A patient with acute kidney injury presents with hyperkalemia, as indicated by a potassium level of 5.8 mEq/L. Which nursing intervention is most appropriate to prioritize in this situation to prevent cardiac complications?

A) Administer intravenous calcium gluconate

B) Restrict dietary potassium intake

C) Initiate hemodialysis immediately

D) Encourage increased fluid intake

A patient with acute kidney injury presents with a serum creatinine level of 3.8 mg/dL, BUN of 48 mg/dL, and potassium level of 5.8 mEq/L. The nurse notes the patient has hypertension and is on multiple antihypertensives. Based on the lab findings and current medications, which nursing intervention is most appropriate to prioritize?

D) Consult with the healthcare provider to adjust antihypertensive medications considering nephrotoxicity.

A) Administer a potassium-sparing diuretic to help lower blood pressure.

B) Initiate a fluid challenge to improve renal perfusion.

C) Prepare the patient for dialysis to rapidly correct electrolyte imbalances.

D) Consult with the healthcare provider to adjust antihypertensive medications considering nephrotoxicity.

A patient with persistent hyperkalemia and metabolic acidosis has been receiving calcium gluconate and sodium polystyrene sulfonate with marginal improvement in potassium levels. Urine output remains low, and the patient exhibits fluctuating blood pressure with episodes of hypotension. What is the most appropriate next step in managing this patient's condition?

B) Initiate intermittent hemodialysis

A) Increase the dose of sodium polystyrene sulfonate

B) Initiate intermittent hemodialysis

C) Administer additional IV fluids to improve renal perfusion

D) Start a high-dose loop diuretic therapy

A patient with oliguria, fluctuating blood pressure, and persistent hyperkalemia despite initial treatment is being evaluated for further management. Which intervention should the nurse anticipate as the next priority to address the patient's condition?

A) Initiating intermittent hemodialysis

B) Increasing the dose of sodium polystyrene sulfonate

C) Administering additional calcium gluconate

D) Adjusting the antihypertensive medication regimen

A nurse is caring for a patient with acute kidney injury who has been initiated on intermittent hemodialysis due to fluid overload, hyperkalemia, and metabolic acidosis. The patient also exhibits signs of mild pulmonary congestion and increased work of breathing. Which nursing intervention is most appropriate to address the patient's respiratory status while preparing for dialysis?

B) Position the patient in a high Fowler's position during dialysis.

A) Encourage the patient to perform incentive spirometry every hour.

B) Position the patient in a high Fowler's position during dialysis.

C) Administer a bronchodilator before starting dialysis.

D) Restrict the patient’s fluid intake to 500 mL per day.

A patient with acute kidney injury is experiencing fluid overload and has been scheduled for intermittent hemodialysis. Which nursing intervention should the nurse prioritize to prevent complications during the dialysis session?

B) Monitor the patient's blood pressure closely throughout the dialysis session

A) Administer a diuretic to manage fluid overload before the procedure

B) Monitor the patient's blood pressure closely throughout the dialysis session

C) Increase the patient's fluid intake to prevent dehydration

D) Encourage high-protein snacks to promote healing

A patient undergoing intermittent hemodialysis experiences hypotension with a blood pressure of 90/60 mmHg and elevated serum potassium levels at 5.2 mEq/L. Which nursing intervention should the nurse prioritize to address the patient's current condition?

C) Reassess the ultrafiltration rate and adjust it to prevent further hypotension.

A) Administer a potassium-binding resin to lower serum potassium levels.

B) Increase the ultrafiltration rate to remove excess fluid more rapidly.

C) Reassess the ultrafiltration rate and adjust it to prevent further hypotension.

D) Administer a bolus of intravenous fluids to raise blood pressure immediately.

A patient undergoing intermittent hemodialysis begins to exhibit a drop in blood pressure to 90/60 mmHg and occasional premature ventricular contractions (PVCs). Which nursing intervention is the priority in this situation?

B) Administer a bolus of normal saline to address hypotension.

A) Increase the ultrafiltration rate to remove more fluid.

B) Administer a bolus of normal saline to address hypotension.

C) Reposition the patient to improve venous return.

D) Prepare to administer calcium gluconate to stabilize cardiac rhythm.

A patient with acute kidney injury is experiencing increased fatigue, confusion, and altered consciousness post-dialysis. Vital signs show hypotension and tachycardia. Laboratory results indicate hyperkalemia and slightly decreased sodium levels. What is the most appropriate initial nursing intervention to address the patient's current condition?

B) Increase the rate of intravenous fluids to rapidly correct hypotension.

C) Administer sodium bicarbonate to correct acidosis and shift potassium intracellularly.

D) Prepare the patient for an emergency dialysis session to rapidly remove excess potassium.

A patient presents with increased fatigue, confusion, and hypotension two hours post-dialysis. Lab results indicate hyperkalemia and slight hyponatremia. Which nursing intervention should be prioritized to address the patient's current condition?

