Laboratory tests of hemostasis. The relation to hemorrhage in liver disease

I, Spector

doi:10.1001/archinte.119.6.577

Cited by 22 publications

(8 citation statements)

References 13 publications

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“…Coagulation factors other than factor XI11 have been shown to be synthesized by the isolated perfused liver (Olson et d, 1966) and these factors may be diminished in liver disease (Rapaport et aZ, 1960;Kupfer et al, 1964;Deutsch, 1965 ;Spector & Corn, 1967)~ presumably as the result of impaired synthesis. Although direct evidence for the synthesis of factor XI11 by the liver is not available, it is a protein and therefore may well be produced by the liver, and liver damage might thus be accompanied by diminished synthesis of factor XIII.…”

Section: Discussionmentioning

confidence: 99%

Mechanisms of Acquired Defects of the Stabilization of Fibrin

Losowsky

Walls

1971

Br J Haematol

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Summary. The causes of undemonstrable plasma fibrin‐stabilizing‐factor (FSF, factor XIII) activity in various diseases have been investigated. Results suggest impaired synthesis of the enzyme in three patients with portal cirrhosis, and one with acute hepatic necrosis. Impaired activation of factor XIII seems a possible explanation in one patient with portal cirrhosis. Evidence of a plasma inhibitor of factor XIII was obtained in six patients with chronic renal failure and two with acute hepatic necrosis. The inhibitor present in renal failure was non‐dialysable, relatively heat labile and not adsorbed by either aluminium hydroxide or bentonite.

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Section: Discussionmentioning

confidence: 99%

Mechanisms of Acquired Defects of the Stabilization of Fibrin

Losowsky

Walls

1971

Br J Haematol

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“…Fibrinogen level is normal or increased in most patients with stable disease, but hypofibrinogenaemia is seen with advanced cirrhosis 33. This may be due to impaired synthesis, loss into extravascular spaces (ascites), increased catabolism or massive haemorrhage 34. Dysfibrinogenaemia, where the function of the fibrinogen is impaired, is also one of the earliest clotting abnormalities seen in chronic liver disease 35.…”

Section: The “Other Factors” In Haemostatic Dysfunctionmentioning

confidence: 99%

Relevance of clotting tests in liver disease

Thachil¹

2008

Postgraduate Medical Journal

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Liver disease is associated with impairment of the haemostatic function due to the abnormal and decreased synthesis of the clotting factors. It is thus only logical to have considered assessment of the clotting profile (to include prothrombin time (PT) and activated partial thromboplastin time (aPTT)) to be an integral part of the comprehensive assessment of a patient who presents with liver impairment. Laboratory abnormalities of coagulation are considered to be a predictive risk factor for bleeding, but patients with liver disease do not have bleeding pattern as those who have coagulation factor deficiencies. Recent experiments have cast doubts over the use of PT and aPTT as a marker of bleeding in liver disease and the use of such tests to decide the need for plasma replacement before interventions like liver biopsy. This article reviews the relevance of the clotting profile in liver disease, the other factors involved in the haemostatic failure associated with it, and the technical problems in the interpretation of these results. Most importantly, it stresses the need for more trials to help us guide the management of bleeding in patients with liver impairment.

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“…To monitor UFH, the (aPTT) activated partial thromboplastin time was evaluated by a traditional method, 19 using the HemosIL SynthASil kit (Instrumentation Laboratory, Milan, Italy) and an Electra 1400 coagulometer (Instrumentation Laboratory), as well as by a Rapidpoint ® Coagulation analyzer, consisting of a microprocessor-based analyzer and single-use assay-specific test cards: the analyzer photo-mechanically monitors fibrin clot formation in a flat capillary chamber on the surface of a test card. [20][21][22] Values of the aPTT <35 s were considered normal, and values >40 s were considered in the therapeutic range.…”

Section: Coagulation Testsmentioning

confidence: 99%

Surgical bleeding after pre-operative unfractionated heparin and low molecular weight heparin for coronary bypass surgery

Renda¹,

Pillo²,

D‘Alleva³

et al. 2007

Haematologica

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Background and ObjectivesSince the impairment of platelet function may cause excess peri-operative bleeding, pre-operative discontinuation of aspirin and heparin bridging are common for cardiac surgery. We evaluated the impact of pre-operative administration of enoxaparin and unfractionated heparin (UFH) on coagulation parameters and peri-operative bleeding in patients undergoing elective coronary artery bypass grafting (CABG) surgery after discontinuation of aspirin. Design and MethodsForty-three patients with three-vessel coronary artery disease undergoing elective CABG surgery discontinued aspirin and were randomized to receive either UFH 180 UI/Kg × 2/day s.c. or enoxaparin 100 UI/Kg × 2/day s.c. until 12 h before surgery (median pre-operative treatment 8 days, range 6-12 days). Surgery was performed as usual with UFH. Neither UFH nor any low molecular weight heparin was given in the immediate post-operative period. The effects of UFH and enoxaparin were monitored by the activated partial thromboplastin time (aPTT) and the Enox-test (sensitive to factor Xa inhibition) using a Rapidpoint®Coagulation Analyzer. aPTT and factor Xa activity were also measured by standard methods. Peri-operative bleeding and the nadirs of hemoglobin concentration, hematocrit and platelet count were monitored post-operatively. ResultsPatients in the two groups were similar for number of bypasses, on-pump time, total surgery time, and time from the last heparin administration. Coagulation parameters increased significantly and similarly at 30 min and 6 h with both treatments, but returned within the normal range at 12 h. Hemoglobin, hematocrit and platelet counts significantly decreased to the same extent after CABG and re-normalized at the same time. Transfusional requirements of blood and plasma units were similar in the two groups. Interpretation and ConclusionsFrom the kinetics of coagulation parameters and the evaluation of bleeding, enoxaparin is a safe alternative to UFH as a bridging therapy to CABG after discontinuation of aspirin.

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Laboratory tests of hemostasis. The relation to hemorrhage in liver disease

Cited by 22 publications

References 13 publications

Mechanisms of Acquired Defects of the Stabilization of Fibrin

Mechanisms of Acquired Defects of the Stabilization of Fibrin

Relevance of clotting tests in liver disease

Surgical bleeding after pre-operative unfractionated heparin and low molecular weight heparin for coronary bypass surgery

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