Chapter 26: Concurrent Disorders during Pregnancy Flashcards

1
Q

CHO metabolism in normal pregnancy

A
  • First Trimester:
    • inc insulin release–>hypoglycemia especially w/ a problem w/ n/v
  • Second & Third Trimester:
    • placental hormones (hPL) inc resistance to insulin and dec glucose tolerance –> dec effectiveness of insuiln
      • allows glucose to be available to the fetus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

etiology of DM

A
  • caused by partial or complete lack of insulin secretion by the beta cells of the pancreas
    • w/o insulin glucose accumulates –> energy depletion and hyperglycemia
  • body tries to dilute glucose load by any means:
    • polydopsia: inc thirst
    • fluid from intracellular space drawn into vascular bed–>dehydration at cellular level but fluid vol excess in vessels
      • kidneys attempt to excrete large vols of fluid and heavy solute load of glucose –> polyuria and glucosuria
  • b/c glucose stays in blood and can’t be metabolized, the body breaks down fat and protein to get energy –> ketosis
  • complications of hyper/hypoglycemia fluctuations which can cause vascular damage (esp in the kidneys, eyes, heart)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

effects of DM on early pregnancy

A
  • during early pregnancy, maternal metabolic rates and energy needs change little
    • but insulin release in response to glucose levels accelerates –> significant hypoglycemia may occur (esp in women experiencing nausea, vomiting)
  • in an uncomplicated pregnancy, availability of glucose and insulin favors the development and storage of fat during the 1st half pregnancy which prepares the mother for rise in energy use by the fetus during the 2nd half of pregnancy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

effects of DM on late pregnancy

A
  • when fetal growth accelerates during 2nd half of pregnancy, levels of placental hormones (hPl, estrogen, and progesterone) create resistance to insulin in maternal cells
    • allows for more glucose available for fetus –> so hormones are diabetogenic effect and leave the woman with insufficient insulin and episodes of hyperglycemia
  • the fetus continues to draw nutrients (glucose and AAs) from maternal blood –> earlier than normal switch from CHO metabolism by gluconeogensis (so form glucose form fat/protein)
    • causes high levels of fatty acids which inhibits uptake of glucose–>more glucose available for fetus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

effects of DM on birth

A
  • maintenance of normal maternal glucose levels is essential during birth to reduce neonatal hypoglycemia
    • women with DM usually maintain glucose testing and administration of insulin to day before scheduled induction or C/S
  • after admission with NPO, glucose level is checked and continuous infusion of insulin and glucose is started based on hourly glucose levels
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

effects of DM on postpartum period

A
  • need for additional insulin falls during postpartum period
    • BF is encouraged for newborn and also b/c added calorie intake by mom helps lower the amount of insulin needed in women with type 1 or 2 DM
      • in women with GDM, usually need no insulin after birth but inc risk for later development of type 2 DM
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

classification of DM

A
  • Type 1: insulin dependent, b/c pancreas makes no insulin
    • obtain HgA1C
    • prone to ketosis
  • Type 2: non insulin dependent
    • insulin is required to contorl maternal blood glucose levels
      • insulin does not cross placenta
    • oral hypoglycemics are NOT taken during pregnancy b/c potential teratogen
  • GDM: inset of glucose interolerance during pregnancy
    • may be asymptomatic
    • disappears but inc risk of DM later in life
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

influence of pregnancy on diabetes

A
  • symptoms: polyphagia, polyuria, polydipsia
  • hypoglycemia is common during 1st trimester
    • insulin needs may dec
  • hyperglycemia is common during 2nd and 3rd trimester
    • insulin needs may inc
  • illness, diarrhea, n/v complicate control
  • exercise: assists in regulation of hyperglycemia and may keep off GDM
  • if hypoglycemic rxn occurs, drink OJ then low fat milk
  • possible induction b/w 38-40 wks as long as metabolic control is maintained and fetal growth w/in stds
  • labor inc energy needs and inc needs for insulin
  • once placenta is delivered insulin needs drop–>risk for hypoglycemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

