Textbook Of Gynecology. Dc Dutta’s

Chapter 10. Pelvic Infection

DEFENCE OF THE GENITAL TRACT

As there is free anastomosis between the lymphatics and blood vessels, the infection of one pelvic organ usually spreads to the other more frequently. There is direct communication of the peritoneal cavity to the exterior through the vagina. In spite of these, the frequency and intensity of pelvic infection is kept lowered by the defence mechanism.

Vulval Defence

Anatomic: (i) Apposition of the cleft by labia; (ii) Compound racemose type of Bartholin’s glands.

Physiologic: (i) Fungicidal action of the secretion (undecylenic acid) of the apocrine glands; (ii) Natural high resistance to infection of the vulval and perineal skin.

Vaginal Defence

Anatomic: (i) Apposition of the anterior and posterior walls with its transverse rugae; (ii) Strati-fied epithelium devoid of glands.

Physiologic: This is maintained by the hormone oestrogen (Table 10.1).

At Birth, under the influence of maternal estrogen circulating into the newborn, the vaginal epithelium becomes multilayered. The desquamated epithelium containing glycogen is converted into lactic acid probably by enzymatic action for the first 48 hours. Subsequently, the Doderlein’s bacilli appear probably from the gut and convert the glycogen into lactic acid. As a result, for about 10-12 days following birth, the vaginal defence is good and infection is unlikely.

Thereafter and upto puberty, there is no circulatory estrogen. The vaginal epithelium is reduced to few layers; glycogen is absent and so also the Doderlein’s bacillus. The vaginal pH becomes neutral or alkaline. During the reproductive period with highoestrogen, the vaginal defence is fully restored. But again in postmenopause, after the withdrawal of estrogen, the vaginal defence is lost.

It should be emphasized that only the Doderlein ’ s bacilli can grow in the acidic media with pH 4-4.5. But when the pH increases, the other organisms normally present in the vagina will grow.

Phases of Life when Defence is lost:

(i)Following 10 days of birth till puberty is reached.

TABLE 10.1

DEFENCE OF THE VAGINA IN RELATION TO AGE

 

Newborn (0-10 days)

Up to puberty

Childbearing period

Postmenopause

Epithelium

Multilayered

Thin

Multilayered

Thin

Glycogen

++

(-)

++

(-)

Doderlein’s bacillus

+

(-)

++

(-)

pH

Acidic (4-5)

Neutral or alkaline (6-8)

Acidic (4-5)

Neutral (6-7)

(ii) During reproductive period—in the following situation:

● During menstruation: The vaginal pH becomes increased due to contaminated blood and fall of oestrogen. The protective cervical mucus disappears and the endometrium sheds.

● Following abortion and childbirth: The contaminated lochia increases the pH. The raw placental site, inevitable tear of the cervix, bruising of the vagina and presence of blood clots or remnants of decidua favor nidation of the bacterial growth.

(iii) During menopause.

Cervical defence: Anatomic—(i) Racemose type of glands, (ii) mucus plug.

Physiologic—Bactericidal effect of the mucus.

Uterine defence: (i) Cyclic shedding of the endometrium (ii) Closure of the uterine ostium of the fallopian tube with slightest inflammatory reaction in the endometrium.

Tubal defence: Anatomic—Integrated mucus plicae and epithelial cilia.

Physiologic—Peristalsis of the tube and also the movement of the cilia are towards the uterus.

Causative organisms: The bacterial pathogens involved in upper genital tract infections are principally derived from the normal flora of the vagina and endocervix. Exogenous sources are sexually transmitted or following induced or unsafe abortion or during delivery in unhygienic surroundings.

ORGANISMS

1. Pyogenic (50%): This is the commonest type - the organisms responsible are:

Aerobes

The gram-positive organisms are Staphylococcus. The gram-negatives are E. coli, Pseudomonas, Klebsiella, N. gonorrhoeae, etc.

Anaerobes

The gram-positives are anaerobic Streptococcus. Clostridium welchii, Cl. tetani, etc. The gram-negatives are mainly bacteroides group of which Bactero- ides fragilis is the commonest.

2. Sexually transmitted disease (STD): The organisms are N. gonorrhoeae, Chlamydia trachomatis, Treponema pallidum, Herpes simplex virus type II, Human papilloma virus, Gardnerella vaginalis (Haemophilus vaginalis), Haemophilus ducreyi, Donovan bodies, HIV I or II, etc.

3. ParasiticTrichomonas vaginalis

4. Fungal: Candida albicans

5. ViralHerpes simplex virus type II, Human papilloma virus, HIV, Condylomata accuminata, etc.

6. TubercularMycobacterium tuberculosis.

MODES OF SPREAD OF INFECTIONS

The route of infection is most commonly ascending in nature. However, the classic modes of infection of some specific organisms are:

• Through continuity and contiguity—gonococcal infection (Fig. 10.1).

• Through lymphatics and pelvic veins—post- abortal and puerperal infection—by pyogenic organisms other than gonococcus (Fig. 10.2).

• Through blood stream—tubercular

• From adjacent infected extra-genital organs like intestine.

ACUTE PELVIC INFECTION

• Pelvic inflammatory disease (PID).

• Following delivery and abortion.

• Following gynecological procedures.

• Following IUD.

• Secondary to other infections—appendicitis.

PELVIC INFLAMMATORY DISEASE (PID)

DEFINITION

PID is a disease of the upper genital tract. It is a spectrum of infection and inflammation of the upper genital tract organs typically involving the uterus (endometrium), fallopian tubes, ovaries, pelvic peritoneum and surrounding structures. It is attributed to the ascending spread of microorganisms from the cervicovaginal canal to the contiguous pelvic structures. The clinical syndrome is not related to pregnancy and surgery.

But, as the terminology fails to pinpoint the precise organ or organisms involved, it is better to use the anatomical terminology in relation to which organ is involved in the infectious process. Thus, the better terminology should be either endometritis, salpingitis, pelvic peritonitis or tuboovarian abscess. The cervicitis is not included in the list.

Many, however, prefer the term salpingitis as because it ultimately bears the brunt of acute infection.

From a clinical perspective, it is more pragmatic to describe acute salpingitis as sexually transmitted or not.

Epidemiology: Despite better understanding of the etiology, pathogenesis, improved diagnostic tools such as sonar or laparoscopy and advent of wide range of antimicrobials, it still constitutes a health hazard both in the developed and more so in the developing countries. The incidence of pelvic infection is on the rise due to the rise in sexually transmitted diseases.

The ready availability of contraception together with increased permissive sexual attitude has resulted in increased incidence of sexually transmitted diseases and, correspondingly, acute PID (more in p. 147).

The incidence varies from 1-2 per cent per year among sexually active women. About 85 per cent are spontaneous infection in sexually active females of reproductive age. The remaining 15 per cent follow procedures, which favors the organisms to ascend up. Such iatrogenic procedures include endometrial biopsy, uterine curettage, insertion of IUD and hysterosalpingography. Two-thirds are restricted to young women of less than 25 years and the remaining one-third limited among 30 years or older.

Pelvic inflammatory disease is a major problem to the reproductive health of young women. PID may be asymptomatic or subclinical. Currently there is certain changes in the epidemiology of PID. (A) Shift from inpatient PID to outpatient PID. (B) Change in clinical presentation. Less severe disease is commonly seen. (C) Shift in the microbial etiology of more Chlamydia trachomatis than gonococcus and others.

