N330 Ob Ch. 19-22 Lowdermilk Exam 4

Front 1

Eclampsia

Back 1

The occurrence of seizure activity/coma/convulsions unrelated to other cerebral conditions with evidence of preeclampsia. Occurs in 2-4% of preeclamptics.

Its occurrence is usually unpredictable, but is usually associated with significant proteinuria. Headache, visual symptoms, and severe RUQ/epigastric pain, hyperreflexia, and hemoconcentrations, are the most common premonitory symptoms.
Convulsions are usually short, lasting 60-75 seconds.

Treatment consists of the usual ABCs and MgSO4.

Front 2

Ch. 19

When is abdominal ultrasound more useful?

Back 2

After 1st trimester

Front 3

Gestational Hypertension

Back 3

BP > = 140/90 after 20 weeks gestation (elevation must be present on 2 measurements taken at least 6 hours apart to avoid spurious results)
OR systolic increase of 30 mmHg or a diastolic increase of 15 mmHg from prepregnancy baseline

No proteinuria or edema.

-Must have no evidence of preexisting hypertension and return to normal levels within 6 weeks after giving birth
-Women who are diagnosed with gestational hypertension before 35 weeks are more likely to result in preeclampsia than woman whose onset of hypertension is closer to term

Front 4

Ch. 19

Should a woman have a full bladder when using abdominal ultrasound to visualize the fetus?

Back 4

Yes, b/c a full-bladder displaces the uterus upward to provide a better image of the fetus.

Front 5

Preeclampsia

Back 5

The diagnosis based on hypertension as well as the presence of proteinuria.

BPs = 140/90 after 20 weeks gestation (2 measurements at least 6 hours apart)

Proteinuria = 300 mg of spilled protein in a 24 hour urine collection or 0.1g/L on a spot specimen (urine dipstick)

Front 6

Ch. 19

Which type of ultrasound is useful for an obese woman?

Back 6

Transvaginal. When thick abdominal layers can't be penetrated w/ an abdominal ultrasound.

Front 7

Chronic hypertension

Back 7

Hypertension present before pregnancy or before 20 weeks gestation. Hypertension persisting for more than 6 weeks postpartum is also classified as chronic HTN.

Gravidas with this are at risk for developing superimposed preeclampsia and that diagnosis is made by a change in hypertension accompanied by proteinuria.

Front 8

Ch. 19

What does a high AFP result potentially indicate?
What about a low AFP?

Back 8

Hi: NTD
Low: Trisomy 21

Front 9

Gestational hypertension

Back 9

Development of HTN during pregnancy or immediately postpartum without other signs of preeclampsia or preexisting HTN.

Front 10

CH. 19

When can you obtain an amniocentesis?

Back 10

Possible after week 14, when uterus becomes an abdominal organ, & sufficient amniotic fluid is available for testing.

Front 11

HELLP Syndrome

Back 11

Stands for hemolysis, elevated liver enzymes, and low platelets. It is a unique variant of preeclampsia (2-12%) and is considered to be evidence of severe preeclampsia. It can involve DIC, periportal liver necrosis and hemorrhage, and microangiopathic hemolytic anemia. Rarely, complications of HELLP can include hypoglycemia, coma, nephrogenic diabetes insipidus, subcapsular liver hematoma.

Unlike "normal" preeclampsia, HELLP can present with little or no HNT or proteinuria. More than half present with epigastric/RUQ pain or nausea/vomiting.

H- Hemolysis resulting in anemia & jaundice
EL - elevated liver enzymes resulting in elevated (ALT) or AST, epigastric pain, and n/v
LP - low platelets (<100,000/mm3), resulting in thrombocytopenia, abnorm bleeding & clotting time, bleeding gums, petechiae, and possibily DIC.

Front 12

Ch. 19

When would you want to perform an amniocentesis?

Back 12

Indicated for prenatal dx of genetic disorder or congenital anomalies (NTDs particularly), assessment of pulmonary maturity, & dx of fetal hemolytic dx

Front 13

Criteria for severe preeclampsia

Back 13

BP > = 160/100
Proteinuria = 5 grams/24 hour urine collection or dip of +3 to +4
Oliguria
serum creatinine > 1.2 mg/dl
Cerebral or visual disturbances
Hyperreflexia w/ possible ankle clonus, pulm, or cardiac involvement
Extensive peripheral edema
Hepatic dysf
Epigastric and RUQ pain
Thrombocytopenia
Eclampsia

Hint 13

consists of BP 160/100 or greater, proteinuria 3+ to 4+, oliguria, elevated serum creatine >1.2 mg/dl, cerebral or visual disturbances (H/A, blurred vision), hyperreflexia w/ possible ankle clonus, pulmonary or cardiac involvement, extensive peripheral edeam, hepatic dysfunction, epigastric and upper quadrant pain, and thrombocytopenia.

