Neuromuscular blocking drugs (NMBD) are administered intra-operatively to facilitate intubation and to achieve muscle relaxation for surgical procedures. Incomplete reversal of NMBD can lead to adverse events in the postoperative period. Patients with obstructive sleep apnea (OSA) may be at higher risk of complications related to the use of NMBD. The objectives of this systematic review were to determine whether: 1) OSA patients are at higher risk of postoperative complications from the use of NMBD than non-OSA patients, and 2) the choice of NMBD reversal agent affects the risk of postoperative complications in OSA patients.
A literature search of multiple databases was conducted up to April 2017. The inclusion criteria were: (1) adult surgical patients (≥18 years old) with OSA diagnosed by polysomnography, or history, or suspected by screening questionnaire; (2) patients who were given NMBD and/or NMBD reversal agents intraoperatively; (3) reports on postoperative adverse events, particularly respiratory events were available; (4) published studies were in English; and (5) RCTs or observational cohort studies. The quality of evidence was determined by the Oxford Center for Evidence Based Medicine levels of evidence.
Out of 4123 studies, five studies (2 RCTs and 3 observational studies) including 1126 patients were deemed eligible. These studies were heterogeneous precluding a meta-analysis of the results. Two of three studies (1 RCT, 2 observational studies) reported that OSA patients given NMBD may be at higher risk of developing postoperative pulmonary complications (PPCs) like hypoxemia, residual neuromuscular blockade or respiratory failure compared to non-OSA patients. Two studies (1 RCT, 1 observational study) reported that OSA patients who were reversed with sugammadex vs. neostigmine had less PPCs and chest radiographic changes, but the quality of the included studies was Oxford level of evidence: low to moderate.
OSA patients who receive intraoperative NMBD may be at higher risk for postoperative hypoxemia, respiratory failure and residual neuromuscular blockade compared to non-OSA patients. There is some, albeit very limited evidence that NMBD reversal with sugammadex may be associated with less PPCs than neostigmine in patients with OSA. More high-quality studies are needed.

OBJECTIVE: Patients complaining of a dry mouth can present themselves to various clinicians such as the primary care physician, dentists, otolaryngologists and/or oral surgeons. The aim of our review is to provide a systematic method of assessing and managing these patients based on current best evidence published in the literature.
METHODS: A literature search was performed on 20th April 2009 using MEDLINE and EMBASE using the terms dry mouth and xerostomia in combination with diagnosis, management, investigations and treatment.
RESULTS: There appears to be little correlation between patient symptoms and objectives tests of salivary flow. Therefore clinical management should be based on patient symptoms. There is good evidence to support that xerostomia is commonly associated with anticholinergic drugs, and altering such agents plays an important role in the management of these patients. In patients with residual salivary gland function, the use of salivary stimulants appears to be more beneficial than salivary substitutes.
CONCLUSIONS: Xerostomia can be debilitating and primarily affects the middle aged and elderly population. The most common causes of xerostomia include medications with anticholinergic properties, dehydration, diabetes and radiotherapy for head and neck cancer. Treatment of xerostomia essentially involves addressing the cause followed by salivary substitutes and/or salivary stimulants.

The Sjogren\'s syndrome (SS) is an chronic inflammatory autoimmune disease of the exocrine glands as well as of internal apparatus. The therapy of exocrinopathy is represented by parasympathomimetic drugs such as pilocarpine and cevimeline. The therapy of systemic manifestations, actually is represented by the inhibitors of TNF alfa, as well as leflunomide, methotrexate and cyclosporine-A, but the results are quite insufficient and disappointed. In order to the involvement of B-cell function in the pathogenesis of SS, one of the most important option in the future should be specific inhibitors of that cells.

Acute colonic pseudo-obstruction is the clinical syndrome of acute large bowel dilatation without mechanical obstruction that is an important cause of morbidity and mortality. Acute colonic pseudo-obstruction occurs in hospitalized or institutionalized patients with serious underlying medical and surgical conditions. The pathogenesis of acute colonic pseudo-obstruction is not completely understood but likely results from an imbalance in the autonomic regulation of colonic motor function. Metabolic or pharmacological factors, as well as spinal or retroperitoneal trauma, may alter the autonomic regulation of colonic function, leading to excessive parasympathetic suppression or sympathetic stimulation. This imbalance results in colonic atony and dilatation. Early recognition and appropriate management are critical to minimizing morbidity and mortality. The mortality rate is estimated at 40% when ischaemia or perforation occurs. The best-studied treatment of acute colonic pseudo-obstruction is intravenous neostigmine, which leads to prompt colon decompression in the majority of patients after a single infusion. In patients failing or having contraindications to neostigmine, colonoscopic decompression is the active intervention of choice. Surgery is reserved for those with peritonitis or perforation.

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OBJECTIVE: (1) To describe the demographic features of patients with voiding dysfunction associated with herpes zoster; (2) to discuss the pathophysiology of voiding dysfunction associated with herpes zoster; and (3) to suggest the best management policy.
METHODS: A retrospective study.
METHODS: A university-affiliated medical center in Taiwan.
METHODS: Four hundred twenty-three patients (mean age, 55.5y) admitted with the diagnosis of herpes zoster from 1988 to 2000.
METHODS: Not applicable.
METHODS: Dermatomal distribution of skin eruptions, urologic symptoms, treatment (catheterization, urecholine), clinical course of voiding dysfunction, and outcome.
RESULTS: Seventeen (mean age, 61.2+/-14.1y) of 423 patients (4.02%) with voiding dysfunction related to this virus infection were identified. Ten (58.8%) were men, and 7 (41.2%) were women. The incidence of dysfunction was as high as 28.6% if only lumbosacral dermatome-involved patients were considered. We classified urologic manifestations caused by herpes zoster into 3 groups: cystitis-associated (n=12), neuritis-associated (n=4), and myelitis-associated (n=1). Urinalysis revealed pyuria in all patients with cystitis-associated voiding dysfunction and microscopic hematuria in all patients with neuritis-associated voiding dysfunction. All patients, although receiving different treatment regimens for voiding dysfunction, regained a normal or balanced bladder within 8 weeks. No major urologic sequelae were noted.
CONCLUSIONS: Voiding dysfunction, although a transient course, is not uncommon in patients with herpes zoster involving lumbosacral dermatomes. Treatment with intermittent catheterization (our preferred choice) or indwelling catheter placement is recommended if the patients have prolonged difficulty in urination. This disease entity usually has a benign clinical course, and almost every patient will either regain normal voiding or, at least, balanced bladder function.

