TOPIC 9: COLLABORATIVE MANAGEMENT OF RENAL FAILURE

REVIEW: KIDNEY FUNCTION

1. Elimination of wastes:
 Urea (end product of protein metabolism), Creatinine (end product of endogenous muscle metabolism) uric acid, toxins,
other wastes
2. Regulates BP (via RAAS)
 If pressure low → kidney retains water, if pressure high → excretes more urine
 Renin is released from juxtaglomerular apparatus of nephron in response to ↓ arterial BP and renal ischemia
3. Erythropoietin production: stimulates production of RBC in bone marrow
 Deficiency of erythropoietin in renal failure → anemia
4. Activates Vit D to utilize Ca
 Vit D is obtained from food intake and by an interaction with cholesterol in skin after exposure to sunlight
o Metabolites of vit D are essential for absorption of Ca+ from GI tract
 2 more reactions (first in liver, then kidneys) are needed for those forms to become active metabolites or steroid hormone
 Pt with renal failure have a deficiency of active metabolite of vit D and manifest problems related to altered Ca+ and
phosphate balance
5. Maintain Acid-base balance: regulates bicarbonate to maintain pH at normal range. In resp distress → kidney compensates
6. Maintain balance of electrolyte levels
7. Urine production & elimination
8. Fluid balance

RENAL FAILURE
 Results in partial or complete impairment of kidney function
 May be acute (AKI) or chronic (CKD) in nature

COMPARISON
AKI CKD
Onset Sudden Gradual, over years
Common Cause ATN (Acute tubular necrosis) Diabetic nephropathy
Diagnostic Criteria Acute ↓ U/O and/or ↑ serum Cr GFR< 60mL/min and/or kidney damage for > 3mths
Reversibility Potentially Progressive & reversible
Mortality High (~60%) (why? - AKI happens in every life- 19-24% (pt on dialysis)
threatening condition e.g. shock, nephrotoxic)
Primary cause of Infection (b/c pt is immunocompromised) CV disease (HF – heart overcompensation for
death prolonged period of time)

AKI (ACUTE KIDNEY INJURY)

 Characterized by abrupt decline in kidney function d/t to an ↑ serum Cr or ↓ in u/o, or both
 Changes are acute & occur over 48 hr period, due to structural or functional change in kidney caused by injury/insult
 Severity of dysfunction may be mild, calling for little intervention, to severe, necessitating RRT (renal replacement therapy)

ETIOLOGY
 severe, prolonged ↓ BP
 severe, prolonged hypovolemia/dehydration
 exposure to a nephrotoxic agent
o NSAIDs (Aspirin, Ibuprofen (Advil/Motrin), Naproxen, celecoxib etc)
o Antibiotics (Aminoglycosides)- gentamycin, vancomycin, neomycin; acetaminophen.
o digoxin, oral glycemic agents (metformin, glyburide), opioids (dilaudid, morphine),
 ARF (acute renal failure) associated with AKI usu develops over hours or days with progressive elevations of BUN, Cr, and
K+ with or without oliguria
 Severe AKI develops in over 60% of Intensive Care Unit (ICU) patients, with mortality rates of 70 to 80%.

CLASSIFICATION: RIFLE CRITERIA (FYI)

 Most commonly used classification systems for renal diseases
 Uses serum Cr, GFR, and u/o to identify
 R = Risk, I = Injury, F = Failure , L = Loss, E = End-stage kidney disease

CAUSES OF AKI
1. Prerenal
 Most common cause of AKI, usually reversible
 Conditions that ↓ renal blood flow → ↓ perfusion and GFR
o Renal tubular and glomerular function is preserved unless prolonged, then → ATN
o Renal hypoperfusion, hypovolemia, ↓BP, vascular obstruction, Low cardiac output, shock (heart not pumping),
GI fluid loss, poor fluid intake, L and R HF, excessive vasodilation, (septicemia, anaphylaxis – fluid shift)
 o vasoactive mediators ie antihypertensives ACE-I, ARBs, epinephrine, ↑Dopamine) → intrarenal vasoconstriction
→ hypoperfusion
o thrombosis & emboli
 Compensation: RAAS, ADH release to attempt to preserve blood flow
 Note: Post-surgical pt have low circulation → nurses need to watch u/o and BP
o Prevention: ensure pt not hypovolemic (may need extra fluid), ambulate to improve circulation
2. Intrarenal:
 Conditions that cause direct damage to renal tissue (parenchyma) → impaired nephron function
 prolonged ischemia,
 nephrotoxins,
 crushed injuries- Hb released from hemolyzed RBC or myoglobin released from necrotic muscle cells (Hb and myoglobin
block tubules causing renal vasoconstriction)
 Acute Tubular Necrosis is most common intrarenal cause and is primarily result of ischemia, nephrotoxins, or sepsis
o Also: damage to glomeruli, tubular or interstitial, glomerulonephritis, tumour lysis syndrome, kidney stones; lupus
 drug induced nephrotoxicity-
o antibiotics Aminoglycosides- (gentamycin, vancomycin, neomycin);,
o contrast-induced nephropathy- d/t to contrast dye- Iodine,
o NSAID (Aspirin, Ibuprofen (Advil/Motrin), Naproxen, celecoxib etc)

