CKD - Nursing Case Study

Pathophysiology

• Primary mechanism: CKD primarily results from longstanding damage to glomeruli and tubules due to chronic diseases such as diabetes and hypertension. Persistent hyperglycemia or hypertension damages the nephrons, leading to their gradual loss and reduced renal function.

• Secondary mechanism: As renal function declines, the kidneys struggle to maintain homeostasis. They're unable to effectively filter waste and excess fluid, leading to uremia. They also fail to synthesize sufficient erythropoietin, causing anemia.

• Key complication: CKD may progress to end-stage renal disease. Accumulation of waste products can lead to various complications like cardiovascular disease, bone disorders, and electrolyte imbalances. Dialysis or kidney transplantation is required in end-stage.

Patient Profile

Demographics:

67-year-old male, retired coal miner

History:

• Key past medical history: Type 2 diabetes, hypertension, heart disease, anemia, and history of smoking

• Current medications: Metformin, Lisinopril, Aspirin, Iron supplements

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Shortness of breath, extreme fatigue, and swelling in the ankles

• Key symptoms: Decreased urination, persistent itching, and nausea

• Vital signs: Blood pressure: 180/110 mmHg, heart rate: 110 bpm, respiratory rate: 24 breaths per minute, body temperature: 98.6F, oxygen saturation: 88%

Section 1

Change in Patient Status:

The patient's condition worsened over the next 24 hours. He became increasingly dyspneic even at rest, with his oxygen saturation dropping to 82% on room air. His blood pressure remained elevated at 190/115 mmHg, despite the administration of his regular antihypertensive medication, Lisinopril. His heart rate climbed to 120 bpm, and he developed tachypnea with a respiratory rate of 30 breaths per minute. He also reported worsening nausea and decreased appetite.

On physical examination, his ankles were markedly swollen and pitting edema was noted up to the level of his knees. Auscultation of his chest revealed crackles in both lower lung fields. He appeared pale and fatigued, with dry mucous membranes. His level of consciousness fluctuated, with periods of confusion and disorientation. His urine output dropped significantly, with only 200 ml recorded over the past 24 hours. The patient's worsening clinical status is suggestive of severe fluid overload and uremic symptoms, indicating progression of his chronic kidney disease towards end-stage renal disease. The development of these symptoms highlights the need for urgent intervention and potential initiation of renal replacement therapy.

Section 2

New Diagnostic Results:

The results of the patient's blood tests were alarming. His blood urea nitrogen (BUN) had risen to 80 mg/dL and his serum creatinine level was 6.5 mg/dL, both significantly higher than the normal range, indicative of severely impaired renal function. His estimated glomerular filtration rate (eGFR) was calculated as less than 15 mL/min/1.73 m2, confirming the progression to end-stage renal disease. His serum potassium level was also elevated at 6.0 mEq/L, putting him at risk for life-threatening arrhythmias. Additionally, his hemoglobin level was low at 8.5 g/dL, suggestive of anemia secondary to chronic kidney disease.

The echocardiogram showed left ventricular hypertrophy and an estimated ejection fraction of 40%, indicating the presence of cardiac dysfunction, likely secondary to longstanding hypertension. The chest X-ray confirmed the presence of pulmonary edema. The patient's arterial blood gas showed a pH of 7.28, a PaCO2 of 38 mmHg, and a HCO3 of 17 mEq/L, suggestive of metabolic acidosis, another complication of advanced renal disease. These new diagnostic results highlight the critical condition of the patient, and the need for immediate and aggressive interventions. The complex interplay between chronic kidney disease, hypertension, and heart failure presents a significant challenge to the management of the patient's condition, requiring a multifaceted therapeutic approach.

Section 3

Change in Patient Status:

Within 24 hours, the patient's condition deteriorated rapidly. His blood pressure readings were consistently high at 190/100 mmHg, despite being on antihypertensive therapy. This was accompanied by increasing shortness of breath and a further decrease in urine output to less than 20 mL/hr. Crackles were heard bilaterally on auscultation, pointing towards worsening pulmonary edema. His mental status also began to fluctuate, with periods of confusion and disorientation, likely due to the build-up of toxins in his blood.

