Chronic pelvic pain is constant or intermittent pain persisting greater than 6 months in the pelvic or lower abdominal region.

This definition features wide variation worldwide and lacks a clear standard classification method even agreed among various scientific institutions worldwide.

Chronic pelvic pain is estimated to affect 4% of all women and 15% of reproductive age women.

Chronic pelvic pain is a symptom of a condition, not a diagnosable condition in itself.

Obesity is the excess accumulation of adipose tissue.

WHO 2016 estimated 40% of women worldwide were overweight with 15% classified as obese.

These numbers represent a tripling since 1975 from 650million to 1.9billion.

The most common measurement of obesity is a body mass index (BMI) value greater than 30 kg/m ² , however this does not effectively account for gender.

More female specific measures of obesity are

• a.
  

  Waist circumference greater than 88 cm (35inches)

  
  
• b.
  

  Waist-to-hip ratio greater than 0.85

  
  
• c.
  

  Greater than 30% body fat percentage.

There is a shortage of existing research in the field of obesity and chronic pelvic pain relationship.

In the passing comments which do mention the relationship, the implication is that increased BMI causes increased severity of chronic pelvic pain.

Most information regarding chronic pelvic pain and obesity is extrapolated from other chronic pain syndromes.

Pain is the stimulation of nociceptors, transmitting impulses via spinal cord, thalamus, and limbic system to its perception portion of the cerebral cortex.

Chemical mediators are released in the offending area and can manipulate the signal all the way through the passage from receptor to brain.

Adipose tissue is a source of inflammatory proteins such as tumour necrosis factor alpha (TNF-α), interleukin-6 (IL-6), and IL-1 beta (IL-1β).

Common regulators of body homeostasis have shown involvement with inflammation and pain sign modulation.

Leptin, produced to inhibit hunger, may also increase C reactive protein (CRP) levels increasing pain perception.

Ghrelin is secreted in the stomach to increase hunger and glucose metabolism; its levels are decreased in obesity.

Ghrelin also inhibits IL-6, IL-1β, and TNF-α reducing inflammation.

Ghrelin increases nitric oxide synthase production which modulates μ-opioid receptors and produces an antinociceptive effect.

All these effects cause an increased level of inflammation and susceptibility to pain in obese people due to the reduction of ghrelin secretion.

Appetite is also stimulated by neuropeptide Y (NPY).

NPY stimulates appetite and reduces energy expenditure.

NPY also stimulates glucocorticosteroid production, gluconeogenesis, and glycogen storage.

Interactions with ghrelin, leptin, and insulin-like growth factor further contribute NPY to obesity.

Nociceptive effects of NPY appear to be linked to the site of the receptor, CNS NPY stimulate analgesia, peripheral postsynaptic receptors stimulate hyperalgesia.

Obese women have higher serum NPY levels.

The orexinergic system consisting of neuropeptides, orexin A and B stimulate appetite and reduce pain perception.

Orexin systems are stimulated in stress times, acute or chronic pain, to inhibit pain transmission and improve physical performance.

Due to this stimulation, chronic pain can contribute to weight gain.

Due to these associations, obesity is being considered a proinflammatory state.

Obese people are at greater risk of neuropathic pain development, for example, peripheral neuropathy.

The effect of obesity on pain is unclear with studies finding opposite results in terms of the relation between BMI and pain effects.

Obesity is more prevalent in chronic pain sufferers, pain limits physical activity.

This limited activity leads to weight gain and deconditioning.

This creates a cycle for pain and weight gain.

Weight can cause structural changes making development of pain more likely.

Quality of life surveys show that weight loss can significantly improve bodily pain scores.

Genetics is thought to play a role in obesity, pain perception, and sensitivity.

Studies indicate there is likely a heritable component to pelvic pain, through a heightened level of pain perception and sensitivity.

No current studies have been done to investigate the genetic link of obesity and chronic pelvic pain.

However, there is growing research showing a genetic link between obesity and pain in other areas, for example, lower back pain.

Melanocortin receptor 4 (MC4R) mutation cause appetite dysregulation and hyperphagia; incidence of MC4R deficiency is noticeably greater in obese populations compared to the general population.

Melanocortin receptors are also implicated in regulation of pain and chronic pain syndromes.

Another pathway may be glucocorticoid receptor gene polymorphisms.

