HTN disorders

are a major cause of perinatal morbidity and mortality. [uteroplacental insufficiency, preterm birth]

HTN disorders

can happen with uteroplacental insufficiency

IUGR

are one of the top causes of maternal morbidity and mortality, Death related to: Renal Failure, Coagulopathy, Cardiac or Liver Failure, Placental abruption, Eclampsia (seizures) and Stroke

HTN disorders

classifications of HTN disorders during pregnancy:

gestational, chronic

gestational hypertensive disorders include:

gestational HTN, pre-E, eclampsia

chronic hypertensive disorders include:

chronic HTN, superimposed pre-E

Onset of hypertension after 20 weeks gestation, BP > 140/90 (only one pressure needs elevation; systolic OR diastolic; or both can be elevated), Need two elevated measures at least 4 hours apart, BP returns to normal within 12 weeks postpartum, 50% of patients diagnosed with this go on to develop preeclampsia, is just the HTN, pre-E has to have another symptom accompanied with it

gestational HTN

HTN and proteinuria OR HTN with thrombocytopenia, impaired liver function, persistent RUQ/epigastric pain, renal insufficiency, pulmonary edema, new-onset cerebral or visual disturbances - normal or severe features

preeclampsia

BP reading (same as gestational HTN) for pre-E w/o severe features: —- mm Hg × 2, at least 4hrs apart after 20 weeks of gestation in a previously normotensive woman

>140/90

proteinuria for pre-E w/o severe features: >—- mg in a 24 hr specimen, or > —- on a dipstick (used only if quantitative measures are not available)

300, 2+

pre-E with severe features: massive proteinuria over —- g in 24 hr specimen - no longer used as diagnostic criterion because pre-E can still cause life threatening damage without protein in the urine

5

thrombocytopenia levels for pre-E and pre-E with severe features:

<100,000

pre-E w/o severe features: Protein/creatinine ratio ≥—- (with each measured as mg/dL)

0.3

Elevated blood levels of liver enzymes (AST/ALT) to twice the upper limit of normal concentration - bilirubin can also be elevated but when that starts to happen points to development of HELLP syndrome

preeclampsia

Abnormal liver function not accounted for by alternative diagnoses and as indicated by abnormally elevated blood concentrations of liver enzymes to twice the normal concentration; severe persistent epigastric or right upper quadrant abdominal pain unresponsive to medication and not accounted for by alternative diagnoses, or both

pre-E with severe features

for both pre-E and pre-E with severe features (more progressive obviously): New development of serum creatinine >— mg/dL or a doubling of the serum creatinine concentration in the absence of other renal disease

1.1

pulmonary edema is —- in both pre-E and pre-E with severe features

present

same for pre-E and pre-E with severe features: New-onset headache unresponsive to medication and not accounted for by alternative diagnoses or visual symptoms/disturbances

cerebral/visual disturbances

BP for pre-E with severe features: ≥—- mm Hg × 2, at least 4 h apart (unless antihypertensive therapy has already been initiated)

160/110

Seizure activity (generalized tonic-clonic) or coma in a patient with preeclampsia with no history of a preexisting condition or seizure disorder, Occurs before, during, or after birth

eclampsia

Hypertension persisting longer than —-postpartum is classified as chronic hypertension

12 wks

associated with adverse maternal and fetal outcomes, Diagnoses is based on one or both- (1) sudden increase in BP that previously well controlled or (2) new-onset proteinuria or a sudden increase in proteinuria in a patient known to have proteinuria before conception or early in pregnancy

chronic HTN with superimposed pre-E

risk factors for pre-E:

nulliparity, AMA, hx, family hx, first pregnancy with new partner, partner who fathered a pre-E pregnancy in another woman, multifetal gestation, obesity, assistive reproductive tech

preexisting medical conditions that are risk factors for pre-E:

