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medical complication Flashcards

1
Q

mild and severe chronic HTN in pregnancy

A
  1. Mild hypertension – systolic of > 140-180 mmHg or diastolic > 90-100 mmHg or both
  2. Severe hypertension - systolic of > 180 mmHg or diastolic > 100 mmHg
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2
Q

Preeclampsia

A

i. Preeclampsia - new onset of hypertension and either proteinuria or end-organ dysfunction after 20 weeks of gestation in a previously normotensive woman

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3
Q

Gestational HTN/Pregnancy Induced HTN

A

HTN that develops after 20 weeks of gestation in the absence of proteinuria and returns to normal postpartum

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4
Q

Gestational HTN/Pregnancy Induced HTN is most commonly seen in these types of pregnancy

A

Develops in 5-10% of pregnancies that go beyond first trimester

30% incidence in multiple gestations

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5
Q

burden of dz with preeclampsia

A

Women with preeclampsia are at an increased risk for life-threatening events:

placental abruption, ARF, cerebral hemorrhage, hepatic failure or rupture, pulmonary edema, DIC, and progression to eclampsia.

1 of 4 leading causes of death of maternal women

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6
Q

preeclampsia -severe features (7)

A
  1. Blood pressure of > 160mm Hg systolic or > 110 mmHg diastolic
  2. Progressive renal insufficiency (serum creatinine >1.1 mg/dL or doubling of serum creatinine concentration in the absence of other renal disease)
  3. Cerebral or visual disturbances (headache and scotomata)
  4. Pulmonary edema or cyanosis
  5. Epigastric or RUQ pain
  6. Evidence of hepatic dysfunction (transaminases doubled)
  7. Thrombocytopenia (<100,000)
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7
Q

RF for preeclampsia (12)

A
  1. Nulliparity – women who have never been pregnant
  2. Age <20 y.o., >35 y.o.
  3. New paternity/partner related factors
  4. Family history of preeclampsia
  5. Chronic renal disease, chronic HTN
  6. Prolonged interpregnancy interval
    a. Long periods of time between pregnancies
  7. Antiphospholipid syndrome
  8. Diabetes mellitus
  9. Multi-fetal gestation
  10. High BMI
  11. Black race
  12. Connective tissue disorders (RA, SLE)
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8
Q

what decreases risk of preeclampsia

A

Smoking DECREASES risk, ASA for high risk

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9
Q

spiral arteries, how do they lead to preeclampsia

A

– coiled arteries which temporarily supply blood to the endometrium during the luteal phase of the menstrual cycle. They are converted and loose their smooth muscle, dilate 5-10 times in order to ensure adequate placental blood flow.

If this doesn’t happen, then there will be complications like preeclampsia

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10
Q

pathophysiology

A

spiral arteries

changes in immune factors

systemic inflammatory

antibodies leading to vessel constriction

increased risk of dementia later in life

under profusion–> hypoxia and ischemia

placental tissue causes the disease and is always cured after the delivery of the placenta

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11
Q

Immunologic factors that lead to preeclampsia

A

 nulliparous women/women who change partners b/w pregnancies, have long interpregnancy intervals, use barrier contraception, and conceive via intracytoplasmic sperm injection have less exposure to paternal antigens and higher risks of developing preeclampsia

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12
Q

immunological abnormalities that lead to preeclampsia

A

similar to those observed in organ rejection graft versus host disease, have been observed in preeclamptic women

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13
Q

genetic factors that lead to preeclampsia

A

Although most cases of preeclampsia are sporadic, genetic factors are thought to play a role in disease susceptibility

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14
Q

Systemic endothelial dysfunction that lead to preeclampsia

A

imbalance between vasodilating and vasoconstricting factors that act on the endothelium

Headache, seizures, visual symptoms, epigastric pain, and IUGR are the sequelae of endothelial dysfunction in the vasculature of target organs, such as the brain, liver, kidney, and placenta.

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15
Q

lab changes you can see in preeclampsia

A

Decreased production of endothelial-derived vasodilators (nitric oxide and prostacyclin), and increased production of vasoconstrictors (endothelins and thromboxanes).

