Acute kidney failure (AKF), clinically referred to as acute kidney injury (AKI), is a critical condition characterized by the sudden loss of kidney function. This abrupt decline impairs the kidneys’ ability to filter waste products and excess fluids from the blood, leading to a rapid accumulation of toxins in the body. Developing within hours or days, AKI is particularly prevalent among critically ill individuals and demands immediate attention and proficient nursing care.
If left unaddressed, acute kidney failure can trigger a cascade of complications affecting multiple organ systems and pose a significant threat to life. Recognizing the signs and symptoms is crucial for prompt intervention. Common indicators include decreased urine output (oliguria), fluid retention manifesting as edema, shortness of breath (dyspnea), confusion, persistent fatigue, nausea, generalized weakness, and in severe cases, seizures and coma.
Effective nursing care is paramount in managing AKI and improving patient outcomes. This guide provides a comprehensive overview of acute kidney failure nursing diagnoses, care plans, and essential interventions for nurses.
Understanding the Causes of Acute Kidney Failure
Several factors can precipitate acute kidney failure, broadly categorized into three main groups based on the location of the underlying issue:
1. Prerenal Causes: Impaired Blood Flow to the Kidneys
These conditions reduce blood flow to the kidneys, hindering their ability to filter waste effectively. Common prerenal causes include:
- Blood Loss (Hemorrhage): Significant blood loss reduces overall blood volume, decreasing renal perfusion.
- Dehydration: Severe dehydration leads to decreased blood volume and subsequently reduced blood flow to the kidneys.
- Heart Failure: Ineffective heart pumping reduces cardiac output, leading to decreased blood supply to the kidneys.
- Liver Failure: Liver failure can cause fluid shifts and reduced blood volume, impacting renal blood flow.
- Myocardial Infarction (Heart Attack): A heart attack can weaken the heart’s pumping ability, reducing blood flow to the kidneys.
- Blood Pressure Medications (e.g., ACE inhibitors, ARBs): While often beneficial, these medications can sometimes reduce blood flow to the kidneys, especially in vulnerable individuals.
2. Intrarenal Causes: Direct Damage to the Kidneys
These conditions involve direct damage to the kidney tissues themselves, impairing their filtering capabilities. Intrarenal causes include:
- Blood Clots in Kidney Blood Vessels: Blockage of blood vessels within the kidneys disrupts blood flow and causes damage.
- Glomerulonephritis: Inflammation of the glomeruli (filtering units of the kidneys) impairs kidney function.
- Lupus: This autoimmune disease can attack the kidneys, causing inflammation and damage.
- Medications (Nephrotoxic Drugs):
- Chemotherapy Drugs: Many chemotherapy agents can be toxic to the kidneys.
- IV Contrast Dye: Contrast media used in imaging procedures can sometimes cause kidney damage, especially in patients with pre-existing kidney conditions.
- Nonsteroidal Anti-inflammatory Drugs (NSAIDs): Prolonged use or high doses can harm the kidneys.
- Alcohol and Drug Abuse: Certain substances can directly damage kidney tissues.
- Rhabdomyolysis: Muscle breakdown releases substances that can harm the kidneys.
- Sepsis: Severe infection can lead to kidney damage due to inflammation and reduced blood flow.
3. Postrenal Causes: Urinary Tract Obstruction
These conditions involve blockage of urine flow after it leaves the kidneys, causing back pressure and kidney damage. Postrenal causes include:
- Cancer of the Bladder, Cervix, Colon, and Prostate: Tumors in these areas can obstruct the urinary tract.
- Kidney Stones: Stones can block the ureters or urethra, preventing urine outflow.
- Enlarged Prostate (Benign Prostatic Hyperplasia – BPH): In men, an enlarged prostate can compress the urethra and obstruct urine flow.
- Nerve Damage Affecting Bladder Control (Neurogenic Bladder): Conditions like spinal cord injury or multiple sclerosis can disrupt bladder function and lead to urinary retention and backflow.
