Macroscopically, focal, focal-confluent, and polysegmental pneumonia, on the background of pronounced pulmonary edema, looked like compaction areas ranging in size from 1 to 5 cm in diameter, from grayish-red to dark-red. These areas protruded above the surface of the incision of the lungs. Histologically, in the alveoli, exudates with a predominance of fibrin and a small number of neutrophils were found. There were signs of circulatory disorders on the periphery of the alveoli filled with exudate. A number of patients were diagnosed with resorption of fibrinopurulent exudate and growth in these areas of granulation and connective tissue in the form of Masson’s bodies (carnification, organization). Changes in the bronchi were local in the area of ​​chronic inflammation. Peribronchial changes prevailed: peribronchial tissue thickening,deformation and constriction of the bronchi with unevenly expanded gaps. In areas of carnification, clusters of alveolar macrophages and desquamated type 2 alveolocytes, the formation of granulation tissue inside the alveoli and respiratory bronchioles, and focal pulmonary fibrosis were detected in the lumen of the alveoli. The organization of exudate in the alveoli was detected against the background of marked infiltration of the interalveolar septa with lymphocytes. Clutches of lymphocytes were formed around small vessels. Often, interlobular, intersegmental, peribronchial fibrosis and obliteration of the terminal and respiratory bronchioles were noted. Microscopic examination of lymphoid infiltration of interalveolar septa, signs of “organizing pneumonia” and obliterating bronchiolitis were detected by microscopic examination of the majority of patients who died of CLL with severe pneumonia.In blood vessels of various calibers, leukostasis was noted with infiltration of the vessel walls with lymphocytes. In the centers of carnification and pneumosclerosis, cavities having a rounded or convoluted shape were often detected. These cavities were islands of preserved alveoli. In the areas of granulation tissue, the formation of a large number of capillaries was noted. In a number of pneumosclerosis foci, in a number of patients, vascular reduction and the appearance of arteriovenous anastomoses were detected. Morphological changes in the lungs (lymphoid infiltration of the interalveolar septa, impaired microhemocirculation and tissue trophism, “organized pneumonia”, bronchiolitis obliterans) contributed to the severe and prolonged course of pneumonia in these patients.In the centers of carnification and pneumosclerosis, cavities having a rounded or convoluted shape were often detected. These cavities were islands of preserved alveoli. In the areas of granulation tissue, the formation of a large number of capillaries was noted. In a number of pneumosclerosis foci, in a number of patients, vascular reduction and the appearance of arteriovenous anastomoses were detected. Morphological changes in the lungs (lymphoid infiltration of the interalveolar septa, impaired microhemocirculation and tissue trophism, “organized pneumonia”, bronchiolitis obliterans) contributed to the severe and prolonged course of pneumonia in these patients.In the centers of carnification and pneumosclerosis, cavities having a rounded or convoluted shape were often detected. These cavities were islands of preserved alveoli. In the areas of granulation tissue, the formation of a large number of capillaries was noted. In a number of pneumosclerosis foci, in a number of patients, vascular reduction and the appearance of arteriovenous anastomoses were detected. Morphological changes in the lungs (lymphoid infiltration of the interalveolar septa, impaired microhemocirculation and tissue trophism, “organized pneumonia”, bronchiolitis obliterans) contributed to the severe and prolonged course of pneumonia in these patients.In a number of pneumosclerosis foci, in a number of patients, vascular reduction and the appearance of arteriovenous anastomoses were detected. Morphological changes in the lungs (lymphoid infiltration of the interalveolar septa, impaired microhemocirculation and tissue trophism, “organized pneumonia”, bronchiolitis obliterans) contributed to the severe and prolonged course of pneumonia in these patients.In a number of pneumosclerosis foci, in a number of patients, vascular reduction and the appearance of arteriovenous anastomoses were detected. Morphological changes in the lungs (lymphoid infiltration of the interalveolar septa, impaired microhemocirculation and tissue trophism, “organized pneumonia”, bronchiolitis obliterans) contributed to the severe and prolonged course of pneumonia in these patients.

In all CLL patients who died when pneumonia was attached, there was an increase in the lymph nodes in the chest cavity, 14 of them had sarcomal transformation of these lymph nodes. Enlarged, sarcomotransformed, dense lymph nodes with Richter syndrome squeezed the lung tissue and bronchi, which contributed to impaired lung ventilation function, bronchial drainage function and the emergence of the inflammatory process.

As an example, here are two extracts from archival case histories.

Extract from the case history No 14267. Patient G., born in 1936. Diagnosis: chronic lymphocytic leukemia, tumor form, stage C according to the classification of J. Binet. The diagnosis of CLL was made in 2002, confirmed by histological examination of the lymph node and immunophenotyping of peripheral blood lymphocytes (CD5 +, CD19 +, CD20 +, CD22 +, CD23 +). Concomitant diseases: ischemic heart disease, circulatory failure IIA.

