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Obstetric Emergencies 

Obstetric Emergencies
Chapter:
Obstetric Emergencies
Author(s):

Robert R. Gaiser

DOI:
10.1093/med/9780199377275.003.0008
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date: 21 September 2020

Accidental Dural Puncture

Definition

Accidental dural puncture occurs when the both the dura and subarachnoid maters are punctured unintentionally during epidural catheter placement.

Presentation

Any one of the following signs indicates accidental dural puncture:

  • Free flowing cerebrospinal fluid (CSF) from the epidural needle

  • Test dose of 3 mL 1.5% lidocaine with epinephrine 1:200,000 through the epidural catheter produces evidence of a sensory and motor block

  • Cerebrospinal fluid is aspirated from the catheter

    • Cerebrospinal fluid may be distinguished from normal saline or local anesthetic by the presence of protein (15–45 mg/dL) and glucose (50–80 mg/dL).

  • Presence of a frontal-occipital headache 24–48 hours after epidural anesthesia

Pathophysiology

The distance from the ligamentum flavum to the dura mater in the lumbar spine averages 4–6 mm. Dural puncture generally occurs when the person performing the procedure fails to recognize that the needle is in the epidural space or advances the local anesthetic infiltration needle too far. The hole in the dura and arachnoid maters makes it possible for local anesthetic to enter the subarachnoid space, causing high sensory and motor levels. Headache tends to occur 24–48 hours after accidental dural puncture and is caused by CSF leaking into the epidural space. The loss of CSF from the intrathecal space results in a decrease in intracranial pressure, causing traction on pain-sensitive structures, including the dura and meninges. This mechanism is proposed for the etiology of the headache. Other symptoms accompanying the headache include visual disturbances (diplopia) and hearing alteration, as cranial nerves III, IV, VI, and VIII are frequently involved.

Differential Diagnosis

Injecting local anesthetic into the subdural space (between the dura and arachnoid mater) may result in a high blockade that may also cause profound hypotension but differs by causing a patchy, weak block.

Immediate Management

  • If the provider notes free-flowing CSF from the epidural needle, there are two courses of management:

    • Immediately remove the needle and redo the procedure at another location and slowly titrate the local anesthetic

      • This approach has the risk of a repeat accidental dural puncture.

      • Use caution when injecting local anesthetic through the resited epidural catheter

    • Thread an epidural catheter intrathecally as rapidly as possible to limit loss of CSF. The catheter should be threaded only 3–4 cm into the intrathecal space. The catheter is then managed as continuous spinal analgesia.

      • Insertion of an intrathecal catheter does not prevent the development of a headache.

      • Limit the number of times the catheter hub is disconnected from the continuous infusion to prevent infection when using continuous spinal anesthesia.

Diagnostic Studies

Cerebrospinal fluid contains both protein (15–45 mg/dL) and glucose (50–80 mg/dL). Both of these may be measured in the laboratory. A simpler approach would be to use a dipstick for the presence of protein or glucose or to use a glucometer to measure the glucose concentration.

Subsequent Management

  • If the epidural catheter was threaded intrathecally, it should be managed as a continuous spinal catheter.

    • The medication administered through an intrathecal catheter is the same as one would use for epidural analgesia, starting at a lower rate. The usual starting rate is 1–2 cc/h and adjusted based upon patient response.

  • If the epidural space was relocated with the catheter threaded epidurally, the amount of local anesthetic used for the initial bolus should be decreased because it may leak through the hole into the dura and arachnoid maters.

  • In both situations the patient should be evaluated daily for 48 hours and also should receive a follow-up phone call once discharged.

    • If the patient develops a headache (risk factors include young age, female gender, and vaginal delivery), the patient should be offered an epidural blood patch. There is no value to conservative measures. Caffeine has not been shown to be beneficial.

    • An epidural blood patch involves the injection of 20 mL of autologous blood into the epidural space. Blood compresses the thecal sac, forcing CSF cephalad; a clot forms at the dural hole preventing further leakage.

Risk Factors

  • For accidental dural puncture

    • Previous accidental dural puncture—patients who had one accidental dural puncture are at increased risk for a second puncture, suggesting a possible anatomic cause.

  • For postdural puncture headache

    • Young age (10–40 years)

    • Female gender

    • Vaginal delivery

Prevention

There are no effective means to prevent the development of a postdural puncture headache. A prophylactic epidural blood patch through the catheter is not effective. Inserting an intrathecal catheter decreases the risk of the patient experiencing a second puncture during relocating the epidural space, but does not decrease the incidence of headache. The use of cosyntropin has been investigated but has not gained widespread acceptance.

Special Considerations

  • Cerebrospinal fluid may be aspirated either through the epidural needle or epidural catheter. Patients occasionally develop symptoms consistent with accidental dural puncture even though CSF is not aspirated. This may be due to a nick in the dura that was caused by either the epidural needle or the needle used for local anesthetic infiltration. The major concern after accidental dural puncture is postdural puncture headache, which tends to be bilateral, positional, and located in the frontal-occipital area. Neck stiffness and nausea may also occur. If the patient has an accidental dural puncture and becomes febrile in the postoperative period, meningitis must be strongly considered and diagnosed with lumbar puncture.

Further Reading

Agerson AN, Scavone BM. Prophylactic epidural blood patch after unintentional dural puncture for the prevention of postdural puncture headache in parturients. Anesth Analg. 2013; 115: 133–136.Find this resource:

Bradbury CL, Singh SI, Badder SR, et al. Prevention of post-dural puncture headache in parturients: A systematic review and meta-analysis. Acta Anaesthesiol Scand. 2013; 57: 417–430.Find this resource:

Russell IF. A prospective controlled study of continuous spinal analgesia versus repeat epidural analgesia after accidental dural puncture in labour. Int J Obstet Anesthesiol. 2012; 21: 7–16.Find this resource:

Breech Presentation

Definition

Breech presentation is the fetal position in which the presenting part is not the head. A breech presentation occurs whenever the fetal buttocks descend into the maternal pelvis before the fetal head. Breech presentations are typically classified according to the position of the fetus within the uterus.

  1. 1. Frank breech: the fetal hips are both flexed and both knees are extended. This is the most common type of breech presentation and accounts for 70% of all breech presentations.

  2. 2. Complete breech: both the fetal hips and fetal knees are flexed. Complete breech accounts for 25% of all breech presentations.

  3. 3. Footling breech: one or both hips are extended. With the hip or hips being extended, one or both feet are lowermost in the birth canal. Footling breech is a more common presentation for premature fetuses rather than a term fetus and accounts for 5% of all breech presentations.

Pathophysiology

The etiology of breech presentation is unknown but is more likely when the fetus is premature or in a multigestation pregnancy. Women with a previous cesarean delivery have an increased incidence of breech presentation. A fetus found to be in the breech position prior to 24 weeks’ presentation will most likely turn itself into a cephalic position.

The major concern with delivery of the breech fetus is fetal head entrapment. In a cephalic presentation, the obstetrician will be able to detect that the head is too large for the pelvis because labor will progress poorly or the fetus will not descend into the birth canal. A fetus in the breech presentation can deliver through a partially dilated cervix but the head will be trapped. This causes compression of the umbilical cord against the cervix, which leads to decreased fetal blood flow and to fetal hypoxia.

Differential Diagnosis

The type of breech is diagnoses by ultrasound examination.

Immediate Management

  • Prepare for Level 1 cesarean delivery in instances of footling breech or a premature breech fetus.

  • If an epidural catheter is in place, it may be used for the delivery. If an epidural catheter is not in place, then general anesthesia is usually used.

  • If the fetus is breech and if it is not footling or premature, management may differ. Vaginal delivery may be attempted. If vaginal delivery is attempted, both the anesthesiologist and the obstetrician must be prepared to perform a rapid cesarean delivery. Monitoring of the fetal heart tones must occur throughout the entire procedure.

Diagnostic Studies

Ultrasound is used to confirm physical examination.

Subsequent Management

Following delivery, the infant should be resuscitated by individuals skilled in neonatal resuscitation. Breech infants have more neonatal complications than neonates that have a vertex presentation, regardless of the route of delivery.

Risk Factors

  • Maternal

    • Uterine anomalies

    • Mulitparity

    • Pelvic tumors

  • Fetal

    • Anencephaly

    • Microcephaly

    • Neuromuscular disorders

    • Polyhydramnios

    • Oligohydramnios

  • Placental

    • Placenta previa

Prevention

Prior to delivery, the obstetrician may attempt an external version to turn the fetus from the breech presentation to cephalic presentation. This is a painful procedure, so epidural analgesia is beneficial. The use of epidural analgesia increases the success but does not increase the risk of abruption placenta from excessive pressure.

Special Considerations

  • Before 28 weeks’ gestation, approximately 40% of fetuses are in the breech position. At term, however, only 3%–4% of singleton pregnancies have a breech presentation. Due to the risks of breech vaginal delivery, the majority of breech presentations are delivered via elective cesarean sections. If a woman with a breech presentation begins to labor, the obstetrician will perform a cesarean section before the fetus becomes engaged. Breech delivery increases the risk of infection and perineal laceration for the mother. Footling breech may occur following rupture of the amniotic membranes. Footling breech is considered an obstetric emergency and will result in a Level 1 cesarean delivery. For other types of breech, the obstetrician will decide whether or not to proceed to cesarean delivery.

  • There are circumstances in which a parturient and her obstetrician will decide to attempt a vaginal breech delivery, such as delivery of a nonvertex second twin, a multigravid parturient who has had several previous vaginal deliveries, or if the mother refuses a cesarean delivery. The Term Breech Trial randomized parturients with breech fetuses at 37 or more weeks’ gestation to either planned cesarean delivery or planned breech vaginal delivery. There was an increased incidence of neonatal morbidity and mortality with attempted vaginal delivery. A breech vaginal delivery should only be considered for a nonviable fetus, delivery of a second nonvertex twin, or advanced labor with a breech presentation.

