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Aicu rp-1 pregancy

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Page 1: Aicu rp-1 pregancy

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Page 2: Aicu rp-1 pregancy

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

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Slide 3

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.

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Slide 4

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)

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Slide 5

Common Reasons for ICU Transfer

30%

29%

17%

14%

10%

HTNHemorrhageRespiratoryInfectionCardiac

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Slide 6

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

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Slide 7

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

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Slide 8

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

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Slide 9

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

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Slide 10

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

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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

• Blood pressure decreases 10-20%, with diastolic more affected; returns toward non-pregnant norms by the end of the third trimester

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Slide 12

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

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Slide 13

Central Hemodynamics

• Cardiac output 50%

• Stroke volume 25%

• Heart rate 25%

• LVEDV, EF

• CVP,PAoP, PAdP, LVSWI:

• SVR, PVR 20%

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Slide 14

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

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Slide 15

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

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Slide 16

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

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Slide 17

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

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Slide 18

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

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Slide 19

Changes in Liver Function

• Alkaline phosphatase: x 2-4

• Total cholesterol x 2

• Fibrinogen 50%

• Albumin, total protein 20%

• Transaminases no change

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Slide 20

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

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Slide 21

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

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Slide 22

Fetoplacental Perfusion andFetal 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

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Slide 23

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

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Slide 24

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

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Slide 25

Assessment of Fetal Oxygenation

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Slide 26

Ionizing Radiation in Pregnancy

• 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

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Slide 27

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 1.7

Pelvis 1.1

IVP1.7

CT examination Mean fetal dose

Head <0.005 mGy

Chest 0.06

Abdomen 8.0

Lumbar spine 2.4

Pelvis 25

Pelvimetry 0.2

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Slide 28

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

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Slide 29

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.

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Slide 30

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

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Slide 31

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.

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Conditions Not Specific to Pregnancy

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Slide 33

Management of the PregnantTrauma Patient

• 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.

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Slide 34

Sepsis

• 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

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Slide 35

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%

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Slide 36

Management of Septic Shock inOB 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.

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Slide 37

Management of Septic Shock inOB 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

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Slide 38

Management of Septic Shock inOB Patients

• Stress dose steroids can be used if patient would otherwise qualify

• Recombinant activated protein C…?

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Slide 39

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

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Slide 40

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

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Slide 41

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%

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Slide 42

ARDS in Pregnancy

• Antepartum:

– Infectious causes 66% (8% PIH, 8% aspiration)

– Mortality 25%

• Postpartum:

– Infection 35%, PIH 29%, shock 18%

– Mortality 50%

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Slide 43

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

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Slide 44

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

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Slide 45

Airway Management

• Higher risk of failed intubation in pregnancy (even for the professionals)

• Be prepared for trouble

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Slide 46

Ventilator Management in Pregnancy

• Decreased FRC means more likely to desaturate on disconnect

• Use sedation/paralysis as appropriate; fetus is not a consideration

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Problems Unique to Obstetrics

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Slide 48

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

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Slide 49

Treatment of Preeclampsia

• DELIVERY

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

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Slide 50

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)

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Slide 51

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

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Slide 52

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

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Slide 53

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

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Slide 54

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

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Slide 55

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

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Slide 56

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

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Slide 57

DDx of HELLP Syndrome

• Easy to confuse with:

– ITP

– Chronic renal disease

– Pyelonephritis

– Cholecystitis

– Gastroenteritis

– Hepatitis

– Pancreatitis

– TTP

– HUS

– Acute fatty liver of pregnancy

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Slide 58

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

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Slide 59

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%

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Slide 60

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

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Slide 61

Acute Fatty Liver of Pregnancy

• 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

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Slide 62

“Amniotic Fluid Embolus”

• A misnomer

• Better: anaphylactoid syndrome of pregnancy

• Characterized by sudden development of hypoxia, hypotension and cardiovascular collapse, coagulopathy

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Slide 63

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)

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Slide 64

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.

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Slide 65

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.

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Slide 66

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

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Slide 67

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.

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Slide 68

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.

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Slide 69

Managing a Pregnant Patient

• At all costs, avoid sacrificing the

• mother for the sake of the fetus

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Slide 70

Case Studies

The following are case studies that can be used for review of this presentation.

Review Cases

End

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Slide 71

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

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Slide 72

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. Lung-protective 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

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Slide 73

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-to-end 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

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Slide 74

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

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Slide 75

Self Assessment

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References

• Afessa B, Green B, Delke I, Koch K. Systemic inflammatory response syndrome, organ failure, and outcome in critically ill obstetric patients treated in an ICU. Chest 2001; 120: 1271-7

• Bouvier-Colle M-H, Salanave B, Ancel P-Y, Varnoux N, Fernandez H, Papiernik E, Reart G, Benhamou D, Boutroy P, Caillier I, Dumoulin M, Fournet P, Elhassani M, Puech F, Poutot C. Obstetric patients treated in intensive care units and maternal mortality. Eur J Obstet Gynecol Reprod Biol 1996; 65: 121-5

• Brace V, Penney G, Hall M. Quantifying severe maternal morbidity: a Scottish population study. BJOG 2004; 111: 481-4

• Collop NA, Sahn SA. Critical illness in pregnancy: an analysis of 20 patients admitted to a medical intensive care unit. Chest 1993; 103: 1548-52

• Gilbert TT, Smulian JC, Martin AA, Ananth CV, Scorza W, Scardella AT. Obstetric admissions to the intensive care unit: outcomes and severity of illness. Obstet Gynecol 2003; 102: 897-903

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References

• Graham SG, Luxton MC. The requirement for intensive care support for the pregnant population. Anaesthesia 1989; 44: 581-4

• Hazelgrove JF, Price C, Pappachan VJ, Smith GB. Multicenter study of obstetric admissions to 14 intensive care units in southern England. Crit Care Med 2001; 29: 770-5

• Heinonen S, Tyrvainen E, Saarikoski S, Ruokonen E. Need for maternal critical care in obstetrics: a population-based analysis. Int J Obstet Anesth 2002; 11: 260-4

• Karnad D, Guntupalli KK. Critical illness and pregnancy: review of a global problem. Crit Care Clin 2004; 20: 555-76

• Keizer JL, Zwart JJ, Meerman RH, Harinck BIJ, Feuth HDM, van Roosmalen J. Obstetric intensive care admissions: a 12-year review in a tertiary care centre. Eur J Obstet Gynecol Reprod Biol 2006; 128: 152-6

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References

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