3. Postrenal:
 Mechanical obstruction of urinary outflow → urine refluxes back into renal pelvis → impairs kidney function
(hydronephrosis)
o Almost always treatable if identified before permanent damage occurs
 Obstructive nephropathy: BPH/prostate cancer, nephrolithiasis/renal calculi//kidney stones, ureter and bladder tumours,
intra-abdominal and pelvic cancer

CLINICAL MANIFESTATIONS
 AKI resolves quickly unless ATN (acute tubular necrosis) has occurred → prolongs course of AKI. If unresolved → CKD
ATN progresses through 3 Phases
1. Initiation phase: ↑ serum Cr (>106) & BUN (>7.1) and ↓ U/O(<30ml/hr), Metabolic acidosis- Ph <7.35 d/t retention of H+→
important for nurse to identify early

2. oliguric -Maintenance phase: (lasts days-weeks)

A. Urinary output  Most common initial mani: Oliguria (<400mL/day), usu lasts 10-14 days (but can go for months)
changes: o can also see anuria (<100 mL/day), or nonoliguria
o Good renal function- 1500ml urine in 24hrs
 Dilute urine being made but uremic toxins not being removed
  urine sediment may show casts ie RBCs & WBCs, and proteinuria
 High specific gravity d/t dehydration/hypovolemia concentration
B. Fluid volume  From fluid retention → distended neck veins and edema, S3 heart sound (if fluid in circulatory
excess: volume), bounding pulse and HTN, CHF, pulmonary edema, and pericardial and pleural effusions
C. Hyperkalemia (one  d/t impaired kidney ability to regulate & excrete K+
of biggest complications  Massive tissue trauma → release of additional K+ into ECF by damaged cells,
of AKI)  acidosis worsens hyperkalemia (H+ ions enter cells, K+ leaves),
 May see weakness with severe hyperkalemia
 Monitor for cardiac dysrhythmias and ECG: tall, peaked T waves; widening QRS complex; ST
depression/elevation
D. Metabolic acidosis  Kidneys unable to produce ammonia (→ needed for H+ ion excretion)
o Serum bicarb level ↓ (bicarb used up in buffering H+ ions)
o Defective reabsorption and regeneration of bicarbonate
 Kussmaul’s respirations (rapid, deep) to excrete Co2 as compensation for acidosis
 Lethargy and stupor will occur if treatment is not started
E. Sodium Balance  Damaged tubules can’t conserve Na+ → may ↑ Na+ excretion → normal Na+ or hyponatremia
 Avoid excessive salt intake as it can → volume expansion, HTN, CHF
F. Hematological  Anemia secondary to impaired erythropoietin production
disorder  Uremia → ↓ platelet adhesiveness → bleeding from multiple sources (e.g. intestines, brain)
 Altered WBCs → immunodeficiency, infection
G. Ca+ deficit and  Cannot activate Vit D → hypocalcemia → tetany, tingling, numbness
phosphate excess  In response to low Ca+ → PTH causes Ca+ release from bones (damaging bones)
o Phosphate is released as well, leading to hyperphosphatemia (worsened by ↓ excretion of
phosphate by kidneys)
H. Waste product  Bun (Normal: 3.6-7.1 mmol/L) and Cr high (M: 53-106 mcmol/L; F: 44-97 mcmol/L)
accumulation  Cr is the better measure as it is not significantly altered by other factors (unlike BUN)
 Note: Cr in OA will be lower than younger person with same degree or muscle dysfunction
because decreased muscle mass from aging (Cr is end product of muscle metabolism)
Neuro changes  d/t nitrogenous waste product accumulation- Azotemia
 Neuro changes → fatigue and difficulty concentrating or can escalate to seizures, stupor, coma
3. Recovery Phase-
 Return of Bun/CR and GFR to normal ranges
 Diuretic phase may be present (gradual ↑ from 1-3L/day to > 3-5L/day) → can result in F&E imbalance
o High urine volumes d/t osmotic diuresis r/t to high urea conc. in the glomerular filtrate and the inability of the tubules
to concentrate the urine.
o Hypovolemia and hypotension can occur from massive fluid losses/diuresis → watch VS
 Monitor for hyponatremia, hypokalemia and dehydration (from F&E loss)
 Renal fx may take up to 12 months to stabilize

