Volume 69(4), October 2010, pp 976-990

Damage Control Resuscitation:

The New Face of Damage Control

Hemorrhage accounts for 40% of all trauma-associated deaths.

Damage control resuscitation (DCR) is a treatment strategy that targets the conditions that exacerbate hemorrhage in trauma patients.

Topics reviewed and discussed will include DCR and surgery, transfusion ratios, permissive hypotension, recombinant factor VIIa (rFVIIa), hypertonic fluid solutions, and the destructive forces of hypothermia, acidosis, and coagulopathy.

Originally coined by the US Navy in reference

to techniques for salvaging a ship.

Damage Control

“Damage control” has been adapted to truncating initial surgical procedures on severely injured patients to provide only interventions necessary to control hemorrhage and contamination to focus on reestablishing a survivable physiologic status.

These temporized patients would then undergo continued resuscitation and aggressive correction of their coagulopathy, hypothermia, and acidosis in the ICU before returning to the OR for the definitive repair of their injuries.

Discussions of damage control surgery usually

center on the type and timing of surgical

procedures.

Recently, methods of resuscitation of patients with

exsanguinating hemorrhage have come under

increasing scrutiny for their ability to adequately

correct the acidosis, hypothermia, and

coagulopathy seen in these patients.

DCR differs from current resuscitation

approaches by attempting an earlier and more

aggressive correction of coagulopathy and

metabolic derangement.

DCR centers on the application of several key

concepts, the permissive hypotension, the use

of blood products over isotonic fluid for volume

replacement, and the rapid and early correction

of coagulopathy with component therapy.

PERMISSIVE HYPOTENSION

Keep the blood pressure low enough to avoid

exsanguination while maintaining perfusion of

end organs.

Injection of a fluid that will increase blood

pressure has dangers in itself.

If the pressure is raised before the surgeon is

ready to check bleeding, blood that is sorely

needed may be lost.

PERMISSIVE HYPOTENSION

Endpoint of resuscitation before definitive hemorrhage control was a systolic pressure of 70 to 80 mmHg, using a crystalloid/ colloid mixture as his fluid of choice.

Cannon WB. JAMA. 1918;70:618.

“When the patient must wait for a considerable period, elevation of his SBP to 85 mmHg is all that is necessary … and when profuse internal bleeding is occurring, it is wasteful of time and blood to attempt to get a patient’s blood pressure up to normal. One should consider himself lucky if a systolic pressure of 80 to 85 mmHg can be achieved and then surgery undertaken.”

Beecher HK. U.S. Government Printing Office; 1952:6

Regardless of the victim’s blood pressure,

survival was better in their urban “scoop and

run” rapid transport system when no attempt

at prehospital resuscitation was made.

Immediate vs. delayed fluid resuscitation for hypotensive

patients with penetrating torso injuries.

N Engl J Med. 1994;331:1105–1109.

Trauma patients without definitive

hemorrhage control should have a

limited increase in blood pressure until

definitive surgical control of bleeding

can be achieved.

ISOTONIC

CRYSTALLOIDS

Isotonic fluid administration in large boluses

for acute hemorrhagic loss or severe

traumatic injury requiring massive

transfusion is the optimal therapy.

ISOTONIC CRYSTALLOIDS

Crystalloids can cause dilutional coagulopathy and do little for the oxygen carrying capacity needed to correct anaerobic metabolism and the oxygen debt associated with shock.

The use of unwarmed fluids can also be implicated as a major cause for hypothermia.

Crystalloids have been associated with hyperchloremic acidosis and the worsening of trauma patients existing acidosis.

Isotonic, hypotonic, and colloid solutions given post-injury have been shown to leak and cause edema with only a fraction remaining within the intravascular system.

HYPERTONIC

SALINE

HTS attractive for its ability to raise blood pressure

quickly at much lower volumes of infusion than

isotonic fluids and, thus, potentially easier to use

and transport into combat.

HYPERTONIC SALINE

Risks and concerns associated with HSD

Uncontrolled bleeding

Hyperchloremic acidosis

Central pontine myelinolysis (CPM)

– Keeping serum Na <155 and not raising >10 mEq/d

HTS with dextran (HSD)

COMPONENTS OF COAGULOPATHY

TRAUMA

Hem

orr

hag

e

Coagulopathy Acidosis

Hypothemia

• Fluid administration

• Operative exposure

Severe hypothermia is associated with a high

mortality.

Most cases of hypothermia

– ER: resuscitation period

– OR: exposure of the peritoneum

Hypothermic patients were hypocoagulable with

body temperatures < 34.0°C

Hypothermia

Metabolic acidosis is the predominant physiologic defect resulting from persistent hypoperfusion.

Acidosis at pH < 7.2 is associated with decreased contractility and cardiac output, vasodilation, hypotension, bradycardia, increased dysrhythmias, and decreased blood flow to the liver and kidneys.

Acidosis can also act synergistically with hypothermia in its detrimental effect on the coagulation cascade.

Acidosis

More sensitive measures of the adequacy of

cellular oxygenation are the base deficit and

serum lactate.

The base deficit and lactate serve as a useful

guide for the adequacy of resuscitation

efforts.

Lactate has been demonstrated to have the

best association with hypovolemic shock and

death and is a useful marker as an endpoint of

resuscitation.

Injury and Ischemia

Hypoperfusion

Base Deficit > -6

Endothelium expresses

thrombomodulin (TM)

TM complexes with thrombin

Protein C pathway activated

Extrinsic pathway inhibited

Systemic

anticoagulation

Endothelium

releases tPA

Hyperfibrinolysis

Fibrinogen

Depletion

Trauma-Induced

Coagulopathy

The coagulopathy of trauma is one of the single

most accurate predictors of prognosis in trauma

and is one of the most significant challenges to

any DCR effort.

