POLYTRAUMA AND DCO: RECENT

CONCEPTS

Polytrauma Injury to 2 or more organ systems

leading potentially to a life threatening condition

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 CARSSy

stem

ic Re

spon

se

SIRS

CARS

D14D7

Adaptive Immune Response

Innate ImmuneResponse

Resolution

Resolution

Insu

lt

Homeostasis

Mild-Moderate Injury

Pro-

infla

mm

ator

yAn

ti-in

flam

mat

ory

Balanced SIRS-CARS maintains homeostasis

Pathological immune response

1st Hit

Moderate Injury

1st Hit

Amplification of SIRSDelayed-onset MODS/death

Incomplete Resolution

2nd Hit

2nd Operation within D3-5Sepsis

Severe injury

Intense CARSEarly MODS/death

IMBALANCE BETWEEN SIRS AND CARS

Pathological immune response

Syst

emic

Resp

onse SIRS

CARS

Adaptive Immune Response

Innate Immune

Response

Insu

ltSevere Injury

Pro-

infla

mm

ator

yAn

ti-in

flam

mat

ory

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

Early MODS

Pathological immune response

Syst

emic

Resp

onse

SIRS

CARS

Adaptive Immune Response

Insu

ltModerate to severe injury

Pro-

infla

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ator

yAn

ti-in

flam

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ory

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

Late MODS

Innate ImmuneResponse

2nd H

it

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 - DIVC

Polytrauma (2 hit phenomenon)

‘First Hit’ Impacts by Trauma The Limb/Organ System

The Patient

Polytrauma (2 hit phenomenon)

‘Second Hit’ Impacts by Surgery and Resuscitation

The Limb The Patient

New concept in resuscitation

First Hit Impacts

How do you decide your fluid replacement?

What is your fluid replacement regimen?

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 >140Blood pressure Normal Normal Decreased DecreasedPulse pressure Normal or inc Decreased Decreased DecreasedRespiratory rate 14-20 20-30 30-40 >35Urine output > 30 ml/hr 20-30 5-15 NegligibleMental status Slightly

anxiousMildly

anxiousAnxious/confused Confused/

lethargicFluid Replacement

Crystalloid Crystalloid Crystalloid and blood

Crystalloid and Blood

Classification of Hypovolaemic Shock and Physiologic Changes

What is your fluid replacement regimen?

Fluid resuscitation Bolus administration of saline? Colloids? GXM or GSH?

Fluid resuscitation

Shock due to primary

haemorrhage Ongoing bleeding 2O

resuscitation regimen Lethal Triad of Death

First Hit

Second Hit?

AcidosisHypothermia

Coagulopathy

Voluminous crystalloid ● dilutes coagulation factors ● causes hyperchloremic and lactate acidosis● supplies inadequate O2 to under-perfused tissue

DCR Priorities Beyond ABCDE of ATLS

On-going BleedingHypoperfusion

ExposureSIRS/CARS

ResuscitationContamination

Balanced Resuscitation or

Permissive Hypotension

Haemostatic Resuscitation

Damage Control Surgery

Paradigm Shift in ResuscitationFrom ATLS in 1980s

EARLY TOTAL CARE (ETC) ATLS concept of Primary Survey

followed by Secondary SurveyTimely debridement within 6-hour Early definitive fracture fixation within 24 hours (ETC)

EDCBA

Paradigm Shift in Resuscitation To DCR in 1990s

HD Triage: Stable, Borderline, Unstable and In Extremis DAMAGE CONTROL RESUSCITATION

Permissive hypotension and haemorrhage control Haemostatic resuscitation in ICU Damage Control Surgery Definitive fracture fixation after D5

DCBAC E

HAEMODYNAMIC ‘TRIAGE’ PROTOCOL

Stable Borderline Unstable In ExtremisNo clinical signs

of hypovolaemicshock

SBP 80-100mmHgAIS > 2Blood transfusion 2-8/2h

Absent vital signsSevere shockUncontrolled h’hageneeding mechanical resuscitationrepeated CA infusion despite complete blood volume replacement within 2h (>12 blood transfusion/2h

Unable to maintain SBP >90mmHgPulse <100/min CVP>5cm H20 UO>30ml/hDespite adequate fluid resuscitation and bloodtransfusion over 2h

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-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

Non-surgical DCR

Damage control orthopaedics

Damage Control Orthopaedics An approach to contain and stabilize an

orthopaedic injury to improve patient’s physiology

Designed to avoid worsening pt’s 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 - evolution1960s 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 categorizationParameter Stable Borderlin

eUnstable In Extremis

Shock SBP (mmHg)Blood unit/2hLactate Base deficitUO ml/hClass

100 or more0-2< 2.0Normal>150I

80-1002-82.5No data50-150II-III

60-805-15>2.5No data<100III-IV

50-60>15Severe>6-18<50IV

Coagulation

PlateletsFactors II/VFibrinogend-Dimer

>110,00090-100%>1 g/dLNormal

90-110,00070-80%1 g/dLAbnormal

70-90,00050-70%<1 g/dLAbnormal

<70,000<50%DICDIC

Temperature

>340C 33-350C 30-320C <300C

Soft TissueInjuries

Chest AIS TTSAbd (Moore)Pelvic AOLimb AIS

2 or 20<IIAI-II

2 or moreI-II<IIIB or CII-III

2 or moreII-IIIIIICIII-IV

3 or moreIVIII or >IIICCrush

Borderline patients (ISS>18)

Bone et al. Early versus delayed stabilization of fractures. A prospective randomized studyJ Bone Joint Surg. 1989; 71-A: 336-40Reynold et al. Is timing of fracture fixation important for the patient with multiple trauma?Ann Surg. 1995; 222:470-81

Femoralshaft #sN=105

<24 hr

24-48 hr

> 48 hr

ReamedIMN

ISS<18 ISS>18

Complications

Complications

Ecke et al. 1985

n=1127

AO Foundation

ETC vs DCO

ETC ETC DCO DCO OR OR OR OR ICU

Stable Borderline Unstable ExtremisHaemorrhage control and/orDecompression in the ER

20 survey (end of ER workup)ABG, FAST, I/O ratio, ABP

Stable Uncertain

Ext-Fix(distractor)

DCO surgery External fixation Nailing if ISS<25

Unreamed/retrograde Usage of new One-step Reamer-Irrigator-

Aspirator (RIA by Synthes)

Application of DCO

Stage 1 Stage 3Stage 2

Definitive # fixation once the patient is

optimized(avoid day 2-5)

Resuscitation and ICU management1.Close monitoring2.Repletion of blood product3.Further hemodynamic stabilization

10 rapid temporary # stabilization(in trauma room/ICU/OR)

1.Control h’hage e.g. ext-fix pelvis2.Debridement of open wound3.Spanning ext-fix or unreamed nailing or reamed nailing using RIA

Timing of surgeryTiming Physiological Status Surgical Intervention

Day 1 Normal response to resuscitation Early Total Care

Day 1Partial response to resuscitation

Damage Control Surgery

Day 1No response to resuscitation Life-saving surgery

Day 2-5 Hyperinflammation ‘Second-look’ onlyDay 6-10 Window of

opportunityDefinitive surgery

Day 12-21

Immunosuppression No surgeryWeek 3+ Recovery 20 reconstructive

surgeryAO Philosophy