Back To Basics: Acidosis and Alkalosis
Back To Basics: Acidosis and Alkalosis
BACK TO
BASICS Acidosis and Alkalosis
Andrew L. Schwaderer, MD,* George J. Schwartz, MD†
acidosis. In type II (proximal) RTA the kidney or liver underuses excess vated anion gap metabolic acidosis.
and with the use of carbonic anhy- lactate. Type A lactic acidosis occurs When the glomerular filtration rate
drase inhibitors such as acetazol- from tissue hypoxia or hypoperfu- falls below 25 mL/min per 1.73 m2,
amide, reabsorption of filtered bicar- sion. Type B lactic acidosis results insufficient excretion of ammonium
bonate is impaired. Distal (type I) from systemic disease, drugs, toxins, and acids prevents bicarbonate re-
RTA is characterized by a defect in and inborn errors of metabolism. generation.
distal acid secretion resulting in de- Inborn errors of metabolism in
creased urinary levels of acid and am- the newborn period can be divided Management
monium. The urine net charge into urea cycle abnormalities or er- Management of metabolic acidosis
[(urine Na⫹ ⫹ urine K⫹) - (urine rors in amino acid, carbohydrate, or usually is directed toward addressing
Cl⫺)] can be used to identify a type II organic acid metabolism. Symptoms the underlying condition. Correc-
RTA. Because ammonium (an un- often include poor feeding, failure to tion of the underlying insulin, vol-
measured cation) accompanies chlo- thrive, seizures, and vomiting. Inges- ume, and electrolyte deficiencies
ride, the concentration of chloride tion of salicylates is another cause of treats diabetic ketoacidosis. Adminis-
should be greater than the sum of the an elevated anion gap acidosis in chil- tration of saline generally is adequate
sodium and potassium, and the net dren, although in adults and older treatment for alcoholic ketoacidosis.
charge should be negative. A positive children, stimulation of the respira- Therapy for lactic acidosis focuses on
net charge indicates impaired ammo- tory center causes primary respiratory restoring adequate tissue oxygen-
nium secretion and, therefore, im- alkalosis. ation and identifying and treating the
paired distal acidification. The use of Overdoses of ibuprofen (a nonste- underlying cause. Treatment of salic-
potassium-sparing agents may re- roidal anti-inflammatory agent and a ylate ingestion involves treating the
duce distal proton secretion. Treat- weak acid) and toluene inhalations underlying acidosis and promoting
ment of patients who have cirrhosis have been associated with a high an- an alkaline diuresis to enhance renal
with spironolactone has caused met- ion gap metabolic acidosis. Ethylene acid and salicylate excretion. In se-
abolic acidosis, which resolves with glycol (antifreeze), methanol (wood vere cases, dialysis may be required.
discontinuation of the spironolac- alcohol), and paraldehyde produce Management of ethylene glycol tox-
tone. acidic byproducts that cause a meta- icity consists of hemodialysis, which
bolic acidosis. These substances pro- removes both the substance and me-
ELEVATED ANION GAP duce an osmolar gap in addition to an tabolites from the serum, and etha-
When an elevated anion gap occurs anion gap. Serum osmolality is ap- nol administration, which competes
with an acidosis, the cause usually is proximated by the formula: Calcu- for alcohol dehydrogenase, resulting
increased organic acid production or lated serum osmolality⫽2 x [Na⫹] ⫹ in increased renal excretion. Re-
ingestion, inborn errors of metabo- glucose/18 ⫹ BUN/2.8. Unmea- cently, fomepizole, a potent inhibi-
lism, or decreased excretion of acid sured solutes such as ethylene glycol tor of alcohol dehydrogenase that re-
due to renal failure. Increased pro- and methanol are not included in this duces the generation of toxic
duction of acid may result in ketoac- formula and would account for an metabolites, has become available.
