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Nursing Care of the with Client
Acute Renal Failure
 Christine R. McMurtrie RN, MSN
 Professor, Nursing
 Nursing Institute
 Brevard Community College
 433-7538
 mcmurtriec@brevardcc.edu


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Longitudinal Section of the Kidney
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The Nephron
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Kidney Functions
 Maintain homeostasis
 Excretion of waste products
 Fluid & Electrolyte Balance
 Acid-Base Balance
 Blood Pressure Regulation
 Hormonal Balance
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Age Related Changes
 Loss of glomeruli
 Decreased glomerular filtration rate
 Decreased production of creatinine
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Effects of renal function Changes
in the Elderly
 Altered ability to concentrate urine and
compensate for Na excess or loss
 Decreased response to ADH
 Decreased thirst response
 Decreased aldosterone levels leading to
hypokalemia
 Altered drug excretion & renal toxicity
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Classification of Renal Diseases
 Congenital
 Disorders of the glomerulus
 Vascular Disorders
 Trauma
 Neoplasms
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ACUTE RENAL FAILURE
 Patho: Abrupt (hours to a few days) decrease in
renal function sufficient to result in retention of
nitrogenous waste (BUN & creat) in the body
 Hallmark of ARF is progressive azotemia caused by
accumulation of nitrogenous end products of
metabolism
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Nephron Destruction in Acute Renal
Failure
 A. Normal nephron.
 B Damage from renal
ischemia results in patchy
necrosis of the tubule.
The lumen may also be
blocked by casts.
 C. Damage from
nephrotoxic agents.

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Etiology
 Three categories of causation
 Prerenal - Decrease renal blood flow
 hypovolemia, CV failure, MI (↓CO)
 dehydration, shock, trauma with bleeding
 Quick response & resolution with intervention
 Intrarenal - Produce a renal parenchymal
insult
 glomerulonephritis, drugs, chemicals, diabetes,
lupus, infections, ATN
 ischemic and nephrotoxic
 Prolonged recovery
 Postrenal - Obstructs urine flow
kidney stones, clots, tumors, neurogenic bladder
Quick response & resolution with intervention

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Management:
 Health Prevention and Promotion
 Determine and treat the cause
 Initiate proper therapy
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ARF Progression
 Initiating Phase (onset until s & s)
 Oliguric Phase (onset 1-7 d; lasts 10-14 d
 Diuretic Phase (1-3 weeks)
 Recovery Phase (1 wk to 1 yr)
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Initiating Phase (Hrs to days)
 Begins at time of insult
 Continues until clinical manifestations appear
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Oliguric Phase
Oliguria = uo < 400 mL/24h
*Most common initial manifestation
 Prerenal
 No damage to renal tissue
 Autoregulation
 Vasoconstriction
 Na & H2O retention
 Urine
 Sp gr > 1.015 (high)
 Na < 10-20 mEq/L (low)
 Intrarenal
 Renal damage
 Autoregulation fails
 Can’t concentrate urine
so lose Na
 Urine
 Sp gr WNL (1.010)
 Na > 40 mEq/L (high)
 Ischemia or toxins
 Urine contains RBC’s
and WBC’s
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Clinical Manifestations Oliguric
Phase (begins 1-7 d; duration 10-14 d
or longer)
 Oliguric Phase
 Urinary changes – 50% experience oliguria
 Fluid volume excess – JVD, bounding P, edema, htn, chf, pul ed,
effusions
 Metabolic acidosis – Kussmaul resp, lethargy, stupor
 Sodium balance – serum Na nml or below nml
 Potassium excess – leading cause of death; see table 475, p. 1202
 Hematologic disorders – pancytopenia *Infection main cause of
death
 Calcium deficit and phosphate excess
 Waste product accumulation – creatinine best indicator
 Neurologic disorders – fatigue, concentration, seizures, stupor, coma

