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• W1694976382 abstract "Currently, there is increasing interest on the optimal use of blood components for two mean reasons: first of all, due to potential complications in recipients, and secondly, diminishing blood supplies are an increasing problem [1]. Clinically significant haemorrhage is a major cause of morbidity and mortality in extremely preterm infants and is a rare event in terms of neonates, older infants and adolescents. Therapeutic options, such as fresh-frozen plasma (FFP), cryoprecipitate, platelet concentrates and other specific plasma derived or recombinant protein products are used to treat bleeding patients (Table 1). FFP is available in all hospitals and is most often used to stop or prevent bleeding. Transfusions of large amounts of blood products have the risk of transfusion-related reactions and disease transmission. In hospital settings, most of the FFP are used for the newborns and small infants (Fig. 1), and most of FFP transfusions are used for surgical procedures, of which cardiac surgery is the most common indication [2]. Age of the FFP recipients in Institute for Mother and Child Health Care of Serbia (n = 148 patients; 1 January to 31 December 2010). Fresh-frozen plasma is blood product produced by centrifugation of donated whole blood or by plasmapheresis, frozen within 8 h from collection, stored in frozen state and used after thawing. FFP contains adequate levels of all soluble coagulation factors (≥70% fibrinogen, factors VIII, II, VII, V, IX, X, XI, XII and XIII) as well as albumin, immunoglobulin’s and naturally occurring anticoagulants (protein C, protein S, antithrombin, plasminogen) [3]. FFP should be of the same ABO group as the patient and the therapeutic dose is usually 10–20 ml/kg. FFP can be standard or kept in quarantaine and released after retesting or pathogen inactivated. Standard FFP is prepared from whole blood donation. It carries a small residual risk of transmitting transfusion transmissible diseases (TTD) [4]. Use of pathogen-inactivated plasma in paediatric patients has been recommended [5,6]. Current methods for pathogen inactivation of plasma involve processes using solvent detergent (SD), methylene blue (MB), amotosalen and riboflavin as additives [7–11]. All methods have some effect on coagulation parameters, resulting in reduction in protein values with the per cent retention of FVIII activity in the range of 67–78% [7]. Limited data on the use of pathogen-inactivated plasma in paediatric patients show no untoward effects following transfusion. However, in many countries, pathogen-inactivated plasma is unavailable. Therefore, many general safety procedures should be implemented in blood screening, such as critical donor selection (no first time donor, male donor), a donor self-exclusion opportunity, the storage of quarantined plasma and to implement screening assay with maximum analytical sensitivity and analytical specificity to reduce the diagnostic window period as much as possible. In addition, adult dose FFP can be divided into small aliquots, about 40–60 ml and used for several transfusions for one neonate or infant as a means to decrease donor expositure [12]. The use FFP is not without hazards (Table 2), and side-effects are seen in relevant number recipients [13]. Reactions to FFP and platelet concentrate are approximately 5–6 times more frequent as after red blood cell (RBC) products. Per blood product transfused a severe transfusion reaction occurred in 0.013% in adults and 0.018% in children less than 18 years old. A three times higher incidence of 0.037% in newborns and infants <12 months was observed [14]. Risk on TTD has decreased because of sophisticated blood screening and pathogen inactivation processes. But, risk from TTD is still present in under-resourced countries, and an restrictive transfusion policy could improve safety of patents [15]. One must always realize that an infected unit of FFP may contain a greater viral load than RBC and may thus run a greater risk of transmitting blood-borne viruses, but also of other plasma-mediated adverse effects. Besides TTD, most important side-effect of FFP is transfusion-related acute lung injury (TRALI). TRALI is a serious, life-threatening pulmonary transfusion reaction characterized by non-cardiogenic lung oedema, hypoxemia and respiratory distress in temporal associated with blood transfusion, most often FFP. The incidence per unit transfused has been calculated as 1:58 000–1:88 000 for FFP [16]. When administering large volumes of FFP it is important to take into account that there is more citrate in FFP than there is in citrated RBCs. If the metabolic capacity of the liver to metabolize the citrate is exceeded citrate toxicity can occur leading to hypocalcaemia, hypomagnesaemia and a metabolic alkalosis. This has many implications of particular importance in newborn infants, because neonate is particularly poor at metabolizing citrate. Hypocalcaemia can contribute to a coagulopathy itself. Indeed, immunological complications including allergic reaction as a haemolytic transfusion reaction in a case transfusion of ABO incompatible plasma can occur [17,18]. Currently, FFP is used for treatment excessive bleeding associated with abnormal coagulation or to prevent bleeding in this clinical setting (Table 3). Accepted indications