SPONTANEOUS ABORTION INTRODUCTION  Loss of pregnancy < 20 weeks or < 500g  Incidence of 15% of clinically recognized pregnancies  Incidence of 30 - 50% of overall pregnancies  Rates dramatically decrease after documentation of FHR with 8wk U/S (3-5%)  PV bleeding occurs in 25% of pregnancies  PV bleeding (early) leads to abortion rate of 30 - 50%  80% of abortions occur in the 1st trimester  Definitions (< 20 weeks)  Threatened abortion: closed cervix, NO passage of POCs  Inevitable abortion: cervix open, NO passage of POCs  Incomplete abortion: cervix open, passage of some but not all POCs  Complete abortion: cervix closed, passage of all POCs  Septic abortion: maternal infection  Missed abortion: no FHR, no passage of POCs and failure of uterine growth overtime (should be called 1st/2nd trimester fetal death)  Blighted ovum = anembryonic gestation: suspected with gestational sac > 25 mm with no fetal pole Complete abortion cannot be diagnosed unless an intact gestational sac is seen, pathologic confirmation of POCs on D&C specimen, or conversion of pregnancy test to negative (4weeks) CLINICAL FEATURES  History  Gestational age, LMP, ectopic RF, syncope, blood type  Pain, bleeding, fever, cramps  Threatened abortion has dull ache b/c uterus not contracting; inevitable and incomplete have crampy pain b/c uterus is contracting; no pain w/ complete  Physical Exam  Vitals: stable? orthostatic changes? fever?  Abdomenal exam: masses, peritonitis, tenderness  Pelvic: cervix open, bleeding, tissue, uterus size/tenderness, adnexal mass or tenderness, remove tissue present in vagina or cervix, may probe cervix gently if open to search for tissue and to see if internal os is open (not in 2nd b/c risk of low placenta)   Investigations     CBC, Type and screen (? needs rhogam): crossmatch if unstable BHCG: urine qualatative, serum quantitative Blood cultures if fever/septic Saline preparation of tissue: chorionic villi, present in 50%, rules out ectopic except in rare circumstance of co-existing ectopic and IUP  Other: CA-125, low progesterone, low urinary HCG have been used as indicators of miscarriage  Ultrasound all should get an ultrasound b/c of possibility of ectopic no FHR = fetal loss only if length > 15mm or gest sac >25mm unstable: to OR without ultrasound stable: urgent ultrasound or RTED in am for ultrasound (significant pain or bleeding should not be sent home) NO FHR: careful distinction b/w fetal loss vs too early to see fhr Differential Diagnosis: PV bleed  Early pregnant: abortion, ectopic, “normal pregnancy bleeding”, corpus luteum cyst, molar pregnancy  Late pregnant: abruption, placenta previa, vasa previa, uterine rupture, PTL  NonPregnant: PID, DUB, anovulatory bleeding, trauma, etc  Ovarian torsion: adnexa pain >> bleeding, increased risk in early pregnancy MANAGEMENT  Make sure to give Rhogam to all Rh-ve patients (50ug 1st trimester, 300ug thereafter)  May require urgent OR for D&C or laparotomy/laparoscopy with heavy bleeding  Ultrasound for all: safe for u/s within 48hrs if minimal pain, minimal bleeding, easy to RTED, no strong risks for ectopic, no strong findings of ectopic (unilateral pain, tenderness, mass)  Threatened Abortion  Discharge home  NO D&C  Serial U/S and BHCG if no definitive IUP seen on u/s (r/o out ectopic)  Inevitable/Incomplete Abortion  D&C for: significant bleeding or pain, suspected infection, patient preference  Observation: rule out ectopic and let nature take its course, ensure follow up  Complete Abortion (presumed)  Send tissue to pathology; usually NOT obviously POCs  D&C: significant bleeding, pt preference, infected (some do routinely)  Observation: BHCG level < 1000, no endometrial tissue on U/S, mild bleeding, gestational age < 8 wks  Follow serial BHCG b/c could be ectopic  Missed Abortion  D&C: significant bleeding, pain, pt preference (decreased risk of infection, bl)  Observation: same as above  Septic Abortion  Admission for Mx of sepsis with iv Abx and fluids/etc  Gram +ves, -ves, anaerobes, STD bugs: clindamycin + gentamycin  Needs D&C as emergent procedure   Discharge Advice  RTED: pain, bleeding, syncope, fevers  F/U: for ultrasound, serial BHCG, pregnancy test at 4wks to r/o retained POCs  Education: reassurance, normal ADLs OK for threatened abortion, no sexual activity or tampons while bleeding, keep tissue if passing any, common problem, not the fault of the patient Hemorrhagic Shock from presumed Miscarriage  Large ivs, fluid, +/- blood, crossmatch, check