SPECIAL INTEREST
Timing of Fixation of Major Fractures in Blunt Polytrauma
Role of Conventional Indicators in Clinical Decision Making
Hans-Christoph Pape, MD,* Peter V. Giannoudis, MD,† Christian Krettek, MD, FRACS,*
and Otmar Trentz, MD‡
Summary: Grading of the clinical status in patients with multiple
trauma is important regarding the treatment plan. In recent years,
4 different clinical conditions have been described: stable, borderline,
unstable, in extremis. Clinical parameters have been widely used in
patients with penetrating injuries, and 3 categories were found to
be important: shock, hypothermia, coagulopathy. However, in blunt
trauma patients, the role of conventional parameters for decision
making regarding the timing of fracture treatment is poorly described.
After blunt trauma, additional factors seem to play a role, because the
injuries affect multiple body regions. These additional factors are
summarized under the term, ‘‘soft-tissue injuries,’’ which may include
the soft tissues of the extremities, lung, abdomen, and pelvis. The study
describes four pathophysiologic cascades that are relevant to the
clinical conditions listed above. Threshold values for separation of the
patient conditions are documented, leading to a staged surgical strategy.
Key Words: polytrauma, multiple injuries, major fractures, scoring,
clinical judgment, clinical status, borderline patient, damage control
orthopaedic surgery, early total care
(J Orthop Trauma 2005;19:551–562)
D uring the past two decades, advances have been made in
prehospital care, perioperative management, intensive care,
and primary definitive stabilization of long bone fractures by
intramedullary nailing. These advances have contributed to im-
proved survival rates and a reduction in acute respiratory dis-
tress syndrome (ARDS) and multiple organ failure (MOF).1–3
There is increasing understanding of the phenomenon
that primary definitive surgery may be too much of an addi-
tional physiologic insult to the polytrauma patient (a ‘‘second
hit’’).4–6 Many recommendations for trauma patients are based
on the experience in abdominal surgery with penetrating
trauma. In the treatment of these patients, the term ‘‘triad of
death’’ (hypothermia, coagulopathy, and acidosis) has been
coined and is indicative of an adverse outcome.7,8 These three
parameters are useful indicators in the care of patients with
acute severe blood loss, as seen in penetrating injuries or
Accepted for publication February 23, 2005.
From the *Department of Trauma Surgery, Hannover Medical School,
Hannover, Germany, †Department of Trauma, Leeds, Great Britan, and
‡Department of Trauma, Zurich, Switzerland.
Reprints: Hans-Christoph Pape, MD, Professor of Orthopaedics Surgery,
Department of Trauma Surgery, Hannover Medical School, Carl-
Neubergstr. 1, 30625 Hannover, Germany.
Copyright Ó 2005 by Lippincott Williams & Wilkins
J Orthop Trauma  Volume 19, Number 8, September 2005
vascular lesions in which rapid blood loss can result in death
by exsanguination.12 In these patients, a staged approach, termed
‘‘damage control’’ (bailout) surgery, has been advocated and
shown to be useful.9
However, blunt trauma patients (as opposed to pene-
trating trauma patients) represent a unique cohort of trauma
patients, and usually develop subacute complications, such as
ARDS and MOF. These complications are associated with
severe soft-tissue extremity and thoracic injuries.10–12 In
critical patients with major fractures, a spanning external
fixateur has been recommended to maintain the principle of
immediate fracture stabilization. Because of the wide range of
injury patterns in blunt trauma, it is useful to attempt to
recognize the clinical parameters in these patients (Table 1).
Recent studies have demonstrated that immunologic changes
occur during this time and are relevant for the patient’s
subsequent clinical course.13,14
Grading of the overall clinical status of patients with
severe blunt trauma is difficult. Two decades ago, it was
recommended to use only systolic blood pressure,15 but even
today there has been a lack of sound recommendations
regarding indicators for standardized patient assessment. To
our knowledge, the first criteria ascertaining the suitability of
blunt trauma patients for orthopaedic surgery were published
in 1979. The authors recommended the use of systolic blood
pressure, heart rate, central venous pressure, and hematocrit
for basic evaluation. In addition, cardiac index, pulmonary
arterial pressure, coagulation status, and acid-base parameters
were found to be of value for the early period after trauma.16
A goal of this review is to better understand several
pathophysiologic mechanisms that we will define as the ‘‘four
pathophysiologic cascades in polytrauma,’’ which are relevant
to the clinical course of the blunt trauma patient. The clinical
consequences of these four cascades have as their common end
point inflammatory changes that result in endothelial damage
(Fig. 1).17–19 Associated with these cascades are conventional
parameters, indicative of adverse outcomes.20
Our purpose is to make recommendations for clinical
decision making concerning the optimal timing of the
operative stabilization of fractures in blunt trauma patients
with orthopaedic injuries. A list of parameters is provided that
indicate a stable clinical condition, which allows for early
definitive fracture stabilization.