Further Reading

Azria E, Le Meaux JP, Khoshnood B, et al. Factors associated with adverse perinatal outcomes for term breech fetuses with planned vaginal delivery. Am J Obstet Gynecol. 2012; 207: 285.e1–9.Find this resource:

Weiniger CF. Analgesia/anesthesia for external cephalic version. Curr Opin Anaesthesiol. 2013; 26: 278–287.Find this resource:

Embolism: Thrombus, Amniotic Fluid, Air

Definition

Entry of solid (thrombus), liquid (amniotic fluid), or gas (air) into the maternal vascular system. Thromboembolism is the most common cause of maternal mortality and is also the most common form of embolism in pregnant patients.

Presentation

  • Common to all:

    • Dyspnea

    • Chest pain

    • Tachypnea

    • Tachycardia

    • Increased central venous pressure

    • Dilated external jugular veins

    • Hypotension

  • Amniotic fluid embolism includes all of the preceding and

    • Bleeding

    • Disseminated intravascular coagulopathy

Pathophysiology

After entry into the venous system, emboli lodge in the pulmonary vascular system, causing occlusion of the vessels and increased central venous blood pressure, decreased cardiac output, and hypotension. The resultant ventilation/perfusion mismatch causes hypoxemia. In contrast, amniotic fluid embolism is more consistent with an anaphylactoid reaction to one of the many possible mediators in amniotic fluid. The precise mechanism of the coagulopathy in amniotic fluid embolism is unknown but is postulated to be due to tissue factor, which is present in amniotic fluid, activating the extrinsic pathway by binding with Factor VII, activating Factor X, leading to clotting and a consumptive coagulopathy.

Immediate Management

  • Thrombus

    • Increase FiO2 to maintain oxygenation.

    • Consider endotracheal intubation if respiratory failure is imminent.

    • Provide hemodynamic support with fluids, inotropes, or vasopressors.

    • Anticoagulation with unfractionated heparin will be initiated by the obstetrician following resuscitation.

    • In the setting of profound hemodynamic compromise, consider thrombolysis or surgery.

  • Amniotic fluid

    • Increase FiO2 to maintain oxygenation.

    • Consider endotracheal intubation if respiratory failure is imminent.

    • Provide hemodynamic support with fluids, inotropes, or vasopressors.

    • Consider insertion of an intra-arterial catheter and establishing central venous access.

    • The patient will develop a cogulopathy. Administer cryoprecipitate early to maintain an adequate fibrinogen level.

  • Air

    • Inform the obstetrician and position the patient with the surgical site below the level of the heart. Placing the patient in reverse Trendelenburg position or returning the uterus into the abdomen will prevent the further entrainment of air.

    • Increase FiO2 to maintain oxygenation. Intubation is usually not required.

    • Provide hemodynamic support with fluids, inotropes, or vasopressors.

    • Although a multi-orifice central venous catheter permits aspiration of air from the right atrium, the provider is usually too busy managing the hemodynamic consequences to attempt insertion.

    • The uterus should be wrapped in moist gauze to cover the open venous sinuses.

    • Consider hyperbaric oxygen postoperatively in severe cases.

Differential Diagnosis

  • Asthma

  • Anaphylaxis

  • Sepsis

  • Aspiration

  • Peripartum cardiomyopathy

  • Uterine rupture

  • Placental abruption

  • Hemorrhage

  • Myocardial infarction

Diagnostic Studies

  • Thrombus

    • Arterial blood gas analysis detects a decrease in PaO2 and an increase in PaCO2

    • V/Q scan

    • Spiral computed tomographic pulmonary angiography

    • Doppler ultrasound or magnetic resonance imaging to locate the source (usually the lower extremities)

  • Amniotic fluid

    • The diagnosis of amniotic fluid embolism is primarily based upon clinical presentation and is one of exclusion. The diagnosis includes the presence of at least one of the following conditions: cardiac arrest, severe respiratory distress, seizure, or disseminated intravascular coagulopathy during pregnancy.

    • The aspiration of amniotic fluid debris from a catheter is not diagnostic for amniotic fluid embolism. The aspiration of squamous cells and lanugo hair has been aspirated from patients without amniotic fluid embolism.

    • Transesophageal echocardiography findings typically include a four-chamber view with right ventricular failure, suprasystemic right-sides pressures, bulging of the interatrial and interventricular septae, severe tricuspid regurgitation, and pericardial effusion.

  • Air

    • Arterial blood gas analysis reveals a decrease in PaO2 and an increase in PaCO2.

    • If general anesthesia is being used, there will be an abrupt decrease in end-tidal CO2.

    • Transesophageal and transthoracic echocardiography is both sensitive and specific. Transesophageal echocardiography requires general anesthesia for probe insertion.

Subsequent Management

  • The most common cause of embolism in pregnancy is thrombus because pregnancy causes a hypercoagulable state with increased levels of Factors I, VII, VIII, X, and XII.

  • Parturients with thromboembolism require anticoagulation. Prior to delivery, the patient is anticoagulated with low molecular weight heparin (warfarin is a teratogen). Follow guidelines for withholding low molecular weight heparin prior to attempting regional anesthesia or neuraxial labor analgesia.

  • The hemodynamic and hematologic consequences of amniotic fluid embolism mandate that the patient be managed in the intensive care unit.

  • Inhaled nitric oxide may be indicated for the pulmonary hypertension accompanying amniotic fluid embolism.

  • If air embolism is suspected, take steps to stop vascular entrainment. Air enters the vascular circulation because of a pressure differential. Air entrainment occurs when the veins are stented open and the surgical site is above the level of the heart (negative venous pressure). Position the patient so that the surgical site is lower than the heart.

Risk Factors

  • Thrombus: Age >35 years, obesity (BMI >30 kg/m2), cesarean delivery, current infection, parity >3, immobility, thrombophilia

  • Amniotic fluid: Advanced maternal age, multiparity, tumultuous labor, trauma, multiple gestation, polyhydramnios, fetal macrosomia, augmentation of labor

  • Air: Cesarean delivery (usually between delivery of infant to closure of hysterotomy), uterine exteriorization

Prevention

  • Thrombus

    • Use of compression stockings during cesarean delivery

    • Mobility

    • SQ heparin

    • Antepartum pharmacologic thromboprophlaxis in patients with several risk factors or a history of thrombus

  • Amniotic fluid

    • There is no proven means of prevention. Maintain a high index of suspicion.

    • Amniotic fluid embolism is a diagnosis of exclusion. Rule out other causes of hypotension and disseminated intravascular coagulation (DIC) before making the diagnosis of amniotic fluid embolism.

  • Air

    • Position the surgical site below the level of the heart.

Special Considerations

  • Embolism is the leading cause of maternal mortality in the United States. Air embolism is common during cesarean delivery, but typically does not result in clinical consequences. Air can be demonstrated by transesophageal echocardiography in 93%–100% of cesarean deliveries. The most common time for air embolism is when the uterus is exteriorized to be repaired. At this point, the uterus and surgical incision are above the level of the heart, causing the entrainment of air. The pathophysiology of amniotic fluid embolism syndrome may be due to the immunologic reaction rather than to the embolism itself. Insulin-growth factor binding protein-1, which is a specific marker of amniotic fluid, is currently being evaluated. The use of recombinant Factor VIIa for the treatment of the bleeding accompanying amniotic fluid embolism is controversial. Although it decreases the amount of bleeding, it may also increase the risk of thromboembolism.

Further Reading

Brennan MC, Moore LE. Pulmonary embolism and amniotic fluid embolism in pregnancy. Obstet Gynecol Clin North Am. 2013; 40: 27–35.Find this resource:

Clark SL. Amniotic fluid embolism. Obstet Gynecol. 2014; 123: 337–348.Find this resource:

Leighton BL, Wall MH, Lockhart EM, et al. Use of recombinant factor VIIa in patients with amniotic fluid embolism: a systematic review of case reports. Anesthesiology. 2011; 115: 1201–1208.Find this resource:

Marik PE, Plante LA. Venous thrombembolic disease and pregnancy. N Engl J Med. 2008; 359: 2025–2033.Find this resource:

Walsh CA, Walsh SR. Extraabdominal vs intraabdominal uterine repair at cesarean delivery: a meta-analysis. Am J Obstet Gynecol. 2009; 100: 625.e1–8.Find this resource:

Failed Intubation

Definition

Inability to intubate the trachea. The most common causes in the pregnant patient are pharyngeal, laryngeal, or tracheal edema.

Presentation

  • Hypoxemia

  • Difficulty with mask ventilation

  • Difficulty with intubation

  • Depending upon the degree of the hypoxemia, hypotension, hypertension, tachycardia, and bradycardia may occur.

Pathophysiology

During pregnancy, capillary engorgement of the mucosa throughout the respiratory tract causes swelling of the nasal and oral pharynx, larynx, and trachea, increasing the incidence of grade IV airways by 34% from the first to the third trimester. Pregnant patients also become hypoxic more rapidly. The gravid uterus displaces the diaphragm 4–7 cm cephalad, decreasing functional residual capacity. Oxygen consumption is increased because of the developing fetus. Labor itself may also exacerbate an already difficult airway.

Differential Diagnosis

Failed intubation may occur during induction of general anesthesia or management complications such as oversedation or high spinal anesthesia. Loss of the airway may also occur at the end of general anesthesia if the patient is extubated prematurely.

Immediate Management

  • If intubation is not possible

    • Call for help.

    • Attempt mask ventilation.

  • If mask ventilation is possible, consider using cricoid pressure and mask ventilation for the cesarean delivery.

  • If mask ventilation is not possible, follow the ASA Difficult Airway Algorithm.

  • Consider using a laryngeal mask airway that allows for passage of a gastric tube.

  • Consider inserting another type of supraglottic airway.

  • Consider transtracheal jet ventilation.

  • Consider a surgical airway (i.e., cricothyroidotomy).

Diagnostic Studies

  • Mallampati classification and other features of the airway examination

    • Able to visualize

      • Faucial pillars, soft palate, uvula (Class 1)

      • Faucial pillars, soft palate (Class 2)

      • Soft palate only (Class 3)

      • Hard palate only (Class 4)

  • The airway must be examined in every parturient before induction of anesthesia, regardless of whether the airway was examined previously.

Subsequent Management

Patients with difficult intubation should not be extubated until they have recovered sufficiently from anesthesia. Parturients who had received large quantities of intravenous fluids or blood products may require postoperative intubation and mechanical ventilation until airway edema has resolved.