DIAGNOSTIC STUDIES
 Hx and PE
 Identify precipitating cause
 Serum Cr/ BUN, electrolytes
 Urinalysis: for colour, specific gravity, abundant cells, casts, protein, blood
o Collect first urinated morning specimen → more likely to contain abnormal constituents if present
o Examine within 1 hr of urinating. If not → bacteria multiply, RBC hemolyze, casts disintegrate, urine becomes
alkaline (from urea-splitting bacteria)
 Refrigerate if unable to send to lab
 Renal u/s: provides info on anatomy and function, no contrast needed, no bowel prep
 Renal scan (as indicated): assess renal blood flow and integrity of collecting system
 CT scan (as indicated and without contrast if possible): for lesions and masses, obstruction
 Retrograde pyelogram (as indicated)
o Radiograph of UT after injection of contrast material into kidneys: cystoscope inserted → ureteral catheters inserted
through it into renal pelvis → inject contrast material thru catheter
o Assess renal fx: if ↑ BUN/Cr → contrast dye not safe (nephrotoxic) and cannot be properly excreted
o Evening before: cathartic or enema, NPO 8hr before
o Assess iodine sensitivity
o Pt may feel warmth, facial flushing, and salty taste
 After: encourage fluids to flush out contrast dye

COLLABORATIVE MANAGEMENT
 Goals: eliminate cause, manage S&S, prevent complications when kidneys recover
1. ENSURE ADEQUATE PERFUSION OF KIDNEYS
 Ensure sufficient intravascular volume to maintain CO
 Monitor fluid intake carefully = Rule for intake: previous 24 hr fluid loss + 600mL insensible
loss
o E.g. if pt excreted 300mL urine with no other losses, fluid intake for next day
restricted to 900mL
 Improve CO

2. DIURETIC THERAPY
 Challenge kidneys to get rid of fluid
 Often administered along with volume expanders to prevent fluid overload
 Drug of choice is Lasix**
o Note: Mannitol (osmotic diuretic) only added if lasix not working for long period of
time

3. INITIATE EARLY RRT (CONTROLLED DIALYSIS)

 To minimize symptoms and prevent complications
Indications:
 Volume overload resulting in compromised cardiac or  BUN > 43 mmol/L
pulmonary status  Significant change in mental status
 Elevated K+ levels  Pericarditis, pericardial effusion, or cardiac
 Metabolic acidosis (serum bicarb < 15 mmol/L) tamponade

4. HYPERKALEMIA (> 6mmol)

 (only the last 3 actually remove K+ from body):
Calcium gluconate IV  Glue down those deadly heart muscles with gluconate
 Give if ECG shows hyperkalemia-related abnormalities
 MOA: Stabilizes myocardium by increasing threshold potential to tolerate
dysrhythmias will occur, thereby protecting heart and counteracts effects of K+
Regular IV insulin + IV 50%  Insulin puts sugar and potassium out of the blood and into the cell to lower blood
Dextrose - glucose
 NaHco3 potassium. And the Insulin to manage the lower blood sugar
Salbutamol  MOA: temporarily shift K+ into cells
 K+ will rebound out in < 2 hours if Hemodialysis or urine excretion does not occur
 Glucose given to prevent hypoglycemia
 This is the go-to treatment when K+ very high e.g. > 7mmol (will shift K+ the fastest)
Sodium polystyrene sulphonate  Enhance K+ removal by exchanging K+ for Na+ (binds to K+ in gut) and gets rid of it
(Kayexalate) by PO or enema  Do not give if pt does not have normal bowel function (auscultate bowel sounds first)
 Takes hours to days
Loop diuretics (Lasix)  ↑ K+ excretion in urine if pt has u/o
Dialysis  Brings K+ levels to normal within 30 min-2 hr -fastest (hemodialysis)

TIP- HIGH K + ECG DYSRYTHMIAS - NO ECG DYSRYTHMIAS MENTIONED

Long-term Treatment
 Dietary restriction of K+ to 40 mmol/day
 Limit/discontinue ACE-I, ARBs, and potassium-sparing diuretics

5. NUTRITIONAL THERAPY
 High calorie (25-35 kcal/kg) to prevent catabolism
 Protein dosage varies with stage of AKI and RRT requirement to decrease muscle breakdown  more urea
 Dietary fat intake is ↑ so at least 30-40% of total calories from fat
 K+ regulations accordance with K+ levels (do not take anything with K+ in it)
 Na+ is restricted as needed to prevent edema, HTN and CHF -
 Monitor and regulate hyperphosphatemia, hypocalcemia, and hypermagnesemia
 If PO not option → enteral. If GI not functional → TPN (may need daily HD or CRRT to remove excess fluid)

