Early and Intensive Therapy of Intravascular Coagulation in Acute Liver Failure

Rake, M. O.; Shilkin, K. B.; Winch, J. E.; Flute, P.T.; Lewis, M. L.; Williams, Roger

doi:10.1016/s0140-6736(71)90540-x

Cited by 90 publications

(45 citation statements)

References 8 publications

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“…Coagulopathy in this setting further complicates patient management because of attendant bleeding risks, increased risks of procedures, alterations of risk assessment for transplant selection, and complications related to treatment of the coagulopathy. 2 Although hyperfibrinolysis 2,15,16 and disseminated intravascular coagulation 17 are important considerations, the most common coagulation abnormality in these patients is prolongation of the PT because of decreased synthesis of vitamin K-dependent coagulation factors (factors II, VII, IX, X). 2,4 Although laboratory abnormalities do not allow absolute prediction of bleeding risks, it is widely accepted that severe prolongation of the PT or INR carries increased risks for bleeding in patients with FHF.…”

Section: Discussionmentioning

confidence: 99%

“…rFVIIa is believed to act mainly by binding to TF-bearing cells, predominantly monocytes, at the site of injury. 17,18 Factors IX and X then are activated and generate a critical amount of thrombin (thrombin burst), which activates platelets and other coagulation factors. 19 rFVIIa does not act as a replacement factor alone, but initiates a site-specific burst of coagulation activity.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Recombinant activated factor VII for coagulopathy in fulminant hepatic failure compared with conventional therapy

Shami

Caldwell

Hespenheide

et al. 2003

Liver Transplantation

219

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Severe coagulopathy in fulminant hepatic failure (FHF) is difficult to correct by conventional means. Recombinant activated factor VII (rFVIIa) is an antihemophilic factor that has shown promise in treating coagulopathy in liver disease. Our aim is to review our experience with rFVIIa in treating the coagulopathy of FHF and compare these results with those of conventional therapy. Fifteen patients with FHF who met King's College criteria for orthotopic liver transplantation were studied. All were ascertained from our liver disease registry. Eight consecutive patients were administered fresh frozen plasma (FFP) alone, whereas seven consecutive patients were administered FFP and rFVIIa (40 g/kg intravenous bolus). The two groups, with similar demographic characteristics, were compared in terms of measured parameters of coagulopathy (prothrombin time and international normalized ratio), amount of plasma infused, development of anasarca, ability to undergo intracranial pressure (ICP) transducer placement, bleeding complications, ability to undergo transplantation, and survival. All patients administered rFVIIa (after a single dose) versus none administered FFP alone had temporary (2-to 6-hour) correction of coagulopathy (P < .0002). All patients administered rFVIIa versus 38% administered FFP alone were able to have an ICP transducer placed (P ‫؍‬ .03). The rFVIIa group had less anasarca (P ‫؍‬ .04). An equal number of patients underwent transplantation from each group, but overall survival was slightly better in the rFVIIa group (P ‫؍‬ .04). Five of seven patients in the rFVIIa group were administered one or more subsequent doses of rFVIIa after placement of the ICP monitor (two patients, for additional procedures; three patients, prophylactically in the first 24 hours after ICP transducer placement) at the discretion of the attending physicians. We conclude that rFVIIa is effective in transiently correcting laboratory parameters of coagulopathy in patients with FHF. It facilitates the performance of invasive procedures and is associated with less frequent anasarca compared with conventional therapy. Our preliminary experience supports the need for further studies to define the optimal dosing, safety, and efficacy of rFVIIa in patients with FHF. (Liver Transpl 2003;9:138-143.)

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Recombinant activated factor VII for coagulopathy in fulminant hepatic failure compared with conventional therapy

Shami

Caldwell

Hespenheide

et al. 2003

Liver Transplantation

219

View full text Add to dashboard Cite

show abstract

“…In fact, fibrin deposition has been shown in areas of hepatocellular necrosis during acute hepatitis and in several models of liver injury. [27][28][29][30][31] More recently, Neubauer et al 32 reported that fibrin deposits accumulate in necrotic areas during acute liver injury and within fibrotic septa during long-term damage in the rat. Together, these studies indicate that thrombin is generated in response to liver injury, resulting in the produc- tion of fibrin.…”

Section: Discussionmentioning

confidence: 99%

Expression of the thrombin receptor in human liver: Up-regulation during acute and chronic injury

et al. 1998

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Thrombin is generated during tissue damage in several organs, including the liver, and participates in the process of tissue repair through proteolytic activation of a specific thrombin receptor (TR). The aim of this study was to investigate TR expression in human liver by immunohistochemistry and in situ hybridization. In normal liver, immunostaining for TR was present in the endothelial lining of the hepatic sinusoids. During chronic hepatitis, several cells expressing the TR were detected in the inflammatory infiltrate of portal tracts. In cirrhosis with chronic active hepatitis, expression of the TR was also present in mesenchymal cells of fibrous septa. TR expression was markedly up-regulated during fulminant hepatitis, with the highest expression in mesenchymal cells in areas of regeneration. Up-regulation of TR expression was associated with increased levels of TR messenger RNA (mRNA), as assessed by in situ hybridization and RNAse protection assay of liver RNA. Immunostaining of serial sections using specific cellular markers showed that different nonparenchymal cells contribute to TR expression during liver injury. TR expression was also shown in cultured human hepatic stellate cells, with increasing signal comparing activated versus quiescent cells. Because thrombin is rapidly generated after tissue damage, regulated TR expression may be involved in tissue remodeling and/or scarring during liver damage. (HEPATOLOGY 1998;27:462-471.)

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“…In LC, immunostaining for VWF antigen (VWF:Ag) shows positive cells predominantly at the scar-parenchyma interface, within the septum, and in the sinusoidal lining cells (Knittel, et al, 1995), and many fibrin thrombi are demonstrated in the hepatic sinusoid in patients with fulminant hepatitis (Rake et al, 1971), and in rats with dimethylnitrosamine (DMN) induced acute hepatic failure (Fujiwara et al, 1988). Portal or hepatic vein thrombosis is often observed in advanced LC (Amitrano et al, 2004;Wanless et al, 1995), and microthrombi formation is seen in one or multiple organs in one-half of autopsied cirrhotic patients (Oka & Tanaka, 1979).…”

Section: Hepatic Microcirculation and Microcirculatory Disturbances Imentioning

confidence: 99%

Crucial Role of ADAMTS13 Related to Endotoxemia and Subsequent Cytokinemia in the Progression of Alcoholic Hepatitis

Uemura¹,

Fujimura²,

Matsuyama³

et al. 2012

Trends in Alcoholic Liver Disease Research - Clinical and Scientific Aspects

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Early and Intensive Therapy of Intravascular Coagulation in Acute Liver Failure

Cited by 90 publications

References 8 publications

Recombinant activated factor VII for coagulopathy in fulminant hepatic failure compared with conventional therapy

Recombinant activated factor VII for coagulopathy in fulminant hepatic failure compared with conventional therapy

Expression of the thrombin receptor in human liver: Up-regulation during acute and chronic injury

Crucial Role of ADAMTS13 Related to Endotoxemia and Subsequent Cytokinemia in the Progression of Alcoholic Hepatitis

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