Text of Venous Thromboembolism (VE)- Deep Vein Thrombosis (DVT) and Pulmonary Embolus (PE) Victoria E. Judd...
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Venous Thromboembolism (VE)- Deep Vein Thrombosis (DVT) and
Pulmonary Embolus (PE) Victoria E. Judd M.D.
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Objectives Discuss common presentation of Deep Vein Thrombosis
(DVT) and Pulmonary Embolism (PE) Describe evidence-based
diagnostic and therapeutic strategies for DVT/PE Identify when to
screen for a hypercoaguable state
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Causes of Thromboembolism Inherited Acquired
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Inherited VE Inherited thrombophilia Factor V Leiden mutation
Prothrombin gene mutation Protein S deficiency Protein C deficiency
Antithrombin (AT) deficiency Rare disorders Dysfibrinogenemia
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Other Plasma Factors In a single, large, population- based case
control study performed in the Netherlands, a two to threefold
increased risk for a first episode of venous thrombosis was found
for elevated levels of a number of plasma components, coagulant
factors, and inflammatory chemokines.
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Other Plasma Factors Plasma factor IX antigen Plasma factor XI
antigen Thrombin activatable fibrinolysis inhibitor (TAFI)
Interleukin 8 Fibrinogen Low levels of tissue factor pathway
inhibitor Low plasma fibrinolytic activity Elevated plasma
fibronectin levels
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Acquired VE Malignancy Presence of a central venous catheter
Surgery, especially orthopedic Trauma Pregnancy Oral contraceptives
Hormone replacement therapy
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Categories of risk for venous thromboembolism in surgical
patients Low risk: Minor surgery in patients
Categories of risk for venous thromboembolism in surgical
patients High risk: Surgery in patients >60, or Surgery in
patients aged 40-60 with additional risk factor* Risk of calf DVT:
20-40 percent Risk of proximal DVT: 4-8 percent Risk of clinical
PE: 2-4 percent Risk of fatal PE: 0.4-1.0 percent
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Categories of risk for venous thromboembolism in surgical
patients Highest risk: Surgery in patients >40 with multiple
risk factors*, or Hip or knee arthroplasty, hip fracture surgery,
or Major trauma, spinal cord injury Risk of calf DVT: 40-80 percent
Risk of proximal DVT: 10-20 percent Risk of clinical PE: 4-10
percent Risk of fatal PE: 0.2-5 percent
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Categories of risk for venous thromboembolism in surgical
patients * Additional risk factors include one or more of the
following: advanced age, cancer, prior venous thromboembolism,
obesity, heart failure, paralysis, or presence of a molecular
hypercoagulable state (e.g., protein C deficiency, factor V
Leiden). Data from Geerts, WH, et al. Chest 2004; 126:3385.
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Acquired VE Oral contraceptive pills that contain third-
generation progestins are the most important cause of thrombosis in
young women. The risk of thrombosis increases within four months of
the initiation of therapy and is unaffected by duration of use. The
risk decreases to previous levels within three months of cessation.
An increased risk for VTE has also been found in women using
contraceptive transdermal patches and ring.
Causes of Thromboembolism Fifty percent of thrombotic events in
patients with inherited thrombophilia are associated with the
additional presence of an acquired risk factor (e.g., surgery,
prolonged bed rest, pregnancy, oral contraceptives).
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Causes of Thromboembolism Some patients have more than one form
of inherited thrombophilia or more than one form of acquired
thrombophilia and appear to be at even greater risk for
thrombosis.
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Causes of Thromboembolism In a population-based study of the
incidence of venous thromboembolism (VTE), 56 percent of the
patients had three or more of the following six risk factors
present at the time of VTE:
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Causes of Thromboembolism >48 hours of immobility in the
preceding month Hospital admission Surgery Malignancy Infection in
the past three months Current hospitalization
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Incidence of pulmonary embolism according to distance traveled
by air
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This figure indicates the incidence of pumonary embolism per
million passenger arrivals, arranged according to flight distance
in kilometers. Error bars indicate 95 percent confidence limits. To
convert kilometers to miles, multiply by 0.62. Data from
Lapastolle, F, et al. N Engl J Med 2001; 345:779.
