Transcript Document

Metabolic Acidosis
Alex Flaxman, MD, MSE
Presentation
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 doesn’t eat, NBNB. Has
been able to tolerate Gatorade, and has increased his
intake of Gatorade.
Pain:
– R-sided, underneath ribs, occ rad to L
“Prior’s”
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
ROS
General:
CV:
Resp:
GI:
GU:
-chills, +fatigue
CP
SOB, Cough
N/V, abd pn, -diarrhea, -blood
-freq/hematuria/urgency
All:
PMH:
PSH:
Meds:
PMD:
NKDA
Depression x2yrs, hyperchol, disc
herniations L3, L4, L5 s/p bk inj
Laminectomy x2, UGI, LGI,
EGD 6 wks ago
Compazine x1d, Nexium, Zoloft,
Vicodin, Somma
@BI
Tobacco:
EtOH:
Drugs:
1 ppd, h/o 2-3 ppd
Denies
Denies
Vital Signs
BP
P
R
O2
T
Pn
161/103
129
24
97%
99.4 PR
10/10
Exam
General:
Pul:
CV:
Abd:
Rectal:
Ext:
WDWN, NAD, tachypneic
CTAB
Tachy, reg, S1, S2, -m/r/g
NABS, RUQ tend, epig tend, +massesliver edge ~ 9 cm inf to costal margin
Guaiac neg w/ no stool
-edema, hyperpig L foot cool
R
PT 2+
DP +Doppler
L
PT +Doppler
DP +Doppler
EKG
SR @ 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
What labs do you want?
Labs
136
112
3
179
4.3
6
1
17.1
16.3
50.9
10.3
13.6
1.2
31.5
Lipase 159
Troponin 0.02
465
N 96
L3
M3
More Labs
AST
ALT
Alk
TB
DB
Alb
TP
74
6
163
3.6
0
5.2
9.7
UA
Cloudy
Prot 100
WBC 0-5
RBC 0-3
Hyaline Casts 0-5
Lactate 2.2
Acetone neg
EtOH 0
Serum osmolarity 290
Now What?
ABG
7.12 / 18 / 105 / RA / 8.3
Recall
136
112
6
Rule 1: Acidosis or Alkalosis
7.12 / 18 / 105 / RA / 8.3
Acidosis
Rule 2: Metabolic, Respiratory, Both
7.12 / 18 / 105 / RA / 8.3
Metabolic
Rule 3: Anion Gap
AG = ?
7.12 / 18 / 105 / RA / 8.3
136
112
6
= Na – Cl – HCO3
= 136 – 112 – 6
= 18
So we have an…
Anion Gap Metabolic Acidosis
Rule 4: Degree of Compensation
For metabolic acidosis,
Expected PCO = 1.5(HCO3) + 8 ± 2
2
= 1.5(6) + 8 ± 2
=9+8±2
= 17 ± 2
= 15, 19
7.12 / 18 / 105 / RA / 8.3
Actual PCO is 18  appropriate compensation
2
Rule #5: δ/δ
7.12 / 18 / 105 / RA / 8.3
136
112
6
AG
Any takers?
= 18 (nl 6.6-10.6)
HCO3 = 6
(nl 24)
Rule #5: δ/δ
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.
Causes of AG Metabolic Acidosis
MUD 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
Other causes
“P” – Phenformin
Toluene poisoning (glue sniffing)
Other organic acids
– Lactic acid
– Acetone
– Ketoacids: hydroxybutyrate / acetoacetate
– Hippuric Acid
– 5-oxyproline
– Salicylates
Lactic 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
D-Lactate
D-Lactate: External Sources
Ingestion of fermented fruits and
vegetables: pickles, yogurt, sauerkraut
LR and dialysate contain dl-lactate (50/50)
Propylene glycol ?metabolism?
D-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)
D-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
D-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
D-Lactic Acidosis
An increase in D-Lactate (duh)
Symptoms
Tachypnea
AMS
Slurred speech
Confusion
Inability to
concentrate
Somnolence
Hallucinations
Clumsiness
Weakness
Ataxia / unsteady gait
Nystagmus
Irritable
Abusive behavior
Ptosis
Asterixis
Risk Factor
Anything that results in increased delivery of
undigested carbohydrates to the colon
Risk Factors
Short Bowel Syndrome
#1 Surgical resection
#2 Intestinal bypass (bariatric surgery)
– Feeding tube placement
Intestinal malabsorption?
– Chronic pancreatitis
Risk Factors Not from the H&P
Alteration of normal colon flora to a
predominance of Gm+ anaerobes
(lactobacillus)
? Colonic stagnation
Impaired metabolism
Precipitating Factors
Excessive oral food intake
– Especially carbohydrates (like Gatorade)
Change in enteral feeding formula
Labs
Renal function normal or abnormal
AG Metabolic acidosis
– Can have non-AG metabolic acidosis
Elevated serum or urine D-lactate
– Serum level > 3 mmol/L
Ancillary 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
Immediate Treatment
A-B-C
NPO
IV dextrose (e.g. D5NS)
Treatment
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
Treatment
Increase luminal pH
– CaCO3, MgCl2
– HCO3
Abx
– Oral vanco, metro, or neomycin
Although can cause overgrowth of lactobacillus
Dialysis
– Corrects acidosis
– Clears d-Lactate
Other 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
Final dorky Interesting Point
7.12 / 18 / 105 / RA / 8.3
136
112
6
AG metabolic acidosis and concurrent
non-AG metabolic acidosis
Why?
Final 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.
Final dorky Interesting Point
1. Much lower renal threshold for d-lactate
than for l-lactate
2. 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
Take Home Points- General
1.
Consider ABG’s more often
2.
Look for causes of metabolic acidosis
3.
In unclear cases, or cases where MUD PILES
fails, send tests for organic acids (e.g. dlactate and ß-hydroxybutyrate)
4.
Involve intensivist early
Take Home Points- d-Lactate
1. For patients with short bowel (or other
malabsorption risks), consider D-lactic
acidosis.
2. Also consider when AG acidosis and:
a) Nl “lactate” levels and no acetone
b) Short bowel or other malabsorption syndrome
c) Preceded by food ingestion (and symptoms
improve after discontinuation)
d) Characteristic neurological findings