C) Administer calcium gluconate to stabilize cardiac function

A) Administer an additional dose of diuretics to reduce fluid overload

B) Increase the rate of oxygen delivery to improve oxygen saturation

C) Administer calcium gluconate to stabilize cardiac function

D) Restrict fluid intake to prevent further hyponatremia

Acute Kidney Disease - Nursing Case Study

Pathophysiology

• Primary mechanism: Acute kidney injury (AKI) often results from decreased blood flow to the kidneys, known as prerenal azotemia. This can be due to conditions like dehydration or heart failure, leading to inadequate perfusion and impaired filtration.

• Secondary mechanism: Intrinsic damage to the kidney tissue, such as acute tubular necrosis (ATN), occurs when prolonged ischemia or exposure to nephrotoxins damages the renal tubules, reducing their ability to reabsorb and concentrate urine effectively.

• Key complication: If untreated, AKI can progress to fluid overload, electrolyte imbalances (like hyperkalemia), and metabolic acidosis, significantly impacting cardiovascular function and requiring prompt medical intervention.

Patient Profile

Demographics:

52-year-old male, 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 swelling in the lower extremities

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

• Vital signs: Blood pressure 160/95 mmHg, heart rate 105 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, the healthcare team prioritized obtaining laboratory tests to further evaluate the patient's renal function and electrolyte balance. The results revealed a serum creatinine level of 3.8 mg/dL, significantly elevated from his baseline and indicating a marked decline in renal clearance. Blood urea nitrogen (BUN) was also notably high at 48 mg/dL. Electrolyte analysis showed a potassium level of 5.8 mEq/L, suggesting emerging hyperkalemia, a common complication in acute kidney injury that can predispose the patient to cardiac arrhythmias. Metabolic panel results indicated mild metabolic acidosis with a bicarbonate level of 18 mEq/L, reflecting impaired acid-base balance due to decreased renal excretion of hydrogen ions.

In addition to these laboratory findings, a urinalysis was performed, revealing a low urine sodium concentration and high urine osmolality, suggesting prerenal causes of AKI, likely exacerbated by the patient's hypertension and possible volume depletion. An ultrasound of the kidneys ruled out obstructive causes, such as nephrolithiasis or hydronephrosis, further supporting a prerenal or intrinsic etiology like acute tubular necrosis (ATN).

These diagnostic results necessitated prompt medical intervention to prevent further renal damage and associated complications. The patient's elevated blood pressure and lab findings pointed towards a need for careful fluid management and possible adjustment of antihypertensive therapy, considering his current medications and potential nephrotoxicity. The healthcare team began planning for possible renal replacement therapy if his condition continued to decline, while closely monitoring cardiac function due to the risk of arrhythmias from hyperkalemia. This approach required ongoing assessment and recalibration of treatment strategies to stabilize the patient and prevent progression to more severe renal impairment.

Section 2

As the healthcare team initiated treatment, the patient's condition began to shift, indicating a change in status that required immediate attention. Despite initial fluid resuscitation efforts to address potential prerenal causes, the patient's urine output remained low, measuring less than 400 mL over the past 24 hours, indicative of oliguria. Concurrently, the patient's blood pressure fluctuated, recorded at 160/95 mmHg, which, while elevated, showed an erratic pattern with episodes of hypotension, dropping to 85/55 mmHg at times. This instability suggested a complex interplay between fluid status and vascular resistance, complicating the management plan.

In light of the patient's persistent hyperkalemia, additional treatment strategies were employed, including the administration of calcium gluconate to stabilize cardiac membranes and sodium polystyrene sulfonate to promote potassium excretion. However, a repeat lab test revealed that potassium levels had decreased only marginally to 5.5 mEq/L, indicating a partial response to interventions. Meanwhile, the patient's acid-base status deteriorated, with bicarbonate levels dropping to 16 mEq/L, exacerbating the metabolic acidosis. The respiratory rate increased to 24 breaths per minute, a compensatory mechanism to counteract the acidosis, yet it led to respiratory fatigue and further clinical concern.

These developments underscored the need for a reevaluation of the treatment regimen, particularly the consideration of renal replacement therapy options, such as intermittent hemodialysis, to more effectively manage the profound electrolyte imbalances and acidosis. The team also deliberated the adjustment of antihypertensive medications, weighing the risk of further renal insult against the need to control blood pressure. Continuous monitoring of the patient's cardiac rhythm was prioritized to promptly detect any arrhythmias, given the persistent hyperkalemia and fluctuating blood pressure. This comprehensive reassessment aimed to stabilize the patient's condition and prevent further deterioration, while preparing for potential escalation of care.

Section 3

As the healthcare team continued to monitor the patient's condition, a new set of diagnostic results prompted a reassessment of the treatment strategy. The latest lab tests indicated a further drop in glomerular filtration rate (GFR), now calculated at 20 mL/min/1.73m², confirming a progression in acute kidney injury severity. Additionally, serum creatinine levels had risen to 3.2 mg/dL, suggesting deteriorating renal function. Despite ongoing efforts to manage fluid balance, the patient's weight had increased by 2 kg over the past 48 hours, likely due to fluid retention. A chest X-ray revealed mild pulmonary congestion, raising concerns about the risk of pulmonary edema, especially in light of the patient's compromised renal function and fluid management challenges.

