List of Abbreviations
LD – labor dystocia
ULD – uncoordinated labor dystocia
UID – uterine inertia dystocia
EA – epidural anesthesia
Terms and Definitions
Labor dystocia (LD) – pathological slowing, arrest, or excessively rapid cervical dilation (opening of the uterine os) and/or fetal descent due to impaired uterine contractile function during labor (myometrial tone, strength, duration, and rhythmicity of contractions/pushing efforts).
Uterine inertia (UI) is a form of labor abnormality characterized by insufficient intensity, duration, frequency, and periodicity of uterine contractions, while the processes of effacement, cervical dilation, and descent of the presenting part proceed at a slowed pace. Uterine inertia is the most common labor anomaly.
"Precipitate labor", "rapid labor" or "very rapid labor" are not strictly differentiated from each other, and minor differences in the periods of their duration are of little significance. The definitions of precipitate and rapid labor are used as synonyms; labor lasts 2–3 hours. In English-language literature, it refers to labor with a total duration of generally less than 3–4 hours.
Uterine dyscoordination (UD) is a type of labor abnormality in which coordinated contractions between the upper and lower segments or among all segments of the uterus are disrupted.
1. Brief information on the disease or condition
1.1 Definition of the disease or condition
Labor abnormality (LA) is a pathological slowing, arrest, or excessively rapid dilation of the cervix (uterine os) and/or descent of the fetus due to a disorder of the uterine contractile function during labor (myometrial tone, strength, duration, and rhythm of contractions/pushing efforts).
In foreign literature, the phrase "labor dystocia" is used to describe LA, along with terms such as: inefficient uterine contractions, failure to progress, protracted or arrested labor, prolonged labor, dysfunctional labor, inadequate expulsive effort-ineffective pushing, protracted or arrested descent.
In domestic literature, a specific variant of uterine contractile dysfunction was distinguished: the pathological preliminary period (PPP). This term referred to the activation of unbalanced uterine contractile activity against the background of increased myometrial excitability and tone at term pregnancy [1]. At the same time, contractions are painful, remain irregular for a long time (more than 24 hours), are not accompanied by adequate structural changes in the cervix and descent of the fetal presenting part into the pelvis, and disrupt the psychoemotional state of the pregnant woman. However, in the International Classification of Diseases, the pathological preliminary period is not classified as an independent type of uterine contractility pathology. Such activation of uterine contractile activity at term pregnancy is considered a variant of "false labor" or a prolonged latent phase of labor [2].
Uterine inertia (UI) is a form of labor abnormality characterized by insufficient intensity, duration, frequency, and periodicity of uterine contractions, while the processes of effacement, cervical dilation, and descent of the presenting part proceed at a slowed pace. Uterine inertia is the most common labor anomaly.
Delaying maternal pushing/laboring down (primary or secondary) is characterized by insufficient pushing efforts due to weakness of the abdominal wall muscles or fatigue [3].
"Precipitate labor", "rapid labor" or "very rapid labor" (uterine hyperstimulation, hypercontractility, and excessive uterine activity) are not strictly differentiated from each other, and minor differences in the periods of their duration are of little significance. The concepts of precipitate and rapid labor are used as synonyms; labor lasts 2–3 hours. In English-language literature (precipitate descent, precipitous labor, or short labor), it refers to labor with a total duration of less than 3–4 hours [4][5][6].
Uterine dyscoordination (UD) (Asymmetrical Uterine Contraction/Incoordinate uterine action/Uncoordinated Uterine Action/Colicky uterus/Hyperactive lower uterine segment/Constriction ring) is an abnormal labor activity in which coordinated contractions between the upper and lower segments or among all segments of the uterus are disrupted [7][8].
1.2 Etiology and pathogenesis of the disease or condition (group of diseases or conditions)
The causes of labor abnormalities are numerous; the main ones are:
excessive neuropsychic stress (anxiety, negative emotions, adverse trace reactions) [9][10];
endocrine and metabolic disorders in the pregnant woman's body [11];
pathological changes in the myometrium: endomyometritis, sclerotic and dystrophic changes, defective uterine scar, malformations, uterine hypoplasia [12];
uterine overdistension due to polyhydramnios, multiple pregnancy, macrosomia [13];
genetic (congenital) pathology of myocytes, in which the excitability of myometrial cells is absent or sharply reduced [14][15][16];
primigravida age of 30 years and older and young age (under 18 years) [17][18];
mechanical obstacles to cervical dilation and fetal descent [1];
iatrogenic factors: unjustified or excessive use of labor stimulants, tocolytics, spasmolytics, and analgesics [19][20].
