A patient with acute kidney injury (AKI) presents with elevated serum creatinine and BUN levels, hyperkalemia, and proteinuria. Which nursing intervention is most appropriate to address the hyperkalemia and prevent cardiac complications?

A) Administer intravenous calcium gluconate

B) Restrict dietary protein intake

C) Encourage increased oral fluid intake

D) Initiate a high-potassium diet

A patient with acute kidney injury (AKI) and hyperkalemia has a potassium level of 5.8 mEq/L. Which nursing intervention should be prioritized to prevent cardiac complications related to hyperkalemia?

C) Place the patient on a cardiac monitor

A) Restrict dietary potassium intake

B) Administer sodium polystyrene sulfonate (Kayexalate)

C) Place the patient on a cardiac monitor

D) Encourage increased oral fluid intake

A patient with acute kidney injury is experiencing fluid overload and hyperkalemia. Which action should the nurse prioritize to address the immediate risks to the patient's health?

B) Prepare the patient for urgent renal replacement therapy.

A) Administer intravenous furosemide to reduce fluid overload.

B) Prepare the patient for urgent renal replacement therapy.

C) Increase the patient's oxygen flow rate to improve oxygen saturation.

D) Administer sodium polystyrene sulfonate to lower potassium levels.

A patient with acute kidney injury is experiencing fluid overload and hyperkalemia, evidenced by bilateral crackles, decreased urine output, and peaked T waves on ECG. Which nursing intervention should be prioritized to address the hyperkalemia and prevent cardiac complications?

B) Prepare the patient for urgent renal replacement therapy as recommended by nephrology.

A) Administer a loop diuretic to promote renal excretion of potassium.

B) Prepare the patient for urgent renal replacement therapy as recommended by nephrology.

C) Encourage increased oral fluid intake to dilute serum potassium levels.

D) Apply supplemental oxygen to maintain adequate oxygenation.

A patient undergoing renal replacement therapy shows improvement in fluid status and electrolyte balance. However, urine output remains low, and blood pressure is elevated. What is the most appropriate nursing intervention to address these concerns while supporting renal recovery?

C) Adjust antihypertensive medications to optimize blood pressure control.

A) Increase fluid intake to improve hydration and urine output.

B) Administer a diuretic to enhance renal excretion and reduce edema.

C) Adjust antihypertensive medications to optimize blood pressure control.

D) Restrict dietary potassium further to prevent hyperkalemia recurrence.

A patient with acute kidney injury (AKI) has just undergone renal replacement therapy. Following the treatment, there is significant improvement in fluid status and serum potassium levels, but the patient's urine output remains low. What is the most appropriate nursing intervention to support renal function in this patient?

B) Monitor and adjust antihypertensive medications to maintain stable blood pressure.

A) Increase oral fluid intake to stimulate urine production.

B) Monitor and adjust antihypertensive medications to maintain stable blood pressure.

C) Administer a diuretic to promote urine output.

D) Restrict fluid intake to prevent further fluid overload.

A patient with acute kidney injury is experiencing metabolic acidosis, as indicated by an arterial blood gas analysis. The healthcare team is adjusting the dialysis prescription and considering sodium bicarbonate supplementation. Which clinical indicator should the nurse prioritize to assess the effectiveness of these interventions in managing the patient's metabolic acidosis?

C) Normalization of arterial blood pH

A) Improvement in blood pressure

C) Normalization of arterial blood pH

D) Decrease in serum potassium levels

A patient with acute kidney injury has developed metabolic acidosis, as indicated by a pH of 7.30, bicarbonate level of 18 mEq/L, and PCO2 of 35 mmHg. The healthcare team is planning to adjust the dialysis prescription. Which additional nursing intervention is most appropriate to implement in this situation to address the metabolic acidosis?

B) Administer sodium bicarbonate as prescribed.

A) Increase the frequency of blood glucose monitoring.

B) Administer sodium bicarbonate as prescribed.

C) Restrict fluid intake to prevent fluid overload.

D) Initiate a low-protein diet to reduce uremic toxins.

A patient with metabolic acidosis and hyperkalemia is undergoing intensified dialysis and receiving intravenous sodium bicarbonate. Which of the following nursing interventions is most critical to monitor in this patient to prevent potential complications?

