**4.3 Clinical diagnostic criteria**

The clinical presentation of PE is nonspecific, which, like many other conditions, makes diagnosis more difficult. Therefore, the current diagnostic method is to assess the risk of PE, thereby recommending appropriate follow-up tests to confirm the diagnosis. According to Ceriani et al., there is currently no best model, although many probabilistic models have been developed to help clinicians easily access the diagnosis of PE. It is recommended to use a scale that is widely used in studies (such as the Wells and Geneva criteria) (**Table 1**) [31].


**Table 1.**

*Clinical prediction scores for PE: the revised Geneva score and the Wells score.*

*Molecular Histopathology and Cytopathology in Cardiovascular Diseases DOI: http://dx.doi.org/10.5772/intechopen.110503*

In patients with a shock state, besides PE, other causes that should be considered are acute myocardial infarction, cardiac tamponade, acute aortic syndrome, and acute valvular disease. Therefore, echocardiography should be the first choice for differential diagnosis. For unstable patients who cannot be transported to CT immediately, when echocardiography is suggestive (right ventricular overload), the diagnosis of PE can be accepted. After resuscitation, the patient can be transported for a diagnostic CT scan. In stable patients, diagnosis by Christopher's Algorithm (**Figure 17**) [36].

#### **4.4 Histopathology**

Pulmonary thromboembolism can form due to stagnation and inflammation or coagulopathy in the large veins in the legs and pelvis. Observed in the pulmonary artery in the left lung on the cut section is massive pulmonary thromboembolism (**Figure 18A**). The "saddle embolus" (**Figure 18B**) is a bridge from the heart across the pulmonary artery and divides into the right and left main pulmonary arteries. This thromboembolism displays a typical gross appearance, irregular surface, and pale tan to white, admixed with dark red areas. It often causes sudden death.

Thrombus layered is typical of a thrombus that forms in a large vein of the pelvis or lower extremity. It has migrated up the inferior vena cava, through the right heart, and into a pulmonary artery (**Figures 18C**–**23**).

**Figure 17.** *Christopher's Algorithm.*

#### **Figure 18.**

*A: Large pulmonary thromboembolus. B: "Saddle Embolus". C: Thrombus layered. D: PE with right ventricular thrombus.*

#### **Figure 19.**

*Thromboembolism is packed into a pulmonary artery.Thromboembolism packs into a pulmonary artery, and thromboembolism forms the organization and dissolution. The interdigitating area of pale pink and red forms the "lines of Zahn" characteristic of a thrombus. These lines represent layers of red cells, platelets, and fibrin laid down in the vessel as the thrombus forms.*

*Molecular Histopathology and Cytopathology in Cardiovascular Diseases DOI: http://dx.doi.org/10.5772/intechopen.110503*

#### **Figure 20.**

*Fat emboli: The round holes in the vascular spaces of the lung are fat emboli. Fat emboli often occur following trauma with a fracture of long bones. It releases fat globules into the circulation trapped in pulmonary capillaries.*

#### **Figure 21.**

*A: Amniotic fluid embolization (H&E stain). B: Amniotic fluid embolization (Immunohistochemistry CK +) Amniotic fluid embolization: It is an obstetric complication. The pulmonary artery branch is an amniotic fluid embolus with layers of fetal squames, and the outcome is a massive pulmonary embolism.*

#### **Figure 22.**

*Pulmonary Arterial Thrombosis due to SARS-CoV-2. Macroscopically: The massive bilateral congestion is grayishred. The most structural feature is the presence of thrombotic in branches of the pulmonary arteries, varied from focal to extensive in all sizes of the vessels. The bronchial system contains viscous mucus and pleural effusion.*

#### **Figure 23.**

*Pulmonary Arterial Thrombosis due to SARS-CoV-2. Microscopic: Diffuse alveolar damage is a consistent feature of COVID-19, to exudative, proliferative, and fibrotic phases with the alveolar multinucleated giant cells and interstitial and alveolar inflammation. Blood vessels may show fibrinoid necrosis, wall thickening, luminal stenosis, or occlusion. The frequent presence of micro pulmonary thrombosis further supports hypercoagulative status.*

*Molecular Histopathology and Cytopathology in Cardiovascular Diseases DOI: http://dx.doi.org/10.5772/intechopen.110503*
