This document provides a review of a case involving a 25-year-old woman with vaginal spotting who is possibly experiencing an early pregnancy complication. It summarizes the patient's medical history and physical exam findings. The rest of the document discusses various conditions that could cause bleeding in early pregnancy like miscarriage, ectopic pregnancy, molar pregnancy and provides details on approaches to diagnosis and treatment of each.
This document provides a review of a case involving a 25-year-old woman with vaginal spotting who is possibly experiencing an early pregnancy complication. It summarizes the patient's medical history and physical exam findings. The rest of the document discusses various conditions that could cause bleeding in early pregnancy like miscarriage, ectopic pregnancy, molar pregnancy and provides details on approaches to diagnosis and treatment of each.
This document provides a review of a case involving a 25-year-old woman with vaginal spotting who is possibly experiencing an early pregnancy complication. It summarizes the patient's medical history and physical exam findings. The rest of the document discusses various conditions that could cause bleeding in early pregnancy like miscarriage, ectopic pregnancy, molar pregnancy and provides details on approaches to diagnosis and treatment of each.
UST OB-GYN June 9, 2010 Bleeding in the 1 st Half of Pregnancy A 25 y/o G3P1 (1011) w/ vaginal spotting. She had (+) pregnancy test since her menses was 2 weeks delayed. She underwent D&C in Sept 2009 after passing grape like tissues. BP-100/70, PR- 98/min, RR- 30/min in respiratory distress Abdomen: slightly tender on the right & hypogastric area, no palpable mass Cervix - bluish w/ brownish discharge, soft Uterus- soft, slightly enlarged w/ mild tenderness Adnexae- no palpable mass, slightly tender right ABORTION ECTOPIC PREGNANCY GTD (H Mole) Termination of pregnancy before 20 weeks AOG Implantation of the fertilized ovum outside the endometrium Proliferative abnormalities of the trophoblast w/c retains its ability to secrete HCG Abnormal zygote or embryonic development +/- passage of meaty tissues Colicky abdominal pain, amenorrhea, vaginal spotting Passage of grape-like tissues; Hyperemesis gravidarum Cervix closed or dilated; Uterus compatible or incompatible with AOG (+) wiggling tenderness; Uterus smaller than AOG; (+) Adnexal tenderness/mass; +/- fullness of the cul de sac Cervix dilated; Uterus enlarged than AOG Ballooning of the lower uterine segment UTZ: +/- fetal cardiac activity; Retained products of conception UTZ: (+) adnexal mass, (-) gestational sac when HCG >2500 mIU/mL; Lower HCG & progesterone UTZ: Snow storm appearance, uterus larger than AOG, theca lutein cysts; High HCG levels; Bed rest/Observation/ Curettage/Prostaglandin/ Cerclage (depending on the type of abortion) Methotrexate; Salpingostomy/ Salpingotomy/ Salpingectomy Suction curettage/ Hysterectomy; Prophylactic chemotherapy; Serial monitoring of B HCG Ovular or Fetal Factors: early fetal wastage (gross defects in the ovum or fetus) autosomal trisomy most common chromosomal abnormality interference with the circulation faulty placental formation Maternal Factors: infection maternal hypoxia and shock acute or chronic respiratory disease, heart failure, severe anemia chronic illness endocrine factors hypo- hyperthyroidism, DM toxic agents blood incompatibility Abortion Paternal Factors : defective sperm, contributing half of the chromosomes to the ovum Unknown Causes: immunological causes Common Known Causes:
Delay or prevent migration salpingitis 50% iatrogenic BTL, tubal plastic surgery, adhesions, IUCD, use of progestin only OC developmental defects or distortion of the tubes transmigration of the ovum tubal spasm Risk Factors for Ectopic Pregnancy HIGH RISK - tubal corrective surgery - tubal sterilization - previous ectopic pregnancy - in utero DES exposure - IUD - documented tubal pathology MODERATE RISK - infertility - previous genital infection - multiple partners SLIGHT RISK - previous pelvic / abdominal surgery - smoking - douching - Early sexual contact ( < 18 y/o) Signs and Symptoms Classic triad of symptoms: Abdominal pain Amenorrhea Vaginal bleeding
Clinical signs: Abdominal tenderness Cervical wiggling tenderness Uterus smaller than AOG Fullness of cul-de-sac Diagnosis hCG Assays lower levels than those in normal intrauterine pregnancies In normal intrauterine pregnancies, hCG levels doubles every 2 days Serial hCG assay is not recommended because of delay in the diagnosis Serum Progesterone Lower levels < 5ng/ml - no viable pregnancy Facilitates diagnosis with a single measurement
Ultrasonography Used to confirm intrauterine pregnancy TVUS - used to visualize an intrauterine pregnancy by 24 days post-ovulation, or 38 days after LMP Its value is highlighted further in its ability to demonstrate free fluid in the cul-de-sac Culdocentesis Aspiration of fluid contents from the cul-de- sac stabbed through the posterior vaginal fornix (+) hemoperitoneum upon aspiration of laked or non-clotting blood 10-14% false negative rates Only done if US or hormonal assays are not available
Laparoscopy Gold standard because it allows assessment of the pelvic structures, size and exact location of ectopic pregnancy or presence of hemoperitoneum
Performed on hemodynamically stable patients Management Medical therapy Indications: Unruptured ectopic pregnancy Hemodynamically stable Size of gestation < 3.5 cm by US measurement Absence of cardiac activity in the ectopic sac
Methotrexate antimetabolite chemotherapeutic agent binds to dihydrofolate reductase, which is involved in the synthesis of purine nucleotides interferes with DNA synthesis and disrupts cell multiplication given as single 50 mg/m 2 IM injection Leucovorin is added to decrease adverse effects
