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20.
DISRUPTION OFDIFFUSION
INFLAMMATION
Shahzad Shae and AaronMittel
CLINICALCASE
In current practice, a wide variety of medical and surgi-
cal conditions are known to precipitate ARDS. Sepsis is the
You are requested to provide anesthesia for an urgent case:a
68- year- old man who has been intubated in the intensive care
most common of these risk factors. Patients with higher bur-
dens of comorbid illnesses are more likely to developARDS.
4
unit (ICU) for the past 3days with multiorgan failure and
suspected abdominal sepsis. He has required 4 units of packed
red blood cells in the past 4 hours for acute anemia and hypotension. Pulse oximetry shows a saturation of 88% despite an
inspiratory oxygen fraction of 80%. e surgical team would
like to perform an urgent exploratory laparotomy.
Underlying Mechanism
As emphasized by the Berlin criteria, the impairment in gas
exchange caused by ARDS is secondary to nonhydrostatic
pulmonary edema, itself caused by underlying pulmonary
inammation. Triggering factors for ARDS may be pul-
INTRODUCTION
Acute respiratory distress syndrome (ARDS), transfusionrelated acute lung injury ( TRALI), and transfusion- associated
circulatory overload (TACO) share a common theme of lifethreatening hypoxemia secondary to acute pulmonary edema
and oen have similar antecedent events. An understanding
of their pathophysiology and clinical presentation is necessary to deliver eective, appropriate perioperativecare.
monary in origin (“pulmonary ARDS”) or nonpulmonary
in origin (“extrapulmonary ARDS”). Pulmonary ARDS is
derived from a direct insult to the lungs, while extrapulmo-
nary ARDS indirectly leads to lung damage via bloodstream
transmission of inammatory mediators. Regardless of the
origin, injury to the lung precipitates an intense inam-
matory cascade leading to damage of microvascular archi-
tecture and transmembrane water permeability. Alveolar
macrophages respond to lung injury by releasing proinam-
matory cytokines, including tumor necrosis factor alpha and
interleukin (IL)- 1, IL- 6, and IL- 8. ese cytokines attract
PATHOPHYSIOLOGY OFDISEASE STATE— ARDS
e denition of ARDS has been modied slightly since its
original identication in 1967, undergoing dramatic update
in 2012. As specied by this current “Berlin denition,”
ARDS is an acute onset of bilateral pulmonary opacities
and noncardiogenic respiratory failure which impairs oxygenation.1 Specic details of the Berlin criteria are shown in
Figure20.1.
neutrophils, which promote cell death and perpetuate fur-
ther inammation by releasing additional cytokines, reactive
oxygen species, eicosanoids, phospholipids, and granular
enzymes (e.g., neutrophil elastase). Death of type II alveo-
lar epithelial cells leads to a decrease of qualitatively eective
surfactant as well as dysregulation of transpulmonary ion
transport. A characteristic exudative edematous state ensues,
followed swily by alveolar collapse and associated respira-
tory failure, as shown in Figure 20.2.
5
Epidemiology/ Risk
Up to 10% of patients admitted to the ICU meet criteria
for ARDS.2 In- hospital death is estimated to occur in 25%–
65% of cases.
156
3
Assessment ofthe Patient:Presenting Signs
and Symptoms
Physical signs of ARDS begin within 1 week of the initial
insult, as outlined in the Berlin denition, and consist of
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Figure20.1 Berlin criteria for ARDS.
ARDS is bilateral, noncardiac, lung
injury leading to hypoxemia, which
occurs within 1 week of inciting event.
ARDS=acute respiratory distress
syndrome; PaO2=arterial partial
pressure of oxygen; FiO2=inspiratory
fraction of oxygen. SOURCE:ARDS Denition
Task Force, Ranieri VM, Rubenfeld GD, etal.
Acute respiratory distress syndrome:the Berlin
denition. JAMA. 2012;307:2526– 33.
hypoxemia despite corrective measures in the setting of presumed lung injury and radiographic observation of bilateral
inltrates. e dierential diagnosis includes multifocal pneumonia, chronic obstructive pulmonary disease (COPD) exacerbation, cardiogenic pulmonary edema, and many others.
tidal volumes while limiting plateau pressure and applying
progressive amounts of positive end- expiratory pressure
(PEEP) to enhance oxygenation. is approach has been
shown to signicantly reduce morbidity and mortality
from ARDS.6 e precise mechanism for improved clinical outcome with a lung- protective strategy is not under-
Management— Initial TreatmentSteps
If a known ARDS risk factor is present, steps should be
taken to correct the underlying physiologic disturbance
(e.g., broad- spectrum antibiotics, if sepsis is suspected).