idosis and lactic acidosis. The over- osmolar gap (osmolal gap ⫽ Assuming an adequate ventilatory
production of ketoacids, such as measured osmolality ⫺ calculated os- response, a metabolic acidosis is se-
acetoacetic and hydroxybutyric ac- molality). Exogenous osmolal sub- vere when the serum bicarbonate
ids, causes the elevated anion gap. stances such as sulfates and concentration is 8 mEq/L (8 mmol/
Diabetic ketoacidosis often is seen phosphates result in a normal osmo- L) or less. With an increased anion
in children. Alcoholic ketoacidosis is lal gap of 10 mOsm/L. The osmolal gap acidosis, treatment of the under-
more common in adults, but can oc- gap must be used cautiously because lying disorder may correct the acido-
cur at any age. Alcoholic ketoacidosis a normal gap has an inadequate neg- sis within hours. In a normal anion
develops a few days after a prolonged ative predictive value. Massive inges- gap acidosis (hyperchloremic), sev-
alcoholic binge (when serum ethanol tion of creams containing propylene eral days may be required for correc-
levels frequently are normal). Keto- glycol, such as silver sulfadiazine, tion. With the low serum bicarbon-
acidosis also results from vomiting- may cause an increased anion gap ate of 4 mEq/L (4 mmol/L)
induced starvation, often presenting metabolic acidosis. The inability to described in the case report, hydra-
as abdominal pain. Lactic acidosis excrete hydrogen ions in acute or tion alone would be inadequate
causes an elevated anion gap, when chronic renal failure results in an ele- treatment. Exogenous sodium bicar-
administered to avoid a concurrent Suggested References Gluck SL. Acid-base. Lancet. 1998;352:
metabolic alkalosis. Supplemental Adrogue HJ, Horacio J, Madias NE. Med- 474 – 479
ical progress: management of life- Greenberg A. Diuretic complications. Am J
oxygen should be provided if hypox- Med Sci. 2000;319:10 –24
threatening acid-base disorders: second
emia is present. If the respiratory ac- of two parts. N Engl J Med. 1998;338: Hanna JD, Scheinman JI, Chan JM. The
idosis is severe, ventilatory support 107–111 kidney in acid-base balance. Pediatr
may be needed. Alkali therapy is not Adrogue HJ, Madias NE. Medical progress: Clin North Am. 1995;42:1365–1395
management of life-threatening acid- Khanna A, Kurtzman N. Metabolic alkalo-
used to treat a primary respiratory sis. Resp Care. 2001;46:354 –365
base disorders: first of two parts. N Engl
acidosis. Treatment of a respiratory J Med. 1998;338:26 –34 Narins RG, Emmett M. Simple and mixed
alkalosis also is directed at treatment Badrick T, Hickman E. The anion gap: a acid-base disorders: a practical approach.
of the underlying cause. Often, sim- reappraisal. Am J Clin Pediatr. 1992;98: Medicine. 1980;59:161–187
249 –252 Oh MS, Carrol HJ. Current concepts: the
ple observation or use of a rebreath- anion gap. N Engl J Med. 1977;297:
Chabali R. Diagnostic use of anion and os-
ing bag is adequate in hyperventila- molal gaps in pediatric emergency med- 814 – 817
tion syndrome. In the case of high- icine. Ped Emerg Care. 1997;13: Relman AS. Metabolic consequences of
altitude hypoxia (acute mountain 204 –210 acid-base disorders. Kidney Int. 1972;1:
Epstein SK, Singh N. Respiratory acidosis. 347–359
sickness), acetazolamide can be ad-
Resp Care. 2001;46:366 –383 Rose BD, Post TW. Clinical Physiology of
ministered prior to ascent to prevent Foster GT, Vaziri ND, Sasoon CS. Respira- Acid-Base and Electrolyte Disorders. 5th
or mitigate symptoms of respiratory tory alkalosis. Resp Care. 2001; 46: ed. New York, NY: McGraw-Hill; 2001;
alkalosis. 384 –391 328 –347
PIR Quiz
Quiz also available online at www.pedsinreview.org.
