Obesity hypoventilation syndrome

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Obesity hypoventilation syndrome
ICD-10 E66.2
ICD-9 278.8
OMIM 257500
DiseasesDB 32243
eMedicine ped/1627 
MeSH D010845

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The obesity hypoventilation syndrome, also known as Pickwickian syndrome, is the combination of obesity (body mass index above 30 kg/m2), falling oxygen levels in blood (hypoxia) during sleep and increasing carbon dioxide levels (hypercapnia); this is the result of hypoventilation (excessively slow or shallow breathing) during sleep.[1] Obstructive sleep apnea is often but not necessarily present.[2]

It may cause dyspnea (difficulty breathing), poor sleep with daytime tiredness, leg swelling and various other symptoms. The main treatments are weight loss and nocturnal ventilation (with CPAP or related methods). The exact cause is unknown.[2]

Signs and symptoms

Most people with obesity hypoventilation syndrome have concurrent obstructive sleep apnea, a condition characterized by snoring, brief episodes of apnoea (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, hypertension (high blood pressure) that is difficult to control with medication and headaches occuring in the morning.[2] Blurring of vision and visual obscurations may result from papilledema (swelling of the optic disc) in response to the raised carbon dioxide levels.[3]

The low oxygen and elevated carbon dioxide levels lead to excessive strain on the right side of the heart, known as "cor pulmonale". Symptoms of this disorder include edema (swelling) of the legs, decreased exercise tolerance, ascites (accumulation of fluid in the abdominal cavity) and exertional chest pain.[2]

Diagnosis

If OHS is suspected, various tests are required for its confirmation. Arterial blood gas levels are determined to measure oxygen and carbon dioxide levels; this requires a blood sample from an artery, usually the radial artery. 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 modalities.[2] To distinguish between OHS and various other lung diseases that can cause similar symptoms, computed tomography (CT/CAT scan) and spirometry may be performed.

Criteria

Formal criteria for diagnosis of OHS are:[1]

  • Body mass index over 30 kg/m2 (a measure of obesity, obtained by taking ones weight in kilograms and dividing it by ones height in meters squared)
  • Arterial carbon dioxide level over 45 mmHg or 6.0 kPa as determined by arterial blood gas measurement
  • No alternative explanation for hypoventilation, such as use of narcotics

Two subtypes are recognized. 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 (1.3 kPa) after sleep compared to awake measurements and overnight drops in oxygen levels without simultaneous apnea or hypopnea.[1] In many patients, both phenomena are present.[2]

Pathophysiology

Despite many studies, it is still unclear why some obese people develop hypoventilation and others do not. Impairment of lung expansion by adipose tissue means that one need to breathe faster and deeper to still absorb sufficient amounts of oxygen and remove adequate amounts of carbon dioxide. It appears that the respiratory center (an area in the brain stem that regulates breathing) becomes relatively insensitive to normal stimuli, leading to a decreased response to low oxygen levels. While this may be the result of obstructive sleep apnea, it does not explain why some people with OHS have no features of obstruction. Recent studies postulate that there is a vicious cycle in which low oxygen levels make the respiratory center progressively more insensitive to hypoxia, impairing normal compensatory mechanisms normally in place to prevent hypercapnia. It appears that insensitivity to the hormone leptin, which is elevated in obesity, plays a role in this process, but there is no conclusive evidence that this is the case.[2]

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 cavity. The dysfunction of the right ventricle improves with treatment.[4]

Treatment

Reduction in weight, either through a regimen of diet and exercise, medication or sometimes through bariatric surgery, 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.[2]

Overnight mask ventilation with positive airway pressure may lead to an improvement in most symptoms of OHS. The type of mask ventilation depends on the underlying problem. If the main abnormality on investigations is obstructive sleep apnea, CPAP (continuous PAP) may be sufficient; this involves sleeping with a face mask connected to a machine that delivers a continuously high atmospheric pressure; this stops tissues in the mouth and throat area from collapsing and obstructing air flow.[2] If sleep hypoventilation is the predominant problem, CPAP may be insufficient, and increased pressure ("pressure support") needs to be delivered during inspiration to allow more airflow into the alveoli (the sacs of the lung where gas transport takes place). This is referred to as BIPAP ("bi-level" PAP).[5][2] In patients whose symptoms are highly disabling but are unable to tolerate CPAP or BIPAP, ventilation through a tracheostomy (opening in the windpipe) is sometimes required.[2]

Despite some initial positive reports about improvement of OHS with medroxyprogesterone,[3] this is not recommended in practice.[2]

Epidemiology

The exact prevalence of OHS is unknown. In patients with a BMI over 35 who were admitted to hospital, 31% had elevated carbon dioxide levels. It is not known whether men or women are at greater risk. The presence of OHS is associated with an increased risk of death compared to those with obesity but no OHS (24% vs 9% over an 18 month period).[2]

History

The condition was first described in 1956 in a patient 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 newly described 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.[6]

References

  1. 1.0 1.1 1.2 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.
  2. 2.00 2.01 2.02 2.03 2.04 2.05 2.06 2.07 2.08 2.09 2.10 2.11 2.12 Olson AL, Zwillich C (2005). "The obesity hypoventilation syndrome". Am. J. Med. 118 (9): 948–56. doi:10.1016/j.amjmed.2005.03.042. PMID 16164877.
  3. 3.0 3.1 Reeve P, Harvey G, Seaton D (1985). "Papilloedema and respiratory failure". Br Med J (Clin Res Ed). 291 (6491): 331–2. PMID 3926184. PMC 1416589
  4. Nahmias J, Lao R, Karetzky M (1996). "Right ventricular dysfunction in obstructive sleep apnoea: reversal with nasal continuous positive airway pressure" (PDF). Eur. Respir. J. 9 (5): 945–51. PMID 8793456.
  5. Piper AJ, Sullivan CE (1994). "Effects of short-term NIPPV in the treatment of patients with severe obstructive sleep apnea and hypercapnia" (PDF). Chest. 105 (2): 434–40. PMID 8306742.
  6. 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. 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. PMID 16353591.

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