Maternal conditions Notes


Osmosis High-Yield Notes

This Osmosis High-Yield Note provides an overview of Maternal conditions essentials. All Osmosis Notes are clearly laid-out and contain striking images, tables, and diagrams to help visual learners understand complex topics quickly and efficiently. Find more information about Maternal conditions:

Cervical incompetence

Intrauterine growth restriction





Preeclampsia & eclampsia

Gestational diabetes

Gestational hypertension

Hyperemesis gravidarum

NOTES NOTES MATERNAL CONDITIONS GENERALLY, WHAT ARE THEY? PATHOLOGY & CAUSES ▪ Group of disorders occurring during gestation which potentially have adverse maternal, fetal, neonatal health effects DIAGNOSIS OTHER DIAGNOSTICS ▪ Preconception, prenatal, obstetric history ▪ Physical examination of mother; assessment of fetal well-being SIGNS & SYMPTOMS ▪ See individual disorders TREATMENT OTHER INTERVENTIONS ▪ Interventions focused on pregnancy maintenance, fetal viability, safe delivery, reduced neonatal complications CERVICAL INCOMPETENCE PATHOLOGY & CAUSES ▪ The inability of the cervix to retain pregnancy during second trimester → premature cervical os opening, fetal expulsion ▫ In absence of clinical contractions/labor ▪ Usually < 24 weeks of gestation CAUSES ▪ Exact mechanism not well-understood ▫ Involves structural abnormality presence, factors such as infection, inflammatory processes; weaken cervix integrity RISK FACTORS ▪ ▪ ▪ ▪ ▪ ▪ ▫ Loop electrosurgical excision procedure (LEEP), cone biopsy Spontaneous/induced abortion history Previous forceps/vacuum-assisted birth Uterine anomalies Genetic predisposition Defective cervical collagen (e.g. Ehlers– Danlos syndrome) Idiopathic COMPLICATIONS ▪ Premature membrane rupture, birth ▫ Fetal loss, morbidity related to prematurity ▪ Chorioamnionitis ▪ Cerclage procedure ▫ Cervical lacerations ▪ Prior cervical surgery OSMOSIS.ORG 773
TREATMENT SIGNS & SYMPTOMS ▪ Often asymptomatic until pregnancy is lost ▪ Mild symptoms ▫ Pelvic pressure, cramping, backache, vaginal discharge ▪ Signs of painless cervical changes ▫ Shortening, funneling at internal os; cervical canal dilation ▪ Bulging amniotic membranes ▪ Short duration from symptom onset → fetal loss DIAGNOSIS DIAGNOSTIC IMAGING Serial transvaginal ultrasound ▪ Cervical shortening, funneling, dilation in the absence of significant uterine contractions ▫ Findings unexplained by other preterm birth causes ▪ Treatment aimed at reinforcing cervical structural integrity MEDICATIONS ▪ Post-cerclage ▫ Indomethacin: enhances fetal lung development ▫ Progesterone: helps maintain pregnancy SURGERY ▪ Cervical cerclage: concentric suture placement at cervical os (McDonald technique) ▫ 36–37 weeks of gestation → sutures removal ▪ Prior failed cervical cerclage → abdominal cerclage ▫ Circumferential Mersilene tape around uterine isthmus OTHER DIAGNOSTICS ▪ History of recurrent (≥ two) consecutive pregnancy losses/extremely preterm births (<28 weeks) accompanied by no/minimal mild symptoms ▪ Tocodynamometry ▫ Excludes labor Figure 128.1 A transvaginal ultrasound scan of the cervix (outlined) in the sagittal plane demonstrating proximal coning of the cervical canal leaving only 10mm of functional cervix. 774 OSMOSIS.ORG
