burns 37 (2011) 742–752                                                               available at www.sciencedirect.com  ...
burns 37 (2011) 742–752                                                                                                   ...
744                                                  burns 37 (2011) 742–752transfusion with that of low haemoglobin conce...
burns 37 (2011) 742–752                                                             745 Table 2 – Red blood cells transfus...
746                                                   burns 37 (2011) 742–752of blood flow and influx of extravascular fluid ...
burns 37 (2011) 742–752                                                        747    Upper and lower extremity use of a t...
748                                                  burns 37 (2011) 742–7521:50,000–1:150,000 in the Western countries [1...
burns 37 (2011) 742–752                                                        749    Analysis of existing transfusion lit...
750                                                    burns 37 (2011) 742–752[28] Sittig KM, Deitch EA. Blood transfusion...
burns 37 (2011) 742–752                                                       751[71] Achauer BM, Hernandez J, Parker A. B...
752                                                 burns 37 (2011) 742–752[111] Shorr AF, Jackson WL, Kelly KM, Fu M, Kol...
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Transfusion

  1. 1. burns 37 (2011) 742–752 available at www.sciencedirect.com journal homepage: www.elsevier.com/locate/burnsReviewRed blood cell transfusion following burnGiuseppe Curinga b,*, Amit Jain c, Michael Feldman a, Mark Prosciak a,Bradley Phillips d, Stephen Milner aa Johns Hopkins Burn Center, MD, Baltimore, USAb Civico and Benfratelli Hospital Burn Center, Palermo, Italyc Johns Hopkins University School of Medicine, Baltimore, MD, USAd Swedish Medical Center, Denver, CO, USAarticle info summaryArticle history: A severe burn will significantly alter haematologic parameters, and manifest as anaemia,Accepted 20 January 2011 which is commonly found in patients with greater than 10% total body surface area (TBSA) involvement. Maintaining haemoglobin and haematocrit levels with blood transfusion hasKeywords: been the gold standard for the treatment of anaemia for many years.Blood transfusion While there is no consensus on when to transfuse, an increasing number of authors haveBlood in burn expressed that less blood products should be transfused.Blood management Current transfusion protocols use a specific level of haemoglobin or haematocrit, whichBlood loss dictates when to transfuse packed red blood cells (PRBCs). This level is known as the trigger.Anemia in burn patients There is no one ‘common trigger’ as values range from 6 g dlÀ1 to 8 g dlÀ1 of haemoglobin.Unnecessary transfusion The aim of this study was to analyse the current status of red blood cell (RBC) transfu-Appropriate transfusion sions in the treatment of burn patients, and address new information regarding burn andin burn population blood transfusion management.Red blood cells transfusion Analysis of existing transfusion literature confirms that individual burn centres trans-in burn patients fuse at a lower trigger than in previous years.Physiologic transfusion trigger The quest for a universal transfusion trigger should be abandoned. All RBC transfusions should be tailored to the patient’s blood volume status, acuity of blood loss and ongoing perfusion requirements. We also focus on the prevention of unnecessary transfusion as well as techniques to minimise blood loss, optimise red cell production and determine when transfusion is appropriate. # 2011 Elsevier Ltd and ISBI. All rights reserved.Contents 1. Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 743 2. Definition of anaemia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 743 3. Review of the literature . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 743 4. Management: treatment and prevention of anaemia in the burn patient . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 744 4.1. When to transfuse? . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 744 * Corresponding author. Tel.: +39 3204748193. E-mail address: giuseppecuringa@venuslab.it (G. Curinga).0305-4179/$36.00 # 2011 Elsevier Ltd and ISBI. All rights reserved.doi:10.1016/j.burns.2011.01.016
  2. 2. burns 37 (2011) 742–752 743 4.2. Strategy to minimise blood loss . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 746 4.2.1. Blood conservation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 746 4.2.2. Estimation of blood loss . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 746 4.2.3. Reduction of blood loss . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 746 4.2.4. Optimisation of red cell production . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 747 5. Adverse events associated with RBC transfusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 747 5.1. Infections. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 747 5.2. Immunosuppression . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 748 5.3. Transfusion-related acute lung injury (TRALI) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 748 5.4. Transfusion errors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 748 6. Conclusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 748 References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7491. Introduction shown that a restrictive red blood cell (RBC) transfusion policy reduces complications.A severe burn will significantly alter haematologic param- While a consensus on when to transfuse has been elusiveeters. This manifests as anaemia, which is commonly found in even until today, an increasing number of authors are agreeingpatients with greater than 10% total body surface area (TBSA) that less blood products should be transfused.involvement [1–3]. The aetiology of anaemia in severe burns is Current transfusion protocols use a specific level ofmultifactorial (Table 1). This is important because blood haemoglobin or haematocrit, which dictates when to trans-transfusions have potential complications and collateral fuse PRBCs. This level is known as the trigger. There is no oneeffects [4–6]. Despite the potential complications, blood ‘common trigger’ as values range from a 6 g dlÀ1 to 8 g dlÀ1 oftransfusion remains common, with approximately 12 million haemoglobin.units of packed red blood cells (PRBCs) transfused each year in The aim of this article is to analyse the current status of RBCthe United States [7]. transfusions in the treatment of burn patients and address This practice can have an immunomodulatory effect, by new information regarding burn and blood transfusiondecreasing cell-mediated immunity, increasing a proinflam- management. We also focus on the prevention of unnecessarymatory state, augmenting the risk of infection, increasing the transfusion as well as techniques to minimise blood loss,risk of acute respiratory distress syndrome (ARDS) and optimise