Lung contusion is when, as a result of chest trauma, there is direct or indirect damage of the parenchyma of the lung that leads to oedema or alveolar haematoma and loss of physiological structure and function of the lung. Acute respiratory distress syndrome (ARDS) is an acute, diffuse, inflammatory form of lung injury that is associated with a variety of etiologies.

1. B Y D R . R U T A Y I S I R E F R A N Ç O I S X A V I E R
P G Y 1 N E U R O S U R G E R Y R E S I D E N T
U N I V E R S I T Y O F R W A N D A
Lung contusion and ARDS
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2. Outline
 Introduction
 Epidemiology
 Etiology
 Types
 Pathophysiology
 Clinical presentation
 Investigations
 Management
 Complications
 Prognosis
 ARDS
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3. Lung contusion
 Lung contusion is when, as a result of chest trauma,
there is direct or indirect damage of the parenchyma
of the lung that leads to oedema or alveolar
haematoma and loss of physiological structure and
function of the lung
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5. History
 They were first described by Morgagni, an Italian
anatomist in 1761, and the term pulmonary
contusion was coined in the 19th century by French
military surgeon, Dupuytren.
 Widespread use of explosives at the time of World
War 1 and 2, lead to increased recognization of
pulmonary contusion due to blast injuries. Many
soldiers with blast injuries developed pulmonary
bleeding without apparent external injuries.
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6. Epidemiology
 Common (30% to 75%) in blunt chest traumas with a
mortality rate of 10-25%.
 Severe contusions seen in children without any
obvious external injuries after blunt chest trauma.
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7. Etiology
 Blunt chest trauma
 Penetrating, or
 Combination of both can lead to a pulmonary
contusion.
 Explosions, falls from great heights, sports injuries
and assaults are other identified causes.
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8. Types of Pulmonary Contusions
 Type I
Due to direct chest wall compression against the lung
parenchyma; this accounts for the majority of cases.
 Type II
Due to shearing of lung tissue across the vertebral bodies
 Type III
Localized lesions due to fractured ribs, which directly
injure the underlying lung
 Type IV
Due to underlying pleuropulmonary adhesions from prior
lung injury tearing the parenchyma
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9. Mechanisms
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Three possible mechanisms of development of contusion
are:
1. Inertial effect: The lighter alveolar tissue is sheared from the
heavier hilar structures, due to different tissue densities at
different areas of lung and therefore different rates of acceleration
or deceleration.
2. Spalling effect: Lung tissue bursts or is sheared where a shock
wave meets the lung tissue, at interfaces between gas and liquid.
The spalling effect occurs in areas with large differences in
density; particles of the spalled denser tissue are thrown into the
less dense particles.
3. Implosion effect: It occurs when a pressure wave passes
through a tissue containing bubbles of gas: the bubbles first
implode, then rebound and expand beyond their original volume.
The overexpansion of gas bubbles stretches and tears alveoli.

10. Pathophysiology
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11. Clinical presentation
 Depend on the extent of the injury.
 Patients present with varying degrees of respiratory
difficulty.
 Symptoms include: respiratory distress, coughing up
blood or bloody sputum, bronchorrhea (production of
watery sputum), wheezing
 Signs include: dyspnea, tachypnea, tachycardia,
hypotension, ecchymosis
 RS: ↓breath sounds on ipsilateral side, crackles and
tenderness may be elicited if there is associated chest
wall injury.
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12. Investigations
 CXR (but underestimate the size of contusion and
usually lags behind the clinical picture. True extent
not apparent on X-ray film until 24-48 hours
following injury.
 CT is very sensitive for diagnosing pulmonary
contusion, its size and 3D assessment. Detect the
contusion almost immediately after the injury.
 Mild (<18%), Moderate (18 –28%) and severe
(>28%)
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13. LUNG CONTUSION & IMAGING
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14. Management
 Mostly heals by its own with supportive care,
supplemental oxygen and close monitoring,
but intensive care may be required.