Adverse effects: nausea, vomiting, stomatitis, diarrhea, gastric distress, and dizziness bone marrow suppression, dermatitis, pleuritis, pneumonitis, and alopecia, can occur with higher doses Surgical Management of Ectopic Pregnancy SALPINGOSTOMY SALPINGOTOMY SALPINGECTOMY - to remove a small pregnancy < 2 cm in length & located in the distal 1/3 of the fallopian tube - basically the same as salpingostomy EXCEPT that the incision is closed with 7.0 vicryl - used for both ruptured & unruptured ectopic pregnancies - LINEAR INCISION, 10 to 15 mm in length or less at the ANTIMESENTERIC BORDER immediately over the ectopic pregnancy - tubal resection through a laparoscope - the products usually will extrude from the incision & can be carefully removed or flushed out - wedge resection of the outer 1/3 (or less) of the interstitial portion of the tube - cornual resection done to minimize the rare occurrence of pregnancy in the tubal stump - may cause: - scarring - narrowing of small isthmic lumen Gestational Trophoblastic Diseases ( GTD ) refers to the spectrum of proliferative abnormalities of the trophoblast associated with pregnancy. contrary to normal pregnancy, in GTD abnormal growth and development of the trophoblast continue even beyond the end of pregnancy Classification of Gestational Trophoblastic Disease Hydatidiform Mole Complete Partial
Gestational trophoblastic tumors Nonmetastatic Metastatic Low riskno risk factors High riskany risk factor Pretherapy hCG level > 40,000 mIU/mL Duration > 4 months Brain or liver metastases Prior chemotherapy failure Antecedant term pregnancy Hydatidiform mole: Risk factors Extremes of maternal age highest among >45 yr old age group
History of prior hydatidiform mole
Unclear role of gravidity, parity, estrogen status, OCP use & dietary factors Complete H Mole Chorionic villi are converted to a mass of clear vesicles Purely avascular cystic villi Histologic structure: Hydropic degeneration & swelling of the villous stroma Absence of blood vessels in the swollen villi Proliferation of trophoblastic epithelium to a varying degree Absence of fetus & amnion Partial H Mole Presence of some villi which are normal with nucleated RBC and others which are cystic and vascular Gestational sac with or without a fetus may be identified Histologic structure: Slowly progressing hydatidiform swelling of some usually avascular villi, while some vascular villi with a functioning fetal-placental circulation are spared
History and PE Uterine bleeding Rapid uterine enlargement Absence of fetal heart activity Pregnancy-induced hypertension: preeclampsia developing before the 24 th
Ancillary Procedures B-hCG measurement normal pregnant levels peak at 10-14 wks rarely exceeds 100,000mIU/mL Levels > 100,000mIU/mL suggest GTD A single determination is not diagnostic May be elevated in a normal twin gestation Lower levels in partial moles Ultrasound snow storm pattern, multicystic appearance , with no fetal echo Absence of fetus (complete mole) If (+) fetal sac, possible partial mole Chest Radiograph cannon- ball exudates
Pre-operative Work-ups CBC, Blood Typing
SGOT, SGPT, BUN, Creatinine
TSH, FT3 and T4 Hydatidiform mole: Management Principles:
Immediate evacuation of the mole Suction curettage Mole in-situ(TAH)
Hydatidiform mole: Follow-up
Serial determination of serum - hCG to monitor potential development of malignant sequelae (GTT) Chest X-ray Avoid pregnancy for 6-12 months (Natural Family Planning)
Management: Follow-up B-hCG measurement Every 2 weeks till normal for 3 determinations then: Monthly for 6 months; every 2 months for the next 6 months Every 3 months in the 2 nd year of follow-up Every 6 months thereafter
Prophylactic Chemotherapy Uterine size larger than AOG of 6 weeks HCG titer of 100,000 mIU/mL Theca lutein cysts > 6 cms Maternal age > 35 yrs Gravida 4 and above Recurrent molar pregnancy Medical complications from the trophoblasts (DIC, Pre-eclampsia, Thyrotoxicosis, Pulmonary Insufficiency) Anticipated poor follow up due to geographic location Disturbing histopathology report like moderate to severe trophoblastic proliferation Chemotherapy Methotrexate 0.3-0.4 mgs/KBW IM for 5 days
Actinomycin-D 10-12 ugs/KBW IV for 5 days Prognosis Nearly 20% of complete moles progress to GTT Good prognosis: Disease duration< 4 mos Initial BhCG titer < 100,000 Decrease to normal levels in 4 wks
Residual Trophoblastic Disease - retention of molar tissue with continued elevation of serum or urine HCG levels 8 weeks post evacuation of H-Mole
Diagnosis: continued vaginal bleeding; persistent soft and enlarged uterus Invasive Mole: prominent features are its invasiveness and destructive potentialities abnormal penetration through the muscle layers of the uterus Choriocarcinoma Presence of exuberant trophoblastic growth lack of villous architecture propensity to invasive growth & blood vessel necrosis no integral vascular stroma may exhibit distant metastases w/o trace of residual disease in the uterus FIGO Classification System of GTT Stage Anatomic Location I Confined to corpus uteri II Metastases outside uterus confined to vagina or pelvic structures III Metastases to lungs IV Distant metastases to other sites Chemotherapy principal mode of treatment Low risk- Good Prognosis GTT-- single agent chemotherapy
High risk Poor Prognosis GTT drug combinations Chemotherapeutic Drugs Used: Methotrexate Actinomycin-D Cyclophosphamide Chlorambucil EMA-CO Chemotherapy Etoposide Dactinomycin Methotrexate + folinic acid Vincristine & Cyclophosphamide Bleeding in the 2 nd Half of Pregnancy LR 32 y/o G3P2(2002) 36 wks had profuse vaginal bleeding upon waking up. Previous 2 LTCS, 1 st due to CPD BP- 100/70, PR- 100/min, RR- 20/min FH- 32 cm, FHR- 142/min LM1(-), LM2- head on the right side of the mother, breech on the left side, LM3(-) PLACENTA PREVIA ABRUPTIO PLACENTA Painless vaginal bleeding Vaginal bleeding abdominal pain Uterine size compatible w/ gestational age Uterine size may be bigger/ Smaller than gestational age Associated w/ prior CS, multiparity, advanced maternal age Associated w/ Hypertensive disorders, abnormal fetal presentations, smoking, PROM Localization by ultrasound History and signs/symptoms Maternal hypovolemia; Fetal demise Shock, DIC, Couvelaire uterus
