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Initial administration of hydroxyl starch vs lactated Ringer after liver trauma in the pig
- Morten Zaar, Brian Lauritzen, Niels H. Secher, Torben Krantz, Henning B. Nielsen, Per L. Madsen, and Pär I. Johansson (2 March 2009)
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Hydroxyethyl starch vs lactated Ringer after liver trauma
- R Jonathan T Wilson (2 February 2009)
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Initial administration of hydroxyethyl starch vs lactated Ringer after liver trauma in the pig
- James Geoghegan (2 February 2009)
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Morten Zaar Rigshospitalet, Brian Lauritzen, Niels H. Secher, Torben Krantz, Henning B. Nielsen, Per L. Madsen, and Pär I. Johansson
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We thank Wilson (1) and Geoghegan (2) for their interest in the acute treatment of haemorrhage. We were not a priori for or against the use of colloids for trauma patients, but considered that the volume expansion effect of hydroxyethyl starch 130/0.4 (HES; Voluven®, Fresenius Kabi; HES 130/0.4 60 mg ml-1, Na+ 154 mmol l-1, Cl- 154 mmol l-1, osmolarity 308 mosm l-1, pH 4.0-5.5) might provide for cardiovascular stability during ongoing haemorrhage as exemplified by a liver trauma (3). With the smaller volume expansion effect of lactated Ringer’s solution (RL; Fresenius Kabi; Na+ 130 mmol l-1, K+ 4 mmol l-1, Ca2+ 1.5 mmol l-1, Cl- 109 mmol l-1, lactate 28 mmol l-1, osmolarity 260 mosm l-1, pH ~6), we can state only that it was a surprise that the crystalloid solution was associated with a better outcome in regard to the time oxygen uptake was maintained. In addition, in the group for whom RL was administrated, bleeding was terminated in six of the seven pigs. Volume treatment was delayed to reflect the assumed response time of a critical care team and the aim was to set up a time frame for cardiovascular stability that would allow transport to where definitive surgery could be performed. That the variables were followed until death was, therefore, a result of the experimental design rather than being a predefined aim of the study. Accordingly, the total amount of fluid provided is somewhat irrelevant, considering that for the trauma patient, blood, plasma, and thrombocytes would be, provided in a balanced order, as soon as the patient arrives at the emergency room (4). Only the volume resuscitation regime until arrival at the trauma centre is considered to reflect what the patient might be exposed to and although that regime was chosen somewhat arbitrary, we were inspired by Ferreira et al. addressing near-fatal experimental shock (5). As Geoghegan (2) suggests, a strategy that excludes aggressive resuscitation would be of interest. Such an evaluation has been carried out in dogs and demonstrated that with a target MAP of 60 mm Hg, oxygen delivery is larger when resuscitation is with HES than with RL (6). The presented results (3) show that oxygen delivery and uptake were maintained during initial fluid resuscitation for both the HES- and RL-group, although the blood loss for the HES-group exceeded that of the RL-group and, because of the uncontrolled blood loss, oxygen delivery and, importantly, uptake decreased shortly after the initial resuscitation phase in the HES-group. Table 1 aimed to illustrate to what extent the two groups of pigs were comparable (3). In order to provide information relevant to the time at which transport to a hospital might have taken place, volume of fluid, bicarbonate, base excess, ionized calcium, and pH at the 37th min are provided (Table). The range of the fluid volume reflects that in the HES- group, pigs developed uncontrolled haemorrhage, while in the RL-group, six pigs ceased to bleed. We did not analyse for chloride levels but agree that a balanced resuscitation fluid would be preferred. Thrombelastography evaluated whether coagulation competence would be affected by the blood loss. Others show that HES may have a detrimental effect on the coagulation competence, while RL provides some assistance to the coagulation competence at low levels of haemodilution (7, 8). We agree that the chosen regime was extreme by focusing on the volume expansion effect of HES and in consequence of the results we do not recommend such a strategy. In fact, a consequence of the present findings could be that for patients for whom bleeding is the main acute problem, HES should be avoided and, as mentioned, we focus on balanced blood administration to not only trauma patients but also to patients with a ruptured aortic aneurism and for both groups of patients survival seems to be enhanced (4, 9). The most important message of the study is that it is important which strategy is chosen for treatment of haemorrhage. Considering that RL was able to terminate haemorrhage in only six of seven pigs it is, at least to us, interesting whether treatment should include immediate administration of e.g. tranexamic acid or NovoSeven®. References 1. Wilson RJT. Hydroxyethyl starch vs lactated Ringer after liver trauma. Br J Anaesth 2009 2. Geoghegan J. Initial administration of hydroxyethyl starch vs lactated Ringer after liver trauma in the pig. Br J Anaesth 2009 3. Zaar M, Lauritzen B, Secher NH, et al. Initial administration of hydroxyethyl