Fluid and Electrolyte Imbalance - Renal Flashcards
Acute kidney injury onset
sudden - hours to days
AKI percent of nephron involvement
about 50%
AKI duration
2-4 wks; less than 3 months
AKI prognosis
good for return of kidney function with supportive care; high mortality in some situations
Chronic kidney disease onset
gradual - months to years
CKD percent of nephron involvement
90-95%
CKD duration
permanent
CKD prognosis
fatal without renal replacement therapy such as dialysis or transplantation
Prerenal AKI
result from conditions that reduce blood flow to the kidneys
Intrarenal AKI
result from damage to the glomeruli, interstitial tissue, or tubules
Postrenal AKI
result from obstruction of urine flow
Oliguria
Less than 400 mL/day
Anuria
Less than 100 mL/day
Pressure in kidney tubules > glomerular pressure
glomerular filtration stops
General manifestations of intrarenal and postrenal azotemia
generalized edema, weight gain
RIFLE Classification
R - Risk, I - Injury, F - Failure, L - Loss, E - End-stage kidney disease
R - Risk
serum creatinine = 1.5 times above normal;
GFR = decreased by >25% of normal (>90 mL/min);
urine output
I - Injury
serum creatinine = 2.5 times above normal;
GFR = decreased by >50% of normal (60-89 mL/min);
urine output
F - Failure
serum creatinine = 3 times above normal;
GFR = decreased by >50% of normal (30-59 mL/min);
urine output
L - Loss
complete loss of kidney function that persists for >4 wks;
GFR 15-29 mL/min;
no urine output without renal replacement therapy
E - End-stage kidney disease
complete loss of kidney function lasting more than 3 mos;
GFR
Prerenal azotemia
caused by poor blood flow to the kidneys that leads to ischemia in the nephrons
Causes of prerenal azotemia
heart failure, sepsis, shock, PE, anaphylaxis, pericardial tamponade
Reversal of prerenal azotemia
correct blood volume, increase blood pressure, improve cardiac output
Intrarenal AKI
caused by actual physical, chemical, hypoxic, or immunologic damage directly to the kidney tissue
Causes of intrarenal AKI
acute interstitial nephritis, exposure to nephrotoxins, acute glomerular nephritis, vasculitis, acute tubular necrosis, renal artery or vein stenosis or thrombosis, formation of crystals or precipitates in the nephron tubules
Postrenal azotemia
develops from obstruction to the outflow of formed urine anywhere within the kidney or urinary tract
Causes of postrenal azotemia
ureter, bladder, or urethral cancer, kidney, ureter, or bladder stones, bladder atony, prostatic hyperplasia or cancer, urethral stricture, cervical cancer
Prevention of progression to severe level of kidney injury
restore circulating volume, improve cardiac output, increase blood pressure
Manifestations of prerenal azotemia
hypotension, tachycardia, decreased cardiac output, decreased central venous pressure, decreased urine output, lethargy
Renal manifestations of intrarenal and postrenal azotemia
oliguria or anuria
Cardiac manifestations of intrarenal and postrenal azotemia
hypertention, tachycardia, JVD, increased ICP, tall T-waves on ECG
Respiratory manifestations of intrarenal and postrenal azotemia
SOB, orthopnea, crackles, pulmonary edema, friction rub
Gastrointestinal manifestations of intrarenal and postrenal azotemia
anorexia, nausea, vomiting, flank pain
Neurologic manifestations of intrarenal and postrenal azotemia
lethargy, HA, tremors, confusion
General manifestations of intrarenal and postrenal azotemia
generalized edema, weight gain
Serum sodium
136-145 mEq/L; remains normal, increases, or decreases
Serum potassium
3.5-5 mEq/L; increases in kidney disease
Serum phosphorus
3.0-4.5 mg/dL; increases in kidney disease
Serum magnesium
1.3-2.1 mEq/L; increases in kidney disease
Serum bicarbonate
23-30 mEq/L; decreases in kidney disease
Arterial blood pH
7.35-7.45; decreases in metabolic acidosis, or remains normal
Arterial blood HCO3
21-28 mEq/L; decreases in kidney disease
Arterial blood PaCO2
35-45 mm Hg; decreases in kidney disease
Hemoglobin
12-18 g/dL; decreases in kidney disease
Hematocrit
37-52%; decreases to 20% in kidney disease
Blood osmolarity
285-295 mOsm/kg; increases in volume depleted states
X-rays
check the size of the kidneys; may show stones
Renal ultrasonography
diagnosis of urinary tract obstruction; dilation of the renal calyces and collecting ducts, and visualization of stones; shows kidney size and patency of ureters
CT scans without contrast dye
identifies obstruction or tumors
Continuous arteriovenous hemofiltration with dialysis (CAVHD)
dialysate delivery system removes waste products in addition to plasma water; used in pts with limited CO, severe hypotension, those who don’t respond to diuretic therapy
