Tuesday, August 7, 2012
Premenstrual Syndrome
Essentials of Diagnosis
• Symptoms include mood symptoms (irritability, mood swings, depression, anxiety), physical symptoms (bloating, breast tenderness, insomnia, fatigue, hot flushes, appetite changes), and cognitive changes (confusion and poor concentration).
• Symptoms must occur in the second half of the menstrual cycle (luteal phase).
• There must be a symptom-free period of at least 7 days in the first half of the cycle.
• Symptoms must occur in at least two consecutive cycles.
• Symptoms must be severe enough to require medical advice or treatment.
General Considerations
Premenstrual syndrome (PMS) is a psychoneuroendocrine disorder with biologic, psychologic, and social parameters. It is both difficult to define adequately and quite controversial. One major difficulty in detailing whether PMS is a disease or a description of physiologic changes is its extraordinary prevalence. Up to 75% of women experience some recurrent PMS symptoms; 20–40% are mentally or physically incapacitated to some degree, and 5% experience severe distress. The highest incidence occurs in women in their late 20s to early 30s. PMS is rarely encountered in adolescents and resolves after menopause. Evidence suggests that women who have suffered with PMS and premenstrual dysphoric disorder are more likely to suffer from perimenopausal symptoms.
The symptoms of PMS may include headache, breast tenderness, pelvic pain, bloating, and premenstrual tension. More severe symptoms include irritability, dysphoria, and mood lability. When these symptoms disrupt daily functioning, they are clustered under the name premenstrual dysphoric disorder (PMDD).
Other symptoms commonly included in PMS are abdominal discomfort, clumsiness, lack of energy, sleep changes, and mood swings. Behavioral changes include social withdrawal, altered daily activities, marked change in appetite, increased crying, and changes in sexual desire. In all, more than 150 symptoms have been related to PMS. Thus the symptom complex of PMS has not been clearly defined.
Pathogenesis
The etiology of the symptom complex of PMS is not known, although several theories have been proposed, including estrogen–progesterone imbalance, excess aldosterone, hypoglycemia, hyperprolactinemia, and psychogenic factors. A hormonal imbalance previously was thought to be related to the clinical manifestations of PMS/PMDD, but in the most recent consensus, physiologic ovarian function is believed to be the trigger. This is supported by the efficacy of ovarian cyclicity suppression, either medically or surgically, in eliminating premenstrual complaints.
Further research has shown that serotonin (5-hydroxytryptamine [5-HT]), a neurotransmitter, is important in the pathogenesis of PMS/PMDD. Both estrogen and progesterone have been shown to influence the activity of serotonin centrally. Many of the symptoms of other mood disorders resembling the features of PMS/PMDD have been associated with serotonergic dysfunction.
Diagnosis
No objective screening or diagnostic tests for PMS and PMDD are available; thus special attention must be paid to the patient's medical history. Certain medical conditions (eg, thyroid disease and anemia) with symptoms that can mimic those of PMS/PMDD must be ruled out.
The patient is instructed to chart her symptoms for at least 2 symptomatic cycles. The classic criteria for PMS require that the patient have symptoms in the luteal phase and a symptom-free period of at least 7 days in the first half of the cycle for a minimum of 2 consecutive symptomatic cycles. To meet the criteria for PMDD, in addition to the criteria for PMS, she must have a chief complaint of at least 1 of the following: irritability, tension, dysphoria, or mood lability; and 5 of 11 of the following: depressed mood, anxiety, affective lability, irritability, decreased interest in daily activities, concentration difficulties, lack of energy, change in appetite or food cravings, sleep disturbances, feeling overwhelmed, or physical symptoms (eg, breast tenderness, bloating).
Clinical Findings
A careful history and physical examination are most important to exclude organic causes of PMS localized to the reproductive, urinary, or gastrointestinal tracts. Most patients readily describe their symptoms, but careful questioning may be needed with some patients who may be reluctant to do so. Although it is important not to lead a patient to exaggerate her concerns, it is equally important not to minimize them.
Symptoms of PMS may be specific, well localized, and recurrent. They may be exacerbated by emotional stress. Migrainelike headaches may occur, often preceded by visual scotomas and vomiting. Symptomatology varies among patients but often is consistent in the same patient.
A psychiatric history should be obtained, with special attention paid to a personal history of psychiatric problems or a family history of affective disorders. A mental status evaluation of affect, thinking, and behavior should be performed and recorded. A prospective diary correlating symptoms, daily activities, and menstrual flow can be useful to document changes and to encourage patient participation in her care.
If underlying psychiatric illness is suspected, a psychiatric evaluation is indicated. The most common associated psychiatric illness is depression, which generally responds to antidepressant drugs and psychotherapy. Recall that psychiatric illnesses have premenstrual exacerbations, so medications should be altered accordingly.
Treatment
Treatment of PMS/PMDD depends on the severity of the symptoms. For some women, changes in eating habits—limiting caffeine, alcohol, tobacco, and chocolate intake, and eating small, frequent meals high in complex carbohydrates—may be sufficient. Decreasing sodium intake may alleviate edema. Stress management, cognitive behavioral therapy, and aerobic exercise have all been shown to improve symptoms.
Low-risk pharmacologic interventions that may be effective include calcium carbonate (1000–1200 mg/d) for bloating, food cravings, and pain; magnesium (200–360 mg/day) for water retention; vitamin B6 (note that prolonged use of 200 mg/d may cause peripheral neurotoxicity) and vitamin E; nonsteroidal anti-inflammatory drugs (NSAIDs); spironolactone for cyclic edema; and bromocriptine for mastalgia. Herbal preparations have been proposed. St. John's wort has potential given its selective serotonin reuptake inhibitor (SSRI)-like effects but should be used with caution given its enzyme-inducing property on cytochrome P450. Chaste berry fruit (Vitex agnus-castus) 20 mg/day has been shown to be more effective than placebo and has minimal side effects but is not as effective as fluoxetine.
For symptoms of severe PMS and PMDD, further pharmacologic intervention may be necessary. Psychotropic medications that are effective include SSRIs, desipramine, and L-tryptophan. SSRIs have minimal side effects and provide symptom improvement in more than 60% of patients studied. Treatment should be given 14 days prior to the onset of menstruation and continued through the end of the cycle. Anxiolytics such as alprazolam and buspirone also have been shown to be efficacious, but their side effects and potential for dependence must be seriously considered.
Hormonal interventions have been shown to be effective. Use of gonadotropin-releasing hormone (GnRH) agonists leads to a temporary "medical menopause" and an improvement in symptoms. Their limitations lie in a hypoestrogenic state and a risk for osteoporosis, although "add-back" therapy with estrogen and progesterone may obviate these problems. Danazol may improve mastalgia. Finally, bilateral oophorectomy is a definitive surgical treatment option; again, estrogen replacement would be recommended.
Use of oral contraceptives has been suggested because they suppress ovulation. However, studies have found little difference between women taking a low-dose birth control pill and women who do not take pills, and oral contraceptives currently are not recommended for treatment of PMS/PMDD.
