ABSTRACT
Clinical findings Onset Tends to be abrupt early; tightness Usually subtle; dyspnea on exer Symptoms in chest, cough, dyspnea tion; cough (often productive)
Hematological Leukocytosis Normal Physiological Oxygen desaturation Normoxia until late
Radiological Primarily restrictive disease Diffuse infiltates, effusions
Primarily obstructive disease No abnormality until late
Histological Perivascular mononuclear cell infil Obliterative bronchiolitis; venous
Response to therapy
trates ± airway inflammation
Usually responds briskly to pulsed
and arterial sclerosis ± perivas cular mononuclear cell infiltrates
Progressive decline in lung func doses of steroids but often re curs (most recipients have more than one episode)
tion over months to years is the rule
primary histological abnormality is obliterative bronchiolitis (OB), but there is also dam age to blood vessels, particularly veins, which undergo sclerosis. At many centers, transbronchial lung biopsy is not sensitive in detecting OB. In addition, there are other causes for this histological finding that are not due to an immunological response to donor antigen, such as infection, chronic aspiration of gastric contents, and drug reactions. For this reason there has been strong movement toward defining late graft dysfunction due to airflow obstruction as the bronchiolitis obliterans syndrome (BOS) when no other cause for the decline in lung function can be demonstrated. This diagnosis does not require confirmation of histological OB, but it does depend on the exclusion of other conditions in the allograft, such as acute rejection and infection, which usually requires bronchoscopy with bronchoalveolar lavage and transbronchial lung biopsy.
