medical complication Flashcards
mild and severe chronic HTN in pregnancy
- Mild hypertension – systolic of > 140-180 mmHg or diastolic > 90-100 mmHg or both
- Severe hypertension - systolic of > 180 mmHg or diastolic > 100 mmHg
Preeclampsia
i. Preeclampsia - new onset of hypertension and either proteinuria or end-organ dysfunction after 20 weeks of gestation in a previously normotensive woman
Gestational HTN/Pregnancy Induced HTN
HTN that develops after 20 weeks of gestation in the absence of proteinuria and returns to normal postpartum
Gestational HTN/Pregnancy Induced HTN is most commonly seen in these types of pregnancy
Develops in 5-10% of pregnancies that go beyond first trimester
30% incidence in multiple gestations
burden of dz with preeclampsia
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
preeclampsia -severe features (7)
- Blood pressure of > 160mm Hg systolic or > 110 mmHg diastolic
- Progressive renal insufficiency (serum creatinine >1.1 mg/dL or doubling of serum creatinine concentration in the absence of other renal disease)
- Cerebral or visual disturbances (headache and scotomata)
- Pulmonary edema or cyanosis
- Epigastric or RUQ pain
- Evidence of hepatic dysfunction (transaminases doubled)
- Thrombocytopenia (<100,000)
RF for preeclampsia (12)
- Nulliparity – women who have never been pregnant
- Age <20 y.o., >35 y.o.
- New paternity/partner related factors
- Family history of preeclampsia
- Chronic renal disease, chronic HTN
- Prolonged interpregnancy interval
a. Long periods of time between pregnancies - Antiphospholipid syndrome
- Diabetes mellitus
- Multi-fetal gestation
- High BMI
- Black race
- Connective tissue disorders (RA, SLE)
what decreases risk of preeclampsia
Smoking DECREASES risk, ASA for high risk
spiral arteries, how do they lead to preeclampsia
– 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
pathophysiology
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
Immunologic factors that lead to preeclampsia
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
immunological abnormalities that lead to preeclampsia
similar to those observed in organ rejection graft versus host disease, have been observed in preeclamptic women
genetic factors that lead to preeclampsia
Although most cases of preeclampsia are sporadic, genetic factors are thought to play a role in disease susceptibility
Systemic endothelial dysfunction that lead to preeclampsia
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.
lab changes you can see in preeclampsia
Decreased production of endothelial-derived vasodilators (nitric oxide and prostacyclin), and increased production of vasoconstrictors (endothelins and thromboxanes).
signs and sxs you want to ask about in preeclampsia
- Signs/symptoms include: visual disturbances, severe/persistent HA, RUQ pain, Hx of LOC/seizures, dizziness
how can weight change in a pt with preeclampsia
water weight and edema
STR and edema in preeclampsia
unresponsive to rest in supine position especially in upper extremities, sacral region and face
DTRs - hyperreflexia or clonus at ankle worrisome
what lab evaluation would you want to get in a pt with preeclampsia
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
why would you get a platelet count in a pt with preeclampsia
thrombocytopenia
why would you get uric acid levels
promotes inflammation and you can see this before the onset of preeclampsia
trend of hmg in pregnant pt without preeclampsia
- Usually the hemoglobin goes down as the blood volume starts expanding
rising hct can indicate worsening vaso constriction
The NST evaluates f
fetal heart rate and response to fetal movement.
The five discrete biophysical variables you are looking at in a NST
- Fetal movement
- Fetal tone
- Fetal breathing
- Amniotic fluid volume
- Fetal Heart Rate
components of a biophysical profile (BPP)
4 ultrasound (US) assessments and a nonstress test (NST).
fetal studies for for fetal weight and growth, and amniotic fluid volume
ULS
indirect assessment of placental status
ii. NST (non stress test) and/or biophysical profile
reassuring BPP result
8 or 10
when would you do labor induction in response to . a BPP
if 4
Labor induction if gestational age >32 weeks
Repeating test same day if <32 weeks, then delivery if BPP <6
definitely 2
if BPP 6
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
A BPP normally is not performed before
A BPP normally is not performed before the second half of a pregnancy, since fetal breathing movements do not occur in the first half.
