Nursing Notes

1. Acute Kidney Injury

2. Acute Kidney Injury
Description
• Acute kidney injury (AKI) is the rapid loss of kidney function from
renal cell damage.
• Occurs abruptly and can be reversible
• AKI leads to cell hypoperfusion, cell death, and decompensation of
renal function.
• The prognosis depends on the cause and the condition of the client.
Near-normal or normal kidney function may resume gradually.

3. • Acute renal failure (ARF) occurs suddenly as a result of physical injury,
infection, inflammation, or damage from toxic chemicals.
• Nephrotoxic agents are those that are poisonous to kidney cells and
include many drugs, iodine substances used as radiographic contrast
media, heavy metals, snake venom, or exposure to industrial chemicals.
• These toxins may inflict damage on the renal tubules, causing acute
tubular necrosis (ATN) and loss of function.
• They can also indirectly harm the tubules by causing severe constriction of
blood vessels that serve the kidney, producing renal ischemia. ATN is
responsible for 90% of acute renal failure.
• Other causes of renal ischemia include circulatory collapse, severe
dehydration, and prolonged hypotension in compromised surgical or
trauma patients.

4. Causes
1. Prerenal:
Outside the kidney; caused by intravascular volume depletion such as
with blood loss associated with trauma or surgery
• Dehydration,
• Decreased cardiac output (as with cardiogenic shock),
• Decreased peripheral vascular resistance,
• Decreased renovascular blood flow,
• Prerenal infection or obstruction.

5. 2. Intrarenal
Within the parenchyma of the kidney (occurs from glomerular damage)
• Tubular necrosis,
• Prolonged prerenal ischemia,
• Intrarenal infection or obstruction,
• Nephrotoxicity.

6. 3. Postrenal:
Between the kidney and urethral meatus,
• Bladder neck obstruction,
• Bladder cancer,
• Calculi, and postrenal infection
ARF is potentially reversible, especially if identified early; patients often
regain kidney function.

7. ACUTE RENAL FAILURE

8. Phases of AKI
1. Onset: Begins with precipitating event
2. Oliguric phase
a. For some clients, oliguria does not occur and the urine output is normal;
otherwise, the duration of oliguria is 8 to 15 days; the longer the duration, the
less chance of recovery.
b. Sudden decrease in urine output; urine output is less than 400 mL/day.
c. Signs of excess fluid volume: Hypertension, edema, pleural and pericardial
effusions, dysrhythmias, heart failure, and pulmonary edema
d. Signs of uremia: Anorexia, nausea, vomiting, and pruritus
e. Signs of metabolic acidosis: Kussmaul’s respirations

9. Phases of AKI
f. Signs of neurological changes: Tingling of extremities, drowsiness
progressing to disorientation, and then coma
g. Signs of pericarditis: Friction rub, chest pain with inspiration, and
low-grade fever
In this phase uremic symptoms first appear and life threatening
conditions such as hyperkalemia develop.

10. Intervention
With early recognition or potential for AKI, client may be treated with
fluid challenges (IV boluses of 500 to 1000 mL over 1 hour).
Restrict fluid intake; if hypertension is present, daily fluid allowances
may be 400 to 1000 mL plus the measured urinary output.
Administer medications, such as diuretics, as prescribed to increase
renal blood flow and diuresis of retained fluid and electrolytes.

11. 3. Diuretic phase
a. Urine output rises slowly, followed by diuresis (4 to 5 L/day).
b. Excessive urine output indicates that damaged nephrons are
recovering their ability to excrete wastes.
c. Dehydration, hypovolemia, hypotension, and tachycardia can occur.
d. Level of consciousness improves.

12. INTERVENTION
• Laboratory analysis
• Administer IV fluids as prescribed, which may contain electrolytes to
replace losses.

13. 4. Recovery phase (convalescent)
a. Recovery is a slow process; complete recovery may take 1 to 2 years.
b. Urine volume returns to normal.
c. Memory improves.
d. The older adult is less likely than a younger adult to regain full kidney
function.