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Diuretic Phase (lasts 1-3 wks)
 Osmotic Diuresis
 UO 1-5 L/day (kidneys excrete)
 Tubules cannot concentrate urine
 Fluid loss
 Hypovolemia
 Hypotension
 Electrolyte Imbalances
 Hyponatremia, hypokalemia, dehydration
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Recovery (up to 1 yr)
 BUN & creat plateau, then decrease
 May progress to CRF
 Elderly at risk
 May achieve normal kidney function
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Health Promotion/Prevention
 Monitor high risk populations
 Elderly
 Trauma
 Surgical procedures; dyes used in dx tests
 Extensive burns
 CHF
 Sepsis
 OB
 Renal insufficiency due to htn, DM
 Monitor nephrotoxic drugs, chemicals
 Prevent prolonged hypotension and hypovolemia
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Health Promotion
 Medication SE
 OTC Drugs
 Chemical and Environmental Exposure
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Assessment

 Diagnostic Studies
 H & P (Differential Dx)
 UA
 Urine osmolality
 Renal ultrasound
 Renal perfusion scan
 CT scan
 MRI
 Nsg Assessment
 Clin Manifestations (table 47-3,
p. 1201)
 VS, EKG
 I & O, wt, oral mucosa
 Urine color, sp gr, glucose,
protein, blood, sediment
 Skin color, edema, JVD,
bruises
 CV, Resp status
 Lab values/dx test results

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Planning Outcomes ARF
 Preservation of renal function
 Maintanence of fluid and electrolyte and
nutritional balance
 Decreased anxiety
 Adherence to medical regimen and follow-up
care

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Potential Complication:
arrhythmias R/T electrolyte
imbalances
 Insulin & D5H
2
O
 NaHC0
3
– correct acidosis
 Calcium gluconate – prevents arrhythmias
 Dialysis
 Sodium Polystyrene sulfonate (Kayexalate)
 *DO NOT GIVE TO PT WITH PARALYTIC ILEUS
 Dietary restriction K+ to 40 mEq daily
 Phosphate and Na restriction
 Calcium supplements, phosphate binding agents
 Cardiac monitoring, check pulse freq.
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Decreased Renal Perfusion R/T
underlying problem
 Treat underlying cause
 Prevent ATN (acute tubular necrosis)
 Rapid blood loss replacement
 Toxicology for nephrotoxic drugs
 Mannitol, furosemide (SE: Tinnitus and hearing impairment with IV
furosemide)
 Potassium replacement
 Dopamine (low dose)
 I & 0, daily wt, renal function studies, labs
 Prevention of uremic syndrome (fig.47-5, p. 1206)
 Sx:
 early -nausea, anorexia, vomiting
 late - stupor, convulsions, coma, bleeding abnormalities, uremic
pneumonitis, pericarditis, pleuritis

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Potential complication: Metabolic acidosis R/T
inability to excrete H+, impaired HCO3
reabsorption, and decreased NH3 synthesis
 Control of acidosis
 Sodium bicarbonate 30-60 meq/d if bicarb falls below
15-18 meq/L
 Monitor Kussmaul resp, lethargy, stupor
 Dialysis or CRRT

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Excess Fluid Volume R/T renal fx
and fluid retention
 Monitor cardiac function , VS, labs, sx fluid overload
 Cardiac monitoring
 Therapy which promotes increasing urinary sodium excretion
 increase CO, diuretics (lasix, bumex, mannitol)
 aldactone (blocks tubular effect of aldosterone)
 *can cause hyperkalemia
 I & O, daily wt
 *Fluid & Salt restriction (I = O + 600 mL)
 Elevate legs, teds, scds
 Dialysis
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Imbalanced Nutrition: LBR R/T
altered metabolic state and dietary
restrictions
 Adequate calories to prevent catabolism
 30-35 kcal/kg body wt
 CHON -0.6 g/kg, increased if catabolic
 30-40% total cal from fat (fat emulsions)
 Enteral nutrition or TPN if indicated (essential
amino acids)
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Risk for Infection R/T leukopenia,
invasive lines, uremic toxins
 Strict aseptic technique
 Crowd and exposure control
 Monitor local and systemic S & S
 Nephrotoxic drugs as last resort

