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Lauren A. Plante, MD, MPH, FACOG
Department of Obstetrics & Gynecology
Department of Anesthesiology
Division of Maternal-Fetal Medicine
Thomas Jefferson University

1. Explain hemodynamic, respiratory, and metabolic changes in the pregnant patient;
2. Identify determinants of fetal oxygen transport and how to assess and manage poor fetal oxygenation;
3. Identify two disease processes in the pregnant patient, describe how they differ compared to the non-pregnant patient, and understand how to manage the patient; and
4. Describe complications of preeclampsia/eclampsia and their management.
Slide 3

• 0.2-0.5% of obstetrical admissions require transfer to an intensive care unit
• One-third are admitted to ICU antepartum
– Half are delivered while still in the ICU (or in ICU care)
• Mortality among OB patients admitted to ICU is 5-6% (cf. overall maternal mortality <1 per 10,000)
Slide 4

14%
10%
30%
HTN
Hemorrhage
Respiratory
Infection
Cardiac
17%
29%
Slide 5

• Two patients rather than one
• Interests may not coincide exactly, but maternal needs take precedence
• Fetal health, as a rule, is maximized when maternal medical condition is optimized
• Changes in maternal physiology; therefore, changes in normal values
Slide 6

• Oxygen consumption increases by 40-60% during pregnancy
• Primarily due to metabolic needs of fetus, uterus, and placenta
• Secondarily because of increased cardiac and respiratory work
Slide 7

• Tidal volume increases 45%
• No change in FEV1
• No change FEV1/FVC ratio
• FRC reduced by 20%
• FRC further decreased
(another 30% ) in the supine position
Slide 8

• Increase in oxygen consumption (~20%)
• Small increase in PaO2: usually >100 mm Hg on room air
• Reduced A-V O2 difference
• Widening of A-a gradient
• Slight decrease in affinity of hemoglobin for oxygen
Slide 9

• Mild chronic compensated respiratory alkalosis
• pH ~7.44
• PaCO2 28-32 mm Hg
• PaO2 >100 mm Hg
• HCO3- 18-22 mEq/L
Slide 10

• Plasma volume increases 40-50%
– Greater increase with multiple gestations
• Red cell mass increases 20-30%
• Physiologic hemodilution (not iron-deficiency anemia) and decrease in blood viscosity
• Blood pressure decreases 10-20%, with diastolic more affected; returns toward non-pregnant norms by the end of the third trimester
Slide 11

• Plasma volume increases 40-50%
– Greater increase with multiple gestations
• Red cell mass increases 20-30%
• Physiologic hemodilution (not iron-deficiency anemia) and decrease in blood viscosity
Slide 12

• Cardiac output
• Stroke volume
• Heart rate
• LVEDV, EF
• CVP,PAoP, PAdP, LVSWI:
• SVR, PVR
50%
25%
25%
20%
Slide 13

• Effect of Supine Position on Hemodynamics: Enlarging uterus can compress vena cava when patient is supine
(less commonly, aortic compression)
– Effects: decreased preload, decreased CO, decreased BP (“supine hypotension”)
– After 20 weeks, maintain left uterine displacement while recumbent
Slide 14

• Further increase in CO (40-70%)
– Increased sympathetic tone augments stroke volume
– Additional effect during contraction: autotransfusion of
300-500 ml blood
Slide 15

• Relative hypervolemia and increased venous return
• Attributed to relief of caval compression, loss of intervillous circuit and, thus, autotransfusion
• CVP rises
• SV and CO increase by up to an additional 75% immediately postpartum
Slide 16

• Anatomic: dilation of the collecting system
• Renal plasma flow & GFR: increase 50%
– Serum creatinine <0.6 mg/dl, BUN <10
• Renal tubular function: increased sodium reabsorption, increased glucose excretion, decrease in uric acid reabsorption
Slide 17

• Decrease in LES tone, increase in resting intragastric pressure => favor reflux
• Decreased gastric motility => delayed gastric emptying
• Acid secretion higher in third trimester than nonpregnant
• Overall effect: more prone to acid aspiration
Slide 18

• Alkaline phosphatase: x 2-4
• Total cholesterol x 2
• Fibrinogen 50%
• Albumin, total protein 20%
• Transaminases no change
Slide 19

