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12 Intensive Care: Principles andTherapy
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sive routine use of inferior vena cava lters in trauma patients
who cannot initially be anticoagulated, there is actually no
data to support this practice, and therefore, this intervention
cannot be recommended at this time. Use of IVC lters may
be considered, however, in patients with pelvic fractures and
moderate-to-severe traumatic brain injuries.
There remains confusion regarding the need for prophylaxis against stress ulceration in intensive care unit patients.
Absolute indications for prophylaxis include intubated patients
for ≥48 h, coagulopathy, active upper GI hemorrhage, or
known gastritis. The following are relative indications: current
steroid use, traumatic brain injury, major burn injury, polytrauma, or sepsis. H2-antagonists are typically used for stress
ulcer prophylaxis, and proton-pump inhibitors (PPIs) are
reserved for those patients who were being previously treated
with these medications, have active upper GI bleeding, and
develop thrombocytopenia after introduction of H2-antagonists
or those who have interactions with another medications. PPIs
have been shown to increase ventilator- associated pneumonia
as well as the development of Clostridium difcile in the ICU;
therefore, they should be avoided as rst-line therapy.
12.12 Multiple Organ Failure
This syndrome is a devastating consequence of our improved
ICU technology and ability to keep patients alive longer. It
remains one of the most challenging conditions to treat for
intensivists, even as its incidence has decreased over the last
decade. This syndrome is characterized by sequential progressive organ dysfunction involving the lungs, kidneys,
liver, gastrointestinal tract, and coagulation cascade.
Mortality has been reported to be as high as 80%, but more
recent studies have suggested mortality rates of 30–50%.
Prevention is the key to this syndrome as there are no treatment modalities to specically reverse this syndrome. If this
syndrome develops, the best management is to support the
patient and attempt to optimize as many organ systems as
possible. To date, there are no effective pharmacological
agents for therapy and the focus remains on early and adequate resuscitation (with much recent research focusing on
more aggressive use of blood and blood products in the early
phases) as well as avoiding secondary insults. Patients with
higher physiologic reserve are more likely to pull through
and heal during the aggressive support provided in the ICU.
12.13 Complications ofICU Care
With the multitude of invasive devices, drains, and catheters, one must be continuously vigilant to prevent them from
becoming dislodged or pulled out. It is important to ensure
that they are adequately secured after insertion with sutures,
the liberal use of adhesive tape or securing devices. Simple
measures such as a note at the head of the bed will communicate to all members of the team looking after the patient
which tubes are vital and/or tenuous.
Self-extubation is usually a consequence of inadequate
sedation. The reported incidence has decreased over the past
decade and ranges from 0.7% to 15.9% with few consistent
predictive risk factors. Although the ICU length of stay is
longer in these patients, this does not seem to come with
increased mortality directly related to the extubation itself.
Self-extubations often occur during nursing care hand- offs
and special attention should be paid during this time. The
incidence of re-intubation for these patients has also
improved over the past decade and is currently 21%, an
improvement from the previously quoted rate of 50%, within
the ensuing 48 hours. Any patient who has self-extubated
should be watched carefully in the ICU for signs of respiratory distress and the necessity for re-intubation.
12.14 Ethical andFamily Issues
One of the hardest aspects of dealing with the critically ill
patient is interfacing with the family. This interaction can
vary from being conducted entirely long distance by telephone with relatives to trying to control an excessive number
of visitors to the patient’s bedside, all of whom are emotional
and some of whom may not be on good terms with the
patient. One of the most important roles of the intensive care
physician is to help the family negotiate this difcult time by
providing timely information, support, and enough time to
visit with their family member.
Futility of care is often a source of conict between the
family and the clinician when there is a difference of opinion
regarding the possibility of a successful outcome. Although
this needs to be approached in a sensitive manner, it usually
requires time on the part of a family to adjust to the reality of
the situation. It is recommended that an ethics committee
consult be obtained in these difcult situations, especially
when rational decision making has been completely overrun
with emotion. Rarely, a legal approach may be necessary in
the case of intransigent or belligerent families where consensus simply cannot be reached.
The clinician needs to remain acutely aware of sudden complications, which can occur at any time in critically ill
patients. Two iatrogenic complications, in particular, tube/
catheter dislodgements and self-extubation, can result in
serious consequences.
12.15 Conclusions
Intensive care has become increasingly complex and
technology- driven such that it has become a multidisciplinary
specialty in its own right. While most surgeons enjoy the
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Z. M. Bauman and T. O’Keee
challenge of managing their own patients through the period
of their critical illness, it has been demonstrated in the literature that a dedicated critical care service is necessary to provide the minute-to-minute care that these patients require. A
thorough and up-to-date knowledge of the medical literature
is also vital, and as you have probably realized, this chapter
only briey discusses some of the important principles a clinician should be aware of when managing trauma patients in
the ICU.Remember these are some of the sickest patients in
the hospital, and the most demanding of our attention, but the
rewards are immense whether it is saving a life or helping a
family come to terms with the death of their loved one.
Important Points
• Noninvasive monitoring is increasing in popularity, especially the use of POCUS.
• Avoid benzodiazepines and work with patients to prevent
ICU delirium.