mainstay of mngmt of preeclampsia
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
how often would you do a non stress test in mother with preeclampsia
how frequently ULS
2x weekly nonstress tests, biophysical profiles or both
U/S q 3 weeks for fetal growth and amniotic fluid assessment
Management – Severe Preeclampsia
- Best managed in a tertiary - care setting
- Daily lab tests and fetal surveillance
- Antihypertensive therapy if indicated
goal of preeclampsia drug therapy
Goal of therapy is to reduce diastolic pressure to 90 - 100 mmHg range
prevention of seizures
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
what do you want to worry about as far as urine output goes with maintenance while on mag sulfate
- Maintenance of urine output of at least 25 mL/hour will avoid accumulation in kidneys
reversal of mag sulfate
reversal of effects done with slow IV of 10% calcium gluconate, along with O2 supplementation
eclampsia is most commonly seen when
Most cases occur within 24 hours of delivery but approximately 3% of cases diagnosed between 2 and 10 days postpartum
management in mother with eclampsia to prevent musculoskeletal injury
Insert padded tongue blade
Restrain gently as needed
Maintain adequate airway
Gain IV access
Presentation of HELLP
RUQ
nausea, vomiting, generalized malaise, they don’t “feel well”, epigastric pain
RX given in eclampsia
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
other management strategies for Eclampsia
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
when does HELLP present
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
why would you see RUQ in HELLP
rupture of liver capsule
presentation with HELLP, who gets this
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.
women with HELLP die from
- Usually these women die from stroke or liver rupture
Labs in assessment of HELLP
LABS - CBC, CMP, coag studies, fibrin degredation products
tx of HELLP
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
management of DIC
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)
PROM
PROM is the rupture of chorioamniotic membranes before the onset of labor
amniotic fluid pH
Amniotic fluid protects against infection, fetal trauma and umbilical cord compression, pH 7.5
amt of amniotic fluid seen at 20 wks and 28 wks
400mL by 20wks,
plateau of 800mL at 28wks
Polyhydramnios
what is it and when do we see this
- AFI >20cm – assoc. with Down’s/Edwards, GDM
Oligohydramnios
what is it and when do we see this
AFI (Amniotic fluid index) <5cm – urinary tract abnormalities (bilat. renal agenesis - Potter’s syndrome), maternal dehydration
Major complication of PROM
Major complication of PROM is intrauterine infection (also cord prolapse, compression, fetal malpresentation)
the leading cause of neonatal morbidity and mortality
PROM
TERM prom
> 37
Preterm PROM
<37 weeks
etiology of PROM
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
RF for PROM
smoking during pregnancy prior PROM prior pre term delivery short cervical length, polyhydramnios multiple gestations bleeding in early pregnancy (threatened abortion)
Diagnosis of PROM
Diagnosis of PROM
1. Fluid passing though the vagina must be presumed to be amniotic fluid UNTIL proven otherwise
evaluation of PROM
Sterile Speculum examination
Nitrazine test
Fern test
Ultrasonography
Sterile speculum exam for PROM should include
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
differentiating amniotic fluid from
amniotic fluid is alkaline
pH > 7.1
vaginal secretions pH - 4.5 to 6.0 and
urine pH - < 6.0
evaluation of fluid pH
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
fern testing
named for pattern of arborization occurs when amniotic fluid is placed on slide and allowed to dry in room air
ULS evaluation of PROM
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
management of PROM
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
tocolytics
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
what is the first sign of toxicity of mag sulfate and what is the remedy
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
For stable patients with PPROM <34 weeks
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
PPROM
preterm premature rupture of membranes 20-22 weeks
Associated with substantial serious pediatric morbidity and mortality (prematurity and infection)
PPROM mngmt
These pts should be counseled regarding impact of immediate delivery and potential risks/benefits of expectant management, usually managed expectantly until viability
at what gestational age would you administer corticosteroids
24-34 weeks
NOT after 34 weeks
Cervical insufficiency
- 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.
mngmt of cervical insufficiency
cerclage at 12-14 weeks, and treatment with hydroxyprogesterone caproate weekly from 16-36 weeks, or..
Ultrasound surveillance and possible US-indicated cerclage
SROM
sudden rupture of membranes
AROM
artificial rupture of membranes
Prolonged PROM
18 hours before onset of labor
