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Nursing care plan renal failure acute

Written by ncp nursing care plan on April 21st, 2012

I. Pathophysiology
a. Sudden decrease in kidney function, which may or may not
be associated with a decrease in urine output and results in a
buildup of toxic wastes, such as urea and creatinine in the
blood
b. Three well-defined stages: oliguric or anuric, diuretic, and
convalescent (Choka, 2005)
i. Oliguric
1. Filtration capability is reduced because of debris and
damage to renal tubules.
2. Output is greatly reduced—may be less than
400 mL/day.
3. If anuria present, catastrophic injury has likely
occurred in both kidneys—as in obstructive uropathy
or, less commonly, in bilateral renal artery occlusion,
acute cortical necrosis, or rapidly progressive
glomerulonephritis (Agraharkar & Gupta, 2007).
ii. Diuretic
1. May skip oliguric phase and begin to make large
quantities (may be several liters) of urine
2. Client with oliguria will progress through diuretic
phase during recovery.
3. Urine is dilute because of kidney’s inability to
concentrate.
iii. Convalescent
1. Renal blood flow and filtration improves.
2. Process of recovery is gradual, often weeks to
months; in many cases, some degree of renal
insufficiency persists.

II. Classification—dependent on site
a. Prerenal failure (azotemia): decreased renal perfusion
manifested by reduced urine output because of decreased
glomerular filtration rate (GFR)
b. Renal or intrinsic failure: associated with parenchymal
changes with damage to the renal tubules (acute tubular
necrosis [ATN]) caused by ischemia or nephrotoxic
substances
c. Postrenal failure: results from an obstruction in the urinary
tract anywhere from the tubules to the urethral meatus

III. Etiology
a. Multiple causes: ischemia and toxicity (most common),
obstructions
i. Prerenal failure: blood volume depletion due to hemorrhage,
“third-space” sequestration of fluid as in edema or
ascites in advanced liver disease, or burns; dehydration
due to gastrointestinal (GI) losses or overuse of diuretics;
septic or anaphylactic shock; heart failure (HF) with renal
insufficiency, myocardial infarction (MI), trauma; renal
artery obstruction; and use of certain drugs, such as
nonsteroidal anti-inflammatory drugs (NSAIDs),
cyclooxygenase inhibitors, angiotensin-converting enzyme
(ACE) inhibitors
ii. Intrinsic failure: ischemia and hypoperfusion similar to
prerenal hypoperfusion (except that correction of the
causative factor may be followed by continued oliguria
for up to 30 days) associated with prolonged acute renal
failure (ARF), blood transfusion reaction, or renal artery
stenosis; and direct damage from nephrotoxic substances,
such as radiocontrast media, cyclosporine,
heavy metals (e.g., lead, mercury), cytotoxic drugs
(e.g., certain chemotherapy agents), certain antibiotics
(e.g., carbenicillins, aminoglycosides)
iii. Postrenal failure: most commonly occurs with stones in
the ureters, bladder, or urethra; from trauma or edema
associated with infection, prostatic hypertrophy, or
cancer; cervical cancer; strictures of renal artery
iv. If underlying cause is corrected, the nephrons may
recover; however, in some cases, damage is permanent
and renal failure becomes chronic.
b. Community- or hospital-acquired
i. Most community-acquired ARF is secondary to volume
depletion; as many as 90% of cases are estimated to
have a potentially reversible cause (Sinert & Peacock,
2006).
ii. Hospital-acquired ARF often occurs in the intensive
care unit (ICU) setting and is commonly the end result
of multiorgan failure.
c. Risk factors: advanced age, chronic infection, diabetes, hypertension,
immune disorders such as lupus or scleroderma

IV. Statistics (Agraharkar & Gupta, 2007; Sinert, 2006)
a. Morbidity: Upon hospital admission, approximately 1% of
clients have ARF, whereas during hospitalization, the
estimated incidence of ARF is 2% to 5%.
b. Mortality: The rate for hospital-acquired ARF is as high as
40% to 80% and is directly correlated to the severity of
comorbidities; with the advent of dialysis, the most common
causes of death associated with ARF include sepsis, cardiac
failure, and pulmonary failure; rates are generally lower for
nonoliguric ARF than for oliguric ARF because the former
is usually caused by drug-induced nephrotoxicity and
interstitial nephritis, which are associated with fewer systemic
complications; individuals with ARF who are older
than age 80 have mortality rates similar to younger adults.

Care Setting
Client will be treated in inpatient acute medical or surgical
unit.

Related Concerns
Metabolic acidosis—primary base bicarbonate deficiency,
Fluid and electrolyte imbalances,
Psychosocial aspects of care,
Renal dialysis—general considerations,
Renal failure: chronic,
Sepsis/septicemia,
Total nutritional support: parenteral/enteral feeding,
Upper gastrointestinal/esophageal bleeding,

Nursing Priorities
1. Reestablish or maintain fluid and electrolyte balance.
2. Prevent complications.
3. Provide emotional support for client and significant
other (SO).
4. Provide information about disease process, prognosis,
and treatment needs.

Discharge Goals
1. Homeostasis achieved.
2. Complications prevented or minimized.
3. Dealing realistically with current situation.
4. Disease process, prognosis, and therapeutic regimen
understood.
5. Plan in place to meet needs after discharge.