• Gunshot wounds to the head should be aggressively
resuscitated with blood products and hypertonic saline
and coagulopathy should rapidly be corrected to improve
survival.
• If a gunshot wound to the head is deemed fatal, the “T4
protocol” should be initiated to increase chances for organ
procurement.
• Low tidal volume ventilation and proning are used for the
treatment of ARDS.
• Prevention is the most important management strategy for
ARDS.
• ECMO can provide additional recovery from ARDS, but
patient selection is key given the various complications
from ECMO itself.
• Daily spontaneous breathing trials are necessary for extubation assessment and delirium prevention.
• Enteral feeding should be started as soon as possible.
• Hypertonic saline should be reserved for patients with
traumatic brain injury.
• Aim for a target glucose of less than 180mg/dL.
• Surgical control of bleeding is the most important management for hemorrhaging trauma patients.
• Blood product transfusions should be given in a ratio of
1:1:1 (platelets to plasma to pack red blood cells), and the
use of whole blood for resuscitation is safe and as effective as component resuscitation.
• Additional agents such as factor VIIa, cryoprecipitate,
prothrombin complex concentrates, and tranexamic acid
should be considered with continued hemorrhage.
• It is important to familiarize yourself with the various
anticoagulation reversal agents your institution has on
formulary to quickly utilize them when needed.
• The use of TEG or ROTEM can be very benecial in
guiding resuscitation efforts related to hemorrhage and
should be utilized when available.
• Central lines and Foley catheter should be removed as
quickly as possible.
• Patients should be extubated as soon as possible when
deemed appropriate.
• Treating the family is an important part of ICU care.
Suggested Reading
American College of Chest Physicians/Society of Critical Care
Medicine. Consensus conference: denitions for sepsis and organ
failure and guidelines for the use of innovative therapies in sepsis.
Crit Care Med. 1992;20:864–74.
ARDS Denition Task Force, Ranieri VM, Rubenfeld GD, Thompson
BT, etal. Acute respiratory distress syndrome: the Berlin Denition.
JAMA. 2012;307(23):2526–33.
Barr J, Pandharipande PP. The pain, agitation, and delirium care bun-
dle: synergistic benets of implementing the 2013 pain, agitation,
and delirium guidelines in an integrated and interdisciplinary fashion. Crit Care Med. 2013;41:S99–S115.
Bauer M, Gerlach H, Vogelmann T, etal. Mortality in sepsis and septic
shock in Europe, North America and Australia between 2009 and
2019 – results from a systematic review and meta-analysis. Crit
Care. 2020;24:239.
Bohan PMK, McCarthy PM, Wall ME, etal. Safety and efcacy of low-
titer O whole blood resuscitation in a civilian level 1 trauma center.
J Trauma Acute Care Surg. 2021;91:S162–8.
Cemaj S, Visenio MR, Sheppard OO, et al. Ultrasound and other
advanced hemodynamic monitoring techniques in the intensive care
unit. Surg Clin N Am. 2022;102:37–52.
Ciesla DJ, Moore EE, Johnson JL, Burch JM, Cothren CC, Sauaia A.A
12-year prospective study of postinjury multiple organ failure: has
anything changed? Arch Surg. 2005;140:432–8; discussion 8–40
Ciesla MFDJ, Moore EE. Multiple organ failure. In: Feliciano M,
Moore EE, editors. Trauma. 6th ed. NewYork: McGraw Hill; 2008.
p.1359–80.
Cohn SM, Nathens AB, Moore FA, etal. Tissue oxygen saturation pre-
dicts the development of organ dysfunction during traumatic shock
resuscitation. J Trauma. 2007;62:44–54; discussion 5
Dezfulian C, Shojania K, Collard HR, Kim HM, Matthay MA, Saint
S.Subglottic secretion drainage for preventing ventilator-associated
pneumonia: a meta-analysis. Am J Med. 2005;118:11–8.
Evans L, Rhodes A, Alhazzani W, et al. Surviving sepsis campaign:
international guidelines for management of sepsis and septic shock
2021. Intensive Care Med. 2021;47:1181–247.
Finfer S, Chittock DR, Su SY, etal. Intensive versus conventional glucose
control in critically ill patients. N Engl J Med. 2009;360:1283–97.
Guérin C, Reignier J, Richard JC, et al. Prone positioning in
severe acute respiratory distress syndrome. N Engl J Med.
2013;368(23):2159–68.
Holcomb JB, Tilley BC, Baraniuk S, etal. Transfusion of plasma, plate-
lets, and red blood cells in a 1:1:1 vs. a 1:1:2 ration and mortality in
patients with severe trauma: the PROPPR randomized clinical trial.
JAMA. 2015;313(5):471–82.
Huang DD, Fischer PE.Management of delirium in the intensive care
unit. Surg Clin N Am. 2022;102:139–48.
Ince C.Hemodynamic coherence and the rationale for monitoring the
microcirculation. Crit Care. 2015;19(suppl 3):S8.
Joseph B, Aziz H, Moutamn S, etal. Fatal gunshot wound to the head:
the impact of aggressive management. Am J Surg. 2014;207:
89–94.
