Physiology of blood
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal in Principles of Physiology for the Anaesthetist, 2015
Following damage to the vascular epithelium, a cascade of events is initiated leading to the formation of a blood clot. Platelet adhesion, release and activation occur. Platelet aggregation at the site of injury occurs within seconds. Current theories on the coagulation cascade are based on the cell-based theory involving three phases: initiation, amplification and propagation. Tissue-factor-bearing cells and activated factor VII initiate the process by generating small amounts of factors Xa and IIa on platelets, monocytes, macrophages or subendothelial fibroblasts. The IIa primes the activated platelets with factors VIIIa, Va and XIa, and this generates the IXa–VIIIa complex on platelets and elicits the propagation phase via Va–Xa (prothrombinase) complex, which generates large amounts of thrombin (IIa) that activates fibrinogen to fibrin. The clotting mechanism requires calcium ions and phospholipids present in the membranes of the platelets. The fibrin threads trap blood cells to form a stronger clot which retracts by shrinkage. The blood clot is then dissolved by plasmin. Undamaged vascular endothelial cells prevent clotting by releasing natural anticoagulants, such as heparin and prostacyclins, and by expressing thrombomodulin, a protein that binds thrombin and activates protein C, an activator of plasmin.
Cardiovascular risk management
Janet Titchener in Diabetes Management, 2020
Most of us think of cholesterol as being a problem because it builds up on the inside of our blood vessel walls. This cholesterol plaque, as we call it, narrows the blood vessels, making it harder for the heart to pump the blood around the body, i.e. cholesterol build-up increases blood pressure. If the cholesterol plaque builds up a lot, it can become quite unstable and bits of plaque can flick off, travel downstream in the blood and lodge in smaller blood vessels, blocking off the blood supply. If this occurs in the heart or brain, the person experiences a heart attack or stroke. Cholesterol build-up also disrupts the regular flow of blood. When blood flows irregularly, blood clots can form. These, like the bits of plaque, can sail off downstream and lodge in smaller blood vessels, again increasing the risk of having a heart attack or stroke.
Principles of laparoscopic and robotic surgery
Professor Sir Norman Williams, Professor P. Ronan O’Connell, Professor Andrew W. McCaskie in Bailey & Love's Short Practice of Surgery, 2018
The best way of dealing with blood clots is to avoid them. As mentioned, careful dissection and identification of the cystic artery and its branches, as well as identifying and carrying out dissection of the gallbladder in the correct plane, help to prevent bleeding from the cystic vessels and the hepatic bed. Nevertheless, clot formation takes place when unsuspected bleeding occurs or when inflammation is severe and a clear plane is not present between the gallbladder and the hepatic bed. The routine use of 5000-7000 units of heparin per litre of irrigation fluid helps to avoid the formation of clots. When extra bleeding is foreseen, a small pool of irrigation fluid can be kept in the operative field to prevent clot formation. After clots have formed, a large bore suction device should be used for their retrieval. Care should be taken to avoid suctioning in proximity to placed clips.
Thrombotic events in children and adolescent patients with SARS-CoV-2 infection: a systematic review with meta-analysis on incidence and management
Published in Expert Review of Hematology, 2022
Giovanna Vitaliti, Valentina Giacchi, Monica Sciacca, Martino Ruggieri, Raffaele Falsaperla
The hemostatic system usually forms blood clots. Hemostasis has a complementary role in developing a barrier against pathogen invasion, sustaining innate immunity. This immune function has been described in several studies, who gave to this phenomenon the name of ‘immunothrombosis concept’ [9]. The different elements of the hemostatic system are all involved in the immune network and they explain the function of chemotactic to immune cells, stimulating different immune elements. Moreover, the immune system itself is important for the activation of coagulation factors [10–12]. Thrombosis, particularly microvascular thrombosis, is the leading cause of morbidity and mortality in COVID-19, as the ‘immunothrombotic’ cascade involves positive feedback loops among inflammatory, coagulation, and complement cascades. In this regard, Magro C et al. described a pauci-inflammatory thrombogenic vasculopathy, with deposition of fragments of complement C5b-9 and C4d in both grossly involved and normally-appearing skin. In addition, the authors found the co-localization of COVID-19 spike glycoproteins with C4d and C5b-9 in the interalveolar septa and the cutaneous microvasculature of two cases examined. Therefore, the authors concluded that COVID-19 may define a type of microvascular injury syndrome mediated by complement activation and an associated procoagulant state [11]. This mutual relationship could explain some common findings between the two systems in COVID-19 infection.
Caveolae, caveolin-1 and lung diseases of aging
Published in Expert Review of Respiratory Medicine, 2019
Sarah A. Wicher, Y.S. Prakash, Christina M. Pabelick
Pulmonary hypertension is defined as pulmonary pressures >25 mmHg at rest or 30 mm Hg with exercise. Pulmonary hypertension is likely multifactorial in origin and can be idiopathic in nature. Although rare compared to other lung or vascular diseases, its occurrence (often in young women) and limited medical therapy make it a devastating disease. Pulmonary arterial hypertension is a disease of the blood vessels of the lungs that results in elevated arterial pressures. In pulmonary hypertension per se, elevation of pressures is caused by another disease extrinsic to the pulmonary vasculature which are themselves not diseased [111]. The World Health Organization (WHO) categorizes pulmonary hypertension in the following five groups: 1. Pulmonary Arterial Hypertension, 2. Pulmonary Hypertension due to left heart disease, 3. Pulmonary Hypertension due to lung disease, 4. Pulmonary Hypertension due to blood clots in the lungs, and 5. Blood and other rare disorders that lead to Pulmonary Hypertension [112].
Risk factors for in-hospital mortality among acute ischemic stroke patients in China: a nationwide prospective study
Published in Neurological Research, 2021
Zhi-Xin Huang, Hong-Qiu Gu, Xin Yang, Chun-Juan Wang, Yong‐Jun Wang, Zi‐Xiao Li
Platelets are necessary for normal hemostasis, but may also be involved in thrombosis. Antiplatelet therapy (APT) has recently gained popularity due to its beneficial effects on cerebrovascular disease, especially in the acute phase of cerebral infarction. Our study suggests that in patients with AIS, APT can reduce the incidence of IHM and may improve the prognosis. Our study also confirms that IHM occurred 1.51-fold more often in AF patients compared with patients without AF, which can be attributed to its increased incidence of heart failure or embolic events [36].To reduce these complications, anticoagulant therapy is recommended as the preferred treatment for secondary prevention. Oral anticoagulant therapy should be started between 4 and 14 days after AIS to ensure the best efficacy and safety [37].AIS patients are at increased risk for pulmonary embolism due to limb paralysis, bed rest and an increased pro-thrombotic state [38]. Because blood clots can block blood flow to parts of the lungs, pulmonary embolism is often a fatal vascular disease. Our study confirms that PE was a strong and independent predictor of IHM.