Is vomiting responsible for the high bicarbonate, low chloride, elevated anion gap, and increased creatinine in this patient?

Vomiting Can Cause High Bicarbonate and Low Chloride, But Does NOT Explain the Elevated Anion Gap and Creatinine

Vomiting produces hypochloremic metabolic alkalosis (high bicarbonate, low chloride), but the presence of an elevated anion gap indicates a concurrent high anion gap metabolic acidosis from a separate process—most likely diabetic ketoacidosis, lactic acidosis, uremic acidosis, or toxic ingestion—while the elevated creatinine reflects acute kidney injury from volume depletion. 1

Understanding the Acid-Base Picture

What Vomiting Actually Causes

• Vomiting causes loss of gastric hydrochloric acid (HCl), resulting in hypochloremic metabolic alkalosis characterized by elevated bicarbonate (>26 mmol/L), low chloride, and elevated pH. 1, 2
• The kidneys normally correct metabolic alkalosis by excreting excess bicarbonate, but volume depletion from vomiting impairs this mechanism, causing the alkalosis to persist. 1
• Severe protracted vomiting can cause volume depletion leading to prerenal acute kidney injury with elevated creatinine, as demonstrated in cases where creatinine normalized after saline resuscitation. 3

The Problem: Elevated Anion Gap

• An elevated anion gap (>12 mEq/L) indicates accumulation of unmeasured anions such as ketoacids, lactate, uremic toxins, or ingested toxins—none of which are caused by vomiting itself. 4, 5
• When a patient presents with both metabolic alkalosis (from vomiting) AND an elevated anion gap, this represents a mixed acid-base disorder requiring identification of the high anion gap acidosis source. 6
• The anion gap is calculated as Na⁺ − (Cl⁻ + HCO₃⁻), with normal values of 10–12 mEq/L. 5

Diagnostic Algorithm for This Patient

Step 1: Confirm the Mixed Disorder

• Obtain arterial or venous blood gas to measure pH and PaCO₂; venous pH is acceptable and typically 0.03 units lower than arterial. 5, 7
• Calculate the expected bicarbonate from the anion gap: for every 1 mEq/L increase in anion gap above 12, bicarbonate should decrease by approximately 1 mEq/L in pure high anion gap acidosis. 5
• If the measured bicarbonate is higher than expected from the anion gap calculation, a concurrent metabolic alkalosis (from vomiting) is present. 1, 6

Step 2: Identify the High Anion Gap Acidosis Source

In a patient with diabetes (controlled or not):

• Measure serum and urine ketones, specifically beta-hydroxybutyrate, to evaluate for diabetic ketoacidosis (DKA). 8, 7
• DKA can occur with relatively normal glucose levels (euglycemic DKA), especially in patients taking SGLT2 inhibitors. 7
• DKA diagnostic criteria include glucose >250 mg/dL (or lower with SGLT2 inhibitors), pH <7.3, bicarbonate <18 mEq/L, positive ketones, and anion gap >10 mEq/L. 8

In all patients:

• Measure serum lactate to evaluate for lactic acidosis from tissue hypoperfusion, sepsis, or medications. 4, 7
• Assess renal function with BUN and creatinine; chronic kidney disease with GFR <30 mL/min can cause uremic acidosis. 5, 7
• If toxic ingestion is suspected (history, osmolar gap >10), measure serum osmolality and consider ethylene glycol, methanol, or salicylate levels. 4

Step 3: Assess Volume Status and Renal Function

• Elevated creatinine with BUN/creatinine ratio >20:1, orthostatic hypotension, decreased skin turgor, and dry mucous membranes indicate prerenal acute kidney injury from volume depletion. 5, 3
• Volume depletion from vomiting impairs renal bicarbonate excretion (maintaining the alkalosis) and reduces GFR (worsening any uremic acidosis). 3, 1

Management Approach

Immediate Resuscitation

• Administer isotonic saline (0.9% NaCl) at 15–20 mL/kg/h during the first hour to restore intravascular volume and renal perfusion. 4, 8
• After initial resuscitation, switch to balanced crystalloids (Lactated Ringer's or Plasma-Lyte) to avoid iatrogenic hyperchloremic acidosis from continued normal saline. 5
• Monitor urine output; once established, add potassium chloride 20–30 mEq/L to IV fluids if serum potassium >3.3 mEq/L. 4, 8

Treat the High Anion Gap Acidosis

If DKA is confirmed:

• Start continuous IV regular insulin at 0.1 units/kg/h after confirming serum potassium >3.3 mEq/L. 8
• Bicarbonate therapy is NOT indicated unless pH <6.9–7.0; the mixed picture with concurrent alkalosis makes bicarbonate even less appropriate. 4, 8
• Monitor venous pH and anion gap every 2–4 hours; resolution criteria are glucose <200 mg/dL, bicarbonate ≥18 mEq/L, and pH ≥7.3. 8

If lactic acidosis is present:

• Focus on restoring tissue perfusion with fluid resuscitation and vasopressors if needed; sodium bicarbonate is not recommended for lactic acidosis from sepsis. 5

If uremic acidosis from acute kidney injury:

• Volume resuscitation typically improves prerenal AKI; if creatinine remains elevated after adequate hydration, consider nephrology consultation. 3

Address the Vomiting

• Control vomiting with antiemetics (ondansetron, metoclopramide) and H₂ blockers or proton pump inhibitors to reduce gastric acid production. 9
• Investigate the underlying cause of vomiting (gastritis, obstruction, medication side effect, pregnancy). 3
• In cases of severe refractory vomiting with structural abnormalities (pyloric stenosis, duodenal scarring), surgical correction may be necessary. 3

Common Pitfalls to Avoid

• Do not assume vomiting explains the entire clinical picture when an elevated anion gap is present; this represents a dangerous mixed disorder requiring urgent evaluation. 6
• Do not administer bicarbonate therapy for the high anion gap acidosis when concurrent metabolic alkalosis is present; treat the underlying cause instead. 5, 8
• Do not continue normal saline beyond initial resuscitation, as large-volume 0.9% NaCl can worsen hyperchloremic acidosis and impair renal function. 5
• Do not overlook euglycemic DKA in diabetic patients taking SGLT2 inhibitors; glucose may be <200 mg/dL despite significant ketoacidosis. 7
• Monitor serum potassium every 2–4 hours during treatment, as correction of acidosis and insulin therapy drive potassium intracellularly, risking life-threatening hypokalemia. 4, 8

Key Monitoring Parameters

• Venous pH and anion gap every 2–4 hours until the anion gap normalizes to ≤12 mEq/L. 5, 8
• Serum electrolytes (Na⁺, K⁺, Cl⁻, HCO₃⁻) every 2–4 hours during acute treatment. 5, 8
• Blood glucose hourly if treating DKA; when glucose reaches 250 mg/dL, reduce insulin and add dextrose to IV fluids. 8
• Serial creatinine to assess renal recovery after volume resuscitation. 3