for educational purpose only..

1. Prepared by:
BSN, Level IV
Sarah Jane A. Cristobal

2. Is the rapid breakdown of renal (kidney)
function that occurs when high levels of uremic toxins
(waste products of the body's metabolism)
accumulate in the blood. ARF occurs when the
kidneys are unable to excrete (discharge) the daily
load of toxins in the urine.
DEFINITION

3. Based on the amount of urine that is excreted over a 24-
hour period, patients with ARF are separated into two groups:
 Oliguric: patients who excrete less than 500 milliliters
per day (< 16 oz/day)
 Nonoliguric: patients who excrete more than 500
milliliters per day (> 16 oz/day)
DEFINITION

4. Acute kidney failure almost always occurs in connection
with another medical condition or event. Conditions that can
increase your risk of acute kidney failure include:
Being hospitalized, especially for a serious condition that
requires intensive care
 Advanced age
 Blockages in the blood vessels in your arms or legs
(peripheral artery disease)
 Diabetes
 High blood pressure
 Heart failure
 Kidney diseases
 Liver diseases
RISK FACTORS

5. A detailed and accurate history is crucial
for diagnosing acute kidney injury (AKI) and
determining treatment. Distinguishing AKI from
chronic kidney disease is important, yet making the
distinction can be difficult.
PHYSICAL
EXAMINATION

6. A history of chronic symptoms—months
of fatigue, weight loss, anorexia, nocturia, sleep
disturbance, and pruritus—suggests chronic kidney
disease. AKI can cause identical symptoms, but over a
shorter course.
PHYSICAL
EXAMINATION

7. It is important to elicit a history of any of the following
etiologic factors:
 Volume restriction (eg, low fluid intake,
gastroenteritis)
 Nephrotoxic drug ingestion
 Trauma or unaccustomed exertion
 Blood loss or transfusions
 Exposure to toxic substances, such as ethyl alcohol or
ethylene glycol
 Exposure to mercury vapors, lead, cadmium, or other
heavy metals, which can be encountered in welders
and miners
PHYSICAL
EXAMINATION

8. Urine output history can be useful. Oliguria
generally favors AKI. Abrupt anuria suggests acute
urinary obstruction, acute and severe
glomerulonephritis, or embolic renal artery occlusion.
A gradually diminishing urine output may indicate a
urethral stricture or bladder outlet obstruction due to
prostate enlargement.
PHYSICAL
EXAMINATION

9. Prerenal failure
Patients commonly present with symptoms related to
hypovolemia, including thirst, decreased urine output,
dizziness, and orthostatic hypotension. Ask about
volume loss from vomiting, diarrhea, sweating, polyuria,
or hemorrhage. Patients with advanced cardiac failure
leading to depressed renal perfusion may present with
orthopnea and paroxysmal nocturnal dyspnea.
PHYSICAL
EXAMINATION

10. Elders with vague mental status change are
commonly found to have prerenal or normotensive
ischemic AKI. Insensible fluid losses can result in
severe hypovolemia in patients with restricted fluid
access and should be suspected in elderly patients
and in comatose or sedated patients.
PHYSICAL
EXAMINATION

11. Intrinsic renal failure
Patients can be divided into those with glomerular
etiologies and those with tubular etiologies of AKI.
Nephritic syndrome of hematuria, edema, and
hypertension indicates a glomerular etiology for AKI.
Query about prior throat or skin infections.
PHYSICAL
EXAMINATION

12. A history of prior gynecologic surgery or
abdominopelvic malignancy often can be helpful in
providing clues to the level of obstruction.
Flank pain and hematuria should raise a concern
about renal calculi or papillary necrosis as the source
of urinary obstruction.
PHYSICAL
EXAMINATION

13. Postrenal failure
Postrenal failure usually occurs in older men with
prostatic obstruction and symptoms of urgency,
frequency, and hesitancy. Patients may present with
asymptomatic, high-grade urinary obstruction
because of the chronicity of their symptoms.
RISK FACTORS

14. The interaction of tubular and vascular
events result in ARF. The primary cause of ATN is
ischemia. Ischemia for more than two hours
results in severe and irreversible damage to the
kidney tubules. Significant reduction in glomular
filtration rate (GFR) is a result of (1) ischemia, (2)
activation of the renin-angiotensin system , and
(3) tubular obstruction by cellular debris
PATHOPHYSIOLOGIC
MECHANISM

15. As nephrotoxins damage the tubular
cells and these cells are lost through necrosis,
the tubules become more permeable. This results
in filtrate absorption and a reduction in the
nephrons ability to eliminate waste.
PATHOPHYSIOLOGIC
MECHANISM

