High Risk: Care for Gestational Conditions
High Risk: Care for Gestational Conditions
Learning Objectives
Differentiate among gestational hypertension, preeclampsia, and chronic hypertension.
Describe etiologic theories and pathophysiology of preeclampsia.
Explain the effects of hyperemesis gravidarum on maternal and fetal well-being.
Differentiate causes, signs, symptoms, possible complications, and management of bleeding disorders: spontaneous abortion, ectopic pregnancy, cervical insufficiency, and hydatidiform mole.
Compare and contrast placental disorders: placenta previa and placental abruption regarding signs, symptoms, complications, and management.
Discuss the diagnosis and management of disseminated intravascular coagulation.
Discuss implications of trauma on mother and fetus during pregnancy.
Hypertension in Pregnancy
Most common gestational complication, occurring in 5-10% of all pregnancies.
Major cause of maternal and perinatal morbidity and mortality worldwide.
Classifications of Pregnancy Hypertension
Gestational Hypertension
Preeclampsia
Eclampsia
Chronic Hypertension
Chronic Hypertension with Superimposed Preeclampsia or Eclampsia
Gestational Hypertension
Onset after 20 weeks gestation.
Defined as Blood Pressure (BP) > 140/90 mmHg.
Blood pressure should be recorded on two separate occasions at least 4-6 hours apart but within a week.
Diagnosis Criteria: Only one of the pressures (systolic or diastolic) needs to meet the criteria.
Classification:
Mild: BP > 140/90 mmHg
Severe: BP > 160/110 mmHg
Preeclampsia
Defined as systolic or diastolic hypertension with proteinuria.
Previously, a patient did not have hypertension or proteinuria.
Proteinuria: A sign of organ damage from hypertension.
Severity Classification:
Mild:
BP > 140/90
Kidneys: Proteinuria > 1+ on dipstick twice or 24-hour urine > 300 mg.
Urine output > 25-30 ml/hr.
Does Not Have:
Severe headache
Visual problems
Epigastric or right upper quadrant (RUQ) pain, nausea, vomiting
Thrombocytopenia
Impaired liver function
Fetal Effects: Reduced placental perfusion.
Severe (only one criterion required):
BP > 160/110
Kidneys: Proteinuria > 3+ on dipstick twice or > 5 grams in 24-hour collection.
Urine output < 500 ml/24 hr.
Neurological: Persistent and severe headaches, blurred vision, light sensitivity, or photophobia.
Hyperreflexia: Increased deep tendon reflexes (DTR) and clonus.
Liver: Enlarged with epigastric or RUQ pain, nausea, vomiting, impaired liver function (elevated liver enzymes).
Thrombocytopenia.
Fetal Effects: Intrauterine growth restriction (IUGR), abnormal antepartum testing (non-stress tests, biophysical profiles, contraction stress tests, etc.).
Eclampsia
Defined as new onset seizures or coma in a woman with preeclampsia.
Eclamptic seizures can occur:
Before labor
During labor
Postpartum (approximately 1/3 of eclamptic seizures occur after birth, usually within 48 hours after delivery).
Chronic Hypertension
Present before 20 weeks gestation or lasting longer than 12 weeks postpartum.
Most women with mild chronic hypertension experience uncomplicated pregnancies.
Severe chronic hypertension increases the risk of perinatal mortality.
Chronic Hypertension with Superimposed Preeclampsia
Defined as having hypertensive conditions before 20 weeks + proteinuria.
Case Study and Assessment for Gestational Hypertension Progression
The nurse evaluates a client with gestational hypertension for possible progression to eclampsia by assessing for:
A. Severe headache
B. New onset of seizures
C. Proteinuria
D. Thrombocytopenia
Further Exploration of Preeclampsia
Signs and symptoms develop only with pregnancy and tend to disappear shortly after the birth of the fetus and placenta.
Etiology Theories:
Unknown causes involving abnormal placental invasion.
Immunologic response to foreign genes of fetus and placenta.
Stimulation of the inflammatory system by vascular changes.
Potential dietary deficiencies (e.g., protein, calcium).
Genetic abnormalities indicating a familial component.
Preeclampsia Risk Factors
Primigravida (first pregnancy).
Age extremes:
<19 years old or >40 years old.
History of severe preeclampsia in a previous pregnancy.
Family history of preeclampsia (mother or sister).
Paternal history of fathering a preeclamptic pregnancy in another woman.
African American ethnicity.
Multifetal gestation (twins).
Maternal infection/inflammation during current pregnancy (e.g., UTI, periodontal disease).