factors associated with DM

A
  • family hx
  • hx of more than 2 spontaneous abortions
  • hydramnios
  • previous baby w/ a weight over 4000 g
  • previous baby w/ unexplained congenital anomalies
  • high parity
  • obesity
  • recurrent monilial vaginitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

maternal effects r/t preexisting DM

A
  • hypoglycemia, hyperglycemia, and ketosis inc incidence of spontaneous abortion or major fetal malformations
  • pre-eclampsia
  • ketoacidosis is a threat to woman with Type 1 DM and is often precipitated by missed doses of insulin or infection
    • can lead to fetal/maternal death if untreated
  • UTIs and monilial vaginitis
  • hydramnios
  • premature ROM
  • during labor, if child has macrosomia–>difficult labor, dystocia, consequent injury to the infant
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

fetal effect r/t pre-existing maternal DM

A
  • effects on fetus depend on timing and severity of maternal hyperglycemia and degree of vascular impairment
  • risks:
    • malformations of the fetus (dec risk if woman maintains normal blood glucose): NTDs, caudal regression syndrome, cardiac defects
    • variations in fetal size: related to maternal vascular integrity
      • fetal macrosomia results when elevated levels of blood glucose stimulate excess fetal insulin production –> C/S and shoulder dystocia
    • vascular impairment leads to dec placental perfusion
      • can be caused by vasoconstriction which occurs in preeclampsia
      • dec supply of glucose and O2 –> IUGR and oligohydramnios
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

fetal surveillance done on IDM

A
  • U/S: starting at 20-22 weeks
    • can also help document fetal growth rates
  • AFP
  • NST
  • CST
  • kick counts
  • BPP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

4 major neonatal effects r/t pre-existing maternal DM

A
  • hypoglycemia: high risk b/c of accelerated fetal insulin production during pregnancy
    • constant stimulation of hyperglycemia leads to hyperplasia and hypertrophy of pancreas
  • hypocalcemia
    • during last half of pregnancy, large amounts of calcium are transported across the placenta from the mother to the fetus
      • at birth, the transfer is stopped, leading to dramatic dec in amount of calcium
    • assoc with preterm birth, perinatal asphyxia
  • hyperbilirubinemia
    • fetus experiencing recurrent hypoxia compensates by production of add’l RBCs (polycythemia)–>excess RBCs broken done–>more bilirubin
  • RDS
    • fetal hyperinsulinemia retards cortisol production which is necessary for synthesis of surfactant
  • maintain normal blood glucose in mom to reduce incidence and severity of neonatal complications
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

lab test for maternal assessment of DM

A
  • baseline renal function should be assessed w/ a 24 hour urine collection for total protein excretion and creatinine clearance and protein excretion
    • random urine sample checked at each prenatal visit for UTIs which are common in diabetes
  • thyroid function tests: inc risk of co-existing thyroid fcn dz
  • HbA1C: accurate msmt of avg glucose concentrations during the preceding 2-3 mos
    • not affected by intake or restriction of food
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

therapeutic mgmt of DM

A
  • goals: maintain normal blood glc, facilitate the birth of a healthy baby, avoid accelerated impairment of blood vessels
  • preconception: establish optimal time to undertake pregnancy, identifying if diabetes complications, determining degree of glycemic control, instruct a woman how to use glucometer, having the woman take a daily prenatal vitamin 400 mcg folic acid
  • diet: 30 kcal/kg/day
    • 40-45% carbs, 12-20% protein (60 g), up to 40% dat
    • 3 meals w/ 2 snacks: bedtime snack should include a complex carb and a protein
  • SMBG
  • insulin therapy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

GDM: risk factors

A
  • overweight or obese
  • maternal age >25 yo
  • previous birth outcome often assoc with GDM: neonatal macrosomia, maternal HTN, infant with unexplained congenital anomalies, previous fetal death
  • GDM in prior pregnancy
  • hx of abnormal glucose tolerance
  • hx of diabetes in first degree relative
  • member of African American, Hispanic/Latino, American Indian, Asian American, or Pacific Islanders
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Diagnostic Testing for DM

