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a paradoxical embolism ( pde ) is defined as a systemic arterial embolism that enters from the venous thrombi into the arterial circulatory system through a right - to - left shunt .
the most common right - to - left shunt , associated with pdes , is patent foramen ovale ( pfo ) , which has been reported as an important cause of cryptogenic strokes.1 - 3 ) in addition to the isolated cryptogenic strokes , related to pfos , the coexistence of pulmonary thromboembolisms ( pte ) and deep vein thromboses ( dvt ) have also been reported,4 - 6 ) as rare cases of arterial systemic embolic involvement through pfo.7 - 9 ) here , we report a rare case of cryptogenic stroke , caused by a pde through pfo , which is complicated with massive pte , dvt , and renal infarctions .
a 52-year - old woman was transferred to our emergency room ( er ) with a 10-hour history of left - side weakness , and a sudden onset of slurred speech , with a clear mental state . her previous medical , medication , and familial histories were unremarkable , and she was a non - smoker .
upon arrival in the er , she was hemodynamically stable and her electrocardiogram showed a normal sinus rhythm . however , a magnetic resonance diffusion image of her brain revealed an infarction of the right middle cerebral artery territory ( fig .
1a ) , and a magnetic resonance angiogram of the cerebral and carotid arteries showed a total obstruction of the genu branch of the right middle cerebral artery ( fig .
she was immediately admitted to the neurologic intensive care unit , with a diagnosis of acute cerebral infarction .
further studies were then ordered , since the etiology of the cerebral infarction was unclear . to evaluate the intracardiac source of the embolism , a transthoracic echocardiogram ( tte ) and transesophageal echocardiogram ( tee ) were performed after 1 week .
the tte revealed no evidence of embolism ; however , the tee revealed separation of the septum primum from the septum secundum that constitutes a pfo , up to 6 mm , according to the pressure variance ( fig .
2a ) , and an agitated saline injection test was used to identify the right - to - left microbubble shunting , during a valsalva maneuver used to confirm the pfo presence ( fig .
2b ) . based on these tests , we subsequently recommended an anticoagulation therapy based on warfarinization . the day after these initial tests ,
she then displayed severe hypoxemia and hypotension , and was immediately intubated and initiated the ventilator care .
a computed tomography ( ct ) image of her chest was taken after starting the ventilator care , which showed massive thromboembolisms in the right pulmonary artery and left pulmonary segmental artery ( fig .
3a ) , indicating an acute pte . because she was in a hemodynamically compromised state , we considered the use of thrombolytic therapy , in spite of the general contraindication of a recent cerebral infarction .
after the discussion with a neurologist , we decided to treat her with a half dosage of recombinant tissue plasminogen activator { rtpa , actylase ( boehringer ingelheim , ingelheim , germany ) ; 45 mg total } in order to treat the massive pte . within 2 - 3 hours after an intravenous infusion of the thrombolytic agent , hypoxemia and hypotension symptoms returned to a normal state .
after stabilization of her vital signs , we checked for the presence of dvt ; the ct venogram of her lower extremities showed thrombi on her left iliac vein and both peroneal veins ( fig .
4a and b ) . on the arterial phase of this ct , previous thrombi in the right main pulmonary and left segmental arteries were resolved ( fig .
3b ) . in addition , there were newly developed multiple wedge - shaped hypoperfusion lesions in both kidneys , compatible with an acute renal infarction ( fig .
4c ) . a work - up of vasculopathies , hypercoagulable states , and hematologic disorders proved unremarkable .
as a result of this treatment plan , the patient was discharged 20 days after admission , and has since been visiting the out - patient department on a regular basis without recurrence of these ischemic events .
because there is considerable evidence suggesting that pfo is highly associated with cryptogenic strokes , pfo detection during the evaluation of a patient having a cryptogenic stroke is not surprising .
but , when the pfo is detected in a patient having a cryptogenic stroke , the presence of dvt and pte always have to be a matter of concern .
in our case , dvt was detected after the event of a massive pte , without previous definitive symptoms or signs of dvt .
