Case Presentation: An 82 year old male with unknown PMH presented with worsening dry cough and dyspnea. 1 week course of antibiotics provided minimal relief. Patient was febrile/tachycardic on arrival with rhonchi appreciated on bilateral lower lung field auscultation. His oxygen saturation was found to be dipping below 90% on room air for which he was placed on a high-flow nasal cannula in the ED. Laboratory findings significant WBC 14.3 x10^3/mcL, Hgb 12.6g/dL and PLT 82 x 10^3/mcL. Coagulation showed PT 57.1s, INR 5.92, PTT 52.5s, D-dimer > 35 mg/L and fibrinogen < 60 mg/dL. Haptoglobin 234 mg/dL, CRP 16.86mg/dL, and Ferritin 2363 ng/mL. Schistocytes were seen on peripheral blood smear. Patient was suspected to be undergoing diffuse intravascular coagulation (DIC); he was then transfused 3 units of FFP, 2 units Cryoprecipitate, and Vitamin K. No evidence of obvious bleeding could be appreciated, however. Abdominal ultrasound was performed and was unremarkable. Patient was started on Dexamethasone, Baricitinib, and Remdesivir for COVID pneumonia; due to worsening kidney function over the next few days (Cr rising up to 5.4 from normal levels) decision was made to hold his Baricitinib and Remdesivir. Patient was given aggressive hydration secondary to worsening kidney function and hypernatremia. He proceeded to have increased oxygen requirements and CXR showed evidence of pulmonary vascular congestion. He was started on diuretics for which he responded well to. Patient’s conditions slowly improved, and his oxygen requirements decreased after treatment.
Discussion: Coagulopathies have been associated with a wide variety of bleeding/inflammatory disorders, but one interesting association is COVID-19’s potential to produce a DIC-like presentation. Stages have been divided into mild, moderate, and severe; each progressively requiring more supplemental oxygen and the coagulopathy from localized to more systemic. As per its mimicking findings of DIC, a study analyzing 10 autopsies of COVID patients showed similar elevations in LDH, D-Dimer, CRP, as well as thrombocytopenia. What differentiated this patient, however, was his elevated haptoglobin levels which would have likely been decreased if DIC was occurring (Beusekom, 2020). DIC coagulopathy is also usually associated with more severe thrombocytopenia and lower levels of clotting factors/coagulation inhibitors in comparison (Levi et al., 2021). Elevation of certain markers, especially D-dimer, have been noted to be correlated to worsening of severity of COVID coagulopathy. These patients should be particularly monitored for evidence of clotting (Covid-19 and coagulopathy, 2021). At this time, guidelines indicate starting patients on therapeutic Heparin regimen for those with history of or at high risk of thrombotic events (Chandra et al., 2021).
Conclusions: Besides its association with pneumonia, COVID has the ability to appear as a pro-thrombotic inflammatory condition. Although similar, certain markers can help differentiate COVID coagulopathy with DIC. Some, such as D-dimer, have been associated with increased disease severity. At this time, however, their elevations should not guide anticoagulation therapy; decisions should be on a patient specific basis regarding their risk of a thrombotic event.