Venous thromboembolism (VTE), which includes of deep vein thrombosis (DVT) and pulmonary embolism (PE), is one of the most common cardiovascular diseases and is a leading cause of maternal death. VTE accounted for 3% of maternal deaths in developing countries, while the proportion is estimated to be 14% in developed countries. In a recent multicenter analysis of pregnancy-related hospitalizations, the rate of pregnancy-related acute PE was 19.36 per 100,000 hospitalizations, which rate was low but had not decreased over the past decade. Although advanced therapies are used, the rate of in-hospital mortality from acute PE during pregnancy and puerperium has not improved. Pregnancy is a hypercoagulable state that protects women from delivery-related bleeding, but the pathophysiological changes include increased clotting factors and decreased fibrinolysis. Additionally, venous flow velocity in the lower limbs is reduced because of physiological vasodilation, compression of the vena cava by the gravid uterus, and compression of the left iliac vein by the right iliac artery. Alterations in haemostasis and vein blood flow with pregnancy all increase the risk of thrombosis in gestation and the perinatal period. Caesarean section (CS) is associated with higher maternal and perinatal mortality and morbidity than vaginal delivery. The incidence of maternal VTE after caesarean delivery is approximately four times greater than that after traditional vaginal delivery. The risk of CS-associated VTE seems independent of other risk factors. Besides haemostatic modifications induced by pregnancy, the CS procedure itself may lead to greater activation of coagulation.
The differential diagnosis of VTE in pregnant and postpartum women must be made carefully. The symptoms and signs of VTE often overlap with the physiological changes of pregnancy, including tachycardia, dyspnea and lower extremity oedema, which might lead to misdiagnosis. The majority of published prediction models for the diagnosis of pulmonary embolism have not been validated in pregnant women. D-dimer is not helpful for diagnosing PE in pregnant/postpartum women, as D-dimer levels increase throughout pregnancy. Duplex ultrasonography (DUS) is the standard protocol for the diagnosis of DVT in symptomatic pregnant woman. It is widely available and carries a low risk for both mother and fetus. The Use of bilateral lower extremity venous compression ultrasonography (CUS) before chest imaging has been advocated. However, the sites of DVT in pregnant women are common in left lower extremity veins but also exist in iliac veins owing to compression of the left iliac vein by the gravid uterus, that is sort of completely different from the DVT within the general population, which is usually located within the calf. The deeper, intrapelvic-located iliofemoral veins always hinder the gravid uterus, making it difficult to acquire clear images during the compression manoeuvre of venous duplex ultrasonography. CUS of the symptomatic leg along the length of the femoral vein to the level of the calf vein combined with Doppler imaging of the iliac veins was confirmed to reliably exclude clinically important DVT. The diagnosis of symptomatic DVT by DUS not only establishes the diagnosis of DVT but also circumvents further radiological examinations if PE is clinically suspected. Additional diagnostic methods to assess PE via chest imaging CTPA and/or lung perfusion scintigraphy (V/Q scan) are required.
Acute PE always leads to RV pressure overload and dysfunction, which can be detected by echocardiography, but there are no standard echocardiographic parameters that provide reliable information on RV size or function. Therefore, a negative RV result cannot exclude PE. Furthermore, TTE shows no significant abnormalities of PE in a large proportion of patients with confirmed acute PE. Studies of acute PE detected by TTE always focus on image of right heart size and function. LV dilated and hypokinesis in echocardiography often help in the differential diagnosis of severe global or regional LV dysfunction. Dilated LV is rare in pulmonary embolism and can mislead the clinician to diagnose cardiomyopathies. The haemodynamic changes of pregnancy include blood volume increases, cardiac output increases and oxygen consumption. The detrimental effects of acute PE on the myocardium may impair LV blood flow output, which causes LV pressure overload. Cardiovascular changes in pregnancy include haemodynamic, neurohumoral, renin/angiotensin, RBC changes and cardiac structural changes. Left ventricular wall thickness and left ventricular mass increase throughout pregnancy . Plasma volume increases may result in a relatively deteriorated cardiac workload that has been damaged by acute PE. We extrapolated the LV dilation from decreased myocardial contractility and systemic afterload overload. Although the results of echocardiography were not consistent with the usual results of acute PE, we accepted the diagnosis of acute PE because DUS showed left iliac vein thrombus and clinical symptoms of acute PE. In this case, TTE also found patent foramen ovale(PFO) with a left-to-right shunt. PFO is a highly prevalent condition in the adult population[25, 26]. Although most individuals with PFO are asymptomatic, a PFO can serve as a pathway for a transient right-to-left gradient during early ventricular systole and with the Valsalva manoeuver, which depends on the pressure in the right atrium exceeding that in the left atrium. The left-to-right shunting in this case indicated that the pressure in the left atrium exceeded that in the right, which is rarely reported and indirectly reflects an overloaded afterload and left heart dilation.
Many cardiac emergencies, including myocardial infarction, peripartum cardiomyopathy, acute myocarditis, dilated cardiomyopathy and Takotsubo cardiomyopathy, ought to be considered, as all of them are life-threatening illnesses that could afflict patients with symptoms of left heart failure, such as onset dyspnoea and hypotension, which mimic acute PE. Most peripartum cardiomyopathies are diagnosed by individual history, cardiac biomarkers, cardiography, and echocardiography. Practitioners should endeavour to better understand these rare conditions to provide timely high-quality service to pregnant women who suffer life-threatening situations.
The backbone of treatment for acute PE in pregnancy is anticoagulation, which includes the primary selection of low-molecular-weight heparin (LMWH) and also the second alternative of unfractionated heparin (UFH). High-risk hemodynamically unstable PE patients should receive advanced therapies, including systemic and catheter-based thrombolysis, as well as surgical embolectomy. In addition, extracorporeal membrane oxygenation can be a rescue treatment for life-threatening situations. Inferior vena cava (IVC) filers during pregnancy can prevent additional venous clots causing pulmonary embolism, with few complications.
In conclusion, acute PE is a life-threatening scenario in the perinatal period. TTE is a standard imaging protocol for confirming the diagnosis of PE and evaluating heart function. However, negative results, even left ventricular dilation, do not fully rule out the PE diagnosis, as physiological changes in pregnant women may further influence cardiac structure and function. In some emergency situations, patients have haemodynamic instability and a risk of cardiac arrest. Catheter-directed angiography, as the gold standard, can be performed at first, when the patient’s symptoms and other results point to PE as the suspected diagnosis.