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Additional Nursing Implications
Acute Renal Failure
 Precautions with drugs
 Avoid: antacids containing magnesium (Mg
intoxication)
 Smaller doses for digoxin, nephrotoxic
antibiotics
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Dialysis
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Dialysis - Review definitions, benefits, procedure,
preparation, patient education, and complications
for:
 Hemodialysis
 Peritoneal
 Continuous Peritoneal

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Hemodialysis
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Vascular Access
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Temporary Hemodialysis Catheters
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Right IJ Temporary HD Catheter
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Peritoneal Dialysis
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Continuous Renal Replacement
Therapy
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The End

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Chronic Renal Failure
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Chronic Renal Failure
 Progressive, irreversible destruction of kidney
tissue by disease which is fatal unless treated by
dialysis or transplant
 Defined as kidney damage or GFR < 60
mL/min for > = 3 months
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Causes CRF
 Metabolic Diseases
 *Diabetic Nephropathy
 *Uncontrolled hypertension
 Infection
 UTI
 *Glomerulonephritis
 Urinary tract obstruction
 Exposure to nephrotoxic agents
 Dehydration
 Multiple myeloma
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Classification Systems - STAGES
CRF (5) – Table 47-6, p. 1205
 Stage 1:
 Asymptomatic, functions intact
 BUN, creat nml
 GFR > = 90
 Dx and Tx comorbid conditions
 CVD risk reduction
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Stage 2
 Mild Decrease GFR with kidney damage
 GFR 60-89
 Estimation of progression
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Stage 3

 Moderate decrease in GFR 30-59
 Evaluation and treatment of complications


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Stage 4
 Severe decrease GRF 15-29
 Preparation for renal replacement therapy
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Stage 5
 Kidney Failure GFR < 15
 Dialysis or renal replacement (if uremia present)
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Biochemical Consequences
 Waste Product Accumulation
 Altered CHO metabolism
 Elevated triglycerides
 Occ Hypermagnesiumemia
 Bleeding tendencies
 Infection
 Increased cancer incidence
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Biochemical Consequences
 Sodium & Water
 Sodium can still be reabsorbed
 Renal tubules lose ability to concentrate urine by
reabsorbing water (sp gr 1.010)
 Should produce polyurea if GFR high enough
 May become rapidly fluid overloaded or depleted
 Eventually oliguria and anuria (UO < 400 mL/d)
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CRF Biochem. Consequences
 Potassium * most serious electrolyte disturbance
 GFR low, nephron loss increases, less potassium is
excreted, develop hyperkalemia
 Acid/Base Balance
 Loose ability to regenerate bicarbonate and excrete
hydrogen ions so develop metabolic acidosis

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Renal Osteodystrophy
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CRF Biochem. Consequences
 Calcium & Phosphate metabolism
 With increased nephron loss, have less
synthesis of VIT D so less Ca reabsorbed from
gut causing hypocalcemia
 PTH levels rise in an attempt to restore serum
Ca
 Leads to secondary hyperparathyroidism and
bone loss (renal bone dystrophy)
 Erythropoietin Synthesis
 impairment leads to normochromic, normocytic
anemia
 Epogen, Procrit
 *Replace folic acid if on dialysis (dialyzable)
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Systemic Manifestations CRF
 Neuro/Psychological: fatigue, lethargy,
depression, poor concentration, involuntary
movements, paresthesias, neuropathy
 CV: HTN, LVH, pericarditis, cardiac
tamponade, hyperlipidemia
 Resp: Kussmaul breathing, Dyspnea, Pleurisy,
pul ed, pneumonia
 Skin: Pruritis, purpura, pigmentation, pallor,
dry, yellowish, uremic frost

