1. Apa saja perubahan fisiologis dan anatomi yang terjadi pada fase nifas?

Bedanya multipara dan

nulipara

Overview
Puerperium is defined as the time from the delivery of the placenta through the first few weeks after the delivery. This period is
usually considered to be 6 weeks in duration. By 6 weeks after delivery, most of the changes of pregnancy, labor, and delivery have
resolved and the body has reverted to the nonpregnant state.

An overview of the relevant anatomy and physiology in the postpartum period follows.

Uterus
The pregnant term uterus (not including baby, placenta, fluids, etc) weighs approximately 1000 g. In the 6 weeks following delivery,
the uterus recedes to a weight of 50-100 g.

Immediately postpartum, the uterine fundus is palpable at or near the level of the maternal umbilicus. Thereafter, most of the
reduction in size and weight occurs in the first 2 weeks, at which time the uterus has shrunk enough to return to the true pelvis. Over
the next several

weeks, the uterus slowly returns to its nonpregnant state, although the overall uterine size remains larger than prior to gestation.

The endometrial lining rapidly regenerates, so that by the seventh day endometrial glands are already evident. By the 16th day, the
endometrium is restored throughout the uterus, except at the placental site.

The placental site undergoes a series of changes in the postpartum period. Immediately after delivery, the contractions of the
arterial smooth muscle and compression of the vessels by contraction of the myometrium ("physiologic ligatures") result in
hemostasis. The size of the placental bed decreases by half, and the changes in the placental bed result in the quantity and quality
of the lochia that is experienced.

Immediately after delivery, a large amount of red blood flows from the uterus until the contraction phase occurs. Thereafter, the
volume of vaginal discharge (lochia) rapidly decreases. The duration of this discharge, known as lochia rubra, is variable. The red
discharge progressively changes to brownish red, with a more watery consistency (lochia serosa). Over a period of weeks, the
discharge continues to decrease in amount and color and eventually changes to yellow (lochia alba).[1] The period of time the lochia
can last varies, although it averages approximately 5 weeks.[2]

The amount of flow and color of the lochia can vary considerably. Fifteen percent of women have continue to have lochia 6 weeks or
more postpartum. Often, women experience an increase in the amount of bleeding at 7-14 days secondary to the sloughing of the
eschar on the placental site. This is the classic time for delayed postpartum hemorrhages to occur.

Cervix
The cervix also begins to rapidly revert to a nonpregnant state, but it never returns to the nulliparous state. By the end of the first
week, the external os closes such that a finger cannot be easily introduced.

Vagina
The vagina also regresses but it does not completely return to its prepregnant size. Resolution of the increased vascularity and
edema occurs by 3 weeks, and the rugae of the vagina begin to reappear in women who are not breastfeeding. At this time, the
vaginal epithelium appears atrophic on smear. This is restored by weeks 6-10; however, it is further delayed in breastfeeding
mothers because of persistently decreased estrogen levels.

Perineum
The perineum has been stretched and traumatized, and sometimes torn or cut, during the process of labor and delivery. The swollen
and engorged vulva rapidly resolves within 1-2 weeks. Most of the muscle tone is regained by 6 weeks, with more improvement over
the following few months. The muscle tone may or may not return to normal, depending on the extent of injury to muscle, nerve, and
connecting tissues.

Abdominal wall
The abdominal wall remains soft and poorly toned for many weeks. The return to a prepregnant state depends greatly on maternal
exercise.

Ovaries
The resumption of normal function by the ovaries is highly variable and is greatly influenced by breastfeeding the infant. The woman
who breastfeeds her infant has a longer period of amenorrhea and anovulation than the mother who chooses to bottle-feed. The
mother who does not breastfeed may ovulate as early as 27 days after delivery. Most women have a menstrual period by 12 weeks;
the mean time to first menses is 7-9 weeks.

In the breastfeeding woman, the resumption of menses is highly variable and depends on a number of factors, including how much
and how often the baby is fed and whether the baby's food is supplemented with formula. The delay in the return to normal ovarian
function in the lactating mother is caused by the suppression of ovulation due to the elevation in prolactin. Half to three fourths of
women who breastfeed return to periods within 36 weeks of delivery.

Breasts
The changes to the breasts that prepare the body for breastfeeding occur throughout pregnancy. If delivery ensues, lactation can be
established as early as 16 weeks' gestation. Lactogenesis is initially triggered by the delivery of the placenta, which results in falling
levels of estrogen and progesterone, with the continued presence of prolactin. If the mother is not breastfeeding, the prolactin levels
decrease and return to normal within 2-3 weeks.

The colostrum is the liquid that is initially released by the breasts during the first 2-4 days after delivery. High in protein content, this
liquid is protective for the newborn. The colostrum, which the baby receives in the first few days postpartum, is already present in
the breasts, and suckling by the newborn triggers its release. The process, which begins as an endocrine process, switches to an
autocrine process; the removal of milk from the breast stimulates more milk production. Over the first 7 days, the milk matures and
contains all necessary nutrients in the neonatal period. The milk continues to change throughout the period of breastfeeding to meet
the changing demands of the baby.

http://emedicine.medscape.com/article/260187-overview#aw2aab6b3
http://www.unfoldbirthservices.com/uploads/1/2/7/7/12776207/hendrick_hormonal_changes.pdf

2. Bagaimana penurunan tinggi fundus uteri setelah persalinan?

3. Jelaskan macam-macam kelainan masa nifas
4. Jelaskan macam-macam lokhea
 The lochia is the physiological postpartum uterine discharge consisting mainly of blood and necrotic tissue that occur during the first 4-6
weeks after delivery of the baby.

The discharge consists of (1) discharge and blood from the area on the uterine wall to which the placenta is attached during the pregnancy
(2)the sloughed off endometrium which gets considerably thickened during pregnancy, (3) blood, mucus from the healing cervix and (4) dead
tissue.

The blood in the lochia comes mainly from the large raw area left in the uterine wall after the placenta detaches from it. While bleeding from
this area is controlled by contraction of the uterine muscles immediately after delivery, it takes about 2 weeks for this area to heal.

This is why bleeding is maximum in the fist 2-3 days after birth and then decreases over the next two weeks.

The lochia is sterile for the first 2-3 days but then becomes colonised by bacteria giving off a typical lochial smell which is normal and should
not be confused with the bad odor from lochia in postpartum infection.

The quantity of lochia may be scanty after a premature delivery but more than normal after a twin pregnancy or other conditions in which the
uterus becomes larger than an average-size pregnancy uterus.

Types of Lochia
Depending on the color, lochia can be of three types:

Lochia Rubra: Lochia rubra occurs in the first 3-4 days after childbirth. It is reddish in colour hence the term 'rubra'. It is made
up of mainly blood, bits of fetal membranes, decidua, meconium and cervical discharge.
Lochia Serosa: The lochia rubra gradually changes colour to brown and then yellow over a period of about I week. It is called
lochia serosa at this stage. The lochia serosa contains less red blood cells but more white blood cells, wound discharge from the
placental and other sites, and mucus from the cervix.
Lochia Alba: The Lochia alba is a whitish, turbid fluid which drains from the vagina for about another 1 - 2 weeks. It mainly
consists of decidual cells, mucus, white blood cells, and epithelial cells.

Amount of Bleeding/Lochia
The amount of lochia will may vary from time to time. In some women, painful contraction of the uterus after delivery ('afterpains')
may lead to a gush of heavy bleeding with clots which decreases spontaenously.

Sometimes getting up from a sitting down or lying down position may lead to a rush of blood - this is just drainage of the collected blood in
the vagina and is not a cause for worry.

Management of Lochia
Lochia does not need any specific management. One thing which should be remembered is that the placental area as well as the sites of
sloughing endometrium are raw and open during this time and bacteria can easily spread from the vagina. So, use of tampons should be
avoided - sanitary pads are the best options to be used at this time.

Sex should also be avoided during this time due to the same reason - to avoid spread of bacteria.

Bathing in public pools are also best avoided until the lochia has completely stopped.

Using a Sitz bath may help to clean out the vagina and also soothe the episiotomy stitches , if any.

Abnormalities of of Lochia
The lochia may be abnormal if infection occurs at this time. Infection can be suspected when :
The Lochia continues to remain bright red even after the first week from childbirth.
The lochia becomes bright red again after having become paler over the previous days.
There is abnormally heavy bleeding causing a sanitary pad to soak through within 1 hour or
less or there is passage of blood clots larger than a golf ball. This is a sign of secondary
postpartum hemorrhage and needs emergency treatment.
It has an unpleasant smell.
There is fever with chills.
There is pain in the lower abdomen which increases over the days.