Preexisting medical or genetic conditions:
Chronic hypertension
Renal disease
Pregestational diabetes
Connective tissue disease (hems, rheumatoid arthritis)
Obesity.
Preeclampsia Pathophysiology
Changes occur long before diagnosis during the first trimester.
Starts with poor circulation to the placenta, leading to endothelial cell dysfunction.
Results in
Generalized vasospasm, causing poor perfusion in all organ systems.
Increased peripheral resistance (BP rises).
Loss of protein and water from blood vessels results in decreased plasma volume and hemoconcentration.
Reduced kidney perfusion decreases glomerular filtration rate causing oliguria.
Proteinuria due to protein loss in urine.
Elevated serum uric acid levels.
Sodium and water retention causing edema.
Renal failure might occur.
Important Notes on Treatment
It is crucial to note that this is not essential hypertension; it cannot be treated identically with just medication.
Plasma volume is expected to increase, and blood vessels should dilate in the middle of pregnancy to ensure good circulation to the placenta.
In hypertensive disorders of pregnancy, this physiological response does not occur, preventing the usual dip in BP. Therefore, the body compensates by raising BP to maintain placental perfusion, requiring gentle management of antihypertensive drugs.
The only definitive "cure" is ending the pregnancy.
Pathophysiology Effects:
Decreased liver perfusion can lead to impaired liver function and elevated liver enzymes.
Liver edema and hemorrhage may result in RUQ pain and rupture of liver hematoma, representing a life-threatening surgical emergency.
Neurological complications may arise such as cerebral edema, hemorrhage, and increased CNS irritability.
Symptoms include severe headaches, hyperreflexia, positive ankle clonus, seizures, and visual disturbances (scotomata).
HELLP Syndrome
Severe preeclampsia characterized by:
Hemolysis (H),
Elevated liver enzymes (EL),
Low platelets (LP).
Occurs in 10-20% of women with severe preeclampsia.
Associated risks include:
Maternal death,
Adverse perinatal outcomes such as pulmonary edema, acute renal failure, disseminated intravascular coagulopathy, placental abruption, and severe IUGR.
Common Laboratory Changes in Preeclampsia
Lab | Preeclamptic | HELLP |
|---|---|---|
LDH | Elevated >600 | |
AST | Elevated >70 | |
ALT | Elevated | Elevated |
Uric Acid | >5.9 | >10 |
Platelets | Unchanged or <100,000 | <100,000 |
Hemoglobin | May increase | Decreased |
Assessments for Preeclampsia Clients
Objective Assessments:
Blood Pressure: manual, same position.
Edema: present, generalized.
Deep Tendon Reflexes: assess popliteal reflex.
Clonus: assess presence and beats.
Proteinuria: urine dip or 24-hour collection.
Subjective Assessments:
Are there headaches?
Is there epigastric pain?
Are there right upper quadrant pains?
Are vision changes (scotomata, photophobia, double vision) present?
Precautions with Preeclampsia
Environment:
Maintain a quiet and non-stimulating environment; lighting should be subdued.
Seizure Precautions:
Ensure suction equipment and oxygen administration equipment are available.
Call buttons must be within reach.
Siderails should be padded; bed should be low to the ground.
Emergency medications such as hydralazine, labetalol, nifedipine, magnesium sulfate, and calcium gluconate should be readily accessible.
Emergency birth pack must be easily accessible due to the necessity of potential rapid labor.
Considerations for Magnesium Sulfate
Administered via IV pump with loading and maintenance doses.
Functions to prevent or reduce cerebral edema, acting as a central anticonvulsant.
Must track hourly intake and output (I/O).
Common Side Effects:
Feelings of warmth, flushing, diaphoresis, burning at the IV site, and warmth in the perineum.
Signs of Magnesium Toxicity:
Lethargy, muscle weakness, decreased or absent DTRs, double vision, slurred speech, maternal hypotension, maternal bradycardia, decreased respiratory rate, and potential cardiac arrest.
Eclampsia Interventions
Maintain airway patency by turning the head to one side.
Use a pillow under one shoulder or back if feasible.
Call for assistance and do not leave the bedside.
Ensure protection with padded side rails up, observing and recording convulsion activity.
Hyperemesis Gravidarum
Normal nausea and vomiting occur in up to 80% of all pregnancies, typically beginning at week 4 and ending by week 20.
Result of relaxation of the smooth muscle of the stomach caused by increasing levels of estrogen, progesterone, and hCG.
Hyperemesis Gravidarum: Excessive vomiting, resulting in:
Weight loss.