Rupture of the Uterus
Essentials of Diagnosis
- Fetal heart rate abnormalities.
- Increased suprapubic pain and tenderness with labor.
- Sudden cessation of uterine contractions with a "tearing" sensation.
- Vaginal bleeding (or bloody urine).
- Recession of the fetal presenting part.
Rupture
of the pregnant uterus is a potential obstetric catastrophe and a major cause
of maternal death. The incidence of uterine rupture is 0.8% for women with a
prior low-transverse uterine scar and 4–8% for women with a prior classic scar.
Complete rupture includes the entire thickness of the uterine wall and, in most
cases, the overlying serosal peritoneum (broad ligament) (Fig 20–5). Occult
or incomplete rupture is a term usually reserved for dehiscence of a
uterine incision from previous surgery, in which the visceral peritoneum
remains intact. Such defects usually are asymptomatic unless converted to
complete rupture during the course of pregnancy or labor.
Risk factors
Risk factors for uterine rupture include history of
hysterotomy (cesarean section, myomectomy, metroplasty, cornual resection),
trauma (motor vehicle accident, rotational forceps, extension of a cervical
laceration), uterine overdistention (hydramnios, multiple gestation,
macrosomia), uterine anomalies, placenta percreta, and choriocarcinoma.
Ruptures usually occur during the
course of labor. One notable exception is scars from a classic cesarean section
(or hysterotomy), one-third of which rupture during the third trimester before
term and before the onset of labor. Other causes of rupture without labor are
placenta percreta, invasive mole, choriocarcinoma, and cornual pregnancy.
Complete ruptures can be classified as
traumatic or spontaneous. Traumatic ruptures occur most commonly as a result of
motor vehicle accidents, improper administration of an oxytocic agent, or an
inept attempt at operative vaginal delivery. Breech extraction through an
incompletely dilated cervix is the type of operative vaginal delivery most
likely to produce uterine rupture. Other maneuvers that impose risk of rupture
are internal podalic version and extraction, difficult forceps, destructive
operations, and cephalic replacement to relieve shoulder dystocia. Neglected
obstructed labor may be responsible for rupture of the uterus. Causes of
obstructed labor include contracted pelvis, fetal macrosomia, brow or face
presentation, hydrocephalus, or tumors involving the birth canal. The vast
majority of uterine ruptures are associated with prior uterine surgery. Previous
uterine surgery includes both classic and low cervical section, intramural or
submucous myomectomy, resection of the uterine cornu, metroplasty, and
trachelectomy. Other operative procedures that may have damaged the uterus are
vigorous curettage, induced abortion, and manual removal of the placenta.
There are no reliable signs of
impending uterine rupture that occurs before labor, although the sudden
appearance of gross hematuria is suggestive.
Rupture may produce local pain and
tenderness associated with increased uterine irritability and, in some cases, a
small amount of vaginal bleeding. Premature labor may follow. As the extent of
the rupture increases, more pain, more bleeding, and perhaps signs of
hypovolemic shock will occur. Exsanguination prior to surgery is unlikely
because of the reduced vascularity of scar tissue, but the placenta may be
completely separated and the fetus extruded partially or completely into the
abdominal cavity.
By far the most common clinical
setting for rupture of the uterus is rupture of a low cervical scar; this
almost always occurs during active labor. Clearly identifiable signs and
symptoms may be lacking. However 78–90% of patients have FHR abnormalities as
the first sign of rupture. Although it is possible that labor will progress to
the vaginal birth of an unaffected infant, rupture may lacerate a uterine
artery, producing exsanguination, or the fetus may be extruded into the
abdominal cavity. If a defect is palpated in the lower uterine segment following
vaginal delivery, laparotomy may be necessary to assess the damage. Laparotomy
is mandatory if continuing hemorrhage is present. If such a defect is palpated
in a stable patient who does not require exploration, a subsequent trial of
labor is contraindicated.
Although much less common than FHR
abnormalities, other findings of spontaneous rupture during labor are
suprapubic pain and tenderness, cessation of uterine contractions,
disappearance of fetal heart tones, recession of the presenting part, and
vaginal hemorrhage—followed by the signs and symptoms of hypovolemic shock and
hemoperitoneum. Ultrasound examination might confirm an abnormal fetal position
or extension of the fetal extremities. Hemoperitoneum can sometimes be seen on
ultrasound.
The clinical picture depends on the
extent of rupture. Unfortunately, valuable time is often lost because the
rupture was not diagnosed at the time of initial examination. Whenever a newly
delivered patient exhibits persistent bleeding or shock, the uterus must be
carefully reexamined for signs of a rupture that may have been difficult to
palpate because of the soft, irregular tissue surfaces.
Whenever an operative delivery is
performed—especially if the history includes events or problems that increase
the likelihood of uterine rupture—the initial examination of the uterus and
birth canal must be diligent. A dehiscence of the lower uterine segment
contained only by a layer of visceral peritoneum is not an uncommon finding at
time of repeat cesarean section.
Treatment is dictated by clinical
scenario and can range from simply repairing the defect and obtaining
hemostasis to removing the entire uterus. If hysterectomy is deemed necessary,
either total hysterectomy or the subtotal operation can be performed, depending
on the site of rupture and the patient's condition. The most difficult cases
are lateral ruptures involving the lower uterine segment and a uterine artery
with hemorrhage and hematoma formation obscuring the operative field. Care must
be taken to avoid ureteral damage by blind suturing at the base of the broad
ligament. If there is a question of ureteral occlusion by a suture, it is best
to perform cystotomy to observe the bilateral appearance of an intravenously
injected dye such as indigo carmine. If doubt still exists, a retrograde
ureteral catheter can be passed upward through the cystotomy wound.
If childbearing is important and the
risks—both short and long term—are acceptable to the patient, rupture repair
can be attempted. Many ruptures can be repaired. Successful pregnancies have
been reported following uterine repair; however, the risk of rupture in a
subsequent pregnancy is at least as high as the risk with a prior classic
cesarean section. Occult ruptures of the lower uterine segment encountered at
repeat section can be treated by freshening the wound edges and secondary
repair, but the newly repaired incision is at increased risk for rupture, and a
subsequent trial of labor is contraindicated.
Most causes of uterine rupture can be
avoided by carefully selecting patients for trial of labor. Thorough and
well-documented informed consent that includes mention of fetal or maternal
death is needed. The ideal candidate will have a single prior low-transverse
cesarean for a nonrepetitive indication (eg, breech), will have a prior vaginal
delivery, will present in active labor, and will not require augmentation
during labor. The further the characteristics diverge from those of this ideal
patient, the greater the chance of a failed trial of labor and complications
including uterine rupture. Continuous FHR monitoring by fetal scalp electrode
as soon as feasible is the best means of detecting evolving rupture during
labor. Two-layer closure of the uterine incision and increasing interval
between pregnancies appears to decrease the risk of subsequent rupture of the
low-transverse scar.
The complications of ruptured uterus
are hemorrhage, shock, postoperative infection, bladder or ureteral damage,
thrombophlebitis, amniotic fluid embolus, DIC, pituitary failure, and death.
