|Year : 2020 | Volume
| Issue : 4 | Page : 123-125
Concomitant acute aortic thrombosis and pulmonary embolism complicating COVID-19 pneumonia
Hassan H Allam1, Abdulhalim Jamal Kinsara2, Amt Alkhaliq A Alrajawi1, Tareq Tuiama1
1 King Abdullah Medical Complex, Ministry of Health, King Abdullah International Medical Research Center, Jeddah, Saudi Arabia
2 Ministry of National Guard-Health Affairs, King Saud Bin Abdulaziz University for Health Sciences, COM-WR, King Abdullah International Medical Research Center, Jeddah, Saudi Arabia
|Date of Submission||03-Sep-2020|
|Date of Acceptance||10-Oct-2020|
|Date of Web Publication||24-Dec-2020|
Dr. Abdulhalim Jamal Kinsara
Department of Cardiology, King Abdullah International Medical Research Center, Ministry of National Guard-Health Affairs, King Saud Bin Abdulaziz University for Health Sciences, COM-WR, Jeddah
Source of Support: None, Conflict of Interest: None
There is rapidly accumulating literature regarding the hypercoagulable state associated with patients diagnosed with COVID-19 infection. Pulmonary, cardiac, and visceral involvement has been described. We describe a middle-aged male, with a background of diabetes and hypertension, diagnosed with severe COVID-19, who passed away despite maximum support. He had concomitant aortic and pulmonary thrombus. This is a devastating, poorly understood complication of severe COVID-19, adding to the body of medical literature related to severe COVID-19. COVID-19 is a hypercoagulable disease, and multi-organ involvement should be considered. Aortic imaging during a computed tomography pulmonary angiography can add additional information to the risk stratification and clinical implications in a patient diagnosed with COVID-19, with a suspected hypercoagulable state and possible multi-organ involvement.
Keywords: Aortic thrombosis, COVID-19, pulmonary embolism
|How to cite this article:|
Allam HH, Kinsara AJ, A Alrajawi AA, Tuiama T. Concomitant acute aortic thrombosis and pulmonary embolism complicating COVID-19 pneumonia. Heart Mind 2020;4:123-5
| Introduction|| |
A hypercoagulable state is recognized as a complication in COVID-19 positive patients. There is a high incidence of pulmonary embolism with or without underlying deep venous thrombosis. Wichmann et al. reported that massive pulmonary embolism was the cause of death in a third of the cases., With the spread of the disease, abnormal coagulation variables and a high incidence of venous thromboembolic (VTE) complications have been observed. This complication necessitates the development of specific VTE diagnostic and therapeutic strategies. Widespread atherothrombosis is probably a clinical manifestation of the prothrombotic state, described in patients with COVID-19. The rate of arterial thrombosis in intensive care units is reported as 2%–6%, with the venous rates 17%–31% in intensive care units without surveillance with duplex ultrasound performed from thigh to ankle and 69% in units with surveillance., The combination of more than one manifestation of the hypercoagulable state is a challenge for diagnosis and therapy and exacerbates the outcome if not promptly recognized. It also emphasizes the need for protocols in anticoagulation.
| Case Report|| |
A 51-year-old male patient, previously diagnosed with diabetes and hypertension, was diagnosed with COVID-19, based on a nasal swab. He was referred from a secondary hospital with a 6-day history of fever, shortness of breath, and cough before presentation. He received oxygen with a face mask, self-pronation, and commenced on ceftriaxone 1 g twice daily, azithromycin 500 mg once daily, and heparin 5000 subcutaneous every 8 h. On the 2nd day, the patient developed progressive hypoxemia, his oxygen requirement increased, and his medication was changed to enoxaparin 60 mg once daily. On day 3, he was intubated and mechanically ventilated and transferred to our hospital on day 4.
On arrival, the body mass index was 26 kg/m2, the initial blood pressure was 100/60 mmHg, and the heart rate was 108 per minute. The inspired oxygen fraction was 70%, the tidal volume 450, and the positive end-expiratory pressure 10. An arterial blood gas was done with the following results: pH 7.30, partial pressure of CO2 (PCO2) 28 mmHg, partial pressure of oxygen (P02) 72 mmHg, bicarbonate (HCO3) 21.2 mEq/L, base excess 3.2, and arterial oxygen saturation (SPO2) 92%.
