Amniotic fluid diseases
Normal amniotic fluid dynamics
• Before the eighth week, the amniotic fluid is formed by the fluid transuded from the amniotic and fetal skin. During the second trimester, the fetus begins urinating, swallowing, and inspiring amniotic fluid, but before the second trimester, the major source of amniotic fluid is not fetal urine. In the third trimester of pregnancy, while the main mechanism in amniotic fluid production is fetal urine, fetal swallowing plays a fundamental role in resorption {
• Normally, amniotic fluid volume becomes 30 ml at the 10th week, 200 ml at the 16th week, and 800 ml in the middle of the third trimester. It decreases after 36 weeks of gestation and decreases below 200 ml at 42 weeks of gestation.
functions of amniotic fluid
1. Protecting the fetus from external trauma
2. Protecting the umbilical cord from compression
3. Ensuring the development of the fetal musculoskeletal system by allowing fetal movements
4. Contributing to fetal pulmonary development
5. Lubricating fetal skin
6. Protect from chorioamnionitis and fetal infection due to its bacteriostatic property
7. Aiding fetal temperature control
• Measurement of amniotic fluid:
► Amniotic fluid index (ASI): The uterus is divided into 4 equal quadrants and the largest vertical depth in each quadrant is measured and summed. ASI: If S is 5 cm, oligohydramnios; If ASI 2:: 25 cm, hydramnios is diagnosed.
► Measurement of the deepest single amnion pocket: The normal value of the deepest vertical pocket is 2-8 cm
between.
hydramnios
etiology
► The degree and prognosis of hydramnios are dependent on the etiological factor. Hydramnios is most commonly observed as idiopathic (50%). Cases of hydramnios with determined causative agents are usually associated with fetal malformations, especially CNS and GIS.
0 Common reasons·
- GIS anomalies (esophageal atresia)
- CNS anomalies (anencephaly, spina bifida)
- Maternal diabetes
- Non-immune hydrops fetalis and isoimmunization
- Chromosomal anomalies; Trisomy 18 should be considered in case of IUGR and polyhydramnios.
- Thoracic anomalies (cystic adenomatoid malformation, pulmonary sequestration and diaphragmatic hernia)
- Skeletal system anomalies
- Cardiac malformations
- Multiple pregnancies (twin to twin transfusion syndrome)
0 Rare causes:
- Pseudohypoaldosteronism, fetal Batter syndrome (hyperprostaglandin E syndrome), fetal nephrogenic diabetes insipidus, placental chorioangioma, fetal sacrococcygeal teratoma, maternal substance abuse, congenital infections (parvovirus, CMV, syphilis and toxoplasma), fetal mesoblastic nephroma.
Complications
► Edema of lower extremities, vulva and abdominal wall
► Dyspnea
► Ureteral pressure
► Ablation placenta (detachment)
► Uterine atony
► Increased cesarean rate as a result of malpresentations
► Preterm action
► Cord prolapse
► Increase in perinatal mortality
Treatment
► Mild hydramnios rarely requires treatment. Antepartum treatment options are limited. Indomethacin reduces the amount of fetal urine; however, it causes premature closure of the ductus arteriosus, so it cannot be used after 34 weeks.
► Removal of fluid with amnioreduction is only temporarily effective. Controlled amniotomy during labor can reduce the incidence of complications resulting from rapid decompression (ablation placenta, cord prolapse, etc.).
Oligohydramnios
etiology
► Oligohydramnios is almost always present in cases of obstruction of the fetal urinary system and renal agenesis.
Fetal Causes
- Chromosome anomalies
- Congenital anomalies
- IUGG
- intrauterine death
- Postterm pregnancy
- Premature rupture of membranes
0 Maternal Causes
- Uteroplacental insufficiency
- hypertension
- Preeclampsia
- Overt diabetes
- AFAS
0 Placental Causes
- Ablation placenta (detachment)
- Twin-to-twin transfusion
0 Drugs
- Prostaglandin synthesis inhibitors
- ACE inhibitors
- Trastuzumab
0 idiopathic
15-25% of oligohydramnios cases are associated with congenital anomalies.
Anhydramnios resulting from bilateral renal agenesis leading to extremity contractures, facial compression and pulmonary hypoplasia is called Potter's syndrome.
Complications
► Amniotic band syndrome
► Musculoskeletal deformities due to uterine compression (such as clubfoot)
► Increase in umbilical cord compression and cesarean section rate
► Pulmonary hypoplasia
Treatment
► It should be evaluated in terms of fetal anomalies and fetal growth retardation. Morbidity is increased in IUGR cases complicated with oligohydramnios. Antepartum treatment options are limited, but inutero surgery may have a chance to correct some structural defects (such as posterior urethral valve repair in male fetuses).
► Timing of delivery depends on gestational age, fetal well-being and etiology. Infusion of crystalloid solution into the amniotic cavity during labor
Cord compression can be prevented, the risk of cesarean section can be reduced and the risk of neonatal meconium aspiration can be minimized by performing (amnioinfusion). Amnioinfusion is not recommended in the treatment of oligohydramnios other than labor.
PLACENTA AND CORD ANOMALIES
Abnormal Placenta Types
• Bilobular Placenta {Plasenta Bipartita): The placenta is almost in the form of two equal lobes.
• Multilobile Placenta: It is a placenta with three or more lobes.
• Placenta Su centriata: It is the presence of one or more small accessory lobes connected to the main placenta with the fetal vessels on the membranes. It is more common in twin pregnancy. It may cause postpartum hemorrhage due to the fact that the accessory lobe remains in the uterus after delivery. It can also cause fetal bleeding by causing vasa previa. It may be related to abortions.
• Membranous Placenta: Most or all of the fetal membranes are covered with functioning villi.
• Annular Placenta The placenta is annular and sometimes the placental tissue forms a complete ring. The probability of antepartum and postpartum bleeding is increased and is associated with IUGR.
Penned Placenta {Planta Fenestrata) The disc-shaped placenta has no middle part, but often the defect contains only villous tissues and the chorionic plate remains intact.
• Extrachorial Placenta: The chorionic layer on the fetal surface of the placenta, the placenta on the maternal side! It is the condition that the peripheral surface of the placenta cannot be covered because it remains smaller than the basal layer. There are two types:
Circumvallate placenta: It is the presence of a central collapsed area on the fetal face surrounded by a thick, gray-white, degenerate decidua and fibrin-containing chorion and a double folded ring formed by the amnion. There is an increased risk of antepartum hemorrhage (both abruption and fetal hemorrhage), preterm delivery, perinatal mortality, and congenital anomalies.
Circummarginate placenta is the absence of a central collapsed area between the membrane folds in this ring. Poor clinical outcomes are less.
placentomegaly
• Etiology
► Maternal diabetes
► Severe fetal anemia
► Fetal hydrops
► Placental hemorrhage
► Erythroblastosis fetalis
► Intrauterine infections (syphilis, toxoplasmosis, CMV and parvovirus infection)
► Chromosome! anomalies
► Molar pregnancies
► Severe maternal anemia
Placental Tumors
• Gestational trophoblastic neoplasms
• Chorioangioma: It is the only benign tumor of the placenta. It may be associated with antepartum hemorrhage, preterm labor, amniotic fluid abnormalities, and IUGR, polyhydramnios, fetal anemia, and fetal heart failure.
