obstetrics - puerperal infection

nianderthalNOTES

OBSTETRICS: Puerperal Infection

PUERPERAL INFECTION: Introduction

PUERPERAL INFECTION

a general term used to describe any bacterial infection of the genital tract after delivery

-PAST: constitutes the LETHAL TRIAD of maternal death, along with preeclampsia and obstetrical hemorrhage

-PRESENT: maternal deaths from infection have become uncommon due to effective antimicrobials (13% of maternal deaths)

PUERPERAL INFECTION: Puerperal Fever

Puerperal Fever -A temperature of 38.0°C or higher in the puerperium -Common causes of puerperal fever: 1. Genital tract infection -Cause most persistent fevers after childbirth 2. Breast engorgement -in 15% of women who don’t breastfeed -rarely exceeds 39.0°C 3. Pyelonephritis -fever: first sign of renal infection -signs and symptoms that follow: costovertebral

angle tenderness, nausea and vomiting

PUERPERAL INFECTION: Puerperal Fever

Puerperal Fever -Common causes of puerperal fever: 4. Respiratory complications after cesarean delivery -atelectasis: caused by hypoventilation and

best prevented by coughing and deep breathing on a fixed schedule following surgery

-fever: follows infection by normal flora that proliferate distal to obstructing mucus plugs

5. Superficial or deep-venous thrombosis of the legs -occasionally cause minor temperature

elevations in the puerperium

PUERPERAL INFECTION: Uterine Infection

-Postpartum uterine infection has been called variously endometritis, endomyometritis and endoparametritis

-Preferred term: metritis with pelvic cellulitis

-because infection does not only involve the decidua but also the myometrium and parametrial tissues


Predisposing Factors

1. Route of delivery -single most significant factor for the development of uterine

infection

-25-fold increased infection-related mortality with cesarean versus vaginal delivery

-manual removal of the placenta increase puerperal metritis 3-fold

-metritis following vaginal delivery is relatively uncommon

RISK FOR METRITIS

Low risk women without complications 1-2%

High risk women due to membrane rupture, prolonged labor, and multiple cervical exams

5-6%

Women with intrapartum chorioamnionitis 13%


Predisposing Factors 1. Route of delivery

-single-dose perioperative prophylaxis is given almost universally at cesarean delivery

-Risk factors for infection following surgery include: -prolonged labor -membrane rupture -multiple cervical examinations -internal fetal monitoring

-Increased risk of infection include cesarean delivery for: -multifetal gestation -young maternal age -nulliparity -prolonged labor induction -obestiy -meconium-stained amnionic fluid


Predisposing Factors 2. Lower socioeconomic status 3. Anemia and Poor Nutrition -in very rare cases 4. Previous bacterial colonization if the lower genital

tract with certain microorganisms like: -Group B streptococcus -Chlamydia trachomatis -Mycoplasma hominis -Ureaplasma urealyticum -Gardnerella vaginalis


Bacteriology -Most female pelvic infections are caused by bacteria indigenous to

the female genital tract -Reports show that group A -hemolytic streptococcus may cause

toxic shock-like syndrome and life-threatening infection -Prematurely ruptured membranes is a prominent risk -Women in whom group A streptococcal infection was manifested

before, during, or within 12 hours of delivery had a maternal mortality rate of almost 90% and fetal mortality rate of >50%

-Skin and soft-tissue infections due to community-acquired methicillin-resistant Staphylococcus aureus—CA-MRSA—have become common NOT for puerperal metritis, but for incisional wound

-Study: A woman with episiotomy cellulitis with CA-MRSA had hematogenously spread necrotizing pneumonia


Common Pathogens -Infections are polymicrobial which promotes bacterial synergy -Other factors that promote virulence are hematomas and

devitalized tissue -The cervix and vagina routinely harbor such bacteria BUT the

uterine cavity is usually sterile before rupture of the amnionic sac

-The amnionic fluid and uterus commonly become contaminated with anaerobic and aerobic bacteria as the consequence of labor and delivery and associated manipulations

