Injury, Int. J.

Care Injured (2004) 35, 713—722

Damage control surgery and intensive care

Michael J.A. Parra,b,*, Tareq Alabdia

a
Department of Intensive Care, Liverpool Hospital, Sydney, Australia
b
University of New South Wales, Sydney, Australia

KEYWORDS Summary The introduction and establishment of the ‘damage control surgery’ con-
Damage control surgery cept has led to increasing numbers of severely injured and unstable patients being
(DCS); presented to Intensive Care Units (ICU) for ongoing resuscitation. These patients
Hypovolaemia; present many challenges for the Intensive Care team and emphasise the need for a
Intensive Care Unit multidisciplinary approach to optimise trauma patient management. Multiple issues
need to be addressed simultaneously while the overall aim is to rapidly achieve a
physiological environment that will allow the best possible recovery. The ‘lethal triad’
of hypothermia, acidosis, and coagulopathy due to initial hypovolaemia require
aggressive correction. From the outset ICU management must also attempt to minimise
the complications of these injuries and the resuscitative process. This review will
address some of the key issues relating to the care of these patients in the ICU.
ß 2004 Elsevier Ltd. All rights reserved.

Introduction contributing to the significant improvements in out-

The introduction and establishment of the damage
control surgery (DCS) has led to severely injured and
unstable patients being presented to Intensive Care
Units for ongoing resuscitation. These patients pre-
sent many challenges for the Intensive Care team
and emphasise the need for a multidisciplinary
approach to optimise patient management. Multi-
ple issues need to be addressed simultaneously
while the overall aim is to rapidly achieve a phy-
siological environment that will allow the best pos-
sible recovery. The ‘lethal triad’ of hypothermia,
acidosis, and coagulopathy due to initial hypovo-
laemia require aggressive correction. From the out-
set ICU management must also attempt to minimise
the complications of these injuries and the resusci-
tative process. This review will address some of the
key issues related to the care of these patients in
the ICU. Improved ICU management is credited as
*Corresponding author. Tel.: þ612-9828-3000;
fax: þ612-9828-3551.
E-mail address: m.parr@unsw.edu.au (M.J.A. Parr).
0020–1383/$ — see front matter ß 2004 Elsevier Ltd. All rights reserved.
doi:10.1016/j.injury.2004.03.010
come from DCS in recent years.33
The concepts of damage control
applied to intensive care
The principles at the core of damage control phi-
losophy are not foreign to current ICU practice. The
concept of delay in definitive therapy while systems
support is maintained is in fact the core principle of
management for many intensive care patients. The
quote from Voltaire, ‘‘The art of medicine consists
of amusing the patient while nature curses the
disease’’ remains not too far from the truth. Often
there is no definitive procedure that is curative and
there is great reliance on the system and organ
support therapy available in intensive care while
the initial inflammatory, infective or traumatic pro-
cess resolves. Clearly the level of system or organ
support can be very intensive or even complete and
as with DCS is aimed at rapidly reversing abnormal
physiology to produce the best possible environ-
ment for optimal recovery. Within this philosophy
714
there are clear circumstances when, as with DCS,
procedures and treatments may be delayed and
deferred until more stability or improvement has
been achieved. The following will serve as exam-
ples: the trauma patient with a severe brain injury
will not be put through extensive radiology to
attempt to clear the thoracolumbar spine when
the priority of management is to achieve a stable
intra-cranial pressure. Field cannulae and resusci-
tation cannulae are not changed and procedures
that may involve bleeding are delayed until coagu-
lopathy is fully reversed. For the medical hypother-
mic patient, all non-life-saving procedures are
delayed until effective rewarming has taken place.
In essence the principles proposed by the DCS
approach are fully consistent with current high
quality Intensive Care Medicine.
Handover to the intensive care team
DCS patients will have been in the operating room
for a significant period of time and the decision to
adopt a DCS strategy should be communicated to
the ICU team prior to patient arrival in the ICU. This
will provide the opportunity for the ICU team to
prepare for optimal care of the patient. In alerting
the ICU team, details of the trauma, initial resusci-
tation and surgical intervention will be described.
The extent of the acidosis, coagulopathy and
hypothermia can be discussed and the strategies
to reverse these can then be planned. This may
include such issues as preparing an isolation room
to high ambient temperature, preparing warming
devices, obtaining warm fluids, preparing special
equipment (e.g. ventilators and renal replacement
therapy (RRT) machines) and alerting the Blood
bank to the likely on-going requirement for blood
products. Early discussion may also help in identify-
ing patients that require angiography with a view to
embolisation of identified active haemorrhage.
Table 1 Key issues for early ICU management
Identifying patients who may benefit from surgical re-exploration or
radiology/angiographic guided haemorrhage control procedures
Correction of hypothermia
Correction of coagulopathy
Correction of acidosis
Fluid and blood product therapy
Monitoring resuscitation end points
Assessing for missed injuries (tertiary survey)
Planing return to OR
Initiating specific therapy to reduce complications (ACS, peptic ulceration, thrombo-prophylaxis, protective lung
ventilation, infection control and appropriate antimicrobial therapy)
Maintaining effective communication
M.J.A. Parr, T. Alabdi
Upon arrival in the ICU, a brief primary survey,
confirming the ABCD status of the patient should be
repeated. These patients are often unstable during
transfer and serious things can happen in transit
that require immediate attention on arrival in the
ICU. Following this, there are a number of key issues
to be identified early and addressed during ICU
management (Table 1).