16. The clinical course of ARF is characterized by the
following three phases:
Phase 1. Onset
ARF begins with the underlying clinical
condition leading to tubular necrosis, for example
hemorrhage, which reduces blood volume and
renal perfusion. If adequate treatment is provided
in this phase then the individual's prognosis is
good.
PATHOPHYSIOLOGIC
MECHANISM

17. Phase 2. Maintenance
A persistent decrease in GFR and tubular
necrosis characterizes this phase. Endothelial
cell necrosis and sloughing lead to tubular
obstruction and increased tubular permeability.
Because of this, oliguria is often present during
the beginning of this phase. Efficient elimination
of metabolic waste, water, electrolytes, and acids
from the body cannot be performed by the kidney
during this phase.
PATHOPHYSIOLOGIC
MECHANISM

18. Therefore, azotemia, fluid retention,
electrolyte imbalance and metabolic acidosis
occurs. The patient is at risk for heart failure and
pulmonary edema during this phase because of
the salt and water retention. Immune function is
impaired and the patient may be anemic because
of the suppressed erythropoietin secretion by the
kidney and toxin-related shorter RBC life.
PATHOPHYSIOLOGIC
MECHANISM

19. Phase 3. Recovery
Renal function of the kidney improves
quickly the first five to twenty-five days of this
phase. It begins with the recovery of the GFR and
tubular function to such an extent that BUN and
serum creatinine stabilize. Improvement in renal
function may continue for up to a year as more
and more nephrons regain function.
PATHOPHYSIOLOGIC
MECHANISM

20. If your signs and symptoms suggest that you have
acute kidney failure, your doctor may recommend tests
and procedures to verify your diagnosis. These may
include:
 Urine output measurements. The amount of urine you
excrete in a day may help your doctor determine the
cause of your kidney failure.
 Urine tests. Analyzing a sample of your urine, a
procedure called urinalysis, may reveal abnormalities
that suggest kidney failure.
DIAGNOSTIC
EXAMINATION

21.  Blood tests. A sample of your blood may reveal
rapidly rising levels of urea and creatinine — two
substances used to measure kidney function.
 Imaging tests. Imaging tests such as ultrasound
and computerized tomography (CT) may be used to
help your doctor see your kidneys.
DIAGNOSTIC
EXAMINATION

22.  Removing a sample of kidney tissue for testing. In
certain situations, your doctor may recommend a
kidney biopsy to remove a small sample of kidney
tissue for lab testing. To remove a sample of kidney
tissue, your doctor may insert a thin needle
through your skin and into your kidney.
DIAGNOSTIC
EXAMINATION

23. Drugs that are renally excreted may need
to have their doses reduced in patients with renal
insufficiency or end-stage renal disease:
MEDICATIONS

24. For prescribing purposes renal impairment is usually
divided into three grades:
 Mild: GFR 20-50 ml/minute; serum creatinine
approximately 150-300 µmol/l.
 Moderate: GFR 10-20 ml/minute; serum creatinine
approximately 300-700 µmol/L.
 Severe: GFR less than 10 ml/minute; serum
creatinine >700 µmol/L.
MEDICATIONS

25. Nephrotoxic drugs should, if possible, be
avoided in patients with renal disease because the
consequences of nephrotoxicity are likely to be more
serious when the renal reserve is already reduced.
MEDICATIONS

26. The situation may change if a patient
begins dialysis, since some drugs will be removed by
the dialysis. Dialysis may lead to the loss of therapeutic
effect for some drugs.
MEDICATIONS

27. Drugs to which particular attention must
be given include many antibiotics, histamine H2-
receptor antagonists, digoxin, anticonvulsants and non-
steroidal anti-inflammatory drugs (NSAIDs).
MEDICATIONS

28. 1. Excess Fluid Volume May be relate to
Compromised regulatory mechanism (renal failure)
Possibly evidenced by
 Intake greater than output, oliguria;
 changes in urine specific gravity
 Venous distension;
 blood pressure (BP)/central venous pressure (CVP)
changes
 Generalized tissue edema, weight gain
Changes in mental status, restlessness
NURSING
DIAGNOSIS

29. 2. Risk for Decreased Cardiac Output
Risk factors may include
 Fluid overload (kidney dysfunction/failure, overzealous
fluid replacement)
 Fluid shifts,
 fluid deficit (excessive losses)
 Electrolyte imbalance (potassium, calcium); severe
acidosis
 Uremic effects on cardiac muscle/oxygenation
Possibly evidenced by
[Not applicable; presence of signs and symptoms
establishes an actual diagnosis.]
NURSING
DIAGNOSIS