Chapter 128 Maternal Conditions CHORIOAMNIONITIS (IAI) PATHOLOGY & CAUSES ▪ Intra-amniotic infection (IAI) of fetal membranes, amniotic fluid, fetus, umbilical cord, placenta ▫ Caused by invading microorganism (most often) ▫ Also caused by sterile inflammation (AKA histologic chorioamnionitis) ▫ AKA triple I: intrauterine infection/ inflammation/both; highlights condition heterogeneity ▪ Most common labor/delivery-diagnosed infection; uncomplicated IAI resolves postpartum ▪ Microbial invasion avenues ▫ Vaginal canal most common (e.g. group B Streptococcus, bacterial vaginosis) ▫ Hematogenous spread ▫ Invasive diagnostic procedures (e.g. amniocentesis) ▫ Other organs (e.g. abdomen, fallopian tubes—rare) ▪ Intra-amniotic structure leukocytosis → inflammatory response → cytokine release ▫ Fever RISK FACTORS ▪ Premature/prolonged membrane rupture, frequent pelvic examination, vaginal infection, cervical insufficiency, alcohol/ tobacco use COMPLICATIONS Maternal ▪ ↑ abnormal labor risk ▫ Premature labor, ↑ cesarean delivery risk, ↑ uterine atony risk → postpartum bleeding ▪ ↑ local infection risk ▫ Endometritis, pelvic abscess ▪ Death ▪ Sepsis → disseminated intravascular coagulation (DIC) Neonatal ▪ Preterm birth, related morbidity/mortality ▪ Perinatal asphyxia ▫ Meconium aspiration syndrome (MAS) ▪ Sepsis, septic shock; pneumonia; meningitis ▪ ↑ neurological damage risk ▫ Intraventricular hemorrhage (IVH), cerebral white matter damage → longterm disability (e.g. cerebral palsy SIGNS & SYMPTOMS ▪ ▪ ▪ ▪ ▪ May be asymptomatic Fever Tachycardia (maternal, fetal) Uterine tenderness Amniotic fluid ▫ May have foul odor/appear purulent DIAGNOSIS LAB RESULTS ↑ white blood cell (WBC) count ↑ Erythrocyte sedimentation rate (ESR) Culture (bacteremia) ↑ lactic acid (indicates sepsis) Amniotic fluid ▫ Positive gram stain/culture ▫ ↓ glucose ▫ ↑ WBC count ▪ Inflammatory markers ▫ IL-6, MMP-8; may be present in cervicovaginal fluid ▪ ▪ ▪ ▪ ▪ OTHER DIAGNOSTICS ▪ Histopathologic infection/inflammation evidence (placenta, fetal membranes, umbilical cord vessels) OSMOSIS.ORG 775
TREATMENT MEDICATIONS ▪ Antibiotics, antipyretics SURGERY ▪ Labor-induction/cesarean section OTHER INTERVENTIONS ▪ Continuous intrapartum electronic fetal monitoring ▪ Address maternal, neonatal complications Figure 128.2 The histological appearance of the membranes in a case of chorioamnionitis. The amnion (light pink) and the chorion (dark pink) both display an acute inflammatory cell infiltrate. ECLAMPSIA PATHOLOGY & CAUSES ▪ New-onset generalized, tonic-clonic seizures/coma in association with preeclampsia ▫ Symptomatic of severe end preeclampsia spectrum ▫ May develop any time before/during labor, up to 24 hours postpartum ▪ Seizure pathogenesis not fully understood ▫ May be related to cerebral circulatory autoregulatory disruption, hypo-/ hyperperfusion, endothelial dysfunction, cerebral inflammation, vasogenic/ cytotoxic edema 776 OSMOSIS.ORG RISK FACTORS ▪ Severe preeclampsia (may occur with “mild” preeclampsia) ▪ Nulliparity ▪ Non-white people of European descent ▪ Lower socioeconomic background ▪ Peak incidence ▫ Adolescents, biologically-female individuals in their early 20s; risk ↑ > 35 years COMPLICATIONS ▪ Status epilepticus (eclampticus), placental abruption, intrauterine asphyxia, maternal/ fetal death