coags, STAT O/G consult  Oxytocin 20 - 40 units/ 1L NS: run at 500-1000 ml/hr Uterine contraction and vasoconstriction\  Methyergonovine 02. Mg im/po/iv Vasoconstriction and increased uterine contractions Watch for hypertension, tachycardia, ischemia, etc - - HOW CAN YOU R/O ECTOPIC?? Obvious passage of POCs POCs seen on saline prep Path report of POCs post abortion Path report of POCs post D&C IUP seen on ultrasound (except IVF) Normal BHCG doubling time NOTABLES IUP + ectopic: 1/4000 -1/70000 unless IVF (1/100) Declining BHCG does not r/o ectopic Plateau, Rising, failure to decline to zero diagnoses an ectopic Low BHCG does not r/o ectopic (most ectopics have Beta <1000) Ectopic can occur with painless bleeding (uncommon) thus all 1st trimester bleeds need an ultrasound ECTOPIC PREGNANCY INTRODUCTION  Definition = any gestation that implants outside the endometrial cavity  Incidence 1/60; rising incidence  2nd leading cause of maternal death  10% of maternal mortality  Most seen in women 25 - 35 but rate highest in older women  Simultaneous intra and extrauterine pregnancies: 1/4000 —> 1/70000 (?) depending on reference  High rate of intra and extrauterine pregnancies with fertility management (1/100) RISK FACTORS (NO Rfs in 50% of confirmed ectopics)  P PID (strongest risk factor: 50% of ectopics have PID hx)  P Previous ectopic (2nd strongest RF; 15% chance of next pregnancy being ectopic)  P Pelvic surgery (tubal ligation, other)  P Previous infertility or current infertility treatment  P Prior abortion (recent) that actually was a missed ectopic  P People: low SES, smoking  P Pill morning after that failed PATHOPHYSIOLOGY  Location  Tubal: ampullary (95%), fibrial, infundibular, ischmic, interstitial  Cervical  Ovarian  Abdominal  Intraligamentous  Ectopic growth  The embryo grows at a slow rate usually resulting in a low BHCG level  Leakage of blood intermitently into the tubal wall or out the fimbrial ends with spillage into the peritoneal cavity; symptoms are intermittent  The embryo may abort, spill into the peritoneum, or grow until rupture  Rupture may cause minor or major hemorrhage  Uterine horn (cornual) ectopics use the myometrial blood supply and allows the embryo to grow larger before rupture at 10 - 14 weeks with massive hemorrhage: CORNUAL ECTOPICS ARE PARTICULARLY DANGEROUS Consider the diagnosis of ECTOPIC PREGNANCY in any female of reproductive age in the ED with abdo pain, vaginal bleeding, shock syncope --------> MUST check urine BHCGs 28yo Female syncope, found down --------> PEA arrest CONSIDER ECTOPIC PRESENTATION  Classic Triad: abdominal pain, vaginal bleeding, delayed/abnormal periods (amenorrhea)  No combination of hx/pe findings can rule out an ectopic (all need an ultrasound)  History  Pain: abdominal or pelvic; severe, constant, peritoneal is most common  Shoulder tip pain: intraperitoneal blood irritating the diaphragm  History unreliable: pain may be intermittent, crampy, or even absent  80% have missed a period; 20% have not  Risk factors occur in 50% (ask about risk factors)  May not give hx of vaginal bleeding  Passage of “tissue” by history does not r/o ectopic  Syncope or postural symptoms  Note: pain may be absent, bleeding may be absent  Unilateral pain more worrisome than bilateral pain  Physical  Abdominal tenderness 90% (peritoneal signs common)  Adnexal mass 50% (often the corpus luteum of pregnancy is palpable thus an adnexal mass is not sensitive or specific)  Vaginal bleeding: often minimal (heavy vag bleed more consistent with miscarriage but can occur with ectopic)  Tissue present on pelvic does not r/o ectopic (dropping hormonal levels with an ectopic can lead to endometrial sloughing which leads to passage of tissue)  Obvious passage of products of conception does r/o ectopic (can do a saline wet mount and the presence of chorionic villi r/o ectopic)  Minimally enlarged uterus  Most afebrile  Signs of shock variable, even with hemorrhage (VAGAL STIMULATION THUS NO TACHYCARDIA IS A COMMON FINDING) HISTORY and PHYSICAL EXAMINATION are INSENSITIVE and NONSPECIFIC for the diagnosis of ectopic pregnancy DIFFERENTIAL DX  Vaginal bleeding: miscarriage, ruptured corpus luteal cyst, acute PID, molar pregnancy  Abdominal pain: acute PID, adnexal torsion, ruptured luteal cyst, appy, pyelo, pancreatitis, etc  Ruptured corpus luteal cyst  On ddx of 1st trimester pv. bleeding and abdominal pain  Rupture causes sudden peritoneal irritation  Ultrasound shows