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CLINICAL REVIEW: Jan O Jansen, Rhys Thomas, Malcolm A Loudon, and Adam Brooks Damage control resuscitation for patients with major trauma BMJ 2009; 338: b1778 [Full text]

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Lessons from Formula one for damage control resuscitation

Jecko Thachil   (12 June 2009)

Are civilians any different?

Ronan O'Leary   (16 June 2009)

Consider radiology in resuscitation for civilian major trauma

Ian A Zealley   (22 June 2009)

In response to Damage control resuscitation 2009

Kai Zacharowski, Rolf Zander   (30 July 2009)

Re: Management of acidosis in trauma.

Richard G Fiddian-Green   (1 August 2009)

Lessons from Formula one for damage control resuscitation 12 June 2009
Jecko Thachil, Research Fellow University of Liverpool Send response to journal: Re: Lessons from Formula one for damage control resuscitation	Jansen and colleagues give a clear and thorough discussion on the management of major trauma with resuscitation aimed at damage control.1 One of the key issues in this resuscitative effort is time management – the quicker the better; leading to less adverse consequences from the lethal triad. Also the co-ordination of the different groups, including the anaesthetist, trauma surgeon, emergency staff and the blood bank and other laboratories is critical for the best outcome. Lots can be learnt in this respect from the flamboyant Formula one circuit where the pit stop car management is a crucial part of the team success. The role of a “person in charge” to coordinate all the resuscitation measures is as important in saving lives as the resuscitation measures themselves. Also designated members to deal with the different aspects of the management can provide a smoother, and less complicated setting in what can otherwise be a chaotic resuscitation room. The key person could also keep records of the amount of the fluids and blood products administered (a legal requirement according to new European directive on traceability of blood products) 2, monitor the progress and outcome of the resuscitation measures, contact the relevant specialist, when necessary and coordinate with the laboratory and the blood bank, as required. Major trauma resuscitation drills in much the same way as the familiar fire drills can keep the team well-alert for the trauma situation. The Formula one has become a much safer circuit and hopefully lessons from their efforts can help us save many more lives through “well- coordinated” damage control resuscitation. References 1. Jan O Jansen, Rhys Thomas, Malcolm A Loudon, and Adam Brooks. Damage control resuscitation for patients with major trauma. BMJ 2009; 338: b1778 2. D. Stainsby, S. MacLennan, D. Thomas, J. Isaac and P.J. Hamilton, BCSH guidelines on the management of massive blood loss. Br J Haematol 2006; 135: 634–641 Competing interests: None declared
Are civilians any different? 16 June 2009
Ronan O'Leary, Registrar in anaesthesia and intensive care medicine West Yorkshire, UK Send response to journal: Re: Are civilians any different?	The review on the limitation of injury in severely injured patients by Jensen is fascinating and thought provoking1. We need to be cautious, however, about wide ranging application of the military experience to civilian medicine. There are a multitude of differences between military and civilian patients. Civilian patients are from a wider age range and include both children and the elderly, they suffer a range of co-morbidities, may be intoxicated and can present many hours after injury. Military patients are, typically, young men who are extremely physically fit with significant physiological reserve and very low rates of co-existent disease. The logistical framework for the management of military patients differs from that seen in civilian practice2. In the military there is a high degree of the awareness of the importance of the immediate management of injured soldiers. One in four soldiers are trained in the stabilisation of battlefield causalities. These soldiers can provide immediate haemorrhage control, administer potent opioid