ACUTE NURSING INTERVENTIONS

 Monitor VS, I&O, F&E balance, daily weight for early detection and prompt replacement of significant fluid loss during
oliguric & diuretic phases- 1KG =1 LITER OF FLUID RETAINED
 Monitor patient's general appearance including skin colour, peripheral edema, neck vein distension, and bruises.
 Avoid infections (leading cause of AKI death) by ensuring meticulous aseptic technique
 protect from infection- Monitor for s/s of infections- swelling, redness, pain etc
 Aggressive diuretic therapy can → ↓ renal blood flow (careful treatment)
 Diagnostic studies with IV contrast media (e.g. MRI & CT with contrast) contraindicated
o IV contrast is nephrotoxic, so avoid
o If test unavoidable, adequate hydration before and after test and use acetylcysteine (mucomyst) as prescribed
 Mucomyst protects kidneys from dye
 Pt w/ UTI need prompt treatment and careful follow-up care,
 Drugs that potentially nephrotoxic should be avoided, including OTC (e.g. metformin, ACE-I, NSAIDs, aspirin, Milk of
magnesia, Antibiotics- aminoglycosides- vancomycin/gentamicin),
 Skin care to prevent pressure ulcers because pt usu develops edema and decreased muscle tone

CKD (CHRONIC KIDNEY DISEASE)

 Progressive, irreversible loss of kidney function (destruction of nephrons)
 Leading causes of End-stage renal disease (ESRD) are uncontrolled diabetes- hyperglycemia, HTN, unchecked
autoimmune diseases, infection, AKI, Polycystic kidney disease, ,
o If CKD progresses to stage 5 (worst functioning), RRT is necessary for long-term survival
 Kidneys have good functional reserve → up to 80% of GFR can be lost with few changes in functioning of body
o Early stages unrecognized because nephrons hypertrophy to compensate
 o RRT not required until 90% of nephrons are lost
 Identifying the stage of CKD allows for early intervention to reduce cardiovascular risk, delay progression, and prevent the
need for RRT

CLINICAL MANIFESTATIONS
 As renal fx deteriorates → excretory, regulatory, and endocrine fx are lost and manifested in every body system
 Uremia: urine in blood- S&S that result from buildup of waste products and excess fluid associated with kidney failure
o E.g., ↑ Cr/BUN, lytes imbalance, acidosis, anemia, fluid volume excess, nausea, anorexia, fatigue, pruritus,
neuropathy, ↓ LOC
 Priority complication- Hypertensive crisis- Headache/N& V/Change in mental status
1. Urinary system  Early:
o Polyuria: just water, inability of kidneys to concentrate urine, occurs most often at night
o Specific gravity fixed around 1.010
 Later as CKD worsens: Oliguria, then Anuria: <400 mL/day with possible proteinuria, casts, pyuria,
hematuria
2. Metabolic  1. Waste product accumulation
disturbance o As GFR ↓, BUN/Cr ↑ → N/V, lethargy, fatigue, impaired thought processes & headache
 2. Altered carbohydrate metabolism
o Caused by impaired glucose use (cells insensitive to insulin i.e. resistance – unknown)
 → see Hyperglycemia, hyperinsulinemia, abnormal GTT
o Diabetics require ↓ insulin than before onset of CKD (impaired Insulin excretion by kidneys
thus insulin stays in circulation longer)
 3. Elevated triglycerides
o With insulin resistance → Hyperinsulinemia stimulates hepatic production of triglycerides
3. Electrolyte and  ↑ K+: Hyperkalemia >5.0 d/t ↓ excretion & metabolic acidosis, Fatal dysrhythmias (if 7-8 mmol/L)
Acid-Base  ↓ Na+ <135: Impaired excretion → Na+ & water retention → dilution and hyponatremia
Imbalance  ↓ Ca+ and ↑ phosphate >4.5
 Mg excreted by kidneys but also binds phosphate, thus hypermagnesemia not a problem unless Pt
ingesting magnesium (e.g. antacids)
 Metabolic acidosis (<7.35) results from inability of kidneys to excrete acid load (mainly ammonia) and
from defective reabsorption/regeneration of bicarbonate (↓)
4. Hematological  1. Anemia (normocytic normochromic)
System o d/t ↓ erythropoietin, and deficient iron (which can be removed in dialysis)
 2. Bleeding Tendencies
o Defect in platelet function
 3. Infection
o Change in leukocyte function, diminished inflammatory response, altered immune response
5. CV  HTN → most common, worsened by Na+ retention and excess fluid volume, renin
o Leads to LV hypertrophy and CHF, peripheral edema
 Cardiac dysrhythmias like Vtach, [Link] from hyperkalemia, hypocalcemia, and ↓ coronary artery
perfusion
 Uremic pericarditis
 PRIORITY↑ K+: Hyperkalemia >5.0  high pumps of the heart, tall, peaked T waves; widening QRS
complex; ST depression/elevation

