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Pregnancyreview

N. Petrenko, MD, PhD

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Signs of pregnancy

Presumptive (generally subjective) Probable (objective) Positive (diagnostic)

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Presumptive symptoms of pregnancy (felt by woman):

• Cessation of menses• Nausea with or without vomiting• “Morning sickness”• Frequent urination• Fatigue• Breast tenderness, fullness, tingling• Maternal perception of fetal movement

(“Quickening”) 18-20w, 16 w

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Presumptive signs of pregnancy

• Increased skin pigmentation – chloasma, linea nigra

• Appearance of striae on abdomen and breasts

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Probable signs of pregnancy

(observed by examiner):• Changes in the size, shape, and consistency of

the uterus (Hegar sign-softening of the cervix )• Enlargement of the abdomen

• Changes in the cervix (Goodell sign-softening of the cervix )

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Probable signs of pregnancy

(observed by examiner):• Bluish or purplish coloration of the vaginal

mucosa and cervix (Chadwick’s sign-a dark blue to purplish-red congested appearance of the vaginal mucosa )

• Palpation of Braxton-Hicks contractions

• Outlining the fetus manually

• Endocrine tests of pregnancy

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Positive signs of pregnancy(noted by examiner, confirm pregnancy)

• Identification of the fetal heart beat separately and distinctly from that of the mother (10-12 w)

• Perception of fetal movements by the examiner (18-20 w)

• Visualization of pregnancy on ultrasound• Fetal recognition on X-ray

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Gravida and Para

• Gravida means a woman who has been, or currently is, pregnant

• Para means a woman who has given birth

• Nulligravida – never been pregnant• Primigravida – pregnant for the first time• Primipara – has delivered once• Multipara – has delivered more than once

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G T P A L

• G – GRAVIDA (how many pregnancies)

• T – TERM (how many term deliveries)

• P – PRETERM (how many preterm deliveries)

• A – ABORTIONS (how many abortions, spontaneous or induced)

• L – LIVING – how many children currently living

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Term, Preterm, Abortion

• TERM means delivery occurring in weeks 38-42

• PRETERM means delivery occurring in weeks 20-37

• ABORTION means delivery occurring before 20 weeks

• POSTTERM means delivery occurring after week 42

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• Duration 280 days =40 weeks= 10 lunar months = 9 calendar month

• 1st Trimester 1-13 weeks– Accepting reality of pregnancy

• 2nd Trimester 14-26 weeks– Resolving feelings about her own mother;

defining herself as a mother

• 3rd Trimester 27-40 weeks– Active preparation for childbirth and baby

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Assessment of Gestational Age

• By LMP

• By physical exam

• By ultrasound

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Nagele’s Rule

Subtract 3 months from that date then add 7 days

1st day of LNMP (last normal menstrual period)

Example: LNMP: September 10, 2006

Expected Due Date (EDD): June 17, 2007

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Uterine Sizing• 6 weeks – globular with softening of the

isthmus, size of a tangerine

• 8 weeks – globular, size of a baseball

• 10 weeks – globular with irregularity around one cornua (Piskacek’s sign), size of a softball

• 12 weeks – globular, size of a grapefruit

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Uterine Sizing• Uterine enlargement

• 12 weeks – At Symphysis

• 16 weeks – Midway between symphysis and umbilicus

• 20 weeks – At the umbilicus

• 36 weeks - Near xyphoid process

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Uterine Sizing

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Accuracy of Dating by Ultrasound

Gestational Age weeks)

Ultrasound Measurements

Range of Accuracy

< 8 Sac size + 10 days

8-12 CRL + 7 days

12-15 CRL, BPD + 14 days

15-20 BPD, HC, FL, AC + 10 days

20-28 BPD, HC, FL, AC + 2 weeks

> 28 BPD, HC, FL, AC + 3 weeks

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Nausea with or without Vomiting

• Starts at 4-6 weeks, peaks at 8-12 weeks, resolves by 14-16 weeks

• Causes: unknown; may be rapidly increasing and high levels of estrogen, hCG, thyroxine; may have a psychological component

• Rule out: hyperemesis gravidarum

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• Most cases of nausea and vomiting in pregnancy will resolve spontaneously within 16 to 20 weeks of gestation.

• Nausea and vomiting are not usually associated with a poor pregnancy outcome.

Nausea and vomiting in early pregnancy

A

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Nausea and vomiting in early pregnancy

• If a woman requests or would like to consider treatment, the following interventions appear to be effective in reducing symptoms:

• non-pharmacological

– ginger – P6 acupressure

• pharmacological

– antihistamines. A

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Ptyalism

• Excessive salivation accompanied by nausea and inability to swallow saliva

• Cause: unknown; may be related to increased acidity in the mouth

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Fatigue

• Causes: unknown; may be related to gradual increase in BMR

• Rule out: anemia, thyroid disease

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BackacheWomen should be informed

that exercising in water, massage therapy might help to ease backache

during pregnancy. A

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Upper Backache

• Cause: increase in size and weight of the breasts

• Relief: well-fitting, supportive bra

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Low Backache

• Cause: weight of the enlarging uterus causing exaggerated lumbar lordosis

• Rule out: pyelonephritis (CVAT)

