DAMAGE CONTROL SURGERY 0039-6109/97 $0.00 + .

20

THE DAMAGE CONTROL

SEQUENCE AND
UNDERLYING LOGIC
Michael F. Rotondo, MD, FACS, and David H. Zonies, BA, MS

THE CHANGING SCOPE OF INJURY

The damage control approach was born out of a need to meet the
challenge of the changing scope and severity of injury in America in the
last 10 years. With the rising tide of violence in the streets and the easy
accessibility of semiautomatic handguns came the inevitable increase in
admissions of severely injured patients to trauma centers. During the
previous 20 years, civilian gunshot wound victims were most frequently
injured with single-shot revolvers of low muzzle velocity. However, the
modern era of violence has been heralded by an onslaught of injury
from multiple penetrations with altered ammunition, delivered at a
greater muzzle velocity.51 This subjective observation, held by many
practicing trauma surgeons in the late 1980s, was verified in a landmark
report by McG~nigal;~which described a significant increase in homi-
cides in Philadelphia County, Pennsylvania, between 1985 and 1990,
referable to a significant increase in semiautomatic weapons. Moreover,
a review of 551 gunshot wound victims admitted to the Trauma Center
at the University of Pennsylvania between June, 1992, and August, 1993,
revealed an average of 2.7 penetrations per patient, a large number of
which resulted from semiautomatic weapons.'j7As expected, an increase
has been seen in the number of patients with exsanguination and physio-
logic instability, correlating with the shift in wounding patterns and the
increase in tissue destruction.
During that time and to the present, injuries as a result of blunt

From the Division of Trauma and Surgical Critical Care, Department of Surgery, University
of Pennsylvania Medical Center, Philadelphia, Pennsylvania

SURGICAL CLINICS OF NORTH AMERICA

VOLUME 77 * NUMBER 4 * AUGUST 1997 761

762 ROTONDO & ZONIES

mechanisms have continued unabated. Falls, blunt assaults, motor vehi-

cle crashes, and pedestrians struck all continue to result in a significant
number of patients sustaining major torso trauma and exsanguination,
yielding another cohort of patients with a high degree of physiologic
instability on presentation.
Despite the organization of ”trauma systems,” the development
of “trauma centers,” and the application of standardized methods of
resuscitation and operative intervention, the mortality rate in patients
with devastating torso trauma and exsanguination remains high. The
challenge lies in the maintenance of physiologic stability during the
struggle for surgical control of hemorrhage. Best efforts at resuscitation
and operation often lead to a lethal cascade of events, including meta-
bolic acidosis, hypothermia, and coagulopathy-a sequence some have
termed the ”lethal triad of death” (Fig. 1).This pattern of physiologic
perturbations is predictable and all too frequently reproduced. Each of
the factors in this pattern must be understood in order to establish
specific interventions designed to combat them. Each must be explored
individually as it applies to the exsanguinating trauma patient. Under-
standing this pattern forms the foundation and underlying logic upon
which the damage control approach was built.

PHYSIOLOGIC PERTURBATIONS OF DEATH BY

EXSANGUINATION

Metabolic Acidosis

The predominant physiologic defect resulting from persistent or

repetitive bouts of hypoperfusion is metabolic acidosis. From the mo-
ment of energy transfer, normal cell physiology is altered and a shift
from aerobic to anaerobic metabolism takes place, resulting in lactic
acidosis (Fig. 2). This association between high lactate levels and hypo-
volemic shock was described nearly 40 years Moreover, the rela-

ACIDOSIS

HYPOTHERMIA 4-& COAGULOPATHY

Figure 1. The lethal triad: physiologic perturbations in death by exsanguination.

 THE DAMAGE CONTROL SEQUENCE AND UNDERLYING LOGIC 763

Figure 2. Cellular metabolism in the shock state.

tionship between high lactate levels and death has been appreciated for
well over 25 years.78The pathophysiologic basis for this relationship is
slowly unfolding in the context of major trauma. Lactate clearance has
been closely correlated with the degree of oxygen delivery and oxygen
consumption as endpoints of resuscitation. In 1993, Abramson et all
demonstrated that the rate of lactate clearance predicts survivorship in
severely injured trauma patients. Whereas 100% of patients survived
with clearance of lactate at 24 hours, only 14% survived with clearance
at 48 hours. Other investigators have demonstrated that the degree of
acidosis, demonstrated as base deficit, is an accurate predictor of total
764 ROTONDO & ZONIES

resuscitation volume, the presence of significant abdominal injury, and

o~tcome.14. 15. 17,24,62

Although much of the clinical research performed in the last 20

years has focused on quantifiable markers of the shock state, a host of
factors are altered in the metabolic response to injury, the clinical sig-
nificance of which remains unclear. Further studies on the changes in
microvascular flow as a result of shock are needed to elucidate the role
of these important factors. Elevations in catecholamines and free fatty
acids, alterations in protein metabolism, changes in amino acid concen-
trations, perturbations in carbohydrate and fat metabolism, increases in
catabolic counterregulatory hormones, and priming of the inflammatory
response through peptide regulatory factor activation are all important
yet unquantified factors.

