Transcript Gestational Hypertension

Complications of Pregnancy
Author: Evelyn M. Hickson, RN, MSN, CNS, WCC
Objectives
Describe and define the following complications of
pregnancy; discuss predisposing factors, and
management of:
 Preterm Labor
 Premature Rupture of Membranes
 Diabetes
 Thrombophelias
 Pulmonary Edema
 Bleeding Complications of Pregnancy (Placenta
previa, Abruption, DIC)
Preterm Labor
Definition: Persistent uterine
contractions that are accompanied
by dilatation and/or effacement as
detected by digital exam (Gonik and
Creasy 1986)
Preterm Labor
One of the most common
complications during pregnancy
 Issue is the appropriate diagnosis
and monitoring
 Treatment modalities still have not
been proven to work
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Definitions: Preterm
Delivery
Any birth, regardless of birth weight,
that occurs before 37 completed
weeks from the first day of the last
menstrual period
 Beginning at 20 weeks and ending
at 36 6/7 weeks (Creasy and
Resnik, 2004)
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Risk Factors Contributing to
Preterm Delivery
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Hypertension
Systemic infections
Pyelonephritis
Drug abuse
Maternal race
Previous preterm birth
Low prepregnancy weight
Absent or inadequate PNC
<18yrs >35yrs
Strenuous work
High personal stress
Anemia
Smoking
Bacteriuria
Genital colonization or infection
Cervical injury or abnormality
Uterine anomaly
Low socioeconomic status
Risk Factors Contributing to
Preterm Delivery
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Preterm labor
Ruptured membranes
Multiple gestation
Preeclampsia
Abrupto placenta
Placenta previa
Vaginal bleeding
Growth restriction
Oligo, polyhydramnios
Fetal anomalies
Uterine anomalies
Chorioamnionitis
Incompetent cervix
Diabetes
Connective tissue disorders
Poor nutrition
Peridonal disease
Fibroids
Spontaneous Preterm Labor
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Risk factors
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preterm rupture of membranes
incompetent cervix
amnionitis
genital tract infection
nonwhite race
multiple gestation
second trimester bleeding
low prepregnancy weight
previous preterm birth
About 75% of preterm births fall into the spontaneous
category (Creasy and Resnik)
Epidemiology
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Poorly understood
Recent Studies have theorized:
Response to chronic intrauterine
inflammatory insult
Influenced by fetal and maternal immune
response
Infection induced activation for the fetal
hypothalamic-pituitary-adrenal axis, the
fetal membranes and decidua produce
cytokines which initiate labor or rupture
of membranes.
Signs and Symptoms
-Nonspecific and not necessarily those of
labor at term
-Pelvic pressure
-Increased vaginal discharge
-Backache
-Menstrual-like cramps
-Painful or painless contractions,
different from Braxton-Hicks only in their
persistence
Difficulty with Accurate
Diagnosis
Fetal fibronectin test – can improve
accuracy of diagnosis—negative
 Predictive value with dilatation
<3cm and effacement <80% for
delivery
 Within 7-14 days good, positive
predictive value not good
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Difficulty with Accurate
Diagnosis
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High prevalence of S&S among healthy
women not in preterm labor
Imprecision of digital exam
Contraction frequency (4 or more per
hour ) has low sensitivity and low positive
predictive value
Endovaginal ultrasonography cervical
length of 30mm or greater has very high
negative predictive value in symptomatic
women
Diagnosis
Cervical effacement of 80% or
greater
 Dilation of more than 2 cm
 Change in dilation of 1 cm or more
 Sonographic cervical length under
30mm or a positive fetal fibronectin
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Management
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Variety of drugs available-no clear first
line drug-clinical situation and
physician preference
Antibiotics do not appear to prolong
gestation, should be used for GBS
prophylaxis if delivery is imminent
Maintenance or repeated acute
tocolysis doesn’t improve perinatal
outcome used generally
Managment
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Tocolytic drugs may prolong pregnancy 27 days which may allow for steroids to
improve lung maturity, and transport to a
tertiary center
Antenatal corticosteroids significantly
reduce the incidence and severity of
neonatal RDS. Also reduce incidence of
IVH and necrotizing enterocolitis.
