Damage Control Resuscitation: The New Face of Damage Control J. trauma Volume 69(4), October 2010, pp 976-990

1. Damage Control Resuscitation:
The New Face of Damage Control
Volume 69(4), October 2010, pp 976-990

2. 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.

3. Damage Control
Originally coined by the US Navy in reference
to techniques for salvaging a ship.

4. “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.

5. 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.

6. 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.

7. PERMISSIVE HYPOTENSION

8. 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.

9. 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

10. 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.

11. Trauma patients without definitive
hemorrhage control should have a
limited increase in blood pressure until
definitive surgical control of bleeding
can be achieved.

12. ISOTONIC
CRYSTALLOIDS

13. ISOTONIC CRYSTALLOIDS
Isotonic fluid administration in large boluses
for acute hemorrhagic loss or severe
traumatic injury requiring massive
transfusion is the optimal therapy.

14. 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.

15. HYPERTONIC
SALINE

16. 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.

17. HTS with dextran (HSD)
Risks and concerns associated with HSD
Uncontrolled bleeding
Hyperchloremic acidosis
Central pontine myelinolysis (CPM)
– Keeping serum Na <155 and not raising >10 mEq/d

18. COMPONENTS OF COAGULOPATHY

19. TRAUMA
• Fluid administration
Hemorrhage
• Operative exposure
Coagulopathy Acidosis
Hypothemia

20. Hypothermia
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

21. Acidosis
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.

22. 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.

23. Injury and Ischemia
Hypoperfusion
Base Deficit > -6
Endothelium Endothelium expresses
releases tPA thrombomodulin (TM)
TM complexes with thrombin
Hyperfibrinolysis
Protein C pathway activated
Fibrinogen
Depletion
Extrinsic pathway inhibited
Trauma-Induced Systemic
Coagulopathy anticoagulation

24. 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.

25. 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.

26. A Blood- and Coagulation Factor-
Based Resuscitation Strategy

27. Early Identification of Shock
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.

28. ABC Scoring
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.

29. DAMAGE CONTROL
RESUSCITATION

30. Resuscitation With FFP
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.

31. The optimal ratio of FFP to PRBC was 1:1
and that this should be given early in
the course.

32. Resuscitation With Blood
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.

33. 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.

34. FWB transfusion is currently primarily
limited to the most severely injured
military combat casualties.

35. Recombinant Factor VIIA
The rFVIIa is currently only approved by the FDA
for the treatment of hemophilia, with all trauma
uses being off-label.

36. 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.

37. 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.

38. rFVIIa seems to be safe and possibly
decreases transfusion in blunt trauma.
rFVIIa has not shown any efficacy in
penetrating trauma.

39. DAMAGE CONTROL
SURGERY

40. 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.

41. Three Phases of 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

42. 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.

43. 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.

44. 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.

45. CONCLUSION
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.