 IVF is required to ensure adequate blood volume, but
this should be done carefully as fluid overload can
worsen pulmonary edema, which may be damaging.
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15. Other Supportive care:
 Pain control
 Pulmonary toilet –suctioning, deep breathing,
coughing
 Chest physiotherapy –breathing exercises,
percussion
 Optimal positioning –placing the good lung in a
dependent position
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16. Complications
 Acute respiratory distress syndrome(ARDS) –in up
to 38% of patients
 Pneumonia –inability to clear bacteria and
secretions; intubation and mechanical ventilation
further increases the risk. Up to 50% of patients tend
to develop a bacterial respiratory infection.
 Long-term respiratory dysfunction.
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17. Prognosis
 Most resolve 5 to 7 days after injury
 Signs detectable by radiography are usually gone
within 10 days after injury
 Lung fibrosis with decreased functional residual
capacity can occur up to 6 years after injury
 Contusion can also permanently reduce the
compliance of the lungs
 A larger contusion is associated with an increased
risk.
 Associated with 10 to 25% mortality rate
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18. What is ARDS
 Acute respiratory distress syndrome (ARDS) is an
acute, diffuse, inflammatory form of lung injury that
is associated with a variety of etiologies.
 Recognizing and promptly treating ARDS is critical
to reduce the associated high mortality.
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19. Clinical Risk Factors:
Direct Lung Injury Indirect Lung Injury
Common Causes
Pneumonia (Bacteria, Viruses, Fungi)
Aspiration of Gastric Contents
Uncommon Causes
Pulmonary Contusion
Fat Embolism
Amniotic Fluid Embolism
Near-drowning
Inhalational Injury (Smoke, NH3)
Reperfusion Injury after Transplant
Common Causes
Sepsis
Severe Trauma with Shock
Acute Pancreatitis
Uncommon Causes
Multiple Transfusions
Drug Overdose
Diffuse Intravascular Coagulation
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20. Pathophysiology ARDS
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 Neutrophils release inflammatory mediators -->degrading
integrity of capillary endothelial cells--->capillary permeability,
interstitial edema.
 Influx of proteinaceous plasma fluid, erythrocytes, and
inflammatory cells into the interstitium
 destroyed surfactant and type 1 and 2 pneumocyte
 Increases alveolar surface tension, thus producing alveolar collapse
Asensio J, Trunkey D: Current Therapy Trauma & Surgical Critical Care
Civetta: Critical Care,4th edition Chapter 136: Acute Lung Injury & Acute Respiratory Distress Syndrome
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21. 21
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22. Evolution of Pathogenesis:
Exudative Phase
(7 Days)
Proliferative Phase
(14 Days)
Fibrotic Phase
(21 Days)
Alveolar Wall Damage
With Flooding
Type II Alveolar Cell Hyperplasia
Myofibroblast Infiltration
Resolution of Edema
Extensive Fibrosis
With Loss of Normal Lung
Architecture
↓↓ Pa02
↓ Compliance
Bilateral Infiltrates
↓ ↓ Pa02
↓ Compliance
Bilateral Infiltrates
↓ ↓ Pa02
↓ Compliance
Infiltrates ± Bullae
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23. ALI V/ARDS
 ALI is the term used for patients with significant
hypoxemia (PaO2/FiO2 ratio of ≤ 300)
 ARDS is the term used for a subset of ALI patients
with severe hypoxemia (PaO2/FiO2 ratio of ≤ 200)
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24. ARDS ALI
 Acute
 PaO2/FiO2 < 200
 B/l interstitial
/alveolar infiltrates
 PCWP <18mmHg
 Acute
 PaO2/FiO2 <
300mmHg
 B/l interstitial
/alveolar infiltrates
 PCWP <18mmHg
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25. Calculating PaO2 / FiO2
ratio
 It is important to consider how
much oxygen a patient requires to
achieve their PaO2 on an ABG.