Risk Factors

  • Obesity

  • Previous airway surgery

  • Diabetes mellitus

  • Pre-eclampsia

  • Inability to visualize oropharyngeal structures

  • Receding mandible

  • Short neck

Prevention

Be alert to the presence of risk factors that place the parturient at increased risk of complications from general anesthesia. In patients who have a suspected or known difficult airway, the obstetric team should encourage early initiation of epidural analgesia and the anesthesia team should ensure that the catheter is functional. Labor and delivery units should have equipment and the personnel readily available to manage airway emergencies. Basic airway equipment should be immediately available during the provision of regional anesthesia and include:

  • Oxygen

  • Suction

  • Self-inflating bag and mask for positive pressure ventilation

  • Laryngoscopes and assorted blades

  • Videolaryngoscopy device

  • Endotracheal tubes with stylets

  • Medications for blood pressure support, muscle relaxation, and hypnosis.

In addition, portable equipment for difficult airway management should be readily available in the operative area of labor and delivery units to include:

  • Rigid laryngoscope blades and handles of alternate design and shape

  • Endotracheal tubes of assorted size

  • Laryngeal mask airways of assorted sizes

  • At least one device for emergency nonsurgical airway ventilation

    • Hollow jet ventilation stylet

    • Cricothyrotomy kit with or without a transtracheal jet ventilator

  • Endotracheal tube guides

  • Equipment suitable for emergency surgical airway access

  • Topical anesthetics and vasoconstrictors

Special Considerations

  • The most recently reported incidence of failed intubation in the obstetric population is 1:224 intubations. Appropriate training in emergency airway management will improve mortality from failed intubation.

  • Pregnancy itself does not result in full stomach considerations. Pregnancy is associated with a shift in the position of the stomach that is caused by the gravid uterus. Although the angle of the gastroesophageal junction changes, this does not cause the pregnant patient to have a full stomach. If the pregnant patient has symptoms of a full stomach (e.g., frequent regurgitation, heartburn), she should be considered to be at risk for aspiration. All laboring patients should be considered a full stomach and at increased risk of aspiration. They should receive aspiration prophylaxis (sodium bicitrate solution 30 mL and H2 antagonists) prior to the induction of general anesthesia. If general anesthesia is required for a symptomatic pregnant patient or a patient in labor, a rapid sequence is indicated.

  • Despite the advent of videolaryngoscopy, management of the difficult airway continues to be a problem in obstetric anesthesia. Videolaryngoscopy increases the chance of success with intubation but does not guarantee it.

Further Reading

Aziz MF, Kim D, Mako J, et al. A retrospective study of the performance of video laryngoscopy in an obstetric unit. Anesth Analg. 2012; 115: 904–906.Find this resource:

Quinn AC, Milne D, Columb M, et al. Failed tracheal intubation in obstetric anaesthesia: 2 yr national case-control study in the UK. Br J Anaesthesiol. 2013; 110: 74–80.Find this resource:

Fetal Bradycardia

Definition

An abnormal baseline heart rate that is <110 beats per minute (bpm). Absence of baseline variability is highly predictive of abnormal fetal acid-base status. Currently, fetal heart rate (FHR) patterns are classified into one of three categories.

Category I (Figure 8.1):


Figure 8.1 Category I. Presences of fetal heart rate variability and lack of decelerations.

Figure 8.1 Category I. Presences of fetal heart rate variability and lack of decelerations.

  • Baseline FHR 110–160 bpm

  • Moderate FHR variability

  • Lack of late or variable decelerations

  • Early decelerations are present or absent

  • Accelerations are present or absent

Category II (Figure 8.2):


Figure 8.2 Category II. No fetal heart rate variability and subtle late decelerations.

Figure 8.2 Category II. No fetal heart rate variability and subtle late decelerations.

  • Fetal heart rate tracing not predictive of abnormal fetal acid-base status or indeterminate

  • Not enough evidence to place in Category I or Category III

  • Requires continued surveillance and re-evaluation

  • Interpreted in the context of the clinical setting

Category III:

  • Abnormal tracing

  • Predictive of abnormal fetal acid-base status

  • Absent baseline fetal heart rate variability (and any of the following):

    • Recurrent late decelerations

    • Recurrent variable decelerations

    • Bradycardia

  • Sinusoidal pattern

Presentation

Clinical diagnosis is based on the FHR tracings.

Pathophysiology

Fetal bradycardia, when accompanied with decreased baseline variability or late decelerations, is associated with fetal acid-base abnormalities from fetal hypoxia. The etiology may be maternal (hypoxemia, hypotension, aortocaval compression, decreased hemoglobin), uterine (placental abruption, pre-eclampsia), or fetal (umbilical cord occlusion from knot or compression).

Differential Diagnosis

  • Malpositioned sensor detecting maternal heart rate

  • Maternal administration of beta-blockers

  • False recording

Immediate Management

  • Prepare for urgent cesarean delivery.

  • Treat factors that may be contributing to fetal distress.

    • Administer supplemental oxygen.

    • Treat hypotension with fluid loading and incremental doses of phenylephrine (100 mcg) or ephedrine (ephedrine in large doses may decrease umbilical cord pH).

    • Left uterine displacement to treat aortocaval compression.

  • If urgent delivery is required, consider aspiration prophylaxis with sodium bicitrate.

  • If a functioning epidural catheter is present, extend the sensory level with 3% 2-chloroprocaine or 2% lidocaine, depending upon the urgency of the case (2-chloroprocaine requires 2 minutes to achieve a satisfactory sensory level; lidocaine requires 4–6 minutes to achieve an appropriate sensory level).

  • If no epidural catheter is in place, evaluate the maternal airway.

    • If the airway exam is suggestive of possible difficult intubation, consider regional anesthesia or videolaryngoscopy.

    • If airway exam does not suggest a possible difficult intubation, consider rapid sequence induction with cricoid pressure.

  • If nonurgent delivery is planned, administer supplemental maternal oxygen and alter maternal position to prevent aortocaval obstruction.

Diagnostic Studies

The FHR may be confirmed with ultrasonography.

Subsequent Management

In case of urgent delivery, either general or regional anesthesia is administered, depending upon the amount of time available and the maternal airway examination. Communication between the obstetrician and anesthesiologist is critical in cases of fetal bradycardia. The obstetrician must convey the urgency of the delivery, and the anesthesiologist must convey his or her concerns.

Risk Factors

  • Maternal hemorrhage

  • Hypovolemia

  • Maternal asthma

  • Polyhydramnios

  • Placental abruption

  • Maternal cardiac disease

  • Maternal cocaine use

  • Maternal trauma

  • Rupture of membranes with the fetal head not engaged

  • Prematurity

Prevention

Maintaining uterine perfusion and fetal oxygen delivery decreases the risk of fetal bradycardia. Left uterine displacement helps to prevent aortocaval compression. Administer incremental doses of phenylephrine (100 mcg IV) or ephedrine (5 mg IV) to treat hypotension caused by neuraxial anesthesia. The use of supplemental oxygen is debatable because the impact on fetal oxygenation is minimal.

Special Considerations

  • The baseline FHR is determined by approximating the FHR for a 10-minute window. Despite the presence of fetal bradycardia, the anesthesiologist may elect to perform regional anesthesia if a difficult airway is suspected in order to avoid failed intubation. Early initiation of epidural analgesia in patients with a Category II tracing is strongly recommended because it decreases the probability that general anesthesia will be required if the tracing progresses to Category III.

Further Reading

Blackwell SC, Grobman WA, Antoniewics L, et al. Interobserver and intraobserver reliability of the NICHD 3-Tier fetal heart rate interpretation system. Am J Obstet Gynecol. 2011; 205: 378.e1–5.Find this resource:

Jackson M, Holmgren CM, Esplin MS. Frequency of fetal heart rate categories and short-term neonatal outcomes. Obstet Gynecol. 2011; 118: 803–808.Find this resource:

Schnettler WT, Rogers J, Barber RE, Hacker MR. A modified fetal heart rate tracing interpretation system for prediction of cesarean section. J Matern Fetal Neonatal Med. 2012; 25: 1055–1058.Find this resource:

Hypotension

Definition

A systolic blood pressure <90 or 100 mm Hg or a decrease of 20% from its baseline.

Presentation

Maternal effects of hypotension are light headedness, dizziness, and nausea. The uterus does not autoregulate blood pressure, so hypotension that decreases uterine blood flow may result in a Category III FHR. A decrease in uterine blood also increases the risk of fetal acidosis.

Pathophysiology

Hypotension is caused by one of two mechanisms: a decrease in systemic vascular resistance or a decrease in cardiac output. In obstetric anesthesia, there are two main causes of hypotension: aortocaval compression and sympathectomy from neuraxial anesthesia. If the parturient lies on her back, the gravid uterus compresses the vena cava against the lumbar vertebra, decreasing venous return and cardiac output. This usually occurs after 20–24 weeks gestation. Aortocaval compression may be avoided by tilting the uterus to the left (uterine displacement) by placing a wedge beneath the right hip. Both epidural and spinal anesthesia can produce a sympathectomy, which decreases systemic vascular resistance. The uterus does not autoregulate blood flow, so blood flow is dependent upon the blood pressure.

Immediate Management

  • Administer bolus doses of phenylephrine (100 mcg) or ephedrine (10 mg). Phenylephrine is preferred.

  • Consider a starting phenylephrine infusion (50–100 mcg/min) for hypotension associated with spinal anesthesia.

Differential Diagnosis

  • Aortocaval compression

  • Sympathectomy from neuraxial anesthesia

  • Anaphylaxis

  • Sepsis

  • Iatrogenic

  • Concurrent medication

  • Hemorrhage

  • Hypovolemia

  • Cardiac arrythmia

  • Pulmonary embolism

  • Pneumothorax

Diagnostic Studies

  • If aortocaval compression or neuraxial anesthesia are causing hypotension, no further studies are indicated.

  • If another cause is suspected, serum hemoglobin or serum tryptase may be indicated.

  • Additional studies include a blood gas, electrocardiogram, or chest X-ray, depending upon physical examination.

