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      Massive Transfusion of 5 U Packed Redblood Cells, 3 U Fresh Frozen Plasma, and 160 cc of Platelets in a 14-Month-Old Patient

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          Abstract

          Patient: Female, 1

          Final Diagnosis: Parietooccipital brain tumor

          Symptoms: Drowsiness • failure to thrive • irritability • seizure-like activity

          Medication: —

          Clinical Procedure: Massive transfusion during tumor resection

          Specialty: Anesthesiology

          Objective:

          Management of emergency care

          Background:

          We present a case in which extremely rapid massive transfusion was successfully used to combat severe acute bleeding during a parietooccipital tumor resection in a 14-month-old patient.

          Case Report:

          An 8-kg patient was found to have a 4×5×5-cm parietooccipital tumor on computed tomography scan, for which resection was urgently planned. Sudden acute bleeding was encountered, which was communicated to the anesthesia team. Transfusion was initiated and a total of 5 units of packed red blood cells, 3 units of fresh frozen plasma, 160 ml of platelets, 200 ml of albumin, and 500 ml of 0.9% normal saline were transfused during a 4-h period. We administered 4 g of mannitol and 0.8 mg of furosemide to deal with anticipated fluid overload. The patient was sent to the intensive care unit and extubated the next day. No clinically significant hemostatic or fluid overload complications were noted after the treatment.

          Conclusions:

          Massive transfusion (MT) was found to be safe and effective in this case. Most of what we know about pediatric MT is an extrapolation of data from adult studies. Although practical, it might not be ideal due to the differences in the physiology and incomplete development of hemostatic mechanisms in children, especially those younger than 12 months. Studies evaluating the use of pediatric MT protocols have not shown a significant advantage over transfusion per clinician discretion.

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          Most cited references10

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          Acute traumatic coagulopathy: initiated by hypoperfusion: modulated through the protein C pathway?

          Coagulopathy following major trauma is conventionally attributed to activation and consumption of coagulation factors. Recent studies have identified an acute coagulopathy present on admission that is independent of injury severity. We hypothesized that early coagulopathy is due to tissue hypoperfusion, and investigated derangements in coagulation associated with this. This was a prospective cohort study of major trauma patients admitted to a single trauma center. Blood was drawn within 10 minutes of arrival for analysis of partial thromboplastin and prothrombin times, prothrombin fragments 1+2, fibrinogen, thrombomodulin, protein C, plasminogen activator inhibitor-1, and D-dimers. Base deficit (BD) was used as a measure of tissue hypoperfusion. A total of 208 patients were enrolled. Patients without tissue hypoperfusion were not coagulopathic, irrespective of the amount of thrombin generated. Prolongation of the partial thromboplastin and prothrombin times was only observed with an increased BD. An increasing BD was associated with high soluble thrombomodulin and low protein C levels. Low protein C levels were associated with prolongation of the partial thromboplastin and prothrombin times and hyperfibrinolysis with low levels of plasminogen activator inhibitor-1 and high D-dimer levels. High thrombomodulin and low protein C levels were significantly associated with increased mortality, blood transfusion requirements, acute renal injury, and reduced ventilator-free days. Early traumatic coagulopathy occurs only in the presence of tissue hypoperfusion and appears to occur without significant consumption of coagulation factors. Alterations in the thrombomodulin-protein C pathway are consistent with activated protein C activation and systemic anticoagulation. Admission plasma thrombomodulin and protein C levels are predictive of clinical outcomes following major trauma.
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            Development of the human coagulation system in the full-term infant.

            The investigation of many hemostatic defects in the newborn is limited by the lack of normal reference values. This study was designed to determine the postnatal development of the human coagulation system in the healthy full-term infant. Consecutive mothers of healthy full-term infants born at St Joseph's Hospital in the city of Hamilton were approached for consent. One hundred eighteen full-term infants (37 to 42 weeks' gestational age) were entered into the study. Demographic information and a 2-mL blood sample were obtained in the postnatal period on days 1, 5, 30, 90, and 180. Between 40 and 79 full-term infants were studied on each day for each of the coagulation tests. Plasma was fractionated and stored at -70 degrees C for batch assaying of the following tests: prothrombin time, activated partial thromboplastin time, thrombin clotting time, and factor assays (biologic): fibrinogen, II, V, VII, VIII, IX, X, XI, XII, and high-molecular weight kininogen. Factor XIII subunits A and S, von Willebrand factor, and the inhibitors antithrombin III, alpha 2-antiplasmin, alpha 2-macroglobulin, alpha 1-antitrypsin, C1 esterase inhibitor, protein C, and protein S were measured immunologically. Plasminogen, prekallikrein, and heparin cofactor II were measured by using chromogenic substrates. The large number of infants studied at each time point allowed us to determine the following: the range of normal for each test at five time points in the postnatal period; that coagulation tests vary with the postnatal age of the infant; that different coagulation factors show different postnatal patterns of maturation; and that near-adult values are achieved for most components by 6 months of life. In summary, this large cohort of infants studied consecutively in the postnatal period allowed us to determine the normal development of the human coagulation system in the full-term infant.
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              Complications of massive transfusion.

              Massive transfusion (MT) is a lifesaving treatment of hemorrhagic shock, but can be associated with significant complications. The lethal triad of acidosis, hypothermia, and coagulopathy associated with MT is associated with a high mortality rate. Other complications include hypothermia, acid/base derangements, electrolyte abnormalities (hypocalcemia, hypomagnesemia, hypokalemia, hyperkalemia), citrate toxicity, and transfusion-associated acute lung injury. Blood transfusion in trauma, surgery, and critical care has been identified as an independent predictor of multiple organ failure, systemic inflammatory response syndrome, increased infection, and increased mortality in multiple studies. Once definitive control of hemorrhage has been established, a restrictive approach to blood transfusion should be implemented to minimize further complications.
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                Author and article information

                Journal
                Am J Case Rep
                Am J Case Rep
                amjcaserep
                The American Journal of Case Reports
                International Scientific Literature, Inc.
                1941-5923
                2016
                01 April 2016
                : 17
                : 211-213
                Affiliations
                [1 ]Department of Anesthesiology, University of Texas Health Science Center at Houston, Houston, TX, U.S.A.
                [2 ]Department of Anesthesiology, University of Texas Health Science Center at Houston, Houston, TX, U.S.A.
                Author notes

                Authors’ Contribution:

                [A]

                Study Design

                [B]

                Data Collection

                [C]

                Statistical Analysis

                [D]

                Data Interpretation

                [E]

                Manuscript Preparation

                [F]

                Literature Search

                [G]

                Funds Collection

                Conflict of interest: None declared

                Corresponding Author: Tanaya Sparkle, e-mail: tanaya.sparkle@ 123456uth.tmc.edu
                Article
                896820
                10.12659/AJCR.896820
                4824341
                27032708
                3d65ebba-6e84-41e8-972a-b7cfbaf5ea00
                © Am J Case Rep, 2016

                This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 3.0 Unported License

                History
                : 12 November 2015
                : 03 January 2016
                Categories
                Articles

                anesthesia,anesthesiology,blood loss, surgical,blood transfusion,hospitals, pediatric,pediatrics

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