A
  • 1 hr glucose screen - routine test on all pregnant women between 24 & 26 weeks
    • Non-fasting
    • Glucola
      • 50 g of glucose is given, blood draw 1 hr later
    • If greater than 140mg/dl then GTT
  • Elevated hA1C will show blood glucose level for 6-8 weeks
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Glucose Tolerance Test

A
  • 3 hour glucose tolerance test: gold standard for dx of diabetes
    • fasting
    • ingest 100 grams or oral glucose solution
    • dx if FBS > or equal to 95 or
      • 2 or more of these values occur:
        • 1 hour >180
        • 2 hour >155
        • 3 hour >140
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

maternal, fetal, and neonatal effects of GDM

A
  • similar to preexisting DM
  • but GDM is not assoc with an inc risk of ketoacidosis or spontaneous abortion
  • b/c GDM develops after 1st trimester (critical period of fetal organ development) is usually not assoc with an inc in congenital malformations
  • poorly controlled GDM assoc with inc neonatal morbidity and mortality
  • fetal complications: macrosomia (leads to birth injuries or C/S), neonatla hypoglycemia, hypocalcemia, hyperbilirubinemia, and RDS
  • BF may reduce later development of Type 2 DM in the baby
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

mgmt of diet with GDM

A
  • should provide calories and nutrients for maternal and fetal health, result in euglycemia, avoid ketosis, and promote appropriate weight gain
  • eliminate simple sugars from sweets
  • 30 kcal/kg/day is recommended
    • if a woman is obese, restricted to 25 kcal/kg/day
  • smaller percent of carbs to limit hyperglycemia
    • carbs at breakfast limited to 30 g b/c of inc levels of cortisol and growth hormone at that time of day
    • protein foods to help satisfy hunger
    • evening snack to prevent ketosis at night
  • divide calories among 3 meals and at least 3 snacks
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

exercise and SMBG with GDM

A
  • exercise can improve cardiorespiratory fitness
    • graduated exercise program should be recommended
  • evaluate blood glucose: fasting blood glucose (no food for previous 4 hours) and postprandial blood glucose (2 hrs after each meal)
    • if fasting is above 95 or postprandial above 120 repeatedly, then insulin is started
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

fetal surveillance with GDM

A
  • begin to identify fetal compromise as early as 28 weeks if woman has poor glycemic control or by 34 weeks in low risk women
  • includes:
    • kick counts
    • U/S for fetal growth and amniotic fluid vol
    • BPP
    • NST
    • CST
    • amniocentesis for lung maturity
23
Q

nursing care during labor with DM

A
  • short acting (regular) insulin
  • maintain blood glucose b/w 70-90
  • hourly fingersticks
  • position left side: b/c of large fetus or hydramnios
  • check urine for ketones hourly (report 2+)
  • continuous EFM
24
Q

nursing care post delivery with DM

A
  • sliding scale insulin
  • continuous IV with 5% glucose
  • check for ketones
  • encourage BF
25
Q

chorioamnionitis

A
  • bacterial infection of the amniotic cavity
  • chorioamnionitis –> postpartum endometritis
  • inc risk of sepsis in the newborn
26
Q

assessment findings with chorioamnionitis

A
  • uterine tenderness and contractions
  • inc temperature
  • maternal and fetal tachycardia
  • foul odor to amniotic fluid
  • inc WBC count
27
Q

nursing considerations w/ chorioamnionitis

A
  • monitor:
    • maternal V/S and FHR
    • uterine contractions and activity
    • results of blood culture
  • medications: abx after cultures
  • prepare for:
    • amniocentesis for gram stain and WBC
    • delivery of the fetus
    • neonatal cultures after delivery
28
Q

cytomegalovirus (CMV)

