By Lisa Linegar-Johnson
For clinicians evaluating obese patients for possible obstructive sleep apnea, diagnosis and treatment is not as clear-cut for patients with a normal BMI. Obesity Hypoventilation Syndrome (OHS), characterized by awake hypercapnia (defined by a PaCO2≥45 mm Hg) and a BMI of ≥ 30 kg/m^2, when other potential causes such as neuromuscular or lung disease have been ruled out, is increasing in the population. Diagnosis and treatment guidelines are complex, with variable patient presentation.
There are two typical pathways for a patient with potential OHS to sleep evaluation. One is a referral to a sleep clinic after a hospital discharge in which the patient has been admitted for respiratory failure. These patients may have typical co-morbidities such as hypertension, CHF and diabetes. Other patients may arrive at a sleep clinic, looking like any other sleepy, obese OSA patient. Studies estimate that approximately 0.3% to 0.4% of the general population has OHS. Of those going to a clinic for a sleep study, studies estimate that 10-20% of this patient population have OHS. Fifty percent of patients with a BMI of 50 kg/m^2 or more that are admitted to the hospital have OHS.
The most reliable way to determine if an obese patient has OHS is a daytime ABG to determine if PaCO2 levels are ≥ 45 mm Hg. Pulse oximetry showing less than 94% SpO2 may prompt some clinicians to order an ABG. Absent that, a serum bicarbonate level as part of a metabolic panel can also help screen for OHS. If your patient has a serum bicarbonate level of 27 mEq/L or greater, this may be an indicator of possible OHS.
A basic visual of patients may also help screen for OHS. Patients with central fat distribution are more likely to have OHS. Central fat pushes the diaphragm towards the head, causing decreased lung compliance. Higher waist/hip ratios and larger neck circumference are both indicators of a greater likelihood of OHS. All these factors combine to increase the work of breathing, meaning smaller lung volumes and small airway closure, leading to air trapping.
The sleep study of a patient with OHS will most likely show apneas and hypopneas caused by upper airway obstruction. One large study revealed that 73% of patients diagnosed with OHS had severe sleep apnea (AHI≥30). However, a patient with OHS will also show longer periods of apnea or abnormal breathing, followed by short periods of breathing that are not adequate to offload accumulating CO2 in the body. This leads the body to compensate by increasing renal bicarbonate levels, causing a decreased response to CO2 when the patient is awake. This problem is compounded by the fact that obese people consume more oxygen and produce more carbon dioxide sim due to their higher body mass. Those who cannot compensate for this with an increased respiratory drive usually develop OHS.
While there are currently no specific guidelines for the treatment of OHS from the AASM, the typical first step is to place the patient on a CPAP to eliminate apneas and hypopneas, and bring O2 saturations to >90%. If this treatment is adequate, daytime blood gases will improve within several days. Should this step fail to resolve oxygen desaturation, the elimination of upper airway obstruction through CPAP has not been enough, and additional treatment is needed to increase ventilation. BIPAP may be prescribed, with the EPAP level set the same as the CPAP setting needed to treat upper airway obstruction, and the IPAP level increased until SpO2=90%. A back-up respiratory rate may also be needed as an additional tool to prevent hypoventilation. Supplementary oxygen is usually only used if the patient has additional lung or heart disease present.
The consequences of OHS are severe. In one study, patients that were diagnosed with OHS had a 23% mortality rate 18 months after hospital discharge, compared with 9% of patients that were simply obese. Patients with OHS have greater cardiometabolic morbidity than patients with OSA or severe obesity alone. Notably, in one study, almost half the patients diagnosed with OHS who refused NIV treatment died within a 50 month period, “compared with 3 of the 54 patients managed with positive pressure therapy.”
With this in mind, researchers have evaluated the best way to treat OHS, both when diagnosed with severe sleep apnea and without. In one study, reported in 2014, OHS patients without severe sleep apnea were separated into three groups: lifestyle modification alone (1000 calorie diet, correct sleep hygiene and habits), lifestyle modification and CPAP, and a third group, which was assigned lifestyle modification and the use of a BIPAP with a back-up respiratory rate. In each group, PaCO2 improved, but the improvement was greatest in the group that used the NIV, especially in comparison with the lifestyle modification only group.
Similar results were seen in a study of patients diagnosed with OHS, who were also diagnosed with severe sleep apnea (AHI≥30). Again, patients were separated into three groups: lifestyle modification alone, lifestyle modification and CPAP, and a third group, which performed lifestyle modifications and used a BIPAP with a back-up respiratory rate. Once again, the greatest improvement was seen in the group that used BIPAP in comparison with the lifestyle modification only group. It is worth noting that in each study, patients using BIPAP only had a slight improvement in comparison with the CPAP group.
In closing, patients that show signs of possible OHS should be identified early in their evaluation for sleep-disordered breathing. The implications of untreated OHS are severe; increased morbidity and more frequent hospitalizations. Evaluating ABG’s and serum bicarbonate levels, as well as looking for the presence of central fat distribution in the patient can help identify this population. Sleep studies may also show prolonged periods of apnea or abnormal breathing, in addition to apneas and hypopneas.
Lisa Linegar-Johnson is a respiratory therapist who has worked in home health and currently works as a Pulmonary Function Technologist for the Multicare System in the Tacoma, Washington area.
Sources:
“Non-invasive Ventilation in Obesity Hypoventilation Syndrome without Severe Obstructive Sleep Apnea” http://thorax.bmj.com/content/71/10/899
“Efficacy of Different Treatment Alternatives for Obesity Hypoventilation Syndrome. Pickwick Study” http://www.atsjournals.org/doi/10.1164/rccm.201410-1900OC
“Obesity Hypoventilation Syndrome, Mechanisms and Management” http://www.atsjournals.org/doi/abs/10.1164/rccm.201008-1280CI
“Obesity Hypoventilation Syndrome” https://pdfs.semanticscholar.org/74ac/c1aff29dcbab3a3baab19dda6345ed2c3086.pdf
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