QJM: An International Journal of Medicine, 2015, 839–840 doi: 10.1093/qjmed/hcv075 Advance Access Publication Date: 13 May 2015 Clinical picture
CLINICAL PICTURE
Black oesophagus poor general conditions (including malnutrition, multiple comorbidity), excessive alcohol abuse and immunocompromised state.3 Opportunistic cytomegalovirus and herpes simplex virus infections were also reported to be the possible etiologies.4,5 Clinical history of caustic ingestion or previous foreign body associated injury should be first taken and excluded. Other diagnostic considerations to exclude include acanthosis nigricans, pseudomelanosis, melanosis and malignant melanoma. Except for intravenous PPI, no standardized treatment therapy is recommended for treating AEN. Removal of the identified etiology, maintain perfusion and supportive care are best strategies. Surgery is only preserved for those with severe complications. As Ben Soussan6 reported in a prospective 1-year study, the mortality rate of AEN is 50% (4/8). However, all the mortality cases were attributed to coexist illness instead of the disease itself. In conclusion, we present a case of AEN. Our patient’s gender, advanced age, habit of alcohol abuse and debilitating medical conditions (HCVD, diabetes, Af, malignancy) fit well with risks factors of AEN. Now, he remains symptom free and recovery from endoscopy. Photographs and text from: M.-C. Lin, Division of Gastroenterology, Department of Internal Medicine, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan and Department of Internal Medicine, Taichiung Armed Forces General Hospital, Taichiung, Taiwan; H.-C. Chu and P.-J. Chen, Department of Internal Medicine, Tri-Service
Figure 1. (a, b) Endoscopic views of esophageal findings. (a) black-brownish appearing of the esophageal mucosa with abrupt ending at the GE junction, (b) healing ulceration in distal esophagus.
C The Author 2015. Published by Oxford University Press on behalf of the Association of Physicians. V
All rights reserved. For Permissions, please email: [email protected]
839
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A 70-year-old male with medical history of hypertensive cardiovascular disease, diabetes mellitus with chronic renal insufficiency, atrial fibrillation, sick sinus syndrome and adenocarcinoma of prostate presented with a 2-day history of melena and hematemesis. On examination, he was afebrile and hemodynamically stable. Except for slight tachycardia (HR: 110 beats/ min) and epigastric tenderness, no other abnormalities were noted. Laboratory analysis revealed hemoglobin of 14.5 g/dl, and creatinine of 1.7 mg/dl, respectively. The fecal occult blood test is positive. Esophagogastroduodenoscopy (EGD) revealed diffuse black pigmentation with extensive ulcerative mucosa in the mid-to-distal esophagus as well as sharp demarcation at the gastroesophageal (GE) junction, which were suggestive of acute necrotizing esophagus (Figure 1a). However, tissue sampling was not performed due to multiple comorbidity and potential perforation. After combination treatment with oral sucralfate and proton-pump inhibitor (PPI) for 2 weeks, a follow-up EGD showed complete resolution of previous black mucosa (Figure 1b). Acute esophageal necrosis (AEN), also known as ‘black esophagus’ or ‘acute necrotizing esophagitis’, is a rare clinical scenario with hemorrhagic manifestations mostly.1 The exact pathophysiology of AEN still remains unclear. However, it is believed to be multifactorial. It is generally seen in individual with ischemia-associated phenomena, such as unstable hemodynamic compromise, back flow injury due to transient gastric outlet obstruction and cardiovascular event, and excessive alcohol abuse.2 Generally, risk factors of AEN are male, the elderly,
840
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QJM: An International Journal of Medicine, 2015, Vol. 108, No. 10
General Hospital, National Defense Medical Center, Taipei, Taiwan. email: [email protected]
Conflict of Interest: None declared.
References 1. Reichart M, Busch OR, Bruno MJ, Van Lanschot JJ. Black esophagus: a view in the dark. Dis Esophagus 2000; 13:311–13. 2. Endo T, Sakamoto J, Sato K, Takimoto M, Shimaya K, Mikami T, et al. Acute esophageal necrosis caused by alcohol abuse. World J Gastroenterol 2005; 11:5568–70.
3. Gurvits GE, Shapsis A, Lau N, Gualtieri N, Robilotti JG. Acute esophageal necrosis: a rare syndrome. J Gastroenterol 2007; 42:29–38. 4. Cattan P, Cuillerier E, Cellier C, Carnot F, Landi B, Dusolel A, et al. Black esophagus associated with herpes esophagitis. Gastrointest Endosc 1999; 49:105–7. 5. Barjas E, Pires S, Lopes J, Valente A, Oliveira E, Palma R Cytomegalovirus acute necrotizing esophagitis. Endoscopy. 2001; 33:735. 6. Ben Soussan E, Savoye G, Hochain P, Herve´ S, Antonietti M, Lemoine F, et al. Acute esophageal necrosis: a 1-year prospective study. Gastrointest Endosc 2002; 56:213–17.
