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Year : 2015  |  Volume : 5  |  Issue : 1  |  Page : 50-52

An uncommon pulmonary embolism

1 Department of Respiratory, Hospital, Pellegrin; Université Bordeaux-II Segalen, Bordeaux, France
2 Department of Cardiology, Groupe Hospitalier Paris Saint Joseph; University of Paris Descartes, Sorbonne Cite, Paris, France
3 Department of Critical Care, Groupe Hospitalier Paris Saint Joseph, Paris, France

Date of Web Publication2-Mar-2015

Correspondence Address:
François Philippart
Critical care department, Groupe Hospitalier Paris Saint Joseph, 185 Rue R. Losserand, 75014 Paris
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/2229-5151.152345

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Objectives: To report an unusual case of suicide attempt secondary complicated of pulmonary and systemic embolisms.
Data Source: A 49-year-old-woman, with a factor V Leiden mutation and a notion of chronic depression, admitted to our intensive care unit for a suicide attempt by ingestion ofmepronizine and lormetazepam.
Data Extraction: We report the rare evolution of this patient with a persistent alteration of consciousness associating a respiratory degradation. Despite the drug intoxication and possibility of aspiration, we performed a computed tomography (CT) angiography which confirmed the presence of a bilateral, proximal, pulmonary embolism suspected on transthoracic echocardiography. A cerebral CT showed left sylvian and cerebellar infarctions complicated of perilesional edema. Association of stroke and pulmonary embolism led us to suspect a patent foramen ovale (PFO). There was also a context of genetical perturbation of hemostasis. Transesophageal echocardiography confirmed the presence of a PFO undiagnosed by transthoracic echography. The PFO was complicated by an entrapped thrombus. The thrombotic complications were treated by unfractionated heparin.
Data Synthesis: Neurological and respiratory degradation following voluntary drug intoxication led to the discovery of both a pulmonary and cerebral embolism secondary to a PFO entrapped thrombus.
Conclusions: An entrapped thrombus in a PFO is a rare and dangerous situation, associated with many complications. Association of systemic and pulmonary embolisms should lead to PFO detection to guide therapeutic interventions.

Keywords: Patent foramen ovale, pulmonary embolism, stroke, thrombophilia

How to cite this article:
Prevel R, Garcon P, Philippart F. An uncommon pulmonary embolism. Int J Crit Illn Inj Sci 2015;5:50-2

How to cite this URL:
Prevel R, Garcon P, Philippart F. An uncommon pulmonary embolism. Int J Crit Illn Inj Sci [serial online] 2015 [cited 2022 Dec 7];5:50-2. Available from: https://www.ijciis.org/text.asp?2015/5/1/50/152345

   Case report Top

A 49-year-old-woman was found at home presenting neurological distress with a Glasgow score of 11 caused by mepronizine and lormetazepam (supposed ingested doses: 12 g and 32 mg, respectively) poisonings and was brought to our intensive care unit. She already tried to kill herself by voluntary drug intoxication (chronic depression) and was known to have a factor V Leiden mutation.

Her initial physical examination at admission showed tachycardia (143 bpm) and tachypnea (respiratory rate 30 cycles/min) with an oxygen saturation of 75% in room air. A worsened Glasgow score of 5 was observed at that time. Due to those respiratory and neurological failures, the patient was intubated, but her respiratory parameters did not improve. The transthoracic echocardiography revealed enlarged right cardiac chambers and an elevated pulmonary artery pressure (sPAP 50mmHg). Considering the severity of respiratory failure and normality of chest X-ray, a spiral computed tomography (CT) was performed revealing a massive bilateral proximal pulmonary embolism.

Increased neurological distress was suggested by anisocoria with areactive left mydriasis and body-part pyramidal syndrome. A cerebral CT scan showed left sylvian and cerebellar infarctions. Those infarctions were complicated by a perilesional edema which caused an under falcorial engagement. No hemorrhagic part was found. Association of stroke and pulmonary embolism led us to suspect a PFO responsible for a cerebral paradoxical embolism.

This diagnosis was confirmed by transesophageal echocardiography with an entrapped thrombus (supplementary video) and positive agitated saline contrast injection. Both pulmonary embolism and brain infarction were treated by unfractioned heparin due to the probable embolic origin of the stroke. The cerebral edema was treated by injection of mannitol.

The further care took place in a neurosurgery unit, but she unfortunately died 2 days after admission.

Despite the confirmation of etiological diagnosis, we were unable to reconstruct the natural history of events: Did the suicide attempt lead to a coma with prolonged immobility favoring thromboembolic complications? Was an embolic complication (stroke) or pulmonary embolism the first event, leading to feeling unwell which triggered the suicide attempt? Were embolic complications and suicide attempt completely independent?"

Importance of patent foramen ovale

We described here a rare but potentially life-threatening event. PFO is present in more than 25% of adults [1] and is the cause of about 95% of the right-to-left shunts. Several previous reports described a straddling thrombus within a PFO with pulmonary and coronary [2] or cerebral embolism. [3] Cryptogenic strokes represent about 40% of strokes and paradoxical embolism via a PFO seems to be responsible of 50% of them leading to 40,000-160,000 such cerebral accidents per year in the United States. [4]

The principal cause of elevated right cardiac chambers pressure is pulmonary embolism and presence of a PFO in patients with clinically apparent pulmonary embolism increases systemic embolism from 2% to 28% (P < 0.02). [5] Size of the PFO might also affect the embolic risk. [4] On the contrary, venous thrombosis, oral contraceptives, or recent surgery can increase the risk of paradoxical embolism through PFO as factor V Leiden mutation (known in our case) and prothrombin G20210A mutation that seems to play a critical role [6] increased about fivefold the risk of stroke in these patients. [6] Those findings show that estimation of paradoxical embolism risk level should simultaneously take into account both the presence of PFO and risk factors for right cardiac chambers pressure elevation.

