OB Review

Placenta Accreta

Abnormally adherent placenta Characterized by amount of invasion into the uterine wallPlacenta Accreta VeraAdheres to myometrium without involvement of uterine wall“A’s” Accreta AdheresPlacenta IncretaInvades the uterine myometrium into the muscle“I’s” go together Increta InvadesPlacenta PercretaMost problematicInvades uterine serosa or other structures outside of the pelvis, it penetrates“P’s” Percreta Penetrates

Without prenatal diagnosis placenta accreta may be found after delivery of the baby Surgeon will be unable to remove the placentaHistory of cesarean section and placental previa increases risk Anesthetist should be highly suspicious of presenting parturient with history of cesarean and current

placenta previa Attempting to remove placenta can result in hemorrhageTreatment usually requires hysterectomyPrenatal diagnosis allows the obstetrician to proceed to peripartum hysterectomy, decreasing incidence of

hemorrhage

Two obstetricians maybe present for high risk accreta Diagnosis of previa and accreta are both done with trans vaginal ultra sound

Advancement in diagnoses decrease the occurrence of double set up examsIf unable to dx with ultrasound, obstetrician and anesthesia set up for possible cesarean sectionObstetrician performs a vaginal exam If placental previa dx or bleeding begins, the teams continue with cesarean delivery

Intubation of the OB pt.

• Airway difficulties are often unexpected and are 3x more likely!!• Changes in the airway

• Airway edema• Decreased FRC Increased closing capacity= desat quickly• Increased O2 consumption• Weight gain • Enlarged breasts• Decreased LES tone, increased intragastric pressure• Decreased emptying

• Always considered to be a full stomach and 6 weeks post delivery• Decreased GI motility, decreased food absorption and decreased LES pressure are d/t elevated

levels of circulating progesterone.• Elevated gastrin produced by the placenta increases intragastric pressure resulting in higher risk

for reflux→ always considered full stomach. Also, gastric acid secretion increases secondary to gastrin secretion.

Parameter: % Change:

Diaphragm excursion ↑

Chest wall excursion ↓

Pulmonary resistance ↓ by 50%

FEV1 No change

FEV1/FVC No change

Flow volume loop No change

Closing capacity No change

Pitocin (Oxytocin)

Drug of choice for labor induction, and prevention/treatment of uterine atony Routine use of oxytocin has been shown to reduce the incidence of PPH by as much as 40 percent Exogenous oxytocin stimulates the force and frequency of uterine contractions MOA: Enhances the activation of voltage-gated calcium channels, and increases local prostaglandin production Oxytocin IV infusion is started after placenta delivery in vaginal birth, or immediately after

umbilical cord clamping in cesarean delivery20-30 U added to 1L NS, in continuous IV infusion Bolusing oxytocin IV causes peripheral vasodilation, which can result in hypotension Various EKG changes may occur with oxytocin administration, but they are transient due to oxytocin’s

short plasma half-life

OB ANESTHESIA

Respiratory-----

-Since the diaphragm pushes up against the lungs by expanding uterus- There is a 20% decrease in FRC (Valley) Chestnut claims 25% in ERV and 15% RV- 45% decrease all the way up to 80% of prepreg. Capacity at term!!

-There is NO CHANGE in TLC, VC, and Insp. Capacity cause of increase in thoracic anteropost. Diameter. – How can the body do this? -- Relaxin – relaxes ligamentous attachments of ribs.

-Tidal volume increases by 45%- half of this occurs during first trimester- so with this- increase in minute ventilation obviously

-ESTROGEN plus more blood-----Airway edema!!!!- Capillary engorgement of larynx- begins early- MOST EVIDENT during third trimester, ironic as this is the time we are usually screwing around w/their airway.

- PROGESTERONE is a direct respiratory stimulant- increases MV, increases chemo sensitivity to CO2-

- SO… PROGESTERONE helps cause left-shift of CO2 curve

-There is a respiratory alkalosis- PaCO2 30- metabolic acidosis keeps pH normal.

