Case Of Acute Esophageal Necrosis Research Articles

A Strange Case of Acute Esophageal Necrosis

Gurvits Syndrome or Acute Esophageal Necrosis (AEN) is an uncommon disease de- scribed as a “black esophagus” in Esophagogastroduodenoscopy (EGD).

S2430 A Rare Case of Acute Esophageal Necrosis Precipitated by Klebsiella pneumoniae

S2430 A Rare Case of Acute Esophageal Necrosis Precipitated by Klebsiella pneumoniae

Gurvits syndrome: a case of acute esophageal necrosis associated with diabetic ketoacidosis

BackgroundAcute esophageal necrosis (AEN), commonly referred to as Gurvits syndrome or “black esophagus”, is a rare clinical disease. We present a case of AEN associated with diabetic ketoacidosis (DKA).Case presentationA 66-year-old male came to our hospital with coffee-ground emesis, dyspnea, and general malaise. He was treated for type 2 diabetes mellitus using insulin and had not been taking his medication, including insulin, for several days. Laboratory analysis revealed severe hyperglycemia (730 mg/dL), normocytic anemia (hemoglobin level, 7.7 g/dL; mean corpuscular volume, 100.4 fL), high serum potassium (7.6 mEq/L), and a high level of blood urea (98.7 mg/dL). Ketones and glucose were detected in the urine, and serum β-hydroxybutyrate was elevated (2132 µmol/L). Arterial blood gas analysis confirmed metabolic acidosis (pH, 7.29; HCO3, 10.5 mmol/L). Collectively, the patient was diagnosed with DKA and upper gastrointestinal bleeding. The patient’s condition improved with intravenous fluids, and he received intravenous insulin to treat DKA. According to these findings, the patient was diagnosed with DKA and upper gastrointestinal bleeding. The patient underwent esophagogastroduodenoscopy (EGD) which revealed a circumferential necrosis of the middle and distal esophagus, immediately proximal to the gastroesophageal junction. The patient was then treated with an intravenous proton pump inhibitor. The patient continued to improve with conservative treatment and was subsequently discharged in a stable condition. An EGD repeated 14 days after discharge showed complete healing of the necrotic-like mucosal change without stricture formation of the esophagus.ConclusionsAEN is rare but potentially life-threatening case of upper gastrointestinal bleeding. Therefore, a clinician should be aware of AEN as a potential cause of upper gastrointestinal bleeding in elderly patients with poorly controlled diabetes and significant comorbidities.

S2074 A Case of Acute Esophageal Necrosis in the Setting of a Paraesophageal Hernia

S2074 A Case of Acute Esophageal Necrosis in the Setting of a Paraesophageal Hernia

S3430 A Case of Acute Esophageal Necrosis in a Male Patient With Prostate Cancer

S3430 A Case of Acute Esophageal Necrosis in a Male Patient With Prostate Cancer

S1925 A Case of Acute Esophageal Necrosis (Black Esophagus) Managed With Fully Covered Self-Expandable Stent

