Injury to type Table 24.1 Diagnostic criteria for acute lung injury ALI and adult respiratory distress syndrome ARDS.. Among the more frequently reported causes of respiratory distr
Trang 1II cells in ALI/ARDS can disrupt removal of alveolar fl uid and impair normal surfactant production and turnover, contributing
to the alveolar collapse, gas exchange abnormalities, and loss of lung compliance characteristic of this syndrome [9,13 – 15]
A number of human and animal studies have implicated the neutrophil as one of the key cellular mediators of this early phase
of acute lung injury Histological examinations and analysis of bronchoalveolar lavage fl uid from lungs of patients with ARDS have demonstrated increased numbers of neutrophils Neutrophils are thought to contribute to lung injury through release of pro-teases, reactive oxygen species, leukotrienes, platelet - activating
tachypnea, and tachycardia, and physical examination signs of
pulmonary edema (bilateral crackles and/or wheezes on chest
auscultation) without signs of left - sided heart failure (e.g absent
S3, elevated jugular venous pressure, and peripheral edema)
Chest radiography will show diffuse bilateral alveolar and/or
interstitial infi ltrates, typically without cardiomegaly Although
plain chest radiographs in ALI/ARDS suggest a diffuse process,
studies utilizing computed tomography of the chest (CT scans)
have shown that in fact lung involvement in ALI and ARDS is
inhomogeneous, with alveolar infi ltrates, consolidation, and
atel-ectasis that are worst in the dependent lung zones while other
areas of the lung may appear to be spared [8,9] Figure 24.1 shows
examples of typical fi ndings on plain chest radiography and CT
scan of the chest in ARDS It should be noted that studies of
bronchoalveolar lavage fl uid from patients with ARDS have
shown that even areas of the lung that appear relatively clear on
radiographic examinations may have signs of signifi cant infl
am-mation [10]
A detailed review of the pathogenesis of ALI and ARDS has
been published recently by Ware and Matthay [9] ALI and ARDS
are characterized by three distinct stages, although not all patients
will progress through all stages The initial stage is an acute
exuda-tive phase , which again presents clinically as acute onset of
respi-ratory distress and hypoxemia refractory to supplemental oxygen,
most often resulting in respiratory failure requiring mechanical
ventilation The term “ non - cardiogenic pulmonary edema ” has
also been applied to this clinical picture, and the radiographic
fi ndings may be indistinguishable from those of congestive heart
failure This acute phase is characterized by increased
permeability of the alveolar – capillary barrier leading to leakage of protein
-rich edema fl uid into the alveolar spaces, accompanied by a
pattern of diffuse alveolar damage with increased numbers of
neutrophils, macrophages, and erythrocytes, and varying degrees
of hyaline membrane formation [9,11,12] Injury to the alveolar
epithelium is a key step in the pathogenesis of ALI and ARDS,
and a greater degree of alveolar epithelial injury has been
corre-lated with worse outcomes Injury to type I alveolar epithelial cells
(which make up the majority of alveolar surface area) contributes
to alveolar fl ooding following endothelial injury and increased
vascular permeability Alveolar type II epithelial cells normally
function to produce surfactant, transport ions, and differentiate
into type I cells as part of recovery from any injury Injury to type
Table 24.1 Diagnostic criteria for acute lung injury ( ALI ) and adult respiratory
distress syndrome ( ARDS )
Acute onset of respiratory distress
Bilateral pulmonary infi ltrates on chest X - ray
PAOP ≤ 18 mmHg or absence of clinical evidence of left atrial hypertension
P a O 2 /F i O 2 ratio of ≤ 200 for ARDS or ≤ 300 for ALI, regardless of PEEP
PAOP, pulmonary artery occlusion (wedge) pressure; PEEP, positive
end - expiratory pressure
(a)
(b)
Figure 24.1 (a) Chest radiograph of a woman at 26 weeks gestation with
pre - eclampsia and acute non - cardiogenic pulmonary edema (ALI), showing the typical fi ndings of bilateral alveolar and interstitial infi ltrates in a perihilar distribution as well as bilateral pleural effusions (b) Chest CT scan image from the same patient demonstrating the atelectasis/consolidation and small pleural effusions in a predominantly dependent lung zone distribution bilaterally, with areas of relatively normal - appearing lung above Note that many of the same radiographic fi ndings may be seen with primarily cardiogenic pulmonary edema (see text)
Trang 2aspiration, drowning, or inhalation exposures of smoke or irri-tant chemicals, all of which may cause direct injury to the lung
In contrast, the extrapulmonary causes trigger a systemic infl am-matory cascade that in turn mediates the lung injury; some common extrapulmonary causes include sepsis, acute pancreati-tis, massive trauma, burns, and shock of any cause Some clinical and radiographical differences have been noted between ARDS due to direct versus indirect lung injury, including differences in responsiveness to PEEP and the presence of more lung consolida-tion on CT scans of the chest in ARDS due to direct lung injury versus a more diffuse pattern of ground glass opacifi cation and pulmonary edema in ARDS due to indirect lung injury The most common cause of ARDS is sepsis (from pulmonary or extrapul-monary sources), accounting for up to 50% of all cases [9,21] The risk of developing ARDS has been shown to increase with the presence of multiple risk factors, as well as with concomitant chronic alcohol abuse and chronic lung disease [22,23]