-PaO2 is higher- higher alveolar ventilation. –CO2 lower- Progesterone, higher PaO2

-ENHANCED uptake of inhaled anesthetics- Increase in O2 consumption- higher alveolar vent and MV, TV, RR- faster uptake of gas

SOOO... challenging airway, prone to mucosal bleeding. Engorge breasts, full dentition and weight gain- good luck with DL. Difficult airway algorithm, have LMA, advanced airway techniques. Better yet, don’t DL at all!

-LOWER MAC- increased MV, decreased FRC. Decreased by 40%.

-Ventilation during general anesthesia adjust so that PaCO2 is maintained at 30mmHg- remember that is their normal level, AND they have a reduced serum bicarb level- so increasing PaCO2 to nonpreg levels will make Acidosis.

Have a smaller ETT 6.5 or 7 and always have 6.0 ready if needed.

DESATURATE FAST!!!! Why? — Less FRC, Increase O2 consumption, and their swollen airways obstruct easy. Why else? --- When lying flat may get venocaval compression- reduction in O2 delivery.

-AIRWAY complications are the LEADING cause of anesthesia related mortality in OB, and the rest of the population for that matter.

PRE-ECLAMPSIA----- Now we are talking retention of extra fluid, low plasma oncotic, ---- TISSUE EDEMA- --- AIRWAY EDEMA, narrowing all the way up to airway compromise.

O2-Hgb dissociation curve lie to right- P50 30.4mmHg vs. normal 26.7mmHg

Higher P50 aids DO2 to uteroplacental unit.

Resp. alkalosis of Preg. Pushes O2-Hbg dissociation to left- increase in 2, 3, DPG- brings curve back to right.

Cardiac changes OB

Pregnancy- Cardiac Hypertrophy- Greater blood volume increased stretch and force of contraction. Eccentric LV hypertrophy- bigger existing cardiomyocytes.

3rd heart sound in 3rd trimester. Benign. S1 accentuation. Elevation of diaphragm- heart shift anterior and to left- PMI displaces to 4th ICS and left to midclavic. Line.

-CO INCREASES to 30-40% during 1st trimester due to increase in HR, decrease in afterload.

-CO during LABOR-

Latent phase 15% increaseActive phase 30% increaseSecond stage 45% increasePOSTPARTUM 80% INCREASE

-Changes in CV System-

Blood volume 35%increasePlasma volume 45% increaseRBC volume 20% increase

Increase in blood volume, however, bigger increase in plasma volume---- Relative Anemia seen in pregnancy

Decrease in PVR seen so HTN doesn’t occur from increased blood volume

Hemodynamics at Term----

CO 50% increase SV 25% increase HR 25% increase LVEDV increase+LVESV unchanged =EF% increase SVR 20% decrease

-Rise in CO- more perfusion to uterus, kidneys, extremities- higher skin temp

Uterine blood flow increase from 50ml/min to 700-900ml/min at term- 90% of this goes to the intervillous space.

Why decrease in SVR? --- Development of low-resistance vascular bed (intervillous space) and vasodilation from prostacyclin, estrogen, and progesterone

-Maternal supine hypotensive syndrome---- Compression of IVC decreases venous return- decreases CO- decreases BP- hypotension.

SOOO----- Venodilation- increase risk of epidural vein puncture

Healthy parturient tolerates up to 1500 blood loss. Transfusion rare.

Higher Hgb of 14 or up- consider low-volume state from pathology- HTN, pre-eclampsia, too much diuretic

- There is a gestational thrombocytopenia- enhanced plt turnover, clotting and fibrinolysis. A state of accelerated, compensated intravascular coagulation Factors XI and XIII DECREASE, Factor I and V unchanged.

GI SYSTEM OB

-Stomach displaced up and to left, axis rotation to left- Esophageal displacement INTO THORAX-

-This REDUCES ton of the lower esophageal high-pressure zone (LEHPZ)

PROGESTINS decrease this zone, and the LES tone, decreases GI motility, food absorption and LES pressure

GASTRIN elevation- Increases gastric acid. Intragastric pressure increase, decreases oblique angle of GE-junction- High risk of GERD.

30-50% pregnant patients get GERD.

