Acute Renal Failure– Reversable- Sudden and almost complete loss of kidney fxn over hours to days.
Increase in serum creatnine and BUN
3 Types ARF:
Pre-Renal– This is everything before the kidneys-ex. Hypovolemia/dehydration, hemorrhage, renal losses-diuretics, vomiting, diarrhea, prolonged fever (sepsis), n/v, hypotension, decreased c.o., MI, diabetes type 1 and type 2. Is the result of impaired blood flow that leads to hypoperfusion of the kidney and a decrease in the GFR.
Intra-renal– Also called ARF or ATN-this is when there is damage to the kidney that causes a nephritic infection. Ex. Medications such as nephrotoxic episodes, (gentimyacin, NSAIDS), transfusion reaction, hypercalcemia, and trauma..
Post-renal– This is after the kidneys and is usually the result of an obstruction somewhere distal to the kidney. Pressure rises in the kidney tubules and eventually, the GFR decreases. Ex: infection in the ureters or bladder such as stones, obstruction, tumor or stricture, BPH, or a blood clot.
Phases of ARF:
Initiation phase– (onset)- Begins with the initial insult and ends when oliguria develops.
increase in BUN and Creatinine that can last hours to days.
Urine output is 30 ml or less per hour- 50% of the pts. Are noted to be oliguric
Oliguric phase– Decrease in urine output approx. 100-400 ml/24 hours. It doesn’t respond to fluid challenges and diuretics.
increase in creatinine, BUN, Potassium, and Magnesium.
Decrease in bicarb and calcium, and GFR.
F&E abnormalities, and metabolic acidosis.
Can last from 1-2 weeks.
Uremic symptoms first appear and life-threatening conditions such as hyperkalemia develop.
Diuretic phase-Occurs when the source of the obstruction has been removed but there is residual scarring and edema of the renal tubules remains.
A gradual increase in u.o. which signal that GFR has started to recover. The pt. will have a lot of urine in this phase-about 4 L in 24 hours. pt. just can’t concentrate their urine (Increased Specific gravity).
Gradual onset-(2-6 weeks) after the oliguric phase.
Electrolyte losses because they are putting out so much urine.
Monitor them for dehydration-administer crystalloids (D5W or NS) to prevent dehydration.
Monitor their BUN and creatinine levels-these will level off at a lower level and plateau up and plateau down.
GFR will be increased (this increase contributes to the passive loss of electrolytes which requires the admin of IV crystalloids), u.o. will be 2-4 L per day, and the
Recovery period phase-This phase can last up to a year.
Renal tubules begin to function adequately
F&E balance are restored.
GFR has returned to 70% to *0% of normal.
Non-oliguirc phase- May take the place of oliguric phase.
Urine output remains near normal. The pt. still puts out urine but their kidneys are just not working.
Decreased renal function with increasing nitrogen retention, yet actually excrete normal amounts of urine.
This occurs predominantly after exposure of the pt. to nephrotoxic agents.
Assess S&S- fever, dehydration, and sustained hypotension.
Always monitor pt’s labs-if there is a decrease in urine-check specific gravity-the kidney loses the ability to concentrate urine.
Monitor the pt’s fluid status–the best way to monitor this is taking the pt’s weight!! Also take accurate I&O’s
Nephrotoxic meds- such as gentomyacin and tobimyocin, immunoglycosides, contrast dyes. Dr. will take baseline BUN and Creatnine before giving med- will recheck weekly.
Assessment/ Dx of ARF:
History: Ask about voiding (color, clarity, problems, etc). Surgeries or trauma, blood transfusions, HTN or diabetes, meds (otc and prescribed), allergies.
**One of the earliest manifestations of tubular damage is the inability to concentrate urine.
Flat plate of abdomen x-ray – Renal Scan
Renal ultrasound – Renal Angiogram
CT and MAG3 – Renal Biopsy
Creatnine (0.6-1.2)- gradual increase over hours
BUN- (10-20)- value may reach as high as 80-100 within one week
Serum Sodium- pre-renal= low serum Na; intra-renal= high; post-renal= high or normal serum Na.
Serum Potassium– increased
Serum Phosphorous–increased **Everything high
Serum Calcium–decreased except for calcium
Serum Magnesium–increased and gasses**
Arterial Ph–decreased-è metabolic acidosis
arterial blood PaCO2-decreased
glomerular damage–protein in urine
glucose in urine–ph of 5 or 6
Cation Exchange Resins: Kayexalate and Sorbitol-
Both can be given PO or rectally as an enema-the pt. needs to hold onto it as long as possible.
