Chapter 71: Care Of Pts With Acute And Chronic Kidney Disease

Question 1

Azotemia

Answer 1

˜Azotemia is the retention and buildup of nitrogenous wastes in the blood.
˜
Prerenal azotemia is kidney injury caused by poor blood flow to the kidneys. Usually caused by hypovolemic shock and heart failure. Bowel preparation, NPO, and fluid lost during surgery can cause this.

Question 2

Causes of AKI

Answer 2

˜Causes: The most common problems leading to AKI are:
ØHypovolemic shock
ØHeart failure
˜Early AKI (levels R & I-see table 71-2) often can be reversed by correcting blood volume, increasing blood pressure, and improving cardiac output. When the reduced blood flow is prolonged, the kidneys are severely damaged and intrarenal kidney injury results.

Question 3

Intra and post renal AKI

Answer 3

˜Intrarenal AKI is often referred to as oliguric AKI in the clinical setting (infections, bacteria, viral, fungi), drugs especially aminoglycoside antibiotics and NSAIDs), invading tumors can cause acute interstitial nephritis.

˜Postrenal azotemia develops from obstruction to the outflow of formed urine anywhere within the kidney or urinary tract.

Question 4

Nonoliguric AKI

Answer 4

˜Nonoliguric form of AKI in which urine output remains near normal but serum creatinine levels rise. Interventions are to restore circulating volume, improve cardiac output, and increase blood pressure to prevent progression to a more severe level of kidney injury.

Question 5

Phases of AKI

Answer 5

˜Rapid decrease in kidney function lead to collection of metabolic wastes in the body
˜Phases (see table 71-4)
ØOnset phase begins with precipitating event and continues until oligurai develops. Last hours to days
ØOliguric characterized by a urine output of 100-400 ml?24 hours that does not respond to fluid challenges or diuretics. Lasts 1-3 weeks.
ØDiuretic often has a sudden onset within 2-6 weeks after oliguric stage. Urine flow increases rapidly over a period of several days. The diuresis can result in an output of up to 10 L/day of dilute urine
ØRecovery in this phase the patient begins to return to normal levels of activity. Complete recovery may take up to 12 months
˜Acute syndrome may be reversible with prompt intervention

Question 6

Manifestations of acute renal failure

Answer 6

They are related to the buildup of nitrogenous waste/azotemia As well as the underlying cause.

Prerenal azotemia are hypotension, tachycardia, decreased urine output, decreased cardiac output, decreased central venous pressure, lethargy. Similar to heart failure or dehydration

Intrarenal include oliguria or anuria, edema, hypertension, tachycardia, shortness of breath, distended neck veins, elevated central venous pressure, weight gain, respiratory crackles, anorexia, nausea and vomiting, lethargy, ECG changes from electrolyte imbalance.

Post Reno olguria or intermittent anuria, symptoms of uremia, lethargy. Report changes in urine stream or difficulty starting urination.

See chart 71-1 pg 1604

Question 7

Interventions AKI

Answer 7

˜Nursing interventions for:
ØElectrolyte imbalances
ØThe patient with AKI may move from the oliguric phase (in which fluid and electrolytes are retained) to the diuretic phase. In the oliguric phase, the plan of care focuses on close monitoring for life-threatening electrolyte changes and nitrogen retention that may require intervention. During the diuretic phase, hypovelemia and electrolyte loss are the main problems. The patient in the diuretic phase of AKI needs a plan of care that focuses on fluid and electrolyte replacement and monitoring.
ØNutritional considerations
•Patients with AKI often have a high rate of protein breakdown. The cause of this is unknown. Need adequate caloric intake of protein, sodium, and fluids. For patient who does not require dialysis 40 g/day of protein, 60 to 90 mEq/day, if high blood potassium levels present, restrict dietary potassium to 60 to 70 mEq/day. The amount of fluid permitted is calculated to be equal to urine volume plus 500 mL.
•If too ill to eat, nutritional support such as TPN or hyperalimentation.
ØDialysis therapies
ØHemodialysis and peritoneal dialysis are used for patients with AKI. Indications for dialysis use include the presence of uremia, persistent high potassium levels, metabolic acidosis, continued fluid overload, uremic pericarditis, and encephalopathy.

Teach patients continuing dialysis to limit foods high in potassium and sodium and to observe protein restrictions. Teach about fluid intake limitation.