-Cultured amnionic fluid obtained at cesarean delivery in women in labor with membranes ruptured more than 6 hours all had bacterial growth and an average of 2.5 organisms was identified from each specimen


Common Pathogens -Anaerobes included Peptostreptococcus and Peptococcus species,

Bacteroides species and Clostridium species -Aerobes included Enterococcus, group B streptococcus, and

Escherichia coli -Chlamydial infections have been implicated in late-onset, indolent

metritis -When cervical colonization of U. urealyticum is heavy, it may

contribute to the development of metritis - Threefold risk of puerperal infection in women in whom

bacterial vaginosis was identified in early pregnancy


NORMAN FLORA CERVICOVAGINAL BACTERIA

Cervical Examinations Internal Monitoring

Prolonged Labor Uterine incision

INNOCULATION

ANAEROBIC CONDITIONS

Surgical Trauma Sutures

Devitalized Tissue Blood and Serum

CLINICAL INFECTION

BACTERIAL PROLIFERATION


Aerobes -Gram-positive cocci — group A, B, and D streptococci,

enterococcus, Staphylococcus aureus, Staphylococcus epidermidis

-Gram-negative bacteria — Escherichia coli, Klebsiella,Proteus species

-Gram-variable — Gardnerella vaginalis Others -Mycoplasma and Chlamydia species, Neisseria gonorrhoeae Anaerobes -Cocci — Peptostreptococcus and Peptococcus species -Others — Clostridium and Fusobacterium species Mobiluncus

species


Bacterial Cultures

-Routine pretreatment genital tract cultures are of little clinical use and add significant costs

-Routine blood cultures seldom modify care

-Before perioperative prophylaxis: blood cultures were positive in 13 percent of women with postcesarean metritis

-Bacteremia in only 5 percent of almost 800 women with puerperal sepsis.

PUERPERAL INFECTION: Pathogenesis

-Puerperal infection following vaginal delivery primarily involves:

-placental implantation site -decidua and adjacent myometrium -cervicovaginal lacerations -The pathogenesis of uterine infection following cesarean

delivery is that of an infected surgical incision -Bacteria that colonize the cervix and vagina gain access to

amnionic fluid during labor and invade devitalized uterine tissue postpartum

-Parametrial cellulitis next follows with infection of the pelvic retroperitoneal fibroareolar connective tissue

-With early treatment, infection is contained within the paravaginal tissue but may extend deeply into the pelvis

PUERPERAL INFECTION: Clinical Course

-Fever is the MOST IMPORTANT criterion for the diagnosis of postpartum metritis

-Degree of fever is believed proportional to the extent of infection and sepsis syndrome

-Temperatures commonly are 38 to 39°C -Chills that accompany fever suggest bacteremia -Women usually complain of: -abdominal pain -parametrial tenderness on abdominal and bimanual examination -offensive odor of lochia (but many women have foul-smelling lochia

without evidence for infection) *those due to group A -hemolytic streptococci, are frequently

associated with scanty, odorless lochia -Leukocytosis may range from 15,000 to 30,000 cells/L *cesarean delivery itself increases the leukocyte count

PUERPERAL INFECTION: Treatment

-Mild metritis following vaginal delivery: outpatient treatment with an oral antimicrobial agent is usually sufficient

-Moderate to severe infections: intravenous therapy with a broad-spectrum antimicrobial regimen is indicated

-Improvement follows in 48 to 72 hours in nearly 90% of women treated with one of several regimens

-Persistent fever after 48 to 72 hours mandates a careful search for causes of refractory pelvic infection including:

-Parametrial phlegmon—an area of intense cellulitis -Abdominal incisional or pelvic abscess -Infected hematoma -Septic pelvic thrombophlebitis -Antimicrobial-resistant bacteria or drug side effects SELDOM -Patient may be discharged home after she has been afebrile for at least 24

hours and further oral antimicrobial therapy is NOT needed


Choice of Antimicrobials

-Although therapy is empirical, initial treatment following cesarean delivery is directed against most of the mixed flora which typically cause puerperal infections

