Faculty Bibliography

BACKGROUND AND AIMS:Acute esophageal necrosis (AEN) in the setting of gastric volvulus is a rare condition with only a handful of cases reported. Volvulus may contribute to AEN by limiting tissue perfusion and promoting massive reflux of gastric contents on compromised esophageal mucosa. METHODS:We reviewed 225 original articles, literature reviews, case series, brief reports, case reports, and discuss six total cases of co-occurring esophageal necrosis and gastric volvulus. RESULTS AND CONCLUSIONS:We present the first comprehensive analysis of all reported cases in the literature to date and formulate management strategies for the co-occurrence of AEN and volvulus. Management of AEN should be directed at correcting underlying medical conditions, providing hemodynamic support, initiating nil-per-os restriction, and administering high-dose proton pump inhibitor therapy. Surgical intervention is typically reserved for cases of esophageal perforation with mediastinitis and abscess formation.

Acute oesophageal necrosis, black oesophagus (BE) or Gurvits syndrome (GS) is a rare form of severe oesophagitis appearing as a striking circumferential discolouration of distal mucosa with various proximal extensions abruptly terminating at the gastro-oesophageal junction. It is most commonly associated with acute exacerbations of medical comorbidities, while associations with altered gut anatomy are rare. We present a unique constellation of BE, Cameron ulcers (CU), and gastric volvulus from a large paraesophageal hiatal hernia. Our patient recently recovered from COVID-19 and was malnourished and frail, while the expanding paraesophageal hiatal hernia turned into an acute organoaxial gastric volvulus with accompanying outlet obstruction. In low-flow post-COVID coagulopathic states, compensatory mechanisms may lack against gastric stunning and sudden massive reflux on the oesophagus. We additionally performed a systematic review and discovered additional cases with coexistent volvulus and paraesophageal hernia, although there are no previous reports of BE with CU, which makes this study the first.

GOALS AND BACKGROUND/OBJECTIVE:Studies analyzing artificial intelligence (AI) in colonoscopies have reported improvements in detecting colorectal cancer (CRC) lesions, however its utility in the realworld remains limited. In this systematic review and meta-analysis, we evaluate the efficacy of AI-assisted colonoscopies against routine colonoscopy (RC). STUDY/METHODS:We performed an extensive search of major databases (through January 2021) for randomized controlled trials (RCTs) reporting adenoma and polyp detection rates. Odds ratio (OR) and standardized mean differences (SMD) with 95% confidence intervals (CIs) were reported. Additionally, trial sequential analysis (TSA) was performed to guard against errors. RESULTS:Six RCTs were included (4996 participants). The mean age (SD) was 51.99 (4.43) years, and 49% were females. Detection rates favored AI over RC for adenomas (OR 1.77; 95% CI: 1.570-2.08) and polyps (OR 1.91; 95% CI: 1.68-2.16). Secondary outcomes including mean number of adenomas (SMD 0.23; 95% CI: 0.18-0.29) and polyps (SMD 0.23; 95% CI: 0.17-0.29) detected per procedure favored AI. However, RC outperformed AI in detecting pedunculated polyps. Withdrawal times (WTs) favored AI when biopsies were included, while WTs without biopsies, cecal intubation times, and bowel preparation adequacy were similar. CONCLUSIONS:Colonoscopies equipped with AI detection algorithms could significantly detect previously missed adenomas and polyps while retaining the ability to self-assess and improve periodically. More effective clearance of diminutive adenomas may allow lengthening in surveillance intervals, reducing the burden of surveillance colonoscopies, and increasing its accessibility to those at higher risk. TSA ruled out the risk for false-positive results and confirmed a sufficient sample size to detect the observed effect. Currently, these findings suggest that AI-assisted colonoscopy can serve as a useful proxy to address critical gaps in CRC identification.