If hemodynamically unstable (low BP, changes in mental status, and dysrrythmias) – give IV D50, insulin, and calcium replacements may be administered to shift potassium back into the cells. They will give pt. 50% dextrose and insulin IV-this pushes the K back into the cells.
Vitamins and minerals– Folic acid and iron. Kidneys produce erythropoietin (hormone that regulates RBC production)-if kidneys are not producing this-pt. will need iron supp-pt. may be anemic.
Biological Response Modifiers–Epogen and procrit-both of these will increase the RBC’s.
Phosphate binders–Amphojel, Renegel and Tums-these meds are absorbed in the GI tract-they don’t cause diarrhea like K. They absorb Phosphate-so Ca levels will rise.
Stool softeners/laxatives–Colace and Dulcolax
Diuretics–Lasix-this is given to improve the renal blood flow-if the pt. is oliguric they should not use it.
Nutrition: No protein- High-carb meals, because carbs have a protein sparing effect; Restricted potassium and phosphorus
Other causes include HTN, glomerular nephritis, certain meds over a long time
There has to be 95% damage to the millions of nephrons to be dx with CRF.
Normal GFR is 125 ml/min
Stages in CRF:
Stage 1-GFR > 90 ml/min-normal renal function
Stage 2-GFR 60-89 ml/min- mild decrease in GFR. No build up of waste but nephrons are still working overtime, may have an increase in BP which causes an increase in glomerular pressure on healthy nephrons. There is no S&S of renal failure in this phase.
Stage 3-GFR 30-59 ml/min- moderate decrease in GFR. Will see a build up of waste- Not enough healthy nephrons to prevent it. There is an increase in BUN, creatinine, uric acid and phosphorous. An increase managing fluid volume and an increase in BP and edema. There are F&E changes. **If the pt. can manage their BP and diet, they can slow down the progression.
Stage 4-GFR 15-29 ml/min-there is a severe decrease in GFR.
Stage 5-the GFR is less than 15 ml/min. Will see S&S and kidney failure. ESRF will result from severe F&E imbalances.
Diagnostic findings of CRF:
GFR– The lower the GFR, the more kidney damage is done.
Electrolytes-Na and K-early chronic renal failure-hyponatremic. In the later stages, pt’s are hypernatremic and K will go up.
Acid-base balance-as nephrons die-acid builds up and the pt. gets metabolic acidosis.
Hematological-the pt. is anemic because of a decrease in erythropoietin and RBC
Calcium and phosphorous-these lab values go hand in hand. The lower the Ca values, the more at risk the pt. is for sucking Ca out of the bone and increasing the serum Ca
Effects on phosphate:
phosphate retention àhyperphosphatemia.
Binding of phosphate with calcium. This decreases the serum calcium. The pt. is not making good ca because of low Vitamin D. (High phosphate levels=low Ca levels.)
The parathyroid gland releases PTH-the parathyroid gland controls the amount of phosphate excreted. In CRF, the parathyroid gland is not doing its job. So, the more the body secretes PTH, the more Ca is released from the bones. So this gives you an increased serum Ca level which will cause binding of phosphate with calcium and cause metastatic calcification. With increased serum ca levels-crystals can lodge in your heart, brain etc., so it puts you at risk for metastatic calcification(crystal like clots-detrimental to pt’s.)
Effects on calcium
There is a decreased production of vitamin Dà leads to a decreased absorption of calcium from the GI tractà decreased serum calcium levelà causes a release of PTH from the parathyroid gland-which controls the amount of phosphorous excretedà which causes a release of calcium stored in the bonesà leads to an increased serum calcium levelà So there is binding of phosphorous with calcium
Meds for CRF ***KNOW***
Calcium and phosphate binders: **Give both with food**
If calcium is LOW- give Oscal (calcium carbonate) and Phos-lo
If calcium is HIGH – give Renegel
Antihypertensive and CV agents
Lanoxin, Dobutamine, and diuretics
These prevent heart failure and pulmonary edema and control BP
Valium and Dilantin
Give to patient in ESRF
Watch if patient’s sodium is low
Epogen- give 3x a week- SQ or IV
Nutrition with CRF
Protein-restricted; complete proteins only (dairy products, eggs, meats only)
Fluids – 500-600ml more thank the previous days 24-hour urine output
Nursing Interventions with CRF
daily weight- assess for manifestations of volume excess-assess by pt. weight. 1 kg of extra weight=1 liter of fluid. Weigh the pt. at the same time, with the same clothes on the same scale.
fluid restriction-assess the pt. for fluid excess-crackles-they will start at the base of the lungs. The more fluid the pt. retains the more the crackles will move up the lung. S/S include restlessness, agitation, anxious- feels like pt. can’t breathe.
