Acute kidney disease - Nursing Case Study
Pathophysiology
• Primary mechanism: Acute kidney injury (AKI) is primarily caused by reduced blood flow to the kidneys (prerenal), leading to decreased glomerular filtration rate. This can result from dehydration, heart failure, or blood loss, impairing the kidneys' ability to filter waste effectively.
• Secondary mechanism: Tubular injury is another crucial factor, often due to toxins or ischemia. Damage to the renal tubules compromises their function, resulting in the back-leakage of filtrate and the loss of essential substances, further reducing renal clearance.
• Key complication: If not addressed promptly, AKI can lead to fluid overload, electrolyte imbalances like hyperkalemia, and metabolic acidosis. These complications can significantly impact cardiac function and overall patient stability, emphasizing the need for early detection and intervention.
Patient Profile
Demographics:
56-year-old male, construction worker
History:
• Key past medical history: Hypertension, Type 2 Diabetes
• Current medications: Lisinopril, Metformin, Atorvastatin
• Allergies: Penicillin
Current Presentation:
• Chief complaint: Reduced urine output and swelling in legs
• Key symptoms: Fatigue, nausea, difficulty breathing, confusion
• Vital signs: Blood pressure 160/95 mmHg, heart rate 105 bpm, respiratory rate 22 breaths per minute, temperature 99.1°F, oxygen saturation 90% on room air
Section 1
As the case progresses, the patient undergoes an initial assessment to evaluate the extent of his acute kidney injury (AKI) and associated complications. Upon physical examination, the patient demonstrates bilateral pitting edema up to the mid-calf, suggesting significant fluid retention. Auscultation reveals crackles at the lung bases, indicating potential pulmonary congestion, which correlates with his difficulty in breathing. Given his history of hypertension and diabetes, these findings raise concern for possible heart failure exacerbating the prerenal cause of his AKI. The patient's fatigue and confusion further suggest underlying metabolic disturbances, likely due to the accumulation of waste products and electrolyte imbalances.
Laboratory tests reveal crucial data to guide further management. Serum chemistry indicates elevated blood urea nitrogen (BUN) and creatinine levels, confirming impaired renal function. Notably, the potassium level is 5.8 mEq/L, revealing hyperkalemia, which poses a risk for cardiac dysrhythmias. The arterial blood gas analysis shows a pH of 7.32, consistent with mild metabolic acidosis, implicating decreased bicarbonate due to impaired renal excretion. These laboratory findings underscore the need to address the electrolyte imbalances and acid-base disturbance promptly to prevent further complications.
The healthcare team initiates interventions targeting the underlying causes and complications of AKI. Intravenous fluid therapy is cautiously administered to improve renal perfusion while monitoring for signs of fluid overload given the patient's compromised cardiac function. A low-potassium diet is implemented alongside medications such as calcium gluconate and insulin with glucose to stabilize cardiac membranes and reduce serum potassium levels. The patient is placed on supplemental oxygen to improve oxygen saturation, and close monitoring of vital signs and urine output is maintained to assess response to treatment. These interventions aim to stabilize the patient's condition and prevent progression to more severe complications, setting the stage for reevaluation and potential escalation of care if necessary.
Section 2
As the healthcare team continues to manage the patient's acute kidney injury and its complications, a new diagnostic test result provides critical insights into his evolving condition. An echocardiogram is performed to assess cardiac function, revealing a reduced ejection fraction of 40%, which confirms the suspicion of heart failure with reduced ejection fraction (HFrEF). This finding suggests that the patient's heart is not pumping efficiently, contributing to the fluid overload and pulmonary congestion observed during the initial assessment. These results necessitate a modification in the treatment plan to address the cardiac component of his condition more aggressively.
In response to these findings, the medical team decides to initiate treatment with a loop diuretic, such as furosemide, to help reduce fluid overload and alleviate the pulmonary congestion. This intervention is carefully titrated to balance the need for diuresis with the risk of exacerbating renal impairment. The patient is also started on an ACE inhibitor, such as lisinopril, to support heart function and control blood pressure, which is monitored closely to avoid further renal perfusion compromise. The team continues to track serum electrolytes and renal function indicators, adjusting therapies as needed to maintain electrolyte balance and prevent worsening of metabolic acidosis.
Despite these interventions, the patient begins to exhibit signs of new complications. Over the next 24 hours, he reports increasing fatigue and experiences a decline in urine output, which drops to less than 20 mL/hour, indicating potential progression to oliguric renal failure. Blood pressure readings reveal hypotension at 98/58 mmHg, raising concern for decreased renal perfusion. Additionally, repeat laboratory tests show a further increase in creatinine to 3.2 mg/dL and potassium to 6.2 mEq/L, with a corresponding drop in bicarbonate to 18 mEq/L, intensifying the metabolic acidosis. These changes prompt the healthcare team to consider the need for renal replacement therapy, such as dialysis, to manage the severe electrolyte imbalances and acidosis, as well as to support renal function. This development underscores the complexity of the patient's condition and the necessity for ongoing, dynamic clinical reasoning to guide his care.