• Hgb, Hct decrease as plasma volume increases
• Overall enhanced platelet turnover, clotting, and fibrinolysis
• Hypercoagulability
• Placenta contains thromboplastin, which can induce formation of fibrin and bypass intrinsic pathway
Slide 20

• No autoregulation in uterine vascular bed => uterus behaves like a fully dilated system
• Uteroplacental perfusion is pressure-dependent (cannot compensate for abrupt drop in BP)
• Uterine vasculature unresponsive to changes in PO2 or
PCO2
Slide 21

• Placenta is metabolically active; consumes a large fraction of the oxygen delivered to the gravid uterus
• Human placenta is probably a venous equilibrator: uterine venous PO2 is the upper limit fetal (umbilical) venous PO2
Slide 22

• Uterine venous PO2, not maternal arterial PO2, determines fetal oxygenation
• Factors affecting uterine venous PO2:
– SvO2 in uterine venous blood
• SaO2, uteroplacental perfusion, placental and fetal O2 consumption, O2 capacity of maternal blood
– Oxyhemoglobin dissociation curve (maternal)
• Hb structure, temperature, pH, 2,3-DPG
Slide 23

• Fetal blood has a very low
PO2, but oxygen transport from placenta to sites of fetal need is efficient
• Fetal Hgb has high O2 affinity
• Fetus has very high cardiac output relative to size and metabolic rate
• Uterine arterial PO2: 100 mm
Hg
• Umbilical venous PO2: 28 mm
Hg (70% saturation)
• Umbilical arterial PO2: 19 mm
Hg (40% saturation)
• Uterine venous PO2: 35 mm
Hg
Slide 24

Slide 25

• First 2 weeks after conception (4 weeks from LMP): potential for loss of conceptus
• Weeks 2-10 after conception (4-12 weeks from LMP): period of organogenesis  teratogenesis possible
• After 10 weeks (12 weeks from
LMP): minimal teratogenesis potential, but risk of impaired fetal growth, childhood leukemia
• Adverse effects unlikely at radiation doses less than 50-100 mGy (5-10 rad)
• Typical AP pelvis film ~0.16 mGy dose to fetus
• Typical CT of pelvis 20-50 mGy
(depends on number of cuts, size of area studied)
• Radiation physicist or dosimetrist can help calculate dose, estimate risk
• Can substitute other modalities:
US, MR; shield abdomen/pelvis unless direct need to image
Slide 26

X-ray examination Mean fetal dose CT examination Mean fetal dose
Skull <0.01 mGy
<0.005 mGy
0.06
Chest
Abdomen
Thoracic spine
Lumbar spine
Pelvis
<0.01
1.4
<0.01
1.7
1.1
Head
Chest
Abdomen
Lumbar spine
Pelvis
Pelvimetry
8.0
2.4
25
0.2
IVP1.7
Slide 27

• Cognitive impairment
– Dose-response with exposure 10-17 weeks
– Loss of ~30 IQ points per 1,000 mGy fetal exposure
• Childhood cancers
– Dose-response
– One excess fatal childhood cancer per 33,000 population for each mGy intrauterine exposure
– Not an indication to offer termination (ACOG 2004)
• ?Contrast media?
– Gadolinium is OK
Slide 28

• Most drugs given to the mother do cross into the fetal compartment. This is not necessarily a problem.
• FDA classification A-B-C-D-X is not helpful, except: avoid category X.
• Teratogenesis is a theoretical concern with drug exposures in the first trimester. The extent and nature of the risk vary widely.
Slide 29

• Motherisk (a project of the Hospital for Sick Children, University of
Toronto)
– http://www.motherisk.org/prof/drugs.jsp
– (416) 813-6780 (phone)
• Reprotox (database available free to residents in training, otherwise by subscription; hospital or university libraries may maintain a multiuser subscription)
– http://www.reprotox.org
• Teris (computerized database available by subscription; your hospital or university library may keep a subscription)
– http://depts.washington.edu/~terisweb/teris
Slide 30

• Increased total body water increases volume of distribution.
• Increased cardiac output and GFR speeds excretion of water-soluble drugs.
• Dilutional hypoalbuminemia decreases drug binding and increases free drug; may alter acceptable therapeutic range.
Slide 31

