DOCSLIB.ORG

Neurologic Urinary and Faecal Incontinence

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Neurologic Urinary and Faecal Incontinence Committee 10 Neurologic Urinary and Faecal Incontinence Chairman J.J. WYNDAELE (Belgium) Members A. KOVINDHA (Thailand), H. MADERSBACHER (Austria), P. R ADZISZEWSKI (Poland), A. RUFFION (France), B. SCHURCH (Switzerland) Consultants D. CASTRO (Spain), Y. IGAWA (Japan), R. SAKAKIBARA (Japan) Advisor I. PERKASH (USA) 793 ABBREVIATIONS Most abbreviations used in the text are given here, MUP: motor unit potential some in the beginning of the chapter where they are MRI: magnetic resonance imaging used MS: multiple sclerosis Ach: acetylcholine MSA: multiple system atrophy AchE: acethylcholine esterase NBo: neurogenic bowel AD: autonomic dysreflexia NBoD: neurogenic bowel dysfunction ADL: activities of daily living NDO: neurogenic detrusor overactivity ALD: Alzheimer’s disease NLUTD: neurological lower urinary tract dysfunction AS: anal sphincter NUI: neurogenic urinary incontinence AUS: artificial urethral sphincter NVC: natural fill cystometry BCR: bulbocavernosus reflex OR: odd ratio BST: bethanechol supersensitivity test PD: Parkinson’s disease CC: cystometriccapacity PF: pelvic floor CIC: clean intermittent catheterization PFD: pelvic floor dysfunction CMG: cystometrogram PSP: progressive supranuclear palsy CPG: clinical practice guideline Psym: parasympathetic CPT: current perception threshold PVR: post void residual CT: computer tomography QoL: quality of life CTT: colonic transit time RCT: randomised controlled trial CUM: continuous urodynamic monitoring SARS: sacral anterior root stimulation CVA: cerebro vascular accident SCI: spinal cord injury CVC: conventional cystometry SCL: spinal cord lesion DI: double incontinence SDAF: sacral deafferentation DLB: dementia with Lewy bodies SIC: sterile intermittent catheterization DOA: detrusor over activity DRS: digital rectal stimulation SLE : systemic lupus erythematosis DSD: detrusor sphincter dyssynergia SNS: sacral nerve stimulation ES: electrical stimulation SOM: somatic EAS: external anal sphincter SPC: suprapubic catheter EMG: electromyography SSEP: somatosensory evoked potentials EPT: electric perception threshold SSR: sympathetic skin response FI: faecal incontinence SUI: stress urinary incontinence FTD : fronto temporal dementia Sym: sympathetic GBS: Guillain Barre Syndrome TBI: traumatic brain injury ID: indwelling catheter TRI: transrectal irrigation IC: intermittent catheterization TURS: transurethral sphincterotomy IVES: intravesical electrical stimulation UFM: uroflowmetry IWT: ice water test UI: urinary incontinence LBT: lower bowel tract UMN: upper motor neuron LMNL: lower motor neuron lesion US: urethral sphincter LOE: level of evidence USo: ultrasound LS: lumbosacral UTI: urinary tract infection LUT: lower urinary tract UUT: upper urinary tract LUTD: lower urinary tract dysfunction VCUG: voiding cystourethrogram LUTS: lower urinary tract symptoms VSD: vesicosphincteric disorders MPdet: maximum detrusor pressure VSU: vecicoureteral reflux MMC: meningomyelocoele WBC: white blood cells 794 CONTENTS A. INTRODUCTION E. SPECIFIC NEUROLOGIC DISEASES B. PATHOPHYSIOLOGY I. DEMENTIA I. SUPRAPONTINE LESIONS II. MULTIPLE SYSTEM ATROPHY II. SPINAL CORD LESIONS III. PARKINSONS DISEASE III. SUBSACRAL LESIONS (CAUDA IV. CEREBRAL LESIONS AND EQUINA OR PERIPHERAL NERVES) CEREBRO-VASCULAR ACCIDENTS C. NEUROLOGIC URINARY V. MULTIPLE SCLEROSIS INCONTINENCE VI. SPINAL CORD LESION I. EPIDEMIOLOGY VII. SPINAL CANAL STENOSIS II. SPECIFIC DIAGNOSTICS VIII. GUILLAIN-BARRE SYNDROME III. CONSERVATIVE TREATMENT IX. LUMBAR DISC PROLAPSE IV. SURGICAL TREATMENT X. MENINGOMYELOCOELE D. NEUROLOGIC FAECAL INCONTINENCE XI. DIABETES MELLITUS I. EPIDEMIOLOGY XII. PERIPHERAL NEUROPATHY DUE TO IATROGENIC LESION (FOCAL NEUROPATHY) II. SPECIAL DIAGNOSIS OF FAECAL INCONTINENCE IN NEUROPATHIC PATIENTS XIII. SYSTEMIC LUPUS ERYTHEMATOSIS III. CONSERVATIVE TREATMENT XIV. HERPES ZOSTER IV. SURGICAL TREATMENT XV. HIV 795 796 Neurologic Urinary and Faecal Incontinence J.J. WYNDAELE, A. KOVINDHA, H.MADERSBACHER, P. RADZISZEWSKI, A.RUFFION, B.SCHURCH, Y. IGAWA, R.SAKAKIBARA Table 1. Overview of function of the abdominal sympathetic (Sym), the pelvic parasympathetic A. INTRODUCTION (PSym) and somatic (Som) nerves in the LUT and LBT. US= urethral sphincter, AS= anal sphincter. Exp= only suggested in animal experiments, no This chapter deals with all aspects of neurologic clinical evidence. urinary and faecal incontinence. To combine this information related to two different structures makes Sym PSym Som this chapter rather unique though there are sufficient Th 10-L 1 S2-S4 S3-S5 arguments to do so, as presented below. Bladder - + Its content is written from data found in literature with Bladder neck + - the keywords “neurologic”, neurogenic”, “bladder”, “bowel”, “lower