Subsequent Management

If the patient develops hypotension, maintain left uterine displacement and administer additional intravenous fluids. Determine the etiology of the hypotension.

Risk Factors

Beginning at 20–24 weeks gestation, the uterus becomes enlarged enough to result in aortocaval compression in the supine position (supine hypotensive syndrome). Many patients do not exhibit these symptoms when not anesthetized because the sympathetic nervous system is intact. However, with general or neuraxial anesthesia, the sympathetic nervous system is attenuated, making them more likely to develop supine hypotension.

Prevention

Originally, fluid loading with crystalloid solutions prior to neuraxial anesthesia for cesarean delivery was thought to decrease the incidence and severity of hypotension. However, fluid loading with these solutions does not prevent the development of hypotension. Colloid solutions have been demonstrated to decrease the incidence and severity of hypotension prior to neuraxial anesthesia. Colloid solutions are more expensive and have the risk of increased anaphylaxis. The routine administration of colloid prior to epidural or spinal anesthesia is not done. Prophylactic administration of vasopressors prior to neuraxial anesthesia is not recommended because they may cause hypertension. Most practitioners do not administer a fluid load prior to the initiation of epidural analgesia for labor.

Special Considerations

  • The sympathetic nervous system runs from T1 to L2. The degree of hypotension is related to the degree of sympathetic block. The innervations for the first stage of labor is T10 to L1, making a high block unnecessary in the management of the pain of first stage. Limiting the degree of sympathectomy will decrease the risk of hypotension. For cesarean section, a T4 sensory level is required, causing a greater degree of hypotension as compared to analgesia for labor.

  • Treatment with phenylephrine is associated with a higher umbilical cord blood pH than is ephedrine. Therefore, phenylephrine is preferred for the management of hypotension accompanying spinal anesthesia. This difference is not due to an effect on uterine blood flow. Ephedrine crosses the placenta and stimulates the fetal sympathetic nervous system when administered in large quantities.

  • Many practitioners initiate a continuous infusion of phenylephrine for the treatment of hypotension accompanying spinal anesthesia during cesarean section. A continuous infusion of phenylephrine decreases the incidence of maternal nausea/vomiting as compared to intermittent boluses.

Further Reading

Cooper DW. Caesarean delivery vasopressor management. Curr Opin Anaesthesiol. 2012;25:300–8.Find this resource:

Habib AS. A review of the impact of phenylephrine administration on maternal hemodynamics and maternal and neonatal outcomes in women undergoing cesarean delivery under spinal anesthesia. Anesth Analg. 2012; 114: 377–390.Find this resource:

Local Anesthetic Toxicity

Definition

Unintended systemic effects of local anesthetics usually due to unintended intravascular injection; also may occur from systemic absorption of excessive amounts.

Presentation

The symptoms from local anesthetic occur when various concentrations are achieved in the blood. Toxicity may present with central nervous system and cardiovascular symptoms. Typically, central nervous system effects occur before cardiovascular effects.

  • Low blood concentrations: The patient may note tongue numbness, metallic taste, or tinnitus.

  • High blood concentrations: As the concentrations increase, the patient will seize before becoming comatose.

  • Very high blood concentrations: If the concentrations of the local anesthetic continue to increase, the patient will develop cardiovascular symptoms in the form of myocardial depression, dysrhythmias, and cardiovascular collapse. These effects occur because of the local anesthetic impairing electrical conduction in the myocardium with ventricular tachycardia and ventricular fibrillation, and myocardial depression.

Pathophysiology

Local anesthetics cause reversible blockade of the sodium channels. They act on the central and peripheral nervous system, myocardial muscle, and the conduction system in the myocardium. Seizures are caused by the local anesthetic blocking inhibitory neurons within the central nervous system, resulting in unopposed excitatory impulses. Eventually, these too are blocked, resulting in coma. Cardiovascular toxicity results from blockade of the sodium channels in the muscle and conduction system of the heart, leading to myocardial depression and dysrhythmias.

Immediate Management

  • Halt the injection of local anesthetic.

  • Prepare for maternal cardiac arrest and initiation of cardiopulmonary resuscitation.

  • If the patient is seizing, administer either a benzodiazepine (e.g., midazolam 2 mg IV) or propofol 1–2 mg/kg. Prepare to secure the airway.

  • Check for a maternal pulse. If there is no pulse, begin cardiopulmonary resuscitation and prepare for cesarean delivery (see section on maternal cardiac arrest).

  • Administer 20% intralipid 1.5 mL/kg IV bolus followed by 0.25 mL/kg/min for 30–60 minutes.

  • Additional boluses of 20% intralipid may be indicated if the symptoms persist.

Differential Diagnosis

  • Eclampsia

  • Underlying seizure disorder

  • Toxic from other drugs

  • Metabolic from electrolyte or glucose abnormalities

  • Alcohol/drug withdrawal

  • Pulmonary embolism

  • Cardiac arrest

  • Myocardial infarction

  • Underlying cardiac disease

Diagnostic Studies

There are no diagnostic studies for local anesthetic toxicity. If local anesthetic toxicity is suspected, the administration of intravenous intralipid should not be delayed.

Subsequent Management

  • If symptoms persist, administer a second dose of intralipid.

  • If the patient’s symptoms do not respond to intralipid, another etiology of the seizure or myocardial arrhythmia should be considered.

  • Following resolution of the symptoms, a neurologic examination should be performed. If the patient had a cardiac arrhythmia, the patient should have continuous cardiac monitoring as well as laboratory testing for myocardial infarction.

Risk Factors

Parturients are at risk for intravascular placement of epidural catheters due to dilation of the epidural veins.

Prevention

Prior to the administration of local anesthetic for cesarean delivery, a test dose of 3 mL 1.5% lidocaine with epinephrine 1:200,000 should be administered. If the catheter is intravascular, there will be an increase in maternal heart rate of 10–15 bpm. It is common for the maternal heart rate to vary during labor due to the pain of contractions. If a patient should experience a contraction during the administration of the test dose and the heart rate increases, this increase may be a “false positive,” meaning that the increase was because of pain, not because of intravascular injection.

Fractionate the dose of local anesthetic and ask the patient about tinnitus and check for tachycardia during injection. Subsequent doses of epidural anesthesia should be fractionated. Administer 3–5 mL increments, waiting several minutes between doses. An intravascular injection may be detected prior to giving the full dose of local anesthetic.

Special Considerations

  • Any location in which local anesthetics are administered should have the 20% intralipid in a sufficient quantity to treat toxicity readily available. There should also be a card with instructions for its use.

Further Reading

Barrington MJ, Kluger R. Ultrasound guidance reduces the risk of local anesthetic systemic toxicity following peripheral nerve blockade. Reg Anesth Pain Med. 2013; 38: 289–297.Find this resource:

Killoran PV, Cattano D. From bedside to bench and back: perfecting lipid emulsion therapy for local anesthetic toxicity. Anesthesiology. 2011; 115: 1151–1152.Find this resource:

Neal JM, Mulroy MF, Weinberg GL. American Society of Regional Anesthesia and Pain Medicine checklist for managing local anesthetic systemic toxicity: 2012 version. Reg Anesth Pain Med. 2012; 37: 16–18.Find this resource:

Maternal Cardiac Arrest

Definition

Absence of a palpable maternal pulse requiring cardiopulmonary resuscitation.

Presentation

The mother has no palpable pulse. The electrocardiogram will reveal pulseless electrical activity, ventricular fibrillation, or asystole.

Pathophysiology

The most common cause is venous thromboembolism. The American Heart Association uses the mnemonic to assist with the diagnosis of the etiology of maternal cardiac arrest: BEAUCHOPS. The letters correspond to the following etiologies: B—bleeding; E—embolism (venous and amniotic fluid); A—anesthetic complications; U—uterine atony (most likely leading to bleeding); C—cardiac disease (myocardial infarction, pre-existing cardiac disease, cardiomyopathy); H—hypertension (pre-eclampsia and eclampsia, intracerebral bleed); O—other (differential diagnosis of standard ACLS guidelines); P—placental abruption/previa (bleeding and possible disseminated intravascular coagulation); and S—sepsis. The anatomic and physiologic changes of pregnancy and labor result in significantly decreased cardiovascular and pulmonary reserves, which may complicate the resuscitation, and both the mother and fetus must be considered.

Differential Diagnosis

  • Hemorrhage

  • Total spinal anesthesia

  • Local anesthetic toxicity

  • Anaphylaxis

  • Embolism

  • Maternal cardiac disease

  • Sepsis

  • Eclampsia

  • Intracerebral hemorrhage

Immediate Management

  • The goal of resuscitating the parturient is the return of maternal circulation. Follow the American Heart Association ACLS algorithm.

  • Begin chest compressions immediately.

  • Left uterine displacement should be used to relieve aortocaval compression. Left uterine displacement is best achieved manually rather than tilting the bed. Tilting the bed or a wedge may decrease the effectiveness of chest compressions.

  • For chest compressions, the hands may need to be placed higher on the sternum than usual due to the gravid uterus.

  • Ventilate the patient. Intubation of the pregnant patient may be more difficult. Use capnography to document adequate ventilation and chest compressions.

  • If indicated, defibrillate the patient. The energy required for defibrillation does not change during pregnancy. The energy settings recommended in the ACLS algorithm apply for pregnant patients.

  • Medications should be administered in the same doses as would be used for a nonpregnant patient. Although the physiologic changes of pregnancy may alter the volume of distribution of the various medications, no adjustment is required.

  • If local anesthetic toxicity is suspected, intravenous intralipid is the indicated treatment.

  • Use the “5-minute rule” during resuscitation of the pregnant patient. If the maternal circulation has not returned by 4 minutes of cardiopulmonary resuscitation, cesarean delivery should be performed with delivery of the infant by minute 5.

Diagnostic Studies

An automated external defibrillator will determine whether the cardiac rhythm is treatable with electricity. The etiology of pulseless electrical activity should be investigated with additional laboratory information such as arterial blood gas analysis and transthoracic echocardiography.

Subsequent Management

If the maternal circulation has not been restored by 4 minutes, the obstetrician should perform cesarean delivery with the goal of delivery of the baby by minute 5. Performance of cardiopulmonary resuscitation in a pregnant patient is difficult due to the gravid uterus causing vena cava compression and inhibiting effective chest compressions.

