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Metabolic AcidosisMetabolic Acidosis
Alex Flaxman, MD, MSEAlex Flaxman, MD, MSE
PresentationPresentation
50 yo M, 4d h/o 50 yo M, 4d h/o vomitingvomiting & R inf chest/RUQ pn & R inf chest/RUQ pn
Wife adds 10-15 lb wt loss x4d and Wife adds 10-15 lb wt loss x4d and lethargiclethargic, , sleeping “23 hrs/day”sleeping “23 hrs/day”
Vomiting:Vomiting:– After eating, but also when doesn’t eat, NBNB. Has After eating, but also when doesn’t eat, NBNB. Has
been able to tolerate Gatorade, and has been able to tolerate Gatorade, and has increased his increased his intake of Gatorade.intake of Gatorade.
Pain:Pain:– R-sided, underneath ribs, occ rad to LR-sided, underneath ribs, occ rad to L
““Prior’s”Prior’s”
Pt in ED Pt in ED MICU 8/04 for same MICU 8/04 for same– S/p CTAP, UGI & LGI endoscopyS/p CTAP, UGI & LGI endoscopy– Investigated for Investigated for toxidrometoxidrome– Denies EtOH, home-made alcohol, antifreeze, Denies EtOH, home-made alcohol, antifreeze,
ethylene glycol, MeOH, pica, or other tox ethylene glycol, MeOH, pica, or other tox exposures. exposures. DOH visit to home.DOH visit to home.
EGD 6 wks agoEGD 6 wks ago for N/V, neg as per pt for N/V, neg as per pt
Travel 3 wks ago to Palm Beach, FLTravel 3 wks ago to Palm Beach, FL
ROSROS
General: -chills, +fatigueGeneral: -chills, +fatigue
CV:CV: CP CP
Resp:Resp: SOB, Cough SOB, Cough
GI:GI: N/V, abd pn, -diarrhea, -blood N/V, abd pn, -diarrhea, -blood
GU:GU: -freq/hematuria/urgency -freq/hematuria/urgency
All:All: NKDANKDAPMH:PMH:Depression x2yrs, hyperchol, discDepression x2yrs, hyperchol, disc
herniations Lherniations L33, L, L44, L, L55 s/p bk inj s/p bk inj
PSH:PSH: Laminectomy x2, UGI, LGI,Laminectomy x2, UGI, LGI,EGD 6 wks agoEGD 6 wks ago
Meds:Meds: Compazine x1d, Nexium, Zoloft,Compazine x1d, Nexium, Zoloft,Vicodin, SommaVicodin, Somma
PMD:PMD:@BI@BI
Tobacco:Tobacco: 1 ppd, h/o 2-3 ppd1 ppd, h/o 2-3 ppd
EtOH:EtOH: DeniesDenies
Drugs:Drugs: DeniesDenies
Vital SignsVital Signs
BP BP 161/103161/103
P P 129129
RR 2424
OO22 97%97%
TT 99.4 PR99.4 PR
PnPn 10/1010/10
ExamExam
General:General: WDWN, NAD, WDWN, NAD, tachypneictachypneicPul:Pul: CTABCTAB
CV:CV: Tachy, reg, STachy, reg, S11, S, S22, -m/r/g, -m/r/g
Abd:Abd: NABS, RUQ tend, epig tend, NABS, RUQ tend, epig tend, +masses-+masses-
liver edge ~ 9 cm inf to costal marginliver edge ~ 9 cm inf to costal marginRectal:Rectal: Guaiac neg w/ no stoolGuaiac neg w/ no stoolExt:Ext: -edema, hyperpig L foot cool-edema, hyperpig L foot cool
R R PT 2+PT 2+ DP +DopplerDP +DopplerLL PT +DopplerPT +Doppler DP +DopplerDP +Doppler
EKGEKGSR @ 124 w/ LAESR @ 124 w/ LAE
? Q II, aVF (new from 8/31/04)? Q II, aVF (new from 8/31/04)
? ST elev V2, V3? ST elev V2, V3
Sinus tach new from 8/21/04Sinus tach new from 8/21/04
CXRCXRNAD, -free airNAD, -free air
NG LavageNG Lavage
Yellow-green material, no bloodYellow-green material, no blood
What labs do you want?What labs do you want?