Question 8

Med therapy for AKI

Answer 8

˜Preazotemia, fluid challenges and diuretics are often used to promote kidney blood flow. In patient without fluid overload, 500 ml to 1000 mL if NS may be infused over 1 hour. The patient responds by producing urine soon after the initial bolus. Diuretics such as Lasix may be prescribed. Assess for I & O may be at risk for hypovolemia due to increased urine output.
˜Oliguric kidney is diagnosed, the fluid challenges and diuretics are discontinued. Will require CVP monitoring or measurement of pulmonary arterial pressure by means of a pulmonary artery catheter for accurate evaluation of hemodynamic status. Watch for signs of fluid overload.
˜Calcium channel blockers may be used and work by preventing the movement of calcium into the kidney cells, maintain kidney cell integrity, and improve glomerular filtration rate by improving kidney flow.

Question 9

Health promotion and maintenance for acute renal failure

Answer 9

Severe volume depletion can lead to renal failure. Urge all people to drink at least 2 to 3 L of fluid daily, especially athletes. In the hospital early recognize signs by physical assessment and laboratory values. Accurately measure I and O. Check bodyweight. Decreased specific gravity is the earliest sign of renal tubular damage. Be aware of nephrotoxic substances.

Question 10

Continuous renal replacement therapy

Answer 10

The standard for acute renal failure. They are tolerated better than hemodialysis for critically ill patients. There used is temporary. They are used for patients who have fluid volume overload, are resistant to diuretics, have unstable blood pressures and cardiac output.

They must have a map of at least 60. Requires an arterial and a venous catheter. There is a risk for bleeding caused by anticoagulants.

Question 11

Pathophysiology of chronic kidney disease

Answer 11

˜Progressive, irreversible kidney injury; kidney function does not recover
˜When kidney function is too poor to sustain life, CKD becomes end-stage kidney disease (ESKD)
˜Azotemia (buildup of nitrogen-based wastes in the blood)
˜Uremia (azotemia with clinical symptoms)
˜Uremic syndrome

The two main causes are hypertension and diabetes mellitus. Infection and genetic can lead to it. African-American patients are four times higher because of their hypertension.

Question 12

Uremia

Answer 12

Azotemia: Build up of nitrogen-based wastes in the blood

Azotemia with clinical symptoms such as metallic taste in the mouth, anorexia, nausea and vomiting, muscle cramps, itching, fatigue, lethargy, hiccups, edema, dyspnea, paresthesias

Question 13

Stages of CKD

Answer 13

5 stages:

1. At risk; normal kidney function and GFR (> 90 ml/min)and no kidney disease, however, reduced renal reserve in which reduced kidney function occurs without buildup of wastes in the blood because the unaffected nephrons overwork to compensate for the diseased nephrons. Stress such as infection, fluid overload, pregnancy, or dehydration can appear to reduce kidney function.
2. Mild CKD, GFR (60-89)is reduced and kidney nephron damage has occurred, and may be slight elevations of metabolic wastes in the blood because not enough healthy nephrons remain to compensate completely for the damaged nephrons. Increased output of dilute urine. Manage fluid volume, blood pressure, electrolytes, dietary intake, and other diseases can prevent further damage and slow progression
3. Moderate CKD, GFR (30-59) reduction continues and nephron damage has continued ,and the remaining nephrons cannot manage metabolic wastes, fluid balance, and electrolyte balance. Restriction of fluids. Proteins, and electrolytes is needs.
4. Severe CKD GFR continues to decline and interventions are to manage complications, and prepare for eventual renal replacement therapy
5. End-stage kidney disease (ESKD) excessive amounts of urea and creatinine build up in the blood, and the kidneys cannot maintain homeostasis. Severe fluid., electrolyte, and acid-base imbalances occur. Without renal replacement therapy, fatal complications occur.

Question 14

CKD kidney changes

Answer 14

Kidney dysfunction with greatly reduced GFR causes many problems, including abnormal urine production, poor water excretion, electrolyte imbalances, and metabolic abnormalities. As disease progresses, the ability to produce dilute urine is reduced. As kidney function continues to decline, the BUN increases and urine output decreases. The patient is at risk for fluid overload.
˜

Question 15

CKI metabolic changes

Answer 15

Metabolic changes include urea and creatinine excretion are disrupted by kidney dysfunction. Creatinine comes from proteins present in skeletal muscle. The rate of creatinine excretion depends on the muscle mass, physical activity, and diet. Without major changes in diet or physical activity, the serum creatinine level is constant.

Question 16

CKD electrolyte changes

Answer 16

˜Electrolyte changes
ØSodium excretion changes are common. Early in CKD the patient is at risk for hyponatremia (sodium depletion) because there are fewer healthy nephrons to reabsorb sodium. Sodium is lost in the urine; the polyuria of early kidney dysfunction also causes sodium loss.
ØIn later stages of CKD, kidney excretion of sodium is reduced as urine production decreases. Then sodium retention and high serum sodium levels (hypernatremia) can occur with only modest increases in dietary sodium intake. Sodium retention causes hypertension and edema.
ØPotassium excretion occurs mainly through the kidney. Any increase in potassium load during the later stages of CKD can lead to hyperkalemia. If urine output is below 500 mL in 24 hours, high serum potassium levels develop quickly reaching 7 to 8 m Eq/L or greater and severe ECG changes result from this elevation and fatal dysrhythmias can occur. Other factors that can contribute to high potassium levels in CKD are ingestion of potassium drugs, failure to restrict dietary potassium, tissue breakdown, blood transfusions, and bleeding or hemorrhage.

