Acute pain in adults admitted to the emergency room: development and implementation of abbreviated guidelines.

AIM: Although acute pain is frequently reported by patients admitted to the emergency room, it is often insufficiently evaluated by physicians and is thus undertreated. With the aim of improving the care of adult patients with acute pain, we developed and implemented abbreviated clinical practice guidelines (CG) for the staff of nurses and physicians in our hospital's emergency room. METHODS: Our algorithm is based upon the practices described in the international literature and uses a simultaneous approach of treating acute pain in a rapid and efficacious manner along with diagnostic and therapeutic procedures. RESULTS: Pain was assessed using either a visual analogue scale (VAS) or a numerical rating scale (NRS) at ER admission and again during the hospital stay. Patients were treated with paracetamol and/or NSAID (VAS/NRS <4) or intravenous morphine (VAS/NRS > or =04). The algorithm also outlines a specific approach for patients with headaches to minimise the risks inherent to a non-specific treatment. In addition, our algorithm addresses the treatment of paroxysmal pain in patients with chronic pain as well as acute pain in drug addicts. It also outlines measures for pain prevention prior to minor diagnostic or therapeutic procedures. CONCLUSIONS: Based on published guidelines, an abbreviated clinical algorithm (AA) was developed and its simple format permitted a widespread implementation. In contrast to international guidelines, our algorithm favours giving nursing staff responsibility for decision making aspects of pain assessment and treatment in emergency room patients.

Pain: a common symptom in human immunodeficiency virus-infected Thai children.

AIM: To determine the prevalence and characteristics of pain in Thai human immunodeficiency virus-infected children. METHODS: A cross-sectional study was performed at the HIV/AIDS outpatient clinic at the Queen Sirikit National Institute of Child Health, Bangkok, Thailand from November 2002 to January 2003. Sixty-one human immunodeficiency virus-infected patients aged 4 to 15 y, an equal number of age-matched children with no chronic disease and their caregivers participated. We interviewed children and their caregivers using a structured questionnaire on pain. The main outcome measure was the percentage of human immunodeficiency virus-infected children reporting pain. RESULTS: Forty-four percent of the human immunodeficiency virus-infected children reported pain compared to 13% of the children with no chronic disease (odds ratio, OR = 5.3; 95% CI: 2.0-14.3). Seven percent of the infected children experienced chronic pain. Children in human immunodeficiency virus clinical categories B and C reported more pain than children in categories N and A (OR = 4.0, 95% CI: 1.1-14.7). Pain in infected children tended to occur in the abdomen, lower limbs or head. Only 44 percent of the infected children experiencing pain received analgesic medication. CONCLUSION: Despite being a common experience, pain is insufficiently taken into account and treated in Thai children with HIV/AIDS. Therefore, adequate pain identification, assessment and management should be systemically considered in their routine care.

Do glial cells control pain?

Management of chronic pain is a real challenge, and current treatments focusing on blocking neurotransmission in the pain pathway have only resulted in limited success. Activation of glia cells has been widely implicated in neuroinflammation in the central nervous system, leading to neruodegeneration in many disease conditions such as Alzheimer's and multiple sclerosis. The inflammatory mediators released by activated glial cells, such as tumor necrosis factor-α and interleukin-1β can not only cause neurodegeneration in these disease conditions, but also cause abnormal pain by acting on spinal cord dorsal horn neurons in injury conditions. Pain can also be potentiated by growth factors such as BDNF and bFGF that are produced by glia to protect neurons. Thus, glia cells can powerfully control pain when they are activated to produce various pain mediators. We will review accumulating evidence supporting an important role of microglia cells in the spinal cord for pain control under injury conditions (e.g. nerve injury). We will also discuss possible signaling mechanisms in particular MAP kinase pathways that are critical for glia control of pain. Investigating signaling mechanisms in microglia may lead to more effective management of devastating chronic pain.

