During the 13-year study period, a fatal outcome was found in 95 CLL patients. The mortality of patients with CLL was analyzed and morphological changes in the lungs, bronchi, and pleura in these patients were studied according to autopsy data. The terminal stage of CLL is more often manifested by the transformation into a large cell lymphosarcoma, the development of cachexia. Prolymphocytic crisis was observed in only two patients. Blast crisis CLL in our study is not registered. The immediate causes of death of patients with CLL are given.
Histological examination of autopsy material showed lymphoid infiltration of the lungs and bronchi in 43 patients (45%). However, only 5 patients had massive leukemic infiltration, which was radiologically detected in the form of focal or infiltrative shadows, and then the diagnosis was made after long-term follow-up of the disease and exclusion of other local processes in the lungs. In the same patients, lymphoid infiltration was diagnosed macroscopically at autopsy. Histological examination of the lungs in these situations revealed a total monomorphic leukemic infiltration along the interalveolar septa, filling the lumen of the alveoli and vessels with lymphocytes . In all other cases, lymphoid infiltration was detected only with microscopic Optical research . Lymphoid infiltration in the lungs was predominantly interstitial. Often, in the stage of malignant transformation, there was a total infiltration of the interstitial lung tissue. Lei goat infiltration was very pronounced along the bronchi, small vessels and in the interalveolar septa, often it was of a confluent nature. Hemorrhages were observed in the interstitial and respiratory tissue with a perivascular edema. Foci of leukemic infiltration in respiratory structures were less frequently observed.
Histological examination in the lungs showed an expansion and congestion of blood vessels, the lumens of many vessels were filled with lymphocytes (leukostasis) . Leukostasis was especially frequently detected in small-caliber vessels. The accumulations of lymphocytes in these situations completely blocked the gaps of small vessels, causing a significant disruption of microcirculation . In some patients, infiltration of the walls of the pulmonary vessels with tumor cells and multiple perivascular arteries of lymphoid cells were noted.
Peribronchial, perivascular, interstitial sclerosis was revealed in many patients. Multiple atelectasis of the lung tissue alternated with areas of emphysematous dilatation of the alveoli, as well as edema and sclerosis of the interalveolar septa . In patients with CLL, it is possible to express an assumption about the compensatory nature of the localized pulmonary emphysema. In some areas, in the presence of diffuse lymphoid infiltration of the pulmonary tissue and an increase in bronchopulmonary lymph nodes, alveoli are excluded from ventilation due to atelectasis. A decrease in the area and ventilation capacity of other alveoli due to edema, sclerosis of the interalveolar septa, lymphoid infiltration of the interalveolar septa, desquamation of the alveolar epithelium is noted. In the remaining parts of the lung, the expansion of the alveoli occurs compensatory. These changes are more pronounced in CLL patients in the later stages of the tumor progression. Speaking of emphysema in patients with CLL, it is also necessary to take into account the elderly age of most patients,in this case, senile emphysema may occur.
Morphometric studies were conducted in patients who died in the presence of CLL. When performing a morphometric study of the bronchi and alveoli, a comparative analysis was carried out with similar indicators of 30 absolutely healthy people, equal in age and sex, who died from injuries incompatible with life and who did not have a history of hemoblastosis and bronchopulmonary pathology (control group).