When women said there is absolutely no way they can be pregnant, they were wrong 10% of the time (Ann Emerg Med 1989;18(1):48)<\/p>\n
<\/span>1st Trimester Vaginal Bleeding\/ABD Pain<\/span><\/h2>\nBleeding: Ectopic vs. Abnormal Pregnancy (Abortion) vs. Normal Pregnancy<\/p>\n
Pain:\u00a0 Torsion, ruptured cyst, TOA, endometriosis, and the normal surgical causes<\/p>\n
<\/h3>\n
History: heavy bleeding more suggestive of spontaneous abortion; worrisome sign if pain persistent and worsens over time; typically associated with crescendo-decrescendo pattern in which pain and bleeding peak over course of 1 to 2 hr and drop off abruptly<\/p>\n
Spontaneous Miscarriage<\/p>\n
up to 1\/3 of pregnancies.\u00a0 If Rh neg, give rhogam (50 ug if 1st trim., 300 after)<\/p>\n
\n- Threatened Ab <\/b>– any amount of uterine bleeding in the first 20 weeks of pregnancy without passage of tissue or cervical dilation.\u00a0 Should see FHTs if appropriate fetal size.\u00a0 85% will progress to full term.<\/li>\n
- Completed <\/b>– closed os, history of bleed, decreasing hCG, no products on UTS.<\/li>\n
- Incomplete\/Inevitable Ab <\/b>– open os with continued tissue passage; use uts to quantify residual.<\/li>\n
- Missed Ab <\/b>– os closed, embryo or products still present.\u00a0 No FHTs.<\/li>\n
- Blighted Ovum <\/b>– large sac, no fetus<\/li>\n<\/ul>\n
Miscarriage can become superinfected (septic miscarriage.)\u00a0 This diagnosis can be confused for PID.<\/p>\n
<\/span>Ectopic Pregnancy<\/span><\/h3>\nAlways consider heterotopic pregnancy.<\/p>\n
UTS-use trans vaginal<\/p>\n
The beta-hCG level should increase by 66% every 1.8-3 days for the first 6-7 weeks beginning 8-9 days after ovulation.<\/p>\n
\n- Get ICON\/UA\/T+H\/CBC\/Serum hCG<\/li>\n<\/ul>\n
Risk Factors:\u00a0 History of PID, infertility for > 2 years, tubal surgery or ligation, prior ectopic pregnancy, and use of an IUD. Recently the history of vaginal douching and smoking have also been implicated as risk factors for ectopic pregnancy in African American women. Only about half of women with ectopic pregnancy have one or more of these risk factors and 25% of patients with threatened abortions have one or more risk factors for ectopic pregnancy, as well. Therefore,\u00a0\u00a0 practically speaking, the presence or absence of risk factors for\u00a0 ectopic pregnancy is not helpful in the differentiation between\u00a0 ectopic pregnancy and threatened abortion.\u00a0 Adnexal tenderness and\/or fullness is present in about 50% of patients with ectopic pregnancy, but also in about 15% of patients with threatened abortions.<\/p>\n
<\/p>\n
Pregnant women presenting with abdominal pain or vaginal bleeding with bHCG<1500 are much more likely to have an ectopic or abnormal pregnancy than a normal one (2.24 likelihood ratio for ectopic, 25% had ectopics, 16% normal IUPs, and the rest abnormal pregnancies)<\/p>\n
In fact, symptomatic<\/p>\n
patients with \u00df-hCG levels less than 1000 mIU\/mL are<\/p>\n
four times more likely to have an ectopic pregnancy than<\/p>\n
those with higher \u00df-hCG values.\u00a0 (em practice Nov 2003)<\/p>\n
<\/p>\n
Heterotopic pregnancies, which traditionally occur in only 1\/30,000 to 1\/3,000 pregnancies, are more common in patients being treated for infertility<\/p>\n
<\/p>\n
All women should receive UTS regardless of b-hCG. (Acad Emerg Med 10:2, 119)<\/p>\n
<\/p>\n
Approximately 15% of ectopic pregnancies will have a<\/p>\n
“normal” rise in their \u00df-hCG value at the first follow-up<\/p>\n
blood draw. In fact, in the setting of an empty uterus on<\/p>\n
ultrasound, a “normal” \u00df-hCG rise increases the likelihood<\/p>\n
of an ectopic pregnancy being present.<\/p>\n
<\/p>\n
<\/p>\n
<\/p>\n
hysterectomy with oophrectomy rules out pregnancy, tubal ligation does not.<\/p>\n
Differential<\/h4>\n
Ovarian cysts-pelvic pain, no bleeding<\/p>\n
UTI\/Pyelo<\/p>\n
Appendicitis<\/p>\n
Kidney Stone<\/p>\n
Ovarian torsion-especially in women undergoing fertility treatment, up to 10% will develop OHSS ovarian hyper-stimulation syndrome resulting in ovarian enlargement and possible torsion.<\/p>\n
Progesterone<\/h4>\n
Serum Progesterone<\/p>\n
1)\u00a0\u00a0 Very low values (<5 ng\/ml) predictive of abnormal pregnancy in 97-100% of patients<\/p>\n
2)\u00a0\u00a0 High values (>25ng\/ml) predictive of normal pregnancy in 97% of patients<\/p>\n
3)\u00a0\u00a0 Intermediate values not helpful in evaluation<\/p>\n
4)\u00a0\u00a0 Recent study found a value < 22 ng\/ml to be 100% sensitive (CI down to 98%) and 25% specific. It’s unclear how, if at all, this will be used by ED physicians. (Ann Emerg Med 2000;36:95-100)<\/p>\n
UTS<\/h4>\n
>5 weeks double ring sign<\/p>\n
>6.5 should see cardiac activity<\/p>\n
1200-1500=endovaginal, >6500=transabdominal<\/p>\n
though this study (J Ultrasound Med 2011;30(12):1637) shows that high HCG with no sac doesn’t rule out a viable IUP. 4336 was the highest level that resulted in a live pregnancy.<\/p>\n
Culdocentesis<\/h4>\n
positive if non-clotting blood is aspirated, >1\/2 cc Crit<12%=ruptured corpus luteum cyst Crit>12%=interuterine bleeding Negative-serous fluid <5cc Indeterminate->5cc serous fluid or clotted blood<\/p>\n
Laparoscopy<\/h4>\n
Diff-threatened abortion, ruptured cyst<\/p>\n
If HCG<1000 and nothing seen, 2 day follow-up c GYN<\/p>\n
Adnexal fullness is on the side opposite the ectopic 20% of the time (Obstet Gynecol Surv 1985;40:259)<\/p>\n
<\/p>\n
Methotrexate<\/h4>\n
is most appropriate for women who are hemodynamically stable, would prefer to avoid surgery,<\/p>\n
are reliable, are available for weekly follow-up visits, have a \u00df-hCG of 3000 mIU\/mL or less, and have ultrasoundexaminations that reveal no fluid outside of the pelvis and a mass less than 4.0 cm maximal diameter(< 3.5 cm if a fetal heartbeat is present on ultrasound). Contraindications to primary methotrexate therapy include neutropenia, thrombocytopenia, liver dysfunction, and kidney disorders with serum creatinine greater than 1.5 mg\/dL. Although a number of predictors of the success of primary methotrexate therapy have been<\/p>\n
studied,78-82 the best predictor of success is a low \u00df-hCG.80<\/p>\n
Methotrexate has been reported to be 98% successful with<\/p>\n
\u00df-hCG levels less than 1000 mIU\/mL, 92% successful<\/p>\n
with \u00df-hCG values of 1000-4999 mIU\/mL, and 76%<\/p>\n
successful with \u00df-hCG values of 5000 mIU\/mL orgreater.80 Patients who are given methotrexate must be told to avoid vitamins containing folic acid (because it counteracts the action of the methotrexate), avoid alcohol, and refrain from intercourse until the \u00df-hCG returns to normal.<\/p>\n
Methotrexate has a variety of side-effects, including<\/p>\n
an increase in abdominal pain, which occurs in about<\/p>\n
30%-60% of patients who are successfully treated.<\/p>\n
<\/p>\n
Methotrexate treatment: usually not performed in emergency department (ED), but these women often present to ED after methotrexate treatment because of persistent vaginal bleeding and\/or pain; watch for rupture (usually occurs in first 2 wk, reported as far out as 42 days); do not perform pelvic examination (may cause rupture); perform abdominal examination; obtain ultrasonography and hematocrit to determine if bleeding in abdomen; if patient has methotrexate pain, treat with analgesic and send home; women with rupture go directly to OR; if unsure, admit and observe using serial examinations and hematocrits<\/p>\n
Do not do the pelvic exam on a woman who comes in with bleeding s\/p methotrexate treatment<\/p>\n
<\/p>\n
15 % of indeterminate scans wound up being ectopic (Acad Emerg Med 2004 11: 912-917)<\/p>\n
<\/p>\n
<\/h3>\n<\/span>Molar Pregnancy<\/span><\/h3>\nAbnormal proliferation of chorionic villi<\/p>\n
Complete mole-no fetal tissue<\/p>\n
Incomplete mole-has fetal tissue<\/p>\n
15-20% become neoplastic (choriocarcinoma), get chest x-ray to evaluate for pulmonary mets, TFTs as high HCG levels can act like TSH, and LFTs for baseline.<\/p>\n
Uterine size will be larger than expected, snowstorm on UTS, elevated bHCGs<\/p>\n
Early preeclampsia, hyperemesis, PE from tropho cells, bleeding.\u00a0 Also ovarian torsion from >6 cm theca lutein cysts.<\/p>\n
acts like 1st trimester preeclampsia<\/p>\n
![](\"\/wp-content\/images\/part3\/09f1_small.jpeg\")
<\/a><\/p>\n ![](\"\/wp-content\/images\/part4\/mole%20uts_small.gif\")
<\/a><\/p>\n<\/span>Nausea and Vomiting of Pregnancy \/ Hyperemesis Gravidum<\/span><\/h2>\nGood review article (Am Fam Phys 68(1):121, 2003) Small meals, avoidance of provoking smells, high carbs, low fats, Vitamin B6, 25 mg TID, Unisom 25 mg OD, and Ginger.\u00a0 Get ketones and electrolytes with prolonged symptoms.\u00a0 Can give antiemetics (chlorpromazine, prochlorperazine, promethazine, trimethobenzamide), antihistamines (diphenhydramine, meclizine, dimenhydrinate) or metoclopramide.<\/p>\n