In response to these findings, the healthcare team decided to initiate renal replacement therapy, opting for intermittent hemodialysis to address the persistent hyperkalemia, metabolic acidosis, and fluid overload. This decision was made after careful consideration of the patient's fluctuating hemodynamics and the potential benefits of more aggressive removal of toxins and excess fluid. The team also adjusted the patient's antihypertensive regimen, introducing a low-dose vasodilator to better manage blood pressure without further compromising renal perfusion. Continuous cardiac monitoring remained a priority, with particular vigilance for any signs of arrhythmias, as the patient's serum potassium level remained at the upper limit of normal at 5.5 mEq/L.

As the team prepared to commence dialysis, they engaged in thorough communication with the patient and family, outlining the procedure, potential benefits, and risks involved. This collaborative approach aimed to ensure informed decision-making and enhance the patient's understanding of the evolving treatment plan. Meanwhile, the nursing staff focused on meticulous monitoring of the patient's respiratory status, given the increased work of breathing and potential for respiratory fatigue. Through these coordinated efforts, the healthcare team endeavored to stabilize the patient's condition, proactively addressing complications while preparing for the next critical phase of care.

Section 4

As the healthcare team initiated intermittent hemodialysis, they closely monitored the patient's response to the treatment. Initially, the dialysis session proceeded smoothly, but midway through, the patient began exhibiting signs of hypotension, with blood pressure dropping to 90/60 mmHg. This development prompted an immediate reassessment of the patient's fluid status and hemodynamic stability. The sudden drop in blood pressure was concerning, given the patient's ongoing challenges with fluid management and the risk of further renal compromise. In response, the team adjusted the ultrafiltration rate during dialysis to mitigate the risk of further hypotension and ensured the patient was positioned comfortably to optimize venous return.

Concurrently, new lab results indicated a slight improvement in metabolic acidosis, with serum bicarbonate levels rising to 18 mEq/L, reflecting partial correction of the acid-base imbalance due to the dialysis. However, serum potassium levels remained elevated at 5.2 mEq/L, necessitating vigilance for any signs of cardiac arrhythmias. Continuous cardiac monitoring revealed occasional premature ventricular contractions (PVCs), which, while not immediately alarming, required ongoing observation to prevent potential progression to more serious arrhythmias.

The nursing team also noted a subtle increase in the patient's respiratory rate, now at 24 breaths per minute, with mild use of accessory muscles, suggesting increased respiratory effort. This change, coupled with the known pulmonary congestion, reinforced the need for frequent respiratory assessments to preempt any progression to respiratory distress. As the immediate post-dialysis period concluded, the healthcare team focused on stabilizing the patient's cardiovascular status and optimizing electrolyte balance, while planning for the next dialysis session. This phase emphasized the importance of dynamic clinical reasoning to adapt the treatment strategy to the patient's evolving needs, aiming to improve renal function and overall stability.

Section 5

As the healthcare team continued to monitor the patient post-dialysis, they noted a change in the patient's status that warranted immediate attention. Approximately two hours after the session, the patient began to experience increased fatigue and confusion, with an altered level of consciousness. The nursing team promptly conducted a neurological assessment, revealing that the patient was oriented only to person and was unable to follow complex commands, a notable decline from the baseline mental status. Vital signs indicated persistent hypotension with a blood pressure of 92/58 mmHg, a heart rate of 110 beats per minute, and a respiratory rate now increased to 26 breaths per minute. Oxygen saturation remained stable at 95% on 2L of supplemental oxygen via nasal cannula, but the patient's use of accessory muscles had become more pronounced.

Recognizing the potential for both fluid and electrolyte imbalances contributing to these changes, the team reviewed the latest laboratory results. Serum electrolyte analysis showed a further increase in potassium to 5.5 mEq/L, heightening the risk for more significant cardiac complications. Serum sodium was slightly decreased at 132 mEq/L, indicating possible dilutional hyponatremia, potentially exacerbating the patient's neurological symptoms. Given these findings, the healthcare team initiated a careful balance of intravenous fluids to address the hypotensive state while avoiding further fluid overload. They also administered a calcium gluconate infusion to stabilize cardiac membranes and prevent arrhythmias, alongside plans to adjust the dialysate composition for the next session to more effectively manage potassium levels.

This evolving clinical picture highlighted the intricate interplay between renal, cardiovascular, and neurological status in acute kidney injury. The team prioritized dynamic reassessment and fine-tuning of interventions, emphasizing the importance of an integrated approach to patient management. As they prepared for the next dialysis session, the focus remained on stabilizing the patient’s hemodynamic status, optimizing electrolyte balance, and closely monitoring neurological function, ensuring that any subtle changes would be promptly addressed to prevent further complications.