AT THE FOCAL POINT Lawrence J. Brandt, MD, Associate Editor for Focal Points
A case of acute necrotizing esophagitis
A
D
B
C
E
A 74-year-old man presented to the emergency department with hematemesis and epigastric pain. His medical history included cerebral infarctions, parkinsonism, dysphagia, and osteoporosis. Medications on admission included aspirin and alendronate. Vital signs were normal except for a low-grade fever. EGD revealed black pigmentation that involved the entire esophagus. In the upper esophagus, the blackness appeared as many small spots, each surrounded by white erosive mucosa (A). In the mid-esophagus, there were many wide and longitudinal black areas (B). The lower esophagus was entirely black (C). Multiple ulcers were seen in the duodenum, but the gastric mucosa appeared normal. Biopsy specimens from the esophagus showed necrosis (D). We diagnosed acute necrotizing esophagitis, possibly associated with
www.giejournal.org
F
aspirin and alendronate, both of which have esophageal toxicity. He was treated with total parenteral nutrition, omeprazole, and cefmetazole. Endoscopy and gastrografin esophagram 2 weeks after admission revealed healing esophagitis with multiple scars and a 9-cm stricture in the lower esophagus (E, F). Balloon dilation was performed weekly for 2 months with no improvement in the stricture, and the patient underwent percutaneous endoscopic gastrostomy.
DISCLOSURE All authors disclosed no financial relationships relevant to this publication.
Volume
-,
No.
-
: 2014 GASTROINTESTINAL ENDOSCOPY 1
At the Focal Point
Yoshito Kimura, MD, Hiroshi Seno, MD, PhD, Department of Gastroenterology and Hepatology, Kyoto University Graduate School of Medicine, Kyoto, Japan, Yukimasa Yamashita, MD, PhD, Department of Gastroenterology
and Hepatology, Kobe City Medical Center West Hospital, Kobe, Japan http://dx.doi.org/10.1016/j.gie.2014.03.041
Commentary First described in 1990 by Goldenberg, acute esophageal necrosis (AEN), commonly referred to as “black esophagus,” is a rare clinical entity. The typical patient is a debilitated man in his 60s, perhaps with alcohol intoxication, and often with a history of diabetes, hypertension, and vascular disease, in whom malignancy or multiorgan failure, hypotension, or sepsis has developed. The most common GI presentation is upper GI bleeding with or without abdominal pain, vomiting, dysphagia, and nausea. AEN is typified by a diffuse circumferential black mucosal discoloration in the distal esophagus that may extend proximally to a variable length. Tissue damage in AEN is likely multifactorial, resulting from a combination of tissue hypoperfusion, impaired local defense barriers, and reflux of gastric contents. Back diffusion of hydrogen ions also may downregulate any augmentation in arterial supply needed for reparative processes. The striking predilection of AEN for the distal esophagus may have its basis in the lesser degree of vascularization of this area, relative to more proximal regions of the esophagus. The distal esophagus receives its blood supply from the left gastric artery or left inferior phrenic artery, but variations are common and small branches off the celiac, splenic, short gastric, or left hepatic arteries may provide alternative paths. The mid-esophageal blood supply is derived from the bronchial arteries, the right third or fourth intercostal arteries, and numerous small esophageal arteries off the descending aorta. The upper esophagus is mainly supplied from the descending branches of the inferior thyroid arteries, with additional contributions from the subclavian, common carotid, and superior thyroid arteries. Histologically, mucosal necrosis is found, although deeper esophageal tissue layers may be involved. In a staging system proposed by Gurvits et al, stage 0 designates a prenecrotic viable esophagus. Stage 1 refers to a diffuse, circumferential, black-appearing esophageal mucosa with occasional yellow exudates and signs of friability; findings begin at the gastroesophageal junction and extend proximally to various lengths. Stage 2 describes the healing phase, which is dominated by residual black areas with thick white exudates composed of necrotic debris that cover friable pink mucosa; the findings in this case are redolent of the “chess-board” appearance that characterizes this stage. In stage 3, the esophageal mucosa regains its normal appearance. Treatment is directed at correcting coexisting clinical conditions, restoring hemodynamic stability, and intravenous acid suppression with proton pump inhibitors. Adverse events include esophageal perforation with mediastinal infection/abscess, stricture formation, superinfection (bacteria, virus, and fungus), and death. Mortality is usually related to underlying comorbid disease, and although overall prognosis is poor, mortality specific to the AEN is less than 10%. In Principles of Philosophy, Descartes wrote, “When we say we perceive colors in objects, it is really just the same as saying that we perceived in objects something as to whose nature we are ignorant but which produces in us a very clear and vivid sensation, what we call the sensation of color.” When we look at a black esophagus, we may be ignorant of its naturedit may be a melanoma or AENdbut we do know it isn’t something of which to be desirous. Fortunately, this badness usually doesn’t dictate the clinical course; it just complicates it. Lawrence J. Brandt, MD Associate Editor for Focal Points
2 GASTROINTESTINAL ENDOSCOPY Volume
-,
No.
