Chronic Renal Failure
1
RENAL FAILURE
Prof. Stroehlein
2
OBJECTIVES
Identify patients with Actual /Potential Acute or Chronic Renal
Failure and respond with appropriate care
Describe alterations in body functions related to Renal self care
deficits.
Discuss and interpret diagnostic tests related to Renal self care
deficits.
Discuss social, economical, cultural factors that impact an
individuals self care.
Use effective teaching and therapeutic communication skills with
parents ,patients families and significant others
3
ANATOMY
4
Kidney System Functions
1.
Eliminate water-soluble nitrogenous end- products of protein metabolism; Excretion of waste products
2.
Maintain electrolyte balance in body fluids
3.
Get rid of the excess electrolytes …show more content…
4.
Discharge excess water in the urine.
5.
Maintain acid-base balance in body fluids and tissue.
6.
Control of blood pressure
7.
Regulation of red blood cell production
8.
Synthesis of vitamin D to active form
9.
Regulates calcium and phosphorus balance
5
RENAL FAILURE
Defined:
Sudden inability of kidneys to regulate fluid and
electrolyte balance and remove toxic waste products from the body.
Glomerular Filtration Rate(GFR):
Volume of blood filtered at the glomerulus into the
kidney tubules each minute;normal rate is approximately 120ml/minute.
6
Renal Failure
Severe impairment or total lack of kidney function
Inability to excrete metabolic waste products and
water
Classified as acute or chronic
May manifest as oliguria, anuria, or normal urine
volume
7
Important Lab Values
BUN - Blood urea nitrogen.
measure of the kidneys' ability to excrete urea, the chief waste product of protein breakdown
Elevated in renal failure and dehydration
Normal range 7 - 20 mg/dl
Creatinine: A waste product from protein in the diet and from the muscles of the body.
removed from the body by the kidneys
Increased in kidney disease
Normal range 0.5 to 1.0 mg/dL
8
Important Test
Creatinine Clearance Test
compares the level of creatinine in urine with the creatinine
level in the blood
24-hour urine sample
Male: 97 to 137 ml/min.
Female: 88 to 128 ml/min.
Estimate the glomerular filtration rate (GFR) -- the standard by which kidney function is assessed range 90 120 mL/min
9
Glomerular Filtration Rate
(GFR)
Levels below 60 mL/min for 3 or more months are a sign of
chronic kidney disease.
Those with GFR results below 15 mL/min are a sign of kidney
failure
10
11
Definitions
Parenchyma - The key elements of an organ essential to its functioning Uremia –retention in the bloodstream of waste products normally excreted in the urine: urea, creatinine and other nitrogen containing waste products of proteins .
Also called Azotemia.
results from kidney disease
Anuria - total urine output less than 50 mL in 24 h
Oliguria - total urine output less than 400 mL in 24 h
12
12
Mechanisms:
Pre-renal -- volume depletion,
poor cardiac efficiency, vasodilation Intra-renal -- prolonged
ischemia, myoglobinuria, infections, nephrotoxins, glomerulonephritis Post-renal -- obstruction from
stone, tumor MECHANICAL
OBSTRUCTION from the tubules to urethra. BPH-most common Fall 2011 NU 202
Renal Failure
13
Clinical Manifestations
Four clinical phases:
1. Initiation: Initial insult to oliguria -≤400ML/24hrs
2. Oliguria: ↑Bun/Creatinine, Rise in serum concentration of substances excreted by kidney K+, Magnesium, ↓U/O
3. Diuresis: Gradually increasing U/O lab values stabilize
4. Recovery: Improvement of renal function
3-12 months
Permanent 1-3% reduction in GFR
14
INITIATION-OLIGURIC PHASES