for use of FFP in paediatric patients is treatment of bleeding in the presence of PT (INR) and aPTT (R) greater than 1.5 or requiring invasive surgery in case of multiple factor deficiency or specific factor deficiency <35% of normal for which a factor concentrate is unavailable. FFP can be used as replacement therapy for plasma exchange in thrombotic thrombocytopenic purpura (TTP), protein C or S deficiency, preparation of reconstituted whole blood for extracorporeal membrane oxygenation (ECMO), cardiopulmonary bypass, (CPB), exchange transfusion (ESTR) and for children with marked coagulopathy at risk for intracranial or other organ haemorrhage in an intensive care unit [19–25]. About 6–8 of 1000 newborns have congenital heart disease often requiring surgery [26]. Severe bleeding is a major complication in postoperative paediatric surgery patients with an incidence of significant haemorrhage as high as 40%. Mediastinal blood loss as high as 15–110 ml/kg has been reported [27]. Hypofibrinogenemia and inadequate heparin reversal are two important factors contributing to perioperative bleeding after paediatric CPB surgery. FFP, platelets, cryoprecipitate, RBCs and antifibrinolytic drugs are administered to correct the coagulopathy and stop bleeding. Bleeding and blood product use are associated with considerable morbidity, mortality and cost [28,29]. Re-exploration of the chest in neonates and infants with severe bleeding reveals a surgically manageable source of bleeding in less than 50% cases [30]. Children with excessive bleeding exhibit hypofibrinogenemia at the end of CPB and have to be treated with cryoprecipitate. Severe hypofibrinogenemia exacerbate bleeding tendency because fibrinogen is vital for clot formation. Bleeding risk will likely be increased with concurrent thrombocytopenia, which is a common finding in these patients. Platelet transfusion in these settings is appropriate. The contribution of fibrinolysis to bleeding during paediatric CPB is controversal. Diagnosed hyperfibrinolysis is seen in only 16% of infants and children on CPB decreasing to 3% post-CPB and is not associated with clinical bleeding [31,32]. However, ongoing fibrinolysis contributes to exacerbating bleeding. This could explain the efficacy of antifibrinolytics in reducing perioperative bleeding, after cardiac surgery [33]. During CPB complex coagulopathy occurs and the predictive value of the routine parameters of PT, PTT and platelet count is rather weak. Miller et al. demonstrated the importance of targeted blood product usage post-CPB, where inappropriate administration of FFP was associated with a paradoxal worsening manifested as increased hypocoagulability [34]. The clinical effectiveness of FFP in cardiac surgery was addressed in several trials. Results of comparison of the use and no use of FFP during and at the end of CPB did not support use of FFP [35]. Studies that evaluated FFP usage in small children, as part of the priming volume prior to initiating CPB showed that blood loss was not different. In contrast, the findings rather suggested that transfusions requirements might be greater in children receiving FFP [36,37]. Use of the rVIIa to treat uncontrolled bleeding after CPB was published, but randomized studies are not available [38,39]. Bleeding most frequently occurs during and after surgical interventions or traumas, in situations where secondary alterations are added to the disposition of the patients. Blood loss, possible acidosis, hypothermia and other metabolic disturbances, not primarily induced by coagulation-activating substances can provocate bleeding. Inadequate volume resuscitation and poor tissue perfusion not only promote the release of tissue procoagulant material leading to disseminated intravascular coagulation (DIC), but also result in lactic acidosis and acidaemia [40–42]. Newborns and small infants do not compensate for hypovolemia as well as adults. After 10% volume depletion to maintain systemic blood pressure peripheral vascular resistance increases and combined with the diminished cardiac output, results in poor tissue perfusion, low tissue oxygenation and metabolic acidosis. Hypothermia enhances several effects, such as increased metabolic rate, hypoglycaemia, metabolic acidosis and a tendency towards apneic episodes that may lead to hypoxia, hypotension and cardiac arrest [43]. In planned surgery, the aim should be to perform major surgical procedures with few or no transfusion. This can be achieved by a commitment to good blood management, with attention to all the details of the patient’s care that together can avoid the need to transfuse. Keep the patient warm as cold impairs blood clotting [44,45]. Congenital coagulation disorders are characterized by defects in factor synthesis. Haemophilia A and B, along with von Willebrand disease, represent 80–85% of the inherited bleeding disorders. Haemophilia A and B may present with bleeding symptoms in newborn period, as a homozygous form of factors II, V, VII, X and XIII deficiency. Intracranial haemorrhage at birth may be the presenting feature in infants with severe forms of inherited coagulation factor deficiencies, although most infants with this conditions do not have bleeding in the perinatal period, unless they undergo an invasive procedure or venipuncture. The other 15% are represented by the rare deficiencies, such as