SEMINAR

ON
PULMONARY EMBOLISM

SUBMITTED TO ; SUBMITTED BY:

Mrs. Kavitha mam, C.Madhubala,

Associate professor M.Sc . Nursing II yr,

Dept. of OBG, Dept. of OBG,

MTPG&RIHS MTPG&RIHS
 PULMONARY EMBOLISM
Development Overview

Week 4 - laryngotracheal groove forms on floor foregut.

Week 5 - left and right lung buds push into the pericardioperitoneal canals
(primordia of pleural cavity)

Week 6 - descent of heart and lungs into thorax. Pleuroperitoneal foramen closes.

Week 7 - enlargement of liver stops descent of heart and lungs.

Month 3-6 - lungs appear glandular, end month 6 alveolar cells type 2 appear and
begin to secrete surfactant.

Month 7 - respiratory bronchioles proliferate and end in alveolar ducts and sacs.

Mechanisms

 Initiation - Budding of foregut endoderm to generate the trachea.

 Branching - A repeated mechanism of branching that is ongoing throughout
development to form the conducting bronchioles then alveolar ducts.
 Surface area increase - Expansion of the surface area in late development
generating eventually the thin air–blood barrier for gas exchange in the
acini.
 Vascular development - Extension of a vascular capillary tree within the
connective tissue and wall of the acini for gas exchange, and the lymphatic
development for immunology of the lungs.
 Surfactant development - allows lung inflation and decreases the work of
breathing and also related to immunology of the lungs.
 Musculoskeletal development - contributes the mechanical elements of
ribs, intercostals and diaphragm required for breathing.
Lung Development Stages

The sequence is most important rather than the actual timing, which is variable
both in development and in the existing literature.
Human Lung Stages

Lung Stage Human Features Vascular

lung buds originate as an outgrowth extra pulmonary

week 4 to
Embryonic from the ventral wall of the foregut artery then
5
where lobar division occurs lobular artery

conducting epithelial tubes surrounded

week 5 to Pre-acinar
Pseudoglandular by thick mesenchyme are formed,
17 arteries
extensive airway branching

bronchioles are produced, increasing

number of capillaries in close contact
week 16 Intra-acinar
Canalicular with cuboidal epithelium and the
to 25 arteries
beginning of alveolar epithelium
development

week 24 alveolar ducts and air sacs are alveolar duct

Saccular
to 40 developed arteries

secondary septation occurs, marked

late fetal alveolar
Alveolar increase of the number and size of
to 8 years capillaries
capillaries and alveoli

Embryonic stage
Human embryonic lung development

 Endoderm - tubular ventral growth from foregut pharynx.

 Mesoderm - mesenchyme of lung buds.
 Intraembryonic coelom - pleural cavities elongated spaces connecting
pericardial and peritoneal spaces.
 Vascular - extra pulmonary artery then lobular artery.
Pseudoglandular stage
 week 5 – 17
 tubular branching of the human lung airways continues
 by 2 months all segmental bronchi are present.
 lungs have appearance of a glandlike structure.
 stage is critical for the formation of all conducting airways.
 lined with tall columnar epithelium, the more distal structures are lined with
cuboidal epithelium.
 Vascular - Pre-acinar arteries.

Canalicular stage

 week 16 - 24
 canalicular phase of the bronchus can be mixed with the pseudoglandular
phase.
 Lung morphology changes dramatically, beginning of alveolar epithelium
development.
 differentiation of the pulmonary epithelium results in the formation of the
future air-blood tissue barrier.
 Surfactant synthesis.
 future gas exchange regions can be distinguished from the future conducting
airways of the lungs.
 Vascular - Intra-acinar arteries, canalization of the lung parenchyma by
capillaries begins, increasing number of capillaries in close contact with
cuboidal epithelium.