IUP, culdocentesis shows Hct < 12% and serous fluid in 50%  If IUP cannot be seen on ultrasound laparoscopy/laparotomy needed to distinguish b/w ectopic; these can bleed and pt may be unstable requiring laparotomy (significant bleeding relatively rare;ie, <1% of ruptured cysts( INVESTIGATIONS  Saline Slide    Laboratory    Ultrasound               Saline preparation slide of passed material to look for chorionic villi Presence of POCs will exclude ectopic except in heterotropic pregnancies Urine BHCG (qualatative): put in foley and cath if unstable Type and screen if stable, type and cross if unstable, check Rh status Transabdominal (TAS) versus transvaginal (TVS) an important distinction Gestational sac should be seen by 5 weeks TVS and 6 weeks TAS Fetal heart activity should be seen by 7 weeks TVS and 8 weeks TAS Used in combination with quantitative BHCG (Discriminatory Zone) Who? all with first trimester vaginal bleeding should get ultrasound When? hemodynamically stable, no peritonitis, minimal pain/bleeding can return in am for ultrasound as long as specific discharge instructions given Transabdominal: indeterminate in 50% of ectopics Transvaginal: better, less indeterminate studies Diagnostic of ectopic: ectopic fetal heart or fetal pole Diagnostic of IUP: double ring sign, double gestational sac, IU heart, IU pole Suggestive of ectopic: cul-de-sac fluid with NO IUP, adnexal mass with NO IUP Indeterminate: no IU findings, single gestational sac, multiple intrauterine echoes, abnormal sac, echogenic material, nonspecific fluid collection Role of ultrasound < 5 weeks: do ultrasound and BHCG, in No IUP seen you follow BHCG and repeat ultrasound when BHCG > discrimnatory zone BHCG              - Hormone secreted by synctytiotrophoblast to support the corpus luteum Blood assays are 99% sensitive and 99% specific Detectable by 7 days after ovulation which is shortly after implantation False -ve urine BHCGs dilute urine (SG < 1.010, use 20 drop test) gross hematuria\ protein > 2+ Levels rise after 8 - 9 days, and double every 1.8 - 3.0 days for the first 6 - 7 wks Majority (85%) increase by > 66% q48hr Minority (15%) increase by < 66% q48hr Increase by < 50% in 48hr is a non-viable pregnancy (m/c or ectopic) Decrease by 50% q48hrs (T1/2 is 48hrs): failure to decline = retained POCs Used in combination with ultrasound: discriminatory zone: discrimnatory zones vary with different references (sensitivity/specificity varies with levels) TVS: BHCG > 1500 mIU/ml (5.5 weeks) + no uterine sac = ectopic TAS: BHCG > 6500 mIU/ml (6.5 weeks) + no uterine sac = ectopic Ectopic pregnancy and BHCG most ectopics have low levels of BHCG (doesn’t r/o ectopic) ectopics can have VERY low levels (case reports of zero!) declining BHCG can be miscarriage or ectopic ectopics can have slowly rising BHCG (or plateud) normal doubling time does R/O ectopic minority of ectopics will reach 6500 (25%) Serial levels can be followed in a stable patient: MUST follow to ZERO HCG > expected (esp > 100,000): think MOLAR PREGNANCY HCG +ve in males: testicular tumor    Serum progesterone  Low level (< 25 ng/ml) consistent with ectopic, abortion  Level > 25 ng/ml r/o ectopic but < 25 ng/ml not helpful b/c many normal IUP have level < 25  Positive predictive value of IUP with progesterone > 25 was reported to be 99.6% in one study with ectopic incidence of 8.9% Culdocentesis  Aspiration of fluid from pouch of Douglas by inserting needle through posterior vaginal fornix and into peritoneal cavity  Used less now: replaced by serial BCHCG and ultrasound  Consider in unstable patient who cannot tolerate the time for ultrasound or ultrasound is not readily available  Ruptured ectopic: 85 - 90% with positive culdocentesis (sensitivity)  Unruptured ectopic: 65 - 70% with positive culdocentesis  Positive culdocentesis: nonclotting blood is aspirated through the posterior cul-desac of the vagina: blood should not clot b/c of the presence of defibrinators in the peritoneum; clotting blood indicates aspiration of pelvic veins without a true peritoneal sample. Very rapid intraperitoneal bleeding can overcome the peritoneal anticoagulants but the clinical picture should be obvious. Culdocentesis hematocrit > 12% suggests ectopic.  