Normal and Abnormal Puerperium

No Results

No Results

processing….

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.

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.

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.

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.

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.

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

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 use formula. 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.

The changes to the breasts that prepare the body for breastfeeding occur throughout pregnancy. Lactogenesis, which is the development of the ability to secrete milk, occurs as early as 16 weeks gestation. The placenta supplies high levels of circulating progesterone which activates mature alveolar cells in the breast to secrete small amounts of milk. After delivery of the placenta, there is a rapid decline in progesterone which triggers the onset of milk production and subsequent swelling, or engorgement, of breasts in the postpartum period. The colostrum is the liquid that is initially released by the breasts during the first 2-4 days after delivery. High in protein content and antibody rich, 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 nutritional demands of the baby.

Lactation is the process of continued secretion of copious milk. Lactation requires regular removal of milk (ie breast emptying) which triggers prolactin release from the anterior pituitary gland.  It also requires nipple stimulation (ie suckling) which triggers oxytocin from the posterior pituitary gland.  Oxytocin release after tactile stimulation of the nipple-areolar complex causes myoepithelial cells of the breasts to contract, which forces milk into the alveolar lumens and then  into the ducts, prior to moving out through the nipple. If the mother is not breastfeeding, the absence of milk removal leads to elevated intramammary pressure as the milk accumulates within the alveolar lumen.  Alveolar distention restricts blood flow to the alveoli and interferes with milk production. Additionally, the increase in pressure triggers an inhibitor of lactation (FIL) which decreases prolactin levels and triggers mammary involution within 2-3 weeks.

The immediate postpartum period most often occurs in the hospital setting, where the majority of women remain for approximately 2 days after a vaginal delivery and 3-4 days after a cesarean delivery. During this time, women are recovering from their delivery and are beginning to care for the newborn. This period is used to make sure the mother is stable and to educate her in the care of her baby (especially the first-time mother). While still in the hospital, the mother is monitored for blood loss, signs of infection, abnormal blood pressure, contraction of the uterus, and ability to void.  There is also attention to Rh compatibility, maternal immunization statuses and breastfeeding.

After a vaginal delivery, most women experience swelling of the perineum and consequent pain. This is intensified if the woman has had an episiotomy or a laceration. Routine care of this area includes ice applied to the perineum to reduce the swelling and to help with pain relief. Conventional treatment is to use ice for the first 24 hours after delivery and then switch to warm sitz baths. However, little evidence supports this method over other methods of postpartum perineum treatment. Pain medications are helpful both systemically as nonsteroidal anti-inflammatory drugs (NSAIDs) or narcotics and as local anesthetic spray to the perineum.

Hemorrhoids are another postpartum issue likely to affect women who have vaginal deliveries. Symptomatic relief is the best treatment during this immediate postpartum period because hemorrhoids often resolve as the perineum recovers. This can be achieved by the use of corticosteroid creams, witch hazel compresses, and local anesthetics in addition to a bowel regimen that avoids constipation.

Tampon use can be resumed when the patient is comfortable inserting the tampon and can maintain it without discomfort. This often takes longer for the woman who has had an episiotomy or a laceration than for one who has not. The vagina and perineum should first be fully healed, which takes several weeks. Tampons must be changed frequently to prevent infection.

The woman who has had a cesarean delivery understandably will experience post-op pain at the abdominal incision. This, too, can be treated with heat or ice to the incision site, abdominal binder support, and use of systemic pain medication. Activities of daily living should be resumed as tolerated but without unnecessary delay.

Sexual intercourse may resume when bright red bleeding ceases, the vagina and vulva are healed, and the woman is physically comfortable and emotionally ready. Physical readiness varies greatly among women but may take several weeks. Birth control is important to protect against pregnancy because the first ovulation is very unpredictable.

Substantial education takes place during the hospital stay, especially for the first-time mother. The mother (and often the father) is taught routine care of the baby, including feeding, diapering, and bathing, as well as what can be expected from the baby in terms of sleep, urination, bowel movements, and eating.

Providing education, support, and guidance to the breastfeeding mother is especially important during this time. Multiple international and national government health agencies including The World Health Organization (WHO), the American Academy of Pediatrics (AAP), the American College of Obstetricians and Gynecologists (ACOG), and the United States Preventive Services Task Force recommend exclusive breastfeeding for the first six months of life. In 1991 The World Health Organization (WHO) and the United Nations Children’s Fund (UNICEF) launched a global program called The Baby-Friendly Hospital Initiation (BFHI) that aims to increase the numbers of infants who are exclusively breastfed worldwide. The BFHI program developed “Ten Steps to Successful Breastfeeding” which are evidence-based practices which are recommended for health care facilities to implement in an effort to protect, promote, and support breastfeeding. More than 152 countries now qualify as “Baby-Friendly” by the standards set forth under the BFHI protocol which can be found at the WHO Baby-friendly Hospital Initiative website ^[3] : http://www.who.int/nutrition/topics/bfhi/en/. 

Breastfeeding is neither easy nor automatic. It requires much effort on the part of the mother and her support team. Breastfeeding should be initiated as soon after delivery as possible; in a normal, uncomplicated vaginal delivery breastfeeding is possible almost immediately after birth. Encourage the mother to feed the baby every 2-3 hours (at least while she is awake during the day) to stimulate milk production. Long feedings are unnecessary, but they should be frequent. Milk production should be well established by 36-96 hours. Lactation consultants have special training in breast feeding support and are an important resource for new mothers.

In women who choose not to breastfeed, the care of the breasts is quite different. Care should be taken not to stimulate the breasts in any way in order to prevent milk production. Ice packs applied to the breasts and the use of a tight brassiere or a binder can also help to prevent breast engorgement. Acetaminophen or NSAIDs can alleviate the symptoms of breast engorgement (eg, tenderness, swelling, fever) if it occurs. Bromocriptine was formerly administered to suppress milk production; however, its use has diminished because it requires 2 weeks of administration, does not always work, and can produce adverse reactions.

For excellent patient education resources, visit eMedicineHealth’s Pregnancy Center. Also, see eMedicineHealth’s patient education articles Postpartum Perineal Care, Birth Control Methods, Birth Control Overview, Birth Control Spermicides, and Breastfeeding.

The new mother should be given discharge instructions and expectations/precautions to consider once leaving the hospital. The most important information is who and where to call if she has problems or questions. She also needs details about resuming her normal activity. Instructions vary, depending on whether the mother has had a vaginal or a cesarean delivery and any comorbidities that may have been part of her care.

The woman who has had a vaginal delivery may resume all physical activity, including using stairs, riding or driving in a car, and performing muscle-toning exercises, as long as she experiences no limiting pain or discomfort. The key counseling is to progressively resume normal activity while being mindful of the common fatigue and exhaustion experienced while caring for a newborn. Pregnancy, labor, delivery, and care of the newborn are strenuous and stressful, and the mother needs sufficient rest to recover. The woman who has had a cesarean delivery must be more careful about resuming some of her activities in the postoperative period. She must avoid overuse of her abdomen until her incision is well healed in order to prevent an early surgical complications. Women are typically scheduled for a routine comprehensive postpartum evaluation between 4 to 6 weeks after delivery. Earlier postpartum follow-up is recommended in women at high risk of postpartum complications who require problem-oriented visits for closer management of hypertensive issues, postpartum depression, wound infections, lactation difficulties, or comorbidities that require postpartum medication changes (i.e. seizure disorder, diabetes). ^[4] The postpartum visit is also an important time to identify the patient’s primary care provider and communicate any recommendations for follow-up on ongoing medical problems or pregnancy-related issues. This better facilitates the patient’s transfer of care and helps optimize maternal health during the interconception period.

Unfortunately, there is a poor attendance rate at scheduled postpartum visits, with approximately 40% of individuals missing their follow-up appointment. Several strategies for increasing attendance include discussing the importance of this visit during prenatal care, scheduling postpartum visits before hospital discharge, using technology to send reminders to patients about their appointment. ^[4]

A comprehensive postpartum visit includes evaluation of the patient’s physical and psychological well-being, review of vaccination history, review of cervical cancer screening history, and discussion about future fertility desires with appropriate contraception counseling. Depression screening is recommended at least once during the perinatal period with a validated instrument, such as the Edinburgh Postnatal Depression Scale. ^{[4, 5]}  The Edinburgh Postnatal Depression scale is a 10-item self-report questionnaire that includes symptoms of both anxiety and depression with exclusion of constitutional symptoms of mood disorders (i.e. change in sleep and eating patterns) that tend to be common in the postpartum period. It is recommended that providers who screen for depression have resources to initiate treatment and provide resources for those who screen positive for postpartum depression.

For women with gestational diabetes, the postpartum period is an important time to screen for impaired glucose tolerance or Diabetes Mellitus Type 2. The Fifth International Workshop on Gestational Diabetes Mellitus recommends that women with GDM undergo a 75-g, 2 hour oral glucose tolerance test between 6-12 weeks postpartum. ^[6]  Approximately one third of women with GDM will have diabetes or impaired glucose metabolism at postpartum screening. These individuals should be appropriately counselled on lifestyle interventions or medical management options (i.e. metformin, insulin) to optimize their glycemic control. Those who have a normal postpartum glucose tolerance test should be appropriately counselled that there is still a 7 fold risk of developing type 2 diabetes later in life and up to 50% of women with GDM will develop diabetes over 20 years after her pregnancy. ^[6]  Therefore the American Diabetes Association (ADA) recommends patients with GDM and normal results of postpartum screening have repeat testing every 3 years because of the increased risk of developing diabetes in the future. ^[7]

 Contraception options should be discussed before the mother leaves the hospital. Although she may not be ready to decide about which method to initiate, she should be educated about the options that are safe based on any medical comorbidities and consistent with her future fertility desires.  It is important to initiate contraception during the postpartum period to prevent unintended pregnancy and reduce the risks associated with pregnancies of short birth intervals; specifically, when the interconception interval is less than 6 months there is a greater incidence of subsequent pregnancies with low birth weight and preterm birth. ^[4]

A systemic review of ovulation and menses in nonlactating women found that although most women begin ovulation at least 6 weeks postpartum, with mean day of first ovulation occurring 45-94 days postpartum, a limited number ovulate sooner. ^[8] Two studies reporting earliest day of first ovulation reported it occurring on days 25 and 27 postpartum, emphasizing the need for early postpartum contraception discussion and method initiation to decrease the risk of pregnancy soon after delivery.

