Acute kidney injury (AKI) is the contemporary name for what was formerly termed acute renal failure. The new name more accurately describes the process of all phases of acute injury to the kidney. The definition of AKI can be referred to as RIFLE, representing three levels of renal dysfunction. These levels are described in the following categories: risk of renal dysfunction, injury to the kidney, failure of kidney function, loss of function, and end-stage renal disease, the later two representing outcome categories (Table 18-1). Dialysis is often necessary for the treatment of AKI. The most common indications include uremia, hyperkalemia, acidosis, fluid overload, and drug overdose.
Table 18-1 Risk, Injury, Failure, Loss, and End-Stage Renal Diseases (RIFLE) Classification
|
Class |
Glomerular filtration rate criteria |
Urine output criteria |
|
Risk |
Serum creatinine × 1.5 |
< 0.5 mL/kg/h × 6 h |
|
Injury |
Serum creatinine × 2.0 |
< 0.5 mL/kg/h × 12 h |
|
Failure |
Serum creatinine × 3 |
< 0.5 mL/kg/h × 24 h, or anuria × 12 h |
|
Loss |
Persistent acute renal failure = complete loss of kidney function > 4 weeks |
|
|
End-stage renal disease |
End-stage renal disease > 3 months |
For conversion of creatinine expressed in conventional units to SI units, multiply by 88.4. RIFLE class is determined based on the worst of either glomerular filtration criteria or urine output criteria. Glomerular filtration criteria are calculated as an increase of serum creatinine above the baseline serum creatinine level.
From Clarkson MR, Brenner BM, Magee C: Pocket companion to Brenner and Rector’s the kidney, ed 2, St. Louis, 2010, Saunders.
What is acute kidney injury?
AKI is the rapid deterioration of renal function. It is usually reversible if diagnosed and treated early. Signs and symptoms of AKI are a urine output of less than 400 mL/day (oliguria), or less than 20 mL/h for an adult; an increase in blood urea nitrogen (BUN); and creatinine, hyperkalemia, and acidosis.
What are the types of acute kidney injury?
AKI is divided into three categories: prerenal, intrarenal, and postrenal (Box 18-1) (see Chapter 4).
Prerenal. Prerenal renal failure accounts for approximately 70% of AKI cases. Prerenal events result in a decrease in blood flow to the kidney. Examples include congestive heart failure, hypovolemia, sepsis, myocardial infarction, prolonged hypotension, and vascular disorders of the renal artery or vein.
Intrarenal. Approximately 25% of AKI cases are caused by intrarenal factors. Any event that damages the kidney tissue, structure, and function is categorized as intrarenal AKI. The damage, which may involve the glomeruli, the tubules, or both, interferes with the ability of the kidneys to carry out their normal functions. The most common cause of intrarenal failure is damage to the tubules. This is called acute tubular necrosis (ATN). ATN is caused by severely reduced blood flow leading to prolonged ischemia, or by direct toxic insult to tubular cells. In oliguric ATN, urine flow falls to about 20 mL/h, and BUN, serum creatinine, phosphate, and potassium levels rise. With nonoliguric AKI, the patient may remain in better fluid balance, but elimination of waste products is impaired. Ischemic injury to the kidneys can occur when the mean arterial blood pressure drops below 60 mm Hg for more than 30 minutes. Massive hemorrhage, transfusion reaction, sepsis, cardiovascular collapse, or major trauma can cause ischemic renal injury.
Substances that injure the kidneys are called nephrotoxins. The most common are medications, such as antibiotics and nonsteroidal antiinflammatory agents (NSAIDs). Other medications, including anesthetics and cancer chemotherapy agents, as well as street drugs, are toxic to the kidney in varying degrees. Radiologic contrast dye used for intravenous pyelography, cardiac catheterization, and computed tomography is potentially nephrotoxic. Other nephrotoxins include hemoglobin (from hemolysis of red blood cells) and myoglobin from muscle breakdown (rhabdomyolysis), caused by crush injury, heatstroke, or seizure.
Postrenal. Postrenal causes account for approximately 5% of AKI cases. Postrenal failure is usually the result of obstruction in the flow of urine anywhere from the kidney to the urinary meatus. The obstruction can be functional or mechanical. Functional causes include diabetic nephropathy, such medications as ganglionic blocking agents that block the autonomic nerve supply to the urinary system, and neurogenic bladder subsequent to spinal cord injury or cerebrovascular accident. Tumors, stones, prostatic hypertrophy, and urethral strictures are some mechanical causes of postrenal failure.
Box 18-1 Etiologies of Acute Kidney Injury
Prerenal (decreased renal perfusion)
• Hypovolemia
• Hemorrhage
• Shock
• Third spacing (edema, ascites)
• Burns
• Dehydration (gastrointestinal losses, overuse of diuretics)
• Decreased cardiac output
• Cardiogenic shock
• Dysrhythmias
• Cardiac tamponade
• Congestive heart failure
• Myocardial infarction
• Thromboembolic obstruction of the renal vasculature
Intrarenal (damage to the nephron)
• Acute tubular necrosis
• Ischemic
• Prolonged prerenal acute kidney injury
• Transfusion reaction
• Rhabdomyolysis
• Nephrotoxic
• Prolonged postrenal acute kidney injury
• Antibiotics (aminoglycosides, carbenicillin, amphotericin B)
• Contrast media
• Heavy metals (lead, mercury)
• Carbon tetrachloride
• Insecticides, fungicides
• Cytotoxic drugs (certain chemotherapeutic agents)
• Hemolytic-uremic syndrome
• Inflammatory
• Acute glomerulonephritis
• Acute pyelonephritis
Postrenal (obstruction)
• Benign prostatic hypertrophy
• Calculi (stones)
• Urinary tract infection
• Tumors
• Strictures
• Altered bladder contraction (neurogenic bladder from medication or injury/disease)
Modified from Copstead LC, Banasik JL: Pathophysiology, ed 4, St. Louis, 2010, Mosby.
