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1
STANTON, PAUL E., JAMES R. EVANS, ARMAND A. LEFEMINE, NGHIA M. VO, GILBERT A. RANNICK, CALVIN V. MORGAN, PHILIP J. HINTON, and MARTHA READ. "White Clot Syndrome*." Southern Medical Journal 81, no. 5 (May 1988): 616–20. http://dx.doi.org/10.1097/00007611-198805000-00018.
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Miller, Peggy, and Sheryl Yardley. "WHITE CLOT SYNDROME." AJN, American Journal of Nursing 85, no. 10 (October 1985): 1051. http://dx.doi.org/10.1097/00000446-198510000-00003.
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Miller, Peggy, and Sheryl Yardley. "WHITE CLOT SYNDROME." AJN, American Journal of Nursing 85, no. 10 (October 1985): 1051. http://dx.doi.org/10.1097/00000446-198510000-00005.
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Chang, Jae C. "White clot syndrome." Postgraduate Medicine 87, no. 1 (January 1990): 293–98. http://dx.doi.org/10.1080/00325481.1990.11704541.
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Mallios, Alexandros, and William Jennings. "White Clot Syndrome." European Journal of Vascular and Endovascular Surgery 55, no. 3 (March 2018): 404. http://dx.doi.org/10.1016/j.ejvs.2017.09.007.
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Daubert, G. P. "The white clot syndrome." Journal of Clinical Pharmacy and Therapeutics 30, no. 6 (December 2005): 503. http://dx.doi.org/10.1111/j.1365-2710.2005.00675.x.
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Somers, D. L., C. Sotolongo, and J. A. Bertolatus. "White clot syndrome associated with renal failure." Journal of the American Society of Nephrology 4, no. 2 (August 1993): 137–41. http://dx.doi.org/10.1681/asn.v42137.
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In a minority of patients, heparin administration is associated with thrombocytopenia and this thrombocytopenia may be associated with thromboembolic events. Heparin-associated thromboembolism is described as heparin-associated thrombocytopenia and thrombosis or white clot syndrome. White clot syndrome is caused by antibodies to a heparin-platelet membrane complex. The diagnosis carries a high mortality and morbidity from limb thromboembolism. Treatment includes discontinuation of heparin, use of alternate anticoagulants, and aggressive treatment of thromboses. A case in which acute renal failure occurred in the setting of heparin treatment and thrombocytopenia is described, and evidence that renal failure was a result of white clot syndrome is provided.
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Kuhar, Peggy A., and Kathleen M. Hill. "White Clot Syndrome: When Heparin Goes Haywire." American Journal of Nursing 91, no. 3 (March 1991): 59. http://dx.doi.org/10.2307/3426548.
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Broughan, Thomas A., Kandice Kottke-Marchant, and David P. Vogt. "THE ???WHITE CLOT SYNDROME??? IN HEPATIC TRANSPLANTATION." Transplantation 61, no. 6 (March 1996): 982–84. http://dx.doi.org/10.1097/00007890-199603270-00027.
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Kuhar, Peggy A., and Kathleen M. Hill. "White Clot Syndrome: When Heparin Goes Haywire." AJN, American Journal of Nursing 91, no. 3 (March 1991): 59–60. http://dx.doi.org/10.1097/00000446-199103000-00019.
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Batra, Munish K., Michael D. Adolph, James C. Thornton, Aspi M. Byramjee, Alan O. Oliver, and Helmut Schreiber. "Antithrombin III Deficiency and White Clot Syndrome." Vascular Surgery 30, no. 1 (January 1996): 37–44. http://dx.doi.org/10.1177/153857449603000107.
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Köppel, C., D. Barckow, and H. Riess. "Severe white-clot syndrome after unfractionated heparin." Intensive Care Medicine 17, no. 3 (March 1991): 185. http://dx.doi.org/10.1007/bf01704726.
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Shelly, M. P., R. V. Majer, C. Perkins, T. Pierce, and M. S. Nielsen. "White clot syndrome and continuous arteriovenous haemofiltration." Intensive Care Medicine 16, no. 5 (May 1990): 334–35. http://dx.doi.org/10.1007/bf01706362.
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AbuRahma, Ali F., James P. Boland, and Todd Witsberger. "Diagnostic and therapeutic strategies of white clot syndrome." American Journal of Surgery 162, no. 2 (August 1991): 175–79. http://dx.doi.org/10.1016/0002-9610(91)90183-e.
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Adebonojo, Samuel A., George Nova, and Ishwar N. Visweshwar. "White Clot Syndrome-Heparin-Induced Platelet Aggregation: A Case Report." Annals of Saudi Medicine 11, no. 6 (November 1991): 698–700. http://dx.doi.org/10.5144/0256-4947.1991.698.
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Melanson, Scott W., Barry Silver, and Michael B. Heller. "Deep vein thrombosis, pulmonary embolism, and the white clot syndrome." American Journal of Emergency Medicine 14, no. 6 (October 1996): 558–60. http://dx.doi.org/10.1016/s0735-6757(96)90098-4.
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Desmet, G., A. Louwagie, A. Criel, M. Hidayat, and A. Van Hoof. "Heparin-Induced Thrombocytopenia With Disseminated Intravascular Coagulation And White Clot Syndrome A Case Report." Acta Clinica Belgica 43, no. 6 (January 1988): 419–22. http://dx.doi.org/10.1080/17843286.1988.11717969.
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Pfeiffer, G., J. Eberhardt, and R. Hamann. "White-clot-syndrome in heparin-induced thrombocytopenia type II with cross reactivity to danaparoid." Gefässchirurgie 5, no. 2 (May 12, 2000): 125–29. http://dx.doi.org/10.1007/s007720050192.
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Kleinschmidt, S., T. Ziegenfuß, U. Seyfert, and A. Greinacher. "Septisch-toxisches Herz-Kreislauf-Versagen als Folge einer Heparin-induzierten Thrombozytopenie mit „White-Clot-Syndrome”." AINS - Anästhesiologie · Intensivmedizin · Notfallmedizin · Schmerztherapie 28, no. 01 (February 1993): 58–60. http://dx.doi.org/10.1055/s-2007-998879.
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Claeys, L. G. Y. "Multiple Postoperative Thromboembolic Events and Fatal Pulmonary Embolism : the White Clot Syndrome. A Case Report." Acta Chirurgica Belgica 101, no. 3 (June 1, 2001): 139–40. http://dx.doi.org/10.1080/00015458.2001.12098604.
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Soetrisno, Coco Kokarkin. "NON-CLOTTING HAEMOLYMPH OF WSSV-INFECTED SHRIMP: IS IT A FACTOR IN INFECTION PROCESSES?" Indonesian Aquaculture Journal 4, no. 2 (December 31, 2009): 109. http://dx.doi.org/10.15578/iaj.4.2.2009.109-119.
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White spot syndrome virus is recognized as the most prominent pathogen of penaeid shrimp and has been affecting this shrimp farming industry around the world. The virus may reduce the shrimp’s immune response and alter enzymatic and biochemical composition of tissues. Similar to other environmental stressed or other pathogeninfected shrimp, in late stages of WSSV infection, shrimp will fail to clot the haemolymph, so any minor injury will lead to increased haemolyph loss. A series of experiments to determine the effect of non-clotting haemolymph on WSSV infection were carried out in controlled facilities in Indonesia. The preliminary test showed that normal clotting time was 13.3 seconds while WSSV-injected shrimp mostly failed to clot their haemolymph 16 hours post infection (hpi). Some other clinical signs such as abnormal swimming, red discoloration, white spots and mortality were consistent with those observed by previous studies. Three shrimp species: banana shrimp (P. merguiensis) 9 g , white leg shrimp (P. vannamei) 7 g and the tiger shrimp (P. monodon) 16.5 g were water-borne-challenged with non-clotting, WSSV-infected haemolymph (NCH) from tiger shrimp donor in duplicate tanks each with 12 shrimp. The control were tiger shrimps fed with WSSV-infected tissue at the rate of 40% of bodyweight (BW) and other tiger shrimps were used as negative controls fed with commercial feed only.The study revealed that NCH dosages of 1.46%; 2.03%; and 2.06% (v/v) for eachspecies were sufficient to infect and kill all shrimps in less than two days comparedto eight days for the shrimps fed on infected tissue. The WSSV in non-clottedhaemolymph eventuallyattaches into the living tissues of healthy shrimp. This modeof infection is likely more difficult to control by the ordinary fine mesh screeningmethod.
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Celińska-Löwenhoff, Magdalena, Teresa Iwaniec, Agnieszka Padjas, Jacek Musiał, and Anetta Undas. "Altered fibrin clot structure/function in patients with antiphospholipid syndrome: association with thrombotic manifestation." Thrombosis and Haemostasis 112, no. 08 (2014): 287–96. http://dx.doi.org/10.1160/th13-11-0980.
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SummaryWe tested the hypothesis that plasma fibrin clot structure/function is unfavourably altered in patients with antiphospholipid syndrome (APS). Ex vivo plasma clot permeability, turbidity and susceptibility to lysis were determined in 126 consecutive patients with APS enrolled five months or more since thrombotic event vs 105 controls. Patients with both primary and secondary APS were characterised by 11% lower clot permeability (p<0.001), 4.8% shorter lag phase (p<0.001), 10% longer clot lysis time (p<0.001), and 4.7% higher maximum level of D-dimer released from clots (p=0.02) as compared to the controls. Scanning electron microscopy images confirmed denser fibrin networks composed of thinner fibres in APS. Clots from patients with “triple-antibody positivity” were formed after shorter lag phase (p=0.019) and were lysed at a slower rate (p=0.004) than in the remainder. Clots from APS patients who experienced stroke and/or myocardial infarction were 8% less permeable (p=0.01) and susceptible to lysis (10.4% longer clot lysis time [p=0.006] and 4.5% slower release of D-dimer from clots [p=0.01]) compared with those following venous thromboembolism alone. Multivariate analysis adjusted for potential confounders showed that in APS patients, lupus anticoagulant and “triple-positivity” were the independent predictors of clot permeability, while “triple-positivity” predicted lysis time. We conclude that APS is associated with prothrombotic plasma fibrin clot phenotype, with more pronounced abnormalities in arterial thrombosis. Molecular background for this novel prothrombotic mechanism in APS remains to be established.
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Fernandez-Bello, Ihosvany, Raul Justo Sanz, Elena Monzón Manzano, Francisco García Río, Carolina Cubillos, Cristina Balbás-García, Teresa Álvarez-Roman, et al. "Platelet Dysfunction and Cellular Microparticles May be Involved in the Hipercoagulable State Observed in Obstructive Sleep Apnea Syndrome." Blood 132, Supplement 1 (November 29, 2018): 5048. http://dx.doi.org/10.1182/blood-2018-99-116018.
