Research PE Pathophysiology, diagnosis, treatment option and occurrence of PE in Covid 19 patients.

The incidence of PE in COVID patients is significantly elevated, with two studies showing incidences of between 20-25% of ICU patients, who were already on thromboprophylaxis. When compared to the ICU population at the same time last year as a control, it was over double for COVID patients. COVID patients at the highest risk for PE include males, those on mechanical ventilation, and the obese. These studies both had small sample sizes, thus further research is warranted. 

 

 The pathophysiology of increased PE incidence in COVID-19 is not fully understood but the growing belief is that coronavirus causes a hypercoagulable state. Activation of coagulation pathways is part of the immune response to infection and results in the cytokine storm which may lead to multi-organ damage (thrombin can increase inflammation via proteinase-activated receptors (PAR). Furthermore, many of the natural mechanisms to combat coagulation, such as antithrombin III, Protein C, etc. are in short supply because of underproduction and increased consumption. 

Upon suspicion of PE, initial labs to be ordered are CBC, coagulation panel, and d-dimer. If the d-dimer is significantly elevated, a CTPA is the gold standard for diagnosis and some researchers are recommending to use contrast when doing a standard chest CT, considering the high incidence of PE in COVID patients. A VQ scan is another option, however it may not be useful in those with extensive lung involvement.

Prophylaxis is indicated for all patients in inpatient services unless there is a contraindication, using LMWH, which also helps decrease inflammation. Considering the high incidence of PE in obese patients, it may be reasonable to use a higher dose on these patients. If the patient cannot take heparin, fondaparinux is an alternative. Those with kidney issues should be on unfractionated heparin. 

The treatment for PE in COVID patients is the standard PE treatment: enoxaparin 1 mg/kg every 12 hours for stable PE and tPA for unstable PE. These patients should continue coagulation for at least three months after, as long as the patient has fully recovered and is no longer at increased risk of thrombus formation.

 

https://wwwnc.cdc.gov/eid/article/26/8/20-1477_article

https://pubs.rsna.org/doi/10.1148/radiol.2020201544

https://www.ahajournals.org/doi/pdf/10.1161/CIRCULATIONAHA.120.047430

https://www.hematology.org/covid-19/covid-19-and-pulmonary-embolism

https://www.thelancet.com/journals/lanres/article/PIIS2213-2600(20)30216-2/fulltext

https://www-uptodate-com.york.ezproxy.cuny.edu/contents/coronavirus-disease-2019-covid-19-hypercoagulability?search=covid%20pulmonary%20embolism&source=search_result&selectedTitle=3~150&usage_type=default&display_rank=3#H172461532

 

What is D-Dimer and significance

Fibrin D-dimer is a product made when plasmin breaks up cross-linked fibrin, indicating that there is some process of clot formation and degradation. This is elevated in PE, DVT, DIC, and other pathologies involving clotting. This can also be elevated in inflammatory and infectious processes including coronavirus. High d-dimer can indicate poor prognosis for COVID patients, with a study of 234 intubated COVID patients having markedly elevated d-dimer levels: mean of 4877 ng/mL, ranging between 1197 to 16,954. D-dimer is very sensitive and thus useful in ruling a pathology out but has very low specificity. Normal value is under 250.

The coagulation panel in general tends to  have high fibrinogen and d-dimer, normal or mildly elevated PT and PTT, and platelets ranging from mildly low to mildly elevated. 

https://www.hematology.org/covid-19/covid-19-and-d-dimer

https://www-uptodate-com.york.ezproxy.cuny.edu/contents/coronavirus-disease-2019-covid-19-hypercoagulability?search=d%20dimer%20covid&source=search_result&selectedTitle=2~150&usage_type=default&display_rank=2