-
: 2014
www.giejournal.org
A case of acute necrotizing esophagitis
A
D
B
C
E
A 74-year-old man presented to the emergency department with hematemesis and epigastric pain. His medical history included cerebral infarctions, parkinsonism, dysphagia, and osteoporosis. Medications on admission included aspirin and alendronate. Vital signs were normal except for a low-grade fever. EGD revealed black pigmentation that involved the entire esophagus. In the upper esophagus, the blackness appeared as many small spots, each surrounded by white erosive mucosa (A). In the mid-esophagus, there were many wide and longitudinal black areas (B). The lower esophagus was entirely black (C). Multiple ulcers were seen in the duodenum, but the gastric mucosa appeared normal. Biopsy specimens from the esophagus showed necrosis (D). We diagnosed acute necrotizing esophagitis, possibly associated with
www.giejournal.org
F
aspirin and alendronate, both of which have esophageal toxicity. He was treated with total parenteral nutrition, omeprazole, and cefmetazole. Endoscopy and gastrografin esophagram 2 weeks after admission revealed healing esophagitis with multiple scars and a 9-cm stricture in the lower esophagus (E, F). Balloon dilation was performed weekly for 2 months with no improvement in the stricture, and the patient underwent percutaneous endoscopic gastrostomy.
DISCLOSURE All authors disclosed no financial relationships relevant to this publication.
Volume
-,
No.
-
: 2014 GASTROINTESTINAL ENDOSCOPY 1
At the Focal Point
Yoshito Kimura, MD, Hiroshi Seno, MD, PhD, Department of Gastroenterology and Hepatology, Kyoto University Graduate School of Medicine, Kyoto, Japan, Yukimasa Yamashita, MD, PhD, Department of Gastroenterology
and Hepatology, Kobe City Medical Center West Hospital, Kobe, Japan http://dx.doi.org/10.1016/j.gie.2014.03.041
Commentary First described in 1990 by Goldenberg, acute esophageal necrosis (AEN), commonly referred to as “black esophagus,” is a rare clinical entity. The typical patient is a debilitated man in his 60s, perhaps with alcohol intoxication, and often with a history of diabetes, hypertension, and vascular disease, in whom malignancy or multiorgan failure, hypotension, or sepsis has developed. The most common GI presentation is upper GI bleeding with or without abdominal pain, vomiting, dysphagia, and nausea. AEN is typified by a diffuse circumferential black mucosal discoloration in the distal esophagus that may extend proximally to a variable length. Tissue damage in AEN is likely multifactorial, resulting from a combination of tissue hypoperfusion, impaired local defense barriers, and reflux of gastric contents. Back diffusion of hydrogen ions also may downregulate any augmentation in arterial supply needed for reparative processes. The striking predilection of AEN for the distal esophagus may have its basis in the lesser degree of vascularization of this area, relative to more proximal regions of the esophagus. The distal esophagus receives its blood supply from the left gastric artery or left inferior phrenic artery, but variations are common and small branches off the celiac, splenic, short gastric, or left hepatic arteries may provide alternative paths. The mid-esophageal blood supply is derived from the bronchial arteries, the right third or fourth intercostal arteries, and numerous small esophageal arteries off the descending aorta. The upper esophagus is mainly supplied from the descending branches of the inferior thyroid arteries, with additional contributions from the subclavian, common carotid, and superior thyroid arteries. Histologically, mucosal necrosis is found, although deeper esophageal tissue layers may be involved. In a staging system proposed by Gurvits et al, stage 0 designates a prenecrotic viable esophagus. Stage 1 refers to a diffuse, circumferential, black-appearing esophageal mucosa with occasional yellow exudates and signs of friability; findings begin at the gastroesophageal junction and extend proximally to various lengths. Stage 2 describes the healing phase, which is dominated by residual black areas with thick white exudates composed of necrotic debris that cover friable pink mucosa; the findings in this case are redolent of the “chess-board” appearance that characterizes this stage. In stage 3, the esophageal mucosa regains its normal appearance. Treatment is directed at correcting coexisting clinical conditions, restoring hemodynamic stability, and intravenous acid suppression with proton pump inhibitors. Adverse events include esophageal perforation with mediastinal infection/abscess, stricture formation, superinfection (bacteria, virus, and fungus), and death. Mortality is usually related to underlying comorbid disease, and although overall prognosis is poor, mortality specific to the AEN is less than 10%. In Principles of Philosophy, Descartes wrote, “When we say we perceive colors in objects, it is really just the same as saying that we perceived in objects something as to whose nature we are ignorant but which produces in us a very clear and vivid sensation, what we call the sensation of color.” When we look at a black esophagus, we may be ignorant of its naturedit may be a melanoma or AENdbut we do know it isn’t something of which to be desirous. Fortunately, this badness usually doesn’t dictate the clinical course; it just complicates it. Lawrence J. Brandt, MD Associate Editor for Focal Points
2 GASTROINTESTINAL ENDOSCOPY Volume
-,
No.
-
: 2014
www.giejournal.org