The P/F ratio is a very useful tool
to monitor your patient’s
oxygenation status.
 PaO2 / FiO2= P/F Ratio
 Healthy adult PaO2 = 80-100
mmHg
 Room air = 21 percent oxygen
 100/.21 = P/F ratio 476 for a
healthy adult
P/F ratio
PaO2
FiO2
= P/F ratio
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26. 26
Lung Injury Score
Chest radiographic score
0 No alveolar consolidation
1 Alveolar consolidation in one quadrant
2 Alveolar consolidation in two quadrants
3 three quadrants
4 four quadrants
Hypoxemia score
0 PaO2/FiO2 ≥300
1 PaO2/FiO2 225–299
2 PaO2/FiO2 175–224
3 PaO2/FiO2 100–174
4 PaO2/FiO2 <100
Respiratory system compliance score (mL/cm H2O)
0 ≥80 1 60–79 2 40–59 3 20–39 4 ≤19
PEEP score (cm H2O)
0 ≤5 1 6–8 2 9–11 3 12–14 4 ≥15
Final value
0 No lung injury 1–2.5 Acute lung injury (ALI)
2- >2.5 Severe lung injury (ARDS)
Murray JF, et al. An expanded definition of the adult respiratory distress syndrome. Am Rev Respir Dis.
1988;138:720
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27. 2012 Berlin ARDS definition
2012 BERLIN ARDS DEFINITION
Mild Moderate Severe
Timing
Acute onset within 1 week of known clinical consult or
new/worsening symptoms
Hypoxemia
PaO2 / FiO2
<300->200
with PEEP ≥ 5
PaO2 / FiO2
<200->100
with PEEP ≥ 5
PaO2 / FiO2
≤100
with PEEP ≥ 5
Origin of Edema
Respiratory failure not fully explained by cardiac failure or fluid overload
objective assessment if no risk factors present
Radiologic
Abnormalities
Bilateral chest opacities Bilateral chest opacities
Opacities involving at least
3 quadrants
1. Munro, C.L. and Savel, R. H. A, Journal of Critical Care, Sept. 2012. http://ajccjournals.org/content/21/5/305.
2. European Society of Intensive Care. Medicine, Journal of American Medical Association, June 2012: 307 (23).
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28. ARDS DIAGNOSTIC CRITERIA
 Acute Onset 6-72 Hours (in setting of a risk factor).
 Chest X-ray: Diffuse Bilateral Infiltrates.
 Hypoxemia.
PaO2/FIO2 <300: Acute Lung Injury
PaO2/FIO2 <200: Acute Respiratory Distress Syndrome
 Non-Cardiogenic Pulmonary Edema. PCWP <18
Example: PaO2=60 on 50% FiO2 P/F ratio= 120
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29. Low Tidal Volume
Ventilation
(4-8ml/kg IBW)
IV Steroid Inhaled Pulmonary
Vasodilator
(Nitric/Flolan)
Advanced Ventilatory
Management
(APRV/Bilevel/PRVC/HFOV)
ECMO
Increase PEEP
Prone Positioning
Neuromuscular Blockade
Management
.
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31. References
 Ventilation with lower tidal volumes as compared with
traditional tidal volumes for acute lung injury and the
acute respiratory distress syndrome. The Acute
Respiratory Distress Syndrome Network. N Engl J
Med. 2000;342(18):1301-8. PMID: 10793162.
 2.http://www.cardiothoracicsurgery.org/content/6/1/73
.http://en.wikipedia.org/wiki/Pulmonary_contusion
 Putensen C, Theuerkauf N, Zinserling J, et al. Meta-
analysis: ventilation strategies and outcomes of the
acute respiratory distress syndrome and acute lung
injury. Ann Intern Med. 2009;151(8):566-76. PMID:
19841457.
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