A patient has been diagnosed with acute kidney injury (AKI) characterized by elevated serum creatinine and potassium levels, along with the presence of muddy brown casts in the urine. What is the most appropriate nursing intervention to prioritize in order to prevent potential complications?

B) Providing calcium gluconate to stabilize cardiac membranes

A) Administering a diuretic to increase urine output

B) Providing calcium gluconate to stabilize cardiac membranes

C) Encouraging the patient to increase fluid intake to enhance renal perfusion

D) Preparing the patient for dialysis to immediately remove toxins

A patient with acute kidney injury (AKI) presents with serum creatinine levels of 3.5 mg/dL, BUN levels of 45 mg/dL, potassium levels of 5.9 mEq/L, and urinalysis showing muddy brown casts. What is the priority nursing intervention to address the immediate risk associated with these findings?

C) Administer calcium gluconate to stabilize cardiac membranes

A) Administer furosemide to promote diuresis

B) Prepare the patient for hemodialysis

C) Administer calcium gluconate to stabilize cardiac membranes

D) Restrict dietary potassium intake

A patient with acute kidney injury and fluctuating blood pressure is being monitored. Despite initial interventions, the urine output has decreased significantly, and serum creatinine and BUN levels continue to rise. Which nursing intervention should be prioritized to address the current renal function issues?

D) Evaluate and discontinue any nephrotoxic medications the patient may be receiving.

A) Increase the rate of intravenous fluids to improve renal perfusion.

B) Prepare the patient for potential initiation of renal replacement therapy.

C) Administer antihypertensive medication to manage fluctuating blood pressure.

D) Evaluate and discontinue any nephrotoxic medications the patient may be receiving.

A patient with acute kidney injury is experiencing significant fluctuations in blood pressure and decreased urine output. After successfully lowering the serum potassium levels, the healthcare team must now address the renal impairment and hemodynamic instability. Which of the following interventions should the nurse anticipate as a priority to promote renal perfusion and stability in this patient?

C) Titrate intravenous fluids based on blood pressure trends.

A) Administer a diuretic to increase urine output.

B) Initiate low-dose dopamine to enhance renal blood flow.

C) Titrate intravenous fluids based on blood pressure trends.

D) Start renal replacement therapy immediately.

A patient has developed signs of pulmonary congestion with bilateral pulmonary edema due to fluid overload and impaired renal function. Which nursing intervention should be prioritized to address the patient's respiratory distress while also considering the patient's renal status?

A) Administer prescribed low-dose diuretics and monitor urine output closely

B) Increase the patient's fluid intake to improve renal perfusion

C) Restrict sodium intake to help manage fluid balance

D) Position the patient in a supine position to aid breathing

A patient with bilateral pulmonary edema and impaired renal function has developed increasing respiratory distress. The healthcare team has initiated low-dose diuretic therapy. Which of the following assessments is the most critical for the nurse to perform to ensure the safe management of this patient's condition?

A) Monitor the patient's urine output and daily weight

B) Assess the patient's blood glucose levels

C) Evaluate the patient's skin turgor and mucous membranes

D) Check the patient's bowel sounds and abdominal distension

A patient with fluid overload and pulmonary edema is initiated on continuous renal replacement therapy (CRRT) due to oliguria and metabolic acidosis. An echocardiogram shows a reduced left ventricular ejection fraction. Which nursing intervention is most appropriate to monitor the effectiveness of the CRRT and the patient's cardiac status?

D) Evaluate the patient's arterial blood gases and electrolyte levels every 4 hours.

A) Monitor the patient's weight daily and compare it to baseline levels.

B) Assess the patient's urine output every hour and document changes.

C) Check the patient's blood pressure and heart rate every 15 minutes.

D) Evaluate the patient's arterial blood gases and electrolyte levels every 4 hours.

A patient with heart failure and renal impairment is undergoing continuous renal replacement therapy (CRRT) due to oliguria and metabolic acidosis. The patient's echocardiogram shows a reduced left ventricular ejection fraction. Which nursing intervention is the priority to monitor for complications during CRRT?

A) Assessing for signs of electrolyte imbalances, such as muscle cramps or arrhythmias

B) Monitoring urine output to evaluate the effectiveness of diuretic therapy

C) Checking for peripheral edema to assess fluid overload

D) Evaluating the patient's weight daily to track fluid balance

A patient receiving continuous renal replacement therapy (CRRT) presents with a potassium level of 5.8 mEq/L, a calcium level of 7.9 mg/dL, and decreased oxygen saturation. Which of the following interventions should the nurse prioritize to address these complications while considering the patient's cardiovascular status?