˜Calcium and phosphorus balance is disrupted by CKD. In CKD, phosphate retention and a deficiency of active vitamin D disrupt the calcium phosphate balance. CKD reduces phosphate excretion and phosphate levels increase, calcium levels decrease. Bone reabsorption occurs as calcium is released from the bones, reduced production of vitamin D and less calcium absorbed from intestinal tract. Renal osteodystrophy occurs with bone mineral loss that causes bone pain, spinal sclerosis, fractures, bone density loss, osteomalacia, and tooth calcium loss.

Question 17

CKD acid/base changes

Answer 17

ØAcid-base imbalance is affected by CKD. In early stages, blood pH changes little because the remaining healthy nephrons increase their rate of acid excretion. As more nephrons are lost, acid excretion is reduced and metabolic acidosis results. Many factors lead to acidosis in CKD. The kidneys cannot excrete excessive hydrogen ions (acid).
In patients with CKD, ammonium production is decreased and reabsorption of bicarbonate does not occur. The process leads to a buildup of hydrogen ions and reduced levels of bicarbonate (base deficit). High potassium levels further reduce kidney ammonium production and excretion.
As CKD worsens and acid retention increases, increased respiratory action is needed to keep blood pH normal. The respiratory system adjusts or compensates for the increased blood hydrogen ion levels (decreased pH) by increasing the rate and depth of breathing to excrete carbon dioxide through the lungs. This breathing pattern Kussmaul respirations, increases with worsening kidney disease. Although hydrogen ions (acids) can leave the body this way, when too much carbon dioxide is “’blown off” respiratory alkalosis results.

Question 18

CKD cardiac changes

Answer 18

˜Cardiac changes:
Ø Hypertension is common in most patients with CKD
Ø Hyperlipidemia occurs in CKD from changes in fat metabolism that increase triglyceride, total cholesterol, and low density lipoprotein (LDL) levels. Increase risk for coronary artery disease and acute cardiac events
Ø Heart failure CKD increases the workload on the heart as a result anemia, hypertension, and fluid overload. Left ventricular enlargement and heart failure are common.
Ø Pericarditis sac becomes inflamed by uremic toxins or infection. If not treated can lead to pericardial effusion, cardiac tamponade, and death.

Question 19

CKD hematologic changes

Answer 19

˜Hematologic changes such as anemia include decreased erythropoietin level that decreased red blood cell production, decreased RBC survival time resulting from uremia, iron and folic acid deficiencies, and increased bleeding as a result of impaired platelet function

Question 20

CKD GI changes

Answer 20

Uremia affects the entire GI system. The normal flora of the mouth changes with uremia. The mouth contains the enzyme urease, that breaks down into ammonia. The ammonia creates bad breath (halitosis) and mouth inflammation (stomatitis).
Anorexia, n/v, and hiccups are common. Uremic colitis with watery diarrhea and constipation may also be present. Blood loss caused by erosions may lead to hemorrhagic shock from severe GI bleeding

Question 21

Manifestations of CKD

Answer 21

˜Neurologic lethargy and daytime drowsiness, inability to concentrate or decreased attention span, seizures, coma, slurred speech, myoclonus, ataxia, and parathesis
˜Cardiovascular cardiomyopathy, hypertension, peripheral edema, heart failure, uremic pericarditis, pericardial effusion, pericardial friction rub, and cardiac tamponade
˜Respiratory uremic halitosis, tachypnea, deep sighing, yawning, Kussmaul respirations, uremic pneumonitis, SOB, pulmonary edema, pleural effusion, depressed cough reflex
˜Hematologic anemia, abnormal bleeding and bruising
˜Gastrointestinal anorexia, n/v, metallic taste in mouth, changes in taste acuity and sensation, uremic colitis (diarrhea), constipation, uremic gastritis, uremic fetor (breath odor), stomatitis
˜Skeletal muscle weakness, cramping, bone pain, pathologic fractures, renal osteodystrophy
˜Urinary polyuria, nocturia, oliguria, proteinuria, hematuria, diluted, straw-colored appearance, concentrated and cloudy
˜Skin decreased skin turgor, yellow-gray, dry, puritis, ecchymosis, purpura,

