ACID-BASE DISORDERS

CHAPTER 44
Stephen L. Adams, MD, FACP, FACEP, and Morris S. Kharasch, MD, FACEP

1. Name the four types of acid-base disorders seen in the ED, and give a
common example of each.
Actually, there are five:
n Metabolic acidosis (e.g., cardiac arrest)

n Respiratory acidosis (e.g., chronic obstructive pulmonary disease with carbon dioxide

[CO2] retention)
n Metabolic alkalosis (e.g., protracted vomiting)

n Respiratory alkalosis (e.g., hyperventilation syndrome)

n Mixed acid-base disorder (e.g., respiratory alkalosis and metabolic acidosis, as seen in an

adult with salicylate intoxication; metabolic acidosis with respiratory compensation)

2. What does pulse oximetry contribute to the understanding of the patient’s

acid-base status?
Nothing. Pulse oximetry measures oxygen saturation and does not provide a measurement of
acid-base or ventilatory status. Arterial blood gas analysis is necessary to determine acid-base
status.

3. What are the most commonly cited causes of an elevated anion gap?
An elevated anion gap, usually indicating a low bicarbonate level, should give the clinician
cause to consider the presence of a metabolic acidosis. The differential diagnoses may be
remembered by the mnemonic DR. MAPLES:
D 5 Diabetic ketoacidosis (DKA)
R 5 Renal failure
M 5 Methanol
A 5 Alcoholic ketoacidosis
P 5 Paraldehyde
L 5 Lactic acidosis
E 5 Ethylene glycol
S 5 Salicylate intoxication
These are only some of the causes of a metabolic acidosis.

4. Name some obscure causes of an elevated anion gap metabolic acidosis.

Sulfuric acidosis, short bowel syndrome (D-lactic acidosis), nalidixic acid, methenamine,
mandelate, hippuric acid salt, rhubarb (oxalic acid) ingestion, and inborn errors of
metabolism, such as the methylmalonic acidemias and isovaleric acidemia. Toluene
intoxication (glue sniffing) can cause either an elevated anion gap metabolic acidosis or a
hyperchloremic metabolic acidosis (no anion gap).

5. Is the size of the anion gap clinically useful?

In one study, an anion gap of greater than 30 mEq/L was usually the result of an identifiable
organic acidosis (i.e., lactic acidosis or ketoacidosis). Almost 30% of patients with an anion
gap of 20 to 29 mEq/L had neither a lactic acidosis nor a ketoacidosis.

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6. What are some causes of lactic acidosis?

Shock, seizure, hypoxemia, isoniazid (INH) toxicity, metformin, cyanide poisoning, ritodrine,
inhaled industrial acetylene, phenformin ingestion, iron intoxication, ethanol abuse, and carbon
monoxide poisoning. Sodium nitroprusside, povidone-iodine ointment, sorbitol, xylitol, and
streptozocin are other drugs that have been listed as causing increased lactic acid formation.

7. Name a vitamin deficiency associated with a fatal metabolic acidosis.

Thiamine deficiency (vitamin B1 deficiency), which is associated with neurological deficits (e.g.
Wernicke’s encephalopathy, Korsakoff syndrome), high output cardiac failure (Beriberi), and
lactic acidosis, has been cited as a cause of fatal metabolic acidosis. Thiamine deficiency
should be considered in such high-risk populations as those who have a history of alcohol
abuse or nutritionally deficient states. Wernicke’s encephalopathy has also been associated with
an anion-gap primary metabolic acidosis in conjunction with a primary respiratory alkalosis.

8. How severe is the acid-base disturbance that results from a grand mal
seizure? How long does it take to resolve the acidosis?
A grand mal seizure can result in a profound lactic acidosis. The pH levels may plummet to
6.9 or lower. The acidosis in an uncomplicated seizure usually resolves spontaneously within
1 hour.

