+ All Categories
Home > Documents > Malpresentation and Malposition.postmaturity

Malpresentation and Malposition.postmaturity

Date post: 19-Dec-2015
Category:
Upload: nishathakuri
View: 18 times
Download: 1 times
Share this document with a friend
Description:
general health caremal presentation and mal position
40
Diagnosis of malpresentations Symptoms and Signs Figure BROW PRESENTATION is caused by partial extension of the fetal head so that the occiput is higher than the sinciput (Fig S-16). On abdominal examination, more than half the fetal head is above the symphysis pubis and the occiput is palpable at a higher level than the sinciput. On vaginal examination, the anterior fontanelle and the orbits are felt. For management FIGURE S-16 FACE PRESENTATION is caused by hyper- extension of the fetal head so that neither the occiput nor the sinciput are palpable on vaginal examination (Fig S-17 and Fig S-18). On abdominal examination, a groove may be felt between the occiput and the back. On vaginal examination, the face is palpated, the examiner’s finger enters the mouth easily and the bony jaws are felt. For management FIGURE S-17 FIGURE S-18 COMPOUND PRESENTATION occurs when an arm prolapses alongside the presenting part. Both the prolapsed arm and the fetal head present in the pelvis simultaneously (Fig S-19). For management FIGURE S-19
Transcript

Occipito posterior position

Diagnosis of malpresentations

Symptoms and Signs Figure

BROW PRESENTATION is caused by partial extension of the fetal head so that the occiput is higher than the sinciput (Fig S-16).

On abdominal examination, more than half the fetal head is above the symphysis pubis and the occiput is palpable at a higher level than the sinciput.

On vaginal examination, the anterior fontanelle and the orbits are felt.

For managementFIGURE S-16

FACE PRESENTATION is caused by hyper-extension of the fetal head so that neither the occiput nor the sinciput are palpable on vaginal examination (Fig S-17 and Fig S-18).

On abdominal examination, a groove may be felt between the occiput and the back.

On vaginal examination, the face is palpated, the examiners finger enters the mouth easily and the bony jaws are felt.

For managementFIGURE S-17

FIGURE S-18

COMPOUND PRESENTATION occurs when an arm prolapses alongside the presenting part. Both the prolapsed arm and the fetal head present in the pelvis simultaneously(Fig S-19). For management FIGURE S-19

BREECH PRESENTATION occurs when the buttocks and/or the feet are the presenting parts. On abdominal examination, the head is felt in the upper abdomen and the breech in the pelvic brim. Auscultation locates the fetal heart higher than expected with a vertex presentation. On vaginal examination during labour, the buttocks and/or feet are felt; thick, dark meconium is normal.For management

COMPLETE (FLEXED) BREECH PRESENTATION occurs when both legs are flexed at the hips and knees (Fig S-20).FRANK (EXTENDED) BREECH PRESENTATIONoccurs when both legs are flexed at the hips and extended at the knees (Fig S-21).

FOOTLING BREECH PRESENTATION occurs when a leg is extended at the hip and the knee (Fig S-22). FIGURE S-20

FIGURE S-21

FIGURE S-22

TRANSVERSE LIE AND SHOULDER PRESENTATION occur when the long axis of the fetus is transverse (Fig S-23). The shoulder is typically the presenting part. On abdominal examination, neither the head nor the buttocks can be felt at the symphysis pubis and the head is usually felt in the flank. On vaginal examination, a shoulder may be felt, but not always. An arm may prolapse and the elbow, arm or hand may be felt in the vagina.

For managementFIGURE S-23

Top of page

Introduction

Postterm pregnancy is defined as a pregnancy that extends to 42 0/7 weeks and beyond.1 The reported frequency of postterm pregnancy is approximately 3-12%.1,2 However, the actual biologic variation is likely less since the most frequent cause of a postterm pregnancy diagnosis is inaccurate dating.3,4,5,6 Risk factors for actual postterm pregnancy include primiparity, prior postterm pregnancy, male gender of the fetus, and genetic factors.7,8,9,2,1

Laursen et al studied monozygotic and dizygotic twins and their subsequent development of prolonged pregnancies. They found that maternal but not paternal genetic factors influenced the rate of postterm pregnancies and accounted for the etiology in as many as 30% of these pregnancies.10 A more recently described risk factor is obesity, which appears to increase the risk of pregnancies progressing beyond 41 or 42 weeks of gestation.11,12,13 Although the last menstrual period (LMP) has been traditionally used to calculate the estimated due date (EDD), many inaccuracies exist using this method in women who have irregular cycles, have been on recent hormonal birth control, or who have first trimester bleeding. In particular, women are more likely to be oligo-ovulatory than polyovulatory, so cycles longer than 28 days are not uncommonly seen.4 If such a cycle is 35 days instead of 28 days, a second trimester ultrasound will not be powerful enough to redate the pregnancy. Thus, not only the LMP date, but the regularity and length of cycles must be taken into account when estimating gestational age.