Eort should be taken to eliminate alternative sources of
hypoxemic respiratory failure, some of which are described
in the dierential diagnosis list above. To this end, imaging
should be performed to evaluate for presence of bilateral
inltrates. Objective exclusion of hydrostatic pulmonary
edema, such as by cardiac catheterization or echocardiography, should be considered if an obvious risk factor for
ARDS is not present. Ultimately, ARDS therapy is largely
supportive. e PaO2/ FiO2 ratio (see Figure 20.1) is useful to categorize the severity of ARDS, and should be followed when observing response to therapy.
Management— Subsequent TreatmentSteps
1
e mainstay of ARDS therapy is lung- protective ventilation. is strategy focuses on delivery of relatively low
stood, but may be due to reduced systemic inammation
secondary to diminished lung stretch and injury (as may
occur with use of higher, traditional tidal volumes).
Practically speaking, the ARDS patient should be
ventilated with initial tidal volumes of 6– 8 mL/ kg of
predicted body weight, with titration of respiratory rate
as necessary to deliver the expected minute ventilation
requirement. e PEEP should be at least 5 cmH2O,
though more may be required. In conjunction, the inspiratory fraction of oxygen (FiO2) should be adjusted to
achieve an arterial oxygen saturation of 88%– 95%; this
will help to limit hyperoxic injury. Further ventilation
adjustments should be made as dictated by the patient’s
transpulmonary compliance, with the primary goal of
keeping plateau pressure less than 30cmH2O. Reduction
in tidal volume may be necessary to achieve this goal.
Sedation may also be required to limit patient– ventilator
dyssynchrony.
Lung- protective ventilation may lead to hypoventilation
and associated respiratory acidosis. Permissive hypercapnia
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NONPULMONARY ORIGIN
PULMONARY ORIGIN
• Aspiration
• Near drowning
• Major surgery
• pneumonia
LUNG INJURY
• Sepsis
• Multiple transfusions
• Severe trauma
• Drug ovedose
• Burns
• Cardiopulmonary bypass
• Pancreatitis
Alveolar
macrophage
Release of proinflammatory cytokines
IL-1
IL-6
Chemoattraction
IL-8
TNF-a
Neutrophil
Degranulation
Elastase
Interleukins
Eicosanoids
Phospholipids
Cell injury
ROS
DEATH OF ALVEOLAR CELLS
Decreased surfactant, disruption of ion transport, increased alveolar-capillary permeability
EXUDATIVE EDEMA
Figure20.2 Pathophysiology of ARDS. Lung injury, which can come from pulmonary or extrapulmonary sources, leads to an intense inammatory
cascade mediated by macrophage activation and eventual neutrophil degranulation. Release of inammatory mediators from neutrophils leads to
alveolar cell death and microvascular injury. Acharacteristic exudative edema ensues; respiratory failure follow swiftly.
ARDS=acute respiratory distress syndrome; IL=interleukin; TNF- a=tumor necrosis factor alpha; ROS=reactive oxygen species. Sources:Estenssoro E, Dubin A,
Laffaire E, etal. Incidence, clinical course, and outcome in 217 patients with acute respiratory distress syndrome. Critical Care Medicine. 2002;30:2450– 6. Fujishima S.Pathophysiology
and biomarkers of acute respiratory distress syndrome. Journal of Intensive Care. 2014;2:32– 7.
is therefore a hallmark of this strategy. ere is not a known
maximum safe PaCO2. Actual PaCO2 is probably of little
importance; arterial pH should be allowed to fall to 7.15
or lower before considering administration of sodium
158 PART IV. PULMONARY CRISES
RESPIRATORY FAILURE
bicarbonate (or other alkalemic solution). Certainly, hypercarbia should be avoided in specic instances in which it
could be harmful, such as elevated intracranial pressure, status epilepticus, arrhythmias, or others.
6
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159
A number of adjunctive strategies have been shown to
be useful to improve mortality rates from ARDS, most of
them aimed at optimizing the eects of lung- protective
ventilation. Using higher levels of PEEP has been shown
to improve mortality in patients with moderate or severe,
but not mild, ARDS.7 Titration of PEEP using esophageal pressure as a surrogate for transpulmonary pressure
has been shown to improve gas exchange,8 and provides
reassurance against alveolar barotrauma. Use of neuromuscular blocking drugs in patients with severe ARDS
may facilitate patient synchrony with lung- protective ventilation settings (or perhaps decreases systemic inammation), and is associated with improved mortality.9 Prone
positioning may improve ventilation- perfusion matching and reduces the transpulmonary pressure gradient.10
When performed at centers adept at caring for patients in
the prone position, it improves mortality in patients with
severe ARDS.