Risk Factors

Parturients with congenital heart disease are at particular risk for cardiac arrest during pregnancy. Pregnancy is associated with an increase in coagulation factors, including fibrinogen (Factor 1), proconvertin (Factor VII), antihemophilic factor (Factor VIII), Christmas factor (Factor IX), Stuart-Prower factor (Factor X), and Hageman factor (Factor XII). The concentrations of Factors I and VIII increase by >100%. Parturients are more likely to be hypercoagulable and at risk for thromboembolism because factor concentrations are increased.

Prevention

Appropriate testing of the epidural catheter may reduce the incidence of total spinal anesthesia and local anesthetic toxicity. Due to aortocaval compression by the gravid uterus, the epidural veins are dilated and are easily punctured during epidural catheter placement. Dosing in an epidural catheter should always in a divided fashion, eliciting symptoms from the patient. Also, a high level of suspicion in parturients with cardiac disease, hemorrhage, or hypertensive disorders of pregnancy should be maintained throughout the peripartum period.

Special Considerations

  • The incidence of cardiac arrest in the pregnant patient is estimated to be <1:20,000 women. The most important step in the resuscitation of the parturient is the early delivery of the fetus if there is no return of maternal circulation. Effective cardiopulmonary resuscitation in the pregnant patient is difficult because chest compressions are less effective and the gravid uterus obstructs the vena cava. Early delivery decreases the risk of neurologic injury in the infant and may improve the likelihood of successful maternal resuscitation by decreasing aortocaval compression and improving maternal compression. Estimated gestational age is an important factor in predicting prognosis for infants after perimortem cesarean deliveries. The threshold for expected fetal viability is considered to be around 24 weeks’ gestation. Although emergency delivery performed between 20 and 23 weeks may produce a nonviable infant, it may enable successful resuscitation of the mother.

Further Reading

Lipman S, Cohen S, Einav S, et al. The Society for Obstetric Anesthesia and Perinatology Consensus Statement on the Management of Cardiac Arrest in Pregnancy. Anesth Analg. 2014; 118: 1003–1016.Find this resource:

Mhyre JM, Tsen LC, Einav S, et al. Cardiac arrest during hospitalization for delivery in the United States, 1998–2011. Anesthesiology. 2014; 120: 810–818.Find this resource:

Maternal Hemorrhage

Definition

The definition of hemorrhage is difficult because the parturient undergoes several physiologic changes of pregnancy, which result in an increase in blood volume to compensate for the blood loss during delivery. Most physicians use as a definition a blood loss of 500 mL for a vaginal delivery and 1000 for a cesarean delivery as a definition, but the majority of deliveries have this amount of blood loss. Symptoms such as hypotension or oliguria do not occur until a blood loss >10% blood volume.

Presentation

Parturients with obstetric hemorrhage present with:

  • Increased maternal heart rate (sinus tachycardia)

  • Maternal hypotension

  • Fetal tachycardia

Pathophysiology

At term, uterine blood flow is approximately 500–700 mL/min. Hemorrhage during delivery may be either antepartum or postpartum. The two major causes of antepartum hemorrhage are placenta previa and placental abruption. The major causes of postpartum hemorrhage are uterine atony, retained placenta, and placenta accreta. Placenta previa occurs when the placenta overlies the cervical os, or is proximate to the internal os of the cervix. Placental abruption refers to separation of the placenta after 20 weeks gestation but before the birth of the fetus. Placenta accreta is defined as implantation directly onto the myometrium (accreta), into the myometrium (increta), or through the myometrium (percreta). If the placenta is implanted into the myometrium, the uterus cannot contract, causing hemorrhage. The incidence of postpartum hemorrhage is increasing; the etiology is unclear. A soft, poorly contracted uterus is referred to as uterine atony.

Differential Diagnosis

  • Antepartum hemorrhage: Placenta previa results in painless vaginal bleeding with no concealed bleeding. Placental abruption is very painful, but the blood loss may be retroplacental and concealed.

  • Postpartum hemorrhage: The incidence of postpartum hemorrhage is increasing. Many attribute it to the increase in labor induction, making the uterus resistant to oxytocin.

Immediate Management

  • Manage the hemorrhage:

    • Obtain large-bore intravenous access.

    • Initiate fluid resuscitation.

    • Initiate rapid transfusion protocol.

      • Every labor floor should have a rapid transfusion protocol that will allow the provider to access packed red blood cells, fresh-frozen plasma, and platelets. As most cases of obstetric hemorrhage are accompanied by a low fibrinogen, the use of cryoprecipitate should be used early in the resuscitation.

    • Use cross-matched blood if possible. If the blood type is unknown, O-blood should be used.

  • Management of uterine atony:

    • Uterine atony results from the lack of uterine contraction. The obstetrician will initially attempt manual massage (fundal massage) to get the uterus to contract. If that is unsuccessful, the choice of medication depends upon the practitioner as there is no study demonstrating the superiority of one medication over another.

      • Oxytocin, 20–40 U, is added to 1 L crystalloid solution and this solution is administered intravenously. Rapid administration may cause hypotension.

      • Methylergonovine 0.2 mg IM. Increased blood pressure is a relative contraindication.

      • Prostaglandin F2α‎ 0.25 mg IM. Asthma is a contraindication.

  • Management of placenta accreta:

    • Prepare for significant hemorrhage: Establish large-bore IV access.

    • Significant hemorrhage may occur during the hysterectomy. Fluid replacement should consist of packed red blood cells, fresh-frozen plasma, and platelets in a 1:1:1 fashion. Strong consideration should be given to the administration of cryoprecipitate (hypofibrinogenemia). Recombinant Factor VII decreases bleeding but may increase the risk of thromboembolism.

    • Consider general anesthesia. Although a gravid hysterectomy may be performed under regional anesthesia, the provider will be transfusing blood products and may have difficulty managing the airway if this becomes necessary.

Diagnostic Studies

  • Placenta previa is diagnosed via ultrasound. If the patient has a placenta previa, a cervical exam is not performed due to risk of causing bleeding.

  • Placental abruption and retained placenta are diagnosed with ultrasound.

  • Uterine atony is a diagnosis of exclusion.

Subsequent Management

  • If the patient has a placenta previa, cesarean delivery is necessary. For placenta previa, the patient will bleed only when the cervix begins to dilate. As such, the patient will not bleed if not in labor. The goal for the obstetrician is to allow the fetus to mature in utero as long as possible, but not so long as to allow the mother to begin to labor and to hemorrhage.

  • If the patient has a placenta abruption, delivery may be by vaginal or cesarean delivery. Placental abruption is the leading cause of disseminated intravascular coagulation. Therefore, coagulation studies and platelet count should be followed if placental abruption is suspected.

  • The management of uterine atony will depend upon subsequent events. If the uterus begins to contract after a period of atony, no further intervention is required. Oxytocin may be continued to maintain uterine tone. If retained products are suspected, intravenous nitroglycerin provides uterine relaxation and allows the obstetrician to explore the uterus manually, potentially avoiding dilation and evacuation.

    • The obstetrician will request additional medications such as methylergonovine or prostaglandin F2α‎.

    • For continued bleeding without hemodynamic instability, the obstetrician may request an interventional radiology consultation for arterial embolization.

Risk Factors

  • Placenta previa

    • Previous cesarean delivery

    • Previous uterine surgery

    • Older maternal age

    • Multiple pregnancy

  • Placental abruption

    • Pre-eclampsia

    • Hypertension

    • History of placental abruption

    • Cocaine

    • Trauma

  • Placenta accreta

    • Previous cesarean section and placenta previa

  • Uterine atony

    • Multiparity

    • Multiple gestation

    • Infection

    • Magnesium

    • Fetal macrosomia

    • Polyhydramnios

Prevention

There are no specific means to prevent obstetric hemorrhage, but early identification of risk factors and preparation for extensive blood loss are essentials. Establish large-bore IV access in patients who are at risk, and verify that blood products are immediately available. In patients with placenta accreta, consider an interventional radiology consultation prior to cesarean delivery to insert balloon catheters in the iliac arteries. These catheters may be inflated after delivery to decrease uterine blood flow.

Special Considerations

  • The use of cell saver in obstetrics is controversial because of the theoretical risk of infection and amniotic fluid embolism. Both the American Congress of Obstetricians and Gynecologists and the American Society of Anesthesiologists guidelines state that the use of a cell saver should be considered if available. Recombinant Factor VIIa has been used, but may exacerbate a pre-existing hypercoagulable state.

Further Reading

Bryant A, Mhyre JM, Leffert LR, et al. The association of maternal race and ethnicity and the risk of postpartum hemorrhage. Anesth Analg. 2012; 115: 1127–1136.Find this resource:

Committee on Obstetric Practice. Committee opinion no. 529: placenta accreta. Obstet Gynecol. 2012; 120: 207–211.Find this resource:

Shields LE, Smalarz K, Reffigee L, et al. Comprehensive maternal hemorrhage protocols improve patient safety and reduce utilization of blood products. Am J Obstet Gynecol. 2011; 205: 368.e1–8.Find this resource:

Neonatal Resuscitation

Definition

During the transition from intrauterine to extrauterine life, the neonate is required to make rapid and profound physiologic changes as the neonate transfers from receiving oxygen from uterine blood flow and nonfunctioning lungs to receiving oxygen completely from respiration. Approximately 10% of newborns require some assistance to initiate respiration, whereas about 1% of newborns need extensive resuscitative measures

Presentation

  • Failure to initiate spontaneous ventilation after being stimulated (usually by gentle rubbing and suctioning)

  • Heart rate <100 bpm

Pathophysiology

Before birth, the fetus depends completely on uterine blood flow for delivery of oxygen to the developing tissues. The transition to postnatal circulation, fluid in the alveoli must be absorbed into the lung tissue and replaced by air. The umbilical arteries and vein are clamped, removing the low-resistance placental circuit and increasing systemic blood pressure. Vasodilation decreases pulmonary artery resistance, resulting in increased pulmonary blood flow and decreased flow through the ductus arteriosus, which begins to constrict. At the completion of this transition, the baby is breathing spontaneously and maintaining the oxygen saturation on room air. If this sequence is interrupted, the pulmonary arterioles may remain constricted and the systemic arterial blood will not become oxygenated.

