RESUMEN

INTRODUCTION: Catheter ablation of atrial fibrillation (AF) may lead to collateral damage to the esophagus. We tested the hypothesis that luminal esophageal temperature (LET)-guided esophageal cooling might reduce the incidence of esophageal thermal lesions (ETL). METHODS: Seventy-six patients from August 2015 to March 2017 with paroxysmal or persistent AF underwent a first-time catheter ablation procedure with or without LET-guided active esophageal cooling through an orogastric tube placed in the esophagus. Esophageal cooling occurred if and only if LET exceeded 0.5 °C from baseline while ablating the LA posterior wall. All patients underwent esophagogastric endoscopy the next day. RESULTS: Of the 76 patients studied, 38 (50%) patients underwent esophageal cooling. Baseline characteristics of the non-cooled and cooled groups were comparable. Of these, 59% of patients had ETL. There was a non-significant trend for more severe lesions (grades 3, 4) in the non-cooled group (29% vs. 13.5%, p = 0.10). Average power delivered on the left atrial posterior wall (27 ± 1.8 W vs. 27 ± 3.8 W, p = 0.34) and average force of contact (10.1 g vs. 9.8 g, p = 0.38) were similar in both groups while more time was spent ablating on the posterior wall in the non-cooled group (24.6 ± 7.3 min vs. 20.4 ± 5.9 min, p = 0.014). In a multivariate analysis, esophageal cooling had no significant effect on the esophageal lesion grade post-ablation. CONCLUSION: The incidence of ETL in patients undergoing left atrial posterior wall isolation is substantial. Our method of esophageal cooling did not decrease the incidence of ETL. There was a non-significant trend toward fewer severe lesions with cooling, but one cannot conclude the value of cooling from this pilot study.

Asunto(s)

Asunto(s)

Asunto(s)

RESUMEN

BACKGROUND: Clostridium difficile infection (CDI) is the leading cause of hospital-associated gastrointestinal illness. Previous studies reported that patients with active malignancy are at high risk for CDIs, and yet they are still classified as nonsevere CDI and initially treated with metronidazole. Our aim is to investigate the need for the escalation of antibiotic therapy in patients with CDI and active cancer treated with oral metronidazole versus oral vancomycin. METHODS: This is a retrospective study of adult patients admitted with CDI and any underlying active malignancy at Beaumont Hospital, Royal Oak, Michigan, from January 2008 to December 2014. Inclusion criteria included age > 18 years old, polymerase chain reaction- (PCR-) proven CDI, and active malignancy. RESULTS: 197 patients were included in the final analysis. 44.8% of the metronidazole group required escalation of therapy compared to 15.2% in the vancomycin group (p value = 0.001). 29.8% of the combination group (metronidazole and vancomycin) underwent deescalation of antibiotics, which was significantly higher compared to 2.2% of patients in the vancomycin group (p value < 0.001). DISCUSSION: Our results support the initial use of vancomycin or a combination (metronidazole and vancomycin) versus metronidazole in patients with CDI and active malignancy.

Asunto(s)

RESUMEN

BACKGROUND: An association between inlet patches and proximal esophageal adenocarcinomas is currently suspected because of numerous case reports of simultaneous occurrence of both diseases. AIMS: To analyze whether inlet patches are significantly associated with proximal esophageal adenocarcinomas in a large population. METHODS: Computerized search of pathology and EGD reports revealed 398 cases of esophageal adenocarcinomas among 156,236 EGDs (performed on 106,510 patients) diagnosed by histopathology performed at Royal Oak/Troy, William Beaumont Hospitals, 2003-2016. Adenocarcinomas localized as distal, middle, or proximal; and characterized as associated versus unassociated with inlet patches. Medical records were reviewed. Endoscopic photographs, radiologic images, and pathologic slides were re-reviewed. Two researchers independently performed systematic computerized literature searches; cases of simultaneous diseases identified by consensus. RESULTS: Adenocarcinoma locations included: distal-381, middle-14, and proximal esophagus-3. Five patients had inlet patches with esophageal adenocarcinomas located at: distal-2, middle-0, and proximal esophagus-3 (relative frequency of inlet patches with cancers of distal/middle esophagus = 2/395 [.5%] vs. proximal esophagus = 3/3 [100%], p < .000001, 95% OR CI > 50.1, Fisher's exact test). Cases of proximal esophageal adenocarcinomas within inlet patches included: (1) Seventy-eight-year-old man presented with dysphagia. Neck CT showed proximal esophageal mass. EGD revealed semi-circumferential, multinodular, 3.0 × 1.5 cm mass within inlet patch. Histopathology of biopsies revealed moderately-to-poorly differentiated adenocarcinoma. Patient received chemoradiotherapy and expired 2 years later. (2) Seventy-nine-year-old man presented with anorexia and weight loss. EGD demonstrated proximal esophageal mass within inlet patch. Histopathology of biopsies revealed poorly differentiated, signet ring cell adenocarcinoma. Chest CT revealed 3.4 × 2.1-cm-proximal esophageal mass. Patient expired 4 months later. (3) Sixty-year-old man presented with dysphagia. EGD revealed 4-cm-long, semi-circumferential, proximal esophageal mass within inlet patch. Histopathology of biopsies revealed poorly differentiated adenocarcinoma. Patient underwent emergency esophagectomy for esophageal perforation 2 weeks after initiating chemoradiotherapy, and died shortly thereafter. Literature review revealed 39 cases of simultaneous disease. STUDY LIMITATIONS: Potential underreporting by endoscopists of inlet patches at EGD. CONCLUSIONS: Study supplements 39 previously reported cases of simultaneous disease, by adding three new cases, and by novel report of statistically significant association between these two entities, which has important implications in the pathophysiology of proximal esophageal adenocarcinoma.