deficiencies of fibrinogen, prothrombin, factors V, combined FV/FVIII, FVII, FX, FXI and FXIII. Manifestations of these uncommon disorders vary from a mild to moderate bleeding tendency to potentially life-threatening haemorrhages. Newborns and young infants with severe haemorrhage due to congenital factor deficiency usually receive FFP at admission in hospital, while awaiting results of coagulation factor assays. Once the diagnosis of congenital bleeding disorder has been determined it is appropriate to use specific factor replacements if available (factors VIII, IX, VII, XIII, fibrinogen, von Willebrand) [46]. In rare factor deficiencies due to the rarity of each of the individual factor deficiencies, purified factor concentrates are not as readily available. Depending on which factor is deficient, purified virus-inactivated products, cryoprecipitate, or FFP can be used [47]. FFP is the only component for clinically significant deficiency of FII, FV, FX and FXI. Families, with certain FXI genotypes, may have bleeding problems and excessive bleeding with surgery, whereas other families do not. Although plasma-derived FXI concentrates are available, FFP (either donor retested Q-FFP or solvent-detergent treated) is generally used if treatment is judged indicated. Disseminated intravascular coagulation in newborn is usually secondary to perinatal asphyxia, sepsis, schlock, severe hypothermia or necrotizing enterocolitis. In older infants and adolescents, DIC most often occurs in malignancy. These children are usually critically ill and may exhibit widespread bleeding from multiple sites. The diagnosis of DIC is based on laboratory findings of low platelet count, prolonged PT, PTT and decreased fibrinogen. Fibrin degradation products can be elevated [48,49]. The primary goal of therapy is treating underlying condition and control of bleeding by replacement therapy with FFP, cryoprecipitate and platelet concentrates as necessary [50,51]. The dose of FFP administered usually is 10–20 ml/kg, with further doses being determined by the clinical situation, underlying disease process and laboratory monitoring. The amelioration of haemostatic problem by the transfusion of FFP in neonates with DIC is only temporary and hence multiple transfusions may be required until the underlying cause resolves. The outcome of DIC has been found to be dependent on the success of treatment of the underlying pathologic process and aggressive supportive care, and is not altered by therapy specifically directed at coagulopathy. Clinical trials with the use of antithrombin concentrate and protein C concentrate in neonates with DIC observed improvement in survival [52,53]. However, evidence-based recommendations for use of this concentrates in sick infants with sepsis and DIC are not available. The levels of vitamin K-dependent coagulation factors II, VII, IX i X are around half of normal adult level at birth in term infants and even lower in preterm infants. Classical haemorrhagic disease of the newborn occurs due to the transient deficiency of vitamin K-dependent factors and characterized by bruising and gastrointestinal haemorrhage in neonates around 2–5 days of age, now has been effectively prevented by routine administration of vitamin K at birth [54]. Early haemorrhagic disease, presenting within 24 h of birth, is associated with the ingestion in pregnancy of drugs which interfere with vitamin K metabolism. Late haemorrhagic disease appears between 2 and 8 weeks after birth and may be secondary to vitamin K malabsorbtion. In all conditions, life-threatening intracranial haemorrhage may occur. When vitamin K deficiency is suspected, vitamin K should be given as soon as possible. This will result in improvement of coagulation tests within a few hours. Neonates with severe bleeding or intracranial haemorrhage need FFP to be given in addition to vitamin K to arrest bleeding as soon as possible [55]. Coagulopathy may be secondary to acute or chronic liver disease. Cases of acute liver failure in neonate include viral infections, metabolic disease and asphyxia. Hepatic failure is associated with significant reduction in synthetic capacity of procoagulant and anticoagulant factors, hypo- and dysfibrinogenemia, thrombocytopenia and platelet dysfunction, reduction of gamma-carboxylation of proteins dependent of vitamin K, and by hyperfibrinolysis. In case of fulminant hepatic failure, bleeding can be the cause of exanguinatuin and death [56,57]. Treatment includes support of circulation and respiration, replacement of coagulation factors by FFP and cryoprecipitate transfusions, correction of metabolic abnormalities and electrolyte disturbance. The correction of coagulopathy secondary to liver failure is temporary in the absence of recovery of hepatic function. Response to FFP in hepatic dysfunction is variable, both in terms of correction of PT and cessation of bleeding. At present, there is no evidence to support the use FFP in patients with liver disease who has no bleeding nor is undergoing an invasive procedure. Some paediatric patients with liver-associated coagulopathy and bleeding have been successfully treated with rVIIa [58,59]. However, evidence-based recommendations regarding the use of VIIa await prospective randomized clinical trials in which outcomes are objectively assessed in well-matched groups of children with liver