Introduction
Acute pulmonary thromboembolism is a common disease in emergency centers that is a diagnostic challenge for clinicians. Pulmonary embolism (PE) remains a significant cause of morbidity and mortality that requires prompt diagnosis and treatment. PE is a disorder of pulmonary circulation as a result of thrombus formation. Thrombus formation may be due to hypercoagulability, blood stasis, or damage to the endothelium of blood vessels, a set of changes known as the Virchow’s triad. Predisposing factors may be: deep vein thrombosis, excessive obesity, immobilization, intervention procedures, advanced age, use of contraceptives, use of some drugs (such as hormone, glucocorticoid therapy, etc.). The most common clinical symptoms are syncope, dyspnea, anginal pain, hemoptysis, and sudden cardiac death. The clinical course can be: fulminant (syncopal), acute (massive), subacute (submassive), and chronic (chronic pulmonary heart). The therapy is mainly fibrinolytic and anticoagulant, with rotablation fragmentation as well as certain surgical procedures including embolectomy, thrombendarectomy, implantation of venous filters, etc. (1-8)
Case report
A 79-year-old patient came to the emergency room because of sweating, vomiting, chest pain, and shortness of breath. Symptoms began with sweating and vomiting the day before admission, while chest pain and shortness of breath began a few hours before admission. The patient reported a history of hypertension several years ago, which was well controlled, and a condition after stenting the circumflex artery 10 years ago. Additionally, the patient reported taking a corticosteroid prescribed by a dermatologist for the last 6 months due to a diagnosis of pemphigus. The patient denied any addictions and allergies to drugs, food, etc. Family history was negative for any relevant diseases. After the initial examination in the emergency room and due to the general severe condition with signs of cardiogenic shock: blood pressure 90/50 mmHg, oxygen saturation 55%, ECG on admission, sinus rhythm with a frequency of 118 / min, with right bundle branch block morphology (Figure 1); the patient was admitted to the Intensive and Coronary Care Unit for further examination and treatment.
Samples were taken at admission and D-dimers were examined because there was a suspicion of PE according to the clinical picture of the patient. Oxygen support was included via an oxygen mask, and the oxygen saturation was increased by up to 80%. Intravenous heparin 5000 IU intravenous was given. An emergency echocardiogram was performed with the following observation:
Echocardiographic finding in addition to the right ventricular load.
Increased dimensions of the right ventricle up to 50 mm at the level of the base.
Right atrium 55 mm. Reduced value of TAPSE 10 mm, STDI 7, FAC reduced by about 30%.
Reduced free wall kinetics of the right ventricle are noted.
Severe tricuspid regurgitation present with a maximum gradient of about 40 to 50 mmHg.
Boundary dimension of the inferior vena cava, non-collapsible.
Pulmonary arterial hypertension present, approximately 70 mmHg. In the pulmonary artery on the hand, a hyperechoic shadow is visible, mobile with a size of 13×14 mm looking like a thrombus and the pulmonary artery somewhere at the level of the aorta (parasternal cortical axis) presents a small echogenic shape in addition to the thrombus.
On the parasternal short axis at the level of the left ventricle, there is a push from the right ventricle – a D-shape phenomenon (Figure 2).
The left ventricle has regular dimensions, function, and kinetics.
In the meantime, we got the results of the D-dimers, with were increased – 8600 ngr/mL. Due to the deterioration of the patient’s condition and according to the new recommendations for pulmonary thromboembolism from the European Society of Cardiology from 2019 (9), we started applying fibrinolysis without prior confirmation of the diagnosis with CT. (1,6) Alteplase 100 mg was immediately given to the patient for a period of 2 hours, according to the protocol for pulmonary thromboembolism. Fibrinolytic therapy was continued for another 24 hours with application of another anticoagulant (saline 500 mL + heparin 25000 IU intravenous / 24h) and gastroprotective therapy. Due to the unclear clinical picture and the situation with the COVID-19 pandemic, a rapid test was performed for COVID-19 which was negative. In the meantime, the results of the blood tests arrived: RBC 5.83 1012/L, Hgb 150 g/L, WBC 15.2 109/L, PLT 193 109/L, Troponin I (s) 152.28 ng/L, CRP 6.0 mg/L, potassium 4.8 mmol/L, natrium 140 mmol/L, serum creatinine 80 µmol/L, and serum urea 6.8 mmol/L. Due to leukocytosis, antibiotic therapy was included. The next day, after the patient’s condition improved, we performed a CT angiography according to the protocol for PE, which confirmed the diagnosis of PE. The findings of the CT were as follows:
At the bifurcation of pulmonary trunk there was a filling defect without obstruction of the flow through the lumen.
