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136 Cards in this Set
- Front
- Back
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Ureteral Bud |
•Starts as outpouching of wolffians •Kidneys migrate up from pelvis |
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Urogenital Sinus 6 Wks Mens |
•Caudal end narrows/elongates •Forms urethra/neck of bladder |
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Allantois |
•Forms the rest of the bladder |
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Ureteral Bud Grows & Branches |
•Ureter, pelvis, calyces, tubules •W/o bud, kidneys don't form |
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Nephrons |
•10 mens wks, 3-5 bud branchings •Seen 15 wks, 13 on TV |
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Normal Kidneys |
•Hypoechoic cortex •See sinus fat & pyramids develop |
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Kidney Development |
•Pelvis may dilate, not > 6mm •NL size in Trans: 1/3 of fetal abd |
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Amniotic Fluid Volume Controlled By |
•Renal output in 2nd half of gestation •Normal with at least 1 NL kidney |
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Polyhydramnios |
•CNS ABNL, poor swallowing •Upper GI ABNL |
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Oligo in 2nd Tri |
•Poor prognosis from pulmonary hypoplasia |
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Oligo Causes |
•Demise, infection, UT anomalies, pre eclampsia, IUGR, PROM |
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AFV at 12 Wks |
•60 ml, increaes 20-26 ml/wk •16 wks: 50-100 ml/wk |
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AFV at 20 Wks |
•500 ml •Late 3rd tri: 450 ml/day |
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Before end of 2nd Tri |
•AFV > fetus volume |
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At End of 2nd Tri |
•AFV = Fetus volume |
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In 3rd Tri |
•AFV < Fetus volume |
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Fetal Bladder |
•Cystic structure in pelvis •Fills/empties every 25 mins |
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3 Areas for UT Evaluation |
•Amniotic fluid volume •For UT anomalies •Other anomalies |
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Syndromes Assoc With Urinary System |
•Meckel's, VACTERL |
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Bilateral Renal Agenesis |
•Absent ureteral bud, 1:4000 •Death from pulm hypoplasia |
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Signs of Agenesis |
•Oligo, absent bladder •Seeing bladder excludes agenesis |
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Bowel/Adrenals vs Kidneys |
•Color helps ID renal arteries •Look for hypoechoic pyramids |
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Unilateral Renal Agenesis |
•1:1000, antenatal diagnosis hard •Bowel/adrenal mistaken for kidney •Bladder fills/empties |
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Urinary Tract Dilatation |
•Can be NL physiologic •4-5 mm 15-24 wks •6-8 mm 24-30 wks •8-10 mm >30 wks |
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Pelvocaliectasis |
•Seen antenatal, f/u 48 postpartum •Can be reflux |
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Posterior Urethral Valves |
•Most common urethral obstruction •Flap of skin on post. urethra |
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Posterior Urethral Valves U/S |
•Persistent dilated bladder •Thick bladder wall, > 2mm •Severe hydro, oligo |
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Oligo with Posterior Urethral Valves |
•95% won't survive |
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UVJ Obstruction |
•Duplicated collecting system •UP obstructs, LP refluxes •Ectopic ureterocele |
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UVJ Obstruction U/S |
•Dilated pelvis, megaureter •Normal AFV, unless bilateral UVJ |
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UPJ Obstruction |
•Biggest cause of neonatal hydro •Pelvis, infundibula, calyces dilated |
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UPJ Obstruction U/S |
•Can appear as giant abd cyst •Ureters not dilated •Other kidney & bladder work |
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Unilateral UPJ Assoc With |
•Contra multicystic dysplasia, renal agenesis or oligo, if severe |
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Obstructive Renal Dysplasia(Potter's IV) |
•From UPJ, UVJ or bladder obs |
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Obstructed Renal Dysplasia U/S |
•Obstructed pelvis •Severely hyperechoic cortex •Cortical cysts |
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MCDK(Potter's II) |
•From atresia of upper uereter, pelvis, infundibulum |
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MCDK U/S |
•NV pelvis, unilateral, macrocysts •Contra renal anomalies, agenesis |
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Inherited Syndrome with MCDK |
•Meckel Gruber, short rib polydactyly, Trisomy 13 |
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PCKD |
•Rec or dom, both kidneys •Low chance of survival if severe |
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Infantile PCKD(Potter's I) |
•Autorecessive, non obstructive •Oligo, hyperechoic, large kidneys |
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Adult PCKD(Potter's III) |
•Bilateral large hyperechoic kidneys •Cysts don't dominate kidneys •Normal AFV, not seen antenatally |
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Prune Belly Syndrome |
•Urethral obstruction •Anterior abd wall distended •Cryptorchidism |
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Prune Belly U/S |
•Oligo, distended, thick bladder •Hydroureter, bilat hydro •Patent urachus, small thorax |
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Mesoblastic Nephroma |
•Mostly solid mass in kidney •May be cystic, assoc w/ poly |
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Hydrops Fetalis |
•Excessive fluid in fetus •Edema, ascites, effusions, poly |
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Fetal Ansarca |
•Generalized edema |
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Immune Hydrops |