9. Can a patient have a metabolic acidosis without evidence of an elevated anion

gap?
Yes. A patient with a hyperchloremic metabolic acidosis may have no evidence of an elevated
anion gap. This condition is caused, in effect, by adding hydrogen chloride to the serum. The
fall in serum bicarbonate is offset by the addition of Cl2; consequently, there is no increased
anion gap.

10. How can I remember some of the causes of a normal anion gap metabolic
acidosis?
Use the mnemonic USED CARP:
U 5 Ureteroenterostomy
S 5 Small bowel fistula
E 5 Extra chloride
D 5 Diarrhea
C 5 Carbonic anhydrase inhibitors
A 5 Adrenal insufficiency
R 5 Renal tubular acidosis
P 5 Pancreatic fistula

11. In a patient with DKA who is improving with appropriate therapy, why might
the measurement of serum ketones show an increase?
There are three ketone bodies: b-hydroxybutyrate (BHB), acetoacetate (AcAc), and acetone.
BHB and AcAc are acids; acetone is not. The proportion of BHB to AcAc depends on the
oxidation-reduction status of the patient. A patient who is in DKA on presentation often is
severely dehydrated, and the preponderance of ketone bodies may be in the form of BHB. The
test by which ketones are noted is the nitroprusside reaction test (Acetest, Ketostix), which
measures AcAc and acetone but is not sensitive to BHB. In the patient with DKA, as fluids and
insulin therapy are instituted, the amount of BHB converted to AcAc increases, and the
nitroprusside reaction, which initially may have been weakly positive or even negative,
becomes increasingly positive.

12. List nine disorders that can cause a hyperketonemic state.

n Isopropyl alcohol intoxication

n DKA

n Alcoholic ketoacidosis
 Chapter 44  ACID-BASE DISORDERS 309

n Starvation
n Paraldehyde intoxication (pseudoketosis)
n Cyanide intoxication
n Industrial acetylene inhalation
n Hyperemesis gravidarum
n Bovine ketosis
n Stress hormone excess

13. What may contribute to metabolic acidosis in an abuser of alcohol?

Ketoacidosis has been well documented in the chronic alcoholic who binges, then presents
with nausea, vomiting, abdominal pain, and poor caloric intake. Lactic acid, acetic acid, and
indirect loss of bicarbonate in the urine (nonanion gap metabolic acidosis) also may
contribute to an alcoholic acidosis.

14. Which electrolyte is affected most commonly by a change in acid-base status?

Serum potassium. Patients with severe acidosis tend to have elevated serum K1 levels,
whereas patients with severe alkalosis tend to have low serum K1 levels. A change of pH of
0.10 is consistent with a corresponding change in serum K1 of about 0.5 mEq/L (range,
0.3–0.8 mEq/L). If the pH is elevated by 0.10, the serum K1 falls by about 0.5 mEq/L. If the
pH is diminished by 0.10, the serum K1 rises by about 0.5 mEq/L. This concept is well known
to clinicians who treat patients who present in DKA. Although the patient’s total body K1 may
be severely depleted, initial serum K1 levels may be elevated in the severely acidotic patient.
As the patient is treated appropriately and acidosis resolves, K1 supplementation is indicated
because serum levels may fall precipitously.

15. What is a pseudometabolic acidosis?

Underfilling of Vacutainer tubes can cause a significant decline in bicarbonate and an increase
in anion gap that may be mistaken for metabolic acidosis. It is theorized that because
atmospheric pressure contains less than 5% CO2, the lower partial pressure of CO2 over the
blood in an underfilled tube causes CO2 to diffuse out of the venous solution, decreasing the
bicarbonate with which it is in equilibrium. Tubes should be filled completely to prevent
creating a pseudometabolic acidosis.

16. Are there any potential ill effects of using paper bag rebreathing in the
treatment of hyperventilation syndrome?
Yes. When normal volunteers hyperventilated into a brown paper bag, inspired oxygen was
decreased sufficiently so as to endanger hypoxic patients. Paper bag rebreathing therapy
probably should not be used unless myocardial ischemia can be ruled out and arterial blood
gas analysis or pulse oximetry excludes hypoxia.

