Title: Metabolic Acidosis
1Metabolic Acidosis
2Presentation
- 50 yo M, 4d h/o vomiting R inf chest/RUQ pn
- Wife adds 10-15 lb wt loss x4d and lethargic,
sleeping 23 hrs/day - Vomiting
- After eating, but also when doesnt eat, NBNB.
Has been able to tolerate Gatorade, and has
increased his intake of Gatorade. - Pain
- R-sided, underneath ribs, occ rad to L
3Priors
- Pt in ED ? MICU 8/04 for same
- S/p CTAP, UGI LGI endoscopy
- Investigated for toxidrome
- Denies EtOH, home-made alcohol, antifreeze,
ethylene glycol, MeOH, pica, or other tox
exposures. DOH visit to home. - EGD 6 wks ago for N/V, neg as per pt
- Travel 3 wks ago to Palm Beach, FL
4ROS
- General -chills, fatigue
- CV CP
- Resp SOB, Cough
- GI N/V, abd pn, -diarrhea, -blood
- GU -freq/hematuria/urgency
5- All NKDA
- PMH Depression x2yrs, hyperchol, disc
- herniations L3, L4, L5 s/p bk inj
- PSH Laminectomy x2, UGI, LGI,
- EGD 6 wks ago
- Meds Compazine x1d, Nexium, Zoloft,
- Vicodin, Somma
- PMD _at_BI
6- Tobacco 1 ppd, h/o 2-3 ppd
- EtOH Denies
- Drugs Denies
7Vital Signs
- BP 161/103
- P 129
- R 24
- O2 97
- T 99.4 PR
- Pn 10/10
8Exam
- General WDWN, NAD, tachypneic
- Pul CTAB
- CV Tachy, reg, S1, S2, -m/r/g
- Abd NABS, RUQ tend, epig tend, masses-
- liver edge 9 cm inf to costal margin
- Rectal Guaiac neg w/ no stool
- Ext -edema, hyperpig L foot cool
- R PT 2 DP Doppler
- L PT Doppler DP Doppler
9- EKG
- SR _at_ 124 w/ LAE
- ? Q II, aVF (new from 8/31/04)
- ? ST elev V2, V3
- Sinus tach new from 8/21/04
- CXR
- NAD, -free air
- NG Lavage
- Yellow-green material, no blood
10What labs do you want?
11Labs
Lipase 159Troponin 0.02
12More 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
13Now What?
14ABG
15Rule 1 Acidosis or Alkalosis
7.12 / 18 / 105 / RA / 8.3
16Rule 2 Metabolic, Respiratory, Both
7.12 / 18 / 105 / RA / 8.3
17Rule 3 Anion Gap
7.12 / 18 / 105 / RA / 8.3
Na Cl HCO3
136 112 6 18
- So we have an
- Anion Gap Metabolic Acidosis
18Rule 4 Degree of Compensation
- For metabolic acidosis,
- Expected PCO2 1.5(HCO3) 8 2
1.5(6) 8 2 9 8 2 17 2
15, 19
7.12 / 18 / 105 / RA / 8.3
Actual PCO2 is 18 ? appropriate compensation
19Rule 5 d/d
7.12 / 18 / 105 / RA / 8.3
AG 18 (nl 6.6-10.6) HCO3 6 (nl 24)
20Rule 5 d/d
- AG should be 10 but is now 18, for a difference
of 8 - The AG went up by 8, so the HCO3 should go down
by 8. - So HCO3 should be 24 8 16 but is really 6.
The HCO3 is lower than predicted so there is also
a concurrent non-AG metabolic acidosis.
21Causes of AG Metabolic AcidosisMUD PILES
- Methanol wood alcohol, grain alcohol
(moonshine), paint thinners, windshield washer
fluid - Uremia
- DKA, AKA
- Paraldehyde, propylene glycol
- Ingestions (INH, iron, XTC, cocaine)
- Lactic Acidosis
- EtOH, Ethylene glycol
- Salicylates
22Other causes
- P Phenformin
- Toluene poisoning (glue sniffing)
- Other organic acids
- Lactic acid
- Acetone
- Ketoacids hydroxybutyrate / acetoacetate
- Hippuric Acid
- 5-oxyproline
- Salicylates
23Lactic Acidosis
- Usually increase in the L isomer
- Type A
- 2 to hypoxia (hypoperfusion, sepsis)
- Type B
- Not d.t. hypoxia seizures, liver failure,
thiamine deficiency - D-Lactic Acidosis- increase in the D isomer
24D-Lactate
25D-Lactate External Sources
- Ingestion of fermented fruits and vegetables
pickles, yogurt, sauerkraut - LR and dialysate contain dl-lactate (50/50)
- Propylene glycol ?metabolism?
