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A sacrococcygeal teratoma (SCT) is a type of tumor arising from the tailbone of a developing fetus. This type of teratoma can either grow externally from the tailbone or internally into the pelvis.
While many sacrococcygeal teratomas are small and can be managed after birth, some may need fetal treatment. As a parent, learning your baby may have a sacrococcygeal teratoma can be frightening. But the Colorado Fetal Care Center is at the forefront of treatment and care for this condition.
One of the most common types of congenital germ cell tumors, a sacrococcygeal teratoma (SCT) is a mass located on the base of the tailbone, or coccyx, of a baby. It occurs in an average of one in every 35,000 births and is seen in three times more females than males.
It can vary in size, shape and consistency. While most are small and benign, some fetuses can develop larger growths or may have islands of malignant cells. There are a wide variety of types and sizes of tumors associated with this condition, however they are predominantly benign (non-cancerous) and can be successfully removed after birth in many cases.
Causes of sacrococcygeal teratomas are unknown, though there are many theories.
Depending on the size of the sacrococcygeal teratoma, complications can vary. If the mass is small, often times there are no complications and the pregnancy will continue without problems. In these cases, the tumor can be successfully removed after birth with no prolonged impact to the baby or mother.
If, however, the tumor grows rapidly during the pregnancy, it can create a variety of complications that impact both the mother and baby. Because these tumors can become very large, severe cases put the fetus and mother at risk of:
Sacrococcygeal teratomas can also be tied to other congenital abnormalities such as myelomeningocele, so it's important to conduct a thorough examination to rule out additional complications.
Many sacrococcygeal teratomas are discovered through blood work or a routine ultrasound. At around 16 weeks of pregnancy, blood is drawn from an expectant mother to examine her levels of alpha-fetoprotein (AFP). A high amount of AFP may be one indicator of this condition. Alternatively, the mass can also be detected through an ultrasound, appearing as a fluid-filled cyst on the baby's tailbone.
After a diagnosis, both mother and baby will be monitored often to watch the progression of the mass. A fetal echocardiogram will also be used to monitor the teratoma during pregnancy to track the development of heart failure and any risk of hydrops (fluid buildup).
Our fetal care team will also work with families to provide informed treatment plans based on the type, size, and composition of a fetal sacrococcygeal teratoma (verified by a fetal MRI). They'll also take into account the complications the mass is causing to determine if fetal surgery is required.
The standard treatment process for small, benign fetal sacrococcygeal teratomas includes:
However, for larger or malignant tumors that are posing a risk to cardiac, lung or bowel functions, prenatal surgery may be recommended by our fetal care team.
Treatment for these types of sacrococcygeal teratomas include:
Treatment for sacrococcygeal teratomas at the Colorado Fetal Care Center has proven very successful. Thanks to our amazing team, sacrococcygeal teratoma surgeries have improved outcomes for our tiniest patients and their mothers.
Retrospective prenatal diagnosis of SCT was first made in the mid-1970s, and the first prospective prenatal diagnosis was reported by Horger and McCarter in 1979. They described a 13-cm complex mass at the caudal end of the fetus, with solid and cystic areas and bizarre internal echoes associated with polyhydramnios. This typical prenatal sonographic appearance has been confirmed by other authors and over 60 cases of prenatally diagnosed SCT have been described (Seeds et al., 1982; Grisoni et al., 1988; Bond et al., 1990). The most common clinical presentation is uterine size greater than dates due to polyhydramnios, initiating an ultrasound examination (Seeds et al., 1982). To date, the earliest diagnosis of SCT that has been made is 12 3/7 weeks of gestation (Roman et al., 2004).
SCTs can grow at an unpredictable rate to tremendous dimensions. Several case reports note fetal tumors as large as 25 by 20 cm (Heys et al., 1967; Weiss et al., 1976). These tumors are generally exophytic (AAPSS type I), but may extend retroperitoneally displacing pelvic (type II) or abdominal structures (type III) (Litwiller, 1969).