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Abstract Introduction: Obstructive sleep apnea syndrome (OSA) is a common disorder characterized by repetitive episodes of nocturnal breathing cessation due to upper airway collapse that cause intermittent hypoxia. Because of this, there is an increase in oxidative stress, endothelial damage and mortality associated with the incidence of thrombotic events. The evaluation of platelet function by flow cytometry (FCM) and hemostatic capacity through global hemostasis tests have been successfully used in the study of the prothrombotic state associated to numerous diseases. We anticipate that these techniques may help to clarify the mechanism involved in the prothrombotic state of OSA. Materials and Methods: We included 16 OSA patients diagnosed in the Pneumology Unit of the University Hospital La Paz and 59 healthy controls recruited in the Donor Unit of the same Hospital. Platelet surface receptors were analysed by FCM (FACScan, BD Biosciences) with specific monoclonal antibodies (mAbs) against CD41/αIIb and CD61/β3, CD42a and CD42b. Platelet activation was assessed by FCM through PAC1-FITC binding (mAbs that recognizes activated conformation of fibrinogen receptor), P-selectin and CD63 exposure in baseline condition and after stimulation with 100 µM TRAP (agonist of the PAR-1 receptor) and 10 µM ADP. Platelet apoptosis was analysed by FCM through FITC-annexin V (BD Pharmingen) binding to phosphatidylserine (PS) exposed on platelet membrane under basal conditions and by determination of activity of caspases -3/7, -8, and -9 (BD Millipore). The overall hemostatic capacity was determined by the evaluation of thrombin generation using the Calibrated Automatic Thrombinography (CAT) with fresh platelet-poor plasma (obtained after double centrifugation of whole blood at 2500g, 20 minutes and 24ºC) and by the assessment of kinetics of clot formation using Rotational Thromboelastometry (ROTEM® Gamma, Tem Innovations GmbH, Spain) using whole blood and activation by recalcification (naTEM® test, Tem Innovations GmbH, Spain). The statistical analysis was performed using SPSS 9.0 software (SPSS Inc., Chicago, Illinois, USA). Statistical significance was established at p <0.05. Results: No significant differences in age or sex were found between groups. Patients presented anxiety-depressive disorder (15%), ischemic cardiomyopathy (8%), dyslipidemias (38%), arterial hypertension (69%) and lower minimum oxygen pressures during sleep (mean±SD; patients: 76±8 % vs controls: 89±1 %; p< 0.001) indicating hypoxia. In basal conditions, an increase of CD42a subunit of the von Willebrand factor receptor was observed in patients with OSA but no differences were found in the exposure of fibrinogen receptor either at basal condition or after activation with TRAP or ADP (Table 1 and Figure 1). Platelet PS exposure before and after TRAP stimulation was higher in the patient group (Figure 1) but no differences between groups were observed in caspase activities (Table 2). Clotting time (CT), maximum clot firmness (MCF) and MP-associated thrombin generation were higher in patients with OSA (Figure 2). Conclusion: Mechanisms related to the mobilization of P-selectin to platelet surface and with the maintenance of phospholipids distribution in platelet membrane might be altered in OSA. The increment of P-selectin exposure may favor the interaction between white cells and platelets through PSGL-1 ligand from lymphocytes which in turn may produce endothelial damage explaining part of OSA's pathophysiology. A lower CT and higher MCF reflected a hypercoagulable state in patients, perhaps related to their higher MP-associated thrombin generation and, at least in part, due to the enhanced platelet-PS exposure. Our results also suggest that both ROTEM and CAT are useful tools for characterizing prothrombotic states in OSA patients. Work supported by grant from FIS-FEDER PI15/01457. NB holds a Miguel Servet II (FIS-FEDER CP14/00024). Disclosures Álvarez-Roman: Shire: Consultancy; NovoNordisk: Consultancy; SOBI: Consultancy. Jimenez-Yuste:Grifols: Consultancy, Research Funding; Octapharma: Consultancy, Research Funding; CSL Behring: Consultancy; Bayer: Consultancy, Research Funding; Roche: Consultancy, Research Funding; Shire: Consultancy, Research Funding; Pfizer: Consultancy, Research Funding; NovoNordisk: Consultancy, Research Funding; Sobi: Consultancy, Research Funding. Butta:FIS-Fondos FEDER: Research Funding.
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Johnston, Ian, Vincent M. Hayes, Douglas B. Cines, and Mortimer Poncz. "A Targeted Photochemical Microfluidic Vascular Injury Model for in Vitro Thrombosis Studies: Usage in Heparin-Induced Thrombocytopenia (HIT)." Blood 126, no. 23 (December 3, 2015): 212. http://dx.doi.org/10.1182/blood.v126.23.212.212.
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Abstract Replicating the complexities of the human blood vessel include the establishment of a 3-D confluency of viable endothelial cells (ECs) on an appropriate matrix, use of human whole blood or specific components of blood, varied shear stresses, and the induction of a localized and controlled injury within the observable field to understand and intervene in hemostatic events. This array of complexities have made vascular modeling an important unmet challenge. Such a model would enhance our understanding of the pathogenesis of diverse coagulation disorders, such as the prothrombotic disorder HIT. In HIT, the platelet-rich clots lead to its other designation as the "white clot syndrome". To provide an improved injury model, we adapted a hematoporphyrin-photochemical injury using a Fluxion Bioflux microfluidic system. When illuminated with 405 nm light, hematoporphyrin releases reactive oxygen species, inducing localized EC injury within the exposed field, but without denuding ECs. Unlike rose bengal, hematoporphyrin does not cause fluorescent interference with quantitative analysis of the developing thrombus. We propose that the model permits refined analysis of ECs transitioning from areas of quiescence to injury to quiescence, allowing us to localize and quantify the contribution of various components to the growing thrombus. In HIT, patients form antibodies to complexes of the platelet-specific chemokine, platelet factor 4 (PF4), and negatively-charged molecules such as infused heparin and heparans found on the surface of platelets and monocytes. ECs also bind PF4 immune complexes due to their highly negatively charged glycocalyx-rich surface. Prior murine cremaster laser injury studies showed that HIT antibodies bind predominantly to the EC surface rather than platelet within the thrombus itself. Was this observation related to the nature of the cremaster injury? Would antibody binding to the EC lining also be important in a wholly human HIT detection system? Using the described photochemical microfluidic system, we created a localized injury in human umbilical vein EC-lined channels through which we flowed whole human blood. Activated platelets established growing aggregates at the site of EC injury, releasing more PF4 that then bound to non-activated ECs downstream of the injury. Whole blood containing a HIT-like antibody to simulate the prothrombotic state of HIT was then flowed over this injured vasculature. HIT antibodies and then platelets bound sequentially to this new site of HIT antigen, allowing the thrombus to propagate downstream. We have named this phenomenon "rolling barrage" and suggest that a key part of the prothrombotic nature of HIT lies in antibody-mediated activation of downstream EC with subsequent thrombus propagation. HIT often occurs in the setting in surgery, which might prime EC dysfunction. We therefore treated the ECs (TNF-α) prior to injury and introducing the HIT-like antibody. TNF-α activated the EC lining, leading to loss of the anticoagulant EC surface, which enhanced clot formation downstream of the site of photochemical injury. Therefore, in a prothrombotic state such as HIT, we propose that a local injury acts as a nidus for thrombus initiation. The procoagulant process spreads distally in part because of released PF4 adhering to the downstream EC glycocalyx, which is exacerbated by mediators of inflammation. We anticipate that the described model can be used to study novel interventions to block this cycle in a wholly human system with control over the contribution of individual cellular elements, and will further understanding of the importance of this mechanism in other prothrombotic disorders. Disclosures No relevant conflicts of interest to declare.
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Waller, Amanda P., Katelyn J. Wolfgang, and Bryce A. Kerlin. "The Hypofibrinolytic Defect of Nephrotic Syndrome Is Directly Proportional to Fibrin Network Density." Blood 132, Supplement 1 (November 29, 2018): 1218. http://dx.doi.org/10.1182/blood-2018-99-119947.
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Abstract Introduction Nephrotic syndrome (NS) is characterized by massive proteinuria (secondary to podocyte injury), hypoalbuminemia, and edema. Importantly, NS is associated with a complex acquired hypercoagulopathy and a high incidence (~25%) of life-threatening thrombotic complications. Both hypercoagulopathy and hypofibrinolysis are described contributors to NS-related VTE risk. However, the mechanisms underlying the latter are poorly understood. We previously showed NS disease severity is directly proportional to both hypercoagulopathy and fibrinolytic resistance There is evidence that fibrin clot structural density contributes to clot stability and has been observed in the presence of both increased plasma thrombin generation and fibrinogen levels, both of which we have previously demonstrated in NS. Thus the aim of the present study was to investigate the mechanistic relationship between fibrin clot structure and fibrinolysis using two rodent models of NS and a cohort of human NS patients. We hypothesized that hypofibrinolysis arises from increased fibrin network density in a manner directly proportional to NS disease severity. Methods Using two well-established rat models of NS, transgenic diphtheria toxin receptor (DTR) and puromycin aminonucleoside (PAN), we compared fibrinolytic markers to disease severity. A range of severity was induced by a single injection of diphtheria toxin (0-75 ng/kg IP) or PAN (0-150 mg/kg IV). On day 10 post-injection, morning spot urines were collected and analyzed for protein:creatinine ratio (uPr:Cr). Rats were then anesthetized and venous blood (IVC) was collected into 0.32% NaCitrate/1.45 µM Corn Trypsin Inhibitor and spun down to platelet poor plasma (PPP). Samples were also collected from a local cohort of pediatric and adult NS patients (n=23), along with the corresponding clinical lab data for each patient. Plasma clot lysis assay (CLA) was performed using urokinase (50 IU) +/- plasminogen (2.4 uM), on clots initiated with high (20 nM) or low (5 nM) thrombin. Clot fibrin network structure was visualized/assessed by laser scanning confocal microscopy using fluorescently-labeled fibrinogen as a tracer. Fibrinolytic markers in plasma were measured by ELISA. Results Hypofibrinolysis: Previous findings of a hypofibrinolytic defect was confirmed with the CLA, such that plasma clot lysis at 60 min was significantly negatively correlated with proteinuria (R2=0.196; P=0.007 & R2=0.214; P=0.010) and significantly positively correlated with hypoalbuminemia (R2=0.310; P<0.001 & R2=0.240; P=0.006), in the DTR & PAN models, respectively. Additionally, plasma clot lysis by CLA was decreased in NS patients with uPrCr ≥2 (n=16) vs. <2 mg/mg (n=7) (96.1 vs 55.2 %, respectively; P=0.041). Similar results were found when the assay was repeated using high or low thrombin concentrations or increased UK (200 IU), with and without the addition of physiologic amounts of plasminogen. When the assay was performed in the absence of UK (0 IU), lysis at 60 min was drastically reduced (~17%) with no difference between groups. Mechanisms of Hypofibrinolysis: Fibrin network density increased with disease severity such that it was positively correlated with proteinuria (P=0.022) and negatively correlated with hypoalbuminemia (P=0.01) in our DTR rat model, with similar results seen in our human samples (Figure). As expected, fibrin network density was negatively correlated with plasma clot lysis (P=0.04), while plasma fibrinogen concentration (P=0.017), and thrombin generation (P=0.047) were positively correlated with fibrin density. There was no correlation with plasma uPA, PAI-1, a2AP, tPA, TAFI, or plasminogen. Conclusions These data suggest that nephrotic plasma forms thrombi with a denser fibrin network that is resistant to fibrinolysis, in a manner that is proportional to disease severity. The significant correlation between thrombin generation and fibrin network density suggest that plasma thrombotic potential may be a key mechanism contributing to the altered clot structure and impaired clot lysis of NS. Current studies are exploring the mechanisms underlying and in vivo significance of fibrinolytic resistance in our rat NS models. Disclosures No relevant conflicts of interest to declare.