Differential Diagnosis

  • Maternal opioid consumption

  • Other causes of apnea include general anesthesia administered to the mother, congenital heart defects or other malformations, and neonatal sepsis.

Immediate Management

  • Place the infant on a radiant warmer to prevent hypothermia.

  • Dry and stimulate the infant for 20 seconds.

  • If the infant remains apneic following stimulation, assume that the neonate is experiencing secondary apnea and requires positive pressure ventilation.

  • Attach a pulse oximeter.

  • Ventilation should be with room air for term neonates and with a mixture of room air/oxygen for premature infants. If the neonate requires chest compression, ventilation should be with 100% oxygen.

  • Administer intravenous naloxone, 0.1 mg/kg, if maternal opioid consumption is suspected.

  • Initiate positive pressure ventilation at a rate of 40–60 breaths per minute at a pressure <20 cm H2O (a pressure manometer must be used during neonatal resuscitation).

  • After initiation of ventilation, assess the heart rate by auscultation or electrocardiogram (preferred). (An increasing heart rate is the most reliable indication of effective ventilation.)

    • If the heart rate is <100 bpm, assess adequacy of ventilation and make necessary adjustments.

    • If the heart rate is <60 bpm, initiate chest compressions. Chest compressions may be performed by having the hand encircle the chest with the two thumbs performing the compressions or by two fingers compressing the lower sternum. The two-thumb technique is preferred because it generates greater systolic and coronary perfusion pressures.

    • The rate of compression is one breath after every third compression, for a total of 30 breaths and 90 compressions per minute.

  • If the heart rate is >60 bpm, chest compressions are stopped but ventilation is continued.

  • If the heart rate is >100 bpm and the baby begins to breathe spontaneously, positive ventilation is stopped.

  • If the heart rate remains <60 bpm despite effective ventilation, epinephrine 1:10,000 0.1–0.3 mL/kg is administered intravenously.

Subsequent Management

If the infant responds to drying or to positive pressure ventilation, no further workup is necessary. After resuscitation, the infant should be admitted to the neonatal intensive care unit for further management.

It is permissible to withhold resuscitation if the infant’s age, weight, or coexisting condition is associated with a high mortality. If the infant does not have an established heart rate following 10 minutes of resuscitation, it is permissible to discontinue resuscitative efforts. In both of these situations, a consistent and coordinated approach that considers the available medical literature must be followed.

Risk Factors

  • Maternal diabetes

  • Pre-eclampsia

  • Maternal infection

  • Maternal drug overdose

  • Post-term gestation

  • Fetal malformation

  • Meconium

  • Nonreassuring fetal heart tracing during delivery

  • Emergency cesarean delivery

  • Prolonged rupture of membrane

  • Premature labor

  • Instrumental delivery (forceps or vacuum)

Prevention

If the need for neonatal resuscitation is anticipated because of the presence of a risk factor, equipment and personnel should be immediately available at delivery. The absence of a risk factor does not guarantee that the infant will not require resuscitation. Individuals capable of providing neonatal resuscitation should be available in every delivery unit.

Special Considerations

  • Respirations are the first vital sign to be affected when a newborn is deprived of oxygen. After an initial period of attempts to breathe, there is a period of primary apnea. During primary apnea, stimulation, such as drying the infant, will cause a resumption of breathing. If hypoxia continues, the baby gasps and enters a period of secondary apnea. During secondary apnea, stimulation will not restart respiratory efforts. The only therapeutic for secondary apnea is positive pressure ventilation. At least one person (not the anesthesia provider) whose primary responsibility is the neonate and who is capable of initiating resuscitation should be present at every delivery.

  • Laryngeal mask airways have proven effective in the management of ventilation of infants >2 kg or 34 weeks gestation. The use of the laryngeal mask airway for smaller or younger infants has limited data.

Further Reading

Kattwinkel J, Perlman JM, Aziz K, et al. Neonatal resuscitation: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Pediatrics. 2010; 126: 1400–1413.Find this resource:

Louis D, Sundaram V, Kumar P. Pulse oximeter sensor application during neonatal resuscitation: a randomized controlled trial. Pediatrics. 2014; 133: 476–482.Find this resource:

Zaichkin J, Weiner GM. Neonatal Resuscitation Program (NRP) 2011: new science, new strategies. Adv Neonat Care. 2011; 11: 43–51.Find this resource:

Pre-eclampsia

Definition

Pre-eclampsia is a multisystem disorder associated with increased blood pressure, proteinuria, and edema. Blood pressure must be ≥140 mm Hg systolic or ≥90 mm Hg diastolic on two measurements that are at least 4 hours apart. Hypertension must be accompanied by proteinuria (as defined as ≥300 mg/24 hours or protein/creatinine ratio >0.3) or in the absence of proteinuria, have any of the following: thrombocytopenia, renal insufficiency (creatinine >1.1 mg/dL), impaired liver function, pulmonary edema, or cerebral or visual symptoms. Severe pre-eclampsia occurs with one of the following symptoms: systolic blood pressure of >160 mm Hg or diastolic blood pressure of >110 mm Hg, thrombocytopenia, impaired liver function, progressive renal insufficiency, pulmonary edema, or new-onset cerebral or visual disturbances. Eclampsia includes these findings as well as central nervous system involvement leading to seizures not from other cerebral conditions.

Presentation

Pre-eclampsia

  • Systolic blood pressure >140 mm Hg

  • Diastolic blood pressure >90 mm Hg

  • Proteinuria >300 mg/24 hours

  • If no proteinuria, may still diagnose pre-eclampsia if any of the following symptoms exist:

    • Platelet count <100,000/µL

    • Liver transaminases twice normal concentration

    • Creatinine >1.1 mg/dL

    • Pulmonary edema

    • New-onset cerebral or visual disturbance

Severe pre-eclampsia

  • Increased blood pressure and any of the following:

    • Systolic blood pressure >160 mm Hg

    • Diastolic blood pressure >110 mm Hg

    • Platelet count <100,000/µL

    • Right upper quadrant pain and elevated liver enzymes

    • Serum creatinine >1.1 mg/dL

    • Pulmonary edema

    • New-onset cerebral or visual disturbances

Pathophysiology

Hypertension during pregnancy has four potential causes: 1) pre-eclampsia-eclampsia, 2) chronic hypertension, 3) chronic hypertension with superimposed pre-eclampsia, and 4) gestational hypertension. The etiology of pre-eclampsia remains unknown, but the disease most likely begins at implantation, well before clinical symptoms appear. The placenta is the most likely source of the disease because molar and abdominal pregnancies have also been associated with pre-eclampsia. The leading theory involves an immunologic alteration of trophoblast function and decreased vascularity. The decrease in vasculature leads to ischemia and the generation of free radicals, which causes the symptoms. There is an abnormal response to the angiogenic proteins produced by the placenta, resulting in the abnormal vasculature.

Immediate Management

  • Pre-eclampsia after 36 weeks gestation or the presence of severe pre-eclampsia is an indication for delivery either by induction of labor or cesarean section.

  • Intravenous magnesium is administered to women with pre-eclampsia to prevent the progression of the disease to eclampsia (seizures). As it is not possible to determine who will develop eclampsia, all women with pre-eclampsia should receive magnesium. While other anticonvulsants have been studied, none has been as effective as magnesium.

  • Consider epidural labor analgesia or neuraxial anesthesia (including spinal anesthesia) for cesarean delivery, even if the patient has severe pre-eclampsia.

  • Check the platelet count in all patients before attempting regional anesthesia.

Differential Diagnosis

  • Local anesthetic toxicity

  • Gestational hypertension

  • Hypertension

  • Acute cocaine toxicity

  • Pain

  • Pre-existing kidney disease

  • Toxic/metabolic

  • Alcohol/drug withdrawal

Diagnostic Studies

  • Proteinuria is diagnosed with a timed urine collection. Proteinuria up to 300 mg/24 hours is normal. Proteinuria >300 mg/24 hours is abnormal. Using a dipstick of the urine for protein is too nonspecific for the diagnosis. A protein/creatinine ratio of at least 0.3 is also consistent with pre-eclampsia, but it is possible for a patient to have pre-eclampsia without proteinuria.

  • Complete blood count including the platelet count.

  • The hemoglobin level may be increased due to hypovolemia or it may be decreased if hemolysis is occurring.

  • If a patient seizes, a head computed tomography scan will rule out an anatomic etiology.

  • Although placental growth factor and sFlt-1 may be measured in the blood or the urine, their variability makes them unsuitable for the diagnosis or for the prediction of the disease at this point. It is unclear of the role of these blood tests in the future.

Subsequent Management

  • Magnesium sulfate is started for seizure prophylaxis in all pre-eclamptic patients. In patients with normal renal function, use a loading dose of 4 grams intravenously followed by an infusion of 1–2 g/h.

  • The diagnosis of severe pre-eclampsia indicates that the mother is at risk of end-organ damage and is an indication for delivery.

  • Parturients with preeclampsia are at risk for the development of eclampsia in the postpartum period, especially during the first 24 hours. Patients must be monitored and magnesium should be continued for 24 hours after delivery.

  • If a patient develops thrombocytopenia after an epidural catheter has been inserted, removal should be delayed until the platelet count begins to normalize, which may take up to 3 days postpartum.

Risk Factors

  • First pregnancy

  • Previous pre-eclampsia

  • Chronic hypertension or chronic renal disease

  • History of thrombophilia

  • Multigestation pregnancy

  • Family history of pre-eclampsia

  • Diabetes mellitus

  • Obesity

  • Systemic lupus erythematosus

  • Advanced maternal age (>40 years)

Prevention

There is no known intervention that prevents pre-eclampsia. For women with a history of early onset pre-eclampsia and a preterm delivery in more than one prior pregnancy, the daily administration of aspirin 60–80 mg is indicated, starting in the first trimester.

Special Considerations

  • The incidence of pre-eclampsia in the United States is increasing and has increased by 25% over the past 20 years. It is the leading cause of maternal and perinatal morbidity and mortality, and is a risk factor for future cardiovascular disease. It complicates up to 10% of pregnancies and is more likely to occur at both extremes of reproductive age.

