eMedicine Specialties > Pediatrics: Cardiac Disease and Critical Care Medicine > Critical Care

Alkalosis, Metabolic

Lennox H Huang, MD, Associate Clinical Chair, Assistant Professor, Department of Pediatrics, McMaster University; Deputy Chief of Pediatrics, McMaster Children's Hospital
Margaret A Priestley, MD, Assistant Professor of Clinical Anesthesiology and Critical Care, University of Pennsylvania School of Medicine; Clinical Director, Pediatric Intensive Care Unit, The Children's Hospital of Philadelphia

Updated: Aug 13, 2008

Introduction

Background

Metabolic alkalosis is an acid-base disturbance caused by an elevation in plasma bicarbonate (HCO₃) concentration. This condition is not a disease; it is a sign or state encountered in certain disease processes. Although metabolic alkalosis may not be referred to as often as metabolic acidosis, it is the most common acid-base abnormality in hospitalized adults. Alkalosis refers to a loss of acid or gain of base in the extracellular fluid (ECF); alkalemia refers to a change in blood pH. Alkalosis is not necessarily accompanied by alkalemia.

The 2 types of metabolic alkalosis (ie, chloride-responsive, chloride-resistant) are classified based on the amount of chloride in the urine.

Chloride-responsive metabolic alkalosis involves urine chloride levels of less than 10 mEq/L and is characterized by decreased ECF volume and low serum chloride levels, such as occurs with vomiting. This type responds to administration of chloride salt.

Chloride-resistant metabolic alkalosis involves urine chloride levels of more than 20 mEq/L and is characterized by increased ECF volume. As the name implies, this type resists administration of chloride salt. Primary aldosteronism is an example of chloride-resistant metabolic alkalosis.

Pathophysiology

In most cases, metabolic alkalosis is caused by loss of hydrochloric acid (HCl) through the kidney or GI tract, especially due to vomiting. Occasionally, the condition is caused by disproportionate loss of chloride. Metabolic alkalosis is rarely caused by actual gain from administered HCO₃.

Other causes of metabolic alkalosis include (1) loss of hydrogen ions (eg, due to vomiting or renal acid losses that exceed acid production from cellular metabolism), (2) disproportionate chloride loss compared with HCO₃ loss (ie, the plasma concentration of HCO₃ increases upon restriction to a smaller space of distribution), and (3) HCO₃ administration (unusual because additional HCO₃ is very quickly eliminated by the kidneys).

The consequences of metabolic alkalosis on organ systems depend on the severity of the alkalemia and the degree of respiratory compensation. If the elevated plasma HCO₃ concentration is not accompanied by a rise in PCO₂, the elevation of pH is much more severe.

• Effects of severe alkalemia
  • Respiratory: An increase in blood pH shifts the oxygen-hemoglobin dissociation curve to the left. This creates a tighter bond between hemoglobin and oxygen, causing decreased oxygen delivery to tissues. Hypoxemia is worsened by a compensatory hypoventilation to elevate PCO₂. Hypoventilation may be severe enough to cause apnea and respiratory arrest.
  • Cardiovascular system: Life-threatening arrhythmias are the most significant adverse effect of metabolic alkalosis. Direct arteriolar constriction is further worsened by electrolyte disturbances. Ventricular and supraventricular arrhythmias that are often unresponsive to antiarrhythmic agents can occur.
  • Neuromuscular system: Patients with severe metabolic alkalosis can develop headache, seizures, and obtundation and marked muscle weakness that resolve only with correction of the pH.
  • Electrolytes: Metabolic alkalosis may cause a decrease in ionized calcium levels due to increased binding of calcium to plasma proteins; consequences include tetany and seizures. Total-body potassium loss may contribute to alkalemia, and serum potassium is intracellularly shifted in alkalemia. Weakness and cardiac arrhythmias may result from severe hypokalemia.
  • Other effects: Metabolic alkalosis may also increase lactic acid production by stimulating the action of phosphofructokinase, with conversion of fructose-6-phosphate to fructose-1,6-diphosphate. Alkalemia also increases renal tubular reabsorption of calcium, resulting in decreased renal excretion.
• Compensation mechanisms
  • Buffering of excess HCO₃: Intracellular buffering occurs through sodium/hydrogen and potassium/hydrogen ion exchange, with eventual formation of CO₂ and water from HCO₃.
  • Hypoventilation: Within several hours, elevated levels of HCO₃ and metabolic alkalosis stimulate a chemoreceptor inhibition of the respiratory center, resulting in hypoventilation and increased PCO₂ levels. This mechanism produces a rise in PCO₂ of as much as 0.7 mm Hg for each 1-mEq/L increase in HCO₃. Hypoventilation may cause hypoxemia.