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Seasonal variation in venous thromboembolism
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Depicted are the monthly percentage variations in French
hospital admissions for deep vein thrombosis and pulmonary
embolism. Hospital admissions for venous thromboembolism were most
frequent in the winter and least frequent in the summer. Reproduced
with permission from: Boulay, F, Berthier, F, Schoukroun, G, et al.
Seasonal variations in hospital admission for deep venous
thrombosis and pulmonary embolism: analysis of discharge data. BMJ
2001; 323:601. Copyright 2001, BMJ.
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Risks Factors for DVT The risk of thrombosis is increased in
all forms of major injury. In one study of 716 patients admitted to
a regional trauma unit, DVT in the lower extremities was found in
58 percent of patients with adequate venographic studies; 18
percent had proximal vein thrombosis.
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Risks factors for DVT Thrombi were detected in: 54 percent of
patients with major head injuries 61 percent of patients with
pelvic fracture 77 percent of patients with tibial fracture 80
percent of those with femoral fracture.
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Risk Factors for DVT Minor injuries A large population- based
study investigated the VTE risk following a minor injury (i.e., one
not requiring surgery, a plaster cast, hospitalization, or extended
bed rest at home for at least four days). A minor injury occurring
in the preceding 3 to 4 weeks was associated with a 3- to 5-fold
increase in DVT risk. In carriers of factor V Leiden, this risk was
increased 50-fold.
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Risks Factors for DVT Intravenous drug use Direct trauma,
irritation, and infection may be responsible for the high incidence
of DVT noted in young drug users who inject these agents directly
into their femoral veins.
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Risk Factors for DVT Pregnancy Pregnancy is associated with an
increased risk of thrombosis that may be due in part to obstruction
of venous return by the enlarged uterus, as well as the
hypercoagulable state associated with pregnancy. Estimates of the
age-adjusted incidence of VTE range from 5 to 50 times higher in
pregnant versus non-pregnant women.
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Pathophysiology VIRCHOW'S TRIAD A major theory delineating the
pathogenesis of venous thromboembolism (VTE), often called
Virchow's triad, proposes that VTE occurs as a result of:
Alterations in blood flow (i.e., stasis) Vascular endothelial
injury Alterations in the constituents of the blood (i.e.,
inherited or acquired hypercoagulable state)
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Deep Vein Thrombosis (DVT) The thrombotic risk associated with
the inherited thrombophilias has been assessed in two ways:
evaluation of patients with deep vein thrombosis, and evaluation of
families with thrombophilia.
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DVT In a Spanish study of 2132 consecutive unselected patients
with venous thromboembolism, for example, 12.9 percent had an
anticoagulant protein deficiency (7.3 percent with protein S, 3.2
percent with protein C, and 0.5 percent with antithrombin). An
additional 4.1 percent had antiphospholipid antibodies (aPL).
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Risks and incidence of a first episode of venous thrombosis
Adult subjects only. Data from the Leiden Thrombophilia Study.
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Condition/risk factor(s)Relative risk Incidence, percent per
year Normal 10.008 Hyperhomocysteinemia (MTHFR 677T mutation)
2.50.02 Prothrombin gene mutation 2.80.02 Oral contraceptives 40.03
Factor V Leiden (heterozygous) 70.06 Oral contraceptives plus
heterozygous factor V Leiden 350.29 Factor V Leiden (homozygous)
800.5-1.0
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DVT Similar findings were noted in a series of 277 Dutch
outpatients with deep vein thrombosis: 8.3 percent had an isolated
deficiency of antithrombin, protein C, protein S, or plasminogen
compared to 2.2 percent of controls. The incidence of a protein
deficiency was only modestly greater in "high risk" patients with
recurrent, familial, or juvenile onset deep vein thrombosis (9, 16,
and 12 percent respectively).