17.1
50.916.3 465
N 96L 3M 3
136 3112
6 1179
10.3
4.3
LabsLabs
13.6
31.51.2
Lipase 159Troponin 0.02
More LabsMore Labs
UACloudyProt 100WBC 0-5RBC 0-3Hyaline Casts 0-5
AST 74ALT 6Alk 163TB 3.6DB 0Alb 5.2TP 9.7
Lactate 2.2
Acetone neg
EtOH 0
Serum osmolarity 290
Now What?Now What?
ABGABG
136 112
6
RecallRecall
7.12 / 18 / 105 / RA / 8.37.12 / 18 / 105 / RA / 8.3
Rule 1: Acidosis or AlkalosisRule 1: Acidosis or Alkalosis
AcidosisAcidosis
7.12 / 18 / 105 / RA / 8.37.12 / 18 / 105 / RA / 8.3
Rule 2: Metabolic, Respiratory, BothRule 2: Metabolic, Respiratory, Both
MetabolicMetabolic
7.12 / 18 / 105 / RA / 8.37.12 / 18 / 105 / RA / 8.3
AG = ?AG = ?
Rule 3: Anion GapRule 3: Anion Gap
= Na – Cl – HCO= Na – Cl – HCO33
136 112
6
7.12 / 18 / 105 / RA / 8.37.12 / 18 / 105 / RA / 8.3
= 136 – 112 – 6= 136 – 112 – 6= 18= 18
So we have an…So we have an…
Anion Gap Metabolic AcidosisAnion Gap Metabolic Acidosis
Rule 4: Degree of CompensationRule 4: Degree of Compensation
For metabolic acidosis,For metabolic acidosis,
Expected PExpected PCOCO22 = 1.5(HCO3) + 8 = 1.5(HCO3) + 8 ± 2± 2
= 1.5(6) + 8 ± 2= 1.5(6) + 8 ± 2
= 9 + 8 ± 2= 9 + 8 ± 2
= 17 ± 2= 17 ± 2
= 15, 19= 15, 19
Actual Actual PPCOCO22 is 18 is 18 appropriate compensation appropriate compensation
7.12 / 18 / 105 / RA / 8.37.12 / 18 / 105 / RA / 8.3
Rule #5: Rule #5: δδ//δδ
Any takers?Any takers?
136 112
6
7.12 / 18 / 105 / RA / 8.37.12 / 18 / 105 / RA / 8.3
AG = 18 (nl 6.6-10.6)
HCO3 = 6 (nl 24)
Rule #5: Rule #5: δδ//δδ
AG should be 10 but is now 18, for a AG should be 10 but is now 18, for a difference of difference of 88
The AG went up by The AG went up by 88, so the , so the HCOHCO33 should should go down by go down by 88..
So HCOSo HCO33 should be 24 – should be 24 – 88 = 16 but is = 16 but is really 6.really 6.
The HCO3 is lower than predicted so there is also a concurrent non-AG metabolic acidosis.
Causes of AG Metabolic AcidosisCauses of AG Metabolic AcidosisMUD PILESMUD PILES
Methanol: wood Methanol: wood alcohol, grain alcohol alcohol, grain alcohol (moonshine), paint (moonshine), paint thinners, windshield thinners, windshield washer fluidwasher fluid
UremiaUremia
DKA, AKADKA, AKA
Paraldehyde, Paraldehyde, propylene glycolpropylene glycol
Ingestions (INH, iron, Ingestions (INH, iron, XTC, cocaine)XTC, cocaine)
Lactic AcidosisLactic Acidosis
EtOH, Ethylene glycolEtOH, Ethylene glycol
SalicylatesSalicylates
Other causesOther causes
““P” – PhenforminP” – PhenforminToluene poisoning (glue sniffing)Toluene poisoning (glue sniffing)Other organic acidsOther organic acids– Lactic acidLactic acid– AcetoneAcetone– Ketoacids: hydroxybutyrate / acetoacetateKetoacids: hydroxybutyrate / acetoacetate– Hippuric AcidHippuric Acid– 5-oxyproline5-oxyproline– SalicylatesSalicylates
Lactic AcidosisLactic Acidosis
Usually increase in the L isomerUsually increase in the L isomer– Type AType A
2° to hypoxia (hypoperfusion, sepsis)2° to hypoxia (hypoperfusion, sepsis)
– Type BType BNot d.t. hypoxia: seizures, liver failure, thiamine Not d.t. hypoxia: seizures, liver failure, thiamine deficiencydeficiency
D-Lactic AcidosisD-Lactic Acidosis- increase in the D - increase in the D isomerisomer
D-LactateD-Lactate
D-Lactate: External SourcesD-Lactate: External Sources
Ingestion of fermented fruits and Ingestion of fermented fruits and vegetables: pickles, yogurt, sauerkrautvegetables: pickles, yogurt, sauerkraut
LR and dialysate contain dl-lactate (50/50)LR and dialysate contain dl-lactate (50/50)
Propylene glycol ?metabolism?Propylene glycol ?metabolism?
