INTRODUCTION: Mobile right heart thrombi (MRHT) have been observed in patients with severe pulmonary embolism (PE), and are associated with a poor prognosis. The incidence is unclear and no widely accepted guidelines exist regarding optimal therapy. We present a case of venous thromboembolism complicated by MRHT successfully treated with systemic thrombolysis.
CASE PRESENTATION: 48-year-old male presented with acute onset of dyspnea of 1 day duration, accompanied by chest pain, productive cough and chills. On admission he was afebrile, tachycardic 105 per minute, tachypneic, blood pressure was 98/60 mm Hg and pulse oximetry 93% on room air. Initial laboratory values included creatinine = 1.8mg/dl, leukocytosis and transaminatis. Chest X-Ray showed pulmonary artery enlargement. Ventilation–perfusion (V/Q) scan was obtained, with a preliminary report of low-probability for PE. Initial therapy consisted of 2.5 L of normal saline heparin and antibiotics with improvement of blood pressure and tachypnea. Overnight patient became hypotensive and cyanotic despite volume expansion, and transferred to MICU. Laboratory analysis revealed lactic acidosis, elevated brain natriuretic peptide level. Arterial blood gases revealed respiratory alkalosis and hypoxia. Transthoracic echocardiography (TTE) showed right atrial and ventricular dilatation with mobile clot in hepatic vein, inferior vena cava (IVC), right atrium and ventricle. Alteplase (10 mg IV bolus, 90 mg IV over the next 2 hours) was administrated, with the initial development of hypotension and chest pain, requiring norepinephrine. Symptoms resolved, repeated TTE after thrombolysis completion documented complete resolution of MRHT. Doppler ultrasound of lower extremities has shown bilateral, near-occlusive and mobile popliteal thrombosis. Temporary IVC filter was placed. V/Q scan interpretation was subsequently revised as high- probability for PE. Renal function normalized and patient was discharged home on warfarin.
DISCUSSIONS: The incidence of MRHT ranges between 3 and 23% with some data suggesting that transesophageal echocardiography is more sensitive than TTE. We are aware of no randomized, controlled trials of treatment of MRHT. Proposed treatment recommendations include surgery, thrombolysis and anticoagulation and are based on case series with no clear consensus (1). Analysis of a European multicenter PE registry showed no overall difference in mortality between these treatment modalities. However, subgroup analysis showed increased mortality in comparable groups of patients with and without MRHT treated with heparin alone (23.5% vs. 8% respectively)(2). These findings suggest that anticoagulation alone may not be sufficient treatment for patients with PE and MRHT. A large metanalysis(1) summarized 177 cases from 95 studies between 1966 and 2000. Mortality post thrombolysis was significantly lower than with surgery or anticoagulation alone (11.3% vs. 23.8% and 28.6% respectively). It is unknown if new MRHT caused late clinical deterioration in our patient or MRHT was present during the initial evaluation. The later case, if true, may argue for consideration of more aggressive therapy in hemodynamically stable patients with PE and documented MRHT.
CONCLUSION: MRHT seems to be a sign of a severe PE. TTE is a safe test that may be useful to establish diagnosis and guide a treatment in patients with suspected PE. It may be particularly helpful in the settings of initially non-conclusive studies when use of contrast–utilizing modalities is undesirable. MRHT can embolize both prior to and after the thrombolysis. Alteplase may be an effective and safe treatment option in this patient group.
DISCLOSURE: Mikhail Gabrilovich, None.