starch vs lactated Ringer after liver trauma in the pig. Br J Anaesth 2009; 102: 221-6 4. Johansson PI, Stensballe J. Effect of haemostatic control resuscitation on mortality in massively bleeding patients: a before and after study. Vox Sang 2009; 96: 111-8 5. Ferreira EL, Terzi RG, Silva WA, de Moraes AC. Early colloid replacement therapy in a near-fatal model of hemorrhagic shock. Anesth Analg 2005; 101: 1785-91 6. Friedman Z, Berkenstadt H, Preisman S, Perel A. A comparison of lactated ringer's solution to hydroxyethyl starch 6% in a model of severe hemorrhagic shock and continuous bleeding in dogs. Anesth Analg 2003; 96: 39-45 7. Roche AM, James MF, Bennett-Guerrero E, Mythen MG. A head-to-head comparison of the in vitro coagulation effects of saline-based and balanced electrolyte crystalloid and colloid intravenous fluids. Anesth Analg 2006; 102: 1274-9 8. Nielsen VG. Colloids decrease clot propagation and strength: role of factor XIII-fibrin polymer and thrombin-fibrinogen interactions. Acta Anaesthesiol Scand 2005; 49: 1163-71 9. Johansson PI, Swiatek F, Jørgensen L, Jensen LP, Secher NH. Intraoperative platelet and plasma improves survival in patients operated for a rAAA: A follow-up evaluation. Eur J Vasc Endovasc Surg 2008; 36: 397 -400 Conflict of Interest:None declared |
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R Jonathan T Wilson, Consultant Anaesthetist York Hospital
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I read the article by Zaar and colleagues in this month's BJA with great interest, and particularly as a signed up member of the pro-colloid school - of-thought in the great fluid debate(1). There are serious flaws in both the design of this study, and in the presentation of the data, which make this particular laboratory study of very limited use, and may even precipitate harmful practice if incorrectly interpreted by the inexperienced anaesthetist. In the study pigs were haemorrhaged and then given either colloid (HES) or Ringer's lactate (RL) in a fixed recipe approach in order to expand the circulation. The findings were that HES was associated with a greater degree of ongoing uncontrolled haemorrhage in comparison to RL. The design has no applicability to a real trauma scenario, as the volumes of fluid given in the first 30 minutes were unrealistically large and dangerous. This was particularly so for the HES group, who received the maximum 24-hour recommended dose (50 ml/kg/24 hours) in the first 30 minutes alone, an average dose of 50.6 ml/kg, in response to an initial bleed of 6.5 ml/kg, a colloid:blood loss ratio of 7.7, which in clinical practice should be nearer 1.0, in the absence of goal-directed monitoring. It is not surprising that such a massive over-transfusion of fluid, which tends to stay in the intra- vascular compartment, would precipitate failure of the clotting system, let alone cardiovascular collapse. At least the RL given to the other group would have been distributed within the interstitial compartment to an extent. I am curious as to why the authors chose such an extreme protocol. A second factor is the carrier solution for the starch colloid. We are not given details of this, but if it is normal saline, as is reasonable to assume, then this may disrupt coagulation more than equivalent balanced solutions, such as the RL used in this study(2). In addition, due to the volumes given, the HES group will have received 1.8 times more chloride ions than the RL group in the first 30 minutes alone, which may lead to ongoing hyperchloraemic acidosis. In addition to the above concerns, there seems to be a curious lack of data presented in this paper. Table 1 gives us baseline cardiovascular and biochemical data for both study groups, but there is no presentation of the same variables at the end of the experiment or at any time between, aside from some figures of haemodynamic data. What is the point of telling us what the baseline base excess is, for example, when we are not told the values at the end of the study? Likewise, calcium and chloride levels should have been presented at end of study as well. We are presented with thromboelastography data at baseline and 7 minutes, but not at any time after, despite the large differences in observed blood loss. Of most concern of all though, we are not even presented with the final total amount of fluids given by the study end, which is quite extraordinary, given that this is the primary intervention in this study! As a manuscript reviewer for the BJA, I am quite surprised that these omissions were allowed by the editorial process. In summary, I think that the combination of the omission of important data, and, most importantly, a study protocol that is so far removed from clinical trauma practice, renders the results of this study irrelevant for the working anaesthetist. 1. Zaar M, Lauritzen B, Secher, NH, Krantz T, Nielsen HB, Madsen PL, Johansson PI. Initial administration of hydroxyethyl starch vs lactated Ringer after liver trauma in the pig. Br J Anaesth 2009; 102:221-6. 2. Gan TJ, Bennett-Guerrero E, Phillips-Bute B, Wakeling H, Moskowitz DM, Olufalabi y, Konstadt SN et al. Hextend, a physiologically balanced plasma expander for large volume use in major surgery: a randomized Phase III clinical trial. Anesth Analg 1999; 88:992-8. Conflict of Interest:None declared |
