RESUMO
OBJECTIVE: Acute mesenteric ischemia (AMI) is a surgical emergency for which delays in treatment have been closely associated with high morbidity and mortality. Although the duration of ischemia as a determinant of outcomes for AMI is well known, the objective of this study was to identify hospital-based determinants of delayed revascularization and their effects on postoperative morbidity and mortality in AMI. METHODS: All patients who underwent any surgery for AMI from a multi-center hospital system between 2010 and 2020 were divided into two groups based on timeliness of mesenteric revascularization after presentation. Early revascularization (ER) was defined as having both vascular consultation ≤12 hours of presentation and vascular surgery performed at the patient's initial operation. Delayed revascularization (DR) was defined as having either delays to vascular consultation or vascular surgery. A retrospective review of demographic and postoperative data was performed. The effect of DR on major postoperative outcomes, including 30-day and 2-year mortality, total length of bowel resection, and development of short bowel syndrome, were analyzed. Effects of delayed vascular consultation alone, delayed vascular surgery alone, no revascularization during admission, and admitting service on outcomes were also examined on subgroup analyses. RESULTS: A total of 212 patients were analyzed. Ninety-nine patients received ER, whereas the remaining 113 patients experienced a DR after hospital presentation. Among the DR group, 55 patients (25.9%) had delayed vascular consultation, whereas vascular surgery was deferred until after the initial operation in 37 patients (17.4%). Fifty-one patients (24.0%) were never revascularized during admission. DR was a significant predictor of 30-day (odds ratio [OR], 2.09; 95% confidence interval [CI], 1.4-4.9; P = .03) and 2-year mortality (hazard ratio, 1.55, 95% CI, 1.0-2.3; P = .04). DR was also independently associated with increased bowel resection length (OR, 7.47; P < .01) and postoperative short bowel syndrome (OR, 2.4; P = .03) on multivariate analyses. When examined separately on subgroup analysis, both delayed vascular consultation (OR, 3.38; P = .03) and vascular surgery (OR, 4.31; P < .01) independently increased risk of 30-day mortality. Hospital discharge after AMI without mesenteric revascularization was associated with increased risk of short bowel syndrome (OR, 2.94; P < .01) and late mortality (hazard ratio, 1.60; P = .04). CONCLUSIONS: Delayed vascular consultation and vascular surgery are both significant hospital-based determinants of postoperative mortality and short bowel syndrome in patients with AMI. Timing-based management protocols that emphasize routine evaluation by a vascular surgeon and early, definitive mesenteric revascularization should be established and widely adopted for all patients with clinically suspected AMI at presentation.
Assuntos
Isquemia Mesentérica , Oclusão Vascular Mesentérica , Síndrome do Intestino Curto , Hospitais , Humanos , Isquemia/diagnóstico , Isquemia/etiologia , Isquemia/cirurgia , Isquemia Mesentérica/diagnóstico por imagem , Isquemia Mesentérica/cirurgia , Oclusão Vascular Mesentérica/complicações , Oclusão Vascular Mesentérica/diagnóstico por imagem , Oclusão Vascular Mesentérica/cirurgia , Estudos Retrospectivos , Fatores de Risco , Síndrome do Intestino Curto/complicações , Síndrome do Intestino Curto/diagnóstico , Fatores de Tempo , Resultado do Tratamento , Procedimentos Cirúrgicos VascularesRESUMO
La isquemia mesentérica aguda (IMA) es consecuencia de la oclusión de la arteria mesentérica superior (AMS) por trombosis o embolia, y es considerada la más letal del síndrome de abdomen agudo. Se presenta el caso de paciente femenina de 69 años con clínica difusa y confirmación diagnóstica radiológica, El objetivo de este caso clínico es proporcionar una revisión bibliográfica actual del tema y facilitar la adecuada actuación ante este problema de salud de amplio compromiso sistémico, y de aparición no tan infrecuente. (AU)