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DVT The overall 8 to 13 percent incidence of an isolated
anticoagulant protein deficiency in patients with deep vein
thrombosis does not include the contribution of factor V Leiden or
the prothrombin gene mutation, now considered to be the most common
causes of inherited thrombophilia.
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DVT The Physicians' Health Study and the Leiden Thrombophilia
Study found a 12 to 19 percent incidence of heterozygosity for the
factor V Leiden mutation in patients with a first DVT (or pulmonary
embolism in the Physicians' Health Study) compared to 3 to 6
percent in controls.
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DVT The incidence reached 26 percent in the Physicians' Health
Study in 31 men over the age of 60 with no identifiable
precipitating factors. The incidence of the prothrombin gene
mutation is approximately 6 to 8 percent in patients with deep vein
thrombosis compared to 2 to 2.5 percent in controls.
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DVT The total incidence of an inherited thrombophilia in
subjects with a deep vein thrombosis ranges from 24 to 37 percent
overall compared to about 10 percent in controls. Another 25
percent of patients appear to have elevated factor VIII levels,
although it has not been proven that this is an inherited
characteristic.
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DVT There are a number of questions that arise when a patient
is suspected of having deep vein thrombosis (DVT) of the lower
extremity.
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DVT What is the differential diagnosis and what are the
possible risk factors for DVT? What is the best way to diagnose or
exclude DVT?
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DVT What is the appropriate initial therapy for DVT; when is
hospitalization not required? What is the recommended long- term
treatment for DVT (e.g., agents to use, monitoring the degree of
anticoagulation, length of time treatment is needed)?
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DVT When should one screen for the presence of a
hypercoagulable state, not only in the patient, but also in family
members?
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DVT INITIAL APPROACH When approaching the patient with
suspected DVT of the lower extremity, it is important to appreciate
that only a minority of patients actually have the disease and will
require anticoagulation.
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DVT This illustrates the importance of using validated
algorithms to evaluate patients with suspected DVT, along with
objective testing to establish the diagnosis. Given the potential
risks associated with proximal lower extremity DVT that is not
treated (e.g., fatal pulmonary emboli) and the potential risk of
anticoagulating a patient who does not have a DVT (e.g., fatal
bleeding), accurate diagnosis is essential.
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DVT History Classic symptoms of DVT include swelling, pain, and
discoloration in the involved extremity. There is not necessarily a
correlation between the location of symptoms and the site of
thrombosis.
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DVT History Symptoms in the calf alone are often the presenting
manifestation of significant proximal vein involvement, while some
patients with whole leg symptoms are found to have isolated calf
vein DVT.
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DVT History A complete thrombosis history includes the age of
onset, location of prior thromboses, and results of objective
diagnostic studies documenting thrombotic episodes in the patient,
as well as in any family members. A positive family history is
particularly important, since a well documented history of venous
thrombosis in one or more first-degree relatives strongly suggests
the presence of a hereditary defect.
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DVT History Recent potential precipitating conditions
Underlying conditions: i.e. cancer, collagen-vascular disorders
Medications
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DVT Physical Exam Special attention should be directed to: The
vascular system Extremities (e.g., looking for signs of superficial
or deep vein thrombosis) Chest Heart Abdominal organs Skin (e.g.,
skin necrosis, livedo reticularis).
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DVT Physical Exam There may be pain and tenderness in the thigh
along the course of the major veins ("painful deep vein syndrome").
Tenderness on deep palpation of the calf muscles is suggestive, but
not diagnostic. Homan's sign is unreliable.
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DVT Physical Exam A 2005 meta-analysis of diagnostic cohort
studies of patients with suspected DVT concluded the following
concerning these physical findings: Only a difference in calf
diameters (likelihood ratio, LR 1.8; 95% CI 1.5- 2.2) was of
potential value for ruling in DVT.
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DVT Physical Exam Only absence of calf swelling (LR 0.67; 95%
CI 0.58-0.78) and absence of a difference in calf diameters (LR
0.57; 95% CI 0.44-0.72) were of potential value for ruling out DVT
Individual clinical features are poorly predictive of DVT when not
combined in a formal prediction rule (e.g., Wells score, see
below).