Identifying patients for surgical re-
exploration or angiography-guided
haemorrhage control procedures
The principles of damage control surgery dictate
that there is no further benefit to the patient from
continued operative intervention and definitive sur-
gical procedure should be carried out after correc-
tion of the serious metabolic abnormalities. There
may however be situations where these patients do
require further surgical or radiology-guided hae-
morrhage control procedures.
Occasionally a patient who has been returned to
the ICU for correction of acidosis, hypothermia and
coagulopathy will suddenly haemorrhage from a
vessel that was not identified at the initial opera-
tion. This may be revealed as haemodynamic
instability with rapid filling of drains left at opera-
tion or a distending abdomen. This may be in rela-
tion to vessels not identified as bleeding due to
vasospasm and the poor perfusion at operation
which now with improving temperatures and reper-
fusion are revealed as active bleeding sites. Urgent
re-exploration to stop the haemorrhage may be
lifesaving. Usually however all surgically controlla-
ble bleeding will have been dealt with at the time of
operation and the ongoing haemorrhage is likely to
represent bleeding from a site that cannot be man-
aged in the operating room. Some of these patients
may benefit from interventional radiology with
angiography followed by embolisation of identified
Damage control surgery and intensive care
actively bleeding vessels. This strategy has been
credited with improved outcomes.15,27,36 This
approach of urgent post-operative angiography
should be considered for patients with complex
hepatic injury (e.g. for deep or transhepatic
GSW), when intrahepatic arterial bleeding or an
AV fistula can be embolised/occluded. Hepatic
angiography appears to be a safe adjunct to the
principles of damage control.32 Angiography should
also be considered for patients with significant
retroperitoneal, pelvic or deep muscle injuries
identified at surgery. A contrast blush seen at angio-
graphy indicates active arterial bleeding and the
need for embolisation. Angiography before damage
control laparotomy may also be indicated if there is
a very high suspicion of a bleeding lesion that may
be amenable to embolisation.
Clearly, safe patient transfer to the angiography
suite will require a coordinated approach between
intensive care, surgical and radiology staff. The
monitoring, ongoing resuscitation, and medical
and nursing supervision of these patients in the
radiology department needs to be of the same
standards as the ICU and OR for optimal outcome
and serves to emphasise the importance of seeing
‘intensive/critical care as a process and not a loca-
tion’. Therefore, patients should be transferred
with full monitoring in place and with the equip-
ment to provide optimal care including a high capa-
city fluid warmer and a forced air heating device
that can be used in the radiology department. This
will require a large team of individuals to coordinate
safe transfer.
Return to operating room
Planning for return to the OR for definitive care
follows successful resuscitation, when the patient
is normothermic, with corrected coagulation and
platelet count, and resolved acidosis. This resus-
citation may occasionally be achieved over a few
hours but is usually optimal at 24—48 h. Compro-
mising and returning to the OR before adequate
resuscitation will leave the patient less likely to
withstand the prolonged procedure of definitive
surgery. Early re-operation may, however, be
appropriate if gross contamination was initially
present, to reduce the incidence of subsequent
infection. Prior to returning to the OR, the route
for on-going feeding should be considered as it
may be appropriate to place a nasojejunal or
enterostomy feeding tube at the time of definitive
surgery. Abdominal closure is performed when
oedema has resolved enough to allow closure with-
out tension.
715
Abdominal compartment syndrome
Patients managed by damage control laparotomy
are at high risk of intra-abdominal hypertension and
abdominal compartment syndrome. 30 For this rea-
son the abdomen is only partially (or temporarily)
closed. Despite this, intra-abdominal hypertension
and abdominal compartment syndrome may still
occur because of increasing visceral swelling,
expanding haematomata, and the use of abdominal
packs. Signs of a distended abdomen, increased
ventilator inspiratory pressure requirement, raised
intracranial pressure, oliguria progressing to anuria,
a decreased cardiac output and hypotension may
occur insidiously and can also be associated with
other pathologies than intra-abdominal hyperten-
sion and abdominal compartment syndrome.48
An objective assessment of intra-abdominal pres-
sure is therefore required. Intra-abdominal pres-
sure can be estimated most conveniently from
the transduced pressure of an indwelling urinary
catheter.29 This is usually done by intermittent
measurement but it is also possible to monitor
continuously using a three-way irrigation cathe-
ter.35 A pressure >30 mmHg confirms ACS and
requires return to OR for initial or further decom-
pression. Decompression should lead to improved
visceral perfusion, cardiac function, and ventilatory
mechanics. Occasionally complex pelvic injuries
may need fascial closure to achieve pelvic tampo-
nade at the cost of renal dysfunction and this may
be an indication for early RRT to optimise the
metabolic and fluid status of the patient.
Resuscitation: physiological
optimisation
During the ICU resuscitation phase, procedures and
interventions should be limited to those that are
essential for the correction of the triad of acidosis,
hypothermia and coagulopathy while ensuring
patient stability. The components of the triad
should not be looked at in isolation and require
simultaneous management. Exposure of the patient
should be kept to absolute minimum to allow effec-
tive rewarming. Non-essential mobile X-rays (e.g. to
clear the thoraco-lumbar spine) should be post-
poned.
