DOCSLIB.ORG

The Effects of Red Blood Cells on Coagulation: a Thromboelastographic Study

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
The Effects of Red Blood Cells on Coagulation: a Thromboelastographic Study Anesth Pain Med 2009; 4: 133～137 ￭실험연구￭ The effects of red blood cells on coagulation: a thromboelastographic study Department of Anesthesiology and Pain Medicine, Sungkunkwan University School of Medicine, *The Catholic University of Korea College of Medicine, Seoul, Korea Sangmin Maria Lee, M.D., Joo Yeon Lee, M.D., Daemyoung Jeong, M.D., and Keon Hee Ryu, M.D.* Background: There are reports suggesting the effect of red blood platelet-rich plasma (PRP).9) In patients with sickle cell disease, cells (RBCs) on blood coagulation. The effects of red blood cells the change in RBC membrane that occurs in deoxygenated (RBCs) on coagulation were investigated in vitro while maintaining sickle RBCs was shown to release platelet factor 3, and, sub- other coagulation elements constant. Methods: Twenty-five healthy male volunteers were enrolled. sequently, to activate platelets to cause vasoocclusive crisis in Citrated fresh whole blood was drawn from each subjects and hypoxic condition.10) The RBC membrane normally has two processed into washed RBCs and platelet-rich plasma (PRP). To aminophospholipids (phosphatidyl serine and phosphatidyl etha- make six different hematocrit groups with each blood, PRP was mixed with the same volume of serially diluted washed RBCs. nolamine) in inner leaflet of the membrane bilayer, and they Reaction time, coagulation time, clot formation rate, and maximum are exposed to outer membrane leaflet of deoxygenated and ir- amplitude were measured using recalcified TEG. reversibly sickled RBCs and senescent normal cells.8,11) Results: The mean ± SD of six different hematocrit was 38.0 ± Phosphatidyl serine provides a catalytic surface for coagulation 2.3% (group 1), 28.9 ± 2.2% (group 2), 21.3 ± 1.9% (group 3), 12) 13.8% ± 1.6% (group 4), 7.1 ± 1.0% (group 5), and 0 ± 0% (group factors and thus can exhibit the procoagulant activity. Others, 6). The platelet count ranged from 141,000 to 292,000/mm3. however, proposed that hemodilution may increase blood Maximum amplitude (r = −0.4213, P ＜ 0.001) and alpha angle coagulability.13) Tocantins et al14) demonstrated hypercoagulable (r = −0.216, P ＜ 0.05) showed statistically significant negative changes after hemodilution of whole blood up to 40% with linear relationship with hematocrit. Conclusions: A gradual reduction in hematocrit was associated crystalloids. Additionally, hemodilution of blood up to 20% with a shortened coagulation time, no changes in reaction time. This with either crystalloid or colloid improved coagulation profile study results suggest that a gradual reduction in the RBC mass in an in vivo study.15) The precise mechanism of the effects of in vitro accelerates coagulation and forms stronger fibrin strands. hemodilution is unclear, but a relative decrease in antithrombin (Anesth Pain Med 2009; 4: 133∼137) concentration was speculated to be the cause, and the proper- Key Words: coagulation, red blood cell, thromboelastography. ties of diluent itself do not appear to play an important role. This discrepancy may be stemming from the fact that in INTRODUCTION most studies the effects of RBCs on coagulation have been in- vestigated by comparing a limited number of blood test results, A number of reports suggested the red blood cells (RBCs) although homeostasis of coagulation is achieved by an appro- 1-8) affect blood coagulation via various mechanisms. The pro- priate balance between procoagulants and anticoagulants with coagulant activity of RBCs was shown by a shortened onset interactions of endothelium, blood cellular components (platelets time of coagulation in whole blood of patients suffering from and RBCs), and coagulation proteins in plasma. For example, deep vein thrombosis or preeclampsia, compared with that of the role of RBCs in uremia and in severe anemia was tested using bleeding time and/or platelet adhesiveness.16,17) There was 논문접수일：2009년 3월 12일 a negative correlation between the log value of bleeding time 책임저자：이상민, 서울시 강남구 일원동 50번지 and the hematocrit in uremic patients, and transfusion of RBCs 삼성서울병원 마취통증의학과 우편번호: 135-230 increased the platelet adhesiveness and returned the bleeding Tel: 02-3410-0319, Fax: 02-3410-0369 time to normal in spite of a reduction of the total platelet E-mail: [email protected] count by 20%. 