One of the major mechanical complications associated with severe obesity is the obesity hypoventilation syndrome – sometimes referred to as “Pickwickian Syndrome” in allusion to Joe, the rather stout kid in Charles Dickens’ Pickwick Papers.
A paper by Edmond Chau and colleagues from the University of Toronto, published in Anaesthesiology, reviews the epidemiology, pathophysiology, and perioperative considerations of this syndrome.
The obesity hypoventilation syndrome (OHS) is defined by
“the triad of obesity, daytime hypoventilation, and sleep-disordered breathing without an alternative neuromuscular, mechanical, or metabolic cause of hypoventilation. It is a disease entity distinct from simple obesity and obstructive sleep apnea.”
As the authors point out,
“OHS is often undiagnosed but its prevalence is estimated to be 10-20% in obese patients with obstructive sleep apnea and 0.15-0.3% in the general adult population.”
Patients present with hypercapnia (which, in part explains the extreme drowsiness) resulting from severe upper airway obstruction, restrictive chest physiology, blunted central respiratory drive, and pulmonary hypertension.
Not surprisingly, it is associated with a vastly increased risk of mortality.
The mainstay of conservative therapy is noninvasive positive airway pressure, which can markedly reduce the symptoms and quite possibly reduce overall risk.
The most effective treatment, however, is bariatric surgery, where weight loss is accompanied by often dramatic improvement in pulmonary function.
However, operating on patients with severe OHS also has its risks.
Perioperative management begins by having a high level of suspicion as this syndrome is often undiagnosed.
The definitive test for hypoventilation is an arterial blood gas performed on room air during wakefulness.
Patients may also have increased serum bicarbonate level due to metabolic compensation of chronic respiratory acidosis. A serum HCO3- threshold of 27 mEq/L demonstrated a 92% sensitivity in predicting hypercapnia on arterial blood gas. Together with an elevated apnea-hypopnea index (AHI), elevated serum HCO3 has a specificity of 95% with a sensitivity of 100%.
In addition, hypoxemia (SpO2 <90%, corresponding to PaO2 < 60 mmHg)99 during wakefulness should lead clinicians to suspect OHS in patients with OSA.
Thus, the authors recommend that all patients presenting with a high BMI and AHI should be screened for OHS, serum HCO3- level being the easiest test for hypercapnia before elective surgery.
Once hypercapnia is confirmed with an arterial blood gases, referral to sleep medicine and further testing, such as pulmonary function testing, chest imaging, thyroid-stimulating hormone, and clinical assessment of neuromuscular strength, is recommended to rule out other important causes of hypoventilation.
The article goes on to make specific recommendations for pre-, intra- and post-operative management of patients with OHS – something perhaps all health professionals dealing with severely obese patients should be aware of.
Chau EH, Lam D, Wong J, Mokhlesi B, & Chung F (2012). Obesity hypoventilation syndrome: a review of epidemiology, pathophysiology, and perioperative considerations. Anesthesiology, 117 (1), 188-205 PMID: 22614131