7.29.08 peery. metabolic acidosis
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ANION GAP METABOLIC ACIDOSISMore then just a mud pile
Anne Peery, MD
July 29, 2008
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Metabolic acidosis
Overproduction or ingestion of fixed acid or loss of
base which produces an increase in arterial pH (an
acidemia)
HCO3 is used to buffer the extra fixed acid.
As a result, the arterial HCO3 decreases.
Acidemia causes hyperventilation (Kussmaul
breathing), which is the respiratory compensationfor metabolic acidosis.
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The anion gap
An estimate of the unmeasured anions.
Used to determine if a metabolic acidosis is due to
an accumulation of non-volatile acids (e.g. lactic
acid) OR a net loss of bicarbonate (e.g. diarrhea)
Anion gap = Na (Cl + HCO3)
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The influence of albumin
Albumin is a major source of unmeasured anions!
If a patients serum albumin is low, then the patient
has more unmeasured anions then the anion gap
predicts.
Corrected AG = Observed AG + 2.5 x (4.5
measured albumin)
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More then one problem?
The gap-gap or delta-delta
In the presence of a high AG metabolic acidosis, it
is possible to detect another metabolic acid base
disorder by comparing the AG excess to the HCO3
deficit
Delta-Delta = (Measured AG 12)/(24-measured
HCO3)
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Mixed Disorders
When a fixed acid accumulates in extracelluar fluid, the
decrease in serum HCO3 is equivalent to the increase
in AG and the gap-gap ratio = 1
When a hypercholemic acidosis appears, the decreasein HCO3 is greater then the increase in AG, and the
gap-gap 1 (i.e. coexistent metabolic
alkalosis)
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Differential for AG Metabolic Acidosis
1. Ketoacidosis
2. Lactic acid acidosis
3. Toxin-induced metabolic acidosis4. Renal failure acidosis
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Ketosis
Occurs in conditions of reduced nutritient intake,
adipose tissues release free fatty acids, which are
taken up in the liver and metabolized to form the
ketones, acetoacetate and B-hydroxybutyrate.
The ACETEST a nitroprusside reaction detects
acetoacetate NOT hydroxybutyrate.
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Ketosis
Diabetic ketoacidosis
Alcoholic ketoacidosis
Starvation ketosis
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Alcoholic Ketoacidosis
Some chronic alcoholics, esp binge drinkers, who
discontinue solid food intake while continuing EtOH
consumption develop this form of ketoacidosis when
EtOH ingestion is curtailed abruptly.
Metabolic acidosis may be severe but is
accompanied by only a modest derangement in
glucose levels (usually low but may be slightlyelevated).
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Alcoholic Ketoacidosis
Presentation may be complex because a mixed
disorder is often present
Metabolic alkalosis from emesis
Respiratory alkalosis from EtOH liver disease
Lactic acid acidosis from hypoperfusion
Therapy includes IV glucose and saline
Check electrolytes frequently High potential for refeeding syndrome
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Lactic Acid Acidosis
Lactic acid can exist in two forms: L-lactate and D-
Lactate. In mammals, only the levorotary form is a
product of metabolism.
D-Lactate can accumulate in humans as a byproduct
of metabolism by bacteria, which accumulate and
overgrow in the GI tract with jejunal bypass or short
bowel syndrome. The lab measures only L-lactate!
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L-Lactic Acidosis
Tissue underperfusion (Type A)
Shock, shock, shock
Hypoxia
Asthma
CO poisoning
Severe anemia
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L-Lactic Acidosis
Medical conditions (w/o tissue hypoxia) Hepatic failure
Thiamine deficiency (co-factor for pyruvate dehyrogenase)
Malignancy
Bowel ischemia Seizures
Heat stroke
Tumor lysis
Drugs/Toxins Metformin (particulary associated with hypovolemia and dye) NRTI (especially stavudine and zidovudine)
Propofol
Nitroprusside
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L-Lactic Acidosis
Propylene Glycol toxicity
An alcohol used to enhance water solubility of many
hydrophobic IV medications (lorazepam, diazepam,
esmolol, nitroglycerin) Propylene glycocol toxicity from solvent accumulation
has been reported in 19% to 66% of ICU patients
receiving high dose lorazepam or diazepam for more
then 2 days. Signs of toxicityagitation, coma, seizures,
tachycardia, hypotension
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Toxic-Induced Metabolic Acidosis
Salicylates
More common in children then in adults
May result in high AG metabolic acidosis
Most commonly associated with respiratory alkalosis
due to direct stimulation of the respiratory center
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Osmolar Gap
Under most physiologic conditions, Na, urea andglucose generate the osmotic pressure of blood .
Serum OSM = 2 (Na) + BUN/2.8 + glc/18
Calculated and determined OSM should agreewithin 10 to 15 mOsm/kg.
If not, then serum Na may be spuriously low ORosmolytes other then Na, glc or urea have
accumulated. The osmolar gap is a reliable and helpful tool when
screening for toxin-associated high AG acidosis.
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Toxic-Induced Metabolic Acidosis
Ethanol
In general does not cause high AG metabolic acidosis
Oxidized to acetaldehyde, acetyl CoA and CO2
Acetaldehyde levels increase significantly if
acetaldehyde dehydrogenase inhibited by disulfiram,
insecticides or a sulfonurea.
Paraldehyde Very rare
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Toxic-Induced Metabolic Acidosis
Methanol
Causes metabolic acidosis in addition to severe optic nerve
and CNS manifestations
High osmolar gap
Ethylene Glycol
Leads to high AG metabolic acidosis in addition to severe
CNS, cardiopulmonary and renal damage.
Recognizing oxalate crystals in urine facilitates diagnosis.
High osmolar gap
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Uremia
At a GFR < 20 mL/min, the inability to excrete H+
with retention of acid anions such as phosphate and
sulfate results in an increased anion gap acidosis,
which RARELY is severe.
The unmeasured anions replace bicarbonate
(which is consumed as a buffer).
Hyperchloremic normal anion gap acidosis developsin milder cases of renal insufficiency.
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References
Marino, P. 2007. The ICU Book. 3rd Edition. Philadelphia. Lippincott.
Brenner and Rector. 2007. The Kidney. 8th Edition. New York. Saunders.
McPhee S andPapadakis M. 2007. Current Medial Diagnosis and
Treatment. New York. McGraw-Hill.
Up to Date 2008.
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