Diagnosis of AKI typically involves a combination of assessments, including blood work to measure kidney function (creatinine, BUN), urinalysis to check for abnormalities, and imaging studies like ultrasounds or CT scans to visualize the kidneys and urinary tract. In some cases, a kidney biopsy may be necessary to determine the specific cause of kidney damage.
The Essential Role of Nursing Process in Acute Kidney Failure Care
The nursing process is fundamental to providing comprehensive care for patients with AKI. Nurses play a vital role in all aspects of AKI management, from early detection to ongoing monitoring and treatment. Given the rapid progression and potential complications of AKI, vigilant assessment and monitoring are paramount. Even subtle changes in a patient’s condition can indicate disease progression or the development of serious complications.
Nurses are actively involved in the medical treatment of AKI, administering prescribed medications such as diuretics to manage fluid overload, potassium-lowering drugs to address hyperkalemia, and calcium supplements to correct electrolyte imbalances. In severe cases of AKI, dialysis becomes necessary to filter waste products and excess fluids from the blood artificially. Nurses are essential in providing care before, during, and after dialysis treatments, ensuring patient comfort and safety.
Furthermore, patient and family education is a critical component of nursing care. Nurses address knowledge deficits regarding the causes of AKI, preventive measures, and the importance of adherence to the treatment plan. Empowering patients and their families with knowledge promotes informed decision-making and active participation in care.
Acute Kidney Failure Nursing Care Plans: Prioritizing Patient Needs
Once nursing diagnoses are identified for a patient with acute kidney failure, nursing care plans serve as roadmaps for prioritizing assessments and interventions. These plans guide nurses in setting both short-term and long-term goals of care, ensuring a structured and patient-centered approach.
Here are examples of common nursing diagnoses and associated care plans relevant to acute kidney failure:
1. Nursing Diagnosis: Decreased Cardiac Output
Decreased cardiac output is a significant concern in AKI patients and can arise from underlying conditions such as heart failure, acute myocardial infarction, or pulmonary embolism. Fluid overload and electrolyte imbalances associated with AKI can further exacerbate cardiac dysfunction, leading to reduced heart pumping efficiency and compromised blood flow to vital organs.
Related Factors:
- Fluid overload
- Fluid shifts, fluid deficits
- Electrolyte imbalance (hyperkalemia, hypocalcemia)
As Evidenced By:
- Dysrhythmias, EKG changes (tachycardia, bradycardia, irregular rhythms)
- Jugular vein distention (JVD)
- Decreased central venous pressure (CVP)
- Dyspnea (shortness of breath)
- Prolonged capillary refill (>3 seconds)
- Color changes (pallor, cyanosis)
- Decreased peripheral pulses (weak or thready pulses)
- Crackles in lungs (rales)
- Cough (may be productive of frothy sputum in pulmonary edema)
Expected Outcomes:
- Patient will maintain adequate cardiac output as evidenced by stable heart rate and blood pressure, palpable peripheral pulses, and urine output within acceptable limits.
- Patient will demonstrate improved activity tolerance, performing activities of daily living (ADLs) without experiencing dyspnea or excessive fatigue.
Nursing Assessments:
- Assess and monitor heart rate and blood pressure frequently (every 1-4 hours, or more often as needed). Rationale: Excess fluid volume and hypertension, common in AKI, increase cardiac workload and can precipitate or worsen heart failure.
- Continuously monitor heart sounds and EKG. Rationale: The appearance of new heart sounds such as gallop rhythms (S3, S4), fine crackles in the lungs, and tachycardia can indicate the onset of heart failure or pulmonary edema. Dysrhythmias can signal cardiac muscle dysfunction due to electrolyte imbalances or hypoxia.
- Assess for peripheral edema and jugular vein distention. Rationale: These are classic signs of fluid overload and increased central venous pressure, indicating compromised cardiac output.
- Monitor urine output closely (hourly if indicated). Rationale: Urine output is a sensitive indicator of renal perfusion, which is directly affected by cardiac output. Decreased urine output may signal worsening cardiac function.