red cell production and determine when transfusionultimately causing multi-system organ failure (MOF) [8–10]. is appropriate. Historically, blood is transfused when the haemoglobin(Hb) level falls below 10 g dlÀ1 or the haematocrit (Htc) is lessthan 30%. Maintaining haemoglobin and haematocrit levels 2. Definition of anaemiawith blood transfusion has been the gold standard fortreatment of anaemia for many years [11–17]. Multicentre The World Health Organization (WHO) defines anaemia as atrials have shown that a restricted blood transfusion protocol haemoglobin value of <13 g dlÀ1 (haematocrit <39%) for anis associated with a lower in-hospital mortality rate, cardiac adult male and <12 g dlÀ1 (haematocrit <36%) for an adultcomplication rate and organ dysfunction compared with a non-pregnant female [20]. The haemoglobin concentration orliberal transfusion group [8,11,13,14]. Similar results were haematocrit used to define anaemia and classify its severity inshown in a cohort of burn patients and in paediatric burn critical care patients is less clear. While this may be apatients [18,19]. Over the past few years, several studies have convenient and useful parameter in the non-injured, euvo- lemic patient, it is not a reliable indicator of anaemia in trauma or burn patients. Furthermore, the restrictive strategy (to maintain the haemoglobin at 7–9 g dlÀ1) of red-cell transfusion Table 1 – Causes of anaemia in burn patients. is at least as effective as and possibly superior to a liberal transfusion strategy (to maintain haemoglobin at 10–12 g dlÀ1) # Production Delayed decreased erythropoiesis in critically ill patients [8,11,13,14,21,22]. " Destruction Anaemia is also defined as a decrease in the oxygen-carrying Thermal injury capacity of blood. The oxygen-carrying capacity of blood is a Injury related coagulopathy function of the total volume of circulating RBCs, so anaemia can Hypotermic coagulopathy be defined as a decrease in the total cell volume [23]. Thrombocytopenia DIC " External loss 3. Review of the literature Wounds Iatrogenic Initial excision, multiple One of the cornerstones of the management of a severe burn debridements involves resuscitation to restore an adequate vascular volume Donor site bleeding for perfusion [24]. An acceptable haemoglobin concentration Phlebotomy/lab draw is the degree of anaemia that balances the risk of red-cell
  3. 3. 744 burns 37 (2011) 742–752transfusion with that of low haemoglobin concentration. An patients) and reported that patients suffering from a 60% TBSAoptimal transfusion protocol has not yet been described. with inhalation injury had an 8% risk of developing sepsis in There is currently little debate about the need for the low group (PRBCs received < 20 U), which increased to 58%restricting blood transfusions. Blood products remain a vital in the high group (PRBCs received > 20 U). This directlyresource and its judicious use in trauma and burn patients has correlated the use of high amounts of blood products withto be applied. an increased likelihood to develop sepsis, thus showing that With the goal of decreasing transfusion-associated morbidi- PRBC transfusion causes an immunocompromising state.ty and mortality, some researchers have focused on safely RBCs can be minimised using a clear protocol of haemos-reducing the amount of blood transfused [25,26]. Mann et al. [27] tasis. O’Mara et al. [36] analysed two 3-year periods before andcompared the quantity of blood given to burn patients in 1980 after institution of a protocol to reduce blood loss and blood(haematocrit greater than 30%) with that given in 1990. In 1980, use. In early period, methods of excision and grafting were133 ml blood was transfused per patient per percent burn more variable. In the later period, a protocol to reduce bloodduring acute hospitalisation, compared with 20 ml in 1990. loss was implemented. All patients were transfused for aThere were no instances of myocardial infarction or congestive haemoglobin below 8.0 g dlÀ1. Overall unit transfused perheart failure related to the maintenance of lower haematocrits. operation decreased from 1.56 to 1.25 units after instituting In 1994, Sittig and Deitch [28] compared the results of a the protocol. They concluded that when using a clear protocolselective transfusion policy in which 14 patients were of haemostasis, technique and transfusion trigger, it istransfused when their haemoglobin levels went below 6 g dlÀ1 possible to decrease overall use of blood for burn patients,1 versus previous routine transfusion policy in which the and in particular to eliminate transfusion requirements in ahaemoglobin levels of 38 patients were routinely maintained great part of the burn population.at 10 g dlÀ1. No differences were found in the length of hospital Another protocol was proposed by Losee et al. [37] forstay. The patients treated with the liberal strategy received 3.5 treating the paediatric burn population. Using electrocauterytimes as much blood as their restrictive counterparts. They for the debridement of full-thickness burns, and dermabra-proposed that prophylactic transfusions to increase the sion for the partial thickness burns, treated immediately withoxygen-carrying capacity of blood are not indicated in epinephrine solution, they showed that intra-operative bloodasymptomatic anaemic patients (without coronary artery loss requiring transfusion can be minimised or eliminated.disease) with haemoglobin levels greater than 6 g dlÀ1. Table 2 summarises the literature on burn patients on RBC Palmieri et al., in a multicentre study of transfusion among transfusion.666 patients in 21 North American Burn Centers with 20% orgreater TBSA showed that the number of transfusionsreceived was associated with mortality and infectious epi- 4. Management: treatment and prevention ofsodes in patients with major burns even after factoring for anaemia in the burn patientindices of burn severity. The risk of infection was increased by13% per unit transfused [18]. Criteria for the optimal management of anaemia in trauma The haemoglobin transfusion threshold was reported by and burn patients are poorly defined. The management ofthe majority of physicians. Mean haemoglobin transfusion anaemia in burn patients must follow a two-prongedthreshold was 8.1 g dlÀ1. The most frequent reasons for approach: treatment and prevention.transfusion were ongoing blood loss (22%), anaemia (20%),hypoxia (13%) and cardiac disease (12%). Age, TBSA burn, the 4.1. When to transfuse?need for further operative intervention, the presence of ARDS,sepsis and evidence of cardiac ischaemia were also deemed The concept of an appropriate ‘transfusion trigger’ for RBCimportant [29]. transfusion in burns is not well described in the literature. As Kwan et al. [30] in a retrospective study, evaluated the shown in Table 1, the trigger most often cited is haemoglobineffects of a restrictive transfusion strategy in two group of or haematocrit. The reason for this may be that there is no onepatients with burns >20%. The restrictive group (REST group discrete ‘transfusion trigger’.135 patients, Hb transfusion trigger 7.0 g dlÀ1) received fewer Since the late 1980s, haemoglobin and haematocrit levels oftransfusion than the liberal group (LIB group 37 patients, Hb 8–10 g dlÀ1 and 32–35%, respectively, have generally beentransfusion trigger 9.2 g dlÀ1) and appeared to have signifi- accepted as being adequate in most patients. More recently,cantly better organ function. There were no differences this threshold has been lowered even further to 7 g dlÀ1 inbetween the groups in the incidence of cardiac disease. response to compelling large trials conducted in medical and A retrospective study conducted on 1615 patients admitted surgical intensive care unit (ICU) patients. The Transfusionto the burn unit showed that patients with small burns or no Requirements in Critical Care (TRICC) trial is the most citedcomorbidities were also at risk of transfusion, especially if clinical trial evaluating RBC transfusion threshold. The TRICCthey required debridement and grafting. This study also investigators allocated 838 critically ill patients who hadreaffirmed that patients with comorbidities, who required baseline haemoglobin concentrations of less than 9 g dlÀ1 totransfusions, were at a higher risk of mortality [31]. two transfusion groups. The ‘liberal’ strategy allowed transfu- Studies conducted on animal burn models demonstrate sions if the haemoglobin concentration decreased belowthat blood transfusion depresses immune function and 10 g dlÀ1, with a target haemoglobin concentration of 10–increases the risks of infectious complication [32–35]. Jeschke 12 g dlÀ1. The ‘restrictive’ strategy allowed transfusions only ifet al. [19] performed a retrospective study (252 paediatric the haemoglobin concentration decreased below 7 g dlÀ1, and
  4. 4. burns 37 (2011) 742–752 745 Table 2 – Red blood cells transfusion in burn patients: review of the literature. Author Pt Transfusion trigger Study Graves et al. [5] 594 A cross-tabulation of predicted mortality, no of transfusions, and infectious complications revealed a significant positive correlation between transfusion number and infectious complications Mann et al. [27] 79 Guidelines suggested: Comparative study between two group (41 patients in 1980, 38 patients in 1990) – Healthy Pt who will undergo a 1980 group received 1321 Æ 154 ml single operation 15% < Ht < 20% – Healthy with multiple operations 1990 group 207 Æ 62 ml Ht < 25% – Critically ill patient or with limited cardiovascular reserve Ht < 30% Sittig et al. [28] 14 Hb < 6 g/dl Retrospective comparative study. The length of hospital stay was similar Prophylactic transfusion to increase oxygen carrying capacity of blood are not indicated in asymptomatic anaemic patients 38 Hb > 9.5–10 g/dl Palmieri et al. [29] Hb 8.1 g/dl, mean transfusion Multicentre survey of North American Centers threshold Criswell et al. [25] 107 1.78 U PRBCs were transfused Retrospective chart review with TBSA > 20%, to evaluate for 1000 cm2 as the estimation of excision area can predict transfusion need excised to maintain 25% < Ht < 31% O’Mara et al. [36] Hb < 8 g/dl Two 3-year time periods were analyzed, before and after implementation of intraoperative protocol to reduce blood loss Kwan et al. [30] 37 Liberal group Retrospective comparison of adults with >20% TBSA Hb 9.2 g/dl Restrictive group appeared to have significantly better organ function 135 Restrictive group Hb 7 g/dl Palmieri et al. [18] 666 Mean Hb 9.2 g/dl Multicentre retrospective cohort analysis; TBSA > 20%; infections per patient increased with each unit of blood transfused Palmieri et al. [26] 584 Traditional policy Retrospective study on paediatric population Hb < 10 g/dl Twice number of pulmonary complications in traditional group 556 Restrictive group Restrictive transfusion policy in children decrease in transfusion-related costs Hb < 7 g/dl Jeschke et al. [19] 252 Hb < 8 g/dl Retrospective, cohort study in paediatric burn population. Patients with TBSA > 60% and concomitant inhalation injury are more likely to develop sepsis if they are given high amount of blood Boral et al. [31] 1615 – Hypovolemic shock in Retrospective review. Patients with small burns or no comorbidities currently bleeding patients were also at risk of transfusion, especially if they required debridment and grafting. Patients with comorbidities, who required transfusions, were at higher risk for mortality – Preoperative Hb < 8 g/dl or Ht < 24% Pt, number of patients; Hb, haemoglobin; Ht, haematocrit.the target haemoglobin concentration was 7–9 g dlÀ1 [38]. The and that purported cardiac risks with anaemia have been30-day mortality rates were similar for these groups (81% with overemphasised. Although cardiovascular disease could in-the restrictive strategy and 77% with the liberal strategy). crease the risk of anaemia because of restricted oxygen In 2007, results were published on a trial in children in the delivery to the myocardium [42], a more recent article showedICU. The authors compared a 7 g dlÀ1 threshold on the rate of that a restrictive RBC transfusion strategy seemed safe in mostmultiple-organ dysfunctions with a 9.5 g dlÀ1 threshold [39]. critically ill patients with cardiovascular disease, with theThe TRICC trial outcomes were very similar in patients possible exception of patients with acute myocardial infarctsallocated to liberal transfusion threshold and restrictive and unstable angina [43].transfusion and were associated with a 44% drop in the Regardless, an important consideration for any decision tonumber of RBC transfusions. give blood is the acuity of the blood loss. Patients with acute, These combined findings, showed in critically ill patients massive haemorrhage show signs of haemodynamic instabil-and in-burn patients, suggest that many patients are receiving ity early in their presentation. The clinical picture depends onmore RBCs than is necessary. the amount of blood loss. Loss of about 20% of blood volume As reported by several authors in the recent literature elicits compensatory increases in heart rate and cardiac[40,41] transfusion for a set transfusion trigger is ill-advised, output, as well as a rise in vasoactive hormones, redistribution
