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Damage control orthopedics
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.
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Damage control orthopedics
- 1. CONTROL ORTHOPAEDICS(D CO) Presented By Hany A.Y. Al-Dakar Consultantof Orthopedic& Traumatology Al-Mahmoudia General Hospital
- 3. OBJECTIVES By the endof 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.
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- 5. IN 1960S RATIONALE FORDELAYED 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 studiesshowed that early stabilization of femoral fractures reduces dramatically the incidence of Fat Emb. Syndrome, pulmonary failure (ARDS) and postoperative complications
- 7. IN1980S RATIONALE OF EARLYFIXATION (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 ofunexpected 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 tothe 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 OFDAMAGE 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
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- 12. Damage Control is aNavy term defined as “the capacity of a ship to absorb damage and maintain mission integrity”
- 13. SAVE THESHIPE 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: Itspriorities 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 OFDAMAGE 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
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- 20. TRAUMA MORTALITY Bimodal Early death –Blood loss – Brain injury Late death – Secondary brain injury – Host defense failure -sepsis
- 21. TWO-HITS THEORY “Hits” Inducea 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 Earlyinnate response Systemic Inflammatory Response Syndrome (SIRS) Delayed adaptive Compensatory Anti-inflammatory Response Syndrome (CARS) Multi Organ Dysfunction Syndrome (MODS)
- 23. EARLY INNATE IMMUNERESPONSE 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/deadcells (Non-apoptotic) produce Endogenous triggers → auto- immune tissue destruction Considered Compensatory Anti- inflammatory Response Syndrome (CARS)
- 26. MULTI ORGAN DYSFUNCTIONSYNDROME (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 1stHit 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 SIRSAND 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 AdaptiveImmune 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 AdaptiveImmune 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 LIMITTHE 2ND HIT
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- 33. Poly-trauma Patient ASyndrome 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 ASSESSEDABOUT 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 StableBorderline 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 OPRATIVETIME > 6H HAEMODYNAMIC INSTABILITY EXAGGERATED INFLAMMATORY RESPONSE
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- 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 DCOSTRATEGY 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 ControlBleeding 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
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- 45. TIMING OF SURGERY TimingPhysiological 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
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- 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 KILLYOUR BORDERLINE PATIENT BY (ETC) HELP HIM TO LIVE BY (DCO) GIVE HIM THE CHANCE TO FIGHT ANOTHER DAY
- 49. Ortho team mustbe resuscitators and stabilizers: not “fixers”