INTRODUCTION: Acute esophageal necrosis (AEN) is a rare but serious endoscopic finding characterized by diffuse inflammation and black appearance of the esophageal mucosa. It mainly affects the distal esophagus and discontinues at the gastroesophageal junction (GEJ). We report a case of AEN presenting in the setting of extensive inferior vena cava thrombosis and alcohol intoxication. CASE DESCRIPTION/METHODS: 58-year-old male with history of alcohol abuse presented with 4 days of constant, severe, epigastric pain. The patient was sedentary for approximately four months following a fall from second floor. CT scan revealed inferior vena cava thrombosis at the level of the renal veins extending to the left iliac vein. Anticoagulation with IV heparin was initiated; however, it was discontinued when the patient developed hematemesis. Emergent upper endoscopy demonstrated diffuse necrosis and black discoloration in the entire lower and middle third of the esophagus to the GEJ. Additionally, actively oozing mucosa was found in the middle esophagus. The decision was made to immediately place a fully covered self-expandable esophageal stent to tamponade the bleeding and prevent complications. The patient was then transferred to interventional radiology. On left gastric arteriogram, he was found to have faint arterial extravasation in the distal esophageal area. This was successfully embolized. The patient stabilized and was later discharged on oral anticoagulation and acid suppression therapy. Repeat endoscopy three months later for stent removal showed complete healing of the esophagus with normal appearing mucosa. DISCUSSION: While the exact etiology of AEN is unknown, it is suspected to be multifactorial. It carries poor prognosis thus initial management includes aggressive resuscitation, correction of underlying medical conditions, and aggressive acid suppression and monitoring for signs of infection or perforation. We present a case managed with fully covered self-expandable stent at the time of diagnosis which prevented complications, allowed early feeding and ultimately complete healing.Figure 1.: Acute Necrotizing Esophagitis (Black Esophagus).Figure 2.: Fully Covered Self-Expandable Esophageal Stent Placed In The Distal Esophagus.Figure 3.: Healed Esophagus On Three Month Follow-Up.

1801 A Rare Case of Acute Esophageal Necrosis

INTRODUCTION: AEN is a rare disease with an incidence ranging from 0.01% to 0.28% of all upper GI endoscopies. AEN occurs in the setting of underlying critical illnesses. Upon review of the English literature, only 14 cases of AEN associated with DKA have been published over the past 50 years. CASE DESCRIPTION/METHODS: A 61 yo M with a PMH: HTN, HTN, GERD, ETOH abuse, and obesity presented to the hospital with severe SOB, worsening mid-back pain, and a 1.5 wk hx of GERD symptoms. T 97.8 F, BP 183/85, HR 141, RR 31/min. BG of 833 mg/dL, arterial blood gas (ABG) pH of 7.164, pCO2 of 11.1 mmHg, HCO3 of 4 mEq/L, and PO2 of 128 mmHg with an anion gap of 25, serum Beta-Hydroxybutyrate of 4.9 mmol/L, 2+ urine ketones. (WBC) of 30.2 K/uL, Hb 13.5 K+ 5.8, Cr: 2.7. Admitted for DKA on day 2 of his hospital stay he developed N/V and hematemesis. He denied melena. On day 3 he had hematemesis and complained of feeling that food was getting stuck in his mid-chest upon swallowing. On day 4 his Hb dropped from 12.8 to 10.7 g/dL and he began to complain of chest pain and discomfort. (EGD) showed severe necrotizing esophagitis along entire length of esophagus with normal stomach and duodenum. Patient was started on oral (PPI) therapy and oral sucralfate therapy. DKA resolved, anion gap closed, AKI resolved, WBC normalized, and he was weaned off the insulin infusion. He was discharged on hospital day 8 with 6 weeks of oral PPI and sucralfate therapy. DISCUSSION: The pathogenesis is hypothesized to be due to the distal portion of the esophagus being a watershed area due to lower levels of vascularization compared to the upper and middle portions. In one case series, 4 out of 16 cases (25%) of AEN occurred in the setting of diabetic ketoacidosis (DKA), and 14% of cases of DKA involved AEN. AEN is more likely to occur in men than women with a 4:1 ratio, and the ages of presentation ranged from 19-91 with a mean of 68 years. It is diagnosed by upper endoscopy which shows circumferential black necrosis in the distal third of the esophagus that may extend along the length of the esophagus into the upper third but will not extend into the gastric mucosa. Mortality is as high as 32% and the mortality specific to AEN is closer to 6%. Complications can include esophageal perforation, mediastinitis, and abscess formation in up to 6%. Late complications include esophageal strictures and stenoses which are seen in 10.2% of cases and appear as early as 7-12 days. AEN is typically managed with high dose PPI and sucralfate.