Umbilical Cord Prolapse
Umbilical cord prolapse is defined as descent of
the umbilical cord into the lower uterine segment, where it may lie adjacent to
the presenting part (occult cord prolapse) or below the presenting part (overt
cord prolapse) . In occult prolapse, the umbilical cord cannot be palpated
during pelvic examination, whereas in funic presentation, which is
characterized by prolapse of the umbilical cord below the level of the
presenting part before the rupture of membranes occurs, the cord often can be
easily palpated through the membranes. Overt cord prolapse is associated with
rupture of the membranes and displacement of the umbilical cord into the
vagina, often through the introitus.
Prolapse of the umbilical cord to a level at or below the
presenting part exposes the cord to intermittent compression between the
presenting part and the pelvic inlet, cervix, or vaginal canal. Compression of
the umbilical cord compromises fetal circulation and, depending on the duration
and intensity of compression, may lead to fetal hypoxia, brain damage, and
death. In overt cord prolapse, exposure of the umbilical cord to air causes
irritation and cooling of the cord, resulting in further vasospasm of the cord
vessels.
The incidence of overt umbilical cord
prolapse in cephalic presentations is 0.5%, frank breech 0.5%, complete breech
5%, footling breech 15%, and transverse lie 20%. The incidence of occult
prolapse is unknown because it can be detected only by fetal heart rate changes
characteristic of umbilical cord compression. However, some degree of occult
prolapse appears to be common, given that as many as 50% of monitored labors
demonstrate fetal heart rate changes compatible with umbilical cord
compression. In most cases, the compression is transient and can be rectified
simply by changing the patient's position.
Whether occult or overt, umbilical
cord prolapse is associated with significant rates of perinatal morbidity and
mortality because of intermittent compression of blood flow and resultant fetal
hypoxia. The perinatal mortality rate associated with all cases of overt
umbilical cord prolapse approaches 20%. Prematurity, itself a contributor to
the incidence of umbilical cord prolapse, accounts for a considerable portion
of this perinatal loss.
Causes
Any obstetric condition that predisposes
to poor application of the fetal presenting part to the cervix can result in
prolapse of the umbilical cord. Cord prolapse is associated with prematurity
(< 34 weeks' gestation), abnormal presentations (breech, brow, compound,
face, transverse), occiput posterior positions of the head, pelvic tumors,
multiparity, placenta previa, low-lying placenta, and cephalopelvic
disproportion. In addition, cord prolapse is possible with hydramnios, multiple
gestation, or premature rupture of the membranes occurring before engagement of
the presenting part. A recent study revealed that obstetric intervention
contributes to nearly half of cases of umbilical cord prolapse. Examples cited
include amniotomy, scalp electrode application, intrauterine pressure catheter
insertion, attempted external cephalic version, and expectant management of
preterm premature rupture of membranes.
Overt cord prolapse can be diagnosed
simply by visualizing the cord protruding from the introitus or by palpating
loops of cord in the vaginal canal.
The diagnosis of funic presentation is
made by pelvic examination if loops of cord are palpated through the membranes.
Antepartum detection of funic presentation is discussed below.
Occult prolapse is rarely palpated
during pelvic examination. This condition can be inferred only if fetal heart
rate changes (variable decelerations, bradycardia, or both) associated with
intermittent compression of the umbilical cord are detected during monitoring.
The fetus in good condition whose
well-being is jeopardized by umbilical cord compression may exhibit violent
activity readily apparent to the patient and the obstetrician. Variable fetal
heart rate decelerations will occur during uterine contractions, with prompt
return of the heart rate to normal as each contraction subsides. If cord
compression is complete and prolonged, fetal bradycardia occurs. Persistent,
severe, variable decelerations and bradycardia lead to development of hypoxia,
metabolic acidosis, and eventual damage or death. As the fetal status
deteriorates, activity lessens and eventually ceases. Meconium staining of the
amniotic fluid may be noted at the time of membrane rupture.
Cesarean section is a major operative
procedure with known anesthetic, hemorrhagic, and operative complications.
These risks must be weighed against the real risk to the fetus of continued
hypoxia if labor were to continue.
Maternal risks encountered at vaginal
delivery include laceration of the cervix, vagina, or perineum resulting from a
hastily performed delivery.
The neonate at delivery may be
hypoxic, acidotic, or moribund. A pediatric team should be present to effect
immediate resuscitation of the newborn.
Patients at risk for umbilical cord
prolapse should be treated as high-risk patients. Patients with
malpresentations or poorly applied cephalic presentations should be considered
for ultrasonographic examination at the onset of labor to determine fetal lie
and cord position within the uterine cavity. Because most prolapses occur
during labor as the cervix dilates, patients at risk for cord prolapse should
be continuously monitored to detect abnormalities of the fetal heart rate.
Artificial rupture of membranes should be avoided until the presenting part is
well applied to the cervix. At the time of spontaneous membrane rupture, a
prompt, careful pelvic examination should be performed to rule out cord
prolapse. Should amniotomy be required and the presenting part remains
unengaged, careful needling of the membranes and slow release of the amniotic
fluid can be performed until the presenting part settles against the cervix.
The diagnosis of overt cord prolapse
demands immediate action to preserve the life of the fetus. An immediate pelvic
examination should be performed to determine cervical effacement and
dilatation, station of the presenting part, and strength and frequency of
pulsations within the cord vessels. If the fetus is viable, the patient should
be placed in the knee–chest position, and the examiner should apply continuous
upward pressure against the presenting part to lift and maintain the fetus away
from the prolapsed cord until preparations for cesarean delivery are complete.
Alternatively, 400–700 mL of saline can be instilled into the bladder in order
to elevate the presenting part. Oxygen should be given to the mother until the
anesthesiologist is prepared to administer a rapid-acting inhalation anesthetic
for delivery. Successful reduction of the prolapsed umbilical cord has been
described, but such an attempt may worsen fetal heart rate changes and should
not delay preparation for cesarean delivery. Abdominal delivery should be
accomplished as rapidly as possible through a generous midline abdominal
incision, and a pediatric team should be on standby in the event immediate
resuscitation of the newborn is necessary.
If cord compression patterns (variable
decelerations) of the fetal heart rate are recognized during labor, an
immediate pelvic examination should be performed to rule out overt cord
prolapse. If occult cord prolapse is suspected, the patient should be placed in
the lateral Sims or Trendelenburg position in an attempt to alleviate cord
compression. If the fetal heart rate returns to normal, labor can be allowed to
continue, provided no further fetal insult occurs. Oxygen should be
administered to the mother, and the fetal heart rate should be continuously
monitored electronically. Amnioinfusion can be performed via an intrauterine
pressure catheter in order to instill fluid within the uterine cavity and
possibly decrease the incidence of variable decelerations. If the cord
compression pattern persists or recurs to the point of fetal jeopardy (moderate
to severe variable decelerations or bradycardia), a rapid cesarean section
should be accomplished.
The patient at term with funic
presentation should be delivered by cesarean section prior to membrane rupture.