• Metastatic tumors: Tumors that most commonly metastasize to the placenta; melanoma, leukemia, lymphoma and breast cancer. Metastatic cells are located in the intervillous space. The most common tumor that metastasizes to the fetus is melanoma.
Single Umbilical Artery
• It is due to secondary atrophy of the previously normal umbilical artery. Cases of increased incidence; diabetes, epilepsy, preeclampsia, antepartum hemorrhage, oligohydramnios, hydramnios, pregnancies with chromosomal anomalies, twin pregnancies.
• It is an isolated finding in most cases, but 1/3 of the cases have additional anomalies (most frequently cardiovascular and genitourinary anomalies). In addition, there is no increase in the risk of aneuploidy unless other structural anomalies are accompanied.
• It may also be associated with IUGR and perinatal mortality.
Cord insertion Anomalies
Marginal insertion (Battledore placenta)
► It is the insertion of the cord into the edge of the placenta. It is common in multiple pregnancies and ivf pregnancies. Marginal insertion rarely causes problems.
Valemento (membranous) insertion
► Umbilical vessels separate from the umbilical cord away from the edge of the placenta and reach the placenta only surrounded by the amniotic remnant. The incidence increases in placenta previa and multiple pregnancies. The risk of vasa previa is high. A low apgar score may be associated with stillbirth, preterm birth, and SGA.
ANTEPARTUM BLEEDINGS
• Bleeding in the genital system after the 28th week. It is one of the important causes of maternal mortality.
Causes of antepartum bleeding
Obstetrical Causes (95%)---------------------Non-obstetrics (5%)
Ablation placenta (30-50%)------------------- Cervicitis, cervical erosion and polyps
Placenta previ-a (-10-15%)-------------------- Vaginal laceration, trauma and varicose veins
Yasa previa / Velamentous insertion---------- Vaginal malignant/benign neoplasms
Uterine rupture------------------------------------Cervical malignant/-ben-ign neoplasms -
--------------------------------------------------------Coagulation disorders
The most common cause of antepartum hemorrhages is detachment.
Detachment (Ablation - Abruptio Placenta)
• It is the early separation of the placenta from the implantation site before the birth of the fetus. Separation can be total or partial. 37-39 of pregnancy most. observed between weeks.
Risk factors
Ablation Placenta Risk Factors Relative Risk
1. Ablation history -------------------------------► 10-188
2. Low birth weight-----------------------► 14
3. Multiple pregnancies ---------------------------------► 2 - 8
4. Hydramnios-----------------------------------------► 2 - 8
5. Preterm premature rupture of membranes -------------------- 2.4 - 4.9
6. Preeclampsia--------------------------------► 2.1- 4.0
7. Single umbilical artery------------------------------► 3,4
8. Chorioamnionitis------------------------------------------- 3
9. Chronic hypertension------------------------► 1.8 - 3
1 O. Advanced age (> 35) and multiparity -----------------► 1.3- 2.3
11. Smoking ------------------------------------------------► 1.4- 1.9
12. Cocaine -------------------------------------------► -
13. Leiomyoma (at implantation site)-------------► -
The most increasing risk in the etiology of detachment: history of detachment
Pathology
► It begins with bleeding into the decidua basalis. The decidua then separates, leaving a thin layer adjacent to the myometrium. The result is a decidual hematoma. Retroplacental hematoma enlarges and causes separation of the adjacent placenta.
► Bleeding is almost always maternal (because the separation occurs in the maternal decidua), but fetal bleeding may also occur in traumatic cases (from the placental damaged area).
Clinic
► Vaginal bleeding: Accumulated blood can separate the membranes from the uterine wall and external bleeding may occur (78%) (overt bleeding) or remain completely inside the uterus (occult bleeding). While there is overt bleeding and the fetus may not be in danger, there may be no overt bleeding and the fetus may be lost.
► Courvelaire uterus (uteroplacental apoplexy): Widespread extravasation to the uterine musculature and below the serosa. It may rarely cause uterine atony and is not an indication for hysterectomy.
► There is uterine tenderness, frequent uterine contractions and hypertonicity (uterus tetanic and contracted) (66%). For this reason, preterm labor may be misdiagnosed (20%) until fetal distress develops.
► Fetal distress is common (60%) and fetal death may occur.
► In severe cases, hypovolemic shock, acute renal failure and Sheehan's syndrome may occur due to bleeding. Detachment is the most common cause of acute cortical necrosis in pregnancy.
► The most common cause of DIC due to obstetric causes is detachment. The risk is greater in occult separation and is less common when the fetus is alive. It develops as a result of tissue thromboplastins passing into the maternal circulation.
Diagnosis and Differential Diagnosis
► In live pregnancies with vaginal bleeding, placenta previa and other causes of bleeding should be excluded by ultrasonography. However, the diagnosis of abruptio placentae, especially in the early period, can be made rarely (2%) by ultrasonography. MR imaging is very successful in the diagnosis of detachment.
► Painful uterine bleeding should suggest detachment and painless bleeding should suggest previa; however, it should not be forgotten that painful bleeding may occur in preterm labor accompanied by placenta previa.
► Depending on the level of bleeding, anemia and thrombocytopenia can be observed among the laboratory findings. While fibrinogen and coagulation factors decrease, fibrin degradation products may increase. Coagulation tests are helpful in diagnosis.
Treatment
► In the presence of a history of detachment, delivery should be planned at 37-38 weeks. In other patients, treatment should be tailored to the gestational age and the condition of the mother and fetus.
0 Approach in term pregnant: If the fetus is not live and vaginal delivery is not close, emergency cesarean section is preferred.
0 Approach in preterm pregnancy: Obvious placenta! Tocolysis is contraindicated in separations.
► Mode of delivery: If the fetus is alive but in distress, it should be delivered by cesarean section. Vaginal delivery is usually preferred if separation is severe enough to kill the fetus. Vaginal delivery is contraindicated in the presence of severe bleeding and other obstetric complications that cannot be overcome even with intensive blood replacement.
Complications
► Maternal complications:
0 Increased maternal mortality (0.5%-5%) (hemorrhage, heart and kidney failure). Clinically significant coagulopathy (DIC) may be seen in 10% of cases.
► Fetal complications:
0 Perinatal morbidity and mortality increase. Fetal mortality in severe detachments is 50%-SO. Causes of high mortality; placenta! separation, preterm birth, and an increase in the incidence of IUGG. Survivors have an increased risk of significant neurological sequelae.
0 Increase in congenital anomalies
The incidence of malpresentation does not increase in ablation.
PLACENTA PREVIA
• It is the placement of the placenta on or very close to the internal cervical os. Incidence of l'dit per 300 births
• Classification of placenta previa;
► Placenta previa: Internal cervical os completely {total) or partially
It is closed with a (partial) placenta.
► Lower placed placenta: The internal cervical os is not covered by the placenta, but the tip of the placenta is closer than 2 cm to the internal cervical os.