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Leukorrhea

• Definition: a profuse, thin or thick white vaginal discharge consisting of white blood cells, vaginal epithelial cells, and bacilli; acidic due to conversion of an increased amount of glycogen in vaginal epithelial cells into lactic acid by Doderlein’s bacilli

• Rule out: vaginitis, STI, ruptured membranes

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Urinary Frequency• 1st trimester: increased

weight, softening of the isthmus, anteflexion of the uterus

• 3rd trimester: pressure of the presenting part

• Rule out: UTI

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Heartburn• Relaxation of the cardiac

sphincter due to progesterone• Decreased GI motility due to

smooth muscle relaxation (progesterone)

• Lack of functional room for the stomach because of its displacement and compression by the enlarging uterus

• Rule out: GI disease

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Heartburn• Women who present with symptoms

of heartburn in pregnancy should be offered information regarding lifestyle and diet modification.

• Antacids may be offered to women whose heartburn remains troublesome

GPP

A

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Constipation

• Decreased peristalsis due to relaxation of the smooth muscle of the large bowel under the influence of progesterone

• Displacement of the bowel by the enlarging uterus

• Administration of iron supplements

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Constipation

Women who present with constipation in pregnancy

should be offered information regarding diet modification, such as bran or wheat fibre

supplementation. A

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Hemorrhoids• Relaxation of vein walls and

smooth muscle of large bowel under influence of progesterone

• Enlarging uterus causes increased pressure, impeding circulation and causing congestion in pelvic veins

• Constipation

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Hemorrhoids• Women should be offered

information concerning diet modification.

• If clinical symptoms remain troublesome, standard hemorrhoids creams should be considered. GPP

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Leg Cramps• Cause: unknown. ? inadequate calcium, ? Imbalance in

calcium-phosphorus ratio

• Relief: straighten the leg and dorsiflex the foot:

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Dependent Edema

• Cause: impaired venous circulation and increased venous pressure in the lower extremities

• Rule out: preeclampsia

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Varicosities

• Impaired venous circulation and increased venous pressure in lower extremities

• Relaxation of vein walls and surrounding smooth muscle under the influence of progesterone

• Increased blood volume• Familial predisposition

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Varicose veins• Varicose veins are a common

symptom of pregnancy that will not cause harm and

• Compression stockings can improve the symptoms but will not prevent varicose veins from emerging. A

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Insomnia

• Discomfort of the enlarged uterus• Any of the common discomforts of pregnancy• Fetal activity• Psychological causes

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Round Ligament Pain• Round ligaments attach

on either side of the uterus just below and in front of insertion of fallopian tubes, cross the broad ligament in a fold of peritoneum, pass through the inguinal canal, insert in the anterior portion of the labia majora

• When stretched, they hurt!

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Supine Hypotensive Syndrome

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Screening for fetal anomalies

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Screening for structural anomalies

Pregnant women should be offered an ultrasound scan to screen for structural anomalies, ideally between 18 and 20 weeks’

gestation, by an appropriately trained sonographer and with equipment of

an appropriate standard. A

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Screening for Down’s syndrome

Pregnant women should be offered screening for Down’s syndrome with a test which

provides the current standard of a detection rate above 60% and a false-positive rate of less

than 5%. B

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The following tests meet this standard:• from 11 to 14 weeks– nuchal translucency (NT)– the combined test (NT, hCG and PAPP-A)• from 14 to 20 weeks– the triple test (hCG, AFP and uE3)– the quadruple test (hCG, AFP, uE3,

inhibin A) B

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Early pregnancy Early pregnancy bleedingbleeding

Spontaneous abortionSpontaneous abortionIncompetent cervixIncompetent cervixEctopic pregnancyEctopic pregnancyHydatiform moleHydatiform mole

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AbortionAbortion

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Abortion miscarriageAbortion miscarriage• End of pregnancy before 20 weeks

• Fetal weight less than 500 mg

• Result of natural cause

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miscarriagemiscarriage• 10-15% of recognize pregnancy end in miscarriage• Early (till 12 weeks)• before 8 weeks• 50% - result from chromosomal abnormalities• endocrine imbalance (luteal phase defects, insulin-

dependent diabetes mellitus with high blood glucose levels in the first trimester),

• immunologic factors (antiphospholipid antibodies), • Infections (bacteriuria and Chlamydia trachomatis), • Systemic disorders (lupus erythematosus), • genetic factors

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miscarriagemiscarriage• Late 12 - 20 weeks • Result from maternal causes:• advancing maternal age and parity, • chronic infections, • premature dilation of the cervix and other

anomalies of the reproductive tract,• chronic debilitating diseases, • nutrition, and recreational drug use

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miscarriagemiscarriage• Little can be done to avoid genetically

caused pregnancy loss, but correction of maternal disorders, immunization against infectious diseases, adequate early prenatal care, and treatment of pregnancy complications can do much to prevent miscarriage.

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miscarriagemiscarriageTypes of miscarriage

• threatened,

• inevitable,

• incomplete,

• complete,

• missed.

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miscarriagemiscarriage

missed.

• threatened

• inevitable

incomplete

complete

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miscarriagemiscarriageClinical manifestation

• uterine bleeding,• uterine contractions, • uterine pain are ominous• before the sixth week - a heavy menstrual flow.• between the sixth and twelfth weeks - moderate

discomfort and blood loss. • After the twelfth week – more severe pain, similar to that

of labor, because the fetus must• be expelled.

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miscarriagemiscarriage• threatened miscarriage - spotting of blood but with the

cervical os closed, Mild uterine cramping• Inevitable and incomplete - a moderate to heavy amount

of bleeding with an open cervical os, Tissue may be present with the bleeding, Mild to severe uterine cramping

• An inevitable miscarriage is often accompanied by rupture of membranes (ROM) and cervical dilation; passage of the products of conception is a certainty.

• An incomplete miscarriage involves the expulsion of the fetus with retention of the placenta

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miscarriagemiscarriage• complete miscarriage all fetal tissue is passed, the cervix

is closed, • slight bleeding, mild uterine cramping • missed miscarriage - fetus has died but the products of

conception are retained in utero for several weeks. • It may be diagnosed by ultrasonic examination after the

uterus stops increasing in size or even decreases in size. • no bleeding or cramping, and the cervical os remains

closed.• Recurrent early (habitual) miscarriage is the loss of three

or more previable pregnancies. Women having three or more miscarriages are at increased risk for preterm birth, placenta previa, and fetal anomalies in subsequent pregnancies

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miscarriagemiscarriage• Assessment

• Complain (pain, bleeding)• LMP• Vital sign (t, Ps, BP)• Previous pregnancy• hCG• US• CBC (Hb, Ht, WBC, ESR)• Blood type & Rh

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miscarriagemiscarriage• Management

• Threatened – bed rest supportive therapy

• inevitable, incomplete, complete, missed – D&C

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miscarriagemiscarriage• Postoperative care

• Oxiticin 10-20 U in 1000 ml of fluid

• Antibiotics

• Analgetics

• Transfusion

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miscarriagemiscarriage• Discharge

• Rest• Iron supplementation• Sexual behavior• Emergency sign• Contraception

• http://www.youtube.com/watch?v=9LJESmC5-wA

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Incompetent cervixIncompetent cervix

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Incompetent cervixIncompetent cervix• passive and painless dilation of the cervix during the

second trimester. • Etiology.• a history of previous cervical lacerations during childbirth,• excessive cervical dilation for curettage or biopsy, • ingestion of diethylstilbestrol by the woman's mother while

being pregnant with the woman. • a congenitally short cervix or cervical or uterine anomalies.

• Clinical diagnosis based on:• history of short labors and recurring loss of pregnancy at

progressively earlier gestational ages are characteristics of reduced cervical competence.

• Ultrasound: cervix (less than 20 mm in length) is indicative of reduced cervical competence.

• Often, but not always, the short cervix is accompanied by cervical fanneling, or effacement of the internal cervical os

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Incompetent cervixIncompetent cervix

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Incompetent cervixIncompetent cervix• Conservative management• bed rest, hydration, and tocolysis (inhibition of uterine contractions). • A cervical cerclage may be placed around the cervix beneath the

mucosa to constrict the internal os of the cervix • Prophylactic cerclage is placed at 10 to 14 weeks of gestation, after

which the woman is told to refrain from intercourse, prolonged (more than 90 minutes) standing, and heavy lifting. She is followed during the course of her pregnancy with ultrasound scans to assess for cervical shortening and funneling.

• The cerclage is electively removed (usually an office or a clinic procedure) when the woman reaches 37 weeks of gestation, or it may be left in place and a cesarean birth performed. If removed, cerclage placement must be repeated with each successive pregnancy.

• Risks r/t of the procedure:• premature rupture of membranes,• preterm labor,• chorioamnionitis. • Because of these risks, and because bed rest and tocolytic therapy

can be used to prolong the pregnancy cerclage is rarely performed after 25 weeks of gestation

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Ectopic pregnancyEctopic pregnancy

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Ectopic pregnancyEctopic pregnancy• Implantation of the fertilized ovum outside

the uterine cavity

• uterine (fallopian) tube 95%, with most located on the ampullar

• abdominal cavity (3% to 4%),

• ovary (1%),

• and cervix (1%).

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Ectopic pregnancyEctopic pregnancy

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Ectopic pregnancyEctopic pregnancy• Clinical manifestation & assessment

• missed period,• Adnexal fullness, and tenderness • The tenderness can progress from a dull pain to a colicky pain when the

tube stretches. Pain may be unilateral, bilateral, or diffuse over the abdomen.

• Abnormal vaginal bleeding that is dark red or brown occurs in 50% to 80% of women.

• If the ectopic pregnancy ruptures, pain increases. This pain may be generalized, unilateral, or acute deep lower quadrant pam caused by blood irritating the peritoneum. Referred shoulder pain can occur as a result of diaphragmatic irritation caused by blood in the peritoneal cavity.

• The woman may exhibit signs of shock related to the amount of bleeding in the abdominal cavity and not necessarily related to obvious vaginal bleeding.

• An ecchymotic blueness around the umbilicus (Cullen sign), indicating hematoperitoneum, may develop in a neglected ruptured intraabdominal ectopic pregnancy.