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Tyukachev, V. E., D. A. Oks, and A. A. Butylkin. "A case of successful systemic thrombolysis in massive thromboembolia of pulmonary artery against the background of pregnancy." Patologiya krovoobrashcheniya i kardiokhirurgiya 21, no. 3 (November 22, 2017): 95. http://dx.doi.org/10.21688/1681-3472-2017-3-95-99.
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<p>We present a clinical case of successful systemic thrombolysis in a pregnant patient with massive pulmonary embolism. A 29-year old patient at 28 weeks of pregnancy was hospitalized 2 hours after sudden suffocation in a presyncopal state and hypotension of 90/50 mm Hg. ECG showed the signs of overload of right heart chambers in the form of a typical S1-Q3-T3 (McGinn–White) syndrome, as well as the Kosuge sign. Echocardiography verified pulmonary 3 Grade hypertension (81 mm Hg), enlargement of the right atrium and ventricle, 3 Grade tricuspid regurgitation and paradoxical movement of the interventricular septum. Multislice computed tomography of the chest with contrast of the pulmonary artery revealed a defect of contrast in the right main pulmonary artery, occlusive clearance, and thrombotic mass, extending to the bifurcation of the left main pulmonary artery ("clot - rider"). Thrombolytic therapy was started with recombinant tissue plasminogen activator (alteplase 10 mg bolus, then 90 mg for 2 hours). The patient was daily examined by a gynecologist. The viability of the fetus, monitoring of possible hemorrhagic complications of the placenta were evaluated. After thrombolysis, the patient began to note clinical improvement in the form of a regression of dyspnea. According to echocardioscopy control, the signs of overload of right heart chambers completely regressed. There were no complications both in the mother and in the fetus during the subsequent days until discharge. On 25.05.16 there was uncomplicated delivery vaginally of live full-term girl. Thus, when there is life-threatening massive pulmonary embolism, the application of General principles of diagnosis and treatment of this disease in patients with pregnancy is warranted. The carrying out of thrombolytic therapy in massive pulmonary embolism enables to reduce the manifestations of pulmonary hypertension, right ventricular failure, and to conduct births on time. Used intravenous thrombolytics have no teratogenic effect in the later stages of pregnancy.</p><p>Received 18 April 2017. Accepted 5 June 2017.</p><p><strong>Funding:</strong> The study did not have sponsorship.<br /><strong>Conflict of interest:</strong> The authors declare no conflict of interest.</p>
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Baranova, Anastasya A., Ilya G. Pochinka, Leonid G. Strongin, Ksenia N. Jurkova, and Maya I. Dvornikova. "Clinical correlates of thrombodynamics in men with metabolic syndrome: the impact of insulin resistance." Problems of Endocrinology 62, no. 5 (September 22, 2016): 24–25. http://dx.doi.org/10.14341/probl201662524-25.
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Background. Hypercoagulation is one of the cardiovascular risk factors in patients with metabolic syndrome (MS). It results from various factors including hyperhomocysteinemia, endothelial dysfunction, non-enzymatic glycation of proteins etc.The aim of this study was to assess clinical correlates of thrombodynamics in insulin resistant and non insulin resistant men with metabolic syndrome.Methods. We investigated 79 patients with MS diagnosed in accordance with IDF criteria (2009). The main group consisted of 44 men with MS including insulin resistance. The control group consisted of 35 men with MS not including insulin resistance. In addition to routine clinical tests we performed thrombodynamics assay and measured serum levels of asymmetric dimethylarginine (ADMA) and homocysteine. Mann-Whitney U-test and Spearmen’s correlation coefficient (rs) were used for statistical analysis.Results. There was no significant difference between thrombodynamics parameters, ADMA and homocysteine levels between the two groups. In both groups thrombodynamics parameters had no correlations with body mass index, hemoglobin level, platelet count and serum ADMA level. In patients with insulin resistance clot density correlated positively with serum level of C-reactive protein (rs=0.621, p=0.007); average and initial rates of clot growth correlated positively with homocysteine level (rs=0.539, p=0.017, and rs=0.554, p=0.014, respectively). In patients with insulin resistance clot density and rates of clot growth were not interrelated with the above mentioned parameters.Conclusions. The results of the study suggest that insulin resistant men with MS are characterized by clinical correlates between thrombodynamics parameters, homocysteine and C-reactive protein levels while patients without insulin resistance have other, unestablished determinants of clot density and rates of clot growth.
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Pchelin, Ivan Y., Natalia V. Hudiakova, and Alexander N. Shishkin. "Clinical correlates of thrombodynamics in men with metabolic syndrome: the impact of insulin resistance." Problems of Endocrinology 62, no. 5 (September 22, 2016): 25–26. http://dx.doi.org/10.14341/probl201662525-26.
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Background. Hypercoagulation is one of the cardiovascular risk factors in patients with metabolic syndrome (MS). It results from various factors including hyperhomocysteinemia, endothelial dysfunction, non-enzymatic glycation of proteins etc.The aim of this study was to assess clinical correlates of thrombodynamics in insulin resistant and non insulin resistant men with metabolic syndrome.Methods. We investigated 79 patients with MS diagnosed in accordance with IDF criteria (2009). The main group consisted of 44 men with MS including insulin resistance. The control group consisted of 35 men with MS not including insulin resistance. In addition to routine clinical tests we performed thrombodynamics assay and measured serum levels of asymmetric dimethylarginine (ADMA) and homocysteine. Mann-Whitney U-test and Spearmen’s correlation coefficient (rs) were used for statistical analysis.Results. There was no significant difference between thrombodynamics parameters, ADMA and homocysteine levels between the two groups. In both groups thrombodynamics parameters had no correlations with body mass index, hemoglobin level, platelet count and serum ADMA level. In patients with insulin resistance clot density correlated positively with serum level of C-reactive protein (rs=0.621, p=0.007); average and initial rates of clot growth correlated positively with homocysteine level (rs=0.539, p=0.017, and rs=0.554, p=0.014, respectively). In patients with insulin resistance clot density and rates of clot growth were not interrelated with the above mentioned parameters.Conclusions. The results of the study suggest that insulin resistant men with MS are characterized by clinical correlates between thrombodynamics parameters, homocysteine and C-reactive protein levels while patients without insulin resistance have other, unestablished determinants of clot density and rates of clot growth.
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Steffel, J., and T. F. Lüscher. "Individualized antithrombotic therapy." Hämostaseologie 36, no. 01 (2016): 26–32. http://dx.doi.org/10.5482/hamo-14-12-0080.
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SummaryClot formation in the circulation is a physiological mechanism preventing bleeding at sites of loss of vascular integrity. Clot formation may also occur intravascularly under pathological conditions, e. g. leading to myocardial infarction, stroke, and critical limb ischaemia. Clot formation involves activation of the coagulation cascade and of platelets eventually leading to an occlusive clot. In the venous circulation, clots are rich in erythrocytes and fibrin, while in the arterial circulation platelets predominate. Accordingly, drugs have been developed to interfere with the activation of the coagulation and/or platelets. As several coagulation factors such as factor VII, VIIII, X and thrombin (factor II) are vitamin K-dependent, drugs interfering with the effects of the vitamin (VKAs), i. e. warfarin, marcoumar or sintrom have been used for decades to prevent thromboembolism and embolic stroke. With the advent of selective inhibitors of factor X (apixaban, edoxaban and rivaroxaban) or factor II (dabigratan) the therapeutic spectrum of anti-thrombotic therapy has been expanded. On the other hand, platelet inhibitors such as aspirin and thienopyridines, i.e. clopidogrel, prasugrel, and ticagrelor have extensively been used to treat arterial disease in the coronary, cerebrovascular and peripheral circulation. Individualized antithrombotic therapy considers (1) characteristics of the disease and (2) those of the patient. Such a decision tree first separates “arterial” and “venous” thrombi. For the prevention of arterial thrombi that occur in acute myocardial infarction and certain forms of stroke and critical limb ischemia, platelet inhibitors are indicated. The first line drug is aspirin which interferes with thromboxane A2 (TXA2) formation and partially inhibits platelet activation. In patients receiving a stent or in acute coronary syndromes (ACS), the combination of aspirin with a thienopyri-dine is indicated. On the other hand, patients with venous clots should be treated with anticoagulants interfering with the activation of the coagulation cascade. While the longest experiences exist with vitamin K antagonists, the novel oral anticoagulants (NOACs) are at least as effective, but associated with less intracerebral and life-threatening bleeding. VKAs remain the treatment of choice in patients receiving artificial heart valves or with renal failure (in general a GFR of 30 ml/min/KG or less). In the remaining patients, current evidence suggests that NOACs should be preferred. The NOACs are well documented in patients with thromboembolism and atrial fibrillation. Whether patients with an acute ACS should receive dual antiplatelet drugs plus a low dose NOAC is a matter of debate, although conceptually it is an attractive concept. In patients after stent implantation with atrial fibrillation, in which a triple therapy with dual antiplatelet drugs and an anticoagulant is indicated, bleeding is an issue. Recent data suggest that administering a thienopyridine plus warfarin (or possibly a NOAC), while at the same time skipping aspirin may be an alternative to avoid severe bleeding and to maintain antithrombotic efficacy. Conclusion: An extensive therapeutic arsenal to interfere with clot formation requires an individualized approach considering the disease condition and co-morbidities of the patient, the anticoagulants’ and patient characteristics. This review builds on and extends previous publications of the authors on this topic.
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Cayla, Guillaume, Pierre Sie, Johanne Silvain, Delphine Brugier, Jean-Pierre Cambou, Daniel Thomas, Ana Pena, et al. "Short-term effects of the smoke-free legislation on haemostasis and systemic inflammation due to second hand smoke exposure." Thrombosis and Haemostasis 105, no. 06 (2011): 1024–31. http://dx.doi.org/10.1160/th11-02-0062.
