Uterine contractions serve as the primary driving force throughout the entire process of labor, characterized by rhythmicity, symmetry, polarity, and the involvement of contraction and retraction mechanisms. Any disruption in the rhythmicity, symmetry, or polarity of uterine contractions, as well as abnormalities in the intensity or frequency of contractions, is referred to as abnormal uterine action, or labor force abnormalities.
Clinically, uterine contraction abnormalities are categorized primarily into two types: uterine inertia (weak uterine contractions) and uterine hypercontraction (excessive uterine contractions). Each type can be further divided into coordinated uterine contraction abnormalities and uncoordinated uterine contraction abnormalities.
Uterine Inertia (Weak Uterine Contractions)
Etiology
Various factors impacting the function of uterine contractions contribute to uterine inertia:
Myogenic Causes
Factors that compromise the normal contractile ability of uterine muscle fibers can lead to uterine inertia. These include overstretching of uterine muscle fibers (as seen in polyhydramnios, macrosomia, or multiple pregnancies), uterine anomalies, uterine fibroids, adenomyosis, multiparity, and advanced maternal age.
Cephalopelvic Disproportion or Fetal Malposition
Obstructions to fetal descent can prevent the presenting part from closely pressing against the lower uterine segment and internal cervical os, thereby hindering uterine stimulations necessary for strong contractions.
Endocrine Imbalance
Imbalances in endocrine factors, such as decreased synthesis or release of acetylcholine, oxytocin, or prostaglandins in women with abnormal fetal engagement, or a reduced number of oxytocin receptors and decreased sensitivity of the uterus to oxytocic agents, can contribute to uterine inertia. Inadequate synthesis and secretion of dehydroepiandrosterone sulfate (DHEA-S) by the fetus and placenta can also impair cervical ripening, directly or indirectly leading to uterine inertia.
Psychological Factors
Psychological disturbances, including fear and tension associated with labor, can disrupt cortical functions in the brain, leading to primary uterine inertia. Prolonged waiting, fatigue, sleep deprivation, excessive physical exertion, an overfilled bladder, and electrolyte or fluid imbalances can also result in uterine inertia.
Other Factors
The early or excessive use of uterine relaxants, antispasmodics, sedatives, or analgesics during labor can directly inhibit uterine contractions.
Clinical Features and Diagnosis
Coordinated Uterine Inertia
Also known as hypotonic uterine inertia, this type is characterized by normal rhythmicity, symmetry, and polarity of uterine contractions but reduced contraction strength. The pressure generated is typically below 180 Montevideo units, with fewer than 2 contractions every 10 minutes, shorter durations of contractions, and longer intervals between contractions. During the contraction peak, the uterus does not feel firm and exhibits depressibility upon palpation.
- Primary Uterine Inertia: This type of uterine inertia occurs early in labor.
- Secondary Uterine Inertia: Normal uterine contractions during early labor weaken later, typically during the late active phase of the first stage or the second stage of labor, resulting in prolonged or arrested labor. This is often associated with fetal malposition or pelvic abnormalities. Coordinated uterine inertia is commonly secondary and does not significantly affect the fetus.
Uncoordinated Uterine Inertia
Also known as hypertonic uterine inertia, this type is characterized by a loss of normal rhythmicity, symmetry, and especially polarity of uterine contractions. Excitation points in the uterus originate from one or multiple locations in the lower uterine segment, causing uncoordinated, high-frequency contraction waves that travel upward rather than downward, thereby failing to generate an effective downward force.
The fundal contractions become weaker than those in the lower uterine segment, and the uterus does not properly relax during intervals between contractions. This limits cervical dilation and prevents timely descent of the presenting part, leading to ineffective contractions.
Maternal symptoms include persistent abdominal pain, abdominal tenderness on palpation, restlessness, and irritability. Severe cases may present with fluid and electrolyte imbalances, urinary retention, intestinal bloating, fetal-placental circulatory disturbances, and elevated intrauterine resting pressures. Fetal heart rate abnormalities may also occur.
Unlike coordinated uterine inertia, uncoordinated uterine inertia is often primary in nature.
Impact on Labor Progress, Maternal Health, and Fetal Well-Being
Impact on Labor Progress
Uterine inertia slows or halts labor progression. Primary uterine inertia causes prolonged latent phases, while secondary uterine inertia leads to prolonged or arrested labor depending on its timing, affecting the first or second stage of labor.
