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INTRODUÇÃO: Na presença de sepse, choque séptico ou foco infeccioso evidente, antimicrobianos devem ser administrados imediatamente. Entretanto, poucos estudos avaliaram essa conduta na suspeita de infecção sem foco infeccioso evidente e sem sepse. O objetivo do presente estudo foi avaliar se há associação entre postergar a administração de antibioticoterapia empírica precoce em pacientes críticos cirúrgicos com suspeita de infecção nosocomial, porém sem disfunções orgânicas agudas e sem foco óbvio de infecção, com progressão de disfunções orgânicas. MÉTODOS: Estudo retrospectivo observacional, incluindo pacientes que tiveram culturas coletadas devido a hipótese diagnóstica de infecção nosocomial. Grupo Terapia Antimicrobiana Empírica Precoce (GTEP): indivíduos que receberam antibióticos com espectro de ação ativo para tratamento de infecções nosocomiais em até 24 horas após coleta de culturas. Grupo Conservador (GC): pacientes que receberam antibióticos somente após 24 horas de coleta de culturas, ou que não receberam antimicrobianos. Os principais critérios de exclusão foram: sepse, choque séptico ou foco de infecção evidente. O desfecho primário foi composto por: aumento da escala SOFA acima de um ponto (sepse); hipotensão, hiperlactatemia e uso de vasopressores (choque séptico); ou morte em até 14 dias após a inclusão. Análise Multivariada foi prevista devido aos desbalanços entre os grupos. RESULTADOS: De 2007 admissões na UTI no período, 751 apresentaram suspeita de infecção nosocomial e 340 pacientes foram elegíveis para inclusão (74% vítimas de trauma). A maior parte das exclusões ocorreu devido a sepse (221 pacientes), choque séptico (81 pacientes) ou foco óbvio de infecção (51 pacientes). Idade, sexo, motivo de admissão hospitalar, escala Simplified Acute Physiology Score (SAPS3), escala Sequential Organ Failure Assessment (SOFA), uso de vasopressor ou de ventilação mecânica não foram diferentes entre os grupos. No GC, 57% dos pacientes receberam antibióticos em até 14 dias da inclusão (vs. 100% no GTEP). O desfecho composto ocorreu em 40% dos indivíduos no GC e 56% no GTEP (p

Objective Multiple factors have been identified as causes of intracranial compliance impairment (ICCI) among patients with obesity. On the other hand, obesity has been linked with worst outcomes in COVID‐19. Thus, the hypothesis of severe acute respiratory syndrome (SARS) conducing to cerebral hemodynamic disorders (CHD) able to worsen ICCI and play an additional role on prognosis determination for COVID‐19 among obese patients becomes suitable. Methods 50 cases of SARS by COVID‐19 were evaluated, for the presence of ICCI and cerebrovascular circulatory disturbances in correspondence with whether unfavorable outcomes (death or impossibility for mechanical ventilation weaning [MVW]) within 7 days after evaluation. The objective was to observe whether obese patients (BMI ≥ 30) disclosed worse outcomes and tests results compared with lean subjects with same clinical background. Results 23 (46%) patients among 50 had obesity. ICCI was verified in 18 (78%) obese, whereas in 13 (48%) of 27 non‐obese (p = 0,029). CHD were not significantly different between groups, despite being high prevalent in both. 69% unfavorable outcomes were observed among obese and 44% for lean subjects (p = 0,075). Conclusion In the present study, intracranial compliance impairment was significantly more observed among obese subjects and may have contributed for SARS COVID‐19 worsen prognosis.

Intracranial hypertension (IH) is a common and significant secondary insult in patients with acute neurologic injury. Clinical signs in patients with altered level of consciousness poorly predict IH, except in advanced stages. Head computed tomography (CT) scans are the initial examination in these patients since it can detect structural causes for IH and provides surgery indication. Optic nerve sheath ultrasound has good accuracy for detecting IH and can be useful as a triage tool in some settings.