Many options are available, as follows:

Natural methods can be used in highly motivated couples, to include the use of monitoring the basal body temperature and the quality and quantity of the cervical mucus to determine what phase of the menstrual cycle the woman is in and if it is safe to have intercourse.

Barrier methods of contraception, such as condoms, are widely available, as are vaginal spermicides. Condoms are available over-the-counter, while diaphragms and cervical caps must be fitted.

Hormonal methods of contraception are numerous. Combined estrogen-progestin agents are taken daily by mouth or monthly by injection. Progestin-only agents are available for daily intake or by long-acting injections that are effective for 12 weeks.

Intrauterine devices can be placed immediately post partum (after delivery of the placenta) or after uterine involution occurs typically 4-6 weeks after delivery. Immediate postpartum insertion is associated with an increased risk of expulsion, approximately 24%. Immediate insertion is contraindicated in those with any postpartum infection including peripartum chorioamnionitis, endometritis or puerperal sepsis. ^[9]

Permanent methods of birth control (ie, tubal ligation, vasectomy) are options for those who are certain they do not desire more children.

The CDC has published “The United Stated Medical Eligibility Criteria for Contraceptive Use (US MEC)” which are evidence-based guidelines that assist health care providers in recommending a safe of contraceptive method for an individual based on medical comorbidities. ^[10] Recommendations are provided using a 4-point categorical grading system which takes into account an individual’s risks of using certain contraceptive agents depending on their medical comorbidities. Specifically, “category 1” identifies a contraception that is safe for use in a patient without restriction versus a “category 4” designation which represents an unacceptable health risk to an individual and should therefore be avoided based on their medical history.

The US MEC should be utilized for patients in the postpartum period in order to select the safest contraception option at time of discharge from delivery. The risk for a venous thromboembolism, or a blood clot, is highest among women in the first 21 days postpartum. and declines gradually until returning to a woman’s baseline risk at around 42 days postpartum. ^[11] Therefore, in women who are less than 21 days postpartum, combined hormonal contraceptives are a category 4 option and not recommended due to the unacceptable health risk in immediate postpartum patients. After that time, combined hormonal contraceptives may be considered without restriction based on an individual’s nursing method and/or other medical risk factors for complications. Among women who are breastfeeding within the first postpartum month, combined hormonal contraception is considered a category 3 option because of possible association on breastfeeding duration and success. Alternatively, progestin-only hormonal methods such as the minipill, depo medroxyprogesterone acetate injections, intrauterine device and Nexplanon implant can be safely initiated immediately postpartum even in those women who are breastfeeding (category 1 and 2).

Postpartum hemorrhage is defined as excessive blood loss during or after the third stage of labor. The average blood loss is 500 mL at vaginal delivery and 1000 mL at cesarean delivery. Since diagnosis is based on subjective observation, it is difficult to define clinically.

Objectively, postpartum hemorrhage is defined as a 10% change in hematocrit level between admission and the postpartum period or the need for transfusion after delivery secondary to blood loss. ^[12]

Early postpartum hemorrhage is described as that occurring within the first 24 hours after delivery. Late postpartum hemorrhage most frequently occurs 1-2 weeks after delivery but may occur up to 6 weeks postpartum.

Early postpartum hemorrhage may result from uterine atony, retained products of conception, uterine rupture, uterine inversion, placenta accreta, lower genital tract lacerations, coagulopathy, and hematoma. Causes of late postpartum hemorrhage most commonly include retained products of conception, infection, subinvolution of placental site, and coagulopathy.

Uterine atony and lower genital tract lacerations are the most common causes of postpartum hemorrhage. Factors predisposing to uterine atony include overdistension of the uterus secondary to multiple gestations, polyhydramnios, macrosomia, rapid or prolonged labor, grand multiparity, oxytocin administration, intra-amniotic infection, and use of uterine-relaxing agents such as terbutaline, magnesium sulfate, halogenated anesthetics, or nitroglycerin. In uterine atony, lack of closure of the spiral arteries and venous sinuses coupled with the increased blood flow to the pregnant uterus causes excessive bleeding.

Active management of the third stage of labor with administration of uterotonics before the placenta is delivered (oxytocin still being the agent of choice), early clamping and cutting of the umbilical cord, and traction on the umbilical cord have proven to reduce blood loss and decrease the rate of postpartum hemorrhage.

Lower genital tract lacerations, including cervical and vaginal lacerations (eg, sulcal tears), are the result of obstetrical trauma and are more common with operative vaginal deliveries, such as with forceps or vacuum extraction. Other predisposing factors include macrosomia, precipitous delivery, and episiotomy.

Vaginal delivery is associated with a 3.9% incidence of postpartum hemorrhage. ^[12] Cesarean delivery is associated with a 6.4% incidence of postpartum hemorrhage. Delayed postpartum hemorrhage occurs in 1-2% of patients.

In the United States, postpartum hemorrhage is responsible for 5% of maternal deaths. Other morbidities associated with hemorrhage include the need for blood transfusions and/or subsequent surgical interventions that may lead to future infertility.

The antepartum or early intrapartum identification of risk factors for postpartum hemorrhage allows for advanced preparation and possible avoidance of severe sequelae.

Every patient must be interviewed upon admission to the labor floor. Request information about parity, multiple gestation, polyhydramnios, previous episodes of postpartum hemorrhage, history of bleeding disorders, and desire for future fertility.

Note the use of prolonged oxytocin administration, as well as the use of magnesium sulfate during the patient’s labor course.

Simulation training for postpartum hemorrhage management and standardized management protocols (including massive transfusion protocols) are now part of many resident training and hospital safety programs.

Patients with postpartum vaginal bleeding that is persistent or greater than anticipated should be urgently evaluated in order to identify the etiology of bleeding and facilitate appropriate interventions. This can be done simultaneously with initiation of any resuscitative measures in order to maintain hemodynamic stability. Additional personnel should be called to bedside in order to facilitate urgent evaluation of a patient with inappropriate postpartum bleeding. Initial assessment should include review of vital signs with careful note of any signs of hypovolemia including tachycardia, hypotension, tachypnea, low oxygen saturation, and oliguria. A thorough physical exam including abdominal exam (incision check and uterine tone), vaginal exam, and rectal examination should be performed to localize any laceration that is the source of bleeding. It is important to obtain IV access in any patient with concerning bleeding or unstable vital signs. Preferably a patient will have two large bore catheters in this situation to aid in the administration of blood products, fluids, and medications.  Supplemental oxygenation by a high-flow face mask (10 to 15 liters/minute) improves oxygen-carrying capacity and delivery.  The anesthesiology team should also be aware of any patient with a postpartum hemorrhage to better assess the patient’s airway, breathing, and indication for intubation.

It is important to check a hemorrhaging patient’s complete blood count and coagulation studies (fibrinogen, prothrombin time/activated partial thromboplastin time) to exclude resulting anemia or coagulopathy, which may require further treatment with blood products. It is also important that any patient admitted to the labor and delivery unit have an active blood sample (type and screen) available if the need for urgent transfusion arises. A “clot observation test” has been used to detect coagulation problems prior to the return of laboratory studies; specifically 5 mL of blood is observed in a red top tube. If clotting occurs within 8-10 minutes and the clot remains intact, the patients fibrinogen stores are likely adequate and functioning. When a patient requires multiple units of blood products, electrolytes should also be monitored serially with immediate treatment of any abnormalities. Hyperkalemia and low levels of ionized calcium are the most common electrolyte disturbances; if untreated the patient is at risk for depressed cardiac function and possible cardiac arrest.  A multidisciplinary team approach involving intensive care specialists is often required for patient management in severe cases.

Initial therapy may include supplemental oxygenation, identification and repair of obstetric lacerations, bimanual uterine massage for atony, manual sweep to remove any retained products of conception or blood clots from the uterus, and administration of uterotonic agents. Ultrasonography can aid in identifying retained products prior to bimanual exam especially in the patient without regional anesthesia. If retained products of conception are noted despite manual removal, a uterine curettage may be necessary to control hemorrhage.

The most common cause of immediate postpartum hemorrhage is atony; therefore uterotonic agents should be readily available for quick access and prompt administration in order to control bleeding. Dilute oxytocin infusion (10-40U in 1000mL of lactated ringer solution [LRS] or isotonic sodium chloride solution) is an effective uterotonic agent for both prevention and treatment of a postpartum hemorrhage. Routine postpartum administration of oxytocin is recommended as a key measure in active management of the third stage of labor to reduce the average risk of maternal hemorrhage at birth and possibly shorten the third stage of labor. ^[13] The rate of oxytocin administration can be increased to correct uterine atony however rapid infusion of high-dose oxytocin can be associated with significant risk of cardiovascular collapse. If IV access is not obtained, 10 units of oxytocin is appropriate. Additionally, if poor uterine tone is noted at time of cesarean section, 10 unites of intrauterine oxytocin may be administered directly into the myometrium.

