Fig. 22.1
Uterine atony during cesarean section: postpartum hemorrhage (PPH) was usually defined as a maternal blood loss ≥500 mL after vaginal birth or ≥1,000 mL after delivery
PPH can also be classified as primary or secondary: primary (or early) PPH occurs in the first 24 h after the delivery, while secondary (or delayed) PPH occurs between 24 h and 12 weeks after the delivery. Common causes of primary PPH are uterine atony, spontaneous or iatrogenic uterine lesions, cervical or vaginal lacerations, and coagulopathies.
Causes of secondary PPH are usually infections, retained products of conception (Fig. 22.2), and rarely a choriocarcinoma or a uterine vascular anomaly like pseudoaneurysms of a uterine artery or arteriovenous malformations.
Fig. 22.2
Among the secondary causes of postpartum hemorrhage is the retention of the uterine cotyledon uterus after afterbirth: (a) placental residues, (b) fragment of cotyledon removed, and (c) chorionic villi, which confirm the diagnosis. Modified from: Antonio Malvasi Gian Carlo Di Renzo, Semeiotica Ostetrica. C.I.C. International Publisher, Rome, Italy, 2012
Secondary PPH has its peak incidence 1–2 weeks postpartum and affects 0.2–2 % of women [3]. A personal history of PPH is a risk factor for developing primary or secondary PPH after a following pregnancy [4].
A reasonable diagnostic approach to a patient with secondary PPH must include:
Basic laboratory screening for bleeding diathesis, with blood and platelet count, prothrombin time, and activated partial thromboplastin time (these tests can be normal even in women with bleeding diathesis, such as Von Willebrand disease). Also, we suggest to perform a quantitative pregnancy test, in order to exclude choriocarcinoma, retained products of conception, or a new pregnancy.
Ultrasound examination: it’s mandatory, because it can directly detect the cause of bleeding or exclude some potential bleeding sources in the differential diagnosis (Fig. 22.3). In fact the uterus may look empty or can contain gas, liquids, or echogenic material. Positivity of this material on color Doppler suggests retained products of conceptions, while lack of Doppler findings is related to blood clots, but cannot exclude the presence of necrotic placental tissue.
Fig. 22.3
Transvaginal ultrasonographic scan showing placental residues
Ultrasonographic evidences of intrauterine accumulations of clots and fluids are common findings in an involving uterus, so ultrasound may not be exhausting in order to understand if surgical or medical is indicated [5, 6]. Moreover, there are no randomized controlled trials regarding the optimal management of a secondary PPH [7]. Endometritis should always be suspected if bleeding is not excessive, and uterine tenderness, fever, and/or malodorous discharge are present. These patients should be treated with broad-spectrum antibiotic therapy, even to prevent potentially lethal causes like Clostridium infections and streptococcal or staphylococcal toxic shock syndrome [8, 9]. If uterine atony is suspected, uterotonic agents should be administered, like oxytocin or methylergonovine (oxytocin can be prescribed in breastfeeding mothers). Women with bleeding diathesis should be treated as appropriate for the underlying disorder, and hematologic consultation should be offered. Surgical procedures (like dilatation and curettage) are often effective in case of unsuccessful medical therapy and can be the first choices when retained products of conception must be evacuated from uterine cavity. Curettage should be performed under sonographic guidance, in order to minimize the rate of uterine perforation and to confirm the complete evacuation of retained products of conception [10].
22.4 Uterine Inversion
Uterine inversion or prolapse is a rare puerperal complication and an obstetrical emergency which can lead to severe hemorrhage and shock. It occurs when the uterine fundus collapses into the cavity, turning the organ partially or entirely inside out, and is a complication of both cesarean and vaginal delivery. The classification of uterine inversion is based on the extension [11]: it can be divided into 4° (Figs. 22.4 and 22.5):
First degree or incomplete inversion: the uterine fundus is within the endometrial cavity.
