A nurse is caring for Mr. Johnson, who presents with acute kidney injury and associated complications. His laboratory results show hyperkalemia with a potassium level of 6.2 mEq/L. Which of the following nursing interventions should be prioritized to address this condition?

A) Administer calcium gluconate to stabilize cardiac membranes.

B) Restrict oral potassium intake to reduce further increases.

C) Provide a potassium-binding resin to enhance elimination.

D) Monitor fluid intake and output to assess kidney function.

A nurse is reviewing the care plan for Mr. Johnson, a patient with acute kidney injury and notable fluid overload. Which nursing intervention is most critical to prevent potential complications related to his hyperkalemia?

B) Administer calcium gluconate and insulin with glucose as prescribed.

A) Monitor intake and output closely to ensure fluid balance.

B) Administer calcium gluconate and insulin with glucose as prescribed.

C) Encourage the patient to ambulate to reduce lower extremity edema.

D) Provide high-potassium foods to prevent hypokalemia.

Mr. Johnson's respiratory distress is worsening despite initial interventions. Which action should the nurse anticipate the healthcare team will prioritize to address both his respiratory and renal status effectively?

C) Start renal replacement therapy to manage fluid overload and metabolic acidosis.

A) Increase the dose of diuretics to further reduce fluid overload.

B) Initiate non-invasive ventilation to improve oxygenation.

C) Start renal replacement therapy to manage fluid overload and metabolic acidosis.

D) Administer bronchodilators to relieve respiratory distress.

Mr. Johnson is experiencing worsening respiratory distress and persistent fluid overload despite diuretic therapy. Which intervention should the nurse anticipate as a priority to address his current condition?

D) Prepare the patient for renal replacement therapy to address fluid overload and electrolyte imbalances.

A) Increase the dosage of diuretics to manage fluid overload.

B) Prepare for the initiation of non-invasive ventilation to improve respiratory status.

C) Administer sodium bicarbonate to correct metabolic acidosis.

D) Prepare the patient for renal replacement therapy to address fluid overload and electrolyte imbalances.

Mr. Johnson is experiencing tachycardia and hypertension due to increased cardiac workload and fluid overload. After initiating renal replacement therapy, which nursing intervention should be prioritized to monitor for potential complications related to his cardiac status?

C) Monitor ECG for arrhythmias continuously

A) Monitor intake and output every shift

B) Assess lung sounds for crackles every 4 hours

C) Monitor ECG for arrhythmias continuously

D) Check peripheral pulses every 8 hours

A patient with acute kidney injury (AKI) is exhibiting tachycardia, hypertension, and nonspecific ST segment changes on an ECG. Laboratory results show hyponatremia and metabolic acidosis. Which nursing intervention is most appropriate to prioritize at this time?

B) Monitor cardiac rhythm closely and prepare for renal replacement therapy

A) Administer a diuretic to manage fluid overload

B) Monitor cardiac rhythm closely and prepare for renal replacement therapy

C) Increase sodium intake to correct hyponatremia quickly

D) Administer potassium supplements to prevent hypokalemia

Mr. Johnson is showing occasional premature ventricular contractions (PVCs) after initiating renal replacement therapy. Which nursing intervention is most appropriate to address this cardiac complication?

B) Review and adjust Mr. Johnson's electrolyte levels, particularly potassium and magnesium.

A) Administer an antiarrhythmic medication to suppress the PVCs.

B) Review and adjust Mr. Johnson's electrolyte levels, particularly potassium and magnesium.

C) Increase the rate of renal replacement therapy to remove excess fluid more rapidly.

D) Encourage Mr. Johnson to ambulate to improve cardiac function and reduce PVCs.

A nurse is reviewing Mr. Johnson's case after the initiation of renal replacement therapy (RRT). Considering his current symptoms and lab results, which of the following actions should the nurse prioritize to prevent potential complications?

C) Monitor cognitive function closely and ensure gradual correction of sodium levels to prevent central pontine myelinolysis.

A) Increase the rate of sodium correction to quickly resolve hyponatremia.

B) Initiate antiarrhythmic therapy immediately to address the premature ventricular contractions.

C) Monitor cognitive function closely and ensure gradual correction of sodium levels to prevent central pontine myelinolysis.

D) Adjust the RRT settings to enhance the correction of metabolic acidosis more rapidly.

A nurse is caring for Mr. Johnson, who is experiencing neurological changes and an increase in PVCs. The healthcare team has decided to slow down the correction of his sodium levels and initiate potassium and magnesium replacement. Which nursing action is most critical in managing Mr. Johnson's care at this time?

C) Perform a neurological assessment every hour.

A) Monitor Mr. Johnson's urine output every 2 hours.

B) Adjust the intravenous fluid rate as per the physician's order.

C) Perform a neurological assessment every hour.

D) Educate Mr. Johnson about the importance of electrolyte balance.

A client with a history of electrolyte imbalance is experiencing neurological changes and increased PVCs. The healthcare team has adjusted intravenous fluid therapy and is administering potassium and magnesium. What should be the nurse's priority action to ensure patient safety?

