Manometric aspects of Zenker's diverticulum.

Zenker's diverticulum is thought to result from disordered coordination between the pharynx and upper esophageal sphincter. Manometric studies of the upper esophagus have been helpful in testing the hypothesis of dysmotility in the formation and growth of a Zenker's diverticulum; however, the data have provided conflicting evidence. Manometric studies show that resting upper esophageal sphincter pressure is normal in some patients with Zenker's diverticulum and decreased in others. Abnormal premature relaxation and contraction of the upper esophageal sphincter seen in some patients with Zenker's diverticulum may be accompanied by pharnygeal contractions against a closed sphincter. This abnormality is thought by some investigators to be the cause of Zenker's diverticulum, but not by others who have found normal upper sphincter relaxation. Future manometric studies will very likely elucidate the pathogenesis of Zenker's diverticulum.     

Radiological aspects of Zenker's diverticulum.

In a retrospective study of 143 patients with Zenker's diverticulum followed for a period of 20 years, we classified the diverticula into 4 categories (A, B, C and D) using Brombart's scheme as a basis; the difference between the first two categories, however, was made on the basis of a morphological-dynamic criterion rather than a purely morphological one. Furthermore, a quantitative index was introduced to define the size of the diverticulum. In two cases we noted a substantial increase in volume with the transition from category C to D after more than 3 years, but we were unable to demonstrate an evolution from category A to B, nor from B to C. Our study confirms, on a large scale, the presence of three possible pathogenetic mechanisms, as proposed earlier in the literature: decreased relaxation of the upper esophageal sphincter as the most frequent factor in all categories except category A, and delayed opening or early closing of this sphincter as less frequent factors. The good relaxation of the upper esophageal sphincter in our category A, the different sex ratio and the absence of evolution in this category suggest that category A does not necessarily evolve further.     

Zenker's diverticulum and reflux.

The interrelationship between gastroesophageal reflux and Zenker's diverticulum remains unclear. The view that cervical diverticula are induced by gastroesophageal reflux disease (GER) is apparently supported by epidemiologic observations indicating that they occur only in populations with a high incidence of GER. However, it is difficult to prove causality on the basis of currently available physiological and pathophysiological investigations. The few data published to date now end to support a cryptogenic change in upper esophageal sphincter (UES) muscle motility characteristics instead of a reflux induced lesion to the UES. Clinical experience also shows that GER does not play a major role in individual cases of Zenker's diverticula, nor do many surgeons consider it a risk following cervical myotomy. This is confirmed by a very low complication rate even in large series of patients in whom no attempt was made preoperatively to rule out concomitant reflux disease. In conclusion, some facts suggest that reflux disease may be a cause of the development of Zenker's diverticulum. In the majority of cases, however, autochtonic structural lesions to the UES muscle fibers or other, as yet unknown, reasons are more probable.     

Pharyngoesophageal (Zenker's) diverticulum: a reappraisal

Manometric evaluation of pharyngeal contraction and upper esophageal sphincter relaxation was performed in a group of patients with Zenker's diverticulum using a specially designed low compliance manometric recording system. The results were compared with those in normal controls. In all cases, the upper esophageal sphincter showed complete relaxation during swallowing and no incoordination between pharyngeal contraction and upper esophageal sphincter relaxation could be demonstrated compared to time intervals found in the control group. Resting upper esophageal sphincter pressures were significantly lower in diverticulum patients than in controls. It is concluded that symptomatic patients with Zenker's diverticulum have normal pharyngeal-upper esophageal sphincter coordination, exhibit complete upper esophageal sphincter relaxation on swallowing, and have low resting upper esophageal sphincter pressures. These results seriously question the previous concept of abnormalities of pharyngeal-upper esophageal sphincter coordination in patients with Zenker's diverticulum.     

