acute kidney injury - Nursing Case Study

Pathophysiology

• Primary mechanism: Decreased renal perfusion - Acute kidney injury (AKI) often begins with reduced blood flow to the kidneys, leading to insufficient oxygen and nutrient delivery. This causes ischemic injury, primarily affecting the renal tubules and impairing their function.

• Secondary mechanism: Tubular obstruction and back-leak - Damaged renal cells can slough off and obstruct tubules, increasing intratubular pressure. This obstruction, along with cellular injury, leads to the back-leak of filtrate into the bloodstream, further reducing effective filtration.

• Key complication: Accumulation of waste products - As filtration decreases, waste products like urea and creatinine build up in the bloodstream, causing systemic effects such as metabolic acidosis and electrolyte imbalances, which can affect multiple organ systems.

Patient Profile

Demographics:

65-year-old male, retired construction worker

History:

• Key past medical history: Hypertension, type 2 diabetes mellitus, and hyperlipidemia

• Current medications: Lisinopril, Metformin, Atorvastatin

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Decreased urine output and swelling in legs

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

• Vital signs: Blood pressure 160/95 mmHg, heart rate 102 bpm, respiratory rate 24 breaths per minute, temperature 37.8°C, oxygen saturation 92% on room air

Section 1

As the nursing team conducts an initial assessment, they note that the patient's peripheral edema has worsened, with pitting edema now evident up to his mid-calves. His jugular venous pressure is elevated, suggesting fluid overload. Lung auscultation reveals bilateral crackles, more pronounced at the bases, indicating potential pulmonary congestion. The patient is visibly dyspneic, with labored breathing and an increased use of accessory muscles. Despite these signs, he remains alert and oriented, though he reports increased fatigue and persistent nausea.

Laboratory results return, showing a significant rise in serum creatinine to 3.2 mg/dL from a baseline of 1.1 mg/dL, and blood urea nitrogen (BUN) has elevated to 62 mg/dL. Electrolyte imbalances are also present, with hyperkalemia (potassium level of 5.9 mEq/L) and mild hyponatremia (sodium level of 132 mEq/L). Arterial blood gas analysis indicates metabolic acidosis, with a pH of 7.30 and bicarbonate level of 18 mEq/L. These findings confirm a worsening acute kidney injury, likely compounded by the patient's pre-existing conditions and current symptoms of fluid overload.

The focus shifts to managing the patient's fluid status and electrolyte imbalances while monitoring for further complications. Diuretics are cautiously considered to reduce fluid overload, but the risk of exacerbating renal perfusion issues must be weighed. The healthcare team initiates a regimen of supplemental oxygen to address hypoxia and contemplates renal replacement therapy if the patient's condition does not improve. Attention is given to dietary modifications and medication adjustments to mitigate hyperkalemia and acid-base disturbances. The patient's progress will be closely monitored, with repeat laboratory assessments scheduled to guide ongoing treatment decisions and ensure prompt identification of any new complications.

Section 2

As the nursing team continues to monitor the patient, they observe a change in his status over the next 24 hours. Despite the initiation of supplemental oxygen, the patient's respiratory distress has not significantly improved, and he exhibits persistent use of accessory muscles. Vital signs reveal a heart rate of 112 beats per minute, blood pressure of 148/92 mmHg, respiratory rate of 28 breaths per minute, and an oxygen saturation of 90% on 4 liters per minute via nasal cannula. The patient's fatigue has worsened, and he now reports mild chest discomfort, which prompts further assessment.

In response to the fluid overload and electrolyte imbalances, the healthcare team decides to administer a low-dose loop diuretic. However, subsequent laboratory results indicate only a modest decrease in serum potassium, now at 5.5 mEq/L, and no significant improvement in metabolic acidosis. The patient's serum creatinine has further increased to 3.6 mg/dL, and BUN has risen to 70 mg/dL, indicating ongoing renal impairment. Despite the cautious use of diuretics, there is a concern for decreased renal perfusion, as evidenced by a drop in urine output to 20 mL/hour.

Given these developments, the healthcare team considers the possibility of initiating renal replacement therapy to manage the escalating fluid overload and severe electrolyte disturbances. The patient's clinical status suggests a high risk for developing further complications such as cardiac arrhythmias due to hyperkalemia and respiratory failure due to worsening pulmonary congestion. The team discusses the need to re-evaluate the patient's medication regimen and dietary intake to address the persistent metabolic acidosis and electrolyte imbalances, while also preparing for potential escalation of care. The priority remains to stabilize the patient's condition and prevent any further decline in renal function.