chronic HTN, pre gestational DM, connective tissue disease, thrombophilia

inadequate vascular remodeling > decreased placental perfusion/hypoxia > endothelial cell dysfunction > vasospasm, increased peripheral resistance, increased endothelial cell permeability > decreased tissue perfusion (at the same time we don’t really know if this is for sure, only suspected)

etiology of pre-E

1-2 wks (up to 6 wks) PP - persistent headache not relieved with tylenol = Will be readmitted with —— for 24 hrs

mag sulfate

Vasospasms cause increased BP, Arteriolar vasospasms results in decreased perfusion of placenta, kidneys, liver, and brain, Decreased perfusion in placenta leads to early degenerative aging of the placenta, and decreased oxygen and nutrients to fetus resulting in IUGR

pre-E patho

HELLP syndrome stands for: ——- Sx of hepatic damage (R upper quadrant or epigastric pain; hyperbilirubinemia)

hemolysis of RBCs, elevated liver enzymes, low platelets

normal AST levels: — (U/L)

4-20

normal ALT levels: —- (U/L)

3-21

normal LDH (released when RBCs burst): —- (U/L)

45-90

AST levels in HELLP:

>70

LDH levels in HELLP:

>600

ALT levels in HELLP:

>50

Clinical presentation nonspecific, May report h/o malaise, flu-like symptoms, epigastric or RUQ pain, Symptoms tend to worsen at night and improve during the daytime, Occurs more often in Caucasian women, hemolysis of RBCs, elevated liver enzymes, low platelets - Don’t have to have all symptoms, just one counts

HELLP syndrome

HCT/HGB and fibrinogen will —— in HELLP

decrease

fibrinogen will increase in pre-E with levels at —— (normal 200-400)

300-600

BUN/creatinine will —— in both pre-E and HELLP

increase

burr cells or schistocytes are present in —

HELLP syndrome

assessment for hypertensive disorders includes:

BP, edema, DTRs, clonus, 24 hr urine collection, other s/s

Low dose aspirin around —- if hx of HTN disorders

12 wks

Teach BP at home - use same arm, rest 10 mins before taking it, arm resting on surface + level with heart =

standardized method

testing for hyperreflexia, count how many times foot hits your hand again after moving up, Positive it hits more than once

clonus

Can be managed at home if: BP less than 155/105 mmHg, No increase in proteinuria, Normal platelet count, Normal liver enzymes, Pregnant patient needs to be well educated

gestational HTN, pre-E w/o severe features

initial maternal labs:

creatinine, platelet count, liver enzymes, 24 hr urine

weekly interventions for gestational HTN/pre-E w/o severe complications: —— (NST or BPP weekly or biweekly)

labs, s/s of severe features, proteinuria

interventions for gestational HTN/pre-E w/o severe features: BP monitored —

2x/wk

interventions for gestational HTN or pre-E w/o severe features (not any labs):

daily fetal movements, amniotic fluid index, estimated fetal weight, gentle exercise, relaxation

how often is amniotic fluid index and estimated fetal weight taken after initial diagnosis of gestational HTN or pre-E w/o severe features

q3wks

(also for severe gestational HTN) Hospitalized immediately for a thorough evaluation of maternal-fetal status, Magnesium Sulfate (prevent eclampsia- seizure), Antihypertensive Meds (if needed), Maternal assessment- monitoring BP, UO, cerebral status, epigastric pain, labor, vaginal bleeding, maternal labs, BPP, U/S for amniotic fluid index/fetal growth

pre-E with severe features

severe gestational HTN/pre-E with severe features: ——= expedite birth after pregnant patient is stabilized (risks of continuing the pregnancy are considered greater than the risks of preterm birth)

>34 wks

severe gestational HTN/pre-E with severe features: —— and no indication for giving birth immediately are candidates for expectant management