Question 22

Assessment CKD

Answer 22

˜Psychosocial: Chronic kidney disease and its treatment disrupt many aspects of a patient’s life. Many patient’s are in denial, experience depression, and anxiety, and it is important the patient and family understand the treatment regimen of diet, drugs, and dialysis. The long term nature of severe CKD and EKSD, the many treatment options, and uncertainties about the course and its treatment require ongoing psychosocial assessment and intervention (i.e., psychiatric nurse practitioner, or other healthcare members to perform psychosocial assessment)

Question 23

Tests for CKD

Answer 23

˜Laboratory: CKD causes extreme changes in many laboratory values. Creatinine, blood urea nitrogen (BUN) sodium, potassium, calcium, phosphate, bicarbonate, hemoglobin, and hematocrit and GFR for trends.
˜Imaging: Few x-ray findings are abnormal with CKD. Long term ESKD kidneys have shrunk except with polycystic disease.
˜Review priority problems in “Analysis”
˜Fluid overload, potential pulmonary edema, decreased cardiac output, inadequate nutrition, potential for infection, potential for injury bone density, blood clotting, drug elimination, fatigue anemia, anxiety.

Question 24

CKD diet changes

Answer 24

˜Dietary restrictions: Vary according to degree of remaining kidney function. Control of protein intake; fluid limitation; restriction of potassium, sodium, and phosphorus intake; vitamin and mineral supplements. Protein restriction will vary if patient is on hemodialysis or peritoneal dialysis.

Question 25

Uremic frost CKD

Answer 25

˜Uremic frost, a layer of urea crystals from evaporated sweat, may appear on the face, eyebrows, axilla, and groin in patients with advanced uremic syndrome. Assess for bruises, purple patches, and rash.

Question 26

CKD musckuloskeletal

Answer 26

˜Muscle strength, energy and fatigue are due to vitamin deficiency, poor nutrition, anemia, and buildup or urea. Patients are given vitamin and mineral supplements due to diet restrictions and vitamin loss due to dialysis. Do not give before dialysis as will be removed and no benefit. Erythropoietin (Epogen, Procrit) is given for anemia to maintain hematocrit of 30%-35%

Question 27

CKD excess fluid

Answer 27

Excess fluid volume monitor the patient’s intake and output and hydration status. Assess for fluid overload (crackles at base of lungs, edema, and distended neck veins). Drug therapy with diuretics to manage fluid retention or help control blood pressure. The increased urine output produced from these drugs helps reduce fluid overload in patients who still have some urine output. Diuretics are seldom used in ESKD after dialysis because kidney function is reduced, these drugs have can have harmful side-effects on remaining kidney cells and on patient’s hearing.
˜Assess fluid status by obtaining daily weights and review intake and output. Daily weight gain in these patients indicates fluid retention rather than true body weight gain.
˜1 kg of weight equals about 1 L of fluid retained. Weigh daily at same time, same scale, same clothes and after voiding.
˜Fluid restriction is often needed and consider all forms oral, IV, gastric tubes over a 24 hour period.
˜Pulmonary edema can result from left-sided heart failure, the heart is unable to eject blood adequately from the left ventricle, leading to an increased pressure in the atrium and in the pulmonary vessels. The increased pressure causes fluid to cross the capillaries into the pulmonary tissue, forming edema.
˜Decreased cardiac output

Question 28

Hemodialysis

Answer 28

Hemodialysis (HD) is the most common renal replacement therapy used with ESKD and kidney failure. Dialysis removes excess fluids and waste products and restores chemical and electrolyte balance. HD involves passing the patient’s blood through artificial semipermeable membrane to perform the filtering and excretion functions of the kidney.
˜Patient selection: Any patient may be considered for HD therapy. Starting this therapy depends on symptoms, not on the glomerular filtration rate (GFR).
˜Dialysis is started immediately for patients who have the following: fluid overload that does not respond to diuretics, pericarditis, uncontrolled hypertension, neurologic problems, and development of bleeding.
˜Most commonly, dialysis is started when uremic manifestations, such as nausea and vomiting, decreased attention span, decreased cognition, worsening anemia, and puritis, are present.
˜Many patients survive for years with HD therapy, and others may live only a few months. How long the individual lives depends on age, the cause of kidney failure, other diseases such as CAD, diabetes and hypertension.
˜Dialysis settings: Patients with CKD may receive HD treatments in many settings, depending on specific needs. Regardless of the setting for therapy, the need for ongoing nursing support to maintain complex and lifesaving treatment.
˜Hospital-based center for recently started treatment or have complicated condition that requires close supervision
˜Community or freestanding HD center for stable patients not requiring intense supervision
˜Complete or partial self-care in an outpatient center of in in-home HD for selected patients. In-home HD least disruptive, most cannot participate in in-home HD because they lack a skilled partner to assist with the therapy and manage the dialysis machine; too stressful

