Relevant bibliographies by topics / Pulmonary failure

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Pulmonary failure'

Author: Grafiati
Published: 4 June 2021
Last updated: 15 February 2022

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Journal articles on the topic "Pulmonary failure"

1

Runcie, C., and G. Ramsay. "Intraabdominal infection: Pulmonary failure." World Journal of Surgery 14, no. 2 (1990): 196–203. http://dx.doi.org/10.1007/bf01664873.

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Suderman, Valerie, and Edward Crosby. "Pulmonary artery catheter failure." Canadian Journal of Anaesthesia 37, no. 3 (1990): 388–89. http://dx.doi.org/10.1007/bf03005603.

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Pinard, Brian, and Evan Geller. "Nutritional Support During Pulmonary Failure." Critical Care Clinics 11, no. 3 (1995): 705–15. http://dx.doi.org/10.1016/s0749-0704(18)30060-5.

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4

Piazza, Gregory, and Samuel Z. Goldhaber. "Pulmonary Embolism in Heart Failure." Circulation 118, no. 15 (2008): 1598–601. http://dx.doi.org/10.1161/circulationaha.108.803965.

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5

West, J. B., K. Tsukimoto, O. Mathieu-Costello, and R. Prediletto. "Stress failure in pulmonary capillaries." Journal of Applied Physiology 70, no. 4 (1991): 1731–42. http://dx.doi.org/10.1152/jappl.1991.70.4.1731.

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In the mammalian lung, alveolar gas and blood are separated by an extremely thin membrane, despite the fact that mechanical failure could be catastrophic for gas exchange. We raised the pulmonary capillary pressure in anesthetized rabbits until stress failure occurred. At capillary transmural pressures greater than or equal to 40 mmHg, disruption of the capillary endothelium and alveolar epithelium was seen in some locations. The three principal forces acting on the capillary wall were analyzed. 1) Circumferential wall tension caused by the transmural pressure. This is approximately 25 dyn/cm (25 mN/m) at failure where the radius of curvature of the capillary is 5 microns. This tension is small, being comparable with the tension in the alveolar wall associated with lung elastic recoil. 2) Surface tension of the alveolar lining layer. This contributes support to the capillaries that bulge into the alveolar spaces at these high pressures. When protein leakage into the alveolar spaces occurs because of stress failure, the increase in surface tension caused by surfactant inhibition could be a powerful force preventing further failure. 3) Tension of the tissue elements in the alveolar wall associated with lung inflation. This may be negligible at normal lung volumes but considerable at high volumes. Whereas circumferential wall tension is low, capillary wall stress at failure is very high at approximately 8 x 10(5) dyn/cm2 (8 x 10(4) N/m2) where the thickness is only 0.3 microns. This is approximately the same as the wall stress of the normal aorta, which is predominantly composed of collagen and elastin. The strength of the thin part of the capillary wall is probably attributable to the collagen IV of the basement membranes. The safety factor is apparently small when the capillary pressure is raised during heavy exercise. Stress failure causes increased permeability with protein leakage, or frank hemorrhage, and probably has a role in several types of lung disease.
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Park, Bernard J. "Respiratory Failure Following Pulmonary Resection." Seminars in Thoracic and Cardiovascular Surgery 19, no. 4 (2007): 374–79. http://dx.doi.org/10.1053/j.semtcvs.2007.10.003.

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Kasai, Takatoshi. "Pulmonary Dysfunction and Heart Failure." Journal of Cardiac Failure 23, no. 10 (2017): S11. http://dx.doi.org/10.1016/j.cardfail.2017.08.037.

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Cundrle, Ivan, Lyle J. Olson, and Bruce D. Johnson. "Pulmonary Limitations in Heart Failure." Clinics in Chest Medicine 40, no. 2 (2019): 439–48. http://dx.doi.org/10.1016/j.ccm.2019.02.010.

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Guglin, Maya, and Hammad Khan. "Pulmonary Hypertension in Heart Failure." Journal of Cardiac Failure 16, no. 6 (2010): 461–74. http://dx.doi.org/10.1016/j.cardfail.2010.01.003.

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Guazzi, Marco, and Robert Naeije. "Pulmonary Hypertension in Heart Failure." Journal of the American College of Cardiology 69, no. 13 (2017): 1718–34. http://dx.doi.org/10.1016/j.jacc.2017.01.051.

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Dissertations / Theses on the topic "Pulmonary failure"

1

Hawkins, Nathaniel Mark. "Heart failure and chronic obstructive pulmonary disease : common partners, common problems." Thesis, University of Glasgow, 2010. http://theses.gla.ac.uk/1574/.