Ultrasonographic dating early in pregnancy can improve the reliability of the EDD; however, it is necessary to understand the margin of error reported at various times during each trimester. A calculated gestational age by composite biometry from a sonogram must be considered an estimate and must take into account the range of possibilities.

Estimation range varies. For example, crown-rump length (CRL) is 3-5 days, ultrasonography performed at 12-20 weeks of gestation is 7-10 days, at 20-30 weeks is 2 weeks, and after 30 weeks is 3 weeks. Thus, a pregnancy that is 35 weeks by a 31-week ultrasound could actually be anywhere from 32 weeks to 38 weeks (35 wk +/-3 wk). If the calculated ultrasonographic gestational age varies from the LMP more than the respective range of error, it is used instead to establish the final EDD. The importance of determining by what method a pregnancy is dated cannot be overemphasized because this may have significant consequences if the physician delivers a so-called term pregnancy that is not or observes a so-called term pregnancy that is very postterm.

When determining a management plan for an impending postterm pregnancy (>40 wk of gestation but 4,500 g)35 , they are, in turn, at greater risk for other complications.36,37 Such complications associated with fetal macrosomia include prolonged labor, cephalopelvic disproportion, and shoulder dystocia with resultant risks of orthopedic or neurologic injury.

Approximately 20% of postterm fetuses have fetal dysmaturity (postmaturity) syndrome, which describes infants with characteristics of chronic intrauterine growth restriction from uteroplacental insufficiency.38 These pregnancies are at increased risk of umbilical cord compression from oligohydramnios, nonreassuring fetal antepartum or intrapartum assessment, intrauterine passage of meconium, and short-term neonatal complications (such as hypoglycemia, seizures, and respiratory insufficiency).

Meconium aspiration syndrome refers to respiratory compromise with tachypnea, cyanosis, and reduced pulmonary compliance in newborns exposed to meconium in utero and is seen in higher rates in postterm neonates.39 Indeed, the 4-fold decrease in the incidence of the meconium aspiration syndrome in the United States from 1990-1998 has been attributed primarily to a reduction in the postterm delivery rate21 with very little contribution from conventional interventions designed to protect the lungs from the chemical pneumonitis caused by chronic meconium exposure, such as amnioinfusion40,41 or routine nasopharyngeal suctioning of meconium-stained neonates.42

Postterm pregnancy is also an independent risk factor for neonatal encephalopathy43 and for death in the first year of life.16,17 While much of the work above has been conducted in postterm pregnancies. Some of the fetal risks such as presence of meconium, increased risk of neonatal academia, and even stillbirth have been described as being greater at 41 weeks ofgestation and even at 40 weeks of gestation as compared with 39 weeks gestation.22,23 For example, in one study, the rates of meconium and neonatal academia both increased throughout term pregnancies beyond 38 weeks of gestation.In addition to stillbirth being increased prior to 42 weeks of gestation, one study found that the risk of neonatal mortality also increases beyond 41 weeks of gestation.44 Thus, 42 weeks does not represent a threshold below which risk is uniformly distributed. Indeed, neonatal morbidity (including meconium aspiration syndrome, birth injury, and neonatal acidemia) appears to be the lowestat around 38 weeks and increase in a continuous fashion thereafter.45 Maternal risks and mode of deliveryThe maternal risks of postterm pregnancy are often underappreciated. These include an increase in labor dystocia (9-12% vs 2-7% at term), an increase in severe perineal injury (3rd and 4th degree perineal lacerations) related to macrosomia (3.3% vs 2.6% at term) and operative vaginal delivery, and a doubling in the rate of cesarean delivery (14% vs 7% at term).18,27,28,29 The latter is associated with higher risks of complications such as endometritis, hemorrhage, and thromboembolic disease.28,46

In addition to the medical risks, the emotional impact (anxiety and frustration) of carrying a pregnancy 1-2 weeks beyond the estimated due date should not be underestimated. In a randomized, controlled trial of women at 41 weeks of gestation, women who were induced would desire the same management 74% of the time, whereas women with serial antenatal monitoring only desired the same management 38% of the time.47

