Author : Philippine Heart Center Vascular CRFs
Ken Nacional, MD
Nestor Subong, MD,
Kevin Ramos, MD
Our patient is a 70 year old male who is non-hypertensive, non-diabetic, and nonsmoker who was rushed to the emergency room due to
shortness of breath. His illness started 1 week prior to admission when the patient complained of fever associated with productive cough,generalized weakness and anorexia. Patient initially did not sought consult nor took medications but was noted to have persistence of symptomwith associated shortnes
s of breath hence consult. At the emergency room, patient was noted to be in respiratory distress. Vital signs were measured with the following results: normotensive at 120-130/80, tachycardic at 110 bpm, tachypneic at 30 cpm and desaturated at 74% on room air. Physical examination of the chest revealed use of accessory muscle on respiration and presence of bilateral rales on auscultation.
Patient was intubated and hooked to mechanical ventilator.
The patient was initially assessed to have Acutac wall motion and contractility of transthoracic echocardiogram and SARS COV 2 RNA positive on antigen detection. Patient was admitted in the intensive care unit and was started on Tociluzimab, broad spectrum antibiotics and enoxaparin (prophylactic dose).
COVID 19 pneumonia is caused by SARS COV 2 virus which was first recognized in Wuhan, China on December 2019. Transmission of the
virus occurs via respiratory droplets, direct contact with infected patient and contact with contaminated surfaces. Clinical manifestation is protean with the most common being fever, cough and anorexia. Pathogenesis of the disease commences with antigen presentation at the angiotensin converting enzyme receptor 2 leading to viral RNA replication and cellular exocytosis and ultimately inducing humoral and cellular immunity to produce cytokine storm.
Patients with COVID 19 presents with laboratory abnormalities compatible with a hypercoagulable state including increased fibrinogen level,elevated d dimer and enhanced platelet activation. Small and large vessel thromboembolism could ensue due to activated coagulation,fibrinolytic suppression, endothelial cell damage and thrombocytosis. Coagulopathy in patients infected with COVID 19 is one of the significant features of poor prognosis, hence, prophylaxis and proper treatment via anticoagulation must be ensured. The role of anticoagulation in patients with COVID 19 syndromes depends on the severity of the disease according to the Philippine Society of Vascular Medicine. Patients with mild COVID 19 must be risk stratified for venous thromboembolism via Padua scoring. A score of more than 4 requires prophylactic anticoagulation with enoxaparin, fondaparinaux or unfractionated heparin whose dose depends on the creatinine clearance. Patients with moderate, severe and critical COVID 19 syndrome and those with D dimer levels more than or equal to 1500 ng/ml with no contraindication for anticoagulation must be given prophylactic dose regardless of Padua score. Therapeutic dose of enoxaparin,
unfractionated heparin or fondaparinaux must be given to COVID 19 patients diagnosed with venous thromboembolism or those with high
index of suspicion. Dose adjustments of anticoagulation has no definite guidelines but can be necessary depending on the creatinine
clearance and patient risk assessment for thrombosis.
In the case, our patient initially received a prophylactic dose of anticoagulation (enoxaparin 40mg every 12 hours) due to severe COVID 19 syndrome but was eventually escalated to therapeutic dose (enoxaparin 1mg/kg every 12 hours) immediately after the presentation and diagnosis of deep venous thrombosis and small vessel disease. Post discharge, anticoagulation will be continued depending of the patient’s bleeding risk and venous thromboembolism (VTE) risk factors. Patients with low bleeding risk and with moderate venous thromboembolism risk can be discharged with one of the following for 1-2 weeks:
enoxaparin 40 mg subcutaneously once a day, unfractionated heparin 5000 units subcutaneously twice or thrice a day, fondaparinaux 2.5 mg subcutaneously once a day or rivaroxaban 10mg per orem once a day. On the other hand, patients with low bleeding risk and high venous thromboembolism risk should be given with rivaroxaban 10mg per orem once a day for 6-7 weeks. Our patient was categorized under low bleeding risk with moderate VTE risk, hence, he was given rivaroxaban 10mg once a day for 2 weeks on discharge.
The pandemic involving SARS COV 2 infection presents with multiple complications involving various organ systems. Coagulopathy is one of the commonly observed complication among confirmed COVID 19 patients, and its presence entails a poor prognosis. It is therefore
important that appropriate anticoagulation prophylaxis be given to diagnosed moderate to severe COVID 19 patients and to those with high risk for VTE.