The same conditions mentioned above that predispose to the development of ALI and ARDS in non - pregnant patients can also lead to these complications in the obstetric population, but there are also several conditions unique to pregnancy that have been associated with the development of ALI/ARDS Among the more frequently reported causes of respiratory distress during preg-nancy are sepsis - induced ARDS, pre - eclampsia and eclampsia, pulmonary edema associated with tocolytic therapy, gastric aspi-ration, and amniotic fl uid embolism (Table 24.2 )
Severe sepsis , particularly septic shock, is the most common
cause of ARDS described in obstetric patients [24] Acute pyelonephritis seems to be an especially important cause of sepsis related ARDS in pregnancy, perhaps because this is one of the more common infections that may complicate pregnancy [25,26] Acute respiratory failure has been reported as a complication in
up to 7% of pregnant women with pyelonephritis [24 – 26]
factor, and other proinfl ammatory molecules in the pulmonary
capillary bed and alveolar spaces On the other hand, ALI and
ARDS can develop in severely neutropenic patients, and
neutro-phil - independent animal models of ALI also have been
devel-oped; thus, whether neutrophils are truly a cause of lung injury
in ALI/ARDS or in fact part of the host response is not entirely
clear [9]
Other mechanisms implicated in the development of ALI/
ARDS include a number of proinfl ammatory cytokines (such as
interleukin - 8 and tumor necrosis factor α ) that may be produced
locally in the lung and also may be regulated by extrapulmonary
factors [9] Disruption of the balance between proinfl ammatory
and anti - infl ammatory mediators is likely also important in the
development of acute lung injury Some of the important
endog-enous inhibitors of these proinfl ammatory molecules include
IL - 1 receptor antagonist, autoantibodies against IL - 8, and the
anti - infl ammatory cytokines IL - 10 and IL - 11 [9] Other pathways
which may be important in the propagation of acute lung injury
include secondary abnormalities of the coagulation system which
can result in formation of platelet – fi brin thrombi in small vessels
and impaired fi brinolysis, leading to further disruption of the
pulmonary capillary bed and contributing to the gas exchange
abnormalities seen clinically [9,16]
In many patients, the acute phase of ALI/ARDS resolves
com-pletely, but in a subset of cases it progresses into a so - called
fi broproliferative phase (also described as fi brosing alveolitis by
some authors), typically beginning 5 – 7 days after the initial
insult This phase may be characterized by persistent hypoxemia,
further increase in physiologic dead space, and worsening lung
compliance, often associated with pulmonary hypertension
secondary to obliteration of the pulmonary capillary bed
Histopathology in this stage may reveal interstitial fi brosis with
acute and chronic infl ammation [9,11,12,17] Patients who
survive this phase typically go on to a recovery phase , which is
perhaps the least well - characterized of the phases of ALI/ARDS
[9] In this phase, there is gradual recovery of lung function, with
improvements in lung compliance and hypoxemia Radiographic
abnormalities often resolve completely in survivors, although
data on the degree of histologic resolution is limited Some
studies of pulmonary function tests in survivors of ARDS have
found return to near - normal pulmonary function after 6 – 12
months [18] , but other investigators have shown that the
major-ity has residual abnormalities of diffusing capacmajor-ity, while 20%
have restrictive ventilatory defects and 20% signs of airfl ow
obstruction [19,20]
Etiology
A number of conditions can result in the injury to the alveolar –
capillary interface that is characteristic of ALI and ARDS These
are frequently divided into direct, or pulmonary, and indirect, or
extrapulmonary, causes of lung injury Examples of pulmonary
causes of ALI/ARDS include pneumonia, lung contusion, gastric
Table 24.2 Causes of acute lung injury and adult respiratory distress syndrome
in pregnancy
Independent of pregnancy Specifi c to pregnancy
Sepsis Pre - eclampsia and eclampsia Pneumonia Tocolytic - induced pulmonary edema Aspiration of gastric contents Aspiration pneumonitis (Mendelson ’ s
syndrome) Lung contusion Amniotic fl uid embolism Acute pancreatitis Placental abruption Inhalational injury Chorioamnionitis Fat embolism Endometritis Severe trauma Retained placental products Transfusion - related acute lung
injury (TRALI)
Other infections more frequent or more severe in pregnancy (e.g pyelonephritis, varicella pneumonia, malaria) Drug overdoses
Trang 3changes), myocardial dysfunction due to prolonged exposure to catecholamines, increased capillary permeability due to occult infection, and aggressive volume resuscitation in response
to maternal tachycardia or hypotension Possible risk factors for the development of tocolytic - induced acute pulmonary edema include multiple gestation, maternal infection, and corticosteroid therapy [30 – 32] In part due to this complication of β 2 adrenoceptor agonist use, magnesium sulfate has increasingly been used in place of these agents for tocolysis Management of tocolytic - induced pulmonary edema includes immediately stop-ping the drug, followed by supportive care and diuresis Most cases resolve rapidly, usually within 12 hours; however, in cases
of delayed resolution consideration must be given to possible alternate causes of acute pulmonary edema
Aspiration of gastric contents is another important cause of
ARDS during pregnancy While this complication is not unique