analgesia (thus reducing the sympathetically mediated stress response), and can co-ordinate evacuation to definitive treatment. When evacuation occurs it is frequently by a team which includes a senior clinician experienced in the management of trauma. Finally, within the emergency department, the injured soldiers are managed by staff with considerable experience in the management of trauma. Furthermore the ED is located close to instantly available facilities and staff for cross sectional imaging and definitive surgical treatment. This is not to say that there is little that can be learned from military practice, on the contrary, military conflict has always driven innovation and technical advances, as the authors say. We should, however, be judicious about the rapid application of treatment strategies without careful research. 1. Jansen, J.O. et al. (2009). Damage control resuscitation for patients with major trauma. British Medical Journal, 338: b1778. 2. Mahoney, P.F. et al. (2007). The combat casualty care special edition. Journal of the Royal Army Medical Corps 153: 235-236. Competing interests: None declared
Consider radiology in resuscitation for civilian major trauma 22 June 2009
Ian A Zealley, Consultant Radiologist Ninewells Hospital, Dundee, DD1 9SY Send response to journal: Re: Consider radiology in resuscitation for civilian major trauma	Trauma patients who remain haemodynamically unstable during resuscitation are, in essence, bleeding to death. The recent review of resuscitation techniques for patients with major trauma (1) promotes the incorporation of damage control surgery into resuscitation pathways but does not mention the alternative of radiologically-guided endovascular haemostasis techniques. This is disappointing but unsurprising. A recent NCEPOD study of 795 episodes of trauma care (injury severity score 16 or greater) identified only one case in which interventional radiology techniques were applied (2). It is appropriate to re-quote from a paper cited by Kessel and Nicholson in their response (3) to the previous article in this series (4) that "therapeutic interventional radiology techniques have now become essential in the management of severely injured patients" (5). Although the review sets out to illustrate how lessons learned in military trauma management may be applied to civilian trauma care it should be borne in mid that a wider range of diagnostic and therapeutic options are generally available in the civilian setting. The current review describes damage control surgery as a potentially therapeutic elaboration of the secondary survey but, as the authors acknowledge, presents the already injured patient with a further major insult and is consequently associated with potential morbidity. The aim of damage control surgery is to stop haemorrhage and minimise contamination. Endovascular interventional radiology techniques can achieve both of these aims, either as the definitive haemostatic procedure or as a bridge to surgery in patients who are severely physiologically impaired and in whom surgery is undesirable in the hyperacute resuscitation setting. In one hospital the introduction of interventional radiology into a trauma care pathway for patients with splenic injuries led to a reduction in the average number of laparotomies per patient from 1.0 (range 0-7) to 0.6 (range 0-4) (p=0.02) accompanied by an increase in the spleen salvage rate from 57% to 74% (p=0.02) (6). Site(s) of bleeding in haemodynamically unstable trauma patients are most reliably identified by CT scanning (5). CT scanning should be incorporated into the secondary survey during resuscitation (3) as CT images provide the most comprehensive non-invasive assessment available and can guide good decision-making regarding the choice of surgical or endovascular haemostatic techniques in individual patients (5). Further, in the severely injured polytrauma patient CT scanning may also identify other unsuspected significant injuries which reveal that further resuscitation is futile, for instance major intracranial haemorrhage. CT scanning should form part of the secondary survey during the ongoing resuscitation of trauma patients and consideration should be given to endovascular radiologically-guided haemostatic techniques as a minimally invasive alternative to damage control surgery. 