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16
Q

signs and sxs you want to ask about in preeclampsia

A
  1. Signs/symptoms include: visual disturbances, severe/persistent HA, RUQ pain, Hx of LOC/seizures, dizziness
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17
Q

how can weight change in a pt with preeclampsia

A

water weight and edema

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18
Q

STR and edema in preeclampsia

A

unresponsive to rest in supine position especially in upper extremities, sacral region and face

DTRs - hyperreflexia or clonus at ankle worrisome

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19
Q

what lab evaluation would you want to get in a pt with preeclampsia

A

i. CBC – rising HCT signals worsening vasoconstriction and intravascular volume or hemolysis
ii. Platelet count
iii. Coagulation profile (PT, PTT) – coagulopathy
iv. LFTs – hepatocellular dysfunction
v. Serum creatinine – decreasing renal function
vi. Uric acid –>happens d/t altered renal fxn
vii. 24 hour urine
viii. Creatinine clearance
ix. Total urinary protein

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20
Q

why would you get a platelet count in a pt with preeclampsia

A

thrombocytopenia

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21
Q

why would you get uric acid levels

A

promotes inflammation and you can see this before the onset of preeclampsia

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22
Q

trend of hmg in pregnant pt without preeclampsia

A
  1. Usually the hemoglobin goes down as the blood volume starts expanding

rising hct can indicate worsening vaso constriction

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23
Q

The NST evaluates f

A

fetal heart rate and response to fetal movement.

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24
Q

The five discrete biophysical variables you are looking at in a NST

A
  1. Fetal movement
  2. Fetal tone
  3. Fetal breathing
  4. Amniotic fluid volume
  5. Fetal Heart Rate
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25
Q

components of a biophysical profile (BPP)

A

4 ultrasound (US) assessments and a nonstress test (NST).

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26
Q

fetal studies for for fetal weight and growth, and amniotic fluid volume

A

ULS

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27
Q

indirect assessment of placental status

A

ii. NST (non stress test) and/or biophysical profile

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28
Q

reassuring BPP result

A

8 or 10

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29
Q

when would you do labor induction in response to . a BPP

A

if 4
Labor induction if gestational age >32 weeks

Repeating test same day if <32 weeks, then delivery if BPP <6

definitely 2

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30
Q

if BPP 6

A

Labor induction if >36 weeks if favorable cervix and normal AFI

Repeating test in 24 hours if <36 weeks and cervix unfavorable; then delivery if BPP <6, and follow-up if >6

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31
Q

A BPP normally is not performed before

A

A BPP normally is not performed before the second half of a pregnancy, since fetal breathing movements do not occur in the first half.

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32
Q

mainstay of mngmt of preeclampsia

A

Care is individualized

Mainstay of management is rest and frequent monitoring of mother and fetus

Daily kick counts

Hospitalization initially recommended for new onset preeclampsia

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33
Q

how often would you do a non stress test in mother with preeclampsia

how frequently ULS

A

2x weekly nonstress tests, biophysical profiles or both

U/S q 3 weeks for fetal growth and amniotic fluid assessment

34
Q

Management – Severe Preeclampsia

A
  1. Best managed in a tertiary - care setting
  2. Daily lab tests and fetal surveillance
  3. Antihypertensive therapy if indicated
35
Q

goal of preeclampsia drug therapy

A

Goal of therapy is to reduce diastolic pressure to 90 - 100 mmHg range

36
Q

prevention of seizures

A

Stabilization with magnesium sulfate (IM/IV)

don’t use for more than 5 days

98% of cases, seizures will be prevented

Therapeutic levels are 4 - 6 mg/dL, toxic concentrations have predictable consequences

37
Q

what do you want to worry about as far as urine output goes with maintenance while on mag sulfate

A
  1. Maintenance of urine output of at least 25 mL/hour will avoid accumulation in kidneys
38
Q

reversal of mag sulfate

A

reversal of effects done with slow IV of 10% calcium gluconate, along with O2 supplementation

