Control Orthopedics (DCO) provides guidelines for treating orthopedic injuries in polytrauma patients. It recognizes that definitive surgical stabilization can worsen a physiologically compromised patient's condition. DCO aims to 1) control hemorrhage and provisionally stabilize fractures, 2) avoid further physiological insult through delayed definitive repair, and 3) get the patient's condition optimized before further surgery. For unstable patients, DCO relies on external fixation and temporary stabilization rather than immediate internal fixation to minimize surgical impact. The approach balances fracture management with the overall goal of stabilizing the patient's physiology.

1. CONTROL
ORTHOPAEDICS(D
CO)
Presented
By
Hany A.Y. Al-Dakar
Consultant of Orthopedic&
Traumatology
Al-Mahmoudia General Hospital

3. OBJECTIVES
By the end of this lecture the Trainees will be
able to :
1) Know the history of damage control
orthopedics (DCO).
2) Understand the pathophysiology of DCO.
3) Define poly-trauma patient.
4) Know steps of DCO strategy.

4. HISTORICAL
REVIEW

5. IN 1960S
RATIONALE FOR DELAYED FIXATION-:-
 The philosophy prevailed that the poly-
trauma patient was ‘too sick to operate
on’
 The development of fat embolism
syndrome and pulmonary dysfunction
was feared
 Definitive surgical stabilization was often
delayed to 10-14 days
 Cast and skeletal tractions preferred

6. 1970S :-
Pioneering studies showed
that early stabilization of
femoral fractures reduces
dramatically the incidence of
Fat Emb. Syndrome,
pulmonary failure (ARDS) and
postoperative complications

7. IN1980S
RATIONALE OF EARLY FIXATION
(ETC) EARLY TOTAL CARE):-
“There is a beneficial effect of early stabilization of fractures
on both mortality and morbidity and length of hospital stay.”
This new philosophy was named Early Total Care ( ETC ).
“The patient is too sick not to be treated surgically”
Surgeries were done within 24 hrs of admission

8. A variety of unexpected complications related to the early
stabilization of fractures of long bones was described.
These complications mainly developed in patients with
severe chest injuries,
severe hemodynamic shock
post reamed intramedullary nailing without thoracic
trauma.
IN THE EARLY 1990S

9. This led to the conclusion that the
method of stabilization and the timing
of surgery may have played a major
role in the development of such
complications.

10. 1990S
THE EVOLUTION OF DAMAGE CONTROL
ORTHOPAEDICS
 An approach to achieve rapid skeletal
stabilization of major orthopedic
injuries to stop the cycle of ongoing
musculo -skeletal injury and to control
hemorrhage
 Its purpose is to avoid worsening of
the patient's condition by the "second
hit" of a major orthopedic procedures

11. WHAT IS
DAMAGE CONTROL ?

12. Damage Control
is a Navy term defined as
“the capacity of a ship to absorb damage and
maintain mission integrity”

13.  SAVE THE SHIPE
 LIMIT THE DAMAGE
 EMERGENCY REPAIR
 FINISH THE MISSION

14. I. Contains & Stabilizes Orthopedic Injuries so that the
Patient’s Overall Physiology can improve
II. Avoid worsening of the patient’s condition by a
major Orthopedic Procedure
III. Delay Definitive Fracture Repair in borderline or
unstable patient till condition is optimized
DAMAGE CONTROL ORTHOPAEDICS (DCO)
Relatively recent concept in Orthopedic
practice that:

15. DAMAGE CONTROL ORTHOPAEDICS (DCO)
Indications:
 Critically ill polytrauma patient
 Unfavorable surgical environment
 Battlefield limb injuries & mass
casualties

16. DAMAGE CONTROL ORTHOPEDICS:
Its priorities are:
• Control of hemorrhage
• Provisional stabilization of major skeletal
fractures
• Management of soft-tissue injuries
• Minimizing the degree of surgical insult
to the patient.