Saccular stage
 week 24 to near term.
 most peripheral airways form widened airspaces, termed saccules.
 saccules widen and lengthen the airspace (by the addition of new
generations).
 future gas exchange region expands significantly.
 Fibroblastic cells also undergo differentiation, they produce extracellular
matrix, collagen, and elastin. May have a role in epithelial differentiation
and control of surfactant secretion
 Vascular - alveolar duct arteries, vascular tree also grows in length and
 diameter during this time.

Alveolar stage
 near term through postnatal period.
 1-3 years postnatally alveoli continue to form through a septation process
increasing the gas exchange surface area.
 microvascular maturation occurs during this period.
 respiratory motions and amniotic fluid are thought to have a role in lung
maturation.
 Vascular - alveolar capillaries.

Lungs:

A major organ of the respiratory system, each lung houses structures of both the
conducting and respiratory zones. The main function of the lungs is to perform the
exchange of oxygen and carbon dioxide with air from the atmosphere. To this end,
the lungs exchange respiratory gases across a very large epithelial surface area—
about 70 square meters—that is highly permeable to gases.

Gross Anatomy of the Lungs

The lungs are pyramid-shaped, paired organs that are connected to the trachea by
the right and left bronchi; on the inferior surface, the lungs are bordered by the
diaphragm. The diaphragm is the flat, dome-shaped muscle located at the base of
the lungs and thoracic cavity. The lungs are enclosed by the pleurae, which are
attached to the mediastinum. The right lung is shorter and wider than the left lung,
and the left lung occupies a smaller volume than the right. The cardiac notch is an
indentation on the surface of the left lung, and it allows space for the heart . The
apex of the lung is the superior region, whereas the base is the opposite region near
the diaphragm. The costal surface of the lung borders the ribs. The mediastinal
surface faces the midline.

Each lung is composed of smaller units called lobes. Fissures separate these lobes
from each other. The right lung consists of three lobes: the superior, middle, and
inferior lobes. The left lung consists of two lobes: the superior and inferior lobes.
A bronchopulmonary segment is a division of a lobe, and each lobe houses
multiple bronchopulmonary segments. Each segment receives air from its own
tertiary bronchus and is supplied with blood by its own artery. Some diseases of
the lungs typically affect one or more bronchopulmonary segments, and in some
cases, the diseased segments can be surgically removed with little influence on
neighboring segments. A pulmonary lobule is a subdivision formed as the bronchi
branch into bronchioles. Each lobule receives its own large bronchiole that has
multiple branches. An interlobular septum is a wall, composed of connective
tissue, which separates lobules from one another.