-Anaerobic coverage is included for infections following cesarean delivery

-Such broad-spectrum antimicrobial coverage is often not necessary to treat infection following vaginal delivery respond to regimens such as ampicillin plus gentamicin


Antimicrobial Regimens for Pelvic Infection Following Cesarean Delivery

Regimen Comments

Clindamycin 900 mg + gentamicin 1.5 mg/kg, q8h intravenously

"Gold standard" 90–97% efficacy, once-daily gentamicin dosing acceptable

+

Ampicillin added to regimen with sepsis syndrome or suspected enterococcal infection

Clindamycin + aztreonam Gentamicin substitute with renal insufficiency

Extended-spectrum penicillins Piperacillin, ampicillin/sulbactam

Extended-spectrum cephalosporins Cefotetan, cefoxitin, cefotaxime

Imipenem + cilastatin Reserved for special indications


Choice of Antimicrobials -Clindamycin-gentamicin – 95% response rate, and this regimen -still considered by most to be the standard by which others are

measured -Enterococcal infections: add ampicillin to the clindamycin-gentamicin

regimen, either initially or if there is no response by 48 to 72 hours -Serum gentamicin levels be periodically monitored or only with altered

renal function *Once-daily dosing has a cure rate similar to 8-hour dosing -Gentamicin: potential nephrotoxicity and ototoxicity in the event of

diminished glomerular filtration -Alternatives in altered renal function: -Clindamycin and a second-generation cephalosporin -Clindamycin and aztreonam (monobactam with aminoglycoside-like

action)


Choice of Antimicrobials -The spectra of -lactam antimicrobials include activity against many anaerobic

pathogens and are inherently safe and free of major toxicity except for allergic reactions

-cephalosporins such as cefoxitin, cefotetan, and cefotaxime -extended-spectrum penicillins such as piperacillin, ticarcillin, and mezlocillin -The -lactamase inhibitors, clavulanic acid, sulbactam, and tazobactam, have been

combined with ampicillin, amoxicillin, ticarcillin, and piperacillin to extend spectra of lactams

-Metronidazole has superior in vitro activity against most anaerobes -Given with ampicillin and an aminoglycoside to provide coverage against most

organisms encountered in serious pelvic infections -Imipenem is a carbapenem that has broad-spectrum coverage against most

organisms associated with metritis -Used with cilastatin, which inhibits renal metabolism of imipenem *Combination is effective in most cases of metritis, it seems reasonable

from both a medical and an economic standpoint to reserve it for more serious infections

PUERPERAL INFECTION: Prevention

Perioperative Antimicrobial Prophylaxis -Administration of antimicrobial prophylaxis at the time of cesarean

delivery reduce the rate of pelvic infection by 70 to 80 *Observed benefit applies to both elective and nonelective

cesarean delivery and also includes a reduction in abdominal incisional infections

-Single-dose prophylaxis with ampicillin or a first-generation cephalosporin is ideal, and both are as effective as broad-spectrum agents or a multiple-dose

-Extended-spectrum prophylaxis with azithromycin added to standard single-dose prophylaxis showed a significant reduction in postcesarean metritis

-Women known to be colonized with methicillin-resistant Staphylococcusaureus—MRSA—are given vancomycin in addition to a cephalosporin


Perioperative Antimicrobial Prophylaxis -Infection rate is lowered more if the selected antimicrobial is given

before the skin incision compared with cord clamping -A number of locally applied antimicrobials have been evaluated to

prevent puerperal infection -Intrapartum vaginal irrigation with chlorhexidine did not reduce

the incidence of postpartum infection -Conflicting studies on use of Povidone-iodine: -vaginal irrigation before cesarean delivery had no effect on

the incidence of fever, metritis, or abdominal incisional infection -Preoperative vaginal cleansing with povidone-iodine had

a significantly lower infection rate following cesarean delivery—7 versus 14 percent

-Metronidazole gel: reduction in rate of metritis but no significant effect on febrile morbidity or wound infections


