Keeler: Obstetrical hemorrhage, GDM and PPROM Flashcards
preggo crazy bleeding, still have fetal heartbeat, dx?
Placenta previa
Abruptio placentae
Vasa previa
US = total placenta previa
(no evidence for “invasive” placenta)
gal has placenta previa and lots of bleeding. What do we do for it?
Steroids given Bleeding slowed/stopped Admitted for prolonged antepartum stay @ 36 weeks, amniocentesis = + FLM Low vertical cesarean delivery
Placenta previa info- risk factors, types, signs
Multiparity, adv maternal age, infertility Tx
Non-white, smoking, cocaine, male baby??
Prior C/S - red light red light red light
Partial, total, marginal, low lying
Second trimester US will find it
No digital exam unless results of 2nd tri US are known
Painless bleeding after 20 weeks
preggo in car accident, abdomen diffusely and markedly tender, no rebound. 30 minutes later– prolonged FHR deceleration with increase in pain and more bleeding
what do we do?
immediate c section under gen anesthesia
50% of maternal surface of placenta ended up being occupied by clotted blood
this was abruptio placentae
Abruptio placentae (Abruption) associated stuff
Associated with HTN/PIH, trauma, smoking, cocaine abuse, some - etiology = unclear
Varying degrees
Delivery – it depends on the case
Can have DIC, massive blood loss
gal has great normal delivery. after placenta 1 L of blood, what’s the possible ddx?
Uterine atony
Retained placental fragment
Obstetrical laceration
The four T’s
Tone, trauma, tissue, thrombus
post partum hemorrhage (PPH) – atony – a different physiology
“Hemostasis” after birth is achieved because the MYOMETRIUM contracts and closes off the SPIRAL ARTERIES that feed the placental bed.
Thus is a “mechanical” event and not a “biochemical” event (coagulation = biochemical)
what we can do for post-partum hemorrhage
Massage/evacuate clots Intrauterine exam Bimanual massage Extra oxytocin Methylergonovine (Methergine®) IM Inspect for lacerations (above perineum) – none are found
what to do when usual measures fail for postpartum hemorrhage
Bleeding continues, or abates only to resume
Curettage for fragment
Code “White”
Prostaglandin agonists (Cytotec PO/PR, Hemabate IM) see 2 slides hence……..
Bakri balloon
Embolization in radiology ????? - NOT for massive acute PPH
finally: Ligation hypogastric (internal iliac) arteries
“B-Lynch” suture
HYSTERECTOMY - have the COURAGE to do this in time !!!!!!!!!!!!!!!!!!!!!!!!!
Prostaglandins for PPH
Cytotec (misoprostol) = analog of prostaglandin E
Hemabate (carboprost) = analog of prostaglandin F2α. ** Do not use this one if patient has asthma. This one can also cause fever and diarrhea. **
PPH risk factors….
Multiparity IOL Prolonged labor – or rapid labor (<3 hrs) Prior hx of PPH Use of oxytocin, esp prolonged Older maternal age Large infant, overdistended uterus Multiple gestations Magnesium sulfate Chorioamnionitis Leiomyomata (fibroids) Halogenated anesthetics
“Uneventful” labor and delivery then... As placenta delivers, mother…….. Takes a deep breath, coughs up a little blood Turns dusky and pale Eyes roll back in head Becomes unintelligible BP = 80/P P = 140 SAO2 = 83% on RA – O2 immediately started
most likely dx?
AFE =
Amniotic fluid embolism
Anaphylactoid reaction of pregnancy
Exact pathophysiology is unclear!!