Does a patient with acute kidney injury have urine output?
Some patients with AKI have significant urine output, referred to as nonoliguric renal failure. Most patients progress through several stages from oliguria to anuria to polyuria, depending on the phase of AKI (Table 18-2).
Oliguric-anuric phase. Oliguria is defined as urine volume less than 400 mL/day. Anuria is a urine output of less than 50 mL/day. This phase can last from 2 days to 30 days or longer. The longer the oliguria or anuria continues, the more the prospect of returning to normal urine output worsens. Proper management of fluid volume is essential.
Diuretic phase. This phase begins when the urine output reaches 1 L/day. The renal indices may stabilize and then start to approach normal with gradual return of renal function. A 24-hour urine volume can increase to as much as 4 to 5 L. Accurate evaluation of the patient’s status to avoid dehydration leading to hypoperfusion of the kidneys is mandatory. Laboratory values are monitored closely with the expectation that they will return to normal in the late phase of AKI.
Convalescent phase. This period begins with the stabilization of serum chemistries and gradual return of normal kidney function. This phase may last from three to six months. Return to normal glomerular filtration rate, if it occurs, may take up to a year.
Table 18-2 Phases of Acute Kidney Injury
What are the clinical presentations of acute kidney injury?
The clinical presentations of AKI include all of the symptoms, signs, and findings of rapidly developing uremia (see Chapter 5).
What biochemical changes are present in acute kidney injury?
The damaged kidneys are unable to excrete the products of normal body metabolism. There is elevation of the serum urea and creatinine, and altered electrolyte levels. Increased hydrogen ion concentration causes acidosis and a low serum pH. Hyperkalemia, hypokalemia, hypocalcemia, hyperphosphatemia, hypermagnesemia, and low bicarbonate may be observed.
How is acute kidney injury treated?
Many treatment options are available depending on the cause of the renal failure, the severity of symptoms, and the overall condition of the patient. Options include hemodialysis, isolated ultrafiltration (UF), peritoneal dialysis, continuous renal replacement therapy (CRRT), and charcoal hemoperfusion.
What are the indications for treatment?
The most common indications for acute dialysis include the following:
Uremia. Acute dialysis is initiated when a patient becomes symptomatically uremic (see Chapter 5) regardless of BUN or creatinine level. Dialysis may be started prophylactically when the BUN reaches 100 mg/dL, even if the patient has few or no symptoms.
Pulmonary edema. Acute pulmonary edema is a life-threatening complication of AKI that necessitates immediate dialysis. Acute pulmonary edema can result from fluid overload directly attributable to AKI or as the result of an acute myocardial infarction or from overzealous administration of fluid.
Hyperkalemia. Hyperkalemia is a result of the damaged kidney’s inability to secrete potassium and the release of intracellular potassium (because of acidosis and tissue breakdown). Hemodialysis is effective in lowering potassium and is initiated when rapid reduction of plasma potassium is indicated. Peritoneal dialysis is an acceptable treatment option, although its effects are slower than that of hemodialysis. Hyperkalemia can be managed in an emergency, while waiting for hemodialysis, by intravenous administration of glucose and insulin in combination with intravenous sodium bicarbonate. These shift extracellular potassium into the cell, where it cannot cause cardiac arrhythmia. Calcium gluconate may be given intravenously to reduce myocardial irritability. Sodium polystyrene sulfonate cation exchange resin (Kayexalate) by mouth or by enema can be administered when slower correction of potassium is acceptable or in the initial management of hyperkalemia.
Acidosis. Metabolic acidosis is caused by the inability of the kidneys to excrete hydrogen ion and to reabsorb bicarbonate. Acidosis can be treated temporarily by intravenous sodium bicarbonate. Hemodialysis may be required because of the added sodium, which increases the danger of volume overload.
Neurologic changes. Toxic effects of uremia can result in central nervous system changes. Headache, insomnia, and drowsiness are early symptoms; confusion, convulsions, and coma may occur later. Dialysis is indicated when any of these serious symptoms are seen, and preferably before they occur.
Drug overdoses and poisonings. Dialysis is indicated for the treatment of some drug intoxications. Drugs normally excreted by the kidneys, or water-soluble drugs of low molecular weight, will diffuse rapidly across cellulosic dialysis membranes. Such drugs are readily removed with hemodialysis. Examples include ethanol, lithium, methanol, and salicylates. Water-soluble drugs with high molecular weight, such as vancomycin and amphotericin B, diffuse across cellulosic membranes much more slowly and are less well removed. If the intoxicant is protein bound (e.g., digoxin and acetylsalicylic acid) or lipid soluble (e.g., glutethimide), hemodialysis is not useful. However, both of these intoxicants are removed by hemoperfusion with a charcoal cartridge or with a plasma membrane filter.
What type of vascular access is used for acute dialysis?
The most common access to the circulation for acute dialysis is a double-lumen venous catheter. The catheter may be placed in the subclavian, internal jugular, or femoral vein. Insertion of a catheter into the subclavian or internal jugular vein must be followed by an x-ray examination to determine correct placement and to rule out pneumothorax or hemothorax before the catheter is used (see Chapter 12).
Can an arteriovenous fistula or graft be used for acute dialysis?
Patients with an arteriovenous (AV) fistula or graft may require acute dialysis, and the fistula or graft may be used after its patency is determined (see Chapter 12 for additional information).