133 134 Anesth Pain Med Vol. 4, No. 2, 2009 Thromboelastography (TEG) which measures the dynamic and calcium chloride (0.2 M, 0.03 ml, Haemoscope corpo- viscoelasticity during whole blood clotting process has been ration) was added for recalcification. The blood and calcium widely used in investigational and clinical field,1,3,4,18) and ap- chloride were mixed by moving the TEG pin up and down pears to have advantages over other techniques in assessing five times, and TEG was maintained at 37oC. Four drops of blood coagulability. In this technique, coagulation is activated mineral oil was added to the surface of the blood to prevent when the blood contacts with inner surface of cup of TEG evaporation. TEG recording began 4 min after recalcification, rather than vascular endothelium. Several TEG variables have and measured variables were reaction time (r, min), coagulation been used to elucidate the blood clotting process. Briefly, the time (k, min), clot formation rate (α, o ), and maximum ampli- reaction time (r) is the time taken to form the initial clot by tude (MA, mm). activation of coagulation factors together with interaction with Data were analyzed using a statistical package (SPSS 7.5 for ionized calcium and platelets. Coagulation time (k) is the time windows; SPSS, Chicago, IL). Analysis of variance of TEG taken to reach an amplitude of 20 mm and is considered the variables was performed to test the dilutional effect on function of coagulation factors and platelets. The clot formation coagulation. For comparison of groups, analysis of variance rate (α angle) represents the rate of clot formation and is the was performed based on ranks followed by Dunnetts’ method. function of fibrinogen and platelets. The maximum amplitude The relationship between hematocrit and each of four TEG (MA) mainly depends on the quantitative and qualitative func- variables were obtained by regression analysis calculating tion of platelets. correlation. All data are presented as means ± SD, and P ＜ The specific objective of the study was to investigate the 0.05 was considered significant. hypothesis that blood coagulability (the rate of clot formation and/or the strength of clot formed) is affected by the amount RESULTS of RBCs while other coagulation elements (coagulation factors and platelets) remain relatively constant. One subject with severe thrombocytopenia (platelet count, 26,000/mm3) was excluded from analysis. Average age of the − MATERIALS AND METHODS 24 subjects was 33 ± 7 years (range, 21 45 years), platelet count was 222,000 ± 40,000/mm3 (range, 141,000 − 292,000/ After the approval of the Institutional Research Review mm3) and hematocrit was 38 ± 2 % (range, 33.5−44%). The Board and obtaining written informed consent, 25 healthy vol- RBC dilutional effects on coagulation of 24 patients are shown unteers were included in this study. They were adult male in Fig. 1. Reaction time and coagulation time remained un- subjects with no history of smoking, coagulation disorder, ane- changed at different levels of RBC concentration, but clot for- mia, liver disease, and any recent medications within two mation rate (α) and maximum amplitude (MA) decreased weeks. Aseptic venopuncture was made in the antecubital vein using a 20-guage venous catheter. The first 2 ml of blood was discarded to avoid tissue contamination, and 9 ml of blood was collected in a test tube containing sodium citrate solution (1 ml, 3.8%). The citrated whole blood sample was centrifused immediately at 300 g for two minutes to separate the PRP from the packed RBCs (pRBCs). Separated pRBCs were wash- ed three times by adding the same volume of normal saline, centrifusing it at 3,000 g for two and half minutes, and