Ventilation in chest trauma

Abstract

Chest trauma is one important factor for total morbidity and mortality in traumatized emergency patients. The complexity of injury in trauma patients makes it challenging to provide an optimal oxygenation while protecting the lung from further ventilator-induced injury to it. On the other hand, lung trauma needs to be treated on an individual basis, depending on the magnitude, location and type of lung or chest injury. Several aspects of ventilatory management in emergency patients are summarized herein and may give the clinician an overview of the treatment possibilities for chest trauma victims.

Full text

Journal of
Emergencies,
Trauma, and Shock
Synergizing Basic Science, Clinical Medicine, & Global Health
ISSN : 0974-2700
www.indusem.com
Published by Medknow Publications
Official Publication of INDO-US Emergency and Trauma Collaborative
Online full text & article submission at
www.onlinejets.org
Volume 4
Issue 2
Apr-Jun 2011
www.indusem.com
INDO-US
Y
&
C
N
T
E
R
G
A
R
U
E
M
M
A
E
Journal of Emergencies, Trauma, and Shock • Volume 4 • Issue 2 • April-June 2011 • Pages 159-****
I
N
N
G
I
A
A
N
R
D
T
R
C
I
E
F
S
I
E
T
A
N
R
E
C
I
H
C
S
O
P
N
U
O
S
I
T
1
A
2
D
F
N
O
U
**
E
s
t
.
1
9
5
9
1
2
www.opus12.org

251
Journal of Emergencies, Trauma, and Shock I 4:2 I Apr - Jun 2011
all organs of the thoracic cavity can be involved in chest trauma.
The most common types of collateral damage that result from chest
trauma include injuries to ribs, lung contusion, hematoma of the
chest wall, pleural effusion, pneumothorax and hematothorax.[4-6]
PATHOPHYSIOLOGICAL ASPECTS
Respiratory impairment
Damage to the osseous structure of the thorax by rib and
sternum fractures destabilizes the rib cage and impairs
spontaneous breathing mechanics substantially. This condition
is amplied by pain, which further reduces breathing function.
Direct traumatic damage to the lung (i.e., lung contusion), in
combination with a concurrent increase in vascular permeability
of the lung capillaries in the injured area, leads to an extravasation
of protein-rich uid with an altered surfactant composition,
eventually resulting in slow but progressive respiratory failure.[7,8]
INTRODUCTION
The lethality of isolated chest traumas is about 5% to 8%. Up to
25% of all deaths caused by trauma are related to chest injuries,[1]
and mortality dramatically increases as a function of increased
chest trauma force.[2] Direct forces, abrupt deceleration and other
mechanisms can cause injury to thoracic structures like major
intrathoracic vessels or the heart. Chest injuries often occur in
combination with other severe injuries, such as extremity, head
and brain and abdominal injuries.[1]
Chest trauma, as shown in Table 1, can occur after vehicle
collisions, assaults, falls and explosive blasts via a variety of
different mechanisms.[3] In elderly patients, a minor trauma can
cause a more serious injury due to the increased stiffness of the
rib cage as a function of advanced age. In contrast, in children,
the elasticity of the osseous structures of the chest can lead to
an underestimation of parenchymateous injuries.
Penetrating injuries are mostly caused by gunshot, stitch or
impalement damage, and the impact of a blunt trauma is typically
conducted to many different intrathoracic structures; hence nearly
Symposium
Ventilation in chest trauma
Torsten Richter, Maximilian Ragaller
Department of Anesthesiology and Intensive Care Medicine, University Hospital Dresden Carl Gustav Carus, Technical University, Dresden, Germany
ABSTRACT
Chest trauma is one important factor for total morbidity and mortality in traumatized emergency patients. The complexity
of injury in trauma patients makes it challenging to provide an optimal oxygenation while protecting the lung from further
ventilator-induced injury to it. On the other hand, lung trauma needs to be treated on an individual basis, depending on
the magnitude, location and type of lung or chest injury. Several aspects of ventilatory management in emergency patients
are summarized herein and may give the clinician an overview of the treatment possibilities for chest trauma victims.
Key Words: Chest trauma, instability of rib cage, mechanical ventilation, pneumothorax, spontaneous breathing
Address for correspondence:
Prof. Maximilian Ragaller, E-mail: maximilian.ragaller@uniklinikum-
dresden.de
Access this article online
Quick Response Code:
Website:
www.onlinejets.org
DOI:
10.4103/0974-2700.82215
Table 1: Injuries after chest trauma
Osseous injuries Rib fractures
Sternal fractures
Scapular fractures
Spine fractures
Heart and vessel injuries Aortic injury (rupture/dissection)
Cardiac contusion
Myocardial rupture
Myocardial infarction
Pulmonary injury Pneumothorax
Hematothorax
Pulmonary contusion
Pulmonary parenchymal injuries
Tracheobronchial injuries
Injury of the esophagus Fistula, mediastinitis
Injury of the diaphragm Enterothorax, herniation, bleeding

252 Journal of Emergencies, Trauma, and Shock I 4:2 I Apr - Jun 2011
The disturbance of diffusion, the reduction of compliance and
functional residual capacity and ventilation-perfusion mismatch
create an intrapulmonary shunt with subsequent elevated PaCO2
levels and reduced oxygenation.[9,10] After severe chest trauma,
intrapulmonary shunting can also be caused by a disruption of
pulmonary capillaries and extravasation into the alveolar spaces.
Aspiration of blood and/ or gastric contents, fat embolism to
the lung due to long bone fractures and systemic inammatory
response syndrome may additionally exacerbate respiratory
deficits and may lead to acute lung injury (ALI) or acute
respiratory distress syndrome (ARDS).[11]
After alveolar overdistension and rupture, extra-alveolar gas has
the potential (supported by mechanical ventilation) to move along
the pressure gradient through the damaged alveolar wall into
the bronchovascular space and pulmonary interstitium, causing
pulmonic interstitial emphysema.[12] The extra-alveolar gas may
push further into the pleural cavity, mediastinum and subcutaneous
tissues. As a consequence, bronchoalveolar stula, pneumothorax
or tension pneumothorax, and emphysema may develop.
Cardiovascular impairment
A reduction in normal intraventricular filling by tension
pneumothorax, pericardial tamponade or massive hemorrhage
may result in a life-threatening reduction in cardiac output.
Moreover, intracardiac structural damage or heart contusions
with concomitant arrhythmias are additional contributors to
reduced cardiac output.