Acute mesenteric ischemia (IMA) is a consequence of occlusion of the superior mesenteric artery (AMS) by thrombosis or embolism; and it is considered the most lethal of acute abdomen syndrome. The case of a 69 years old female patient with diffuse clinic and radiological diagnostic confirmation is presented. The objective of this clinical case is to provide a current bibliographic review of the topic and facilitate adequate action in the face of this health problem with a broad systemic commitment, and with no appearance so infrequent. (AU)
Assuntos
Humanos , Feminino , Idoso , Artéria Mesentérica Superior/diagnóstico por imagem , Isquemia Mesentérica/diagnóstico por imagem , Oclusão Vascular Mesentérica/complicações , Doença Aguda , Artéria Mesentérica Superior/cirurgia , Tomografia Computadorizada Multidetectores , Isquemia Mesentérica/etiologia , Isquemia Mesentérica/terapiaRESUMO
RESUMEN Se presentó un caso de una paciente de 78 años de edad, procedente del municipio de Calimete, con antecedentes patológicos personales de infarto agudo miocárdico sin elevación del segmento ST e hipertensión arterial. Llegó a la Unidad de Cuidados Intensivos de Emergencia, de Colón con un estado toxico infeccioso severo. Fue intervenida quirúrgicamente con el diagnóstico presuntivo de una trombosis mesentérica. Se constató dicho diagnóstico complementario a una neoplasia maligna de colon sigmoides. Falleció producto a un shock séptico refractario a aminas. En la necropsia se reportaron hallazgos de interés.
ABSTRACT The authors present the case of a 78-years-old female patient from the municipality of Calimete, with personal pathological antecedents of acute myocardial infarct without ST segment elevation and arterial hypertension. She arrived to the Emergency Intensive Care Unit of Colon with a severe toxic-infectious status. She underwent a surgery with a presumptive mesenteric thrombosis. It was stated that diagnosis, complementary to a sigmoid colon malignant neoplasia. She died as a product of an amine-refractory septic shock. The autopsy showed findings of interest.
Assuntos
Humanos , Feminino , Idoso , Doenças do Colo Sigmoide/complicações , Doenças do Colo Sigmoide/diagnóstico , Neoplasias do Colo Sigmoide/cirurgia , Neoplasias do Colo Sigmoide/complicações , Neoplasias do Colo Sigmoide/diagnóstico , Neoplasias do Colo Sigmoide/mortalidade , Neoplasias Colorretais/complicações , Neoplasias Colorretais/diagnóstico , Oclusão Vascular Mesentérica/complicações , Oclusão Vascular Mesentérica/diagnóstico , Peritonite , Choque Séptico , Colostomia , Sistema Cardiovascular/fisiopatologia , Dor Abdominal/diagnóstico , Sigmoidoscopia , Taxa de Filtração Glomerular , Falência Renal Crônica , Laparotomia , NeoplasiasRESUMO
PURPOSE: To determine the role of mesenteric lymph reperfusion (MLR) on endotoxin translocation in brain to discuss the mechanism of brain injury subjected to superior mesenteric artery occlusion (SMAO) shock. METHODS: Twenty-four rats were randomly assigned to MLR, SMAO, MLR+SMAO and sham groups. MLR was performed by clamping the mesenteric lymph duct (MLD) for 1 h and then allowing reperfusion for 2 h in the MLR group; SMAO involved clamping the superior mesenteric artery (SMA) for 1 h, followed by reperfusion for 2 h in the SMAO group; occlusion of both the SMA and MLD for 1 h was followed by reperfusion for 2 h in the MLR+SMAO group rats. RESULTS: SMAO shock induced severe increased levels of the endotoxin, lipopolysaccharide receptor, lipopolysaccharide-binding protein, intercellular adhesion molecule-1 and tumor necrosis factor-α. Concurrently, MLR after SMAO shock further aggravates these deleterious effects. CONCLUSION: Mesenteric lymph reperfusion exacerbated the endotoxin translocation in brain; thereby increased inflammatory response occurred, suggesting that the intestinal lymph pathway plays an important role in the brain injury after superior mesenteric artery occlusion shock.