1743 From Red to Black: A Deadly Case of Acute Esophageal Necrosis

INTRODUCTION: Black Esophagus, or acute esophageal necrosis (AEN), is a rare but deadly clinical syndrome appearing as diffuse circumferential black necrotic mucosa on esophagogastroduodenoscopy (EGD). It is associated with comorbidities that cause hypoperfusion and ischemia to the esophageal mucosa. It has a reported incidence rate of about 0.001% to 0.2%. We report a case of black esophagus in a patient with fulminant hepatic failure related to nonalcoholic steatohepatitis (NASH) cirrhosis. CASE DESCRIPTION/METHODS: A 75-year-old female with a history of diabetes mellitus, hypertension, gastroesophageal reflux disease, NASH-related cirrhosis, and GI bleeding due to esophageal varices presented to the hospital with altered mental status and increased lethargy of 2 weeks’ duration. Her initial lab workup revealed a calculated MELD score of 36. She was diagnosed with an NSTEMI and hepatic encephalopathy in the setting of fulminant hepatic failure. During her hospital stay, she developed coffee ground emesis and melena with resultant drop in hemoglobin requiring transfusion with multiple units of blood. An EGD performed in order to find the source of her apparent upper GI bleeding revealed diffuse circumferential black discoloration of the mucosa at the middle and inferior third of the esophagus demarcated clearly from the normal-appearing mucosa of the cardia at the gastroesophageal junction (Figure 1). Unfortunately, she developed hepatorenal syndrome due to worsening liver function. Due to the poor prognosis, the patient’s family chose to request “do not resuscitate” (DNR) status. Severe hypoxia failing noninvasive positive-pressure ventilation ultimately led to cardiac arrest and death. DISCUSSION: This case emphasizes the need to include black esophagus on the differential of upper GI bleeding in a patient with a history of esophageal varices and NASH cirrhosis and highlights the high mortality rate, estimated at about 32%, associated with this condition. Documented cases exist of black esophagus in patients with alcohol-related cirrhosis, but we found no others reporting this condition in a patient with NASH-related cirrhosis. There is no direct treatment for black esophagus; recommendations are to treat comorbidities, suppress acid production, and optimize vascular perfusion. Complications include stricture, infection, perforation and death. This case clearly demonstrates that early detection through endoscopy and active management of its underlying cause is critical to improving patient outcomes.

Clinical presentations, management, and outcomes of acute esophageal necrosis: a systemic review

ABSTRACTBackground: To review all the reported literature on acute esophageal necrosis.Research methods: Databases were searched using the special Medical Subject Heading (MeSH) terms. All the available reported cases of acute esophageal necrosis were analyzed.Results: A total of 154 cases were identified and 130 cases were analyzed. The mean age of presentation was 61 years, and 70% of cases were males. The most common presenting symptoms were hematemesis in 66%, shock in 36%, melena in 33%, abdominal or substernal pain in 28%. The most common comorbidities reported were diabetes in 38%, hypertension in 37%, alcohol abuse in 25%, and chronic kidney disease in 16%. On upper endoscopy, 51% had a distal disease, 36% had pan esophageal, and only 2% had a proximal disease. 84% of patients were treated with IV Proton Pump Inhibitors, 22% received transfusions, 23% got antibiotics for underlying sepsis, 14% also received sucralfate, and 4% required surgery for treatment. The mortality rate was 32%, while perforation was reported in 5% and stricture formation reported in 9% of patients.Conclusions: Patients with acute esophageal necrosis can have a favorable outcome if treated appropriately.

