A not-so-black-and-white case of gastrointestinal bleeding

Correct answer: D.

Discussion

Acute oesophageal necrosis (AEN), more frequently known as black oesophagus, was first described in 1990.¹It has been also described as Gurvits syndrome, after the physician whodescribed itin depthand studied it thoroughly.²As seen in the case patient, AEN is characterized by the conspicuous endoscopic finding of diffuse and circumferential black ulcero-necrotic oesophageal mucosa, almost always involving the distal oesophagus and with an abrupt demarcation line at the gastro-oesophageal junction.³

Biopsy samples are not required for confirmation of diagnosis unless there is a high degree of suspicion for the presence of atypical forms of infection (e.g. CMV or HSV oesophagitis). When biopsy samples are taken tissue necrosis of variable depth is noted, with accompanying ulcerations and deposits of hemosiderin.⁴

AEN is a rare entity, with an incidence of only 0.1–0.28%, being encountered most frequently in the older population (mean age 67 years) and with a predilection for the male sex.⁵Around 220 cases have been presented so far worldwide.²The vast majority of patients (>90%) present with signs of upper gastrointestinal bleeding. Other less frequent symptoms include nausea, fever, dysphagia and abdominal pain.^6–8

Correct answer: B.

Discussion

The pathogenesis of AEN seems to be multifactorial.⁸It has been suggested that an event of transient or extended mucosal hypoperfusion (in the setting of underlying vascular disease), in combination with impaired local defence mechanisms, leads to the inability of the tissue to cope with increased exposure to toxic gastric contents (i.e. gastrin and pepsin). Thus, the damage to the mucosa is devastating, leading to variable degrees of necrosis. 

Several medical conditions/situations have been described to contribute to development of AEN:^2,5,6

• Diabetes mellitus (especially ketoacidosis)
• Hypertension
• Alcohol abuse
• Malignancy
• Malnutrition
• Sepsis
• Gastric volvulus or gastric outlet obstruction
• Immunosuppression
• Corrosive agent ingestion

Correct answer: C.

Discussion

Although the oesophagus is the organ most obviously affected by this condition, treatment should target the underlying medical conditions and restoring hemodynamic stability. Treatment involves bowel rest, aggressive fluid resuscitation (with blood transfusion as needed) and high-dose IV acid suppression with PPIs to decrease oesophageal acid exposure. In severe cases total parenteral nutrition may be necessary.⁹ 

Use of antibiotics (including antivirals and antifungals) is generally not recommended. Antibiotics may even be detrimental, as cases complicated by C. difficileinfection have shown, unless there is a confirmed diagnosis of, or a high degree of clinical suspicion for, underlying significant infection or sepsis, perforation or the patient is immunocompromised.³Surgery is required only in highly selected cases (e.g. those complicated by perforation, abscess formation or a stricture). Complications are rare, but they usually involve stenosis or stricture formation. Prognosis is poor, with a high mortality rate of 32% due to the severity of the comorbidities present, despite specific AEN-related mortality being quite low at 6%. Treatment should, therefore, be prompt, aggressive and aimed at the conditions that have caused the AEN, to achieve better recovery rates.⁶