Acute kidney injury (AKI), also known as Acute Renal Failure (ARF) occurs when the kidneys lose their filtering ability resulting in the build-up of waste products in the blood. This condition develops rapidly, in hours or days, and is common in critically ill patients.
This condition affects other organs in the body if not treated promptly and can be life-threatening. Common signs and symptoms include oliguria, fluid retention, edema, dyspnea, confusion, fatigue, nausea, weakness, and seizures and coma in severe cases.
Advanced age, already being hospitalized, and chronic conditions like diabetes, hypertension, heart failure, and liver disease increase the risk of AKI. The causes of AKI are categorized into 3 sections.
1. Impaired blood flow from:
- Blood loss
- Liver failure
- Severe dehydration
- Myocardial infarction
- Blood pressure medications
2. Direct kidney damage due to:
- Blood clots
- Medications like chemotherapy drugs or IV contrast
- Alcohol or drug use
3. Urinary blockage from:
The diagnosis of AKI can be confirmed through blood work, urinalysis, ultrasounds or CT scans, and biopsy.
Assessment and monitoring play an essential role in the nursing care for patients with AKI, as subtle changes can signal progression of the disease or the development of complications. Nurses are involved in treatment by administering medications like diuretics, potassium-lowering drugs, and calcium supplements. In severe cases, dialysis is indicated to help remove toxins from the blood. Nurses may care for patients before, during, and after dialysis treatments.
Patient education is also important to address the patient’s and the family member’s knowledge deficits related to the causes and prevention of AKI.
Nursing Care Plans
Once the nurse identifies nursing diagnoses for acute kidney injury, nursing care plans help prioritize assessments and interventions for both short and long-term goals of care. In the following section, you will find nursing care plan examples for acute kidney injury.
Decreased Cardiac Output
Decreased cardiac output in patients with acute kidney injury may be caused by heart failure, acute myocardial infarction, or pulmonary embolus. This results in decreased pumping of the heart and reduced blood flow to the rest of the body.
Nursing Diagnosis: Decreased Cardiac Output
- Fluid overload
- Fluid shifts, fluid deficits
- Electrolyte imbalance
As evidenced by:
- Dysrhythmias, EKG changes
- Jugular vein distention
- Decreased central venous pressure
- Prolonged capillary refill
- Color changes (pallor, cyanosis)
- Decreased peripheral pulses
- Crackles in lungs
- Patient will maintain normal cardiac output as evidenced by stable heart rate and blood pressure along with renal perfusion observed by urine output
- Patient will demonstrate activity tolerance as evidenced by performing ADLs without dyspnea
1. Assess and monitor heart rate and blood pressure.
Excess fluid volume and hypertension can increase cardiac workload which may lead to cardiac failure.
2. Monitor heart sounds and EKG.
The new onset of gallop (S3, S4) rhythm, fine crackles in the lungs, and tachycardia can indicate the onset of heart failure. In pulmonary edema, the patient will exhibit coarse crackles during inspiration and severe dyspnea. The development of dysrhythmias can signal cardiac dysfunction.
1. Administer oxygen.
High-flow oxygen or a ventilator may be necessary to increase oxygenation for cardiac function and tissue perfusion.
2. Encourage bed rest.
Frequent rest is required to prevent overexertion and stress on the heart. Group activities and assessments to reduce interruptions and maximize sleep.
3. Monitor electrolytes.
Increased and decreased levels of potassium can affect the heart muscle and cause arrhythmias. Calcium has cardiac effects and decreased levels can enhance the toxic effects of potassium.
4. Administer medications as indicated.
Inotropic agents may be prescribed to improve cardiac output though care must be taken to preserve renal function. Antidysrhythmics, vasopressors, and blood products may be required. Monitor administration closely to prevent fluid overload.
Deficient Fluid Volume
Intravascular volume depletion is a risk factor for acute kidney injury. During the diuretic phase of acute kidney injury, the patient’s daily urine output can reach up to 5 L or more due to osmotic diuresis and the inability of the tubules to concentrate urine.
Nursing Diagnosis: Deficient Fluid Volume
- Disease process
- Kidney dysfunction
- Blood loss
- Excessive fluid loss
As evidenced by:
- Altered mental status
- Altered skin turgor
- Decreased blood pressure
- Decreased pulse pressure
- Decreased urine output
- Dry skin
- Dry mucous membranes
- Increased temperature
- Patient will maintain a urine output of 0.5 to 1.5 mL/kg/hr.