re- moving supernatant at each time. The washed pRBCs were divided into six alliquotes (0.3 ml each), and normal saline was added to make pRBCs and normal saline in a ratio of 5：0, 4：1, 3：2, 2：3, 1：4, and 0：5. Each reconstituted pRBC samples (0.3 ml) were mixed with autologous PRP (0.3 Fig. 1. The relationship between hematocrit and four TEG variables. ml) to maintain the same amount of autologous PRP. Each ci- Maximum amplitude (MA, r=−0.4213, P ＜ 0.001) and alpha angle (r= trated blood specimen (0.33 ml) was placed into the TEG cup, −0.216, P ＜ 0.05) showed negative linear relationship with hematocrit. Sangmin Maria Lee, et al：RBC effects on coagulation 135 steadily with hemoconcentration (P ＜ 0.05). Hematologic and respectively), indicating stronger fibrin strands. TEG variables of 24 subjects at six different dilutions are shown in Table 1. Hematocrit decreased gradually by the study DISCUSSION design as blood was diluted, while platelet count was similar in all six dilutions. Except for blood specimens containing no In this study, a gradual hemodilution increased the rate of RBCs, hemodilution decreased the reaction time (at dilution clot formation and the strength of clot formed, when the 1:4) and coagulation time (at all dilutions) and increased the amount of platelets and coagulation factors remained unchang- clot formation rate (at all dilutions) and maximum amplitude ed. However, the procoagulant activity of hemodilution was not (at dilutions 3:2, 2:3, and 1:4), suggesting increased coagula- observed in platelets and PRP without RBCs. bility with hemodilution compared with the blood with no This observation is different from results of other studies dilution. that proposed the procoagulant effects of RBCs, and several Because of the difference in the baseline hematocrit of all mechanisms are proposed. First, in the biochemical mechanism, subjects, the 144 data points were divided into six groups RBCs appear to stimulate platelet activation and aggregation.
Load more

Recommended publications
  • Recombinant Factors for Hemostasis
    University of Nebraska - Lincoln DigitalCommons@University of Nebraska - Lincoln Chemical & Biomolecular Engineering Theses, Chemical and Biomolecular Engineering, Dissertations, & Student Research Department of Summer 2010 Recombinant Factors for Hemostasis Jennifer Calcaterra University of Nebraska at Lincoln, [email protected] Follow this and additional works at: https://digitalcommons.unl.edu/chemengtheses Part of the Biochemical and Biomolecular Engineering Commons Calcaterra, Jennifer, "Recombinant Factors for Hemostasis" (2010). Chemical & Biomolecular Engineering Theses, Dissertations, & Student Research. 5. https://digitalcommons.unl.edu/chemengtheses/5 This Article is brought to you for free and open access by the Chemical and Biomolecular Engineering, Department of at DigitalCommons@University of Nebraska - Lincoln. It has been accepted for inclusion in Chemical & Biomolecular Engineering Theses, Dissertations, & Student Research by an authorized administrator of DigitalCommons@University of Nebraska - Lincoln. Recombinant Factors for Hemostasis by Jennifer Calcaterra A DISSERTATION Presented to the Faculty of The Graduate College at the University of Nebraska In Partial Fulfillment of Requirements For the Degree of Doctor of Philosophy Major: Interdepartmental Area of Engineering (Chemical & Biomolecular Engineering) Under the Supervision of Professor William H. Velander Lincoln, Nebraska August, 2010 Recombinant Factors for Hemostasis Jennifer Calcaterra, Ph.D. University of Nebraska, 2010 Adviser: William H. Velander Trauma deaths are a result of hemorrhage in 37% of civilians and 47% military personnel and are the primary cause of death for individuals under 44 years of age. Current techniques used to treat hemorrhage are inadequate for severe bleeding. Preliminary research indicates that fibrin sealants (FS) alone or in combination with a dressing may be more effective; however, it has not been economically feasible for widespread use because of prohibitive costs related to procuring the proteins.