• hCG, US, CBC• Ps, BP

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Ectopic pregnancyEctopic pregnancy• Differential diagnosis

• miscarriage, ruptured corpus luteum cyst, appendicitis, salpingitis, ovarian cysts, torsion of the ovary, and urinary tract infection

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Ectopic pregnancyEctopic pregnancy• Management

• Surgery (tubeectomy, remove ectopic pregnancy)

• Methotrexate

• Antibiotics

• Transfusion

• Contraception

• Restoring of fertility

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Ectopic pregnancyEctopic pregnancy• Nursing Interventions with Ectopic

Pregnancy• Prepare patient for surgery.• Institute measures to control bleeding/treat

shock if hemorrhage severe and continue to monitor postoperatively

• May be given methotrexate instead of surgery

• Allow patient to express feelings about loss of pregnancy and concerns about future pregnancies.

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Hydatidiform moleHydatidiform mole

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Hydatidiform moleHydatidiform mole• is a gestational trophoblastic disease. There are two distinct

types of hydatidiform moles: complete (or classic) mole and partial mole.

• The etiology is• unknown, • may be • an ovular defect or a nutritional deficiency. • Using clomiphene (Clomid) • early teens or older than 40 years of age. • Chromosomal abnomalities

• Types. The complete mole results from fertilization of an egg whose nucleus has been lost or inactivated nucleus.

• The mole resembles a bunch of white grapes .• The fluid-filled vesicles grow rapidly, causing the uterus to

be Rupture of uterus

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Hydatidiform moleHydatidiform mole• Clinical manifestations• early stages same as normal pregnancy. • Later, vaginal bleeding (dark brown (resembling prune juice) or

bright red and either scant or profuse. It may continue for only a few days or intermittently for weeks.

• Early in pregnancy the uterus in approximately half of affected women is significantly larger than expected from menstrual dates.

• The percentage of women with an excessively enlarged uterus increases as length of time since LMP increases. Approximately 25% of affected women have a uterus smaller than would be expected from menstrual dates.

• Anemia from blood loss, excessive nausea and vomiting (hyperemesis gravidarum), and abdominal cramps caused by uterine distention are relatively common findings.

• Preeclampsia occurs in approximately 15% of cases, usually between 9 and 12 weeks of gestation, but any symptoms of PIH before 20 weeks of gestation may suggest hydatidiform mole.

• Hyperthyroidism and pulmonary embolization of trophoblastic elements occur infrequently but are serious complications of hydatidiform mole. Partial moles cause few of these symptoms and may be mistaken for an incomplete or missed miscarriage.

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Hydatidiform moleHydatidiform mole• Management• US (snowstorm pattern)• hCG• Uterine height• D&C• Induced labour• Contraception• hCG level control 1 year

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Late pregnancy Late pregnancy bleedingbleeding

Placenta previaPlacenta previaAbruptio placentaAbruptio placenta

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Placenta previaPlacenta previa

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Placenta previaPlacenta previa• the placenta is implanted in the lower uterine

segment near or over the internal cervical os. • Total or complete placenta previa - if the internal

os is entirely covered by the placenta when the cervix is fully dilated.

• Partial placenta previa implies incomplete coverage of the internal os.

• Marginal placenta previa indicates that only an edge of the placenta extends to the internal os but may extend onto the os during dilation of the cervix during labor.

• The term low-lying placenta is used when the placenta is implanted in the lower uterine segment but does not reach the os.

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Placenta PraeviaPlacenta Praevia

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Placenta PraeviaPlacenta Praevia• Etiology / risk factors • previous placenta previa,• previous cesarean birth,• induced abortion, possibly related to endometrial

scarring• multiple gestation (because of the larger

placental area), • advanced maternal age (older than 35 years), • African or Asian ethnicity,• smoking, and cocaine us

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Placenta PraeviaPlacenta Praevia• painless vaginal bleeding• vaginal bleeding associated with uterine activity.• after 24 weeks of gestation. • This bleeding is associated with the stretching and thinning of

the lower uterine segment that occurs during the third trimester. • It is bright red in color. • Vital signs may be normal, even with heavyblood loss, because

a pregnant woman can lose up to 40% of blood volume without showing signs of shock.

• Clinical presentation and decreasing urinary output may be better indicators of acute blood loss than vital signs alone.

• The fetal heart rate is reassuring unless there is a major detachment of the placenta.

• Abdominal examination usually reveals a soft, relaxed, nontender uterus with normal tone. If the fetus is lying longitudinally, the fundal height is usually greater than expected for gestational age because the low placenta hinders descent of the presenting fetal part. Leopold's maneuvers may reveal a fetus in an oblique or breech position or lying transverse because of the abnormal site of placental implantation.

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Placenta PraeviaPlacenta Praevia• Related risk: mother• premature ROM,• preterm birth, • surgery-related trauma to structures adjacent to

the uterus, anesthesia complications, blood transfusion reactions, overinfusion of fluids, abnormal placental attachments to the uterine wall (e.g., placenta accreta), postpartum hemorrhage, thrombophlebitis, anemia, and infection.

