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Pathophysiology
Published in Burkhard Madea, Asphyxiation, Suffocation,and Neck Pressure Deaths, 2020
Wolfgang Keil, Claire Delbridge
The venae vertebrales consist of an inner and an outer plexus. The inner system runs in the spinal canal and cannot be compressed by strangulation. The outer part of the venous plexus is located in the vertebral muscles and apparently has a larger cross-section than the venae jugulares. However, compression of the neck can significantly impede blood flow from the brain. If the impairment of the blood flow is greater than the reduction of the inflow, a considerable passive hyperaemia develops above the compression. In this case, considerably more O2 is withdrawn from the accumulated blood than normally, so that cyanosis develops in the head and neck region. If the obstruction persists, oxygenated blood cannot enter and cerebral hypoxia occurs. Due to the suppressed cleansing function of the blood, mainly acidic metabolites accumulate, resulting in particularly pronounced cell damage. In addition, tissue fluid can be expressed, which can lead to swelling of the face.
Anatomy of the Pharynx and Oesophagus
Published in John C Watkinson, Raymond W Clarke, Terry M Jones, Vinidh Paleri, Nicholas White, Tim Woolford, Head & Neck Surgery Plastic Surgery, 2018
Venous drainage is via the internal submucosal and the external pharyngeal venous plexus, which sits predominantly on the posterior aspect of the middle constrictor. The venous plexus drains into the internal jugular vein and, to an extent, connects with the pterygoid venous plexus. The venous plexus is a common cause of significant bleeding in operations of the pharynx and can, on occasion, be very difficult to control.
Complications of mitral stenosis
Published in Neeraj Parakh, Ravi S. Math, Vivek Chaturvedi, Mitral Stenosis, 2018
Senguttuvan Nagendra Boopathy, Ambuj Roy
The bronchial arterial circulation forms the bronchial venous plexus, which is connected to the pulmonary venous circulation. Approximately two-thirds of the blood from this venous plexus drains to the pulmonary veins and thus to the LA.23,24 An increase in pulmonary venous pressure due to MS leads to a reverse flow of blood from the pulmonary veins to the bronchial venous plexus, visible as engorged bronchial vasculature. When there is a sudden increase in LA pressure, these veins are prone to rupture, leading to hemoptysis, which can be massive and require blood transfusion and surgery.25 In rare cases, this may be the only presenting feature of MS. This complication occurs more commonly early in the course of the disease when the bronchial veins are more prone to rupture. Long-standing PVH leads to thickening of these veins and thus they are able to withstand greater pressure. Susceptibility to tuberculosis in patients with MS is much debated. Rokitansky, in 1846, enunciated the theory that chronic passive congestion of the lungs excludes probability of tuberculosis of the lungs.26 However, this concept has been argued against and patients of MS in endemic areas are as susceptible to it. Pulmonary thromboembolism may also occur in these patients especially in untreated cases with PAH and right-heart failure. The resulting pulmonary infarct can be a cause of hemoptysis.
Clinicopathological Analysis of Sturge–Weber Syndrome with Focal Cortical Dysplasia FCD IIIc
Published in Fetal and Pediatric Pathology, 2023
Juan Cao, Guocheng Yang, Shoujun Xu, Pengyue Tang, Yue Wang, Yingying Shan, Yongxian Chen, Peng He
In this study, SWS was associated with FCD type IIIc. In the early stages of embryonic development, the primitive venous plexus diverges into three branches, which supply blood to different parts. The outer branch supplies the face and scalp, the middle branch supplies the meninges, and the inner branch supplies the brain tissue. The origin of SWS is thought to be a developmental disorder of the primitive venous plexus of the head, which persists without regression and causes dysmorphic hemangiomas on the skin and meninges. Children with SWS have vascular malformations in the cerebral cortex that cause hypoperfusion, ischemia, and hypoxia in brain tissue, as well as neuronal migration disorders, a reduction in the number of neurons, and a disorder in the arrangement of neurons, which may contribute to SWS with FCD IIIc. SWS can be accompanied by FCD, while FCD is the epileptogenic focus of partial SWS.
Technical note: Novel use of recombinant tissue plasminogen activator for the evacuation of an acute extensive spinal epidural haematoma in a patient with coagulopathy
Published in British Journal of Neurosurgery, 2023
Stavros Koustais, Kieron J. Sweeney, Ciaran Bolger
Spinal epidural haematoma is a rare entity, usually isolated to a few vertebral levels, which may potentially lead to long-term neurological disability.1 The estimated incidence is 1 per million patients2 and is most common in the fourth and fifth decades of life.3 The majority are associated with trauma, anticoagulation therapy and arteriovenous malformations.4 The exact pathogenesis of spontaneous spinal epidural haematoma remains unclear, however the epidural venous plexus has been thought to be the main source of haemorrhage by many authors. This valveless venous plexus is thought to be at risk of rupture and haemorrhage following activities that may result in increase in the intraluminal pressure, such as straining, coughing and voiding.5 Patients may present with back pain followed by symptoms and signs of neural compression. Neurological recovery has been reported in selected patients who had been managed conservatively, having exhibited early signs of improvement,6,7 however in patients without early neurological improvement or with deteriorating neurological function, the long term neurological outcome depends on the degree of initial neurological deficit and the timing of surgical intervention.1
Effects of CYP2C11 gene knockout on the pharmacokinetics and pharmacodynamics of warfarin in rats
Published in Xenobiotica, 2019
Huanying Ye, Danjuan Sui, Wei Liu, Yuannan Yuan, Zhen Ouyang, Yuan Wei
In the PD study, the rats were divided into four groups comprised of five each and were fasted for 12 h, but allowed free access to water before the experiment. An aqueous solution of warfarin (2 mg/mL) was orally administered to each animal at a dose of 1.0 mg/kg. Plasma samples were collected through the posterior venous plexus at 0, 0.5, 1, 2, 4, 8, 12, 24, 36, 48 and 72 h after treatment and immediately mixed thoroughly with 0.109 mol/L sodium citrate. The whole blood samples were centrifuged at 4000×g for 10 min. The plasma sample (0.1 mL) and reconstituted thromboplastin reagent (Sunbio, Shanghai, China) were incubated separately at 37 °C for 3 min prior to mixing. The time required to form a clot was recorded after adding thromboplastin kinase to the plasma. The clotting time was recorded in seconds and the test was duplicated for each sample to ensure accuracy. PT was measured and reported both in seconds and as the international normalized ratio (INR), after calibration of the thromboplastin used in the laboratory against an international reference preparation (Am, 1985; Loeliger et al., 1985a,b).