A
  • type of herpesvirus
  • isolated from urine, saliva, blood, cervical mucus, semen, breast milk, and stool
  • transmission may occur thru contamination of any of these fluids, but close personal contact is required
  • children often can acquire CMV in a day care center
    • inc risk again at adolescence w/ activities such as kissing, sexual intercourse
  • after a primary infection, the virus becomes latent, but can become periodically reactivated and shedding of the virus can occur
    • primary infection more likely to cross placenta
  • seroconversion (change in blood test from negative to positive indicates development of Abs in response to infection) and a rise in IgM Abs can detect a primary infection that has occurred in the last 4-8 mos
29
Q

fetal and neonatal effects of CMV

A
  • 10% of newborns are symptomatic at birth
    • these infants show full cytomegalic inclusion dz
  • another 10% of the group showing CMV infection at birth will develop late onset signs like developmental delay, seizure activity, enlargement of the spleen and liver, chorioretinitis, dental defects, and hearing loss
30
Q

therapeutic mgmt of CMV

A
  • no effective therapy is available for congenital CMV
  • U/S may identify manifestations like cranial abnormalities or growth restriction
  • antiviral agents (ganciclovir or foscarnet) can be used for severe infections, but these drugs are toxic and only temporarily stop the shedding
  • primary prevention (hand washing, warning about risk of multiple sexual partners) is most effective
31
Q

Rubella

A
  • caused by a virus transmitted from person to person thru droplets or thru direct contact with articles contaminated thru nasopharyngeal secretions
  • congenital rubella could have serious consequences
  • S/S: fever, general malaise, characteristic maculopapular rash that begins on the face and migrates over the body
32
Q

fetal and neonatal effects of rubella

A
  • crosses the placenta and causes fetal infection
  • greatest risk during 1st trimester when organs forming
    • if occurs during this time, often leads to spontaneous abortions
  • common complications:
    • deafness
    • developmental delay
    • cataracts
    • cardiac defects
    • IUGR
    • microcephaly
    • infect other adults and infants after birth
33
Q

therapeutic mgmt of rubella

A
  • rubella titer of 1:8 or greater provides evidence of immunity
  • if not immune, should be vaccinated before they become pregnant
    • should not become pregnant for 28 days after receiving vaccination
    • can be given during postpartum period
    • do not give during pregnancy
34
Q

Varicella Zoster Virus

A
  • VZV causes chickenpox
  • herpesvirus transmitted by direct contact or thru the respiratory tract
  • after primary infection, it can become latent in the nerve ganglia
    • if VZV is reactivated, herpes zoster (shingles) can result
  • maternal complications:
    • preterm labor
    • encephalitis
    • varicella pneumonia
  • can be vaccinated against this
35
Q

fetal and neonatal effects of VZV

A
  • effects depend on time of maternal infection
  • if during 1st trimester, can cause congenital varicella syndrome
    • greatest risk during 13-20 weeks
    • clinical findings: limp hypoplasia, cutaneous scars, chorioretinitis, cataracts, microcephaly, IUGR
  • later in pregnancy: transplacental passage of maternal antibodies usually protects the fetus
  • infant infected during perinatal period (5 days before thru 2 days after birth) will not have benefit of maternal Abs
    • 4 days before birth is not sufficient time for mother to develop Abs to VZV and pass them to the fetus
      • if there is an infection of VZV in the perinatal period, then it can be passed to the infant and cause neonatal varicella infection
    • VZIG: indicated for infant infected perinatally
      • also for those born earlier 28 weeks or who weigh 1000 g or less b/c of maternal Abs to VZV earlier in pregnancy have not yet crossed the placenta
36
Q

therapeutic mgmt of VZV

A
  • immune testing may be done for women who are presumed susceptible
  • VZIG should be given if the woman has been exposed and who fetuses are at high risk for congenital rubella syndrome
  • if infected during pregnancy, report pulmonary symptoms immediately
    • hospitalization, fetal surveillance, full respiratory support, and hemodynamic monitoring should be done for those women with VZ pneumonia
  • acyclovir primary drug to tx varicella
  • if an infant born to a mother with varicella in perinatal period, immunize with VZIG ASAP but w/in 96 hours of birth to provide passive immunity
    • place women and infants with varicella in airborne and contact precautions
  • immunization with the live attenuated varicella vaccine is recommended for nonpregnant adults
    • do not administer to pregnant women
    • can receive in postpartum period and booster 4-8 weeks later but don’t become pregnant for 28 days after each
37
Q

