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Obesity hypoventilation syndrome

obesity hypoventilation syndrome, obesity hypoventilation syndrome icd 10
Obesity hypoventilation syndrome also known as Pickwickian syndrome is a condition in which severely overweight people fail to breathe rapidly enough or deeply enough, resulting in low blood oxygen levels and high blood carbon dioxide CO2 levels Many people with this condition also frequently stop breathing altogether for short periods of time during sleep obstructive sleep apnea, resulting in many partial awakenings during the night, which leads to continual sleepiness during the day1 The disease puts strain on the heart, which eventually may lead to the symptoms such as heart failure, leg swelling and various other related symptoms The most effective treatment is weight loss, but it is often possible to relieve the symptoms by nocturnal ventilation with positive airway pressure CPAP or related methods12

Obesity hypoventilation syndrome is defined as the combination of obesity body mass index above 30 kg/m2, hypoxemia falling oxygen levels in blood during sleep, and hypercapnia increased blood carbon dioxide levels during the day, resulting from hypoventilation excessively slow or shallow breathing23 The disease has been known since the 1950s, initially as "Pickwickian syndrome" in reference to a Dickensian character but currently under a more descriptive name2


  • 1 Classification
  • 2 Signs and symptoms
  • 3 Mechanism
  • 4 Diagnosis
  • 5 Treatment
    • 51 Positive airway pressure
    • 52 Other treatments
  • 6 Prognosis
  • 7 Epidemiology
  • 8 History
  • 9 References


Obesity hypoventilation syndrome is a form of sleep disordered breathing Two subtypes are recognized, depending on the nature of disordered breathing detected on further investigations The first is OHS in the context of obstructive sleep apnea; this is confirmed by the occurrence of 5 or more episodes of apnea, hypopnea or respiratory-related arousals per hour high 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 13 kPa after sleep compared to awake measurements and overnight drops in oxygen levels without simultaneous apnea or hypopnea13 Overall, 90% of all people with OHS fall into the first category, and 10% in the second2

Signs and symptomsedit

Most people with obesity hypoventilation syndrome have concurrent obstructive sleep apnea, a condition characterized by snoring, brief episodes of apnea cessation of breathing during the night, interrupted sleep and excessive daytime sleepiness In OHS, sleepiness may be worsened by elevated blood levels of carbon dioxide, which causes drowsiness "CO2 narcosis" Other symptoms present in both conditions are depression, and hypertension high blood pressure that is difficult to control with medication1 The high carbon dioxide can also cause headaches, which tend to be worsening in the morning4

The low oxygen level leads to excessive strain on the right side of the heart, known as cor pulmonale1 Symptoms of this disorder occur because the heart has difficulty pumping blood from the body through the lungs Fluid may, therefore, accumulate in the skin of the legs in the form of edema swelling, and in the abdominal cavity in the form of ascites; decreased exercise tolerance and exertional chest pain may occur On physical examination, characteristic findings are the presence of a raised jugular venous pressure, a palpable parasternal heave, a heart murmur due to blood leaking through the tricuspid valve, hepatomegaly an enlarged liver, ascites and leg edema5 Cor pulmonale occurs in about a third of all people with OHS2


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 adipose tissue restricts the normal movement of the chest muscles and makes the chest wall less compliant, the diaphragm moves less effectively, respiratory muscles are fatigued more easily, and airflow in and out of the lung is impaired by excessive tissue in the head and neck area Hence, people with obesity need to expend more energy to breathe effectively67 These factors together lead to sleep-disordered breathing and inadequate removal of carbon dioxide from the circulation and hence hypercapnia; given that carbon dioxide in aqueous solution combines with water to form an acid CO2g + H2Ol + excess H2Ol --> H2CO3aq, this causes acidosis increased acidity of the blood Under normal circumstances, central chemoreceptors in the brain stem detect the acidity, and respond by increasing the respiratory rate; in OHS, this "ventilatory response" is blunted28

The blunted ventilatory response is attributed to several factors Obese people tend to have raised levels of the hormone leptin, which is secreted by adipose tissue and under normal circumstances increases ventilation In OHS, this effect is reduced28 Furthermore, episodes of nighttime acidosis eg due to sleep apnea lead to compensation by the kidneys with retention of the alkali bicarbonate This normalizes the acidity of the blood However, bicarbonate stays around in the bloodstream for longer, and further episodes of hypercapnia lead to relatively mild acidosis and reduced ventilatory response in a vicious circle28

Low oxygen levels lead to hypoxic pulmonary vasoconstriction, the tightening of small blood vessels in the lung to create an optimal distribution of blood through the lung Persistently low oxygen levels causing chronic vasoconstriction leads to increased pressure on the pulmonary artery pulmonary hypertension, which in turn puts strain on the right ventricle, the part of the heart that pumps blood to the lungs The right ventricle undergoes remodeling, becomes distended and is less able to remove blood from the veins When this is the case, raised hydrostatic pressure leads to accumulation of fluid in the skin edema, and in more severe cases the liver and the abdominal cavity2

The chronically low oxygen levels in the blood also lead to increased release of erythropoietin and the activation of erythropoeisis, the production of red blood cells This results in polycythemia, abnormally increased numbers of circulating red blood cells and an elevated hematocrit2


Formal criteria for diagnosis of OHS are:123

  • 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 mmHg or 60 kPa as determined by arterial blood gas measurement
  • No alternative explanation for hypoventilation, such as use of narcotics, severe obstructive or interstitial lung disease, severe chest wall disorders such as kyphoscoliosis, severe hypothyroidism underactive thyroid, neuromuscular disease or 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 measured2

