China
Africa
Explore chapters and articles related to this topic
Cardiovascular Disease
Published in John S. Axford, Chris A. O'Callaghan, Medicine for Finals and Beyond, 2023
Increased pericardial fluid above the normal 15–50 mL can occur with many conditions. Whether clinical symptoms develop depends on: Volume of fluidRate of accumulationResponse of the pericardium to the fluid
Pericardial Disease
Published in Paul Schoenhagen, Frank Dong, Cardiac CT Made Easy, 2023
CT allows reliable identification of pericardial anatomy on non–contrast-enhanced scans. CT scans performed with intravenous contrast administration provide additional anatomic information, including associated myocardial disease and evidence of inflammation with pericardial enhancement.Congenital or postsurgical absence of the pericardium is identified by complete or focal discontinuity of the pericardial layer (Figures 5.2 and 5.3). Pericardial thickening can be identified (Figure 5.4), and local pattern of thickening and calcification is clearly seen on scans with and without contrast (Figure 5.5). The identification of pericardial effusion, description of distribution adjacent to the left and right ventricles, quantification of the amount, and basic characteristics of pericardial fluid are possible (Figures 5.6–5.9). Indirect evidence of tamponade can be identified. Pericardial cysts can be identified defined in relation to adjacent structures (Figures 5.10 and 5.11). Pericardial primary or metastatic pericardial tumours (Chapter 11) can be described.
Bunny Suit
Published in R. Annie Gough, Injury Illustrated, 2020
As we methodically carried out the steps of the post, the coroner stopped cold. “Wait a minute,” she said, staring me down, “What did we forget?” She stared at her hands, confused. She verbally repeated the steps we had completed: Toxicology samples taken, skin incision, rib cage removed, initial inspection of the thoracic cavity. She went to cut the pericardial sac and lift the apex of the heart to withdraw blood for the DNA lab. She looked again, forceps in hand, lifting the heart. Where was the pericardial sac? Why didn't we cut the pericardial sac? As it turned out, there was no pericardial sac. This young man had survived 27 years without the fibrous envelope around his heart. Known for secreting pericardial fluid and lubricating the heart, the pericardial sac allows the heart to pump and turn with minimal friction. Considering the vital importance of your heart, this was a significant anatomical structure to be missing. As we removed the lungs, it was clear his heart was quite enlarged, large enough to end his life. The conclusion was that this was a natural death; a heart attack in the spice factory. No homicide. No vicious smothering in chili powder. No Colonel Mustard in the library with a candlestick. The policemen sighed with disappointment, pulled off their masks, and left the autopsy suite.
Retrospective study of risk factors for pericardial effusion after haematopoietic stem cell transplantation in children
Published in Hematology, 2023
Ke Tong, Yan Meng, Luying Zhang, Xiaoying Lei, Xianmin Guan, Li Xiao, Jie Yu, Ying Dou
The causes of PE (n = 45) were as follows: infection (n = 23, 51%), hypoalbuminaemia (n = 16, 36%), capillary leakage syndrome (CLS) (n = 31, 69%), and post-transplant lymphoproliferative disorder (PTLD) (n = 2, 4%). Regarding treatment, all patients with PE were given albumin and diuresis, 31 were given methylprednisolone, and 11 were infused with hydroxyethyl starch; 3 patients with cardiac insufficiency were treated with phentolamine and dobutamine (2 patients) or milrinone (1 patient). Three patients with large PE were treated with pericardial puncture and drainage; 2 of these patients had negative pericardial fluid aetiology, and 1 patient died of aggravated pericardial tamponade and did not undergo pericardial fluid aetiological examination. Among the 45 patients, PE disappeared in 24 patients after treatment, and the outcomes of PE could not be confirmed in 21 patients because of death without echocardiography. The clinical data of patients with moderate to large PE and small PE are summarized in Table 2 and Supplemental Table 1.
Pericardial Anatomy, Interventions and Therapeutics: A Contemporary Review
Published in Structural Heart, 2021
Reza Reyaldeen, Nicholas Chan, Saberio Lo Presti, Agostina Fava, Chris Anthony, E. Rene Rodriguez, Carmela D. Tan, Walid Saliba, Paul C Cremer, Allan L. Klein
Distinct histologic changes are often noted in the setting of pericardial pathology. For instance, in the progression of pericarditis, the pathophysiologic process consists of first deposition of fibrinous material and recruitment of inflammatory cells, then disintegration of mesothelial cells, followed by organization with ingrowth of fibroblasts and neovascularization.8 The main response to pericardial injury is the production of pericardial fluid, which often manifests as effusion and is readily identified by echocardiography. Inflammation can be detected by more advanced cardiovascular imaging techniques, particularly cardiac MRI and to a lesser extent CT, with pericardial neovascularization in the setting of pericarditis correlating with delayed pericardial hyperenhancement on MRI.9 Healing through organization can result in the formation of adhesions between the parietal and visceral pericardial layers, disrupting and obliterating the pericardial cavity space, which can lead to eventual constriction. Calcification represents an end-stage response to repeated and progressive pericardial injury.1
Acute purulent pericarditis treated conservatively with intrapericardial fibrinolysis and intrapericardial and systemic antibiotics
Published in Baylor University Medical Center Proceedings, 2021
Mahmoud Abdelnabi, Abdallah Almaghraby, Yehia Saleh, Alyaa El Sayed, Judy Rizk
Purulent pericarditis is typically present as an acute illness characterized by high-grade fever, tachycardia, cough, and less commonly chest pain. In the postoperative setting, most patients with purulent pericarditis also have signs of mediastinitis or sternal wound infection. Cardiac tamponade may also occur.3S. aureus is the most common implicated pathogen, while Streptococcus pneumoniae is the most common organism in the setting of direct extension of an intrathoracic infection. Other causes include gram-positive organisms, fungi, and Mycobacterium tuberculosis. Polymicrobial infections are uncommon.4–6 Pericardial fluid analysis including chemical testing (for protein and glucose content as well as white cell count), microscopy (gram stain, acid-fast stain, and fungal stain), and culture and sensitivity is the mainstay for the diagnosis of purulent pericarditis.7