From the Guidelines
Polycythemia can develop as a complication of sleep apnea due to intermittent hypoxia during apneic episodes, and the primary treatment is addressing the underlying sleep apnea, typically with continuous positive airway pressure (CPAP) therapy. When sleep apnea causes repeated drops in oxygen levels during sleep, the body responds by increasing red blood cell production (erythropoiesis) to improve oxygen-carrying capacity. This secondary polycythemia is the body's compensatory mechanism to chronic intermittent hypoxemia. The relationship between sleep-disordered breathing (SDB) and pulmonary artery hypertension (PAH) has been studied, and it has been found that SDB is a common condition in the United States and western nations, with a prevalence of sleep apnea syndrome estimated to be 4% in middle-aged men and 2% in middle-aged women 1. Several studies have examined the relationship between obstructive sleep apnea (OSA) and PAH, and it has been found that OSA is a risk factor for hypertension, myocardial infarction, heart failure, and stroke 1. The use of CPAP therapy has been shown to lower systolic blood pressure and improve quality of life in patients with OSA. Most patients will see normalization of their hemoglobin and hematocrit levels within 3-6 months of consistent CPAP use. For severe cases with hematocrit above 55-60%, therapeutic phlebotomy might be temporarily needed while CPAP therapy takes effect. Weight loss, positional therapy, oral appliances, or surgical interventions may also help manage sleep apnea and consequently improve polycythemia. Regular monitoring of complete blood counts is important to track improvement. Untreated, this condition increases risks of cardiovascular complications including stroke, heart attack, and venous thromboembolism due to increased blood viscosity and hypercoagulability. Some studies have reported a higher BMI in patients with PAH compared to patients without PAH, and lower daytime Po2 and oxygen saturation during sleep were consistent predictors of PAH in sleep apnea 1. The apnea-hypopnea index (AHI) was predictive of PAH in two of the studies, and spirometric abnormalities have also been strongly associated with PAH in OSA 1. In general, patients with OSA and PAH tended to be older, heavier, and have worse lung function compared to patients with OSA and without PAH. Nocturnal desaturation was a determinant of the presence of PAH in OSA, and the degree of PH associated with SDB is not as severe as that associated with idiopathic pulmonary arterial hypertension (IPAH) or many other forms of PAH 1. The stimulus for PH is thought to be hypoxic pulmonary vasoconstriction and subsequent vascular remodeling, and studies have highlighted the role of increased tone of the autonomic nervous system, inflammatory mediators, and reactive oxygen species in the upregulation of peripheral vascular tone in patients with SDB 1. Ip and colleagues recently demonstrated that nitric oxide activity is suppressed in OSA, and that this reduction in nitric oxide expression is rapidly reversible with CPAP therapy 1. In addition to the aforementioned pathogenic stimuli, a genetic susceptibility may also contribute to a PAH predisposition in response to the chronic sustained or intermittent hypoxia that occurs in SDB. Polycythemia vera (PV) is a chronic myeloproliferative disorder (CMPD) that can cause an increased risk of thrombosis, and the management of PV involves phlebotomy, myelosuppressive agents, and low-dose aspirin 1. However, the relationship between PV and sleep apnea is not well established, and further studies are needed to determine the optimal management of patients with both conditions. In the meantime, the primary treatment for polycythemia secondary to sleep apnea should focus on addressing the underlying sleep apnea with CPAP therapy, and monitoring for cardiovascular complications.
From the Research
Relationship Between Polycythemia and Sleep Apnea
- Polycythemia is reported to be a condition that can be caused by obstructive sleep apnea (OSA) 2.
- The prevalence of polycythemia in patients with OSA is estimated to be around 2%, with a higher prevalence in severe OSA cases (6%) 2.
- Continuous positive airway pressure (CPAP) treatment has been shown to reduce hemoglobin and hematocrit levels in patients with OSA, suggesting a link between OSA treatment and polycythemia management 2, 3.
Effects of CPAP Treatment on Blood Parameters
- CPAP treatment has been found to reduce mean platelet volume (MPV) values, but increase platelet distribution width (PDW) and red cell distribution width (RDW) in patients with severe OSA 3.
- CPAP treatment has also been shown to reduce hemoglobin levels by 3.76 g/L and hematocrit levels by 1.1% in patients with OSA 2.
Case Studies and Observations
- A case study reported a patient with hemodialysis-dependent stage 5 chronic kidney disease who developed polycythemia due to OSA, which was successfully treated with CPAP therapy 4.
- Another study found that OSA severity was not directly associated with hematocrit or clinically significant erythrocytosis, but rather with hypoxemia as measured by awake and mean nocturnal oxygen saturation 5.
Treatment and Management
- Positive airway pressure (PAP) therapy is considered first-line therapy for moderate to severe OSA and may also be considered for mild OSA, particularly if it is symptomatic or there are concomitant cardiovascular disorders 6.
- Close follow-up of patients is important to evaluate adherence to and effectiveness of PAP treatment 6.