11
Extracorporeal membrane oxygenation (ECMO) is a
potentially eective option for patients with severe ARDS
who are not improving, and ECMO has been shown to
improve survival for patients with potentially reversible
causes of ARDS. is requires highly specialized care, and
transfer to a center capable of providing ECMO should be
considered for appropriate patients.12 Figure 20.3 provides
a broad summary of the approach to perioperative ARDS
management.
Most other interventions for ARDS are of little benet
with respect to mortality. Future anti- ARDS therapy may
include targeting of the biochemical mediators of ARDS,
such as anti- interleukin antibodies. However, this remains
hypothetical.
Consider objectively eliminating
hydrostatic cause of edema
• echocardiogram
• cardiac catheterization
Figure20.3 Summary of treatment approach to
ARDS. Correction of the underlying problem is
of paramount importance when treating ARDS.
Effective therapies include lung- protective
ventilation, increased PEEP, neuromuscular
blockade, prone positioning, and ECMO if needed.
ARDS=acute respiratory distress syndrome;
TV=tidal volume; PBW=predicted body weight;
RR=respiratory rate; PEEP=positive endexpiratory pressure; FiO2=inspiratory fraction
of oxygen; PaO2=arterial partial pressure of
oxygen; ECMO=extracorporeal membrane
oxygenation. Sources:The Acute Respirator y Distress
Syndrome Network. Ventilation with lower tidal volumes
as compared with traditional tidal volumes for acute lung
injury and the acute respiratory distress syndrome. N Engl
J Med. 2000;342:1301– 8. Briel M, Meade M, Mercat A,
etal. 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– 873. Papazian L, Forel JM, Gacouin
A, etal. Neuromuscular blockers in early acute respiratory
distress syndrome. N Engl J Med. 2010;363:1107– 16.
Beitler JR, Shae S, Montesi SB, etal. Prone positioning
reduces mortality from acute respiratory distress
syndrome in the low tidal volume era:a meta- analysis.
Intensive Care Med. 2014;40:332– 41. Peek GJ, Mugford
M, Tiruvoipati R, etal. Efcacy and economic assessment
of conventional ventilatory support versus extracorporeal
membrane oxygenation for severe adult respiratory
failure (CESAR):a multicentre randomised controlled trial.
Lancet. 2009;374:1351– 63.
Correct underlying
problem
(e.g, antibiotics if septic)
LUNG-PROTECTIVE
VENTILATION
Suspected
ARDS
obvious risk factor
• TV 6-8 mL/kg PBW, titrate RR
as needed
• Plateau pressure <30 cm H
• Permissive hypercapnia
• PEEP at least 5 cm H2O
• Reduce FIO2 as able
If moderate or severe
Increase PEEP
If severe
Consider prone if at
adept center
If not improving
Consider ECMO
no obvious risk factor
Goal:
PaO
55-800 mmHg
2
or
O
2
Trend PaO
Consider neuromusular to
blockade to decrease
dyssynchrony
Consider titration with
esophageal balloon
SpO2 88-95%
Consider sedation to
decrease dyssynchrony
/FiO2 to observe
2
response
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Follow- Up
Patients who survive ARDS remain limited several years
aer discharge, especially with respect to functional capacity. Extrapulmonary symptoms also persist; subjective muscle weakness is especially prominent.13 It is unknown how
early recognition and treatment of ARDS may limit these
impairments.
PATHOPHYSIOLOGY OFDISEASE STATE— TRALI
First described in 1951 as a case report of pulmonary
hypersensitivity in response to a transfusion of blood,
TRALI represents another perioperative pulmonary
inammatory state with potentially lethal consequences.
In 2005, a formal denition was adopted, specifying
TRALI as an acute- onset (within 6 hours) of lung injury
(ALI) following transfusion when no other risk factor
for ALI is present. If a risk factor for ALI is present, the
clinician must assess whether other TRALI- like ndings are present, whether the patient was stable before
transfusion, whether the new ALI developed with the
transfusion, and the incidence of ALI with the given
risk factor.14 Notably, this denition limits identication of TRALI in patients with ARDS. Furthermore,
this denition was operationalized using the 1994 North
American- European Consensus Conference denition
of ALI, which has since been updated to the Berlin denition of ARDS.1 ere is also a considerable degree of
ambiguity when interpreting whether new ALI occurs
secondary to transfusion in a patient with alternative preexisting ALI risk factors. Nevertheless, dening TRALI
using these criteria empowers the perioperative clinician
to recognize and respond appropriately to transfusionprecipitated lung injury.
