End Goals of Dialysis in Oxalic Acid Poisoning
The primary end goals of dialysis in acute oxalic acid poisoning are to normalize the anion gap to <18 mmol/L, correct metabolic acidosis with stable pH >7.35, and achieve clinical improvement with normalization of mental status. 1
Specific Biochemical Targets
The cessation criteria for dialysis in acute oxalic acid poisoning are clearly defined and should guide treatment endpoints:
- Anion gap normalization to <18 mmol/L is the primary biochemical target, as this indicates adequate removal of oxalate and correction of the toxic metabolic derangement 1, 2
- Resolution of metabolic acidosis with stable pH >7.35 must be achieved before discontinuing dialysis 1, 2
- Correction of acid-base abnormalities beyond just pH normalization, ensuring metabolic stability 1
Clinical Endpoints
Beyond laboratory parameters, clinical recovery is essential:
- Normalization of mental status including resolution of altered consciousness, coma, or seizures that prompted dialysis initiation 1, 2
- Clinical improvement with stabilization of neurological function 1
Rationale for High-Flux Hemodialysis
The choice of dialysis modality directly impacts achieving these goals:
- High-flux hemodialysis achieves oxalate clearance of 116 mL/min/1.73 m² BSA, which is vastly superior to peritoneal dialysis (7 mL/min/1.73 m²) 1, 2
- This superior clearance allows rapid removal of both parent compound and toxic metabolites, which is critical for preventing irreversible organ damage 1
- Technical specifications should include high-flux membrane >1m² capillary surface area per 1m² body surface area and blood flow rate >250 mL/min 1, 2
Critical Pitfall to Avoid
Do not delay dialysis waiting for traditional uremic indications - the anion gap >27 mmol/L and pH <7.1 thresholds are absolute indications for immediate dialysis initiation, not endpoints 2. The goal is to reverse these severe derangements, not to wait until they worsen further.
Context: Chronic vs. Acute Poisoning
It is important to distinguish that in chronic hyperoxaluria (such as primary hyperoxaluria), the goals differ substantially - targeting pre-dialysis plasma oxalate levels around 50-70 μmol/L to prevent systemic oxalosis 3, 2. However, in acute oxalic acid poisoning, the endpoints are the normalization parameters described above, as the pathophysiology involves acute toxic ingestion rather than chronic metabolic disease.