Joseph B, Aziz H, Pandit V, et al. Improving survival rates after civil-
ian gunshot wounds to the brain. J Am Coll Surg. 2014;218:
58–65.
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Kollef MH, Afessa B, Anzueto A, et al. Silver-coated endotra-
cheal tubes and incidence of ventilator-associated pneumonia: the NASCENT randomized trial. JAMA. 2008;300:
805–13.
Lee JH, Lee HC, Jeon YT, etal. Clinical outcomes after unplanned
Extubation in a surgical intensive care population. World J Surg.
2014;38:203–10.
Martin M, Salim A, Murray J, Demetriades D, Belzberg H, Rhee P.The
decreasing incidence and mortality of acute respiratory distress
syndrome after injury: a 5-year observational study. J Trauma.
2005;59:1107–13.
Pinsky M, Teboul JL, Vincent JL. Hemodynamic monitoring.
NewYork: Springer; 2019.
Pronovost P, Needham D, Berenholtz S, et al. An intervention to
decrease catheter-related bloodstream infections in the ICU.N Engl
J Med. 2006;355:2725–32.
Roy S, Sadowitz B, Andews P, etal. Early stabilizing alveolar ventila-
tion prevents acute respiratory distress syndrome: a novel timing-
based ventilatory intervention to avert lung injury. J Trauma Acute
Care Surg. 2006;73(2):391–400.
Troianos CA, Hartman GS, Glas KE, et al. Councils on intraopera-
tive echocardiography and vascular ultrasound of the American
Society of Echocardiography. Guidelines for performing ultrasound
guided vascular cannulation: recommendations of the American
Society of Echocardiography and the Society of Cardiovascular
Anesthesiologists. J Am Soc Echocardiogr. 2011;24:1291–318.
Wang JW, Li JP, Song YI, etal. Hypertonic saline in the traumatic hypo-
volemic shock: meta-analysis. Jour Surg Res. 2014;191:448–54.
Whiting D, DiNardo JA.TEG and ROTEM: technology and clinical
applications. Am J Hematol. 2014;89:228–32.
Wrisinger WC, Thompson SL. Basics of extracorporeal membrane
oxygenation. Surg Clin N Am. 2022;102:23–35.
Zieleskiewicz L, Muller L, Lakhal K, etal. Point-of-care ultrasound
in intensive care units: assessment of 1073 procedures in a multicentric, prospective, observational study. Intensive Care Med.
2015;41:1638–47.
Ventilation intheTrauma Patient:
DO
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APractical Approach
GuyA.Richards, TimothyC.Hardcastle,
andRichardE.Hodgson
13
13.1 Introduction
This chapter will provide the trauma surgeon with the basic
guidelines for the provision of appropriate airway management and ventilatory support of the patient being treated for
major trauma with a brief focus on penetrating trauma. The
chapter will be divided into the following sections: background, physiology and theory, emergency airway management, early ventilation strategies in the emergency department
(ED) and intensive care unit (ICU) airway management, and
ventilatory strategies. The chapter will conclude with brief
comments regarding liberation from the mechanical
ventilator.
13.2 Background Physiology andTheory
13.2.1 Whom toVentilate
There are three main indications for ventilation:
1. Hypoxemia from lung pathology resulting from ventilation/perfusion mismatch (V/Q) also called shunt, due to
alveolar collapse or lling of alveoli with uid (exudate,
transudate, or blood)
2. Ventilatory insufciency due to neuromuscular dysfunction resulting in diminished alveolar ventilation (alveolar
hypoventilation) resulting in an increased partial pressure
of carbon dioxide (PaCO2)
3. Airway compromise from direct or indirect airway injury
or neuromuscular dysfunction that impairs airway protection and places the patient at risk of aspiration
Any combination of conditions may coexist and will
inform the decision to provide mechanical ventilation (MV)
after endotracheal intubation.
Prior to a discussion of practical ventilation, an understanding of the terminology used is essential.
13.2.1.1 Hypoxia
The arterial oxygen content (CaO2=16−20mL/blood) consists of hemoglobin (Hb)×1.34mL oxygen×saturation plus
that dissolved in plasma (0.003mL×PaO2). Any reduction
in delivery (DO2) is termed tissue hypoxia and is represented
by the formula cardiac index (CI)×content:
Hypoxia may be caused by any of the components of
delivery as seen below, many of which are frequently encountered in trauma patients:
CI CaO
G. A. Richards (*)
Division of Critical Care, Faculty of Health Sciences, University of
the Witwatersrand, Johannesburg, South Africa
e-mail: Guy.richards@wits.ac.za
T. C. Hardcastle
Trauma, Burns and Trauma Intensive Care Unit, Inkosi Albert
Luthuli Central Hospital, Nelson R Mandela School of Clinical
Medicine, Durban, KZN, South Africa
e-mail: Hardcastle@ukzn.ac.za
R. E. Hodgson
Department of Anaesthesia, Inkosi Albert Luthuli Central Hospital,
Nelson R Mandela School of Clinical Medicine,
Durban, KZN, South Africa
e-mail: eric_hodgson@mweb.co.za
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023
E. Degiannis et al. (eds.), Penetrating Trauma, https://doi.org/10.1007/978-3-031-47006-6_13
(a) Hypoxic hypoxia (sometimes called hypoxemia)— PaO2
low (see causes below)
(b) Anemic hypoxia—low carrying capacity (anemia, car-
boxyhemoglobin, methemoglobinemia)
(c) Circulatory hypoxia—low cardiac output (myocardial
contusion, myocardial infarct, cardiac tamponade, tension pneumothorax)
(d) Histocytotoxic hypoxia—low utilization (mitochondrial
dysfunction, propofol-related infusion syndrome (PRIS),
aspirin, antiretrovirals, severe sepsis)
The latter three present primarily with a metabolic acidosis and have a normal or elevated PaO2. All of these situa-
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tions may be seen by the trauma surgeon, and recognition
that inadequate oxygenation is not the only requirement for
intubation is important.
