DKA - Nursing Case Study

Pathophysiology

• Primary mechanism: Lack of insulin results in the inability to use glucose for energy, causing the body to break down fat as an alternative source. This process produces ketones, a by-product that leads to the acidic condition known as ketoacidosis.

• Secondary mechanism: With glucose unable to enter cells due to insulin deficiency, blood glucose levels rise (hyperglycemia). The kidneys attempt to eliminate excess glucose through urine, leading to increased urine output, dehydration, and electrolyte imbalance.

• Key complication: The combination of ketoacidosis and hyperglycemia can lead to severe dehydration, altered mental status, and shock. If left untreated, it can progress to coma or death. Immediate medical intervention is critical.

Patient Profile

Demographics:

60-year-old male, retired mechanic

History:

• Key past medical history: Type 2 Diabetes Mellitus, Hypertension

• Current medications: Metformin, Lisinopril

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Severe abdominal pain, frequent urination and excessive thirst

• Key symptoms: Dry mouth, rapid and shallow breathing, fruity-scented breath, confusion, fatigue, recurrent urination, increased thirst

• Vital signs: Blood pressure 140/95 mmHg, heart rate 115 bpm, respiratory rate 26 breaths per minute, temperature 37.5 C, SpO2 95%, Blood Glucose Level: 450 mg/dl.

Section 1

New Diagnostic Results:

After initial assessment, the patient is admitted to the hospital for further evaluation. The diagnostic tests results return with an elevated HbA1c of 12.5%, indicating poor blood glucose control over the past three months. The patient's blood gas analysis reveals a pH of 7.25 and bicarbonate level of 18 mEq/L, both lower than normal, suggesting metabolic acidosis. Moreover, the serum ketones test is positive, confirming the presence of ketones in the blood. His urine analysis also reveals glucosuria and ketonuria.

These new findings confirm the diagnosis of diabetic ketoacidosis (DKA). The high glucose levels in his blood and urine, along with the presence of ketones, indicate that his body is using fat for energy due to the lack of insulin. The low pH and bicarbonate level in his blood illustrate the acidosis state of his body due to the accumulation of ketones. The increased HbA1c suggests that the patient's diabetes has been poorly controlled, which may have contributed to the development of DKA. The healthcare team must now focus on managing the patient's DKA and improving his overall diabetes care to prevent further complications. This would involve clinical reasoning to determine the most effective treatment approach considering the patient's history and current status.

Section 2

Change in Patient Status:

Over the next 24 hours, the patient's condition steadily worsens. His vital signs reveal a heart rate of 110 beats per minute, respiratory rate of 24 breaths per minute, blood pressure of 95/60 mmHg, and a body temperature of 37.6 degrees Celsius (99.7 degrees Fahrenheit). His blood glucose levels continue to rise, now at 450 mg/dL. Additionally, the patient complains of increasing abdominal pain and nausea, and has started vomiting.

These changes in the patient's status suggest that his body is struggling to compensate for the metabolic acidosis and hyperglycemia. The elevated heart rate and respiratory rate may indicate the body's attempt to compensate for acidosis through increased cardiac output and rapid, deep breathing (Kussmaul respiration). The persistent hyperglycemia, despite hospital admission, could suggest that the patient's insulin therapy is inadequate or that he is not responding as expected. Moreover, the symptoms of abdominal pain, nausea, and vomiting are likely due to gastric stasis, a common complication in DKA that can worsen the patient's condition by causing dehydration and electrolyte imbalances. This new information demands a reassessment of the current management plan and a consideration of alternative interventions.

Section 3

New Diagnostic Results:

Upon reassessment, the patient's arterial blood gases (ABGs) showed a pH of 7.28, PaCO2 of 25 mmHg, and HCO3 of 13 mEq/L, which confirm metabolic acidosis. His serum electrolyte panel revealed a potassium level of 3.2 mEq/L, sodium of 135 mEq/L, and chloride of 102 mEq/L. The patient's urine output, which was initially normal, had decreased to less than 30 mL/hour, suggesting a decline in kidney function. A repeat blood glucose level showed an increase to 475 mg/dL.

These diagnostic results indicate that the patient's metabolic acidosis and hyperglycemia are worsening, and he is now also displaying signs of hypokalemia and potential renal insufficiency. The presence of hypokalemia in the setting of DKA is concerning as it suggests a total body potassium deficit, which can lead to dangerous cardiac dysrhythmias. The reduced urine output and persistent hyperglycemia may indicate that the patient's kidneys are struggling to excrete the excess glucose and ketones, leading to further acidosis and potential renal damage. These findings call for immediate adjustment of the patient's treatment regimen, with particular attention to fluid management, insulin therapy, and potassium replacement.

Section 4

Change in Patient Status:

Over the next few hours, the patient's condition deteriorated further. He became increasingly lethargic, and his respiratory rate increased to 30 breaths per minute. On physical examination, his skin was cool and clammy, and his capillary refill time was delayed at 3 seconds. His urine output remained less than 30 mL/hour, and his blood glucose was persistently high at 490 mg/dL.

These clinical findings indicate that the patient's metabolic acidosis is progressing, with his increased respiratory rate representing Kussmaul breathing, a compensatory mechanism to blow off excess CO2 and attempt to correct the acidosis. The changes in his skin and capillary refill time suggest poor peripheral perfusion, likely due to hypovolemia from osmotic diuresis and potential renal insufficiency. The persistently high blood glucose level and reduced urine output are further evidence of ongoing DKA and inadequate renal excretion of glucose and ketones. These changes in patient status underscore the need for prompt reassessment of the patient's treatment plan and potentially more aggressive intervention.

Section 5

New Diagnostic Results:

Laboratory results were returned showing a blood gas pH of 7.20, bicarbonate level of 10 mEq/L, and an anion gap of 25 mEq/L. Additionally, his serum potassium level was elevated at 5.5 mEq/L, and his creatinine level was 1.7 mg/dL, up from 1.2 mg/dL on admission. The patient's urine tested positive for ketones.

The blood gas results confirm severe metabolic acidosis, which is consistent with uncontrolled DKA. The increased anion gap suggests that acid is being added to the body, likely due to the production of ketones in DKA. The elevated serum potassium level is indicative of acidosis and renal insufficiency, as the kidneys are unable to excrete potassium effectively. The rise in creatinine level further supports the suspicion of acute kidney injury, likely secondary to hypovolemia and poor perfusion. The presence of urinary ketones verifies the ongoing breakdown of fats for energy, leading to the production of ketones and further exacerbating the patient's metabolic acidosis. These results highlight the urgency in addressing the patient's deteriorating condition.