<\/p>\n
<\/p>\n
Reglan is good:\u00a0 METOCLOPRAMIDE FOR NAUSEA AND VOMITING OF PREGNANCY: A PROSPECTIVE MULTICENTER INTERNATIONAL STUDY (Am J Perinatol 19(6):311, August 2002)<\/p>\n
Magee LA et al:<\/p>\n
Evidence-based view of safety and<\/p>\n
effectiveness of pharmacologic therapy for nausea and vomiting of pregnancy (NVP).<\/p>\n
Am J Obstet Gynecol <\/i>186:S256, 2002; All are safe<\/p>\n
<\/p>\n
<\/span>Complications of Late Pregnancy<\/span><\/h2>\n<\/span>Vaginal Bleeding<\/span><\/h3>\nAbruptio Placentae-separation of placenta from the uterine wall.\u00a0 Early bleeding can not be seen on UTS.\u00a0 Predisposes to amniotic fluid emboli and DIC.<\/p>\n
<\/p>\n
Placenta Previa-painless vaginal bleeding.\u00a0 No digital exam before UTS.<\/p>\n
<\/p>\n
Massive Post-partum Hemorrhage Stuff<\/a><\/p>\n<\/span>Preeclampsia\/Eclampsia<\/span><\/h3>\nCan occur from 20 weeks to 2 weeks post (seizure activity occurring as late as 23 days postpartum have been attributed to eclampsia)<\/p>\n
PIH c proteinuria or edema, from vasospastic cause<\/p>\n
Liver damage, generalized edema, thrombocytopenia, HAs<\/p>\n
HELLP-hemolysis, Elev. LFTs, low platelets<\/p>\n
Eclampsia-give Mg 6 g over 5-15 minutes then 2-3 g\/hr.\u00a0 Looking for Mg of 4-7.\u00a0 Signs of toxicity no patellar reflex(10),<\/p>\n
<\/p>\n
Nimodipine is probably as good, but MgSO4 wins out by a bit (NEJM 348(4):304, 2003)<\/p>\n
<\/p>\n
Resp (12), Urine <100 cc\/hr.\u00a0 Give CaCl<\/p>\n
Admit if BP>140\/90<\/p>\n
Hydralizine or labetolol to decrease BP.<\/p>\n
Amniotic Fluid Embolism<\/p>\n
Sudden hypotension, hypoxia, coagulopathy<\/p>\n
CBC, Coags, ABG, C-XR, uric acid, which has been shown to be elevated in up to 80% of eclamptic patients (JEM Nov 2003)<\/p>\n
ICU Admit, Supportive Care<\/p>\n
<\/p>\n
DELAYED POSTPARTUM PREECLAMPSIA: AN EXPERIENCE OF 151 CASES Matthys, L.A., et al, Am J Obstet Gyn 190:1464, May 2004<\/p>\n
Seizures in a pregnant woman who had not been previously diagnosed with preeclampsia must be accompanied by 2 of the following within 24 hours of presentation to be considered eclamptic: hypertension, proteinuria, thrombocytopenia, or increased aspartate aminotransferase<\/p>\n
up to 23 days post partum<\/p>\n
<\/p>\n
The Journal of Emergency Medicine<\/b>Volume 40, Issue 4, April 2011, Pages 380-384\u00a0 best review of post-partum preeclampsia<\/p>\n
<\/p>\n
<\/span>Neurologic Disorders in the Pregnant and Post-Partum Patient<\/a><\/span><\/h2>\n<\/span>Peripartum Cardiomyopathy<\/span><\/h3>\n(Crit Care Med 2005;33(10):S340) Presents with systemic and pulmonary congestion, low CO, dysrhythmia, and possible systemic or pulmonary embolization Etiology is usually unknown ? of immune, viral, selenium deficiency,<\/p>\n
<\/p>\n
<\/span>HTN in Pregnancy<\/span><\/h3>\n(Crit Care Med 2005;33(10):S307) labetolol onset in 5minutes, peak effect 10-20 minutes, lasts up to 6 hrs<\/p>\n
<\/span>PE during pregnancy<\/span><\/h3>\n(Crit Care Med 2005;33(10):S294) Increased risk during all three semesters and peripartum Most recent study of helical CT in pregnancy for PE calculated 0.00033 Rad in first trim and 0.01308 rad in the third; these are comparable to V\/Q (Radiology 2002;224:487) UFH and LMWH are safe for pregnancy and breastfeeding<\/p>\n
<\/p>\n
<\/span>Neuro disorders during pregnancy<\/span><\/h3>\n(Crit Care Med 2005;33(10):S364) Magnesium for preelampsia 4-6 G of MgSO4 over 20 min followed by 2G\/hr Ther. level 4-8 CaGLUC can be given for cards dysrhythmia Should lower BP as well, if still over 160\/110 use labetolol \u00a0 3-fold increase in risk of SAH, occur during 2nd and 3rd trim<\/p>\n
<\/span>Cerebral Venous Sinus Thrombosis<\/span><\/h3>\n120-300% increae in circulating clotting factors during pregnancy<\/p>\n
levels of protein S are decreased, protein C levels are the same Treat with heparin or LMWH empty delta sign is traingle of clot on contrast scan in the sinus<\/p>\n
<\/span>Post-partum ovarian vein thrombosis (POVT)<\/span><\/h3>\nis uncommon, but the true incidence is not known. Ninety per cent of cases present as right iliac fossa pain within 10 days of delivery. Anti-coagulation and intravenous antibiotics are the mainstay of treatment. We report three cases that were referred to our unit. These cases illustrate the difficulty in the clinical diagnosis of POVT and highlight the importance of its inclusion in the differential diagnoses of an acute abdomen in post-partum patients. POVT can be accurately diagnosed by appropriate non-invasive investigations and a laparotomy avoided.<\/p>\n
<\/p>\n
Post-partum ovarian vein thrombosis has an incidence of 1:2000 deliveries.1 The majority of cases occur within one week of delivery. Ovarian vein thrombosis is also associated with malignancy, pelvic inflammatory disease and gynaecological surgery.2 Eighty to ninety per cent occur in the right ovarian vein.3 This is believed to be due, in part, to the commonly occurring dextrotorsion of the enlarging uterus, which causes compression of the right ovarian vein and right ureter as they cross the pelvic rim.4 Studies have shown that there is retrograde flow in the left ovarian vein and antegrade flow in the right ovarian vein immediately post-partum.2 The right ovarian vein is also longer than the left ovarian vein and has many valves within its length. These valves may act as a nidus for thrombosis. 4 The pathogenesis of thrombus formation in the ovarian vein involves many factors. Along with the hypercoagulable state of pregnancy and the puerperium, there is a decrease in blood flow velocity immediately following delivery. If there is endometritis, blood flowing from the uterus could carry pathogenic bacteria to the right ovarian vein. Other prothrombotic risk factors, e.g. factor V Leidin, and protein S and C deficiency, can congenitally predispose to POVT. The usual clinical features of POVT are as described in the cases above. Eighty per cent of patients present with a pyrexia. Lower quadrant pain and flank pain with associated nausea is common. A mass may be palpable in the right iliac fossa. Among the differential diagnoses of ovarian vein thrombosis are appendicitis, septic pelvic thrombophlebitis, peritonitis, adnexal torsion, pyelonephritis and tubo-ovarian abscess. The diagnosis is made on the clinical features described above. Where the condition is suspected on clinical grounds, the initial investigation should be an ultrasound examination, which may confirm the diagnosis. However, it should be borne in mind that ultrasound examination is operator-dependent, especially with a rare condition. If there is a high index of clinical suspicion a CT or MRI scan, where available, should be requested even with a negative ultrasound, as it is important to avoid surgery, if possible, in POVT. This is well illustrated in Case 2. The condition is treated initially with intravenous heparin and broad-spectrum antibiotics. Once thrombolysis has begun, warfarin is introduced and continued for 3 months. Pulmonary embolism may complicate POVT in up to 13% of cases, and has a mortality of approximately 4%.3 There are no data on the long-term outcome for these patients with regard to subsequent fertility and future pregnancies. Diagnosis and treatment are both non-invasive. Hence, it is important to consider POVT when faced with a post-partum patient with lower quadrant pain and fever. Once the diagnosis is considered, the appropriate investigations can be ordered and a laparotomy can be avoided.<\/p>\n
Anatomy: The ovarian veins form a plexus near the ovary within the broad ligament and communicate with the uterine plexus. These veins ascend in the retroperitoneum adjacent to the psoas muscle in pairs, which combine to form a single vein prior to termination. The right ovarian vein terminates in the inferior vena cava at an acute angle. The left ovarian vein terminates in the left renal vein at a right angle. Occasionally, valves are present in the ovarian veins. The veins enlarge greatly during pregnancy to accommodate increased blood volume. Following childbirth, a period of venous stasis occurs. Clinical Details: The typical patient with clinically significant ovarian vein thrombosis (ie, thrombophlebitis) presents with pelvic pain, fever, and a right-sided abdominal mass. Anticoagulant and intravenous (IV) antibiotic therapy is the treatment of choice. Note that patients who have undergone total abdominal hysterectomy and bilateral salpingo-oophorectomy with retroperitoneal lymph node dissection often demonstrate ovarian vein thrombosis on contrast-enhanced CT. No treatment is necessary in patients in whom the complications of thrombophlebitis or embolism do not occur.<\/p>\n
