3.5.1 - Appreciate the taxonomy of functional gastrointestinal disorders and chronic
pelvic pain syndromes, in particular, the trend to move away from end-organ
nomenclature
The move from end-organ nomenclature has been driven by increasing recognition of pain as a disease state in its own right.
It moves away from a purely biomedical focus and searching for an alternative cause
Previous ICD-10 either had the clear disease, or patients were classified as having a mental disorder. This is clearly incorrect with a newer understanding of pain processes.
Chronic Primary pain was designed to think of conditions as having 'positive' findings rather than being diagnoses of exclusion
Terms such as 'nonspecific' and 'somatoform' and 'functional' are vague and practically often unhelpful
Avoids the dichotomy of physical vs psychological
Visceral pain in ICD-11
Either Primary or Secondary
Secondary is intially described by mechanism (e.g. inflammation, vascular, mechanical) and then from body locations
Reference: IASP Chronic Primary Pain -
3.5.2 Discuss the concurrence of somatic and visceral pain syndromes
These can occur together. See details below regarding referred pain
3.5.3 - Generally describe the innervation of the viscera within the:
Revised version
Innervation of the visceral organs occurs with sensory afferent fibres which travel with sympathetic and parasympathetic efferents. These have usual paths of travel with the long sensory afferent nerve going to the DRG and then synapsing within the dorsal horn.
Colon = Lumbar splanchnic (T10-L2) and sacral pelvic nerves (L5-S1)
Bladder = Lumbar splanchnic (T10-L2) and sacral pelvic nerves (L5-S1)
Second = Lateral spinal nucleus, superficial dorsal horn, and dorsal commissure
Third = PAG
General:
Viscera are innervated by TWO sets of afferent nerves that share overlapping functions
Visceral innervation is sparse compared to sensory innervation of other tissues
Most viscera are derived from midline structures so have innervation bilaterally
Visceral structures also can have their own neural networks e.g. the enteric nervous system
Transduction is thought to occur via unencapsulated 'free' nerve endings in target organs
Other levels of transduction are not fully understood and are complex in nature
Only 5-15% of spinal afferents in the spinal cord arise from the viscera
Most noxious stimuli to the viscera are encoded by mechanoreceptors. However, these are commonly thought to be polymodal and can respond also to thermal and/or chemical stimuli
Vagus nerve
The vagal nerve supplies all internal organs of the chest and abdomen and extending to some pelvic structures
Cell bodies of the vagus nerve are located in the nodose and rostral jugular ganglia
Vagal central afferents project to the nucleus of the solitary tract (The vagus nerve is LONELY and solitary)
Spinal afferents traverse the pre and post paravertebral ganglion en route to the spinal cord
They may send branches into those ganglia but otherwise traverse across
They then typically terminate in the superficial laminae (1 and 2) of the dorsal horn
Thorax (cardiac and non-cardiac)
- Vagal nerve
- Runs with fibres of the upper thorax T1-T5
Abdomen (including peritoneal and retroperitoneal spaces)
Greater splanchnic and small splanchnic --> Coeliac plexus --> Stomach, Oesophagus, liver, pancreas, adrenal, small intestine
Superior mesenteric ganglion supplies first part of large intestine
Inferior mesenteric ganglion supples kidney, bladder, sexual organs and large intestine/rectum
Vagus nerve also has innervation in this region
Pelvis (female and male)
Inferior mesenteric ganglion supplies Rectum, kidney, bladder, an sexual organs
Pelvic nerves (parasympathetic) supply rectum, kidney, bladder, and sexual organs
With particular reference to:
Stellate ganglion
Sympathetic fibres of the head, neck, heart and superior limbs
They arise from the first thoracic segments, ascend in the sympathetic chain, and synapse in the superior, middle, and inferior cervical ganglions
The stellate ganglion is the fusion of the inferior cervical ganglion and first thoracic ganglion
Blocks can help with sympathetically mediated pain from abnormal connections between sympathetic and sensory nervous systems
Stellate ganglion nerve block has low-quality small studies suggestion benefit for CRPS of the upper limb
Splanchnic nerves
Paired autonomic nerves carrying both visceral sympathetic and sensory fibres, except for the pelvic splanchnic that carry parasympathetic fibres
Arise from the sympathetic thoracic trunk to innervate the abdomen
They are the greater, lesser and least splanchnic nerve
Greater = T5-9
Lesser = T10-11
Least = T12
The Greater and lesser join to form the coeliac ganglion and least splanchnic nerve ends by synapsing with the renal ganglion
After the coeliac plexus they move to the organs of the foregut as the coeliac plexus
Lumbar splanchnic nerve forms branches of the L1 and L2 sympathetic chain
Go to the aortic plexus -->
Hypogastric plexus
Inferior hypogastric plexus is otherwise known as the pelvic ganglion
Ganglion impar
Termination of the sympathetic chains causes a fused ganglion called the ganglion impar
Primary visceral afferents from the perineum, distal rectum, distal urethra, vulva, perianal area and distal one-thrird of the vagina travel alongside visceral sympathetic fibres converging on the ganglion impar.