    [Show full text]
  • Section 8: Hematology CHAPTER 47: ANEMIA
    Section 8: Hematology CHAPTER 47: ANEMIA Q.1. A 56-year-old man presents with symptoms of severe dyspnea on exertion and fatigue. His laboratory values are as follows: Hemoglobin 6.0 g/dL (normal: 12–15 g/dL) Hematocrit 18% (normal: 36%–46%) RBC count 2 million/L (normal: 4–5.2 million/L) Reticulocyte count 3% (normal: 0.5%–1.5%) Which of the following caused this man’s anemia? A. Decreased red cell production B. Increased red cell destruction C. Acute blood loss (hemorrhage) D. There is insufficient information to make a determination Answer: A. This man presents with anemia and an elevated reticulocyte count which seems to suggest a hemolytic process. His reticulocyte count, however, has not been corrected for the degree of anemia he displays. This can be done by calculating his corrected reticulocyte count ([3% × (18%/45%)] = 1.2%), which is less than 2 and thus suggestive of a hypoproliferative process (decreased red cell production). Q.2. A 25-year-old man with pancytopenia undergoes bone marrow aspiration and biopsy, which reveals profound hypocellularity and virtual absence of hematopoietic cells. Cytogenetic analysis of the bone marrow does not reveal any abnormalities. Despite red blood cell and platelet transfusions, his pancytopenia worsens. Histocompatibility testing of his only sister fails to reveal a match. What would be the most appropriate course of therapy? A. Antithymocyte globulin, cyclosporine, and prednisone B. Prednisone alone C. Supportive therapy with chronic blood and platelet transfusions only D. Methotrexate and prednisone E. Bone marrow transplant Answer: A. Although supportive care with transfusions is necessary for treating this patient with aplastic anemia, most cases are not self-limited.
    [Show full text]
  • Common Laboratory Values
    AmericAn AcAdemy of PediAtric dentistry Reference Manual 2006-2007 Resource Section 251 Common LaboratoryCommon Values Laboratory Values CBC Test Normal value Function Significance Hemoglobin 12-18 g/100 mL Measures oxygen carrying capacity of blood Low: hemorrhage, anemia High: polycythemia Hematocrit 35%-50% Measures relative volume of cells and plasma in Low: hemorrhage, anemia blood High: polycythemia, dehydration Red blood cell 4-6 million/mm3 Measures oxygen-carrying capacity of blood Low: hemorrhage, anemia High: polycythemia, heart disease, pulmonary disease White blood cell Measures host defense against inflammatory agents Low: aplastic anemia, drug toxicity, Infant 8,000-15,000/mm3 specific infections 4-7 y 6,000-15,000/mm3 High: inflammation, trauma, 8-18 y 4,500-13,500/mm3 toxicity, leukemia Differential Count Test Normal value Significance Neutrophils 54%-62% Increase in bacterial infections, hemorrhage, diabetic acidosis Lymphocytes 25%-30% Viral and bacterial infection, acute and chronic lymphocytic leukemia, antigen reaction Eosinophils 1%-3% Increase in parasitic and allergic conditions, blood dyscrasias, pernicious anemia Basophils 1% Increase in types of blood dyscrasias Monocytes 0%-9% Hodgkin’s disease, lipid storage disease, recovery from severe infections, monocytic leukemia Absolute Neutrophil Count (ANC) Calculation Normal value Significance (% Polymorphonuclear Leukocytes + % Bands)×Total White Cell Count >1500 <1000 Patient at increased risk for 100 infection; defer elective dental care Bleeding Screen Test
    [Show full text]
  • Prolonged Partial Thromboplastin Time Without Bleeding History; Fletcher Factor Deficiency
    Prolonged Partial Thromboplastin Time Without Bleeding History; Fletcher Factor Deficiency Celalettin ÜSTÜN*, Anand JILLELLA*, Linda HENDRIKS*, Mary JONAH**, Ferdane KUTLAR*, Russell BURGESS*, Abdullah KUTLAR* * Section of Hematology Oncology, Department of Medicine, Medical College of Georgia, ** Department of Pathology, Medical College of Georgia, Augusta, USA ABSTRACT A 67-year-old patient was admitted to the hospital to perform an esophagogastrectomy because a lesion at the lower esophagus was strongly suspicious for cancer. Her medical history and her family his- tory were negative for bleeding tendency or thrombosis. Her activated partial thromboplastin time (aPTT) was prolonged (44 s) whereas her prothrombin time (PT) was normal (11 s) presurgery. Mixing of her plasma with normal plasma corrected her prolonged aPTT (27.9 s). Prolonged incubation shortened the patient’s aPTT (36.3 s). Fletcher factor activity was found to be 50%. The patient underwent an esopha- gogastrectomy without bleeding complications under spinal anesthesia. Fletcher factor deficiency, a ra- re disorder, should be considered in patients who have no history of bleeding tendency with a prolonged aPTT. Surgical interventions are safe in these patients. Key Words: aPTT, Surgery, Fletcher factor, Prekallikrein. Turk J Haematol 2002;19(3): 417-419 Received: 20.06.2001 Accepted: 28.07.2001 INTRODUCTION unt[2]. Hematologists are frequently consulted for preoperative coagulation abnormalities. Preoperative evaluation of hemostasis is cru- cial to assess the risk of per-and peri-operative Prolonged aPTT is not an uncommon abnor- bleeding. The most effective screening method is mality encountered during preoperative evaluati- to obtain a thorough history of bleeding[1]. on. It may indicate the presence of antiphospholi- Preoperative screening tests mostly include acti- pid antibodies or a factor deficiency in the intrinsic vated partial thromboplastin time (aPTT), proth- and/or common pathways of blood coagulation.
