A patient with acute kidney injury is displaying signs of fluid overload and hyperkalemia. Which nursing intervention should be prioritized to address the hyperkalemia and prevent cardiac complications?

A) Administer intravenous normal saline to dilute serum potassium levels.

B) Initiate a low-potassium diet and monitor daily serum potassium levels.

D) Encourage oral intake of fluids to promote renal excretion of potassium.

A patient with acute kidney injury presents with hyperkalemia, pulmonary edema, and hypertension. Which nursing intervention should be prioritized to address the patient's current condition?

C) Initiate continuous cardiac monitoring to detect potential dysrhythmias.

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

B) Provide dietary potassium restriction to prevent further hyperkalemia.

C) Initiate continuous cardiac monitoring to detect potential dysrhythmias.

D) Restrict fluid intake to manage fluid overload and prevent pulmonary complications.

A patient with hyperkalemia and hyponatremia is receiving treatment to stabilize cardiac function and correct electrolyte imbalances. Which of the following actions should the nurse prioritize to prevent potential complications associated with the patient's current condition?

B) Monitor cardiac rhythm and administer calcium gluconate as ordered to stabilize cardiac membranes.

A) Administer a rapid IV infusion of normal saline to correct hyponatremia.

B) Monitor cardiac rhythm and administer calcium gluconate as ordered to stabilize cardiac membranes.

C) Increase oral fluid intake to prevent dehydration and further electrolyte imbalance.

D) Hold insulin administration to avoid hypoglycemia and focus on fluid restriction.

A patient with hyperkalemia is being treated with intravenous calcium gluconate, insulin, and glucose. Despite these interventions, the patient continues to display pulmonary crackles and a new S3 heart sound. What is the most appropriate nursing action at this time?

A) Administer a loop diuretic to reduce fluid overload

B) Increase the rate of intravenous fluids to improve renal perfusion

C) Consult with a nephrologist about initiating dialysis

D) Hold all medications and reassess laboratory values

A patient with worsening renal function, characterized by elevated serum creatinine and BUN levels, oliguria, and pulmonary crackles, is being monitored for potential acute tubular necrosis. Which of the following nursing interventions is most appropriate to prioritize in this situation?

B) Monitor daily weights and adjust fluid balance as needed

A) Increase oral fluid intake to promote diuresis

B) Monitor daily weights and adjust fluid balance as needed

C) Administer high-dose loop diuretics to manage fluid overload

D) Encourage ambulation to improve renal perfusion

A patient with worsening renal function and oliguria is being managed with low-dose loop diuretics for fluid overload. Despite fluid restriction, the patient presents with persistent hyponatremia and fluctuating mental status. Which nursing intervention should be prioritized to address the current clinical findings?

B) Implement seizure precautions due to risk of hyponatremia-induced seizures.

A) Increase the diuretic dose to enhance fluid removal.

B) Implement seizure precautions due to risk of hyponatremia-induced seizures.

C) Encourage increased oral fluid intake to correct hyponatremia.

D) Prepare the patient for immediate dialysis to manage electrolyte imbalances.

A patient with persistent hyponatremia and hyperkalemia is being prepared for dialysis due to worsening renal function and neurological symptoms. Which nursing intervention is most critical to ensure patient safety during this time?

C) Observing for cardiac arrhythmias and administering calcium gluconate as prescribed

A) Monitoring for signs of fluid overload, such as edema and crackles

B) Administering lactulose to manage potential hepatic encephalopathy

C) Observing for cardiac arrhythmias and administering calcium gluconate as prescribed

D) Restricting oral fluid intake to manage hyponatremia

A patient with acute kidney injury and liver dysfunction presents with persistent hyponatremia (sodium level of 128 mEq/L) and hyperkalemia (potassium level of 5.6 mEq/L). The patient is also exhibiting increased confusion and asterixis. Which nursing intervention is the highest priority to implement to address these clinical findings?

B) Prepare the patient for dialysis to manage electrolyte imbalances.

A) Administer lactulose to reduce ammonia levels.

B) Prepare the patient for dialysis to manage electrolyte imbalances.

C) Restrict fluid intake to correct hyponatremia.

D) Administer sodium polystyrene sulfonate to lower potassium levels.

A patient undergoing dialysis shows improvement in electrolyte levels but continues to exhibit neurological symptoms such as lethargy and asterixis. Considering the current clinical picture, what is the most appropriate nursing intervention to prioritize at this time?

B) Continue monitoring and administering lactulose for ammonia reduction.

A) Increase fluid intake to correct hyponatremia.

B) Continue monitoring and administering lactulose for ammonia reduction.

C) Administer a potassium supplement to maintain cardiac function.

D) Encourage high protein intake to improve nutritional status.

A patient undergoing dialysis shows improvement in electrolyte balance but continues to exhibit neurological symptoms such as lethargy and asterixis. What is the most appropriate nursing action to address the patient's neurological status?

D) Notify the physician about the persistent symptoms and discuss the addition of rifaximin.

