Chronic Gout - Nursing Case Study

Pathophysiology

• Primary mechanism: Chronic Gout is predominantly due to persistent hyperuricemia, an excess of uric acid in the bloodstream. This happens when the body either overproduces uric acid or has an impaired ability to excrete it through the kidneys.

• Secondary mechanism: The excess uric acid leads to monosodium urate (MSU) crystal deposit in joints and soft tissues. These crystals trigger an inflammatory response, causing acute gouty arthritis.

• Key complication: Over time, the chronic inflammation leads to gouty tophi formation, causing joint deformity and destruction (known as chronic tophaceous gout). This chronic tissue damage can also affect renal function, leading to urate nephropathy.

Patient Profile

Demographics:

68-year-old male, retired construction worker

History:

• Key past medical history: Chronic gout for 20 years, hypertension, type 2 diabetes, and chronic kidney disease stage 3

• Current medications: Allopurinol, Lisinopril, Metformin, Aspirin

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Severe pain in multiple joints, especially the big toe, along with fever.

• Key symptoms: Intense joint pain, joint redness, inflammation, restricted movement, fatigue, loss of appetite, weight loss, persistent low-grade fever.

• Vital signs: Blood pressure 180/100 mmHg, heart rate 110 bpm, respiratory rate 20 breaths per minute, temperature 38.5°C, oxygen saturation 90% on room air, BMI 30.

Section 1

Initial Assessment Findings:

Upon physical examination, the patient's affected joints were visibly swollen and red, particularly the metatarsophalangeal joint of the big toe. There were also palpable nodules (tophi) on the patient's ears and elbows, indicating a progression to chronic tophaceous gout. Additionally, the patient showed signs of fluid retention such as pitting edema of the lower extremities, suggestive of worsening renal function. Auscultation revealed crackles in the lower lobes of the lungs, indicating possible fluid accumulation secondary to compromised kidney function. The patient's elevated blood pressure and rapid heart rate also pointed towards hypertensive urgency, likely exacerbated by pain and overall systemic inflammation.

New Diagnostic Results:

Laboratory results showed an elevated serum uric acid level of 10.2 mg/dL (normal range: 3.4 - 7.0 mg/dL), indicating hyperuricemia. Furthermore, the patient's blood urea nitrogen (BUN) and creatinine levels were also raised to 45 mg/dL (normal range: 7 - 20 mg/dL) and 3.5 mg/dL (normal range: 0.6 - 1.2 mg/dL) respectively, suggestive of further deterioration of renal function. The hemoglobin A1c level was 8.5% (normal range: <5.7%), indicating poor glycemic control. A joint aspiration was performed, which confirmed the presence of negatively birefringent urate crystals, hence confirming a gout flare. Chest x-ray showed signs of pulmonary congestion, possibly due to fluid overload secondary to diminished renal function.

Section 2

Change in Patient Status:

Over the next 24 hours, the patient's condition deteriorated significantly. His pain became increasingly severe, unresponsive to NSAIDs and colchicine, leading to an inability to ambulate. His blood pressure continued to rise, peaking at 190/110 mmHg, and his heart rate remained tachycardic at 120 beats per minute. The patient also developed shortness of breath, with his oxygen saturation dropping to 88% on room air, indicating possible hypoxemia. Repeat auscultation of the lungs revealed increased crackles bilaterally, suggesting further progression of pulmonary congestion.

Response to Interventions:

Initial treatment with intravenous (IV) furosemide resulted in a slight decrease in pitting edema but did not improve the patient's hypoxemia or hypertension. Administration of IV morphine for pain and anxiety relief provided minimal comfort, but the patient's heart rate remained elevated due to persistent pain. The patient was started on oral allopurinol to control hyperuricemia, but this intervention was not expected to provide immediate relief from the acute gout flare. Despite aggressive fluid management and administration of IV insulin for hyperglycemia, the patient's renal function continued to decline, and blood glucose levels remained poorly controlled, with a random blood glucose level of 350 mg/dL. The patient's worsening status necessitated a transfer to the intensive care unit for closer monitoring and consideration for renal replacement therapy.