Electrolyte imbalances and dehydration.
Nutritional deficiencies.
Only occurs in approximately 0.5% of pregnancies.
Risk Factors for Hyperemesis Gravidarum
Hyperthyroidism.
Psychiatric diagnoses.
Previous pregnancy with hyperemesis.
High hCG levels, such as in molar pregnancy or multiple gestation.
Diabetes.
Gastrointestinal disorders.
Complications:
Esophageal rupture.
Vitamin K deficiency.
Unknown causes are thought to possibly involve high levels of estrogen or hCG, transient hyperthyroidism, or esophageal reflux.
Clinical Manifestations of Hyperemesis Gravidarum
Significant weight loss.
Dehydration and electrolyte imbalance.
Inability to retain oral fluids.
Nutritional deficiencies.
Management of Hyperemesis Gravidarum
NPO (nothing by mouth): no food or drink.
Administer IV fluids to compensate for dehydration.
Provide medications such as anti-nausea agents and supplements.
Bleeding in Pregnancy
Maternal Risks:
Decreased oxygen-carrying capacity.
Hypovolemia.
Anemia.
Fetal Risks:
Fetal blood loss or anemia.
Hypoxia and anoxia.
Preterm birth.
Early Pregnancy Bleeding
Spontaneous Abortion (Miscarriage):
Occurs due to natural causes before 20 weeks of gestation.
Common occurrence in 10-15% of clinically recognized pregnancies.
80% of abortions happen before 12 weeks of gestation; 50% due to chromosomal abnormalities.
Late spontaneous abortion may occur after 12 weeks due to maternal causes such as advanced maternal age over 35 years, premature dilation of the cervix, inadequate nutrition, and substance use.
Reduced Cervical Competence
Cervical incompetence is a cause of late spontaneous abortion or preterm birth, characterized by passive, painless dilation of the cervix during the second trimester.
Associated with cervical length, poor integrity of cervical tissue, and stress.
Etiology of Reduced Cervical Competence
History of cervical trauma or treatment for cervical cancer.
Diagnosis:
Based on history of 2nd trimester losses.
Short cervix (less than 25 mm) observed via ultrasound.
Management of Reduced Cervical Competence
Recommended strategies may include bed rest, pessaries, antibiotics, anti-inflammatory drugs, progesterone supplementation, and cerclage (McDonald technique), which should be removed at 36 to 38 weeks.
Critical Instructions: Report symptoms like pain, increased pressure, possible rupture of membranes, or signs of infection.
Ectopic Pregnancy
Commonly referred to as “tubal pregnancy,” though implantation can occur outside of the fallopian tube.
Defined as the fertilized ovum being implanted outside of the uterus, affecting 2% of pregnancies in the U.S.
Accounts for 9% of all pregnancy-related maternal deaths and is a leading cause of infertility.
Ectopic Pregnancy Risk Factors
Current or previous sexually transmitted diseases (STDs).
Use of intrauterine devices (IUDs) and history of tubal ligations.
Procedures involving reproductive technologies.
History of ectopic pregnancy.
Clinical Manifestations of Ectopic Pregnancy
Abdominal pain localized to one side.
Late or light menstrual period.
Abnormal vaginal spotting occurring 6-8 weeks post last menstrual period (LMP).
If ruptured:
Internal bleeding characterized by referred shoulder pain due to blood in the peritoneal cavity and signs of shock.
Management of Ectopic Pregnancy
Medical Management (if small, unruptured):
Methotrexate used to destroy rapidly dividing cells (folate inhibitor).
Patients must avoid alcohol and supplements containing folic acid.
Surgical Management:
Removal of either the tube or the ectopic pregnancy itself.
Hydatidiform Mole (Molar Pregnancy)
A type of Gestational Trophoblastic Disease, which also includes choriocarcinoma (cancer).
Characterized by benign proliferative growth of placental trophoblasts.
Chorionic villi develop into cysts resembling a grape-like cluster.
The embryo fails to develop beyond a primitive state but can become a rapidly metastasizing malignancy (choriocarcinoma).
Clinical Manifestations of Hydatidiform Mole
Early stages resemble a normal pregnancy; however:
95% of cases present with vaginal bleeding.
Uterine size larger than expected for the gestational age.
No fetal heart tones are ever detected.
Symptoms may also include those related to elevated hCG.
Risk Factors for Molar Pregnancy
Age extremes (very young or older mothers).
Use of assisted reproductive medications (e.g., Clomid).