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James Geoghegan, SpR Anaesthetics University Hospital Birmingham NHS Foundation Trust
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I would like to commend Zaar and colleagues for their trial comparing hydoxyethyl starch (HES) with lactated Ringer’s solution (RL) intravenous fluid administration after liver trauma in pigs.1 There are some sections of their paper that I would like to consider in greater detail: Firstly, they hypothesise that the increased blood loss in the HES group may have been due to increased intravascular expansion leading to disruption of haemostatic plugs. This theory is supported by previous studies.2 Other reasons for the increased blood loss in the HES group (who had greater volumes of intravenous fluids administered) maybe because dilution of red blood cell mass may decrease blood viscosity and therefore may increase flow around an incomplete thrombus3 or because dilution of clotting factors may inhibit clot formation.4 Secondly, they state that “..although HES provided effective support to the intravascular volume after a liver trauma in the pig, it also provoked uncontrolled haemorrhage…” Their results section shows a graph detailing changes in blood pressure over time for the two groups. The RL group appear to consistently have a lower blood pressure (BP) (although no mention is made whether this difference is significant or not). I suspect the two findings are related: the HES provided better circulatory support, which caused more blood loss. The dangers of aggressive fluid resuscitation in the trauma patient have been known for some time: “Injection of a fluid that will increase blood pressure has dangers in itself. Haemorrhage in a case of shock may not have occurred to a marked degree because blood pressure has been too low and the flow too scant to overcome the obstacle offered by a clot. If the pressure is raised before the surgeon is ready to check any bleeding that may take place, blood that is sorely needed may be lost”¬.5 Animal models of uncontrolled haemorrhage (which category this study would fall into) show increased mortality and blood loss if there is fluid administration prior to haemorrhage control 6-9 and that aggressive fluid resuscitation increases mortality.3;4;10;11 A recent systematic review of animal trials demonstrated a relative risk of death associated with hypotensive resuscitation of 0.37 (95% CI, 0.27-0.50) when compared with normotensive resuscitation.12 Finally, they state that to distinguish between the effects of HES on increased intravascular expansion and possible effects of HES on coagulation, “more experiments with the use of, for example, albumin are necessary”. I would like to suggest that another area for study would be a repeat of this experiment comparing HES with RL, but rather than giving a fixed formula of each, only give as much fluid as is needed to maintain a predetermined BP. That would then exclude aggressive resuscitation as a cause for the observed uncontrolled haemorrhage. Reference List (1) Zaar M, Lauritzen NH, Secher NH, Krantz T, Nielsen HB, Madsen PL et al. Initial administration of hydroxyethyl starch vs lactated Ringer after liver trauma in the pig. British Journal of Anaesthesia 102[2], 221-226. 2009. (2) Shaftan GW, Chiu CJ, Dennis C, Harris B. Fundamentals of physiologic control of arterial hemorrhage. Surgery 1965; 58(5):851-856. (3) Bickell WH, Bruttig SP, Millnamow GA, O'Benar J, Wade CE. Use of hypertonic saline/dextran versus lactated Ringer's solution as a resuscitation fluid after uncontrolled aortic hemorrhage in anesthetized swine. Annals of Emergency Medicine 1992; 21(9):1077-1085. (4) Bickell WH, Bruttig SP, Millnamow GA, O'Benar J, Wade CE. The detrimental effects of intravenous crystalloid after aortotomy in swine.[see comment]. Surgery 1991; 110(3):529-536. (5) Cannon WB, Fraser J, Cowell EM. The preventive treatment of wound shock. Journal of the American Medical Asociation 1918; 70(9):618-621. (6) Capone A, Safar P, Stezoski SW, Peitzman A, Tisherman S. Uncontrolled hemorrhagic shock outcome model in rats. Resuscitation 1995; 29(2):143-152. (7) Krausz MM, Landau EH, Klin B, Gross D. Hypertonic saline treatment of uncontrolled hemorrhagic shock at different periods from bleeding. Arch Surg 1992; 127(1):93-96. (8) Krausz MM, Bar-Ziv M, Rabinovici R, Gross D. "Scoop and run" or stabilize hemorrhagic shock with normal saline or small-volume hypertonic saline? Journal of Trauma-Injury Infection & Critical Care 1992; 33(1):6-10. (9) Rabinovici R, Krausz MM, Feuerstein G. Control of bleeding is essential for a successful treatment of hemorrhagic shock with 7.5 per cent sodium chloride solution. Surgery, Gynecology & Obstetrics 1991; 173(2):98- 106. (10) Craig RL, Poole GV. Resuscitation in uncontrolled hemorrhage. American Surgeon 1994; 60(1):59- 62. (11) Stern SA, Dronen SC, Wang X. Multiple resuscitation regimens in a near-fatal porcine aortic injury hemorrhage model.[see comment]. Academic Emergency Medicine 1995; 2(2):89-97. (12) Mapstone J, Roberts I, Evans P. Fluid resuscitation strategies: a systematic review of animal trials. [Review] [52 refs]. Journal of Trauma-Injury Infection & Critical Care 2003; 55(3):571-589. Conflict of Interest:None declared |
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