  5. 5. 746 burns 37 (2011) 742–752of blood flow and influx of extravascular fluid to the 4.2. Strategy to minimise blood lossintravascular compartment [44–47]. Therefore, with anaemia, oxygen delivery is maintained 4.2.1. Blood conservationthrough a series of complex interactions and compensatory In attempts to lower the rate of complications reported withmechanisms. the use of PRBCs in burn patients, some authors examined the Blood volume evaluation should be estimated to restore use of autologous blood transfusion [63,64].adequately the circulatory system, preventing complications Samuelsson et al. [63] used auto transfusion in four casesof inadequate or overload fluid resuscitation, which can ranging from 8% to 30% TBSA. The study was limited by andaggravate the anaemic status. abandoned due to the high risk of bacterial contamination of Clinical signs at the bedside have been proven insensitive blood collected intra-operatively.and nonspecific markers of hypoxia; blood pressure, heart Imai et al., in 2007 [64], reported treatment with periopera-rate, changes in mental status and urine output, suffer tive haemodilutional autologous blood transfusion of sevenconfounding factors in their interpretation, and may not cases in burn patients. Patients ranged from 33 to 79 years ofaccurately predict the clinical status [48,49]. age and TBSA ranged from 5.5% to 20%. One patient required Base deficit, a surrogate marker for lactic acidosis, reflects allogenic blood transfusion. The main disadvantage of thisfailing tissue oxygenation, is easily measured but is confounded method was the limitation of the amount of blood that couldby a range of conditions as well as resuscitative efforts [48]. The be withdrawn and transfused. They concluded that thismeasurement of serum lactate has also been proposed as a test technique avoids or minimises the risks of allogenic transfu-to estimate and monitor the extent of bleeding and shock [50]. In sion in burn surgery involving less than 20% TBSA.fact, the clearance of serum lactate to normal levels within 24 his a powerful predictor of mortality in the critically ill patient. 4.2.2. Estimation of blood lossThe amount of lactate produced by anaerobic glycolysis is an In the burn unit, it is essential to be able to estimate theindirect marker of oxygen debt, tissue hypoperfusion and the probable blood requirements of surgery prior to burnsseverity of haemorrhagic shock [51–54]. excision. This can reduce wasting of blood products. Therefore, serum lactate adds another variable to decide Several authors have proposed different and variouswhen to transfuse. systems to estimate blood loss during the surgery [65–69]. Mixed venous oxygen saturation should be the best guide to It is commonly estimated that 117 ml of the blood volume isneed transfusion, but is limited by the need for invasive lost for every 1% of body surface area excised and grafted [66].monitoring using a pulmonary artery catheter or right atrial Desai et al., in 1990, calculated that blood losses in burns ofcentral line [55,56]. Central venous oxygen saturation, a more more than 30% TBSA were 0.75 ml cmÀ2 between 2 and 16 dayseasily measured approximation of mixed venous saturation, after the burn [69].and currently a marker used to guide early goal-directedtherapy in the adult septic shock patients, can be misleading 4.2.3. Reduction of blood loss[56]. A significant amount of blood can be lost with repeated Tissue-specific markers of hypoxia are ST segment changes phlebotomy in the ICU. A policy of obtaining laboratory resultson electrocardiogram and P300 latency on electroencephalo- only when clinically indicated should be followed. This issuegram. may be addressed by drawing a smaller sample using paediatric Myocardial insufficient tissue oxygenation can be detected collection tubes. Another way of reducing blood loss fromby continuous five-lead ECG monitoring as new ST-depression laboratory draws is by sending a single sample for multiple tests>0.1 mV or as new ST-segment elevation >0.2 mV for more (batching of requests for laboratory tests) [70]. Early woundthan a minute [57]. Although authors reported that ST- excision minimises the loss of blood because hyperaemia has notsegment change is a physiological transfusion trigger [58,59] yet occurred [69]. Blood loss in large burns (more than 30% TBSA)it cannot be used to signal the need for transfusion. There are significantly decreased when surgical excision was performedno evidence literature data to support these findings. within the first 24 h after injury compared to those performed Current monitoring techniques that assess the heart for between the second and sixteenth days after injury [69].development of myocardial ischaemia are electrocardiogram Based on these findings, early wound excision mayand transoesophageal echocardiography. Weiskopf et al. [60] decrease the loss of blood. Burn wound excision to fascia,have opened the ‘window to the brain’ with respect to when performed, has been shown to decrease blood loss,monitoring the adequacy of cerebral oxygenation during acute although tangential excision can result in better cosmetic andanaemia. The P300 latency above a certain threshold might functional outcomes [71].serve as a monitor of inadequate cerebral oxygenation and as an New intra-operative techniques and approaches have beenorgan-specific transfusion trigger in the future [49,61]. Blood developed to reduce blood loss and limit the need for allogenictransfusion should be based on a comprehensive assessment of blood transfusions. These approaches include the use ofthe patient, including vital signs, estimation of the amount of surgical instruments that minimise bleeding, and minimallyblood loss and evaluation of blood volume, as well as clinical invasive surgical procedures [72].and laboratory evaluation of end-organ perfusion. Several techniques that use warm saline-soaked pads, The conclusion of the National Institutes of Health tourniquet and topical epinephrine (1:100,000–1:200,000), haveConsensus Conference remains the extremely valid one today: been described to minimise blood loss during burn excisionno single measurement can replace good clinical judgement [73–77]. Subdermal clysis with epinephrine can be used almostconcerning the need for red-cell transfusion [62]. everywhere except the extremities.
  6. 6. burns 37 (2011) 742–752 747 Upper and lower extremity use of a tourniquet allows for incidence of red-cell transfusion among critically ill patients,bloodless debridement. This practice requires close attention to but it may reduce mortality in patients with trauma. At day 29,detail and experience to recognise adequacy of debridement. the increase in the haemoglobin concentration from baseline Even on more difficult sites like the torso and on the graft was greater in the epoetin alfa group than in the placebodonor sites, blood loss can be reduced dramatically with the group. Treatment with epoetin alfa was associated with anuse of a haemostatic agent (such as recombinant thrombin) increase in the incidence of thrombotic events.