Acute and Chronic Renal Failure

1 McMurtrie/Nur 2241/Fall2012
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

Longitudinal Section of the Kidney
The Nephron
Kidney Functions
Maintain homeostasis
Excretion of waste products
Fluid & Electrolyte Balance
Acid-Base Balance
Blood Pressure Regulation
Hormonal Balance
Age Related Changes
Loss of glomeruli
Decreased glomerular filtration rate
Decreased production of creatinine
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
Classification of Renal Diseases
Congenital
Disorders of the glomerulus
Vascular Disorders
Trauma
Neoplasms
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
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.

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

Management:
Health Prevention and Promotion
Determine and treat the cause
Initiate proper therapy
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)
Initiating Phase (Hrs to days)
Begins at time of insult
Continues until clinical manifestations appear
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
Cant concentrate urine
so lose Na
Urine
Sp gr WNL (1.010)
Na > 40 mEq/L (high)
Ischemia or toxins
Urine contains RBCs
and WBCs
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

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
Recovery (up to 1 yr)
BUN & creat plateau, then decrease
May progress to CRF
Elderly at risk
May achieve normal kidney function
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
Health Promotion
Medication SE
OTC Drugs
Chemical and Environmental Exposure
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

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

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.
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

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

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
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)
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

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

Hemodialysis
Vascular Access

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

Chronic Renal Failure
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
Causes CRF
Metabolic Diseases
*Diabetic Nephropathy
*Uncontrolled hypertension
Infection
UTI
*Glomerulonephritis
Urinary tract obstruction
Exposure to nephrotoxic agents
Dehydration
Multiple myeloma
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
Stage 2
Mild Decrease GFR with kidney damage
GFR 60-89
Estimation of progression
Stage 3

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

Stage 4
Severe decrease GRF 15-29
Preparation for renal replacement therapy
Stage 5
Kidney Failure GFR < 15
Dialysis or renal replacement (if uremia present)
Biochemical Consequences
Waste Product Accumulation
Altered CHO metabolism
Elevated triglycerides
Occ Hypermagnesiumemia
Bleeding tendencies
Infection
Increased cancer incidence
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)
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

Renal Osteodystrophy
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)
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

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
Uremia in Chronic Renal Failure
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)
Nursing Interventions CRF
Anemia erythropoetin and iron replacement
Avoid Dig, Aminoglycosides, Meperidine,
NSAIDS
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
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)
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
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)
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)
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

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
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
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)
Dyslipidemia
Goal to keep LDLs less than 100mg/dl and
triglycerides below 200 mg/dl
Statins
fobrates
Drug Excretion & Nephrotoxicity
Drugs Excreted by Kidneys
Digoxin
Narcotic Analgesics
Meperidine (converted to normeperidine)
Oxycodone
MS
Nephrotoxic Drugs
NSAIDS
Amnoglycosides Vanc, Gent
PNC
Tetracyclines

Nsg Management CKD
See Care Plan Lewis pp 1180-1181
Treatment Options CKD
Dialysis
Hemodialysis
Peritoneal Dialysis
Continuous Renal Replacement Therapy
Kidney Transplantation
Renal Transplantation
Review indications for transplantation, patient
preparation, patient education, postoperative
care, immunosuppression, rejection, and
management following transplantation
70% Cadavers donors
30% LRD
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)

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
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)
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
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
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)
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
Discharge Teaching
Corticosteroids
Report cushingoid effects:
Wt gain
Fat redistribution
Hyperglycemia
Sodium and water retention

The End

Acute and Chronic Renal Failure

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1 McMurtrie/Nur 2241/Fall2012

Nursing Care of the with Client

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