However, there is no consensus on management if the fetus is premature. The
most conservative approach is to hospitalize the patient on bed rest in the
Sims or Trendelenburg position in an attempt to reposition the cord within the
uterine cavity. Serial ultrasonographic examinations should be performed to
ascertain cord position, presentation, and gestational age.
Vaginal delivery can be successfully
accomplished in cases of overt or occult cord prolapse if, at the time of
prolapse, the cervix is fully dilated, cephalopelvic disproportion is not
anticipated, and an experienced physician determines that delivery is imminent.
Internal podalic version, midforceps rotation, or any other operative technique
is generally more hazardous to mother and fetus in this situation than is a
judiciously performed cesarean delivery. Cesarean delivery is the preferred
route of delivery in most cases. Vaginal delivery is the route of choice for
the previable or dead fetus.
Maternal complications include those
related to anesthesia, blood loss, and infection following cesarean section or
operative vaginal delivery. Maternal recovery is generally complete.
Although the prognosis for intrapartum
cord prolapse is greatly improved, fetal mortality and morbidity rates still
can be high, depending on the degree and duration of umbilical cord compression
occurring before the diagnosis is made and neonatal resuscitation is started.
If the diagnosis is made early and the duration of complete cord occlusion is
less than 5 minutes, the prognosis is good. Gestational age and trauma at
delivery also affect the final neonatal outcome. If complete cord occlusion has
occurred for longer than 5 minutes or if intermittent partial cord occlusion
has occurred over a prolonged period of time, fetal damage or death may occur.
Thursday, August 2, 2012
Abruptio Placentae
Premature Separation of
the Placenta (Abruptio Placentae, Marginal Sinus Bleed
Essentials of Diagnosis
- Unremitting abdominal (uterine) or back pain.
- Irritable, tender, and often hypertonic uterus.
- Visible or concealed hemorrhage.
- Evidence of fetal distress may or may not be present, depending on the severity of the process.
Premature separation of the placenta is defined as
separation from the site of uterine implantation before delivery of the fetus
The term premature separation of the normally implanted
placenta is most descriptive because it differentiates the placenta that
separates prematurely but that is implanted some distance beyond the cervical
internal os from one that is implanted over the cervical internal os—that is,
placenta previa. This is cumbersome, however, and hence a shorter term abruptio
placenta, or placental abruption, has been used. The Latin abruptio
placentae, which means "rending asunder of the placenta," denotes
a sudden accident, a clinical characteristic of most cases of this
complication.
Two principal forms of premature separation of the placenta
can be recognized, depending on whether the resulting hemorrhage is external or
concealed
Concealed form
Less often, the blood does not escape externally but is
retained between the detached placenta and the uterus, leading to concealed
hemorrhage
Detachment of the placenta may be complete, and the
complications often are severe. Approximately 10% of abruptions are associated
with clinically significant coagulopathies (disseminated intravascular
coagulation [DIC]), but 40% of those severe enough to cause fetal death are
associated with coagulopathy
External form
Some of the bleeding of placental abruption usually
insinuates itself between the membranes and uterus, and then escapes through
the cervix, causing external hemorrhage
Placental detachment is more likely to be incomplete, and
the complications are fewer and less severe. Occasionally, the placental
detachment involves only the margin or placental rim. Here, the most important
complication is the possibility of premature labor.
Etiology
The hypertensive states of pregnancy are associated with
2.5–17.9% incidence of placental separation
Other predisposing factors include advanced maternal age,
multiparity, uterine distention (e.g., multiple gestation, hydramnios),
vascular disease (e.g., diabetes mellitus, systemic lupus erythematosus),
thrombophilias, uterine anomalies or tumors (e.g., leiomyoma), cigarette
smoking, alcohol consumption (> 14 drinks per week), cocaine use, and
possibly maternal type O blood.
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Pathophysiology & Pathology
Several mechanisms are thought to be
important in the pathophysiology of premature placental separation. One
mechanism is local vascular injury that results in vascular rupture into the
decidua basalis, bleeding, and hematoma formation. The hematoma shears off
adjacent denuded vessels, producing further bleeding and enlargement of the
area of separation.
Another mechanism is initiated by an abrupt rise in
uterine venous pressure transmitted to the intervillous space. This results in
engorgement of the venous bed and separation of all or a portion of the
placenta.
Conditions predisposing to vascular injury and known to be
associated with an increased incidence of placental separation are
preeclampsia–eclampsia, chronic hypertension, diabetes mellitus, chronic renal
disease, cigarette smoking, and cocaine use.
Retained or concealed hemorrhage is likely when:
2.
The placenta is completely separated yet the membranes
retain their attachment to the uterine wall.
4.
The fetal head is so closely applied to the lower
uterine segment that the blood cannot make its way past it.
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Differential
Diagnosis
With severe placental abruption, the
diagnosis generally is obvious. Milder and more common forms of abruption are
difficult to recognize with certainty, and the diagnosis is often made by
exclusion. Unfortunately, neither laboratory tests nor diagnostic methods are
available to detect lesser degrees of placental separation accurately.
Therefore, with vaginal bleeding complicating a viable pregnancy, it often
becomes necessary to rule out placenta previa and other causes of bleeding by
clinical inspection and ultrasound evaluation. It has long been taught, perhaps
with some justification, that painful uterine bleeding means placental
abruption, whereas painless uterine bleeding is indicative of placenta previa.
Unfortunately, the differential diagnosis is not that simple. Labor
accompanying placenta previa may cause pain suggestive of placental abruption.
On the other hand, abruption may mimic normal labor, or it may cause no pain at
all. The latter is more likely with a posteriorly implanted placenta. At times,
the cause of the vaginal bleeding remains obscure even after delivery.
Management
Expectant Management in Preterm Pregnancy
Delaying delivery may prove beneficial
when the fetus is immature, but it is exceptional, not rule. This management
pathway should be attempted only with careful observation of the patient and a
clear clinical picture. In general, expectant management may be appropriate
when the mother is stable, the fetus is immature, and the fetal heart tracing
is reassuring. The patient should be observed in the labor and delivery suite
for 24–48 hours to ensure that further placental separation is not occurring.
Continuous fetal and uterine monitoring should be maintained. Changes in fetal
status may be the earliest indication of an expanding abruption.
Emergency Measures
Most cases of placental abruption are diagnosed as an
acute event (upon presentation to labor and delivery or during the intrapartum
period), making immediate intervention necessary. If the patient exhibits
clinical findings that become progressively more severe or if a major placental
separation is suspected as manifested by hemorrhage, uterine spasm, or fetal
distress, an acute emergency exists.
Blood should be drawn for laboratory
studies and at least 4 units of PRBCs typed and crossed. Two large-bore
intravenous catheters should be placed and crystalloid administered.
Otherwise delivery should be considered either with
caesarian section or vaginal delivery as patient’s condition and pregnancy
allows.
Vaginal Delivery
An attempt at vaginal delivery is
indicated if the degree of separation appears to be limited and if the
continuous FHR tracing is reassuring. When placental separation is extensive
but the fetus is dead or of dubious viability, vaginal delivery is indicated.