OBJECTIVEThe present study was designed to answer several concerns disclosed by systematic reviews indicating no evidence to support the use of computed tomography angiography (CTA) in the diagnosis of brain death (BD). Therefore, the aim of this study was to assess the effectiveness of CTA for the diagnosis of BD and to define the optimal tomographic criteria of intracranial circulatory arrest.METHODSA unicenter, prospective, observational case-control study was undertaken. Comatose patients (Glasgow Coma Scale score ≤ 5), even those presenting with the first signs of BD, were included. CTA scanning of arterial and venous vasculature and transcranial Doppler (TCD) were performed. A neurological determination of BD and consequently determination of case (BD group) or control (no-BD group) was conducted. All personnel involved with assessing patients were blinded to further tests results. Accuracy of BD diagnosis determined by using CTA was calculated based on the criteria of bilateral absence of visualization of the internal cerebral veins and the distal middle cerebral arteries, the 4-point score (4PS), and an exclusive criterion of absence of deep brain venous drainage as indicated by the absence of deep venous opacification on CTA, the venous score (VS), which considers only the internal cerebral veins bilaterally.RESULTSA total of 106 patients were enrolled in this study; 52 patients did not have BD, and none of these patients had circulatory arrest observed by CTA or TCD (100% specificity). Of the 54 patients with a clinical diagnosis of BD, 33 met the 4PS (61.1% sensitivity), whereas 47 met the VS (87% sensitivity). The accuracy of CTA was time related, with greater accuracy when scanning was performed less than 12 hours prior to the neurological assessment, reaching 95.5% sensitivity with the VS.CONCLUSIONSCTA can reliably support a diagnosis of BD. The criterion of the absence of deep venous opacification, which can be assessed by use of the VS criteria investigated in this study, can confirm the occurrence of cerebral circulatory arrest.Clinical trial registration no.: 12500913400000068 (clinicaltrials.gov)

Background: Anemia is frequent among patients with traumatic brain injury (TBI) and is associated with an increased risk of poor outcome. The optimal hemoglobin concentration to trigger red blood cell (RBC) transfusion in patients with TBI is not clearly defined. Methods: All eligible consecutive adult patients admitted to the intensive care unit (ICU) with moderate or severe TBI were randomized to a "restrictive" (hemoglobin transfusion threshold of 7 g/dL), or a "liberal" (threshold 9 g/dL) transfusion strategy. The transfusion strategy was continued for up to 14 days or until ICU discharge. The primary outcome was the mean difference in hemoglobin between groups. Secondary outcomes included transfusion requirements, intracranial pressure management, cerebral hemodynamics, length of stay, mortality and 6-month neurological outcome. Results: A total of 44 patients were randomized, 21 patients to the liberal group and 23 to the restrictive group. There were no baseline differences between the groups. The mean hemoglobin concentrations during the 14-day period were 8.4 ± 1.0 and 9.3 ± 1.3 (p < 0.01) in the restrictive and liberal groups, respectively. Fewer RBC units were administered in the restrictive than in the liberal group (35 vs. 66, p = 0.02). There was negative correlation (r = - 0.265, p < 0.01) between hemoglobin concentration and middle cerebral artery flow velocity as evaluated by transcranial Doppler ultrasound and the incidence of post-traumatic vasospasm was significantly lower in the liberal strategy group (4/21, 3% vs. 15/23, 65%; p < 0.01). Hospital mortality was higher in the restrictive than in the liberal group (7/23 vs. 1/21; p = 0.048) and the liberal group tended to have a better neurological status at 6 months (p = 0.06). Conclusions: The trial reached feasibility criteria. The restrictive group had lower hemoglobin concentrations and received fewer RBC transfusions. Hospital mortality was lower and neurological status at 6 months favored the liberal group. Trial registration: ClinicalTrials.gov, NCT02203292. Registered on 29 July 2014., SCOPUS: ar.j, info:eu-repo/semantics/published

RESUMO Objetivo: avaliar epidemiologia, características anatômicas, manejo e prognóstico de pacientes críticos com fraturas de esterno. Métodos: análise retrospectiva de pacientes internados em unidade de terapia intensiva (UTI) de emergências cirúrgicas e trauma de um centro de trauma Tipo III em São Paulo, Brasil. Resultados: foram admitidos 1552 pacientes traumatizados no período de janeiro de 2012 a abril de 2016. Desses, 439 apresentavam trauma torácico e 13 apresentavam fratura de esterno, configurando 0,9% das admissões de trauma e 3% dos traumas torácicos. Desses pacientes, três apresentavam tórax instável e dois foram submetidos à conduta cirúrgica para fixação da fratura. A mortalidade de pacientes com fratura de esterno foi de 29% (três pacientes). Em um dos óbitos pôde-se atribuir a fratura do esterno como contribuinte principal para o desfecho. Conclusão: a fratura de esterno foi diagnosticada em 0,9% dos pacientes críticos vítimas de trauma em UTI especializada. Somente 15% dos pacientes necessitaram de conduta cirúrgica específica na fase aguda e a mortalidade foi decorrente das outras lesões na maior parte dos casos. ABSTRACT Objective: to evaluate epidemiology, anatomical characteristics, management, and prognosis of critical patients with sternum fractures. Methods: retrospective analysis of patients admitted to intensive care unit (ICU) of a Level III trauma center in Sao Paulo, Brazil. Results: 1552 trauma patients were admitted from January 2012 to April 2016. A total of 439 patients had thoracic trauma and among these, 13 patients had sternum fracture, making up 0.9% of all trauma admissions and 3% of all thoracic trauma cases. Three of these 13 patients had unstable chest, two underwent surgical management for fracture fixation, and three died (mortality was of 29%). In one of the deaths, sternum fracture was assessed as the main contributor to the outcome. Conclusion: sternum fracture was diagnosed in 0.9% of critical trauma patients in a specialized ICU. Only 15% of patients required specific surgical management in the acute phase. In most cases, mortality was due to other injuries.