How often are patients dialyzed?
Frequency of dialysis is determined by the patient’s response to treatment. Patients may be hemodialyzed daily for a few days until the BUN, serum creatinine, potassium level, and acidosis are considered acceptable. Daily dialysis may be necessary for volume overload or if parenteral nutrition is to be given.
What complications may occur with acute kidney injury?
Congestive heart failure is a common occurrence. It is most often caused by hypertension, volume excess, and/or anemia.
Hypertension. Fluid removal by dialysis may correct the hypertension. Antihypertensive medication may be necessary.
Hypotension. Hypotension may result from blood loss, a strict fluid restriction, sepsis, myocardial infarction, or pericarditis. To prevent additional kidney damage, the underlying cause of the hypotension must be corrected to maintain adequate renal perfusion. The use of a vasopressor, such as dopamine, may be necessary.
Anemia. In AKI the release of erythropoietin is decreased. The usual response to therapy with recombinant erythropoietin or epoetin alfa requires three to four weeks, so it is not of immediate help. Uremic red blood cells also have a shortened life span. Blood loss from bleeding is often present (see Chapter 5 for additional information about complications).
What is the most serious complication of acute kidney injury?
Infection is the leading cause of death in AKI. Uremia causes immune suppression, which predisposes the patient to sepsis. Strict aseptic technique must be used for all invasive procedures, including initiating and discontinuing dialysis, starting an intravenous line, and caring for the bladder catheter.
Are there special considerations when dialyzing a patient for the first time?
An infrequent syndrome known as the “first-use” syndrome results from an allergic-type reaction to new dialyzers and is characterized by itching, hypotension, chest and back pain, and breathing difficulties. In severe cases, cardiopulmonary arrest may occur. Symptoms are usually manifested during the first 15 to 30 minutes of dialysis. Cuprophan dialyzers are most often implicated. Cellulose acetate, modified cellulosic and synthetic membranes (polysulfone, polyamide, and polyacrylonitrile) are less likely to cause first-use syndrome.
What is the treatment for first-use syndrome?
When the symptoms are severe, the blood must not be returned to the patient and the dialyzer is discarded. The physician should be notified and an assessment of symptoms, particularly cardiopulmonary status, should be performed. The use of a more biocompatible membrane may be necessary. When the symptoms are less severe, symptomatic treatment (e.g., nasal oxygen or oral diphenhydramine [Benadryl]) is adequate. In this situation, dialysis can continue because the symptoms usually subside after the first hour.
Are there special precautions when dialyzing someone with acute kidney injury?
Patients requiring acute dialysis are generally critically ill with multisystem failure. A thorough and accurate total assessment of the patient is essential before initiating dialysis (see Chapter 13). The nephrology nurse must be highly cognizant of changes, be prudent in assessing and monitoring the patient’s vital signs, and respond appropriately.
Controlled anticoagulation with heparin may be necessary to minimize clotting of the dialyzer; however, dialysis can be performed with little or no heparin. Careful monitoring of clotting times may be necessary to prevent complications related to heparinization during hemodialysis. A baseline clotting time must be obtained before the start of dialysis; a normal activated clotting time (ACT) is 60 to 90 seconds. The Clinical Laboratory Improvement Act (CLIA) now requires quality control checks for ACT machines to meet CLIA requirements. These requirements are resource intensive and may not permit bedside monitoring of ACT levels during dialysis (see Chapter 11).
The physician determines the technique of anticoagulation. “Tight” or no heparin may be used for patients at high risk for bleeding. In tight heparinization, clotting times are performed every 30 minutes. The ACT is kept at 1.25 times the baseline with additional heparin, as indicated when the ACT falls below the 1.25 baseline value. With systemic heparinization, generally the ACT values are allowed to range from 2.5 to 3 times the baseline.
“No heparin” dialysis requires a blood flow between 250 and 300 mL/min, otherwise significant dialyzer clotting will occur. The dialyzer is flushed every 20 to 30 minutes with 100 mL of normal saline so that it can be easily examined visually for clotting and so that proteins and clotting factors will be moved away from the dialyzer membrane surface. Before the start of dialysis this extra volume is calculated into the required fluid loss to achieve the planned fluid removal goal. The risk of clotting the dialyzer, resulting in an average blood loss of 150 mL, must be weighed against the risk of administering an anticoagulant to a high-risk patient.
Patients in an intensive care unit are often attached to a cardiac monitor. It is important to watch for arrhythmias during dialysis because these may relate to the dialysis. However, it is not uncommon to see some aberrant beats or premature ventricular beats during dialysis.
What measures may be taken during acute dialysis to counteract hypotension?
Abnormalities causing hypotension must be identified and corrected as much as possible. These usually involve intravascular volume, cardiac output, and/or vasomotor tone. Although patients are often overhydrated and edematous, some may have hypotension from low intravascular volume and need infusion of normal saline or dextrose and water. Patients who do not respond to normal saline infusion may require colloid or hyperosmolar products such as human plasma protein fraction (Plasmanate) or albumin. These colloids will increase the oncotic pressure and attract fluid from the extracellular space into the vascular space. Hypotension resulting from decreased red blood cell mass from hemorrhage or other causes may require transfusion of red blood cells. When hypotension is caused by low cardiac output, cardiotonic drugs, particularly inotropic (dopamine) and antiarrhythmic (lidocaine) agents may be helpful. It may be appropriate to reduce the blood flow rate to between 150 and 200 mL/min for an apparent decrease in cardiac output. The physician will need accurate assessment data on duration of dialysis, blood flow rate, UF estimate (or weight), blood pressure readings, and all medications administered to determine the most appropriate treatment. Note that when the blood flow is lowered, dialysis efficiency is reduced; that is, there is a decrease in urea reduction, Kt/V, and creatinine clearance. If hypotension is caused by poor vasomotor tone, patients may be maintained above their ideal weight to promote vascular filling and normotensive blood pressure.