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Heart failure (HF) and chronic obstructive pulmonary disease (COPD) are common partners with common problems. Both are chronic systemic disorders incurring significant morbidity and mortality. Although around one third of patients with HF have concurrent COPD,1 remarkably few reports have addressed this often ignored combination. The systematic review presented within this thesis defines the diagnostic challenges, prevalence and prognostic implications of HF with coexistent COPD. I then critically appraise the twin controversies of β-blockade in COPD and β-agonists in HF. The two are inextricably linked, each therapy exerting the reverse pharmacologic activity of the other. The evidence for symptomatic or prognostic benefit from either therapy is limited, and in the case of β-agonists adverse consequences appear more likely. A Cochrane meta-analysis concluded that long term cardioselective β-blockade is safe and well tolerated in patients with moderate to severe or reversible COPD.2 Although often cited,3 these conclusions are simply not true. Of the 20 randomised controlled trials included in the meta-analysis, 11 involved single doses and only one lasted longer than a month. The 9 ‘long term’ studies (defined as more than a single treatment dose) involved 147 young, predominantly male patients with moderate airways obstruction (mean forced expiratory volume in 1 second (FEV1) 1.8 litres). The effect on health status has never been assessed in any cohort with COPD. The long term impact of β-blockade on pulmonary function, symptoms and quality of life is therefore largely unknown. Most importantly, no study has included patients with HF. I randomised 27 patients with HF and coexistent moderate or severe COPD to receive bisoprolol or placebo, titrated to maximum tolerated dose over 4 months. Patients were elderly and predominantly male. Cardiovascular comorbidity, smoking history and pulmonary function were similar in each group (mean FEV1 1.37L vs 1.26L). There were several key findings. A reduction in FEV1 occurred after 4 months following treatment with bisoprolol compared with placebo (–70 ml vs +120 ml, p=0.01). Reversibility following inhaled β2-agonist and static lung volumes were not impaired by bisoprolol. All measures of health status exhibited a consistent non-significant improvement, including the Short Form 36 physical and mental component scores, Minnesota Living with Heart Failure Questionnaire, and Chronic Respiratory Questionnaire. The mean number of COPD exacerbations was similar in the bisoprolol and placebo groups. Although recruitment was limited, the results pose crucial questions and provide direction for larger randomised controlled trials. I analysed cross-sectional data from 61 primary care practices (377,439 patients) participating in the Scottish Continuous Morbidity Recording scheme. The prevalence of COPD in patients with HF increased year on year from 19.8% in 1999 to 23.8% in 2004. These changes may previously have been attributed to an ageing population or increasing age of presentation. However, the trend remained significant after age standardisation. A clear socioeconomic gradient was observed, with prevalence greatest in the most deprived. Consultation rates for HF or COPD in those with both conditions were greater than disease specific contact rates in patients with either condition alone. Cardiovascular comorbidity was similar in HF patients with and without COPD, despite differences in smoking history (respectively 76% vs 47%, p<0.001). This is concerning and suggests that common cardiovascular conditions are being under diagnosed (and likely under treated) in patients with HF and COPD. Although overall β-blocker prescribing increased over time, the adjusted odds of β-blocker prescription in patients with COPD was low (odds ratio 0.30 [95% CI 0.28–0.32], p<0.001). Whether the gap between patients with and without COPD is improving was previously unknown. Despite the overall improvement in beta-blocker prescribing, the relative difference in prescribing between those with and without COPD remained unchanged. By 2004, only 18% of individuals with HF and COPD were prescribed β-blockers. COPD is consistently an independent predictor of death and HF hospitalisation in patients with HF. However, the causes of increased mortality were unclear. I examined the relationship between COPD and cardiovascular outcomes in patients with myocardial infarction (MI) complicated by heart failure, left ventricular systolic dysfunction (LVSD), or both enrolled in the Valsartan in Acute Myocardial Infarction (VALIANT) trial. COPD was an independent predictor of mortality, largely due to increased non-cardiovascular (HR 1.86 [1.43–2.42]) and sudden death (HR 1.26 [1.03–1.53]). However, after multivariate adjustment COPD was not an independent predictor of atherosclerotic events (MI or stroke: HR 0.98 [0.77–1.23]). This is an important finding, as atherosclerotic consequences of chronic systemic inflammation in COPD have been postulated. These appear of limited clinical significance, at least during intermediate follow-up. Part of the adverse risk associated with COPD may be attributable to bronchodilators. The prognosis of patients with HF prescribed bronchodilators is however ill defined. I examined the prognostic implications of bronchodilator use in patients with HF enrolled in the Candesartan in Heart failure Assessment of Reduction in Mortality and morbidity (CHARM) programme. The diversity and magnitude of adverse outcomes associated with bronchodilator therapy was surprising. Bronchodilator use was associated with increased all cause mortality (HR 1.26 [1.09–1.45]), cardiovascular death (HR 1.21 [1.03-1.42]), death due to HF progression (HR 1.40 [1.07-1.82]) and HF hospitalisation (HR 1.49 [1.29-1.72]). Although association is not causation, it is possible that bronchodilators compound maladaptive remodeling and further depress myocardial function. Finally, β-blockers were independently associated with better survival in both VALIANT and CHARM. No significant interaction was observed between either COPD or bronchodilators and β-blockade with respect to mortality. Furthermore, β-blocker use was not associated adversely with any pre-specified outcome in patients with COPD or those prescribed bronchodilators, including non-cardiovascular mortality. Although recruitment bias and the absence of spirometry limit inference to patients with severe or reversible airflow obstruction, the results should encourage β-blockade in patients with COPD. In summary, the studies presented in this thesis extend our understanding of HF with concurrent COPD. Only large randomised controlled trials will solve the quandary of β-blockers and β-agonists. Justification for these trials evolves from observational data and smaller prospective studies such as my own. In the meantime, I hope the evidence presented will stimulate physicians to re-evaluate the management of patients with HF and COPD.
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Aikio, O. (Outi). "Pulmonary nitric oxide in preterm and term infants with respiratory failure." Doctoral thesis, University of Oulu, 2002. http://urn.fi/urn:isbn:9514268512.