The underlying principle of the ICU resuscitation
is to provide physiological optimisation that will
allow the best chance for recovery. At the centre
of this principle is the aim of reversing hypovolae-
mia which then allows adequate cardiac output and
oxygen delivery with the resultant correction of
metabolic acidosis, coagulopathy and hypothermia.
716
Assessment of the adequacy of the circulating
volume accompanies active rewarming and correc-
tion of coagulopathy. If these issues are correctly
addressed the metabolic acidosis will gradually
improve.
Rewarming
Temperature control is dependent on a balance
between heat generation, CNS temperature control
and heat loss by conduction, convection, evapora-
tion, and radiation. Heat loss commences at the site
of trauma and is compounded by the degree of
reduced perfusion, prolonged exposure, immobility,
resuscitative fluid and procedures. The very young
and very old are particularly at risk. In the absence
of preemptive treatment, this process continues in
the emergency department, where the patient is
uncovered and exposed to a large patient—room
temperature gradient. This is continued into the
OR where general anaesthesia, blood loss, and
further exposure, now with open body cavities,
rapidly results in severe hypothermia.22
Core temperature decreases precipitously for 1 h
and then decreases slowly for 2—3 h in a predictable
manner following the induction of general anaes-
thesia in normal circumstances, which emphasises
the need for awareness and the use of preventative
strategies.54 A temperature <35 8C is associated
with reduced cardiac output, increased SVR, risk
of arrhythmia, cold diuresis, metabolic acidosis,
left-shift of the oxygen-haemoglobin dissociation
curve and coagulopathy in it’s own right. These
patients have increased fluid, transfusion, vaso-
pressor and inotropic requirements, and more organ
dysfunction, mortality, and prolonged intensive
care unit stay.37,51 A temperature <34 8C is further
associated with inhibition of platelet aggregation
and dysfunction of intrinsic and extrinsic coagula-
tion factors and is used as an indicator for DCS.19
These processes emphasize the need for prevention
and effective warming strategies (Table 2).
Maintaining a room temperature >28 8C may be
impractical for multi-bed space ICUs but feasible for
ICUs with single rooms. Keeping the patient covered
and dry needs particular emphasis if effective
warming is to be achieved. Ventilated patients
should have gases humidified and warmed and in
this situation the heated water bath humidifiers will
be more efficient than heat and moisture exchange
(HME) devices. Warming gases is however, an inef-
ficient method of warming hypothermic patients
compared with forced air warming devices. Forced
air warming devices are an increasingly popular and
efficient method of warming from hypothermia.
M.J.A. Parr, T. Alabdi
Table 2 Strategies to correct hypothermia
Warm room
Room T > 28 8C, may not be feasible in many ICUs
Cover/insulate patient
Reduces convection, conduction and radiant
heat loss
Prevent unnecessary exposure
Dry patient
Remove any wet sheets/clothing to reduce
evaporative heat loss
Active warming
External
Forced air warming device (e.g. Bair HuggerTM)
Warm water blanket
Radiant heaters
Internal
Use pre-warmed fluids
High capacity fluid warmer (e.g. Level 1TM,
Rapid Infusion System [RIS])
Warmed ventilator gases (warm water
reservoir/HME)
Peritoneal or pleural lavage
Extracorporeal rewarming
They result in less core temperature after-drop
and a 6—10 fold faster rate of warming when com-
pared with passive and inhalation warming techni-
ques.21 The majority of patients can be rapidly
rewarmed by using these techniques and ensuring
all fluids administered are warm.
Cold temperature IV fluid administration is a very
rapid way of accelerating hypothermia. Therefore, all
fluids administered should be warm and there are
numerous devices on the market to provide consistent
warming of fluids at both low and high infusion rates.
High capacity fluid warmers (e.g. Level 1 and rapid
infusion system (RIS)) are capable of warming fluid
from 4 8C to body temperature at flow rates up to
0.5 l/min (Level 1) and 1.5 l/min (RIS). These devices
have been credited with improved resuscitation of
major trauma, reduced requirements for fluid/blood
products, less coagulopathy, more rapid correction of
acidosis and hypothermia, and fewer hospital com-
plications when compared to conventional methods
of fluid/blood product administration .5,14 However,
there may also be potential for overly aggressive fluid
administration that may worsen outcome .23
There may be potential for an adverse response to
surface warming when cold, acidotic blood returns
to the central circulation further lowering core
temperature, and precipitating life-threatening
arrhythmias. With severe hypothermia (T < 33 8C)
there is an increasing risk of cardiac depression and
arrhythmias and the more extreme the hypothermia,
Damage control surgery and intensive care
the more justification for aggressive warming,
including extracorporeal techniques. A variety of
invasive techniques of rewarming have been
described including gastric lavage, bladder irriga-
tion, and peritoneal or pleural lavage. While all may
have potential uses, they are often difficult to man-
age effectively especially in the multi-trauma situa-
tion. Extracorporeal rewarming is possible using
several techniques and is likely to see increased
popularity given the increasing availability of simple
pumps and heparin-bonded circuits. The need for
anticoagulation however, may restrict use. Contin-
uous arteriovenous rewarming has been achieved
using a heparin-bonded circuit without a pump
where flow is driven by the patient’s own blood
pressure. This technique rewarms at a rate of 4—
5 8C/h, which is more efficient than many other
methods. Because the warmed blood is sent directly
to organs, continuous arteriovenous rewarming
rapidly increases core temperature without shiver-
ing .20 Depending on the technique used extracor-
poreal rewarming can achieve warming rates of 4—
50 8C/h. Advocates suggest that if the temperature
drops below 33 8C, aggressive extracorporeal
rewarming (arteriovenous or veno-venous) rewarm-
ing should be considered.20,26,43 The fact that
despite aggressive replacement of clotting factors
and platelets, normal coagulation may not occur
until the core temperature exceeds 34 8C adds sup-
port to this suggested approach.44
Coagulopathy
The incidence of early coagulation abnormalities
after trauma is high and they are independent pre-
dictors of mortality. An initial abnormal PT
increases the adjusted odds of dying by 35% and
an initial abnormal APTT increases the adjusted
odds of dying by 326%.40 The late coagulopathy
associated with DCS is multifactorial in origin
(Table 3).