If uterine atony persists, alternative uterotonic agents should be considered. These include methylergonovine (ie Methergine), carboprost tromethamine (15 methyl-PG2alpha, Hemabate), or misoprostol (PGE1). Carboprost tromethamine (methylergonovine) is administered as an injection of 250mcg in 20mL normal saline intramuscularly; it may be administered at least 15 minutes apart for eight total doses. Methylergonovine 0.2mg is administered intramuscularly every two to four hours. It is important to consider contraindications to certain uterotonics when using pharmacotherapy to control bleeding.  For example, carboprost tromethamine should not be given to individuals with asthma and methylergonovine is contraindicated in hypertension.

Misoprostol may be administered sublingually, orally, or rectally for postpartum hemorrhage treatment. Vaginal administration in the setting of postpartum hemorrhage is not recommended due to impaired absorption. The optimum dose depends on route of misoprostol administration because of varying rates of absorption and time to peak concentration. Although misoprostol is a less effective than the injectable uterotonics for postpartum hemorrhage treatment, it is commonly used in low resource settings because of its widespread availability, low cost, ease of storage (i.e. heat stable) and ease of administration. ^[14] The 2010 Monte Carlo study reported 70% reduction in mortality among 10,000 women delivering at home in rural India with a $6 incremental cost per disability-adjusted life year (DALY). ^[15]

A Foley catheter with a large bulb (#24 Foley catheter with a 30 mL balloon or a Sengstaken-Blakemore tube) can be used as an alternative to uterine packing. ^[17] .This tamponading technique can be highly effective, is inexpensive, requires no special training, and may prevent the need for surgery.

A Bakri tamponade balloon is a silicone fluid-filled balloon that may also provide control of uterine bleeding in cases where other interventions have failed. A deflated silicone balloon is inserted into the uterus and then filled to a recommended volume of 500cc to allow the balloon to adapt to the configuration of the uterine cavity. ^[18]  The Bakri balloon is connected to a 24 French silicone catheter which allows drainage of the uterine cavity for measurement of ongoing bleeding. Maximum intrauterine time is 24 hours but it may be removed prior to this time.

Uterine artery embolization, which is performed under local anesthesia, is a minimally invasive technique performed by trained interventional radiologists. ^[19] The success rate is greater than 90%. ^[20] This procedure is believed to preserve fertility. ^{[20, 19]} Complications are low (6-7%) and include fever, infection, and nontarget embolization. In patients at high risk for postpartum hemorrhage, such as those with placenta previa, placenta accreta, coagulopathy, or cervical pregnancy, the catheter can be placed prophylactically prior to delivery. ^[20]

The B-Lynch suture technique ^[21] : A suture is passed through the anterior uterine wall in the lower uterine segment approximately 3 cm medial to the lateral edge of the uterus. The suture is wrapped over the fundus 3–4 cm medial to the cornual and inserted into the posterior uterine wall again in the lower uterine segment approximately 3 cm medial to the lateral edge of the uterus and brought out 3 cm medial to the other edge of the uterus. The suture is wrapped over the fundus and directed into and out of the anterior uterine wall parallel to the previous anterior sutures. The uterus is compressed in an accordion-like fashion and the suture is tied across the lower uterine segment. The B-Lynch suture technique and other compression suture techniques are operative approaches to postpartum hemorrhage that have proven to preserve fertility. ^{[22, 23]} As practitioners become proficient in this technique, it may be considered before uterine artery or hypogastric artery ligation and hysterectomy.

When conservative therapy fails, the next step is surgery with either bilateral uterine artery ligation or hypogastric artery ligation. Uterine artery ligation is thought to be successful in 80-95% of patients. If this therapy fails, hypogastric artery ligation is an option however most obstetricians have little to no experience with this technique. This approach is technically difficult and is only successful in 42-50% of patients. ^[24] Instead, stepwise devascularization of the uterus is now thought to be the next best approach, with possible ligation of the utero-ovarian and infundibulopelvic vessels. ^[25]

When all other therapies fail, emergency hysterectomy is often a necessary and lifesaving procedure.

Lacerations are a common sequelae of vaginal childbirth due to strain on the perineum and pelvic floor muscles, with 53-79% of women sustaining some type of laceration during a vaginal delivery. ^[26] Perineal lacerations are distinct from an episiotomy which is a purposeful surgical incision of the posterior aspect of the vagina in order to enlarge the perineum for childbirth during the second stage of labor. An epidemiologic study in 2012 reported approximately 12% of vaginal births included an episiotomy. ^[27]

Perineal tears are classified into four categories depending on the depth of tissue involvement. First degree lacerations involve superficial injury to the skin and subcutaneous perineal tissue or vaginal epithelium only. Second degree lacerations extend into the musculature of the perineal body, including the deep and superficial transverse perineal muscles, the bulbocavernosus muscle, and the pubococcygeus muscle. Obstetric anal sphincter injuries (OASIS), which are third and fourth degree perineal lacerations are considered more severe forms of obstetric tears. Third degree lacerations extend beyond the muscles and involve the anal sphincter. There are three subdivisions of a third degree tear depending on degree of involvement of the external and/or internal anal sphincter. Specifically less than 50% of the external anal sphincter is torn in a 3A tear. In a 3b tear, greater than 50% of the external anal sphincter is torn. A 3c tear includes complete rupture of the external anal sphincter as well as involvement of the internal anal sphincter. Lastly, a fourth degree laceration is an injury involving the entire anal sphincter complex as well as the anal epithelium. Any deep perineal laceration noted after a delivery warrants a thorough evaluation including a digital rectal exam to improve the diagnosis of OASIS. Approximately 4% of women have a clinically recognized OASIS immediately after time of vaginal delivery. ^[26] Other tears after childbirth include periclitoral, periurethral, and labial lacerations; these should only be repaired to achieve hemostasis or to correct distorted anatomy. Additionally, lacerations to the vulva, vagina, and cervix also occur and should be repaired based on clinical assessment of bleeding or distorted anatomy.

Those who had an OASIS are at greatest risk of complications from lacerations including include pain, bleeding and/or hematoma formation, localized infection (20%), and wound breakdown (25%). ^[26] Immediate care of OASIS includes pain control and avoidance of constipation with a prescribed bowel regimen. These individuals should have early and consistent follow up in the postpartum period to evaluate wound healing and any development of anal incontinence.  In individuals with a severe perineal laceration, the absolute risk of OASIS in a subsequent pregnancy is approximately 3%. Moreover, 67-90% of women with a previous OASIS have a subsequent vaginal delivery. ^[26] It is reasonable to offer a cesarean delivery in those who sustained an OASIS in the following circumstances: women with anal incontinence after delivery, women who had further complications including wound infection or need for repeat laceration repair, women who experienced psychological trauma due to significant laceration tear at time of delivery. However, those who desire a cesarean delivery should be appropriately counseled on the increased morbidity of this mode of delivery compared to a vaginal delivery.

Delivery by cesarean section is the single most important risk factor for postpartum maternal infection. In the absence of antimicrobial prophylaxis, women who have a cesarean delivery have a five to 20-fold greater chance of a postpartum infection compared to those who delivery vaginally. ^[28] Therefore ACOG recommends the routine administration of prophylactic antibiotics in women undergoing cesarean section. ^[29] In a large Cochrane review of 95 studies including over 15,000 women who had cesarean deliveries, there was a 60-70% reduction in postpartum complications after the use of prophylactic antibiotics including wound infection and endometritis. ^[28]

The American College of Obstetricians and Gynecologist recommend a single dose of a targeted antibiotic, such as a first-generation cephalosporin, as first-line antimicrobial prophylaxis in women undergoing a cesarean section due to its narrow spectrum of activity, efficacy, and low cost. ^[29]  Guidelines set forth by the Society of Health-System Pharmacists (ASHP), the Infectious Diseases Society of America (IDSA), the Surgical Infection Society (SIS), and the Society for Healthcare Epidemiology of America (SHEA) recommend cefazolin 2 grams for patients .</i> ^[30]

In those individuals with a severe allergy to penicillin or cephalosporin (ie a history of anaphylaxis, angioedema, respiratory distress or urticarial reaction) a combination of clindamycin (900mg) with an aminoglycoside (ie gentamicin 5mg/kg IV) is recommended for broad coverage antibiotic prophylaxis. ^{[29, 30]} The prophylactic agent should be administered within 60 minutes prior to skin incision to ensure adequate drug tissue levels; in emergent cases when this is not possible antibiotic administration should occur as soon as possible after the start of the cesarean delivery. ^[29] Compared to multidose therapy, single-dose antibiotic administration is preferred because it just as effective with a reduction in costs, associated toxicity and risk of colonization with resistant organisms.

Endometritis is an ascending polymicrobial infection. The causative agents are usually normal vaginal flora or enteric bacteria.

Endometritis is the primary cause of postpartum infection. The most common organisms are divided into 4 groups: aerobic gram-negative bacilli, anaerobic gram-negative bacilli, aerobic streptococci, and anaerobic gram-positive cocci. Specifically, Escherichia coli, Klebsiella pneumoniae, and Proteus species are the most frequently identified organisms.

Endometritis occurring on postpartum day 1 or 2 most frequently is caused by group A streptococci. If the infection develops on day 3 or 4, the causative organism is frequently enteric bacteria, most commonly E coli, or anaerobic bacteria. Endometritis that develops more than 7 days after delivery is most frequently caused by Chlamydia trachomatis. Endometritis following cesarean delivery is most frequently caused by anaerobic gram-negative bacilli, specifically Bacteroides species.