to pregnancy, pregnant patients are at increased risk of pulmo-nary aspiration of gastric contents because of some of the physi-ologic and anatomic changes occurring during pregnancy and immediately postpartum Reduced gastroesophageal sphincter tone, increased intragastric pressure due to the enlarged uterus, reduced gastric motility, and reduced gastric emptying during labor all predispose to aspiration When it occurs during obstetric anesthesia, aspiration of gastric acid resulting in acute lung injury has been termed Mendelson ’ s syndrome, after the classic descrip-tion of 66 cases published in 1946 [33] Mendelson reported an incidence of 1 case per 668 deliveries, with only two fatalities attributed to pulmonary aspiration A more recent study of peri-operative aspiration pneumonitis in pregnant patients reported
an incidence of 0.11% for cesarean deliveries and 0.01% for vaginal deliveries [34] The diagnosis of acid aspiration - induced acute lung injury may be straightforward in cases of witnessed aspiration, but it is important to remember that aspiration may also occur unwitnessed Occasionally, the only clue for aspiration may be the visualization of gastric contents in the pharynx during laryngoscopy at the time of endotracheal intubation The degree
of lung injury due to aspiration is positively correlated with higher volume and lower pH of aspirated material, and with more particulate matter aspirated
Amniotic fl uid embolism (AFE) is a pregnancy - specifi c cause of
ALI/ARDS which carries a high mortality rate This condition is discussed in detail in another chapter, and thus will be only men-tioned briefl y here The mechanisms underlying AFE are still not fully understood, but it is thought to occur when elements from amniotic fl uid enter the maternal circulation, most often at the time of labor or delivery This can lead to mechanical disruption
of pulmonary blood fl ow as a result of the embolic events and can also trigger release of proinfl ammatory cytokines that lead to disruption of the alveolar – capillary interface and produce a sys-temic infl ammatory response The classic clinical presentation
of AFE includes acute hypoxemic respiratory distress, hemody-namic collapse (often resulting in cardiac arrest), and dissemi-nated intravascular coagulation, occurring most often during labor or delivery Reported mortality rates with AFE are generally
Pregnancy - associated dilatation of the ureters and increased
collecting system volume have been suggested as reasons for
the increased frequency of acute pyelonephritis resulting from
untreated bacteruria during pregnancy [24] Besides
pyelone-phritis, other infections linked to development of ALI and ARDS
during pregnancy include viral and bacterial pneumonias,
liste-riosis, fungal infections with blastomycosis and
coccidioidmyco-sis, and malaria [21] Chorioamnionitis is another important
pregnancy - specifi c infectious complication to consider in the
dif-ferential diagnosis of the obstetric patient with ALI/ARDS and
clinical suspicion of sepsis without a clear source Clinical
indica-tions of chorioamnionitis include fever, fetal tachycardia, uterine
tenderness, and foul - smelling amniotic fl uid, but the
presenta-tion may be more subtle, and diagnostic amniocentesis should be
considered in pregnant patients with ALI/ARDS without a clear
cause [21,24]
Preeclampsia , characterized by hypertension, proteinuria, and
edema, occurs in up to 8% of pregnancies [24] Pulmonary
edema has been reported to occur in about 3% of patients with
severe pre - eclampsia, with most cases (70%) occurring in the
immediate postpartum period [27] Risk factors include older
age, multiple prior pregnancies, pre - existing chronic
hyperten-sion, and infusion of excessive volumes of crystalloid or colloid
[21,27] A combination of reduced plasma oncotic pressure,
altered permeability of pulmonary capillary membranes, and
elevated pulmonary vascular hydrostatic pressure have been
implicated as factors contributing to the development of
pulmo-nary edema complicating pre - eclampsia/eclampsia [28,29]
Details on the management of pre - eclampsia and eclampsia are
discussed in a separate chapter However, when pulmonary
edema complicates these conditions, management is similar to
that for pulmonary edema due to other causes, and includes
supplemental oxygen, mechanical ventilation when needed, and
judicious use of diuretics Invasive hemodynamic monitoring
using a pulmonary artery catheter may be helpful in
distinguish-ing fl uid overload and cardiogenic pulmonary edema from
ALI/ARDS, but does not seem to impact the outcome of these
patients Therefore, the decision to place these catheters must be
individualized
Tocolytic - induced pulmonary edema is another important
preg-nancy - specifi c cause of non - cardiogenic pulmonary edema The
β 2- adrenoceptor agonists terbutaline and ritodrine were until
recently used frequently for tocolysis, and their use has been
associated with various adverse effects including hyperglycemia,
hypokalemia, sodium and water retention, tachycardia, and
arrhythmias In addition, acute pulmonary edema can complicate
up to approximately 10% of cases where a β 2 - adrenoceptor
agonist is used for inhibition of premature labor This
complica-tion can occur during the infusion of these agents or up to 12
hours after their discontinuation [21,24] The mechanism of
tocolysis - related pulmonary edema is not fully understood, but
several contributing factors have been suggested, including a
combination of medication - induced increases in heart rate
and cardiac output (on top of pregnancy - related cardiovascular
Trang 4randomized study of a specifi c strategy of mechanical ventilation