Table 3 Factors contributing to coagulopathy
Hypothermia
Dilution of coagulation factors
Continued loss of coagulation factors from bleeding
Thrombocytopaenia
Non-functional platelets
Acidosis
Hypocalcaemia
Reduced synthesis of coagulation factors due to liver
dysfunction secondary to hypoxic/ischaemic insult
Fibrinolysis
Disseminated intravascular coagulation (DIC)
717
Dilution of coagulation factors and platelets
occurs early and abnormal prolonged coagulation
studies may be demonstrated after even small
volume fluid resuscitation. The clinically observed
coagulopathy however, may not be confirmed by
laboratory investigation, demonstrating that ele-
ments other than levels of clotting factors and
platelet count are involved in haemostatic failure.
Hypothermia results in dysfunction of intrinsic and
extrinsic coagulation cascades that will not be
demonstrated by laboratory prolongation of pro-
thrombin time (PT) and activated partial thrombo-
plastin time (APTT) because coagulation testing is
normally performed at 37 8C rather than at the
patient’s core temperature.44,45
Hypothermia causes a temperature-dependent
defect in thromboxane B2 production and altered
enzyme kinetics which delay the initiation and
propagation of platelet aggregation.53 Resultant
platelet dysfunction is seen despite adequate repla-
cement of platelet number.18 Also the increasing
use of non-steroidal anti-inflammatory drugs and
aspirin impair platelet activity prior to the trauma
incident.
As there is often poor correlation between plate-
let count and ability to form clots in patients who
have received massive transfusion, the presence of
continued haemorrhage in this setting is an indica-
tion for platelet transfusion even with a ‘‘normal’’
platelet count.
Many coagulation factors and enzyme reactions
are pH dependent and the presence of severe meta-
bolic acidosis may directly contribute to the coa-
gulation failure.8 Citrate present in transfused
blood may decrease calcium concentration and
add to the coagulopathy,12 rapid plasma protein
administration may also decrease ionised calcium
levels, presumably as a consequence of the binding
of calcium ions to anionic sites on plasma protein. In
most situations this is a transient phenomenon and
dependent on the total dose of citrate administered
and the rate of infusion. Often calcium is given in an
empiric fashion during massive and continuing high
volume transfusion but rational calcium replace-
ment may be based on direct ionised calcium mea-
surement. Interestingly, Haemaccel, a gelatin
colloid solution has a calcium concentration of
6.25 mmol/l, and its use during trauma resuscita-
tion has been associated with transient hypercal-
caemia.17
Increased fibrinolysis is seen in hypothermia and
imbalances in the production and degradation of
fibrin may also lead to excessive bleeding.16,49
Fibrinolysis may also be excessive due to extensive
tissue damage and hypotension, and is particularly
seen in head injury and lung injury and results in a
718
DIC with prolonged coagulation, low fibrinogen,
elevated D dimers and thrombocytopaenia.
As conventional laboratory assessments of coa-
gulation function have limitations in the DCS situa-
tion, thrombelastography has been advocated as a
technique to determine coagulation abnormalities
and give information about fibrinolytic activity
and platelet function.34,41 Thromboelastography
assesses the clotting from initial platelet-fibrin
interaction, through platelet aggregation, clot
strengthening, and fibrin cross-linking, to clot lysis,
within around 20 minutes. It is practical for use in
the ICU and OR, simplifies the diagnosis of coagulo-
pathy, and may be an early predictor of the need for
transfusion. However, despite the availability of
thromboelastography technology it has not become
popular. Recently, the activated coagulation time
(ACT) has been assessed in relation to global coa-
gulation status. The investigators suggest that an
elevated ACT (which only takes a few minutes to
perform) is an objective indicator that the coagula-
tion system reserve is near exhaustion and may
represent an indication for considering damage
control manoeuvres or more aggressive resuscita-
tion.3
There are no simple strategies to correct coagu-
lopathy that can be applied to all trauma patients.
Computer modelling has generated suggested pre-
ventive strategies recognising that existing proto-
cols underestimate the dilution of clotting factors in
severely bleeding patients.25 Again a number of
strategies (Table 4) may need to be implemented
simultaneously and enrolling the help of experi-
enced haematologist should be considered at an
early stage.