Known risk factors for endometritis include cesarean delivery, young age, low socioeconomic status, prolonged labor, prolonged rupture of membranes, multiple vaginal examinations, placement of an intrauterine catheter, preexisting infection or colonization of the lower genital tract, twin delivery, and manual removal of the placenta. It has also been shown that manual removal of the placenta at cesarean delivery increases the incidence of endometritis.

Endometritis complicates less than 3% of all vaginal deliveries. Cesarean delivery is the most important risk factor for development of postpartum endometritis and therefore significantly increases the risk of endometritis after delivery, particularly when performed after the onset of labor and without antibiotic prophylaxis. Among women who receive standard antibiotic prophylaxis prior a cesarean section delivery in the absence of labor, the frequency of postpartum endometritis is 1.7%; this increases to 11% in patients have a cesarean delivery after the onset of labor and 28% in those who do not receive antibiotic prophylaxis after the onset of labor that resulted in a cesarean section. ^[28]

Following 48-72 hours of intravenous antibiotic therapy, 90% of women clinically improve. Fewer than 2% of patients develop life-threatening complications such as septic shock, pelvic abscess, or septic pelvic thrombophlebitis. ^[31]

A patient may report any of the following symptoms: fever, chills, lower abdominal pain, malodorous lochia, increased vaginal bleeding, anorexia, and malaise.

A focused physical examination is important and should include vital signs, an examination of the respiratory system, breasts, abdomen, perineum, and lower extremities. A patient with endometritis typically has a fever of 38°C or greater, tachycardia, and fundal tenderness. Some patients may develop mucopurulent vaginal discharge, whereas others have scant and odorless discharge.

See the list below:

Urinary tract infection

Acute pyelonephritis

Lower genital tract infection

Wound infection

Atelectasis

Pneumonia

Thrombophlebitis

Mastitis

Appendicitis

See the list below:

Laboratory tests: The appropriate tests for a febrile postpartum patient may include a CBC count with differential, urinalysis, urine culture, and blood cultures.

Imaging: If a respiratory process is high on the differential, obtain a chest radiograph.

Treatment of endometritis is with intravenous antibiotics. Parenteral antibiotics are usually stopped once the patient is afebrile for 24-48 hours, tolerating a regular diet, and ambulating without difficulty. ^[32] In general, an extended course of oral antibiotics has not been found to be beneficial, ^[33] although 2 exceptions have been noted. In patients who respond quickly to intravenous antibiotics and who desire early discharge, a short course of oral antibiotics may be substituted for continued intravenous therapy. The other exception includes patients with staphylococcal bacteremia requiring an extended period of treatment.

Broad spectrum coverage with a combination of clindamycin and gentamicin is a commonly used and highly effective regimen for the treatment of endometritis with a cure rate of greater than 90%. ^[34] Clindamycin is typically administered as 900 mg intravenously every eight hours. The most cost efficient and convenient gentamycin regimen is extended interval dosing of gentamicin with 5mg/kg every 24 hour, however 1.5mg/kg every 8 hours is also an acceptable regimen with equal efficacy. Gentamicin should be avoided in those with impaired renal function; instead reasonable alternative regimens include ampicillin-sulbactam (1.5g every 6 hours) or clindamycin and a second-generation cephalosporin. Ampicillin-sulbactam should also be considered in regions with a significant clindamycin resistant B. fragilis. ^[35] Ampicillin (or vancomycin for patients with a penicillin allergy) should be considered when the patient does not respond to the initial therapy of gentamicin and clindamycin to cover Enterococcus faecalis, which may be the cause of up to 25% of postpartum endometritis infections. ^[36] In a Cochrane review of endometritis treatment regimens, there were significantly more treatment failure rates in those treated with a regimen with poor activity against penicillin-resistant anaerobic bacteria as compared to those treated with a regimen with coverage against penicillin-resistant anaerobic bacteria with no difference in side effects. ^[34]

A urinary tract infection (UTI) is defined as a bacterial inflammation of the bladder or urethra. Greater than 105 colony-forming units from a clean-catch urine specimen or greater than 10,000 colony-forming units on a catheterized specimen is considered diagnostic of a UTI.

Risk factors for postpartum UTI include cesarean delivery, forceps delivery, vacuum delivery, tocolysis, induction of labor, maternal renal disease, preeclampsia, eclampsia, epidural anesthesia, bladder catheterization, length of hospital stay, and previous UTI during pregnancy. ^[37]

The most common pathogen is E coli. ^[38] In pregnancy, group B streptococci are a major pathogen. Other causative organisms include Staphylococcus saprophyticus, E faecalis, Proteus, and K pneumoniae.

Postpartum bacteruria occurs in 3-34% of patients, resulting in a symptomatic infection in approximately 2% of these patients.

A patient may report frequency, urgency, dysuria, hematuria, suprapubic or lower abdominal pain, or no symptoms at all.

On examination, vital signs are stable and the patient is afebrile. Suprapubic tenderness may be elicited on abdominal examination.

See the list below:

Acute cystitis

Acute pyelonephritis

Appropriate laboratory tests include urinalysis, urine culture from either a clean-catch or catheterized specimen, and CBC count.

Treatment is started empirically in uncomplicated infection because the usual organisms have predictable susceptibility profiles. When sensitivities are available, use them to guide antimicrobial selection. Treatment is with a 3- or 7-day antibiotic regimen. ^[37] Commonly used antibiotics include trimethoprim/sulfamethoxazole, ciprofloxacin, and norfloxacin. Amoxicillin is often still used, but it has lower cure rates secondary to increasing resistance of E coli. The quinolones are very effective but are considerably more expensive than amoxicillin and trimethoprim/sulfamethoxazole and should not be used in breastfeeding mothers.

Mastitis is defined as inflammation of the mammary gland.

Milk stasis and cracked nipples, which contribute to the influx of skin flora, are the underlying factors associated with the development of mastitis. Mastitis is also associated with primiparity, incomplete emptying of the breast, and improper nursing technique. The most common causative organism, isolated in approximately half of all cases, is Staphylococcus aureus. ^[39] Other common pathogens include Staphylococcus epidermidis, S saprophyticus, Streptococcus viridans, and E coli.

In the United States, the incidence of postpartum mastitis is 2.5-3%. ^{[40, 39]} Mastitis typically develops during the first 3 months postpartum, with the highest incidence in the first few weeks after delivery.

Neglected, resistant, or recurrent infections can lead to the development of an abscess, requiring parenteral antibiotics and surgical drainage. Abscess development complicates 5-11% of the cases of postpartum mastitis and should be suspected when antibiotic therapy fails.

The diagnosis of mastitis is solely based on the clinical picture.

Fever, chills, myalgias, erythema, warmth, swelling, and breast tenderness characterize this disease.

Focus examination on vital signs, review of systems, and a complete examination to look for other sources of infection. Typical findings include an area of the breast that is warm, red, and tender. When the exam reveals a tender, hard, possibly fluctuant mass with overlying erythema, a breast abscess should be considered.

See the list below:

Mastitis

Breast abscess

Cellulitis

No laboratory tests are required. Expressed milk can be sent for analysis, but the accuracy and reliability of these results are controversial and aid little in the diagnosis and treatment of mastitis.

Milk stasis sets the stage for the development of mastitis, which can be treated with moist heat, massage, fluids, rest, proper positioning of the infant during nursing, nursing or manual expression of milk, and analgesics.

When mastitis develops, penicillinase-resistant penicillins and cephalosporins, such as dicloxacillin or cephalexin, are the drugs of choice. Erythromycin, clindamycin, and vancomycin may be used for infections that are resistant to penicillin. Resolution usually occurs 48 hours after the onset of antimicrobial therapy. Lactation efforts should continue and the milk is still safe for newborn ingestion.

Wound infections in the postpartum period include infections of the perineum developing at the site of an episiotomy or laceration, as well as infection of the abdominal incision after a cesarean birth. Wound infections are diagnosed on the basis of erythema, induration, warmth, tenderness, and purulent drainage from the incision site, with or without fever. This definition can be applied both to the perineum and to abdominal incisions.

Perineal infections: Infections of the perineum are rare. In general, they become apparent on the third or fourth postpartum day. Known risk factors include infected lochia, fecal contamination of the wound, and poor hygiene. These infections are generally polymicrobial, arising from the vaginal flora.

Abdominal wound infections: Abdominal wound infections are most frequently the result of contamination with vaginal flora. However, S aureus, either from the skin or from an exogenous source, is isolated in 25% of these infections. ^[41] Genital Mycoplasma species are commonly isolated from infected wounds that are resistant to treatment with penicillins. ^[42] Known risk factors include diabetes, hypertension, obesity, treatment with corticosteroids, immunosuppression, anemia, development of a hematoma, chorioamnionitis, prolonged labor, prolonged rupture of membranes, prolonged operating time, abdominal twin delivery, and excessive blood loss.

The incidence of perineal infections is 0.35-10%. The incidence of incisional abdominal wound infections is 3-15% and can be decreased to approximately 2% with the use of prophylactic antibiotics.

The most common consequence of wound infection is increased length of hospital stay or hospital readmission. About 7% of abdominal wound infections are further complicated by wound dehiscence. More serious sequelae, such as necrotizing fasciitis, are rare, but patients with such conditions have a high mortality rate.

Patients with perineal infections may complain of an inordinate amount of pain, malodorous discharge, or vulvar edema.

Abdominal wound infections develop around postoperative day 4 and are often preceded by endometritis. These patients present with persistent fever despite antibiotic treatment.

Perineal infections: An infected perineum often looks erythematous and edematous and may be accompanied by purulent discharge. Perform an inspection to identify hematoma, perineal abscess, or stitch abscess.