New Complications:

The patient's latest ECG showed tall, peaked T-waves and a widened QRS complex, signs of hyperkalemia’s effect on the heart. Additionally, he developed a fever of 38.6°C, with increased WBC count at 18,000 cells/mm3 and significantly elevated procalcitonin levels suggestive of a possible systemic infection. His already low hemoglobin dropped further to 7.2 g/dL, and platelet count dropped to 95,000 cells/mm3, indicating possible bone marrow suppression, another complication of end-stage renal disease. The new findings necessitate immediate therapeutic interventions to manage the hyperkalemia, hypertension, possible sepsis, and worsening anemia, along with renal replacement therapy to manage the end-stage renal disease. It is clear that the patient is now in a critical condition, with multi-organ dysfunction, and requires intensive care and monitoring.

Section 4

Change in Patient Status:

Despite aggressive interventions, the patient's condition continued to decline. He became increasingly lethargic and unresponsive, and his Glasgow Coma Scale (GCS) dropped to 8, indicating a decreased level of consciousness. The patient's blood pressure remained elevated at 200/110 mmHg, and his heart rate increased to 120 beats per minute. His respiratory rate increased to 28 breaths per minute with an oxygen saturation of 88% on 2L of oxygen via nasal cannula. The patient's skin became cool, clammy, and pale, and capillary refill time was delayed. His urine output further decreased to less than 10 mL/hr.

New Diagnostic Results:

Further laboratory tests showed a potassium level of 7.0 mEq/L, a significant rise from the previous reading, indicating severe hyperkalemia. His creatinine and BUN levels were also significantly elevated at 8.0 mg/dL and 80 mg/dL respectively, confirming worsening renal function. The patient's arterial blood gas (ABG) analysis showed a pH of 7.25, PaCO2 of 50 mmHg, and HCO3 of 20 mEq/L, indicating a mixed respiratory and metabolic acidosis. Blood cultures were drawn, and initial results showed gram-negative bacilli, suggesting a possible source of the patient's sepsis. His hemoglobin continued to drop, now at 6.5 g/dL, and his platelet count was down to 80,000 cells/mm3. These clinical findings signal a progression of multi-organ failure, with the patient's respiratory, cardiovascular, renal, and hematological systems severely compromised. This calls for a heightened level of critical thinking and an urgent need for multidisciplinary team collaboration to manage the patient's condition.

Section 5

Change in Patient Status:

The patient's condition took a further turn for the worse. He developed a fever of 39.2°C, raising concerns of a systemic inflammatory response driven by the identified sepsis. He became hypotensive with a blood pressure of 90/50 mmHg, and his pulse rate rose further to 140 beats per minute - a combination indicative of septic shock. The patient's respiratory status also deteriorated with an increase in respiratory rate to 35 breaths per minute, accompanied by decreasing oxygen saturation levels, now at 82% on 4L of oxygen via nasal cannula. Examination revealed the presence of crackles in both lung fields suggestive of pulmonary edema. His level of consciousness dropped further with a GCS of 6, and his urine output remained low at less than 10ml/hr.

Response to Interventions:

Despite administering intravenous fluids and aggressive vasopressor therapy to counter the septic shock, the patient's blood pressure remained critically low. Supplemental oxygen was increased to 6L, but his oxygen saturation levels continued to fluctuate dangerously. In response to the worsening renal function and oliguria, the nephrology team initiated emergent hemodialysis, with the dual aim of managing the hyperkalemia and aiding fluid removal to alleviate the pulmonary edema. A transfusion of packed red blood cells was ordered to address the severe anemia, but the patient's hemoglobin levels remained persistently low at 6.8 g/dL post-transfusion, raising the possibility of ongoing blood loss or hemolysis. This complex clinical scenario necessitates a continual reassessment and adjustment of the therapeutic strategy while maintaining an ongoing dialogue with the patient's family about the gravity of his situation and potential outcomes.