The exception to vaginal delivery is the patient in whom hemorrhage is
uncontrollable and operative delivery is necessary to save the life of the
fetus or mother.
Induction of labor with an oxytocin
infusion should be instituted if active labor does not begin shortly after
amniotomy. In practice, augmentation often is not needed because usually the
uterus is already excessively irritable. If the uterus is extremely spastic,
uterine contractions cannot be clearly identified unless an internal monitor is
used, and the progress of labor must be judged by observing cervical
dilatation. Pudendal block anesthesia is recommended. Conduction anesthesia is
to be avoided in the face of significant hemorrhage because profound,
persistent hypotension may result. However, in the volume-repleted patient in
early labor, a preemptive epidural should be considered because rapid
deterioration of maternal or fetal status can occur as labor progresses.
Cesarean Section
The indications for cesarean section
are both fetal and maternal. Abdominal delivery should be selected whenever
delivery is not imminent for a fetus with a reasonable chance of survival who
exhibits persistent evidence of distress. Cesarean section also is indicated if
the fetus is in good condition but the situation is not favorable for rapid
delivery in the face of progressive or severe placental separation. This
includes most nulliparous patients with less than 3–4 cm of cervical
dilatation. Maternal indications for cesarean section are uncontrollable
hemorrhage from a contracting uterus, rapidly expanding uterus with concealed
hemorrhage (with or without a live fetus) when delivery is not imminent,
uterine apoplexy as manifested by hemorrhage with secondary relaxation of a
previously spastic uterus, or refractory uterus with delivery necessary (20%).
Complications
Placental abruption can lead to
initiation of the coagulation cascade by release of tissue thromboplastin into
the maternal circulation. Consumption of coagulation factors and platelets is
followed by coagulopathic hemorrhage. A cycle ensues as further bleeding
worsens the depletion of coagulation factors. Continuous monitoring for
evidence of a clotting deficiency is mandatory from the time the diagnosis of
placental abruption is considered well into the postpartum period. Treatment
will depend not only on the demonstration of hematologic deficiencies but also
on the amount of active bleeding and the anticipated route of delivery.
Reference
Tenth edition of Current Diagnosis & Treatment
Obstetrics & Gynecology.
Twenty second edition Williams Obstetrics
Placenta Previa
Essentials of Diagnosis
- Spotting during first and second trimesters.
- Sudden, painless, profuse bleeding in third trimester.
- Initial cramping in 10% of cases.
In
placenta previa, the placenta is implanted in the lower uterine segment within
the zone of effacement and dilatation of the cervix, constituting an
obstruction to descent of the presenting part
Etiology
The
incidence of placenta previa is increased by multiparity, advancing age, and
previous cesarean delivery. Thus, possible etiologic factors include scarred or
poorly vascularized endometrium in the corpus, a large placenta, and abnormal
forms of placentation such as succenturiate lobe. The incidence of placenta
previa is slightly higher in multiple gestation. A cesarean section scar
triples the incidence of placenta previa. Another contributory factor is an
increased average surface area of a placenta implanted in the lower uterine
segment, possibly because these tissues are less well suited for nidation.
Bleeding
in placenta previa may be due to any of the following causes: (1) mechanical
separation of the placenta from its implantation site, either during the
formation of the lower uterine segment or during effacement and dilatation of
the cervix in labor, or as a result of intravaginal manipulation; (2)
placentitis; or (3) rupture of poorly supported venous lakes in the decidua
basalis that have become engorged with venous blood.
1. Complete
placenta previa: The placenta completely covers the internal cervical os.
2. Marginal
placenta previa: The placenta is implanted at the margin of the internal
cervical os, within 2 cm. If the placenta is seen to be more than 2 cm from the
internal os, the rate of antepartum or intrapartum hemorrhage is not increased.
Every
patient suspected of placenta previa should be hospitalized, and cross-matched
blood should be at hand. To avoid provoking hemorrhage, both vaginal and rectal
examination should not be performed.
Painless
hemorrhage is the cardinal sign of placenta previa. Although spotting may occur
during the first and second trimesters of pregnancy, the first episode of
hemorrhage usually begins after the 28th week and is characteristically
described as sudden, painless, and profuse. With the initial bleeding episode,
clothing or bedding may be soaked by an impressive amount of bright red,
clotted blood, but the blood loss usually is not extensive, seldom produces
shock, and almost never is fatal. In approximately 10% of cases there is some
initial pain, probably because of coexisting placental separation and localized
uterine contractions. Spontaneous labor can be expected over the next few days
in 25% of patients. In a small minority of cases, bleeding is less dramatic or
does not begin until after spontaneous rupture of the membranes or the onset of
labor. A few nulliparous patients even reach term without bleeding, possibly
because the placenta has been protected by an uneffaced cervix.
The
uterus usually is soft, relaxed, and nontender. A high presenting part cannot
be pressed into the pelvic inlet. The infant will present in an oblique or
transverse lie in approximately 15% of cases. FHR abnormalities are unlikely
unless there are complications such as hypovolemic shock, placental separation,
or a cord accident.
Bedside transabdominal ultrasonography can
definitively identify 95% of placenta previas. Transvaginal or transperineal
studies can make the diagnosis in virtually every case. This approach is particularly
helpful with the posterior placenta previa.
During the middle of the second trimester, the placenta is
observed by ultrasound to cover the internal cervical os in approximately 30%
of cases. With development of the lower uterine segment, almost all of these
low implantations will be carried to a higher station. An early ultrasonic
diagnosis of placenta previa requires the confirmation of an additional study
before definitive action is taken.
Placental causes of bleeding other
than placenta previa include partial premature separation of the normally
implanted placenta or circumvallate placenta.
The treatment depends on the amount of
uterine bleeding; the duration of pregnancy and viability of the fetus; the
degree of placenta previa; the presentation, position, and station of the
fetus; the gravidity and parity of the patient; the status of the cervix; and
whether or not labor has begun. The patient must be admitted to the hospital to
establish the diagnosis and ideally should remain in the hospital once the
diagnosis is made. Blood should be readily available for transfusion.
The initial hemorrhage of placenta
previa may occur before pulmonary maturity is established. In such cases, fetal
survival can often be enhanced by expectant therapy. Early in pregnancy,
transfusions to replace blood loss and the use of tocolytic agents to prevent
premature labor are indicated to prolong pregnancy to at least 32–34 weeks.
After 34 weeks, the benefits of further maturation must be weighed against the
risk of major hemorrhage. The possibility that repeated small hemorrhages may
be accompanied by intrauterine growth retardation also must be considered.
Approximately 75% of cases of placenta previa are now delivered between 36 and
40 weeks.
In selecting the optimum time for
delivery, tests of fetal lung maturation, including assessment of amniotic
fluid surfactants and ultrasonic growth measurements, are valuable adjuvants.
If the patient is between 24 and 34
weeks' gestational age, a single course of betamethasone (2 doses of 12 mg
intramuscularly separated by 24 hours) or dexamethasone (4 doses of 6 mg
intravenously or intramuscularly separated by 12 hours) should be given to
promote fetal lung maturity. Repeat courses of steroids are not necessary and
usually are considered only for patients who initially present and receive
treatment with steroids at less than 24 weeks.