Right lung
The right lung has both more lobes and segments than the left. It is divided into
three lobes, an upper, middle, and a lower lobe by two fissures, one oblique and
one horizontal. The upper, horizontal fissure, separates the upper from the middle
lobe. It begins in the lower oblique fissure near the posterior border of the lung,
and, running horizontally forward, cuts the anterior border on a level with
the sternal end of the fourth costal cartilage; on the mediastinal surface it may be
traced back to the hilum.
The lower, oblique fissure, separates the lower from the middle and upper lobes
and is closely aligned with the oblique fissure in the left lung.
The mediastinal surface of the right lung is indented by a number of nearby
structures. The heart sits in an impression called the cardiac impression. Above the
hilum of the lung is an arched groove for the azygos vein, and above this is a wide
groove for the superior vena cava and right brachiocephalic vein; behind this, and
close to the top of the lung is a groove for the brachiocephalic artery. There is a
groove for the esophagus behind the hilum and the pulmonary ligament, and near
the lower part of the esophageal groove is a deeper groove for the inferior vena
cava before it enters the heart.
The weight of the right lung varies between individuals, with a standard reference
range in men of 155–720 g (0.342–1.587 lb) and in women of 100–590 g (0.22–
1.30 lb).
Left lung
The left lung is divided into two lobes, an upper and a lower lobe, by the oblique
fissure, which extends from the costal to the mediastinal surface of the lung both
above and below the hilum. The left lung, unlike the right, does not have a middle
lobe, though it does have a homologous feature, a projection of the upper lobe
termed the "lingula". Its name means "little tongue". The lingula on the left serves
as an anatomic parallel to the right middle lobe, with both areas being predisposed
to similar infections and anatomic complications. There are two bronchopulmonary
segments of the lingula: superior and inferior.
The mediastinal surface of the left lung has a large cardiac impression where the
heart sits. This is deeper and larger than that on the right lung, at which level the
heart projects to the left.
On the same surface, immediately above the hilum, is a well-marked curved
groove for the aortic arch, and a groove below it for the descending aorta. The left
subclavian artery, a branch off the aortic arch, sits in a groove from the arch to near
the apex of the lung. A shallower groove in front of the artery and near the edge of
the lung, lodges the left brachiocephalic vein. The esophagus may sit in a wider
shallow impression at the base of the lung.
The weight of the left lung, by standard reference range, in men is 110–675 g
(0.243–1.488 lb) in women 105–515 g (0.231–1.135 lb).
Respiratory tract
The lower respiratory tract is part of the respiratory system, and consists of
the trachea and the structures below this including the lungs. The trachea receives
air from the pharynx and travels down to a place where it splits (the carina) into a
right and left bronchus. These supply air to the right and left lungs, splitting
progressively into the secondary and tertiary bronchi for the lobes of the lungs, and
into smaller and smaller bronchioles until they become the respiratory bronchioles.
These in turn supply air through alveolar ducts into the alveoli, where the exchange
of gases take place. Oxygen breathed in, diffuses through the walls of the alveoli
into the enveloping capillaries and into the circulation, and carbon dioxide diffuses
from the blood into the lungs to be breathed out.
Estimates of the total surface area of lungs vary from 50 to 75 square metres (540
to 810 sq ft); roughly the same area as one side of a tennis court.
The bronchi in the conducting zone are reinforced with hyaline cartilage in order to
hold open the airways. The bronchioles have no cartilage and are surrounded
instead by smooth muscle. Air is warmed to 37 °C (99 °F), humidified and
cleansed by the conducting zone; particles from the air being removed by
the cilia on the respiratory epithelium lining the passageways.
Pulmonary stretch receptors in the smooth muscle of the airways initiate
a reflex known as the Hering–Breuer reflex that prevents the lungs from over-
inflation, during forceful inspiration.

Blood Supply and Nervous Innervation of the Lungs

The blood supply of the lungs plays an important role in gas exchange and serves
as a transport system for gases throughout the body. In addition, innervation by the
both the parasympathetic and sympathetic nervous systems provides an important
level of control through dilation and constriction of the airway.

Blood Supply
The major function of the lungs is to perform gas exchange, which requires blood
from the pulmonary circulation. This blood supply contains deoxygenated blood
and travels to the lungs where erythrocytes, also known as red blood cells, pick up
oxygen to be transported to tissues throughout the body. The pulmonary artery is
an artery that arises from the pulmonary trunk and carries deoxygenated, arterial
blood to the alveoli. The pulmonary artery branches multiple times as it follows the
bronchi, and each branch becomes progressively smaller in diameter. One arteriole
and an accompanying venule supply and drain one pulmonary lobule. As they near
the alveoli, the pulmonary arteries become the pulmonary capillary network. The
pulmonary capillary network consists of tiny vessels with very thin walls that lack
smooth muscle fibers. The capillaries branch and follow the bronchioles and
structure of the alveoli. It is at this point that the capillary wall meets the alveolar
wall, creating the respiratory membrane. Once the blood is oxygenated, it drains
from the alveoli by way of multiple pulmonary veins, which exit the lungs through
the hilum.
Nervous Innervation
Dilation and constriction of the airway are achieved through nervous control by the
parasympathetic and sympathetic nervous systems. The parasympathetic system
causes bronchoconstriction, whereas the sympathetic nervous system
stimulates bronchodilation. Reflexes such as coughing, and the ability of the
lungs to regulate oxygen and carbon dioxide levels, also result from this autonomic
nervous system control. Sensory nerve fibers arise from the vagus nerve, and from
the second to fifth thoracic ganglia. The pulmonary plexus is a region on the lung
root formed by the entrance of the nerves at the hilum. The nerves then follow the
bronchi in the lungs and branch to innervate muscle fibers, glands, and blood
vessels.