Lochia after a Cesarian Section

Many women believe that the flow of lochia is less after a cesarian section since the
uterine cavity is cleaned out after the birth of the baby. This is not true. The flow of
lochia is not dependent on the type of delivery - normal vaginal childbirth or C-section.
The amount and duration is the same in both cases.
http://www.gynaeonline.com/lochia.htm
5. Kenapa ditemukan pendarahan semakin memberat disertai demam?
Pada kasus post SC (perdarahan dan TFU) bedanya sama pervaginam
Perawatan masa nifas (post natal care)

Lochia after a Cesarian Section

Many women believe that the flow of lochia is less after a cesarian section since the
uterine cavity is cleaned out after the birth of the baby. This is not true. The flow of
lochia is not dependent on the type of delivery - normal vaginal childbirth or C-section.
The amount and duration is the same in both cases.
http://www.gynaeonline.com/lochia.htm
6. Tindakan awal apa yang dilakukan dokter untuk menghentikan perdarahan?
7. Bagaimana interpretasi dari PF yang didapat?
8. DD
 Postpartum hemorrhage, the loss of more than 500 mL of blood after delivery, occurs in up to 18
percent of births and is the most common maternal morbidity in developed countries. Although
risk factors and preventive strategies are clearly documented, not all cases are expected or
avoidable. Uterine atony is responsible for most cases and can be managed with uterine
massage in conjunction with oxytocin, prostaglandins, and ergot alkaloids. Retained placenta is a
less common cause and requires examination of the placenta, exploration of the uterine cavity,
and manual removal of retained tissue. Rarely, an invasive placenta causes postpartum
hemorrhage and may require surgical management. Traumatic causes include lacerations,
uterine rupture, and uterine inversion. Coagulopathies require clotting factor replacement for the
identified deficiency. Early recognition, systematic evaluation and treatment, and prompt fluid
resuscitation minimize the potentially serious outcomes associated with postpartum hemorrhage.

Postpartum hemorrhage, defined as the loss of more than 500 mL of blood after delivery, occurs
in up to 18 percent of births.1,2 Blood loss exceeding 1,000 mL is considered physiologically
significant and can result in hemodynamic instability.3Even with appropriate management,
approximately 3 percent of vaginal deliveries will result in severe post-partum hemorrhage.4 It is
the most common maternal morbidity in developed countries and a major cause of death
worldwide.1,3

Complications from postpartum hemorrhage include orthostatic hypotension, anemia, and fatigue,
which may make maternal care of the newborn more difficult. Post-partum anemia increases the
risk of post-partum depression.5 Blood transfusion may be necessary and carries associated
risks.6 In the most severe cases, hemorrhagic shock may lead to anterior pituitary ischemia with
delay or failure of lactation (i.e., postpartum pituitary necrosis).7,8 Occult myocardial ischemia,
dilutional coagulopathy, and death also may occur.9 Delayed postpartum hemorrhage, bleeding
after 24 hours as a result of sloughing of the placental eschar or retained placental fragments,
also can occur.10

SORT: KEY RECOMMENDATIONS FOR PRACTICE

CLINICAL EVIDENCE
RECOMMENDATION RATING REFERENCES

Active management of the A 2,17

third stage of labor
decreases postpartum blood
loss and the risk of
postpartum hemorrhage
(number needed to
treat=12).

Active management of the A 2,17,18

third stage of labor does not
 CLINICAL EVIDENCE
RECOMMENDATION RATING REFERENCES

increase the risk of retained

placenta.

Oxytocin (Pitocin) is the first A 2,25,26

choice for prevention of
postpartum hemorrhage
because it is as effective or
more effective than ergot
alkaloids or prostaglandins
and has fewer side effects.

Misoprostol (Cytotec) may A 27

be used when other oxytocic
agents are not available for
prevention of postpartum
hemorrhage (number
needed to treat=18).

Misoprostol may be used for A 37

treatment of postpartum
hemorrhage, but this agent
is associated with more side
effects than conventional
uterotonic drugs.

Routine episiotomy A 11,40

increases anal sphincter
tears and blood loss.

A = consistent, good-quality patient-oriented evidence; B = inconsistent or limited-quality patient-

oriented evidence; C = consensus, disease-oriented evidence, usual practice, expert opinion, or
case series. For information about the SORT evidence rating system, see page 789
or http://www.aafp.org/afpsort.xml.

SORT: KEY RECOMMENDATIONS FOR PRACTICE

View Table
 Prevention
Jump to section +

Risk factors for postpartum hemorrhage include a prolonged third stage of labor, multiple
delivery, episiotomy, fetal macrosomia, and history of postpartum
hemorrhage.3,4,11,12 However, postpartum hemorrhage also occurs in women with no risk
factors, so physicians must be prepared to manage this condition at every delivery.13 Strategies
for minimizing the effects of postpartum hemorrhage include identifying and correcting anemia
before delivery, being aware of the mother's beliefs about blood transfusions, and eliminating
routine episiotomy.1416 Reexamination of the patient's vital signs and vaginal flow before
leaving the delivery area may help detect slow, steady bleeding.

The best preventive strategy is active management of the third stage of labor (number needed to
treat [NNT] to prevent one case of postpartum hemorrhage = 12).17,18 Hospital guidelines
encouraging this practice have resulted in significant reductions in the incidence of massive
hemorrhage.19 Active management, which involves administering a uterotonic drug with or soon
after the delivery of the anterior shoulder, controlled cord traction, and, usually, early cord
clamping and cutting, decreases the risk of postpartum hemorrhage and shortens the third stage
of labor with no significant increase in the risk of retained placenta.17,18Compared with
expectant management, in which the placenta is allowed to separate spontaneously aided only
by gravity or nipple stimulation, active management decreases the incidence of postpartum
hemorrhage by 68 percent.17

Early cord clamping is no longer included in the International Federation of Gynecology and
Obstetrics (FIGO) definition of active management of the third stage of labor, and uterine
massage after delivery of the placenta has been added.20 Delaying cord clamping for about 60
seconds has the benefit of increasing iron stores and decreasing anemia, which is especially
important in preterm infants and in low-resource settings.16,2123 The delay has not been
shown to increase neonatal morbidity or maternal blood loss.16,21,23

Prophylactic administration of oxytocin (Pitocin) reduces rates of postpartum hemorrhage by 40

percent24; this reduction also occurs if oxytocin is given after placental delivery.2,18 Oxytocin is
the drug of choice for preventing postpartum hemorrhage because it is at least as effective as
ergot alkaloids or prostaglandins and has fewer side effects.2,25,26 Misoprostol (Cytotec) has a
role in the prevention of postpartum hemorrhage (NNT = 18)16; this agent has more side effects
but is inexpensive, heat- and light-stable, and requires no syringes.27

Diagnosis and Management

Jump to section +
The diagnosis of postpartum hemorrhage begins with recognition of excessive bleeding and
methodic examination to determine its cause (Figure 1). The Four Ts mnemonic (Tone, Trauma,
Tissue, and Thrombin) can be used to detect specific causes (Table 1).

Management of Postpartum Hemorrhage

Figure 1.

Algorithm for management of postpartum hemorrhage. Many of the steps involved in diagnosing and treating
postpartum hemorrhage must be undertaken simultaneously. Although the steps in maternal resuscitation are
consistent (bold arrows) other actions may differ based on the actual cause. (IV = intravenous; IU =
international units; CBC = complete blood count; IM = intramuscularly; RBC = red blood cells; ICU = intensive
care unit)

View Large
Management of Postpartum Hemorrhage

Figure 1.

Algorithm for management of postpartum hemorrhage. Many of the steps involved in diagnosing
and treating postpartum hemorrhage must be undertaken simultaneously. Although the steps in
maternal resuscitation are consistent (bold arrows) other actions may differ based on the actual
cause. (IV = intravenous; IU = international units; CBC = complete blood count; IM =
intramuscularly; RBC = red blood cells; ICU = intensive care unit)
TABLE 1

The Four Ts Mnemonic Device for Causes of Postpartum Hemorrhage

APPROXIMATE INCIDENCE
FOUR TS CAUSE (%)

Tone Atonic uterus 70

Trauma Lacerations, 20
hematomas,
inversion,
rupture

Tissue Retained tissue, 10

invasive
placenta

Thrombin Coagulopathies 1

TABLE 1 The Four Ts Mnemonic Device for Causes of Postpartum Hemorrhage

View Table

TONE

Uterine atony is the most common cause of postpartum hemorrhage.28 Because hemostasis
associated with placental separation depends on myometrial contraction, atony is treated initially
by bimanual uterine compression and massage, followed by drugs that promote uterine
contraction.

Uterine Massage
Brisk blood flow after delivery of the placenta should alert the physician to perform a bimanual
examination of the uterus. If the uterus is soft, massage is performed by placing one hand in the
vagina and pushing against the body of the uterus while the other hand compresses the fundus
from above through the abdominal wall (Figure 2).29 The posterior aspect of the uterus is
massaged with the abdominal hand and the anterior aspect with the vaginal hand.
Figure 2.

Technique of bimanual massage for uterine atony. Bimanual uterine compression massage is performed by
placing one hand in the vagina and pushing against the body of the uterus while the other hand compresses the
fundus from above through the abdominal wall. The posterior aspect of the uterus is massaged with the
abdominal hand and the anterior aspect with the vaginal hand.

Redrawn with permission from Anderson J, Etches D, Smith D. Postpartum hemorrhage. In: Baxley E.
Advanced Life Support in Obstetrics course syllabus. 4th ed. Leawood, Kan.: American Academy of Family
Physicians, 2001.

View Large

Figure 2.

Technique of bimanual massage for uterine atony. Bimanual uterine compression massage is
performed by placing one hand in the vagina and pushing against the body of the uterus while the
other hand compresses the fundus from above through the abdominal wall. The posterior aspect
of the uterus is massaged with the abdominal hand and the anterior aspect with the vaginal hand.

Redrawn with permission from Anderson J, Etches D, Smith D. Postpartum hemorrhage. In:
Baxley E. Advanced Life Support in Obstetrics course syllabus. 4th ed. Leawood, Kan.: American
Academy of Family Physicians, 2001.