Pathogenesis and endoscopic treatment of the hypopharyngeal (Zenker's) diverticulum

The authors review the literature about the pathogenesis -still unknown- of Zenker's diverticulum as well as their experience of endoscopic treatment of this disease. From 1964 till 1988, they have treated endoscopically 507 patients, 323 by electrocoagulation, 184 by CO2-laser. The endoscopic procedure is described, consisting in precise division of the tissue bridge between the oesophagus and the diverticulum by micro-endoscopic surgery under general anesthesia. In recent years, the CO2-laser was found preferable, since it may cause less tissue necrosis and consequently less fibrous scar tissue. The results were very favourable, with more than 99% of the patients satisfied. Although many patients were old and in poor condition, only one patient died two days after operation because of cardiac failure. Complications such as bleeding, emphysema, mediastinitis and stenosis were seen in 5% of the patients, but in most cases there complications were mild and conservative therapy was sufficient. Stenosis occurred in 8 patients treated by electrocoagulation and in none of the patients treated by laser. Microendoscopic surgery is a safe and efficient method of therapy for the hypopharyngeal diverticulum.     

Flexible endoscopic and surgical management of Zenker's diverticulum

Zenker's diverticulum is an outpouching of the mucosa through the Killian's triangle. The etiology of Zenker's diverticulum is not well understood. It is thought to be due to the incoordination or incomplete relaxation of the cricopharyngeal muscle. Most patients are men who present with symptoms of dysphagia between the seventh and eighth decades of life. The diagnosis is made with a dynamic contrast swallowing study. Treatment options include open surgical diverticulectomy and diverticulopexy with myotomy or myotomy alone using flexible or rigid endoscopes. Rigid endoscopic treatment is currently the preferred initial choice for Zenker's diverticulum of any size. The flexible endoscopic technique is used when there is a high risk of general anesthesia, or neck extension is contraindicated. Some centers use flexible endoscopy as the initial treatment option. Due to a lack of prospective studies, the treatment choice should be tailored to the individual patient and local expertise.     

Endoscopic treatment of the hypopharyngeal (Zenker's) diverticulum.

Over the years the techniques for endoscopic treatment of Zenker's diverticulum have been improved. Initially, in 1964, we used the electrocoagulation technique as described by Dohlman, but currently we prefer to sever the tissue bridge between the diverticulum and esophagus with the CO2 laser under microscopic control. The results of endoscopic treatment in 507 patients with a diverticulum are discussed. It is concluded that endoscopic treatment can readily be performed with good results, especially in the case of elderly patients in a poor general condition.     

Zenker's diverticulum. The clinical manifestations and treatment]

Clinical manifestations and surgical results are analyzed in a retrospective study of 16 patients with a Zenker's diverticulum. Pharyngoesophageal diverticulum are an uncommon anomaly, producing cervical dysphagia and recurrent airway infections. Treatment should be surgical, as earliest as possible. Morbidity is very low and mortality very rare.     

Clinical, diagnostic, and therapeutic aspects of familial hypercholesterolemia

Heterozygous familial hypercholesterolemia (FH) is a common inherited disorder of lipoprotein metabolism. FH is characterized by elevated levels of low-density lipoprotein cholesterol, the presence of tendon xanthomas, and premature cardiovascular disease. The underlying molecular defect of FH consists of mutations in the gene coding for the low-density-lipoprotein-receptor protein, detection of which provides the only unequivocal diagnosis. Although the cause of FH is monogenic, there is wide variation in the onset and severity of atherosclerotic disease in these patients. Additional atherogenic risk factors of environmental, metabolic, and genetic origin are presumed to influence the clinical phenotype in FH. Criteria used to identify individuals with FH include a combination of clinical characteristics, personal and family history of early coronary artery disease, and biochemical parameters. Since the introduction in 1989 of statins, which have been shown to be effective and to delay or prevent the onset of cardiovascular disease, drug treatment of FH has greatly improved. New lipid-lowering agents are presently being developed for clinical use. This review provides an update on the clinical, diagnostic, and therapeutic aspects of heterozygous familial hypercholesterolemia.     

Clinical, immunologic and therapeutic aspects of endangiitis obliterans

In the period of 1975-1983 twenty-three patients with thromboangiitis obliterans were examined at the Surgical Clinic of the Medical Academy of Magdeburg. The diagnosis was established clinically, angiographically histologically and immunologically. In 7 out of 12 patients histology revealed inflammatory vascular alterations including lymphocyte infiltrates throughout the entire vessel wall and also in the perivascular area. Immunohistology showed in 10 out of 15 patients segmental granular fluorescence identifiable as deposits of IgM and IgG. In 6 cases a complement formation was found. The endangiitis group revealed more frequent and increased immune complexes concentrations. Circulating immune complexes were established by phase-locked radio-immunoassay. The therapy is depended on the localization of the obliteration and can be a lumbar sympathectomy or a vascular reconstruction.     

