A 27-year-old man with type 1 diabetes mellitus that was diagnosed 15 years ago comes to the emergency department due to abdominal pain, nausea, and vomiting. The patient takes insulin glargine at night and insulin lispro before meals 3 times a day, but has not been compliant with his insulin injections. He stopped taking his insulin for the last 2 days due to not feeling well and inability to eat. The patient's medical history is otherwise unremarkable. He does not use tobacco or alcohol. Temperature is 36 C (96.8 F), blood pressure is 102/60 mm Hg, pulse is 110/min, and respirations are 26/min. The patient appears lethargic and dehydrated. The lungs are clear to auscultation. The abdomen is soft, nontender, and nondistended. Laboratory results are as follows:
| Sodium | 128 mEq/L |
| Potassium | 5.4 mEq/L |
| Chloride | 90 mEq/L |
| Bicarbonate | 10 mEq/L |
| Blood glucose | 550 mg/dL |
Which of the following is the most appropriate next step in management of this patient?
Management of diabetic ketoacidosis | |
IV fluids |
|
Insulin |
|
Potassium |
|
Bicarbonate |
|
Phosphate |
|
IV = intravenous; SQ = subcutaneous. | |
This patient with nausea, vomiting, and abdominal pain has metabolic acidosis (low bicarbonate) with an elevated anion gap (sodium – [chloride + bicarbonate]; 128 – [90 + 10] = 28 [normal 10-14]). In light of his hyperglycemia and type 1 diabetes, this is consistent with diabetic ketoacidosis (DKA). DKA can be precipitated by discontinuation of insulin, especially in the setting of infection or other stressors. It is more common in patients with type 1 diabetes due to absolute insulin deficiency, which leads to accumulation of ketoacids. A diagnosis can often be made provisionally based on bedside capillary blood glucose and confirmed with venous glucose, serum or urine ketones, and arterial blood gas analysis.
Essential measures in DKA include:
Insulin deficiency causes an extracellular shift of potassium, and serum potassium levels may be normal or elevated despite a total body deficit. Administration of insulin drives potassium into cells, resulting in hypokalemia. Potassium should be added to intravenous fluids once serum potassium is <5.3 mEq/L. When glucose reaches <200 mg/dL, patients also should be given dextrose-containing fluids to avoid hypoglycemia, but insulin should be continued to ensure resolution of ketosis.
(Choice A) After intravascular volume is restored, if serum sodium is normal or elevated, the intravenous fluid is changed to 0.45% saline. Normal saline is used initially regardless of sodium levels.
(Choices B and E) A solution of 5% dextrose provides only limited volume resuscitation because as dextrose is metabolized the solution becomes hypotonic, promoting water shift out of the intravascular space. NPH and glargine have a long duration of action and do not allow rapid dose titration; they are usually restarted when DKA has resolved. Finally, intravenous insulin is preferred to subcutaneous insulin (except in very mild DKA) due to the latter's unpredictable absorption (erratic skin perfusion).
(Choice C) Patients with DKA can have pseudohyponatremia due to hyperglycemia; this patient's corrected sodium (observed sodium + ~2 mEq/L for every 100 mg/dL glucose is over 100 mg/dL) is normal (128 + ~2 x 4.5 = 128 + ~9 = ~137 mEq/L). Hypertonic saline is reserved for moderate to severe (true) hyponatremia.
(Choice F) In most patients with DKA, administration of bicarbonate is not beneficial and may lead to cerebral edema, reduced tissue oxygenation, hypokalemia, and alkalosis. Bicarbonate is reserved for severe acidosis (pH ≤6.9), plasma bicarbonate <5 mEq/L, or severe hyperkalemia.
Educational objective:
Essential measures in diabetic ketoacidosis include: