DCO VS ETC

RH/JA/RK
 Definition of Polytrauma
A syndrome of multiple injuries (ISS>17), with systemic
traumatic reaction, which may lead to dysfunction or
failure organs and vital system, which had not
themselves been directly injured.

Damage Control Orthopaedics. Evolving Concepts in the Treatment of Patients Who Have Sustained Orthopaedic
Trauma,J Bone Joint Surg Am. 87:434-449, 2005.
Polytrauma
Injury to 2 or more organ systems leading
potentially to a life threatening condition
Physiological response to injury
Inflammatory immune response
Innateimmune response : Systemic Inflammatory
Response Syndrome (SIRS)

Adaptive immune response: Compensatory Anti-

inflammatory Response Syndrome (CARS)

Multi Organ Dysfunction Syndrome (MODS)

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
 Systemic Response
Anti-inflammatory Pro-inflammatory

Insult
SIRS

CARS
D7
Response

Response
Innate Immune

Adaptive Immune
D14

Balanced SIRS-CARS maintains homeostasis

Interplay of SIRS and CARS

Homeostasis
Mild-Moderate Injury

Damage Control Orthopaedics. Evolving Concepts in the Treatment of Patients Who

Have Sustained Orthopaedic Trauma,J Bone Joint Surg Am. 87:434-449, 2005.
Pathological immune response

Severe Injury
Anti-inflammatory Pro-inflammatory

SIRS
Systemic Response

Insult

Innate Immune
Response

Adaptive Immune
Response

CARS

Imbalanced CARS>SIRS leads to hypo-inflammation or early MODS

Pathological immune response

Moderate to severe injury

Anti-inflammatory Pro-inflammatory

SIRS
2nd Hit
Systemic Response

Insult

Innate Immune
Response

Adaptive Immune
Response

CARS

Imbalanced SIRS>CARS leads to hyper-inflammation or delayed MODS

Damage Control Orthopaedics. Evolving Concepts in the Treatment of Patients Who Have Sustained Orthopaedic
Trauma,J Bone Joint Surg Am. 87:434-449, 2005.
Balance between SIRS and
CARS
induce reparative
mechanisms
limit entry or overload of
microorganisms
avoid auto-aggressive
inflammation, with
secondary tissue damage
Avoid susceptibility to
infection
MODS
Cerebral - Cerebral edema
CVS - Hypotension and shock
Respiratory - Acute lung injury, ARDS
Liver - High LFT 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

Polytrauma (2 hit phenomenon)

Second Hit Impacts by Surgery and Resuscitation

The Patient The Limb

New concept in resuscitation

First Hit Impacts

How do you decide your fluid replacement?

What is your fluid replacement regimen?

 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

Coagulopathy

Lethal
Voluminous crystalloid Triad of
dilutes coagulation factors Death
causes hyperchloremic and lactate acidosis
supplies inadequate O2 to under-perfused Hypothermia Acidosis
tissue
 DCR Priorities Beyond ABCDE of ATLS

On-going Bleeding
Hypoperfusion
Exposure
SIRS/CARS
Resuscitation
Contamination

Balanced Resuscitation or Haemostatic Damage Control

Permissive Hypotension Resuscitation Surgery
HAEMODYNAMIC TRIAGE PROTOCOL

Stable Borderline Unstable In Extremis

No clinical signs SBP 80-100mmHg Unable to maintain Absent vital signs
of hypovolaemic AIS > 2 SBP >90mmHg Severe shock
shock Blood transfusion Pulse <100/min Uncontrolled hhage
2-8/2h CVP>5cm H20 needing mechanical
UO>30ml/h resuscitation
Despite adequate fluid repeated CA
resuscitation and blood infusion despite
transfusion over 2h complete blood
volume replacement
within 2h (>12 blood
transfusion/2h
 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 (Hemoglobin based oxygen carrier)
transfusion decreases MODS
Packed RBC, FFP and Platelets in 1:1:1 ratio
Cryoprecipitate, Tranexamic acid, Recombinant factor-VIIa
Storage blood of < 2 weeks to minimise TRALI, MODS
 Non-surgical DCR