Hypothermia

Hypothermia is an inevitable pathophysiologic consequence of se-

vere injury and subsequent resuscitation. Heat loss in the field, resuscita-
tion maneuvers, injury severity, age, exposure of body cavities during
surgery, impaired thermogenesis, and degree of transfusion have all
been implicated as important fact01-s.~. 29, 40, 71 These multifactorial causes
contribute to the relationship between hypothermia and death demon-
strated in a number of studies. In 1985, Slotman et a170identified a 40%
mortality in 100 postoperative patients admitted to the intensive care
unit with hypothermia (defined as temperature < 97°F) for more than 4
hours. In 1987, Luna's analysis of 94 severely injured patients demon-
strated that 66% were hypothermic on admission.46Subsequently, a
report by Jurkovich et ala elucidated the consequences of hypothermia
in trauma patients. In this study of 71 severely injured adult trauma
patients, mortality increased from 40% to 100% when patients with core
temperatures of 34°C were compared with patients with temperatures
of 32°C or less. Although a 1990 study by Steineman et a171 could not
demonstrate an independent effect of hypothermia on outcome when
patients were stratified by physiologic and anatomic indicators, the
authors clearly acknowledge the deleterious effects of hypothermia in
severely injured patients.
Little has been done to elucidate the relationship between the devel-
opment of complications and the degree of hypothermia in severely
injured patients. Adverse effects such as cardiac arrhythmias, reduction
in cardiac output, increase in systemic vascular resistance, and a left
shift in the oxygen-hemoglobin saturation curve have been described.25,
41, 52 However, understanding of the relationship between hypothermia
and clinical morbidity is in its infancy. Bush et a17 in a study of 262
elective abdominal aortic aneurysm repairs, demonstrated that hypo-
thermic patients (temperature < 34.5"C) had a greater frequency of
organ dysfunction in the first 24 hours following admission to the
intensive care unit and a greater need for crystalloid resuscitation as
 THE DAMAGE CONTROL SEQUENCE AND UNDERLYING LOGIC 765

well as vasopressor and inotropic support. Moreover, lengths of stay

and the rate of multiple organ dysfunction syndrome were increased in
hypothermic patients. Similar rates of morbidity have yet to be defined
for severely injured patients.

Coagulopathy

It is clear that virtually every aspect of normal physiologic clotting

is affected in the cold, acidotic, exsanguinating trauma patient. It is
also clear that a predominant factor governing coagulation is body
temperature. The clotting cascade, governed by a series of temperature-
sensitive serine-dependent esterase reactions, becomes relatively inhib-
ited during hyp0therrnia.5~In fact, Reed et a158described clotting abnor-
malities equivalent to profound factor deficiencies during hypothermia.
However, the extent to which hypothermia exacerbates coagulopathic
bleeding remains unclear. The standard assays used to assess clotting
function, such as the partial thromboplastin time (PTT), prothrombin
time (PT), and bleeding time (BT), are all performed at a standardized
temperature of 37°C. Although this provides useful quantitative informa-
tion regarding clotting factors, it does not take into account the qualita-
tive dysfunction due to hypothermia. This fact was demonstrated in a
recent study by Rohrer and Natale,6O which showed a dramatic increase
in mean PT and PTT with a decreasing assay temperature in pooled
plasma from normal volunteers. Rohrer and Natale concluded that the
contribution of hypothermia to a bleeding diathesis may potentially be
overlooked on the basis of testing at standardized temperatures. Previ-
ous clinical studies have demonstrated a quantitative decrease in clotting
factors as a result of hemorrhagic shock and massive resuscitati~n.~~, 33, 78
Although most of these studies were uncontrolled for temperature, it
stands to reason that hypothermia has both a qualitative and a quantita-
tive effect on the clotting cascade, resulting in a decrease in the rate of
cascade reaction and a decrease in the production of factors.
Platelet function is also affected by hypothermia. In 1987, Valeri
et a176demonstrated that cutaneous hypothermia in an animal model
decreased plasma thromboxane levels and increased bleeding times.
This implies that the cyclo-oxygenase pathway and hence the balance
between thromboxane and prostacyclin are affected by changes in tem-
perature. Furthermore, a number of in vitro studies describe the temper-
ature-sensitive nature of the inositol triphosphate messenger system at
the GPIIb-IIIa platelet-thrombin receptor site for the release of intracellu-
lar calcium. This is a critical step in the activation of protein kinase C
for phosphorylation of cytosolic proteins that initiate platelet adherence,
aggregation, and release.5o Although in vivo studies have not been
performed to confirm this finding, it is likely that in addition to varia-
tions in prostanoid production, platelet adherence and receptor complex
formation are altered in the hypothermic state. These observations may
766 ROTONW & ZONIES