Uterotonic Agents
Uterotonic agents include oxytocin, ergot alkaloids, and prostaglandins. Oxytocin stimulates the
upper segment of the myometrium to contract rhythmically, which constricts spiral arteries and
decreases blood flow through the uterus.30 Oxytocin is an effective first-line treatment for
postpartum hemorrhage31; 10 international units (IU) should be injected intramuscularly, or 20 IU
in 1 L of saline may be infused at a rate of 250 mL per hour. As much as 500 mL can be infused
over 10 minutes without complications.10

Methylergonovine (Methergine) and ergometrine (not available in the United States) are ergot
alkaloids that cause generalized smooth muscle contraction in which the upper and lower
segments of the uterus contract tetanically.32 A typical dose of methylergonovine, 0.2 mg
administered intramuscularly, may be repeated as required at intervals of two to four hours.
Because ergot alkaloid agents raise blood pressure, they are contraindicated in women with
preclampsia or hypertension.33 Other adverse effects include nausea and vomiting.33

Prostaglandins enhance uterine contractility and cause vasoconstriction.34 The prostaglandin

most commonly used is 15-methyl prostaglandin F2a, or carboprost (Hemabate). Carboprost can
be administered intramyometrially or intramuscularly in a dose of 0.25 mg; this dose can be
repeated every 15 minutes for a total dose of 2 mg. Carboprost has been proven to control
hemorrhage in up to 87 percent of patients.35 In cases where it is not effective, chorioamnionitis
or other risk factors for hemorrhage often are present.35 Hypersensitivity is the only absolute
contraindication, but carboprost should be used with caution in patients with asthma or
hypertension. Side effects include nausea, vomiting, diarrhea, hypertension, headache, flushing,
and pyrexia.34

Misoprostol is another prostaglandin that increases uterine tone and decreases postpartum
bleeding.36 Misoprostol is effective in the treatment of postpartum hemorrhage, but side effects
may limit its use.28,37 It can be administered sublingually, orally, vaginally, and rectally. Doses
range from 200 to 1,000 mcg; the dose recommended by FIGO is 1,000 mcg administered
rectally.28,37,38 Higher peak levels and larger doses are associated with more side effects,
including shivering, pyrexia, and diarrhea.28,39 Although misoprostol is widely used in the
treatment of postpartum hemorrhage, it is not approved by the U.S. Food and Drug
Administration for this indication.

TRAUMA
Lacerations and hematomas resulting from birth trauma can cause significant blood loss that can
be lessened by hemostasis and timely repair. Sutures should be placed if direct pressure does
not stop the bleeding. Episiotomy increases blood loss and the risk of anal sphincter
tears,11,12,40 and this procedure should be avoided unless urgent delivery is necessary and the
perineum is thought to be a limiting factor.14

Hematomas can present as pain or as a change in vital signs disproportionate to the amount of
blood loss. Small hematomas can be managed with close observation.41 Patients with persistent
signs of volume loss despite fluid replacement, as well as those with large or enlarging
hematomas, require incision and evacuation of the clot.41 The involved area should be irrigated
and the bleeding vessels ligated. In patients with diffuse oozing, a layered closure will help to
secure hemostasis and eliminate dead space.

Uterine Inversion
Uterine inversion is rare, occurring in 0.05 percent of deliveries.10 Active management of the
third stage of labor may reduce the incidence of uterine inversion.42 Fundal implantation of the
placenta may lead to inversion; the roles of fundal pressure and undue cord traction are
uncertain.10 The inverted uterus usually appears as a bluish-gray mass protruding from the
vagina. Vasovagal effects producing vital sign changes disproportionate to the amount of
bleeding may be an additional clue. The placenta often is still attached, and it should be left in
place until after reduction.42 Every attempt should be made to replace the uterus quickly. The
Johnson method of reduction begins with grasping the protruding fundus Figure 3A29) with the
palm of the hand and fingers directed toward the posterior fornix (Figure 3B29). The uterus is
returned to position by lifting it up through the pelvis and into the abdomen (Figure
3C29).43 Once the uterus is reverted, uterotonic agents should be given to promote uterine tone
and to prevent recurrence. If initial attempts to replace the uterus fail or a cervical contraction ring
develops, administration of magnesium sulfate, terbutaline (Brethine), nitroglycerin, or general
anesthesia may allow sufficient uterine relaxation for manipulation. If these methods fail, the
uterus will need to be replaced surgically.42
Figure 3.

Reduction of uterine inversion (Johnson method). (A) The protruding fundus is grasped with fingers directed
toward the posterior fornix. (B, C) The uterus is returned to position by pushing it through the pelvis and into the
abdomen with steady pressure towards the umbilicus.

Redrawn with permission from Anderson J, Etches D, Smith D. Postpartum hemorrhage. In: Baxley E.
Advanced Life Support in Obstetrics course syllabus. 4th ed. Leawood, Kan.: American Academy of Family
Physicians, 2001.

View Large
Figure 3.

Reduction of uterine inversion (Johnson method). (A) The protruding fundus is grasped with
fingers directed toward the posterior fornix. (B, C) The uterus is returned to position by pushing it
through the pelvis and into the abdomen with steady pressure towards the umbilicus.

Redrawn with permission from Anderson J, Etches D, Smith D. Postpartum hemorrhage. In:
Baxley E. Advanced Life Support in Obstetrics course syllabus. 4th ed. Leawood, Kan.: American
Academy of Family Physicians, 2001.

Uterine Rupture
Although rare in an unscarred uterus, clinically significant uterine rupture occurs in 0.6 to 0.7
percent of vaginal births after cesarean delivery in women with a low transverse or unknown
uterine scar.4446 The risk increases significantly with previous classical incisions or uterine
surgeries, and to a lesser extent with shorter intervals between pregnancies or a history of
multiple cesarean deliveries, particularly in women with no previous vaginal deliveries.44
48 Compared with spontaneous labor, induction or augmentation increases the rate of uterine
rupture, more so if prostaglandins and oxytocin are used sequentially. However, the incidence of
rupture is still low (i.e., 1 to 2.4 percent).46,48 Misoprostol should not be used for cervical
ripening or induction when attempting vaginal birth after previous cesarean delivery.48

Before delivery, the primary sign of uterine rupture is fetal bradycardia.45Tachycardia or late
decelerations can also herald a uterine rupture, as can vaginal bleeding, abdominal tenderness,
maternal tachycardia, circulatory collapse, or increasing abdominal girth.47 Symptomatic uterine
rupture requires surgical repair of the defect or hysterectomy. When detected in the postpartum
period, a small asymptomatic lower uterine segment defect or bloodless dehiscence can be
followed expectantly.47

TISSUE

Classic signs of placental separation include a small gush of blood with lengthening of the
umbilical cord and a slight rise of the uterus in the pelvis. Placental delivery can be achieved by
use of the Brandt-Andrews maneuver, which involves applying firm traction on the umbilical cord
with one hand while the other applies suprapubic counterpressure (Figure 429).49 The mean
time from delivery until placental expulsion is eight to nine minutes.4 Longer intervals are
associated with an increased risk of postpartum hemorrhage, with rates doubling after 10
minutes.4 Retained placenta (i.e., failure of the placenta to deliver within 30 minutes after birth)
occurs in less than 3 percent of vaginal deliveries.50 One management option is to inject the
umbilical vein with 20 mL of a solution of 0.9 percent saline and 20 units of oxytocin. This
significantly reduces the need for manual removal of the placenta compared with injecting saline
alone.51Alternatively, physicians may proceed directly to manual removal of the placenta, using
appropriate analgesia. If the tissue plane between the uterine wall and placenta cannot be
developed through blunt dissection with the edge of the gloved hand, invasive placenta should be
considered.

Figure 4.

Brandt-Andrews maneuver for cord traction. Firm traction is applied to the umbilical cord with one hand while
the other applies suprapubic counterpressure.

Redrawn with permission from Anderson J, Etches D, Smith D. Postpartum hemorrhage. In: Baxley E.
Advanced Life Support in Obstetrics course syllabus. 4th ed. Leawood, Kan.: American Academy of Family
Physicians, 2001.

View Large
Figure 4.

Brandt-Andrews maneuver for cord traction. Firm traction is applied to the umbilical cord with one
hand while the other applies suprapubic counterpressure.

Redrawn with permission from Anderson J, Etches D, Smith D. Postpartum hemorrhage. In:
Baxley E. Advanced Life Support in Obstetrics course syllabus. 4th ed. Leawood, Kan.: American
Academy of Family Physicians, 2001.

Invasive placenta can be life threatening.50 The incidence has increased from 0.003 percent to
0.04 percent of deliveries since 1950s; this increase is likely a result of the increase in cesarean
section rates.49 Classification is based on the depth of invasion and can be easily remembered
through alliteration: placentaaccreta adheres to the myometrium, placenta increta invades the
myometrium, and placenta percreta penetrates the myometrium to or beyond the serosa.10 Risk
factors include advanced maternal age, high parity, previous invasive placenta or cesarean
delivery, and placenta previa (especially in combination with previous cesarean delivery,
increasing to 67 percent with four or more).49 The most common treatment for invasive placenta
is hysterectomy.49 However, conservative management (i.e., leaving the placenta in place or
giving weekly oral methotrexate52 until human chorionic gonadotropin levels are 0) is
 sometimes successful.53 Women treated for a retained placenta must be observed for late
sequelae, including infection and late postpartum bleeding.52,53

THROMBIN

Coagulation disorders, a rare cause of post-partum hemorrhage, are unlikely to respond to the
measures described above.10 Most coagulopathies are identified before delivery, allowing for
advance planning to prevent postpartum hemorrhage. These disorders include idiopathic
thrombocytopenic purpura, thrombotic thrombocytopenic purpura, von Willebrand's disease, and
hemophilia. Patients also can develop HELLP (hemolysis, elevated liver enzyme levels, and low
platelet levels) syndrome or disseminated intravascular coagulation. Risk factors for disseminated
intravascular coagulation include severe pre-eclampsia, amniotic fluid embolism, sepsis,
placental abruption, and prolonged retention of fetal demise.54,55 Abruption is associated with
cocaine use and hypertensive disorders.54 Excessive bleeding can deplete coagulation factors
and lead to consumptive coagulation, which promotes further bleeding. Coagulation defects
should be suspected in patients who have not responded to the usual measures to treat post-
partum hemorrhage, and in those who are not forming blood clots or are oozing from puncture
sites.

