Neurologic Urinary and Faecal Incontinence
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A Clever Technique for Placement of a Urinary Catheter Over a Wire
[Downloaded free from http://www.urologyannals.com on Monday, August 24, 2015, IP: 107.133.192.199] Original Article A clever technique for placement of a urinary catheter over a wire Joel E. Abbott, Adam Heinemann, Robert Badalament, Julio G. Davalos1 Department of Urology, St. John Providence, Michigan State University, Detroit, MI 48071, 1Chesapeake Urology Associates, University of Maryland, Baltimore, MD 21061, USA Abstract Objective: The objective was to present a straightforward, step-by-step reproducible technique for placement of a guide-wire into any type of urethral catheter, thereby offering a means of access similar to that of a council-tip in a situation that may require a different type of catheter guided over a wire. Materials and Methods: Using a shielded intravenous catheter inserted into the eyelet of a urinary catheter and through the distal tip, a “counsel-tip” can be created in any size or type of catheter. Once transurethral bladder access has been achieved with a hydrophilic guide-wire, this technique will allow unrestricted use of catheters placed over a wire facilitating guided catheterization. Results: Urethral catheters of different types and sizes are easily advanced into the bladder with wire-guidance; catheterization is improved in the setting of difficult urethral catheterization (DUC). Cost analysis demonstrates benefit overuse of traditional council-tip catheter. Conclusion: Placing urinary catheters over a wire is standard practice for urologists, however, use of this technique gives the freedom of performing wire-guided catheterization in more situations than a council-tip allows. This technique facilitates successful transurethral catheterization over wire in the setting of DUC for all catheter types and styles aiding in urologic management of patients at a cost benefit to the health care system. -
The National Drugs List
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CMS Manual System Human Services (DHHS) Pub
Department of Health & CMS Manual System Human Services (DHHS) Pub. 100-07 State Operations Centers for Medicare & Provider Certification Medicaid Services (CMS) Transmittal 8 Date: JUNE 28, 2005 NOTE: Transmittal 7, of the State Operations Manual, Pub. 100-07 dated June 27, 2005, has been rescinded and replaced with Transmittal 8, dated June 28, 2005. The word “wound” was misspelled in the Interpretive Guidance section. All other material in this instruction remains the same. SUBJECT: Revision of Appendix PP – Section 483.25(d) – Urinary Incontinence, Tags F315 and F316 I. SUMMARY OF CHANGES: Current Guidance to Surveyors is entirely replaced by the attached revision. The two tags are being combined as one, which will become F315. Tag F316 will be deleted. The regulatory text for both tags will be combined, followed by this revised guidance. NEW/REVISED MATERIAL - EFFECTIVE DATE*: June 28, 2005 IMPLEMENTATION DATE: June 28, 2005 Disclaimer for manual changes only: The revision date and transmittal number apply to the red italicized material only. Any other material was previously published and remains unchanged. However, if this revision contains a table of contents, you will receive the new/revised information only, and not the entire table of contents. II. CHANGES IN MANUAL INSTRUCTIONS: (N/A if manual not updated.) (R = REVISED, N = NEW, D = DELETED) – (Only One Per Row.) R/N/D CHAPTER/SECTION/SUBSECTION/TITLE R Appendix PP/Tag F315/Guidance to Surveyors – Urinary Incontinence D Appendix PP/Tag F316/Urinary Incontinence III. FUNDING: Medicare contractors shall implement these instructions within their current operating budgets. IV. ATTACHMENTS: Business Requirements x Manual Instruction Confidential Requirements One-Time Notification Recurring Update Notification *Unless otherwise specified, the effective date is the date of service. -
Autonomic Nervous System Dysfunction Involving the Gastrointestinal and the Urinary Tracts in Primary Sjögren’S Syndrome
Autonomic nervous system dysfunction involving the gastrointestinal and the urinary tracts in primary Sjögren’s syndrome L. Kovács1, M. Papós2, R. Takács3, R. Róka2, Z. Csenke4, A. Kovács1, T. Várkonyi3, L. Pajor5, L. Pávics2, G. Pokorny1 Department of Rheumatology1, Department of Nuclear Medicine2, 1st Department of Internal Medicine3 and Department of Urology5, University of Szeged, Faculty of Medicine, Szeged; Division of Urology, Municipial Clinic, Szeged, Hungary4 Abstract Objective Antibodies reacting with the m3 subtype muscarinic acetylcholine receptor appear to be an important patho- genic factor in primary Sjögren’s syndrome (pSS). As this receptor subtype is functionally important in the gastrointestinal and urinary tracts, and very little is known about the autonomic nervous system function in these organs in pSS patients, the occurrence and clinical significance of an autonomic nervous