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Sepsis and myocardial dysfunction
Rafaela Deczka Morsch,Nelson Akamine,Constantino José Fernandes Junior
Einstein (S?o Paulo) , 2006,
Abstract: Sepsis and septic shock are prevalent in the intensive care setting,accounting for more than 40% of mortality in this scenario. Theappropriate management and recognition of sepsis-inducedmyocardial dysfunction are paramount for its proper treatmentand probably impact mortality rates. The objective of this articleis to review its definition, pathophysiologic mechanisms, possibletreatments and current research on the subject according to acritical view.Cellular signaling involved in myocardial depression is not fullyunderstood. Disturbances in calcium homeostasis,cardiodepressant circulating factors, inflammatory mediators,nitric oxide and apoptosis act as synergistic pathways that leadto severely depressed cardiac function. The diagnosis ofmyocardial dysfunction during sepsis carries a worse prognosisand increased mortality.Myocardial dysfunction plays an important role in morbidity andmortality rate of critically ill patients. Current research in thisarea will continue to evolve; we will, therefore, soon have moreinsights into potential novel therapies that can change its mortalityrates.
Decreased Autophagy Contributes to Myocardial Dysfunction in Rats Subjected to Nonlethal Mechanical Trauma  [PDF]
Jie Wang, Keyi Lu, Feng Liang, Xiaoyu Li, Li Wang, Caihong Yang, Zi Yan, Suli Zhang, Huirong Liu
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0071400
Abstract: Autophagy is important in cells for removing damaged organelles, such as mitochondria. Insufficient autophagy plays a critical role in tissue injury and organ dysfunction under a variety of pathological conditions. However, the role of autophagy in nonlethal traumatic cardiac damage remains unclear. The aims of the present study were to investigate whether nonlethal mechanical trauma may result in the change of cardiomyocyte autophagy, and if so, to determine whether the changed myocardial autophagy may contribute to delayed cardiac dysfunction. Male adult rats were subjected to nonlethal traumatic injury, and cardiomyocyte autophagy, cardiac mitochondrial function, and cardiac function in isolated perfused hearts were detected. Direct mechanical traumatic injury was not observed in the heart within 24 h after trauma. However, cardiomyocyte autophagy gradually decreased and reached a minimal level 6 h after trauma. Cardiac mitochondrial dysfunction was observed by cardiac radionuclide imaging 6 h after trauma, and cardiac dysfunction was observed 24 h after trauma in the isolated perfused heart. These were reversed when autophagy was induced by administration of the autophagy inducer rapamycin 30 min before trauma. Our present study demonstrated for the first time that nonlethal traumatic injury caused decreased autophagy, and decreased autophagy may contribute to post-traumatic organ dysfunction. Though our study has some limitations, it strongly suggests that cardiac damage induced by nonlethal mechanical trauma can be detected by noninvasive radionuclide imaging, and induction of autophagy may be a novel strategy for reducing posttrauma multiple organ failure.
Myocardial dysfunction in malnourished children
Faddan Nagla Hassan,El Sayh Khalid,Shams Hamdy,Badrawy Hosni
Annals of Pediatric Cardiology , 2010,
Abstract: Background : Malnourished children suffer several alterations in body composition that could produce cardiac abnormalities. Aim : The aim of the present study was to detect the frequency of myocardial damage in malnourished children as shown by echocardiography and cardiac troponin T (cTnT) level. Methods : Forty-five malnourished infants and young children (mean±SD of age was 11.24 ±7.88 months) were matched with 25 apparently healthy controls (mean±SD of age was 10.78±6.29 months). Blood sample was taken for complete blood picture, liver and kidney function tests, serum sodium, potassium, calcium levels and cTnT. All the malnourished children were subjected to echocardiographic evaluation. Results : Malnourished children showed a significantly lower left ventricular (LV) mass than the control group. The LV systolic functions were significantly impaired in patients with severe malnutrition. The cTnT level was higher than the upper reference limits in 11 (24.44%) of the studied malnourished children and all of them had a severe degree of malnutrition. The cTnT level was significantly higher in patients with anemia, sepsis and electrolyte abnormalities and it correlated negatively with LV ejection fraction (EF). Six of the studied children with high cTnT levels (54.5%) died within 21 days of treatment while only one case (2.9%) with normal level of cTnT died within the same period. Conclusions: LV mass is reduced in malnourished children. Children with severe malnutrition have a significant decrease in LV systolic functions. Elevated cTnT levels in malnourished children has both diagnostic and prognostic significance for cardiomyocyte damage.
