Use of rivaroxaban in an elderly patient with intermediate-low early mortality risk due to pulmonary embolism: a case report
An 80-year-old white man was admitted to our emergency department (DEA) presenting
with dyspnea; this symptom appeared 2 weeks before and worsened a few days prior to
hospital admission. He did not present other symptoms or signs; in particular he did
not report thoracic pain or unilateral extremity swelling. He had no previous episodes
of VTE, major trauma, immobilization or any other risk factors, such as obesity, cancer
or family history suggestive of inherited thrombophilia.
His main predisposing factor for VTE was advanced age. His medical history included
arterial hypertension, previous left varicectomy and right saphenectomy. On examination,
his systolic blood pressure was 130/80 mmHg and pulse rate was 100 beats per minute.
His respiratory rate was 24 breaths/minute and arterial oxyhemoglobin saturation was
90 % at room air. His oral temperature was 36 °C and his mental status was preserved.
Chest auscultation did not reveal pathological lung sounds. An electrocardiogram (ECG)
showed a normal sinus rhythm with inversion of T waves in leads V3 to V6 (Fig. 1a) not detected in previous recordings (Fig. 1b). Arterial blood gas analysis revealed a mild hypoxemia with respiratory alkalosis.
His chest X-ray was normal. No supplemental oxygen was administered.
Fig. 1. Electrocardiogram on admission and previous electrocardiogram without pathological
features. a Electrocardiogram on admission: sinus rhythm with inversion of T waves in anterior
and lateral leads. b Previous electrocardiogram without pathological features
Laboratory findings on admission revealed a high serum D-dimer level (6987 ng/L),
elevated high-sensitivity cardiac troponin concentration (137 ng/l) and increased
serum level of pro-B-type natriuretic peptide (pro-BNP; 6166 ng/L), while renal (creatinine
1.53 mg/dl and glomerular filtration rate 43 ml/minute/1.73m
2
) and liver function were normal. The focused assessment with sonography for trauma
(FAST) scan performed in DEA showed a moderate right ventricular (RV) dilation and
hypokinesia with flattening of his interventricular septum and dilated inferior vena
cava.
Together, these findings led to the suspicion of PE, subsequently confirmed by a CT
pulmonary angiography (Fig. 2).
Fig. 2. Computed tomographic pulmonary angiography on admission: multiple filling defects
within the pulmonary trunk and the right pulmonary artery. Left pulmonary artery presents
similar features. These computed tomography findings are suggestive of pulmonary thromboembolism
(Miller index 17)
According to the simplified PE Severity Index (sPESI; Table 1), an extensively validated prognostic tool for predicting death and adverse outcome
events in patients with PE, our patient had a score of 0. This data, in combination
with the hemodynamic status of our patient, signs of RV dysfunction and cardiac laboratory
biomarkers, allowed us to classify our patient as having an intermediate to low risk
of early mortality.
Table 1. Simplified Pulmonary Embolism Severity Index score
Given the diagnosis of bilateral PE and encouraged by the results of the EINSTEIN
PE trial 5], we decided to start therapy with rivaroxaban (15 mg, twice daily). In the following
days the patient showed a progressive improvement of clinical status and laboratory
tests. His troponin levels decreased from 905 ng/L on day 2 to 26 ng/L on day 4, pro-BNP
from 6166 ng/L on day 1 to 543 ng/L on day 4 and D-dimer from 6987 ng/L to 1385 ng/L
(Table 2). Furthermore, his partial pressure of oxygen (pO
2
) increased from 68.9 to 136.4 mmHg and the following parameters remained in the normal
range; pH, partial pressure of carbon dioxide (pCO
2
) and fraction of inspired oxygen (FiO
2
). Supplemental oxygen was not administered.
Table 2. Laboratory findings on admission (27 January 2014) and the next 3 days
Five days after starting therapy, we performed another echocardiography showing a
normalized RV function: ejection fraction (EF) of 55 %, systolic pulmonary artery
pressure (PAPs) of 30 mmHg, and tricuspid annular plane systolic excursion (TAPSE)
of 26 mm.
Seven days after starting treatment, the patient underwent a CT pulmonary angiography
that revealed a significant improvement of filling defects in the lower lobes (Fig. 3).
Fig. 3. Computed tomographic pulmonary angiography at the 7-day follow-up: partial reperfusion
of lower lobe pulmonary arteries. The other computed tomography findings appear unchanged