Pathophysiology 2 Flashcards
Eclampsia
- presence of new-onset grand mal seizures in a woman with preeclampsia
- more likely in cases in which new-onset seizures occur after 48-72hrs postpartum
Causes of seizures in addition to eclampsia?
- bleeding arteriovenous malformation
- ruptured aneurysm
- idiopathic seizure disorder
Pathophysiology of Hemotologic Changes?
-both thrombocytopenia and hemolysis may occur as part of unknown HELLP syndrome (unknown etiology)
Effect of Preeclampsia on baby?
- impaired uteroplacental blood flow or placental infarction
- intrauterine growth restriction
- oligohydramnios
- placental abruption
- non-reassuring fetal status demonstrated on antepartum surveillance
Treatment of Preeclampsia?
-delivery: balance both maternal/fetal risks
How common is HTN in pregnancy?
12-22%
What % of maternal deaths is HTN responsible for?
17.6%
HTN disorders of Pregnancy?
- Gestational HTN (PIH)
- Preeclampsia
- Superimposed Preeclampsia
- Eclampsia
Gestational HTN
- BP>140/90 after 20 wga
- no protein
- NL BP within 12 weeks postpartum
- 25% of women with gestational hypertension will develop proteinuria (preeclampsia)
Hysterotomy
-like a C/S but need to get the baby out
Herpes Virology
- large, enveloped, double-stranded DNA virus
- glycoproteins 1 & 2 differentiates HSV 1 & 2
- replicated in host cell
- can form latent infection in dorsal root ganglion
HSV Epidemiology
-among most common STD
-HSV 1: 75-90% abs by age 10
-HSV 2: 25-60% reported prevalence of abs in young women, seroprevalence correlates with number of sexual partners
80% of new genital infections may be caused by HSV 1, may have surpassed HSV 2 as primary cause of genital herpes
HSV Epidemiology in Pregnancy
-incidence of new 1 or 2 in pregnancy is 2%
-about 10% of women who are seronegative have + partners
-with recurrent HSV
75% will have at least 1 recurrence during pregnancy
14% will have prodromal symptoms or lesions at delivery
Risk factors of HSV
- minority ethnicity
- previous genital infection
- lower family income
- # of sexual partners
- duration of sexual activity
HSV Treatment in Pregnancy
- at 37 weeks go on suppression therapy
- Acyclovir & Valacyclovir
Suppression therapy of HSV
- > 6 episodes a day that isn’t pregnant
- 1 or more episodes in pregnancy
- ACOG-pregnant women with history of recurrent HSV
- if mother is -, partner is + give suppression to partner
Invasive procedures in HSV
- if active: cesarean delivery
- if no lesions: “reasonable” to sue fetal scalp monitoring if indicated, invasive monitoring increases risk of neonatal infection
CMV Virology
- double stranded DNA enveloped
- Member of B-herpesvirus group
- primary & latent infections
CMV risk factors in pregnancy
- lower socioeconomic status
- birth outside US
- first pregnancy < 15 years old
- child care workers
- families with young children
Diagnosis of Maternal CMV
- incubation period: 28-60 days
- viremia can be detected 2-3 weeks following primary infection
- lab abnormalities: leukocytosis, lymphocytosis, elevated transaminases
Congenital CMV
- vertical transmission (transplacental infection, exposure to contaminated genital tract secretions during delivery, breastfeeding)
- hematogenous spread of virus across placenta (GREATEST RISK)
Diagnosis of CMV in pregnancy?
ultrasound
Ultrasound findings in CMV?
- cerebral calcifications
- microcephaly
- ventriculomegaly
- hepatosplenomegaly
- ascites
- hydrops
- echogenic bowel
- growth restrictions
- oligohydramnios
KEY points of diagnosis of CMV?
- amniotic fluid for PCR is more sensitive than culture
- fetal blood sampling is less sensitive than fluid
- fetal infection may occur weeks to months after maternal infection (may need to repeat testing)
- timing of testing important (21 weeks, likely due to immaturity of fetal immune system & lag b/w maternal & fetal infection)
- detection of CMV in the amniotic fluid does not predict severity of disease
What predicts the severity of CMV?
-how early the baby was exposed in womb (early worse)
Intrauterine growth restriction is?
