PLENO GROUP 9 B

PLENO

GROUP 9 BZULHERMANRAHMI FITRIDENADA LEONAAULIA RAHMINOVA SURYATIHIDAYATURAHMIULFIA RAHMANITAFITRA KURNIAFEBY RAHMA ASTRI

Learning objective1. Vaginal Bleeding During Pregnancy2. IUGR3. Examination in pathological pregnancy

4. The maternal mortality ratio and child mortality rate5. Preeclapmsia dan eclampsi6. Treatment of pathological pregnancy7. Case referred to pregnancy

1. Vaginal Bleeding During Pregnancy

1.Bleeding in early pregnancy.2.Bleeding in late pregnancy ( ante partum hemorrhage). 3. Examination in pregnancy pathology

1-Bleeding In Early Pregnancy (Before 20 weeks Gestation)CausesAbortion.Vesicular mole.Ectopic pregnancy.Local lesions cervical polyps cervical cancer.

abortion It is the termination of pregnancy before 24 weeks, or products of conception weighing below 500 grams.

The termination is either spontaneous or induced, before the fetus develops sufficiently to survivecauses 50%-80% of abortions in the first 12 weeks of pregnanacy result from Chromosomal anomalies.FetalChromosomal anomalies.Diseases of the fertilized ovum.Hypoxia.

MaternalInfections e.g. influenza, malaria, syphilis ,HIV.Disease such as chronic nephritis,TB.Drug intake during pregnancy.Rh and ABO incompatibility.Incompetent cervix.Uterine malformation.Aquired uterine defect as uterine fibroid or adhesionsTrauma - criminal interference,Endocrinal disorder as hypothyrodism , daibetes mellitus

Patoloy of abortionFirst 8 weeks gestation Separation of decidua basalies and expulsion of the ovumIf retained within the uterus, the ovum becomes surrounded by decidua and blood clot 8-12 weeks of gestation Rupture of decidua capsularis and expuslion of the product of conception After 12 weeksRupture of membranes followed expulsion of the product of fetus and the placenta retained in uterus

Type abortionSpontaneous abortionThreatened abortion: Missed abortionInevitable abortion Complete abortion

Hydatidiform Mole (Vesicular Mole) Hydatidiform mole is a gross malformation of the trophoblast in which the chorionic villi proliferate and become avascular. causeThe exact cause is unknown.Risk factors are:Maternal age above 40 years or below 19 years.Malnutrition Types 1- partial mole 2- complete mole

Ectopic Pregnancypregnancy occurring outside the normal uterine cavity Ectopic pregnancy usually occurs 99% of cases in the uterine tube.

Tubal PregnancyCausesImpaired tubal ciliary action.Impaired tubal contractility.Decreased sperm mobility.The use of intrauterine contraceptive device.

2-Bleeding in late pregnancy Antepartum hemorrhage is defined as bleeding from the genital tract between 28th week of pregnancy and onset of labor.Classification Placenta previa Abruptio placenta Extraplacental bleeding (cervical polyp) Plasenta previaplacenta is partly or totally implanted over the lower uterine segment.

causes No specific cause can be detected for most of the cases, while the predisposing factors are:Large placentaprevious uterine scarringMultiparaDegreesComplete central placenta previa Placenta previa partialisPlacenta previa marginalis Low lying placenta

Abruptio Placenta (Accidental Hemorrhage) bleeding during the last three months of pregnancy, the first or second stage of labor, due to premature separation of a normally implantated placenta

CausesThe most important cause is hypertension.The second most common cause is traumadeficiencies in vitamins C and K.Traction on a short umbilical cord.Sudden reduction of the size of the uterus.

typesRevealed: almost all the blood expelled through the cervix.Concealed: almost all the blood is retained inside the uterus.Combined: some blood is retained inside the uterus and some is expelled through the cervix.

2. IUGRIUGR: Failure of normal fetal growth caused by multiple adverse effects on the fetus.SGA: Infant with wt < 10% ile for GA, or > 2 SDs below mean for GA.

INCIDENCE3 - 10 % of all pregnancies.20 % of stillborns are growth retarded.30 % of infants with SIDS were IUGR.1/3 of infants with BW < 2800 gms are growth retarded and not premature.9 - 27 % have anatomic and/or genetic abnormalities.Perinatal mortality is 8 - 10 times higher for these fetuses.

