Maternal-Fetal Medicine
224
Maternal-Fetal Medicine
224Paperback
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Overview
Product Details
| ISBN-13: | 9780521709347 |
|---|---|
| Publisher: | Cambridge University Press |
| Publication date: | 07/30/2007 |
| Series: | Cambridge Pocket Clinicians |
| Pages: | 224 |
| Product dimensions: | 4.96(w) x 7.09(h) x 0.43(d) |
Read an Excerpt
Cambridge University Press
978-0-521-70934-7 - Maternal–Fetal Medicine - by Mary E. D’alton, Errol Norwitz and Thomas F. Mcelrath
Excerpt
ACUTE ASTHMA EXACERBATION
BAKGROUND
■ 4% of adult population has asthma
■ In general, sx often worsen during 28–36 wk of pregnancy; acute exacerbations rare in last 4 wk or in labor
DIAGNOSIS
History
■ Sx include cough, dyspnea, wheezing; fever, chills, malaise less common
■ Ask about prior attacks, current Rx, baseline peak expiratory flow rate (PEFR), precipitating events (upper respiratory tract infection, allergen exposure)
Physical examination
■ Check temp, pulse oximetry (note: pulse oximetry does not assess pt’s ability to clear CO2)
■ Examine for cyanosis, hyperinflation, use of accessory muscles, pulsus paradoxus
Diagnostic tests
■ Laboratory tests: ABG, CBC
■ Specific diagnostic tests: decrease in PEFR, FEV1
■ Screening tests: daily PEFR
DIFFERENTIAL DIAGNOSIS
■ Pulmonary edema
■ Pulmonary embolism
■ Bronchitis
■ Pneumonia
COMPLICATIONS
■ Maternal complications: respiratory failure, preterm birth
■ Fetal complications: prematurity, low birthweight, increased perinatal mortality (esp. w/ severe disease)
PROGNOSIS
■ Pregnancy represents a state of compensated respiratory alkalosis; maternal PCO2 >=35 mmHg in room air suggests impending respiratory failure
MANAGEMENT
General measures
■ O2 supplementation to maintain O2 saturation >=95%, PO2 >=70%
■ Continuous pulse oximetry to follow oxygenation
■ Adequate hydration
■ Serial ABGs
SPECIFIC TREATMENT
■ Inhaled beta-2-agonist (bronchodilator) Rx q 20–30 min * 3 doses
■ If initial response adequate (ie, increase in PEFR to >=70% predicted or baseline, if known), continue bronchodilator Rx & follow as outpatient
■ If response inadequate, continue Rx for 2–3 h; consider admission for measured PEFR <70% predicted
■ Consider Ⅳ corticosteroid Rx for PEFR 40–70% baseline (or predicted) after 2–3 h
■ Stress-dose steroids (Ⅳ hydrocortisone 80 mg q8h) in labor if history of steroid Rx in last 6 mo
Contraindications
■ Cardiogenic disease relative contraindication to beta-agonist Rx
Side effects & complications of treatment
■ Maternal adrenal suppression (can be avoided w/ stress-dose steroids in labor)
Follow-up care
■ Regular outpatient visits
■ Referral to pulmonologist
SUBSEQUENT MANAGEMENT
■ Severity & frequency of acute exacerbations similar in subsequent pregnancies
ACUTE CYSTITIS
BACKGROUND
■ Most common medical complaint of pregnancy
■ Incidence: 1–4% of all pregnancies
■ Organisms: Escherichia coli (90%), Staphylococcus saprophyticus (4–7%)
DIAGNOSIS
History
■ Sx may include frequency, dysuria, urgency, suprapubic pain
■ Risk factors: diabetes, urinary tract anomaly, prior urinary tract infection/pyelonephritis in index pregnancy, sickle cell trait/disease
Physical examination
■ Suprapubic tenderness
■ Flank pain, costovertebral angle tenderness, fever, systemic complaints usually absent
Diagnostic tests
■ Urine dip can be positive for nitrates, leukocyte esterase
■ Definitive Dx made by urinalysis (>=100,000 colony-forming units/mL of single pathogenic organism in midstream clean-catch urine specimen)
■ Imaging studies not indicated
■ Check CBC if patient febrile
DIFFERENTIAL DIAGNOSIS
■ Mycotic/bacterial vaginosis w/ contamination of urine specimen
■ Asymptomatic bacteriuria
■ Pyelonephritis
COMPLICATIONS
■ Maternal complications: progression to pyelonephritis, urosepsis, ARDS, preterm labor
■ Fetal complications: preterm birth, low birthweight
PROGNOSIS
■ Full resolution can be expected w/ adequate Rx; increased risk of pyelonephritis/urosepsis if Rx inadequate
■ Screening/treatment prevents 80% of pyelonephritis in pregnancy
MANAGEMENT
General measures
■ Aggressive oral hydration
■ Outpatient Rx acceptable in absence of pyelonephritis
Specific treatment
■ Antibiotic Rx for 3 d adequate for otherwise healthy women (consider 5-d course for women w/ concurrent chronic disease); single-dose Rx assoc. w/ increased failure rate in pregnancy
■ Rx options include trimethoprim/sulfamethoxazole 160/180 mg po bid, nitrofurantoin monohydrate/macrocrystals 100 mg po bid, cephalexin 500 mg po qid
■ Adjust Rx according to culture results, if indicated
Prevention
■ Periodic screening urinalysis in women at high risk for urinary infections
SUBSEQUENT MANAGEMENT
■ Repeat urine culture in 10 d after completion of Rx (“test of cure”)
■ If Rx unsuccessful, consider noncompliance, failed Rx (poor antibiotic selection, antibiotic resistance)
■ Consider suppressive Rx for 6 wk if repeat culture positive w/ same organism.
