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CBP: Obstetrics

CBP: Obstetrics. April 30 2009. CASE # 1.

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CBP: Obstetrics

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  1. CBP: Obstetrics April 30 2009

  2. CASE # 1 • It’s 5 pm on Friday at St Paul’s and you’re going home early. Just as you hit the metal plate that lets you out of the unit, your anesthesia R2 catches up to you and tells you that he just got called for a 26-week pregnant woman in severe respiratory distress. • You decide to head down with your resident to take a look at her before leaving, and realizing you haven’t seen a pregnant let alone a premenopausal patient during your three years of internal medicine training, you pimp your R2 on the physiologic changes seen in pregnancy:

  3. Question # 1 • Summarize relevant physiologic changes in pregnancy giving normal values for important vital signs and relevant lab tests. (Scot)

  4. Hemodynamic changes in normal pregnancy Normal pregnancy is characterized by an increase in cardiac output, a reduction in systemic vascular resistance, and a modest decline in mean blood pressure. These changes are associated with a 10 to 15 beat/min increase in heart rate.

  5. Expansion of the plasma volume and an increase in red blood cell mass begin as early as the fourth week of pregnancy, peak at 28 to 34 weeks of gestation, and then plateau. Plasma volume expansion exceeds the increase in red cell volume, leading to "physiologic anemia". • The major hemodynamic changes induced by pregnancy include an increase in cardiac output and reductions in systemic vascular resistance and systemic blood pressure. Cardiac output peaks a few minutes after delivery, before gradually returning to prepregnancy levels. • Changes in several coagulation factors produce a hypercoagulable state. • Labor and delivery is associated with significant hemodynamic changes due to anxiety, exertion, pain, uterine contractions, uterine involution, and bleeding. Infection, hemorrhage, and the administration of anesthesia or analgesia also play a role.

  6. Gastrointestinal • Oropharyngeal changes in pregnancy include epulis, gingivitis, and increased salivation. • Gastrointestinal reflux is common in pregnancy because of decreased lower esophageal sphincter pressure and inhibition of the adaptive responses of the sphincter. • Pregnant women are predisposed to gastric aspiration due to increased intraabdominal pressure and relaxation of the lower esophageal sphincter. • Abdominal bloating and constipation during pregnancy are probably caused by hormonal changes that reduce small bowel and colonic motility. • 30 to 40 percent of pregnant women are bothered by hemorrhoids.

  7. Nephrologic • Ureteral dilatation during pregnancy results from hormonal effects, external compression, and intrinsic changes in the ureteral wall. Intermittent vesicoureteral reflux is also common. • Urinary frequency and nocturia are among the most common pregnancy-related complaints. Urinary incontinence also increases during pregnancy. • Glomerular filtration rate (GFR) and renal blood flow rise markedly during pregnancy. Other renal changes in pregnant women include increased renal size, chronic respiratory acidosis, mild hyponatremia, and fall in plasma osmolality. Fractional absorption of glucose, amino acids, and beta microglobulin are decreased. Protein excretion is increased. • The release of vasopressinases from the placenta results in an approximate four-fold increase rate of vasopressin catabolism, but plasma vasopressin levels remain normal because of a fourfold rise in the production of vasopressin by the pituitary gland. Women who have higher than normal vasopressinase levels or decreased vasopressin reserves may develop gestational diabetes insipidus. The high urine output in this setting is generally resistant to the administration of vasopressin, but patients generally remain responsive to desmopressin.

  8. Hematologic • Blood Volume increases: magnitude varies according to size, number of pregnancies, number deliveries, and one or multiple foetuses. Increases in blood volume progress until term;the average increase in volume at term is 45-50%. Needed for extra blood flow to the uterus, extra metabolic needs of foetus, and increased perfusion of others organs, especially kidneys. Also compensate for maternal blood loss at delivery. • Red Blood Cells The increase in red blood cell mass is about 33%. Since plasma volume increases early in pregnancy and faster than red blood cell volume, the hematocrit falls until the end of the second trimester, when the increase in the red blood cells is synchronized with the plasma volume increase. The hematocrit then stabilizes or may increase slightly near term. • Iron With the increase in red blood cells, the need for iron for the production of hemoglobin increases. If supplemental iron is not added to the diet, iron deficiency anemia will result. Maternal requiriments can reach 5-6mg/d in the latter half of pregnancy. If iron is not readly available, the fetus uses iron from maternal stores. Thus, the production of fetal hemoglobin is usually adequate even if the mother is serely iron deficient. Maternal iron deficiency may cause preterm labour and late spontaneus abortion.

