A patient with acute kidney injury and heart failure presents with hyperkalemia (potassium level of 6.2 mEq/L) and metabolic acidosis (pH 7.28). What is the priority nursing action to address the hyperkalemia?

C) Administer insulin and glucose infusion

A) Administer sodium bicarbonate to correct acidosis

B) Prepare the patient for dialysis

C) Administer insulin and glucose infusion

D) Implement a low-potassium diet

A patient is admitted with acute kidney injury and heart failure, presenting with hyperkalemia and metabolic acidosis. Which of the following interventions should the nurse prioritize to stabilize the patient's condition?

C) Administer insulin and glucose to facilitate the shift of potassium into cells.

A) Administer sodium bicarbonate to correct metabolic acidosis.

B) Prepare the patient for hemodialysis to rapidly remove excess potassium.

C) Administer insulin and glucose to facilitate the shift of potassium into cells.

D) Increase intravenous fluid rate to enhance renal perfusion.

A patient is experiencing oliguria, metabolic acidosis, and declining respiratory status with increased work of breathing and low oxygen saturation. Which nursing intervention should be prioritized to address the patient's current condition?

B) Prepare the patient for non-invasive ventilation support to improve oxygenation

A) Administer a bronchodilator to improve respiratory function

B) Prepare the patient for non-invasive ventilation support to improve oxygenation

C) Increase the rate of intravenous fluids to improve urine output

D) Administer sodium bicarbonate to correct metabolic acidosis

A patient with a diagnosis of acute kidney injury is experiencing oliguria, metabolic acidosis, and respiratory distress. Which intervention should the nurse prioritize to address the patient's deteriorating respiratory status?

C) Initiate non-invasive positive pressure ventilation (NIPPV).

A) Administer sodium bicarbonate to correct the metabolic acidosis.

B) Prepare for intubation and mechanical ventilation.

C) Initiate non-invasive positive pressure ventilation (NIPPV).

D) Increase the diuretic dose to reduce pulmonary congestion.

A patient with acute kidney injury and respiratory distress shows signs of pulmonary edema and an increasing anion gap metabolic acidosis. The healthcare team is considering initiating renal replacement therapy. Which of the following clinical findings is the MOST indicative of the need to commence renal replacement therapy?

D) Persistent oliguria despite conservative management

A) Bilateral pulmonary infiltrates confirmed by chest X-ray

B) Anion gap metabolic acidosis with an anion gap of 18 mEq/L

C) Rising creatinine level now at 3.5 mg/dL

D) Persistent oliguria despite conservative management

A patient with acute kidney injury and respiratory distress is being evaluated for renal replacement therapy. The healthcare team has noted bilateral infiltrates on chest X-ray and a rising anion gap metabolic acidosis. Which nursing intervention is most important to prioritize before initiating renal replacement therapy?

B) Assess the patient's hemodynamic stability and perfusion status.

A) Administer sodium bicarbonate to correct the metabolic acidosis.

B) Assess the patient's hemodynamic stability and perfusion status.

C) Restrict fluid intake to prevent further fluid overload.

D) Increase the frequency of monitoring vital signs and oxygen saturation.

A patient undergoing continuous renal replacement therapy (CRRT) has developed hypokalemia with a serum potassium level of 3.2 mEq/L and hypotension. Which nursing intervention is the priority to address these complications?

A) Administer intravenous potassium chloride as prescribed

B) Increase the rate of CRRT to remove excess fluid

C) Hold vasopressor administration to avoid further hypotension

D) Encourage the patient to increase dietary potassium intake

A patient undergoing continuous renal replacement therapy (CRRT) for fluid overload and acute kidney injury presents with a potassium level of 3.2 mEq/L, hypotension, and metabolic acidosis. What should be the priority nursing intervention to address the patient's current condition?

C) Initiate vasopressor support to manage hypotension.

A) Increase the rate of CRRT to enhance metabolic waste removal.

B) Administer potassium supplements to correct hypokalemia.

C) Initiate vasopressor support to manage hypotension.

D) Reduce the CRRT fluid removal rate to stabilize blood pressure.

A patient with acute kidney injury (AKI) on continuous renal replacement therapy (CRRT) has rising BUN and creatinine levels along with metabolic acidosis. What is the most appropriate nursing intervention to address the metabolic acidosis in this patient?

B) Collaborate with the healthcare team to adjust the bicarbonate concentration in the dialysate solution.

A) Increase the rate of CRRT to enhance clearance of metabolic waste.

B) Collaborate with the healthcare team to adjust the bicarbonate concentration in the dialysate solution.

C) Encourage the patient to increase oral fluid intake to dilute blood urea nitrogen.

D) Administer sodium bicarbonate intravenously to quickly correct acidosis.

A patient with acute kidney injury (AKI) on continuous renal replacement therapy (CRRT) has a blood urea nitrogen (BUN) level of 68 mg/dL and a creatinine level of 5.4 mg/dL. The patient's arterial blood gas shows a pH of 7.25, bicarbonate level of 18 mEq/L, and PaCO2 of 32 mmHg. Given these findings, which nursing intervention should take priority to address the patient's metabolic acidosis and deteriorating renal function?