Fig. 10.1 : Mode of spread in gonococcal infection

RISK FACTORS

 Menstruating teenagers.

 Multiple sexual partners.

 Absence of contraceptive pill use.

● Previous history of acute PID.

 IUD users.

 Area with high prevalence of sexually transmitted diseases.

Teenagers have got low hormonal defence in response to genital tract infection. Wider area of cervical epithelium allows colonisation of Chlamydia trachomatis and N. gonorrhoeae (See p. 147).

PROTECTIVE FACTORS

■ Contraceptive practice

 Barrier methods, specially condom, diaphragm with spermicides (see p. 476).

 Oral steroidal contraceptives have got two preventive aspects.

- Produce thick mucus plug preventing ascent of sperm and bacterial penetration (see p. 485).

- Decrease in duration of menstruation, creates a shorter interval of bacterial colonization of the upper tract.

 Monogamy or having a partner who had vasectomy.

■ Others

 Pregnancy

 Menopause

 Vaccines: hepatitis B, HPV (p. 326).

MICROBIOLOGY

Acute PID is usually a polymicrobial infection caused by organisms ascending upstairs from downstairs.

The primary organisms are sexually transmitted and limited approximately to N. gonorrhoeae in 30 per cent, Chlamydia trachomatis in 30 per cent and Mycoplasma hominis in 10 per cent.

The secondary organisms normally found in the vagina are almost always associated sooner or later. These are:

Aerobic organisms—non-hemolytic Streptococcus.

E. coli, group B Streptococcus and Staphylococcus.

Anaerobic organisms—Bacteroides species - fra- gilis and bivius, Peptostreptococcus and Peptococcus.

MODE OF AFFECTION

• The classic concept is that the gonococcus ascends up to affect the tubes through mucosal continuity and contiguity. This ascent is facilitated by the sexually transmitted vectors such as sperm and trichomonads.

• Reflux of menstrual blood along with gonococci into the fallopian tubes is the other possibility.

• Mycoplasma hominis probably spreads across the parametrium to affect the tube.

• The secondary organisms probably affect the tube through lymphatics.

• Rarely, organisms from the gut may affect the tube directly.

PATHOLOGY

The involvement of the tube is almost always bilateral and usually following menses due to loss of genital defence.

The pathological process is initiated primarily in the endosalpinx. There is gross destruction of the epithelial cells, cilia and microvilli. In severe infection, it invades all the layers of the tube and produces acute inflammatory reaction; becomes edematous and hyperemic. The exfoliated cells along with the exudate pour into the lumen of the tube and agglutinate the mucosal folds. The abdominal ostium is closed by the indrawing of the edematous fimbriae and by inflammatory adhesions. The uterine end is closed by congestion. The closure of both the ostia results in pent up of the exudate inside the tube. Depending upon the virulence, the exudate may be watery producing hydrosalpinx or purulent producing pyosalpinx. The purulent exudate then changes the microenvironment of the tube which favors growth of other pyogenic and anaerobic organisms resulting in deeper penetration and more tissue destruction. The organisms spontaneously die within 2-3 weeks. As the serous coat is not much affected, the resulting adhesions of the tube with the surrounding structures are not so dense, in fact flimsy, unlike pyogenic or tubercular infection.

On occasions, the exudate pours through the abdominal ostium to produce pelvic peritonitis and pelvic abscess or may affect the ovary (the organisms gain access through the ovulation rent) producing ovarian abscess. A tubo-ovarian abscess is thus formed (Fig. 10.1).

CLINICAL FEATURES

SYMPTOMS

Patients with acute PID present with a wide range of non-specific clinical symptoms. Symptoms usually appear at the time and immediately after the menstruation.

► Bilateral lower abdominal and pelvic pain which is dull in nature. The onset of pain is more rapid and acute in gonococcal infection (3 days) than in chlamydial infection (5-7 days).

► There is fever, lassitude and headache.

► Irregular and excessive vaginal bleeding is usually due to associated endometritis.

► Abnormal vaginal discharge which becomes purulent and or copious.

► Nausea and vomiting.

► Dyspareunia.

► Pain and discomfort in the right hypochondrium due to concomitant perihepatitis (Fitz-Hugh-Curtis syndrome) may occur in 5-10 per cent of cases of acute salpingitis. The liver is involved due to transperitoneal or vascular dissemination of either gonococcal or chlamydial infection.

SIGNS

► The temperature is elevated to beyond 38.3°C.

► Abdominal palpation reveals tenderness on both the quadrants of lower abdomen. The liver may be enlarged and tender.

► Vaginal examination reveals: (1) Abnormal vaginal discharge which may be of purulent. (2) Congested external urethral meatus or openings of Bartholin’s ducts through which pus may be seen escaping out on pressure. (3) Speculum examination shows congested cervix with purulent discharge from the canal. (4) Bimanual examination reveals bilateral tenderness on fornix palpation, which increases more with movement of the cervix. There may be thickening or a definite mass felt through the fornices.

CLINICAL DIAGNOSTIC CRITERIA OF PID (CDC-2006)

► Minimum Criteria

 Lower abdominal tenderness.

 Adnexal tenderness.

 Cervical motion tenderness.

► Additional Criteria

 Oral temperature > 38.3°C.

 Mucopurulent cervical or vaginal discharge.

 Raised C-reactive protein and/or ESR.

 Laboratory documentation of positive cervical infection with Gonorrhoea or C. trachomatis.

 Definitive Criteria

 Histopathologic evidence of endometritis on biopsy.

 Imaging study (TVS/MRI) evidence of thickened fluid filled tubes ± tubo-ovarian complex.

 Laparoscopic evidence of PID (see below).

INVESTIGATIONS

Identification of organisms: For identification of organisms, the materials are collected from the following available sources:

1. Discharge from the urethra or Bartholin’s gland.

2. Cervical canal.

3. Collected pus from the fallopian tubes during laparoscopy or laparotomy.

The material so collected is subjected to Gram stain and culture (aerobic and anaerobic). The findings of gram-negative diplococci is very much suggestive of gonococcal infection. Except in highly sophisticated centers, the detection of Cl. trachomatis is difficult (for diagnosis see p. 150). As the process of investigation is not specific and is time consuming, treatment for Cl. trachomatis should be started from the clinical diagnosis. A positive Gram stain smear from endocervical mucus is non-specific and a negative smear does not rule out upper genital tract infection. Blood: Leucocyte count shows leucocytosis to more than 10,000 per cu mm and an elevated ESR value of more than 15 mm per hour. The results correlate with the severity of the inflammatory reactions of the fallopian tubes as seen on laparoscopy. Serological test for syphilis should be carried out for both the partners in all cases.

Laparoscopy: Laparoscopy is considered the "gold standard". While it is the most reliable aid to support the clinical diagnosis but it may not be feasible to do in all cases. It is reserved only in those cases in which differential diagnosis includes salpingitis, appendicitis or ectopic pregnancy. Nonresponding pelvic mass needs laparoscopic clarification (also see p. 141).

Laparoscopic findings and severity of PID:

 Mild: Tubes: Edema, erythema, no purulent exudates and mobile.

 Mod: Purulent exudates from the fimbrial ends, tubes not freely movable.

 Severe: Pyosalpinx, inflammatory complex, abscess.

 ‘Violin string’ like adhesions in the pelvis and around the liver suggests chlamydial infection.