Nursing Interventions:
- Administer supplemental oxygen as prescribed. Rationale: High-flow oxygen or mechanical ventilation may be necessary to improve oxygenation, supporting cardiac function and tissue perfusion. Hypoxia can further compromise cardiac output.
- Promote rest and reduce activity. Rationale: Frequent rest periods minimize cardiac workload and prevent overexertion. Cluster nursing activities to allow for uninterrupted rest and sleep.
- Monitor serum electrolyte levels, particularly potassium and calcium. Rationale: Hyperkalemia and hypocalcemia, common in AKI, can significantly affect cardiac muscle contractility and rhythm, predisposing to arrhythmias. Calcium imbalances can exacerbate the toxic effects of potassium on the heart.
- Administer medications as ordered, such as inotropic agents, antidysrhythmics, vasopressors, and diuretics. Rationale: Inotropic agents (e.g., dobutamine, dopamine) may be prescribed to enhance cardiac contractility and output, while carefully monitoring renal function. Antidysrhythmics are used to manage arrhythmias. Vasopressors (e.g., norepinephrine) may be needed to support blood pressure. Diuretics (e.g., furosemide) help manage fluid overload, but their use in AKI requires careful consideration of renal function and electrolyte balance.
2. Nursing Diagnosis: Deficient Fluid Volume
Intravascular volume depletion is a significant risk factor for the development and progression of acute kidney injury. Paradoxically, during the diuretic phase of AKI, patients can experience excessive fluid loss through urine, exacerbating fluid volume deficit. This phase is characterized by osmotic diuresis and the kidneys’ impaired ability to concentrate urine, potentially leading to urine output as high as 5 liters or more per day.
Related Factors:
- Disease process (AKI-induced diuresis)
- Kidney dysfunction (impaired urine concentration)
- Blood loss
- Dehydration (inadequate fluid intake)
- Excessive fluid loss (vomiting, diarrhea, excessive sweating)
As Evidenced By:
- Altered mental status (confusion, lethargy)
- Altered skin turgor (poor skin elasticity)
- Decreased blood pressure (hypotension, orthostatic hypotension)
- Decreased pulse pressure (narrowed difference between systolic and diastolic pressures)
- Tachycardia (rapid heart rate)
- Decreased urine output (oliguria)
- Dry skin and mucous membranes
- Increased body temperature (hyperthermia)
- Thirst
- Weakness
Expected Outcomes:
- Patient will maintain adequate fluid volume as evidenced by urine output of at least 0.5 to 1.5 mL/kg/hr, stable vital signs (heart rate, blood pressure, temperature) within normal limits, and improved skin turgor and mucous membrane hydration.
- Patient will exhibit balanced fluid intake and output over 24 hours.
Nursing Assessments:
- Monitor laboratory values, particularly serum osmolality, BUN, creatinine, and hematocrit. Rationale: Elevated serum osmolality, BUN, creatinine, and hematocrit are indicative of hemoconcentration and decreased intravascular volume.
- Assess and monitor vital signs frequently, including orthostatic blood pressure. Rationale: Patients with deficient fluid volume often exhibit tachycardia, orthostatic hypotension (drop in blood pressure upon standing), and decreased pulse pressure as compensatory mechanisms to maintain blood pressure in the face of reduced fluid volume.
- Assess and monitor urine characteristics, including urine output and specific gravity. Rationale: Decreased urine output (<0.5 mL/kg/hr) is a hallmark of fluid volume deficit. Urine specific gravity measures the kidney’s ability to concentrate urine; a specific gravity above 1.030 and dark-colored urine suggest dehydration.
- Assess skin turgor and mucous membranes. Rationale: Poor skin turgor (tenting) and dry mucous membranes are clinical signs of dehydration.