<\/p>\n
<\/span>Tocolytics Can induce Pulmonary Edema<\/span><\/h2>\n <\/p>\n
<\/p>\n
<\/span>Rh Immunization in Preg<\/span><\/h2>\nGive Rhogam 50 for first trimester, 300 past the first<\/p>\n
<\/span>ABD Pain<\/span><\/h2>\nAppendicitis-moves to RUQ, pyuria s bacteria<\/p>\n
Gall Bladder Disease<\/p>\n
Acute fatty liver of pregnancy (can be fatal)<\/p>\n
Liver or Splenic Rupture-can be spontaneous, often assoc c PIH<\/p>\n
<\/span>Genitourinary Infections<\/span><\/h2>\nUTI-10 days of cephalosporin or nitrofurantoin<\/p>\n
<\/span>STDs<\/span><\/h2>\nBacterial Vaginosis-2 weeks of amoxicillin<\/p>\n
Chorioamnionitis-fever, uterine tenderness<\/p>\n
<\/p>\n
<\/p>\n
<\/span>When Pregnancy Tests Turn Negative<\/span><\/h2>\nfrom LitFL Blog
\nWorking a few Peds shifts lately I\u0092ve run into the same question: when should your urine pregnancy test (or quantitative serum hCG) be negative after a regular pregnancy, a termination, or a miscarriage (meaning, could she really already be pregnant\u00a0again<\/em>)? I hear different answers depending on the obstetrical consultant I ask, so I decided to do a little literature search myself. It\u0092s really only been looked at in very small studies;\u00a0I\u0092ve got the specific numbers if you want them, but based on the studies I found, it looks something like this:<\/p>\nAfter a Full-Term Pregnancy:<\/p>\n
\n- Should be 3 weeks or less. In some women, ovulation may occur as early as 3 weeks after delivery.<\/li>\n<\/ul>\n
After a Termination with Misoprostol\/Mifepristone:<\/p>\n
\n- In one study, following up at 6-18 days, if the hCG level was 80% lower than the initial hCG level, there was a positive predictive value for successful expulsion of 0.995. There was no information on when the level dropped to 0 or <5.<\/li>\n<\/ul>\n
After a D&C Termination:<\/p>\n
\n- Depends on the initial hCG, but mean time was 35 days, but could be up to 60 days.<\/li>\n<\/ul>\n
After Miscarriage in Women Who Then Had a D&E for Continued Bleeding:<\/p>\n
\n- Median ~20 days, range 9-22 days.<\/li>\n<\/ul>\n
After Ectopic with Laparotomy:<\/p>\n
\n- Ectopics had the lowest hCG to begin with, reached 0 by 1-31 days, median 8.5 days.<\/li>\n<\/ul>\n
References:<\/p>\n
\n- Routine terminations of pregnancy\u0097should we screen forgestational trophoblastic neoplasia? The Lancet, 2004.<\/li>\n
- Human chorionic gonadotropin in maternal plasma after induced abortion, spontaneous abortion, and removed ectopic pregnancy. Obstetrics and Gynecology, 1984.<\/li>\n
- Verifying the effectiveness of medical abortion; ultrasound versus hCG testing. European Journal of Obstetrics and Gynecology, 2003.<\/li>\n<\/ol>\n
<\/p>\n
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Miscarriage can become superinfected (septic miscarriage.)\u00a0 This diagnosis can be confused for PID.<\/p>\n
<\/span>Ectopic Pregnancy<\/span><\/h3>\nAlways consider heterotopic pregnancy.<\/p>\n
UTS-use trans vaginal<\/p>\n
The beta-hCG level should increase by 66% every 1.8-3 days for the first 6-7 weeks beginning 8-9 days after ovulation.<\/p>\n
\n- Get ICON\/UA\/T+H\/CBC\/Serum hCG<\/li>\n<\/ul>\n
Risk Factors:\u00a0 History of PID, infertility for > 2 years, tubal surgery or ligation, prior ectopic pregnancy, and use of an IUD. Recently the history of vaginal douching and smoking have also been implicated as risk factors for ectopic pregnancy in African American women. Only about half of women with ectopic pregnancy have one or more of these risk factors and 25% of patients with threatened abortions have one or more risk factors for ectopic pregnancy, as well. Therefore,\u00a0\u00a0 practically speaking, the presence or absence of risk factors for\u00a0 ectopic pregnancy is not helpful in the differentiation between\u00a0 ectopic pregnancy and threatened abortion.\u00a0 Adnexal tenderness and\/or fullness is present in about 50% of patients with ectopic pregnancy, but also in about 15% of patients with threatened abortions.<\/p>\n
<\/p>\n
Pregnant women presenting with abdominal pain or vaginal bleeding with bHCG<1500 are much more likely to have an ectopic or abnormal pregnancy than a normal one (2.24 likelihood ratio for ectopic, 25% had ectopics, 16% normal IUPs, and the rest abnormal pregnancies)<\/p>\n
In fact, symptomatic<\/p>\n
patients with \u00df-hCG levels less than 1000 mIU\/mL are<\/p>\n
four times more likely to have an ectopic pregnancy than<\/p>\n
those with higher \u00df-hCG values.\u00a0 (em practice Nov 2003)<\/p>\n
<\/p>\n
Heterotopic pregnancies, which traditionally occur in only 1\/30,000 to 1\/3,000 pregnancies, are more common in patients being treated for infertility<\/p>\n
<\/p>\n
All women should receive UTS regardless of b-hCG. (Acad Emerg Med 10:2, 119)<\/p>\n
<\/p>\n
Approximately 15% of ectopic pregnancies will have a<\/p>\n
“normal” rise in their \u00df-hCG value at the first follow-up<\/p>\n
blood draw. In fact, in the setting of an empty uterus on<\/p>\n
ultrasound, a “normal” \u00df-hCG rise increases the likelihood<\/p>\n
of an ectopic pregnancy being present.<\/p>\n
<\/p>\n
<\/p>\n
<\/p>\n
hysterectomy with oophrectomy rules out pregnancy, tubal ligation does not.<\/p>\n
Differential<\/h4>\n
Ovarian cysts-pelvic pain, no bleeding<\/p>\n
UTI\/Pyelo<\/p>\n
Appendicitis<\/p>\n
Kidney Stone<\/p>\n
Ovarian torsion-especially in women undergoing fertility treatment, up to 10% will develop OHSS ovarian hyper-stimulation syndrome resulting in ovarian enlargement and possible torsion.<\/p>\n
Progesterone<\/h4>\n
Serum Progesterone<\/p>\n
1)\u00a0\u00a0 Very low values (<5 ng\/ml) predictive of abnormal pregnancy in 97-100% of patients<\/p>\n
2)\u00a0\u00a0 High values (>25ng\/ml) predictive of normal pregnancy in 97% of patients<\/p>\n
3)\u00a0\u00a0 Intermediate values not helpful in evaluation<\/p>\n
4)\u00a0\u00a0 Recent study found a value < 22 ng\/ml to be 100% sensitive (CI down to 98%) and 25% specific. It’s unclear how, if at all, this will be used by ED physicians. (Ann Emerg Med 2000;36:95-100)<\/p>\n
UTS<\/h4>\n
>5 weeks double ring sign<\/p>\n
>6.5 should see cardiac activity<\/p>\n
1200-1500=endovaginal, >6500=transabdominal<\/p>\n
though this study (J Ultrasound Med 2011;30(12):1637) shows that high HCG with no sac doesn’t rule out a viable IUP. 4336 was the highest level that resulted in a live pregnancy.<\/p>\n
Culdocentesis<\/h4>\n
positive if non-clotting blood is aspirated, >1\/2 cc Crit<12%=ruptured corpus luteum cyst Crit>12%=interuterine bleeding Negative-serous fluid <5cc Indeterminate->5cc serous fluid or clotted blood<\/p>\n
Laparoscopy<\/h4>\n
Diff-threatened abortion, ruptured cyst<\/p>\n
If HCG<1000 and nothing seen, 2 day follow-up c GYN<\/p>\n
Adnexal fullness is on the side opposite the ectopic 20% of the time (Obstet Gynecol Surv 1985;40:259)<\/p>\n
<\/p>\n
Methotrexate<\/h4>\n
is most appropriate for women who are hemodynamically stable, would prefer to avoid surgery,<\/p>\n
are reliable, are available for weekly follow-up visits, have a \u00df-hCG of 3000 mIU\/mL or less, and have ultrasoundexaminations that reveal no fluid outside of the pelvis and a mass less than 4.0 cm maximal diameter(< 3.5 cm if a fetal heartbeat is present on ultrasound). Contraindications to primary methotrexate therapy include neutropenia, thrombocytopenia, liver dysfunction, and kidney disorders with serum creatinine greater than 1.5 mg\/dL. Although a number of predictors of the success of primary methotrexate therapy have been<\/p>\n
studied,78-82 the best predictor of success is a low \u00df-hCG.80<\/p>\n
Methotrexate has been reported to be 98% successful with<\/p>\n
\u00df-hCG levels less than 1000 mIU\/mL, 92% successful<\/p>\n
with \u00df-hCG values of 1000-4999 mIU\/mL, and 76%<\/p>\n
successful with \u00df-hCG values of 5000 mIU\/mL orgreater.80 Patients who are given methotrexate must be told to avoid vitamins containing folic acid (because it counteracts the action of the methotrexate), avoid alcohol, and refrain from intercourse until the \u00df-hCG returns to normal.<\/p>\n
Methotrexate has a variety of side-effects, including<\/p>\n
an increase in abdominal pain, which occurs in about<\/p>\n
30%-60% of patients who are successfully treated.<\/p>\n
<\/p>\n
Methotrexate treatment: usually not performed in emergency department (ED), but these women often present to ED after methotrexate treatment because of persistent vaginal bleeding and\/or pain; watch for rupture (usually occurs in first 2 wk, reported as far out as 42 days); do not perform pelvic examination (may cause rupture); perform abdominal examination; obtain ultrasonography and hematocrit to determine if bleeding in abdomen; if patient has methotrexate pain, treat with analgesic and send home; women with rupture go directly to OR; if unsure, admit and observe using serial examinations and hematocrits<\/p>\n