Myocardial dysfunction in septic shock: A case report  [PDF]
Popovi? Nada,Miju?kovi? Dragan,Ne?kovi? Vojislava,Arsenijevi? Ljubica
Medicinski Pregled , 2008, DOI: 10.2298/mpns0804187p
Abstract: Introduction Sepsis is characterized by generalized inflammatory respons induced by infection. The incidence of myocardial dysfunction m sepsis is unknown as well as its impact on survival, independently other organ system dysfunction. Case report A female patient, age 36, with clinical signs of septic shock was admitted to the Intensive Care Unit. After initial therapy of septic shock, patient was still haemodynamically unstable. Transthoracic echocardiography showed left ventricular dysfunction (EF=20%), with mitral regurgitation 2-3+, tricuspid regurgitation 3+, and estimated systolic right ventricular pressure of 53 mm Hg. Inotropic drug, dobutamin, was initiated, which led to significant improvement of hemodynamic parameters. Eight days after the initiation of therapy the clinical improvement was observed and the control transthoracic echocardiography was performed. It showed the improvement in left ventricular size and function, with EF of 57%. and reduced mitral regurgitation to 2+, and tricuspide regurgitation to 1+. Discussion A hyperdynamic state is typically present in sepsis. Myocardial dysfunction in sepsis is characterized by decreased ejection fraction, ventricular dilatation and impaired contaractile response to volume loading. Cardiac output can be measured using pulmonary artery catheter, transthoracic and transoesophageal echocardiography, or by pulse contour analysis. In this patient, myocardial dysfunction was detected by echocardiography, which helped in clinical decision making to administer inotropic agent. The recovery of myocardial function was also confirmed by echocardiography. Conclusion Echocardiography can be used in septic patient for diagnosis of myocardial dysfunction, decision making, follow-up of the response to inotropic therapy, and detection of the complete recovery of cardiac function.
Myocardial Dysfunction in Sepsis: A Large, Unsolved Puzzle  [PDF]
Constantino Jose Fernandes Jr.,Murillo Santucci Cesar de Assuncao
Critical Care Research and Practice , 2012, DOI: 10.1155/2012/896430
Abstract: Sepsis has high incidence and mortality rates around the world. The role of cardiac depression in myocardial dysfunction during sepsis remains to be elucidated. This review attempts to summarize our understanding of the anatomical, histopathological, and pathophysiological mechanisms behind cardiac dysfunction. Biomarkers to detect cardiac depression have been used to recognize developing problems, but the actual impact of these tools remains unclear. 1. Introduction Sepsis and sepsis-induced mortality are major health concerns worldwide [1–3]. Septic shock is the most severe form of sepsis and is one of the most significant causes of death among critically ill patients. It is characterized by hemodynamic changes and the dysfunction of one or more organs. Septic shock is a kind of distributive shock, but it can contain components from other forms of shock, such as hypovolemic, cardiogenic, and obstructive shock, which can manifest in the form of profound hypovolemia, severe cardiac failure, or pulmonary arterial hypertension, respectively. Cardiovascular changes are important in septic shock; peripheral vascular dysfunction, which can result in heterogeneous microcirculatory flow, can frequently induce myocardial depression. In this population, cardiovascular collapse can increase the risk of death in sepsis as much as two times, and myocardial depression occurs in almost 40% of septic patients. Myocardial depression is characterized by a cardiac output that fails to meet metabolic demands [4, 5]. In a recent, elegant study, Vieillard-Baron et al. observed a reduced left ventricular ejection fraction (LVEF < 45%) in 60% of patients during the first 3 days of the treatment of septic shock. Curiously, 39% of these patients had presented with left ventricular hypokinesia at admission, suggesting that the development of LVEF can occur in the earliest sepsis stage [6]. In general, approximately 15% of the deaths related to septic shock are secondary to myocardial depression [5]. Myocardial dysfunction can determine whether a patient survives. In survivors, ventricular compliance is increased with a higher end-diastolic volume that helps maintain an adequate stroke volume. Nonsurvivors, in contrast, are progressively unable to maintain the same stroke volume because of reduced diastolic compliance [7]. Reversible myocardial depression also plays a role in survival. It is transient in survivors, typically with a limited duration of 7 to 10 days after the onset of sepsis. As the inflammatory response is attenuated, myocardial dysfunction decreases in a