The chest X-ray revealed bilateral diffuse increased pulmonary opacity [Figure 1]. The admission laboratory results are summarized in [Table 1]. The patient was prescribed antibiotic treatment (tazocin and azithromycin) and intravenous (IV) unfractionated heparin. The dose was guided with the activated partial thromboplastin time every 6 h, with a target of approximately 70 s. No steroid was prescribed. After admission, the patient became more hypotensive with acute kidney injury, requiring norepinephrine and continuous renal replacement therapy (CRRT). An echocardiogram indicated a normal left ventricle. There was no evidence of a thrombus or intracardiac shunt.
|Figure 1: Chest X-ray showing bilateral diffuse increased pulmonary opacity|
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A computed tomography pulmonary angiography was done, which revealed large filling defects in the left main pulmonary artery, suggestive of a recent embolus. Subtle filling defects were observed in the right distal upper lobe segmental artery as well as a proximal abdominal aortic filling defect. There was no evidence of atherosclerotic changes in the aorta [Figure 2] and [Figure 3]. IV tissue plasminogen activator (tPA) 100 mg over 2 h was given without a significant improvement in the patient's saturation or hemodynamic status. Unfortunately, the next day, the patient developed cardiac arrest and died.
|Figure 2: Computed tomography angiography showing large PE and clot in the abdominal aorta (yellow arrow points to pulmonary thrombosis and white arrow points to aortic thrombosis)|
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|Figure 3: Computed tomography angiography showing large pulmonary embolism (short and long axis – yellow) and abdominal aorta clot (short and long axis – white)|
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| Discussion|| |
Our case demonstrated a concomitant pulmonary and aortic thrombosis. There is only one case in the literature describing a concomitant pulmonary and aortic thrombosis in COVID-19 patients. Hypoxemia, secondary to respiratory failure, results in microvascular thrombosis in some patients with COVID-19. An autopsy revealed large-vessel and microvascular thrombosis, pulmonary hemorrhage, and a high prevalence of VTE complications.
Abnormal coagulation parameters, such as elevated D-dimers, have been reported and are possibly associated with a higher risk for the development of acute respiratory distress syndrome (ARDS) and death in patients diagnosed with COVID-19. Therapeutic anticoagulation may be considered in patients at a high risk for coagulopathy (including CRRT). The coagulopathy status should be weighed against the risk of bleeding. It is noteworthy that some centers are therapeutically prescribing anticoagulants for all patients on admission, if no absolute contraindication exists., The use of an anticoagulant appears to be associated with decreased mortality in all patients and particularly in patients with a sepsis-induced coagulopathy score > 3. The inference from the study is prone to bias, as there is no randomized control trial evidence available, regarding therapeutic anticoagulation in the absence of a thrombus.
Some early reports support an extended-infusion tPA as a potential approach to refractory ARDS cases or catheter-directed thrombectomy., Patients with COVID-19 may be at risk of acute pulmonary embolism, however, the prevalence of this association with aortic thrombosis is yet to be determined. This report is, to our knowledge, the second to report an acute aortic thrombosis related to COVID-19. This complication may reflect the potential hypercoagulability associated with SARS-CoV-2 infection and raises the question of using early markers of a hypercoagulable state and the initiation of early and high dose of therapeutic anticoagulation.,,
Development of coagulopathy is a significant indicator of a poor prognostic outcome in patients with COVID-19. It mandates the consideration of prophylactic anticoagulation, based on risk stratification, for all admitted COVID-19 patients. The risk stratification should be based on the clinical severity of the disease and laboratory parameters (D-dimer, prothrombin time, and platelet count). Therapeutic intensity anticoagulation, in the absence of confirmed or suspected VTE in critically ill COVID-19 patients, is currently unknown.
| Conclusion|| |
COVID-19 is a hypercoagulable disease, and multi-organ involvement should be considered. Aortic imaging during a computed tomography angiography pulmonary study can add additional information to the risk stratification and clinical implications in a patient diagnosed with COVID-19.
Our institution does not require ethical approval for reporting individual cases or case series.
Full written informed consent was obtained from the patient family in using clinical data images and radiologic images after discussing the details of the case report contents.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given his consent for his images and other clinical information to be reported in the journal. The patient understands that name and initials will not be published and due efforts will be made to conceal identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
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[Figure 1], [Figure 2], [Figure 3]
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