Treatment of Vaginitis -Prenatal treatment of asymptomatic vaginal infections has

not been shown to prevent postpartum pelvic infections -No beneficial effects for women treated for asymptomatic

bacterial vaginosis -Similar postpartum infection rate in women treated for 2nd

trimester asymptomatic Trichomonas vaginalis infection compared with that of placebo-treated women


Operative Technique -Allowing the placenta to separate spontaneously compared with

removing it manually lowers the risk of infection -Changing gloves by the surgical team after placental delivery DOES

NOT lower infection rates -Exteriorizing the uterus to close the hysterectomy may decrease

febrile moridity -Single versus 2-layer uterine closure: no difference in

postoperative infection rate -Closure versus Non-closure of Peritoneum: no effect on infection

rates -Closure of subcutaneous tissue in obese women: does NOT lower

infection rate but LOWERS incidence of wound separation

PUERPERAL INFECTION: Complications of Pelvic Infections

Wound Infection -When prophylactic antimicrobials are given, incidence of

abdominal incisional infections following Cesarean delivery is less than 2%

-Wound infection is a common cause of persistent fever in women treated for metritis

-Risk factors: -Obesity -Diabetes -Corticosteroid therapy -Immunosuppression -Anemia -Hypertension -Inadequate hemostasis with hematoma formation


Wound Infection -Incisional abscesses that develop following cesarean delivery

usually cause fever or cause persisting fever beginning on the 4th day – may be accompanied by wound erythema and drainage

-Treatment for abscess include antimicrobials and surgical drainage, with careful inspection to ensure that fascia is intact

-Wound care given 2-3 times daily: secondary en bloc closure at 4-6 days of tissue involved in superficial wound infection

-After closure: polypropylene or nylon suture of appropriate gauge enters 3 cm from one wound edge crosses the wound to incorporate the full wound thickness emerges 3 cm from the other wound edge – placed in series to close the opening

-Sutures may be removed on postprocedural day 10


Wound Dehiscence -Disruption or Dehiscence refers to separation of the fascial

layer -Requires secondary closure of the incision in the operating

room -Most disruptions manifested on 5th postoperative day and

is often accompanied by a serosanguineous discharge -May be associated with concurrent fascial infection and

tissue necrosis


Necrotizing Fasciitis of Abdominal Wall Incisions -Uncommon, severe wound infection with necrosis associated with

high mortality -may involve abdominal incisions, or may complicate episiotomy or

other perineal lacerations -Risk factors: Diabetes, Obesity, Hypertension -Usually are polymicrobial and are caused by organisms that

comprise normal vaginal flora -Can also be caused by single virulent bacterial species such as

group A β-hemolytic streptococcus -Treatment consists of broad-spectrum antibiotics along with

prompt fascial debridement until healthy bleeding tissue is encountered

-In extensive resection, synthetic mesh may be required


Peritonitis -unusual to develop following cesarean delivery -invariably preceded by metritis and uterine incisional necrosis and

dehiscence -may be due to: -inadvertent bowel injury at cesarean delivery -after rupture of parametrial or adnexal abscess -vaginal delivery (very rare) -Abdominal rigidity MAY NOT be prominent with puerperal peritonitis

because of abdominal wall laxity from pregnancy -Severe pain may be experienced, but FIRST SYMPTOM is frequently

adynamic ileus -Bowel distention may develop -Treatment: antimicrobial treatment alone may suffice for infections that

begin with an intact uterus and extend to peritoneum -surgical treatment is for peritonitis caused by uterine incisional necoris or

bowel perforation


Adnexal Infections -Ovarian abscess rarely develops in the puerperium -Presumed to be caused by bacterial invasion through a rent

in the ovarian capsule -Usually unilateral -Present 1-2 weeks after delivery -Rupture is common and peritonitis may be severe


Parametrial Phlegmon -Phlegmon: an area of induration within the leaves of the

broad ligament in those with parametrial cellulitis -Develops following cesarean delivery in women with

metritis -Considered when fever persists after 72 hours despite IV

antibiotics -Phlegmons are usually unilateral, frequently limited to the

parametrial area at the base of the broad ligament -In intense cases, cellulitis extends along natural lines of

cleavage – most common of which is laterally along broad ligament with tendency to extend to pelvic sidewall