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DVT Physical Exam Many patients are asymptomatic; however, the
history may include the following: Edema, principally unilateral,
is the most specific symptom. Massive edema with cyanosis and
ischemia (phlegmasia cerulea dolens) is rare. Leg pain occurs in
50% of patients, but this is entirely nonspecific. Pain can occur
on dorsiflexion of the foot (Homans sign).
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DVT Physical Exam Homans sign Discomfort in the calf muscles on
forced dorsiflexion of the foot with the knee straight has been a
time-honored sign of DVT. However, this sign is present in less
than one third of patients with confirmed DVT. The Homans sign is
found in more than 50% of patients without DVT and, therefore, is
nonspecific.
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DVT Physical Exam -Tenderness occurs in 75% of patients but is
also found in 50% of patients without objectively confirmed DVT.
-Clinical signs and symptoms of PE as the primary manifestation
occur in 10-50% of patients with confirmed DVT. -The pain and
tenderness associated with DVT does not usually correlate with the
size, location, or extent of the thrombus. -Warmth or erythema of
skin can be present over the area of thrombosis
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DVT Physical Exam oSuperficial thrombophlebitis is
characterized by the finding of a palpable, indurated, cordlike,
tender, subcutaneous venous segment. oForty percent of patients
with superficial thrombophlebitis without coexisting varicose veins
and with no other obvious etiology (e.g., intravenous catheters,
intravenous drug abuse, soft tissue injury) have an associated
DVT.
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DVT Differential Diagnosis In one study of 160 consecutive
patients with suspected DVT who had negative venograms, the
following causes of leg pain were identified: Muscle strain, tear,
or twisting injury to the leg 40 percent Leg swelling in a
paralyzed limb 9 percent
DVT Diagnosis The clinical assessment of patients with
suspected DVT is often difficult because of the interplay between
risk factors and the nonspecific nature of the physical findings.
Clinicians have observed that a discordance is often present
between the clinical assessment and the results of objective
testing.
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DVT Diagnosis One report of 593 patients with suspected DVT
validated a measure of pretest probability in conjunction with an
algorithm designed to minimize the use of venography or repeat
ultrasonography. The measure of pretest probability is referred to
as the Wells score or Wells criteria for DVT probability:
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DVT Diagnosis The Wells clinical prediction guide quantifies
the pretest probability of DVT. The model enables providers to
reliably stratify their patients into high-, moderate-, or low-risk
categories. Combining this with the results of objective testing
greatly simplifies the clinical workup of patients with suspected
DVT. The Wells clinical prediction guide incorporates risk factors,
clinical signs, and the presence or absence of alternative
diagnoses.
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DVT Diagnosis For example, patients deemed to be at high risk
for DVT may have a negative finding on duplex ultrasonographic
study. In this case, the probability of DVT is still greater than
20% when the known sensitivity, specificity, and negative
likelihood ratio of duplex ultrasonography are considered. Having
an objective method to determine pretest probability simplifies
clinical management.
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Wells Score Paralysis, paresis, or recent orthopedic casting of
a lower extremity (1 point) Recently bedridden for longer than
three days or major surgery within the past four weeks (1 point)
Localized tenderness in the deep vein system (1 point) Swelling of
an entire leg (1 point)
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Wells Score Calf swelling 3 cm greater that the other leg,
measured 10 cm below the tibial tuberosity (1 point) Pitting edema
greater in the symptomatic leg (1 point) Collateral non-varicose
superficial veins (1 point)
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Wells Score Active cancer or cancer treated within six months
(1 point) Alternative diagnosis more likely than DVT (e.g., Baker's
cyst, cellulitis, muscle damage, post phlebitic syndrome, inguinal
lymphadenopathy, external venous compression (-2 points)
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Clinical Parameter ScoreScore Active cancer (treatment ongoing,
or within 6 mo or palliative)+1 Paralysis or recent plaster
immobilization of the lower extremities+1 Recently bedridden for
>3 d or major surgery 3 cm compared with the asymptomatic leg+1
Pitting edema (greater in the symptomatic leg)+1 Previous DVT
documented+1 Collateral superficial veins (nonvaricose)+1
Alternative diagnosis (as likely or greater than that of DVT)-2
Total of Above Score High probability>3>3 Moderate
probability1 or 2 Low probability95 percent) and specific (>95
percent) for proximal vein thrombosis.">
Compression Ultrasonography Prospective studies have
demonstrated that lack of compressibility of a vein with the
ultrasound probe is highly sensitive (>95 percent) and specific
(>95 percent) for proximal vein thrombosis.
