Low Serum Bicarbonate
HCO3 <22 mEq/L or pH <7.35 with metabolic component
All Pathways
NephrologyDiagnostic
Metabolic Acidosis Evaluation & Management
Metabolic Acidosis Evaluation & Management: Low Serum Bicarbonate → Confirm Metabolic Acidosis → Calculate Anion Gap → Anion Gap Elevated? → High Anion ...
Pathway Overview
16 steps
Algorithm Steps
16 total
01Start 02Action Confirm Metabolic Acidosis
Review ABG and basic metabolic panel
- Check arterial or venous blood gas
- pH <7.35 confirms acidemia
- Low HCO3 with appropriate pCO2 response
- Expected pCO2 = 1.5 × [HCO3] + 8 (±2) - Winter's formula
- If pCO2 different: Mixed disorder
03Action Calculate Anion Gap
AG = Na - (Cl + HCO3)
- Normal AG: 8-12 mEq/L
- MUST correct for albumin:
- Corrected AG = AG + 2.5 × (4 - albumin g/dL)
- Each 1 g/dL decrease in albumin lowers AG by ~2.5
04Decision Anion Gap Elevated?
Corrected AG >12 mEq/L
05Action High Anion Gap Metabolic Acidosis (HAGMA)
MUDPILES or GOLDMARK mnemonic
- M - Methanol
- U - Uremia (renal failure)
- D - DKA/Diabetic ketoacidosis
- P - Propylene glycol, Paraldehyde
- I - INH, Iron
- L - Lactic acidosis
- E - Ethylene glycol
- S - Salicylates
- Order: Lactate, ketones, BUN/Cr, osmolar gap, toxicology
06Action Calculate Delta-Delta Ratio
Check for concurrent metabolic disorders
- Delta AG = (AG - 12)
- Delta HCO3 = (24 - HCO3)
- Ratio = Delta AG / Delta HCO3
- <1: Concurrent NAGMA
- 1-2: Pure HAGMA
- >2: Concurrent metabolic alkalosis
07Decision Elevated Lactate?
Lactate >2 mmol/L
08Warning Lactic Acidosis
Most common cause of HAGMA
- Type A (hypoxic): Shock, hypoxia, sepsis, seizures
- Type B (non-hypoxic): Metformin, malignancy, liver failure
- Treatment: Address underlying cause
- Bicarb controversial, consider if pH <7.0-7.1
09Action Treatment Approach
Treat underlying cause first
- Primary: Address underlying etiology
- Bicarbonate therapy:
- - Generally reserved for pH <7.1-7.2 or HCO3 <8
- - Calculate deficit: 0.5 × wt × (24 - HCO3)
- - Give 50% of deficit, reassess
- - Caution: Volume overload, overshoot alkalosis
- RTA: Oral bicarbonate or citrate supplementation
10Outcome Acidosis Corrected
pH normalizing, address underlying cause
11Outcome Ongoing Management
Chronic RTA, CKD, or recurrent episodes
12Action Ketoacidosis
DKA, AKA, or starvation
- DKA: Hyperglycemia, check beta-hydroxybutyrate
- AKA: Recent alcohol binge, often normal glucose
- Starvation ketosis: Usually mild
- Treatment: Insulin (DKA), fluids, correct electrolytes
- Path rejoins step 09Shared downstream outcome
13Warning Toxic Alcohol Ingestion?
Check osmolar gap if suspected
- Osmolar gap = Measured osm - Calculated osm
- Calculated = 2×Na + Glu/18 + BUN/2.8
- Gap >10: Consider methanol, ethylene glycol
- Treatment: Fomepizole, HD if severe
- Poison control consultation
- Path rejoins step 09Shared downstream outcome
14Action Normal Anion Gap Metabolic Acidosis (NAGMA)
Also called hyperchloremic acidosis
- GI losses: Diarrhea, fistulas, ureteral diversion
- Renal: RTA types 1, 2, 4
- Dilutional: Large volume NS resuscitation
- Early renal failure
- Carbonic anhydrase inhibitors (acetazolamide)
- Check: Urine anion gap, urine pH
15Action Calculate Urine Anion Gap
UAG = (Urine Na + Urine K) - Urine Cl
- Negative UAG: GI losses (appropriate NH4 excretion)
- Positive UAG: Renal cause (impaired NH4 excretion)
- - RTA Type 1 (distal): UAG positive, urine pH >5.5
- - RTA Type 2 (proximal): UAG variable, bicarbonaturia
- - RTA Type 4: UAG positive, hyperkalemia
16Action RTA Classification
Based on urine studies and serum K+
- Type 1 (Distal): Cannot acidify urine, urine pH >5.5, hypokalemia
- - Causes: Autoimmune, drugs, obstruction
- Type 2 (Proximal): Bicarbonate wasting, urine pH <5.5 eventually
- - Causes: Fanconi, drugs, myeloma
- Type 4: Aldosterone deficiency/resistance, hyperkalemia
- - Causes: Diabetes, ACEi/ARB, adrenal insufficiency
- Path rejoins step 09Shared downstream outcome
Guideline Source
Clinical approach to metabolic acidosis - evidence-based synthesis
Clinical Safety Information
Clinical Decision Support — Not a Substitute for Clinical Judgment
Individual patient factors may require deviation from these recommendations.
Known Limitations
- Anion gap must be corrected for albumin
- Mixed acid-base disorders common and complex
- Does not address respiratory compensation in detail
- Stewart approach provides alternative framework
Applicable Regions
EUUSglobal
global: Traditional anion gap approach widely used
Version 1Next review: 2027-01-01
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Frequently Asked Questions
What is the Metabolic Acidosis Evaluation & Management?
The Metabolic Acidosis Evaluation & Management is a diagnostic clinical algorithm for Nephrology. It provides a structured decision tree to guide clinical decision-making, based on Clinical approach to metabolic acidosis - evidence-based synthesis.
What guideline is the Metabolic Acidosis Evaluation & Management based on?
This algorithm is based on Clinical approach to metabolic acidosis - evidence-based synthesis (DOI: 10.1056/NEJMra1003327).
What are the limitations of the Metabolic Acidosis Evaluation & Management?
Known limitations include: Anion gap must be corrected for albumin; Mixed acid-base disorders common and complex; Does not address respiratory compensation in detail; Stewart approach provides alternative framework. Individual patient factors may require deviation from these recommendations.
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