Herpes Simplex Virus (HSV)

A
  • genital herpes, usually caused by HSV type 2
  • result of direct contact of the skin or mucous membrane w/ an active lesion
    • lesions form at the site of contact and begin as painful papules that progress to become vesicles, shallow ulcers, pustules, and crusts
    • virus then migrates along the sensory nerves to reside in the sensory ganglion and then the dz is latent
  • often have no S/S
  • vertical transmission from mom to infant can occur by:
    • after ROM, when virus ascends from active lesions
    • during birth, when fetus comes in contact with genital secretions
  • definitive dx from culture of virus from active lesions
38
Q

fetal and neonatal effects of HSV

A
  • if primary infection occurs during pregnancy, rates of spontaneous abortions, IUGR, and preterm labor inc
  • neonatal herpes infection is uncommon but potentially devastating
    • can be limited to skin lesions or systemic (disseminated)
    • S/S appear w/in 1st week and dz progresses rapidly
    • risk is greater if mother has a primary infection during perinatal period
  • transmission to infant:
    • after ROM
    • during birth
    • placement of FSE
39
Q

therapeutic mgmt of HSV

A
  • acyclovir: prescribed to reduce S/S and shorten duration of lesions
    • may be given tduring pregnancy to reduce possibility of active lesions at birth
  • no vaginal delivery w/ active lesions
    • bright light exam
    • C/S necessary if active lesions are present
  • should allow woman time to dicuss their feelings
  • mother may breast feed if no lesions on the breast
  • assess infant for signs of infection:
    • temp instability
    • lethargy
    • poor sucking reflex
    • jaundice
    • seizure
    • herpetic lesions
40
Q

hepatitis B

A
  • transmitted via blood, saliva, vaginal secretions, semen, or breast milk
    • readily crosses placenta
  • inc risk of cirrhosis, hepatocelluular carcinoma, or liver dz
  • preventable w/ a vaccine that can be given during pregnancy
  • newborn vaccine starts before discharge
    • 2nd dose: 1-2 most later
    • 3rd dose: 6-18 mos after first dose
41
Q

fetal and neonatal effects of Hep B

A
  • when mom has hep B infection during pregnancy, risk of:
    • prematurity
    • low birth weight
    • neonatal death
  • infection of newborn whose mother is known to be positive for Hep B can be prevented with administration of Hep B immune globulin (HBIG) followed by Hep B vaccine w/in 12 hrs of birth
    • newborn must be carefully bathed before any contaminations by the virus
    • BF is safe as long as newborn has been vaccinated
42
Q

therapeutic mgmt of hep B

A
  • preventable infection
  • simple hygiene measures such as safe sex and use of std precautions w/ bodily fluids
  • vaccines available in a series of 3 IM injections into the deltoid for adults
    • second dose given 1 mos after first
    • third dose given 6 mos after first
  • recommended for anyone who comes into contact w/ bodily fluids
  • all pregnant women should be screened for Hep B Ags
    • rescreen in the 3rd trimester if high risk
43
Q

human immunodeficiency virus (HIV)

A
  • time from infection with HIV to development of AIDS is approx 11 yrs w/ antiretrovirals
  • transmission of infection thru 3 modes:
    • heterosexual exposure to genital secretions of an infected person
    • parenteral exposure to infected blood or tissue
    • perinatal exposure of the infant thru infected maternal secretions thru birth (vertical transmission)
      • breast milk or prechewed food from infected person can cause infant infection
44
Q

fetal and neonatal effects of HIV

A
  • antiretroviral therapy during pregnancy should include 3 drugs, including the primary drug Zidovudine (ZDV)
  • infant infection may occur during pregnancy, labor and birth, or BF
  • infant HIV tests can remain positive for up to 18 mos after birth b/c of passive maternal Abs
    • an infected newborn is asymptomatic at birth, but S/S may be come obvious during the first year of life
      • early S/S: enlargement of liver and spleen, lymphadenopathy, failure to thrive, persistent thrush, and extensive seborrheic dermatitis (cradle cap)
        • also often have bacterial infections of meningitis, pneumonia, osteomyelitis, septic arthritis, and septicemia
45
Q