13.2.1.2 Measures ofAdequacy ofOxygenation
Clearly, the partial pressure of oxygen (PaO2) in the arterial
blood alone is of no value as the PaO2 must be related to the
fraction of inspired oxygen (FiO2) and whether or not the
patient is receiving positive pressure ventilation (PPV).
Additionally PaO2 is far less important than saturation. The
most commonly used means of assessment is the PaO2/FiO2
(P/F) ratio where:
• Normal: 400–500
• <300: Mild lung injury/acute respiratory distress syndrome (ARDS)
• <200>100: Moderate lung injury/ARDS
• <100: Severe lung injury/ARDS
This does not take into account the mean airway pressure
(MAP), and as such, the oxygenation index is a useful parameter. This includes both the P/F ratio and the MAP, and a
reduction in the oxygenation index (OI) signies improvement, whereas a value ≥25 indicates severe hypoxemic
respiratory failure:
MAPFiO PaO
22
100/
Another useful bedside calculation which gives an indica-
tion of the degree of shunt can be achieved simply in the
following manner; the difference between the calculated
alveolar oxygen (PAO2) and the actual PaO2 [P(A−a)O2] is
measured. This would normally be in the range of
10–15 mmHg, but it is also dependent on age [predicted
PaO2=103.5−0.42(age)±4] and the degree of pulmonary
parenchymal disease.
The PAO2 is calculated by means of the Bohr equation:
• PAO2=partial pressure of inspired oxygen (PiO2)−PCO2/
respiratory quotient (usually taken to be 0.8).
• The PiO2 is calculated as follows: atmospheric pressure–
47 (for warm moist air)×FiO2.
• At sea level if one presumes the pCO2 is 35mmHg, this
equation would read [(760−47)×0.21]−35/0.8 giving
a value of 106mmHg.
A further emerging index is the ROX score which is cal-
culated as the (saturation/FiO2)/PaO2 and the trend may be
useful when assessment of the need for invasive ventilation
in trauma patients.
13.2.1.3 The Causes ofHypoxic Hypoxia
(Hypoxemia) Are asFollows
• Shunt—alveoli that are perfused but not ventilated due to:
– Alveolar collapse—lung that may be recruited by
application of positive airway pressure
– Alveolar lling—lung that is not recruitable by appli-
cation of positive pressure but requires resolution of
the underlying condition due to:
Inammatory exudate: aspiration and pneumonia
Transudate: increased ltration across the alveolar
endothelium due to raised pulmonary capillary
pressure as seen in cardiac failure
Blood: due to pulmonary contusion
• Partial pressure of inspired oxygen (PiO2) seen in where
an individual has been trapped in a conned space and
in locations at altitude including Johannesburg, Quito,
and Kathmandu
• Alveolar hypoventilation [overdose of drugs or alcohol,
head injury, respiratory center control, airway obstruction, weakness (cord transection, pain, splinting), metabolic alkalosis/vomiting]
Less common causes of hypoxia that should be considered, if the causes above have been treated, include the
following:
• Alveolar diffusion defect.
• Anatomical/cardiac shunt.
• Reduced cardiac output (CO) in the presence of V/Q mis-
match [low CO] decreases central venous saturation
(ScvO2) such that if V/Q mismatch is present, hypoten-
sion causes hypoxemia.
13.2.2 PaCO
2
The PaCO2 represents a balance between production through
metabolism and excretion through alveolar ventilation.
13.2.2.1 Production: VCO
2
• Increased (catecholamine inotropes, shivering, high car-
bohydrate diet)
• Decreased (paralysis/sedation)
13.2.2.2 Alveolar Ventilation
• Alveolar ventilation is reduced by neuromuscular disor-
ders that include the following:
– Drug or alcohol overdose
– High spinal cord injury or any other causes of
paralysis
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– Acute severe metabolic alkalosis such as prolonged
vomiting due to anatomical or functional gastric outlet
obstruction
• Increased physiological dead space: alveoli that are ventilated but not perfused: ventilation/dead space ratio
(VD/VT):
– Preexisting chronic obstructive pulmonary disease,
especially emphysema
– Severe asthma
– Iatrogenic due to the use of excessive positive pressure
in an attempt to reduce shunt by alveolar recruitment
which results in overdistension of ventilated alveoli
increasing physiological dead space and reducing
effective alveolar ventilation
It is important to note however that an elevated pCO2
alone is not an absolute indication for ventilation provided
that:
• There is no acidosis indicating that the patient may be tir-
ing and that the minute ventilation is insufcient relative
to demand.