  • One percent of parturients with pre-eclampsia them will develop eclampsia.

  • Spinal anesthesia is not contraindicated in patients with severe pre-eclampsia, nor is it associated with a greater degree of hypotension or pulmonary edema.

  • Thrombocytopenia is the most common hematologic abnormality in patients with pre-eclampsia. Its incidence depends upon the severity of the disease and the presence of placental abruption. The platelet count should be checked prior to the initiation of neuraxial anesthesia. The American Society of Anesthesiologists has not recommended a safe limit for the platelet count in patients with pre-eclampsia, and there are numerous case reports of epidural placement in patients with low platelet counts.

  • Magnesium sulfate significantly potentiates nondepolarizing neuromuscular blocking drugs. If the patient receives general anesthesia for cesarean delivery, nondepolarizing neuromuscular blocking drugs should be avoided if possible.

Further Reading

Homer CS, Brown MA, Mangos G, et al. Non-proteinuric pre-eclampsia: a novel risk indicator in women with gestational hypertension. J Hypertens. 2008; 26: 295–302.Find this resource:

Lindheimer MD, Taler SJ, Cunningham FG. Hypertension in pregnancy. J Am Soc Hyptens. 2010; 4: 68–78.Find this resource:

Rana S, Powe CE, Salahuddin S, et al. Angiogenic factors and the risk of adverse outcomes in women with suspected preeclampsia. Circulation. 2012; 125: 911–919.Find this resource:

Van Veen JJ, Nokes TJ, Makris M. The risk of spinal haematoma following neuraxial anaesthesia or lumbar puncture in thrombocytopenic individuals. Br J Haematol. 2010; 148: 15–25.Find this resource:

Sepsis

Definition

Puerperal sepsis is an infection of the genital tract occurring at any time between rupture of the membranes and 42 days postpartum.

Presentation

The patient should have two or more of the following: pelvic pain, fever >38.5° C, abnormal vaginal discharge, and delay in the reduction of the size of the uterus. Systemic inflammatory response syndrome (SIRS) is an inflammatory process with two or more of the following clinical findings are present: temperature >38.5° C, heart rate >90 bpm, respiratory rate >20/min, and white blood cell count >12 × 109/dL. Sepsis is SIRS with an infection. In septic shock, the patient is hypotensive.

Pathophysiology

The majority of cases of sepsis during pregnancy involved Group A streptococcus. Approximately 5%–30% of the population is thought to be asymptomatic carriers. Group B streptococcus may cause urosepsis or endometritis with approximately 20%–30% of women of reproductive age having these bacteria in the vagina. Influenza A and B are the most common pathogens of pneumonia in pregnancy.

Immediate Management

  • Draw blood for culture and blood count.

  • Obtain uterine swabs for culture.

  • Begin high dose broad spectrum antibiotics. Note: Blood cultures should be obtained before initiation of antibiotics.

  • Septic shock is treated with vasopressors such as phenylephrine and intravenous fluids.

  • Antibiotics should be continued for 7–10 days.

Differential Diagnosis

  • Asthma

  • Anaphylaxis

  • Hypovolemia

  • Hemorrhage

  • Thromboembolism

  • Pneumothorax

  • Pericardial effusion

Diagnostic Studies

  • Obtain cultures, including blood, vaginal swabs, surgical sites, and urine.

  • Draw blood for blood count, electrolytes, C-reactive protein, and lactacte.

  • Obtain an arterial blood gas analysis if pneumonia is suspected.

  • Radiographic studies of the chest or abdomen are guided by the patient’s symptoms.

Subsequent Management

Continue treatment with intravenous fluids. Both colloids and crystalloids have been used for the fluid resuscitation. If the patient remains hypotensive, initiate treatment with one or more vasopressors as required (e.g., norepinephrine, epinephrine, or phenylephrine). Follow serum lactates to determine the response to therapy. Broad-spectrum antibiotics should be initiated.

Risk Factors

  • History of group B streptococcal infection

  • Vaginal discharge

  • History of pelvic infection

  • Prolonged rupture of membranes

  • Cesarean delivery

  • Recent upper respiratory infection

  • Diabetes

  • Human immunodeficiency virus

  • Maternal age >35 years

  • Low socioeconomic factors

Prevention

Preoperative skin preparation prior to cesarean delivery should include hair removal with an electric razor and antiseptic (chlorhexidine). All patients having cesarean delivery should receive prophylactic antibiotics. A surgical mask and gown should be worn by all personnel during both vaginal delivery and cesarean delivery. Hand hygiene should be enforced throughout the labor suite.

Special Considerations

  • Sepsis remains a major cause of maternal mortality. The physiologic changes of pregnancy result in an increase in maternal heart rate and respiratory rate, making the diagnosis of SIRS difficult. Pregnancy and labor also increase the white blood cell count in some individuals. A low threshold for the diagnosis of sepsis should be maintained given the associated high mortality.

Further Reading

Acosta CD, Knight M. Sepsis and maternal mortality. Curr Opin Obstet Gynecol. 2013; 25: 109–116.Find this resource:

Bamfo JE. Managing the risks of sepsis in pregnancy. Best Pract Research Clin Obstet Gynaecol. 2013; 27: 583–595.Find this resource:

Shoulder Dystocia

Definition

Shoulder dystocia occurs when gentle downward traction on the fetal head by the obstetrician fails to result in delivery of the shoulders. The most common reason is impaction of the anterior shoulder under the public bone. Less commonly, the posterior shoulder becomes impacted on the sacral promontory.

Presentation

  • Prolonged second stage of labor

  • Following delivery of the fetal head, gentle traction on the head fails to result in delivery of the shoulder.

  • The obstetrician does not apply excessive force to the fetal head to prevent brachial plexus injury.

Pathophysiology

During a normal delivery, the fetal head and shoulders rotate to allow for its descent and passage through the maternal pelvis. If the shoulder should rotate into the anterior-posterior diameter before entering the pelvis, the shoulders may become impacted on the pelvic bone. Another concern with shoulder dystocia is compression of the umbilical cord against the maternal pelvis with no flow of oxygenated blood to the fetus.

Differential Diagnosis

  • Poor maternal pushing effort

  • Absence of maternal contraction

Immediate Management

  • Delivery must be expedited to prevent hypoxic brain injury.

  • Prepare for emergency cesarean delivery.

  • To assist with the vaginal delivery, the obstetrician will perform the McRoberts maneuver, in which the maternal legs are hyperflexed to the maternal abdomen. This increases the size of the maternal pelvis by flattening of the maternal lumbar lordosis and cephalad rotation of the symphysis. Another individual will apply suprapubic pressure to decrease the diameter of the shoulders. If attempts to deliver the neonate fail, the obstetrician may return the fetal head into the maternal pelvis and perform cesarean delivery (the Zavenelli maneuver). Both require maternal analgesia.

Diagnostic Studies

Clinical diagnosis is made by the obstetrician.

Subsequent Management

Following delivery, the infant should be evaluated by a neonatal resuscitation team. The mother should be informed of the event with the medical record documenting the times and the maneuvers used.

Risk Factors

  • Fetal macrosomia

  • Abnormal maternal pelvic anatomy

  • Gestational diabetes

  • Postdates pregnancy

  • Maternal obesity

  • Prolonged second stage

  • Previous shoulder dystocia

Prevention

Assess fetal position during labor and delivery. The obstetrician will strongly consider elective cesarean delivery in patients at risk for shoulder dystocia. Simulation training improves the management of shoulder dystocia by improving the functioning of a multidisciplinary team.

Special Considerations

  • Shoulder dystocia complicates an estimated 0.6%–1.4% of all vaginal deliveries and requires an immediate and coordinated response. The anesthesia provider must be prepared to provide analgesia if an epidural catheter is present and to provide anesthesia if urgent cesarean delivery is required.

  • Potential maternal complications include:

    • Hemorrhage

    • 4° vaginal laceration with the potential for the development of a rectovaginal fistula

    • Pubic symphyseal separation

    • Uterine rupture

  • Potential neonatal complications include:

    • Hypoxic encephalopathy

    • Brachial plexus injury

Further Reading

Grobman W. Shoulder dystocia. Obstet Gynecol Clin North Am. 2013; 40: 59–67.Find this resource:

Ouzounian JC, Korst LM, Miller DA, Lee RH. Brachial plexus palsy and shoulder dystocia: obstetric risk factors remain elusive. Am J Perinatol. 2013; 30: 303–307.Find this resource:

Total/High Spinal Anesthesia

Definition

Extensive spread of local anesthetic within the subarachnoid space that is caused by excessive volume of local anesthetic injected into the epidural space in a patient with a previous accidental dural puncture, intrathecal injection of local anesthetic following the administration of large volumes of epidural local anesthetic, or injection of a large amount of local anesthetic into the subarachnoid space.

Presentation

  • The patient may be conscious but have difficulty speaking or breathing, or the patient may become unconscious.

  • The patient will be unable to move her upper extremities.

  • Bradycardia is common from blockade of cardiac accelerator fibers (level higher than T1).

  • Hypotension caused by extensive sympathetic blockade

  • Respiratory distress caused by motor blockade of muscles of respiration.

  • Patients with a total spinal anesthetic may have fixed and dilated pupils.

Pathophysiology

Total or high spinal anesthesia is caused by unintentional injection of large amounts of local anesthetic into the subarachnoid space. It may also occur when spinal anesthesia is performed after the administration of large volumes of local anesthetic is administered epidurally, as when an epidural catheter fails to produce adequate anesthesia for cesarean delivery, necessitating a spinal anesthetic. The previously administered epidural local anesthetic compresses the intrathecal space in the lumbar area, causing greater cephalad spread from the intrathecal injection. Another cause of total or high spinal anesthesia is administration of epidural local anesthetic following an accidental dural puncture with an epidural needle. A hyperbaric local anesthetic solution can migrate cephalad if the patient is placed in Trendelenburg position, or a hypobaric solution may rise if the patient is placed into a head-up position.

Differential Diagnosis

  • Myocardial infarction

  • Local Anesthetic toxicity

  • Vasovagal

  • Hemorrhage

  • Intracerebral bleed

Immediate Management

  • Recognize that the patient has a total or high spinal anesthetic.