1. Jansen JO, Thomas R, Loudon MA, Brooks A. Damage control resuscitation for patients with major trauma. BMJ 2009;338:1436-40. 2. Trauma: Who cares? http://www.ncepod.org.uk/2007report2/Downloads/SIP_report.pdf (accessed 22 June 2009) 3. Kessel DO and Nicholson AA. Trauma services must improve. BMJ 2008;336:1205. 4. Jansen JO, Yule SR, Udon MA. Investigation of blunt abdominal trauma. BMJ 2008;336:9382-942. 5. Pryor JP, Braslow B, Reilly PM, Gullamondegi O, Hedrick JH, Schwab CW. The evolving role of interventional radiology in trauma care. J Trauma 2005;59:102-4. 6. Gaarder C, Dormagen AB, Eken T et al. Non-operative management of splenic injuries: improved results with angioembolization. J Trauma 2006;61:192-8. Competing interests: None declared
In response to Damage control resuscitation 2009 30 July 2009
Kai Zacharowski, Professor and Director Clinic of Anaesthesia, Intensive Care Medicine and Pain Therapy University Hospital Frankfurt, 60590 Frankfurt, Germany, Rolf Zander Send response to journal: Re: In response to Damage control resuscitation 2009	The current article ‘management of major trauma’ [5] requires essential additional information. Although the definition of “lethal triad” has been established and described as a combination of acute coagulopathy, hypothermia and acidosis during exsanguination of trauma patients, it is still deceptive. We define “lethal triad” differently; a better word would be causality and not combination. Coagulopathy in exsanguinating patients is almost always caused by acidosis and hypothermia and this is well documented. Coagulation activity declines by 10% when temperature declines by 1 °C [11]. Furthermore, the activity of three clotting factors is reduced by 50% at a pH of 7.2 (base deficit 12.5 mmol/l) and doubled at pH 7.6 (base excess 16.5 mmol/l) [8]. Therefore, we suggest the following: Major bleeding – reversing hypothermia, prevents acidosis! The reversal and the prevention of hypothermia can be accomplished quite easily. We recommend the early application of measures to reduce heat loss, whilst warming the hypothermic patient in order to achieve and maintain normothermia [11]. In contrast, the prevention (not management and treatment) of acidosis [5] is the key to effective therapy of coagulopathy during exsanguination. Contrary to in vitro findings, several studies in vivo revealed that despite successful correction of acidosis, coagulopathy was still present up to 12-18 hrs [4, 6, 7, 9]. What causes acidosis during major haemorrhage? The facts [14]: 1. As a result of blood loss, haemorrhagic shock is associated with hypoxia, and hence metabolic acidosis with an increased base deficit (BD, negative base excess) and lactate levels. 2. Recently, volume replacement solutions augmented preexisting acidosis via additional infusion- and dilution acidosis. Ringer’s lactate given during shock with consecutive lactic acidosis, causes additional calcium binding and thus leads to coagulopathy (10 mmol/l lactate levels cause a 50% decrease of ionized calcium). 3. The production and storage of packed red blood cells (RBCs) is associated with ‘RBC aging’. In freshly prepared RBCs, a BD of 20 mmol/l was classed as normal, while in 21-days old RBCs a BD of 40 mmol/l was measured. In contrast, freshly frozen plasma (FFP) presented high levels of citrate [12] and has alkalescent potential. 4. 21-days old RBCs induce hypocalcaemia due to their high lactate levels of 20 mmol/l. 5. The average age of RBCs at the time of transfusion is currently 20 days world-wide (90,000 RBCs units studied in 3 trials). The transfusion of 3 RBCs (approximately 1 litre) causes a ‘load’ of 40 mmol of H+-ions to the patient, while the kidney purges only 50 mmol of H+-ions daily. 