Case Study: 28-Year-Old Patient With 12-Year History

Case Study 2dkamrs S Is A 28 Year Old Patient With A 12 Year Histor

Case Study #2 DKA Mrs. S is a 28-year-old patient, with a 12-year history of type I diabetes mellitus. Her husband states that she has had a “bad cold” for several days. Yesterday she stayed in bed and slept all day. She was “too ill” to check her blood sugar, and since she was not really eating, she did not take her insulin.

This morning, she was not able to stand up and vomited twice. A Gram stain of Mrs. S’s blood contains gram-positive cocci in clusters. Her admission vital signs are: BP = 90/60; HR = 118 bpm (sinus tachycardia); RR = 32/min; T = 102.3° F; O2 sat via pulse oximetry = 96%. Her serum glucose is 398 mg/dl, and she is positive for serum ketones.

She is admitted with a diagnosis of diabetic ketoacidosis (DKA). Her baseline arterial blood gases (ABGs) on 2 L of oxygen are: pH = 7.25; PCO2 = 28 mm Hg; HCO3 = 14 mEq/L; PaO2 = 92 mm Hg; O2 sat = 96%. Her respirations are deep, rapid, and labored. She has bronchial breath sounds in the right axillary area. There is bilateral chest expansion and no evidence of cyanosis.

A regular insulin bolus is given, and a regular insulin drip is initiated. Mrs. S’s IV fluids are infusing at 800 ml/hr. Her vital signs after 2 hours in the unit are: BP = 120/70; HR = 78 bpm (normal sinus rhythm); RR = 22/min; O2 sat = 100%. Her serum glucose is 250 mg/dl and serum potassium is 4.0 mEq/L.

She is more alert and is feeling hungry. The case prompts several questions about the physiological mechanisms of insulin, DKA pathogenesis, clinical signs, and management strategies, requiring an understanding of complex metabolic processes and nursing considerations.

Paper For Above instruction

Insulin plays a critical role in maintaining glucose homeostasis in the body by facilitating cellular uptake and utilization of glucose, especially in muscle and adipose tissues. It promotes glycogen synthesis in the liver and muscle, stimulates protein synthesis, and inhibits lipolysis and gluconeogenesis (American Diabetes Association [ADA], 2020). Without sufficient insulin, glucose remains in the bloodstream, leading to hyperglycemia, and the body shifts to alternative energy sources such as lipids, resulting in ketoacidosis (Mastrototaro et al., 2021). This metabolic shift underscores the importance of insulin in both glucose regulation and the prevention of metabolic derangements.

The most significant basic defect in the development of diabetic ketoacidosis (DKA) is absolute or relative insulin deficiency concurrent with an increase in counter-regulatory hormones such as glucagon, catecholamines, cortisol, and growth hormone (Kitabchi et al., 2009). These hormones antagonize insulin actions, stimulate hepatic glucose production, and promote lipolysis, resulting in elevated free fatty acids that the liver converts into ketone bodies. The accumulation of these acids causes metabolic acidosis, characteristic of DKA. The deficiency of insulin prevents glucose uptake into cells, thus perpetuating hyperglycemia and further stimulating osmotic diuresis, dehydration, and electrolyte imbalances (Umpierrez et al., 2019).

Mrs. S experienced DKA primarily because her insulin intake was disrupted during her illness—she was too sick to administer insulin and was not eating, leading to an energy deficit. Her infection, indicated by symptoms and positive blood cultures, likely increased her secretory stress response, raising counter-regulatory hormones, thereby exacerbating hyperglycemia and ketone production. The body's response to illness—via cytokine release and immune activation—further aggravates insulin resistance, compounding her risk of developing DKA (Ball and Dhatemz, 2021). Moreover, her poor oral intake and subsequent omission of insulin created the conditions for unchecked lipolysis and ketogenesis, typical of DKA pathophysiology.

Classic signs and symptoms of DKA include polyuria, polydipsia, dehydration, abdominal pain, nausea, vomiting, rapid deep respirations (Kussmaul respirations), fruity odor of acetone on the breath, and altered mental status in severe cases (Umpierrez et al., 2019). In Mrs. S’s case, symptoms such as vomiting, tachypnea, fever, dehydration evidenced by hypotension and tachycardia, and altered mental status (noted as she was sleeping all day) reflect the severe metabolic disturbance characteristic of DKA. Her deep, rapid respirations are a direct compensatory response to metabolic acidosis aimed at exhaling CO2 to raise blood pH.

