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DAMAGE CONTROL
ORTHOPAEDICS
Presenter - Dr Akhil John
Moderator - Dr N Ravinder Kumar
Contents
• Definition
• Polytrauma
• Physiological Response
• Triage protocol
• Damage control orthopaedics
• Management
Definition
• is an approach that contains and stabilizes orthopaedic injuries so
that the patient’s overall physiology can improve.
• purpose :
- avoid worsening of the patient's condition by the “second hit” of a
major orthopaedic procedure
- delay definitive fracture repair until a time when the overall condition
of the patient is optimized
• Basic principles include arresting hemorrhage;
• restoring blood volume;
• and correcting Coagulopathy, Acidosis and Hypothermia.
• Early rapid fracture stabilization by external fixation
• Avoiding prolonged operative times
• Preventing the onset of thelethal triad ( Coagulopathy, Acidosis &
Hypothermia )
WHAT IS POLYTRAUMA
• Polytrauma and multiple trauma are medical terms
describing the condition of a person who has been subjected
to multiple traumatic injuries, The term is defined via an
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)
⚫Todescribe the overall condition of the pt many trauma scoring
systems have been developed like-
1. Abbrevieted injury scale(AIS)
2. Injury severity scale(ISS)
3. Revised trauma score
4. Anatomic profile
5. Glasgow coma scale
ABBREVIATED INJURY SCALE(AIS):
•AIS is an anatomical scoring
system first introduced in 1969
Injuries are ranked on a scale of 1
to 6,
• with 1 being minor, 5 severe, and
6 a nonsurvivable injury.
Injury severity score(ISS)-
⚫ISS is an anatomical scoring system that provides an overall score for
patients with multiple injuries.
⚫Each injury is assigned an AIS and is allocated to one of six body
regions (Head,Face, Chest, Abdomen, Extremities (including
Pelvis), External).
⚫ Only the highest AIS score in each body region is used.
⚫The 3 most severely injured body regions have their score
• squared and added together to produce the ISS score.
• The ISS score takes values from 0 to 75. If an injury is assigned an AIS
of
• 6 (unsurvivable injury), the
• ISS score is automatically assigned to 75
Physiological response to injury
 Inflammatory immune response
• Innate immune response
• Adaptive immune response
 Systemic Inflammatory Response Syndrome (SIRS)
 Compensatory Anti-inflammatory Response Syndrome (CARS)
 Multi Organ Dysfunction Syndrome (MODS)
Inflammatory immune response
 EARLY innate immune response
 DELAYED adaptive immune response
• Innate = Hyperinflammation = SIRS
• Adaptive = Immunosuppression = CARS
Early innate immune response
 Neutrophils (major cellular ‘player’) are drawn to the site of injury by
IL-8 and C5a (chemokines)
 Priming neutrophils for defence and debridement of injured
tissue, and mediating inflammation
 Activation of PMN, monocytes, macrophages, NKC and endothelial
cells
 Release of pro-inflammatory mediators (cytokines and
molecular mediators)
 Considered the hyperinflammatory period
SIRS DEFINITION
 Heart rate: > 90 bpm
 WBC: <4000/mm3 or >12000/mm3 or >10% immature PMNs
 Respiratory rate: >20/min with PaCO2<32mmHg
 Core temperature: <360C or >380C
• 2 of 4 parameters = SIRS
Delayed adaptive immune response
 Non-apoptotic necrotic/dead cells produce alarmins plus
Endogenous triggers (DAMPs = damage-associated molecular
patterns)
 CD5+ B-cells to produce natural antibody without prior exposure and
subsets of T- cells to inflict self-reactivity → autoimmune tissue
destruction
 Considered the immunosuppression period or CARS
Interplay of SIRS and CARS
2- 4 Days
24
–
48
H.