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SummaryIt was the objective of this study to assess the effect of the implementation of the smoke-free legislation on haemostasis and systemic inflammation in second-hand smoking (SHS)-exposed healthy volunteers. Fibrin-rich clot properties, platelet reactivity and inflammatory biomarkers were measured before and four months following the implementation of the smoke-free legislation in gender and age-matched healthy volunteers exposed (n=23, exposed) and unexposed (n=23, controls) to occupational SHS. The primary objective was to compare fibrin-rich clot stiffness before and after implementation of the smoke-free legislation. There was 40% reduction in fibrin-rich clot stiffness following the implementation of the smoke-free legislation in SHS-exposed volunteers (17 ± 7 vs. 10.6 ± 7 dynes/cm², before and after, respectively, p=0.001). These dramatic changes were associated with a 20% reduction in fibrin fiber density (p<0.01) and a 20% reduction inclot lysis time (p=0.05). No change in fibrin properties was observed in the control group of SHS-unexposed volunteers related to the implementation of the smoke-free legislation. Of interest, neither platelet reactivity nor systemic inflammatory biomarkers were changed in either group. The smoke-free legislation is associated with significant changes in fibrin-rich clot properties toward a less thrombogenic conformation with a better fibrinolysis response while neither platelet reactivity nor systemic inflammatory biomarkers are modified. These improvements may explain the observed reduction in acute coronary syndrome following the implementation of the smoke-free legislation.
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Vorobev, Alexander Viktorovich, Alexander Davidovich Makatsaria, Andrey Mikhailovich Chabrov, and Alexander Anatol’evich Savchenko. "Pathogenesis of Trousseau’s syndrome." Journal of obstetrics and women's diseases 64, no. 4 (September 15, 2015): 85–94. http://dx.doi.org/10.17816/jowd64485-94.
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Malignancies and thrombosis have common pathogenetic features that was shown by A. Trousseau in 1865. There is now no doubt that the cancer patients occur much more frequently thromboembolism, and migratory venous thrombosis is a manifestation of paraneoplastic syndrome in cancer patients. In general, any manifestation of thrombohemorrhagic complications in cancer patients called Trousseau’s syndrome. While thrombotic complications such as venous thromboembolism are most frequent in cancer patients, may also experience severe bleeding symptoms due to systemic coagulopathies, including disseminated intravascular coagulation, haemolytic thrombotic microangiopathy, and hyperfibrinolysis. The basis of the pathophysiology of Trousseau’s syndrome, except the classic triad of Virchow, is overproduction of tissue factor (TF), the main initiator of extrinsic coagulation pathway. Thus a significant release of microparticles from tumor cells bearing tissue factor is critical not only for the formation of a blood clot, but the growth and progression of tumors. Tumor cells activate the coagulation cascade or fibrinolysis system, providing conditions for its further spread, stimulation of angiogenesis, increased vascular permeability, which in turn promotes metastasis.
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Hamarshi, Majdi, Tasma Harindhanavudhi, Maha Abu Kishk, Ammar Hamad, and Joseph Pyle. "Lymphoplasmacytic Lymphoma with IgA Gammopathy, Case Report and Review of Literature." Blood 110, no. 11 (November 16, 2007): 4409. http://dx.doi.org/10.1182/blood.v110.11.4409.4409.
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Abstract The Second International Workshop on Waldenstrom’s macroglobulinemia Consensus Panel has recommended diagnostic criteria that have been modified by the Mayo Clinic and large cohort studies 1–5. Essential to the criteria: IgM monoclonal gammopathy regardless of the size of the M protein, 10% or greater bone marrow infiltration by small lymphocytes that exhibit plasmacytoid or plasma cell differentiation with an intertrabecular pattern, and typical immunophenotype. We present a 72 year old WM who is free of any past medical history, presented with worsening ataxic gait for four months, mild headache, and frequent urination at night. No history of fever, weight loss, bone pain, numbness, muscle weakness, or back pain. On examination, patient had ataxic gait, positive Romberg test, otherwise normal exam, patient had no palpable lymph nodes, spleen or liver. Ophthalmic exam was normal. His Haemoglobin was 14.7 g/dl, white cell count was 9.9 × 109/l, no shift in neutrophils, no abnormal cells were seen, MCV was 92.4 fL, and no rouleaux formation. 24 Hour total urine protein is 66 mg/24 hours, no free monoclonal light chains (BJP). BUN, creatinine and electrolytes were normal, serum calcium 9.8 mg/dl, albumin 3.8 g/dl, and globulin 3.6 g/dl. After an extensive neurological work up including LP, CSF viral, bacterial, and fungal cultures and radiological studies that were all negative a thinking started about paraneoplastic syndrome. Serum protein electrophoresis was obtained and showed monoclonal paraproteinemia of 0.24 g/dL, immunofixation sowed IgA of 1110 mg/dl, 953 mg/dl, and 1190 mg/dl on three different occasions. IgM, and IgG were within normal limits. Anti Hu,”ANNA-1” and anti Ri “ANNA-2” were negative. Viscosity was 1.6 centipoises. Absence of anemia, bone lytic lesions, renal failure and normal serum calcium levels made Multiple Myeloma “MM” diagnosis less likely. Bone Marrow biopsy “BMB” was done and showed typical diffuse proliferation of small lymphocytes, plasmacytoid lymphocytes, and plasma cells which is the morphologic features of lymphoplasmacytic lymphoma “LPL”. The B cells expressed CD19, CD20, and CD138 without expression of CD5, CD10, CD11c, CD23, or CD25. Immunostains on the clot sections for IGA, kappa, lambda, CD20 and CD138 revealed up to 20 percent B lymphocytes with cytoplasmic and membrane kappa and IgA expression consistent with LPL. The challenge became how to explain such a combination between IgA gamopathy and LPL which classically has IgM macroglobulinemia. The patient was given a regimen of six cycles of cyclophosphamide, prednisone and rituxan, a follow up of six months showed dramatic improvement of his neurological symptoms, a second BMB was done after the chemotherapy course and showed no more evidence of LPL. Few case reports of LPL has been described and showed that monoclonal gammopathy isn’t restricted to the IgM class, it could be IgA 6–13, IgG 8, 10, 12, or non at all 12, all these cases were not given the diagnosis of Waldenstrom’s macroglobulinemia for the abscnce of IgM gammopathy.
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Fitzmaurice, David, Kate Fletcher, Sheila Greenfield, Sue Jowett, Alison Ward, Carl Heneghan, Eve Knight, et al. "Prevention and treatment of venous thromboembolism in hospital and the community: a research programme including the ExACT RCT." Programme Grants for Applied Research 8, no. 5 (May 2020): 1–104. http://dx.doi.org/10.3310/pgfar08050.
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Background Deep-vein thrombosis and pulmonary embolism, collectively known as venous thromboembolism when clots are formed in the venous circulation, are common disorders that are often unprovoked (i.e. there is no obvious reason for the clot occurring). Some people, after having an unprovoked clot, are at a high risk of developing another, or at risk of developing a secondary clot, most importantly in the lungs. Furthermore, in the long term, some patients will develop circulation problems known as post-thrombotic syndrome. The aim of this programme was to improve the understanding of both the prevention and the treatment of thrombosis in people at the highest risk of recurrence. Objectives To clarify if it is possible to identify those people at the highest risk of having a recurrent venous thromboembolism, and if it is possible to prevent this happening by giving anticoagulation treatment for longer. To clarify if it is possible to identify those people at the highest risk of developing post-thrombotic syndrome. To document the current knowledge level about prevention and treatment of venous thromboembolism. To find what the barriers are to implementing measures to prevent venous thromboembolism. To find the most cost-effective means of treating venous thromboembolism. Design Mixed methods, comprising a randomised controlled trial, qualitative studies, cost-effectiveness analyses and questionnaire studies, including patient preferences. Setting UK general practices and hospitals, predominantly from the Midlands and Shropshire. Participants Adults attending participating anticoagulation clinics with a diagnosis of first unprovoked deep-vein thrombosis or pulmonary embolism, and health-care professionals, patients and other stakeholders who were involved in the prevention and treatment of venous thromboembolism. Intervention Extended treatment with oral anticoagulation therapy (2 years) versus standard care (treatment with oral anticoagulation therapy for at least 3 months). Results Work package 1 demonstrated that extended anticoagulation for up to 2 years was clinically effective and cost-effective in reducing the incidence of recurrent venous thromboembolism, with a small increase in the risk of bleeding. There was no difference in post-thrombotic syndrome incidence or severity, or quality of life, between those undergoing the extended treatment and those receiving the standard care. Work package 2 identified five common themes with regard to the prevention of hospital-acquired thrombosis: communication, knowledge, role of primary care, education and training, and barriers to patient adherence. Work package 3 suggested that extended anticoagulation with novel oral anticoagulants was cost-effective only at the £20,000-per-quality-adjusted life-year level for a recurrence rate of between 17.5% and 22.5%, depending on drug acquisition costs, while identifying a strong patient preference for extended anticoagulation based on a fear of recurrent venous thromboembolism. Limitations The major limitation was the failure to reach the planned recruitment target for work package 1. Conclusions Extended anticoagulation with warfarin for a first unprovoked venous thromboembolism is clinically effective and cost-effective and is strongly preferred by patients to the alternative of not having treatment. There are significant barriers to the implementation of preventative measures for hospital-acquired thrombosis. Further research is required on identifying patients in whom it is safe to discontinue anticoagulation, and at what time point following a first unprovoked venous thromboembolism this should be done. Trial registration Current Controlled Trials ISRCTN73819751 and EudraCT 2101-022119-20. Funding This project was funded by the National Institute for Health Research (NIHR) Programme Grants for Applied Research programme and will be published in full in Programme Grants for Applied Research; Vol. 8, No. 5. See the NIHR Journals Library website for further project information.
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Seredavkina, N., T. Reshetnyak, T. Lisitsyna, and A. Lila. "AB0305 IS THERE HYPERCOAGULATION IN PATIENTS WITH ANTIPHOSPHOLIPID SYNDROME AND BEHCET’S DISEASE?" Annals of the Rheumatic Diseases 80, Suppl 1 (May 19, 2021): 1178.2–1179. http://dx.doi.org/10.1136/annrheumdis-2021-eular.1319.