TRAUMA-INDUCED COAGULOPATHY

In severely injured patients, coagulopathy can

be exacerbated during initial care, resuscitation,

and stabilization.

More than 5 units of pRBC will lead to a

dilutional coagulopathy, that prolongation of

the PT was a sentinel sign of dilutional

coagulopathy, and that this phenomenon occurs

early.

A Blood- and Coagulation Factor-

Based Resuscitation Strategy

The combination of altered mental status,

cool/clammy skin, and an absent radial pulse

is a well-established triad, indicating

hypovolemic shock.

When examining vital signs, the shock index

(SI= HR/SBP) is a better indicator of shock than

hypotension and is more sensitive than

individual vital signs analysis.

Laboratory findings indicative of hypoperfusion

include bicarbonate, base deficit, and lactate.

Early Identification of Shock

1. Penetrating mechanism

2. Positive FAST

3. SBP ≦ 90 mmHg on arrival

4. Heart rate ≧120 bpm on arrival

Score ≧ 2 is 75% sensitive and 86% specific for predicting massive transfusion

Early prediction of massive transfusion in trauma: Simple as ABC (assessment of blood consumption)?

J Trauma. 2009;66:346–352.

ABC Scoring

DAMAGE CONTROL

RESUSCITATION

Hewson et al. recommended that FFP and pRBCs be given at a ratio of 1:1

Crit Care Med. 1985;13:387–391.

Hirshberg et al. concluded that to avoid coagulopathy, RBCs and FFP must be given in a 3:2 ratio.

J Trauma. 2003;54:454–463.

Patients receiving a “high” ratio of FFP to pRBC (1:1.4) had the lowest overall mortality rates and hemorrhage-related mortality rates and concluded that high FFP to RBC ratio is independently associated with improved survival to hospital discharge.

J Trauma. 2007;63:805–813.

Resuscitation With FFP

The optimal ratio of FFP to PRBC was 1:1

and that this should be given early in

the course.

Fresh whole blood (FWB) was historically used

in transfusion until it fell out of favor in the middle

of the 20th century.

By the late 1980s, component therapy had

almost completely replaced whole blood therapy.

Resuscitation With Blood

Theoretically, FWB replaces all the blood components lost to trauma, including platelets and fully functional clotting factors.

In addition, the components of FWB are more functional than their stored counterparts.

Separating blood into components results in dilution and loss of about half of the viable platelets (88K/L in 1 unit of component therapy vs. 150–400 K/L in 500 mL of FWB), PRBCs (Hct 29% in component therapy vs. 38–50% in FWB), and clotting factors decreasing the coagulation activity of the separated components to 65% when giving a 1:1:1 ratio of component therapy.

FWB transfusion is currently primarily

limited to the most severely injured

military combat casualties.

The rFVIIa is currently only approved by the FDA

for the treatment of hemophilia, with all trauma

uses being off-label.

Recombinant Factor VIIA

Recombinant factor VIIa as adjunctive therapy

for bleeding control in severely injured

trauma patients: two parallel randomized,

placebo-controlled, double-blind clinical trials. J Trauma. 2005;59:8–15; discussion 15–18.

One arm of the trial evaluated its use in blunt trauma

whereas the other assessed its utility in penetrating

trauma. Although there was no change in mortality,

the trial demonstrated a statistically significant

reduction in transfusion required in the blunt trauma

group, whereas the results for the penetrating trauma

group showed no benefit.

Use of activated recombinant coagulation

factor VII in patients undergoing

reconstruction surgery for traumatic fracture

of pelvis or pelvis and acetabulum: a double-

blind, randomized, placebo-controlled trial. Br J Anaesth. 2005;94:586–591.

In a cohort of patients requiring pelvic surgery

demonstrated no significant reduction in

transfusion requirement.

rFVIIa seems to be safe and possibly

decreases transfusion in blunt trauma.

rFVIIa has not shown any efficacy in

penetrating trauma.

DAMAGE CONTROL

SURGERY

Victims of penetrating torso trauma or multiple

blunt trauma with hemodynamic instability are

generally better served with abbreviated

operations that control hemorrhage allowing for

subsequent focus on resuscitation, correction of

coagulopathy, and avoiding hypothermia.

DAMAGE CONTROL SURGERY

1. Initial operation with hemostasis and packing

2. Transport to the ICU to correct the conditions of

hypothermia, acidosis, and coagulopathy

3. Return to the OR for definitive repair of all

temporized injuries

Ann Surg. 1988;208:362–370

Three Phases of Damage Control Surgery

In the case of laparotomy, once a damage

control approach has been initiated, the initial

procedure is directed toward controlling surgical

bleeding.

Bleeding is controlled with either ligation of

vessels, balloon catheter tamponade, or packing.

Splenic and renal injuries are treated with rapid

resections, non-bleeding pancreatic injuries are

simply drained, and liver injuries are packed.

The treatment of hollow viscus perforations

includes either a simple suture closure or rapid

resection of the involved segment.

No anastomoses are performed, and ostomies

are not matured.

At the completion of this portion of the procedure,

the patient can either be transported to the ICU

or to the interventional radiology suite for

embolization of arterial hemorrhage that could

not be controlled during the open procedure,

such as pelvic fracture or liver trauma

involving the arterial circulation.

DCR focuses on early, aggressive

correction of the components of the

lethal triad, hypothermia, coagulopathy,

and acidosis.

This strategy must start in the ER and

continue through the OR and ICU until

the resuscitation is complete.

CONCLUSION