  9. Hematologic cont’d • White Blood Cells Increases from a pre-pregnancy level of 4300-4500/mL to 5000-12000/mL in the last trimester. Lymphocyte and monocyte numbers stay essentially the same throughout pregnancy; polymorphonuclear leucocytes are the primary contributors to the increase. • Clotting Factors Marked increases in fibrinogen and factor8. Factors VII, IX, X, and XII also increased but to a lesser extent. • Fibrinolytic activity is depressed during pregnancy and labor, although the precise mechanism is unknown. The placenta may be partially responsible for this alteration in fibrinolytic status. Plasminogen levels increase concomitantly with fibrinogens levels, causing an equilibration of clotting and lysing activity. • Coagulation and fibrinolytic systems undergo major alterations during pregnancy. Understanding these physiologic changes is necessary to manage two of the more serious problems of pregnancy: haemorrhage and thromboembolic disease, both caused by disorders in the mechanism of haemostasis.

  10. CASE # 1 (cont’d) …Walking confidently into the ER with your rediscovered knowledge of obstetric physiology, you do your best to look bored and ask the ER doc where your pregnant patient is. The doc thanks you for coming so quickly, and promptly tells you that the patient was just brought in by ambulance with acute onset shortness of breath. She is on 100% oxygen via non-rebreather, with an O2 sat of 89%, and a soft blood pressure that’s responded to boluses so far. You manage to whimper “Is that all?” and promptly turn to your R2 to pimp him some more:

  11. Question #2 • What’s the differential for shortness of breath in a pregnant woman? (Naisan)

  12. What’s the differential for shortness of breath in a pregnant woman? Crit Care Med 2005; 33[Suppl.]:S248 –S255

  13. CASE # 1 (cont’d) • The patient looks like she’s tiring, and can barely answer the nurse’s questions when the doc interrupts your educational moment and says: “I was going to intubate her, but since you’re here… You are a fellow right?”. • You reassure her that you are in fact a fellow as of 5 days ago and thank her for letting you in on all the “fun”. You then turn to your R2 and tell him to get ready to intubate while you go change your underwear.

  14. Question # 3 • What are the anatomic and physiologic changes in pregnancy that can make intubation more challenging? What drugs are safe for induction? What considerations apply when mechanically ventilating a pregnant patient? (Neil)

  15. What are the anatomic and physiologic changes in pregnancy that can make intubation more challenging? • May need smaller Ett 6 or 7 • Peripheral and pulmonary vascular resistance is decreased so decreased BP and inc PP • Vena caval compression in supine position • BVM more difficult

  16. What drugs are safe for induction? • Little evidence that a single dose of any currently available IV induction agents is harmful to the fetus • Thiopental has most evidence • Propofol and benzos are ok • Rocuronium has a longer half life, so adjust dose (75%)

  17. What considerations apply when mechanically ventilating a pregnant • Aim for pCO2 28 – 35 mmHg • PO2 > 90 mmHg • Permissive hypercapnea may be harmful to fetus (animal studies) • Monitor fetal heart • May need to allow plateau pressures >30

  18. Case # 1 (cont’d) • Thanks to your superb supervision, the intubation goes smoothly without a drop in pressure, and the patient’s FiO2 comes down to 0.6. • The CXR shows that the tube is in good position, and otherwise looks remarkably clean. • Her vitals are HR 130, BP 100/70, RR 32, PS 18/5, T= 38.2. Her JVP is elevated at 6 cm ASA, she has a loud P2, and what you think is a right-sided S3. Her lungs are clear, and her legs look remarkably svelte for a pregnant woman.