39
Q

eclampsia is most commonly seen when

A

Most cases occur within 24 hours of delivery but approximately 3% of cases diagnosed between 2 and 10 days postpartum

40
Q

management in mother with eclampsia to prevent musculoskeletal injury

A

Insert padded tongue blade

Restrain gently as needed

Maintain adequate airway

Gain IV access

41
Q

Presentation of HELLP

A

RUQ

nausea, vomiting, generalized malaise, they don’t “feel well”, epigastric pain

42
Q

RX given in eclampsia

A

Tx directed to initiation of magnesium sulfate to prevent further seizures

If pt already receiving magnesium sulfate, additional 2g can be given (slowly) and blood level obtained

43
Q

other management strategies for Eclampsia

A

a. Transient uterine hyperactivity for approx. 15 min associated with fetal heart changes (i.e.bradycardia, decreased variability and late decelerations)
i. Usually self limited, not dangerous unless > 20 minutes
ii. Delivery during this time unnecessary and should be avoided
b. Foley catheter should be placed to monitor urinary output
c. Central venous catheter or continuous EKG may be appropriate if BP to high, urinary output low, or evidence of cardiac disturbance

44
Q

when does HELLP present

A

Generally presents in the third trimester of pregnancy, although it occurs at less than 27 weeks in 11% of patients
viii.

Presents antepartum in 69% of patients and postpartum in 31% of patients - Postpartum onset is typically within the first 48 hours after delivery, but signs and symptoms may not become apparent until as long as seven days after delivery

45
Q

why would you see RUQ in HELLP

A

rupture of liver capsule

46
Q

presentation with HELLP, who gets this

A

Pts usually multiparous and blood pressure readings lower than those of preeclamptic pts

Initial symptoms may be vague

Nausea and vomiting, viral - like syndrome

90 % of patients present with generalized malaise

65 % with epigastric pain, 30 % with nausea and vomiting, and 31 % with headache.

47
Q

women with HELLP die from

A
  1. Usually these women die from stroke or liver rupture
48
Q

Labs in assessment of HELLP

A

LABS - CBC, CMP, coag studies, fibrin degredation products

49
Q

tx of HELLP

A

Tx consists of cardiovascular stabilization, correction of coagulation abnormalities and delivery – DIC occurs in 20% of HELLP pts.

Platelet perfusion before/after delivery indicated if platelet <20,000/mm3

50
Q

management of DIC

A

Patients with DIC should be given fresh frozen plasma and packed RBCs

Lab abnormalities typically worsen after delivery, resolve 3-4 days PP

Treatment – Prompt delivery of the baby!

Magnesium sulfate - decrease risk of seizures
xxiv. Blood transfusions - anemia

DIC - Fresh frozen plasma

Antihypertensives (labetalol, hydralazine, nefedipine)

51
Q

PROM

A

PROM is the rupture of chorioamniotic membranes before the onset of labor

52
Q

amniotic fluid pH

A

Amniotic fluid protects against infection, fetal trauma and umbilical cord compression, pH 7.5

53
Q

amt of amniotic fluid seen at 20 wks and 28 wks

A

400mL by 20wks,

plateau of 800mL at 28wks

54
Q

Polyhydramnios

what is it and when do we see this

A
  • AFI >20cm – assoc. with Down’s/Edwards, GDM
55
Q

Oligohydramnios

what is it and when do we see this

A

AFI (Amniotic fluid index) <5cm – urinary tract abnormalities (bilat. renal agenesis - Potter’s syndrome), maternal dehydration

56
Q

Major complication of PROM

A

Major complication of PROM is intrauterine infection (also cord prolapse, compression, fetal malpresentation)

57
Q

the leading cause of neonatal morbidity and mortality

A

PROM

58
Q

TERM prom

A

> 37

59
Q

Preterm PROM

A

<37 weeks

60
Q

etiology of PROM

A

Causes not clearly understood

Sexually transmitted diseases and other lower genital tract conditions (i.e. BV) commonly found in women with PROM