Pudendal nerve
S2-4 nerve that traverses the pelvis and terminates into the inferior rectal nerve, perineal nerve, and dorsal nerve of the clitoris
3.5.4 - Demonstrate an understanding of the neurobiology underlying:
Visceral pain
Visceral fibres complete sensory and efferent functions
They are c-fibres and thinly myelinated Adelta fibres
Silent Abeta fibres can become sensitised and undergo phenotypic switching in times of sensitisation
Can be triggered by mechanical, chemical or thermal triggers.
Some visceral organ pain sensations are more completely received as pain than others e.g. liver tissue pain versus bladder wall
Visceral hyperalgesia
Pain or discomfort associated with non-noxious stimuli
E.g. Enhanced perception of afferent stimuli from the GI tract and genitourinary structures
Can manifest as lower thresholds, increased intensity, and/or atypical viscera-somatic referral areas
Peripheral sensitisation
Acute inflammation and tissue injury results in recruitment of previously mechano-insensitive afferent in addition to sensitisation of mechanically responsive afferents
Central sensitisation
Reduced descending inhibitory control and neuroplastic changes
Risk factors for visceral sensitisation to occur include:
Female sex
Duration of inciting event
Psychosocial stressors at the time
Psychological factors such as depression and anxiety
3.5.5 - Discuss current concepts of referred pain:
Mechanism of REFERRED pain:
Viscero-somatic convergence of afferent fibres in the dorsal horn
Signal misinterpreted by the brain as originating from a site distant from the original noxious stimulus
Mechanism of ALLODYNIA sensation:
Convergence-facilitation is where the nociceptive input from the viscera may sensitise dorsal horn neurons that also process somatic input
Sensitised second-order neurons are now responsible for non-noxious somatic input being perceived as painful.
Viscero-somatic
Pain felt in the skin, subcutis or muscle from a visceral source
Viscero-visceral
One sensitised organ causes sensitisation of another organ
Somato-somatic
Pain from one somatic site is also felt in a secondary somatic site
3.5.6 - Discuss the “brain-gut axis” and the neurohumoral functions of the gut
Gut-Brain Axis
Vagus nerve feedback from brain to gut (ANS, ENS, HPA axis)
Gut feedback to the brain - Immune, endocrine and neural pathways of feedback
Epigenetics – phenotypic expression of genes
Often environmental changes
Methylation can be induced by maternal neglect, emotional deprivation etc
Widespread changes in the glial cells and other CNS cells
Can impact upon the way we behave and perceive the world
3.5.7 - Elicit a history of painful visceral dysfunction, including but not limited to:
Dysuria - Painful urination
Dyschezia - Painful defecation
Dysmenorrhoea - Painful periods
Dyspareunia - Painful sexual intercourse
3.5.8 - Identify ‘red flag’ features that suggest active visceral disease.