What measures are appropriate for hypertension?
Most hypertension in acute dialysis patients is related to fluid excess and responds to UF. If it is not controlled through fluid removal, the physician may prescribe an antihypertensive medication. Patients on antihypertensive agents may be subject to hypotensive episodes. Administration of antihypertensive agents may need to be deferred prior to hemodialysis if ordered accordingly by the physician.
What is disequilibrium syndrome?
Disequilibrium syndrome is a complex of signs and symptoms ranging from headache, restlessness, and impaired mental concentration to confusion, twitching, jerking, and occasionally culminating in a grand mal seizure. It may occur during or soon after dialysis.
What causes dialysis disequilibrium?
Disequilibrium is believed to be related to cerebral edema. The blood-brain barrier has a selective effect on the transfer of solute and water between the plasma and the brain. During dialysis, plasma solute concentration is lowered faster than brain solute concentration and the plasma becomes hypotonic in relation to the brain cell water, causing water to shift from the plasma to the brain.
When should disequilibrium be anticipated?
Disequilibrium is most common in the more severely catabolic patient or in those in whom azotemia is severe (BUN greater than 200 mg/100 mL).
What are ways to prevent or minimize disequilibrium?
Prevention is best. Care must be taken not to lower the urea level too rapidly; it is best to do short (2- to 3-hours) dialysis at 24-hour intervals for the first few treatments. A reduced blood flow rate of 150 to 200 mL/min may lessen the risk of dialysis disequilibrium by slowing the rate of solute shift. Using a small dialyzer with lower clearance properties will help. Configuring the extracorporeal blood circuit with the dialysate flow concurrent—rather than countercurrent—to the blood flow is an easy means of decreasing the rapid removal of urea by lowering clearance throughout the treatment. Decreasing the dialysate flow rate also will lead to decreased removal of urea. The physician may also prescribe a high osmotic solution, such as 25% mannitol, intravenously at the beginning of treatment. Disequilibrium manifested by seizures and coma is unusual with frequent and less aggressive dialysis. Early detection of the potential for severe neurologic changes must be promptly reported to the physician.
Procedures
What is isolated ultrafiltration?
Isolated UF is a process by which excess fluid is removed with little or no change in solute concentrations of the blood. Very small amounts of urea and creatinine are removed from the patient’s serum passively along with the ultrafiltrate. The rate and amount at which the fluid can be removed depend in part on the amount of excess extracellular fluid present, the patient’s intravascular volume, and cardiovascular stability.
What are the indications for using isolated ultrafiltration?
Isolated UF is indicated to remove fluid when the removal of solute is not a priority. Isolated UF can be performed immediately before, after, or independent of hemodialysis treatment.
What equipment is needed for ultrafiltration?
Isolated UF is performed with the same dialyzer and tubing used for hemodialysis. The dialysate flow is turned off or placed in bypass mode. The dialyzer membrane does not come into contact with the dialysate solution. With conventional equipment, the total of the negative pressure applied to the dialysate side of the membrane plus the venous pressure represents the transmembrane pressure and determines the amount of UF. With volumetric equipment, the set value for UF determines the fluid to be removed. A blood pump, air detector, blood leak detector, and pressure monitors are standard equipment to perform the procedure safely.
Are there complications with isolated ultrafiltration?
Rapid removal of fluid can cause hypotension and muscle cramps.
What is continuous renal replacement therapy?
CRRT provides a gentle treatment and is used primarily to treat patients with AKI, particularly those with multiple organ failure. Such individuals tend to be hemodynamically unstable, to have cardiac insufficiency, and to tolerate hemodialysis poorly. Various hemofilters are available, hollow-fiber or plate design, and are characterized by small contained blood volume and low resistance to flow. There is increasing evidence that CRRT is improving patient survival in acute renal failure.
What treatments besides hemodialysis are available to treat acute kidney injury?
There are many alternatives to conventional hemodialysis. CRRT is the umbrella acronym for the five approaches for this treatment, such as slow continuous ultrafiltration (SCUF), continuous arteriovenous hemofiltration (CAVH), continuous arteriovenous hemodialysis (CAVHD), continuous venovenous hemofiltration (CVVH), and continuous venovenous hemodialysis (CVVHD). Originally SCUF, CAVH, and CAVHD were very popular because they do not require special equipment or the constant attention of nephrology personnel. Now CVVH and CVVHD are being prescribed more often. The principles of CRRT are the same, but special equipment is necessary for CVVH or CVVHD. The procedures are limited to the critical care setting for the treatment of AKI. A collaborative approach using the collective expertise of critical care and nephrology personnel is strongly recommended.
CAVH requires both arterial and venous access but does not use a blood pump. If solute removal by convective transport is not sufficient, diffusive transport is added by also using hemodialysis. CVVH and CVVHD do not require arterial access, with its attending problems, but instead use double lumen catheters in major venous sites. In each person, flow is controlled with a blood pump (Fig. 18-1).
Figure 18-1 Continuous renal replacement therapy (CRRT) using hemofiltration. A, Continuous arteriovenous hemofiltration (CAVH). B, Continuous venovenous hemofiltration (CVVH).
What are problems in the use of continuous renal replacement therapy?