Nursing Interventions:
- Administer intravenous fluid replacement as prescribed. Rationale: Fluid administration is crucial in AKI to restore circulating volume, enhance cardiac output, improve renal perfusion pressure, and ultimately promote renal blood flow and function. The type and rate of fluid administration will be guided by the patient’s hemodynamic status and electrolyte balance. Blood products may be necessary if fluid volume deficit is due to blood loss.
- Encourage adequate oral fluid intake when appropriate and as indicated. Rationale: During the diuretic phase, maintaining adequate fluid intake is vital to prevent progression to the oliguric phase and further kidney damage. Provide fresh water and offer foods with high water content throughout the day. However, fluid intake may be restricted in the oliguric phase.
- Insert a urinary catheter if indicated to monitor urine output accurately. Rationale: A urinary catheter allows for precise measurement of urine output, which is essential for guiding fluid replacement and monitoring kidney function in AKI. However, the necessity and duration of catheterization should be carefully considered to minimize the risk of urinary tract infection.
- Identify and treat underlying factors contributing to fluid volume deficit. Rationale: Address underlying causes of fluid loss such as vomiting, diarrhea, fever, and inadequate oral intake to prevent further dehydration and support fluid balance.
3. Nursing Diagnosis: Excess Fluid Volume
Excess fluid volume is a common complication of AKI, stemming from the kidneys’ compromised ability to filter and eliminate excess fluid from the body. Effective management requires careful assessment of volume status, appropriate fluid resuscitation when needed (especially in the early phases), and meticulous management of fluid overload once it develops. Prevention of nephrotoxicity from medications and careful adjustment of medication dosages based on renal function are also crucial aspects of managing fluid volume in AKI.
Related Factors:
- Compromised regulatory mechanism (kidney/renal failure)
- Excess fluid intake (IV fluids, oral intake)
- Excess sodium intake (dietary sodium, sodium-containing medications)
As Evidenced By:
- Fluid intake greater than output; oliguria (decreased urine output)
- Jugular vein distention (JVD)
- Blood pressure changes (hypertension)
- Generalized edema (peripheral, pulmonary, sacral)
- Weight gain (rapid weight gain over short period)
- Restlessness, anxiety
- Changes in mental status (confusion, lethargy)
- Adventitious lung sounds (crackles/rales, wheezing)
- Dyspnea (shortness of breath, orthopnea, paroxysmal nocturnal dyspnea)
Expected Outcomes:
- Patient will achieve balanced fluid volume as evidenced by balanced fluid intake and output, stable weight without rapid weight gain, resolution of edema, and clear lung sounds.
- Patient will maintain stable vital signs within acceptable limits, with blood pressure controlled and absence of dyspnea.
Nursing Assessments:
- Accurately assess and monitor intake and output (I&O) every 1-2 hours or more frequently as needed. Rationale: Normal urine output is at least 30 mL/hour. Meticulous I&O monitoring is crucial for assessing fluid balance, guiding fluid management, and preventing both fluid deficit and overload in AKI.
- Assess for edema in dependent areas (hands, feet, ankles, sacrum) and periorbital edema. Rationale: Edema is a hallmark of fluid overload in AKI, typically manifesting initially in dependent tissues. Patients can retain significant fluid (approximately 4.5 kg or 10 lbs) before pitting edema becomes clinically apparent.
- Assess and monitor level of consciousness and mental status. Rationale: Changes in level of consciousness, confusion, and restlessness may indicate fluid shifts, accumulation of metabolic toxins (uremia), developing hypoxia, and electrolyte imbalances associated with fluid overload.
- Monitor and review laboratory tests, including serum creatinine, BUN, electrolytes, and hematocrit. Rationale: Elevated serum creatinine and BUN levels confirm AKI and impaired kidney function. Electrolyte imbalances (hyperkalemia, hyponatremia) are common with fluid overload. Decreased hematocrit may indicate hemodilution.
- Auscultate lung sounds for adventitious sounds (crackles, wheezes) and heart sounds for S3 gallop. Rationale: Fluid overload can lead to pulmonary edema and heart failure, manifested by crackles in the lungs and S3 gallop heart sound.
