubular injury.51 The objectives of volume replacement are to replace fluid and electrolyte losses and to prevent ongoing loss. Maintenance intravenous fluid therapy is initiated when oral (PO) fluid intake is inadvisable. Maintenance fluids are calculated with consideration for individual body surface area. Adults require approximately 1500 mL/m²/24 hr; fever, burns, and trauma significantly increase fluid requirements. Other important criteria in the calculation of fluid volume replacement include baseline metabolism, environmental temperature, and humidity. The rate of replacement depends on cardiopulmonary reserve, adequacy of kidney function, urine output, fluid balance, ongoing loss, and type of fluid replaced.

Diuretics are used to stimulate urinary output in the fluid overloaded patient with functioning kidneys. Care must be taken in their use to avoid the creation of secondary electrolyte abnormalities (Table 20-7). Diuretics reduce volume overload and are helpful for symptoms such as pulmonary edema, but they have not been shown to prevent AKI.⁵⁶ Diuretics are used in many patient populations other than those with incipient kidney failure.

Low-dose dopamine (2 to 3 mcg/kg/min), previously known as renal-dose dopamine, is infused to stimulate blood flow to the kidney. Dopamine is effective in increasing urine output in the short term, but tolerance of the dopamine renal receptor to the drug is theorized to develop in the critically ill patients who are most at risk for AKI.64 A meta-analysis of related research studies determined that renal-dose dopamine did not prevent onset of AKI and did not decrease the need for dialysis or reduce mortality.⁶⁵ At this point, the support for routine use of low-dose dopamine for the prevention of AKI remains anecdotal only.⁶⁶ See Table 13-16 and the Priority Medications Box: Dopamine in Chapter 13 for more information on dopamine.

N-Acetylcysteine (Mucomyst, Mucosil) is an N-acetyl derivative of the amino acid L-cysteine. It has been used for many years as a mucolytic agent to assist with expectoration of thick pulmonary secretions. It is also frequently prescribed for patients with mildly elevated serum creatinine values before a radiologic study using contrast dye.67 In research trials, the addition of N-acetylcysteine to normal saline hydration has not showed a reduction in the incidence of contrast-induced AKI.^37,39,67 In clinical trials enrolling cardiac surgery patients, prophylactic use of N-acetylcysteine did not decease the rate of AKI.^67,68 Most studies suggest that N-acetylcysteine does not prevent AKI during radiologic procedures or after cardiac surgery.

Fenoldopam mesylate (Corlopam) is a dopamine 1 (D₁) receptor agonist similar in structure to dopamine and dobutamine. It is used to lower blood pressure. Claims that this drug would prevent contrast-induced nephrotoxicity in high-risk patients have not been supported by clinical trial results.40

Many patients with kidney failure are prescribed a dietary phosphorus–binding medication (see earlier “Dietary-Phosphorus Binding Drugs”).⁵⁰ Many dietary phosphorus–binding drugs are available, and some important issues concern all of them. The dietary phosphorus binder must be taken at the time of the meal. If it is taken 2 hours later, it will increase only the level of the binding substance (e.g., calcium) in the bloodstream and will not lower the serum phosphorus level. Related issues such as the quantity of phosphorus in the diet should be discussed with a clinical nutritionist (dietitian).

Some individuals are at increased risk for AKI as a complication during hospitalization, and the alert critical care nurse recognizes potential risk factors and acts as a patient advocate.19,20 Patients at risk include older persons because their GFR may be decreased,⁵ dehydrated patients with kidney hypoperfusion, patients who have increased creatinine values before hospitalization, and patients undergoing a radiologic procedure involving contrast dye.

Hyperkalemia, hypocalcemia, hyponatremia, hyperphosphatemia, and acid-base imbalances occur during AKI (see Table 20-4). Clinical manifestations of these electrolyte imbalances must be prevented and their associated side effects controlled. The more likely imbalances are hyperkalemia and hypocalcemia, which can result in life-threatening cardiac dysrhythmias. Dilutional hyponatremia may develop as fluid overload worsens in the patient with oliguria. Monitoring the serum sodium level is important to prevent this complication. Hyperphosphatemia results in severe pruritus. Nursing care is directed at soothing the itching by performing frequent skin care with emollients, discouraging scratching, and administering phosphate-binding medications.⁵⁰ The acid-base imbalances that occur with AKI are monitored by arterial blood gas (ABG) analyses. The goal of treatment is to maintain the pH within the normal range.

Anemia is an expected side effect of kidney failure that occurs because the kidney no longer produces the hormone erythropoietin.70 As a result, the bone marrow is not stimulated to produce red blood cells (RBCs). Decreased RBC production by the bone marrow also occurs as a consequence of critical illness.⁷¹ Care is taken to prevent blood loss in the patient with AKI, and blood withdrawal is minimized as much as possible. Irritation of the GI tract from metabolic waste accumulation is expected, and stress ulcer prophylaxis must be prescribed. Gastrointestinal bleeding remains a possibility. Stool, nasogastric tube drainage, and emesis are routinely tested for occult blood. Anemia may be treated pharmacologically by the administration of recombinant human erythropoietin (rhEPO), epoetin alfa (Procrit, Epogen), to stimulate erythrocyte production by the bone marrow and if required by RBC transfusion. Treatment of anemia early in the course of AKI (before dialysis) appears to slow the progression of the kidney failure and delays the initiation or renal replacement therapies.⁷² Even in anemic, critically ill patients without kidney failure, administration of rhEPO weekly significantly decreases the number of blood transfusions.⁷³ However, this therapy is not recommended for anemia related to sepsis in the critically ill.²⁸

Accurate and uncomplicated information must be provided to the patient and family about AKI, including its prognosis, treatment, and possible complications.7 Education of the patient can be challenging because elevations of BUN and creatinine can negatively affect the level of consciousness. Sleep-rest disorders and emotional upset often occur as complications of AKI and can disrupt short-term memory. Encouraging the patient and family to voice concerns, frustrations, or fears and allowing the patient to control aspects of the acute care environment and treatment are essential.