Introduction: Acute esophageal necrosis (AEN) is an emerging cause of gastrointestinal bleeding with an increasing incidence over the past two decades. It appears as a circumferential necrotic lesion encircling the distal esophagus with various proximal extensions. It is most commonly associated with exacerbations of medical co-morbidities such as diabetes, renal failure, coronary disease; however cases of AEN due to mechanical alteration in gut anatomy are exceedingly rare and its prognosis is less defined. We present a unique constellation of AEN, Cameron ulcers (CU), and gastric volvulus from a large paraesophageal hiatal hernia. Case Description/Methods: A 77-year-old female began experiencing abdominal pain and repeated emesis. She had a history of COPD, GERD, episodes of bleeding ulcers, hiatal hernia, malnutrition, and recently COVID-19. She was hemodynamically stable, ill-appearing with tenderness to abdominal palpation and a negative stool guaiac. BP 106/48 mm/Hg, HR 107, requiring oxygen. Investigations revealed WBC 18.5 k/uL, Hgb 9.8 g/dL, and acute renal failure. A CT abdomen revealed complete herniation of the stomach into the posterior mediastinum, dilated esophagus, organoaxial gastric volvulus, and gastric distension [Figure 1 - Pane A-C]. IV fluids, pantoprazole 80 mg, and ondansetron 4 mg were given. An EGD revealed a large hiatal hernia, Cameron ulcers (CU), and necrotic ulceration along the mid-to-lower third of the esophagus. The patient deferred surgical intervention and was discharged home on hospice.
Discussion(s): These constellations represent a common underlying pathophysiologic mechanism that stems from large hiatal hernias and their effect on surrounding structures in our case, precipitated by a paraesophageal hiatal hernia that became too large causing acute gastric volvulus. In severe presentations, the stomach may herniate into the posterior mediastinum known as an upside-down stomach requiring surgery while CU represents trauma to the mucosa from the hernia sliding. In our patient, lower esophagus blood flow traversing through the lesser gastric curvature may have been compromised during gastric necrosis. Simultaneously, sudden gastric stunning from acute outlet obstruction can lead to prolonged acidic bathing of the esophageal mucosa. Often the esophagus can compensate for this by increasing blood flow, however, this is compromised in low-flow states. Limitations of our study include lack of follow-up. A systematic review of all cases of AEN and gastric volvulus are in Table 1

INTRODUCTION: Pseudomelanosis duodeni is identified by a tigroid mucosa with brown-black or grey-black speckling. It is not associated with laxatives, unlike its colonic variant. Over the years, isolated reports of pseudomelanosis across the duodenum, jejunum, and ileum have been reported that were not captured in previous reviews. We aim to summarize all affected cases and provide clinical characteristics of this visually striking disease.
METHOD(S): We conducted a systematic review to identify all published reports of pseudomelanosis in the small bowel. A search string ("pseudomelanosis duodeni") OR ("duodenal melanosis") OR ("melanosis duodeni") OR ("melanosis ilei") OR ("pseudomelanosis ilei") OR ("melanosis intestini") OR ("pseudomelanosis intestini") OR ("melanosis jejuni") OR ("pseudomelanosis jejuni") was applied across databases (Figure 1). All cases were analyzed for characteristics with outcomes.
RESULT(S): 134 patients were identified. 82% of cases were identified by an EGD, while 5% used capsule endoscopy. Commonly affected segments were duodenum (70%), ileum (11%), stomach (7%), jejunum (5%), while 7% appeared endoscopically unaffected. Histology revealed a lack of fibrosis or cellular injury, reacting to prussian blue (43%), Fontana-Masson (27%), and PAS (16%) stains. Iron accumulations were frequently noted in samples (34%). The mean age was 61.23 +/- 17 years, with 56% males. The most common coexisting comorbidities were HTN (63%), CKD (55%) with 13% on hemodialysis, iron deficiency anemia (23%), diabetes mellitus (22%), and heart failure (6%). Hiatal hernias were seen in less than 10% of cases. Anti-hypertensives (44%), iron supplements (41%), diuretics (31%), beta-blockers (26%), and multivitamins (12%) were most commonly implicated. Anti-reflux therapy was used in less than 5% of patients, while mortality was seen in 5% of all cases, mainly to renal failure (42%) and sepsis (14%).
CONCLUSION(S): Pseudomelanosis of the upper GI tract maintains a distinct pathophysiology. The majority are diagnosed on endoscopy, and tissue diagnosis can be reassuring to the patient. There seems to be a firm association with chronic illness, that may contribute to impaired iron utilization. It is possible that defects in absorption can affect nutrients as well, contributing to GI symptoms of dyspepsia and abdominal discomfort, although the majority remain asymptomatic. Most cases resolve spontaneously, although the persistence of deposits is an emerging feature of this disease