Nursing Interventions:
- Monitor weight daily at the same time each day, using the same scale. Rationale: Daily weights are a sensitive indicator of fluid status. A sudden weight gain of more than 0.5 kg (1 lb) per day suggests fluid retention.
- Auscultate lung and heart sounds regularly, especially before and after fluid administration or diuretic therapy. Rationale: Early detection of adventitious lung sounds and abnormal heart sounds allows for prompt intervention to prevent or manage pulmonary edema and heart failure.
- Administer or restrict fluids as prescribed, carefully calculating and monitoring fluid balance. Rationale: Fluid management is central to AKI treatment. Fluid restriction is often necessary in the oliguric phase to prevent fluid overload. Fluid administration must be carefully calculated, especially during fluid resuscitation or diuretic therapy, to avoid exacerbating fluid imbalances.
- Administer prescribed medications, such as diuretics (e.g., furosemide, bumetanide), with careful monitoring of renal function and electrolytes. Rationale: Loop diuretics are commonly used to promote urine output and reduce edema. However, their effectiveness may be limited in severe AKI, and they can contribute to electrolyte imbalances. Dosage and frequency must be adjusted based on renal function and patient response.
- Implement sodium restrictions in diet as prescribed. Rationale: Reducing sodium intake helps minimize fluid retention. Educate the patient and family about sodium-rich foods and hidden sources of sodium.
- Prepare for and assist with dialysis as indicated. Rationale: In severe fluid overload unresponsive to diuretics, dialysis (hemodialysis or peritoneal dialysis) may be necessary to remove excess fluid and waste products from the blood.
4. Nursing Diagnosis: Imbalanced Nutrition: Less Than Body Requirements
AKI significantly impacts nutritional status. The condition is associated with increased protein catabolism (breakdown) and decreased protein synthesis, leading to muscle wasting, protein depletion, and weight loss. As kidney function deteriorates, protein-energy wasting accelerates. Anorexia, nausea, and vomiting, common symptoms of AKI, further contribute to decreased oral intake and malnutrition. Dietary restrictions, often necessary to manage electrolyte imbalances and azotemia (build-up of nitrogenous waste products), can also contribute to inadequate nutrient intake if not carefully planned and monitored.
Related Factors:
- Dietary restrictions (protein, potassium, phosphorus, sodium)
- Increased metabolic needs (due to illness and catabolism)
- Anorexia, nausea, vomiting
- Uremic toxins affecting appetite and taste
As Evidenced By:
- Unintentional weight loss
- Muscle weakness and wasting
- Fatigue, lethargy
- Lack of appetite, anorexia
- Decreased serum albumin and prealbumin levels
- Electrolyte imbalances affecting appetite and nutrient absorption
Expected Outcomes:
- Patient will maintain or improve nutritional status as evidenced by stable weight, improved muscle strength, adequate energy levels, and serum albumin and prealbumin levels within acceptable limits.
- Patient will demonstrate adequate oral intake to meet nutritional needs within dietary restrictions.
Nursing Assessments:
- Assess and monitor weight trends regularly (daily or at least 2-3 times per week). Rationale: Weight loss is a key indicator of malnutrition. Monitor for both weight loss and rapid weight gain (which may indicate fluid overload). Compare current weight to baseline weight.
- Assess and document dietary intake, including appetite, food preferences, and any barriers to adequate intake (nausea, vomiting, anorexia, dietary restrictions). Rationale: Detailed dietary assessment helps identify nutritional deficits and guide interventions. Assess the patient’s ability to chew and swallow, cultural and religious dietary preferences, and food allergies.
- Monitor laboratory studies relevant to nutritional status, including serum albumin, prealbumin, transferrin, iron, glucose, BUN, creatinine, and amino acid levels. Rationale: Serum albumin and prealbumin are indicators of protein status. Transferrin and iron levels assess iron stores. Glucose levels are important for managing diabetes and nutritional support. BUN and creatinine reflect kidney function and protein catabolism. Amino acid levels can provide a more detailed assessment of protein metabolism.