Abruptio Placenta
premature detachment of a normally implanted placenta maybe partial or total
Bleeding maybe: Concealed blood does not escape externally and is retained between the placenta and the uterus External Blood insinuates itself between the membranes and uterus and escapes through the cervix Etiology : Relation with PIH Trauma Sudden uterine decompression Short cord Supine hypotension syndrome Folic Acid deficiency Pathogenesis : Bleeding is from torn uterine sinuses and blood loss is proportionate to the extent of placental separation In some cases, degeneration and necrosis of decidua basalis as in PIH. Disruption of vessels with formation of decidual hematoma leads to placental separation. Etiology : Dropping down theory poor decidual reaction in upper segment Persistence of chorionic activity in the decidua capsularis and its subsequent development Defective decidua Clinical Features : painless vaginal bleeding general condition proportionate to visible blood loss relaxed uterus malpresentation floating presenting part Placenta Previa 3 rd Stage Bleeding/ Postpartum Hemorrhage MD 35 y/o had continuous vaginal bleeding following spontaneous vaginal delivery to an 8 lb baby after labor induction for 15 hrs due to EROM. BP- dropped to 90/60, PR- 100/min T- 38.5 Definition Mean blood loss with vaginal delivery: 500cc > 1000cc is hemorrhage Mean blood loss with C/S: 1000cc >1500cc is hemorrhage
Prenatal Risk Factors for hemorrhage Most patients with hemorrhage have none. Pre-eclampsia Previous postpartum hemorrhage Multiple gestation Previous C/S Multiparity Intrapartum Risk Factors Prolonged 3rd stage (>30 min) Medio-lateral episiotomy Midline episiotomy Arrest of descent Lacerations Augmented labor Forceps delivery
ALSOs 4 Ts Tone (Uterine tone)
Tissue (Retained tissue--placenta)
Trauma (Lacerations and uterine rupture)
Thrombin (Bleeding disorders) TONE TONE Rule out Uterine Atony Palpate fundus. Massage uterus. Oxytocin 40U/L @ 250cc / h. Methergine one amp IM (not in hypertensives) Hemabate IM q 15min TISSUE Tissue R/O retained placenta Inspect placenta for missing cotyledons. Explore uterus. Treat abnormal implantation. TRAUMA TRAUMA R/o cervical or vaginal lacerations. Obtain good exposure. Inspect cervix and vagina. Worry about slow bleeders. Treat hematomas. THROMBIN THROMBIN Check labs if suspicious. Puerperal Infection ZG 34 y/o G1P1 (0101) was noted to be febrile T- 38.9 C. She underwent LTCS 2 days ago due to PROM of 24 hrs. BP- 110/70, PR- 110/min, RR-23/min Abdomen- (+) tenderness at the hypogastrium wound dry Foul lochia rubra Cervix- soft,long,closed Uterus- (+) tenderness at hypogastrium & adnexae PUERPERAL INFECTIONS Temperature of 38 o C on any 2 days of 1 st 10 days after delivery exclusive of 1 st 24 hours Endometritis most common cause of puerperal fever CS major predisposing factor for pelvic infection Risk Factors: Prolonged labor PROM Repeated IE Organisms: Aerobic S. pyogenes, E. Coli, Pseudomonas, S. Aureus Anaerobic Strep, B. fragilis Spread of Infection: pelvic cellulitis, parametritis, salpingitis, peritonitis, thrombophlebitis, septicemia Treatment Proper antibiotics ( clindamycin + gentamycin) Dystocia DYSTOCIA POWERS PASSENGER PASSAGE Causes of Dystocia Abnormalities of the expulsive forces >Uterine dysfunction uterine forces insufficiently strong or inappropriately coordinated to efface and dilate the cervix >Inadequate voluntary muscle effort during the second stage of labor Abnormalities of presentation, position, or fetal development Abnormalities of the maternal bony pelvis Abnormalities of the birth canal PASSAGES Diameter Pelvic Inlet Contraction Normal Value AP (obstetrical conjugate) <10 cm 12 cm Diagonal conjugate <11.5 cm 12 cm Transverse diameter <12 cm 13 cm R & L oblique 13 cm Diameter Contracted midpelvis Normal Value AP Transverse (interischial spinous) <10 cm 10.5 cm Posterior sagittal +transverse <13.5 cm 4.5 cm Clinical pelvimetry Ischial spines prominent, pelvic sidewalls convergent Clinical Assessment of Adequate Pelvis sacral promontory accessible
ischial spines not prominent
pelvic sidewalls not convergent
sacrum curve
sub-pubic arch wide 3 Stages of Labor Stage 1 Latent Phase Active Phase Stage 2 Stage 3 Begins Regular contractions 3 or > cm cervical dilatation 10 cm cervical dilatation Delivery of neonate Ends 3 or > cm cervical dilatation 10 cm cervical dilatation Delivery of neonate Delivery of placenta Normal duration < 14 hrs in multipara < 20 hrs in primipara < 4 hrs in multipara (CD 1.5 or > cm/ hr) < 5 hrs in primipara (CD 1.2 or > cm/hr) < 30 mins in multipara < 60 mins in primi < 30 mins Stages of labor First Stage - begins with onset of labor and ends when cervix is fully dilated to 10cm Latent Phase - onset of labor to approx. 4cm cervical dilatation Nulli = 20hrs Multi = 14hrs Active Phase - rapid dilatation; from 4- 10cm Nulli - 1.2cm/hr Multi - 1.5cm/hr
Factors influencing the 1 st
stage of labor uterine contractions cervical resistance forward pressure by the fetal head Second Stage - from full cervical dilatation to delivery of fetus
Duration: Nulliparas 50 mins 2 hrs Multiparas 20 mins 1 hr *additional hour allowed in the presence of epidural anesthesia Criteria for diagnosing arrest in 1 st stage labor 1. latent phase has been completed with the cervix dilated to 4cm or more.
