ESRD - Nursing Case Study

Pathophysiology

• Primary mechanism: Progressive nephron loss leads to decreased glomerular filtration rate (GFR), impairing the kidneys' ability to filter waste and maintain fluid, electrolyte, and acid-base balance, culminating in end-stage renal disease (ESRD).

• Secondary mechanism: Compensatory hyperfiltration in remaining nephrons initially maintains function but eventually causes glomerular sclerosis and further nephron loss, accelerating progression to ESRD.

• Key complication: Accumulation of toxins and fluid overload from reduced renal clearance results in uremia, hypertension, and electrolyte imbalances, significantly impacting cardiovascular health and necessitating renal replacement therapy.

Patient Profile

Demographics:

62-year-old male, retired construction worker

History:

• Key past medical history: Type 2 diabetes mellitus, hypertension, stage 4 chronic kidney disease

• Current medications: Lisinopril 20 mg daily, Metformin 1000 mg twice daily, Erythropoietin injections weekly, Furosemide 40 mg daily

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Increasing fatigue and swelling in legs

• Key symptoms: Shortness of breath, decreased urine output, persistent nausea

• Vital signs: Blood pressure 168/92 mmHg, heart rate 96 bpm, respiratory rate 20 breaths per minute, temperature 98.6°F, oxygen saturation 93% on room air

Section 1

New Complications:

As the clinical team continues to monitor the patient, new complications arise indicative of further progression towards end-stage renal disease. The patient begins to exhibit signs of worsening fluid overload, evidenced by increased peripheral edema extending to the thighs and sacral region. Upon auscultation, bilateral crackles are heard in the lung bases, suggesting pulmonary congestion. These findings, coupled with the patient's ongoing shortness of breath, raise concerns about impending congestive heart failure, a common cardiovascular complication associated with advanced kidney disease.

Laboratory results return, showing a significant elevation in serum creatinine at 7.2 mg/dL, and blood urea nitrogen (BUN) at 80 mg/dL, confirming reduced renal clearance. Electrolyte analysis reveals hyperkalemia with a serum potassium level of 5.8 mEq/L, posing a risk for cardiac arrhythmias. The patient's hemoglobin is critically low at 9.0 g/dL, reflecting persistent anemia despite erythropoietin therapy, likely exacerbated by uremic toxins inhibiting erythropoiesis. These lab findings corroborate the clinical picture of uremia and fluid-electrolyte imbalance, necessitating urgent intervention.

In response to these developments, the healthcare team considers initiating renal replacement therapy, such as dialysis, to manage the patient's accumulating toxins and fluid status. Meanwhile, immediate steps are taken to address the hyperkalemia with dietary potassium restrictions and potential pharmacological interventions like calcium gluconate or insulin with glucose. The escalation in symptoms and lab values underscores the importance of timely intervention to avert further complications, such as life-threatening cardiac events or severe pulmonary edema, while also highlighting the need for comprehensive management of the patient's multiple comorbidities.

Section 2

The healthcare team swiftly implements the planned interventions to address the patient's hyperkalemia and fluid overload. The patient is started on a regimen of calcium gluconate intravenously to stabilize cardiac membranes, followed by a combination of insulin and glucose to facilitate the intracellular shift of potassium. Concurrently, the patient's fluid intake is meticulously restricted, and a loop diuretic is administered to promote diuresis, aiming to reduce peripheral edema and pulmonary congestion. Despite these efforts, the patient begins to demonstrate new complications, indicating the challenges of managing advanced ESRD.

Within 24 hours of initiating treatment, the patient's vital signs reveal a new development. The patient exhibits tachycardia with a heart rate of 112 beats per minute and an elevated blood pressure of 168/98 mmHg, suggestive of increased sympathetic activity and fluid overload strain on the cardiovascular system. The respiratory rate has increased to 26 breaths per minute, with accompanying use of accessory muscles, indicating worsening respiratory distress. Repeat laboratory tests show a slight decrease in serum potassium to 5.5 mEq/L, but the patient's serum bicarbonate level is now noted at 18 mEq/L, pointing to a developing metabolic acidosis.

These changes prompt the clinical team to consider the possibility of dialysis initiation to effectively manage the patient's metabolic derangements and fluid status. Given the patient's escalating symptoms and the partial response to pharmacological interventions, immediate hemodialysis is proposed as a critical step in preventing further deterioration. This decisive move not only addresses the acute complications but also sets a new direction in the patient's management plan, requiring careful consideration of long-term dialysis options and potential lifestyle adjustments. This progression in the patient's condition emphasizes the need for ongoing assessment and adaptation of treatment strategies to ensure optimal care and stability.