Renal scan
determine whether blood flow to the kidneys is sufficient
Cytoscopy/retrograde pyelography
identify obstructions of lower urinary tract
Kidney biopsy
performed if the cause of AKI is uncertain, immunologic disease is suspected, or if the reversibility needs to be determined
Diuretics (furosemide)
administered to pt without fluid overload; discontinued if diagnosed with oliguric kidney injury; monitor for signs of fluid overload
Calcium Channel Blockers
used to treat AKI resulting from nephrotoxic acute tubular necrosis; prevents the movement of Ca into the kidney cells, maintain kidney cell integrity, and improves the GFR by improving kidney blood flow
Vitamins/minerals (folic acid, FeSO4)
when on dialysis essential vitamins and minerals are removed from the blood; replacement is needed to prevent deficiencies; teach to take after dialysis, take iron with meals and to take stool softeners with iron
Synthetic erythropoietin (epoetin alfa, darbopoetin alfa)
prevents anemia by stimulating RBC growth and maturation in bone marrow; teach to have Hgb monitored weekly
Phosphate binders (aluminum hydroxide gel, aluminum carbonate gel)
high blood phosphate levels cause hypocalcemia and osteogystrophy; lowers serum phosphate by binding phosphorus present in food; teach to take with meals, separate digoxin by 2 hrs, take stool softeners, and report muscle weakness, slow or irregular pulse, or confusion
Cardiac glycosides (digoxin)
used when heart failure induces kidney injury/disease or makes it worse; improves ventricular contraction, increasing stroke volume and cardiac output; teach to check HR daily and not to take antacids within 2 hrs of digoxin
Dialysis therapy
used for pts with L and E levels of AKI; indications include uremia, persistent high K+, metabolic acidosis continued fluid overload, uremic pericarditis, and encephalopathy
Hemodialysis lasting several weeks vascular access
subclavian, internal jugular vein or femoral vein (for 1 or 2 treatments)
Subclavian vascular access for HD
inserted at the bedside; covered with sterile dressing; monitor for pneumothorax and subcutaneous emphysema; checked by X-ray before use
Femoral vascular access for HD
avoided for more than 1 or 2 HD treatments d/t restrictions of mobility, hematomas, and infection
Internal jugular vascular access
segment of catheter within the subcutaneous tissue before the jugular vein reduces risk of infection; placed in the radiology dept
Hemodialysis catheter
has 2 lumens (inflow/outflow); 3 lumen is available for drawing venous blood or giving drugs and fluid without interrupting HD
Peritoneal dialysis
uses the peritoneum as the dialyzing membrane; dialysate is infused through a catheter implanted in the peritoneum; fluid stays in cavity for specified time; fluid drains into a drainage bag; repeated as physician prescribes
Continuous Renal Replacement Therapy (CRRT)
better tolerated than HD for critically ill pts because it avoids rapid shifts of fluids and electolytes
Continuous venovenous hemofiltration (CVVH)
used with critically ill pts; powered by a pump; pump increases risk for air embolus; requires the use of anticoagulants; used in critical care units; pts require more continuous nursing care
Continuous venovenous hemodiafiltration (CVVHD)
uses infusion pump, hemodialysis membrane, and dialysate solution; adds the dialysis membrane and dialysate soln instead of just filtering the blood; increases the efficiency of removing waste products; less efficient than CVVH; fewer adverse changes in blood volume and blood pressure
Continuous arteriovenous hemofiltration (CAVH)
for pts with fluid volume overload, resistant to diuretics, have unstable BP and CO; placement of arterial and venous catheters; MAP must be at least 60; continuously removes plasma water, wastes, and electrolytes; risk for bleeding caused by anticoagulants used to prevent membrane clotting
Continuous arteriovenous hemofiltration with dialysis (CAVHD)
dialysate delivery system removes wast products in addition to plasma water; used in pts with limited CO, severe hypotension, those who don’t respond to diuretic therapy
Chronic kidney disease
progressive, irreversible disorder and kidney function does not recover
Azotemia
buildup of nitrogen-based wastes in the blood
Uremia
azotemia with clinical symptoms (metallic taste, anorexia, n/v, muscle cramps, “frost” on skin, itching, fatigue, lethargy, hiccups, edema, dyspnea, paresthesias)
Main causes of ESKD
hypertension and diabetes mellitus; infection and genetic kidney disease
Appearance of urine
note any changes in color, clarity, or odor