to demonstrate convincingly an improvement in mortality in ARDS, and this method of ventilation has now become the stan-dard against which all new ventilatory modes for ALI/ARDS must
be compared
Unfortunately, there are no randomized trials in obstetric patients with ALI/ARDS to guide our approach to mechanical ventilation (or other aspects of management) in this population; indeed, pregnancy has been an exclusion criterion in almost all the clinical trials of therapies for ALI/ARDS Since maintaining the best environment for the fetus generally requires optimizing intrauterine conditions by supporting the hemodynamic and other organ function of the mother until delivery is feasible, the overall approach to management of ARDS in pregnancy closely parallels the management in non - pregnant patients [24] There are, however, some important aspects of maternal physiology that may dictate modifi cations of the targets of mechanical ventilation
in this group During pregnancy, driven in part by progesterone production by the placenta, maternal minute ventilation increases
by 50% compared with the non - pregnant state due to increased tidal volume and to a lesser extent increased respiratory rate The result is mild chronic (compensated) respiratory alkalosis, with
P a CO 2 dropping from 35 – 45 mmHg at baseline to the 27 –
34 mmHg range during pregnancy The renal compensatory response is to increase bicarbonate excretion to maintain normal
pH, resulting in normal serum bicarbonate levels in the 18 –
21 mEq/L range during pregnancy Lung volumes are also affected
by pregnancy, with total lung capacity, functional residual capac-ity, expiratory reserve volume, and residual volume all decreasing
by 4% to 20% from baseline, or non - pregnant values [43,44] The general approach to mechanical ventilation in the obstetric patient with ARDS is the same as in the general population, aiming to optimize blood gas parameters while preventing ventilator - induced lung injury However, although volume - controlled mechanical ventilation using the low - tidal volume (target 6 mL/kg ideal body weight) approach should be the goal given the proven mortality benefi t in non - pregnant populations, the degree of respiratory acidosis that may be tolerated during pregnancy may be lower as compared with the general popula-tion In fact, the effect of maternal hypercapnia on uteroplacental blood fl ow is not well understood Animal studies suggest that with maternal P a CO 2 > 60 mmHg, uterine vascular resistance increases and uterine blood fl ow decreases However, these animal models generally examined the impact of acute increases
in maternal P a CO 2 , whereas with the controlled hypoventilation strategy in ALI/ARDS the effect on P a CO 2 is usually more gradual
In ventilating obstetric patients with ALI/ARDS, maintaining maternal P a CO 2 < 45 – 50 mmHg has been suggested as a general rule [24] Excessive maternal hyperventilation and hypocapnia also should be avoided when managing mechanical ventilation in pregnancy, as these have been associated with uteroplacental vasoconstriction, decreased uteroplacental blood fl ow, and fetal hypoxia and acidosis [45 – 47] Thus, respiratory alkalosis beyond what is normal in pregnancy also should be avoided
very high (up to 80%), although more recent reports have
dis-puted this [24]
Management of ALI and ARDS
Mechanical v entilation
The management of patients with acute lung injury and ARDS is
largely supportive, in combination with specifi c therapies directed
toward the underlying cause whenever possible Especially
impor-tant is identifying infections when present, and treating them
expeditiously with appropriate antimicrobials and, if necessary,
surgical intervention (e.g abscess drainage) The mainstay in
supportive care for patients with ALI/ARDS is positive - pressure
ventilation Soon after the initial descriptions of ARDS,
investiga-tors made the observation that application of positive end -
expi-ratory pressure (PEEP) could produce dramatic improvements in
oxygenation [35] More recently, the application of ventilatory
support in ALI and ARDS has evolved further with increased
understanding of the potential adverse effects of alveolar
overdis-tention due to the use of excessively high tidal volumes Ample
evidence from animal models has shown that mechanical
ventila-tion using large tidal volumes and high airway pressures can
produce lung injury characterized by increased capillary
perme-ability and non - cardiogenic pulmonary edema, even in
previ-ously normal lungs [36,37] This type of lung injury has been
termed ventilator - induced lung injury (VILI) In addition to
alveo-lar overdistention, evidence suggests that repetitive opening and
closing of surfactant - depleted atelectatic alveoli during
mechani-cal ventilation can itself contribute to VILI, and furthermore can
initiate the release of a cascade of proinfl ammatory cytokines that
contributes to a systemic infl ammatory response and resulting
multiorgan failure [38 – 40] A “ lung protective ” ventilation
strat-egy which aims to avoid both overdistention of alveoli and the
repetitive opening and closing of atelectatic lung units has been
associated with reductions in this pulmonary and systemic
cyto-kine response [41]
A number of early trials in small numbers of patients using
either low tidal volume ventilation or pressure control modes
with low target airway pressures in ARDS produced confl icting
results as to effect on clinical outcomes However, the benefi t of
a low tidal volume approach was clearly demonstrated in the
landmark NIH - sponsored ARDS Network randomized trial
using volume - controlled mechanical ventilation with 12 mL/kg