17. 5 TENETS OF DAMAGE CONTROL
ORTHOPAEDICS
1. Recognize who needs damage control.
2. Salvage operations.
3. Keep the patient alive.
4. Accept morbidity of the salvage procedures.
5. 5. Definitive repair later

18. PATHOPHYSIOLOGY

19. HYPOTHERMIA
COAGULOPATHY
BLOOD
TRANSFUSION
BLEEDING
THE BLOODY VICIOUS CIRCLE

20. TRAUMA MORTALITY
Bimodal
Early death
– Blood loss
– Brain injury
Late death
– Secondary brain injury
– Host defense failure -sepsis

21. TWO-HITS THEORY
“Hits” Induce a Host Immune Response
First Hit (Trauma)
 Hypoxia
 Hypotension
 Organ & soft tissue injury
 Fractures
Second Hit (operation)
 Ischemia/reperfusion injury
 Compartment syndrome
 Operative intervention
 Infection

22. PHYSIOLOGICAL RESPONSE TO
INJURY
Early innate response
Systemic Inflammatory Response Syndrome (SIRS)
Delayed adaptive
Compensatory Anti-inflammatory Response
Syndrome (CARS)
Multi Organ Dysfunction Syndrome (MODS)

23. EARLY INNATE IMMUNE RESPONSE
Activation of
PMN
Monocytes
Macrophages
Endothelial cells
Release of
pro-inflammatory mediators
o Cytokines and
o Molecular mediators
Considered Systemic Inflammatory Response
Syndrome (SIRS)

24. PARAMETERS IN TRAUMA
PATIENT
1. Heart rate:
> 90 bpm
2. WBC:
<4000/mm3 or
>12000/mm3 or
>10% immature
PMNs
3. Respiratory rate:
>20/min with
PaCO2<32mmHg
4. Core temperature:
<360C or
 >380C

25. DELAYED ADAPTIVE IMMUNE
RESPONSE
Necrotic/dead cells (Non-apoptotic)
produce Endogenous triggers → auto-
immune tissue destruction
Considered Compensatory Anti-
inflammatory Response Syndrome (CARS)

26. MULTI ORGAN DYSFUNCTION SYNDROME
(MODS)
Pathology
Organ
Cerebral edema
Cerebral
Hypotension and shock
CVS
Acute lung injury, ARDS
Respiratory
hepatocytes dysfunction
Liver
Increased mucosal Bacterial
translocation
GI permeability
Renal tubular necrosis, acute
renal failure
Renal
DIVC
Hematologic

27. PATHOLOGICAL IMMUNE RESPONSE
1st Hit
Moderate Injury 1st Hit
Amplification of SIRS
Delayed-onset MODS/death
Incomplete Resolution
2
nd
Hit
2nd Operation within D3-5
Sepsis
Severe injury Intense CARS
Early MODS/death
IMBALANCE BETWEEN SIRS AND CARS

28. INTERPLAY OF SIRS AND CARS
Systemic
Response
SIRS
CARS
D14
D7
Adaptive Immune
Response
Innate Immune
Response
Insult
Homeostasis
Mild-Moderate Injury
Pro-inflammatory
Anti-inflammatory
Balanced SIRS-CARS maintains homeostasis

29. PATHOLOGICAL IMMUNE RESPONSE
Systemic
Response
SIRS
CARS
Adaptive Immune
Response
Insult
Moderate to severe injury
Pro-inflammatory
Anti-inflammatory
Imbalanced SIRS>CARS leads to hyper-inflammation or delayed MODS
Innate Immune
Response
2
nd
Hit

30. PATHOLOGICAL IMMUNE RESPONSE
Systemic
Response
SIRS
CARS
Adaptive Immune
Response
Innate Immune
Response
Insult
Severe Injury
Pro-inflammatory
Anti-inflammatory
Imbalanced CARS>SIRS leads to hypo-inflammation or early MODS

31. WE‘VE To LIMIT THE 2ND HIT

32. PATIENT SELECTION

33. Poly-trauma Patient
 A Syndrome of Multiple Injuries exceeding a defined
Injury Severity Score ISS > = 17
 Sequential Post traumatic Systemic Inflammatory
Reactions (SIRS)
 Dysfunction or failure of Remote Systems or Organs
which are not injured (MODS – MOF)