• Severity of maternal injuries determines both maternal and fetal outcome.
• However, even minor maternal injury can be associated with fetal loss.
• All pregnant patients with major traumatic injury require admission to a facility with both trauma and obstetrical services.
• Neonatal intensive care services may also be required.
• Assess and resuscitate the mother first.
• Then may assess fetus (if at or near viability).
• Then proceed with secondary survey of the mother.
Slide 33

• OB patients with clinical evidence of local infection: 8-
10% risk bacteremia
• OB patients with bacteremia rarely progress to sepsis: overall about 4%
• OB patients with septic shock: <20% mortality
Slide 34

• Chorioamnionitis
• PP endometritis: SVD
• PP endometritis: CS
• Urinary
• Septic abortion
• Necrotizing fasciitis
0.5-10%
<10%
12-50%
1-3%
1-2%
<1%
Slide 35

• Treat as if non-pregnant: fluids, antibiotics, etc; appropriate imaging; ventilatory support, hemodynamic monitoring as needed.
• Fetoplacental perfusion is dependent on adequate uterine blood flow —maintain BP.
• If still pregnant and uterus source of infection, delivery is indicated regardless of gestational age.
Slide 36

• What MAP to target?
• Can you distinguish central hemodynamics of normal pregnancy from those of sepsis?
• No human data on vasopressors
• Some animal data on dopamine
• All will increase resting uterine tone and decrease uteroplacental perfusion
• Use electronic fetal monitoring to help titrate
• Probably cannot use long-term
Slide 37

• Stress dose steroids can be used if patient would otherwise qualify
• Recombinant activated protein C…?
Slide 38

• Incidence has been decreasing in US
• Probably 1/5,000 pregnancies currently
• Current mortality rate in US: 15%
OB causes
Preeclampsia
HELLP
Non-OB causes
Prerenal
ATN
AFLP Acute interstitial nephritis
Postpartum HUS Glomerulonephritis
Bilateral renal cortical necrosis
Acute obstruction
Slide 39

• Similar to that in non-pregnant patients
• Both hemodialysis and peritoneal dialysis acceptable
– Recommend intensive dialysis (?effect of azotemia on fetus): usually daily
– Maintain BUN <70 mg/dl, Cr <5 mg/dl
• If obstetric cause for renal failure, delivery may be indicated
Slide 40

• Incidence low (1/6,000-10,000 deliveries)
• Spectrum of causes widened: aside from usual causes
ARDS, consider preeclampsia-eclampsia-HELLP, AFLP, anaphylactoid syndrome of pregnancy, tocolytic therapy
• Maternal mortality ~30%
Slide 41

• Antepartum:
– Infectious causes 66% (8% PIH, 8% aspiration)
– Mortality 25%
• Postpartum:
– Infection 35%, PIH 29%, shock 18%
– Mortality 50%
Slide 42

• Management similar to non-pregnant patient
• Lung-protective strategy has not been widely tested in pregnant patients with ARDS
– Historical data: pregnancy increases barotrauma risk
– Theoretical concerns with acidemia 2 • hypercapnia
• Fetal oxygenation OK with maternal PaO2>60 but perfusion essential
• Delivery does not improve maternal condition or survival
Slide 43

• Common reasons for mechanical ventilation: asthma,
ARDS, altered level of consciousness
• When deciding whether intubation is needed, remember pregnancy norms for ventilation
• When setting ventilator, remember pregnancy norms for
PaO2, PaCO2
• PEEP is not contraindicated
• Use the fetal monitor
Slide 44

• Higher risk of failed intubation in pregnancy (even for the professionals)
• Be prepared for trouble
Slide 45

• Decreased FRC means more likely to desaturate on disconnect
• Use sedation/paralysis as appropriate; fetus is not a consideration
Slide 46

• Affects 5-10% of pregnancies in US
• Syndrome of hypertension, proteinuria, and pathologic edema
• Unique to human pregnancy
• Exact etiology unknown
– ?immunologic contributions
– ?endothelial dysfunction
– ?uteroplacental ischemia
Slide 48

• DELIVERY
• If mild, remote from term, some place for expectant management
Slide 49

