end stage renal disease - Nursing Case Study

Pathophysiology

• Primary mechanism: Glomerular Damage - Chronic diseases such as hypertension and diabetes mellitus cause deleterious changes in glomerular structure, leading to glomerulosclerosis. This fibrous hardening of the glomeruli impairs the kidney's ability to filter waste products, leading to accumulation of toxins in the body.

• Secondary mechanism: Tubulointerstitial fibrosis - Persistent glomerular damage induces inflammation and fibrosis in the surrounding tubulointerstitial area. This fibrotic process further impairs kidney function by obstructing the tubules and reducing their ability to reabsorb vital substances.

• Key complication: Uremia - The gradual decline in renal function leads to uremia, a severe complication where waste products build up in the bloodstream. Symptoms include nausea, vomiting, fatigue and neurologic abnormalities. It can progress to life-threatening conditions like heart failure and pulmonary edema.

Patient Profile

Demographics:

62-year-old male, retired construction worker

History:

• Key past medical history: Hypertension for 20 years, Type II diabetes mellitus for 15 years, chronic kidney disease stage 4 diagnosed 5 years ago.

• Current medications: Metformin, Lisinopril, Amlodipine, Furosemide, Erythropoietin, Calcium carbonate

• Allergies: Penicillin, causes rash

Current Presentation:

• Chief complaint: Severe fatigue, reduced appetite, nausea, vomiting, difficulty in breathing

• Key symptoms: Swelling in legs and feet (edema), confusion, irregular heartbeat, chest pain, high blood pressure, weight loss, dry skin, frequent urination, muscle cramps

• Vital signs: Blood pressure 186/110 mmHg, pulse 102 beats per minute irregular, respiratory rate 30 breaths per minute, oxygen saturation 90% on room air, body temperature 37.8°C, weight 80 kg, height 170 cm.

Section 1

Change in patient status:

The patient's condition deteriorated over the course of the next 24 hours. His respiratory rate increased to 35 breaths per minute and oxygen saturation dropped to 85% on room air. The patient complained of worsening shortness of breath and appeared increasingly anxious. Additionally, his blood pressure remained persistently elevated at 188/115 mmHg despite antihypertensive therapy. His consciousness level also dropped, with a Glasgow Coma Scale of 13/15, demonstrating confusion and disorientation. He also exhibited new onset of pericardial rub on auscultation, suggestive of uremic pericarditis.

New complications:

The patient's renal function tests showed a sharp increase in serum creatinine to 7.2 mg/dL from a baseline of 4.2 mg/dL and blood urea nitrogen to 120 mg/dL, indicating rapid progression of kidney failure. His serum potassium level was also elevated at 6.5 mEq/L, indicating hyperkalemia, a life-threatening electrolyte imbalance. An electrocardiogram showed tall, peaked T waves, a classic sign of hyperkalemia. Additionally, his hemoglobin level dropped to 9 g/dL, suggesting worsening anemia. The development of these complications indicates the progression towards end stage renal disease and the need for immediate intervention.

Section 2

New diagnostic results:

The patient's deteriorating condition necessitated further diagnostic tests. A chest X-ray revealed bilateral pulmonary edema, a common complication of kidney disease, which explained his increased respiratory rate and decreased oxygen saturation. A transthoracic echocardiogram showed pericardial effusion with signs of cardiac tamponade, correlating with the previous finding of pericardial rub. This condition, characterized by fluid accumulation in the pericardial sac, could explain his elevated blood pressure and decreased level of consciousness due to reduced cardiac output.

Change in patient status:

Despite aggressive diuretic therapy, the patient's pulmonary edema did not improve significantly, and his oxygen saturation dropped further to 82% even with supplemental oxygen. He became hypotensive with a blood pressure of 90/60 mmHg, likely secondary to decreased cardiac output from cardiac tamponade. His mental status continued to decline with a Glasgow Coma Scale of 11/15, demonstrating increased confusion and lethargy. The patient's increasing hyperkalemia, despite treatment with sodium polystyrene sulfonate, was also concerning. His serum potassium level rose further to 7 mEq/L, and the ECG now showed a widening QRS complex, indicating severe hyperkalemia. His renal function tests remained poor, with a further increase in serum creatinine to 8.5 mg/dL and blood urea nitrogen to 150 mg/dL. These developments signaled an urgent need for renal replacement therapy.