Begins with the onset of the event causing tubular
necrosis
Ends when tubular injury occurs
Oliguria develops
Elevated serum Creatinine, BUN, K+, Mg. ,acidosis
Nonoliguric form-urine output WNL( associated
with nephrotoxic ABT, Burns,Trauma, Halothane)
15
INITIATION-OLIGURIC PHASES
Begins with the onset of the event causing tubular
necrosis
Ends when tubular injury occurs
Oliguria develops
Elevated serum Creatinine, BUN, K+, Mg. ,acidosis
Nonoliguric form-urine output WNL( associated
with nephrotoxic ABT, Burns,Trauma, Halothane)
16
DIURESIS PHASE
Increased urine output
Serum Creatinine, BUN K+ decrease
Uremic symptoms improve
17
RECOVERY PHASE
GFR IMPROVES
May take up to 1 year
18
Clinical MANIFESTATIONS
Altered Mental Status (AMS)-lethargy,
fatigue
HTN, Hypotension
Edema
Decreased urinary output
CHF
19
Clinical Manifestations
19
Every system of the body is affected:
CNS-Lethargy, Confusion, Headache ,Seizures
CV-Congestive Heart Failure , HTN
Lungs- SOB
Skin/Hair/Nails-Dry thin scaly
GI- Diarrhea ,Nausea, Vomiting, Uremic GI lesions
GU-Oliguria , Anuria , Hematuria
Fall 2011 NU 202
20
Abnormal lab values
20
Hyperkalemia as result of the ↓ in GFR
Patients can not excrete K+ normally
↑Protein catabolism ↑K+ = in body fluid
Can cause dysrhythmias and cardiac arrest
Source of K+ is GI blood loss, dietary, extracellular shift
related to metabolic acidosis
Fall 2011 NU 202
21
Metabolic Acidosis
21
Related to oliguria
Unable to eliminate acids
Normal renal buffering system fails
Fall in CO2 combining power
Progressive
Can cause cardiac arrhythmias
Fall 2011 NU 202
22
22
Changes in Calcium and Phosphorus
Increase in serum phosphate
Decrease in calcium levels
Decreased CA++ absorption from GI tract
At risk for stress fractures
Fall 2011 NU 202
23
Medical Management
23
Restore normal electrolyte balance
Prevent complications
Prevent anuria if possible
Allow kidneys time to regenerate until
normal kidney function resumes
Fall 2011 NU 202
Summary of ARF Categories 24
Characteristics
PreRenal
Intrarenal
Postrenal
Etiology
Hypo-perfusion Parenchymal damage Obstruction
BUN
Increased
Increased
(out of normal
20:1 proportion to creatinine)
Increased
Creatinine
Increased
Increased
Increased
Urine output
Decreased
Varies, often decreased Varies, may be decreased, or sudden anuria Urine sodium
Decreased to
<20 mEq/L
Increased to >40 mEq/L Varies, often decreased to 20 mEq/L or less
Urinary sediment Normal, few hyaline casts
Abnormal casts & debris Usually normal
Urine osmolality Increased to
500 mOsm
About 350 mOsm similar to serum
Varies, increased or equal to serum
Urine specific gravity Increased
Low normal
Varies
25
Pre-Renal
Intra-Renal
Increase renal perfusion
Supportive
Blood loss – Blood transfusion Restrict meds that are excreted by kidneys
Hypovolemia -Infuse
Albumin ,Normal Saline
Remove causative agent
25
Treatment
Remove obstruction
Post-Renal
Avoid Complications
Aggressive Management of prerenal and post renal causes Management
Fluid balance based on daily body weight, CVP, serum and urine concentrations, losses,
B/P
Measure all output
Fall 2011 NU 202
26
URINE ANALYSIS
Fixed specific gravity1.010 due to inability to
concentrate urine
+protein if glomerular damage is cause of ARF
Microscopic RBC’S if inflammatory process
Renal tubular epithelial cells indicates acute tubular
necrosis
Cast cells are protein and cellular debris
27
Serum Electrolytes
K+=elevated
Na+=depends on phase
Phosphorus=elevates, Calcium decreases
BUN=elevated; measurement of nitrogen portion of
urea-a product formed from protein metabolism.
Normal=10-20.