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Background:Whereas antiphospholipid syndrome (APS) is a non-inflammatory vasculopathy and is associated with thrombosis in 98% of cases, Behcet’s disease (BD) is a systemic vasculitis of unknown etiology, characterized by vascular damage of any calibre. Both venous and arterial thromboses occur in 45% of BD patients and are associated not with hypercoagulable disease but with inflammatory changes in the vascular wall mediated by hypersecretion of pro-inflammatory cytokines and endothelial cells dysfunction. Thrombodynamics (TD) is a new global test for diagnosing plasma haemostasis disorders, identifying bleeding and thrombosis risks, and can be used to detect a prothrombotic state and assess the influence of disease activity and course on the hypercoagulation process.Objectives:comparative assessment of TD in patients with APS and BD before anticoagulant therapy (AC).Methods:The study included 20 patients (9 APS and 11 BD) and 8 age and sex-matched healthy controls (HC). None of the subjects received AC. Thromboses in past history were registered in 5/9 (55%) APS patients and 2/11 (18%) BD patients and none of HC. Fetal loss occurred only in women with APS (4/4 (100%) who had pregnancy during the disease). All the patients were hospitalized and underwent fool investigation according to the diagnosis including TD, local coagulation tests and antiphospholipid antibodies profile.Results:the velocity of clot growth in APS was lower, than in BD and in HC: 23.7 [22.6; 24.7] vs 29.0 [28.2; 34.4] and 31.1 [28.9; 33.5] Um/min, respectively (р=0.001). Clot size at 30 minutes in APS also was lower, than in BD and HC: 972.1 [921.3; 1007.4] vs 1152.7 [1098.3; 1225.4] and 1226.6 [1140.5; 1295.1] Um, respectively (р=0.001). Spontaneous clotting was registered only in 2 BD patients in mean time 2 minutes. Clot density and lag time (Tlag, the delay between the test start and the onset of clot formation) were the same in all three groups. Prolonged APTT was found in APS (33.7 [30.6; 47.1] sec) and normal APTT - in BD (30.9 [29.1; 31.1] sec) and HC (29.7 [28.2; 30.8] sec). Increased soluble fibrin-monomer complexes were revealed in all APS patients (100%), 91% BD patients and 25% HC (р=0.01). After interpretation the TD results were distributed as follows: hypocoagulation was noted in 1 APS patient with a positive lupus anticoagulant, while all other APS patients had normocoagulation. Thrombotic readiness status (TRS) was diagnosed only in 2 BD patients. The frequency of normocoagulation and hypercoagulation did not differ between BD and HC. Local coagulation tests (APTT, thrombin time, prothrombin time) were the same depending on hypo- and hypercoagulation by TD results. Fibrinogen level in BD patients with hypercoagulation was higher, than in BD patients with normocoagulation and TRS: 4.2 [3.6; 4.7] vs 2.8 [2.7; 3.0] and 2.8 [2.7;2.8] g/l respectively, р=0.04. BD activity by Behcet’s Disease Current Activity Form correlated with stationary velocity of clot growth (Rs = 0.68, p<0.05).Conclusion:Thrombodynamics results showed: before anticoagulant therapy there were normocoagulation with a tendency to hypocoagulation in APS and hypercoagulation in BD. In BD hypercoagulation associated with disease activity.Disclosure of Interests:None declared
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Yeh, C., B. Camilotti, H. Hanif, R. Mohindra, C. Sun, P. Kim, S. Lin, and M. Sholzberg. "P001: Proof-of-principle in a large animal pilot: cardiac arrest may be associated with acute, transient coagulopathy that may drive post-cardiac arrest syndrome." CJEM 22, S1 (May 2020): S64—S65. http://dx.doi.org/10.1017/cem.2020.209.
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Introduction: Many cardiac arrest survivors die later due to hemorrhage or thromboembolism, thought to be caused by acquired coagulopathy in post-cardiac arrest syndrome (PCAS) from shock and reperfusion injury. Understanding PCAS is a priority identified by the AHA for the prevention of complications in cardiac arrest survivors. Shock dysregulates both coagulation and fibrinolysis. The key effector enzyme thrombin (Th), is responsible for both up- and down-regulating coagulation and fibrinolysis. Measuring early Th activity may allow for predicting PCAS coagulopathy, and early medical intervention in the ED. Therefore, we aimed to characterize the time-course profile of early coagulation using an established pig model of cardiac arrest. Methods: Yorkshire pigs were anaesthetised and intubated, had VF-arrest induced by pacing, and were resuscitated per ACLS. Rotational thromboelastometry (ROTEM) was performed on whole blood at four times: baseline, intra-arrest, post-arrest, and death, using the fibrin-based test with tissue factor to initiate clotting in the presence of a platelet inhibitor cytochalasin D (FIBTEM). Clot time (CT), clot formation time (CFT), alpha-angle during clot formation (Alpha), clot amplitude at 10 min (A10), maximum clot firmness (MCF), and maximum lysis as total percentage (ML%) were quantified. The primary outcome is the overall coagulation initiation measured by CFT, while secondary outcomes include ROTEM parameters reflecting Th activity. Parameters are compared over time in SPSS using repeated measures ANOVA and Bonferroni correction. Results: Pilot data from one experiment show that cardiac arrest causes immediate early changes to coagulation that subsequently normalized with ROSC (Figure 1). CFT was impaired immediately upon cardiac arrest (2.3-fold increase), normalized with ROSC, and impaired again at death when compared with baseline. Consistent with clotting impairment, A10, Alpha, and MCF were all reduced with cardiac arrest, normalized with ROSC, and impaired again at death. Conclusion: Higher initial indices of coagulopathy in patients with cardiac arrest appear to correlate with death and thromboembolism. In this pilot, CFT is acutely modified by cardiac arrest. Since CFT is affected by overall Th activity, early Th dysregulation may be a critical driver of coagulopathy. Th may therefore be a lead target that is modifiable in the emergency post-arrest setting to decrease morbidity and mortality from PCAS in cardiac arrest survivors.
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Sedney, Cara L., Brenton R. Coger, and Julian E. Bailes. "Posterior Fossa Subdural Hematoma Resulting in Locked-in Syndrome: Case Report." Neurosurgery 69, no. 2 (March 30, 2011): E497—E500. http://dx.doi.org/10.1227/neu.0b013e318218cf85.
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Abstract BACKGROUND AND IMPORTANCE: Locked-in syndrome (LIS) is a well-known and devastating clinical entity, of which stroke is the most common cause; the distant second, trauma, usually results in LIS from basilar artery dissection. Our case report describes a posterior fossa subdural hematoma causing LIS, likely by direct compression of neural structures, which is a unique etiology and prognosis compared with other causes. CLINICAL PRESENTATION: A 34-year-old female experienced a posterior fossa subdural hematoma. She was taken emergently for evacuation, and on postoperative examination was found to be locked-in. The symptom complex, while classic for LIS, resolved at an accelerated rate compared with previous reports. Emergent evacuation of clot and rehabilitation were performed. CONCLUSION: Prompt treatment allowed this patient to experience an accelerated and more complete recovery compared with the ischemic causes of LIS.
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Swanepoel, Albe C., Amcois Visagie, and Etheresia Pretorius. "Synthetic Hormones and Clot Formation." Microscopy and Microanalysis 22, no. 4 (August 2016): 878–86. http://dx.doi.org/10.1017/s1431927616011478.
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AbstractCombined oral contraceptives (COCs), colloquially referred to as “the pill,” have been regarded as a medical breakthrough, as they have improved the lives of countless women, from simplifying family planning to the treatment of acne, endometriosis, polycystic ovarian syndrome, and dysmenorrhea. Unfortunately, COC usage has been associated with an increased occurrence of venous thrombosis and therefore a systemic hypercoagulable state in susceptible females. Here we discuss the health risks of COC usage and use viscoelastic and morphological techniques to investigate the effect of different COC constituents on clot formation, particularly fibrin network packaging and whole blood viscoelasticity. Viscoelastic properties of whole blood showed gender-specific changes while morphological alterations were person-specific, regardless of gender. Using scanning electron microscopy and thromboelastography provides great insight regarding fibrin packaging and the development of a hypercoagulable state in high-risk individuals. We proposed a three-step approach where (1) an individual’s coagulation profile baseline is determined, after which (2) the “ideal” combination of constituents is prescribed, and (3) the coagulation profile of the individual is monitored to assess possible risk of thrombosis. Only in following such an individualized patient-oriented approach will we be able to avoid the many health issues due to COC usage in susceptible females.
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Ringer, Coral N., Rebecca J. Engberg, Kristen E. Carlin, Kellie J. Micheletti, Dianna L. Shankland, and Robert M. DiBlasi. "Assessment of mask efficiency for preventing transmission of airborne illness through aerosols and water vapor." Gates Open Research 5 (July 20, 2021): 105. http://dx.doi.org/10.12688/gatesopenres.13318.1.
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Background: Currently the Center for Disease Control has advised the use of face coverings to prevent transmission of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) to those who are unvaccinated. This study seeks to evaluate if cloth masks have increased efficiency with the addition of a filter material. Methods: An adult airway and test lung model were exposed to nebulized ‘coarse’ aerosol droplets (0.5-11 µm) and humidified ‘fine’ water vapor particles (0.03-0.05 µm). Aerosol was quantified based on particles deposited on the face, airway and lung model. Tracheal humidity levels characterized fine particle permeability. Both phases of testing were conducted by evaluating the following testing conditions: 1) no mask; 2) cloth mask; 3) cloth mask with Swiffer™ filter; 4) cloth mask with Minimum Efficiency Reporting Value (MERV) 15 filter; 4) cloth mask with PM2.5 filter 5) surgical mask and 6) N95 respirator. Results: All mask conditions provided greater filtration from coarse particles when compared to no mask (P<0.05). All cloth mask with filter combinations were better at stopping fine particles in comparison to no mask. A cloth mask without a filter and surgical mask performed similarly to no mask with fine particles (P<0.05). The cloth mask with MERV 15 filter and the surgical mask performed similarly to the N95 with course particles, while the cloth mask with Swiffer™ performed similarly to the N95 with the fine particles (P<0.05). Conclusions: Respiratory viruses including SARS-CoV-2 and influenza are spread through exposure to respiratory secretions that are aerosolized by infected individuals. The findings from this study suggest that a mask can filter these potentially infectious airborne particles.
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Odani, Kentaro, Junya Abe, Yoshiaki Tsuyuki, Soshi Yanagita, Kazuya Shiogama, Mitsuhiro Tachibana, and Yutaka Tsutsumi. "Acute Coronary Syndrome in Acute Myeloid Leukemia with Maturation Accompanying Megakaryocytic Differentiation." Case Reports in Pathology 2020 (September 21, 2020): 1–7. http://dx.doi.org/10.1155/2020/8886298.