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Abstract The aim of the study was to evaluate pulmonary endogenous and inhaled nitric oxide (NO) in neonates with severe respiratory failure. Infant autopsy documents were reviewed for fulminant early-onset bacterial pneumonia. 12 infants with the onset at &lt; 72 h of age and three control groups were identified. Immunohistochemistry revealed that 11 of the infants with early-onset pneumonia (92%) had no or faint inducible nitric oxide synthase (NOS2) staining in their alveolar macrophages (AM). All control infants, regardless of their postnatal age, had NOS2-positive AM. The marker of NO-toxicity, nitrotyrosine, was low in all specimens. To confirm this finding, airway specimens of 21 newborns requiring mechanical ventilation were examined. Seven of them had fulminant early-onset pneumonia with maternal ascending intra-uterine infection (IUI). The controls had no infection at birth despite IUI or neither infection nor IUI. In early-onset pneumonia, NOS2 and nitrotyrosine immunoreactivity were low at birth and increased during the recovery phase (p &lt; 0.05). Analyses of interleukin-1 and surfactant protein A showed the same pattern of age-dependent change. Of the autopsied infants, 12 had received inhaled NO (iNO) before death. Each case was paired with a matched control. Additional five infants without respiratory failure prior to death were also studied. The iNO-treated ones tended to have more intensive NOS2 staining in the bronchiolar epithelium and adjacent tissue than the controls. No differences in other NOS isoforms or nitrotyrosine were detected. A novel method for exhaled NO measurements of intubated infants was developed. Six preterm and six term newborns were prospectively recruited for expired and nasal NO measurements. During the first week of life, the preterm infants showed a different pattern of exhaled NO excretion compared to the term infants. For the pilot intervention study on very early iNO, the eligible patients had a birth weight &lt; 1500 g and progressive, therapy-resistant respiratory failure before five hours of age. Five infants received iNO, showed immediately improved oxygenation and survived without deleterious side effects. Deficient production of NO in small premature infants is associated with severe infection and respiratory failure. Very early iNO therapy may be exceptionally effective in a select group of infants, and did not appear to cause oxidation lung injury.
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Kjellström, Barbro. "The usefulness of continuous hemodynamic monitoring to guide therapy in patients with cardiopulmonary disease /." Stockholm, 2007. http://diss.kib.ki.se/2007/978-91-7357-225-5/.

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Roberts, Clare Elizabeth. "Characterisation of pulmonary inflammation in an 'in vivo' model of chronic heart failure." Thesis, Imperial College London, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.415719.

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Zelt, Jason. "Risk Factors, Mechanisms and Therapeuthic for Right Heart Failure Associated with Pulmonary Hypertension." Thesis, Université d'Ottawa / University of Ottawa, 2020. http://hdl.handle.net/10393/40737.

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Right ventricular function (RV) is one of the most important predictors of prognosis in many cardiovascular disease states. Despite the significance of RV function to survival, there are no therapies that directly nor selectively improve RV function. As well, the basis for RV failure is poorly understood. This is particularly relevant for patients with pulmonary arterial hypertension (PAH), where RV failure in the setting of pressure overload is the leading cause of death. PAH will be introduced in the 2nd chapter of this thesis by comparing and refining contemporary mortality risk assessment strategies. I will then explore 1) RV neurohormonal function and, 2) RV energetics, two molecular pathways thought to be involved in the pathogenesis and progression of maladaptive RV failure. I employed small animal molecular imaging using positron emission tomography (PET) to non-invasively investigate these pathways. The PET imaging techniques employed in this thesis have the unique potential for translation to human studies, to further explore disease mechanisms.
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Evans, Rachael Andrea. "Generic exercise rehabilitation for patients with chronic obstructive pulmonary disease and chronic heart failure." Thesis, University of Leicester, 2009. http://hdl.handle.net/2381/7559.

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Background: Exertional breathlessness and fatigue are common disabling symptoms of patients with Chronic Obstructive Pulmonary Disease (COPD) and Chronic Heart Failure (CHF). The mechanisms behind these symptoms are similar including skeletal muscle dysfunction. Exercise training at least partially reverses the skeletal muscle abnormalities and improves exercise performance and health related quality of life in both conditions. Pulmonary rehabilitation, with exercise training as a core component, is an integral part of the management of COPD, but a service for CHF has not developed in the same way. The hypothesis, for the main studies described in this thesis, was that the successful model of pulmonary rehabilitation could be applied to patients with CHF and patients with COPD and CHF could be beneficially trained together. Methods: Two main studies were undertaken; 1) a randomised controlled trial of pulmonary rehabilitation (PR) vs. normal care (NC) in patients with CHF 2) a comparative observational study of PR between COPD and CHF. Alongside these studies, the outcome measures commonly used for COPD were applied to patients with CHF. Two pilot studies were performed investigating the effect of exercise training on other systemic manifestations of COPD and CHF. Results: Patients with CHF made significant improvements in exercise performance and health status with PR compared to NC. The improvements were similar to those seen in the patients with COPD. Measures of exercise performance and health status were applied successfully to patients with CHF. Conclusions: Patients with COPD and CHF can be successfully trained together demonstrating the feasibility of generic exercise rehabilitation for exertional breathlessness. Further work would need to investigate whether combined exercise programmes for COPD and CHF provides economies of scale for both populations. The work in this thesis highlights the possibility of organising services for chronic disease around a disability rather than an individual disease.
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Gorst, Sarah L. "What predicts optimal telehealth usage among heart failure and chronic obstructive pulmonary disease patients?" Thesis, University of Sheffield, 2015. http://etheses.whiterose.ac.uk/9511/.