2. uterine contraction pattern of 200 Montevideo units or more in a 10- min period of observation POWERS Adequate uterine contractions
Occur at least once every 3 minutes, last 50- 60 secs and are moderate to strong (at least 50 mm above baseline) or greater than 250 Montevideo Units ( average intensity X frequency/10 min). Patients whose contractions do not meet these criteria may benefit from labor augmentation. 3 cm/min. 1 minute 1cm/min. EFM Uterine Dysfunction hypotonic hypertonic oxytocin sedation no basal hypertonus elevated basal tone synchronous asynchronous insufficient to cause cervical dilatation distorted pressure gradient Passenger A. Abnormalites in fetal presentation 1. Breech more common during 1 st & 2 nd
Malpresentation 2. Face Etiology: contracted pelvis face is very large pendulous abdomen cord coils anencephalic fetuses
Malpresentation 3. Transverse lie Etiology: relaxation of the abdominal wall preterm placenta previa abnormal uterus contracted pelvis
Recommendation for delivery: CS Malpresentation 4. Shoulder dystocia Antepartum factors: maternal obesity DM post-term pregnancy Intrapartum: prolonged 2 nd stage of labor oxytocin induction or augmentation use of midforceps or vacuum
Recommendation for delivery: CS B. Abnormalities in fetal development 1. Fetal macrosomia BW >4,000g Etiology: multiparity large parents maternal obesity maternal DM postdatism Prognosis: increased perinatal loss severely depressed at birth neurological complications JS, 24 y/o G1P0, 39-40 wks was admitted because of labor pains BP- 110/70, PR- 85/min., T- 36.5 C FH- 35 cms, LM3- cephalic, FHR- 135/min UC q 5-7 mins,moderate, 40 secs duration Cx: 3-4 cm dilated, 80% effaced, LOT, St (- 3), (+) BOW Prominent ischial spines, convergent pelvic side walls, sacrum straight
3 hrs after admission UC q 3-4 mins, 50 secs moderate Repeat IE: cervix 5 cm dilated, 80% effaced, ST(-3) Epidural anesthesia was given for intrapartum pain relief 2 hrs later BOW spontaneously ruptured Repeat IE no change in cervical dilatation LATENT PHASE ACTIVE PHASE Acceleratio n Phase Phase of Maximun Slope Deceleratio n Phase
Prerequisites for forceps application Fully dilated cervix Ruptured membranes Empty bladder Engaged head, > st +2, in vertex presentation Preferably in occiput anterior position Preferably epidural anesthesia, low spinal or pudendal block Indications for Forceps/Vacuum Delivery Fetal indication: Non- reassuring FHR patterns Maternal indications: Maternal exhaustion To shorten the second stage of labor and avoid bearing down efforts: Cardiac disease Preeclampsia Pulmonary disorders
Trial of Forceps: - entails successful forceps application but undue amount of force is required to extract the head
Failed Forceps: Failure of application - forceps cannot be applied properly Failure of extraction successful forceps application but delivery of the head unsuccessful
Breech Delivery Breech Presentation Frank breech variety ideal for vaginal delivery Indications for CS: preterm footling primi LGA Partial Breech Extraction best vaginal delivery Pipers forceps for delivery of aftercoming head Maneuvers for delivery of after-coming head Mauriceaus Brachts Pragues Breech decomposition conversion of frank to double footling variety Pinards bringing down of legs during breech decomposition Cesarean Delivery DEFINITION: -birth of a fetus through incisions in the abdominal wall (laparotomy) and the uterine wall (hysterotomy) Indications for Cesarean Section Labor Dystocia Fetal Distress Abnormal Presentation (Breech in a primi or transverse lie) Prior Cesarean Delivery
Cesarean Section LTCS CCS Technique Slightly difficult Easy Less bloody More Apposition is perfect Coaptation not PF Post-op Hemorrhage is less More Less infection More Less adhesion More Better convalescence Relatively poorer Lower mortality Higher Better wound healing Poorer Preterm Labor/ PROM RV, 17 y/o G1P0, 31 wks consulted because of hypogastric pains FHx: (-) DM, Asthma,HPN Personal Hx: (+) smoker pack/day non- alcoholic drinker BP- 110/70, PR- 78/min, RR- 21/min, T- 36.7 c FH- 31 cm ;UC q 4-5 mins, 30 secs duration,moderate ; LM3- breech Cervix- violaceous w/ white mucoid discharge soft, long, closed before 37 weeks AOG at least one painful uterine contraction in 10 minutes progressive cervical dilatation and effacement Etiology: Infection Low socio-economic and nutritional Maternal factors uterine anomalies Fetal multiple pregnancies, PROM, congenital malformations Predictors : Biochemical Fibronectin, Estriol Sonographic cervical funneling, cervical length Preterm Labor Management of Preterm Labor: Tocolysis Steroid administration Diagnosis of Preterm Labor Regular contractions after 20 weeks & before 37 weeks which are 5-8 mins or less accompanied by one or more of the ff. : 1. Progressive change in the cervix 2. Cervical dilatation of 2 cm or more 3. Effacement of 80 percent or more