[78–80]. All fascial excisions should be performed with Contrarily, two previous trials involving critically illelectrocautery such that perforating vessels can be immedi- patients showed that treatment with epoetin alfa reducedately coagulated [81]. the number of red-cell transfusions and raised the haemo- It is a crucial and often overlooked point to maintain globin concentration [96,97].euthermia, principally through operating room heating. These A randomised, double-blind, placebo-controlled, multi-patients are particularly susceptible to intra-operative hypo- centre trial in anaemic critically ill patients demonstrated athermia as massive evaporative heat loss can occur through 29-day survival benefit in the trauma subgroup receivingtheir wounds. The heat loss rate is related to TBSA and the epoetin alfa [98].temperature gradient between body and the environment. It has also been reported that EPO administration exertsThe induction of anaesthesia results in relative ablation of protective effects on apoptosis induced by ischaemic reperfu-thermoregulatory mechanism and puts the patient at further sion injury, in the brain, spinal cord, skeletal muscle and therisk for developing hypothermia. Actions such as maintaining myocardium [99–103].higher ambient air temperature, covering extremities andhead, applying warm blankets, utilising radiant heaters andforced air warming gases are usually effective in maintaining 5. Adverse events associated with RBCcore temperature if applied aggressively. Body temperature transfusionshould be maintained at or above 37 8C in burn patients.Hypothermia is a contributing factor to platelet and coagula- The transfusion of blood and blood products is associated withtion factor dysfunction; patients should be aggressively several well-documented adverse effects, which can be dividedwarmed during surgery [82]. into transfusion-associated infections, immunological risks, By keeping the patient euthermic, we can minimise the metabolic complications and transfusion errors (Table 3) [84].need to transfuse blood products. Optimal timing and quantity of RBCs, plasma and platelets 5.1. Infectionsin the treatment of hypothermia is unclear. It is unclear ifcurrent component therapy is equivalent to whole blood Estimated risks of transfusion–transmitted disease for immu-transfusion. In fact, data from the current war in Iraq and nocompetent patients are lower than ever before. Since 1999,Afghanistan suggest otherwise [83]. the risks have been declining substantially with the imple- Timely use of FFP, prevention of hypothermia and correction mentation of NAT (nucleid acid testing), which has shortenedof acidosis through PRBC resuscitation are important strategies infectious periods and dramatically reduced the currentin preventing coagulopathy. Transfusing FFP and PRBC in an 1:1 estimated risks of post-transfusion hepatitis C virus (HCV)strategy may prevent some of the coagulopathic effects [84]. and HIV. Current estimates of the risk per unit of blood are approximately 1:1,900,000 for HIV and 1:1,600,000 for HCV4.2.4. Optimisation of red cell production [104–106]. In contrast to the reduction of infection for HIV andTo promote haematopoiesis, supplementation with vitamin HCV, the risk of hepatitis B virus remains approximatelyB12 and folate should be considered as part of routineperioperative care of burn patients. Iron supplementation hasbeen proposed as adjuvant treatment [85,86]. However, there is Table 3 – Estimated risks in transfusions per unitexperimental evidence that iron therapy in the critically ill transfused.patient may enhance the risk of infections and the production offree radicals [87,88]. Iron is required for microbial growth. Adverse effect Estimated riskInflammatory cytokines increase the synthesis of ferritin, Urticaria or other cutaneous reaction 1 in 33–100which may serve as a protective function by binding iron and Febrile reaction 1 in 18–300reducing its availability for microbial growth [89]. Iron appears TRALI 1 in 5000 Haemolytic reaction 1 in 6000–70,000to stimulate bacterial virulence, and impair cellular immunity Mistransfusion 1 in 14,000–18,000via inhibition of phagocytosis by neutrophils [90]. Before Anaphylaxis 1 in 20,000–50,000routinely supplementing anaemic burn patients with iron, we Bacterial infections 1 in 5,000,000need additional studies to clarify the risk of infection. HTLV I and II 1 in 641,000 Recombinant human erythropoietin (r-HuEPO) in acutely Hepatitis B 1 in 50,000–150,000burned patients did not prevent the development of postburn Fatal haemolysis 1 in 1,000,000 Hepatitis C 1 in 1,600,000anaemia or decrease transfusion requirements. Several HIV 1 in 1,900,000studies reported a statistically significant increase of reticu-locytosis, but no change in the haemoglobin, haematocrit or TRALI, transfusion-related acute lung injury; HTLV, human T- lymphotropic virus; HIV, human immunodeficiency virus (Ref.RBC count [90–94]. In a prospective randomised placebo- [84]).controlled trial [95], the use of epoetin alfa does not reduce the
  7. 7. 748 burns 37 (2011) 742–7521:50,000–1:150,000 in the Western countries [106]. Bacterial 5.4. Transfusion errorscontamination of red blood occurs 1:500,000. The mostcommonly implicated organism in bacterial contamination Human errors are responsible for more than half of allis Yersinia enterocolitica [106]. transfusion-related fatalities [115]. They have been estimated to be one in 14,000 units in the United States, and one in 18,0005.2. Immunosuppression in the United Kingdom [116]. Mistransfusion, defined as an ABO-incompatible reaction owing to an error, is a leadingThere is also evidence that red-cell transfusions are associated cause of morbidity and mortality from transfusion because itwith an immunomodulatory effect. Transfusion-related can lead to a major haemolytic reaction. Non-ABO acuteimmunomodulation has been noted to be clinically important haemolytic reactions and febrile nonhaemolytic reactions arein renal transplantation patients and in women with multiple much more common but are generally mild and self-limitingmiscarriages [107,108]. in nature. Mistransfusion may lead to an acute haemolytic Allogenic blood transfusions have also been associated reaction, which is characterised by fever, chills, pain, nausea,with a reduction of cell-mediated immunity, increased rates of vomiting, hypotension, tachycardia, renal failure and dissem-postoperative infection and early recurrences of malignancy inated intravascular coagulation [113].[109–111].5.3. Transfusion-related acute lung injury (TRALI) 6. ConclusionPresenting signs and symptoms of TRALI include dyspnoea, Blood transfusion is not a benign therapy. Patients who receivehypotension and fever, caused by noncardiogenic pulmonary PRBCs have an increased incidence of complications. Theoedema. Symptoms begin during, or shortly after transfusion, optimal transfusion strategy for burn patients has not yet beentypically within 4 h after receiving blood. definitively determined, and additional clinical research is The mechanism of transfusion-related acute lung injury needed.(TRALI) is not completely understood, but it appears to involve The most important physiologic consequence of anaemialocalisation of antibody-coated leucocytes to pulmonary is a reduction in the oxygen-carrying capacity of blood. Thesevasculature resulting in increased permeability and oedema changes are accompanied by increased cardiac output, a shift[112]. Its estimated frequency is approximately 1 in 5000 of the oxyhaemoglobin dissociation curve and increasedtransfusions, and it is fatal in 5–10% of cases [113]. The actual oxygen extraction.reported mortalities underscores the fact that this complica- Anaemia is well tolerated as long as intravascular volumetion evades clinical recognition, it may be responsible for more is maintained. Blood volume evaluation should be evaluatedserious adverse events and fatalities than are reported [114]. and corrected based on the length and severity of the anaemia.[()TD$FIG]Fig. 1 – Limit and prevent unnecessary transfusion in burn patient reduce the RBC exposure: uniform application of bloodconserving techniques, optimization of red blood cell production, and an adequate and ‘‘physiologic’’ evaluation of theanaemic status of the patient. *R-HuEPO = recombinant human erythropoietin.