17. How does core temperature affect arterial blood gases?

Uncorrected arterial blood gases yield a falsely elevated pH and a falsely decreased PO2
and PCO2 in hypothermia. For every 1°C decrease in body temperature, the pH is elevated
0.015, PCO2 (mm Hg) decreases 4.4%, and PO2 decreases 7.2% (37°C reference).
Hyperthermia decreases the pH and increases the PCO2 and PO2 by an equivalent amount.
The clinical use of corrected versus uncorrected pH determinations in hypothermia is
controversial.

18. What acid-base alterations are seen commonly in heatstroke?

Metabolic acidosis (81% of patients in one study) and respiratory alkalosis (55% of patients).
The prevalence of metabolic acidosis was associated significantly with the degree of
hyperthermia. Of patients, 63% with a rectal temperature of 41°C, 95% with a temperature of
42°C, and 100% with a temperature of 43°C had a metabolic acidosis. This association was
not true for respiratory alkalosis. Patients who had a metabolic acidosis had a large anion gap
(24 6 5).
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19. What disease process can present with an anion gap higher than the serum
glucose?
Alcoholic ketoacidosis, a well-known cause of an elevated anion gap metabolic acidosis,
may present with hypoglycemia. One case report presented a patient with alcoholic
ketoacidosis and a concomitant illness, pneumonia, with an anion gap of 36 and a serum
glucose of less than 20 mg/dL. Severe hypoglycemia may cause a lactic acidosis and
usually occurs in the setting of a defect in gluconeogenesis, which may be seen in a
patient with chronic alcohol ingestion. A concomitant illness commonly is seen in the
patient with alcoholic ketoacidosis.

KEY POINTS: ACID-BASE DISORDERS

1. Patients with a metabolic acidosis may have an elevated serum K1 even though they may
have a low total body K1.
2. Patients with alcoholic ketoacidosis should appropriately be treated with crystalloids
containing glucose.
3. Thiamine deficiency should be considered in the appropriate clinical setting and treated in
those at risk for the consequences of same.

20. How can patients with HIV have an abnormality in the anion gap?
A patient with HIV may have a low anion gap. Hypergammaglobulinemia, resulting
from an increased number of immunoglobulin-secreting b-cells because of failure in
immunoregulation, has been reported in patients with HIV. Consequently, an elevation
of immunoglobulin G (IgG) and immunglobulin A (IgA) may occur. The anion gap may
be low because of the cationic charge of IgG. One case report described a patient with
HIV with lactic acidosis, which should elevate the anion gap, who had a “deceptively”
normal anion gap. A patient with hyperlactacidemia and a normal anion gap acidosis
should prompt an evaluation of coexisting illnesses that may be responsible for the low
anion gap.

21. What is the most common cause of metabolic acidosis in the pediatric
population?
Significant diarrheal illnesses in this population may produce a starvation ketosis.

22. In addition to the toxic alcohols, name two entities causing a metabolic
acidosis with an elevated anion gap that have been associated with an
elevated osmolal gap.
Alcoholic ketoacidosis and lactic acidosis. It has been speculated that, in patients
with lactic acidosis, organic substances of low molecular weight are released from
ischemic tissues, accounting for unmeasured osmols. In alcoholic ketoacidosis, it has
been speculated that an increased osmolal gap could be attributed to acetone, an
uncharged ketone of low molecular weight that may be elevated if the ketoacidosis is
severe and prolonged. The exact pathogenesis of the gap in these two entities is not
certain, however. As can be seen, the elevated osmolal gap is not specific for a toxic
alcohol ingestion.

23. Name a base and an outfielder.

Al Kaline (Detroit Tigers 1953–1974, Hall of Fame 1980).
 Chapter 44  ACID-BASE DISORDERS 311

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