AFE
Sudden hypoxia + CV collapse
Profound DIC
Massive blood loss
90+% mortality
AFE - Tx
Get help – a LOT of help
Second IV line/central line
Massive transfusion protocol (1:1:1 of packed red cells, platelets, FFP)
** “Rescues” have been reported with HEART-LUNG MACHINE. Busy OB units have pre-arranged with CV Dept for this
** Early recognition is vital
eklampsis means
a shining forth or
strikes like lightning
Maternal physiology gone off the rails!
some terminology about eclampsia
Toxemia (no “toxin” ever discovered)
Pre-eclampsia
Pregnancy-induced hypertension = “PIH”
17 y/o preggers with high BP, pretibial edema, narrowing of arterioles in retina
PIH, pre-eclampsia, etc.
admit, induce labor.
expect post partum hemorrhage due to MgSO4
Pre-eclampsia - facts
Leading cause of maternal morbidity/mortality worldwide
Up by 25% in US in past 20 years
At risk for future CVD + metabolic disorders
risk factors for pre-eclampsia
Nulliparity Hx of PIH Age < 18, >40 \+ FHx Chronic HTN/renal dis Thrombophilias Vascular/CT diseases Diabetes/ high BMI Multiple gestation African-Am race Male history Fetal hydrops IUGR/ mom was LBW Long interval between Molar pregnancy ? Genetic mutation ? Partner factors Suggestive hx in prior Pg
Diagnosis of HTN
Pre-eclampsia / Eclampsia
(aka “Pregnancy-Induced Hypertension” = PIH)
Chronic HTN (existed before Pg, or < 20 wks)
Chronic HTN w/ “superimposed” pre-eclampsia
“Gestational hypertension”
Triad of Pre-eclampsia
Hypertension > 140/90 after 20 weeks
Proteinuria > 0.3gm/24H (~ 1+ dip)
Edema
physiology of pre-eclampsia
Fundamental process = VASOSPASM
Why? How?
Theory after theory after theory
Mysterious correlation w/ HCG + trophoblast, increased w/ twins, molar pregnancy
Mysterious “male factor”??
Goals with pre-eclampsia
Term or near-term birth Prevent significant IUGR Prevent abruption of placenta Prevent maternal seizures or CVA Prevent rupture of maternal liver capsule
ONLY ONE CURE for pre-eclampsia
DELIVER THE BABY !!!!!!
THUS, YOU ALSO DELIVER THE PLACENTA !!
pre-eclampsia DELIVERY - WHEN
Once the Dx is made, it becomes “all about” “how soon can we get this baby delivered?”.
Factoring in: prematurity, fetal condition, maternal condition
When does risk (of waiting) become > the risk of ACTING?
“Severe Pre-eclampsia” – any 1 of:
BP > 160/110
Platelets < 100,000
Liver impairment (RUQ pain or 2x ↑ in transaminases)
Renal impairment (creatinine > 1.1 mg/dl)
Pulmonary edema
(New) cerebral or visual disturbances
HELLP
hemolysis
elevated
liver-function tests
low Platelet count
if we have Severe pre-eclampsia or HELLP is going on…
The FUSE is LIT
DELIVERY is indicated !
May or may not be “time” for steroids
Get MFM consult liberally
May or may not be time for IOL
Ancillary treatments for pre-eclampsia
Remember – ultimate TX = delivery
Seizure prophylaxis = MgSO4 through delivery + 24-48 hours after
Hypertension control – hydralazine IV – don’t “bottom it out”
HTN control – labetolol PO
Prenatal overwatch (pre-eclampsia)
A big goal of prenatal care is to find this complication EARLY – if you suspect it:
More frequent visits
Rest
US for growth
Baseline labs – CBC, LFT’s, Cr, 24 hr urine
Counseling as to Sx to watch for, esp HA and RUQ/epigastric pain
pre-eclampsia: Beware the “headache”
HA’s = very common
This Sx should always → check BP
Ask about vision – scotomata, blurry, double?
HA, esp w/ visual disturbances may be a sign of cerebral edema and a warning about impending ECLAMPSIA
pre-eclampsia: Beware the “swelling”
“Swelling” is very common and normal
Sudden-onset of new swelling and weight gain is a warning sign – see patient that day!
Rest may help
A/C in summer may help
“NAS” diet = borderline help
pre-eclampsia: Beware the RUQ !!
Acid reflux (GERD) and GB sx are common Reported RUQ or epigastric pain should be treated as an emergency!
See pt immediately
A potential WARNING SIGN of expansion of liver capsule and impending RUPTURE. = The worst-imaginable catastrophe.
pre-eclampsia: Beware of Post-partum!
