Small incision transcutaneous levator aponeurotic repair for blepharoptosis

PURPOSE: Patients presenting with blepharoptosis due to disinsertion or thinning of the levator aponeurosis require surgical repair. A minimally invasive approach directed specifically at the levator aponeurotic anatomic defect may provide benefits to the patient. Proposed advantages of a small eyelid incision (8-13 mm) include less local anesthetic and tissue distortion, less ecchymosis and edema, decreased operative times, a shortened recovery period, and improved surgical results. We describe our results with the use of a small incision ptosis repair in select patients. SUBJECT AND METHODS: A retrospective chart review between January 2000 and September 2001 included 91 patients and 118 eyelids with blepharoptosis due to aponeurotic disinsertion, corrected by a minimally invasive approach. The small incision technique comprised levator aponeurotic resection and advancement. Pre- and postoperative upper eyelid marginal reflex distances (MRD1), eyelid contour, need for reoperation, and complications (overcorrection, undercorrection, hematoma, and infection) were recorded. RESULTS: The average preoperative MRD1 measured 0.5 +/- 1.1 mm, with a range of -2.0 to 2.5 mm. The average postoperative MRD1 measured 2.6 +/- 0.8 mm, with a range of 1 to 5.5 mm (P < 0.0001). Of the 118 eyelids corrected by a small incision technique, there were 4 overcorrections, 3 undercorrections, 1 failure, 1 postoperative ptosis procedure of the contralateral upper eyelid secondary to Hering's law ptosis, and 4 patients requesting surgical treatment of dermatochalasis. No symptomatic dry eye, exposure keratopathy, or other complication resulted in association with the overcorrections. No contour abnormalities, infections, hematomas, or other complications were noted. CONCLUSION: Our experience suggests that utilization of a small skin incision is safe, precise, and efficient and allows for more rapid recovery from surgery. The authors note a decreased incidence of reoperation and postoperative complaints compared with historical larger-incision cases.     

Etiology and pathogenesis of pouchitis

Restorative proctocolectomy with ileal pouch-anal anastomosis (IPAA) is the preferred surgery for ulcerative colitis (UC) and familial adenomatous polyposis (FAP). While this surgical therapy is effective and results in good clinical outcomes and quality of life, patients experience complications, the most common of which is pouchitis. While most pouchitis is considered idiopathic, there is mounting evidence that pouchitis results from aberrant immune response to the bacterial populations found in the pouch in a genetically predisposed patient. Dysbiosis and decreased diversity of the microbiota seem to contribute to this process. Risk factors for pouchitis including inflammatory bowel disease and obesity provide further clues to the etiology of pouchitis. In conclusion, we seek to understand the pathogenesis of pouchitis as both a post-operative complication and a form of inflammatory bowel disease (IBD).     

Etiology and pathogenesis of spondyloarthritides

Seronegative spondyloarthritides are inflammatory rheumatic diseases which are classified together because of numerous common and similar clinical, epidemiologic and genetic characteristics. Pathogenesis of seronegative spondyloarthritides is usually described as development of clinical characteristics of the disease in genetically susceptible person in the presence of favorable environmental factors. Development of seronegative spondyloarthritides, notably ankylosing spondylitis, is strongly connected with presence of the HLA-B27 gene. There are clear evidence that HLA-B27 positive individuals have significantly higher risk for disease development. The role of infection in occurence of seronegative spondyloarthritides is not completely understood--its role is better clarified in the case of reactive arthritis than in ankylosing spondylitis. The relation between HLA-B27 gene and infection is not clarified. Molecular mimicry theory is based on similarities between HLA-B27 molecule and microbial particle.     

Upgaze eyelid position allows differentiation between congenital and aponeurotic blepharoptosis according to the neurophysiology of eyelid retraction

To differentiate between congenital and aponeurotic blepharoptosis, we investigated whether upgaze with stretching of the mechanoreceptor of Mueller muscle increases involuntary reflex contraction of the levator slow-twitch muscle fibers.In 50 cases each of unilateral congenital blepharoptosis and of asymmetric aponeurotic blepharoptosis, the mean increases by upgaze in the upper eyelid margin to the line between the medial and lateral canthi as upper eyelid retraction distance (UERD) of the ptotic eyelid 0.4 mm and 2.9 mm, respectively. These were significantly smaller and significantly larger than those of the corresponding nonptotic eyelid, 2.0 mm and 2.3 mm, respectively.Worsening of ptosis on upgaze is common in congenital ptosis and is an abnormal differentiating sign, lacking the involuntary reflex contraction. Improvement of ptosis on upgaze is common in aponeurotic blepharoptosis and likely represents a normal physiological process, restoring the involuntary reflex contraction.     

