Diabetes - Nursing Case Study

Pathophysiology

• Primary mechanism: Insufficient insulin production or ineffective insulin utilization. In Type 1 diabetes, the immune system destroys insulin-producing beta cells in the pancreas, leading to insulin deficiency. In Type 2 diabetes, the body develops resistance to insulin, meaning cells can't use it properly and blood glucose levels rise.

• Secondary mechanism: Chronic hyperglycemia. Persistently high blood glucose levels lead to glucose toxicity, damaging various organs and tissues. This contributes to long-term complications like retinopathy, nephropathy, and neuropathy.

• Key complication: Cardiovascular disease. Diabetes significantly increases the risk of various cardiovascular problems, including coronary artery disease, heart attack, stroke, and atherosclerosis. This is due to the damaging effects of sustained high blood glucose levels on blood vessels and nerves.

Patient Profile

Demographics:

57-year-old female, working as a school teacher

History:

• Diagnosed with Type 2 Diabetes 15 years ago

• Currently on Metformin and Glipizide

• Allergic to Penicillin

Current Presentation:

• Chief complaint is frequent urination, excessive thirst and unexplained weight loss

• Patient also reports blurry vision and feeling frequently tired

• Vital signs reveal blood pressure of 150/95 mmHg, heart rate of 85 beats per minute, temperature of 98.6°F, respiratory rate of 16 breaths per minute, and a blood glucose level of 260 mg/dL

Section 1

Change in Patient Status:

Over the next 24 hours, the patient's condition worsens. Her blood glucose levels remain persistently elevated, with a morning reading of 280 mg/dL, despite adherence to her medication regimen. She also complains of increasing thirst and urination, and a feeling of weakness in her legs. Additionally, she reports experiencing episodes of chest discomfort, describing it as a "heavy feeling" that seems unrelated to physical exertion. Her blood pressure is now 160/100 mmHg, while her heart rate has increased to 90 beats per minute.

New Complications:

With the persistence of hyperglycemia and the new-onset chest discomfort, there is a concerning possibility of acute coronary syndrome (ACS). This is a range of conditions caused by a sudden, reduced blood flow to the heart, which can lead to myocardial infarction, commonly known as a heart attack. Diabetes, especially uncontrolled, significantly increases the risk of ACS. Furthermore, the patient's elevated blood pressure may indicate hypertensive urgency, which can further exacerbate the potential cardiovascular complication. The weakness in her legs could also be an early sign of diabetic neuropathy, a condition caused by long-term damage to the nerves due to sustained high blood glucose levels.

These new complications necessitate immediate actions including further diagnostic tests such as an electrocardiogram (ECG) and cardiac enzymes to evaluate for possible ACS, as well as aggressive blood glucose and blood pressure management. The patient's symptoms, combined with her history of diabetes and recent vitals, require attention to prevent severe outcomes.

Section 2

New Diagnostic Results:

The ECG results indicate slight ST-segment elevation, which suggests that the patient may be experiencing an acute myocardial infarction (MI). The blood tests show elevated cardiac enzymes, specifically creatine kinase-MB (CK-MB) and troponin I, which further supports the suspicion of an acute MI. These cardiac markers are typically elevated in the blood following damage to the heart muscle, such as that incurred during a heart attack. Additionally, the patient's glycosylated hemoglobin (HbA1c) level is 9.5%, indicating poor long-term blood glucose control.

Further tests are run to assess the patient's renal function, as uncontrolled diabetes can also lead to nephropathy. The results show elevated levels of both serum creatinine (2.5 mg/dL) and blood urea nitrogen (BUN; 28 mg/dL), which suggest impaired kidney function. This is a significant finding, as renal dysfunction can complicate the management of both diabetes and ACS, and increases the patient's risk for further complications.

In light of these results, the patient's condition is discussed with a cardiologist and an endocrinologist. The team agrees that immediate intervention is necessary to manage the patient's ACS and uncontrolled diabetes, and to prevent further damage to her heart and kidneys. A strategy of aggressive medical management is decided upon, with the aim of stabilizing the patient's condition before considering more invasive procedures such as cardiac catheterization or revascularization.

Section 3

Change in Patient Status:

After initiation of aggressive medical management, the patient's blood glucose levels begin to decrease, reaching a more acceptable range of 150-180 mg/dL. However, her chest pain persists and her blood pressure remains elevated at 160/90 mmHg. Respiratory rate is noted to be slightly increased at 22 breaths per minute and oxygen saturation has dropped to 92% on room air. The patient reports feeling short of breath and her skin appears pale and cool to touch. On auscultation, crackles are heard at the bases of both lungs, suggesting fluid accumulation.

New Complications:

Given the patient's clinical presentation and the presence of crackles on lung auscultation, a chest X-ray is ordered to assess for signs of pulmonary edema, a potential complication of impaired heart function. The X-ray reveals increased opacities in the lower lung fields, consistent with pulmonary edema. This new complication suggests that the patient's heart function may be deteriorating, leading to fluid backup into the lungs. This could be a result of uncontrolled blood pressure, ongoing myocardial damage, or a combination of both. This development prompts the healthcare team to consider additional interventions to manage the patient's heart failure and pulmonary edema, while still addressing her diabetes and renal impairment.

Section 4

New Diagnostic Results:

A 12-lead EKG is ordered to further evaluate the patient's heart function. The EKG reveals evidence of left ventricular hypertrophy and nonspecific T wave changes, which can be indicative of myocardial ischemia or strain. Lab results also come back with elevated B-type natriuretic peptide (BNP) levels at 890 pg/mL, significantly above the normal range of 0-100 pg/mL. BNP is a hormone secreted by the heart in response to changes in pressure that occur when heart failure develops or worsens. The increase suggests that heart failure is indeed contributing to the patient's condition.

Given the continued chest pain, elevated blood pressure, and now pulmonary edema and abnormal EKG findings, the healthcare team suspects that the patient may be experiencing a myocardial infarction (MI). Troponin levels are ordered and come back elevated at 0.5 ng/mL, above the reference range of 0.00-0.04 ng/mL. The elevated troponin levels confirm the diagnosis of an MI.

These new diagnostic results indicate that the patient's condition is more serious than initially thought. The team must now prioritize interventions to manage the MI and heart failure, while also continuing to address the patient's diabetes and renal impairment.

Section 5

Change in Patient Status:

As the day progresses, the patient's condition deteriorates. He becomes increasingly short of breath, even at rest, and complains of persistent chest pain despite administration of nitroglycerin. His blood pressure further increases to 180/100 mmHg, and his heart rate spikes to 120 beats per minute. On physical examination, bilateral crackles are heard in the lower lung fields and the patient appears anxious and diaphoretic. His oxygen saturation levels drop to 88% on room air, and his blood glucose level remains elevated at 300 mg/dL.

The clinical team recognizes these signs as indicative of worsening heart failure and uncontrolled diabetes. The worsening shortness of breath and persistent chest pain suggest that the myocardial infarction may be more extensive than initially thought. The team decides to escalate care, moving the patient to the intensive care unit for closer monitoring and management. This change in status necessitates a reevaluation of the patient's current treatment plan and possible initiation of additional interventions.