Do not do the pelvic exam on a woman who comes in with bleeding s\/p methotrexate treatment<\/p>\n
<\/p>\n
15 % of indeterminate scans wound up being ectopic (Acad Emerg Med 2004 11: 912-917)<\/p>\n
<\/p>\n
<\/h3>\n<\/span>Molar Pregnancy<\/span><\/h3>\nAbnormal proliferation of chorionic villi<\/p>\n
Complete mole-no fetal tissue<\/p>\n
Incomplete mole-has fetal tissue<\/p>\n
15-20% become neoplastic (choriocarcinoma), get chest x-ray to evaluate for pulmonary mets, TFTs as high HCG levels can act like TSH, and LFTs for baseline.<\/p>\n
Uterine size will be larger than expected, snowstorm on UTS, elevated bHCGs<\/p>\n
Early preeclampsia, hyperemesis, PE from tropho cells, bleeding.\u00a0 Also ovarian torsion from >6 cm theca lutein cysts.<\/p>\n
acts like 1st trimester preeclampsia<\/p>\n
<\/a><\/p>\n <\/a><\/p>\n<\/span>Nausea and Vomiting of Pregnancy \/ Hyperemesis Gravidum<\/span><\/h2>\nGood review article (Am Fam Phys 68(1):121, 2003) Small meals, avoidance of provoking smells, high carbs, low fats, Vitamin B6, 25 mg TID, Unisom 25 mg OD, and Ginger.\u00a0 Get ketones and electrolytes with prolonged symptoms.\u00a0 Can give antiemetics (chlorpromazine, prochlorperazine, promethazine, trimethobenzamide), antihistamines (diphenhydramine, meclizine, dimenhydrinate) or metoclopramide.<\/p>\n
<\/p>\n
<\/p>\n
Reglan is good:\u00a0 METOCLOPRAMIDE FOR NAUSEA AND VOMITING OF PREGNANCY: A PROSPECTIVE MULTICENTER INTERNATIONAL STUDY (Am J Perinatol 19(6):311, August 2002)<\/p>\n
Magee LA et al:<\/p>\n
Evidence-based view of safety and<\/p>\n
effectiveness of pharmacologic therapy for nausea and vomiting of pregnancy (NVP).<\/p>\n
Am J Obstet Gynecol <\/i>186:S256, 2002; All are safe<\/p>\n
<\/p>\n
<\/span>Complications of Late Pregnancy<\/span><\/h2>\n<\/span>Vaginal Bleeding<\/span><\/h3>\nAbruptio Placentae-separation of placenta from the uterine wall.\u00a0 Early bleeding can not be seen on UTS.\u00a0 Predisposes to amniotic fluid emboli and DIC.<\/p>\n
<\/p>\n
Placenta Previa-painless vaginal bleeding.\u00a0 No digital exam before UTS.<\/p>\n
<\/p>\n
Massive Post-partum Hemorrhage Stuff<\/a><\/p>\n<\/span>Preeclampsia\/Eclampsia<\/span><\/h3>\nCan occur from 20 weeks to 2 weeks post (seizure activity occurring as late as 23 days postpartum have been attributed to eclampsia)<\/p>\n
PIH c proteinuria or edema, from vasospastic cause<\/p>\n
Liver damage, generalized edema, thrombocytopenia, HAs<\/p>\n
HELLP-hemolysis, Elev. LFTs, low platelets<\/p>\n
Eclampsia-give Mg 6 g over 5-15 minutes then 2-3 g\/hr.\u00a0 Looking for Mg of 4-7.\u00a0 Signs of toxicity no patellar reflex(10),<\/p>\n
<\/p>\n
Nimodipine is probably as good, but MgSO4 wins out by a bit (NEJM 348(4):304, 2003)<\/p>\n
<\/p>\n
Resp (12), Urine <100 cc\/hr.\u00a0 Give CaCl<\/p>\n
Admit if BP>140\/90<\/p>\n
Hydralizine or labetolol to decrease BP.<\/p>\n
Amniotic Fluid Embolism<\/p>\n
Sudden hypotension, hypoxia, coagulopathy<\/p>\n
CBC, Coags, ABG, C-XR, uric acid, which has been shown to be elevated in up to 80% of eclamptic patients (JEM Nov 2003)<\/p>\n
ICU Admit, Supportive Care<\/p>\n
<\/p>\n
DELAYED POSTPARTUM PREECLAMPSIA: AN EXPERIENCE OF 151 CASES Matthys, L.A., et al, Am J Obstet Gyn 190:1464, May 2004<\/p>\n
Seizures in a pregnant woman who had not been previously diagnosed with preeclampsia must be accompanied by 2 of the following within 24 hours of presentation to be considered eclamptic: hypertension, proteinuria, thrombocytopenia, or increased aspartate aminotransferase<\/p>\n
up to 23 days post partum<\/p>\n
<\/p>\n
The Journal of Emergency Medicine<\/b>Volume 40, Issue 4, April 2011, Pages 380-384\u00a0 best review of post-partum preeclampsia<\/p>\n
<\/p>\n
<\/span>Neurologic Disorders in the Pregnant and Post-Partum Patient<\/a><\/span><\/h2>\n<\/span>Peripartum Cardiomyopathy<\/span><\/h3>\n(Crit Care Med 2005;33(10):S340) Presents with systemic and pulmonary congestion, low CO, dysrhythmia, and possible systemic or pulmonary embolization Etiology is usually unknown ? of immune, viral, selenium deficiency,<\/p>\n
<\/p>\n
<\/span>HTN in Pregnancy<\/span><\/h3>\n(Crit Care Med 2005;33(10):S307) labetolol onset in 5minutes, peak effect 10-20 minutes, lasts up to 6 hrs<\/p>\n
<\/span>PE during pregnancy<\/span><\/h3>\n(Crit Care Med 2005;33(10):S294) Increased risk during all three semesters and peripartum Most recent study of helical CT in pregnancy for PE calculated 0.00033 Rad in first trim and 0.01308 rad in the third; these are comparable to V\/Q (Radiology 2002;224:487) UFH and LMWH are safe for pregnancy and breastfeeding<\/p>\n
<\/p>\n
<\/span>Neuro disorders during pregnancy<\/span><\/h3>\n(Crit Care Med 2005;33(10):S364) Magnesium for preelampsia 4-6 G of MgSO4 over 20 min followed by 2G\/hr Ther. level 4-8 CaGLUC can be given for cards dysrhythmia Should lower BP as well, if still over 160\/110 use labetolol \u00a0 3-fold increase in risk of SAH, occur during 2nd and 3rd trim<\/p>\n
<\/span>Cerebral Venous Sinus Thrombosis<\/span><\/h3>\n120-300% increae in circulating clotting factors during pregnancy<\/p>\n
levels of protein S are decreased, protein C levels are the same Treat with heparin or LMWH empty delta sign is traingle of clot on contrast scan in the sinus<\/p>\n
<\/span>Post-partum ovarian vein thrombosis (POVT)<\/span><\/h3>\nis uncommon, but the true incidence is not known. Ninety per cent of cases present as right iliac fossa pain within 10 days of delivery. Anti-coagulation and intravenous antibiotics are the mainstay of treatment. We report three cases that were referred to our unit. These cases illustrate the difficulty in the clinical diagnosis of POVT and highlight the importance of its inclusion in the differential diagnoses of an acute abdomen in post-partum patients. POVT can be accurately diagnosed by appropriate non-invasive investigations and a laparotomy avoided.<\/p>\n
<\/p>\n
Post-partum ovarian vein thrombosis has an incidence of 1:2000 deliveries.1 The majority of cases occur within one week of delivery. Ovarian vein thrombosis is also associated with malignancy, pelvic inflammatory disease and gynaecological surgery.2 Eighty to ninety per cent occur in the right ovarian vein.3 This is believed to be due, in part, to the commonly occurring dextrotorsion of the enlarging uterus, which causes compression of the right ovarian vein and right ureter as they cross the pelvic rim.4 Studies have shown that there is retrograde flow in the left ovarian vein and antegrade flow in the right ovarian vein immediately post-partum.2 The right ovarian vein is also longer than the left ovarian vein and has many valves within its length. These valves may act as a nidus for thrombosis. 4 The pathogenesis of thrombus formation in the ovarian vein involves many factors. Along with the hypercoagulable state of pregnancy and the puerperium, there is a decrease in blood flow velocity immediately following delivery. If there is endometritis, blood flowing from the uterus could carry pathogenic bacteria to the right ovarian vein. Other prothrombotic risk factors, e.g. factor V Leidin, and protein S and C deficiency, can congenitally predispose to POVT. The usual clinical features of POVT are as described in the cases above. Eighty per cent of patients present with a pyrexia. Lower quadrant pain and flank pain with associated nausea is common. A mass may be palpable in the right iliac fossa. Among the differential diagnoses of ovarian vein thrombosis are appendicitis, septic pelvic thrombophlebitis, peritonitis, adnexal torsion, pyelonephritis and tubo-ovarian abscess. The diagnosis is made on the clinical features described above. Where the condition is suspected on clinical grounds, the initial investigation should be an ultrasound examination, which may confirm the diagnosis. However, it should be borne in mind that ultrasound examination is operator-dependent, especially with a rare condition. If there is a high index of clinical suspicion a CT or MRI scan, where available, should be requested even with a negative ultrasound, as it is important to avoid surgery, if possible, in POVT. This is well illustrated in Case 2. The condition is treated initially with intravenous heparin and broad-spectrum antibiotics. Once thrombolysis has begun, warfarin is introduced and continued for 3 months. Pulmonary embolism may complicate POVT in up to 13% of cases, and has a mortality of approximately 4%.3 There are no data on the long-term outcome for these patients with regard to subsequent fertility and future pregnancies. Diagnosis and treatment are both non-invasive. Hence, it is important to consider POVT when faced with a post-partum patient with lower quadrant pain and fever. Once the diagnosis is considered, the appropriate investigations can be ordered and a laparotomy can be avoided.<\/p>\n