I. Pathophysiology
a. Sudden decrease in kidney function, which may or may not
be associated with a decrease in urine output and results in a
buildup of toxic wastes, such as urea and creatinine in the
blood
b. Three well-defined stages: oliguric or anuric, diuretic, and
convalescent (Choka, 2005)
i. Oliguric
1. Filtration capability is reduced because of debris and
damage to renal tubules.
2. Output is greatly reduced—may be less than
400 mL/day.
3. If anuria present, catastrophic injury has likely
occurred in both kidneys—as in obstructive uropathy
or, less commonly, in bilateral renal artery occlusion,
acute cortical necrosis, or rapidly progressive
glomerulonephritis (Agraharkar & Gupta, 2007).
ii. Diuretic
1. May skip oliguric phase and begin to make large
quantities (may be several liters) of urine
2. Client with oliguria will progress through diuretic
phase during recovery.
3. Urine is dilute because of kidney’s inability to
concentrate.
iii. Convalescent
1. Renal blood flow and filtration improves.
2. Process of recovery is gradual, often weeks to
months; in many cases, some degree of renal
insufficiency persists.
II. Classification—dependent on site
a. Prerenal failure (azotemia): decreased renal perfusion
manifested by reduced urine output because of decreased
glomerular filtration rate (GFR)
b. Renal or intrinsic failure: associated with parenchymal
changes with damage to the renal tubules (acute tubular
necrosis [ATN]) caused by ischemia or nephrotoxic
substances
c. Postrenal failure: results from an obstruction in the urinary
tract anywhere from the tubules to the urethral meatus

III. Etiology
a. Multiple causes: ischemia and toxicity (most common),
obstructions
i. Prerenal failure: blood volume depletion due to hemorrhage,
“third-space” sequestration of fluid as in edema or
ascites in advanced liver disease, or burns; dehydration
due to gastrointestinal (GI) losses or overuse of diuretics;
septic or anaphylactic shock; heart failure (HF) with renal
insufficiency, myocardial infarction (MI), trauma; renal
artery obstruction; and use of certain drugs, such as
nonsteroidal anti-inflammatory drugs (NSAIDs),
cyclooxygenase inhibitors, angiotensin-converting enzyme
(ACE) inhibitors
ii. Intrinsic failure: ischemia and hypoperfusion similar to
prerenal hypoperfusion (except that correction of the
causative factor may be followed by continued oliguria
for up to 30 days) associated with prolonged acute renal
failure (ARF), blood transfusion reaction, or renal artery
stenosis; and direct damage from nephrotoxic substances,
such as radiocontrast media, cyclosporine,
heavy metals (e.g., lead, mercury), cytotoxic drugs
(e.g., certain chemotherapy agents), certain antibiotics
(e.g., carbenicillins, aminoglycosides)
iii. Postrenal failure: most commonly occurs with stones in
the ureters, bladder, or urethra; from trauma or edema
associated with infection, prostatic hypertrophy, or
cancer; cervical cancer; strictures of renal artery
iv. If underlying cause is corrected, the nephrons may
recover; however, in some cases, damage is permanent
and renal failure becomes chronic.
b. Community- or hospital-acquired
i. Most community-acquired ARF is secondary to volume
depletion; as many as 90% of cases are estimated to
have a potentially reversible cause (Sinert & Peacock,
2006).
ii. Hospital-acquired ARF often occurs in the intensive
care unit (ICU) setting and is commonly the end result
of multiorgan failure.
c. Risk factors: advanced age, chronic infection, diabetes, hypertension,
immune disorders such as lupus or scleroderma

IV. Statistics (Agraharkar & Gupta, 2007; Sinert, 2006)
a. Morbidity: Upon hospital admission, approximately 1% of
clients have ARF, whereas during hospitalization, the
estimated incidence of ARF is 2% to 5%.
b. Mortality: The rate for hospital-acquired ARF is as high as
40% to 80% and is directly correlated to the severity of
comorbidities; with the advent of dialysis, the most common
causes of death associated with ARF include sepsis, cardiac
failure, and pulmonary failure; rates are generally lower for
nonoliguric ARF than for oliguric ARF because the former
is usually caused by drug-induced nephrotoxicity and
interstitial nephritis, which are associated with fewer systemic
complications; individuals with ARF who are older
than age 80 have mortality rates similar to younger adults.

Care Setting
Client will be treated in inpatient acute medical or surgical
unit.

Related Concerns
Metabolic acidosis—primary base bicarbonate deficiency,
Fluid and electrolyte imbalances,
Psychosocial aspects of care,
Renal dialysis—general considerations,
Renal failure: chronic,
Sepsis/septicemia,
Total nutritional support: parenteral/enteral feeding,
Upper gastrointestinal/esophageal bleeding,

Nursing Priorities
1. Reestablish or maintain fluid and electrolyte balance.
2. Prevent complications.
3. Provide emotional support for client and significant
other (SO).
4. Provide information about disease process, prognosis,
and treatment needs.

Discharge Goals
1. Homeostasis achieved.
2. Complications prevented or minimized.
3. Dealing realistically with current situation.
4. Disease process, prognosis, and therapeutic regimen
understood.
5. Plan in place to meet needs after discharge.

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Source Credits: Nursing Care Planning Guides: For Adults in Acute, Extended and Home Care Settings by S. P. Ulrich and S. W. Canale BSN MSN / Nursing Care Plans by M. Doenges MF Moorehouse Alice Murr