Case Presentation: Our patient is a 24-year-old male with a family history of Antithrombin III (ATIII) deficiency and cerebral aneurysm. He was transferred to our hospital for management of syncope in the setting of a pulmonary embolism (PE). While at work as a landscaper, he felt lightheaded and diaphoretic. The following day, he syncopized, had bladder incontinence, without seizure-like activity, tongue biting, preceding chest pain or palpitations. Prior to his transfer, the patient syncopized twice, both in the setting of standing from a supine position. On admission, vital signs were notable for a heart rate of 123, but he was otherwise stable. He endorsed dyspnea and anxiety, but denied pre-syncope, chest pain, or palpitations while supine. EKG showed sinus tachycardia, and the S1Q3T3 morphology of right heart strain (see Figure). The Troponin-T was 0.508. CTA-Chest showed bilateral saddle PE, extending into the segmental and subsegmental branches. Bedside transthoracic echocardiography (TTE) confirmed right heart strain. He was monitored in the ICU on systemic heparin, with the anticipation that if he decompensated, he would immediately receive systemic fibrinolysis.

Discussion: In a young, otherwise healthy patient with a submassive PE the role of systemic fibrinolysis is often controversial. According to the PEITHO trial, among patients with submassive PE, systemic fibrinolysis prevents hemodynamic decompensation. However, this was associated with an increased risk of major adverse bleeding. The MOPETT Trial later showed that administration of tissue plasminogen activator (tPA) in addition to anticoagulation decreased the long-term risk of pulmonary artery hypertension. However, given the often unpredictable clinical course of such patients, there remain uncertainties regarding the optimal timing of systemic thrombolysis. Thus, in addition to serologic and radiographic considerations, the decision to administer tPA relies on intensive clinical monitoring to detect subtle changes that could signal impending hemodynamic collapse. This would make tPA more palatable, especially in a patient like ours with a family history significant for cerebral aneurysm. After 36 hours in the ICU, the patient began to have episodes of severe hypoxia and chest pain, which prompted the administration of tPA. His symptoms resolved completely thereafter, and he had considerable improvement in right heart size and function. While testing could not be done in the setting of an acute thromboembolic event, in the absence of other risk factors, ATIII deficiency was likely the culprit of his thrombosis.

Conclusions: The decision to administer systemic thrombolytics in patients with submassive PE must weigh the benefits of preventing immediate hemodynamic compromise and the risks of pulmonary hypertension, with the grave risks of severe complications such as intracranial hemorrhage. However, there may be a subgroup of patients with submassive PE in whom the benefits of thrombolysis far outweigh the risks, beyond rigid parameters outlined by research trials to date.