Decrease neonatal mortality.
Tocolytics
Tocolytic
Agent
Dosage and
Administration
Contraindications
Maternal Side
Effects
Fetal and
Neonatal Side
Effects
Betamimetic
Terbutaline .25mg
sub Q every 20 min
to 3 hrs hold for
pulse >120
Cardiac
arrhythmias
Cardiac arrhythmia
Pulmonary edema
Fetal tachycardia
Hyperinsulinemia
Hyperglycemia
Myocardial and septal
hypertrophy
Myocardial ischemia
Magnesium
Sulfate
4-6 g bolus for 20
min, then 2-3 g/hr
Myasthenia gravis
Flushing,lethargy,
Headache,muscle
weakness, diplopia,
dry mouth,
pulmonary edema,
cardiac arrest
Lethargy, hypotonia,
respiratory depression
prolonged use
demineral-ization with
Tocolytics
Calcium
channel
blockers
Nifedipine 30mg
loading dose, then
10-20mg q 4-6 hr
Cardiac disease,
use caution with
renal disease,
hypotension ,90/50
mm HG avoid
concomitant use
with magnesium
sulfate
Flushing, headache,
diaainess, nausea,
transient
hypotension
None noted
Prostaglandin
gynthetase
inhibitors
Indomethacin
loading dose of 50
mg rectally or 50100mg orally, then
25-50mg orally
every 6hrx48hrs
Sig. Renal or
hepatic impairment
Nausea, heartburn
Constriction of ductus
arteiosus, pulmanary
hypertension,
reversible decrease in
renal function with
oligo, IVH,
hyperbilirubinemia,
necrotizing
enterocolitis
Nursing Care:
Evaluation for Preterm Labor
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History (risk factors)
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S&S
S&S
S&S
S&S
S&S
of preterm labor
UTI
vaginitis/cervicitis/STDs
viral or bacterial infection
PROM
Physical Exam
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VS
Evaluate gestational age
Electronic monitor and palpate contractions
Electronic monitor of FHR and pattern
Abdominal palpation for presentation, position,
multiple gestation, EFW, pain
Costovertebral angle tenderness
Low back or suprapubic pain
Evaluation for Preterm Labor
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Pelvic Exam
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Speculum exam for vaginitis,cervicitis,STDs,PROM,
bloody show, meconium
Digital exam for cervical changes (not done if PROM
found on spec exam)
Lab tests
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UA, urine culture and sensitivity
Wet mount for Bacterial Vaginosis or Trichomonas
GBS cultures and cultures of any lesions
GC and chlamydia cultures
CBC with differential
Nitrazine and ferning if appropriate
Nursing Care of Woman
in Preterm Labor
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Bedrest, lateral position
IV, hydration has not been shown to be
effective in stopping labor and increases
risk of pulmonary edema
Continuous uterine and fetal monitoring
Medications as ordered
Arrange for transport if planned
Arrange for care of infant, staffing,
pediatrician, respiratory therapy,
equipment
Premature Rupture of
Membranes (PROM)
Definition: Rupture of membranes
before the onset of labor
 Preterm premature rupture of
membranes (PPROM)is rupture of
membranes before the onset of
labor at <37 weeks gestation
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Term PROM
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Complicates 8% of pregnancies
Generally followed by onset of labor and
delivery
In a large randomized study, with
expectant management, and ½ of women
with PROM delivered within 5 hours, and
95% delivered within 28 hours.