tidal volumes as compared with 6 mL/kg tidal volumes in 861
patients with ALI and ARDS This study demonstrated a 22%
relative risk reduction in mortality rate in the low tidal volume
group (absolute mortality rates 39.8% versus 31.0%, p = 0.007)
[42] In this study a detailed algorithm was used to titrate F i O 2
and PEEP, and plateau pressures were maintained below
30 cmH 2 O, with use of sodium bicarbonate infusions if needed to
manage severe respiratory acidosis resulting from the controlled
hypoventilation caused by low tidal volume ventilation The
ARDS Network trial of low tidal volume ventilation was the fi rst
Trang 5ARDS; in the FACTT protocol, the conservative fl uid strategy targeted a CVP < 4 mmHg or a PAOP < 8 mmHg, as long as the
patient was not in shock and maintained adequate renal perfu-sion and effective circulation (defi ned for the protocol as mean arterial pressure > 60 mmHg without vasopressors, urine output
≥ 0.5 mL/kg/h, and cardiac index ≥ 2.5 L/min/m 2 or capillary refi ll
time < 2 s and the absence of cold, mottled skin) While this study excluded pregnant patients with ALI/ARDS, it suggests that avoidance of volume overload, together with judicious diuresis and fl uid restriction, should be the approach to fl uid manage-ment in this population as well At the same time, avoidance of maternal hypotension and careful attention to end - organ perfu-sion parameters as suggested by the FACTT protocol is critical to avoid compromising uteroplacental blood fl ow
Prone p ositioning
Studies have shown improved oxygenation in as many as 70 – 80%
of patients with ALI when ventilated in the prone position [54] Several factors may be involved in producing the improvement
in gas exchange, which interestingly may be sustained for several hours even after return to the supine position Reduced ventro-dorsal pleural pressure gradient and removal of the effects of compression by heart and mediastinum on dorsal lung units leading to increased recruitment of these previously atelectatic areas of lung, increased functional residual capacity due to the unsupported abdomen in the prone position, and better mobili-zation of secretions are among the proposed mechanisms for the improvement in oxygenation described with prone positioning [55,56] However, no randomized trials have demonstrated an impact on mortality or other clinically important outcomes with this approach Special beds and other devices have been devel-oped to aid in prone positioning of patients, but extreme caution
is warranted in order to avoid inadvertent loss of the artifi cial airway or other support catheters or monitoring equipment, and
to prevent the development of pressure ulcers [21] For obvious reasons, prone positioning is not likely to be a very practical option in the obstetric patient with ARDS, at least not in later stages of pregnancy In cases where the mother is close to term, maintaining the patient in the left lateral decubitus position will
be more important in order to limit the hemodynamic conse-quences of vena caval compression by the gravid uterus
Inhaled n itric o xide
Inhaled nitric oxide (NO) has been used in several studies in patients with ARDS and shown to produce improvements in oxygenation NO is a potent vasodilator, and when administered via the inhaled route produces fairly selective pulmonary vasodilation with minimal effects on systemic blood pressure Improvement in oxygenation in ALI/ARDS following inhaled NO administration results from improvements in ventilation – perfu-sion matching through greater vasodilation in the well - ventilated areas of lung [57] Unfortunately, randomized multicenter trials
in adults with ALI and ARDS have failed to show any improve-ment in mortality or other clinically important outcomes with
For the most part, providing positive - pressure ventilatory
support in pregnant patients with ALI/ARDS will require
estab-lishing an artifi cial airway fi rst (i.e endotracheal intubation)
Non - invasive positive - pressure ventilation (NIPPV), where
ven-tilatory support is provided by means of a tight - fi tting nasal or
full - face mask, has only a limited role in the management of
care-fully selected hemodynamically stable patients with ALI/ARDS
[48,49] Studies in other forms of respiratory failure have shown
reduced complications with NIPPV as compared with invasive
positive - pressure ventilation (principally reduced nosocomial
pneumonias, and also reduced mortality rates in patients with
hypercarbic respiratory failure due to COPD) However, NIPPV
should not be used in hemodynamically unstable patients or in
those with impaired respiratory drive or in patients at increased
risk of aspiration, and there are no studies evaluating NIPPV in
the management of hypoxemic respiratory failure during
preg-nancy In the obstetric population, a trial of NIPPV may be
con-sidered in carefully selected patients with a rapidly reversible cause
for the pulmonary edema, but close monitoring is always
war-ranted due to the increased risk of gastric aspiration during
preg-nancy In general, early endotracheal intubation by a clinician
experienced in the management of the obstetric airway will be
preferable in most cases, especially given the increased risk of
encountering a diffi cult airway in this population
Fluid m anagement
Optimal fl uid management in patients with ALI/ARDS has been
another area of controversy over the years, with advocates of fl uid
restriction pointing to improvements in pulmonary edema and
oxygenation with this approach and opponents emphasizing the
potential detrimental effects of fl uid restriction on cardiac output,