explain the frequent clinical observation of persistent bleeding in the

hypothermic patient despite a normal quantitative platelet level.
Activation of the fibrinolytic system has been demonstrated in an
animal model of massive transfusion, shock, and hypothermia,8O but
clinical studies of fibrinolysis after major injury are far less clear. Evi-
dence indicates that changes in fibrolysis after major injury contribute
to the coagulopathic state by an increase in fibrinolysis. This is particu-
larly true in selected injury complexes. Keamey et a142demonstrated
that head injury is associated with elevation of D-dimer levels (fibrinogen
degradation products), prolongation of the PT, and reduction of both
antithrombin I11 and fibrinogen levels. This may explain the findings of
a recent study in which blood samples were obtained at the scene and
on admission from a random selection of severely injured trauma pa-
tients. High levels of D-dimer were identified in the initial samples.44It
appears then, that severe injury and perhaps specific injury complexes
alter the fibrinolytic system from the moment of energy transfer. How-
ever, evidence indicates that the increase in fibrinolysis is not a sustained
effect. Shortly after injury, a hypercoagulable state is achieved marked
by a decrease in both endogenous fibrinolytic activity and antithrombin
III.l7,34, 53, In short, although most would agree that an early increase
in fibrinolysis is followed by a decrease, no controlled prospective clini-
cal studies precisely demonstrate these changes.
The dilutional effects of massive transfusion, defined as replace-
ment of greater than 100% of a patient’s blood volume, have been
previously described. In this setting, thrombocytopenia and reduction
in factors V and VIII have been well documented.l2.33, 56, 63, 79 More
recently, Gubler and demonstrated that simultaneous hypo-
thermia and hemodilution have an independent additive effect on
coagulopathy. This study, performed using hemodiluted samples from
critically ill patients, measured both PT and PTT over a decreasing
temperature range. As expected, hypothermia alone increased both PT
and PTT. However, the effect was even more dramatic when combined
with hemodilution. The results of this study corroborate previous in-
vestigations and demonstrate the contribution of hemodilution to the
coagulopathic state.
The complexity of the multifactorial interactions leading to coagulop-
athy in the exsanguinating trauma patient can be overwhelming. Clearly,
the large number of in vitro, in vivo, and clinical studies relative to
this topic do not provide a clear cohesive physiologic picture of the
coagulopathic state. We are left, instead, with a series of observations
that lead us to believe that metabolic acidosis, hypothermia, and dilution
all contribute in varying amounts to the development of coagulopathy
and the progression to death. With this in mind, each of these factors
must be controlled or prevented to stop this lethal cascade of events in
exsanguinating trauma victims.
 THE DAMAGE CONTROL SEQUENCE AND UNDERLYING LOGIC 767

HISTORICAL PERSPECTIVES-ALTERNATIVE
APPROACHES

Feliciano and co-workers' 1988 investigationz1of 300 consecutive

abdominal gunshot wounds provides an excellent description of the
"tried and true approach' to managing penetrating injury. In this series,
exploration, control, and definitive repair were achieved in a majority
of cases, yielding an overall survival rate of 88.3%. However, in patients
with major vascular injuries, the survival rate decreased to 60%, and in
those with concomitant multiple visceral injuries, survival rate plum-
meted further. The authors correctly concluded that acidosis, hypother-
mia, and coagulopathy contributed to 85% of deaths that occurred in the
study population. They suggested that alternative surgical techniques to
reduce operative times contributed to the overall high survival rate.
These alternative techniques included packing of exsanguinating injuries
and rapid closure using towel clips.
The concept of rapid termination of operation after intra-abdominal
packing in the face of massive hemorrhage followed by delayed re-
exploration for definitive repair has been part of the surgeon's armamen-
tarium for many years. The introduction of the technique by Pringle5I in
1908 focused on the management of hepatic hemorrhage using sutures
above gauze packing. This was later described in detail and modified by
Halsted31in 1913. As surgical techniques and primary repair improved,
packing for control of hepatic hemorrhage fell out of favor and by the
end of World War 11, the technique was almost universally condemned.
In 1955, Maddinf wrote that "temporary packs may be effective in
checking bleeding," but he went on to emphasize that the packs must
be removed prior to completion of the operation. By the early 1970s, a
few centers were using this technique in selected situations to arrest
hemorrhage. Reports began to surface of success in small groups of
patients. In 1976, Lucas and L e d g e r w ~ o ddescribed
~~ a prospective 5-
year evaluation of 637 patients treated for severe liver injury. Three
patients were deemed candidates for insertion of perihepatic packs, and
all three patients survived. Calne et a1,8 in 1979, reviewed four such
cases, all of whom survived after application of intra-abdominal packing
and returned for definitive operation. In 1981, Feliciano et alZ3reported
a 90% survival rate in 10 patients in whom intra-abdominal packing for
control of exsanguinating hepatic hemorrhage was used. These authors
pointed out that this maneuver may be life saving in highly selected
patients in whom coagulopathy, hypothermia, and acidosis make further
surgical efforts likely to increase hemorrhage. In 1983, Stone et a17*
described a stepwise approach using intra-abdominal packing and rapid
termination of a laparotomy, with suggestions for temporizing maneu-
vers for other injured organs such as the intestines and the urinary tract.
He suggested that after correction of coagulopathy, definitive surgery
could be completed and reported a 65% survival rate in 17 patients
treated with this approach. Between 1984 and 1993, varying success was
reported in a number of studies that focused on packing for the control
768 ROTONDO & ZONIES

Table 1. CUMULATIVE REVIEW OF PACKING FOR HEPATIC INJURIES

Year Author Number Mortality (%) Morbidity (%)

1976 Lucas 3 0/3 (0) - (-)
1979 Calne 4 0/4 (0) - (-)
1981 Feliciano 10 1/10 (10) 6/9 (67)
1982 Svoboda 12 2/12 (17) - (-1
1984 Carrnona 17 2/17 (12) 5/15 (33)
1986 Baracco 36 6/36 (17) 4/36 (11)
1986 lvatuty 14 8/14 (57) 5/6 (83)
1986 Feliciano 66 38/66 (58) 9/49 (19)
1988 Cogbill 52 31/52 (60) 3/21 (14)
1990 Saifi 9 2/9 (22) 6/9 (67)
1990 Beal 49 19/49 (39) 7/30 (23)
1990 Apraharnian 20 4/20 (20) 9/16 (56)
1990 Cue 35 17/35 (49) 19/21 (90)
1992 Krige 22 6/22 (27) 12/16 (75)
1992 Sharp 39 17/39 (44) 6/22 (27)
1993 Morris 107 64/107(60) 22/43 (51)
Totals 495 217/495 (44) 113/293 (39)