MATERIALS AND METHODS
A search of the English literature was performed by
using the PubMed database of the United States National
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Pape et al
TABLE 1. Summary of Parameters Associated With Adverse
Outcome in Multiply Injured Patients (30, 144 [previously
156])
Criteria
ISS 40 or above in the absence of additional thoracic injury
Polytrauma +ISS .20 and additional thoracic trauma (AIS .2)
Multiple long bone fractures + truncal injury AIS 2 or more
Polytrauma with abdominal/pelvic trauma (.Moore 3) and hem. shock (initial
RR ,90 mm Hg)
Bilateral lung contusion on first plain film
Presumed operation time .6 hours
Initial mean pulmonary arterial pressure .24 mm Hg
PA-pressure increase during intramedullary nailing .6 mm Hg
ISS, injury severity score; AIS, abbreviated injury scale; PA, pulmonary arterial
pressure.
Library of Medicine with combinations of the terms poly-
trauma, outcome, prediction, hypothermia, transfusion, acido-
sis, acid-base balance, coagulopathy, platelets, inflammation,
immune response, and interleukin as search criteria to identify
a group of relevant publications. Methodologic filters relating
to outcome prediction were used to exclude publications that
did not contain information about the value of prediction of
physiologic parameters.
A total of 114 potentially applicable publications were
identified. Of these, 51 contained evidence on outcome pre-
diction in polytrauma patients from initial laboratory or
clinical findings. The majority of patients included in these
publications were the victims of blunt trauma. Many authors
used an injury severity score $16 for patient inclusion. Some
looked at a specific group of patients, such as severe liver or
pelvic injuries, or trauma patients requiring intubation, inva-
sive monitoring, or ICU care.
Four Pathologic Cascades of Polytrauma
In patients with penetrating trauma, the lethal triad
consisting of shock, hypothermia, and coagulopathy has been
shown to be of clinical value.7,8,21,22 In addition, the presence
FIGURE 1. Four pathophysiologic cascades relevant for the
development of posttraumatic complications and outcome.
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J Orthop Trauma  Volume 19, Number 8, September 2005
of soft-tissue injuries to extremities and lungs are other factors
that are equally relevant to the patient’s clinical course. We are
aware that the 4th entity (soft-tissue injuries) represents a term
that describes a number of clinical diagnoses rather than
a cascade system. However, we feel that the presence of such
diagnoses is relevant as an initiating factor for pathophysio-
logic events based on clinical experience with these patients.
The four entities are hemorrhagic shock, hypothermia,
coagulopathy, and soft-tissue injuries.7,8,23–25
The premise was substantiated with a literature search.
Critical analysis of the studies that met these selection criteria
was performed. Data were sorted by each of the four
parameters.
Furthermore, we recognize that inflammatory changes
are important in the clinical course of the blunt trauma patient
with orthopaedic injuries.26–29 However, daily clinical mea-
surement of inflammation is not practical at the present time
for several reasons. First, laboratory testing of inflammatory
mediators, such as interleukin (IL)-6, are not routinely in-
cluded in standard laboratory tests. Second, the cost-
effectiveness of each of these tests is unverified. Third, the
clinical relevance of these tests has not been fully established.
Integration of Four Pathologic Cascades of
Polytrauma into the Concept of a Staged
Surgical Treatment Plan
We have previously separated four different grades to
describe the clinical status of a patient with blunt multiple
injuries (Tables 2 and 3).30 According to these clinical dif-
ferentiations, different indications for stabilization of major
fractures have been assigned and clinical approaches to these
patients have been recommended accordingly (Fig. 2). In this
article, relationships are established between the pathologic
cascades of polytrauma and patient categories. Patients may be
categorized into 1 of 4 different classes (stable, borderline,
unstable, in extremis) if they meet the criteria in 3 of 4
categories. However, it is important to notice that individual
variations exist.
Also, the values listed in Tables 2 and 3 do not represent
mandatory thresholds. They should be used in the context of
other factors known to influence the patient’s clinical
condition, such as comorbidities, rescue conditions, or other
adverse effects.
The severity of injury was categorized using the
abbreviated injury scale and the injury severity score.31
Multiple organ failure was defined as organ dysfunction in
an accepted scoring system32 if at least 3 organs demonstrated
a grade II dysfunction. Adult respiratory distress syndrome
was determined as discussed previously.33 Chest trauma was
assessed using the thoracic trauma score.34 The severity of
abdominal trauma was determined as described by Moore
et al.35
RESULTS
Hemorrhagic Shock
The criteria for the diagnosis of hemorrhagic shock have
evolved. Border et al15 in 1975 defined a patient to be in shock
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J Orthop Trauma  Volume 19, Number 8, September 2005 Fixation of Major Fractures in Blunt Polytrauma

TABLE 2. Time Sequence of Parameters Indicative of the Four Pathophysiologic Cascades in Polytrauma
Parameter Indicative of Parameter indicative of
Time to Normalization in
High-risk Patients High-risk Patients
Case of an Uneventful
Pathophysiology Admission (day 1) Course Clinical Course (.day 2) Comment
Shock BP ,90 mm ,1 day Catecholamine dependency Irrelevant after
HG .5 blood Units/2 hours .2 days resuscitation
Lactate .2.5 mmol/L
Base excess .8 mmol/L
Coagulation Platelet count ,90,000 1–2 days .3 days below 100.000 or Simple parameter,
failure to increase good indicator
Core temperature ,33°C Hours Irrelevant after rewarming Irrelevant after rewarming
Soft-tissue injuries PaO2/FiO2 ,300 ,2–4 days PaO2/FiO2 ,300 for .2 days Lung function often close
Lung contusions, AIS .2 pathologic extravascular lung to normal for 2–3 days
Chest trauma score; TTS .II water (.10 ml/kg BW) (PaO2/FiO2 .300)
Abdominal trauma (Moore .II)
Complex pelvic trauma
Arbitrary threshold values are documented that indicate a high-risk situation on admission and during the further course in regards to the development of organ dysfunction.