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Lovell, Sharon Lynne. "The role of nitric oxide and endothelin in the regulation of pulmonary arterial pressure in man." Thesis, Queen's University Belfast, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.322648.

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Gustafson, Torbjörn. "Causes and treatment of chronic respiratory failure : experience of a national register." Doctoral thesis, Umeå universitet, Folkhälsa och klinisk medicin, 2007. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-1473.

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Long-term oxygen therapy (LTOT) or home mechanical ventilation (HMV) can improve survival time in chronic respiratory failure. A national quality register could be an aid to identifying risk markers and optimizing therapy for respiratory failure. Aims: ▪To identify risk markers for chronic respiratory failure, especially when triggered by chronic obstructive pulmonary disease (COPD) and idiopathic pulmonary fibrosis (IPF). ▪To predict sex-related differences in the future need of LTOT for COPD and to study sex related survival rate in COPD patients starting LTOT. ▪To investigate if HMV is more effective than LTOT alone in treating chronic respiratory failure caused by kyphoscoliosis. ▪To evaluate the use of quality indicators in LTOT. Methods: Swedish national registers for LTOT and HMV were established in 1987 and 1996 respectively. They were reconstructed in 2004 to form the web-based register Swedevox. Indications for LTOT were based on the guidelines from the Swedish Society for Respiratory Medicine. The incidence and prevalence of LTOT for COPD were measured annually from 1987 to 2000, and the future need for LTOT was estimated on the basis of the frequency of ever smoking in Sweden in 2001 in different age groups. A postal questionnaire on occupational exposures was completed by 181 patients with severe pulmonary fibrosis who started LTOT between 1997 and 2000, and by 757 controls. Odds ratios (ORs) were calculated. Time to death was evaluated in kyphoscoliotic patients starting HMV or LTOT alone in 1996-2004. Ten quality indicators were defined and evaluated based on data from patients starting LTOT in 1987-2005. Results: The incidence each year of LTOT in COPD patients increased more rapidly in women than in men (from 2.0 and 2.8/100,000 in 1987 to 7.6 and 7.1/100,000 in 2000 respectively, (p < 0.001)). Women ran a 1.9 times higher risk than men to develop chronic hypoxemia from COPD and had a higher survival rate during LTOT. In men, IPF was associated with exposure to birch dust with an OR 2.7, (95% confidence interval (CI) 1.30–5.65) and with hardwood dust, OR 2.7 (95% CI 1.14–6.52). Patients with kyphoscoliosis showed a better survival rate with HMV than with LTOT alone with a hazard ratio of 0.30 (95%CI 0.18-0.51), adjusted for age, sex, concomitant respiratory diseases, and blood gas levels. There were improvements in the following eight quality indicators for LTOT: access to LTOT, PaO2 ≤ 7.3 kPa without oxygen, no current smoking, low number of thoracic deformity patients without concomitant HMV, LTOT > 16 hours of oxygen/day, mobile oxygen equipment, reassessment of hypoxemia when LTOT was not started in a stable state COPD, and avoidance of continuous oral steroids in COPD. There was a decline in the indicator PaO2 > 8 kPa on oxygen. First-year survival rate in COPD was unchanged. Conclusions: The incidence and prevalence of LTOT increase more rapidly in women than in men. Survival rate during LTOT in COPD is better in women than in men. Exposure to birch and hardwood dust may contribute to the risk of IPF in men. Survival rate in patients with kyphoscoliosis was three times better with HMV than with LTOT alone. The national quality register for LTOT showed improvements in eight out of ten quality indicators. Levels for excellent quality in the indicators are suggested.
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Haghighi, Masoud Kavoli. "Analysis of the role of endothelial nitric oxide in regulating the tone and responses of pulmonary artery rings to drugs." Thesis, University of Glasgow, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.295321.

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Books on the topic "Pulmonary failure"

1

Pulmonary Hypertension. W.B. Saunders Company, 2012.

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Excerpts from pulmonary SCOR progress reports: Respiratory failure. The Division, 1987.

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Jean-Philippe, Derenne, Similowski Thomas 1961-, and Whitelaw William A. 1941-, eds. Acute respiratory failure in chronic obstructive pulmonary disease. M. Dekker, 1996.

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Kreit, John W. Right Ventricular Failure. Edited by John W. Kreit. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190670085.003.0014.

