scholarly journals Conservative management of abnormally invasive placenta complicated by local hyperfibrinolysis and beginning disseminated intravascular coagulation

Author(s):  
C. Biele ◽  
L. Kaufner ◽  
A. Schwickert ◽  
A. Nonnenmacher ◽  
K. von Weizsäcker ◽  
...  

Abstract Introduction Abnormally invasive placenta (AIP) is often associated with high maternal morbidity. In surgical treatment, caesarean hysterectomy or partial uterine resection may lead to high perioperative maternal blood loss. A conservative treatment by leaving the placenta in utero after caesarean delivery of the baby is an option to preserve fertility and to reduce peripartum hysterectomy-related morbidity. Nevertheless, due to increased placental coagulation activity as well as consumption of clotting factors, a disseminated intravascular coagulation (DIC)-like state with secondary late postpartum bleeding can occur. Purpose Systematic review after the presentation of a case of conservative management of placenta percreta with secondary partial uterine wall resection due to vaginal bleeding, complicated by local hyperfibrinolysis and consecutive systemic decrease in fibrinogen levels. Methods Systematic PubMed database search was done until August 2019 without any restriction of publication date or journal Results Among 58 publications, a total of 11 reported on DIC-like symptoms in the conservative management of AIP, in the median on day 59 postpartum. In most cases, emergency hysterectomy was performed, which led to an almost immediate normalization of coagulation status but was accompanied with high maternal blood loss. In two cases, fertility-preserving conservative management could be continued after successful medical therapy. Conclusion Based on these results, we suggest routinely monitoring of the coagulation parameters next to signs of infection in the postpartum check-ups during conservative management of AIP. Postpartum tranexamic acid oral dosage should be discussed when fibrinogen levels are decreasing and D-Dimers are increasing.

Author(s):  
Anne Craig ◽  
Anthea Hatfield

Part one of this chapter tells you about the physiology of blood and oxygen supply, about anaemia and tissue hypoxia, and the physiology of coagulation. Drugs that interfere with clotting are discussed. Bleeding, coagulation, and platelet disorders are covered as well as disseminated intravascular coagulation. Part two is concerned with bleeding in the recovery room: how to cope with rapid blood loss, managing ongoing blood loss, and how to use clotting profiles to guide treatment. There is also a section covering blood transfusion, blood groups and typing. Massive blood transfusion is clearly described, there are guidelines about when to use fresh frozen plasma, when to use platelets, and when to use cryoprecipitate. The final section of the chapter is about problems with blood transfusions.


Blood ◽  
2011 ◽  
Vol 118 (7) ◽  
pp. 1943-1951 ◽  
Author(s):  
Oliver Grottke ◽  
Till Braunschweig ◽  
Henri M. H. Spronk ◽  
Stephanie Esch ◽  
Annette D. Rieg ◽  
...  

Abstract Despite increasing use of prothrombin complex concentrate (PCC) to treat hemorrhage-associated coagulopathy, few studies have investigated PCC in trauma, and there is a particular lack of safety data. This study was performed to evaluate PCC therapy in a porcine model of coagulopathy with blunt liver injury. Coagulopathy was induced in 27 anesthetized pigs by replacing approximately 70% blood volume with hydroxyethyl starch 130/0.4 and Ringer's lactate solution; erythrocytes were collected and retransfused. Ten minutes after trauma, animals randomly received PCC (35 or 50 IU/kg) or saline. Coagulation parameters including thromboelastometry, thrombin generation, and blood loss were monitored for 2 hours. Internal organs were examined macroscopically and histologically to determine the presence of emboli and assess liver injury. Total blood loss was significantly lower and survival was higher in both PCC groups versus the control group (P < .05). These outcomes appeared to be dose-independent. Thromboembolism was found in all animals treated with 50 IU/kg PCC; 44% also showed signs of disseminated intravascular coagulation. Liver injury was similar in all animals. In conclusion, 35 IU/kg PCC safely improved coagulation and attenuated blood loss. However, the higher dose of PCC (50 IU/kg) appeared to increase the risk of thromboembolism and disseminated intravascular coagulation.


2018 ◽  
Vol 24 (9_suppl) ◽  
pp. 8S-28S ◽  
Author(s):  
Chrysoula Papageorgiou ◽  
Georges Jourdi ◽  
Eusebe Adjambri ◽  
Amanda Walborn ◽  
Priya Patel ◽  
...  