Pleura of the Lungs

Each lung is enclosed within a cavity that is surrounded by the pleura. The pleura
(plural = pleurae) is a serous membrane that surrounds the lung. The right and left
pleurae, which enclose the right and left lungs, respectively, are separated by the
mediastinum. The pleurae consist of two layers. The visceral pleura is the layer
that is superficial to the lungs, and extends into and lines the lung fissures. In
contrast, the parietal pleura is the outer layer that connects to the thoracic wall,
the mediastinum, and the diaphragm. The visceral and parietal pleurae connect to
each other at the hilum. The pleural cavity is the space between the visceral and
parietal layers.

The pleurae perform two major functions: They produce pleural fluid and create
cavities that separate the major organs. Pleural fluid is secreted by mesothelial
cells from both pleural layers and acts to lubricate their surfaces. This lubrication
reduces friction between the two layers to prevent trauma during breathing, and
creates surface tension that helps maintain the position of the lungs against the
thoracic wall. This adhesive characteristic of the pleural fluid causes the lungs to
enlarge when the thoracic wall expands during ventilation, allowing the lungs to
fill with air. The pleurae also create a division between major organs that prevents
interference due to the movement of the organs, while preventing the spread of
infection.

Everyday connection:

The Effects of Second-Hand Tobacco Smoke

The burning of a tobacco cigarette creates multiple chemical compounds that are
released through mainstream smoke, which is inhaled by the smoker, and through
sidestream smoke, which is the smoke that is given off by the burning cigarette.
Second-hand smoke, which is a combination of sidestream smoke and the
mainstream smoke that is exhaled by the smoker, has been demonstrated by
numerous scientific studies to cause disease. At least 40 chemicals in sidestream
smoke have been identified that negatively impact human health, leading to the
development of cancer or other conditions, such as immune system dysfunction,
liver toxicity, cardiac arrhythmias, pulmonary edema, and neurological
dysfunction. Furthermore, second-hand smoke has been found to harbor at least
250 compounds that are known to be toxic, carcinogenic, or both. Some major
classes of carcinogens in second-hand smoke are polyaromatic hydrocarbons
(PAHs), N-nitrosamines, aromatic amines, formaldehyde, and acetaldehyde.

Tobacco and second-hand smoke are considered to be carcinogenic. Exposure to

second-hand smoke can cause lung cancer in individuals who are not tobacco users
themselves. It is estimated that the risk of developing lung cancer is increased by
up to 30 percent in nonsmokers who live with an individual who smokes in the
house, as compared to nonsmokers who are not regularly exposed to second-hand
smoke. Children are especially affected by second-hand smoke. Children who live
with an individual who smokes inside the home have a larger number of lower
respiratory infections, which are associated with hospitalizations, and higher risk
of sudden infant death syndrome (SIDS). Second-hand smoke in the home has also
been linked to a greater number of ear infections in children, as well as worsening
symptoms of asthma.

PULMONARY EMBOLISM

Pulmonary embolism occurs when a clot (thrombus) breaks free from the
vessel wall (most commonly from the pelvic vein), travels to the heart, and then
through the pulmonary circulation, where it lodges and interrupts the blood flow to
the lungs. (The clot that migrates and cre- ates a blockage is called a pulmonary
embolus.) If a large area of lung tissue is deprived of blood flow, cardiovas- cular
collapse ultimately occurs, which can be fatal.
Pulmonary embolism is the leading cause of maternal deaths in many centers
especially in the developed countries after the sharp decline of maternal mortality
due to hemorrhage, hypertension and sepsis. While deep venous thrombosis in the
leg or in the pelvis is most likely the cause of pulmonary embolism, but in about
80–90%, it occurs without any previous clinical manifestations of deep vein
thrombosis. The predisposing factors are those already mentioned in venous
thrombosis. The clinical features depend on the size of the embolus and on the
preceding health status of the patient. The classical symptoms of massive
pulmonary embolism are sudden collapse with acute chest pain and air hunger.
Death usually occurs within short time from shock and vagal inhibition
Although it causes approximately 10 percent of maternal deaths, pulmonary
embolism is relatively uncommon during pregnancy and the puerperium. The
incidence averages 1 in 7000 pregnancies. According to Marik and Plante (2008),
70 percent of gravidas presenting with a pulmonary embolism have associated
clinical evidence of deep-vein thrombosis. And recall that between 30 and 60
percent of women with a deep-vein thrombosis will have a coexisting silent
pulmonary embolism.