Frequency

United States

Because metabolic alkalosis is a manifestation of a disease process rather than a disease itself, the incidence is unknown. In a review of 2000 hospitalized adults, Hodgkin et al noted that metabolic alkalosis was the most common acid-base disorder.¹

Mortality/Morbidity

Severe metabolic alkalosis is associated with increased morbidity and mortality, probably because of its profound influences on multiple organ systems and, more importantly, because of tissue anoxia caused by hypoventilation and shift of the oxygen-dissociation curve to the left.

Race

No racial predilection has been reported.

Sex

Incidence is equal in males and females.

Age

Metabolic alkalosis can occur in people of any age. A higher incidence of metabolic alkalosis after cardiac surgery in younger children has been reported.

Clinical

History

Obtain historical data to pinpoint the nature of the disease causing metabolic alkalosis.

• Ask the patient about history of vomiting, other gastric fluid loss, and diuretic use. Loss of gastric fluid and HCl due to vomiting is the most common cause of metabolic alkalosis.
  • Vomiting may be caused by pyloric stenosis or ulcers. Occasionally, it may be self-induced.
  • Significant gastric fluid loss can occur via long-term nasogastric (NG) tube drainage.
  • Diuretic use may lead to increased chloride losses.
• Obtain information about specific disease states such as primary hyperaldosteronism, reninism, hyperglucocorticoidism, Bartter syndrome, and deoxycorticosterone (DOC) excess syndromes.
• Because hypokalemia may lead to metabolic alkalosis, ask about the use of diuretics because these lead to potassium loss.

Physical

Increased neuromuscular excitability sometimes causes tetany or seizures. Generalized weakness may be noted if the patient also has hypokalemia. Signs and symptoms observed with metabolic alkalosis usually relate to the specific disease process that caused the acid-base disorder.

• Patients who develop metabolic alkalosis from vomiting can have symptoms related to severe volume contraction, with signs of dehydration that include tachycardia, dry mucous membranes, decreased skin turgor, postural hypotension, poor peripheral perfusion, and weight loss.
• Although diarrhea typically produces a hyperchloremic metabolic acidosis, diarrheal stools may rarely contain significant amounts of chloride, as in the case of congenital chloride diarrhea. Children with this condition present at birth with watery diarrhea, metabolic alkalosis, and hypovolemia.
• Weight gain and hypertension may accompany metabolic alkalosis that results from a hypermineralocorticoid state.

Causes

• Chloride-responsive type
  • Gastric fluid loss (eg, vomiting, NG drainage)
  • Volume contraction (eg, secondary to loop or thiazide diuretics)
  • Congenital chloride diarrhea
  • Posthypercapnia syndrome (especially in mechanically ventilated patients with chronic lung disease)
  • Cystic fibrosis (in toddlers)
• Chloride-resistant type
  • Primary aldosteronism
  • Bartter syndrome (renal sodium, potassium, and chloride wasting; often presents as failure to thrive)
  • DOC excess syndrome (congenital adrenal hyperplasia variant)
  • Liddle syndrome (autosomal dominant; unregulated sodium resorption in renal collecting duct)
  • Excessive ingestion of licorice
  • Chronic potassium depletion (eg, anorexia nervosa)
  • Primary reninism
  • Hyperglucocorticoidism
  • Milk-alkali syndrome (excess calcium plus bicarbonate intake and vomiting)
• Further discussion
  • Gastric losses (eg, vomiting, NG drainage): One mEq of HCO₃ is generated in response to each mEq of hydrogen ion produced by the gastric mucosa. Although this can generate a large amount of HCO₃, it is counteracted by the gastric stimulation of the pancreas to produce HCO₃. When gastric acid is removed by suctioning or lost through vomiting, the stimulus for the pancreas is lost, thus allowing plasma HCO₃ levels to increase. In addition, the loss of potassium and volume contraction due to vomiting potentiate metabolic alkalosis.
  • Diuretics: This class of drugs produces increased renal losses of sodium, which is followed by excretion of chlorides. To maintain electrical neutrality in the ECF, HCO₃ reabsorption in renal tubules increases. Additionally, increased sodium in the distal tubules increases sodium-potassium exchange. The loss of potassium, in turn, leads to intracellular accumulation of hydrogen ions and its secretion in the distal tubules. Diuretics also promote the loss of magnesium in the urine, which further lowers potassium levels through an unknown mechanism.
  • Decrease in ECF volume (ie, volume contraction): Volume contraction concentrates the existing levels of HCO₃ and stimulates release of renin-angiotensin, which causes increased potassium and hydrogen ion losses in the kidney.
  • Posthypercapnia syndrome: Chronic CO₂ retention causes a compensatory increase in HCO₃ levels. Metabolic alkalosis becomes evident when a patient with chronic CO₂ retention receives treatment that abruptly drops the CO₂ level.