of devastating hepatic injuries.* Since that time, this technique has been
extended to a wide array of injury complexes. In 1992, Burch et a16
described 200 patients treated with abbreviated laparotomy and planned
reoperation and reported a 33% overall survival rate. In 1993, we coined
the term damage contro2 and detailed a standardized approach that
yielded a 58% survival rate. When applied to select cohorts of patients,
survival increased further.61Similar results have been reported by a
number of other centers.10,26*35,69,
74
A cumulative 20-year review of the mortality and morbidity rates
for the damage control approach in patients with devastating hepatic
injury is reported in Table 1. A total of 495 patients undergoing damage
control specifically for hepatic injury have been reported. The overall
mortality rate is 449'0, and the overall abdominal complication rate in
this group is 39%. A similar analysis, provided in Table 2, provides a
cumulative report of patients in whom damage control was used in a
wide variety of injury complexes. In this review, a 60% mortality in 466
patients occurred, with a concomitant 43% abdominal complication rate.
A comparison of these two groups of studies is provided in Table 3. In
total, 961 patients have been reported, with an overall mortality rate of
52% and an overall complication rate of 40%.
A cumulative analysis such as this has obvious limitations. It is very
difficult to discern the timing of the application of the damage control
approach on review of these studies. Damage control was applied as a
primary technique, as an adjunctive technique, and, at times, as a desper-
ation maneuver. Furthermore, the grading and multiplicity of injuries
were also difficult to determine. Frequently, extra-abdominal sites of

*References2-4, 9, 11, 13, 22, 39, 43, 54, 64, 68, 73.
 THE DAMAGE CONTROL SEQUENCE AND UNDERLYING LOGIC 769

Table 2. CUMULATIVE REVIEW OF PACKING FOR MULTIPLE INJURIES

Year Author Number Mortality (%) Morbidity (%)

1983 Stone 17 6/17 (35) 11/11 (100)
1992 Burch 200 134/200(67) 38/86 (44)
1992 Shen 6 3/6 (50) - (-1
1992 Talbert 11 4/11 (36) 3/7 (43)
1993 Carillo 14 2/14 (14) 9/12 (75)
1993 Rotondo 24 10/24 (42) 5/14 (36)
1994 Hirshberg 124 72/124(58) - (-1
1996 Garrison 70 47/70 (67) 6/38 (16)
Totals 466 2781466 (60) 72/168 (43)

exsanguination, potentially contributing to worsening physiologic status,

are not reported, and the sequencing of the treatment of injuries is
unclear. All of these unreported and uncontrolled factors affect survival.
Moreover, complications were not consistently reported throughout
the studies; therefore, only abdominal complications were tabulated. A
total of 193 complications were identified in 185 patients who were
reported to have survived long enough to develop complications. The
frequency of those complications is summarized in Table 4. Intra-abdom-
inal abscess or fluid collection was by far the most frequent complication,
occurring in 24% of patients. Careful review of the literature reveals that
virtually every abdominal complication that could occur, did occur.
However, there is an absence of standardized abdominal complication
reporting, and few studies have commented on overall complications.
The high complication rate comes as no surprise. The damage
control approach is grounded in the principle that the potential for
increasing survivorship takes priority over the potential for increasing
morbidity. In essence, in an effort to prevent rapid impending death,
the focus of the resuscitation shifts from completing the operation to
the fundamental goal of preserving life. This allows the acceptance
of incomplete operations, complicated intensive care unit courses, and
multiple operative procedures.%Although our own study in 1993 dem-
onstrated a high abdominal complication rate of 36%, this was still
less than that predicted by the penetrating abdominal trauma index.
Furthermore, overall survival, when compared with a definitive opera-
tion control group, was significantly increased for those patients with
both major vascular and multiple visceral injuries.'jl

Table 3. SUMMARY REVIEW

Injury Number Mortality (Yo) Morbidity (Yo)

Hepatic 495 217/495(44) 1 1 3/293(39)

Multiple 466 278/466(60) 72/168(43)
Total 961 495/961 (52) 185/461 (40)
770 ROTONDO & ZONIES

Table 4. ABDOMINAL COMPLICATIONS RANKED BY FREQUENCY

Total No. Frequency (YO)

Complication (n = 185) (n = 461)
Abdominal abscesskollection 109 24
Wound infection/dehiscence 38 8.2
Bile leak 17 3.7
Intestinal fistula 11 2.4
Intestinal necrosis 7 1.5
Intestinal obstruction 4 0.8
Pancreatic fistula 2 0.4
Renal leak 2 0.4
Cholecystitis 1 0.2
Gastritis 1 0.2
Pancreatic pseudocyst 1 0.2
Total 193* 40

'Complications occurred in 185 patients.

THE DAMAGE CONTROL APPROACH

The term damage control describes a systematic three-phase approach

designed to disrupt the lethal cascade of events leading to the death by
exsanguination (Fig. 3).61The first, damage control part I, consists of
immediate exploratory laparotomy for control of hemorrhage and con-
tamination using the simplest techniques. Definitive reconstruction is
delayed, and the application of intra-abdominal packing to all dissected
surfaces and injured organs is followed by a rapid, simple closure.
Damage control part I1 consists of a secondary resuscitation in the
intensive care unit that is characterized by maximization of hemodynam-
ics, core rewarming, correction of coagulopathy, complete ventilatory
support, and continued injury identification. When normal physiology
has been restored, damage control part 111, reoperation for removal of
intra-abdominal packing with definitive repair of abdominal injury and
closure, can take place. If necessary, extra-abdominal injuries may be
repaired at this time.

