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Objectives To prospectively determine the incidence of venous thromboembolism (VTE) following major head and neck surgery. At the midpoint of enrollment, an interim analysis was performed to determine if it was ethical to continue this study as an observational study without routine anticoagulation. Design Prospective, observational cohort study. Setting Academic surgical center. Patients The interim analysis comprised 47 subjects. Main Outcome Measure The total number of new cases of VTE (superficial and deep) identified within 30 days of surgery and confirmed on diagnostic imaging. These cases were further categorized as clinically relevant and nonclinically relevant. Clinically relevant VTEs were those requiring more than 6 weeks of anticoagulation or were associated with any negative impact on clinical course. On postoperative day 2 or 3, subjects were clinically examined and received duplex ultrasonography. Subjects with negative findings from examination and ultrasonography were followed up clinically; subjects with evidence of deep venous thrombus or pulmonary embolism were given therapeutic anticoagulation. Subjects with superficial VTE received repeated ultrasonography on postoperative days 4 to 6. Subjects were monitored for 30 days after surgery. Results Three subjects (6%) were identified as having clinically significant VTE: 2 cases of deep venous thrombus and 1 case of pulmonary embolism. Two additional subjects had lower extremity superficial VTE without clinical findings, which were detected by ultrasonography alone. No statistically significant differences were seen between patients with VTE and those without VTE. Conclusions This interim analysis of the first prospective study of the incidence of VTE in patients with head and neck cancer showed a VTE rate slightly higher than previously estimated in retrospective studies. There have been no unexpected serious adverse events and no rationale for early termination of the study.

Methods: Patients were identified as being referred for cough between 2005 and 2010. Initial consultation and clinical encounters were reviewed and diagnostic studies/therapies recorded. Findings on diagnostic studies were noted if they aided in treatment. Response to therapies was determined by reviewing clinical encounter documentation and therapies were rated: no response, partial response, or complete response.

INTRODUCTION: Distortion of esophagogastric junction (EGJ) architecture, caused by repeated proximal gastric distention, creates susceptibility to GERD; the end result is permanent dilation of the gastric cardia which is directly proportional to disease severity, with the largest circumference present in those with Barrett's esophagus (BE). Because of their propensity to reflux in the upright position, it is unclear whether cardia dilation with resultant anatomic valve deformation is also present in patients with laryngopharyngeal reflux (LPR) symptoms. METHODS: In a prospective study, 113 patients recruited from ENT (N=87) and Gastroenterology Clinics (N=26) underwent unsedated upper endoscopy in the upright position after completing validated questionnaires for GERD and LPR symptoms. Exclusions were made for a poor endoscopic view of the gastric cardia. Three populations were stratified based on symptom complex: 1) LPR symptoms only (Pure LPR), 2) Typical GERD symptoms only (GERD), and 3) Both LPR and typical GERD symptoms (Mixed). The primary outcome was cardia circumference (mm) as measured by an observer blinded to symptom complex using previously validated software. The secondary outcome was the prevalence of biopsy proven BE within each group as a proxy for disease severity and cancer risk. RESULTS: The Pure LPR group (N=32) had a mean gastric cardia circumference of 33.6 ± 7.3 mm. Similarly, the values in GERD (N=41) and Mixed (N=40) groups were 36.5 ± 9.6mm and 35.1 ± 8.0 mm, respectively (p=0.347, One Way ANOVA). Hiatal hernia size positively correlated with cardia circumference (r=0.219, p=0.02, Pearson's). The overall prevalence of BE was 20.4%. BE was present in 15.6%, 34.2%, and 10.0% of Pure LPR, GERD, and Mixed patients, respectively (p

44-YEAR-OLD man presented with a 1year history of progressive right-sided hearing loss that developed after a syncopal episode during which he suffered blunt trauma to his occiput. He was unconscious briefly and was taken to the emergency department for evaluation. On arrival, he noted complete deafness in the left ear and marked hearing loss in the right ear, with tinnitus bilaterally. At that time, he denied vertigo. The physical examination was significant for hemotympanum in the left ear, with scant blood in the external auditory canal, no cerebrospinal fluid leak, normal facial strength, and a wide-based gait. A computed tomographic (CT) scan showed intraparenchymal hemorrhages in the frontal and temporal lobes bilaterally with associated edema and a right temporal subdural hematoma. Audiologic testing demonstrated profound hearing loss in the left ear and moderately severe sensorineural hearing loss (SNHL) in the right ear, with a speech discrimination score of 96% and a threshold of 60 dB. The patient received a short course of prednisone for presumed right auditory nerve traction, with modest improvement in his hearing. One year after the injury, the patient was referred to our clinic for fluctuating right-sided hearing loss. The patient reported that his hearing loss remained profound in the left ear and was worsening in a stepwise pattern in the right ear. His tinnitus persisted (greater in the left ear than in the right), and anosmia and dysgeusia had developed soon after the fall. He also complained of disequilibrium, which had improved with vestibular rehabilitation exercises. He reported no other syncopal events or neurologic symptoms. He had no significant history of noise exposure. He denied recent use of ototoxic agents and was taking no prescribed medications. The findings of a review of systems were noncontributory, and the results of otoscopy were normal. Audiologic testing showed a sloping moderate to profound right-sided SNHL, with a speech discrimination score of 30% (speech reception threshold, 65 dB); tympanometry revealed no abnormalities. Vestibular testing showed signs of persistent left vestibular hypofunction. The CT scans of the left temporal bone that were obtained immediately after the injury occurred are shown in the Figure. The right side was noted to have an enlarged vestibular aqueduct that was consistent with a congenital variation, but was otherwise normal. What is your diagnosis?