Sonographic assessment of cervical dilatation and effacement (TYVU) Management of Preterm Labor In the absence of maternal / fetal indications warranting intentional delivery:
cornerstone is to forestall preterm delivery prior to 35 weeks; and
to enhance infants ability to cope with extrauterine environment
To Avoid Preterm Delivery
Bedrest Hydration and sedation ? Cerclage Active treatment of bacteria vaginosis Tocolytics
Tocolytics: Beta-Adrenergic Receptor Agonists: MOA: Adrenergic receptors located on outer surface of smooth muscles are coupled with agonists activating adenyl cyclase in cell membrane which enhances convertion of ATP to cyclic AMP which in turn initiates a number of reactions that reduce intracellular ionized calcium and thereby prevent activation of contractile proteins. Types: B1 receptor- heart and intestine B2 receptor- myometrium Beta Receptor Agonists A. Ritodrine B. Terbutaline C. Isoxsuprine
Only delay delivery for at least 48 hours
1.Allow maternal transport to tertiary care centers 2.Effect fetal maturation with glucocorticoids 3.To achieve adequate antibiotic level to control infection
Side Effects of beta-agonists Maternal and fetal tachycardia Hypotension and arrythmias Chest tightness (MI) Pulmonary edema Maternal metabolic effects Emesis, fever, tremulousness,headache
Tocolytics Magnesium Sulfate: MOA: Calcium agonist Delay delivery by at most 48 hours Side effects: Pulmonary edema Respiratory depression Hypotension Profound muscular paralysis Maternal tetany Cardiac arrest Tocolytics: Calcium Channel-Blocker Drugs:
MOA: Act to inhibit entry of calcium thru the cell membrane channels. Ex: Nifedipine
Side effects: Maternal Hypotension Headache Tocolytics: Prostaglandin Inhibitors: MOA: Inhibits synthesis of prostaglandins or by blocking the action of prostaglandins on target organs Ex: Salicylates, Indomethacin, Naproxen sulindac Side Effects: - closure of ductus arteriosus - necrotizing enterocolitis - intracranial hemorrhage
Other Tocolytics: Atosiban: competitive oxytocin vasopresin antagonist
Nitric oxide donor drugs: potent endogenous smooth muscle relaxant in the vasculature ex: Nitroglycerine Steroid Therapy NIH CONSENSUS 1994:
- Given to 28-34 wks gestation - 24 mg IM dexamethasone or betamethasone in 24 hours - Birth delayed for at least 24 hours after completion
Premature Rupture of Membranes Causes: friability of membranes tensile strength of membrane Chorioamnionitis Hydramnios Cervical incompetence Diagnosis : Fluid coming out of the os Ferning, pH determination, Nitrazine test Amnionitis
Presence of intrauterine infection associated with: maternal fever maternal tachycardia fetal tachycardia uterine tenderness leukocytosis foul smelling vaginal discharge Pathophysiology: from pathogens of the vaginal flora PGF synthesis release of lipopolysaccharides and release of cytokines interleukin 6 PGE2 weakened membranes due to type II collagen or Proteolytic activity in chorioamnionic membrane Diagnosis of PPROM History of watery vaginal discharge
Physical examination: vital signs fundic height usually small for AOG uterine contractions, FHT single speculum examination Suggested PPROM Protocol Ultrasound Examination (mainly for prognostication) Confirm gestational age Get estimated fetal weight Identify presenting part Assess amniotic fluid volume Suggested PPROM Protocol Assessment of Labor (fetal monitoring) No labor ------ Watch out for: infection fetal jeopardy onset of labor With labor----- Ampicillin 2g. IV. Q 6 (for prevention of group B strep in Neonates) - Minimize maternal hypotension/infection - Prevent fetal hypoxia and acidosis PPROM Management 1. Below 25 weeks: -Expectant ?Hospitalization II. 26-34 weeks: - Antibiotics - hospitalization - corticosteroids - tocolysis III. After 34 weeks: - Hospitalization - Antibiotics and delivery Chorioamnionitis (intraamniotic infection) Fever only reliable indicator(>38c ) Maternal tachycardia Fetal tachycardia Uterine tenderness Foul smelling vaginal discharge
FHR abnormalities (fetal distress) macrosomia (shoulder dystocia) meconium passage (aspiration syndrome) Multiple Pregnancy MULTIFETAL PREGNANCY More than one fetus being borne by a pregnant woman Includes twins and higher order multiples (eg, triplets, quadruplets).
The 2 types of twins are monozygotic and dizygotic. DIZYGOTIC TWINS = FRATERNAL TWINS
Two sperms fertilize 2 ova Separate amnions, chorions, and placentas are formed The placentas in dizygotic twins may fuse if the implantation sites are proximate. The fused placentas can be separated easily after birth. MONOZYGOTIC TWINS = IDENTICAL TWINS
single fertilized ovum splits after conception. First 2 days dichorionic diamniotic 30% 3-8 days monochorionic diamniotic 70% 9-12 days monochorionic monoamniotic > 12 days conjoined twins
evaluate the placenta(s) after the birth of all multifetal pregnancies in order to determine zygosity.
