Initial workup
• ✓ anion gap (AG) Na - (CI » HCOs) unmeasured anions - unmeasured cations if t glc. use measured not corrected Na expected AG is [albumin] - 2.5 (ie. 10 if albumin is 4 g dl. 7.5 if albumin is 3 g dl) T AG t unmeasured anions such as organic acids, phosphates, sulfates . AG -»I alb or t unmeasured cations (Ca. Mg, K. Li. immunoglobulin)
• If T AG. ✓ delta-delta (aa aAG aHCOj) to assess if there is an additional metabolic acid-base disturbance: aAG (calculated AG - expected AG). aHCOj (24 - HCOj) aa 1-2 — pure AG metabolic acidosis
AA 1 — AG metabolic acidosis and simultaneous non-AG acidosis AA 2 AG metabolic acidosis and simultaneous metabolic alkalosis
Etiologies of AG Metabolic Acidosis
Ketoacidosis Diabetes mellitus, alcoholism, starvation
Lactic Type A: impairment in tissue oxygenation, eg. circulatory or acidosis respiratory failure, sepsis, ischemic bowel, carbon monoxide
Type B: no impairment in tissue oxygenation, eg. malignancy, alcoholism, meds (metformin. NRTIs. salicylates) D-lactic acidosis: short bowel syndrome — gk metab by colonic bacteria to D-lactate. which is absorbed; not detected by standard lactate assay Renal failure Accumulation of organic anions such as phosphates, sulfates, etc. Ingestions Methanol: manifestations include blurred vision
Ethylene glycol: manifestations include aMS. cardiopulmonary failure.
calcium oxalate crystals and renal failure Paraldehyde
Salicylates: metabolic acidosis (from lactate, ketones) • respiratory alkalosis due to stimulation of CNS respiratory center Acetaminophen: glutathione depletion — accumulation of the endogenous organic acid 5-oxoproline in susceptible host
Workup for AG metabolic acidosis
• ✓ for ketonuria (dipstick acetoacetate) or plasma P-hydroxybutyrate (pOHB)
nb. urine acetoacetate often not present in early ketoacidosis due to shunting to [iOHB: acetoacetate may later turn 0. but does not signify worsening disease
• If e ketones. ✓ renal function, lactate, toxin screen, and osmolal gap
• Osmolal gap (OG) measured osmoles - calculated osmoles calculated osmoles (2 x Na) . (glucose 18) ♦ (BUN 2.8) ♦ (EtOH 4.6) OG >10 — suggests ingestion (methanol, ethylene glycol)
Etiologies of Non-AG Metabolic Acidosis | |
Gl losses of HCOj |
Diarrhea, intestinal or pancreatic fistulas or drainage |
RTAs |
See section on renal tubular acidoses below |
Early renal failure |
Impaired generation of ammonia |
Ingestions |
Acetazolamide, sevelamer, cholestyramine, toluene |
Dilutional |
Due to rapid infusion of bicarbonate-free intravenous fluids |
Post-hypocapnia Ureteral diversion |
Respiratory alkalosis — renal wasting of HCOj; rapid correction of resp. alk transient acidosis until HCOj regenerated Colonic CI HCOj exchange, ammonium reabsorption |
Workup for non-AG metabolic acidosis
• Evaluate history for causes (see above)
UAG unmeasured anions - unmeasured cations.as NH«" is primary unmeasured cation. UAG is indirect assay for renal NH«' excretion (nejm 1988:318594)
• © UAG -• T renal NH«' excretion — appropriate renal response to acidemia
Gl causes, type II RTA. ingestions or dilutional
type I or IV RTA. early renal failure; plasma K usually i in type I and T in type IV
• UAG interpretation assumes Pt not volume deplete and w o AG met. acidosis -»© UAG
Renal tubular acidoses (RTAs)
• Type I (distal): defective distal H" secretion
1°. autoimmune (Sjogren's, RA). nephrocalcinosis. meds (ampho, Li, ifosfamide). associated with * K (sickle cell, obstruction. SLE. renal transplant)
• Type II (proximal): i proximal reabsorption of HCOj
1° (Fanconi's syndrome), paraprotein (multiple myeloma, amyloidosis), meds (acetazolamide. heavy metals, ifosfamide). renal transplant
• Type IV (hypoaldo): TK 1 NHj synthesis delivery I urine acid carrying capacity i renin: diabetic nephropathy, NSAIDs. chronic interstitial nephritis. HIV
normal renin, 1 aldo synthesis: 1° adrenal disorders. ACEI. ARBs, heparin i response to aldosterone meds: K-sparing diuretics.TMP-SMX. pentamidine, calcineurin inhibitors tubulointerstitial disease: sickle cell. SLE. amyloid, diabetes
Renal Tubular Acidosis | ||||||
Type |
Location |
Acidosis |
UAG |
UpH |
FeHCO,' |
Serum K |
I |
Distal |
severe |
® |
>5.3 |
<3% |
»' |
II |
Proximal |
moderate |
í |
<5.3' |
>15% |
i |
IV |
Hypoaldo |
mild |
ffi |
<5.3 |
<3% |
t |
•urine pH w»B roe above 5.3 In the jetting of HCOj load
;FeHCOj should be checked after an HCO) toad
'see above for causes of type I RTA associated with hyperkalemia
Figure 4-2 Approach to metabok acidosis
•urine pH w»B roe above 5.3 In the jetting of HCOj load
;FeHCOj should be checked after an HCO) toad
'see above for causes of type I RTA associated with hyperkalemia
Figure 4-2 Approach to metabok acidosis
Metabolie Acidosis
1 AG
AG Metabolic Acidosis
0 ketones
DKA AKA
Starvation (SaVcylaiOT) (Par»Wehydo)
® lactate
Lactic uremia *
Renal failure normal AG
. Non-AG Metabolic Acidosis
©fox screen i
Ingestions / \
Methanol Salicylates Ethylene glycol Paraldehyde 5-oxoprolinuria
. Non-AG Metabolic Acidosis
FeHC03>i5% Diarrhea urine pHvar. Fistulas * t Ingestions
Dilutional Type "
Post-hypocapnia
FeHC03>i5% Diarrhea urine pHvar. Fistulas * t Ingestions
Dilutional Type "
Treatment of severe metabolic acidoses (pH <7.2) (NEjm 1998.338 26)
• DKA: insulin. IVF; AKA: dextrose. IVF. replete K. Mg. PO< as needed
• Lactic acidosis: treat underlying condition, avoid vasoconstrictors
• Renal failure: hemodialysis
• Methanol & ethylene glycol: saline diuresis, thiamine, vit B6. fomepizole. hemodialysis
• Alkali therapy: NaHCOj (eg. 3 50-mmol amp in 1 L DsW) to get serum HCO] -8
and pH -7.2 (estimate mmol of HCOj needed as 8-[HCOj]„n«n x wt > 0.5) side effects: volume overload, hypernatremia. i ICa. T P.COj (and .. possibly intracellular acidosis), overshoot: no proven benefit in lactic acidosis (A/woh 1990.112:492)
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