A 23 year old Type 1 diabetic with DKA develops complication of AKI - Nursing Case Study

Pathophysiology

• Primary mechanism: Dehydration - In DKA, hyperglycemia leads to osmotic diuresis, increasing urine output and causing severe dehydration. This decreases kidney perfusion, leading to ischemic injury and Acute Kidney Injury (AKI).

• Secondary mechanism: Ketoacidosis - The body's inability to use glucose for energy in type 1 diabetes leads to fat metabolism and production of ketone bodies, causing metabolic acidosis. Acidosis can cause vasoconstriction of renal arterioles, reducing renal blood flow and causing AKI.

• Key complication: Hyperkalemia - As AKI progresses, the kidneys' ability to excrete potassium decreases, leading to hyperkalemia. This can further deteriorate kidney function and potentially lead to life-threatening cardiac arrhythmias.

Patient Profile

Demographics:

23-year-old female, university student

History:

• Key past medical history: Diagnosed with Type 1 Diabetes Mellitus at age 8, has a history of poor glycemic control.

• Current medications: Insulin Glargine 20 units daily, Insulin Lispro sliding scale

• Allergies: No known allergies

Current Presentation:

• Chief complaint: Nausea, vomiting, increased thirst, frequent urination and abdominal pain for the past 3 days.

• Key symptoms: Dry skin, rapid heart rate, fruity-scented breath, confusion and fatigue.

• Vital signs: Blood pressure 100/60 mmHg, heart rate 120 bpm, respiratory rate 24 bpm, temperature 37.8°C, blood glucose 450 mg/dl, severe metabolic acidosis with a pH of 7.1 and bicarbonate of 10 mmol/L. Urine test reveals presence of ketones.

Section 1

New Diagnostic Results:

The patient's lab results have come back and are concerning. Her blood glucose remains elevated at 400 mg/dl, despite the administration of insulin. Her potassium level is alarmingly high at 6.5 mEq/L, indicating severe hyperkalemia. The patient's BUN and creatinine levels are elevated as well, at 35 mg/dL and 3.1 mg/dL respectively, which is indicative of further decline in renal function. The arterial blood gas (ABG) analysis reveals a pH of 7.0, signifying continued severe metabolic acidosis.

Change in Patient Status:

The patient's condition seems to be deteriorating. She is increasingly confused and fatigued, which may be a sign of worsening metabolic acidosis and hyperkalemia. Her heart rate has increased to 130 bpm, and blood pressure has dropped further to 90/58 mmHg, suggesting hypovolemia due to persistent osmotic diuresis. She complains of muscle weakness and palpitations, which are symptoms of hyperkalemia. Her breath continues to have a fruity odor, and her skin is warm and flushed due to the ongoing fever. The patient's condition necessitates immediate intervention to prevent further complications and potential cardiac arrest due to hyperkalemia and acidosis.

Section 2

Response to Interventions:

Despite the continuous insulin infusion, the patient's blood glucose levels remain persistently high. The healthcare team decides to increase the insulin dosage while closely monitoring her vital signs and blood glucose levels. A potassium-lowering medication, sodium polystyrene sulfonate, is administered to address hyperkalemia.

The patient is also started on intravenous fluid resuscitation with normal saline to combat hypovolemia. This is expected to help restore her blood pressure and improve kidney function. Given her severe metabolic acidosis, sodium bicarbonate is also added to her treatment regimen.

New Complications:

Unfortunately, the patient's renal function continues to deteriorate despite interventions, and she develops oliguria. Her urine output has decreased to less than 20 ml per hour, indicating acute kidney injury. This could be resulting from persistent hyperglycemia, hyperkalemia, and hypovolemia.

Her respiratory rate has also increased to 28 breaths per minute, a condition known as Kussmaul breathing, which is the body's attempt to compensate for the severe metabolic acidosis by expelling more carbon dioxide. This new development raises concern for possible progression to diabetic ketoacidosis-related respiratory failure. Further evaluation and immediate intervention are needed to manage these complications.