6-8 Days
Pathological immune response
• IMBALANCE BETWEEN SIRS AND CARS
• Severe injury 1st Hit Intense CARS
Early MODS/death
• Moderate Injury 1st Hit Incomplete Resolution
• 2nd Operation within D3-5 Sepsis
Amplification of SIRS
Delayed-onset MODS/death
•
MODS
 Cerebral - Cerebral edema
 CVS - Hypotension and shock
 Respiratory- Acute lung injury, ARDS
 Liver - High APR and cytokines, hepatocytes dysfunction
 GI - Increased mucosal permeability , Bacterial translocation
 Renal - Renal tubular necrosis, acute renal failure
 Hematologic - DIC
Polytrauma (2 hit phenomenon)
‘First Hit’ Impacts by Trauma
The Patient The Limb/Organ System
‘Second Hit’ Impacts by Surgery and Resuscitation
The Patient The Limb
First Hit Impacts - How do you decide your
fluid replacement?
• Classification of Hypovolaemic Shock and Physiologic Changes
Class I Class II Class III Class IV
Blood loss (liter) Up to 0.75 0.75-1.5 1.5-2.0 > 2
% TBV 15% 30% 40% >40%
Pulse rate < 100 > 100 >120 >140
Blood pressure Normal Normal Decreased Decreased
Pulse pressure Normal or inc Decreased Decreased Decreased
Respiratory rate 14-20 20-30 30-40 >35
Urine output > 30 ml/hr 20-30 5-15 Negligible
Mental status Slightly anxious Mildly anxious Anxious/confused Confused/lethargic
Fluid Replacement Crystalloid Crystalloid Crystalloid and blood Crystalloid and blood
What is your fluid replacement regimen?
• Fluid resuscitation
• Shock due to primary haemmorrhage
Ongoing bleeeding 2o resuscitation regimen
Lethal triad Coagulopathy , acidosis ,
hypothermia
Voluminous crystalloid
• Dilutes coagulation factors
• Causes hypochloremic and lactate acidosis
• Supplies inadequate O2 to under perfused tissue
HAEMODYNAMIC ‘TRIAGE’ PROTOCOL
PATIENT CLINICALLY ASSESSED ABOUT THEIR PHYSICAL STATUS
AND CLASSIFIED AS:-
1. STABLE: GRADE 1
2. BORDERLINE: GRADE2
3. UNSTABLE: GRADE 3
4. EXTREMIS: GRADE 4
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
Temperature >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
Non-surgical DCR
1. Fluid Replacement in Balanced Resuscitation
● Initial fluid replacement with up to 2L crystalloid
Permissive hypotension to achieve SBP to 80- 90mmHg
• (radial pulse) until definitive control of bleeding is obtained
● Role of fluid challenge (250-500ml) tests to stratify responder, transient
responder, non-responder
2. Haemostatic Resuscitation
● Early blood versus HBOC transfusion decreases MODS
● Packed RBC, FFP and Platelets in 1:1:1 ratio
● Cryoprecipitate, Tranexamic acid, Recombinant factor-
3. Correction of Metabolic Derangement
● Role of THAM (Tris-hydroxmethyl-amino-methane)
● Use of NaHCO3 to correct acidosis causes
hypercapnia?
4.Hypothermia Prevention and Treatment Strategies
● Limit casualties’ exposure
● Warm IV fluids and blood products before transfusion
● Use forced air warming devices before and after surgery
● Use carbon polymer heating mattress
Application of DCO
Stage 1
10 rapid temporary # stabilization (in trauma room/ICU/OR)
• 1.Control hemmorhage e.g. ext-fix pelvis
• 2.Debridement of open wound
• 3.Spanning ext-fix or unreamed nailing or reamed nailing using RIA
Stage 2
Resuscitation and ICU management
• 1.Close monitoring
• 2.Repletion of blood product
• 3.Further hemodynamic stabilization
Stage 3
• Definitive # fixation once the patient is optimized (avoid day 2-5)
Injury complexes
suitable for damage
control orthopaedics
Femur Fracture
• Femoral fractures in a multiply injured patient are not
automatically treated with intramedullary nailing because :
-second hit’
- fat emboli
• Patients with a chest injury are most prone to deterioration
after an intramedullary nailing procedure
• Bilateral femoral fracture is associated with a higher mortality rate
and incidence of adult respiratory distress syndrome than is a
unilateral femoral fracture
• Increase in mortality may be more closely related to associated
injuries and physiologic parameters than to the bilateral femoral
