Diverticula arising in the esophagus are mainly categorized as pulsion and traction diverticula [1]. Pulsion diverticula usually occur in elderly people and commonly seen in men. They almost always arise in the cervical esophagus and arise usually at a constant level, opposite the cricoids cartilage from the posterior esophageal wall at the pharyngo-esophageal junction. Initially the sac lies at the mid line behind the esophagus, as it gradually increases in size it protrudes to a side of the esophagus usually to the left side of esophagus. When the sac increases in size it descends inferiorly to the mediastinum and become intrathoracic. Pulsion diverticula are protrusions of wall or a part of the wall due to increase intraluminal pressure [1]. Traction diverticula occur due to cicatricial contraction of a chronic inflammatory process drawing the wall of the esophagus outward, giving a characteristic tent like appearance. They are commonly seen in mid esophagus contain all three layers of wall [1]. Diverticula are also categorized as true and false according to the contents of the diverticula wall. If the wall of the diverticula consists all three layers of the esophageal wall, it is considered a true diverticula. False diverticulum contains protrusion of mucosa and submucosa, without the involvement of muscle layer [2]. In 1887 Zenker and Ziemssen described a diverticula which is known as Zenker’s or pharyngo-esophageal diverticulum. Zenker’s diverticula is the commonest type of diverticula arise in the esophagus [1]. It is defined as a protrusion of mucosa through the posterior wall of the esophagus, at the transition of hypopharynx to the esophagus. Killans space is a triangular space between the oblique muscle fibres of the inferior constrictor muscle and the transverse muscle of the cricopharyngeus muscle. This potentially weak area allows the protrusion of the wall and formation of Zenker’s diverticula [3]. The Pathophysiology of developing the Zenker’s diverticulum is thought to be due to an in coordination between the contraction of pharyngeal musculature and relaxation of the cricopharyngeus muscle leading to increase intraluminal pressure and protrusion of esophageal wall through the Killan space [3]. Patients typically presents with dysphagia, regurgitation of undigested food, choking, borborygmi in the cervical region, cough, aspiration, halitosis and weight loss. Less commonly they can present with horseness of voice and malnutrition. On examination rarely a swelling can be felt (Boyce’s sign) [4]. Complications reported with zenker’s diverticula are aspiration pneumonia (30%), abscess formation, ulceration, perforation, fistula and rarely development of squamous carcinoma (0.48%) [4,5,2]. Diagnosis is made by upper esophageal contrast study. Contrast video fluoroscopy allows contrast monitoring of the swallowing mechanism and better identification of the diverticula compared to the single shot barium swallow study. Contrast study shows a contrast filled out pouch with smooth outline [4]. Loss of smooth interior contour indicates a possibility of developing a carcinoma. A malignant change of a diverticula commonly arise in the distal two thirds of the pouch. Appearance of diverticula in a barium study also can be simulated by a hypertrophied cricopharyngeas muscle which is known as transient diverticula and should not be named as a zenker’s diverticula unless its growth and symptoms progress [4]. Other differential considerations of Zenker’s diverticulum are strictures following caustic ingestion, plummer Vinson syndrome, cricopharyngeal achalasia, carcinoma of cervical esophagus [3]. Killian-Jamieson diverticula also named as proximal lateral cervical esophageal diverticula arise from the antero lateral wall of the esophagus and protrude through the Killan Jamieson space. This is smaller than the Zenker’s diverticula and rarely causes symptoms [6].