nephrotic syndrome - Nursing Case Study
Pathophysiology
• Primary mechanism: Loss of glomerular filtration barrier integrity leads to increased permeability, allowing proteins like albumin to leak into the urine (proteinuria), reducing plasma oncotic pressure and causing edema.
• Secondary mechanism: The liver compensates for hypoalbuminemia by increasing lipoprotein production, causing hyperlipidemia and further contributing to cardiovascular risk.
• Key complication: Increased susceptibility to infections due to urinary loss of immunoglobulins and complement proteins, which impairs the body's ability to mount an effective immune response.
Patient Profile
Demographics:
45-year-old male, construction worker
History:
• Key past medical history: Hypertension, type 2 diabetes diagnosed 5 years ago
• Current medications: Lisinopril 20 mg daily, Metformin 500 mg twice daily, Atorvastatin 10 mg daily
• Allergies: Penicillin
Current Presentation:
• Chief complaint: Swelling in legs and fatigue
• Key symptoms: Edema in lower extremities, foamy urine, weight gain, decreased urine output
• Vital signs: Blood pressure 150/95 mmHg, heart rate 88 bpm, respiratory rate 20 breaths per minute, temperature 98.6°F, oxygen saturation 97% on room air
Section 1
During the initial assessment, the healthcare team noted significant bilateral lower extremity edema, with pitting present up to the mid-calf. The patient reported persistent fatigue, which he described as a constant feeling of being drained, impacting his ability to work. Upon auscultation, mild crackles were heard in the lower lung fields, suggesting the possibility of fluid overload. The patient's abdominal examination revealed mild ascites, further indicative of significant fluid retention. Despite his normal oxygen saturation, the respiratory rate was slightly elevated, hinting at compensatory mechanisms due to increased fluid burden.
Laboratory results reinforced the clinical findings: the patient's serum albumin was markedly low at 2.1 g/dL, corroborating the hypothesis of nephrotic syndrome with significant proteinuria. Urinalysis demonstrated massive proteinuria of over 3.5 g/day, consistent with the diagnosis. Additionally, elevated serum cholesterol levels at 280 mg/dL reflected the hyperlipidemia expected in nephrotic syndrome. Importantly, the patient's creatinine level had increased to 1.6 mg/dL, suggesting declining renal function. Given these findings, the healthcare team recognized the need to address both the fluid overload and the potential for progressive renal impairment.
In response to these assessment findings, the clinical team initiated a treatment plan focusing on dietary modifications, including sodium and fluid restriction, to manage edema. Diuretics were prescribed to facilitate fluid removal, with close monitoring of electrolyte balance. Additionally, the increase in blood pressure despite antihypertensive therapy prompted a review of the current regimen, considering the potential need for adjustments. As part of the comprehensive care plan, the patient was educated about signs of infection, emphasizing the importance of early detection given his increased susceptibility. This strategic approach aimed to stabilize the patient's condition while mitigating the risk of further complications, setting the stage for evaluating the effectiveness of these interventions in the following days.
Section 2
Over the next few days, the healthcare team closely monitored the patient's response to the interventions. Initially, there was some improvement in the patient's edema with the diuretic therapy, as noted by a reduction in the extent of the pitting edema in his lower extremities. However, on the third day of treatment, the patient began to experience new symptoms, including increasing shortness of breath and a persistent cough. Upon reassessment, his respiratory rate had increased to 24 breaths per minute, and mild hypoxia was noted with an oxygen saturation dropping to 92% on room air. Auscultation revealed more pronounced crackles in the lung bases, raising concern for worsening pulmonary edema.
Additionally, repeat laboratory tests indicated a concerning trend: the patient's creatinine level had risen further to 2.0 mg/dL, suggesting continued decline in renal function. Electrolyte imbalances were also noted, with a low potassium level of 3.2 mEq/L, likely secondary to aggressive diuresis. These findings prompted the clinical team to reconsider the current diuretic regimen, balancing the need to manage fluid overload with the risk of further renal impairment and electrolyte disturbances.
Given the new development of respiratory symptoms and laboratory changes, the healthcare team conducted a thorough review of the patient's fluid management strategy and considered the potential need for advanced therapies, such as albumin infusion or adjusted diuretic dosing. They also emphasized the importance of monitoring the patient for signs of acute kidney injury and potential cardiovascular complications, given the interplay between fluid overload and renal function. This evolving scenario required careful clinical reasoning to prioritize interventions that would stabilize the patient's condition while minimizing the risk of further complications.
Section 3
On the fourth day of treatment, the healthcare team noted a further change in the patient's status. Despite previous interventions, the patient's respiratory symptoms worsened, with his respiratory rate climbing to 28 breaths per minute and oxygen saturation dropping to 89% on room air. The patient appeared visibly distressed, with increased use of accessory muscles for breathing and audible wheezing upon auscultation. These signs suggested a concerning progression of pulmonary edema, likely exacerbated by the cumulative effects of nephrotic syndrome and aggressive diuretic use.