Impaired receptor function creates glucocorticoid resistance.

Negative feedback because of this causes excessive production of glucocorticoids causing inflammatory cytokine stimulation such as CRP and visceral fat accumulation.

Many of the comorbidities of chronic pain and obesity are also implicated.

There is a likely bidirectional effect between psychiatric disorders and both obesity and chronic pelvic pain.

Either reduce a person’s quality of life and both likely cause an additive effect.

Both obesity and chronic pelvic pain demonstrate body image distortion elements.

There is minimal research investigating the psychological effect of both obesity and chronic pelvic pain in combination.

It has been suggested that obese women with chronic pelvic pain experience show an increase in depressive symptoms but not anxiety symptoms.

Chronic pain and obesity show a cumulative negative effect on psychological morbidity.

Anxiety and depression increase circulating levels of CRP and IL-6 in the obese individual.

Weight-loss treatments have been shown to improve quality of life and pain management in chronic pain management sufferers.

Pain treatments effect on weight loss has not been studied.

In developed countries, women from low socioeconomic backgrounds are more likely to be obese.

There is also a negative relationship between socioeconomic status and chronic pelvic pain.

Economic hardship has a negative effect on mental health.

In low socioeconomic groups there is potential for a compound effect of economic hardship, chronic pelvic pain, and obesity on mental health.

The excess adipose tissue in obesity increases the difficulty and limits the effectiveness of the pelvic examination which is necessary to distinguish between various aetiologies of pelvic pain.

This is compounded by the lack of appropriate equipment, such as larger instruments and bariatric examination couches.

The pitfalls and barriers present in obesity, chronic pelvic pain, and low socioeconomic groups have many similarities.

In groups with overlaps between these three conditions the barriers are raised due to the compound effect.

Due to difficulties in pelvic examination, imagining is becoming more prevalent. Ultrasound is the method of choice; however, alterations need to be made to minimise the effects of excess fat on the quality of images.

Experience in working with these images also presents a challenge.

Excess fat also presents an increased risk of muscular strain to the sonographer.

CT and MRI can produce better images, however there are restrictions on their use and there is an upper limit of capacity for weight and gantry diameter in these machines.

The supine position inside the machine can potentially cause hypoxia and hypotension secondary to aorto-caval compression by a large pannus.

Estimation of contrast dose for CT scan is challenging as it is based on lean body weight, and the increased radiation exposure, which is required for optimisation of image quality.

The oral contraceptive pill (OCP) is often used as an empirical treatment of chronic pelvic pain as oestrogen is a pain modulator.

Obesity and OCP both increase risk of venous thromboembolism (VTE) by two to three times, respectively.

Both obesity and OCP are likely to cumulatively increase the risk of VTE.

Obese OCP users are 10 times more likely to have a VTE event than normal nonusers.

Obese OCP users are also thought to potentially have an increased risk of acute myocardial infarction.

Hormonal treatment is the first line of common potential gynaecological conditions (endometriosis and adenomyosis),

The effect of OCP has not been adequately assessed in the treatment of chronic pelvic pain.

Progesterone -only subdermal implants and intrauterine devices are preferred methods of hormone suppression in obese patients.

Dosing recommendations of analgesic are based on total body weight from studies that do not include obese cohorts.

Obese people have a large magnitude of changes affecting clinical efficacy and drug metabolism, thought to be associated with lipophilicity of the drug.

Opioids and other sedating analgesics may exacerbate existing abnormal breathing patterns, thus compounding the risk of hypoxemia via central sleep apnoea, OSA, and ataxic breathing.

Neuropathic pain medications and hormonal suppressants may promote weight gain.

Psychological component of chronic pelvic pain in obese patients must be considered as pain management success is reduced in this combination.

Cognitive behavioural therapy, goal setting techniques, and development of coping strategies have been shown to be effective in obese chronic pelvic pain sufferers.

Investigation and management of chronic pelvic pain may require diagnostic laparoscopy.

Laparoscopy requires a steep Trendelenburg position which can be difficult in obese patients, this is worsened by the excess adipose tissue viscerally as well as externally obscuring view and increasing the risk of injury.

The gastric changes in obese patients increases the risk of gastric aspiration during laparoscopy in this cohort.

Detrimental respiratory changes of obesity are compounded by the effects of the general anaesthesia, increasing the risk of hypoxemia and the degree of intrapulmonary shunting.