6. Resp  Dyspnea from FVE
 Pulmonary edema, pleural effusion, uremia pleuritis (pleurisy), predisposition to resp infections
 Kussmaul’s in advanced CKD
7. GI  Excessive urea → mucosal inflammation → stomatitis, ulcers, GI bleeding, uretic fetor (urinous odour
of breath)
 N&V & anorexia as CKD progresses d/t irritation by waste products
8. Neuro  D/t azotemia, acidosis, lytes imbalance
 CNS depression → fatigue, irritability, altered mental ability, seizures and coma if rapidly increasing
BUN and hypertensive encephalopathy
 Peripheral neuropathy → c/o of restless legs syndrome (bugs crawling inside leg)
 Dialysis or transplant is necessary to treat neuro problems
9. MSK  Systemic disorder involving bone abnormalities, changes in mineral balance, and calcification
(CKD-MBD -  As kidney declines → hypocalcemia, hyperphosphatemia, ↓ Vit D → excess PTH
Mineral and Bone  Leads to skeletal complications → osteitis fibrosa (↑ bone turnover), osteomalacia (low bone turnover)
Disorder)  Extra skeletal complications → excess phosphate → calcifications in vascular and soft tissue (e.g. GI,
lungs, BV)- risk for fractures
10. Integumentary  Pruritus, uremic frost (when urea crystallizes on skin d/t very ↑↑ BUN)
 11. Repro  Infertility (M & F), ↓ libido, low sperm counts, menstrual changes, sexual dysfunction
12. Psychological  Emotionally labile, personality changes, withdrawal, depression, changes in body image

DIAGNOSIS
 Hx and PE  Creatinine clearance test
 Identify reversible renal disease o 24hrs urine collection- put on ice to
 Dipstick evaluation → proteinuria is earliest marker of o Discard 1st urine specimen when test
kidney damage begins- We do not use mid stream
o Screen those at high risk (DM, HTN)  Renal ultrasound: check obstruction and size
 Albumin-Cr ratio (First morning void)  Renal scan, CT scan, Renal biopsy
better than dipstick. measure urine  Bloodwork: Lytes, Hb, iron
protein (albumin) to Cr  Urine analysis and culture → RBC/WBC, casts,
 GFR: measure kidney fx protein, glucose

COLLABORATIVE MANAGEMENT
 Focus: prevention and early identification. Upon diagnosis → detect and treat reversible causes
 Goal: preserve existing renal function, delay progression of renal disease, treat clinical manifestations, prevent
complications, educate pt and families, prepare pt for RRT
o Care of pt must be tailored to stage for CKD
o Note: treatment focuses on urea in CKD vs AKI which focuses on Cr

DRUG THERAPY
Calcium carbonate Reduces cramping/tetany in hypocalcaemia pt.
phosphate binders (Caltrate) binds phosphate in bowel and excretes via stool
Calcitriol (Rocaltrol) Supplementing vitamin D
Serum phosphate level must be lowered before calcium or vitamin D is administered (drug
can contribute to soft tissue calcification if both Ca+ and phosphate are elevated
Erythropoietin: Epoetin alfa  Treat anemia
(Epogen, Procrit)  Do not give if significantly ↑ BP as ESA accelerates HTN (d/t ↑ blood viscosity when anemia
Erythropoietin stimulating is corrected)
agents (ESA)  SE: iron deficiency because of ↑ demand for iron to support erythropoiesis
o Give iron supplements
ACE-I & ARB  ↓ proteinuria and delays progression of renal failure as first line
 Caution with use because can further ↓ GFR and ↑ K+
 Note: altered kidney fx → delayed and decrease elimination of drug → drug toxicity
 Need to adjust dose and frequency based on kidney fx. Dialysis may remove or lower drug levels
 Caution with: digoxin, oral glycemic agents (metformin, glyburide), antibiotics, opioids (dilaudid, morphine), aspirin
 Avoid NSAIDs: these block synthesis of renal prostaglandins that promote vasodilation → worsens kidney perfusion

1. HYPERKALEMIA  Antihypertensives: ACE-I & ARB (First-line), CCBs

 Dietary restriction of high-K+ foods if 5.5-5.9 mmol/L;
pharm management once ≥ 6 (same as AKI)
 Monitor ECG changes → if present, give calcium
gluconate
2. DYSLIPIDEMIA 4. ANEMIA
 Statins- atorvastatin/rosuvastatin  ESAs, Iron supplements (esp If on HD)
o Side effects: gastric irritation, constipation,
may make stool dark in colour
3. MANAGE HTN  Folic acid supplements: b/c folic acid is removed by
 Weight loss, lifestyle changes, dietary Na+ and fluid dialysis and is needed for RBC formation
restriction, home BP measurements  Avoid blood transfusions (d/t suppression of
 Diuretics for fluid overload erythropoiesis)

5. CKD-MBD
 Chronic Kidney Disease–Mineral and Bone Disorder
 Phosphate intake restricted (< 1000mg/d)
 Calcium carbonate phosphate binders (Caltrate), Calcitriol (Rocaltrol)
 Controlling secondary hyperparathyroidism → parathyroidectomy
6. NUTRITION THERAPY
Restrict:
 Protein  Sodium: 2-4 g/d (depending on pt; avoid salt
o Because BUN is end product of protein substitutes) because of renal failure and HTN
metabolism o High salt foods: cured/processed meats,
o Calorie-protein malnutrition is a potential pickled foods, cold cuts, canned soup, salad
problem (substitute fat) dressing,soy sauce
o Restrict protein- lower workload-  Potassium: Low potassium foods 2-4g/d
o For dialysis, protein is not routinely restricted. o Avoid oranges, bananas, melons, tomatoes,
o low chicken, steak, pork prunes, raisins, deep green/yellow
 Fluid vegetables, beans, legumes, strawberries
o If not on dialysis → diuretics and low o Apples- best choice
sodium diet to manage fluid retention o No salt substitutes
o If dialysis → restrict to previous 24 hr u/o +  Phosphate (<1000mg/d)
600mL o Avoid: dairy products (milk, ice cream,
 Space this throughout day so pt is pudding, yoghurts)
not thirsty o Most foods high in phosphate are also high in
calcium (thus will also restrict calcium intake)