Laparoscopy helps to aspirate fluid or pus for microbiological study from the fallopian tube, ovary or pouch of Douglas.

Sonography: It is of limited value. Dilated and fluid- filled tubes, fluid in the pouch of Douglas or adnexal mass are suggestive of PID. It may be employed where clinical examination is difficult or is not informative because of acute tenderness or obesity.

Culdocentesis: Aspiration of peritoneal fluid and its white cell count, if exceeds 30,000 per mL. is significant in acute PID. Bacterial culture from the fluid is not informative because of vaginal contamination.

Investigations are also to be extended to male partner and smear and culture are made from urethral secretion.

DIAGNOSIS

The anatomic diagnosis of infection to the upper genital tract is made from the following clinical features (Table 10.2).

Microbial diagnosis is difficult. But as already emphasized, one should not wait for the report, instead treatment should be started empirically. The materials for identification of organisms are from the cervical and urethral discharge and secretion from the Bartholin’s gland, and laparoscopic or laparotomy collection of pus from the fallopian tubes. The materials are to be subjected to Gram stain and culture (aerobic and anaerobic).

Gram stain of the discharge may be positive for gram-negative intracellular diplococci of N. gonorrhoeae. Bacteriologic diagnosis of Chlamydia trachomatis is difficult. However, the status of the sexual partner is the single most important clue to the diagnosis of chlamydial infection. If the woman has a stable sexual relationship with asymptomatic man, the clinical manifestations are unlikely to be due to chlamydial infection.

DIFFERENTIAL DIAGNOSIS

The clinical condition may be confused with: (1) Appendicitis, (2) Disturbed ectopic pregnancy, (3) Torsion of ovarian pedicle, haemorrhage or rupture of ovarian cyst, (4) Endometriosis, (5) Diverticulitis and (6) Urinary tract infection (Table 10.3).

TABLE 10.3

CLINICAL FEATURES OF ACUTE SALPINGITIS, ACUTE APPENDICITIS AND DISTURBED ECTOPIC

Symptoms and signs

Acute salpingitis (Table 12.3)

Acute appendicitis

Disturbed ectopic

♦ Pain

Acute lower abdominal on both sides

Starts near umbilicus but settles to right iliac fossa

Acute lower abdomen on one side

♦ Amenorrhea and bleeding PV

Unrelated

Unrelated

Usually present

♦ GI symptoms such as nausea, vomiting

Inconsistently present

Usual

Absent

♦ General look

Face-flushed

Toxic

Pale

♦ Tongue

No significant change

Furred

Pale

♦ Pulse

Rapid but proportionate with temperature

Rapid, out of proportion to temperature

Persistent rise even with normal temperature

♦ Temperature

More raised

Slightly raised

Not raised

♦ Tenderness

Lower abdomen on both sides

On McBurney’s point may have muscle guard

Lower abdomen more on one side

♦ Per vaginum

Tenderness on both fornices. A mass may be felt

Tenderness on right fornix and high up

Mass may be felt through one fornix extending up to pouch of Douglas

The two conditions—acute appendicitis and disturbed ectopic pregnancy must be ruled out, because both the conditions require urgent laparotomy whereas acute salpingitis is to be treated conservatively.

COMPLICATIONS OF PID

Immediate: (1) Pelvic peritonitis or even generalized peritonitis. (2) Septicemia—producing arthritis or myocarditis.

Late: (1) Dyspareunia. (2) Infertility rate is 12 per cent, after two episodes increases to 25 per cent and after three raises to 50 per cent. It is due to tubal damage or tubo-ovarian mass. (3) Chronic pelvic inflammation is due to recurrent or associated pyogenic infection. (4) Formation of adhesions or hydrosalpinx or pyosalpinx and tubo-ovarian abscess. (5) Chronic pelvic pain and ill health. (6) Increased risk of ectopic pregnancy (6-10 fold).

TREATMENT

Essential steps in the prevention are:

● Community based approach to increase public health awareness.

● Prevention of sexually transmitted diseases with the knowledge of healthy and safer sex.

● Liberal use of contraceptives.

● Routine screening of high-risk population.

The principles of therapy are:

● To control the infection energetically.

● To prevent infertility and late sequelae.

● To prevent reinfection.

Outpatient therapy: Apart from adequate rest and analgesic, antibiotics are to be prescribed even before the microbiological report is available. As because the infection is polymicrobial in nature, instead of single, combination of antibiotics should be prescribed. Outpatients antibiotic therapy for acute PID is given in the Table 10.4.

All patients treated in the outpatients are evaluated after 48 hours and if no response, are to be hospitalised.

Inpatient therapy: The patients are to be hospitalized for antibiotic therapy in the conditions as mentioned in Table 10.5.

Bed rest is imposed. Oral feeding is restricted. Dehydration and acidosis are to be corrected by intravenous fluid.

Intravenous antibiotic therapy is recommended for at least 48 hours but may be extended to 4 days, if necessary (Table 10.6).

Improvement of the patient is evidenced by remission of temperature, improvement of pelvic tenderness, normal white blood cell count and negative report on bacteriological study.

Indications of surgery: The indications of surgery are comparatively less. The unequivocal indica-tions are:

 Generalized peritonitis.

 Pelvic abscess.

 Tubo-ovarian abscess which does not respond (48-72 hours) to antimicrobial therapy.

To prevent reinfection: The following formalities are to be rigidly followed to prevent reinfection:

 Educating the patient to avoid reinfection and the potential hazards of it.

 The patient should be warned against multiple sexual partners.

 To use condom.

 The sexual partner or partners are to be traced and properly investigated to find out the organism(s) and treated effectively. If they have got nongonococcal urethritis, they should be treated with tetracycline 500 mg 6 hourly or doxycycline 100 mg twice daily for 7 days.

FOLLOW UP

Repeat smears and cultures from the discharge are to be done after 7 days following the full course of treatment. The tests are to be repeated following each menstrual period until it becomes negative for three consecutive reports when the patient is declared cured. Until she is cured and her sexual partner(s) have been treated and cured, the patient must be prohibited from intercourse.

The only unequivocal proof of successful treatment after salpingitis is an intrauterine pregnancy.

PELVIC INFECTION FOLLOWING DELIVERY AND ABORTION

The common organisms producing acute infection following delivery are anaerobic Streptococcus, Staphylococcus pyogenes, non-hemolytic streptococcus, E. coli and Bacteroides group. Too often, multiple organisms are present and it is difficult to pinpoint a particular organism responsible for a particular type of infection.

As previously mentioned, the defence is lost following childbirth and abortion. Malnutrition, unhygienic environment during delivery, dehydration and ketoacidosis during labor are the additional factors in underprivileged women. Infections are common following cesarean section. Following abortion, specially when induced criminally, exogenous infection is quite likely and potentially virulent.

Pathology

The infection is either localized to the cervix, producing acute cervicitis or may affect the placental site producing endometritis. The infection may spread to the myometrium producing endomyometritis which is limited by a leucocytic barrier. On occasion, the infection spreads to the parametrium, usually to one side, through lymphatics or directly through the tear of the cervix; thereby gaining access to the base of the broad ligament. The infection may also spread upwards through the tubal openings into the tubal lumen producing endosalpingitis. Thus, the fallopian tube is affected either from outside following parametritis, through lymphatics producing perisalpingitis or through endosalpingitis. The ovary may be affected through involvement of the tube or following pelvic peritonitis. Thus, an acute tubo-ovarian mass is formed (Fig. 10.2).

