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Amniotic fluid and it,s abnormality The amniotic fluid initially is secreted by the amnion but by the 10th week it,s mainly atransudate of fetal serum via the skin and umbilical cord ;from 16th wk. the fetal skin becomes impermeable to water and net increasein amniotic fluid is through asmall imbalance between the contributions of fluid through the kidneys and lung fluids and removal by fetal swallowing. AF increases progressively: 10 wk.:30 ml 20wk.:300ml 30wk:600ml 38wk:1000ml But post-term,there is arapid fall in volume(40wk:800ml,42wk:350ml). The reason for the late reduction in AF volume has not been explained. The function of the amniotic fluid is to : *Protect the fetus from mechanical injury. *permit movement of the fetus while preventing limb contracture. *It provides an even temperature.. *It is also bacteriostatic,providing some protection against bacteria. *prevent adhesions between fetus and amnion . *permit fetal lung development in which there is two way movement of fluid into the fetal bronchioles . Absence of AF in the second trimester is associated with pulmonary hypoplasia. *In labor,the even distribution of fluid allows for the force of uterine contraction to be applied evenly to the cervix when the presenting part is high. *The presence of AF provides the ultrasonographer with an excellent view of the fetus by transmitting sound freely. *The volume of the AF presents an important indicator of fetal condition(as in cases with increase or decrease in AF volume) *It is useful in fetal diagnosis.Access to AF by amniocentesis,chromosomal abnormalities,isoimmunization,lung maturity and infection . Abnormalities of amniotic fluid: Polyhydramnios; About 1% of pregnant women have polyhydramnia,most cases are minor and result from agradual buildup of excess fluid in the second half of pregnancy. However ,asmall number of women have arapid buildup of fluid occurring as early as 16 weeks of gestation that usually results in very early delivery. The amount of AF in the amniotic cavity is variable dependant on maternal and fetal factors,the alteration of any factor that regulate the fetomaternal equilibrium may induce an abnormal increase in AFvolume,the factors involved in this regulation are fetal swallowing,micturition,respiratory movements and uteroplacental blood flow. Causes of polyhydramnia are ; *Maternal. *Fetal. *Placental. *Idiopathic. Maternal causes;15% 1-Rh isoimmunization ;is uncommon now due to the use of Rh(D)immunoglobulin. 2-Diabetes :form about 14% of cases with polyhydramnia,the etiology is unknown,fetal hyperglycemia with polyuria and increased osmolarity of the AFcaused by high glucose concentration has been proposed *Placental causes:<1% 1-placental chorioangioma. 2-Circumvallate placenta syndrome. Fetal causes 18%: A-multiple pregnancy esp.in monozygotic twins with twin to twin transfusion syndrome,multiple pregnancy accounts for 4.9% of all cases of polyhydramnia. B-Fetal infection ,such as with parvovirus B19(which in childhood commonly causes amild illness called fifth disease) Rubella,syphilis and toxoplasmosis. C-Fetal anomalies,12.7% the most common lesions are : 1-Abnormalities of the central nervous system including anencephaly,hydrocephaly,encephalocele,spina bifida and microcephaly. 2-Gastrointestinal abnormalities:include esophageal atresia,annular pancreas,jejunal atresia,diaphragmatic hernia and duodenal atresia. 3-Genitourinary abnormalities include partial or complete urinary atresia,most commonly ureteropelvic obstruction. 4-Skeletal malformations:osteogenesis imperfecta and achondroplasia. 5-Fetal tumors:include cystic congenital adenomatoid malformation of the lung,sacrococcygeal teratoma. 6-Cardiac abnormalities:severe congenital heart disease and persistent cardiac arrhythmia. 7-Chromosomal abnormalities:the most frequent are Down syndrome and trisomies 13 and 18. 8-Genetic syndromes:include hydrocephalus syndrome,multiple congenital anomalies and myotonia dystrophica. 9-Hematological disorders:homozygous alpha thalassemia and fetomaternal hemorrhage. D-Miscellaneous:non immune hydrops fetalis. *Idiopathic causes:65% most mild cases of polyhydramnios are idiopathic. Diagnosis of polyhydramnia: 1-Clinically: *uterine size larger than expected for gestational age. *easy ballotment of the fetus. *difficulty in defining fetal parts. *faded heart tones. 2-Ultrasound:by finding apocket of fluid measuring 8cm or more in vertical diameter. The vertical measurement of the largest single pocket of amniotic fluid free of fetal parts is used to classify poly hydramnia into mild(8-11cm),moderate(12-15cm) and severe(16cm or more). Another ultrasound definition is by finding an amniotic fluid index(AFI) greater than 25cm. AFI:AFvolume is measured with the four quadrant technique which consist of measuring the largest pool of fluid found in each of the four quadrants of the uterus,the measurement are added and the result is the AFI. Traditionally any volume of AF greater than 2000ml has been considered as polyhydramnia and there is two types of polyhydramnia:either acute when it occur before 24wk of gestation or chronic when the diagnosis is made in the third trimester. Complications of polyhydramnios: Maternal complications include: 1-pregnancy induced hypertention. 2-preterm labor. 3-premature rupture of membrane. 4-respiratory discomfort. 5-Intrapartum complications include placental abruption,cord prolapse,placental insufficiency and increased incidence of ClS 6-postpartum hemorrhage. Fetal morbidity and mortality: The major cause of mortality is congenital abnormality incompatible with life. Morbidity usually is associated with minor abnormalities and with prematurity and its complications. Management: 1-U\S examination to detect congenital and placental abnormalities and to confirm gestational age. 2-Fetal karyotyping using amniocentesis,cordocentesis or placental biopsy. 