What your doctor is reading on Medscape.com:
APRIL 14, 2020 — COVID-19 infection may represent a “hypercoagulable” state, new research suggests.
Researchers from China describe three patients admitted to the intensive care unit (ICU) with confirmed SARS-CoV-2 infection, severe COVID-19, and clinically significant coagulopathy, antiphospholipid antibodies, and multiple cerebral infarcts.
“Antiphospholipid antibodies abnormally target phospholipid proteins, and the presence of these antibodies is central to the diagnosis of the antiphospholipid syndrome,” write Yan Zhang, MD, and colleagues from Peking Union Medical College Hospital in Beijing, China.
“However, these antibodies can also arise transiently in patients with critical illness and various infections,” they add.
The findings were published online April 8 as a correspondence letter in the New England Journal of Medicine.
The first patient described in the report was a 69-year-old man with a history of hypertension, diabetes, and stroke who presented with fever, cough, dyspnea, diarrhea, and headache.
Initial treatment for COVID-19 was supportive. However, the patient deteriorated to hypoxemic respiratory failure and he was put on a ventilator. Imaging showed ground-glass opacity and bilateral pulmonary infiltrates.
The patient had evidence of ischemia in both lower limbs and in digits two and three of the left hand. Brain imaging revealed bilateral cerebral infarcts in multiple areas.
Pertinent laboratory results on ICU admission included leukocytosis, thrombocytopenia, an elevated prothrombin time and partial thromboplastin time, and elevated levels of fibrinogen and D-dimer. Serologic tests were positive for anticardiolipin IgA and anti-β2-glycoprotein I IgA and IgG.
The two other patients were a 65-year-old woman and a 70-year-old man. They had similar findings to the first patient, including positive tests for anticardiolipin IgA and anti-β2-glycoprotein I IgA and IgG.–
Presence of antibodies “may rarely lead to thrombotic events that are difficult to differentiate from other causes of multifocal thrombosis in critically patients, such as disseminated intravascular coagulation, heparin-induced thrombocytopenia, and thrombotic microangiopathy,” the researchers write.
Carlos del Rio, MD, Division of Infectious Diseases, Emory University School of Medicine, Atlanta, Georgia, singled out this report during an April 10 media briefing hosted by the Infectious Diseases Society of America to discuss emerging issues with COVID-19.
The issue of hypercoagulability with COVID-19 is “really interesting,” del Rio noted.
“We are seeing a hypercoagulable state in this condition and it’s something we don’t yet fully understand. We are seeing people present with pulmonary emboli. Also, some of the renal insufficiency that we are seeing…is related to microemboli at the level of the kidneys,” he said.
“We know that infections can cause a hypercoagulable state. Understanding the hypercoagulability in this condition is going to be critical,” said del Rio.
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