Spread of infection: Depending upon the virulence of the organisms and resistance of the host, the following events may occur.

The infection is localized principally to the cervix and subsequently develops into chronic cervicitis. The parametrial exudate may resolute completely leaving behind scarring or fibrosis or may undergo suppuration. The abscess so formed usually points above the inguinal ligament. The tubal affection results in cornual block, hydro-salpinx or pyosalpinx following blockage of the fimbrial end. There may be peritonitis either localized or at times generalized. In others, the tube may be adherent with the ovary, intestine and omentum producing tubo-ovarian mass, the abdominal ostium usually remaining patent. The pelvic veins may be involved producing thrombophlebitis, which is either confined to the pelvis or spreads upwards along the ovarian veins or downwards along the iliofemoral veins. The systemic effect varies from minimal to a fatal one, specially with gramnegative organisms following criminal abortion. The serious complications include septic shock, acute renal failure and disseminated intravascular coagulopathy.

Fig. 10.2 : Mode of spread in postabortal or puerperal infection

Clinical features

The onset may be acute or insidious and the clinical picture varies widely depending upon the severity and spread of infection. But the chief complaints of varying magnitude are fever, lower abdominal and pelvic pain and offensive vaginal discharge following delivery or abortion.

On examination, the patient looks ill and may be restless. She likes to lie on her back with the legs flexed. Pulse rate is rapid and is out of proportion to the temperature. Abdominal examination reveals tenderness or even rigidity on lower abdomen.

Vaginal examination is painful. The discharge is offensive. The uterus is tender, more with movement of the cervix. The fornices are tender. Depending upon the spread, there may be unilateral or bilateral mass (tubo-ovarian), an unilateral tender indurated mass pushing the uterus to the contralateral side (parametritis) or a bulging fluctuating mass felt through the posterior fornix (pelvic abscess). Rectal examination is useful to corroborate the pelvic findings.

Complications of Acute PID following Delivery or Abortion

(1) Endotoxic shock. (2) Oliguria or anuria. (3) Disseminated intravascular coagulopathy. These are predominantly due to gram-negative organisms and are too often associated with unsafe abortion. (4) Tubo- ovarian abscess. (5) Peritonitis. (6) Parametritis. (7) Thrombophlebitis—features usually appear 7-10 days following the initial events. (8) Pulmonary embolism.

TREATMENT

Prevention: (1) To maintain asepsis and antiseptic measures during labor. (2) To avoid traumatic and difficult vaginal deliveries. (3) To use prophylactic antibiotic when labor is delayed following rupture of the membranes or when there are intrauterine manipulations like forceps or manual removal of placenta. (4) To encourage family planning acceptance to prevent the unwanted pregnancies.

Curative

 Hospitalization: The patient may be admit-ted if clinically indicated (p. 132).

 Triple swabs are to be taken—one from high vagina, one from the endocervix and the third from the urethra. These are to be sent for aerobic and anaerobic culture, drug sensitivity test and Gram stain. The swabs are to be taken prior to bimanual examination.

● Vaginal and rectal examinations are then made to note the extent of pelvic infection.

■ Investigations

Routine: (a) Blood is sent for hemoglobin estimation, total and differential count of white cells, depending on severity of infection blood culture and serum electrolytes are done. (b) Urine analysis including culture.

Special investigations are to be done as required: (a) Ultrasonography of abdomen and pelvis to detect physometra or presence of any foreign body left behind in the uterus or in the abdominal cavity used for criminal interference.

Definitive treatment

● Antibiotics: Pending sensitivity report, potent bactericidal drugs such as gentamicin 2 mg/kg body weight and clindamycin IV 600 mg daily with IV metronidazole 500 mg are to be administered at every 6-8 hours interval. If the temperature does not subside by 48 hours, the antibiotic should be changed according to microbiology and sensitivity report.

Supportive therapy

 Blood transfusion for anemia.

 Treatment for endotoxic shock, renal failure or disseminated intravascular coagulopathy need intensive care management.

Indications of surgery in septic abortion are:

(1) Injury to the uterus. (2) Suspected injury to the gut. (3) Presence of foreign body in the abdomen as evidenced by the USG or felt through the fornix on bimanual examination. (4) Unresponsive peritonitis suggestive of collection of pus. (5) Patient’s clinical condition not responding to the conservative treat-ment.

Active surgery includes:

 Evacuation of uterus

 Posterior colpotomy

 Laparotomy—in a suspected case of acute appendicitis or ruptured tubo-ovarian abscess.

LATE SEQUELAE OF PID

 Infertility either due to cornual block, or damage to the wall of the tube.

 Chronic infection

 Chronic pelvic pain, dysmenorrhea

 Pelvic adhesive disease

 Ectopic pregnancy

 Residual infection with periodic acute exacerbation.

 Intestinal obstruction.

 Chronic ill health.

 Dyspareunia and marital disharmony.

PELVIC INFECTION FOLLOWING GYNECOLOGICAL PROCEDURES

Infection of the residual pelvic organs or cellular tissues is not uncommon following hysterectomy, more in vaginal than abdominal one. It is more common in infected or potentially infected cases than in ‘elective’ non-infective cases.

Organisms: Escherichia coli and Bacteroides fragilis are the predominant organisms.

Pathology: The vaginal cuff may be indurated due to infected hematoma → cellulitis → abscess. The infection may spread to produce pelvic cellulitis, thrombophlebitis or tubo-ovarian mass.

Clinical features: Fever and lower abdominal or pelvic pain of varying degrees appear few days (3-4) following surgery.

Per vaginam: Discharge is offensive and the vaginal vault is indurated and tender. Speculum examination may reveal exposed vaginal cuff with purulent discharge coming through the gaping vault. Rectal examination reveals induration on the vault or its extension to one side (parametritis). Rarely, a fluctuant mass may be felt (pelvic abscess).

TREATMENT: Prophylactic

Preoperative cleaning of the vagina with antiseptic lotion, perfect hemostasis during surgery and leaving behind the vault open in infected cases could reduce the postoperative infection. Chemoprophylaxis in potentially or actually infected cases using intravenous metronidazole 500 mg 8 hourly for 3 such and intravenous ceftriaxone 1 g, given during the operation and 1-2 doses after the operation is quite effective to lower the risk of infection.

Definitive treatment: Appropriate antibiotic and drainage of pus through the vault are enough to arrest the infection. However, in parametritis and thrombophlebitis, the response is poor. Adnexal abscess requires urgent exploration and removal of the infected mass.

IUD AND PELVIC INFECTION

IUD is one of the iatrogenic causes of pelvic infection in gynecology (see ch. 29). All types of IUDs are responsible. The incidence ranges from 2-10 per cent. The risk is, however, more in nulliparae. It may flare up pre-existing pelvic infection. IUD tail may be implicated in ascent of the organisms from the vagina in infections long after insertion. The bacteria may be carried from the cervix into the endometrium during insertion. Actinomycosis has been found rarely infection coagulates, which later either completely resolutes or becomes fibrotic. The fibrosis pulls the uterus, the cervix in particular to the same side.

As a preventive measure, it is better not to insert in nulliparae or in cases with previous history of pelvic inflammatory disease. Insertion should be carried out under strict aseptic condition. Once the pelvic infection occurs, the device should be removed in addition to antibiotic and supportive therapy. Actinomycosis responds well with penicillin.

