Managing a Pregnant Patient - Thomas Jefferson University
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Critical Care in Pregnancy
Lauren A. Plante, MD, MPH, FACOG
Department of Obstetrics & Gynecology
Department of Anesthesiology
Division of Maternal-Fetal Medicine
Thomas Jefferson University
Objectives
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
Critical Care in Obstetrics
• 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
Common Reasons for ICU
Transfer
10%
30%
14%
HTN
Hemorrhage
Respiratory
Infection
Cardiac
17%
29%
Slide 5
Basic Principles in OB Critical
Care
• 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
Metabolism & Respiration
• 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
Lung Volumes and Capacities
• 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
Oxygen Changes In Pregnancy
• 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
Normal Arterial Blood Gas in
Pregnancy
• Mild chronic compensated respiratory alkalosis
• pH ~7.44
• PaCO2 28-32 mm Hg
• PaO2 >100 mm Hg
• HCO3- 18-22 mEq/L
Slide 10
Cardiovascular Changes
• 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
Cardiovascular Changes
• 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
Central Hemodynamics
• Cardiac output
50%
• Stroke volume
25%
• Heart rate
25%
• LVEDV, EF
• CVP,PAoP, PAdP, LVSWI:
• SVR, PVR
20%
Slide 13
Aortocaval Compression:
• 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
Hemodynamic Changes in Labor
• Further increase in CO (40-70%)
– Increased sympathetic tone augments stroke volume
– Additional effect during contraction: autotransfusion of
300-500 ml blood
Slide 15
Hemodynamic Changes in
Puerperium
• 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
Changes in Renal Function
• 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
GI and Hepatic Changes
• 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
Changes in Liver Function
• Alkaline phosphatase:
x 2-4
• Total cholesterol
x2
• Fibrinogen
50%
• Albumin, total protein
20%
• Transaminases
no change
Slide 19
Hematology and Coagulation
Changes
• 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
Fetoplacental Perfusion
• 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
Fetoplacental Perfusion and
Fetal Oxygenation
• 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
Determinants of Fetal
Oxygenation
• 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 Oxygen Transport
• 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
Assessment of Fetal
Oxygenation
Slide 25
Ionizing Radiation in Pregnancy
•
First 2 weeks after conception (4
weeks from LMP): potential for
loss of conceptus
•
Adverse effects unlikely at
radiation doses less than 50-100
mGy (5-10 rad)
•
Weeks 2-10 after conception (4-12
weeks from LMP): period of
organogenesis teratogenesis
possible
•
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
•
After 10 weeks (12 weeks from
LMP): minimal teratogenesis
potential, but risk of impaired fetal
growth, childhood leukemia
Slide 26
National Radiologic Protection
Board, 1998
X-ray examination
Mean fetal dose
Skull
<0.01 mGy
Chest
<0.01
Abdomen
1.4
Thoracic spine
<0.01
Lumbar spine
Pelvis
1.7
1.1
CT examination
Mean fetal dose
Head
<0.005 mGy
Chest
Abdomen
0.06
8.0
Lumbar spine
2.4
Pelvis
25
Pelvimetry
0.2
IVP1.7
Slide 27
Additional Radiation Worries
• 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
Pharmacology in Pregnancy
• 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
Resources for Drugs in
Pregnancy
• 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
Perinatal Pharmacology
• 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
Conditions Not Specific
to Pregnancy
Management of the Pregnant
Trauma Patient
• Severity of maternal injuries
determines both maternal and
fetal outcome.
• Assess and resuscitate the
mother first.
• However, even minor maternal
injury can be associated with
fetal loss.
• Then may assess fetus (if at or
near viability).
• Then proceed with secondary
survey of the mother.
• 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.
Slide 33
Sepsis
• OB patients with clinical evidence of local infection: 810% risk bacteremia
• OB patients with bacteremia rarely progress to sepsis:
overall about 4%
• OB patients with septic shock: <20% mortality
Slide 34
Infections Associated with
Septic Shock in Pregnancy
• Chorioamnionitis
0.5-10%
• PP endometritis: SVD
<10%
• PP endometritis: CS
12-50%
• Urinary
1-3%
• Septic abortion
1-2%
• Necrotizing fasciitis
<1%
Slide 35
Management of Septic Shock in
OB Patients
• 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
Management of Septic Shock in
OB Patients
• 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
Management of Septic Shock in
OB Patients
• Stress dose steroids can be used if patient would
otherwise qualify
• Recombinant activated protein C…?