34. PATIENT CLINICALLY ASSESSED ABOUT THEIR
PHYSICAL STATUS AND CLASSIFIED AS:-
1. STABLE: GRADE I
2. BORDERLINE: GRADE II
3. UNSTABLE: GRADE III
4. EXTREMIS: GRADE VI

35. PATIENT CATEGORIZATION
Parameter Stable Borderline Unstable In Extremis
Shock SBP (mmHg)
Blood unit/2h
Lactate
Base deficit
UO ml/h
Class
100 or more
0-2
< 2.0
Normal
>150
I
80-100
2-8
2.5
No data
50-150
II-III
60-80
5-15
>2.5
No data
<100
III-IV
50-60
>15
Severe
>6-18
<50
IV
Coagulation Platelets
Factors II/V
Fibrinogen
d-Dimer
>110,000
90-100%
>1 g/dL
Normal
90-110,000
70-80%
1 g/dL
Abnormal
70-90,000
50-70%
<1 g/dL
Abnormal
<70,000
<50%
DIC
DIC
Temperatur
e
>340C 33-350C 30-320C <300C
Soft Tissue
Injuries
Chest AIS
TTS
Abd (Moore)
Pelvic AO
Limb AIS
2 or 2
0
<II
A
I-II
2 or more
I-II
<III
B or C
II-III
2 or more
II-III
III
C
III-IV
3 or more
IV
III or >III
C
Crush

36. BORDER LINE
PATIENTS
COAGULOPATHIC
HYPOTHERMIA
(T <32)
ACIDOSIS
SHOCK
OPRATIVE TIME > 6H
HAEMODYNAMIC
INSTABILITY
EXAGGERATED
INFLAMMATORY
RESPONSE

37. MANAGMENT

38. ORTHOPEDIC INJURY COMPLEX
PROBLEMS
 Femoral fractures in a multiply injured patient
 Pelvic ring injuries with shock
 Poly-trauma in a geriatric patient
 Long bone fractures with chest or head injuries
 Mangled extremities

39. APPLICATION OF DCO STRATEGY
 Multiply injured patient
 Physiologically unstable
 Severe chest injury
 Severe hemorrhage
 Mass casualty situation

40.  Stage 1: early temporary External Fixation,
Stabilization of unstable fractures and the
control of hemorrhage and, if indicated,
decompression of intracranial lesion.
 Stage 2: resuscitation of the patient in ICU and
optimization of his condition.
 Stage 3: delayed definitive management of
the fracture
STATGED TREATMENT

41. Stable
WHAT TO DO ? - CLINICAL STATUS
ETC
Unstable or
In extremis
DCO
OP – ICU ?
Borderline
Resuscitate
Reevaluate

42. Steps of Damage
Control
Orthopaedics
Control Bleeding
Manage Soft tissues
Spanning Ex. Fixator
Antibiotic Pouch
Vacuum Dressings

43. 1. Control Bleeding
2. Manage Soft tissues
3. Spanning External Fixator
4. Antibiotic Pouch
5. Vacuum Dressings

44. SECONDARY PROCEDURE
WHEN?

45. TIMING OF SURGERY
Timing Physiological Status Surgical Intervention
Day 1 Normal response to
resuscitation
Early Total Care
Day 1 Partial response to
resuscitation
Damage Control Surgery
Day 1 No response to
resuscitation
Life-saving surgery
Day 2-5 Hyper-inflammation ‘Second-look’ only
Day 6-10 Window of opportunity Definitive surgery
Day 12-
21
Immunosuppression No surgery
Week 3+ Recovery 20 Reconstructive surgery

46. CONCLUSION

47. DAMAGE CONTROL ORTHOPAEDICS (DCO)
Is a Way of thinking aiming to Save lives not just fixing a
fracture in a limb
Early Skeletal external fixation (DCO) is appropriate as Early
Total Care may be very risky in
Hemodynamic instability
Pulmonary instability
Sever head injury
Lethal triad (Coagulopathy, Hypothermia & Acidosis)

48. DO NOT KILL YOUR
BORDERLINE PATIENT BY
(ETC)
HELP HIM TO LIVE BY (DCO)
GIVE HIM THE CHANCE TO
FIGHT ANOTHER DAY

49. Ortho team must be resuscitators
and stabilizers: not “fixers”