All plasma- containing products have been implicated
in TRALI. In the perioperative sphere, this is usually limited to whole blood, packed red blood cells, platelets, fresh
frozen plasma (FFP), and cryoprecipitate. Nevertheless,
sources such as intravenous immunoglobulin have also
been described.14 e greatest risk of serious TRALI (i.e.,
that which requires mechanical ventilation and may lead to
death) occurs when transfusingFFP.
17
Underlying Mechanism
ere are two suggested underlying mechanisms for
TRALI pathogenesis, the antibody- mediated model and
the “two- hit” model. Regardless of the precise mechanism,
the clinical outcome is ALI, with accumulation of a proteinaceous edema uid in the pulmonary interstitium secondary to increased microvascular permeability, as shown
in Figure20.4.
In the antibody- mediated model of TRALI, antibodies
in the donor plasma are passively transfused into the recipient’s serum. ese antibodies bind to recipient endothelial cells, monocytes, and neutrophils to cause neutrophil
activation. As in ARDS, neutrophil activation results in
release of cytotoxic and inammatory agents, which damage microvascular and alveolar surfaces and lead to pulmonary edema. Transfusion of products from female donors
has been especially linked with TRALI. is is presumably
due to a higher antibody burden aer alloimmunization
during pregnancy.
18
In the “two- hit” hypothesis of TRALI, a rst insult
(such as major surgery, trauma, multiple transfusions, or
other risk factors for lung injury) leads to lung injury and
sequestration of neutrophils on the endothelial lining of
lung tissue. e second hit, the blood transfusion itself,
activates these neutrophils via inammatory mediators that
have accumulated during blood storage (lipid degradation
Epidemiology/ Risk
products). Again, microvascular and alveolar injury occurs,
with subsequent development of pulmonary edema and
By denition, TRALI is a clinical diagnosis that is easily
loss of surfactant.
19
confounded by the presence of comorbid reasons for lung
injury, and is likely underreported. e exact incidence of
TRALI is unknown, but according to the Food and Drug
Administration (FDA), TRALI caused the highest number of transfusion- related fatalities from 2009 to 2013 in
the United States, representing 72 out of a total of 190
transfusion- related deaths (38%).15 Fortunately not all cases
of TRALI lead to death, though the risk is up to 40% in
critically ill patients who develop TRALI. Unsurprisingly,
sicker patients have a higher risk of TRALI, which occurs
in 8% of transfused ICU patients.
16
Assessment ofthe Patient:Presenting Signs
and Symptoms
e presenting signs and symptoms are nearly identical to
those of early ARDS, with the added time- factor of recent
transfusion. e dierential diagnosis of TRALI includes
transfusion- associated circulatory overload, anaphylactic
transfusion reaction, sepsis (including bacterial contamination of transfused blood), acute le ventricular failure,
ARDS from alternative triggers (i.e., precipitated by an
160 PART IV. PULMONARY CRISES
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161
Figure20.4 Pathophysiology of TRALI.
In the antibody mediated model,
antibodies from the donor serum lead
to recipient neutrophil activation. In
the two- hit model, a rst insult injures
the lung and “primes” it for further
injury. Asecond insult, transfusion of
inammatory mediators such as lipid
degradation products, then leads to
neutrophil activation. Both models
culminate in microvascular and alveolar
injury and subsequent exudative
edema. TRALI=transfusion- related
acute lung injury; ROS=reactive oxygen
species. Sources:Vlaar AP, Juffermans NP.
Transfusion- related acute lung injur y:a clinical
review. Lancet. 2013;382:984– 94. Silliman
CC. The two- event model of transfusionrelated acute lung injury. Crit Care Med.
2006;34:S124– 31.
alternative lung injury risk factor, coincidentally associated
with transfusion), and many others.
from male donors only, which has been shown to have up to
a two- thirds reduction in TRALI incidence.18 eoretically,
using fresher products (i.e., which have not had time to form
Management— Initial TreatmentSteps
Initial treatment of TRALI is largely focused on excluding
lipid degradation products) may reduce the risk of TRALI
with each transfusion, according to the “two- hit” hypoth-
esis. is has not been fully investigated, however.
other etiologies for acute pulmonary failure, with appropriate resuscitation if the patient is unstable.