Gene expression mapping in neuropathic pain : molecular plasticity in nociceptors and superficial dorsal horn

RESUME : La douleur neuropathique est le résultat d'une lésion ou d'un dysfonctionnement du système nerveux. Les symptômes qui suivent la douleur neuropathique sont sévères et leur traitement inefficace. Une meilleure approche thérapeutique peut être proposée en se basant sur les mécanismes pathologiques de la douleur neuropathique. Lors d'une lésion périphérique une douleur neuropathique peut se développer et affecter le territoire des nerfs lésés mais aussi les territoires adjacents des nerfs non-lésés. Une hyperexcitabilité des neurones apparaît au niveau des ganglions spinaux (DRG) et de la corne dorsale (DH) de la moelle épinière. Le but de ce travail consiste à mettre en évidence les modifications moléculaires associées aux nocicepteurs lésés et non-lésés au niveau des DRG et des laminae I et II de la corne dorsale, là où l'information nociceptive est intégrée. Pour étudier les changements moléculaires liés à la douleur neuropathique nous utilisons le modèle animal d'épargne du nerf sural (spared nerve injury model, SNI) une semaine après la lésion. Pour la sélection du tissu d'intérêt nous avons employé la technique de la microdissection au laser, afin de sélectionner une sous-population spécifique de cellules (notamment les nocicepteurs lésés ou non-lésés) mais également de prélever le tissu correspondant dans les laminae superficielles. Ce travail est couplé à l'analyse à large spectre du transcriptome par puce ADN (microarray). Par ailleurs, nous avons étudié les courants électriques et les propriétés biophysiques des canaux sodiques (Na,,ls) dans les neurones lésés et non-lésés des DRG. Aussi bien dans le système nerveux périphérique, entre les neurones lésés et non-lésés, qu'au niveau central avec les aires recevant les projections des nocicepteurs lésés ou non-lésés, l'analyse du transcriptome montre des différences de profil d'expression. En effet, nous avons constaté des changements transcriptionnels importants dans les nocicepteurs lésés (1561 gènes, > 1.5x et pairwise comparaison > 77%) ainsi que dans les laminae correspondantes (618 gènes), alors que ces modifications transcriptionelles sont mineures au niveau des nocicepteurs non-lésés (60 gènes), mais important dans leurs laminae de projection (459 gènes). Au niveau des nocicepteurs, en utilisant la classification par groupes fonctionnels (Gene Ontology), nous avons observé que plusieurs processus biologiques sont modifiés. Ainsi des fonctions telles que la traduction des signaux cellulaires, l'organisation du cytosquelette ainsi que les mécanismes de réponse au stress sont affectés. Par contre dans les neurones non-lésés seuls les processus biologiques liés au métabolisme et au développement sont modifiés. Au niveau de la corne dorsale de la moelle, nous avons observé des modifications importantes des processus immuno-inflammatoires dans l'aire affectée par les nerfs lésés et des changements associés à l'organisation et la transmission synaptique au niveau de l'aire des nerfs non-lésés. L'analyse approfondie des canaux sodiques a démontré plusieurs changements d'expression, principalement dans les neurones lésés. Les analyses fonctionnelles n'indiquent aucune différence entre les densités de courant tétrodotoxine-sensible (TTX-S) dans les neurones lésés et non-lésés même si les niveaux d'expression des ARNm des sous-unités TTX-S sont modifiés dans les neurones lésés. L'inactivation basale dépendante du voltage des canaux tétrodotoxine-insensible (TTX-R) est déplacée vers des potentiels positifs dans les cellules lésées et non-lésées. En revanche la vitesse de récupération des courants TTX-S et TTX-R après inactivation est accélérée dans les neurones lésés. Ces