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Acidosis Correction Tool

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Neonatal Acid–Base · Decision Support

Acidosis Correction Tool

Models a NaAcetate infusion running at a chosen rate and strength — and shows the base, the sodium, and the fluid that ride along with it. Bicarbonate is available for the rare acute case.

⚠ Decision support — not a directive. Treat the cause first (sepsis, hypovolemia, hypoxia, GI/renal losses, hyperchloremia). Acetate is for slow correction of persistent/loss-driven acidosis; it acts over hours via hepatic metabolism, not minutes. Outputs are estimates — confirm against your unit protocol, total daily sodium/fluid goals, and serial gases.

Patient & blood gas

Values from the gas (Epic) and serum chemistry.

Epic reports Base Excess, Blood (BEB) — enter it with its sign. A negative value is a base deficit (what acetate makes up); positive means no deficit. Prefer a standard/ECF base excess when available (less PaCO₂-distorted), and cross-check a serum HCO₃.

Acetate infusion

Set the running line, then read off what the baby is getting.

NaAcetate is 1:1 sodium-to-acetate, and acetate → bicarbonate 1:1 in the Krebs cycle. So the base, the sodium, and (per strength) the mEq/L are the same number. Strength changes Na/base without changing fluid; rate changes all three.

Result Sodium acetate

Evidence, formulas & physiology

The acetate model

  • Concentration from strength: Na (mEq/L) = strength × full-strength conc. Full → 154, ½ → 77, ¼ → 38.5 mEq/L (editable).
  • Base / sodium per hour: = conc (mEq/L) × rate (mL/hr) ÷ 1000. Acetate → HCO₃ is 1:1, and NaAcetate is 1 Na : 1 acetate, so base mEq = Na mEq.
  • Per kg per day: = (conc × rate × 24 ÷ 1000) ÷ weight. This is the number to weigh against daily sodium and fluid goals.
  • Fluid: mL/kg/day = rate (mL/hr) × 24 ÷ weight — unchanged by strength, only by rate.
  • One-time deficit: base needed (mEq) = 0.3 × weight × base deficit (standard Vd = 0.3 L/kg, full deficit). Hours of the running line to deliver that = needed ÷ (base mEq/hr) — a gross reference; ongoing acid load and renal handling make real correction slower.
  • Projected pH (Henderson–Hasselbalch, once the deficit's base is replaced): pH = 6.1 + log₁₀( HCO₃ ÷ (0.03 × PaCO₂) ).

Why acetate over bicarbonate

Acetate is a bicarbonate precursor, not a buffer: it's metabolized through the Krebs cycle to HCO₃ + CO₂ over hours. That slow, hepatic conversion avoids the abrupt extracellular HCO₃ rise that drives paradoxical intracellular acidosis (CO₂ diffuses into cells faster than HCO₃), the high osmolar load, and the cerebral blood-flow swings linked to IVH in preterm infants — the harms that make bolus bicarbonate hazardous. Substituting acetate for chloride in PN also corrects the hyperchloremic component that NaCl-heavy fluids create, and offsets the renal bicarbonate wasting of the immature kidney. RCT and interventional data show higher pH and reduced bicarbonate need with acetate in PN.

Where bicarbonate still has a narrow role

Severe, persistent metabolic acidosis with hemodynamic compromise (critical CHD, severe PPHN, septic shock) — small, slow doses (the review favors ~0.5–2 mEq/kg over 30–60 min, reassessing) with secured ventilation, while the cause is treated. Not for resuscitation, and not when the acidosis is respiratory.

Primary source: Dhugga G, Sankaran D, Lakshminrusimha S. “ABCs of base therapy in neonatology: role of acetate, bicarbonate, citrate and lactate.” J Perinatol 2025;45(3):298–304. Supporting: Peters et al. Arch Dis Child Fetal Neonatal Ed 1997 and Ali et al. 2020 (acetate in PN); BASE trial protocol (NIHR/NPEU 2024); Katheria et al. J Perinatol 2017. Confirm ranges and the definition of “full” NaAcetate against your local protocol.