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Chapter

Mechanical Ventilation in the

Trauma Patient
Jessica Lovich-Sapola, Jonathan A. Alter and Maureen Harders

Abstract

In this chapter, we discuss the unique ventilatory strategies of the trauma

patient. Injuries can be direct to the lung resulting from the trauma or indirect
because of other injury to the body. We will discuss the airway and ventilation
management and concerns in a patient with chest trauma, abdominal trauma, head
trauma, orthopedic, and burn injury. The chapter will explain lung-protective
strategies as well as innovative ventilation management techniques including
extracorporeal membrane oxygenation.

Keywords: trauma, ventilation, burn, anesthesia, chest

1. Introduction

Trauma lung injury can result from a direct injury to the lung or secondary to
injury elsewhere. The trauma and the associated aggressive resuscitation lead to
bleeding, edema, and inflammation of the lungs. The trauma can result in acute
lung injury (ALI) and acute respiratory distress syndrome (ARDS). The goal of
the ventilation is to preserve the lung as well as the brain and other organs that are
injured. Each form of traumatic injury results in an individualized approach to
mechanical ventilation [1].

1.1 Lung-protective ventilation strategies in the trauma patient

The primary goal of the trauma patient is to avoid hypoxia and secondary tissue
injury. Mechanical ventilation may be initiated for reasons other than respiratory
compromise, such as brain injury, shock, intoxication, agitation, or combative-
ness. Lung-protective ventilation strategies aim to reduce the volume and pressure
delivered to the lung. For example, the goal tidal volume is 6–8 mL/kg of predicted
body weight regardless of the type of ventilation [1].

1.2 Modes of ventilation in the trauma patient

Volume-controlled ventilation (VCV) is the most used form of ventilation in

the operating room. The tidal volume (Vt), respiratory rate, and FiO2 are set by the
operator. This mode guarantees delivery of a set Vt and minute ventilation. The Vt is
not reached if the peak inspiratory pressure (PIP) exceeds a set limit [1].

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Mechanical Ventilation

Pressure-controlled ventilation (PCV) can be used. In this type of ventilation,

the Vt delivered is variable and depends on the airway resistance and the lung/chest
wall compliance. This mode is recommended in the case of severe ARDS to promote
better gas exchange [1].
Airway pressure release ventilation (APRV) is useful for the patient that has
suffered a blunt trauma, with pulmonary contusions and severe atelectasis. APRV
is also indicated for patients with morbid obesity and pregnancy. This mode of ven-
tilation is a time-triggered, pressure-limited, and time-cycled mode of ventilation.
The patient is able to breathe spontaneously. This mode is excellent for recruitment
of the collapsed lung [1].
High-frequency oscillation ventilation (HFOV) results in the rapid delivery of
very small tidal volumes with the application of high mean airway pressures. This
type of ventilation results in active exhalation and therefore reduces air trapping.
This type of ventilation is useful for patients with severe pulmonary contusion,
ALI/ARDS, and smoke inhalation injury [1].
Noninvasive positive-pressure ventilation (NIPPV) including continuous posi-
tive airway pressure (CPAP) and bi-level airway pressure (BiPAP) can be used to
treat acute respiratory failure. This mode of ventilation can be used in the trauma
patient as well. This is not recommended for patients with brain injury, intoxica-
tion, or facial trauma. It is also not recommended for patients that are at increased
risk of aspiration [1].

2. Chest trauma

Chest trauma, and the subsequent complications of chest injury, is significantly

prevalent and the second most common cause of mortality in trauma. Injury
sustained to the thorax can cause enormous damage to the heart, lungs, and major
vasculature.
Any mechanism of injury to the chest wall or underlying organ systems has the
potential to cause acute life-threatening issues with respiration. Mechanical ven-
tilation, as it relates to the resulting complications of contusions, hypoxemia, and
hemorrhage that occupy the spaces left behind by traumatic events, will be dis-
cussed throughout this chapter. Understanding the pernicious effects on respiratory
mechanics and respiratory physiology helps the clinician to determine the timing of
intubation and where the patient would most benefit on the spectrum of invasive
ventilation.