Upon admission to the hospital (March 12, 2006), there is an increase in the lymph nodes of all peripheral groups up to 5–6 cm in diameter with a densely elastic consistency, soldered between each other, form “packages”, with surrounding tissues are not soldered, without painful. Packings of enlarged abdominal lymph nodes are palpable through the anterior abdominal wall. The lower edge of the liver is palpated 8 cm below the costal arch. The spleen is palpable 13 cm below the left costal margin. In the lungs, vesicular breathing and wheezing are not heard. Heart sounds are muffled, the rhythm is right. Blood pressure 150/90 mm. Hg Art.HR – 88 beats per minute. A blood test (from 13.03.2006): hemoglobin – 68 g / l, red blood cells – 2.7 × 10 12 / l, leukocytes – 166.7 × 10 9 / l, platelets – 90 × 10 9 / l, lymphocytes – 98%, segmented – 2%, ESR – 10 mm / h. CCFG: lungs without focal and infiltrative shadows, the roots of the lungs are enlarged. ERTGS – an increase in mediastinal lymph nodes. Immunogram: CD 3 – 29.0%, CD 4 – 19.1%, CD 8 – 19.0%, CD 4 / CD 8 – 1.0, CD 20 – 63.1%, CD 22 – 30.2 %, immunoglobulins: A – 1.1 g / l, M – 1.0 g / l, G – 8.0 g / l. The patient underwent a course of therapy with fludararabine (Fludar tablet tablets, at a dose of 30 mg / m 2 , 1 – 5 days) in combination with cyclophosphate (at a dose of 200 mg / m 2 , 1 – 5 days), red blood cell transfusions, etc. Positive dynamics was observed: the lymph nodes of all peripheral groups decreased to 2–2.5 cm in diameter. The size of the liver and spleen has decreased. The lower edge of the liver protrudes 5 cm from the edge of the costal arch, the lower edge of the spleen is palpable 4 cm below the left costal edge. A blood test (from March 25, 2006): hemoglobin – 104 g / l, erythrocytes – 3.3 × 10 12 / l, leukocytes – 27.9 × 10 9 / l, platelets – 100 × 10 9 / l, lymphocytes – 96%, segmented – 4%, ESR – 18 mm / h. The patient notes improvement in well-being, preparing for discharge. On March 28, 2006, the temperature suddenly rose to 39 С. Chills. Tachycardia up to 120 beats per minute. Severe weakness, indisposition, shortness of breath at rest, feeling of lack of air. A decrease in blood pressure to 100 and 50 mm Hg is noted. During auscultation in the lower parts of the right lung moist rales are heard. An x-ray examination of the lungs was performed (March 29, 2006). Conclusion: focal-confluent pneumonia in the lower lobe of the right lung. In the clinical analysis of blood from March 29, 2006, the number of leukocytes decreased to 2.5 × 10 9 / l. KHS and blood gas composition: pH – 7,323; pCO 2 – 48.6 mm. Hg Art., pO 2 – 56.6 mm. Hg Art., O 2 SAT – 88%, O 2 CONT – 12.7 vol /%, AaDO 2 – 44.9 mm. Hg Art. In the sputum and bronchial washings, the pathogen was not detected in the pathogenic titer. Empirical therapy with broad-spectrum antibiotics was performed. Initially, the combination of ciprofloxacin (0.4 × 2 p / day, IV drip) and medocef (2.0 × 2 p / day, IV drip) was prescribed, followed by the combination of sulperazone (4.0 × 2 p / day, iv drip) and amikacin (1.5 g. 1p. per day). Immunomodulatory (immunoglobulins), antimycotic (mycosyst, mycoflucan) and detoxification therapy were prescribed. Blood pressure values ​​normalized on the fifth day, dyspnea stopped on the 10th day of treatment, the temperature returned to normal on the 18th day, wheezing stopped listening on the 16th day. Weakness, malaise persisted. 04/29/2006, a repeated X-ray of the lungs was taken.On control radiographs in the frontal and lateral projections, a decrease in pneumonic infiltration in the lower part of the right lung was determined (S 4-5-10). Conclusion: right-sided foci-confluent pneumonia in the resolution stage. For 4 weeks, pneumonia was not completely resolved, took a protracted course. The treatment was continued – a combination of fortum (2g. × 2 p / day, intravenous droplet) and ciprofloxacin in the same dose (given the good effect of prescribing this antibiotic). Immunomodulatory and detoxification therapy was continued. On radiographs from 13.05.2006, infiltration is not determined. As a complication, the development of focal pneumofibrosis is noted. Full normalization of well-being (the absence of all extrapulmonary manifestations of pneumonia) was also noted at the beginning of May 2006.In this case, classical nosocomial pneumonia took place in a patient with CLL that developed after a course of polychemotherapy, which has a heavy and protracted course.