Clinical Presentation

In almost 2500 nonpregnant patients with a proven pulmonary embolism,

symptoms included dyspnea in 82 percent, chest pain in 49 percent, cough in 20
percent, syncope in 14 percent, and hemoptysis in 7 percent (Goldhaber, 1999).
Pollack and coworkers (2011) found similar symptoms. Other predominant clinical
findings typically include tachypnea, apprehension, and tachycardia. In some
cases, an accentuated pulmonic closure sound, rales, and/or friction rub is heard.

Right axis deviation and T-wave inversion in the anterior chest leads may be
evident on the electrocardiogram. In at least 40 percent, chest radiography results
are normal. In others, nonspecific findings may include atelectasis, an infiltrate,
cardiomegaly, or an eusion (Pollack, 2011). Vascular markings in the lung region
supplied by the obstructed artery can be lost. Although most women are
hypoxemic, a normal arterial blood gas analysis does not exclude pulmonary
embolism. Approximately a third of young patients have Po2 values >80 mm Hg.
Thus, the alveolar-arterial oxygen tension dierence is a more useful indicator of
disease. More than 86 percent of patients with acute pulmonary embolism will
have an alveolar-arterial dierence >20 mm Hg (Lockwood, 2012). Even with
massive pulmonary embolism, signs, symptoms, and laboratory data to support the
diagnosis may be deceptively nonspecific.

INCIDENCE AND MORTALITY OF PE

While no exact epidemiological data are available, the incidence of PE is estimated

to be approximately 60 to 70 per 100,000, and that of venous thrombosis
approximately 124 per 100,000 of the general population . The European
guidelines for the diagnosis and management of PE report annual incidence rates
of venous thrombosis and PE of approximately 0.5 to 1.0 per 1000 inhabitants .
However, the actual figures are likely to be substantially higher because silent PE
can develop in up to 40% to 50% of patients with deep vein thrombosis (DVT) . In
addition, autopsy studies have shown that PE had been diagnosed before death in
30% to 45% of patients . After coronary artery disease and stroke, acute PE ranks
third among the most common types of cardiovascular diseases. While clinical data
indicate that most cases of PE occur at 60 to 70 years of age, autopsy data show the
highest incidence among individuals 70 to 80 years of age. If untreated, acute PE is
associated with a significant mortality rate (as high as 30%), whereas the death rate
of diagnosed and treated PE is 8%. Up to 10% of acute PE patients die suddenly.
Two of three patients succumbing to PE die within 2 h after presentation.
Risk Factors :

