Introduction

Heyde syndrome is the co-occurrence of aortic stenosis and gastrointestinal bleeding secondary to vascular lesions, including angiodysplasias. Several studies have demonstrated cessation of gastrointestinal bleeding after transcatheter aortic valve implantation (TAVI), but the etiology and effects on vascular lesions are largely unknown.

Aims & Methods

We aimed to establish the effects of TAVI on gastrointestinal vascular lesions and identify the factors associated with recovery. In this prospective, single-center cohort study, patients with iron-deficiency anemia on the TAVI waitlist from September 2020 to February 2022 were assessed by capsule endoscopy. Those with vascular lesions were reassessed six months after TAVI. Endoscopic images were anonymized and evaluated by two independent researchers.

Results

Twenty-four patients underwent capsule endoscopy, and vascular lesions were present in 18 (prevalence 75%). TAVI was performed in 15/18 patients with vascular lesions, of which 11 agreed to a second capsule endoscopy. The mean number of vascular lesions across the gastrointestinal tract decreased from 6.4 (SD 5.6) to 2.0 (SD 2.1) (P = .036). The number of vascular lesions decreased in 9/11 (82%) patients, including 6/11 (55%) who no longer had typical angiodysplasias. Cessation of angiodysplasias was less frequent in patients who had multiple valvular heart disease before TAVI (0/3 [0%] vs 6/8 [75%]) and patients with significant paravalvular leakage after TAVI (2/5 [40%] vs 4/6 [67%]).

Conclusion

Angiodysplasias are present in 75% of anemic patients with severe aortic stenosis. TAVI effectively reduces the size and number of angiodysplasias in these patients.

Disclosure

Lia Goltstein, Maxim Rooijakkers, Naomi Thierens, Selene Schoormans, Charles Houdeville, Marlijn Hoeks, and Sanna Rijpma do not have potential conflicts of interest or disclosures to report. Hanneke Beaumont has received speaker fees from Medtronic. Erwin van Geenen has received research funding from Viatris, Boston Scientific, and Olympus and serves as a consultant for MTW-Endoskopie and Microtech. Xavier Dray is cofounder and shareholder of Augmented Endoscopy, has served as a consultant for Norgine and Provepharma, and received speaker fees from Bouchara Recordati, Fujifilm, Medtronic, Norgine, and Sandoz. Niels van Royen has received research funding from Abbott, Philips, Medtronic, and Biotronik, has served as a consultant for RainMed, Castor, and Medtronic, and received speaker fees from Abbott. The Radboudumc, on behalf of Joost Drenth, has received research funding from Gilead to support Hepatitis C elimination in The Netherlands.

Clinical Case Summary

Introduction: A rare but serious side effect of SGLT-2 inhibitors is the euglycemic diabetic ketoacidosis (DKA), which is usually triggered by acute disease (e.g. infection), reduced food and fluid intake, reduced insulin doses, or alcohol consumption.^1-4
Case report: A 53-year-old patient, with a history of type 2 diabetes mellitus treated with metformin and empagliflozin, presented with abdominal pain, jaundice and abnormal liver function tests (AST: 338 U/l, ALT: 508 U/l, γ-GT: 2020 U/l, ALP: 483 U/l, TBL: 2.65 mg/dl, DBL: 2 .22 mg/dl). Abdominal U/S revealed intrahepatic and extrahepatic bile duct dilatations. The patient underwent ERCP (Figure A) where a stenosis in the intrapancreatic segment of the bile duct was revealed and a fully covered metal stent of 6 cm length was placed, while a cytological smear was positive for adenocarcinoma. Abdominal CT scan (Figure B) revealed a hypodense lesion (d. 3cm) in the head of the pancreas. Postoperatively, the patient manifested abdominal pain, fever, vomiting, lethargy, tachypnea and tachycardia with increased inflammatory markers and cholestatic enzymes and normal serum glucose. Arterial blood gases revealed metabolic acidosis (PH: 7.21, HCO3: 13 mmol/l, Lac: 0.8 mmol/l) with an increased anion gap (25 mmol/l) and ketonuria (ketone > 43 mg/dl). Euglycemic diabetic ketoacidosis was treated with an insulin pump with co-administration of glucose solution and intravenous administration of crystalline fluids and potassium replenishment. SGLT-2 inhibitor was discontinued. Microbemia due to Pseudomonas aeruginosa was detected and due to lack of apyrexia, an imaging re-evaluation with CT scan was performed where a liver abscess was detected (Figure C). Eventually, liver abscess was treated with drainage under CT guidance (Figure D).
Conclusion: Euglycemic diabetic ketoacidosis is a rare but serious complication of SGLT-2 inhibitors, which requires a high level of awareness from physicians for early recognition.

References

1. Sethi SM, Vohra M, Ali SA. EUGLYCEMIC DIABETIC KETOACIDOSIS (EDKA) IN A PATIENT RECEIVING DAPAGLIFLOZIN. Acta Endocrinol (Buchar). 2021 Apr-Jun;17(2):266-269.
2. Acevedo-Mendez BA, Ye Y, Hajizadeh N, Myers A. Hypertriglyceridemia-Induced Acute Pancreatitis, Euglycemic Diabetic Ketoacidosis and COVID-19 Infection in a Patient With Type 2 Diabetes Taking a Sodium-Glucose Cotransporter 2 Inhibitor. Cureus. 2021 Nov 23;13(11):e19828.
3. Sampani, E., Sarafidis, P., Dimitriadis, C. et al. Severe euglycemic diabetic ketoacidosis of multifactorial etiology in a type 2 diabetic patient treated with empagliflozin: case report and literature review. BMC Nephrol 21, 276 (2020).
4. Yii ESS, Azli AW, Sitaram PN. Sodium-glucose cotransporter 2 inhibitor-induced euglycemic diabetic ketoacidosis in a patient with coronavirus disease 2019: a case report. J Med Case Rep. 2022 Jan 4;16(1):17.