BP, blood pressure; AIS, abbreviated injury scale; TTS, thoracic trauma score; BW, body weight.

when there was a loss of 1 to 2 L of blood volume.15 The
systolic blood pressure (BP) for many years has been the
single most important parameter used to quantify the degree of
hemorrhagic shock. Most authors have agreed that a systolic
BP ,90 mm Hg adequately diagnoses the presence of hem-
orrhagic shock,36 and vital signs were frequently thought to
predict outcome in trauma patients.37–39 The most commonly
described correlation has been between hypotension (systolic
BP ,90 mm Hg) on admission and adverse outcome.40–42 In
addition, several authors found that the duration of shock was
more important than the initial value, and a critical interval of
70 minutes was discussed as the threshold value.6,43 Admis-
sion pulse and respiratory rate also were found to be predictive
in several studies, often forming part of the SIRS score,44–46
although their sensitivity has been questioned when used
alone.47 Both cardiovascular parameters and metabolic chan-
ges have been used to quantify the degree of shock.
Cardiovascular Parameters
The cardiovascular system is able to maintain an ade-
quate systolic blood pressure in young patients. Because the
compensatory mechanism often is an increase in heart rate,
some authors have argued that volume depletion may occur
despite a normal blood pressure. Allgower’s group developed
a simple score that uses the ratio between the systolic blood
pressure and the heart rate. If this ratio drops below a value of 1,
they defined the patient to be in shock.48 In North America,
the revised trauma score has been widely used and summarizes

TABLE 3. Assessment of Four Different Clinical Grades and Ranges of Clinical Parameters Determining These Grades
Parameter Stable (Grade 1) Borderline (Grade II) Unstable (Grade III) In Extremis (Grade IV)
Shock Blood pressure (mmHg) 100 or more 80–100 60–90 ,50–60
Blood units (2 h) 0–2 2–8 5–15 .15
Lactate levels normal range approximately 2.5 .2.5 severe acidosis
Base deficit (mmol/L) normal range no data no data .6–18
ATLS classification I II–III III–IV IV
Urine output (mL/h) .150 50–150 ,100 ,50
Coagulation Platelet count (mg/mL) .110,000 90,000–110,000 ,70,000–90,000 ,70,000
Factor II and V (%) 90–100 70–80 50–70 ,50
Fibrinogen (g/dl) .1 approximately 1 ,1 DIC
D-Dimer normal range abnormal abnormal DIC
Temperature .34°C 33°C–35°C 30°C–32°C 30°C or less
Soft-tissue injuries Lung function; PaO2/FiO2 .350 300 200–300 ,200
Chest trauma scores; AIS AIS I or II AIS 2 or more AIS 2 or more AIS 3 of more
Thoracic trauma score; TTS 0 I–II II–III IV
Abdominal trauma (Moore) #II #III III III or .III
Pelvic trauma (AO class.) A type (AO) B or C C C (crush, rollover abd.)
Extremities AIS I–II AIS II–III AIS III–IV Crush, rollover extrem.
Surgical strategy Damage control (DCO) or DCO if uncertain
(Fig. 2) Definitive surgery (ETC) ETC ETC if stable DCO DCO

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Pape et al
FIGURE 2. Treatment protocol for major fractures in poly-
trauma.30
information on the respiration, circulation, and neurologic
status.49 In a similar fashion, the criteria proposed by the
advanced trauma life support program also includes four
different stages of hemorrhage.50 For the determination of
blood loss from parenchymal organs, an estimated overall
blood loss of .2000 mL (class III and IV) has been used for
classification of instability. To estimate the degree of blood
loss, the requirement of mass transfusion (10 units/12 h) has
been advocated to guide surgical strategy by some authors.51
Sauaia et al52 described that an excess of 6 units of blood is
associated with a higher risk of organ failure and death and
used this threshold value as a predictive parameter.
