Diabetic Ketoacidosis (DKA)
Patient Presentation:
M.B., a 28 y/o female presents to the ED with general weakness and vomiting. Her PMH includes IDDM. ROS is positive for polyuria, and polydipsia. Pt also reports dysuria that started 3 days prior. Pt denies SOB or cough, chest pain, abdominal pain, bloating, change in bowel habits; and reports taking her insulin regularly. M.B. also denies alcohol and drug use.
VS: T 101.2, BP 120/80, HR 120, RR 24, SpO2 98% RA
Neuro: AAOx3, but drowsy
Lungs: CTAB. No wheezes or crackles.
Heart: S1, S2, Tachycardic but with Regular Rhythm. No murmur, rubs, or clicks.
Abdomen: soft, non-tender, non-distended. BS(bowel sounds) present.
Differential List:
DKA vs. HHS (Hyperglycemic Hyperosmolar State)
Diagnosis:
Tests: EKG was normal; chest x-ray was clear without infiltrate
Labs: Urinalysis was positive for ketones, leukocyte esterase, nitrites, and WBCs.
Na+: 149 mEq/L; K+: 3.2 mEq/L; HCO3-: 16 mEq/L; pH: 7.2; Anion gap: 18; plasma glucose: 455 mg/dL; troponin: <0.04; urine drug screen: normal; etoh: 0.0
Based on the elevated blood glucose and the high anion gap acidosis, the diagnosis was DKA.
Treatment:
M.B. admitted to ICU. Urine culture ordered (results generally take 2 days but will tell us which abx to use). Pending urine culture, empirically treat underlying UTI with broad spectrum abx with urinary coverage, ceftriaxone, as the UTI is a likely precipitant of the DKA. Treat DKA with: aggressive hydration (NS 10-14 mL/kg/h); insulin (10 U IV push followed by 0.1 U/kg/h) and continue insulin drip until anion gap is normal; electrolyte repletion (add K+ 20-40 mEq/L IVF if serum K <4.5).
Outcome:
M.B.’s DKA resolved and pt discharged home the next day. Pt also educated to be alert for signs of infection and to stay well hydrated by drinking sugar free fluids throughout the day.
Summary:
★ Severe hyperglycemia (>250 mg/dL) should lead to consideration of DKA and HHS.
★ Initial lab tests include: plasma glucose, ABGs, electrolytes, BUN, creatinine, serum anion gap, plasma osmolality, urine/serum ketones, CBC and differential, and urinalysis.
★ DKA is characterized by the triad of hyperglycemia, ketosis, and metabolic acidosis.
★ Hyperglycemia in HHS tends to be more severe than DKA; acidosis and ketosis are not major features of HHS.
★ While hyperosmolality is a feature of HHS, note that DKA patients may also present with an elevated serum osmolality.
★ Since DKA (and HHS) can be precipitated by infection and myocardial infarction, additional evaluation should always be considered, including: EKG, chest x-ray, and cultures. The underlying precipitant would need to be corrected.
★ DKA has additional known precipitants including drugs and ETOH, which is why a drug screen and ETOH level was done. If either of these were positive it would be imperative that she receives counseling on how these increase her risk for DKA.
Case created by Mimi Balaji, 2011.