Charles Dickens’ Character “Fat Joe” Appeared in The Pickwick Papers in 1836
Fat Joe was Known for Overeating and Falling Asleep at Any Time of the Day
Burwell First Coined the Term “Pickwickian Syndrome” to Describe Patients with What is Now Termed Obesity-Hypoventilation Syndrome (Am J Med, 1956) [MEDLINE]
Centers for Disease Control and Prevention (CDC) Statistics Related to Obesity (JAMA, 2014) [MEDLINE]
Approximately 34.9% of US Adults are Obese: accounts for 78.6 million people
Approximately 6.4% of US Adults are Severely Obese (BMI ≥40 kg/m2)
Prevalence of Severe Obesity in Non-Hispanic Black Adults: 12.2%
Prevalence
Approximately 0.15-0.3% of the Adult Population in the US Have OHS (Respir Care 2010) [MEDLINE]
The Prevalence of OHS Increases with Body Mass Index (BMI) (Chest, 2005) [MEDLINE]
BMI 30-35: prevalence of OHS is 8-12%
BMI ≥40: prevalence of OHS is 18-31%
BMI ≥50: prevalence of OHS is 50%
Physiology
Factors Involved with the Pathogenesis of Obesity-Hypoventilation Syndrome
Impaired Control of Ventilation
Decreased Neural Drive Has Been Observed in OHS: in contrast, obese patients without OHS normally have increased neural drive, as compared to normal patients
Decreased Ventilatory Responsiveness to Hypoxemia/Hypercapnia are Decreased in OHS During Sleep
Leptin Resistance May Occur in OHS:
Increased Carbon Dioxide Production Due to Increased Body Surface Area (Ann Am Thorac Soc, 2014) [MEDLINE]
Altered Pulmonary Mechanics Due to Body Habitus
Restrictive Pulmonary Function Tests (PFT’s)
V/Q Mismatch with Decreased Lower Lung Zone Ventilation and Increased Lower Lung Zone Perfusion: ventilation abnormalities are due to decreased lung compliance, difficulty mobilizing the ribcage/diaphragm, and/or alveolar closure prior to the end of expiration
Modestly Decreased Respiratory Muscle Strength (Which is Worse in the Supine Position): this occurs despite increased inspiratory loads created by obesity
Sleep-Disordered Breathing
Approximately 90% of Patients with OHS Have Associated OSA, While 10% of Patients with OHS Have Sleep-Associated Hypoventilation Alone (without Airway Obstruction)
Inadequate Carbon Dioxide Clearance Occurs During Sleep: resulting in worsening of nocturnal hypercapnia (with resulting renal bicarbonate retention)
Nocturnal Hypoxemia Occurs During Sleep: the percentage of time spent with SaO2 <90% correlates with the development of daytime hypercapnia
Development of Pulmonary Hypertension (see Pulmonary Hypertension, [[Pulmonary Hypertension]])
Acute Respiratory Failure (see Respiratory Failure, [[Respiratory Failure]])
Epidemiology
Females with OHS Tend to Present Later in the Disease Course More Frequently than Do Males with OHS (Respir Med, 2016) [MEDLINE]: they more frequently present with acute on chronic respiratory failure
Approximately 90% of Patients with OHS Have Associated OSA, While 10% of Patients with OHS Have Sleep-Associated Hypoventilation Alone (without Airway Obstruction)
Treatment
Treatment of Nocturnal Sleep-Disordered Breathing (with Positive-Pressure Ventilation, Tracheostomy) is Also Effective in the Treatment of OHS
While Oxygen Therapy May Improve Daytime Hypoxemia, it Can Acutely Worsen Hypoventilation (Via Worsening of the Dead Space Fraction)
Supplemental Oxygen Therapy (100%) in Stable OHS Has Been Demonstrated to Worsen Hypercapnia, Up to 10 mm Hg in Some Cases (Chest, 2011) [MEDLINE]\
Generally, Maintenance of SaO2 of 89-92% is Recommended to Avoid Hyperoxia in These Patients: these thresholds should be similarly applied in patients on noninvasive mechanical ventilation
Avoid Excessive Nocturnal Oxygen Therapy: while oxygen improves nocturnal hypoxemia, it can worsen nocturnal hypoventilation
Diuretics
Avoid Creation of Pre-Renal Azotemia in the Setting of an Acute Illness
