At the end of the 19th century the first microscopic examinations of uterine-placental specimens were conducted, derived from patients, in which the placenta could not be removed during delivery. Histological evidence of an “attached placenta” was brought to light.¹ In 1922, Dietrich totally traced 19 cases of placenta accreta in which the diagnosis had been histologically verified.² He documented that all of these cases were multiparas with history of previous surgical interventions, such as manual removal of the placenta in one or more previous pregnancies, or endometrial ablation.

It was not until the year 1978 when Larsen and Solomon reported the first case of cesarean scar pregnancy (CSP). The first review article by Fylstra summarized a total of 18 cases up to 2002.^3,4 Although cesarean scar pregnancy was first considered a different clinical entity, Timor-Tritsch et al showed it to be the histopathological expression of a placental attachment disorder (PAD) in the first trimester.⁵ Today we use the term “placenta attachment disorders” (PADs) to refer to the whole spectrum of disorders concerning abnormal placental implantation into the uterine wall. Collins et al suggested using “abnormally invasive placenta (AIP)” as the clinical term to describe any placenta that does not separate spontaneously during a delivery and that causes pathological high blood loss if forcefully separated.⁶

PADs present serious clinical conditions that can lead to massive blood loss and even death. Torrential bleeding occurs when there is forceful separation of an abnormally implanted placenta from the uterine wall. With increasing depths of invasion, morbidity and mortality rate increases.^7,8 The term placenta accreta is used if histopathologically the placenta attaches directly to the myometrium, placenta increta if there is deep myometrial invasion, and placenta percreta if the placenta is perforating through the full thickness of the myometrium and uterine serosa with possible involvement of adjacent organs.⁹ Out of all cases with PAD in the third trimester, 75% are placenta accreta, 18% placenta increta, and 7% placenta percreta.⁷

Worldwide the incidence of AIP has increased over the past decades. In 1977, Breen et al reported an incidence of placenta accreta of 1 in 7000 pregnancies.¹⁰ In a cohort between 1985 and 1994, the PAD rate was reported as 1 in 2500 pregnancies.⁷ In a study between 1982 and 2002, there was a documented increase to 1 in 533 pregnancies.¹¹ PAD were seen to have increased parallel to the increasing rate of cesarean deliveries (CDs). In 2013, an Italian study reported PAD rates as high as 1 in 322 pregnancies and a cesarean section rate of 64%, compared to incidence of 1 in 833 and a cesarean section rate of 17% in 1976.¹²

The incidence of CSP was estimated to range from 1:1800 to 1:2216 pregnancies. Rotas et al reported the increasing number of CSP since 1978, which might reflect not only the increased number of CDs but also the improved diagnostic accuracy, as well as the higher index of suspicion.¹³ The increased clinical awareness of the CSP in the obstetric and gynecologic community may be reflected in the number of publications. Timor-Tritsch et al reported increasing numbers of publications about CSP. From 1990 until 1999, 19 articles regarding CSP were found, between 2000 and 2005, 48 articles, and from 2006 to 2011, 104 articles.¹⁴

Knowing the risk factors is fundamental for every clinician. The risk assessment helps to detect patients who might need a detailed ultrasound to rule out PAD.

Placenta previa is a risk factor. The risk of placenta accreta in patients with placenta previa alone, without previous surgery, is increased and ranges from 2% to 6.3%, depending upon whether maternal age is under or over 35 years.⁷ Wu et al found that the likelihood ratio of placenta previa for PAD was 51.4—by far the highest of any factors studied.¹¹

Uterine surgeries, such as cesarean section, myomectomy, uterine curettage, endometrial ablation, and radiation, are strong risk factors for PAD because of possible damage to the endometrium.^15-21 Prior cesarean delivery, especially multiple cesarean deliveries, is a major risk factor.^16,22,23 In patients with placenta previa, the risk for placenta accreta was 3%, 11%, 40%, 61%, and 67% for first, second, third, fourth, and fifth or more repeat cesarean deliveries.²⁴ Clark et al found that one prior cesarean section in patients with placenta previa increased the risk to 24% while 4 or more cesarean deliveries increased the risk to 67% (and was increased even if the placenta does not lie over the uterine scar).²² However, the risk increases fivefold if the placenta actually lies over the scar itself,⁷ probably due to lower uterine segment location typical of placenta previa, in addition to a surgically disturbed area of myometrium.

Prior placenta accreta is also a risk factor. In a group of patients with presumed placenta accreta due to difficulty removing the placenta, 16% of patients had previous events of placenta accreta.¹⁸

Maternal age, high gravity and parity, and multiple abortions were found to significantly correlate with severe outcome of placenta accreta.¹⁸ Maternal age over 35 years can double or triple baseline risk.⁷

Cryopreserved embryo transfer is a strong independent risk factor for placenta accreta among patients using in vitro fertilization (IVF) and/or intracytoplasmic sperm injection (ICSI).²⁵ Patients’ age may be a cofactor since the overall age of patients in the group treated by reproductive techniques tends to be increased.