ACUTE INTERVENTION
 Daily weight, I&O, monitor edema, daily BP as indicators of FVE
o Identify S&S of fluid overload and hyperkalemia
 Strict dietary/fluid adherence to control edema and HTN
 Assess indicators of anemia: dyspnea, fatigue, palpitations, tachycardia, chest pain
o Monitor trends in Hb and iron stores

HEALTH PROMOTION
 Identify individuals at risk for CKD: Hx of renal disease, HTN, DM, repeated UTI
o Regular checkups → BUN/Cr, urinalysis
o Changes in urinary appearance (colour/odour), frequency, and volume should be reported
o Glycemic control (if diabetic), BP control, lifestyle (smoking cessation)

AMBULATORY AND HOME CARE

 When conservative therapy is no longer effective, HD, PD, and transplantation are treatment options
 Patient/family need clear explanation of dialysis and transplantation early in order to make informed decision
 DIALYSIS
 Movement of fluid and molecules across a semipermeable membrane from one compartment to another
 Substances move from blood thru semipermeable membrane (dialyzer) and into dialysis solution (dialysate)
 Corrects F&E imbalances & removes waste products in renal failure (via osmosis and diffusion)
o Wastes move from blood to dialysate with net effect of lowering their blood
o Indicated in certain uremic complications (neuro, uncontrolled hyperkalemia, accelerated HTN)
 Ultrafiltration (water and fluid removal) results when there is an osmotic gradient (usu glucose is used) or pressure gradient
across the membrane → this pulls excess fluid from blood allowing for fluid removal

2 TYPES OF DIALYSIS:
1. PERITONEAL DIALYSIS (PD)
 Removing waste and excess fluid using natural semipermeable membrane – the peritoneum
o Dialysis fluid infused into peritoneal cavity → excess fluid and waste pass across membrane into fluid → drained
and discarded
Catheter Placement:
 Peritoneal access obtained by inserting catheter thru anterior abdo wall
 Catheter connected to sterile tubing system and secured to abdo with tape
o Catheter irrigated immediately with heparinized dialysate to clear blood and fibrin
 Pt d/c with instructions: keep dressing dry, avoid pulling, wait 7-14 days before starting PD for proper sealing of catheter
(fibrous tissue starts growing around catheter to hold in place), routine care everyday (soap), monitor S&S of infection

3 phases of PD cycle (called exchange):

 A. Inflow (fill): a prescribed solution (usu 2L), is infused thru established catheter over ~ 10 min
 B. Dwell (equilibration): diffusion and osmosis occur between pt’s blood and peritoneal cavity (20-30mins to > 8hours)
o Allows for removal of waste and excess fluid
 C. Drain: removing solution from peritoneal cavity (~15 – 30mins)
o If 2L goes in, slightly more than 2L should come out

2 main types (FYI)

A. Automated peritoneal dialysis (APD), (continuous cycling PD)
 Done while pt sleeps (times the 3 phases)
 Cycles 4 or more exchanges/night with 1-2 hrs/exchange
B. Continuous ambulatory peritoneal dialysis (CAPD)
 Done during the day. Dialysis fluid is always in peritoneal cavity so dialysis is continuously going on
 Manually by exchanging 1.5 to 3 L of peritoneal dialysate at least 4x daily, with dwell times averaging 4 hours

PD CONTRAINDICATIONS
 Hx of multiple abdo surgical procedures  Excessive obesity with large abdo wall and fat
 Severe abdo pathological conditions (e.g. severe deposits
pancreatitis: risk of abscess formation as it may  Pre-existing vertebral disease (e.g., chronic back
spread; diverticulitis) problems)
 Recurrent abdo wall or inguinal hernias  Severe obstructive pulmonary disease