Extract from the case history No 4239. Patient K., born in 1955. Diagnosis: Chronic lymphocytic leukemia, progressive form, stage C according to the J. Binet classification. CLL was diagnosed in 2004. Clinical blood test from 2004. – hemoglobin – 135g / l, erythrocytes – 3.9 × 10 12 / l, leukocytes – 35 × 10 9 / l, lymphocytes 73%, choke-core – 2%, segmented core – 20%, monocytes – 5%, platelets – 180 × 10 9 / l. Immunophenotype of peripheral blood lymphocytes – CD5 +, CD19 +, CD20 +, CD22 +, CD23 +. Expressed expression of CD38 was not observed at that time. Peripheral lymph nodes of all groups in 2004 did not exceed 1.5 – 2 cm. Liver, spleen were not enlarged. At that time, the stage A CLL was classified according to the Binet classification. Within two years, there was no significant progression of hemoblastosis, cytostatic therapy was not prescribed, and patients were monitored dynamically. Deterioration since September 2006: peripheral lymph nodes, liver, spleen began to increase; leukocytosis increased progressively; anemia and thrombocytopenia increased. Blood count: hemoglobin – 89g / l, erythrocytes – 2.78 × 10 12 / l, leukocytes – 134.16 × 10 9 / l, lymphocytes 86%, prolymphocytes – 8%, segment-nuclear – 6%, platelets – 70 × 10 9 / l. The patient was prescribed mono-therapy with fludarabine, subsequently the FCR protocol. But a persistent therapeutic effect was not observed. In June 2007 Clinical and X-ray studies diagnosed destructive pneumonia in the S 6 segment. left. Pulmonary tuberculosis was excluded (sputum and bronchial lavages at KUM, CT of the lungs were repeatedly examined, consultation with a phthisiologist). From the bronchial washings, S. pneumoniae and neisseria were sown. In the treatment of pneumonia, a combination of broad-spectrum antibiotics was used to identify the causative agent; after the causative agent was detected, antibiotic therapy was corrected taking into account its sensitivity. Immunomodulatory, antimycotic, anti-inflammatory therapy was prescribed. Fully clinical and radiological manifestations of pneumonia resolved in August 2007. October 18, 2007 He was taken to the therapeutic department of the CRH (at the place of residence) by an ambulance in a critical condition. There was an increase in body temperature to 39 – 40 ̊С, a decrease in blood pressure, severe shortness of breath. Clinical blood test:red blood cells – 2.4 × 10 12 / l, hemoglobin – 67 g / l, leukocytes – 274 × 10 9 / l, lymphocytes – 87%, prolymphocytes – 10%, segmented cells – 3%, platelets – 50 × 10 9 / l, ESR – 61 mm / h . During the X-ray examination, pneumonia was again diagnosed in the S 6 segment on the left. Despite the conduct of adequate antibacterial, anti-inflammatory, immunomodulating, detoxification therapy, 20.10.2007. a lethal outcome was established with the phenomena of bacterial toxic shock. Histological examination of tissue S 6 the left lung revealed lymphoid infiltration of the pulmonary interstitium; in the alveoli exudate was found with a significant predominance of fibrin, a small number of neutrophils, accumulations of bacteria. In this case, the focus of inflammation was localized in the area of ​​lymphocytic infiltration of the lung, which, along with pronounced immunodeficiency, caused severe and recurrent pneumonia.

Based on a study of the clinical and morphological features of the course of pneumonia in CLL patients, the following conclusion can be drawn : 1. Pneumonia is the most common infectious complication of CLL (103 patients out of 228 examined, which is 45%). As CLL progresses, the incidence of pneumonia increases. Patients with CLL have a high incidence of nosocomial pneumonia (36%).
 
 
 For patients with CLL, the prevalence of prolonged (53.4%), severe (60%) and atypical (27.6%) course of pneumonia is characteristic. The causes of atypical, severe, and protracted pneumonia in CLL are: a) pronounced secondary immunodeficiency, primarily neutrophil deficiency and hypo-immunoglobulinemia, b) courses of chemotherapy and glucocorticoid therapy, which contribute to the development of an ammunition deficit, aggravating the development of the ammunition and corticosteroids, which contribute to the development of an inadequate case of chemotherapy and glucocorticoid therapy, which contribute to the inadequacy of cortical diseases, which contribute to the development of an obstructive, severe and prolonged course of pneumonia in CLL; lung tissue and bronchi, d) significant microcirculation in the lungs and bronchi, e) pulmonary ventilation disturbance and perfusion, e) elderly rast of most CLL patients, g) presence of concomitant diseases (COPD, IHD, diabetes, etc.), pulmonary ventilation function and bronchial drainage function. Gram-negative flora occupies an important place among pneumonia pathogens in patients with CLL – 56% of the total number of hospital pneumonia and 26.3% of cases of community-acquired pneumonia. In accordance with the occurrence of pneumonia in the hospital or outside the hospital, the suspected causative agent, the clinical and pathogenetic situation and the presence of underlying diseases, an empirical antibiotic therapy of pneumonia has been compiled in patients with CLL
 identifying the pathogen and determining its sensitivity to antibiotics, as well as for those situations when it is impossible to establish the etiological diagnosis of pneumonia.