Concurrent with these respiratory changes, the patient's blood pressure was found to be elevated at 160/100 mmHg, likely reflecting a combination of fluid shifts and stress response. Repeat laboratory tests showed a further decline in renal function, with a creatinine level of 2.3 mg/dL. Electrolyte imbalances persisted, with potassium levels remaining low despite supplementation efforts. Given these developments, the clinical team decided to adjust the fluid management strategy, opting to initiate a carefully monitored administration of intravenous albumin to address hypoalbuminemia and facilitate better diuretic response. Alongside this, diuretic therapy was recalibrated to reduce the risk of further renal impairment and electrolyte disturbances.
As the team implemented these changes, they also prioritized continuous monitoring of the patient's cardiac and renal status, given the potential for acute kidney injury and cardiovascular strain. Echocardiography was ordered to assess cardiac function and rule out any underlying cardiac causes of pulmonary edema. With these adjustments, the team aimed to stabilize the patient's condition, mitigate the evolving complications, and create a pathway toward recovery. The response to these interventions would guide the next steps in managing this complex case of nephrotic syndrome with moderate complications.
Section 4
As the healthcare team closely monitored the patient's response to the adjusted treatment plan, initial signs of improvement were noted within the first 24 hours. The administration of intravenous albumin appeared to stabilize the patient's blood pressure, which decreased to 145/90 mmHg, and facilitated a more effective diuretic response, as evidenced by a gradual increase in urine output. However, the patient's respiratory status remained a significant concern. Despite some stabilization of oxygen saturation levels, which improved slightly to 91% on supplemental oxygen, the patient continued to exhibit pronounced respiratory distress, with a respiratory rate still elevated at 26 breaths per minute and persistent wheezing.
New diagnostic results from the echocardiography provided critical insights into the patient's condition. The echocardiogram revealed mild left ventricular hypertrophy with preserved ejection fraction, suggesting that while cardiac function was not the primary driver of pulmonary edema, the stress of fluid overload was impacting cardiac workload. Additionally, repeat laboratory tests showed a slight improvement in creatinine levels, now at 2.1 mg/dL, indicating a cautious positive trend in renal function as a result of intervention adjustments. However, the potassium levels remained marginally low at 3.3 mEq/L, necessitating continued monitoring and supplementation.
In response to these findings, the clinical team decided to continue with the current therapeutic approach, emphasizing careful balance in fluid management and diuretic use. They also initiated a respiratory therapy consult to optimize oxygen delivery and alleviate breathing effort. As the patient navigated these challenges, the team remained vigilant for any new complications, aware of the delicate interplay between nephrotic syndrome, renal function, and cardiovascular health. The next critical step involved assessing the patient's ongoing response to treatment and adjusting care plans as needed to prevent further deterioration and promote recovery.
Section 5
Change in Patient Status:
As the clinical team continued to monitor the patient, they noted a change in the patient's status that warranted immediate attention. Over the next 48 hours, the patient's respiratory distress showed signs of exacerbation. The respiratory rate increased to 30 breaths per minute, and oxygen saturation levels fluctuated, dipping to 88% despite continued supplemental oxygen. The persistent wheezing was now accompanied by the development of a productive cough with frothy sputum, suggesting worsening pulmonary congestion. These changes prompted a repeat chest X-ray, which revealed an increase in bilateral pleural effusions and interstitial edema, confirming the suspicion of ongoing fluid overload despite diuretic therapy.
Concurrently, the patient's blood pressure began to trend upward again, with readings consistently around 160/95 mmHg, indicating potential challenges in maintaining hemodynamic stability. The patient also reported new onset of mild headache and dizziness, raising concerns about potential secondary complications such as hypertensive urgency. Despite these setbacks, creatinine levels remained stable at 2.2 mg/dL, suggesting that renal function was relatively preserved, though the low potassium persisted at 3.2 mEq/L, necessitating continued supplementation and vigilance for signs of hypokalemia.
In response to these developments, the healthcare team decided to reassess the diuretic regimen, considering the addition of a potassium-sparing diuretic to enhance fluid removal while addressing the hypokalemia. Additionally, they arranged for a nephrology consult to evaluate the need for further adjustments in the treatment plan, particularly in light of the patient's complex fluid status and cardiovascular implications. The team emphasized the importance of closely monitoring the patient's vital signs, respiratory function, and laboratory values to guide ongoing management and prevent further deterioration. This change in patient status highlighted the intricate balance required in managing nephrotic syndrome, especially when complicated by cardiovascular and respiratory challenges.