Pneumoperitoneum pressures necessary for laparoscopy further exacerbate the physiological changes of obesity.

Compromise between anaesthetist and surgeon regarding depth of incline and insufflation pressures are necessary to trade between surgeon fatigue and impact on respiratory physiology.

Laparoscopy is preferred to laparotomy due to the lower complication rate.

Robot-assisted laparoscopy may decrease operation time, blood loss, and length of hospital stay.

However, only literature for oncological problems is available and nothing specifically relating to chronic pelvic pain.

Endometriosis is an oestrogen-dependent inflammatory condition and the most common gynaecological disease among reproductive age women with chronic pelvic pain.

Increased levels of adipose tissue in obese women results in increased levels of aromatase expression, causing higher oestrogen levels by the following mechanisms:

• a.
  

  the increased numbers of adipose cells result in increased aromatase enzyme activity resulting in increased circulating oestrogen;

  
  
• b.
  

  increased conversion of the less active oestrone to the more active oestradiol by the β-hydroxy steroid dehydrogenase type 1 enzyme;

  
  
• c.
  

  increased number of oestrogen receptors;

  
  
• d.
  

  decreased numbers of progesterone receptors;

  
  
• e.
  

  higher levels of leptin and lower levels of ghrelin in the peritoneal fluid of women with endometriosis show higher levels of CRP and IL-6.

These higher levels of oestrogen show the link between obesity and endometriosis, and other oestrogen-related cancers of ovary, breast, and endometrium are seen more often among obese women,

It is not yet proven if it is a causality or merely an association in this similar risk profile group.

However the correlation between higher BMI and the severity of endometriosis is controversial.

It is more likely that higher levels of oestradiol can result in neuromodulation with enhanced sensitivity of peripheral nerves and modulate CNS activity.

Minimal to mild disease can not be identified with imaging modalities, and MRI is more likely to identify endometriosis than transvaginal ultrasound.

Endometriosis requires long-term hormone suppression therapy, as previously discussed OCP increases VTE risk so therefore progesterone-only suppression is recommended.

Oophorectomy may be used as a last resort for treatment of endometriosis.

Recurrence of symptoms within 5 years may be due to increased aromatase enzymes in obese women.

Menopause increases risk of several other conditions also exacerbated by obesity (coronary heart disease, depression, anxiety, and all-cause mortality).

Adenomyosis is the presence of ectopic endometrial-like tissue within the myometrium.

Adenomyosis has a higher incidence in obese women.

Most symptoms of adenomyosis can be managed with hormone suppression or hysterectomy.

The challenges with hormonal suppression and surgical treatment are the same as endometriosis.

MRI preferable to ultrasound in cases of suspected adenomyosis because of greater sensitivity and positive predictive value.

Abdominal myofascial pain syndrome can affect up to 93% of women attending pain clinic.

The syndrome causes inflammation and intense pain in the pelvis activated by trigger points in muscle fascia, which can be palpated as taut bands or spasm of the rectus abdominus and pelvic floor muscles.

Pelvic organ prolapse, which obesity increases the risk of, may also be a cause of this pain.

Diagnosis of this condition is difficult due to the earlier challenges in pelvic examination as well as the thickening of subcutaneous layer.

Non gynaecological causes can be urological, gastrointestinal, musculoskeletal, or psychological.

Interstitial cystitis and irritable bowel syndrome, although commonly seen in women with chronic pelvic pain and endometriosis, have questionable links to obesity as causes of pelvic pain.

Lower back pain is directly related to BMI and obesity and may refer to pelvic pain.

Victims of sexual, verbal, or physical abuse may be obese and have chronic pain including pelvic pain.

The inconsistency of the definition of chronic pelvic pain is problematic to coalescing ideas.

Although poorly researched, there are several probable links between obesity and chronic pelvic pain.

Multidisciplinary management of chronic pain results in reduced pain, somatisation, use of hospital resources, and increased mood and speed of return to work.

Obesity proves challenging for the assessment and management of chronic pelvic pain, as such adequate equipment is vital.

MRI is the preferred method of imaging.

Progesterone-only hormone suppression is more beneficial as it avoids complications.

Patient education, respectful communication, legitimisation of their pain, and multidisciplinary holistic care overcomes the barriers of management of chronic pelvic pain in obese women.