Amniotic fluid embolism (AFE) is one of the catastrophic complications of pregnancy in which amniotic fluid, fetal cells, hair, or other debris enters into the maternal pulmonary circulation, causing cardiovascular collapse. Etiology largely remains unknown, but may occur in healthy women during labour, during cesarean section, after abnormal vaginal delivery, or during the second trimester of pregnancy. It may also occur up to 48 hours post-delivery. It can also occur during abortion, after abdominal trauma, and during amnio-infusion. The pathophysiology of AFE is not completely understood. Possible historical cause is that any breach of the barrier between maternal blood and amniotic fluid forces the entry of amniotic fluid into the systemic circulation and results in a physical obstruction of the pulmonary circulation. The presenting signs and symptoms of AFE involve many organ systems. Clinical signs and symptoms are acute dyspnea, cough, hypotension, cyanosis, fetal bradycardia, encephalopathy, acute pulmonary hypertension, coagulopathy etc. Besides basic investigations lung scan, serum tryptase levels, serum levels of C3 and C4 complements, zinc coproporphyrin, serum sialyl Tn etc are helpful in establishing the diagnosis. Treatment is mainly supportive, but exchange transfusion, extracorporeal membrane oxygenation, and uterine artery embolization have been tried from time to time. The maternal prognosis after amniotic fluid embolism is very poor though infant survival rate is around 70%.

In patients with diabetes, metabolic disorders disturb the physiological balance of coagulation and fibrinolysis, leading to a prothrombotic state characterized by platelet hypersensitivity, coagulation disorders and hypofibrinolysis. Hyperglycemia and insulin resistance cause changes in platelet number and activation, as well as qualitative and/or quantitative modifications of coagulatory and fibrinolytic factors, resulting in the formation of fibrinolysis-resistant clots in patients with diabetes. Other coexisting factors like hypoglycemia, obesity and dyslipidemia also contribute to coagulation disorders in patients with diabetes. Management of the prothrombotic state includes antiplatelet and anticoagulation therapies for diabetes patients with either a history of cardiovascular disease or prone to a higher risk of thrombus generation, but current guidelines lack recommendations on the optimal antithrombotic treatment for these patients. Metabolic optimizations like glucose control, lipid-lowering, and weight loss also improve coagulation disorders of diabetes patients. Intriguing, glucose-lowering drugs, especially cardiovascular beneficial agents, such as glucagon-like peptide-1 receptor agonists and sodium glucose co-transporter inhibitors, have been shown to exert direct anticoagulation effects in patients with diabetes. This review focuses on the most recent progress in the development and management of diabetes related prothrombotic state.

The values of hematological and coagulation biomarkers were evaluated as predictors of in hospital mortality and complications, in patients with acute coronary syndromes (ACS). This retrospective observational study enrolled 936 ACS subjects admitted to the Clinical Emergency Hospital of Oradea, Romania, between January-December 2019. Hematological and coagulation parameters were obtained at admission. During hospitalization, the following adverse events were recorded: death, ventricular rhythm disturbances, atrial fibrillation, heart failure, re-infarction, and stroke. Accuracy of hematological and coagulation parameters as predictors of adverse outcome were also evaluated. The diagnosis was unstable angina in 442 patients (47.22%), non-ST-elevation myocardial infarction (NSTEMI) in 113 patients (12.1%) and ST-elevation myocardial infarction (STEMI) in 381 patients (40.70%); 87 patients (9.29%) died during hospitalization and 193 (20.7%) developed complications. Predictors for in hospital mortality were as follows: red cell distribution width (RDW) (AUC 0.691, < 0.0001), white blood cells (WBC) (AUC 0.684, < 0.0001), neutrophils (NEU) (AUC 0.684, < 0.0001), and prothrombin time (PT) (AUC 0.765, < 0.0001). WBC (AUC 0.659, < 0.0001), NEU (AUC 0.664, < 0.0001), RDW (AUC 0.669, < 0.0001), and PT (AUC 0.669, 95% CI 0.622-0.714, < 0.0001) also had accuracy for complications prediction. RDW had a good ability to predict heart failure in NSTEMI patients (AUC 0.832, < 0.0001). An acceptable ability to predict ventricular rhythm disturbances occurrence had WBC (AUC 0.758, < 0.0001) and NEU (AUC 0.772, < 0.0001). Hematological and coagulation parameters can help in risk stratification of ACS patients. RDW, WBC, NEU, and PT were able to predict mortality and in-hospital complications in ACS patients. RDW has a good accuracy in predicting complications and heart failure in NSTEMI patients. WBC and NEU are good predictors for ventricular rhythm disturbances.