The anion gap is a calculated measure used to identify unmeasured anions in the blood, indicative of metabolic acidosis. It is calculated by subtracting the sum of serum chloride and bicarbonate from serum sodium (Anion Gap = Na+ – [Cl– + HCO3–]) (Kirk, 2020). An elevated anion gap indicates the presence of excessive acids, such as ketone bodies in DKA. Monitoring this parameter guides clinicians in assessing the severity of acidosis, tracking response to treatment, and determining when the acidosis has resolved. A decreasing anion gap suggests effective clearance of ketones and correction of metabolic acidosis.

Ms. S is experiencing metabolic acidosis, as indicated by her low pH (7.25) and decreased bicarbonate (14 mEq/L). Her respiratory compensation manifests as Kussmaul respirations—deep, rapid breathing—that help expel CO2 and temporarily stabilize her blood pH. These are involuntary responses mediated through the respiratory center in the brainstem, attempting to compensate for the primary metabolic disturbance (Kirk, 2020). These mechanisms are crucial for maintaining acid-base balance until definitive correction with insulin therapy and fluid resuscitation can restore metabolic homeostasis.

The primary nursing diagnosis for Ms. S is "Deficient Fluid Volume related to osmotic diuresis secondary to hyperglycemia and ketonemia." Goals for treatment include restoring circulatory volume, correcting hyperglycemia, resolving acidosis, and preventing complications such as electrolyte imbalances and cerebral edema (Kitabchi et al., 2009). Initial independent nursing interventions focus on assessing vital signs, initiating IV fluids for hydration, monitoring blood glucose and electrolytes, and providing oxygen therapy as needed. Collaborative interventions involve administering insulin as prescribed, correcting electrolyte disturbances, and managing the underlying infection.

Immediate interventions necessary include continuous cardiac and respiratory monitoring, fluid resuscitation with isotonic saline, insulin therapy initiation, and regular laboratory assessments. Within 12-24 hours, priorities include ongoing assessment of fluid status, electrolyte replacement (especially potassium), monitoring for signs of fluid overload or cerebral edema, and addressing precipitating factors such as infection. Ensuring patient understanding of disease management and adherence to insulin therapy is vital for discharge planning (Umpierrez et al., 2019).

Potential laboratory abnormalities in DKA include hyperglycemia, elevated serum ketones, increased anion gap metabolic acidosis, electrolyte disturbances (hyperkalemia or hypokalemia, depending on treatment phase), and dehydration markers such as elevated BUN and serum creatinine (American Diabetes Association, 2020). Nursing considerations for discharge planning involve patient education on blood glucose monitoring, insulin administration, recognition of early symptoms of DKA, and strategies to prevent future episodes. Follow-up with healthcare providers, nutritional counseling, and infection prevention are essential components of comprehensive care (Mastrototaro et al., 2021).

The American Association of Critical-Care Nurses (AACN) Synergy Model emphasizes patient-centered care through aligning nurses' competencies with patients’ needs. For Ms. S, this model advocates assessing her physiological stability, emotional status, learning needs, and cultural background to inform personalized interventions (AACN, 2018). Such an approach ensures holistic care, promotes optimal recovery, and enhances patient safety by fostering effective nurse-patient collaboration, especially upon transition from intensive to outpatient settings.

References

• American Diabetes Association. (2020). Standards of Medical Care in Diabetes—2020. Diabetes Care, 43(Supplement 1), S1–S212.
• American Association of Critical-Care Nurses (AACN). (2018). Synergy Model for Patient Care. AACN.
• Kirk, S. (2020). Acid-base balance. Critical Care Nurse, 40(2), 33-40.
• Kitabchi, A. E., Umpierrez, G. E., Miles, J. M., & Fisher, J. N. (2009). Hyperglycemic crises in adult patients with diabetes. Diabetes Care, 32(7), 1335–1343.
• Mastrototaro, J., et al. (2021). Pathophysiology of diabetic ketoacidosis. Journal of Endocrinology & Diabetes, 8(2), 45-52.
• Umpierrez, G. E., et al. (2019). Diabetic ketoacidosis: Patient management. Endocrinology and Metabolism Clinics, 50(1), 183-193.