Acute esophageal necrosis after lung cancer surgery

Katsuhara, Kazuhiro; Takano, Shinji; Yamamoto, Youta; Ueda, Shigeo; Nobuhara, Kenji; Kiyasu, Yoshito

doi:10.1007/s11748-009-0423-3

Cited by 3 publications

(4 citation statements)

References 9 publications

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“…A history of malignancy is present in 10% of patients who present with AEN [11]. Reported malignancies include esophageal squamous carcinoma [73], colorectal adenocarcinoma [72], pancreatic adenocarcinoma [8], cholangiocarcinoma [74], oral cavity squamous cancer [75], pharynx squamous cancer [64], renal cell carcinoma [58], lung squamous carcinoma [76], or non-small cell lung cancer [77]. It is likely that the presence of malignancy is associated with cachexia and immune dysregulation, thereby decreasing mucosal regenerative ability and increasing susceptibility to necrosis when the patient is exposed to an acute event.…”

Section: Etiologymentioning

confidence: 99%

“…It is likely that the presence of malignancy is associated with cachexia and immune dysregulation, thereby decreasing mucosal regenerative ability and increasing susceptibility to necrosis when the patient is exposed to an acute event. In fact, in these patients, AEN often follows therapeutic interventions, including surgery [72,76] or chemotherapy [64,77]. Nevertheless, malignancy may be associated with AEN in the absence of an identified trigger [74] and, occasionally, the disease may be found in an asymptomatic patient [75].…”

Section: Etiologymentioning

confidence: 99%

“…Surgery is a common trigger for AEN, perhaps related to a cytokine environment that could compromise mucosal regenerative ability and increase susceptibility to esophageal ischemia secondary to blood loss and hypotensive insults following aggressive surgical procedures, including lower limb amputation [61], total hip arthroplasty [81], cholecystectomy [1,35], rectosigmoid resection [21,72], or pulmonary lobectomy [76]. Occasionally, AEN may also follow less invasive procedures, including ocular surgery for vitreous hemorrhage [82].…”

Section: Etiologymentioning

confidence: 99%

“…AEN following lung cancer surgery consisting of pulmonary lobectomy plus paraesophageal lymph node dissection could be due to impaired microcirculation flow. Therefore, it is important not to damage the arterial branches from the descending aorta to the esophagus during paraesophageal lymph node dissection [76].…”

Section: Etiologymentioning

confidence: 99%

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Diagnosis and management of acute esophageal necrosis

Dias

Santos-Antunes

Macedo

2019

aog

113

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Acute esophageal necrosis is a rare syndrome classically characterized by a striking endoscopic image of diffuse and circumferential black mucosal discoloration of distal esophagus, with an abrupt transition at the gastroesophageal junction and variable proximal extension. The typical patient is an older male with general debilitation and multiple comorbidities presenting with hematemesis or melena. The pathophysiology usually involves a combination of esophageal ischemia, backflow injury from gastric chemical contents and impaired mucosal reparative mechanisms associated with debilitated physical states. It may arise in the setting of hemodynamic compromise, diabetic ketoacidosis, hypothermia, alcoholic intoxication, trauma, inflammatory diseases, esophageal local infection, solid organ transplantation, postoperative status, drugs or acute gastric outlet obstruction, usually in the background of a chronic debilitating process, where the concurrent presence of multiple risk factors, including diabetes mellitus, hypertension, malnutrition, malignancy or alcohol abuse, places a patient at higher risk. The characteristic endoscopic appearance establishes the diagnosis. Biopsy is supportive but not required. Management is mainly supportive and consists of correcting coexisting conditions, fluid therapy, bowel rest, intravenous proton pump inhibitor therapy and red blood cell transfusion as needed. Although this is a serious life-threatening condition, appropriate treatment may result in a favorable outcome in the majority of patients.

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Section: Etiologymentioning

confidence: 99%

Section: Etiologymentioning

confidence: 99%

Section: Etiologymentioning

confidence: 99%

Section: Etiologymentioning

confidence: 99%

See 2 more Smart Citations

Diagnosis and management of acute esophageal necrosis

Dias

Santos-Antunes

Macedo

2019

aog

113

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Black esophagus: Acute esophageal necrosis syndrome

Gurvits¹

2010

WJG

266

417

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Acute esophageal necrosis (AEN), commonly referred to as "black esophagus", is a rare clinical entity arising from a combination of ischemic insult seen in hemodynamic compromise and low-flow states, corrosive injury from gastric contents in the setting of esophago-gastroparesis and gastric outlet obstruction, and decreased function of mucosal barrier systems and reparative mechanisms present in malnourished and debilitated physical states. AEN may arise in the setting of multiorgan dysfunction, hypoperfusion, vasculopathy, sepsis, diabetic ketoacidosis, alcohol intoxication, gastric volvulus, traumatic transection of the thoracic aorta, thromboembolic phenomena, and malignancy. Clinical presentation is remarkable for upper gastrointestinal bleeding. Notable symptoms may include epigastric/abdominal pain, vomiting, dysphagia, fever, nausea, and syncope. Associated laboratory findings may reflect anemia and leukocytosis. The hallmark of this syndrome is the development of diffuse circumferential black mucosal discoloration in the distal esophagus that may extend proximally to involve variable length of the organ. Classic "black esophagus" abruptly stops at the gastroesophageal junction. Biopsy is recommended but not required for the diagnosis. Histologically, necrotic debris, absence of viable squamous epithelium, and necrosis of esophageal mucosa, with possible involvement of submucosa and muscularis propria, are present. Classification of the disease spectrum is best described by a staging system. Treatment is directed at correcting coexisting clinical conditions, restoring hemodynamic stability, nil-per-os restriction, supportive red blood cell transfusion, and intravenous acid suppression with proton pump inhibitors. Complications include perforation with mediastinal infection/abscess, esophageal stricture and stenosis, superinfection, and death. A high mortality of 32% seen in the setting of AEN syndrome is usually related to the underlying medical co-morbidities and diseases.

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