Prenatal sonographic image demonstrating a large type III sacrococcygeal tumor in a 24-week fetus. In this view, a primarily cystic tumor with internal and external components can be seen.
Image of a 24-week fetus in a spine up position demonstrating a large type III sacrococcygeal tumor.
Most SCTs are solid or mixed solid and cystic, consisting of randomly arranged irregularly shaped cysts (Seeds et al., 1982; Chervenak et al., 1985). Purely cystic SCT has also been described prenatally (Seeds et al., 1982; Hogge et al., 1987). Calcifications can be seen microscopically, although the majority are not visible on prenatal ultrasound examination. Most prenatally diagnosed SCTs are extremely vascular, which is easily demonstrated with the use of color flow Doppler studies. Three-dimensional power Doppler has been suggested to demonstrate the large vascular volume in SCT (Sciaky-Tamir et al., 2006). Polyhydramnios has been noted in most cases of prenatally diagnosed SCT and, although the mechanisms for this are not known, it is likely secondary to renal hyperfiltration occurring as a result of high-output state (Chervenak et al., 1985).
Hepatomegaly, placentomegaly, and nonimmune hydrops are also seen in association with SCT and appear to be secondary to high-output cardiac failure (Heys et al., 1967; Cousins et al., 1980; Gergely et al., 1980; Kapoor and Saha, 1989; Bond et al., 1990; Flake, 1993; Hedrick et al., 2004). High-output failure may be due to tumor hemorrhage or arteriovenous shunting within the tumor (Cousins et al., 1980; Flake et al., 1986; Alter et al., 1988; Schmidt et al., 1989; Bond et al., 1990). Some authors have attributed heart failure with subsequent hydrops to severe fetal anemia secondary to tumor hemorrhage and resulting anemia (Alter et al., 1988). However, normal fetal hematocrits have also been reported, suggesting that congestive heart failure is more often due to high-output cardiac state from arteriovenous shunting within the tumor (Schmidt et al., 1989). The demonstration of heart failure or hydrops on ultrasound examination is usually a preterminal event (Flake et al., 1986; Kuhlmann et al., 1987; Bond et al., 1990).
Controversy exists regarding the presence of associated anomalies and the need for chromosome analysis. The incidence of coexisting anomalies is 11% to 38%, primarily involving the nervous, cardiac, gastrointestinal, genitourinary, and musculoskeletal systems (Hickey and Layton, 1954; Schiffer and Greenberg, 1956; Carney et al., 1972; Fraumeni et al., 1973; Altman et al., 1974; Izant and Filston, 1975; Gonzalez-Crussi et al., 1978; Ein et al., 1980; Holzgreve et al., 1985; Kuhlmann et al., 1987; Werb et al., 1992). Several authors postulate that at least some of these anomalies are related to tumor development. Others have reported an increased incidence of spinal deformities (Ewing, 1940; Gruenwald, 1941; Alexander and Stevenson, 1946; Bentley and Smith, 1960; Wilson et al., 1963; Carney et al., 1972). Most authors agree with the Berry et al. (1970) observation that local abnormalities such as rectovaginal fistula and imperforate anus are thought to be directly related to tumor growth during fetal development. Aneuploidy has not been reported with SCT and we do not recommend amniocentesis for karyotype analysis unless there are multiple anomalies, advanced maternal age or if fetal surgery is contemplated.
Fetal MRI has emerged as an adjunctive imaging modality that can provide important anatomical detail in cases of SCT (Avni et al., 2002; Hedrick et al., 2004; Nassenstein et al., 2006). MRI may be particularly useful in defining the pelvic component of SCT and impact on other pelvic structures (Garel et al., 2005). In cases in which fetal surgery is being considered, fetal MRI provides a broader field of view than ultrasound and may be helpful in operative planning. In cases in which SCT has a pelvic component or there is polyhydramnios, oligohydramnios, hydronephrosis or hydrocolpos, fetal MRI may provide additional information on the anatomical relationships not apparent on ultrasound alone (Danzer et al., 2006). Fetal MRI in cases of cystic SCT may be particularly helpful in excluding myelomeningocele from the differential diagnosis (Yoon and Park, 2005; Danzer et al., 2006). Fetal MRI can also be used to assess the SCT for evidence of hemorrhage into the tumor.