Evaluation should include a platelet count and measurement of prothrombin time, partial
thromboplastin time, fibrinogen level, and fibrin split products (i.e., D-dimer). Management
consists of treating the underlying disease process, supporting intravascular volume, serially
evaluating coagulation status, and replacing appropriate blood components. Administration of
recombinant factor VIIa or clot-promoting medications (e.g., tranexamic acid [Cyklokapron]) may
be considered.33,54,56

http://www.aafp.org/afp/2007/0315/p875.html

EARLY INFECTION

Early infections most frequently result from subclinical infection or from excessive bacterial colonization of amniotic
fluid and the endometrical deciduae prior to delivery, both of which are frequently caused by prolonged labor or
ruptured membranes. Usually organisms that produce early infections are able to divide rapidly or produce toxin.
Organisms, toxins, or both easily gain access to the vascular system of postpartum patients because of the large
exposed venous channels in the uterus or because of interruption of natural barriers.

A thorough assessment of the patient by a complete history and physical examination is essential when symptoms or
signs of severe infection develop. Symptoms of severe pain that appear out of proportion to that usually expected may
occur with severe infection. Sudden pain with diaphoresis can indicate a sudden event. The more common symptoms
and signs associated with severe infection are listed in Table 1. Unusual anxiety or disorientation may indicate
impending circulatory shock. Prostration indicates a serious condition. Unusual temperature elevations, leukocytosis,
leukopenia, hemoconcentration, low hematocrits, or poor urinary output should prompt close scrutiny for severe
infection. Additional unusual manifestations indicate serious infection in the septic patient: septic shock, adult
respiratory distress syndrome, disseminated intravascular coagulation, pulmonary emboli, hemolysis, sudden
anasarca, or cardiac failure. Increasing areas of cellulitis with adequate antibiotic therapy or necrosis of tissue also
indicates a severe infection. As stressed later, surgical removal of infected areas is required when these additional
signs occur. Intensive care monitoring should be undertaken so that vital signs, blood gases, and urine function can
be closely documented (Table 2). Ultrasound or imaging tests may be indicated. Patients with symptoms and signs of
serious infection should have consultation with an infectious disease specialist or be transferred to a tertiary center
once the clinical condition is stable.

TABLE 1. Common Manifestations That Indicate Severe Postpartum Infection

Physical Examination Laboratory Examination

Anxiety
Marked leukocytosis ( ;25,000)
Disorientation Marked leukopenia (<1,000)
Prostration Hemoconcentration (hematocrit > 45%)
Severe tenderness Low hematocrit (<20%)
Low urinary output (<20 ml/hr)
Unusual temperature elevation ( ;39C)
Cardiac failure

TABLE 2. Unusual Signs That Virtually Always Indicate a Serious Infection Which Usually Requires Surgical Removal

Septic Shock Hemolysis

Adult respiratory distress syndrome Increasing area of cellulitis
Necrosis of tissue
Disseminated intravascular coagulation

ENDOMETRITIS (UTERINE-PERITONEAL INFECTIONS)

Early postpartum endometritis usually results from colonization or infection of the amniotic fluid prior to
delivery.8 Often amniotic fluid infection will not be recognized during labor, particularly if fever has not developed.
Risk factors important for amniotic fluid infection are also important for early postpartum endometritis and include
those events likely to contaminate amniotic fluid (i.e., prolonged labor, prolonged rupture of the membranes, multiple
cervical examinations, and lower socioeconomic status).9 Patients in lower socioeconomic groups probably have
increased rates of virulent vaginal organisms that produce upper tract infection.10 Prolonged labor and rupture of
membranes contribute to amniotic fluid colonization from organisms colonizing the lower genital tract. Colonizing
organisms usually do not invade the endometrium or produce infection if patients deliver vaginally, because the
contaminated amniotic fluid drains into the vagina in these cases. However, during cesarean section, bacteria in the
amniotic fluid no longer remain within the uterus but have the potential to contaminate the peritoneal cavity and
incisions of the uterus and abdominal wound. In fact, postpartum endometritis (uterine-peritoneal infections) is
tenfold to 20-fold more common in patients delivered by cesarean section than among patients who deliver
vaginally.2

Early postpartum endometritis is usually diagnosed on the basis of a temperature of 38.5C or higher in the first 24
hours or 38C or higher for 4 consecutive hours beyond the first 24 hours from delivery. Uterine tenderness is
expected because most patients will have both a uterine and an abdominal wound from the cesarean section. Since
wide variations occur in the degree of uterine tenderness, the finding of uterine tenderness is not a precise guide to
establish whether or not uterine infection is present. Some organisms, particularly streptococci, may produce little or
no uterine tenderness. Careful physical examination will usually reveal signs of peritonitis with an ileus and rebound
tenderness in both upper and lower quadrants of the abdomen. It is important during the physical examination to
exclude other sources of fever, particularly from wound, intravenous line, or lung infection.
Many physicians do not routinely obtain endometrial cultures because the organisms that cause early postpartum
endometritis have been well described and, until recently, have been relatively similar between hospitals. Certainly
unreliable culture results occur when cervicovaginal cultures are used or transcervical endometrial cultures are
obtained by pushing an unprotected swab through the cervix.11 Instead, protected swabs should be used to obtain
endometrial culture, because they reduce (although they do not eliminate) cervicovaginal contamination. Endometrial
or amniotic fluid cultures taken at the time of delivery accurately reflect the endometrial flora for 24 hours post
partum and can be substituted for a transcervical endometrial culture during this period. However, endometrial
cultures should be obtained for the remaining patients to detect an unusual or particularly virulent organism.
Organisms that are commonly isolated from patients with postpartum endometritis have been described elsewhere in
these volumes and are not discussed in detail here. Cultures typically recover a wide variety of facultative bacteria,
including group B streptococci, other facultative streptococci, Gardnerella vaginalis, and Escherichia coli, and a wide
variety of anaerobic bacteria, including Bacteroides and Peptostreptococcus species.6,12 Blood cultures recover similar
organisms from approximately 15% to 25% of febrile patients.6 Bacteremia per se does not predict the severity or the
course of infection, although the isolation of certain virulent organisms can be predictive of severe infection. Despite
the high frequency of positive blood cultures, young, otherwise healthy patients rarely develop septic shock.

A wide variety of antibiotics have been used to successfully treat postpartum endometritis. The antibiotic should be
active against the most common facultative and anaerobic bacteria.13 Over 90% of patients with postpartum
endometritis readily respond to antibiotic therapy. Several possibilities must be checked when patients do not
respond to antibiotic therapy (Table 3). The administration of too low an antibiotic dose is the most common cause of
treatment failure. Pregnant and postpartum women require a 40% increase in antibiotic dose over that required when
they are no longer pregnant.14 The 40% increase in blood volume, extracellular volume, and glomerular filtration rate
that occurs during pregnancy is maintained in the immediate postpartum period, and antibiotic concentrations must
be high enough to achieve bacterial inhibition in the postpartum patient. Thus, most antibiotics, particularly those
excreted through the kidneys, need to be administered at a high dosage. For example, the increased doses that should
be given post partum calculate to between 8 and 12 g/day of a -lactam (penicillin or cephalosporin) antibiotic. Other
causes of antibiotic treatment failure include infection from resistant organisms (unusual), wound infection, abscess
formation, and the development of septic thrombophlebitis.13

TABLE 3. Possibilities to Check When Patients Fail to Respond to Antibiotic Therapy

Subtherapeutic antibiotic dose Wound infection

Resistant organisms Septic thrombophlebitis
Abscess formation

URINARY TRACT INFECTION

Approximately 5% of the patients who develop immediate and postpartum infections have a sterile endometrial cavity
but 105 organisms or more per milliliter in the urine culture.6 Most of these patients will have had asymptomatic
antepartum bacteriuria, which becomes symptomatic following bladder catheterization or the trauma of delivery.
Costovertebral angle tenderness and other clinical signs of acute pyelonephritis are not usually present. Therefore, on
the basis of clinical signs, these patients are difficult to differentiate from those with early postpartum endometritis.
Urine sediments usually contain large numbers of white blood cells, and urine cultures are positive for uropathogens.
Urinary tract infection usually responds readily to common antibiotics used to treat endometritis. However. an
unusual serious antepartum complication of pyelonephritis has been reported with severe respiratory distress and
disseminated intravascular coagulopathy requiring prolonged assisted ventilation.15 Physicians must be aware that
similar severe manifestations of pyelonephritis could occur in the early postpartum period.