When pt. goes to dialysis hold all meds. Will get meds when they get back from dialysis..
Meticulous/ preventative skin care- due to uremic frost and itching (keep nails cut short)
Inspection of vascular access site
Monitoring of v/s- pt’s temp and heart rate will increase after dialysis.
Cardiac monitor- look at T-waves- cardiac issues- biggest cause of death in pt’s
Pt’s go to dialysis 3x/week.
Works by using passive transfer of toxins by diffusion. Some use anticoagulation (Heparin)- newer machines don’t.
Arteriovenous fistula- the preferred method of permanent access that is created surgically.
Join an artery to a vein usually an anastomosis between the radial artery and cephalic vein.
Most of the time, they will start the pt’s off with a fistula.
Arteriovenous graft- Can be created subcutaneously interposing a biologic (silicone tube) graft material between an artery and vein.
Usually created when the patient’s vessels are not suitable for creation of a fistula.
Acute dialysis- used for QUICK fluid changes
High potassium – Increasing acidosis
Fluid overload – Pericarditis
Pulmonary Edema – Severe confusion
Chronic or Maintenance dialysis
ESRD – fluid overload not responsive to diauretics and fluid restrictions
Presence of uremic S/S affecting all body systems (N/V)
Hyperkalemia – pericardial friction rub
Hemodialysis– Used to extract toxic nitrogenous substances from the blood and to remove excess water.
Used for pt’s not responding to tx.
If the K+ is 7 and not responding to tx such as kayexelate and they can’t get the K+ down, they will start the pt. on dialysis.
If the BUN is too high they will also start dialysis.
If pt. has ARF- this dialysis tx will be short-term
Cath. will be in subclavian or jugular with an inflow/outflow lumen
If pt. only has dialysis 1 or 2 times, will put cath. in femoral artery- not used longterm d/t risk for infection and kinking.
Peritoneal Dialysis– used to remove toxic substances and metabolic wastes and to re-establish normal F&E balance.
May be used for pt’s with renal failure who are unable to undergo hemodialysis or renal x-plant.
Will put dialysate into the abdomen- let it sit and well- then the drainage tube is unclamped and fluid drains from the peritoneal cavity. Uses a Tenkoff catheter
Usually takes 36 to 48 hours to achieve what Hemodialysis accomplishes in 6-8 hours.
High risk for peritonitis- infection comes from insertion site- STERILE technique is used.
Dialysate is warmed prior to administration to prevent discomfort and abdominal pain and to dilate the vessels of the peritoneum to decrease urea clearance.
3 Phases of peritoneal dialysis:
Infusion: 2-3 Liters – takes 5-20 minutes. The docs can add different things to dialysate (ex: insulin, antibiotics, or dextrose- 4.25à the higher the dextrose concentration, the more water will be removed.
Dwell– solution sits in the abd. Cavity for 20-30 mins
Drain– should look colorless, pale, straw with a little blood.
Don’t want to see cloudy fluid- Indicates infection **exam**
Two types of peritoneal dialysis:
Continuous ambulatory PD: 5 different exchanges per day.
Can be done at home-it allows more flexibility and remains in the ab for 4 to 5 hours.
Less extreme fluctuations in the pt’s lab values occur because dialysis is constantly in progress.
Because of protein loss with CAPD, the pt. needs to eat high protein, and increase daily fiber to help prevent constipation, which can impede the flow of dialysate into or out of the peritoneal cavity.
May be asked to limit their carb intake to avoid excessive wt. gain. Potassium, sodium, and fluid restrictions are not normally needed
Continuous cycle PD: This combines overnight intermittent peritoneal dialysis with a prolonged dwell time during the day
Need a very stable pt. to do this.
The peritoneal cath is connected to a cycler machine every evening and the pt receives 3 to 5 exchnages during the night. In the morning the pt. caps off the cath after infusing 2 to 3 L of fresh dialysate. This dialysate remains in the ab cavity until the tubing is reattached to the cycler machine at bedtime
Complications of Peritoneal Dialysis:
Peritonitis/ Infection-this is the most common-due to connection contamination. Characterized by cloudy dialysate, drainage, diffuse abdominal pain, and rebound tenderness. Can teat this by using dextrose alone to clear system and then add ATBX if not helping take out TEEKOFF cath and get rid of catheter.
pain– usually goes away with time. Heat/warm dialysate-wrap in heating pad and then infuse it.
poor dialysate flow-make sure bag is lower, no kinks or blocks in tubing. Constipation can also cause this. Have a good bowel regimen and stool softener. Also have pt. turn from side to side. The catheter should never be pushed further into the peritoneal cavity.
dialysate leakage-this is common at the beginning of dialysis. 1 to 3 L exchange. Body has a hard time adapting to large amounts of volume. Leakage can be avoided by using small volumes (500 ml) of dialysate and then gradually increasing the volume.