Acute (gangrenous) esophageal necrosis (black esophagus). A rare form of injury with specific histologic features and diverse clinical associations with a common pathogenesis

Acute esophageal necrosis (AEN) also known as black esophagus is a rare form of injury to the esophageal mucosa that complicates a variety of clinical conditions. It is characterized by circumferential black discoloration of the mucosa. There is little information relating to the histopathologic features and pathogenesis of this condition. In this study we describe the histopathologic features of six cases of AEN (3 autopsy and 3 biopsy cases) and compared the finding to 26 cases of ulcerated esophagitis. Cases and controls were assessed for type of necrosis, inflammatory cells, vascular thrombi, pigment deposits, granulation tissue and presence of viable mucosa. Cases were evaluated with histochemical stains for iron and microorganisms and immunohistochemical stains to inflammatory cells (myeloperoxidase, CD20, CD3 and CD163), squamous cells (pancytokeratin and p40) and muscle (smooth muscle actin). Most patients were males (60%) with an average age of 58 years. All specimens show the characteristic black discoloration of the mucosa. Microscopic examination revealed a distinct band of basophilic necrosis, Prussian blue-negative pigment deposits and fibrin thrombi in vessels. Myeloperoxidase-positive neutrophils were seen beneath the area of necrosis and CD163-positive macrophages throughout the esophagus. Basophilic necrosis was never seen in control cases. Only one control case showed intravascular thrombi and pigment deposits. We conclude that the combination of basophilic necrosis, intravascular thrombi and pigment deposits are diagnostic of AEN. We theorize that microvascular occlusion is the unifying lesion that explains the diversity of conditions associated with this disorder.

A Case of Acute Esophageal Necrosis in a Patient With Multiple Sclerosis

Introduction: Acute esophageal necrosis (AEN) is a rare syndrome with incidence of .01 to .28% on endoscopic series and mortality of 32%. Known as “Black Esophagus,” it's characterized endoscopically by circumferential black mucosa ending abruptly at the gastroesophageal junction. It has been postulated that precipitating events include hypoperfused states and gastric outlet obstruction with concurrent esophageal reflux. Case: A 77-year-old Caucasian female with remote history of peptic ulcer disease and progressive multiple sclerosis (MS) presented with diffuse abdominal pain, nausea, and vomiting. Urinalysis was suggestive of a urinary tract infection (UTI) and she was discharged on five-days of cephalexin. She delayed taking cephalexin and returned four days later with fatigue, worsening dysphagia, and melena. She was hypotensive and labs revealed leukocytosis, acute blood loss anemia, and acute kidney injury. Urine culture grew extended-spectrum beta lactamase producing multi-drug resistant proteus mirabilis. She was admitted for septic and hypovolemic shock secondary to multi-drug resistant UTI and suspected upper gastrointestinal bleeding. Ertapenem was started in light of the resistance and sensitivity pattern of the causative organism. Upper endoscopy revealed diffuse mucosal changes characterized by black discoloration throughout the esophagus and obstructive duodenal ulcer with adherent clot (Figure 1). Endoscopic findings and presentation was consistent with AEN. She improved with vasopressor support, fluid resuscitation, and 14-days of ertapenem. Discussion: AEN is a multifactorial syndrome with notable morbidity. Risk factors include alcohol abuse, hypertension, male gender, diabetes, dyslipidemia, malnourishment, and chronic kidney disease. The most common presentation is upper GI hemorrhage but dysphagia, chest and epigastric pain can also occur. Diagnosis is made endoscopically and histologic confirmation of tissue necrosis is recommended but not required. Treatment involves management of inciting insult(s), acid suppression with intravenous proton pump inhibitor therapy and “nil per os.” A video swallow study revealed mild oral and moderate pharyngeal dysphagia that was attributed to MS. Dysphagia and regurgitation of stomach contents from gastric outlet obstruction predisposed patient to hypovolemia. Septic shock and an obstructive duodenal ulcer with blood loss anemia culminated to promote the development of AEN.1793 Figure 1. Black discoloration of mucosa in the upper third of the esophagus (A), and the middle third of the esophagus (B), normal mucosa at the gastroesophageal junction as seen in retroflexion (C), and duodenal bulb ulcer (D).

A Rare Case of Acute Esophageal Necrosis

A Rare Case of Acute Esophageal Necrosis

An Eye on Necrosis

We present a case of acute esophageal necrosis (black esophagus) caused by iron pill esophagitis in a patient thirteen days status post combined heart and bilateral lung transplant who was supplemented with oral iron for anemia due to intraoperative blood loss. This case illustrates an unusual cause of acute esophageal necrosis and should be on the differential for patients with unexplained findings of esophageal necrosis who are also on iron supplementation. Case A 52 year old man with chronic right ventricular failure due to class I pulmonary hypertension and unrepaired total anomalous pulmonary venous return with Eisenmenger physiology underwent combined heart and bilateral lung transplantation. He received standard infectious prophylaxis, and started oral ferrous sulfate for anemia after passing a swallow evaluation. On postoperative day (POD) 11, he developed dysphagia and odynophagia. Esophagogastroduodenoscopy (EGD) performed on POD 13 showed circumferential necrosis of the esophagus with tongues of esophagitis proximally (Figure 1), and a stricture with luminal diameter of 6mm. Biopsies revealed necrotic tissue and brown pigment/crystalline material consistent with iron pill-induced esophageal necrosis (supported by positive iron stain) (Figure 2). Ischemia and infection were ruled out. Four months after discharge, EGD showed a 3 cm long fibrotic stricture 25 cm from the incisors 6 mm in diameter. There was mild erythema adjacent to the stricture with otherwise normal esophageal mucosa. Biopsies demonstrated normal squamous mucosa. He will undergo temporary esophageal stenting to treat the stricture. Discussion Ferrous sulfate was first reported to cause ulcerations of the hypopharynx and cervical esophagus in 1976. Severe gastrointestinal necrosis has been seen with iron overdose, however, not with therapeutic doses. In one series of 33 patients with iron pill induced upper gastrointestinal injury, 83% of biopsies contained ulcerative or erosive mucosal injury, but none contained necrosis. Acute esophageal necrosis remains a rare entity with well characterized clinical manifestations but poorly understood pathophysiology. It is suspected to result from ischemia and decreased mucosal defenses. Currently there are no reported cases of iron pill induced acute esophageal necrosis in the literature. This was a surprising finding and should be considered in patient with severe esophagitis or acute esophageal necrosis taking oral iron supplements.1770_A Figure 1 No Caption available.1770_B Figure 2 No Caption available.

Acute Esophageal Necrosis: A Case Report

Acute esophageal necrosis, also known as black esophagus and necrotizing esophagitis, is a rare esophageal disease, characterized by diffuse inflammation and black appearance of the esophageal mucosa. It mainly affects the distal esophagus and discontinue at the gastroesophageal junction. Etiology is thought to be due to ischemia in the presence of acid reflux into the esophagus. The usual clinical presentation is hematemesis and melena. The mainstay of treatment is fluid resuscitation and proton pump inhibitors. Mortality rate is 13 to 35 %, mainly due to underlaying cause. We describe a case of Acute esophageal necrosis in a 60-year-old male. A 60-year-old male with a significant history of hypertension, coronary artery disease, diverticulosis, gastro esophageal reflux disease, indeterminate colitis. Two weeks prior to presentation he has severe watery diarrhea with no bleeding or melena. patient also has vomiting and had two episodes of presyncope. at the EC, he developed hematemesis, he was then admitted to ICU and given IV fluids, 2 units of PRBC, and IV proton punp inhibtors. Blood culture were negarive so septecmia was unlikely cause of his low blood pressure.Esophagogastroduodenoscopy Showed diffusely congested, black esophageal mucosa (image 1, 2) in the middle and lower thirds of the esophagus. These ulcerations stop at gastro esophageal junction. Biopsy was contraindicated because of the severe esophagitis. Gastrografin esophagogram showed no perforation. Patient was kept NPO and had parentral nutirion for 5 days, he was able to have liquid diet at the 6th day of his stay. A repeat endoscopy 12 days later showed almost complete healing of the esophagus with reflux esophagitis (image 3). subsequently patient clinical condition has improved and was discharged home after 18 days of hospital stay. The black esophagus is one of the rare esophageal diseases. In this case the probable cause was hypovolemic shock from severe diarrhea, and hemorrhage in the presecne of reflux disease. The underlying vascular diseases also put the patient at higher risk to develop necrotizing esophagitis. This patient was treated with early resuscitative management which resulted in significant improvement in endoscopic findings and the overall survival. The key factors which contributed to survival are early detection and aggressive management in the resuscitation as the cause of ischemia needs to be corrected in order to increase perfusion to the esophageal mucosa.1828_A Figure 1. Image showing gangrenous esophageal mucosa, the likely cause of patient's bleeding1828_B Figure 2. esophageal necrosis.1828_C Figure 3. Esophageal healing 12 days later.