3-Fetal swallowing studies are also indicated.. 4-Basic laboratory studies include maternal antibody screen,diabetic screening and TORCH serology.If these evaluations are negative ,the case should be considered as idiopathic. 5-serial amniotic fluid decompression is the treatment of choice relieves maternal discomfort and also reduces excessive intrauterine pressure that can induce preterm labor. 6-Prostaglandin synthetase inhibitors(Indomethacine) have been proven in reducing the amount of amniotic fluid,it probably acts by decreasing the fetal urinary output or by increasing the reabsorption of fluid via the lung .the dose is 2.2mg/kg/day orally every 6 hr.this treatment should be suspended at 32wk of gestation to avoid neonatal hemodynamic complications. This drug may cause fetal ductal constriction and close monitoring by serial fetal echocardiographic studies is necessary. 7-Prenatal therapy:the aim is to reduce the risk of very premature delivery,treatment will depend on the diagnosis and will include better glycemic control of maternal D.M,antiarrhythmic medication for fetal hydrops due to dysrrhythmias,thoracoamniotic shunt for fetal pulmonary cysts or pleural effusions. In twin to twin transfusion syndrome ,presenting with acute polyhydramnia at 18-22wks of gestation endoscopic laser occlusion of placental anastomoses or serial amniodrainage may be carried out. Oligohydramnios; About 4% of pregnant women have oligohydramnios,it can develop at any time during pregnancy,although it is most common in the last trimester,some 12% of women whose pregnancies last about 2wks beyond their due dates(42wks gestation) develop oligohydramnios. Defined asAFI of less than 5cm in severe cases and less than 10 cm in mild cases. Causes: 1-postterm pregnancy. 2-PROM 3-maternal health condition such as chronic hypertension,severe PET,SLE and chronic renal disease 4-fetal congenital abnormalities,such as renal agenesis,obstructive uropathy,multicystic,dysplastic kidney,skeletal dysplasia,congenital heart block and multiple anomalies. 5-certain medications,like angiotensin converting enzyme inhibitors(captopril) used to treat hypertension,can damage the fetal kidneys and cause severe oligo hydramnios and fetal death. 6-leaking fluid following amniocentesis and chorionic villi sampling. 7-uteroplacental insufficiency. Diagnosis: 1-Largest single pocket of AF being 1cm or less. 2-AFI of 5 cm. 4-in uteroplacental insufficiency,Doppler blood flow studies will often demonstrate high impedence to flow in the placental circulation and redistribution in the fetal circulation. 5-In the remaining cases,intraamniotic instillation of normal saline may help improve ultrasonographic examination and lead to the diagnosis of fetal abnormalities like renal agenesis. Risk of oligohydramnios: Oligohydramnios is more likely to have serious consequences if it occur in the first half of pregnancy than if it occur in the last trimester,these consequences include; *Birth defect:too little amniotic fluid early in pregnancy can lead to compression of fetal organs,resulting in lung and limb defects. *Miscarriage. *Premature birth. *Stillbirth. When oligo hydramnia occurs in the 2nd half of pregnancy,it may be associated with poor fetal growth.Near term it may increase the risk of complication of labor and delivery,including compression of the umbilical cord.This can deprive the baby of oxygen ,sometimes resulting in stillbirth,women with oligohydramnios are more likely than un affected women to need c/s. Treatment: Women with normal pregnancies who develop oligohydramnios near term need no treatment and their babies are likely to be born healthy,they need weekly or more frequent u/s examination to see if the level of amniotic fluid is decreasing to adangerous point that necessate termination of pregnancy. Nearly half the cases of oligohydramnios resolves themselves without treatment. Tests of fetal well being such as non stress test,if the test show that the baby is having difficulties ,then delivery help to prevent serious problems. Afetus with poor growth whose mother has oligohydramnios is at high risk of complication such as asphyxia before and during birth,mothers with these conditions are monitored very closely,they sometimes need to be hospitalized. If awoman has severe oligohydramnios near the time of delivery,infusing salty water through the cervix into the uterus(amnioinfusion) may help to reduce complications during labor and delivery and reduce the need for c/s. Some studies suggest that women with oligohydramnia can help increase their level of amniotic fluid by drinking extra water. Prognosis: The prognosis of patients with oligohydramnios in the 2nd trimester is poor because the 2 most common causes,PROM and fetal congenital anomally are not amenable to successful treatment.Also pulmonary hypoplasia occurs frequently in fetuses deprived of amniotic fluid for several weeks. The best outcomes are obtained in fetuses with severe IUGR that occasionally can be saved by early delivery and intensive neonatal care. Pulmonary hypoplasia is alethal neonatal condition characterized by small anatomically immature lungs,pulmonary hypertension and surfactant deficiency,it affects fetuses with prolonged oligohydramnios before 28wks. The option of termination of pregnancy should be offered to patients with lethal fetal abnormalities or PROM before 20wks. One exception is those patients with PROM following amniocentesis or CVS in whom recovery is the rule. For patient with PROM after fetal viability ,the management will be according to gestational age.