  8. 8. burns 37 (2011) 742–752 749 Analysis of existing transfusion literature confirms severity, is associated with worse outcome in trauma. Jthat individual burn centres transfuse at a lower trigger Trauma 2003;54:898–907. [9] Kauvar DS, Lefering R, Wade CE. Impact of hemorrhage onthan in previous years. However, the quest for a universal trauma outcome: an overview of epidemiology, clinicaltransfusion trigger should be abandoned. All RBC transfu- presentations, and therapeutic considerations. J Traumasions should be tailored to the patient’s blood volume 2006;60:S3–11.status, acuity of blood loss and ongoing perfusion require- [10] Khan H, Belsher J, Yilmaz M, Afessa B, Winters JL, Moorements. SB, et al. Fresh-frozen plasma and platelet transfusions The indication for and the degree of urgency of RBC are associated with development of acute lung injury intransfusions cannot be defined only on the basis of the values critically ill medical patients. Chest 2007;131:1308–14. [11] Chohan SS, McArdle F, McClelland DB, Mackenzie SJ,of Hb or the Htc, but must be based on a complete evaluation of Walsh TS. Red cell transfusion practice following thethe patient’s clinical condition and the possible presence of transfusion requirements in critical care (TRICC) study:mechanisms compensating for anaemia. A systematic analy- prospective observational cohort study in a large UKsis of clinical status should be made in conjunction with an intensive care unit. Vox Sang 2003;84:211–8.analysis of volume status, pulmonary function, cardiovascular [12] Corwin HL, Gettinger A, Pearl RG, Fink MP, Levy MM,status, duration of anaemia and the need for further surgical Abraham E, et al. The CRIT study: anemia and blood transfusion in the critically ill-current clinical practice inintervention. the United States. Crit Care Med 2004;32:39–52. Uniform application of blood-conserving techniques, opti- [13] Hebert PC. Red cell transfusion strategies in the ICU,misation of RBC production and an adequate and ‘physiologic’ Transfusion Requirements in Critical Care Investigatorsevaluation of the anaemic status of the patient can be used to and the Canadian Critical Care Trials Group. Vox Sangreduce the RBC exposure (Fig. 1). 2000;78:167–77. The ‘physiologic’ transfusion trigger could be based on [14] ´ Hebert PC, Wells G, Tweeddale M, Martin C, Marshall J,signs and symptoms of impaired global (lactate, SvO2 or ScvO2) Pham B, et al. Does transfusion practice affect mortality in critically ill patients? Transfusion Requirements in Criticalparameters. No standard care exists despite current literature Care (TRICC) Investigators and the Canadian Critical Careimplying the efficacy of minimising transfusions to critically ill Trials Group. Am J Respir Crit Care Med 1997;155:1618–23.patients. Complication rates and costs associated with blood [15] Napolitano LM, Corwin HL. Efficacy of red blood celltransfusion should be reduced with a comprehensive strategy transfusion in the critically ill. Crit Care Clin 2004;20:255–of blood conservation. 68. [16] Wallace EL, Churchill WH, Surgenor DM, Cho GS, McGurk S. Collection and transfusion of blood and bloodConflict of interest components in the United States, 1994. Transfusion 1998;38:625–36. [17] Wallace EL, Sullivan MT. New beginnings: the NationalDr. Giuseppe Curinga was supported in part from ISBI Blood Data Resource Center. Transfusion 1998;38:622–4.Travelling Fellowship. Dr. Giuseppe Curinga wants to dedicate [18] Palmieri TL, Caruso DM, Foster KN, Cairns BA, Peck MD,this article in memory of his father. Gamelli RL, et al. American Burn Association Burn Multicenter Trials Group, effect of blood transfusion on outcome after major burn injury: a multicenter study. Crit Care Med 2006;34:1602–7.references [19] Jeschke MG, Chinkes DL, Finnerty CC, Przkora R, Pereira CT, Herndon DN. Blood transfusions are associated with increased risk for development of sepsis in severely [1] Loebl EC, Baxter CR, Curreri PW. The mechanism of burned pediatric patients. Crit Care Med 2007;35: erythrocyte destruction in the early post-burn period. Ann 579–83. Surg 1973;178:681–6. [20] Emmanuel JE, McClelland B, Page R, editors. The clinical [2] Topley E, Jackson DM, Cason JS, Davies JW. Assessment of use of blood in medicine, obstetrics, paediatrics, surgery red cell loss in the first two days after severe burns. Ann anaesthesia. Trauma & Burns: World Health Organisation; Surg 1962;155:581–90. 1997. p. 337. [3] Shankar R, Amin CS, Gamelli RL. Hematologic, [21] DeBellis RJ. Anemia in critical care patients: incidence, hematopoietic and acute phase response. In: Herndon etiology, impact, management, and use of treatment DN, editor. Total burn care. London: Saunders Co; 2002. p. guidelines and protocols. Am J Health Syst Pharm 331–2. 2007;64:S14–21. [4] Alvarez G, Hebert PC, Szick S. Debate: transfusing to [22] Walsh TS, Saleh EE. Anaemia during critical illness. Br J normal haemoglobin levels will not improve outcome. Crit Anaesth 2006;97:278–91. Care 2001;5:56–63. [23] Marino PL, Sutin KM. The ICU book, third ed., Lippincott [5] Graves TA, Cioffi WG, Mason Jr AD, McManus WF, Pruitt Jr Williams & Wilkins; 2006. BA. Relationship of transfusion and infection in a burn [24] Feldschuh J, Katz S. The importance of correct norms in population. J Trauma 1989;29:948–52. blood volume measurement. Am J Med Sci 2007;334:41–6. [6] Triulzi DJ, Blumberg N, Heal JM. Association of transfusion [25] Criswell KK, Gamelli RL. Establishing transfusion needs in with postoperative bacterial infection. Crit Rev Clin Lab Sci burn patients. Am J Surg 2005;189:324–6. 1990;28:95–7. [26] Palmieri TL, Lee T, O’Mara MS, Greenhalgh DG. Effects of a [7] Comprehensive report on blood collection and transfusion restrictive blood transfusion policy on outcomes in in the United States in 2001. Bethesda, MD: National Blood children with burn injury. J Burn Care Res 2007;28:65–70. Data Resources Center; 2002. [27] Mann R, Heimbach DM, Engrav LH, Foy H. Changes in [8] Malone DL, Dunne J, Tracy JK, Putnam AT, Scalea TM, transfusion practices in burn patients. J Trauma Napolitano LM. Blood transfusion, independent of shock 1994;37:220–2.