COMPLICATIONS- know- ALWAYS ASSESS PT B4 DEVICES, ALSO ALWAYS ASSESS B4 INTERVENTION- ADPIE
1. Exit-site  Assess: redness, tenderness, cloudy drainage, fever, tachycardia
infection  Tx: Abx, maintain aseptic technique when spiking bag to avoid peritonitis- report to HCP immediately
2. Peritonitis  Assess: cloudy peritoneal effluent (fluid in lower bag) with WBC > 0.1 x 109/L or bacteria in culture,
abdo pain, diarrhea, vomiting, distension, hyperactive bowel sounds, fever may or may not be present
 Tx: Abx
3. Abdo pain  Tx: change catheter position, do not infuse air or infuse too rapidly (slow infusion)
4. Outflow  Assess causes: abdo distention & constipation; catheter kinks & obstructions, migration
problems  Tx: reposition to side-lying; laxatives, surgical manipulation of catheter,
5. Hernias  Caused by ↑ intra-abdominal pressure during infusion
 Tx: small dialysate volumes, keep pt supine
6. Lower back  Caused by ↑ intra-abdominal pressure
problems  Tx: orthostatic binders, regular exercise program to strengthen back muscles
7. Bleeding  Assess: BP and Hb, bleeding
8. Pulmonary  Caused by rapid infusion /over filling the abdomen, upward displacement of diaphragm
/respiratory  Signs: Crackles in lung bases, rapid respirations, dyspnea- diff. breathing
distress  Tx: elevate HOB ; reposition, deep breathing,
9. Protein Loss  Tx: adequate protein intake
via osmosis
10. Carbohydrate  Caused by glucose in dialysate being absorbed via peritoneum → hyperinsulinemia → stimulates
and Lipid hepatic production of triglycerides
 Abnormalities
Effectiveness of and Adaptation to Chronic PD
 Advantages: PD provides independence to be at home,
fewer dietary restrictions, greater mobility
o Better for vascular access problems or responds
poorly to hemodynamic stresses (e.g. OA with
CVD)
o Less hemodynamic instability because fluid shifts
are gradual
 Main disadvantage: developing peritonitis

2. HEMODIALYSIS (HD)
 Waste and fluid removed from blood using machine to
pump blood thru artificial membrane
 To carry out HD: very rapid blood flow required, access to
large BV essential (subclavian or IJ)
o IV heparin is added to the bag to prevent clotting
 Not necessary to give another form of
blood thinner before dialysis

3 VASCULAR ACCESS SITES:

1A. AVF (arteriovenous fistulas)
 Superior to the other 2 → best patency, lower infection
and complications (e.g. clot)
 Surgically connects a vein & an artery (in forearm)
o Preferred sites for AVF are wrist (radiocephalic)
and elbow (brachiocephalic)
 How the fistula works:
o Provides for arterial blood flow thru vein →
Increased pressure (turbulence) of arterial blood
flow causes vein to dilate and become tough,
making it amenable to repeated venipuncture
 Vein is accessed using 2 large-gauge needles
o 1 needle to draw blood and circulate through
dialyzer, other needle to return the blood
 Best to create 3-4 months before HD to give vein time to
dilate/toughen
 Difficult to create in: severe peripheral vascular disease,
DM, prolonged IV drug use, previous multiple IV
procedures in forearm → may need AVG
 Teach pt to
o squeeze or grip rubber ball/sponge to help blood flow and strengthen new site;
o that pitting edema is normal here- resolves on its own
 Complication
o Pale skin/pallor, paresthesia-numbness & tingling, diminished pulse, poor cap refill and pain distant to shunt.
 Monitor- for infection, bleeding & always feel a thrill; monitor for stiffening and blood clotting at site
 Prevent- no restrictive dressing, no blood cuffing, no sleeping on the arm, no lifting over 5lbs, no purses, no creams, lotions

1B. AVG (arteriovenous grafts)

 Used in absence of a suitable vessel for an AVF
 Surgically created synthetic graft (anastomosis) attached to an artery and a vein (in forearm)
o Graft is under the skin & accessed using 2 needles
 The graft material is self-healing, meaning it should close over any puncture site after needle is removed
 Infections in other parts of the body can result in infection and damage to graft and have a tendency to be thrombogenic
AVF & AVG Special Considerations:
 A thrill can be felt by palpating area of anastomosis, Bruit can be heard with a stethoscope
 BPs, IV insertion, and venipuncture should not be performed on an extremity with an AVF or AVG
o To prevent thrombosis and infection in vascular access (more common in AVG than AVF)
Complications
 AVFs and AVGs can cause the development of distal ischemia b/c too much arterial blood is shunted from distal extremity
 Check perfusion to hand esp after surgery
 Aneurysms can also develop at the fistula site

1C. CVCS: Tunnelled and nontunneled central venous catheters:

 When immediate vascular access is required
  Percutaneous cannulation of the internal jugular or the femoral vein - IJ cannulation has lower incidence of thrombosis
than subclavian vein (→ use subclavian as last resort due to risk for pneumothorax and brachial plexus)
 Potential complications of femoral catheterization: femoral vein thrombosis with pulmonary emboli infections, immobility,
and inadvertent blood vessel punctures with hematoma formation
 Proper catheter position should be confirmed using radiography