AMNIOTIC FLUID EMBOLISM
BACKGROUND
■ Rare, unpredictable, catastrophic obstetric event
■ 10% of maternal mortality in U.S.
■ Incidence: 1/8,000–1/85,000 births
DIAGNOSIS
History
■ Prodromal sx may include sudden chills, sweating, anxiety
■ Risk factors: multiparity, advanced maternal age, hypertonic labor, male fetus, intrauterine fetal demise, oxytocin, am-niotomy, abruption, intrauterine pressure catheter, chorioamnionitis, cesarean, preeclampsia, intrauterine saline injection (abortion)
Physical examination
■ Clinical: Dx characterized by acute-onset respiratory distress, cyanosis, hypotension, tachycardia, hypoxemia, neurologic manifestations (seizures, coma), hemorrhage in labor/delivery or early puerperium
Diagnostic tests
■ Laboratory tests: check CBC, DIC panel
■ Specific diagnostic tests: clinical Dx, identification of amniotic fluid (mucin, fetal squames) in pulmonary vasculature at postmortem not pathognomonic
■ Imaging: check CXR, V/Q scan (shows decreased perfusion); of little value in acute setting. Transesophageal ultrasound useful in acute assessment of pulmonary embolism in intubated pt.
DIFFERENTIAL DIAGNOSIS
■ Pulmonary embolism
■ Pulmonary edema
■ Venous air embolism (assoc w/ ruptured uterus, placenta previa, persistent atrial septal defect)
■ Aspiration
■ Eclampsia
■ Drug overdose/withdrawal
■ Other causes of DIC
COMPLICATIONS
■ Maternal complications: shock, DIC, blood transfusion; very high maternal mortality rate (60–90%), permanent neurologic sequelae (85% of survivors)
■ Fetal complications: intrauterine fetal demise, hypoxic ischemic cerebral injury if fetus undelivered
PROGNOSIS
■ Death not inevitable if early Dx, aggressive management, including intubation and possible pulmonary bypass
MANAGEMENT
General measures
■ High index of suspicion, early Dx
■ Monitor vital signs, O2
■ Anesthesia consult, central hemodynamic monitoring, Ⅳ access
■ Immediate delivery regardless of gestational age
■ Rx primarily supportive
Specific treatment
■ CPR, Rx hypoxemia (supplemental O2, mechanical ventilation)
■ Control bleeding (correct DIC, uterotonic Rx)
■ Correct anemia/coagulopathy w/ aggressive blood product transfusion
■ Maintain arterial PO2 >60 mmHg, O2 saturation >90%; Rx bronchospasm (terbutaline, aminophylline, ? steroids)
■ Maintain SBP >90 mmHg, urine output >25 mL/h; inotropic support (dopamine) as needed
Contraindications
■ Regional anesthesia contraindicated in acute setting; general endotracheal anesthesia for cesarean
➢ Airway management crucial and intubation highly likely
➢ Pressor support likely to be acutely needed
➢ May require pulmonary bypass
■ Avoid heparin in established DIC
SUBSEQUENT MANAGEMENT
■ Recurrence rate not clear, likely low.
