The problem of obesity has already affected almost all corners of the world, thus causing emergence of syndromes and symptoms in all known diseases creating new comorbidities as well as separate ailments. Therefore, innovations and alterations in medical management of various illnesses are required. In 2015, approximately 1 in 3 adults on the planet were predicted to suffer from excess body mass (BMI>25kg/m2) and 10% of the world population was diagnosed as having obesity (BMI>30kg/m2). One of the syndromes that come with being obese is obesity hypoventilation syndrome (OHS) stipulated by a quotidian alveolar hypoventilation (PCO2 >45mm Hg), while other conventional reasons for the condition are absent. OHS is the causative factor of intensive usage of hospital beds nowadays. In addition, it is a leading factor in the development of cardiorespiratory diseases.

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Obese teenagers male overweight fat front belly

Image: “Obese boy 16 years old, weight 136kg – 300lbs height 185cm – 6ft” by FatGiVi – Own work. License: CC BY-SA 4.0


Definition and Background of Obesity Hypoventilation Syndrome

Alveolar hypoventilation occurs due to several disorders that are referred to as hypoventilation syndromes. Alveolar hypoventilation is an insufficient ventilation leading to hypercapnia, which is determined by arterial blood gas analysis (PaCO2), hence, it is an increase in the partial pressure of carbon dioxide. Therefore, obesity hypoventilation syndrome (OHS) manifests as the development of pronounced hypoxemia, lack of oxygen in the blood affecting all parts of the body.

OHS may be acute or chronic; there are a number of mechanisms that affect the development of both conditions. First of all, the main triggers of OHS are the disturbance of the central ventilator drive and an increased body weight.

OHS encompasses obesity itself accompanied by disordered breathing during sleep, BMI > 30kg/m2, and hypercapnia PaCO2 > 45 mm Hg. The majority of patients with OHS (90%) suffer from obstructive sleep apnea (OSA) respectively.

Etiology of Obesity Hypoventilation Syndrome

Owing to the increased energy needed for breathing, weakening of the inspiratory muscles occurs accompanied by low resting tidal volumes in patients with OHS, leading to respiratory and cardiovascular disorders.

Obesity & BMI

Image: “Obesity & BMI.” by BruceBlaus – Own work. License: CC BY-SA 4.0

Patients with OHS tend to have 20% decreased lung capacity40% lower maximal voluntary ventilation and lower pulmonary compliance than people with obesity who do not suffer from hypoventilation. OHS triggers intensive breathing, as the lack of oxygen in the blood elevates the quantity of carbon dioxide, thus stimulating the respiratory center in the brain leading to additional breathing in.

Carbon dioxide retention may be stipulated by the scarcity of leptin or its resistance in the case of OHS patients.

Nevertheless, the central respiratory control disorder remains the most contributing factor in the development of OHS, as overweight individuals that hyperventilate tend to have abnormal body reaction to hypoxia and are less responsive to CO2 rebreathing.

Epidemiology of Obesity Hypoventilation Syndrome

According to the US Centers of Disease Control and Prevention (CDC), the occurrence of OHS ranges from 10% to 20% because 30% of American citizens are obese. The figures characterizing the disorder tend to elevate as obesity rate grows from year to year at an alarming rate.

OHS often remains undiagnosed; the prevalence of OHS is 10-20% in patients with obstructive sleep apnea and 0.15-0.3% in the adult population. OHS is more common in males, with a ratio of 2:1 male-to-female. Also, patients older than 50 years tend to have OHS.

Presentation of Obesity Hypoventilation Syndrome

History

OHS is usually a secondary syndrome for a main condition, of which the flow is characterized by the stage of hypoventilation and hypercapnia as well as the body’s ability to recovery from respiratory acidosis.

OHS sufferers tend to develop signs of OSA, namely, hypersomnolence, daytime sleepiness, tiredness, especially during daytime even after minimal physical activity, disturbing snoring, poor sleeping patterns, night choking – sleep apnea, frequent depression attacks, and headaches, especially in the morning. Fatigue usually follows shortness of breath which is a symptom of low blood oxygen levels (chronic hypoxia).

Pulmonary hypertension and chronic right-sided heart failure (cor pulmonale) are some of the major complications of OHS in obese patients, further aggravated by peripheral edema, leading to emergence of swellings in the limbs. Also, there can be presence of cyanosis-bluish color on the lips, fingers, toes, or skin.

barrel chest

Image: “A lateral CXR of a person with emphysema. Note the barrel chest and flat diaphragm.” by James Heilman, MD – Own work. License: CC BY-SA 3.0

Physical examination

Physical examinations are not clinically articulate, are non-specific, and are characterized by comorbidities:

Thoracic examination

During thoracic examination, patients who are at different stages of OHS have diffuse wheezing, hyperinflation, a specific appearance of the chest, “barrel chest”, percussion produces hyperresonance; there is prolonged expiration and breath sounds are diffusely decreased.

Also, there are coarse crackles during inspiration, followed by wheezes during expiration. In addition to thoracic examination, there may be clubbing and cyanosis indicating the rate of hypoxia.