• Fetus• death is caused by preterm birth. • hypoxia in utero • Congenital anomalies. • IUGR

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Placenta PreviaPlacenta PreviaNursing Management

Assess the amount and character of bleeding

• Monitor Fetal Heart Tones (FHT) and activity monitoring (kick count)

• Bedrest and no sexual activity

• Report signs of preterm labor

• Conservative management of pregnancy

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Placenta PraeviaPlacenta Praevia• Management based on:

• Gestational age

• Amount of bleeding

• Fetal condition

• CS

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ManagementManagement• Hospitalize if actively bleeding; if not minimal

activity at home is OK---pelvic rest• Check Hgb & Hct routinely• Transfusion may be necessary to maintain

maternal and fetal stability (goal is to keep maternal Hct between 30-35%)

• If bleeding is severe, delivery is indicated regardless of gestational age or fetal lung maturity

• Birth by cesarean if cervix is >30% covered or if bleeding is excessive; otherwise, attempt at vaginal delivery is indicated (double set-up)

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Placenta PreviaPlacenta Previa• Nursing Care of the Patient Maintain IV

access

• O2 PRN

• Continuous fetal monitoring if active bleeding

• Hourly pad count noting color and amount• Digital cervical exams are contraindicated!!

– Evaluation of cervical dilatation is obtained visually with a speculum

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Placenta abruptioPlacenta abruptio

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Placenta abruptioPlacenta abruptio• Risk factors –• Multiparity, • PIH, • Polyhydramnios, • Trauma, • Smoking, • Malnutrition, • Previous abruption, • Idiopathic

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Placenta abruptioPlacenta abruptio• Grades 1 (mild), vaginal bleeding with

uterine tendeness, no distress, 10-20 %• 2 (moderate), uterine tendeness and

tetany with or with out external bleeding, fetal distress, 20-50%

• 3 (severe) severe uterine tetany, schock, fetal is dead, coagulopathy, greater than 50%

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Placenta abruptioPlacenta abruptio• Clinical symptoms

• Vaginal bleeding

• Abdominal pain

• Uterine tenderness

• Uterine contraction

• Couvelaire uterus

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Placenta abruptioPlacenta abruptio• Outcomes• Maternal mortality• Renal failure • pituitary necrosis• Rh negative woman with Rh positive fetus can become

sensitized if fetal-to-maternal hemorrhage • fetal hypoxia, • preterm birth, • Risk for neurologic defects• Perinatal mortality

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Placental Abruption

• Expectant management- if small bleed, and maternal and fetal condition satisfactory. Monitor well-being and induce labour >37weeks. Anti-D if indicated.

• Active Management- if severe abruption. Resuscitate and correct shock & DIC. Perform ARM and deliver fetus asap. IV Oxytocics to prevent PPH. Anti-D as above.

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Abruptio Placenta

• Complete of partial premature separation of the placenta from uterus

• Precipitating Factors– Blunt trauma to abdomen– Drug abuse, especially cocaine– Hypertension– Premature rupture of membrane– Smoking

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Abruptio Placenta (continued)

• Medical emergency because of the risk of maternal hemorrhage and fetal demise

• May develop Disseminated Intravascular Coagulation (DIC)

• Bleeding may be obvious or concealed

• Concealed bleeding may lead to uterine tenderness and abdominal pain

• Monitoring may reveal elevated uterine resting tone and a rising FHT

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Nursing Management of Abruptio Placenta

• Assess amount and character of bleeding• Assess abdominal/uterine tenderness,

contractions and resting • Monitor for shock • Assess FHT and activity • Measure fundal height since concealed bleeding

may be present• Provide emotional support • Prepare for possible C-Section

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Clinical Manifestations

• Vaginal bleeding (external)– May not be present in concealed abruptions

(occult bleeding)

• Abdominal pain (sudden onset/often severe)

• Uterine tenderness• Uterine CTXs/hypertonus/hyperactivity• Hemorrhagic shock• Ischemic necrosis of distant organs• Fetal distress or death

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Management• Hospitalize• Large-bore (16-guage) IV access (2 preferable)• Assess Bleeding

– Hgb & Hct monitoring– Coagulation factor monitoring (fibrinogen, platelets,

fibrin split products, PT, PTT)– Transfuse if necessary

• Frequent VS• O2 if necessary• Continuous Fetal Monitoring• Rhogam if necessary

– Rhogam covers 30cc fetal whole blood

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Management—cont.• Identify appropriate timing of delivery

– Decision is based on condition of mother and fetus, gestational age of fetus, dilation of cervix

– Possibly use betamethasone to accelerate fetal lung maturity in preparation for delivery

• Type of delivery– Vaginal delivery may be attempted if

abruption is moderate (stable mother and no signs of fetal distress)

– Cesarean section if fetal distress is present

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Hypertension in Pregnancy Classification

• Chronic hypertension• Pregnancy-induced hypertension

– Gestational hypertension– Preeclampsia– Eclampsia

• Preeclampsia superimposed on chronic hypertension

• Standard definitions are not consistently used by health care providers

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Chronic hypertension

– Present before the pregnancy or diagnosed before week 20 of gestation

– or continuing beyond 42 days postpartum

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Gestational hypertension

– Onset of hypertension without proteinuria after the 20th week of pregnancy

• Systolic BP > 140 mm Hg• Diastolic BP >90 mm Hg

– Diagnosis of onset during pregnancy based on two measurements that meet criteria for gestational BP elevation within a 1-week period

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Preeclampsia– Pregnancy-specific syndrome– Hypertension develops after 20 weeks of gestation in

previously normotensive woman– Proteinuria may be present – Multisystem, vasospastic disease process

characterized by hemoconcentration, hypertension, and proteinuria

– Disease of reduced organ perfusion with presence of hypertension and proteinuria

– Complicates 3% to 7% of all pregnancies

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Proteinuria

• is a concentration of 0.1 g/L (1+ to 2+ on dipstick measurement) or more in at least two random urine specimens collected at least 6 hours apart.

