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Acute necrotizing esophagitis. Case Report.

Pierini Angel, Imhof Hugo*, Burlando Eduardo, Gianinetti Leonardo, Pierini Leandro.
Endoscopy Service. Nefrology, Urology and Cardiovascular Diseases Clinic. Santa Fe –
Argentina.

Introduction
Acute necrotizing esophagitis, also known as Black Esophagus (BE), represents a highly
infrequent clinical entity, defined by the balck pigmentation of the esophagus, secondary to
necrosis of the mucosa, detectable at endoscopic procedure(2-3-6-9).
It was first described by Goldenberg et al

(1-3-4)

in 1990. Its incidence is 0.01 to 0.2 %. It

generally occurs in male adults, with co-morbidities (2-3-7).
Although its pathogenesis is unknown, it is believed to have a multi-factorial origin
associated to systemic hypo-perfusion, obstruction of the gastric outflow tract, malnutrition
and infectious processes (1-7).
The prognosis is regarded as unfavourable, with a mortality rate ranging from 30 to 50%,
generally related to these patients’ co-morbidities (2-3).
The aim of this study is to present a clinical case, outlining its manifestation, diagnosis,
treatment and a review of the literature.
* Reference Author: Imhof Hugo - email: hugoimhof@hotmail.com Address: Av. Freyre 3074, 3 Piso, Santa Fe (CP: 3000) – Phone.: 0342-4535741.
Key words: Endoscopy, Acute necrotizing esophagitis, Black esophagus.

referred to our centre. . and laboratory studies are conducted. This alteration extends to the cardia. The patient is transferred to Intermediate Care Unit. and slipped??? hiatal hernia. receiving chemotherapy. 24-hour evolution clinical manifestation. manifesting hematemesis. Conservative medical treatment begins: broad spectrum intravenous antibiotics (ampicillin – sulbactam). respecting (not affecting??) the gastric mucosa which is unaltered (Figure 2). The patient presents a pathological history that includes Stage IV Renal Cell Carcinoma. treated with fluconazole (100 mg/day). which shows a diffused thickening of the esophageal wall on the distal third. with sloughing and isolated bleeding (Foco de sangrado en napa?? ) . intravenous proton pump inhibitors (omeprazole 40 mg/24 hs). 3 months prior to her referral.Biopsies are taken for anatomopathological study. extending continuously and symmetrically. Besides. rational. Endoscopic diagnosis is carried out: Acute Necrotizing Esophagitis.3 mg. From them. Video-gastroscopy is carried out. Leukocytes: 14000 and Albumin: 2. During physical examination the patient was hemodynamically stable.CASE 70-year-old female patient. Stage III Esophageal Candidiasis had been diagnosed through endoscopy (Figure 1). in regular general conditions. Hemoglobin: 9. diagnosed with high tract digestive hemorrhage. sucralfate (10 ml/ 12hs) and calorie-free diet / absolute fasting?? Thorax CT is done. due to oncological illness. Blackish mucosa is observed in lower esophageal third. There are no signs of mediastinal involvement?? (Figure 3). the following relevant data emerges: Hematocrit: 30.

confirming the diagnosis. with ischemic injury of the esophageal mucosa. and it is found that only 88 cases were described (2-3-7). its incidence being 0. oral feeding begins. Gurvits et al reviewed world literature in the year 2007. this would be amplified in cases of low cardiac output. Its association with candidiasis. Its pathogenesis is unknown and it is believed to have a multi-factorial origin. Seven days after admission. without new hematemesis episodes. It is an infrequent pathology. extending in a circumferential and symmetric pattern. vascular disease. with associated illnesses such as: cancer. pyloric syndrome and hypersensitivity reactions to drugs (Steven-Johnson syndrome) has also been described (1-2-6). It generally involves (Comprometiendo??) the lower third up to the cardia. alcoholism and cirrhosis. the pathology appears in male adults. It is defined by the black coloring of the esophagic mucosa. diabetes. 72 hs later. infections and malnutrition (2-3-5). . associated to systemic hypo-perfusion.2% of the gastroscopies done. shock. Besides. showing a good clinical evolution. kidney failure. Anatomical Pathology informs: esophageal mucosal necrosis. vomiting.The patient progressed well. diabetic ketoacidosis. Discussion Acute Necrotizing Esophagitis or Black Esophagus (BE) was first described in 1990 by Goldenberg et al (4) . In 90% of the cases. hypothermia. hospital discharge is ordered. with good subsequent tolerance. obstruction of the gastric outflow tract or gastroparesis with a prolonged gastroesophageal reflux that could injure the mucosa by exceeding protection mechanisms or clearance. herpetic esophagitis.01 – 0. where it abruptly changes to normal gastric mucosa (2-3-6-9).