• BP >160 systolic or 110 diastolic
• Proteinuria >5 g/24 hours
• Oliguria (<500 ml/ 24 hours)
• Cerebral or visual disturbances
• Pulmonary edema or cyanosis
• HELLP syndrome
• Fetal growth restriction
• Eclampsia (seizures)
Slide 50

• Brain:
• Eyes: edema, hemorrhage, infarction retinal detachment, cortical blindness, papilledema
• CV: severe HTN, pulmonary edema
• Lung:
• Liver: pulmonary edema, aspiration hemorrhage, infarction, rupture
• Kidney: nephrotic syndrome, ARF
• Blood: thrombocytopenia, DIC, microangiopathic hemolytic anemia
Slide 51

• Inadequate plasma volume expansion
• Increased vasoconstriction
• Hyperdynamic LV function
• Further decrease in colloid oncotic pressure
• Decreased COP-PCWP gradient
• Poor correlation between CVP and PCWP
Slide 52

• Reported as high as 2-3%
– 70% develop postpartum
• Contributing factors include decreased COP, alteration of capillary membrane permeability, elevated pulmonary vascular hydrostatic pressures
• Can be iatrogenic
Slide 53

• Renal plasma flow and GFR are diminished
• Oliguria in preeclampsia:
– Most commonly prerenal
– Up to one-third may manifest disproportionate vasospasm
– <10%: decreased ECV because of LV dysfunction
Slide 54

• H emolysis
• E levated L iver enzymes
• L ow P latelets
• A variant of severe preeclampsia…?
• Unlike most preeclampsia, not a disease of primigravidas
• May not meet BP criteria for preeclampsia
Slide 55

• Acute renal failure in 7% (usually ATN)
• Hepatic compromise is common
• Maternal mortality 1-3%
• Perinatal mortality 7-30%
• Resolves after delivery
Slide 56

• Easy to confuse with:
– ITP
– Chronic renal disease
– Pyelonephritis
– Cholecystitis
– Gastroenteritis
– Hepatitis
– Pancreatitis
– TTP
– HUS
– Acute fatty liver of pregnancy
Slide 57

• Convulsions or coma, not attributed to any other cause, in a woman with signs or symptoms of preeclampsia
• Average rate in US 1/2,000 deliveries
• May occur antepartum, intrapartum, or up to 4 weeks postpartum
• Maternal mortality in US 0.5-2%
• Perinatal mortality in US 7-16%
• Treatment: magnesium; anti-hypertensives if needed;
DELIVERY
Slide 58

• Abruptio placentae
• HELLP syndrome
• DIC
• Pulmonary edema
• Neuro deficit
• ARF
• Cardiopulmonary arrest
• Death
6-17%
14-20%
6-7%
5-6%
2-9%
2-8%
2-6%
<1%
Slide 59

• Rare (1/7,000 to 1/13,000) but potentially fatal
• Maternal mortality until 1980 as high as 80%; more recently <20%
• Characterized by jaundice, coagulopathy, CNS disturbance, microvesicular fatty infiltration of liver
Slide 60

• Initial manifestations mild, nonspecific: nausea/vomiting
(70%); RUQ or epigastric pain
(50%)
• Jaundice follows in 1-2 weeks
• DDx includes viral hepatitis, cholestasis of pregnancy, atypical preeclampsia/HELLP
• Typical picture of hepatic failure: hypoglycemia, coagulopathy, encephalopathy, etc.
• Usually resolves after delivery
(may take days or, rarely, weeks)
• Stabilize mother, then deliver
• Care like any other hepatic failure
• Limited role for transplantation
Slide 61

• A misnomer
• Better: anaphylactoid syndrome of pregnancy
• Characterized by sudden development of hypoxia, hypotension and cardiovascular collapse, coagulopathy
Slide 62

• Mortality 60-80%
• No improvement in survival when event occurs in tertiary care centers
• No predictability
• Clinical and hemodynamic similarities to other types of distributive shock (septic, distributive)
Slide 63

• General treatment strategies:
• Supportive care with initial insult; CPR if needed, ventilation with high FIO2, correct any dysrhythmias.
• Optimize preload; inotropic support if needed.
• Consider steroid administration.
Slide 64

