Persistent Pelvic P ain - PowerPoint Presentation

1. Persistent Pelvic Pain Beyond the initial causeD. halmagiu

2. Our Patients

3. IntroductionPersistent pelvic pain (PPP) affects 15–26% of women. It is defined by pelvic pain for more than 3–6 months that is not solely related to menstruation, sexual activity or bowel movements.PPP is caused by a complex combination of visceral and musculoskeletal pain, central sensitisation and pelvic floor hypertonicity, often accompanied by evolving psychological dysfunction.

4. Persistent Pelvic Pain (PPP)ProblemsLack of robust classification - epidemiology studies difficultSubjectivity of syndromes - inter-clinician variabilityGeneral absence of understanding Complicated patient journey Protracted referral process Loss of faith and disengagement Late or wrong treatment initiated

5. Source of Persistent Pelvic Pain (PPP)pain from end organs (pelvic organs)musculoskeletal response to paincentral and peripheral sensitisation of nerve pathwayspsychosocial sequelae of the pain conditionpsychosocial context

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7. PPP - Co-existing Pain Conditions= Central SensitizationVulvodyniaPainful bladder syndromeIBSFibromyalgiaMigraine, tension headacheCLBPChronic neck painChronic fatigue related to painTMJ pain

8. Persistent Pelvic Pain (PPP) Pain is often the disease, a diagnosis in its own right

9. Visceral HyperalgesiaVisceral hyperalgesia is a pain state caused by peripheral and central sensitization, leading to abnormal perception of both painful and non-painful stimuli (primary hyperalgesia in the involved viscous)Increased sensory input to interneurons and/or projection neurons in the dorsal horn of SCMay cause secondary hyperalgesia – adjacent, undamaged visceral tissue develops sensitivity to normally innocuous stimuli (peripheral sensitization)May cause central hyperexcitability – including plastic changes in the synaptic circuitry of the dorsal horn for visceral inputs and convergent somatic inputs. Refers to increased pain sensation in response to gastrointestinal sensory stimulusStimulus can be: pressure, stimulation, distensionDue to an abnormal process arising from any level of the visceral nociceptive pathwayEven non-pathological, normal stimuli may produce pain from that organ

10. Peripheral SensitizationPersistent noxious stimulation of visceral nociceptors can produce hyperalgesia via: Inflammatory mediators (sensitize nociceptors by reducing threshold for activation, and increase response to stimuli)Inflammatory soup: K+, H+, ATP, 5-hydroxytryptamine, bradykinin, prostaglandin, serotonin (released by injured afferent fibres, damaged tissues, inflammatory cells)Ectopic activityNoxious stimuli (chemical stimuli, mechanical stimulation)Decrease in intensity of stimulus required to initiate depolarisationIncrease in number and amplitude of neuronal discharges in response to stimulusIf prolonged, these mediators induce changes including: Activating nociceptive afferentsSensitizes peripheral nociceptive afferents (reduce transduction thresholds)Enhanced excitability of afferent neurons in DRGRecruits previously silent nociceptors (tissue damage, inflammation, ischemia  becomes spontaneously active or respond to previously ineffective adequate stimuli)Increase input to 2nd order neurons in dorsal horn  Results in hyperalgesiaEnsuing disruption of cells, degranulation of mast cells, secretion by inflammatory cells, induction of enzymes changes the chemical milieu at site of injury  peripheral hyperalgesia

11. Central sensitizationAltered afferent input and release of neuroactive chemicals in the spinal cord dorsal horn Neuroactive chemical increase the excitability of spinal neurons which can develop either in response to peripheral tissue irritation or in response to descending influences originating in the brainstem. Prolonged noxious stimulation of viscera and peripheral sensitization of visceral nociceptors can promote excitability of the SC and higher centre neurons that mediate nociceptive processing (aka central sensitization)Characterised by increased spontaneous activity of central neuronsDecreased threshold for stimulation (innocuous afferent stimuli able to excite previously unexcitable nociceptive pathways)Increased receptor field sizeIncrease in magnitude of responseProlonged facilitation of reflexesAs hyperalgesia develops, several CNS changes occur including: Activation of NMDA receptor complexes (as hyperalgesia develops)Excitotoxicity causing cell death secondary to persistent barrage of SC by noxious stimuliDevelopment of a pain memory leading to persistent pain even though the primary cause has goneVoltage gated sodium channels (Nav1.8) may contribute to sensitization of visceral nociceptors (Nav1.8) TRPV1 expression upregulated in patients with IBS, correlates significantly with visceral pain

12. Autonomic InvolvementNervous system mediated degranulation of mast cells will results in release of histamine – shown to sensitize peripheral terminals of primary afferent fibres. Sympathetically maintained pain - Release of catecholamines and PG from sympathetic nerve terminals (in close proximity to the terminals of damaged primary afferent nerves) results in direct activation of afferent fibres that have developed (or upregulated) α adrenergic receptors

13. Bulbospinal pain inhibitory pathwaysRole in modulating the excitability of dorsal horn neurons receiving converging somato-visceral inputDetermines the:Size of receptive fieldsReferral areasPain thresholdsSignificant genetic, age, gender differences in activity of these pathways have been reported 

14. Causes of visceral hyperalgesia (theories)Alterations in visceral sensory processing from a perinatal event or during infancy (time when neuroplastic changes may permanently alter sensory processing)Permanent central, neuroplastic changes from excitotoxicity to inhibitory interneurons in SC (from surgical damage to afferent nerves)Stress induced alterations in the activity of descending inhibitory and/or facilitatory modulating systemsGenetic differences in the activity and responsiveness of descending modulating pain systems. Pain arising from nerves of cells lining the internal organChanges to micro RNA molecules of these cellsChanges in neurotransmitter and other receptors within these cellsChanges in interactions between CNS and PNSIncreased intestinal permeabilityInflammation (transient or chronic)

15. We Sometimes Struggle to See the Whole Picture

16. PPP Team ApproachGPGynaecologistPhysiotherapistPsychologistPain physicianUrologist?GastroenterologistDietician

17. Need for Multidisciplinary ManagementLifestyle advice:Gentle physical activityDiet (avoid high GI foods, processed, …)Sleep hygieneMindfulness, meditationPhysical means ; heat, hydrotherapy,TENS

18. Aims in ManagementManage pain (decrease, not eliminate) Decrease anxiety about painManage stressIncrease function despite painSupport, empathizeHelp with hyperactive bladder, IBS, sexPharmacotherapy Procedures only later

19. Pharmacological Treatment aiming to:Treat original cause if still activeTreat painTreat sensitization (amitriptyline, nortriptyline)Treat anxiety/depressionTreat bowel/IBSTreat hyperactive bladder

20. Really ImportantNeed for awarenessNeed for validation and supportEarly diagnosis if possible and treatmentEarly referral to multidisciplinary teamsEarly education to prevent and minimize psychological problemsLook for psycho-social context as it is often part of the picture

21. PPP - GP RoleRefer to find source, etiology , treat and resolve/improveReassure, educate, avoid catastrophizingSometimes discordance between severity of pathology and severity of painRefer to multidisciplinary teamEMPATHY - Listen, make them feel heard

22. PPP - SummaryWe often cannot sort out every pain!We aim to teach patients to manage pain and improve functionDespite medical training, this situation is not a binary one:Believing their pain does not have to mean to operate or medicate;Not operating or medicating does not mean we do not believe their pain.Believing their pain can mean to refer to another colleagueRefer early to multidisciplinary team (it might help with assessing multifaceted character of the problem)

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