• In a 24-hour specimen, proteinuria is a concentration of 0.3 g/L per 24 hours

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Edema• Pathologic edema is clinically evident,

generalized accumulation of fluid of the face, hands, or abdomen that is not responsive to 12 hours of bed rest. It may also be manifested as a rapid weight gain of more than 2 kg in 1 week. The presence of edema is no longer considered necessary for the diagnosis of preeclampsia

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MILD PREECLAMPSIA SEVERE PREECLAMPSIA

MATERNAL EFFECTS

Blood pressure BP reading of 140/90 mm Hg x2, 4-6 hr apart Rise to >160/110 mm Hg on two separate occasions 4-6 hr apart with pregnant woman on bed rest

Mean arterial pressure (MAP)

>105 mm Hg >105 mm Hg

Weight gain Weight gain of more than 0.5 kg/wk during the second and third trimesters or sudden weight gain of 2 kg/wk at any time

Same as mild preeclampsia

Proteinuria— Qualitative dipstick— Ouantitative 24 hr analysis

Proteinuria of 0.3 g/L in a 24 hr specimen or >0.1 g/L in a random day-time specimen on two or more occasions 6 hr apart (because protein loss is variable); with dipstick, values varying from 1+ to 2 +

Proteinuria of >0.5 g/L in 24 hr or >4+ protein on dipstick

Edema Dependent edema, some puffiness of eyes, face, fingers; pulmonary edema absent

Generalized edema, noticeable puffiness; eyes, face, fingers; pulmonary edema possibly present

Reflexes May be normal Hyperreflexia ≥3+, possible ankle clonus

Preeclampsia

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MILD PREECLAMPSIA SEVERE PREECLAMPSIA

MATERNAL EFFECTS

Reflexes May be normal Hyperreflexia ≥3+, possible ankle clonus

Urine output Output matching intake, ≥30 ml/hr or <650 ml/24 hr

<20 ml/hr or <400 ml to 500 ml/24 hr

Headache Absent/transient Severe

Visual problems Absent Blurred, photophobia, blind spots on funduscopy

Irritability/changes in affect

Transient Severe

Epigastric pain Absent Present

Serum creatinine Normal Elevated

Thrombocytopenia Absent Present

AST elevation Normal or minimal Marked

Preeclampsia

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MILD PREECLAMPSIA SEVERE PREECLAMPSIA

FETAL EFFECTS

Placental perfusion Reduced Decreased perfusion expressing as IUGR in fetus; FHR: late decelerations

Premature placental aging

Not apparent At birth placenta appearing smaller than normal for duration of pregnancy, premature aging apparent with numerous areas of broken syncytia, ischemic necroses (white infarcts) numerous, intervillous fibrin deposition (red infarcts)

Preeclampsia

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HELLP syndrome

• is a laboratory diagnosis for a variant of severe preeclampsia characterized by hemolysis (H), elevated liver enzymes (EL), and low platelets (LP)

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Eclampsia

– Seizure activity or coma in woman diagnosed with preeclampsia

– No history of previous seizure disorder– Presentation varies

• One third in labor• One third during delivery• One third within 72 hours postpartum

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Chronic hypertension with superimposed preeclampsia

– Women with chronic hypertension may acquire preeclampsia or eclampsia

– Increases morbidity for mother and fetus

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Etiology– Unique to human pregnancies– Signs and symptoms develop only during

pregnancy and disappear after birth of the fetus and passage of placenta

– The cause is unknown– Associated high risk factors

• Primigravidity • Multifetal pregnancy• Preexisting medical condition (Obesity, Chronic renal

disease, Chronic hypertension, Diabetes)• Preeclampsia in a prior pregnancy or Family history of

PIH• Maternal age <19 years; >40 years• Rh incompatibility

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Etiology

• Current theories

• Increase vasoconstrictor tone

• Abnormal prostaglandin action

• Endotelian cell activation

• Immunologic factor

• Genetic disposition

• diet

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Pathophysiology

May be caused by disruptions in placental perfusion and endothelial cell dysfunction

• Main pathogenic factor is not an increase in BP, but poor perfusion resulting from vasospasm

• Arteriolar vasospasm diminishes diameter of blood vessels, which impedes blood flow to all organs and increases BP

• Significant decreases in placental, kidney, liver, and brain function

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Pathophysiology• reflects alterations in the normal adaptations of pregnancy. • Normal physiologic adaptations to pregnancy include

increased blood plasma volume, vasodilatation, decreased systemic vascular resistance, elevated cardiac output, and decreased colloid osmotic pressure

• Pathologic changes in the endothelial cells of the glomeruli (glomeruloendotheliosis) are uniquely characteristic of preeclampsia, particularly in nulliparous women (85%).

