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Program Information. 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.

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    1. Program Information

    2. 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

    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.

    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)

    5. Common Reasons for ICU Transfer

    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

    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

    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

    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

    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

    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

    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

    13. Cardiac output 50% Stroke volume25% Heart rate25% LVEDV, EF CVP,PAoP, PAdP, LVSWI: SVR, PVR20% Central Hemodynamics

    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

    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

    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

    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

    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

    19. Changes in Liver Function Alkaline phosphatase: x 2-4 Total cholesterolx 2 Fibrinogen50% Albumin, total protein20% Transaminasesno change

    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

    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

    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

    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

    24. 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 Fetal Oxygen Transport

    25. Assessment of Fetal Oxygenation

    26. 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 Ionizing Radiation in Pregnancy

    27. National Radiologic Protection Board, 1998 X-ray examination Mean fetal dose Skull<0.01 mGy Chest<0.01 Abdomen1.4 Thoracic spine<0.01 Lumbar spine1.7 Pelvis1.1 IVP1.7 CT examination Mean fetal dose Head <0.005 mGy Chest 0.06 Abdomen8.0 Lumbar spine 2.4 Pelvis 25 Pelvimetry 0.2

    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

    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.

    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

    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.

    32. Conditions Not Specific to Pregnancy

    33. 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. Management of the PregnantTrauma Patient

    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

    35. Infections Associated with Septic Shock in Pregnancy Chorioamnionitis 0.5-10% PP endometritis: SVD<10% PP endometritis: CS12-50% Urinary 1-3% Septic abortion 1-2% Necrotizing fasciitis <1%

    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.

    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

    38. Management of Septic Shock inOB Patients • Stress dose steroids can be used if patient would otherwise qualify • Recombinant activated protein C…?

    39. Incidence has been decreasing in US Probably 1/5,000 pregnancies currently Current mortality rate in US: 15% OB causesNon-OB causes PreeclampsiaPrerenal HELLPATN AFLPAcute interstitial nephritis Postpartum HUSGlomerulonephritis Bilateral renal cortical necrosis Acute obstruction Acute Renal Failure in Pregnancy

    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

    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%

    42. ARDS in Pregnancy • Antepartum: • Infectious causes 66% (8% PIH, 8% aspiration) • Mortality 25% • Postpartum: • Infection 35%, PIH 29%, shock 18% • Mortality 50%

    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

    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

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

    46. Ventilator Management in Pregnancy • Decreased FRC means more likely to desaturate on disconnect • Use sedation/paralysis as appropriate; fetus is not a consideration

    47. Problems Unique to Obstetrics

    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

    49. Treatment of Preeclampsia • DELIVERY • If mild, remote from term, some place for expectant management

    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)