Because of the costs of
hospitalization, patients with a presumptive diagnosis of placenta previa are
sometimes sent home on strict bed rest after their condition has become stable
under ideal, controlled circumstances. Such a policy is always a calculated
risk in view of the unpredictability of further hemorrhage, but the practice
has been studied and is an acceptable alternative.
Cesarean section is the delivery
method of choice with placenta previa. Cesarean section has proved to be the
most important factor in lowering maternal and perinatal mortality rates (more
so than blood transfusion or better neonatal care).
If possible, hypovolemic shock should
be corrected by administration of intravenous fluids and blood before the
operation is started. Not only will the mother be better protected, but an
at-risk fetus will recover more quickly in utero than if born while the mother
is still in shock.
The choice of anesthesia depends on
current and anticipated blood loss. A combination of rapid induction,
endotracheal intubation, succinylcholine, and nitrous oxide is a suitable
method for proceeding in the presence of active bleeding.
The choice of operative technique is
of importance because of the placental location and the development of the
lower uterine segment. If the incision passes through the site of placental
implantation, there is a strong possibility that the fetus will lose a
significant amount of blood—even enough to require subsequent transfusion. With
posterior implantation of the placenta, a low-transverse incision may be best
if the lower uterine segment is well developed. Otherwise, a classic incision
may be required to secure sufficient room and to avoid incision through the
placenta. Preparations should be made for care and resuscitation of the infant
if it becomes necessary. In addition, the possibility of blood loss should be
monitored in the newborn if the placenta has been incised.
In a small percentage of cases,
hemostasis in the placental bed is unsatisfactory because of the poor
contractility of the lower uterine segment. Mattress sutures or packing may be
required in addition to the usual oxytocin, prostaglandins, and
methylergonovine. If placenta previa accreta is found, hemostasis may
necessitate a total hysterectomy. Puerperal infection and anemia are the most
likely postoperative complications.
Vaginal delivery usually is reserved
for patients with a marginal implantation and a cephalic presentation. If
vaginal delivery is elected, the membranes should be artificially ruptured
prior to any attempt to stimulate labor (oxytocin given before amniotomy likely
will cause further bleeding). Tamponade of the presenting part against the
placental edge usually reduces bleeding as labor progresses.
Because of the possibility of fetal
hypoxemia due to either placental separation or a cord accident (as a result of
either prolapse or compression of low insertion of the cord by the descending
presenting part), continuous fetal monitoring must be used. If FHR
abnormalities develop, a rapid cesarean section should be performed unless
vaginal delivery is imminent.
Deliver the patient in the easiest and
most expeditious manner as soon as the cervix is fully dilated and the
presenting part is on the perineum. For this purpose, a vacuum extractor is
particularly valuable because it expedites delivery without risking rupture of
the lower uterine segment.
Maternal hemorrhage, shock, and death
may follow severe antepartum bleeding resulting from placenta previa. Death may
occur as a result of intrapartum and postpartum bleeding, operative trauma,
infection, or embolism.
Premature separation of a portion of a
placenta previa occurs in virtually every case and causes excessive external
bleeding without pain; however, complete or wide separation of the placenta before
full dilatation of the cervix is uncommon.
Placenta previa accreta is a serious
abnormality in which the sparse endometrium and the myometrium of the lower
uterine segment are penetrated by the trophoblast in a manner similar to
placenta accreta higher in the uterus. In patients with 1 prior cesarean
section, the rate of accreta in the presence of previa is 20–25% and rises to
50% with 2 or more prior cesarean sections.
Prematurity (gestational age < 36
weeks) accounts for 60% of perinatal deaths due to placenta previa. The fetus
may die as a result of decreased oxygen delivery intrapartum or birth injury.
Fetal hemorrhage due to tearing of the placenta occurs with vaginal
manipulation and especially upon entry into the uterine cavity as cesarean section
is done for placenta previa. About half of these cesarean babies lose some
blood. Fetal blood loss is directly proportional to the time that elapses
between lacerating the cotyledon and clamping the cord.
With rapid recourse to cesarean
section, use of banked blood, and expertly administered anesthesia, the overall
maternal mortality has fallen to less than 1 in 1000.
The perinatal mortality rate
associated with placenta previa has declined to approximately 1%. Although premature
labor, placental separation, cord accidents, and uncontrollable hemorrhage
cannot be avoided, the mortality rate can be greatly reduced if ideal obstetric
and newborn care is given.
Wednesday, August 1, 2012
Breech presentation
Breech presentation, which complicates
3–4% of all pregnancies, occurs when the fetal pelvis or lower extremities
engage the maternal pelvic inlet. Three types of breech are distinguished,
according to fetal attitude (Fig 21–1). In frank breech, the hips
are flexed with extended knees bilaterally. In complete breech, both
hips and knees are flexed. In footling breech, 1 (single footling
breech) or both (double footling breech) legs are extended below the level of
the buttocks.
In singleton breech presentations in which the infant
weighs less than 2500 g, 40% are frank breech, 10% complete breech, and 50%
footling breech. With birth weights of more than 2500 g, 65% are frank breech
, 10% complete breech, and 25% footling breech.
Fetal position in breech presentation is determined
by using the fetal sacrum as the point of reference to the maternal pelvis.
This is true for frank, complete, and footling breeches. Eight possible
positions are recognized: sacrum anterior (SA), sacrum posterior (SP), left
sacrum transverse (LST), right sacrum transverse (RST), left sacrum anterior
(LSA), left sacrum posterior (LSP), right sacrum anterior (RSA), and right
sacrum posterior (RSP). The station of the breech presenting part is the
location of the fetal sacrum with regard to the maternal ischial spines.
Causes
Before 28 weeks, the fetus is small
enough in relation to intrauterine volume to rotate from cephalic to breech
presentation and back again with relative ease. As gestational age and fetal
weight increase, the relative decrease in intrauterine volume makes such
changes more difficult. In most cases, the fetus spontaneously assumes the
cephalic presentation to better accommodate the bulkier breech pole in the
roomier fundal portion of the uterus.
Breech presentation occurs when
spontaneous version to cephalic presentation is prevented as term approaches or
if labor and delivery occur prematurely before cephalic version has taken
place. Some causes include oligohydramnios, hydramnios, and uterine anomalies
such as bicornuate or septate uterus, pelvic tumors obstructing the birth
canal, abnormal placentation, advanced multiparity, and a contracted maternal
pelvis.
In multiple gestations, each fetus may
prevent the other from turning, with a 25% incidence of breech in the first
twin, nearly 50% for the second twin, and higher percentages with additional
fetuses. Additionally, 6% of breech presentations are found to have congenital
malformations, which include congenital hip dislocation, hydrocephalus, anencephalus,
familial dysautonomia, spina bifida, meningomyelocele, and chromosomal
trisomies 13, 18, and 21. Thus, those conditions that alter fetal muscular tone
and mobility increase the likelihood of breech presentation.