A) Monitor for signs of hypocalcemia such as tetany and seizures

B) Regularly assess the patient's blood glucose levels to prevent hypoglycemia

C) Frequently check the patient's blood pressure to avoid hypotension

D) Evaluate the patient's level of consciousness to detect worsening confusion

Acute Kidney Injury - Nursing Case Study

Pathophysiology

• Primary mechanism: Acute kidney injury (AKI) often results from decreased blood flow to the kidneys, known as prerenal AKI. Hypoperfusion leads to reduced glomerular filtration rate, causing waste accumulation and electrolyte imbalances.

• Secondary mechanism: Intrinsic AKI occurs when direct damage to kidney tissue happens, often due to ischemia or nephrotoxins. This results in tubular cell injury, impairing reabsorption and secretion functions and exacerbating waste retention.

• Key complication: If untreated, AKI can progress to chronic kidney disease or cause systemic complications like fluid overload, hypertension, and heart failure, emphasizing the importance of early intervention and monitoring.

Patient Profile

Demographics:

68-year-old female, retired school teacher

History:

• Key past medical history: Hypertension, Type 2 Diabetes Mellitus, Chronic Osteoarthritis

• Current medications: Lisinopril, Metformin, Ibuprofen as needed

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Decreased urine output and fatigue

• Key symptoms: Nausea, swelling in the legs, shortness of breath, confusion

• Vital signs: Blood pressure 150/95 mmHg, heart rate 92 bpm, respiratory rate 20 breaths per minute, temperature 99.1°F, oxygen saturation 93% on room air

Section 1

New Diagnostic Results:

Following the initial presentation of symptoms consistent with acute kidney injury (AKI), a series of diagnostic tests were conducted to further assess the patient's renal function and overall status. The laboratory results reveal a significant elevation in serum creatinine at 3.2 mg/dL (baseline approximately 1.0 mg/dL), indicating a marked decline in kidney filtration capabilities. Blood urea nitrogen (BUN) is also elevated at 48 mg/dL. Electrolyte imbalances are apparent, with hyperkalemia noted at a potassium level of 5.8 mEq/L, posing a risk for cardiac complications. Additionally, a urinalysis shows proteinuria and the presence of granular casts, suggesting possible intrinsic renal damage.

Imaging studies, including renal ultrasound, reveal no evidence of obstructive uropathy, ruling out postrenal causes. However, there is evidence of mild bilateral renal cortical thinning, which may be indicative of chronic changes superimposed on the acute process. The combination of these findings suggests a mixed etiology for the AKI, likely involving both prerenal and intrinsic factors. The nephrology team is consulted to evaluate the need for potential renal replacement therapy, considering the patient's declining urine output and rising creatinine levels.

These diagnostic results necessitate a prompt and focused intervention strategy to address the underlying causes and prevent further complications. The healthcare team must consider the risk of progressing to chronic kidney disease and the implications of fluid overload on the patient's cardiovascular status. Close monitoring of renal function and electrolytes, along with judicious management of blood pressure and fluid balance, will be critical in stabilizing the patient's condition and guiding further therapeutic decisions.

Section 2

Change in Patient Status

Over the next 24 hours, the patient's condition begins to deteriorate, highlighting the complexity of managing their acute kidney injury. The patient develops signs of fluid overload, evident by increasing peripheral edema and mild dyspnea on exertion. Lung auscultation reveals bilateral basal crackles, suggesting pulmonary congestion. Vital signs show a blood pressure of 168/92 mmHg, heart rate of 102 beats per minute, respiratory rate of 22 breaths per minute, and oxygen saturation dropping to 91% on room air. These clinical findings raise concerns about the patient's cardiovascular stability and the risk of progressing to pulmonary edema.

Laboratory results reveal that despite initial interventions, the patient's serum potassium level has risen further to 6.2 mEq/L, exacerbating the risk for potentially life-threatening cardiac arrhythmias. An urgent electrocardiogram (ECG) is performed, which shows peaked T waves consistent with hyperkalemia. The patient's urine output continues to decrease, now measuring only 300 mL over the past 24 hours, underscoring the severity of renal impairment and further complicating fluid management strategies.

These developments necessitate an immediate escalation in care, with the healthcare team prioritizing measures to address the hyperkalemia and fluid overload. The nephrology team recommends the initiation of urgent renal replacement therapy to manage the electrolyte imbalance and prevent further complications, while continuous cardiac monitoring is implemented to detect any arrhythmias promptly. This change in patient status underscores the need for dynamic clinical reasoning and swift adjustments in the treatment plan to stabilize the patient and prevent irreversible damage.