    [Show full text]
  • TEG: the Abcs of Implementing Thromboelastography in a Trauma Center
    TEG: The ABCs of Implementing Thromboelastography in a Trauma Center Mary Kay Bader RN, MSN, CCNS, FNCS, FAHA Neuro/Critical Care CNS Mission Hospital Learning Objectives • Implement TEG into a Trauma Center • Describe the normal/abnormal dynamic clotting parameters of Thromboelastography (TEG) and propose treatment using an algorithm • Strategize treatment options involving actual cases of hemorrhage Disclosure Statement • Bader • Board of Directors: Secretary • Neurocritical Care Society • Honorarium • Bard • Integra • Medical Advisory Board • Brain Trauma Foundation and Neuroptics • Scientific Advisory Board • Cerebrotech • Stock options • Neuoptics and Cerebrotech Hemorrhage States • Trauma – Traumatic Brain Injury • Intracranial Hemorrhage – ICH – SAH • GI Bleeding • Liver disease/disorders • OB Hemorrhage • Ruptured vessels Trauma Injury, Hemorrhage, & TBI • Trauma/Injury is the 2nd leading cause of death globally – 40% of mortality associated with injury due to uncontrollable hemorrhage • 1/3 of severely injured trauma patients sustain Trauma Induced coagulopathy (TIC) – Poorly understood mechanisms – Several theories • Coagulopathy of TBI (CTBI) is a component of TIC – Multiple theories contribute to early platelet dysfunction – Correlation between severity of TBI and platelet dysfunction Coagulopathy of TBI (CTBI) • Presence of CTBI ranges 10-97% in ROL due to many factors – Heterogeneity of patients, types of lab tests, timing of tests, and lack of clear defined consensus to define CTBI – Associated with poor outcomes – Blunt
    [Show full text]
  • Hematopoiesis and Hemostasis
    Hematopoiesis and Hemostasis HAP Susan Chabot Hematopoiesis • Blood Cell Formation • Occurs in red bone marrow – Red marrow - found in flat bones and proximal epiphyses of long bones. • Each type of blood cell is produced in response to changing needs of the body. • On average, an ounce of new blood is produced each day with about 100 billion new blood cells/formed elements. Hemocytoblast • Hemo- means blood • Cyto- means cell • -blast means builder • Blood stem cell found in red bone marrow. • Once the precursor cell has committed to become a specific blood type, it cannot be changed. Hemocytoblast Erythropoiesis • Erythrocyte Formation • Because they are anucleated, RBC’s must be regularly replaced. – No info to synthesize proteins, grow or divide. • They begin to fall apart in 100 - 120 days. • Remains of fragmented RBC’s are removed by the spleen and liver. • Entire development , release, and ejection of leftover organelles takes 3-5 days. Normal RBC’s Reticulocytes • The stimulus for RBC production is the amount of OXYGEN in the blood not the NUMBER of RBC’s. • The rate of RBC production is controlled by the hormone ERYTHROPOIETIN. Leuko- and Thrombopoiesis • Leukopoesis = WBC production • Thrombopoesis = platelet production • Controlled by hormones Leukopoesis Thrombopoesis • (CSF) Colony • Thrombopoetin stimulating factor • Little is known • Interleukins about this – Prompts WBC process. production – Boosts other immune processes including inflammation. HEMOSTASIS Hemostasis • Hemo- means blood • -stasis means standing still – Stoppage of bleeding • Fast and localized reaction when a blood vessel breaks. • Involves a series of reactions. • Involves substances normally found in plasma but not activated. • Occurs in 3 main phases Phases of Hemostasis • Step 1: Vascular Spasm – Vasoconstriction, narrowing of blood vessels.