urinary tract”, “anorectal”, Extern US exp exp + “incontinence“, “continence”, “urinary”, “faecal”, Bowel + “paralysis”, “dysfunction”, “retention”, “constipation” and the list of the specific neurologic diseases as Intern AS + - described in chapter E. Important information from Extern AS exp exp + the previous ICI report was used as starting point and some is used as such in this chapter, which is intended Pelvic floor + to be able to stand alone. For some topics more elaborate information will be found in other chapters Central control of both continence and evacuation is as on neurophysiology, diagnostics, urodynamic similar and is discussed in the chapter on physiology testing, female, male , frail elderly, faecal incontinence [2]. and more. To look up the related information in these chapters will be worthwhile. Also in chapter E not all Very generally LUT and LBT act quite similar, both are neurologic diseases will be found as we decided in autonomic organs regulated to necessary social consensus to look into the most prevalent or consisting requirements by a somatic innervation. The voluntary of the more challenging in diagnosis and or treatment control depends on accurate sensation [3]. Continence of incontinence. Other colleagues might have made relates to contraction of smooth closing structures a different choice. (bladder neck and internal bowel sphincter) and striated urethral and anal sphincters. An inhibitory It is known that the lower urinary tract (LUT) and the effect on detrusor and lower rectum resulting from lower bowel tract (LBT) are interrelated structures. contraction of the pelvic floor and anal or urethral Embryologically bladder and rectum originate from sphincter has been named a “procontinence” reaction. the same basic structure, the cloaca [1]. Anatomically Micturition and defaecation need a proper relaxation both viscera lay in close communication and share of these latter structures to permit a physiological muscular structures of the pelvic floor. reflex evacuation of urine or faeces. The innervation of both systems depends on Interactions between both functions have been autonomic and somatic nerves (Figure 1) that carry demonstrated. The filling status of the bladder fibres of both. In table 1 a simplified overview is given influences sensation in the rectum and vice versa [4]. of the action linked to different peripheral nerves. A vesico-ano-rectal reflex permits voiding without 797 Figure 1: Schematic overview of innervation of LUT and LBT Figure 2 : Frequent sites of neurologic pathology causing neurologic urinary and faecal incontinence. 798 defaecation [5]. When the bladder is full, sensation of tight thereby retaining stool (Dyssynergia). The rectal filling is decreased. When healthy people visit connections between the spinal cord and the colon the toilet to defaecate, the initiation of micturition often remain intact, permitting reflex coordination and stool precedes that of defaecation, even if both organs are propulsion. This type of lesion provokes faecal considered equally full [6]. The prevalence of both retention at least in part due to the activity of the anal urinary and bowel dysfunction is high in many sphincter. Incontinence can be a consequence of neurological diseases. faecal impaction and constipation. There is no study so far on correlation between both 2. CONUS LESION functions in patients with neurological pathology. If the nuclei of the pelvic nerves are destroyed, the In this chapter levels of evidence (LOE) and grades detrusor becomes areflexic. Retention of urine can of recommendation (A) are used as described in the provoke stress incontinence (formerly termed overflow general introduction of this book. incontinence). III. SUBSACRAL LESIONS (CAUDA B. PATHOPHYSIOLOGY EQUINA OR PERIPHERAL NERVES) The same effect as from lesions of the conus With a neurologic lesion the type of dysfunction that medullaris can result from lesions of the subsacral follows in LUT and LBT will depend on the site, the nerves (cauda equina or peripheral nerves). If the extent and the evolution of the lesion. nuclei of the pudendal nerves are harmed, a paralysis of the urethral sphincter and pelvic floor muscles will Traditionally neurological pathology has been divided occur often with loss of outflow resistance and stress in suprapontine, suprasacral spinal cord and subsacral incontinence. (cauda equina and peripheral nerve) lesions (Figure 2). A neurological lesion affecting the parasympathetic cell bodies in the conus medullaris will eliminate the pelvic I. SUPRAPONTINE LESIONS nerve function of the bowel. No spinal-cord mediated peristalsis will occur. It will be the myenteric plexus that coordinates segmental colonic peristalsis. If the Patients with lesions above the pons usually continue pudendal
Load more

Recommended publications
  • 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.