Front 14

Ch. 19

What important nursing intervention should be performed after an amniocentesis?

Back 14

Fetomaternal hemorrhage risk standard practice, after an amniocentesis, to administer RhoD immunoglobulin to the woman who is Rh(-)

Front 15

Ch. 19

What is one of the biggest problems in the US today that place pregnancies at risk?

Back 15

Access to prenatal care

Front 16

Ch. 21

Mild preeclampsia

Back 16

Gestation HTN w/ the addition of proteinuria of 1-2 + and wt. gain of more than 2 kg (4.4 lb) per wk in the 2nd and 3rd trimesters, mild edema will begin to appear in the upper extremities or face

Front 17

Ch. 21

How can you tell/differentiate between mild and severe preeclampsia?

(how can you tell it's getting worse)

Back 17

Mild: 140/90, protein > 1 + on dipstick, output matches intake (25-30ml/hr)

Severe: 160/110, protein > 3+ on dipstick, urine output 400-500 ml/24 hours.

Indications of worsening liver involvement renal failure, worsening HTN, cerebral involvement, and developing coagulopathies

Front 18

Ch. 21

What is the main underlying factor of preeclampsia?

Back 18

Main factor is not ↑ in BP but rather poor perfusion as a result of VASOSPASM with reduced plasma volume

Front 19

Ch. 21
Hyperemesis Gravidarum

Back 19

excessive vomiting lasting past 12 weeks causing weight loss, electrolyte imbalance, nutritional deficiencies, and ketonuria (0.5% of all live births)

Front 20

Ch. 21
Who are more likely to get Hyperemesis Gravidarum?

Back 20

More likely when are you carrying a female baby

Associated with: nulliparous, increased body weight, history of migraines, fetus with chromosomal abnormalities, multiple gestations, gestational trophoblastic disease, family history,transient hyperthyroidism, interrelated psychologic component must be assessed, high stress levels, younger than 20, vitamin B deficiencies

Front 21

Ch. 21
How long does Hyperemesis Gravidarum last?

Back 21

Usually begins in the first trimester and lasts until the end of pregnancy

Front 22

Ch. 21
How is Hyperemesis Gravidarum managed?

Back 22

o Assessment
 Frequency of vomiting, severity, during of episodes, precipitating factors, all medications, weight loss during pregnancy
 Lab test: ketonuria, thyroid levels
 Psychosocial assessment: anxiety, fears, concerns related to her health

o Initial Care
 IV therapy LR’s to correct fluid and electrolyte imbalances
 NPO for 24-48 hours
 Caution with antiemetics
 Vitamin B6
 Advance to clear diet after 24 hours of no vomiting
 Medications for nausea and vomiting
 Monitor for signs of complications: metabolic acidosis secondary to starvation, jaundice, or hemorrhage.
 Monitor I & O including the amount of emesis
 Oral hygiene
 Relaxing environment, free from odors
 Once vomiting stops
• Small meals at frequent intervals
• Limited oral fluids and bland foods ( crackers, toast, chicken)
• Diet is progressed as tolerated
• Promote adequate rest

o Diet for Hyperemesis
 Eat frequently at least 2-3 hours, separate liquids from solids and alternate every 2-3 hours
 Eat a snack at bedtime
 Dry, bland, high protein foods, cold foods
 Eat what sounds goods to you
 Follow the salty-sweet approach, junk foods are okay
 Eat protein after sweets
 Dairy might stay down better than other foods
 If you vomit even when your stomach is empty, try sucking on a popsicle
 Try ginger tea
 Warm ginger ale
 Drink liquids from a cup with a lid

o Follow Up Care
 Tell women about the diet for hyperemesis
 Advise to have another person cook for her
 Contact doctor is vomiting recurs
 Calm, compassionate, and sympathetic care

Front 23

Ch. 21

What is the criteria for Chronic Hypertension with superimposed preeclampsia?

Back 23

 HTN before 20 weeks and new-onset proteinuria ( >0.5 g protein in 24 hours)
 Women with both hypertension and proteinuria before 20 weeks of gestation, , sudden increase in hypertension, plus one of the following:
o New onset of symptoms
o Thrombocytopenia
o Elevated liver enzymes

Front 24

Ch. 21

PROM vs PPROM?

What is the most common maternal complication of PROM?

Back 24

•Premature rupture of membranes (PROM) is the spontaneous rupture of the amniotic sac and leakage of amniotic fluid before the onset of labor at any gestational age.

Preterm premature rupture of membranes (PPROM) is a rupture before 37 weeks of gestation.