A Rare Case of Acute Esophageal Necrosis Due to Gastric Outlet Obstruction From a Malignant Duodenal Ulcer

A Rare Case of Acute Esophageal Necrosis Due to Gastric Outlet Obstruction From a Malignant Duodenal Ulcer

Acute esophageal necrosis: A new case

Acute esophageal necrosis is an uncommon clinical entity. It is diagnosed with upper gastrointestinal endoscopy with the presence of strikingly black necrotic esophagus. Very often no definite etiology is identified, even though a large list of potential associations has been postulated. His treatment is primarily medical. A high mortality is usually related to the underlying medical co-morbidities and diseases. We report a case of acute esophageal necrosis occurring in a patient undergoing Fournier’s gangrene intervention.

A Rare Case of Acute Esophageal Necrosis in a Patient with Alcoholic Cirrhosis

A 55-year-old man with alcoholic cirrhosis presents after being found unresponsive at home. On route to the hospital, he had multiple episodes of coffee ground emesis. On admission, he was hemodynamically unstable and remained unresponsive. He was intubated, given packed red blood cells, started on nexium, octreotide and norepinephrine drips, and admitted to the MICU. An upper endoscopy revealed diffuse necrotic appearing esophagus, with confluent dark black areas and intermittent pale mucosal patches throughout the entire esophagus, but sparing the gastroesophageal (GE) junction. Hematin with diffuse moderate inflammation was seen in the gastric fundus and duodenum. Esophageal biopsies showed extensive necrotic debris with inflammation and black pigment deposition along the surface, consistent with acute esophageal necrosis (AEN). CT abdomen/pelvis showed a new pancreatic body mass with diffuse lymphadenopathy and nodules in lung, liver and adrenals. Superclavicular lymph node biopsy was consistent with pancreatic adenocarcinoma. Following biopsy, he remained encephalopathic and in persistent hemorrhagic and cardiogenic shock. He was transitioned to comfort care and expired from multi-system organ failure. Acute esophageal necrosis, or “black esophagus,” is a rare disorder, with a prevalence of approximately 0.2 percent.1 The condition is described as diffuse, circumferential black mucosal discoloration predominantly affecting the distal third of the esophagus and sparing the GE junction. The etiology is multifactorial and includes ischemic injury, corrosive injury from gastric contents in the setting of impaired motility, and impaired mucosal barrier systems.2 The most common risk factors include underlying malignancy and alcoholic cirrhosis. 70% of cases present with hematemesis and melena. Esophageal biopsies, however, are necessary to differentiate AEN from other etiologies.2 Management is largely supportive, aimed at correcting coexisting clinical conditions, as well as bowel rest and intravenous acid suppression with proton pump inhibitors. Complications include strictures, superinfections and perforation. While AEN does have a high mortality rate of 32%, it is largely due to the underlying clinical disease.2 Overall, acute esophageal necrosis is a rare condition, which should be viewed as a poor prognostic factor.Figure 1