Patient Selection

The success of the damage control approach depends on judicious

selection of patients and careful timing based on the development of
abnormal physiology. Early identification of patients who require dam-
age control promotes optimal results. In an effort to identify these
patients, conditions, complications, and critical factors must be considered
(Table 5).
Certainly, the condition of hemodynamic instability as manifested
by hypotension, tachycardia, tachypnea, and altered mental status
should alert the surgeon to the potential need for damage control. This
 THE DAMAGE CONTROL SEQUENCE AND UNDERLYING LOGIC 771

3
Figure 3. The damage control sequence.

Table 5. KEY FACTORS IN PATIENT SELECTION FOR DAMAGE CONTROL

Conditions
High-energy blunt torso trauma
Multiple torso penetrations
Hemodynamic instability
Presenting coagulopathy and/or hypothermia
Complexes
Major abdominal vascular injury with multiple visceral injuries
Multifocal or multicavitary exsanguination with concomitant visceral injuries
Multiregional injury with competing priorities
Critical Factors
Severe metabolic acidosis (pH < 7.30)
Hypothermia (temperature < 35°C)
Resuscitation and operative time > 90 minutes
Coagulopathy as evidenced by development of nonmechanical bleeding
Massive transfusion (> 10 units packed red blood cells)
772 ROTONDO & ZONIES

occurs in patients with high-energy blunt torso trauma or multiple torso

penetrations. Moreover, presenting coagulopathy and/ or hypothermia
as a result of the initial injury or a co-morbidity must be considered an
important indicator pointing down the damage control path.
An acute awareness of the injury complex may also alert the surgeon
to the need for damage control. Any patient with major abdominal
vascular injuries and multiple visceral injuries should be considered for
the procedure.lO,61 Moreover, patients with multifocal and multicavitary
sources of exsanguination represent suitable candidate^.^^ In this situa-
tion, the control of hemorrhage takes priority within a cavity and across
multiple cavities so that time spent on nonbleeding injuries is mini-
mized.
After consideration of conditions and complexes preoperatively,
several critical factors must be considered intraoperatively. Injury pattern
recognition may be of utmost importance in the decision to embark on
the damage control approach and, ideally, should be made within the
first few minutes of operation. Injury to the pancreatic head requiring
pancreatectomy, retrohepatic caval injuries, ruptured pelvic hematomas,
open pelvic fractures, and severe hepatic injuries all represent important
injury patterns indicating the need for the damage control approach.
Most importantly, the key physiologic triggers for damage control in-
clude pH less than 7.30, temperature less than 35"C, and coagulopathy
as evidenced by the presence of nonmechanical bleeding6,lo, 13, 26, 35, 54,
Additional factors should be considered, such as total resuscitation and
operative times greater than 90 minutes and transfusion requirement of
10 units of packed cells.

Damage Control Part I: Initial Laparotomy

The success of damage control part I depends on a disciplined

approach, which includes expeditious operative control and immediate
termination of the operative procedure. Emergency celiotomy for evacu-
ation of hematoma and four quadrant packing are performed. Initial
control of hemorrhage is achieved with packing, ligation, clamps, or
balloon catheter tamponade for all vascular injuries.16,48, 75 Only the
simplest vascular repairs are performed, complex reconstruction is virtu-
ally always deferred, and, when necessary, temporary vascular shunts
are used.59Hollow viscus injuries are temporarily controlled with liga-
tion, staples, or simple running suture. Resection can be deferred, and
reconstruction is virtually always deferred. When both hemorrhage and
contamination are controlled, the procedure is rapidly terminated and
the remaining definitive repairs are delayed. Rapid closure of the abdo-
men can be achieved using towel clips or nonabsorbable sutures in the
skin only. Temporary silos can be sewn to the skin if necessary.
Resuscitation volumes are typically quite high during damage con-
trol part I. Crystalloid infusions of 8 to 12 liters with 18 to 22 units of
packed cells and 8 to 10 units of platelets are not unusual. Operative
 THE DAMAGE CONTROL SEQUENCE AND UNDERLYING LOGIC 773

times may vary from 60 to 180 minutes, average PT and PTT are most
frequently elevated to 1.5 to 2 times control levels, and pH is on average
7.3 or lower.6,26, 35, If there is lingering concern that ongoing solid-
organ hemorrhage is present, adjunctive angiography for embolizationzO
may be helpful prior to transfer to the intensive care unit for damage
control part 11.