Urinary output also may be used as a parameter to
determine volume depletion, provided that the urinary
production is not altered by an injury to the genitourinary
system. Urinary output ,25 mL per 1/2 hour in the emergency
room has been determined to represent an indicator for urgent
increase in volume therapy.53
Metabolic Changes
Metabolic end points induced by shock have been
considered sensitive guides to therapy.54–56 These parameters
were frequently used in patients presenting with rapid blood
loss (vascular injuries, penetrating trauma). Lactate values
.2.5 mmol/L and a base excess .8 mmol/L are thought to
represent important threshold levels for patients with blunt
trauma. Acidosis on admission was shown to be a significant
marker of outcome with a general consensus of ,7.2 being used
as a cut off,57 other studies used alternative values of ,7,21
,7.18,30 and ,7.32 combined with lactate .5.58 Demsar’s
computer model identified a pH ,7.2 as the most important
predictor of outcome among 174 variables tested.59,60 Inter-
estingly, several reports have discarded a correlation between
abnormal pH and outcome.61 Thus, a low pH alone should not
be used as an indication to withdraw or withhold treatment.21 To
increase the sensitivity of this parameter, a combination of
shock, defined by a blood loss of 4 to 5 L, hypothermia (core
temperature ,34°C), and acidosis (pH ,7.25) as diagnostic of
a critical situation has been advocated.62
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Base deficit is used as an alternate marker of abnormal
tissue perfusion. A threshold value of .623,36,63 was described,
although figures ranging from .3 to .12 have been quoted.64,65
A more abnormal base excess was found to be associated with
increases in mortality rates.36,40,12,21 It has been proposed that
the time to normalize base excess is more important than the
absolute value being a marker of the patients’ response to re-
suscitation and correction of their state. A continuing abnormal
base deficit at 24 hours also has been associated with an
increased rate of complications and mortality.66,67
Lactate levels have been used as a marker of ongoing
tissue hypoperfusion because lactate levels are not normalized
by the body’s buffer systems, and therefore may be more
representative of the current overall state of tissue perfusion.
Lactate clearance times of .24 hours have been reported to be
most significantly associated with outcome, rather than using
admission values.68,69 Blow et al55 used lactate levels to guide
resuscitation. Claridge et al70 later confirmed these results
when lactate levels .2.5 did not respond to fluid challenge;
then invasive monitoring (PA catheter) and aggressive re-
suscitation (vasopressor and inotropic agents) were performed.
Patients treated in this manner seemingly had improved
survival rates.31,46
Transfusion Requirements
Transfusion requirements have been considered as end
points and predictors of outcome.13,71,72 Several studies looked
at a group of patients receiving .20 units. In these patients,
mortality was greatly increased, with some studies finding
little difference once this boundary had been crossed.18,73 An
increasing mortality was observed when the number of blood
transfusions exceeded 40.48 A significant increase in mortality
was described in other studies, when .9 units,16,33 .6 units,43
or .2 units49 were received. Transfusion requirements alone
should not be used to prompt withdrawal of treatment (ie, stop
resuscitation), because some patients survive massive trans-
fusions.15,18,41
Whether the overall transfusion requirements correlates
with outcome is controversial. It has been suggested that
failure of hemostasis and ongoing blood loss affect outcome
rather than absolute transfusion requirements.74 Nonetheless,
transfusion requirements have been identified as an in-
dependent risk factor for adverse outcome (eg, multiple organ
failure).33,75
In summary, the diagnosis of volume depletion should
be based on several parameters, including the systolic BP, the
need for transfusions, and urine output. More invasive
monitoring may be required for the calculation of stroke
volumes.43,44,46,48
Coagulopathy
Changes in hemostasis occur within minutes after severe
trauma. Repeated investigations have demonstrated that
platelet counts are a stable and reliable parameter to measure
the consumption of platelets. A decreased systemic platelet
count on day 1 (,80)20,76 was associated with multiple organ
failure and death, as was decreased platelet function and in-
creased activation.77 Abnormal values of the partial thrombo-
plastin time (PTT) and the prothrombin time (PT) were
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studied. An admission PT .15 or a PTT .5030 and PT .19 or
a PTT .606,19 were found to be predictors of adverse outcome.
Demsar et al59 used computer modeling with 174 variables and
found a PTT .78.8 (worst value after admission) to be the
second most important predictor of MOF and death. Other
investigators have concurred that coagulation parameters are
significantly altered in patients who developed complications
or died.13,52
The diagnosis of disseminated intravascular coagulation
is based on parameters that may not always be available within
the first hour after the injury. Before D-dimers or prothrombin
fragments were available for testing, the diagnosis of post-
traumatic alterations of the coagulatory response was made
based on the changes of factor V, fibrinogen levels, and AT
III.78 Nowadays, serum levels of D-dimers are considered
sensitive indicators of the fibrinolytic cascade. The serum
levels of D-dimers have been suggested to be valuable
screening markers for perioperative complications, such as
ARDS and MOF.29,31,32 Furthermore, D-dimer concentrations
have been described as a marker for the extent of the soft-
tissue injury.79–81
In summary, the best screening marker for coagulopathy
and adverse outcomes is the platelet count performed on
admission or shortly thereafter. In addition, this seems to be
true later in the patient’s clinical course, in which a failure to
normalize is a warning signal for adverse outcomes.
