A patient with acute kidney injury (AKI) is admitted to the hospital with laboratory findings indicating hyperkalemia and metabolic acidosis. Which intervention should the nurse prioritize to address the patient's hyperkalemia?

C) Administer calcium gluconate intravenously to stabilize cardiac membranes.

A) Administer sodium bicarbonate intravenously to correct metabolic acidosis.

B) Initiate continuous renal replacement therapy (CRRT) to manage fluid overload.

C) Administer calcium gluconate intravenously to stabilize cardiac membranes.

A patient with acute kidney injury presents with hyperkalemia, hyponatremia, and metabolic acidosis. Which of the following interventions should the nurse prioritize to address the patient's hyperkalemia while monitoring for potential complications?

B) Administer calcium gluconate and monitor for cardiac arrhythmias

A) Administer sodium polystyrene sulfonate and monitor for bowel movements

B) Administer calcium gluconate and monitor for cardiac arrhythmias

C) Provide a sodium-restricted diet to prevent further hyponatremia

D) Administer bicarbonate to correct metabolic acidosis

A patient with worsening renal function and metabolic acidosis is experiencing altered mental status, tachycardia, and increased respiratory rate. Which of the following interventions should the nurse anticipate as the priority to address the patient's hemodynamic instability and respiratory distress?

B) Prepare the patient for hemodialysis

A) Administer intravenous sodium bicarbonate

B) Prepare the patient for hemodialysis

C) Increase oxygen therapy to 100% via non-rebreather mask

D) Administer intravenous diuretics for fluid overload

A patient with worsening renal function and metabolic acidosis is displaying altered mental status, hypotension, tachycardia, and respiratory distress. Which intervention should the nurse prioritize to stabilize the patient’s condition?

B) Begin continuous renal replacement therapy (CRRT) to address fluid overload and electrolyte imbalances.

A) Administer a rapid IV fluid bolus to increase blood pressure.

B) Begin continuous renal replacement therapy (CRRT) to address fluid overload and electrolyte imbalances.

C) Increase supplemental oxygen to improve oxygen saturation levels.

D) Administer sodium bicarbonate IV to correct metabolic acidosis.

A patient diagnosed with partially compensated metabolic acidosis and cardiac dysfunction is being managed with a low-dose inotropic agent. Which nursing intervention is most appropriate to monitor for potential complications associated with this treatment?

C) Observe for signs of tachyarrhythmias

A) Monitor for signs of hypoglycemia

B) Assess for increased peripheral edema

C) Observe for signs of tachyarrhythmias

D) Check daily body weight for weight loss

A patient with a diagnosis of partially compensated metabolic acidosis, reduced ejection fraction, and pulmonary edema is receiving low-dose inotropic support. The nurse is monitoring the patient's response to treatment. Which assessment finding would indicate an effective response to the inotropic therapy?

B) Increase in blood pressure and urine output

A) Decrease in serum lactate levels

B) Increase in blood pressure and urine output

C) Development of new onset arrhythmias

D) Worsening of pulmonary crackles on auscultation

A patient receiving inotropic support for heart failure exhibits worsening pulmonary edema, hypotension, and elevated potassium levels. Continuous renal replacement therapy (CRRT) is initiated to manage fluid overload and electrolyte imbalances. Which nursing intervention is most critical to prioritize at this time?

B) Closely monitor cardiac telemetry for signs of arrhythmias.

A) Administer prescribed diuretics to reduce fluid overload.

B) Closely monitor cardiac telemetry for signs of arrhythmias.

C) Increase the rate of inotropic infusion to improve blood pressure.

D) Collaborate with respiratory therapy to increase oxygen flow rate.

A patient receiving inotropic support is experiencing worsening pulmonary edema, hypotension, and electrolyte imbalances. Which nursing intervention should be prioritized to address the patient's current condition?

B) Initiate continuous renal replacement therapy (CRRT) as recommended by nephrology to manage fluid overload.

A) Increase the infusion rate of the inotropic medication to support blood pressure.

B) Initiate continuous renal replacement therapy (CRRT) as recommended by nephrology to manage fluid overload.

C) Administer a diuretic to rapidly reduce pulmonary edema and improve breathing.

D) Provide supplemental oxygen to maintain adequate oxygen saturation levels.

A patient undergoing continuous renal replacement therapy (CRRT) for acute kidney injury presents with a persistent potassium level of 5.4 mEq/L, occasional premature ventricular contractions (PVCs), and low blood pressure. Which nursing intervention is most appropriate to address the risk of cardiac complications while maintaining hemodynamic stability?

B) Administer calcium gluconate to stabilize cardiac membranes

A) Increase the rate of CRRT to enhance potassium removal

B) Administer calcium gluconate to stabilize cardiac membranes

C) Initiate a potassium-restricted diet and consult a dietitian

D) Increase inotropic support to raise blood pressure and improve renal perfusion

A patient undergoing continuous renal replacement therapy (CRRT) presents with persistent hyperkalemia and episodes of premature ventricular contractions (PVCs). What is the priority nursing intervention to address the patient's elevated potassium level and reduce the risk of cardiac complications?