Delivery is great, but……
The DANGER is not over!!!!
Pre-eclampsia can seem to be getting better, only to WORSEN after patient goes home
*** Some cases do not even begin until post-partum
Good News about pre-eclampsia
Usually a disease of First term pregnancy
Usually does not mean HTN-for-life
Usually OK to use OCP’s after
MgSO4
write it out in hand-written notes so as not so confuse with MSO4, morphine sulfate
goals in treating gestational diabetes
Reduce birth defects
Reduce/dx early – pre-eclampsia
Reduce hydramnios (aka “polyhydramnios”)
Reduce/eliminate stillbirths
Reduce macrosomia (→ a ↓ in C/S, shoulder dystocia)
Reduce neonatal hypoglycemia/hypocalcemia
TWO Types of diabetes in pregnancy
Gestational = “GDM”
“Pre-existing” DM
White classifications – no test questions
Pre-conception control + planning = critical
Gestational DM – risk factors
GDM in prior pregnancy High BMI Prior large infant (> 9 lbs) Prior shoulder dystocia Family Hx of (any) DM Older age (30? 35? 40?)
Gestational DM - screening
“Challenge” test all by 28 weeks “GCT” = glucose challenge test 50 gm glucose, get plasma glucose = “BS” one hour later Fasting/special diet not necessary (Limiting conc. CHO’s may ↓ false +) under 130-140 = normal
GDM - workup
If GCT is abnormal……….
If ≥ 140 but < 200 —– do 3 hour GTT
If > 200, do NOT do GTT – may get ↑↑ BS
If > 200, you have your dx
If + dx: LFT’s, BMP, HgbA1C
GDM management
Strongly consider med endocrinology consult
Diet ~ 2500 Cal
Self-monitoring
FBS HgbA1C each visit
Dietitian/nutritionist, endocrinol NP
Diet may not be enough: insulin, glyburide po
GDM – OB monitoring
Serial US to assess growth (not absolute)
FM chart
Warn about pre-eclampsia sx
NST’s weekly, biweekly – when to start? (34)
IOL at term
(C/S if EFW > 4000 gm)
Pre-existing DM (Or, “early dx” GDM)
Control is the goal 2 week visits, weekly in 3rd tri Monitoring (FM, NST, US) starts sooner Assess FLM Role of “early” delivery
GDM – postpartum + beyond
GDM moms are @ higher risk of DM later
FBS + HgbA1C @ 6 week PP appt
Recheck annually
importance of FHT/FHR
it is a VITAL SIGN
gal thinks her water broke early. DDX?
PPROM
Urinary incontinence
Vaginal discharge
Perspiration
testing results in PPROM
alkaline pH
Estrogen causes salt in fluid to crystallize in a unique pattern: fern testing
PPROM
accounts for ~1/2 of preterm births
PROM = Premature Rupture of Membranes (defined as prior to onset of labor) PPROM = Preterm PROM (<37 weeks)
“mid-trimester PROM” = PROM between 14 and 26 weeks (pre-viable)
PROM risk factors
Genital tract infections Previous PPROM Antepartum bleeding Cigarette smoking/cocaine Mechanical Stress Most patients have no identifiable risk factors
Not so fun FACTS about PPROM
About 1/3 of women with PPROM develop potentially serious intrauterine infections Increased risk of: - Placental abruption - Umbilical cord prolapse - Pulmonary hypoplasia
Tx = Expeditious delivery, esp if after 34 weeks
PROM - Expectant vs Delivery
If < 24-26 weeks – delivery
If 26-34 weeks – expectant
If 34+ weeks - delivery
Surfactant
It’s all about SURFACE TENSION
Soap bubble effect in the ALVEOLI
HMD = hyaline membrane disease = collapse of alveoli due to low surface tension
Surfactant in alveoli keeps them expanded!!
Steroids and surfactant
Liggins and Howe, British physiologists
Late 1960’s
Fetal lambs, intentional premature delivery
Steroids to ewe = much less premature lung disease in her premature lambs
“Fools” alveolar lining into producing surfactant
UC inhibitors used to allow steroids to work