- a fetus who fails to reach its growth potential
- less than 10th percentile of weight class (linked to morbidity & mortality)
Extrinsic Risk Factors of Intrauterine Growth Restriction
- Maternal Health: HTN, renal disease, constrictive lung disease, diabetes, cyanotic heart disease, collagen-vascular disease, hemoglobinopahties
- smoking/substance ebuse
- severe malnutrition
- infections
Intrinsic Risk Factors of Intrauterine Growth Restriction
- aneuploidy
- genetic syndromes
- congential anomalies
- primary placental disease
- multiple gestation
Maternal Vascular Disease: Intrauterine Growth Restriction
- 25-30% of all IUGR
- most common cause of IUGR in nonanomalous infants
- decrease in uteroplacental perfusion
- most common etiology (early onset severe preeclampsia, CHTN/SIP)
Maternal Nutrition Abnormalities: Intrauterine Growth Restriction
- first dem. in WWII in Russia/Holland
- birth weight declined when under nutrition occurred in 3rd
- also gave evidence to importance of prepregnancy nutritional status
- 10,000ft, cyanotic heart disease, hemoglobinopahties, chronic pulmonary disease
Infection: Intrauterine Growth Restriction
- Rubella (60%), capillary endothelial damage, hypoplasia, necrotizing angiopathy
- CMV - cytolysis, localized necrosis of organs
- Toxoplasma gondii, Plasmodium, Trypanosoma cruzi, syohilis
- Bacterial infections have not been linked
Placental Disease: Intrauterine Growth Restriction
-placental weight increases throughout gestation
-not to same degree as fetal weight
-IUGR placentas 24% smaller when compaired to AGA
(chorioangioma, placenta previa, abnormal cord insertions)
Toxins/Teratogens: Intrauterine Growth Restriction
- tobacco
- alcohol ingestion
- cocain
- anticonvulsants (phenytoin)
- warfarin
- heroin
Biophysical Profile of Fetal Wellbeing
- Tone: extension with rapid return to flexion
- Gross body movement: 4 discrete body movements in 30 min
- Fetal Breathing movement: 30 sec of breathing, intermittent, hiccups cont.
- Amniotic Fluid Evaluation: one pocket >2cm without cord
Genetic Factors: Intrauterine Growth Restriction
-overall chromosomal/multifactorial anomalies account for 20% of IUGR
-if early onset IUGR (<26 wks) up to 25% have abnormal karyotype (trisomy 13, 18, 21, Turners)
-cardiac malformations, anencephaly, pyloric stenosis
INTRINSIC
Multiple Gestation: Intrauterine Growth Restriction
TTTS Congential anomalies maternal comlications multifetal reduction growth rate differences INTRINSIC
Diagnosis of IUGR: Ultrasound
- fetal biometry (HC/BPD/AC/FL): best if growth followed at 2-4 week intervals
- Amniotic fluid volume: deepest pocket/AFI both acceptable
- Doppler studies
- Biophysical Profile
- Amniocentesis for genetic/infectious etiology
Diagnosis of IUGR: Fetal biometry
- confirms weight at less than 10th percentile
- should be followed by serial growth (if interval <2 weeks, risk or erroneous values)
Criteria for Diagnosis of Preeclampsia
- systolic bp >140, diastolic >90 at more than 20 weeks of gestation in a women with previously normal blood pressure
- proteinuria (0.3g protein or higher in 24hr urine)
- may be associated with myriad other signs and symptoms, such as visual disturbances, headache, & epigastric pain, & edema
Lab abnormalities in Preeclampsia
-hemolysis
-elevated liver enzymes
-low platelet counts
(HELLP syndrome)
Disgnosis of Severe Preeclampsia
1 or more
- BP>160 (systolic), >110 (diastolic) (at least 2 times, 6hr apart on bed rest)
- > 5g protein in 24hrs or 3+ greater on 2 random urine samples collected more than 4 hrs apart
- oliguria of less then 500mL in 24hrs
- serum creatinine>1.2mg/dL
- cerebral or visual distrubances
- pulmonary edema/cyanosis
- epigastric or right upper-quadrant pain