fracture itself
Pelvic Ring Injuries
• Exsanguinating haemorrhage associated with pelvic fracture
• Conditions where haemorrhage can be expected, when
there is pelvic injury :
• -Posterior pelvic ring injuries
• -Anterior-posterior compression type III injuries, lateral compression
injuries
• -Pelvic fracture in patients over 55 years old
Mangement
• Minimally invasive pelvic stabilisation
 Pelvic binder
 External fixator
 Pelvic c-clamp
 Pelvic stabilizer
• Angiography and embolisation Indications :
1.Initial treatment of pelvic fractures associated with hypotension that
have not responded to the placement of a pelvic binder, external fixator,
pelvic c- clamp, or pelvic stabilizer and transfusion of four units or more
of blood
2. expanding retroperitoneal hematoma,
3. a vascular blush seen on CT
4. a massive retroperitoneal hematoma observed on CT
- Timing is important
- Embolisation later than 3 hours after injury increased risk of mortality
• -Average procedure time is 90 minutes
• Pelvic Packing Indication :
• 1. Patient with severe hypotension and a pelvic fracture that is unresponsive
to other initial treatment measures, associated with imminent risk of death
Chest Injuries
• Treatment of multiply injured patients with long bone fractures and a
chest injury:
• early fracture stabilisation (within 48 hours)is safe and may be
beneficial
• early fracture stabilisation is safe and maybe beneficial
Head Injuries
• Early stabilisation doesn’t enhance or worsen the outcome in
patients with head injury.
• Management :
• Based on the individual clinical assessment and
treatment requirements
• Damage control orthopaedics can provide temporary
osseous stability to an injured extremity, functioning as a
temporary bridge to staged definitive osteosynthesis,
without worsening the patient's head injury or overall
condition.
• Aggressive management of intracranial pressure
• Maintenance of cerebral perfusion pressure at >70 mm Hg
and intracranial pressure at <20 mm Hg
Mangled Extremities
• DCO approach to save the limb :
a) Spanning external fixator
b)Antibiotic bead pouches
c) Vacuum assisted wound closure
Antibiotic bead pouch for
treatment of an open
proximal tibial fracture
Isolated Complex Lower-Extremity Trauma
• “limb damage control orthopaedics”
• Proximal tibial articular and metaphyseal fractures,
metaphyseal fractures, distal tibial pilon fractures
• Useful for preventing soft-tissue complications by spanning the
articular segment with an external fixator and avoiding areas of
future incisions.
• Then minimally invasive plate osteosynthesis can be performed at a
stage when the condition of the soft tissue envelope is optimized.
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 Hyperinflammation ‘Second-look’ only
Day 6-10 Window of opportunity Definitive surgery
Day 12-21 Immunosuppression No surgery
Week 3+ Recovery 20 reconstructive surgery
DCO surgery
 External fixation
 Nailing if ISS<25
• 🞑 Unreamed/retrograde
• 🞑 Usage of new One-step Reamer-Irrigator- Aspirator
Mangled extremities -
Amputations vs Reconstruction
• Amputation group have a better
functional outcome rather than
the reconstruction and rapid
return to work
• Reconstruction group have
higher complication rate ,needs
more surgeries , more hospital
admissions
• 6.4% risk of amputation
Minimally invasive operations
External fixation of femur-
35 minutes 90 ml blood loss
Intramedullary nailing of
femur-130 minutes 400 ml blood
loss
Reamed IMN vs Ex Fix
• Reamed Intramedullary nailing Has been associated with
development of “second hit” phenomena
 Primary external fixation
• has not stimulated any inflammatory reaction“second hit”
Skeletal traction vs External fixation
External fixation of femur fractures in severely injured patients offers
no significant advantages compared with skeletal traction. The use of
ST as a temporization method remains a practical option.