Introduction: One of the possible mechanisms by which the new coronavirus (SARS-Cov2) could induce brain damage is the impairment of cerebrovascular hemodynamics (CVH) and intracranial compliance (ICC) due to the elevation of intracranial pressure (ICP). The main objective of this study was to assess the presence of CVH and ICC alterations in patients with COVID-19 and evaluate their association with short-term clinical outcomes. Methods: Fifty consecutive critically ill COVID-19 patients were studied with transcranial Doppler (TCD) and non-invasive monitoring of ICC. Subjects were included upon ICU admission, CVH was evaluated using mean flow velocities in the middle cerebral arteries (mCBFV), pulsatility index (PI), and estimated cerebral perfusion pressure (eCPP), while ICC was assessed by using the P2/P1 ratio of the non-invasive ICP curve. A CVH/ICC score was computed using all these variables. The primary composite outcome was unsuccessful in weaning from respiratory support or death on day 7 (defined as UO). Results: At the first assessment (n = 50), only the P2/P1 ratio (median 1.20 [IQRs 1.00–1.28] vs. 1.00 [0.88–1.16], p = 0.03) and eICP (14 [11–25] vs. 11 [7–15] mmHg, p = 0.01) were significantly higher among patients with an unfavorable outcome (UO) than others. Patients with UO had a significantly higher CVH/ICC score (9 [8–12] vs. 6 [5–7], p &lt, 0.001) than those with a favorable outcome, the area under the receiver operating curve (AUROC) for CVH/ICC score to predict UO was 0.86 (95% CIs 0.75–0.97), a score &gt, 8.5 had 63 (46–77)% sensitivity and 87 (62–97)% specificity to predict UO. For those patients undergoing a second assessment (n = 29), after a median of 11 (5–31) days, all measured variables were similar between the two time-points. No differences in the measured variables between ICU non-survivors (n = 30) and survivors were observed. Conclusions: ICC impairment and CVH disturbances are often present in COVID-19 severe illness and could accurately predict an early poor outcome.

to evaluate epidemiology, anatomical characteristics, management, and prognosis of critical patients with sternum fractures.retrospective analysis of patients admitted to intensive care unit (ICU) of a Level III trauma center in Sao Paulo, Brazil.1552 trauma patients were admitted from January 2012 to April 2016. A total of 439 patients had thoracic trauma and among these, 13 patients had sternum fracture, making up 0.9% of all trauma admissions and 3% of all thoracic trauma cases. Three of these 13 patients had unstable chest, two underwent surgical management for fracture fixation, and three died (mortality was of 29%). In one of the deaths, sternum fracture was assessed as the main contributor to the outcome.sternum fracture was diagnosed in 0.9% of critical trauma patients in a specialized ICU. Only 15% of patients required specific surgical management in the acute phase. In most cases, mortality was due to other injuries.avaliar epidemiologia, características anatômicas, manejo e prognóstico de pacientes críticos com fraturas de esterno.análise retrospectiva de pacientes internados em unidade de terapia intensiva (UTI) de emergências cirúrgicas e trauma de um centro de trauma Tipo III em São Paulo, Brasil.foram admitidos 1552 pacientes traumatizados no período de janeiro de 2012 a abril de 2016. Desses, 439 apresentavam trauma torácico e 13 apresentavam fratura de esterno, configurando 0,9% das admissões de trauma e 3% dos traumas torácicos. Desses pacientes, três apresentavam tórax instável e dois foram submetidos à conduta cirúrgica para fixação da fratura. A mortalidade de pacientes com fratura de esterno foi de 29% (três pacientes). Em um dos óbitos pôde-se atribuir a fratura do esterno como contribuinte principal para o desfecho.a fratura de esterno foi diagnosticada em 0,9% dos pacientes críticos vítimas de trauma em UTI especializada. Somente 15% dos pacientes necessitaram de conduta cirúrgica específica na fase aguda e a mortalidade foi decorrente das outras lesões na maior parte dos casos.