renal and other organ perfusion [50,51] The role of invasive
hemodynamic monitoring using pulmonary arterial catheters in
this population also has been debated extensively In an attempt
to answer these questions, the NIH ARDS Network undertook
the Fluid and Catheter Treatment Trial (FACTT), a randomized
multicenter trial involving 1000 patients with ALI and ARDS,
which compared a conservative versus liberal fl uid management
strategy and hemodynamic monitoring with a pulmonary artery
catheter (PAC; using primarily the pulmonary artery occlusion
pressure, or PAOP, and cardiac index, or CI) versus monitoring
with a central venous catheter (CVC; measuring central venous
pressure, or CVP) [52,53] This trial demonstrated that PAC
guided therapy was not associated with any improvements in
survival or organ function as compared with CVC - guided
therapy, but rather with more catheter - related complications
than seen with CVC - guided therapy [53] In addition, the
com-parison of fl uid management strategies revealed no signifi cant
difference in 60 - day mortality (the primary outcome), but the
conservative fl uid strategy was associated with improvement in
oxygenation and reduction in ventilator - free days as compared
with the liberal fl uid strategy without any adverse effect on non
pulmonary organ function [52] These results lend support to a
conservative strategy of fl uid management in patients with ALI/
Trang 6Fetal m onitoring and p otential e ffects of m aternal ARDS on p regnancy
The potential effects of maternal ARDS on a pregnancy include: (i) fetal distress due to maternal hypoxemia, (ii) premature labor triggered by the stress of the maternal condition, (iii) fetal expo-sure to medications used in management of ARDS, and (iv) inter-ference with assessment of fetal well - being by therapies used to treat the mother [21] Fetal assessment should be part of the management of any pregnant woman with ALI/ARDS If the fetus
is not yet at the gestational age of viability (at least 24 – 26 weeks
in most centers), assessment may be limited to periodic Doppler auscultation or ultrasonography to determine if the fetal heart tones are still present However, later in pregnancy, more fre-quent fetal assessment is needed to help guide decisions regarding the possible need for delivery, especially in the event of changes
in the maternal condition such as worsening maternal hypoxemia
or acidosis or addition of therapies which may adversely affect the fetus such as use of high doses of vasopressors Typically such ongoing fetal assessment will be done using continuous fetal heart rate monitoring and periodic ultrasonography with biophysical profi le scoring [21,24] It is important to remember that fetal movements may be affected by sedatives and other medications given to the mother Furthermore, the mother ’ s critical illness may trigger premature labor, and uterine contractions may in turn worsen maternal hypoxia due to the resulting increased maternal oxygen consumption; in this case, pharmacologic sup-pression of contractions may be necessary In cases of maternal ARDS where the fetus is potentially viable, decisions regarding optimal timing of delivery and mode of delivery must be indi-vidualized based on the condition of the mother and fetus, and
in general the indications for delivery will be the usual obstetric indications [24]
Prognosis of ALI and ARDS
Most epidemiologic studies suggest improvements in survival of patients with ALI/ARDS since the syndrome was fi rst recognized This is thought to be due to improvements in supportive critical care Stapleton and colleagues, in a retrospective single - institution study of mortality in patients with ARDS using a uniform defi nition, describe an overall reduction in mortality rate from 68% in 1981 – 1982 to a low of 29% in 1996 [69] Sepsis with multiple organ failure was the most common cause of death (30 – 50%) and respiratory failure accounted for a smaller propor-tion (13 – 19%) of deaths The ARDS network low tidal volume trial found an overall mortality rate of 31% in the intervention group, and multiple other studies have shown reductions in mor-tality rates from 50 – 60% up until the 1980s, down to the 30 – 40% range since the 1990s [42,70,71] Several investigators have shown that the mortality for sepsis - related ARDS is higher than that from ARDS associated with trauma and other non - sepsis risk factors [69,72] Older age ( > 65), higher elevations in dead space ventilation, and presence of other comorbidities are also
impor-inhaled NO use despite short - term improvements in oxygenation
[58 – 60] Thus, there is no evidence to support its use in the
routine management of patients with ALI/ARDS [61]
Surfactant t herapy
Surfactant therapy has been another potential intervention of
great interest in the management of ALI and ARDS Pulmonary
surfactant contains a combination of phospholipids and
apopro-teins and is produced by alveolar type II epithelial cells It
nor-mally lines the alveoli and respiratory bronchioles and serves to
reduce surface tension and stabilize the alveoli, preventing
alveo-lar collapse at low lung volumes As discussed earlier, loss of
surfactant in ALI and ARDS contributes to the atelectasis, gas
exchange abnormalities, and reduced lung compliance seen
in this syndrome Exogenous surfactant is routinely used in
managing respiratory distress syndrome (RDS) in premature
infants, having been shown to improve outcomes in this
popula-tion However, a large multicenter randomized trial of exogenous
surfactant administered by aerosolization in adults with ARDS
failed to show any improvement in outcomes [62] More
recently, small studies suggesting benefi ts when surfactant