system dysfunction involving the gastrointestinal and urinary tracts were investigated. Methods Data on clinical symptoms attributable to an autonomic dysfunction were collected from 51 pSS patients. Gastric emptying scintigraphy and urodynamic studies were performed on 30 and 16 patients, respectively, and the results were correlated with patient characteristics and with the presence of autonomic nervous system symptoms. Results Gastric emptying was abnormally slow in 21 of the 30 examined patients (70%). Urodynamic findings compatible with a decreased detrusor muscle tone or contractility were found in 9 of the 16 patients tested (56%). Various symptoms of an autonomic nervous system dysfunction were reported by 2-16% of the patients. Conclusion Signs of an autonomic nervous system dysfunction involving the gastrointestinal and the urinary systems can be observed in the majority of pSS patients. -
Urinary Tract Infection (UTI): Western and Ayurvedic Diagnosis and Treatment Approaches
Urinary tract infection (UTI): Western and Ayurvedic Diagnosis and Treatment Approaches. By: Mahsa Ranjbarian Urinary system Renal or Urinary system is one of the 10 body systems that we have. This system is the body drainage system. The urinary system is composed of kidneys (vrikka), ureters (mutravaha nadis), bladder(mutrashaya) and urethra(mutramarga). The kidneys are a pair of bean-shaped, fist size organs that lie in the middle of the back, just below the rib cage, one on each side of the spine. Ureters are tubes that carry the wastes or urine from the kidneys to the bladder. The urine finally exit the body from the urethra when the bladder is full.1 Urethras length is shorter in women than men due to the anatomical differences. Major function of the urinary system is to remove wastes and water from our body through urination. Other important functions of the urinary system are as follows. 1. Prevent dehydration and at the same time prevent the buildup of extra fluid in the body 2. Cleans the blood of metabolic wastes 3. Removing toxins from the body 4. Maintaining the homeostasis of many factors including blood PH and blood pressure 5. Producing erythrocytes 6. make hormones that help regulate blood pressure 7. keep bones strong 8. keep levels of electrolytes, such as potassium and phosphate, stable 2 The Urinary system like any other systems of our body is working under the forces of three doshas, subdoshas. Mutravaha srotas, Ambuvahasrota and raktavahasrota are involved in formation and elimination of the urine. Urine gets separated from the rasa by maladhara kala with the help of pachaka pitta and samana vayu and then through the mutravaha srota(channels carrying the urine) it is taken to the bladder. -
A Sign It's Time for BOTOX®
When OAB* due to MS† makes matters worse… A sign it’s time for BOTOX® Ask your patients if they still have leakage or can’t tolerate their current OAB medication *Overactive bladder. †Multiple sclerosis. Indication Detrusor Overactivity Associated With a Neurologic Condition BOTOX® for injection is indicated for the treatment of urinary incontinence due to detrusor overactivity associated with a neurologic condition (eg, SCI, MS) in adults who have an inadequate response to or are intolerant of an anticholinergic medication. IMPORTANT SAFETY INFORMATION, INCLUDING BOXED WARNING WARNING: DISTANT SPREAD OF TOXIN EFFECT Postmarketing reports indicate that the effects of BOTOX® and all botulinum toxin products may spread from the area of injection to produce symptoms consistent with botulinum toxin effects. These may include asthenia, generalized muscle weakness, diplopia, ptosis, dysphagia, dysphonia, dysarthria, urinary incontinence, and breathing difficulties. These symptoms have been reported hours to weeks after injection. Swallowing and breathing difficulties can be life threatening, and there have been reports of death. The risk of symptoms is probably greatest in children treated for spasticity, but symptoms can also occur in adults treated for spasticity and other conditions, particularly in those patients who have an underlying condition that would predispose them to these symptoms. In unapproved uses and in approved indications, cases of spread of effect have been reported at doses comparable to those used to treat Cervical Dystonia -
Autonomic Dysreflexia – a Medical Emergency a Guide for Patients
