Looping of a subclavian catheter: An unusual presentation (original) (raw)
Related papers
Changes in the inflammatory response during and after cardiac surgery
2000
Background A prospective randomised trial was carried out to evaluate whether heparin-coated extracorporeal circuits for patients undergoing coronary artery surgery could improve the clinical outcome. Methods Hundred-sixteen low-risk patients were randomly allocated to either a heparin-coated (n=55, Duraflo® II) or uncoated circuit (n=61). Systemic hepat izat ion was identical in both groups. Patient characteristics, differences in postoperative recovery and clinical chemistry were scored. In addition, we also evaluated patients with and without adverse events, independent of the used circuit. Results No significant differences in adverse events, blood loss, or blood transfusions, except for transfusion of platelets were observed. Fifty-seven adverse events occurred in 35 patients in the uncoated group and 47 adverse events in 30 patients in the heparin-coated group. Sixty-five patients encountered one or more than one adverse event. Regardless of the coating, differences were obser...
Impaired anti-platelet effect of aspirin, inflammation and platelet turnover in cardiac surgery
2010
A reduced platelet inhibitory response to acetyl salicylic acid (ASA) has been associated with an increased risk of graft thrombotic occlusion after coronary artery bypass grafting (CABG). We performed a prospective, observational study of 18 patients on 100 mgyday ASA before and after CABG. We assessed antiplatelet response to ASA and its relationship with platelet turnover, inflammatory markers, and soluble thrombomodulin (sTM) levels. All patients showed optimal response to ASA preoperatively but had higher values during follow-up. Platelet aggregation and platelet count in the perioperative period were significantly associated (Ps0.05). Platelet turnover was defined as the average daily turnover (ADTO). The lowest inhibitory value (28% of patients G6 V) was recorded at the same time of the highest platelet turnover ()10% daily in 77.77% of patients), one week after CABG. ADTO)10% was associated with an increased risk of platelet aggregation G6 V. Levels of sTM were significantly higher one week after CABG (median 13 vs. 3 ngyml preoperatively, Ps0.0011). There is a transient impairment in ASA antiplatelet effect after CABG related to an increased platelet turnover caused by the inflammatory process. This could be responsible for the high risk of occlusive thrombosis.
Journal of Thrombosis and Haemostasis, 2007
Objectives: Myocardial ischemia is the leading cause of postoperative mortality and morbidity in patients undergoing major vascular surgery. Platelets have been implicated in the pathogenesis of acute thrombotic events. We hypothesized that platelet activity is increased following major vascular surgery and that this may predispose patients to myocardial ischemia. Methods: Platelet function in 136 patients undergoing elective surgery for subcritical limb ischemia or infrarenal abdominal aortic aneurysm repair was assessed by P-selectin expression and fibrinogen binding with and without adenosine diphosphate (ADP) stimulation, and aggregation mediated by thrombin receptor-activating peptide and arachidonic acid (AA). Cardiac troponin-I (cTnI) was performed. Results: P-selectin expression increased from days 1 to 3 after surgery [median increase from baseline on day 3: 53% (range:)28% to 212%, P < 0.01) for unstimulated and 12% (range:)9% to 45%, P < 0.01) for stimulated]. Fibrinogen binding increased in the immediate postoperative period [median increase from baseline: 34% (range:)46% to 155%, P < 0.05)] and decreased on postoperative day 3 (P < 0.05). ADP-stimulated fibrinogen binding increased on day1 (P < 0.05) and thereafter decreased. Platelet aggregation increased on days 1-5 (P < 0.05). Twenty-eight (21%) patients had a postoperative elevation (> 0.1 ng mL)1) of cTnI. They had significantly increased AA-stimulated platelet aggregation in the immediate postoperative period and on day 2 (P < 0.05), and non-response to aspirin (48% vs. 26%, P = 0.036). Conclusions: This study has shown increased platelet activity and the existence of non-response to aspirin following major vascular surgery. Patients with elevated postoperative cTnI had significantly increased AA-mediated platelet aggregation and a higher incidence of non-response to aspirin compared with patients who did not.