Blood tinged drainage is common-if yellow like urine color-pt could have bladder perforation; if brown-pt could have bowel perforation.
Nursing Interventions during PD
always evaluate baseline v.s., weight and lab values before and after treating the pt.
continue to monitor the pt for resp distress, pain and discomfort
always monitor prescribed dwell time and initiate outflow
observe the outflow for amount and pattern of fluid.-document I&O, pt’s response to tx, how long it took the fluid to go in, color that came out, how much fluid came out.
Want to see more fluid come out than you instill (ex: if you put in 3L- you want to see 4L come out). Can use a stronger dextrose solution if you need to pull more fluid off.
Treatment of choice in pt’s with ARF:
Continuous venovenous hemofiltration (CVH)-
don’t have arterial access-
only removes fluid – very slowly
is tolerated better by the patient
It is done in the ICU setting. It is used to manage acute renal failure.
This provides continuous slow fluid removal. Therefore hemodynamic effects are mild and better tolerated by pt’s with unstable conditions.
Continuous Venovenous Hemodialysis ***EXAM***
You will see this used in ******UNSTABLE PATIENTS****
It removes fluid and uremic waste.
Blood is pumped from a double-lumen venous catheter through a hemofilter and returned to the patient through the same catheter.
In addition to the benefits of filtration, CVVHD uses a concentration gradient to facilitate the removal of uremic toxins and fluid. No arterial access is required.
Short term catheters are placed at the bedside and are used for 1-week because of infection. Veins used are subclavian, internal jugular or femoral vein.
Perm caths can last longer. There is a notch/cuff which is used for infection. This helps micro-organisms from entering the wound. Want the notch to be inside the pt.
Complications of dialysis ***EXAM***
atherosclerotic cardiovascular disease-caused by disturbances of lipid metabolism
coronary artery disease
anginal pain/chest pain-occur in pt’s with anemia or arteriosclerotic heart disease
peripheral vascular insufficiency
hypotension-n/v, diaphoresis, tachycardia, dizziness-all S&S of hypotension
painful muscle cramping-this occurs usually late in dialysis as F&E rapidly leave the extra-cellular space
exsanguinations- occurs if blood lines separate or dialysis needle become dislodged
****Dialysis disequilibrium-cerebral fluid shifts-this can cause cerebral edema. S&S include headache, n/v, restlessness, LOC changes (1st symptom), seizures, and death. Can prevent this by having shorter dialysis treatment with lower blood volume shifts. Can cause Increased ICP.
Complications of having a vascular access device, fistula or graft?***EXAM***
Thrombus- **most common** Due to reduced blood flow- due to the muscles in the vein thickening up. They will use decreased doses of TPA to treat.
Infection-usually cause by staph aurus-use sterile technique when accessing a graft.
Aneurysms-repeated needle sticks can weaken the vein/fistula
Ischemia-this is a rarer complication. There is decreased arterial blood flow. See diminished pulses, discoloration, cool skin-this can progress to gangrene if you don’t catch it in time.
Safety measures when a pt. undergoes dialysis
No BP, no blood draws, no IV fluids through fistula
No tight dressings, restraints, or jewelry
Assess bruit or thrill over the site at least every 8 hours-absence may indicate clot or blockage
Assess site for infection-pts with renal disease are more prone to infection-they have low WBC counts, low RBC counts, and impaired platelet function.
Weight is taken before and after dialysis- it’s is a good indication of how dialysis worked.
Drop in weight and drop in blood pressure is good sign- showed it worked.
Glomerulonephritis– inflammation of the capillaries of the glomerulus
Acute: –see more in children
if severe it can progress to acute renal failure.
Most common cause is strep throat. You see this about 2-3 weeks after the infection.
The kidney becomes large, edematous, and congested.
Can also see this after viral infections but not as common.
S/S: hematuria-blood in urine-coca cola urine, proteinuria-protein in urine, edema-will see this in orbital area, face and hands-watch out for fluid overload and SOB, HTN, Azotemia-this is the build up of urea and nitrogenous waste
Labs: Decreased GFR, blood and protein in urine, increased BUN and creatinine, hypoalbumin-pt. losing all protein, urine output will decrease-may do renal biopsy to make a definitive diagnosis, anemia may be present
Tx: infection management-treat the pt. with ANTBX-penicillin, arythromycin, zithromycin-use good hygiene to prevent spread of this. May also use steroids and immunosuppressants. Prevent complications with diuretics(get rid of protein-prevent fluid overload-also helps with HTN and edema); Na, H2O, K and protein restrictions(pt. needs a diet high in carbs-give energy and decrease the catabolism (break down) of protein; dialysis and plasmapheresis(usually if pt. has fluid overload and uremic symptoms-take off fluid and antibodies if immunosuppressive component);pt. education-teach diet and nutrition-teach that if the pt. has a sore throat then he needs to take an ANTBX.