For those procedures requiring arterial access, such as CAVH and CAVHD, there is risk of damage to the artery itself, as well as danger of hemorrhage if a connection is faulty or a leak develops in the blood circuit. Critically ill patients are often hypotensive, with the blood flow rate inadequate for effective filtration. In addition, correction of electrolyte imbalance and/or fluid overload may be slower than desired. Clotting problems are frequent.
For systems using venovenous flow, a blood pump is needed. Monitoring is required to avert air being drawn into the blood circuit and to watch for bleeding from a loose connection on the downstream side. Staff must be trained to perform this treatment and the system must be closely monitored.
What is slow continuous ultrafiltration?
SCUF is a method of gradual fluid removal. As with isolated UF, little solute removal takes place; therefore, intermittent hemodialysis may be needed to treat azotemia and to maintain electrolyte balance. The amount of fluid removed is usually 2 to 6 L in a 24-hour period.
What are the indications for slow continuous ultrafiltration?
Many patients with AKI have a high rate of protein breakdown and require large volumes of total parenteral nutrition fluid. A few hours of hemodialysis may be inadequate to remove such large volumes of fluid, particularly in the patient with hypotension and hemodynamic instability. SCUF allows for the slow continuous removal of fluid, alleviating the large volume administered.
What equipment is used in slow continuous ultrafiltration?
A highly permeable hemofilter, similar to a dialyzer, is used in SCUF. SCUF can be performed without blood pump assistance, relying on the patient’s cardiac output and mean arterial pressure (MAP) to provide adequate blood flow through the filter. The hydrostatic pressure of the blood forces the ultrafiltrate across the membrane, and it is collected in a drainage bag for disposal. The length of tubing from the hemofilter to the fluid collection device creates a negative pressure that supports the UF rate. SCUF may also be performed with blood pump assistance from the Prisma machine.
Do patients require heparin during slow continuous ultrafiltration?
Usually an initial bolus of 500 to 2000 units of heparin is injected, followed by a continuous drip of 250 to 500 units/h, or 5 to 10 units/kg/h. Clotting times are monitored. SCUF can be used without heparin by using normal saline flushes, but the chances of clotting the hemofilter are greatly increased.
What problems are associated with slow continuous ultrafiltration?
The most common problem associated with SCUF is failure to obtain the desired quantity of ultrafiltrate. The reasons are usually clotting of the hemofilter or decrease in blood flow through the circuit. A problem with the patient’s access, a kink in the tubing, or a drop in the patient’s arterial pressure can also result in a low UF rate.
What is continuous arteriovenous hemofiltration?
CAVH is the continuous flow of blood through an extracorporeal circuit to remove excess fluid and solutes over an extended period. Specific hemofilters in different sizes are available to perform CAVH. Product specifications, membrane properties, and hemofilter sizes vary considerably.
What are the indications for continuous arteriovenous hemofiltration?
CAVH is indicated when large volumes of fluid must be removed from hemodynamically unstable patients. Fluid loss is generally 8 to 15 L/day for adult patients. The large amount of fluid loss allows the removal of solutes from the blood. The solutes are removed by convection in proportion to their plasma water concentration.
What equipment is used during continuous arteriovenous hemofiltration?
CAVH (Fig. 18-2) is also performed without blood pump assistance and is dependent on the adequacy of the patient’s blood pressure to push the blood through the circuit. As with SCUF, the patient’s MAP must be maintained at greater than 60 mm Hg, or ideally 70 mm Hg. A drainage bag is attached to a port on the filter to collect the ultrafiltrate. Ultrafiltrate is replaced before the hemofilter (predilution) or after the hemofilter (postdilution).
Figure 18-2 Continuous arteriovenous hemofiltration (CAVH) schematic.
What is continuous arteriovenous hemodialysis?
CAVHD (Fig. 18-3) is a modification of CAVH, with the addition of dialysate flowing through the filter at a slow rate, for combined removal of fluid and solutes by diffusion (dialysis) and by convection (UF).
Figure 18-3 Continuous arteriovenous hemodialysis (CAVHD).
(From Lewis SM, Heitkemper, MM, Dirksen SR: Medical-surgical nursing, ed 6, St. Louis, 2004, Mosby.)
What are the indications for continuous arteriovenous hemodialysis?
When CAVH does not provide adequate waste product removal, CAVHD becomes the preferred treatment option. CAVHD may be more appropriate for patients who are anuric, hyperkalemic, or severely acidotic.
How is the procedure different from continuous arteriovenous hemofiltration?
The procedures for CAVH and CAVHD are similar except that dialysate is circulated around the hemofilter membrane in CAVHD for more efficient clearance of urea and creatinine. The dialysate used may be standard peritoneal dialysis solution containing 1.5% to 2.5% dextrose, which is infused into the hemofilter via one of the ultrafiltrate ports at a rate of 15 to 40 mL/min, or 1 to 4 L/h. Custom dialysate fluid may be necessary to avoid hyperglycemia and lactic acidosis, or for patients with liver failure. The increased solute removal reduces uremia, acidosis, and potential electrolyte imbalance so that replacement fluid may not be necessary.
What type of access is required for these treatments?
Access to the arterial circulation is necessary because no blood pump is used. Generally, a single lumen catheter is inserted into the femoral artery, with the blood returning to the femoral vein via another catheter. The subclavian vein can also be used for the return of the blood.
What is continuous venovenous hemofiltration?
CVVH (Fig. 18-4) is a form of continuous therapy, similar to its predecessor, CAVH, but a blood pump is used to control the blood flow through the hemofilter. CVVH is a venous therapy so the access used for this therapy is the subclavian, internal jugular, or femoral vein. Solute removal is through convection and fluid removal is achieved using UF with replacement fluid administered. The replacement fluid composition may vary and can be infused prefilter or postfilter to maintain intravascular volume.
