Gynecological pain
Gynecological pain
Gynecological pain may be one of three:
- Cyclic (primary dysmenorrhea, secondary dysmenorrhea, mid cyclic pain and early endometriosis.
- Acute (disturbed ectopic, adnexal torsion, labor pain and complication of ovarian cyst or fibroid)
- Chronic pelvic pain persistent non cyclic pain for at least 6 months affecting general condition of patients. Moderate or severe endometriosis, pelvic congestion syndrome and nerve trapping.
- Pain has been described as an “unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage”.
Pain pathway:
- Pain pathways, is a complex pathway. The major pathway which transmits pain (and temperature) from the body to the brain is known as the spinothalamic tract and consists of several components :
- Nociceptors, which then enter the spinal cord through the lateral division of the dorsal horns. These axons then form the Tract of Lissauer which travels up and down for one or two spinal segments on the same (ipsilateral) side of the spinal cord. These axons then enter the gray matter of the spinal cord and send projections to neurons in Rexed’s laminae I (also known as the marginal zone), II (also known as the substantia gelatinosa), III, and IV.
- Axons in Rexed’s laminae I–IV synapse with second-order neurons in Rexed’s laminae V, VI, VII, and VIII, which are collectively known as the nucleus proprius. Some of the axons in Rexed’s lamina I synapse with second-order neurons located within the same lamina. These second-order neurons from Rexed’s laminae V–VIII along with second-order neurons from Rexed’s lamina I have axons, which cross the midline in the anterior white commissure and ascend to the brainstem and thalamus in the anterolateral quadrant on the contralateral half of the spinal cord as the spinothalamic tract. Pain fibers from the sacral and lower areas of the body are located laterally in the spinothalamic tract, whereas those transmitting pain from the upper half of the body are found on the medial side of the tract.
- Once in the brain, the second-order neurons synapse and terminate with neurons found in the ventro posterolateral nucleus (VPL) of the thalamus. These third order neurons have projections to various parts of the brain such as the frontal cortex and the anterior cingulate gyrus which then modulate both the emotional and behavioral response to pain via descending pathways.
Two types of pain could be perceived:
1. Visceral pain—this is the pain transmitted by nociceptors from internal organs and may be referred to areas of the body distant to the organ. This type of pain is typically vague and difficult to localize. Usually referred to the corresponding dermatome innervated by the same root.
2. Somatic pain—this is the pain transmitted by nociceptors in the skin and deep tissues. The pain by comparison with visceral pain is localized to the area where the nociceptors have been stimulated.
Innervation of the Uterus and Cervix:
The uterus is functionally formed of two components: the cervix and the body (corpus uteri).
- The uterus is supplied by both somatic and autonomic nerve fibers from the hypogastric plexus.
- The hypogastric plexus is a continuation of the aortic plexus and is found anterior to the terminal aorta, fifth lumbar vertebra, and the sacral promontory.
- The afferent (sensory) fibers, which transmit pain from the uterus, travel in close association with sympathetic nerve fibers in the hypogastric plexus to the sympathetic chain before entering the spinal cord.
- In addition, efferent nerve fibers travel from the spinal cord via the hypogastric plexus to modulate smooth muscle activity in the cervix.
- The parasympathetic supply to the uterus is from the second, third, and fourth sacral segments, collectively known as the pudendal nerve .
In summary, the nerves derive from the inferior hypogastric plexus. Sympathetic innervation originates from the T12 and L1 spinal segments, while the parasympathetic nervous supply is provided by the S2 to S4 spinal segments. All vessels and nerves run through the lateral ligaments, a broad duplication of the peritoneum connecting the lateral wall of the uterus with the pelvic wall.
Primary Spasmodic Dysmenorrhea:
- It is defined as Painful menstruation without underlying pathology.
- It is Commonest in teens/early twenties
- Onset 1 or more years after menarche as its affecting ovulatory cycle. In other words, non-ovulatory cycle are usually painless.