Chronic-This will progress to renal failure.
The cause includes repeated episodes of acute glomerular nephritis, hypertensive nephrosclerosis (hardening of renal arteries) hyperlipidemia and other causes of glomerular damage.
The pt. may be without symptoms for years.
S/S: first symptoms-sudden nose bleed, stroke or seizure, swollen feet at night, gradual weight loss, decreased strength, increased irritability, confusion, nocturis-getting up more at night to go to the bathroom, complain of HA and dizziness, will look poorly nourished, skin-yellow.grayish color, orbital edema, s&s of heart (or renal) failure
Labs: decreased urine output, protein and RBC’s in urine, increased K and phosphorous, decreased GFR, increased BUN and creatinine, may be anemic because of epotien, metabolic acidosis, decreased serum calcium
NI’s- slow the progression of the disease, prevent complications through management of symptoms-if pt has hypertension-reduce BP with sodium and water restrictions, high carbs and good complete proteins (eggs and dairy products), restrict K and Na, have pt. limit fluid intake-monitor it along with weight daily, the pt. may or may not use diuretics as drug therapy. Will be on anti-HTN meds, dialysis and transplant is needed for the pt. to survive.
Nephrotic Syndrome: Increased glomerular permeability that allows larger molecules to pass through the membrane into the urine and be removed from the blood.
An immune or inflammatory response (ex. Lupus, multiple myloma).
Cluster of findings r/t this syndrome including proteinuria (severe loss of protein in urine), hypoalbumemia, edema and hyperlipidemia.
Without treatment this will lead to ESRD
S/S: massive proteinuria, hypoalbuminia, lipiduria-protein and lipids in urine, edema-periorbital and in dependent areas
Tx: use immunosuppressive agents-steroids. ACE inhib and loop diuretics to decrease proteinuria-takes about 6 weeks to be effective. Heparin-.this reduces protein in urine and reduces the risk of renal insufficiency. Diet changes-if the pt. is not hyperkalemic-decrease Na and increase K in diet. This helps get rid of Na and help edema-use ONLY if K is not high! The pt. should be on a low protein diet. Mild diuretics.
Teach Importance of following all medication and dietary regimens so that their condition can remain stable as long as possible.
Treatment of choice for pt’s with ESRD
Live /related donor-pt. will have good urine output after surgery.
If kidney from cadaver-may take 2 weeks for kidney to wake up. If kidney does not produce urine output after surgery, pt may need to go on dialysis until the kidney wakes up.
Make sure pt is free from infection before transplant. Meds are prescribed after surgery to immunosuppress the pt’s immune system so that transplant rejection will not occur.
Pt’s are tx for dental cavities and gingival infections as well (make sure you look in pt’s mouth).
It is preferred to avoid dialysis before transplant.
Meds after transplant:
Cyclosporine (immunosuppressive agent) are used with other medications to prevent transplant rejection
Pt’s receiving cyclosporine may not exhibit the ususal signs and symptoms of acute rejection.
The pt. is closely monitored for infection because of susceptibility to impaired healing and infection r/t immunosuppressive therapy and complications of renal failure.
Tacrolimus (Prograf) similar to cyclosporine and about 100 times more potent. Given in smaller doses than cyclosporine.
Mycophenolate (CellCept)- immunosuppressive. Don’t want to open if pregnant.
Doses are gradually reduced- but the pt is required to take immunosuppressives for the rest of their life.
Risks of meds: *nephrotoxicity*, HTN, hyperlipidemia, hirsutism-excessive hair, tremor, several types of cancer
S/S transplant rejection: fever (one of the first signs), oliguria, edema, increasing BP, weight gain, swelling or tenderness over the transplanted kidney
S/S Infection: shaking chills, fever, rapid heartbeat, tachypnea, increase or decrease in WBC’s-leukocytosis or leucopeniaà need freq. urine cultures.
Chase Urine: ***EXAM*** The pts. will need a lot of IV fluids. Need to adjust the IV fluids based on what the pt’s urine output is. Check urine output every 1 to 2 hours and follow protocol. Keep the kidney good and hydrated!!!