Hypothermia
There are many known causes of hypothermia in the
trauma patient: blood loss, environmental exposure, prolonged
rescue times, and metabolic changes. Heat production for
maintenance of euthermia in the presence of surrounding low
temperatures increases oxygen requirements. If tissue oxygen
consumption is limited as a result of hemorrhagic shock, heat
production cannot offset ongoing losses. This scenario results
in hypothermia. Hypothermia also can be induced by anes-
thetic agents, leading to a decrease in heat production by as
much as one-third.82
Inadequate resuscitation and oxygen delivery also lead
to metabolic failure and lactic acid accumulation. A drop in
tissue oxygen delivery below a critical level exceeds the
maximum ability of the maximum tissue oxygen extraction
capability, thus leading to a decrease in oxygen consumption
and heat production. The frequent presence of lactic acid
accumulation in cold, seriously injured patients supports this
hypothesis.83,84 The consequences of decreased body temper-
ature for the other cascade systems are best described for the
coagulatory response. Hypothermic coagulopathy rises sig-
nificantly whenever the core temperature drops below 34°C.85
Admission temperature was studied in 15 publications in
the available literature. Threshold values for the development
of complications ranged between 32°C and 36°C.16,30,33,86,87
Rewarming time also has been associated with outcome. In
a randomized, controlled trial investigating the effect of arte-
riovenous rewarming, a 100% mortality was found in patients
failing to rewarm.88 In a computer model of damage-control
laparotomy, patients demonstrating an initial temperature
of 36°C survived a 66-minute laparotomy compared with a
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Fixation of Major Fractures in Blunt Polytrauma
36-minute cutoff for those presenting with a temperature
of 34°C.89
Soft-Tissue Injuries (Extremity and Truncal
Soft-Tissue Damage, Lung Contusion)
The term, soft-tissue injuries, as used in this article
summarizes different categories: soft-tissue damage to the
abdomen, chest, and extremities. It is common sense that
severe abdominal trauma and other injuries to the trunk
implicate sustained shock states and severe soft-tissue injuries.
We assume that the importance of these injuries and of
abdominal injuries is widely recognized.90–94 This article
focuses on information relevant for orthopaedic surgeons to
facilitate the management of major fractures.
Although extremity soft-tissue lesions imply direct
surgical consequences (eg, debridement or amputation), lung
injuries most often can be handled by insertion of chest tubes
and alterations in the ventilator settings. The indications for
surgical management of severe chest trauma are limited.51,95
Moreover, for many years, chest trauma has not been
thought to represent an important factor in the decision-
making process regarding the surgical treatment of extremity
injuries. Yet none of the studies dealing with this subject is
a prospective trial and the comparability of the patient groups
is limited.96,97 Likewise, the degree of chest trauma has not
been quantified in the available studies and the clinical
relevance of these studies has been criticized.98 Recently, an
increased awareness toward the importance of chest injuries
has been recognized.99
On the basis of numerous publications, we believe that
both factors—soft-tissue injuries and severe chest trauma—
have to be considered when establishing general management
principles. The lung is a soft-tissue organ whose immunologic
properties are well described for patients who develop
a respiratory distress syndrome.100 Unfortunately, the effect
of these immunologic alterations and the effects of thoracic
trauma on the systemic response have been sparsely described.
We only found one clinical study investigating this
entity: polytraumatized patients with associated thoracic
trauma demonstrated a significantly higher incidence of
posttraumatic organ dysfunction than polytraumatized patients
with the same injury severity, but without thoracic trauma. The
authors discussed that thoracic trauma is a precursor of other
complications, such as multiple organ failure.101
Most of the clinical studies available in the current
literature investigate the effects of chest trauma on the lung. It
is obvious that direct or indirect injury to the lung has negative
effects on pulmonary function. In a series of 203 patients with
pulmonary contusion, an overall mortality of 20% was found,
and the presence of additional injuries was associated with
a substantial increase in mortality.102,103 The impact velocity
has been stressed.104 In a rabbit model, low impact velocity
mainly caused bronchial injury, whereas high energy impact
was associated with alveolar injury.105 Clemedson and
Jonsson106 found that direct crushing of lung parenchyma
occurs if the compression of the chest exceeds 40%. Kroell107
and Stalnaker et al108 investigated human torsos and found that
primarily bronchial or alveolar contusion occurred if the
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impact velocity was ,6 milliseconds or .9 milliseconds,
respectively.
The time course of changes after chest trauma has been
shown to be relevant. Fulton and Peter109 reported that despite
severe pulmonary injury, dysfunction was not fully detectable
early after trauma. They found only a moderate decrease of
pulmonary blood flow, and an increase of pulmonary vascular
resistance and pulmonary edema. However, all of these param-
eters continue to deteriorate as time proceeds. Oppenheimer
et al110 described that hypoxemia increases with time, which
was explained by intrabronchial bleeding and flooding of air
spaces with blood and plasma.