Performance of Leopold's maneuvers and
ballottement of the uterus may confirm breech presentation. The softer, more
ill-defined breech may be felt in the lower uterine segment above the pelvic
inlet. Diagnostic error is common, however, if these maneuvers alone are used
to determine presentation.
During vaginal examination, the round,
firm, smooth head in cephalic presentation can easily be distinguished from the
soft, irregular breech presentation if the presenting part is palpable.
However, if no presenting part is discernible, further studies are necessary
(ie, ultrasound).
X-ray studies will differentiate
breech from cephalic presentations and help determine the type of breech by
locating the position of the lower extremities. X-ray studies can reveal
multiple gestation and skeletal defects. Fetal attitude may be seen, but fetal
size cannot readily be determined by x-ray film. Because of the risks of
radiation exposure to the fetus with this technique, ultrasonography is now
used instead of radiography to determine fetal presentation or malformations.
Ultrasonographic scanning by an
experienced examiner will document fetal presentation, attitude, and size;
multiple gestation; location of the placenta; and amniotic fluid volume.
Ultrasound also will reveal skeletal and soft-tissue malformations of the
fetus.
Following confirmation of breech
presentation, the mother must be closely followed to evaluate for spontaneous version
to cephalic presentation. If breech presentation persists beyond 36 weeks,
external cephalic version should be considered (see below).
In women considering a vaginal breech
delivery, radiographic pelvimetry using x-ray, computed tomography, or magnetic
resonance imaging should be performed to rule out women with a borderline or
contracted pelvis. Attempts at vaginal delivery with an inadequate pelvis are
associated with a high rate of difficulty and significant trauma to mother and
fetus. Difficult vaginal delivery may still occur in women with adequate pelvic
measurements.
Patients with singleton breech
presentations are admitted to the hospital with the onset of labor or when
spontaneous rupture of membranes occurs because of the increased risk of
umbilical cord complications. Upon admission, a repeat ultrasound is obtained
to confirm the type of breech presentation and to ascertain head flexion. The
fetus is again screened for lethal congenital malformations, such as
anencephaly, which would preclude cesarean delivery for fetal indications. A
thorough history is taken, and a physical examination is performed to evaluate
the status of mother and fetus. Based on these findings, a decision must be
made regarding the route of delivery (see below).
Continuous electronic fetal heart rate
monitoring is essential during labor. If a fetal electrocardiographic electrode
is needed, care should be taken to avoid injury to the fetal anus, perineum, and
genitalia when attaching the electrode to the breech presenting part. An
intrauterine pressure catheter can be used to assess the frequency, strength,
and duration of uterine contractions. With the catheter in place, fetal
distress or dysfunctional labor can easily be identified and the decision to
proceed with a cesarean section made expeditiously to optimize fetal outcome.
The use of oxytocin in the management
of breech labor is controversial. Although some obstetricians condemn its use,
others use oxytocin with benefit and without complications. Generally, oxytocin
should be administered only if uterine contractions are insufficient to sustain
normal progress in labor. Continuous fetal and uterine monitoring should be
used whenever oxytocin is administered.
The decision regarding route of
delivery must be made carefully on an individual basis. Criteria for vaginal or
cesarean delivery are outlined in Table.
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Cesarean Delivery
The type of incision chosen is
extremely important. If the lower uterine segment is well developed, as is
usually the case in women at term in labor, a transverse "lower
segment" incision is adequate for easy delivery. In premature gestations,
in an unlabored uterus, or in many cases of malpresentation, the lower uterine
segment may be quite narrow, and a low vertical incision is almost always
required for atraumatic delivery.
Obstetricians who contemplate
performing a vaginal breech delivery should be experienced in the maneuver and
should be assisted by 3 physicians: (1) an experienced obstetrician who will
assist with delivery; (2) a pediatrician capable of providing total
resuscitation of the newborn; and (3) an anesthesiologist, to ensure that the
mother is comfortable and cooperative during labor and delivery. The type of
anesthesia required depends on the type of breech delivery. Multiparous women
undergoing spontaneous breech delivery may require no anesthesia or only
intravenous analgesia for pain relief during labor and a pudendal anesthetic
during delivery. Epidural anesthesia may also be administered during labor or
in anticipation of partial breech extraction, including application of Piper
forceps to the aftercoming head. In emergency circumstances, complete
relaxation of the perineum and uterus is essential for a successful outcome.
This is accomplished by immediate induction of inhalation anesthesia or by
administration of intravenous nitroglycerin.
During spontaneous delivery of an
infant in the frank breech position, delivery occurs without assistance, and no
obstetric maneuvers are applied to the body. The fetus negotiates the maternal
pelvis as outlined below, while the operator simply supports the body as it
delivers.
Engagement occurs when the
bitrochanteric diameter of the fetus has passed the plane of the pelvic inlet.
As the fetus descends into the pelvis (Fig 21–2), the buttocks reach the
levator ani muscles of the maternal pelvis. At this point, internal rotation
occurs, whereby the anterior hip rotates beneath the pubic symphysis, resulting
in a sacrum transverse position. The bitrochanteric diameter of the fetal
pelvis is now in an anteroposterior position within the maternal pelvis. The
breech then presents at the pelvic outlet and, upon emerging, rotates from
sacrum transverse to sacrum anterior. Crowning occurs when the bitrochanteric
diameter passes under the pubic symphysis. As this occurs, the shoulders enter
the pelvic inlet with the bisacromial diameter in the transverse position. As
descent occurs, the bisacromial diameter rotates to an oblique or
anteroposterior diameter, until the anterior shoulder rests beneath the pubic
symphysis. Delivery of the anterior shoulder occurs as it slips beneath the
pubic symphysis. Upward flexion of the body allows for easy delivery of the
posterior shoulder over the perineum.
As the shoulders descend, the head engages the pelvic
inlet in a transverse or oblique position. Rotation of the head to the occiput
anterior position occurs as it enters the midpelvis. The occiput then slips
beneath the pubic symphysis, and the remainder of the head is delivered by
flexion as the chin, mouth, nose, and forehead slip over the maternal perineum.
As delivery of the breech occurs,
increasingly larger diameters (bitrochanteric, bisacromial, biparietal) of the
body enter the pelvis, whereas in cephalic presentation, the largest diameter
(biparietal diameter) enters the pelvis first. Particularly in preterm labors,
the head is considerably larger than the body and provides a better
"dilating wedge" as it passes through the cervix and into the pelvis.
The smaller bitrochanteric and bisacromial diameters may descend into the
pelvis through a partially dilated cervix, but the larger biparietal diameter
may be trapped. Delivery in these cases is described in the following.
Partial breech extraction (assisted
breech extraction) is used when the operator discerns that spontaneous delivery
will not occur or that expeditious delivery is indicated for fetal or maternal
reasons. The body is allowed to deliver spontaneously up to the level of the
umbilicus. The operator then assists in delivery of the legs, shoulders, arms,
and head.