Question 29

Hemodialysis procedure

Answer 29

Procedure: Dialysis works by using the passive transfer of toxins by diffusion. Diffusion is the movement of molecules from an area of higher concentration to an area of lower concentration.
˜When HD is started, blood and dialysate (dialysing solution) flow in opposite directions across an enclosed semipermeable membrane. The dialysate contains a balanced mix of electrolytes and water that closely resemble human plasma. The other side of the membrane is the patient’s blood, which contains nitrogen waste products, excess water, and excess electrolytes. During HD, the waste products move from the blood into the dialysate because of the difference in their concentrations (diffusion).
˜The HD system includes a dialyzer (artificial kidney), dialysate, vascular access routes, and an HD machine
˜Dialysate is made from clear water and chemicals and is free of waste products and drugs. Bacteria and other organisms are too large to pass through the membrane, dialysate is not sterile. Dialysate is warmed to 100° F to prevent hypothermia. Patient’s temperature may rise due to this.
˜The HD machine has alarms to monitor for potential problems, including changes in dialysate temperature, air in the blood tubing, a blood leak in the dialysate compartment, changes in the pressure in either compartment, and changes in composition of the blood or dialysate.
˜The number and length of treatments depends on the amount of wastes and fluid to be removed, the clearance capacity of the dialyzer, and the blood flow rate to and from the machine.
˜Most patients require about 12 hours per week of total dialysis time. This time is divided into three 4-hour treatments. For those with some ongoing urine production 5-6 hour treatments a week may be adequate.
˜If a patient gains large amounts of fluid weight, a longer treatment time may be needed to remove the fluid without hypotension or severe side effects.
˜Anticoagulation: To prevent blood clots from forming within the dialyzer or the blood tubing, anticoagulation is needed during HD treatments. Heparin is the most commonly used drug to prevent clots from forming with blood comes in contact with foreign surfaces.
˜Heparin remains active in the body for 4 to 6 hours after dialysis, making the patient at risk for hemorrhage during and immediately after HD treatments. Invasive procedures must be avoided during that time. Monitor for signs of bleeding and clotting times can be monitored and Protamine sulfate is an antidote to heparin and should always be available in the dialysis setting.

Question 30

Vascular access for hemodialysis

Answer 30

˜Vascular access is required for hemodialysis. The procedure requires the easy availability of a large amount of blood flow: at least 250 to 300 mL/minute, usually for a period of 3 to 4 hours. Normal venous cannulation does not provide this high rate of blood flow.
˜Long-term vascular access is internal for most patients having long-term HD. The two most common choices are an internal arteriovenous (AV) fistula or the AV graft. AV fistulas are formed by surgically connecting an artery to a vein. The vessels most often used are the radial or brachial artery and the cephalic vein of the non-dominant arm.
˜Time is needed for anastomosis for the AV fistula to develop. As the AV fistula “matures,” the increased pressure of the arterial blood flow into the vein causes the vessel walls to thicken. Some fistulas may take up to 4 months after surgery to be ready.
˜Hemodialysis catheter, dual or triple lumen, or AV shunt for temporary access until AV fistula ready. Can be inserted into the subclavian, internal jugular, or femoral vein (only a couple treatments). The lumens of these are smaller than permanent accesses, and more time (4 to 8 hours) is required to complete each dialysis session.
˜Precautions: Some precautions are needed to ensure the functioning of an internal AV fistula or AV graft.
˜1. First assess for adequate circulation in the fistula or graft as well as in the lower portion of the arm.
˜2. Check distal pulses and capillary refill in the arm with the fistula or graft.
˜3. Check for a bruit (swishing sound) by auscultating over access site or a thrill (vibration) by palpating over it.
˜The fistula changes in appearance over time as it dilates, and skin stretching increases the risk for injury in the area.

Question 31

Vascular access complications

Answer 31

˜Because repeated compression can result in the loss of the vascular access, avoid taking the blood pressure or performing venipunctures in the arm with the vascular access. Do not use AV fistula or graft for delivery of IV fluids.
˜Complications: Complications can occur with any type of access. The most common problems are thrombosis or stenosis, infection, aneurysm formation, ischemia, and heart failure.
˜Thrombosis, or clotting of the AV access, is the most frequent complication. Most grafts fail because of high-pressure arterial flow entering the venous system. The vein react by thickening and this occludes blood flow. tPA can be used to dissolve the clot within minutes and a stricture is revealed at the point of where the vein and artery connect. The stricture is corrected by balloon angioplasty.
˜Infection: Most infections of the vascular access are caused by Staphylococcus aureus introduced during cannulation. Use sterile technique during to prevent infection.
˜Aneurysms: Can form in the fistula and are caused by repeated needle punctures at the same site. Rotate needlw insertion sites with each HD treatment. Large aneurysms may cause loss of the fistula’s function and require surgical repair.
˜Ischemia: Occurs in a few patients with vascular access when the fistula decreases arterial blood flow to areas below the fistula. Symptoms include cold or numb fingers to gangrene.
˜Heart failure: The shunting of blood directly from the arterial system to the venous system, through the fistula, can cause heart failure in patients with limited cardiac function. Is rate and fistula can be revised to reduce artrial blood flow.