To optimize early blood product resuscitation, a
local ‘trauma exsanguination policy’ needs to be
agreed that can be activated to allow rapid blood
product availability during DCS and ICU care. This
protocol should only require a single phone call for
activation and should result in the expedited deliv-
ery of blood and blood products to the OR. A reason-
able approach for a major trauma centre would
Table 4 Strategies to correct coagulopathy
Reverse hypothermia and maintain an effective circulating blood volume and oxygenation
Preferably use whole blood and/or the freshest available
Give FFP to replace coagulation factors (10—15 ml/kg approx. 2 units will achieve 30% factor activity in adults)
Give platelets
Give cryoprecipitate if fibrinogen level is <1 g l1
Give calcium (10 mmol) to reverse hypocalacaemia
Consider the use of adjuncts to promote coagulation/reduce fibrinolysis (e.g. aprotinin)
Consider the use of rVIIa
Give Vitamin K
Repeat coagulation tests and blood count and modify treatment accordingly
M.J.A. Parr, T. Alabdi
include the provision of up to 10 units of group
O, non-cross-matched packed red blood cells
(PRBCs), 6 units of platelets, and 4 units of stored
(previously thawed) fresh frozen plasma (FFP) as
the initial response.33 A further 4 units of FFP should
be thawed to replace the dispensed FFP and five
more units of group O blood should be available on
request. The cycle should repeat automatically
until discontinued by the trauma team. The ongoing
availability of blood products needs to be con-
firmed, particularly for hospitals that may be large
distances from a central blood transfusion service.
Prolonged turn around times from request to infu-
sion of blood products will not help these patients.
Guidelines for the administration of blood pro-
ducts vary on what is the ideal red blood cell,
platelet and clotting factor replacement regimen
and the ideal endpoints. Again a locally agreed
policy is the way to appropriately plan for and
provide the optimal chances of survival for these
patients.28
The rheological effect of anaemia (platelet func-
tion is inversely related to haematocrit) is com-
pounded by thrombocytopenia < 100  109 l1
resulting in an increasingly prolonged bleeding
time. It follows that during continued haemorrhage
and instability especially if head injury is present
that the haematocrit should be maintained >30 and
the platelet count > 100  109 l1. These values
correlate with the minimum value recommended
by the British Committee for Standards in Haema-
tology for intracranial or eye surgery.6
DCS patients should receive the freshest blood
available and as whole blood if possible. However
the increasing use of donated blood to provide blood
components has lead to whole blood availability
being very limited.
Platelet counts of < 100  109 l1 can be antici-
pated when between 1 and 1.5 blood volumes have
been replaced.9 Initially platelets will be given
empirically and repeated according to ongoing
blood loss, transfusion requirement and platelet
counts. In the face of massive transfusion and
Damage control surgery and intensive care
DCS aiming for an early platelet count > 100 
109 l1 will provide a margin of safety. With resolu-
tion of the acidosis, coagulopathy and approaching
normothermia lower platelet counts (50—
75  109 l1) may be a more suitable level to aim
for. Platelets are presented in different volumes
and platelet yields depend on their method of pre-
paration (either single donor, apheresis or pooled).
A standard single donor unit (average platelet
yield ¼ 55  109 unit) can be expected to raise
the platelet count by 5—10  109 l1 in marrow
failure patients, but in the DCS patient this level
of effect may be unlikely as they are rapidly con-
sumed. The initial adult dose will be 4 units or one
adult therapeutic dose for pooled packs and apher-
esis packs (average platelet yield > 240  109 unit).
The requirement for FFP is less predictable as the
labile factors V and VIII have wide normal ranges and
levels down to 20% of normal may not result in
coagulopathy if the haematocrit and platelet count
are maintained. FFP should also be given initially
empirically in massive transfusion (defined as the
replacement of one blood volume in 24 h) and then
laboratory tests should be used to assist with
ongoing requirements. FFP 10—15 ml/kg or an
empiric approach of giving 4 units initially and then
at a ratio of 2:5 for FFP:PRBCs is often practiced
once one blood volume has been replaced and
bleeding is not under control. Frequent samples
should be taken for the usual clotting assays includ-
ing fibrinogen. Because FFP may not supply enough
fibrinogen in the massive transfusion situation
cryoprecipitate (10 units) should be given if the
measured fibrinogen levels is <1 g l1. If the
hypothermia is not corrected the administered pla-
telets and coagulation factors will remain ineffec-
tive. Blood components are administered until the PT
and APTT reach less than 1.25 times control levels,
the platelet count is more than 100  109 l1, and
the fibrinogen is greater than 1 g l1.
Recently, recombinant activated factor VII
(rFVIIa) has been reported as useful for adjunctive
treatment of coagulopathy in trauma patients and is
undergoing trials. rFVIIa was originally developed as
a pro-hemostatic agent for the treatment of hae-
mophilia patients who had become sensitised to
donated factor VIII or IX. rFVIIa has been successfully
used, with impressive clinical resolution of bleeding
in moribund trauma patients in whom standard pro-
cedures had failed. Various dosage regimens have
been used and clinical studies are under way.38,39 In
the absence of definitive studies local agreed poli-
cies on the use of rFVIIa need to be formulated. Our
current approach is that if after the administration
of 10 units of PRBCs, 10 units of platelets, 10 units of
FFP, and 10 units of cryoprecipitate, bleeding con-
719
tinues despite all attempts at correcting coagulation
and all attempts at surgery and embolisation; then
rVIIa is administered in a dose of 100 mg kg1. Higher
doses or repeated doses have been used and remain
an option.42 A haemotologist should be involved in
the decision making process.
There is also anecdotal evidence (including the
authors experience) that aprotinin, the protease
inhibitor may have a role as adjunctive therapy in
the presence of ongoing coagulopathy and potential
DIC by decreasing fibrinolysis.52
Acidosis
All patients having DCS have a lactic acidosis that
reflects the degree of anaerobic metabolism in the
presence of inadequate oxygen delivery. The acido-
sis also contributes to coagulopathic bleeding
resulting in a vicious cycle of continued blood loss,
coagulopathy, hypovolaemia and worsening acido-
sis. The correction of this acidosis therefore
requires control of haemorrhage and optimization
of oxygen delivery, initially by blood and fluid
administration. Inotropic/vasopressor should be
considered if the patient does not respond ade-
quately to volume and red cell loading and myo-
cardial depression may be seen at pH < 7:2.
However, the need for inotropes and vasopressors
correlates with poor outcomes for these patients.
The acidosis puts a large burden on the respiratory
system and continued ventilatory support is
required. The direct use of IV sodium bicarbonate
to raise the pH > 7:2 remains an option but may be
better avoided (particularly for patient who appear
to be stable) because of well recognised adverse
effects of bicarbonate administration. Some
patients will have established acute renal failure
and the early commencement of RRT may benefit
these patients with more rapid correction of acido-
sis (particularly if a bicarbonate dialysis fluid is
used) and provision of an optimal metabolic envir-
onment. The persistence of a metabolic acidosis
and base deficit are negative prognostic indicators
in trauma patients10,11,46 and although the initial
lactate level may not be predictive, lack of clear-
ance of lactate within 48 h is strongly predictive of
mortality.1 Clearance of lactic acidosis in DCS
patients suggests that optimal resuscitation has
occurred while persistent acidosis is generally a sign
of hypovolaemia. Persistent acidosis may also
represent reduced cardiac output, reduced oxygen
delivery or abnormal oxgen utilisation and empha-
sises the need for continuous monitoring, repeated
objective assessment and setting appropriate resus-
citation endpoints.
720
Monitoring of resuscitation end points
The response to therapy is monitored initially by
observing vital signs and urine output. However,
even in young trauma patients, these signs may
be unreliable and fail to demonstrate significant
cardiac depression.47 These patients may therefore
benefit from invasive (PA catheter) or non-invasive
(echocardiography) repeated assessments of car-
diac filling and contractility. A number of resusci-
tative end points have been proposed that go
beyond conventional ‘‘vital signs’’, including serum
lactate and base deficit as stated above, mixed
venous oxygen saturation in conjunction with oxy-
gen delivery and consumption4 and gastric mucosal
pH31. No particular strategy has been shown to be
universally applicable and all have potential limita-
tions or risks that need to be considered but aggres-
sive therapy, continuous assessment and repeated
laboratory evaluations are well justified. The abso-
lute level of haemoglobin required in the acute
setting is controversial and while much has been
written on the tolerance of restrictive transfusion
strategies in critically ill patients 24, the unstable
DCS patient at high risk of organ failure is not a
suitable candidate for this strategy in the immedi-
ate ICU phase. Maintaining a haemoglobin level
>10 g dl1/haemotocrit >30% will provide a margin
of safety in the initial ICU phase.
Specific strategies to reduce
complications
Given the critical condition of DCS patients it is not
surprising that the overall mortality rate is high
(12—67%) and complications are frequent50. How-
ever many of the complications are predictable
(Table 5) and strategies can be commenced early
in the ICU phase to reduce the risks (Table 6).
All patients should have IAP measured and pro-
phylaxis from peptic ulceration should be com-
menced on admission (H2 blocker or proton pump
inhibitor)7. Early enteral nutrition is also protective
Table 5 Predictable complications seen in DCS
patients
ACS
Peptic ulceration
Venous thromboembolism
ARDS
Nosocomial infection
Intra-abdominal infection, fistula, dehiscence
Nutritional failure
Critical illness myoneuropathy
M.J.A. Parr, T. Alabdi
Table 6 Strategies to reduce complications
Measurement of IAP
Peptic ulceration prophylaxis
Thromboprophylaxis
Protective lung ventilation
Infection control and appropriate antimicrobial
therapy
Early nutritional support (preferably enteral)
but may be better delayed until the acidosis is
corrected and splanchnic perfusion is deemed to
be adequate. Compression stockings should be
applied initially and calf compressors added at an
early stage, heparin will be withheld until the coa-
gulopathy is corrected. Low molecular weight
heparin may be an option but renal impairment
and repeated surgery restrict is use in the early
days post injury. These patients are at high risk
of acute respiratory distress syndrome (ARDS)
because of chest trauma, aspiration, hypotension
and large IV fluid administration or transfusion
associated lung injury (TRALI), in which case a lung
protective ventilatory strategy will be appropriate.2
Scrupulous infection control is required and the
rational use of antibiotics is particularly important.
Positioning the patient head up will reduce the rate
of nosocomial pneumonia. Antimicrobial prophy-
laxis should be limited and proven infection should
be appropriately targeted. The indisciminant use of
braod spectrum antimicrobials will promote bacter-
ial resistance and must be avoided. General nursing
and pressure area care must be meticulous and
neuromuscular blockade should be avoided. Ade-
quate sedation and analgesia will be required. A
tertiary survey should be performed within 24 h to
ensure that all injuries have been identified and the
priorities of interventions and ongoing management
are agreed. It is not uncommon for these patients to
have been incompletely assessed on admission
because of haemodynamic instability requiring
immediate surgery. It may be only after resuscita-
tion in the ICU that the patient is deemed stable
enough to be transferred for further radiology ima-
ging if needed.