Determine chorionicity as soon as possible US at 10-14 weeks: twin peak sign
Monoamnionic Diamnionic Monochorionic Diamnionic Dichorionic Hypertension in Pregnancy IL, 17 y/o, 34-35 wks was brought to UST- ER due to upward rolling of eyeballs. No antenatal care BP- 210/170, PR-100/min, RR- 24/min, T- 37 C FH- 28 cms, LM3-cephalic, FHR- 145/min, No UC noted Cervix- long, closed Leg edema +2, DTRs +3
Classification of Hypertensive disorders in Pregnancy 1. Gestational HPN- formerly PIH that included transient HPN 2. Preeclampsia 3. Eclampsia 4. Preeclampsia superimposed on chronic HPN 5. Chronic HPN
Gestational HPN
BP 140/90 mmHg for the first time during pregnancy No proteinuria BP returns to N < 12 weeks postpartum Preeclampsia
Minimum Criteria BP 140/90 mmHg after 20 weeks gestation Proteinuria 300mg/24 hours or 1+ dipstick Preeclampsia Increased certainty of preeclampsia BP 160/110 mmHg Proteinuria 2.0g/24 hours or 2 + dipstick Serum creatinine 1.2 mg/dL Platelets < 100,000/mm Microangiopathic hemolysis (increased LDH) Elevated ALT or AST Persistent headache or other cerebral or visual disturbance Persistent epigastric pain
Indications of Severity of Hypertensive Disorders During Pregnancy ABNORMALITY MILD SEVERE Diastolic BP 100 mmHg 110mmHg Proteinuria Trace to 1 + 2+ Headache absent present Visual disturbance absent present Upper abdominal pain absent present Oliguria absent present Convulsion (eclampsia) absent present Serum creatinine normal elevated Thrombocytopenia absent present Liver enzyme elevation minimal marked Fetal growth restriction absent obvious Pulmonary edema absent present Eclampsia Seizures/convulsions + preeclampsia
Preeclampsia superimposed on chronic HPN New-onset proteinuria 300mg/24 hours in hypertensive women but no proteinuria before 20 weeks gestation
A sudden in proteinuria or BP or platelet count < 100,000mm in women with HPN and proteinuria before 20 weeks gestation Chronic HPN BP 140/90 mmHg before pregnancy or before 20 weeks gestation not attributable to GTD
or first diagnosed after 20 weeks gestation and persistent after 12 weeks postpartum/long after delivery
Nulliparity Chronic HPN Maternal age > 35 Obesity Genetic predisposition Hyperplacentosis states (multifetal pregnancy, H-mole, hydrops) African-american ethnicity Renovascular disease Dietary factors (low protein, low calcium) Low socioeconomic status
Risk factors
Etiology HPN disorders due to pregnancy are likely to develop in women who: - are exposed to chorionic villi for the first time - are exposed to superabundance of chorionic villi, as with twins or H. mole - have preexisting vascular disease - are genetically predisposed to HPN developing during pregnancy Mechanisms 1. abnormal trophoblastic invasion 2. immunological factors 3. vasculopathy & inflammatory changes 4. dietary deficiencies 5. genetic influences Associated Changes: 1. plasma uric acid 2. plasma creatinine 3. Glomerular endotheliosis 4. Periportal hemorrhagic necrosis of the liver SGOT, SGPT 5. Subcapsular hemorrhage of the liver 6. Brain edema, hemorrhages 7. Blurring of vision due to edema; retinal detachment Objectives of Treatment: control of hypertension prevent convulsion delivery of healthy, if possible term baby avoid residual effects Drugs Used: MagSO4- control & prevention of convulsion Hydralazine, Nifedipine, Ca-channel blockers Three Cardinal Principles
1. control of convulsions 2. control of hypertension 3. optimum mode and time of delivery
Anti-convulsant Therapy MgSo4 Diazepam Phenytoi n given in 2 ways : 1. continuous IV infusion 2. intermittent IM injections Magnesium sulfate drug of choice MOA: cerebral vasodilator increases uterine blood flow reduces level of plasma endothelin 1 increases renal and extrarenal prostacyclin central anticonvulsant effect increases levels of endothelium- derived relaxing factor precursors
MgSO 4
Therapeutic Level: 4-7 mEq/L Loss of Patellar Reflex: 10 mEq/L Respiratory Depressions: > 10 mEq/L Respiratory Paralysis and Arrest:> 12 mEq/L
Precautions for succeeding doses:
1. presence of patellar reflex 2. respirations are not depressed 3. urine output 30 ml for the past hour or 100 ml for the past 4 hours 4. IV Ca-gluconate ( 10 ml of 10% solution) available at bedside for MgS04 overdose
MgS04 therapy is continued for 24 hours after delivery and is administered for 24 hours after the onset of convulsions if eclampsia develops postpartum.