PROCESS
 Before HD:
o assess
 current & previous fluid status (wt, BP, edema, lung & heart sounds),
 Last post dialysis weight and present predialysis weight represents amount of fluid weight gained
since last treatment → determines amount of fluid to be removed (i.e. ultrafiltration)
 vital signs,
 vascular access,
 temp,
 general skin condition
o Assess Fistula- Should feel a thrill/vibration & hear a bruit/swoosh- Report if not present
o Hold Meds that:
 cause hypotension- Antihypertensives,
 A- Aces & Arbs- “prils/Sartan- since they retain K+
 B-Beta-blockers- “olol – low bp and Hr
 C- Calcium channel blockers- “dipine; ‘amil, ‘zem-
 D- diuretics- Furosemide & thiazides
 D- dilators- nitroglycerine- dilate vessels to make bp low
 Can be washed out-
 Antibiotics- penicillin, cephalosporins.
 Digoxin (for heart contraction);
 water-soluble vitamins (b, c & folic acid)
o Never hold Ca supplements - they bring down phosphrus in the blood
o Never hold Insulin- It is absorbed fast
 During HD: VS q30-60 min because rapid changes in BP

HD COMPLICATIONS- know
1. Muscle cramping:  Caused by rapid removal of Na+/water
F&E imbalance  Tx: reduce UF rate, infuse hypertonic NS or NS bolus
2. Hypotension  Caused by rapid removal of vascular volume
 Assess: lightheadedness, N&V, seizures, vision changes, chest pain (cardiac ischemia)
 Tx: ↓ volume of fluid removal, infuse 100-300mL 0.9% NS, hold BP drugs before HD
3. Loss of blood  Caused by accidental separation or blood not being rinsed completely from dialyzer, clotting
problems, too much heparin
 Tx: monitor heparinization, rinse back all blood, hold firm pressure on access sites
 Note: if a clot is present, get rid of the blood in the machine because do not want to risk giving
clot back to pt
4. Sepsis  Caused by infection of vascular access
 Assess: fever, hypotension, elevated WBC
 Tx: aseptic technique
5. Hepatitis  Tx: isolate pt, good infection control practice
6. Disequilibrium  Caused by rapid changes in composition of ECF where urea, Na+ removed faster than CSF
syndrome → high osmotic gradient in brain causing fluid shift into brain → cerebral edema/ICP coma,
death
 More common in first treatment → first treatment purposely short to prevent this
 Assess: Vomiting, disorientation/confusion, restlessness confusion, headache, twitching,
seizures, muscle cramps, hypotension
 Tx:
o slow or stop HD,
o infuse hypertonic NS/albumin/mannitol to draw fluid back into blood
o report to hcp
o never trendburg – leads to more icp;

Effectiveness of and Adaptation to HD

 Ambivalence as to whether HD is worthwhile (5 yr survival rate ~40%) as there is dependence on machine → depression
CRRT (CONTINUOUS RENAL REPLACEMENT THERAPIES) – for AKI
 Alternative method for treating AKI, used in hemodynamically unstable pt
o Slow removal of fluid while acid-base and electrolytes adjusted slowly and continuously
 Continuous rather than intermittent
 Large volumes of fluid can be removed over longer periods
 Causes less hemodynamic instability (e.g. hypotension)
 Requires trained ICU nurse
o Hourly U&O, VS, hemodynamic status are essential. Also check patency, prevent infection

KIDNEY TRANSPLANTATION
 Goal: watch for rejection → temp symptoms (fever, WBC), ↓ u/o
 If you see these come on more abruptly → this is rejection rather than an actual infection which comes days later

NURSING MANAGEMENT
A. PREOPERATIVE CARE
 ECG, CXR, Lab studies, may need dialysis before, maintain patency of vascular access because may need dialysis after sx
B. POSTOPERATIVE CARE
 Living donor or cadavre
o Monitor renal fx for impairment, Hb for bleeding
 Kidney transplant recipient
o Diuresis may occur because of new functioning kidney → maintain F&E balance by replacing u/o mL to mL hourly
for first 12-24 hours
o Assess dehydration, hyponatremia, hypokalemia associated with rapid diuresis
o ATN can occur (days to weeks) and may need dialysis to maintain F&E balance
o Catheter insitu 3-5 days to allow bladder anastomosis to heal – watch for clots in catheter, ↓ u/o
 Immunosuppressive therapy
o Prevent rejection by giving anti-rejection agents (corticosteroids) to prevent excessive inflammatory process in body
 Methylprednisolone (Solu-medrol)
 SE: PUD, glucose intolerance and DM, cataracts, dyslipidemia, ↑ infection and malignancies
o Still want to maintain sufficient immunity to prevent overwhelming infection
o Higher risks for cancer,

COMPLICATIONS
 Rejection
 Infection (d/t surgery, immunosuppressive therapy)
 CV disease
 Malignancies (d/t immunosuppressive therapy)
 Recurrence of original renal disease
 Corticosteroid-related complications → aseptic necrosis of joints
o Prevent with Ca+ and vit D supplements to minimize bone disorders, wt-bearing exercise, limit alcohol/smoking