Figure 18-4 Continuous venovenous hemofiltration (CVVH).
(Courtesy Baxter Healthcare, Renal Division, McGraw Park, IL.)
What is the objective of continuous venovenous hemofiltration?
The objective of CVVH is to provide CRRT, allowing the removal of solutes, balance of fluid and electrolytes, and stabilization of azotemia. Because this occurs evenly over time, this is a therapy of choice for those patients who are unable to tolerate rapid fluid and solute concentration shifts similar to those that occur with hemodialysis.
What are the indications for continuous venovenous hemofiltration?
CVVH is indicated when large volumes of fluid must be removed from hemodynamically unstable patients. CVVH is a recommended therapy to treat AKI patients who exhibit cardiovascular instability. Other indications include fluid removal (carcinogenic shock), increased intracranial pressure (subarachnoid hemorrhage, hepatorenal syndrome), shock (sepsis, adult respiratory distress syndrome), and nutrition (burns). CVVH is also indicated for multiorgan failure, nonoliguric patients who require large volumes of intravenous fluids. CVVH is frequently employed in the care of critically ill and unstable pediatric patients.
What equipment is used during continuous venovenous hemofiltration?
The blood pump equipment includes an arterial pressure monitor, a venous pressure monitor, and a venous drip chamber with an air alert detector. The use of a blood pump replaces the patient’s MAP as the driving force for the extracorporeal system, which is a significant advantage when treating a patient with decreased blood pressure.
What are some other advantages of continuous venovenous hemofiltration?
Because a blood pump is used with this therapy, higher blood flow rates can be achieved, permitting higher UF rates and urea clearance. The increased blood flow also helps to decrease clotting of the hemofilter. CVVH has the ability to remove larger molecular weight solutes because of the more porous nature of the hemofilter used in this treatment.
What is continuous venovenous hemodialysis?
CVVHD (Fig. 18-5) is similar to CAVHD in principle but, as with CVVH, a blood pump is employed to control the blood flow rate. Unlike CVVH, CVVHD requires the use of dialysate running countercurrent to the blood flow through the extracorporeal circuit. The indications for CVVHD are the same as for CAVHD. Intermittent hemodialysis would be insufficient therapy for these patients, plus they may be too unstable to tolerate aggressive hemodialysis.
Figure 18-5 Continuous venovenous hemodialysis (CVVHD).
(From Lewis SM, Heitkemper MM, Dirksen SR: Medical-surgical nursing, ed 7, St. Louis, 2007, Mosby.)
What are the primary advantages of cvvh or cvvhd over cavh or cavhd?
Arteriovenous extracorporeal circuits require the prolonged cannulation of an artery. This can lead to compromised blood flow to the extremities, infection, and impaired ability to move the patient. Venovenous extracorporeal circuits do not require use of an artery. A single dual lumen catheter can be used. Preferred sites are the subclavian or internal jugular vein. Blood flow through the hemofilter is consistent and controlled by the nurse, generally between 100 to 200 mL/min.
What are the disadvantages of venovenous access?
CVVH and CVVHD require more bedside equipment that must be monitored by the critical care nurse. In-service education must be provided to assist the critical care nurses to be comfortable with the system.
Is the anticoagulation the same for cavh/cavhd and cvvh/cvvhd?
The entire system must be constantly monitored for changes in pressure, clotting in the dialyzer or lines, and dark streaks in the dialyzer filters. These and frequent blood pump alarms may be warnings of a clotted system. Heparin is the primary anticoagulant used with all approaches of CRRT. Generally a bolus of 500 to 2000 units is administered into the blood circuit upon initiation of therapy, followed by a heparin infusion of 5 to 10 units/kg/h. If ACTs are permitted in the institution, an appropriate range for CRRT would be 150 to 200 seconds. An alternative or adjunct therapy is to routinely flush the hemofilter and blood circuit with normal saline. This may prolong the life of the hemofilter. Trisodium citrate anticoagulation has been used successfully but requires additional monitoring of serum sodium, calcium, and bicarbonate to avoid compromising the patient. Citrate can be used on those patients with an allergy to heparin. Venovenous circuits have fewer clotting problems because of the consistent blood flow.
What are the complications associated with continuous renal replacement therapy?
Patient complications include hypotension, cardiac dysrhythmias, dehydration, electrolyte imbalance, blood loss, infection, and air embolism. There are technical complications that include blood leak, membrane rupture, clotted hemofilter, disconnection of the arterial or venous tubing, equipment malfunction, position of catheters, kinked tubing, and inexperienced personnel.
Who is responsible for continuous renal replacement therapy?
The ideal situation is for the critical care and nephrology professionals to work collaboratively. Generally the nephrologist prescribes the therapy and then shares the monitoring and appropriate interventions with the intensivists. The nephrology nurses set up the system, provide in-service education, assist with nursing interventions (such as catheter dressing changes), and remain on call for troubleshooting or problem solving. The critical care nurses are responsible for 24-hour monitoring, documentation of intake and output, replacement fluids, heparinization, and discontinuing a clotted circuit. CRRT offers an approach that focuses on providing the patient with 24-hour renal replacement, rather than attempting to correct a multitude of problems in a 3- or 4-hour hemodialysis treatment. The delineation of clinical responsibilities must be decided upon before initiating a CRRT program for critically ill patients.
What is sustained low-efficiency dialysis?