    [Show full text]
  • Notch and TLR Signaling Coordinate Monocyte Cell Fate and Inflammation
    RESEARCH ARTICLE Notch and TLR signaling coordinate monocyte cell fate and inflammation Jaba Gamrekelashvili1,2*, Tamar Kapanadze1,2, Stefan Sablotny1,2, Corina Ratiu3, Khaled Dastagir1,4, Matthias Lochner5,6, Susanne Karbach7,8,9, Philip Wenzel7,8,9, Andre Sitnow1,2, Susanne Fleig1,2, Tim Sparwasser10, Ulrich Kalinke11,12, Bernhard Holzmann13, Hermann Haller1, Florian P Limbourg1,2* 1Vascular Medicine Research, Hannover Medical School, Hannover, Germany; 2Department of Nephrology and Hypertension, Hannover Medical School, Hannover, Germany; 3Institut fu¨ r Kardiovaskula¨ re Physiologie, Fachbereich Medizin der Goethe-Universita¨ t Frankfurt am Main, Frankfurt am Main, Germany; 4Department of Plastic, Aesthetic, Hand and Reconstructive Surgery, Hannover Medical School, Hannover, Germany; 5Institute of Medical Microbiology and Hospital Epidemiology, Hannover Medical School, Hannover, Germany; 6Mucosal Infection Immunology, TWINCORE, Centre for Experimental and Clinical Infection Research, Hannover, Germany; 7Center for Cardiology, Cardiology I, University Medical Center of the Johannes Gutenberg-University Mainz, Mainz, Germany; 8Center for Thrombosis and Hemostasis, University Medical Center of the Johannes Gutenberg-University Mainz, Mainz, Germany; 9German Center for Cardiovascular Research (DZHK), Partner Site Rhine Main, Mainz, Germany; 10Department of Medical Microbiology and Hygiene, Medical Center of the Johannes Gutenberg- University of Mainz, Mainz, Germany; 11Institute for Experimental Infection Research, TWINCORE, Centre for
    [Show full text]
  • Human Alveolar Macrophages Synthesize Factor VII in Vitro
    Human alveolar macrophages synthesize factor VII in vitro. Possible role in interstitial lung disease. H A Chapman Jr, … , O L Stone, D S Fair J Clin Invest. 1985;75(6):2030-2037. https://doi.org/10.1172/JCI111922. Research Article Both fibrin and tissue macrophages are prominent in the histopathology of chronic inflammatory pulmonary disease. We therefore examined the procoagulant activity of freshly lavaged human alveolar macrophages in vitro. Intact macrophages (5 X 10(5) cells) from 13 healthy volunteers promoted clotting of whole plasma in a mean of 65 s. Macrophage procoagulant activity was at least partially independent of exogenous Factor VII as judged by a mean clotting time of 99 s in Factor VII-deficient plasma and by neutralization of procoagulant activity by an antibody to Factor VII. Immunoprecipitation of extracts of macrophages metabolically labeled with [35S]methionine by Factor VII antibody and analyzed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis revealed a labeled protein consistent in size with the known molecular weight of blood Factor VII, 48,000. The addition of 50 micrograms of unlabeled, purified Factor VII blocked recovery of the 48,000-mol wt protein. In addition, supernatants of cultured macrophages from six normal volunteers had Factor X-activating activity that was suppressed an average of 71% after culture in the presence of 50 microM coumadin or entirely by the Factor VII antibody indicating that Factor VII synthesized by the cell was biologically active. Endotoxin in vitro induced increases in cellular tissue factor but had no consistent effect on macrophage Factor VII activity. We also examined the tissue factor and Factor VII activities […] Find the latest version: https://jci.me/111922/pdf Human Alveolar Macrophages Synthesize Factor VII In Vitro Possible Role in Interstitial Lung Disease Harold A.