Second degree or complete: the fundus protrudes through the cervical os.
Third degree or uterine prolapse: the fundus protrudes beyond the introitus.
Fourth degree or total uterine and vaginal: both the uterus and vagina are turned inside out.
Fig. 22.4
On the left, a first degree or incomplete inversion; on the right, second degree or complete uterine inversion
Fig. 22.5
On the left, third degree or uterine prolapse; on the right, fourth degree or total uterine and vaginal prolapse
Moreover, we can also divide the types of uterine inversion by the time of occurrence: acute (within 24 h of delivery), subacute (between 24 h and 4 weeks postpartum), and chronic (1 month or more postpartum) [12].
The incidence is between 1 in 1,200 and 57,000 deliveries; risk factors are fetal macrosomia, retained placenta, short umbilical cord, fast labor and delivery, use of uterine relaxants, leiomyomas, and other uterine anomalies.
Uterine inversion is also supposed to be related to incorrect obstetric maneuvers during of third stage of labor, in particular an excessive fundal pressure (Kristeller maneuver) and excessive cord traction [13]; this relationship has never been proved [14], and the pathogenesis of uterine inversion is not yet completely understood.
Presentation of uterine inversion varies by the extension of the pathology: the most common is the complete variant, with the fundus absent on transabdominal palpation, but present on transvaginal examination (Fig. 22.6), lower abdominal pain, and severe hemorrhage often leading to hypovolemic shock.
Fig. 22.6
Initial uterine inversion detected by transabdominal ultrasound
An incomplete inversion occurs in 10 % of cases, and its presentation is more devious than the complete one: blood loss can be minimal, and just a little fundus defect can be noticed on transabdominal palpation.
When not promptly recognized, uterine inversion usually requires a surgical intervention.
The diagnosis is usually based upon the clinical findings listed above, and radiographic imaging is usually used to confirm the diagnosis when the patient is stable, but because uterine inversion is an obstetrical emergency, radiologic exams are not mandatory.
The management of uterine inversion consists in replacing the uterus in its correct position and correct postpartum hemorrhage and shock (if present) and prevents recurrency. These objectives can be achieved using the following passages:
- •
Discontinue uterotonic drugs.
- •
Call for assistance.
- •
Establish intravenous access and fluid resuscitation.
- •
The placenta must not be removed, because its removal before the correction of the uterine inversion is related to a more severe blood loss [15, 16]. Removal of placenta must be attempted only after the uterus has been replaced and after its spontaneous detachment. Alternatively, manual removal should be attempted in the operating room, with a hemodynamically stable patient under anesthesia. If the detachment of placenta doesn’t happen, a placenta accreta must be suspected.
- •
Immediately attempt to manually replace the inverted uterus by placing a hand in the vagina and pushing the fundus along the vaginal axis toward the umbilicus (Johnson maneuver). Prompt replacement is critical since the lower uterine segment and the cervix will contract, making this maneuver more difficult as time passes by.
- •
When uterine replacement is unsuccessful, an alternative option can be to give uterine relaxants, like nitroglycerin, terbutaline, or magnesium sulfate, and then reattempt to replace manually the uterus.
In case of failing of the above procedure, the patient should be promptly taken to the operating room, and a surgical correction of the inversion must be attempted, using Huntington procedure (simultaneous gentle traction with two Allis or Babcock clamps of the two round ligaments, which are usually involved into the inversion) or the Haultain procedure (incision of the posterior uterine surface and manual reduction with Huntington procedure).
Uterine atony is a common complication after repositioning of the uterus. For that reason uterotonic agents are administered to induce uterine contraction, avoid reinversion, and reduce hemorrhage.
Main uterotonic agents are oxytocin (20–40 units in 1 L of crystalloid infused at 150–200 mL per hour), misoprostol (800 μg intravaginally or rectally), dinoprostone (20 mg rectally), and methylergonovine (200 mcg intramuscularly up to four doses per day).