TYPE OF IUGRSymmetric IUGR: weight,length and head circumference are all below the 10 th percentile. (33 % of IUGR Infants)Asymmetric IUGR: weight is below the 10 th percentile and head circumference and length are preserved. (55 % of IUGR) Combined type IUGR: Infant may have skeletal shortening, some reduction of soft tissue mass. (12 % of IUGR)

Normal Intrauterine Growth patternStage I (Hyperplasia) - 4 to 20 weeks - Rapid mitosis - Increase of DNA contentStage II (Hyperplasia & Hypertrophy) - 20 to 28 weeks - Declining mitosis. - Increase in cell size.

Stage III ( Hypertrophy) - 28 to 40 weeks - Rapid increase in cell size. - Rapid accumulation of fat, muscle and connective tissue.95% of fetal weight gain occurs during last 20 weeks of gestations.

EtiologyGrowth inhibition in stage I: - Undersized fetus with fewer cells. - Normal cell size.Result in symmetric IUGR.Associated conditions: - Genetic - Congenital anomalies - Intrauterine infections - Substance abuse - Cigarette smoking - Therapeutic irradiation

Growth Inhibition in Stage II/III -Decrease in cell size and fetal weight- Less effect on total cell numeric, fetal length, head circumferance. Result in asymmetric IUGR. Associated Conditions: - Uteroplacental insufficiency.Combination above associated mixed type IUGR.

PATOPHISIOLOGY1) Fetal factors:Genetic Factors: - Race, ethnicity, nationality- sex ( male weigh 150 -200 gm more than female )- parity ( primiparous, weigh less than subsequent siblings) -genetic disorders ( Achondroplasia, Russell - silver syn.)Chromosomal anomalies: - Chromosomal deletions - trisomies 13,18 & 21

Congenital malformations: examples:Anencephaly, GI atresia, potters syndrome, and pancreatic agenesis.Fetal Cardiovascular anomaliesCongenital Infections: mainly TORCH infections.Inborn error of metabolism: - Transient neonatal diabetes- Galactosemia - PKU

Maternal hypoxemia- Hemoglobinopathies - High altitudesOthers- Short stature- Younger or older age (45)- Low socioeconomic class- Primiparity- Grand multiparity- Low pregnancy weight- Previous h/o preterm IUGR baby - Chronic illness ( DM, renal failure, cyanotic heart disease etc.)

3) Placental Factors:Placental insufficiency ( most imp in 3rd trimester)Anatomic problems: Multiple infarctsAberrant cord insertionsUmbilical vascular thrombosis & hemangiomasPremature placental separationSmall Placenta

Postnatal AssessmentGrowth parameters: weight, height, HCAssess GA with Ballard score.Plotted growth parameters in growth chart

Physical appearance:

Heads are disproportionately large for their trunks and extremities Facial appearance has been likened to that of a wizened old man.Long nails.Scaphoid abdomen

Signs of recent wasting - soft tissue wasting - diminished skin fold thickness - decrease breast tissue - reduced thigh circumferenceSigns of long term growth failure - Widened skull sutures, large fontanelles - shortened crown heel length - delayed development of epiphysesComparison to premature infants,IUGR has brain and heart larger in proportion to the body weight, in contrast the liver, spleen, adrenals and thymus are smaller.

3. EXAMINATION IN PREGNANCY pathologyPelvic examination in ectopic pregnancy

Unilateral or bilateral exquisite tenderness especially on motion of the cervixAdnexal massEnlarged uterus Tenderness and painful of the posterior fornix

Signs of internal hemorrhages which provoke hypovolemic shock are the more prominent the more closely fertilized ovum localized near the uterus

Diagnostic procedures Complete blood count Positive urinary test fir estimation of chorionic gonadotropin (hCG) levels UltrasonographyCuldocentesisCurettage of the uterine cavity can also rule out ectopic pregnancy

Culdocentesis is the simplest technique for identifying hemoperitoneum Bloody fluid that does not clot result of hemoperitoneum resulting from an ectopic pregnancy

Hydatidiform MoleIs an abnormal conceptus with loss of villus vascularity and without an embryo or fetus.Most of symptoms are presented thanks to markedly elevated hCG levels.

Hydatidiform MoleIs an abnormal conceptus with loss of villus vascularity and without an embryo or fetus.Most of symptoms are presented thanks to markedly elevated hCG levels.

Signs of Hydatidiform MoleVaginal bleeding with molar elementsPreeclampsia In pelvic exam - uterus larger than expected, Ovarian enlargement due to bilateral theca lutein cystsUltrasonography snow-storm appearance

Clinical findings and Diagnosis : plasenta previaPainless bleeding It almost always ceases spontaneously, unless digital examination or other trauma occurs. Ultrasonography has been of enormous benefit in localizing the placenta.