Similar to neonatal outcomes, maternal morbidity also increases in term pregnancies prior to 42 weeks of gestation. Such complications as chorioamnionitis, severe perineal lacerations, cesarean delivery rates, postpartum hemorrhage, and endomyometritis all increase progressively after 39 weeks ofgestation.23,30,31,32,21 Timing of Delivery

The first decision that must be made when managing an impending postterm pregnancy is whether to deliver. In certain cases (eg, nonreassuring surveillance, oligohydramnios, growth restriction, certain maternal diseases), the decision is straightforward. In these high-risk situations, the time at which the risks of remaining pregnant begin to outweigh the risks of delivery may come at an earlier gestational age (eg, 39 weeks of gestation). However, frequently several options can be considered when determining a course of action in the low-risk pregnancy. The certainty of gestational age, cervical examination findings, estimated fetal weight, patient preference, and past obstetric history must all be considered when mapping a course of action.

The main argument against a policy of routine induction of labor at 41 0/7 to 41 6/7 weeks has been that induction increases the rate of cesarean delivery without decreasing maternal and/or neonatal morbidity. Some of the studies that failed to show a reduction in fetal/neonatal morbidity were diluted by poorly dated pregnancies that were not necessarily postterm. In addition, the potential for increasing the risk for cesarean delivery with a failed induction is far less likely in the era of safe and effective cervical ripening agents.

To date, more than 10 studies have been published of elective induction of labor, many of them at 41 weeks of gestation.48,34,49,50,51,52 The preponderance of the evidence from these studies, including meta-analyses, find that not only israte of cesarean delivery not increased in women who were randomized to routine induction of labor, but alsomore cesarean deliveries were performed in the noninduction groups, and the most frequent indication was fetal distress. Even with multiple studies, very few neonatal differences have been demonstrated. However, the reduction in meconium is statistically significant andtherate of neonatal mortality is lower.

In summary, routine induction at 41 weeks ofgestation does not increase the cesarean delivery rate and may decrease it without negatively affecting perinatal morbidity or mortality. In fact,both the woman and theneonate benefitfrom a policy of routine induction of labor in well-dated, low-risk pregnancies at 41 weeks' gestation. A policy of routine induction at 40 weeks' has few benefits, and there are multiple reasons not to allow a pregnancy to progress beyond 42 weeks.

Prior to 41 weeks of gestation, the evidence becomes more scant with only 3 small, non-US, randomized, controlled trials comparing elective induction of labor to expectant management of pregnancy.51 However, elective induction of labor is increasingly being used as a management strategy.53,54 While this management may be reasonable in a practice that allows 48 hours or more for the management of the latent phase and the first stage of labor overall, in a setting where induction of labor is called a failure after 18-24 hours, it will likely further increase the cesarean delivery rate.

Prevention of Postterm Pregnancy

As noted above, the most decisive way to prevent postterm pregnancy is induction of labor prior to 42 weeks gestation. However, since complications rise during 40 and 41 weeks' gestation and both clinicians and patients are concerned about the risks of induction of labor, it is perceivably better for women to go into spontaneous labor at 39 weeks of gestation on their own. Several minimally invasive interventions have been recommended to encourage the onset of labor at term and prevent postterm pregnancy, including membrane stripping, unprotected coitus, and acupuncture.

Stripping or sweeping of the fetal membranes refers to digital separation of the membranes from the wall of the cervix and lower uterine segment. This technique, which likely acts by releasing endogenous prostaglandins from the cervix, requires the cervix to be sufficiently dilated to admit the practitioners finger. Although stripping of the membranes may be able to reduce the interval to spontaneous onset of labor, a reduction in operative vaginal delivery, cesarean delivery rates, or maternal or neonatal morbidity has not been consistently proven.55,56,57

Unprotected sexual intercourse causes uterine contractions through the action of prostaglandins in semen and potentially release of endogenous prostaglandins similar to stripping of the membranes. Indeed, prostaglandins were originally isolated from extract of prostate and seminal vesicle glands, hence their name. Despite some conflicting data, it appears that unprotected coitus may lead to the earlier onset of labor, reduction in postterm pregnancy rates, and less induction of labor.58,59,60

In a small randomized trial that attempted to address this question, women were randomized to a group advised to have coitus versus a control group that was not. In this study, the women advised to have coitus did so more often (60% vs 40%), the difference in the rate of spontaneous labor was not measurablein this underpowered study.61 Similarly, the efficacy of acupuncture for induction of labor cannot be definitively assessed because of the paucity of trial data; this requires further examination.62,63 Cervical Ripening and Intrapartum Management

Once the decision to deliver a patient has been made, the management of the labor induction depends on the clinical setting, and a brief review of cervical ripening agents and potential complications of induction of labor is appropriate. A comprehensive review of all available methods for cervical ripening, indications, contraindications, and dosing is beyond the scope of this article.

