Glucose is an effective osmole — it does not freely cross cell membranes. In hyperglycaemia, the elevated extracellular osmolality draws water out of cells into the plasma compartment by osmosis, diluting the measured sodium. This is a translocation hyponatraemia, not true sodium deficit.
The Katz correction (0.016/mmol glucose) was derived empirically from human studies and has been used for decades. Hillier et al. (1999) showed that the true correction factor is closer to 0.024 — especially at very high glucose levels (>400 mg/dL) — and this is now recommended by most guidelines for DKA and HHS management.
The corrected sodium reflects the patient's underlying sodium status once the dilutional effect is removed. In DKA, as glucose normalises with insulin therapy, the measured sodium should rise — failure to rise suggests excess free-water administration.
| Osmolar Gap | Interpretation |
|---|---|
| <10 mOsm/kg | Normal — no significant unmeasured osmoles |
| 10–20 mOsm/kg | Borderline — repeat or investigate further |
| >20 mOsm/kg | Significant — unmeasured osmoles present |
Causes of elevated osmolar gap:
DKA management: Monitor the corrected sodium trend throughout insulin and fluid resuscitation. A rising corrected Na during treatment is expected and reassuring; a persistently falling value may indicate cerebral oedema risk, particularly in children.
HHS diagnosis: Effective serum osmolality >320 mOsm/kg is a diagnostic criterion for HHS. Use the calculated osmolality to screen; measure directly when toxic alcohol ingestion is suspected.
Unit conversions: Glucose mmol/L × 18 = mg/dL. Urea (SI, mmol/L) is equivalent to BUN (US, mg/dL) ÷ 2.8 — make sure to select the correct unit toggle.