A) Increase the frequency of lactulose administration to reduce ammonia levels.

B) Encourage the patient to drink more fluids to improve hydration status.

C) Elevate the head of the bed to 30 degrees to enhance cerebral perfusion.

D) Notify the physician about the persistent symptoms and discuss the addition of rifaximin.

acute kidney injury - Nursing Case Study

Pathophysiology

• Primary mechanism: Ischemia - Reduced blood flow to the kidneys decreases oxygen delivery, impairing renal cell function and causing cell death. This often results from conditions like severe dehydration, heart failure, or sepsis, leading to inadequate perfusion pressure.

• Secondary mechanism: Nephrotoxic injury - Exposure to harmful substances, such as certain medications (e.g., NSAIDs, aminoglycosides) or contrast dyes, damages renal tubular cells, leading to cell necrosis and impaired filtration capacity.

• Key complication: Tubular obstruction - Dead cells and debris can obstruct renal tubules, further reducing urine output and exacerbating kidney injury. This can lead to fluid overload, electrolyte imbalances, and increased risk of chronic kidney disease if not addressed promptly.

Patient Profile

Demographics:

45-year-old male, construction worker

History:

• Key past medical history: Hypertension, type 2 diabetes

• Current medications: Lisinopril, Metformin

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Decreased urine output and fatigue

• Key symptoms: Nausea, mild swelling in legs, confusion

• Vital signs: Blood pressure 160/95 mmHg, heart rate 105 bpm, respiratory rate 22 breaths per minute, temperature 100.4°F

Section 1

As the patient's condition is further evaluated, the initial assessment findings reveal significant clinical insights. Physical examination confirms moderate pitting edema in the lower extremities, indicating fluid retention likely due to impaired renal function. Auscultation of the lungs reveals bilateral crackles at the bases, suggestive of fluid accumulation and possible pulmonary edema. This is compounded by elevated blood pressure at 170/100 mmHg, indicating worsening hypertension possibly due to fluid overload and heightened systemic vascular resistance. The patient is also increasingly lethargic, with a noticeable decline in mental clarity, suggesting potential uremic encephalopathy as waste products accumulate in the bloodstream.

Laboratory tests reveal a marked elevation in serum creatinine and blood urea nitrogen (BUN), confirming the diagnosis of acute kidney injury. Serum electrolytes show hyperkalemia, with potassium levels at 6.1 mEq/L, posing a risk for cardiac arrhythmias. Additionally, the patient exhibits hyponatremia at 130 mEq/L, indicating potential dilutional effects from fluid retention. Urinalysis shows the presence of muddy brown casts, aligning with acute tubular necrosis as a key pathological process. These findings emphasize the need for immediate intervention to address the electrolyte imbalances and prevent further deterioration.

The healthcare team initiates a plan to manage the patient's complications, including cautious fluid management to prevent overload, administration of diuretics to enhance renal excretion, and potential dialysis consideration if renal function does not improve. The patient's medication regimen is reviewed, with temporary discontinuation of nephrotoxic agents and careful monitoring of blood pressure. Close observation is warranted to assess the efficacy of interventions and to detect any new complications, such as worsening fluid status or cardiac effects of hyperkalemia. This stage of the case demands careful clinical reasoning to optimize treatment outcomes and mitigate the risk of progression to chronic kidney disease.

Section 2

As the healthcare team closely monitors the patient's condition, new diagnostic results offer further insights into the evolving clinical picture. A repeat set of laboratory tests indicates that, despite initial interventions, the patient's serum potassium level remains critically elevated at 6.3 mEq/L, necessitating immediate action to prevent cardiac complications. Electrocardiogram findings reveal peaked T-waves, a classic sign of hyperkalemia, reinforcing the urgency of addressing this electrolyte imbalance. The team initiates treatment with intravenous calcium gluconate to stabilize cardiac membranes, along with insulin and glucose to facilitate intracellular potassium shift, while preparing for potential dialysis should these measures prove insufficient.

Additionally, the patient's serum sodium level has decreased further to 128 mEq/L, exacerbating concerns about hyponatremia. This raises the possibility of syndrome of inappropriate antidiuretic hormone secretion (SIADH) as a concurrent complication, possibly triggered by stress or medications. The management plan is adjusted to include fluid restriction to address dilutional hyponatremia, while ensuring adequate renal perfusion. Continuous reassessment of fluid status and electrolyte levels is crucial to guide ongoing treatment decisions.

Clinically, the patient's mental status shows slight improvement following interventions, with more coherent speech and improved responsiveness, suggesting partial alleviation of uremic encephalopathy. However, the persistence of pulmonary crackles and the development of a new S3 heart sound on auscultation highlight the ongoing risk of heart failure due to fluid overload. These findings necessitate a balanced approach to fluid management, ensuring diuretic therapy is optimized without compromising renal perfusion. The healthcare team remains vigilant for any signs of worsening renal function or new complications, emphasizing the need for dynamic clinical reasoning to navigate this complex presentation.