    [Show full text]
  • Ferric Sulfate Hemostasis: Effect on Osseous Wound Healing, II, with Curettage and Irrigation
    0099-2399/93/1904-0174/$03.00/0 JOURNAL OF ENDODONTICS Printed in U.S.A. Copyright © 1993 by The American Association of Endodontists VOL. 19, No. 4, APRIL 1993 Ferric Sulfate Hemostasis: Effect on Osseous Wound Healing, II, With Curettage and Irrigation Billie G. Jeansonne, DDS, PhD, William S. Boggs, DDS, MS, and Ronald R. Lemon, DMD Hemorrhage control is often a problem for the clini- MATERIALS AND METHODS cian during osseous surgery. Ferric sulfate is an effective hemostatic agent, but with prolonged ap- The experiments were performed in 12 New Zealand White plication to an osseous defect can cause persistent rabbits (2.3 to 3.7 kg). Anesthesia was obtained by the intra- inflammation and delayed healing. The purpose of muscular injection of a combination of xylazine (7 mg/kg), ketamine (30 mg/kg), and atropine (0.3 mg/kg). On both this investigation was to evaluate the effectiveness sides of the mandible, an incision was made along the alveolar of ferric sulfate as a hemostatic agent and to deter- crest in the naturally edentulous space between the incisor mine its effect on healing after thorough curettage and premolar teeth. An envelope flap was reflected to expose and irrigation from osseous surgical wounds. Stand- the alveolar cortical bone. An osseous defect (3 mm in di- ard size osseous defects were created bilaterally in ameter, 2 mm into cancellous bone) was created on each side the mandibles of rabbits. Ferric sulfate was placed with a #8 round bur. All defects were curetted and irrigated in one defect until hemostasis was obtained; the with saline.
    [Show full text]
  • Effect of Thromboelastography (TEG®) and Rotational Thromboelastometry (ROTEM®) on Diagnosis of Coagulopathy, Transfusion Guid
    Da Luz et al. Critical Care 2014, 18:518 http://ccforum.com/content/18/5/518 RESEARCH Open Access Effect of thromboelastography (TEG®) and rotational thromboelastometry (ROTEM®) on diagnosis of coagulopathy, transfusion guidance and mortality in trauma: descriptive systematic review Luis Teodoro Da Luz1, Bartolomeu Nascimento2, Ajith Kumar Shankarakutty3, Sandro Rizoli4 and Neill KJ Adhikari1* Abstract Introduction: The understanding of coagulopathies in trauma has increased interest in thromboelastography (TEG®) and thromboelastometry (ROTEM®), which promptly evaluate the entire clotting process and may guide blood product therapy. Our objective was to review the evidence for their role in diagnosing early coagulopathies, guiding blood transfusion, and reducing mortality in injured patients. Methods: We considered observational studies and randomized controlled trials (MEDLINE, EMBASE, and Cochrane databases) to February 2014 that examined TEG®/ROTEM® in adult trauma patients. We extracted data on demographics, diagnosis of early coagulopathies, blood transfusion, and mortality. We assessed methodologic quality by using the Newcastle-Ottawa scale (NOS) for observational studies and QUADAS-2 tool for diagnostic accuracy studies. Results: Fifty-five studies (12,489 patients) met inclusion criteria, including 38 prospective cohort studies, 15 retrospective cohort studies, two before-after studies, and no randomized trials. Methodologic quality was moderate (mean NOS score, 6.07; standard deviation, 0.49). With QUADAS-2, only three of 47 studies (6.4%) had a low risk of bias in all domains (patient selection, index test, reference standard and flow and timing); 37 of 47 studies (78.8%) had low concerns regarding applicability. Studies investigated TEG®/ROTEM® for diagnosis of early coagulopathies (n = 40) or for associations with blood-product transfusion (n =25)ormortality(n =24).Most(n = 52) were single-center studies.