• There is no evidence of CO2 narcosis.
• There is no traumatic brain injury (TBI) where hypercap-
nia is undesirable.
13.2.3 Ventilator-Induced Lung Injury
Reduction of lung injury means that alveolar distension on
inspiration and atelectasis on expiration should be avoided.
This essentially means that one should restrict the tidal volume (TV) to 6mL/kg ideal body weight (IBW) and utilize a
positive end-expiratory pressure (PEEP) designed to avoid
expiratory atelectasis. Reduction of the “driving pressure” is
critical. This is the difference between the PEEP and the plateau (volume modes) or peak (pressure modes) pressures. If
this can be restricted to <16 or even lower, lung injury can be
minimized.
The IBW can be simply estimated by utilizing the last two
gures of the height in centimeters, e.g., if the height is
1.55m, the IBW is in the region of 55kg. One can add on
10% for males as this really does not add much to the delivered volumes.
13.2.4 Recruitment andRecruitment
Maneuvers
In acute lung injury (ALI) of any type, three lung zones
potentially exist; these are as follows:
1. Ventilated alveoli with reduced perfusion increasing
physiological dead space that are commonly found in
nondependent zones of the lung.
2. Lungs that are ventilated and perfused—this zone is commonly reduced in ALI.
3. Lungs that are perfused but not ventilated with associated
physiological shunting and is most commonly found in
the dependent lung regions. This zone is increased due to:
(a) Atelectasis—collapsed alveoli that may be reinated
by application of positive pressure, either in the form
of a recruitment maneuver or PEEP or both.
(b) Alveolar lling—as outlined above, uid in the alve-
oli cannot be displaced by positive airway pressure,
making these alveoli non-recruitable.
The clinical assessment contributes to the likelihood of
recruitability.
ALI or ARDS may be due to primary lung pathology
(pneumonia, aspiration, contusion, drowning) which is less
likely to be recruitable or secondary lung injury where the
alveolar endothelium is disrupted and capillary leak occurs
as a component of a systemic disease process (major trauma,
sepsis, pancreatitis, burns) in which there is disruption of the
endothelial glycocalyx, a 1-mm-thick, noncirculating, intravascular uid layer that maintains the oncotic pressure. The
distribution of alveolar uid is also gravitationally dependent, particularly in secondary ARDS, the so-called sponge
lung.
However, regardless of how meticulous the clinical
assessment, it is impossible to predict how much of the lung
is actually recruitable. Because the amount of lung that is
available for ventilation is reduced in both forms of ARDS
(as represented by zones 1 and 2 above), it can be said (as per
Luciano Gattinoni) that a “baby lung” exists. It is necessary
to apply a positive pressure to improve recruitment, but at the
same time, overdistension of nondependent alveoli should be
avoided as this increases physiologic dead space and results
in ventilator-induced lung injury (VILI). As such a recruitment maneuver is applied early in patients that are hypoxemic with pulmonary inltrates. Recruitment is thereafter
maintained by judicious application of PEEP to prevent
repetitive tidal collapse and recruitment (pulmonary biotrauma). PEEP “splints” alveoli open by increasing the functional residual capacity (FRC) but lacks efcacy in opening
already atelectatic lung.
The main adverse effect of PEEP is to unmask intravascular hypovolemia by impeding venous return. In the early
resuscitative phase, PEEP may need to be limited until normovolemia has been achieved. As there is a balance between
recruitment and overdistension, there is a balance between
oxygenation and hemodynamics. Any reduction in mean air-
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way pressure (MAP) designed to improve perfusion may be
associated with a reduction in oxygenation as derecruitment
occurs. The hemodynamic effects of PEEP can usually be
corrected with uids or pressors and are also less profound
when applied to the relatively noncompliant lung.
If the lung is relatively non-recruitable, tidal volumes
even in the region of 6mL/kg can result in hemodynamic
compromise and elevation of PCO2. It is preferable in this
setting to consider a reduction of PEEP or an increase in
respiratory rate rather than an increase in TV as this causes
overdistension of functional alveoli with an even greater
increase in PCO2 due to the increase in the physiologic dead
space.
Recruitment maneuvers work by the application of a
raised mean airway pressure over a prolonged period, often
in association with restriction of anterior motion of the chest
wall by placing the patient in the prone position. The most
frequently employed method is the application of a positive
pressure of 30–40 cmH2O for at least 30–40 s, and this is
usually employed when the patient has been sedated and
paralyzed and on an FiO2 of 1. Failure to recruit may indicate
that there is no recruitable lung or may require turning the
patient into the prone position, particularly with secondary
ARDS (sponge lung) where the nondependent lung volume
may be substantially increased by anterior redistribution of
alveolar uid. Alternative methods of ventilation such as airway pressure release ventilation (APRV) have been used
with some success as well.