2.1 Respiratory physiology in chest trauma

Injuries to the chest requiring mechanical ventilation may affect respirations

in a variety of ways. Damage to the integument, musculoskeletal, nervous, or
circulatory supply confined within and around the thoracic cavity can vastly change
the physiology of respirations. Similarly, damage to the airways and lungs can
significantly impede proper ventilation and oxygenation. As such, we can reduce
respiratory compromise into two distinct circumstances: respirations compromised
by altered mechanics of breathing, and respirations compromised by direct damage
to the airway and lungs. Injuries to the respiratory system can also be categorized
as being either penetrating or blunt in origin; however, the need for mechanical
ventilation may exceed this distinction.
Integument provides a barrier from foreign organisms and elasticity, which
is essential for expansion and contraction of the lungs; hindrance of integument

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Mechanical Ventilation in the Trauma Patient
DOI: http://dx.doi.org/10.5772/intechopen.101578

by injuries, such as in the case of burns or circumferential eschars, limits the

compliance of the respiratory system and often necessitates positive pressure
ventilation.
Skeletal trauma most commonly involves rib fractures. Splinting, caused by
painful respirations and often associated with factures involving the ribs, sternum,
vertebrae, clavicles, or scapulae as well as injuries to soft tissue or muscle, can lead
to atelectasis, hypoxemia, and pneumonia. Disruption to breathing mechanics by a
flail chest, when two or more ribs are fractured in two or more places, and by hemo-
pneumothorax, whereby the thoracic cavity is occupied by blood or air, may impede
lung expansion and limit tidal volumes as well as oxygenation. Massive thoracic
trauma is often accompanied by significant abdominal trauma. Diaphragmatic
injury inhibits the lungs’ ability to expand and contract. Invasion of the lung cavity
by penetrating wounds, bone spurs, and the like creates a discordance within the
respiratory system, inhibiting lung expansion, and reversing physiology to an open
cavity [2].
Damage to respiratory parenchyma, including alveoli, alveolar ducts, and bron-
chioles, will impede gas exchange. High kinetic energy to the chest wall commonly
causes pulmonary contusions and is the most frequently diagnosed intrathoracic
injury associated with blunt trauma.
Tracheobronchial wounds, and more rarely esophageal damage, can have
profound consequences. Structural damage may result in tension pneumothorax,
pneumomediastinum, and subcutaneous emphysema. Most importantly, damage
to the tracheobronchial tree can create an immediate threat to oxygenation and
perfusion, a situation requiring swift discovery, appropriate intubation technique
in a patient with diminished respiratory reserve, and isolation of injury for surgical
manipulation, exposure, and repair.
Vascular injury, cardiac injury, and cardiac tamponade may impair circulation
via massive hemorrhage, diminished preload because of decreases in venous return,
and impediments to cardiac ejection from impedance on myocardium [3, 4].

2.2 Pulmonary contusion

Blunt trauma often results in pulmonary contusion. The early signs of tachy-
pnea, rhonchi, wheezing, or hemoptysis may indicate pulmonary contusion.
Changes may not be visible on a chest X-ray for up to 4–6 hours. Pulmonary contu-
sions usually resolve in 7 days, which are managed easily by treating with permissive
hypercapnia, conservative fluids, routine lung recruitment, positive end-expiratory
pressure (PEEP), and lung-protective ventilation [1].

2.3 Hemothorax

The most common cause of a hemothorax is the rupture of intercostal vessels.

Chest tube placement is recommended to access the rate of blood loss. Massive
hemothorax, >1500 ml or one third of a patient’s blood volume, often requires
emergent surgery [1].

2.4 Bronchopleural fistulas

Bronchopulmonary fistula is a communication between proximal and distal

airways and the pleural space. Mechanical ventilation can be difficult. The mean
airway pressure should be kept low. Some experts recommend PCV due to the abil-
ity to control the pressure gradient more precisely. Lung isolation may be required

3
Mechanical Ventilation

if the leak is too large for proper ventilation. This can be achieved with main stem
intubation, double-lumen tube, or bronchial blocker depending on the location of
the fistula. The use of HFOV has been reported in some cases in addition to extra-
corporeal membrane oxygenation (ECMO) [1].

2.5 Choosing the appropriate mechanical ventilation for a chest trauma

patient

2.5.1 Non-invasive ventilation

Provided the patient is hemodynamically stable without significant associated

injury such as traumatic brain injury or severe abdominal trauma, non-invasive
ventilation (NIV) techniques should be attempted. NIV has become common in
acute chest trauma as it limits the hazard of further damaging the contused lung,
which is at risk for diminished oxygenation and diffusion issues. Furthermore, NIV
removes the risk of ventilator-induced lung injury, and many of the complications
associated with endotracheal intubation should be considered prior to intubation
attempts [5].