- It is associated vomiting and faintness due to vaso-vagal stimulation
RISK FACTORS:
1.Age < 20 years
2.Attempts to lose weight
3.Depression / anxiety
4.Disruption of social networks
5.Heavy menses
6.Nulliparity
7.Smoking
CLINICAL PRESENTATION:
- Usually presents during adolescence, within three years of menarche. Unusual for symptoms to start within the first six months after menarche. Pain usually develops within hours of the start of menstruation and peaks as the flow becomes heaviest during the first day or two of the cycle Symptoms of nausea, vomiting, diarrhea, fatigue, fever, headache or lightheadedness. Pain character is as follow.
- It is colicky (Spasmodic) in character, started at onset of menstruation then it is reaching to peak in intensity till establishing in flow, radiated to inner aspect of thigh and to the back may be associated with nausea and vomiting, usually patient is nullipara.
Causes of pain may be ischemia of the myometrium. Contraction of the myometrium against closed cervix,
It is pathogenesis due to disturbances in prostaglandins in favour of PG F2α and drops of PGE2. Prostaglandin F2 alpha has a contraction effect on the smooth muscle fibers of the uterus. While PGE has its effect on the blood vessels only.
Management Primary Spasmodic Dysmenorrhea:
Diagnosis :
No abnormalities should be detected in Examination., investigation.
Treatment:
Prevention of primary (spasmodic dysmenorrhea:
- Various measures have been used to manage dysmenorrhea in the outpatient setting, including the following:
- Lifestyle modification seems to be helpful.
- Smoking cessation should be encouraged, in that smoking may be a risk factor for dysmenorrhea.
- Exercise has been shown to alleviate symptoms of dysmenorrhea, though the mechanism is not well understood.
- Education and reassurance.
Physiotherapy treatment:
- Acupuncture, acupressure, various herbal medicines and dietary supplements, transcutaneous electrical nerve stimulation (TENS) units, and massage therapy and isometric exercise have been suggested for therapeutic use in this setting. Topical application of continuous low-level heat may be beneficial for some patients. Interruption of nerve pathways has been performed.
Treatment of pain:
- Prostaglandin synthetase inhibitors.
- Spasmolytic.
- Nitrous oxide donors.
- Ca channel Blockers; transdermal nitroglycerin, blockers, beta-adrenergic agonists, antileukotrienes.
- Combined oral contraceptive pill-choose a progestagen dominant pill
- “Bicycle” or “Tricycle” pill.
- Failure to respond to Pill increases likelihood of underlying pathology.
- LUNA laparoscopic utero-sacral nerve ablation.
Secondary (Congestive) Dysmenorrhea:
Painful menstruation secondary to a cause. The presence of pathology will lead to hyperaemia and congestion of vessels. These hyperaemiae and congestion of vessels will result in ill defined dull aching pain in the pelvis and the back.
Dysmenorrhea ( painful menstruation) | Primary (spasmodic) dysmenorrhea | Secondary (congestive) dysmenorrhea |
Onset | Sudden at time of start of menstruation | Gradua l7 days before menstruation |
Age | Less than 20 | More than 20 |
Character of the pain | Colicky (spasmodic) | Heaviness dull aching |
Peak of pain | First day | Before start of menstruation |
End of pain | Establishment of flow | End of menstruation |
Pathology | No pathology | Present (fibroid, endometriosis , adenomyosis, PID, …..etc) |
Pathogenesis | disturbance in the level of prostaglandin PG F 2 α > PG E2 | Congestion of pelvic blood vessels |
Site of pain | Suprapubic | Back |
referral | Inner aspect of the thigh and back | No |
What increase | Heavy menstruation or passage of clot | Constipation |
What decrease | Re-assurance, exercise, TENSE, Acupuncture, | |
Treatment | Anti spasmodic anti prostaglandin ca channel blocker, nitrous relasing, LUNA | Treat the cause |
Risk factor | Nulliparity, smoker, depreesion, positive family history | Multiparity, infertility |
Due to a cause e.g.
- Endometriosis: Endometrial gland outside the uterus
- Fibroids: benign tumour of smooth muscle of the myometrium
- Adenomyosis: endometrial gland embedded deep in the myometrium
- Pelvic Inflammatory Disease
- Uterine anomalies
Treatment of secondary (Congestive) dysmenorrhea:
- Treatment of the cause is the main line of management of congestive dysmenorrhea.
