diabetes and sepsis - Nursing Case Study

Pathophysiology

• Primary mechanism in diabetes: Insulin deficiency or resistance leads to chronic hyperglycemia, causing endothelial dysfunction and impaired immune response, increasing susceptibility to infections and complications like sepsis.

• Secondary mechanism in sepsis: Systemic inflammatory response to infection results in vasodilation, increased vascular permeability, and coagulation abnormalities, leading to multi-organ dysfunction.

• Key complication in diabetes and sepsis: Hyperglycemia exacerbates immune dysfunction and inflammation, worsening sepsis outcomes by promoting oxidative stress and further endothelial damage, increasing morbidity and mortality risk.

Patient Profile

Demographics:

56-year-old male, construction worker

History:

• Key past medical history: Type 2 diabetes mellitus for 15 years, hypertension, chronic kidney disease stage 3

• Current medications: Metformin, insulin glargine, lisinopril, amlodipine, atorvastatin

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Severe abdominal pain and high fever

• Key symptoms: Confusion, shortness of breath, increased heart rate, high blood glucose levels

• Vital signs: Temperature 39.4°C (103°F), heart rate 130 bpm, blood pressure 85/60 mmHg, respiratory rate 28 breaths per minute, SpO2 88% on room air

Section 1

The initial assessment reveals a rapidly deteriorating clinical picture. The patient is diaphoretic and appears lethargic, scarcely able to answer questions. On examination, his skin is cool and clammy, and capillary refill is delayed at more than 3 seconds. Auscultation of the lungs reveals crackles at the bases, and the abdomen is distended with hypoactive bowel sounds, indicating potential ileus or impending bowel ischemia. The extremities are cold to the touch, suggesting poor perfusion, consistent with the hypotensive state noted in his vital signs.

Laboratory tests return with critical findings: a blood glucose level of 450 mg/dL, lactate level of 4.5 mmol/L, and a white blood cell count of 24,000/mm³, suggesting a robust inflammatory response. Blood cultures are pending, but given the patient's presentation and history of diabetes, a gastrointestinal source of sepsis is suspected. Renal function tests show a worsening of chronic kidney disease, with a serum creatinine of 3.2 mg/dL and a blood urea nitrogen of 68 mg/dL, indicating acute kidney injury superimposed on chronic kidney disease, likely due to hypoperfusion and dehydration.

The patient is started on aggressive fluid resuscitation with isotonic crystalloids, and broad-spectrum intravenous antibiotics are initiated, mindful of his penicillin allergy. Despite these interventions, his blood pressure remains critically low, necessitating initiation of vasopressor support with norepinephrine. With these measures, there is a slight improvement in his mental status, but he remains tachycardic and tachypneic, with ongoing hypoxemia requiring supplemental oxygen. This scenario demands advanced critical thinking to manage not only the sepsis but also to adjust diabetic management in the context of acute kidney injury and potential fluid overload, underscoring the complexity and interdependence of the patient's conditions.

Section 2

As the patient remains under close observation, there's a notable change in his status. Despite the initial improvement in mental clarity, he begins to exhibit signs of respiratory distress. His respiratory rate climbs to 32 breaths per minute, and his oxygen saturation drops to 88% on 4 liters of oxygen via nasal cannula. On auscultation, the crackles in his lungs have progressed, now audible throughout both lung fields, suggesting worsening pulmonary edema. The patient's heart rate remains elevated at 125 beats per minute, and his blood pressure, although slightly improved with vasopressors, is still tenuous at 92/56 mmHg.

New diagnostic imaging, including a chest X-ray, reveals bilateral infiltrates consistent with acute respiratory distress syndrome (ARDS), likely secondary to sepsis and fluid resuscitation. Given his deteriorating respiratory status and the potential for further decompensation, the decision is made to intubate and mechanically ventilate the patient to ensure adequate oxygenation and ventilation. This intervention is critical to prevent further hypoxemic damage, but it also complicates the management of his hemodynamics and fluid status.

Concurrently, updated lab results highlight a further increase in serum creatinine to 4.0 mg/dL, indicating worsening renal function, and a bicarbonate level of 15 mmol/L, suggesting metabolic acidosis. The patient's blood glucose remains elevated despite insulin therapy, and ketones are detected in the urine, raising concerns for diabetic ketoacidosis (DKA) superimposed on his septic state. This necessitates a recalibration of his insulin regimen, close monitoring of his electrolyte levels, and a delicate balance of fluid management to prevent exacerbating his ARDS while also addressing his kidney function. The complex interplay of these conditions requires continuous reassessment and adjustment of the treatment plan, highlighting the intricate decision-making process essential in managing such a critically ill patient.

Section 3

As the medical team continues to navigate the complexities of the patient's condition, a new complication arises. Despite the initiation of mechanical ventilation, the patient's oxygenation status remains precarious. His PaO2 levels, measured via arterial blood gas analysis, remain at a concerning 58 mmHg, even with increased positive end-expiratory pressure (PEEP) settings. This indicates persistent hypoxemia and suggests refractory ARDS, requiring further fine-tuning of ventilator settings and potential consideration of advanced therapies such as prone positioning or extracorporeal membrane oxygenation (ECMO) consultation. Additionally, the patient's lactate levels have risen to 5.2 mmol/L, indicative of worsening tissue perfusion and ongoing septic shock, necessitating a reevaluation of both his vasopressor support and fluid management strategy.