Negative culdocentesis: serous fluid < 5.0 ml  Indeterminate: dry tap, clotted blood, serous fluid > 5.0 ml Laparoscopy  Extremely accurate and useful  Last step b/c of surgical, anesthetic risk  Diagnostic and therapeutic MANAGEMENT  Hemodynamically unstable or Frank peritonitis  ABCs, brief history and physical examination  Investigations: baseline CBC, type and cross, urine BHCG (cath if necc)  Stat consult to O&G  Two large bore ivs: fluid +/- blood resuscitation  Laparotomy  Stabilized, Peritonitis  Same approach  Consider ultrasound or culdocentesis  Stable patient  Goal: localize the pregnancy and r/o ectopic  Investigations: quantitative BHCG and ultrasound  Consider admission: unreliable pt, high risk for ectopic, significant pain/bleeding  Three outpatient approaches .... U/S w/i 24 - 48hrs: if no IUP seen, measure quantitative BHCG or progesterone to define IUP (progesterone > 25) or determine when U/S should be repeated (BHCG > discriminatory zone which is 1500 - 2000 mIU/ml for transvaginal U/S) Serial BHCG levels: if level rises > 1500 then U/S is repeated; if levels plateau or decline then d/c is done to differentiate ectopic vs abortion Serum progesterone: progesterone < 25 referred for U/S, levels > 25 likely IUP (3% of ectopics can have progesterone > 25), level < 5 likely miscarriage : D&C    Miscellaneous  Fertility patients considered high risk and less role for outpt management  Give RHIG to all Rh-ve moms (50ug IM) unless father known to be Rh-ve Medical Management  Methotrexate: folic acid inhibitor that blocks nucleic acid synthesis in trophoblasts, given once im (80% effective); repeat dose needed in 15%  Side effects: n/v/d/abdo pain, stomatitis, hepatotoxicity, cp/cough/sob  Need to avoid folic acid supplementation while on methotrexate  Must follow BHCGs to zero  RU 486 will replace methotrexate in future  Criteria for medical management stable hemodynamically small: < 3.5 cm small bhcg level: < 15,000 (success rates decline with increasing betas: 95% if < 1000, 85% < 10,000, 80% < 15,000, etc) no c/i to methotrexate: leukopenia, thrombocytopenia, liver dz, renal dz (must check CBC, SCR, BUN, AST) Surgical Management  Contraindications to medical management  Laparoscopy preferred if stable  Laparotomy necessary for ... hemodynamically unstable ectopic > 3.5 cm extensive pelvic adhesions failure of laparoscopy ANTEPARTUM HEMORRHAGE (APH) INTRODUCTION  Incidence: 4% of pregnancies  Definition: vaginal bleeding in the 2nd half of pregnancy (>20wks)  Bleeding < 20wks is an abortion (miscarriage) not APH  Incidence: 5% of pregnancies  Importance: increased risk of prematurity, perinatal and maternal morbidity/mortality  Serious life-threatening disorder thus any bleeding in pregnancy, pt MUST come to hospital  Etiology of APH  Unknown (50%)  Abruptio placenta (30%)  Placenta previa (20%)  Vasa previa (fetal vessel rupture)  Uterine rupture  Cervical/vaginal lesion (polyp, ulcer, abrasion)  Rectal lesion (hemorrhoids etc)  Early labor (bloody show)  Occult placental separations  Approach to APH           Quick look, ABCs, vitals to determine full resuscitation vs hx/PE/invest Unstable: large IV lines, stat blood work, stat O&G consult, fluids, consider blood and FFP/platelets for coagulopathies Fetal monitoring Hx: amount and duration of bleeding, hx of trauma/sex, abdominal pain, UT contractions, obstetrics hx (previous C/S, preterm labour, previa, etc), recent ultrasounds (has a recent U/S ruled out previa??) PE: vitals, orthostatic changes? (NO pelvic if the hx is painless bleeding unless there has been definitive recent U/S that did NOT show a placenta previa) US to localize the placenta (best test) Labs: CBC, type and screen/cross, and coags looking for evidence of DIC (PTT, INR, fibrinogen, d-dimer) Management depends on etiology, maternal status, fetal age and status RhIG to all Rh-ve moms with Rh+ve dad or unknown dad Transfer to obstetrical unit MUST RULE OUT PLACENTA PREVIA IN THIRD TRIMESTER BLEEDING BEFORE DOING A PELVIC EXAMINATION  NOTE    Consider abruption on ddx of abdominal pain in later pregnancy even without hx of vaginal bleeding (may be concealed) May be confused with early labor Hypotension, shock, syncope: Abruption, Amniotic Fluid Embolus, UT rupture ABRUPTIO PLACENTA (30%)  Definition: partial or complete separation of a normally situated placentia  Also called accidental hemorrhage  Incidence 1 in 200 deliveries  Etiology: unknown (MC), HTN thought to be most common cause, blunt trauma  Associations: folate def, advanced maternal age, acute decompression, short cord  Classification  Partial vs complete separation  Concealed (internal) vs revealed (external) vs mixed (MC)  Couvelaire UT: complete separation usu w/ intrauterine death  Presentation  Vaginal bleeding in 80% (can be totally concealed): dark blood, often minimal  Abdominal pain 60%, abdominal tenderness60%  Hard, tender, tetanic uterus in 30%  Fetal distress -------> fetal death (15%)  Hypovolemia not in proportion to amount of bleeding  May have complications of renal failure, DIC, AFE (increased risk)  Abruption is the most common cause of DIC in pregnancy  Consider with abdopain even w/o bleeding; commonly confused with   PTL Grading (clinical)  Grade 0 - I: 40% slight vaginal bleeding minimal or no UT irritability no fetal distress no clotting abnormalities  Grade II: 45% moderate vaginal bleeding uterine irritability +/- uterine tetany maternal tacchycardia fetal distress fibrinogen 150 - 200 mg/dL  Grade III: 15% very painful uterine tetany maternal hypotension fibrinogen < 150 high risk of fetal death Approach  Stratify into stable or unstable  ABCs + IVs and correct hypovolemia + fetal monitoring + stat O&G consult  MOM: hx, PE, coags, foley, fluids, blood, FFP, platelets prn  FETUS: NST, BPP, US (must do U/S b/f pelvic)  Ultrasound: unreliable, done to r/o placenta previa, clinical diagnosis; unreliable b/c echogenicity of blood = placenta, sensitivity 2-20%  Apt test: confusion of maternal vs fetal blood (vasa previa); blood on slide and mix with NaOH, maternal blood hemolyses to produce yellow supernatant (“moms are yellow”), fetal blood does not hemolyse and supernatant will be pink (“babies are pink”)  Obstetrical Mx: C/S for fetal distress, continued bleeding or obstetric indications; otherwise, vag delivery by induction; MUST watch for DIC and post partum hemorrhage PLACENTA PREVIA (20%)  Definition: partial or complete implantation of the placenta in the lower segment of the uterus  Also called the inevitable hemmorrhage  1 in 250 live births  Etiology unknown  Types: central vs marginal; 1st degree ------> 4th degree  Risk Factors: multiparous, older age, previous hx. multiple gestation, prior C/S  Pathophysiology  Tearing of placental vessels as UT wall elongates or cervix dilates  Bleeding usually self limites unless increased by cervical probing  History  PAINLESS, CAUSLESS, RECURRENT vaginal bleeding  20% have contractions with previa :. MAY have pain (usually minor)  Mean onset of bleeding is 30wks (1/3 b/f 30)  Physical Exam  Hypovolemia related to amount of bleeding        Non-tender UT Abnormal lie, high presenting part Never do a digital or speculum vaginal examination in a third trimester patient w/ hx of vaginal bleeding until you have R/O placenta previa: superficial speculum examination safe if you don’t have access to U/S or O&G consult Approach    ABCs + large IVs + fetal monitoring and crossmatch blood Hx + PE w/o pelvic + labs including crossmatch and coag/DIC W/U US (gold standard for dx b/c 95%-100% accurracy; do b/f pelvic); empty bladder for U/S will decrease false -ve rate  Gestational age important At or Near Term  US shows significant placenta previa -------> delivery by C/S  US shows minor placenta previa ------------> attempt V/D+double setup _ go to OR w/ cross-matched blood and prepare for a C/S _ carefully examine pt and do C/S if you feel placenta _ attempt V/D if no placenta felt _ not used much b/c US accurately defines placental position Immature fetus (30wks)  Hospitalize and monitor + IVs while waiting for delivery  Outpatient Mx possible if pt is able to come to hospital very quickly w/ L/D  Must do C/S for lifethreatening bleeding Unique concerns  Placenta accreta: placental implantation into wall of uterus myometrium vs just being attached, serious bleeding can occur at delivery, hysterectomy may be a life saving procedure  Postpartum hemorhage UTERINE RUPTURE  Complete separation of uterine musculature through all of its layers  Prior UT scar in 40%  Risk with classic C/S is 5% (vs 0.5% with lower C/S)  Hx: sudden onset intense abdominal pain and some vag bleed  PE: presenting part retracts on pelvic exam, fetal parts easily palpated transabdominally. Impending rupture - restless, hyperventilation, agitation, taccy  Mx: STAT laparotomy usu w/ TAH VASA PREVIA  Occurs with villamentous insertion :. unprotected vessels pass over the cervical os and increase risk of rupture  Bleeding is from fetus therefore potential for distaster  Painless vaginal bleeding and fetal distress (tacchy or brady)  APT test makes dx (NaOH + blood ------> pink supernatant is baby)  Wright’s stain on blood smear and look for nucleated rbc.s  Mx: stat C/S  Px: 50% perinatal mortality MISCELLANEOUS TOPICS POST D&C BLEEDING  Must consider that ECTOPIC pregnancy has been missed  R/O ectopic by D&C path report, ultrasound showing IUP  Consider that patient has RETAINED PRODUCTS OF CONCEPTION  Ultrasound (really necessary?)  