Abdominal wound infections: Infected incisions may be erythematous, warm, tender, and indurated. Purulent drainage may or may not be obvious. A fluid collection may be appreciated near the wound, which, when entered, may release serosanguineous or purulent fluid.

The diagnosis of wound infection is often made based on the clinical findings. Serial CBC counts with differentials may be helpful, especially if a patient does not respond to therapy as anticipated. CT imaging of the abdomen may be indicated if an abscess is suspected after a cesarean delivery.

Perineal infections: Treatment of perineal infections includes symptomatic relief with NSAIDs, local anesthetic spray, and sitz baths. Identified abscesses must be drained, and broad-spectrum antibiotics may be initiated.

Abdominal wound infections: These infections are treated with antibiotics as well as drainage and inspection of the fascia to ensure that it is intact. Antibiotics may be used if the patient is afebrile.

Most patients respond quickly to the antibiotic once the wound is drained. Antibiotics are generally continued until the patient has been afebrile for 24-48 hours. Patients do not require long-term antibiotics unless cellulitis has developed. Studies have shown that closed suction drainage or suturing of the subcutaneous fat decreases the incidence of wound infection when the subcutaneous tissue is greater than 2 cm in depth. ^{[43, 44]}

Septic pelvic thrombophlebitis is defined as venous inflammation in the abdomen/pelvis with thrombus formation. It is associated with fevers and is unresponsive to antibiotic therapy.

Bacterial infection of the endometrium seeds organisms into the venous circulation, which damages the vascular endothelium and in turn results in thrombus formation. The thrombus acts as a suitable medium for proliferation of anaerobic bacteria. Ovarian veins are often involved because they drain the upper half of the uterus. When the ovarian veins are involved, the infection is most often unilateral, involving the right more frequently than the left. Occasionally, the thrombus has been noted to extend to the vena cava or to the left renal vein. Ovarian vein involvement usually manifests within a few days postpartum. Disease with later onset more commonly involves the iliofemoral vein.

Risk factors include low socioeconomic status, cesarean birth, prolonged rupture of membranes, and excessive blood loss.

Septic pelvic thrombophlebitis occurs in 1 of every 2000-3000 pregnancies and is 10 times more common after cesarean birth (1 per 800) than after vaginal delivery (1 per 9000). ^[45] The condition affects less than 1% of patients with endometritis.

Septic thrombophlebitis may result in the migration of small septic thrombi into the pulmonary circulation, resulting in effusions, infections, and abscesses. Only rarely is a thrombus large enough to cause death.

Septic pelvic thrombophlebitis usually accompanies endometritis. Patients report an initial improvement after an intravenous antibiotic is initiated for treatment of the endometritis. The patient does not appear ill. Patients with ovarian vein thrombosis may describe lower abdominal pain, with or without radiation to the flank, groin, or upper abdomen. Other symptoms include nausea, vomiting, and bloating. Frequently, patients with enigmatic fever are asymptomatic except for chills.

Vital signs demonstrate fever greater than 38°C and resting tachycardia. If pulmonary involvement is significant, the patient may be tachypneic and stridulous. On abdominal examination, 50-70% of patients with ovarian vein thrombosis have a tender, palpable, ropelike mass extending cephalad beyond the uterine cornu.

See the list below:

Ovarian vein syndrome

Pyelonephritis

Appendicitis

Broad ligament hematoma

Adnexal torsion

Pelvic abscess

Enigmatic fever

Drug fever

Viral syndrome

Collagen vascular disease

Pelvic abscess

See the list below:

Important laboratory studies included urinalysis, urine culture, and CBC count with differential.

Imaging: CT scan and MRI are the studies of choice for the diagnosis of septic pelvic thrombophlebitis. ^{[45, 46]} MRI has 92% sensitivity and 100% specificity, and CT imaging has a 100% sensitivity and specificity for identifying ovarian vein thrombosis. These imaging modalities are capable of identifying both ovarian vein and iliofemoral involvement.

The standard therapy after diagnosis of septic pelvic thrombophlebitis includes anticoagulation with intravenous heparin to an aPTT that is twice normal and continued antibiotic therapy. A therapeutic aPTT is usually reached within 24 hours, and heparin is continued for 7-10 days. In general, long-term anticoagulation is not required. Antibiotic therapy is most commonly with gentamicin and clindamycin. Other choices include a second- or third-generation cephalosporin, imipenem, cilastin, or ampicillin and sulbactam. All of these antibiotics have a cure rate of greater than 90%. Initially, it was thought that patients defervesce within 24-28 hours. ^[47] More recent studies show that it takes 5-6 days for the fevers to resolve. ^{[47, 48]}

In a 1999 prospective randomized study, women who were treated with heparin in addition to antibiotics responded no faster than patients treated with antibiotics alone. ^[45] These findings do not support the empiric practice of heparin therapy for septic pelvic thrombophlebitis and raise the question of whether a new standard protocol should be developed. ^[45]

Prevalence and Types  Postpartum thyroid dysfunction can occur any time in the first postpartum year. Clinical or laboratory dysfunction occurs in 5-10% of postpartum women and may be caused by primary disorders of the thyroid, such as postpartum thyroiditis (PPT) and Grave’s disease, or by secondary disorders of the hypothalamic-pituitary axis, such as Sheehan syndrome and lymphocytic hypophysitis. ^[49]

PPT is a transient destructive lymphocytic thyroiditis occurring within the first year after delivery.

PPT develops 1-8 months postpartum and is an autoimmune disorder in which microsomal antibodies of the thyroid play a central role. PPT has 2 phases: thyrotoxicosis and hypothyroidism.

Thyrotoxicosis occurs 1-4 months postpartum and is always self-limited. The condition is caused by the increase release of stored hormone as a result of disruption of the thyroid gland.

Hypothyroidism arises between the fourth and eighth month postpartum.

Risk factors for development of PPT include a positive antithyroid antibody test finding, history of PPT, and family or personal history of other thyroid or autoimmune disorders.

Approximately 4% of women develop transient thyrotoxicosis in the postpartum period. Of these, 66-90% return to a euthyroid state; 33% progress to hypothyroid. Approximately 2-8% of women develop hypothyroidism in the postpartum period. A third of these patients experience transient thyrotoxicosis, whereas 10-30% go on to develop permanent thyroid dysfunction.

Patients with high antithyroid antibody levels during pregnancy, multiparity, and history of spontaneous abortions are at high risk for permanent hypothyroidism. Having developed PPT, these women are at significant risk for recurrent disease after subsequent pregnancies. ^[50]

Patients with thyrotoxicosis may report fatigue, palpitations, heat intolerance, tremulousness, nervousness, and emotional lability. Patients in the hypothyroid phase often complain of fatigue, dry skin, coarse hair, cold intolerance, depression, and memory and concentration impairment. Because many of these symptoms are mild and nonspecific and are often associated with the normal postpartum state, PPT may go undiagnosed.

On examination, a patient may have tachycardia, mild exophthalmos, and a painless goiter.

The first laboratory test to be performed should be the thyroid-stimulating hormone (TSH) test. ^[51] TSH is decreased during the thyrotoxicosis stage and increased during the hypothyroid phase. If the TSH level is abnormal, check thyroid stimulating antibodies, free thyroxine index (FTI), and radioactive iodine uptake (RIU) in order to distinguish this disorder from Graves disease. In PPT, RIU is low, thyroid-stimulating antibodies are undetectable, and FTI is high. Referral to an endocrine specialist is appropriate.

A thorough, cost-effective screening test for PPT does not exist; therefore, limit screening to high-risk patients such as those with previous PPT or other autoimmune disorders. ^[52]

No treatment is available to prevent PPT. ^[52]

Thyrotoxicosis phase: No treatment is required for the thyrotoxicosis phase unless the patient’s symptoms are severe. In this case, a beta-blocker is useful. For example, propranolol can be started at 20 mg every 8 hours and can be doubled if the patient remains symptomatic. Propylthiouracil (PTU) has no role in the treatment of PPT because the disorder is caused by the release of hormone from the damaged thyroid and is not secondary to increased synthesis and secretion.

Hypothyroid phase: Since the hypothyroid phase of PPT is often transient, no treatment is required unless necessitated by the patient’s symptoms. Treatment is with thyroxine (T4) replacement. T4 is most often given for 12-18 months, then gradually withdrawn. The starting dose is 0.05-0.075 mg, which may be increased by 0.025 mg every 4-8 weeks until a therapeutic level is achieved.

Postpartum Graves disease is not as common as PPT, but it accounts for 15% of postpartum thyrotoxicosis. Similar to classic Graves disease, postpartum Graves disease is an autoimmune disorder characterized by diffuse hyperplasia of the thyroid gland caused by the production of antibodies to the thyroid TSH receptor, resulting in increased thyroid hormone production and release. No clinical features distinguish postpartum Graves disease from Graves disease in other settings; therefore, diagnosis and management of this disorder is beyond the scope of this article (see Graves Disease).

Lymphocytic hypophysitis is a rare autoimmune disorder causing pituitary enlargement and hypopituitarism, leading to a decrease in TSH and to hypothyroidism. Symptoms include headache, visual field deficits, difficulty lactating, and amenorrhea. Diagnosis requires histopathologic examination. Most patients do not require transsphenoidal hypophysectomy, so diagnosis is based on history, physical, diagnostic imaging, and the temporal relationship to pregnancy. Identification of the disorder becomes clearer as the pituitary reverts to its normal size and recovers some of its normal function. During the acute phase of this disease, hormone replacement is often necessary.