During Acute Illness, Worsening Hypoxemia and Hypercapnia Can Result in an Increase in Catecholamines, Resulting in Increased Renal Vascular Resistance: during this illness, diuretics may exacerbate the azotemia
For This Reason, Diuresis May Need to Be Withheld Until the Acute Hypoxemia/Hypercapnia Improve
Avoid Excessive Diuresis/Contraction Alkalosis During the Treatment of Peripheral Edema (see Metabolic Alkalosis, [[Metabolic Alkalosis]])
Excessive Alkalemia Blunts the Ventilatory Response, Worsening Hypercapnia
For This Reason, Periodic Acetazolamide (Diamox) Therapy May Be Useful to Avoid an Excessive Increase in Serum Bicarbonate Which Occurs in the Setting of Diuretic Use, Restoring the Reactivity of the Respiratory Drive to Carbon Dioxide (see Acetazolamide, [[Acetazolamide]]) (Respir Care, 2010) [MEDLINE] and (Respir Care, 2010) [MEDLINE]
Sedatives/Opiates
Avoid (or Minimize) the Use of Any Agents Which Depress the Central Respiratory Drive
Treatment of Acute (on Chronic) Respiratory Failure
Careful Consideration of the Approach to Airway Management is Crucial in These Patients
Awake Fiberoptic Intubation with Concomitant Nasal BiPAP Ventilation is Usually the Preferred Approach: as sedation/paralysis (per standard rapid sequence intubation methods) may result in airway compromise with difficulty bag-mask ventilating (and intubating) the patient
References
Extreme obesity associated with alveolar hypoventilation: a Pickwickian syndrome. Am J Med 1956;21:811–818 [MEDLINE]
The obesity-hypoventilation syndrome revisited: a prospective study of 34 consecutive cases. Chest. 2001;120(2):369 [MEDLINE]
Daytime hypercapnia in adult patients with obstructive sleep apnea syndrome in France, before initiating nocturnal nasal continuous positive airway pressure therapy. Chest. 2005;127(3):710 [MEDLINE]
The effects of body weight on airway calibre. Eur Respir J 2005;25:896–901 [MEDLINE]
Short-term and long-term effects of nasal intermittent positive pressure ventilation in patients with obesity-hypoventilation syndrome. Chest. 2005 Aug;128(2):587-94 [MEDLINE]
Obesity hypoventilation syndrome: prevalence and predictors in patients with obstructive sleep apnea. Sleep Breath. 2007;11(2):117 [MEDLINE]
Assessment and management of patients with obesity hypoventilation syndrome. Proc Am Thorac Soc. 2008;5:218–225 [MEDLINE]
Obesity hypoventilation syndrome: a state-of-the-art review. Respir Care 2010;55:1347–1362 [MEDLINE]
Hypercapnic respiratory failure in obesity-hypoventilation syndrome: CO2 response and acetazolamide treatment effects. Respir Care 2010;55:1442–1448 [MEDLINE]
Obesity hypoventilation syndrome: bicarbonate concentration and acetazolamide. Respir Care 2010;55: 1504–1505 [MEDLINE]
The effect of supplemental oxygen on hypercapnia in subjects with obesity- associated hypoventilation: a randomized, crossover, clinical study. Chest 2011;139:1018–1024 [MEDLINE]
Noninvasive ventilation in acute hypercapnic respiratory failure caused by obesity hypoventilation syndrome and chronic obstructive pulmonary disease. Am J Respir Crit Care Med. 2012 Dec;186(12):1279-85. Epub 2012 Oct 26 [MEDLINE]
Diagnostic predictors of obesity-hypoventilation syndrome in patients suspected of having sleep disordered breathing. J Clin Sleep Med. 2013 Sep;9(9):879-84 [MEDLINE]
Prevalence of childhood and adult obesity in the United States, 2011-2012. JAMA 2014;311: 806–814 [MEDLINE]
Respiratory determinants of diurnal hypercapnia in obesity hypoventilation syndrome. What does weight have to do with it? Ann Am Thorac Soc. 2014 Jul;11(6):945-50 [MEDLINE]
Obesity hypoventilation syndrome: current theories of pathogenesis. Curr Opin Pulm Med. 2015;21:557–562 [MEDLINE]
Avoiding management errors in patients with obesity hypoventilation syndrome. Ann Am Thorac Soc. 2016;13:109–114 [MEDLINE]
Gender differences in patients starting long-term home mechanical ventilation due to obesity hypoventilation syndrome. Respir Med. 2016 Jan;110:73-8. Epub 2015 Nov 26 [MEDLINE]