Chapter 128 Maternal Conditions DIAGNOSIS SIGNS & SYMPTOMS Seizure ▪ May be preceded by certain signs/ symptoms ▫ May occur in asymptomatic individual ▫ Headache: persistent, frontal, occipital, thunderclap ▫ Visual disturbances: scotoma, cortical blindness, photophobia, blurred vision, visual field defect (e.g. homonymous hemianopsia) ▫ Right upper quadrant (epigastric) pain ▫ Ankle clonus Generalized tonic-clonic seizure onset ▪ Tonic phase ▫ Abrupt consciousness loss; extremities/ chest/back stiffening; possible cyanosis ▪ Clonic phase ▫ Muscle twitching/jerking; frothy/bloody sputum may be present ▪ Postictal phase ▫ Muscle movements stop ▪ Responsiveness resumes (usually) within 10–20 minutes; neurologic findings may include altered mental status, memory/ visual deficits, ↑ deep tendon reflexes Fetal seizure response ▪ Bradycardia → tachycardia + heart rate variability loss → maternal/fetal stabilization → improvement ▪ Clinical diagnosis based on new-onset of seizure in preeclamptic individual DIAGNOSTIC IMAGING MRI ▪ Can visualize posterior reversible encephalopathy syndrome (PRES) ▪ Patchy T2/FLAIR hyperintensity in subcortical white matter; also in adjacent parietal, occipital lobes’ gray matter ▪ Posterior cerebral hemispheres show localized vasogenic edema TREATMENT MEDICATIONS ▪ Antihypertensives ▪ Seizure prophylaxis ▫ Magnesium sulfate IV; diazepam/ lorazepam SURGERY ▪ Prompt delivery ▫ Induced vaginal/cesarean (gestationdependent) OTHER INTERVENTIONS ▪ Supplemental oxygen GESTATIONAL DIABETES (GDM) PATHOLOGY & CAUSES ▪ Glucose intolerance onset during pregnancy → maternal, fetal hyperglycemia ▫ Adverse fetal/neonatal effects depend on glycemic derangement degree/ duration ▪ Normal pregnancy: characterized by progressive insulin resistance, pancreatic β-cell hyperplasia ▫ Hyperplasia: influenced by chorionic somatomammotropin (hCS) AKA human placental lactogen (hPL) ▪ Gestational diabetes develops when insulin resistance overcomes pancreatic β-cell OSMOSIS.ORG 777
ability to maintain normoglycemia ▪ Resistance begins in second trimester, peaks in third (fetal weight gain) ▫ Maternal hormonal, metabolic changes support steady glucose supply for fetal growth, cell proliferation, tissue development, differentiation. ▫ After fetus, placenta delivery → hCS no longer produced → ↓ pregnancyassociated insulin resistance ▪ Maternal hyperglycemia → fetal hyperglycemia → macrosomia (birth weight > 90th percentile on population-appropriate growth chart/> 4kg/8.82lbs) ▫ Hyperinsulinemia → ↓ surfactant production → impaired lung development ▫ ↑ fetal metabolic rate → ↑ oxygen consumption → fetal hypoxemia → metabolic acidosis ▫ ↑ erythropoiesis → polycythemia → hyperviscosity; iron redistribution secondary to accelerated erythropoiesis → ↓ iron available for developing organs → cardiomyopathy, altered neurodevelopment (reactive oxygen species → cardiac remodeling → transient hypertrophic cardiomyopathy) RISK FACTORS ▪ Respiratory distress ▫ ↓ fetal surfactant development ▪ Hypoglycemia ▫ Hyperinsulinemia + placental glucose delivery loss ▪ Hyperbilirubinemia ▫ Polycythemia, excess red blood cell (RBC) breakdown ▪ ↑ stillbirth risk ▫ Often cardiomyopathy + ↓ ability to tolerate macrosomia-related difficult labor → failure to progress, shoulder dystocia → perinatal asphyxia ▪ ↑ obesity risk (later in life) SIGNS & SYMPTOMS Maternal ▪ May be asymptomatic ▪ Severe hyperglycemia manifests with polyuria, polydipsia, polyphagia Neonatal (infant of diabetic mother) ▪ Low APGAR score ▪ Large for gestational age; > 4kg/8.82lbs ▪ Plethora ▪ Hypoglycemia (may be jittery on delivery) DIAGNOSIS ▪ Polygenic influence; age > 25 years; nonwhite people of European descent; BMI > 25kg/m²; polycystic ovary syndrome; hypertension; multiple gestation; personal/ family glucose-intolerance history; previous macrosomic infant/unexplained fetal loss DIAGNOSTIC IMAGING COMPLICATIONS Pulse oximetry ▪ Neonatal: ↓ oxygen saturation Maternal ▪ ↑ risk of preeclampsia, polyhydramnios, developing type 2 diabetes mellitus Neotatal ▪ Macrosomia/large for gestational age (LGA) ▫ ↑ cesarean delivery risk; ↑ shoulder dystocia risk → ↑ maternal trauma risk (e.g. lacerations, hematoma); fetal birth trauma (brachial plexus injury, facial palsy, clavicular/humeral fractures, cephalohematoma, subdural hematoma) 778 OSMOSIS.ORG Fetal ultrasound ▪ Prenatal: fetal size, weight estimation LAB RESULTS Prenatal (maternal) ▪ Glucose tests: random capillary glucose, fasting glucose, hemoglobin A1c, oral glucose tolerance testing (OTT) ▪ Serum, urinary ketone bodies