Anatomy: The ovarian veins form a plexus near the ovary within the broad ligament and communicate with the uterine plexus. These veins ascend in the retroperitoneum adjacent to the psoas muscle in pairs, which combine to form a single vein prior to termination. The right ovarian vein terminates in the inferior vena cava at an acute angle. The left ovarian vein terminates in the left renal vein at a right angle. Occasionally, valves are present in the ovarian veins. The veins enlarge greatly during pregnancy to accommodate increased blood volume. Following childbirth, a period of venous stasis occurs. Clinical Details: The typical patient with clinically significant ovarian vein thrombosis (ie, thrombophlebitis) presents with pelvic pain, fever, and a right-sided abdominal mass. Anticoagulant and intravenous (IV) antibiotic therapy is the treatment of choice. Note that patients who have undergone total abdominal hysterectomy and bilateral salpingo-oophorectomy with retroperitoneal lymph node dissection often demonstrate ovarian vein thrombosis on contrast-enhanced CT. No treatment is necessary in patients in whom the complications of thrombophlebitis or embolism do not occur.<\/p>\n
<\/p>\n
<\/span>Tocolytics Can induce Pulmonary Edema<\/span><\/h2>\n <\/p>\n
<\/p>\n
<\/span>Rh Immunization in Preg<\/span><\/h2>\nGive Rhogam 50 for first trimester, 300 past the first<\/p>\n
<\/span>ABD Pain<\/span><\/h2>\nAppendicitis-moves to RUQ, pyuria s bacteria<\/p>\n
Gall Bladder Disease<\/p>\n
Acute fatty liver of pregnancy (can be fatal)<\/p>\n
Liver or Splenic Rupture-can be spontaneous, often assoc c PIH<\/p>\n
<\/span>Genitourinary Infections<\/span><\/h2>\nUTI-10 days of cephalosporin or nitrofurantoin<\/p>\n
<\/span>STDs<\/span><\/h2>\nBacterial Vaginosis-2 weeks of amoxicillin<\/p>\n
Chorioamnionitis-fever, uterine tenderness<\/p>\n
<\/p>\n
<\/p>\n
<\/span>When Pregnancy Tests Turn Negative<\/span><\/h2>\nfrom LitFL Blog
\nWorking a few Peds shifts lately I\u0092ve run into the same question: when should your urine pregnancy test (or quantitative serum hCG) be negative after a regular pregnancy, a termination, or a miscarriage (meaning, could she really already be pregnant\u00a0again<\/em>)? I hear different answers depending on the obstetrical consultant I ask, so I decided to do a little literature search myself. It\u0092s really only been looked at in very small studies;\u00a0I\u0092ve got the specific numbers if you want them, but based on the studies I found, it looks something like this:<\/p>\nAfter a Full-Term Pregnancy:<\/p>\n
\n- Should be 3 weeks or less. In some women, ovulation may occur as early as 3 weeks after delivery.<\/li>\n<\/ul>\n
After a Termination with Misoprostol\/Mifepristone:<\/p>\n
\n- In one study, following up at 6-18 days, if the hCG level was 80% lower than the initial hCG level, there was a positive predictive value for successful expulsion of 0.995. There was no information on when the level dropped to 0 or <5.<\/li>\n<\/ul>\n
After a D&C Termination:<\/p>\n
\n- Depends on the initial hCG, but mean time was 35 days, but could be up to 60 days.<\/li>\n<\/ul>\n
After Miscarriage in Women Who Then Had a D&E for Continued Bleeding:<\/p>\n
\n- Median ~20 days, range 9-22 days.<\/li>\n<\/ul>\n
After Ectopic with Laparotomy:<\/p>\n
\n- Ectopics had the lowest hCG to begin with, reached 0 by 1-31 days, median 8.5 days.<\/li>\n<\/ul>\n
References:<\/p>\n
\n- Routine terminations of pregnancy\u0097should we screen forgestational trophoblastic neoplasia? The Lancet, 2004.<\/li>\n
- Human chorionic gonadotropin in maternal plasma after induced abortion, spontaneous abortion, and removed ectopic pregnancy. Obstetrics and Gynecology, 1984.<\/li>\n
- Verifying the effectiveness of medical abortion; ultrasound versus hCG testing. European Journal of Obstetrics and Gynecology, 2003.<\/li>\n<\/ol>\n
<\/p>\n
|\u00a0\u00a0 \u00a0\u00a0 |\u00a0\u00a0 \u00a0\u00a0 |<\/p>\n","protected":false},"excerpt":{"rendered":"
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Risk Factors:\u00a0 History of PID, infertility for > 2 years, tubal surgery or ligation, prior ectopic pregnancy, and use of an IUD. Recently the history of vaginal douching and smoking have also been implicated as risk factors for ectopic pregnancy in African American women. Only about half of women with ectopic pregnancy have one or more of these risk factors and 25% of patients with threatened abortions have one or more risk factors for ectopic pregnancy, as well. Therefore,\u00a0\u00a0 practically speaking, the presence or absence of risk factors for\u00a0 ectopic pregnancy is not helpful in the differentiation between\u00a0 ectopic pregnancy and threatened abortion.\u00a0 Adnexal tenderness and\/or fullness is present in about 50% of patients with ectopic pregnancy, but also in about 15% of patients with threatened abortions.<\/p>\n
<\/p>\n
Pregnant women presenting with abdominal pain or vaginal bleeding with bHCG<1500 are much more likely to have an ectopic or abnormal pregnancy than a normal one (2.24 likelihood ratio for ectopic, 25% had ectopics, 16% normal IUPs, and the rest abnormal pregnancies)<\/p>\n
In fact, symptomatic<\/p>\n
patients with \u00df-hCG levels less than 1000 mIU\/mL are<\/p>\n
four times more likely to have an ectopic pregnancy than<\/p>\n
those with higher \u00df-hCG values.\u00a0 (em practice Nov 2003)<\/p>\n
<\/p>\n
Heterotopic pregnancies, which traditionally occur in only 1\/30,000 to 1\/3,000 pregnancies, are more common in patients being treated for infertility<\/p>\n
<\/p>\n
All women should receive UTS regardless of b-hCG. (Acad Emerg Med 10:2, 119)<\/p>\n
<\/p>\n
Approximately 15% of ectopic pregnancies will have a<\/p>\n
“normal” rise in their \u00df-hCG value at the first follow-up<\/p>\n
blood draw. In fact, in the setting of an empty uterus on<\/p>\n
ultrasound, a “normal” \u00df-hCG rise increases the likelihood<\/p>\n
of an ectopic pregnancy being present.<\/p>\n
<\/p>\n
<\/p>\n
<\/p>\n
hysterectomy with oophrectomy rules out pregnancy, tubal ligation does not.<\/p>\n
Differential<\/h4>\n
Ovarian cysts-pelvic pain, no bleeding<\/p>\n
UTI\/Pyelo<\/p>\n
Appendicitis<\/p>\n
Kidney Stone<\/p>\n
Ovarian torsion-especially in women undergoing fertility treatment, up to 10% will develop OHSS ovarian hyper-stimulation syndrome resulting in ovarian enlargement and possible torsion.<\/p>\n
Progesterone<\/h4>\n
Serum Progesterone<\/p>\n
1)\u00a0\u00a0 Very low values (<5 ng\/ml) predictive of abnormal pregnancy in 97-100% of patients<\/p>\n
2)\u00a0\u00a0 High values (>25ng\/ml) predictive of normal pregnancy in 97% of patients<\/p>\n
3)\u00a0\u00a0 Intermediate values not helpful in evaluation<\/p>\n
4)\u00a0\u00a0 Recent study found a value < 22 ng\/ml to be 100% sensitive (CI down to 98%) and 25% specific. It’s unclear how, if at all, this will be used by ED physicians. (Ann Emerg Med 2000;36:95-100)<\/p>\n
UTS<\/h4>\n
>5 weeks double ring sign<\/p>\n
>6.5 should see cardiac activity<\/p>\n
1200-1500=endovaginal, >6500=transabdominal<\/p>\n
though this study (J Ultrasound Med 2011;30(12):1637) shows that high HCG with no sac doesn’t rule out a viable IUP. 4336 was the highest level that resulted in a live pregnancy.<\/p>\n
Culdocentesis<\/h4>\n
positive if non-clotting blood is aspirated, >1\/2 cc Crit<12%=ruptured corpus luteum cyst Crit>12%=interuterine bleeding Negative-serous fluid <5cc Indeterminate->5cc serous fluid or clotted blood<\/p>\n
Laparoscopy<\/h4>\n
Diff-threatened abortion, ruptured cyst<\/p>\n
If HCG<1000 and nothing seen, 2 day follow-up c GYN<\/p>\n
Adnexal fullness is on the side opposite the ectopic 20% of the time (Obstet Gynecol Surv 1985;40:259)<\/p>\n
<\/p>\n
Methotrexate<\/h4>\n
is most appropriate for women who are hemodynamically stable, would prefer to avoid surgery,<\/p>\n
are reliable, are available for weekly follow-up visits, have a \u00df-hCG of 3000 mIU\/mL or less, and have ultrasoundexaminations that reveal no fluid outside of the pelvis and a mass less than 4.0 cm maximal diameter(< 3.5 cm if a fetal heartbeat is present on ultrasound). Contraindications to primary methotrexate therapy include neutropenia, thrombocytopenia, liver dysfunction, and kidney disorders with serum creatinine greater than 1.5 mg\/dL. Although a number of predictors of the success of primary methotrexate therapy have been<\/p>\n
studied,78-82 the best predictor of success is a low \u00df-hCG.80<\/p>\n