Damage Control Part II: The Secondary Resuscitation

Upon completion of damage control part I, the patient is transferred

to the intensive care unit, where the resuscitation team labors to re-
establish normal physiology. The first several hours require the efforts
of at least two nurses and a full critical care team to successfully carry
out the secondary resuscitation. In an effort to maximize hemodynamics,
early use of an oximetric, flow-directed pulmonary artery catheter is
helpful. In general, efforts are made to restore volume to a non-flow-
dependent state of oxygen consumption. Lactate levels can be followed
as one of a number of important endpoints of resuscitation.’ Core re-
warming can be accomplished using radiant heaters, warming blankets,
a warmed ventilator circuit, and, in some instances, placement of chest
tubes for warm saline pleural lavage.28.A number of other techniques
such as arteriovenous rewarming using a Level I infuser or venovenous
rewarming with a Level I infuser and a roller pump may be
Aggressive infusion of fresh frozen plasma and platelets is key in the
correction of coagulopathy. Laboratory values are followed and, when
a normal PT and PTT are achieved and thrombocytopenia has resolved,
efforts at rewarming are continued until no evidence of clinical coagu-
lopathy remains and normal temperature is re-established. Complete
ventilatory support of the patient is used, and, if necessary, the patient
is sedated and paralyzed after a brief window of time for neurologic
examination.
Two cohorts of patients exist who require unplanned reoperation
prior to completion of the secondary resuscitation. The first consists of
those in whom a normal temperature and coagulation profile have been
achieved but who nonetheless have ongoing transfusion requirements.%
In this group, complete surgical control of bleeding may not have been
achieved at the time of the first operation. Mortality in this subgroup is
extremely high. The second group consists of those in whom abdominal
compartment syndrome develops. Typically, these patients develop a
tensely distended abdomen, low urinary output, ventilatory insuffi-
ciency with markedly elevated peak inspiratory pressures, and dimin-
ished cardiac output on the basis of decreased venous 65 The
diagnosis can be confirmed by measurement of intra-abdominal pressure
via urinary catheter.38Immediate re-exploration is indicated and, if ongo-
ing bleeding is identified, expeditious control should be obtained. If
elevated intra-abdominal pressure is secondary to massive edema, the
abdomen should remain open. Reopening of the abdomen is best accom-
774 ROTONDO & ZONES

plished in the operating room, but it can also be performed in the

intensive care unit if necessary. Average time of the secondary resuscita-
tion is 24 to 48 hours, and 8 to 10 units of packed cells with 8 to 10 units
of fresh frozen plasma are typically required to re-establish "normal"
physiology.6,54, 61
During the course of damage control part 11, a careful tertiary
survey for additional injuries should be conducted.18In anticipation of
return to the operating room, occult injury should be diagnosed, appro-
priate radiographic examinations performed, and operative planning for
damage control part I11 completed.

Damage Control Part 111: Definitive Operation

When fully resuscitated, warm, and no longer coagulopathic, pa-

tients are returned to the operating room for removal of packing and
completion of the definitive surgical procedures. During this phase,
packing is removed, the abdominal cavity is irrigated, and previously
repaired injuries are reassessed. Most importantly, a thorough search
for intra-abdominal injuries overlooked during damage control part I is
carried out. Ongoing surgical bleeding is controlled, definitive vascular
repairs can be performed, and the gastrointestinal tract can be placed in
continuity. Operative times may be between 2 and 4 hours, and resusci-
tation needs may be substantial.6,54, 61 If physiologic instability develops,
the principles of damage control part I should be applied.
When all definitive procedures have been completed, the abdominal
wall can be evaluated for the possibility of primary closure. It is of
utmost importance that no tension be placed on the anterior abdominal
wall at the time of closure. This only leads to failure and ultimately to
significant tissue loss. If peak inspiratory pressures rise to the point of
impaired ventilation, efforts at definitive closure should be terminated
and simple skin suturing should be used if possible. If not, the abdomen
should be left open. At this time, if a patient remains physiologically
stable, definitive treatment of extra-abdominal injuries may ensue.

SUMMARY

With the growing understanding of the pathophysiology of exsan-

guination has come the evolution of extraordinary surgical techniques
designed to improve survival. As the success of damage control has
grown, so has its acceptance in the traditional surgical community.
Our challenge now is to scientifically define patient selection, refine
intraoperative techniques, and acquire a greater clinical and basic science
understanding of the physiology of exsanguination and reperfusion
injury in resuscitation. In these efforts, overall survival should continue
to increase and morbidity should continue to decrease.
 THE DAMAGE CONTROL SEQUENCE AND UNDERLYING LOGIC 775

