Thrombotic microangiopathy in intensive care units

Thrombotic microangiopathy (TMA) is a clinical entity characterised by endothelial lesions and the consequent formation of thrombi, with rapid progression and where clinical manifestations are generally severe due to the presence of organic dysfunctions. It is important to know and understand that the aetiology is multifactorial and clinically overlaps and that there are many mechanisms of the disease. The TMA disease complex requires an adequate differentiation between primary and secondary thrombocytopenia. This requires reviewing any underlying and reversible causes with the management of multisystem support in the ICU, leading to a marked improvement in patient outcomes. The current classification is determined by the aetiology and clinical association, requiring the multiple causes of TMA to be investigated and to treat the underlying causes of each. A correct differential diagnosis is essential as the pathophysiological changes, such as pregnancy, infections, medications, etc., can be confusing or, in turn, trigger a TMA. Similarly, in the presence of a thrombotic thrombocytopenic purpura due to ADAMTS 13 protein deficiency, the starting of plasmapheresis is fundamental. Also, in view of the clinical diagnosis of atypical haemolytic uremic syndrome, the prescribing of eculizumab is a priority and definitive, since early treatment is key to changing the prognosis and improving the morbidity and mortality reported in the studies.