6. A massive transfusion leads to metabolic acidosis and, hence coagulopathy. Mortality is strongly associated with the number and age of transfused RBCs; the latter fact is present when more than 5 RBC units are transfused (14,500 patients from 4 trials). What is the impact of acidosis following major haemorrhage? The facts [14]: 1. In 8,000 patients with polytrauma (4 trials) it has been shown that at the time of hospitalization, a BD of 15 mmol/l predicts a mortality rate of 50%. This number is comparable to 3,300 patients suffering from blunt trauma or gunshot wound. 2. Aside to age, injury severity score (ISS), Glasgow coma score (GCS) and pattern of injuries (head and extremity), the two most important predictive factors of mortality, i.e. BD and pro-thrombin time (PT) show a significant correlation in 4,000 poly-traumatic patients; inversely at a BD of 15 mmol/l the PT values averages to 50%. 3. Trauma patients with massive transfusion develop coagulopathy depending on the BD level. Survivors and non-survivors can be differentiated by observing their BD alone. A BD of approximately 20 mmol/l is predictive of limited survival. So how should major haemorrhage be treated? Do not start fluid therapy with crystalloids (only 20% remain intravascular) as previously recommended [11]; begin with balanced colloids [13] insuring that electrolytes (in particular calcium) and the acid-base state is not compromised (e.g. steady isotonic solutions such as HES 130/0.4 with BEpot of ~ 0 mmol/l). Potential BE (BEpot) describes the possible impact of a solution following infusion; this also includes anion metabolization and effects on the patient’s acid-base state. Balanced fluids containing acetate are superior to lactate preparations due to faster turnover of acetate in all organs. Lactate is degraded almost uniquely in the liver (by 80%). Therefore acetate solutions are also effective during shock. Furthermore, calcium binding and functional reduction of relevant levels does not exist for acetate. To summarize, the pattern of volume- or blood component therapy requires an urgent revision [10]: First balanced colloids, followed by plasma (volume, coagulation factors, acidosis prevention) and than fresh RBCs. We now raise the subject of "early or delayed” and, “deferring or restricting fluid administration" by "successful or less successful acidosis- prevention via an optimal volume regime". Is there a place for haemostatic agents? Additional attempts using clotting factors are limited: a massive transfusion limits the effectiveness of rFVIIa (NovoSeven) due to the fact that old RBCs maintain the acidosis. rFVIIa has its therapeutic window in patients with blunt or penetrating trauma, however, administration is required prior RBC transfusion and not after the 8th pack of RBCs [3]. As coagulation activity is strongly depending on the pH, one can assume that fibrinolysis as well as drugs modifying it (i.e. aprotinin, - aminocaproic acid, tranexamic acid) are influenced by the base deficit. How much FFP should one give? It seems that numerous groups have empirically approached the problem of the relation of FFP:RBC [references no. 15-20 in (5)]. The most impressive case numbers have been generated by Maegele et al. in 2008 [reference no. 20 in (5)] for massive transfusion (> 10 RBCs). The higher the ratio of FFP:RBC is inversely correlated to a fall in mortality, e.g. 24 h mortality is reduced from 33 to 11 %. This is of logical consequence owing to the fact that during massive transfusion (10 RBCs) with a ratio of 1:1 (FFP:RBC), the “fresh” RBC exhibit a BD of 6 mmol/l while 3 weeks “old” RBC exhibit a BD of 11 mmol/l in the patient (75 kg BW, ECFV 15 l). Lactate levels of the same patient increased by 5 mmol/l in the ECFV, which subsequently causes additional calcium binding of 0.25 mmol/l. In addition, simultaneous supply of lactate (via RBC) and citrate (via FFP) maintains the coagulopathy. Conclusion The key to effective treatment of haemorrhagic shock is by prevention of acidosis and hence of coagulopathy: This could be achieved by administration of first balanced acetate- and calcium-containing colloids, followed by FFPs (coagulation factors, volume substitution, alkalescent) and finally with only fresh RBCs. This subject has recently been addressed in The New England Journal, titled "New blood, old