Risks—intrauterine infection—increases
with duration of membrane rupture,
umbilical cord compression (ACOG
practice bulletin)
Etiology of Membrane
Rupture at Term
Combination of stretching with
uterine growth, strain from uterine
contractions and fetal movement
 Biochemical changes, including a
decrease in collagen content
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Management PROM
May induce labor immediately
 Observe for the onset of
spontaneous labor for up to 24-72
hours (if observing need to avoid
digital exams which increase the
risk of infection)
 Antibiotics if GBS positive or if
rupture >18 hours
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Risk Factors
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Smoking
Multiple gestation
Abruptio placenta
Cocaine use
Previous PPROM
Previous cervical operations or lacerations
Occupational fatigue, long working hours
Vitamin C and E deficiencies
Management
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Antibiotics—prolongs latency period and
improve perinatal outcome with expectant
management prior to 35 weeks
Administration of corticosteroids if <32
weeks (some recommend <34 weeks*)
Avoid digital exams if not in labor and
immediate induction is not planned
Nursing Care
Accurate history: time, amt, color,
odor, intercourse
 Physical Exam: VS,FHR,
contractions, abdominal palpation
 Sterile Speculum Exam: vulva,
vaginal pooling, fluid from os, cord,
fetal part, nitrazine, fFN, amnitoic
protein, cervical cultures, GBS
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Nursing Care continued
In labor assess temp q2 hrs,
otherwise q 4 hrs
 Monitor FHR, cord compression or
tachycardia
 Avoid unnecessary vaginal exams
 Watch hydration, dehydration can
cause a temp elevation
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Diabetes Mellitus
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Definition: Gestational Diabetes is the
presence of carbohydrate intolerance of
varying degrees of severity with an onset
or first recognition during pregnancy.
(Varney)
Incidence: Averages about 7%, varies
with ethnicity
Increased in Hispanic, African, Native
American, South or Eastern Asian, or
Pacific Islander
Pregestational Diabetes: Diabetes which
antedates the pregnancy
Pre-Gestational Diabetes
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Type I or Type II
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Type I: True insulin-dependent, typically
develops prior to adolescence, usually
diagnosed prior to pregnancy.White
classification of B,C,D,F and above
Type II: Not necessarily insulin dependent and
usually begins after age 40
Risk Factors
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Marked obesity
Hx GDM prior pregnancy
Strong family Hx
Previous infant >4000 gm
Hx unexplained stillbirth
Poor OB Hx, SABs, congenital anomalies
Recurrent glycosuria (2 positive tests)
unexplained by diet
Physiology Gestational Diabetes
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Similar to type II Diabetes: Insulin is
available
Hormonal changes alter receptivity to
insulin
<20 weeks cells more responsive to
insulin
>20 weeks, as placenta grows, production
of human placental lactogen (HPL)
increases
Physiology of Gestational
Diabetes
HPL increases cellular resistance to
insulin
 When production of insulin cannot
keep up with rising need
hyperglycemia results
 Peak effect of HPL 26 to 28 weeks
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Risks of Diabetes
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Pregestational Diabetes: Congenital
anomalies,spontaneous AB, stillbirth,
IUGR, HTN, preeclampsia
Gestational Diabetes: If early pregnancy
blood sugars not elevated, no increase in
anomalies, but increase in macrosomic
infants, protracted labor, shoulder
dystocia, operative delivery HTN and
preeclampsia, Type II Diabetes later in
life
Macrosomic Infant
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Insulin similar to Human Growth
Hormone
Glucose crosses the placenta
Fetus increases insulin production to
metabolize glucose
Hyperplasia and hypertrophy of cells
causing lifelong change increasing risk of
obesity as well as diabetes
Screening tests
ADA recommends random
nonfasting 1hour post 50 gram
glucola <130-140
(early with risk factors, 24-28
weeks for everyone)
 3 hour glucose tolerance test
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Management
 ADA
diet—same nutrition requirements as
nondiabetic women —2000 to 2200k cal diet, may
consider caloric restriction in obese women no
