In-depth explanation of labor divided into two extensive parts. A thorough examination of proper procedure, care, and health for expecting mothers. Delicate consideration must be taken to insure the safety of the baby and promote the best chances for a healthy delivery. Topics such as biochemical messengers, hormonal balance, preterm conditions, fetal position, and cardinal movements.

1. Labor: Part 1 by La Lura White MD Maternal Fetal Medicine

2. Labor: Part 1 Labor is a remarkable natural experience. A sequence of timed events, correlate with biochemical and hormonal messengers to develop synchronized contraction patterns. These contractions become stronger, more regulated and lead to the progressive dilation and effacement of the cervix , and ultimately the delivery of a neonate. Understanding these interactions and recognizing their normal and abnormal manifestations are paramount in the appropriate management of the obstetrical patient.

3. Labor: Part 1 The onset of labor occurs around 280 days, or 40 weeks, from the first day of a patient's last menstrual period (LMP), and serves the basis for the EDC or estimated date of confinement. Actually, only 5% of births occur on the assigned due date (EDC). 50% occur within a week. Almost 90% within 2 weeks of an EDC.

4. Labor: Part 1 According to Gabbe: Labor occurs in the term patient when she is between 37 0/7 (36 completed weeks) – 42 0/7 weeks (41 completed weeks). Pre-term or premature labor: occurs prior to 37 0/7 (36 completed weeks). Post-dates: gestation that continues past the assigned EDC. Post-term (prolonged): pregnancy progresses beyond 42 0/7. Obstetrics: Normal and Problem Pregnancies, Gabbe.

5. Labor: Part 1 Adequate dating early in pregnancy is important to distinguish term from preterm conditions that may occur later in gestation, and avoid unnecessary tocolysis or labor inductions based on erroneous dating. Pregnancy dating should also use the earliest accurate information and not be changed on later less accurate data, or represent developing conditions like macrosomia or IUGR conditions. The EDC can be calculated using an appropriate pregnancy wheel. or LMP EDC

6. Labor: Part 1 Nagele’s rule = LMP-3 months + 7 days+1 year Ex: LMP = 8 May 2007 8 May 2007 (LMP) -3 months = 8 February 2007 Add 7 days = 15 February 2007 Add 1 year = 15 February 2008 EDC=15 February 2008

7. Labor: Part 1 Using these dating methods assumes the patient has a regular menstrual cycle, a 28 day interval and an anticipated ovulation at day 14. The patient should have not recently discontinued oral contraceptives, which may affect ovulation time. If the cycles are irregular, they are adjusted based onvariations in the follicular or pre-ovulatory phase (first half of the cycle). For example, if a patient has a cycle that last 34 days (34-28=6), ovulation may have occurred 6 days later, and those 6 days may need to be added to the assigned EDC.

8. Labor: Part 1 If using ultrasound data to determine a patients gestational age, use only the earliest ultrasound information, and change the EDC if and only if that early information falls outside the normal margin of error for ultrasound. The 1st trimester (conception to 13 weeks) scan should correlate within one week of EDC by LMP. The 2nd trimester(14-27 weeks) scan should correlate within two weeks of EDC by LMP. 3rd trimester (28 weeks-delivery) should correlate within three weeks of EDC by LMP, but a single femur length may be a more accurate determination of gestational age in this late ultrasounds, if no earlier data available. PATIENTS SHOULD ONLY HAVE ONE EDC

9. Labor: Part 1Uterine Changes in Pregnancy The uterus is made primarily of smooth muscle. Increase in weight 4-70g (non-pregnant) to 1100-1200g (at term). Initial myometrial hyperplasia (increase in number cells) then hypertrophy (increase in cell size). Volume increases from 10ml to 5 L. 10 times increase in uterine blood flow, with 80-90% directed to the placenta.