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An autopsy case (85-year-old Japanese male) of myeloperoxidase- (MPO-) positive acute myeloid leukemia with maturation (M1) accompanying megakaryocytic differentiation is presented. The patient manifested acute coronary syndrome. Even after emergent percutaneous coronary intervention, his performance status remained poor, so no chemotherapy against leukemia was given. The final white blood cell count reached 291,700/μL, and the platelet count was elevated to 510,000/μL. No cytogenetic studies were performed. He died at the 25th day of hospitalization. Autopsy revealed marked leukemic infiltration to the endocardium and subendocardial myocardium. Subendocardial myonecrosis was surrounded or replaced by the leukemic blasts, and neither granulation tissue reaction nor fibrosis was observed. In the cardiovascular lumen, lard-like blood clots were formed and microscopically consisted of leukemic blasts and platelets (leukemic thrombi). Infiltration of leukemic blasts was seen in the body cavities and systemic organs including the lung. The MPO-positive blasts lacked azurophilic granules and expressed the stem cell markers, CD34 and CD117 (c-kit). No features of myelofibrosis were seen in the 100% cellular marrow. In the endocardium, liver, lymph nodes, and bone marrow, megakaryocytic cells (CD42b/CD61+, MPO-) were distributed, while the small-sized blastic cells in the blood and tissues predominantly expressed MPO. The blasts lacked expression of CD42b/CD61. Megakaryocytic differentiation might be stimulated by certain tissue factors. AML accompanying megakaryocytic differentiation in certain tissues and organs should be distinguished from acute megakaryoblastic leukemia. The mechanisms provoking acute coronary syndrome in acute myeloid leukemia are discussed.
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Dobesh, Paul P., and Julie H. Oestreich. "Novel Direct-Acting Anticoagulants for Risk Reduction in ACS." Journal of Pharmacy Practice 26, no. 4 (November 19, 2012): 358–66. http://dx.doi.org/10.1177/0897190012465954.
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Acute coronary syndrome (ACS) is a devastating adverse cardiovascular event with a massive burden on patient morbility and mortality, as well as the economy. Approximately 1.2 million people are hospitalized annually for ACS in the United States, with direct medical costs estimated at $150 billion in 2009. Rehospitalization is common, often as the result of recurrence of the initial event or complications of ACS or its therapy. Thrombosis is central to the pathogenesis of ACS. The current standard of care includes dual antiplatelet therapy, which reduces platelet activation and aggregation, integral steps for forming a thrombus. However, antiplatelet therapy does not prevent continued thrombin generation or the deposition of fibrin in the clot and residual risk of a recurrent event remains high. New oral anticoagulants offer a mechanism of action that is different from and complementary to that of antiplatelet agents. The ATLAS ACS-TIMI 51 (Anti-Xa Therapy to Lower Cardiovascular Events in Addition to Standard Therapy in Subjects with Acute Coronary Syndrome–Thrombolysis in Myocardial Infarction 51) trial, using rivaroxaban, is the first trial of the new oral anticoagulants to show a benefit when added to antiplatelet therapy in reducing ACS events and mortality. While there was more major bleeding with the addition of rivaroxaban, fatal bleeding was not increased. These agents, if added to the current standard of care, might substantially reduce the high clinical and economic consequences of ACS.
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Kemerov, S. V., V. M. Vorobjev, M. R. Karpova, M. M. Solov᾿ev, and G. Tz Dambaev. "Prevention of pathological syndromes and post-morbidity rehabilitation of patients with heavy surgical infection on the basis of the complications development prediction index." Bulletin of Siberian Medicine 17, no. 3 (September 29, 2018): 70–79. http://dx.doi.org/10.20538/1682-0363-2018-3-70-79.
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Purpose of the study: working out an easy-to-use complication development index (CDI), designing a program for post morbidity rehabilitation of patients with surgical infection to improve the results of its treatment and reduce lethality.Materials and methods. A retrospective results analysis of treatment of 320 patients for purulent peritonitis and abdominal sepsis was carried out, including 268 patients (the comparison group) and 52 (the core group) with whom the complications development index was calculated. While studying this group of patients, the same protocol was used to prevent and treat complications on the basis of a complex individual program. In the comparison group, the patients were divided according to the severity of their condition in compliance with generally accepted clinical criteria: medium-heavy (98), severe (86) and extremely severe (84 patients, respectively).We have studied general clinical and biochemical indices, as well as the results of instrumental studies of the function of vital organs and body systems. The following indices were calculated: the prothrombin index; the integral index of thromboelastography (IIT), J = [R (min) × K (min)] : mA (mm), where R is the clotting time, K is the clot formation time, mA is the clot density); the general condition severity APACHE II (Acute physiology and chronic health evaluation); the degree of organ dysfunction SOFA (Sepsis organ failure assessment); leukocyte index of intoxication (LII). The PIRO concept (predisposition, infection, response, organ dysfunction) was used for clinical interpretation of the received research results.Results. The prediction index of complications of surgical infection was proposed. It is based on the results of clinical analysis the results of patient treatment and calculated by using the severity of the underlying pathological process, as well as the number of concomitant diseases, pathological syndromes and aggravating factors. As a result of the complication development prediction index use along with the implementation of the complex program for prevention and treatment of complications, the number went down from 50% to 90% in different groups under observation.
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Johansen, Max E., Wenche Jy, Lawrence L. Horstman, Carlos Bidot, and Yeon S. Ahn. "Red Cell-Derived Microparticles (RMP) Correct or Improve Abnormal Coagulation Profiles in TEG in a Variety of Disorders of Different Pathology." Blood 118, no. 21 (November 18, 2011): 2277. http://dx.doi.org/10.1182/blood.v118.21.2277.2277.
Full textAbstract:
Abstract Abstract 2277 Introduction: Thromboelastography (TEG) reports several viscoelatstic changes during clot formation, giving useful information on multiple parameters, and can give information on effects of therapeutic measures. We previously demonstrated that RMP can improve clotting parameters in selected bleeding disorders, judging by TEG. In this report we characterize the abnormalities seen in TEG in several disease states, and how RMP can modify or correct the abnormal parameters. Methods: (i) The following patient groups were studied by TEG: Patients with ITP (n=10), other non immune TP (n=10), thrombocytopenia from aplastic anemia (AA, n=3), antiphospholipid syndrome (APS, n=10), systemic lupus erythmatosus (SLE, n=8), hemophilia (n=3), hemolytic anemia (HA, n=4) and healthy controls (n=84). (ii) RMP were produced from washed, packed RBC by high-pressure extrusion and were added at 1×10E8/mL f.c. to the test samples. (iii) TEG was performed on whole citrated blood, each in presence and absence (+/−) of added RMP. Parameters measured were R (lag time), k (clot formation time), A, angle (initial rate of clot growth), MA (maximum amplitude, or clot strength), G (shear elastic modulus, another measure of clot strength) and CI (coagulation index), a composite measure. Results: (1) Baseline findings (absence of RMP). All disease groups except HA had longer R (lag) time than controls (p≤0.03), but only AA, ITP, and SLE had longer k times (p≤0.03). HA had a significantly shorter k time and higher angle A (initial rate) compared to controls, both at p<0.01. Angle A was lower in Hemophilia, TP, ITP, AA and SLE (all p≤0.05 or better). APS did not differ from controls. Finally, MA (amplitude) and G (elastic modulus) were lower in TP, ITP, and AA than controls (p≤0.04), while the other diseases did not differ from controls in this measure. (2) Effect of RMP. The R and k parameters of all disease groups except HA were significantly shortened upon addition of RMP (p≤0.05 or better). RMP also shortened R and k of healthy controls (p<0.01, n=84). TP, ITP, AA, hemophilia APS, and controls also had shorter R+k time, and steeper angle A (p≤0.05 or better for all measures). HA had a shorter R+k time (p<0.05) but angle A remained unaffected. Additionally, modest increases in MA and G were seen in hemophilia and APS in the presence of RMP (p<0.04 or better). (3) Global measures. The CI (coagulation index) was significantly improved (p<0.05 or better) by addition of RMP in TP, ITP, APS, and SLE, indicating a better global coagulation profile in those diseases. (4) Combined groups. When all of the hematologic disorders were combined, significant differences in R, k, R+k, A, and G were observed in the presence of RMP (p≤0.02), but no difference in MA was seen, although it was very close to significance (p=0.051). CI was also markedly improved by RMP (p=0.02). (5) General observation. It is important to add that in nearly all groups, some patients responded strongly to RMP but others weakly or not at all, indicating different status of the disorder, possibly reflecting a state of platelet activation, inflammation, or disease activity. Conclusions/Discussion: RMP appear to have broad efficacy in correcting abnormal coagulation profiles in several disorders with differing pathologies. The parameter most strongly affected was time for initial fibrin formation, R. Effect on clot strength (G, MA) was statistically significant but varied among individual patients. RMP could correct abnormal clotting parameters in blood from differing pathologies, although there were individual variations. These data support the hypothesis that RMP can serve as a useful hemostatic agent to reduce bleeding in a variety of conditions of differing etiology. However, the factors responsible for such variations remain unknown. Elucidation of underlying factors influencing the effect of RMP will further improve and refine its therapeutic benefit and indications of its application. Disclosures: No relevant conflicts of interest to declare.
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Brooks, Marjory B., James L. Catalfamo, H. Alex Brown, Pavlina Ivanova, and Jamie Lovaglio. "A hereditary bleeding disorder of dogs caused by a lack of platelet procoagulant activity." Blood 99, no. 7 (April 1, 2002): 2434–41. http://dx.doi.org/10.1182/blood.v99.7.2434.
Full textAbstract:
We have discovered a novel canine hereditary bleeding disorder with the characteristic features of Scott syndrome, a rare defect of platelet procoagulant activity. Affected dogs were from a single, inbred colony and experienced clinical signs of epistaxis, hyphema, intramuscular hematoma, and prolonged bleeding with cutaneous bruising after surgery. The hemostatic abnormalities identified were restricted to tests of platelet procoagulant activity, whereas platelet count, platelet morphology under light microscopy, bleeding time, clot retraction, and platelet aggregation and secretion in response to thrombin, collagen, and adenosine diphosphate stimulation were all within normal limits. Washed platelets from the affected dogs demonstrated approximately twice normal clotting times in a platelet factor 3 availability assay and, in a prothrombinase assay, generated only background levels of thrombin in response to calcium ionophore, thrombin, or combined thrombin plus collagen stimulation. While platelet phospholipid content was normal, flow cytometric analyses revealed diminished phosphatidylserine exposure and a failure of microvesiculation in response to calcium ionophore, thrombin, and collagen stimulation. Pedigree studies indicate a likely homozygous recessive inheritance pattern of the defect. These findings confirm the importance of platelet procoagulant activity for in vivo hemostasis and provide a large animal model for studying agonist-induced signal transduction, calcium mobilization, and effector pathways involved in the late platelet response of transmembrane phospholipid movement and membrane vesiculation.