-Changes in GI physiology during Pregnancy

Parameter First trimester Second trimester

Third trimester

Labor Postpartum

Barrier pressure

Decrease Decrease Decrease Decrease

Gastric emptying

Unchanged Unchanged Unchanged Delayed Unchanged

Gastric acid secretion

No change or decrease

No change or decrease

No change or decrease

?? increase

Amount of women with gastric volume >25ml

Unchanged Unchanged Unchanged Increased No change

Amount with pH<2.5 gastric

Unchanged Unchanged Unchanged Decreased No change

These patients are ALWAYS considered full stomach and risk for aspiration!!!

ON top of this, narcotics, valium and atropine all further decrease LES tone and increase GI emptying-

Renal OB

Increase in total vascular volume--- renal vascular volume and interstitial volume increase- Enlarged Kidneys

-Hydronephrosis may occur in 80% of women by mid-pregnancy

-GFR and renal plasma flow INCREASE MARKEDLY. GFR increase 50%, plasma blood flow increase 75%.

-GFR does not decrease until 3 months postpartum.

With the above- creat. Clearance increased to 150-200ml/min- this is up from normal `120ml/min.

With the above- reduction in nitrogenous metabolites- BUN decreases to 8-9mg/dlring

Proteinuria also occurs during pregnancy

-GREATER BICARBONATE EXCRETION--- metabolic acidosis- this is a compensatory response to the resp. alkalosis

- With the above- there is a decreased ability to buffer an acid load

Drugs Passing Placenta Review

• The transfer mechanisms used for the transfer of substances across the placental barrier: simple diffusion; simple diffusion through channels; facilitated diffusion; active transport; endocytosis.

• Drug dose.

• Maternal protein binding- reduces the amount of available drug (only free drug will transfer).

• Non-ionized drugs cross the placenta.

• Highly charged drugs do not cross placenta easily NDMR do not cross.

• Rapid biotransformation & excretion speed the decline of drug levels & limit transfer; i.e.: Succinylcholine.

• Route is important ( less drug transfer epidurally than intravenously)

• Dependent on uterine blood flow

• Placental blood flow decreases with uterine contractions

• Molecular weights - heavier molecules do not cross as easily as lighter molecules

• Lipid solubility: the more lipid soluble the molecule, the faster it crosses the placental membrane.

- Fetal academia can result in the ion trapping of both local anesthetics and opioids.

- Drugs that pass placenta - Drugs that don’t pass placentaAnticholinergics- atropine scopolamineAntiHTN agents- B-antagonists, nipride, nitroglycerinBenzos- Diazepam, MidazolamInduction- Propofol, STP, ketamine, methohexital, etomidateAll inhalationalLocal anesthetics----

Amides greatest to least ability to cross-

Mepiv>Etidocaine>Lidocaine>Ropivicaine>Bupivicaine

Ester LAs don’t transfer as much due to metabolization by plasma pseudochol.OpioidsMEPERIDINE- neonate and CNS depressionEphedrine

Anticholinergic- GlycopyrrolateHeparinSuccinylcholineAll NDMRs

OB Review

Stages of labor review,

1st (cervical): perception of regular contractions → complete cervical dilation (10 cm)o Allows fetal movement from uterus to vaginao Active phase, 1st stage: nullipara should dilate cervix at 1.2 cm/hr, parous at 1.5 cm/hro –If pt doesn’t dilate at appropriate rate during active phase, said to have 1o dysfunctional laboro Membranes generally rupture at onset of labor or near full cervical dilation

2nd (pelvic): complete cervical dilation to birth of babyo Cervix completely retracted to form lower uterine segment

o –Full dilationo When complete, increased bloody show and vomiting may occuro Strong uterine contractions w/pushing cause fetal presenting part to descend through pelvis,

resulting in deliveryo 2nd stage > 2 hrs prolonged for nullipara w/out epidural, 3 hrs w/epiduralo Cord arterial pH varies inversely w/length of 2nd stage duration

3rd (placental): birth of baby to placental deliveryo Time from delivery of baby to delivery of placentao •Placenta usually separates from uterine wall w/in few contractions after delivery of babyo •Signs of placental separation:

Uterus rises in maternal abdomen Shape of uterus changes from discoid to globular Umbilical cord lengthens Gush of blood

o •If no separation of placenta after 30 min, or significant bleeding, manual removal indicated If placenta can’t be separated from uterine wall, may have some retention and ↑ bleeding

o •After placenta removed, uterotonic given to decrease bleedingo •Oxytocin 20U/1L