Surgical therapy of Zenker's diverticulum: Low risk and high efficiency

Surgery for the treatment of Zenker's diverticulum was performed at our institution in a total of 43 patients over 6½ years. Cervical myotomy with diverticulectomy was performed in 32 of the patients and myotomy alone in 11. Mortality totaled 0%, with a reversible lesion of the recurrent nerve occurring in 7%. In 60% of the cases investigated preoperatively (N=40), motility disorders of the upper esophageal sphincter (UES) could be demonstrated using manometry as well as with cineradiography in 92% of the patients. Follow-up studies in 39 of the cases 25 months (mean) postprocedure indicated 82% of the patients to be symptom-free, with the remaining 18% demonstrating a marked improvement. Postoperative manometry as well as cineradiography carried out in 12 patients revealed the presence of UES motility dyscoordination in 8% and 25%, respectively. There were, however, no signs of recurrence of the diverticulum. The high number of patients in our study group demonstrating motility disorders of the UES emphasizes the need for cervical myotomy as part of the surgical therapy for Zenker's diverticulum.     

Pharyngeal (Zenker's) diverticulum is a disorder of upper esophageal sphincter opening.

Pharyngeal coordination, sphincter opening, and flow pressures during swallowing were investigated in patients with pharyngeal (Zenker's) diverticula. Fourteen patients with diverticula and 9 healthy age-matched controls were studied using simultaneous videoradiography and manometry. Pharyngeal and upper esophageal sphincter pressures were recorded by a perfused side hole/sleeve assembly. Temporal relationships among swallowing events, extent of sphincter opening during swallowing, and intrabolus pressure during bolus passage across the sphincter were measured. The timing among pharyngeal contraction and sphincter relaxation, opening, and closure did not differ between patients and controls. Sphincter opening was significantly reduced in patients compared with controls in sagittal (P = 0.0003) and transverse (P = 0.005) planes. Manometric sphincter relaxation was normal in patients. Intrabolus pressure was significantly greater in patients than in controls (P = 0.001). It is concluded that Zenker's diverticulum is a disorder of diminished upper esophageal sphincter opening that is not caused by pharyngosphincteric incoordination or failed sphincter relaxation. Incomplete sphincter opening is likely to cause dysphagia. Increased hypopharyngeal pressures during swallowing are probably important in the pathogenesis of the diverticulum.     

Clinical, microbiologic and therapeutic aspects of purulent pericarditis.

Twenty-six patients with purulent pericarditis were seen at the Massachusetts General Hospital between 1960 and 1974. The diagnosis was made in 18 of them during life, but only 6 survived, with an over-all mortality rate of 77 per cent. In eight patients, purulent pericarditis developed in the early postoperative period after thoracic surgery. In seven, purulent pericarditis was the result of contiguous spread of infection from a pleural, mediastinal or pulmonary focus in nonsurgical patients. In five patients, it was the result of direct spread to the pericardium from an intracardiac infection. In the remaining six patients, purulent pericarditis developed as the result of a systemic bactermia. Immunosuppressive therapy, extensive thermal burns, lymphoproliferative disease and other systemic processes affecting host resistance were present in at least half the patients. Staphylococcus aureus was the etiologic agent in the largest number of patients (8 of 26 in this report). However, in contrast to previous studies, in a significant number of the patients (five), purulent pericarditis was the result of fungal infection (in three patients subjected to thoracic surgery and in two immunosuppressed patients). This report confirms that purulent pericarditis is an acute disease with a fulminant course. The diagnosis is easily missed since classic signs of pericarditis (including chest pain, friction rub and diagnostic electrocardiographic abnormalities) may be absent. The echocardiogram shows considerable promise in allowing earlier diagnosis of the pericardial effusion which accompanies purulent pericarditis. Optimal therapy consists of prolonged antibiotic therapy and aggressive drainage of the pericardium. In this series, there were 6 survivors among the 11 patients (55 per cent) who received appropriate therapy.