The problem in the daily care of the multiple trauma
patient is to recognize the severity of pulmonary damage. In
this context, it is important to mention that the mechanisms
initiated by pulmonary contusion are comparable after severe
injury; in patients with pulmonary contusion, an unusually
high incidence of interstitial edema has been found. Mecha-
nisms known to be present in patients with severe injury may
lead to activation in the immune response systems.111,112 Thus,
although triggered differently, the host response to pulmonary
contusion is similar to that of a nonpulmonary injury, resulting
in an increased risk of ARDS. It is of note that a lung contusion
has been judged to be more relevant for the development of
complications in the clinical course than the bony lesion.113
Although it is common sense that isolated soft-tissue
lesions are a concern for orthopaedic surgeons because of local
complications, these injuries may be even more relevant in
terms of systemic effects in the polytrauma situation. Even
though this issue has been poorly investigated, we believe that
it has to be considered. Local tissue hypoxia and necrosis may
spread systemically, and changes induced by fractures and by
other injuries may have additive effects.
On one hand, nonextremity soft-tissue injuries can add
further systemic insults to that already present from the soft-
tissue injuries from extremity trauma.114 On the other hand,
some systemic sequelae of major fractures are well described.
Intramedullary contents after long bone fractures enter the
bloodstream,115 which may induce the formation of thrombi as
a result of a high thromboplastin content.116 In unreduced
fractures, nursing causes additional local soft-tissue trauma,
muscle necrosis, and pain. These mechanisms alter the
systemic immunologic response.117 The effects of blunt
trauma on the hemostatic response are well known and range
from blockage of the pulmonary microvasculature118 to
disseminated intravascular coagulation.78 Hauser et al12
convincingly demonstrated that fracture fluid and adjacent
soft tissues also contain inflammatory mediators. It has been
discussed that these are indicative of the hypoxic and necrotic
changes and a systemic spread can occur. Among the sequelae
known to occur in response to major fractures associated with
severe soft-tissue injuries and after torso trauma are necrosis,
inflammation, and systemic acidosis.119,120 However, quanti-
fication of severe soft-tissue injuries with regard to the clinical
course is difficult.121,122
In addition to the factors described above, it has been
argued that a close relationship between extremity injuries and
lung function exists, as debris from open wounds and from the
fracture site enters the venous circulation and the lungs. The
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lung was named a ‘‘filter organ,’’ preventing these substances
from entering the arterial bloodstream.123 Trauma-induced
hemorrhage causes an increase in microvascular permeability
that occurs in all organs including the lung,124,125 although it
has an extraordinary ability to clear interstitial fluid via the
lymphatic systems.126 The lung contains the largest micro-
vascular bed in the body. Therefore, an increase in interstitial
edema and a reduction of oxygenation capacity may occur.20
External pathogens may enter the blood stream in shock
states127 and are usually inactivated by the reticuloendothelial
system. However, nonsurviving trauma patients showed an
inadequate reticuloendothelial system function,128 which may
enable these pathogens to cause adverse effects in the lung.
Additional immunologic changes of the circulating immune
system have been discussed.129,130
DISCUSSION
Criteria for the Primary Assessment of the
Trauma Patient in the Emergency Room
The patient’s clinical condition may range from stable to
a state named in extremis, in which there is imminent danger
of death. Patients in extremis have been well-classified by
general surgeons (early blood loss of 4–5 L, core temperature
of 34°C, and pH ,7.25).131 We have coined the term
‘‘borderline’’ for the situation in which a patient is in an
apparently stable condition preoperatively, but deteriorates
subsequently and may develop organ dysfunction.132 As
described in MATERIALS AND METHODS, the current list
of parameters of the 4 pathophysiologic cascades has been
attributed to the clinical grades described. It is understood that
individual variations exist because of cofactors, such as rescue
conditions, genetic differences, and other factors that clini-
cians may not be aware of today. We believe that the assess-
ment of these parameters and cascade systems represents a
helpful tool regarding patient classification during the emer-
gency room management period.
According to the current literature, the following clinical
parameters in addition to those listed in Table 1 define the
status of the patient in the emergency room.
Shock
Patients presenting with a systolic blood pressure
,90 mm Hg are regarded as volume-depleted. Likewise,
vasopressor dependency and low urinary output are important.
In young patients who have excellent compensatory mecha-
nisms, an increased heart rate may be an important sign if the
systolic pressure is approximately 100 mm Hg. These patients
may temporarily compensate a low cardiac output by a
tachycardia for some time and then deteriorate acutely.
Hypothermia
Decreased body temperature is known as a signal for
various complications (cardiac arrhythmias, cardiac arrest,
coagulopathy). The most important lower limit is a core
temperature of ,33°C.
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J Orthop Trauma  Volume 19, Number 8, September 2005
Coagulopathy
In addition, the hemostatic response can be of value.
The most simple and rapidly available parameter in the
emergency room is the systemic platelet count. Initial platelet
values ,90,000 indicate impending disseminated intravascu-
lar coagulopathy, provided that no other cause of coagulopathy
is present.
Soft-Tissue Injuries
The effects of severe extremity soft-tissue lesions
usually do not become evident until days after injury. The
same holds true for lung contusions. Quantification of soft-
tissue injury to the extremities and the lungs continues to be
a challenge.
The initial patient assessment can be structured
according to the 4 categories described above. The parameters
of these 4 cascades are summarized as: soft-tissue injuries
(major extremity fractures, crush injuries, severe pelvic
fractures, lung contusions abbreviated injury scale (AIS)
.2), coagulopathy (platelets ,90,000), and shock (systolic
BP ,90 mm Hg, requirement of vasopressors) contribute to
hypothermia (core temperature ,33°C) and are dangerous.