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Kotova, Yana N., Nadezhda A. Podoplelova, Sergey I. Obydennyy, Elizaveta A. Kostanova, Alexander A. Ryabykh, Aleksandra S. Demyanova, Maria I. Biriukova, et al. "Binding of Coagulation Factor XIII Zymogen to Activated Platelet Subpopulations: Roles of Integrin αIIbβ3 and Fibrinogen." Thrombosis and Haemostasis 119, no. 06 (April 1, 2019): 906–15. http://dx.doi.org/10.1055/s-0039-1683912.
Full textAbstract:
AbstractFactor XIIIa (fXIIIa) is a transglutaminase that plays a crucial role in fibrin clot stabilization and regulation of fibrinolysis. It is known to bind to procoagulant platelets. In contrast, the zymogen fXIII interaction with platelets is not well characterized. We investigated the interaction of zymogen fXIII with activated platelet subpopulations. Confocal microscopy and flow cytometry using fluorescently labelled factors and antibodies. Phosphatidylserine (PS)-positive activated platelets bound 700 to 800 molecules/cell of fXIII at 100 nM, while both PS-negative activated platelets and resting platelets bound 200 to 400 molecules/cell. The binding was reversible, calcium-independent and linear within the fXIII concentration range of up to 1,000 nM. fXIII predominantly bound to the caps of procoagulant platelets and co-localized with fibrinogen. Exogenous fibrinogen promoted fXIII binding by activated PS-negative platelets; this effect was abolished by the integrin αIIbβ3 antagonist monafram. The fXIII binding was 1.5- to 3-fold decreased for platelets from four patients with grey platelet syndrome, and was variable for platelets from six patients with Glanzmann's thrombasthenia. Strong platelet stimulation, fibrinogen and αIIbβ3 play essential roles in fXIII binding, without any of them fXIII does not bind to platelets. The preferential binding in the cap-like structures might be important for increasing local fXIII concentration in platelet thrombi.
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Matusik, Pawel, Bartlomiej Guzik, Christian Weber, and Tomasz J. Guzik. "Do we know enough about the immune pathogenesis of acute coronary syndromes to improve clinical practice?" Thrombosis and Haemostasis 108, no. 09 (2012): 443–56. http://dx.doi.org/10.1160/th12-05-0341.
Full textAbstract:
SummaryMorbidities related to atherosclerosis, such as acute coronary syndromes (ACS) including unstable angina and myocardial infarction, remain leading causes of mortality. Unstable plaques are inflamed and infiltrated with macrophages and T lymphocytes. Activated dendritic cells interact with T cells, yielding predominantly Th1 responses involving interferon-gamma (IFN-γ) and tumour necrosis factor-alpha (TNF-α), while the role of interleukin 17 (IL-17) is questionable. The expansion of CD28nullCD4 or CD8 T cells as well as pattern recognition receptors activation (especially Toll-like receptors; TLR2 and TLR4) is characteristic for unstable plaque. Inflammation modifies platelet and fibrin clot characteristics, which are critical for ACS. Understanding of the inflammatory mechanisms of atherothrombosis, bridging inflammation, oxidative stress and immune regulation, will allow for the detection of subjects at risk, through the use of novel biomarkers and imaging techniques including intravascular ultrasound, molecular targeting, magnetic resonance imaging (MRI) and 18F-fluorodeoxyglucose (18F-FDG) positron emission tomography (PET). Moreover, understanding the specific inflammatory pathways of plaque rupture and atherothrombosis may allow for immunomodulation of ACS. Statins and anti-platelet drugs are anti-inflammatory, but importance of immune events in ACS warrants the introduction of novel, specific treatments directed either on cytokines, TLRs or inflammasomes. While the prime time for the introduction of immunologically inspired diagnostic tests and treatments for atherosclerosis have not come yet, we are closer than ever before to finally being able to benefit from this vast body of experimental and clinical evidence. This paper provides a comprehensive review of the role of the immune system and inflammation in ACS.Note: The review process for this manuscript was fully handled by G. Y. H. Lip, Editor in Chief.
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Cacciapuoti, Federico. "Thrombophilias: therapeutic employment of direct oral anticoagulants in venous hypercoagulable states." Italian Journal of Medicine 14, no. 3 (September 17, 2020): 136–42. http://dx.doi.org/10.4081/itjm.2020.1296.
Full textAbstract:
Thrombophilia or hypercoagulable state is a predisposition to form clots. Thrombophilia can be inherited or acquired, and prevalently involves venous vessels. Inherited thrombophilia consists of congenital conditions, as methylenetetrahydrofolate reductase polymorphism, Factor V Leiden and prothrombin gene mutations, natural anticoagulant deficiencies, high level of factor VIII, or dysfibrinogenemia. These congenital disorders can be responsible for venous thromboembolism, particularly deep venous thrombosis, pulmonary embolism, and, less frequently, mesenteric veins thrombosis, kidneys’ veins thrombosis or retinal vein occlusion. Acquired thrombophilia can be associated both with venous and arterial thrombosis and may be caused by antiphospholipid syndrome, aging, some malignancies, oral contraceptive use, heparin-induced thrombocytopenia, and human immunodeficiency virus. Antiplatelets’ drugs are employed in arterial thrombosis, while, heparins/oral vitamin K antagonists are indicated for acute and long-term anticoagulation. However, new oral anticoagulants can be usefully used for venous thromboembolic events. Recent experiences demonstrated that their employment is useful in some thrombophilias only, whereas other investigations are requested to evaluate their use in all hypercoagulable disorders.
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Chen, PP, M. Wu, and BH Hahn. "Some antiphospholipid antibodies bind to various serine proteases in hemostasis and tip the balance toward hypercoagulant states." Lupus 19, no. 4 (March 30, 2010): 365–69. http://dx.doi.org/10.1177/0961203310361488.
Full textAbstract:
The body has an elaborate system that maintains blood circulation and rapidly stops bleeding when vessels are damaged. Abnormalities that disrupt this balance may lead to thrombosis. While β2-glycoprotein I is generally accepted as the major antigen for antiphospholipid antibodies in the antiphospholipid syndrome, our accumulated studies show that some antiphospholipid antibodies bind homologous enzymatic domains of several serine proteases involved in hemostasis and fibrinolysis. Functionally, some of the protease-reactive antiphospholipid antibodies hinder anticoagulant regulation and resolution of clots, thus tip the balance toward thrombosis. Intriguingly, several serine protease-reactive antiphospholipid antibodies also react with β2-glycoprotein I, and interactions between antiphospholipid antibodies and antigens are cross-inhibited, indicating that these antiphospholipid antibodies recognize conformational epitope(s) on β2-glycoprotein I and target serine proteases. Viewed as a whole, these results extend previous reports that antiphospholipid antibodies bind to various hemostasis factors, and provide a new perspective about some antiphospholipid antibodies in terms of their binding specificities and related functional properties in promoting thrombosis.
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Kunk, Paul, B. Gail Macik, and Melissa Rice. "Non-Warfarin Oral Anticoagulants in Anti-Phospholipid Syndrome." Blood 126, no. 23 (December 3, 2015): 1133. http://dx.doi.org/10.1182/blood.v126.23.1133.1133.
Full textAbstract:
Abstract Introduction: Anti-Phospholipid Syndrome (APS) is a serious and deadly disorder leading to a significant risk of thrombi, requiring lifelong therapeutic anticoagulation. Traditionally, the vitamin K antagonist (VKA) warfarin has been considered standard of care in this patient population. However, the VKAs require frequent laboratory monitoring, have a narrow therapeutic window, numerous drug interactions and dietary restrictions. Due to these factors, many patients suffer recurrent thrombi and/or major bleeding, warranting therapy modification or switching to parenteral anticoagulants. The non-warfarin oral anticoagulants (NOACs), specifically the direct Xa inhibitors apixaban and rivaroxaban, have been approved for the treatment of venous thromboembolism and represent attractive options for these patients. Methods: We designed a retrospective analysis of all patients at the University of Virginia with APS that were treated with either apixaban or rivaroxaban since September 2011. All patients were required to have a definitive diagnosis of APS [defined by the Sydney criteria as an arterial or venous thrombosis and IgM and/or IgG anti-cardiolipin antibody >40GLP, IgG and/or IgM beta-2 glycoprotein >99th percentile, and/or positive lupus anticoagulant (e.g. prolonged silica clot time or dilute Russell viper venom time)]. Patients were reviewed for recurrent thrombi, severe bleeding or other complications that led to changes in their management. Results: Sixty-six patients were identified with suspected APS, with 18 being treated with a NOAC. Of these, 10 had definitive APS per the Sydney criteria and were analyzed. 6/10 (60%) were treated with apixaban and 4/10 (40%) were treated with rivaroxaban. No patients developed severe bleeding or thrombotic complications and none required changes of their therapy. 30% started a NOAC as the first line outpatient regimen with the remaining 70% being previously treated with other anticoagulants. 7/10 (70%) were treated with warfarin and 3 patients were treated with fondaparinux before changing to a NOAC. Reasons for stopping warfarin were difficulty managing INRs (33%) or thrombi while on warfarin (66%). Of those previously on fondaparinux, reasons for changing therapy were transient ischemic attack (33%), difficulty with injections (33%) and cost (33%). Of these 10 patients, safe and effective anticoagulation with a NOAC was noted for up to 36 months without adverse effects. Conclusion: Apixaban and rivaroxaban showed to be a safe and effective first line outpatient regimen for patients with APS or patients with APS who develop recurrent thrombi on warfarin or parenteral anticoagulation. Further prospective studies are needed before their use should be considered standard of care. Table 1. Patients with Anti-Phospholipid Syndrome Treated with Non-Warfarin Oral Anticoagulant Patient First Positive Test Second Positive Test Serum Testing Performed off Warfarin Anticoagulant Length of Treatment (in months) Bleeding Complications Thrombotic Complications Prior Anticoagulant Use Reason Therapy was Changed 1 Cardiolipin IgG 52, β2 IgG >112 Cardiolipin IgG 76, β2 IgG >112; RVVT prolonged No Apixaban 8 None None Yes (warfarin) Difficult to control INR 2 Cardiolipin IgG >15;RVVT prolonged Cardiolipin IgG >15;RVVT prolonged Yes Apixaban 6 None None Yes (warfarin) Difficult to control INR 3 Cardiolipin & β2 >112 Cardiolipin & β2 >112 Yes Apixaban 2 None None Yes (warfarin) Stroke while on warfarin 4 Cardiolipin IgM 66, β2 IgM 68 Cardiolipin IgM 98, β2 IgM 87 Yes Apixaban 8 None None No N/A 5 β2 IgG 122;+ LA Cardiolipin & β2 >112 No Apixaban 7 None None Yes (warfarin) Multiple strokes while on warfarin 6 β2 IgM 29;+ LA Cardiolipin IgM 50, β2 IgM 74RVVT prolonged Yes Apixaban 4 None None Yes (Fondaparinux) Difficulty with injections 7 Cardiolipin IgG 73 Cardiolipin IgG & β2 IgG>112;RVVT prolonged Yes Rivaroxaban 36 None None Yes (warfarin & fondaparinux) Thrombi on warfarin & fondaparinux 8 Cardiolipin IgG>112;RVVT prolonged Cardiolipin IgG>112 Yes* Rivaroxaban 2 None None Yes (warfarin) Difficult to control INR 9 Cardiolipin IgM & β2 IgM>112 Cardiolipin IgM & β2 IgM>112 Yes* Rivaroxaban 15 None None No N/A 10 β2 IgG>100RVVT prolonged β2 IgG>100;RVVT prolonged No Rivaroxaban 31 None None Yes (warfarin & fondaparinux) Thrombi on warfarin & fondaparinux *Second serum testing drawn while on rivaroxaban Disclosures Off Label Use: Apixaban and rivaroxaban use in patients with Anti-phospholipid Syndrome.