changements pourraient être à l'origine de l'altération de l'activité électrique des neurones sensoriels dans le contexte des douleurs neuropathiques. En résumé, ces résultats suggèrent l'existence de mécanismes différenciés affectant les neurones lésés et les neurones adjacents non-lésés lors de la mise en place la douleur neuropathique. De plus, les changements centraux au niveau de la moelle épinière qui surviennent après lésion sont probablement intégrés différemment selon la perception de signaux des neurones périphériques lésés ou non-lésés. En conclusion, ces modulations complexes et distinctes sont probablement des acteurs essentiels impliqués dans la genèse et la persistance des douleurs neuropathiques. ABSTRACT : Neuropathic pain (NP) results from damage or dysfunction of the peripheral or central nervous system. Symptoms associated with NP are severe and difficult to treat. Targeting NP mechanisms and their translation into symptoms may offer a better therapeutic approach.Hyperexcitability of the peripheral and central nervous system occurs in the dorsal root ganglia (DRG) and the dorsal horn (DH) of the spinal cord. We aimed to identify transcriptional variations in injured and in adjacent non-injured nociceptors as well as in corresponding laminae I and II of DH receiving their inputs.We investigated changes one week after the injury induced by the spared nerve injury model of NP. We employed the laser capture microdissection (LCM) for the procurement of specific cell-types (enrichment in nociceptors of injured/non-injured neurons) and laminae in combination with transcriptional analysis by microarray. In addition, we studied functionál properties and currents of sodium channels (Nav1s) in injured and neighboring non-injured DRG neurons.Microarray analysis at the periphery between injured and non-injured DRG neurons and centrally between the area of central projections from injured and non-injured neurons show significant and differential expression patterns. We reported changes in injured nociceptors (1561 genes, > 1.5 fold, >77% pairwise comparison) and in corresponding DH laminae (618 genes), while less modifications occurred in non-injured nociceptors (60 genes) and in corresponding DH laminae (459 genes). At the periphery, we observed by Gene Ontology the involvement of multiple biological processes in injured neurons such as signal transduction, cytoskeleton organization or stress responses. On contrast, functional overrepresentations in non-injured neurons were noted only in metabolic or developmentally related mechanisms. At the level of superficial laminae of the dorsal horn, we reported changes of immune and inflammatory processes in injured-related DH and changes associated with synaptic organization and transmission in DH corresponding to non-injured neurons. Further transcriptional analysis of Nav1s indicated several changes in injured neurons. Functional analyses of Nav1s have established no difference in tetrodotoxin-sensitive (TTX-S) current densities in both injured and non-injured neurons, despite changes in TTX-S Nav1s subunit mRNA levels. The tetrodotoxin-resistant (TTX-R) voltage dependence of steady state inactivation was shifted to more positive potentials in both injured and non-injured neurons, and the rate of recovery from inactivation of TTX-S and TTX-R currents was accelerated in injured neurons. These changes may lead to alterations in neuronal electrogenesis. Taken together, these findings suggest different mechanisms occurring in the injured neurons and the adjacent non-injured ones. Moreover, central changes after injury are probably driven in a different manner if they receive inputs from injured or non-injured neurons. Together, these distinct and complex modulations may contribute to NP.