Fortunately, the majority of patients belong to the group
classified as ‘‘stable’’ or to the ‘‘borderline’’ patient group
(grade I or II, if stable after resuscitation) that can be safely
stabilized during the course of the emergency treatment. These
patients should undergo early fracture stabilization to benefit
from the advantages of this approach. If patients are in an
unstable condition or do not respond to resuscitation at all
(grade II (if uncertain after resuscitation), III, IV), they should
not undergo prolonged surgical therapy and their fractures
should be treated by early temporary measures, such as exter-
nal fixation.
Treatment Principles: Effect of
Fracture Fixation
Stabilization of major long bone fractures during the first
24 hours continues to represent the ‘‘gold standard’’ for any
trauma patient.2,3 However, a discussion has evolved during
the last few years about whether initial definitive treatment
should be performed in all patients, or whether some patients
should undergo a staged approach using damage control or-
thopaedic surgery (Fig. 2).133,134 Some authors argued that the
degree of initial surgery may represent an additional burden to
a subset of patients with blunt trauma who are at special risk
for complications.135,136 Others described that the pathophys-
iologic effects induced by hypothermia, blood loss, coagul-
opathy, and soft-tissue damage can become clinically
relevant.137–139 Moreover, further authors suggested that early
definitive treatment of all fractures may not be the best
treatment of all patients. The local and systemic effects of early
definitive surgery in patients with certain injury patterns have
been investigated in detail and were thought to be potentially
harmful.140–142
Although the effect of early definitive orthopaedic sur-
gery is difficult to assess on the basis of clinical parameters,
the duration of this type of surgery may be used as an indirect
indicator. When 3 groups of patients with similar injuries were
separated according to the duration of initial surgery, patients
q 2005 Lippincott Williams & Wilkins
Fixation of Major Fractures in Blunt Polytrauma
with the longest initial surgery (.6 hours) developed
a significantly higher complication rate, namely ARDS and
MOF.143
These results support the idea that orthopaedic surgeons
play a pivotal role in influencing the course of the path-
ophysiologic cascades mentioned above. Although further
therapeutic measures (rewarming, replacement of blood
products, etc.) are important, they must be viewed as adjuncts
of the principal treatment, fracture stabilization, and soft-tissue
management by the orthopaedic trauma surgeon. Orthopaedic
surgery affects all 4 pathophysiologic pathways described
above. By recognizing this, it is evident that early hemorrhage
control and limitation of soft-tissue injuries limits the degree
of coagulopathy and, if performed in a timely fashion, prevents
further temperature lowering. In addition, it is important to
monitor the patient during the surgical procedure. Several
conventional parameters have been used intraoperatively to
determine the clinical status of a patient.156 These are listed in
Table 4.
Timing of Secondary Major Fracture Surgery
(Acetabular Fracture Fixation, Reconstruction
of Large Joints) Based on Clinical Parameters
The timing of the definitive procedure is critical.144 It
was previously advocated that major surgeries should be
performed within 24 hours after injury, or several days
thereafter. Special care should be taken at days 2 to 4 after the
injury, because the parameters described above often have not
normalized.16 In line with these recommendations, clinical
data clearly document an increase in the incidence of organ
failures when major surgeries were performed at days 2 to 4
after trauma.145
Similar time-dependent recommendations have been
made for patients with neurotrauma.140 Intracranial pressure
reaches maximum values during days 2 to 5 as a result of
permeability shifts. Therefore, neurosurgeons have advised to
carefully evaluate patients during this time period to minimize
the risk of further intraoperative pressure increases. If in doubt,
it was recommended to delay craniotomies until the risk of
worsening cerebral edema has decreased.146
TABLE 4. Indicators for Increased Risk for Development of
Organ Dysfunction to Be Assessed Repeatedly and
Intraoperatively
Intraoperative
Parameter Threshold Value Assessment Available?
Platelet count ,90,000/mL Yes
I/O ratio .+5 liters/6 hours Limited
after the initial injury
Urinary output ,50 ml/hour Yes
Lactate levels .2.5 mmol/L Yes
Base excess .8 mmol/L Yes
Body temperature ,33°C Yes
Transfusion .3 Units/hour Yes
PaO2/FiO2 ,250 Yes
Age (yr) .55 Yes
557
Pape et al
Early after trauma, multiple pathophysiologic changes
occur simultaneously. The resulting systemic response pro-
gresses toward the common end point of endothelial cell
damage and a generalized endothelial permeability leak,
associated with an increased inflammatory response. In this
line, a pathologic increase in organ size and interstitial edema
in all organs after severe trauma has been shown in autopsy
studies.147–149 As a result of the pathophysiologic changes
induced by the initial injury, the development of the interstitial
edema increases within the first days. Early clinical signs
usually are subtle, and consist of a positive fluid balance and
increased interstitial markings on the chest radiograph, al-
though not associated with functional alterations at that time
point. In an uneventful course, improvement of endothelial
permeability within 3 to 6 days after the injury indicates clinical
improvement. A continuous pathologic elevation of the per-
meability defect is an important warning signal for adverse
outcome and organ failure.20
In the patient with multiple injuries, the following time-
sensitive changes should be considered to minimize the risk of
postoperative complications:
Shock
Complete restoration of the intravascular and extravas-
cular volume usually occurs within 6 to 12 hours, unless the
patient continues to demonstrate ongoing active and sustained
bleeding. The shock-induced permeability changes normalize
within 3 to 4 days after the injury in an uneventful course.150
These may be visible on chest x-ray and also may induce
pulmonary dysfunction in the absence of pulmonary injuries
(lung contusion). A fluid balance after day 4 (. +500 mL)
represents a warning sign of the threat of later organ failure.