Autonomic Dysreflexia – A Medical Emergency A guide for patients Only applicable to T6 level and above Key Points • Autonomic Dysreflexia (AD) is a medical emergency that occurs due to a rapid rise in blood pressure in response to a harmful or painful stimulus below the level of your Spinal Cord Injury (SCI) • It occurs in people with SCI at T6 and above but has in rare occasions been reported in individuals with SCI as low as T8 • If left untreated your blood pressure can rise to dangerous levels, risking stroke, cardiac problems, seizures, even death • Typically there is a pounding headache as your blood pressure rises. Other symptoms can include redness and sweating above the level of your SCI, slow heart rate, goosebumps, nausea, nasal congestion, blurred vision, shortness of breath and anxiety • Some or all of the symptoms may be present • AD can be triggered by any continuous painful or irritating stimulus below the level of your lesion. The most common causes are related to the bladder or bowel • Relieving the cause of the AD will resolve your AD episode • If the cause cannot be found or treated, medication is required to lower your blood pressure which may require a visit to your nearest emergency department • All people with SCI at T6 and above should carry their Autonomic Dysreflexia Medical Emergency Card at all times • The best treatment for AD is prevention • People at risk of AD often carry an ‘AD Kit’ with them – items useful to resolve AD such as catheters and prescribed medication 1 What is Autonomic Dysreflexia? Autonomic Dysreflexia (AD) is a medical emergency. -
Treatment of Autonomic Dysreflexia for Adults & Adolescents with Spinal
Treatment of Autonomic Dysreflexia for Adults & Adolescents with Spinal Cord Injuries Authors: Dr James Middleton, Director, State Spinal Cord Injury Service, NSW Agency for Clinical Innovation. Dr Kumaran Ramakrishnan, Honorary Fellow, Rehabilitation Studies Unit, Sydney Medical School Northern, The University of Sydney, and Consultant Rehabilitation Physician & Senior Lecturer, Department of Rehabilitation Medicine, University Malaya. Dr Ian Cameron, Head of the Rehabilitation Studies Unit, Sydney Medical School Northern, The University of Sydney. Reviewed and updated in 2013 by the authors. AGENCY FOR CLINICAL INNOVATION Level 4, Sage Building 67 Albert Avenue Chatswood NSW 2067 PO Box 699 Chatswood NSW 2057 T +61 2 9464 4666 | F +61 2 9464 4728 E [email protected] | www.aci.health.nsw.gov.au Produced by the NSW State Spinal Cord Injury Service. SHPN: (ACI) 140038 ISBN: 978-1-74187-972-8 Further copies of this publication can be obtained from the Agency for Clinical Innovation website at: www.aci.health.nsw.gov.au Disclaimer: Content within this publication was accurate at the time of publication. This work is copyright. It may be reproduced in whole or part for study or training purposes subject to the inclusion of an acknowledgment of the source. It may not be reproduced for commercial usage or sale. Reproduction for purposes other than those indicated above, requires written permission from the Agency for Clinical Innovation. © Agency for Clinical Innovation 2014 Published: February 2014 HS13-136 ACKNOWLEDGEMENTS This document was originally published as a fact sheet for the Rural Spinal Cord Injury Project (RSCIP), a pilot healthcare program for people with a spinal cord injury (SCI) conducted within New South Wales involving the collaboration of Prince Henry & Prince of Wales Hospitals, Royal North Shore Hospital, Royal Rehabilitation Centre Sydney, Spinal Cord Injuries Australia and the Paraplegic & Quadriplegic Association of NSW. -
Guidelines for Management of Acute Renal Failure (Acute Kidney Injury)
Guidelines for management of Acute Renal Failure (Acute Kidney Injury) Children’s Kidney Centre University Hospital of Wales Cardiff CF14 4XW DISCLAIMER: These guidelines were produced in good faith by the author(s) reviewing available evidence/opinion. They were designed for use by paediatric nephrologists at the University Hospital of Wales, Cardiff for children under their care. They are neither policies nor protocols but are intended to serve only as guidelines. They are not intended to replace clinical judgment or dictate care of individual patients. Responsibility and decision-making (including checking drug doses) for a specific patient lie with the physician and staff caring for that particular patient. Version 1, S. Hegde/Feb 2009 Guidelines on management of Acute Renal Failure (Acute Kidney Injury) Definition of ARF (now referred to as AKI) • Acute renal failure is a sudden decline in glomerular filtration rate (usually marked by rise in serum creatinine & urea) which is potentially reversible with or without oliguria. • Oliguria defined as urine output <300ml/m²/day or < 0.5 ml/kg/h (<1 ml/kg/h in neonates). • Acute on chronic renal failure suggested by poor growth, history of polyuria and polydipsia, and evidence of renal osteodystrophy However, immediately after a kidney injury, serum creatinine & urea levels may be normal, and the only sign of a kidney injury may be decreased urine production. A rise in the creatinine level can result from medications (e.g., cimetidine, trimethoprim) that inhibit the kidney’s tubular secretion. A rise in the serum urea level can occur without renal injury, such as in GI or mucosal bleeding, steroid use, or protein loading. -
Increase Thirst and Urination (Polydyspsia and Polyuria)