C) Evaluate the patient's cardiac rhythm and rate every hour.

A) Monitor the patient's neurological status every four hours.

B) Assess the patient's urine output hourly.

C) Evaluate the patient's cardiac rhythm and rate every hour.

D) Check the patient's serum electrolyte levels daily.

acute kidney injury - Nursing Case Study

Pathophysiology

• Primary mechanism: Acute tubular necrosis (ATN) - Ischemia or nephrotoxic injury causes damage to renal tubular cells, leading to cell death and loss of function. This results in impaired reabsorption and filtration, causing an accumulation of waste products and fluid imbalances.

• Secondary mechanism: Reduced renal perfusion - Conditions like hypotension or severe dehydration decrease blood flow to the kidneys. Inadequate perfusion leads to hypoxia and further tubular damage, exacerbating kidney injury.

• Key complication: Fluid overload and electrolyte imbalances - As kidney function declines, the body struggles to excrete excess fluid and maintain electrolyte balance, potentially leading to complications like pulmonary edema, hyperkalemia, and metabolic acidosis.

Patient Profile

Demographics:

65-year-old male, retired factory worker

History:

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

• Current medications: Lisinopril, Metformin, Albuterol inhaler, Aspirin

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Decreased urine output and swelling in lower extremities

• Key symptoms: Fatigue, nausea, shortness of breath, confusion, elevated blood pressure

• Vital signs: Blood pressure 160/95 mmHg, heart rate 105 bpm, respiratory rate 22 breaths per minute, temperature 37.8°C, oxygen saturation 90% on room air

Section 1

As the clinical team conducts a thorough assessment of Mr. Johnson, they note several critical findings that help elucidate the severity of his acute kidney injury and its complications. The physical examination reveals notable bilateral pitting edema in the lower extremities, extending up to the knees, and crackles can be auscultated in the lung bases, indicating potential pulmonary congestion due to fluid overload. His skin appears cool and clammy, and there is jugular venous distension, further reinforcing concerns about fluid retention and compromised cardiac function.

Laboratory results return, providing additional insight into Mr. Johnson's condition. His serum creatinine is markedly elevated at 4.5 mg/dL, indicating significant renal impairment, while blood urea nitrogen (BUN) has risen to 68 mg/dL, reflecting impaired waste elimination. Electrolyte analysis reveals hyperkalemia, with a potassium level of 6.2 mEq/L, posing a risk for cardiac dysrhythmias. Additionally, the patient's arterial blood gas analysis shows metabolic acidosis, with a pH of 7.28 and a bicarbonate level of 18 mEq/L, suggesting that the kidneys are unable to adequately excrete acid and maintain electrolyte balance.

With these findings, the healthcare team initiates interventions aimed at managing fluid overload and stabilizing electrolyte imbalances. Diuretics are cautiously administered to facilitate fluid removal, while careful monitoring of cardiac and respiratory status is prioritized to prevent further complications. The elevation in potassium levels necessitates immediate attention, leading to the administration of calcium gluconate and insulin with glucose to temporarily shift potassium into cells. These measures, while addressing the immediate concerns, prompt consideration of dialysis as a potential intervention if Mr. Johnson's renal function continues to deteriorate. As the team monitors his response to treatment, they remain vigilant for any changes in his clinical status, understanding that swift adaptation to new developments is crucial in the management of acute kidney injury.

Section 2

As Mr. Johnson's clinical team continues to monitor his condition, they observe a change in his status that warrants immediate attention. Over the course of several hours, Mr. Johnson begins to exhibit signs of worsening respiratory distress. His respiratory rate increases to 28 breaths per minute, and he becomes increasingly tachypneic, with oxygen saturation dropping to 89% on room air. Auscultation of his lungs reveals worsening crackles, now extending to the mid-lung fields, suggesting an escalation of pulmonary edema. Despite the cautious administration of diuretics, Mr. Johnson's fluid overload seems to persist, raising concerns about the effectiveness of current interventions and prompting consideration of alternative strategies.

In response to the deteriorating respiratory status, supplemental oxygen is administered, and the team considers non-invasive ventilation to support Mr. Johnson's breathing. Concurrently, a repeat set of laboratory tests is ordered to reassess his electrolyte balance and renal function. The results show a slight improvement in hyperkalemia, with a potassium level now at 5.8 mEq/L, thanks to earlier treatments. However, his renal function remains critically impaired, with serum creatinine still elevated at 4.3 mg/dL, indicating no significant improvement. The metabolic acidosis persists, with a pH of 7.30 and bicarbonate level of 19 mEq/L.

Faced with these developments, the healthcare team deliberates the possibility of initiating renal replacement therapy earlier than anticipated to manage both the fluid overload and metabolic derangements more effectively. As they weigh the benefits and risks, they remain vigilant for further complications, such as potential cardiac instability or infection, that could arise from Mr. Johnson's compromised state. This decision-making process underscores the importance of a dynamic approach to acute kidney injury management, relying on continuous assessment and timely intervention to optimize patient outcomes.