DIAGNOSTIC STRATEGIES
Patient history can provide clues about the severity of trauma and
the resultant injuries. Instability of the thorax, signs of hemorrhagic
shock, low cardiac output and intrathoracic bowel sounds indicating
diaphragm rupture are the clinical signs of severe chest trauma.
Table 2 provides an overview of chest injury indicators.
The location of a chest injury may provide signs of associated
injuries. Fractures of the 1st to 3rd ribs indicate severe causative
forces because of their protected location and may be associated
with mediastinal injury. Therefore, injuries of large blood vessels
(aorta) or tracheal/ bronchial structures may be associated and
must be specically excluded. Lower rib (9th to 12th ribs)[13]
fractures are more often associated with hepatic injury on the
right side, splenic laceration on the left side or renal injury on
the posterior lower chest wall.
Exact preclinical diagnosis is typically difcult. A spiral computed
tomography (CT) scan of the chest and an echocardiogram
provide the most diagnostic information concerning intrathoracic
injuries. If necessary, chest x-ray, bronchoscopy, pulmonal angio-
CT, and an electrocardiogram may provide further diagnostic
information. Clinicians must be aware that patients remain at risk
for deterioration and that radiographic ndings may develop with
a time delay of up to four hours or more after injury.
THERAPEUTIC STRATEGIES FOR SELECTED
INJURIES
1) Chest wall osseous injuries
Injuries of one or two ribs are typically not dangerous and can be
handled without hospital admission; however, at any level of rib
fracture, the risk of pneumothorax and pulmonary contusion exists.
More than two rib fractures put the patient at signicant risk
of complications.
Fractures of more than two adjacent ribs at two different
locations result in thorax instability with paradoxical motion. This
ail chest condition is most often accompanied by an underlying
pulmonary parenchymal injury and can be life threatening.
The pleural cavity generates negative pressure during inspiration,
and the chest wall moves outwards during inspiration; however, in
the case of ail chest, the oating segment of chest wall and soft
tissue will move paradoxically in an inward direction, resulting in
elevated respiratory effort, dyspnea and hypoxemia.[14]
Therapeutic aspects
A sufcient reduction in pain is critical to optimizing patient
ventilation. Therein, the systemic administration of painkillers,
regional anesthesia with intercostal blockades, pleural catheters
and thoracic epidurals as well as paravertebral blockades may
be helpful.
Epidural analgesia has been demonstrated to benecially impact
ventilatory function in patients suffering from blunt chest
trauma[15] and is associated with a decreased rate of nosocomial
pneumonia and a reduced duration of mechanical ventilation in
patients after rib fractures.[16] Pneumatic stabilization is based on
the use of positive intrathoracic pressure provided by noninvasive
positive-pressure ventilation (NPPV) by mask; or after intubation,
by invasive positive-pressure ventilation (IPPV).[17]
Preventing atelectasis and pneumonia requires additional
chest physiotherapy. Frequent exible bronchoscopy typically
provides sufcient removal of secretions and blood from the
lungs. In severe cases of chest wall instability, reconstruction of
vertebrosternal ribs 3, 6 and 9 at an early stage may be required.
[18]
Surgical stabilization has been found to be associated with a
faster recovery of pulmonary function and a shorter ICU time
in a select group of ail chest patients who required prolonged
ventilatory support.[17,19]
Table 2: Clinical signs of chest trauma
External signs of contusion, lesion, gash, external bleeding, instability of thorax
Dyspnea, hemoptysis
Hypoxemia
Tracheal deviation
Emphysema
Side-specic breathing sounds
Vena cava superior syndrome
Intrathoracic bowel sounds
Richter and Ragaller: Chest trauma ventilation

253
Journal of Emergencies, Trauma, and Shock I 4:2 I Apr - Jun 2011
2) Pneumothorax
Injuries of the lungs or the thoracic wall can create a pleural
injury, resulting in the collection of air in the pleural space,
which is associated with a collapse of the lung. Consequently,
all penetrating thoracic injuries and most blunt chest injuries are
associated with pneumothorax. Occult pneumothorax among
victims of blunt trauma appears in 2% to 55% of patients who
undergo CT scans.[20] The closed form, or a small pneumothorax,
is mostly inconspicuous; however, tension pneumothorax may
occur when the amount of air in the pleural space increases and
the loss of air is impaired or impossible due to a valve mechanism.
This results in a displacement of the mediastinal structures and
the lungs and induces a reduction of venous ow to the heart,
reducing cardiac output. Clinical signs of pneumothorax, which
can vary depending on its extent, are summarized in Table 3.
Many patients after penetrating trauma have been diagnosed
to have a hemopneumothorax, in the absence of clinical
ndings. Chest radiograph or CT scan should be the initial
test for all patients with penetrating chest injuries[21] or blunt
thoracic trauma.[22] Ultrasound is also useful in the diagnosis of
pneumothorax and hematothorax.[6,23]
Therapeutic aspects
Thorax drainage should be performed except in asymptomatic
patients with occult pneumothorax, although they should be
closely observed.[24] Patients who are mechanically ventilated
should be treated immediately with a tube thoracostomy to
prevent the development of tension pneumothorax.
Suspected tension pneumothorax is typically treated with
immediate decompression of the pleural space by blunt
dissection and nger decompression. This is a reliable and safe
procedure prior to chest tube insertion. Needle thoracocentesis
should be the technique of last resort during hospital and trauma
reception, because of signicant failure rates; and the delay in
providing formal pleural decompression, caused due to incorrect
needle placement.[25]
Thorax drainage is typically performed to drain air as well as
blood and to reduce the air leak due to bronchopulmonal stulas.
The optimal tube size depends on the air leakage rate, wherein a
tube size of 28 or 32 French is normally sufcient for patients
who develop pneumothorax during mechanical ventilation or for
traumatic pneumothoraces with the risk of a large air leak due
to bronchopulmonal stulas. Larger chest tubes or an additional
chest tube should be considered if an additional drainage of
blood is necessary.
The application of negative pressure to the drainage system may
be necessary to maintain lung expansion, but it has the potential
to increase stula ow and retard closure.[26] Pleural drainage
systems can vary in their ability to evacuate large gas ows
(6- 50 L/min).[27] Some patients have highly variable stula ows,
which can be inuenced by body position. These patients should
choose a body position that produces the smallest possible stula
gas ow. Patients with high stula ows, wherein reexpansion
of the lungs cannot be achieved, may require further surgical
treatment (i.e., stula closure or lobectomy).