There is no consensual definition of refractory shock. The use of more than 0.5 mcg/kg/min of norepinephrine or epinephrine to maintain target blood pressure is often used in clinical trials as a threshold. Nearly 6% of critically ill patients will develop refractory shock, which accounts for 18% of deaths in intensive care unit. Mortality rates are usually greater than 50%. The assessment of fluid responsiveness and cardiac function can help to guide therapy, and inotropes may be used if hypoperfusion signs persist after initial resuscitation. Arginine vasopressin is frequently used in refractory shock, although definite evidence to support this practice is still missing. Its associations with corticosteroids improved outcome in observational studies and are therefore promising alternatives. Other rescue therapies such as terlipressin, methylene blue, and high-volume isovolemic hemofiltration await more evidence before use in routine practice.

There are few reports in the literature regarding the use of venoarterial extracorporeal membrane oxygenation (ECMO) for double-dysfunction from both heart and lung contusions in polytrauma patients. This article reports a 48-year-old patient admitted after a traffic accident. He rapidly progressed to shock with low cardiac output due to myocardial contusion and refractory hypoxemia due to pulmonary contusion, an unstable chest wall and bilateral pneumothorax. ECMO was an effective rescue procedure in this dramatic situation and was successfully discontinued on the fourth day after the trauma. The patient also developed an extensive brain infarction and eventually died on the seventh day after admission.

Objective— We hypothesized that reactive oxygen species (ROS) contribute to progression of aortic valve (AV) calcification/stenosis. Methods and Results— We investigated ROS production and effects of antioxidants tempol and lipoic acid (LA) in calcification progression in rabbits given 0.5% cholesterol diet +10 4 IU/d Vit.D 2 for 12 weeks. Superoxide and H 2 O 2 microfluorotopography and 3-nitrotyrosine immunoreactivity showed increased signals not only in macrophages but preferentially around calcifying foci, in cells expressing osteoblast/osteoclast, but not macrophage markers. Such cells also showed increased expression of NAD(P)H oxidase subunits Nox2, p22phox, and protein disulfide isomerase. Nox4, but not Nox1 mRNA, was increased. Tempol augmented whereas LA decreased H 2 O 2 signals. Importantly, AV calcification, assessed by echocardiography and histomorphometry, decreased 43% to 70% with LA, but increased with tempol ( P ≤0.05). Tempol further enhanced apoptosis and Nox4 expression. In human sclerotic or stenotic AV, we found analogous increases in ROS production and NAD(P)H oxidase expression around calcifying foci. An in vitro vascular smooth muscle cell (VSMC) calcification model also exhibited increased, catalase-inhibitable, calcium deposit with tempol, but not with LA. Conclusions— Our data provide evidence that ROS, particularly hydrogen peroxide, potentiate AV calcification progression. However, tempol exhibited a paradoxical effect, exacerbating AV/vascular calcification, likely because of its induced increase in peroxide generation.

