Can a pulmonary arteriovenous malformation (AVM) cause elevated white and red blood cell counts?

Pulmonary AVMs Do Not Directly Cause Elevated White or Red Blood Cell Counts

Pulmonary arteriovenous malformations (AVMs) are not a recognized cause of elevated white blood cell (WBC) or red blood cell (RBC) counts. The pathophysiology of pulmonary AVMs involves abnormal direct connections between pulmonary arteries and veins that bypass the capillary bed, leading to right-to-left shunting and hypoxemia—not hematologic abnormalities 1, 2.

Why Pulmonary AVMs Don't Cause Blood Count Elevations

Mechanism of Pulmonary AVMs

• Pulmonary AVMs create direct vascular communications between pulmonary arteries and veins, bypassing the normal capillary bed where gas exchange occurs 2, 3
• This anatomic shunt results in deoxygenated blood flowing directly into the pulmonary veins without oxygenation, causing hypoxemia in 27-71% of patients 1, 2
• The primary pathophysiologic consequence is impaired oxygenation and loss of the pulmonary capillary filter function—not stimulation of bone marrow or inflammatory responses 1

Expected Clinical Manifestations

• Hypoxemia is the hallmark finding, manifesting at rest or during exercise 1
• Orthodeoxia and platypnea occur characteristically because 65-83% of pulmonary AVMs are located in the lower lung lobes, causing gravity-dependent worsening of shunting 1, 2
• Paradoxical emboli leading to transient ischemic attacks and strokes occur in 3.2-55% of patients due to loss of the pulmonary capillary bed's filtering function 1
• Cerebral abscesses develop in 0-25% of cases from systemic infections bypassing pulmonary filtration 1

When to Consider Alternative Diagnoses

If Leukocytosis is Present

• Infection/abscess: Cerebral abscesses occur in up to 25% of pulmonary AVM patients and would cause elevated WBC counts 1
• Concurrent infection: Pulmonary infections or empyema can occur alongside AVMs (as documented in tuberculosis-related cases) and would elevate WBC 4
• Inflammatory conditions: Hereditary hemorrhagic telangiectasia (HHT), present in 70-90% of pulmonary AVM cases, does not itself cause leukocytosis 1, 5

If Erythrocytosis is Present

• Secondary polycythemia: Chronic hypoxemia from large or multiple pulmonary AVMs could theoretically trigger compensatory erythropoietin production and secondary polycythemia, though this is not a documented typical feature 1, 2
• Unrelated primary hematologic disorder: The elevated counts likely represent a separate pathologic process requiring independent evaluation

Critical Clinical Pitfall

Do not attribute elevated blood counts to the pulmonary AVM itself. Instead, investigate for:

• Infectious complications of the AVM (particularly cerebral abscess) if WBC is elevated 1
• Chronic hypoxemia-driven secondary polycythemia if RBC is elevated (though this would require significant shunting) 2
• Completely unrelated hematologic conditions that coincidentally coexist with the AVM

Context from Related Conditions

The provided evidence discusses chronic thromboembolic pulmonary hypertension (CTEPH), which mentions "hypercoagulation, 'sticky' red blood cells, high platelet counts" as contributing factors to pulmonary artery obliteration 6. However, this refers to CTEPH pathophysiology, not pulmonary AVMs, which are entirely different entities with distinct mechanisms. CTEPH involves chronic thrombotic obstruction, while AVMs are abnormal vascular connections—these should not be conflated.