Black esophagus and diabetes: a close relationship

Abstract

The black esophagus is a rare clinical entity, down to 0.2% in autopsy series and 0.001–0.2% in series of endoscopies. Although it is an entity that has already been reported in the literature, its etiopathogenesis is not completely known. Different theories have been proposed to clarify their cause. One of these theories makes a hypothesis of a viral infection as the underlying cause; this theory can be seen in the literature extensively, but only two cases were reported. The first case is a case with histopathological confirmation of Herpes virus infection. The second is a case in which vascular deterioration has been the main cause of esophageal necrosis. In both cases, diabetes is the factor that determines a bad evolution of the disease.

The black esophagus, also known as necrotizing esophagitis or acute esophageal necrosis, is a rare entity described in patients for the first time in 1990, although previously it had been reported postmortem cases [1]. Its prevalence is low, up to 0.2% in series of autopsies [2] and 0.001–0.2% in series of endoscopies [3]. It is associated with high mortality, close to 35%, which is related to the underlying pathology and the comorbidity of the patient. It is more frequent in men than women, diabetic patients, with an average age of 70 years at the time of diagnosis. Its pathogenesis is not completely known, mechanisms related to situations of tissue hypoperfusion and viral infections are proposed [4]. The diagnosis of this entity is made by endoscopy, with this technique an esophageal mucosa with a blackish, friable and hemorrhagic coloration can be observed, which is generally found in the distal esophagus. The diagnosis for confirmation requires histopathological confirmation by biopsy [5].

Case presentation

We present two cases, the first of them, an 81-year-old male who was admitted due to disorientation with visual hallucinations and incontinence of the sphincters after diarrhea at home with signs of dehydration for a week. In the medical history highlights: hypertension, dyslipidemia, diabetes mellitus type 2 (20 years of evolution in treatment with oral antidiabetics and poor control), chronic alcoholism. Analytical studies included leukocytosis of 14.670 × 10³/µL, PCR 68.3 mg/L: normal value (VN: <5 mg/L), glucose 264 mg/dl (VN: 110 mg/dl) without ketoacidosis and renal insufficiency (creatinine clearance:54 mml/min). During admission, a respiratory infection was diagnosed, with good adherence to antibiotic treatment, and poor glycemic control despite continuous therapeutic adjustments. After 3 days of evolution, he had black stools, suggesting a high digestive hemorrhage, so gastroscopy was performed. Lesions compatible with black esophagus and esophagitis were observed (Fig. 1a), thereafter, histopathological analysis of esophageal tissue confirmed the etiology of herpes simplex virus (Fig. 1b). The patient received treatment with proton pump inhibitors and antiviral treatment. Five days after the completion of the endoscopy the patient died after an episode of massive hematemesis.

Fig. 1.

(a) Endoscopy image of the esophagus showing areas of black color that correspond to the necrosis. (b) Fragment of esophageal tissue with the replacement of squamous epithelium by dense transmural infiltrated with the presence of syncytial groups, formed by multinucleated giant cells with cores in ground glass and with intranuclear inclusion bodies, typical of herpes esophagitis.

The second case is a 61-year-old male, a history of ex-smoker, hypertensive, long-term diabetic, more than 20 years, with stage 5 chronic kidney disease secondary to diabetic nephropathy in hemodialysis for 5 years. He was hospitalized for renal transplantation, at 9 days he presented organ rejection secondary to renal artery thrombosis, which led to the removal of the transplant the postoperative period, the patient begins with abundant bilious vomiting, in the analytical increase of the infectious parameters and in the results of the abdominal ultrasound compatible with acute cholecystitis, so we begin the empirical antibiotic therapy. After 2 days of treatment, the patient began with melanic depositions, decreased blood pressure and decreased hemoglobin of 5 g/dl, an urgent endoscopy was performed. In the endoscopy, it was observed lesions with complete esophageal involvement from the proximal area are visualized, it is provisionally diagnosed with a black esophagus while waiting for the results of the biopsy. The patient has an unfavorable evolution in successive hours, persistence of melanin depositions and anemization despite treatment with proton pump inhibitors, vasopressor support and blood transfusions, after a sudden hypotension and absence of improvement, an abdominal CT scan was performed objectifying Paralytic and ischemic colitis with involvement of up to 8 cm of left colon dying within a few hours of the study.

Discussion

The black esophagus is an infrequent entity. In many cases, it is underdiagnosed or endoscopic findings are confused with other entities such as reflux esophagitis. Acute esophageal necrosis is often diagnosed incidentally in patients who undergo upper endoscopy for evaluation of upper gastrointestinal bleeding [6]. Diagnostic suspicion can be made because of the endoscopic aspect given that it is highly suggestive, but for the diagnosis of certainty, esophageal biopsies are needed since it is the only way to make the differential diagnosis with other entities such as melanosis or pseudomelanosis, acanthosis nigricans, intake of coal, caustic and corrosive agents.

Mortality is related in large part to the underlying disease or comorbidities that the patient presents and not to the esophageal necrosis itself [7]. Only 6% of deaths are directly attributable to complications such as perforation (6.8%). Other associated complications are esophageal stenosis (10.8%), mediastinitis and abscesses (5.7%) [6,8,9].

To clarify the etiopathogenesis, an ischemic origin had been suggested, supported by the usual affectation of the distal esophageal third in vascular diseases, which is the territory with the least vascularization, as well as in the histopathological findings found very similar to those found in ischemic colitis. The predisposing conditions that lead to its development described in the literature are multiple: hypersensitivity to some broad-spectrum antibiotics, obstruction to the gastric outlet tract, rupture or aortic dissection, hyperglycemia, neoplasms, Stevens-Johnson syndrome, hypothermia, shock, vomiting severe, liver disease, diabetic ketoacidosis, coagulopathies and viral infections (cytomegalovirus and herpes virus) [7]. The viral etiology is one of the most mentioned causes, but only two cases have been reported to date in the literature [10–12].

Diabetes must be highlighted as underlying pathology in a large number of cases. Gurvits et al. [12] have recently found that nearly 90% of the patients are moderately hyperglycemic in a large series of reviewed cases with black esophagus. Also, it has been shown that necrotizing esophagitis may complicate acute hyperglycemic states, such as diabetic ketoacidosis [13]. This association of both pathologies has the pathophysiological basis in the greater damage that diabetic patients present in the arteries, especially those of small caliber, a fact that occurs in many other vascular territories such as the heart or the retina. It is known that patients with diabetes mellitus have greater endothelial damage and greater atherosclerotic disease, which translates into a greater number of vascular events. Therefore, it is essential to consider the association between diabetes and black esophagus, in order to its early recognition and proper treatment.

Acknowledgements

Conflicts of interest

There are no conflicts of interest.