    [Show full text]
  • Role of Thromboelastography As an Early Predictor of Disseminated Intravascular Coagulation in Patients with Septic Shock
    Journal of Clinical Medicine Article Role of Thromboelastography as an Early Predictor of Disseminated Intravascular Coagulation in Patients with Septic Shock Sang Min Kim 1, Sang-Il Kim 2, Gina Yu 3, June-Sung Kim 1, Seok In Hong 1 , Bora Chae 1 , Yo Sep Shin 1 , Youn Jung Kim 1, Seongsoo Jang 4 and Won Young Kim 1,* 1 Department of Emergency Medicine, University of Ulsan College of Medicine, Asan Medical Center, Seoul 05505, Korea; [email protected] (S.M.K.); [email protected] (J.-S.K.); finefi[email protected] (S.I.H.); [email protected] (B.C.); [email protected] (Y.S.S.); [email protected] (Y.J.K.) 2 Department of Emergency Medicine, Soonchunhyang University Seoul Hospital, Seoul 04401, Korea; [email protected] 3 Department of Emergency Medicine, University of Yonsei College of Medicine, Seoul 06273, Korea; fl[email protected] 4 Department of Laboratory Medicine, University of Ulsan College of Medicine, Asan Medical Center, Seoul 05505, Korea; [email protected] * Correspondence: [email protected]; Tel.: +82-2-3010-3350 Received: 12 November 2020; Accepted: 27 November 2020; Published: 29 November 2020 Abstract: (1) Background: The currently proposed criteria for diagnosing overt disseminated intravascular coagulation (DIC) are not suitable for early detection of DIC. Thromboelastography (TEG) rapidly provides a comprehensive assessment of the entire coagulation process and is helpful as a guide for correcting consumptive coagulopathy in sepsis-induced DIC. This study aimed to investigate the role of TEG in the prediction of DIC in patients with septic shock. (2) Methods: TEG was conducted prospectively in 1294 patients with septic shock at the emergency department (ED) between January 2016 and December 2019.
    [Show full text]
  • Pulmonary Megakaryocytes in Coronavirus Disease 2019 (COVID-19): Roles in Thrombi and Fibrosis
    Published online: 2020-09-03 Commentary 831 Pulmonary Megakaryocytes in Coronavirus Disease 2019 (COVID-19): Roles in Thrombi and Fibrosis Jecko Thachil, MD, FRCP1 Ton Lisman, PhD2 1 Department of Haematology, Manchester Royal Infirmary, Address for correspondence Jecko Thachil, MD, FRCP, Department of Manchester, United Kingdom Haematology, Manchester Royal Infirmary, Oxford Road, Manchester 2 Surgical Research Laboratory and Section of Hepatobiliary Surgery M13 9WL, United Kingdom (e-mail: [email protected]). and Liver Transplantation, Department of Surgery, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands Semin Thromb Hemost 2020;46:831–834. Coronavirus disease 2019 (COVID-19) has already claimed karyocyte presence in the lungs assert that lung megakaryo- many lives and continues to do so in different parts of the cytes just represent a gravity phenomenon noted at autopsy. world. Autopsy reports of patients who succumbed to this viral The mostelegant (and latest)study for validating thelungorigin infection have been published despite concerns about health of platelets comes from Lefrançais et al who directly imaged the care professional safety. One of the unusual findings in COVID- lung microcirculation in mice to provide definite proof for the 19 lung autopsy reports is the increase in pulmonary mega- existence of lung megakaryocytes.8 They also proved that karyocytes.1,2 Although the presence of megakaryocytes in the approximately halfof the total number of platelets or 10 million lungs is a well-established concept in the medical literature, it platelets per hour would be produced by these cells.8 is still not widely accepted in the clinical fraternity.
    [Show full text]