• The main pathogenic factor is not an increase in blood pressure but poor perfusion as a result of vasospasm. Arteriolar vasospasm diminishes the diameter of blood vessels, which impedes blood flow to all organs and raises blood pressure

• Function in organs such as the placenta, kidneys, liver, and brain is depressed by as much as 40% to 60%

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HELLP syndrome

– Laboratory diagnostic variant (not clinical) variant of severe preeclampsia involves hepatic dysfunction, characterized by:

• Hemolysis (H)• Elevated liver enzymes (EL)• Low platelets (LP)

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HELLP syndrome

• epigastric or right upper quadrant abdominal pain (possibly related to hepatic ischemia) 65%

• nausea and vomiting 50%

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Severe preeclampsia and HELLP-syndrome

Magnesium sulfate• As prophylaxis against convulsion• I/V as a secondary infusion to the main intravenous (IV) line

by volumetric infusion pump • An initial loading dose of 4 to 6 g of MgSO4 per protocol or

physician's order is infused over 20 to 30 minutes. This dose is followed by a maintenance dose of magnesium sulfate that is diluted in an IV solution per physician's order (e.g., 40 g of magnesium sulfate in 1000 ml of lactated Ringer's solution) and administered by infusion pump at 1 to 3 g/hr.

• This dose should maintain a therapeutic serum Mg level of 4 to 8 g/dl.

• Serum magnesium levels are obtained after the patient has received magnesium sulfate for 4 to 6 hours.

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Severe preeclampsia and HELLP-syndrome Magnesium sulfate

• Intramuscular (IM) MgSO4 is seldom used because absorption rate cannot be controlled, injections are painful, and tissue necrosis may occur.

• However, the IM route may be used with some women who are being transported to a tertiary care center.

• The IM dose is 4 to 5 g given in each buttock, a total of 10 g (with 1% procaine possibly being added to the solution to reduce injection pain), and can be repeated at 4-hour intervals.

• Z-track technique should be used for the deep IM injection, followed by gentle massage at the site.

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Severe preeclampsia and HELLP-syndrome Magnesium sulfate

• Magnesium sulfate interferes with the release of acetylcholine at the synapses,

• decreasing neuromuscular irritability, • depressing cardiac conduction, • and decreasing CNS (central nervous system) irritability. • Because magnesium circulates free and unbound to protein and is

excreted in the urine, accurate recordings of maternal urine output must be obtained.

• Diuresis is an excellent prognostic sign; however, if renal function declines, all of the magnesium sulfate will not be excreted and can cause magnesium toxicity.

• Serum magnesium levels are obtained on the basis of the woman's response and if any signs of toxicity are present.

• Early symptoms of toxicity include nausea, a feeling of warmth, flushing, muscle weakness, decreased reflexes, and slurred speech.

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Severe preeclampsia and HELLP-syndrome Magnesium sulfate

• Deep tendon reflexes• Urine output• Respiration rate• Consciousness

• If magnesium toxicity is suspected, the infusion should be discontinued immediately.

• Calcium gluconate, the antidote for magnesium sulfate, may also be ordered (10 ml of a 10% solution, or 1 g) and given by slow IV push (usually by the physician) over at least 3 minutes to avoid undesirable reactions such as arrhythmias, bradycardia, and ventricular fibrillation.

• Because magnesium sulfate is also a tocolytic agent, its use may increase the duration of labor. A preeclamptic woman receiving magnesium sulfate may need augmentation with oxytocin during labor. The amount of oxytocin needed to stimulate labor may be more than that needed for a woman who is not on magnesium sulfate.

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Severe preeclampsia and HELLP-syndrome

antihypertensive agent• Starts if diastolic pressure is higher than 100 to 110 mm Hg• Order to decrease the diastolic blood pressure to 90 to 100

mm Hg • Prevent left ventricular failure and cerebral hemorrhage. • decrease the arterial pressure too much or too rapidly• agent of choice is • hydralazine IV • labetalol hydrochloride IV • methyldopa orally • Nifedipine orally

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Diabetes Mellitus Pathogenesis

• Group of metabolic diseases characterized by hyperglycemia resulting from defects in insulin secretion, insulin action, or both

• Insulin, produced by the beta cells in the islets of Langerhans in the pancreas, regulates blood glucose levels by enabling glucose to enter adipose and muscle cells, where it is used for energy.

• When insulin is insufficient or ineffective in promoting glucose uptake by the muscle and adipose cells, glucose accumulates in the bloodstream, and hyperglycemia results.

• Hyperglycemia causes hyperosmolarity of the blood, which attracts intracellular fluid into the vascular system, resulting in cellular dehydration and expanded blood volume.

• Consequently, the kidneys function to excrete large volumes of urine (polyuria) in an attempt to regulate excess vascular volume and to excrete the unusable glucose (glycosuria).

• Polyuria, along with cellular dehydration, causes excessive thirst (polydipsia).