RESUMO Objetivo: Avaliar o impacto do monitoramento da pressão intracraniana nos desfechos em curto prazo de pacientes com lesão encefálica traumática. Métodos: Estudo retrospectivo e observacional que incluiu 299 pacientes consecutivos admitidos por lesão cerebral traumática entre janeiro de 2011 e julho de 2012 em um centro de trauma Nível 1 localizado em São Paulo (SP). Os pacientes foram categorizados em dois grupos, segundo a mensuração da pressão intracraniana (grupos com mensuração da pressão intracraniana e sem mensuração da pressão intracraniana). Aplicamos uma análise de propensão pareada para ajustar quanto a possíveis fatores de confusão (variáveis contidas no algoritmo prognóstico CRASH Score). Resultados: A mortalidade global aos 14 dias (16%) foi equivalente à observada em países desenvolvidos no estudo CRASH, e melhor que o previsto com base na calculadora de escore CRASH (20,6%), com uma proporção padronizada de mortalidade de 0,77. No total, 28 pacientes receberam monitoramento da pressão intracraniana (grupo com mensuração da pressão intracraniana), dos quais 26 foram pareados em proporção 1:1 com pacientes do grupo sem mensuração da pressão intracraniana. Não houve melhora no grupo com mensuração da pressão intracraniana em comparação àquele sem mensuração da pressão intracraniana quanto à mortalidade hospitalar, à mortalidade aos 14 dias, ou à mortalidade combinada hospitalar e em hospital de retaguarda. A sobrevivência até 14 dias foi também similar entre os grupos. Conclusão: Os pacientes que receberam monitoramento da pressão intracraniana tendem a ser portadores de lesões encefálicas mais graves. Porém, após ajustar quanto a múltiplos fatores de confusão com a utilização de um escore de propensão, não se observou qualquer benefício em termos de sobrevivência entre os pacientes com monitoramento da pressão intracraniana em relação aos tradados segundo um protocolo clínico sistematizado. ABSTRACT Objective: To assess the impact of intracranial pressure monitoring on the short-term outcomes of traumatic brain injury patients. Methods: Retrospective observational study including 299 consecutive patients admitted due to traumatic brain injury from January 2011 through July 2012 at a Level 1 trauma center in São Paulo, Brazil. Patients were categorized in two groups according to the measurement of intracranial pressure (measured intracranial pressure and non-measured intracranial pressure groups). We applied a propensity-matched analysis to adjust for possible confounders (variables contained in the Crash Score prognostic algorithm). Results: Global mortality at 14 days (16%) was equal to that observed in high-income countries in the CRASH Study and was better than expected based on the CRASH calculator score (20.6%), with a standardized mortality ratio of 0.77. A total of 28 patients received intracranial pressure monitoring (measured intracranial pressure group), of whom 26 were paired in a 1:1 fashion with patients from the non-measured intracranial pressure group. There was no improvement in the measured intracranial pressure group compared to the non-measured intracranial pressure group regarding hospital mortality, 14-day mortality, or combined hospital and chronic care facility mortality. Survival up to 14 days was also similar between groups. Conclusion: Patients receiving intracranial pressure monitoring tend to have more severe traumatic brain injuries. However, after adjusting for multiple confounders using propensity scoring, no benefits in terms of survival were observed among intracranial pressure-monitored patients and those managed with a systematic clinical protocol.

On January 2013, a disaster at Santa Maria (RS) due to a fire in a confined space caused 242 deaths, most of them by inhalation injury. On November 2013, four individuals required intensive care following smoke inhalation from a fire at the Memorial da América Latina in São Paulo (SP). The present article reports the clinical progression and management of disaster victims presenting with inhalation injury. Patients ERL and OC exhibited early respiratory failure, bronchial aspiration of carbonaceous material, and carbon monoxide poisoning. Ventilation support was performed with 100% oxygen, the aspirated material was removed by bronchoscopy, and cyanide poisoning was empirically treated with sodium nitrite and sodium thiosulfate. Patient RP initially exhibited cough and retrosternal burning and subsequently progressed to respiratory failure due to upper airway swelling and early-onset pulmonary infection, which were treated with protective ventilation and antimicrobial agents. This patient was extubated following improvement of edema on bronchoscopy. Patient MA, an asthmatic, exhibited carbon monoxide poisoning and bronchospasm and was treated with normobaric hyperoxia, bronchodilators, and corticosteroids. The length of stay in the intensive care unit varied from four to 10 days, and all four patients exhibited satisfactory functional recovery. To conclude, inhalation injury has a preponderant role in fires in confined spaces. Invasive ventilation should not be delayed in cases with significant airway swelling. Hyperoxia should be induced early as a therapeutic means against carbon monoxide poisoning, in addition to empiric pharmacological treatment in suspected cases of cyanide poisoning.

Vascular calcification decreases compliance and increases morbidity. Mechanisms of this process are unclear. The role of oxidative stress and effects of antioxidants have been poorly explored. We investigated effects of the antioxidants lipoic acid (LA) and tempol in a model of atherosclerosis associated with elastocalcinosis. Male New Zealand white rabbits (2.5-3.0 kg) were fed regular chow (controls) or a 0.5% cholesterol (chol) diet+104 IU/day vitamin D2 (vitD) for 12 weeks, and assigned to treatment with water (vehicle, n=20), 0.12 mmol·kg-1·day-1 LA (n=11) or 0.1 mmol·kg-1·day-1 tempol (n=15). Chol+vitD-fed rabbits developed atherosclerotic plaques associated with expansive remodeling, elastic fiber disruption, medial calcification, and increased aortic stiffness. Histologically, LA prevented medial calcification by ∼60% and aortic stiffening by ∼60%. LA also preserved responsiveness to constrictor agents, while intima-media thickening was increased. In contrast to LA, tempol was associated with increased plaque collagen content, medial calcification and aortic stiffness, and produced differential changes in vasoactive responses in the chol+vitD group. Both LA and tempol prevented superoxide signals with chol+vitD. However, only LA prevented hydrogen peroxide-related signals with chol+vitD, while tempol enhanced them. These data suggest that LA, opposite to tempol, can minimize calcification and compliance loss in elastocalcionosis by inhibition of hydrogen peroxide generation.