Control of Hypertension Hydralazine (initial dose 5 mg IV Bolus followed by 5 mg increments every 30 min to total 20 mg IF DBP does not improve Labetalol adverse effects of fetal growth and hemodynamics Nifedepine Nicardipine ACE Inhibitors NOT USED (Teratogenic)
Optimum time and mode of delivery Five considerations in terminating pregnancy:
1. age of gestation 2. disease severity 3. status of fetus 4. condition of the mother 5. nursery capabilities Diabetes in Pregnancy LP, 28 y/o, G2P1(1001) 24 wks came in for antenatal care FHx: (+) HPN and DM OBHx: 2007 NSD term 8 lbs baby boy BP- 110/70, PR- 78/min, RR- 21/min, T- 36.6 C FH- 25 cm, FHR- 130-140/min Cervix- violaceous, (+) curdlike vaginal discharge Cervix- soft, long, closed GLYCOSURIA IN PREGNANCY Causes: 1. Renal renal threshold is due to glomerular filtration and impaired tubular reabsorption of glucose 2. Impaired glucose tolerance Due to accelerated absorption of glucose from GIT Complex endocrinal changes delay utilization of glucose to form liver glycogen due to anti-insulin activity 3. Clinical diabetes either pre-existing or detected for 1 st time 4. Lactosuria glucose in converted into lactose Screening Test: all patients 50 grams oral glucose at 24-28 weeks w/o regard to last meal > 130 mg 2 hrs after = OGTT If FBS value is >130 mg - NO need to do OGTT + acetone in urine confirms overt Diabetes Complications: perinatal loss, macrosomia Hydramnios, congenital fetal malformation
Glycosylated Hgb ( HbA1c) > 9.5 % severe malformation Diagnosis Low risk status requires no glucose testing but this category is limited to those women meeting all of the ff. characteristics: < 25 years old Weight normal before pregnancy Member of an ethnic group with a low prevalence of GDM No known diabetes in first-degree relatives No history of abnormal glucose tolerance No history of poor obstetric outcome
Diagnosis Low Risk Pregnancies A. Screening: A 50 gram glucose load is given orally, irrespective of the last meal. One hour later, venous plasma is obtained for glucose determination. B. When done: At the time of initial visit
Diagnosis
C. Results: a value of 129 mgs% and below is considered negative, but test must be repeated at 26 weeks of gestation. If the value is 130 mgs% or more, a glucose tolerance test is performed right away. If negative, the GTT is repeated anytime after the 26 th week of gestation.
D. Glucose tolerance Test Glucose Tolerance Test 100-g oral glucose load mgs/dl mmol/l Fasting 95 5.3 1-h 180 10.0 2-h 155 8.6 3-h 140 7.8 75-g oral glucose load mgs/dl mmol/l Fasting 95 5.3 1-h 180 10.0 2-h 155 8.6 Two or more of the venous plasma concentrations must be met or exceeded for a positive diagnosis. The test should be done in the morning after an overnight fast of at least 3 days of unrestricted diet (> 150 g CHO per day) and unlimited physical activity. The subject should remain seated and should not smoke throughout the test. American Diabetes Association Diagnosis
High risk for GDM Marked obesity Personal history of GDM Glycosuria Strong family of GDM
A glucose tolerance test is done at initial visit. If negative and if performed before the 26 th week, this should be repeated anytime after the 26 th week ( at 2 different time intervals)
Diagnosis
Symptomatic Patients A random plasma glucose of 200 mgs% establishes the diagnosis of GDM. If between 140-199mgs, a glucose tolerance test is done. Renal & Urinary Tract Disorders PP, 32 y/o, G2P1(1001) 11-12 wks complained of right flank pain BP- 100/70, PR- 96/min,RR- 21/min, T-38.4 c (+) RCVA tenderness Cervix- soft, long, closed; Uterus- enlarged to 3 mos size; Adnexae negative for mass & tenderness Asymptomatic Bacteriuria Most common; 2-10% of pregnant women 40% if untreated symptomatic UTI Urinalysis test for Bacteriuria Leucocyte esterase nitrite cost effective 100,000 organisms per mL = Bacteriuria E. coli organism associated w/ ASB Complications : Preterm births, LBW, Hypertension, Preeclampsia, Maternal Anemia, Symptomatic UTI Cystitis and Urethritis Dysuria, urgency and frequency Pyuria, bacteriuria, hematuria 3-day regimen Chlamydia Trachomatis cause of urethritis w/o growth on culture Untreated UTI associated w/ mental retardation in 23% of women Acute Pyelonephritis Occurs at the 2 nd trimester unilaterally and right-sided Ascending infection from untreated ASB Characterized by fever, chills, nausea, vomiting, lumbar pain CVA tenderness Organisms E.Coli 75-80% Klebsiella 10% Enterobacter 10% Proteus 10%
Management of Acute Pyelonephritis Hospitalization IV Hydration IV antimicrobials until for 24-48 hrs after fever lyses and CVA tenderness resolves Oral antimicrobials for 2 weeks Blood C&S if no response to initial anti- microbials Ampicillin + Gentamicin, Cefazolin or Ceftriaxone
Nephrolithiasis during Pregnancy Physiologic changes increase risk for stone formation: - Increase progesterone levels - Hydroureter Urinary stasis - GFR Na , Ca, UA filtration Presents with gross hematuria Sonography confirms suspected stone Intravenous Hydration & Analgesics Lithotripsy Acute Nephritic Syndrome Characterized by hematuria and proteinuria with renal insufficiency and salt-water retention edema, hypertension and circulatory congestion Acute poststreptococcal glomerulonephritis Membranous IgA and mesangial glomerulonephritis are seen on renal biopsy Associated with fetal loss and perinatal mortality, preterm delivery and growth restriction Connective Tissue Disorders GM 34 y/o G5P0 (0040) 9-10 wks sought prenatal care. BP-110/70, PR- 76/min, RR- 21/min, T- 36.7 C Heart & Lungs were unremarkable On speculum examination, cervix was violaceous w/ brownish mucoid discharge Cervix- soft, long, closed Uterus- enlarged to 2 mos size Adnexae- no tenderness Antiphospholipid Syndrome (APS) Antiphospholipid Syndrome Autoimmune disorder defined by the presence of characteristic clinical features and specified level of circulating antiphospholipid antibodies. Platelets may be damaged directly by antiphospholipid antibody or indirectly binding B2 glycoprotein I which causes platelets to be susceptible to aggregation.