26D-Lactate Internal Sources
- In the gut, glucose is metabolized by flora to
lactate - l-Lactate
- d-Lactate
- Produced via the methyl-glyoxal pathway (part of
threonine catabolism) - (threonine is an essential amino acid)
27D-Lactate Internal Sources
- Pyruvate ? dl-Lactate via Lactate Dehydrogenase
- BUT
Pyruvate ? l-Lactate requires l-LDH Pyruvate ?
d-Lactate requires d-LDH Mammals do not have d-LDH
28D-Lactate Getting rid of it
- Slowly metabolized? Not.
- d-hydroxy-acid-dehydrogenase
- Mitochondrial enzyme
- In many tissues (especially liver and kidney)
- Converts d-lactate (and other substrates) to
pyruvate - But overall, d-lactate is metabolized more slowly
than l-lactate
29D-Lactic Acidosis
- An increase in D-Lactate (duh)
30Symptoms
- AMS
- Slurred speech
- Confusion
- Inability to concentrate
- Somnolence
- Hallucinations
- Clumsiness
- Weakness
- Ataxia / unsteady gait
- Nystagmus
- Irritable
- Abusive behavior
- Ptosis
- Asterixis
31Risk Factor
- Anything that results in increased delivery of
undigested carbohydrates to the colon
32Risk Factors
- Short Bowel Syndrome
- 1 Surgical resection
- 2 Intestinal bypass (bariatric surgery)
- Feeding tube placement
- Intestinal malabsorption?
- Chronic pancreatitis
33Risk Factors Not from the HP
- Alteration of normal colon flora to a
predominance of Gm anaerobes (lactobacillus) - ? Colonic stagnation
- Impaired metabolism
34Precipitating Factors
- Excessive oral food intake
- Especially carbohydrates (like Gatorade)
- Change in enteral feeding formula
35Labs
- Renal function normal or abnormal
- AG Metabolic acidosis
- Can have non-AG metabolic acidosis
- Elevated serum or urine D-lactate
- Serum level gt 3 mmol/L
36Ancillary Tests
- LP CSF D-lactate levels same as serum
- EEG b/l diffuse, high-voltage slow waves
without focal abnormality - Stool culture predominance of Gm anaerobic
organisms - Lactobacillus
- Bifidobacterium
- Eubacterium
37Immediate Treatment
- A-B-C
- NPO
- IV dextrose (e.g. D5NS)
38Treatment
- Supportive
- Adjust feeding tube
- Adjust enteral feeding formula
- Change diet to starch instead of carbohydrates ?
recurrent attacks - Surgical reanastomosis
- Oral abx neomycin, vanco, kanamycin, metro
- Bicarb- unclear
39Treatment
- Increase luminal pH
- CaCO3, MgCl2
- HCO3
- Abx
- Oral vanco, metro, or neomycin
- Although can cause overgrowth of lactobacillus
- Dialysis
- Corrects acidosis
- Clears d-Lactate
40Other Interesting Points
- d-Lactate levels correlate poorly with symptoms
- Normal humans infused with d-lactate do not
develop symptoms - Other acidoses to the same pH do not cause
similar symptoms
41Final dorky Interesting Point
7.12 / 18 / 105 / RA / 8.3
- AG metabolic acidosis and concurrent non-AG
metabolic acidosis - Why?
42Final dorky Interesting Point
- In D-lactate acidosis the increase in the AG
tends to be less than the decrease in the HCO3. - In L-lactic acidosis where the increase in the AG
tends to be greater than the reduction in the
bicarb.
43Final dorky Interesting Point
- Much lower renal threshold for d-lactate than for
l-lactate - Loss of the sodium salt of D-lactic acid in the
stool (the H is resorbed from the lumen or
reacts with secreted HCO3) but the organic ion
does not
44Take Home Points- General
- Consider ABGs more often
- Look for causes of metabolic acidosis
- In unclear cases, or cases where MUD PILES fails,
send tests for organic acids (e.g. d-lactate and
ß-hydroxybutyrate) - Involve intensivist early
45Take Home Points- d-Lactate
- For patients with short bowel (or other
malabsorption risks), consider D-lactic acidosis. - Also consider when AG acidosis and
- Nl lactate levels and no acetone
- Short bowel or other malabsorption syndrome
- Preceded by food ingestion (and symptoms improve
after discontinuation) - Characteristic neurological findings
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