■ Normal physiological changes in coagulation related to pregnancy

■ Cesarean birth, which has a risk five times greater than vaginal birth

■ Endometritis, which can spread to the vascular system causing thrombophlebitis

and can lead to thrombosis

■ Decreased mobility, which increases the risk for venous stasis

■ Obesity, which places extra pressure on pelvic vessels, causing venous stasis

■ Increased parity
PATHOPHYSIOLOGY

PE occurs when clots formed in the deep venous system dislodge or break loose,
travel through the heart, and become lodged in the pulmonary vasculature. While
small PE can frequently lyse spontaneously, larger PE can cause a sudden and
persistent rise in pulmonary artery pressure, which can lead to circulatory collapse.
Clot formation usually begins at sites of tissue or vascular trauma where recruited
activated monocytes expose blood to tissue factor on their surfaces and overwhelm
the body’s natural anticoagulant and fibrinolytic mechanisms. These deep venous
thrombi (DVT), composed mainly of red blood cells, platelets, and fibrin, tend to
form in the venous sinuses or cusps of the lower extremity deep veins. While the
main concern is that part or all of a DVT will embolize to the pulmonary
vasculature, the vascular congestion caused by DVT also has multiple effects on
the limb. There is often associated swelling and discomfort, as well as eventual
loss of valve competency. This allows for lack of forward flow causing more
swelling, stasis, and thrombus propagation.
A longer-term complication is “post-thrombotic syndrome” which can result if
these changes persist over time. Post-thrombotic syndrome consists of a
constellation of symptoms including calf pain, swelling, and stasis skin changes,
especially hyperpigmentation at the medial malleolus. It affects approximately half
of patients who suffer DVT, although the onset can be delayed several years
following DVT formation .
Once a clot becomes lodged in the pulmonary vasculature, it causes obstruction.
The extent of this obstruction, combined with the presence of any underlying
cardiopulmonary disease are the most important factors in determining whether
right ventricular dysfunction will develop [4]. The blockage, combined with the
release of vasoactive mediators, causes a sudden rise in pulmonary artery pressure,
which increases right ventricular afterload. The right ventricle, a thin-walled
structure compared to the robust left ventricle, can dilate and become hypokinetic
in response to the rapid rise in afterload. Right ventricular dilatation can ultimately
lead to under-filling of the left ventricle as the interventricular septum protrudes
into the left ventricle, decreasing cardiac output and coronary perfusion which, in
turn, can lead to eventual circulatory collapse .
Assessment Findings:

 Positive Homans’sign
 Tenderness and heat over the affected area
 Leg pain with walking
 Swelling in the affected leg

Massive Pulmonary Embolism

This is defined as embolism causing hemodynamic instability (Tapson, 2008).

Acute mechanical obstruction of the pulmonary vasculature causes increased
vascular resistance and pulmonary hypertension followed by acute right ventricular
dilation. In otherwise healthy patients, significant pulmonary hypertension does not
develop until 60 to 75 percent of the pulmonary vascular tree is occluded (Guyton,
1954). Moreover, circulatory collapse requires 75- to 80-percent obstruction. This
is depicted schematically in Figure 52-4 and emphasizes that most acutely
symptomatic emboli are large and likely a saddle embolism. These are suspected
when the pulmonary artery pressure is substantively increased as estimated by
echocardiography.

If there is evidence of right ventricular dysfunction, the mortality rate approaches

25 percent. This compares with a 1-percent rate without such dysfunction (Kinane,
2008). It is important in these cases to infuse crystalloids carefully and to support
blood pressure with vasopressors. As discussed in Management, oxygen treatment,
endotracheal intubation, and mechanical ventilation are completed preparatory to
thrombolysis, filter placement, or embolectomy (Tapson, 2008).

Diagnosis

In most cases, recognition of a pulmonary embolism requires a high index of

suspicion that prompts objective evaluation. Exposure of the mother and fetus to
ionizing radiation is a concern when investigating a suspected pulmonary
embolism during pregnancy. However, this concern is largely overruled by the
hazards of missing a potentially fatal diagnosis. Moveover, erroneously assigning a
diagnosis of pulmonary embolism to a pregnant woman is also fraught with
problems. It unnecessarily exposes the mother and fetus to the risks of
anticoagulation treatment and will impact delivery plans, future contraception, and
thromboprophylaxis during subsequent pregnancies. Therefore, investigations
should aim at diagnostic certainty (Konstantinides, 2014).