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Right ventricular (RV) failure is common in the ICU. Chronic RV failure is most often due to long-standing left ventricular (LV) systolic or diastolic failure or other causes of chronic pulmonary hypertension. Acute RV failure can result from massive pulmonary embolism, ARDS, RV infarction, and acute LV failure. Finally, acute-on-chronic RV failure can be precipitated by any disorder that leads to an abrupt rise in pulmonary vascular resistance (PVR) and RV afterload. Right Ventricular Failure provides an in-depth review of the adverse hemodynamic effects of mechanical ventilation and PEEP in patients with right ventricular failure. The chapter explains the effect of positive pressure ventilation and PEEP on pulmonary vascular resistance and RV afterload and describes how to adjust the ventilator to minimize these hemodynamic effects.
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Lee, Jae Myeong, and Michael R. Pinsky. Cardiovascular interactions in respiratory failure. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0087.

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Acute respiratory failure not only impairs gas exchange, but also stresses cardiovascular reserve by increasing the need for increased cardiac output (CO) to sustain O2 delivery in the face of hypoxaemia, increased O2 demand by the increased work of breathing and inefficient gas exchange, and increased right ventricular afterload due to lung collapse via hypoxic pulmonary vasoconstriction. Mechanical ventilation, though often reversing these processes by lung recruitment and improved arterial oxygenation, may also decrease CO by increasing right atrial pressure by either increasing intrathoracic pressure or lung over-distention by excess positive end-expiratory pressure or inadequate expiratory time causing acute cor pulmonale. Finally, spontaneous negative swings in intrathoracic pressure also increase venous return and impede left ventricular ejection thus increasing intrathoracic blood volume and often precipitating or worsening hydrostatic pulmonary oedema. Positive-pressure breathing has the opposite effects.
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Torbicki, Adam, Marcin Kurzyna, and Stavros Konstantinides. Pulmonary embolism. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0066.

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Pulmonary embolism is usually a consequence of deep vein thrombosis, and together the two conditions are known as venous thromboembolism. Non-thromboembolic causes of pulmonary embolism are rare. Pulmonary thromboembolism is a potentially life-threatening disease, if left untreated. This is due to a natural tendency towards early recurrence of pulmonary emboli which may lead to fatal right ventricular failure. In more severe cases, secondary right ventricular failure may result from myocardial ischaemia and injury caused by systemic hypotension and adrenergic overstimulation. Clinical presentation of pulmonary embolism is non-specific and may include dyspnoea, chest pain, haemoptysis, syncope, hypotension, and shock. Patients with suggestive history, symptoms, and signs require an immediate triage which determines further management strategy. Computerized tomographic angiography has become the mainstay of diagnosis. However, depending on the clinical presentation, treatment decisions may also be made based on results from other tests. In particular, in high-risk patients with persistent hypotension or shock, bedside echocardiography may be the only available test to identify patients in need of primary thrombolysis, surgical embolectomy, or percutaneous intervention which will stabilize the systemic cardiac output. For most normotensive patients, anticoagulation is sufficient as initial treatment. However, in the presence of signs of right ventricular dysfunction and myocardial injury monitoring is recommended to allow prompt rescue reperfusion therapy in case of haemodynamic decompensation.
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Torbicki, Adam, Marcin Kurzyna, and Stavros Konstantinides. Pulmonary embolism. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199687039.003.0066_update_001.

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Pulmonary embolism is usually a consequence of deep vein thrombosis, and together the two conditions are known as venous thromboembolism. Non-thromboembolic causes of pulmonary embolism are rare. Pulmonary thromboembolism is a potentially life-threatening disease, if left untreated. This is due to a natural tendency towards early recurrence of pulmonary emboli which may lead to fatal right ventricular failure. In more severe cases, secondary right ventricular failure may result from myocardial ischaemia and injury caused by systemic hypotension and adrenergic overstimulation. Clinical presentation of pulmonary embolism is non-specific and may include dyspnoea, chest pain, haemoptysis, syncope, hypotension, and shock. Patients with suggestive history, symptoms, and signs require an immediate triage which determines further management strategy. Computerized tomographic angiography has become the mainstay of diagnosis. However, depending on the clinical presentation, treatment decisions may also be made based on results from other tests. In particular, in high-risk patients with persistent hypotension or shock, bedside echocardiography may be the only available test to identify patients in need of primary thrombolysis, surgical embolectomy, or percutaneous intervention which will stabilize the systemic cardiac output. For most normotensive patients, anticoagulation is sufficient as initial treatment. However, in the presence of signs of right ventricular dysfunction and myocardial injury monitoring is recommended to allow prompt rescue reperfusion therapy in case of haemodynamic decompensation.
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Torbicki, Adam, Marcin Kurzyna, and Stavros Konstantinides. Pulmonary embolism. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199687039.003.0066_update_002.

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Pulmonary embolism is usually a consequence of deep vein thrombosis, and together the two conditions are known as venous thromboembolism. Non-thromboembolic causes of pulmonary embolism are rare. Pulmonary thromboembolism is a potentially life-threatening disease, if left untreated. This is due to a natural tendency towards early recurrence of pulmonary emboli which may lead to fatal right ventricular failure. In more severe cases, secondary right ventricular failure may result from myocardial ischaemia and injury caused by systemic hypotension and adrenergic overstimulation. Clinical presentation of pulmonary embolism is non-specific and may include dyspnoea, chest pain, haemoptysis, syncope, hypotension, and shock. Patients with suggestive history, symptoms, and signs require an immediate triage which determines further management strategy. Computerized tomographic angiography has become the mainstay of diagnosis. However, depending on the clinical presentation, treatment decisions may also be made based on results from other tests. In particular, in high-risk patients with persistent hypotension or shock, bedside echocardiography may be the only available test to identify patients in need of primary thrombolysis, surgical embolectomy, or percutaneous intervention which will stabilize the systemic cardiac output. For most normotensive patients, anticoagulation is sufficient as initial treatment. However, in the presence of signs of right ventricular dysfunction and myocardial injury monitoring is recommended to allow prompt rescue reperfusion therapy in case of haemodynamic decompensation.
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Torbicki, Adam, Marcin Kurzyna, and Stavros Konstantinides. Pulmonary embolism. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0066_update_003.