Nonconventional efforts were made to decrease
bronchopulmonary ow. The principle behind these methods
is either an intermittent thoracostomy tube closure during
mechanical inhalation and a release during exhalation[28,29]; or a
“counter-pressure” in the form of positive intrapleural pressure,
similar to the positive intrapulmonary pressure at the end of
expiration (PEEP).[30,32] Such methods are only allowed under
careful monitoring in the ICU setting.
If mechanical ventilation is needed, the ventilator setting should
support stula closure and limit inationary pressure (peak,
plateau and end-expiratory) and volume. Early spontaneous
breathing might support stula closure.
3) Hematothorax or hematopneumothorax
Sources of massive bleeding can include aortic rupture,
myocardial rupture and injuries to hilar structures. Other sources
could be injuries to the chest wall with lesions on intercostal or
mammary blood vessels. The hemodynamic reduction of cardiac
output may reach the level of hemorrhagic shock.
Therapeutic aspects
Thoracic drainage is the therapy of choice. The intent of
thoracic draining is the drainage and quantication of blood,
removal of possible coexisting pneumothorax, and tamponade
of the bleeding source. Arterial hemorrhage is life threatening;
therefore, the amount of blood loss must be closely monitored.
An initial blood loss in excess of 1,500 mL (≥20 mL/kg) or a
blood loss of about 300-500 mL/h via the chest tube should
lead to a surgical thoracotomy to stop bleeding.[33,34]
If a hematothorax is not drained, coagulated blood can produce
a clotted hemothorax, empyema and fibrothorax, with a
prolonged disturbance of ventilation, which results in extended
hospitalization. If the chest tube does not effectively drain the
blood, thoracoscopic drainage is a further possibility within the
rst week.[18]
4) Respiratory duct injury
Tracheal or bronchial injuries mostly occur as a component of
Table 3: Clinical signs of pneumothorax
Dyspnea
Diminished or absent sounds of breathing on the aected side
Unilateral hyperresonance to percussion
Pleuratic pain
Tracheal deviation
Hypotension
Pulsus paradoxus
Elevated central venous pressure, superior vena cava syndrome
Increased pressure on ventilator
End-tidal CO2 elevation, decreased PaO2 and SpO2 levels
Richter and Ragaller: Chest trauma ventilation

254 Journal of Emergencies, Trauma, and Shock I 4:2 I Apr - Jun 2011
multiple trauma, and the majority of patients with such injuries
die before hospital admission.[35] Injuries of the upper airways are
usually caused by blunt or, to a lesser extent, penetrating chest
traumas. Injury of the cranial part of the trachea is uncommon,
but it can occur even from a direct, low-energy blow.
Approximately 80% of tracheobronchial ruptures are located
around the carina (approximately a 2-cm radius) and are caused
by high-energy trauma. The right main bronchus is involved
more often than the left main bronchus.[36,37] Such injuries usually
involve the pars membranacea of the trachea; whereas in the main
bronchi, the ruptures are transversal between two chondral rings.
Dyspnea, hemoptysis, emphysema, pneumothorax and
pneumomediastinum that reaccumulates despite tube
thoracostomy and continuous air loss after placement of a chest
tube are clinical manifestations of tracheobronchial injury.
[38]
Diagnosis is achieved by bronchoscopy and is often difcult.
Signs of airway-vascular communication — such as hemoptysis
and sudden cardiovascular or neurologic dysfunction; air in
arterial aspiration; and air in retinal vessels — may alert the
clinician to symptoms of life-threatening systemic air embolism.
Therapeutic aspects
Intubation should be performed during spontaneous breathing
if possible because positive-pressure ventilation may enlarge an
incomplete rupture and may worsen symptoms. Ruptures above
the carina can be protected with a single- or double-lumen tube,
whereas ruptures at the carina level or more distal ones make a
double-lumen tube indispensable.[39] Further distally, a univent
bronchial blocker may be necessary to isolate the affected
bronchopulmonary segment and to promote healing.
[40,41] Surgical
closure is usually necessary.[33] In cases of systemic air embolism
where the source is suspected on one side, one-lung ventilation
may be applied. In cases of bilateral sources of airway-vascular
communication, the ventilation pressure should be kept as low
as possible to decrease a further collection of air in the vascular
system.
5) Lung contusion
Lung contusion is the most frequently diagnosed intrathoracic
injury that results from blunt trauma.[42] Isolated lung contusions
are considered more benign.[43] The risk of pulmonary contusion
appears to correlate with the severity of forces and the proximity
of the zone of the impact to the patient.[44] In the early phase of
injury, the impairment of oxygenation seems to correlate with
the involved lung tissue.[45] Clinically, gas exchange impairment
is obvious. Chest x-ray with irregular, nonlobular opacication
provides no indication of the severity of contusion and cannot
lead to a reliable prognosis. Thorax CT scan and blood gases are
better indicators of the grade of lung contusion.[46,47]
Therapeutic aspects
Respiratory relief can be achieved by positive-pressure ventilation
(i.e., continuous positive airway pressure, CPAP), sufcient pain
management, physiotherapy and pulmonary drainage (to prevent
pneumonia). Pulmonary drainage may be successfully supported
by high-frequency chest wall oscillation (HFCWO).[48] In severe
cases, the need for volume and blood substitution can add further
damage to the lung parenchyma by capillary leakage. In cases of
impaired gas exchange, intubation and mechanical ventilation are
necessary. Additionally, early xation of concomitant long bone
fractures may prevent further pulmonary complications, such as
acute respiratory distress syndrome (ARDS).
Other related injuries after chest trauma include rare traumatic
diaphragmatic rupture, which requires surgical repair.[49]
VENTILATION STRATEGIES
The presence of pulmonary contusion with or without ail chest
is usually associated with a high incidence of ventilatory support
requirements[50]; however, there is often no clear correlation
between the affected lung volume and the severity and duration
of hypoxemia.[3] Respiratory support can avoid asynchronous
paradoxical movements and can achieve pneumatic stabilization.
A general optimal ventilatory strategy that is applicable to all
patients after chest trauma does not exist. Understanding the
pathophysiology of individual patients, with their specic kinds
of lung damage after trauma, and accordingly devising and
implementing ventilation strategies may support the respiratory
system and prevent further ventilator-associated lung injury
(VALI). VALI has the potential to induce acute lung injury (ALI)
or ARDS, as well as multiple organ failure.[51,52]
The risk factors for developing trauma-associated ARDS
include direct pulmonary injury, direct chest wall injury,
aspiration, hemorrhagic shock, massive transfusion, old age,
underlying diseases, malignancy, severe traumatic brain injury,
and quadriplegia.[53,54]
Clinicians need to be aware that barotrauma, as well as VALI in
general, results from elevated pulmonary pressures, large tidal
volumes, overdistension and an increased fraction of inspired
oxygen, viz., FiO2 >0.6. Limiting plateau airway pressures
and reducing tidal volumes help minimize the risk of VALI.