Section 3

As the healthcare team continues to closely monitor the patient, new diagnostic results offer further insights into the evolving clinical picture. A repeat set of laboratory tests indicates that, despite initial interventions, the patient’s renal function is deteriorating. The serum creatinine level has increased to 3.8 mg/dL from the previous 3.2 mg/dL, and the blood urea nitrogen (BUN) has climbed to 45 mg/dL, both suggestive of worsening renal impairment. Additionally, the patient’s urine output has decreased to less than 400 mL over the past 24 hours, confirming oliguria and raising concerns about the progression to acute tubular necrosis.

In terms of fluid status, the patient's blood pressure remains stable at 130/85 mmHg, but the heart rate has increased slightly to 102 beats per minute, possibly indicating early signs of compensatory mechanisms to maintain cardiac output amidst fluid shifts. Given the pulmonary crackles and the S3 heart sound, the team carefully adjusts diuretic therapy, opting for a low-dose loop diuretic to mitigate fluid overload while avoiding excessive volume depletion. The decision to initiate dialysis is revisited, with plans to proceed should renal function and electrolyte imbalances fail to improve.

Clinically, the patient's mental status continues to fluctuate. Although there was an initial improvement, periods of confusion and lethargy persist, suggesting the need for a comprehensive neurological assessment to rule out other contributing factors such as electrolyte imbalances or medication effects. The interdisciplinary team discusses the potential for SIADH as a complicating factor, given the persistent hyponatremia and recent fluid restriction. The focus remains on achieving a delicate balance between addressing fluid overload and ensuring adequate renal perfusion, with frequent reassessment guiding the dynamic treatment plan. The healthcare team remains vigilant for new complications, prepared to adapt the management strategy as the patient's condition evolves.

Section 4

As the patient's condition continues to evolve, new diagnostic results reveal a concerning development in the clinical picture. A recent electrolyte panel indicates a sodium level of 128 mEq/L, confirming persistent hyponatremia despite fluid restriction efforts. In addition to the low sodium level, the potassium level has risen to 5.6 mEq/L, raising the specter of hyperkalemia, which could further complicate cardiac function. These findings necessitate immediate adjustments to the treatment plan, as the risk of life-threatening arrhythmias increases. The healthcare team decides to initiate measures to stabilize the potassium level, including administering calcium gluconate for cardiac protection and considering the use of sodium polystyrene sulfonate for potassium removal.

The patient's neurological status continues to ebb and flow, with increased episodes of confusion and lethargy. A further assessment is conducted to explore potential causes, revealing asterixis on examination, suggesting hepatic involvement or perhaps a more profound metabolic disturbance. Given these findings, an ammonia level is obtained, which returns elevated, hinting at possible hepatic encephalopathy or a significant uremic component due to the acute kidney injury. This prompts the team to initiate lactulose therapy to address the potential buildup of toxins contributing to the mental status changes.

In response to these new complications, the interdisciplinary team convenes to re-evaluate the patient's management plan. The decision is made to escalate to dialysis, given the worsening renal function, persistent electrolyte imbalances, and neurological deterioration. This intervention aims to provide symptomatic relief while removing excess fluid and correcting metabolic derangements. As preparations for dialysis commence, the team emphasizes continued monitoring of vital signs, laboratory values, and neurological status to tailor ongoing interventions and prevent further complications, ensuring a comprehensive approach to the patient's complex and dynamic condition.

Section 5

As the patient undergoes dialysis, the healthcare team closely monitors the response to this critical intervention. In the immediate aftermath of the first dialysis session, there is a notable improvement in the patient's electrolyte profile. The potassium level decreases to 4.8 mEq/L, alleviating the immediate cardiac risk. However, the sodium level remains at 130 mEq/L, indicating that while there is slight improvement, the hyponatremia persists and requires ongoing attention. The patient's blood pressure stabilizes to 118/76 mmHg, and heart rate is 82 bpm, suggesting a positive hemodynamic response.

Despite these encouraging signs, the patient's neurological status remains concerning. Although there is a slight reduction in episodes of confusion, the patient continues to exhibit lethargy and intermittent asterixis. An updated ammonia level shows a decrease, but it remains elevated at 65 µmol/L, supporting the hypothesis of a significant metabolic disturbance contributing to the encephalopathy. The team decides to continue lactulose therapy, while also considering the possibility of adding rifaximin should the neurological symptoms persist.

Throughout this period, continuous reassessment is crucial. The nursing staff pays close attention to the patient's fluid status, monitoring for signs of fluid overload or dehydration, both of which could complicate the clinical picture. The patient's urine output remains scant, reinforcing the need for ongoing renal support. Daily weight measurements and careful input-output tracking become essential components of care. As the team prepares for the next dialysis session, the focus shifts to optimizing the patient's nutritional status and addressing any further electrolyte imbalances, ensuring that each aspect of the patient's condition is managed in a coordinated and comprehensive manner.