28
Summary of ARF Categories
29
CBC
RBC decreased-anemia secondary to
decreased production of erythropoitin
HCT decreased
30
DIAGNOSTIC TESTS
ULTRASOUND KIDNEYS-UTETERS-BLADDER
Large kidneys-acute problem
Small kidneys-chronic problem
CT pelvis/abdomen
IVP
Retrograde pyelography
Renal Biopsy
Renal Scan
31
Nursing Diagnosis
Altered thought process R/T excess
metabolic wastes
Fluid volume excess
Altered nutrition
Risk for infection
Knowledge deficit
32
MANAGEMENT
Altered mental status
Goal: reduce urea
PLAN- ASSESS V/S, NEURO status,
Maintain safety
33
Fluid volume excess
Monitor v/s- (adm.dopamine prn hypotension)
Diuresis-adm. Lasix or atrial naturetic peptide
which inihibits Na+ and water absorption and dilates afferent arterioles, therefore increasing blood flow
HTN-adm. Anti HTN meds-ACEI (check serum
BUN/creatinine ratio20:1)
Maintain fluid restriction
Monitor weight daily
MAINTAIN ACCURATE INTAKE AND OUTPUT
34
FVE/CV
Hyperkalemia- adm.kayexalate po/pr
Combine with sorbital to prevent constipation
Adm. Glucose and insulin to drive K+ back into
intracellular space or
Calcium gluconate
Metabolic acidosis(ABG)-adm. Sodium bicarbonate
DIALYSIS
Hyperphosphotemia- administer Phosphorus
binding agents(antacids bind with phosphorous in
G.I. tract, then are excreted in feces) calcium carbonate :administer with food
35
Alt. Nutrition
G.I=adm H2 blockers or proton
pump inhibitors-prevent GI bleed
Low protein ,low NA+,K+,high carb,fld.restriction(500ml. +u.o./24hr)Dietary consult
Monitor nausea/vomitingadm.antiemetic
36
Alt. Nutrition
Adm. and monitor parenteral nutrition
Provide oral care
Adm. meds with meals
Encourage small meals or snacks
37
Knowledge deficit
ASSESS pts. Level of anxiety
Assess pts. Knowledge and understanding
Explain therapeutic procedures and diagnostic
tests
Reinforce dietary and fluid restrictions
Instruct pt. to avoid nephrotoxic drugs
Review S&S of ARF
38
Risk for Infection
Teach pt. handwashing
Teach pt.S&S of infection
Reinforce importance of iron supplement,
multivitamin daily to improve anemia and improve immune status
Prevent skin breakdown
39
Supportive care
Dialysis:removes excess fluid and metabolic waste products Hemodialysis
Peritoneal Dialysis
Continuous Arteriovenous
Hemofiltration(CAVH)
40
Chronic Renal Failure
End Stage Renal Disease-silent disease
Develops slowly and insidiously
Functional capacity of nephrons is lost
Glomerular filtration(GRF) decreases
41
Conditions Causing ESRD
Diabetic Nephropathy
HYPERTENSION
Glomerulonephritis
Cystic kidney disease
Other urologic diseases
Etiology unknown
Other
42
Stages of Chronic Renal Failure
Stage 1
Reduced renal reserve
40-75%nephron loss
Usually asymptomatic
43
Stage 2
Renal Insufficiency
75-90% nephron function loss
Elevated BUN and Creatinine
Anemia; inability to concentrate urine
May c/o polyuria and nocturia
44
Stage 3
End stage real disease (ESRD)
Final stage; less than 10% nephron function
Elevated BUN and Creatinine;Elevated K+
Dialysis is indicated
Metabolic acidosis
45
ESRD
Elevated serum phosphate level
Reciprocal low calcium level
Decreased serum calcium level causes
increased secretion of parathormone,causing calcium to leave the
bone.
Vitamin D decreases causing osteodystrophy 46
Pathophysiology of CRF
As nephrons are destroyed, remaining nephrons
hypertrophy
Glomerular capillary flow and pressure increase in
these nephrons
Remaining nephrons predisposed to …show more content…
glomerular
sclerosis/scarring
CRF is identified when uremic stage is reached
47
MANIFESTATIONS OF CRF
Uremia
Alteration in fluid and electrolytes
Early S&S include nausea, apathy, weakness
and fatigue
Progresses to vomiting, increased
weakness , lethargy and confusion
48
Cardiovascular and Hematologic
Effects
Hypertension
Hyperlipidemia,Anemia
Coronary artery disease, Impaired clotting
Dysrhythmias
Pericarditis
Pericardial effusion
Cerebral Vascular Disease,CHF
49
Neurologic and Musculoskeletal
Effects
Altered mental status
Fatigue , Seizures, Coma
Peripheral neuropathy
Osteodystrophy, Bone pain, Fractures
Muscle Weakness
50
Fluid and Electrolyte Effects
Proteinuria, Hematuria
Inability to concentrate urine
Dehydration
Polyuria,nocturia
Na and H2O retention, Hyperkalemia
Hyperphosphatemia, Hypocalcemia
Acidosis, Hyperlipidemia, Hyperuricemia
51
Respiratory and GI Effects
Respiratory Distress Syndrome
Pulmonary edema
Pleural effusion, Pleuritis
Kuss maul respirations
Anorexia ,N/V, Hiccups
Gastroenteritis, GI Bleed, Peptic ulcer
Uremic fetor
Abdominal pain
52
Endocrine,Metabolic and
Dermatologic Effects
Significantly elevated BUN and creatinine
Glucose intolerance
Elevated uric acid level=Gout
Menstrual irregularities
Reduced testosterone levels
Uremic frost, dry itchy skin, poor turgor, bruising
53
Dialysis
A process of diffusion by which dissolved particles can
be transported across a semipermeable membrane.