The antenatal natural history of prenatally detected SCT is not as favorable as that of SCT presenting at birth. Well-defined prognostic factors for SCT diagnosed postnatally, as outlined in the AAPSS classification system, do not necessarily apply to fetal cases (Altman et al., 1974; Bond et al., 1990). While the mortality rate for SCT diagnosed in the newborn is at most 5%, the mortality rate for fetal SCT approaches 50% (Flake et al., 1986; Bond et al., 1990; Flake, 1993; Hedrick et al., 2004).
Most SCTs are histologically benign. The incidence of malignant elements present in fetal SCT has ranged from 7% to 30% (Hedrick et al., 2004; Heerema-McKenny et al., 2005). Malignancy appears to be more common in males, especially with solid versus complex or cystic tumors (Schey et al, 1977). The presence of histologically immature tissue does not necessarily signify malignancy (Carney et al., 1972; Gonzalez-Crussi, 1982). Calcifications occur more often in benign tumors but may also be seen in malignant tumors and are unreliable indicators of malignant potential (Hickey and Layton, 1954; Waldhausen et al., 1963; Grosfeld et al, 1976; Schey et al., 1977; Horger and McCarter, 1979). Although there is one reported case of malignant yolk sac differentiation in a fetal SCT, there has not been a case of metastatic teratoma in a neonate with a prenatally diagnosed SCT (Holzgreve et al., 1985; Flake, 1993).
The prenatal history of SCT is quite different from postnatal natural history. Flake et al. (1986) reviewed 27 cases of prenatally diagnosed SCT. Five cases were electively terminated and 15 of the remaining 22 died, either in utero or shortly after delivery. The majority of these patients presented between 22 and 34 weeks of gestation with a uterus large for gestational age secondary to severe polyhydramnios. The International Fetal Medicine and Surgery Society reported a mortality rate of 52% among cases of prenatally diagnosed SCT (Bond et al., 1990). When SCT was seen in association with placentomegaly or hydrops, all affected fetuses died in utero. The indication for ultrasound examination was also found to be a predictive factor. If SCT was an incidental finding, the prognosis was favorable at any gestational age. However, if the ultrasound examination was performed for maternal indications, 22 of 32 (69%) fetuses died. In addition, diagnosis prior to 30 weeks was associated with a poor outcome.
Sheth et al. (1988) also reported significant perinatal mortality associated with SCT, with only 6 survivors among 15 cases diagnosed prenatally. Three of four cases associated with hydrops were rapidly fatal. The sole survivor was salvaged by emergency cesarean section at 35 weeks. This series was unusual because three cases had severe obstructive uropathy and secondary renal dysplasia. A more favorable outcome was reported by Gross et al. (1987) in which 8 of 10 fetuses with prenatally diagnosed SCT survived. However, no fetus had hydrops or placentomegaly, and the two nonsurvivors were electively terminated.
Hydrops in SCT is usually, but not always, fatal. Nakoyama et al. (1991) reported survival in two fetuses with SCT presenting with hydrops at 27 and 30 weeks of gestation. In addition, Robertson and Crombleholme (1995) were able to salvage a hydropic fetus at 26 weeks of gestation by staged resection of the SCT in the neonatal period. In this case, acute rapid growth of the SCT led to polyhydramnios and preterm delivery. After delivery, the newborn was noted to be in a high-output state from shunting through the tumor. In a staged resection, the tumor was initially devascularized by ligation of both internal iliac arteries. Twenty-four hours later, the external portion of the mass was resected. The infant subsequently underwent resection of the intrapelvic portion of the tumor at 3 months of age and did well.