In tandem with managing his respiratory and hemodynamic challenges, the patient's metabolic derangements demand urgent attention. Despite aggressive insulin therapy, his blood glucose levels are erratic, hovering around 280-320 mg/dL, and his anion gap remains elevated, pointing to the ongoing DKA. Potassium levels are fluctuating, with a recent lab showing a drop to 2.9 mmol/L, necessitating cautious replacement to avoid cardiac complications, especially in the context of his tachycardia and hypotension. Continuous renal replacement therapy (CRRT) is considered to address both his worsening renal function and acidosis, but this requires careful coordination with his fluid and electrolyte needs, particularly given the risks of volume overload in the setting of ARDS.

The evolving clinical picture presents a significant challenge, requiring the healthcare team to employ advanced critical thinking and clinical judgment. Continuous reassessment and dynamic adaptation of the treatment plan are imperative to stabilize the patient. The integration of multidisciplinary care, including input from nephrology, endocrinology, and critical care specialists, becomes essential in orchestrating a cohesive approach to his multifaceted condition. As the team deliberates on the next best steps, they remain vigilant for any further complications that may arise, ready to pivot strategies as needed to optimize the patient's chances of recovery.

Section 4

As the medical team continues to closely monitor the patient, a new complication emerges that demands immediate attention. During a routine assessment, the patient's blood pressure suddenly drops to 78/50 mmHg, accompanied by a heart rate that spikes to 140 beats per minute. These changes suggest a further deterioration in his hemodynamic status, potentially indicating a progression of septic shock or a new onset of cardiac dysfunction. The team swiftly performs a bedside echocardiogram, revealing decreased left ventricular ejection fraction, suggestive of stress-induced cardiomyopathy or septic cardiomyopathy. This finding necessitates a rapid reassessment of his vasopressor regimen, with consideration for adding an inotropic agent to support his myocardial function.

Meanwhile, the patient's laboratory results continue to reflect his precarious metabolic state. His blood glucose remains difficult to control, with levels fluctuating despite adjustments to his insulin infusion rate. The anion gap metabolic acidosis persists, with recent lab values showing a bicarbonate level of 14 mmol/L and a pH of 7.25, further complicating his metabolic profile. Concurrently, his potassium levels, though supplemented, have only modestly improved to 3.1 mmol/L, highlighting the delicate balance required in managing his electrolyte status. Given the combination of refractory acidosis, electrolyte imbalances, and renal impairment, the nephrology team recommends initiating continuous renal replacement therapy (CRRT) to help stabilize his metabolic environment and improve his overall condition.

The integration of these new findings into the patient's evolving clinical picture challenges the healthcare team to adjust their management strategy dynamically. The consideration of advanced interventions such as ECMO for refractory ARDS becomes more pressing as his oxygenation remains inadequate despite maximal ventilatory support. As they navigate these complexities, the team remains vigilant for signs of further deterioration or new complications, ready to pivot their approach in a coordinated, multidisciplinary effort to optimize the patient's chances of stabilization and recovery.

Section 5

As the team implements continuous renal replacement therapy (CRRT) to address the patient's metabolic derangements, they vigilantly monitor for changes in his clinical status. Over the next few hours, there is a notable improvement in his acid-base balance, with his bicarbonate level rising to 18 mmol/L and pH improving to 7.32. However, despite these positive changes, his hemodynamic status remains a significant concern. The addition of an inotropic agent has stabilized his heart rate at 120 beats per minute, but his blood pressure continues to fluctuate, with readings occasionally dropping to 82/54 mmHg. These fluctuations suggest that his cardiac output remains compromised, likely due to ongoing stress-induced cardiomyopathy compounded by septic shock.

Simultaneously, the patient's respiratory status continues to deteriorate. Despite maximal ventilatory support, his PaO2 remains critically low at 58 mmHg, and his PaCO2 has risen to 55 mmHg, indicating worsening hypercapnia. The team also notes the development of new bilateral infiltrates on a repeat chest X-ray, raising concerns for refractory acute respiratory distress syndrome (ARDS). In light of these findings, the potential need for extracorporeal membrane oxygenation (ECMO) becomes increasingly urgent, prompting the team to consult with the ECMO specialist to evaluate the patient's candidacy for this advanced intervention.

As the multidisciplinary team strategizes the next steps, they remain acutely aware of the delicate balance required to manage the patient's complex condition. The integration of CRRT has offered some metabolic stability, yet the persistent hemodynamic and respiratory challenges necessitate ongoing reassessment of his therapeutic plan. The decision to initiate ECMO could represent a pivotal intervention, offering a potential lifeline as they seek to optimize oxygenation and cardiac function. The team prepares to mobilize resources swiftly, understanding that timely intervention is critical to improving the patient's chances of recovery.