scholarly journals Alternating therapeutic plasma exchange (TPE) with double plasma molecular adsorption system (DPMAS) for the treatment of fulminant hepatic failure (FHF)

2021 ◽  
Vol 9 (12) ◽  
Author(s):  
Yan Lei ◽  
Yuling Liang ◽  
Xuemei Zhang ◽  
Xiaohua Wang ◽  
Yu Zhang ◽  
...  
Keyword(s):  
Plasma Exchange ◽  
Fulminant Hepatic Failure ◽  
Hepatic Failure ◽  
Therapeutic Plasma Exchange ◽  
Molecular Adsorption ◽  
Adsorption System

Hemostatic Changes After Plasma Exchange Therapy For Fulminant Hepatic Failure

1981 ◽  
Author(s):  
N Takata ◽  
S Kusumi ◽  
K Fujimura ◽  
A Kuramoto
Keyword(s):  
Plasma Exchange ◽  
Fulminant Hepatic Failure ◽  
Hepatic Failure ◽  
Enzyme Inhibitor ◽  
Life Time ◽  
Hepatic Necrosis ◽  
Plasma Exchange Therapy ◽  
Post Transfusion Hepatitis ◽  
Bedside Diagnosis ◽  
And Control

Although it is well known that fulminant hepatic failure (FHF)might be often complicated with disseminated intravascular coagulation (DIC), its bedside diagnosis and control are rather confused. Hemostatic change after replacement therapy might be helpful to distinguish wheather the abnormal clotting tests are owing to the defects of protein synthesis or to excessive consumption. A 38-year-old woman with relapse of acute myeloblastic leukemia and FHF(post-transfusion hepatitis, type of non-A,non-B) received 2 courses of plasma exchange therapy (4 and 3L) using Hemonetics M-30 with 6,000 U/day of heparin sodium continuous i.v. and died on 4th hospital day. Postmortem necropsy revealed massive hepatic necrosis and fibrin thrombi in kidneys. Before the beginning of plasma exchange, results of bedside tests were as follow;platelets 44×109/l(decreased from 240 within a week ), PT over 90", aPTT 26", fibrinogen 120 mg/dl and serum FDP 10 mcg/ml. Serial observations of hemostatic parameters 1, 4, 8 and 12 hours after the end of exchange therapy disclosed that apparent half life time of each factors were remarkably shortened. For example, T 1/2 of factor I, E, VE, XI, antithrombin EE (AT IE) and alpha-2 plasmin inhibitor(AP) were 4, 14.5, 1-5, 4.7, 15 and 2.6 hours, respectively. In crossed immunoelectrophoresis of AT III and AP, patient plasma showed abnormal peaks of each protein which were considered to be enzyme-inhibitor complexes. Plasminogen was not detected before therapy(0 % by S-2251 and less than 5 % by Rocket IEP) in spite of AP remaining (16 % by S-2251, 25 % by Rocket IEP) and FDP was elevated to 80 mcg/ml at 4 hours after exchange. These findings indicated that, in some case of FHF, FDP did not increase because of absence of plasminogen even if accompanied with DIC.

scholarly journals Single Pass Albumin Dialysis and Plasma Exchange for Copper Toxicity in Acute Wilson Disease

2019 ◽  
Vol 9 (2) ◽  
pp. 55-63
Author(s):  
Shireen Bakhsh ◽  
Chia Wei Teoh ◽  
Elizabeth A. Harvey ◽  
Damien G. Noone
Keyword(s):  
Liver Transplantation ◽  
Plasma Exchange ◽  
Hemolytic Anemia ◽  
Fulminant Hepatic Failure ◽  
Hepatic Failure ◽  
Wilson Disease ◽  
Serum Copper ◽  
Albumin Dialysis ◽  
Single Pass ◽  
Rebound Increase

Background: Wilson disease (WD) is a disorder of copper metabolism that results in accumulation of copper in tissues. In acute WD, patients present with fulminant hepatic failure, encephalopathy, and hemolytic anemia due to copper release from necrotic hepatocytes. Many will require life-saving liver transplantation. Extracorporeal liver support systems can provide a bridge to transplantation for critically ill patients. We report our experience with 2 patients for whom we used a combination of plasma exchange (PLEX) and single pass albumin dialysis (SPAD), or SPAD alone as a bridge to liver transplantation. Case Reports: A 17-year-old girl (patient 1) and a 12-year-old boy (patient 2) presented with fulminant hepatic failure, hemolytic anemia, and acute kidney injury. Patient 1 received SPAD on days 2 and 3 (total 32 h). Serum copper decreased from 22.3 to 15.9 µmol/L (28.7% decrease), measured after 28 h of continuous SPAD. She underwent successful liver transplantation on day 4 after presentation. Patient 2 was treated with PLEX on days 1, 3, 4, and 5 and with SPAD on days 3–6. Serum copper decreased from 48.7 to 25.8 µmol/L (47% decrease) after the first session of PLEX and from 35.5 to 21.5 µmol/L (39.4% decrease) after the second session. The serum copper level was 16.2 µmol/L after 4 sessions of PLEX (and ongoing SPAD), with an overall 66.7% reduction in copper levels over 5 days combining both therapies. He underwent successful liver transplantation on day 6. Conclusion: We conclude that SPAD, with or without PLEX, is effective in reducing serum copper levels as a bridge to liver transplantation in WD. PLEX may be more efficient at removing copper but is associated with a rebound increase in copper levels between sessions.

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