10. Labor: Part 1 Uterine tonicity changes from the non-pregnant muscular uterus that has a normal but significant resting tone, to a functional uterine quiescence during pregnancy, secondary to negative inhibitory factors and finally towards the end of pregnancy to an activated, stimulated responsive uterus that is able to contract. These physiological changes are divided into four phases: Phase 0: (inhibitory) Uterine maintains functional quiescence secondary to multiple agents that exert an inhibitory and includes: progesterone, prostacyclin, prostaglandin, relaxin, parathyroid hormone-related peptide, nitric oxide, calcitonin gene-related peptide, adrenomedullin and vasoactive intestinal peptide.

11. Labor: Part 1 Before term, there is a release of this negative inhibition Phase 1: (activation) Initiate by uterotopins, like estrogen and possibly progesterone, prostaglandins and corticotrophin-releasing hormone. Increased expression of contraction associated proteins, including myometrial receptors for prostaglandin and oxytocin. Activation of certain ion channels. Increase in connexin-43 (key component for gap junctions). Increase in the number of gap junctions. This primed uterus can now be stimulated to contract.

12. Labor: Part 1 Phase 2: (stimulation) Myometrium is stimulated by uterotropins like stimulatory prostaglandin (PGE2 and PGF2 alpha) and oxytocin. Previously formed Gap junctions facilitate the passage of electrical activity. Improved synchrony between myometrial contractions, leads to a progression in myometrial activity.

13. Labor: Part 1 This results in the development of initially Braxton-Hicks contractures that are irregular, low frequency, disco-ordinate and painless) to true labor contractions (regular, painful, high intensity, high frequency). Phase 3 Occurs after delivery. Involution of uterus. Mediated by oxytocin and possibly thrombin.

14. Labor: Part 1 This uterine activity is coordinated with cervical changes: The cervix, composed some smooth muscle (greatest amount found at internal os) is mainly an extracellular connective tissue matrix. It’s major component are type 1 and type 3 collagen, with a small amount of type 4 collagen at the basement membrane. In addition, this matrix includes glycosaminoglycans and proteoglycans, predominantly dermatan sulfate, hyaluronic acid, and heparin sulfate.

15. Labor: Part 1 Collagen fibers are tightly wound into a tubular configuration that maintains a tight sphincter, protected by a mucus plug, that maintains the fetus in utero during pregnancy. Fibronectin and elastin are also found among these collagen fibers, with the highest ratio of elastin to collagen at the internal os. The actual amount of elastin and smooth muscle decrease progressively from the internal to the external os of the cervix.

16. Labor: Part 1 In late pregnancy, the hyaluronic acid content in the cervix increases that leads to increased accumulation of water molecules that intersperse among the collagen fibers. Dermatan sulfate decreases, causing reduced bridging among the collagen fibers and a decrease in cervical firmness. The amount of collagen and collagen fibrils also decrease and disperse secondary to increased decorin, a proteoglycan that coats and separates collagen fibrils.

17. Labor: Part 1 Leading to a rearrangement and realignment of the collagen molecules with diminished collagen fiber and tensile strength. The cervix becomes thinner, softer, shorter and more pliable, leading to cervical ripening. Now if coordinated with regular uterine contractions, these changes allow easier progressive dilatation and effacement of the cervix, an efficient labor and a successful delivery.

18. Labor: Part 1 The “parturition cascade” thought to recruit the factors that moves uterine activity from an irregular to a more regular contraction pattern involves activation of fetal-hypothalamic-pituitary-adrenal axis. Once activated, the fetal adrenal assist the placenta in its production of steroid hormones, especially estrogens, E1 ( estrone ) E2 (estradiol ) and E3 (estriol). However, the fetal adrenals and placenta are incomplete steridogenic organs and dependent on precursors from each other in order to complete their respective steroid synthesis.

19. Labor: Part 1 The fetal adrenals are functional early in pregnancy. Fetal pituitary basophilic cells at about 7 weeks begins to produce fetal ACTH to stimulate the fetal adrenal cortex. The placenta, because of its access to these steroid precursors, can now begins to dominate steroid production, a previous function of the corpus luteum. This is also when estrogen first appears in the maternal circulation.