Sustained low-efficiency dialysis (SLED) is an AKI modality choice that is becoming increasingly popular, particularly in the intensive care unit setting. It is an acceptable compromise between intermittent hemodialysis and CRRT. It is also known as extended daily dialysis. This form of treatment employs dialysis over a prolonged duration (8 to 12 hours) with modified blood and dialysate flow rates (≤ 200 mL/min blood flow rate and 100 to 300 mL/min dialysate flow rate). Conventional dialysis machines preclude the need for costly CRRT machines, filters, and tubing. Hemodynamic stability is a benefit of SLED, allowing the patient to achieve the desired UF goal. SLED is an alternative for the critically ill patient who has had poor outcomes on intermittent hemodialysis therapy. SLED is a slow and gentle therapy and assists with fluid and electrolyte control and solute clearance.
Other extracorporeal treatment modalities
There are techniques other than dialysis for removing metabolic wastes, toxic materials, and/or excess water. Some of these are very useful in the intensive care unit for the patient with complex problems or multiple organ failure.
What are some of these techniques?
The following three basic modalities are in clinical use:
• Hemofiltration
• Hemoperfusion
• Apheresis
Hemofiltration
What is hemofiltration?
In conventional hemodialysis, diffusion or conductive transfer accounts for the major portion of solute movement across the membrane. The natural kidney in its process of glomerular filtration actually uses UF, or convective transfer. Convective transfer across a synthetic membrane is also used to remove uremic wastes from blood. This is the process of hemofiltration, or diafiltration.
How effective is hemofiltration?
Using membrane or hollow fibers of polyacrylonitrile, polyamide, polysulfone, or polycarbonate, UF of more than 100 mL/min is possible at blood flow rates of 200 to 350 mL/min. If the BUN were 50 mg/dL, that amount of BUN would also be removed in one minute. The removal of creatinine and middle and large molecules, such as β2-microglobulin, with hemofiltration far exceeds that of conventional hemodialysis.
What problems may occur with hemofiltration?
The following problems may occur with hemofiltration:
• The infusion of replacement fluid must be carefully and continually monitored to avoid underhydration or overhydration.
• Blood leak can be a serious hazard when negative pressure is applied to the filtrate bag to enhance UF.
• The serum level of various beneficial medications (antibiotics, cardiac drugs, anticonvulsants) may be adversely altered.
• The essential sterile replacement fluids are expensive.
What are clinical advantages of hemofiltration?
Several low-flow modalities of hemofiltration are useful for critically ill individuals who need multisystem support. Hemofiltration offers the following clinical advantages:
• Hypotension is less of a problem than with hemodialysis, even though a large volume of fluid is removed.
• Disequilibrium and other systems or findings of intracellular osmolar shift are rare.
• Large volumes of parenteral nutrition may be given; fluid balance is maintained at a stable level.
• Improved blood pressure control in hypertensive individuals during periods between treatments has been attributed to better sodium and volume control and to improved autonomic stability.
• Hemofiltration allows removal of harmful substances of large molecular size, such as myocardial depressant factor.
These positive attributes of hemofiltration have resulted in the development of CRRT.
Hemoperfusion
In hemoperfusion blood is brought in direct contact with a sorbent material, packaged in a cartridge or column. Most devices use 70 to 300 g of activated charcoal coated with a polymer film to reduce embolism by tiny carbon particles and to decrease platelet and cellular element buildup.
What are the indications for using hemoperfusion?
Hemoperfusion is used primarily for drug overdose or toxic exposure of great severity. Activated charcoal binds most chemicals in the range of 100 to 20,000 Da. Most medications have molecular weights of 500 to 2000 Da. Hemoperfusion is more effective than hemodialysis for removal of most sedatives, theophylline, digoxin, and some pesticides and herbicides.
In association with deferoxamine chelation, charcoal may be used to remove excess aluminum or iron from body tissue.
What are the adverse effects of hemoperfusion?
A transient decrease in platelets is frequent; it corrects within 24 hours in most instances. Some patients have a fall in white blood cell count. Hemolysis or red blood cell damage is unusual. Hypotension is frequent, as the poisoned patient is already very brittle. Heavy anticoagulation is needed, and postprocedure bleeding may be prolonged.
Is there a limit to the capacity of the cartridges?
Adsorptive capacity of the cartridges is limited and is difficult to determine in advance. The kinetics of adsorption is complex. Overall mass transfer relates to a fluid transfer rate and an intraparticle transfer rate, which depend on microcapillary size and solute diffusion. Clearance of some solutes may decrease gradually over time until the sorbent is filled; for other solutes, clearance may fall off rapidly even though considerable sorbent capacity remains.
Apheresis
The term apheresis is a Greek expression that means “taking something away.” Plasmapheresis has been conducted for a number of years to separate plasma protein components using special centrifuges. Synthetic hollow-fiber technology produces filters of selectively permeable capability to remove specific blood constituents (e.g., antibodies and immunoglobulins).
Plasmapheresis has been used experimentally for a variety of conditions, including transplant rejection by reducing antibody titer. Plasmapheresis removes the plasma portion of the blood where the antibody is located. The blood and albumin are returned to the patient and the normal function of the immune system is unaffected. The technique is of definite value in hyperviscosity syndrome, cryoglobulinemia, thrombotic thrombocytopenic purpura, myasthenia gravis crisis, Guillain-Barré syndrome, refractory idiopathic—or autoimmune—hemolytic anemia, multiple myeloma with renal failure, and Goodpasture syndrome.
What substances can be removed by either dialysis or hemoperfusion?