CHRONIC PELVIC INFECTION

Chronic pelvic infection is a distressing clinical entity not only to the patients but also to the physicians. It results:

 Following acute pelvic infection—the initial treatment was delayed or inadequate.

 Following low grade recurrent infection.

 Tubercular infection.

The first two types are predominantly due to pyogenic organisms. There is often history of previous acute pelvic infection. Tubercular infection is chronic from the beginning and is described as a separate entity.

PYOGENIC

Pathology

The pathology in the uterus is most often spared because of periodic shedding of the endometrium. The tubal changes are secondary to the changes induced by previous acute salpingitis. The tubal epithelium is usually lost, specially in gonococcal infection; the wall gets thickened with plasma cell infiltration and the openings are blocked. These result in hydrosalpinx, with loss of the lining mucosa with its plicae. The peritoneal surface is involved in recurrent infection producing either flimsy (gonococcal) or dense (nongonococcal pyogenic) adhesions. The tubes are thus kinked and may get adherent to the ovaries, uterus, intestine, omentum and pelvic peritoneum. A tubo-ovarian mass or a frozen pelvis results. The serum and lymphatic exudate in the parametrium of acute in association with the use of copper devices. Risk of PID is highest in the first month after insertion. Again risk of PID is highest when the patient has multiple sexual partners.

Clinical features

‣ The entity may remain asymptomatic.

‣ There may be previous history of acute pelvic infection following childbirth or abortion. Recurrent episodes of reinfection is often present. The use of IUCD is highly corroborative.

Symptoms

 Chronic pelvic pain of varying magnitude and the pain aggravates prior to menstruation due to congestion.

 Dyspareunia, which is deep and may be located unilaterally or bilaterally.

 Congestive dysmenorrhea.

 Lower abdominal pain.

 Menorrhagia or polymenorrhagia are due to congestion.

 Vaginal discharge is almost a constant manifestation and may be mucoid or mucopurulent.

 Infertility, which may be primary or more commonly secondary.

Important factors for infertility are—cornual block (Fig. 37.69), loss of cilia, loss of peristalsis due to thickening of the tubal wall, closure of the abdominal ostium and distortion of the tube due to peritubal adhesions.

On examination

Per abdomen: There may be tenderness on one or both iliac fossa. An irregular tender pelvic mass may be felt.

Per vaginam: The findings are as mentioned in page 130.

Rectal examination corroborates the findings of vaginal examination and should not be omitted (p. 108). The involvement of the parametrium and uterosacral ligaments are better assessed rectally.

Investigations

 Blood examination for evidences of leucocytosis, Hb estimation and ESR. Urine examination— routine and, if necessary, culture sensitivity.

Laparoscopy: This is helpful to confirm the diagnosis and to know the extent of the lesion specially in cases of infertility. However, in cases where too much adhesions are anticipated, diagnostic laparotomy is a safer substitute.

Management: • General • Specific • Surgery

■ General

► Improvement of general health and anemia.

► Analgesics as required, may be prescribed. Pelvic heat application by short wave diathermy is comforting to the patient.

■ Specific

► The IUCD is to be removed, if it is still inside.

► Antibiotic therapy has got little benefit unless there is recent acute exacerbation. The longterm broad spectrum antibiotics to be administered include doxycycline or tetracycline or cephalosporin for three weeks. In proved cases of gonococcal infection, specific therapy is directed as outlined in acute infection (p. 148).

■ Surgery: Surgery may be needed either by laparoscopy or by laparotomy in a few selected cases.

Indications:

• Persistence of symptoms in spite of adequate conservative treatment.

• Recurrence of acute attacks.

• Increase in size of the pelvic mass despite treatment.

• Infertility for restorative tubal surgery or for adhesiolysis.

Nature of surgery: Due consideration should be given to age, parity and extent of the lesion.

Laparoscopic adhesiolysis, tubal restorative and reconstructive surgery are commonly done. Few cases may need salpingectomy or salpingo-oophore-ctomy.

In general, the ideal surgery should be total hysterectomy with bilateral salpingo-oophorectomy for women that they have completed their family.

GENITAL TUBERCULOSIS

INCIDENCE

The incidence of genital tuberculosis varies widely with the social status of the patient and her environment. The incidence is about 1 per cent amongst the gynecological patients attending the outpatient department in the developing countries. Incidence is high (5-10%) amongst the patients with infertility. With the prevalence of HIV infection incidence of genital tuberculosis is rising. About 10 per cent of women with pelvic tuberculosis, have urinary tract tuberculosis.

PATHOGENESIS

The causative organism is Mycobacterium tuberculosis of human type. Very rarely the bovine type may affect the vulva. Genital tuberculosis is almost always secondary to primary infection elsewhere in the extragenital sites such as lungs (50%), lymph nodes, urinary tract, bones and joints. The fallopian tubes are invariably the primary sites of pelvic tuberculosis from where secondary spread occurs to other genital organs.

MODE OF SPREAD

Hematogenous: From any of the primary sites, the pelvic organs are involved by hematogenous spread in about 90 per cent cases. If the post-primary hematogenous spread coincides with the growth spurt of the pelvic vessels, the genital organs, the tubes in particular, are likely to be affected. Thus, the pelvic organs are infected during puberty. If the spread precedes the growth phase, the genital organs are spared. The infection remains dormant for a variable period of time (4-6 years) until clinical manifestations appear (Fig. 10.3).

Lymphatic or direct: The pelvic organs are involved directly or by lymphatics from the infected organs such as peritoneum, bowel or mesenteric nodes.

Ascending: Although difficult to prove but sexual transmission from a male with urogenital tuberculosis is possible in vulval, vaginal or cervical lesion.

PATHOLOGY OF PELVIC ORGANS

Fallopian tube: The commonest site of affection is the fallopian tubes (100%). Both the tubes are affected simultaneously. The initial site of infection is in the submucosal layer (interstitial salpingitis) of the ampullary part of the tube.

Fig. 10.3 : Mode of spread in tubercular infection through blood-stream

Fig. 10.4: Miliary tuberculosis. Tubercles are seen over the uterus and the tube. Note also the peritoneum and intestines which are all studded with miliary tubercules. [By courtesy Dr. H. Roy, Patna]

The infection may spread medially along the wall causing destruction of the muscles which are replaced by fibrous tissue. The walls get thickened, become calcified or even ossified. The thickening may at time become segmented. The infection may spread inwards; the mucosa gets swollen and destroyed. The fimbria are everted and the abdominal ostium usually remains patent. The elongated and distended distal tube with the patent abdominal ostium gives the appearance of “tobacco-pouch”. Occlusion of the ostium may however occur due to adhesions. The tubercles burst pouring the caseous material inside the lumen producing tubercular pyosalpinx, which may adhere to the ovaries and the surrounding structures. Often the infection spreads outwards producing perisalpingitis with exudation, causing dense adhesions with the surrounding structures— tubercular tubo-ovarian mass. Rarely, miliary tubercles may be found on the serosal surface of the tubes, uterus, peritoneum or intestines. These are often associated with tubercular peritonitis (Fig. 10.4).

However, not infrequently the tubes may look absolutely normal or nodular at places. If the nodules happen to be present in the isthmus near the uterine cornu, it constitutes salpingitis isthmica nodosa.