Impact on Maternal Health
Prolonged labor results in inadequate rest for the mother, along with excessive physical and emotional fatigue. Symptoms such as mental exhaustion, weakness, difficulty in urination, and intestinal bloating may occur due to moaning, hyperventilation, reduced food intake, and dehydration. Severe cases can result in maternal dehydration, hypokalemia, or acidosis, which can further weaken uterine contractions and increase the likelihood of operative deliveries. Prolonged second-stage labor may lead to postpartum urinary retention caused by prolonged pressure on the birth canal. Long-term ischemia of compressed tissues can result in edema, necrosis, soft birth canal injuries, or even genital fistulas. Additionally, postpartum hemorrhage and puerperal infections may occur.
Impact on the Fetus
In cases of uncoordinated uterine inertia, the uterine wall cannot completely relax during the intervals between contractions, which significantly affects uteroplacental circulation and can lead to fetal distress. Prolonged labor increases the length of time the fetal head and umbilical cord are compressed, raising the risk of operative deliveries. This, in turn, can lead to neonatal complications such as birth asphyxia, birth trauma, intracranial hemorrhage, or aspiration pneumonia.
Management
Management of Coordinated Uterine Inertia
The primary step in management involves identifying the underlying cause. Clinical vaginal examination is performed to assess cervical dilation and fetal descent, with attention to detecting cephalopelvic disproportion or fetal malposition. If vaginal delivery is deemed unlikely, cesarean section is advised. If there is no cephalopelvic disproportion, fetal malposition, or signs of fetal distress, and vaginal delivery appears feasible, uterine contractions may be strengthened.
First Stage of Labor
General Measures
Addressing psychological fears and tension related to childbirth, ensuring rest, maintaining hydration and nutritional intake, and facilitating bowel and bladder emptying are primary goals. Intravenous supplementation of fluids or nutrition and catheterization may be implemented as needed. In cases of uterine inertia during the latent phase, strong sedatives such as 100 mg of pethidine or 10 mg of morphine administered intramuscularly can often help patients transition naturally to the active phase following sufficient rest.
Augmentation of Contractions
Artificial Rupture of Membranes is applicable when cervical dilation exceeds 3-5 cm, cephalopelvic disproportion is excluded, fetal engagement is present, and labor is delayed. Rupture of membranes allows the fetal head to press directly against the lower uterine segment and internal cervical os, reflexively stimulating uterine contractions and accelerating labor progress. Prior to rupture, fetal heart monitoring is required to exclude cord prolapse. Membrane rupture is typically performed during the intervals between contractions, with close observation of amniotic fluid characteristics, quantities, and fetal heart changes afterward. If contractions remain insufficient post-rupture, oxytocin infusion can be considered.
Oxytocin Infusion is appropriate for cases of coordinated uterine inertia with normal fetal heart rates, fetal position, and proportions between the fetal head and pelvis. The dosage begins with 1-2 mU/min, adjusted at intervals of 15-30 minutes by increments of 1-2 mU/min. The maximum dose typically does not exceed 20 mU/min. The goal is to achieve contractions with an intrauterine pressure of 50-60 mmHg, a frequency of 2-3 contractions every 2-3 minutes, and durations of 40-60 seconds. Insufficient responses can warrant cautious dose increases. Monitoring includes uterine contractions, fetal heart rates, blood pressure, and labor progress either manually, via electronic fetal monitoring, or intrauterine pressure catheter assessments. Montevideo units (MU) are calculated by summing the pressures (mmHg) generated by uterine contractions over a 10-minute period. Effective contractions during the active phase typically reach 200-250 MU, while induction using oxytocin requires reaching 200-300 MU. If more than five contractions occur within 10 minutes, last more than one minute, or result in fetal heart abnormalities, oxytocin infusion should be discontinued immediately. As oxytocin has a short maternal half-life (1-6 minutes), its effects diminish quickly upon cessation.
Notable side effects of oxytocin include increased water absorption due to its antidiuretic effects, which may result in oliguria and, in severe cases, signs of water intoxication. It should not be used in cases of significant birth canal obstruction.
Second Stage of Labor
For uterine inertia without cephalopelvic disproportion, oxytocin infusion is used to enhance uterine contractions while guiding the patient to coordinate pushing efforts with contractions. If maternal and fetal conditions are favorable and the fetal head descends to a station of S+3 or lower, spontaneous vaginal delivery or assisted vaginal delivery may be possible. If no progress is observed, with the fetal head remaining at an S+2 station or higher, cesarean section is indicated.
Third Stage of Labor
After delivery of the fetal shoulders, 10-20 U of oxytocin may be administered intravenously to prevent postpartum hemorrhage. Prolonged labor, extended rupture of membranes, or operative deliveries warrant prophylactic administration of antibiotics to prevent infection.