Risk factors
► History of placenta previa
► advanced maternal age; Incidence after 35 years 1:100
► Multiparity
► Multiple pregnancy (40%)
► previous cesarean section history (the higher the number, the higher the risk;)
► Cigarettes (increase 2 times)
► Uterine leiomyomas
► History of curettage
► Assisted reproductive techniques
Clinic
► It is characterized by painless, red vaginal bleeding and the bleeding is of maternal origin. Bleeding is not usually seen until the end of the second trimester or later. Bleeding can range from mild to severe but usually stops spontaneously to recur.
► Coagulation disorders are very rare, even with excessive separation; because tissue thromboplastins are expelled with bleeding.
► Bleeding may continue after the placenta is removed. It may even be associated with placental invasion defects.
The risk of placental invasion anomalies (acreta, increta, percreta) increases in pregnant women with a previous cesarean section history and diagnosed with placenta previa.
► Fetal malpresentation is common because the placenta prevents engagement of the presenting part.
tan
► Placenta previa must be ruled out ultrasonographically in pregnant women who have bleeding in the second half of pregnancy. Placental localization can almost always be determined by ultrasonography i. MRI can be used if a clear diagnosis cannot be made by ultrasonography or in the presence of a posteriorly located placenta. MRI is also helpful in the diagnosis of placenta accreta.
► Placenta previa is observed in 30% of the cases in the first half of pregnancy. In most of these cases, the placenta is pulled upward while the lower uterine segment is formed. Therefore, the diagnosis of placenta previa should be made after the 24th gestational week.
T d vi
► Birth 36-38. should be planned in the week and all cases with placenta previa are cesarean section.
should be born with
► In case of severe bleeding, delivery should be considered regardless of gestational age. In the absence of severe bleeding, the decision is made according to the condition of the fetus. If the fetus is mature; birth should be planned. If the fetus is premature and there is no other indication for delivery, close follow-up can be done. Tocolysis can be performed if necessary during follow-up.
Complications
Maternal complications:
0 Maternal mortality and morbidity have increased. Neonate options:
0 Preterm birth
0 IUGR
0 2.5-fold increase in congenital anomaly risk
Vasa Previa
• It is the presence of fetal vessels on the cervical os, passing through the membranes. It is bleeding from the umbilical vessels and the bleeding is of fetal origin.
• The placenta type with the highest risk of vasa previa is velamentous (membranous) insertion. There is also an increased risk of placenta suxentriata and bilobular placenta. Other conditions that increase the risk are placenta previa (2nd trimester), IVF pregnancies and multiple pregnancies.
• Fetal mortality is 75% due to fetal blood loss. 34-35 in case of prenatal diagnosis. Elective cesarean section should be performed during the gestational week. The diagnosis can also be made in case of heavy bleeding in light red color with the discharge of amniotic fluid following amniotomy during labor. In this case, an emergency cesarean section should be performed.
EARLY MEMBRANE RUPTURE AND PRETERM ACTION
Fetal Lung Maturation
• Respiratory distress syndrome (RDS) occurs due to pulmonary surfactant deficiency. Surfactant prevents alveolar collapse and consists mainly of phospholipids (dipalmitoyl-lecithin, phosphatidyl glycerol (PG) and phosphatidyl inositol
{Pi). Fetal cortisol stimulates surfactant synthesis, while insulin inhibits it.
• Amniotic fluid taken by amniocentesis is used in fetal lung maturation tests.
Lung maturation tests
► Lecithin / sphingomyelin ratio: 32-34 of pregnancy. After the first week, the lecithin level starts to rise rapidly and if the L/S ratio is above 2, the lungs are highly mature.
► Phosphatidylglycerol (PG): Phosphatidylglycerol is not seen in the amnion until the 35th gestational week, then its amount increases. In PG amniocentesis fluid (+), the lungs are mature, (-) they are immature.
► Fluorescent polarization test: Amniotic fluid is put into an automatic device without centrifugation and 30 min. It gives results according to the surfactant/albumin ratio. When the ratio is above 55, 100% lungs are mature. It gives better results than any of the other tests. It is also successful in diabetic women and those with blood contamination.
► Foam stability (shaking) test: It is based on the ability of the surfactant to form stable foam with 1 ml of amniotic fluid + 1 ml of 95% ethanol.
► Coverslip cell count: It is a fast and effective method.
Lung maturation induction
► 24-34. Corticosteroids should be administered to increase lung maturation (surfactant synthesis) in cases where delivery is expected in gestational weeks. Steroid administration can also be considered in pregnancies at 23 weeks of expected delivery. The benefit of using steroids after 34 weeks is controversial. Some authors 34-37. recommends a single dose of steroids, if it has not been done before, between weeks.
► Corticosteroids; RDS, intraventricular hemorrhage, necrotizing enterocolitis,
and reduces neonatal mortality. steroid therapy bronchopulmonary dysplasia
does not reduce the incidence
► Useful even 4 hours after application; however, preferably 48 hours are desired. Betamethasone or dexamethasone is used as iM. Repeated doses are not recommended as they may slightly increase the risk of cerebral palsy. Prednisone is not given for this purpose as it does not cross the placenta.
Premature Membrane Rupture (EMR)
• It is the rupture of membranes before labor starts after 37 weeks of pregnancy. If membrane rupture occurs before 37 weeks of gestation, it is called preterm premature rupture of membranes. Spontaneous rupture of membranes occurs physiologically at the end of the first stage of labor.
• Active labor often begins immediately after the arrival of the amniotic fluid. If there is still no delivery 12-24 hours after the waters come, the possibility of intrauterine infection increases significantly.
etiology
► Idiopathic (most common)
► History of premature rupture of membranes
► Intraamniotic infections (considered as the most important risk factor)
► Unexplained vaginal bleeding
► Low socioeconomic level
► Low body mass index (< 19.8)
► Nutritional disorders
► Smoking
tan
► It is placed clinically. Vaginal fluid accumulation and turning the litmus (nitrazine) paper blue of the vaginal fluid is valuable in sterile speculum examination. The pH of the vaginal secretions is 4.5-6.0, while the pH of the amniotic fluid is 7.1-7.3. The microscopic ferning pattern (which crystallizes when dry) is also significant. Decreased amniotic fluid index in abdominal ultrasonography also supports the diagnosis (I).
Complications
eona I o m ions depend on the severity of prematurity and oligohydramnios. These include RDS, intraventricular hemorrhage, periventricular leukomalacia, sepsis, convulsions, pulmonary hypoplasia (only at or below 23 weeks), cord prolapse, extremity deformities (related to the duration and severity of oligohydramnios).
Matern I complications: Chorioamnionitis and postpartum endometritis.
► Chorioamnionitis when one or more of the following clinical findings are present
diagnosis is made.