ANTENATAL FETAL TESTING
BACKGROUND
■ Goal: early identification of fetus at risk for preventable morbidity due to hypoxemia
■ Assumptions: (1) hypoxemia leads to permanent injury; (2) tests discriminate between asphyxiated, nonasphyxiated fetuses; (3) early detection can prevent adverse outcome
■ At most, 15% of cerebral palsy due to intrapartum hypoxemia
DIAGNOSIS
History
Indications for testing:
1. Maternal factors: diabetes, hypertension, hyperthyroidism
2. Fetal factors: intrauterine growth restriction, increased fetal activity, oligo/polyhydramnios
3. Pregnancy-associated: placental abruption, postterm pregnancy
Physical examination
■ Usually unhelpful
Diagnostic tests
1. Fetal movement charts (“kick counts”): count all movements in 1 h or count time for 10 kicks; 2–3 times/d; any decreased movement requires further evaluation
2. Contraction stress test (CST): measures response of fetal heart rate to contractions (3/10 min required to interpret test); (+) CST defined as decelerations w/ >=50% contractions
3. Nonstress test (NST): changes in fetal heart rate pattern w/ time; reflects maturity of fetal autonomic nervous system; absence of reactivity (2 accelerations of 15 bpm * 15 sec in 20 min) depends on gestational age: 50% at 24–28 wk, 15% at 28–32 wk
4. Biophysical Profile (BPP): NST + 4 sonographic variables: breathing >=30 sec/30 min, movements >=3/30 min, tone (flexion/extension) >=1/30 min, amniotic fluid volume >=2 cm single vertical pocket
DIFFERENTIAL DIAGNOSIS
Causes of irreversible cerebral injury other than hypoxia:
■ Congenital abnormalities
■ Intracerebral hemorrhage
■ Infection
■ Drugs
■ Trauma
■ Hypotension
■ Metabolic (thyroid, hypoglycemia)
COMPLICATIONS
■ Maternal complications: increased cesarean delivery rate
■ Fetal complications: iatrogenic prematurity due to false-positive testing
PROGNOSIS
■ Negative predictive value (intrauterine fetal demise <1 wk following (–)/reassuring testing) consistent for all tests at 0.3–1.9/1,000 pregnancies
■ Positive predictive value varies widely; severely abnormal fetal testing associated w/ adverse outcome in only 25–40% of cases
■ Interpret testing in light of gestational age, underlying clinical risk factors, congenital anomalies
MANAGEMENT
General measures
■ All antenatal tests probably equally efficacious
Contraindications
■ Contraindications to CST: preterm premature rupture of membranes, previa, preterm labor, prior cesarean
SUBSEQUENT MANAGEMENT
■ Specific to suspected pathology.
ANTIPHOSPHOLIPID ANTIBODY SYNDROME
BACKGROUND
■ Autoimmune disorder characterized by circulating antibodies against membrane phospholipid & one or more specific clinical syndromes
■ Incidence depends on population screened (0.5–3% of nonpregnant, 2–4% of pregnant, & 4–5% of women w/ prior pregnancy loss have low-titer anticardiolipin antibody [ACA] IgG; among women w/ recurrent pregnancy loss, 5–20% have moderate to high titer ACA, & 5–10% are + for lupus anticoagulant [LAC])
DIAGNOSIS
Two elements are required for Dx:
1. Appropriate clinical setting:
➢ Recurrent pregnancy loss
➢ Unexplained thrombosis
➢ Autoimmune thrombocytopenia
➢ ? Preeclampsia
➢ ? Intrauterine growth restriction
AND
2. A confirmatory serologic test:
➢ LAC is an unidentified antibody causing increases of phospholipid-dependent coagulation tests (aPTT, Russel Viper Venom test) by binding to prothrombin-activator complex; in vivo, LAC causes thrombosis; LAC results reported as present or absent (no titers)
➢ Specific antiphospholipid antibodies measured by ELISA (most commonly ACA) assoc. w/ anticoagulant activity in vitro but procoagulant activity in vivo; ACA IgM alone &/or low-positive IgG may be nonspecific; moderate to high levels of ACA IgG required for Dx
➢ ACA & LAC similar but not identical antibodies; may coexist in vivo (70–80% of women w/ LAC are ACA (+); 10–30% of ACA (+) women have LAC)
➢ False-positive test for syphilis common but not sufficient to make Dx of antiphospholipid antibody syndrome (APS)
DIFFERENTIAL DIAGNOSIS
■ SLE (10–30% of women w/ SLE have antiphospholipid antibodies; 60–90% of women w/ APS are ANA (+) but w/ insufficient criteria for Dx of SLE)
■ Other causes of thrombocytopenia
© Cambridge University Press