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Disseminated intravascular coagulation (DIC) is a condition in which blood clots form throughout the body, blocking small blood vessels. [1] Symptoms may include chest pain, shortness of breath, leg pain, problems speaking, or problems moving parts of the body. [1] As clotting factors and platelets are used up, bleeding may occur. [1]
It is characterized by overwhelming bacterial infection meningococcemia leading to massive blood invasion, organ failure, coma, low blood pressure and shock, disseminated intravascular coagulation (DIC) with widespread purpura, rapidly developing adrenocortical insufficiency and death.
Hemolysis, shock, ischemia, acute respiratory distress syndrome, disseminated intravascular coagulation, [1] and acute renal failure. [2] Usual onset: Hours to months (various types of hypersensitivities reactions)of the initial drug exposure. [1] Causes: Antimicrobials, nonsteroidal anti-inflammatory drugs, antineoplastic drugs, and other ...
People with AHTR are managed with supportive care, which may include diuretics, blood pressure support, and treatment of disseminated intravascular coagulation (with fresh frozen plasma, cryoprecipitate, and platelet transfusion). [6] The use of steroids, intravenous immune-globulins or plasma exchange is not supported by evidence. [6]
This leads to the sequelae of DIC or Disseminated intravascular coagulation. [5] [7] It is also supposed that endothelin a potent vasoconstrictor is upregulated during the course of the amniotic fluid embolism in the maternal circulation. This endothelin acts in an antagonistic fashion to blood vessels causing intense vasoconstriction. [5]
Splenic infarction can be due to vasculitis or disseminated intravascular coagulation. Various other conditions have been associated with splenic infarction in case reports, for example granulomatosis with polyangiitis [ 15 ] or treatment with medications that predispose to vasospasm or blood clot formation , such as vasoconstrictors used to ...
The pathophysiology behind septic shock is as follows: 1) Systemic leukocyte adhesion to endothelial cells [18] 2) Reduced contractility of the heart [18] 3) Activation of the coagulation pathways, resulting in disseminated intravascular coagulation [18] 4). Increased levels of neutrophils [18]
Early PCAS (first 24 hours) is generally defined by hyperfibrinolysis, due to increased tissue plasminogen activator activity, resulting in a risk of disseminated intravascular coagulation. However late PCAS generally presents with hypofibrinolysis, due to increased PAI-1 levels, resulting in a risk of multiorgan dysfunction. [20]