2.5.2 Indications for intubation

Respiratory compromise is depicted in many facets. Decreased tidal volume,

increased respiratory rate, inadequate chest compliance, pleural compromise,
failed lung mechanics, high oxygen requirements, and severe associated injuries
(e.g., head trauma) are all situations that could require intubation. These indica-
tions are not absolute. These situations can quickly spiral out of ventilatory control.
Surmounting a response prior to catastrophic failure and respiratory compromise is
essential (Table 1) [6–8].

2.5.3 Ventilator settings in chest trauma

Initial ventilator settings in chest trauma are based on a lung-protective strategy.

The Vt should be set between 4 and 8 mL/kg of ideal body weight with the plateau
pressure < = 30 cm H20. While positive end-expiratory pressure (PEEP) has well-
established benefits in ICU and ARDS patients, it is initially withheld to evaluate
the level of pulmonary injury, barotrauma, air leaks, and pulmonary shunt. The
FiO2 should be set = 1.0 and then titrated to an appropriate arterial oxygenation
(PaO2). The respiratory rate should be set to 15–25 breaths per minute and then
increased as need to achieve the desired PaCO2. Limiting plateau pressure to 30 cm
H20 will help protect lung physiology (Table 2) [6–8].

Indications for intubation in a chest trauma patient

• Hemodynamic instability
• Decreased respiratory reserves
• Hypoxemia (PaO2 < 60 mmHg)
• Tachypnea
• Hypercarbia
• Glasgow coma scale of 8 or less

Table 1.
Indications for intubation in a chest trauma patient [6–8].

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Mechanical Ventilation in the Trauma Patient
DOI: http://dx.doi.org/10.5772/intechopen.101578

Initial ventilator settings in the chest trauma patient

• Tidal volumes between 4 and 8 mL/kg of ideal body weight

• FiO2 = 1.0, titrated to arterial oxygenation
• Avoid PEEP
• Rate 15–25 breaths per minute

Table 2.
Initial ventilator settings in the chest trauma patient [6–8].

3. Abdominal trauma

Abdominal trauma can result from compression of the organs, deceleration

injury, or penetrating trauma such as a stab or gunshot. It is important to first
determine whether the injury is superior (above the diaphragm), inferior (inguinal
ligament and symphysis pubis), or lateral (anterior axillary lines). The location of
the injury helps to determine the organs involved [9].
The pain from an abdominal trauma can lead to poor shallow respirations,
increased respiratory rate, and a decreased ability to clear secretions. This can result
in a secondary pneumonia. The use of early mechanical ventilation has been cor-
related with a decreased risk of pneumonia, but after 5 days of ventilation that risk
of pneumonia begins to increase again [10].
A patient presenting to the operating room with an abdominal injury requires a
rapid sequence induction with intubation secondary to the high risk of aspiration.
Most trauma patients are considered a “full stomach” and have delayed gastric emp-
tying secondary to the high catecholamine levels from the stress of the trauma [9].

3.1 Abdominal compartment syndrome

Abdominal compartment syndrome can result from increased intra-abdominal

pressure secondary to massive fluid resuscitation (bowel edema) or continued
bleeding. Intra-abdominal pressures exceeding 20–25 mmHg can result in poor
circulation and tissue perfusion as well as decreased cardiac output. The abdominal
compartment syndrome can lead to respiratory dysfunction that will present as
high peak pressures, decreased tidal volume, worsening atelectasis, and hypercar-
bia. Emergent surgery is required to release the abdominal pressure [9].

4. Head trauma

Traumatic brain injury (TBI) resulting from a trauma has a primary and sec-
ondary injury component. The primary injury results from the initial trauma and
resulting mechanical deformation of the skull and brain tissue. The secondary
injury is a result of the progressive insult to the neurons (Table 3) [11].