Observation Closed os, no tissue or blood Mild symptoms Minimal bleeding No evidence of infection U/S mass small (<3cm)  Indications for repeat D&C Open os, tissue at os Significant cramping Significant bleeding Evidence of infection Large mass (>3cm) on U/S  Follow up  Preg test at 4 weeks  +ve indicates that tissue hasn’t been passed  Specific RTED instructions required  NOTE: 75% of patients with retained products post D&C will have spontaneous passage within 3 days (was U/S really necessary?) CHORIOAMNIONITIS  Fever and uterine tenderness > 16 weeks  Maternal clues: PROM, malodorous vag d/c, UT tenderness, fever, maternal tachycardia, wbc  Fetal clues: fetal tachy, decreased movement, decreased variability, abnormal BPP  Bugs: GBS, E.coli, GC, chlamydia, mycoplasma  Dx: amniocentesis for definitive dx  Antibiotics: ampicillin/erythromycin iv X 2/7 then po X 7 doses GENITAL TRACT INFECTIONS AND PREGNANCY  Bacterial Vaginosis  20% of pregnancies  Risks: PTL, PROM, abortion, cuff cellulitis, peripeural infection, chorioamnin  Rx even if asymptomatic b/c of risks  Rx with flagyl po 7/7, or gel 5/7 (clinda po 7/7)  Candida  Increased because of estrogen  NO association with PTL or LBW  Rx with vaginal imidazoles  Trichomonas: Rx flagyl 2gm po X 1 or 7/7 course  Chlamydia: Rx erythromycin or amoxil 7/7 (risks PTL, PROM, LBW, endometritis, chorio)  HSV: Rx acyclovir po for first episode  Gonorrhea: Rx the same (risks same as chlamydia)  PID: rare in pregnancy, doesn’t occur after 1st trimester GESTATIONAL TROPHOBLASTIC DISEASE  Tumors arisiong from fetal chorion: spectrum of disease from benign to malignant  1/1000 pregnancies, more common in very young and older  Complete mole: no fetal tissue (majority)  Incomplete mole: fetal tissue present (rare)  Gestational choriocarcinoma: malignant transformation from molar tissues, very aggressive  History  Irregular or heavy vaginal bleeding in 1st/2nd trimester (think with abortions)  Usually painless  May have expulsion of molar vesicles  Excessive N/V due to excess BHCG (hyperemesis gravidarum)  Associated with PIH  Partial mole generally presents as late miscarriage  Can be incidental finding on U/S  Can develop after delivery  Physical  Uterus large for dates (>4weeks) in 50% in complete  Uterus small for dates in partial mole  NO fetal heart tones  Grape-like vesicles on pelvic  Ovarian enlargement by thecal lutean cysts in 30%  Wheezing, SOB from trophoblastic emboli  Diagnosis/Management  Quantitative BHCG higher than expected (consider GTD and mult gestations)  Ultrasound: hydropic vesicles with “snowstorm”appearance  D&C indicated, watch for DIC, monitor BHCG, prophylactic chemo not indicated, Rx with oxytocin  Choriocarcinoma  SOB, hemoptysis, wheezing common from lung mets  Presents with s/s of mets to lung, brain. Can present with acute abdomen from rupture of UT, liver, or thecal lutein cyts.  “The great imitator” b/c of unusual presentation ........Screen for this with BHCG level in any female of reproductive age with unusual symptoms  Needs LP for investigation of BHCG in CSF  Rx: chemo + hysterectomy HYPEREMESIS GRAVIDARUM  Definition = nausea and vomiting leading to starvation metabolism, weight loss, dehydration, prolonged ketosis in a pregnant female  Due to rapid increase in BHCG (? association with H.pylori)  Mx: iv prn, antiemetic, assess po intake, consider admission for iv rehydration and enteral feeding, consider diclectin, note that oral methylprednisone has been used URINARY TRACT INFECTIONS  Most common complication of pregnancy  Actual rates of asymptomatic bactururia do not increase but rates of symptomatic UTIs does  Why?  Hormonal: progesterone decreases ureteral peristalsis  Mechanical: pressure on ureters, urethra and dilatation and distortion of ureters, renal pelvis, and ureteral insertion on bladder  Asymptomatic UTI  > 10^6 with NO symptoms  Note: lab may not report low culture counts  30% will develop UTI thus Rx indicated (vs nonpregnant)  Same bugs  Chose an antibiotic safe in pregnancy for 7 - 10d (ampicillin, ancef, keflex, ?cipro, NO sulphas in 3rd trimester - OK in 1st or 2nd trimester)  F/U culteures at one month  Acute Cystitis  Dysuria, frequency, urgency, hematureia but no fever, back pain  Same tx as asymptomatic UIT  Acute Pyelonephritis  Lower UTI symptoms + fever, rigors, back/flank pain, N/V, dehydration  Fever, CVA tenderness on exam  Note predominance of right sided symptoms (?why)  Urine CAN be negative if there is an obstruction  Remember: 20% of appendicitis have pyuria without bactururia!!  