What are the typical presentation and management of a patient with contraction alkalosis?

Clinical Presentation of Contraction Alkalosis

Patients with contraction alkalosis typically present with symptoms of volume depletion (lightheadedness, weakness, orthostatic hypotension) combined with metabolic alkalosis, characterized by elevated serum bicarbonate and CO2 levels, along with hypochloremia and often hypokalemia. 1, 2

Key Clinical Features

Volume Status and Hemodynamic Findings

• Orthostatic symptoms including lightheadedness, dizziness, and cloudy judgment due to effective volume contraction 3
• Reduced plasma volume despite potential normal or near-normal body weight 4
• Blood pressure may be variable—can be elevated (if diuretic-induced hypertension is the cause) or low (if severe volume depletion) 3
• Signs of dehydration including decreased skin turgor, dry mucous membranes, and reduced urine output 5

Laboratory Abnormalities

The hallmark laboratory pattern includes: 1, 2

• Elevated serum bicarbonate (typically >30 mEq/L) and CO2 levels
• Hypochloremia (serum chloride often <95 mmol/L)
• Hypokalemia (serum potassium typically <3.5 mmol/L) 6
• Elevated arterial pH (>7.45) with compensatory respiratory acidosis 2
• Low urinary chloride (<20 mEq/L) in classic contraction alkalosis, distinguishing it from other causes 6

Neurological Manifestations

• Confusion, altered mental status, or cloudy judgment secondary to alkalemia 3
• Potential for seizures in severe cases due to decreased ionized calcium 7
• Paresthesias and muscle cramps from electrolyte disturbances 7

Gastrointestinal Symptoms

• Nausea and vomiting may be both a cause and consequence of the alkalosis 3
• Abdominal pain can occur, particularly in severe cases 3
• Decreased gastrointestinal motility due to hypokalemia 7

Respiratory Findings

• Compensatory hypoventilation with elevated PaCO2 to maintain pH homeostasis 2
• Dyspnea or difficulty breathing may be reported, though this seems paradoxical given the alkalosis 3
• Respiratory rate is typically reduced as a compensatory mechanism 7

Common Clinical Scenarios

Diuretic-Induced Contraction Alkalosis

The most common presentation involves: 1, 2

• Recent or ongoing loop or thiazide diuretic therapy
• Progressive volume contraction with chloride depletion
• Activation of the renin-angiotensin-aldosterone system
• Enhanced distal tubular hydrogen ion secretion despite systemic alkalosis

Vomiting-Related Alkalosis

• History of persistent vomiting with loss of gastric hydrochloric acid 8
• Volume depletion from fluid losses
• Paradoxical aciduria (acid urine despite alkalemic blood) due to volume contraction 1

Bartter Syndrome Presentation

In genetic salt-wasting tubulopathies, patients present with: 5

• Polyuria and polydipsia from impaired urinary concentrating ability
• Failure to thrive and growth retardation in children
• History of polyhydramnios and premature birth (important historical clue) 6
• Persistent hypokalemic metabolic alkalosis despite treatment
• Elevated urinary chloride (>20 mEq/L) despite volume depletion, distinguishing it from contraction alkalosis 1
• Hypercalciuria and potential nephrocalcinosis in certain subtypes 5

Paradoxical Aciduria

A critical diagnostic feature is paradoxical aciduria—the presence of acid urine (pH <6.0) despite systemic alkalosis: 1

• Occurs due to volume depletion driving enhanced sodium reabsorption in the distal tubule
• Aldosterone activation increases hydrogen ion secretion to maintain electrical neutrality
• This phenomenon helps distinguish volume-responsive (contraction) alkalosis from other causes

Cardiovascular Manifestations

• Cardiac arrhythmias, particularly in the setting of severe hypokalemia 5
• Decreased cardiac output in severe cases 9
• Increased risk of digitalis toxicity if patient is on cardiac glycosides 7

Critical Pitfall to Recognize

The severity of symptoms does not always correlate with the degree of alkalemia—patients may have profound metabolic alkalosis (pH >7.55) with relatively mild symptoms, or conversely, significant symptoms with moderate alkalosis. 8 The rate of development matters more than the absolute values, with acute alkalosis causing more severe symptoms than chronic, compensated states. 7

The key to diagnosis is recognizing the triad of volume depletion, hypochloremic hypokalemic metabolic alkalosis, and low urinary chloride (<20 mEq/L), which distinguishes chloride-responsive contraction alkalosis from chloride-resistant causes. 1, 2