Hedrick et al. (2004) reviewed their experiences with 30 cases of prenatally diagnosed SCT and reported 4 terminations, 5 fetal deaths, 7 neonatal deaths and only 14 survivors (47%). Among the 26 patients continuing the pregnancy, 81% experienced obstetric complications including polyhydramnios (n=7), oligohydramnios (n=4), preterm labor (n=13), pre-eclampsia (n=4), gestational diabetes (n=1), HELLP syndrome (n=1) and hyperemesis (n=1).
Sonographic features of SCT such as size, AAPSS classification, solid or cystic composition or presence or absence of calcifications have not been predictive of either fetal survival or future malignant potential (Altman et al., 1974; Flake, 1993). One exception to this may be the unilocular cystic form of SCT, which has a relatively favorable prognosis because of benign histology and limited vascular and metabolic demand (Horger and McCarter, 1979; Mintz et al., 1983). The growth of the SCT in relation to the size of the fetus is also unpredictable and may increase, decrease or stabilize as gestation proceeds. However, a rapid phase of tumor growth usually precedes the development of placentomegaly and hydrops. Highly vascular lesions are more likely to undergo rapid tumor growth and to be associated with the development of placentomegaly and hydrops. The prenatal mortality, unlike postnatal mortality, is not due to malignant degeneration but to complications of tumor mass or tumor physiology (Flake et al., 1993). The tumor mass may result in malpresentation or dystocia, which in turn may result in tumor rupture and hemorrhage during delivery. Dystocia has been reported in 6% to 13% of cases in postnatal series (Giugiaro et al., 1977; Musci et al., 1983; Gross et al., 1987). SCTs may also spontaneously rupture in utero leading to significant fetal anemia or death (Sy et al., 2006). The most important benefit of prenatal diagnosis is prevention of dystocia by elective or emergency cesarean section. Tumor mass effect may also result in uterine instability and preterm delivery because of uterine distention (Flake et al., 1986; Bond et al., 1990). Massive polyhydramnios is frequently seen in large fetal SCTs, which also predisposes to uterine irritability and preterm delivery.
SCT may occur in twins further complicating the prenatal management. In the series of Hedrick et al., 10% of the cases occurred in twin gestations (Hedrick et al., 2004). The presence of SCT in a twin gestation increases the risk of preterm delivery. Because SCT is associated with an increased risk of fetal death, intrauterine demise of a monochorionic twin with SCT places the surviving unaffected co-twin at risk of adverse neurologic outcome (Ayzen et al., 2006).
The physiologic consequence of fetal SCT depends on the metabolic demands of the tumor, blood flow to the tumor and the presence and degree of anemia. The features of the SCT (i.e. whether cystic or solid, size and rate of growth) all affect the metabolic demands of fetal SCT. While classically thought to derive its blood supply from the middle sacral artery (Smith et al., 1961), these large tumors often parasitize blood supply from the internal and external iliac systems. This may result in vascular "steal" from the umbilical artery blood flow to the placenta. As an SCT outgrows its blood supply, tumor necrosis may occur leading to tumor rupture and hemorrhage. The high-output cardiac failure in fetal SCT can be diagnosed by fetal echocardiography and Doppler studies (Flake et al., 1986; Langer et al., 1989; Schmidt et al., 1989). When hydrops develops in fetuses with SCT, all have dilated ventricles and dilated inferior venae cavae due to increased venous return from the lower body (Flake, 1993). Serial sonographic examinations in fetal SCT often show progressive increases in combined ventricular output and descending aortic flow velocity. In general, placental blood flow is decreased by the vascular steal by the SCT (Schmidt et al., 1989; Flake, 1993) and may lead to the finding of end-diastolic flow reversals in the umbilical artery.