•Maternal blood cells destroy others •Fetal cells enter maternal system |
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Immune Response Setup |
•During delivery(most common) •Fetal-maternal hemorrhage |
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Subsequent Pregnancies |
•MNL antibodies cross P-F barrier •Antibodies attach to antigens •Attack cells, fetal anemia results |
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Erythroblastosis Fetalis |
•Immature RBCs produced •Hepatomegaly, placental edema, pleural effusions |
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Hydrops Fetalis U/S |
•Ascites, skin edema, PE •Poly, placenta edema/enlargement •Pericardial effusion |
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Immune Hydrops Prevention |
•Rhogam, amniocentesis |
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Non-Immune Hydrops |
•Not immunologic, other causes •No lab tests, high mortality •Non immune if absent antibodies |
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Non-Immune Hydrops U/S |
•Same as immune •Structural anomalies, most heart •Can have oligo |
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Non-Immune Hydrops Structural Anomalies |
•Congenital lymphangiectasia, arrhythmias, CCAM |
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Non-Immune Hydrops Causes |
•TORCH, Parvovirus |
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Maternal Hypertensive Disease |
•Chronic hypertension disease •Pregnancy induced hypertension |
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Pregnancy Induced Hypertension |
•Appears late in preg, disappears postpartum |
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Pre Eclampsia |
•Hypertension, proteinuria, edema •During last 20 wks |
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Eclampsia |
•Convulsions, coma |
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PIH Onset Signs |
•Sudden weight gain/high BP, edema, proteinuria •Headaches, blurred vision, EG pain |
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PIH Fetus |
•Decreased liver blood flow •Low oxygen/nourishment •Premature labor, abruptions |
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If Patient Becomes Eclamptic |
•Deliver fetus ASAP |
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PIH U/S |
•IUGR, oligo •Hetero placenta, early separation, decreased volume, increased vasc resistance |
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Diabetes Maternal Complications |
•Hypoglycemia, poly, PIH, vasc disease, renal dysfunction |
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Diabetes Fetal Complications |
•Defects, IUGR, SUA, macrosomia |
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Assoc With SUA |
•Cardiac anomalies, pulmonary hypoplasia, polydactyly |
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IUGR |
•Uteroplacental vasc insufficiency |
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Macrosomia |
•Fetal hyperinsulinemia from maternal hyperglycemia •>4000g, or above 90th percentile |
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Gestaional Diabetes |
•Develops during pregnancy •25 in 1000 pregnancies |
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Gestational Diabetes Risk Factors |
•Previous stillbirth, F/Hx of diabetes •Prior macrosomia or anomalies |
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IUGR Considered |
•Small for gestational age •<2500g(5lbs8ozs), or 10th percentile |
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IUGR Etiologies |
•Maternal disease states •Congenital anomalies/infection •Primary placental pathology |
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Maternal Disease States |
•Diabetes mellitus, chronic HTN, Rh disease, drugs, high altitude |
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Maternal Disease States Results |
•Uteroplacental insufficiency •Poor placental perfusion •Oxygen/nutrition deprivation |
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Congenital Anomalies/Infection |
•CHD, CNS anomalies, 21, 18, 13 •TORCH |
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Primary Placental Pathology |
•Infarction, previa, abruption •Leads to uteroplacental insufficiency |
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Symmetrical IUGR |
•Proportionately small fetus •All measurments below 10th % •As early as 20 weeks MA |
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Symmetrical IUGR Causes |
•Congenital anomalies, trisomies, intrauterine infection, FAS, maternal malnutrition |
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Asymmetrical IUGR |
•Disproportion between head/body •Body severely affected, liver 1st •Brain sparing |
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Brain Sparing |
•Head last affected to prevent brain damage |
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Asymmetrical IUGR MDS |
•Chronic HTN/renal disease, severe diabetes, cardiovascular disease |
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Asymmetrical IUGR Placental Abruption |
•Smoking, drugs, multiple pregnancies |
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IUGR U/S Exam |
•Compare interval growth •HC/AC, FL/AC, FL/BPD, weight •Doppler MCA, umbilical artery |
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Uterine Artery Doppler 1st Tri |
•Persistent diastole with early notch |
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S/D Ratios |
•10 wks: 3 •13 wks: 2.6 •26 wks: 2 |
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Uterine Artery PI |
•NL: <1.24 •Abnl: >1.67 •AMA: high risk SGA, preterm |
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IUGR Treatment |
•Bed rest on left side, relieves IVC •Anti-coagulants: heparin |
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IUGR Outcomes |
•More often in males •Speech defects, CNS abnormalities |
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Fetal Maladaption Syndrome |
•Fetus unable to compensate •Oligo, abnl fetal/umbilical Doppler |
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Perinatal IUGR |
•Intrapartum fetal stress •Hypo/hyperglycemia •Hypothermia, encephalopathy |
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Childhood IUGR |