Assuntos
Translocação Bacteriana/fisiologia , Lesões Encefálicas/etiologia , Endotoxinas/fisiologia , Vasos Linfáticos/fisiologia , Oclusão Vascular Mesentérica/fisiopatologia , Mesentério , Traumatismo por Reperfusão/fisiopatologia , Proteínas de Fase Aguda/análise , Animais , Lesões Encefálicas/metabolismo , Proteínas de Transporte/análise , Modelos Animais de Doenças , Endotoxinas/análise , Ensaio de Imunoadsorção Enzimática , Molécula 1 de Adesão Intercelular/análise , Ligadura , Receptores de Lipopolissacarídeos/análise , Vasos Linfáticos/cirurgia , Masculino , Glicoproteínas de Membrana/análise , Artéria Mesentérica Superior , Oclusão Vascular Mesentérica/complicações , Distribuição Aleatória , Ratos Wistar , Traumatismo por Reperfusão/complicações , Fatores de Tempo , Fator de Necrose Tumoral alfa/análiseRESUMO
PURPOSE: To determine the role of mesenteric lymph reperfusion (MLR) on endotoxin translocation in brain to discuss the mechanism of brain injury subjected to superior mesenteric artery occlusion (SMAO) shock. METHODS: Twenty-four rats were randomly assigned to MLR, SMAO, MLR+SMAO and sham groups. MLR was performed by clamping the mesenteric lymph duct (MLD) for 1 h and then allowing reperfusion for 2 h in the MLR group; SMAO involved clamping the superior mesenteric artery (SMA) for 1 h, followed by reperfusion for 2 h in the SMAO group; occlusion of both the SMA and MLD for 1 h was followed by reperfusion for 2 h in the MLR+SMAO group rats. RESULTS: SMAO shock induced severe increased levels of the endotoxin, lipopolysaccharide receptor, lipopolysaccharide-binding protein, intercellular adhesion molecule-1 and tumor necrosis factor-α. Concurrently, MLR after SMAO shock further aggravates these deleterious effects. CONCLUSION: Mesenteric lymph reperfusion exacerbated the endotoxin translocation in brain; thereby increased inflammatory response occurred, suggesting that the intestinal lymph pathway plays an important role in the brain injury after superior mesenteric artery occlusion shock. .
Assuntos
Animais , Masculino , Translocação Bacteriana/fisiologia , Lesões Encefálicas/etiologia , Endotoxinas/fisiologia , Vasos Linfáticos/fisiologia , Mesentério , Oclusão Vascular Mesentérica/fisiopatologia , Traumatismo por Reperfusão/fisiopatologia , Proteínas de Fase Aguda/análise , /análise , Lesões Encefálicas/metabolismo , Proteínas de Transporte/análise , Modelos Animais de Doenças , Ensaio de Imunoadsorção Enzimática , Endotoxinas/análise , Molécula 1 de Adesão Intercelular/análise , Ligadura , Vasos Linfáticos/cirurgia , Artéria Mesentérica Superior , Glicoproteínas de Membrana/análise , Oclusão Vascular Mesentérica/complicações , Distribuição Aleatória , Ratos Wistar , Traumatismo por Reperfusão/complicações , Fatores de Tempo , Fator de Necrose Tumoral alfa/análiseRESUMO
The intestinal lymph pathway plays an important role in the pathogenesis of organ injury following superior mesenteric artery occlusion (SMAO) shock. We hypothesized that mesenteric lymph reperfusion (MLR) is a major cause of spleen injury after SMAO shock. To test this hypothesis, SMAO shock was induced in Wistar rats by clamping the superior mesenteric artery (SMA) for 1 h, followed by reperfusion for 2 h. Similarly, MLR was performed by clamping the mesenteric lymph duct (MLD) for 1 h, followed by reperfusion for 2 h. In the MLR+SMAO group rats, both the SMA and MLD were clamped and then released for reperfusion for 2 h. SMAO shock alone elicited: 1) splenic structure injury, 2) increased levels of malondialdehyde, nitric oxide (NO), intercellular adhesion molecule-1, endotoxin, lipopolysaccharide receptor (CD14), lipopolysaccharide-binding protein, and tumor necrosis factor-α, 3) enhanced activities of NO synthase and myeloperoxidase, and 4) decreased activities of superoxide dismutase and ATPase. MLR following SMAO shock further aggravated these deleterious effects. We conclude that MLR exacerbates spleen injury caused by SMAO shock, which itself is associated with oxidative stress, excessive release of NO, recruitment of polymorphonuclear neutrophils, endotoxin translocation, and enhanced inflammatory responses.