The most common maternal complication of preterm PROM is infection of the amniotic cavity, called chorioamnionitis.

Front 25

Ch. 21

Explain the pathophysiology behind preeclampsia

Back 25

 Can progress from mild to severe
 Caused by disruptions in placental perfusion and endothelial cell dysfunction
 The arteries in the uterus do not widen and thin out so this decreases placental perfusion and hypoxia results
 Placental ischemia is thought to cause endothelial cell dysfunction by stimulating the release of a substance that is toxic to endothelial cells, this causes vasospasm which results in poor tissue perfusion in all organ systems, increased peripheral resistance and BP and increased endothelial cell permeability, leading to intravascular protein and fluid loss and ultimately to less plasma volume.
 Main factor is not ↑ in BP but rather vasospasm with reduced plasma volume
 Decreased kidney perfusion can lead to oliguria

Front 26

Ch. 21

What are the 3 classic symptoms of ectopic pregnancies?

Back 26

1. Abdominal pain: dull, lower quadrant pain to a colicky pain when the tube stretches to a sharp stabbing pain

2. Delayed menses

3. Abnormal abdominal bleeding (spotting) that occurs 6-8 weeks after the last normal menstrual period

Front 27

Ch. 21
What are the consequences of ruptured ectopic pregnancies?

Back 27

fatal hemorrhage

Front 28

Ch. 21
What is a Hydatidiform Mole (Molar Pregnancy)?

Back 28

a benign proliferative growth of the placental trophoblast in which chorionic villi develop into edematous, cystic, avascular transparent vesicles that hang in a grapelike cluster

Front 29

Ch. 21
How is Hydatidiform Mole (Molar Pregnancy) diagnosed?

Back 29

o Transvaginal ultrasound and serum hCG levels are used for diagnosis
o Transvaginal is the most accurate
o Characteristic pattern of multiple diffuse intrauterine masses, often called snowstorm pattern is seen with or without a fetus
o The trophoblastic tissue secretes the hCG
o hCG levels are persistently high or rising beyond 10-12 weeks of gestation, which is the time when levels should start to decline in a normal pregnancy.

Front 30

Ch. 21
What is the tx for Hydatidiform Mole (Molar Pregnancy) ?

Back 30

o Most abort spontaneously, but suction offers safe, rapid method to remove the mole
o Do not induce labor with oxytocin or prostaglandins due to increased risk of embolization of trophoblastic
o Administer RhD immunoglobin to women who are Rh negative to prevent isoimmunization
o Nurses must provide support to the women
o Explain the importance of avoiding pregnancy: to avoid confusion with signs of pregnancy, pregnancy should be avoided for 6 months-1 years. Don’t use IUD for contraception, use oral birth control
• Follow up Care
o Frequent physical and pelvic examinations along with bi-weekly measurements of hCG levels until they decrease to normal and remain normal for 3 weeks
o Monthly measurements for 6 months and then every 2 months for a total of 1 year

**A rising titer and an enlarging uterus may indicate choriocarcinoma ( malignant GTD). Women with complete molar pregnancy are at a 15-28% risk of requiring further management with chemotherapy for persistent trophoblastic disease

Front 31

Ch. 21
What are the risk factors of Hydatidiform Mole (Molar Pregnancy) ?

Back 31

o  Women who have had ovulation stimulation with clomiphene (Clomid)
 Age: Early teens or over 40
 History of miscarriage
 Nutritional factors: deficient intake or carotene and animal fats

Front 32

Ch. 21
If mom presented to L & D with bleeding. How do you tell the difference between placenta abruption and placenta previa?

Back 32

PP: o Painless, bright red vaginal bleeding during the second or third trimester
o (most cases are diagnosed by ultrasound before bleeding occurs)
o Bleeding is associated with the disruption of blood vessels that occur with stretching an thinning of the lower uterine segment, usually small amount and stops when clots form
o Vital signs may be normal, b/c woman blood volume increases by 40% so she can lose a lot of blood before shock
 Clinical presentation and urine output may be better predictors of acute blood loss than vital signs
o The FHR is fine unless a major detachment of the placenta occurs
o Abdominal examination:
 Soft, relaxed, non tender uterus, normal tone
 Presenting part is high b/c the placenta occupies the lower uterine segment
 Fundal height is greater than expected for gestational age
 Fetal malpresentation is common ( breech or transverse or oblique lie)

PA: o Vaginal bleeding, localized abdominal pain, uterine tenderness, contractions
o Bleeding may result in maternal hypovolemia, and coagulopathy.
o Mild to severe uterine hypertonicity is present
o Pain is mild to severe and localized over one region of the uterus or diffuse over the uterus with a board like abdomen
o Couvelaire Uterus: blood accumulates in between the separated placenta and the uterine wall, uterus appears purple or blue rather than the usual bubble gum pink and contractility is lost
o Laboratory findings: positive Apt test (blood in the amniotic fluid), clotting defects ( 40% have DIC)

Front 33

Ch. 21
What is Placenta Previa?