Therefore, it is helpful that physiological parameters (e.g.,
SpO2, CO2, pH) need not be corrected to physiologic norms,
as previously described.[55] One exception involves patients with
elevated intracranial pressures (ICPs), where normoventilation
should be achieved. In trauma patients, wherein thorax injury is
combined with head injuries (about 18% of fatally injured car
drivers),[56] an additional goal is to optimize the cerebral perfusion
pressure. Hypercapnia and acidosis compromise cerebral
perfusion and should therefore be avoided in these patients.
In addition to VALI, other problems can occur in combination
with mechanical ventilation. One important complication is the
reduction of cardiac output due to elevated intrathoracic pressure
created by positive-pressure ventilation with resultant reduced
venous return and hypotension. The challenge for the physician
Richter and Ragaller: Chest trauma ventilation

255
Journal of Emergencies, Trauma, and Shock I 4:2 I Apr - Jun 2011
is to achieve the ne balance between ventilation, oxygenation
and adequate cardiac output in chest trauma patients.
Clinicians can select between two different strategies to apply
mechanical ventilation: noninvasive positive-pressure ventilation
(NPPV) and invasive positive-pressure ventilation (IPPV).
Noninvasive positive-pressure ventilation
NPPV delivers positive pressure to patients through nasal,
facial or helmet interfaces, without an endotracheal airway, and
should be used in cooperative patients without hemodynamic
instability, facial injuries and a risk of aspiration. NPPV is typically
associated with fewer serious complications, a shorter stay at
the ICU, shorter periods of ventilation and improvements in
oxygenation.[57,58] NPPV may reduce the incidence of intubation
in patients with chest trauma–induced hypoxemia.[59] Therefore,
NPPV should be considered the rst choice in the absence of
contraindications. In the event of noncompliance or failure to
respond, intubation and IPPV are indicated.
The advantages of noninvasive ventilation are the avoidance of
complications related to endotracheal intubation, avoidance of
sedation and paralysis and the easy removal and reinstitution
of NPPV, if needed. There are no guidelines for administering
continuous or intermittent NPPV therapy, and so it should be
adapted to the patient’s needs.
The disadvantages of NPPV are typically related to the interface
(a mask with an air leak and necrosis) and the lack of a protected
airway. However, tracheal intubation should never be delayed if
the respiratory status worsens under NPPV.
Invasive positive-pressure ventilation
The choice of endotracheal tube depends on the type of injury
and the requirements of further surgery. Trauma patients with
maxillofacial injury, full stomach, cervical spine instability, neck
hematoma, laryngeal injury or respiratory distress may require
more extensive airway management.[50,61] IPPV should be
primarily selected in patients who need a denitive airway and
need to be protected from aspiration.
Ventilator setting
NPPV is part of a noninvasive technique that delivers continuous
PEEP or CPAP, or it is used to maintain two positive airway
pressures [pressure support ventilation (PSV) and PEEP]. The
avoidance of airway and alveolar collapse by CPAP prevents
atelectasis, maintains functional residual capacity and increases
cardiac output. In the PSV mode, the patient triggers the
ventilator to provide a variable ow of gas that increases until
airway pressure reaches a selected limit. Patients with PSV control
the respiratory rate and the inspiratory and expiratory times.
The setting should be adjusted to provide the lowest inspiratory
pressures or volumes needed to obtain improved gas exchange
and patient comfort.[62] A pressure differential of 5 cm H2O
should be maintained between the inspiratory positive airway
pressure and expiratory positive airway pressure (EPAP), starting
with an EPAP of 3 cm H2O. Inspiratory and expiratory pressures
can be gradually increased over the course of 5 minutes if
necessary. The impact of these pressure changes on oxygenation
improvement should be monitored by using continuous pulse
oximetry and end-tidal CO2.
Higher EPAP levels (≥12 cm H2O) may require IPPV. The
implementation of the open lung concept with a PEEP ≥10
cm H2O increases normally aerated lung volume and arterial
oxygenation in patients with severe chest trauma.[63] Otherwise,
patients with significant lung contusion and poor lung
compliance have an increased risk of barotrauma. In patients
with hemorrhagic shock, PEEP levels higher than 5 cm H2O
can exacerbate hypotension.
Therefore, this type of trauma patient needs a ventilator strategy
that minimizes airway pressure[64] and incorporates permissive
hypercapnia, meaning that the strategy of protective mechanical
ventilation should be applied by limiting peak lung distension and
preventing end-expiratory collapse with —
1
. Low tidal volumes
Tidal volumes of 6 mL/kg of predicted body weight;
for men = [50+0.91 • (body height in cm − 152.4)] and
for women = [45.5+0.91 • (body height in cm − 152.4)].
2
. Limited plateau pressure viz., <30 cm H2O
A plateau pressure <28 cm H2O is associated with less tidal
hyperinflation and is even more protective than a plateau
pressure (Pplat) <30 cm H2O in patients with a large, dependent
and nonaerated lung compartment.[65] To adequately distend
the lung, in several types of patients (e.g., with morbid obesity),
higher, additional pressures [including elevated PEEP (as the
rst choice)] might be needed to lift the restricted chest wall
away from the lung.
3
. An FiO2 that is as low as possible
Unclear initial situations in polytraumatized patients require high
FiO2 values. This is supported by studies that have shown a lower
mortality in animals with hemorrhagic shock and with high FiO2
levels,[66] and a better prognosis in patients with head and brain
injuries.[67] Under controlled conditions of an ICU, FiO2 should
be adapted to obtain a PaO2 of 8-10 kPa per 60-80 mm Hg (or
oxygenation saturation ≥90%). This can be optimized by using
closed-loop control systems.[68]
4
. Optimal PEEP
PEEP should be incrementally added to optimize oxygenation
and CO2–elimination and may reach a range of 14-16 cm H2O
in patients with severe lung injury.[69] A meta-analysis of the
treatment of patients with acute lung injury and ARDS (which
includes a fraction of patients with multiple trauma) compared
the outcomes after treatment with higher (11-15 cm H2O) vs.
lower (8-9 cm H2O) PEEP levels and showed that higher levels
of PEEP were associated with improved hospital survival only
among the subgroup of patients with ARDS.[70] However, severe
Richter and Ragaller: Chest trauma ventilation

256 Journal of Emergencies, Trauma, and Shock I 4:2 I Apr - Jun 2011
hypotension and a substantial reduction of cardiac output have
to be avoided.