Communication
Given the complexity of the management of DCS
patients it is not surprising that one of the crucial
factors in optimising care is communication. This is
often overlooked.13 Whether it is the timely avail-
ability of blood products, the comprehensive
assessment of all injuries, the coordinated return
Damage control surgery and intensive care
to the OR for definitive care or the urgent inter-
ventions required to save life, the need for clear and
effective communication between emergency phy-
sicians, surgeons, anaesthetists, intensivists, radi-
ologists, haematologists, nurses, laboratory staff,
and all others involved should be at the forefront of
management. This is often an area of trauma care
that can easily be improved.
Conclusion
Damage control surgery is a significant advance in
trauma patient management. The central principle
of damage control surgery is that patients are more
likely to die from a triad of coagulopathy, hypother-
mia and metabolic acidosis than from a failure to
complete operative repairs. If the patient is to
survive, definitive surgery must wait until hypother-
mia, acidosis and coagulopathy are corrected.
These corrections should occur over a period of
hours in the ICU and result in rapid and complete
reversal of metabolic failure. A multidisciplinary
coordinated approach is needed to optimize out-
come.
References
1. Abramson D, Scalea TM, Hitchcock R, et al. Lactate
clearance and survival following injury. J Trauma
1993;35:584—9.
2. Anonymous. Ventilation with lower tidal volumes as
compared with traditional tidal volumes for acute lung
injury and the acute respiratory distress syndrome. The
Acute Respiratory Distress Syndrome Network. NEJ Med
2000:342;1301—8.
3. Aucar JA, Norman P, Whitten E, et al. Intraoperative
detection of traumatic coagulopathy using the activated
coagulation time. Shock 2003;19:404—7.
4. Bishop MH, Shoemaker WC, Appel PL, et al. Prospective
randomized trial of survivor values of cardiac index, oxygen
delivery and oxygen consumption as resuscitation endpoints
in severe trauma. J Trauma 1995;38:780—7.
5. Booke M, Sielenkamper A. Massive transfusion with the
Rapid Infusion System. Its effect on core body temperature.
German Anaesthesist 2001;50:926—9.
6. British Committee for Standards in Haematology. Guidelines
for platelet transfusions. Transfus Med 1992;2:311—8.
7. Cook DJ, Reeve BK, Guyatt GH, et al. Stress ulcer
prophylaxis in critically ill patients. Resolving discordant
meta-analyses. JAMA 1996;275:308—14.
8. Cosgrif N, Moore EE, Sauaia A, et al. Predicting life-
threatening coagulopathy in the massively transfused
patient: hypothermia and acidoses revisited. J Trauma
1997;42:857—62.
9. Counts RB, Haisch C, Simon TL, et al. Hemostasis in
massively transfused trauma patients. Ann Surg 1979;190:
91—9.
10. Davis JW, Kaups KL. Base deficit in the elderly: a marker of
severe injury and death. J Trauma 1998;45:873—7.
721
11. Davis JW, Shackford SR, Mackersie RC, Hoyt DB. Base deficit
as a guide to volume resuscitation. J Trauma 1988;28:
1464—7.
12. Denlinger JK, Nahrwold ML, Gibbs PS, Lecky JH. Hypocal-
caemia during rapid blood transfusion in anaesthetized
man. Br J Anaesth 1976;48:995—1000.
13. Donchin Y, Gopher D, Olin M, et al. A look into the nature
and causes of human errors in the intensive care unit.
Quality and safety in health. Care 1995;12:143—7.
14. Dunham CM, Belzberg H, Lyles R, et al. The rapid infusion
system: a superior method for the resuscitation of hypovo-
lemic trauma patients. Resuscitation 1991;21:207—27.
15. Dutton RP, Mackenzie CF, Scalea TM. Hypotensive resusci-
tation during active hemorrhage: impact on in-hospital
mortality. J Trauma 2002;52:1141—6.
16. Enderson B, Chen J, Robinson R, et al. Fibrinolysis in multi-
system trauma patients. J Trauma 1991;31:1240—6.
17. Evans PA, Madira W, Riyatt MS, et al. Changes in plasma
ionised calcium within 24 h of trauma in patients infused
with the calcium containing colloid Haemaccel during fluid
resuscitation. J Acc Emerg Med 1997;14:73—5.
18. Ferrara A, MacArthur J, Wright H, et al. Hypothermia and
acidosis worsen coagulopathy in the patient requiring
massive transfusion. Am J Surg 1990;160:515—8.
19. Garrison J, Richardson D, Hilakos A, et al. Predicting the
need to pack early for severe intra-abdominal haemorrhage.
J Trauma 1996;40:923—9.
20. Gentilello I, Rifley. Continuous arteriovenous rewarming:
report of a new technique for treating hypothermia. J
Trauma 1991;31:1151—54.
21. Goheen MS, Ducharme MB, Kenny GP, et al. Efficacy of
forced-air and inhalation rewarming by using a human model
for severe hypothermia. J Appl Physiol 1997;83: 1635—40.
22. Gregory J, Flancbaum L, Townsend M, et al. Incidence and
timing of hypothermia in trauma patients undergoing
operations. J Trauma 1991;31:795—800.