Question 32

Hemodialysis nursing care

Answer 32

˜Many drugs, such as antibiotics, or dialyzable can be removed from the blood during dialysis and should not be administered just before or during dialysis.
˜Vasoactive drugs can cause hypotension during HD and may be held until after treatment
˜Post dialysis assessment: Closely monitor the patient immediately and for several hours after dialysis for any side effects from treatment. Common problems include:
ØHypotension
ØHeadache
ØNausea, vomiting
ØMalaise, dizziness
ØMuscle cramps or bleeding

Question 33

Complications from hemodialysis

Answer 33

˜Many fluid-related and infectious complications can occur from HD. The most common complications include:
1. Dialysis disequilibrium syndrome may develop during HD or after HD. The cause appears to be the rapid decrease in fluid volume and blood urea nitrogen (BUN) levels during HD. The change in the urea levels can cause cerebral edema and increased intracranial pressure. Neurologic symptoms result of headache, n/v, restlessness, decreased LOC, seizures, coma, or death. Recognition and treatment with anticonvulsants and barbituartes may prevent a life-threatening situation
2. Infectious disease transmitted by blood transfusion are a serious complication of long-term HD. Two of the most serious blood transmitted infections are hepatitis and HIV.
ØHepatitis B & C has decreased because of the use of erythropoietin has reduced the need for blood transfusions to maintain RBC counts.
ØHIV risks reduced by consistent use of Standard Precautions, screening of donated blood for HIV and decreased need for blood.

Question 34

Peritoneal dialysis

Answer 34

Peritoneal dialysis (PD) allows exchanges of wastes, fluids, and electrolytes to occur in the peritoneal cavity. PD is slower than HD, and more time is needed to achieve the same affect. The advantages of PD is more flexibility and freedom is scheduling PD, a machine is not needed for PD, as PD is ambulatory, and there a fewer dietary restrictions
˜PD can be performed on those who are unstable, cannot tolerate anticoagulation, chronic infection, vascular access issues, waiting for VA to mature , older adults, and less hazardous than HD.
˜Procedure: Each PD exchange process consists of three phases: fill, dwell, and drain.
˜1. Involves siliconized rubber catheter placed into abdominal cavity for infusion of dialysate. Usually 1 to 2 L of dialysate is infused by gravity (fill) into the peritoneal space over a 10-20 minute period, according to patient tolerance.
˜2. The fluid stays (dwells) in the cavity for a specified time prescribed.
˜3. The fluid then flows out of the body (drains) by gravity into a drainage bag.
˜This is repeated as prescribed by physician.
˜Dialysate additives: Heparin may be added to the dialysate to prevent clotting of the catheter or tubing. Usually intraperitoneal (IP) heparin is needed only after a new catheter placement or peritonitis. IP heparin is not absorbed systemically and does not affect blood clotting.
˜Other agents that may be given in the dialysate are potassium and antibiotics. Potassium may be added to the dialysate to prevent hypokalemia, and antibiotics for peritonitis. Potassium and antibioitics are not mixed in the same dialysate bag due to interactions may reduce the antibiotic affect.

˜Many types of PD are available:
ØContinuous ambulatory (CAPD) is performed by the patient with the infusion of four 2-L exchanges. Each time the dialysate remains for 4 to 8 hours, and these exchanges occur 7 days a week.
ØAutomated can be used in the acute care setting, the outpatient dialysis center, or the patient’s home. A cycling machine with preset times allows dialysis while sleeping so can be dialysis free during waking hours.
ØIntermittent 3 times weekly
ØContinuous-cycle exchanges occur at night allows for 24 hour dialysis.

Question 35

Complications of temporary vascular access

Answer 35

Pneumothorax: reduce breath sounds, tracheal deviation away from midline, prominence, and poor movement of one side of the chest. Subcutaneous emphysema: crackling, swelling of tissue around the site. Check placement by chest x-ray before using.