C) Administer calcium gluconate to stabilize cardiac membranes

A) Increase the diuretic dosage to enhance fluid removal

B) Adjust the CRRT dialysate to correct electrolyte imbalances

C) Administer calcium gluconate to stabilize cardiac membranes

D) Increase supplemental oxygen to improve oxygen saturation

A patient undergoing continuous renal replacement therapy (CRRT) begins to exhibit a potassium level of 5.8 mEq/L and a calcium level of 7.9 mg/dL. The patient also shows signs of pulmonary congestion with decreased oxygen saturation to 88%. Which intervention should the nurse prioritize to address these complications?

C) Collaborate with the healthcare team to adjust the dialysate composition to correct electrolyte imbalances.

A) Increase the rate of fluid removal on CRRT to reduce pulmonary congestion.

B) Administer a potassium-sparing diuretic to manage electrolyte imbalance.

C) Collaborate with the healthcare team to adjust the dialysate composition to correct electrolyte imbalances.

D) Initiate high-flow oxygen therapy to improve oxygen saturation.

Acute kidney injury - Nursing Case Study

Pathophysiology

• Primary mechanism: Acute tubular necrosis (ATN) is a leading cause of acute kidney injury (AKI), resulting from ischemia or nephrotoxic injury. This leads to the death of tubular epithelial cells, causing obstruction and back-leakage of filtrate, impairing kidney function.

• Secondary mechanism: Reduced renal perfusion, often due to hypovolemia or heart failure, decreases glomerular filtration rate (GFR). This triggers compensatory mechanisms like vasoconstriction, which further exacerbates kidney damage by limiting blood flow.

• Key complication: If untreated, these mechanisms can progress to chronic kidney disease (CKD), increasing the risk of fluid overload, electrolyte imbalances, and accumulation of waste products, which are critical concerns for patient management.

Patient Profile

Demographics:

65-year-old male, retired construction worker

History:

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

• Current medications: Lisinopril, Metformin, Atorvastatin

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Decreased urine output and fatigue

• Key symptoms: Oliguria, generalized weakness, swelling in legs, nausea

• Vital signs: Blood pressure 160/95 mmHg, Heart rate 92 bpm, Respiratory rate 22 breaths per minute, Temperature 37.8°C, Oxygen saturation 94% on room air

Section 1

New Diagnostic Results:

Following the initial assessment and presentation of symptoms indicative of acute kidney injury, the healthcare team proceeded with a comprehensive evaluation to better understand the underlying pathology and extent of kidney impairment. Laboratory tests revealed significantly elevated serum creatinine levels at 3.5 mg/dL, indicating a marked decline in renal function from the patient's baseline. Blood urea nitrogen (BUN) levels were also elevated at 45 mg/dL, further corroborating the diagnosis of AKI. An electrolyte panel showed hyperkalemia, with potassium levels at 5.9 mEq/L, posing an immediate risk for cardiac complications. Urinalysis revealed muddy brown casts, characteristic of acute tubular necrosis, and a fractional excretion of sodium (FENa) greater than 2%, suggesting intrinsic renal damage.

In addition to laboratory findings, imaging studies including a renal ultrasound were conducted to assess structural changes. The ultrasound indicated normal kidney size without evidence of hydronephrosis, ruling out obstructive uropathy. However, Doppler studies showed reduced renal blood flow, supporting the secondary mechanism of decreased perfusion contributing to the acute tubular necrosis. These findings highlighted the complex interplay between ischemic injury and nephrotoxic effects in this patient's condition.

This diagnostic information prompted the care team to consider targeted interventions to address the underlying causes and complications. The elevation in potassium levels necessitated immediate intervention to prevent cardiac arrhythmias, with plans to administer calcium gluconate and initiate insulin with glucose to drive potassium back into cells. The team also deliberated on optimizing fluid management to improve renal perfusion while avoiding fluid overload, particularly given the patient's history of hypertension and potential diastolic dysfunction. These decisions underscored the need for careful monitoring and adjustment of the therapeutic approach based on ongoing clinical assessments and laboratory results, paving the way for the next steps in managing the patient's acute kidney injury.

Section 2

As the healthcare team implemented the initial interventions, the patient's condition was closely monitored for any changes or signs of improvement. Within the first 24 hours, the response to treatment was mixed, indicating a need for further clinical reasoning and adjustment of the care plan.

The administration of calcium gluconate and insulin with glucose successfully lowered the serum potassium levels to a safer range of 4.8 mEq/L, reducing the immediate risk of cardiac arrhythmias. However, the patient's blood pressure readings remained unstable, fluctuating between hypotensive episodes with systolic measurements dropping to 90 mmHg and periods of hypertension reaching 160 mmHg systolic. This variability suggested ongoing challenges with fluid balance and potential cardiac involvement, necessitating careful titration of intravenous fluids and consideration of adjunctive therapies to support hemodynamic stability.