Characterization of Nedd4-2 ubiquitin ligase expression in experimental neuropathic pain

Background: Neuropathic pain is associated with altered expression of voltage-gated sodium channels (VGSCs). The ubiquitin ligase Nedd4-2 regulates sodium channels and we have previously demonstrated in expression systems that this protein decreases the Nav1.7 current. Nav1.7 is the most abundant VGSC in dorsal root ganglion (DRG) and is a major contributor to pain perception. We hypothesize that Nedd4-2 modulates Nav1.7 channel density at the neuronal cell membrane and the goal of this present experiment is to characterize Nav1.7 and Nedd4-2 expression in the context of neuropathic pain. Methods: Biotinylation, Western Blot and Immunohistochemistry experiments for Nav1.7 and Nedd4-2 were performed in HEK transfected cells or in rodent DRGs 7 days after SNI surgery. We used antibodies against Nedd4-2 and Nav1.7 and several comarkers of DRG neurons (Peripherin for nociceptors, NF-200 for large myelinated cells, ATF3 for injured neurons). Data are expressed in proportion of positive cells (%) and protein signal ratio } SEM, n = 3-4 in each condition. Results: In HEK293 cells, upon co-expression of Nedd4-2, a decrease of 50% of Nav1.7 signal at the membrane is demonstrated (p ≤0.005). Immunofluorescence on DRGs neurons reveals a decreased number of positive Nedd4-2 cells in the SNI model (27.0 } 1.2%) versus sham group (43.4 } 3.5%) (p <0.005). Nedd4-2 is mainly colocalized with markers of small neurons and almost absent in large neurons. In addition, Nedd4-2 is predominantly decreased in injured ATF3 positive cells. Conclusion: Our results indicate that Nedd4-2 decreases Nav1.7 channels and currents at the cell membrane and that it is mainly expressed in nociceptors and downregulated after nerve injury. Taken together, our data suggest that the reduction of Nedd4-2, after nerve injury, modulates Nav1.7 activity and can contribute to neuropathic pain. We will further try to restore a normal level of Nedd4.2 via a gene therapy approach with viral vectors in order to soothe symptoms of neuropathic pain.

Anaesthetics, Pain Relief and Critical Care Follow Up (PDF 797 KB)

In 2003/2004 the Department of Health, Social Services and Public Safety commissioned a value for money follow-up audit of Anaesthetics, Pain Relief and Critical Care (APRCC) services at twelve Trusts and covering fourteen hospital sites. The original study had reported in 1999/2000. Detailed follow-up reports, together with action plans have been agreed locally with Trusts. The objectives of the follow-up review were to: • Ascertain the progress made in implementing recommendations from the original study; • Provide data to compare performance across Trusts in areas such as: - Pre-operative assessments; - Organisation of post-operative pain relief; - Organisation of chronic pain services; - Levels of admissions to critical care units; - Occupancy in critical care units; and åÊ • Assess the extent of progress made by Trusts in the implementation of the Chief Medical Officer’s (CMO) recommendations from ‘Facing the Future –Building on the Lessons of Winter 1999/2000’. To enable comparisons across Trusts, data was collected for the financial year 2002/2003. In addition, relevant findings from the Audit Commission’s Acute Hospitals Portfolio have also been included. The Acute Hospital Portfolio is a collection of reviews that are undertaken at acute and specialist Trusts. They focus on key service areas and are reported along the key performance criteria of patient experience, efficiency and capacity. åÊ

Anaesthetics, Pain Relief and Critical Care Services in Northern Ireland - Regional Summary (May 2002)

Anaesthetics, Pain Relief and Critical Care Services in Northern Ireland - Regional Summary (May 2002) Pages 1 to 7 (PDF 276 KB)åÊ Pages 8 to 14 (PDF 392 KB)åÊ Pages 15 to 20 (PDF 265 KB)

Managing Your Cancer Pain in Hospital and at Home (PDF 32 KB)

The purpose of this booklet is to give you information about pain. It will help you understand how to describe pain, and how the pain may be treated.

General Palliative Care Guidance for Control of Pain in Patients with Cancer (PDF 56 KB)

This document is intended to be a practical clinical guideline for the control of pain in patients with cancer. Its target group is hospital staff, primary care team members and nursing home staff. It attempts to apply the clinical principles outlined in the document 'Control of Pain in Patients with Cancer' published by "Scottish Intercollegiate Guidelines Network" (SIGN). This document has been adapted with the permission of SIGN. Rigour of Development A full evidence based reference list is available with the SIGN document. This can be accessed at www.sign.ac.uk. Contents not based on the SIGN document are referenced separately. This document has been developed as one part of the recommendations identified in the Regional Review of Palliative Care Services, 'Partnerships in Caring'. The development of these Pain Guidelines was led by the Northern Ireland Group of the National Council for Hospice and Specialist Palliative Care, whose membership is detailed in Appendix 4. They will be reviewed and updated in two years. A wide consultation process with potential users was undertaken. åÊ åÊ

