What are the differences between Obstructive Sleep Apnea (OSA) and Obesity Hypoventilation Syndrome (OHS) in terms of diagnosis, treatment, and management in obese patients?

OSA vs Obesity Hypoventilation Syndrome: Key Differences

Obesity Hypoventilation Syndrome (OHS) is a distinct and far more severe condition than OSA alone, defined by the triad of obesity (BMI > 30 kg/m²), sleep-disordered breathing, and daytime hypercapnia (PaCO₂ > 45 mm Hg), representing the most severe form of obesity-induced respiratory compromise with significantly higher morbidity and mortality. 1, 2

Fundamental Pathophysiologic Distinction

OSA involves recurrent upper airway obstruction during sleep causing apneas and hypopneas, while OHS represents chronic hypercapnic respiratory failure that persists during wakefulness due to multiple failing compensatory mechanisms. 1

Key pathophysiologic differences include:

• OSA patients maintain normal daytime ventilation and gas exchange through compensatory mechanisms 1
• OHS develops when multiple mechanisms fail simultaneously: impaired central respiratory drive, severe mechanical respiratory dysfunction, inadequate respiratory muscle strength, and chronic nocturnal hypoventilation 1, 2
• Approximately 90% of OHS patients also have coexistent OSA (AHI > 5), with nearly 70% having severe OSA (AHI > 30), but the reverse is not true—most OSA patients do not have OHS 1, 2

Diagnostic Criteria

OSA Diagnosis

• Characterized by recurrent upper airway obstruction during sleep measured by apnea-hypopnea index (AHI) 1
• Diagnosed via polysomnography or home sleep testing 3
• No requirement for blood gas abnormalities during wakefulness 1

OHS Diagnosis

The American Thoracic Society requires three mandatory components for OHS diagnosis: 1, 2

1. Obesity: BMI > 30 kg/m² (though most have BMI > 35 kg/m²) 3, 1
2. Sleep-disordered breathing (documented by sleep study) 1, 2
3. Awake daytime hypercapnia: PaCO₂ > 45 mm Hg at sea level 1, 2
4. Exclusion of other causes of hypoventilation (neuromuscular disease, severe COPD, chest wall disorders) 1, 2

Screening Algorithm for OHS

For obese patients with suspected sleep-disordered breathing: 1

• High pretest probability: Measure arterial PaCO₂ directly via arterial blood gas 1, 4
• Low-to-moderate pretest probability: Use serum bicarbonate as initial screen 1, 4
  • If serum bicarbonate < 27 mmol/L, OHS is very unlikely 4
  • If serum bicarbonate > 27 mmol/L: 85.7% sensitivity and 89.5% specificity for OHS diagnosis 5
• Do not rely on SpO₂ alone to decide when to measure PaCO₂ 4

Clinical Consequences and Prognosis

OHS carries substantially worse prognosis than OSA alone, with significantly increased mortality rates. 1, 2

Cardiovascular Complications

• Pulmonary hypertension develops in 30-88% of OHS patients versus lower rates in OSA alone 1
• Chronic heart failure and cor pulmonale from chronic hypoxemia and hypercapnia are more common in OHS 1
• Left ventricular dysfunction develops from chronic heart strain 3

Perioperative Risk

• OSA doubles the incidence of postoperative desaturation, respiratory failure, cardiac events, and ICU admission 3
• OHS patients are particularly susceptible to anaesthetic agents and opioids, which may precipitate acute respiratory arrest in the early postoperative period 3
• The combination of chronic hypoxemia and hypercapnia in OHS creates extreme sensitivity to opioid-induced respiratory depression 3

Treatment Differences

OSA Treatment

CPAP is the standard first-line treatment for OSA, with BiPAP not typically required unless CPAP fails. 1

• If identified pre-operatively and treated with CPAP, risk of complications is much reduced 3
• Approximately 50% of OSA patients are poorly compliant with CPAP therapy, usually due to mask fitting problems 3

OHS Treatment Algorithm

The American Academy of Sleep Medicine recommends treatment based on OSA severity: 1, 2

1. OHS with severe OSA (AHI > 30): CPAP as first-line treatment 1, 2
2. OHS without severe OSA: BiPAP (noninvasive ventilation) is recommended 1, 2
3. For patients with both OHS and COPD with severe OSA: CPAP is suggested as first-line rather than NIV 4

Definitive Treatment

Weight loss interventions producing sustained weight loss of 25-30% of actual body weight can achieve resolution of OHS, representing definitive treatment. 4, 2

• Bariatric surgery is most likely to achieve this degree of sustained weight loss 2

Critical Clinical Pitfalls

OHS is largely underdiagnosed despite its severity, with prevalence of 10-20% among obese patients with OSA but only 0.15-0.4% diagnosed in the general population. 2, 6

Common diagnostic errors to avoid:

• Assuming all obese patients with sleep-disordered breathing have simple OSA without checking daytime blood gases 1, 2
• Relying on oxygen saturation alone rather than measuring PaCO₂ 4
• Failing to screen obese patients (especially BMI > 35 kg/m²) for hypercapnia before surgery 3
• Treating OHS patients with CPAP alone when they have non-severe OSA (should receive BiPAP) 1
• Underestimating perioperative risk—OHS patients require heightened vigilance with opioid administration and postoperative monitoring 3