DISTURBED ABSCESSES

lntra-abdominal abscesses are unusual during pregnancy. Appendicitis and, rarely, abscess from
salpingitis16 constitute the most likely sources of an intra-abdominal abscess. Relatively asymptomatic abscesses
occur because infection within the abscesses remains separated from the vasculature and from adjacent organs by the
abscess wall. During pregnancy, the uterus usually constitutes part of the abscess wall. At delivery, the uterine portion
of the abscess wall is disturbed by the collapse of the uterus, and pus leaks into the peritoneal cavity. Infection can
then spread, causing frank peritonitis, bacteremia, or both. A ruptured abscess may be difficult to recognize,
particularly if the leak is slow and there are no sudden peritoneal findings. Prompt recognition of a ruptured abscess
from the history and physical findings can prevent uncontrolled and potentially fatal sepsis. The patient may have had
vague lower abdominal pain or even an episode resembling appendicitis during pregnancy. Unsuspected rupture of an
abscess occurs among vaginally delivered patients because the abscess would have been discovered during cesarean
section. Possible abscess rupture is most easy to recognize in vaginally delivered patients without prolonged labor or
rupture of membranes who otherwise would not be expected to suddenly develop septic shock or signs of sepsis.
Recognition becomes more difficult when patients have recognized risk factors for infection. Immediate abdominal
exploration under antibiotic coverage is necessary to control sepsis from a disturbed ruptured abscess (Table 4).

TABLE 4. Most Common Cause of Serious Infection Occurring Early in the Postpartum Period (<48 Hours of
Delivery)

Postpartum endometritis
Urinary tract infection
Disturbed abscess
Rapidly developing soft tissue infection
Necrotizing fasciitis
Intravenous fluid contamination
Intravenous catheter infection

RAPIDLY DEVELOPING SOFT TISSUE INFECTION

Rapidly developing soft tissue infections are potentially lethal infections of the subcutaneous tissue, muscle, or
myometrium, most commonly caused by clostridia or group A streptococci. Patients with these rapidly developing
infections usually have a history and physical examination similar to patients with other causes of postpartum
infection. These infections commonly masquerade as postpartum endometritis, and patients may have the usual risk
factors for infection, including prolonged labor or rupture of membranes, although many others will have no
particular risk factors. However, two clinical features suggest a more serious infection: the severity of clinical
manifestations and indications of septic shock. Patients with these infections invariably exhibit marked systemic signs
and symptoms, including severe pain out of proportion to that usually expected, prostration, and, at times,
disorientation initially or later in the course of infection. Temperature may be high ( 40C), leukocytosis may be
marked (>30,000), and hemoconcentration may occur as large shifts of fluid leak from the vascular compartment
infected area. These patients frequently develop the features of particularly severe infection, including adult
respiratory distress syndrome, disseminated intravascular coagulopathy, or renal shutdown. Signs of septic shock
often eventually develop.

A relatively high (approximately 20%) bacteremic rate occurs with postpartum endometritis.6 However, few otherwise
healthy postpartum women with uncomplicated postpartum endometritis or uncomplicated postpartum infection
develop septic shock. Even in young patients without underlying disease, the mortality rate remains between 20% and
30% when septic shock occurs.17 Patients in septic shock require immediate resuscitation with fluids, respiratory
support, circulatory support, and antibiotics. Intensive care monitoring becomes mandatory. The differential
diagnosis includes amniotic fluid embolism, pulmonary embolism, cardiogenic shock (from drugs, cardiac disease, or
aortic dissection), and diabetic ketoacidosis. Although unusual, rupture of an abscess with release of gram-negative
anaerobic and aerobic bacteria must also be considered if septic shock occurs. The causative organism and the
infectious source must be identified with certainty using physical examination, diagnostic tests, and appropriately
obtained cultures. Poor prognostic signs include leukopenia, severe disseminated intravascular coagulopathy, high
levels of lactate, and adult respiratory distress syndrome. Successful outcome usually depends on surgical removal of
the source of infection. Virtually all postpartum septic shock develops from a source of infection that is amenable to
surgical drainage or removal. Therefore it becomes the duty of the surgeon-obstetrician to absolutely exclude the
possibility of surgically treatable infection when signs of severe infection occur. The surgeon must not relinquish this
responsibility when the patient with shock is transferred to an intensive care specialist. Fluid resuscitation often
restores the blood pressure to normal, giving a false sense of security. Thus, unless it can be established that the
infection originates from the lung, kidney, or heart or from another site outside the pelvis, wound exploration, an
examination under anesthesia, curettage, or exploratory laparotomy may be necessary for diagnosis and treatment.
Surgery should be performed as soon as possible after restoration of adequate circulation. Surgery that becomes
necessary despite a deteriorating circulatory function is hazardous but occasionally lifesaving if a defined focus of
infection exists. Endotracheal intubation with minimal balanced general anesthesia is preferable to regional
anesthesia.
Some causes of rapidly developing infection or shock are more common than others. Among these, myonecrosis
caused by either Clostridium perfringens or other clostridia, including C. sordellii, is high on the list of possibilities,
particularly if an unusual amount of tissue trauma has resulted from a difficult forceps delivery or during cesarean
section. Other evidence of clostridial infection includes the classic signs of severe pain, hemolysis, renal shutdown,
and gas formation. Other toxin-producing organisms, such as group A streptococci, or other organisms,
including E.coli, can produce rapidly developing cellulitis without myonecrosis. Bacterial toxins usually produce
necrosis in the area of cellulitis, and the combination of tissue necrosis and the systemic release of toxins causes
unusually severe manifestations. Necrosis can occur in subcutaneous tissue, striated muscle, or myometrial tissue.
Patients with necrosis exhibit progressive local infection and the alarming systemic signs previously noted. The
source of infection may be particularly difficult to locate for physical or imaging examination if group A streptococci
or clostridia produce deep striated muscle or uterine muscle necrosis. Necrotizing fasciitis from either an abdominal
or an episiotomy wound is another cause of rapidly developing infection and shock that will be covered in more detail
below.

Immediate antibiotic therapy must cover gram-negative facultative and anaerobic bacteria and clostridia, in
particular. Three antibiotics are initially indicated for patients with septic shock or the severe manifestations of
infection described above. Either an aminoglycoside or a first-generation cephalosporin is chosen to inhibit
facultative aerobic bacteria. Clindamycin, imipenem-cilastatin, or metronidazole is given to inhibit anaerobic
bacteria, and either penicillin or ampicillin is used for its effect on clostridia and for its synergistic action with
aminoglycosides against enterococci. However, it cannot be overemphasized that antibiotic therapy alone in these
serious infections is almost never sufficient to control sepsis, and surgical exploration is usually required (Table 5).
Failure to recognize myonecrosis or necrotic cellulitis often proves fatal for patients with these serious infections.
Antibiotics alone are without effect in necrotic tissue.

TABLE 5. Therapy for Rapidly Developing Soft Tissue Infections and Necrotizing Fasciitis

Three antibiotics

1. Choice of one to inhibit gram-negative and gram-positive facultative aerobic bacteria

Gentamicin
Tobramycin
Amikacin

2. Choice of one to inhibit anaerobic bacteria

Clindamycin
Imipenem-cilastatin
Metronidazole

3. Choice of one to inhibit enterococci and clostridia

Penicillin
Ampicillin

Surgical removal of infected tissue

Obvious cellulitis of the subcutaneous tissue needs to be explored with the patient under general anesthesia, as
described for necrotizing fasciitis. Tissue culture and Gram stain are required to identify the responsible organisms.
Frozen tissue section may be required to identify necrosis.18Necrotic tissue needs to be removed to the point of
viability. Debridement serves to remove both necrotic tissue and the source of bacterial toxins. The involved area may
be small in cases of early necrotizing cellulitis or extensive when infection has gone uncontrolled. Clostridial
myonecrosis can involve muscles in the uterus or elsewhere in the pelvic diaphragm or sacral area.

Exploratory laparotomy can be lifesaving for patients with unchecked bacteremia and uncontrolled intra-abdominal
sepsis. Laparotomy should be particularly considered when no apparent source of infection is evident. Obviously
infected or necrotic structures need to be removed, whereas normal organs and tissue should be conserved. Removal
or drainage of an abscess can be undertaken without removal of the uterus or fallopian tubes, if these organs are not
extensively infected. The extensively infected uterus is usually pale, yellow, or obviously necrotic, often with extensive
thrombosis of ovarian and adnexal vessels. When these findings are present and patients have increasingly severe and
life-threatening disseminated coagulopathy or respiratory distress, hysterectomy can be lifesaving. The uterus usually
contains areas of frank necrosis or micro-abscesses in the myometrium. Life-threatening coagulopathy or respiratory
distress from sepsis slowly resolves with removal of infected tissue.

On the other hand, there are rare circumstances in which ascites and edematous bowel, uterus, and adnexae are
present without obviously infected tissue. Considerable clinical judgment is required. We have had these rare cases
that have progressive life-threatening coagulopathy and adult respiratory distress at maximal levels of oxygen and
positive end-expiratory pressure in which the uterus contained only normal necrotic deciduae. Resolution of these
life-threatening signs began immediately although slowly following hysterectomy. It is likely that in these rare
circumstances the sepsis that began the coagulopathy and respiratory distress was successfully treated with
antibiotics but the normal necrosis of deciduae continued to release enough thromboplastin or other factors to
maintain the vicious cycle of coagulopathy and respiratory distress.