B) Administer sodium polystyrene sulfonate as prescribed

A) Increase the rate of CRRT to enhance potassium removal

B) Administer sodium polystyrene sulfonate as prescribed

C) Initiate a low-potassium diet immediately

D) Request an increase in inotropic support to stabilize blood pressure

acute kidney injury - Nursing Case Study

Pathophysiology

• Primary mechanism: Reduced renal perfusion leads to prerenal acute kidney injury (AKI). This occurs when there's a significant drop in blood flow to the kidneys, often due to dehydration, heart failure, or blood loss, causing insufficient oxygen and nutrient delivery.

• Secondary mechanism: Direct kidney damage, known as intrinsic AKI, arises from conditions like acute tubular necrosis (ATN), which is caused by toxins or ischemia damaging kidney tubules. This results in impaired filtration and waste accumulation.

• Key complication: The accumulation of waste products and fluid imbalance can lead to electrolyte disturbances and acid-base imbalances, exacerbating potential for systemic complications like metabolic acidosis or hyperkalemia, which are critical for nursing assessment and intervention.

Patient Profile

Demographics:

65-year-old male, retired construction worker

History:

• Key past medical history: Hypertension, Type 2 Diabetes, Chronic Obstructive Pulmonary Disease (COPD)

• Current medications: Lisinopril, Metformin, Albuterol inhaler

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Decreased urine output and fatigue

• Key symptoms: Swelling in legs, nausea, shortness of breath, confusion

• Vital signs: Blood pressure 150/95 mmHg, heart rate 105 bpm, respiratory rate 22 breaths per minute, temperature 99.1°F, oxygen saturation 92% on room air

Section 1

New Diagnostic Results:

Upon admission to the hospital, a series of diagnostic tests are conducted to further evaluate the extent of the patient's acute kidney injury and its systemic effects. Laboratory results reveal a blood urea nitrogen (BUN) level of 45 mg/dL and a creatinine level of 3.2 mg/dL, indicating significant renal impairment. The patient's estimated glomerular filtration rate (eGFR) is calculated at 25 mL/min, confirming a marked reduction in kidney function. Electrolyte analysis shows hyperkalemia with a potassium level of 5.8 mEq/L and hyponatremia with a sodium level of 130 mEq/L. These findings suggest potential risks for cardiac arrhythmias and neurological symptoms, necessitating close monitoring and prompt intervention.

Further urinalysis reveals proteinuria and the presence of granular casts, consistent with acute tubular necrosis (ATN). Arterial blood gas (ABG) analysis indicates metabolic acidosis, with a pH of 7.31 and bicarbonate level of 18 mEq/L, highlighting the patient's compromised acid-base balance. Chest X-ray shows bilateral lower lobe infiltrates, raising concerns about possible fluid overload or developing pulmonary complications. These diagnostic results guide the medical team to prioritize fluid management, electrolyte correction, and renal support, while also considering the patient's existing comorbidities of hypertension, diabetes, and COPD in their treatment plan.

The healthcare team initiates a multi-faceted approach to address these issues. Aggressive management of hyperkalemia is critical, involving the administration of calcium gluconate to stabilize cardiac membranes, insulin with glucose to shift potassium intracellularly, and sodium polystyrene sulfonate to enhance potassium elimination. Diuretic therapy is cautiously considered to manage fluid overload, but care is taken to avoid exacerbating renal perfusion deficits. These interventions are complemented by continuous monitoring of renal function and electrolytes, ensuring timely adjustments to the treatment regimen as the patient's condition evolves. This diagnostic information provides a critical foundation for ongoing clinical reasoning and decision-making, influencing both immediate and long-term management strategies for the patient.

Section 2

Change in Patient Status

Over the next 24 hours, the patient's condition evolves, presenting new challenges requiring vigilant reassessment and adaptation of the care plan. The patient begins to exhibit signs of altered mental status, including confusion and lethargy, which can be attributed to the ongoing electrolyte imbalances and the metabolic acidosis. Vital signs reveal hypotension, with a blood pressure of 95/60 mmHg, and tachycardia, with a heart rate of 105 beats per minute. The respiratory rate has increased to 24 breaths per minute, suggesting compensatory mechanisms in response to the acid-base imbalance. Oxygen saturation remains stable at 94% on room air, but the patient reports increased shortness of breath, prompting concerns about potential fluid overload and pulmonary congestion.

Laboratory tests are repeated to reassess the patient's renal and electrolyte status. The BUN level has risen to 55 mg/dL, and creatinine has increased to 3.8 mg/dL, indicating worsening renal function. Potassium levels have decreased slightly to 5.5 mEq/L following initial interventions, but sodium levels persist at 128 mEq/L, and bicarbonate has further declined to 16 mEq/L, exacerbating the metabolic acidosis. A repeat chest X-ray shows progression of the bilateral lower lobe infiltrates, raising the suspicion of pulmonary edema.