Careful vaginal examination in labor.

Diagnosis and management of Genital Tract Trauma Diagnosis speculum inspectionManagement - ligation and suturing of all ruptures of the vagina, cervix and perineum. In the case of uterine rupture hysterectomy should be performed

Diagnosis abnormal placental adherence1. Absence of the signs of placental separation during 30 minutes.2. External bleeding in the case of partial adherence, absence of the bleeding in the case of total placenta accreta.3. Manual removal of the placenta confirms the diagnosis of different types of abnormal placental adherence.In the case of partial placental adherence it stops bleeding, but in the case of placenta accreta, increta and percrata it increases bleeding. Attempts at manual removal are futile. Thats why in these cases manual removal of the placenta should be stopped immediately and hysterectomy should be performed.

4. THE MATERNAL MORTALITY RATIO AND CHILD MORTALITY RATE

THE MATERNAL MORTALITY RATIO

Maternal death is the death of a woman while pregnant or within 42 days of termination of pregnancy, irrespective of the duration and site of the pregnancy, from any cause related to or aggravated by the pregnancy or its management but not from accidental or incidental causes.

Where do maternal deaths occur?

The high number of maternal deaths in some areas of the world reflects inequities in access to health services, and highlights the gap between rich and poor. Almost all maternal deaths (99%) occur in developing countries. More than half of these deaths occur in sub-Saharan Africa and almost one third occur in South Asia.

The maternal mortality ratio in developing countries is 240 per 100 000 births versus 16 per 100 000 in developed countries. There are large disparities between countries, with few countries having extremely high maternal mortality ratios of 1000 or more per 100 000 live births. There are also large disparities within countries, between people with high and low income and between people living in rural and urban areas.

Women die as a result of complications during and following pregnancy and childbirth. Most of these complications develop during pregnancy. Other complications may exist before pregnancy but are worsened during pregnancy.

Why do women die?The major complications that account for 80% of all maternal deaths are: severe bleeding (mostly bleeding after childbirth)high blood pressure during pregnancy (pre-eclampsia and eclampsia) infections (usually after childbirth)unsafe abortion. The remainder are caused by or associated with diseases such as malaria, and AIDS during pregnancy.

CHILD MORTALITY RATE

The status of child health in Indonesia has been improving. This is indicated by declining rates of neonatal, infant, and under-five mortality.Under-five mortality declined sharply from 97 per 1,000 live births in 1991 to less than half, which were 44 in 2007. Infant mortality rate significantly declined from 68 per 1,000 live births in 1991 to 34 per 1,000 live births in 2007. Over the same period neonatal mortality rate also declined from 32 per 1,000 live births to 19 per 1,000 live births.

Why do child die?The main cause of under-5 mortality was neonatal complications (asphyxia, low birth weight, and neonatal infections), infectious diseases (primarily diarrhea and pneumonia) as well as closely related to nutritional problems (malnutrition). Other issues were the disparity among provinces on neonatal mortality, infant mortality and under-5 mortality are relatively high. This condition was caused by issues of quality and access to health services, socio economic and cultural issues, infrastructure development as well as the openness of areas to educational and economic development.

5.Preeclampsia and EclampsiaPREECLAMPSIA

The presence of hypertension of at least 140/90 mm Hg recorded on two separateoccasions at least 4 hours apart and in the presence of at least 300 mg protein in a 24 hours collection of urine arrising de novo after the 20th week gestation in a previouslynormotensive women and resolving completetly by the sixth postpartum week.Classification of hypertensive disorders of pregnancyPreeclampsia / eclampsiaChronic hypertensionChronic hypertension with superimposed preeclampsiaGestational or transient hypertension

Etiology of preeclampsia:-(Genetic predisposition)(Abnormal immunological response)(Deficient trophoplast invasion)(Hypoperfused placenta)(Circulating factors)(Vascular endothelial cell activation)(Clinical manifestations of the disease)

Incidence 3% of pregnancies.EpidemiologyMore common in primigravidThere is 3-4 fold increase in first degree relatives of affected women.

pathophisiologyDefective trophoplast invasion hypoperfused placenta release factors (growth factors,Cytokines) vascular endothelial cellactivation.Vasospasm hypertensionEndothelial cell damage oedema, hemoconcentrationKidneys,glomeruloendotheliosis proteinuria,reduced uric excretion and oliguria.