Pyelo increases risk of PTL (contractions very common)  Ddx of dysuria: remember vaginitis, herpes and other STDs, torsion  Mx: usually admitted for iv antibiotics after cultures (ampicillin + gentamycin), monitor for PTL, D/C when afebrile X 48hrs ABDOMENAL PAIN IN THE PREGNANT PATIENT DIFFERENTIAL DIAGNOSIS  Pregnancy Related  Abortion  Ectopic  Corpus luteal cyst rupture  Abruption  UT rupture  Chorioamnionitis  PIH  Labor  Acute Fatty Liver of pregnancy  Spontaneous liver bleed/rupture  Spontaneous spleen bleed/rupture  Gyne  PID  Ovarian cyst   Nongyne        Ovarian torsion Appy Chole Pyelo Renal colic Hepatitis Gastro ETC APPENDICITIS  Increased rates of perforation  Presentation similar in 1st tri  Displaced appendix counterclockwise out of pelvis in 2nd/3rd  Sterile pyuria in 20% because of inflammation of ureter/kidney (close approximation)  THINK of appendicitis in flank pain, fever, abdotenderness + pyruria with NO bactururia  Physiologic leukocytosis  Physiologic tachycardia  Physiologic N/V of pregnancy  Fever/tachycardia can be less common b/c of increased maternal steroids  Uterus obscures normal physical findings of peritoneal irritation :. presents late, pain and tenderness are more diffuse and atypical locations (RUQ in late pregnancy), perforation rate is higher  Dx: ultrasound, CT less useful (5 rads to fetus), laparotomy/laparoscopy  Mx: NPO, iv, consultation with surgery +/- obstetrics HEPATITIS  MC liver disease in pregnancy  Causes, dx, tx unchanged GALL BLADDER DISEASE  Gall stones 5%, symptomatic in 50%  Hormonal changes, steroid increase :. increased gall bladder volume and decreased contractility and more stasis and more cholelithiasis  Note physiologic leukocytosis, increased amylase, and ALP (2Xs, produced by placenta)  U/S shows stones but doesn’t tell you if they are symptomatic  Ddx: hepatitis, AFL of pregnancy, appy, pyelo, spont liver bleed all can give RUQ pain  Mx: admit, observe, antibiotics if infected, try to avoid surgery b/c of anesthetic risk to fetus ACUTE FATTY LIVER OF PREGNANCY  Fulminant hepatic failure in 3rd trimester with complicated labor and increased maternal and fetal mortality with unknown etiology (note similarity to Reye’s)  More common in primips and multiple gestations  Pathology: fatty liver infiltrate with NO necrossis  Liver function returns to normal after pregnancy  N/V in third trimester is historical clue  Presentation: N/V, anorexia, fatigue, H/A, jaundice, tender liver, coagulopathy/SZ/coma, 50% associated with PIH  Labs: leukocytosis, thrombocytopenia, incr bili/PT/PTT/FDPs/uric acid/AST/ALT (< 500)    Dx: ultrasound normal, CT normal, bx required for dx Ddx: viral infection, PIH with congested liver shouldn’t cause hepatic failure, drugs/toxins possible, cholecystitis doesn’t cause liver failure Mx: stabilize and deliver, follow coags and replace blood products prn INTRAHEPATIC CHOLESTASIS OF PREGNANCY  Idiopathic jaundice, pruritis gradivarum  Cholestasis, jaundice, pruritis in 3rd trimester  Mild incr bili and ALP, normal AST/ALT  Must exclude other liver conditions  Mx: antihistamine, cholestyramine HEPATIC/SPLENIC RUPTURE  Case reports of spontaneous hepatic or splenic hematomas/rupture  Usually associated with PIH and DIC  Dx usually requires CT b/c organs hidden by ribs and not always seen on U/S  Intraperitoneal —> peritonitis  Consider UT rupture and conceal abruption PREGNANCY INDUCED HYPERTENSION (PIH) INTRODUCTION  7% of pregnancies  PIH = > 140/90 during pregnancy (after 20wks) and resolves postpartum  Prenancy aggravated chronic hypertension  Preeclampsia (Toxemia) = old terminology for HTN + proteinuria + edema  Eclampsia = preeclamsia + seizures  Classification (CMAJ 1997)  Preexisting HTN: diastolic HTN dx before 20 weeks  Prexisting HTN w/ superimposed gestational HTN with proteinuria: dx before pregnancy  Gestational HTN: develops > 20 weeks With or without proteinuria (> 0.3gm in 24hr) With or without adverse conditions (sz, DBP>110, plt <100, oliguria, pulmn edema, incr AST/ALT, severe N/V, persistant RUQ pain, frontal