Patient with DKA complicating into developing AKI - Nursing Case Study
Pathophysiology
• Primary mechanism: In DKA, hyperglycemia results in osmotic diuresis, causing significant fluid and electrolyte loss. This volume depletion can reduce renal blood flow, leading to pre-renal acute kidney injury (AKI).
• Secondary mechanism: Persistent hyperglycemia leads to glycosuria, which increases medullary solute delivery. This, combined with volume depletion, can cause tubular injury, leading to intrinsic AKI.
• Key complication: AKI in DKA exacerbates metabolic acidosis and hyperkalemia, increasing the risk of arrhythmias and cardiac arrest. Furthermore, it slows recovery from DKA by impairing excretion of glucose and ketones.
Patient Profile
Demographics:
56 year old, male, truck driver
History:
• Key past medical history: Uncontrolled Type 1 Diabetes, Hypertension, Chronic kidney disease stage 3
• Current medications: Insulin, Lisinopril, Metoprolol
• Allergies: Penicillin
Current Presentation:
• Chief complaint: Severe abdominal pain, frequent urination
• Key symptoms: Intense thirst, blurred vision, vomiting, weakness, confusion
• Vital signs: Blood pressure 160/90 mmHg, Heart rate 110 bpm, Respiratory rate 26 breaths per minute, Temperature 38.5°C, Blood glucose level >600 mg/dL, Serum ketone level significantly high, Serum creatinine level elevated.
Section 1
Change in Patient Status:
Despite the initiation of insulin therapy and fluid resuscitation, the patient's condition starts to deteriorate. His blood pressure drops to 90/60 mmHg, heart rate increases to 130 bpm, and respiratory rate rises to 32 breaths per minute. He becomes increasingly lethargic and confused, raising concerns over cerebral edema, a potentially fatal complication of DKA. In addition, despite initial fluid resuscitation, his urine output remains low at 20 ml per hour, indicating ongoing renal impairment.
New Complications:
On re-testing, his serum potassium level is found to be 6.5 meq/L, consistent with hyperkalemia. Acidosis-mediated shift of potassium from intracellular to extracellular compartment coupled with decreased renal excretion due to AKI is likely contributing to this rise. Furthermore, his blood gas analysis reveals a worsening metabolic acidosis with a pH of 7.15, bicarbonate of 12 meq/L, and an increased anion gap of 28. His blood glucose level remains persistently high at 550 mg/dL, and serum creatinine level has further increased, indicating a worsening of AKI. EKG shows tall, peaked T waves - an alarming sign of hyperkalemia-induced cardiac toxicity.
Section 2
Response to Interventions:
The patient is transferred to the intensive care unit (ICU) for close monitoring and aggressive management. The insulin infusion rate is increased to help lower blood glucose levels and shift potassium back into cells. Despite these efforts, the patient's blood glucose remains persistently high, indicating an inadequate insulin response, possibly due to insulin resistance, a common feature in patients with severe DKA. The ICU team considers the addition of an insulin sensitizer, such as metformin, to enhance the effectiveness of insulin.
However, the patient's hyperkalemia remains a pressing concern. Standard treatment with calcium gluconate, sodium bicarbonate, and insulin with glucose is initiated to stabilize the myocardium, buffer the extracellular acidemia, and promote the intracellular shift of potassium, respectively. Despite these interventions, the patient's potassium level remains elevated, necessitating the initiation of emergency hemodialysis.
At this stage, the patient's clinical status is precarious. His worsening metabolic acidosis, possible cerebral edema, persistent hyperglycemia, and severe hyperkalemia present a complex challenge, requiring advanced clinical reasoning and prompt, aggressive interventions to prevent a fatal outcome. The next steps in his management will require a careful balance of treating the underlying DKA, managing the complications of AKI and hyperkalemia, and monitoring for the development of insulin resistance and potential neurological complications.