failure. Extra-corporeal membrane oxygenation is used to provide temporary life support in patients with profound cardio respiratory failure who fail to respond to conventional therapy [28]. Infants placed on ECMO are critically ill and already may have a disturbed haemostasis secondary to sepsis, shock or profound hypoxia, predisposing them to intracranial haemorrhage [60,61]. The continuous contact of blood with the surface of the ECMO circuit results in activation of the coagulation cascade. The use of heparin to prevent clot formation in the circuit and the decrease in platelet number and function from interaction with the circuit put the patient at risk for bleeding. FFP support is variable, with postsurgical infants, patients with sepsis, or those on prolonged bypass requiring considerably more transfusions [62]. The necessity for multiple blood components for neonates on ECMO often result in high donor exposures. Strategies for limiting donor exposure include using small paediatric aliquots from the same blood unit for subsequent transfusions, using standard FFP units up to 24 h after thawing, and eliminating the empirical use of FFP and cryoprecipitate [12]. Exchange transfusion for the management of severe unconjugated hyperbilirubinaemia of the neonate is more often required in the setting of alloimmune Rh- or ABO haemolytic anaemia. Clinical trials determined that clinical outcomes in newborns were equivalent by the use of blood reconstituted from FFP and RBCs as compared with fresh whole blood for ESTR [63]. Fresh-frozen plasma is used as a replacement solution in children undergoing therapeutic plasma exchange (TPE) in treatment of TTP [64]. TPE is recommended as the first line treatment of choice for TTP. FFP is a source of ADAMTS 13 and is preferred replacement solution in this life-treating condition [65]. As these patients need very large volume of FFP for regulatory TPE, pathogen-inactivated FFP has been recommended [66]. Monitoring of blood coagulation is critical to better understanding causes of bleeding, to guide haemostatic therapies and to predict the risk of bleeding [67]. Overall, haemostasis depends on a complex inter-relationship among endothelium, platelets, RBC, inflammatory cells, fibrinolysis and inhibitors as well as procoagulant factors. The PT and aPTT are routine laboratory tests used to investigate coagulation factor deficiency in patient with bleeding by providing an end assessment of thrombin generation by fibrin formation. The value of these tests has been questioned in the acute perioperative setting because there are delays from blood sampling to obtaining results (45–60 min), tests are determined in plasma rather than in whole blood, give no information on platelet function and the assays are performed at a temperature of 37°C rather than the patient’s temperature. In addition, PT and PTT coagulation tests vary in sensitivity for reduced levels of coagulating factors. According to published trials, new methods of global haemostasis assessment (thrombelastometry, thrombin generation tests) can better determine cause of bleeding and predict clinical bleeding risk as well as clinical outcome after haemostatic therapies, such as FFP transfusion in cardiac and liver surgery patients [68]. Large prospective clinical trials in different clinical settings, not only surgical have to be conducted to conclude whether tests of global haemostasis are better than routinely used coagulation screening tests to guide blood component therapy. There are insufficient scientific evidences on efficacy of FFP transfusion on the outcome of bleeding [69]. A very few researchers compared paediatric patients treated with FFP to the ones without such treatment, the number of patients is usually small, details on FFP regimen and transfused dose are not known [70]. Also, there are usually no data on bleeding extend before and after FFP, and the efficacy was estimated by the results of the routine coagulation tests [67]. From the clinical point of view, if FFP is given to stop the bleeding in the above-mentioned indications, stopping of bleeding and improvement of coagulation tests occur in majority of patients. Only in small number of patients the bleeding continues and laboratory tests worsen [71]. It is not possible to say whether the FFP was inefficient in these cases, or the result should be considered within the course of disease and other therapeutical and supportive measures [72,73]. Preliminary results of the new diagnostic methods point-of-care promise better monitoring of coagulation in patients with bleeding and more rational treatment with blood components. Indications for FFP in newborns, infants and adolescents are limited. In patients with bleeding caused by multiple deficiency of coagulation factors, FFP lead to cessation of bleeding and improvement of coagulation tests in majority of patients. Efficacy of preventive plasma transfusion is not proven [74]. The author declares that there are no potential conflicts of interest." @default.
• W1694976382 created "2016-06-24" @default.
• W1694976382 creator A5044808756 @default.
• W1694976382 date "2011-05-13" @default.
• W1694976382 modified "2023-09-27" @default.
• W1694976382 title "Use fresh-frozen plasma in newborns, older infants and adolescents on the outcome of bleeding" @default.
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