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Clinical Manifestations CRF
(Cont.)
 GI: anorexia, N & V, GI bleed, peptic ulcers,
constipation, diarrhea, metal taste in mouth
 GU: Nocturia, polyurea, sp gr 1.010, oliguria, anuria,
impotence
 Musc./Sk.: Myopathy, bone pain, renal osteodystrophy
 Heme: Normochromic, normocytic anemia, depressed
platelet production due to uremic toxins, easy bruising
and bleeding, Altered WBC production and function
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Uremia in Chronic Renal Failure
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Nursing Interventions CRF
 Prevent sodium overload
 Dietary sodium restriction
 Diuretics
 Control htn (diuretics, beta blockers, ace inhibitors) and
anemia (Epogen, Procrit)
 Control hyperkalemia (Kayexalate)
 Control hyperphosphatemia with oral calcium based
phosphate binders to sequester ingested phosphate in
the gut (Tums, PhosLo, Renagel)
 Vit D supplements, (Calcitrol, Calcifediol, Rocaltrol)
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Nursing Interventions CRF
 Anemia – erythropoetin and iron replacement
 Avoid Dig, Aminoglycosides, Meperidine,
NSAIDS
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National Renal Diet
 Established for pre-ESRD, hemodialysis, & PD
 Goals: Decrease build-up of urea and
nitrogenous wastes
 Delay progression of renal disease
 prevent wasting and malnutrition
 restriction of protein to prevent accumulation
of nitrogenous wastes
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Diet in CRF – Table 47-8, p. 1212
 Comparison of diets for ESRD, PD, HD, ESRD
 ESRD
 CHON (0.6-1 g/kg/d)
 Unrestricted for fluid
 Individualized for K, Na, Phosphorus
 If Phosphorus restriction (avoid organ meats, fish,
poultry, milk, milk products, whole grains, nuts,
eggs, dried beans)
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Diet in CRF
 PD
 CHON – 1.2-1.3 g/kg (nml diet .8 g/kg)
 No added salt in diet (2-4 gm)
 Phosphorus restriction same as HD <= 17 g
 Fluid unrestricted if wt & B/P controlled
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Diet in CRF
 HD
 CHON – 1.1-1.4 g/kg
 Sl less than PD
 Individualized Phosphorus restriction
 Sodium – based on body wt & B/P
 Fluid = 0utput previous 24 hr + insensible loss
(600 mL)
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Electrolyte Imbalances in the Pt
with Renal Fx
 Hyperkalemia - impaired excretion of K
 Sx: Irritability, nausea, diarrhea, abd cramps, dysrhythmias,
ECG changes
 Hyponatremia - water retention (sodium leaves vascular
compartment and moves to interstitial space)
 Sx: Nausea, vomiting, headache, CNS involvement causing
lethargy, confusion, seizures, & coma
 Hyperphosphatemia - decreased excretion of phosphate
in urine
 Sx: Hyperreflexia, paraesthesias, tetany (same sx as
hypocalcemia)
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Dietary Goals:
 Encourage foods low in K and Na
 avoid salt substitutes and processed foods
 2-4 g/d K and sodium restriction
 1 g NaCl = 400 mg Na
 Avoid foods high in phosphorus
 Restrict P to 1 G/d
 nuts, anchovies, organ meat, bran, cheese, dairy
products, poultry

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Phosphorus/Ca- (moves in
opposition to Ca)
 Encourage Low phos foods and Ca
supplements
 Hyperphosphatemia occurs with hypocalcemia
(tetany)- Nml phosphate 2.5-4.5
 Avoid vegetarian diets (high in Phosphates)
 Tetany SX: muscle cramps, paresthesias, convulsions,
calcification in soft tissue
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Diet CRF
 Calcium carbonate or calcium acetate (bind
phosporus)
 Calcium supplements (dairy products are
restricted)
 Vitamin D (lose ability to produce Vit D)
 Give Vit D
 Rocaltrol
 Calcijex
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Anemia
 Fe supplements (FeTinic)
 Tarry stools, constipation, GI irritation
 Do not take at same time as phosphate binders
 Folic acid – RBC formation and dialysis
 Epogen (EPO), Procrit
 (adverse effects= htn, increased blood viscosity, iron
deficiency)
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Dyslipidemia
 Goal to keep LDL’s less than 100mg/dl and
triglycerides below 200 mg/dl
 Statins
 fobrates
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Drug Excretion & Nephrotoxicity
 Drugs Excreted by Kidneys
 Digoxin
 Narcotic Analgesics
 Meperidine (converted to normeperidine)
 Oxycodone
 MS
 Nephrotoxic Drugs
 NSAIDS
 Amnoglycosides – Vanc, Gent
 PNC
 Tetracyclines