Effectiveness of Optic Decompression by Endoscopic Endonasal Approach on Patients with Traumatic Fracture of Optic Canal
Rongjiang Luo, Zhichao Yan, Wentong Xia, Xianping Zeng, Rui Xu, Hexin Chen
Open Access Library Journal (OALib Journal) , 2017, DOI: 10.4236/oalib.1103682
Abstract:
Traumatic fracture of optic canal is a severe injury to the optic nerve and often causes permanent visual loss, and it is difficult to treat. This study is to evaluate the effectiveness of decompression of optic canal by nasal endoscope. Operation of optic canal decompression was performed on 210 cases (212 sides) with traumatic fracture of optic canal. Clinical effectiveness was assessed based on improvement of visual acuity. After following up for 6 months to 2 years, visual improvement with more than one visual acuity level was observed on 101 sides (47.6%). Among them, an excellent effect (increasing 2 levels of visual acuity) was achieved on 72 sides (34.0%). Among 133 sides performed within 5 days of injury, 61 sides (45.9%) showed excellent effect (improved 2 levels of visual acuity). In contrast, when operation was performed after 5 days of injury, only 11 out of 79 sides (13.9%) showed excellent effect with improvement of 2 levels of visual acuity. And the overall effectiveness between the operations were performed within and after 5 days of injury was different significantly (P < 0.05). Therefore, endonasal endoscopic optic decompression for traumatic optic neuropathy is an effective measure for patients with traumatic optical canal fracture. Operation within 5 days of injury significantly increases the success rate.
Total Facial Nerve Decompression for Severe Traumatic Facial Nerve Paralysis: A Review of 10 Cases  [PDF]
Sertac Yetiser
International Journal of Otolaryngology , 2012, DOI: 10.1155/2012/607359
Abstract: Management of traumatic facial nerve disorders is challenging. Facial nerve decompression is indicated if 90–95% loss of function is seen at the very early period on ENoG or if there is axonal degeneration on EMG lately with no sign of recovery. Middle cranial or translabyrinthine approach is selected depending on hearing. The aim of this study is to present retrospective review of 10 patients with sudden onset complete facial paralysis after trauma who underwent total facial nerve decompression. Operation time after injury is ranging between 16 and105 days. Excitation threshold, supramaximal stimulation, and amplitude on the paralytic side were worse than at least %85 of the healthy side. Six of 11 patients had HBG-II, one patient had HBG-I, 3 patients had HBG-III, and one patient had HBG-IV recovery. Stretch, compression injuries with disruption of the endoneurial tubules undetectable at the time of surgery and lack of timely decompression may be associated with suboptimal results in our series.
Disfunción miocárdica en la sepsis Myocardial dysfunction in sepsis  [cached]
MAX ANDRESEN,TOMáS REGUEIRA
Revista médica de Chile , 2010,
Abstract: Myocardial dysfunction appears in 25% of patients with severe sepsis and in 50% of patients with septic shock, even in the presence of hyper dynamic states. It is characterized by a reduction in left ventricle ejection fraction, that reverts at the seventh to tenth day of evolution. Right ventricular dysfunction and diastolic left ventricular dysfunction can also appear. There is no consensus if an increase in end diastolic volume is part of the syndrome. High troponin or brain natriuretic peptide levels are associated with myocardial dysfunction and a higher mortality. The pathogenesis of myocardial dysfunction is related to micro and macro circulatory changes, infammatory response, oxidative stress, intracellular calcium management disturbances, metabolic changes, autonomic dysfunction, activation of apoptosis, mitochondrial abnormalities and a derangement in catecholaminergic stimulation. Since there is no specifc treatment for myocardial dysfunction, its management requires an adequate multi systemic support to maintain perfusion pressures and systemic fows suffcient for the regional and global demands.
