DKA - Nursing Case Study

Pathophysiology

• Primary mechanism: Insulin deficiency leads to impaired glucose uptake by cells, resulting in hyperglycemia as glucose accumulates in the bloodstream instead of being used for energy.

• Secondary mechanism: To compensate for cellular energy deficits, the body breaks down fat, leading to increased production of ketone bodies. This causes metabolic acidosis as ketones accumulate, lowering blood pH.

• Key complication: The combination of hyperglycemia, ketosis, and acidosis can lead to severe dehydration and electrolyte imbalances, presenting as confusion, abdominal pain, and rapid breathing, necessitating urgent medical intervention.

Patient Profile

Demographics:

45-year-old female, high school teacher

History:

• Key past medical history: Type 1 Diabetes Mellitus diagnosed 10 years ago, hypertension

• Current medications: Insulin glargine, lisinopril

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Nausea and vomiting for the past 24 hours

• Key symptoms: Abdominal pain, deep rapid breathing, fatigue, fruity-scented breath

• Vital signs: Temperature 99.5°F, Heart rate 120 bpm, Respiratory rate 28 breaths per minute, Blood pressure 95/60 mmHg, Blood glucose level 450 mg/dL

Section 1

As the medical team begins to address the patient's diabetic ketoacidosis (DKA), initial interventions include fluid resuscitation with isotonic saline and insulin therapy to reduce blood glucose levels. Despite these efforts, the patient exhibits a concerning change in status. Two hours into treatment, she becomes increasingly lethargic, and her vital signs show further deterioration: her heart rate has climbed to 130 bpm, respiratory rate remains at 30 breaths per minute, and her blood pressure has dropped further to 90/55 mmHg. This progression suggests a potential complication of hypovolemic shock due to severe dehydration and electrolyte imbalances, which are common in DKA.

Lab results reveal a significant anion gap metabolic acidosis, with a pH of 7.25 and bicarbonate level of 12 mEq/L. Additionally, serum potassium is noted to be 3.0 mEq/L, indicating hypokalemia. This is a critical finding, as insulin therapy can exacerbate potassium depletion by driving potassium back into cells, further compromising cardiac function. The nursing team must prioritize careful monitoring of electrolyte levels and adjust treatment to include potassium replacement to prevent potential cardiac arrhythmias. This scenario underscores the need for vigilant assessment and timely intervention to manage the dynamic and interrelated complications of DKA.

Section 2

As the patient's condition continues to deteriorate, the nursing team conducts a thorough reassessment to identify any new developments. The patient remains lethargic, with increasingly shallow respirations, and her skin is cool and clammy to the touch, suggesting poor perfusion. Her capillary refill time is delayed at approximately 4 seconds, indicative of compromised circulation. Auscultation of the chest reveals diminished breath sounds bilaterally, and there is no evidence of jugular venous distention. The nursing staff notes decreased urine output, with only 10 mL in the past hour, highlighting the severity of the patient's hypovolemia.

New diagnostic results arrive, providing further insights into the patient's condition. Repeat blood gas analysis shows a worsening metabolic acidosis with a pH now at 7.20, while the bicarbonate level has fallen to 10 mEq/L. Serum potassium has decreased to 2.8 mEq/L, underscoring the urgency for potassium supplementation. The patient's electrocardiogram reveals flattened T-waves and the presence of U-waves, classic signs of hypokalemia that raise the concern for potential cardiac arrhythmias. Additionally, the serum lactate level is elevated at 4.5 mmol/L, suggesting the onset of lactic acidosis, which may be contributing to the patient's persistent hemodynamic instability.

In response to these findings, the medical team intensifies their intervention strategy. They increase the rate of intravenous fluid administration, switching to a balanced electrolyte solution to address both dehydration and electrolyte deficiencies. Potassium chloride is added to the IV fluids to correct hypokalemia promptly, and the insulin infusion rate is carefully titrated to avoid exacerbating the potassium deficit. The nursing staff is tasked with continuous cardiac monitoring to detect any arrhythmias early and ensure close observation of the patient's response to treatment. This careful balancing act between correcting acidosis, maintaining optimal glucose control, and stabilizing electrolyte levels is critical in steering the patient towards recovery.

Section 3

As the interventions proceed, the patient's condition shows mixed signs of improvement and concern. Over the next few hours, the increased fluid administration seems to improve her circulatory status slightly, evidenced by a capillary refill time that has decreased to approximately 3 seconds. Her skin, while still cool, begins to show signs of improved perfusion, with a slightly warmer touch. However, the patient's respiratory status remains a point of concern. Although her respirations are no longer as shallow, she begins to exhibit more pronounced Kussmaul breathing, an indication of the body's attempt to compensate for persistent metabolic acidosis.