Section 3

In light of the patient's deteriorating condition and the decision to initiate hemodialysis, the healthcare team conducts a thorough initial assessment to establish a baseline for treatment effectiveness. Upon examination, the patient appears anxious and fatigued, with persistent peripheral edema and jugular venous distention, further confirming fluid overload. Auscultation of the lungs reveals diffuse crackles, more pronounced at the bases, suggesting the persistence of pulmonary congestion. The patient's skin is cool and clammy, indicative of compromised peripheral perfusion. Neurologically, the patient reports mild confusion and difficulty concentrating, raising concerns about uremic encephalopathy as the metabolic waste products accumulate.

Emerging laboratory results provide additional insight into the patient's status. Serum creatinine levels have soared to 8.2 mg/dL, and blood urea nitrogen (BUN) is markedly elevated at 102 mg/dL, reflecting significant renal impairment. Despite the slight improvement in potassium levels, the metabolic acidosis is more pronounced, with an arterial blood gas showing a pH of 7.25 and a bicarbonate level of 15 mEq/L. The patient's hemoglobin has dropped to 9.8 g/dL, hinting at anemia of chronic disease, which may exacerbate the patient's fatigue and shortness of breath.

The synthesis of these findings underscores the urgency of dialysis initiation to address the multifaceted complications of ESRD. The healthcare team must carefully weigh the benefits and risks of different dialysis modalities, considering the patient's current health status and long-term prognosis. This critical juncture in the patient's treatment plan emphasizes the necessity for a coordinated approach to stabilize the patient, including adjustments in medication, nutritional support, and dialysis scheduling. The team's clinical reasoning will be pivotal in optimizing the patient's care, with close monitoring to evaluate the response to hemodialysis and anticipate potential complications.

Section 4

Following the initiation of hemodialysis, the healthcare team closely monitors the patient for any changes in status and response to the intervention. Within the first session, the patient experiences a mild reduction in peripheral edema, and there is a slight decrease in jugular venous distention, suggesting some relief of the fluid overload. However, the patient remains fatigued and anxious, with ongoing difficulty concentrating, which continues to indicate possible uremic encephalopathy.

New diagnostic results reveal a modest improvement in metabolic acidosis, with the arterial blood gas showing a pH of 7.30 and bicarbonate level of 17 mEq/L, demonstrating that the dialysis is beginning to address the acid-base imbalance. Despite these positive changes, the patient's blood pressure remains low, averaging 90/60 mmHg, which raises concerns about the potential for intradialytic hypotension. This requires the team to adjust the ultrafiltration rate and consider the use of volume expanders if necessary to maintain hemodynamic stability.

Unexpectedly, the patient begins to exhibit signs of pruritus and skin irritation, which are common complications associated with dialysis treatment due to the accumulation of certain metabolic byproducts. This new complication prompts the healthcare team to review the patient's medication regimen and consider the addition of phosphate binders or antihistamines to alleviate symptoms. As the team continues to evaluate the patient's response to treatment, these new findings will guide further adjustments in the patient's care plan, emphasizing the need for ongoing assessment and adaptation to optimize outcomes.

Section 5

As the healthcare team continues to monitor the patient's response to hemodialysis, they observe new diagnostic results indicating hyperphosphatemia, with serum phosphate levels rising to 6.5 mg/dL. This finding suggests that the dialysis is not fully effective in managing the patient's phosphate levels, likely contributing to the pruritus and skin irritation. The nephrologist recommends initiating phosphate binders to help control the phosphate levels in conjunction with dietary modifications, emphasizing the importance of a low-phosphate diet to prevent further complications.

In addition to addressing hyperphosphatemia, the team notes a change in the patient's neurological status. The patient reports increased difficulty with concentration and memory, which are potential signs of worsening uremic encephalopathy. To evaluate this, a repeat set of neurocognitive tests is ordered along with a review of the patient's current medication regimen, ensuring no nephrotoxic or centrally acting drugs are contributing to these symptoms. The team also considers adjusting the dialysis prescription to increase the frequency or duration of sessions, aiming to enhance clearance of uremic toxins.

With these findings, the interdisciplinary team holds a meeting to adjust the care plan, focusing on the newly identified complications. The plan includes close monitoring of vital signs, particularly blood pressure, to prevent hypotension during dialysis sessions, along with regular assessment of skin integrity and neurological status. The patient's fluid and electrolyte balance will be closely tracked, with specific attention to phosphate and calcium levels to prevent mineral-bone disorders. These efforts are crucial in managing the complexities of end-stage renal disease and optimizing the patient's overall well-being as they continue their dialysis journey.