14. INTERVENTION
• Laboratory analysis
• AKI can progress to chronic kidney disease (CKD).

15. DIAGNOSIS
• BUN (increases depends on the degree of catabolism(protein
breakdown), renal perfusion, and protein intake.
• Serum creatinine levels
• radiologic studies (such as ultrasound,CT, or MRI)(show evidence for
anatomical changes)
• A renal biopsy may be obtained to assist in determining the cause or
to evaluate the extent of kidney damage.
• CBC (anemia can occur as a results of reduced erythropoietin
production, reduced RBC lifespan)

16. Prevention
• Continually assess renal function( urine output, laboratory
values)when appropriate
• Monitor central venous and arterial pressure and hourly urine output
of critically ill patient
• Prevent and treat infections promptly. Infection can produce
progressive kidney damage.
• Prevent and treat shock promptly with blood and fluid replacement.
• Provide adequate hydration to patients at risk for dehydration,

17. Prevention
• Avoid severe transfusion reaction
• Prevent ascending urinary tract infection
• To prevent toxic drug effect, dosage, duration and blood levelsof all
medications metabolized or excreted by the kidneys
• Treat hypotension promptly

18. Medical management
Treatment of ARF is aimed toward correcting the underlying cause and preventing
or controlling complications and maintaining a tolerable internal environment until
the kidneys are able to recover and resume their normal functions
Symptomatic treatment includes
• correction of fluid and electrolyte balances,
• management of anemia and hypertension, and
• cleansing the blood and tissues of waste products with hemodialysis (filtration of
blood across a semipermeable membrane) or peritoneal dialysis (filtration of
blood across the peritoneal membrane).
• Pharmacologic therapy.
IV dextrose 50%, insulin, and calcium replacement may be administered
to shift potassium back into cells;
• diuretic agents are often administered to control fluid volume.

19. Medical management contd
• Volume overload is treated with diuretics and sometimes low-dose
dopamine to promote better kidney perfusion.
• Dialysis is also used to reduce volume overload if it cannot be reduced
with drugs. Electrolyte imbalances (hyperkalemia, hypocalcemia,
hyperphosphatemia, and mild hypermagnesemia) are monitored and
treated.
• Metabolic acidosis, if severe, is treated with IV sodium bicarbonate
• Replacement of dietary proteins is individualized to provide the
maximum benefit and minimize uremic symptoms; likewise, caloric
requirements are met with high-carbohydrate meals, because
carbohydrates have a protein-sparing effect; foods and fluids
containing potassium or phosphorus are restricted; and after diuretic
phase, the patient is placed on a high-protein, high-calorie diet.

20. Assessment
Patient's history, include questions that relate to
• fluid imbalance (e.g., changes in voiding patterns, weight gain,
muscle cramps, cardiac arrhythmia or palpitations, vomiting, or
edema) and
• potential risk factors (e.g., patient or family history of renal disease
or hypertension; recent surgery, trauma, or anesthesia; and exposure
to nephrotoxic substances or any medications).
• Complete head-to-toe assessment
• Laboratory investigation

21. Diagnosis
• Fluid volume excess due to decreased kidney function.
• Altered nutrition due to nausea and loss of appetite.
• Altered activity tolerance due to metabolic changes.
• Potential for infection due to indwelling urinary catheter.

22. Nursing Interventions
1. Monitor vital signs, especially for signs of hypertension, tachycardia,
tachypnea, and an irregular heart rate.
2. Monitor urine and intake and output hourly and urine color and
characteristics.
3. Monitor daily weight (same scale, same clothes, same time of day), noting
that an increase of 0.5 to 1 lb/day (0.25 to 0.5 kg/day) indicates fluid
retention.
4. Monitor for changes in the BUN, serum creatinine, and serum electrolyte
levels.
5. Monitor for acidosis (may need to be treated with sodium bicarbonate).

23. 6. Monitor urinalysis for protein level, hematuria, casts, and specific gravity.
7. Monitor for altered level of consciousness caused by uremia.
8. Monitor for signs of infection because the client may not exhibit an
elevated temperature or an increased WBC count.
9. Monitor the lungs for wheezes and rhonchi and monitor for edema, which
can indicate fluid overload.
10. Administer the prescribed diet, which is usually a low to moderate-
protein (to decrease the workload on the kidneys) and high-carbohydrate
diet; ill clients may require nutritional support with supplements, enteral
feedings, or parenteral nutrition.

24. 11. Restrict potassium and sodium intake as prescribed based on the
electrolyte level.
12. Administer medications as prescribed; be alert to the mechanism
for metabolism and excretion of all prescribed medications.
13. Be alert to nephrotoxic medications, which may be prescribed

25. 15. Prepare the client for dialysis if prescribed; continuous renal
replacement therapy may be used in AKI to treat fluid volume overload
or metabolic acidosis.
16. Provide emotional support by allowing opportunities for the client
to express concerns and fears and by encouraging family interactions.