13.2.5 Fluid Overload andAtelectasis
Alveolar derecruitment is minimized by early application of
PEEP and by limiting unnecessary administration of crystalloid, which merely enhances leak across the damaged alveolar endothelium even in the absence of increased hydrostatic
pressures, thereby worsening the ARDS and increasing mortality. A patient that is edematous (sacral edema) is by denition uid overloaded, and in addition to avoidance of
crystalloid, gentle diuresis should be considered, or if in
renal failure, renal replacement therapy could be utilized.
Time must be allowed for redistribution of uid from the
extravascular space to the intravascular compartment in
order to prevent hypotension; however in our experience,
hemodynamics actually improve when uid overload is corrected. Fluid boluses in an already edematous patient may
transiently increase the stroke volume but ultimately worsen
pulmonary function and overall outcome. In this setting,
alternative causes for hypotension such as vasodilatation as a
component of the inammatory response, myocardial contusion, intra-abdominal compartment syndrome, and pulmonary embolus should be sought.
13.3 Practical Application ofVentilation
Strategies
13.3.1 Specic Indications forVentilation
• Apnea or severe chest pathology provided treatable causes
(tension pneumothorax or massive hemothorax) are
excluded rst
• Tachypnea (in the adult >30 or<10/min or child RR>40
or <15/min)
• Mechanical ventilatory compromise (such as severe ail
chest and pulmonary contusion)
• Hypoxemia (pO2 < 8 kPa or 60 mmHg on a reservoir
mask (FiO2=0.6) or a saturation that is decreasing)
• Hypercarbia (pCO2>6.5kPa or 50mmHg), especially in
the context of associated TBI or where an associated acidosis indicates ventilatory insufciency
• Mental compromise (Glasgow Coma Score (GCS)<9/15)
• Hemodynamic instability/cardiac arrest
13.3.2 Initiation ofVentilation
Once it has been decided that the patient should be mechanically ventilated, the following steps should be considered.
13.3.2.1 Airway Management
With blunt trauma it should be assumed that there may be
associated injury to the C-spine and therefore a risk to the
spinal cord, so extreme caution is required. This is less true
for penetrating trauma where airway control must not be
delayed or impeded by the necessity for restriction of spinal
motion.
Assess the airway for:
• Patency and maintenance of patency: does the patient
need a denitive airway emergently?
• Protection: is there an aspiration risk?
• Gas exchange: does the patient need an airway to opti-
mize ventilation? Are there any possible complications in
the near future, i.e., identication of a potentially threatened airway from injuries that might cause swelling?
Prepare for intubation and have alternatives available:
• STOP-IC-BARS is a useful mnemonic:
– S—suction: with Yankauer catheter and soft-suction
catheters.
– T—tubes: expected size and one 0.5mm smaller and
bigger.
– O—oxygen source: ideally nasal prongs and bag mask
to enable apneic passive oxygenation.
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– P—pharmaceuticals for rapid sequence intubation:
either etomidate (0.4mg/kg) used as a sole agent or ketamine 1mg/kg with a muscle relaxant, either succinylcholine (1mg/kg) or rocuronium 1mg/kg. Drugs should
be available for ongoing sedation if relaxants are used,
to avoid the medicolegal hazard of awake paralysis.
– I—intravenous access: at least one functional large-
bore intravenous (IV) line with appropriate uid—a
250mL uid bolus prior to drug-assisted induction is
advised.
– C—conrmatory devices: end-tidal CO2 capnography
or color change devices are acceptable.
– B—bougies (long introducers) reduce intubation fail-
ure and alternative blades for the laryngoscope should
be available: place the patient at the belt height of the
intubator for best view; bimanual laryngoscopy, best-
look ramping of shoulders to ensure there is a horizontal line between the earlobe and sternum.
– A—alternative airway devices: supraglottic airway
(SGA), e.g., intubating laryngeal mask airway (LMA),
video laryngoscope (e.g., GlideScope, C-MAC), and
exible scope, available on a difcult airway trolley.
– R—rescue devices, such as standard LMA or laryngeal-
tracheal tube.
– S—surgical airway equipment: for emergency
cricothyroidotomy.
Once the airway is secured, one must provide ventilatory support—a T-piece alone will lead to progressive atelectasis due to nitrogen washout and
absence of PEEP.Auto-PEEP is normally provided
by the vocal cords which are bypassed by the tube.
Dead space however is actually reduced once one is
intubated.
13.3.3 The Initial Ventilator Settings
Patients frequently decrease their oxygen saturation following intubation. This is related to application of a minute ventilation that is less than that generated by the patient prior to
intubation and by drug-induced hypotension with a decreased
central venous saturation (ScvO2) in the presence of V/Q
mismatch. The operator should be prepared for and respond
to this.
The actual settings on the ventilator are determined by the
pO2, the pCO2, and ability to trigger the ventilator.
Most trauma patients that require ventilation are intubated
and initiated on full mechanical ventilation (MV) as opposed
to noninvasive ventilation (NIV). Continuous positive airway pressure (CPAP) or noninvasive pressure support ventilation (PSV), by face mask or helmet, should be reserved for
patients with mild pathology where support is predicted to be
of short duration. If this modality is utilized and, despite this,
the PCO2 increases or the PaO2 or saturation decreases, MV
should ensue. It is far safer to intubate early than to try to
recover from a sequential failure of face or rebreather mask
and noninvasive ventilation particularly if eventual respiratory arrest occurs. The latter group of patients also have longer ICU stay.
