Diabetic Ketoacidosis - Nursing Case Study

Pathophysiology

• Primary mechanism: In diabetic ketoacidosis (DKA), a lack of insulin leads to hyperglycemia. The body uses fat as an alternative energy source, leading to excess production of ketones, acidic byproducts of fat metabolism, resulting in metabolic acidosis.

• Secondary mechanism: The kidney excretes glucose and ketones to compensate for hyperglycemia and acidosis but can't keep up, leading to osmotic diuresis, dehydration, and electrolyte imbalance (primarily sodium and potassium).

• Key complication: Progressive acidosis and electrolyte imbalance can cause nausea, vomiting, and altered mental status, potentially leading to coma and death if not timely treated.

Patient Profile

Demographics:

52-year-old female, high school teacher

History:

• Key past medical history: Diagnosed with Type 2 Diabetes 10 years ago, High Blood Pressure, History of Obesity

• Current medications: Metformin, Lisinopril for blood pressure

• Allergies: No known drug allergies

Current Presentation:

• Chief complaint: Frequent urination, extreme thirst, nausea, abdominal pain, shortness of breath

• Key symptoms: Increasing fatigue, confusion, dry skin, rapid breathing, fruity-smelling breath

• Vital signs: Blood pressure 140/90, pulse 110, respirations 24, temperature 98.6°F, blood sugar 350 mg/dL

Section 1

Change in Patient Status:

The patient's condition begins to deteriorate rapidly. Her heart rate elevates to 120 bpm, and her blood pressure drops to 100/60 mm Hg. Her respiratory rate is also high at 30 breaths per minute. Upon assessment, she appears lethargic and her level of consciousness has decreased. She is unable to answer simple questions correctly and is becoming progressively more confused. Her skin is cool and clammy to the touch. Her urine output has significantly decreased to less than 30ml per hour, indicating possible renal dysfunction.

The patient's blood sugar level has increased further to 400 mg/dL, and a bedside urine ketone test shows large amounts of ketones. Her arterial blood gas (ABG) results show a pH of 7.20, PaCO2 of 25 mm Hg and HCO3 of 12 mEq/L, indicating severe metabolic acidosis. Her serum potassium is 3.0 mEq/L, and sodium is 130 mEq/L, indicating electrolyte imbalances. These findings suggest that the patient's DKA is progressing, leading to worsening acidosis, electrolyte imbalance, and possible renal impairment. Immediate medical intervention is necessary to prevent further complications and potential risk of coma or death.

Section 2

Change in Patient Status:

Despite the ongoing interventions, the patient's condition takes a turn for the worse. Her heart rate continues to climb, reaching 140 bpm, and her blood pressure further drops to 90/50 mm Hg. Her respiratory rate is now at 35 breaths per minute, and she becomes increasingly somnolent and less responsive to verbal stimuli. Her skin has become paler and cooler to touch, and her urine output has further decreased to less than 20ml per hour.

Her blood sugar level has now risen to 450 mg/dL, and a repeat ABG shows a pH of 7.15, PaCO2 of 22 mm Hg, and HCO3 of 10 mEq/L, suggesting deepening metabolic acidosis. Her serum potassium is now at 2.8 mEq/L, and her sodium level is 128 mEq/L. The worsening vital signs, lab values, and decreased level of consciousness demonstrate that the patient's DKA is not responding to current interventions and is progressing rapidly. The patient is now at a higher risk of developing shock, renal failure, or falling into a diabetic coma. This rapid deterioration necessitates urgent re-evaluation of the current treatment plan and consideration of more aggressive therapeutic measures.

Section 3

Change in Patient Status:

As the night shifts into early morning, the patient's condition continues to deteriorate. She is now lethargic and only arousable to painful stimuli. Her heart rate has now spiked to 155 bpm, and her blood pressure has plummeted further to 85/45 mm Hg. She is breathing at a rate of 40 breaths per minute, and her oxygen saturation has dropped to 88% on 2 liters of oxygen via nasal cannula. Her skin is now cold and clammy, and she is not producing any urine.

New Diagnostic Results:

Repeat lab work shows a further increase in her blood sugar to 500 mg/dL, and her serum potassium has dropped to 2.5 mEq/L. Her sodium level has further decreased to 125 mEq/L. A repeat ABG now shows a pH of 7.10, PaCO2 of 20 mm Hg, and HCO3 of 8 mEq/L, indicating worsening metabolic acidosis. Her blood ketone level is now at 5 mmol/L, indicating severe ketosis. Urinalysis shows large amounts of glucose and ketones, and her serum creatinine has risen to 2.5 mg/dL, suggesting acute kidney injury. The patient's worsened clinical status and lab values indicate a progressing DKA and the possible development of other complications such as shock and kidney failure. The healthcare team must urgently reassess and modify the treatment approach, considering more aggressive interventions to prevent further deterioration.

Section 4

New Complications:

The patient's condition further deteriorates as she develops seizures, likely due to severe hyponatremia and metabolic acidosis. She is immediately administered a bolus of normal saline and 10% dextrose. Intravenous diazepam is given to control the seizures, and an urgent computed tomography (CT) scan of the head is ordered to rule out cerebral edema.

Initial Assessment Findings:

Post-seizure, the patient is now unresponsive and her Glasgow Coma Scale score has dropped to 6, indicating a severe decrease in the level of consciousness. Her heart rate has increased to 165 bpm and blood pressure further decreased to 80/40 mmHg. Respiratory rate is now 45 breaths per minute with decreased breath sounds bilaterally, and oxygen saturation has dropped to 84% on 4 liters of oxygen via nasal cannula. Her skin is mottled and extremities are cool to touch. A repeat ABG shows a pH of 7.05, PaCO2 of 18 mm Hg, and HCO3 of 5 mEq/L, indicating a further deterioration in metabolic acidosis. Serum potassium is now critically low at 2.0 mEq/L, and her serum sodium remains at 125 mEq/L. The patient's worsening clinical status indicates the possible development of other severe complications such as cerebral edema, multi-organ failure, and septic shock secondary to DKA. The healthcare team must urgently decide on the next course of action and potentially prepare for emergency measures.

Section 5

New Diagnostic Results:

The CT scan results come back, showing signs of cerebral edema, confirming the team's suspicions due to the patient’s declining level of consciousness and seizures. Lab results also show an elevated white blood cell count of 18,000 cells/mcL and a high C-reactive protein level of 18 mg/dL, indicating possible infection. Blood culture results are not yet available. The critical potassium level might be causing her heart to beat irregularly and too fast. The respiratory rate remains alarmingly high, and her oxygen saturation levels continue to drop despite the oxygen therapy.

Response to Interventions:

In response to these findings, the team increases the oxygen flow rate to 6 liters via nasal cannula and orders IV potassium replacement. The patient is then started on empirical broad-spectrum antibiotics, pending the results of the blood culture. In order to manage cerebral edema, mannitol is administered and the patient is closely monitored for signs of increased intracranial pressure. The healthcare team is also prepared to intubate and mechanically ventilate the patient if her respiratory status continues to worsen. Despite these interventions, the patient's blood pressure remains low, necessitating the consideration of vasopressor administration. The patient's condition is critical, and the healthcare team must continue to monitor her closely, adapt their plan as necessary, and prepare for potential further deterioration.