Archives of Medical Science
Introduction: Despite therapy, patients operated using a cardiopulmonary bypass demonstrate increased platelet aggregation, which rebounds to above preoperative levels. The aim of the study was to test the interaction between platelet reactivity/activation and selected inflammatory markers in the post-operative period. Material and methods: In total, 103 patients with non-ST elevation acute coronary syndrome (NSTE-ACS) who were not eligible for percutaneous coronary interventions (PCI), and required urgent revascularization, were included. Platelet reactivity was measured using the PFA-100 platelet analyser, multiple electrode aggregometry, and was expressed as a novel platelet reactivity score (PRS). Patients were divided using their PRS scores into high platelet relativity or low platelet reactivity subgroups (HPR or LPR). Platelet basal activation was measured using immunoassays for soluble P-selectin and soluble CD40L. We measured high-sensitivity C-reactive protein (CRP), and used immunoassays for tumour necrosis factor α (TNF-α) and interleukin 6 (IL-6) as inflammation markers. Results: Significant differences between HPR and LPR groups were found for CRP (mg/l): 81.5 vs. 44.6, p < 0.02; and TNF-α (pg/l): 3.51 vs. 2.37, p < 0.02. A significant association was found between CRP, TNF-α, IL-6 and platelet reactivity (platelet reactivity score). Cohen's k showed: CRP = 0.49, p < 0.0001, TNF-α = 0.37, p < 0.002. Perioperative myocardial infarction and rhythm disturbances occurred more frequently in the high platelet reactivity group: 7 (16.3%) vs. 2 (3.3%), p < 0.04, and 9 (20.9%) vs. 4 (6.7%), p < 0.04, respectively. Conclusions: Inflammatory parameters CRP and TNF-α are strongly associated with platelet reactivity (expressed as PRS) in cardiopulmonary bypass graft patients. Platelet hyperreactivity in the early post-operative period combined with a systemic inflammatory state correlates with a higher risk of post-operative rhythm disturbances and myocardial infarction.
Increased Inflammation in Pericardial Fluid Persists 48 Hours After Cardiac Surgery
Circulation, 2017
C ardiac surgery causes direct trauma to cardiac tissue, breaches the pericardium, and disrupts the normal composition of the fluid largely produced from the myocardial interstitium and epicardial and visceral pericardium. This leaves the heart exposed to pericardial fluid (PCF) and mediastinal contents comprising inflammatory cells and their products that now bathe the heart. This can potentially have adverse effects on the thin-walled atria leading to postoperative atrial fibrillation (AF). 1 After cardiac surgery, the pericardium remains open, and chest drains are routinely placed to prevent fluid accumulation around the heart. Here, we describe the concentration and trajectory of blood proinflammatory factors in the PCF after cardiac surgery over time. The study protocol was approved by the University of Alabama at Birmingham. Institutional Review Board approval and informed consent were obtained from all patients. PCF (n=19) was collected immediately after pericardiotomy (time 0) and from the pericardial drains at times 4, 12, 24, and 48 hours after surgery. The patient population (mean age, 60±3 years) included 26.3% women and 26.3% blacks undergoing cardiac surgery (coronary artery bypass graft, n=14; coronary artery bypass graft+valve procedure, n=3; valve procedure alone, n=2). Patients with ventricular assist devices, AF surgery, thoracic aorta surgery, and AF within 6 months prior were excluded. All participants who had valve replacement (with or without coronary artery bypass graft) underwent on-pump surgeries. Of the patients undergoing coronary artery bypass graft only, 7 underwent on-pump and 7 underwent off-pump surgeries. Blood samples were collected in parallel with PCF. ELISA analysis 2 revealed that neutrophil products (myeloperoxidase and neutrophil-gelatinase-associated lipocalin), neutrophil chemotactic factors (C-X-C motif chemokine ligand 6 and interleukin-8), and cardiac inflammatory factors (tumor necrosis factor-α and oncostatin