What diagnosis best fits a morbidly obese, CPAP‑non‑compliant obstructive sleep apnea patient with flu‑like symptoms, positive rapid strep A, and an arterial blood gas showing acidemia, hypercapnia and elevated bicarbonate (metabolic compensation)?

Obesity Hypoventilation Syndrome (OHS) with Acute-on-Chronic Hypercapnic Respiratory Failure

This patient has obesity hypoventilation syndrome (OHS) presenting with acute-on-chronic hypercapnic respiratory failure, triggered by a Streptococcus A infection in the setting of morbid obesity, untreated obstructive sleep apnea, and CPAP non-compliance.

Diagnostic Reasoning

The arterial blood gas reveals the key diagnostic features:

• Respiratory acidosis with metabolic compensation: pH 7.31 (acidemic), pCO₂ 67 mmHg (severe hypercapnia), and HCO₃ 33.3 mmol/L (elevated bicarbonate indicating chronic compensation). 1

• OHS diagnostic criteria are met: This morbidly obese patient has daytime hypercapnia (pCO₂ >45 mmHg) with a serum bicarbonate >27 mmol/L, which is highly suggestive of OHS when combined with known OSA. 1, 2

• The elevated bicarbonate (33.3 mmol/L) indicates chronic CO₂ retention: A bicarbonate ≥27 mmol/L has 76.6% sensitivity and 74.6% specificity for diagnosing OHS in obese patients with OSA. 2

• Adequate oxygenation (pO₂ 109.3 mmHg) with severe hypercapnia confirms hypoventilation: The patient is not primarily hypoxemic but rather has ventilatory failure, distinguishing OHS from pure OSA. 3

Clinical Context

The flu-like symptoms and positive Strep A represent an acute infectious trigger superimposed on chronic baseline hypoventilation:

• CPAP non-compliance is a critical factor: Untreated OSA in morbidly obese patients leads to progressive daytime hypercapnia and eventual OHS development. 4, 5

• The pH of 7.31 with pCO₂ 67 mmHg indicates acute-on-chronic respiratory failure: While the bicarbonate is elevated (chronic compensation), the pH remains acidemic, signaling acute decompensation requiring immediate intervention. 1

Immediate Management Algorithm

Step 1: Oxygen Titration (Critical First Action)

• Target SpO₂ 88–92% using controlled oxygen delivery (Venturi mask 24–28% or nasal cannula 1–2 L/min). Excessive oxygen (current pO₂ 109.3 mmHg) worsens hypercapnia by suppressing hypoxic respiratory drive and increasing V/Q mismatch. 6, 7, 3

Step 2: Assess for Non-Invasive Ventilation (NIV/BiPAP)

This patient requires NIV based on American Thoracic Society criteria:

• pH <7.35, pCO₂ >6.5 kPa (48.75 mmHg), and clinical respiratory distress mandate NIV initiation after one hour of optimal medical therapy. 6, 7

• The pH of 7.31 is above the threshold of 7.25 that mandates immediate intubation, allowing a trial of NIV if no absolute contraindications exist. 6, 7

Contraindications to assess before NIV:

• Impaired mental status (drowsiness/somnolence) is an absolute contraindication—if present, proceed directly to intubation. 6, 7
• Copious secretions, hemodynamic instability, or inability to protect airway also preclude NIV. 6, 7

If NIV is appropriate:

• Initial settings: IPAP 12–15 cm H₂O, EPAP 4–5 cm H₂O, backup rate 12–15 breaths/min. 6, 7
• Deliver supplemental O₂ through BiPAP circuit to maintain SpO₂ 88–92%. 6, 7
• Obtain repeat ABG in 1–2 hours: If pH worsens or no improvement after 4–6 hours, proceed to intubation. 6, 7

Step 3: Concurrent Medical Therapy

• Nebulized bronchodilators: Salbutamol 2.5–5 mg and/or ipratropium 0.25–0.5 mg every 2–4 hours using compressed air (not oxygen). 6

• Systemic corticosteroids: Prednisolone 30–40 mg orally daily or hydrocortisone 100 mg IV for 10–14 days. 6

• Antibiotics for Strep A infection: Amoxicillin/clavulanate or respiratory fluoroquinolone (levofloxacin/moxifloxacin) based on local resistance patterns. 6

Step 4: Intubation Criteria (If NIV Fails or Contraindicated)

Proceed to immediate intubation if:

• pH <7.25 with pCO₂ >60 mmHg (8 kPa). 6, 7
• Worsening mental status, respiratory arrest, or cardiovascular instability. 6, 7
• NIV failure (worsening ABG within 1–2 hours or no improvement after 4–6 hours). 6, 7
• Severe tachypnea (>35 breaths/min) or life-threatening hypoxemia. 7

Long-Term Management Considerations

• Sleep study and PAP titration within 3 months: Confirm OHS diagnosis and determine if severe OSA is present (requiring CPAP) versus mild/moderate OSA (requiring NIV). 1

• Weight loss interventions: Sustained weight loss of 25–30% of actual body weight is required to achieve resolution of OHS; consider bariatric surgery (sleeve gastrectomy or Roux-en-Y gastric bypass) when benefit outweighs risk. 1

• Long-term NIV or CPAP therapy: If OHS with severe OSA, initiate CPAP; if OHS with no/mild OSA, initiate NIV. 1

Critical Pitfalls to Avoid

• Do not continue high-flow oxygen without ventilatory support—this patient's pO₂ of 109.3 mmHg is excessive and likely worsening hypercapnia. Immediately reduce oxygen to target SpO₂ 88–92%. 6, 7, 3

• Do not delay NIV initiation—a pH of 7.31 requires immediate ventilatory support in a high-dependency or ICU setting with intubation capability. 6, 7

• Do not assume drowsiness automatically precludes NIV—assess the patient's ability to cooperate and protect the airway; only complete unresponsiveness or inability to follow commands is an absolute contraindication. 6, 7

• Do not manage on a general ward—pH <7.35 mandates HDU/ICU-level care with immediate intubation capability. 6, 7

• Do not target SpO₂ >92%—over-oxygenation suppresses respiratory drive and worsens V/Q mismatch, increasing CO₂ retention and mortality risk. 6, 7, 3