Obesity hypoventilation syndrome

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Obesity hypoventilation syndrome
Other namesPickwickian syndrome
Respirology
Risk factorsObesity

Obesity hypoventilation syndrome (OHS) is a condition in which severely overweight people fail to breathe rapidly or deeply enough, resulting in low oxygen levels and high blood carbon dioxide (CO2) levels. The syndrome is often associated with obstructive sleep apnea (OSA), which causes periods of absent or reduced breathing in sleep, resulting in many partial awakenings during the night and sleepiness during the day.[1] The disease puts strain on the heart, which may lead to heart failure and leg swelling.

Obesity hypoventilation syndrome is defined as the combination of obesity and an increased blood carbon dioxide level during the day that is not attributable to another cause of excessively slow or shallow breathing.[2]

The most effective treatment is weight loss, but this may require bariatric surgery to achieve.[3] Weight loss of 25 to 30% is usually required to resolve the disorder.[3] The other first-line treatment is non-invasive positive airway pressure (PAP), usually in the form of continuous positive airway pressure (CPAP) at night.[4][5] The disease was known initially in the 1950s, as "Pickwickian syndrome" in reference to a Dickensian character.[5]

Signs and symptoms

Most people with obesity hypoventilation syndrome have concurrent

control with medication.[4] The high carbon dioxide can also cause headaches, which tend to be worsening in the morning.[6]

The low oxygen level leads to physiologic constriction of the pulmonary arteries to correct ventilation-perfusion mismatching, which puts excessive strain on the right side of the heart. When this leads to right sided heart failure, it is known as

blood leaking through the tricuspid valve, hepatomegaly (an enlarged liver), ascites and leg edema.[7] Cor pulmonale occurs in about a third of all people with OHS.[5]

Mechanism

It is not fully understood why some obese people develop obesity hypoventilation syndrome while others do not. It is likely that it is the result of an interplay of various processes. Firstly, work of breathing is increased as

brain stem detect the acidity, and respond by increasing the respiratory rate; in OHS, this "ventilatory response" is blunted.[5][10]

The blunted ventilatory response is attributed to several factors. Obese people tend to have raised levels of the hormone

vicious circle.[5][10]

Low oxygen levels lead to

hydrostatic pressure leads to accumulation of fluid in the skin (edema), and in more severe cases the liver and the abdominal cavity.[5]

The chronically low oxygen levels in the blood also lead to increased release of

erythropoeisis, the production of red blood cells. This results in polycythemia, abnormally increased numbers of circulating red blood cells and an elevated hematocrit.[5]

Diagnosis

Formal criteria for diagnosis of OHS are:[4][5][11]

  • Body mass index over 30 kg/m2 (a measure of obesity, obtained by taking one's weight in kilograms and dividing it by one's height in meters squared)
  • Arterial carbon dioxide level over 45 
    arterial blood gas
    measurement
  • No alternative explanation for hypoventilation, such as use of
    congenital central hypoventilation syndrome

If OHS is suspected, various tests are required for its confirmation. The most important initial test is the demonstration of elevated carbon dioxide in the blood. This requires an

arterial blood gas determination, which involves taking a blood sample from an artery, usually the radial artery. Given that it would be complicated to perform this test on every patient with sleep-related breathing problems, some suggest that measuring bicarbonate levels in normal (venous) blood would be a reasonable screening test. If this is elevated (27 mmol/L or higher), blood gasses should be measured.[5]

To distinguish various subtypes,

pulse oximetry (measurement of oxygen levels) and often other modalities.[4] Blood tests are also recommended for the identification of hypothyroidism and polycythemia.[4][5]

To distinguish between OHS and various other lung diseases that can cause similar symptoms,

CT/CAT scan), spirometry, electrocardiography and echocardiography may be performed. Echo- and electrocardiography may also show strain on the right side of the heart caused by OHS, and spirometry may show a restrictive pattern related to obesity.[5]

Classification

Obesity hypoventilation syndrome is a form of

apnea-hypopnea index) during sleep. The second is OHS primarily due to "sleep hypoventilation syndrome"; this requires a rise of CO2 levels by 10 mmHg (1.3 kPa) after sleep compared to awake measurements and overnight drops in oxygen levels without simultaneous apnea or hypopnea.[4][11] Overall, 90% of all people with OHS fall into the first category, and 10% in the second.[5]

Treatment

In people with stable OHS, the most important treatment is

exercise, with medication, or sometimes weight loss surgery (bariatric surgery). This has been shown to improve the symptoms of OHS and resolution of the high carbon dioxide levels. Weight loss may take a long time and is not always successful.[4] If the symptoms are significant, nighttime positive airway pressure (PAP) treatment is tried; this involves the use of a machine to assist with breathing. PAP exists in various forms, and the ideal strategy is uncertain. Some medications have been tried to stimulate breathing or correct underlying abnormalities; their benefit is again uncertain.[5]