Pulmonary hypertension

While auscultating:

  • the second heart sound has a characteristic split and pronounced pulmonary component (P2)
  • the left parasternal (right ventricular) heave has an S4 of right ventricular origin
  • the jugular venous pulse has a large a-wave component
  • the pulmonic valve regurgitation is reflected by a diastolic murmur

Advanced stages of the disease

  • There are usually signs of right ventricular failure (cor pulmonale) coupled with V wave upon increased jugular venous pressure.
  • Swelling of the limbs aggravates.
  • There is severe tricuspid regurgitation that manifests as a systolic murmur as a result of a pulsatile liver.
  • Hepatosplenomegaly

Differential Diagnosis

  • Infectious diseases: botulism
  • Respiratory system disorders: bronchitis, chronic obstructive pulmonary disease (COPD), diaphragm disorders, diaphragmatic paralysis, emphysema
  • Digestive system disorders: obesity
  • Substances usage: opioid abuse
  • Metabolic disorders: respiratory acidosis
  • Medication induced disorders: sedative, hypnotic, and anxiolytic intake disorders
  • ALA dehydratase deficiency porphyria

Diagnosis of Obesity Hypoventilation Syndrome

Diagnosis is established based on the results of physical, laboratory and imaging examinations, namely:

  • Arterial blood gas is compulsory while conducting OHS diagnosis
  • CT scan/chest x-ray either of them are conducted in order to exclude comorbidities and other ailments
  • MRI
  • ECG helps to detect signs of right heart strain, right atrial enlargement and right ventricular hypertrophy.
  • Echocardiography looks for evidence of pulmonary hypertension and right ventricular enlargement.
  • Electromyography and nerve conduction velocity is informative in neuromuscular disorders, such as myasthenia gravis, Guillain-Barré syndrome, and amyotrophic lateral sclerosis, this method allows differentiation of neuropathic and myopathic patterns of the disorders.
  • Lung function tests (pulmonary function tests)
  • Polysomnography is sleep pattern study, which is often disordered in OHS followed by OSA.

Laboratory studies

  • Serum biochemical examination: elevated concentration of serum bicarbonate (HCO3) as a response to respiratory acidosis, as well as high volumes of serum Ca and K, hypercalcemia and hyperkalemia
  • Complete blood cell count: due to hypoxia, there may be polycythemia and an increased level of hematocrit.
  • Thyroid function studies: Decline in the functioning of the thyroid gland, hypothyroidism, leads to development of obesity and OHS. Those who are suspected to have developed OSA have to undergo thyroid function examination.
  • Arterial blood gas analysis: OHS is represented by hypercapnia/high PaCO2 >45mmHg.
  • The development of acute and chronic acidosis as well as the rate of their compensation are determined via estimation of HCO3 and PH.
  • Transdiaphragmatic pressure is informative while monitoring muscular weakness; it helps to distinguish the etiology of the disorder (diaphragmatic dysfunction and paralysis).

Imaging studies

  • Chest radiography is administered in order to exclude pulmonary diseases; it helps to determine the etiology of hypoventilation.
  • Fluoroscopy is informative while looking for unilateral diaphragmatic paralysis, and is used as an additional measure of chest radiography.
  • Chest CT scanning has better sensitivity and may detect abnormalities that are not found on a chest radiography (emphysema, diaphragm and skeletal thoracic abnormalities).
  • Brain CT scanning is indicated if a physician suspects a central cause of hypoventilation; it may also help to rule out cerebrovascular accidents and CNS tumors or trauma, various lesions of the brainstem in the area of the pons and medulla.
  • Brain MRI is useful when a CT scan of the brain is negative but a central etiology of OHS has not yet been ruled out.

Management of Obesity Hypoventilation Syndrome

Management of OHS includes a combination of different medical and surgical methods. The sufferers require the intervention of different specialists:

  • Physicians and endocrinologists regarding probability of diabetes mellitus, hypertension, elevated blood pressure, hyperlipidemia, heart failure and hypothyroidism therapy
  • A dietician for the correction of daily nutrition in order to lose weight
  • A respirologist for the management of respiratory failure
  • A surgeon considering potential bariatric surgery

    Tracheostomy

    Image: “Figure A shows a side view of the neck and the correct placement of a tracheostomy tube in the trachea, or windpipe. Figure B shows an external view of a patient who has a tracheostomy.” by National Heart Lung and Blood Institute (NIH). License: Public Domain

Based on the severity of OHS there are certain steps required:

  1. Correction of weight gain towards reduction
  2. Therapy with oxygen
  3. Positive pressure ventilation
  4. Medication
  5. Tracheostomy
  6. OHS complications and comorbid illnesses management

Advanced cases of OHS require ICU admission. Such cases include: If the patient is confused and lethargic, respiratory acidosis reflected by a pH of less than 7.3, there is fatigue of the respiratory muscles, aggravation of hypoxia in the form of hypercapnia.

Pharmacotherapy

  • Medroxyprogesterone acetate, a synthetic progesterone, a breathing stimulator: This remedy has been efficiently used in patients with OHS, and elevates ventilatory response to hypercapnia. Administration of medroxyprogesterone acetate leads to a decrease in PaCO2 and an elevation in PaO2. A possible side effect is hypercoagulation, especially in those who are predisposed to this condition.
  • Acetazolamide is the carbonic anhydrase inhibitor; a moderate diuretic may become the reason for metabolic acidosis leading to an increase in minute ventilation, thus reducing PaCO2 level. In addition, acetazolamide stipulates decline of serum bicarbonate level.
  • Beta-2 agonists: albuterol, metaproterenol, atrovent affect beta-2 receptors in the bronchial smooth muscle, bronchospasm relief.

Surgical intervention

  • Vertical banded gastroplasty (VBG) allows restriction of the volume of the stomach.
  • Adjustable gastric banding (AGB)
  • Roux-en-Y gastric bypass (RYGB) is the most common procedure that provides short- and long-term after-effects regarding safety, efficiency, and durability; it is performed laparoscopically.
  • Biliopancreatic diversion (BPD) and biliopancreatic diversion with duodenal switch (BPD-DS) leading to malabsorption.
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