Corrects fluid, electrolyte and acid-base
Imbalances
Severe fluid and electrolyte imbalances, hyperkalemia,
acidosis and uremic manifestations
54
Hemodialysis
Uses the principles of diffusion and ultrafiltration to
remove electrolytes, waste products and excess water from the body
Blood>Venous access>dialyzing membrane unit
Semipermeable membrane has large pores allowing
small particles to pass thru
(e.g. blood cells and plasma proteins)
55
Considerations
Vascular access
Acute or temporary access may be gained
using subclavian or internal jugular venous catheter Arteriovenous (AV) fistula most commonly
used long term access
56
Internal AV Fistula and Graft
56
Fall 2011 NU 202
57
Systemic Complications
Hypotension
Bleeding
Infection
Dialysis dementia
58
AV Fistula
Non dominant arm is used
No blood draws, IV access or blood pressure
Fistula is created by anastomosis of artery and vein
Takes approx.1 month
Assess for Bruit (auscultate) and Thrill(pulsation)
)
59
Peritoneal Dialysis
Peritoneal dialysis use the pt’s own peritoneal
lining as a semi permeable membrane thru which diffusion, osmosis, and filtration occurs
Warmed dialyzing fluid. placed into peritoneal
cavity via a permanent indwelling catheter
Metabolic wastes and excess electrolytes
diffuse into the dialasate
FLD. drained by gravity out of peritoneal cavity
into sterile bag
60
Peritoneal Dialysis
60
The patient must be alert
and have good fine motor skills Pt must be independently able to perform dialysis at home
Risk of peritonitis from
introduction of bacteria into the peritoneal cavity
The higher the dialysate
the greater the osmotic gradient the more water is removed Solutions used 1.5% 2.5%
4.25%
Fall 2011 NU 202
61
Complications of P.D.
Peritonitis-abdominal pain, tenderness,
fever, cloudy drainage
Alt in gas exchange due to abdominal
distention
Increased protein loss
Perforation
62
Nursing management
Teaching regarding disease process
Teaching regarding diet
Teaching regarding Meds
Teaching regarding technique especially for
Peritoneal Dialysis
Evaluation of teaching via return demonstration
63
Fall 2011 NU 202
63
64
Renal Transplantation
Solid organ most successful of transplanted
Most successful of transplantation procedures
Surgical insertion of a functioning kidney
Improved quality of life
Lifelong immunosuppressive therapy
Most from cadavers; rest related living donors
65
Renal Transplantation
Recipients in good physical health, except for primary
kidney disease and pts. betw,.5 and 50 yrs. of age have best prognosis
66
Types of transplants
Living Donor- Relative
Cadaver
Living Donor- Non Relative
67
Renal Transplantation
Tissue antigens must be as close to the
recipient’s as possible
Live donor must be in good phy. Condition
Have the same ABO blood group
Cadaver kidney requires human leukocyte
antigen(HLA) compatibility
Cadaver donors must be brain dead,<65years of
age, no disease,malignancy,infection(HIV-HBVHCV)
68
Patient Positioning and Incisional
68
Approaches
Fall 2011 NU 202
69
Renal Transplantation
70
Kidney Surgery
Pre-operative considerations
Peri-operative concerns
Post-operative management
Potential hemorrhage and shock
Potential abdominal distention and paralytic ileus
Potential infection
Potential thromboembolism
71
Kidney Transplant Explained
http://www.nlm.nih.gov/medlineplus/ency/presen
tations/100087_1.htm
72
Immunosupressive Therapy
The presence of foreign tissue in the body stimulates a
normal immune response to reject the transplanted organ Immunosuppressive therapy reduces rejection
response
Therapy suppresses a portion of the immune system
and the inflammatory response
73
Case Presentation
80 yo active male with a Hx.
of Left Nephrectomy
2@ry to Ca 10 years ago,and a Hx.HTN,is noted to have STEMI on EKG w/o S/S in his PMD’s office. Patient sent via EMS to ED,then transferred to the cath lab where an angiography w contrast and a stent placement was performed.
74
Case Presentation
Post Procedure Labs:
K*5.7
Na145
BUN 50
Creat 2.5
What caused this change from previous
normal values?
What else would you want to look at?