5
. Permissive hypercapnia
Elevated PaCO2 levels can be tolerated, so long as the pH is greater
than 7.2, except in patients with elevated intracranial pressures.
Ventilator modes
Unfortunately, there is a limited amount of scientic data that can
be used to guide the practitioner in the selection of the best mode
of ventilation. Despite the several ventilator modes introduced
into the clinical routine, there is no evidence that the choice
between a volume-controlled mode and a pressure-controlled
mode inuences the mortality or morbidity of patients.[71] PSV
assists respiratory muscles during noninvasive and invasive
ventilation and is patient-triggered and ow-cycled (see above).
In the event of leakage (i.e., bronchopulmonal stula), PSV
with an adjustable termination ow should be used to prevent
prolonged inspiration.
Airway pressure release ventilation (APRV) is a mode that
can permit spontaneous breathing at any time throughout the
respiratory cycle. Airway pressure is transiently released to a
lower level to create a deep expiration and to support the patient
effort during CPAP breathing. Hereby, the lower pressure level
is extremely shorter than the time of the upper pressure level.
APRV has been shown to improve oxygenation in trauma patients
and therefore may be a good option.[72-74]
High-frequency oscillation ventilation (HFOV) is an additional
option for mechanical ventilation and is typically used as a
rescue mode of ventilation in patients with severe respiratory
distress.
[75] With HFOV, the lung achieves a higher mean airway
pressure in comparison to conventional mechanical ventilation
and very low tidal volumes (44-210 mL),[76] preventing cyclical
lung de-recruitment and overdistension. The potential benecial
effects of HFOV still need elaboration and evaluation in the
chest trauma population.[77]
Under the assumption that mechanical ventilation patterns that
produce variable airway pressures and inspiratory times may be
advantageous to maximize lung recruitment and stabilization,[78] a
new mode of "noisy ventilation" with variable tidal volumes and
xed respiratory frequencies to improve respiratory function has
been introduced. However, this mode has not been demonstrated
in human patients.[79,80]
Gas exchange through an artificial lung
Extracorporeal membrane oxygenation (ECMO) or
extracorporeal life support (ECLS) is benecial in treating ALI
and ARDS after trauma[81-84] and can improve the survival of
trauma patients.[85] Extracorporeal oxygenation needs systemic
anticoagulation and is therefore difcult to apply in patients
with multiple trauma[86] and is only provided in specialized
centers.
Independent lung ventilation
Chest trauma can lead to disproportionate or unilateral lung
trauma. In such cases, the affected lung cannot be sufciently
ventilated without compromising the healthy lung with VALI.
Conventional respiration methods may fail in such a condition
of the lungs. Here independent lung ventilation should be
considered to optimize the respiratory and hemodynamic
situations. Non-synchronized independent ventilation can be
used to provide the lungs with selective ventilator management,
according to the different statuses of the affected and non-
affected lungs.[87,88] In this way, after intubation with a double-
lumen tube, two ventilators that are independently attached to
the lungs can provide different ventilator modes, ows, pressure
levels, rates, volumes and inspired oxygen. Independent lung
ventilation provides the option of combining high-frequency jet
ventilation to the affected side with protective lung ventilation
to the non-affected side.[89-92]
The use of differential PEEP is another important factor for
improving gas exchange in unilateral parenchymal lung injuries
after trauma.[93-95] In bronchopleural stula, the positive pressure
(PEEP/ CPAP) and inationary volume should be limited, and
inverse-ratio inationary holds should be avoided on the affected
side. Further limitation in positive pressure can be achieved by
reducing the rate of positive-pressure breaths with the affected
lung. In very severe cases, the affected side may be left open
to the atmosphere or connected to an oxygen-rich gas source,
whereas the non-affected side is ventilated.[32,96]
CONCLUSIONS
Ventilation in patients after chest trauma is challenging because of
the difculty in achieving balance between sufcient ventilation
and the avoidance of further harm to the lungs. Coexisting
neurologic, osseous and vascular injuries may require more
attention by the emergency physician than the pulmonary trauma
itself. The goal of rst-line clinical therapy for chest trauma
patients is to achieve an adequate level of oxygenation and to
protect the lungs from further injury using reduced tidal volumes
(6 mL/kg pbw), a pressure limit below 30 cm H2O and a level
of FiO2 as low as possible. The magnitude, location and type of
lung or chest injury require a gradually adapted therapy tailored
to individual patient’s needs and which includes NIPPV or IPPV
with i.e. APRV. Additionally, ECMO should be considered, as
should independent, side-specic lung ventilation in combination
with HFOV. Chest tube management, chest physiotherapy,
extensive bronchial drainage, bronchial alveolar lavage sampling
and other options, such as the use of bronchial blockers and the
performance of a tracheostomy, should be incorporated into the
management of ventilation in chest trauma patients.
REFERENCES
1. Devitt JH, McLean RF, Koch JP. Anaesthetic management of acute blunt
thoracic trauma. Can J Anaesth 1991;38:506-10.
Richter and Ragaller: Chest trauma ventilation

257
Journal of Emergencies, Trauma, and Shock I 4:2 I Apr - Jun 2011
2. Pape HC, Remmers D, Rice J, Ebisch M, Krettek C, Tscherne H. Appraisal
of early evaluation of blunt chest trauma: Development of a standardized
scoring system for initial clinical decision making. J Trauma 2000;49:
496-504.
3. Cohn SM. Pulmonary contusion: Review of the clinical entity. J Trauma
1997;42:973-9.
4. Szucs-Farkas Z, Kaelin I, Flach PM, Rosskopf A, Ruder TD, Triantafyllou
M, et al. Detection of chest trauma with whole-body low-dose linear
slit digital radiography: a multireader study. AJR Am J Roentgenol
2010;194:W388-95.
5. Wustner A, Gehmacher O, Hammerle S, Schenkenbach C, Hafele H,
Mathis G. Ultrasound diagnosis in blunt thoracic trauma. Ultraschall Med
2005;26:285-90.
6. Brooks A, Davies B, Smethhurst M, Connolly J. Emergency ultrasound in
the acute assessment of haemothorax. Emerg Med J 2004;21:44-6.