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Compression Ultrasonography Color flow imaging, in addition to
duplex Doppler ultrasound, is a less demanding study and is also
highly accurate for the diagnosis of above the knee DVT.
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Duplex-Doppler ultrasound image of an acute superficial femoral
vein thrombosis (labeled "V") Blue color indicates venous blood
flow and red indicates arterial blood flow (labeled "A"). Echogenic
white speckles are seen in the vein which was non- compressible
with the ultrasound probe.
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Compression Ultrasonography In comparison, the presence of an
echogenic band, although sensitive for DVT, has a specificity of
only about 50 percent. The variation of venous size with the
Valsalva maneuver has a low sensitivity and specificity for the
presence of DVT and is not performed in many centers.
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Compression Ultrasonography Serial studies need to be performed
when the initial test is negative; approximately 2 percent of
patients with an initially negative ultrasound develop a positive
study when retested seven days later. A single repeat study that is
negative five to seven days after an initial negative study
predicts a less than 1 percent likelihood of venous thromboembolism
over months of follow-up.
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Compression Ultrasonography oDuplex ultrasonography is also
helpful to differentiate venous thrombosis from hematoma, Baker
cyst, abscess, and other causes of leg pain and edema. oDiagnostic
accuracy varies depending on local expertise.
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MRI oMRI is the diagnostic test of choice for suspected iliac
vein or inferior vena caval thrombosis when CT venography is
contraindicated or technically inadequate. oIn the second and third
trimester of pregnancy, MRI is more accurate than duplex
ultrasonography because the gravid uterus alters Doppler venous
flow characteristics. oExpense, lack of general availability, and
technical issues limit its use.
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Screening For A Hypercoaguable State A biologic risk factor for
venous thrombosis can be identified in over 60 percent of Caucasian
patients with idiopathic DVT. In addition, there is often more than
one factor at play in a given patient. As an example, 50 percent of
thrombotic events in patients with inherited thrombophilia are
associated with an accompanying acquired risk factor (e.g.,
surgery, pregnancy, use of oral contraceptives).
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Screening For A Hypercoaguable State There is currently no
consensus regarding whom to test for inherited thrombophilia. The
likelihood of identifying an inherited thrombophilia is increased
several-fold by screening only patients with one or more of the
following:
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Screening For A Hypercoaguable State Initial thrombosis
occurring prior to age 50 without an immediately identified risk
factor (i.e., idiopathic or unprovoked venous thrombosis) A family
history of venous thromboembolism
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Screening For A Hypercoaguable State Recurrent venous
thrombosis Thrombosis occurring in unusual vascular beds such as
portal, hepatic, mesenteric, or cerebral veins A history of
warfarin-induced skin necrosis, which suggests protein C
deficiency
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Screening For A Hypercoaguable State Patients at increased risk
for inherited thrombophilia can be identified. There is no clear
clinical value to screening for the following reasons: Even if a
hypercoagulable workup uncovers abnormalities predisposing to VTE,
the strongest risk factor for VTE recurrence is the prior VTE event
itself, particularly if idiopathic.
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Screening For A Hypercoaguable State Patients with idiopathic
VTE, whether or not they have an identifiable inherited
thrombophilia, are at high risk for recurrence (as high as 7 to 8
percent per year in some studies) after warfarin is discontinued,
at least for the first few years after the event. Thus, the
presence or absence of an inherited thrombophilia will usually not
change the decision regarding length of warfarin therapy.
