Case Study 1 Diabetes Complications Case Scenario Mrs Guadal
Case Study 1diabetes Complicationscase Scenariomrs Guadalupe Hernan
Mrs. Guadalupe Hernandez, a 65-year-old woman diagnosed with adult onset diabetes mellitus (AODM) at age 51, is hospitalized with complications related to her diabetes. She has been prescribed glyburide 10 mg daily but does not possess a home glucose monitor. Recently, she developed a foot ulcer on her left great toe, which she has been self-treating at home. She reports difficulty visualizing her feet and suspects the ulcer is worsening, with red streaks extending from her ankle to mid-calf. She has experienced increased thirst, frequent urination, nausea, vomiting, and fatigue. On presentation to the emergency room, her vital signs include a temperature of 100.1°F, pulse of 102 bpm, respiratory rate of 28 breaths per minute, and blood pressure of 96/62 mm Hg. Her BMI is 32, indicating obesity.
Physical examination shows a tired woman with limited responsiveness, an ulcer on her left great toe measuring approximately 5 cm with full-thickness skin involvement, yellow-green exudate, surrounding induration, and warmth. She reports little sensation in her feet and admits the ulcer may have been present for some time. She has not eaten or taken medication since yesterday morning, consuming a diet of two corn tortillas with cheese and refried beans, along with coffee with milk and sugar. Laboratory evaluation reveals a blood glucose of 480 mg/dL, pH of 7.0, serum bicarbonate of 12 mEq/L, positive serum ketones, serum potassium of 3.7 mEq/L, sodium of 140 mEq/L, calcium of 10 mg/dL, and a leukocyte count of 22,000 cells/mm³ with a shift to the left.
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Introduction
Diabetes mellitus is a chronic metabolic disorder characterized by hyperglycemia resulting from defects in insulin secretion, insulin action, or both. It predisposes individuals to various acute and chronic complications, including infections, neuropathy, and vascular diseases. This case study highlights the complexity of diabetic emergencies, particularly diabetic ketoacidosis (DKA), as well as the interplay of infection, metabolic derangements, and neuropathy. Understanding the pathophysiology, clinical manifestations, laboratory abnormalities, and nursing management strategies is essential to optimize patient outcomes and prevent recurrence.
Abnormal Laboratory Values and Their Significance
The laboratory data reveal several abnormal findings in Mrs. Hernandez. Notably, her blood glucose level of 480 mg/dL indicates severe hyperglycemia. Her serum pH of 7.0 signifies acidemia, and the bicarbonate level of 12 mEq/L confirms metabolic acidosis. The presence of serum ketones and a low pH collectively point toward diabetic ketoacidosis (DKA). The serum potassium is within the normal range but warrants close monitoring because acidosis and insulin deficiency typically cause shifts of potassium extracellularly, risking arrhythmias if not managed properly. The elevated white blood cell count of 22,000 with a shift to the left suggests an ongoing infection, likely cellulitis or osteomyelitis related to the ulcer.
Clinical Manifestations Corresponding to Laboratory Abnormalities
The hyperglycemia manifests clinically as increased thirst (polydipsia), frequent urination (polyuria), and dehydration, predisposing to tachycardia and hypotension. The metabolic acidosis contributes to Kussmaul respirations—deep, rapid respirations designed to compensate for the acidemia. The fruity odor on her breath is characteristic of ketone production. Elevated serum ketones further confirm DKA. The infection indicated by leukocytosis and erythema with streaking underscores the systemic inflammatory response and risk of sepsis. These manifestations reflect the body's attempt to eliminate excess acids and manage hyperglycemia but can lead to significant fluid shifts, electrolyte abnormalities, and hemodynamic instability.
Pathophysiology of the Abnormal Values
Severe hyperglycemia in diabetes results from insufficient insulin to facilitate glucose uptake into cells. Elevated blood glucose increases osmotic diuresis, leading to dehydration and electrolyte loss. In DKA, insulin deficiency, combined with elevated counter-regulatory hormones (glucagon, catecholamines, cortisol, growth hormone), stimulates lipolysis. The breakdown of triglycerides releases free fatty acids, which are converted by the liver into ketone bodies, causing metabolic acidosis. The decreasing serum bicarbonate reflects buffering of excess acids. The acidosis and hyperglycemia impair cellular function and contribute to systemic symptoms like nausea, vomiting, and altered mental status.
The infection from the foot ulcer likely compounded the metabolic disturbance, as infection-induced stress hormones further elevate glucose levels. The leukocytosis with a shift to the left indicates an active bacterial invasion, fueling systemic inflammatory response syndrome (SIRS), which can precipitate DKA in diabetic patients.
Nursing Care and Management
Nursing management of this patient must be multifaceted, focusing on correcting metabolic abnormalities, controlling infection, and preventing complications. Immediate priorities include fluid resuscitation with isotonic saline to restore circulating volume and improve perfusion, which aids in reducing serum glucose and ketone concentrations. Close monitoring of vital signs, mental status, and input/output is vital to detect hypovolemia or electrolyte imbalances.
Electrolyte management is crucial, especially potassium. Despite normal serum levels, potassium shifts from intracellular to extracellular during acidosis, and insulin therapy can cause rapid intracellular shifts, risking hypokalemia. Therefore, serum electrolytes should be monitored closely, and potassium replacement initiated if needed.
Insulin therapy is essential to inhibit lipolysis, stop ketone production, and lower blood glucose levels. Regular insulin via intravenous infusion allows precise titration based on blood glucose and ketone levels. Additionally, correcting acid-base imbalances with bicarbonate may be considered in severe acidosis, but only under strict medical supervision.
Addressing the infection is equally critical. Empiric broad-spectrum antibiotics should be administered after obtaining appropriate cultures, and wound care optimized to prevent further spread of infection. The patient's nutritional status must be improved gradually, starting with small, easily digestible meals once stabilized.
Patient education plays a vital role in preventing future episodes. This includes instruction on blood glucose monitoring, foot care, recognizing signs of infection or hyperglycemia, medication adherence, and lifestyle modifications such as diet and exercise.
Nursing Diagnosis
Impaired tissue integrity related to ulceration and infection secondary to diabetes mellitus as evidenced by foot ulcer, erythema, warmth, yellow-green exudate, and systemic signs of infection.
Conclusion
This case underscores the importance of comprehensive nursing care in managing diabetic emergencies. Early recognition of abnormal laboratory values and understanding their relationship with clinical manifestations aid in prompt treatment. Interventions aimed at correcting metabolic derangements, preventing infection progression, and educating the patient can significantly improve outcomes and quality of life for individuals with diabetes.
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