In 2011, the American Thoracic Society and the Society of Thoracic Radiology
developed an algorithm—shown in Figure 52-5 for the diagnosis of pulmonary
embolism during pregnancy (Leung, 2011). In addition to compression
ultrasonography, which was previously discussed (Deep-Vein Thrombosis), the
algorithm includes computed-tomographic pulmonary angiography (CTPA) and
ventilation-perfusion scintigraphy.
Computed Tomographic Pulmonary Angiography

Multidetector computed tomography with pulmonary angiography is currently the

most commonly employed technique used for pulmonary embolism diagnosis in
nonpregnant patients (Bourjeily, 2012; Pollack, 2011). The estimated fetal
radiation exposure averages 0.45 to 0.6 mGy. The estimated maternal breast dose
is 10 to 70 mGy (Waksmonski, 2014).

Bourjeily and colleagues (2012) performed a follow-up study of 318 pregnant

women who had a negative CTPA performed for a suspected pulmonary
embolism. All were seen 3 months following their initial presentation or at 6 weeks
postpartum. None of these women were subsequently diagnosed with a
thromboembolism.

CTPA has many advantages, but we find that the higher resolution allows detection
of previously inaccessible smaller distal emboli that have uncertain clinical
significance. Similar observations have been reported by others (Anderson, 2007;
Hall, 2009). Also, the hyperdynamic circulation and augmented plasma volume
associated with pregnancy leads to a higher number of nondiagnostic studies
compared with nonpregnant patients (Ridge, 2011; Scarsbrook, 2006).

Ventilation–Perfusion Scintigraphy—Lung Scan

This technique involves a small dose of radiotracer such as intravenously

administered technetium-99m–macroaggregated albumin. There is negligible fetal
and maternal breast radiation exposure—0.1 to 0.4 mGy. The scan may not provide
a definite diagnosis because many other conditions can cause perfusion defects.
Examples are pneumonia or local bronchospasm. Chan and coworkers (2002)
found that a fourth of ventilation-perfusion scans in pregnant women were
nondiagnostic. In these instances, CTPA is preferred (Tromeur, 2017).

To compare the performance of lung scintigraphy and CTPA, Revel and colleagues
(2011) evaluated 137 pregnant women with suspected pulmonary embolism. The
two modalities performed comparably and had no significant dierences between
the proportions of positive, negative, or indeterminate results. Specifically, the
proportion of indeterminate results for both approximated 20 percent. By way of
comparison, about a fourth of the nonpregnant population had indeterminate
studies. The investigators attributed this dierence to the younger age of the
pregnant patients. Similarly, one systematic review concluded that both CTPA and
lung scintigraphy seem appropriate for exclusion of pulmonary embolism during
pregnancy (van Mens, 2017).

Intravascular Pulmonary Angiography

This requires catheterization of the right side of the heart and is considered the
reference test for pulmonary embolism. With newer generation multidetector CT
scanners, however, the role of invasive pulmonary angiography has been
questioned. This is especially true given the higher radiation exposure for the fetus
(Konstantinides, 2014; Kuriakose, 2010). Other detractions are that it can be time
consuming, uncomfortable, and associated with dye-induced allergy and renal
failure. Indeed, the procedure-related mortality rate approximates 1 in 200 (Stein,
1992). It is reserved for confirmation when less invasive tests are equivocal.
Management

Immediate treatment for pulmonary embolism is full anticoagulation similar to that

for deep-vein thrombosis as discussed in Unfractionated Heparin. Several
complementary procedures may be indicated.

Vena Caval Filters

The woman who has very recently suered a pulmonary embolism and who must
undergo cesarean delivery presents a particularly serious problem. Reversal of
anticoagulation may be followed by another embolus, and surgery while fully
anticoagulated frequently results in life-threatening hemorrhage or troublesome
hematomas. In these cases, placement of a vena caval filter should be considered
before surgery (Marik, 2008). Moreover, in the very infrequent circumstances in
which heparin therapy fails to prevent recurrent pulmonary embolism from the
pelvis or legs, or when embolism develops from these sites despite heparin
treatment, a vena caval filter may also be indicated. Such filters can also be used
following massive emboli in patients who are not candidates for thrombolysis
(Deshpande, 2002).