Restoration of involuntary tonic contraction of the levator muscle in patients with aponeurotic blepharoptosis or Horner syndrome by aponeurotic advancement using the orbital septum.

Müller's muscle can be thought of as a large serial type of muscle spindle of the levator muscle. Effective stretching of the mechanoreceptor in the proximal part of Müller's muscle by voluntary phasic contraction of the levator muscle for initial opening of the eye induces involuntary tonic contraction of the levator muscle as a stretch reflex via the mesencephalic trigeminal nucleus, to maintain an adequate visual field. After disinsertion of the levator aponeurosis from the tarsus by habitual rubbing, elongation of Müller's muscle secondary to thinning (aponeurotic blepharoptosis) or paralysis (Horner syndrome) desensitises the mechanoreceptor of Müller's muscle, resulting in blepharoptosis. Shortening of the elongated and thinned Müller's muscle by instillation of phenylephrine, and surgical shortening, and fixation of the disinserted, elongated, and thinned aponeurosis using the orbital septum, restored involuntary tonic contraction of the levator muscle in nearly all of 2000 patients with aponeurotic blepharoptosis and in 11 patients with Horner syndrome.     

慢性胰腺炎的病因和发病机制

慢性胰腺炎可由多种因素所致,以胰腺组织结构的进行性、不可逆性损害和内外分泌功能不全为主要表现。胰腺纤维化为其典型的病理学改变,临床表现有反复发作的腹痛及胰腺内、外分泌功能不全等。与慢性胰腺炎相关的病因及危险因素主要包括胆石病、酗酒、遗传因素、自身免疫因素等,其发病机制仍不甚明确,临床中慢性胰腺炎的发生更是多种病因、多种发病机制共同作用的结果。进一步研究慢性胰腺炎的具体病因及发病机制,对预防和治疗慢性胰腺炎具有重要意义。     

Etiology and pathogenesis of Mallory-Weiss syndrome

Treatment results of 405 patients with Mallory-Weiss syndrome, X-ray gastric investigation in patients with severe bloating reflex were analyzed. Experimental part of the study involved rats and pigs, modeling esophageal and gastric rupture. Cardioesophageal and gastric cardial rupture happen in case of simultaneous sudden intragastric and intraabdominal hypertension, following the rule of Laplace.     

Etiology and pathogenesis of overactive bladder

The symptom complex??overactive bladder?? (OAB) affects more than 10% of adult individuals. The etiopathology is complex and multifactorial. Foremost, urinary tract infection, bladder cancer, foreign bodies, and history of radiation or intravesical instillation of chemotherapeutics must be excluded. In many cases, OAB is caused by neurogenic disorders that activate involuntary detrusor contractions (detrusor overactivity, DO). Also, non-neurogenic disorders such as bladder outlet obstruction or dysfunctions of the female pelvic floor/slack ligaments that affect the urothelium, suburothelium, detrusor and bladder afferents are substantially involved in the pathogenesis of OAB. Until now, circulatory disorders have not been adequately taken into consideration but seem to be another etiological factor that causes OAB. Henceforth, molecular changes of bladder afferents and circulatory disorders in patients suffering from OAB have to be investigated in more detail.     

对胰性脑病病因和发病机制的认识

胰性脑病作为重症急性胰腺炎发展到一定阶段产生神经精神障碍的综合症 ,一直受到临床医师的关注。 194 1年首次由Ｒｏｔｈｅｒｍｉｃｈ[1] 提出胰性脑病的概念 ,发现 8例急性胰腺炎病人出现精神和神经异常 ,定向力障碍、激动、妄想、幻觉甚至意识模糊 ,其中 5例病人脑组织病理切片显示散在瘀斑、小出血灶、神经轴突脱髓鞘等改变。然而对胰性脑病的病因和发病机制至今尚不明确 ,有多种假说予以解释 ,认为本病可能与胰酶、真菌感染、电解质紊乱、维生素缺乏、酒精中毒、低氧血症等有关。以下综述胰性脑病的可能病因和发生机制 ,希望对胰性脑病…