4.1 Brain injury and acute lung injury (ALI)

Head injury can occur as an isolated trauma or along with other injuries to the
trauma patient. Isolated head injuries have been shown in clinical and experimental
studies to cause lung damage soon after the injury. Neurogenic pulmonary edema
can occur due to the release of catecholamines. In addition, the injured brain
can display a systemic inflammatory response, which can result in injury to the

5
Mechanical Ventilation

Causes of brain injury

Primary brain injury • Disruption of vascular structure

• Compression of neuronal and glial tissue
• Axonal injury

Secondary brain injury • Astrocyte and neuronal swelling

• Hypoperfusion
• Increased free radicals
• Inflammation
• Cellular necrosis
• Axonal degeneration
• Systemic insults: hypotension, hypoxemia, hypoglycemia, hypocarbia,
and hypercarbia

Table 3.
Causes of brain injury [11].

epithelial cells in the lungs. Subsequent mechanical ventilation (MV) can cause
further pulmonary injury and strategies to minimize further damage to the lungs
should be employed [12].
Mechanical ventilation in a patient with both a brain injury and ALI requires a
balance between the principles that guide brain injury and the mechanical ventila-
tion required to be protective of the lung. High PEEP can lead to elevated intratho-
racic pressure, which results in decreased cerebral venous drainage and therefore
poor cerebral perfusion. This effect is seen less in patients with ALI and ARDS;
therefore, PEEP can often be safely applied in these patients. The key is to maintain
the patient’s volume status and mean arterial pressure. Also, the PEEP must be
lower than the patient’s intracranial pressure (ICP). The goal is to apply the lowest
level of PEEP possible to still maintain oxygenation. Head elevation, avoiding tight
endotracheal ties around the neck, and maintaining normocapnia are all important
measures to monitor when ventilating a patient with head and lung injury [13].
Hypoxia, hypercarbia, and hypocarbia should be avoided in patients with a brain
injury. Oxygenation should be monitored with a continuous pulse oximeter (goal
>90%) and the PaO2 should be >60 mmHg. Hyperventilation can result in cerebral
vasoconstriction and brain ischemia. Prolonged hyperventilation is not recom-
mended and should be avoided in the first 24 hours after injury. Hyperventilation
should only be used as a temporizing measure [11].

4.2 Prolonged mechanical ventilation in the head injury patient

Prolonged mechanical ventilation in the patient with a traumatic brain injury

presents a unique set of goals, first, to avoid further increased ICP and to optimize
cerebral blood flow (CBF). Maintaining adequate oxygenation is critical to ensuring
adequate cerebral perfusion pressure (CPP). Another goal is to reduce the risk of
ARDS. In a multicenter study of ventilated patients with severe brain injury, higher
tidal volumes were associated with increased risk of ALI. Lower PaO2/FiO2 ratio
and higher respiratory rate were also independent predictors of ALI in the same
study [14]. Low tidal volumes and permissive hypercapnia are recommended. One
systemic review of intubated patients showed a tidal volume range of 6–8 ml/kg
may reduce the risk of ARDS [15].
When ARDS develops along with TBI, management can be more difficult. ARDS
NET strategies to improve ventilation can conflict with the goal of maintaining CPP.

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DOI: http://dx.doi.org/10.5772/intechopen.101578

Increasing PEEP up to 15 cm H2O has a clinically insignificant effect on CPP; how-

ever, permissive hypoxia can lead to increased cerebral blood flow and increased
CPP. ICP monitoring is suggested to monitor the effects of MV on CPP [12].

4.3 High-frequency percussive ventilation (HFPV) in head injury

Some studies show good results with HFPV in trauma patients with or without
head injury. Using HFPV has resulted in improved oxygenation and reduced ICP [13].

5. Orthopedic trauma

Trauma management of a multiply-injured patient will require stabilization of

pelvic and long bone fractures in as timely a manner that is safely possible. Research
has shown that early stabilization of these fractures can reduce pain and improve
patient outcomes. This includes a decrease in length of hospital stay and a reduction
in pulmonary complications [16].
Patients with pre-existing pulmonary disease are at an even greater risk for sig-
nificant pulmonary complications after a polytrauma. A chest X-ray or computed
tomography (CT) scan is recommended on arrival to determine a baseline [16].