Assuntos
Animais , Masculino , Linfa/metabolismo , Oclusão Vascular Mesentérica/complicações , Traumatismo por Reperfusão/etiologia , Reperfusão/efeitos adversos , Baço/lesões , Proteínas de Fase Aguda/análise , Adenosina Trifosfatases/análise , /análise , Proteínas de Transporte/análise , Endotoxinas/análise , Molécula 1 de Adesão Intercelular/análise , Intestinos/irrigação sanguínea , Artéria Mesentérica Superior , Malondialdeído/análise , Glicoproteínas de Membrana/análise , Óxido Nítrico Sintase/análise , Óxido Nítrico/análise , Peroxidase/análise , Ratos Wistar , Baço/patologia , Superóxido Dismutase/análise , Fator de Necrose Tumoral alfa/análiseRESUMO
The intestinal lymph pathway plays an important role in the pathogenesis of organ injury following superior mesenteric artery occlusion (SMAO) shock. We hypothesized that mesenteric lymph reperfusion (MLR) is a major cause of spleen injury after SMAO shock. To test this hypothesis, SMAO shock was induced in Wistar rats by clamping the superior mesenteric artery (SMA) for 1 h, followed by reperfusion for 2 h. Similarly, MLR was performed by clamping the mesenteric lymph duct (MLD) for 1 h, followed by reperfusion for 2 h. In the MLR+SMAO group rats, both the SMA and MLD were clamped and then released for reperfusion for 2 h. SMAO shock alone elicited: 1) splenic structure injury, 2) increased levels of malondialdehyde, nitric oxide (NO), intercellular adhesion molecule-1, endotoxin, lipopolysaccharide receptor (CD14), lipopolysaccharide-binding protein, and tumor necrosis factor-α, 3) enhanced activities of NO synthase and myeloperoxidase, and 4) decreased activities of superoxide dismutase and ATPase. MLR following SMAO shock further aggravated these deleterious effects. We conclude that MLR exacerbates spleen injury caused by SMAO shock, which itself is associated with oxidative stress, excessive release of NO, recruitment of polymorphonuclear neutrophils, endotoxin translocation, and enhanced inflammatory responses.