Total Facial Nerve Decompression for Severe Traumatic Facial Nerve Paralysis: A Review of 10 Cases  [PDF]
Sertac Yetiser
International Journal of Otolaryngology , 2012, DOI: 10.1155/2012/607359
Abstract: Management of traumatic facial nerve disorders is challenging. Facial nerve decompression is indicated if 90–95% loss of function is seen at the very early period on ENoG or if there is axonal degeneration on EMG lately with no sign of recovery. Middle cranial or translabyrinthine approach is selected depending on hearing. The aim of this study is to present retrospective review of 10 patients with sudden onset complete facial paralysis after trauma who underwent total facial nerve decompression. Operation time after injury is ranging between 16 and105 days. Excitation threshold, supramaximal stimulation, and amplitude on the paralytic side were worse than at least %85 of the healthy side. Six of 11 patients had HBG-II, one patient had HBG-I, 3 patients had HBG-III, and one patient had HBG-IV recovery. Stretch, compression injuries with disruption of the endoneurial tubules undetectable at the time of surgery and lack of timely decompression may be associated with suboptimal results in our series. 1. Introduction Indication and timing of the facial nerve decompression for facial paralysis and the anatomical extent of decompression has been a subject of controversy for years. Studies indicate that the number of surgical interventions has decreased over decades. In an analysis of large volume of published data between 1966 and 1999 regarding the management of facial nerve injury due to temporal bone trauma, Chang and Cass have reported that the patients with normal facial nerve function after injury regardless of progression, those with presentation of incomplete paralysis with no progression to complete paralysis, and those with less than 95% degeneration on ENoG at initial admission usually do not require surgical intervention. However, they have also reported that no data were available to provide information on exactly how much the return of function will be for the remaining patients who presumably have poorer prognosis [1]. Brodie and Thompson have reviewed 58 facial nerve injuries and reported that all patients with incomplete paralysis in the beginning recovered and 8 of 9 patients with delayed and 3 of 5 patients with sudden onset facial paralysis recovered after surgical decompression. But 2 of those (40%) patients with immediate-onset complete paralysis presented poor prognosis [2]. McKennan and Chole have compared recovery of patients with delayed and immediate-onset traumatic facial paralysis and have found that recovery is likely to occur in 94% of delayed-onset facial paralysis without surgical intervention [3]. Darrouzet et al. have
Endotoxin-induced myocardial dysfunction in senescent rats
Sandrine Rozenberg, Sophie Besse, Hélène Brisson, Elsa Jozefowicz, Abdelmejid Kandoussi, Alexandre Mebazaa, Bruno Riou, Beno?t Vallet, Beno?t Tavernier
Critical Care , 2006, DOI: 10.1186/cc5033
Abstract: Senescent (24 month) and young adult (3 month) male Wistar rats were treated with intravenous lipopolysaccharide (LPS) (0.5 mg/kg (senescent and young rats) or 5 mg/kg (young rats only)), or saline (senescent and young control groups). Twelve hours after injection, cardiac contractility (isolated perfused hearts), myofilament Ca2+ sensitivity (skinned fibers), left ventricular nitric oxide end-oxidation products (NOx and NO2) and markers of oxidative stress (thiobarbituric acid reactive species (TBARS) and antioxidant enzymes) were investigated.LPS (0.5 mg/kg) administration resulted in decreased contractility in senescent rats (left ventricular developed pressure (LVDP), 25 ± 4 vs 53 ± 4 mmHg/g heart weight in control; P < 0.05) of amplitude similar to that in young rats with LPS 5 mg/kg (LVDP, 48 ± 7 vs 100 ± 7 mmHg/g heart weight in control; P < 0.05). In contrast to young LPS rats (0.5 and 5 mg/kg LPS), myofilament Ca2+ sensitivity was unaltered in senescent LPS hearts. Myocardial NOx and NO2 were increased in a similar fashion by LPS in young (both LPS doses) and senescent rats. TBARS and antioxidant enzyme activities were unaltered by sepsis whatever the age of animals.Low dose of LPS induced a severe myocardial dysfunction in senescent rats. Ca2+ myofilament responsiveness, which is typically reduced in myocardium of young adult septic rats, however, was unaltered in senescent rats. If these results are confirmed in in vivo conditions, they may provide a cellular explanation for the divergent reports on ventricular diastolic function in septic shock. In addition, Ca2+-sensitizing agents may not be as effective in aged subjects as in younger subjects.Impairment in cardiac function is one of the most recognized organ dysfunctions in sepsis. Although the mechanism of myocardial dysfunction is complex and remains incompletely defined, increasing experimental evidence suggests that the main subcellular mechanisms include decreased cardiac myofilament responsivenes
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