Anticholinergics and prokinetics are mainstays of therapy for Irritable Bowel Syndrome (IBS) patients despite their limited efficacy and troublesome side-effect profile. The clinical limitations of these drugs are a result of their relative broad and nonspecific pharmacologic interaction with various receptors. Recent advances in gut physiology have led to the identification of various receptor targets that may play a pivotal role in the pathogenesis of IBS. Medicinal chemists searching for safe and effective IBS therapies are now developing compounds targeting many of these specific receptors. The latest generation of anticholinergics, such as zamifenacin, darifenacin, and YM-905, provide selective antagonism of the muscarinic type-3 receptor. Tegaserod, a selective 5-HT4 partial agonist, tested in multiple clinical trials, is effective in reducing the symptoms of abdominal pain, bloating, and constipation. Ezlopitant and nepadudant, selective antagonists for neurokinin receptors type 1 and type 2, respectively, show promise in reducing gut motility and pain. Loperamide, a mu (mu) opioid receptor agonist, is safe and effective for IBS patients with diarrhea (IBS-D) as the predominant bowel syndrome. Fedotozine, a kappa (kappa) opioid receptor agonist, has been tried as a visccral analgesic in various clinical trials with conflicting results. Alosetron, a 5-HT3 receptor antagonist, has demonstrated efficacy in IBS-D patients but incidents of ischemic colitis seen in post-marketing follow-up resulted its removal from the market. Compounds that target cholecystokinin. A, N-methyl-D-aspartate, alpha 2-adrenergic, and corticotropin-releasing factor receptors are also examined in this review.

BACKGROUND: There are many agents in clinical use that manipulate central nervous system levels of epinephrine, dopamine, and serotonin. However, development of pharmacological options to manipulate central acetylcholine systems has lagged behind because of poor penetration of the blood-brain barrier and significant peripheral nervous system side effects. Newer agents have demonstrated some efficacy in the management of behavioral and cognitive side effects in Alzheimer\'s disease, and preliminary data in traumatic brain injury suggest acetylcholine esterase inhibitors may play a significant role in the treatment of this patient population as well.
CONCLUSIONS: In this article, the basic neuroanatomy and pharmacology of the central acetylcholine system are reviewed, along with agents currently available for clinical use.

Xerostomia may result from salivary dysfunction secondary to a variety of conditions, including medications, autoimmune disease, and tumoricidal therapy. As the geriatric population increases, the incidence of xerostomia will increase and the oral manifestations will continue to be a challenge to the clinician. Common oral manifestations resulting from decreased salivary flow include increased dental caries, fungal infections, and dysphagia. Treatment for salivary gland dysfunction is currently limited because of a lack of controlled clinical trials. Medications that have been studied in clinical trials are emphasized in this article. The aim of this article is to briefly review salivary gland physiology and to summarize the suggested systemic treatment modalities for xerostomia that emphasize controlled clinical trials.

For some time the medical treatment of glaucoma has consisted of topical beta-blockers, adrenergic agents, miotics and oral carbonic anhydrase inhibitors (CAIs). However, the therapeutic arsenal available for the medical treatment of glaucoma has recently extended with new classes of ocular hypotensive agents i.e. prostaglandins, local CAIs and alpha2-adrenergic agents. Beta-blockers are still the mainstay in glaucoma treatment and are first line drugs. However, even if they are applied once daily, as with timolol in gel forming solution and levobunolol, the possible cardiopulmonary adverse effects of beta-blockers remain a cause for concern. When monotherapy with beta-blockers is ineffective in reducing intraocular pressure (IOP) or is hampered by adverse effects, a change of monotherapy to prostaglandins, local CAIs, alpha2-adrenergic agonists (brimonidine) or to dipivalyl epinephrine is advised. Prostaglandins, local CAIs and alpha2-adrenergic agonists, such as brimonidine, may in time become first line drugs because they reduce IOP effectively and until now systemic adverse effects have rarely been reported with these agents. The development of a pro-drug of either a local CAI or an alpha2-adrenergic agonist with a sustained and continuous effect on IOP level, which could be applied once a day is suggested. Because of these new developments, miotics, i.e. pilocarpine and carbachol, are recommended as second or third line drugs. The cholinesterase inhibitors are considered third line drugs as better agents with fewer local and systemic adverse effects have become available. Oral CAIs may be used temporarily in patients with elevated IOPs e.g. postsurgery or post-laser, or continuously in patients with glaucoma resistant to other treatment. Combining ocular hypotensive drugs is indicated when the target pressure for an individual patient cannot be reached with monotherapy. Combination therapy of beta-blockers is additive with prostaglandins, topical CAIs and miotics. Prostaglandins such as latanoprost can be combined with beta-blockers, adrenergic agents, local CAIs and miotics. Combinations with brimonidine or local CAIs need further investigation. Treatment of glaucoma with the new ocular hypotensive agents, either in monotherapy or combination therapy, may provide lower IOPs and delay or postpone the need for surgery.