as such , we are not able to explain precisely whether these dvt and subsequent pte were present before the stroke , or produced during her admission and immobilization . however , searching for the coexistence of pte or dvt and their prophylaxis with anticoagulation could be a more important process . in literature , clergeau et al.4 )
demonstrated that pfo is an independent predictor of the silent brain ischemia in patients with pte , and concluded that patients having cryptogenic stroke and pfo may require a systematic search for silent thromboembolisms .
tanislav et al.10 ) reported that the silent ptes frequently occur in patients with cryptogenic strokes and pfos . also , the paradoxical embolism from large veins in ischemic stroke study addressed direct evidence of the increased frequency of dvt , among patients with cryptogenic strokes and pfos.6 ) this patient in our case had a recent stroke and experienced a hemodynamically compromised state , due to a massive pte .
in this situation , we had difficulty in making a therapeutic decision between the beneficial effects of thrombolysis on the hemodynamic instability of the massive pte , and the potentially catastrophic effect of a cerebral hemorrhage .
as such , after the discussion with a neurologist , we administrated a half dose of rtpa , and this modified thrombolytic therapy enabled the patient to make a good recovery from hemodynamic instability . in literature , there are number of case reports presenting similar situations.5)11 ) however , our case was notably different from these cases , both in terms of the timing of the stroke and the treatment modality .
therefore , other therapeutic options , including surgical or catheter embolectomy , must be considered when there are contraindications for systemic thrombolysis , like in our case.12 ) however , because there was a lack of experience of invasive embolectomy in our center , and these kinds of modalities are traditionally chosen in case of failure of systemic thrombolysis , we chose a systemic thrombolytic therapy .
also , there is no strong evidence to support a particular therapeutic option under the specific conditions of a stroke on a pfo , associated with pte .
thus , every treatment modality ranging from a more conservative approach with anticoagulation alone to a more aggressive approach with invasive thrombectomy should be considered on a case - by - case basis . in this case , there was an acute renal infarction , detected on the arterial phase of the ct venogram , suspected to be a result of a pde ; this renal infarction was not detected on the first ct angiogram when the pulmonary embolism was diagnosed .
the mechanism of the renal infarction in our case was considered that transiently increased right arterial hypertension , due to acute pulmonary embolism induced continuous opening of pfo and permitted a passage of the thrombi in deep vein into the arterial system.11 ) it should also be noted that though there have been several case reports of systemic pdes with pte associated with pfo,7)8)13 ) cases of non - cerebral , systemic pdes , associated with pfo , are relatively lower than for cerebral pdes .
one report showed that only 2.9% of patients with pfo presented with a presumptive diagnosis of systemic embolism,14 ) though when patients with major pulmonary embolism have pfo , the incidence of peripheral artery embolisms , can significantly be increased ( up to 15%).15 ) we are following up this patient with anticoagulation using warfarin , and this patient has not shown recurrent cerebral ischemia or thrombotic events .
however , the closure of pfo is considered to eliminate the risk of pde , and to no longer require the use of warfarin .
also , many studies have shown the favorable outcomes of percutaneous device closure of pfo.16)17 ) so , we plan to recommend a percutaneous pfo closure to this patient , after confirming the nonexistence of dvt for several months . in conclusion , this report describes a rare case of cryptogenic stroke , associated with pfo and coexisting pte , dvt , and renal infarctions .
when pfo is suspected as a cause of the cryptogenic stroke , it is considered here that seeking the presence of pte , dvt , and other systemic arterial embolisms , using an imaging modality is useful for the prediction and prevention of adverse outcomes .
a paradoxical embolism is defined as a systemic arterial embolism requiring the passage of a venous thrombus into the arterial circulatory system through a right - to - left shunt , and is commonly related to patent foramen ovale ( pfo ) . however , coexisting pulmonary embolisms , deep vein thromboses ( dvt ) , and multipe systemic arterial embolisms , associated with pfo , are rare . here , we report a patient who had a cryptogenic ischemic stroke , associated with pfo , which is complicated with a massive pulmonary thromboembolism , dvt , and renal infarctions , and subsequently , the patient was treated using a thrombolytic therapy .