D-Lactate: Internal SourcesD-Lactate: Internal Sources
In the gut, glucose is metabolized by flora In the gut, glucose is metabolized by flora to lactate:to lactate:
l-Lactatel-Lactate
d-Lactated-Lactate
Produced via the methyl-glyoxal pathway Produced via the methyl-glyoxal pathway (part of threonine catabolism)(part of threonine catabolism)(threonine is an essential amino acid)(threonine is an essential amino acid)
D-Lactate: Internal SourcesD-Lactate: Internal Sources
Pyruvate ↔ Pyruvate ↔ dl-Lactate via Lactate Dehydrogenasedl-Lactate via Lactate Dehydrogenase
BUTBUT
Pyruvate ↔ l-Lactate requires l-LDHPyruvate ↔ l-Lactate requires l-LDH
Pyruvate ↔ d-Lactate requires d-LDHPyruvate ↔ d-Lactate requires d-LDH
Mammals do not have d-LDHMammals do not have d-LDH
D-Lactate: Getting rid of itD-Lactate: Getting rid of it
Slowly metabolized? Not.Slowly metabolized? Not.
d-hydroxy-acid-dehydrogenased-hydroxy-acid-dehydrogenase– Mitochondrial enzymeMitochondrial enzyme– In many tissues (especially liver and kidney)In many tissues (especially liver and kidney)– Converts d-lactate (and other substrates) to Converts d-lactate (and other substrates) to
pyruvatepyruvate
But overall, d-lactate is metabolized more But overall, d-lactate is metabolized more slowly than l-lactateslowly than l-lactate
D-Lactic AcidosisD-Lactic Acidosis
An increase in D-Lactate (duh)An increase in D-Lactate (duh)
SymptomsSymptoms
AMSAMSSlurred speechSlurred speechConfusionConfusionInability to Inability to concentrateconcentrateSomnolenceSomnolenceHallucinationsHallucinationsClumsinessClumsiness
WeaknessWeaknessAtaxia / unsteady gaitAtaxia / unsteady gaitNystagmusNystagmusIrritableIrritableAbusive behaviorAbusive behaviorPtosisPtosisAsterixisAsterixis
TachypneaTachypnea
Risk FactorRisk Factor
Anything that results in increased delivery of Anything that results in increased delivery of undigested carbohydrates to the colonundigested carbohydrates to the colon
Risk FactorsRisk Factors
Short Bowel SyndromeShort Bowel Syndrome#1 Surgical resection#1 Surgical resection
#2 Intestinal bypass (bariatric surgery)#2 Intestinal bypass (bariatric surgery)– Feeding tube placementFeeding tube placement
Intestinal malabsorption?Intestinal malabsorption?– Chronic pancreatitisChronic pancreatitis
Risk Factors Not from the H&PRisk Factors Not from the H&P
Alteration of normal colon flora to a Alteration of normal colon flora to a predominance of Gm+ anaerobes predominance of Gm+ anaerobes (lactobacillus)(lactobacillus)
? Colonic stagnation? Colonic stagnation
Impaired metabolismImpaired metabolism
Precipitating FactorsPrecipitating Factors
Excessive oral food intakeExcessive oral food intake– Especially carbohydrates (like Especially carbohydrates (like GatoradeGatorade))
Change in enteral feeding formulaChange in enteral feeding formula
LabsLabs
Renal function normal or abnormalRenal function normal or abnormal
AG Metabolic acidosisAG Metabolic acidosis– Can have non-AG metabolic acidosisCan have non-AG metabolic acidosis
Elevated serum or urine D-lactateElevated serum or urine D-lactate– Serum level > 3 mmol/LSerum level > 3 mmol/L
Ancillary TestsAncillary Tests
LP: CSF D-lactate levels same as serumLP: CSF D-lactate levels same as serum
EEG: b/l diffuse, high-voltage slow waves EEG: b/l diffuse, high-voltage slow waves without focal abnormalitywithout focal abnormality
Stool culture: predominance of Gm+ Stool culture: predominance of Gm+ anaerobic organismsanaerobic organisms– LactobacillusLactobacillus– BifidobacteriumBifidobacterium– EubacteriumEubacterium
Immediate TreatmentImmediate Treatment
A-B-CA-B-C
NPONPO