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Abstract:
Pulmonary embolism is usually a consequence of deep vein thrombosis, and together the two conditions are known as venous thromboembolism. Non-thromboembolic causes of pulmonary embolism are rare. Pulmonary thromboembolism is a potentially life-threatening disease, if left untreated. This is due to a natural tendency towards early recurrence of pulmonary emboli which may lead to fatal right ventricular failure. In more severe cases, secondary right ventricular failure may result from myocardial ischaemia and injury caused by systemic hypotension and adrenergic overstimulation. Clinical presentation of pulmonary embolism is non-specific and may include dyspnoea, chest pain, haemoptysis, syncope, hypotension, and shock. Patients with suggestive history, symptoms, and signs require an immediate triage which determines further management strategy. Computerized tomographic angiography has become the mainstay of diagnosis. However, depending on the clinical presentation, treatment decisions may also be made based on results from other tests. In particular, in high-risk patients with persistent hypotension or shock, bedside echocardiography may be the only available test to identify patients in need of primary thrombolysis, surgical embolectomy, or percutaneous intervention which will stabilize the systemic cardiac output. For most normotensive patients, anticoagulation is sufficient as initial treatment. However, in the presence of signs of right ventricular dysfunction and myocardial injury monitoring is recommended to allow prompt rescue reperfusion therapy in case of haemodynamic decompensation.
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Millar, Professor Ann B., Dr Richard Leach, Dr Rebecca Preston, et al. Respiratory diseases and respiratory failure. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199565979.003.0005.

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Chapter 5 covers respiratory diseases and respiratory failure, including clinical presentations of respiratory disease, assessment of diffuse lung disease, hypoxaemia, respiratory failure, and oxygen therapy, pneumonia, mycobacterial infection, asthma, chronic obstructive pulmonary disease (COPD), lung cancer, mediastinal lesions, pneumothorax, pleural disease, asbestos-related lung disease, diffuse parenchymal (interstitial) lung disease, sarcoidosis, pulmonary hypertension, acute respiratory distress syndrome, bronchiectasis and cystic fibrosis, bronchiolitis, eosinophilic lung disease, airways obstruction, aspiration syndromes, and near-drowning, pulmonary vasculitis, the immunocompromised host, sleep apnoea, and rare pulmonary diseases.
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Book chapters on the topic "Pulmonary failure"

1

Wiedenroth, Christoph B., and Eckhard Mayer. "Pulmonary Hypertension." In Heart Failure. Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-98184-0_22.

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Vanzeller, Mafalda, Marta Drummond, and João Carlos Winck. "Chronic respiratory failure – pathophysiology." In Pulmonary Rehabilitation. CRC Press, 2020. http://dx.doi.org/10.1201/9781351015592-41.

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Ramani, Gautam V., and Myung H. Park. "Pulmonary Hypertension." In Management of Heart Failure. Springer London, 2015. http://dx.doi.org/10.1007/978-1-4471-6657-3_9.

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Mador, M. J., and M. J. Tobin. "Acute Respiratory Failure." In Chronic Obstructive Pulmonary Disease. Springer US, 1995. http://dx.doi.org/10.1007/978-1-4899-4525-9_19.

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Medinger, Ann. "Extrapulmonic Ventilatory Failure." In Handbook of Pulmonary Emergencies. Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-5125-2_3.

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Söderberg, Stefan, and Michael Y. Henein. "Pulmonary Arterial Hypertension." In Heart Failure in Clinical Practice. Springer London, 2010. http://dx.doi.org/10.1007/978-1-84996-153-0_7.

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Rodriguez-Roisin, R., J. Roca, and J. A. Barbera. "Extrapulmonary and Intrapulmonary Determinants of Pulmonary Gas Exchange." In Ventilatory Failure. Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-84554-3_2.

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Krowka, Michael J., and Aynur Okcay. "Pulmonary Alterations in Chronic Liver Failure." In Chronic Liver Failure. Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-866-9_18.

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Krüger, Wolfgang. "Pulmonary Hypertension in Left Heart Disease." In Acute Heart Failure. Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-54973-6_6.

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Ntiloudi, Despina, and George Giannakoulas. "Pulmonary Arterial Hypertension." In Heart Failure in Adult Congenital Heart Disease. Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-77803-7_8.

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Conference papers on the topic "Pulmonary failure"

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Sanders, DB, RC Bittner, and CH Goss. "Failure to Recover to Baseline Pulmonary Function after Cystic Fibrosis Pulmonary Exacerbation." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a1206.

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Holgado, S., A. Olivé, M. Gumà, et al. "AB0080 Treatment failure pulmonary haemorrhage of sistemic lupus." In Annual European Congress of Rheumatology, Annals of the rheumatic diseases ARD July 2001. BMJ Publishing Group Ltd and European League Against Rheumatism, 2001. http://dx.doi.org/10.1136/annrheumdis-2001.125.