- impaired liver function (elevated AST/ALT)
- microangiopathic hemolysis, increased LDH
- thrombocytopenia, platelets less than 100,000
Diagnostic Criteria for Superimposed Preeclampsia
- new onset proteinuria >300mg/24hrs in a women with HTN before 20 weeks of gestation, but no proteinuira prior to 20wga
- a sudden increase in proteinuria if already present in early gestation
- a sudden increase in HTN or dev. of HELLP syndrome
- onset of headache, scotomata, or epigastric pain
Risk factors for Preeclampsia
- primigravida
- multifetal gestations
- H/o preeclampsia
- chronic hypertension
- pregestational diabetes
- vascular/connective tissue disease
- nephropathy
- antiphospholipid antibody syndrome
- BMI >34 or <19.8
- 35 or older
- African-American race
- may have genetic basis
- thrombophilias
Pathophysiology of Preeclampsia
- invasion by the trophoblast appears to be incomplete
- severity of HTN may be related to degree of trophoblastic invasion
1. abnormal trophoblastic invasion of uterine vessels
2. immunological intolerance b/w maternal & fetalplacntal tissue
3. maternal maladaptation to cardiovascular or inflammatory changes in pregnancy
4. dietary deficiencies
5. genetic influences
Hemotologic changes in preeclampsia
- both thrombocytopenia & hemolysis may occur as part of HELLP syndrome, etiology is unknown
- hematocrit may be very low because or very high secondary to hemoconcentration in absence of hemolysis
- lactate dehydrogenase is present in erythrocytes in high conc. (or a sign of hemolysis)
HELLP Syndrome
- hemolysis
- elevated liver enzymes
- low platelets
Hepatic Changes in Preeclampsia
- hepatic function may be altered
- alanine aminotransferase & aspartate aminotransferase may be elevated
- hyperbilirubinemia
- hepatic hemorrhage (subcapsular hematoma)
- rare: hepatic rupture (high mortality)
Incidence of HELLP with preeclampsia?
-20%
HELLP increases risk of?
- placental abruption
- renal failure
- subcapsular hepatic hematoma
- recurrent preeclampsia
- preterm delivery
- fetal or maternal death
Neurologic issues with preeclampsia?
- intracranial hemorrhage
- temporary blindness (hours to week)
- headache
- blurred vision
- scotomata
- hyperreflexia
Treatment of Preeclampsia
- delivery
- continued observation with preterm fetus (if mild)
- weekly nonstress tests, biophysical profiles
- testing twice weekly for suspected fetal gorwth restriction or oligohydramnios
- ultrasound every 3 weeks
- platelet count, renal function, urine protein - repeat as needed
Treatment with HELLP syndrome
-delivered regardless of gestational age
Management of preeclampsia during labor
- prevent seizures
- control of HTN
(Mg sulfate)
Peripartum Cardiomypathy
- development of cardiac failure in the last month of pregnancy or within 5 months after delivery
- absence of an identifiable cause for the cardiac failure
- absence of recognizable heart disease prior to the last month or pregnancy
- left ventricular systolic dysfunction demonstrated by classic echocardiographic criteria such as depressed shortening fraction or ejection fraction
Diagnosis of Peripartum Cardiomyopathy
- diagnosis of exclusion
- similar to those in nonpregnant adults
- acute disease
Risk Factors for Peripartum Cardiomyopathy
- CHTN
- Superimposed Pre-E
- obesity
- obestiy + CHTN
- H/o Peripartum Cardiomyopathy
- AMA
- Extremes of Age
- AA
- Multiple Gestation
- Genetic???
Most common cause of heart failure during pregnancy?
-chronic HTN with superimposed preeclampsia
Obesity and Peripartum Cardiomyopathy
- common cofactor with chronic HTN (cause/contribute to underlying ventricular HTN)
- Framingham increased by 2x risk in nonpregnant
Dilated Cardiomyopathy is also found in???