In labor abnormalities, the conduction system of the uterus, built on gap junctions with intercellular channels, becomes disorganized. Impairment of the conduction system and displacement of the center of formation and generation of electrical impulses (the contraction "pacemaker") leads to uncoordinated, asynchronous labor activity, where individual myometrial zones contract and relax at different rhythms and at different time intervals, which is accompanied by sharp pain during contractions and a lack of labor progress.
An important link in the pathogenesis of uterine inertia is hypocalcemia. Calcium ions play a major role in signal transmission from the plasma membrane to the contractile apparatus of smooth muscle cells. Muscle contraction requires the influx of calcium ions from extracellular or intracellular stores. The metabolism of cyclic AMP (cAMP) in muscles is closely linked to calcium ion exchange. In uterine inertia, there is a decrease in cAMP, suppression of the tricarboxylic acid cycle, and an increase in the content of lactate and pyruvate in myocytes. A decrease in the formation of $\alpha$-adrenergic receptors, weakening of the function of the myometrial adrenergic mechanism, and a decrease in the estrogen balance play a role in the pathogenesis of uterine inertia. A reduction in the "density" of specific $\alpha$- and $\beta$-adrenergic receptors makes the myometrium insensitive to uterotonic agents. Impaired blood flow in the myometrium, which is combined with hypotonic and/or hypertonic uterine dysfunction, sometimes leads to such profound metabolic disorders that the synthesis of $\alpha$- and $\beta$-adrenergic receptors may be disrupted [21]. Persistent uterine inertia resistant to labor stimulation develops [22].
1.3 Epidemiology of the Disease or Condition
The frequency of LA ranges from 5.8 to 37%, depending on the definition used [23][24][25][26][27].
According to the Russian Ministry of Health (main indicators of maternal and child health, activities of the child and obstetrical care service in the Russian Federation for 2021), the frequency of labor abnormalities in the Russian Federation is 7.6%. The proportion of uterine inertia is 67.9%, uterine dyscoordination is 16.2%, and precipitate labor is 15.9% [28].
Labor abnormalities account for 25–55% of primary cesarean deliveries [3].
An increase in the duration of labor during dilation from 4 to 6 cm by more than 10 hours (which constitutes the 90th percentile) is associated with an increased rate of cesarean section, OR 2.05 (95% CI 1.67–2.52), obstetric and neonatal complications, OR 1.48 (95% CI 1.10–2.00) and OR 1.92 (95% CI 1.52–2.4) [29][30].
An increase in the duration of the second stage of labor by each subsequent hour is associated with an increased risk of obstetric anal sphincter injury, RR 1.21 (95% CI 1.16–1.25), episiotomy, RR 1.48 (95% CI 1.45–1.52), postpartum hemorrhage, RR 1.27 (95% CI 1.25–1.30) [31], instrumental delivery, RR 3.93 (95% CI 3.62–4.25), and emergency cesarean section, RR 9.08 (95% CI 8.00–10.29) [32].
An increase in the duration of the second (expulsive) stage of labor from 15 to 60 minutes increases the incidence of neonatal acidosis from 0.57 to 1.69%, RR 2.55 (95% CI 1.51–4.30) [33].
1.4 Features of Coding the Disease or Condition
O62.0 Primary uterine inertia
O62.1 Secondary uterine inertia
O62.2 Other uterine inertia
O62.3 Precipitate labor
O62.4 Hypertonic, uncoordinated, and prolonged uterine contractions:
O62.8 Other abnormalities of forces of labor
O62.9 Abnormality of forces of labor, unspecified
O63 Long labor
O63.0 Prolonged first stage (of labor)
O63.1 Prolonged second stage (of labor)
O63.9 Long labor, unspecified
1.5 Classification of the disease or condition
Classification of the disease or condition (group of diseases or conditions) [34][35].
primary uterine inertia;
secondary uterine inertia;
excessively strong labor activity (uterine hyperactivity);
uterine dyscoordination (hypertonic uterine dysfunction), uterine tetanus.