Fever above 0 38°C (the most important and only reliable finding suggesting the development of chorioamnionitis)
0 Maternal leukocytosis (> 18,000/mm3) (Unreliable alone.)
0 Foul-smelling vaginal discharge
0 Maternal (100 beats/min) and/or fetal tachycardia (more than 160 beats/min)
0 Uterine tenderness
0 CRP increase in amniotic fluid, leukocyte increase, IL-6 increase, glucose decrease, positive Gram staining and culture/catalase positivity (N ı ı J
Routine amniocentesis is not recommended to detect infection, but a negative result on Gram staining of amniotic fluid excludes the presence of bacteria in 99% amniotic fluid. In addition, culture negativity is the most reliable method to exclude the presence of bacteria.
► Risk factors for chorioamnionitis;
0 prolonged EMR
0 prolonged action
0 Multiple vaginal exams
0 low parity
0 Internal fetal monitoring
0 Bacterial vaginosis
► In all cases with clinical diagnosis of chorioamnionitis, emergency delivery is the basis of treatment to minimize the infectious morbidity of mother and baby, regardless of gestational age . If there are no signs of fetal distress in monitoring with NST, labor is induced and the patient is delivered vaginally. However, if there are signs of fetal distress, cesarean section is preferred.
► Broad-spectrum antibiotics are given to the mother in the intrapartum and postpartum period.
Group B and D streptococci are most commonly isolated in amniotic fluid culture in chorioamnionitis.
Treatment
|
EMR'de
tedavi yaklasım |
|
|
Gestasyonel yaÅŸ |
treatment approach |
|
34 hafta ve üstü |
Birth; Induction if no contraindications |
|
24 ile 33 haftalar arası |
Follow-up until lung maturity (34 weeks) |
|
24. haftanın alti |
Follow-up or termination under 24 weeks should be
based on the family's decision. |
In premature rupture of membranes; ampicillin + erythromycin (7 days), ampicillin
± sulbactam (3-7 days) or erythromycin can be used. Amoxicillin + clavulanate should not be used because it increases the risk of NEC.
Preterm Action
• It is the onset of labor before 37 weeks of gestation. 34-36 days of labor. It is called late preterm labor and it constitutes 70-75% of all preterm labors. Preterm labor is the most common cause of perinatal morbidity and mortality.
Causes of preterm birth
► There are 4 main causes directly related to preterm birth:
0 Unexplained (idiopathic) spontaneous preterm birth without membrane rupture (40-45%)
0 Preterm premature rupture of membranes (30-35%)
0 Preterm births due to maternal or fetal indication (30-35%)
0 Multiple pregnancies
Risk factors
► History of preterm labor; It is a major risk factor and the risk increases 3 times.
► Intrauterine infections (25-40%)
► Bacterial vaginosis
► Abortion imminens
► Smoking, illegal drug use
► Young or advanced maternal age
► Low socioeconomic level, insufficient weight gain, vitamin C deficiency, obesity
► Heavy working conditions
► Psychological factors such as depression, anxiety, chronic stress
► Physical trauma
► Black race and short stature
► Chronic periodontal diseases
► Congenital anomalies
► < 18th month or >59th of pregnancy interval. be the moon
The most frequently isolated microorganisms in amniotic fluid in cases of preterm labor are; Ureaplasma urealyticum, Gardnerella vaginalis, Fusobacterium and Mycoplasma hominis
Diagnosis
► For a definitive diagnosis, uterine contractions (4 in 20 minutes or 8 in 60 minutes), cervical dilation (more than 1 cm) and cervical effacement (80% and above) are required.
► Another approach is to measure the cervical canal length by ultrasonography.
While it is normal to be >35 mm at the 24th gestational week; If it is <25 mm, cervical length is shortened. Funneling of the cervix on ultrasound is a harbinger of preterm labor.
► Detection of fetal fibronectin, a glycoprotein secreted from the amnion, in the cervicovaginal fluid before the 37th week of pregnancy is also a powerful method for diagnosing preterm labor.
prophylaxis
► Prophylaxis can be successful in selected patients. For this purpose, progesterone or
cervical cerclage can be used.
0 Progesterone can be given IM or vaginally between 16-36 weeks in pregnant women with a history of spontaneous preterm delivery.
0 In patients with a cervical length of <25 mm and a history of preterm birth, cervical cerclage should be applied in addition to progesterone.
Treatment
► Tocolytic agents; They do not significantly prolong the gestation period. and they are used to temporarily stop uterine contractions and to gain 48 hours for corticosteroids to take effect.
► Routine antibiotic use has no place in the treatment of preterm labor.
Preterm marriage treatment approach
Gestational grief -----------Treatment
34th week and above: Fetal monitoring and fetal follow-up, between 34-37 weeks; Never done job corticosteroid
24 to 33 weeks: Group B streptococcal prophylaxis, Corticosteroid, 24-31 weeks; magnesium sulfate for neuroprotection (if delivery is planned), Tocolysis
Below 24 weeks: Pregnancy is terminated
Tocolytics and their maternal-fetal effects
MgSO4
Maternal effect:
hypermagnesemia
pulmonary edema
cardiac arrest
hot flashes
diplopia
Fetal effect:
Protects against cerebral palsy (neuroprotective between 24-31 weeks)
Ca channel blockers
Maternal effect: None
Fetal effect: Reliable
Pg inhibitors (Indomethacin)
Maternal effect:
Oligohydramnios
Fetal effect:
Closure of the ductus arteriosus
Necrotizing enterocolitis
Intraventricular bleeding
Beta-mimetics (Ritodrin, Terbutaline)
Maternal effect:
Sodium and water retention
hypokalemia
pulmonary edema
cardiac arrhythmia
MI
Maternal sepsis
hyperglycemia
Fetal effect:
Myocardial necrosis
Oxytocin antagonist (Atosiban)
Maternal effect: none
Fetal effect: increased neonatal morbidity
Oral terbutaline has no tocolytic effect.
· Beta mimetics should not be preferred in diabetics as they disrupt glucose regulation
POSTTERM PREGNANCY
• It is the name given to the fact that the birth has not occurred despite the completion of the 42nd week (294th day) of the pregnancy.
• The most effective method in determining or confirming the gestational age is the first trimester ultrasonographic measurement. If available, the last menstrual period and first trimester ultrasonographic measurements are compared. The only exception to this is the pregnancies that occur with assisted reproductive techniques, and the embryo age or transfer date is used to determine the gestational age in these pregnancies.
Risk factors
• Postterm pregnancy history (the situation that increases the risk the most}
• Those with a body mass index of 25 and above
• Nulliparity
• Fetal anencephaly
• Fetal adrenal hypoplasia
• X-dependent placenta! sulfatase deficiency
Complications
• Oligohydramnios
• Macrosomia
• Fetal distress
• Placenta! failure
• Meconium aspiration
• Increase in cesarean section rate
Treatment
• If there is no hypertension, oligohydramnios or decreased fetal movements, normal pregnancy follow-up is performed until the 42nd week is completed. If labor has not started yet, an induction delivery is performed.
FETAL DEVELOPMENT DISORDERS
Normal Fe I growth
• Cellular hyperplasia in the first 16 weeks of fetal growth during pregnancy, 16-32. Cellular hyperplasia and hypertrophy are effective in weeks, and cellular hypertrophy is effective from 32 weeks to delivery.
