Management of esophageal perforation after pneumatic dilation for achalasia.

Current management of esophageal perforation after pneumatic dilation for achalasia is thoracotomy and repair with myotomy. This study aims to assess the outcome of patients managed by laparotomy, and the role of laparoscopic repair. The study was carried out by means of retrospective case review and prospective follow-up with a symptom questionnaire. Results were compared with results in patients undergoing elective Heller myotomy. Over a 20-year period, 445 dilations for achalasia were performed in 371 patients. There were 10 esophageal perforations. Nine patients were referred for surgery and were successfully managed with a transabdominal repair. Laparoscopic repair was attempted in four patients but was successful in only one because of the perforation site. After a mean follow-up of 5.4 years, grade 1 or 2 Visick scores were recorded in all patients. Residual symptoms of dysphagia occurred in 67% in the emergency group and 88% in the elective group. There was an increased incidence of heart-burn compared to elective myotomy. Early operation after perforation provides good results for treatment of achalasia. Mild dysphagia persists and there is an increasing sensation of heartburn. The site of perforation is typically posterolateral, which makes laparoscopic repair difficult.

Predictors of outcome following cricopharyngeal disruption for pharyngeal dysphagia.

The indications for, and predictors of outcome following cricopharyngeal disruption in pharyngeal dysphagia are not clearly defined. Our purpose was to examine the symptomatic response to cricopharyngeal disruption, by either myotomy or dilatation, in patients with oral-pharyngeal dysphagia and to determine pre-treatment manometric or radiographic predictors of outcome. Using simultaneous pharyngeal videoradiography and manometry, we studied 20 patients with pharyngeal dysphagia prior to cricopharyngeal dilatation (n = 11) or myotomy (n = 8), and 23 healthy controls. We measured peak pharyngeal pressure, hypopharyngeal intrabolus pressure, upper esophageal sphincter diameter, and coordination. Response rate to sphincter disruption was 65%. The extent of sphincter opening was significantly reduced in patients compared with controls (p = 0.004), but impaired sphincter opening was not a predictor of outcome. Increased hypopharyngeal intrabolus pressures (> 19 mmHg for 10 ml bolus; > 31 mmHg for 20 ml bolus) was a significant predictor of outcome (p = 0.01). Neither peak pharyngeal pressure nor incoordination were predictors of outcome. In pharyngeal dysphagia, hypopharyngeal intrabolus pressure, and not peak pharyngeal pressure, is a predictor of response to cricopharyngeal disruption. The relationship between intrabolus pressure and impaired sphincter opening is an indirect measure of sphincter compliance which helps predict therapeutic response.

Mechanisms of oral-pharyngeal dysphagia in patients with Parkinson's disease.

BACKGROUND & AIMS: Oral-pharyngeal dysphagia in Parkinson's disease is well recognized. The aim of this study was to establish the mechanisms of oral-pharyngeal dysphagia in these patients. METHODS: Using simultaneous videoradiography and pharyngeal manometry, we studied 19 patients with Parkinson's disease (12 with oral-pharyngeal dysphagia and 7 without oral-pharyngeal dysphagia) and compared them with 23 healthy controls. RESULTS: the clinical severity of Parkinson's disease predicted neither the presence nor the severity of dysphagia. Minor alterations in oral function were common in controls and patients, but pharyngeal dysfunction was significantly more prevalent in patients. Incomplete upper esophageal sphincter (UES) relaxation was present in 4 patients (21%), all of whom showed increased hypopharyngeal intrabolus pressure, but not all of whom had a diminished UES opening. The patients had a reduced UES diameter (P = 0.004) and a higher intrabolus pressure compared with the controls (P = 0.007). Pharyngeal contraction pressures were lower in patients, but 6 patients with dysphagia and an abnormal pharyngeal wall motion had normal peak pressures. CONCLUSIONS: An incomplete UES relaxation and a reduced UES opening, both associated with high intrabolus pressure, are prevalent in Parkinson's disease. Oral-pharyngeal dysphagia in Parkinson's disease is multifactorial, with the majority of patients showing oral and pharyngeal dysfunction, even before the clinical expression of dysphagia. Impaired pharyngeal bolus transport is the major determinant of dysphagia.

Influence of cold stimulation on the normal pharyngeal swallow response.

We examined the potential influence of cold stimulation of the anterior tonsillar pillars, before and after topical anesthesia, on the temporal linkage between the oral and pharyngeal components of the swallow. We hypothesized that if elicitation of the pharyngeal swallow were dependent upon stimulation of faucial mucosal receptors this response would be facilitated by cold tactile stimulation and inhibited by topical anesthesia. In 14 healthy volunteers undergoing simultaneous videoradiography and manometry we measured and compared regional transit and clearance times, and the timing of hyoid motion, upper esophageal sphincter relaxation, and opening within the swallow sequence. There was a significant, volume-dependent forward shift in timings of hyoid motion, upper esophageal sphincter (UES) relaxation profile, and opening which were influenced neither by cold stimulation nor topical anesthesia. Regional transit and clearance times and UES coordination were not influenced by cold stimulation. Pharyngeal clearance time was prolonged by tonsillar pillar anesthesia due to earlier arrival of the bolus head at this region (p = 0.002). We conclude that the normal pharyngeal swallow response is neither facilitated nor inhibited by prior cold tactile stimulation or topical anesthesia to the tonsillar pillars, respectively. These observations do not support the hypothesis that elicitation of the pharyngeal swallow response is dependent upon stimulation of mucosal receptors in the tonsillar arches.

Esophageal achalasia and coexistent upper esophageal sphincter relaxation disorder presenting with airway obstruction.

Acute airway obstruction associated with esophageal achalasia is an uncommon but life-threatening complication. The pathophysiology of this phenomenon has not been fully defined. A fully documented case of coexistent esophageal achalasia and upper esophageal sphincter relaxation abnormality presenting with airway obstruction is reported. The patient was initially treated with Heller's myotomy but had a recurrence of respiratory distress. She was successfully treated by cricopharyngeal myotomy. The causes of gas entrapment and respiratory distress are likely to be due to failure of both swallow- and distention-induced upper esophageal sphincter relaxation. Cricopharyngeal myotomy is an effective treatment for this complication, probably by facilitating esophagopharyngeal gas venting.

Influence of mucosal receptors on deglutitive regulation of pharyngeal and upper esophageal sphincter function.

The potential influence of mucosal sensory receptors on the regulation of oral-pharyngeal swallow events was studied in 15 healthy volunteers using simultaneous videoradiography and manometry. We determined the effects of selective pharyngeal and oral plus pharyngeal anesthesia on the following temporal and manometric measures in response to liquid and viscous swallows: regional transit and clearance times; motion of hyoid and larynx; upper esophageal sphincter relaxation, opening, and closure; and pharyngeal contraction wave characteristics. Under the influence of mucosal anesthesia no subjects demonstrated aspiration during deglutition. Neither regional transit and clearance times nor pharyngosphincteric coordination was influenced significantly by pharyngeal mucosal anesthesia or oral plus pharyngeal anesthesia. Although midpharyngeal and distal pharyngeal contraction amplitudes were not influenced by mucosal anesthesia, midpharyngeal contraction wave duration was reduced significantly by both pharyngeal (P = 0.02) and oral plus pharyngeal anesthesia (P = 0.0005). We conclude that 1) neither elicitation of the pharyngeal swallow response nor temporal regulation among swallow events is dependent on mucosal sensory receptors and 2) duration of the pharyngeal contraction is influenced by sensory input from the oral-pharyngeal mucosa.