more than 33%
 Balance of calories from carbohydrate, fat and
protein
 Home glucose monitoring Fasting <95mg/dl, 1 hr
<140, 2hr <120
 Careful evaluation of fetal size and fluid volume,
ultrasound if necessary but poor predictor of EFW
 Optimal antenatal testing for diet controlled GDM
with no other risk factors not established
 Usually recommend DFMC from 34 to 36 wks on at
40 weeks NST or BPP
Management
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Mild to moderate exercise
If well controlled with diet alone, await
spontaneous labor
Insulin or glyburide if poorly controlled with diet
Consider C-Section if EFW >4500 gm
6 week postpartum glucose testing
Labor management the same as nondiabetic
with higher level of suspicion for shoulder
dystocia
IV fluids should not contain glucose
Nursing Care
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Same as any woman in labor
Notify pediatrician of diabetic mom
Anticipate shoulder dystocia and be prepared to
help
Avoid glucose containing IV fluids unless on
insulin drip and NPO
If on insulin, periodic blood glucose checks and
insulin as ordered
Anticipate postpartum uterine atony/hemorrhage
if macrosomic infant
Watch vital signs closely and be aware of
increased risk for HTN
Thrombophilia
Definition: Tendency toward blood clot
formation
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Most common inherited are:
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Factor V Leiden
Prothrombin G20210A mutation
Less common inherited are:
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Deficiency of anticoagulants protein C,
proteinS, and antithrombin III
Thrombophilia
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Most common acquired:
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Antiphospholipid antibody syndrome
Lupus Anticoagulant
Anticardiolipin antibodies
Less common acquired:
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Lupus Anticoagulant
Anticardiolipin Antibodies
Risk Factors for Deep Vein Thrombosis
and Thromboembolic Disorders
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Hereditary thrombophilia
Acquired thrombophilia
Mechanical heart valve
Atrial fibrillation
Trauma/prolonged immobilization/major
surgery
History of deep vein thrombosis
Strong family history of thrombosis or
thromboembolic events
Pregnancy
Oral contraceptive use
Testing for Thrombophilias
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History of thrombosis
First degree relative with thrombophilia
Recurrent fetal loss
History of early or severe preeclampsia
Severe unexplained IUGR
Signs and Symptoms Superficial Thrombophlebitis
Leg pain
 Localized heat, tenderness or
inflammation at site
 Palpation of knot or cord
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Signs and Symptoms DVT
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Slight temperature elevation
Mild tachycardia
Abrupt onset with severe leg pain worse
with motion or standing
Edema of ankle,leg,thigh
Positive Homan’s sign
Pain with calf pressure
Tenderness along entire course of involved
vessel with palpable cord
Signs and Symptoms of
Pulmonary Embolism
Dyspnea
 Tachycardia
 Tachypnea
 Breath sounds few rales or wheezes
 Low PO2 and O2 saturation
 Hemoptysis
 Pleuritic chest pain
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Signs and Symptoms of
Pulmonary Embolism
Pleural friction rub or signs of
effusion
 Hypoxia
 Hypotension
 Cyanosis
 Jugular venous distention
 Right ventricular heave (lower left
sternal border)
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Management of
Thrombophilias
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Appropriate testing for thrombophilias
High index of suspicion with risk factors
Occasional prophylactic anticoagulation
with sub q heparin injection
During labor, if anticoagulant therapy is
required, IV heparin is used
Postpartum, switch back to sub q heparin
overlapping with coumadin
With some anticoagulants neuraxial
blocks should not be used for 24 hours
after last injection
Nursing Care
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Recognize increased risk for
thromboembolic events and be
prepared
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If on anticoagulants, recognize
increased risk for bleeding and be
prepared
Pulmonary Edema
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Usually due to excess capillary pressure
as in cardiomyopathy, mitral stenosis or
due to a disruption of alveolar capillary
membrane integrity as in pneumonia,