Patient being mechanically ventilated may not tolerate abdominal distention that occurs with peritoneal dialysis

Question 36

Complications of peritoneal dialysis

Answer 36

˜Complications are possible with PD, but many can be prevented with meticulous care.
˜Peritonitis due to connection site contamination. Meticulous sterile technique when caring for PD catheter and when hooking up or clamping off dialysate bags.
˜Manifestations of peritonitis include cloudy dialysate outflow (effluent), fever, abdominal tenderness, abdominal pain, general malaise, n/v.
˜Pain during inflow of dialysate is common when patients are first started on PD therapy. Subsides within a week or two. Cold dialysate increases discomfort; warm in heating pad or warming chamber. Do not warm in a microwave!
˜Exit site/tunnel infections (ESIs) are serious complications. The exit site from a PD catheter should be clean, dry, and without pain or inflammation. Leakage, pulling, or twisting of the catheter increase the risk of ESIs
˜Poor dialysate flow is usually related to constipation. To prevent constipation, a bowel preparation is prescribed before placement of the PD. Enemas, high-fiber diet and stool softeners are helpful. Other flow difficulties include kinked or clamped connection tubing, patient’s position, fibrin clot formation, and catheter displacement.
˜Dialysate leakage is seen as clear fluid coming from the catheter exit site. Takes 1-2 weeks to tolerate full exchange and for leakage to stop.
˜Other complications
˜Bleeding which is expected when the catheter is first placed and outflow may be bloody or blood tinged for the first 1-2 weeks. After that the effluent should be clear and light yellow. Document any change color in outflow and notify physician. A C&S may be obtained. Brown colored affluent is a bowel perforation and serious. If outflow is the same color as urine and has the same glucose level, a bladder perforation is probable.
˜Cloudy or opaque effluent indicates infection; send for culture and sensitivity.

Question 37

Nursing care during peritoneal dialysis

Answer 37

˜Before treatment—evaluate baseline vital signs, weight, laboratory tests
˜Continually monitor patient for respiratory distress, pain, discomfort
˜Monitor prescribed dwell time, initiate outflow
˜Observe outflow amount and pattern of fluid

Question 38

Kidney transplant

Answer 38

Dialysis and kidney transplant are life-sustaining treatments for end-stage-kidney disease. Kidney transplant is not considered “a cure.”
˜Candidate selection criteria:
˜Candidates for transplantation must be free of medical problems that might increase the risks from the procedure.
˜Are accepted up to 70 years of age; older than 70 years on an individual basis more complications with older adult
˜Advanced, uncorrectable cardiac disease excluded
˜Metastatic cancer, chronic infection, severe psychosocial problems such as alcoholism or substance abuse, long standing pulmonary disease, certain GI diseases exclude.
˜Diabetes mellitus and other endocrine problems cause greater risks and complications. Determined on an individual basis.

˜Donors may be:
1. Living donors (either related or unrelated to the patient)
2. Non-heart beating donors ( NHBDs)
3. Cadaveric donors
˜The available kidneys are matched on the basis of tissue type similarity between the donor and the recipient.
˜Living donors are most often blood relatives, but unrelated donors have been used
˜NHBDs are persons declared dead by cardiopulmonary criteria. Kidneys from NHBDs are removed (harvested) immediately after death in cases in which patients have previously given consent for organ donation.
˜Cadaveric donors are usually individuals who suffered irreversible brain injury and brain death, most often as a result of trauma. These donors are maintained with mechanical ventilation and must have sufficient renal perfusion for the kidneys to remain viable.

Question 39

Kidney transplantation

Answer 39

Preoperative care: Many issues related to patient health and the actual transplant procedure must be addressed before surgery
˜Immunologic studies: are needed because the major barrier to transplant success after a suitable donor kidney is available is the body’s ability to reject “foreign” tissue. The immunologic process can attack the transplanted kidney and destroy it. Tissue typing is done on all candidates. A donated kidney must come from a donor who is the same blood type as the recipient. The more similar the human leukocyte antigen (HLA) of the donor are to those of the recipient, the more likely the transplant will be successful and rejection will be avoided.

˜Surgical team members for transplantation include circulating and scrub nurses, clinical nurse specialists, transplant surgeons, anesthesiologists, and nephrologists.
˜The patient usually requires dialysis within 24 hours of the surgery, the recipient often receives a blood transfusion before surgery, this procedure increases graft survival of organs from living related donors.
˜Operative procedure: The donor nephrectomy procedures varies depending on whether the donor is a non-heart-beating donor (NHBD), cadaveric donor, or living donor.
˜Living donors 3-4 hour procedure, flank incision, careful to avoid scarring. More pain after surgery and provide psychological support to adjust to loss of body part.
˜Recipient transplantation surgery 4-5 hours. New kidney is placed in right or left anterior iliac fossa for easier connection of the ureter and the renal artery and vein, and easier palpation. Non-functioning kidney remains. Note-if chronic kidney infection or enlarged kidneys (polycystic) will remove as these can cause pain.