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
Damage control orthopaedics
Damage Control Orthopaedics
An approach to contain and stabilize an
orthopaedic injury to improve patients physiology
Designed to avoid worsening pts condition due to
second hit phenomenon
Delay definitive surgery until pt condition is
optimized
Focuses on hemorrhagic control, management of
soft-tissue injury and provisional fracture stability
DCO - evolution
1960s Delayed Surgery (too sick to operate on)
Preliminary traction delayed definitive fixation

1980s Early Total Care within 24 hours

(too sick not to operate on)
ATLS concepts plus
Advancement in anaesthesiology and ICU care
early fixation prevents FES
early mobilization facilitates nursing care and
early mobilization prevents pneumonia, sepsis, TED
Patients with ISS>17 (borderline patients) are at
high risk of complications

1990s Damage Control Orthopaedics

Patient categorization
Parameter Stable Borderline Unstable In Extremis
Shock SBP (mmHg) 100 or more 80-100 60-80 50-60
Blood unit/2h 0-2 2-8 5-15 >15
Lactate < 2.0 2.5 >2.5 Severe
Base deficit Normal No data No data >6-18
UO ml/h >150 50-150 <100 <50
Class I II-III III-IV IV
Coagulation Platelets >110,000 90-110,000 70-90,000 <70,000
Factors II/V 90-100% 70-80% 50-70% <50%
Fibrinogen >1 g/dL 1 g/dL <1 g/dL DIC
d-Dimer Normal Abnormal Abnormal DIC
Temperature >340C 33-350C 30-320C <300C
Soft Tissue Chest AIS 2 or 2 2 or more 2 or more 3 or more
Injuries TTS 0 I-II II-III IV
Abd (Moore) <II <III III III or >III
Pelvic AO A B or C C C
Limb AIS I-II II-III III-IV Crush
 Sustained Orthopaedic Trauma,J Bone Joint Surg Am. 87:434-449, 2005.
Damage Control Orthopaedics. Evolving Concepts in the Treatment of Patients Who Have
ETC vs DCO
Stable Borderline Unstable Extremis
Haemorrhage control and/or
Decompression in the ER

20 survey (end of ER workup)

ABG, FAST, I/O ratio, ABP Ext-Fix
(distractor)

Stable Uncertain

ETC ETC DCO DCO

OR OR OR OR ICU
DCO surgery
External fixation
Nailing if ISS<25
Unreamed/retrograde

Usage of new One-step Reamer-Irrigator-Aspirator

(RIA by Synthes)
Application of DCO

10 rapid temporary # stabilization

(in trauma room/ICU/OR)
1.Control hhage e.g. ext-fix pelvis
2.Debridement of open wound Definitive # fixation once the
3.Spanning ext-fix or unreamed nailing patient is optimized
or reamed nailing using RIA (avoid day 2-5)

Stage 1
Stage 2 Stage 3

Resuscitation and ICU management

1.Close monitoring
2.Repletion of blood product
3.Further hemodynamic stabilization
Timing of surgery
Timing Physiological Status Surgical Intervention
Normal response to resuscitation
Day 1 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

AO Philosophy
Damage Control Orthopaedics. Evolving Concepts in the Treatment of Patients Who Have Sustained Orthopaedic
Trauma,J Bone Joint Surg Am. 87:434-449, 2005.
Algorithm initial assessment, life support
& day 1 surgery

Damage Control Orthopaedics. Evolving Concepts in the Treatment of Patients Who Have Sustained Orthopaedic
Trauma,J Bone Joint Surg Am. 87:434-449, 2005.
Fixation method (Pro and Cons)
Nailing
Pro : the method of choice for shaft femur or tibia fracture
Cons : Reamed or unreamed Has an adverse effect pulmonary embolism
Platting
Pro : allow better bleeding control, permit debridement and
fasciotomies
Cons : Requires major surgical access
External fixation
Pro : its fast !!!
Cons : insufficient for definitive treatment, pin track infection

Damage Control Orthopaedics. Evolving Concepts in the Treatment of Patients Who Have Sustained Orthopaedic
Trauma,J Bone Joint Surg Am. 87:434-449, 2005.
THANK YOU