Despite therapeutic interventions, mortality vary from 14% to 33% during the hospital stay [5] , impending paradoxical embolism being associated with a 30-day mortality rate is 18.4%. There is no modification of mortality between thromboembolectomy, anticoagulation, or thrombolysis. [7] High level evidence for impending paradoxical embolism treatment need has to be investigated and treatment has to be adapted to the characteristics of the patients and care center resources and expertise.

The first PFO treatment was cardiac surgery, but it is no longer indicated as an isolated procedure. Guidelines remain ambiguous concerning secondary prevention of complications. No prospective randomized long-term study has ever proved a benefit from closing the PFO. PFO can be treated by percutaneous therapy with low morbidity and mortality rates [8] and recurrent neurological or peripheral embolic event in 0%-3.8% per year. Nonetheless, the interest of a PFO closure after a stroke remains debatable as a recent study did not show a significant benefit, using a composite end-point mixing mortality and stroke recurrence in a 2 years follow-up period. [9] Two more recent trials confirmed these observations. [10],[11] Nonetheless, per-protocol and as-treated analysis showed significant improvement in the risk of recurrent stroke. [11] Pooling these data suggesta probable benefit of the percutaneous closure of PFO. These works confirmed a previous propensity score-matched comparison showing a mortality reduction. [12] Local radiofrequency application and percutaneous intracardiac suture are still being evaluated clinically. [9],[13] At last, medical strategy by lifelong anticoagulants such as warfarin is preferable to acetylsalicylic acid as it reduces the risk of recurrent ischemic events. [14]

A risk stratification at the base of treatment strategy was proposed as a compromise. [15]

   Conclusion Top

PFO is a frequent condition, but an entrapped thrombus is a rare and life-threatening situation that should be sought for in a suspicious clinical situation such as the one described here (pulmonary and systemic embolism and a coagulation factor mutation).

   References Top

Homma S, Sacco RL. Patent foramen ovale and stroke. Circulation 2005;112:1063-72.  Back to cited text no. 1
Pilgrim T, Meier B, Khattab AA. Death by patent foramen ovale in a soccer player. J Invasive Cardiol 2013;25:162-4.  Back to cited text no. 2
Chow V, Wang W, Wilson M, Yiannikas J. Thrombus in transit within a patent foramen ovale: An argument for consideration of prophylactic closure? J Clin Ultrasound 2012;40:115-8.  Back to cited text no. 3
Rosamond W, Flegal K, Furie K, Go A, Greenlund K, Haase N, et al., American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Heart disease and stroke statistics--2008 update: A report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Circulation 2008;117:e25-146.  Back to cited text no. 4
Konstantinides S, Geibel A, Kasper W, Olschewski M, Blumel L, Just H. Patent foramen ovale is an important predictor of adverse outcome in patients with major pulmonary embolism. Circulation 1998;97:1946-51.  Back to cited text no. 5
Botto N, Spadoni I, Giusti S, Ait-Ali L, Sicari R, Andreassi MG. Prothrombotic mutations as risk factors for cryptogenic ischemic cerebrovascular events in young subjects with patent foramen ovale. Stroke 2007;38:2070-3.  Back to cited text no. 6
Myers PO, Bounameaux H, Panos A, Lerch R, Kalangos A. Impending paradoxical embolism: Systematic review of prognostic factors and treatment. Chest 2010;137:164-70.  Back to cited text no. 7
Butera G, Carminati M, Chessa M, Youssef R, Drago M, Giamberti A, et al. Percutaneous versus surgical closure of secundum atrial septal defect: Comparison of early results and complications. Am Heart J 2006;151:228-34.  Back to cited text no. 8
Furlan AJ, Reisman M, Massaro J, Mauri L, Adams H, Albers GW, et al. Closure or medical therapy for cryptogenic stroke with patent foramen ovale. N Engl J Med 2012;366:991-9.  Back to cited text no. 9
Meier B, Kalesan B, Mattle HP, Khattab AA, Hildick-Smith D, Dudek D, et al. Percutaneous closure of patent foramen ovale in cryptogenic embolism. N Engl J Med 2013;368:1083-91.  Back to cited text no. 10
Carroll JD, Saver JL, Thaler DE, Smalling RW, Berry S, MacDonald LA, et al., RESPECT Investigators. Closure of patent foramen ovale versus medical therapy after cryptogenic stroke. N Engl J Med 2013;368:1092-100.  Back to cited text no. 11
Wahl A, Juni P, Mono ML, Kalesan B, Praz F, Geister L, et al. Long-term propensity score-matched comparison of percutaneous closure of patent foramen ovale with medical treatment after paradoxical embolism. Circulation 2012;125:803-12.  Back to cited text no. 12
Meier B. Catheter-based closure of the patent foramen ovale. Circulation 2009;120:1837-41.  Back to cited text no. 13
Schuchlenz HW, Weihs W, Berghold A, Lechner A, Schmidt R. Secondary prevention after cryptogenic cerebrovascular events in patients with patent foramen ovale. Int J Cardiol 2005;101:77-82.  Back to cited text no. 14
Mas JL, Arquizan C, Lamy C, Zuber M, Cabanes L, Derumeaux G, et al. Recurrent cerebrovascular events associated with patent foramen ovale, atrial septal aneurysm, or both. N Engl J Med 2001;345:1740-6.  Back to cited text no. 15

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[Pubmed] | [DOI]


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