Benachi et al. (2006) have suggested a prenatal prognostic classification system based on tumor diameter, vascularity and rapidity of growth. In a group of 44 fetal SCTs divided into group A (tumor <10 cm, absent or mild vascularity and slow growth), group B (tumor >10 cm, pronounced vascularity or high output cardiac failure and rapid growth), and group C (tumor >10 cm, predominantly cystic lesion with absent or mild vascularity and slow growth). Groups A and C did well with gestational age at delivery of 38 and 37 weeks, respectively, while group B delivered prematurely at 31 weeks of gestation. There was no mortality in either group A or C but there was 52% for group B. The newborns in group B also have a much longer length of stay postnatally (Benachi et al. 2006). Postnatal measurements of umbilical arterial blood gases before and after removal of a large SCT demonstrate that the tumor acts as a large arteriovenous shunt.
The uniformly dismal outcome in fetuses with SCT complicated by placentomegaly and hydrops has been the impetus for resection of this tumor in utero. Harrison was the first to attempt antenatal resection of an SCT (Langer et al., 1989). In this first case, a fetus was noted to be markedly hydropic with a significantly elevated combined ventricular output (972 mL per kilogram of body weight per minute) at 24 weeks (Langer et al., 1989; Flake, 1993). In addition, the mother had mild hypertension, edema and proteinuria. Preterm labor developed and was controlled with tocolytic agents. At surgery, the exophytic portion of the tumor was dissected free of the anus and rectum and amputated at its base with a stapling device. Despite the resection, the fetus remained hydropic with an elevated combined ventricular output of 869 mL per kilogram of body weight per minute. Percutaneous umbilical cord blood sampling showed the fetal hematocrit to be only 16%. This was increased to 27% by blood transfusion. The fetus subsequently improved significantly with sonographic resolution of hydrops and a decrease in descending aortic flow to 524 mL/kg of body weight per minute. However, the maternal mirror syndrome progressed to pulmonary edema and, on postoperative day 12, a 26-week-gestation fetus was delivered by cesarean section and died of pulmonary immaturity at 6 hours of age. The mother's illness resolved within 2 days. Autopsy showed no evidence of hydrops and no residual tumor.
A second case was attempted at 26 weeks of gestation when dramatic enlargement of the tumor resulted in early hydrops, elevated combined ventricular output and severe polyhydramnios (Flake, 1993). The surgery went uneventfully and the base of the tumor was stapled to excise the exophytic portion and reverse the hyperdynamic state. The fetus did well until postoperative day 8, when irreversible preterm labor developed and the fetus was delivered by emergency cesarean section. Because the histology of the resected specimen was interpreted as an immature teratoma grade with predominance of neuroepithelial elements and foci of yolk sac differentiation, resection of residual tumor was attempted on the 13th day of postnatal life. During dissection of the presacral space, the baby experienced complete cardiovascular collapse due to a paradoxical air embolism. The histology of the tumor revealed grade immature teratoma but the residual tumor was more mature than the previous tumor specimen and contained no foci of yolk sac differentiation.
The first successful resection of fetal SCT with long-term survival was reported by Adzick and Crombleholme (1997). At 25 weeks of gestation, a type II SCT had rapid enlargement and development of polyhydramnios and placentomegaly, with associated maternal tachycardia and proteinuria suggesting impending maternal mirror syndrome. At surgery, the exophytic portion of the tumor was dissected free of the anus and rectum and the base of the tumor excised with a thick tissue stapling device. The mother and fetus did well postoperatively, with resolution of hydrops and placentomegaly within 10 days. Pathology of the tumor showed immature teratoma without evidence of yolk sac differentiation. At 29 weeks of gestation, preterm labor prompted cesarean delivery. Postnatally, the female infant underwent resection of the coccyx and surrounding tissue at 2 months of age but no residual tumor was found. She did well until 1 year of age when AFP levels became elevated to 22,000 ng/mL and she presented with pleural effusions, lung nodules and a recurrent buttock mass from a metastatic yolk sac tumor. She has had an excellent response to chemotherapy. Hedrick et al. subsequently reported their experience with four open fetal surgeries for SCT with all four surviving the procedure to delivery at an average gestational age of 29 weeks (range 27.6-31.7 weeks). There was one neonatal death due to premature closure of the ductus arteriosus thought to be secondary to indomethacin exposure as a tocolytic following fetal surgery. Other complications experienced in these fetal surgery patients included tumor embolism resulting in renal infarction and multiple jejunal atresias (n=1), chronic lung disease (n=1), and development of metastatic endodermal yolk sac tumor (n=1) (Hedrick et al., 2004).