  9. 9. 750 burns 37 (2011) 742–752[28] Sittig KM, Deitch EA. Blood transfusions: for the thermally [49] Vallet B, Adamczyk S, Barreau O, Lebuffe G. Physiologic injured or for the doctor? J Trauma 1994;36:369–72. transfusion triggers. Best Pract Res Clin Anaesthesiol[29] Palmieri TL, Greenhalgh DG. Blood transfusion in burns: 2007;21:173–81. what do we do? J Burn Care Rehabil 2004;25:71–5. ´ [50] Spahn DR, Cerny V, Coats TJ, Duranteau J, Fernandez-[30] Kwan P, Gomez M, Cartotto R. Safe and successful ´ Mondejar E, Gordini G, et al. Task force for advanced restriction of transfusion in burn patients. J Burn Care Res bleeding care in trauma, management of bleeding 2006;27:826–34. following major trauma: a European guideline. Crit Care[31] Boral L, Kowal-Vern A, Yogore 3rd M, Patel H, Latenser BA. 2007;11:R17. Transfusions in burn patients with/without comorbidities. [51] Wilson M, Davis DP, Coimbra R. Diagnosis and monitoring J Burn Care Res 2009;30:268–73. of hemorrhagic shock during the initial resuscitation of[32] Waymack JP, Rapien J, Garnett D, Tweddell JS, Alexander multiple trauma patients: a review. J Emerg Med JW. Effect of transfusion on immune function in a 2003;24:413–22. traumatized animal model. Arch Surg 1986;121:50–5. [52] Baron BJ, Scalea TM. Acute blood loss. Emerg Med Clin[33] Winslow GA, Shelby J, Nelson EW, Saffle JR. Influence of North Am 1996;14:35–55. allogeneic blood transfusion on natural killer cell activity [53] Porter JM, Ivatury RR. In search of the optimal end points in burn injured mice. J Burn Care Rehabil 1996;17:117–23. of resuscitation in trauma patients: a review. J Trauma[34] Waymack JP, Robb E, Alexander JW. Effect of transfusion 1998;44:908–14. on immune function in a traumatized animal model, II. [54] Bilkovski RN, Rivers EP, Horst HM. Targeted resuscitation Effect on mortality rate following septic challenge. Arch strategies after injury. Curr Opin Crit Care 2004;10: Surg 1987;122:935–9. 529–38.[35] Waymack JP, Gallon L, Barcelli U, Alexander JW. Effect of [55] Klein HG. Blood avoidance for the critically ill: another blood transfusions on macrophage function in a burned blow to liberalism? Crit Care Med 2006;34:2013–4. animal model. Curr Surg 1986;43:305–7. [56] Wang JK, Klein HG. Red blood cell transfusion in the[36] O’Mara MS, Hayetian F, Slater H, Goldfarb IW, Tolchin E, treatment and management of anaemia: the search for Caushaj PF. Results of a protocol of transfusion threshold the elusive transfusion trigger. Vox Sang 2009 [Aug 4, Epub and surgical technique on transfusion requirements in ahead of print]. burn patients. Burns 2005;31:558–61. [57] Madjdpour C, Heindl V, Spahn DR. Risks, benefits,[37] Losee JE, Fox I, Hua LB, Cladis FP, Serletti JM. Transfusion- alternatives and indications of allogenic blood free pediatric burn surgery: techniques and strategies. transfusions. Minerva Anestesiol 2006;72(May (5)):283–98. Ann Plast Surg 2005;54:165–71. [58] Spahn DR. Perioperative transfusion triggers for red blood ´[38] Hebert PC, Wells G, Blajchman MA, Marshall J, Martin C, cells. Vox Sang 2000;78:163–6. Pagliarello G, et al. A multicenter, randomized, controlled [59] Spahn DR, Smith LR, Veronee CD, McRae RL, Hu WC, clinical trial of transfusion requirements in critical care, Menius AJ, et al. Acute isovolemic hemodilution and blood Transfusion Requirements in Critical Care Investigators, transfusion. Effects on regional function and metabolism Canadian Critical Care Trials Group. N Engl J Med in myocardium with compromised coronary blood flow. J 1999;340:409–17 [Erratum in: N Engl J Med 1999;340:1056]. Thorac Cardiovasc Surg 1993;105:694–704. ´[39] Lacroix J, Hebert PC, Hutchison JS, Hume HA, Tucci M, [60] Weiskopf RB, Toy P, Hopf HW, Feiner J, Finlay HE, Ducruet T, et al. TRIPICU Investigators; Canadian Critical Takahashi M, et al. Acute isovolemic anemia impairs Care Trials Group; Pediatric Acute Lung Injury and Sepsis central processing as determined by P300 latency. Clin Investigators Network, Transfusion strategies for patients Neurophysiol 2005;116:1028–32. in pediatric intensive care units. N Engl J Med [61] Spahn DR, Madjdpour C. Physiologic transfusion triggers: 2007;356:1609–19. do we have to use (our) brain? Anesthesiology[40] Klein HG, Spahn DR, Carson JL. Red blood cell transfusion 2006;104:905–6. in clinical practice. Lancet 2007;370:415–26. [62] Consensus conference on perioperative red blood cell[41] Grottke O, Henzler D, Rossaint R. Use of blood and blood transfusion. JAMA 1988;260:2700–2. products in trauma. Best Pract Res Clin Anaesthesiol [63] Samuelsson A, Bjornsson A, Nettelblad H, Sjoberg F. ¨ ¨ 2007;21:257–70. Autotransfusion techniques in burn surgery. Burns[42] Carson JL, Duff A, Poses RM, Berlin JA, Spence RK, Trout R, 1997;23:188–9. et al. Effect of anaemia and cardiovascular disease on [64] Imai R, Matsumura H, Uchida R, Watanabe K. surgical mortality and morbidity. Lancet 1996;348:1055–60. Perioperative hemodilutional autologous blood[43] Hebert PC, Yetisir E, Martin C, Blajchman MA, Wells G, transfusion in burn surgery. Injury 2008;39:57–60. Marshall J, et al. Is a low transfusion threshold safe in [65] Snelling CFT. Quantitative evaluation of blood loss critically ill patients with cardiovascular diseases? Crit during debridement and grafting of burns. Can J Surg Care Med 2001;29:227–34. 1982;25:416.[44] Howarth S, Sharpey-Schafer EP. Low blood pressure [66] Budny PG, Regan PJ, Roberts AH. The estimation of blood phases following haemorrhage. Lancet 1947;1:18–20. loss during burns surgery. Burns 1993;19:134–7.[45] Skillman JJ, Lauler DP, Hickler RB, Lyons JH, Olson JE, Ball [67] Brown RA, Grobbelaar AO, Barker S, Rode H. A formula to MR, et al. Hemorrhage in normal man: effect on renin, calculate blood cross-match requirements for early burn cortisol, aldosterone, and urine composition. Ann Surg surgery in children. Burns 1995;21:371–3. 1967;166:865–85. [68] Warden GD, Saffle JR, Kravitz M. A two stage technique for[46] Skillman JJ, Awwad HK, Moore FD. Plasma protein kinetics excision and grafting of bum wounds. J Trauma of the early transcapillary refill after hemorrhage in man. 1982;22:98–103. Surg Gynecol Obstet 1967;125:983–96. [69] Desai MH, Herndon DN, Broemeling L, Barrow RE, Nichols[47] Meyers RL, Paulick RP, Rudolph CD, Rudolph AM. Jr RJ, Rutan RL. Early burn wound excision significantly Cardiovascular responses to acute, severe haemorrhage in reduces blood loss. Ann Surg 1990;211:753–9 [discussion fetal sheep. J Dev Physiol 1991;15:189–97. 759–62].[48] Maar SP. Searching for the Holy Grail: a review of markers [70] Smoller BR, Kruskall MS. Phlebotomy for diagnostic of tissue perfusion in pediatric critical care. Pediatr Emerg laboratory tests in adults. Pattern of use and effect on Care 2008;24:883–7. transfusion requirements. N Engl J Med 1986;314:1233–5.