Section 3

New complications:

Amidst the aggressive treatment, the patient developed sudden onset chest pain, radiating to the left arm, accompanied by diaphoresis, suggestive of an acute coronary syndrome. An immediate EKG was ordered, which revealed ST-segment elevation in the anterolateral leads, suggestive of ST-Elevation Myocardial Infarction (STEMI). The cardiac troponin level was significantly elevated at 8 ng/mL, further confirming the diagnosis of a myocardial infarction. The combination of his kidney disease, pulmonary edema, pericardial effusion, and now STEMI made the situation extremely complicated.

Meanwhile, the patient's acid-base balance was also deteriorating. An arterial blood gas (ABG) analysis showed a pH of 7.20, PaCO2 of 30 mmHg, and a bicarbonate level of 12 mEq/L, indicative of metabolic acidosis, likely secondary to his renal dysfunction. The patient's respiratory rate increased further to 28 breaths per minute, suggesting compensatory hyperventilation. This development necessitated additional interventions, such as bicarbonate administration, to correct the acidosis and further underscored the urgency for renal replacement therapy. However, the new onset of myocardial infarction posed a significant challenge to the initiation of dialysis. It was a race against time to stabilize the patient's cardiac condition while mitigating his renal failure and its associated complications.

Section 4

Change in Patient Status:

Despite aggressive medical management, the patient's condition continued to deteriorate. His blood pressure fell to 85/55 mmHg, likely due to the combined effects of his myocardial infarction and renal failure. The patient also became increasingly agitated and disoriented, indicative of uremic encephalopathy, a severe complication of renal failure. His Glasgow Coma Scale (GCS) dropped to 10, a significant decline from his previous score of 15. This progressive neurologic decline further complicated the clinical scenario and necessitated immediate protective measures for airway management and prevention of aspiration.

New Diagnostic Results:

A new set of blood tests revealed a potassium level of 6.5 mEq/L, significantly higher than the upper normal limit of 5.0 mEq/L, indicating hyperkalemia, another life-threatening complication of renal failure. The patient's BUN and creatinine levels also continued their upward trend, reaching 85 mg/dL and 7.2 mg/dL respectively. The electrocardiogram showed a new development of peaked T waves, a classical sign of hyperkalemia. These findings suggested the urgent need for renal replacement therapy, but the patient's hemodynamic instability and acute myocardial infarction posed significant challenges in initiating dialysis. It was a critical juncture in the patient's clinical course, where the benefits and risks of each intervention had to be weighed meticulously.

Section 5

Change in Patient Status:

As the patient's condition continued to decline, he developed acute pulmonary edema, a severe complication of both renal failure and myocardial infarction. His respiratory rate increased to 32 breaths per minute, and he exhibited severe dyspnea and pink-tinged, frothy sputum. His oxygen saturation dropped to 85% on room air, prompting immediate supplemental oxygen therapy. The patient's new symptomatology, along with a chest X-ray confirming the presence of pulmonary edema, further complicated the clinical picture. This life-threatening situation demanded immediate response to ensure patient stability, adding a new layer of complexity to the management of his concurrent renal failure and myocardial infarction.

Response to Interventions:

In response to the acute pulmonary edema, the patient was immediately placed on high-flow oxygen therapy, which increased his oxygen saturation to 94%. However, despite the administration of intravenous diuretics, the patient's renal response was inadequate, likely due to his advanced renal failure. The decision was made to initiate ultrafiltration therapy to remove excess fluid, despite the risk of further hemodynamic instability. The patient's blood pressure was closely monitored, revealing an initial improvement to 95/60 mmHg, but subsequent readings showed a concerning downward trend. His agitation and disorientation persisted, and his GCS further declined to 8, indicating the increasing severity of his uremic encephalopathy. This response underscored the need for immediate and aggressive intervention to address his deteriorating renal function while managing his concurrent complications.