A Case of Acute Esophageal Necrosis (AEN) in a Hypothermic Patient: The Grave Prognosis of the Black Esophagus

Introduction: Acute Esophageal Necrosis (AEN) is a syndrome characterized by diffuse, necrotic, circumferentially black distal esophageal mucosa on esophagogastroduodenoscopy (EGD) that ends at the gastroesophageal junction (GEJ).The exact etiology is unknown, with hypoperfusion predisposing the less vascularized distal esophagus to acute necrosis plays a rule. 70% of AEN cases present with upper gastrointestinal bleeding (UGIB) and melena. We describe a case of AEN caused by severe hypothermia in an alcoholic patient presenting with UGIB. Case Report: 62 year-old lady with history of liver cirrhosis secondary to heavy alcohol intake presented with change in mental status and hematemesis. Vital signs were consistent with temporal temperature of 29.9 C, heart rate of 61 bpm, and blood pressure of 86/49. Bedside pulse oximetry recorded 84% on room air. She was confused, icteric with distended abdomen, and bilateral lower extremity pitting edema. She was admitted to the intensive care unit after intubation. Hemogram showed a hemoglobin of 5.1 g/dL, platelet count of 62, INR 7.2, total bilirubin 8.9, AST/ ALT 154/59, albumin 2.1. Model for End stage Liver Disease (MELD) score at presentation was 33. Patient was resuscitated with warm crystalloid fluids and 2 units of packed RBCs, and started on Octreotide and Pantoprazole drip. EGD showed normal looking proximal third of the esophagus, with diffuse mucosal ulceration of the middle and lower third of the esophagus (figures 1, 2) without varices, and sharp demarcation of affected areas noted in the GEJ (figure 3). Patient's clinical condition deteriorated over the next 24 hours and she deceased despite aggressive supportive therapy with vasopressors, packed RBC, platelets, and fresh frozen plasma transfusion.Figure 1Figure 2Figure 3Discussion: AEN is a rare syndrome with significant morbidity and mortality. It is found in patients undergoing upper endoscopy for evaluation of UGIB. EGD shows diffuse, circumferential, black pigmentation of the distal esophagus, ending sharply at the Z-line of the GEJ. Medical management is supportive with aggressive hemodynamic support, intravenous proton pump inhibitors, and treatment of underlying illness. Mortality rates in patients with AEN reported to range from 13 to 35%. Over 90% of death cases were secondary to their underlying serious illness. In our case, the patient's clinical condition continued to deteriorate due to multi-organ failure despite aggressive medical intervention.

Black Esophagus: A Case of Acute Esophageal Necrosis Following Orthopedic Injury

Black Esophagus: A Case of Acute Esophageal Necrosis Following Orthopedic Injury

Necrose esofágica aguda secundária a endoprótese: relato de caso de primeiro sobrevivente

<p>A necrose esofágica aguda é uma das mais graves complicações associadas ao tratamento endovascular da aorta descendente com colocação de endoprótese. Sua ocorrência é rara, com apenas 3 casos descritos na literatura, entretanto em todos a complicação mostrou-se fatal. O presente trabalho descreve, até onde se sabe, o primeiro caso de necrose esofágica aguda secundária a endoprótese de aorta na qual o paciente sobrevive. Paciente masculino de 53 anos com dissecção de aorta, de artéria subclávia esquerda até bifurcação de artérias ilíacas, realizou tratamento endovascular de colocação de endoprótese. Evoluiu com lesão isquêmica de esôfago médio e distal, para a qual foi indicada esofagectomia total. Após um ano e dois meses, foi submetido a esofagogastroplastia para reconstrução do trato gastrointestinal, com transposição de tubo gástrico retroesternal, a partir da qual permanece praticamente oligossintomático. O presente trabalho consiste no primeiro relato de caso na qual o paciente sobreviveu à necrose esofágica aguda secundária à colocação de endoprótese de aorta torácica.</p>