5.1 Fat embolism

Fat embolism syndrome (FES) is a result of the micro-embolism of fat and

bone marrow from a patient’s long bones [16]. Intraoperative transesophageal
echocardiography performed on patients undergoing a long bone repair shows that
most have some microembolization of fat and marrow [17]. This embolization can
result in a varying degree of symptoms, including a significant acute inflamma-
tory response [16, 17]. Most patients will not have a clinical impact. About 3–10%
of patients will have clinically significant symptoms. The symptoms are usually
progressive and develop over 12–72 hours. The most significant symptoms result in
acute respiratory arrest and cardiac arrest [16].
The patient can present with hypoxia, tachycardia, mental status change, and a
petechial rash. The rash is usually present on the upper body, including the conjunc-
tiva, oral mucosa, neck, axilla, chest, and arms. Elevated pulmonary artery pressure
and decreased cardiac output are seen with direct monitoring. When these symp-
toms arise, there are tests that can help confirm the diagnosis. These include testing
for fat globules in the blood and urine, anemia, thrombocytopenia, and elevated
ESR. A chest X-ray will often show bilateral alveolar infiltrates [16, 17].
The treatment for FES is supportive. The treatment for hypoxia requires early
recognition and supplemental oxygenation, and may require ventilation manage-
ment. Patients often require oxygen and PEEP. They may need long-term mechani-
cal ventilation [16].

6. Burn injury

6.1 Smoke inhalational injury

Smoke inhalation is associated with increased mortality in a burn patient.

Inhalational injury can be caused by the superheated air or the toxic compounds
found in the smoke. These toxic compounds can include ammonia, sulfur, chlorine,
and nitrogen dioxide [18].

7
Mechanical Ventilation

There should be an increased suspicion of inhalational injury in any burn patient

that presents with singed facial hair, carbonaceous deposits in the oropharynx, and
blood carboxyhemoglobin levels greater than 10%. The chemical components of
smoke can cause a significant inflammatory response that can lead to bronchospasm
and impaired ciliary function. Lung necrosis and edema can lead to airway obstruc-
tion and atelectasis [19].
Signs and symptoms of inhalational injury include increased respiratory rate,
increased secretions, stridor, dyspnea, use of accessory muscles, and facial burns.
The first phase of inhalational injury includes asphyxia and acute toxicity. The
second phase of inhalational injury begins at 24–96 hours after the injury and is
the result of cellular level damage to the lungs. The treatment of inhalational injury
includes ventilatory support, early pulmonary toilet, and nebulization therapy [18].

6.2 Carbon monoxide toxicity

Carbon monoxide is a byproduct of combustion. It is the cause of 80% of deaths

associated with smoke inhalation from its ability to saturate hemoglobin at very low
partial pressures. Burn patients with carbon monoxide toxicity may present with a
normal pulse oximeter reading. It is important to always check arterial concentra-
tions of oxy- and carboxy-hemoglobin. The treatment of carbon monoxide poison-
ing is oxygen therapy (Table 4) [18, 19].

6.3 Airway injury

Upper airway injury is often due to thermal heat injury. This leads to swelling
and upper airway obstruction due to edema of the oropharynx (Table 5) [18].

Carbon monoxide saturation % Symptoms

<15% Rare symptoms

15–20% Headache
Nausea
Confusion
Tinnitus

20–40% Neurological symptoms

Disorientation
Nausea
Fatigue

40–60% Cardiac dysrhythmias

Brain injury
Hallucinations
Combativeness

>60% Death

Table 4.
Carbon monoxide toxicity symptoms [18, 19].

Classic symptoms of impending airway obstruction: • Stridor

• Hoarseness
• Dysphagia

Table 5.
Classic symptoms of impending airway obstruction in the burn patient [19].

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Mechanical Ventilation in the Trauma Patient
DOI: http://dx.doi.org/10.5772/intechopen.101578

Indications for immediate • Respiratory distress and impending airway compromise (increased
tracheal intubation: respiratory rate, increased secretions, stridor, dyspnea, and progressive
hoarseness.)
• TBSA burn >60%
• Evidence of inhalational injury
• Cardiovascular instability
• Central nervous system depression

Table 6.
Indications for immediate tracheal intubation in the burn patient [18, 19].

6.4 Ventilator strategies in the burn patient

Patients with a large percentage of burn, burns to the head and neck, and inha-
lational injury will have an increased likelihood of need for mechanical ventilation.
The large fluid load required to treat a burn can result in fluid overload to the lungs.
Early bronchoscopy after intubation can help with the removal of secretions and
burn-related debris and can help to reduce the length of time required for mechani-
cal ventilation [10].
Non-invasive ventilation can be used for awake patients with minimal facial
trauma that are stable hemodynamically. This can be started early upon arrival to
the hospital (Table 6) [10].
Invasive mechanical ventilation can be lung-protective at low tidal volumes.
Airway pressure release ventilation (APRV), high-frequency percussive ventilation
(HFPV), and high-frequency oscillatory ventilation (HFOV) have been studied and
shown useful in burn patients and to improve morbidity and mortality in com-
parison to VCV. These provide better oxygenation at lower FiO2 than conventional
ventilation with minimal effects on hemodynamics. APRV can be used to improve
lung recruitment and oxygenation. There is no marked improvement in mortality,
but it has been shown to stabilize alveoli, reduce edema of the alveoli, and helps to
prevent the development of ARDS [10, 13].