  • Increase FiO2 to maintain oxygenation.

  • Provide positive pressure ventilation if the patient is in respiratory distress. She may be hand ventilated with a bag/mask or be intubated and ventilated. Although the patient may not be responsive, she is awake. A general anesthetic should be started with caution because the patient will also be hypotensive.

  • Administer vasopressors (ephedrine or epinephrine) to treat the hypotension. Bradycardia may occur if the level of the block extends beyond T1, which may decrease the effectiveness of phenylephrine.

  • Administer additional intravenous fluid.

Diagnostic Studies

No diagnostic studies are indicated for the diagnosis of total/high spinal. If the patient does not respond within the expected time frame following the intrathecal injection, a computed tomography is indicated.

Subsequent Management

  • Hypotension resulting from sympathetic blockade may require continuous infusion of a vasopressor such as phenylephrine or epinephrine.

  • A low concentration of a potent volatile anesthetic or other sedative should be used to provide amnesia if the patient is intubated.

  • If fetal bradycardia occurs, urgent cesarean delivery should be performed.

  • Reverse Trendelenburg position is not recommended to prevent further rostral spread, as it will only worsen venous pooling and further decrease venous return to the heart.

  • Using mask ventilation until the patient is able to protect the airway is not recommended because it may increase the risk of aspiration and make it difficult to perform other tasks.

Risk Factors

  • Short stature

  • Spinal anesthesia following failed epidural anesthesia

  • Epidural anesthesia following accidental dural puncture

Prevention

  • Maintain vigilance while performing neuraxial blocks.

  • Reduce the dose of intrathecal local anesthetic in short patients.

  • Reduce the dose of local anesthesia in patients with failed epidural anesthesia.

  • Always administer a test dose of local anesthetic through the epidural catheter.

  • Fractionate the dose of epidural local anesthetic, always soliciting the patient for symptoms of intrathecal injection.

Special Considerations

  • Cardiac arrest may occur in patients with high/total spinal anesthesia, with the most common preceding sign being bradycardia.

Further Reading

Carvalho B, Collins J, Drover DR, et al. ED(50) and ED(95) of intrathecal bupivacaine in morbidly obese patients undergoing cesarean delivery. Anesthesiology. 2011; 114: 529–535.Find this resource:

Visser WA, Dijkstra A, Albayrak M, et al. Spinal anesthesia for intrapartum Cesarean delivery following epidural labor analgesia: a retrospective cohort study. Can J Anaesthesiol. 2009; 56: 577–583.Find this resource:

Umbilical Cord Prolapse

Definition

The umbilical cord descends in advance of the fetal presenting part during labor, protruding into or through the cervix, becoming compressed between the fetal presenting part and the pelvis. This decreases fetal blood flow.

Presentation

Umbilical cord prolapse typically presents with persistent fetal bradycardia or severe variable decelerations in the setting of ruptured membranes. This fetal heart pattern is due to compression of the umbilical cord against the maternal pelvis with decreased oxygen delivery to the fetus.

Pathophysiology

Umbilical cord prolapse occurs when the amniotic membranes are ruptured prior to engagement of the fetus into the pelvis. Two mechanisms have been postulated. The first step is rupture of the amniotic membranes prior to engagement of the fetal presenting part in the maternal pelvis.

  • The umbilical cord becomes limp after repeated compression and therefore more easily prolapses.

  • Fetal acidosis increases the stiffness of the umbilical cord, which then leads to decreased adaptability and predisposes to cord prolapsed.

Differential Diagnosis

  • Fetal bradycardia

  • Placental abruption

  • Maternal hypotension

  • Oligohydramnios

Immediate Management

  • Ask the obstetrician to elevate the presenting part of the fetus, moving it away from the umbilical cord.

  • Assess fetal heart rate (ask the obstetrician to palpate the umbilical cord pulsations) to determine whether an emergency cesarean section is necessary.

  • Prepare for emergency cesarean delivery. If the patient does not have an epidural catheter in place, consider general anesthesia using rapid sequence induction.

Diagnostic Studies

Consider umbilical cord prolapse in with the setting of fetal bradycardia and ruptured membranes. The diagnosis is confirmed by the obstetrician.

Subsequent Management

If the obstetrician is able to return the umbilical cord back into the uterus and the fetal heart rate improves, it may be possible to perform spinal anesthesia. If an epidural catheter is in place, a local anesthetic with rapid onset of blockade should be used. If no epidural catheter is in place and the fetal heart rate is nonreassuring, general anesthesia may be indicated. The neonate is at high risk for apnea and bradycardia and should be resuscitated by individuals skilled in neonatal resuscitation.

Risk Factors

  • Fetal malpresentation

  • Preterm delivery

  • Low birth weight

  • Contracted pelvis

  • Multiparity

  • Amnioinfusion

  • Polyhdramnios

  • Twin gestation

  • Amniotomy

Prevention

  • A careful vaginal examination should be performed prior to rupture of the membranes to insure that the fetus is engaged in the pelvis.

  • If the fetus develops bradycardia after membrane rupture, an immediate vaginal examination should be performed rule out prolapse.

Special Considerations

  • The incidence of umbilical cord prolapse varies between 0.14% and 0.62% of deliveries and has a high perinatal mortality (approximately 50% due to out of hospital occurrence). If umbilical cord prolapsed occurs in a hospital and a monitored setting, the incidence of perinatal mortality is low (0%–3%). Although spinal anesthesia may be possible, it is technically difficult to position the patient with the obstetrician’s hand in the patient’s vagina.

Further Reading

Holbrook BD, Phelan ST. Umbilical cord prolapsed. Obstet Gynecol Clin North Am. 2013; 40: 1–14.Find this resource:

Kamoshita E, Amano K, Kanai, et al. Effect of the interval between onset of sustained fetal bradycardia and cesarean delivery on long-term neonatal neurologic prognosis. Int J Gynaecol Obstet. 2010; 111: 23–27.Find this resource:

Uterine Rupture

Definition

Uterine rupture is the complete separation of all layers of the uterine wall, resulting in free communication between the uterine and abdominal cavities. Uterine dehiscence is an incomplete disruption of the uterine wall, usually within the serosa overlying the defect in the uterine muscle. A dehiscence is also known as a uterine window.

Presentation

  • Abdominal pain

    • If an epidural catheter is in place and being used for labor analgesia, the patient may experience breakthrough pain because the concentrations of local anesthetic currently used for the management of labor analgesia are inadequate to cover the pain of uterine rupture.

  • Vaginal bleeding

  • Loss of fetal station

  • Abnormal FHR (usually bradycardia)

Pathophysiology

Uterine rupture is exceptionally rare in women who have not undergone previous uterine surgery, and is thought to be due to uterine anomalies or connective tissue disease. Uterine rupture occurs most commonly when a scar on the uterus begins to separate. After uterine surgery, the risk of rupture depends upon the type of uterine scar. A low transverse scar carries a risk of approximately 1%. The risk associated with a low vertical scar increases to 2%, and further increases to 4%–9% with an inverted T-shaped or classic incision. Uterine rupture may occur following myomectomy. Although rupture generally occurs during labor with uterine contractions, it may also occur before the onset of labor.

Differential Diagnosis

  • Placental abruption

  • Placenta prvia

  • Fetal bradycardia

  • Uterine tetany

Diagnostic Studies

There are no diagnostic studies. Suspect uterine rupture in any patient with previous uterine surgery and whose fetus has a Category III fetal heart rate. It also part of the differential in a patient with previous uterine surgery who has breakthrough pain despite an epidural infusion of a low concentration local anesthetic mixture. Ultrasound may be helpful, but is not sensitive for uterine rupture.

Immediate Management

  • Prepare for expeditious cesarean delivery.

  • Establish large bore intravenous access. There is a high risk of significant hemorrhage.

  • Send a maternal blood specimen for type and cross-match.

  • Consider the use of a fluid warmer and rapid infusion system.

  • Epidural anesthesia may be used, but if the hemorrhage is significant, consider general anesthesia.

Subsequent Management

Uterine rupture is not necessarily an indication for hysterectomy if the uterus can be repaired. If a uterine repair is planned, anticipate a prolonged procedure and the patient must deliver via elective cesarean delivery. If gravid hysterectomy is performed, close attention to adequate fluid and blood resuscitation is mandatory.

Risk Factors

  • Prior uterine surgery (risk increases in direct correlation with number of surgeries)

  • Type of scar (classic incision has the highest risk)

  • Pregnancy within 2 years of previous cesarean delivery

  • Induction of labor in patients with previous cesarean delivery

Prevention

A patient who is considering vaginal delivery after cesarean delivery (TOLAC: trial of labor after cesarean) should not undergo induction of labor with prostaglandins. Prolonged use of oxytocin is associated with uterine rupture. Due to the risk of uterine rupture in patients with a previous cesarean delivery, an anesthesiologist and an obstetrician must be available during any attempted TOLAC in case uterine rupture occurs. This requirement has decreased the number of hospitals that are able to offer TOLAC.

Special Considerations

  • Uterine rupture typically occurs in patients who have had previous uterine surgery, although it may rarely occur in a patient who never had previous uterine surgery. Despite the low incidence of uterine rupture during attempted vaginal birth after cesarean delivery, the number of women who attempt vaginal delivery has decreased. A factor in this decrease is the decrease in the number of hospitals where trial of labor after cesarean section is offered. The ability to have an immediately available obstetrician and anesthesiologist limits the ability to offer TOLAC.

Further Reading

Barger MK, Nannini A, DeJoy S, Wisner K, Markenson G. Maternal and newborn outcomes following uterine rupture among women without versus those with a prior cesarean. J Mat Fet Neonat Med. 2013; 26: 183–187.Find this resource:

Charach R, Sheiner E. Risk Factors for peripartum hysterectomy following uterine rupture. J Mat-Fetal Neonat Med. 2013; 26: 1196–1200.Find this resource:

Guise JM, Denman MA, Emeis C, et al. Vaginal birth after cesarean: new insights on maternal and neonatal outcomes. Obstet Gynecol. 2010; 115: 1267–1278.Find this resource: