28th April 2020
Emerging data points to faulty blood clotting system in Covid-19 patients with underlying health issues.
The underlying health issues that increase the risk of Covid-19 severity are high blood pressure, diabetes, heart disease, cerebrovascular disease, respiratory conditions such as chronic obstructive pulmonary disease (COPD), and conditions affecting the kidneys.
Early findings suggest that the hyperactivity of the body’s anticoagulant response may be to blame for the severe bleeding dysfunctions – in other words, an overactive anticlotting system is causing excessive bleeding in Covid-19, the disease caused by the new coronavirus SARS-CoV-2.
Hyperfibrinolysis an indicator
Fibrinolysis is an enzymatic process that serves to limit clot formation. According to research, the over activity of the body’s attempts to remove blood clots is known as hyperfibrinolysis, a mechanism that can result in increased and catastrophic bleeding. Doctors testing the blood of critically ill C-19 patients are finding increased levels of fibrinogen, also known as clotting factor.
Blood clots form on a protein called fibrin. In fibrinolysis, the fibrin is broken down through a process of two opposing forces that regulate the conversion of plasminogen to plasmin – the active enzyme responsible for dissolving a fibrin clot into soluble Fibrin Degradation Products (FDP).
Data shows that people with severe COVID-19 also present with elevated fibrinogen or FDP and reduced platelets (an inability to form clots), which is also considered an indication of hyperfibrinolysis.
Haemorrhage in multiple organs, together with the correlation between fibrinolysis and mortality, supports a growing opinion that hyperfibrinolysis can explain the poor prognosis in people with underlying heath conditions.
Some patients also develop disseminated intravascular coagulopathy (DIC). DIC is a rare but serious disorder in which small blood clots can develop throughout the body.
Furthermore, COVID-19 patients with comorbidities often present with high levels of plasminogen and plasmin. Plasminogen is a non-active substance in the blood. When substances found in the blood vessel cells activate plasminogen, it converts into plasmin — an enzyme that reduces blood clots. However, too much plasminogen and plasmin can cause haemorrhaging.
D-dimer also an indicator
Recent data also shows another protein called D-dimer, which is formed in the blood after enzymes break down a clot, is significantly elevated in patients with severe COVID-19 and is also associated with a poor prognosis.
The more severe the infection becomes, the more D-dimer levels increase, particularly in patients who develop acute respiratory distress syndrome (ARDS).
It is reported that it generally takes at least 1 week for elevated D-dimer to decrease in mild cases but longer for severe patients. Therefore plasmin(ogen) levels and its enzymatic activity are considered important biomarkers of disease severity, in addition to resultant D-dimer.
How does COVID-19 cause blood clots?
It is now understood that COVID-19 causes inflammation, and can include an inflammatory cytokine storm (an overproduction of immune cells and their activating compounds). It is thought that the inflammation caused by COVID-19 sets off a chain of events that causes blood clots to develop – and targeting hyperfibrinolysis with a broad spectrum of specific anti-plasmin compounds may prove to be a promising strategy for improving the clinical outcome of patients with comorbid conditions.
Treatments for COVID-19 patients with blood clots
Clinicians and researchers are using their clinical experience to determine the best way to prevent and manage clot formation in critically ill C-19 patients. Existing anticoagulant medications, such as low molecular weight heparin, are being used.
Whilst a low dose blood thinner is considered low risk, giving larger doses can cause excessive bleeding with poor clinical outcomes. C-19 coagulation guidance therefore advocates stepping-up preventative dosing but reinforces the need for individual patient bleed risk assessment.
In the event of high bleed risk, the guidance supports use of mechanical thromboprophylaxis, e.g. Intermittent pneumatic compression (IPC or SCD) or the geko™ device as an adjunct to drugs, or used alone.
The geko™ device is recommended by NICE and cleared by the FDA for blood clot prevention in combination with drugs or when drugs and other methods of mechanical prophylaxis are impractical or contraindicated.
The geko™ device impact on blood coagulation
The following studies show the geko™ device can increase clot prevention; shifting the balance of coagulation towards a lower risk of thrombosis.
Easy to use, the geko™ is a battery powered, disposable, neuromuscular electro-stimulation device designed to increase blood flow in the deep veins of the leg.
The geko™ device gently stimulates the common peroneal nerve activating the calf and foot muscle pumps resulting in increased blood flow, at a rate equal to 60% of walking, without a patient having to move. The highly portable geko™ device is:
Whilst NICE guidance specifically recommends use of geko™ device in reducing the risk of deadly blood clots, results from other clinical studies, describing the ability for the geko™ device to increase tissue oxygen levels and support kidney function, demonstrates the impact increased systemic blood flow – generated by geko device – can have in an intensive care environment beyond DVT prevention.
Sue Davenport-VP Marketing Communications
28th April 2020