Section 3

Following the initiation of renal replacement therapy, the healthcare team closely monitors the patient's response to the intervention. Within hours, there is a noticeable improvement in the patient's fluid status; peripheral edema begins to decrease, and the patient's respiratory effort eases somewhat, suggesting a reduction in pulmonary congestion. The patient's oxygen saturation improves to 95% on room air, and auscultation of the lungs reveals a slight reduction in crackles, indicating a positive response to the fluid removal.

Laboratory results post-therapy show a reduction in serum potassium levels to 5.5 mEq/L, a significant improvement that reduces the immediate risk of cardiac arrhythmias. The ECG is repeated and demonstrates normalization of the T wave morphology, further alleviating concerns about hyperkalemia-induced cardiac complications. However, despite these improvements, the patient's urine output remains critically low at 200 mL over the subsequent 24 hours, highlighting ongoing challenges in renal recovery and the need for continued renal support.

As the team evaluates the patient's progress, attention turns to the potential underlying causes of the acute kidney injury. Additional diagnostics, including renal ultrasound and serological tests, are planned to assess for potential obstructive or intrinsic renal pathologies. Meanwhile, the patient's blood pressure remains elevated at 160/88 mmHg, necessitating careful titration of antihypertensive medications to optimize cardiovascular stability without compromising renal perfusion. The healthcare team remains vigilant, recognizing the delicate balance required to support renal function while managing the broader systemic impacts of acute kidney injury. This phase of care emphasizes the importance of ongoing assessment and adaptation of the treatment plan to maintain the patient's clinical trajectory towards recovery.

Section 4

As the healthcare team continues to monitor the patient's status, a new complication arises: the development of metabolic acidosis, as evidenced by an arterial blood gas analysis showing a pH of 7.30, a bicarbonate level of 18 mEq/L, and a PCO2 of 35 mmHg. This finding prompts the team to reconsider the patient's metabolic status and the balance of electrolytes and fluids, recognizing the potential impact of acidosis on both renal and systemic function. The patient begins to exhibit signs of increased fatigue and lethargy, suggesting a worsening in overall metabolic state.

In response to these findings, the team initiates a careful adjustment of the dialysis prescription to address the acidosis, aiming to optimize the removal of uremic toxins and correct the acid-base balance. Sodium bicarbonate supplementation is also considered as part of the treatment plan to counteract the acidosis. Concurrently, the patient's antihypertensive regimen is reassessed to ensure it does not exacerbate the patient's renal status, given the potential for some medications to impair renal perfusion further.

The emergence of metabolic acidosis highlights the complexity of managing acute kidney injury and underscores the need for precise clinical reasoning. The team must evaluate the interconnectedness of renal function, fluid balance, and cardiovascular stability, ensuring that each intervention supports the patient’s path towards recovery without introducing additional complications. As the patient's journey progresses, the healthcare providers remain committed to frequent reassessments and tailored interventions, fully aware that each decision can significantly impact the patient's trajectory.

Section 5

As the healthcare team revisits the patient's condition, they note a change in the patient's status that necessitates immediate attention. The patient, previously alert and oriented, now exhibits increased confusion and agitation, raising concerns about potential cerebral effects of the metabolic acidosis. Vital signs reveal a blood pressure of 145/92 mmHg, a heart rate of 110 beats per minute, and a respiratory rate of 28 breaths per minute, suggesting compensatory mechanisms in response to the worsening metabolic derangement. The patient's temperature remains stable at 98.6°F, but oxygen saturation has decreased slightly to 92% on room air, possibly indicating respiratory compensation for the acidosis.

In light of these changes, the team decides to obtain repeat laboratory tests to further elucidate the patient's acid-base status and electrolyte balance. The new results demonstrate a pH of 7.28, a bicarbonate level of 16 mEq/L, and a PCO2 of 32 mmHg, confirming a progression of the metabolic acidosis despite initial interventions. Serum potassium is elevated at 5.8 mEq/L, posing a risk for cardiac arrhythmias, while serum calcium is on the lower end of normal at 8.4 mg/dL, possibly contributing to the neuromuscular symptoms observed.

The clinical team, acknowledging the critical need for rapid correction, intensifies the dialysis regimen to enhance clearance of excess hydrogen ions and uremic toxins. Simultaneously, intravenous sodium bicarbonate is administered cautiously, with careful monitoring to prevent overcorrection and subsequent alkalosis. The patient's antihypertensive medications are adjusted to minimize renal perfusion compromise, and a low-potassium diet is introduced to address hyperkalemia. The team remains vigilant in observing the patient's response, understanding that timely and precise interventions are crucial in steering the patient away from further complications while stabilizing their overall condition.