Also, administration of a single dose of first-generation cephalosporin (cefazolin) is recommended for endometritis prophylaxis.
22.5 Postpartum Preeclampsia and Eclampsia
Preeclampsia and eclampsia can manifest clinically in the antepartum or postpartum period. Most of these cases occur within 48 h of the delivery. Read Chap. 7 for informations about incidence, diagnosis, and management of these complications.
22.6 Postpartum Fever
Postpartum fever is defined as an oral temperature ≥38.0 °C (≥100.4 °F) on any two of the first 10 days postpartum, exclusive of the first 24 h. The first 24 h is excluded because low-grade fever during this period is common and often resolves spontaneously, especially after vaginal birth.
If fever is present, a physical examination should be performed to identify the source of infection and direct optimal therapy (Fig. 22.7). Surgical site infections may occur at sites of episiotomy, lacerations, or cesarean delivery. Typical physical examination findings include cellulitis with redness and induration at the surgical site, which may or be accompanied by tenderness or not. Purulent incisional drainage can also be present.
Fig. 22.7
Postpartum fever due to a thrombophlebitis
In case of postpartum fever, the following conditions should be investigated: urinary tract infections, wound infection (episiotomy or other surgical site infections), mastitis or breast abscess, endometritis or deep surgical infection, septic pelvic thrombophlebitis, drug reaction, clostridium difficile-associated diarrhea, and complications related to anesthesia.
22.7 Dehiscence of Vaginal Lacerations or Episiotomies
Perineal infections, and subsequent breakdown of previously repaired lacerations or episiotomies, are a particularly onerous complication of episiotomy. The incidence is between 0.1 % and 0.2 % of all postpartum sutures [17], and common causes are all the ones who slow wounds healing, e.g., diabetes, obesity, infections, and local ischemia. Diagnosis is made when, on examination, the previously sutured area appears swollen and erythematous with a purulent exudate. Breakdown of perineal laceration repair has been associated with longer second stage of labor, operative vaginal delivery, mediolateral episiotomy, third- and fourth-degree lacerations, and presence of meconium-stained amniotic fluid. In the past, these defects used to be closed after 2 or 3 months after delivery, even if they could also lead to a perineal fistula (Fig. 22.8); nowadays early repair (within 2 weeks) seems to be more effective [18, 19, 20]. Many surgeons suggest to clean the area of necrotic tissue and sutures first than prescribe daily irrigation and antibiotic therapy if necessary; after some days, when the wound is granulating and free to exudate, it is sutured with the same technique of primary repair.
Fig. 22.8
A central perineal fistula, between the vagina and anus, after 12 months from the episiotomy dehiscence
22.8 Vulvar Edema
Vulvar edema has been associated with the use of tocolytics for preterm labor [21], prolonged second stage of labor, and preeclampsia; it is common after delivery and can usually be managed with ice packs in order to relief symptoms.
Rarely a unilateral or bilateral vulvar edema has been associated with maternal mortality [22], and usually these cases are related to obstetric procedures like forceps application, median episiotomy, and perineal injuries [23].
In these cases, especially if necrotizing fasciitis is suspected, clinician must closely monitor the patients, investigating if worsening of the edema, induration, pain, and leukocytosis (>20,000/mm2) are present; fever can be absent. A broad-spectrum empiric antibiotic therapy must be started, and a surgical debridement must be quickly executed in order to ensure correct blood perfusion of the necrotic tissue. In general, empiric treatment of necrotizing infection should consist of broad-spectrum antimicrobial therapy, including activity against gram-positive, gram-negative, and anaerobic organisms; special consideration for group A Streptococcus and Clostridium species should be taken [24]. For these reasons, an acceptable empiric antibiotic regime should include carbapenem or beta-lactamase inhibitor, clindamycin, and vancomycin.