Chapter 128 Maternal Conditions Postnatal ▪ Maternal: serial capillary glucose tests (hyperglycemia initially → resolving after placenta delivery) ▪ Neonatal: blood studies (↓ glucose; ↑ hematocrit; ↑ bilirubin; possible ↓ calcium, magnesium) OTHER DIAGNOSTICS ▪ Postnatal: neonatal weight, gestational age assessment; physical examination TREATMENT MEDICATIONS Prenatal ▪ A2 GDM (requires medical management) ▫ Insulin as required to reach blood glucose target (does not cross placenta) ▫ Oral antidiabetic agents (crosses placenta) Postnatal ▪ Maternal: continue glucose medical management until normalization ▪ Neonatal: supplemental oxygen, oral/ intravenous glucose SURGERY Prenatal ▪ Elective cesarean delivery (estimated fetal weight ≥4.5kg/9.92lbs) OTHER INTERVENTIONS Prenatal ▪ Serial nonstress tests, amniotic fluid index (AMI) ▪ A1 GDM (maintains euglycemia via lifestyle modification) ▫ Labor induction: between 40+0–41+0 weeks of gestation ▪ A2 GDM (requires medical management) ▫ Labor induction: 39+0 weeks of gestation (39+0–39+6 if glucose is well-controlled) GESTATIONAL HYPERTENSION PATHOLOGY & CAUSES ▪ New hypertension onset; develops ≥ 20 weeks of gestation ▫ Systolic blood pressure (≥ 140mmHg)/ diastolic blood pressure (≥ 90mmHg) ▫ No proteinuria/new end-organ dysfunction evidence ▫ Usually resolves by postpartum week 12 ▫ Exact mechanism unclear COMPLICATIONS ▪ Preeclampsia development SIGNS & SYMPTOMS ▪ ↑ blood pressure (≥ 140mmHg)/diastolic blood pressure (≥ 90mmHg) ▪ Severe gestational hypertension (≥ 160mmHg)/diastolic blood pressure (≥ 110mmHg) RISK FACTORS ▪ ↑ prevalence in primigravidas (first pregnancy) ▪ Genetic factors OSMOSIS.ORG 779
DIAGNOSIS LAB RESULTS ▪ Urine dipstick ▫ Negative/trace protein amounts ▪ Normal platelet count ▪ Creatinine, hepatic transaminases ▫ Normal OTHER DIAGNOSTICS ▪ Clinical exclusion diagnosis ▫ Established when preeclampsia eliminated as hypertension cause ▪ Focused history ▫ Cerebral/visual disturbance absence; epigastric/right upper quadrant pain absence Figure 128.3 Histological section of the placenta from an individual with hypertension during pregnancy displaying hypertrophic decidual vasculopathy. There is hypertrophy of the smooth muscle layer and numerous perivascular inflammatory cells. This may also be seen in pre-eclampsia. 780 OSMOSIS.ORG TREATMENT MEDICATIONS ▪ Antihypertensives, antenatal corticosteroids OTHER INTERVENTIONS ▪ Delivery timed in accordance with individual status ▪ Ongoing maternal monitoring ▫ Blood pressure ▫ Proteinuria ▫ Platelet count, liver enzymes ▪ Ongoing fetal well-being monitoring ▫ Biophysical profile/nonstress test ▫ Measure amniotic fluid index (AFI) ▫ Uterine, umbilical artery doppler velocimetry ▫ Monitor fetal growth signs (placental insufficiency)