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Ke, Yunbo, Yue Li, Kamoltip Promnares, Anna Birukova, and Konstantin Birukov. "Esterification of iloprost enhances its protective effects on pulmonary endothelium." In ERS Respiratory Failure and Mechanical Ventilation Conference 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/23120541.rfmvc-2020.21.

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Barbara, S., M. Sebastian, C. Hagl, K. Nikolaus, C. Schneider, and R. Schramm. "The Evolution of Pulmonary Hypertension in Terminal Lung Failure." In 49th Annual Meeting of the German Society for Thoracic and Cardiovascular Surgery. Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0040-1705376.

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Voelkel, Norbert F., Laszlo Farkas, Aysar Alhussaini, et al. "The Microvascular Pathology Of Pulmonary Hypertension-Associated Right Ventricular Failure." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a4986.

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Habib, Shifa, S. M. Asad Zaidi, Wafa Jamal, Imran Zafar, Talha Kazmi, and Muhammad Yasir. "Predictors of treatment failure among pulmonary tuberculosis patients in Pakistan." In ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.pa2950.

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Slepchenko, Nataliia, Yuriy Mostovoy, Nataliia Tsymbaliuk, Andrii Sidorov, and Kostiantyn Dmytriiev. "Does heart failure make a difference in pulmonary function testing?" In ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.172.

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D'Cruz, Rebecca, Richard Morton, Adam Jakes, George Thornton, Jacob De Wolff, and Rachel Tennant. "Respiratory failure as an indication for thrombolysis in pulmonary embolism?" In ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.pa2469.

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Potus, Francois, Evangelos Michelakis, Steeve Provencher, and Sébastien Bonnet. "Epigenetic signature of right ventricular failure in pulmonary arterial hypertension." In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa586.

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Hernández-Urquieta, Luis, Clyo Chávez-Méndez, Arturo Orea-Tejeda, et al. "Body composition in chronic obstructive pulmonary disease and heart failure." In ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.pa713.

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Reports on the topic "Pulmonary failure"

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DePriest, Jack. Work of Breathing as a Predictor of Failure to Wean from Mechanical Ventilation in Patients with Severe Chronic Obstructive Pulmonary Disease. Defense Technical Information Center, 1993. http://dx.doi.org/10.21236/ada274121.

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DePriest, Jack. Work of Breathing as a Predictor of Failure to Wean from Mechanical Ventilation in Patients with Severe Chronic Obstructive Pulmonary Disease. Defense Technical Information Center, 1993. http://dx.doi.org/10.21236/ada268432.

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Treadwell, Jonathan R., James T. Reston, Benjamin Rouse, Joann Fontanarosa, Neha Patel, and Nikhil K. Mull. Automated-Entry Patient-Generated Health Data for Chronic Conditions: The Evidence on Health Outcomes. Agency for Healthcare Research and Quality (AHRQ), 2021. http://dx.doi.org/10.23970/ahrqepctb38.

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Background. Automated-entry consumer devices that collect and transmit patient-generated health data (PGHD) are being evaluated as potential tools to aid in the management of chronic diseases. The need exists to evaluate the evidence regarding consumer PGHD technologies, particularly for devices that have not gone through Food and Drug Administration evaluation. Purpose. To summarize the research related to automated-entry consumer health technologies that provide PGHD for the prevention or management of 11 chronic diseases. Methods. The project scope was determined through discussions with Key Informants. We searched MEDLINE and EMBASE (via EMBASE.com), In-Process MEDLINE and PubMed unique content (via PubMed.gov), and the Cochrane Database of Systematic Reviews for systematic reviews or controlled trials. We also searched ClinicalTrials.gov for ongoing studies. We assessed risk of bias and extracted data on health outcomes, surrogate outcomes, usability, sustainability, cost-effectiveness outcomes (quantifying the tradeoffs between health effects and cost), process outcomes, and other characteristics related to PGHD technologies. For isolated effects on health outcomes, we classified the results in one of four categories: (1) likely no effect, (2) unclear, (3) possible positive effect, or (4) likely positive effect. When we categorized the data as “unclear” based solely on health outcomes, we then examined and classified surrogate outcomes for that particular clinical condition. Findings. We identified 114 unique studies that met inclusion criteria. The largest number of studies addressed patients with hypertension (51 studies) and obesity (43 studies). Eighty-four trials used a single PGHD device, 23 used 2 PGHD devices, and the other 7 used 3 or more PGHD devices. Pedometers, blood pressure (BP) monitors, and scales were commonly used in the same studies. Overall, we found a “possible positive effect” of PGHD interventions on health outcomes for coronary artery disease, heart failure, and asthma. For obesity, we rated the health outcomes as unclear, and the surrogate outcomes (body mass index/weight) as likely no effect. For hypertension, we rated the health outcomes as unclear, and the surrogate outcomes (systolic BP/diastolic BP) as possible positive effect. For cardiac arrhythmias or conduction abnormalities we rated the health outcomes as unclear and the surrogate outcome (time to arrhythmia detection) as likely positive effect. The findings were “unclear” regarding PGHD interventions for diabetes prevention, sleep apnea, stroke, Parkinson’s disease, and chronic obstructive pulmonary disease. Most studies did not report harms related to PGHD interventions; the relatively few harms reported were minor and transient, with event rates usually comparable to harms in the control groups. Few studies reported cost-effectiveness analyses, and only for PGHD interventions for hypertension, coronary artery disease, and chronic obstructive pulmonary disease; the findings were variable across different chronic conditions and devices. Patient adherence to PGHD interventions was highly variable across studies, but patient acceptance/satisfaction and usability was generally fair to good. However, device engineers independently evaluated consumer wearable and handheld BP monitors and considered the user experience to be poor, while their assessment of smartphone-based electrocardiogram monitors found the user experience to be good. Student volunteers involved in device usability testing of the Weight Watchers Online app found it well-designed and relatively easy to use. Implications. Multiple randomized controlled trials (RCTs) have evaluated some PGHD technologies (e.g., pedometers, scales, BP monitors), particularly for obesity and hypertension, but health outcomes were generally underreported. We found evidence suggesting a possible positive effect of PGHD interventions on health outcomes for four chronic conditions. Lack of reporting of health outcomes and insufficient statistical power to assess these outcomes were the main reasons for “unclear” ratings. The majority of studies on PGHD technologies still focus on non-health-related outcomes. Future RCTs should focus on measurement of health outcomes. Furthermore, future RCTs should be designed to isolate the effect of the PGHD intervention from other components in a multicomponent intervention.
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Saldanha, Ian J., Wangnan Cao, Justin M. Broyles, et al. Breast Reconstruction After Mastectomy: A Systematic Review and Meta-Analysis. Agency for Healthcare Research and Quality (AHRQ), 2021. http://dx.doi.org/10.23970/ahrqepccer245.