Sheehan syndrome is the result of ischemia, congestion, and infarction of the pituitary gland, resulting in panhypopituitarism caused by severe blood loss at the time of delivery. Patients have trouble lactating and develop amenorrhea, as well as symptoms of cortisol and thyroid hormone deficiency. Treatment is with hormone replacement in order to maintain normal metabolism and response to stress.

Three psychiatric disorders may arise in the postpartum period: postpartum blues, postpartum depression (PPD), and postpartum psychosis. The American College of Obstetricians and Gynecologist recommend that patients are screened at least once for depression and anxiety symptoms during the perinatal period using a standardized, validated tool. ^[5]

Postpartum blues is a transient disorder the lasts hours to weeks and is characterized by bouts of crying and sadness.

PPD is a more prolonged affective disorder that lasts for weeks to months. PPD is not well defined in terms of diagnostic criteria, but the signs and symptoms do not differ from depression in other settings. Anxiety is a prominent feature of perinatal mood disorders while other “common” symptoms of depression such as changes in sleep, appetite, and libido may be normal in the setting of pregnancy

Postpartum psychosis occurs in the first postpartum year and refers to a group of severe and varied disorders that elicit psychotic symptoms.

The specific etiology of these disorders is unknown. The current view is based on a multifactorial model. Psychologically, these disorders are thought to result from the stress of the peripartum period and the responsibilities of child rearing. Other authorities ascribe the symptoms to the sudden decrease in the endorphins of labor and the sudden fall in estrogen and progesterone levels that occur after delivery. Low free serum tryptophan levels have been observed, which is consistent with findings in major depression in other settings. Postpartum thyroid dysfunction has also been correlated with postpartum psychiatric disorders.

Risk factors include undesired pregnancy, feeling unloved by mate, age younger than 20 years, unmarried status, medical indigence, low self-esteem, dissatisfaction with extent of education, economic problems with housing or income, poor relationship with husband or boyfriend, being part of a family with 6 or more siblings, limited parental support (either as a child or as an adult), and past or present evidence of emotional problems. Women with a history of PPD and postpartum psychosis have a 50% chance of recurrence. Women with a previous history of depression unrelated to childbirth have a 30% chance of developing PPD.

Perinatal depression includes any depressive episode that occurs during pregnancy or in the first 12 months after delivery.

See the list below:

Approximately 50-70% of women who have given birth develop symptoms of postpartum blues.

PPD occurs in 1 of 7 women or approximately 10-15% of new mothers. ^{[53, 5]}

The incidence of postpartum or puerperal psychosis is 0.14-0.26%.

Psychiatric disorders can have deleterious effects on the social, cognitive, and emotional development of the newborn. ^{[54, 55, 56, 57]} These ailments can also lead to marital difficulties.

See the list below:

Postpartum blues is a mild, transient, self-limited disorder that usually develops when the patient returns home. It commonly arises during the first 2 weeks after delivery and is characterized by bouts of sadness, crying, anxiety, irritation, restlessness, mood lability, headache, confusion, forgetfulness, and insomnia.

PPD: Patients suffering from PPD report insomnia, lethargy, loss of libido, diminished appetite, pessimism, incapacity for familial love, feelings of inadequacy, ambivalence or negative feelings toward the infant, and an inability to cope. Consult a psychiatrist when PPD is associated with comorbid drug abuse, lack of interest in the infant, excessive concern for the infant’s health, suicidal or homicidal ideations, hallucinations, psychotic behavior, overall impairment of function, or failure to respond to therapeutic trial.

Postpartum psychosis: The signs and symptoms of postpartum psychosis typically do not differ from those of acute psychosis in other settings. Patients with postpartum psychosis usually present with schizophrenia or manic depression, which signals the emergence of preexisting mental illness induced by the physical and emotional stresses of pregnancy and delivery.

See the list below:

Postpartum blues, which has little effect on a patient’s ability to function, often resolves by postpartum day 10; therefore, no pharmacotherapy is indicated. Providing support and education has been shown to have a positive effect.

PPD generally lasts for 3-6 months, with 25% of patients still affected at 1 year. PPD greatly affects the patient’s ability to complete activities associated with daily living.

Supportive care and reassurance from healthcare professionals and the patient’s family is the first-line therapy for patients with PPD. ^[58] Research on pharmacological treatment for PPD is limited because postpartum women are often excluded from large clinical trials. ^[54] Empirically, the standard treatment modalities for major depression have been applied to PPD.

First-line agents include selective serotonin reuptake inhibitors (SSRIs) or secondary amines. Studies on these drugs show that they can be used by nursing mothers without adverse effects on the infant. LactMed (https://www.nlm.nih.gov/pubs/factsheets/lactmedfs.html) can be referenced for up to date safety considerations. 

Consider electroconvulsive therapy for patients with PPD because it is one of the most effective treatments available for major depression. Treatment is recommended for 9-12 months beyond remission of symptoms, with tapering over the last 1-2 months.

Postpartum psychosis: Treatment of postpartum psychosis should be supervised by a psychiatrist and should involve hospitalization as it is a medical emergency. Specific therapy is controversial and should be targeted to the patient’s specific symptoms. Patients with postpartum psychosis are thought to have a better prognosis than those with nonpuerperal psychosis. Postpartum psychosis generally lasts only 2-3 months.

Secondary to the overlap between the normal sequelae of childbirth and the symptoms of PPD, the former is often underdiagnosed. ^[53] Screening for PPD increases the identification of women suffering from this disorder. ^[53] The Edinburgh Postnatal Depression Scale has proven to be an effective tool for this type of screening. ^{[59, 60, 61]} This scale consists of 10 self-reported items that takes the patient less than 5 minutes to complete. This scale excludes constitutional symptoms of depression, such as changes in sleeping patterns that are common in pregnancy and postpartum period. It requires little extra time, is available in 50 languages,  and is acceptable to both patients and physicians. ^{[61, 62]}  Other screening instruments include the Patient Health Questionnaire 9, the Beck Depression Inventory, and the Center for Epidemiologic Studies Depression Scale. ^[5]

Screening with a standardized instrument should be concomitant with clinical assessment of a patient’s psychosocial wellbeing and support in the postpartum period. It is important that physicians who utilize screening methods are prepared on how to manage those with perinatal depression. Management may include pharmacotherapy, referral to behavioral health resources, and closer follow up in the postpartum period.

Oppenheimer LW, Sherriff EA, Goodman JD. The duration of lochia. Br J Obstet Gynaecol. 1986 Jul. 93(7):754-7. [Medline].

Sherman D, Lurie S, Frenkel E. Characteristics of normal lochia. Am J Perinatol. 1999. 16(8):399-402. [Medline].

Baby-friendly Hospital Initiative. World Health Organization. Available at http://www.who.int/nutrition/topics/bfhi/en/.

Committee Opinion No. 666: Optimizing Postpartum Care. Obstet Gynecol. 2016 Jun. 127 (6):e187-92. [Medline].

Committee on Obstetric Practice. The American College of Obstetricians and Gynecologists Committee Opinion no. 630. Screening for perinatal depression. Obstet Gynecol. 2015 May. 125 (5):1268-71. [Medline].

Committee on Practice Bulletins–Obstetrics. Practice Bulletin No. 137: Gestational diabetes mellitus. Obstet Gynecol. 2013 Aug. 122 (2 Pt 1):406-16. [Medline].

Basevi V, Di Mario S, Morciano C, Nonino F, Magrini N. Comment on: American Diabetes Association. Standards of medical care in diabetes–2011. Diabetes Care 2011;34(Suppl. 1):S11-S61. Diabetes Care. 2011 May. 34 (5):e53; author reply e54. [Medline].

Jackson E, Glasier A. Return of ovulation and menses in postpartum nonlactating women: a systematic review. Obstet Gynecol. 2011 Mar. 117(3):657-62. [Medline].

American College of Obstetricians and Gynecologists. ACOG Practice Bulletin No. 121: Long-acting reversible contraception: Implants and intrauterine devices. Obstet Gynecol. 2011 Jul. 118 (1):184-96. [Medline].

Centers for Disease Control and Prevention (CDC). U S. Medical Eligibility Criteria for Contraceptive Use, 2010. MMWR Recomm Rep. 2010 Jun 18. 59 (RR-4):1-86. [Medline].

Jackson E, Curtis KM, Gaffield ME. Risk of venous thromboembolism during the postpartum period: a systematic review. Obstet Gynecol. 2011 Mar. 117 (3):691-703. [Medline].

Combs CA, Murphy EL, Laros RK Jr. Factors associated with postpartum hemorrhage with vaginal birth. Obstet Gynecol. 1991 Jan. 77(1):69-76. [Medline].

WHO Recommendations for the Prevention and Treatment of Postpartum Haemorrhage. Geneva: World Health Organization; 2012. [Full Text].

Prata N, Bell S, Weidert K. Prevention of postpartum hemorrhage in low-resource settings: current perspectives. Int J Womens Health. 2013. 5:737-52. [Medline].

Sutherland T, Meyer C, Bishai DM, Geller S, Miller S. Community-based distribution of misoprostol for treatment or prevention of postpartum hemorrhage: Cost-effectiveness, mortality, and morbidity reduction analysis. Int J Gynaecol Obstet. 2010 Jan 13. [Medline].

Maier RC. Control of postpartum hemorrhage with uterine packing. Am J Obstet Gynecol. 1993 Aug. 169(2 Pt 1):317-21; discussion 321-3. [Medline].

Marcovici I, Scoccia B. Postpartum hemorrhage and intrauterine balloon tamponade. A report of three cases. J Reprod Med. 1999 Feb. 44(2):122-6. [Medline].