20. Labor: Part 1 In the first 20 weeks of gestation, placental hCG and progesterone, and possibly prolactin help maintain and regulate the fetal adrenal cortex that is later maintained by fetal ACTH. Between 32-36 weeks, there is a marked growth in the fetal adrenal cortex, in response to the increased steroid production required towards the end of gestation. So how does the placenta and the fetal adrenals interact to affect their respective steroidgenesis?

21. Labor: Part 1 The fetal adrenal cortex is deficient in 3-B hydroxysteroid dehydrogenate, the enzyme that converts pregnenolone and DHEA to progesterone and androstendione Therefore, the fetus cannot make progesterone and androstendione But the placenta is abundant in in 3-B hydroxysteroid dehydrogenate

22. Labor: Part 1 So the fetus takes LDL cholesterol from the fetal circulation and converts it to pregnenolone sulfate and DHEA-S. It then sends pregnenolone sulfate to the placenta via the umbilical artery. The placenta converts the pregnenolone to progesterone. The progesterone (that the fetus is unable to make), is sent back to the fetal adrenals where they can proceed to synthesize various mineralcorticoids and glucocorticids.

23. Labor: Part 1 The placenta can also extract LDL cholesterol from the maternal circulation to produce progesterone, so although it uses the precussors produced in the fetal adrenal cortex, it is not dependent on them to synthesize progesterone. As a preservative measure, the placenta lacks 17-alpha hydroxylase, needed to metabolize progesterone.

24. Labor: Part 1 The placenta synthesizes estrogen, but needs external supply C-19 steroid precursor (DHEA: dehydroepiandrostenedione), DHEA is supplied from the fetal adrenal intermediate zone Remember, DHEA-S, was the other byproduct, of the fetal adrenal cortex conversion of LDL cholesterol extracted from the fetal circulation, (LDL cholesterol= pregnenolone sulfate and DHEA-S) Also DHEA-S is the delivered to the fetal liver where it is converted into16-alpha hydroxydehydroepiandrosterone sulfate (16 alpha OHDHEAS) Placenta also uses 16 alpha OHDHEAS from the fetal liver , where it is first converted into 16 alpha-hydroxyandrostenedione and further aromatized to estriol )

25. Labor:: Part 1Maternal Fetal Placental Unit

26. Labor: Part 1 Once a contraction pattern of Labor is established, it is divided into three stages. First Stage: onset of labor until full cervical dilation. Second Stage: full dilation of cervix until delivery of neonate. Third Stage: delivery of neonate to delivery of placenta. Fourth Stage: the hour immediately following delivery of placenta. (originally described by Friedman)

27. Labor: Part 1 First Stage : is further divided into the latent and active phase: Latent phase: onset of labor to beginning of active phase Slower rate of cervical dilation, primarily softening and effacement 14 hours in multigravid patients and up to 20 hours in nulligravida Friedman EA; Labor: clinical evaluation and management, 2nd ed. Norwalk, CT, Appleton Century Crofts, 1978.

28. Labor: Part 1 Transition between the latent and active phases can vary, usually occurs at some time between 2 and 5 cm of cervical dilation in most patients. Important to distinguish between latent phase where slow progression is normal and dysfunctional labor, where labor is abnormal and interventions may be necessary. After the latent phase is the active phase, where there is a faster rate of cervical dilatation.

29. Labor: Part 1 Active phase is further divided into: Acceleration phase: abrupt change in the rate of dilatation Phase of maximum slope: the time of rapid cervical dilation and rapid fetal descent Deceleration phase: decreased rate of dilation of the cervical os Descent phase which coincides with second stage Friedman used the lower limit value of 1cm/hr dilatation in the active phase to refer to the phase of maximum slope, not the entire active phase that many clinicians interpret, but have normally slower cervical dilatation rates

