A thrombotic storm may also occur due to the following precipitating events: alterations in coagulation and fibrinolysis, which induce high mortality rates, and infections amongst pediatric patients where IgM and IgG anti-β2-GPI antibodies induce an endothelial signal, leading to a procoagulant state. It is also hypothesized that thrombotic storms occur due to prothrombotic genetic risk factors, which trigger a sped-up form of thrombosis after its first occurrence, rather than being caused solely by environmental factors. Cardiovascular, nervous, kidney, and lung system complications are common. More specifically with the heart, Ashersons syndrome can lead to complications such as mitral valve regurgitation (MVR) in which the mitral valve does not shut properly allowing backflow of blood into the heart as well as angina (chest pain) and myocardial infarction (heart attack). Furthermore, complications in the kidneys may occur, including low urine production and high blood pressure, while complications with the lungs can result in rapid breathing (hyperventilation) and low oxygen levels (hypoxemia). The affected individual may exhibit skin purpura and necrosis. Cerebral manifestations may lead to encephalopathy and seizures. Myocardial infarctions may occur. Strokes may occur due to the arterial clotting involvement. Death may result from multiple organ failure. Furthermore, the syndrome has been shown to manifest multi-organ failures and miscarriages in the context of pregnancies. 54% of pregnant mothers with the disease experienced fetal loss, and around 50% of pregnant mothers died from complications associated with the syndrome. Diagnosis
Two specific types of blood tests are used to aid in the diagnosis of Ashersons Syndrome.
A coagulation blood test is used to measure and determine the bloods ability to clot and how fast it takes to clot, indicating the presence of lupus anticoagulant in the blood. An Enzyme-Linked ImmunoSorbent Assay (ELISA) test is done to detect anticardiolipin antibodies presence in the blood. Individuals with CAPS often exhibit a positive test to antilipid antibodies, typically IgG. Patients with high aPL(positive antiphospholipid antibodies) must have microthrombosis in multiple organs to definitively be diagnosed with CAPS— a high antilipid antibody count is not sufficient enough for diagnosis. To be diagnosed with CAPS, a patient must have three or more new organ thromboses developing within less than a week, and a biopsy must be later performed testing for microthrombosis in order to accurately diagnose the patient with ‘definite CAPS’. If the patient has two or less new organ thromboses within a week but a biopsy still indicates the presence of microthrombosis, the patient is not considered to have CAPS. Positive test are often repeated due to the fact that antilipid antibodies can be present in the body for short stints due to infection or drug use. Along with that, individuals may or may not have a history of lupus or another connective tissue disease. Association with another disease such as lupus is called a secondary APS unless it includes the defining criteria for CAPS. Treatment
Treatments may involve the following steps:

Prevention includes the use of antibiotics for infection and parenteral anticoagulation for susceptible patients.