Mr. Sweet, 38 years old, is brought to the Emergency Depart…
Mr. Sweet’s presentation in the Emergency Department is concerning for diabetic ketoacidosis (DKA), a life-threatening complication of Type 1 diabetes. DKA is characterized by hyperglycemia, metabolic acidosis, and ketosis. In this case, his blood sugar of 532 mg/dL is significantly elevated, and his arterial blood gas (ABG) results demonstrate metabolic acidosis with a pH of 7.08 and low bicarbonate (12 mEq/L).
The high blood sugar in DKA results from a combination of insulin deficiency and counter-regulatory hormone release, such as glucagon and catecholamines. Insulin deficiency leads to increased hepatic glucose production and impaired glucose utilization by peripheral tissues. Counter-regulatory hormone release further exacerbates hyperglycemia by promoting glycogenolysis, gluconeogenesis, and lipolysis.
Along with hyperglycemia, Mr. Sweet demonstrates profound dehydration and electrolyte imbalances. The elevated potassium level of 7.2 mEq/L indicates a shift of potassium out of the cells, likely due to insulin deficiency and acidosis. Dehydration is reflected by his tachycardia (HR 116) and low blood pressure (107/64 mmHg). Additionally, his deep and rapid respirations with a respiratory rate of 36 suggests compensatory respiratory alkalosis. The increased respiratory rate aims to decrease the arterial partial pressure of carbon dioxide (CO2) and thus raise the pH, which is explained by the Henderson-Hasselbalch equation.
Metabolic acidosis in DKA is primarily caused by an increase in ketone bodies, namely β-hydroxybutyrate and acetoacetate. The accumulation of ketone bodies results from the breakdown of fatty acids in the absence of adequate insulin. In DKA, there is a relative insulin deficiency due to either insufficient insulin administration or increased insulin requirements in the setting of illness or infection.
The ABG results provide further insights into Mr. Sweet’s acid-base status. The pH of 7.08 indicates severe acidosis, with a normal range being 7.35-7.45. A bicarbonate level of 12 mEq/L reflects metabolic acidosis, as the normal range is typically 22-28 mEq/L. The CO2 level of 28 mmHg suggests a compensatory respiratory response to the metabolic acidosis.
The elevated body temperature of 101.5°F is likely due to the underlying infection that precipitated his DKA. Infection is a common trigger for DKA because it increases the body’s insulin requirements and promotes the release of stress hormones, worsening insulin resistance.
The management of DKA involves fluid resuscitation, insulin administration, electrolyte replacement, and treatment of the underlying cause. Mr. Sweet should receive intravenous fluids, typically isotonic saline, to correct his dehydration and restore his intravascular volume. The insulin therapy aims to correct the hyperglycemia by promoting glucose uptake and suppressing hepatic glucose production. Regular insulin is typically administered as an initial bolus followed by a continuous intravenous infusion.
Electrolyte abnormalities, such as hyperkalemia, must be addressed while administering insulin therapy. In DKA, once insulin administration begins, cells take up glucose and potassium, leading to a potential drop in serum potassium levels. However, caution must be exercised as insulin administration can also shift potassium intracellularly, leading to paradoxical hypokalemia. Serial monitoring of potassium levels is, therefore, essential.
In summary, Mr. Sweet’s presentation is consistent with diabetic ketoacidosis, a severe complication of Type 1 diabetes. DKA is characterized by hyperglycemia, metabolic acidosis, ketosis, and electrolyte imbalances. Prompt recognition and appropriate management, including fluid resuscitation, insulin therapy, and electrolyte replacement, are crucial for successful treatment. Additionally, addressing the underlying cause, in this case, a possible infection, is essential for comprehensive management.