A thrombus was detected in the right lobar artery with a partial involvement of the apical and the medial segments of the right lobe, also without significant obstruction of the lumen.
Due to the unclear etiology of PE, other tests were performed to rule out or confirm possible causes of the disease. CT scans of the abdomen and chest CT scans were performed, with no pathological findings. Doppler sonography of the lower extremities was also performed, with a finding of proper arterial circulation of the lower extremities, exclusion of deep venous stasis, and no fresh thrombotic masses in the lumen of the veins of the lower extremities.
Before discharging the patient to his home, we examined him again for D-dimer, which was now reduced to 1462 ngr/mL. Control echocardiography was performed with the following finding: a hyperechoic round formation resembling an older date thrombus. The other shadow previously described at the time of examination was not visualized.
After treatment with anticoagulant therapy, the patient was transferred to oral therapy comprising apixaban 5 mg 2×2 for 7 days and 2×1 after that. Due to improvement of the patient’s condition after 6 days of hospitalization, he was discharged to his home with O2 saturation 98%, blood pressure 120/80 mmHg, ECG sinus rhythm with a frequency of 79 / min, left axis deviation, rS form in II, III, AVF, V1-V3 leads, regular ST-segment and T wave, with a recommendation for regular therapy and a scheduled next visit in our clinic in 3 months.
Discussion
Pulmonary thromboembolism is a very common disorder of pulmonary circulation, often presenting with nonspecific symptoms and signs. (7) It is an urgent medical pathology which, if not diagnosed and treated in time, can have a fatal outcome. Based on to the latest recommendations from the European Society of Cardiology from 2019, the assessment for starting treatment in patients with PE is made on the basis of the hemodynamic condition of patients at admission, i.e. the division of patients into hemodynamically stable or unstable. The patient described herein, who was in cardiogenic shock, belonged to patients at high risk of developing cardiac arrest, according to our estimates based on the latest recommendations (9). Since CT pulmonary angiography could not be performed due to the clinical condition, we administered a bolus anticoagulant therapy of heparin, and we administered an emergency echocardiography which showed that the left ventricle was suppressed by the right ventricle – a D-shape phenomenon with clearly enlarged right ventricular dimensions and clear signs of right ventricular loading. Although we did not have clear evidence that it was caused PE and because of the unclear etiology and inability to organize CT angiography of the lungs, we decided on therapy with fibrinolysis, taking into account all possible contraindications, due to the clinical instability of the patient. After improving the patient’s condition, we discussed his medical history in more detail, and after this second conversation and the examinations we performed to confirm the etiology of PE (COVID-19 test, CT of the chest and abdomen, Doppler sonography of the blood vessels of the lower extremities), we came to the final conclusion that as the etiology of PE in this case was the corticosteroid therapy (prednisolone) that the patient had regularly taken according to the treatment scheme for the last 6 months without interruption, which was prescribed by a dermatologist for the treatment of pemphigus.
Conclusion
Pulmonary thromboembolism is a life-threatening condition that is associated with significant mobility and mortality. Today there are many different diagnostic procedures that maximize the chance of timely diagnosis of this pathology for faster treatment and better prognosis. Taking all these things into consideration, however, the most important factor is the method of treatment, which is based on the hemodynamic clinical picture of the patient. We have shown that timely treatment with fibrinolytic therapy can be lifesaving in patients with PE who are hemodynamically unstable, taking into account all possible contraindications. Care should also be taken with corticosteroid therapy in patients who will be receiving it for a long-time, and more frequent check-ups are required to promptly diagnose possible complications.