Change in frequency or volume of urine passage
more or less frequent voiding not associated with changes in fluid intake may signal potential problems
Discomfort or distress
pain, burning, urgency, aching, or difficulty with initiating urine flow or complete bladder emptying is of concern
Carbonated soft drinks
decrease intake
Kidney function
periodically ask for provider to measure your kidney function with a serum creatinine and urinalysis
Hx of kidney disease, DM, HTN, or family hx of kidney disease
know serum creatinine level and 24-hr creatinine clearance
If identified as having decreased kidney function
ask about whether drugs, diet, diagnostic tests, or therapeutic procedure will present risk to kidney function
Neurological manifestations of CKD
lethargy, inability to concentrate, seizures, coma, slurred speech, asterixis, tremors, twitching, or jerking movements, myoclonus, ataxia, paresthesias
Cardiovascular manifestations of CKD
cardiomyopathy, HTN, peripheral edema, heart failure, uremic pericarditis, pericardial effusion or friction rub, cardiac tamponade
Respiratory manifestations of CKD
uremic halitosis, tachypnea, deep sighing, yawning, Kussmaul respirations, uremic pneumonitis, SOB, pulmonary edema, pleural effusion, depressed cough reflex, crackles
Hematologic manifestations of CKD
anemia, abnormal bleeding and bruising
Gastrointestinal manifestations of CKD
anorexia, n/v, metallic taste, changes in taste acuity and sensation, uremic colitis, constipation, uremic gastritis, uremic fetor, stomatitis
Urinary manifestations of CKD
polyuria, nocturia (early), oliguria, anuria (late), proteinuria, hematuria, diluted straw-colored appearance (early), concentrated cloudy appearance (late)
Integumentary manifestations of CKD
decreased skin turgor, yellow-gray pallor, dry skin, pruritis, ecchymosis, purpura, soft tissue calcifications, uremeic frost
Musculoskeletal manifestations of CKD
muscle weakness and cramping, bone pain, pathologic fractures, renal osteodystrophy
Reproductive manifestations of CKD
decreased fertility, infrequent or missed menses, decreased libido, impotence
Psychosocial assessment of CKD
ask about pts understanding of diagnosis, assess for anxiety and coping styles; requires ongoing psychosocial assessment
FOC: fluid overload
r/t inability of diseased kidneys to maintain body fluid balance; monitor input/output, hydration status, and fluid overload, daily weight; diuretics; fluid restriction
FOC: potential for pulmonary edema
r/t fluid overload; assess for s/s of pulmonary edema; high fowlers; loop diuretics; morphine sulfate; monitor serum electrolytes, ECG tracings, and O2 sat
FOC: decreased cardiac output
r/t reduced stroke volume, dysrhythmias, fluid overload, and increased peripheral vascular resistance; ACEI, ARBs, CCBs; teach to measure BP daily, weigh daily; monitor for manifestations of decreased cardiac output, heart failure, and dysrhythmias
FOC: inadequate nutrition
r/t inability to ingest, digest food, or absorb nutrients as a result of physiologic factors; protein, sodium, potassium, and phosphorus restriction, vitamin supplementation; collaborate with dietitian, give written examples of diet
FOC: potential for infection
r/t skin breakdown, chronic disease, or malnutrition; provide meticulous care where skin is not intact, provide preventative skin care where skin is intact, inspect vascular access site every shift, monitor VS
FOC: potential for injury
r/t effects of kidney disease on bone density, blood clotting, and drug elimination; use lift sheet, observe ROM, unusual surface bumps, depressions over bones; get detailed drug history, assess for drug toxicity
FOC: fatigue
r/t kidney disease, anemia, and reduced energy production; avoid vitamin/mineral supplementation before HD; anemic pt is treated with erythropoietin
FOC: anxiety
r/t threat to or change in health status, economic status, relationships, role function, situational crisis, threat of death, lack of knowledge, loss of control, or disrupted family life; coordinate health care team, perform ongoing assessment of pts anxiety level, observe cues indicating anxiety, evaluate the support system; explain all procedures, tests, and treatments, provide education; encourage pt to discuss current problems, concerns, questions, and fears
Most pts require about 12 hrs/week of total dialysis time
usually divided into 3 4-hr treatments
Prevention of blood clots within the dialyzer
anticoagulation therapy; heparin is most common; pts receiving erythropoietin may need add’l heparin
Heparin during dialysis