Bolus doses cause hypotensiono •If uterus doesn’t respond, consider methergine 0.2 mg IM

Contracts vascular smooth muscleo •15-methylprostaglandin F2α (Hemabate)

Ecbolic agent 0.25 mg IM can be effective uterotonic

4th (1st 60 minutes after delivery of placenta)o 60 min post deliveryo Pt must be watched closely for bleedingo >90% of postpartum hemorrhage due to uterine atony

Regional in OB...Included how the uterine blood flow is affected,

Neuraxial anesthesia:

Regional strongly preferred Neonatal APGAR scores no different at 5 min, but maternal M&M decreased with regional Considerations:

o Pre-hydrationo FHT monitoringo LUDo Vasopressors : ephedrine ( β sympathetic, α indirect) > Neosynephrine ( pure α ₁ agonist)o T4 sensory block

Local Anesthetics and Uterine Blood flowo Pregnancy may enhance uterine vascular reactivity to local anesthetic agents. Exact mechanism

is unknown.o Clinical experience with the use of local anesthetics; clinical concentrations do not adversely

affect the uterine vasculature.o All local anesthetics can reduce uterine blood flow at plasma concentrations that greatly exceed

those occurring during the routine practice of obstetric anesthesiao Regulatory mechanisms that control flow through the umbilical vessels are poorly understood. o Local anesthetics constrict at lower doses and relax vessels at higher doses. ↓↓ Flow with IV

administration.

o Local anesthetics exert direct effects on uterine smooth muscle. o Local anesthetics cross the placenta.o Local anesthetics are weak bases; they have a relatively low degree of ionization and

considerable lipid solubility at physiologic pH.o Maturation of the placenta may affect the rate of drug transfer. Drugs cross the placenta more

rapidly in late pregnancy. Maternal hypotension= >20% decrease in CO > 2 mins of severe hypotension→ fetal acidosis, lower APGAR scores, prolonged time to sustain

respiration SAB for elective or urgent cesarean delivery Epidural→ when rapid blockade is contraindicated : hypovolemia, hemorrhaging patient; good control

over duration

Spinal for C-section:

Metoclopramide 10 mg IV Oral antacid IV volume expansion w/LR or NS 15-20 ml/kg Apply monitors Supplemental O2 Prophylactic IM ephedrine L3-L4:24 or 22 G Sprotte; 25 or 27 G Whitacre Hyperbaric bupivacaine 12 mg +/- morphine 0.25-0.4 mg for postop analgesia ( or 20 mcg fentanyl or

200 mcg astromorph) Aggressive rx hypotension *Exaggerated L uterine displacement *IV fluids *Ephedrine Complications

o Prurituso Nausea/vomitingo Urinary retentiono Uterine hyper stimulation and fetal bradycardia: presumably due to decrease in maternal

catecholamines with opioids causing uterine hypotonicityo Maternal respiratory depression

Epidural for C-section:

Metoclopramide 10 mg IV Oral antacid Volume expansion w/LR or NS, 10-20 ml/kg Supplemental O2 Epidural catheter at L2-3 or L3-4 L uterine displacement Test dose: why? what to expect, what to give Therapeutic dose

o 5 ml boluses of 2% lido with 1:200K/1:400K epi, oro 5 ml boluses of 0.5% bupivacaine or 3% Nesacaineo Boluses of lidocaine or Nesacaine q 1-2 mino Boluses of bupivacaine q 2-5 min

Aggressive rx hypotension

o Exaggerated LUDo IV fluidso Ephedrine

Nerve and dermatome during stages and pain blocking mechanisms

1st Stage – uterine contraction & cervical dilation

Pain initially @ T11-T12, then progresses to T10-L1 with active labor via visceral afferent nerves Dilating cervix & lower uterine segment along with myometrial contraction against resistance of cervix

and perineum play major role in pain2nd Stage – from end of first stage to delivery of baby

Onset of perineal pain @ end of first stage is signal of fetal descent Pudendal nerves (S2-4) provides the sensory innervation of the perineum via somatic nerve fibers,

therefore the 2nd stage of labor involves T10-S4 dermatomes.3rd Stage – delivery of baby until placenta & membranes expelled

Pain perception involves a complex series of nociceptive transmissions that begin with stimulation of sensory nerves in the periphery, resulting in generation of action potentials within the spinal cord and synaptic transmission to other supraspinal sites.