7. Cohn SM, Zieg PM. Experimental pulmonary contusion: Review
of the literature and description of a new porcine model. J Trauma
1996;41:565-71.
8. Aufmkolk M, Fischer R, Voggenreiter G, Kleinschmidt C, Schmit-
Neuerburg KP, Obertacke U. Local effect of lung contusion on lung
surfactant composition in multiple trauma patients. Crit Care Med
1999;27:1441-6.
9. Wanek S, Mayberry JC. Blunt thoracic trauma: Flail chest, pulmonary
contusion, and blast injury. Crit Care Clin 2004;20:71-81.
10. Ullman EA, Donley LP, Brady WJ. Pulmonary trauma emergency
department evaluation and management. Emerg Med Clin North Am
2003;21:291-313.
11. Raghavendran K, Notter RH, Davidson BA, Helinski JD, Kunkel SL,
Knight PR. Lung contusion: Inammatory mechanisms and interaction
with other injuries. Shock 2009;32:122-30.
12. Thibeault DW, Lachman RS, Laul VR, Kwong MS. Pulmonary interstitial
emphysema, pneumomediastinum, and pneumothorax. Occurrence in the
newborn infant. Am J Dis Child 1973;126:611-4.
13. Al-Hassani A, Abdulrahman H, A I, Almadani A, Al-Den A, Al-Kuwari A,
et al. Rib fracture patterns predict thoracic chest wall and abdominal solid
organ injury. Am Surg 2010;76:888-91.
14. Duff JH, Goldstein M, McLean AP, Agrawal SN, Munro DD, Gutelius JR.
Flail chest: A clinical review and physiological study. J Trauma 1968;8:63-74.
15. Mackersie RC, Shackford SR, Hoyt DB, Karagianes TG. Continuous
epidural fentanyl analgesia: Ventilatory function improvement with routine
use in treatment of blunt chest injury. J Trauma 1987;27:1207-12.
16. Bulger EM, Edwards T, Klotz P, Jurkovich GJ. Epidural analgesia improves
outcome after multiple rib fractures. Surgery 2004;136:426-30.
17. Abolhoda A, Livingston DH, Donahoo JS, Allen K. Diagnostic and
therapeutic video assisted thoracic surgery (VATS) following chest trauma.
Eur J Cardiothorac Surg 1997;12:356-60.
18. Tanaka H, Yukioka T, Yamaguti Y, Shimizu S, Goto H, Matsuda H, et al.
Surgical stabilization of internal pneumatic stabilization? A prospective
randomized study of management of severe ail chest patients. J Trauma
2002;52:727-32.
19. Pettiford BL, Luketich JD, Landreneau RJ. The management of ail chest.
Thorac Surg Clin 2007;17:25-33.
20. Ball CG, Kirkpatrick AW, Laupland KB, Fox DI, Nicolaou S, Anderson
IB, et al. Incidence, risk factors, and outcomes for occult pneumothoraces
in victims of major trauma. J Trauma 2005;59:917-24.
21. Bokhari F, Brakenridge S, Nagy K, Roberts R, Smith R, Joseph K, et al.
Prospective evaluation of the sensitivity of physical examination in chest
trauma. J Trauma 2002;53:1135-8.
22. Ho ML, Gutierrez FR. Chest radiography in thoracic polytrauma. AJR Am
J Roentgenol 2009;192:599-612.
23. Dulchavsky SA, Hamilton DR, Diebel LN, Sargsyan AE, Billica RD,
Williams DR. Thoracic ultrasound diagnosis of pneumothorax. J Trauma
1999;47:970-1.
24. Barrios C, Tran T, Malinoski D, Lekawa M, Dolich M, Lush S, et al. Successful
management of occult pneumothorax without tube thoracostomy despite
positive pressure ventilation. Am Surg 2008;74:958-61.
25. Fitzgerald M, Mackenzie CF, Marasco S, Hoyle R, Kossmann T. Pleural
decompression and drainage during trauma reception and resuscitation.
Injury 2008;39:9-20.
26. Powner DJ, Cline CD, Rodman GH, Jr. Effect of chest-tube suction on
gas ow through a bronchopleural stula. Crit Care Med 1985;13:99-101.
27. Baumann MH, Patel PB, Roney CW, Petrini MF. Comparison of function
of commercially available pleural drainage units and catheters. Chest
2003;123:1878-86.
28. Gallagher TJ, Smith RA, Kirby RR, Civetta JM. Intermittent inspiratory
chest tube occlusion to limit bronchopleural cutaneous airleaks. Crit Care
Med 1976;4:328-32.
29. Blanch PB, Koens JC Jr., Layon AJ. A new device that allows synchronous
intermittent inspiratory chest tube occlusion with any mechanical ventilator.
Chest 1990;97:1426-30.
30. Downs JB, Chapman RL Jr. Treatment of bronchopleural stula during
continuous positive pressure ventilation. Chest 1976;69:363-6.
31. Phillips YY, Lonigan RM, Joyner LR. A simple technique for managing a
bronchopleural stula while maintaining positive pressure ventilation. Crit
Care Med 1979;7:351-3.
32. Taylor RW, Dellinger RP. Special Problems in Mechanical Ventilation. In:
Marini JJ, Slutsky AS, editors. Physiological Basis of Ventilatory Support.
New York: Marcel Dekker; 1998. p 1247-61.
33. Castelli I, Schlapfer R, Stulz P. Thoracic trauma. Anaesthesist 1995;44:
513-30.
34. Klein U, Laubinger R, Malich A, Hapich A, Gunkel W. Emergency
treatment of thoracic trauma. Anaesthesist 2006;55:1172-88.
35. Balci AE, Eren N, Eren S, Ulkü R. Surgical treatment of post-traumatic
tracheobronchial injuries: 14-year experience. Eur J Cardiothorac Surg
2002;22:984-9.
36. Cassada DC, Munyikwa MP, Moniz MP, Dieter RA Jr, Schuchmann GF,
Enderson BL. Acute injuries of the trachea and major bronchi: Importance
of early diagnosis. Ann Thorac Surg 2000;69:1563-7.
37. Kiser AC, O'Brien SM, Detterbeck FC. Blunt tracheobronchial injuries:
Treatment and outcomes. Ann Thorac Surg 2001;71:2059-65.
38. Symbas PN, Justicz AG, Ricketts RR. Rupture of the airways from blunt
trauma: Treatment of complex injuries. Ann Thorac Surg 1992;54:177-83.