Differential Diagnoses

Alkalosis, Metabolic
Bartter Syndrome
Cystic Fibrosis
Pyloric Stenosis, Hypertrophic

Other Problems to Be Considered

Liddle syndrome
Primary aldosteronism
Hyperglucocorticoidism
DOC excess syndromes
Gastric fluid losses
Potassium depletion
Congenital chloride diarrhea

Workup

Laboratory Studies

• Measurement of blood gas and serum electrolyte levels, including calcium, are the essential laboratory studies necessary for initial evaluation of metabolic alkalosis. Blood gas measurement shows elevated pH with a high HCO₃ level. With compensation, the PCO₂ level may also be near the reference range or elevated. Serum electrolyte levels may show evidence of hypokalemia, hypercalcemia, hypochloremia, or hyponatremia.
• Spot urine chloride
  • Urine chloride level of less than 10 mEq/L indicates chloride-responsive metabolic alkalosis.
  • Urine chloride level of more than 20 mEq/L indicates chloride-resistant metabolic alkalosis.
• Diagnostic indicators for specific disease states
  • Primary aldosteronism - Metabolic alkalosis, hypokalemia, urine chloride level of more than 20 mEq/L, persistently elevated aldosterone levels despite controlled sodium chloride (NaCl) intake of 12-15 g daily for 5 days
  • Cushing syndrome - Hypersecretion of cortisol
  • Primary reninism - Usually results from renovascular disease with hypertension
  • Bartter syndrome - Hypokalemic metabolic alkalosis with secondary hyperaldosteronism and with renal potassium and chloride wasting
  • Milk-alkali syndrome - Excessive oral intake of calcium, vitamin D metabolites, and absorbable alkali (Metabolic alkalosis is usually accompanied by hypercalcemia.)
  • Pyloric stenosis - Marked hypochloremia (due to loss of HCl in gastric contents) and metabolic alkalosis, generally observed in male infants aged approximately 6-12 weeks (Children present with protracted vomiting and frequently have significant dehydration and cachexia.)

Treatment

Medical Care

Mild or moderate metabolic alkalosis or alkalemia rarely requires correction. For severe metabolic alkalosis, therapy should address the underlying disease state, in addition to moderating the alkalemia. As with correction of any electrolyte or acid-base imbalance, the goal is to prevent life-threatening complications with the least amount of correction. The initial target pH and bicarbonate level in correcting severe alkalemia is approximately 7.55 mmol/L and 40 mmol/L, respectively, not values within the reference range.