H/A, visual disturbances, CP, SOB, suspected abruption, HELLP syndrome, IUGR, oligohydramnios, absent/reverse umbilical artery flow) PATHOPHYSIOLOGY  Starts with uteroplacental ischemia which promotes widespread ischemia, capillary leak and platelet clumping  Vasospasm/Ischemia due to Nitric oxide deficiency and production of endothelin (VC)  Brain: seizures, strokes, headaches, visual symptoms, decreased LOC  Kidneys: renal failure  Placenta: IUGR  Liver: ischemia –> periportal necrosis then hepatic congestion  Heart: chest pain   Capillary leak  Pulmonary edema  Hepatic congestion  Splenic congestion  Hand/face edema Platelet Clumping/Microangiopathy  Thrombocytopenia  Microangiopathic hemolytic anemia CLINICAL FEATURES  Risk Factors  Nulliparous, previous hx, fhx, vasculopath, multiple gestation, molar pregnancy, fetal hydramnios, race, SES, IUGR  History  Headache, visual changes, severe N/V, RUQ or epigastric pain, chest pain, SOB, seizures, face or hand edema change  Physical Exam  Pulmonary edema, RUQ tenderness, facial edema, hand edema, BP > 140/90   Investigations  HELLP: hemolytic anemia, elevated liver enzymes, low platelets (<100)  Hemolysis: anemia, increased bili, increased LDH  Proteinuria: mild 1+, severe > 2+  Oliguria < 500 ml/d  Reduced/reversed umbilical artery flow  IUGR Notes on HELLP  5% of PIH  Increased with multips, > 25, < 36wjks  HTN may be absent (can have HELLP w/o PIH)  PT, PTT, fibrinogen normal (DIC can be similar)  Platelets < 100 COMPLICATIONS  Maternal          Fetal   MANAGEMENT Cerebral hemorrhage Seizures Pulmonary edema CHF Renal Failure DIC HELLP Liver/splenic rupture (congestion) Premature delivery Placental abruption   Mild    < 170/110 and NO adverse conditions Term: deliver Preterm: observe    > 170/110, proteinuria > 5g/24hr, HELLP Stabilize and deliver Treat BP with hydralazine 5mg or labetolol 20 mg Severe PIH RELATED SEIZURES (ECLAMPSIA)  Can occur postpartum (2 - 10 days have been reported although rare)  EXAM CASE: seizure 2 weeks post partum that is ECLAMPSIA!  Retrospective reviews of eclamptic seizure patients  Headache 80%  Hyperreflexia 70% (½ with clonus or Chevostek’s sign)  Generalized edema 50%  Marked proteinuria 50%  Visual changes 40%  Abdomenal pain 20%  Investigation  Must consider ddx of seizures (structural vs metabolic) (AFE - 10% have initial presentation with seizure)  Glucose, lytes, Ca, Mg, P04 for seizures  CBC, Urate, ALT, LD, urinalysis (?protein) for PIH  Head CT: localizing signs, persistent seizure despite Mg, prolonged seizure (eclamptic sz usually short), persitent post-ictal state, suspicious for non-eclamptic seizure, no hx of PIH. Note that pregnant patients with PIH are also at risk for bleeds as well. Probably should do in all  Consider pregnant trauma patient: ? sz as precipitant of trauma.  Management  Eclamptic seizures are brief duration; ie, should spontaneously stop in 12min  Seizure control: Magnesium is drug of choice (benzos second line)  Hypertension control: Labetolol or Hydralazine  Minimize fluids to avoid exacerbating pulmonary edema  Do NOT give diuretics or hyperosmolar agents  Consult O&G and initiate steps toward delivery: don’t forget fetal monitor  Magnesium  Magnesium controls almost all eclamptic seizures thus think of ddx if magnesium is not effective  MOI: acts as a membrane stabilizer and decreases neuromuscular transmission to reduce CNS irritabiltiy; also is a smooth muscles inhibitor :. vasodilation decreases cerebral ischemia  Side-effects: headache, hot flash, N/V, dizzy, lethargy  Complications: hypotension, respiratory depression/arrest, cardiac depression or arrest, pulmonary edema, hypocalcemia, fetal depression  Contraindications: hypocalcemia, myasenia gravis, renal failure  Intravenous: 6 gm over 15 min then 2 gm/hr  Intramuscular: 4 gm iv over 5 min + 10 gm deep im (½ in each buttock), repeat 2 gm iv if seizure lasts > 15 min, 5 gm im q 4hrs      Stop magnesium for (i) areflexia (ii) hypoventilation (iii) u/o < 25 cc/hr Reversal of toxicity with 10 ml of 10% CaGluconate Prophylaxis: ? all patients with severe PIH, let O&G decide Does it work? good literature showing decreased recurrence and that Mg is superior to BZD and dilantin (Coetzee 1998: RCT; Duley 2000 Cochrane review of 5 RCTs; Duley 2000 Cochrane review of 4 RCTs. Hypertensive Mx  Give to all patients with DBP > 105  Labetolol: 20 mg iv q15 min prn to effect  Hydralazine: 1mg iv over 1min then 5 - 25mg iv over 4 min q15 min