CONCLUSION
• Incidence of Polytrauma is rising
• Initial evaluation and stabilisation is of paramount importance
• Changing trends in fluid therapy
• Proper selection of patient for ETC and DCO
• Multidisciplinary approach
DCO principles in polytrauma
Ortho team must be resuscitatorsand
stabilizers: not “fixers”
•THANK YOU

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DAMAGE CONTROL ORTHOPAEDICS.pptx

  • 1. DAMAGE CONTROL ORTHOPAEDICS Presenter - Dr Akhil John Moderator - Dr N Ravinder Kumar
  • 2. Contents • Definition • Polytrauma • Physiological Response • Triage protocol • Damage control orthopaedics • Management
  • 3. Definition • is an approach that contains and stabilizes orthopaedic injuries so that the patient’s overall physiology can improve. • purpose : - avoid worsening of the patient's condition by the “second hit” of a major orthopaedic procedure - delay definitive fracture repair until a time when the overall condition of the patient is optimized
  • 4. • Basic principles include arresting hemorrhage; • restoring blood volume; • and correcting Coagulopathy, Acidosis and Hypothermia.
  • 5. • Early rapid fracture stabilization by external fixation • Avoiding prolonged operative times • Preventing the onset of thelethal triad ( Coagulopathy, Acidosis & Hypothermia )
  • 6. WHAT IS POLYTRAUMA • Polytrauma and multiple trauma are medical terms describing the condition of a person who has been subjected to multiple traumatic injuries, The term is defined via an 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)
  • 7. ⚫Todescribe the overall condition of the pt many trauma scoring systems have been developed like- 1. Abbrevieted injury scale(AIS) 2. Injury severity scale(ISS) 3. Revised trauma score 4. Anatomic profile 5. Glasgow coma scale
  • 8. ABBREVIATED INJURY SCALE(AIS): •AIS is an anatomical scoring system first introduced in 1969 Injuries are ranked on a scale of 1 to 6, • with 1 being minor, 5 severe, and 6 a nonsurvivable injury.
  • 9. Injury severity score(ISS)- ⚫ISS is an anatomical scoring system that provides an overall score for patients with multiple injuries. ⚫Each injury is assigned an AIS and is allocated to one of six body regions (Head,Face, Chest, Abdomen, Extremities (including Pelvis), External). ⚫ Only the highest AIS score in each body region is used.
  • 10. ⚫The 3 most severely injured body regions have their score • squared and added together to produce the ISS score. • The ISS score takes values from 0 to 75. If an injury is assigned an AIS of • 6 (unsurvivable injury), the • ISS score is automatically assigned to 75
  • 11. Physiological response to injury  Inflammatory immune response • Innate immune response • Adaptive immune response  Systemic Inflammatory Response Syndrome (SIRS)  Compensatory Anti-inflammatory Response Syndrome (CARS)  Multi Organ Dysfunction Syndrome (MODS)
  • 12. Inflammatory immune response  EARLY innate immune response  DELAYED adaptive immune response • Innate = Hyperinflammation = SIRS • Adaptive = Immunosuppression = CARS
  • 13. Early innate immune response  Neutrophils (major cellular ‘player’) are drawn to the site of injury by IL-8 and C5a (chemokines)  Priming neutrophils for defence and debridement of injured tissue, and mediating inflammation  Activation of PMN, monocytes, macrophages, NKC and endothelial cells  Release of pro-inflammatory mediators (cytokines and molecular mediators)  Considered the hyperinflammatory period
  • 14. SIRS DEFINITION  Heart rate: > 90 bpm  WBC: <4000/mm3 or >12000/mm3 or >10% immature PMNs  Respiratory rate: >20/min with PaCO2<32mmHg  Core temperature: <360C or >380C • 2 of 4 parameters = SIRS
  • 15. Delayed adaptive immune response  Non-apoptotic necrotic/dead cells produce alarmins plus Endogenous triggers (DAMPs = damage-associated molecular patterns)  CD5+ B-cells to produce natural antibody without prior exposure and subsets of T- cells to inflict self-reactivity → autoimmune tissue destruction  Considered the immunosuppression period or CARS
  • 16. Interplay of SIRS and CARS 2- 4 Days 24 – 48 H. 6-8 Days
