DM2 - Nursing Case Study

Pathophysiology

• Primary mechanism: Insulin resistance - Over time, the body's cells become less responsive to insulin, a hormone that regulates blood sugar levels. Despite the pancreas producing more insulin to compensate, glucose cannot enter the cells efficiently, resulting in high blood sugar levels.

• Secondary mechanism: Pancreatic beta-cell failure - The pancreas initially compensates for insulin resistance by producing more insulin. However, as DM2 progresses, these beta cells can't keep up with the demand for more insulin, eventually leading to their failure.

• Key complication: Chronic Hyperglycemia - Persistently high blood sugar levels can damage blood vessels and nerves over time, leading to complications like heart disease, stroke, kidney disease, vision problems, and nerve damage (neuropathy).

Patient Profile

Demographics:

62-year-old male, retired construction worker

History:

• Key past medical history: Diagnosed with Type 2 Diabetes 12 years ago, hypertension, high cholesterol

• Current medications: Metformin 1000mg twice daily, Lisinopril 20mg daily, Simvastatin 40mg daily

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Persistent numbness and tingling in both feet, increasing fatigue, and worsening vision in the last few months

• Key symptoms: Peripheral neuropathy, blurred vision, fatigue, occasional chest discomfort

• Vital signs: Blood pressure 145/90 mmHg, pulse 80 bpm, respiratory rate 20/min, temperature 98.6°F, BMI 28, fasting glucose 180 mg/dl, HbA1c 8.0%

Section 1

Change in Patient Status:

Over the next few days, the patient's symptoms worsen. He complains of increased numbness and tingling in his feet, and his vision continues to blur. He also reports feeling more fatigued, often falling asleep during the day. His blood pressure has increased to 155/95 mmHg and his fasting glucose levels have risen to 200 mg/dl, indicating poor glucose control.

New Complications:

In addition, the patient has developed new symptoms. He complains of a persistent headache and dizziness. He has also noticed swelling in his ankles, which is a concern for possible heart failure or kidney disease. His urine output has decreased and the color has darkened, raising suspicion for possible kidney involvement. A urine analysis shows proteinuria (3+), indicating kidney damage. His BUN and creatinine levels are also elevated at 25 mg/dL and 2.5 mg/dL respectively, further supporting possible renal impairment. The patient's condition indicates a progression of DM2 complications, with signs of nephropathy and possible cardiovascular involvement. These findings necessitate immediate intervention and adjustment in the management plan.

Section 2

New Diagnostic Results:

The patient's worsening symptoms and new complications necessitated further diagnostic tests. An EKG reveals some irregularities in his heart rhythm, suggesting that there may be strain on his heart. An echocardiogram is ordered to assess his heart function more fully. The results show a left ventricular ejection fraction (LVEF) of 45%, indicating mild heart failure. This likely explains the patient's increased fatigue, swollen ankles, and high blood pressure.

A renal ultrasound also reveals moderate bilateral renal cortical thinning, consistent with chronic kidney disease. The patient's HbA1c level is now at 9.5%, significantly above the target range for individuals with DM2, indicating poor long-term glucose control. Additionally, his lipid panel shows elevated triglycerides at 300 mg/dL and low HDL cholesterol at 35 mg/dL, further increasing his risk for cardiovascular disease.

These new diagnostic results present a complex, interconnected web of complications related to the patient's poorly controlled DM2. This suggests that the current treatment plan is ineffective and that a more aggressive approach to managing his diabetes, kidney disease, and heart failure is needed. The patient's situation clearly illustrates the need for comprehensive management of DM2 and the importance of maintaining good glycemic control to prevent or delay complications.

Section 3

Change in Patient Status:

The patient's condition continues to deteriorate despite the current interventions. His fatigue has increased, and he reports difficulty in completing daily tasks without becoming short of breath. On physical examination, the patient's ankles are noticeably more swollen than at his previous visit, and his blood pressure is now consistently over 150/90 mmHg. His weight has increased by 5 pounds in the past week, which may be due to fluid retention secondary to his heart failure.

Laboratory tests show that his kidney function has further declined, with a serum creatinine now at 2.5 mg/dL. His HbA1c remains at 9.5% despite adjustments to his insulin regimen, and his triglycerides have risen to 320 mg/dL. His urine protein is positive, indicating early nephropathy, a complication of DM2. He also reports intermittent chest discomfort, which is concerning for potential ischemic heart disease. These changes signify that the patient's DM2, heart failure, and kidney disease are not adequately controlled, and his risk for developing further serious complications is high. It's clear that a significant change in his treatment plan is necessary.

Section 4

New Diagnostic Results:

A 12-lead ECG is ordered due to the patient's intermittent chest discomfort, which reveals ST-segment depression and T-wave inversion in leads II, III, and aVF. This suggests possible myocardial ischemia, which could be an indication of coronary artery disease (CAD). To further investigate, the patient undergoes a cardiac stress test, which shows evidence of inducible ischemia. A subsequent cardiac catheterization identifies significant three-vessel CAD.

In addition, an echocardiogram is performed due to the patient's shortness of breath and increasing peripheral edema. The results indicate a left ventricular ejection fraction of 35%, suggesting moderate systolic heart failure. The patient also has signs of left ventricular hypertrophy, likely secondary to his longstanding hypertension.

These new diagnostic results indicate that the patient's cardiovascular complications are progressing. The evidence of CAD puts the patient at a high risk for a myocardial infarction. His worsening heart failure further exacerbates his already compromised renal function. These results necessitate immediate intervention to prevent further deterioration and potentially life-threatening complications. The patient's weight gain, hypertension, and increased shortness of breath are likely due to his declining cardiac function. Furthermore, the combination of DM2 and kidney disease increases his risk for cardiovascular disease, which is now apparent with the diagnosis of CAD and heart failure. The patient's treatment plan will need to be significantly revised to address these new findings and manage his various conditions.

Section 5

Change in Patient Status:

The patient’s condition begins to deteriorate rapidly. He becomes increasingly short of breath, even at rest, and his peripheral edema worsens despite increased diuretic therapy. His blood pressure, previously well-controlled on antihypertensive medication, is now consistently elevated (160/95 mmHg) and his heart rate is tachycardic at 110 beats per minute. His oxygen saturation also drops to 88% on room air. An arterial blood gas (ABG) is ordered, revealing a pH of 7.31, a PaCO2 of 50 mmHg, and a PaO2 of 60 mmHg, suggesting acute on chronic respiratory failure.

In addition to his respiratory complications, the patient's renal function continues to decline. His serum creatinine jumps from 1.8 mg/dL to 2.5 mg/dL within 24 hours, and his urine output falls below 0.5 mL/kg/hr. His glucose levels also become erratic, ranging from 70 to 300 mg/dL despite careful insulin management. These changes in patient status indicate a worsening of his heart failure, renal insufficiency, and poorly controlled DM2. This suggests that his current treatment plan is insufficient and requires immediate reassessment and adjustment. The interdisciplinary team must now consider more aggressive intervention options, such as inotropic support or renal replacement therapy, and potentially refer the patient for evaluation for advanced heart failure therapies or transplantation.