13.3.3.1 Basic Ventilator Settings intheED
FiO
2
If there is no respiratory compromise, initiate at a FiO2 of 0.4
and reduce according to saturation, maintaining the latter at
≥92%. If hypoxemic, initiate at a FiO2 of 0.8 and reduce
according to saturation.
Trigger Setting
This should be set at whatever setting provides the least
effort. Auto-triggering sometimes occurs, but this is more
frequently a consequence of too rapid inspiratory ow rates
rather than the trigger setting.
Mode
The mode of ventilation is less important; pressure or volume modes are acceptable. Assist control modes are used
most frequently due to concerns regarding work of breathing
with those using synchronous intermittent mandatory ventilation (SIMV), plus pressure support ventilation. Differences
in outcome between the two modes have been difcult to
document however. Total thoracic compliance is reected by
the plateau pressure in volume modes and by the peak pressure in pressure modes. Thoracic compliance is determined
by the chest wall, the pulmonary parenchyma, and the intraabdominal pressure. In general the peak or plateau pressure,
depending on mode, should not exceed 30cmH2O; however
in patients with signicant chest wall edema or with an obese
abdomen, this pressure could be exceeded as most of the
compliance is determined by factors other than the pulmonary parenchyma.
Other modes of ventilation that may be utilized include
airway pressure release ventilation (APRV) or bi-level positive airway pressure (BiPAP), but these are for more complex
patients and not appropriate in the early phase of care.
pCO
2
If the pCO2 is elevated and the patient is acidotic, i.e.,
pH<7.35, or if there is a head injury and a slightly lower
pCO2 is required, the pressure control above PEEP or pressure support ventilation (PSV) can be increased if the patient
is breathing spontaneously and is tachypneic, with the proviso that pressure be limited as above, or the respiratory rate
can be increased.
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Tidal Volume
There is evidence that in the early phase (<24h), up to 8mL/
kg TV may be associated with no worse outcomes and better
control of PCO2 and reversal of acidosis than the lungprotective values; however, early application of PEEP generally prevents atelectasis and deterioration of gas exchange,
and as such 6mL/kg with adequate PEEP remains the best
approach.
Rate
In the early phase, particularly if the patient is acidotic, it is
prudent to deliver a rate that would correct hypercarbia. A set
rate of around 12–16/min, adjusted to the desired PCO2 and
utilizing an inspiratory/expiratory (I/E) ratio that avoids
auto-PEEP (failure of airway pressure to return to the baseline by the end of expiration), should be employed. This is
one of the areas of difference from the later ICU phase where
spontaneous modes are encouraged. It is not necessary to
apply a rate if the patient has been intubated for airway control only; such patients determine their own rates on PSV.
PEEP
PEEP should be administered to all patients, even those
without ARDS, to prevent lung injury. Although the ARDSnet
group recommended application of PEEP in proportion to
the degree of hypoxemia, this is seldom possible as PEEP
>12–15cmH2O is frequently accompanied by hypotension
and peak pressures >30 cmH2O. A starting PEEP level of
8–10cmH2O is commonly employed.
13.3.3.2 Sedation andAnalgesia
During the resuscitation phase, analgesia and appropriate
sedation are important to enable the performance of essential
interventions and imaging studies. Infusions are recommended rather than bolus doses. Dexmedetomidine, ketamine (with or without propofol), and opioids are the
mainstay of modern analgo-sedation. Thereafter sedation,
particularly the use of benzodiazepines, should be limited as
they predispose to delirium and have long-term cognitive
side effects. If possible the patient should be awake and ventilated. Paralysis is not routinely advised, except for general
anesthesia.
13.4 Ventilation intheICU Phase
13.4.1 Positioning
If patients have had cervical spinal injuries excluded during
the resuscitation phase, it is essential to place them in a
30–45° head-up position, which improves tolerance for
early enteral feeding and reduces regurgitation, which
might also reduce aspiration and ventilator-associated
pneumonia (VAP). Additionally, avoiding proton pump
inhibitors as stress ulcer prophylaxis, with preferential use
of early enteral feeding with topical mucosal agents, if
required, will further reduce the risks for VAP. Pronepositioning may be used in severe ARDS as a means of
recruitment.
13.4.2 Ventilator Settings
At this juncture if not already at this level, the TV should be
reduced to around 6mL/kg ideal body weight (in the patient
without TBI) and PEEP adjusted to avoid expiratory atelectasis. The PEEP is more difcult to estimate, but a useful rule
of thumb is to administer in an approximate a 1:5 ratio with
the required FiO2, while weaning it down to the minimum
required level as soon as possible. Levels >16 are seldom
required and if too high in a non-recruitable lung may
increase dead space with an increase in pCO2 and cause
hypotension.