Management of Uncoordinated Uterine Inertia
The principle of management involves restoring normal rhythmicity and polarity of uterine contractions. Intramuscular administration of 100 mg of pethidine or 10 mg of morphine can effectively address the condition, allowing most patients to recover coordinated uterine contractions after adequate rest. If contractions remain weak after coordination is restored, they are managed as coordinated uterine inertia. Uterotonics should not be used when uterine contractions are uncoordinated. For cases with fetal distress, cephalopelvic disproportion, or failure to restore coordinated contractions after sedative treatment, cesarean section is recommended.
Excessive Uterine Contractions
Clinical Presentation and Diagnosis
Coordinated Excessive Uterine Contractions
The rhythmicity, symmetry, and polarity of uterine contractions remain normal, but the contractions are excessively strong and frequent. When there is no resistance in the birth canal, labor tends to be accelerated, with the total duration of labor being less than 3 hours, a condition referred to as precipitate delivery. This is more commonly observed in multiparous women. However, in the presence of birth canal obstruction or a scarred uterus, excessively strong contractions may result in the formation of a pathological retraction ring and, in severe cases, uterine rupture.
Uncoordinated Excessive Uterine Contractions
Tetanic Contractions of the Uterus
These contractions lack rhythmicity and occur continuously without intervals, presenting as sustained tetanic contractions. Inappropriate use of uterotonics is a common cause. Patients typically experience continuous abdominal pain, restlessness, and abdominal tenderness. The fetal heart sounds may become inaudible, and fetal positioning is often difficult to ascertain. When combined with birth canal obstruction, signs of impending uterine rupture, such as a pathological retraction ring or hematuria, may occur.
Constriction Ring of the Uterus
This refers to a localized and sustained spasm of the uterine smooth muscle, leading to the formation of a circumferential constriction. Common causes include psychological tension, excessive fatigue, inappropriate use of uterotonics, or rough vaginal maneuvers. The constriction ring often occurs at the narrow part of the fetus or at the transition between the upper and lower uterine segments, such as around the fetal neck or waist, and does not ascend with contractions, distinguishing it from a pathological retraction ring. Symptoms include persistent abdominal pain, restlessness, intermittent fetal heart rate variability, slow cervical dilation, and stalled fetal descent. During manual placental extraction, the constriction ring may be directly palpated above the internal cervical os. In the third stage of labor, this can lead to placental incarceration.
Figure 1 Spastic constriction ring of the uterus
Impact on Labor Progress, Maternal Health, and Fetal Well-Being
Impact on Labor Progress and Maternal Health
Coordinated excessive uterine contractions may result in precipitate labor, increasing the risk of soft birth canal lacerations and even uterine rupture. Uncoordinated excessive uterine contractions, such as those forming a uterine constriction ring or presenting as tetanic contractions, can cause abnormal labor progress, placental incarceration, postpartum hemorrhage, puerperal infection, and a higher likelihood of operative deliveries.
Impact on the Fetus
Strong uterine contractions reduce uteroplacental blood flow, while uterine constriction rings can cause labor to stagnate and prolong, increasing the likelihood of fetal distress, neonatal asphyxia, or even fetal death. Rapid expulsion of the fetus during precipitate labor may result in an abrupt release of pressure within the birth canal, leading to neonatal intracranial hemorrhage. If delivery preparations are inadequate, the newborn is at a higher risk of infection, fractures, and birth trauma.
Management
Preventative Measures
Prevention is a priority, with careful observation and timely correction of abnormalities. A history of precipitate labor or a family history of the same should warrant early admission during the third trimester for delivery preparation. During labor, measures that enhance contractions, such as uterotonics, enemas, or artificial rupture of membranes, should be used cautiously. Preparations for delivery and neonatal resuscitation should be made in advance.
Management of Tetanic Uterine Contractions or Constriction Rings
When tetanic uterine contractions or uterine constriction rings occur, cessation of vaginal manipulations and discontinuation of uterotonics are crucial. Administration of oxygen and uterine relaxation agents such as terbutaline or magnesium sulfate may help alleviate symptoms, with pethidine being an option if necessary. If contractions normalize, the labor process can be allowed to progress naturally or assisted vaginal deliveries may be performed. In cases where contractions fail to resolve, a pathological retraction ring is present without full cervical dilation, the fetal head is high, or fetal distress is evident, cesarean delivery becomes necessary. For intrauterine fetal demise with full cervical dilation, uterine relaxation medications should be administered prior to vaginal assisted delivery, following principles that minimize maternal harm.