• Consider the severity of hypovolemia or hypokalemia and the degree of alkalosis when managing metabolic alkalosis due to chloride loss from vomiting or other GI losses.
• Children with protracted vomiting, whether due to pyloric stenosis or other causes, may develop hypovolemic shock. Intravascular volume expansion with isotonic crystalloid solution is needed, and monitoring of central venous pressure to determine adequacy of volume resuscitation may be indicated.
• Administer potassium as a chloride salt to patients with hypokalemia to help replenish chloride losses. However, remember that using potassium chloride (KCl) alone to correct hypochloremia is limited because the KCl infusion rate cannot exceed prescribed safe levels.
• For persistent severe metabolic alkalosis, administration of HCl or ammonium chloride (NH₄ Cl) may be considered.
• Acetazolamide may help patients with chloride-resistant metabolic alkalosis and has been safely used for treatment of diuretic induced metabolic alkalosis in pediatric cardiac patients.^2,3
• Correction of metabolic alkalosis in patients with renal failure may require hemodialysis or continuous renal replacement therapy with a dialysate that contains high levels of chloride and low levels of HCO₃.
• Temporary discontinuation of chloruretic diuretics (eg, furosemide, bumetanide, ethacrynic acid) may help patients with metabolic alkalosis due to long-term diuretic use. Potassium-sparing diuretics and carbonic anhydrase inhibitors may be used in patients who require continued diuretic therapy. Patients with accompanying ECF volume contraction occasionally require sodium and potassium administration. If continued diuretic use is indicated, potassium salt supplements may help avoid metabolic alkalosis.
• Manage the specific disease that led to metabolic alkalosis.

Surgical Care

Children with pyloric stenosis require surgical intervention (pyloromyotomy) following intravascular fluid expansion and correction of metabolic abnormalities.

Consultations

Severe alkalemia should be initially managed in an ICU setting under the direction of a pediatric intensivist. Subsequent consultations should be obtained with specific specialists (eg, endocrinologist, nephrologist) to manage the underlying etiology responsible for the metabolic alkalosis.

Diet

Tailor dietary changes to the underlying disease.

Medication

Metabolic alkalosis that results from chloride depletion and volume contraction can often be corrected with volume replacement, but persistent severe metabolic alkalosis may require more specific therapy directed at moderating the alkalemia.

Chloride solutions

These solutions are the recommended therapeutic agents for rapid correction of severe metabolic alkalosis, especially metabolic alkalosis due to gastric losses of chloride.

Hydrochloric acid (HCl)

Amount required to correct metabolic alkalosis is determined by estimating the amount of pH deficit, the volume, and the infusion rate of HCl solution.
IV HCl may be indicated in severe metabolic alkalosis (pH >7.55) or when NaCl or KCl cannot be administered because of volume overload or advanced renal failure. May also be indicated if rapid correction of severe metabolic alkalosis is warranted (eg, cardiac arrhythmia, hepatic encephalopathy, digoxin toxicity).
Typical preparation contains 0.1 N solution (ie, 100 mmol H⁺/L [mEq/L]) in D5W or 0.9% NaCl).

Dosing

Adult

IV via central venous catheter: H⁺ ion deficit (mEq) = 0.3 X weight (kg) X (measured HCO₃ - desired HCO₃ [mEq/L])
Rate of H⁺ replacement: 0.1-0.2 mEq/kg/h
For example, 0.1 N solution IV at 100 mL/h provides about 10 mEq/h

Pediatric

Not established, limited data have been reported

Interactions

None reported

Contraindications

Lack of central venous access

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Do not use HCl solutions with concentrations >0.2 N (increased venous irritation and potential hemolysis); concentrations >0.1 N have been reported to cause corrosive effects, even when administered through a central venous catheter; injection of HCl into a peripheral vein may cause extravasation and can produce severe tissue necrosis; monitor ABGs and serum electrolyte levels

Ammonium chloride (NH4Cl)

Administer to correct severe metabolic alkalosis related to chloride deficiency. NH₄ Cl is converted to ammonia and HCl by the liver. By releasing HCl, NH₄ Cl may help correct metabolic alkalosis.
Available as 500-mg tabs and 26.75% parenteral for IV use. Parenteral contains 5 mEq/mL (267.5 mg/mL).