- Assess for signs and symptoms of malnutrition, such as muscle wasting, weakness, edema (may mask weight loss), and poor wound healing. Rationale: Clinical signs of malnutrition provide further evidence of nutritional deficits and guide intervention priorities.
Nursing Interventions:
- Educate the patient and family about appropriate dietary regimens and restrictions for AKI, emphasizing the rationale for each restriction (protein, potassium, phosphorus, sodium). Rationale: Patient education promotes understanding and adherence to dietary recommendations. Recent guidelines often recommend controlled but moderate protein intake in AKI, rather than severe protein restriction. Individualized dietary plans are essential.
- Encourage meticulous mouth care before meals. Rationale: Uremia can cause unpleasant taste changes and mouth sores. Good oral hygiene improves taste and appetite, making eating more palatable.
- Consult with a registered dietitian for comprehensive nutritional assessment and individualized dietary planning. Rationale: Dietitians are experts in medical nutrition therapy and can determine individual calorie, protein, fluid, and electrolyte needs within the patient’s specific dietary restrictions and medical condition. They can recommend optimal routes of nutritional support (oral, enteral, parenteral).
- Encourage and provide small, frequent meals and snacks throughout the day, rather than large meals. Rationale: Small, frequent meals are often better tolerated in patients with anorexia, nausea, or early satiety. They help maintain consistent nutrient intake and minimize gastrointestinal distress.
- Offer nutritional supplements as recommended by the dietitian or physician. Rationale: Oral nutritional supplements (ONS) can help bridge nutritional gaps and increase calorie and protein intake, especially when oral intake is insufficient. Enteral or parenteral nutrition may be necessary in patients unable to meet nutritional needs orally or enterally.
- Administer antiemetics as prescribed to manage nausea and vomiting. Rationale: Effective nausea and vomiting management improves comfort and promotes oral intake.
- Create a pleasant and supportive meal environment. Rationale: Minimize distractions, provide social interaction during meals if appropriate, and offer assistance with feeding if needed. A positive mealtime experience can enhance appetite.
5. Nursing Diagnosis: Risk for Electrolyte Imbalance
Acute kidney injury profoundly disrupts fluid and electrolyte balance, ranging from mild abnormalities to life-threatening derangements. The damaged kidneys lose their ability to regulate electrolyte levels effectively, leading to imbalances that can affect virtually every organ system, particularly the cardiovascular and neurological systems.
Related Factors:
- Disease process (AKI and kidney dysfunction)
- Excess fluid volume or fluid deficit
- Compromised regulatory mechanisms (renal tubules’ impaired function)
- Medications (diuretics, nephrotoxic drugs)
As Evidenced By:
A risk diagnosis is not evidenced by existing signs and symptoms, as the problem has not yet occurred. Nursing interventions are focused on prevention.
Expected Outcomes:
- Patient will maintain serum potassium, sodium, calcium, and phosphorus levels within normal ranges, as evidenced by laboratory values.
- Patient will remain free from signs and symptoms of electrolyte imbalance, including muscle weakness, cramping, cardiac arrhythmias, and neurological changes.
Nursing Assessments:
- Assess the patient’s heart rate and rhythm regularly, and monitor EKG as indicated. Rationale: Potassium and calcium imbalances are common and serious complications of AKI. Hyperkalemia and hypocalcemia can manifest with cardiac arrhythmias, muscle weakness, palpitations, and EKG changes (e.g., peaked T waves in hyperkalemia, prolonged QT interval in hypocalcemia).
- Assess and monitor the patient’s neurological status and level of consciousness frequently. Rationale: Sodium imbalances, particularly hyponatremia and hypernatremia, are associated with AKI and can cause neurological changes ranging from mild confusion and headache to seizures and coma. Hypocalcemia and hypercalcemia also affect neurological function.
- Assess and monitor fluid intake and output balance meticulously. Rationale: Imbalances between intake and output are often indicative of fluid overload or deficit, which directly impact electrolyte concentrations. Fluid overload can dilute electrolytes, while fluid deficit can concentrate them.