Assuntos
Linfa/metabolismo , Oclusão Vascular Mesentérica/complicações , Traumatismo por Reperfusão/etiologia , Reperfusão/efeitos adversos , Baço/lesões , Proteínas de Fase Aguda/análise , Adenosina Trifosfatases/análise , Animais , Proteínas de Transporte/análise , Endotoxinas/análise , Molécula 1 de Adesão Intercelular/análise , Intestinos/irrigação sanguínea , Receptores de Lipopolissacarídeos/análise , Masculino , Malondialdeído/análise , Glicoproteínas de Membrana/análise , Artéria Mesentérica Superior , Óxido Nítrico/análise , Óxido Nítrico Sintase/análise , Peroxidase/análise , Ratos Wistar , Baço/patologia , Superóxido Dismutase/análise , Fator de Necrose Tumoral alfa/análiseRESUMO
Portal venous thrombosis was originally considered to be a contraindication for liver transplantation. Currently, several methods exist to re-establish blood flow to the hepatic portal system. Cavoportal hemitransposition is a surgical procedure that can be used in liver transplantation when the portal venous system is thrombosed and portal flow cannot be re-established from the mesenteric venous system. In cavoportal hemitransposition the blood flow from the inferior vena cava of the recipient is directed to the portal vein of the donor liver to compensate for the lost portal venous supply. This can either be done by end-to-end or end-to-side anastomosis. Seventy-one cases of cavoportal hemitransposition have been reported worldwide. All patients reported had been in a critical and life-threatening condition, presenting with either end-stage-liver disease or acute hepatic failure combined with severe vascular pathology. Of the cases reported, 32 patients died for reasons non-related to the surgical procedure. Seven of the 71 patients had Budd-Chiari syndrome complicated by thrombosis of the portal-venous system. This means thrombosis in two different venous systems at the same time, the mesenteric and main venous system. To date this <
Assuntos
Veias Hepáticas/cirurgia , Transplante de Fígado , Oclusão Vascular Mesentérica/cirurgia , Derivação Portocava Cirúrgica , Veia Porta/cirurgia , Circulação Esplâncnica , Veia Cava Inferior/cirurgia , Trombose Venosa/cirurgia , Síndrome de Budd-Chiari/fisiopatologia , Síndrome de Budd-Chiari/cirurgia , Circulação Colateral , Veias Hepáticas/fisiopatologia , História do Século XIX , História do Século XX , Humanos , Circulação Hepática , Oclusão Vascular Mesentérica/complicações , Oclusão Vascular Mesentérica/fisiopatologia , Derivação Portocava Cirúrgica/efeitos adversos , Derivação Portocava Cirúrgica/história , Veia Porta/fisiopatologia , Radiografia Intervencionista , Terminologia como Assunto , Resultado do Tratamento , Veia Cava Inferior/fisiopatologia , Trombose Venosa/complicações , Trombose Venosa/fisiopatologiaRESUMO
Acute ischemia due to spontaneous dissections of the superior mesenteric artery are uncommon events, with sporadic reports. Therapeutic options include clinical management, direct artery repair, bowel resection, and more recently, endovascular stenting. We present a case of abdominal pain due to superior mesenteric artery spontaneous isolated dissection treated with stent placement and with a favorable 31-month follow-up period.
Assuntos
Dor Abdominal/etiologia , Angioplastia com Balão/instrumentação , Dissecção Aórtica/terapia , Oclusão Vascular Mesentérica/complicações , Stents , Dor Abdominal/patologia , Dor Abdominal/prevenção & controle , Dissecção Aórtica/complicações , Dissecção Aórtica/patologia , Angiografia Digital , Humanos , Masculino , Artéria Mesentérica Superior , Oclusão Vascular Mesentérica/etiologia , Oclusão Vascular Mesentérica/patologia , Oclusão Vascular Mesentérica/terapia , Pessoa de Meia-Idade , Resultado do Tratamento , Ultrassonografia Doppler DuplaRESUMO
We evaluated changes involving the myenteric neurons of the guinea pig after different times of ischemia in situ followed by superfusion in vitro. Intestinal ischemia was produced by clamping the superior mesenteric artery and maintaining it for 5, 10, 20, 40, 80, or 160 min. Myenteric plexus-longitudinal muscle preparations from ischemic and non-ischemic portions, obtained from the same guinea pig, were dissected and mounted in organ baths containing Krebs bicarbonate solution at 37 degrees C, gassed with 95% O(2) and 5% CO(2). After 2 h of superfusion, ischemic and non-ischemic strips were removed, immersed in a fixative solution, and processed for light and electron microscopy. We found that ultrastructural neuronal changes, which corresponded with light microscopy findings, developed over time. Some structural changes started after 10 min of ischemia, including cell swelling, chromatin clumping, vacuolization, and disruption of protoplasmic and mitochondrial membranes. Smooth muscle cells changes paralleled those observed in the myenteric neurons, but were evidenced until 40 min of ischemia were completed. These results show that ischemia produces acute time-dependent structural changes in the guinea-pig small intestine, and that affected cells exhibit primarily morphological changes characteristic of necrosis.