Dosing

Adult

8-12 g/d PO divided q6h
1.5 g IV q6h; dilute solution to concentration <0.4 mEq/mL; not to exceed infusion rate of 1 mEq/kg/h

Pediatric

75 mg/kg/d PO/IV divided q6h; not to exceed 6 g/d and an infusion rate of 1 mEq/kg/h; dilute solution to concentration <0.4 mEq/mL

Interactions

May reduce levels of aspirin, chlorpropamide, ephedrine, methadone, pseudoephedrine, spirolactone, and para-aminosalicylic acid (PSA)

Contraindications

Hepatic or renal failure

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Use with extreme caution in infants; may produce acidosis and hyperammonemia with encephalopathy; may cause GI irritation; monitor chloride levels, serum ammonia levels, and acid-base status

Potassium chloride (Clor-Con, K-Tab, K-Dur)

Essential for transmission of nerve impulses, contraction of cardiac muscle, and maintenance of intracellular tonicity, skeletal and smooth muscles, and normal renal function.

Dosing

Adult

20-120 mEq PO qd
Up to 20 mEq/dose IV; dilute in >500 mL IV fluid for peripheral line infusion or >100 mL for central line infusion; not to exceed administration rate of 10 mEq/h unless cardiac monitoring in place

Pediatric

0.5-1 mEq/kg/dose IV; dilute in adequate IV fluid before administering by either peripheral or central IV; not to exceed administration rate of 10 mEq/h unless cardiac monitoring in place; may be prudent to not exceed 10 mEq in any one total dose, regardless if per Kg calculation indicates higher dose; recheck level, and administer additional dose as needed

Interactions

Concurrent use with ACE inhibitors may result in elevated serum potassium concentrations; potassium-sparing diuretics and potassium-containing salt substitutes can produce severe hyperkalemia; caution if discontinuing potassium administration in patients maintained on digoxin (hypokalemia may result in digoxin toxicity)

Contraindications

Hyperkalemia; renal failure; conditions in which potassium retention is present; oliguria or azotemia; crush syndrome; severe hemolytic reactions; anuria; adrenocortical insufficiency

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Do not rapidly infuse; high plasma concentrations of potassium may cause death due to cardiac depression, arrhythmias, or arrest; plasma levels do not necessarily reflect tissue levels; monitor potassium replacement therapy whenever possible by continuous or serial ECG; when a concentration >40 mEq/L is infused, local pain and phlebitis may also follow

Carbonic anhydrase inhibitors

These agents may be used to treat chloride-resistant metabolic alkalosis.

Acetazolamide (Diamox)

A carbonic anhydrase inhibitor that blocks HCO₃ reabsorption in the proximal renal tubules. A recent study demonstrated that acetazolamide causes increased renal excretion of sodium vs chloride, causing a net increase in serum chloride. Acetazolamide is also a diuretic and, therefore, may help decrease ECF volume that frequently accompanies chloride-resistant metabolic alkalosis.

Dosing

Adult

5-10 mg/kg/d PO/IV divided q6h

Pediatric

5 mg/kg PO qd/qod
8-30 mg/kg/d IV/IM divided q6-8h; not to exceed 1 g/d

Interactions

Can decrease therapeutic levels of lithium and alter excretion of drugs (amphetamines, quinidine, phenobarbital, salicylates) by alkalinizing urine

Contraindications

Documented hypersensitivity; hepatic disease; severe renal disease; adrenocortical insufficiency; severe pulmonary obstruction

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution with respiratory acidosis and diabetes mellitus (may increase blood glucose); IM administration is painful

Follow-up

Further Inpatient Care

• Severe metabolic alkalemia should be monitored in an ICU setting with full noninvasive cardiopulmonary monitoring. Invasive monitoring and specialized vascular access may be necessary, depending on the overall clinical picture.
• Monitor serum electrolyte levels and acid-base status when providing treatment for metabolic alkalosis, particularly when using chloride salts.
• Provide follow-up care specific to the disease that caused metabolic alkalosis.

Further Outpatient Care

• Outpatient care depends on the underlying disease process.

Transfer

• The role of a pediatric tertiary care center where appropriate subspecialists are available in the care of a child with metabolic alkalosis cannot be overemphasized.
• If the patient requires dialysis or has a renal disease, such as Bartter syndrome, transfer the patient to a nephrologist.
• An endocrinologist should manage primary aldosteronism and mineralocorticoid excess states.
• Children who develop hypovolemic shock or those with persistent severe and symptomatic metabolic alkalosis are best monitored in a critical care setting.

Deterrence/Prevention

• Metabolic alkalosis may be avoided by judicious use of long-term diuretics with appropriate monitoring.