Hemodialysis works by circulating blood outside the body through synthetic tubing to a dialyzer, which consists of hollow-fiber tubes. The dialyzer is sometimes described as an artificial kidney (Figure 20-3). While the blood flows through the membranes, which are semipermeable, a fluid (dialysate bath) bathes the membranes and, through osmosis and diffusion, performs exchanges of fluid, electrolytes, and toxins from the blood to the bath, where toxins and dialysate then pass out of the artificial kidney. The blood and the dialysate bath are shunted in opposite directions (countercurrent flow) through the dialyzer to match the osmotic and chemical gradients at the most efficient level for effective dialysis.

Heparin or sodium citrate is added to the system just before the blood enters the dialyzer to anticoagulate the blood within the dialysis tubing. Without an anticoagulant, the blood clots because its passage through the foreign tubular substances of the dialysis machine activates the clotting mechanism. Heparin can be administered by bolus injection or intermittent infusion. It has a short half-life, and its effects subside within 2 to 4 hours. If necessary, the effects of heparin are easily reversed with the antidote protamine sulfate. When there is concern about the development of heparin-induced thrombocytopenia (HIT),75 alternative anticoagulants can be used. Citrate (trisodium citrate) can be infused as an anticoagulant by intermittent bolus or continuous infusion.⁷⁶

Because of the design of the CRRT machine, it is not possible to look at the outside and follow the flow of blood and, if used, dialysate. Each of the CRRT methods is described here, and diagrams are employed to clarify the mode of CRRT that is used (Figure 20-6, A-D).

Continuous Venovenous Hemofiltration

CVVH is indicated when the patient’s clinical condition warrants removal of significant volumes of fluid and solutes (see Figure 20-6, B). Fluid is removed by ultrafiltration in volumes of 5 to 20 mL/min or up to 7 to 30 L/24 hr. Removal of solutes such as urea, creatinine, and other small non-protein-bound toxins is accomplished by convection. The replacement fluid rate of flow through the CRRT circuit can be altered to achieve desired fluid and solute removal without causing hemodynamic instability.

As with other CRRT systems, the blood outside the body is anticoagulated, and the ultrafiltrate is drained off by gravity or by the addition of negative-pressure suction into a large drainage bag. Because large volumes of fluid may be removed in CVVH, some of the removed ultrafiltrate volume must be replaced hourly with a continuous infusion (replacement fluid) to avoid intravascular dehydration. Replacement fluids may consist of standard solutions of bicarbonate, potassium-free LR solution, acetate, or dextrose. Electrolytes such as potassium, sodium, calcium chloride, magnesium sulfate, and sodium bicarbonate may be added. The formula used to calculate the volume removed from the patient follows with an example:

< ?xml:namespace prefix = "mml" />Ultrafiltrate in bag+Other output−(CVVH replacement fluid+intravenous/)oral/nasogastric tube intake=Output

1000mL−800mL=200mL/hr output

Potential problems associated with CRRT and appropriate nursing interventions are listed in Table 20-11. Complications are often related to the rate of flow through the system. If the patient becomes hypotensive or the access lines remain kinked, the ultrafiltration rate will decrease. This can lead to increased clot formation within the hemofilter. As the surface of the hemofilter becomes more clotted, it will not provide effective fluid or solute clearance, and CRRT will be stopped; a new CRRT circuit must then be set up. The critical care nurse keeps track of the pressures displayed on the CRRT machine screen to monitor the positive pressure of fluid going into the hemofilter (inflow) and the pressures coming out of the hemofilter to ensure that that resistance to the negative-pressure pull of the fluid across the hemofilter membrane has not developed. Other patient-related complications include fluid and electrolyte alterations, bleeding because of anticoagulation, and problems with the access site, such as dislodgement and infection.

Critical care nurses play a vital role in monitoring the patient receiving CRRT. In many critical care units, the CRRT system is set up by the dialysis staff but is run on a 24-hour basis by critical care nurses with additional training. Complications may be related to the CRRT circuit, the CRRT pump, or to the patient, as shown in Box 20-6. The critical care nurse monitors fluid intake and output, prevents and detects potential complications (e.g., bleeding, hypotension), identifies trends in electrolyte laboratory values, supervises safe operation of the CRRT equipment, and provides patient and family education about the patient’s condition and the use of CRRT.

Electrolyte balance is also of grave concern. Because of the large volumes of urine produced, the potential exists for hypokalemia, hypomagnesemia, and hypocalcemia, leading to possible cardiac compromise.91 Electrolytes must be monitored at least every 4 to 6 hours and replaced as necessary. Assessment of the BUN and the creatinine concentration also is necessary every 4 to 6 hours to monitor graft function and determine the need for dialysis.

The average length of stay in the hospital after uncomplicated kidney transplantation is 5 to 7 days.92 During the first few days, the patient must learn self-care related to the new organ. Medication regimens are very complicated, and most centers initiate a self-medication program at the patient’s bedside as a training tool. Patients are taught the signs and symptoms of infection and graft rejection, the protocols of the transplant clinic, and new dietary limitations. Frequent transplant clinic visits to check the functioning of the organ and to adjust down the doses of immunosuppressant medications are necessary for the first few months after transplantation.⁹²