Salpingitis isthmica nodosa is the nodular thickening of the tube due to proliferation of tubal epithelium within the hypertrophied myosalpinx (muscle layer). Exact aetiology is unknown. It is diagnosed radiologically as a small diverticulum (Fig. 10.7). It is however not specific to tubercular infection only (see p. 172). It is also observed in pelvic endometriosis.

Uterus: The endometrium is involved in 60 per cent of cases. The infection is from the tubes either by lymphatics or by direct spread through continuity. Cornual ends are commonly affected due to their dual blood supply, as well as their anatomical proximity to tubes. The tubercle is situated in the basal layer of the endometrium only to come to the surface premenstrually. After the endometrium is shed at each menstruation, reinfection occurs from the lesions in the basal layer or from the tubes. Endometrial ulceration may lead to adhesion or synechiae formation (Asherman’s syndrome). This may cause infertility, secondary amenorrhea or recurrent abortion (p. 459). Rarely, the infection spreads to the myometrium (2.5%) and if caseation occurs, a pyometra results, specially in postmenopausal women.

Cervix: The cervical affection is not so uncommon (5-15%). Primary infection of the cervix by sexual intercourse though rare, has been recorded. It may be ulcerative or may be bright nodular in type. Both may bleed to touch, thereby causing confusion with carcinoma. Histologically genital tuberculosis is associated with marked epithelial hyperplasia with some degree of atypia. This may lead to erroneous diagnosis of carcinoma (Fig. 10.8).

Vulva and vagina: The affection of these sites is very rare (1%). The lesion may be ulcerative with undermined edges. Rarely the lesions may be of hypertrophic variety. The diagnosis is made only by histology.

Ovary: The ovaries are involved in about 30 per cent of tubercular salpingitis. The manifestation may be surface tubercles, adhesions, thickening of the capsule or even caseating abscess in the substance of the ovary.

PELVIC PERITONEUM

Pelvic peritonitis is present in about 40-50 per cent of cases. Tuberculous peritonitis may be ‘wet’ (exudative type) or ‘dry’ (adhesive type).

In the ‘wet’ variety there is ascites with straw colored fluid in the peritoneal cavity. The parietal and visceral peritoneum are covered with numerous small tubercles (Fig. 10.4).

In the ‘dry’ variety there is dense adhesion with bowel loops. The adhesion is due to fibrosis when the ‘wet’ variety heals.

Microscopic appearance of the lesion

Microscopic picture of the lesion is very characteristic irrespective of the organ involved. Typical granuloma consists of infiltration of multinucleated giant cells (Langhans), chronic inflammatory cells and epithelioid cells, surrounding a central area of caseation necrosis (Fig. 10.5). Caseation may not be a constant feature.

CLINICAL FEATURES

Patient profile: The infection is restricted mostly (80%) to childbearing period (20-40 years). There may be past history of tubercular affection of the lungs or lymph glands. Genital tuberculosis occurs in 10-20 per cent of patients who have pulmonary tuberculosis in adolescence. A family history of contact may be available. Onset is mostly insidious. A flare up of the infection may occur acutely either spontaneously or following diagnostic endometrial curettage or hysterosalpingography.

Symptoms: Symptoms vary considerably with the severity and stage of the disease. At one extreme, there is neither any symptom nor any palpable pelvic pathology. Sometimes symptoms like weakness, low grade fever, anorexia, anemia or night sweats may be present. The lesion is accidentally diagnosed during investigation for infertility or dysfunctional uterine bleeding. These cases are often designated as “silent tuberculosis”. In others, the clinical manifestations appear. These are:

Infertility: It may be primary or secondary and is present in about 70-80 per cent cases of pelvic tuberculosis. In India, about 10 per cent infertile women have got genital tuberculosis. The causes are predominantly due to tubal blockage, adhesions in the endometrial cavity (uterine synechiae) or associated ovulatory dysfunction.

Menstrual abnormality: In about 50 per cent, the menstrual function is normal.

Fig. 10.5 : A typical tubercular granuloma formed by lymphocytes, epithelioid cells and Langhans giant cells. Central area of caseation necrosis is seen

The menstrual abnormalities include:

‣ Menorrhagia or irregular bleeding is probably due to ovarian involvement, pelvic congestion or endometrial proliferative lesion. It is the early manifestation. These patients fail to respond with hormone therapy. Endometrial tuberculosis is a rare cause of puberty menorrhagia and postmenopausal bleeding.

‣ Amenorrhea or oligomenorrhea: Secon-dary amenorrhea is more common and may be the only presenting symptom that makes the patient seek medical advice. It may be due to suppression of the ovarian function probably by tubercular toxin (oophoritis). Else it may be result of endometrial destruction and uterine synechiae formation. It may be due to general debility also. As such, it is a late manifestation.

Others: Chronic pelvic pain is present in about 20-30 percent cases. It is often associated with tuboovarian mass and may be precipitated by tubal patency test. Secondary infection may aggravate the chronic pain to an acute one. Vaginal discharge—cervical or vaginal tuberculosis may be associated with postcoital bleeding or blood stained discharge. Constitutional symptoms such as loss of weight, malaise, anorexia, pyrexia and anaemia are present in the acute phase of the disease.

SIGNS

Health status: The general health usually remains unaffected. There may be constitutional symptoms like weakness, low grade fever, anorexia, anemia and night sweats. There may be evidences of active or healed extra-genital tubercular lesion.

Per abdomen: Abdominal findings may be negative or rarely one may find an irregular tender mass in lower abdomen arising out of the pelvis. Abdomen may feel doughy due to matted intestines. Evidences of free peritoneal fluid are rare. Tubercular ascites when encysted mimics an ovarian cyst.

Per vaginam: The pelvic findings may be negative in 50 per cent cases. Vulval or vaginal ulcer presents with undermined edges. There may be thickening of the tubes which are felt through the lateral fornices or nodules, felt through posterior fornix. At times, there is bilateral pelvic mass of varying sizes quite indistinguishable from that due to pyogenic infection.

Per rectum, one may confirm the vaginal findings.

INVESTIGATIONS

The aims of investigations are:

● To identify the primary lesion.

● To confirm the genital lesion.

Blood: The leucocyte count and ESR values may be raised. Periodic examination is of value to evaluate the progress of the lesion.

Mantoux test: Positive test with high dilution is suggestive that the patient is sensitized to tuberculoprotein. A negative test excludes tuberculosis.

Chest X-ray is taken for evidence of healed or active pulmonary lesion.

Diagnostic uterine curettage: This is to be done during the week preceding menstruation. The tubercles are likely to come to the surface during this period. The material should be sent to the laboratory in two portions.

a. One part in formol-saline for histopathological examination to detect the giant cell system. Histology could detect tuberculosis in about 10 per cent of cases only. False-positive histology may be due to the presence of chronic lesions (like talc or catgut granuloma) or sarcoidosis. False-negative result is due to improper timing of uterine curettage or due to less incidence of uterine infection.

b. One part in normal saline for:

i. Culture in Lowenstein-Jensen media.

ii. Identification of the acid-fast bacilli by Ziehl- Neelsen’s stain (AFB-Microscopy).

iii. Nucleic acid amplification.

iv. Guineapig inoculation.

A positive culture is suggestive while a positive guineapig inoculation test is diagnostic. Bacteriological test, if positive, should be able to type the bacilli and report on their drug sensitivity.