Methotrexate has been reported to be 98% successful with<\/p>\n
\u00df-hCG levels less than 1000 mIU\/mL, 92% successful<\/p>\n
with \u00df-hCG values of 1000-4999 mIU\/mL, and 76%<\/p>\n
successful with \u00df-hCG values of 5000 mIU\/mL orgreater.80 Patients who are given methotrexate must be told to avoid vitamins containing folic acid (because it counteracts the action of the methotrexate), avoid alcohol, and refrain from intercourse until the \u00df-hCG returns to normal.<\/p>\n
Methotrexate has a variety of side-effects, including<\/p>\n
an increase in abdominal pain, which occurs in about<\/p>\n
30%-60% of patients who are successfully treated.<\/p>\n
<\/p>\n
Methotrexate treatment: usually not performed in emergency department (ED), but these women often present to ED after methotrexate treatment because of persistent vaginal bleeding and\/or pain; watch for rupture (usually occurs in first 2 wk, reported as far out as 42 days); do not perform pelvic examination (may cause rupture); perform abdominal examination; obtain ultrasonography and hematocrit to determine if bleeding in abdomen; if patient has methotrexate pain, treat with analgesic and send home; women with rupture go directly to OR; if unsure, admit and observe using serial examinations and hematocrits<\/p>\n
Do not do the pelvic exam on a woman who comes in with bleeding s\/p methotrexate treatment<\/p>\n
<\/p>\n
15 % of indeterminate scans wound up being ectopic (Acad Emerg Med 2004 11: 912-917)<\/p>\n
<\/p>\n
<\/h3>\n<\/span>Molar Pregnancy<\/span><\/h3>\nAbnormal proliferation of chorionic villi<\/p>\n
Complete mole-no fetal tissue<\/p>\n
Incomplete mole-has fetal tissue<\/p>\n
15-20% become neoplastic (choriocarcinoma), get chest x-ray to evaluate for pulmonary mets, TFTs as high HCG levels can act like TSH, and LFTs for baseline.<\/p>\n
Uterine size will be larger than expected, snowstorm on UTS, elevated bHCGs<\/p>\n
Early preeclampsia, hyperemesis, PE from tropho cells, bleeding.\u00a0 Also ovarian torsion from >6 cm theca lutein cysts.<\/p>\n
acts like 1st trimester preeclampsia<\/p>\n
<\/a><\/p>\n <\/a><\/p>\n<\/span>Nausea and Vomiting of Pregnancy \/ Hyperemesis Gravidum<\/span><\/h2>\nGood review article (Am Fam Phys 68(1):121, 2003) Small meals, avoidance of provoking smells, high carbs, low fats, Vitamin B6, 25 mg TID, Unisom 25 mg OD, and Ginger.\u00a0 Get ketones and electrolytes with prolonged symptoms.\u00a0 Can give antiemetics (chlorpromazine, prochlorperazine, promethazine, trimethobenzamide), antihistamines (diphenhydramine, meclizine, dimenhydrinate) or metoclopramide.<\/p>\n
<\/p>\n
<\/p>\n
Reglan is good:\u00a0 METOCLOPRAMIDE FOR NAUSEA AND VOMITING OF PREGNANCY: A PROSPECTIVE MULTICENTER INTERNATIONAL STUDY (Am J Perinatol 19(6):311, August 2002)<\/p>\n
Magee LA et al:<\/p>\n
Evidence-based view of safety and<\/p>\n
effectiveness of pharmacologic therapy for nausea and vomiting of pregnancy (NVP).<\/p>\n
Am J Obstet Gynecol <\/i>186:S256, 2002; All are safe<\/p>\n
<\/p>\n
<\/span>Complications of Late Pregnancy<\/span><\/h2>\n<\/span>Vaginal Bleeding<\/span><\/h3>\nAbruptio Placentae-separation of placenta from the uterine wall.\u00a0 Early bleeding can not be seen on UTS.\u00a0 Predisposes to amniotic fluid emboli and DIC.<\/p>\n
<\/p>\n
Placenta Previa-painless vaginal bleeding.\u00a0 No digital exam before UTS.<\/p>\n
<\/p>\n
Massive Post-partum Hemorrhage Stuff<\/a><\/p>\n<\/span>Preeclampsia\/Eclampsia<\/span><\/h3>\nCan occur from 20 weeks to 2 weeks post (seizure activity occurring as late as 23 days postpartum have been attributed to eclampsia)<\/p>\n
PIH c proteinuria or edema, from vasospastic cause<\/p>\n
Liver damage, generalized edema, thrombocytopenia, HAs<\/p>\n
HELLP-hemolysis, Elev. LFTs, low platelets<\/p>\n
Eclampsia-give Mg 6 g over 5-15 minutes then 2-3 g\/hr.\u00a0 Looking for Mg of 4-7.\u00a0 Signs of toxicity no patellar reflex(10),<\/p>\n
<\/p>\n
Nimodipine is probably as good, but MgSO4 wins out by a bit (NEJM 348(4):304, 2003)<\/p>\n
<\/p>\n
Resp (12), Urine <100 cc\/hr.\u00a0 Give CaCl<\/p>\n
Admit if BP>140\/90<\/p>\n
Hydralizine or labetolol to decrease BP.<\/p>\n
Amniotic Fluid Embolism<\/p>\n
Sudden hypotension, hypoxia, coagulopathy<\/p>\n
CBC, Coags, ABG, C-XR, uric acid, which has been shown to be elevated in up to 80% of eclamptic patients (JEM Nov 2003)<\/p>\n
ICU Admit, Supportive Care<\/p>\n
<\/p>\n
DELAYED POSTPARTUM PREECLAMPSIA: AN EXPERIENCE OF 151 CASES Matthys, L.A., et al, Am J Obstet Gyn 190:1464, May 2004<\/p>\n
Seizures in a pregnant woman who had not been previously diagnosed with preeclampsia must be accompanied by 2 of the following within 24 hours of presentation to be considered eclamptic: hypertension, proteinuria, thrombocytopenia, or increased aspartate aminotransferase<\/p>\n
up to 23 days post partum<\/p>\n
<\/p>\n
The Journal of Emergency Medicine<\/b>Volume 40, Issue 4, April 2011, Pages 380-384\u00a0 best review of post-partum preeclampsia<\/p>\n
<\/p>\n
<\/span>Neurologic Disorders in the Pregnant and Post-Partum Patient<\/a><\/span><\/h2>\n<\/span>Peripartum Cardiomyopathy<\/span><\/h3>\n(Crit Care Med 2005;33(10):S340) Presents with systemic and pulmonary congestion, low CO, dysrhythmia, and possible systemic or pulmonary embolization Etiology is usually unknown ? of immune, viral, selenium deficiency,<\/p>\n
<\/p>\n
<\/span>HTN in Pregnancy<\/span><\/h3>\n(Crit Care Med 2005;33(10):S307) labetolol onset in 5minutes, peak effect 10-20 minutes, lasts up to 6 hrs<\/p>\n
<\/span>PE during pregnancy<\/span><\/h3>\n(Crit Care Med 2005;33(10):S294) Increased risk during all three semesters and peripartum Most recent study of helical CT in pregnancy for PE calculated 0.00033 Rad in first trim and 0.01308 rad in the third; these are comparable to V\/Q (Radiology 2002;224:487) UFH and LMWH are safe for pregnancy and breastfeeding<\/p>\n
<\/p>\n
<\/span>Neuro disorders during pregnancy<\/span><\/h3>\n(Crit Care Med 2005;33(10):S364) Magnesium for preelampsia 4-6 G of MgSO4 over 20 min followed by 2G\/hr Ther. level 4-8 CaGLUC can be given for cards dysrhythmia Should lower BP as well, if still over 160\/110 use labetolol \u00a0 3-fold increase in risk of SAH, occur during 2nd and 3rd trim<\/p>\n
<\/span>Cerebral Venous Sinus Thrombosis<\/span><\/h3>\n120-300% increae in circulating clotting factors during pregnancy<\/p>\n
levels of protein S are decreased, protein C levels are the same Treat with heparin or LMWH empty delta sign is traingle of clot on contrast scan in the sinus<\/p>\n
<\/span>Post-partum ovarian vein thrombosis (POVT)<\/span><\/h3>\nis uncommon, but the true incidence is not known. Ninety per cent of cases present as right iliac fossa pain within 10 days of delivery. Anti-coagulation and intravenous antibiotics are the mainstay of treatment. We report three cases that were referred to our unit. These cases illustrate the difficulty in the clinical diagnosis of POVT and highlight the importance of its inclusion in the differential diagnoses of an acute abdomen in post-partum patients. POVT can be accurately diagnosed by appropriate non-invasive investigations and a laparotomy avoided.<\/p>\n
<\/p>\n
Post-partum ovarian vein thrombosis has an incidence of 1:2000 deliveries.1 The majority of cases occur within one week of delivery. Ovarian vein thrombosis is also associated with malignancy, pelvic inflammatory disease and gynaecological surgery.2 Eighty to ninety per cent occur in the right ovarian vein.3 This is believed to be due, in part, to the commonly occurring dextrotorsion of the enlarging uterus, which causes compression of the right ovarian vein and right ureter as they cross the pelvic rim.4 Studies have shown that there is retrograde flow in the left ovarian vein and antegrade flow in the right ovarian vein immediately post-partum.2 The right ovarian vein is also longer than the left ovarian vein and has many valves within its length. These valves may act as a nidus for thrombosis. 