39. Benumof JL, Partridge BL, Salvatierra C, Keating J. Margin of safety in
positioning modern double-lumen endotracheal tubes. Anesthesiology
1987;67:729-38.
40. al Jishi N, Dyer D, Sharief N, al-Alaiyan S. Selective bronchial occlusion
for treatment of bullous interstitial emphysema and bronchopleural stula.
J Pediatr Surg 1994;29:1545-7.
41. Sprung J, Krasna MJ, Yun A, Thomas P, Bourke DL. Treatment of a
bronchopleural stula with a Fogarty catheter and oxidized regenerated
cellulose (surgicel). Chest 1994;105:1879-81.
42. Raghavendran K, Davidson BA, Helinski JD, Marschke CJ, Manderscheid
P, Woytash JA, et al. A rat model for isolated bilateral lung contusion from
blunt chest trauma. Anesth Analg 2005;101:1482-9.
43. Rashid MA, Wikström T, Ortenwall P. Outcome of lung trauma. Eur J
Surg 2000;166:22-8.
44. O'Connor JV, Kufera JA, Kerns TJ, Stein DM, Ho S, Dischinger PC,
et al. Crash and occupant predictors of pulmonar y contusion. J Trauma
2009;66:1091-5.
Richter and Ragaller: Chest trauma ventilation

258 Journal of Emergencies, Trauma, and Shock I 4:2 I Apr - Jun 2011
45. Mizushima Y, Hiraide A, Shimazu T, Yoshioka T, Sugimoto H. Changes
in contused lung volume and oxygenation in patients with pulmonary
parenchymal injury after blunt chest trauma. Am J Emerg Med 2000;18:385-9.
46. Omert L, Yeaney WW, Protetch J. Efcacy of thoracic computerized
tomography in blunt chest trauma. Am Surg 2001;67:660-4.
47. Keel M, Meier C. Chest injuries - what is new? Curr Opin Crit Care
2007;13:674-9.
48. Anderson CA, Palmer CA, Ney AL, Becker B, Schaffel SD, Quickel
RR. Evaluation of the safety of high-frequency chest wall oscillation
(HFCWO) therapy in blunt thoracic trauma patients. J Trauma Manag
Outcomes 2008;2:8
49. Cain JG, Tesfaye Y. Pulmonary trauma. Curr Opin Anaesthesiol
2001;14:245-9.
50. Rao PM, Puri GD, Bharadwaj N, Chari P, Acup D. ICU management
of blunt chest trauma: Our experience. Ann Card Anaesth 1998;1:31-5.
51. Gajic O, Frutos-Vivar F, Esteban A, Hubmayr RD, Anzueto A. Ventilator
settings as a risk factor for acute respiratory distress syndrome in
mechanically ventilated patients. Intensive Care Med 2005;31:922-6.
52. Slutsky AS. Ventilator-induced lung injury: From barotrauma to biotrauma.
Respir Care 2005;50:646-59.
53. Hoyt DB, Simons RK, Winchell RJ, Cushman J, Hollingsworth-Fridlund
P, Holbrook T, et al. A risk analysis of pulmonar y complications following
major trauma. J Trauma 1993;35:524-31.
54. Garber BG, Hebert PC, Yelle JD, Hodder RV, McGowan J. Adult respiratory
distress syndrome: A systemic overview of incidence and risk factors. Crit
Care Med 1996;24:687-95.
55. Ragaller M, Richter T. Acute lung injury and acute respiratory distress
syndrome. J Emerg Trauma Shock 210;3:43-51.
56. Ndiaye A, Chambost M, Chiron M. The fatal injuries of car drivers. Forensic
Sci Int 2009;184:21-7.
57. Antonelli M, Conti G, Rocco M, Bu M, De Blasi RA, Vivino G, et al. A
comparison of noninvasive positive-pressure ventilation and conventional
mechanical ventilation in patients with acute respiratory failure. N Engl J
Med 1998;339:429-35.
58. Beltrame F, Lucangelo U, Gregori D, Gregoretti C. Noninvasive positive
pressure ventilation in trauma patients with acute respiratory failure.
Monaldi Arch Chest Dis 1999;54:109-14.
59. Hernandez G, Fernandez R, Lopez-Reina P, Cuena R, Pedrosa A, Ortiz
R, et al. Noninvasive ventilation reduces intubation in chest trauma-related
hypoxemia: A randomized clinical trial. Chest 2010;137:74-80.
60. Smith CE, Dejoy SJ. New equipment and techniques for airway
management in trauma. Curr Opin Anaesthesiol 2001;14:197-209.
61. Abernathy JH 3rd, Reeves ST. Airway catastrophes. Curr Opin Anaesthesiol
2010;23:41-6.
62. Jaber S, Chanques G, Jung B. Postoperative noninvasive ventilation.
Anesthesiology 2010;112:453-61.
63. Schreiter D, Reske A, Stichert B, Seiwerts M, Bohm SH, Kloeppel R, et al.
Alveolar recruitment in combination with sufcient positive end-expiratory
pressure increases oxygenation and lung aeration in patients with severe
chest trauma. Crit Care Med 2004;32:968-75.
64. Sha S, Gentilello L. Pre-hospital endotracheal intubation and positive
pressure ventilation is associated with hypotension and decreased survival
in hypovolemic trauma patients: An analysis of the National Trauma Data
Bank. J Trauma 2005;59:1140-5.
65. Terragni PP, Rosboch G, Tealdi A, Corno E, Menaldo E, Davini O, et al.
Tidal hyperination during low tidal volume ventilation in acute respiratory
distress syndrome. Am J Respir Crit Care Med 2007;175:160-6.
66. Meier J, Kemming GI, Kisch-Wedel H, Blum J, Pape A, Habler OP.
Hyperoxic ventilation reduces six-hour mortality after partial fluid
resuscitation from hemorrhagic shock. Shock 2004;22:240-7.
67. Reinert M, Barth A, Rothen HU, Schaller B, Takala J, Seiler RW. Effects
of cerebral perfusion pressure and increased fraction of inspired oxygen
on brain tissue oxygen, lactate and glucose in patients with severe head
injury. Acta Neurochir (Wien) 2003;145:341-9.
68. Johannigman JA, Branson R, Lecroy D, Beck G. Autonomous control
of inspired oxygen concentration during mechanical ventilation of the
critically injured trauma patient. J Trauma 2009;66:386-92.