Question 40

Postoperative care after kidney transplant

Answer 40

Urologic management: Is essential to graft management. A large bore indwelling (Foley) catheter is placed for accurate measurements of urine output and decompression of the bladder. Decompression prevents stretch on sutures and ureter attachment sites on the bladder.
˜Assessment of hourly urine output x 48 hour: An abrupt decrease in urine output may indicate complications such as rejection, acute kidney injury, thrombosis, or obstruction.
˜Perform routine catheter care, to reduce contamination; the catheter is removed as soon as possible to avoid infection, usually 3-7 days after surgery.
˜Nursing Safety Priority:
˜Notify the physician immediately about hypotension or excessive diuresis in the patient who has had a kidney transplant. Excessive diuresis may cause hypotension; because hypotension reduces blood flow and oxygen to the new kidney, threatening graft survival.

˜Complications:
ØRejection is the most serious complication of transplantation and is the leading cause of graft loss.
ØAcute tubular necrosis after surgery can occur as a result of hypoxic damage when transplantation is delayed after kidney have been harvested.
ØThrombosis of the major renal artery vessels may occur during the first 2 to 3 days after the transplant. A sudden decrease in urine output may signal impaired perfusion.
ØRenal artery stenosis may result in hypertension.
ØOther complications: surgical wound (hematomas, abscesses, and lymphoceles) or urinary tract (ureteral leakage, fistula, or obstruction; stone formation; bladder neck contracture; and graft rupture)
ØImmunosuppressive drug therapy masks usual manifestations of infection. Low grade fevers, mental status changes, and vague reports of discomfort may be the only manifestations of sepsis. Strict aseptic technique and hand washing must be rigorously enforced.
ØImmunosuppressive drugs protect the transplanted organ and are taken by the transplant recipient for the rest of his or her life.
ØPatients taking these drugs are at an increased risk for death by viral, fungal, bacterial, or protozoal infection.
ØPsychosocial preparation for patient and family to help adjust to diagnosis of kidney failure and accept the treatment regimens.
ØMany patients view dialysis as a cure instead of lifelong management. Not unusual for starting HD that patient feels better physically and mood is better and overlook the discomfort and inconvenience of HD (honeymoon period)
ØUse this time to begin health care teaching that uremic symptoms are reduced, and should not expect a complete return to the previous state of well-being.
ØMany patients become discouraged during 1st year of treatment due to the reality of incorporating dialysis into daily life is staggering, and patients become depressed as problems occur. Monitor behavior that contribute to nonadherence, and suggest psychiatric referrals.
ØAfter patients have accepted or become resigned to the chronic aspect of their disease, they attempt to resume previous activities that may not be possible.

Question 41

Pathophysiology of acute kidney injury

Answer 41

˜Pathophysiology
˜Acute kidney injury (AKI) which use to be known as acute renal failure (ARF) is a rapid decrease in kidney function leading to the collection of metabolic wastes in the body.
˜Types:
ØPrerenal: AKI can result from conditions that reduce blood flow to the kidneys (prerenal acute kidney injury)
ØIntrarenal: damage to the glomeruli, interstitial tissue, or tublule (intrarenal/intrinsic acute kidney injury)
ØPostrenal: is obstruction of urine flow (postrenal acute kidney injury)
ØWhen AKI occurs in patients who already have reduced kidney function, it may lead to end-stage kidney disease (ESKD), or it may resolve to nearly the pre-AKI level of kidney function.

If BUN rises faster than the serum creatinine level, the cause is usually related to protein breakdown or volume depletion. When both the BUN and creatinine levels rise and the ratio between the two remains constant, this indicates kidney failure.

Question 45

Erythropoietin/ epogen

Answer 45

Prevent anemia by stimulating red blood cell growth and maturation in the bone marrow.

50 to 100 units per kilogram subcutaneously or IV three times a week for patients on dialysis.

Report chest pain, difficulty breathing, high blood pressure, rapid weight gain, seizures, rash or hives, swelling of the feet or ankles. It can induce cardiovascular problems such as myocardial infarction

Have hemoglobin levels monitored weekly blood viscosity increases, raising blood pressure and increasing the risk for an MI. Dose may need to be reduced to prevent hemoglobin levels higher than 10 to 12.

Question 46

Digoxin/lanoxin

Answer 46

0.0625-0.25 mg orally or IV daily or every other

Used when heart failure induces renal failure or makes it worse. It improves ventricular contraction increasing stroke volume and cardiac output.

Pulse needs to be above 60. It can cause bradycardia. Notify Dr. if changes in color vision such as more yellow color, blurred vision, photophobia, light flashes, halos, changes in behavior, mood, or mental ability, chest pain or palpitations. These are manifestations of toxicity.

Do not take and acids within two hours. They prevent absorption