Voice prosthesis insertion after endoscopic balloon-catheter dilatation in case of a stenotic hypopharyngo-oesophageal junction

Stenosis of the hypopharyngo-oesophageal junction can be a rare complication of laryngectomy and/or partial pharyngectomy and makes the insertion of voice prosthesis extremely difficult. This study describes the authors’ experiences gained by endoscopic balloon-catheter dilatation of hypopharyngo-oesophageal stenoses prior to implantation of voice prostheses in four cases. In two patients a single balloon-catheter dilatation resulted in wide enough pharyngo-oesophageal lumen on the long run. The average prosthesis wearing-times were 6.8 months in case 1 and 4.6 months in case 2, corresponding to the published literature data. In case 3, repeated dilatation of the pharyngo-oesophageal transition had proved to be unsuccessful despite taking every effort with the endoscopic balloon-catheter method. Having excised the stenotic segment, reconstruction with pectoralis major myocutaneous flap (PMMF) was indicated. Eighteen months later, a repeated restenosis was observed and a free jejunal flap needed to be performed as a final solution. In case 4, the insertion was carried out into a previously dilated jejunal free flap, which became gradually ischemic and stenotic since the major head-and neck procedure was carried out that resulted in prosthesis rejection after just 1 week. The authors emphasize that correct indication of pedicled and free flaps in head and neck reconstruction is a prerequisite from the aspect of prevention of pharyngo-oesophageal strictures. Endoscopic balloon-catheter dilatation is a safe and established method for dilatating hypopharyngo-oesophageal stenoses of different origin. The procedure provides maximum patient benefit with minimal trauma and morbidity; moreover, facilitates insertion of voice prostheses. However, a single balloon-catheter dilatation cannot always result in wide enough oesophageal lumen on the long run (case 3). Insertion of a voice prosthesis into a previously dilated ischemic jejunal segment is challenging and avoidable due to risks of complications.     

处女膜修补手术及麻醉方法的改进

目的；增大处女膜粘膜瓣的接触面，减少因麻醉造成的处女膜粘膜水肿，提高修复手术的成功率。方法：手术全部采用1％的卡因行粘膜表面麻醉。53例采用瓦合粘膜瓣法，3例用瓦合粘膜瓣联合阴道粘膜瓣修复法。结果：56例术后一月随访，53例处女膜孔径为一指，成功率94．64％。结论：采用1％的卡因粘膜表面麻醉，瓦合粘膜瓣法及瓦合粘膜联合阴道粘膜瓣修复法对处女膜修复是行之有效的。     

Epiploic appendagitis and omental infarction: pitfalls and look-alikes

Epiploic appendagitis and omental infarction are benign self-limiting conditions that are more frequent than generally assumed. Both disorders frequently mimic symptoms of an abdominal surgical emergency, often leading to clinical misdiagnosis of appendicitis or diverticulitis. Because a misdiagnosis can result in an unnecessary laparotomy, a correct diagnosis is of great importance. Ultrasound and computed tomography can be used to make a reliable diagnosis. This pictorial essay illustrates the various ultrasonographic and computed tomographic appearances of epiploic appendagitis and omental infarction and focuses on their radiologic differential diagnoses and pitfalls. Received: 22 February 2001/Accepted: 18 April 2001     

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角膜损伤后神经再生的实验研究

应用神经组织化学技术观察了兔角膜NA能神经及AchE阳性神经在角膜损伤后的再生,证实术后1月,两种神经均有再生轴突进入植片;术后3月可见交界区和植床内神经密度明显增加;同时,对术后两种神经再生的功能意义进行了讨论。     

Transient Brain Ischaemia Provokes Ca2+, PIP2 and Calpain Responses Prior to Delayed Neuronal Death in Monkeys

To clarify the mechanism of postischaemic delayed cornu Ammonis (CA)-1 neuronal death, we studied correlations among calpain activation and its subcellular localization, the immunoreactivity of phosphatidylinositol 4,5-bisphosphate (PIP₂) and Ca²⁺ mobilization in the monkey hippocampus by two independent experimental approaches: in vivo transient brain ischaemia and in vitro hypoxia-hypoglycaemia of hippocampal acute slices. The CA-1 sector undergoing 20 min of ischaemia in vivo showed microscopically a small number of neuronal deaths on day 1 and almost global neuronal loss on day 5 after ischaemia. Immediately after ischaemia, CA-1 neurons ultrastructurally showed vacuolation and/or disruption of the lysosomes. Western blotting using antibodies against inactivated or activated μ-calpain demonstrated μ-calpain activation specifically in the CA-1 sector immediately after ischaemia. This finding was confirmed in the perikarya of CA-1 neurons by immunohistochemistry. CA-1 neurons on day 1 showed sustained activation of μ-calpain, and increased immunostaining for inactivated and activated forms of μ- and m-calpains and for PIP₂. Activated μ-calpain and PIP₂ were found to be localized at the vacuolated lysosomal membrane or endoplasmic reticulum and mitochondrial membrane respectively, by immunoelectron microscopy. Calcium imaging data using hippocampal acute slices showed that hypoxia-hypoglycaemia in vitro provoked intense Ca²⁺ mobilization with increased PIP₂ immunostaining specifically in CA-1 neurons. These data suggest that transient brain ischaemia increases intracellular Ca²⁺ and PIP₂ breakdown, which will activate calpain proteolytic activity. Therefore, we suggest that activated calpain at the lysosomal membrane, with the possible release of biodegrading enzyme, will cause postischaemic CA-1 neuronal death.