A 67-year-old woman presents to the emergency room complaining of shortness of breath, chest pain, and a cold, painful left arm two weeks after undergoing a right total hip replacement. She had no previous history of cardiothoracic disease.
A 67-year-old woman presents to the emergency room complaining
of shortness of breath, chest pain, and a cold, painful left arm
two weeks after undergoing a right total hip replacement. She had
no previous history of cardiothoracic disease. On physical
examination, the patient was tachycardic at a rate of 110 and
tachypneic at a rate of 30. The woman's left arm was cold to the
touch and her pulses were decreased on the left side compared to
the right. Initial po2 on room air was 41%. Chest x-ray and ECG on
admission were within normal limits.
There was strong clinical concern for a pulmonary embolism, as
well as an arterial embolism, and the patient was sent for a
pulmonary arteriogram. Initially, it was difficult to pass the
catheter tip into the pulmonary artery, as the catheter tip
preferentially entered the left pulmonary vein (figure 1). Contrast
was injected into the right atrium and a communication between the
right and left atrium (patent foramen ovale) was demonstrated
(figure 2). The patient had no documented history of atrial septal
defect. Pulmonary arterial pressures measured 42/20 mm Hg.
Pulmonary arteriogram revealed multiple pulmonary emboli within the
left upper and lower lobes (figure 3).
Using the right femoral artery approach, subselective
catheterization of the left brachial artery was performed.
Arteriogram demonstrated complete occlusion of the left brachial
artery with a clot extending into the forearm (figure 4). The ulnar
artery filled at the wrist. Urokinase therapy was not started due
to the patient's recent postoperative status. An inferior vena cava
filter was placed, and the patient was placed on heparin and
subsequent coumadin therapy. Anticoagulation therapy resulted in
complete resolution of her pulmonary and left upper extremity
Paradoxical embolism, first described in 1877 by Connheim,1
refers to the passage of venous thrombus into the systemic
circulation through a right-to-left shunt. Several conditions must
be met in order to make the diagnosis of paradoxical embolism,
including the presence of venous thrombus; an abnormal
communication between the right and left circulation; a favorable
pressure gradient to promote a right-to-left shunt; and clinical,
angiographic, or pathologic evidence for systemic embolism.2 A
"proved" case of paradoxical embolism is defined as one in which a
venous thrombus is found trapped in an intracardiac defect during
echocardiography or at autopsy.3 Prior to 1980, very few "proved"
cases were documented in living patients. In the early 1980s,
invasve maneuvers performed during echocardiography became
useful for defining a patent foramen ovale in patients with
suspected paradoxical embolism.4-6 This led to an increase in the
number of "proved" cases, although proving the diagnosis of
paradoxical embolism during a patient's life remains a diagnostic
challenge. A "presumptive" diagnosis during life can be made when
the aforementioned conditions are met and when there is a favorable
temporal relationship between pulmonary and systemic emboli.
The diagnosis of paradoxical embolus should be considered in any
postoperative patient who has an unexpected arterial embolism.7
Risk factors are identical to those for pulmonary embolus. In order
for a venous thrombus to cross a patent foramen ovale, a
right-to-left pressure gradient must exist. Elevation of right
atrial pressure may be secondary to a chronic condition such as
chronic obstructive lung disease with cor pulmonale, tricuspid
valve disease, or primary pulmonary hypertension.7 More commonly
though, elevated right atrial pressures are secondary to an acute
process such as substantial pulmonary embolism with acute right
ventricular and atrial hypertension.7 The valsalva maneuver also
has been shown to cause a sudden rise in right sided pressures.
A presumptive diagnosis of paradoxical embolism was made in this
patient based on the temporal relationship between her pulmonary
and systemic emboli without an evident cardiac or systemic source
for the arterial embolus.7 Although this entity is uncommon, it
should be included in the differential diagnosis of arterial
embolism of which there is no obvious source.
1. Connheim J: Thrombose and embolie. VorIesung uber allgemeine
pathologie, Vol. 1, p.134. Berlin, Hirschwald, 1877.
2. Johnson BI: Paradoxical embolism. J Clin Pathol 4:316,
3. Loscalzo J: Paradoxical embolism: Clinical presentation,
diagnostic strategies, and thera-
peutic options. Am Heart J 112(1):141-145,
4. Higgins JR, Strunk BL, Shiller NB: Diagnosis of paradoxical
embolism with contrast echocardiography. Am Heart J 107:375,
5. Cheng TO: Echocardiogram and paradoxical embolism. Ann Intern
Med 95:515, 1981.
6. Rodgers DM, Singh S, Meister SG: Contrast echocardiographic
documentation of paradoxical embolism. Am Heart J 107:1270,
7. Sperber SJ, Horowitz D: Paradoxical embolism after surgery.
Hosp Pract 21(4):159-162, 1986.