A) Increase the bicarbonate concentration in the CRRT dialysate solution.

B) Administer diuretics to enhance urine output and reduce BUN and creatinine levels.

C) Encourage increased oral fluid intake to improve hydration status.

D) Consult with the dietitian to enhance the patient's nutritional intake.

acute kidney injury - Nursing Case Study

Pathophysiology

• Primary mechanism: Acute kidney injury (AKI) commonly arises from reduced renal perfusion, often due to hypovolemia, heart failure, or sepsis. This decreased blood flow results in ischemia, impairing the kidneys' ability to filter waste and maintain fluid balance.

• Secondary mechanism: Tubular injury often follows, especially in prolonged ischemia or exposure to nephrotoxins. Damaged renal tubules can lead to cell death and obstruction, further decreasing glomerular filtration rate (GFR) and exacerbating waste accumulation.

• Key complication: Accumulation of toxins and fluid imbalances can lead to electrolyte disturbances, such as hyperkalemia and acidosis, posing significant risks to cardiac function and overall homeostasis.

Patient Profile

Demographics:

65-year-old male, retired factory worker

History:

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

• Current medications: Lisinopril, Metformin, Atorvastatin

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Decreased urine output and swelling in legs

• Key symptoms: Fatigue, nausea, confusion, shortness of breath

• Vital signs: Blood pressure 160/95 mmHg, heart rate 105 bpm, respiratory rate 22 breaths/min, temperature 99.1°F, oxygen saturation 92% on room air

Section 1

As the medical team conducts an initial assessment, several critical findings emerge that offer insight into the patient's condition. The patient's lower extremity edema is noted to be pitting, with significant swelling extending up to the knees. Lung auscultation reveals bilateral crackles, suggesting pulmonary congestion. A further examination of the cardiovascular system indicates jugular venous distention, pointing towards fluid overload likely secondary to heart failure exacerbating the acute kidney injury. The patient's skin is cool and clammy, and he exhibits signs of mild cognitive impairment, likely related to both fluid and electrolyte imbalances.

Recent laboratory results provide additional clarity. Serum electrolytes reveal hyperkalemia with a potassium level of 6.2 mEq/L, indicating a danger to cardiac stability and requiring urgent attention. Blood urea nitrogen (BUN) and creatinine levels are significantly elevated, confirming the reduced renal clearance and substantiating the diagnosis of acute kidney injury. Arterial blood gas analysis points to metabolic acidosis with a pH of 7.28, further complicating the clinical picture. These findings underscore the need for rapid intervention to prevent further deterioration and stabilize the patient's condition.

In response to these findings, the healthcare team initiates a comprehensive intervention plan. Intravenous fluids are administered cautiously to optimize renal perfusion, while diuretics are considered to alleviate fluid overload and reduce cardiac strain. Continuous cardiac monitoring is essential due to the elevated potassium levels, and measures to lower serum potassium, such as insulin and glucose infusion, are promptly implemented. The patient is closely monitored for changes in mental status and respiratory function, as these parameters will guide the ongoing management and adjustments to the treatment plan. This vigilant approach aims to address the immediate complications while preventing further progression of the acute kidney injury.

Section 2

As the healthcare team monitors the patient's response to the initial interventions, several changes in the patient's condition begin to emerge. Over the next few hours, the patient's vital signs reveal a slight improvement in blood pressure, stabilizing at 110/70 mmHg, suggesting an initial positive response to the cautious fluid management. However, despite the administration of diuretics, the patient's urine output remains scant, with only 200 mL recorded over six hours. The persistent oliguria raises concerns about worsening renal function or possible acute tubular necrosis.

Repeated laboratory tests indicate a slight decrease in serum potassium levels, now at 5.8 mEq/L, demonstrating some efficacy of the insulin and glucose infusion. However, the metabolic acidosis remains unresolved; the arterial blood gas shows a pH of 7.30 with a bicarbonate level that remains low at 18 mEq/L. This persistent acidosis, coupled with the unchanged elevated BUN and creatinine levels, signifies ongoing renal impairment and the need for further intervention to correct the acid-base imbalance and support renal recovery.

New complications arise as the patient's respiratory status begins to decline. The patient exhibits increased work of breathing, with a respiratory rate climbing to 28 breaths per minute, and oxygen saturation dropping to 88% on room air. The bilateral crackles have progressed, indicating worsening pulmonary congestion. In light of these developments, the healthcare team considers the possibility of acute respiratory distress syndrome (ARDS) secondary to fluid overload and metabolic disturbances. This change necessitates a reassessment of the treatment plan, potentially incorporating non-invasive ventilation support, further electrolyte management, and perhaps even renal replacement therapy if renal function continues to deteriorate. These adjustments aim to stabilize the patient while addressing the multifaceted complications that have arisen.