Liver,subendothelial fibrin deposition elevated liver,hemorrhage,infarction,liver rupture and epigastric pain.Blood thrombocytopenia,DIC,HELLP syndrome.Placental vasospasm placental infarction,placental abruptio& uteroplacental perfusion IUGR.CNS vasospasm&oedema headache, visual symptons(blurred vision,spots,

Symptoms of preeclampsiaHeadacheMay be symptomlessVisual symptomsEpigastric and right abdominal pain Signs of preeclampsiaHypertensionNon dependent oedemaBrisk reflexesAnkle clonus(more than 3 beats) Fundal height

Investigations1. MaternalUrinalysis by dipstick24 hours urine collectionFull blood count(platelets&haematocrit)Renal function(uric acid,s.creatinine,urea)Liver function testsCoagulation profile2. Fetal Uss(growth parameters,fetal size,AF) CTG BPP Doppler

Preeclampsia consists of :A Mild preeclampsia Diastolic blood pressure 90-95mmhg minimal proteinurea,normal heamatological and biochemical parameters,no fetal compromise.Deliver at term.B severe preeclampsia (BP>160/110MMHG, urine protein 5grams 3+ ) Abnormal haematological and biochemical parameters,abnormal fetal findings 1. Control blood pressure(aim to keep BP 90-95mmgh )

Complications of preeclampsia:-ECLAMPSIAMaternalCVAHEELP syndromePulmonary oedemaAdult RDSRenal failureFetalIUGRIUFDAbruptio placentaProphylaxis(aspirin,antioxidant)

Eclampsia:- Is a life threatening complications of preeclampsia,defined as tonic,clonic convulsions in a pregnant woman in the absence of any other neurological or metabolic causes.It is an obstetric emergency.It occurs antenatal,intrapartum,postpartum(after delivery 24-48hs)

6. TREATMENT OF pathological pregnancy

Treatment in the case abortion

Bed restSedative drugs Valeriannae, Persen,Novopaside.Spasmolitics Papaverini hydrochlorideAnalgetics Analgin, BaralginProgesterone Utrogestan, Duphastone, ProgesteroneVitamines vit. E Surgical uterine curettage

Hydatidiform Mole Management:Medical care:Correction of:Anemia Dehydration Hyperthyroidismhypertension

Hydatidiform Mole Management:Surgical care:

Suction curettage (with oxytocin or prostaglandin infusion)Suction curettage (with oxytocin or prostaglandin infusion)The method of choiceThe method of choiceTreatment of HypertensionHome ManagementDecrease activities and promote bed rest Sedative drugsLie in left lateral positionRemain quiet and calm restrict visitors and phone calls

Dietary modifications increase protein intake to 70 - 80 g/day maintain sodium intake Caffeine avoidance

Weigh daily at the same time

Keep record of fetal movement - kick counts

Check urine for Protein

HOSPITALIZATIONIf symptoms do not get better then the patient needs to be hospitalized in order to further evaluate her condition.Common lab studies:Renal blood studies -- creatitine, uric acidLiver studies DIC profile -- platelets, fibrinogen, FSP, D-Dimer

MAGNESIUM SULFATEACTION CNS Depressant, reduces CNS irritability Calcium channel blocker- inhibits cerebral neurotransmitter releaseROUTE IV effect is immediate and lasts 30 min. IM onset in 1 hour and lasts 3-4 hours

Prior to administration:Insert a foley catheter with urimeter for assessment of hourly output

MAGNESIUM SULFATENURSING IMPLICATIONS 1. Monitor respirations > 14-16; < 12 is critical

2. Assess reflexes for hyporeflexia -- D/C for hyporeflexia 3. Measure Urinary Output >100cc in 4 hrs.

4. Measure Magnesium levels normal is 1.5-2.5 mg/dl

Have Calcium Gluconate available as antagonist

Control Blood Pressure Check B / P frequently.

Give Antihypertensive Drugs Hydralzine ( apresoline) Labetalol Aldomet Procardia Check Hemocrit * Do NOT want to decrease the B/P too low ortoo rapidly. Best to keep diastolic ~90.Need to maintain uteroplacental perfusion!

Promote Diuresis

Bed rest in left or right lateral position

Check hourly output -- foley cath with urimeter

Dipstick for Protein

Weigh daily -- same time, same scale

7. CASES REFERRED TO PREGNANCY

*Have a history of heart disease, kidney, diabetes, and epilepsy before pregnancy.

*Having a family history of genetic disorders Signs of severe anemia (hemoglobin 200mg/dl) during pregnancy

*Vaginal bleeding or the appearance of blotches of blood during pregnancy.

*Severe headaches, blurred vision or swelling throughout the body.

*Infection during pregnancy.

TERIMA KASIH