30. Labor: Part 1 Friedman (1955) evaluated uncomplicated pregnancies delivering normal infants Primagravidas Multigravidas Min. rate of cervical dilatation (5th %) 1.2cm/h 1.5cm/h Mean rate cervical dilatation 3.0cm/h 5.7 cm/h Descent of fetal head in relation to ischial spines began well before second stage (fully dilated) Rate of descent increased late in first stage and continued linearly into second stage Friedman EA. Primigravid labor; a graphicostatistical analysis. Obstet Gynecol. Dec 1955;6(6):567-89

31. Labor: Part 1 Friedman EA. Primigravid labor; a graphicostatistical analysis. Obstet Gynecol. Dec 1955;6(6):567-89

32. Labor: Part 1 Recent challenges to Friedman’s data on patient’s labor patterns reflects changes over the past 50 years in the patients we see and how we practice. More aggressive medical management, higher induction rates, use of oxytocin, regional anesthesia and continuous fetal monitoring. Maternal characteristics have also changed, with greater body mass index [BMI] and an increase in fetal size.

33. Labor: Part 1 Challenges to Friedman’s Curve: Zhang used a statistical approach to demonstrate contemporary differences in women laboring today. He showed gradual instead of abrupt change from latent to active phase. A longer length of the active labor phase, 5.5 hr. instead of vs. 2.5 hours. No deceleration phase identified. Zhang J et al. Reassessing the labor curve in nulliparous women. Am J Obstet Gynecol 2002 Oct; 187:824-8.

34. Labor: Part 1 Common for two hours to lapse in active phase without cervical change and especially before the patient was 7 cm. was not uncommon 5th percentile for rate of cervical dilatation was determined less than 1 cm/hr. Head can take up to three hours to descend from +0 station to +4 or present at the perineum, and an additional 30 minutes for delivery. Zhang J et al. Reassessing the labor curve in nulliparous women. Am J Obstet Gynecol 2002 Oct; 187:824-8.

35. Labor: Part 1 Rouse developed a protocol requiring a minimum of 12 hours of oxytocin after membrane rupture before failed labor induction could be diagnosed. Found many nulliparas who remained in the latent phase at up to 9 hours still had safe vaginal deliveries Suggest extending the minimum period of oxytocin augmentation for active phase labor arrest from 2 to at least 4 hours was found to be safe and effective Rouse DJ Owen, Hauth JC: Criteria for failed labor induction: Prospective evaluation of a standardized protocol. Obstet Gynecol 96:671,2000.

36. Labor: Part 1 Despite these differences, it is important to have normal parameters to assess the progress of the laboring patient, and identify situations of dysfunctional labor patterns that require re-evaluation and minimize interventions when both mother and fetus are stable.

37. Labor: Part 1 Abnormal Labor Patterns Prolonged Latent Phase: abnormal duration of latent phase of first stage of labor Protraction disorders: ( Slower than normal progress) Primary dysfunctional labor Protraction of descent Arrest disorders (Complete cessation of progress) Arrest of dilatation Arrest of descent

38. Labor: Part 1 Prolonged Latent Phase: Greater than 20 h in nulliparas (mean 8.6 hr.) and 14 h in multiparas (mean 5.3 hr.). May be due to a delay in cervical ripening or change in the cervical tissue biochemistry. Not correlated with adverse outcome. Expectant management. Differentiate latent phase (normal slow progression) from Braxton-Hicks (irregular pre-labor contractions).

40. 15mg with or without phenegram 25mg or vistiril

42. Labor: Part 1 Careful assessment to fetal size and position Augmentation and/or amniotomy if appropriate especially if poor contraction strength Most common cause in nulliparas is inadequate uterine activity and in multiparas is CPD (cephaloelvic disproportion)

43. Labor: Part 1 Arrest Disorders: Secondary arrest: cessation of previously normal active phase dilatation for 2 or more hours. Suggest dystocia in presence of adequate contractions. Requires vaginal exam to verify dilatation, presentation, position and station. Evaluate with clinical pelvimetry to assess adequacy of pelvis.