Nucleic acid amplification (16S ribosomal DNA) techniques with Polymerase Chain Reaction (PCR), can identify M. tuberculosis from endometrium or menstrual blood (clinical specimens). PCR is more sensitive (85-95%) than microscopy and bacteriological culture. This method can detect fewer than 10 organisms in clinical specimens compared to 10,000 necessary for smear positivity. Genital TB is usually paucibacillary.

First day menstrual discharge: This is to be collected by a pipette and the material subjected to mycobacterial nucleic acid amplification, culture and guineapig inoculation. It should be emphasized that while a positive report on AFB-microscopy, PCR, culture and histology gives the diagnosis, a negative report does not rule out tuberculosis.

Sputum and urine are to be cultured for tubercle bacillus.

Lymph node biopsy is to be done, specially from the neck in lymphadenitis.

Biopsy from the lesion in cervix, vagina or vulva.

Hysterosalpingography (HSG): In a proved case, HSG is contraindicated for the risk of reactivation of the lesion. HSG done as a routine work up in the investigation of infertility may reveal the following suggestive features:

♦ Vascular or lymphatic extravasation of dye (Fig. 10.6).

Fig. 10.6: Hysterosalpingogram showing marked extravasation of dye in venous and lymphatic channels. It was proved to be a case of tubercular endometritis [By courtesy Dr. H. Roy, Patna]

♦ Rigid (lead-pipe) tubes with nodulations at places.

♦ ‘Tobacco pouch’ appearance with blocked fimbrial end (Fig. 10.4).

♦ Beaded appearance of the tube with variable filling density (Fig. 10.7).

♦ Distal tube obstruction.

♦ Coiling of the tubes or calcified shadow at places.

♦ Bilateral cornual block (Fig. 37.69).

♦ Tubal diverticula and/or fluffiness of tubal outline.

♦ Uterine cavity—irregular outline, honeycomb appearance or presence of uterine synechiae.

Imaging: Abdominal and pelvic ultrasound, CT or MRI is helpful where a mass and/or ascites is present. However, it cannot confirm the diagnosis.

Laparoscopy: In the absence of endometrial evidence, one may take the advantage of laparoscope for identification of tubercles in the pelvic organs or characteristic segmented nodular appearance of the tubes. Biopsy may be taken from peritoneal tubercles for histology. Aspiration of fluid is done for culture. This may be accidentally discovered during diagnostic laparoscopy for infertility work up or for chronic pelvic pain.

DIAGNOSIS

Fig. 10.7: Hysterosalpingogram showing beaded appearance of the tube with variable filling density. Pelvic tuberculosis was later confirmed

(By courtesy: Dr P Panigrahi, Consultant Gynecologist, JLN Hospital, Bhilai)

Considering the high prevalence of extragenital tuberculosis, pulmonary in particular, the physicians of the Third World Countries should look out for the presence of genital tuberculosis. For this, the following guidelines may be prescribed:

a. The physician should be conscious of the entity.

b. One should suspect and exclude genital tuberculosis in the following conditions:

 Unexplained infertility or amenorrhea.

 Recurrent episodes of pelvic infections, not responding with usual course of antibiotics.

c. Presence of pelvic mass with nodules in the pouch of Douglas.

Differential diagnosis: The pelvic mass is often confused with: (i) Pyogenic tubo-ovarian mass. (ii) Pelvic endometriosis. (iii) Adherent ovarian cyst. (iv) Chronic disturbed ectopic pregnancy.

TREATMENT: • General • Chemotherapy • Surgery

General: In the presence of active pulmonary tuberculosis, hospital admission is preferred. Otherwise, pelvic tuberculosis per se need not require hospitalization or bed rest except in acute exacer bation. To improve the body resistance, due attention is to be paid as regards diet and to correct anemia.

Until the infection is controlled, the husband should use condom during intercourse to prevent possibility of contracting urogenital tuberculosis.

Chemotherapy: Antitubercular chemotherapy is the treatment of first choice.

Initial phase: Four drugs are used for 2 months to reduce the bacterial population and to prevent emergence of drug-resistance. The drugs used are isoniazid, rifampicin, pyrazinamide and ethambutol. Ethambutol is essential to those who have been treated previously or are immunocompromised (HIV positive individual).

Continuation phase: Treatment is continued for a period of further 4 months with isoniazid and rifampicin.

This standard regimen may be used during pregnancy and lactation (Table 10.7).

After about a year of treatment, diagnostic endometrial curettage is to be done. If the histological and/or bacteriological examination becomes positive, the treatment must be continued further. If these are negative, the endometrium is examined at interval of 6 months. A patient may be considered cured, if at least two reports including histological and bacteriological examination become negative. Majority of the patients (90-95 %) respond well to chemotherapy.

TABLE 10.7

ANTITUBERCULAR CHEMOTHERAPY FOR INITIAL TREATMENT

Drug

Daily oral dosage (adult)

Nature

Toxicity

Comments

Isoniazid

5 mg/kg: max. 300 mg

Bactericidal

Hepatitis, Peripheral neuropathy

• Check liver function

• Combine pyridoxin 50 mg daily

Rifampicin

10 mg/kg: max.

600 mg.

Bactericidal

Hepatic dysfunction, orange discolouration of urine.

Febrile reaction

• Drug interaction (p. 487)

• Oral contraceptives to be avoided (p. 487)

• Monitor Liver enzymes (AST)

Pyrazinamide

20-25 mg/kg: max. 2 gm

Bactericidal

Hepatitis, Hyperuricemia, GI upset and Arthralgia

• Active against intracellular dividing forms of Mycobacterium.

• Monitor (AST)

Ethambutol

15-20 mg/kg: max. 2.5 gm.

Bacteriostatic

Visual disturbances, Optic neuritis, Loss of visual acuity.

• Ophthalmoscopic examination prior to therapy.

Intermittent dose schedule is also recommended. Treatment should be supervised by the DOTS provider. Revised National TB Control Program (RNTCP) 1993 and Directly Observed Treatment by Short Course Chemotherapy (DOTS).

♦ Isoniazid: 15 mg/kg, 3 times a week for 6 months.

♦ Rifampicin : 600 mg, 3 times a week for 6 months.

♦ Pyrazinamide: 30 mg/kg, 3 times a week for first 2 months only.

♦ Ethambutol: 30 mg/kg, 3 times a week for first 2 months only.

Multidrug resistant (MDR) tuberculosis is defined as infection with M. tuberculosis that is resistant to two or more agents including isoniazid. HIV negative patients who are MDR have high mortality rate (80%). Such patients are treated with five drug regimens (CDC).

Surgery—Indications: (i) Unresponsiveness of active disease in spite of adequate anti-tubercular chemotherapy. (ii) Tubercular pyosalpinx, ovarian abscess or pyometra (iii) Persistent menorrhagia and/ or chronic pelvic pain causing deteriorating health status.

Contraindications: (i) Presence of active tuberculosis in extragenital site. (ii) Favorable response to antimicrobial therapy with diminishing size of the pelvic mass. (iii) Accidental discovery of tubercular tubo-ovarian mass on laparotomy in young patient. The abdomen is to be closed after taking tissue for biopsy. Precautions: Antitubercular drug therapy in full dosage should be instituted at least 6 weeks prior to surgery and similar treatment should be continued following surgery.