As the umbilicus appears at the
maternal perineum, the operator places a finger medial to 1 thigh and then the
other thigh, pressing laterally as the fetal pelvis is rotated away from that
side by an assistant. Thus, the thigh is externally rotated at the hip and
results in flexion of the knee and delivery of one, then the other, leg. The
fetal trunk is then wrapped in a towel to support the body. When both scapulae
are visible, the body is rotated counterclockwise. The operator locates the
right humerus and laterally sweeps the arm across the chest and out the
perineum (Fig 21–3). In a similar fashion, the body is rotated clockwise to
deliver the left arm. The head then spontaneously delivers by gently lifting
the body upward and applying fundal pressure to maintain flexion of the fetal
head (Fig 21–4). During partial breech extraction, the anterior shoulder may be
difficult to deliver if it is impacted behind the pubic symphysis. In this
event, the body is gently lifted upward toward the pubic symphysis, and the
operator inserts 1 hand along the hollow of the maternal pelvis and identifies
the posterior humerus of the fetus. By gentle downward traction on the humerus,
the posterior arm can be easily delivered, thus allowing for easier delivery of
the anterior shoulder and arm.
Complications of Breech Delivery
Umbilical cord compression and
prolapse may be associated with breech delivery, particularly in complete (5%)
and footling (15%) presentations. This is due to the inability of the
presenting part to fill the maternal pelvis, either because of prematurity or
poor application of the presenting part to the cervix so that the umbilical
cord is allowed to prolapse below the level of the breech (see below). Frank
breech presentation offers a contoured presenting part, which is better
accommodated to the maternal pelvis and is usually well applied to the cervix.
The incidence of cord prolapse in frank breech is only 0.5% (the same as for
cephalic presentations).
Compression of the prolapsed cord may
occur during uterine contractions, causing moderate to severe variable
decelerations in the fetal heart rate and leading to fetal anoxia or death.
Continuous electronic monitoring is mandatory during labor in these cases to
detect ominous decelerations. If they occur, immediate cesarean delivery must
be performed.
The incidence of birth trauma during
vaginal breech delivery is 6.7%, 13 times that of cephalic presentations
(0.51%). Only high forceps and internal version and extraction procedures have
higher rates of birth injury than do vaginal breech deliveries. The types of
perinatal injuries reported in breech delivery include tears in the tentorium
cerebellum, cephalohematomas, disruption of the spinal cord, brachial palsy,
fracture of long bones, and rupture of the sternocleidomastoid muscles. Vaginal
breech delivery is the main cause of injuries to the fetal adrenal glands,
liver, anus, genitalia, spine, hip joint, sciatic nerve, and musculature of the
arms, legs, and back.
Factors contributing to difficult
vaginal breech delivery include a partially dilated cervix, unilateral or
bilateral nuchal arms, and deflexion of the head. The type of procedure used
may affect the neonatal outcome.
Delivery of a breech fetus may progress
even though the cervix is only partially dilated because the bitrochanteric and
bisacromial diameters are smaller than the biparietal diameter. This is true
especially in prematurity. The hips and shoulders may negotiate the cervix, but
the aftercoming head becomes entrapped, resulting in difficult delivery and
birth injury.
During partial breech extraction and
more often in total breech extraction, excessive downward traction on the body
results in a single or double nuchal arm. This occurs because of the rapid
descent of the body, leading to extension of 1 or both arms, which become
lodged behind the neck. When delivery of the shoulder is difficult to
accomplish, a nuchal arm should be suspected. To dislodge the arm, the operator
rotates the body 180 degrees to bring the elbow toward the face. The humerus
can then be identified and delivered by gentle downward traction. In cases of
double nuchal arm, the fetus is rotated counterclockwise to dislodge and
deliver the right arm and rotated clockwise to deliver the left arm. If this
action is unsuccessful, the operator must insert a finger into the pelvis,
identify the humerus, and possibly extract the arm, resulting in fracture of
the humerus or clavicle. Nuchal arms cause a delay in delivery and increase the
incidence of birth asphyxia.
Hyperextension of the head is
defined as deflexion or extension of the head posteriorly beyond the
longitudinal axis of the fetus (5% of all breech deliveries). Causes of
hyperextension include neck cysts, spasm of the neck musculature, and uterine
anomalies, but over 75% have no known cause. Although deflexion may be
documented by ultrasonographic or x-ray studies weeks before delivery, there is
little apparent risk to the fetus until vaginal delivery is attempted. At that
time, deflexion causes impaction of the occipital portion of the head behind
the pubic symphysis, which may lead to fractures of the cervical vertebrae,
lacerations of the spinal cord, epidural and medullary hemorrhages, and
perinatal death. If head deflexion is diagnosed prior to delivery, cesarean
section should be performed to avert injury. Cesarean section cannot prevent
injuries such as minor meningeal hemorrhage or dislocation of the cervical
vertebrae, which may develop in utero secondary to longstanding head deflexion.
More complex delivery procedures have
a higher rate of birth trauma. Whereas few infants are injured during
spontaneous breech births, as many as 6% are injured during partial breech
extraction and 20% during total breech extraction. Injuries associated with
total breech extraction usually are extensive and severe, and this procedure
should never be attempted unless fetal survival is in jeopardy and cesarean
section cannot be immediately performed.
An additional important factor in
breech injury and perinatal outcome is the experience of the operator.
Inexperience may lead to hasty performance of obstetric maneuvers. Delay in
delivery may result in birth asphyxia due to umbilical cord compression, but
haste in the management of breech delivery results in application of excessive
pressure on the fetal body, causing soft-tissue damage and fracture of long
bones. Too-rapid extraction of the body from the birth canal causes the arms to
extend above the head, resulting in unilateral or bilateral nuchal arms and
difficult delivery of the aftercoming head. All breech deliveries should be
performed slowly and methodically by experienced obstetricians who execute the
maneuvers with gentleness and skill—not speed.
The incidence of cesarean section for
breech delivery has been steadily increasing, from approximately 30% in 1970 to
85% in 1999. A recent review of breech deliveries in California revealed an 88%
cesarean section rate, with more vaginal deliveries performed in public
teaching hospitals and far fewer in private facilities. A decreased number of
practitioners currently are skilled in vaginal breech delivery, and although
academic faculty support its teaching, there are insufficient numbers of
vaginal breech deliveries to properly teach this procedure at most institutions.
It should be noted that cesarean section for the immature or malformed fetus
does not improve chances for perinatal survival; vaginal delivery should be
performed in these cases.
The Term Breech Trial Collaborative
Group recently conducted a randomized controlled trial to compare planned
cesarean section with vaginal birth for selected breech presentation
pregnancies. They found that fetuses of women who underwent planned cesarean
sections were less likely to die or to experience poor outcomes in the immediate
neonatal period than were fetuses of women who underwent vaginal birth. There
was no difference in the 2 groups in terms of maternal mortality or serious
morbidity. They concluded that a policy of planned cesarean section will result
in 7 cesarean births to avoid 1 infant death or serious morbidity. Because of
the results of this trial, the American College of Obstetricians and
Gynecologists recommends planned cesarean delivery for persistent breech
presentations at term.
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