the cause of death might be related to the morbidities of these patients (1-2- 5) . melanoma. where the above mentioned features can be validated. dye poisoning. infection and sepsis (2-5).. Although biopsies are recommended. restriction of oral intake. which should be considered in adults with co-morbidities and a . even reaching the muscular …. mortality ranging from 30 to 50 %. it could be said that Acute Necrotizing Esophagitis or BE is a highly infrequent pathology. In cases which are unresponsive to medical treatment. optimizing perfusion. In certain cases. with non-viable squamous epithelium and submucosal compromise. exposure to coal dust. a que refiere con la muscular propia? (1-2-7-9) . they are not exclusive for diagnosis. with hematemesis or melena. vomiting. Of these. necrosis of the mucosa is observed. To conclude. Treatment should be aimed at stabilizing the patient hemodynamically. esophagus intramural hematoma. Acute necrotizing esophagitis’ prognosis is poor. reflux treatment and intravenous broad spectrum antibiotics. injury for caustic chemicals ???. the inhibition of acid secretion. Histologically. surgical treatment is mandatory. the administration of paraenteral nutrition is necessary (2-3-5). Acute necrotizing esophagitis is diagnosed through endoscopy. Complications occur in 25% of patients. which may require reiterated endoscopic dilation. Acantosis nigricans. followed by esophageal perforation in a 7%. necrosis induced by broad spectrum antibiotics and the Steven-Johnson syndrome. Besides patients may present abdominal pain. In the majority of cases. the most frequent is esophageal stricture in a 15%.80 % of cases manifest themselves clinically as Upper Gastrointestinal bleeding. It should be differentiated from other entities such as: melanosis. fever or dysphagia (2-6). Mortality associated to complications of this pathology represent 6%. or esophageal perforation takes place.

and surgical in cases of poor responsiveness to it or when complications arise. Treatment should be conservative at the beginning. . with mucosal edema. FIGURE 1: Video gastroscopy: Linear and conclusive?? white patches. It is diagnosed through endoscopy. compatible with Stage III Esophageal Candidiasis.clinical picture of upper gastrointestinal bleeding.

. extending continuously and symmetrically.FIGURE 2: Video gastrocopy: Blackish mucosa. with sloughing and isolated bleeding (en napa??).

FIGURE 3: Thorax CT: Diffused thickening of the esophageal wall on the distal third. There are no signs of mediastinal involvement?? .

Hochain P. Lau N. Siroký M. Acute esophageal necrosis (Black esophagus): endoscopic and histopathologic appearance. Wain SL. Antonietti M. Finn B. 36: 1133. Lemoine F. Young P. Acute esophageal necrosis: 1-year prospective study. 2008.2002. Marignani P. Reporte de un caso clínico. Yong H. Spacek J. Gualtieri N. Esp. Si Young C. Chueco A. 98: 493-6 5.BIBLIOGRAPHY: 1. Bures J. “Black esophagus” a rare complication of shock. Acute esophageal necrosis: a rare syndrome. Douda T. Reinus C. Ramos J. Gurvits GE. Gastrointest Endosc. Acute esophageal necrosis: a retrospective case series. Duarte C. Wallberg M. 6. Gastroenterology 1990. Villarejo F. 3. Kopácová M. Repák R. World J Gastroenterol 2007.14:5662-5663. Mascarenhas P. 4. Black esophagus with concomitant candidiasis developed after diabetic ketoacidosis. 8. 16: 3219-3225. 100: 583-585. 9. 91: 2432-4. Rev. Nozicka J. Rev. Goldenberg SP. Rejchrt S. Zimmerman J. Haviv YS. World J Gastroenterol 2010. Esófago negro secundario a esofagitis necrotizante aguda. Casteleiro C. Savoye G. . 137: 672-674. 7. J Gastroenterol. 56(2):2137. 2. 2007. 42(1):29-38. Endoscopy 2004. Ducrotté P. Méd. Enfermedades Dig. Ben Soussan E. Thomé M. Chile 2009. Shapsis A. Grigoriy EG. Acute necrotizing esophagitis. Robilotti JG. Black esophagus: Acute esophageal necrosis syndrome. Hervé S. Vicente C. Am J Gastroenterol 1996.