ARDS (Gabbe, Niebyl, Simpson, 2002)
Two general causes alveolar flooding:
caused by heart failure or permeability
edema from alveolar-capillary injury. In
many OB cases both are present
(Williams OB, 2001)
Risk Factors for the Development
of Pulmonary Edema
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Maternal cardiac disease (structural, ischemic or
dysrhythmia)
Eclampsia, severe preeclampsia, or other significant
hypertensive disease
Antepartum hemorrhage
HELLP syndrome
Use of tocolytics, Betamimetics, Magnesium Sulfate
Fluid overload
Infection - occult chorioamnionitis and sepsis
Adult Respiratory Distress Syndrome
Risk Factors/Acute Lung
Injury
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Pneumonia:
Aspiration, bacterial,
viral
Sepsis:
Chorioamnionitis,
pyelonephritis,
puerperal infection,
septic abortion
Hemorrhage: Shock,
massive transfusion
therapy
Arsenic poisoning
Preeclampsia
(Williams OB, 2001)
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Embolism: Amnionic
fluid, trophoblastic
disease, air
Connective-tissue
disease
Substance abuse:
Heroin, methadone
Irritant inhalation and
burns
Pancreatitis
Pheochromocytoma
Signs and Symptoms
Dyspnea
 Cough
 Orthopnea
 Tachycardia
 Hemoptosis (occasionally)
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Management
O2 supplementation
 Diuretics
 Discontinuation of offending agent
 Ventilatory support
 Circulatory support
 Treatment of underlying cause
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Nursing Care
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Unless very mild, requires Intensive
Care with invasive hemodynamic
monitoring
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Labor and Delivery nurses role
primarily in close monitoring of
patient at risk, early recognition of
signs of decompensation, prevention
of iatrogenic causes
Hypertensive Disorders of
Pregnancy
Chronic Hypertension
 Gestational Hypertension
 Preeclampsia
 Eclampsia
 HELLP syndrome
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Effects of HTN on
Pregnancy
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Worsening or malignant HTN
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CNS involvement – stroke,
hemorrhage
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Cardiac decompensation
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Renal deterioration or failure
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Decreased uteroplacental perfusion
Hypertension in Pregnancy
Chronic HTN:
 Present before the 20th week of pregnancy or present
before pregnancy
 Systolic greater than or equal to 140 and/or diastolic
greater than or equal to 90
 Mild=140/90
 Severe=180/110
 Use of antihypertensive meds before pregnancy
 Persistence of HTN beyond postpartum period
Hypertension in Pregnancy
Gestational Hypertension
 Replaces older term PIH
(pregnancy induced hypertension)
 Describes cases in which elevated
blood pressure without proteinuria
develops after 20 weeks and
returns to normal after delivery
(ACOG Practice Bulletin 33)
 25% of these women develop
preeclampsia
Complications of Gestational
Hypertension and
Pre-eclampsia
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At higher risk for  S & S of pulmonary
pulmonary edema edema:
 Decreased SaO2
due to dramatic
 Wheezing/SOB
decrease in colloid
 Neck vein distention
osmotic pressure
 Tachypnea
Highest risk is 6 Tachycardia
24 hours post Lungs dull to
percussion
delivery prior to
 Cough (Productive or
diuresis
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Nonproductive)
Anxiety
Nursing Care
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Monitor:
Signs and symptoms of decline in patient
condition
Maternal and Fetal Well-being (done by
OB)
Strict I & O
Respiratory Status - Pulmonary Edema
Renal and Hepatic Function
Clotting Capability – potential for bleeding
Psych-Social Support of patient and
family
Hypertension in Pregnancy
Preeclampsia
 Definition: Pregnancy specific syndrome that
usually occurs after 20 weeks (except in
trophoblastic disease)
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Characterized by: BP elevation of 140 or greater
systolic or 90 or greater diastolic in previously
normotensive woman, accompanied by
proteinuria of .3g or more in 24 hours, or 1+ or
greater reading on dipstick
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Suspect preeclampsia if elevated BP without
proteinuria but with HA, blurred vision,
abdominal pain, low platelets, abnormal liver
enzymes
Risk Factors for
Preeclampsia