HIV
Signs/Symptoms of Congestive Heart Failure
- dyspnea
- orthopnea
- cough
- palpitations
- chest pain
Clinical Findings of Peripartum Cardiomyopathy
- impressive cardiomegaly
- echo show EF less than 45%
Management for Peripartum Cardiomyopathy
- treatment for heart failure
1. Diuretics: reduce preload
2. Hydralazine: reduce afterload (vasodilator)
3. Digoxin: intropic effects (unless complex arrhythmias) - prophylactic heparin: thromboembolism
Short Term Prognosis for Peripartum Cardiomyopathy
-immediate mortality rate is approximately 2%
Long Term Prognosis for Peripartum Cardiomyopathy
-long term mortality is significant (5-10 yr survival is lower in nonpregnant patients with idiopathic cardiomyopathy)
100% vs 25%
-peripartum that regain ven. function within 6 months have god prognosis (if not, bad)
-if ejection fraction is <50%, be reserved to have another baby
Diagnosis of IUGR
- Clinical Evaluation (fundal height, searching for etiologies)
- Ultrasound (growth, anatomy, genetic testing, amniotic fluid, doppler studies, antenatal testing)
Clinical Evaluation of IUGR
- fundal height for screening only (PE alone misses/inaccurate about 50% of time)
- important in evaluating risk factors
- often with gives an index of suspicion for IUGR
- prompt examination if concern for lagging growth
Diagnosis of IUGR: Amniotic Fluid
- oligohydramnios
- single deepest pocket <5cm
Diagnosis of IUGR: Oligohydramnios
- result of chronic hypoxia with blood diverted from kidneys to vital organs
- increased risk of perinatal mortality
- normal fluid less likely to end in demise
Management of IUGR: Doppler Ultrasonography
-important tool: reduction in number of antenatal admission
induction of labor is decreased
cesarean section for distress is reduced
reduction in perinatal death
Doppler: Umbilical Artery
-placental vascular resistance
reversed flow when >70% of arteries are obliterated
Doppler: Middle Cerebral Artery
-detect “brain sparing effect”
increased blood flow directed away from abdominal organs to the brain
Doppler: Venous Circulation
-reflect cardiac dysfunction
Doppler: Uterine Arteries
-used in high risk pregnancies to predict IUGR, preeclampsia
Components of Doppler Assessment
- arterial circulation: umbilical artery, middle cerebral artery
- venous circulation: umbilical vein, ductus venosus
Delivery Management with HSV
- important facts to remember when managing HSV in pregnancy
- risk of transmission to neonate during primary infection at the time of delivery (30-60%)
- risk of transmission to neonate during recurrent infection at time of delivery 1-3%
- cesarean delivery doesn’t completely prevent vertical transmission
HSV Cesarean Delivery
- active lesions
2. prodromal symptoms-culcar pain & burning w/history of HSV
Women w/history of genital HSV but no active genital lesions at time of delivery?
- risk of vaginal transmission is very low
- sterile speculum exam for lesions
- non-genital lesions should be covered w/occlusive dressing
PPROM
- premature pre-rupture of membranes
- seen with HSV
Risk factors for CMV infection
- 11% childcare workers seroconvert in 10 months of hire
- families with young children
Risk for Congenital CMV
- primary CMV in pregnancy - 1/2 will infect fetus
- risk of transmission is greatest when infection occurs in 3rd trimester
- severe fetal injury is greatest when infection occurs in 1st trimester
- recurrent CMV in pregnancy: 5-10% will infect fetus (rarely symptomatic fetus)
Clinical Manifestations of CMV
- not highly contagious: saliva, urine, sexual, transplantation of organ
- asymptomatic
- mono-like syndrome: fever, malaise, myalgia, chills, cervical lymphadenopathy
- sever: pneumonia, hepatitis, guillian-barre, aseptic meningitis
Diagnosis of Maternal CMV
-serologic studies
CMV specific IgM (first) & IgG (long term)
CMV IgG avidity (how long has it been around, if <25% previous 3 months)
-PCR of blood, urine, salvia, amniotic fluid, cervical secretions
Diagnosis of CMV in pregnancy
- serum samples collected 3-4 weeks apart & tested in parallel CMV spec. IgG
- sero conversion from - to +
Is CMV IgM reliable?
- not completely
1. may not be + during acute infection
2. may persist for several months after primary inf
3. may be + with recurrent infection
4. should not be used alone to diagnose
Treatment of CMV in Pregnancy
- no therapies available
- antiviral treatment with ganciclovir is approved for treatment of CMV retinitis in women with AIDS
- live attenuated vaccine-concern about the ability of the vaccine to reactivate & infect the host