Chapter 128 Maternal Conditions HYPEREMESIS GRAVIDARUM PATHOLOGY & CAUSES DIAGNOSIS ▪ Exaggerated, protracted nausea/vomiting in early pregnancy ▪ Incidence: 1 in 200 pregnancies (Western countries) ▪ Usually between week 4–8 of gestation ▪ May last ≥ 16 weeks DIAGNOSTIC IMAGING CAUSES ▪ ↑ Blood urea nitrogen (BUN), creatinine; urea/creatinine ratio > 25:1; ↓ potassium, sodium; ↑ hematocrit, pH ▪ Urinalysis ▫ ↑ specific gravity, ketones ▪ Multifactorial ▫ E.g. pregnancy-induced hormonal changes, pregnancy-related gastric motility ↓ + other individual factors RISK FACTORS ▪ ▪ ▪ ▪ ▪ Previous hyperemesis gravidarum ↑ human chorionic gonadotropin (hCG) Multiple pregnancy, hydatidiform mole Biologically-female fetus Hyperthyroidism (may be hCG ↑ triggered) COMPLICATIONS ▪ Dehydration, weight loss, electrolyte imbalance, metabolic alkalosis (HCl loss orally), ketosis, Mallory–Weiss esophageal tear (violent vomiting), intrauterine growth restriction (if prolonged) SIGNS & SYMPTOMS ▪ Frequent, severe nausea; vomiting ▪ Dehydration ▫ Tachycardia, palpitations, hypotension, postural hypotension, dry mucous membranes, ↓ skin turgor ▪ ↑ smell sensitivity ▪ Malaise ▪ Weight loss ▪ Ketotic odor Pelvic ultrasound ▪ Excludes molar pregnancy; identifies multiple gestation LAB RESULTS OTHER DIAGNOSTICS ▪ Excessive vomiting history ▫ Sufficient to cause clinically-evident dehydration TREATMENT MEDICATIONS ▪ Antiemetics (off-label for pregnancy) ▪ Vitamin B6 ▫ ↓ nausea ▪ Fluid, electrolyte replacement OTHER INTERVENTIONS ▪ Trigger avoidance ▫ Consume small, frequent meals ▫ Bland food (avoid spicy/greasy food) OSMOSIS.ORG 781
INTRAUTERINE GROWTH RESTRICTION PATHOLOGY & CAUSES ▪ Full fetal growth not accomplished during gestation → ↑ morbidity, mortality risk ▪ AKA fetal growth restriction TYPES ▪ Symmetric ▫ Effects begin early in gestation ▫ Most commonly intrinsic factors (infection, chromosomal abnormality) ▫ Uniform effect (all organ systems) ▫ Body/head circumference, length, weight restricted proportionally ▪ Asymmetric ▫ Affects fetus in late second/third trimester ▫ Commonly ↓ nutrition delivery to fetus (limits glycogen, fat storage; brain sparing) ▫ Head circumference (normal), length (near normal), weight (significantly affected) CAUSES ▪ Fetal factors ▫ Genetic (e.g. aneuploidy, single gene mutations) ▫ Infection (e.g. cytomegalovirus (CMV), toxoplasmosis; rubella) ▫ Multiple gestation (e.g. nutrientcompetition by > one fetus) ▪ Placental factors ▫ Ischemic placental disease (e.g. preeclampsia) ▫ Structural anomalies (e.g. single umbilical artery) 782 OSMOSIS.ORG ▪ Maternal factors ▫ Chronic disease (e.g. renal, cardiac, pulmonary disease) ▫ Substance use/abuse (e.g. alcohol, cigarettes, illicit drugs) ▫ Poor nutritional status/inadequate weight gain ▪ Environmental factors ▫ Teratogen exposure, pollution ▫ Certain maternal therapeutic medication COMPLICATIONS ▪ Preterm birth, related sequelae (e.g. necrotizing enterocolitis, respiratory distress syndrome) ▪ Intrauterine asphyxia ▫ ↓ physiological reserve → poor response to temporary hypoxia secondary to uterine contractions ▫ ↑ meconium aspiration risk → pulmonary hypertension ▪ Impaired thermoregulation ▫ ↓ subcutaneous tissue + ↓ catecholamines (used in non-shivering thermogenesis via brown fat) → ↑ cold stress risk → hypoxia, hypoglycemia, metabolic acidosis ▪ Hypoglycemia ▫ ↓ glycogen, fat, protein reserves ▪ Polycythemia ▫ Chronic hypoxia ▪ Impaired immune function ▫ Inadequate nutrition-related ▪ Hypocalcemia ▫ ↑ serum phosphate load from tissue catabolism, ↓ nutrition, renal insufficiency ▪ ↑ mortality risk