While clinical experience remains limited, there have been other cases of SCT successfully resected in utero at the University of California San Francisco and at Cincinnati Children's Hospital. For the fetus with a large SCT associated with early signs of hydrops or placentomegaly, resection in utero remains a viable option. Primary resection of the external portion of the tumor was performed with interval resection of the pelvic extension of SCT. This approach may be useful in managing the common association of prematurity, large tumor and hyperdynamic state. Because the primary cause of fetal mortality and morbidity is the vascular shunting through the tumor, there have been attempts to embolize or devascularize the tumor using radiofrequency ablation (Paek et al., 2001; Lam et al., 2002). In a report of four patients treated with radiofrequency ablation, two fetuses died secondary to hemorrhage after a significant portion of the tumor mass was ablated. The remaining two fetuses delivered at 28 and 31 weeks' gestation with evidence of extensive necrosis of pelvic and perineal structures, necessitating extensive reconstructive surgery (Ibrahim et al., 2003). The uncontrolled nature of the energy delivered by the radiofrequency ablation device prevents its safe application in SCT and this treatment modality has been abandoned.
The most recent approach to the management of large predominately solid SCTs with polyhydramnios and preterm labor has been the use of EXIT-to-Resection strategy. In our experience, as well as those at CHOP and Cincinnati Children's, these fetuses can exsanguinate into the tumor at the time of delivery, even by very careful cesarean section. In our experience at Cincinnati Children's with four type II and type III solid and very vascular SCTs, all four experienced cardiovascular collapse at the time of delivery due to hemorrhage into the SCT. These infants could be temporarily stabilized by a tourniquet at the base of the SCT, allowing resuscitation. Two of the four did not make it out of the delivery room. One was stabilized for transport to the NICU. The fourth underwent emergency resection in the delivery room. As a result of this experience, we now offer EXIT-to-Resection for these fetuses to prevent hemorrhage into the tumor. We have had excellent results with these cases of SCT managed by EXIT. Not every SCT requires this approach and EXIT-to-Resection should be reserved for large, predominately solid and extremely vascular SCTs.
Although the primary cause of death in neonatal SCT is malignant invasion, in prenatal SCT the complications of prematurity or exsanguinating tumor hemorrhage at delivery predominate (Flake et al., 1986; Bond et al., 1990; Adzick and Harrison, 1994). Weekly sonographic examinations should be performed during pregnancy to assess amniotic fluid index, tumor growth, fetal well-being and early evidence of hydrops (Chervenak et al., 1985; Langer et al., 1989). Serial Doppler echocardiographic evaluations should be performed in all patients to detect early signs of high-output state, as evaluated by an increased diameter of the inferior vena cava (should be >1 cm), increased descending aortic flow velocity (>120cm/s) (Alter et al., 1988; Flake, 1993; Bahlmann et al., 2001) or increased combined ventricular output (>500 mL/kg/min for CVO) (Bahlmann et al., 2001). Evidence of the earliest signs of heart failure, placentomegaly and/or hydrops should be sought, as these may progress rapidly and are harbingers of preterminal events (Langer et al., 1989). Bond et al. (1990) reported a uniformly fatal outcome when SCT was associated with placentomegaly and/or hydrops. Flake et al. (1986) reported seven of seven fetal deaths in pregnancies complicated by placentomegaly and hydrops.
Weekly amniocenteses to determine pulmonary maturity are recommended by some physicians after 36 weeks of gestation, with delivery once fetal lung maturity is established (Adzick and Harrison, 1994). Many pregnancies complicated by SCT do not reach this gestational age, however. Warning signs and symptoms of preterm labor should be stressed at prenatal visits and limitation of activity, treatment and cervical checks may be indicated (Garmel et al., 1994).