While many people with obesity hypoventilation syndrome are cared for on an outpatient basis, some deteriorate suddenly and when admitted to the hospital may show severe abnormalities such as markedly deranged blood acidity (pH<7.25) or depressed

level of consciousness due to very high carbon dioxide levels. On occasions, admission to an intensive care unit with intubation and mechanical ventilation is necessary. Otherwise, "bi-level" positive airway pressure (see the next section) is commonly used to stabilize the patient, followed by conventional treatment.[12]

Positive airway pressure

Positive airway pressure, initially in the form of continuous positive airway pressure (CPAP), is a useful treatment for obesity hypoventilation syndrome, particularly when obstructive sleep apnea coexists. CPAP requires the use during sleep of a machine that delivers a continuous positive pressure to the airways and preventing the collapse of soft tissues in the throat during breathing; it is administered through a mask on either the mouth and nose together or if that is not tolerated on the nose only (nasal CPAP). This relieves the features of obstructive sleep apnea and is often sufficient to remove the resultant accumulation of carbon dioxide. The pressure is increased until the obstructive symptoms (snoring and periods of apnea) have disappeared. CPAP alone is effective in more than 50% of people with OHS.[5]

In some occasions, the oxygen levels are persistently too low (

tracheostomy may be necessary; this involves making a surgical opening in the trachea to bypass obesity-related airway obstruction in the neck. This may be combined with mechanical ventilation with an assisted breathing device through the opening.[5]

Other treatments

People who fail first-line treatments or have very severe, life-threatening disease may sometimes be treated with

progestin, and acetazolamide are both associated with an increased risk of thrombosis and are not recommended.[4][5]

Prognosis

Obesity hypoventilation syndrome is associated with a reduced

type 2 diabetes (in 30–32%). Its main complication of heart failure affects 21–32% of patients.[5]

Those with abnormalities severe enough to warrant treatment have an increased risk of death reported to be 23% over 18 months and 46% over 50 months. This risk is reduced to less than 10% in those receiving treatment with PAP. Treatment also reduces the need for hospital admissions and reduces healthcare costs.[5]

Epidemiology

The exact prevalence of obesity hypoventilation syndrome is unknown, and it is thought that many people with symptoms of OHS have not been diagnosed.[4] About a third of all people with morbid obesity (a body mass index exceeding 40 kg/m2) have elevated carbon dioxide levels in the blood.[5]

When examining groups of people with obstructive sleep apnea, researchers have found that 10–20% of them meet the criteria for OHS as well. The risk of OHS is much higher in those with more severe obesity, i.e. a body mass index (BMI) of 40 kg/m2 or higher. It is twice as common in men compared to women. The average age at diagnosis is 52. American Black people are more likely to be obese than American whites, and are therefore more likely to develop OHS, but obese Asians are more likely than people of other ethnicities to have OHS at a lower BMI as a result of physical characteristics.[5]

It is anticipated that rates of OHS will rise as the prevalence of obesity rises. This may also explain why OHS is more commonly reported in the United States, where obesity is more common than in other countries.[5]

History

The discovery of obesity hypoventilation syndrome is generally attributed to the authors of a 1956 report of a professional poker player who, after gaining weight, became somnolent and fatigued and prone to fall asleep during the day, as well as developing edema of the legs suggesting heart failure. The authors coined the condition "Pickwickian syndrome" after the character Joe from Dickens' The Posthumous Papers of the Pickwick Club (1837), who was markedly obese and tended to fall asleep uncontrollably during the day.[14] This report, however, was preceded by other descriptions of hypoventilation in obesity.[5][15] In the 1960s, various further discoveries were made that led to the distinction between obstructive sleep apnea and sleep hypoventilation.[16]

The term "Pickwickian syndrome" has fallen out of favor because it does not distinguish obesity hypoventilation syndrome and sleep apnea as separate disorders (which may coexist).[16][17]

References

  1. ^ Casey KR, Cantillo KO, Brown LK. Sleep-related hypoventilation/hypoxemic syndromes. Chest. 2007;131(6):1936-48.
  2. ^ American Academy of Sleep Medicine. International Classification of Sleep Disorders. 3rd ed. Darien, IL: American Academy of Sleep Medicine; 2014.
  3. ^
    PMID 31368798
    .
  4. ^
    S2CID 37801868
    .
  5. ^
    PMID 17934118. Archived from the original
    on 2008-12-08. Retrieved 2008-11-22.
  6. ISBN 978-0-7020-2510-5
    .
  7. ISBN 978-0-07-139140-5
    .
  8. ISBN 978-0-8247-9899-4
    .
  9. ISBN 978-0-397-50999-7
    .
  10. ^
    S2CID 32488927
    .
  11. ^
    PMID 10450601
    .
  12. PMID 18250215
    .
  13. ^ Martin TJ, Badr M Safwan, and Finlay G. Treatment and prognosis of the obesity hypoventilation syndrome. UpToDate Aug 6, 2019. https://www.uptodate.com/contents/treatment-and-prognosis-of-the-obesity-hypoventilation-syndrome
  14. PMID 16353591
    .
  15. PMID 13263434
    .
  16. ^
    PMID 16284108
    .
  17. PMID 16353586
    .

Further reading

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