diabetes - Nursing Case Study

Pathophysiology

• Primary mechanism: Insulin deficiency or resistance leads to impaired glucose uptake into cells, resulting in elevated blood glucose levels. In Type 1 diabetes, autoimmune destruction of pancreatic beta cells causes insulin deficiency. In Type 2 diabetes, insulin resistance occurs, often associated with obesity and lifestyle factors.

• Secondary mechanism: Chronic hyperglycemia triggers metabolic stress and inflammation, damaging blood vessels and nerves over time. This process contributes to microvascular complications like retinopathy, nephropathy, and neuropathy, as well as macrovascular complications such as cardiovascular disease.

• Key complication: Persistent high blood glucose levels can cause diabetic ketoacidosis in Type 1 diabetes, characterized by the accumulation of ketones leading to metabolic acidosis. In Type 2 diabetes, hyperosmolar hyperglycemic state can occur, marked by severe dehydration and altered consciousness.

Patient Profile

Demographics:

52-year-old male, office manager

History:

• Type 2 diabetes diagnosed 10 years ago, hypertension, hyperlipidemia

• Metformin, Lisinopril, Atorvastatin, Aspirin

• Allergic to penicillin

Current Presentation:

• Chief complaint: Increasing numbness and tingling in feet

• Key symptoms: Fatigue, blurred vision, frequent urination, slow-healing sores on feet

• Vital signs: Blood pressure 145/90 mmHg, heart rate 88 bpm, respiratory rate 18 breaths per minute, temperature 98.6°F, blood glucose 180 mg/dL fasting

Section 1

Upon initial assessment, the healthcare team noted several key findings that suggested the progression of diabetic neuropathy and potential complications. The patient reported increasing numbness and tingling in his feet, which upon examination, revealed decreased sensation to monofilament testing and diminished vibratory sense. Additionally, the slow-healing sores on his feet raised concerns about potential diabetic foot ulcers, compounded by the patient's slightly elevated blood pressure of 145/90 mmHg and fasting blood glucose level of 180 mg/dL. These factors suggested suboptimal glycemic and blood pressure control, which are critical in managing diabetes complications.

Laboratory results further illuminated the patient's condition. His hemoglobin A1c was notably elevated at 8.5%, indicating poor long-term blood glucose control. Lipid panel results showed an LDL cholesterol level of 130 mg/dL, higher than the target for patients with diabetes, suggesting a need for more aggressive lipid management. The urine albumin-to-creatinine ratio was slightly elevated at 35 mg/g, suggesting early signs of nephropathy. These findings highlighted the interconnected nature of diabetic complications, where poor glucose control can exacerbate vascular damage, leading to both microvascular and macrovascular complications.

Faced with these assessment and diagnostic findings, the healthcare team recognized the need for a comprehensive intervention plan. This plan would aim to tighten glycemic control, potentially through adjustments in medication or lifestyle changes, and address hypertension and hyperlipidemia more aggressively. Patient education on foot care and regular screenings for neuropathy and retinopathy were also emphasized. The team also scheduled follow-up appointments to closely monitor the patient's response to interventions and to prevent further deterioration of his condition. This approach aimed to mitigate the risk of new complications and improve the patient's overall management of his diabetes.

Section 2

Following the comprehensive intervention plan, the patient returned for a follow-up appointment six weeks later. During the visit, the healthcare team conducted a thorough reassessment to evaluate the patient's response to the interventions. The patient reported being more consistent with his medication regimen and had incorporated suggested dietary changes, including reducing carbohydrate intake and increasing fiber-rich foods. However, he noted persistent numbness in his feet and occasional dizziness upon standing, raising concerns about potential orthostatic hypotension.

Vital signs revealed a blood pressure of 138/85 mmHg, indicating some improvement from the previous visit. Fasting blood glucose levels had decreased slightly to 160 mg/dL, demonstrating better but still suboptimal glycemic control. Repeat laboratory tests showed a hemoglobin A1c of 8.1%, suggesting a modest improvement in long-term glucose management. Nevertheless, the LDL cholesterol level remained elevated at 128 mg/dL, prompting consideration of further lipid-lowering strategies. The urine albumin-to-creatinine ratio had increased to 40 mg/g, signaling a progression in nephropathy that warranted closer monitoring and possibly an adjustment in the patient's antihypertensive regimen to include an ACE inhibitor or ARB.

The patient's ongoing symptoms and lab values led the healthcare team to reassess the current management plan. They decided to intensify the pharmacological approach by optimizing the patient's insulin regimen, aiming for tighter glucose control. Additionally, they increased the dosage of his statin medication to address the persistent hyperlipidemia. The team also emphasized the importance of continued foot care and scheduled a referral to a nephrologist for a more detailed evaluation of kidney function. This approach aimed to prevent further complications and stabilize the patient's condition, setting the stage for ongoing management and monitoring in the next phase of his diabetes care.