    [Show full text]
  • The National Drugs List
    ^ ^ ^ ^ ^[ ^ The National Drugs List Of Syrian Arab Republic Sexth Edition 2006 ! " # "$ % &'() " # * +$, -. / & 0 /+12 3 4" 5 "$ . "$ 67"5,) 0 " /! !2 4? @ % 88 9 3: " # "$ ;+<=2 – G# H H2 I) – 6( – 65 : A B C "5 : , D )* . J!* HK"3 H"$ T ) 4 B K<) +$ LMA N O 3 4P<B &Q / RS ) H< C4VH /430 / 1988 V W* < C A GQ ") 4V / 1000 / C4VH /820 / 2001 V XX K<# C ,V /500 / 1992 V "!X V /946 / 2004 V Z < C V /914 / 2003 V ) < ] +$, [2 / ,) @# @ S%Q2 J"= [ &<\ @ +$ LMA 1 O \ . S X '( ^ & M_ `AB @ &' 3 4" + @ V= 4 )\ " : N " # "$ 6 ) G" 3Q + a C G /<"B d3: C K7 e , fM 4 Q b"$ " < $\ c"7: 5) G . HHH3Q J # Hg ' V"h 6< G* H5 !" # $%" & $' ,* ( )* + 2 ا اوا ادو +% 5 j 2 i1 6 B J' 6<X " 6"[ i2 "$ "< * i3 10 6 i4 11 6! ^ i5 13 6<X "!# * i6 15 7 G!, 6 - k 24"$d dl ?K V *4V h 63[46 ' i8 19 Adl 20 "( 2 i9 20 G Q) 6 i10 20 a 6 m[, 6 i11 21 ?K V $n i12 21 "% * i13 23 b+ 6 i14 23 oe C * i15 24 !, 2 6\ i16 25 C V pq * i17 26 ( S 6) 1, ++ &"r i19 3 +% 27 G 6 ""% i19 28 ^ Ks 2 i20 31 % Ks 2 i21 32 s * i22 35 " " * i23 37 "$ * i24 38 6" i25 39 V t h Gu* v!* 2 i26 39 ( 2 i27 40 B w< Ks 2 i28 40 d C &"r i29 42 "' 6 i30 42 " * i31 42 ":< * i32 5 ./ 0" -33 4 : ANAESTHETICS $ 1 2 -1 :GENERAL ANAESTHETICS AND OXYGEN 4 $1 2 2- ATRACURIUM BESYLATE DROPERIDOL ETHER FENTANYL HALOTHANE ISOFLURANE KETAMINE HCL NITROUS OXIDE OXYGEN PROPOFOL REMIFENTANIL SEVOFLURANE SUFENTANIL THIOPENTAL :LOCAL ANAESTHETICS !67$1 2 -5 AMYLEINE HCL=AMYLOCAINE ARTICAINE BENZOCAINE BUPIVACAINE CINCHOCAINE LIDOCAINE MEPIVACAINE OXETHAZAINE PRAMOXINE PRILOCAINE PREOPERATIVE MEDICATION & SEDATION FOR 9*: ;< " 2 -8 : : SHORT -TERM PROCEDURES ATROPINE DIAZEPAM INJ.
    [Show full text]
  • 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.
    [Show full text]
  • 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.
    [Show full text]
  • 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.
    [Show full text]
  • 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
    [Show full text]
  • 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.
    [Show full text]
  • 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.
    [Show full text]
  • 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.
    [Show full text]
  • 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.
    [Show full text]
  • 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.
    [Show full text]
  • 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
    [Show full text]