remains active in body for 4-6 hrs after HD tx; pt is at risk for hemorrhage during this time; avoid invasive procedures for 6 hrs; protamine sulfate is antidote
AV fistula
long-term vascular access formed by surgically connecting an artery to a vein; most often used are the radial or brachial artery and the cephalic vein of non-dominant arm; need maturation time of up to 4 months before use
AV fistula access
cannulate by inserting two needles (one toward venous, one toward arterial)
AV graft
long-term vascular access used when the AV fistula does not develop or when complications limit its use; synthetic material
Precautions of AV fistula/AV graft
assess for circulation; check distal pulses and cap refill; palpate for thrill; auscultate for bruit; skin stretching increases risk for injury in area
Complications of AV fistula/AV graft
thrombosis, stenosis, infection, aneurysm, ischemia, heart failure
Care for pt with AV fistula/AV graft
no BP readings, venipunctures or IV lines in accessed arm; elevate postop; encourage ROM; check for bleeding at needle insertion sites; assess for s/s infections; no heavy objects; sleep on non-accessed side
Post-dialysis care
Monitor for hypotension, HA, nausea, malaise, vomiting, dizziness, muscle cramps, VS, hemorrhage
Dialysis disequilibrium syndrome
caused by rapid decrease in fluid volume ad BUN levels during HD; can cause cerebral edema and increased ICP
Infectious diseases
transmitted by blood transfusion in long-term HD; most common are hepatitis and HIV
Continuous ambulatory peritoneal dialysis (CAPD)
infusion of 4 2-L exchanges of dialysate into the peritoneal cavity; remains for 4-8 hrs; 7 days/week; no machine necessary; allows constant removal of fluid and wastes; resembles kidney action more closely than HD
Continuous-cycle peritoneal dialysis (CCPD)
automated cycling machine; exchanges occur at night; final exchange is left to dwell during the day and is drained the next night
Automated peritoneal dialysis (APD)
uses cycling machine for dialysate inflow, dwell, and outflow according to preset times and volumes; 30-minute exchanges for 8-10 hrs; can be done while pt sleeps
Intermittent peritoneal dialysis (IPD)
combines osmotic pressure gradients with true dialysis; 30-40 exchanges of 2L 3x/week; can be automated or manual
Complication: Peritonitis
major complication of PD; common cause is connection site contamination; use sterile technique when caring for, hooking up, or clamping off
Peritonitis manifestations
cloudy dialysate outflow (first sign), fever, abd tenderness, abd pain, general malaise, n/v; when suspected send specimen for culture and sensitivity, gram stain, and cell count
Complication: pain
common; no longer occurs after a week or two of PD; warm dialysate bags before instillation (no microwaving)
Complication: exit site and tunnel infections
difficult to treat and can become chronic; dialysate leakage and pulling or twisting of catheter increase risk; gram stain and culture should be performed when exit sites have purulent drainage
Tunnel infection manifestations
redness, tenderness, and pain; treated with antimicrobials; deep cuff infection may require catheter removal
Complication: poor dialysate flow
usually r/t constipation; kinked or clamped connection tubing, pts position, fibrin clot formation, catheter displacement
Complication: dialysate leakage
clear fluid coming from catheter exit site; may take pts 1-2 weeks to tolerate a full 2L exchange without leakage; occurs more often in obese pts, diabetics, older adults, and long-term steroid therapy
Other complications
bleeding, bowel perforation (brown effluent), may be blood tinged when PD is first started, bladder perforation (same color outflow as urine and same glucose level), infection (cloudy or opaque effluent)
Nursing care for PD
mask, wash hands, done sterile gloves, remove old dressing, remove contaminated gloves; assess for signs of infection; use aseptic technique, don sterile gloves, clean around catheter site; apply pre-cut gauze over catheter site and tape edges only
Nursing care during PD
VS, breath sounds, and weight before; continually monitor during, VS every 15-30 min, signs of resp distress, pain, or discomfort; outflow pattern should be a continuous stream after the clamp is completely open; measure total outflow after each exchange, inflow/outflow records; weigh daily to monitor fluid status
Exclusion criteria for kidney transplant
advanced uncorrectable cardiac disease, metastatic cancer, chronic infection, alcoholism, chemical dependency
Physical criteria for kidney donor
absence of systemic disease and infection, no hx of cancer, no htn or kidney disease, adequate kidney function