PURPOSE:The diagnostic significance of coagulation parameters in periprosthetic joint infection (PJI) is currently attracting increasing attention. We assessed the diagnostic accuracy of thromboelastography (TEG) for PJI and compared the values of various coagulation indicators for PJI diagnosis and reimplantation timing. METHODS:We enrolled 250 patients undergoing revision for aseptic failure (Group A), revision for PJI (Group B), or reimplantation (Group C) during 2013-2020. C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), representative coagulation-related indicators (reaction time [R], clotting time [K], angle and maximum amplitude [MA]) of TEG and routine coagulation indicators, including fibrinogen, D-dimer, fibrin degradation product (FDP), platelets count (PC), mean platelet volume (MPV), distribution width (PDW) and plateletcrit (PCT) as well as PC/MPV ratio(PVR)were measured preoperatively. Receiver operating characteristic (ROC) curves were used to evaluate the utility of all tested indicators for assessing infection. RESULTS:All the indicators showed significant differences between groups A and B (P < 0.05) and, except for D-dimer, FDP, MPV and R, between groups B and C (P < 0.05). Similar differences were also observed in biomarkers before first-stage revision and second-stage reimplantation. ROC curves showed that fibrinogen, K, angle and MA outperformed the other coagulation indicators, with areas under the curve of 0.864 to 0.893 and threshold values of 3.55 g/L, 1.2 min, 72.4 deg and 69.1 mm, respectively. The multiple tests of TEG indices (K, angle and MA) and traditional inflammatory markers (CRP and ESR) or conventional coagulation indicators (fibrinogen, PC and PVR) had good sensitivity and specificity for PJI diagnosis, and the diagnostic values of TEG and platelet-associated indicators (PC and PVR) varied in the different subgroups. CONCLUSION:TEG was closely related to PJI and could serve as a valuable technique for identifying residual infection before reimplantation. Fibrinogen showed high diagnostic accuracy for PJI and effectively guided the timing of reimplantation.

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.

OBJECTIVES:This article describes the pathophysiology and causes of disseminated intravascular coagulation (DIC). Implications for nurses are also reviewed. DATA SOURCES:Pee-reviewed articles and up-to-date references were used to check accuracy of the information and provide information for current management of this syndrome. CONCLUSION:DIC is an oncologic emergency in which bleeding and clotting occur simultaneously. In the cancer population, the syndrome is frequently associated with certain malignancies or sepsis. If not recognized and treated early, mortality can be high. This article describes the risk factors that contribute to DIC, clinical manifestations of DIC, and its treatment. IMPLICATIONS FOR NURSING PRACTICE:Nurses need to consider the presenting diagnosis of the patient and understand laboratory abnormalities that signify DIC. The nurse plays a key role in early recognition of this syndrome as prompt treatment can reduce fatality.

Aim:In healthy adults, there are sufficient amounts of antithrombin in the blood to regulate thrombin. However, the effects of high concentrations of antithrombin on dose-dependent anticoagulation and platelet function have not been reported. In this study, we assessed platelet function and blood coagulation following high-dose antithrombin supplementation . Methods:Blood samples were collected from 10 healthy volunteers, and samples with different antithrombin concentrations were prepared by adding an antithrombin agent (Neuart). Blood coagulation was assessed by the Thrombus-Formation Analysis System (T-TAS) and Rotational Thromboelastometry (ROTEM) using whole blood samples. Results:The data obtained by the platelet chip, exclusively representing platelet function, revealed that the onset of thrombus formation was significantly delayed in a dose-dependent manner (100%-200%,  = 0.021; 100%-500%,  = 0.011; 200%-500%,  = 0.047). In measurements using the atheroma chip, which enables assessment of blood coagulation, the thrombus formation ability was found to be reduced (100%-200%,  = 0.022; 100%-500%,  = 0.05). In the ROTEM measurements, clotting time was prolonged in a dose-dependent manner (100%-200%:  = 0.203, 200%-500%:  = 0.005, 500%-1000%:  = 0.022), except when comparing with 100% and 200%. Although antithrombin is reportedly saturated in healthy blood, its anticoagulant ability appears to be enhanced depending on its concentration. Furthermore, data obtained from the platelet chip showed that antithrombin might reduce platelet function. Conclusions:Antithrombin suppressed platelet function and blood coagulation in a dose-dependent manner.

Beyond blood pressure control, angiotensin receptor blockers reduce common injury mechanisms, decreasing excessive inflammation and protecting endothelial and mitochondrial function, insulin sensitivity, the coagulation cascade, immune responses, cerebrovascular flow, and cognition, properties useful to treat inflammatory, age-related, neurodegenerative, and metabolic disorders of many organs including brain and lung.