- Closely monitor laboratory values, particularly serum potassium, sodium, calcium, phosphorus, and magnesium levels. Rationale: AKI impairs the renal tubules’ ability to conserve sodium and excrete potassium and phosphorus, leading to hyponatremia, hyperkalemia, and hyperphosphatemia. Calcium levels are often inversely related to phosphorus levels in AKI (hyperphosphatemia leads to hypocalcemia). Magnesium imbalances can also occur.
Nursing Interventions:
- Record accurate intake and output and monitor daily weight changes. Rationale: Meticulous I&O monitoring and daily weights provide sensitive indicators of fluid balance and potential electrolyte shifts. Rapid changes in weight or I&O discrepancies warrant further investigation of electrolyte status.
- Administer intravenous fluids with caution, carefully considering the type and rate of infusion, especially in the oliguric phase of AKI. Rationale: While fluid resuscitation may be necessary in prerenal AKI due to dehydration, rapid or excessive fluid administration can exacerbate electrolyte imbalances, particularly hyponatremia. Isotonic solutions are generally preferred for initial resuscitation. Avoid hypotonic solutions.
- Implement potassium restrictions in the diet as prescribed. Rationale: Hyperkalemia is a life-threatening complication of AKI. Dietary potassium restriction is crucial to minimize potassium intake. Educate the patient and family about potassium-rich foods to avoid.
- Administer potassium-lowering medications as prescribed, such as sodium polystyrene sulfonate (Kayexalate), patiromer (Veltassa), or sodium zirconium cyclosilicate (Lokelma). Rationale: These medications promote potassium excretion from the body through the gastrointestinal tract. Kayexalate is older and less well-tolerated; newer agents like patiromer and sodium zirconium cyclosilicate are often preferred due to better tolerability and effectiveness.
- Administer calcium supplements or phosphate binders as prescribed to manage calcium-phosphorus imbalance. Rationale: Hyperphosphatemia is common in AKI and contributes to hypocalcemia. Phosphate binders (e.g., calcium acetate, sevelamer) are given to reduce phosphate absorption from the gut. Calcium supplements may be needed to treat hypocalcemia, but calcium-containing phosphate binders should be used cautiously to avoid excessive calcium intake.
- Prepare for and assist with dialysis as indicated to correct severe electrolyte imbalances, particularly hyperkalemia unresponsive to medical management. Rationale: Dialysis is highly effective in rapidly removing excess potassium and other electrolytes from the blood in severe cases of electrolyte imbalance.
- Review the patient’s medication list for drugs that can affect kidney function and electrolyte balance, such as diuretics, ACE inhibitors, ARBs, NSAIDs, and certain antibiotics. Rationale: Nephrotoxic medications can worsen AKI and electrolyte disturbances. Dosage adjustments or alternative medications may be necessary.
- Educate the patient and family on the signs and symptoms of electrolyte imbalances and the importance of reporting any new or worsening symptoms promptly. Rationale: Early recognition and reporting of electrolyte imbalance symptoms (muscle weakness, cramps, palpitations, neurological changes) allows for timely intervention and prevents serious complications.
- Implement continuous cardiac monitoring for patients at high risk of electrolyte imbalances, particularly hyperkalemia. Rationale: Continuous EKG monitoring allows for immediate detection of cardiac arrhythmias related to electrolyte imbalances.
Conclusion: Enhancing Nursing Care in Acute Kidney Failure
Effective nursing care is indispensable in managing acute kidney failure and improving patient outcomes. By utilizing comprehensive nursing diagnoses and implementing well-structured care plans, nurses can proactively address the complex needs of AKI patients. Vigilant assessment, prompt intervention, and patient education are cornerstones of nursing practice in this critical area. A deep understanding of acute kidney failure nursing diagnoses empowers nurses to provide optimal, patient-centered care, ultimately contributing to better recovery and reduced morbidity in individuals affected by this serious condition.