Complications

• Severe metabolic alkalosis can lead to hypoventilation; the resultant hypoxemia is compounded by a shift of the oxygen-hemoglobin dissociation curve to the left. In extreme cases, hypoventilation may be severe enough to require mechanical ventilation or to interfere with weaning from existing mechanical ventilation.
• Metabolic alkalosis can also lead to neuromuscular excitability and, if accompanied by hypocalcemia, can result in tetany, seizures, and life-threatening ventricular arrhythmias.
• Intracellular shift of potassium in severe alkalemia may lead to life-threatening arrhythmias or cardiac arrest.

Prognosis

• Overall prognosis depends on the underlying etiology.
• Chloride-responsive metabolic alkalosis responds to volume resuscitation and chloride repletion.
• Chloride-resistant metabolic alkalosis may be more difficult to control. Prognosis is good with prompt treatment and avoidance of hypoxemia.

Patient Education

• Educate patients placed on long-term diuretic therapy and those with diseases that can lead to metabolic alkalosis to recognize the symptoms of moderate-to-severe alkalosis; this knowledge allows them to promptly seek medical care.

Miscellaneous

Medicolegal Pitfalls

• Failure to realize that severe metabolic alkalosis can lead to hypoventilation that may result in hypoxemia could delay treatment and result in hypoxic damage.
• Physicians must be familiar with the complications associated with the use of chloride salts to treat severe metabolic alkalosis. Hydrochloric acid can cause severe tissue necrosis if the solution extravasates into the tissues. In addition, use of high concentrations (ie, >0.1 N) of HCl can corrode central veins and venous catheters.
• Use of NH₄ Cl can result in hyperammonemia and encephalopathy.
• Carefully weigh use of chloride salts against risks. Use chloride salts only when absolutely necessary.

References

1. Hodgkin JE, Soeprono FF, Chan DM. Incidence of metabolic alkalemia in hospitalized patients. Crit Care Med. Dec 1980;8(12):725-8. [Medline].

2. Moviat M, Pickkers P, van der Voort PH, van der Hoeven JG. Acetazolamide-mediated decrease in strong ion difference accounts for the correction of metabolic alkalosis in critically ill patients. Crit Care. Feb 2006;10(1):R14. [Medline].

3. Moffett BS, Moffett TI, Dickerson HA. Acetazolamide therapy for hypochloremic metabolic alkalosis in pediatric patients with heart disease. Am J Ther. Jul-Aug 2007;14(4):331-5. [Medline].

4. Adrogue HJ, Madias NE. Management of life-threatening acid-base disorders. Second of two parts. N Engl J Med. Jan 8 1998;338(2):107-11. [Medline].

5. Finberg L, Kravath RE, Hellerstein S. Metabolic Alkalosis. In: Water and Electrolytes in Pediatrics: Physiology, Pathophysiology, and Treatment. Philadelphia, Pa: WB Saunders; 1993:97-98.

6. Galla JH. Metabolic alkalosis. J Am Soc Nephrol. Feb 2000;11(2):369-75. [Medline].

7. Kokko JP, Tannen RL, eds. Metabolic Alkalosis. In: Fluids and Electrolytes. 1990. Philadelphia, Pa: WB Saunders; 356-376.

8. Maxwell MH, Kleeman CR, eds. Metabolic Alkalosis. In: Clinical Disorders of Fluid and Electrolyte Metabolism. New York, NY: McGraw-Hill; 1994:213-220.

9. Naka T, Bellomo R. Bench-to-bedside review: treating acid-base abnormalities in the intensive care unit--the role of renal replacement therapy. Crit Care. Apr 2004;8(2):108-14. [Medline].

10. Omron EM. Metabolic alkalosis and cystic fibrosis. Chest. Mar 2004;125(3):1169; author reply 1169-70. [Medline].

11. Palmer BF, Alpern RJ. Metabolic alkalosis. J Am Soc Nephrol. Sep 1997;8(9):1462-9. [Medline].

12. Shapiro BA, Harrison RA, Cane RD. Clinical application of blood gases. St. Louis, Mo: Mosby; 1989.

13. Siberry GK, Iannone R. Formulary. In: The Harriet Lane Handbook: A Manual for Pediatric House Officers. St. Louis, Mo: Mosby; 2000:616, 629.

