7.29.08 peery. metabolic acidosis

8/7/2019 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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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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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.

7.29.08 peery. metabolic acidosis

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