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Objectives. This systematic review evaluates breast reconstruction options for women after mastectomy for breast cancer (or breast cancer prophylaxis). We addressed six Key Questions (KQs): (1) implant-based reconstruction (IBR) versus autologous reconstruction (AR), (2) timing of IBR and AR in relation to chemotherapy and radiation therapy, (3) comparisons of implant materials, (4) comparisons of anatomic planes for IBR, (5) use versus nonuse of human acellular dermal matrices (ADMs) during IBR, and (6) comparisons of AR flap types. Data sources and review methods. We searched Medline®, Embase®, Cochrane CENTRAL, CINAHL®, and ClinicalTrials.gov from inception to March 23, 2021, to identify comparative and single group studies. We extracted study data into the Systematic Review Data Repository Plus (SRDR+). We assessed the risk of bias and evaluated the strength of evidence (SoE) using standard methods. The protocol was registered in PROSPERO (registration number CRD42020193183). Results. We found 8 randomized controlled trials, 83 nonrandomized comparative studies, and 69 single group studies. Risk of bias was moderate to high for most studies. KQ1: Compared with IBR, AR is probably associated with clinically better patient satisfaction with breasts and sexual well-being but comparable general quality of life and psychosocial well-being (moderate SoE, all outcomes). AR probably poses a greater risk of deep vein thrombosis or pulmonary embolism (moderate SoE), but IBR probably poses a greater risk of reconstructive failure in the long term (1.5 to 4 years) (moderate SoE) and may pose a greater risk of breast seroma (low SoE). KQ 2: Conducting IBR either before or after radiation therapy may result in comparable physical well-being, psychosocial well-being, sexual well-being, and patient satisfaction with breasts (all low SoE), and probably results in comparable risks of implant failure/loss or need for explant surgery (moderate SoE). We found no evidence addressing timing of IBR or AR in relation to chemotherapy or timing of AR in relation to radiation therapy. KQ 3: Silicone and saline implants may result in clinically comparable patient satisfaction with breasts (low SoE). There is insufficient evidence regarding double lumen implants. KQ 4: Whether the implant is placed in the prepectoral or total submuscular plane may not be associated with risk of infections that are not explicitly implant related (low SoE). There is insufficient evidence addressing the comparisons between prepectoral and partial submuscular and between partial and total submuscular planes. KQ 5: The evidence is inconsistent regarding whether human ADM use during IBR impacts physical well-being, psychosocial well-being, or satisfaction with breasts. However, ADM use probably increases the risk of implant failure/loss or need for explant surgery (moderate SoE) and may increase the risk of infections not explicitly implant related (low SoE). Whether or not ADM is used probably is associated with comparable risks of seroma and unplanned repeat surgeries for revision (moderate SoE for both), and possibly necrosis (low SoE). KQ 6: AR with either transverse rectus abdominis (TRAM) or deep inferior epigastric perforator (DIEP) flaps may result in comparable patient satisfaction with breasts (low SoE), but TRAM flaps probably increase the risk of harms to the area of flap harvest (moderate SoE). AR with either DIEP or latissimus dorsi flaps may result in comparable patient satisfaction with breasts (low SoE), but there is insufficient evidence regarding thromboembolic events and no evidence regarding other surgical complications. Conclusion. Evidence regarding surgical breast reconstruction options is largely insufficient or of only low or moderate SoE. New high-quality research is needed, especially for timing of IBR and AR in relation to chemotherapy and radiation therapy, for comparisons of implant materials, and for comparisons of anatomic planes of implant placement.
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