75
Question
A patient receiving peritoneal dialysis is complaining of pain with rebound tenderness. The dialysate drainage is cloudy. This symptom is indicative of which acute complication? a. Hernia
b. Bleeding
c. Leakage
d. Peritonitis
RENAL FAILURE
Prof. Stroehlein
2
OBJECTIVES
Identify patients with Actual /Potential Acute or Chronic Renal
Failure and respond with appropriate care
Describe alterations in body functions related to Renal self care
deficits.
Discuss and interpret diagnostic tests related to Renal self care
deficits.
Discuss social, economical, cultural factors that impact an
individuals self care.
Use effective teaching and therapeutic communication skills with
parents ,patients families and significant others
3
ANATOMY
4
Kidney System Functions
1.
Eliminate water-soluble nitrogenous end- products of protein metabolism; Excretion of waste products
2.
Maintain electrolyte balance in body fluids
3.
Get rid of the excess electrolytes …show more content…
4.
Discharge excess water in the urine.
5.
Maintain acid-base balance in body fluids and tissue.
6.
Control of blood pressure
7.
Regulation of red blood cell production
8.
Synthesis of vitamin D to active form
9.
Regulates calcium and phosphorus balance
5
RENAL FAILURE
Defined:
Sudden inability of kidneys to regulate fluid and
electrolyte balance and remove toxic waste products from the body.
Glomerular Filtration Rate(GFR):
Volume of blood filtered at the glomerulus into the
kidney tubules each minute;normal rate is approximately 120ml/minute.
6
Renal Failure
Severe impairment or total lack of kidney function
Inability to excrete metabolic waste products and
water
Classified as acute or chronic
May manifest as oliguria, anuria, or normal urine
volume
7
Important Lab Values
BUN - Blood urea nitrogen.
measure of the kidneys' ability to excrete urea, the chief waste product of protein breakdown
Elevated in renal failure and dehydration
Normal range 7 - 20 mg/dl
Creatinine: A waste product from protein in the diet and from the muscles of the body.
removed from the body by the kidneys
Increased in kidney disease
Normal range 0.5 to 1.0 mg/dL
8
Important Test
Creatinine Clearance Test
compares the level of creatinine in urine with the creatinine
level in the blood
24-hour urine sample
Male: 97 to 137 ml/min.
Female: 88 to 128 ml/min.
Estimate the glomerular filtration rate (GFR) -- the standard by which kidney function is assessed range 90 120 mL/min
9
Glomerular Filtration Rate
(GFR)
Levels below 60 mL/min for 3 or more months are a sign of
chronic kidney disease.
Those with GFR results below 15 mL/min are a sign of kidney
failure
10
11
Definitions
Parenchyma - The key elements of an organ essential to its functioning Uremia –retention in the bloodstream of waste products normally excreted in the urine: urea, creatinine and other nitrogen containing waste products of proteins .
Also called Azotemia.
results from kidney disease
Anuria - total urine output less than 50 mL in 24 h
Oliguria - total urine output less than 400 mL in 24 h
12
12
Mechanisms:
Pre-renal -- volume depletion,
poor cardiac efficiency, vasodilation Intra-renal -- prolonged
ischemia, myoglobinuria, infections, nephrotoxins, glomerulonephritis Post-renal -- obstruction from
stone, tumor MECHANICAL
OBSTRUCTION from the tubules to urethra. BPH-most common Fall 2011 NU 202
Renal Failure
13
Clinical Manifestations
Four clinical phases:
1. Initiation: Initial insult to oliguria -≤400ML/24hrs
2. Oliguria: ↑Bun/Creatinine, Rise in serum concentration of substances excreted by kidney K+, Magnesium, ↓U/O
3. Diuresis: Gradually increasing U/O lab values stabilize
4. Recovery: Improvement of renal function