Management— Subsequent TreatmentSteps
Aer initial treatment, focus should shi to preventing
future occurrence. When transfusion is necessary, consideration should be given to using washed red cells and products
Follow- Up
Care of the patient with TRALI is largely supportive; the
mortality risk is high, especially in critically ill patients.
Prevention remains the best method of avoiding TRALI.
Follow- up of suspected TRALI should involve discussion
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a
TRALI
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with the blood bank, with hopes of reducing the risk of
TRALI in future patients who may otherwise be transfused
with products from the samedonor.
PATHOPHYSIOLOGY OFDISEASE STATE— TACO
Transfusion- associated circulatory overload (TACO) is yet
another syndrome seen in perioperative patients which creates
pulmonary edema and limits gas exchange. Distinct from both
ARDS and TRALI, TACO is not mediated by an inammatory or immunologic cascade. Rather, TACO represents a
hydrostatic pulmonary edema akin to acute heart failure.
Epidemiology/ Risk
Underlying Mechanism
e underlying etiology of TACO is volume overload of
the le ventricle caused by increased intravascular volume.
is intravascular volume will lead to a rise in le ventricular and, eventually, le atrial and pulmonary venous
hydrostatic pressures. e Starling relationship, as dened
by the dierence in hydrostatic and oncotic pressures across
capillary walls, dictates that uid move into the pulmonary
interstitium when capillary hydrostatic pressure is elevated.
Ultimately, this will manifest as pulmonary edema and
hypoxic respiratory failure.
21
Assessment ofthe Patient:Presenting Signs
and Symptoms
Similar to TRALI, TACO is likely underrecognized and
therefore underreported. From 2009 to 2013, TACO was
responsible for 45 out of 190 transfusion- related fatalities
in the United States (24%), ranking it just behind TRALI
with respect to frequency of death.15 Transfusion- related
risk factors for development of TACO include a preexisting
positive uid balance, large volume of transfusion, greater
plasma transfusion volume, and a faster transfusion rate.
Patient- related risk factors predisposing toward TACO
included preexisting le ventricular dysfunction and elderly
age. e overall incidence of TACO approaches 8% of all
transfused patients and is more common in theICU.
20
Presenting signs of TACO are comparable to those of
acute left- sided heart failure. The temporal relationship of hypoxemia and fluid overload should nevertheless alert the perioperative provider to the potential of
TACO. The relatively rapid time after transfusion to
development of TACO may necessitate differentiation
from TRALI. Classically, the hypotension seen with
TRALI is not present with TACO, and can help distinguish between the two.22 Figure 20.5 identifies common
findings and pathophysiology associated with TRALI
versusTACO.
TACO
Alveolar duct and
alveoli
Nonhydrostatic
edema
Microvascular injury
• Dyspnea
• Dyspnea
• Fever
• Hypertension
• Hypoxia
• Bilateral infiltrates
• Normal LV function
• Normal PCWP
Figure20.5 TRALI vs. TACO. Both TRALI and TACO follow several hours after transfusion and lead to respiratory failure, thus distinguishing between the two can
be challenging. Fever and hypotension are classically associated with TRALI. The absence of these, plus the presence of cardiac failure, is more commonly
associated with TACO. TRALI=transfusion- related acute lung injury; TACO=transfusion- associated circulatory overload; LV=left ventricle; PCWP=pulmonary
capillary wedge pressure; Pa=arterial hydrostatic pressure; BNP=brain natriuretic peptide. Sources:Vlaar AP, Juffermans NP. Transfusion- related acute lung injur y:a clinical
review. Lancet. 2013;382:984– 94. Li G, Daniels C, Kojicic M, etal. The accuracy of natriuretic peptides (brain natriuretic peptide and N- terminal pro- brain natriuretic) in the differentiation
between transfusion- related acute lung injury and transfusion- related circulatory overload in the critically ill. Transfusion. 2009;49:13– 20.
RESPIRATORY
FAILURE
• Lack of fever
• Hypertension
• Hypoxia
• Bilateral infiltrates
• Normal or
decreased LV
function
• Increased PCWP
• Potentially
increased BNP
Hydrostatic edem
Pa
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163
Management— Initial TreatmentSteps
If the patient is still being transfused, attempts at slowing
the rate of transfusion should be attempted. If appropriate,
volume removal using diuretics may be necessary.
Management— Subsequent TreatmentSteps
20
Once the patient’s uid status has been optimized, the
remainder of management of TACO is supportive.
Optimization of le ventricular function may be required
to limit hydrostatic pulmonaryedema.