Section 3
As the patient's condition evolves, the medical team closely monitors his response to the initiated interventions. Over the following 48 hours, it becomes apparent that the patient's response to the loop diuretic and ACE inhibitor therapy is suboptimal. Despite careful titration of furosemide, the patient's urine output remains low, and his fluid status is not improving as anticipated. The persistent hypotension, alongside a further decline in renal function, suggests that the diuretic is exacerbating his renal impairment rather than alleviating the fluid overload effectively. Consequently, the focus shifts to addressing the pressing issue of electrolyte imbalance and metabolic acidosis, now critical due to the elevated potassium level of 6.2 mEq/L and a bicarbonate level that has dropped further to 16 mEq/L.
Given these complications, the healthcare team contemplates the initiation of renal replacement therapy. However, they recognize that the patient's hypotension complicates the immediate use of conventional hemodialysis. Instead, they consider starting continuous renal replacement therapy (CRRT) as it offers gentle and more controlled fluid removal, better suited for hemodynamically unstable patients. This decision is weighed carefully, taking into consideration the potential benefits of stabilizing electrolyte imbalances and acidosis against the risks involved. The team also reassesses the patient's medication regimen, evaluating the necessity of continuing the ACE inhibitor, given the current hypotension and worsening renal function.
In addition to these intervention adjustments, the team revisits the patient's cardiac management plan, considering the possibility of introducing a beta-blocker, such as carvedilol, to further support heart function and potentially improve ejection fraction over time. This decision is contingent upon stabilizing the patient's blood pressure and ensuring that renal perfusion is not further compromised. The multidisciplinary approach highlights the complexity of managing acute kidney injury in the context of heart failure, emphasizing the importance of dynamic clinical reasoning and the ability to adapt the treatment plan as new challenges arise in this patient's critical care journey.
Section 4
As the healthcare team moves forward with the initiation of continuous renal replacement therapy (CRRT), they closely monitor the patient's response to this intervention. Over the next 24 hours, the patient's vital signs show some stabilization, with blood pressure improving slightly to 98/62 mmHg and heart rate maintaining at 88 beats per minute. The CRRT helps to gradually correct the severe electrolyte imbalance, with potassium levels trending down to 5.5 mEq/L and bicarbonate levels beginning to rise towards 18 mEq/L. Despite these positive changes, the patient's urine output remains minimal, and his creatinine level has increased to 3.8 mg/dL, reinforcing the need for ongoing renal support.
In conjunction with CRRT, the medical team decides to cautiously reintroduce low-dose carvedilol to the patient's medication regimen, aiming to optimize cardiac function without exacerbating hypotension. This decision is made after careful deliberation and consultation with the cardiology team, who concur that potential benefits include improved heart rate control and reduced cardiac workload. The medication is introduced at the lowest effective dose, with plans for gradual titration as the patient's hemodynamic status allows. The multidisciplinary team continues to emphasize the importance of frequent reassessment, recognizing that the patient's response to this adjusted treatment plan will be pivotal in determining subsequent steps.
While there are initial signs of improvement, the team remains vigilant for any new complications that may arise. Notably, they observe the patient's respiratory status, as there is a slight increase in respiratory rate to 24 breaths per minute and mild bilateral crackles on auscultation, indicating potential fluid overload in the lungs. This finding prompts further imaging and laboratory tests to rule out worsening pulmonary edema or infection. The patient's journey remains complex, with each intervention requiring a delicate balance between managing acute kidney injury, heart failure, and maintaining overall stability. As the team navigates these challenges, dynamic clinical reasoning and collaborative decision-making continue to be crucial in guiding the patient's care trajectory.
Section 5
As the healthcare team continues to monitor the patient, new diagnostic results provide critical insights into his evolving condition. A chest X-ray reveals mild pulmonary congestion, consistent with fluid overload, but no evidence of significant pulmonary edema or pneumonia. Laboratory tests show a slight increase in the patient's B-type Natriuretic Peptide (BNP) levels, now at 480 pg/mL, suggesting a strain on the heart due to fluid shifts. Despite the CRRT's effectiveness in managing electrolyte imbalances, the patient's renal function remains severely compromised, as evidenced by a further increase in creatinine levels to 4.1 mg/dL.
Given these findings, the team revisits their fluid management strategy. They decide to adjust the CRRT settings to enhance fluid removal while maintaining electrolyte balance, aiming to reduce the cardiac workload and improve respiratory function. The decision to optimize diuretic therapy is also weighed, considering the patient's low urine output and the potential risk of further hypotension. The nephrology and cardiology teams collaborate closely to ensure that the balance between fluid removal and hemodynamic stability is meticulously maintained.
This multifaceted approach necessitates vigilant monitoring for any signs of hemodynamic instability, such as hypotension or tachycardia, which could complicate the patient's condition. The team also remains alert to any changes in respiratory status, given the patient's increased respiratory rate and crackles on auscultation. As the patient's journey unfolds, these new diagnostic insights guide the interdisciplinary team's ongoing efforts to stabilize his condition and prevent further complications, underscoring the importance of dynamic clinical reasoning and adaptive care strategies.