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Learning Center
Coagulation Corner
Sunday, November 1, 2009
H1N1 & COAGULATION
H1N1- has infected every area of our lives- and I don't mean in the pure definition of infection- you see signs to be cautious at work- every day on the news, you stay away from people who sneeze, coughing into your arm is common place- these are all good practices. Forget epidemic, we want to avoid pandemic! So stay healthy, wash your hands, drink plenty of fluids and stop asking yourself, how does this H1N1 affect the coagulation system- that is what I am hear for!
The notable characteristic of a pandemic quality flu virus is its ability to kill young adults (ages 20 - 45). It does this by "cytokine storm." It is believed that cytokine storms were responsible for many of the deaths during the 1918 influenza pandemic, which killed a disproportionate number of young adults. Here's how:
When the immune system is fighting pathogens, cytokines signal immune cells such as T-cells and macrophages to travel to the site of infection. ... In some instances, the reaction becomes uncontrolled, and too many immune cells are activated in a single place. ... If a cytokine storm occurs in the lungs, for example, fluids and immune cells such as macrophages may accumulate and eventually block off the airways, potentially resulting in death.
The cytokine storm (hypercytokinemia) is the systemic expression of a healthy and vigorous immune system resulting in the release of more than 150 inflammatory mediators (cytokines, oxygen free radicals, and coagulation factors).
Now mind you the research that I found was in pigs (I know we are not supposed to use swine flu), but the coagulation process is explained.
Remember, this is in pigs.
This virus is a member of the Pestivirus (get it, pesti virus) genus in the Flaviviridae family. Cellular response against virus infections includes production of inflammatory and antiviral cytokines, and the induction of cell death through apoptosis. Strains of high virulence cause an acute disease with haemorrhagic fever, thrombocytopenia and disseminated intravascular coagulation (DIC). Vascular endothelial cells maintain balance of the coagulation process by providing an anti-thrombotic barrier as well as activation by pathogens which express a proinflammatory and procoagulant phenotype to eliminate infection. If this system is not controlled, it results in the appearance of microthrombi, DIC, and fibrinolysis. These changes are thought to occur via several factors one by the induction of blood coagulation factors in endothelial cells.
There have been no reported cases of DIC in human cases of HINI.
However it never hurts to review the process.
Disseminated Intravascular Coagulation (DIC) is an acquired syndrome that occurs as a result of an underlying condition. This disorder leads to an unbalance in the coagulation system characterized by the simultaneous activation and consumption of clotting factors and platelets. Consumption results in patients bleeding. While the activation of intravascular coagulation results in fibrin formation which deposits in the microvasculator causing thrombosis.
DIC results from an inappropriate activation of clotting factors or abnormal release of tissue factor into the circulation. The major mechanisms of the coagulation system are activated. The extrinsic pathway is activated as excess tissue factor is released during tissue necrosis and organ failure. This results in the formation of platelet-fibrin rich thrombi in the vasculature. Some of the triggers of DIC that activate the intrinsic pathway are liver disease, immune disorders, burns, shock, OB complications and the most common trigger is sepsis.
Naturally occurring anticoagulants which are inhibitors of coagulation are also impaired. Antithrombin, the most important inhibitor of thrombin, is reduced due to a combination of consumption, degradation, and impaired synthesis. Protein C system is decreased due to impaired synthesis as well as the reduction of protein S which is a cofactor of protein C. There is also evidence that tissue factor pathway inhibitor (TFPI) doesn't regulate tissue factor sufficiently. This further triggers the activation of coagulation in DIC.
Plasminogen activators are released due to bacteremia and endoteoxima. However, the fibrinolytic system, which is responsible for the dissolution of a clot, is mostly shut off during DIC. This is due to suppressed activity resulting from an increase in plasminogen activator inhibitor (PAI-1).
In DIC, bleeding occurs due to deficiencies in multiple coagulation factors (coagulation factors are consumed in thrombi and digested by plasmin) and thrombocytopenia (platelets are consumed in the thrombi). Additionally, intravascular fibrin deposits contribute to organ failure and mortality. All of these processes cause the simultaneous formation of both thrombin and plasmin, resulting in the clinical presentation of bleeding and clotting.
Thrombosis and the Flu
Pulmonary emboli are not known to be a common complication of acute respiratory distress syndrome (ARDS) or of sepsis syndrome, but both ARDS and sepsis represent hypercoagulable states Pulmonary emboli were not noted in patients hospitalized with novel influenza A (H1N1) virus infection in Mexico . One clinical study did not identify any increased risk for pulmonary embolism with seasonal influenza virus infection . However, a report of two patients with rapidly progressive hypoxemia associated with influenza A (H3N2) virus infection noted that they received a diagnosis of acute pulmonary embolism . Clinicians providing care to patients with novel influenza A (H1N1) virus infection should be aware of the potential for patients with ARDS to develop a hypercoagulable state and for pulmonary emboli to cause severe complications, including fatal outcomes.The majority of patients with H1N1 that undergo chest X-rays have normal radiographs. CT scans
One population that might have heightened concern is the bleeding disorder community, There is no threat to the safety of plasma derived clotting factor products. Influenza is a lipid enveloped virus that is inactivated by several steps in the production of products. Additionally, prospective donors who show symptoms of the flu are prevented from donating blood.
So, that is the update on this pesky bug, stay healthy, and
How relevant is it to end with Porky Pig-
That's all folks!
Donna Castellone
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About the Author
Donna Castellone,
MS, MT(ASCP)SH
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