IV dextrose (e.g. D5NS)IV dextrose (e.g. D5NS)
TreatmentTreatment
SupportiveSupportive
Adjust feeding tubeAdjust feeding tube
Adjust enteral feeding formulaAdjust enteral feeding formula
Change diet to starch instead of carbohydrates Change diet to starch instead of carbohydrates recurrent attacksrecurrent attacks
Surgical: reanastomosisSurgical: reanastomosis
Oral abx: neomycin, vanco, kanamycin, metroOral abx: neomycin, vanco, kanamycin, metro
Bicarb- unclearBicarb- unclear
TreatmentTreatment
Increase luminal pHIncrease luminal pH– CaCOCaCO33, MgCl, MgCl22– HCOHCO33
AbxAbx– Oral vanco, metro, or neomycinOral vanco, metro, or neomycin
Although can cause overgrowth of lactobacillusAlthough can cause overgrowth of lactobacillus
DialysisDialysis– Corrects acidosisCorrects acidosis– Clears d-LactateClears d-Lactate
Other Interesting PointsOther Interesting Points
d-Lactate levels correlate poorly with d-Lactate levels correlate poorly with symptomssymptoms
Normal humans infused with d-lactate do Normal humans infused with d-lactate do not develop symptomsnot develop symptoms
Other acidoses to the same pH do not Other acidoses to the same pH do not cause similar symptomscause similar symptoms
Final dorky Interesting PointFinal dorky Interesting Point
AG metabolic acidosis AG metabolic acidosis andand concurrent concurrent non-AG metabolic acidosisnon-AG metabolic acidosis
Why?Why?
136 112
6
7.12 / 18 / 105 / RA / 8.37.12 / 18 / 105 / RA / 8.3
Final dorky Interesting PointFinal dorky Interesting Point
In D-lactate acidosis the increase in the In D-lactate acidosis the increase in the AG tends to be less than the decrease in AG tends to be less than the decrease in the HCO3.the HCO3.
In L-lactic acidosis where the increase in In L-lactic acidosis where the increase in the AG tends to be greater than the the AG tends to be greater than the reduction in the bicarb.reduction in the bicarb.
Final dorky Interesting PointFinal dorky Interesting Point
1.1. Much lower renal threshold for d-lactate Much lower renal threshold for d-lactate than for l-lactatethan for l-lactate
2.2. Loss of the sodium salt of D-lactic acid in Loss of the sodium salt of D-lactic acid in the stool (the H+ is resorbed from the the stool (the H+ is resorbed from the lumen or reacts with secreted HCOlumen or reacts with secreted HCO33) but ) but
the organic ion does notthe organic ion does not
Take Home Points- GeneralTake Home Points- General
1.1. Consider ABG’s more oftenConsider ABG’s more often
2.2. Look for causes of metabolic acidosisLook for causes of metabolic acidosis
3.3. In unclear cases, or cases where MUD PILES In unclear cases, or cases where MUD PILES fails, send tests for organic acids (e.g. d-fails, send tests for organic acids (e.g. d-lactate and ß-hydroxybutyrate)lactate and ß-hydroxybutyrate)
4.4. Involve intensivist earlyInvolve intensivist early
Take Home Points- d-LactateTake Home Points- d-Lactate
1.1. For patients with short bowel (or other For patients with short bowel (or other malabsorption risks), consider D-lactic malabsorption risks), consider D-lactic acidosis.acidosis.
2.2. Also consider when AG acidosis and:Also consider when AG acidosis and:a)a) Nl “lactate” levels and no acetoneNl “lactate” levels and no acetone
b)b) Short bowel or other malabsorption syndromeShort bowel or other malabsorption syndrome
c)c) Preceded by food ingestion (and symptoms Preceded by food ingestion (and symptoms improve after discontinuation)improve after discontinuation)
d)d) Characteristic neurological findingsCharacteristic neurological findings
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