DKA - Nursing Case Study
Pathophysiology
• Primary mechanism: Insulin deficiency leads to decreased glucose uptake by cells, resulting in hyperglycemia as glucose accumulates in the bloodstream. This triggers osmotic diuresis, causing dehydration and electrolyte imbalances.
• Secondary mechanism: The lack of insulin also causes increased lipolysis, leading to the excessive release of free fatty acids that are converted into ketone bodies in the liver. This results in metabolic acidosis due to the accumulation of ketones.
• Key complication: If untreated, the combination of dehydration, electrolyte imbalances, and acidosis can lead to severe complications such as cerebral edema, cardiac arrhythmias, and diabetic coma, highlighting the need for prompt medical intervention.
Patient Profile
Demographics:
45-year-old female, school teacher
History:
• Key past medical history: Type 1 Diabetes Mellitus diagnosed 20 years ago, hypertension
• Current medications: Insulin glargine, insulin lispro, lisinopril
• Allergies: Penicillin
Current Presentation:
• Chief complaint: Nausea and abdominal pain for the past 24 hours
• Key symptoms: Polyuria, polydipsia, fatigue, confusion
• Vital signs: Temperature 99.5°F, heart rate 120 bpm, respiratory rate 24 breaths/min, blood pressure 100/60 mmHg, oxygen saturation 94% on room air
Section 1
Change in Patient Status:
As the healthcare team continues to monitor the patient, there is a noticeable change in her status. Over the next few hours, the patient's confusion worsens, and she becomes increasingly lethargic. Her vital signs show a concerning trend: the heart rate has increased to 130 bpm, respiratory rate has climbed to 28 breaths/min, and her blood pressure has dropped further to 90/55 mmHg. Oxygen saturation remains at 94% on room air, but the increased respiratory effort and Kussmaul breathing pattern suggest worsening metabolic acidosis. These changes signal a progression in the severity of her diabetic ketoacidosis (DKA).
Laboratory results confirm the clinical suspicions, showing a blood glucose level of 450 mg/dL, a serum bicarbonate level of 12 mEq/L, and an anion gap of 22, indicating a high anion gap metabolic acidosis. Serum ketones are significantly elevated, and her potassium level is noted to be 5.6 mEq/L, reflecting a shift due to acidosis. Despite her hyperkalemia, the risk of hypokalemia upon insulin treatment requires careful management. Given her deteriorating hemodynamics, the team decides to initiate fluid resuscitation with isotonic saline to correct dehydration and begin an insulin infusion to address hyperglycemia and acidosis. Continuous cardiac monitoring is imperative due to the risk of electrolyte-induced arrhythmias.
These developments present a critical juncture in the patient's care, demanding meticulous clinical reasoning to balance aggressive intervention with careful monitoring of potential complications. The healthcare providers must anticipate shifts in electrolyte levels as acidosis resolves and monitor for signs of cerebral edema, given her worsening mental status. The next steps in her management will focus on stabilizing her condition while preparing to address any new complications that may arise from the treatment itself.
Section 2
Response to Interventions:
As the insulin infusion progresses, the healthcare team observes initial positive changes in the patient's blood glucose levels, which begin to decrease steadily, reaching 300 mg/dL within the first few hours. The fluid resuscitation efforts also appear effective, as her blood pressure improves to 110/65 mmHg, suggesting a favorable response to volume expansion. However, the team remains vigilant, knowing that as her acidosis corrects and insulin drives potassium back into cells, there is a significant risk of hypokalemia. Repeated electrolyte panels are closely monitored, revealing a downward trend in potassium levels, now at 3.9 mEq/L, necessitating cautious potassium supplementation to prevent cardiac complications.
Despite the initial positive response, the patient's neurological status remains a concern. Her lethargy persists, and she exhibits transient episodes of disorientation. Recognizing the potential risk of cerebral edema, the team initiates neuro checks every hour, assessing her level of consciousness and pupil responses. They also adjust the rate of insulin infusion to ensure a gradual reduction in glucose levels, aiming to minimize rapid osmotic changes that could exacerbate cerebral edema.
Throughout this critical period, the nursing staff remains integral in the coordination of care, meticulously documenting all interventions and patient responses. Their clinical reasoning focuses on balancing the need to correct metabolic derangements while preemptively addressing the cascading effects of electrolyte shifts. As they prepare for the next phase of treatment, the team continues to evaluate the patient’s fluid status, electrolyte balance, and neurological function, ready to intervene swiftly should any new complications arise. This approach ensures they remain one step ahead in managing her complex condition during this vulnerable stage of recovery.
