M.

Bima Mandraguna
Betha Egih R
Teuku Aditya K
 DEFINISI TRAUMA
Semua jenis kekerasan yang menimpa tubuh
sehingga terjadi kerusakan / gangguan pada
struktur dan fungsi jaringan / organ tubuh
yang terkena, bahkan secara sistemik dapat
berdampak pada aspek fisiologis, kejiwaan
dan kondisi sosial penderita yang
bersangkutan.
2
FAKTOR – FAKTOR
YANG BERPERAN
FAKTOR INTERNAL
- Keadaan Umum Penderita, Usia, Status Gizi
- Kondisi Premorbid penderita ( Kehamilan,
Penyakit lain, seperti Peny. Jantung,
Kelainan Ginjal, Kelainan Metabolik )
FAKTOR EKSTERNAL
- Jenis Trauma ( mempengaruhi perjalanan
penyakit dan prognosis, ada tidaknya cedera
inhalasi, shock, cedera penyerta lain )
- Penatalaksanaan ( Resusitasi, Rawat luka )
TRAUMA JARINGAN / ORGAN

 KERUSAKAN
 PERDARAHAN
 NYERI
3
 JENIS TRAUMA
• Ledakan benda berkecepatan tinggi, benda tajam
( tusukan, irisan, sabetan ), benda tumpul
• Suhu tinggi / rendah
 uap panas
 luka bakar
 frostbite ( suhu dingin )
• Arus listrik tegangan tinggi
• Bahan kimia
• Radiasi, ionisasi
• Gigitan, sengatan
4
 KERUSAKAN AKIBAT TRAUMA
BENTUK :
Diastase ( robekan ), memar, erosi, lecet, hancur ( crush injury ),
jaringan hilang

LOKALISASI :
• Jaringan lunak + kulit : - luka terbuka
- luka tertutup

• Tulang / sendi : fraktura / dislokasi

• Organ berongga ( lambung, usus ) : perforasi
• Organ Padat ( hati, limpa, ginjal, otak ) : ruptur, memar

5
6
7
9
16
AKIBAT TRAUMA

 SEMBUH
 CACAT
( anatomis + fisiologis + psikologis )
 MENINGGAL

10
THE RESPONSE
Starts within minutes following the
traumatic impact
Characterized by the immediate activation
of monocytes and granulocytes
Leukocytic activation leads to an increased
synthesis and release of inflammatory and
anti-inflammatory mediators
 Host Stress Response to Injury
Modulation by CNS
Afferent Arc Efferent Arc

Local Endocrine
Wound Response

Systemic Inflammation

Systemic Response
 Demling et al. Surg Clin North Am 74(3); 1994.
Release of Mediators
“First Hit” POST INJURY “Second Hit”
Systemic Activation of
Inflammatory Cells
Primed
Lung Inflammatory
INITIAL INSULT Cells
Primed
Liver
Local Activation of Systemic Release WBCs
Inflammatory Cells of Cytokines Primed
Gut
WBCs

Other Primed
LOCAL
Organs WBCs
TISSUE
RESPONSE
SYSTEMIC RELEASE OF
TOXIC MEDIATORS
 Demling et al. Surg Clin North Am 74(3); 1994.
GENERALIZED TISSUE INJURY
POST INJURY MULTIPLE
ORGAN FAILURE
MOF emerged as a clinical syndrome as a result of
our ability to keep pts alive with advanced technology
It remains the leading cause of late postinjury deaths
in the ICU
The association between the severity of MOF and
outcome is reflected in almost linear relationship
between the number of organs that have failed and
mortality
PREVENTION OF MOF
Prevention of MOF is a paramount importance
A common mistake is the believe that prevention of
MOF begins in the ICU
It does not . In the trauma pts, prevention begins in
the field, with rapid transportation to the hospital,
followed by the rapid institution of volume
resuscitation in the ED, meticulous assessment, early
and appropriate surgical intervention, through ICU
care and prompt reoperation when indicated
PREVENTABLE MISTAKES THAT CAN INCREASE
THE RISK OF MOF
1. Delays in diagnosis
2. Missed injuries
3. Inadequate and/or delayed volume resuscitation
4. Failure to recognize signs of inadequate tissue
perfusion
5. The use of antibiotics in place of adequate surgical
drainage and debridement
6. Delayed recognition of surgical misadventures

Deith EA: Commentary to post injury MOF in Moore FA & Moore

EE : Trauma 5th edit. 2004
 ATP
Ischemia/Reperfusion Injury

AMP
Ischemia

Adenosine
Xanthine dehydrogenase

Inosine
Xanthine oxidase
Hypoxanthine Xanthine
SOD Catalase
O2 O2- H2O2 H2O
Fe++
OH
Tissue
Reperfusion Damage
 Severe SIRS
Early MOF
Moderate SIRS
First
Insult Moderate
2nd CARS
Severe
Insult
CARS

Host Factors
Shock
Tissue injury Infections Late MOF
Second Hits

SIRS : Systemic inflammatory response syndrome Moore & Moore : MODS following trauma, 2004
MOF : Multiple organ failure
CARS: Compensatory anti-inflammatory response syndrome
POST INJURY AUTOCANNIBALISM
CONTRIBUTES TO THE
PATHOGENESIS OF MOF

Musce Mass
Visceral protein
Organ function
Immune response

INFECTION

MULTIPLE ORGAN FAILURE

Moore FA & Moore EE ; Trauma 5th edit. 2004

 Major issues in restoring &
maintaining perfusion after
initial insult
Insult Insult