As a general rule, substances completely or almost completely excreted by the normal kidney will be removed by dialysis. Substances metabolized by the liver, or their by-products, may not be removed by hemodialysis. Information about the site of metabolism and excretion of most drugs is often obtainable from the package insert or from pharmacology texts. The Physicians’ Desk Reference is another quick resource. A computerized textbook of treatment options for drug overdoses and poisonings, or Poisindex, should be available. Information on this system can be very useful because it is updated regularly. Regional poison centers have information on drugs or poisons. The intoxicating substance(s) should be identified and quantified as soon as possible. Often quantitative results may take several hours and are not available when most urgently needed.
What if the substance is not known or cannot be readily verified?
The decision to treat or not treat, and by what modality, becomes a clinical one, to be made by the physician. If the patient is severely ill and the circumstances suggest that one or more of the substances ingested is likely to be removable by hemoperfusion or dialysis, treatment should be started. This is because the duration of coma, morbidity, and mortality may be reduced by early initiation of treatment.
For what toxic agents is dialysis recommended as specific treatment of choice?
Alcohols, such as methyl alcohol and ethylene or propylene glycol (antifreeze), are easily dialyzed. Salicylates (aspirin), lithium carbonate, and aminophylline dialyze well. Certain mushrooms (Amanita phalloides) call for immediate hemodialysis therapy. Early removal of toxins may prevent the blindness, liver necrosis, renal failure, or death that can result from such poisons. Accidental therapeutic intravenous drug overdose from such agents as theophylline, antibiotics, or mannitol may require emergent dialysis to decrease the risk of serious complications.
Is there any particular type of dialyzer preferable for poisonings?
In cases of poisoning, the objective is to remove as much of the offending agent as rapidly as possible. Therefore a dialyzer with the largest surface area the patient will tolerate should be used. High-middle molecule clearance devices (i.e., 500 to 20,000 Da) may be the dialyzer of choice.
What poisonings are best treated by charcoal hemoperfusion?
Sedatives, including barbiturates, ethchlorvynol, and glutethimide, and many insecticides and herbicides have better removal by hemoperfusion than by hemodialysis.
What about bloodstream access for dialysis of poisons?
The most appropriate access, if the patient does not already have a permanent vascular access, is a temporary catheter placed in a large vein, such as femoral, subclavian, or internal jugular. The greater the blood flow, the greater the removal of toxins.
Does peritoneal dialysis have any place in the treatment of poisoning?
Peritoneal dialysis is rarely appropriate in the treatment of poisoning, and only if hemodialysis is not available or will be delayed. Peritoneal dialysis has low clearance rates and takes longer to remove drugs than hemodialysis and hemoperfusion. However, if preparation for hemodialysis will be delayed, and peritoneal dialysis can be instituted at once, it can be a temporary treatment option.
Should hemodialysis and charcoal hemoperfusion be used together?
Hemoperfusion has a greater affinity and faster clearance for many toxins than does hemodialysis. However, hemoperfusion does not provide the UF that may be needed for hypervolemia or pulmonary edema. Perfusion alone does not correct acid-base imbalance or electrolyte abnormalities, which may be very important in the acidosis associated with many intoxications. Sometimes sequential use of hemodialysis and hemoperfusion is recommended. The appropriate treatment is dictated by the properties of the poison or drug that needs to be removed.
What special patient problems may be encountered in dialysis or hemoperfusion of ingested or intravenous poisons or drug overdoses?
Such patients are generally critically ill, possibly with multisystem failure. Most are hemodynamically unstable. Specific patient problems may include the following:
Hypotension. This responds poorly to volume replacement; infusion of a pressor agent, such as dopamine, is frequently necessary. However, the pressor agent’s effect may be reduced by the dialysis or hemoperfusion.
Respiratory depression or apnea. The patient may have an endotracheal tube or tracheostomy and may require ventilatory assistance equipment.
Severe acid-base imbalance. Patients who have an alkalosis from the drug intoxication may experience worsening of the condition with the dialysis treatment. The amount of bicarbonate in the dialysate may have to be adjusted. Often custom dialysate is required with changes during the treatment.
Dialysis in relation to transplant
Many patients receive dialysis as part of the plan for kidney transplant (see Chapter 20). Dialysis may be initiated immediately pretransplant as preparation for surgery, during surgery, or following transplantation as support because of technical complications or complications during rejection episodes. Patients who require dialysis during posttransplant dysfunction or acute rejection require special treatment considerations.
What is posttransplant kidney dysfunction?
Posttransplant kidney dysfunction is a form of AKI seen occasionally with living donor kidneys and more often with deceased donor kidneys. It is usually related to the length of the “warm and cold ischemia time.” This is the time measured from the kidney removal to its revascularization in the transplanted patient. The mechanism is similar to that of acute tubular necrosis. The kidney usually begins to function in about 10 days, occasionally going as long as 3 to 4 weeks before producing quality urine (see Chapter 20).
Dialysis patients with transplant rejection
What are special problems in the dialysis of posttransplant patients?
Maintenance of fluid balance is essential to the function of the transplanted kidney. Care must be taken not to be overly aggressive with fluid removal; the resulting hypotension could cause hypoperfusion of the new organ and lead to renal dysfunction. In the early postoperative period, such patients have all of the problems of recent major surgery. “No heparin dialysis” should be used to prevent bleeding at the operative site. Because of steroids, patients may be intensely catabolic, with BUN disproportionately high in relation to serum creatinine. Hypertension may be aggravated by steroid treatment. Wound healing may be slow, and some drainage is common. Patients who have lost a transplant to severe rejection usually have been treated with steroids. Their tissues are often edematous and extremely friable. Patients with infections and rejection are almost always catabolic, edematous, and hypoproteinemic. Their cardiopulmonary and cardiovascular systems are often labile, and hypotension or cardiac dysrhythmias and pulmonary congestion should be anticipated.