acute kidney injury - Nursing Case Study

Pathophysiology

• Primary mechanism: Acute Tubular Necrosis (ATN) - Often results from ischemia or nephrotoxic injury, leading to damaged renal tubular cells, impaired reabsorption, and obstructed urine flow. This causes decreased glomerular filtration rate (GFR) and the accumulation of waste products in the blood.

• Secondary mechanism: Prerenal Azotemia - Caused by reduced renal perfusion due to factors like dehydration or heart failure. It leads to decreased renal blood flow, triggering compensatory mechanisms (e.g., renin-angiotensin-aldosterone system) that may worsen renal ischemia if unresolved.

• Key complication: Fluid and Electrolyte Imbalance - Impaired kidney function results in fluid overload, electrolyte disturbances (e.g., hyperkalemia, hyponatremia), and metabolic acidosis, posing significant clinical challenges and requiring careful management to prevent further complications.

Patient Profile

Demographics:

55-year-old male, construction worker

History:

• Key past medical history: Hypertension, Type 2 Diabetes, Chronic back pain

• Current medications: Lisinopril, Metformin, Ibuprofen

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Decreased urine output and fatigue

• Key symptoms: Nausea, swelling in legs, shortness of breath

• Vital signs: Blood pressure 150/95 mmHg, Heart rate 110 bpm, Respiratory rate 22 breaths/min, Temperature 37.8°C, Oxygen saturation 91% on room air

Section 1

As the healthcare team progresses with the initial assessment, further diagnostic evaluations are conducted to better understand the extent of the acute kidney injury in this 55-year-old male patient. Laboratory results reveal elevated serum creatinine at 3.2 mg/dL and blood urea nitrogen (BUN) at 52 mg/dL, indicating significant impairment in kidney function. Additionally, serum potassium levels are elevated at 5.8 mEq/L, raising concerns about the risk of cardiac complications. Urinalysis shows muddy brown casts, a hallmark of acute tubular necrosis, supporting the primary mechanism of injury. The patient's electrolytes reveal a sodium level of 130 mEq/L, suggestive of hyponatremia, and a bicarbonate level of 18 mEq/L, indicating metabolic acidosis.

Clinically, the patient displays signs of fluid overload, including persistent lower extremity edema and worsening shortness of breath, now with auscultation revealing bilateral crackles in the lung bases. The patient's blood pressure remains elevated at 155/98 mmHg despite his current antihypertensive regimen, adding to the complexity of his condition. These findings highlight the intricate balance needed to manage this patient's fluid status while addressing the underlying renal impairment and electrolyte imbalances.

The healthcare team initiates a careful approach, adjusting the patient's fluid management strategy by reducing intravenous fluid intake and commencing a diuretic regimen to alleviate fluid overload. Continuous monitoring of the patient's cardiac rhythm is essential due to the hyperkalemia, and measures such as administering calcium gluconate and insulin with glucose are considered to stabilize the potassium levels. With these interventions, the focus remains on optimizing renal perfusion and minimizing further renal injury, while preparing for potential escalation to more intensive renal support should the patient's status not improve. This scenario sets the stage for evaluating the patient's response to treatment and adjusting the care plan as necessary, with emphasis on mitigating the risk of further complications.

Section 2

Following the initial interventions, the healthcare team closely monitors the patient's response, particularly focusing on the reduction of fluid overload and stabilization of electrolytes. Over the next 24 hours, the patient experiences a slight improvement in symptoms of fluid overload, with a decrease in lower extremity edema and some reduction in shortness of breath. However, auscultation still reveals persistent crackles at the lung bases, suggesting ongoing pulmonary congestion. Vital signs show a slight improvement in blood pressure, now reading 148/92 mmHg, yet it remains elevated, indicating a continued need for careful blood pressure management alongside renal function considerations.

New laboratory results reveal a modest decrease in serum potassium levels, now at 5.4 mEq/L, suggesting that the interventions to address hyperkalemia are beginning to take effect. However, the patient's bicarbonate level remains low at 17 mEq/L, indicating persistent metabolic acidosis, and the serum sodium level has decreased further to 128 mEq/L, exacerbating the hyponatremia. These findings prompt the team to reconsider the fluid and electrolyte management strategy, with potential adjustments needed to address the ongoing acid-base and electrolyte imbalances without compromising renal perfusion.

As the team assesses these developments, they recognize the need to balance further diuretic therapy with potential risks of worsening electrolyte disturbances. The consideration of initiating renal replacement therapy becomes more pertinent, especially if the patient's renal function does not show signs of recovery or if metabolic acidosis and electrolyte imbalances continue to pose significant risks. The healthcare team prepares to discuss these options with the patient and his family, emphasizing the goal of preventing further complications while optimizing the current management strategy. This ongoing assessment and adjustment underscore the importance of a dynamic, responsive approach to the patient's complex clinical needs.