prevention of HIV

A
  • prevention remains the only way to control HIV
  • sexual transmission can be avoided by several methods
    • abstinence keeps a person safe from all STDs, including HIV
    • transmission of HIV can be prevented if infected persons do not have vaginal intercourse w/ susceptible persons
      • if intercourse does occur, barrier methods reduce contact
    • IV drug users who refuse rehabilitative tx must be taught to wash equipment with water and soap
46
Q

therapeutic mgmt of HIV

A
  • multiple antiretrovirals from different classes are beneficial
    • ZDV is most effective to reduce vertical transmission from mother to infant
  • if giving ZDV, must consider:
    • if mother has had any antiretrovirals during pregnancy, including ZDV, and when it began
    • if mother had any prenatal care
    • fetal gestational age
    • if membranes have ruptured and how long they have been ruptured
47
Q

nursing considerations for HIV

A
  • issues during PP therapy:
    • whether to continue or stop antiretroviral therpay
    • support services needed after discharge
    • contraceptive counseling, including info that condoms can reduce the risk of acquiring/transmitting STDs
    • comprehensive f/u for infection indicators
  • determine what the family perceives as the most pressing needs and worries incluind loss of control, loss of support, social isolation
  • help woman attain highest possible level of wellness including adequate, high quality nutrition
  • teach about testing
48
Q

toxoplasmosis

A
  • protozoan infection
  • transmitted thru organisms in raw and undercooked meat, thru contact w/ infected cat feces or soil, and across the placental barrier to the fetus if the expectant mother acquires the infection during pregnancy
  • poor handwashing and sanitation of surfaces after food prep inc risk
  • often subclinical
    • S/S: days of fatigue, muscle pains, and swollen galnds, but she may be unaware of dz
49
Q

fetal and neonatal effects of toxoplasmosis

A
  • may cause abortion or result in birth of an infant w/ the dz
  • many infants are asymptomatic at birth, but many have serious effects like:
    • LBW
    • enlarged spleen and liver
    • jaundice
    • anemia or coagulation disorders
  • severe complications for fetus includes:
    • chorioretinitis that leads to blindness, deafness, seizures, hydrocephalus, and microcephaly
50
Q

therapeutic mgmt of toxoplasmosis

A
  • all pregnant women should be advised to:
    • cook meat thoroughly until juices run clear
    • avoid touching mucous membranes of mouth/eyes while handling raw meat
    • wash all surfaces that came into contact w/ raw meat
    • avoid uncooked eggs and unpasteurized milk
    • wash fruits and veggies
    • avoid contact w/ cat feces
  • sulfonamides can be used to tx women infected during pregnancy
51
Q

GBS

A
  • colonizes rectum, vagina, cervix, and urethra of pregnant or nonpregnant woman
    • often asymptomatic, although symptomatic infections, like UTIs, chorioamnionitis, or metritis, can occur
  • risk for infection w/ prolonged ROM or multiple vaginal exams
52
Q

fetal and neonatal effects of GBS

A
  • early onset newborn GBS occurs during 1st week after birth, and often w/in 48 hrs
    • sepsis, pneumonia, and meningitis are primary infections with early onset GBS
  • late onset GBS occurs after the first week of life
    • meningitis is most common clinical manifestation
    • permanent neuro consequences more common in those with meningeal infections
53
Q

therapeutic mgmt of GBS

A
  • optimally identified by rectal and vaginal cultures at 35-37 weeks gestation
  • if had a previous infant w/ GBS or GBS in their urine in any trimester will be considered as GBS+ during delivery
  • higher risk for GBS if:
    • delivers at or before 37 weeks
    • has ROM for more than 18 hrs
    • has a temp over 100.4 deg F
  • penicillin (or cephazolin) during labor
  • C/S before ROM does not require abx therapy
54
Q

listeria

A
  • no lunch meat, sushi, or soft cheese