NECROTIZING FASCIITIS

Necrotizing fasciitis is a rapidly evolving acute infection of the superficial fascia (subcutaneous tissue). The superficial
fascia contains two layers of subcutaneous tissue that become infected: a superficial fascia of Camper and a deeper
Scarpa's fascia. Necrotizing fasciitis usually begins as a wound infection that spreads unchecked in part because of the
lack of natural tissue barriers. In an abdominal wound, infection spreads superiorly, laterally, and inferiorly in the
abdominal wall, and in an episiotomy wound, infection spreads onto the abdominal wall, laterally to the inner thighs,
or posteriorly to the buttocks. More important, the synergistic action of at least two organisms causes tissue necrosis.
A large variety of organisms can combine to produce a synergistic infection, including nonhemolytic streptococci and
staphylococci, mixed aerobic and anaerobic bacteria (including clostridia), and group B hemolytic streptococci and
anaerobes. The combined effect of the organisms produces extensive subcutaneous tissue necrosis and in many cases
toxins that cause further severe systemic effects. Necrosis prevents antibiotics from reaching infected tissue, and
organisms continue to proliferate and release toxin in the necrotic areas. The deep fascia and muscle layers are not
involved unless the infection is totally out of control or clostridia are present. In addition, skin is not primarily
infected. Therefore, the extent of necrosis often cannot be appreciated from the appearance of the skin until late in the
disease when bullae or frank necrosis of the skin appears.

Although infections have been associated with diabetes mellitus,19 most postpartum patients with necrotizing fasciitis
have no preexisting medical disease. Usually the antepartum course and delivery are uncomplicated. Extensive
episiotomy tears are not associated with necrotizing fasciitis. Mortality rates range from 20% to 75%; the mortality
rate is directly related to the promptness of diagnosis and surgical debridement.20 Fatalities occur most frequently 4
days after onset.

Typical clinical features include severe local pain and progressive erythema and edema of the area surrounding the
wound despite appropriate antibiotic therapy. Infection can occur within hours of making the surgical wound. This
progression can be documented over several hours in exceedingly rapid infections, particularly among diabetics. More
often, infection progresses over a period of days. Erythema and woody edema occur beyond the boundary normally
expected for a simple wound infection, and progression is a particularly characteristic feature.21 In addition, any
patient with cellulitis who develops septic shock should be considered to have necrotizing fasciitis. Patients invariably
have marked systemic features, including a high temperature (which occasionally can be normal), marked
prostration, anemia (which may be masked by hemoconcentration as a vast amount of fluid collects within the extra-
cellular compartment), shock, marked leukocytosis (often 20,00075,000), and disseminated intravascular
coagulopathy. Hypocalcemia is common, caused by the action of bacterial lipases, which degrade fat into fatty acids
that in turn combine with calcium to produce soap.

Any patient suspected of having necrotizing fasciitis must have the diagnosis immediately confirmed by wound
exploration under general anesthesia. Wounds should not be opened at bedside without adequate anesthesia because
characteristic findings of infection, such as pus, are not usually present and limited exploration frequently leads to the
conclusion that only minimal infection is present. On opening the wound, a thin, watery, usually nonodorous
dishwater-appearing exudate is present but pus is not found. The tissue does not have an obviously necrotic
appearance, but rather appears edematous. Necrosis is confirmed by easily dissecting tissue free with a blunt
instrument. Frozen tissue diagnosis of suspected necrotic areas may be useful when the clinician is unfamiliar with
the disease or when clinical findings are atypical.18 Tissue culture and immediate Gram stain must be done to exclude
the presence of large gram-positive rods suggesting clostridia. The presence of large rods should prompt a search for
deeper infection, including myonecrosis.

Therapy for this infection is obvious when the correct diagnosis is established. This uncommon disease is usually
unfamiliar to the obstetrician. Many general surgeons have had experience with this infection, but consulting
inexperienced physicians, even infectious disease specialists, may result in misleading recommendations. Therapy
includes immediate debridement of all necrotic tissue. Necrotic tissue must be removed to the point where bleeding
occurs. At times overlying viable skin can be saved and used as a skin graft, since skin is not primarily infected. Even
with proper debridement, only 50% of patients survive.20 However, survival is nearly zero without surgical
debridement. Survival is also low when patients have developed septic shock or clostridial infection. Wide-spectrum
antibiotic therapy needs to be instituted, but it must be emphasized that most people who die of this infection
received optimal antibiotic therapy from the time diagnosis is made. Multiple debridements are often required, and
the patient should have further tissue removed under anesthesia as frequently as needed, often with daily
debridements until the infection stabilizes.

INTRAVENOUS INFECTION

Fluid Contamination

Intravenous fluid contamination is an uncommon but lethal infection in which unusual organisms
(Erwinia sp, Enterobacter cloacae, Pseudomonas stutzeri, Mima sp, or Herellea sp) colonize intravenous fluids and
disseminate intravenously when the fluid is administered.22Organisms in high concentrations or organisms that
produce toxins are especially lethal. It is estimated that a large number of these infections occur annually, but most
episodes go unrecognized because patients who receive intravenous fluids often have debilitating diseases with high
mortality rates. The obstetrician can recognize this infection more readily when a rapid onset of sepsis developed in
an otherwise healthy patient. Intravenous fluid contamination causes a rapid onset of sepsis or a persistent gram-
negative sepsis with a hectic fever, leukocytosis, hypotension, disseminated intravascular coagulation, respiratory
distress, and often renal shutdown. The intravenous bottle is usually not cloudy, and diagnosis requires a high degree
of suspicion and the recovery of the same organism from both the patient's blood and the intravenous fluid. Therapy
includes the immediate change of the intravenous line and bottle; the administration of antibiotics, including
aminoglycosides to cover gram-negative facultative bacteria; and the usual resuscitative therapy for shock and serious
sepsis. In many cases the offending source will not be identified, particularly if manifestations occur late or are
present in a patient who had another apparent source of infection.

Catheter Infection

Intravenous catheter infections are associated with plastic catheters that are in place for more than 48 hours. These
infections are reduced when professionally trained intravenous teams place and care for the catheters. Further
preventive methods include the use of steel needles and upper extremities, careful washing of hands before line
placement, a secure catheter anchoring, and coverage of the site with sterile dressing. Blood should not be drawn
through the intravenous lines. However, changing the catheter site at least every 48 hours provides the most
protection against these infections.

Clinical features of this infection include the presence of a plastic catheter (usually in place for more than 48 hours)
and fever. with tenderness and redness along the vein or pus at the site when the catheter is removed. A palpable vein
cord may also be present. Persistent septicemia or hypotension or multiple pulmonary emboli should also raise
suspicion of this infection. Organisms involved include Staphylococcus aureus (in approximately 50% of cases)
and Klebsiella, Enterobacter, and Serratia species. Therapy includes immediate intravenous catheter removal and
culture of the catheter. Rolling the catheter on a blood plate provides a simple method for semi-quantitative
culture.23 The presence of more than 15 colonies on the blood plate correlates with infection, whereas fewer colonies
indicate colonization of the catheter by skin flora. Appropriate intravenous antibiotic therapy to
inhibit Staphylococcus aureus is required through a new intravenous site. Surgical removal of the vein should be
considered when intraluminal pus is discovered, particularly if pulmonary embolization continues despite
appropriate antibiotic therapy.

LATE INFECTION

In contrast to the early postpartum infections previously discussed, most late postpartum infections do not have an
associated high mortality rate. Many late infections develop slowly and insidiously. Both the pathogenesis and the
microbiology of late postpartum infections differ from those of early postpartum infections. Late infections are often
more difficult to diagnose and include a larger range of possibilities than early postpartum infections. Clinical features
are often less obvious. For example, some patients will lack fever or leukocytosis. Despite the often insidious nature of
late infections, they are still capable of causing serious morbidity (Table 6).

TABLE 6. Most Common Cause of Serious Infections Occurring Late in the Postpartum Period (3 Days to 6 Weeks)

Continuation of postpartum Septic thrombophlebitis

endometritis Pudendal and paracervical
Abscess block infection
Abdominal wound infection Breast infection
Toxic shock syndrome Pseudomembranous colitis
infection Pneumonia
Episiotomy infection
New ascending uterine
infection

CONTINUATION OF EARLY POSTPARTUM ENDOMETRITIS AND SOFT TISSUE

INFECTION

Physical examination of the patient is the key to diagnosing the continuation of the earlier infections. The patient
should be checked carefully for a wound infection and for other sources of fever outside the pelvis. A thorough
physical examination should include a bimanual pelvic examination. If a pelvic examination reveals only minimal
tenderness and no mass; the remaining physical examination reveals no other source of infection, but only a fever;
and the elevated pulse rate, leukocytosis, abdominal tenderness, and ileus have resolved, resolution of fever can be
expected within 24 hours and additional or new antibiotic therapy is not indicated. The patient should be observed
carefully. However, if a fever together with any of the other features remain or reappear, the following checklist
should be used:

1. Check for an appropriate antibiotic dose or level.

2. Check the antibiotic sensitivities for resistant organisms.

3. Thoroughly reexamine for wound infection, including, at times, aspirating the wound with a needle.

4. Search for an abscess, extragenital infection, or septic pelvic thrombophlebitis.13

Two antibiotics should be administered as a rule when patients have a prolonged or serious infection.24 Broad-
spectrum antibiotic coverage with either clindamycin or an aminoglycoside will inhibit the majority of aerobic and
anaerobic bacteria. Metronidazole and a cephalosporin or other antibiotic combinations are other possible choices.
Imipenem-cilastatin, given alone, can also be used.
Rarely, patients with early postpartum endometritis will remain seriously ill with a prolonged course or will develop
signs of uncontrolled sepsis such as persistent bacteremia or increasingly severe disseminated intravascular
coagulopathy or adult respiratory distress syndrome. The same careful clinical judgment needed to manage persistent
early sepsis is also required for persistent late sepsis. Patients with these continued manifestations of infection must
be carefully scrutinized for either a surgically treatable infection or inappropriate antibiotic therapy. As is true of
unchecked early infection, unchecked late infection with these serious manifestations usually represents a collection
of pus or necrotic infected tissue that requires surgical removal. If there is no other obvious source of the infection,
such as a wound or extragenital site, consideration should be given for a laparotomy.