Weight loss
Night sweats
Severe fatigue
Night pain
Visible blood e.g. PV, PR
Anaemia and iron deficiency
3.5.9 - Distinguish clinically between:
Active visceral nociception
Visceral hyperalgesia
Referred pain with and without hyperalgesia:
o Viscero-somatic
o Viscero-visceral
3.5.10 - Demonstrate a mechanistic approach to identifying non-visceral causes of
thoracic, abdominal and pelvic pain, especially post-surgical neuropathic
pain.
Differential diagnosis for non-visceral pain felt in visceral organ areas:
Neurological
Radiculopathy
Herpes Zoster
Abdominal migraine
Tabes Dorsalis
Haematological
HSP
Sickle Cell crises
Metabolic/Endocrinological
DKA
Acute porphyria
Lead poisoning
Addison's disease
Hypercalcaemia
Uraemia
Cancer related
Metastatic bone disease
MMyeloma
MSK
Psychological
Panic attacks
FND
Iatrogenic
Post surgical syndromes
Post-thoracotomy syndrome
Post-sternotomy syndreom
Post-mastectomy pain
Post-Caesarian section pain
Post-inguinal surgery pain
Radiation related
Chemotherapy related
Myopathy
Chronic post-surgical pain mechanisms
Massive injury signal followed by quiescence in peripheral nerve
Neurochemical release with biochemical and morphological CNS changes (plasticity)
Sprouting and microneuromata formation (microneuromata can ectopically fire and over-respond to low-threshold stimuli)
A basket-like spiderwebs of sympathetic nerves grown around the DRG sensitising them
New dendritic growths cause rewiring and convergence
3.5.11 - Demonstrate a mechanistic approach to differentiating causes of pain at the
somatic-visceral interface of the pelvis and perineum, in female and in male
patients.
Uncertain exactly what this is asking.
Remember that visceral pain is poorly localised commonly
True visceral pain is dull/colicky but can transform to sharp
Abdominal - worse with eating
Pelvic - Worse with urination, sexual intercourse, or defecation
Important to ask - Dysautonomia - Nausea, vomiting, pallor, diaphoresis, restlessness
3.5.12 - Discuss the principles of pharmacotherapy for visceral pain and visceral
hyperalgesia.
Evidence in these groups is weak and there are few studies demonstrating benefit for monotherapy
The UPOINT system has been suggested: Urinary, psychosocial, organ-specific, infection, neurologic/systemic and muscle tenderness.
Specific medications and therapies depend upon the condition but may include:
Antispasmodics (peppermint oil)
Hormonal treatments (female)
NSAIDs, paracetamol can be considered
Gabapentinoids, TCAs, SNRIs (<-- if evidence of neuropathic),
Ketamine and lignocaine infusions can be considered
Topical agents are an option
Opioids are last line pharmacologically
NB: TCA for chronic pelvic pain in women NNT = 3 (Cochrane review)
3.5.13 - Discuss the evidence base for the indications, effectiveness and adverse
effects of invasive therapies used for chronic visceral pain.
No evidence for much
SCS - For unrelenting angina
Neurolytic coeliac plexus block for pancreatic cancer ??Chronic pancreatitis
?? Sacral nerve stim for IBS - fairly unclear
Painful bladder syndrome - MAYBE some sacral neuromodulation evidence
Hysterectomy for pelvic pain - 30% are unhappy with the outcome
Neuromodulation for pelvic pain is unclear
Sacral neuromodulation may have benefit in pudendal neuralgia
Chronic prostatitis - Cochrane review suggested pregabalin no better than placebo
3.15.14 - Discuss treatment options for capsular pain associated with liver, spleen and
renal pathology.
Dexamethasone has been used in these settings
Could not find anything more specific
3.5.15 - Discuss the role of exogenous gonadal hormones in the treatment of
gynaecological visceral pain.