Follow- Up
Aer short- term recovery from TACO, the patient may
still be at risk for ARDS or TRALI, and thus perioperative providers should continue to maintain vigilance for
transfusion- related sequelae.
CASE- BASED LEARNING DISCUSSION
1. What are the important considerations in this patient?
What monitoring devices might youneed?
2. What are appropriate ventilator settings for this patient?
3. On postoperative day 2, the patient’s pulse oximetry
readings have failed to rise above 90%, despite initiating
lung- protective ventilation and a high PEEP level.
What should be the nextstep?
4. What diagnostic studies should be considered?
5. Aer several transfusions of platelets, the patient
develops a fever and hypotension on postoperative
day 3.What should be the next step? Should you call
the bloodbank?
6. What should you tell his family regarding his prognosis?
REFERENCES
1. ARDS Denition Task Force, Ranieri VM, Rubenfeld GD, etal.
Acute respiratory distress syndrome: the Berlin denition. Journal
of the American Medical Association. 2012;307:2526– 33.
2. Esteban A, Ferguson ND, Meade MO, etal. Evolution of mechani-
cal ventilation in response to clinical research. American Journal of
Respiratory and Critical Care Medicine. 2008;177:170– 7.
3. Buregeya E, Fowler RA, Talmor DS, Twagirumugabe T, Kiviri W,
Riviello ED. Acute respiratory distress syndrome in the global
context. Global Heart. 2014;9:289– 95.
4. Estenssoro E, Dubin A, Laaire E, etal. Incidence, clinical course,
and outcome in 217 patients with acute respiratory distress syndrome. Critical Care Medicine. 2002;30:2450– 6.
5. Fujishima S. Pathophysiology and biomarkers of acute respiratory
distress syndrome. Journal of Intensive Care. 2014;2:32– 7.
6. e Acute Respiratory Distress Syndrome Network. Ventilation
with lower tidal volumes as compared with traditional tidal volumes
for acute lung injury and the acute respiratory distress syndrome.
New England Journal of Medicine. 2000;342:1301– 8.
7. Briel M, Meade M, Mercat A, et al. Higher vs lower positive
end- expiratory pressure in patients with acute lung injury and
acute respiratory distress syndrome:systematic review and metaanalysis. Journal of the American Medical Association. 2010;
303:865– 73.
8. Talmor D, Sarge T, Malhotra A, etal. Mechanical ventilation guided
by esophageal pressure in acute lung injury. New England Journal of
Medicine. 2008;359:2095– 104.
9. Papazian L, Forel JM, Gacouin A, etal. Neuromuscular blockers in
early acute respiratory distress syndrome. New England Journal of
Medicine. 2010;363:1107– 16.
10. Guerin C, Baboi L, Richard JC. Mechanisms of the eects of prone
positioning in the acute respiratory distress syndrome. Intensive
Care Medicine. 2014;40:1634– 42.
11. Beitler JR, Shae S, Montesi SB, etal. Prone positioning reduces
mortality from acute respiratory distress syndrome in the low
tidal volume era:a meta- analysis. Intensive Care Medicine. 2014;
40:332– 41.
12. Peek GJ, Mugford M, Tiruvoipati R, etal. Ecacy and economic
assessment of conventional ventilatory support versus extracorporeal membrane oxygenation for severe adult respiratory failure (CESAR): a multicentre randomised controlled trial. Lancet.
2009;374:1351– 63.
13. Herridge MS, Tansey CM, Matte A, et al. Functional disability
5 years aer acute respiratory distress syndrome. New England
Journal of Medicine. 2011;364:1293– 304.
14. Toy P, Popovksy MA, Abraham E, et al. Transfusion- related
acute lung injury: denition and review. Critical Care Medicine.
2005;33:721– 6.
15. Fatalities reported to FDA following blood collection and transfusion:annual summary for scal year 2013. Silver Spring, MD:US
Department of Health and Human Services, the Food and Drug
Administration;2013.
16. Gajic O, Rana R, Winters JL, etal. Transfusion- related acute lung
injury in the critically ill: prospective nested case- control study.
American Journal of Respiratory and Critical Care Medicine.
2007;176:886– 91.
17. Eder AF, Herron R, Strupp A, et al. Transfusion- related acute
lung injury surveillance (2003– 2005) and the potential impact of
the selective use of plasma from male donors in the American Red
Cross. Transfusion. 2007;47:599– 607.
18. Vlaar AP, Juermans NP. Transfusion- related acute lung injury: a
clinical review. Lancet. 2013;382:984– 94.
