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Acute coronary syndromes
Published in Henry J. Woodford, Essential Geriatrics, 2022
The key treatment for STEMI is immediate reperfusion by primary PCI. If this is not available in a timely manner then reperfusion by fibrinolytic therapy can be used. Guidelines recommend primary PCI if it can be delivered within 12 hours of symptom onset and within two hours of diagnosis.12 Otherwise, fibrinolysis should be given within 12 hours of symptom onset unless there are contraindications – e.g. bleeding disorders, recent haemorrhage or history of haemorrhagic stroke. PCI might be considered in some cases beyond 12 hours from symptom onset, for example, if there was ongoing pain, ECG changes or complications of ischaemia. PCI is also likely to be better than fibrinolysis for people on oral anticoagulants and a time delay may be less important. People aged over 75 tend to do better with PCI compared to thrombolysis.10,22
Congenital and acquired disorders of coagulation
Published in Jennifer Duguid, Lawrence Tim Goodnough, Michael J. Desmond, Transfusion Medicine in Practice, 2020
Jeanne M Lusher, Roshni Kulkarni
The most common cause of systemic fibrinolysis is liver disease. Plasminogen activator levels are increased owing to decreased clearance coupled with decreased production of PAI-1. Other causes include urogenital neoplasm (associated with increased secretion of urokinase), acute promyelocytic leukaemia (APL cells contain TF and plasminogen activator), primary amyloidosis, immediate Puerperium, cardiopulmonary bypass, and inherited PAI-1 and α2-antiplasmin deficiency. Iatrogenic causes include therapeutic administration of plasminogen activators (t-PA, streptokinase, or urokinase).62
Spontaneous (Unexplained) Thrombosis: The Inherited Basis for the Thrombohemorrhagic Balance
Published in E. Nigel Harris, Thomas Exner, Graham R. V. Hughes, Ronald A. Asherson, Phospholipid-Binding Antibodies, 2020
The fibrinolytic system may also be activated by the so called intrinsic pathway, i.e., the factor XII-prekallikrein (PK)-high molecular weight kininogen (HMWK)-activator mechanism.42 The clinical importance of this mechanism as an activator pathway for fibrinolysis remains obscure.
Ligneous conjunctivitis mimicking preseptal cellulitis in a 3-month-old infant
Published in Ophthalmic Genetics, 2023
Valentien Merlevede, Virginie Ninclaus, Dimitri Roels, Liesbeth Huys, Bert Callewaert, Elke O. Kreps
Different treatment strategies have been reported, consisting of surgery, fibrinolysis or anticoagulation, and immunomodulation (9). Surgical excision is often performed, despite the risk of triggering or aggravating acute flare-ups and must be carefully and thoughtfully performed. Lysis of the accumulated fibrinous material is attempted with topical enzymatic therapy (hyaluronidase, alpha-chymotrypsin), topical heparin or plasminogen. Immunomodulatory therapy options with topical corticosteroids or 2% cyclosporine A may reduce the recurrence risk after surgical excision. Due to the scarcity of cases and the absence of comparative trials, there are no validated therapeutic protocols. Anecdotal treatment options include expensive, pharmacy-prepared eye drops such as topical plasminogen (1 mg/mL) and heparin (1000 or 5000 I.E./ml). We therefore opted for very frequent instillation of commercially available artificial tears containing heparin (HYLO PARIN®, 1300 I.E./ml heparin sodium), combined with low-dose topical corticosteroids to reduce inflammation. In this case, this approach achieved rapid response. In patients with lower systemic plasminogen levels, this approach might not be sufficient for severe acute flare-ups. In such patients, however, HYLO PARIN® eye drops are a good alternative to consider as maintenance therapy, given the low cost and commercial availability.
Survival in Patients with Paramedic-Identified ST-Segment Elevation Myocardial Infarction
Published in Prehospital Emergency Care, 2021
Tan N. Doan, Kirsten Wilson, Brendan V. Schultz, Brett Rogers, William Vollbon, Marcus Prior, Stephen Rashford, Emma Bosley
A total of 1,541 patients were included (Figure 1). Of these, 23.9% (369/1,541) received prehospital fibrinolysis therapy, and the remaining (76.1%, 1,172/1,541) were direct PCI referral. Table 1 compares the characteristics and survival outcomes between prehospital fibrinolysis patients and direct PCI referral patients. Higher proportions of prehospital fibrinolysis patients suffered STEMI in rural areas, had Aboriginal and Torres Strait Islander status, had out-of-hospital cardiac arrest, were younger, obese, and current smokers, compared to direct PCI referral patients. 30-day all-cause mortality was low, being 2.2% (8/369) for prehospital fibrinolysis group and 1.8% (21/1,172) for direct PCI referral group (between-group difference p = 0.661). One-year all-cause mortality for the two groups were 2.7% (10/369) and 3.2% (37/1,172), respectively (p = 0.732). The two groups also had comparable survival times (Figure 2). Among the 369 patients who received prehospital fibrinolysis, minor bleeding was the only observed adverse event, reported in 4 patients (1.1%).
A rare case of eptifibatide-induced thrombocytopenia
Published in Journal of Community Hospital Internal Medicine Perspectives, 2021
Khalil Kamar, Kira MacDougall, Mira Alsheikh, Sara Parylo, Yevgeniy Skaradinskiy
Disseminated intravascular coagulation (DIC) is another likely etiology in this case. DIC is known as consumption coagulopathy; it is an acute life-threatening emergency. It causes a systemic pathologic activation of the coagulation system leading to an extensive formation of thrombi, which in turn leads to consumption of pro- and anticoagulation factors. It also involves fibrinolysis and excessive bleeding. The diagnosis is based on clinical and laboratory criteria. Clinically, the patient should have an underlying condition known to be associated with DIC, either infectious or non-infectious, and present with generalized bleeding and unexplained thrombosis. Laboratory findings include thrombocytopenia, low fibrinogen, elevated prothrombin time (PT), activated partial thromboplastin time (PTT), and D-dimer (a marker of fibrin degradation). These tests should not be taken in isolation. A scoring system was developed by the International Society of Thrombosis and Haemostasis; it includes low platelet count and fibrin-related marker, prolonged PT, and low fibrinogen level. A score greater than or equal to five is compatible with overt DIC[7]. We could not calculate the score in our patient since the D-dimer was not performed. However, it was unlikely, since fibrinogen, international normalized ratio (INR), and PTT were normal (Table 1).