Primary Systemic Secondary

Multiple Organ Stress Multiple Organ
Dysfunction Response Dysfunction
What Endpoints?
What Fluids?
When Inotropes?
When Blood?
What Results?
 Demling et al. Surg Clin North Am 74(3); 1994.
 Primary Secondary organ failure
organ
failure

Progressive organ failure

Systemic inflammatory response syndrome
Response

Shock

Resuscitation

Recovery

Recovery

1 3 10 14 21
Injury Days after injury

 Pasquale et al. Critical Care. In: Basic Surgery 1995. P.195

THE ROLE OF GUT IN DYSFUNCTION
INFLAMMATION TO MOF
Pathophysiology and Prevention
of ARDS in Trauma Patient
ARDS Criteria
American-European Consensus Conference Definitions of Acute
Lung Injury and Acute Respiratory Distress Syndrome
Acute Lung Injury Criteria
Timing: acute onset
Oxygenation: PaO2/FIO2 ≤300 mm Hg (regardless of positive
end-expiratory pressure)
Chest radiograph: bilateral infiltrates on anteroposterior chest
radiograph
Pulmonary artery occlusion pressure: ≤18 mm Hg or no clinical
evidence of left atrial hypertension
ARDS Criteria
Same as acute lung injury except:
Oxygenation: PaO2/FIO2 ≤200 mm Hg (regardless of positive
end-expiratory pressure)
The “DELPHI” Definition of ARDS
Timing: acute onset
Oxygenation: PaO2/FIO2 ≤200 with PEEP ≥10
Chest radiograph: bilateral infiltrates
Absence of CHF OR presence of recognized risk
factor for ARDS
RISK FACTORS
 Clinical Risk Factors for ARDS
 RISK FACTOR
 FREQUENCY OF ARDS (%)
 DIRECT
 Aspiration
 12-36
 Pneumonia
 12-31
 Pulmonary contusion
 5-22
 Toxic inhalation
 2-17
 INDIRECT
 Sepsis syndrome
 11-80
 Multiple transfusions
 5-36
 Multiple fractures
 2-21
 Pancreatitis
 7-18
 Disseminated intravascular coagulation
 23
PATHOGENESIS

Lung injury in ARDS involves :

inflammation,
coagulation,
vasomotor tone,
and other systems .
The pivotal cellular mediators appear to be
leukocytes, with both local and humoral mediators
orchestrating their function. Activation of these
leukocytes results in release or activation of multiple
cytokines, chemokines, oxidants, and proteases that
result in the final common pathway of tissue injury in
ARDS
BIOLOGICAL MARKERS OF ACUTE
RESPIRATORY DISTRESS
SYNDROME
von Willebrand factor antigen (vWF:Ag) has been
studied fairly extensively as a marker of endothelial
dysfunction
PATHOPHYSIOLOGY
ARDS is characterized by diffuse, patchy, panlobar
pulmonary infiltrates on plain chest radiograph
Modern Adult Respiratory Distress
Syndrome (Low-Pressure
Pulmonary Edema)
 Phase 1 (Early Change)

Normal radiograph
Dyspnea, tachypnea, normal chest examination
Mild pulmonary hypertension, normoxemic or mild
hypoxemia hypocarbia
Neutrophil sequestration, no clear tissue damage
Phase II (Onset of Parenchymal Changes)
Patchy alveolar infiltrates begining in dependent lung
Dyspnea, tachypnea, cyanosis, tachycardia, coarse rales
Pulmonary hypertension, normal wedge pressure,
increased lung permeability, increased lung increasing
shunt, progressive decrease in compliance, moderate-
to-serve hypoxemia
Neutrophil infiltration, vascular congestion, fibrin
strands, platelet clumps, alveolar septal edema,
intraalveolar protein, white cells, type 1 epithelial
damage
No perivascular cuffs (unless a component of water,
high-pressure edema is present)
Normal heart size
Phase 3 (Acute Respiratory Failure with Progression, 2-
10 Days)
Diffuse alveolar infiltrates
Tachypnea, tachycardia, hyperdynamic state, sepsis
syndrome, signs of consolidation, diffuse rhonchi
Phase 2 changes persist, progression of symptoms,
increasing shunt fraction, further decrease in compliance,
increased minute ventilation, impaired oxygen extraction of
hemoglobin
Increased interstitial and alveolar inflammatory exudate
with neutrophil and mononuclear cells, type II cell
proliferation, beginning fibroblast proliferation,
thromboembolic occlusion
Air bronchograms
Decreased lung volume
Normal heart size
Phase 4 (Pulmonary Fibrosis-Pneumonia with
Progression, >10 Days)b
Persistent diffuse infiltrates
Symptoms as above, recurrent sepsis, evidence of
multiple-system organ failure
Phase 3 changes persist, recurrent pneumonia,
progressive lung restriction, impaired tissue
oxygenation, impaired oxygen extraction,multiple-
system organ failure
Type II cell hyperplasia, interstitial thickening,
infiltration of lymphocytes, macrophages, fibroblasts,
loculated pneumonia and/or interstitial fibrosis, medial
thickening and remodeling of arterioles
Recurrent pneumothorax
Normal heart size , enlargement with pulmonale
therapy
Inhaled Nitric Oxide (pulmonary hypertension)
SURFACTANT REPLACEMENT THERAPY
CORTICOSTEROIDS
Thank you