Hypothermia
The normalization of decreased body temperatures is
completed within hours after admission and does not play any
role during the remainder of the treatment. At the end of the
first week, hyperthermia may occur secondary to over-
stimulation of the immune system. An infectious cause for
hyperthermia should be excluded.
Coagulation
In an uneventful clinical course, the coagulatory
response is normal within a day after injury. Secondary
worsening of the coagulation parameters can be a late sign of
organ failure, usually after liver and pulmonary failures have
occurred. However, the normalization of the platelet count
continues to be a reliable and easily obtainable clinical
parameter for decision-making. Based on our experience,
major secondary operations should not be performed if the
platelet count fails to increase, especially if the fluid balance
has not become negative at the same time.34,151
Soft-Tissue Injuries
After initial debridement, a re-evaluation of extremity
soft-tissue injuries represents the standard of care to exclude
the development of further tissue necrosis. Therefore,
a planned revision is regarded as a standard procedure for
open fractures. Lung function changes occur as a result of
pulmonary contusions after a time lapse of several days. Also,
558
J Orthop Trauma  Volume 19, Number 8, September 2005
there is a delay between the increase in pulmonary per-
meability, the detection of radiologic signs of permeability
increases and the deterioration of lung function. The earliest
assessments of lung function can be evaluated using a chest
CT, quantification of extravascular lung water, or secondary
ventilation parameters (airway pressures, etc.). Unfortunately,
there are almost no publications available with reference to
these issues. According to our experience, secondary oper-
ations should be performed only when airway pressures, and
oxygenation (PaO2/FiO2 ratios) are normal in the absence of
a pulmonary infection.
In contrast with the initial assessment period, the clinical
relevance of immunologic alterations are better described
during the course of intensive care. The immunologic response
to blunt trauma may lead to an immune state in which the
patient is essentially anergic. This anergic state situation can
lead to infectious complications in those areas accessible to
bacteria. If no infection is present, the activated immune cells
can still mimic a septic state, resulting in temperature elevation
and a hyperdynamic state (endotoxin induced, cytokine
induced).152 Thus, a phase of early hyperreactivity is followed
by a state of anergy, associated with the development of
posttraumatic complications.153,154
The immune response can be altered by a surgical
stimulus and the reaction has been shown to be dependent on
time after injury. When a standardized operation was per-
formed within the first 24 hours after injury, it was associated
with a transient increase in systemic inflammatory markers
(IL-6). However, no increase in IL-6 concentrations was
measured when this operation was performed secondarily.155
Similar observations were made when the immune
response was determined during and after major secondary
operations. When stabilization of a major fracture was per-
formed at days 2 to 4 after trauma, more sustained liberations
of proinflammatory cytokines were measured than when
operations of similar magnitude were performed at days 6 to 8
after the injury.152 These results are in accordance with those
from other research groups who looked at the impact of
secondary operations.42 The preoperative values were com-
pared between patients who did or did not develop post-
operative complications after a secondary orthopaedic
operation. The determining factors demonstrating significant
group differences were C-reactive protein, neutrophil elastase
release, platelet count, and the PaO2/FiO2 ratio. The authors
describe ‘‘a close association between surgery and the onset of
organ failure when surgery was performed within a period of
48 hours after the operation.’’42
Subtle clinical changes should be respected when
planning a secondary definitive procedure. Among these are
a positive fluid balance (I/O ratio above +500 mL/day) that has
not cleared after days 2 to 3 after injury, and airway pressures
(.30 cm H2O), both of which are indicative of systemic and/or
pulmonary interstitial fluid accumulation. Moreover, failure of
the platelet count to rise .100,000 or other evidence of
coagulopathy should be seen as a warning sign. Although there
is no prospective, randomized study available in the literature
that describes the consequences of not respecting these thresh-
old levels, common clinical practice has clearly demonstrated
their value.
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J Orthop Trauma  Volume 19, Number 8, September 2005
In summary, the decision making for both the initial and
secondary operations for fracture stabilization in blunt trauma
patients should be performed carefully. Conventional param-
eters are helpful in determining the appropriate timing and the
degree of surgery. When using a staged surgical approach, the
orthopaedic surgeon is able to maintain the benefits of early
fracture stabilization without risking to cause an additional
surgery-induced burden.
ACKNOWLEDGMENT
The authors thank Dr. Craig Roberts for assistance.
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