What is the most likely diagnosis and initial management for a patient with hyperchloremic metabolic acidosis (chloride 121 mmol/L, bicarbonate 11.4 mmol/L), low‑normal calcium, elevated blood urea nitrogen and normal creatinine indicating volume depletion?

Hyperchloremic Metabolic Acidosis with Volume Depletion

The most likely diagnosis is hyperchloremic (normal anion gap) metabolic acidosis secondary to gastrointestinal bicarbonate loss from diarrhea, and the initial management is aggressive isotonic saline resuscitation at 15–20 mL/kg/h during the first hour to restore intravascular volume and renal perfusion. 1

Diagnostic Interpretation

Calculate the anion gap to confirm normal anion gap acidosis:

• Anion gap = Na⁺ − (HCO₃⁻ + Cl⁻) = (assume Na⁺ ~140) − (11.4 + 121) = ~7.6 mEq/L
• This is below the normal range of 10–12 mEq/L, confirming a hyperchloremic (normal anion gap) metabolic acidosis 1

The elevated BUN (47 mg/dL) with normal creatinine (0.67 mg/dL) indicates prerenal azotemia from volume depletion, producing a BUN/Cr ratio >20:1, which is the hallmark of hypovolemia rather than intrinsic renal disease. 1

The bicarbonate of 11.4 mmol/L represents moderate-to-severe metabolic acidosis, falling well below the threshold of 18 mmol/L where pharmacological intervention is typically considered in chronic conditions. 1

Differential Diagnosis of Hyperchloremic Metabolic Acidosis

Gastrointestinal bicarbonate loss from diarrhea is the most common cause in a volume-depleted patient, as the colon normally secretes bicarbonate-rich fluid and diarrhea results in net bicarbonate loss with relative chloride retention. 1, 2

Renal tubular acidosis (RTA) should be considered but is less likely given the acute presentation with volume depletion; RTA typically presents with chronic acidosis without marked volume loss. 3, 2

Iatrogenic causes from excessive normal saline administration can produce dilutional hyperchloremic acidosis by increasing serum chloride and decreasing the strong ion difference, but this requires prior large-volume saline infusion. 1, 4

Urinary diversion procedures (ileal conduit, ureterosigmoidostomy) cause urinary reabsorption in bowel segments, leading to chloride retention and bicarbonate loss, but require a surgical history. 5

Initial Resuscitation Strategy

Administer isotonic saline (0.9% NaCl) at 15–20 mL/kg/h during the first hour to restore intravascular volume and renal perfusion, as aggressive volume expansion is the cornerstone of initial management in the absence of cardiac compromise. 1

After the initial bolus, switch to balanced crystalloids (Lactated Ringer's or Plasma-Lyte) to avoid iatrogenic hyperchloremic acidosis from continued normal saline, as large-volume 0.9% saline can worsen hyperchloremia and impair renal blood flow. 1

Monitor serum electrolytes (Na⁺, K⁺, Cl⁻, HCO₃⁻) every 2–4 hours during acute resuscitation to assess response and detect complications such as hypokalemia. 1

Measure venous pH and anion gap every 2–4 hours to track resolution of acidosis; repeat arterial blood gases are generally unnecessary once the diagnosis is established. 1

Role of Bicarbonate Therapy

Bicarbonate therapy is NOT indicated for diarrhea-induced hyperchloremic acidosis unless arterial pH falls below 7.0, an extremely rare scenario, as the acidosis typically resolves spontaneously once volume is restored and renal perfusion improves. 1

The bicarbonate level of 11.4 mmol/L, while severe, does not automatically warrant bicarbonate administration in the acute setting of volume depletion, because fluid resuscitation alone will correct the acidosis by restoring renal bicarbonate regeneration. 1

If bicarbonate therapy is considered for pH <7.0, the goal is to achieve pH 7.2–7.3, not normalization, and only in the context of treating severe acidemia while addressing the underlying cause. 1

Addressing the Underlying Cause

Identify and treat the source of gastrointestinal losses:

• Infectious gastroenteritis (viral, bacterial, parasitic) requires supportive care and antimicrobials if indicated 1
• Inflammatory bowel disease exacerbations may require corticosteroids or immunosuppression 1
• Medication-induced diarrhea (magnesium products, metformin, NSAIDs) necessitates discontinuation of the offending agent 1

For mild-to-moderate dehydration (3–9% fluid deficit), oral rehydration solution containing 50–90 mEq/L sodium at 50 mL/kg over 2–4 hours can be used if the patient can tolerate oral intake. 1

Monitoring Parameters During Treatment

Serial serum electrolytes every 2–4 hours initially to ensure appropriate correction of acidosis and to detect hypokalemia, which can develop as acidosis corrects and potassium shifts intracellularly. 1

Daily body weight and strict intake/output monitoring to evaluate fluid balance and adequacy of resuscitation. 6

Urine output should be monitored to confirm restoration of renal perfusion, with a target of at least 0.5 mL/kg/h indicating adequate volume repletion. 1

BUN and creatinine should be rechecked after initial resuscitation to confirm resolution of prerenal azotemia; the BUN should normalize as volume is restored. 1

Common Pitfalls to Avoid

Do not administer bicarbonate empirically for low serum bicarbonate in the setting of volume depletion, as fluid resuscitation alone will correct the acidosis by restoring renal function and bicarbonate regeneration. 1

Avoid continued large-volume normal saline after initial resuscitation, as this can worsen hyperchloremia and create a self-reinforcing cycle of acidosis by impairing renal blood flow and promoting sodium retention. 1

Do not overlook the need to switch to balanced crystalloids after the initial bolus, as Lactated Ringer's or Plasma-Lyte provide a more physiologic chloride concentration and facilitate faster correction of hyperchloremic acidosis. 1

Failure to monitor potassium closely can result in life-threatening hypokalemia as acidosis corrects and potassium shifts intracellularly, particularly if bicarbonate is administered. 1

Special Considerations

If the patient has chronic kidney disease (CKD), the approach differs:

• CKD patients with bicarbonate <18 mmol/L require pharmacological treatment with oral sodium bicarbonate (0.5–1.0 mEq/kg/day) once acute illness resolves 1
• During acute hospitalization, CKD patients should not continue dietary protein restriction, as the catabolic state requires increased protein intake (1.2–1.5 g/kg/day) 1
• Target maintenance is serum bicarbonate ≥22 mmol/L to prevent protein catabolism, bone disease, and CKD progression 1

If the patient has underlying respiratory disease with chronic hypercapnia, avoid excessive oxygen therapy and target SpO₂ 88–92% to prevent worsening respiratory acidosis. 1