There are few reports in the literature regarding the use of venoarterial extracorporeal membrane oxygenation (ECMO) for double-dysfunction from both heart and lung contusions in polytrauma patients. This article reports a 48-year-old patient admitted after a traffic accident. He rapidly progressed to shock with low cardiac output due to myocardial contusion and refractory hypoxemia due to pulmonary contusion, an unstable chest wall and bilateral pneumothorax. ECMO was an effective rescue procedure in this dramatic situation and was successfully discontinued on the fourth day after the trauma. The patient also developed an extensive brain infarction and eventually died on the seventh day after admission.

To the Editor:A healthy 31-year-old man who was the victim of a motorvehicle accident developed multiple-organ failure secondary tocomplications of polytrauma, including acute kidney injuryrequiring continuous renal replacement therapy.Despite regional anticoagulation using citrate (mean postfiltercalcium concentration, 0.43 mmol/L), there was recurrent clottingwithin the circuit. A markedly greasy aspect of coagulated bloodin the dialyzer and bubble trap was noted (Fig 1). Triglycerideconcentration in the dialysis circuit blood was 1,667 mg/dL,which was similar to the serum level (1,772 mg/dL). Propofolwas the presumed cause of hypertriglyceridemia because ithad been used to control intracranial hypertension for the last10 days.Microscopic analysis of the dialyzer membrane revealed clotand fibrin without signs of fat deposition, as demonstrated byhistopathologic analysis with Sudan Black stain. Five days afterceasing propofol therapy, the patient’s blood triglyceride con-centration decreased to 534 mg/dL andfilter patency was bettermaintained. The patient had complete kidney recovery onfollow-up.A similar problem was described by Kazory et al

Introduction Mechanisms underlying inotropic failure in septic shock are incompletely understood. We previously identified the presence of exosomes in the plasma of septic shock patients. These exosomes are released mainly by platelets, produce superoxide, and induce apoptosis in vascular cells by a redox-dependent pathway. We hypothesized that circulating platelet-derived exosomes could contribute to inotropic dysfunction of sepsis.Methods We collected blood samples from 55 patients with septic shock and 12 healthy volunteers for exosome separation. Exosomes from septic patients and healthy individuals were investigated concerning their myocardial depressant effect in isolated heart and papillary muscle preparations.Results Exosomes from the plasma of septic patients significantly decreased positive and negative derivatives of left ventricular pressure in isolated rabbit hearts or developed tension and its first positive derivative in papillary muscles. Exosomes from healthy individuals decreased these variables non-significantly. in hearts from rabbits previously exposed to endotoxin, septic exosomes decreased positive and negative derivatives of ventricular pressure. This negative inotropic effect was fully reversible upon withdrawal of exosomes. Nitric oxide ( NO) production from exosomes derived from septic shock patients was demonstrated by fluorescence. Also, there was an increase in myocardial nitrate content after exposure to septic exosomes.Conclusion Circulating platelet-derived exosomes from septic patients induced myocardial dysfunction in isolated heart and papillary muscle preparations, a phenomenon enhanced by previous in vivo exposure to lipopolysaccharide. the generation of NO by septic exosomes and the increased myocardial nitrate content after incubation with exosomes from septic patients suggest an NO-dependent mechanism that may contribute to myocardial dysfunction of sepsis. Univ São Paulo, Sch Med, Emergency Med Res Lab, BR-05403900 São Paulo, Brazil Hosp Sirio Libanes, Res & Educ Inst, BR-01308060 São Paulo, Brazil Univ São Paulo, Inst Biomed Sci, Dept Pharm, BR-05508900 São Paulo, Brazil Univ São Paulo, Heart Inst InCor, Vasc Biol Lab, BR-05403000 São Paulo, Brazil Universidade Federal de São Paulo, Cardiovasc Physiol Lab, BR-04022000 São Paulo, Brazil Universidade Federal de São Paulo, Cardiovasc Physiol Lab, BR-04022000 São Paulo, Brazil Web of Science