An ultrasound examination of the diaphragm in patients of group I showed no significant changes compared to controls. The thickness of the diaphragm did not change. The position, shape, echogenicity of the diaphragm also did not differ from the control. Excursion of the diaphragm with calm and forced breathing did not differ from control. In patients of group II, the thickness of the diaphragm did not change, but its echo structure became heterogeneous. Marked flattening of the dome of the diaphragm. Significantly decreased excursion of the diaphragm. In group III, the largest morphological changes in the diaphragm were revealed. Its dome was not clear, the echo structure became non-uniform. The mobility of the diaphragm significantly decreased. EDS and EDF were significantly reduced. Decrease in the expansion of the diaphragm and its morphological restructuring, with MM,specific myelomatous damage to the diaphragm (plasma cell and lymphoid infiltration, the presence of protein stasis in vessels with impaired microcirculation, etc.), impaired chest movements in patients with severe osteodestructive process, in the presence of renal failure – uremic defeat afragmal muscle .
In patients of group II, a significant correlation dependence was found between a decrease in EDF and a decrease in the MOB of the lower (r = 0.89; P <0.001) and middle zones of the lungs (r = 0.56; P <0.05), between decrease EDS and a decrease in the MVR of the lower (r = 0.62 P <0.05) and middle zones (r = 0.56; P <0.05) of the lungs. In group III patients, a clear correlation was found between a decrease in EDF and a decrease in the MOBP of the lower lung zones (r = 0.56; P <0.05), between a decrease in the EDS and a decrease in the MOP of the lower lung zones (r = 0.52; P < 0.05). At the same time, no reliable correlation was found between the EDF, EDS and MOVr indices of the upper and middle zones. lungs. Smaller correlation indicators (compared to group II) between the decrease in the excursion of the diaphragm and the ventilation capacity of the lower zones of the lungs, the lack of reliable links between the excursion rates of the diaphragm and the ventilation of the middle zones is explained by the fact that in violation of the ventilation of the lungs, specific bronchopulmonary manifestations of CRF — nephrogenic edema, pneumonitis, calcification, fluid accumulation in the pleural cavities — play.
A significant inverse correlation was established between the decrease in EDF and EDS and the increase in SrDLA in patients II (r = –0.69; P <0.01 and –0.61; P <0.05) and III (r = –0.52 ; P <0.05 and – 0.5; P <0.05) groups. A positive correlation was found between a decrease in the MOVR of the sums and a decrease in the pO 2 of blood in patients of the II (r = 0.89; P <0.001) and III (r = 0.82; P <0.001) groups. A reverse correlation was diagnosed between a decrease in blood pO 2 and an increase in SrDLA in patients of the II (r = –0.96; P <0.001) and III (r = –0.79; P <0.001) groups.
Thus, in patients with MM, impaired functional ability of the diaphragm leads to impaired ventilation of the middle and lower zones of the lungs, resulting in hypoxemia and pulmonary hypertension. However, in patients with MM complicated by CRF, this relationship is less pronounced, since the uremic damage of the bronchopulmonary system plays an important role in impaired respiratory function, and the pH of the blood and endothelial dysfunction of the vessels contribute to the development of PH.
As an example, here is an extract from the outpatient card No 4569. Patient S., born in 1947. Diagnosis: Multiple myeloma, diffuse focal form, secreting P IgG, stage IIIA was exposed in November 1997. In the myelogram, 19% of plasma cells, in the immunogram, IgG is 65 g / l, on radiographs of the skull, pelvic bones and edges multiple destruction. Mild anemia has occurred. During the initial hospitalization in the hospital, treatment was carried out according to the MR protocol. The plateau phase has been reached. She subsequently received maintenance therapy according to the MR protocol for 5 years. In 2002, a relapse of the disease was established. After conducting two courses of therapy under the protocol M 2 – VBMCP reached the second phase of the “plateau”, which lasted until 2006. In 2006 a relapse of the disease developed, which was accompanied by the destruction of flat bones, a pronounced pain syndrome and a pathological fracture of the left shoulder. Attempts to strengthen cytostatic therapy led to the development of serious complications: agranulocytosis, complicated by pneumonia; toxic hepatitis; thrombocytopenia and severe hemorrhagic syndrome. In July 2006 therapy started on the Velc + dexa protocol. A stable plateau phase has been reached.