<34 wks

hospitalization, consult with perinatologist, oral antihypertensive meds, ongoing maternal and fetal assessments, betamethasone, mag sulfate 24 hrs, serial BP q15 mins - done for severe gestational age/pre-E with severe features who are under 34 wks

expectant management

severe gestational HTN/pre-E with severe features: Continuous EFM, CNS, Cardiovascular, Pulmonary, Hepatic, and Renal Systems Assessments/Evaluations, Education and Supportive Measures, Bedrest (quiet, darkened environment)

intrapartum care

Suction equipment tested and ready to use, Oxygen administration equipment tested and ready to use, Call button within easy reach

seizure precautions

—or fewer fetal movements/hr needs to be reported

4

emergency meds for severe gestational HTN/pre-E with severe features on unit: —— (also emergency birth pack ready and easily accessible)

hydralazine, labetalol, nifedipine, mag sulfate, calcium gluconate

arterial vasodilator = decreases cardiac after load and BP, for BP over 160/110, decreases peripheral arterioles in order to decrease pulmonary/systemic/renal resistance, can cause tachycardia in mom and baby, increase in CO, HA, flushing, decrease in uteroplacental blood flow, max dose is 25 mg/hr - wait 20 mins before administered increase in dose (also known as apresoline)

hydralazine

Combined alpha- and beta-blocking agent causing vasodilation without significant change in cardiac output, used to address BP in pre-E, hold dose if HR <60, contraindicated with asthma, heart disease/CHF, can’t exceed 80 mg in single dose or 300 mg in 24 hrs

labetalol

CCB, acts on arterioles: to reduce systemic vascular resistance by relaxation of arterial smooth muscle, oral route only - recommended if no IV access, avoid with concurrent mag sulfate use, avoid with tachycardia/palpitations, aka Procardia

nifedipine

IV fluids and oral fluids max to avoid pulmonary edema (can’t adjust mag sulfate, can’t really adjust pitocin - will decrease LR to meet that):

125 mL/hr

Given to prevent or treat seizures (eclampsia), is not used for BP, Administer IVPB using infusion pump, is not considered toxic to healthy fetus of normal weight but if toxicity in mother occurs, infant may be born with hyporeflexia, bradypnea, etc.

mag sulfate

initial loading dose for mag sulfate: ——-moms get hot/sweaty because it’s run fast (also because of systemic dilation) - stay in the room for time that it’s administered

4-6 g in 100 mL IV fluid over 15-30 mins

maintenance dose for mag sulfate: ——(40 grams in 1000 ml LR)

1-2 g/hr

Therapeutic level: serum Mg level between —- mEq/L

4-7

CNS checks for mag sulfate include:

VS, LOC, reflexes, HA, visual disturbances, lethargy

mag sulfate toxicity assessments at least hourly:

BP/RR, DTRs/clonus, UO, LOC, HA, visual disturbances, epigastric pain, FHR and activity

if BP is over ——- on mag, call doctor for new order

160/110

if UO is less than —— on mag, call doctor

25-30 mL/hr

mag: Lethargy, muscle weakness, decreased/absent DTRs, double vision, slurred speech

mild toxicity

mag: Hypotension, bradycardia, bradypnea, cardiac arrest

increased toxicity

if mag toxicity give calcium gluconate —— (administered slowly to avoid dysrhythmias, bradycardia, and ventricular fibrillation) - infant can be born with hyporeflexia, bradypnea, etc

10 mL of 10% solution IVP over 3 mins

if mag toxicity happens with mom and it reaches baby =

calcium transfusions, mechanical ventilation

mag sulfate contraindicated with: —- (first one because it can cause respiratory failure)

myasthenia gravis, heart block, myocardial insufficiency, renal disease

PP hemorrhage - —- is used for this but cannot use for someone with pre-E or eclampsia

methergine

continue mag sulfate PP for —-

12-24 hrs

S/S of preeclampsia usually resolve within —- after birth

48 hrs

potentiates action of narcotics and CNS depressants and calcium-channel blockers

mag sulfate

chronic HTN associated with these complications:

superimposed pre-E, placental abruption, IUGR, preterm birth

after the eclampsic seizure uterus can be —- from seizure so dilation can advance or ROM - why assessing cervical status

hypertonic