44. Labor: Part 1 Oxytocin with or without amniotomy if suboptimal contractions and candidate for artificial rupture. Greater risk for further labor abnormalities and operative delivery. Arrest 2-4 hours despite adequate contractions, preferably documented with an IUPC, may need to consider cesarean section. With a recently documented 31% cesarean section rate in the U.S., this decision should be made after a thorough evaluation, however it should not be inappropriately delayed.

45. Labor: Part 1 Arrest of descent: No descent of fetal head with an epidural of >3 hours in primips and >2 hours in multips. If no epidural >2 hours in primips and >1 hour in multip.s Usually preceded by a normal pattern of dilatation and descent. Major risk factors nulliparity, fetal macrosomia, epidural analgesia, hydramnios, hypertensive disorders and gestational diabetes mellitus. Careful evaluation with the same caveat, make an appropriate, expedient and supportive decision for further management.

46. Indication Nullipara Multipara Prolonged latent phase >20 h >14 h Average second stage 50 min 20 min Prolonged second stage: without (with) epidural >2 h (>3 h) >1 h (>2 h) Protracted dilation <1.2 cm/h <1.5 cm/h Protracted descent <1 cm/h <2 cm/h Arrest of dilation* >2 h >2 h Arrest of descent* >2 h >1 h Prolonged third stage >30 min >30 min *Adequate contractions >200 Montevideo units [MVU] per 10 minutes for 2 hours.

47. Labor: Part 1 Prevent abnormalities of second stage: “ Aggressiveness may get you in trouble.” Descent and rotation often occurs before the cervix is fully dilated. No impact of duration of second stage if progressing slowly, if mother and fetus are stable. Delayed pushing after the patient is fully dilated, especially if the head is still high , “laboring down” may have better outcome

48. Labor: Part 1 Muueller-Hillis maneuver: apply pressure to uterine fundus with one hand, and with 1-2fingers in the vagina, detect if there is descent of the fetal head. If fetal head descends 1 cm or more with pressure, prognosis for vaginal delivery is good. Once the fetus is delivered……. Remember, its not over! You still need to deliver the placenta

49. Labor: Part 1 Although most placentas deliver within 5 minutes, you have up to 30 minutes Two maneuvers Brandt-Andrews: an abdominal hand is placed on the abdomen to secure the uterus while providing downward traction on the umbilical cord;pt may assist with pushing Créde maneuver: the cord is fixed with the lower hand while the hand on the abdomen secures the uterine fundus and provides upward traction

50. Labor: Part 1 The three classic signs of placental separation will be: Lengthening of the umbilical cord A gush of blood from the vagina signifying the separation of the placenta from the uterine wall A change in the shape of the uterine fundus from discoid to globular, with an elevation of fundal height Uterotonics given after delivery of the fetus (active management can hasten the delivery of the placenta, reduce blood loss and improve uterine contractility Be Patient……………

52. Severe hemorrhage and shock can lead to maternal death

53. Immediate recognition with prompt attention and treatment

55. Remember that the management of labor is an enlightening and rewarding experience between a provider and their patient, make it a positively memorable one. This concludes Labor: Part 1 We invite you to listen to Labor Part 2, where we will further discuss: Mechanics of Labor: Power, Passage and Passenger Calculating Montevideo units Maternal clinical pelvimetry Leopold's Maneuvers Fetal lie, position, presentation Cardinal movements

56. Visit our website @secondopinion2.com Or you can contact Dr. White for teaching and conference opportunities at: Second Opinion 2 1-800-219-0713 e-mail info@secondopinion2

57. Bibliography: 1) Pritchard JA Mac Donald PC (eds): William’s Obstetrics, 16th ed. New York, Appleton-Century-Crogts, 1980. 2) Creasy R.K., Resnik, R., Maternal Fetal Medicine, 6th ed. Saunders Elsvier, 2009. 3) Gibbs, Ronald S.; Karlan, Beth Y.; Haney, Arthur F.; Nygaard, Ingrid E, Danforth's Obstetrics and Gynecology, 10th Edition, Lippincott Williams & Wilkins. 4) Google Images