22.9 Surgical Wound Complications
Wound complications generally develop 4–7 days after cesarean section and are diagnosed in 2.5–16 % of patients [25]: the most common complications are infection, hematoma, and dehiscence. Therapy can vary from ice packing, antibiotic treatment to surgical debridement if necrotizing fasciitis (which is a surgical emergency that affects 0.18 % of cesarean deliveries [26]) is suspected.
Moreover, gynecologic sequelae due to deficient uterine scar healing after cesarean section (which prevalence ranges from 19.4 % to 88 %) [27] are only recently being identified and described: these conditions include infertility, cesarean scar ectopic pregnancy (Fig. 22.9), pelvic pain, and abnormal bleeding.
Fig. 22.9
Transvaginal ultrasonographic scan showing a cesarean scar ectopic pregnancy
An abnormal uterine cesarean scar healing is often related to the development of isthmocele (Fig. 22.10), which is the result of incomplete healing of isthmic myometrium after a low transverse uterine incision performed for cesarean section (Fig. 22.11). Although mostly asymptomatic, it may cause menstrual abnormalities (typically postmenstrual spotting), chronic pelvic pain, secondary infertility, and tissue necrosis.
Fig. 22.10
Transvaginal ultrasonographic scan showing an isthmocele
Fig. 22.11
Transvaginal ultrasonographic scan on the uterus on the 30th after a cesarean section; the images show the presence of stitches on isthmic myometrium
Scar tissue dehiscence, scar pregnancy, and abnormally adherent placenta are some of the obstetric complications associated with isthmocele.
No standardized treatment has yet been accepted: currently, hysteroscopic resection and laparoscopic correction or hysterectomy are the minimally invasive approaches used to repair the defect.
22.10 Postpartum Endometritis
Postpartum endometritis (Fig. 22.12) is characterized by an oral temperature ≥38.0 °C (≥100.4 °F) between the second and tenth day postpartum [28]; in fact, during the first 24 h after delivery, low-grade fever is a common finding that often resolves spontaneously, especially after vaginal birth [29]. Other clinical findings in postpartum endometritis are uterine tenderness, midline lower abdominal pain, purulent lochia (in some women), and leukocytosis.
Fig. 22.12
A scheme depicting a postpartum endometritis: on the left, a uterine cavity rich of bacteria leading to a postpartum fever with patient sweating
Retained products of conception after delivery can cause acute or chronic endometritis because microbes can infect the necrotic tissues retained inside the uterine cavity (e.g., membranes, placental fragments).
It is caused by polymicrobial infection involving various aerobes and anaerobes from the genital tract, which colonize the decidua (the pregnancy endometrium) even extending to myometrium (endomyometritis) or the parametrium (parametritis), and is a common cause of febrile morbidity after delivery.
The main risk factor for postpartum endometritis is cesarean delivery especially if performed after the onset of labor [30]: in fact, before routine antibiotic prophylaxis, the rate of infection was 28 % for cesareans performed after the onset of labor and 3.5 % for those performed electively (now is 11 % and 1.7 %, respectively) [31]. The frequency of postpartum endometritis after vaginal birth is less than 3 % [32].
Other risk factors are prolonged labor, multiple manual examinations, internal uterine fetal monitoring, chorioamnionitis, low socioeconomic status, HIV infection, post-term pregnancy, operative vaginal delivery, manual removal of placenta (Fig. 22.13), and colonization with group B Streptococcus, Streptococcus agalactiae or Escherichia coli [33].
Fig. 22.13
Manual placental removal during cesarean section
In women with postpartum fever and mild uterine tenderness and no purulent loch, other causes than infections should be considered, like a surgical site infection (cesarean incision, episiotomy incision, or perineal lacerations) or a mastitis.
The value of laboratory studies is limited: leukocytosis is a common finding in postpartum period, but a rising of neutrophil count associated with elevated numbers of bands is suggestive of infection.