30. 3. Risk for Imbalanced Nutrition
risk for less than body requirements
Risk factors may include
 Protein catabolism;
 dietary restrictions to reduce nitrogenous waste
products
 Increased metabolic needs
 Anorexia,
 nausea/vomiting;
 ulcerations of oral mucosa
NURSING
DIAGNOSIS

31. 4. Risk for Infection
Risk factors may include
 Depression of immunologic defenses (secondary to
uremia)
 Invasive procedures/devices (e.g., urinary catheter)
 Changes in dietary intake/malnutrition
Possibly evidenced by
[Not applicable; presence of signs and symptoms
establishes an actual diagnosis.]
NURSING
DIAGNOSIS

32. 5. Risk for Deficient Fluid Volume
Risk factors may include
 Excessive loss of fluid (diuretic phase of ARF, with
rising urinary volume and delayed return of tubular
reabsorption capabilities)
Possibly evidenced by
[Not applicable; presence of signs and symptoms
establishes an actual diagnosis.]
NURSING
DIAGNOSIS

33. 6. Deficient Knowledge May be related to
Lack of exposure/recall
Information misinterpretation
Unfamiliarity with information resources
Possibly evidenced by
 Questions/request for information,
 statement of misconception
 Inaccurate follow-through of instructions/development
of preventable
Complications
NURSING
DIAGNOSIS

34. Other Possible Nursing Care Plans
 Fluid Volume, deficient (specify)—dependent on cause,
duration, and stage of recovery.
 Fatigue—decreased metabolic energy production/dietary
restriction, anemia, increased energy requirements, e.g.,
fever/ inflammation, tissue regeneration.
 Infection, risk for—depression of immunologic defenses
(secondary to uremia), changes in dietary
intake/malnutrition, increased environmental exposure.
 Therapeutic Regimen: ineffective management—
complexity of therapeutic regimen, economic difficulties,
perceived benefit.
NURSING
DIAGNOSIS

35. Record accurate intake and output (I&O).
Include “hidden” fluids such as IV antibiotic
additives, liquid medications, ice chips, frozen
treats.
Measure gastrointestinal (GI) losses and
estimate insensible losses, e.g., diaphoresis.
NURSING
INTERVENTIONS

36. Monitor urine specific gravity.
Weigh daily at same time of day, on same scale,
with same equipment and clothing.
Assess skin, face, dependent areas for edema.
NURSING
INTERVENTIONS

37. Evaluate degree of edema (on scale of +1–+4).
Monitor heart rate (HR), BP, and JVD/CVP.
Auscultate lung and heart sounds.
Assess level of consciousness; investigate
changes in mentation, presence of restlessness.
Plan oral fluid replacement with patient, within
multiple restrictions. Intersperse desired
beverages throughout 24 hr. Vary offerings, e.g.,
hot, cold, frozen.
NURSING
INTERVENTIONS

38. Correct any reversible cause of ARF, e.g.,
replace blood loss, maximize cardiac output,
discontinue nephrotoxic drug, relieve obstruction
via surgery.
Monitor laboratory/ diagnostic studies, e.g.:
BUN, Cr; Urine sodium and Cr; Serum sodium;
Serum potassium; Hb/Hct; Serial chest x-rays.
NURSING
INTERVENTIONS

39. Administer/restrict fluids as indicated.
Note occurrence of slow pulse, hypotension,
flushing, nausea/ vomiting, and depressed level
of consciousness (central nervous system [CNS]
depression).
NURSING
INTERVENTIONS

40. Give patient/SO a list of permitted foods/fluids
and encourage involvement in menu choices.
Provide high-calorie, low-/moderate-protein diet.
Include complex carbohydrates and fat sources to
meet caloric needs (avoiding concentrated sugar
sources) and essential amino acids.
NURSING
INTERVENTIONS

41. Avoid invasive procedures, instrumentation, and
manipulation of indwelling catheters whenever
possible. Use aseptic technique when caring
for/manipulating IV/invasive lines. Change
site/dressings per protocol. Note edema, purulent
drainage.
NURSING
INTERVENTIONS

42. Provide routine catheter care and promote
meticulous perianal care. Keep urinary drainage
system closed and remove indwelling catheter as
soon as possible.
Encourage patient to observe characteristics of
urine and amount/frequency of output.
NURSING
INTERVENTIONS

43. Review fluid intake/restriction. Remind patient to
spread fluids over entire day and to include all
fluids (e.g., ice) in daily fluid counts.
Discuss activity restriction and gradual
resumption of desired activity. Encourage use of
energy-saving, relaxation, and diversional
techniques.
NURSING
INTERVENTIONS

44. Determine/ prioritize ADLs and personal
responsibilities. Identify available
resources/support systems.
Recommend scheduling activities with adequate
rest periods.
Establish regular schedule for weighing.
NURSING
INTERVENTIONS