Submitted by Kevin Anderson MD PGY1
HPI
A 63-year-old male with PMH diabetes type 2 and renal failure presents to the ED via EMS with AMS. The patient’s family noted the patient had been feeling ill over the last week, causing him to miss 2 dialysis sessions. Patient has been taking insulin as prescribed. Today, the patient was confused and lethargic with LOC. EMS noted the patient’s blood glucose to be >600.
Vitals HR: 90, BP: 110/70, RR: 30, SpO2: 100%, Rectal Temp: 94F
The patient has peaked T-waves on ECG
Patient is initially given calcium gluconate for suspected hyperkalemia and IVF for suspected Sepsis/DKA. Patient’s labs result:
VBG: pH 6.96, pCO2 20, pO2 41, HCO3 6, K 7.4
BMP: Glucose 1227, BUN 120, Cr 5.90, Na 123, K (hemolyzed), Cl 84, CO2 4, Anion Gap 35
Beta-Hydroxybutyrate: 8.18
Lactate: 2.2
Clinical Course
Patient given additional doses of calcium gluconate for hyperkalemia and IVF for worsening hypotension. Insulin bolus and drip started. Sodium Bicarbonate was given for severe acidosis. Patient started on broad-spectrum antibiotics for sepsis as suspected cause of DKA. Patient was admitted to the ICU for diabetic ketoacidosis and continued to receive insulin until anion gap closed. UTI secondary to urinary retention was identified as the cause of sepsis.
DKA Pearls
Diabetic ketoacidosis is usually secondary to insulin non-adherence or infection DKA is the result of decreased serum insulin, increased gluconeogenesis, accelerated glycogenolysis, and impaired glucose utilization. Utilizing fatty acid metabolism for energy production
Of note, whole-body potassium will be depleted through osmotic diuresis Serum levels may be normal due to large potassium shift into serum- except in patients with renal failure (like this one!) Potassium must be checked and replaced to >3.3 before giving insulin, otherwise patient may go into respiratory arrest, cardiac arrhythmias, or cardiac arrest!
Patients will be tachypneic (Kussmaul respirations), trying to breathe off CO2 to compensate for their metabolic acidosis! AVOID intubating these patients as even seconds of hypoxia will interrupt this crucial compensatory mechanism.
References
Diabetic Ketoacidosis
https://www.emrap.org/episode/icufundamentals/thefulltalk