References

1. Abramson D, Scalea T, Hitchcock R, et al: Lactate clearance and survival following

injury. J Trauma 35:584, 1993
2. Aprahamian C, Wittmann D, Bergstein J, et a 1 Temporary abdominal closure (TAC)
for planned relaparotomy (etappenlavage) in trauma. J Trauma 30:719, 1990
3. Baracco-Gandolfo V, Vidarte 0, Baracco-Miller V, et a1 Prolonged closed liver packing
in severe hepatic trauma: Experience with 36 patients. J Trauma 26754, 1986
4. Beal S Fatal hepatic hemorrhage: An unresolved problem in the management of
complex liver injuries. J Trauma 30363, 1990
5. Bemabei A, Levison M, Bender J: The effects of hypothermia and injury severity on
blood loss during trauma laparotomy. J Trauma 33835, 1992
6. Burch J, Ortiz V, Richardson R, et a 1 Abbreviated laparotomy and planned reoperation
for critically injured patients. Ann Surg 215:476, 1992
7. Bush H, Hydo L, Fischer E, et al: Hypothermia during elective abdominal aortic
aneurysm repair: The high price of avoidable morbidity. J Vasc Surg 21:392, 1995
8. Calne R, McMaster P, Pentlow B The treatment of major liver trauma by primary
packing with transfer of the patient for definitive treatment. Br J Trauma 66:338,1978
9. Carmona R, Peck D, Lim R The role of packing and planned reoperation in severe
hepatic trauma. J Trauma 24:779,1984
10. Carrillo C, Fogler R, Shaftan G: Delayed gastrointestinal reconstruction following
massive abdominal trauma. J Trauma 34:233,1993
11. Cogbill T, Moore E, Jurkovich G, et al: Severe hepatic trauma: A multi-center experi-
ence with 1,335 liver injuries. J Trauma 281433, 1988
12. Collins J: Recent devdopments in the area of massive transfusion. World J Surg
11:75, 1987
13. Cue J, Cryer H, Miller F, et al: Packing and planned reexploration for hepatic and
retroperitoneal hemorrhage: Critical refinements of a useful technique. J Trauma
301007,1990
14. Davis J, Shackford S, Mackersie R, et a1 Base deficit as a guide to volume resuscitation.
J Trauma 28:1464, 1988
15. Davis J, Mackersie R, Holbrook T, et al: Base deficit as an indicator of significant
abdominal injury. Ann Emerg Med 20842, 1991
16. DiGiacomo J, Rotondo M, Schwab C W Transcutaneous balloon catheter tamponade
for definitive control of subclavian venous injuries. J Trauma 37111,1994
17. Enderson B, Chen J, Robinson R, et a1 Fibrinolysis in multi-system trauma patients. J
Trauma 31:1240, 1991
18. Enderson B, Reath D, Meadors J: The tertiary trauma survey: A prospective study of
missed injury. J Trauma 30:666, 1990
19. Falcone R, Santanello S, Schulz M, et al: Correlation of metabolic acidosis with outcome
following injury and its value as a scoring tool. World J Surg 17575, 1993
20. Fandrich B, Gnanadev D, Jaecks R, et a 1 Selective hepatic artery embolization as an
adjunct to liver packing in severe hepatic trauma: Case report. J Trauma 291716, 1989
21. Feliciano D, Burch J, Spjut-Partinely V, et a1 Abdominal gunshot wounds. Ann Surg
208362, 1988
22. Feliciano D, Mattox K, Burch J, et al: Packing for control of hepatic hemorrhage. J
Trauma 26:738, 1986
23. Feliciano D, Mattox K, Jordan G: Intra-abdominal packing for control of hepatic
hemorrhage: A reappraisal. J Trauma 21:285, 1981
24. Ferrara A, MacArthur J, Wright H, et a 1 Hypothermia and acidosis worsen coagulopa-
thy in the patient requiring massive transfusion. Am J Surg 160:515, 1990
25. Frank S, Beattie C, Christopherson R, et al: Unintentional hypothermia is associated
with postoperative myocardial ischemia. Anesthesiology 78:468, 1992
26. Garrison J, Richardson D, Hilakos A, et al: Predicting the need to pack early for severe
intra-abdominal hemorrhage. J Trauma 40:923, 1996
27. Gentile110 L, Jurkovich G, Moujaes S Hypothermia and injury: Thermodynamic princi-
ples of prevention and treatment. Persp Surg 225, 1991
776 ROTONDO & ZONIES

28. Gentilello L, Rifley W: Continuous arteriovenous rewarming: Report of a new tech-

nique for treating hypothermia. J Trauma 31:1151,1991
29. Gregory J, Flancbaum L, Townsend M, et al: Incidence and timing of hypothermia in
trauma patients undergoing operations. J Trauma 31:795,1991
30. Gubler K, Gentilello L, Hassantash S, et al: The impact of hypothermia on dilutional
coagulopathy. J Trauma 36847,1994
31. Halsted W The employment of fine silk in preference to catgut and the advantages of
transfixing tissues and vessels in controlling haemorrhage. Also an account of the
introduction of gloves, gutta-percha tissue and silver foil. JAh4A 60:1119, 1913
32. Harrigan C, Lucas C, Ledgerwood A: The effect of hemorrhagic shock on the clotting
cascade in injured patients. J Trauma 291416, 1989
33. Hewson J, Neame P, Kumar N, et a1 Coagulopathy related to dilution and hypotension
during massive transfusion. Crit Care Med 13:387, 1985
34. Hirsh J, Barlow G, Swann H, et al: Diagnosis of prethrombotic state in surgical patients.
Contemp Surg 16:65, 1980
35. Hirshberg A, Wall M, Allen M, et a1 Double jeopardy: Thoracoabdominal injuries
requiring surgical intervention in both chest and abdomen. J Trauma 39225,1995
36. Hirshberg A, Wall M, Mattox K Planned reoperation for trauma: A two year experi-
ence with 124 consecutive patients. J Trauma 37365,1994
37. Huckabee W: Relationships of pyruvate and lactate during anaerobic metabolism:
Effects of infusion of pyruvate or glucose and of hyperventilation. J Clin Invest
37244, 1958
38. Iberti TJ: A simple technique to accurately determine intra-abdominal pressure. Crit
Care Med 151140, 1987
39. Ivatury R, Nallathambi M, Gunduz Y, et al: Liver packing for uncontrolled hemor-
rhage: A reappraisal. J Trauma 26:744, 1986
40. Jurkovich G, Greiser W, Luterman A, et al: Hypothermia in trauma victims: An
ominous predictor of survival. J Trauma 271019, 1987
41. Just B, Delva E, Camus Y, et a1 Oxygen uptake during recovery following naloxone.
Anesthesiology 7660, 1992
42. Kearney T, Bentt L, Grode M, et al: Coagulopathy and catecholamines in severe head
injury. J Trauma 32608,1992
43. Krige J, Bornman P, Terblanche J: Therapeutic perihepatic packing in complex liver
trauma. Br J Surg 7943,1992
44. Lamp1 L Disorders of hemostasis after polytrauma. Chirurg 63305, 1992
45. Lucas C, Ledgerwood A Prospective evaluation of hemostatic techniques for liver
injuries. J Trauma 16442, 1976
46. Luna G, Maier R, Pavlin E, et a1 Incidence and effect of hypothermia in seriously
injured patients. J Trauma 271014,1987
47. Madding G: Injuries of the liver. Arch Surg 70:748, 1955
48. McAnena 0, Moore E, Moore F Insertion of a retrohepatic vena cava balloon shunt
through the saphenofemoral junction. Am J Surg 158:463, 1989
49. McGonigal M D Urban firearm deaths: A five-year perspective. J Trauma 35:532,1993
50. McGowan E, Detwiler T Modified platelet response to thrombin. Evidence for two
types of receptor or coupling mechanisms. J Biol Chem 261:739, 1986
51. Mendelson JA The relationship between mechanisms of wounding and principles of
treatment of missile wounds. J Trauma 31:1181, 1991
52. Michenfelder J, Uihlein A, Saw E, et al: Moderate hypothermia in man: Hemodynamic
and metabolic effects. Br J Anaesth 37738, 1965
53. Miller R Antithrombin I11 and trauma patients: Factors that determine low levels. J
Trauma 37442, 1994
54. Morris J, Eddy V, Blinman T, et al: The staged celiotomy for trauma: Issues in
unpacking and reconstruction. Ann Surg 217576, 1993
55. Patt A, McCroskey B, Moore E: Hypothermia-induced coagulopathies in trauma. Surg
Clin North Am 68:775, 1988
56. Phillips T, Soulier G, Wilson R Outcome of massive transfusion exceeding two blood
volumes in trauma and emergency surgery. J Trauma 27903, 1987
 THE DAMAGE CONTROL SEQUENCE AND UNDERLYING LOGIC 777