19. Silliman CC. e two- event model of transfusion- related acute lung
injury. Critical Care Medicine. 2006;34:S124– 31.
20. Li G, Rachmale S, Kojicic M, etal. Incidence and transfusion risk
factors for transfusion- associated circulatory overload among medical intensive care unit patients. Transfusion. 2011;51:338– 343.
21. Starling EH. On the absorption of uids from the connective tissue
spaces. Journal of Physiology. 1896;19:312– 26.
22. Li G, Daniels C, Kojicic M, etal. e accuracy of natriuretic peptides (brain natriuretic peptide and N- terminal pro- brain natriuretic) in the dierentiation between transfusion- related acute lung
injury and transfusion- related circulatory overload in the critically
ill. Transfusion. 2009;49:13– 20.
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21.
DISRUPTION OFDIFFUSION
AIRSPACE DISEASES
Nayema Khan and John Pawlowski
CLINICALCASE
structures containing vessels within the lung that allow for
gas to be exchanged from the environment to the body. In
A 68- year- old man presents to the emergency department
(ED) with severe abdominal pain and has been added on to
the operating room (OR) schedule for an urgent repair of
an incarcerated ventral hernia. In the preoperative area, he
is in visible distress with tears present. He is tachypneic, but
is not using any accessory muscles of respiration. He does
not demonstrate peritoneal signs and states that his pain has
improved from a 9/ 10 to a 3/ 10 with pain medication he
received in the ED. He is a 40- pack- year smoker and has had
a productive cough with occasional blood tinged sputum for
the last 3days. is cough is very dierent from his usual dry
cough, and he also reports generalized malaise and a runny
nose. e patient lives on a two- story walk- up and now has
to stop aer one ight of stairs to catch his breath. On questioning, he reports that he does not have any major medical problems, does not see a doctor regularly, and does not
take any daily medications. However, he does report a visit
to the ED 1month ago, when he presented with diculty
breathing that resolved with bronchodilator therapy. He
was supposed to follow up with a primary care doctor at that
time, but has been unable to do so due to insurance reasons.
His BMI is 34, and he has a good airway on exam. Vitals are
notable for a temperature of 101.2oF, blood pressure 108/
65mmHg, pulse 97 beats per minute, respiratory rate 22
breaths per minute, and a saturation of 92% pulse oximetry
on room air. He has diuse rales and end expiratory wheezes
in his lower lung elds. Labs from the ED are notable for a
white blood cell count of 17 and a bicarbonateof35.
order to have adequate gas exchange, there must be a bal-
ance between ventilation (V)of the lungs, that is, the ow
of gas from the environment to the alveoli; diusion of
the gas from the alveolar space into the alveolar capillar-
ies; and perfusion (Q), or the circulation to the pulmonary
capillarybeds.
1
Oxygen moves from the alveolar gas into the plasma
and red blood cells, where it combines with hemoglobin,
and carbon dioxide moves from the plasma into the alveolar space. e diusion of both gases occurs passively, down
each of their respective gradients.1 e lungs are designed to
maximize diusion with a large surface area and relatively
thin membranes. Other factors that inuence diusion
are inherent properties of molecules such as the molecular weight of a gas and their individual solubilities (carbon
dioxide being more soluble than oxygen). Disease states
can adversely aect diusion and subsequently cause a mismatch in ventilation and perfusion (V/ Q mismatch).
In this chapter we focus on airspace diseases, pathological states that impair gas ow to the alveolar interface and,
thus, impair diusion in the lungs. In particular, we will discuss the management of secretions, pneumonia, pulmonary
edema, and hemoptysis. While the underlying pathophysiology of each of these conditions is dierent, collectively they
cause uid in the alveolar spaces and thickening of the alveolar membrane. is results in impaired diusion across the
alveolar capillary membranes and V/ Q mismatch.
General anesthesia itself is associated with impaired
oxygenation and decreased functional residual capacity.
DEFINITION OF AIRSPACE DISEASES
e lungs constitute a spongy air- lled organ that is essential for respiration— the oxygenation of blood and the
elimination of carbon dioxide. e alveoli are thin- walled
Additionally, there is increased airway collapse or atelectasis, decreased respiratory drive/ response to hypoxia,
and inhibition of hypoxic pulmonary vasoconstriction.