3-12 months
Permanent 1-3% reduction in GFR
14
INITIATION-OLIGURIC PHASES
Begins with the onset of the event causing tubular
necrosis
Ends when tubular injury occurs
Oliguria develops
Elevated serum Creatinine, BUN, K+, Mg. ,acidosis
Nonoliguric form-urine output WNL( associated
with nephrotoxic ABT, Burns,Trauma, Halothane)
15
INITIATION-OLIGURIC PHASES
Begins with the onset of the event causing tubular
necrosis
Ends when tubular injury occurs
Oliguria develops
Elevated serum Creatinine, BUN, K+, Mg. ,acidosis
Nonoliguric form-urine output WNL( associated
with nephrotoxic ABT, Burns,Trauma, Halothane)
16
DIURESIS PHASE
Increased urine output
Serum Creatinine, BUN K+ decrease
Uremic symptoms improve
17
RECOVERY PHASE
GFR IMPROVES
May take up to 1 year
18
Clinical MANIFESTATIONS
Altered Mental Status (AMS)-lethargy,
fatigue
HTN, Hypotension
Edema
Decreased urinary output
CHF
19
Clinical Manifestations
19
Every system of the body is affected:
CNS-Lethargy, Confusion, Headache ,Seizures
CV-Congestive Heart Failure , HTN
Lungs- SOB
Skin/Hair/Nails-Dry thin scaly
GI- Diarrhea ,Nausea, Vomiting, Uremic GI lesions
GU-Oliguria , Anuria , Hematuria
Fall 2011 NU 202
20
Abnormal lab values
20
Hyperkalemia as result of the ↓ in GFR
Patients can not excrete K+ normally
↑Protein catabolism ↑K+ = in body fluid
Can cause dysrhythmias and cardiac arrest
Source of K+ is GI blood loss, dietary, extracellular shift
related to metabolic acidosis
Fall 2011 NU 202
21
Metabolic Acidosis
21
Related to oliguria
Unable to eliminate acids
Normal renal buffering system fails
Fall in CO2 combining power
Progressive
Can cause cardiac arrhythmias
Fall 2011 NU 202
22
22
Changes in Calcium and Phosphorus
Increase in serum phosphate
Decrease in calcium levels
Decreased CA++ absorption from GI tract
At risk for stress fractures
Fall 2011 NU 202
23
Medical Management
23
Restore normal electrolyte balance
Prevent complications
Prevent anuria if possible
Allow kidneys time to regenerate until
normal kidney function resumes
Fall 2011 NU 202
Summary of ARF Categories 24
Characteristics
PreRenal
Intrarenal
Postrenal
Etiology
Hypo-perfusion Parenchymal damage Obstruction
BUN
Increased
Increased
(out of normal
20:1 proportion to creatinine)
Increased
Creatinine
Increased
Increased
Increased
Urine output
Decreased
Varies, often decreased Varies, may be decreased, or sudden anuria Urine sodium
Decreased to
<20 mEq/L
Increased to >40 mEq/L Varies, often decreased to 20 mEq/L or less
Urinary sediment Normal, few hyaline casts
Abnormal casts & debris Usually normal
Urine osmolality Increased to
500 mOsm
About 350 mOsm similar to serum
Varies, increased or equal to serum
Urine specific gravity Increased
Low normal
Varies
25
Pre-Renal
Intra-Renal
Increase renal perfusion
Supportive
Blood loss – Blood transfusion Restrict meds that are excreted by kidneys
Hypovolemia -Infuse
Albumin ,Normal Saline
Remove causative agent
25
Treatment
Remove obstruction
Post-Renal
Avoid Complications
Aggressive Management of prerenal and post renal causes Management
Fluid balance based on daily body weight, CVP, serum and urine concentrations, losses,
B/P
Measure all output
Fall 2011 NU 202
26
URINE ANALYSIS
Fixed specific gravity1.010 due to inability to
concentrate urine
+protein if glomerular damage is cause of ARF
Microscopic RBC’S if inflammatory process
Renal tubular epithelial cells indicates acute tubular
necrosis
Cast cells are protein and cellular debris
27
Serum Electrolytes
K+=elevated
Na+=depends on phase
Phosphorus=elevates, Calcium decreases
BUN=elevated; measurement of nitrogen portion of
urea-a product formed from protein metabolism.
Normal=10-20.