• Those that are effective in fetal growth; insulin, IGF 1-11, leptin. Leptin increases during the first two trimesters of pregnancy and correlates with birth weight.
Developmental Retardation
• Fetal weight below the 10th percentile (2 standard deviations) for gestational age is defined as small for gestational age (SGA), and perinatal morbidity and mortality increase significantly below the 3rd percentile. A history of IUGG increases the risk of recurrence by 20%.
• Intrauterine growth restriction is classified as symmetrical and asymmetrical.
► Symmetrical growth retardation (20%): Both cell number and cell size decrease due to factors in early pregnancy weeks. This results in a proportional reduction in both head and body size. It can be seen in the presence of chemical exposure, viral infections or aneuploidy.
► Asymmetric growth retardation (80%): As a result of uteroplacental insufficiency due to factors in late pregnancy, cell size is affected, not cell number. Accordingly, while normal brain and head development continues (brain protective effect), abdominal circumference (liver size) measurements are delayed.
Risk factors
► Non-pathological factors affecting birth weight include maternal and paternal height and weight, parity, ethnicity, geographical location and fetal sex.
0 Fetal Causes
- Genetic factors: Autosomal trisomies (t18, t13, t22, t21), Turner syndrome, osteogenesis imperfecta and chondrodystrophies
- Fetal structural anomalies: Gastroschisis
- Multiple pregnancies
Trisomy 18 can cause severe IUGR, while Klinefelter syndrome does not.
Uteroplacental Causes
- Preeclampsia, chronic vascular diseases, chronic hypertension, placenta previa, chronic ablation placenta, placenta! infarct, placenta circumvallata, chorioangioma, marginal or velamentous location of umbilical cord, umbilical artery thrombosis
0 Maternal Causes
- History of giving birth to a baby with IUGR
- The mother is small
- Malnutrition
- A history of infertility
- AFAS
- Infections (Rubella, CMV infection, hepatitis A, hepatitis B, listeria, tuberculosis, syphilis, toxoplasma, malaria)
- Teratogens (anticonvulsants, antineoplastics, smoking, alcohol, opiates, cocaine, caffeine)
- Diseases (CKD, hypertension-related chronic nephropathy, asthma, cyanotic heart diseases, sickle cell anemia, pregestational diabetes)
- Living at high altitude
physiopathology
► As a result of the effect on uteroplacental blood flow, insufficient nutrients (glucose, amino acids) pass to the fetus. First, subcutaneous tissue, liver stores, skeletal system development stops, then vital organs (brain, heart, kidney) stop their development.
► As a result, hypoxia, acidosis and death develop in the fetus.
GLUT-3 expression in the placenta increases in intrauterine growth retardation.
Diagnosis
► The most important factor in the diagnosis of growth retardation is the correct calculation of the gestational age. Ultrasonography performed in the early period (10-12 weeks) is more valuable than the last menstrual period in determining the gestational age.
► In the ultrasonographic determination of gestational age, the head-rump distance (CRL) in the first trimester gives the most valuable information. Abdominal circumference (AC) is the most valuable parameter for fetal growth and weight. It is recommended to use the HC/AC ratio in the determination of symmetric-asymmetric growth retardation.
► In ultrasonography, amniotic fluid index and Doppler flow velocity should also be evaluated. Perinatal mortality increases as the amniotic fluid index decreases (oligohydramnios).
► End-diastolic flow loss and reverse flow pattern are associated with developmental delay in Doppler USG.
► According to the severity of the retardation in the Doppler flow pattern, the affected vessels are respectively; umbilical artery, middle cerebral artery (MCA), aorta, pulmonary artery and ductus venosus. Defects in the ductus venosus doppler indicate myocardial damage and acidemia.
The most important cardiovascular parameter in predicting newborn outcomes
ductus venosus Doppleri.
Treatment
► IUGR near term (>=34th week):
0 If there is oligohydramnios or NST disorder over the 34th week, or if there is a defect in the umbilical artery Doppler examination, delivery is performed. Except in these situations, follow-up is recommended.
IUGR far from term (< 34 weeks):
0 If there is NST disorder or reverse flow in umbilical artery Doppler before 34 weeks, delivery is performed. If the NST, biophysical profile and Doppler are normal and the fetus continues to grow, follow-up is continued until fetal maturity is achieved.
,. Labor and birth:
The incidence of cesarean section has increased in 0 IUGR pregnancies. Because the placenta! insufficiency becomes evident in labor and if oligohydramnios is present, the risk of cord compression is increased.
macrosomia
• Fetal macrosomia is defined as an absolute birth weight of 4.500 g and above. Fetal macrosomia affects all organs of the fetus except the brain. f, J0J
Risk factors
► Obesity
► Diabetes {gestational and Type 2)
► Postterm pregnancy
► Multiparity
► Large parents and gaining a lot of weight during pregnancy
► Advanced maternal age
► History of previous macrosomic birth
► Racial and ethnic factors
Complications
► Macrosomic fetuses have a high risk of birth trauma, especially shoulder dystocia and brachial plexus paralysis.
► Increased maternal morbidity due to the delivery of a macrosomic baby is mainly related to the incidence of cesarean section. Other maternal complications are postpartum hemorrhage, perineal trauma and puerperal infection.
Treatment
► In order to prevent shoulder dystocia, elective cesarean section should be performed when the estimated birth weight is 5000 g and above (for diabetics, it should be 4500 g and above).
HYDROPS FETALIS
• It is edema of the fetus. There is abnormal accumulation of fluid in multiple fetal extravascular compartments such as the abdomen, thorax, and skin. It is often accompanied by hydramnios and a hydropic thickened placenta.
• Prenatal diagnosis can be made in 60% of cases with effusion in two or more regions (pleural, pericardial, or ascites) or anasarca-like edema accompanying effusion in one region on ultrasonography.
Non-immune Hydrops Fetalis
• It constitutes 90% of all hydrops. It is hydrops that develops without an immune etiology. While the most common cause of non-immune hydrops fetalis is cardiac anomalies (22%), the most common infection causing non-immune hydrops is parvovirus B-19 infection.