  • 17. Pathological immune response • IMBALANCE BETWEEN SIRS AND CARS • Severe injury 1st Hit Intense CARS Early MODS/death • Moderate Injury 1st Hit Incomplete Resolution • 2nd Operation within D3-5 Sepsis Amplification of SIRS Delayed-onset MODS/death •
  • 18. MODS  Cerebral - Cerebral edema  CVS - Hypotension and shock  Respiratory- Acute lung injury, ARDS  Liver - High APR and cytokines, hepatocytes dysfunction  GI - Increased mucosal permeability , Bacterial translocation  Renal - Renal tubular necrosis, acute renal failure  Hematologic - DIC
  • 19. Polytrauma (2 hit phenomenon) ‘First Hit’ Impacts by Trauma The Patient The Limb/Organ System
  • 20. ‘Second Hit’ Impacts by Surgery and Resuscitation The Patient The Limb
  • 21. First Hit Impacts - How do you decide your fluid replacement? • Classification of Hypovolaemic Shock and Physiologic Changes Class I Class II Class III Class IV Blood loss (liter) Up to 0.75 0.75-1.5 1.5-2.0 > 2 % TBV 15% 30% 40% >40% Pulse rate < 100 > 100 >120 >140 Blood pressure Normal Normal Decreased Decreased Pulse pressure Normal or inc Decreased Decreased Decreased Respiratory rate 14-20 20-30 30-40 >35 Urine output > 30 ml/hr 20-30 5-15 Negligible Mental status Slightly anxious Mildly anxious Anxious/confused Confused/lethargic Fluid Replacement Crystalloid Crystalloid Crystalloid and blood Crystalloid and blood
  • 22. What is your fluid replacement regimen? • Fluid resuscitation • Shock due to primary haemmorrhage Ongoing bleeeding 2o resuscitation regimen Lethal triad Coagulopathy , acidosis , hypothermia
  • 23. Voluminous crystalloid • Dilutes coagulation factors • Causes hypochloremic and lactate acidosis • Supplies inadequate O2 to under perfused tissue
  • 24. HAEMODYNAMIC ‘TRIAGE’ PROTOCOL PATIENT CLINICALLY ASSESSED ABOUT THEIR PHYSICAL STATUS AND CLASSIFIED AS:- 1. STABLE: GRADE 1 2. BORDERLINE: GRADE2 3. UNSTABLE: GRADE 3 4. EXTREMIS: GRADE 4
  • 25. 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 Temperature >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
  • 26. Non-surgical DCR 1. Fluid Replacement in Balanced Resuscitation ● Initial fluid replacement with up to 2L crystalloid Permissive hypotension to achieve SBP to 80- 90mmHg • (radial pulse) until definitive control of bleeding is obtained ● Role of fluid challenge (250-500ml) tests to stratify responder, transient responder, non-responder 2. Haemostatic Resuscitation ● Early blood versus HBOC transfusion decreases MODS ● Packed RBC, FFP and Platelets in 1:1:1 ratio ● Cryoprecipitate, Tranexamic acid, Recombinant factor-
  • 27. 3. Correction of Metabolic Derangement ● Role of THAM (Tris-hydroxmethyl-amino-methane) ● Use of NaHCO3 to correct acidosis causes hypercapnia? 4.Hypothermia Prevention and Treatment Strategies ● Limit casualties’ exposure ● Warm IV fluids and blood products before transfusion ● Use forced air warming devices before and after surgery ● Use carbon polymer heating mattress
  • 28. Application of DCO Stage 1 10 rapid temporary # stabilization (in trauma room/ICU/OR) • 1.Control hemmorhage e.g. ext-fix pelvis • 2.Debridement of open wound • 3.Spanning ext-fix or unreamed nailing or reamed nailing using RIA Stage 2 Resuscitation and ICU management • 1.Close monitoring • 2.Repletion of blood product • 3.Further hemodynamic stabilization
  • 29. Stage 3 • Definitive # fixation once the patient is optimized (avoid day 2-5)
  • 30. Injury complexes suitable for damage control orthopaedics
  • 31. Femur Fracture • Femoral fractures in a multiply injured patient are not automatically treated with intramedullary nailing because : -second hit’ - fat emboli • Patients with a chest injury are most prone to deterioration after an intramedullary nailing procedure
  • 32. • Bilateral femoral fracture is associated with a higher mortality rate and incidence of adult respiratory distress syndrome than is a unilateral femoral fracture • Increase in mortality may be more closely related to associated injuries and physiologic parameters than to the bilateral femoral fracture itself