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Nulliparity
Trophoblastic disease
Multiple pregnancy
CHTN
Preexisting renal disease
Pregestational diabetes
Family history of preeclampsia or eclampsia
Hx of preeclampsia in previous pregnancy
Multipara with new sexual partner
African or Asian ethnicity
Thrombophilia
Signs and Symptoms
Persistent HA
 Dizziness, blurred vision, scotomata
 Persistent epigastric pain
 BP elevation
 Ophthalmic Exam: Papilledema, A-V
nicking, vessel; narrowing,
hemorrhagic areas
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Lab Value Changes
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Platelets - Low
> 100 K is severe disease
Serum Uric Acid – High
BUN – Normal to High
Serum Creatinine – Normal to High
Liver Function – Elevated
Urine Protein – Increased
3-4+ with 5 Grams/L in 24 hrs = severe
disease
2-3+ with 1 Grams/L in 24 hrs diagnostic of
preeclampsia
Treatment
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Magnesium Sulfate 4-6 Gram IV load over
20 minutes followed by 2 Grams /hr and
maintained for 12-24 hours post partum
Antihypertensive Medications for diastolic
>105-110
If still pregnant with viable baby –
determine severity of disease, risk to
mother and to baby and determine if
mom needs to be delivered
If baby has demised, deliver
Eclampsia
Preeclampsia disease process that
progresses to convulsions
 Most common prior to delivery but
may occur to 10+ days post partum
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Seizure Aura
“Worst Headache Ever”
 Feeling Weird
 Ringing in ears
 Visual Disturbance
 Epigastric / Right Upper Quadrant
Pain
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Seizure Characteristics
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Fixation of diaphragm during seizure
Respirations may cease during seizure
Duration vary
Cyanosis
Fetal Bradycardia (if still pregnant)
Potential for:
Sudden Death
Massive Cerebral Hemorrhage
Blindness due to retinal detachment, occipital
lobe
ischemia, infarction or edema
Cerebral Edema
Treatment
If still pregnant and baby alive and
viable:
 Reload with Magnesium Sulfate 4-6
Grams
 Magnesium Sulfate drip rate at 2
Grams/hour
 No use of Valium – use Ativan
 Deliver
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HELLP Syndrome
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Combination of hemolysis(H), elevated
liver enzymes(EL), and low platelets
(LP)
Liver involvement in preeclampsiaeclampsia
May occur in as many as 20% of
women with severe preeclampsia
HELLP Syndrome
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Increased risk of averse outcomes
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Increased risk of abruptio placenta
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Renal failure
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Subcapsular hepatic hematoma
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Recurrent preeclampsia
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Preterm delivery
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Fetal and maternal death
Signs and Symptoms
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Upper abdominal pain, epigastric or right
upper quadrant
Thrombocytopenia
Elevated liver enzymes aspartate
aminotransferase typically less than 200
to 500U/L
Sometimes serum bilirubin is elevated,
seldom greater than 2-4 mg/dL
Intrahepatic and subcapsular hemorrhage
Liver rupture, fatal hemorrhage
Signs and Symptoms
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Most cases obvious preeclampsia
Patients either present with or report
having symptoms of “flu”
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Most have no symptoms relating to liver,
but if there is pain liver more likely
involved
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Hepatic failure with encephalopathy and
consumptive coagulopathy are not usual
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Patient may become comatose if HELLP
severe enough
Management
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Prompt delivery
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Lab abnormalities peak by 23-48
hours and begin to normalize in 2-3
days
References
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Burrow, G.N., MD; Duffy, T.D., MD (Eds.) (1999). Medical Complications
During Pregnancy fifth edition. Pennsylvania: W.B. Saunders Company.
Creasy, R.K., MD; Resnik, R., MD (Eds.) (2004) Maternal-fetal Medicine,
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