Furthermore, shunt, or the area of the lung that is perfused but not ventilated (V/ Q ratio=0), increases during
general anesthesia.1 Shunt may be caused by atelectasis or
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consolidation, as seen in pneumonia and edema. Secretions,
edema of the airway walls, and increased bronchial muscle
tone or spasms reduce the lumen of the airways and facilitate premature closure. Bronchospasm aects gas distribution by decreasing or eliminating ventilation in regions
aected by airway obstruction and by increasing it in less
obstructed areas. In individuals with preexisting pulmonary
disease, gas exchange is further compromised in the anesthetized state compared to the awakestate.
sputum, fever, chills, and pleuritic chest pain. Physical
exam ndings include fevers, tachycardia, and tachypnea
(seen in 70% of adults older than 65years).3 Lung examination may be notable for decreased or asymmetrical breath
sounds, rales, or bronchial breath sounds, dullness to percussion, egophony, and increased fremitus.3 An inltrate
is oen seen on chest x- ray imaging. Lobar consolidation,
cavitation, and pleural eusions may also be seen in more
extensive disease. It is important to note that radiographic
evidence is a late sign, which lags behind clinical presenta-
RETAINED SECRETIONS
e lungs are exposed to 500 L of air an hour, or 12,000 L
a day, which includes up to 25million inhaled particles a
day containing dust, irritants, and microbes. ese particles
can damage the epithelial lining of the airway.2 e lungs’
rst line of defense against the accumulation of damaging
particles and pathogens is the secretion of mucus from goblet cells, which line the epithelial cells of the cartilaginous
portion of the airway (the trachea down to the terminal
bronchi). Mucus is a viscoelastic gel that acts as a physical
barrier, entrapping foreign material. With the assistance of
ciliary cells, debris is swept away to the more proximal portion of the airway.
tion of the disease. Individuals with pneumonia have a widening of the V/ Q distribution, and a pure shunt is caused by
areas of consolidation that are perfused but not ventilated.
1
Pneumonia in an otherwise healthy individual may
present with mild symptoms and is oen treated with a
course of outpatient antibiotics. Its presentation can also
be quite severe, as in hospitalized patients and those with
multiple medical comorbidities. According to the Centers
for Disease Control (CDC), pneumonia and inuenza
were the eighth leading cause of death in 2013.4 Prediction
tools such as the CURB- 65 and SMART- COP have been
developed to assess the need for hospitalization, including
intensive respiratory or vasopressor support and to predict
3
death.
While mucus has an important homeostatic role,
overproduction or hypersecretion of mucus can lead to
impaired mucociliary clearance and obstruction of airow.
is can subsequently lead to diculty breathing, morbidity, and even death. Hypersecretion is seen in individuals
with asthma, chronic bronchitis, and cystic brosis. Oen
the initial production of mucus is thought to be an acute
response to increased irritant exposure that becomes maladaptive.2 In smaller or more reactive airways, excess mucus
can form an obstruction or “plug” that prevents the movement of gas distal to the obstruction.
PULMONARYEDEMA
Pulmonary edema is the accumulation of uid in the interstitial and alveolar spaces. Histologically, there is dilation
of the alveolar veins and capillaries due to acute distention and thickened alveolar walls from increased interstitial uid. Alveolar lumens become lled with transudate,
which replaces the air, creating a barrier to diusion.5
us, like pneumonia, the diusion impairment seen
with pulmonary edema is associated with V/ Q mismatch
andshunt.
PNEUMONIA
Pneumonia is caused by inammation of the lung parenchyma, oen due to bacterial or viral etiologies, resulting
in capillary congestion and consolidations of the airspaces
due to exudate and polymorphonuclear cells. Aspiration of
organisms from the upper respiratory tract and intrusion
of bacteria into the lower respiratory tract are thought to
be the main causes of this disease. Classication of pneu-
In the normal lung, there is constant ow of uid and
solute ltered from the pulmonary capillaries in the alveolar walls and absorbed by the pulmonary lymphatic system in the interstitial space. e ow of uid in the lungs
is classically described by the Starling forces, which take
into account the hydrostatic and oncotic pressure gradients
between the alveolar capillaries and the adjacent interstitial
space, as well as the endothelial permeability to both water
and proteins.
monia as community- acquired, healthcare- associated, and
ventilator- associated pneumonia depends on the patient’s
Rateof filtrationof fluid( )
KP P[]
fcap is ca
s
exposure and clinical risk factors.
Pneumonia is a clinical diagnosis that presents most
commonly with a cough productive of mucopurulent
Starlings forces equation:where P
is the capillary hydro-
cap
static pressure, Pis is the interstitial hydrostatic pressure,
DISRUPTION OF DIFFUSION:AIRSPACE DISEASES 165
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