Diagnosis and Treatment of Molar Pregnancy
Diagnosis:
Elevated hCG levels.
Uterus larger than expected with no fetal heart tones.
Ultrasound may show the uterine cavity filled with vesicles without an embryo.
Treatment:
Suction and curettage to evacuate tissue from the uterus.
Weekly serum hCG monitoring for 3 weeks, followed by monthly monitoring for 6 months.
Advised to avoid pregnancy until cleared.
Late Pregnancy Bleeding
1. Placenta Previa
Characterized by the placenta implanted in the lower uterine segment.
Can completely cover or partially cover the cervical os (marginal placenta previa).
Dilation of the cervix causes vaginal bleeding; diagnosed via ultrasound.
Affects approximately 1 in 200 women with pregnancies at term.
Placenta Previa Risk Factors
Previous cesarean birth or scarring on the uterus.
Advanced maternal age.
Multiparity (multiple pregnancies).
History of D&C (dilation and curettage).
Tobacco use.
Residing at a higher altitude (oxygen levels).
Clinical Manifestations of Placenta Previa
Bright red vaginal bleeding after 20 weeks, which is typically painless.
Vital signs may remain normal until up to 40% of blood volume is lost.
The fundus palpates as soft; fetal heart tones may be normal unless the placenta detaches completely.
Fetal malpresentation is common (e.g., breech or transverse lie).
Maternal and Fetal Outcomes of Placenta Previa
Maternal Outcomes:
Major complication is maternal hemorrhage; potential for abnormal placental attachment.
Possible hysterectomy if bleeding cannot be controlled.
Fetal Outcomes:
Greatest risk includes preterm birth, possible stillbirth, malpresentation, and fetal anemia.
Management of Placenta Previa
NOTHING should be placed in the vagina.
Avoid vaginal exams and intercourse; constant monitoring for bleeding with pad counts and weighing.
Administer corticosteroids (e.g., betamethasone) for lung maturity if under 34 weeks.
Bed rest is often recommended.
Cesarean birth is always indicated.
2. Abruptio Placentae (Placental Abruption)
Premature separation of the placenta, which can be partial or complete.
Bleeding can be concealed (internal) or evident (vaginally).
High maternal and fetal morbidity and mortality rates; affects approximately 1 in 75 to 1 in 226 pregnancies.
Risk Factors for Placental Abruption
Maternal hypertension or vascular problems.
Cocaine use or blunt external trauma.
Tobacco abuse and previous abruption.
Thrombophilia (blood clotting disorders).
Clinical Manifestations of Placental Abruption
Bright red vaginal bleeding (may be concealed).
Painful: abdominal pain, uterine tenderness, contractions, and uterine hypertonicity.
Can result in a board-like abdomen (uterus).
Diagnosis and Maternal/Fetal Outcomes of Placental Abruption
Diagnosis: typically via ultrasound showing separation and bleeding.
Maternal Outcomes: depend on the extent of placental detachment, overall blood loss, and coagulopathy.
Fetal Outcomes: may include IUGR, preterm birth, possible neurological defects (cerebral palsy), or fatal outcomes post-birth due to SIDS.
Management of Placental Abruption
Critical nursing assessment is crucial!
Monitor pain, bleeding amount, fetal status (electronic fetal monitoring immediately), and uterine tone.
Laboratory evaluation: hemoglobin and hematocrit (H&H), decreased coagulation factors, type, and cross-match.
Time Critical: Prepare for an emergency cesarean section or possible vaginal delivery.
Disseminated Intravascular Coagulation (DIC)
A form of consumptive coagulopathy that consumes clotting factors leading to widespread bleeding.
In pregnancy, potential causes include:
Retained Dead Fetus Syndrome.
Amniotic fluid embolus.
Severe preeclampsia.
HELLP syndrome.
Obstetrical Surgical & Trauma Emergencies
Appendicitis: affects 1 in 1000 pregnancies; requires prompt surgical intervention.
Gallbladder issues: cholelithiasis and cholecystitis often see surgical intervention postponed until postpartum.
Trauma in Pregnancy: occurs in 5-15% of all pregnancies, most commonly due to motor vehicle accidents or falls. Leading cause of non-obstetric maternal death in the U.S. with an increased incidence of domestic violence.
Nursing Considerations for Trauma
Risk of aspiration if the patient is unconscious; elevate the head if possible.
Assess for possible placental abruption (uterine tenderness, pain, bleeding, leaking of amniotic fluid).
Fetal assessment includes monitoring fetal heart tones.
Priority care should stabilize the mother before considering the fetus.