blood, or no blood?" [1]. References 1. Adamson JW: New blood, old blood, or no blood? N Engl J Med 2008; 358; 1295 – 1296 2. Basran S, Frumento RJ, Cohen A et al.: The association between duration of storage of transfused red blood cells and morbidity and mortality after reoperative cardiac surgery. Anesth Analg 2006; 103: 15-20 3. Boffard KD, Riou B, Warren B, et al: Recombinant factor VIIa as adjunctive therapy for bleeding control in severely injured trauma patients: two parallel randomized, placebo-controlled, doubleblind clinical trials. J Trauma 2005; 59: 8-15 4. Dunn EL, Moore EE, Breslich DJ et al.: Acidosis-induced coagulopathy. Surg Forum 1979; XXX: 471-473 5. Jansen JO, Thomas R, Loudon MA, Brooks A: Damage control resuscitation for patients whit major trauma. BMJ 2009; 338: b1778 6. Martini WZ, Dubick MA, Pusateri AE et al.: Does bicarbonate correct coagulation function impaired by acidosis in swine? J Trauma 2006; 61: 99- 106 7. Martini WZ, Dubick MA, Wade CE et al.: Evaluation of tris- hydroxymethylaminomethane on reversing coagulation abnormalities caused by acidosis in pigs. Crit Care Med 2007; 35:1568-1574 8. Meng, ZH, Wolberg AS, Monroe DM et al.: The effect of temperature and pH on the activity of factor VIIa: Implications for the efficacy of high- dose factor VIIa in hypothermic and acidotic patients. J Trauma 2003; 55: 886-891 9. Rutherford RB, West RL, Hardaway RM: Coagulation changes during experimental hemorrhagic shock. Ann Surg 1966; 164: 203-214 10. Spahn DR, Rossaint R: Coagulopathy and blood component transfusion in trauma. Br J Anaesth 2005; 95: 130-139 11. Spahn DR, Cerny V, Coats TJ et al.: Management of bleeding following major trauma: European guideline. Crit Care 2007; 11: (R17) 1-22 12. Zander R, Sümpelmann R: Säure-Basen-Status gelagerter und gewaschener Erythrozyten. Anästhesiol Intensivmed Notfallmed Schmerzther 2001: 36 (Suppl. 1): 25-30 13. Zander R: Infusion fluids: Why should they be balanced solutions? EJHP Practice 2006; 6: 60–62 14. Zander R: Fluid Management (2nd expanded ed.) Bibliomed - Med. Verlagsgesellschaft, Melsungen (Germany) 2009. Available (as pdf document) under www.Physioklin.de Competing interests: None declared
Re: Management of acidosis in trauma. 1 August 2009
Richard G Fiddian-Green, FRCS, FACS None Send response to journal: Re: Re: Management of acidosis in trauma.	In his rapid response Kai Zacharowski, Professor and Director Clinic of Anaesthesia, Intensive Care Medicine and Pain Therapy at University Hospital Frankfurt, concluded that, "The key to effective treatment of haemorrhagic shock is..[the] prevention of [an arterial] acidosis..". This is not enough (1,2) neither does it address the need to reduce the time for a abnormally low intramucosal pH to be returned to normality (3). Most importantly it does not address the adverse effects current forms of volume and haemodynamic management administered by "intensivists" have had upon the gastric intramcuosal pH after patients have been returned to the ICU (4,5). 1. C. Hamilton-Davies, M. G. Mythen, J. B. Salmon, D. Jacobson, A. Shukla and A. R. Webb. Comparison of commonly used clinical indicators of hypovolaemia with gastrointestinal tonometry. Intensive Care Medicine. 1997;23:276-281. 2. R. G. Fiddian-Green. Splanchnic ischaemia and multiple organ failure in the critically ill. Ann R Coll Surg Engl. 1988 May; 70(3): 128–134. 3. Ivatury, Rao R, Simon, Ronald J, Havriliak, Damien, Garcia, Carlos, Greenbarg, James, Stahl, William M. Gastric Mucosal pH and Oxygen Delivery and Oxygen Consumption Indices in the Assessment of Adequacy of Resuscitation after Trauma: A Prospective, Randomized Study The Journal of Trauma: Injury, Infection, and Critical Care: 1995;39:128- 136. 4. Nicholas Maynard, David Bihari,Richard Beale, Mark Smithies, Graham Baldock, Robert Mason, Ian McColl. Assessment of Splanchnic Oxygenation by Gastric Tonometry in Patients With Acute Circulatory Failure. JAMA. 1993;270(10):1203-1210. 5. RG Fiddian-Green. Haemodynamic and/or tonometric monitoring in cardiac surgery. Br J Anaesth. 2000 Jan;84(1):128. Competing interests: Tonometric patents issued in my name