  10. 10. burns 37 (2011) 742–752 751[71] Achauer BM, Hernandez J, Parker A. Burn excision with [93] Wallner SF, Vautrin R. The anemia of thermal injury: intraoperative vasopressin. J Burn Care Rehabil mechanism of inhibition of erythropoiesis. Proc Soc Exp 1989;10:375–8. Biol Med 1986;181:144–50.[72] Goodnough LT, Shander A, Spence R. Bloodless medicine: [94] Still Jr JM, Belcher K, Law EJ, Thompson W, Jordan M, Lewis clinical care without allogeneic blood transfusion. M, et al. A double-blinded prospective evaluation of Transfusion 2003;43:668–76. recombinant human erythropoietin in acutely burned[73] Gomez M, Logsetty S, Fish JS. Reduced blood loss during patients. J Trauma 1995;38:233–6. burn surgery. J Burn Care Rehabil 2001;22:111–7. [95] Corwin HL, Gettinger A, Fabian TC, May A, Pearl RG, Heard[74] Sheridan RL, Szyfelbein SK. Staged high-dose epinephrine S, et al. EPO Critical Care Trials Group. Efficacy and safety clysis is safe and effective in extensive tangential burn of epoetin alfa in critically ill patients. N Engl J Med excisions in children. Burns 1999;25:745–8. 2007;357:965–76.[75] Robertson RD, Bond P, Wallace B, Shewmake K, Cone J. [96] Corwin HL, Gettinger A, Rodriguez RM, Pearl RG, Gubler The tumescent technique to significantly reduce blood KD, Enny C, et al. Efficacy of recombinant loss during burn surgery. Burns 2001;27:835–8. humanerythropoietin in the critically ill patient: a[76] Marano MA, O’Sullivan G, Madden M, Finkelstein J, randomized, double-blind, placebo-controlled trial. Crit Goodwin CW. Tourniquet technique for reduced blood Care Med 1999;27:2346–50. loss and wound assessment during excisions of burn [97] Corwin HL, Gettinger A, Pearl RG, Fink MP, Levy MM, wounds of the extremity. Surg Gynecol Obstet Shapiro MJ, et al. Efficacy of recombinant human 1990;171:249–50. erythropoietin in the critically ill patient: a randomized[77] Rosenberg JL, Zawacki BE. Reduction of blood loss using controlled trial. JAMA 2002;288:2827–35. tourniquets and ‘compression’ dressings in excising limb [98] Napolitano LM, Fabian TC, Kelly KM, Bailey JA, Block EF, burns. J Trauma 1986;26:47–50. Langholff W, Enny C, Corwin HL. Improved survival of[78] Greenhalgh DG, Gamelli RL, Collins J, Sood R, Mozingo DW, critically ill trauma patients treated with recombinant Gray TE, et al. Recombinant thrombin: safety and human erythropoietin. J Trauma 2008;65(August (2)):285– immunogenicity in burn wound excision and grafting. J 97 [discussion 297–9]. Burn Care Res 2009;30:371–9. [99] Siren AL, Fratelli M, Brines M, Goemans C, Casagrande S,[79] Pallua N, Wolter T, Markowicz M. Platelet-rich plasma in Lewczuk P, et al. Erythropoietin prevents neuronal burns. Burns 2010;36:4–8. apoptosis after cerebral ischemia metabolic stress. Proc[80] Comments on ‘‘Platelet-rich plasma in burns’’ Curinga G, Natl Acad Sci USA 2001;98:4044–9. Scherer SS, Rusciani A, Gherardini G, Pietramaggiori G. [100] Celik M, Gokmen N, Erbayraktar S, Akhisaroglu M, Konakc Burns. 2009 Dec 18 [Epub ahead of print]. S, Ulukus C, et al. Erythropoietin prevents motor neuron[81] Sheridan RL, Szyfelbein SK. Trends in blood conservation apoptosis and neurologic disability in experimental spinal in burn care. Burns 2001;27:272–6. cord ischemic injury. Proc Natl Acad Sci USA 2002;99:2258–[82] Woodson LC, Sherwood ER, Aarsland A, Talon M, Kinsky 63. MP, Morvant EM. Anesthesia for burned patients. In: [101] Grimm C, Wenzel A, Groszer M, Mayser H, Seeliger M, Herndon DN, editor. Total burn care. London: Saunders Samardzija M, et al. HIF-1-induced erythropoietin in the Co; 2007. p. 221. hypoxic retina protects against light-induced retinal[83] Holcomb JB, Spinella PC. Optimal use of blood in trauma degeneration. Nat Med 2002;8:718–24. patients. Biologicals 2010;38(January (1)):72–7 [Epub 2010 [102] Ogilvie M, Yu X, Nicolas-Metral V, Pulido SM, Liu C, Ruegg Jan 13]. UT, et al. Erythropoietin stimulates proliferation and[84] Fraga GP, Bansal V, Coimbra R. Transfusion of blood interferes with differentiation of myoblast. J Biol Chem products in trauma: an update. J Emerg Med 2009 [Epub 2000;275:39754–61. ahead of print Apr 1]. [103] Calvillo L, Latini R, Kajstura J, Leri A, Anversa P, Ghezzi P,[85] Curreri PW, Richmond D, Marvin J, Baxter CR. Dietary et al. Recombinant human erythropoietin protects the requirements of patients with major burns. J Am Diet myocardium from ischemia–reperfusion injury and Assoc 1974;65:415–8. promotes beneficial remodeling. Proc Natl Acad Sci USA[86] Hanumadass ML, Kagan RJ, Matsuda T. Management of 2003;100:4802–6. pediatric burns. In: Vidyasagar D, Sarnaik AP, editors. [104] McIntyre LA, Hebert PC. Can we safely restrict transfusion Neonatal and pediatric intensive care. Littleton: PSG; 1985. in trauma patients? Curr Opin Crit Care 2006;12: p. 215–26. 575–83.[87] Bobbio-Pallavicini F, Verde G, Spriano P, Losi R, Bosatra [105] Goodnough LT, Shander A, Brecher ME. Transfusion MG, Braschi A, et al. Body iron status in critically ill medicine: looking to the future. Lancet 2003;361:161–9. patients: significance of serum ferritin. Intensive Care Med [106] Goodnough LT. Risks of Blood Transfusion. Anesthesiol 1989;115:171–8. Clin N Am 2005;23:241–52. ´˜[88] Belmonte JA, Ibanez L, Ras MR, Aulesa C, Vinzo J, Iglesias J, [107] Opelz G, Terasaki PI. Improvement of kidney-graft et al. Iron metabolism in burned children. Eur J Pediatr survival with increased numbers of blood transfusions. N 1999;158:556–9. Engl J Med 1978;299:799–803.[89] Patruta SI, Horl WH. Iron and infection. Kidney Int Suppl ¨ [108] Mowbray JF, Gibbings C, Liddell H, Reginald PW, 1999;69:S125–30. Underwood JL, Beard RW. Controlled trial of treatment of[90] Rudis MI, Jacobi J, Hassan E, Dasta JF. Managing anemia in recurrent spontaneous abortion by immunization with the critically ill patient. Pharmacotherapy 2004;24:229–47. paternal cells. Lancet 1985;1:941.[91] Fleming RY, Herndon DN, Vaidya S, Nichols RJ, Desai MH, [109] Bordin JO, Heddle NM, Blajchman MA. Biologic effects of Rutan RL, et al. The effect of erythropoietin in normal leukocytes present in transfused cellular blood products. healthy volunteers and pediatric patients with burn Blood 1994;84:1703–21. injuries. Surgery 1992;112:424–31 [discussion 431–2]. [110] Gong MN, Thompson BT, Williams P, Pothier L, Boyce PD,[92] Wallner S, Vautrin R, Katz J, Murphy J. The anemia of Christiani DC. Clinical predictors of and mortality in acute thermal injury: partial characterization of an erythroid respiratory distress syndrome: potential role of red cell inhibitory substance. J Trauma 1987;27:639–45. transfusion. Crit Care Med 2005;33:1191–8.
  11. 11. 752 burns 37 (2011) 742–752[111] Shorr AF, Jackson WL, Kelly KM, Fu M, Kollef MH. report of a clinical look-back investigation. JAMA Transfusion practice and blood stream infections in 2002;287:1968–71. critically ill patients. Chest 2005;127:1722–8. [115] Sazama K. Transfusion errors: scope of the problem,[112] Kopko PM. Leukocyte antibodies and biologically active consequences, and solutions. Curr Hematol Rep mediators in the pathogenesis of transfusion-related 2003;2:518–21. acute lung injury. Curr Hematol Rep 2004;3:456–61. [116] Williamson LM, Lowe S, Love E, Cohen H, Soldan K,[113] Janatpour K, Holland PV. Noninfectious serious hazards of McClelland DBL, et al. Serious hazards of transfusion. transfusion. Curr Hematol Rep 2002;1:149–55. Initiative: analysis of first two annual reports. BMJ[114] Kopko PM, Marshall CS, MacKenzie MR, Holland PV, 1999;319:16–9. Popovsky MA. Transfusion-related acute lung injury:

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