Therapeutic apheresis in the treatment of acute lung injuries

Acute   lung   injuries  —  respiratory   distress   syndrome  (RDS) —  rather   frequent and severe complications of acute pneumonia and other diseases (acute inflammatory diseases   of   abdominal   organs,   severe   traumas,   burns,   eclampsia,   septical   shock   and other).  RDS   is   the   major   causes   of   unfavorable   outcomes,   despite   the   use   of   most modern medicaments.       Our     previous     experimental      studies    have    demonstrated      that    endotoxicosis developed   in   animals   since   first   minutes   of   acute   pneumonia   modeling.   There   are many   pathogenous   factors   of   endotoxicosis:   bacterial   endo-  and   exogenous   toxins, inflammatory         toxic   metabolites,     products      of   proteolisis,    activation     of   lipid peroxydation       and   decrease     of  anti-oxidation     protection,   toxic    middle     molecular weight compounds (oligopeptids), lysosomal enzymes.       As     a  result   arise   some    complications      of   endotoxicosis:     increase     vascular permeability      (microvascular      leaking),   hypoproteinemia,       hypooncotic      hypovolemia, low blood pressure, toxic pulmonary edema —  respiratory distress syndrome, acute respiratory insufficience, disseminated vascular coagulations syndrome and, as result – multiple organ failure.       Patients and methods. We analyzed the therapy of 153 RDS patients: 99 with moderate,   44   with   severe   and   10   with   extremely   severe   degree   of   lung  injury.   67 patients   received   the   conventional   therapy   only   (antibiotics   and   other   drugs,   and   in severe degree of RDS — mechanical lung ventilation).       76    patients   received    an   additional    detoxication   therapy    –  hemadsorption        or plasma exchange (membrane plasmapheresis with “Hemofenix” device end exchange  1.5–2.5   l   of   plasma).   10   patients   with   extremely   severe   RDS   were   underwent   the extracorporeal membrane oxigenation of the blood (ECMO) with hemoadsorption.       Results. In moderate RDS group there were no lethal outcomes. But the duration of   hospital   stay   was   significantly   lower   in   patients   underwent   detoxication  than   in ones of control group (28,9±1,5 versus 40,3±3,3 days; p < 0,05), and there were no destructive processes in lungs. 
 In   patients   with   severe   RDS   and   only   conventional  therapy   the   lethality   level attained 74% while additional using of hemoadsorption or plasmapheresis allowed to decrease       it  to  31%.     We    failed    to  save    just   patients    in   which     detoxication       was performed   in   more   late   terms   after   the   disease         onset.   The   extremely   severe   RDS degree   was   characterized   by   practically   total   injury   of   lung   parenchyma   and   severe respiratory      failure,    which      was    not   corrected     with    mechanical       ventilation.      Using ECMO during from 15 to 44 hours with 3–4 hemoadsorption procedures allowed to save 7 of 10 these patients.        Conclusion.  The   results   of   the   study   performed  demand   a   radical   revision   of fixed therapeutic schemes for acute pneumonias and RDS, still based predominantly on   antibacterial   therapy.   However,   the   most   powerful   antibiotic   don’t   eliminate   the endotoxines        but   can    even    aggravate      it  due   to   massive      bacteria    death    and    lysis. However, in most of these cases the fact of progressing course of the acute respiratory syndrome         indicates     an    initial   lack     of   defense      systems.      Medicament         immune stimulation   is   also   unable   to   restore   suppressed   mechanisms   of   immune   defense. Under      these    conditions      is  pathogenetically        well-founded        conducting       of  a   special detoxication        therapy     based    on    plasma     exchange       with    compensation       of    removed volume (up to 1– 1.5 of circulating plasma volume) with donor plasma. 
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