The device is inserted through either the jugular or femoral vein and can be
inserted during labor (Jamjute, 2006). Routine filter placement has no added
advantage to heparin given alone (Decousus, 1998). Retrievable filters may be
used as short-term protection and then removed 1 to 2 weeks later (Liu, 2012).
From their systematic review, Harris and associates (2016) found that complication
rates in pregnant women with vena caval filters are comparable to those in
nonpregnant patients.

Thrombolysis

Compared with heparin, thrombolytic agents provide more rapid lysis of

pulmonary clots and improvement of pulmonary hypertension (Tapson, 2008).
Konstantinides and coworkers (2002) studied 256 nonpregnant patients receiving
heparin for an acute submassive pulmonary embolism. They also were randomly
assigned to a placebo or the recombinant tissue plasminogen activator a l t e p l a s
e . Those given the placebo had a threefold greater risk of death or treatment
escalation compared with those given alteplase. Agnelli and associates (2002)
performed a metaanalysis of trials involving 461 nonpregnant patients. They
reported that the risk of recurrence or death was significantly lower in patients
given thrombolytic agents and heparin compared with those given heparin alone—
10 versus 17 percent. Importantly, however, there were five—2 percent—fatal
bleeding episodes in the thrombolysis group and none in the heparin-only group.

In their review, Leonhardt and colleagues (2006) identified 28 reports of tissue

plasminogen activator use during pregnancy. Ten cases were for
thromboembolism. Complication rates were similar to those in nonpregnant
patients, and the authors concluded that such therapy should not be withheld during
pregnancy if indicated. However, Akazawa and Nishida (2017) reviewed 13 cases
of systemic thrombolytic therapy administered during the first 48 hours aer
delivery. Blood transfusion was required in five of the eight cesarean deliveries,
including three cases of hysterectomy and two cases of hematoma removal.

Embolectomy

Given the eicacy of thrombolysis and filters, surgical embolectomy is uncommonly

indicated. Published experience with emergency embolectomy during pregnancy is
limited to case reports (Colombier, 2015; Saeed, 2014). From their review, Ahearn
and associates (2002) found that although the operative risk to the mother is
reasonable, the stillbirth rate is 20 to 40 percent.
Nursing Actions :

■ Review prenatal and labor records for risk factors.

■ Monitor women who are at greater risk for thrombosis more frequently.

■ Apply compression stockings as per orders.

■ Assist with ambulation. Early ambulation increases circulation and decreases the
risk of venous stasis.

■ Report assessment finding of possible signs of thrombosis to the physician or

CNM for further evaluation.

■ Administer medications as per orders, which include analgesia for pain and
anticoagulants.
Prevention

Pulmonary embolism may be preventable in those with risk factors. People

admitted to hospital may receive preventative medication, including
unfractionated heparin, low molecular weight heparin (LMWH), or fondaparinux,
and anti-thrombosis stockings to reduce the risk of a DVT in the leg that could
dislodge and migrate to the lungs.
Following the completion of anticoagulation in those with prior PE, long-term
aspirin is useful to prevent recurrence.

COMPLICATION:

A pulmonary embolism (PE) can cause a lack of blood flow that leads to lung
tissue damage. It can cause low blood oxygen levels that can damage other organs
in the body, too.

A PE, particularly a large PE or many clots, can quickly cause serious life-
threatening problems and, even death.

Treatment of a PE often involves anti-coagulation medicines or blood thinners.

These medicines can put you at a risk for excessive bleeding if they thin the blood
too much. Excessive bleeding is bleeding that won't stop after applying pressure
for 10 minutes. Other symptoms of bleeding to watch for include:

Signs of bleeding in the digestive system:

 Bright red vomit or vomit that looks like coffee grounds

 Bright red blood in your stool or black, tarry stools
 Abdominal pain

Signs of bleeding in the brain:

 Severe headache
 Sudden vision changes
 Sudden loss of movement or feeling in your legs or arms
 Memory loss or confusion

If you have any of these, you need to get treatment right away.