As many as 80% of patients who reach 42 weeks' gestation have an unfavorable cervical examination (ie, Bishop Score 160 beats per minute

2. Dinoprostone Hyperstimulation Incidence: 17%

3. Misoprostol Hyperstimulation Incidence

1. Intravaginal gel or tablet: 8%

2. Oral crushed form or tablet: 1 to 2%

3. Uterine Rupture in VBAC

1. Risk: 2.5% in Trial of Labor after Cesarean

4. References

1. Crane (2001) Obstet Gynecol 97:926

2. Ravasia (2000) Obstet Gynecol 183:1176

7. Complications: Hyperstimulation Management

1. Consider Terbutaline SQ

2. Dinoprostone (Cervidil): Remove

3. Misoprostol (Cytotec): Irrigate vagina

1. Use Normal Saline via 100 cc Syringe (no needle)

2. Repeat several times until pill fragments recovered

8. References

1. Adair (2000) Clin Obstet Gynecol 43:447

2. Crane (2001) Obstet Gynecol 97:926

3. Sanchez-Ramos (1997) Obstet Gynecol 89:633

4. Tenore (2003) Am Fam Physician 67(10):2123

Dinoprostone (C0012472)

Definition (MSH)The most common and most biologically active of the mammalian prostaglandins. It exhibits most biological activities characteristic of prostaglandins and has been used extensively as an oxytocic agent. The compound also displays a protective effect on the intestinal mucosa.

Definition (NCI)A synthetic prostaglandin E2 (PGE2) analogue with smooth muscle contraction inducing property. It has been suggested that PGE2 regulates the intracellular levels of cyclic 3, 5-adenosine monophosphate (cAMP) by activating adenylate cyclase and thereby increases cellular membrane calcium ion transport. By acting directly on the myometrium, dinoprostone induces uterine and gastrointestinal smooth muscle contractions.

1. Indications

1. Bishop Score 10 contractions in 20 minutes

2. Dinoprostone Tachysystole Incidence: 33%

3. Misoprostol Tachysystole Incidence

1. Intravaginal gel or tablet: 31 to 49%

2. Oral crushed form or tablet: 16 to 22%

2. Hyperstimulation

1. Criteria

1. Exaggerated uterine response (i.e. Tachysystole)

2. Concerning Fetal Heart Rate tracing

1. Late Decelerations

2. Fetal Tachycardia >160 beats per minute

2. Dinoprostone Hyperstimulation Incidence: 17%

3. Misoprostol Hyperstimulation Incidence

1. Intravaginal gel or tablet: 8%

2. Oral crushed form or tablet: 1 to 2%

3. Uterine Rupture in VBAC

1. Risk: 2.5% in Trial of Labor after Cesarean

4. References

1. Crane (2001) Obstet Gynecol 97:926

2. Ravasia (2000) Obstet Gynecol 183:1176

7. Complications: Hyperstimulation Management

1. Consider Terbutaline SQ

2. Dinoprostone (Cervidil): Remove

3. Misoprostol (Cytotec): Irrigate vagina

1. Use Normal Saline via 100 cc Syringe (no needle)

2. Repeat several times until pill fragments recovered

8. References

1. Adair (2000) Clin Obstet Gynecol 43:447

2. Crane (2001) Obstet Gynecol 97:926

3. Sanchez-Ramos (1997) Obstet Gynecol 89:633

4. Tenore (2003) Am Fam Physician 67(10):2123

Dinoprostone (C0012472)

Definition (MSH)The most common and most biologically active of the mammalian prostaglandins. It exhibits most biological activities characteristic of prostaglandins and has been used extensively as an oxytocic agent. The compound also displays a protective effect on the intestinal mucosa.

Definition (NCI)A synthetic prostaglandin E2 (PGE2) analogue with smooth muscle contraction inducing property. It has been suggested that PGE2 regulates the intracellular levels of cyclic 3, 5-adenosine monophosphate (cAMP) by activating adenylate cyclase and thereby increases cellular membrane calcium ion transport. By acting directly on the myometrium, dinoprostone induces uterine and gastrointestinal smooth muscle contractions.


Recommended