Complications of Pregnancy

Complications of Pregnancy

Author: Evelyn M. Hickson, RN, MSN, CNS, WCC

ObjectivesDescribe and define the following complications ofpregnancy; discuss predisposing factors, andmanagement 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

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)

Risk Factors Contributing to Preterm Delivery

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

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 Risk factors

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 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

Difficulty with Accurate Diagnosis 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

Management 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 Tocolytic drugs may prolong pregnancy 2-

7 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.

Tocolytic Agent

Dosage and Administration

Contraindica-tions

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 arrhythmiaPulmonary edema

Fetal tachycardia HyperinsulinemiaHyperglycemiaMyocardial and septal hypertrophyMyocardial 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 50-100mg 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

Tocolytics

Nursing Care: Evaluation for Preterm Labor

History (risk factors) S&S of preterm labor S&S UTI S&S vaginitis/cervicitis/STDs S&S viral or bacterial infection S&S PROM

Physical Exam 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

Pelvic Exam 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 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 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

Term PROM 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

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

Risk Factors 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 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

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

Diabetes Mellitus 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

Type I or Type II 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

1. Marked obesity2. Hx GDM prior pregnancy3. Strong family Hx4. Previous infant >4000 gm5. Hx unexplained stillbirth6. Poor OB Hx, SABs, congenital anomalies7. Recurrent glycosuria (2 positive tests)

unexplained by diet

Physiology Gestational Diabetes 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

Risks of Diabetes 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

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

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 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 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 Most common inherited are:

1. Factor V Leiden2. Prothrombin G20210A mutation

Less common inherited are:1. Deficiency of anticoagulants protein C,

proteinS, and antithrombin III

Thrombophilia

Most common acquired:1. Antiphospholipid antibody syndrome2. Lupus Anticoagulant3. Anticardiolipin antibodies

Less common acquired: 1. Lupus Anticoagulant2. Anticardiolipin Antibodies

Risk Factors for Deep Vein Thrombosis and Thromboembolic Disorders

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

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

Signs and Symptoms DVT 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

Pleural friction rub or signs of effusion

Hypoxia Hypotension Cyanosis Jugular venous distention Right ventricular heave (lower left

sternal border)

Signs and Symptoms of Pulmonary Embolism

Management of Thrombophilias

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

Recognize increased risk for thromboembolic events and be prepared

If on anticoagulants, recognize increased risk for bleeding and be prepared

Pulmonary Edema 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

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 Pneumonia:

Aspiration, bacterial, viral

Sepsis: Chorioamnionitis, pyelonephritis, puerperal infection, septic abortion

Hemorrhage: Shock, massive transfusion therapy

Arsenic poisoning Preeclampsia (Williams OB, 2001)

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)

Management O2 supplementation Diuretics Discontinuation of offending agent Ventilatory support Circulatory support Treatment of underlying cause

Nursing Care Unless very mild, requires Intensive

Care with invasive hemodynamic monitoring

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

Effects of HTN on Pregnancy Worsening or malignant HTN CNS involvement – stroke,

hemorrhage Cardiac decompensation Renal deterioration or failure Decreased uteroplacental perfusion

Hypertension in PregnancyChronic 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 PregnancyGestational 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

At higher risk for pulmonary edema due to dramatic decrease in colloid osmotic pressure

Highest risk is 6-24 hours post-delivery prior to diuresis

S & S of pulmonary edema: Decreased SaO2 Wheezing/SOB Neck vein distention Tachypnea Tachycardia Lungs dull to

percussion Cough (Productive or

Nonproductive) Anxiety

Nursing Care 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 PregnancyPreeclampsia Definition: Pregnancy specific syndrome that

usually occurs after 20 weeks (except in trophoblastic disease)

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

Suspect preeclampsia if elevated BP without proteinuria but with HA, blurred vision, abdominal pain, low platelets, abnormal liver enzymes

Risk Factors for Preeclampsia 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

Lab Value Changes 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 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

Seizure Aura “Worst Headache Ever” Feeling Weird Ringing in ears Visual Disturbance Epigastric / Right Upper Quadrant

Pain

Seizure Characteristics 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

HELLP Syndrome

Combination of hemolysis(H), elevated liver enzymes(EL), and low platelets (LP)

Liver involvement in preeclampsia-eclampsia

May occur in as many as 20% of women with severe preeclampsia

HELLP Syndrome Increased risk of averse outcomes Increased risk of abruptio placenta Renal failure Subcapsular hepatic hematoma Recurrent preeclampsia Preterm delivery Fetal and maternal death

Signs and Symptoms 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 Most cases obvious preeclampsia Patients either present with or report

having symptoms of “flu” Most have no symptoms relating to liver,

but if there is pain liver more likely involved

Hepatic failure with encephalopathy and consumptive coagulopathy are not usual

Patient may become comatose if HELLP severe enough

Management

Prompt delivery Lab abnormalities peak by 23-48

hours and begin to normalize in 2-3 days

References 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,

Principles and Practice fifth edition. Pennsylvania: Saunders Cunningham, F.G., Gant, N.F., Leveno, K.J., Gilstrap III, L.C., Hauth, J.C.,

Wenstrom, K.D. (Eds.) (2001) Williams Obstetrics twenty first edition. New York: McGraw-Hill.

Gabbe, S.G., Niebyl, J.R., Simpson J.L. (Eds.) (2002). Obstetrics, Normal and Problem Pregnancies fourth edition. Pennsylvania: Churchhill Livingstone.

Netter, F.H., MD (Ed.) (1965) The CIBA Collection of Medical Illustrations Vol. 2 Reproductive System. New York: CIBA Pharmaceutical Company.

Varney, H.; Kriebs, J.M.; Gegor, C.L., (2004) Varney’s Midwifery fourth edition. Canada: Jones and Bartlett Publishers.

The American College of OB/GYN (Ed.) (2004) 2004 Compendium of Selected Publications. Washington D.C.: The American College of OB/GYN.