ABSCESS FORMATION

Well-recognized clinical features of abscess formation include spiking temperatures despite appropriate antibiotic
coverage, persistent tachycardia, persistent leukocytosis, and a demonstrable mass. The mass may be difficult to feel
on pelvic examination in the early stages of abscess formation, but well-established abscesses may be demonstrated
by either pelvic examination or ultrasound, computed tomography (CT), or magnetic image (MI) scanning. Abscesses
usually contain both aerobic and anaerobic bacteria, including one or more of the Bacteroides species,
usually B. bivius, B. disiens, or B. fragilis.

The therapy for abscesses includes administration of antibiotics and the possibility of surgical drainage if abscesses
are large (greater than 6 cm). Several methods can be chosen for surgical drainage, depending on the clinical situation
and physician experience. Traditionally, abscesses have either been drained vaginally or drained or surgically
removed at laparotomy. In the past, hysterectomy or bilateral salpingo-oophorectomy was also frequently performed.
Hysterectomy usually is not indicated when the abscess is well established and infection of the uterine myometrium
appears unlikely. In recent studies, over 90% of intra-abdominal abscesses have been successfully treated with
percutaneous catheter drainage.25Experience with obstetric and gynecologic infection indicates that similar rates of
success also occur with percutaneous drainage of pelvic abscesses.26 In many cases, catheters can be placed at the time
of minilaparotomy or under ultrasound guidance if the abscess is pointing close to the abdominal surface and bowel is
not present between the abscess and the anterior abdominal wall. Open laparoscopy can also be used to avoid bowel
and the large postpartum uterus and to place percutaneous catheters. The abscess is directly visualized through the
laparoscope, bowel is dissected from the abscess surface, and the abscess is confirmed by the aspiration of pus, using
a percutaneously placed 18-gauge spinal needle. A drainage catheter placed over a sharp trocar can be inserted
through the skin into the abscess under direct vision. Pus is aspirated through the catheter, and sterile water is used
to gently irrigate the abscess cavity. It is important that irrigation fluid not be forced into the abscess cavity, but
rather irrigation fluid should be allowed to flow by gravity to prevent bacteria in the abscess wall from disseminating
into the vascular system and causing septic shock. When the abscess drainage clears, 2 g of a broad-spectrum
cephalosporin can be placed in the abscess through the catheter and the catheter can be clamped for 2 hours. The
catheter is then attached to a closed drainage system bag and allowed to drain to gravity. The catheter is pulled when
drainage has ceased, usually 24 to 48 hours later. A 90% success rate has been achieved in reports of a small number
of patients.26 Percutaneous drainage procedures allow abscess drainage without prolonged hospitalization or
postoperative recovery because of a laparotomy. Contraindications include the absence of a clear-cut source of the
abscess and the possibility of an intestinal source. Close follow-up is required to ensure continued resolution of the
abscess. Systemic antibiotics should be continued until the infection clinically responds.

If the abscess is not surgically treated, it is best to continue intravenous antibiotics until the abscess has been reduced
to 50% or less of its original size. Patients with this degree of resolution who have no fever, leukocytosis, or large
amount of pelvic tenderness may be placed on oral antibiotics for an additional 10 to 14 days. Oral doses of
clindamycin, metronidazole, or Augmentin (amoxicillin and clavulanate potassium) should be used because they are
active against anaerobic bacteria, develop appropriate tissue levels, and penetrate into abscesses. The patient should
be closely followed to ensure total resolution.

ABDOMINAL WOUND INFECTIONS

Approximately 5% (range 2%10%) of women undergoing cesarean section develop an abdominal wound
infection.1,27 Factors that increase the rate of wound infection include amniotic fluid infection, a long duration of labor
or rupture of membranes.27 urgency of operation, obesity, diabetes, preoperative shaving, and the use of wound
drains and electrocautery.28,29 Some factors can be eliminated, including excessively high electrocautery amperage and
the use of drains, particularly Penrose drains brought out through the abdominal excision. If required, drainage
should be established with a closed catheter drain brought out of the wound through a separate skin incision. An
additional measure preventing wound infection includes the use of delayed primary closure whenever patients
manifest well-established infection as determined by either grossly purulent exudate or foul-smelling amniotic fluid
at cesarean section. Wound infection rates in these conditions approach 25% with immediate primary closure.28 The
peritoneum and fascia can be closed, but the subcutaneous tissue and wound should be left open. Delayed primary
closure can be undertaken 2 to 4 days post partum.

Wound infection usually causes erythema and tenderness of the wound and a fever. Pus can usually be demonstrated
with an 18-gauge needle aspiration or with opening of the wound. If pus is not present, streptococcal cellulitis or
necrotizing fasciitis needs to be considered. Wound cultures should be obtained either of tissue removed from the
deep portion of the wound or of a swab taken of pus deep in the wound. Gram stain of the specimen should be
reviewed to identify streptococci or clostridia. Therapy includes the continued use of wide-spectrum antibiotics until
the cellulitis clears, as indicated by resolution of adjacent erythema, edema, and tenderness. Wound infections should
be opened and sharply debrided of all necrotic debris under anesthesia. A wet gauze is packed into the wound, and the
wound is then gently irrigated three times daily. Vigorous brushing, scraping, or other trauma to the wound will only
prevent further wound healing.30 It may be necessary to remove new or necrotic debris surgically with additional
debridement. Following control of the wound infection, the wound can be allowed to close by secondary intent,
although large, open clean wounds can be secondarily closed.

TOXIC SHOCK SYNDROME

Clinical features of toxic shock syndrome have been well described. They include hypotension (<90 mm Hg systolic
or 15 mm Hg orthostatic drop), fever (>38C), diffuse macular rash, multi-system involvement, and desquamation
of the skin, usually the palms and soles,1 to 2 weeks after the onset of infection.31 Toxin-producing Staphylococcus
aureus and, rarely, Staphylococcus epidermidis cause this disease. Toxic shock syndrome has recently been
recognized in post-partum patients.32 Typical clinical features of this syndrome in a postpartum patient should alert
the clinician to the diagnosis. An immediate search needs to be instituted for the source of S. aureus toxin. The site of
infection may be difficult to detect in the postpartum patient. Toxic shock syndrome from S. aureus can occur from
wound, endometrial, or even breast infection. Although signs of typical wound infection may be present, toxic shock
syndrome has also occurred from wounds with minimal erythema or even from initially normal-appearing wounds
that develop manifestations of infection several days after the onset of toxic shock syndrome.33 Thus, diagnosis
depends on finding typical clinical features of the syndrome in a patient with S. aureus infection. Therapy for toxic
shock syndrome includes immediate removal of the source of the toxin. Wound infections should be debrided, and a
search should be made for endometrial, breast, or other infections. Supportive therapy is required, and adequate
volume replacement is crucial; the patient must be closely monitored for renal failure or adult respiratory distress
syndrome. Nafcillin, 1 g every 4 hours, is recommended to prevent recurrent infection, but the value of antibiotics in
the acute phase of the syndrome may be minimal.

EPISIOTOMY INFECTION

Most episiotomy infections represent simple wound infections that can be treated in a manner similar to an
abdominal wound infection. However, extensive cellulitis from toxin-producing organisms and necrotizing fasciitis
can also occur in episiotomy wounds. Patients with serious systemic manifestations, septic shock, or signs of wound
infection beyond the immediate episiotomy area must be scrutinized for these possibilities, particularly necrotizing
fasciitis. Necrotizing fasciitis of the episiotomy wound has the same lethal consequences as necrotizing fasciitis in
other areas of the body, and several deaths have been reported.21

Serious episiotomy infection may be difficult to appreciate. Virtually all episiotomies in primiparous women cause
pain, often severe pain. Edema, bruising, and hematomas following a long second stage of labor are also frequent
causes of discoloration of the area. Most episiotomy infections readily respond to simple drainage and antibiotic
therapy. However, serious episiotomy infection must be considered when systemic toxicity or signs beyond the
immediate episiotomy exist.21 Surgical therapy of clostridial myonecrosis and necrotizing fasciitis is the same as when
these infections are present in other areas.

NEW ASCENDING UTERINE INFECTION

In contrast to early postpartum uterine infections, which are usually related to cesarean section, late-occurring
uterine infections usually develop in patients who delivered vaginally.5 The onset of infection most often occurs 2
weeks (range of 3 days-6 weeks) post partum. It is most likely that the pathogenesis of late uterine infection involves
the ascent of bacteria along mucosal surfaces analogous to that occurring in nonpregnant patients with pelvic
inflammatory disease. Patients usually have mild clinical symptoms with minimal pain. They are usually afebrile, and
they often experience minimal abdominal and uterine tenderness.