• Etiology
► Cardiovascular anatomical and functional causes (21%): Structural defects (Ebstein anomaly, tetralogy of Fallot, hypoplastic left and right heart, premature closure of ductus arteriosus), arteriovenous malformations (vein of galena aneurysm), cardiomyopathies, tachyarrhythmias, bradycardia (heterotaxy syndrome, maternal SLE)
► Chromosomal anomalies (13%): Turner syndrome, triploidy, trisomy 21,18 and 13
► Hematological causes (10%): α-thalassemia, erythrocyte enzyme and membrane diseases, fetomaternal hemorrhage, erythrocyte aplasia/dyserythropoiesis, decrease in erythrocyte production (myeloproliferative diseases)
► Lymphatic anomalies (8%): Cystic hygroma, systemic and pulmonary lymphangiectasia
► Infections (7%): Parvovirus, syphilis, cytomegalovirus, toxoplasmosis, Rubella, Enterovirus, Varicella, HSV, Coxacivirus, Listeriosis, Leptospirosis, Chagas disease, Lyme disease
► Syndromes (5%): Arthrogryposis multiplex congenita, lethal multiple pterygium, congenital lymphedema, myotonic dystrophy type I, Neu-Laxova, Noonan, Pena-Shokeir syndrome
► Thoracic anomalies (5%): Cystic adenomatoid malformation, pulmonary sequestration, diaphragmatic hernia, hydro and chylothorax, congenital airway obstructions, mediastinal tumors, skeletal dysplasias with small thorax
► Placental, cord and twinning-related anomalies (5%): Placenta! chorioangioma, twin-to-twin transfusion syndrome, TRAP sequence, twin anemia polycythemia sequence, thrombosis of cord vessels
► Other rare diseases (5%): Neonatal metabolic diseases (Gaucher's disease, galactosidosis, GM1 gangliosidosis, sialidosis, mucopolysaccharidosis, mucolipidosis), tumors (sacrococcygeal teratoma, Kassabach-Merritt Syndrome accompanied by hemangioendothelioma)
► Renal and urinary system causes (2%): Renal malformations, bladder outlet obstruction, congenital nephrosis, Bartter syndrome, mesoblastic nephroma
► Gastrointestinal causes (1%); Meconium peritonitis, gastrointestinal tract obstruction
► Idiopathic (18%)
• The frequencies of the factors change according to the period of diagnosis;
► In cases diagnosed prenatally, the most common factors are aneuploidies (20%), cardiac anomalies (15%) and infections (14%).
► About half of the cases diagnosed before the 24th gestational week are accompanied by chromosomal anomalies, the most common being Turner syndrome (45XO) and often cystic hygroma is present.
• The prognosis varies according to the etiology, while it is quite poor in alpha thalassemias; those due to infection, chylothorax and tachyarrhythmias can be cured with treatment;
Immune Hydrops Fetalis (RH Isoimmunization)
• Also known as erythroblastosis fetalis. It constitutes 10% of hydrops. Immune hydrops occurs when fetal erythrocytes carry a protein not found in maternal erythrocytes, and protein D is the most antigenic structure on erythrocytes. It is also known as the Rhesus factor.
• Most cases of severe fetal anemia occur against the Kell, D, c or E antigen. Other antigens that can cause severe alloimmunization include group A Duffy, MNS and Kidd antigens. Lewis, I and group B Duffy antigen
It does not cause hemolytic disease.
• If the Rh (-) mother encounters Rh (+) erythrocytes, first IgM and then IgG response develops against these foreign proteins. IgG antibodies formed can cross the placenta and hemolyze fetal erythrocytes, which may cause fetal anemia and high-output cardiac failure. Therefore, Rh incompatibility affects the next pregnancies; however, it can also be seen in first pregnancies since sensitization may occur for reasons other than pregnancy.
etiology
Conditions that may cause fetomaternal hemorrhage that may cause sensitization in the mother
Cordocentesis (state with the greatest risk of immunization)
Abortion (spontaneous or elective)
Chorionic villus sampling
amniocentesis
ectopic pregnancy
Fetal death (in any trimester)
Normal vaginal or cesarean delivery (most common cause of immunization)
external cephalic version
Ablation placenta, placenta previa and vasa previa
Abdominal trauma
Unexplained vaginal bleeding during pregnancy
Molar pregnancy evacuation
Manual removal of the placenta
Determination of fetal risk
► If the expectant mother is Rh (+), there is no fetal risk. In order to determine the fetal risk in the pregnancy of a woman with Rh (-), the father's blood group is checked first, and if Rh (-) there is no fetal risk.
► If the mother candidate is Rh (-) and the father candidate is Rh (+); Analyzing ONA-based zygosity for prenatal paternal D antigen is helpful in determining risk. If the father is homozygous positive, there is absolute fetal risk; If the father is heterozygous positive, fetal blood group determination by amniocentesis (from amniocytes by PCR) or free fetal DNA method in maternal blood should be recommended for fetal antigenic structure. If the fetal blood group is Rh (+), there is a risk; however, if Rh (-) there is no fetal risk.
► Cell-free ONA test can also be used to determine the fetal Rh status in cases with Rh incompatibility.
Diagnosis
► Antibody screening in blood type and Rh (-) patients is recommended in the first prenatal examination for all pregnant women.
► Indirect Coombs (IDC) test is a test used for the determination of free antibodies in maternal blood (E-92, E 93). In cases with positive indirect Coombs test, the titer of specific anti-D antibodies in the IgG structure is checked. The critical titer for these antibodies is 1/16 and higher titer of positivity. In cases with positivity below the critical value, the titer should be repeated every 4 weeks (S-19).
Once the critical value is exceeded, repetition is of no use and further examination is required. requires.
► Direct Coombs test is performed in fetal blood with cordocentesis for the determination of antibodies on erythrocytes in fetal circulation .
► Kleihauer-Betke test; it is a quantitative test to calculate the amount of fetal erythrocytes that have entered the maternal circulation . As hemoglobin F is resistant as a result of acid elution, fetal erythrocytes do not undergo hemolysis, while maternal erythrocytes are hemolyzed and appear in silhouette.
► The deep anemia caused by the sinusoidal heartbeat tracing in fetal monitoring leads to Ultrasonography shows placentomegaly.
Physiopathology and clinical
► The primary factor that determines the severity of acid formed in hydrops is the severity and duration of anemia. Extramedullary hemopoiesis, liver dysfunction and hypoproteinemia occur due to deep anemia and hypoxia. Colloid oncotic pressure decreases due to hypoproteinemia and capillary endothelial leakage occurs. As a result, heart failure develops due to hypoxia and decreased intravascular volume.
► Although the mother's liver has the ability to metabolize excess bilirubin, after birth the fetus, maternal and placenta! Since he is deprived of help, he cannot clear excess bilirubin from his blood and runs the risk of kernicterus (bilirubin encephalopathy) (E-02).
prophylaxis
► When there is a risk of fetomaternal hemorrhage, maternal immune response does not develop if sufficient doses of antibodies are given to the maternal circulation. If the Rh (-} mother is indirect Coombs negative, anti-D IgG must be administered at 28 weeks and within the first 72 hours after birth.Half-life is 16-24 days, with a standard dose of 300 µg, 15 ml Rh (+) fetal erythrocytes and 30 ml Contains enough IgG to neutralize fetal blood
► In only 0.2-0.3% of pregnancies, the amount of fetomaternal bleeding is more than 30 ml. In these patients, a single dose of anti-D IgG may not be sufficient. Therefore, all D-negative women should be screened at birth with the rosette test (a qualitative test that indicates the presence of fetal D-positive cells in the circulation of a D-negative woman). If the test is positive afterwards, the amount of bleeding should be determined by a quantitative test (Kleihauer-Betke Test or flow cytometry) in order to calculate the required dose of anti-D immunoglobulin.
► If the spouse of a pregnant woman with Rh (-) is Rh (+) and the pregnant woman has an indirect Coombs test (-), anti-D IgG must be performed in any situation that may cause sensitization (such as amniocentesis, chorionic villus sampling).