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Screening For A Hypercoaguable State Screening information can
be used to identify family members with an inherited thrombophilia,
but anticoagulant prophylaxis is rarely recommended in asymptomatic
affected family members outside of high risk situations.
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Screening For A Hypercoaguable State Screening test
interference A number of factors can interfere with screening tests
for thrombophilia. Therefore, it is generally best not to undertake
testing at the time of presentation with VTE.
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Screening For A Hypercoaguable State Confounding Factors Acute
thrombosis Heparin therapy Coumadin therapy
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Treatment of DVT The primary objectives of treatment of DVT are
to prevent and/or treat the following complications: Prevent
further clot extension Prevention of acute pulmonary embolism
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Treatment of DVT Reducing the risk of recurrent thrombosis
Treatment of massive iliofemoral thrombosis with acute lower limb
ischemia and/or venous gangrene (i.e., phlegmasia cerulea dolens)
Limiting the development of late complications, such as the
postphlebitic syndrome, chronic venous insufficiency, and chronic
thromboembolic pulmonary hypertension.
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Treatment of DVT Anticoagulant therapy is indicated for
patients with symptomatic proximal DVT, since pulmonary embolism
will occur in approximately 50 percent of untreated individuals,
most often within days or weeks of the event.
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Treatment of DVT The use of thrombolytic agents, surgical
thrombectomy, or percutaneous mechanical thrombectomy in the
treatment of venous thromboembolism must be individualized.
Patients with hemodynamically unstable PE or massive iliofemoral
thrombosis (i.e., phlegmasia cerulea dolens), and who are also at
low risk to bleed, are the most appropriate candidates for such
treatment.
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Treatment of DVT Inferior vena caval filter placement is
recommended when there is a contraindication to, or a failure of,
anticoagulant therapy in an individual with, or at high risk for,
proximal vein thrombosis or PE.
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Treatment of DVT It is also recommended in patients with
recurrent thromboembolism despite adequate anticoagulation, for
chronic recurrent embolism with pulmonary hypertension, and with
the concurrent performance of surgical pulmonary embolectomy or
pulmonary thromboendarterectomy.
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Treatment of DVT Oral anticoagulation with warfarin should
prolong the INR to a target of 2.5 (range: 2.0 to 3.0). If oral
anticoagulants are contraindicated or inconvenient, long- term
therapy can be undertaken with either adjusted-dose unfractionated
heparin, low molecular weight heparin, or fondaparinux.
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Treatment of DVT The general medical management of the acute
episode of DVT is individualized. Once anticoagulation has been
started and the patient's symptoms (i.e., pain, swelling) are under
control, early ambulation is advised.
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Treatment of DVT During initial ambulation, and for the first
two years following an episode of VTE, use of an elastic
compression stocking has been recommended to prevent the
postphlebitic syndrome.
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PE classification Acute vs. chronic Massive vs. submassive
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PE Classification A saddle PE is a PE that lodges at the
bifurcation of the main pulmonary artery into the right and left
pulmonary arteries. Most saddle PE are submassive. In a
retrospective study of 546 consecutive patients with PE, 14 (2.6
percent) had a saddle PE. Only two of the patients with saddle PE
had hypotension.
Slide 134
PE Epidemiology In a study of more than 42 million deaths that
occurred over a 20-year duration, almost 600,000 patients
(approximately 1.5 percent) were diagnosed with PE. PE was the
presumed cause of death in approximately 200,000. This study
certainly underestimates the true incidence and prevalence of PE,
since more than half of all PE are probably undiagnosed.
Slide 135
PE Prognosis PE is associated with a mortality rate of
approximately 30 percent without treatment, primarily due to
recurrent embolism. However, accurate diagnosis followed by
effective anticoagulant therapy decreases the mortality rate to 2
to 8 percent.
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PE Prognosis Poor Prognosis: Elevated Brain Natriuretic Peptide
(BNP) Right Ventricular dysfunction Hypotension RV thrombus
Elevated Troponin I
Slide 137
PE Pathophysiology Most PE arise from thrombi in the deep
venous system of the lower extremities. However, they may also
originate in the right heart or the pelvic, renal, or upper
extremity veins.