1.6 Clinical presentation of the disease or condition
Primary uterine inertia – this anomaly occurs from the very beginning of labor and persists throughout the dilation stage and until the end of labor. As labor progresses, the strength, duration, and frequency of contractions do not increase or increase only slightly. Contractions are regular, painless or mildly painful because myometrial tone is reduced. Contractions may be of satisfactory strength but very infrequent, or conversely, frequent but weak and short. Infrequent contractions of satisfactory strength are more favorable for the outcome of labor. Prolonged staging of the fetal head in the pelvic inlet plane is noted. The amniotic sac is flaccid, filling poorly during contractions. In its absence, the descent of the fetal head through the birth canal is slowed. Upon repeat vaginal examination, there is no progression of cervical dilation; the edges of the cervix are unresponsive and stretch poorly under the force of contractions.
Secondary uterine inertia – secondary uterine inertia often becomes a continuation of primary inertia, but most commonly develops in the active phase of labor or in the second stage of labor. Contractions at the beginning of labor are sufficiently strong, prolonged, and frequent, but become weaker and shorter, and the pauses between contractions become longer; sometimes contractions cease altogether. Dilation of the uterine os slows down or stops. The descent of the fetal presenting part through the birth canal also slows or stops. Particular attention should be paid to "expulsive weakness" («слабость потуг»), a condition in which the weakening of labor activity in the second stage of labor results from weakness of the anterior abdominal wall muscles or general exhaustion of the parturient woman.
Hypertonic uterine activity (precipitate labor) – is observed in rapid/precipitate labor. Labor begins suddenly, strong contractions follow one another at short intervals, leading to cervical effacement and expulsion of the fetus within 1–3 hours. In the second stage of labor, the fetus is born within 1–2 pushes, sometimes along with the placenta.
Uncoordinated uterine activity – this labor anomaly includes contraction disordination, lower segment hypertonus (reverse triple gradient), convulsive contractions (uterine tetanus), and circulatory cervical dystocia. The coordination and synchronicity of uterine contractions are disrupted. In this case, either the pacemaker may shift from the uterine cornu to the lower segment of the uterus, or multiple pacemakers may form, emitting impulses in different directions, thereby disrupting the synchronicity of contraction and relaxation in separate areas of the uterus. Basal myometrial tone becomes inadequately high, leading to a decrease in the effectiveness of contractions. Despite sufficiently strong uterine contractions, cervical os dilation does not occur. As a result, labor activity becomes ineffective.
2. Diagnostics, medical indications and contraindications for diagnostic methods
The diagnosis of labor anomalies is established based on:
Complaints;
Physical examination;
Evaluation of the partogram during labor.
2.1 Complaints and Anamnesis
In uterine inertia, there are generally no complaints; rarely, the parturient woman may note fatigue [36]. In excessively strong and uncoordinated labor activity, the parturient woman typically complains of excessive, incessant pain.
2.2 Physical Examination
The diagnosis of uterine inertia is established based on the characteristic clinical picture (assessment of the main parameters of uterine contractile activity, slowed rate of uterine os dilation, absence of forward movement of the fetal presenting part). Contractions do not increase (2 or fewer per 10 minutes), and their frequency, strength, and duration do not significantly increase (less than 20 seconds) [37]. Proper dilation of the uterine os does not occur. An important role in establishing the diagnosis is played by the lack of proper progression in cervical dilation, the transition from the latent phase to the active phase of labor, low effectiveness of labor activity, and excessively slow descent of the fetus through the birth canal.
The diagnosis of primary uterine inertia (First Stage Prolongation, Protraction, and Arrest) should be suspected in situations where:
the latent phase of labor is:
in nulliparous women, more than 20 hours;
in multiparous women, more than 14 hours.
the active phase of labor is:
in nulliparous women, more than 8.6 hours;
in multiparous women, more than 7.5 hours.
Active phase labor arrest (after cervical os dilation reaches 5–6 cm) is a clinical situation characterized by the absence of cervical os dilation progression in the presence of ruptured membranes or following amniotomy for 4 hours of adequate contractions [38][3].
Secondary uterine inertia in the first stage of labor is characterized by a clinical situation where cervical os dilation corresponded to normal labor progression, but slowed down after 6–7 cm and no longer progressed. Secondary uterine inertia in the second stage of labor is a clinical situation where, despite the absence of signs of fetopelvic disproportion, the presenting part does not advance through the birth canal, halting in one of the planes of the pelvic cavity for >1 hour in both nulliparous and multiparous women [39].
The diagnosis of uterine inertia in the second stage of labor should be suspected in situations where:
in nulliparous women, the duration of the second stage of labor is more than 3 hours without epidural anesthesia (EA), or 4 hours with EA;
in multiparous women, the duration is more than 2 hours without EA, or 3 hours with EA [40][41][38].