Slide 38
Acute Renal Failure in
Pregnancy
• Incidence has been decreasing in US
• Probably 1/5,000 pregnancies currently
• Current mortality rate in US: 15%
OB causes
Non-OB causes
Preeclampsia
Prerenal
HELLP
ATN
AFLP
Acute interstitial nephritis
Postpartum HUS
Glomerulonephritis
Bilateral renal cortical necrosis
Acute obstruction
Slide 39
Management of Acute Renal
Failure in Pregnancy
• 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
Pregnancy and ARDS
• 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
ARDS in Pregnancy
• Antepartum:
– Infectious causes 66% (8% PIH, 8% aspiration)
– Mortality 25%
• Postpartum:
– Infection 35%, PIH 29%, shock 18%
– Mortality 50%
Slide 42
ARDS and Pregnancy
• 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
Ventilator Management In
Pregnancy
• 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
Airway Management
• Higher risk of failed intubation
in pregnancy (even for the
professionals)
• Be prepared for trouble
Slide 45
Ventilator Management in
Pregnancy
• Decreased FRC means more likely to desaturate on
disconnect
• Use sedation/paralysis as appropriate; fetus is not a
consideration
Slide 46
Problems Unique to
Obstetrics
Preeclampsia
• 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
Treatment of Preeclampsia
• DELIVERY
• If mild, remote from term, some place for expectant
management
Slide 49
Severe Preeclampsia
• 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
Complications of Preeclampsia
• Brain:
edema, hemorrhage, infarction
• Eyes:
retinal detachment, cortical
blindness, papilledema
• CV:
severe HTN, pulmonary edema
• Lung:
pulmonary edema, aspiration
• Liver:
hemorrhage, infarction, rupture
• Kidney:
nephrotic syndrome, ARF
• Blood:
thrombocytopenia, DIC,
microangiopathic hemolytic anemia
Slide 51
Cardiovascular Findings in
Preeclampsia
• 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
Pulmonary Edema in
Preeclampsia
• 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 Dysfunction in
Preeclampsia
• 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
HELLP Syndrome
• Hemolysis
• Elevated Liver enzymes
• Low Platelets
• A variant of severe
preeclampsia…?
• Unlike most
preeclampsia, not a
disease of primigravidas
• May not meet BP criteria
for preeclampsia
Slide 55
Complications of HELLP
Syndrome
• Acute renal failure in 7% (usually ATN)
• Hepatic compromise is common
• Maternal mortality 1-3%
• Perinatal mortality 7-30%
• Resolves after delivery
Slide 56
DDx of HELLP Syndrome
• Easy to confuse with:
– Hepatitis
– ITP
– Pancreatitis
– Chronic renal disease
– TTP
– Pyelonephritis
– HUS
– Cholecystitis
– Acute fatty liver of
pregnancy
– Gastroenteritis
Slide 57
Eclampsia
• 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
Eclampsia – Complications
• Abruptio placentae
6-17%
• HELLP syndrome
14-20%
• DIC
6-7%
• Pulmonary edema
5-6%
• Neuro deficit
2-9%
• ARF
2-8%
• Cardiopulmonary arrest
2-6%
• Death
<1%
Slide 59
Acute Fatty Liver of Pregnancy
• 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
Acute Fatty Liver of Pregnancy
• Initial manifestations mild,
nonspecific: nausea/vomiting
(70%); RUQ or epigastric pain
(50%)
• Typical picture of hepatic
failure: hypoglycemia,
coagulopathy, encephalopathy,
etc.
• Jaundice follows in 1-2 weeks
• Usually resolves after delivery
(may take days or, rarely,
weeks)
• DDx includes viral hepatitis,
cholestasis of pregnancy,
atypical preeclampsia/HELLP
• Stabilize mother, then deliver
• Care like any other hepatic
failure
• Limited role for transplantation
Slide 61
“Amniotic Fluid Embolus”
• A misnomer
• Better: anaphylactoid syndrome of pregnancy
• Characterized by sudden development of hypoxia,
hypotension and cardiovascular collapse, coagulopathy
Slide 62
ASP/AFES
• 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
ASP/AFES
• 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
CPR in Pregnancy
• 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
Perimortem Cesarean Section
• 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
Managing the Pregnant Patient
• 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
Managing a Pregnant Patient
• 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
Managing a Pregnant Patient
• At all costs, avoid sacrificing the
• mother for the sake of the fetus
Slide 69
Case Studies
The following are case studies that can be used for review
of this presentation.
Review Cases
End
Slide 70
Case #1
• 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
Case #1
•
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
Case #2
• 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
Case #2
• 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
Self Assessment
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Slide 75
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