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Nsg Management CKD
 See Care Plan Lewis pp 1180-1181
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Treatment Options CKD
 Dialysis
 Hemodialysis
 Peritoneal Dialysis
 Continuous Renal Replacement Therapy
 Kidney Transplantation
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Renal Transplantation
 Review indications for transplantation, patient
preparation, patient education, postoperative
care, immunosuppression, rejection, and
management following transplantation
 70% Cadavers donors
 30% LRD
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Pre-op
 Supportive Care for both donor & recipient
 H & P
 Continue dialysis
 Immunosuppressive therapy to prevent rejection
(can occur hours to years after transplantation)
 Azathioprine (Imuran)
 Prednisone
 Cyclosporine (Sandimmune)

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Rejection
 Mechanism of action of T
cytotoxic lymphocyte
activation and attack of
renal transplanted tissue.
The transplanted kidney
is recognized as foreign
and activates the immune
system. T helper cells are
activated to produce IL-2,
and T cytotoxic
lymphocytes are
sensitized. After these T
cytotoxic cells proliferate,
they attack the
transplanted kidney
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Immunosuppressive therapy
 Suppress proliferation of cells within immune system
 Nsg. Responsibilities
 Monitor WBC (fever), platelets (bleeding gums,
bruising, petechiae, joint pain, hematuria, black or
tarry stools), pul function (cyclophosphamines can
cause pul fibrosis)
 Monitor renal and liver function studies
 Administer meds with food to avoid GI effects
 Give antacids
 Encourage po fluids
 Monitor I & O, hand-washing, prevent infection
(MRSA)
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Patient Teaching –
Immunosuppressive Therapy
 Avoid large crowds and exposure to infection
 Report fever, chills, sore throat, fatigue, malaise
 Use contraceptives to prevent birth defects
 Avoid aspirin, ibuprofen to prevent bleeding
 Females may stop having periods while on
cyclophosphamide; menses resumes after drug is
discontinued
 If on cyclophosphamide, report coughing or
difficulty breathing
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Postoperative Care
 Indwelling urinary catheter; measure hourly,
maintain closed system; foley out after 2-3 days
(monitor voiding)
 Fluid replacement cc/cc
 VS, arterial pressure, PWP (Diuresis can occur
immediately after transplantation)
 Diuretics
 Monitor lytes and urinary function tests
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Postoperative Complications
 Hemorrhage (Swelling of operative site, increased abd
girth, shock, changes in VS, LOC
 Failure of the ureteral anastomosis (leakage of urine
into peritoneal cavity – abd swelling, tenderness,
decreased uo
 Renal artery thrombosis (abrupt htn, reduced GFR)
 Infection from immunosupporession (change in LOC,
cloudy or malodorous urine, purulent incisional
drainage)
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Discharge Teaching
 Emotional support – allow control
 Medications
 Monitor VS and daily wt
 Sx of rejection to be reported immediately:
 Swelling and tenderness of graft site, fever, joint
aching, weight gain, decreased urinary output
 Dietary
 Restricted carbohydrate and increased CHON
 Sodium restriction
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Discharge Teaching
 Corticosteroids
 Report cushingoid effects:
 Wt gain
 Fat redistribution
 Hyperglycemia
 Sodium and water retention

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The End