Asunto(s)

RESUMEN

Atrioesophageal fistula (AEF) is a rare but catastrophic complication of catheter ablation of atrial fibrillation (AF), with an incidence of 0.03% to 1.5% per year. We report two cases and review the epidemiology, clinical features, pathogenesis, and management of AEF after AF ablation. The principal clinical features of AEF include fever, hematemesis, and neurologic deficits within 2 months after ablation. The close proximity of the esophagus to the posterior left atrial wall is considered responsible for esophageal injury during ablation and the eventual development of AEF. Prophylactic proton pump inhibitors, esophageal temperature monitoring, visualization of the esophagus during catheter ablation, esophageal protection devices, esophageal cooling, and avoidance of energy delivery in close proximity to the esophagus are some techniques to prevent esophageal injury. Eliminating esophageal injury during AF ablation is of utmost importance in preventing AEF. A high index of suspicion and early intervention are necessary to prevent fatal outcomes. Early surgical repair is the mainstay of treatment.

Asunto(s)

Asunto(s)

RESUMEN

INTRODUCTION: A novel case is reported of upper gastrointestinal (UGI) bleeding from sinistral portal hypertension, caused by a left gastric artery (LGA) pseudoaneurysm (PA) compressing the splenic vein (SV) that was successfully treated with PA embolization. CASE REPORT: A 41-year-old man with previous medical history of recurrent, alcoholic pancreatitis presented with several episodes of hematemesis and abdominal pain for 48 hours. Physical examination revealed a soft abdomen, with no abdominal bruit, no pulsatile abdominal mass, and no stigmata of chronic liver disease. The hemoglobin declined acutely from 12.3 to 9.3 g/dL. Biochemical parameters of liver function and routine coagulation profile were entirely within normal limits. Abdominal CT revealed a 5-cm-wide peripancreatic mass compressing the stomach and constricting the SV. Esophagogastroduodenoscopy showed blood oozing from portal hypertensive gastropathy, small nonbleeding gastric cardial and fundal varices, gastric compression from the extrinsic mass, and no esophageal varices. MRCP and angiography showed that the mass was vascular, arose from the LGA, compressed the mid SV without SV thrombosis, and caused sinistral portal hypertension. At angiography, the PA was angioembolized and occluded. The patient has been asymptomatic with no further bleeding and a stable hemoglobin level during 8 weeks of follow-up. DISCUSSION: Literature review of the 14 reported cases of LGA PA revealed that this report of acute UGI bleeding from sinistral portal hypertension from a LGA PA constricting the SV is novel; one previously reported patient had severe anemia without acute UGI bleeding associated with sinistral portal hypertension from a LGA PA. CONCLUSION: A patient presented with UGI bleeding from sinistral portal hypertension from a LGA PA compressing the SV that was treated by angiographic obliteration of the PA which relieved the SV compression and arrested the UGI bleeding. Primary therapy for this syndrome should be addressed to obliterate the PA and not the secondarily constricted SV.

Asunto(s)

RESUMEN

A 59-year-old man with past medical history of thoracic aortic aneurysm treated with thoracic endovascular aortic repair presented with melena for 2 weeks. Initial EGD did not reveal the source of bleeding and showed normal esophagus; abdominal arteriogram did not reveal a fistulous communication and initial CTA showed normal position of the aortic graft stent without endoleak. The sixth EGD revealed a submucosal tumor-like projection in the upper esophagus and stigmata of recent bleeding. Another thoracic endovascular aortic repair with stent was placed over the old graft for presumed aortoesophageal fistula. Poststent upper gastrointestinal series with contrast showed extravasation of the contrast from the esophagus and CTA showed fistulous tract between aorta and esophagus. The patient refused definitive surgical repair despite having infected aortic graft; jejunostomy tube was placed and life-long suppressive antibiotic treatment was given and the patient is doing well at 2-year follow-up.