Antiphospholipid Syndrome Antiphospholipid antibodies decreased decidual production of vasodilating PFE2 Uncontrolled placental complement activation by antiphospholipid antibodies may play a role in fetal loss and growth restriction. Lupus anticoagulant (LAC) and anticardiolipin antibodies (ACA)- most widely accepted for clinical use Indications to Identify Lupus Anticoagulant and Antiphospholipid Antibodies Recurrent pregnancy loss Unexplained 2 nd or 3 rd trimester loss Early onset severe preeclampsia Venous or arterial thrombosis Unexplained fetal growth restriction Autoimmune or connective tissue disease False positive serological test for syphilis Prolonged coagulation studies Positive autoantibody test Classification Criteria for the Antiphospholipid Antibody Syndrome Clinical Thrombosis Unexplained venous arterial, or small vessel thrombosis in any organ or tissue Pregnancy One or more unexplained fetal losses after 10 weeks 3 or more consecutive abortions before 10 weeks Preterm delivery for severe preeclampsia Placental insufficiency before 34 weeks
Classification Criteria for the Antiphospholipid Antibody Syndrome Laboratory Anticardiolipin antibodies IgG or IgM isotypes in medium to high titers at least 6 weeks apart
Lupus anticoagulant Partial thromboplastin time, dilute Russel viper venom test (dRVVT) and the platelet neutralization procedure Identified twice at least 6 weeks apart Adverse Effects Arterial and venous thrombosis Autoimmune thrombocytopenia Fetal loss Preeclampsia IUGR Placental insufficiency Preterm delivery Treatment Guidelines Low dose aspirin, 80mg daily - blocks the conversion of arachidonic acid to thromboxane A2 while sparing prostacyclin Heparin, 5000-10,000 units SC q 12hours - prevent venous and arterial thrombotic episodes Glucocorticoids use only if with connective tissue disorder Immunoglobulin therapy 0.4 g/kg daily for 5 days - use when 1 st line therapies have failed Treatment Guidelines Calcium and Vitamin D - prevent osteoporosis Fetal antepartum surveillance - fetal growth monitoring - Biophysical profile scoring - NST, CST - Doppler velocimetry Systemic Lupus Erythematosus Systemic Lupus Erythematosus Multisystemic autoimmune rheumatic diseases with protean and often complex manifestations Chronic or of a relapsing or remitting form Has serious muskuloskeletal, renal and cardiovascular effects Pathogenesis SLE occurs when a patient develops persistent pathogenic autoantibodies and immune complexes These alter the normal anatomy and function of target tissues and organs These gives rise to a constellation of signs and symptoms Clinical Findings May be confined initially to one organ system, with others being involved as the disease progresses.
Alternatively, the disease may initially manifest by multisystem involvement.
Common findings are malaise, fever, arthritis, rash, pleuropericarditis, photosensitivity, anemia, and cognitive dysfunction. Laboratory Findings Screening - Antinuclear antibody (ANA) highly sensitive but not specific
Specific test for Lupus - Double stranded DNA (dsDNA) - Smith (Sm)
1997 Revised Criteria of American Rheumatism Association for Systemic Lupus Eryjthematosus Malar rash Discoid rash Photosensitivity Oral ulcers Arthritis Serositis Renal disorder Neurological disorder Hematological disorder Immunological disorders Antinuclear antibodies
Effect of SLE on Pregnancy If no HPN, renal impairment or APS ---pregnancy outcome is better
Renal disease HPN developed and proteinuria worsened
Increase incidence of preeclampsia SLE Nephritis Require intense fetal and maternal surveillance Pregnancy outcome is better if lupus activity has been quiescent for at least 6 months before pregnancy Pregnancy outcome is better if at conception creatinine </= 1.5 mg/dl; proteinuria is < 3g/24hr and BP is controlled. SLE Nephritis Proteinuria is the most common presentation (75%),followed by hematuria or aseptic pyuria (40%), and followed by urinary cast (33%). Diffuse proliferative glomerulopnephritis most common and most serious histologic category. of women experienced renal deterioration 50% fetal loss rate if creatinine is >1.5mg/dl
Rheumatoid Arthritis Rheumatoid Arthritis Chronic inflammatory/autoimmune disease Characterized by symmetrical polyarthritis of the small joints of hands and feet Cardinal feature is inflammatory synovitis that usually involves the peripheral joints. The disease has a propensity for cartilage destruction, bony erosions, and joint deformities. Rheumatoid Arthritis Genetic predisposition Cigarette smoking increase the risk Protective effect of pregnancy Clinical Manifestations Prodromal phase malaise, weight loss, arthralgias, or joint stiffness The onset is insidous with pain and swelling in one or more joints in the upper extremities Progression is usually centripetal (from small joints to large joints) Clinical improvement during pregnancy American College of Rheumatology Revised 1987 Criteria for Classification of Rheumatoid Arhtritis 1. Morning joint stiffness 2. Arthritis of 3 or more joints 3. Arthritis of wrist, metacarpophalangeal joint or proximal interphalangeal joint 4. Symmetrical arthritis 5. Rheumatoid nodules 6. Serum rheumatoid factor 7. Radiographic changes Management Pain relief Reduction of inflammation Protection of articular structures Preservation of function
Management Systemic and articular rest Use of heat and cold modalities Physical and occupational therapy Aspirin or NSAIDs COX-2 inhibitors Disease modifying antirheumatic drugs (DMARDs) Glucocorticoid therapy
Malnutrition in Hospital Outpatients and Inpatients Prevalence Concurrent Validity and Ease of Use of The Malnutrition Universal Screening Tool Must For Adults