Section 3

As the healthcare team continues to address the patient's evolving condition, new diagnostic results provide further insights into the complications at play. A chest X-ray confirms the presence of bilateral infiltrates consistent with pulmonary edema, reinforcing the suspicion of fluid overload contributing to the patient's respiratory distress. Further laboratory tests reveal an increasing anion gap metabolic acidosis, with the anion gap now at 18 mEq/L, pointing towards an accumulation of unmeasured anions potentially due to renal retention of acidic metabolites.

Meanwhile, a repeat assessment of the patient's renal function through a renal ultrasound shows no signs of obstruction, but the renal cortex appears slightly hyperechoic, suggestive of ongoing acute tubular necrosis. This finding corroborates the clinical picture of persistent oliguria and rising creatinine levels, which have now escalated to 3.5 mg/dL, indicating deteriorating renal function. The patient’s electrolyte panel shows a sodium level of 130 mEq/L, hinting at potential dilutional hyponatremia due to fluid shifts and aggressive fluid management attempts.

In response to these findings, the healthcare team deliberates the initiation of renal replacement therapy, given the continued decline in renal function and the inadequate response to conservative management. They also consider transitioning the patient to high-flow nasal cannula oxygen therapy to improve oxygenation and reduce respiratory effort. The interdisciplinary team, including nephrology and pulmonology specialists, collaborates to refine the treatment strategy, aiming to stabilize the patient’s respiratory status while supporting renal recovery. This strategic adjustment underscores the complexity of managing acute kidney injury with concurrent respiratory compromise and highlights the importance of dynamic clinical reasoning in the face of evolving challenges.

Section 4

The healthcare team decides to initiate continuous renal replacement therapy (CRRT) to address the patient's worsening renal function and fluid overload. Within the first 24 hours of CRRT initiation, there is a noticeable improvement in the patient's fluid balance, with a net negative fluid balance of 1.5 liters. This intervention helps to alleviate the pulmonary edema, as evidenced by a reduction in respiratory distress and improved oxygen saturation levels, now consistently above 92% on high-flow nasal cannula. The patient reports less dyspnea, and auscultation reveals decreased crackles in the lung bases.

However, within this period, new complications arise. The patient's potassium level, initially stable, begins to drop, reaching 3.2 mEq/L, raising concerns about hypokalemia induced by the aggressive dialysis. The team promptly adjusts the CRRT prescription to include potassium supplementation. Additionally, the patient's blood pressure trends lower, with readings fluctuating between 94/58 mmHg and 88/54 mmHg, prompting the need for vasopressor support to maintain adequate perfusion, especially in the context of ongoing fluid removal.

The interdisciplinary team reassesses the treatment plan, emphasizing the need for vigilant monitoring and dynamic adjustments to both the CRRT parameters and supportive measures. They reinforce the importance of balancing electrolyte management while ensuring hemodynamic stability. The patient's continued oliguria and metabolic acidosis, with a current blood pH of 7.28, emphasize the need for ongoing renal support and highlight the interconnected nature of these physiologic challenges. The healthcare team remains focused on optimizing the patient's hemodynamic status and metabolic balance to support recovery, illustrating the delicate balance required in managing complex cases of acute kidney injury with respiratory and metabolic complications.

Section 5

As the healthcare team continues to manage the patient's acute kidney injury with CRRT, they closely monitor for any changes in the patient's status. In the following 24 hours, the patient's blood pressure stabilizes slightly with the administration of vasopressors, now maintaining an average of 98/60 mmHg. However, new diagnostic results reveal a concerning rise in the patient's blood urea nitrogen (BUN) and creatinine levels, indicating a potential worsening of renal function. BUN is noted at 68 mg/dL, and creatinine has increased to 5.4 mg/dL. These findings suggest that despite initial improvements in fluid balance and respiratory status, the underlying renal impairment persists and may be exacerbating.

The patient's metabolic acidosis remains a challenge, with an arterial blood gas showing a pH of 7.25, bicarbonate level of 18 mEq/L, and a partial pressure of carbon dioxide (PaCO2) at 32 mmHg. The healthcare team deliberates on adjusting the CRRT settings to better address the acidosis, considering increasing the bicarbonate buffer in the dialysate solution. Additionally, they explore whether the patient's nutritional needs are being adequately met, as poor nutritional status could hinder recovery and contribute to the acid-base imbalance.

Given the rise in BUN and creatinine, along with persistent oliguria, the team discusses the potential benefits of further nephrology consultation to evaluate the need for additional diagnostic investigations, such as renal ultrasound or biopsy, to rule out any underlying pathologies that may be contributing to the patient's deteriorating renal function. This approach exemplifies the importance of integrating multidisciplinary perspectives and dynamic clinical reasoning to navigate the complexities of acute kidney injury management effectively. The team remains committed to optimizing the patient's treatment plan and closely monitoring for any new complications, understanding the fragile nature of the patient's condition.