28
Summary of ARF Categories
29
CBC
RBC decreased-anemia secondary to
decreased production of erythropoitin
HCT decreased
30
DIAGNOSTIC TESTS
ULTRASOUND KIDNEYS-UTETERS-BLADDER
Large kidneys-acute problem
Small kidneys-chronic problem
CT pelvis/abdomen
IVP
Retrograde pyelography
Renal Biopsy
Renal Scan
31
Nursing Diagnosis
Altered thought process R/T excess
metabolic wastes
Fluid volume excess
Altered nutrition
Risk for infection
Knowledge deficit
32
MANAGEMENT
Altered mental status
Goal: reduce urea
PLAN- ASSESS V/S, NEURO status,
Maintain safety
33
Fluid volume excess
Monitor v/s- (adm.dopamine prn hypotension)
Diuresis-adm. Lasix or atrial naturetic peptide
which inihibits Na+ and water absorption and dilates afferent arterioles, therefore increasing blood flow
HTN-adm. Anti HTN meds-ACEI (check serum
BUN/creatinine ratio20:1)
Maintain fluid restriction
Monitor weight daily
MAINTAIN ACCURATE INTAKE AND OUTPUT
34
FVE/CV
Hyperkalemia- adm.kayexalate po/pr
Combine with sorbital to prevent constipation
Adm. Glucose and insulin to drive K+ back into
intracellular space or
Calcium gluconate
Metabolic acidosis(ABG)-adm. Sodium bicarbonate
DIALYSIS
Hyperphosphotemia- administer Phosphorus
binding agents(antacids bind with phosphorous in
G.I. tract, then are excreted in feces) calcium carbonate :administer with food
35
Alt. Nutrition
G.I=adm H2 blockers or proton
pump inhibitors-prevent GI bleed
Low protein ,low NA+,K+,high carb,fld.restriction(500ml. +u.o./24hr)Dietary consult
Monitor nausea/vomitingadm.antiemetic
36
Alt. Nutrition
Adm. and monitor parenteral nutrition
Provide oral care
Adm. meds with meals
Encourage small meals or snacks
37
Knowledge deficit
ASSESS pts. Level of anxiety
Assess pts. Knowledge and understanding
Explain therapeutic procedures and diagnostic
tests
Reinforce dietary and fluid restrictions
Instruct pt. to avoid nephrotoxic drugs
Review S&S of ARF
38
Risk for Infection
Teach pt. handwashing
Teach pt.S&S of infection
Reinforce importance of iron supplement,
multivitamin daily to improve anemia and improve immune status
Prevent skin breakdown
39
Supportive care
Dialysis:removes excess fluid and metabolic waste products Hemodialysis
Peritoneal Dialysis
Continuous Arteriovenous
Hemofiltration(CAVH)
40
Chronic Renal Failure
End Stage Renal Disease-silent disease
Develops slowly and insidiously
Functional capacity of nephrons is lost
Glomerular filtration(GRF) decreases
41
Conditions Causing ESRD
Diabetic Nephropathy
HYPERTENSION
Glomerulonephritis
Cystic kidney disease
Other urologic diseases
Etiology unknown
Other
42
Stages of Chronic Renal Failure
Stage 1
Reduced renal reserve
40-75%nephron loss
Usually asymptomatic
43
Stage 2
Renal Insufficiency
75-90% nephron function loss
Elevated BUN and Creatinine
Anemia; inability to concentrate urine
May c/o polyuria and nocturia
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Stage 3
End stage real disease (ESRD)
Final stage; less than 10% nephron function
Elevated BUN and Creatinine;Elevated K+
Dialysis is indicated
Metabolic acidosis
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ESRD
Elevated serum phosphate level
Reciprocal low calcium level
Decreased serum calcium level causes
increased secretion of parathormone,causing calcium to leave the
bone.
Vitamin D decreases causing osteodystrophy 46
Pathophysiology of CRF
As nephrons are destroyed, remaining nephrons
hypertrophy
Glomerular capillary flow and pressure increase in
these nephrons
Remaining nephrons predisposed to …show more content…
glomerular
sclerosis/scarring
CRF is identified when uremic stage is reached
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MANIFESTATIONS OF CRF
Uremia
Alteration in fluid and electrolytes
Early S&S include nausea, apathy, weakness
and fatigue
Progresses to vomiting, increased
weakness , lethargy and confusion
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Cardiovascular and Hematologic
Effects
Hypertension
Hyperlipidemia,Anemia
Coronary artery disease, Impaired clotting
Dysrhythmias
Pericarditis
Pericardial effusion
Cerebral Vascular Disease,CHF
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Neurologic and Musculoskeletal
Effects
Altered mental status
Fatigue , Seizures, Coma
Peripheral neuropathy
Osteodystrophy, Bone pain, Fractures
Muscle Weakness
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Fluid and Electrolyte Effects
Proteinuria, Hematuria
Inability to concentrate urine
Dehydration
Polyuria,nocturia
Na and H2O retention, Hyperkalemia
Hyperphosphatemia, Hypocalcemia
Acidosis, Hyperlipidemia, Hyperuricemia
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Respiratory and GI Effects
Respiratory Distress Syndrome
Pulmonary edema
Pleural effusion, Pleuritis
Kuss maul respirations
Anorexia ,N/V, Hiccups
Gastroenteritis, GI Bleed, Peptic ulcer
Uremic fetor
Abdominal pain
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Endocrine,Metabolic and
Dermatologic Effects
Significantly elevated BUN and creatinine
Glucose intolerance
Elevated uric acid level=Gout
Menstrual irregularities
Reduced testosterone levels
Uremic frost, dry itchy skin, poor turgor, bruising
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Dialysis
A process of diffusion by which dissolved particles can
be transported across a semipermeable membrane.
