Metastatic endophthalmitis.
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Biomedical subjects
Publications and source records attributed to J Winch.
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In a group of dogs in whom fulminant liver failure had been induced, perfusion of blood through activated charcoal resulted in a significantly longer survival than that of a similar group of dogs whose blood was not so treated. An otherwise progressive rise in blood ammonia concentration was halted in the treatment group. In another group of dogs with fulminant liver failure perfusion of blood through the resin Amberlite XAD-2 was associated with a fall in the serum bilirubin concentration and complete clearance from the blood of (14)C-labelled sodium glycocholate. Survival in this group of animals was not significantly prolonged. This was due at least in part to the occurrence of haemorrhage due to thrombocytopenia. Platelets adhere to the resin but do not adhere to the same degree to charcoal coated with a thin layer of polymer.
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The use of extracorporeal pig liver perfusion for temporary liver support has been followed not infrequently by major bleeding with a fall in coagulation factors and platelets, rather than a rise as hoped. In 18 experimental perfusions in which (125)I-labelled fibrinogen was used as a marker there was in every instance a significant loss of the fibrinogen into the fluid supporting the liver in the perfusion chamber. Further, in 11 of the perfusions there was an additional loss into liver substance, this being associated with a very rapid fall in (125)I fibrinogen and platelets content of the perfusion fluid. Damage to the sinusoids from ischaemic damage incurred during removal of the liver could explain both the direct loss of fibrinogen and, as a result of intravascular coagulation, the associated loss within the perfused liver. No correlation could be found with biochemical function, but it proved possible to assess haematological safety before connexion of the patient to the perfusion by a shortened (125)I fibrinogen test. This was done in three patients treated by five perfusions and in none was the thrombocytopenia or coagulation disturbance adversely affected.
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Four consecutive patients, three with fulminant hepatic failure and one with a severe relapse of serum hepatitis, who showed evidence of intravascular coagulation, were treated intensively with heparin and fresh frozen plasma. Rapid correction of the coagulation disturbance was achieved, and all four patients recovered completely. The necessity for starting such treatment early in the course of the disease and before the onset of major gastrointestinal bleeding is stressed, and it is suggested that intravascular coagulation may act as an intermediary in the pathogenesis of the hepatic necrosis.
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