Endometrial cultures are not routinely performed due to the difficulty to obtain a correct specimen through the cervix. Moreover, blood culture is not routinely performed because usually an antibiotic therapy must be started before the results are effectively available, and usually these results do not lead to a change of the initial empiric treatment [34].
The initial empiric treatment must include intravenous broad-spectrum antibiotics covering beta-lactamase-producing anaerobes: clindamycin 900 mg every 8 h plus gentamicin is a common effective option, with a cure rate between 90 % and 97 % [35]. The treatment should last until the patient is afebrile and clinically improved for at least 24 h. Alternative options reported to be equivalent include cefotetan, cefoxitin, ampicillin and sulbactam, and piperacillin.
Oral antibiotics after parenteral therapy are not indicated, unless a positive blood culture is obtained; in this case, antibiotic therapy can be prolonged orally for 7 more days [36].
Usually a good response to the therapy is obtained within the first 48–72 h.
In case of retained product of conceptions, ultrasound may detect the retained tissues, and these should be removed in order to resolve the infection with dilatation and curettage procedures [37].
As we previously reported, usually postpartum endometritis develop within the first 7 days after delivery, but 15 % of cases have a late onset between 1 and 6 weeks after delivery.
These women have mild clinical signs and can be treated with oral antibiotic therapy: in order to give protection over facultative and anaerobic bacteria, a therapy with amoxicillin-clavulanate by mouth twice a day for 7 days can be prescribed [38].
22.11 Voiding Difficulty and Urinary Retention
Postpartum urinary retention (PUR) presenting in the puerperium has been explained with several definitions and widely reported rates.
Actually two variants of PUR are considered: overt PUR as the absence of spontaneous micturition after 6 h from vaginal delivery and covert PUR as a post-void residual bladder volume of at least 150 mL after spontaneous micturition, after ultrasonographic diagnosis of bladder distension or catheterization [39]. Its incidence seems to be related to prolonged second stage of labor [40] (Fig. 22.14) and pudendal nerve injury after delivery [41], as well as epidural anesthesia, operative delivery, episiotomy, and primiparity.
Fig. 22.14
A prolonged second stage of labor for a persistent occiput posterior position; on the top, the ultrasonographic image showing the fetal eyes under pubis; in the image below, the bladder catheterization to difficulty emptying the bladder
Usually more than 90 % of PUR resolve spontaneously in 1 week.
Patients may be asymptomatic or refer voiding difficulty with small and frequent amounts of urine, slow or intermittent streams, bladder pain, urinary incontinence, and send of incomplete voiding [42].
Treatment of overt PUR is intermittent catheterization; routine antibiotic therapy is unnecessary, and treatment of overt PUR is intermittent catheterization, every 4–6 h or when the patient has void urgency.
In clinical practice, when the residual urine volume is <150 mL and the patient no longer has significant symptoms of voiding difficulty bladder catheters should be discontinued.
22.12 Hemorrhoids
Hemorrhoids are normal vascular structures in the anal canal (Fig. 22.15) that often produce variety of problems like anal pruritus, prolapse, bleeding, and pain due to thrombosis. Their incidence is higher after delivery than in the late pregnancy and postpartum period: in fact, of those women 91 % referred hemorrhoid complications in the first day after delivery, 30 % at 8 weeks postpartum, and 13–25 % in the first 6 months [43]. Moreover, it has been estimated that 35 % of pregnant women experienced anal lesions after delivery, 20 % external hemorrhoids, 15 % anal fissures, and 7.8 % thrombosed external hemorrhoids during late pregnancy [44]. Risk factors seem to be fetal macrosomia, prolonged second stage of labor, and operative and/or traumatic delivery.
Fig. 22.15
A perineal frontal vision in gynecological position of the patient in the puerperal period: on the left, it shows the vascularization of the perineum; above, it is evident edema and vulvar varicose veins and hemorrhoids below
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