preparations were instilled directly into the lower airways using
bronchoscopy have revived interest in this therapy for acute lung
injury [63,64] However, larger randomized trials using newer
preparations of surfactant and bronchoscopic delivery are still
ongoing [21]
Systemic c orticosteroids
Because of the prominent role of acute infl ammation in the
pathology of acute lung injury and ARDS, there was also early
interest in potential benefi t of anti - infl ammatory therapies, in
particular corticosteroids Several studies of high - dose
corticoste-roids given early in acute - phase ARDS showed no improvement
in outcomes including survival, with some suggesting increased
rates of infection following early high - dose corticosteroid use
[65,66] However, recent small clinical trials focusing on the
administration of corticosteroids in late phase ARDS (the so
called fi broproliferative phase) reported favorable results,
includ-ing one small randomized trial which showed improved survival
in the steroid - treated group [67] The ARDS Network recently
published results of a multicenter double - blind, placebo -
con-trolled, randomized trial of corticosteroids (methyprednisolone)
in persistent ARDS, defi ned in this study as at least 7 days after
the onset of ARDS The mean duration of ARDS prior to
enrol-ment in this study was 11 days There was no signifi cant
differ-ence in the primary endpoint of 60 - day mortality between the
placebo and corticosteroid - treated groups, and when begun
more than 14 days after onset of ARDS, methylprednisone was
associated with signifi cantly increased 60 - and 180 - day mortality
No signifi cant difference in infectious complications was seen,
but rates of neuromuscular weakness were higher in the
corticosteroid - treated group [68] Thus, the routine use of
corticosteroids in the treatment of late - phase ARDS is no longer
recommended
Trang 74 Goss CH , Brower RG , Hudson LD , Rubenfeld GD Incidence of acute lung injury in the United States Crit Care Med 2003 ; 31 ( 6 ):
1607 – 1611
5 Catanzarite V , Willms D , Wong D , Landers C , Cousins L , Schrimmer
D Acute respiratory distress syndrome in pregnancy and the
puerpe-rium: causes, courses, and outcomes Obstet Gynecol 2001 ; 97 ( 5 ):
760 – 764
6 Smith JL , Thomas F , Orme JF Jr , Clemmer TP Adult respiratory distress syndrome during pregnancy and immediately postpartum
West J Med 1990 ; 153 ( 5 ): 508 – 510
7 Mabie WC , Barton JR , Sibai BM Adult respiratory distress syndrome
in pregnancy Am J Obstet Gynecol 1992 ; 167 ( 4 Pt 1 ): 950 – 957
8 Gattinoni L , Bombino M , Pelosi P , Lissoni A , Pesenti A , Fumagalli R ,
et al Lung structure and function in different stages of severe adult respiratory distress syndrome JAMA 1994 ; 271 ( 22 ): 1772 –
1779
9 Ware LB , Matthay MA The acute respiratory distress syndrome
N Engl J Med 2000 ; 342 ( 18 ): 1334 – 1349
10 Pittet JF , Mackersie RC , Martin TR , Matthay MA Biological markers
of acute lung injury: prognostic and pathogenetic signifi cance Am J
Respir Crit Care Med 1997 ; 155 ( 4 ): 1187 – 1205
11 Pratt PC , Vollmer RT , Shelburne JD , Crapo JD Pulmonary morphol-ogy in a multihospital collaborative extracorporeal membrane oxy-genation project I Light microscopy Am J Pathol 1979 ; 95 ( 1 ):
191 – 214
12 Bachofen M , Weibel ER Structural alterations of lung parenchyma
in the adult respiratory distress syndrome Clin Chest Med 1982 ; 3 ( 1 ):
35 – 56
13 Sznajder JI Strategies to increase alveolar epithelial fl uid removal in the injured lung Am J Respir Crit Care Med 1999 ; 160 ( 5 Pt 1 ):
1441 – 1442
14 Greene KE , Wright JR , Steinberg KP , Ruzinski JT , Caldwell E , Wong
WB , et al Serial changes in surfactant - associated proteins in lung and
serum before and after onset of ARDS Am J Respir Crit Care Med
1999 ; 160 ( 6 ): 1843 – 1850
15 Lewis JF , Jobe AH Surfactant and the adult respiratory distress
syn-drome Am Rev Respir Dis 1993 ; 147 ( 1 ): 218 – 233
16 Gunther A , Mosavi P , Heinemann S , Ruppert C , Muth H , Markart P ,
et al Alveolar fi brin formation caused by enhanced procoagulant and depressed fi brinolytic capacities in severe pneumonia Comparison
with the acute respiratory distress syndrome Am J Respir Crit Care
Med 2000 ; 161 ( 2 Pt 1 ): 454 – 462
17 Anderson WR , Thielen K Correlative study of adult respiratory distress syndrome by light, scanning, and transmission electron
microscopy Ultrastruct Pathol 1992 ; 16 ( 6 ): 615 – 628
18 McHugh LG , Milberg JA , Whitcomb ME , Schoene RB , Maunder RJ , Hudson LD Recovery of function in survivors of the acute respiratory
distress syndrome Am J Respir Crit Care Med 1994 ; 150 ( 1 ): 90 –
94
19 Orme J Jr , Romney JS , Hopkins RO , Pope D , Chan KJ , Thomsen G ,
et al Pulmonary function and health - related quality of life in
survi-vors of acute respiratory distress syndrome Am J Respir Crit Care Med
2003 ; 167 ( 5 ): 690 – 694
20 Neff TA , Stocker R , Frey HR , Stein S , Russi EW Long - term assess-ment of lung function in survivors of severe ARDS Chest 2003 ;
123 ( 3 ): 845 – 853
21 Bandi VD , Munnur U , Matthay MA Acute lung injury and acute respiratory distress syndrome in pregnancy Crit Care Clin 2004 ;
20 ( 4 ): 577 – 607
tant independent risk factors for death in patients with ARDS
[3,73,74]
While there are no established registries or studies involving
large numbers of cases of ALI and ARDS in pregnancy, data from
published series suggest outcomes in obstetric patients with this
complication can be expected to be similar or perhaps slightly
more favorable than outcomes in the general population In one
of the more recent published series, Catanzarite and colleagues