- Patient will exhibit heart rate, body temperature, and blood pressure within normal limits.
1. Monitor lab values.
Serum osmolality, BUN, creatinine, and hematocrit will be elevated with decreased intravascular volume.
2. Assess and monitor the patient’s vital signs.
Patients with AKI exhibit alterations in vital signs, including tachycardia, orthostatic hypotension, and decreased pulse pressure to compensate for problems with deficient fluid volume caused by loss of kidney function.
3. Assess and monitor the patient’s urine characteristics.
Assessing and monitoring the patient’s urine characteristics can help determine fluid volume deficits in patients with AKI. A decrease in urine output is less than 0.5mg/kg/hr. Urine specific gravity measures the kidney’s ability to concentrate urine. A urine specific gravity above 1.030 and dark-colored urine signals dehydration.
1. Administer intravenous fluid replacement as indicated.
Fluid administration in AKI is indicated to help optimize circulating volume, increase cardiac output, promote perfusion pressure, and ultimately improve renal blood flow and function. Blood products may also be necessary if fluid volume deficit is caused by blood loss.
2. Encourage adequate fluid intake 24/7 as indicated.
During the diuretic phase, AKI may progress to the oliguric phase if fluid intake is not maintained. Reversal and prevention of hypovolemia are vital in preventing further kidney damage. Provide fresh water and foods with high water content throughout the day.
3. Insert a urinary catheter as indicated.
The placement of a urinary catheter allows for accurate measurement of urine output. Intensive monitoring of urine output is associated with improved outcomes in AKI.
4. Treat factors contributing to deficient fluid volume.
If the patient is experiencing vomiting, diarrhea, and fever and is unable to tolerate PO intake, treat these symptoms to prevent further fluid loss.
Excess Fluid Volume
Excess fluid volume is common in patients with AKI due to the kidneys inability to filter and get rid of excess fluid in the body. Its management will include volume status determination, fluid resuscitation, fluid overload management, nephrotoxicity prevention, and adjustment of medications based on the patient’s renal function.
Nursing Diagnosis: Excess Fluid Volume
- Compromised regulatory mechanism (kidney/renal failure)
- Excess fluid intake
- Excess sodium intake
As evidenced by:
- Fluid intake is greater than output; oliguria
- Jugular vein distention
- Blood pressure changes
- Generalized edema
- Weight gain
- Changes in mental status
- Adventitious lung sounds
- Patient will display balanced fluid volume as evidenced by balanced I&O without weight gain.
- Patient will exhibit stable vital signs with the absence of edema.
1. Assess and monitor intake and output accurately.
Normal urine output is at least 30mL/hour. Accurate monitoring of intake and output is necessary to preserve renal function, replace fluids as needed, and reduce the risk of fluid overload.
2. Assess and observe for edema of the hands, feet, and lumbosacral area.
Edema occurs primarily in dependent tissues throughout the body like the lumbosacral area, feet, and hands. The patient can gain about 10 lbs or 4.5kg before pitting edema occurs.
3. Assess and monitor the patient’s level of consciousness.
Changes in the level of consciousness may indicate fluid shifts, accumulation of toxins, developing hypoxia, and electrolyte imbalance.
4. Monitor and review laboratory tests.
Rises in serum creatinine levels and blood urea nitrogen (BUN) can identify AKI. Proteinuria can also indicate kidney damage.
1. Monitor weight daily.
Daily weights will help monitor fluid status. Sudden weight gain of more than 0.5kg/day can indicate fluid retention.
2. Auscultate lung and heart sounds.
Fluid overload can lead to heart failure and pulmonary edema as evidenced by the development of extra heart sounds and adventitious breath sounds.
3. Administer or restrict fluids as indicated.
Fluid management is essential in the treatment of AKI. Excess fluid volume requires a calculated administration of fluids and also the restriction of fluids orally.
4. Administer prescribed medications as indicated.
Diuretics are prescribed to promote urine output and reduce edema.
Imbalanced Nutrition: Less Than Body Requirements
AKI is associated with the imbalance of protein breakdown and production, resulting in muscle wasting, protein wasting, and weight loss. As kidney function continues to deteriorate, protein-energy wasting accelerates, appetite decreases, and malnutrition will start to develop.