In response to these developments, the healthcare team must refine their management strategy. The priority is to address the patient's hemodynamic instability and respiratory distress, which may involve cautious fluid restriction and the possible initiation of dialysis to manage the worsening renal failure and fluid status. The patient's altered mental status also requires close neurological monitoring and may necessitate further investigation to rule out other causes of encephalopathy. The evolving clinical picture demands ongoing interdisciplinary collaboration and dynamic clinical reasoning to optimize the patient's recovery trajectory and prevent further complications.

Section 3

In the following hours, the patient's condition continues to evolve, and new diagnostic results provide further insight into the underlying issues. A repeat arterial blood gas (ABG) analysis reveals a pH of 7.28, indicating persistent acidosis, with a partial pressure of carbon dioxide (PaCO2) at 32 mmHg, and a bicarbonate (HCO3-) level stabilized at 16 mEq/L. These results confirm a partially compensated metabolic acidosis, aligning with the patient's respiratory compensation efforts. Serum lactate levels are now elevated at 3.2 mmol/L, suggesting a possible component of lactic acidosis due to hypoperfusion and tissue hypoxia. These findings underscore the need to closely monitor the patient's hemodynamic status and consider advanced supportive measures.

Echocardiography is performed to evaluate cardiac function and assess for potential cardiac contributors to the patient's symptoms. The echocardiogram shows a reduced ejection fraction of 45%, indicative of impaired systolic function, which may be contributing to the observed hypotension and fluid overload. This cardiac dysfunction could also explain the patient's increased shortness of breath and the progression of pulmonary edema noted on imaging. These results highlight the necessity of careful fluid management and the potential need for inotropic support to improve cardiac output and stabilize blood pressure.

In light of these diagnostic results, the care team decides to initiate a low-dose inotropic agent to enhance cardiac contractility and support systemic circulation. Additionally, a nephrology consultation is obtained to evaluate the timing and modality of renal replacement therapy, given the worsening renal function and fluid overload. The interdisciplinary team continues to engage in regular discussions to adjust the treatment plan as needed, ensuring a comprehensive approach to address the patient's multi-faceted condition. The focus remains on preventing further complications and optimizing recovery through meticulous monitoring and timely interventions.

Section 4

As the care team closely monitors the patient's response to the initiated inotropic support, new complications begin to emerge. Over the next 12 hours, the patient's respiratory status continues to deteriorate despite previous interventions. The patient exhibits increased work of breathing, with a respiratory rate climbing to 28 breaths per minute. Auscultation reveals diffuse crackles throughout both lung fields, consistent with worsening pulmonary edema. Blood pressure readings fluctuate, with systolic readings ranging from 85 to 95 mmHg, indicating persistent hypotension despite inotropic therapy. Heart rate remains elevated at 110 beats per minute, suggesting ongoing compensatory tachycardia.

Laboratory results reveal a further decline in renal function, with serum creatinine rising to 3.2 mg/dL and blood urea nitrogen (BUN) increasing to 45 mg/dL. Electrolyte imbalances become apparent, with a potassium level of 5.6 mEq/L, raising concerns about the risk of cardiac arrhythmias. The nephrology team recommends initiating renal replacement therapy, opting for continuous renal replacement therapy (CRRT) to gently manage fluid removal and correct metabolic derangements without exacerbating the patient's hemodynamic instability.

The decision to start CRRT marks a pivotal step in addressing the patient's fluid overload and metabolic acidosis. The multidisciplinary team remains vigilant in reassessing the patient's evolving condition, ready to adjust the therapeutic approach as necessary. Efforts are directed toward stabilizing the patient's cardiovascular and renal status, preventing further respiratory compromise, and mitigating the risk of arrhythmias through careful electrolyte management. As these interventions are implemented, ongoing evaluation of the patient's response will be crucial in guiding the next stages of care.

Section 5

As the continuous renal replacement therapy (CRRT) is initiated, the care team closely monitors the patient's response, focusing on fluid balance and electrolyte management. Over the next six hours, there is a subtle shift in the patient's status. The respiratory rate gradually decreases to 24 breaths per minute, and auscultation reveals a slight reduction in crackles, indicating an initial improvement in pulmonary edema. However, blood pressure remains a concern, with systolic readings persistently low at 90 mmHg, despite adjustments in the inotropic support. This necessitates ongoing titration of medications to support hemodynamic stability.

New laboratory results provide further insight into the patient's condition. Serum creatinine stabilizes at 3.2 mg/dL, and BUN decreases to 40 mg/dL, suggesting a positive response to CRRT. However, the potassium level remains elevated at 5.4 mEq/L, despite efforts to manage it through CRRT and medication. This persistent hyperkalemia poses a risk of cardiac complications, prompting the team to consider additional strategies, such as dietary modifications and the administration of potassium-binding agents, to prevent arrhythmias.

Throughout this period, the patient's cardiac status is closely monitored via telemetry, revealing episodes of occasional premature ventricular contractions (PVCs), a potential precursor to more severe arrhythmias if not addressed. The multidisciplinary team discusses the need for further interventions to manage electrolyte imbalances and continues to assess the patient's fluid status, ensuring that fluid removal through CRRT is optimized without compromising blood pressure. This dynamic situation requires ongoing reassessment and adaptation of the treatment plan to improve the patient's overall stability and prevent further complications.