Damage control resuscitation for patients with major traumaBMJ 2009; 338 doi: https://doi.org/10.1136/bmj.b1778 (Published 05 June 2009) Cite this as: BMJ 2009;338:b1778
All rapid responses
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
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.
2. R. G. Fiddian-Green. Splanchnic ischaemia and multiple organ
failure in the critically ill. Ann R Coll Surg Engl. 1988 May; 70(3):
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-
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
5. RG Fiddian-Green. Haemodynamic and/or tonometric monitoring in
cardiac surgery. Br J Anaesth. 2000 Jan;84(1):128.
Tonometric patents issued in my name
Competing interests: No competing interests
The current article ‘management of major trauma’  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
. 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) .
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 .
In contrast, the prevention (not management and treatment) of acidosis 
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 :
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  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 :
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
So how should major haemorrhage be treated?
Do not start fluid therapy with crystalloids (only 20% remain
intravascular) as previously recommended ; begin with balanced
colloids  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 : 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 . 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.
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. 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-
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:
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)
Competing interests: No competing interests
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
3. Kessel DO and Nicholson AA. Trauma services must improve. BMJ
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
6. Gaarder C, Dormagen AB, Eken T et al. Non-operative management of
splenic injuries: improved results with angioembolization. J Trauma
Competing interests: No competing interests
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
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
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
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: No competing interests
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.
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: No competing interests