European Medical Alliance

Metabolic Acidosis

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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