Kaya B, Tuten A, Daglar K, Misirlioglu M, Polat M, Yildirim Y, et al. Balloon tamponade for the management of postpartum uterine hemorrhage. J Perinat Med. 2014 Nov. 42 (6):745-53. [Medline].

Vedantham S, Goodwin SC, McLucas B, Mohr G. Uterine artery embolization: an underused method of controlling pelvic hemorrhage. Am J Obstet Gynecol. 1997 Apr. 176(4):938-48. [Medline].

Hansch E, Chitkara U, McAlpine J. Pelvic arterial embolization for control of obstetric hemorrhage: a five-year experience. Am J Obstet Gynecol. 1999 Jun. 180(6 Pt 1):1454-60. [Medline].

Allam MS, B-Lynch C. The B-Lynch and other uterine compression suture techniques. Int J Gynaecol Obstet. 2005 Jun. 89(3):236-41. [Medline].

El-Hamamy E, B-Lynch C. A worldwide review of the uses of the uterine compression suture techniques as alternative to hysterectomy in the management of severe post-partum haemorrhage. J Obstet Gynaecol. 2005 Feb. 25(2):143-9. [Medline].

Chai VY, To WW. Uterine compression sutures for management of severe postpartum haemorrhage: a 5-year audit. Hong Kong Med J. 2013 Oct 21. [Medline].

Clark SL, Phelan JP, Yeh SY, et al. Hypogastric artery ligation for obstetric hemorrhage. Obstet Gynecol. 1985 Sep. 66(3):353-6. [Medline].

Abd Rabbo SA. Stepwise uterine devascularization: a novel technique for management of uncontrolled postpartum hemorrhage with preservation of the uterus. Am J Obstet Gynecol. 1994 Sep. 171(3):694-700. [Medline].

Practice Bulletin No. 165: Prevention and Management of Obstetric Lacerations at Vaginal Delivery. Obstet Gynecol. 2016 Jul. 128 (1):e1-e15. [Medline].

Friedman AM, Ananth CV, Prendergast E, D’Alton ME, Wright JD. Variation in and factors associated with use of episiotomy. JAMA. 2015 Jan 13. 313 (2):197-9. [Medline].

Smaill FM, Grivell RM. Antibiotic prophylaxis versus no prophylaxis for preventing infection after cesarean section. Cochrane Database Syst Rev. 2014 Oct 28. CD007482. [Medline].

American College of Obstetricians and Gynecologists. ACOG Practice Bulletin No. 120: Use of prophylactic antibiotics in labor and delivery. Obstet Gynecol. 2011 Jun. 117 (6):1472-83. [Medline].

Bratzler DW, Dellinger EP, Olsen KM, et al. Clinical practice guidelines for antimicrobial prophylaxis in surgery. Am J Health Syst Pharm. 2013 Feb 1. 70 (3):195-283. [Medline].

Duff P. Pathophysiology and management of postcesarean endomyometritis. Obstet Gynecol. 1986 Feb. 67(2):269-76. [Medline].

Casey BM, Cox SM. Chorioamnionitis and endometritis. Infect Dis Clin North Am. 1997 Mar. 11(1):203-22. [Medline].

Dinsmoor MJ, Newton ER, Gibbs RS. A randomized, double-blind, placebo-controlled trial of oral antibiotic therapy following intravenous antibiotic therapy for postpartum endometritis. Obstet Gynecol. 1991 Jan. 77(1):60-2. [Medline].

Mackeen AD, Packard RE, Ota E, Speer L. Antibiotic regimens for postpartum endometritis. Cochrane Database Syst Rev. 2015 Feb 2. CD001067. [Medline].

McGregor JA, Crombleholme WR, Newton E, Sweet RL, Tuomala R, Gibbs RS. Randomized comparison of ampicillin-sulbactam to cefoxitin and doxycycline or clindamycin and gentamicin in the treatment of pelvic inflammatory disease or endometritis. Obstet Gynecol. 1994 Jun. 83 (6):998-1004. [Medline].

Brumfield CG, Hauth JC, Andrews WW. Puerperal infection after cesarean delivery: evaluation of a standardized protocol. Am J Obstet Gynecol. 2000 May. 182(5):1147-51. [Medline].

Stray-Pedersen B, Solberg VM, Torkildsen E. Postpartum bacteriuria. A multicenter evaluation of different screening procedures and a controlled short-course treatment trial with amoxycillin. Eur J Obstet Gynecol Reprod Biol. 1989 May. 31(2):163-71. [Medline].

Bacheller CD, Bernstein JM. Urinary tract infections. Med Clin North Am. 1997 May. 81(3):719-30. [Medline].

Marshall BR, Hepper JK, Zirbel CC. Sporadic puerperal mastitis. An infection that need not interrupt lactation. JAMA. 1975 Sep 29. 233(13):1377-9. [Medline].

Kaufmann R, Foxman B. Mastitis among lactating women: occurrence and risk factors. Soc Sci Med. 1991. 33(6):701-5. [Medline].

Emmons SL, Krohn M, Jackson M, Eschenbach DA. Development of wound infections among women undergoing cesarean section. Obstet Gynecol. 1988 Oct. 72(4):559-64. [Medline].

Yamaguchi M, Kikuchi A, Ohkusu K, Akashi M, Sasahara J, Takakuwa K, et al. Abscess formation due to Mycoplasma hominis infection after cesarean section. J Obstet Gynaecol Res. 2009 Jun. 35(3):593-6. [Medline].

Allaire AD, Fisch J, McMahon MJ. Subcutaneous drain vs. suture in obese women undergoing cesarean delivery. A prospective, randomized trial. J Reprod Med. 2000 Apr. 45(4):327-31. [Medline].

Vermillion ST, Lamoutte C, Soper DE, Verdeja A. Wound infection after cesarean: effect of subcutaneous tissue thickness. Obstet Gynecol. 2000 Jun. 95(6 Pt 1):923-6. [Medline].

Brown CE, Stettler RW, Twickler D, Cunningham FG. Puerperal septic pelvic thrombophlebitis: incidence and response to heparin therapy. Am J Obstet Gynecol. 1999 Jul. 181(1):143-8. [Medline].

Brown CE, Lowe TW, Cunningham FG, Weinreb JC. Puerperal pelvic thrombophlebitis: impact on diagnosis and treatment using x-ray computed tomography and magnetic resonance imaging. Obstet Gynecol. 1986 Dec. 68(6):789-94. [Medline].

Witlin AG, Sibai BM. Postpartum ovarian vein thrombosis after vaginal delivery: a report of 11 cases. Obstet Gynecol. 1995 May. 85(5 Pt 1):775-80. [Medline].

Witlin AG, Mercer BM, Sibai BM. Septic pelvic thrombophlebitis or refractory postpartum fever of undetermined etiology. J Matern Fetal Med. 1996 Nov-Dec. 5(6):355-8. [Medline].

Browne-Martin K, Emerson CH. Postpartum thyroid dysfunction. Clin Obstet Gynecol. 1997 Mar. 40(1):90-101. [Medline].

Stagnaro-Green A. Recognizing, understanding, and treating postpartum thyroiditis. Endocrinol Metab Clin North Am. 2000 Jun. 29(2):417-30, ix. [Medline].

Ecker JL, Musci TJ. Treatment of thyroid disease in pregnancy. Obstet Gynecol Clin North Am. 1997 Sep. 24(3):575-89. [Medline].

Davies TF. The thyroid immunology of the postpartum period. Thyroid. 1999 Jul. 9(7):675-84. [Medline].

Stowe ZN, Nemeroff CB. Women at risk for postpartum-onset major depression. Am J Obstet Gynecol. 1995 Aug. 173(2):639-45. [Medline].

Howard LM, Hoffbrand S, Henshaw C, Boath L, Bradley E. Antidepressant prevention of postnatal depression. Cochrane Database Syst Rev. 2005 Apr 18. CD004363. [Medline].

O’Hara MW, Wisner KL. Perinatal mental illness: Definition, description and aetiology. Best Pract Res Clin Obstet Gynaecol. 2013 Oct 7. [Medline].

Misund AR, Nerdrum P, Bråten S, Pripp AH, Diseth TH. Long-term risk of mental health problems in women experiencing preterm birth: a longitudinal study of 29 mothers. Ann Gen Psychiatry. 2013 Oct 31. 12(1):33. [Medline].

Elisei S, Lucarini E, Murgia N, Ferranti L, Attademo L. Perinatal depression: a study of prevalence and of risk and protective factors. Psychiatr Danub. 2013 Sep. 25 Suppl 2:S258-62. [Medline].

Dennis CL. Psychosocial and psychological interventions for prevention of postnatal depression: systematic review. BMJ. 2005 Jul 2. 331(7507):15. [Medline].

Cox JL, Holden JM, Sagovsky R. Detection of postnatal depression. Development of the 10-item Edinburgh Postnatal Depression Scale. Br J Psychiatry. 1987 Jun. 150:782-6. [Medline].

Evins GG, Theofrastous JP, Galvin SL. Postpartum depression: a comparison of screening and routine clinical evaluation. Am J Obstet Gynecol. 2000 May. 182(5):1080-2. [Medline].

Georgiopoulos AM, Bryan TL, Yawn BP, et al. Population-based screening for postpartum depression. Obstet Gynecol. 1999 May. 93(5 Pt 1):653-7. [Medline].

Glaze R, Cox JL. Validation of a computerised version of the 10-item (self-rating) Edinburgh Postnatal Depression Scale. J Affect Disord. 1991 May-Jun. 22(1-2):73-7. [Medline].

