Common contributors include:

1. Higher hematocrit (more red blood cells per volume of blood), a major determinant of whole-blood viscosity. [9][10]
2. Higher plasma protein levels (for example, monoclonal proteins in Waldenström macroglobulinemia or multiple myeloma), which can increase serum/plasma viscosity and cause classic hyperviscosity symptoms. [8][11]
3. Reduced plasma volume (hemoconcentration), which can make lab values (like hemoglobin/hematocrit) appear elevated even without a true increase in red cell mass. [1][12]

1. Dehydration or reduced plasma volume (hemoconcentration)

Fluid loss (or inadequate intake) can reduce plasma volume and concentrate blood components, sometimes raising measured hemoglobin/hematocrit until hydration is restored. [1][7]

2. Polycythemia vera (PV)

PV is a myeloproliferative neoplasm in which the bone marrow produces too many blood cells—most notably red blood cells—often driven by JAK2 variants. Increased hematocrit can increase viscosity and contribute to microvascular symptoms and thrombosis risk. [5][7][9]

3. Chronic low oxygen states (secondary erythrocytosis)

Chronic or intermittent hypoxia (for example, advanced lung disease, some congenital heart disease, or sleep-disordered breathing) may stimulate erythropoietin signaling and increase red cell production, raising hematocrit and viscosity in some patients. [13][14]

4. High altitude adaptation

At higher altitude, lower oxygen availability can drive physiologic changes that may increase red cell production in some people; in a minority, erythrocytosis can become excessive. [14]

5. Erythropoietin-producing tumors or paraneoplastic erythrocytosis (less common)

Some tumors can increase erythropoietin signaling, leading to secondary erythrocytosis. This is uncommon but clinically important when erythrocytosis is unexplained. [1][7]

6. Medication- or hormone-associated erythrocytosis

Exogenous androgens (including testosterone) can increase hemoglobin/hematocrit in some individuals and may contribute to hyperviscosity-related concerns depending on degree and clinical context. [1][7]

7. Inflammation and higher fibrinogen (blood “stickiness”)

Inflammation can increase acute-phase proteins such as fibrinogen, which can raise plasma viscosity and promote red cell aggregation—potentially worsening flow properties. [15][16]

8. Hyperviscosity from high immunoglobulins (plasma cell disorders)

In disorders such as Waldenström macroglobulinemia (and less often multiple myeloma), high immunoglobulin levels can drive symptomatic hyperviscosity (e.g., mucosal bleeding, visual changes, neurologic symptoms) and requires urgent medical care. [8][11]

Symptoms are non-specific and depend on cause and severity. Examples clinicians may consider include bleeding, headache, dizziness, visual disturbances, shortness of breath, and—depending on condition—microvascular symptoms or thrombotic events. Symptoms alone cannot confirm a cause. [7][17]

Persistently increased viscosity (or the conditions associated with it) may increase the likelihood of circulation problems and, in some settings, thrombosis.

For PV specifically, randomized evidence supports maintaining hematocrit below 45% to reduce cardiovascular death and major thrombosis. [7][9]

If “thick blood” is suspected based on symptoms or blood tests, clinicians typically evaluate:

• Whether the finding reflects hemoconcentration (low plasma volume) versus true erythrocytosis [1][6]
• Oxygen status and secondary causes (including sleep-disordered breathing in appropriate cases) [7][13]
• Whether a hematologic disorder such as PV is a concern and whether disease-specific management is needed [5][9]

PV — Polycythemia vera

JAK2 — Janus kinase 2

1. Haider, M. Z., & Anwer, F. (2023, May 8). Secondary polycythemia. In StatPearls [Internet]. StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK562233/
2. Mondal, H., & Zubair, M. (2024, October 6). Hematocrit. In StatPearls [Internet]. StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK542276/
3. Kwaan, H. C. (2010). Role of plasma proteins in whole blood viscosity: A brief clinical review. Clinical Hemorheology and Microcirculation, 44(3), 167–176. https://doi.org/10.3233/CH-2010-1271
4. Taylor, K., & Madden, J. (2025, March 5). Adult dehydration. In StatPearls [Internet]. StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK555956/
5. Lu, X., Alhaj Moustafa, M., et al. (2023, April 24). Polycythemia vera. In StatPearls [Internet]. StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK557660/
6. Mithoowani, S., Laureano, M., Crowther, M. A., & Hillis, C. M. (2020). Investigation and management of erythrocytosis. CMAJ, 192(32), E913–E918. https://doi.org/10.1503/cmaj.191587
7. StatPearls. (n.d.). Polycythemia. In StatPearls [Internet]. StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK526081/
8. Mehta, J., & Singhal, S. (2003). Hyperviscosity syndrome in plasma cell dyscrasias. Seminars in Thrombosis and Hemostasis, 29(5), 467–471. https://doi.org/10.1055/s-2003-44554
9. Marchioli, R., Finazzi, G., Specchia, G., et al. (2013). Cardiovascular events and intensity of treatment in polycythemia vera. The New England Journal of Medicine, 368(1), 22–33. https://doi.org/10.1056/NEJMoa1208500
10. Kishimoto, S., Maruhashi, T., Kajikawa, M., et al. (2020). Hematocrit, hemoglobin and red blood cells are associated with vascular function and vascular structure in men. Scientific Reports, 10, 11467. https://doi.org/10.1038/s41598-020-68319-1
11. Cleveland Clinic. (n.d.). Erythrocytosis. Retrieved February 4, 2026, from https://my.clevelandclinic.org/health/diseases/23468-erythrocytosis
12. Rha, M. S., Jeong, Y., Kim, J., Kim, C. H., Yoon, J. H., & Cho, H. J. (2022). Is obstructive sleep apnea associated with erythrocytosis? A systematic review and meta-analysis. Laryngoscope Investigative Otolaryngology, 7(2), 627–635. https://doi.org/10.1002/lio2.751
13. Villafuerte, F. C., Simonson, T. S., Bermudez, D., & León-Velarde, F. (2022). High-altitude erythrocytosis: Mechanisms of adaptive and maladaptive responses. Physiology, 37(4), 0. https://doi.org/10.1152/physiol.00029.2021
14. Sui, J., Noubouossie, D. F., Gandotra, S., & Cao, L. (2021). Elevated plasma fibrinogen is associated with excessive inflammation and disease severity in COVID-19 patients. Frontiers in Cellular and Infection Microbiology, 11, 734005. https://doi.org/10.3389/fcimb.2021.734005
15. Hoffmeister, A., Hetzel, J., Sander, S., Kron, M., Hombach, V., & Koenig, W. (1999). Plasma viscosity and fibrinogen in relation to haemodynamic findings in chronic congestive heart failure. European Journal of Heart Failure, 1, 293–295. https://doi.org/10.1016/S1388-9842(99)00030-6
16. Perez Rogers, A., & Estes, M. (2023, March 13). Hyperviscosity syndrome. In StatPearls [Internet]. StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK518963/
17. Weaver, A., Rubinstein, S., & Cornell, R. F. (2020). Hyperviscosity syndrome in paraprotein secreting conditions including Waldenstrom macroglobulinemia. Frontiers in Oncology, 10, 815. https://doi.org/10.3389/fonc.2020.00815