INTRODUCTION: As awareness for Acute Esophageal Necrosis syndrome increases, so does our ability to understand its associations and causations. It classically presents as a striking necrotic appearance of black mucosa preferentially affecting the distal esophagus and extending proximally to various degrees while stopping at the GEJ. Its etiology is multifactorial and related to tissue hypoperfusion, massive reflux of gastric contents, and compromised local mucosal barriers. Historically, diabetes mellitus was seen in nearly 36% of AEN cases, although its association with hyperglycemia has never been parsed out. We aim to present a case of diabetic ketoacidosis (DKA) and review the literature with a focus on hyperglycemia and acute esophageal necrosis (AEN). CASE DESCRIPTION/METHODS: A 34-year-old female had called emergency services after experiencing coffee-ground emesis, abdominal pain, and pre-syncopal like symptoms for 5 days. She was found hypotensive, tachycardic with a blood sugar over 400 mg/dL. She was an active smoker with a history of diabetes mellitus type 1 with her last hemoglobin A1c at 16.9%. On arrival to the ED, her labs revealed blood glucose greater than 1000 mg/dL, pH of 7.1, bicarbonate ,10 mEq/L, anion gap over 30 mEq/L with acute kidney injury and cystitis. She was initiated on an insulin drip and antibiotics, made NPO, and IV esomeprazole was started. Esophagogastroduodenoscopy (EGD) revealed circumferential black appearing mucosa and a necrotic complexion in the middle and distal segments (Figures 1-3). She was managed conservatively with antiacid therapy. Enteral feeds were restarted shortly, and she was discharged home. DISCUSSION: Despite growing literature revealing DKA as a common precipitant for black esophagus, a bonafide association to hyperglycemia has not been shown. A literature review across all reported cases revealed diabetes mellitus as its most common risk factor (39%). Blood glucose over 150 mg/dL was seen in 15% of all black esophagus cases, while 67% of all hyperglycemic patients had blood glucose levels over 350 mg/dL. Average hemoglobin A1c was 11.46%, and approximately 13% that met DKA criteria developed black esophagus. Cases of DKA reported unusually high glucose levels, with the highest recorded at 1294 mg/dL. The mortality amongst patients with black esophagus and hyperglycemia nears 19%, while patients that develop concomitant black esophagus and DKA, mortality is 15%. (Figure Presented)

INTRODUCTION: Much has been written about melanosis coli; in contrast, occurrences of pigmentation in the upper gastrointestinal (GI) tract remains relatively rare. Pseudomelanosis duodeni (PD) appears as a striking black-brown speckle across the mucosa, presenting a diagnostic challenge to endoscopists. The paucity of reported cases and minimal understanding makes management arbitrary. Follow-up data on the persistence of these accumulations and its long-term outcomes remain to be explored. CASE DESCRIPTION/METHODS: An 86-year-old female presented with fatigue, dizziness, and melena. She had a history of end-stage renal disease requiring hemodialysis, valvular heart disease, history of recurrent GI bleeding, anemia, and diabetes mellitus. Home medications included amlodipine, carvedilol, hydralazine, insulin (detemir and aspart), and oral iron supplements. On arrival, her vitals read