In OSA the upper airway collapses causing a reduction (hypopnoea) or cessation (apnoea) of breathing during sleep

This leads to fragmentation and intermittent hypoxia during sleep

Patient might suffer from daytime sleepiness, slow reaction time, poor concentration and memory with significant increase for cardio-vascular morbidity and mortality

The prevalence of OSA in adults is estimated to be as high as 15-20%

In some studies the prevalence of OSA is between 64-97% in bariatric surgical candidates

• The risk is higher in males
• 70% of patients with OSA also has obesity

OSA is often under diagnosed sometimes 2/3 are undiagnosed before bariatric surgery

OSA may be asymptomatic even based on the questionnaire (STOPBANG)

OSA is a slowly progressive disease with the patient adapting to the hypoxia

The gold standard is a sleep study test, overnight cardio-respiratory sleep recording which demonstrate at least 5 apnoea or hypopnoea episodes per hour

Weight reduction of >5% has been shown to cure 61% of patients with mild OSA

Long term results of conservative management of obesity is poor especially for more severe OSA

Bariatric and metabolic surgery results in reduction of adipose tissue in the neck and thoracic area, reduce the physical pressure on the upper airways

• Short term results have an overall remission rate of 65%
• Bariatric surgery is an effective treatment for OSA even after 5 years attesting to the sustain benefit of weight loss surgery in the long term

Pulmonary hypertension

Pulmonary HPT is increase in the mean pulmonary arterial pressure of >20mmHg measured with right heart catherization

Causes include:

Group 1: Idiopathic and hereditary

Group 2: Associated left sided heart disease

Group 3: Associated with lung disease

Group 4: Associated with thrombo-embolic disorder

Group 5: Heterogenous conditions

The pathogenesis of pulmonary hypertension include OSA, insulin resistance, metabolic syndrome and obesity

• Obesity is related to visceral or dysfunctional adipose tissue excessive production of adipocytokines causing a chronic low grade systemic inflammation, which induce structural changes to the pulmonary peri-vascular adipose tissues
• Increase secretion of vasoconstrictors and pro-inflammatory factors leading to pulmonary hypertension

Pulmonary HPT is a major risk factor associated with high mortality and morbidity after cardiac and non cardiac operations (14-42% morbidity and 1-18% mortality)