•Hypertension, poor neural outcome |
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Adult IUGR |
•Cardiovascular disease •Hypertension, diabetes |
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Multiple Gestations Incidence |
•1% of all births •Highest in blacks, lowest in Asians |
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Multiple Gestations Increases With |
•AMA, parity, heredity, fertility drugs |
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Multiple Gestations Maternal Risks |
•PIH, preterm labor, edema, 3rd tri hemorrhage, varicosities |
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Multiple Gestations Fetal Risks |
•Congenital anomalies 2× more •IUGR, discordant growth, PROM •Prematurity, RDS, cerebral hem |
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Discordant Growth |
•Smaller, > risk of prenatal anoxia •Normal growth till 31-32 wks |
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Discordant Growth U/S |
•5mm or more diff in BPD •20mm or more diff in AC •Oligo, abnl umb artery Doppler |
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Dizygotic Twins |
•Fraternal, non identical •2 chorions/2 placentas •2 amnions, thick membrane |
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Monozygotic Twins |
•Identical, 1 zygote splits •Single chorion, 1 or 2 sacs •Riskier than dizygotic |
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Twin to Twin Transfusion(Mono Only) |
•Arteriovenous shunt in placenta •Arterial blood of 1 twin pumped into venous system of other |
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TTT Donor Twin |
•Arterial shunted to recipient •Becomes hypovolemic •Stuck twin if severe |
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Hypovolemic Twin |
•Growth retarded, poor renal perfusion, anuria, severe oligo |
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TTT Recipient Twin Hypervolemic |
•Symmetrical size increase •Poly, CHF, hydrops, demise |
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TTT U/S Criteria |
•Same sex fetuses, single placenta •Thin membrane, 20% weight diff •Twin poly-oli sequence(stuck) |
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TTT Doppler |
•Decreased diastolic flow •>.4 S/D difference between twins |
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Quintero Staging System |
•Determines TTT severity •AFV, bladder size, Doppler, hydrops |
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Quintero Stage I |
•Donor twin bladder visible •Poly-oli sequence |
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Quintero Stage II |
•Collapsed/NV donor bladder •No CADS |
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Quintero Stage III |
•CADS: Absent/reverse EDS in UA, reverse DV flow, UV pulsatile |
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Quintero Stage IV |
•Fetal hydrops |
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Quintero Stage V |
•Demise of one or both twins |
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Conjoined Twins |
•Mono/mono gestations •Division after 13th day •Always same sex |
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Conjoined Twins U/S |
•Lack of separating membrane •Heads in same plane, poly •>3 vessel cord |
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Parasitic Twin(Fetus in Fetu) |
•2nd twin in sibling's abd •Benign, distinguish from teratoma |
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Parasitic Twin Characteristics |
•Benign, in upper abd •May have radiographic evidence of vertebrae |
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Teratoma vs Parasitic Twin |
•Teratoma in lower abd, ovaries or sacrococcygeal area |
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TRAP Syndrome |
•Twin Reversed Arterial Perfusion •Results in acardiac twin, 1:3500 |
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TRAP Develops |
•Anastomoses between twins through placenta •Large art-art and ven-ven shunt |
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Acardiac Twin |
•Blood enters through fetal aorta •Well developed lower body •Poor development of head/upper |
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TRAP Donor |
•20% become hydropic due to high output cardiac function |
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Genetic Defects in Mono Twins |
•Nearly 100% with genetic defects •1 normal, 1 Turner's most common •Higher risk of dev abnormalities |
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Genetic Defects Dizy Twins |
•Very low incidence since not genetically similar |
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Multi Gestation Polyhydramnios |
•5-10% of all twins •Chronic or acute |
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Chronic Polyhydramnios |
•Develops over wks in 3rd tri •Increased mortality rate(45%) |
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Acute Polyhydramnios |
•Develops over days, in wks 20-26 •Mostly in dizygotic, 100% mortality |
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Selective Termination |
•Improves best survival chance •Only on confirmed dichorionic |
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Selective Termination Process |
•Inject air into heart or UV •Exsanguination by cardiac puncture |
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Selective Termination in Mono |
•Can cause thromboplastic response from terminated into suriving •Brain/multi organ damage or death |
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Signs of Fetal Demise |
•Coarsing of outline, scalp edema, absent heart/somatic movement •Robert's, Spaulding's, Trunk |
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Coarsing of Outline |
•Edema, AF seeps into skin |
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Scalp Edema |
•May occur with severe diabetes, Rh sensitivity, fetal anemia |
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Robert's Sign |
•Gas in fetal vascular system |
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Spaulding's Sign |
•Overlapping of fetal skull bones •Unable to see falx |
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Trunk Changes |
•Difficult to ID abd organs •Compressed, coarse outline |