Introduction

Chronic liver disease remains one of the most common causes for hospital admission and is associated with high morbidity and mortality rates. Timely and adequate management within the first 24 hours is crucial for improving clinical outcomes in cases of decompensated cirrhosis. This study aimed to evaluate the impact of implementing a care bundle checklist during the first 24 hours of hospital admission on management and outcomes of decompensated cirrhosis.

Aims & Methods

We developed an adapted care bundle (based on the BSG/BASL care bundle, AASLD quality measures proposal, Baveno VII consensus, and EASL guidelines) and compared two patient groups from two Portuguese hospital centers: Group-A (retrospective, pre-care bundle implementation) and Group-B (prospective, post-care bundle implementation).

Results

A total of 224 patients (Group-A: 148; Group-B: 76) were included. More than one decompensation was observed in 118 patients (52.7%), and 69 patients (30.8%) were experiencing their index hospitalization for liver decompensation. Regarding etiology, alcoholic liver disease was the most common (n=200; 89.3%). The groups were similar in terms of gender, age, length of hospital stay, and Child-Pugh and MELD-Na scores at admission. The most common decompensations were gastrointestinal bleeding (n=91; 40.6%), ascites (n=75; 33.5%), and hepatic encephalopathy (n=72; 32.1%). Group B was more likely to present with multiple decompensations at admission and exhibited significantly higher rates of acute kidney injury, hepatocellular carcinoma, acute-on-chronic liver failure, and portal vein thrombosis (p<0.05). Following care bundle implementation, we found significant improvements in patient care. At admission, patients were significantly more likely to undergo urine and blood cultures, chest X-ray, and abdominal ultrasound (p<0.05), receive diagnostic paracentesis (p<0.05), and have an accurate alcohol history documented (p=0.04). During admission, Group-B was significantly more likely to be prescribed lactulose for encephalopathy prophylaxis, vasopressor therapy for gastrointestinal bleeding, and venous thromboembolism prophylaxis, as well as undergo nutritional assessment (p<0.05). While in-hospital mortality rates were similar (4.7% vs. 5.3%; p=1), 6-week mortality rates (8.8% vs. 3.9%; p=0.01) and 3-month readmission rates (31.1% vs. 15.8%; p=0.02) were significantly lower in the post-intervention cohort.

Conclusion

The implementation of a standardized care bundle was associated with higher rates of appropriate investigation and treatment within the first 24 hours of hospital admission and improved patient outcomes, reducing 6-week mortality and 3-month readmission rates.

Clinical Case Summary

A 58-year-old woman with no relevant medical history, presenting with progressive dysphagia and odynophagia over a 2-month period. Upper gastrointestinal endoscopy (UGE) revealed a circumferential lesion with a verrucous appearance and exophytic papillomatous component spanning from 20 to 30 cm from the dental arch. These lesions raised suspicion of malignancy; however, biopsies showed only hyperplastic mucosa with chronic inflammation. In an attempt to obtain histological documentation, additional UGE were performed, with repeat biopsies and macrobiopsy of one of the more exophytic components, all without confirmation of neoplasia by multiple pathologists. Immunohistochemistry showed positivity for p16. Additional imaging studies confirmed extensive and locally invasive neoplastic formation with nodal involvement, leading to an empirical diagnosis of verrucous carcinoma of the esophagus (VCE), prompting initiation of neoadjuvant chemoradiotherapy. Subsequently, exploratory thoracoscopy revealed unresectable disease. Palliative chemotherapy was initiated, and a repeat endoscopy shows regression of the lesion.
Discussion: VCE, an extremely rare variant of squamous cell carcinoma, presents with slow growth, local invasiveness, and rare nodal metastases. Although its exact etiology is uncertain, associations with chronic inflammation caused by factors such as smoking, reflux esophagitis, or alcoholism are reported. Human papillomavirus (HPV) infection has also been suggested as a potential contributor. Due to the proliferative nature of VCE, superficial biopsies often show nonspecific inflammatory changes, making diagnosis challenging. Despite the lack of confirmatory histopathology, the unique endoscopic findings, presence of p16 (associated with HPV-related carcinomas), and clinical deterioration led to the empirical diagnosis of VCE. This case highlights the diagnostic complexity and therapeutic challenge associated with this rare variant of esophageal carcinoma.

References

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• Cappellesso, R. et al. Human papillomavirus infection is not involved in esophageal verrucous carcinoma. Hum Pathol 85, 50–57 (2019).
• Tonna, J. et al. Esophageal verrucous carcinoma arising from hyperkeratotic plaques associated with human papilloma virus type 51. Diseases of the Esophagus 23, (2010).
• Ramani, C., Shah, N. & Nathan, R. S. Verrucous carcinoma of the esophagus: A case report and literature review. World Journal of Clinical Cases : WJCC 2, 284 (2014).
• Osborn, N. K., Keate, R. F., Trastek, V. F. & Nguyen, C. C. Verrucous carcinoma of the esophagus: Clinicopathophysiologic features and treatment of a rare entity. Dig Dis Sci 48, 465–474 (2003).
• Devlin, S., Falck, V., Urbanski, S. J., Mitchell, P. & Romagnuolo, J. Verrucous carcinoma of the esophagus eluding multiple sets of endoscopic biopsies and endoscopic ultrasund: A case report and review of the literature. Canadian Journal of Gastroenterology 18, 459–462 (2004).