[Dacryocystorhinostomy as part of the interdisciplinary treatment of lacrimal duct]. / Dakryozystorhinostomie nach West in der interdisziplinären Behandlung von Tränenwegsstenosen.

INTRODUCTION AND METHODS: Epiphora, which leads to blurry vision, is the leading symptom for intra- and/or postsaccal lacrimal duct stenosis. Due to the anatomy of the tear duct system, which lies between the fields of ophthalmology and otorhinolaryngology, and due to newly available techniques in interventional radiology to diagnose and treat patients with intra- and postsaccal lacrimal duct stenosis, various methods for diagnosis and treatment are available. We report the results of 107 patients who underwent endonasal dacryocystorhinostomy (DCR) between 2005 and 2011. RESULTS: Prior to the DCR, dacryocystography was performed in 95 of the 107 patients. In 68 of these 95 cases, balloon dilatation was unsuccessful. Histological examination of 64 patients showed chronic inflammation in 61 patients, non-Hodgkin's lymphoma was diagnosed in 2 patients and aspergilloma in1 patient. Over a follow-up time of 6 months to a maximum of 7 years we revised 15 of 107 patients, due to reocclusion after removal of the stent. None of these patients showed recurrence of epiphora. DISCUSSION: In comparison to transcutaneous DCR, endonasal DCR has certain benefits: it is less invasive, no visible scars occur because of the endonasal approach, and the function of the lacrimal pump remains uneffected. Furthermore, the possibility of co-treatment of endonasal pathologies during DCR exists. We observed no serious adverse events in our study group and the success rate was similar to other studies.

[Basic diagnostics of tear duct diseases]. / Basisdiagnostik bei Tränenwegserkrankungen.

The two main reasons for tearing are epiphora and excess lacrimation. Epiphora is a result of a failure of tear drainage caused by mechanical obstruction or lacrimal pump failure. Lacrimation is excessive tearing caused by reflex hypersecretion. The goal of the basic examination is to distinguish between epiphora and lacrimation. The clinical history, palpation, inspection, diagnostic probing and syringing are sufficient to evaluate the function of the lacrimal drainage system or to determine location and extension of obstructions in most patients with epiphora. Numerous diagnostic tests are available and the most important tests and their interpretation are described.

Roles for tumor necrosis factor receptor p55 and sphingomyelinase in repairing the cutaneous permeability barrier.

Epidermal TNF expression increases in response to cutaneous permeability barrier disruption and wound healing. TNF signaling is mediated by acid and neutral sphingomyelinases (A- and N-SMase), which generate ceramide, an important regulator of proliferation, differentiation, and apoptosis. In the epidermis, ceramide is known to be an integral part of the extracellular stratum corneum (SC) lipid bilayers that constitute the permeability barrier of the skin. We show here that topical application of TNF after experimental injury to the SC of hairless mice (hr(-/-)) enhances barrier repair. In TNF receptor p55-deficient (TNF-R55-deficient) mice (hr(+/+)), cutaneous barrier repair was delayed compared with wild-type (hr(+/+)) or TNF-R75-deficient (hr(+/+)) animals. After barrier disruption in hairless (hr(-/-)) and wild-type (hr(+/+)), but not in TNF-R55-deficient (hr(+/+)) mice, the enzymatic activities of both A-SMase and N-SMase were significantly enhanced. Stimulation of SMase activities was accompanied by an increase in C(24)-ceramide levels. Most A-SMase activity in hairless mice (hr(-/-)) was found in the outer epidermal cell layers and colocalized in the lamellar bodies with A-SMase and sphingomyelin. Reduction of epidermal A-SMase activity by the inhibitor imipramine resulted in delayed permeability barrier repair after SC injury. Together, these results suggest that TNF-R55 signaling pathways contribute to cutaneous permeability barrier repair through SMase-mediated generation of ceramide.

[Botulinum toxin treatment for crocodile tears, spastic entropion and for dysthyroid upper eyelid retraction]. / Botulinumtoxin bei Uberfunktion der Tränendrüse, spastischem Entropium und Oberlidretraktion bei endokriner Orbitopathie.

After proximal facial nerve lesions, misrouting of nerve fibres may cause the phenomenon of crocodile tears. Transconjunctival injections of botulinum toxin in the palpebral part of the lacrimal gland are the treatment of choice. An initial dose of 2.5 U of toxin is recommended, and injections may be repeated after 6 months if symptoms reoccur. Botulinum toxin A is also a highly effective temporary treatment for involutional (spasmodic) entropion until surgery is performed. A dose of 10 U of botulinum toxin is injected in the pretarsal part of the lower lid near the eyelashes. Botulinum toxin treatment is also effective for dysthyroid upper eye lid retraction, especially in instable thyroid disease or mild retraction. Slight transient ptosis may occur in some cases. Depending on the amount of retraction, a dose of 5 or 7.5 U of toxin is injected into the subconjunctival space at the superior margin of the tarsal plate.