Hofmeyr GJ, Ferreira S, Nikodem VC, Mangesi L, Singata M, Jafta Z, et al. Misoprostol for treating postpartum haemorrhage: a randomized controlled trial [ISRCTN72263357]. BMC Pregnancy Childbirth. 2004 Aug 6. 4(1):16. [Medline]. [Full Text].

Mousa HA, Alfirevic Z. Treatment for primary postpartum haemorrhage. Cochrane Database Syst Rev. 2003. CD003249. [Medline].

Olsen MA, Butler AM, Willers DM, Gross GA, Devkota P, Fraser VJ. Risk factors for endometritis after low transverse cesarean delivery. Infect Control Hosp Epidemiol. 2010 Jan. 31(1):69-77. [Medline].

Noyes N, Berkeley AS, Freedman K, Ledger W. Incidence of postpartum endomyometritis following single-dose antibiotic prophylaxis with either ampicillin/sulbactam, cefazolin, or cefotetan in high-risk cesarean section patients. Infect Dis Obstet Gynecol. 1998. 6(5):220-3. [Medline].

Dinsmoor MJ, Gilbert S, Landon MB, Rouse DJ, Spong CY, Varner MW, et al. Perioperative antibiotic prophylaxis for nonlaboring cesarean delivery. Obstet Gynecol. 2009 Oct. 114(4):752-6. [Medline].

Kaimal AJ, Zlatnik MG, Cheng YW, Thiet MP, Connatty E, Creedy P, et al. Effect of a change in policy regarding the timing of prophylactic antibiotics on the rate of postcesarean delivery surgical-site infections. Am J Obstet Gynecol. 2008 Sep. 199(3):310.e1-5. [Medline].

Yildirim G, Gungorduk K, Guven HZ, Aslan H, Celikkol O, Sudolmus S, et al. When should we perform prophylactic antibiotics in elective cesarean cases?. Arch Gynecol Obstet. 2009 Jul. 280(1):13-8. [Medline].

ACOG. Quality Assurance on Obstetrics and Gynecology. Washington, DC: 1989.

ACOG. Thyroid disease in pregnancy. ACOG Technical Bulletin Number 181–June 1993. Int J Gynaecol Obstet. 1993 Oct. 43(1):82-8. [Medline].

Alamia V Jr, Meyer BA. Peripartum hemorrhage. Obstet Gynecol Clin North Am. 1999 Jun. 26(2):385-98. [Medline].

Bowes WA Jr. The puerperium and its complications. Curr Opin Obstet Gynecol. 1990 Dec. 2(6):780-4. [Medline].

Cronin TJ. Influence of Lactation upon Ovulation. Lancet. 1968 Aug 24. 2(7565):422-4. [Medline].

Cuningham FG, MacDonald PC, Gant NF. Williams Obstetrics. 20th ed. McGraw-Hill; 1997.

Droegemuller W. Cold sitz baths for relief of postpartum perineal pain. Clin Obstet Gynecol. 1980 Dec. 23(4):1039-43. [Medline].

Gabbe SG, Niebyl JR, Simpson JL. Obstetrics Normal and Problem Pregnancies. 2nd ed. Churchill Livingstone; 1991.

Gavin NI, Gaynes BN, Lohr KN, Meltzer-Brody S, Gartlehner G, Swinson T. Perinatal depression: a systematic review of prevalence and incidence. Obstet Gynecol. 2005 Nov. 106(5 Pt 1):1071-83. [Medline].

Gibbs RS. Infection after cesarean section. Clin Obstet Gynecol. 1985 Dec. 28(4):697-710. [Medline].

Gilstrap LC 3rd, Ramin SM. Postpartum hemorrhage. Clin Obstet Gynecol. 1994 Dec. 37(4):824-30. [Medline].

Hellgren M. Hemostasis during normal pregnancy and puerperium. Semin Thromb Hemost. 2003 Apr. 29(2):125-30. [Medline].

Hofmeyr GJ, Walraven G, Gulmezoglu AM, Maholwana B, Alfirevic Z, Villar J. Misoprostol to treat postpartum haemorrhage: a systematic review. BJOG. 2005 May. 112(5):547-53. [Medline].

Holden JM. Postnatal depression: its nature, effects, and identification using the Edinburgh Postnatal Depression scale. Birth. 1991 Dec. 18(4):211-21. [Medline].

Lev-Toaff AS, Baka JJ, Toaff ME. Diagnostic imaging in puerperal febrile morbidity. Obstet Gynecol. 1991 Jul. 78(1):50-5. [Medline].

Lucas A, Pizarro E, Granada ML. Postpartum thyroiditis: epidemiology and clinical evolution in a nonselected population. Thyroid. 2000 Jan. 10(1):71-7. [Medline].

Nothnagle M, Taylor JS. Should active management of the third stage of labor be routine?. Am Fam Physician. 2003 May 15. 67(10):2119-20. [Medline].

Oleen MA, Mariano JP. Controlling refractory atonic postpartum hemorrhage with Hemabate sterile solution. Am J Obstet Gynecol. 1990 Jan. 162(1):205-8. [Medline].

Orrett FA, Premanand N. Postpartum surveillance of bacteriuria in term vaginal deliveries. J Natl Med Assoc. 1998 Mar. 90(3):177-80. [Medline].

Othman S, Phillips DI, Parkes AB. A long-term follow-up of postpartum thyroiditis. Clin Endocrinol (Oxf). 1990 May. 32(5):559-64. [Medline].

Perez A, Vela P, Masnick GS. First ovulation after childbirth: the effect of breast-feeding. Am J Obstet Gynecol. 1972 Dec 15. 114(8):1041-7. [Medline].

Pritchard JA. Blood Volume Changes in Pregnancy and Puerperium. American Journal Obstetrics and Gynecology. 1962. 84:1271.

Sakaihara M, Yamada H, Kato EH. Postpartum thyroid dysfunction in women with normal thyroid function during pregnancy. Clin Endocrinol (Oxf). 2000 Oct. 53(4):487-92. [Medline].

Sapi E. The role of CSF-1 in normal physiology of mammary gland and breast cancer: an update. Exp Biol Med (Maywood). 2004 Jan. 229(1):1-11. [Medline].

Walfish PG, Chan JY. Post-partum hyperthyroidism. Clin Endocrinol Metab. 1985 May. 14(2):417-47. [Medline].

Whitaker-Worth DL, Carlone V, Susser WS, et al. Dermatologic diseases of the breast and nipple. J Am Acad Dermatol. 2000 Nov. 43(5 Pt 1):733-51; quiz 752-4. [Medline].

Younis MN, Abdel-Rahman FM, Khalaf I, et al. Bacteriuria following vaginal delivery. Int J Gynaecol Obstet. 1983 Dec. 21(6):477-9. [Medline].

Iliadis SI, Comasco E, Sylven S, et al. Prenatal and postpartum evening salivary cortisol levels in association with peripartum depressive symptoms. PLoS One. 2015. 10(8):e0135471. [Medline].

Brummelte S, Galea LA. Postpartum depression: etiology, treatment and consequences for maternal care. Horm Behav. 2015 Aug 28. [Medline].

Begley CM, Gyte GM, Devane D, McGuire W, Weeks A. Active versus expectant management for women in the third stage of labour. Cochrane Database Syst Rev. 2015 Mar 2. CD007412. [Medline].

Owens SM, Brozanski BS, Meyn LA, Wiesenfeld HC. Antimicrobial prophylaxis for cesarean delivery before skin incision. Obstet Gynecol. 2009 Sep. 114 (3):573-9. [Medline].

Christine Kansky, MD Resident Physician, Department of Obstetrics and Gynecology, Virginia Commonwealth University School of Medicine

Disclosure: Nothing to disclose.

Christine Isaacs, MD Associate Professor, Department of Obstetrics and Gynecology, Division Head, General Obstetrics and Gynecology, Medical Director of Midwifery Services, Virginia Commonwealth University School of Medicine

Christine Isaacs, MD is a member of the following medical societies: American College of Obstetricians and Gynecologists

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Christine Isaacs, MD Associate Professor, Department of Obstetrics and Gynecology, Division Head, General Obstetrics and Gynecology, Medical Director of Midwifery Services, Virginia Commonwealth University School of Medicine

Christine Isaacs, MD is a member of the following medical societies: American College of Obstetricians and Gynecologists

Disclosure: Nothing to disclose.

Michail Spiliopoulos, MD Clinical Assistant Professor, Department of Obstetrics, Gynecology, and Reproductive Sciences, Temple University Hospital

Michail Spiliopoulos, MD is a member of the following medical societies: American College of Medical Genetics and Genomics, American College of Obstetricians and Gynecologists

Disclosure: Nothing to disclose.

Dimitrios Mastrogiannis, MD, PhD, MBA, FACOG Associate Professor, Department of Obstetrics, Gynecology and Reproductive Sciences, Director of Obstetrics and Maternal-Fetal Medicine, Director of Labor and Delivery, Temple University School of Medicine

Dimitrios Mastrogiannis, MD, PhD, MBA, FACOG is a member of the following medical societies: American College of Obstetricians and Gynecologists, American Institute of Ultrasound in Medicine, American Medical Association, Florida Medical Association, Society for Maternal-Fetal Medicine, Southern Medical Association, AAGL, Society for Reproductive Endocrinology and Infertility

Disclosure: Nothing to disclose.

The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous authors Karin Witt, MD, Natali Franzblau, MD, FACOG, Guillermo M Guzman, MD, and John P O’Grady, MD, MA, to the development and writing of this article.

Normal and Abnormal Puerperium

Research & References of Normal and Abnormal Puerperium|A&C Accounting And Tax Services
Source

Share on Facebook

Tweet

Follow us