6.5 Extubation of the burn patient

Extubation of a burn patient should be based on the patient hemodynamics,

fluid resuscitation, inhalational lung injury, and existing airway abnormalities.
Burn patients often receive large volumes of fluid resuscitation, which can result in
airway edema. Burn patients also require large amounts of opioids for pain control.
This results in burn patients often requiring prolonged intubation and ventilation.
The criteria for extubation should be similar to those of non-burn patients: resolu-
tion of intoxications, ability to follow commands, pain-controlled, gag reflex,
and appropriate cough. Burn patients need to be able to protect their airway from
aspiration. An early tracheostomy should be considered for patients with long-term
respiratory failure. While early tracheostomy has the benefits of improved commu-
nication, oral and tracheal hygiene, and improved patient comfort, it has not been
associated with improved outcome [18, 19].

7. Extracorporeal membrane oxygenation (ECMO) in the trauma patient

Polytrauma is the leading cause of death among adults. This is often second-
ary to hemorrhagic shock, hypoxia, acute respiratory distress syndrome (ARDS),

9
Mechanical Ventilation

hypothermia, coagulopathy, and brain injury. The lung is often the first organ
to fail in a severe trauma. ECMO has been used for nearly two decades, and its
use has been gradually expanded to treat severe trauma patients, but the indica-
tions are uncertain and clinical outcomes are variable. The mortality of a severe
trauma patient on ECMO is still high. There is much research needed on the proper
initiation time for ECMO in the trauma patient and which patients will have
the most benefit from ECMO. The safety and efficacy of ECMO still needs to be
studied [20].

7.1 What is ECMO?

ECMO is a simplified version of the heart-lung machine used in open heart

surgery. It is a method of gas exchange outside the body, so the lungs are exposed
to minimal volume, pressure, rate, Fio2, and they potentially have some time to
recover [10]. ECMO can provide adequate tissue oxygenation, help in rewarming,
and infuse large amounts of blood products quickly [20].

7.2 Complications of the trauma patient on ECMO

Complications associated with a trauma patient on ECMO include bleeding and

thrombotic complications. Patients also presented with abdominal compartment
syndrome, lung and brain edema, and pancreatitis [20].

8. Conclusion

As cases of severe trauma continue to increase, more and more trauma patients
will be arriving in the operating rooms and intensive care units. It is important to
understand how the mechanism of injury in a trauma affects the goals and types of
mechanical ventilation required. The understanding of these individual cases will
lead to improved patient outcomes.

Conflict of interest

The authors declare no conflict of interest.

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Mechanical Ventilation in the Trauma Patient
DOI: http://dx.doi.org/10.5772/intechopen.101578

Author details

Jessica Lovich-Sapola*, Jonathan A. Alter and Maureen Harders

MetroHealth Medical Center, Cleveland, Ohio, USA

*Address all correspondence to: [email protected]

© 2021 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms
of the Creative Commons Attribution License (http://creativecommons.org/licenses/
by/3.0), which permits unrestricted use, distribution, and reproduction in any medium,
provided the original work is properly cited.