Subclinical intraamniotic infection may contribute to PROM

RF

61
Q

RF for PROM

A 
smoking during pregnancy
prior PROM
prior pre term delivery
short cervical length, polyhydramnios
multiple gestations
bleeding in early pregnancy (threatened abortion)
62
Q

Diagnosis of PROM

A

Diagnosis of PROM

1. Fluid passing though the vagina must be presumed to be amniotic fluid UNTIL proven otherwise

63
Q

evaluation of PROM

A

Sterile Speculum examination

Nitrazine test

Fern test

Ultrasonography

64
Q

Sterile speculum exam for PROM should include

A

Obtain cervical or vaginal cultures for N. gonorrheae, B-hemolytic strep, chlamydia trachomatis

Cervix visualized for degree of dilation and free flowing amniotic fluid

Fluid obtained for nitrazine and/or fern testing

65
Q

differentiating amniotic fluid from

A

amniotic fluid is alkaline

pH > 7.1

vaginal secretions pH - 4.5 to 6.0 and

urine pH - < 6.0

66
Q

evaluation of fluid pH

A

Sample of fluid obtained from vagina during speculum exam is placed on nitrazine paper - if pH is 7.1 - 7.3 paper turns dark blue

67
Q

fern testing

A

named for pattern of arborization occurs when amniotic fluid is placed on slide and allowed to dry in room air

68
Q

ULS evaluation of PROM

A

Can be helpful in evaluating the possibility of rupture of membranes

Looking for less than expected amount of fluid around fetus, then ddx of oligohydraminos is considered

Has been shown that labor and infection less likely when adequate volume of amniotic fluid remains within uterus – 800ccs at 34 weeks, 600ccs at term

Also helpful in determining gestational age

69
Q

management of PROM

A

Term PROM – 90% of patients will begin spontaneous labor within 24 hrs

Serial evaluations for the development of intrauterine infection

Induction of labor at any point after PROM considered appropriate

Group B strep (GBS) prophylaxis should be given if appropriate

70
Q

tocolytics

A

beta-mimetics (for example, terbutaline)

calcium channel blockers (for example, nifedipine)

non-steroidal anti-inflammatory drugs or NSAIDs (for example, indomethacin)

allow for the administration of corticosteroids

71
Q

what is the first sign of toxicity of mag sulfate and what is the remedy

A

toxicity is depressed or absent deep tendon reflexes, as in this patient. If left untreated, the toxicity can progress to respiratory depression and even cardiac arrest.

calcium gluconate

72
Q

For stable patients with PPROM <34 weeks

A

Course of antenatal corticosteroids to enhance fetal lung maturation in pregnancies (<34 weeks)

Prophylactic antibiotics

For patients with confirmed GA, delivery at ≥34 weeks without assessment of pulmonary maturity.

If GA is uncertain, attempt to confirm lung maturity before delivery

If amniotic fluid cannot be obtained or the test result demonstrates lung immaturity, delivery at 36 weeks, assuming the mother and fetus are stable

73
Q

PPROM

A

preterm premature rupture of membranes 20-22 weeks

Associated with substantial serious pediatric morbidity and mortality (prematurity and infection)

74
Q

PPROM mngmt

A

These pts should be counseled regarding impact of immediate delivery and potential risks/benefits of expectant management, usually managed expectantly until viability

75
Q

at what gestational age would you administer corticosteroids

A

24-34 weeks

NOT after 34 weeks

76
Q

Cervical insufficiency

A
  • painless cervical dilation leading to recurrent 2nd trimester pregnancy losses/births of otherwise normal pregnancies.

congenital or acquired

Term has also been applied to women with one or two such losses/births or at risk for second-trimester pregnancy loss/birth.

77
Q

mngmt of cervical insufficiency

A

cerclage at 12-14 weeks, and treatment with hydroxyprogesterone caproate weekly from 16-36 weeks, or..

Ultrasound surveillance and possible US-indicated cerclage

78
Q

SROM

A

sudden rupture of membranes

79
Q

AROM

A

artificial rupture of membranes

80
Q

Prolonged PROM

A

18 hours before onset of labor

OB (14 decks)

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