Chapter 128 Maternal Conditions SIGNS & SYMPTOMS ▪ General postnatal appearance ▫ Thin, loose skin; ↓ subcutaneous tissue, skeletal muscle; thin umbilical cord ▪ ↓ weight, length, head, chest circumference ▫ Asymmetric growth restriction (head circumference may be normal; will appear large relative to trunk, extremities) DIAGNOSIS DIAGNOSTIC IMAGING Ultrasound biometry (prenatal) ▪ Correlate estimated date of confinement (EDC) with fetal parameters ▫ Sonographically-estimated fetal weight (SEFW) ▫ Head: biparietal diameter (BPD), head circumference (HC), transcerebellar diameter (TDC) ▫ Abdominal circumference (AC): AC/HC ratio ▫ Amniotic fluid index (AFI): oligohydramnios present if placental pathology Doppler velocimetry (prenatal) ▪ Measure circulatory status ▫ Vascular resistance, placental/cardiac function) LAB RESULTS ▪ Blood studies (postnatal) ▫ ↓ capillary glucose level, serum calcium; ↑ hematocrit OTHER DIAGNOSTICS ▪ Postnatal diagnostics Ponderal index ▪ Low; asymmetric growth restriction especially ▪ Body weight:length ratio ▫ PI = [weight (in g) x 100] ÷ [length (in cm)]3 Ballard score ▪ Gestational age assessment ▫ Small for gestational age ▪ Includes weight, head, chest circumference; physical maturity, neuromuscular maturity indicators TREATMENT MEDICATIONS ▪ Glucose ▫ Intravenous/oral/early feeding OTHER INTERVENTIONS ▪ Maintain neutral thermal environment OSMOSIS.ORG 783
MASTITIS PATHOLOGY & CAUSES ▪ Localized infection: one/more mammary ducts, usually associated with lactation LAB RESULTS ▪ Leukocytosis ▪ Breast milk culture ▫ Identifies causative microorganism CAUSES ▪ Infectious ▫ Microorganism introduction: transferred from breastfeeding infant’s mouth/nose (commonly Staphylococcus aureus, Streptococcus spp.) ▪ Noninfectious ▫ Milk stasis: prolonged engorgement, infrequent/inefficient feedings, clogged ducts RISK FACTORS ▪ Cracked/damaged nipples, poor hygiene, ineffective breastfeeding technique, impaired immunity, diabetes COMPLICATIONS ▪ Infection progression, abscess formation SIGNS & SYMPTOMS ▪ ▪ ▪ ▪ ▪ Localized firmness, redness, swelling, heat Palpable lump Breast pain Tender/enlarged axillary nodes Flu-like symptoms ▫ Fever, malaise, myalgias DIAGNOSIS DIAGNOSTIC IMAGING Ultrasound ▪ Identifies abscess presence 784 OSMOSIS.ORG Figure 128.4 An ultrasound scan of the breast demonstrating a breast abscess, a complication of mastitis. TREATMENT MEDICATIONS ▪ Analgesics ▪ Antibiotics (if conservative measures ineffective) OTHER INTERVENTIONS ▪ Ice, cold compress application ▪ Continue breastfeeding/manual extraction ▪ Lactation consultant referral
Chapter 128 Maternal Conditions OLIGOHYDRAMNIOS PATHOLOGY & CAUSES ▪ ↓ amniotic fluid volume surrounding fetus for gestational age ▫ Can adversely affect fetal development CAUSES ▪ Amniotic fluid production, movement imbalance ▫ ↓ placental blood flow, ↓ fetal urine production, ↑ amniotic fluid loss → ↓ amniotic fluid volume ▫ ↓ fluid cushioning effect → ↑ umbilical cord compression risk ▫ Restricted fetal movement → ↓ musculoskeletal development ▫ Fetal thorax compression → ↓ pulmonary development ▫ ↓ amniotic fluid bacteriostatic effect → ↑ infection risk RISK FACTORS Maternal ▪ Hypertensive disorders, diabetes, preeclampsia, abnormal placentation → uteroplacental insufficiency ▪ Premature rupture of membranes (PROM), amniotic fluid leak → fluid loss ▪ Maternal medications (e.g. ACE inhibitors, NSAIDs) ▪ Post-term pregnancy Fetal ▪ Renal/urinary tract anomalies (e.g. renal agenesis), restricted growth, fetal death → ↓ fetal urine production ▪ Congenital anomalies (e.g. aneuploidy, cardiac, preferential perfusion to brain at kidney’s expense) COMPLICATIONS ▪ Amniotic band syndrome ▫ Adhesions between