reported a mortality rate of 39% in a cohort of 28 pregnant
patients with ARDS, but other investigators reported mortality
rates ranging from a low of 24% up to 44% [5 – 7,75] The most
common cause of death in pregnancy - associated ALI/ARDS cases
has been multiple organ system failure [5]
Summary
Acute lung injury (ALI) and ARDS can complicate the course of
pregnancy and may result from a number of different causes,
which may be unrelated to the pregnancy (such as sepsis, trauma,
severe pancreatitis, or inhalation injury, to name only a few) or
may be unique to pregnancy (such as pre - eclampsia or amniotic
fl uid embolism) Management of these complications is directed
to the prompt treatment of the underlying precipitating cause,
and to supportive care in an intensive care unit In the absence
of pregnancy - specifi c data to guide supportive care, the existing
recommendations are based on evidence from studies in non
obstetric populations with ALI and ARDS Mechanical
ventila-tion is the mainstay of supportive management in severe ALI/
ARDS, and a low tidal volume approach with attention to
mater-nal P a CO 2 and acid – base status to avoid both excessive
hypercar-bia and excessive hyperventilation should be utilized Fluid
management, appropriate hemodynamic support, and
imple-menting measures to avoid nosocomial infections also should be
part of the routine critical care management of these patients
Unfortunately, none of the specifi c therapies which have been
studied (such as inhaled NO, surfactant, and corticosteroids)
have proven to be benefi cial in improving outcomes of ALI and
ARDS in adults
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Trang 10Critical Care Obstetrics, 5th edition Edited by M Belfort, G Saade,
M Foley, J Phelan and G Dildy © 2010 Blackwell Publishing Ltd.
William C Mabie
University of South Carolina, Greenville, SC, USA
Introduction
The clinical circumstances in which pulmonary edema is seen
during pregnancy are summarized in Table 25.1 The
pathophysi-ologic mechanism of the pulmonary edema may sometimes be
gleaned from the history, physical examination, laboratory data,
and chest radiograph For example, pulmonary edema occurring
in the setting of acute pyelonephritis suggests non - cardiogenic or
permeability edema On the other hand, even using
echocardiog-raphy and pulmonary artery catheterization; we have been unable
to fully understand the mechanisms involved in tocolytic - induced
pulmonary edema or that associated with pre - eclampsia, two of
the more common causes of pulmonary edema in pregnancy
Two stages in the formation of pulmonary edema are
recog-nized: interstitial and alveolar The physiology of lung fl uid
clear-ance will be reviewed briefl y The lung is divided into alveoli,
interstitium, and vessels Fluid enters the lung interstitium and is
pumped out by the lymphatics to the thoracic duct at about
20 mL/h at rest With strenuous exercise, interstitial edema may
be cleared at a rate up to 200 mL/h In patients with mitral
ste-nosis or chronic congestive heart failure, compensatory
hypertro-phy of the pulmonary lymphatics and vasculature prevents
alveolar fl ooding even with elevated hydrostatic pressure (e.g
pulmonary artery wedge pressure [PAWP] > 18 mmHg) and
interstitial edema formation rates
If the fl uid clearance mechanisms are exceeded and alveolar
edema results, type I and type II alveolar epithelial cells actively
transport fl uid back into the interstitium Fluid enters the cells
via the apical sodium channel and is extruded at the base of the
cells via the Na,K - ATPase pump with water following
isosmoti-cally (Figure 25.1 )
There are also water channels called aquaporins within cells
and between cells Aquaporins presumably have a role in water
homeostasis as evidenced by their increased expression in the neonatal period during rapid fl uid absorption following the ini-tiation of alveolar respiration [1]
Pathophysiology
Nearly all cases of pulmonary edema may be classifi ed under one
of four mechanisms: hydrostatic, permeability, lymphatic
insuf-fi ciency, and unknown or poorly understood (see Table 25.2 ) [2]
In perhaps 10% of cases, more than one mechanism may be operating (e.g fl uid overload in a septic patient with permeability edema) [3]
Hydrostatic p ulmonary e dema
Hydrostatic pulmonary edema includes cardiogenic causes, colloid osmotic pressure (COP) problems, and rare states result-ing in negative interstitial pressure such as rapid reexpansion of
a pneumothorax or acute airway obstruction (e.g blocked endo-tracheal tube) Excessive intravenous infusions of saline, plasma,
or blood can lead to a rise in PAWP and pulmonary edema Cardiogenic pulmonary edema can be further divided into disease resulting from systolic dysfunction (decreased myocardial squeeze, ejection fraction < 45%), diastolic dysfunction (impaired ventricular muscle relaxation resulting in high fi lling pressures),
or valvular disease (either stenosis or insuffi ciency) Systolic dysfunction is one of the major causes of pulmonary edema in pregnancy (e.g peripartum cardiomyopathy) and is the classic pathophysiologic mechanism of congestive heart failure [4,5] Congestive heart failure may be thought of from different points
of view – backward failure versus forward failure, or left heart failure versus right heart failure Discussing these viewpoints illustrates pathophysiologic mechanisms for the development of the signs and symptoms of heart failure
With backward failure there is accumulation of excess fl uid behind the failing ventricle In backward failure of the left heart, the ventricle does not empty normally Left ventricular end - diastolic pressure, wedge pressure, and pulmonary artery