Despite the initial management efforts, the patient's urine output decreased significantly, falling to less than 20 mL/hr over the past 12 hours, indicating a worsening of the renal function. Repeat laboratory tests showed a further increase in serum creatinine to 4.2 mg/dL and BUN to 58 mg/dL, pointing to a progression of the acute kidney injury. These developments raised concerns about the adequacy of renal perfusion and highlighted the need for re-evaluation of potential contributing factors such as medication effects or undiagnosed underlying conditions. The healthcare team discussed the possibility of initiating renal replacement therapy to manage the escalating renal impairment, balancing this decision with the patient's overall clinical picture and potential for recovery.

Section 3

As the healthcare team continued to monitor the patient, new complications began to emerge, complicating the clinical picture. Over the next 12 hours, the patient developed signs of pulmonary congestion, characterized by increasing respiratory distress, crackles upon auscultation of the lungs, and a new oxygen requirement to maintain adequate saturation levels. The chest X-ray revealed bilateral pulmonary edema, suggesting a fluid overload state likely exacerbated by the impaired renal function and fluctuating blood pressure. This development prompted the team to reconsider the fluid management strategy, as the delicate balance between preventing further kidney damage and avoiding fluid overload became increasingly challenging.

In light of these complications, a decision was made to initiate a low-dose diuretic therapy cautiously, aiming to alleviate the pulmonary congestion without compromising renal perfusion further. Concurrently, a nephrology consultation was sought to evaluate the potential need for renal replacement therapy, given the persistent oliguria and rising creatinine levels. The team also explored the possibility of underlying cardiac dysfunction contributing to the patient's hemodynamic instability, considering further cardiac evaluation to rule out congestive heart failure or other cardiac conditions.

These new developments required the healthcare team to engage in comprehensive clinical reasoning, integrating data from various diagnostic tests, clinical assessments, and response to interventions. The patient's care plan was adjusted to address the complex interplay of renal, cardiac, and fluid balance issues, emphasizing the need for meticulous monitoring and timely interventions. As the team prepared for potential renal replacement therapy, they remained vigilant for any further changes in the patient's condition, recognizing that the path to recovery would require a careful and coordinated approach.

Section 4

As the healthcare team implemented the low-dose diuretic therapy, the patient's response was closely monitored. Over the next few hours, there was a slight improvement in the respiratory distress, with a reduction in crackles upon auscultation and a decreased need for supplemental oxygen. However, the patient's urine output remained low, and creatinine levels continued to rise, indicating persistent renal impairment. The nephrology team assessed the patient and recommended continuous renal replacement therapy (CRRT) as the next step, given the ongoing oliguria and worsening metabolic acidosis, evidenced by arterial blood gases showing a pH of 7.28 and bicarbonate level of 16 mEq/L.

Meanwhile, an echocardiogram was performed to evaluate cardiac function. The results revealed a moderately reduced left ventricular ejection fraction of 40%, suggesting systolic dysfunction contributing to the fluid overload and pulmonary edema. This finding necessitated a modification of the patient's medication regimen to include an ACE inhibitor and optimized beta-blocker therapy to improve cardiac output while minimizing fluid retention. The team also adjusted the diuretic dosing, taking into account the need to balance cardiac support with renal protection.

As the patient transitioned onto CRRT, the healthcare team remained vigilant for any signs of hemodynamic instability, given the patient's fluctuating blood pressure and recent cardiac findings. Regular assessments were conducted to monitor electrolytes, fluid balance, and renal function, ensuring that the interventions were achieving the desired effects without inducing further complications. The careful integration of renal and cardiac management strategies highlighted the complexity of the patient's condition, requiring ongoing collaboration and clinical reasoning to navigate the intertwined challenges effectively.

Section 5

As the patient settled into the continuous renal replacement therapy (CRRT), the healthcare team observed an initial stabilization in vital signs, with blood pressure maintaining at 110/70 mmHg and heart rate steady at 88 beats per minute. However, over the next 24 hours, new complications emerged. The patient began to exhibit signs of electrolyte imbalance, with laboratory results indicating a potassium level of 5.8 mEq/L and a calcium level dropping to 7.9 mg/dL. These changes prompted an immediate reassessment of the CRRT settings and additional interventions to correct the electrolyte disturbances.

Simultaneously, the patient's respiratory status, which had initially improved, began to deteriorate once more. Oxygen saturation decreased to 88% on room air, necessitating an increase in supplemental oxygen support. Upon auscultation, there was a return of scattered crackles in the lung bases, suggesting a recurring pulmonary congestion. This development required the team to revisit the balance between diuretic therapy and fluid removal via CRRT, considering the patient's compromised cardiac function and the need to prevent further exacerbation of heart failure symptoms.

These new complications underscored the intricate interplay between the renal and cardiovascular systems, challenging the team to refine their management approach. The nephrology and cardiology teams collaborated closely to adjust the CRRT parameters, including the dialysate composition, to address the electrolyte imbalances while optimizing fluid removal. This ongoing dynamic management highlighted the necessity for continuous monitoring and the application of clinical reasoning to anticipate and mitigate potential complications, paving the way for the next phase of the patient's care journey.