M) were manyfold higher in PCF than in blood over the 4-to 48-hour time course after cardiac surgery (Figure A). Matrix metallopeptidase-9 (MMP-9), a major product of neutrophils, was significantly higher in blood than in PCF at time 0, but quickly rose in PCF to 2.6-, 2.3-, and 2.7-fold higher than in blood at 4, 12, and 24 hours, respectively. Mast cell chymase activity was increased at 4, 12, and 24 hours in comparison with time 0, whereas MMP-9 activity, which is activated by chymase, was significantly higher than time 0 throughout the 48 hours postsurgery (Figure B). Seven of the 19 patients (37%) had postoperative AF. There was no relationship between AF and PCF proinflammatory proteins at baseline. PCF troponin I levels were significantly higher at 48 hours among those who had postoperative AF (0.22±0.05 µg/mL) than those who did not (0.09±0.07 µg/mL, t=3.125, P=0.01). Troponin I (Figure A, second row, right graph) was markedly elevated in PCF over blood values at 4, 12, 24, and 48 hours after surgery. As opposed to the other PCF constituents that can come from multiple sources, troponin I is solely produced by cardiac myocytes. The persistent 3-fold elevation of troponin as
Platelet–monocyte pro-coagulant interactions in on-pump coronary surgery
European Journal of Cardio-Thoracic Surgery, 2006
Objective: Platelets and monocytes possess haemostatic properties, but the clinical effect of platelet-monocyte interactions on haemostasis following coronary surgery is not known. The study characterises the platelet and monocyte responses in cardiac surgery and its impact on haemostasis. Methods: In 1342 patients, changes in white blood cell counts (WBC), monocyte counts and platelet counts were measured. PMC formation was analysed by flow-cytometry using monoclonal antibodies against pan-leucocyte marker CD45, monocyte marker CD14 and platelet marker CD42. TF expression was determined using monoclonal antibodies against, CD45, CD14 and human-TF. Continuous variables were expressed as mean AE SD. Changes in monocyte and platelet counts over time were considered as repeated measures data, and analysed using Generalised Estimating Equations (GEE). Multivariate regression analysis was used to evaluate the effect of several factors on blood loss. Results: A monocytosis occurs with on-pump coronary surgery, but is less pronounced than with off-pump surgery. No difference was seen in patients having redo-surgery or more complex cardiac surgery. Factors associated with monocytosis on multivariate analysis were higher body mass index ( p = 0.02), diabetes ( p = 0.035) and smoking ( p = 0.01). Older patients manifested a lower response ( p < 0.001). Cross-clamp fibrillation was associated with a lower ( p = 0.048) monocytic response than was cardioplegia. PMC formation dropped following administration of heparin, peaked at 5 min of CPB, and declined by 2 h of CPB ( p = 0.04). A return towards preoperative levels was found during postoperative days 1-5. No significant change in monocyte TF expression occurred. The mean postoperative blood loss was 581.2 AE 292.8 ml, and inversely related to increasing preoperative platelet counts ( p < 0.001), and to higher monocyte % counts ( p = 0.012). Patients, who were female ( p < 0.001), had higher body mass indices ( p < 0.001), and higher core body temperatures during surgery ( p = 0.013), as well as patients having perioperative aprotinin ( p < 0.001) related to less blood loss. Conclusions: A higher postoperative platelet count as well as monocyte% significantly and independently decreases postoperative blood loss following cardiac surgery. #
SMA circuits reduce platelet consumption and platelet factor release during cardiac surgery
The Annals of Thoracic Surgery, 2000
cardiac surgery SMA circuits reduce platelet consumption and platelet factor release during http://ats.ctsnetjournals.org/cgi/content/full/70/6/2075 on the World Wide Web at: The online version of this article, along with updated information and services, is located Print ISSN: 0003-4975; eISSN: 1552-6259. Southern Thoracic Surgical Association.