Slide 138
PE Pathophysiology Iliofemoral veins are the source of most
clinically recognized PE. It is estimated that 50 to 80 percent of
iliac, femoral, and popliteal vein thrombi (proximal vein thrombi)
originate below the popliteal vein (calf vein thrombi) and
propagate proximally. The remainder arise within the proximal
veins. Fortunately, most calf vein thrombi resolve spontaneously
and only 20 to 30 percent extend into the proximal veins if
untreated.
Slide 139
PE Pathophysiology After traveling to the lung, large thrombi
may lodge at the bifurcation of the main pulmonary artery or the
lobar branches and cause hemodynamic compromise. Smaller thrombi
continue traveling distally and are more likely to produce
pleuritic chest pain, presumably by initiating an inflammatory
response adjacent to the parietal pleura.
Slide 140
PE Pathophysiology Only about 10 percent of emboli cause
pulmonary infarction, usually in patients with preexisting
cardiopulmonary disease. Most pulmonary emboli are multiple, with
the lower lobes being involved in the majority of cases.
Slide 141
PE Pathophysiology Impaired gas exchange due to PE cannot be
explained solely on the basis of mechanical obstruction of the
vascular bed and alterations in the ventilation to perfusion ratio.
Gas exchange abnormalities are also related to the release of
inflammatory mediators, resulting in surfactant dysfunction,
atelectasis, and functional intrapulmonary shunting.
Slide 142
PE Risk Factors PE is a common complication of deep vein
thrombosis (DVT), occurring in more than 50 percent of cases with
phlebographically confirmed DVT. This suggests that factors that
promote the development of DVT also increase the risk for PE.
Slide 143
PE Additional Risks Factors in Women Obesity (BMI 29 kg/m2)
Heavy cigarette smoking (>25 cigarettes per day)
Hypertension
Slide 144
PE Symptoms Specific symptoms and signs are not helpful
diagnostically because their frequency is similar among patients
with and without PE. In the Prospective Investigation of Pulmonary
Embolism Diagnosis II (PIOPED II), the following frequencies of
symptoms and signs were noted among patients with PE who did not
have preexisting cardiopulmonary disease:
Slide 145
PE Symptoms Dyspnea at rest or with exertion (73 percent). The
onset of dyspnea was usually within seconds (46 percent) or minutes
(26 percent). Pleuritic pain (44 percent) Cough (34 percent)
>2-pillow orthopnea (28 percent) Calf or thigh pain (44 percent)
Calf or thigh swelling (41 percent), Wheezing (21 percent)
Slide 146
PE Signs The most common signs were Tachypnea (54 percent)
Tachycardia (24 percent) Rales (18 percent) Decreased breath sounds
(17 percent) An accentuated pulmonic component of the second heart
sound (15 percent), Jugular venous distension (14 percent)
Slide 147
PE DVT Symptoms Symptoms or signs of lower extremity deep
venous thrombosis (DVT) were common (47 percent). They included
edema, erythema, tenderness, or a palpable cord in the calf or
thigh.
Slide 148
PIOPED II Clinical characteristics of patients with acute
pulmonary embolism: data from PIOPED II. Stein PD; Beemath A; Matta
F; Weg JG; Yusen RD; Hales CA; Hull RD; Leeper KV Jr; Sostman HD;
Tapson VF; Buckley JD; Gottschalk A; Goodman LR; Wakefied TW;
Woodard PK. Am J Med. 2007 Oct;120(10):871-9.
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PE Labs Routine laboratory findings are nonspecific.
Leukocytosis An increased erythrocyte sedimentation rate (ESR)
Elevated serum LDH or AST (SGOT) Normal serum bilirubin.
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PE Arterial Blood Gases (ABGs) Arterial blood gas (ABG)
measurements and pulse oximetry have a limited role in diagnosing
PE. ABG s usually reveal hypoxemia, hypocapnia, and respiratory
alkalosis.
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PE ABGs Patients with room air pulse oximetry readings