Section 3

As the clinical team continues to monitor Mr. Johnson's condition, they note a concerning change in his cardiac status. Mr. Johnson is now exhibiting signs of increased cardiac workload, with a heart rate that has escalated to 118 beats per minute and blood pressure readings fluctuating between 150/95 mmHg and 160/100 mmHg. The combination of tachycardia and hypertension suggests that his heart is struggling to compensate for the ongoing fluid overload and metabolic stress. An ECG is performed, revealing nonspecific ST segment changes, which raises the suspicion of potential cardiac ischemia exacerbated by his current condition.

Simultaneously, the repeat laboratory tests indicate a worrying trend in his electrolyte balance. While the potassium level shows slight improvement, sodium levels have dropped to 130 mEq/L, indicating the development of hyponatremia. This electrolyte imbalance, coupled with the persistent metabolic acidosis, signals the complexity of Mr. Johnson's condition and the need for a more aggressive intervention strategy. The healthcare team faces the challenge of correcting these imbalances without precipitating further cardiac or renal compromise.

In response to these developments, the decision to initiate renal replacement therapy is made, aiming to address the fluid overload, correct the metabolic acidosis, and stabilize Mr. Johnson's electrolyte levels. The team remains acutely aware of the potential for further complications, such as arrhythmias or worsening cardiac function, and plans to closely monitor Mr. Johnson's cardiac status and overall response to the therapy. This strategic pivot underscores the necessity for a vigilant, adaptive approach in managing complex cases of acute kidney injury, where timely interventions can make a critical difference in patient outcomes.

Section 4

As the renal replacement therapy (RRT) is initiated, the clinical team closely monitors Mr. Johnson's response to the intervention. Within the first few hours, there is a noticeable diuresis, and his fluid overload begins to resolve, evidenced by a gradual reduction in peripheral edema and improved breath sounds on auscultation. However, while the fluid balance appears to be stabilizing, Mr. Johnson's cardiac status remains precarious. His heart rate continues to hover around 115 beats per minute, and although his blood pressure shows a slight downward trend, it remains elevated at 145/92 mmHg. The ECG is repeated, showing persistent nonspecific ST segment changes, but fortunately, no new signs of significant ischemia are noted at this time.

The laboratory results post-RRT indicate partial correction of the metabolic acidosis, with a serum bicarbonate level rising to 18 mEq/L. The sodium level has stabilized at 132 mEq/L, yet the team remains cautious due to the narrow margin for error in correcting the hyponatremia. Mr. Johnson also reports mild confusion and headache, symptoms possibly attributable to the electrolyte shifts or the subtle ongoing cerebral effects of his condition. The healthcare team decides to maintain a delicate balance in correcting his sodium levels, ensuring gradual adjustments to prevent central pontine myelinolysis.

Despite the positive response to RRT, a new complication arises as Mr. Johnson begins to exhibit occasional premature ventricular contractions (PVCs) on the cardiac monitor. This development prompts the team to reassess his electrolyte management and consider the impact of ongoing stress on his cardiac function. The possibility of initiating antiarrhythmic therapy is weighed carefully, with consideration of potential drug interactions and side effects. As the team plans the next steps, they emphasize the importance of continued vigilant monitoring and a multifaceted approach to address the intertwined challenges of cardiac and renal dysfunction in Mr. Johnson's care.

Section 5

As the clinical team continues to monitor Mr. Johnson, they observe a change in his status that requires immediate attention. Over the next 12 hours, his mild confusion progresses to a more pronounced disorientation, with Mr. Johnson becoming increasingly agitated and difficult to redirect. His speech is slurred, and he struggles to follow simple commands. Concerned about these neurological changes, the team conducts a thorough neurological assessment. Mr. Johnson's pupils are equal and reactive, but his Glasgow Coma Scale score has decreased from 15 to 13. The team suspects that the electrolyte imbalance, particularly the sodium level, may be contributing to these symptoms. A repeat serum sodium level shows a slight increase to 134 mEq/L, suggesting that the correction might be occurring too rapidly.

Recognizing the critical nature of these findings, the team decides to slow down the rate of sodium correction to prevent further neurological deterioration. They adjust the intravenous fluid therapy and monitor Mr. Johnson's neurological status hourly. Concurrently, they re-evaluate the cardiac monitor findings, noting that the frequency of PVCs has increased, now recorded at 10 per minute. The cardiology team is consulted, and they recommend magnesium and potassium replacement, given the potential for these electrolytes to stabilize cardiac rhythms. Current laboratory results show a serum potassium level of 3.4 mEq/L and magnesium at 1.7 mg/dL, both slightly below normal.

The healthcare team carefully administers intravenous potassium and magnesium while keeping a close watch on Mr. Johnson's cardiac and neurological status. Throughout this process, they emphasize the importance of careful titration of electrolyte levels to prevent further complications. As they implement these changes, they prepare for possible escalation of care, including considering advanced imaging to rule out any central nervous system pathology if Mr. Johnson's neurological status does not stabilize. The priority remains to restore balance while mitigating risks associated with both cardiac and renal dysfunctions.