The main risk factor for a CSP is prior CD. The literature is not conclusive whether or not the number of prior CD increases the risk for a CSP. Jurkovic reported in his cohort of 18 patients that 13 (72%) of them had multiple CDs.²⁶ Other authors were not able to show that. More than half of the 75 patients in Rotas’ study had one previous CD.¹³

There is also not enough evidence to support that a double-layer closure of the hysterotomy, with sutures inverting the first layer by the second one, which was performed in the past, heals better and therefore might prevent CSPs compared to the single noninverting running suture commonly used today.²⁷

Placenta attachment disorders (PAD) are associated with relevant maternal and fetal morbidity and even mortality. Maternal morbidity is primarily the result of severe hemorrhage. The mean estimated blood loss in patients with PAD ranges from 2000 to 7800 mL, with a mean number of five units of blood transfused.²⁸ The majority of all emergency peripartum hysterectomies and hemorrhages occur in the setting of an abnormally adherent placenta.²⁹

Other relevant complications reported with PAD are disseminated intravascular coagulation, thromboembolism, pyelonephritis, pneumonia, adult respiratory distress syndrome, multiorgan failure, renal failure, infection, and even amniotic fluid embolism.^22,30 Surgical complications reported were injury to the bladder and ureters, as well as injury to the bowel, large vessels, and pelvic nerves.^16,31-33 Maternal deaths due to severe hemorrhage because of PAD have been reported,^16,19,33-35 in one case series as high as 7%.³¹ Neonatal complications are most often the result of preterm birth around 34 weeks of pregnancy.^30,34

The invasion of the myometrium early in the first trimester in a CSP can cause uterine rupture and profuse bleeding as the pregnancy continues.⁴ Also, sometimes a CSP is misdiagnosed as a cervical or aborting pregnancy, and therefore correct diagnosis and treatment is delayed.¹³

In PAD, the Nitabuch’s fibrinoid layer of the decidua basalis between the myometrium and placenta is absent or thinned,³⁶ leaving the trophoblast to lie in direct contact with the myometrium, so there is no natural separation plane, and the placenta is thus firmly adherent to the myometrium. The placental villi may even invade and penetrate through the entire myometrium and serosa.³⁷ This lack of decidua can sometimes involve the whole placenta, sometimes only part of the placental myometrial surface. The term “focal placenta accreta” may apply to such partially adherent placentas. But even a limited area creates a problem if the placenta is forcefully separated from the myometrium. In some cases of placenta percreta, the placental villi may also invade the bladder, making the removal of the uterus difficult and often resulting in loss of parts of the bladder. It can also invade the parametrium, ie, broad ligament, cervix, or uterine artery. In cases of cesarean scar pregnancy, the placental villi invade into the myometrium through the niche in the cesarean scar.^5,38

In CSP the invasion of the pregnancy into the myometrium occurs through a defect in the scar on the basis of incomplete healing. The underlying mechanism is similar as described previously.³⁹

It has to be carefully determined whether the patient has any risk factors for PAD, as mentioned previously. In patients with previous uterine surgery, especially prior CD with low-lying placenta or placenta previa, the placenta has to be examined for signs of placenta accreta.⁴⁰ The bladder should be “comfortably full” (300 cc) in order to have an optimal sight.⁴¹ Low implantation of the gestational sac upon a previous cesarean section scar is the typical first trimester appearance of placenta accreta, in contrast to the usual location of the gestational sac in the fundus.^42,43

Criteria for diagnosing a CSP in a patient with previous cesarean section and a positive pregnancy test, Timor et al⁴¹:

1. 
   

   Visualization of an empty uterine cavity as well as an empty endocervical canal (Figure 8-1).

   
   
2. 
   

   Detection of the placenta and/or a gestational sac embedded in the hysterotomy scar/niche (Figure 8-2). In the gestational sac an embryonic/fetal pole and/or yolk sac with or without heart activity can and be visualized (see Figure 8-1).

   
   
3. 
   

   In early gestations (before postmenstrual 8 weeks), a triangular gestational sac that fills the niche of the scar (see Figure 8-1); at after 8 postmenstrual weeks this shape may become rounded or even oval, and part or the entire chorionic sac may be seen approaching or lying in the uterine cavity (Figure 8-3). Importantly, the placenta and its blood vessels remain attached within or on the scar and define the diagnosis of CSP.

   
   
4. 
   

   A thin (1-3 mm) or absent myometrial layer between the gestational sac and the bladder (Figure 8-4).

   
   
5. 
   

   The presence of a prominent and at times rich vascular pattern in color Doppler at or in the area of a cesarean section scar in the presence of a positive pregnancy test (Figures 8-5 and 8-6).

A simple method to differentiate an intrauterine pregnancy from a CSP in a patient with previous CD is to determine the position of the center of the sac related to the midpoint of the uterine length in a sagittal, longitudinal ultrasound image (Figure 8-7). If the center of the sac is above the midpoint, it is in an intrauterine pregnancy, if it is underneath, close to the cervix, it is a CSP.⁴³