Diagnosis of excessively strong labor activity does not present difficulties. It is based on an objective assessment of the nature of contractions (more than 5 contractions per 10 minutes and/or contraction duration of more than 60 seconds), excessively rapid progression of cervical os dilation and fetal descent through the birth canal [42][43][8]. Sometimes the woman has practically no clinical manifestations of contractions and pushing efforts, nor any painful sensations. An important factor contributing to the short duration of such labor is the lack of resistance from the internal cervical os, which is most often observed in multiparous women and in cervical insufficiency.
The diagnosis of uncoordinated labor activity is established based on the evaluation of the character of labor activity and its effectiveness. Uncoordinated labor activity has various clinical and pathogenetic variants. The following forms are distinguished:
contraction disordination;
cervical dystocia (hypertonus of the lower uterine segment), "rigid cervix";
convulsive contractions (uterine tetanus);
contraction ring.
In uncoordinated labor activity, uterine tone, including that of the lower segment and the internal os, is elevated. The rhythm of contractions is irregular; the periods of uterine contraction and relaxation (systole and diastole of a contraction) are sometimes prolonged, sometimes short. Amplitude (contraction strength) and intrauterine pressure are uneven; contractions are marked by inadequate pain. The parturient woman's behavior is restless. Upon vaginal examination, the cervix is determined to be dense, thick, rigid, edematous, and unevenly dense. Premature pushing efforts frequently occur as a consequence of the cervix being trapped between the fetal head and the pelvic bones. As a result, early caput succedaneum formation occurs on the fetal head, and intracranial hemorrhages or spinal cord injuries may develop [1]. Uncoordinated labor activity disrupts uteroplacental blood flow, which can lead to fetal hypoxia [22].
Partogram
The partogram allows for an objective assessment of labor progression. Labor anomalies of the inertia or uncoordinated type in the active phase are indicated by a labor duration of >6 hours at 5 cm dilation, ≥5 hours at 6 cm, ≥3 hours at 7 cm, ≥2.5 hours at 8 cm, ≥2 hours at 9 cm [37].
In the second stage of labor, a labor anomaly is indicated by the absence of labor progression when all grid cells are filled, which indicates a total dilation duration of more than 3 hours.
2.3 Laboratory Diagnostics
The list of laboratory diagnostic examinations prior to labor must comply with the clinical guidelines "Normal Pregnancy". If examinations required in the 3rd trimester of pregnancy have not been performed, they are carried out upon the patient's admission to the inpatient facility.
2.4 Instrumental Diagnostics
Not applicable.
2.5 Other Procedures
Not applicable.
3. Treatment, including drug and non-drug therapies, diet therapy, and pain management
3.1. Pharmacotherapy
It is recommended, before initiating treatment for a diagnosis of uterine inertia, to take into account that the latent phase of labor is significantly longer in induced labor compared to spontaneous labor, whereas the active phase of labor is similar in both groups [38].
LeveL of Recommendation AGrade of Evidence 2LeveL of Recommendation A (Grade of Evidence - 2).
Comments: the median duration of cervical dilation from 4 cm to full dilation in induced labor among nulliparous women is 5.5 hours versus 3.8 hours in spontaneous labor. In multiparous women, it is 4.4 versus 2.4 hours. At the same time, the rate of cervical dilation after reaching 6 cm does not differ between spontaneous and induced labor [44].
Amniotomy is recommended for the purpose of reducing the duration of labor in women undergoing labor induction and augmentation [38].
LeveL of Recommendation BGrade of Evidence 2LeveL of Recommendation B (Grade of Evidence - 2).
Comments: early amniotomy shortens the time to delivery by more than 2 hours (19.0 versus 21.3 hours) and increases the proportion of induced patients who deliver within 24 hours (68% versus 56%), without significant differences in the rates of cesarean section, chorioamnionitis, placental abruption, and postpartum hemorrhage [45].
It is recommended that in women with uterine inertia following amniotomy, the issue of early labor augmentation with #oxytocin** should be addressed [46] (For the adult population).
GCP CLEL 5Level of Evidence C (Level of Likelihood of Evidence - 5).
Comments: compared to delayed administration (after 2 hours), early initiation of labor augmentation with #oxytocin** after amniotomy in nulliparous women helps reduce the time to delivery by 72 minutes (5.8±1.7 h vs 7.0±1.9 h), reduces the duration of #oxytocin** use to 5.6±4.4 ml/h vs 6.8±5.3 ml/h, and promotes vaginal delivery within 4 hours, without increasing the rate of cesarean section, hyperstimulation, postpartum hemorrhage, or worsening neonatal outcomes [47].