Section 3
Change in Patient Status:
The patient's clinical status deteriorates further. He becomes increasingly somnolent and less responsive to verbal stimuli, raising concerns for the development of cerebral edema, a severe and life-threatening complication of DKA. His Glasgow Coma Scale (GCS) score drops to 9 (E2V2M5) from an initial score of 15. His blood pressure fluctuates, with readings ranging from 90/50 mmHg to 140/90 mmHg, and his heart rate increases to 120 beats per minute, suggestive of possible cardiovascular instability. The patient's breathing pattern also changes, becoming rapid and shallow, indicative of worsening metabolic acidosis. His oxygen saturation drops to 88%, necessitating the initiation of high-flow nasal cannula oxygen therapy.
New Diagnostic Results:
Despite aggressive management, the patient's blood gas analysis reveals a worsening metabolic acidosis with a pH of 7.10 (normal 7.35-7.45), bicarbonate level of 8 mEq/L (normal 22-28 mEq/L), and an increased anion gap of 20 mEq/L (normal 8-16 mEq/L). The blood glucose level remains high at 550 mg/dL, and the serum potassium level is dangerously elevated at 6.5 mEq/L, despite emergency hemodialysis. A computed tomography (CT) scan of the brain is ordered urgently to assess for cerebral edema, which reveals mild cerebral swelling. Collectively, these findings underscore the gravity of the patient's condition and the need for prompt, aggressive intervention to avoid a catastrophic outcome. The management plan will need to be reevaluated swiftly to address the patient's deteriorating status.
Section 4
Change in Patient Status:
The patient's status continues to decline. His GCS deteriorates further to 7 (E1V2M4), indicating a severe level of impaired consciousness. His blood pressure readings become more erratic, spiking to 150/95 mmHg and dropping to as low as 80/45 mmHg. His heart rate also remains elevated at 130 beats per minute. His breathing becomes more labored and rapid, with a respiratory rate of 32 breaths per minute and persistent oxygen saturation levels of 85-88% despite high-flow nasal cannula oxygen support. Furthermore, the patient starts to exhibit signs of respiratory distress, including increased use of accessory muscles and paradoxical chest movements, suggesting impending respiratory failure.
Response to Interventions:
Despite ongoing aggressive treatment, the patient's metabolic acidosis does not improve. His arterial blood gas shows a pH of 7.08, bicarbonate level of 7 mEq/L, and an anion gap of 22 mEq/L. The blood glucose level remains persistently high at 600 mg/dL, and the serum potassium level continues to rise to 6.8 mEq/L after hemodialysis. This lack of significant improvement suggests that the current management strategy may not be sufficient, and more aggressive interventions might be necessary. Given the patient's deteriorating respiratory status, the healthcare team considers intubation and mechanical ventilation to prevent respiratory arrest. They also consider initiating continuous renal replacement therapy (CRRT) to more effectively manage his hyperkalemia and acidosis. These decisions necessitate a multidisciplinary discussion involving the critical care, nephrology, and neurology teams.
Section 5
New Complications:
As the healthcare team deliberates on the next course of action, the patient's clinical status further deteriorates. He becomes increasingly lethargic and difficult to rouse which raises concerns for cerebral edema, a rare but deadly complication of DKA. Additionally, the patient's urine output significantly decreases to less than 0.5 ml/kg/hr over the past six hours, indicating worsening acute kidney injury and possible progression to oliguric renal failure.
Response to Interventions:
Despite the neurology team's administration of hypertonic saline to manage potential cerebral edema, the patient's GCS further decreases to 5 (E1V1M3). A CT scan of the head is urgently performed, revealing signs of cerebral edema, confirming the team's suspicions. Concurrently, the nephrology team initiates CRRT due to the patient's worsening renal function, hyperkalemia, and acidosis. However, the patient's serum potassium levels remain at 6.9 mEq/L and bicarbonate levels at 6 mEq/L, indicating persistent metabolic acidosis and refractory hyperkalemia. The team begins to discuss the possibility of an underlying, undiagnosed condition contributing to the patient's deteriorating status and refractory response to treatments. The patient's deteriorating condition necessitates further investigation and a potential change in the treatment plan.