14. van Thiel RJ, Koopman SR, Takkenberg JJ, Ten Harkel AD, Bogers AJ. Metabolic alkalosis after pediatric cardiac surgery. Eur J Cardiothorac Surg. Aug 2005;28(2):229-33. [Medline].

15. [Best Evidence] Wiedemann HP, Wheeler AP, Bernard GR, Thompson BT, Hayden D, deBoisblanc B, et al. Comparison of two fluid-management strategies in acute lung injury. N Engl J Med. Jun 15 2006;354(24):2564-75. [Medline].

16. Wong HR, Chundu KR. Metabolic alkalosis in children undergoing cardiac surgery. Crit Care Med. Jun 1993;21(6):884-7. [Medline].

Keywords

metabolic alkalosis, plasma bicarbonate, HCO₃, acid-base abnormality, metabolic acidosis, chloride-responsive metabolic alkalosis, chloride-resistant metabolic alkalosis, primary aldosteronism, hypoxemia, arteriolar constriction, hypokalemia, vomiting, pyloric stenosis, primary hyperaldosteronism, reninism, hyperglucocorticoidism, Bartter syndrome, deoxycorticosterone excess syndromes, hypertension, hypermineralocorticoid state, cystic fibrosis, primary aldosteronism, Liddle syndrome, anorexia nervosa, hyperglucocorticoidism, milk-alkali syndrome, hypercalcemia, hypochloremia, hyponatremia

Contributor Information and Disclosures

Author

Lennox H Huang, MD, Associate Clinical Chair, Assistant Professor, Department of Pediatrics, McMaster University; Deputy Chief of Pediatrics, McMaster Children's Hospital
Lennox H Huang, MD is a member of the following medical societies: American Academy of Pediatrics, Canadian Medical Association, Ontario Medical Association, and Society of Critical Care Medicine
Disclosure: Nothing to disclose.

Coauthor(s)

Margaret A Priestley, MD, Assistant Professor of Clinical Anesthesiology and Critical Care, University of Pennsylvania School of Medicine; Clinical Director, Pediatric Intensive Care Unit, The Children's Hospital of Philadelphia
Margaret A Priestley, MD is a member of the following medical societies: American Academy of Pediatrics, American Medical Association, and Society of Critical Care Medicine
Disclosure: Nothing to disclose.

Medical Editor

G Patricia Cantwell, MD, Associate Clinical Professor, Department of Pediatrics, University of Miami; Director of Pediatric Critical Care Medicine, Miller School of Medicine, Jackson Children's Hospital
G Patricia Cantwell, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Emergency Physicians, American Heart Association, American Trauma Society, National Association of EMS Physicians, Society of Critical Care Medicine, and Wilderness Medical Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from broker recommendation; Avanir Pharma Stock Investment from broker recommendation

Managing Editor

Barry J Evans, MD, Assistant Professor of Pediatrics, Temple University Medical School; Director of Pediatric Critical Care and Pulmonology, Associate Chair for Pediatric Education, Temple University Children's Medical Center
Barry J Evans, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Chest Physicians, American Thoracic Society, and Society of Critical Care Medicine
Disclosure: Nothing to disclose.

CME Editor

Mary E Cataletto, MD, Associate Director, Division of Pediatric Pulmonology, Winthrop University Hospital; Professor of Clinical Pediatrics, State University of New York at Stony Brook; Director of Children's Sleep Services, Winthrop University Hospital
Mary E Cataletto, MD is a member of the following medical societies: American Academy of Pediatrics and American College of Chest Physicians
Disclosure: Shering Plough Pharmaceuticals Honoraria Consulting

Chief Editor

Timothy E Corden, MD, Associate Professor of Pediatrics, Co-Director, Policy Core, Injury Research Center, Medical College of Wisconsin; Associate Director, PICU, Children's Hospital of Wisconsin
Timothy E Corden, MD is a member of the following medical societies: American Academy of Pediatrics, Phi Beta Kappa, Society of Critical Care Medicine, and Wisconsin Medical Society
Disclosure: Nothing to disclose.

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