Treatment
► Today, amniocentesis and Liley X-rays are out of practice and replaced by fetal middle cerebral artery (MCA} Doppler examination.Detection of increased systolic velocity (> 1.5 MoM) in fetal MCA with Doppler ultrasonography, which is a completely noninvasive method, establishes the diagnosis of anemia.
► In cases with severe anemia findings (increased systolic velocity in MCA Doppler or development of hydrops findings), treatment is planned according to gestational age and fetal well-being. In order to determine the severity of anemia in preterm fetuses and to determine whether intrauterine transfusion is required, Hb and hematocrit should be measured in fetal blood sample by cordocentesis. Transfusion is recommended if fetal hematocrit is <30%.
► Intrauterine transfusion O-negative, CMV-negative, burned, irradiated and
It is performed with erythrocytes with 80% hematocrit. Today, more intravascular
transfusion is used (intraperitoneal use has decreased).
· Mirror syndrome; It is the presence of maternal edema with fetal hydrops. Edema in the mother, fetus and placenta is called triple edema.
WITH MULTIPLE PREGNANCY
ZIGOSITY
dizygotic twin
► It occurs as a result of maturation of two oocytes and fertilization by two different sperms during a single ovulatory cycle. Therefore, they are not identical. 80% of multiple pregnancies are dizygotic.
► The frequency of dizygotic twins is significantly affected by race, heredity, maternal age, parity and infertility treatments.
monozygotic twin
► It occurs as a result of the division of a single fertilized oocyte into two separate structures. Monozygotic twinning occurs with a constant frequency throughout the world (1/250 births).
► Monozygotic twinning frequency is independent of race, heredity, age and parity. Assisted reproductive techniques can increase the rate of monozygotic twinning.
· Superfecondation: It is the fertilization of two ova in the same cycle in different coituses.
Superfetation: It is the fertilization of two different ova, which are excreted in different cycles, in different coituses. This situation does not occur spontaneously in humans.
Chorionicity
• Chorionicity reflects the arrangement of membranes in multiple pregnancies. Determination of chorionicity is helpful in determining obstetric risks and in the management of multiple pregnancies.
Chorionicity in dizygotic twins
► Dizygotic twins are always dichorionic diamniotic.
Chorionicity in monozygotic scars
► Chorionicity of monozygotic twins changes according to the day of zygotic division.
0 If division occurs within the first 72 hours after fertilization; dichorionic diamniotic monozygotic twin pregnancy occurs.
0 If division occurs 4-8 days after fertilization; monochorionic diamniotic monozygotic twin pregnancy occurs. It is the most common type of monozygotic twins.
0 If division occurs 8-13 days after fertilization; monochorionic monoamniotic monozygotic twin pregnancy occurs (E J 6).
0 If division occurs after 2 weeks, the division of the embryonic disc is incomplete
and conjoined twins occur. It is the type with the highest mortality and the latest onset.
Monochorionic twins are always monozygotic.
► While chorionicity can be detected with an accuracy of 98% by ultrasonographic examination in the first trimester; In the second trimester, more than 10% of wrong evaluations can be made.
► Fetuses of different sexes are almost always dizygotic, therefore dichorionic.
► The presence of two separate placentas and a separating membrane with a thickness of >=2 mm establishes the diagnosis of dichorionicity.
► In the case of a single placenta and same-sex presence, the membranes are placenta! Examination of the starting point on the surface is helpful in diagnosis. Observing the thick chorion between the membranes establishes the diagnosis of dichorionic and indicates the fusion of the two placentas. (Twin peak finding = Lambda finding). Membrane thickness <2 mm and placenta! If the starting point on the face is thin and right-angled (T sign), it is monochorionic.
Risk factors
• Race: Caused by racial variations in FSH levels.
• Heredity: The maternal ancestry is more important and four potential gene regions have been identified. Among these, the most frequent association was seen on the long arm of the 6th chromosome, and the other gene regions were on the 7,9 and 16 chromosomes.
• Maternal age: It is the age with the highest rate of dizygotic twin pregnancies between the ages of 15-37. The incidence of twin pregnancy increases with advancing maternal age. Although there is a relationship with paternal age, its perceptible effect is quite low.
• Parity: The risk increases with increasing parity and is an independent risk factor.
• Nutrition: Those with better nutritional conditions are at increased risk. Tall and overweight women are at greater risk. The incidence may increase slightly in those with folic acid intake.
• Pituitary gonadotropin level: It is associated with high gonadotropin level. The rate of dizygotic twins increased in women who became pregnant within the first month following the discontinuation of oral contraceptive use.
• Infertility treatment: Ovulation induction significantly increases the rate of multiple ovulation (25-30%).
• Assisted reproductive techniques: The more embryos transferred, the higher the risk.
Maternal hCG, AFP and estriol levels are higher in multiple pregnancies than in singleton pregnancies.
Obstetric Complications
Spontaneous abortion
► The probability of spontaneous abortion is increased in multiple pregnancies, and the risk is higher in monochorionic twins and pregnancies with assisted reproductive techniques.
malformations
► The rate of congenital malformations is significantly increased in multiple pregnancies, and the risk is higher in monochorionic twins and pregnancies with assisted reproductive techniques. Cardiac anomaly risk is 73% higher in twin pregnancies compared to singleton pregnancies.
low birth weight
► They are more likely to have low birth weight due to IUGR and preterm labor. The degree of growth restriction is greater in monozygotic twins.
Siscordance
► Explained by more than 25% difference in estimated fetal weights between fetuses or a difference in abdominal circumferences >20 mm
Gestational hypertension and preeclampsia
► Pregnancy-related hypertensive diseases tend to be more frequent, earlier and more severe in multiple pregnancies. BMI>=30 and oocyte donation are independent risk factors for the development of preeclampsia. The risk of preeclampsia increases as the number of fetuses and placental mass increase. There is no relationship between the type of zygosity and the risk of developing preeclampsia.
preterm action
► As the number of fetuses increases, the duration of pregnancy decreases. The most important cause of neonatal morbidity and mortality in twin pregnancies is preterm birth and is seen in 50% of twin pregnancies.
Long-term effects on infant development
► There is no difference in cognitive results and general intelligence levels, but the risk of cerebral palsy is higher.
Specific Fetal Complications
cord entanglement
► It is seen in monochorionic monoamniotic twins (Åž-20).
conjoined twins
► It is seen in monozygotic twins and the most common one is thoracopagus.
twin to twin transfusion syndrome
► It is seen in monochorionic twins and originates from placental vascular anastomoses. In twin-to-twin transfusion syndrome, as a result of arteriovenous anastomosis, blood donor passes from twin to recipient with one-way flow. Recipient fetus; It is larger, has heart failure, hypertensive, polycythemic, polyhydramniotic appearance and hydrops may develop. donor fetus; growth retarded, anemic, dehydrated, hypovolemic and oligohydramniotic (stuck twin).
► Diagnosis: It is made according to two criteria;
0 Monochorionic diamniotic twin pregnancy
0 Polyhydramnios in one twin (largest vertical amniotic fluid measurement >8 cm) and oligohydramnios in the other (largest vertical amniotic fluid measurement)
<2 cm)
► Quintero Classification is used in its evaluation.