Section 3

As the healthcare team deliberates the next steps, they decide to proceed with continuous renal replacement therapy (CRRT) to manage the patient's fluid overload and severe electrolyte imbalances. During the initiation of CRRT, the patient's vital signs remain unstable: heart rate is elevated at 118 beats per minute, blood pressure fluctuates between 140/90 mmHg and 130/85 mmHg, respiratory rate remains high at 30 breaths per minute, and oxygen saturation has dropped further to 88% despite increasing supplemental oxygen to 6 liters per minute via a face mask. The patient continues to exhibit significant fatigue and increased work of breathing.

Laboratory results obtained shortly after initiating CRRT indicate a slight improvement in serum potassium, now at 5.2 mEq/L, but ongoing metabolic acidosis with a bicarbonate level of 18 mEq/L and a pH of 7.31. The patient's serum creatinine has plateaued at 3.6 mg/dL; however, BUN remains high at 72 mg/dL, suggesting persistent renal impairment. The urine output remains low, at 15 mL/hour, confirming the need for ongoing renal support. A chest X-ray reveals worsening pulmonary congestion, consistent with fluid overload, and an echocardiogram shows mild left ventricular hypertrophy with an ejection fraction of 45%, indicating compromised cardiac function likely exacerbated by the patient's current condition.

As CRRT continues, the patient's clinical status requires close monitoring for potential complications such as hypotension or electrolyte shifts associated with the therapy. The team considers the need for potential adjustments in the CRRT prescription to optimize fluid removal and electrolyte balance, while also planning for a comprehensive medication review to address ongoing metabolic acidosis and prevent further cardiac complications. The immediate focus remains on stabilizing the patient's respiratory status and ensuring effective renal support to prevent any further deterioration in his condition.

Section 4

As the CRRT continues, the healthcare team closely monitors the patient for any changes in status. Over the next few hours, there is a notable change in the patient's respiratory condition. The work of breathing has increased, and the patient is now using accessory muscles more prominently, indicative of respiratory distress. Despite supplemental oxygen, the oxygen saturation has decreased further to 85%. This suggests a possible worsening of pulmonary edema or a developing acute respiratory distress syndrome (ARDS), necessitating an urgent reassessment of the patient's respiratory support.

Additional diagnostic results from an arterial blood gas (ABG) analysis show a slight worsening of metabolic acidosis, with the pH now at 7.29 and bicarbonate at 17 mEq/L. PaCO2 is elevated at 55 mmHg, indicating a concurrent respiratory component to the acidosis. These findings suggest that the patient is struggling to maintain adequate ventilation, potentially due to fluid overload and impaired gas exchange. The healthcare team discusses the option of transitioning to non-invasive positive pressure ventilation (NIPPV) to improve oxygenation and reduce the work of breathing, while assessing the risk of further fluid shifts exacerbating the patient's condition.

Meanwhile, the patient's blood pressure has become less stable, with episodes of hypotension occurring during the CRRT sessions, dropping to 105/65 mmHg. This prompts a review of the CRRT settings, considering adjustments to the fluid removal rate to prevent further hemodynamic instability. The team also considers the introduction of vasoactive medications to support blood pressure if needed. This evolving scenario underscores the need for a multidisciplinary approach to manage the complexities of the patient's acute kidney injury, fluid overload, and declining respiratory function, requiring ongoing collaboration and reevaluation of treatment strategies to stabilize the patient and prevent further complications.

Section 5

As the healthcare team implements non-invasive positive pressure ventilation (NIPPV) to address the patient's respiratory distress, there is an initial improvement in oxygenation. Oxygen saturation increases to 90%, and the patient exhibits reduced use of accessory muscles, indicating a decrease in the work of breathing. However, the team remains vigilant for any signs of deterioration, given the patient's precarious condition and the potential for further complications. The patient's blood pressure continues to fluctuate, with episodes of hypotension persisting. Vasoactive medications, such as norepinephrine, are introduced at a low dose to stabilize the mean arterial pressure above 65 mmHg, ensuring adequate organ perfusion.

New diagnostic results, including a repeat chest X-ray, reveal worsening bilateral infiltrates consistent with pulmonary edema, raising concerns about fluid overload exacerbating the respiratory compromise. The decision is made to adjust the CRRT settings, reducing the ultrafiltration rate to mitigate further hemodynamic instability while continuing to monitor fluid balance closely. Laboratory results show a persistent elevation in creatinine at 3.5 mg/dL, and the patient's urine output remains minimal, indicating ongoing acute kidney injury despite interventions.

As the evening progresses, the patient experiences an abrupt change in status, marked by increased agitation and confusion, suggestive of emerging encephalopathy. The healthcare team reassesses the patient's neurological status, considering the possibility of uremic encephalopathy or hypoxic brain injury due to the earlier episodes of hypoxia. A prompt neurological evaluation is initiated, and additional supportive measures are considered to address the potential cerebral complications. This evolving situation highlights the need for continuous monitoring and adaptive management strategies, as the patient's complex clinical scenario requires an integrated, multidisciplinary approach to stabilize their condition and prevent further decline.