Corrects fluid, electrolyte and acid-base
Imbalances
Severe fluid and electrolyte imbalances, hyperkalemia,
acidosis and uremic manifestations
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Hemodialysis
Uses the principles of diffusion and ultrafiltration to
remove electrolytes, waste products and excess water from the body
Blood>Venous access>dialyzing membrane unit
Semipermeable membrane has large pores allowing
small particles to pass thru
(e.g. blood cells and plasma proteins)
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Considerations
Vascular access
Acute or temporary access may be gained
using subclavian or internal jugular venous catheter Arteriovenous (AV) fistula most commonly
used long term access
56
Internal AV Fistula and Graft
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Fall 2011 NU 202
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Systemic Complications
Hypotension
Bleeding
Infection
Dialysis dementia
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AV Fistula
Non dominant arm is used
No blood draws, IV access or blood pressure
Fistula is created by anastomosis of artery and vein
Takes approx.1 month
Assess for Bruit (auscultate) and Thrill(pulsation)
)
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Peritoneal Dialysis
Peritoneal dialysis use the pt’s own peritoneal
lining as a semi permeable membrane thru which diffusion, osmosis, and filtration occurs
Warmed dialyzing fluid. placed into peritoneal
cavity via a permanent indwelling catheter
Metabolic wastes and excess electrolytes
diffuse into the dialasate
FLD. drained by gravity out of peritoneal cavity
into sterile bag
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Peritoneal Dialysis
60
The patient must be alert
and have good fine motor skills Pt must be independently able to perform dialysis at home
Risk of peritonitis from
introduction of bacteria into the peritoneal cavity
The higher the dialysate
the greater the osmotic gradient the more water is removed Solutions used 1.5% 2.5%
4.25%
Fall 2011 NU 202
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Complications of P.D.
Peritonitis-abdominal pain, tenderness,
fever, cloudy drainage
Alt in gas exchange due to abdominal
distention
Increased protein loss
Perforation
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Nursing management
Teaching regarding disease process
Teaching regarding diet
Teaching regarding Meds
Teaching regarding technique especially for
Peritoneal Dialysis
Evaluation of teaching via return demonstration
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Fall 2011 NU 202
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64
Renal Transplantation
Solid organ most successful of transplanted
Most successful of transplantation procedures
Surgical insertion of a functioning kidney
Improved quality of life
Lifelong immunosuppressive therapy
Most from cadavers; rest related living donors
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Renal Transplantation
Recipients in good physical health, except for primary
kidney disease and pts. betw,.5 and 50 yrs. of age have best prognosis
66
Types of transplants
Living Donor- Relative
Cadaver
Living Donor- Non Relative
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Renal Transplantation
Tissue antigens must be as close to the
recipient’s as possible
Live donor must be in good phy. Condition
Have the same ABO blood group
Cadaver kidney requires human leukocyte
antigen(HLA) compatibility
Cadaver donors must be brain dead,<65years of
age, no disease,malignancy,infection(HIV-HBVHCV)
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Patient Positioning and Incisional
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Approaches
Fall 2011 NU 202
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Renal Transplantation
70
Kidney Surgery
Pre-operative considerations
Peri-operative concerns
Post-operative management
Potential hemorrhage and shock
Potential abdominal distention and paralytic ileus
Potential infection
Potential thromboembolism
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Kidney Transplant Explained
http://www.nlm.nih.gov/medlineplus/ency/presen
tations/100087_1.htm
72
Immunosupressive Therapy
The presence of foreign tissue in the body stimulates a
normal immune response to reject the transplanted organ Immunosuppressive therapy reduces rejection
response
Therapy suppresses a portion of the immune system
and the inflammatory response
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Case Presentation
80 yo active male with a Hx.
of Left Nephrectomy
2@ry to Ca 10 years ago,and a Hx.HTN,is noted to have STEMI on EKG w/o S/S in his PMD’s office. Patient sent via EMS to ED,then transferred to the cath lab where an angiography w contrast and a stent placement was performed.
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Case Presentation
Post Procedure Labs:
K*5.7
Na145
BUN 50
Creat 2.5
What caused this change from previous
normal values?
What else would you want to look at?
75
Question
A patient receiving peritoneal dialysis is complaining of pain with rebound tenderness. The dialysate drainage is cloudy. This symptom is indicative of which acute complication? a. Hernia
b. Bleeding
c. Leakage
d. Peritonitis