Ideally support of the patient’s own respiration is preferred. This implies allowing the patient to generate a spontaneous respiratory effort. A ventilator set rate is only utilized
if the patient is not triggering the ventilator. If the patient is
triggering, then PSV should be utilized with the level
adjusted using the rapid shallow breathing index (RSBI)
which is calculated by dividing the respiratory rate by the
tidal volume in liters:
BI respiratory rate TV liters eg
While the RSBI is usually utilized as a cutoff to determine
success of extubation, it may also be utilized to titrate pressure support as follows:
RSBI PSV
>80 Increase 2–4 cmH2O
60–80 Maintain
<60 Decrease 2–4 cmH2O
/,..,/.20 04 80
Once the non-head-injured patient is in the ICU and acute
reversible pathologies have been addressed (including derecruitment), it is reasonable to use lung-protective ventilation,
as applied in the ARDSnet study again with the proviso that
very high PEEP levels >12–14cmH2O may be associated
with hemodynamic compromise.
13.4.3 Paralysis
If the patient has a P/F ratio of <100 and oxygenation is
marginal, paralysis and sedation are recommended, and a
recruitment maneuver should be attempted. Not all patients
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recruit successfully however, and it may be necessary to
accept lower oxygenation in those with severe lung injury.
Injurious ventilator strategies only transiently improve oxygenation and cause signicant long-term pulmonary compromise. There is also evidence that 48h of paralysis with
cisatracurium in patients with ARDS may improve outcome
primarily due to enhancing synchrony, with the recent
Surviving Sepsis 2021 evidence suggesting intermittent
boluses and not continuous infusion as the optimal strategy.
This not an issue however in those breathing spontaneously
with PSV.
13.4.4 Sedation andAnalgesia
Opioid analgesia not only provides pain relief but promotes
endotracheal tube tolerance by peripheral cough suppression
and central respiratory depression. Hypnotic sedation (with
propofol or benzodiazepines) should be minimized and used
for the shortest period and at the lowest dose possible to
ensure a calm but not comatose patient, with ketamine infusion and ideal alternative. Hypnotic sedation should only be
used for procedural sedation, severe agitation, or when neuromuscular paralysis is utilized, to avoid the medicolegal
hazard of awake paralysis.
Avoiding hypnotic sedation facilitates early mobilization, which is an essential component of the weaning and
recovery process, and reduces subsequent cognitive decit
and post-traumatic stress arising from the ICU experience.
Hypnotic sedation may be required with a P/F ratio<100,
where paralysis is required and for delirium or extreme
agitation (if a cause has been sought and if possible corrected and pain and discomfort have been addressed).
Analgesia is essential and should be titrated to levels of
adequate pain control. Early involvement of the physiotherapist is essential for management of the chest and to
ensure maintenance of general range of the movement.
Removal of chest tubes reduced pain and discomfort and
can be safely performed when no longer draining or bubbling and yet still patent, using an inspiratory hold in place
of a Valsalva maneuver. Rib xation also reduces pain and
aids in weaning, although is seldom needed for penetrating
trauma.
13.5 Rescue Therapies forPersistent
Hypoxemia
13.5.1 Ongoing Ventilation
Ongoing requirements are dictated by such factors as degree
of lung injury, thoracic and pulmonary compliance, neuromuscular weakness, and level of consciousness. It is critically important to avoid further lung injury as described
above, and every attempt should be made to wean the patient
as soon as possible.
13.6 The Head-Injured Patient
Patients with TBI should have the end-tidal CO2 controlled
for approximately 48h (neuroprotective ventilation) to optimize neuronal recovery. On the one hand, hyperventilation
lowers intracranial pressure (ICP) by causing cerebral vasoconstriction, but the latter decreases cerebral ow and intracerebral blood volume, leading to ischemia if prolonged. It is
not recommended that chronic prophylactic hyperventilation
be used, although short term it may be of value
preoperatively.
Similarly controversial has been the use of PEEP.It does
appear however that when PEEP is set at levels lower than
ICP, it does not have a signicant effect on ICP. Given the
potential for patients with severe trauma to develop ARDS, it
is advisable that PEEP be used to prevent derecruitment as
described above.
13.7 Monitoring theVentilated Patient
Patients ventilated for chest trauma, or post major abdominal
trauma, are at risk for pulmonary complications due to alterations in thoracic compliance. Capillary leak reduces chest
wall compliance and when patients are mechanically ventilated has the potential to increase intrathoracic pressures,
which along with increased intra-abdominal pressures reduce
venous return. Venous pressures may be falsely elevated due
to reduced abdominal compliance, pneumothorax, hemothorax, or chest wall injuries. If coupled with intravascular volume depletion, hypotension may ensue. Lung contusion,
particularly in the face of uid overload, further reduces lung
compliance. All of these factors may act in concert to increase
measured ventilator pressures (volume modes), reduce tidal
volume (pressure modes), and reduce oxygenation or carbon
dioxide clearance.
Therefore it is essential to monitor:
Interventions include restrictive uid management, recruitment and paralysis (as discussed above), and alternative ventilatory modes such as airway pressure release ventilation
(APRV) and extra corporeal membrane oxygenation
(ECMO).
• Blood gases
• Ventilator pressures
• Invasive and noninvasive blood pressure and to watch for
pulsus paradoxus on the arterial trace as an early indicator
of hypovolemia
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