To distinguish various subtypes, polysomnography is required This usually requires brief admission to a hospital with a specialized sleep medicine department where a number of different measurements are conducted while the subject is asleep; this includes electroencephalography electronic registration of electrical activity in the brain, electrocardiography same for electrical activity in the heart, pulse oximetry measurement of oxygen levels and often other modalities1 Blood tests are also recommended for the identification of hypothyroidism and polycythemia12

To distinguish between OHS and various other lung diseases that can cause similar symptoms, medical imaging of the lungs such as a chest X-ray or 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 obesity2


In people with stable OHS, the most important treatment is weight loss—by diet, through 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 successful1 Bariatric surgery is avoided if possible, given the high rate of complications, but may be considered if other treatment modalities are ineffective in improving oxygen levels and symptoms2 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 uncertain2

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<725 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 treatment9

Positive airway pressureedit

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 co-exists 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 OHS2

In some occasions, the oxygen levels are persistently too low oxygen saturations below 90% In that case, the hypoventilation itself may be improved by switching from CPAP treatment to an alternate device that delivers "bi-level" positive pressure: higher pressure during inspiration breathing in and a lower pressure during expiration breathing out If this too is ineffective in increasing oxygen levels, the addition of oxygen therapy may be necessary As a last resort, 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 opening2

Other treatmentsedit

Medroxyprogesterone acetate, a progestin, has been shown to improve the ventilatory response, but this has been poorly studied and is associated with an increased risk of thrombosis12 Similarly, the drug acetazolamide can reduce bicarbonate levels, and thereby augment to normal ventilatory response, but this has been researched insufficiently to recommend wide application2


Obesity hypoventilation syndrome is associated with a reduced quality of life, and people with the condition incur increased healthcare costs, largely due to hospital admissions including observation and treatment on intensive care units OHS often occurs together with several other disabling medical conditions, such as asthma in 18–24% and type 2 diabetes in 30–32% Its main complication of heart failure affects 21–32% of patients2

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 costs2


The exact prevalence of obesity hypoventilation syndrome is unknown, and it is thought that many people with symptoms of OHS have not been diagnosed1 About a third of all people with morbid obesity a body mass index exceeding 40 kg/m2 have elevated carbon dioxide levels in the blood2

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, ie 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 characteristics2

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 countries2


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 day10 This report, however, was preceded by other descriptions of hypoventilation in obesity211 In the 1960s, various further discoveries were made that led to the distinction between obstructive sleep apnea and sleep hypoventilation12


  1. ^ a b c d e f g h i j k Olson AL, Zwillich C 2005 "The obesity hypoventilation syndrome" Am J Med 118 9: 948–56 doi:101016/jamjmed200503042 PMID 16164877 
  2. ^ a b c d e f g h i j k l m n o p q r s t u v w x y z Mokhlesi B, Tulaimat A October 2007 "Recent advances in obesity hypoventilation syndrome" Chest 132 4: 1322–36 doi:101378/chest07-0027 PMID 17934118 
  3. ^ a b c Anonymous 1999 "Sleep-related breathing disorders in adults: recommendations for syndrome definition and measurement techniques in clinical research The Report of an American Academy of Sleep Medicine Task Force" Sleep 22 5: 667–89 PMID 10450601 
  4. ^ McNicholas, WT; Phillipson EA 2001 Breathing Disorders in Sleep Saunders Ltd p 80 ISBN 0-7020-2510-0 
  5. ^ Braunwald E 2005 "Chapter 216: heart failure and cor pulmonale" In Kasper DL, Braunwald E, Fauci AS, et al Harrison's Principles of Internal Medicine 16th ed New York, NY: McGraw-Hill pp 1367–78 ISBN 0-07-139140-1 
  6. ^ Bray, GA; Bouchard C; James WPT 1998 Handbook of Obesity Marcel Dekker Inc p 726 ISBN 0-8247-9899-6 
  7. ^ Björntorp, P; Brodoff BN 1992 Obesity JB Lippincott p 569 ISBN 0-397-50999-5 
  8. ^ a b c Piper AJ, Grunstein RR November 2007 "Current perspectives on the obesity hypoventilation syndrome" Current Opinion in Pulmonary Medicine 13 6: 490–6 doi:101097/MCP0b013e3282ef6894 PMID 17901754 
  9. ^ Mokhlesi B, Kryger MH, Grunstein RR February 2008 "Assessment and management of patients with obesity hypoventilation syndrome" Proc Am Thorac Soc 5 2: 218–25 doi:101513/pats200708-122MG PMC 2645254 PMID 18250215 
  10. ^ Burwell CS, Robin ED, Whaley RD, Bicklemann AG 1956 "Extreme obesity associated with alveolar hypoventilation; a Pickwickian syndrome" Am J Med 21 5: 811–8 doi:101016/0002-93435690094-8 PMID 13362309  Reproduced in Burwell CS, Robin ED, Whaley RD, Bickelmann AG 1994 "Extreme obesity associated with alveolar hypoventilation--a Pickwickian Syndrome" Obes Res 2 4: 390–7 doi:101002/j1550-85281994tb00084x PMID 16353591 
  11. ^ Auchincloss JH, Cook E, Renzetti AD October 1955 "Clinical and physiological aspects of a case of obesity, polycythemia and alveolar hypoventilation" J Clin Invest 34 10: 1537–45 doi:101172/JCI103206 PMC 438731 PMID 13263434 
  12. ^ Pack AI January 2006 "Advances in sleep-disordered breathing" Am J Respir Crit Care Med 173 1: 7–15 doi:101164/rccm200509-1478OE PMID 16284108 

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