The latest set of vital signs reveals a heart rate of 116 bpm, slightly elevated but stable, and a blood pressure of 90/58 mmHg, which is still on the lower side, suggesting continued attention to her fluid status is necessary. The nursing team is vigilant in monitoring her cardiac status, given her hypokalemic state, and they note occasional premature ventricular contractions on the cardiac monitor. While these arrhythmias are transient, they underscore the importance of maintaining electrolyte balance. Repeat blood work shows a modest improvement in serum potassium, now at 3.2 mEq/L, following the potassium supplementation, but it remains below the normal range, necessitating ongoing replacement and monitoring.

Despite these efforts, the patient's urine output remains critically low at about 15 mL over the last two hours, pointing to potential acute kidney injury. The medical team considers whether the increased serum lactate level, now at 5.0 mmol/L, could be contributing to her renal impairment or if it's primarily due to her ongoing hemodynamic instability. This complexity requires the team to carefully weigh the potential benefits and risks of further increasing fluid administration against the backdrop of possible fluid overload. The situation calls for precise clinical judgment and a nuanced understanding of the interplay between acidosis, electrolyte imbalances, and renal function, as the team strives to stabilize the patient and prevent further complications.

Section 4

As the nursing team continues to monitor the patient, a new complication emerges. Despite ongoing fluid resuscitation and careful electrolyte management, the patient begins to exhibit signs of altered mental status. She becomes increasingly lethargic, responding sluggishly to verbal stimuli. Her Glasgow Coma Scale score drops to 12, with particular concern noted in her eye-opening and verbal response components. This change raises alarms for possible cerebral edema, a rare but serious complication in the context of diabetic ketoacidosis (DKA), especially as her serum glucose levels have been decreasing more rapidly than anticipated to 185 mg/dL.

The medical team promptly orders a head CT to rule out cerebral edema, while also adjusting the rate of insulin infusion to ensure a more gradual reduction in blood glucose levels. Additionally, they decide to initiate mannitol treatment as a precautionary measure to manage potential intracranial pressure increases. The nursing staff is tasked with performing frequent neurological checks to detect any further deterioration in her mental status.

Amid these developments, the respiratory team's involvement becomes crucial as the patient’s Kussmaul breathing persists, and her arterial blood gas shows a pH of 7.25, remaining in the acidotic range. The team evaluates the need for possible intubation should her respiratory effort become insufficient. This juncture requires the interdisciplinary team to integrate their clinical reasoning skills, carefully balancing the ongoing management of her DKA with the emerging neurological concerns, while also addressing her respiratory and renal challenges. The complexity of this situation underscores the importance of a coordinated approach to her care, with each decision potentially impacting multiple aspects of her condition.

Section 5

As the nursing team continues to monitor the patient, her response to interventions becomes the focal point. The mannitol treatment is initiated to address the suspected cerebral edema, and within a few hours, there are observable improvements in her neurological status. The patient’s Glasgow Coma Scale score shows a modest increase to 13, with her eye-opening response improving slightly, although her verbal responses remain somewhat delayed. Her serum glucose level stabilizes around 160 mg/dL, and the insulin infusion rate is adjusted to maintain this steady pace. Despite these positive changes, the patient still exhibits Kussmaul breathing, suggesting that her metabolic acidosis persists. Repeat arterial blood gas analysis reveals a pH of 7.30, with a bicarbonate level of 14 mEq/L, indicating a slight improvement but still within the acidotic range.

The interdisciplinary team remains vigilant, understanding that the patient's respiratory status requires close attention. Her respiratory rate is noted to be 28 breaths per minute, with deep, labored breaths persisting, and her oxygen saturation hovers at 92% on room air. As the respiratory team evaluates her condition, they decide to initiate non-invasive positive pressure ventilation (NIPPV) to support her breathing and potentially prevent the need for intubation. This intervention aims to alleviate the work of breathing and improve gas exchange, thereby addressing the ongoing acid-base imbalance.

As these interventions are implemented, the nursing staff continues to perform regular neurological and respiratory assessments, watching for any signs of further deterioration. The coordinated efforts of the medical, nursing, and respiratory teams highlight the complexity of managing DKA with concurrent complications. Each decision is carefully weighed for its impact on the patient's multifaceted condition, ensuring that her care remains comprehensive and adaptive to her evolving needs. The focus remains on stabilizing her physiological parameters while monitoring for any new complications that may arise as a result of her critical state.