Additional survey methods (July 2006). Roentgenograms of the bones of the skull, pelvis, and ribs – multiple destruction. In myelogram 40% of plasma cells. Immunogram: IgG – 75 g / l, IgA – 0.84 g / l, IgM – 0.58 g / l. Blood count: hemoglobin – 95 g / l, erythrocytes – 3.6 × 10 12 / l, platelets – 120 × 10 9 / l, leukocytes – 3.9 × 10 9 / l, segmented nucleus – 46%, lymphocytes – 45%, eosinophils – 3%, monocytes – 6%, ESR – 65 mm / h. Biochemical analysis of blood: total protein – 95 g / l, creatinine – 90 μm / l, urea – 6 μm / l, Ca – 2.6 mmol / l. Clinical analysis of urine – proteinuria 1000 mg / l. Spirography: VC – 64% D, FEV 1 – 70% D. During peak flowmetry, the PSV indicators were as follows: in the morning hours – 69% D, in the evening hours – 74% D. Daily fluctuations PSV was 5%. During pneumotachography, an increase in bronchial inhalation resistance was observed (3.2 cm water / l / s) and exhalation (3.5 cm water / l / s). When conducting PBS, a bilateral diffuse atrophic endobronitis was diagnosed. The results of endobronchial LDF before treatment with Velcade and Dexamethasone: PM – 35.63 PE; σ – 5.8 PE; Kv – 16.28%; Ae – 1.98 PE; An – 1.93 PE, Am – 3.04 PE; Hell – 2,850 PE; Ac – 1,460 PE. The data of endobronchial LDF in the stable plateau phase: PM — 65.1 PE; σ – 8.1 PE; Kv – 17.9%; Ae – 2.3 PE; An – 2.8 PE, Am – 3.2 PE; Hell – 3.6 PE; Ac – 2,9PE. Zone rheography of the lungs (July 2006). Dore of the right lung: upper zone – 0.5, middle zone – 0.38, lower zone – 0.8 ohm;The depth of the left lung is the upper zone — 0.46, the middle zone — 0.44, the lower zone — 0.44 ohms. Dob sum = 3.02 ohms. MEP of the right lung: upper zone – 8.3, middle zone – 6, lower zone – 11.2 ohm / min; MEP of the left lung: upper zone – 7, middle zone – 8, lower zone – 6.6 ohm / min. MOVr Sum – 47.1 ohm / min. The ratio of the MOV of the upper zones / MOV of the lower zones = 0.86. SCR of the right lung: in the upper zone – 0.09, in the middle zone – 0.05, in the lower zone – 0.1 ohm; The CR of the left lung – in the upper zone – 0.1, in the middle zone – 0.06, in the lower zone – 0.1 ohm. Scr sum = 0.5 ohm MPCr of the right lung: in the upper zone – 7.5, in the middle zone 3.5, in the lower zone 9.7; MPCr of the left lung: in the upper zone – 8.6, in the middle zone 4.5, in the lower zone 9.7 ohms / min. MPKr Sum = 43.5 ohm / min. Ventilation-perfusion ratio: right lung: upper zone 1.1, middle zone 1.7, lower zone 1.15; left lung: upper zone 0.8, middle zone – 1.77, lower zone 0.7. VPO of both lungs 1.1. IKC ultrasound data (July 2006): SrDLA – 23 mm. Hg Art., KDO PZh – 126 ml, KSO PZh – 67 ml, UI PZh – 49 ml / m 2 , SI PZH – 2.6 l / min / m 2 , EF PZH – 41%, E TC – 0.36 m / s, A TC 0.53 m / s, E / A – 0.7. Diagnosed the expansion of all cavities of the heart. Ultrasonic examination of the diaphragm: TD – 6 mm, EDS – 12 mm, EDf – 28 mm.