Intraspinal administration of an opioid exploits the pharmacology of pain-modulating and pain-relieving systems that exist within the spinal cord.

Preeclampsia and magnesium

Magnesium as tocolytic:

Decreases uterine activity during labor Has infrequent cardiovascular side effects, thus is widely used. Although actual mechanism is unknown, calcium antagonism appears to play a role Extracellular Mg++ affects uptake, binding, distribution of cellular Ca++ in vascular smooth muscle→ ↑

intracellular cAMP which inhibits light chain kinase activity and actin-myosin interaction Loading dose = 4 g x 15-20 min Continuous gtt: 1-4 g/hr Serum concentration of 5-7 mg/100 ml needed to inhibit uterine activity •Adverse effects: chest pain, palpitations, nausea, hypotension ( from ↑ed muscle relaxation including

vascular smooth muscle), blurred vision, sedation ( hence, there is a 20% decrease in MAC requirements), pulmonary edema

•Hypermagnesemia results in abnormal neuromuscular functiono Decreases release of ACh at NMJ and sensitivity of endplate to ACh, thus potentiates the action

of both depolarizing and non-depolarizing MRs ( titrate NDMR; avoid defasciculating dose)o May have an effect on platelet function due to calcium antagonism

•Affects action of phenylephrine by increasing uterine vascular resistance →↓UBF; use ephedrine instead

•D/C MgSO4 before epidural (2-4 hrs prior) due to more pronounced hypotension.

Anesthetic Implications of MgSO4

Regionalo Titrate epidural block carefullyo Higher block level + MgSO4 may impair maternal MAP and UBF

•Neuromuscular functiono At motor end plate, Mg++ inhibits Ca++ facilitated presynaptic transmitter release, enhancing

sensitivity to nondepolarizerso Mg++ also potentiates activity of depolarizers

Pre-Eclampsia:

Pregnancy-induced HTNo Preeclampsia

Mild Severe

o Eclampsia Pre-eclampsia

o HTN, proteinuria and/or pathologic edema after 20th week HTN–Diastolic BP at least 90, systolic BP at least 140

Rise of 15 mm Hg diastolic or 30 mm Hg systolic on at least 2 occasions 6 hrs apart

Magnesium as treatment:o Peripheral effects at neuromuscular junctiono Central anticonvulsant effect mediate via NMDA receptors in

hippocampuso Beneficial effects:

Vasodilation, increased cGMP production, attenuation of vascular responses to pressor substances, decreased PRA and ACE levels, increased production of PGI2 by endothelial cells

Severe refractory HTNo Most preeclampsia pts respond well to intermittent boluses of hydralazine

SNP, labetalol, Ca++ channel blockers may all be useful for rx of severe refractory HTN

o ACE inhibitors useful in postpartum periodo Magnesium produces vasodilation

1st line drug before anti-HTN agent Plus proteinuria

≥ 300 mg protein in 24 hr urine collection or ≥ 1 g/L in at least 2 random specimens 6 or more hrs apart

And/or edema Generalized fluid accumulation (> 1+ pitting edema) after 12 hrs bed rest Wt gain of ≥ 5 # (2.27 kg) in 1 wk.

o Severe Symptoms: SBP ≥ 160, DBP ≥ 110 on 2 occasions 6 hrs apart Proteinuria ≥ 5 g in 24 hr urine specimen or 3+-4+ on UA Oliguria: urine output < 400 ml/24hrs

Cerebral or visual disturbances H/A, blurred vision, altered LOC

Pulmonary edema, cyanosis Epigastric or RUQ pain 2o stretching of Glisson’s capsule by hepatic edema Hepatic rupture (rare) Impaired liver function Thrombocytopenia 2̊ platelet adhesion to exposed collagen at sites of endothelial damage

Check Coags before inserting epidural – just because they have platelets doesn’t mean they work well in pre-eclampsia