Section 3

Change in Patient Status:

Despite the aggressive treatment, the patient's condition takes a turn for the worse. Her heart rate increases to 130 beats per minute, and her blood pressure elevates to 150/90 mmHg. She becomes increasingly confused and lethargic, suggesting possible cerebral edema, a life-threatening complication of DKA. The patient's Glasgow Coma Scale (GCS) score drops to 10, further signifying deterioration in her mental status.

In relation to her respiratory status, her respiratory rate spikes to 32 breaths per minute, and her oxygen saturation falls to 88% on room air. Her lab work shows worsening metabolic acidosis with a blood pH of 7.15 and bicarbonate levels dropping to 10 mEq/L. Her blood glucose levels remain elevated at 350 mg/dL despite the increased insulin infusion. Furthermore, her serum potassium levels are still high at 6.2 mEq/L, and creatinine levels have risen to 2.5 mg/dL, indicating ongoing renal dysfunction. These findings suggest that the current treatment regimen is not sufficient to manage her condition, necessitating a reassessment of the management plan.

Section 4

New Complications:

Suddenly, the patient's monitor begins to alarm with a rapid decrease in her oxygen saturation from 88% to 80%. The nurse at bedside notes that her skin is becoming mottled and her extremities are cool to touch, indicating poor perfusion. Upon auscultation, her lung sounds are crackly in the bases, suggesting possible fluid overload or early signs of pulmonary edema. The patient's urine output has also decreased to less than 30 mL/hour over the last 4 hours, further indicating worsening renal function.

The nurse pages the rapid response team due to the sudden change in patient status. Upon arrival, the team leader orders a stat arterial blood gas (ABG), chest x-ray, and an EKG. The ABG results show a further drop in pH to 7.10 and an increase in the partial pressure of carbon dioxide (PaCO2) to 50 mmHg, suggesting that the patient is now in mixed metabolic and respiratory acidosis. The EKG shows peaked T-waves, a sign of hyperkalemia, which is consistent with her lab results showing a serum potassium of 6.5 mEq/L. The chest x-ray reveals bilateral infiltrates, consistent with pulmonary edema. This new constellation of findings suggests that the patient may be developing multiple organ dysfunction syndrome (MODS), a severe and potentially life-threatening complication. This development necessitates an immediate reassessment of the patient's management plan, likely involving more aggressive interventions.

Section 5

Change in Patient Status:

The patient's condition continues to deteriorate. Despite aggressive management, her oxygen saturation level falls to 76%. She becomes increasingly somnolent and less responsive to verbal stimuli. The nurse also notes that her respiratory rate has increased to 30 breaths per minute and her heart rate is now tachycardic at 130 beats per minute. The increase in respiratory rate is likely a compensatory response to her worsening acidosis and hypoxemia.

Her blood pressure also starts to drop, with readings now at 90/50 mmHg from her previous readings of 110/70 mmHg. Her capillary refill time is delayed at 4 seconds, and her peripheral pulses are weak. These findings suggest that she is developing signs of shock, possibly due to inadequate tissue perfusion secondary to her worsening metabolic and respiratory acidosis, pulmonary edema, and AKI.

In addition, her blood glucose levels remain persistently high despite insulin administration, with her latest reading at 300 mg/dL. This could be due to the stress of her critical illness causing insulin resistance or possibly due to her kidneys' impaired ability to excrete glucose due to her AKI.

New Diagnostic Results:

Her repeat ABGs show a further worsening in her acid-base status, with a pH of 6.95 and a PaCO2 of 55 mmHg. Her serum potassium has also risen to 7.0 mEq/L, and her creatinine has increased to 3.0 mg/dL, indicating worsening renal function. Her chest x-ray now shows increased bilateral infiltrates consistent with worsening pulmonary edema. Her EKG shows widening of the QRS complex, a sign of severe hyperkalemia. These findings further confirm the suspicion of MODS and the need for urgent intervention to prevent further deterioration.