OCP - Helpful for endometriosis but limited evidence for non-cyclic pain
Cochrane review suggested moderate evidence in progesterone treatment for chronic pelvic pain (Depo IM every 12 weeks)
If endometriosis-injectable GNRH-agonist (e.g. gosrelin (zoladex) can provide longer-lasting effects) - Primarily used prior to surgery
3.5.16 - Discuss treatment options for the management of irritable bowel syndrome
Suspected IBS pathophysiology:
1. GI motility disorder with altered serotonin signalling
2. Visceral hypersensitivity disorder triggering sensitised nociceptors in gut wall
3. Intestinal barrier disorder with loss of tight-junctions. Inflammatory responses ++
4. Bile acids may affect intestinal permeability in response to different foods
5. Increased intestinal permeability following acute gastroenteritis from infection
6. Bacterial overgrowth
7. Intestinal microbiota imbalance with gut-brain communication complications
8. Low grade mucosal inflammation
9. Genetics contribution
Definition (Rome 4 criteria)
Recurrent abdominal pain 1 day/week over last 3 months with 2 or more of the following:
· Related to defecation
· Associated with change in frequency of stool
· Change in form of stool
Criteria filled for last 3 months and symptoms for 6
Subtypes
· Constipation, diarrhoea, or mixed, or unspecified
Management:
Management directed towards possible alterations in gastrointestinal flora, abnormal colonic transit time, and visceral hyperactivity.
Diet and Lifestyle interventions.
Evidence Summary
FODMAPS NNT = 2.2
General dietary change NNT = 9
Psyllium addition for 12 weeks NNT = 4-7
Probiotics NNT = 7
Antispasmodics NNT = 5
Peppermint oil NNT = 2.5
TCAs NNT = 4
SNRI NNT = 4
Rifaximin NNT = 10
(Camilleri M. (2018). Management Options for Irritable Bowel Syndrome. Mayo Clinic proceedings, 93(12), 1858–1872. https://doi.org/10.1016/j.mayocp.2018.04.032)
Specific foods/substances
•Gluten •Caffeine
•Fibre - conflicting evidence •Carbonated drinks
•Excessive Alcohol: rectal urgency •Smoking/Chewing gum (swallowed air)
•Gas-producing foods (beans, onions, celery, cabbage, Brussel sprouts)
FODMAPS: Fermentable Oligo-Di- Mono - Saccharides and Polyols:
Galactans: legumes Mannitol: corn sugar
Lactose: milk Sorbitol: corn sugar
Fructose: fruits Xylitol: corn sugar
Comorbid conditions
Comorbidities are twice as common as controls and are correlated with
More health-seeking
Worse prognosis
Higher rates of anxiety and depression.
Non-Pharmacological:
Acupuncture – equivocal (Cochrane)
Medication: Cochrane data...
Herbal preparations (data hard to interpret): complementary, alternative - unclear
Antispasmodics:
Peppermint oil NNT 2.5, hyoscine, dicycloverine, cimetropium
Acetylcholine competitors are more effective than placebo.
Antidepressants:
TCA NNT 4
SSRI’s 3.5
Anti- diarrhoeal
Loperamide avoid
No indication for benzodiazepines
Alter the flora of the large intestine - rifaximin (non absorbable antibiotic)
Two weeks treatment significant symptom improvement at 4 and 12 weeks
Probiotic (live or attenuated bacteria)
Anti-inflammatory effect.
Bifidobacteria show a trend towards benefit.
Analgesics
Little or no evidence for opioids - too many side effects, no pain reduction, and no functional or quality of life improvement.
Psychological intervention
Only marginally greater than placebo
CBT, hypnotherapy and multicomponent psychological therapy being more effective than relaxation therapy and self-administered CBT.
Behavioural intervention
Physical exercise as a group activity beneficial in coexisting chronic fatigue and FM symptoms of IBS
Sleep hygiene is beneficial but evidence for specific interventions is unclear. Melatonin may be of some benefit in women more than placebo.
Pain and symptom related education
In a group setting was related to higher rates of symptoms resolution
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