HELLP syndrome: Hemolysis, Elevated Liver enzymes, Low Platelets Eclampsia:

o convulsions w/out coincidental neurologic disease in pt who meets criteria for preeclampsiao Etiology unknowno 85% of preeclampsia cases in 1st pregnancy. Also associated with:

Higher body mass, multiple gestation, chronic HTN

Magnesium Sulfate is cornerstone of seizure prophylaxis

Loading dose 4-6 g IV over 20 min followed by infusion of 1-2 g/hr

o Pts monitored clinically, e.g., patellar reflexes, respiratory rate, urine outputo Therapeutic range: 4-7 mEq/L

Loss of patellar reflexes: 10 mEq/L Respiratory arrest: 12-16 mEq/L Asystole: > 20 mEq/L If suspected toxicity, D/C immediately & treat w/ IV calcium gluconate or chloride

Acceleration – Abrupt increase above the baseline, duration of >/= 15 seconds but </= 2 minutes from onset to return to baseline. Accelerations are usually associated with either spontaneous fetal activity, stimulation, or uterine activity. Acceleration are GOOD

Decelerations- NOT good, ↓ in HR, shows fetal distress, can’t tolerate the contractionsPeriodic (occurring associated with contractions)Episodic (occurring without an association to contractions)

Early deceleration occur simultaneously w/ uterine contractions

Gradual decrease and return to baseline associated with a contraction; the onset, nadir and offset occur coincidentally with the contraction, with the nadir of the deceleration occurring at the peak of the contraction.

Variable Deceleration

Abrupt decrease in FHR of ≥ 15 bpm lasting ≥ 15 seconds but < 2 minutes. May be periodic or episodic. When associated with uterine contractions (periodic), variable decelerations may vary in onset, depth, and duration from contraction to contraction.

Transient umbilical cord compression

Variable decelerations

Change in maternal position (e.g., left or right lateral or Trendelenburg position), amnioinfusion

Return of umbilical blood flow toward normal

Head compression, usually during the second stage of labor

Variable decelerations Pushing only with alternate contractions

Return of umbilical blood flow toward normal

Late Deceleration → begin after the onset of a uterine contraction.

Hypotension (e.g., supine hypotension, neuraxial anesthesia)

Bradycardia, late decelerations

Intravenous fluids, position change, vasopressor (phenylephrine or ephedrine)

Return of uterine blood flow toward normal

Excessive uterine activity (tachysystole)

Bradycardia, late decelerations

Decrease in oxytocin, lateral position, tocolysis (e.g., terbutaline, nitroglycerin)

Return of uterine blood flow toward normal

Decreased uterine blood flow associated with uterine contractions, below limits of fetal basal oxygen needs

Late decelerations

Change in maternal position (e.g., left lateral position), administration of supplemental oxygen

Tocolysis (e.g., terbutaline, nitroglycerin)

Return of uterine blood flow toward normal, increase in maternal-fetal O 2 gradient

Decrease in contractions or uterine tone, thus abolishing the associated drop in uterine blood flow

Baseline Variability-fluctuations in the baseline FHR of two cycles per minute with peak to trough amplitude.

Absent variability = undetectable amplitude range-> sign of fetal compromise Minimal variability = undetectable but ≤ 5 bpm → sign of fetal compromise Moderate variability = amplitude 6-25 bpm → OK Marked variability = amplitude > 25 bpm → bad, baby is working hard

Sinusoidal baseline

- Regular oscillations with an amplitude range of 5-15 bpm. Frequency of undulations of 2-5 cycles per minute. Minimal to absent short term variability. Rhythmic oscillation of a since wave above and below baseline. Absence of FHR accelerations. Extreme regularity and smoothness.

- Is known to occur in the presence of fetal hypoxia, fetal anemia, and chronic fetal bleeds.