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Mechanical Ventilation

References

[1] Dudaryk R, Weyers EW, McCunn M. [8] Rico FR, Cheng JD, Gestring ML,
Mechanical Ventilation of the patient et al. Mechanical ventilation strategies
following traumatic injury. In: in massive chest trauma. Critical Care
Smith CE, editor. Trauma Anesthesia. Clinics. 2007;23:299-315
2nd ed. Cambridge: Cambridge
University Press; 2015. pp. 340-351 [9] Kaslow O. Anesthetic considerations
for abdominal surgery. In: Varon A,
[2] Brasel KJ, Moore EE, Albrecht RA, Smith C, editors. Essentials of Trauma
et al. Western trauma association critical Anesthesia. 2nd ed. Cambridge:
decisions in trauma: Management if rib Cambridge University Press; 2018.
fractures. Journal of Trauma and Acute pp. 232-245
Care Surgery. 2017 Jan;82(1):200-203.
DOI: 10.1097/TA.0000000000001301 [10] Arora S, Singh P, Trikha A.
Ventilatory Strategies in Trauma
[3] Edgecombe L, Sigmon DF, Patients. Journal of Emergencies,
Galuska MA, et al. Thoracic trauma. In: Trauma, and Shock. 2014;7(10):25-31.
StatPearls [Internet]. Treasure Island DOI: 10.4103/0974-2700.125635
(FL): StatPearls Publishing. Last
revision Jan 2021. Available from: [11] Luk KHK, Dagal A. Anesthetic
https://www.ncbi.nlm.nih.gov/books/ considerations for adult traumatic brian
NBK534843/ injury. In: Varon A, Smith C, editors.
Essentials of Trauma Anesthesia. 2nd
[4] Weiser TG. Overview of thoracic ed. Cambridge: Cambridge University
trauma. In: Merck Manual Professional Press; 2018. pp. 173-186
Version. [Internet]. Last full revision
May 2020. Available from: https://www. [12] Koutsoukou A, Katsiari M,
merckmanuals.com/professional/ Orfanos SE, et al. Respiratory
injuries-poisoning/thoracic-trauma/ mechanics in brain injury: A review.
overview-of-thoracic-trauma World Journal of Critical Care Medicine.
2016;5(1):65-73. DOI: 10.5492/wjccm.
[5] Chiumello D, Coppola S, Froio S, v5.i1.65
et al. Noninvasive ventilation in chest
trauma: Systematic review and meta- [13] Mohta M. What’s new in
analysis. Intensive Care Medicine. emergencies, trauma, and shock?
2013;70:1171-1180. DOI: 10.1007/ Mechanical ventilation in trauma
s00134-013-2901-4 patients: A tight-rope walk! Journal of
Emergencies, Trauma, and Shock.
[6] Richter T, Ragaller M. Ventilation in 2014;7(1):1-2. DOI: 10.4103/0974-2700.
chest trauma. Journal of Emergencies, 125630
Trauma, and Shock. 2012;4(2):251-259.
DOI: 10.4103/0974-2700.82215 [14] Mascia L, Zavala E, Bosma K, et al.
High tidal volume is associated with the
[7] Prunet B, Bourenne J, David J-S, development of acute lung injury after
et al. Patters of invasive mechanical severe brain injury: an international
ventilation in patients with severe blunt observational study. Critical Care
chest trauma and lung contusion: A Medicine. 2007;35:1815-1820. DOI:
French multicentric evaluation of 10.1097/01.ccm.0000275269.77467.df
practices. Journal of Intensive Care
Society. 2019;20(1):46-52. DOI: [15] Fuller BM, Mohr NM, Drewry AM,
10.1177/1751143718767060 et al. Lower tidal volume at initiation of

12
Mechanical Ventilation in the Trauma Patient
DOI: http://dx.doi.org/10.5772/intechopen.101578

mechanical ventilation may reduce

progression to acute respiratory distress
syndrome: A systemic review. Critical
Care. 2013;17(1):R11. DOI:
10.1186/cc11936

[16] Lovich-Sapola JA, Smith CE.

Anesthesia for Orthopedic Trauma. In:
Al-Aubaidi Z, editor. Orthopedic
Surgery. Rijeka: InTech; 2012.
pp. 185-220

[17] Lovich-Sapola JA, Smith CE.

Anesthetic considerations for
musculoskeletal trauma. In: Varon A,
Smith C, editors. Essentials of Trauma
Anesthesia. 2nd ed. Cambridge:
Cambridge University Press; 2018.
pp. 246-260

[18] Lovich-Sapola J. Anesthesia for

burns. In: Smith CE, editor. Trauma
Anesthesia. 2nd ed. Cambridge:
Cambridge University Press; 2015.
pp. 666-688

[19] Olivar H, Sharar S. Anesthetic

management of the burn patient. In:
Varon A, Smith C, editors. Essentials of
Trauma Anesthesia. 2nd ed. Cambridge:
Cambridge University Press; 2018.
pp. 261-274

[20] Wang C, Zhang L, Qin T, et al.

Extracorporeal membrane oxygenation
in the trauma patients: A systematic
review. Journal of Emergency Medicine.
2020;15:51. DOI: 10.1186/
s13017-020-00331-2

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