  • 33. Pelvic Ring Injuries • Exsanguinating haemorrhage associated with pelvic fracture • Conditions where haemorrhage can be expected, when there is pelvic injury : • -Posterior pelvic ring injuries • -Anterior-posterior compression type III injuries, lateral compression injuries • -Pelvic fracture in patients over 55 years old
  • 34. Mangement • Minimally invasive pelvic stabilisation  Pelvic binder  External fixator  Pelvic c-clamp  Pelvic stabilizer • Angiography and embolisation Indications : 1.Initial treatment of pelvic fractures associated with hypotension that have not responded to the placement of a pelvic binder, external fixator, pelvic c- clamp, or pelvic stabilizer and transfusion of four units or more of blood
  • 35. 2. expanding retroperitoneal hematoma, 3. a vascular blush seen on CT 4. a massive retroperitoneal hematoma observed on CT - Timing is important - Embolisation later than 3 hours after injury increased risk of mortality • -Average procedure time is 90 minutes • Pelvic Packing Indication : • 1. Patient with severe hypotension and a pelvic fracture that is unresponsive to other initial treatment measures, associated with imminent risk of death
  • 36. Chest Injuries • Treatment of multiply injured patients with long bone fractures and a chest injury: • early fracture stabilisation (within 48 hours)is safe and may be beneficial • early fracture stabilisation is safe and maybe beneficial
  • 37. Head Injuries • Early stabilisation doesn’t enhance or worsen the outcome in patients with head injury. • Management : • Based on the individual clinical assessment and treatment requirements • Damage control orthopaedics can provide temporary osseous stability to an injured extremity, functioning as a temporary bridge to staged definitive osteosynthesis, without worsening the patient's head injury or overall condition. • Aggressive management of intracranial pressure • Maintenance of cerebral perfusion pressure at >70 mm Hg and intracranial pressure at <20 mm Hg
  • 38. Mangled Extremities • DCO approach to save the limb : a) Spanning external fixator b)Antibiotic bead pouches c) Vacuum assisted wound closure Antibiotic bead pouch for treatment of an open proximal tibial fracture
  • 39. Isolated Complex Lower-Extremity Trauma • “limb damage control orthopaedics” • Proximal tibial articular and metaphyseal fractures, metaphyseal fractures, distal tibial pilon fractures • Useful for preventing soft-tissue complications by spanning the articular segment with an external fixator and avoiding areas of future incisions. • Then minimally invasive plate osteosynthesis can be performed at a stage when the condition of the soft tissue envelope is optimized.
  • 40. 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 Hyperinflammation ‘Second-look’ only Day 6-10 Window of opportunity Definitive surgery Day 12-21 Immunosuppression No surgery Week 3+ Recovery 20 reconstructive surgery
  • 41. DCO surgery  External fixation  Nailing if ISS<25 • 🞑 Unreamed/retrograde • 🞑 Usage of new One-step Reamer-Irrigator- Aspirator
  • 42. Mangled extremities - Amputations vs Reconstruction • Amputation group have a better functional outcome rather than the reconstruction and rapid return to work • Reconstruction group have higher complication rate ,needs more surgeries , more hospital admissions • 6.4% risk of amputation
  • 43. Minimally invasive operations External fixation of femur- 35 minutes 90 ml blood loss Intramedullary nailing of femur-130 minutes 400 ml blood loss
  • 44. Reamed IMN vs Ex Fix • Reamed Intramedullary nailing Has been associated with development of “second hit” phenomena  Primary external fixation • has not stimulated any inflammatory reaction“second hit”
  • 45. Skeletal traction vs External fixation External fixation of femur fractures in severely injured patients offers no significant advantages compared with skeletal traction. The use of ST as a temporization method remains a practical option.
  • 46. CONCLUSION • Incidence of Polytrauma is rising • Initial evaluation and stabilisation is of paramount importance • Changing trends in fluid therapy • Proper selection of patient for ETC and DCO • Multidisciplinary approach DCO principles in polytrauma Ortho team must be resuscitatorsand stabilizers: not “fixers”