Quintero classification of twin-to-twin transfusion syndrome
• Stage I: There is discordant amniotic fluid; but the donor has urine in the bladder.
Stage II: There is no urine in the donor bladder.
Stage III: Accompanied by abnormal Doppler finding in umbilical artery, vein or ductus venosus
Stage IV: Accompanied by ascites or significant hydrops in one of the twins
· Stage V: Death of one of the twins.
► Treatment: Amnioreduction, septostomy, laser ablation of vascular anastomoses and selective fetocide
Both donor and recipient twins have an increased risk of brain injury, and cardiac functions of the recipient twin are associated with fetal outcomes.
TRAP (Twin reversed arterial perfusion)
► It is seen in monochorionic twins and originates from placental vascular anastomoses. It is caused by a large artery-to-artery and often accompanying vein-to-vein shunt.
► A donor twin with signs of heart failure and developing normally and his heart (acardia)
and other superstructures are recipient twins.
death of one of the twins
► At birth, a dead fetus may be recognized and markedly crushed (fetus compressus).
In others, the fetus may be markedly flattened (fetus papyraceous).
► The prognosis of the surviving twin depends on the gestational week at which the other twin died, the chorionicity, and the length of time between death and delivery of the living fetus. After intrauterine loss of one fetus in twin pregnancies, the risk of neurological damage such as cerebral palsy in the other baby born alive is increased.
► Risk of loss of living twin following the death of one of the twins
It is highest in monochorionics.
vanishing twin syndrome
► It is the twin syndrome lost in the early period and is seen before the second trimester in 10-40% of all twins. It is observed more frequently in pregnancies using assisted reproductive techniques. The prognosis is generally good. The neurologic prognosis of the survivor is dependent on chorionicity and the risk is greater in monochorionics. The death of one of the fetuses in late pregnancy can theoretically lead to the development of DIC, but it is rare.
Multiple pregnancy risks
Perinatal and neonatal complications ------------Maternal complications
• Preterm birth------------------------------------------ Postpartum atony bleeding
• Very low birth weight (<1500 g)--------• Preeclampsia
• Abortion------------------------------------------------ ------• Hyperemesis
• IUGG------------------------------------------------ ---------- Urinary infection
• Anomaly of presentation ---------------------------- Polyhydramnios
• Congenital anomalies---------------------------------• Abrupt placenta
• Hypoxia and trauma--------------------------------------- Placenta previa
• stillbirth----------------------------------------------- ---• Gestational diabetes
• ------------------------------------------------- ---------------------- Anemia
•------------------------------------------------ -----------------------• Depression
Antenatal Follow-up
• The need for calories, protein, minerals, vitamins and essential fatty acids has increased. Folic acid and iron replacement should be done. Serial sonographic measurements, amniotic fluid volume monitoring, NST and fetal biophysical follow-up should be performed.
• Bed rest, tocolytics, progesterone, pessary and prophylactic cervical cerclage have no significant effect for the prophylaxis of preterm labor. Side effects of tocolytics (especially 3-mimetics) to be used in the treatment of preterm labor
(tachycardia, pulmonary edema) is more common in multiple pregnancies.
The method of administration of steroids for lung maturation is the same as in singleton pregnancies.
If cervical length is >25 mm at 24 weeks and fetal fibronectin is negative
The risk of delivery before 32 weeks is low.
labor and birth
• The recommended mode of delivery depends on the presentation of the twins, gestational age (or expected birth weight), and maternal and fetal well-being. Time of delivery in multiple pregnancies;
► 38th week in uncomplicated dichorionic twins,
► Between 34-37 weeks in uncomplicated monochorionic diamniotic twins
► 32-34 in monochorionic monoamniotic twins. week between birth is recommended.
• Head-to-head presentation is most common in term twin pregnancies (fF 9 i). Cesarean section is recommended in twins with non-vertex presentation of the first presenting fetus and in multiple pregnancies with more than two numbers.
Locking at birth: If the first baby is breech and the second baby is head, the jaws can be locked at birth
Multifetal reduction (fetocyte): It can be done in multichorionic multiple pregnancies, and it is often used between the 10th and 13th days of pregnancy to reduce perinatal risks due to prematurity. It is the reduction of the number of fetuses that are 3 or more between weeks of pregnancy and mostly by the transabdominal route by injecting KCI. The ideal is to achieve a twin or singleton pregnancy. The most common complication is premature rupture of membranes (13%). Because of the vascular anastomoses in monochorionic multiple pregnancy, multifetal reduction can only be performed if there is a dichorionic placenta.
INTRAUTERINE FETAL DEATH
• 20 weeks or more (or 350 g and more) is the loss of the fetus before it is born.
Risk Factors -------------------roactive risk
Renal diseases------------------------------------------------ --------------------► 2.2-30.0
SLE ------------------------------------------------ --------------------------------------► 6.0-20.0
Diabetes (insulin) ---------------------------------------------- ----------------------► 1. 7 -7
Thrombophilia ------------------------------------------------ -----------------------------► 2.8-5.0
IUGG in previous pregnancy ----------------------------------------------- ------------► 2.0-4.6
severe preeclampsia ------------------------------------------------ --------------► 1.8-4.4
Pregnancy cholestasis ------------------------------------------------ -------------------► 1.8-4.4
Mild preeclampsia ------------------------------------------------ ------------------► 1.2-4.0
Triplet pregnancy ------------------------------------------------ --------------------------► 2. 8-3. 7
Maternal age > 40 ----------------------------------------------- --------------------------► 1.8-3.3
Fetal death in previous pregnancy---------------------------------------------- ------► 1.4-3.2
Thyroid diseases------------------------------------------------ -------------------► 2.2-3.0
Smoking (> 10/day) ------------------------------------------ -----------------------► 1. 7-3
BMI (> 30 ) --------------------------------------------- --------------------------------► 2.1-2.8
Chronic hypertension------------------------------------------------ --------------► 1.5-2. 7
black race------------------------------------------------ --------------------------------► 2.0-2.2
Maternal age 35-39 --------------------------------------------- -----------------------► 1.8-2.2
Diabetes (diet)---------------------------------------------- --------------------------► 1.2-2.2
Education (< 12 years)---------------------------------------------------------- --------------------------► 1.6-2.0
Diagnosis
• Decreased beta-hCG levels in early pregnancy may help in diagnosis.
• Absence of fetal heartbeats in ultrasonography is the gold standard for today .
• Microarray analysis is recommended in case of fetal chromosome examination in stillbirths.
Treatment
• Since the risk of DIC is increased in cases of intrauterine fetal death, pregnancy should be terminated and the safest method to terminate the pregnancy after the 20th week is to induce labor.
• Pregnant women with a history of fetal death in their previous pregnancy are considered risky pregnancies. Fetal monitoring is started 2 weeks before the previous week of death and elective labor induction is performed at the 39th gestational week.
OBSTETRIC REASONED CONSUMPTION COAGULOPATHY (E-06)
• Placental abruption (most common obstetric cause)
• Fetal death and delayed delivery
• Amniotic fluid embolism
• Sepsis
• Abortion
• Preeclampsia