4 The pathogenesis of thrombus formation in the ovarian vein involves many factors. Along with the hypercoagulable state of pregnancy and the puerperium, there is a decrease in blood flow velocity immediately following delivery. If there is endometritis, blood flowing from the uterus could carry pathogenic bacteria to the right ovarian vein. Other prothrombotic risk factors, e.g. factor V Leidin, and protein S and C deficiency, can congenitally predispose to POVT. The usual clinical features of POVT are as described in the cases above. Eighty per cent of patients present with a pyrexia. Lower quadrant pain and flank pain with associated nausea is common. A mass may be palpable in the right iliac fossa. Among the differential diagnoses of ovarian vein thrombosis are appendicitis, septic pelvic thrombophlebitis, peritonitis, adnexal torsion, pyelonephritis and tubo-ovarian abscess. The diagnosis is made on the clinical features described above. Where the condition is suspected on clinical grounds, the initial investigation should be an ultrasound examination, which may confirm the diagnosis. However, it should be borne in mind that ultrasound examination is operator-dependent, especially with a rare condition. If there is a high index of clinical suspicion a CT or MRI scan, where available, should be requested even with a negative ultrasound, as it is important to avoid surgery, if possible, in POVT. This is well illustrated in Case 2. The condition is treated initially with intravenous heparin and broad-spectrum antibiotics. Once thrombolysis has begun, warfarin is introduced and continued for 3 months. Pulmonary embolism may complicate POVT in up to 13% of cases, and has a mortality of approximately 4%.3 There are no data on the long-term outcome for these patients with regard to subsequent fertility and future pregnancies. Diagnosis and treatment are both non-invasive. Hence, it is important to consider POVT when faced with a post-partum patient with lower quadrant pain and fever. Once the diagnosis is considered, the appropriate investigations can be ordered and a laparotomy can be avoided.<\/p>\n
Anatomy: The ovarian veins form a plexus near the ovary within the broad ligament and communicate with the uterine plexus. These veins ascend in the retroperitoneum adjacent to the psoas muscle in pairs, which combine to form a single vein prior to termination. The right ovarian vein terminates in the inferior vena cava at an acute angle. The left ovarian vein terminates in the left renal vein at a right angle. Occasionally, valves are present in the ovarian veins. The veins enlarge greatly during pregnancy to accommodate increased blood volume. Following childbirth, a period of venous stasis occurs. Clinical Details: The typical patient with clinically significant ovarian vein thrombosis (ie, thrombophlebitis) presents with pelvic pain, fever, and a right-sided abdominal mass. Anticoagulant and intravenous (IV) antibiotic therapy is the treatment of choice. Note that patients who have undergone total abdominal hysterectomy and bilateral salpingo-oophorectomy with retroperitoneal lymph node dissection often demonstrate ovarian vein thrombosis on contrast-enhanced CT. No treatment is necessary in patients in whom the complications of thrombophlebitis or embolism do not occur.<\/p>\n
<\/p>\n
<\/span>Tocolytics Can induce Pulmonary Edema<\/span><\/h2>\n <\/p>\n
<\/p>\n
<\/span>Rh Immunization in Preg<\/span><\/h2>\nGive Rhogam 50 for first trimester, 300 past the first<\/p>\n
<\/span>ABD Pain<\/span><\/h2>\nAppendicitis-moves to RUQ, pyuria s bacteria<\/p>\n
Gall Bladder Disease<\/p>\n
Acute fatty liver of pregnancy (can be fatal)<\/p>\n
Liver or Splenic Rupture-can be spontaneous, often assoc c PIH<\/p>\n
<\/span>Genitourinary Infections<\/span><\/h2>\nUTI-10 days of cephalosporin or nitrofurantoin<\/p>\n
<\/span>STDs<\/span><\/h2>\nBacterial Vaginosis-2 weeks of amoxicillin<\/p>\n
Chorioamnionitis-fever, uterine tenderness<\/p>\n
<\/p>\n
<\/p>\n
<\/span>When Pregnancy Tests Turn Negative<\/span><\/h2>\nfrom LitFL Blog
\nWorking a few Peds shifts lately I\u0092ve run into the same question: when should your urine pregnancy test (or quantitative serum hCG) be negative after a regular pregnancy, a termination, or a miscarriage (meaning, could she really already be pregnant\u00a0again<\/em>)? I hear different answers depending on the obstetrical consultant I ask, so I decided to do a little literature search myself. It\u0092s really only been looked at in very small studies;\u00a0I\u0092ve got the specific numbers if you want them, but based on the studies I found, it looks something like this:<\/p>\nAfter a Full-Term Pregnancy:<\/p>\n
\n- Should be 3 weeks or less. In some women, ovulation may occur as early as 3 weeks after delivery.<\/li>\n<\/ul>\n
After a Termination with Misoprostol\/Mifepristone:<\/p>\n
\n- In one study, following up at 6-18 days, if the hCG level was 80% lower than the initial hCG level, there was a positive predictive value for successful expulsion of 0.995. There was no information on when the level dropped to 0 or <5.<\/li>\n<\/ul>\n
After a D&C Termination:<\/p>\n
\n- Depends on the initial hCG, but mean time was 35 days, but could be up to 60 days.<\/li>\n<\/ul>\n
After Miscarriage in Women Who Then Had a D&E for Continued Bleeding:<\/p>\n
\n- Median ~20 days, range 9-22 days.<\/li>\n<\/ul>\n
After Ectopic with Laparotomy:<\/p>\n
\n- Ectopics had the lowest hCG to begin with, reached 0 by 1-31 days, median 8.5 days.<\/li>\n<\/ul>\n
References:<\/p>\n
\n- Routine terminations of pregnancy\u0097should we screen forgestational trophoblastic neoplasia? The Lancet, 2004.<\/li>\n
- Human chorionic gonadotropin in maternal plasma after induced abortion, spontaneous abortion, and removed ectopic pregnancy. Obstetrics and Gynecology, 1984.<\/li>\n
- Verifying the effectiveness of medical abortion; ultrasound versus hCG testing. European Journal of Obstetrics and Gynecology, 2003.<\/li>\n<\/ol>\n
<\/p>\n
|\u00a0\u00a0 \u00a0\u00a0 |\u00a0\u00a0 \u00a0\u00a0 |<\/p>\n","protected":false},"excerpt":{"rendered":"
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Abnormal proliferation of chorionic villi<\/p>\n
Complete mole-no fetal tissue<\/p>\n
Incomplete mole-has fetal tissue<\/p>\n
15-20% become neoplastic (choriocarcinoma), get chest x-ray to evaluate for pulmonary mets, TFTs as high HCG levels can act like TSH, and LFTs for baseline.<\/p>\n
Uterine size will be larger than expected, snowstorm on UTS, elevated bHCGs<\/p>\n
Early preeclampsia, hyperemesis, PE from tropho cells, bleeding.\u00a0 Also ovarian torsion from >6 cm theca lutein cysts.<\/p>\n
acts like 1st trimester preeclampsia<\/p>\n
Good review article (Am Fam Phys 68(1):121, 2003) Small meals, avoidance of provoking smells, high carbs, low fats, Vitamin B6, 25 mg TID, Unisom 25 mg OD, and Ginger.\u00a0 Get ketones and electrolytes with prolonged symptoms.\u00a0 Can give antiemetics (chlorpromazine, prochlorperazine, promethazine, trimethobenzamide), antihistamines (diphenhydramine, meclizine, dimenhydrinate) or metoclopramide.<\/p>\n <\/p>\n <\/p>\n Reglan is good:\u00a0 METOCLOPRAMIDE FOR NAUSEA AND VOMITING OF PREGNANCY: A PROSPECTIVE MULTICENTER INTERNATIONAL STUDY (Am J Perinatol 19(6):311, August 2002)<\/p>\n Magee LA et al:<\/p>\n Evidence-based view of safety and<\/p>\n effectiveness of pharmacologic therapy for nausea and vomiting of pregnancy (NVP).<\/p>\n Am J Obstet Gynecol <\/i>186:S256, 2002; All are safe<\/p>\n <\/p>\n Abruptio Placentae-separation of placenta from the uterine wall.\u00a0 Early bleeding can not be seen on UTS.\u00a0 Predisposes to amniotic fluid emboli and DIC.<\/p>\n <\/p>\n Placenta Previa-painless vaginal bleeding.\u00a0 No digital exam before UTS.<\/p>\n <\/p>\n Massive Post-partum Hemorrhage Stuff<\/a><\/p>\n Can occur from 20 weeks to 2 weeks post (seizure activity occurring as late as 23 days postpartum have been attributed to eclampsia)<\/p>\n PIH c proteinuria or edema, from vasospastic cause<\/p>\n Liver damage, generalized edema, thrombocytopenia, HAs<\/p>\n HELLP-hemolysis, Elev. LFTs, low platelets<\/p>\n Eclampsia-give Mg 6 g over 5-15 minutes then 2-3 g\/hr.\u00a0 Looking for Mg of 4-7.\u00a0 Signs of toxicity no patellar reflex(10),<\/p>\n <\/p>\n Nimodipine is probably as good, but MgSO4 wins out by a bit (NEJM 348(4):304, 2003)<\/p>\n <\/p>\n Resp (12), Urine <100 cc\/hr.\u00a0 Give CaCl<\/p>\n Admit if BP>140\/90<\/p>\n Hydralizine or labetolol to decrease BP.