-Posterior extension may involve rectovaginal septum, producing a firm mass on the cervix


Parametrial Phlegmon -Severe cellulitis of uterine incision may lead to

necrosis and separation -Puerperal metritis with cellulitis: typically a

retroperitoneal infection evidence of peritonitis suggests possibility of uterine incisional necrosis, bowel injury, or other lesions

-Treatment: broad-spectrum antimicrobial regimen *Fever resolves in 5-7 days but may last longer -surgery is reserved for uterine incisional necrosis -uterine debridement and resuturing are feasible


Imaging Studies -Persistent puerperal infections can be evaluated using

computed tomography (CT) or magnetic resonance (MR) imaging

-Uterine incisional dehiscence is sometimes suspected by CT scanning images but these must be interpreted within the clinical context because apparent uterine incisional defects thought to represent edema can be seen even on images after uncomplicated cesarean delivery


Pelvic Abscess

-Rarely, a parametrial phlegmon suppurates, forming a fluctuant broad ligament mass that may point above the inguinal ligament

-Abscesses may dissect:

-anteriorly - amenable to CT-directed needle drainage

-posteriorly to the rectovaginal septum - surgical drainage is easily effected by colpotomy incision

-Psoas abscess: rare, may require percutaneous drainage despite antimicrobial therapy


Septic Pelvic Thrombophlebitis

-common complication in the preantibotic era

-Pathogenesis: puerperal infection may extend along venous routes and cause thrombosis

-Lymphangitis often coexists

-Ovarian veins may become involved because they drain the upper uterus and therefore, the placental implantation site

-Puerperal septic thrombophlebitis is likely to involve one or both ovarian venous plexuses

-Clot may extend into the inferior vena cava and occasionally to the renal vein


Septic Pelvic Thrombophlebitis -Incidence: -1:9000 - following vaginal delivery -1:800 - with cesarean delivery -Overall incidence of 1:3000 -Management: -Women with septic thrombophlebitis usually have clinical

improvement of pelvic infection with antimicrobial treatment but they continue to have fever

-Occasionally there is pain in one or both lower quadrants but patients are usually asymptomatic except for chills.

-Diagnosis can be confirmed by either pelvic CT or MR imaging -Before imaging methods were available, the heparin challenge test

was advocated


Infections of the Perineum, Vagina, and Cervix -Episiotomy infections are NOT common because the operation is

performed much less frequently now than in the past -With infection, dehiscence is a concern - 0.5% of episiotomy wounds

dehisced and 80% of these were due to infection -Infection of a fourth-degree laceration is likely to be more serious -Although life-threatening septic shock is rare, it may still occur as a

result of an infected episiotomy -Pathogenesis and Clinical Course: -Factors associated to episiotomy dehiscence: -infection -coagulation disorders -smoking -HPV infection


Infections of the Perineum, Vagina, and Cervix -Pathogenesis and Clinical Course: -Common symptoms of episiotomy dehiscence: -Local pain 65% -Purulent discharge 65% -Fever 44% -dysuria, with or without urinary retention -Edema, ulceration and exudation of the vulva


Infections of the Perineum, Vagina, and Cervix -Pathogenesis and Clinical Course: -Vaginal lacerations may become infected directly or by extension

from the perineum mucosa becomes red and swollen and may then become necrotic and slough

-Parametrial extension may result in lymphangitis. -Cervical lacerations are common but seldom are noticeably

infected and may manifest as metritis -Deep lacerations which extend directly into the tissue at the base

of the broad ligament may become infected and cause lymphangitis, parametritis, and bacteremia


Infections of the Perineum, Vagina, and Cervix -Treatment: -Infected episiotomies are managed like other infected surgical

wounds -Drainage is established -Sutures are removed -Infected wound debrided -Cellulitis but NO purulence: broad-spectrum antimicrobial therapy

with close observation -Dehiscence: local wound care is continued along with intravenous

antimicrobials -Early repair after infection subsided is advocated - average

duration of 6 days from dehiscence to episiotomy repair -Rarely, intestinal diversion may be required to allow healing