9. An 8-month-old Caucasian infant presents with a history of failure to gain weight for the past 4 months.
The infant was born after a term uncomplicated pregnancy. His birthweight was 3.5 kg. He always has
been a poor eater and tends to spit up formula frequently after feeding. Physical examination documents
the weight below the 3rd percentile, height at the 5th percentile, and head circumference at the 25th
percentile. Vital signs include: respiratory rate of 32 breaths/min, heart rate of 110 beats/min, and blood
pressure of 80/45 mm Hg. Other than poor subcutaneous fat, no abnormalities are noted. Laboratory
studies reveal: hemoglobin, 11 g/dL (110 g/L); sodium, 136 mEq/L (136 mmol/L); potassium, 4.0 mEq/L
(4.0 mmol/L); chloride, 112 mEq/L (112 mmol/L); and bicarbonate, 14 mEq/L (14 mmol/L). Venous blood
pH is 7.24 and PCO2 is 26 mm Hg. Blood urea nitrogen and serum creatinine concentrations are normal.
Urinalysis shows a pH of 7.0, specific gravity of 1.015, and no protein or glucose. Of the following, the
most likely diagnosis is:
A. Cystic fibrosis.
B. Gastroesophageal reflux.
C. Obstructive uropathy.
D. Organic acidemia.
E. Renal tubular acidosis. (continued)
10. A 2-year-old girl is brought to the emergency department after being found unconscious in the basement.
On physical examination, she is unresponsive to tactile and verbal stimuli except for withdrawal to pain.
Pupils are equal and reactive. Respirations are 30 breaths/min and deep, heart rate is 130 beats/min,
axillary temperature is 98.2°F (36.8°C), and blood pressure is 90/60 mm Hg. Laboratory studies show:
serum sodium, 138 mEq/L (138 mmol/L); potassium, 3.8 mEq/L (3.8 mmol/L); chloride, 94 mEq/L
(94 mmol/L); bicarbonate, 10 mEq/L (10 mmol/L); blood urea nitrogen, 14 mg/dL (5 mmol/L); blood
glucose, 72 mg/dL (4 mmol/L); serum osmolality, 330 mOsm/kg (330 mmol/kg); venous blood pH, 7.15;
and PCO2, 16 mm Hg. Of the following, the most likely diagnosis is:
A. Carbon monoxide poisoning.
B. Diabetic ketoacidosis.
C. Encephalitis.
D. Ethylene glycol ingestion.
E. Salicylate poisoning.
11. A 6-week-old male infant presents with vomiting and poor weight gain for the last 2 weeks. The
vomiting is described as forceful, and it occurs after every feeding. Physical examination reveals poor
subcutaneous fat. You palpate a 2 ⴛ 2-cm round mass to the right of the midline in the upper abdominal
region. Laboratory studies show: serum sodium, 128 mEq/L (128 mmol/L); potassium, 3.2 mEq/L
(3.2 mmol/L); chloride, 86 mEq/L (86 mmol/L); bicarbonate, 34 mEq/L (34 mmol/L); and calcium, 8.2 mg/
dL (8.2 mmol/L). Venous blood pH is 7.55. Measurement of urine electrolytes document sodium, 12 mEq/L
(12 mmol/L) and chloride, 8 mEq/L (8 mmol/L). Administration of which of the following is most likely to
correct alkalosis in this child?
A. Angiotensin-converting enzyme inhibitors.
B. Calcium chloride.
C. Hydrochlorothiazide.
D. Hydrocortisone.
E. Sodium and potassium chloride.
12. A 12-year-old girl who has steroid-dependent asthma presents with increasing respiratory difficulty for
12 hours. On physical examination, her respiratory rate is 30 breaths/min, heart rate is 160 beats/min, and
blood pressure is 80/50 mm Hg. She is unable to speak a full sentence and has severe suprasternal
retractions. Her extremities are cool, and capillary refill is poor. Chest auscultation reveals bilateral
inspiratory/expiratory wheezing with decreased air entry over the right hemithorax. Arterial blood gases
while receiving oxygen via a face mask reveal: pH, 7.1; PCO2, 50 mm Hg; PCO2, 50 mm Hg, and HCO3ⴚ,
15 mEq/L (15 mmol/L). Which of the following best describes this child’s acid-base disorder?
A. Combined metabolic and respiratory acidosis.
B. Metabolic acidosis with compensated respiratory alkalosis.
C. Metabolic acidosis without respiratory compensation.
D. Respiratory acidosis with compensated metabolic alkalosis.
E. Respiratory acidosis without metabolic compensation.
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