Premenstrual Tension Syndrome:
- Molimina, During the reproductive years, up to 80-90% of menstruating women will experience symptoms [breast pain, bloating, acne, constipation] that forewarn them of impending menstruation, so-called premenstrual molimina.
- Premenstrual Syndrome [PMS], The term PMS continues to be used; however, as it may encompass a wide range of severity and therefore is not particularly useful in defining cohorts for research or in directing the most appropriate therapeutic interventions.
- Premenstrual Dysphoric Disorder [PMDD], should be reserved for a more severe constellation of symptoms, mostly psychiatric, that lead to periodic interference with day-to-day activities and interpersonal relationships. Women with this degree of symptoms probably comprise 3-5% of women in their reproductive years
Etiology:
- Many theories of etiology have been proposed and disproved for this poorly understood condition, contemporary work suggests that PMDD is the result of an aberrant response of central neuro-transmitters to normal changes in gonadal steroids during the menstrual cycle. Other theories, while having some biological plausibility, have not or cannot be confirmed with available diagnostic techniques. No one theory has gained universal acceptance although consensus is developing that in some susceptible women normal swings in gonadal hormones appear to mediate changes in the activity of central neurotransmitters, such as serotonin, that in turn incite profound changes in mood and behaviour. Although it is likely that many of the physical symptoms (breast tenderness, bloating constipation) are the direct effect of gonadal steroids, it is exciting that treatment of PMS with selective serotonin reuptake inhibitors will ameliorate the severity of not only psychological but also physical complaints.
- PMS disappears during suppression of the ovarian cycle (for example, during hypothalamic amenorrhea due to excessive physical, or nutritional stress, during lactational amenorrhea, during pregnancy, and after menopause – either natural or induced). It is useful when evaluating a woman with suspected PMS to confirm that PMS symptoms did indeed disappear in these circumstances. Contrary to the popular belief, there is no convincing evidence that PMS begins after pregnancy or tubal ligation. This belief probably originated when PMS symptoms reappeared and seemed acutely worse after the hormonal “protection” of pre-existing pregnancy or lactation. PMS also, disappears after natural, medically or surgically induced menopause although the reintroduction of exogenous hormone replacement therapy may be associated with the reappearance of symptoms. Typically, the use of sequential progestin triggers PMS symptoms in susceptible women whereas continuous combined hormone replacement therapy is less likely to be associated adverse mood changes.
Symptoms:
A) Affective
1. Anger/irritability
2. Anxiety/tension
3. Tearful/Increased sensitivity to rejection
4. Depressed mood/hopelessness
5. Decreased interest in work activities
6. Decreased interest in home activities
7. Decreased interest in social activities
8. Difficulty concentrating
9. Fatigue/lack of energy
10. Overeating/food cravings
11. Insomnia
12. Hypersomnia (needing more sleep)
13. Feeling overwhelmed or out of control
B) Physical
14. Physical symptoms: breast tenderness, headaches, joint/muscle pain, bloating
weight gain.
Physical finding Examinations:
- There are no characteristic physical findings in women with PMS. When seen in the follicular phase of the cycle, PMS sufferers typically appear entirely normal. Premenstrually, a woman presenting with an acute episode of PMDD may appear anxious, tearful, or angry, depending on the nature of her symptom complex.
Chronic pelvic pain:- Many authors have used duration of at least 6 months that occurs below the umbilicus and is severe enough to cause functional disability or require treatment and the pain is non-cyclic
Population at Increased Risk:
- Demographic profiles of large surveys suggest that women with chronic pelvic pain are no different in terms of age, race and ethnicity, education, socioeconomic status, or employment status
- May be slightly more likely to be separated or divorced
- Tend to be of reproductive age
- Age is not a specific risk factor
Gynecologic Causes of Pelvic Pain:
- Endometriosis[i]
- Adhesions (chronic PID[ii])
- Leiomyomata
- Adenomyosis[iii]
- Pelvic congestion syndrome
- Adnexal masses
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