Introduction
Esophageal varices frequently complicate liver cirrhosis and are commonly related to portal hypertension. Esophageal varices are graded in terms of size and severity.1 Placement of band ligation for the treatment of Grade 2 and greater esophageal varices is a mainstay of therapy and systemic non-selective beta-blocking agents.1 Complications of this common intervention include bleeding, esophageal ulcers, and very rarely esophageal obstruction, which will manifest clinically as dysphagia after the procedure.2
Case Report
A 78-year-old woman with a history of liver cirrhosis, diabetes mellitus, breast cancer, and hypertension presented to the hospital with abdominal pain and distention over several months. She reported weight gain, lower extremity edema, and fatigue. She denied nausea, vomiting, dysphagia, fever, chills, constipation, diarrhea, hematemesis, melena, and hematochezia. She reported accumulation of recurrent abdominal ascites requiring daily diuretic medications. She had no previous history of esophageal varices, hepatic encephalopathy, or other complications of advanced liver cirrhosis.
On physical examination, the patient was afebrile and chronically ill-appearing. Abdominal distention with a fluid wave and lower extremity swelling was noted. Complete blood count and chemistry panel were within normal limits except mild thrombocytopenia, 105 platelets x 109/L. Serum alanine transaminase and aspartate aminotransferase levels were normal. Serum bilirubin levels were normal. Serum albumin level was 3.1 g/dL. Prothrombin time was 17.1 seconds (range 10.0-13.0 seconds). Ascitic fluid analysis revealed ascites albumin level of 1.2 g/dL and 114 nucleated cells/mm3. Gram stain and culture were negative. Computed tomography of the abdomen and pelvis revealed a nodular liver, splenomegaly, and ascites.
An esophagogastroduodenoscopy (EGD) was performed to screen for esophageal varices. During the procedure, grade II esophageal varices were identified in the lower third of the esophagus, and two band ligatures were placed with complete eradication and deflation of varices (Figure 1A). Within 24 hours of the procedure, the patient complained of inability to tolerate oral intake, dysphagia, and nausea with vomiting. Her symptoms went on without improvement for five days of initial conservative management when repeat EGD was performed with the findings of esophageal obstruction and necrosis related to variceal banding (Figure 1B). Esophageal band ligatures were removed, and the esophageal stricture, related to necrosis and banding, was dilated to 15mm with a balloon dilator (Figure 1C). The patient tolerated clear liquids after the procedure and advanced her dietary intake without further complications. She was discharged home in stable condition with a plan for follow-up endoscopy within 4-6 weeks.
Discussion
Esophageal varices frequently complicate liver cirrhosis and are commonly related to portal hypertension.3 Placement of band ligation for the treatment of esophageal varices is a mainstay of therapy, in addition to systemic non-selective beta blocking agents.1 Band ligation of esophageal varix leads to local venous thrombosis followed by sloughing of necrosed tissue into the lumen within 2-3 days.3 This treatment aids in reducing variceal size and risk of future hemorrhage.4 Complications of band ligation include post-procedural pain, hemorrhage, esophageal ulcers, chronic strictures, and acute mechanical obstruction and necrosis of the esophagus.5
Twelve reported cases of esophageal obstruction after band ligature placement were found since the advent of the procedure in 1988.3–14 Review of reported cases reveals that patients are predominantly female, are asymptomatic prior to the band ligation, and typically develop symptoms of severe dysphagia within 1-21 days of the procedure (Table 1). All reported patients were found to have esophageal obstruction on repeat EGD.3–14 A minority responded to conservative management with nil per os, with the majority requiring removal of band ligatures and dilation of the esophagus. All patients could resume oral intake within 1-14 days of treatment initiation. None required surgical intervention, but one case was complicated by intramural esophageal dissection and bleeding.7
Esophageal obstruction should be suspected when dysphagia, odynophagia, inability to tolerate oral intake, and nausea with vomiting occur after band ligation. The pathophysiology involves necrosis of the esophageal mucosa surrounding the banded varix leading to obstruction of the lumen of the esophagus.13 Risk factors for this rare complication have not been identified. However, it may include placement of the band ligature close to the mucosa, which is already exhibiting signs of tissue compromise such as edema or necrosis.11 Other factors may include impaired lower esophageal sphincter function and esophageal motility after esophageal variceal ligation. Notably, dysphagia after esophageal band ligature placement may result from more benign causes such as esophageal spasm and dysmotility, which may be treated supportively.
In conclusion, esophageal obstruction is a rare complication that should be considered in patients who report dysphagia after esophageal variceal banding. Esophageal obstruction after esophageal variceal banding is likely related to mucosal necrosis and edema related to the band ligature. Treatment of esophageal obstruction and necrosis involves removing band ligatures and esophageal dilation if a stricture is present. Reported outcomes suggest that patients generally regain the ability to tolerate an oral diet after band ligatures are removed, as was the case with our patient.
Corresponding Author
Simran Gupta, MD
The Miriam Hospital, 164 Summit Avenue, Providence RI, 02906