amnion, fetus → limb malformation, amputation ▪ Limb position defects (e.g. club foot) ▪ Pulmonary hypoplasia → respiratory distress ▪ Multiple anomalies (Potter sequence) ▫ Pulmonary hypoplasia, oligohydramnios, twisted skin/face, extremity malformation, renal agenesis ▪ Chorioamnionitis ▪ Low birth weight ▪ Meconium aspiration syndrome (MAS) ▪ ↑ fetal/neonatal mortality risk SIGNS & SYMPTOMS ▪ Uterine size/fundal height less than expected for gestational age ▪ Easily palpated fetus ▪ ↓ fetal movement DIAGNOSIS ▪ Targeted history, physical examination → identify specific cause DIAGNOSTIC IMAGING Uterine ultrasound ▪ ↓ amniotic fluid index (AFI) ▫ < 5cm/1.97in total; single deepest pocket < 2cm/0.79in ▪ Amniotic fluid measurement in deepest pocket in each uterine quadrant ▪ Sum of each maximum vertical pocket = AFI OSMOSIS.ORG 785
Fetal ultrasound + biophysical profile ▪ Detects fetal anomalies; assesses degree of fetal well-being LAB RESULTS ▪ Amniotic fluid leak detection: nitrazine, fern tests, AmniSure TREATMENT OTHER INTERVENTIONS ▪ ↑ intrauterine-fluid volume ▫ Maternal hydration ▫ Amnioinfusion POLYHYDRAMNIOS PATHOLOGY & CAUSES ▪ Excessive amniotic fluid amount surrounding fetus for gestational age ▪ Can adversely affect fetal development CAUSES ▪ Amniotic fluid production, movement imbalance ▪ ↑ placental blood flow ▪ ↑ fetal renal perfusion, urine production ▪ ↓ fetal amniotic fluid swallowing/absorption ▪ Idiopathic RISK FACTORS Maternal ▪ Diabetes; chronic/gestational Fetal ▪ Gastrointestinal anomalies (e.g. duodenal, esophageal, intestinal atresia ) ▪ Central nervous system abnormalities ▪ High cardiac-output state ▪ Twin-twin transfusion syndrome ▪ Nonimmune hydrops ▪ Genetic ▫ Aneuploidy, trisomy 18 or 21 COMPLICATIONS Maternal ▪ Placental abruption, umbilical cord prolapse, postpartum uterine atony → hemorrhage, upward diaphragm pressure → respiratory distress Fetal ▪ Preterm birth, fetal anomalies SIGNS & SYMPTOMS ▪ Uterine size/fundal height ↑ than expected for gestational age ▪ Difficulty palpating fetal parts DIAGNOSIS DIAGNOSTIC IMAGING Uterine ultrasound ▪ AFI ≥ 24cm/9.44in ▪ Single deepest pocket ≥ 8cm/3.1in Fetal ultrasound + biophysical profile ▪ Detects fetal anomalies; assesses degree of fetal well-being OTHER DIAGNOSTICS ▪ Focused history, physical examination → identify specific cause 786 OSMOSIS.ORG
Chapter 128 Maternal Conditions TREATMENT ▪ Treatment determined by gestational age, amniotic fluid excess severity, symptom presence, cause MEDICATIONS ▪ Indomethacin ▫ Severe polyhydramnios, preterm labor onset ▫ Fetal antidiuretic response via endogenous vasopressin production ▫ Short duration with monitoring → avoids ductus arteriosus constriction SURGERY ▪ Severe polyhydramnios, preterm labor onset ▫ Amnioreduction (decompression amniocentesis) ▫ Amniotic fluid removal (amniocentesis) Figure 128.5 A fetal ultrasound scan demonstrating polyhydramnios. There is a large hypoechoic region between the fetus and the maternal abdominal wall. There is also the double-bubble sign of duodenal atresia, which is the underlying cause in this case. OTHER INTERVENTIONS ▪ Mild polyhydramnios ▫ Expectant management PRE-ECLAMPSIA PATHOLOGY & CAUSES ▪ New-onset hypertension, proteinuria/endorgan dysfunction > 20 weeks of gestation ▪ Preeclampsia (severe) characteristics ▫ ↑ ↑ blood pressure; thrombocytopenia; hepatic, renal abnormalities; cerebral/ visual dysfunction; pulmonary edema ▫ Often resolves days/weeks after delivery CAUSES ▪ Abnormal placentation ▫ Abnormal spiral artery