Increase Thirst and Urination (Polydyspsia and Polyuria) 803-808-7387 www.gracepets.com What are the causes of increased thirst and urination? These clinical signs are non-specific and can be caused by many different diseases or conditions. Usually it is the production of excess, dilute urine that results in a compensatory increase in water consumption, but occasionally the condition is one of increased water intake resulting in the production of large volumes of dilute urine. The following is not a complete listing of the diseases that may result in increased thirst and urination. However it outlines the most common causes: Conditions related to the urinary and reproductive systems including kidney failure, infections of the kidneys or bladder, and infections of the uterus. Endocrine or hormone related conditions including hyperadrenocorticism and hypoadrenocorticism, hyperthyroidism, diabetes mellitus and diabetes insipidus. Liver disease, certain drugs, fever, pain and certain electrolyte imbalances may also result in increased thirst and urination. Rarely, a behavioral problem is at the root of increased drinking behavior. This list is huge! How can we possibly determine what the cause is in my pet? Certain diseases are more common in certain species (dogs versus cats) so this may narrow down the range of possibilities. In addition, the specific history of the pet, including a list of all medications and supplements that your pet has recently received, is helpful. This information, along with a physical examination, will often narrow the list further. A panel of screening tests will also exclude a large number of these conditions and may even provide a definitive diagnosis. -
Chapter Four – TRPA1 Channels: Chemical and Temperature Sensitivity
CHAPTER FOUR TRPA1 Channels: Chemical and Temperature Sensitivity Willem J. Laursen1,2, Sviatoslav N. Bagriantsev1,* and Elena O. Gracheva1,2,* 1Department of Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, CT, USA 2Program in Cellular Neuroscience, Neurodegeneration and Repair, Yale University School of Medicine, New Haven, CT, USA *Corresponding author: E-mail: [email protected], [email protected] Contents 1. Introduction 90 2. Activation and Regulation of TRPA1 by Chemical Compounds 91 2.1 Chemical activation of TRPA1 by covalent modification 91 2.2 Noncovalent activation of TRPA1 97 2.3 Receptor-operated activation of TRPA1 99 3. Temperature Sensitivity of TRPA1 101 3.1 TRPA1 in mammals 101 3.2 TRPA1 in insects and worms 103 3.3 TRPA1 in fish, birds, reptiles, and amphibians 103 3.4 TRPA1: Molecular mechanism of temperature sensitivity 104 Acknowledgments 107 References 107 Abstract Transient receptor potential ankyrin 1 (TRPA1) is a polymodal excitatory ion channel found in sensory neurons of different organisms, ranging from worms to humans. Since its discovery as an uncharacterized transmembrane protein in human fibroblasts, TRPA1 has become one of the most intensively studied ion channels. Its function has been linked to regulation of heat and cold perception, mechanosensitivity, hearing, inflam- mation, pain, circadian rhythms, chemoreception, and other processes. Some of these proposed functions remain controversial, while others have gathered considerable experimental support. A truly polymodal ion channel, TRPA1 is activated by various stimuli, including electrophilic chemicals, oxygen, temperature, and mechanical force, yet the molecular mechanism of TRPA1 gating remains obscure. In this review, we discuss recent advances in the understanding of TRPA1 physiology, pharmacology, and molecular function. -
Updatirg the Beers Criteria for Potentially Inappropriate Medication Use in Older Adults
Updatirg the BeersCriteria for Potentially InappropriateMedication Use in Older Adults Resultsof a US ConsensusPanel of Experts DonnaM.Fich,PhD,RN;lamesW.Cooper,PhD,RPh;WilliamE.Wade,PhannD,FASHP,FCCP; JenniJerL. Waller, PhD;J, RossMaclean, MD; Marh H. Beers,MD Bcckground: Medication toxic effectsand drug- Reruhr: This study identified 48 individual medica- relatedproblems can have profound medical and safety tions or classeso[ medicationsto avoid in older adults consequencesfor older adults and economically affect the and their potential concernsand 20 diseases/conditions health caresystem. The purpose of this initiative was to and medicationsto be avoidedin older adultswith these reviseand update the Beerscriteria for potentially inap- conditions.Of thesepotentially inappropriate drugs, 66 propriate medicationuse in adults 65 yearsand older in wereconsidered by the panelto haveadverse outcomes the United States. of high severity. lYlcthcdr: This study used a modified Delphi method, a Concludonr: This study is an importantupdate of pre- setof proceduresand methodsfor formulating a groupjudg- viously establishedcriteria that have been widely used ment for a subject matter in which precise information is and cited. The application of the Beerscriteria and other Iacking. The criteria reviewed covered 2 types of state- tools for identifying potentially inapproprlate medica- ments: (l) medicationsor medicationclasses that should tion use will continue to enableproviders to plan inter- grnerally be avoidedin persons 65 years or older because