57. Pringle J: Notes on the arrest of hepatic haemorrhage due to trauma. AM Surg
48:541, 1908
58. Reed R, Bracey A, Hudson J: Hypothermia and blood coagulation: Dissociation be-
tween enzyme activity and clotting levels. Circ Shock 32141, 1990
59. Reilly P, Rotondo M, Carpenter J, et al: Temporary vascular continuity during damage
control: Intraluminal shunting for proximal superior mesenteric artery injury. J Trauma
39:757, 1995
60. Rohrer M, Natale A: Effect of hypothermia on the coagulation cascade. Crit Care Med
201402, 1992
61. Rotondo M, Schwab CW, McGonigal M, et al: "Damage control": An approach for
improved survival in exsanguinating penetrating abdominal injury. J Trauma 35375,
1993
62. Rutherford E, Morris J, Reed G, et al: Base deficit stratifies mortality and determines
therapy. J Trauma 33:417, 1992
63. Rutledge R, Sheldon G, Collins M: Massive transfusion. Crit Care Clin 2791, 1986
64. Saifi J, Fortune J, Graca L, et al: Benefits of intra-abdominal pack placement for the
management of nonchemical hemorrhage. Arch Surg 125:119,1990
65. Schein M, Wittmann D, Aprahamian C, et a1 The abdominal compartment syndrome:
The physiological and clinical consequences of elevated intra-abdominal pressure. J
Am Coll Surg 180745, 1995
66. Schmidt U, Enderson B, Chen J, et al: D-Dimer levels correlate with pathologic throm-
bosis in trauma patients. J Trauma 33:312, 1992
67. Schwab C W Violence: America's uncivil war. Presidential Address, Sixth Scientific
Assembly of the Eastern Association for the Surgery of Trauma. J Trauma 35:657, 1993
68. Sharp K, Locicero R Abdominal packing for surgically uncontrollable hemorrhage.
Ann Surg 215467,1992
69. Shen G, Rappaport W. Control of nonhepatic intra-abdominal hemorrhage with tempo-
rary packing. Surg Gynecol Obstet 174411, 1992
70. Slobnan G, Jed E, Burchard K Adverse effects of hypothermia in postoperative
patients. Am J Surg 149:495, 1985
71. Steinemann S, Shackford S, Davis J: Implications of admission hypothermia in trauma
patients. J Trauma 30200, 1990
72. Stone H, Strom P, Mullins R Management of the major coagulopathy with onset
during laparotomy. Ann Surg 197532, 1983
73. Svoboda J, Peter E, Dang C, et al: Severe liver trauma in the face of coagulopathy. Am
J Surg 144717, 1982
74. Talbert S, Trooskin S, Scalea T, et al: Packing and re-exploration for patients with
nonhepatic injuries. J Trauma 33:121, 1992
75. Thomas S, Dulchavsky S, Diebel L: Balloon tamponade for liver injuries: Case report.
J Trauma 34:448, 1993
76. Valeri C, Cassidy G, Khuri S Hypothermia-induced reversal and platelet dysfunction.
Ann Surg 205:175, 1987
77. Weil M, Afifi A: Experimental and clinical studies on lactate and pyruvate as indication
of the severity of acute circulatory failure. Circulation 41:989, 1990
78. Wilson R, Dulchavsky S, Soullier G: Problems with 20 or more blood transfusions in
24 hours. Am Surg 53:410, 1987
79. Wudel J, Morris J, Yates K, et al: Massive transfusion: Outcome in blunt trauma
patients. J Trauma 31:1, 1991
80. Yoshihara H, Yamamoto T, Mihara H Changes in coagulation and fibrinolysis oc-
curring in dogs during hypothermia. Thromb Res 37503, 1985

Address reprint requests to

Michael F. Rotondo, MD, FACS
Division of Trauma and Surgical Critical Care
Department of Surgery
University of Pennsylvania Medical Center
Philadelphia, PA 19104