Back 33

the placenta is implanted in the lower uterine segment such that it completely or partially covers the cervix or is close enough to the cervix to cause bleeding when the cervix dilates or the lower uterine segment effaces

Front 34

Ch. 21
What is Placenta Abruption?

Back 34

detachment of part or all of a normally implanted placenta from the uterus

• Normally separation occurs in the deciduas basalis after 20 weeks of gestation and before birth of the infant

Front 35

Ch. 21
What is the biggest risk factor for placenta abruption?

Back 35

Maternal hypertension

Others risk factors:
 Cocaine use
 Blunt trauma (abuse, car accident)
 Smoking
 PROM
 Twins
 Previous abruptions ↑ risk of 25%

Front 36

Ch. 21
What is happening in Disseminated Intravascular Coagulation (DIC)?

Back 36

• Pathologic form of clotting that is diffuse and consumes large amount of clotting factor, causing widespread external bleeding, internal bleeding, or both, and clotting.


• DIC is an overactivation of the clotting cascade and the fibrinolyic system, resulting in depletion of platelets and clotting factor, which results in formation of multiple fibrin clots
o Blood cells are destroyed as they pass though these fibrin choked vessels

Front 37

Ch. 21

How is DIC identified?

Back 37

• Clinical Signs
o Clotting
o Bleeding: spontaneous bleeding from gums/nose, oozing blood from a puncture site, petechiae from where a BP cuff was placed, signs of bruising, hematuria, GI bleeding
o Ischemia
o Lab Results: decreased platelets, decreased fibrinogen, prolonged PT & PTT, decreased factor V and factor VIII, increased fibrin degradation products, D-Dimer test increased, red blood smear shows fragmented RBC’s.

• Most often triggered by large amounts of tissue thromboplastin like in placental abruption and in retained dead fetus and anaphylactoid syndrome of pregnancy

Front 38

Ch. 21

How is DIC managed?

Back 38

o Treat the underlying cause ( remove the dead fetus, treat the infection or preeclampsia or eclampsia, removal of the placental abruption)
o Volume replacement, blood component therapy, optimization of oxygenation and perfusion status¸ monitor labs
o Vitamin K and factor VIIa may be considered adjuvant therapies
o Nursing interventions
 Assess for signs of bleeding
 Assess for blood transfusion complications
 Give fluid and blood products
 Cardiac and hemodynamic monitoring
 Prevent injury
 Renal failure is consequence of DIC so monitor urine output with a foley
• Urine must be 30ml/hour
 If DIC occurs before birth: side lying position to maximize blood flow to baby
 Oxygen via nonrebreather mask at 8-10L/ min
 Monitor fetus
 DIC is “cured” with birth and as coagulation abnormalities resolve

Front 39

CH. 21
When is vasa previa usually identified?

Back 39

Not aware of it until the rupture of membranes when heavy bleeding occurs. It is sometimes found on routine anatomic ultrasounds ultrasound.

Front 40

Ch. 21

Women w/ gestational diabetes are at a higher risk for UTI b/c they....

Back 40

Spill more glucose into the urine. Ketoacidosis can result from the diabetoenic effect of pregnancy as insulin resistance increases, commonly resulting from untreated hyperglycemia or inappropriate insulin dosing. There is no fluid restriction for gestational diabetes. Ketones are tested to assess the severity of acidosis

Front 41

Ch. 21
Nursing considerations when administering MgSO4?

Back 41

RR < = 12 breaths/min indicates dangerous CNS depression by MgSO4; soln should be 40 g in 1000 mL of Ringer's lactate, assessment should occur q 15-30 mins & maintenance dosage should be 1-3 g/hr

Inform client of initally feeling flushed, hot, and sedated w/ the bolus

Monitor client's BP, pulse, RR, DTRs, LOC, urinary output (indwelling Foley for accuracy), presence of H/A, visual disturbances, epigastric pain, uterine contractions, & FHR & activity.

Place client on fluid restriction of 100-125 ml/hr & maintaining urinary output @ 30 mL/hr or greater

Front 42

Ch. 21

S/s of MgSO4 toxicity?

Back 42

Absence of pateller DTR
Urine output < 30 ml/hr
RR < 12/min
Decreased LOC

Front 43

Ch. 21

What is the indication for methotrexate? How does it work?

Back 43

ectopic pregnacy; it destroys rapidly growing tissue, in this case the fetus and placenta.