Disseminated intravascular coagulation (DIC) is an acquired clinicobiological syndrome characterized by widespread activation of coagulation leading to fibrin deposition in the vasculature, organ dysfunction, consumption of clotting factors and platelets, and life-threatening hemorrhage. Disseminated intravascular coagulation is provoked by several underlying disorders (sepsis, cancer, trauma, and pregnancy complicated with eclampsia or other calamities). Treatment of the underlying disease and elimination of the trigger mechanism are the cornerstone therapeutic approaches. Therapeutic strategies specific for DIC aim to control activation of blood coagulation and bleeding risk. The clinical trials using DIC as entry criterion are limited. Large randomized, phase III clinical trials have investigated the efficacy of antithrombin (AT), activated protein C (APC), tissue factor pathway inhibitor (TFPI), and thrombomodulin (TM) in patients with sepsis, but the diagnosis of DIC was not part of the inclusion criteria. Treatment with APC reduced 28-day mortality of patients with severe sepsis, including patients retrospectively assigned to a subgroup with sepsis-associated DIC. Treatment with APC did not have any positive effects in other patient groups. The APC treatment increased the bleeding risk in patients with sepsis, which led to the withdrawal of this drug from the market. Treatment with AT failed to reduce 28-day mortality in patients with severe sepsis, but a retrospective subgroup analysis suggested possible efficacy in patients with DIC. Clinical studies with recombinant TFPI or TM have been carried out showing promising results. The efficacy and safety of other anticoagulants (ie, unfractionated heparin, low-molecular-weight heparin) or transfusion of platelet concentrates or clotting factor concentrates have not been objectively assessed.


2015 ◽  
Vol 95 (1) ◽  
pp. 119-119 ◽  
Author(s):  
Shigeki Matsubara ◽  
Hiroyuki Fujiwara ◽  
Akihide Ohkuchi ◽  
Hironori Takahashi ◽  
Alan K. Lefor

2013 ◽  
Vol 92 (4) ◽  
pp. 468-471 ◽  
Author(s):  
Angela Ramoni ◽  
Eva-Maria Strobl ◽  
Johanna Tiechl ◽  
Magdalena Ritter ◽  
Christian Marth

2020 ◽  
Vol 101 (5) ◽  
pp. 704-712
Author(s):  
V M Vdovin ◽  
A P Momot ◽  
D A Orekhov ◽  
I I Shakhmatov ◽  
N A Lycheva ◽  
...  

Aim. To assess the effect of fibrin monomer on the rate of blood loss after controlled liver injury in hypofibrinogenemia induced by systemic administration of Malayan pit viper venom (Agkistrodon rhodostoma). Methods. A placebo-controlled study of the hemostatic effect of fibrin monomer administered intravenously at 0.25 mg/kg, and coagulation parameters in the controlled liver injury with profound hypofibrinogenemia caused by administration of Malayan pit viper venom was conducted in 34 male Chinchilla rabbits. The distribution of the studied parameters was investigated by the ShapiroWilk test. Statistical differences between groups were tested by Students t-test, MannWhitney U test, or Wilcoxon test, as appropriate. Differences in mortality rate were examined using Fisher's exact test. Results. A model of experimental toxogenic disseminated intravascular coagulation was reproduced, manifested by high mortality of animals (50.0%), severe blood loss (increased blood loss by 1.78 times), hemolysis, a decreased platelet count (by 19.6% of median) and platelet dysfunction, fibrinogen consumption (protein content less than 0.9 g/l), hypocoagulation as well as intensive D-dimer production (increased concentration by 25.0 times of median). A high level of the fibrin derivative demonstrated activation of fibrin formation and fibrinolysis in the bloodstream of the animals. Systemic prophylactic administration of exogenous fibrin monomer after receiving snake venom did not lead to a decrease in post-traumatic bleeding, whereas earlier, during reproduction of disseminated intravascular coagulation caused by streptokinase infusion, such a hemostatic effect of fibrin monomer was shown. Conclusion. The absence of fibrin monomer effect (at a dose of 0.25 mg/kg) on the severity of blood loss in toxogenic disseminated intravascular coagulation may be associated with more profound disseminated intravascular coagulation and a sharp 25-fold increase in D-dimer levels that can act as a fibrin monomer polymerization inhibitor.


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