The recommended mode of delivery is determined by the size of the tumor. Vaginal delivery may be possible with some small tumors (Grisoni et al., 1988; Flake, 1993). Complications of vaginal delivery, however, have included fetal death after rupture, avulsion or asphyxia (Schiffer and Greenberg,1956; Heys et al., 1967; Grosfeld et al., 1976; Giugiaro et al., 1977; Chervenak et al., 1985; Holzgreve et al., 1987; Werb et al., 1992). Cesarean delivery is recommended to avoid trauma-induced hemorrhage or dystocia, especially in large (>5-10 cm) tumors (Chervenak et al., 1985; Gross et al., 1987; Hogge et al., 1987; El-Qarmalaui et al., 1990; Flake, 1993). The size of the tumor may also influence the type of uterine incision. A large tumor may warrant a classical uterine incision, especially in a preterm infant (Chervenak et al., 1985).
Dystocia has been reported when the diagnosis of SCT was unsuspected in as many as 6% to 13% of cases (Hickey and Layton, 1954; Schiffer and Greenberg, 1956; Seidenberg and Hurwitt, 1958; Lowenstein et al., 1963; Hickey and Martin, 1964; Abbott et al., 1966; Lu and Lee, 1966; Heys et al., 1967; Desai, 1968; Kowalski and Sokolowska-Pituchowa, 1968; Werner and Swiecicka, 1968; Litwiller, 1969; Weiss et al., 1976; Seeds et al., 1982; Tanaree, 1982; Edwards, 1983; Mintz et al., 1983; Musci et al., 1983; Varga et al., 1987; El-Shafie et al., 1988; Johnson et al., 1988). Transabdominal and transvaginal aspirations of large cysts have been attempted with variable results to facilitate delivery in the face of significant dystocia (Abbott et al., 1966; Desai, 1968; Litwiller, 1969; Weiss et al., 1976; Tanaree, 1982; Edwards, 1983; Mintz et al., 1983; Musci et al., 1983; El-Shafie et al., 1988; Johnson et al., 1988). Cyst decompression has also been used to treat maternal discomfort and, in one case, cyst amniotic shunting was used to treat bladder outlet obstruction due to tumor compression (Garcia et al., 1998; Kay et al., 1999; Jouannic et al., 2001). It is hoped that prenatal detection of SCT will prevent such unforeseen emergencies (Musci et al., 1983).
Fetal SCT is sometimes associated with maternal complications. The mother should be observed for signs and symptoms of pre-eclampsia, such as the "mirror syndrome" described by Nicolay et al. in association with SCT and hydrops (Nicolay and Gainey, 1964; Cousins et al., 1980; Flake et al., 1986; Coleman et al., 1987; Langer et al., 1989; Bond et al., 1990). Delivery should be performed in a tertiary care center with neonatologists and pediatric surgeons available.
A neonatologist should attend the delivery and be prepared to provide respiratory support for babies born with a sacrococcygeal teratoma. Careful handling of the infant is important to prevent exsanguinating hemorrhage into the tumor. Excellent venous access is paramount should hemorrhage in the tumor occur and umbilical artery and umbilical venous catheters should be placed. The infant should be started on pressor agents such as dopamine or dobutamine to support the heart in its hyperdynamic state. Transfusion may be necessary immediately postnatally because hemorrhage into the tumor may have occurred during the delivery.
Severely premature infants should be intubated and treated for respiratory distress with surfactant-replacement therapy. Echocardiography should be obtained to assess the cardiac status of the newborn. Abdominal ultrasound examination can be performed at the bedside to assess the intrapelvic extent of tumor. If there is no high-output state then there is no urgency to resect the tumor and attention should focus on the treatment of respiratory distress and correction of anemia. If a hyperdynamic state exists with an elevated cardiac output, attention should focus on supporting the newborn heart with inotropic agents and urgent resection of the SCT.
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Ob/Gyn Obstetrics & Gynecology
Cardiology - Pediatric, Pediatrics
Maternal-Fetal Medicine, Ob/Gyn Obstetrics & Gynecology