Section 3

Two weeks after the intensified interventions, the patient returned to the clinic reporting new symptoms that had developed over the past few days. He experienced increased frequency of urination, excessive thirst, and fatigue, despite adherence to the adjusted insulin regimen and medication plan. Concerned about these developments, the healthcare team conducted a more detailed assessment to determine the underlying cause.

Vital signs revealed a slight increase in blood pressure to 142/88 mmHg, suggesting the potential impact of ongoing nephropathy despite the introduction of an ACE inhibitor. Fasting blood glucose had risen unexpectedly to 185 mg/dL, indicating a potential mismatch in insulin dosage or adherence issues. A repeat hemoglobin A1c test showed minimal change, holding at 8.2%, hinting at ongoing challenges in achieving optimal glycemic control. Further laboratory tests revealed a rise in urine albumin-to-creatinine ratio to 50 mg/g, signaling a concerning progression of kidney involvement. Moreover, a comprehensive metabolic panel detected an elevated creatinine level of 1.5 mg/dL, underscoring the need for urgent nephrology input.

The healthcare team determined that the patient's symptoms and lab findings indicated a potential worsening of diabetic nephropathy and possible insulin resistance. They decided to refine the insulin regimen further, considering a basal-bolus approach for more precise glucose management. Additionally, they initiated discussions about considering an SGLT2 inhibitor to address both glycemic control and renal protection. The team reinforced the importance of monitoring blood pressure and glucose levels closely, and they expedited the nephrology referral. This proactive strategy aimed to halt the progression of complications and stabilize the patient's condition, setting the stage for further adjustments in his long-term diabetes management.

Section 4

Two weeks after initiating the basal-bolus insulin regimen and introducing an SGLT2 inhibitor, the patient returned to the clinic for a follow-up appointment. During this visit, he reported some improvement in his thirst and urination frequency, yet he continued to experience persistent fatigue. The healthcare team conducted a thorough assessment to evaluate the effectiveness of the recent interventions and identify any emerging issues.

Vital signs revealed that blood pressure had slightly improved to 138/86 mmHg, indicating a positive response to the ACE inhibitor and enhanced blood pressure management. Blood glucose monitoring showed a modest decrease in fasting levels to 165 mg/dL, suggesting partial improvement in glycemic control. However, the hemoglobin A1c remained relatively unchanged at 8.0%, indicating that further adjustments might be needed to achieve optimal glycemic control. Despite these efforts, the urine albumin-to-creatinine ratio had increased to 60 mg/g, pointing to ongoing kidney stress. The patient's creatinine level remained elevated at 1.6 mg/dL, prompting the healthcare team to anticipate nephrology consultation results eagerly.

The team considered the potential for underlying insulin resistance and discussed the possibility of lifestyle modifications, including dietary adjustments and a tailored exercise program, to complement pharmacological interventions. They also emphasized the importance of consistent blood glucose monitoring and maintaining adherence to the medication regimen. Recognizing the need for a comprehensive approach, the team planned to collaborate closely with the nephrologist to refine the patient's management plan further, aiming to curb the progression of nephropathy while safeguarding overall health. The patient's journey underscored the complexity of diabetes management and highlighted the critical need for ongoing, multidisciplinary care to navigate the challenges of chronic complications.

Section 5

Two weeks following the initial follow-up, the patient returned to the clinic, reporting new symptoms of mild swelling in his ankles and an occasional shortness of breath during exertion. These changes raised concerns about potential fluid retention and cardiovascular involvement. The healthcare team conducted a detailed examination and noted that the patient's blood pressure had risen slightly to 142/88 mmHg. His heart rate was regular at 78 beats per minute, but the presence of peripheral edema was confirmed upon physical examination.

New diagnostic results from the nephrology consultation indicated a further increase in urine albumin-to-creatinine ratio to 75 mg/g, suggesting worsening renal function. The patient's estimated glomerular filtration rate (eGFR) had decreased to 45 mL/min/1.73m², reinforcing the suspicion of progressive diabetic nephropathy. Additionally, a recent lipid panel revealed elevated LDL cholesterol at 160 mg/dL, contrasting with the patient's prior stable levels, thereby compounding cardiovascular risk.

In response to these findings, the healthcare team recognized the need for an intensified therapeutic approach. Adjustments to the patient's medication regimen were discussed, including the potential introduction of a statin to address dyslipidemia and a diuretic to manage fluid overload. The team emphasized the importance of dietary sodium restriction and adherence to an exercise routine tailored to the patient's cardiovascular capacity. Collaborative discussions with the cardiologist and nephrologist were prioritized to integrate care strategies, aiming to stabilize renal function while mitigating cardiovascular complications. This phase of the patient's journey highlighted the intricate interplay between diabetes management and its systemic effects, underscoring the necessity for vigilant, interdisciplinary coordination.