Infections of the Perineum, Vagina, and Cervix -Technique for Early Repair:

Before performing early repair, diligent preparation is essential

PREOPERATIVE PROTOCOL for Early Repair of Episiotomy Dehiscence

1. Open wound, remove sutures, begin intravenous antimicrobials

2. Wound care

-Sitz bath several times daily or hydrotherapy

-Adequate analgesia or anesthesia—regional analgesia or general anesthesia may be necessary for the first few debridements

-Scrub wound twice daily with a povidone-iodine solution

-Debride necrotic tissue

3. Closure when afebrile and with pink, healthy granulation tissue

4. Bowel preparation for fourth-degree repairs


Infections of the Perineum, Vagina, and Cervix -Technique for Early Repair: -Most important is that the surgical wound must be properly

cleaned and free of infection -Surface of the episiotomy wound free of infection & exudate and

covered by pink granulation tissue secondary repair can be done -Tissue must be adequately mobilized, with special attention to

identify and mobilize the anal sphincter muscle -Secondary closure of the episiotomy is accomplished in layers -Postoperative care includes: -local wound care -low-residue diet -stool softeners -nothing per vagina or rectum until healed


Infections of the Perineum, Vagina, and Cervix -Necrotizing Fasciitis of Perineal and Vaginal Wound Infections -Fatal complication of perineal and vaginal wound infections is deep

soft-tissue infection involving muscle and fascia -Common in women with diabetes or those immunocompromised

but may develop in otherwise healthy women -Microbiology is similar to those of other pelvic infections, as well

as necrotizing fasciitis of the abdominal wall incision -Necrotizing fasciitis of the episiotomy site may involve any of the

several superficial or deep perineal fascial layers may extend to the thighs, buttocks, and abdominal wall

-Early Postpartum: Group A β-hemolytic streptococci infections typically do NOT cause symptoms until 3 to 5 days after delivery


Infections of the Perineum, Vagina, and Cervix -Necrotizing Fasciitis of Perineal and Vaginal Wound Infections -If myofasciitis progresses, the woman may become ill from

septicemia profound hemoconcentration from capillary leakage with circulatory failure commonly occurs death

-Early diagnosis, surgical debridement, antimicrobials, and intensive care are of paramount importance in the successful treatment of necrotizing soft-tissue infections

-Surgery includes extensive debridement of all infected tissue, leaving wide margins of healthy tissue including extensive vulvar debridement with unroofing and excision of abdominal, thigh, or buttock fascia

-Mortality is virtually universal without surgical treatment, and rates approach 50% even if extensive debridement is performed

PUERPERAL INFECTION: Toxic Shock Syndrome

-Acute febrile illness with severe multisystem derangement has a case-fatality rate of 10-15%

-Presents usually with: -Fever -Headache -Mental confusion -Diffuse macular erythematous rash -Subcutaneous edema -Nausea and vomiting -Watery diarrhea -Marked hemoconcentration -Renal failure followed by hepatic failure, disseminated intravascular

coagulation, and circulatory collapse may follow in rapid sequence


-During recovery, the rash-covered areas undergo desquamation

-Staphylococcus aureus has been recovered from almost all afflicted persons specifically, a staphylococcal exotoxin, termed toxic shock syndrome toxin-1

-TSST-1—causes the clinical manifestations by provoking profound endothelial injury

-A very small amount of TSST-1 has been shown to activate 5-30% of T cells to create a "cytokine storm”

-Other possible causes: Clostridium sordellii colonization, group A β-hemolytic streptococcal infection (more virulent serotypes: M1, M3)


-Delayed diagnosis and treatment may be associated with fetal or maternal mortality

-Principal therapy for toxic shock is supportive, while allowing reversal of capillary endothelial

-Antimicrobial therapy to include staphylococcal and streptococcal coverage is given

-With evidence of pelvic infection, antimicrobial therapy must also include agents used for polymicrobial infections

-Women with these infections often require extensive wound debridement and possibly hysterectomy

obstetrics - puerperal infection

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