Section 3

Over the next 12 hours, the patient's clinical status begins to show signs of new complications. The healthcare team notes that while there is a continued gradual improvement in the patient's fluid overload symptoms, with further reduction in peripheral edema, the patient now reports increasing fatigue and generalized weakness. Upon examination, the nurse observes slight confusion and a delayed response to questions, raising concerns about potential neurological involvement. The patient's vital signs reveal an elevated heart rate of 112 beats per minute, indicating possible compensatory mechanisms in response to underlying issues.

The most recent laboratory results reveal a concerning drop in hemoglobin levels to 9.8 g/dL, suggesting the possibility of anemia, which could be contributing to the patient's fatigue and weakness. Additionally, renal function tests indicate a rise in serum creatinine to 3.2 mg/dL, signaling a worsening of renal impairment. Urinalysis shows new findings of proteinuria, which may be indicative of further kidney damage or an underlying condition affecting renal filtration capabilities. The serum sodium remains low at 126 mEq/L, while serum potassium has stabilized at 4.9 mEq/L, demonstrating a partial response to earlier interventions.

Recognizing the potential for anemia and renal deterioration to complicate the patient's recovery, the team must now consider additional diagnostic evaluations, including a possible hematological assessment to identify the cause of anemia and further imaging to assess renal structure. The possibility of an underlying systemic condition such as glomerulonephritis or another renal pathology must be explored to guide treatment adjustments. The team plans to discuss these findings with the patient and family, explaining the importance of further testing and the potential need for more aggressive interventions, including renal replacement therapy, to address the kidney injury and prevent further complications. This evolving situation demands vigilant monitoring and a coordinated approach to manage the intricate balance of the patient's fluid, electrolyte, and hematological status.

Section 4

The healthcare team decides to prioritize the investigation of the new diagnostic results to better understand the underlying causes of the patient's deteriorating condition. A hematological assessment reveals that the patient's anemia is likely due to a combination of decreased erythropoietin production by the kidneys and possible blood loss, necessitating further evaluation for gastrointestinal bleeding. An abdominal ultrasound is performed to assess renal structure and function, uncovering signs consistent with acute glomerulonephritis, including enlarged kidneys with increased echogenicity. This finding aligns with the proteinuria observed in the urinalysis and suggests an inflammatory process affecting the renal glomeruli.

In light of the suspected glomerulonephritis, the healthcare team initiates a discussion about potential immunosuppressive treatment options to manage the inflammation and prevent further renal damage. The patient and their family are informed about the possible benefits and risks associated with these therapies, such as corticosteroids or other immunomodulatory agents. Meanwhile, supportive care continues, with careful monitoring of fluid and electrolyte balance, as well as the administration of erythropoiesis-stimulating agents to address the anemia and improve the patient's energy levels.

Despite these measures, the patient's clinical status remains tenuous. The persistent low serum sodium levels are suggestive of ongoing hyponatremia, possibly compounded by the patient's fluid management regimen and underlying kidney pathology. The team considers adjusting the fluid restrictions and sodium intake to address this imbalance while remaining vigilant for signs of neurological deterioration. As they await further serological tests to confirm autoimmune markers and narrow down the specific type of glomerulonephritis, the team emphasizes the importance of continued interdisciplinary collaboration and patient education to navigate the complexities of this acute kidney injury case.

Section 5

As the healthcare team continues to navigate the complexities of the patient's condition, new serological test results return, providing a clearer picture of the underlying autoimmune process. The tests reveal elevated levels of anti-neutrophil cytoplasmic antibodies (ANCA), suggesting that the patient may be suffering from an ANCA-associated vasculitis, a condition known to cause rapidly progressing glomerulonephritis. This finding necessitates an immediate reassessment of the treatment plan, as the current supportive measures may not be sufficient to curb the aggressive nature of the autoimmune response. Consequently, the team deliberates the initiation of a more aggressive immunosuppressive protocol, potentially involving a combination of high-dose corticosteroids and cyclophosphamide to halt further renal damage.

Simultaneously, the patient's clinical status reveals subtle yet concerning signs of neurological involvement, likely exacerbated by persistent hyponatremia. The patient begins to exhibit mild confusion and slight disorientation, prompting a reevaluation of their fluid management strategy. Serum sodium levels have dropped to 126 mEq/L, despite efforts to adjust fluid intake. The healthcare team decides to cautiously increase sodium supplementation and modify fluid restrictions, aiming to correct the electrolyte imbalance while closely monitoring for any signs of cerebral edema or other complications. This adjustment underscores the importance of a delicate balance between managing fluid overload and preventing further neurologic compromise.

As these interventions unfold, the patient's family is brought into the conversation to discuss the potential risks and benefits of the revised treatment plan. Emphasizing the critical nature of timely immunosuppressive therapy and vigilant supportive care, the healthcare team ensures that the family is fully informed and engaged in the decision-making process. The next steps will involve closely monitoring the patient's response to the intensified treatment regimen, with particular attention to renal function markers, electrolyte balance, and neurological status, as the team strives to stabilize the patient's condition and prevent further deterioration.