Section 3
As the patient's condition evolves, new diagnostic results reveal additional insights into her ongoing management challenges. A recent arterial blood gas (ABG) analysis indicates a partial correction of her acidosis, with pH rising to 7.32 and bicarbonate levels improving to 18 mEq/L. However, despite these positive changes, her anion gap remains elevated at 16, suggesting persistent metabolic derangements. The team also notes a slight increase in serum creatinine to 1.6 mg/dL, raising concerns about potential renal complications secondary to dehydration and underlying stress from the acute illness.
Concurrently, repeat neurological assessments highlight a troubling development. The patient now exhibits increased confusion, responding inconsistently to verbal commands and displaying sluggish pupillary reactions. Her Glasgow Coma Scale (GCS) score has decreased to 11, prompting immediate consideration of potential cerebral edema or other intracranial processes. A stat CT scan of the head is ordered to rule out any structural abnormalities or edema that may be contributing to her altered mental status.
These findings necessitate a recalibration of the treatment strategy. The healthcare team decides to cautiously adjust the fluid therapy to address renal perfusion, ensuring adequate hydration without overloading the vascular system. Potassium supplementation continues, targeting a level above 4.0 mEq/L to mitigate cardiac risks. Additionally, they re-evaluate the insulin infusion rate, prioritizing a delicate balance between correcting hyperglycemia and preventing rapid osmotic shifts that could worsen neurological outcomes. This comprehensive approach underscores the critical need for continuous assessment and adaptation in managing the multifaceted challenges of diabetic ketoacidosis with emerging complications.
Section 4
As the team closely monitors the patient's response to the adjusted treatment regimen, new diagnostic results begin to provide further clarity. A follow-up CT scan of the head reveals mild cerebral edema, consistent with her altered mental status, though no other structural abnormalities are identified. This finding corroborates the need to maintain cautious fluid management to prevent exacerbating intracranial pressure. The healthcare team initiates a protocol to elevate the head of the bed and administers a low-dose mannitol infusion to help manage the cerebral edema, carefully weighing the risks of fluid shifts against the potential benefits.
Simultaneously, the patient's blood chemistry panel shows a slight improvement in her potassium levels, now at 3.8 mEq/L, although still below the targeted threshold. This necessitates continued potassium supplementation, while ongoing glycemic control is maintained through a finely-tuned insulin drip. The team remains vigilant for signs of insulin resistance or unexpected shifts in glucose levels, understanding that the balance between correcting hyperglycemia and avoiding rapid osmotic changes is critical to her neurological recovery.
Despite these interventions, the patient's vital signs show a concerning trend. Her heart rate has increased to 110 beats per minute, and her blood pressure has decreased to 98/60 mmHg, suggesting possible hemodynamic instability. This prompts the team to reassess her fluid status and consider additional diagnostic tests, such as an echocardiogram, to evaluate cardiac function and potential underlying causes of hypotension. The evolving clinical picture underscores the importance of dynamic, interdisciplinary collaboration in navigating the complexities of diabetic ketoacidosis with secondary complications, with a continued focus on stabilizing the patient while preventing further deterioration.
Section 5
As the healthcare team continues to closely monitor the patient's condition, they observe a subtle but notable change in her respiratory status. The patient begins to exhibit an increased respiratory rate of 28 breaths per minute, with audible wheezing on auscultation. An arterial blood gas analysis reveals a partially compensated metabolic acidosis, with a pH of 7.31, PaCO2 of 30 mmHg, and HCO3- of 14 mEq/L. The presence of ketones remains significant, indicating ongoing ketoacidosis despite partial metabolic improvement. Given the respiratory findings, the team considers the possibility of evolving pulmonary edema or an early sign of acute respiratory distress syndrome (ARDS) as a complication of systemic inflammatory response.
In response to these developments, the team decides to initiate non-invasive positive pressure ventilation (NIPPV) to support the patient's respiratory efforts and improve oxygenation. Concurrently, they reassess her fluid balance, carefully adjusting intravenous fluids to prevent fluid overload while ensuring adequate perfusion. The team also orders a chest X-ray to evaluate for any signs of pulmonary congestion or infiltrates that might indicate infection or fluid overload.
With the patient's hemodynamic parameters still suggesting instability, the team requests a consultation with the cardiology service to provide further insight into her cardiac function, suspecting that underlying cardiac dysfunction could be contributing to her hypotension and increased heart rate. This collaborative approach, integrating respiratory support, fluid management, and cardiac evaluation, aims to address the multifaceted challenges presented by the patient's current condition, ensuring that each aspect of her care is meticulously coordinated to improve her overall prognosis.