Chlamydia trachomatis has been isolated from the cervix and endometrium in half of the patients.34 The remaining
patients have either aerobic or anaerobic bacteria or genital mycoplasmas. It is necessary to obtain cervical cultures
for C. trachomatis and other cultures as indicated. Therapy should be initiated with antibiotics that
inhibit C. trachomatis (erythromycin or, for non-breast-feeding women, tetracyclines). Other broad-spectrum
antibiotics may need to be given in conjunction with these antibiotics, particularly if patients are seriously ill or
require hospital admission. Despite minimal abdominal pain and uterine tenderness, the diagnosis is important to
establish because of possible long-term sequelae. A recent association has been made between chlamydiae and
infertility.35 About half of the patients who are infertile because of tubal obstruction have never had a recognized
episode of pelvic inflammatory disease.35 From one third to two thirds of patients who are infertile because of
obstructed fallopian tubes have been previously pregnant.35 Generally, 5% to 10% of pregnant women
carry C. trachomatis in the cervix. Although the late postpartum infection rates following a normal vaginal delivery
are unknown, salpingitis occurs in up to 20% of women with C. trachomatis following induced abortion.36 If similar
infection rates were to occur post partum in women with C. trachomatis, it is possible that a considerable amount of
infertility results from these late ascending postpartum endometritis-salpingitis infections. Therefore, despite the
often mild clinical features, it seems important that these infections be recognized and treated.

SEPTIC PELVIC THROMBOPHLEBITIS (SPT)

Patients with SPT usually have spiking fever of obscure origin, together with chills and a pulse rate out of proportion
to the degree of fever. Chest symptoms may result if pulmonary emboli occur. The combination of large pelvic veins,
increased blood coagulability, and vessel injury (from infection or surgery) in the postpartum patient makes
thrombosis a threat.37 A significantly increased rate of SPT occurs among women delivered by cesarean sections
compared with those who deliver vaginally. Septic pelvic thrombophlebitis occurs in 1% to 2% of postpartum pelvic
infections.13,24 Two clinically distinct syndromes of SPT exist. The most common syndrome is ovarian vein
thrombosis. These patients have acute onset of abdominal pain and fever, usually 2 to 3 days post partum. They
appear ill and usually have a palpable right-sided lower abdominal mass38 A second septic thrombosis syndrome
develops later and is associated with an obscure, high spiking fever, minimal or no abdominal pain or tenderness, and
usually no abdominal mass.39 It should be noted that most patients who develop persistent fever on antibiotic therapy
do not have SPT but more commonly have persistent endometritis or less frequently another source of infection.

Organisms that have been related to SPT include facultative streptococci, S. aureus, Escherichia coli, anaerobic
streptococci, and Bacteroides sp. The diagnosis can be made in patients with typical clinical features who have no
other apparent source of fever. CT scan and an intravenous pyelogram may help demonstrate ovarian vein
thrombosis. The diagnosis can be confirmed by the prompt resolution, usually within 24 hours, of fever and the signs
and symptoms following the institution of heparin therapy to maintain clotting times or activated partial
thromboplastin times two to three times longer than normal.40 Broad-spectrum antibiotics should be continued to
cover common aerobic and anaerobic bacteria. Heparin is given for 7 to 10 days in usual cases. Prolonged heparin
therapy is required only if pulmonary embolization occurs, in which case coumarin is given for 3 to 6 months. Surgery
should be avoided if the diagnosis can be established prior to surgical exploration.37,41 Occasionally, surgical
exploration will be needed to exclude adnexal torsion, degenerated leiomyomata, pelvic abscess, or appendicitis, and
surgical removal or ligation may occasionally become necessary for patients who continue showering pulmonary
emboli despite full heparinization.

PUDENDAL AND PARACERVICAL BLOCK INFECTIONS

Unusual pudendal and paracervical block infections are caused when the needle used for the nerve block carries
bacteria from the vaginal surface into the retroperitoneal space. The large retroperitoneal space is limited by the
pelvic diaphragm inferiorly, but infection can spread unchecked superiorly along the psoas muscle or laterally along
the trochanter muscle into the hip. Infection is often advanced before recognition occurs. A variety of aerobic and
anaerobic bacteria usually cause infection.

A clinical diagnosis can be made in patients who have had either a pudendal or a paracervical block. Hip tenderness is
the characteristic and prominent feature of this infection. Patients are not able to place extensive weight on the leg of
the affected hip.42 Physical examination reveals tenderness on motion of the hip and tenderness of the hip capsule and
paravaginal and psoas muscles. Occasionally CT scan or MI will reveal an abscess in this space.

In recent experience, early institution of broad-spectrum antibiotic therapy that includes anaerobic coverage usually
prevents serious abscess formation. However, early reports of pudendal and paracervical block infections included
patients who had developed large abscesses.42 Surgical drainage is necessary if large abscesses
occur.43 Retroperitoneal infection is often advanced because an extensive volume (several liters) of pus can collect in
this large space. These infections are potentially serious because large abscesses have ruptured and caused paraplegia
or resulted in extended hospitalization.

BREAST INFECTION

Approximately 2% of breast-feeding mothers develop breast infection. Staphylococcal colonization of the infant's oral
cavity begins a few days after birth.44 Organisms can be introduced into the breast through fissures or by negative
pressure during suckling. Mild milk stasis contributes to infection. Two forms of infection exist. The first and most
common type is endemic mastitis typified by cellulitis in which fissures are frequent and fever with flulike symptoms
occur.45 Some patients will develop fever or flulike symptoms even prior to breast tenderness. A second, less frequent,
epidemic mastitis represents a hospital-acquired infection in which a primary ductal infection exists and pus may be
present at the nipple but fissures are uncommon. Staphylococcus aureus and, less commonly, S. epidermidis are the
usual organisms recovered in these infections. Diagnosis is based on the presence of redness and tenderness in an
area of the breast or a fluctuant breast mass, usually together with fever. Therapy should include the administration
of a broad-spectrum penicillinase-resistant antibiotic. Cloxacillin, dicloxacillin, or cephalexin, 500 mg given orally
every 6 hours, is effective. Local measures should also be instituted to ensure milk drainage. Continued breast-feeding
is helpful to prevent further breast milk stasis. The patient should be encouraged to begin breast-feeding on the
infected breast first to promote adequate drainage. This may be difficult when fissures or excessive tenderness exists.
An exception to continued breast-feeding should be made if a breast abscess is present, because neonatal lung
abscesses have been associated with the presence of maternal breast abscesses .46 Although it is possible that an infant
with lung abscesses infects the mother to cause breast infection, the alternative possibility is that a large
concentration of bacteria in breast abscesses could be aspirated into the infant's lung, causing pulmonary abscesses. A
breast pump should be used to ensure drainage when a breast abscess is present. Surgical drainage of breast
abscesses is often necessary.47 Except for the rare development of toxic shock syndrome, patients with breast infection
usually do not become seriously ill.

PSEUDOMEMBRANOUS COLITIS

Pseudomembranous colitis occurs in patients who received or are still receiving antibiotics. This potentially lethal
infection is caused by an overgrowth of Clostridium difficile in the gastrointestinal tract related to the inhibition of
normal intestinal flora by the antibiotic administered.48Clostridium difficile overgrowth produces sufficient toxin
levels to cause intestinal mucosal sloughing and clinical manifestation. The severity of diarrhea is highly variable,
ranging from mild diarrhea to severe megacolon. The possibility of pseudomembranous colitis needs to be considered
when the patient on antibiotics develops a persistent fever together with other manifestations of this infection. The
infection is associated with odorous, watery diarrhea, sometimes mixed with blood, and with leukocytes in the feces.
High fever, leukocytosis, abdominal distention, and severe abdominal tenderness are common and herald severe
illness in contrast to benign anti-biotic-associated diarrhea.49Manifestations most frequently develop 4 to 9 days after
starting antibiotics, but shorter and longer periods are not uncommon.

Only a small portion of patients with antibiotic-associated diarrhea have pseudomembranous colitis. The more
benign antibiotic-associated diarrhea without pseudomembranous colitis does not produce fever, bloody diarrhea, or
abdominal signs. Although pseudomembranous colitis had initially been noted most commonly with the
administration of clindamycin, virtually all antibiotics (especially ampicillin, cephalosporins, and tetracyclines) have
since been associated with this infection. Pseudomembranous colitis has even been reported following a short course
of cephalosporin antibiotic prophylaxis. Diagnosis can be made by finding mucosal ulcers and pseudomembranous
plaques at sigmoidoscopy and demonstrating C. difficile toxin in diarrhea fluid. However, proximal cecitis may not be
demonstrated at sigmoidoscopy. An increased number of leukocytes can be found in the stool in over 50% of cases.
Although C. difficile can be recovered from these patients, it can also be recovered from approximately 5% of
otherwise normal patients, and isolation of this organism without finding toxin is not sufficiently specific to diagnose
pseudomembranous colitis. Other organisms associated with diarrhea (Salmonella, Shigella, Entamoeba histolytica,
Campylobacter, and Yersinia) should also be sought with severe illness. Toxic megacolon, perforation, secondary
sepsis, and severe hemorrhage are associated with high mortality. Treatment includes discontinuation of the
antibiotic therapy, if possible, and fluid support. Medications that slow peristalsis and hence toxin elimination, such
as diphenoxylate hydrochloride with atropine sulfate (Lomotil), should not be used. Oral vancomycin, 125 mg every 6
hours, or oral metronidazole can be used in patients with serious manifestations. These antibiotics inhibit C. difficile,
and their administration decreases recurrent disease.50

http://www.glowm.com/section_view/heading/Serious%20Postpartum%20Infections/item/177
9. Pemeriksaan penunjang dari scenario
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