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CLINICAL PICTURE
Black oesophagus poor general conditions (including malnutrition, multiple comorbidity), excessive alcohol abuse and immunocompromised state.3 Opportunistic cytomegalovirus and herpes simplex virus infections were also reported to be the possible etiologies.4,5 Clinical history of caustic ingestion or previous foreign body associated injury should be first taken and excluded. Other diagnostic considerations to exclude include acanthosis nigricans, pseudomelanosis, melanosis and malignant melanoma. Except for intravenous PPI, no standardized treatment therapy is recommended for treating AEN. Removal of the identified etiology, maintain perfusion and supportive care are best strategies. Surgery is only preserved for those with severe complications. As Ben Soussan6 reported in a prospective 1-year study, the mortality rate of AEN is 50% (4/8). However, all the mortality cases were attributed to coexist illness instead of the disease itself. In conclusion, we present a case of AEN. Our patient’s gender, advanced age, habit of alcohol abuse and debilitating medical conditions (HCVD, diabetes, Af, malignancy) fit well with risks factors of AEN. Now, he remains symptom free and recovery from endoscopy. Photographs and text from: M.-C. Lin, Division of Gastroenterology, Department of Internal Medicine, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan and Department of Internal Medicine, Taichiung Armed Forces General Hospital, Taichiung, Taiwan; H.-C. Chu and P.-J. Chen, Department of Internal Medicine, Tri-Service
Figure 1. (a, b) Endoscopic views of esophageal findings. (a) black-brownish appearing of the esophageal mucosa with abrupt ending at the GE junction, (b) healing ulceration in distal esophagus.
C The Author 2015. Published by Oxford University Press on behalf of the Association of Physicians. V
All rights reserved. For Permissions, please email: [email protected]
839
Downloaded from by guest on November 14, 2015
A 70-year-old male with medical history of hypertensive cardiovascular disease, diabetes mellitus with chronic renal insufficiency, atrial fibrillation, sick sinus syndrome and adenocarcinoma of prostate presented with a 2-day history of melena and hematemesis. On examination, he was afebrile and hemodynamically stable. Except for slight tachycardia (HR: 110 beats/ min) and epigastric tenderness, no other abnormalities were noted. Laboratory analysis revealed hemoglobin of 14.5 g/dl, and creatinine of 1.7 mg/dl, respectively. The fecal occult blood test is positive. Esophagogastroduodenoscopy (EGD) revealed diffuse black pigmentation with extensive ulcerative mucosa in the mid-to-distal esophagus as well as sharp demarcation at the gastroesophageal (GE) junction, which were suggestive of acute necrotizing esophagus (Figure 1a). However, tissue sampling was not performed due to multiple comorbidity and potential perforation. After combination treatment with oral sucralfate and proton-pump inhibitor (PPI) for 2 weeks, a follow-up EGD showed complete resolution of previous black mucosa (Figure 1b). Acute esophageal necrosis (AEN), also known as ‘black esophagus’ or ‘acute necrotizing esophagitis’, is a rare clinical scenario with hemorrhagic manifestations mostly.1 The exact pathophysiology of AEN still remains unclear. However, it is believed to be multifactorial. It is generally seen in individual with ischemia-associated phenomena, such as unstable hemodynamic compromise, back flow injury due to transient gastric outlet obstruction and cardiovascular event, and excessive alcohol abuse.2 Generally, risk factors of AEN are male, the elderly,
840
|
QJM: An International Journal of Medicine, 2015, Vol. 108, No. 10
General Hospital, National Defense Medical Center, Taipei, Taiwan. email: [email protected]
Conflict of Interest: None declared.
References 1. Reichart M, Busch OR, Bruno MJ, Van Lanschot JJ. Black esophagus: a view in the dark. Dis Esophagus 2000; 13:311–13. 2. Endo T, Sakamoto J, Sato K, Takimoto M, Shimaya K, Mikami T, et al. Acute esophageal necrosis caused by alcohol abuse. World J Gastroenterol 2005; 11:5568–70.
3. Gurvits GE, Shapsis A, Lau N, Gualtieri N, Robilotti JG. Acute esophageal necrosis: a rare syndrome. J Gastroenterol 2007; 42:29–38. 4. Cattan P, Cuillerier E, Cellier C, Carnot F, Landi B, Dusolel A, et al. Black esophagus associated with herpes esophagitis. Gastrointest Endosc 1999; 49:105–7. 5. Barjas E, Pires S, Lopes J, Valente A, Oliveira E, Palma R Cytomegalovirus acute necrotizing esophagitis. Endoscopy. 2001; 33:735. 6. Ben Soussan E, Savoye G, Hochain P, Herve´ S, Antonietti M, Lemoine F, et al. Acute esophageal necrosis: a 1-year prospective study. Gastrointest Endosc 2002; 56:213–17.
Downloaded from by guest on November 14, 2015