Nursing Diagnosis: Imbalanced Nutrition
- Dietary restrictions to reduce nitrogenous waste products
- Increased metabolic needs
As evidenced by:
- Joint and muscle pain
- Lack of appetite
- Decreased albumin
- Patient will remain free of malnutrition as evidenced by nutritional markers and electrolytes within normal limits
1. Assess and monitor weight.
Monitoring the patient’s weight will help determine a loss of weight or weight gain which can signal malnutrition or fluid overload.
2. Assess and document dietary intake.
Monitoring dietary intake will help in identifying the patient’s dietary deficiencies and needs. The patient’s general physical condition and lack of appetite may be affecting intake.
3. Monitor laboratory studies.
Assess albumin, transferrin, iron, glucose, BUN, and amino acid levels to identify gaps in nutrition.
1. Educate the patient about appropriate dietary regimens and restrictions.
This will provide the patient with a certain measure of control within his or her dietary restrictions. Recent dietary guidelines recommend controlled and moderate protein intake for patients with AKI.
2. Encourage mouth care before meals.
Mucous membranes may be cracked or dry and can develop mouth sores. Clean oral hygiene makes eating more pleasant and may help with increasing appetite.
3. Consult with a dietitian for support.
Dietitians can help determine individual calorie and nutrient needs within the patient’s dietary restrictions. They can help formulate the most effective routes and regimens for the patient’s nutritional needs.
4. Encourage and provide small but frequent meals.
Small frequent meals promote appetite, provide nutrients, and reduce nausea and vomiting which are common in patients with AKI.
Risk for Electrolyte Imbalance
Acute kidney injury can range from slight deterioration in kidney function to severe impairment, which can alter the balance of fluid and electrolytes.
Nursing Diagnosis: Risk for Electrolyte Imbalance
- Disease process
- Kidney dysfunction
- Excess fluid volume
- Insufficient fluid volume
- Compromised regulatory mechanism
As evidenced by:
A risk diagnosis is not evidenced by signs and symptoms as the problem has not yet occurred. Nursing interventions are aimed at prevention.
- Patient will maintain serum potassium, sodium, calcium, and phosphorus levels within normal range.
- Patient will remain free from signs of fluid and electrolyte imbalance, including muscle cramping, edema, and irregular heart rate.
1. Assess the patient’s heart rate and rhythm.
Potassium and calcium imbalances are common complications of AKI and will manifest with heart palpitations, muscle pain and spasms, nausea, or paresthesias.
2. Assess and monitor the patient’s neurologic status and alterations in consciousness.
Sodium imbalance is associated with AKI and will cause neurologic changes in patients, including confusion, headache, irritability, and seizures.
3. Assess and monitor the patient’s intake and output.
Intake that doesn’t match output is an obvious sign of fluid overload, which can result in imbalanced electrolytes.
4. Assess laboratory values.
AKI causes damage to the renal tubules, preventing them from conserving sodium and excreting potassium, resulting in low serum sodium and high potassium levels. BUN and creatinine levels will also increase with AKI.
1. Record accurate intake and output and weight changes.
Meticulous intake, output, and daily weight measurements offer a consistent and sensitive indicator of excess fluid volume.
2. Administer IV fluids with caution.
AKI commonly results from severe dehydration. Rapid fluid resuscitation may be necessary but can adversely affect electrolytes.
3. Restrict potassium intake.
Patients with AKI tend to exhibit high levels of potassium as it is not excreted optimally by the kidneys. Potassium restrictions in the diet are vital in reducing the risk of hyperkalemia.
4. Review the effects of the patient’s ordered medications.
Medications such as diuretics, IV contrast, chemotherapy, and some antibiotics can adversely affect the patient’s kidney function and subsequent electrolyte balance.
5. Educate the patient on symptoms of alterations in electrolytes.
Signs and symptoms of hypokalemia include muscle weakness, nausea, vomiting, irregular pulse, and constipation, while symptoms of hyperkalemia include restlessness, slow heart rate, muscle weakness, cramping, and diarrhea. Early signs of hyponatremia include muscle cramps, nausea, disorientation, and mental status changes. Symptoms of hypernatremia include thirst, dry mucous membranes, hypotension, tachycardia, confusion, and seizures.
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