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Diabetes Mellitus

• The body compensates for its inability to convert carbohydrate (glucose) into energy by burning proteins (muscle) and fats. However, the end products of this metabolism are ketones and fatty acids, which, in excess quantities, produce ketoacidosis and acetonuria. Weight loss occurs as a result of the breakdown of fat and muscle tissue. This tissue breakdown causes a state of starvation that compels the individual to eat excessive amounts of food (polyphagia).

• Over time, diabetes causes significant changes in both the microvascular and macrovascular circulations. These structural changes affect a variety of organ systems, particularly the heart, eyes, kidneys, and nerves. Complications resulting from diabetes include premature atherosclerosis, retinopathy, nephropathy, and neuropathy.

• Diabetes may be caused by either impaired insulin secretion, when the beta cells of the pancreas are destroyed by an autoimmune process, or by inadequate insulin action in target tissues at one or more points along the metabolic pathway. Both of these conditions are commonly present in the same person, and it is unclear which, if either, abnormality is the primary cause of the disease

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Diabetes Mellitus Classification

– Type 1 diabetes• Absolute insulin deficiency

– Type 2 diabetes• Relative insulin deficiency

– Pregestational diabetes mellitus– Gestational diabetes mellitus (GDM)

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Diabetes Mellitus

• Metabolic changes associated with pregnancy– Alterations in maternal glucose metabolism, insulin production, and metabolic

homeostasis– During normal pregnancy, adjustments in maternal metabolism allow for

adequate nutrition for both the mother and the developing fetus. Glucose, the primary fuel used by the fetus, is transported across the placenta through the process of carrier-mediated facilitated diffusion. This means that the glucose levels in the fetus are directly proportional to maternal levels. Although glucose crosses the placenta, insulin does not.

– Around the tenth week of gestation the fetus begins to secrete its own insulin at levels adequate to use the glucose obtained from the mother. Thus, as maternal glucose levels rise, fetal glucose levels are increased, resulting in increased fetal insulin secretion.

– During the first trimester of pregnancy the pregnant woman's metabolic status is significantly influenced by the rising levels of estrogen and progesterone. These hormones stimulate the beta cells in the pancreas to increase insulin production, which promotes increased peripheral use of glucose and decreased blood glucose, with fasting levels being reduced by approximately 10%

– There is a concomitant increase in tissue glycogen stores and a decrease in hepatic glucose production, which further encourage lower fasting glucose levels. As a result of these normal metabolic changes of pregnancy, women with insulin-dependent diabetes are prone to hypoglycemia during the first trimester.

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Diabetes Mellitus – During the second and third trimesters, pregnancy exerts a "diabetogenic"

effect on the maternal metabolic status. Because of the major hormonal changes, there is decreased tolerance to glucose, increased insulin resistance, decreased hepatic glycogen stores, and increased hepatic production of glucose. Rising levels of human estrogen, progesterone, chorionic somatomammotropin, prolactin, cortisol, and insulinase increase insulin resistance through their actions as insulin antagonists. Insulin resistance is a glucose-sparing mechanism that ensures an abundant supply of glucose for the fetus. Maternal insulin requirements may double or quadruple by the end of the pregnancy, usually leveling off or declining slightly after 36 weeks

– At birth, expulsion of the placenta prompts an abrupt drop in levels of circulating placental hormones, cortisol, and insulinase. Maternal tissues quickly regain their prepregnancy sensitivity to insulin. For the nonbreastfeeding mother the prepregnancy insulin-carbohydrate balance usually returns in approximately 7 to 10 days.

– Lactation uses maternal glucose; thus the breastfeeding mother's insulin requirements will remain low during lactation. On completion of weaning, the prepregnancy insulin requirement is reestablished

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Diabetes MellitusChanging insulin needs during

pregnancy

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Diabetes MellitusAntepartum care

• Routine visit • every 1-2 weeks at I and II trim• 1-2 times each week at last trim

• Hospitalization• Insulin dose changes

• Maintain constant euglycemia

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Complications requiring Hospitalization

• Complete baseline cardiovascular, renal, ophtalmologic evaluations, balance diet and insulin regiment

• Inections

• Fail to maintain acceptable glucose level

• Before labour

• To confirm fetal lung maturity: lecithin/ sphingomyelin ratio

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Cesarean birth

• Fetal distress

• Estimate fetal weight is 4000-4500 kg

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Risk factors for GDM include

• maternal age over 30 years; • obesity; • family history of type 2 diabetes; • and an obstetric history of an infant weighing more

than 4000 g, • hydramnios, • unexplained stillbirth, • miscarriage, or an infant with congenital

anomalies. • Women at high risk for GDM are often screened at

their initial prenatal visit and then rescreened later in pregnancy if the initial screen is negative

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Maternal-Fetal Risk

• of developing hypertensive disorders compared with normal pregnant women

• fetal macrosomia, which can lead to increased rates of perineal lacerations, episiotomy, and cesarean birth

• macrosomia with associated shoulder dystocia and birth trauma.

• hypoglycemia, hypocalcemia, hyperbilirubinemia, thrombocytopenia, polycythemia, and respiratory distress syndrome

• The overall incidence of congenital anomalies among in fants of women with gestational diabetes approaches that of the general population because gestational diabetes usually develops after the twentieth week of pregnancy—after the critical period of organogenesis (first trimester) has passed.