69. Papadakos PJ, Karcz M, Lachmann B. Mechanical ventilation in trauma.
Curr Opin Anaesthesiol 2010;23:228-32.
70. Briel M, Meade M, Mercat A, Brower RG, Talmor D, Walter SD, et al.
Higher vs lower positive end-expiratory pressure in patients with acute
lung injury and acute respiratory distress syndrome: systematic review and
meta-analysis. JAMA 2010;303:865-73.
71. Esteban A, Alía I, Gordo F, de Pablo R, Suarez J, González G, et al.
Prospective randomized trial comparing pressure-controlled ventilation
and volume-controlled ventilation in ARDS. For the Spanish Lung Failure
Collaborative Group. Chest 2000;117:1690-6.
72. Sydow M, Burchardi H, Ephraim E, Zielmann S, Crozier TA. Long-
term effects of two different ventilatory modes on oxygenation in
acute lung injury. Comparison of airway pressure release ventilation and
volume-controlled inverse ratio ventilation. Am J Respir Crit Care Med
1994;149:1550-6.
73. Davis K Jr., Johnson DJ, Branson RD, Campbell RS, Johannigman
JA, Porembka D. Airway pressure release ventilation. Arch Surg 1993;
128:1348-52.
74. Dart BW 4th, Maxwell RA, Richart CM, Brooks DK, Ciraulo DL, Barker
DE, et al. Preliminary experience with airway pressure release ventilation
in a trauma/surgical intensive care unit. J Trauma 2005;59:71-6.
75. Chan KP, Stewart TE, Mehta S. High-frequency oscillatory ventilation for
adult patients with ARDS. Chest 2007;131:1907-16.
76. Hager DN, Fessler HE, Kaczka DW, Shanholtz CB, Fuld MK, Simon BA,
et al. Tidal volume delivery during high-frequency oscillatory ventilation
in adults with acute respiratory distress syndrome. Crit Care Med
2007;35:1522-9.
77. Siau C, Stewart TE. Current role of high frequency oscillatory ventilation
and airway pressure release ventilation in acute lung injury and acute
respiratory distress syndrome. Clin Chest Med 2008;29:265-75, vi.
78. Pelosi P, Gama de Abreu M, Rocco PR. New and conventional strategies
for lung recruitment in acute respiratory distress syndrome. Crit Care
2010;14:210.
79. Spieth PM, Carvalho AR, Güldner A, Pelosi P, Kirichuk O, Koch T, et al.
Effects of different levels of pressure support variability in experimental
lung injury. Anesthesiology 2009;110:342-50.
80. Spieth PM, Carvalho AR, Pelosi P, Hoehn C, Meissner C, Kasper M, et al.
Variable tidal volumes improve lung protective ventilation strategies in
experimental lung injury. Am J Respir Crit Care Med 2009;179:684-93.
81. Anderson HL 3rd, Shapiro MB, Delius RE, Steimle CN, Chapman RA,
Bartlett RH. Extracorporeal life support for respiratory failure after multiple
trauma. J Trauma 1994;37:266-72.
82. Voelckel W, Wenzel V, Rieger M, Antretter H, Padosch S, Schobersberger
W. Temporary extracorporeal membrane oxygenation in the treatment of
acute traumatic lung injury. Can J Anaesth 1998;45:1097-102.
83. Senunas LE, Goulet JA, Greeneld ML, Bartlett RH. Extracorporeal life
support for patients with signicant orthopaedic trauma. Clin Orthop
Relat Res 1997:339:32-40.
84. Cordell-Smith JA, Roberts N, Peek GJ, Firmin RK. Traumatic lung
injury treated by extracorporeal membrane oxygenation (ECMO). Injury
2006;37:29-32.
Richter and Ragaller: Chest trauma ventilation

259
Journal of Emergencies, Trauma, and Shock I 4:2 I Apr - Jun 2011
85. Michaels AJ, Schriener RJ, Kolla S, Awad SS, Rich PB, Reickert C, et al.
Extracorporeal life support in pulmonary failure after trauma. J Trauma
1999;46:638-45.
86. Marasco SF, Preovolos A, Lim K, Salamonsen RF. Thoracotomy in adults
while on ECMO is associated with uncontrollable bleeding. Perfusion
2007;22:23-6.
87. Katsaragakis S, Stamou KM, Androulakis G. Independent lung ventilation
for asymmetrical chest trauma: effect on ventilatory and haemodynamic
parameters. Injury 2005;36:501-4.
88. Anantham D, Jagadesan R, Tiew PE. Clinical review: Independent lung
ventilation in critical care. Crit Care 2005;9:594-600.
89. Terragni P, Rosboch GL, Corno E, Menaldo E, Tealdi A, Borasio P, et al.
Independent high-frequency oscillatory ventilation in the management of
asymmetric acute lung injury. Anesth Analg 2005;100:1793-6.
90. Miranda DR, Stoutenbeek C, Kingma L. Differential lung ventilation with
HFPPV. Intensive Care Med 1981;7:139-41.
91. Feeley TW, Keating D, Nishimura T. Independent lung ventilation using
high-frequency ventilation in the management of a bronchopleural stula.
Anesthesiology 1988;69:420-2.
92. Rico FR, Cheng JD, Gestring ML, Piotrowski ES. Mechanical ventilation
strategies in massive chest trauma. Crit Care Clin 2007;23:299-315, xi.
93. Zandstra DF, Stoutenbeek CP. Reection of differential pulmonary
perfusion in polytrauma patients on differential lung ventilation (DLV).
A comparison of two CO2-derived methods. Intensive Care Med
1989;15:151-4.
94. Lev A, Barzilay E, Geber D, Bishara H, Prego J. Differential lung ventilation:
A review and 2 case reports. Resuscitation 1987;15:77-86.
95. Siegel JH, Stoklosa JC, Borg U, Wiles CE 3rd, Sganga G, Geisler FH, et al.
Quantication of asymmetric lung pathophysiology as a guide to the use
of simultaneous independent lung ventilation in posttraumatic and septic
adult respiratory distress syndrome. Ann Surg 1985;202:425-39.
96. Bonnet R, Wilms D. Long-term use of asynchronous independent lung
ventilation: Effects on gas exchange and hemodynamics. Pneumologie
1990;44:665-7.
How to cite this article: Richter T, Ragaller M. Ventilation in chest
trauma. J Emerg Trauma Shock 2011;4:251-9.
Received: 09.12.10. Accepted: 09.12.10.
Source of Support: Nil. Conict of Interest: None declared.
Richter and Ragaller: Chest trauma ventilation