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Disseminated Intravascular Coagulation
Published in Hau C. Kwaan, Meyer M. Samama, Clinical Thrombosis, 2019
Thiti Jaojaroenkul, Hau C. Kwaan
Coumarin drugs and antiplatelet agents are not effective in the treatment of DIC. The use of heparin to prevent microthrombi formation in patients with progressive and severe life-threatening DIC is warranted. It has been used with good results in patients with purpura fulminans95–97 and improvement in survival has been reported among septicemic patients who survived more than 24 h after initiating therapy.98 Weber and Blakeley31 successfully treated a case of severe DIC in heat stroke with heparin. Heparin is also being given as an adjuvant therapy for patients with amniotic fluid embolism.99,100 It has corrected hypofibrinogenemia in a 26-week pregnant woman with DIC following death fetus in utero of a single twin,101 while a normal fetus was delivered at 36 weeks along with a stillborn twin. Sack et al.34 used heparin to treat patients with DIC associated with malignancy and found improvement in 29 of 48 patients. When heparin was discontinued, 19 patients had recurrent symptoms. This was also observed by Bell et al. in two other patients.102 Those patients with neoplasia and DIC who are not in complete remission may need prolonged subcutaneous heparin administration.
Drugs causing cutaneous necrosis
Published in Biju Vasudevan, Rajesh Verma, Dermatological Emergencies, 2019
Purpura fulminans is a rapidly progressing thrombotic disorder characterized by skin necrosis and disseminated intravascular coagulation (DIC) [30]. The clinical presentation of purpura fulminans is with acute-onset purpuric rash that rapidly progresses to large ecchymotic areas with sharp, irregular borders (Figure 7.2). In severe cases, gangrene and necrosis of the extremities may be observed [31]. Various drugs have been implicated in the causation of purpura fulminans. Individuals with protein C and protein S deficiencies are predisposed to development of purpura fulminans, including the drug-induced ones. In a study by Bonaldo et al., analyzing the World Health Organization's Global Individual Case Safety Report (ICSR) database, the common drugs implicated in causation of purpura fulminans were antineoplastic agents, antithrombotic agents, and antibacterials for systemic use. Other drugs that were most frequently reported were paracetamol, dabigatran, oxaliplatin, and bevacizumab [32].
Head and neck infections
Published in S. Musheer Hussain, Paul White, Kim W Ah-See, Patrick Spielmann, Mary-Louise Montague, ENT Head & Neck Emergencies, 2018
Muhammad Shakeel, AE Louise McMurran
Purpura fulminans is a rare syndrome of intravascular thrombosis and haemorrhagic infarction of the skin; it is rapidly progressive and accompanied by vascular collapse. Clinically it presents as septic shock, and the newest revolutionary advancement in the treatment of neonatal purpura fulminans is the use of activated protein C.
New-onset diabetic ketoacidosis with purpura fulminans in a child with COVID-19-related multisystem inflammatory syndrome
Published in Infectious Diseases, 2022
Parvathi Parappil, Sushant Ghimire, Apoorv Saxena, Sweta Mukherjee, B. M. John, Vishal Sondhi, P. Sengupta, Suchi Acharya
Immune-triggered, complement-mediated thrombotic microangiopathy is common in patients with SARS-CoV-2-related disease [17,18]. Like the better-known thrombotic microangiopathy syndromes (like HUS, TTP, and DIC), this is characterised by organ failure caused by widespread micro-clots in capillaries and other small vessels [3]. Whether this thrombotic microangiopathy is caused by an autoreactive thrombotic disorder or is secondary to comorbidity (like type 1 diabetes mellitus/diabetic ketoacidosis in our patient) is debatable. Reports of SARS-CoV-2-related thrombotic microangiopathy are emerging in children, wherein thrombotic microangiopathy has been shown to affect both the acute- and post-infectious stage [17]. In our patient, this involvement was in the MIS-C stage. Purpura fulminans, as in our patient, has been scarcely reported in children and adults affected with Covid-19 are likely to be a manifestation of thrombotic microangiopathy [18].
Streptococcal toxic shock syndrome in a returning traveller
Published in Acta Clinica Belgica, 2019
Stéphanie Note, Patrick Soentjens, Marie Van Laer, Philippe Meert, Peter Vanbrabant
Cutaneous manifestation is a common finding in TSS. Typically, the rash will be a diffuse, macular, sometimes pruritic erythroderma, often present at onset of disease [2]. Desquamation of the palms and soles typically develops 1 to 3 weeks later. Superficial ulcerations may occur in severe cases. Non-pitting oedema due to capillary leak can be present [2]. If the pain exceeds what is expected based on clinical examination, and especially at appearance of purpura or ecchymotic plaques, necrotizing fasciitis needs to be suspected [13–15]. If further investigation appears negative, histology can guide into the direction of acute infectious purpura fulminans, as presented in this case. Purpura fulminans is a life-threatening syndrome marked by DIC and endovascular thrombosis, resulting in the characteristic pattern of cutaneous purpura, associated to multiple-organ failure [14–16]. Purpura fulminans can be related to an anticoagulant protein deficiency or a post-infectious context, but most commonly occurs as a severe complication in the acute phase of infection [15,16]. Typically, gram-negative bacteria are the causal organisms, but reports of association with a streptococcal infection were made [16–18].
Disseminated intravascular coagulation: an update on pathogenesis and diagnosis
Published in Expert Review of Hematology, 2018
Marcel Levi, Suthesh Sivapalaratnam
The diagnosis of DIC is based on clinical findings in combination with laboratory parameters [76]. A diagnosis of DIC can only be made if there is a primary condition known to be associated with DIC and clinical signs and symptoms are compatible with this underlying disease. In addition, purpura fulminans or hemorrhagic thrombosis of the skin and underlying tissue can be visible. Thromboembolism of larger vessels will present itself as well by symptomatology compatible with the occlusion in circulation. Widespread bleeding from mucosal tissue (such as gingiva, nose or digestive tract) and from insertion points of indwelling catheters can be another typical finding, particularly in primary hyperfibrinolytic DIC [77]. Characteristic findings in routine laboratory assays are thrombocytopenia or a rapid decrease in subsequent platelet counts, abnormal screening assays (such as PT or aPTT) and a marked elevation of products that are formed during fibrin formation and subsequent degradation (D-dimer or any other form of fibrin degradation products [76]. However, there are alternative diagnoses that can cause these changes (Table 2), and these need to be considered as they may have differential therapeutic consequences [76].