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Santiago, Marc Reinald G., and Natividad A. Almazan. "Gradenigo Syndrome." Philippine Journal of Otolaryngology-Head and Neck Surgery 23, no. 2 (December 27, 2008): 46–48. http://dx.doi.org/10.32412/pjohns.v23i2.747.
Full textAbstract:
Chronic suppurative otitis media (CSOM) has a potential for intratemporal complications. Gradenigo syndrome, lateral sinus thrombosis and cavernous sinus thrombosis must be considered when patients present with ear discharge, headache, fever and lateral rectus palsy. Computed Tomography and Magnetic Resonance Imaging are essential in confirming the diagnosis but do not substitute for a good clinical eye in establishing the diagnosis and initiating proper treatment.
CASE
A 17 year old male with an 11-year history of otorrhea on the right ear was admitted because of on-and-off diffuse headache, drowsiness, occasional sensorial changes, high grade fever and vomiting. Later in the ward, he complained of double vision; anisocoria and lateral rectus palsy were confirmed by active generation test. Associated symptoms included right-sided frontal, orbital and mastoid pain with neck stiffness. Otoscopy showed yellowish foul smelling discharge with a pink, smooth mass partially obstructing the external auditory canal.
Leukocytosis was seen with a count of 32.9 x 103/L. Pure tone audiometry revealed moderate conductive hearing loss on the right ear. CT scan with contrast (Figure 1) showed lytic erosion of the underpneumatized right mastoid bone and sigmoid sinus plates with slightly asymmetric right internal auditory canal (IAC). Penicillin G 5 million “IU” every 6 hours and Chloramphenicol 1.5 grams IV every 8 hours were given for 3 weeks, but he continued to deteriorate and two units of PRBC were transfused. Because of his worsening condition, Penicillin G was shifted to Ceftriaxone 2 grams IV BID while Chloramphenicol IV was continued at the same dose. The patient’s headache and fever steadily lessened after 4 weeks but orbital pain and diplopia persisted. On the 50th hospital day, patient underwent Modified Radical Mastoidectomy, right. Intraoperatively, granulation tissue was noted occupying the enlarged mastoid cavity and antrum. A 0.5 cm break at the sigmoid sinus was also occupied by granulation tissue. IV antibiotics was continued 2 weeks postoperatively and after 64 days of hospitalization he was discharged on oral Ciprofloxacin 500mg BID for 1 month with steroid/antibiotic otic drops.
Regular follow-up documented gradual lessening of diplopia, headache and orbital pain. Complete resolution of diplopia with normal ophthalmologic findings and a dry mastoidectomy cavity were noted on the fourth month of follow-up.
DISCUSSION
In the Philippines, the prevalence of Chronic Suppurative Otitis Media (CSOM) is estimated at 2.5 – 29.5%.1 Complications of chronic otitis media can cause grave morbidity and even mortality2 even though the intratemporal and/or intracranial complications of infectious ear disease have become rarer with the advent of broad spectrum antibiotics.3 The spread of infection can occur by osteothrombosis, bone erosion and when present along preformed pathways.2
The triad of Gradenigo syndrome includes otorrhea, retroorbital pain and abducens nerve palsy. Chole and Donald found that the most common presenting symptom in 22 patients from 1976-1995 was otalgia (72%) followed by deep pain, headache and otorrhea (59%). Cranial nerve VI paralysis was only present in 18.2% of the cases.4 Homer and others reported 3 cases with middle ear infection and 6th nerve palsy without petrositis. 5
MRI and CT are required to identify the deep seated petrous apex as the site of the inflammatory process.6 While CT scans may demonstrate opacification of the air cells of the petrous apex with cortical bone erosion, MRI is very useful for assessing inflammatory soft tissue lesions around the petrous apex.5 Both CT and MRI are essential to establish opacification of air cells in the petrous apex under suspicion, as opposed to assymetric pneumatization.2 However, acute petrositis cannot always be equated with Gradenigo syndrome.7 A study by Back and others documented 8 cases of radiologically confirmed apical petrositis that did not manifest the classical syndrome of deep facial pain, otitis media and ipsilateral abducens nerve palsy.8
Petrous apicitis is essentially mastoiditis that occurs in the petrous apex.2 Because the trigeminal (CN V) or gasserian ganglion lies in Meckel’s cave on the antero-superior aspect of the petrous tip, damage or irritation to the ganglion may explain the deep facial pain in some patients with apicitis. The petroclinoid ligament extends from the tip of the petrous apex to the clinoid. Below this ligament, the gasserian ganglion (CN V) and abducens nerve (CN VI) travel in the small Dorello's canal. Inflammation extending into the canal produces the triad of symptoms recognized by Gradenigo9: lateral rectus (CN VI) palsy, retroorbital pain (CN V), and otorrhea.
Lateral Sinus Thrombophlebitis (LST) or thrombosis of the lateral sinus usually forms as an extension of a perisinus abscess following mastoid bone erosion from cholesteatona, granulation tissue or coalescence which eventually leads to pressure necrosis and mural thrombus formation.2 Classic symptoms of LST include a "picket fence" fever pattern, chills and progressive anemia. Symptoms of septic emboli, headache and papilledema may indicate extension to involve the cavernous sinus4 or sudden intracranial hypertension resulting from decreased venous drainage from the skull.2
The diagnostic procedure of choice is MRI with MR angiography. The thrombus can be identified by its signal intensity on MRI and the flow void in the affected sinus is clearly documented on MR angiography.10 Non-contrast CT findings include dense cord sign, dense dural sinuses, diffuse cerebral edema, non hemorrhagic infarct or multifocal haemorrhages.11 Papilledema and anisocoria may be symptoms of progression of lateral sinus thrombophlebitis or development of cavernous sinus thrombosis.4 Fresh thrombi from the lateral sinus can propagate and extend to the cavernous sinus via the superior and inferior petrosal sinus.
Cavernous Sinus Thrombosis is usually a late complication of an infection of the central face or paranasal sinuses. Other causes include bacteremia, trauma, and infections of the maxillary teeth or ear, as seen in our patient. CST is generally a fulminant process with high rates of morbidity and mortality. Headache is the most common presenting symptom that usually precedes fever, periorbital edema (which may or may not occur) and cranial nerve dysfunction.
This intimate relationship of veins, arteries, nerves, meninges, petrous apex and paranasal sinuses account for the characteristic etiology and presentation of CST. The internal carotid artery with its surrounding sympathetic plexus passes through the cavernous sinus. The third, fourth, and sixth cranial nerves are attached to the lateral wall of the sinus while the ophthalmic and maxillary divisions of the fifth cranial nerve are embedded in the wall.8
Other signs and symptoms include chemosis resulting from occlusion of the ophthalmic veins, lateral gaze palsy (isolated cranial nerve VI), ptosis, mydriasis and eye muscle weakness from cranial nerve III dysfunction. These are followed by manifestations of increased retrobulbar pressure (such as exophthalmos) and increased intraocular pressure (such as sluggish pupil and decreased visual acuity). Systemic signs indicative of sepsis are late findings.
The complications of Gradenigo syndrome, lateral sinus thrombophlebitis and cavernous sinus thrombosis from chronic suppurative otitis media need immediate diagnosis and aggressive medical treatment with broad spectrum antibiotics against gram positive cocci (Staphylococci and Streptococci), gram negative bacilli (Pseudomonas aeruginosa) and to a lesser extent, Anaerobes. These antibiotics should also cross the blood-brain barrier.
Mastoidectomy is required once the patient is neurologically stable.2 In cases of lateral sinus thrombosis, surgical removal of emboli can be done. However, Cummings, Syms and colleagues2 report 6 patients operated on without opening and evacuating the lateral sinus clot who all survived, albeit with a longer 49 day average hospital stay. Once a highly controversial issue, ligation of the internal jugular vein is seldom needed. In the majority of recent cases, anticoagulation has not been found to be necessary.2
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Del Pozzo, Jill, Erica F. Weiss, Diana Bronshteyn, David M. Masur, John J. McGinley, and Ronda F. Facchini. "A-57 The Neuropsychological Impact of Antiphospholipid Antibody Syndrome: A Case Study." Archives of Clinical Neuropsychology 36, no. 6 (August 30, 2021): 1099. http://dx.doi.org/10.1093/arclin/acab062.75.
Full textAbstract:
Abstract Objective Antiphospholipid Antibody Syndrome (APS), also known as Hughes Syndrome, is an autoimmune condition linked to various adverse medical and neurological outcomes affecting 5 in 100,000. APS results from antibodies (aPL) that attack blood proteins that bind to phospholipids (e.g., 2-glycoprotein I and prothrombin), which can cause blood flow problems, increased risk of blood clots, and recurrent vascular thrombotic events. Research suggests APS may lead to various neurologic/medical issues including memory loss, visual disturbances, and dementia. Method Neuropsychological evaluation of 48-year-old female with triple-positive APS and history of bilateral superior parietal chronic ischemic infarctions, multiple bilateral lacunar infarctions, and bilateral encephalomalacia. Reports progressive cognitive changes (< 1 year). Results Neuropsychological evaluation evidenced low average premorbid functioning and currently, extremely low overall cognitive ability. Memory was variable with significant visual and working memory impairment but preserved delayed recall of contextual information. While verbal abilities were intact, deficits were noted in executive functioning, attention, processing speed, visuomotor, visual–spatial, and fine motor skills. Conclusion This 48-year-old woman’s cognitive profile is consistent with findings in the APS literature and is indicative of an early onset major vascular neurocognitive disorder. Retrospective studies suggest that cognitive deficits often precede somatic symptoms of APS and abnormal neuroimaging findings; she presents atypically, as somatic symptoms and abnormal neuroimaging preceded cognitive decline. This case adds to the limited body of neuropsychological data regarding the effects of APS on cognitive functioning, as the pathogenesis of cognitive impairment in APS is unclear and leads to questions regarding differences in, and trajectories of, cognitive deficits in APS.