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Musculoskeletal disorders (MSD) are the most prevalent pain disorders in industrialized countries, and their costs can represent up to 2% of gross national product. MSD are often work associated and recurrent and may lead to disability. In occupational health we are interested in the opposite process : in the return to work (RTW). Different models of disability and RTW exist with different conceptions of psychosocial factors. We therefore propose to analyze the influence of factors from work, patient, health care providers, and broader societal domains along the different phases of the MSD process, adopting a biopsychosocial approach. The analysis of risk factors for the different phases of MSD indicate that work stress factors have an impact on the occurrence of MSD and RTW with MSD, but their effect is low to moderate and nonspecific. Physical work demands, work place adaptation, and pain experience are much stronger predictors of RTW. Lack of modified or adapted work is one of the major factors that hinder RTW. The longer the pain lasts, the longer the patient is out of work, the more personal factors and broader context factors become dominant. There is a clear lack of RTW studies concerning neck and upper limb pain. MSD and especially chronic MSD should be viewed as public health concerns, implying a wider socio-economic and insurance and disability problem. Adequate medical support tailored to the different dimensions and phases of MSD must be on offer, and work accommodations must be promoted and supported.

Chest pain and ST-segment elevation in a patient with Duchenne muscular dystrophy, what really happened?

Introduction: Myocardial infarction is rare in children, if it occurs, findings are almost similar to adults. In Ouchenne muscular dystrophy (OMO), ST segment displacement associated with typical chest pain can occur. We report the case of a young boy with OMO presenting symptoms suggestive of myocardial ischemia. Case report: 7 year old boy, diagnosed with OMO, eoming to the emergency department with complaints of acute chest pain, dyspnoea and anxiety the night before. Clinical examination was not remarkable, with exception of findings of the OMO. ECG showed important ST-segment elevation in right precordial leads. Major increase in troponin 1 42.33 mcg/(normal, <0.04 mcg/I) was found. Echocardiography revealed slight yskinesia of postero-septal wall without decrease in ventricular function. As acute pain had happened more han 12 hours before referral and as the child was asymptomatic, he received anti-platelets therapy. The serum level of troponin 1 declined and the ECG normalised in a few days. Cardiac catheterization did not show any coronary anomaly or eardiac dysfunction. Cardiac biopsy revealed myocardial cell damaged compatible with OMO cardiomyopathy. Tc99m myocardial single-photon emission computed tomography (SPECT) did not show any radionuclide uptake defect. Conclusions: ln this particular context of children with OMO, the classical signs of myocardial ischemia could be misleading, standard investigation failed to demonstrate the cause of chest pain and inerease of troponin l, there was also no evidence of myocarditis. Role of late enhancement (LE) signal in eontrast-enhanced MRI in the understanding of the occurring process has to be evaluated.

Revue critique d'instruments pour evaluer la douleur chez les personnes cérébrolésées non communicantes aux soins intensifs [Critical review of instruments to assess pain in the non communicative brain injured persons in intensive care].

The purpose of this review is to critically appraise the pain assessment tools for non communicative persons in intensive care available in the literature and to determine their relevance for those with brain injury. Nursing and medical electronic databases were searched to identify pain tools, with a description of psychometric proprieties, in English and French. Seven of the ten tools were considered relevant and systematically evaluated according to the criteria and the indicators in the following five areas: conceptualisation, target population, feasibility and clinical utility, reliability and validity. Results indicate a number of well designed pain tools, but additional work is necessary to establish their accuracy and adequacy for the brain injured non communicative person in intensive care. Recommendations are made to choose the best tool for clinical practice and for research.