Uterine Emergencies

Staging Scheme to Assess Obstetric Hemorrhage

Severity of Shock

Findings % blood loss

None None <15%-20%

Mild Tachycardia (< 100), mild hypotensionPeripheral vasoconstriction

20-25%

Moderate Tachycardia (100-120)Hypotension (SBP 80-100), Restlessness, oliguria

Moderate

Severe Tachycardia (> 120), Hypotension (SBP < 60), altered consciousness, anuria

> 35%

Placenta PreviaPlacenta Previa: Anesthetic Management• All pts admitted w/antepartum vaginal bleeding should be

evaluated by anesthesia provider on admission– Airway exam, volume status– At least 1 large-bore IV– Check hgb & hct, type & crossmatch– Volume resuscitation w/crystalloid

• Double set-up– U/s exam results?– Examine pt in OR – all team members present & set up for C-section– Full monitors, 2 large bore IVs, 2 U PRBCs, – C-section if significant bleeding during exam

• RSI preferred for bleeding pts– Ketamine 0.5-1 mg/kg IV

• No hallucinations when < 1 mg/kg• Causes myocardial depression if pt hypovolemic

– Etomidate 0.2-0.3 mg/kg IV• Minimal cardiac depression• Venous irritation, myoclonus, poss adrenal suppression

• Maintenance of anesthesia– Severe fetal distress – no N2O

– Low concentration inhalation agent – D/C after delivery 2o effects on uterus & increase N2O to 70% w/opioids

– Add Pitocin 20U/1L after delivery

Placental Abruption• Separation of placenta before delivery of fetus.• Acute bleeding from exposed decidual vessels.• Fetal distress occurs due to loss of area for maternal-fetal gas exchange.

Anesthetic Management: Placental Abruption• Epidural analgesia if coags and volume status OK• If C-section for fetal distress:

– GA w/RIS, etomidate or ketamine induction– Aggressive volume resuscitation

• Crystalloid, colloid, Level I infuser • Consider invasive monitoring lines

– Risk for persistent hemorrhage 2o uterine atony or coagulopathy• After delivery, add oxytocin 20U/1 L

Uterine Rupture: Etiologies• Previous uterine surgery• Trauma

– Indirect: blunt, e.g., seat belt, excessive manual fundal pressure, extension of cervical laceration– Direct: penetrating wound, intrauterine manipulation, forceps application & rotation, postpartum

curettage, manual placental extraction, version & extraction, external version

• Inappropriate oxytocin use• Grand multiparity• Uterine anomaly• Placenta Percreta• Tumors

– Trophoblastic disease, cervical carcinoma• Fetal problems

– Macrosomia, malposition, anomaly

Anesthetic Management: Uterine Rupture• Hysterectomy is definitive procedure for most cases of uterine rupture• Pt evaluation/preparation begun while pt prepared for emergency laparotomy• If rupture antepartum, fetal distress likely• GA often necessary• Aggressive volume replacement & maintenance of urine output essential• Invasive monitoring if unsure re: adequacy of volume replacement

Vasa Previa• Umbilical vessels separate in membranes distant from placental margin• Some of fetal vessels cross internal os and occupy position ahead of presenting fetal part• Rupture of membranes may be accompanied by tear of fetal vessel leading to exsanguination• Obstetric emergency

– C-section – Ensure fetal survival– Aggressive neonatal resuscitation

Placental Abruption

What is it?Complete or partial separation of the placenta from the uterine wall before delivery of the baby. Maternal hemorrhage may be revealed by vaginal bleeding or may be concealed behind the placenta. Fetal compromise occurs because of the loss of placental surface area for maternal-fetal exchange of oxygen and nutrients.

Risk factorshypertension, pre-eclampsia, advanced maternal age/parity (high number of pregnancies), tobacco use, cocaine use, premature rupture of membranes, chorioamnionitis (infection between maternal and fetal edges of the amniotic membrane), bleeding in early pregnancy and a history of previous abruption.

Incidence0.4-1% of pregnancies, higher in African American women.

DiagnosisPAINFUL VAGINAL BLEEDING, although bleeding may be hidden, uterine tenderness, idiopathic preterm labor

Fetal impactnon-reassuring fetal heart rate (FHR) patterns including bradycardia, late or variable decels, and/or loss of FHR variability, fetal hypoxia, fetal compromise or demise.

Maternal complicationshemorrhagic shock, acute renal failure, & coagulopathy. Most common cause of DIC in pregnancy.