  19. Case # 1 (cont’d) • Your R2 hands you her EKG and your eyes immediately focus on leads I and III which show the following:

  20. Case # 1 (cont’d) • You look back at the film and notice that her left PA is prominent and that her left lower lobe is hyperlucent. • You smile to yourself suddenly feeling like House and inform your R1 that this woman has a PE when you notice him already filling out a heparin protocol, and think to yourself “who is this guy?”.

  21. Question # 4 • What factors place the pregnant woman at higher risk of VTEs? (Scot)

  22. Case # 1 (cont’d) • You tell your resident that you agree with the heparin, but that you’re going to have to actually prove the diagnosis if you’re going to keep her on it.

  23. Question # 5 • How would you work up a pregnant woman for PE? Please discuss imaging strategies and safe levels of radiation exposure in the fetus. (Neil)

  24. How would you work up a pregnant woman for PE? • 5 x increased prevalence in pregnant vs. non-pregnant state • Clinical symptoms • Less specific in preg • Dyspnea, tachypnea, tachycardia, leg sewlling are normal • ECG • cannot rely on usual picture • Preg will show LAD and tachy normally • D-dimer not useful • CT vs VQ

  25. IV Contrast Dye • Class B drug • animal reproduction studies have not demonstrated a fetal risk, but there are no controlled studies in pregnant women and they should be used only after assessing the potential risk/benefit

  26. Take Home • The American College of Obstetricians and Gynecologists published the following policy statement: “Women should be counseled that x-ray exposure from a single diagnostic procedure does not result in harmful fetal effects. Specifically, exposure to less than 5 rad [50 mGy] has not been associated with an increase in fetal anomalies or pregnancy loss.”

  27. Case # 1 (cont’d) • The patient comes up to the unit looking stable, when she suddenly drops her BP to 70 systolic and a her FiO2 requirements go back up to 1.0. • You quickly throw an echo probe on her chest and notice a dilated RV with septal shift, and wonder if you have any more clean underwear in your gym bag.

  28. Question # 6 • What’s the treatment for PE in a pregnant patient? Can thrombolytics be used (if so when)? When should a filter be considered? (Naisan)

  29. What’s the treatment for PE in a pregnant patient? • Incidence of venous thromboembolism is estimated at 0.76 to 1.72 per 1000 pregnancies, • 4 times as great as the risk in the non-pregnant population.

  30. Initial Treatment • Treatment with LMW heparin or unfractionated heparin is recommended until the diagnosis is ruled out by objective testing

  31. Heparin • Neither unfractionated heparin nor LMWH crosses the placenta, • advantages of LMWH • include a reduced risk of bleeding, • Predictable pharmacokinetics allowing weight-based dosing without the need for monitoring, • reduced risk of HIT • and heparin-induced osteoporotic fractures

  32. Heparin • a twice-daily weight-based regimen has been recommended due to increased renal excretion

  33. Fondaparinux • A synthetic pentasaccharide and direct inhibitor of factor Xa, • Suggests that it may be a safe alternative • Passes the placental barrier in vivo, resulting in low but measurable anti–factor Xa activity

  34. Anticoagulant therapy duringlabor and delivery • Advised that once they are in established labor, no further heparin should be taken • Patients commonly are switched to subcutaneous unfractionated heparin for the last few weeks of pregnancy,

  35. The pharmacokinetics and pharmacodynamics of subcutaneous unfractionated heparin are unpredictable during the 3rd trimester, • Meticulous monitoring of the aPTT with dosage adjustment as needed

  36. Post Partum • Treatment with low-molecular-weight heparin may be resumed within 12 hours after delivery in the absence of persistent bleeding. • Should wait >24 hrs if had epidural or poorly controlled bleeding

  37. Duration of Tx • LMWH or warfarin is recommended • For at least 6 weeks post partum and for a total of at least 6 month

  38. Thrombolytics • Experience with thrombolytic therapy in pregnancy is limited, • Due to its large molecular size (72000 kd) rt-PA does not cross the placenta. • Concern that thrombolytic therapy will lead to placental abruption, but this complication has not been reported

  39. Maternal Complications • Complication rates of thrombolytic therapy in pregnant patients are not higher than in the large randomized trials on stroke, myocardial infarction and pulmonary embolism • Comparing case reports though • J Thromb Thrombolysis 21(3), 271–276, 2006.

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