23. Hambly PR, Dutton RP. Excess mortality associated with the
use of a rapid infusion system at a level 1 trauma center.
Resuscitation 1996;31:127—33.
24. Hebert PC, Wells G, Blajchman MA, et al. A multicenter,
randomised, controlled clinical trial of transfusion require-
ments in critical care. NEJ Med 1999;340:409—17.
25. Hirshberg A, Dugas M, Banez EI, et al. Minimizing dilutional
coagulopathy in exsanguinating hemorrhage: a computer
simulation. J Trauma 2003;54:454—63.
26. Hirshberg A, Walden R. Damage control for abdominal
trauma. Surg Clin North Am 1997;77:813—20.
27. Hoey BA, Schwab CW. Damage control surgery. Scand J Surg
2002;91:92—103.
28. Horsey PJ. Multiple trauma and massive transfusion.
Anaesthesia 1997;52:1027—9.
29. Iberti TJ. A simple technique to accurately determine intra-
abdominal pressure. Crit Care Med 1987;15:1140—2.
30. Ivatury RR, Diebel L, Porter JM, et al. Intra-abdominal
hypertension and the abdominal compartment syndrome.
Surg Clin North Am 1997;77:783—800.
31. Ivatury RR, Simon RJ, Islam S, et al. A prospective,
randomized study of endpoints of resuscitation after major
trauma: global oxygen transport indices versus organ-
specific gastric mucosal pH. J Am Coll Surg 1996;183:
145—54.
32. Johnson JW, Gracias VH, Gupta R, et al. Hepatic angio-
graphy in patients undergoing damage control laparotomy.
J Trauma 2002;52:1102—6.
33. Johnson JW, Gracias VH, Schwab CW, et al. Evolution in
damage control for exsanguinating penetrating abdominal
injury. J Trauma 2001;51:261—9.
722
34. Kaufmann CR, Dwyer KM, Crews JD, et al. Usefulness of
thrombelastography in assessment of trauma patient coa-
gulation. J Trauma 1997;42:716—22.
35. Kron IL, Harman PK, Nolan SP. The measurement of intra-
abdominal pressure as a criterion for abdominal reexplora-
tion. Ann Surg 1984;199:28—30.
36. Kushimoto S, Arai M, Aiboshi J, et al. The role of
interventional radiology in patients requiring damage
control laparotomy. J Trauma 2003;54:171—6.
37. Luna G, Maier R, Pavlin E, et al. Incidence and effect of
hypothermia in seriously injured patients. J Trauma
1987;27:1014—8.
38. Lynn M, Jerokhimov I, Jewelewicz D, et al. Early use of
recombinant factor VIIa improves mean arterial pressure
and may potentially decrease mortality in experimental
hemorrhagic shock: a pilot study. J Trauma 2002;52:703—7.
39. Lynn M, Jeroukhimov I, Klein Y, Martinowitz U. Updates in
the management of severe coagulopathy in trauma patients.
Int Care Med 2002;28:S241—7.
40. MacLeod JB, Lynn M, McKenney MG, et al. Early coagulopathy
predicts mortality in trauma. J Trauma 2003;55:39—44.
41. Mallett SV, Cox DJ. Thrombelastography. Br J Anaesth
1992;69:307—13.
42. Martinowitz U, Kenet G, Lubetski A, et al. Posssible role of
recombinant activated factor VII (rFVIIa) in the control of
hemorrhage associated with massive trauma. Can J Anaesth
2002;49:S15—20.
43. Moore EE. Staged laparotomy for the hypothermia, acidosis,
and coagulopathy syndrome. Am J Surg 1996;172:405—10.
M.J.A. Parr, T. Alabdi
44. Reed R, Bracey A, Hudson J. Hypothermia and blood
coagulation: dissociation between enzyme activity and
clotting levels. Circ Shock 1990;32:141—52.
45. Rohrer M, Natale A. Effect of hypothermia on the coagula-
tion cascade. Crit Care Med 1992;20:1402—5.
46. Rutherford EJ, Morris JA, Reed GW, Hall KS. Base deficit
stratifies mortality and determines therapy. J Trauma
1992;33:417—23.
47. Sauaia A, Moore FA, Moore EE, et al. Epidemiology of trauma
deaths: a reassessment, J Trauma 1995;38:185—93.
48. Schein M, Wittmann D, Aprahamian C, et al. The abdominal
compartment syndrome: the physiological and clinical
consequences of elevated intra-abdominal pressure. J Am
Coll Surg 1995;180:745—53.
49. Schmidt U, Enderson B, Chen J, et al. D-Dimer levels
correlate with pathologic thrombosis in trauma patients. J
Trauma 1992;33:312—20.
50. Shapiro MB, Jenkins DH, Schwab CW, Rotondo MF. Damage
control: a collective review. J Trauma 2000;49:969—78.
51. Steinemann S, Davis JW, Shackford SR. Implications of
admission hypothermia in trauma patients. J Trauma 1990;
30:200—2.
52. Valentine S, Williamson P, Sutton D. Reduction of acute
haemorrhage with aprotinin. Anaesthesia 1993;48:405—6.
53. Valeri C, Cassidy G, Khuri S. Hypothermia-induced reversal
and platelet dysfunction. Ann Surg 1987;205:175—81.
54. Yamakage M, Kamada Y, Honma Y, et al. Predictive
variables of hypothermia in the early phase of general
anesthesia. Anesth Analg 2000;90:456—9.