Section 3

New Diagnostic Results:

On the second day in ICU, the patient's lab results showed a significant rise in serum uric acid levels to 15.2 mg/dL, confirming a severe acute gout attack. His renal function worsened, with a creatinine level of 3.5 mg/dL and a glomerular filtration rate of less than 30 mL/min, indicating stage 4 chronic kidney disease. The arterial blood gas (ABG) analysis revealed respiratory acidosis, with a pH of 7.24, a PaCO2 of 58 mmHg, and a bicarbonate level of 24 mEq/L. This was suggestive of inadequate ventilation, possibly due to the patient's severe pain and anxiety, as well as underlying pulmonary congestion. Furthermore, the patient's blood glucose remained elevated at 360 mg/dL despite insulin therapy, and his complete blood count revealed leukocytosis with a white blood cell count of 15,000 cells/mm3, indicating an ongoing inflammatory response.

Change in Patient Status:

The patient's condition continued to deteriorate. He became progressively lethargic, disoriented, and restless, indicating a possible buildup of toxins due to worsening renal function. His blood pressure spiked further to 210/120 mmHg despite antihypertensive therapy. His oxygen saturation levels continued to decrease, falling to 82% on 2 liters of oxygen via nasal cannula, and his respiratory rate increased to 26 breaths per minute. The shortness of breath worsened, and the patient now had difficulty speaking in full sentences. On examination, his jugular venous distension was prominent, and his lower extremity pitting edema had worsened despite diuretic therapy, indicating worsening fluid overload. His cardiac examination was concerning for a new third heart sound (S3 gallop), suggesting acute congestive heart failure.

Section 4

Response to Interventions:

Despite aggressive management, the patient's condition worsened. His hyperuricemia was refractory to allopurinol and colchicine, and the nephrology team started him on rasburicase, an enzyme that converts uric acid to a more soluble and easily excreted compound, allantoin. However, his renal function continued to decline, and the decision was made to start the patient on continuous renal replacement therapy (CRRT) in an effort to control his worsening hyperkalemia and metabolic acidosis.

New Complications:

The patient's clinical status further deteriorated when he developed a fever of 102.2°F (39°C), chills, and a productive cough with yellowish sputum. A chest X-ray revealed new infiltrates in the lower lobes of both lungs, suggestive of hospital-acquired pneumonia. Blood cultures were sent and broad-spectrum antibiotics were initiated. Furthermore, he complained of severe chest pain radiating to his left arm, and his EKG showed new ST-segment elevations in the anterior leads, highly suggestive of an acute myocardial infarction. Emergent cardiology consultation was sought, and he was rushed to the catheterization lab for possible percutaneous coronary intervention. This new sequence of events further complicates the management of this patient with multi-system involvement, requiring a multidisciplinary approach and constant re-evaluation of his treatment plan.

Section 5

Change in Patient Status:

The patient's status continued to worsen over the following hours. His blood pressure plummeted to 85/45 mmHg and his heart rate accelerated to 120 beats per minute. He appeared diaphoretic, confused, and increasingly anxious. His oxygen saturation also decreased to 88% on 4 liters of oxygen via nasal cannula, despite a previous saturation of 95% on the same oxygen settings. His respiratory rate increased to 30 breaths per minute and he developed an increased work of breathing with accessory muscle use, indicating worsening respiratory distress. His Glasgow Coma Scale (GCS) score also dropped from 15 to 12, a sign of declining neurological function.

New Complications:

Upon examination, the patient's abdomen was distended and firm to touch, with diffuse tenderness noted. His white blood cell count spiked to 18,000 /mm3 with a left shift, indicating a systemic inflammatory response. An abdominal CT scan was ordered and revealed signs of intestinal ischemia, a potentially life-threatening condition that requires immediate surgical intervention. His lactate level rose to 6 mmol/L, further suggesting poor tissue perfusion. The surgical team was consulted urgently. The patient's rapidly declining condition and the development of multiple organ dysfunction syndrome (MODS) required immediate and aggressive interventions, necessitating ongoing evaluation and management from multiple disciplines. The complexity of his case also poses significant challenges in balancing the management of his uncontrolled gout, renal failure, pneumonia, myocardial infarction, and now intestinal ischemia.