Type of surgery: The ideal surgery should be total hysterectomy with bilateral salpingo-oopho-rectomy. In young women at least one ovary, if found apparently healthy, should be preserved. Isolated excision of tubo-ovarian mass, drainage of pyometra or repair of fistula may be done in selected cases.

Results of Treatment

In terms of future reproduction, the prognosis is most unfavorable. Pregnancy is rare (5-10 %), and if occurs, chance of ectopic pregnancy is more (40 %). In uterine pregnancy, abortion is likely and a pregnancy going upto term is a rare event.

With the help of assisted reproductive technology (ART) higher pregnancy rate is observed following successful chemotherapy.

VULVAL TUBERCULOSIS

The patient complains of a painful and tender ulcer in the vulva. Confirmation is done by biopsy. The medical treatment is the same as that outlined in pelvic tuberculosis. In unresponsive cases, local vulvectomy is to be done.

CERVICAL TUBERCULOSIS

The presenting complaints are mucopurulent discharge and postcoital bleeding. Cervical tuberculosis on speculum examination (Fig. 10.9) appears as an ulcerated or hypertrophic growth which bleeds on touch.

Cervical cytology: may reveal multinucleated giant cells, epithelioid cells and dyskaryotic cells. Biopsy confirms the diagnosis. Antitubercular drug therapy as outlined in pelvic tuberculosis is prescribed (Table 10.7). In unresponsive cases, hysterectomy is justified.

Chronic PID: The term chronic pelvic inflam-matory disease has largely been abandoned. The longterm sequelae of acute PID such as adhesions or hydrosalpinx are bacteriologically sterile.

True chronic PID such as genital tuberculosis and actinomycosis is less although the former is not infrequent in the developing countries.

ACTINOMYCES INFECTION

It is a rare cause of upper genital tract infection. Infection is caused by Actinomyces israelii, a grampositive anaerobe. It may be associated in IUCD users more with noncopper devices. Actinomyces causes chronic endometritis. There may be foul smelling vaginal discharge. The diagnosis is usually made from tubo-ovarian abscess when the classic “Sulphergranules”are observed histologically along with gram positive filaments. Presence of symptoms like fever, abdominal pain, abnormal uterine bleeding may necessitate the removal of IUCD. It is sensitive to penicillin, doxycycline or fluroquinolones. The treatment should be continued for 12 weeks. Following the course of antibiotic treatment, Pap smear is repeated after 3 months.

KEY POINTS

The vaginal defence is lost following 10 days of birth till puberty, in reproductive period-during menstruation, following abortion and childbirth and following menopause.

Pelvic inflammatory disease according to anatomic location may be in the endometrium (endometritis), the oviducts (salpingitis), the ovary (oophoritis), the myometrium (myometritis), uterine serosa and broad ligaments (parametritis) and the peritoneum (pelvic peritonitis).

The primary organisms of PID are predominantly sexually transmitted. Acute PID is polymicrobial in nature. As the symptoms of PID are nonspecific, over treatment is preferred to missed diagnosis.

Clinical diagnostic criteria for acute PID includes : Minimum and Additional (routine and definitive) criteria (see p. 130).

Laparoscopy is the optimum method for accurately diagnosing acute PID.

Gonococcal affection of the tubes is by direct spread from downstairs to upstairs across the mucosal surface of the endometrium, reflux of the menstrual flow with gonococci into the tubes and carried along the spermatozoa or the trichomonads. The pathological process is initiated primarily in the endosalpinx.

For detection of Gonococcus, the materials are collected from the urethra or Bartholin's duct, cervical smear and laparoscopic collection of pus from the uterine tube. Acute gonorrhoea is treated by drugs (Table 11.2 on p. 148) to both the partners.

In acute condition, the diagnosis is confused with acute appendicitis and disturbed ectopic pregnancy.

Immediate complications include pelvic peritonitis and septicemia and late complications include infertility, chronic pelvic pain and chronic ill-health.

Repeat smears and cultures from the discharge are to be done following each menstrual period until it becomes negative for 3 consecutive reports when the patient is declared cured.

Chlamydia trachomatis — a gram-negative obligatory intracellular bacteria, is now the commonest organism proved to be sexually transmitted from the non-gonococcal urethritis in male consort. The clinical picture is almost the same to that of gonococcal infection but is milder in nature. Perihepatic inflammation (Fitz-Hugh- Curtis syndrome) is observed in 5-10 percent women with acute PID.

The late sequelae include tubal obstruction, infertility, early abortion and ectopic pregnancy.

Detection can be done by tissue culture. The specific antibody can be detected by immunofluorescent test or complement fixation test. Chlamydial nucleic acid amplification and detection by PCR is a very sensitive and specific test. The organism is sensitive to azithromycin, erythromycin or ofloxacin. The same treatment is to be given to the sexual partner.

The commonest organisms producing acute infection following delivery and abortion are anaerobic Streptococcus, Staphylococcus pyogenes, Esch. coli and Bacteroides groups.

The fallopian tube is affected either following parametritis through the lymphatics producing perisalpingitis or through endosalpingitis. Tubal affection to cause infertility depends on the severity and number of episodes of the disease.

Triple swabs are to be taken prior to bimanual examination; one from the high vagina, one from the endocervix and the third from the urethra. These are to be sent for aerobic and anaerobic culture, gram stain and drug sensitivity.

Clinical diagnostic criteria of PID (CDC-2006) include minimum and additional ones (p. 130). Diagnostic laparoscopy is considered the gold standard (p. 130). Women may be given antibiotic therapy either as an outpatient (Table 10.4) or as an inpatient (Table 10.6) depending on her evaluation (Table 10.5).

Few patients need surgical management (pelvic abscess, tubo-ovarian abscess) with laparotomy, posterior colpotomy or laparoscopy.

IUD may produce pelvic infection (2-10 %). The chance is more in nullipara. The highest risk is in the first month after insertion. Bacteria ascends along the nylon threads. Actinomycosis is often implicated.

Combined oral contraceptive use offers some protection against PID causing thick cervical mucus and decrease in duration of menstrual flow. Contact tracing and treatment of sexual partner should be a routine for effective treatment of PID.

The incidence of genital tuberculosis is about 1 per cent amongst the gynecological patient. The pelvic organs are affected secondarily, the primary site is predominantly in lung. The spread is by hematogenous route. Fallopian tube is almost always (100%) affected by interstitial salpingitis, endometrium in 60 per cent and cervix in 15 per cent cases. Infertility is present in 70 per cent. About 10 per cent of the infertile couple have got genital tuberculosis.

Although menorrhagia may be the early symptom but more commonly, the patient presents with oligomenorrhea or amenorrhea. The diagnosis is confirmed by histological examination, culture in Lowenstein-Jensen media and guineapig inoculation and identification of the bacteria by Ziehl-Neelsen's stain from the uterine curettage materials. PCR is more sensitive (p. 141).

The suggestive features of HSG are extravassation of dye, rigid tubes with nodulation at places and tobaccopouch appearance (p. 138). The result in terms of fertility following treatment (Table 10.7) is unsatisfactory. Pregnancy is rare and if occurs, risk of ectopic pregnancy is more. In uterine pregnancy, abortion is likely and a pregnancy upto term is a rarity.

Complications of PID may be — (a) immediate (pelvic peritonitis) or (b) Late (infertility, pelvic pain, dyspareunia, ectopic pregnancy) (p. 132, 135).



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