remodeling into shallow, narrow arteries instead of normally deeply implanted, large, low-resistance arteries → placental, fetal hypoperfusion → gestational age progression → worsening hypoperfusion ▪ Ischemic placenta → release proinflammatory proteins into maternal circulation → generalized endothelial dysfunction → ↑ reactivity to circulating vasoconstrictors + ↓ endogenous vasodilators production + ↑ vascular permeability + abnormal procoagulant expression ▫ Hypertension ▫ Target-organ microangiopathy (kidneys, liver, brain) OSMOSIS.ORG 787
▫ Intravascular fluid leakage into interstitium ▫ Microangiopathic intravascular hemolysis ▫ Placental thrombosis, sclerosis, infarction RISK FACTORS Positive preeclampsia family history Previous pregnancy preeclampsia Nulliparity Age > 40 Biologically-female individuals of AfricanAmerican descent ▪ Chronic disease (e.g. hypertension, diabetes, systemic lupus erythematosus, antiphospholipid syndrome) ▪ ↑ body mass index (BMI) ▪ Assistive reproductive technology use ▪ ▪ ▪ ▪ ▪ COMPLICATIONS Maternal ▪ Cerebral edema/hemorrhage; stroke; hepatic failure; renal failure; hemolysis, elevated liver enzymes, low platelet count (HELLP) syndrome; placental abruption; eclampsia; liver rupture; posterior reversible encephalopathy syndrome (PRES); death Fetal ▪ Intrauterine growth restriction, premature birth, fetal demise SIGNS & SYMPTOMS ▪ Hypertension ▫ Vasoconstriction ▪ Epigastric pain ▫ Liver capsule swelling (advanced disease sign) ▪ Peripheral edema, dyspnea ▫ ↑ vascular permeability ▪ Oliguria, proteinuria ▫ ↓ glomerular filtration rate (GFR), glomerular damage ▪ Severe headache, altered mental status ▫ Cerebrovascular pathology 788 OSMOSIS.ORG ▪ Visual disturbances ▫ E.g. photopsia (flashes of light), scotoma (dark areas/gaps in visual field), blurred vision (retinal arteriolar spasm) ▪ Hyperreflexia, ankle clonus ▫ Neuromuscular irritability ▪ Sudden, rapid weight gain ▫ Fluid retention DIAGNOSIS DIAGNOSTIC IMAGING Pulse oximetry ▪ ↓ oxygen saturation Ultrasound ▪ Fetal ▫ Intrauterine growth restriction, oligohydramnios ▪ Placenta ▫ Infarction, hematoma, cystic lesion ▪ Uterine, umbilical artery doppler studies ▫ ↑ flow resistance ECG ▪ ↓ left ventricular function; ↑ filling pressure LAB RESULTS ▪ Proteinuria ▪ ↑ serum creatinine, liver transaminases, indirect bilirubin; ↓ platelet count ▪ Hyperuricemia ▪ Peripheral blood smear ▫ Schistocytes, helmet cells OTHER DIAGNOSTICS ▪ Low fetal biophysical profile score TREATMENT MEDICATIONS ▪ Antepartum ▫ Antenatal steroids: promote fetal lung development
Chapter 128 Maternal Conditions ▪ Intrapartum ▫ Intravenous magnesium sulfate: bolus, then continuous infusion (seizure prophylaxis) ▫ Intravenous antihypertensives: maintain normal blood pressure ▪ Postpartum ▫ Continue intravenous magnesium sulfate infusion until stable SURGERY ▪ Antepartum ▫ Labor induction/cesarean delivery: progressive placental function deterioration, disease advancement (preeclampsia with severe pathological features) OTHER INTERVENTIONS ▪ Antepartum ▫ Regular maternal status, fetal wellbeing assessments ▪ Intrapartum ▫ Electronic fetal monitoring ▫ Supplemental oxygen OSMOSIS.ORG 789

Osmosis High-Yield Notes

This Osmosis High-Yield Note provides an overview of Maternal conditions essentials. All Osmosis Notes are clearly laid-out and contain striking images, tables, and diagrams to help visual learners understand complex topics quickly and efficiently. Find more information about Maternal conditions by visiting the associated Learn Page.