Curedefinitive treatment=delivery of baby, degree of maternal and fetal compromise determine the timing and route of delivery. Most often, non-reassuring FHR pattern necessitates immediate delivery.

Anesthetic considerations

If mom and baby are stable enough to warrant an attempt at a vaginal delivery adequate volume status and baseline CBC/coagulation panel are essential. Epidural anesthesia will cause a sympathectomy which may impact the maternal response to hemorrhage.

If procedure is urgent d/t fetal distress, general anesthesia is required. RSI should be done with all pregnant patients along with gastric acid neutralization-30mL bicitra. Avoid propofol and thiopental with induction as they may precipitate severe hypotension in hypovolemic patients. Ketamine and etomidate are better options for the hypovolemic patient.

Large gauge IV catheter T/C x at least 2 units, baseline CBC & coags Oxygen Left uterine displacement Aggressive volume resuscitation with crystalloid and colloids. If severe hemorrhage CVC (if coagulopathy present, use an antecubital vein to place 14 g PIV) and

arterial line

Patients are at a high risk for persistent hemorrhage from uterine atony or coagulopathy once the baby is delivered. Immediate infusion of oxytocin (20-30 U/L) should be infused. Can also use misoprostol, methergine or Hemabate for severe uterine atony.

Umbilical Cord Prolapse

Situation in which the umbilical cord passes through the cervix leading to cord compression resulting in fetal hypoxia. Compression of the cord cuts off the supply line for oxygen/nutrients exchange for the baby.

Diagnosiscan be visibly seen protruding out of the vagina or can be found on digital cervical examination. FHR patterns can include decels, variables and/or late, or prolonged bradycardia.

TreatmentDELIVERY

Place the mom on her hands and knees and have a practitioner manually displace the fetal head away from the cervix, relieving pressure on the cord. Do not touch the umbilical cord itself as manipulation of the cord will cause the vessels to vasospasm. The practitioner “rides the bed” with the patient to the OR and does not remove their hand until the fetus is delivered by the surgical team.

If unable to immediately proceed to the OR, place the patient in Trendelenburg and place a foley catheter. Instill the maternal bladder with 500 mL of saline and clamp. This will cause the bladder to displace the baby’s head and keep it from compressing on the cord. Continuous FHR monitoring.

Anesthetic considerations

If patient was laboring, dose epidural, if unable to achieve an adequate surgical block, may have to convert to a general. Can try 5-10 mg of ketamine to make it to delivery of the baby then you can give more narcotics/benzos. Must not sedate patient too much so that they are unable to protect their airway as they are high risk for aspiration.

If patient does not have regional anesthesia already in place, proceed with GETA with RSI and gastric acid neutralization.

Retained Placenta

• Placenta accreta vera:– Adherence to myometrium w/out invasion into/through uterine muscle

• Placenta increta– Invasion in myometrium

• Placenta percreta– Invasion into uterine serosa or other pelvic structures

Retained placenta: anesthetic management• Depends on presence/absence of hemorrhage• Epidural block used for labor/delivery

– Add 2% Nesacaine or lidocaine PRN• SAB good choice for pts not bleeding who don’t have epidural in place• In some cases, 50% N2O adequate or ketamine 10 mg boluses up to 0.5 mg/kg, fentanyl 50-100 μg• May require GA• Consider NTG

Treatment of massive blood loss• Postpartum hemorrhage can lead to massive blood loss• BP may remain close to normal until EBL 1500 ml• Initial resuscitation

– Warmed LR, NS, Hespan– 1 unit RBCs increases hgb by 1.5 g/dL, hct 4-5% – FFP: replaces coag factors in clotting disorders. Doesn’t decrease blood loss in massive EBL

situations.– Platelets: beneficial if platelet count < 50K

• Coagulopathy can develop rapidly– Observe for microvascular bleeding on surgical field

Coagulopathy• Dilutional `

– Results from replacement of blood loss w/ crystalloid and PRBCs• Concentrations of coag factors diluted• Develops gradually after > 1 blood volume loss• Responds to FFP & platelets

• Disseminated– Dramatic decline in coag factors & platelets 2o clotting factor and platelet consumption– Develops rapidly in OB pts, e.g., w/ AFE or abruption– Multiple coag components required (FFP, platelets, cryo)