• Difficult to assure adequate cardiac output in supine position (vena cava and, possibly, aortic compression) => perform CPR with patient in left lateral tilt.
• Fetus is anoxic during maternal cardiac arrest; inadequate uterine perfusion even during effective CPR.
• Interval from maternal arrest to delivery is correlated with neonatal survival: if mother not resuscitated within 4 minutes, effect perimortem cesarean delivery.
• A-B-C-D (for delivery).
• Occasionally, relief of aortocaval compression by uterine evacuation may allow reestablishment of effective CO => improve maternal survival.
Slide 65

• Consider if maternal resuscitation unsuccessful after 4-5 minutes of CPR
• If performed after 24 weeks gestation, perinatal survival is possible
• Even if perinate does not survive, may allow maternal resuscitation
• Speed counts:
– <5 min from arrest to delivery: 70% perinatal survival
6-15 min: 12% perinatal survival
Slide 66

• Multidisciplinary: If unit is closed, must still involve obstetrician in decision-making. After fetal viability, patient needs both critical care nurse and OB nurse.
• Maintain left uterine displacement.
• IM steroids (betamethasone or dexamethasone) after 24 weeks enhance fetal pulmonary maturation and improve neonatal survival.
• Continuous fetal monitoring from viability onward: excellent indicator of regional perfusion.
• No tocolytics to suppress contractions.
Slide 67

• Plan ahead for delivery.
• Careful with diagnosis of “fetal distress”—ominous tracing more likely indicates a need for a change in maternal therapy.
• Can patient be safely transported to, or managed in,
L&D?
• Vaginal delivery can be conducted in ICU.
• Anesthesiology support.
• Avoid cesarean delivery in ICU (unless perimortem)— move patient to L&D or OR.
Slide 68

• At all costs, avoid sacrificing the
• mother for the sake of the fetus
Slide 69

The following are case studies that can be used for review of this presentation.
Review Cases
End
Slide 70

• 26-year-old woman, first pregnancy, admitted to community hospital at 28 weeks of pregnancy, c/o cough, abdominal pain, fever
• W/u suggested community-acquired pneumonia: begun on cephalosporin and azithromycin
• Status deteriorated over ~5 days: transferred to OB at referral center, O2 via facemask, continuous fetal monitoring
• Further deterioration over 48 hr: PaO2 60 mm Hg on
100%NRB, PaCO2 45. Intubated, transferred to MICU.
Dx: ARDS
Slide 71

•
PEEP 15 cm, FIO2 1.0
• Continuous EFM with OB nurse at bedside
•
Dropped BP: normalized with left uterine displacement and decreased PEEP. Lungprotective ventilatory strategy adopted. Sedation (propofol, benzodiazepines)
• Not improved after 2 weeks. No etiology apparent other than severe CAP. Trach,
PEG.
•
Team conference: offer delivery as course & prognosis of disease unclear and no signs improvement. Betamethasone for fetal lung maturity since newborn will be preterm. Deliver 2 days after steroids given.
• Transported back to OB floor for induction of labor & planned vaginal delivery. Critical care nurse at bedside.
•
Induction of labor (<24 hr), forceps-assisted delivery; 1,500g newborn to NICU
• Mother transported back to MICU 2 hours postpartum
•
Gradual improvement over next month
• Discharged home with no sequelae; baby home ~5 weeks
Slide 72

• 37-year-old woman, 26 weeks pregnant, on methadone maintenance, seen for expanding discoloration on abdomen 3 days after minor domestic trauma
• Prior history includes rectovaginal fistula (following anal sphincter laceration at delivery 10 years earlier) that required diverting colostomy to heal, followed by end-toend reanastomosis; later incisional hernia repaired w mesh
• PE: ecchymosis and necrosis in RUQ with purulent malodorous fluid seepage. Patient reported rapid expansion of lesion. BP 90/50, lactate 50
Slide 73

• Likeliest diagnosis: necrotizing soft-tissue infection
• Broad-spectrum antibiotics. Considered abdominal CT vs. direct exploration in OR
• Operative findings: necrotic abdominal wall; perforated ileum
• Resected abdominal wall and 3 feet of bowel; plan to leave abdomen open
• OB proceeded with cesarean delivery at time of exploratory laparotomy
• 900-gram newborn to NICU
• Mother home in 1 week with wound care plan, baby home in 6 weeks
Slide 74

• Ready to test your knowledge?
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Slide 75

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