<\/p>\n Amniotic Fluid Embolism<\/p>\n Sudden hypotension, hypoxia, coagulopathy<\/p>\n CBC, Coags, ABG, C-XR, uric acid, which has been shown to be elevated in up to 80% of eclamptic patients (JEM Nov 2003)<\/p>\n ICU Admit, Supportive Care<\/p>\n <\/p>\n DELAYED POSTPARTUM PREECLAMPSIA: AN EXPERIENCE OF 151 CASES Matthys, L.A., et al, Am J Obstet Gyn 190:1464, May 2004<\/p>\n Seizures in a pregnant woman who had not been previously diagnosed with preeclampsia must be accompanied by 2 of the following within 24 hours of presentation to be considered eclamptic: hypertension, proteinuria, thrombocytopenia, or increased aspartate aminotransferase<\/p>\n up to 23 days post partum<\/p>\n <\/p>\n The Journal of Emergency Medicine<\/b>Volume 40, Issue 4, April 2011, Pages 380-384\u00a0 best review of post-partum preeclampsia<\/p>\n <\/p>\n (Crit Care Med 2005;33(10):S340) Presents with systemic and pulmonary congestion, low CO, dysrhythmia, and possible systemic or pulmonary embolization Etiology is usually unknown ? of immune, viral, selenium deficiency,<\/p>\n <\/p>\n (Crit Care Med 2005;33(10):S307) labetolol onset in 5minutes, peak effect 10-20 minutes, lasts up to 6 hrs<\/p>\n (Crit Care Med 2005;33(10):S294) Increased risk during all three semesters and peripartum Most recent study of helical CT in pregnancy for PE calculated 0.00033 Rad in first trim and 0.01308 rad in the third; these are comparable to V\/Q (Radiology 2002;224:487) UFH and LMWH are safe for pregnancy and breastfeeding<\/p>\n <\/p>\n (Crit Care Med 2005;33(10):S364) Magnesium for preelampsia 4-6 G of MgSO4 over 20 min followed by 2G\/hr Ther. level 4-8 CaGLUC can be given for cards dysrhythmia Should lower BP as well, if still over 160\/110 use labetolol \u00a0 3-fold increase in risk of SAH, occur during 2nd and 3rd trim<\/p>\n 120-300% increae in circulating clotting factors during pregnancy<\/p>\n levels of protein S are decreased, protein C levels are the same Treat with heparin or LMWH empty delta sign is traingle of clot on contrast scan in the sinus<\/p>\n is uncommon, but the true incidence is not known. Ninety per cent of cases present as right iliac fossa pain within 10 days of delivery. Anti-coagulation and intravenous antibiotics are the mainstay of treatment. We report three cases that were referred to our unit. These cases illustrate the difficulty in the clinical diagnosis of POVT and highlight the importance of its inclusion in the differential diagnoses of an acute abdomen in post-partum patients. POVT can be accurately diagnosed by appropriate non-invasive investigations and a laparotomy avoided.<\/p>\n <\/p>\n Post-partum ovarian vein thrombosis has an incidence of 1:2000 deliveries.1 The majority of cases occur within one week of delivery. Ovarian vein thrombosis is also associated with malignancy, pelvic inflammatory disease and gynaecological surgery.2 Eighty to ninety per cent occur in the right ovarian vein.3 This is believed to be due, in part, to the commonly occurring dextrotorsion of the enlarging uterus, which causes compression of the right ovarian vein and right ureter as they cross the pelvic rim.4 Studies have shown that there is retrograde flow in the left ovarian vein and antegrade flow in the right ovarian vein immediately post-partum.2 The right ovarian vein is also longer than the left ovarian vein and has many valves within its length. These valves may act as a nidus for thrombosis. 4 The pathogenesis of thrombus formation in the ovarian vein involves many factors. Along with the hypercoagulable state of pregnancy and the puerperium, there is a decrease in blood flow velocity immediately following delivery. If there is endometritis, blood flowing from the uterus could carry pathogenic bacteria to the right ovarian vein. Other prothrombotic risk factors, e.g. factor V Leidin, and protein S and C deficiency, can congenitally predispose to POVT. The usual clinical features of POVT are as described in the cases above. Eighty per cent of patients present with a pyrexia. Lower quadrant pain and flank pain with associated nausea is common. A mass may be palpable in the right iliac fossa. Among the differential diagnoses of ovarian vein thrombosis are appendicitis, septic pelvic thrombophlebitis, peritonitis, adnexal torsion, pyelonephritis and tubo-ovarian abscess. The diagnosis is made on the clinical features described above. Where the condition is suspected on clinical grounds, the initial investigation should be an ultrasound examination, which may confirm the diagnosis. However, it should be borne in mind that ultrasound examination is operator-dependent, especially with a rare condition. If there is a high index of clinical suspicion a CT or MRI scan, where available, should be requested even with a negative ultrasound, as it is important to avoid surgery, if possible, in POVT. This is well illustrated in Case 2. The condition is treated initially with intravenous heparin and broad-spectrum antibiotics. Once thrombolysis has begun, warfarin is introduced and continued for 3 months. Pulmonary embolism may complicate POVT in up to 13% of cases, and has a mortality of approximately 4%.3 There are no data on the long-term outcome for these patients with regard to subsequent fertility and future pregnancies. Diagnosis and treatment are both non-invasive. Hence, it is important to consider POVT when faced with a post-partum patient with lower quadrant pain and fever. Once the diagnosis is considered, the appropriate investigations can be ordered and a laparotomy can be avoided.<\/p>\n Anatomy: The ovarian veins form a plexus near the ovary within the broad ligament and communicate with the uterine plexus. These veins ascend in the retroperitoneum adjacent to the psoas muscle in pairs, which combine to form a single vein prior to termination. The right ovarian vein terminates in the inferior vena cava at an acute angle. The left ovarian vein terminates in the left renal vein at a right angle. Occasionally, valves are present in the ovarian veins. The veins enlarge greatly during pregnancy to accommodate increased blood volume. Following childbirth, a period of venous stasis occurs. Clinical Details: The typical patient with clinically significant ovarian vein thrombosis (ie, thrombophlebitis) presents with pelvic pain, fever, and a right-sided abdominal mass. Anticoagulant and intravenous (IV) antibiotic therapy is the treatment of choice. Note that patients who have undergone total abdominal hysterectomy and bilateral salpingo-oophorectomy with retroperitoneal lymph node dissection often demonstrate ovarian vein thrombosis on contrast-enhanced CT. No treatment is necessary in patients in whom the complications of thrombophlebitis or embolism do not occur.<\/p>\n <\/p>\n <\/p>\n <\/p>\n Give Rhogam 50 for first trimester, 300 past the first<\/p>\n Appendicitis-moves to RUQ, pyuria s bacteria<\/p>\n Gall Bladder Disease<\/p>\n Acute fatty liver of pregnancy (can be fatal)<\/p>\n Liver or Splenic Rupture-can be spontaneous, often assoc c PIH<\/p>\n UTI-10 days of cephalosporin or nitrofurantoin<\/p>\n Bacterial Vaginosis-2 weeks of amoxicillin<\/p>\n Chorioamnionitis-fever, uterine tenderness<\/p>\n <\/p>\n <\/p>\n from LitFL Blog After a Full-Term Pregnancy:<\/p>\n After a Termination with Misoprostol\/Mifepristone:<\/p>\n After a D&C Termination:<\/p>\n After Miscarriage in Women Who Then Had a D&E for Continued Bleeding:<\/p>\n After Ectopic with Laparotomy:<\/p>\n References:<\/p>\n <\/p>\n |\u00a0\u00a0 \u00a0\u00a0 |\u00a0\u00a0 \u00a0\u00a0 |<\/p>\n","protected":false},"excerpt":{"rendered":" Array<\/p>\n","protected":false},"author":1,"featured_media":0,"comment_status":"closed","ping_status":"closed","sticky":false,"template":"","format":"standard","meta":{"_genesis_hide_title":false,"_genesis_hide_breadcrumbs":false,"_genesis_hide_singular_image":false,"_genesis_hide_footer_widgets":false,"_genesis_custom_body_class":"","_genesis_custom_post_class":"","_genesis_layout":"","footnotes":""},"categories":[12],"tags":[],"yoast_head":"\n![](\"\/wp-content\/images\/part3\/09f1.jpeg\")
<\/a><\/p>\n<\/a><\/p>\n<\/span>Nausea and Vomiting of Pregnancy \/ Hyperemesis Gravidum<\/span><\/h2>\n
<\/span>Complications of Late Pregnancy<\/span><\/h2>\n
<\/span>Vaginal Bleeding<\/span><\/h3>\n
<\/span>Preeclampsia\/Eclampsia<\/span><\/h3>\n
<\/span>Neurologic Disorders in the Pregnant and Post-Partum Patient<\/a><\/span><\/h2>\n
<\/span>Peripartum Cardiomyopathy<\/span><\/h3>\n
<\/span>HTN in Pregnancy<\/span><\/h3>\n
<\/span>PE during pregnancy<\/span><\/h3>\n
<\/span>Neuro disorders during pregnancy<\/span><\/h3>\n
<\/span>Cerebral Venous Sinus Thrombosis<\/span><\/h3>\n
<\/span>Post-partum ovarian vein thrombosis (POVT)<\/span><\/h3>\n
<\/span>Tocolytics Can induce Pulmonary Edema<\/span><\/h2>\n
<\/span>Rh Immunization in Preg<\/span><\/h2>\n
<\/span>ABD Pain<\/span><\/h2>\n
<\/span>Genitourinary Infections<\/span><\/h2>\n
<\/span>STDs<\/span><\/h2>\n
<\/span>When Pregnancy Tests Turn Negative<\/span><\/h2>\n
\nWorking a few Peds shifts lately I\u0092ve run into the same question: when should your urine pregnancy test (or quantitative serum hCG) be negative after a regular pregnancy, a termination, or a miscarriage (meaning, could she really already be pregnant\u00a0again<\/em>)? I hear different answers depending on the obstetrical consultant I ask, so I decided to do a little literature search myself. It\u0092s really only been looked at in very small studies;\u00a0I\u0092ve got the specific numbers if you want them, but based on the studies I found, it looks something like this:<\/p>\n\n
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