It is recommended, in cases of uterine inertia, to initiate labor augmentation with #oxytocin** [38].
LeveL of Recommendation BGrade of Evidence 2LeveL of Recommendation B (Grade of Evidence - 2).
Comments: for every 20 patients who received labor augmentation with #oxytocin**, one vaginal delivery is expected. At the same time, it reduces the duration of labor (median 1.28 hours; 95% CI 1.97–0.59) and the use of antibiotics during labor (RR 0.45; 95% CI 0.21–0.99), but increases the risk of uterine hyperstimulation without worsening neonatal outcomes (RR 2.90; 95% CI 1.21–6.94) [48].
It is recommended during labor augmentation to prefer low doses of #oxytocin** over high doses [49][50]. (For the adult population)
LeveL of Recommendation BGrade of Evidence 2LeveL of Recommendation B (Grade of Evidence - 2).
Comments: the use of high doses of #oxytocin** is an effective method that reduces the duration of labor by 23.4 minutes, but contributes to an increased rate of tachysystole (43.2% vs 33.5%) and an increased rate of operative vaginal delivery due to fetal hypoxia (43.8% vs 22.7%) [51].
It is recommended during labor augmentation with #oxytocin** to titrate the infusion rate according to the contraction pattern [52].
GCR BLEL 3Recommendation Grade B (Level of Evidence — 3).
Comments: #Oxytocin** should be administered IV by drip infusion in a dilution of 1.0 ml (5 IU) in 400 ml of 0.9% sodium chloride solution**, starting at 6 drops/min (3 mIU/min), or using an infusion pump in a dilution of 1.0 ml (5 IU) of #oxytocin** in 50.0 ml of 0.9% sodium chloride solution**, starting at a rate of 1.8 ml/h (3 mIU/min). Increase the #oxytocin** infusion rate every 20–30 minutes by 1 "step" until 4–5 contractions per 10 minutes are achieved under maternal and fetal monitoring, then maintain this minimum effective dose. A dose of 33 mIU/min (19.8 ml/h) is a critically dangerous level [1][53].
It is recommended in cases of uterine tachysystole to determine the fetal heart rate pattern, if conditions permit, using continuous CTG monitoring [54][55].
GCR CLOE 4Grade of Recommendation C (Level of Evidence - 4).
Comments: uterine tachysystole occurs in more than 10% of spontaneous vaginal deliveries [56] and is associated with the risk of fetal hypoxia due to impaired placental blood flow and placental abruption, which is accompanied by an increased number of cesarean sections, low Apgar scores, and NICU admissions [57][58].
It is recommended in cases of uterine tachysystole arising from the use of a dinoprostone** insert [59] or #oxytocin** labor augmentation [60], to remove the insert, reduce the dose of #oxytocin** or discontinue its administration until tachysystole resolves, and if no effect is achieved, consider tocolysis. (For the adult population)
GCP CLEL 5Level of Evidence C (Level of Likelihood of Evidence - 5).
Comments: if uterine contractions return to normal ranges after conservative measures, cautious resumption of #oxytocin** labor augmentation may be considered with continuous monitoring of uterine activity and fetal heart rate [61][62].
In uncomplicated uterine tachysystole without fetal compromise, tocolysis is generally not required, but may be considered if there is a risk that ongoing tachysystole may lead to fetal distress. The following medications are used to stop tachysystole:
Administer 1–2 doses of #Nitroglycerin** (0.4 mg–0.8 mg) as a sublingual spray (#Nitroglycerin** 1% alcohol solution in 96% ethanol) [63][64][65].
#Hexoprenaline** bolus administration of 10 mcg (1 ampoule of 2 ml) of the drug diluted in 10 ml of isotonic sodium chloride solution**, over 5 minutes, followed by an infusion at a rate of 0.3 mcg/min [66][67]. Intravenous tocolysis is performed with the woman in the left lateral position, preferably under cardiotocographic monitoring. Recommended monitoring: maternal heart rate and blood pressure every 15 minutes, lung auscultation, and monitoring of fetal condition and uterine contractility [62].
A 2018 Cochrane review was unable to assess the effect of tocolytics in uterine tachysystole and/or suspected fetal distress during labor [42].
It is recommended to use analgesia for the treatment of uterine dyscoordination [1][68].
GCP CLEL 5Level of Evidence C (Level of Likelihood of Evidence - 5).
Comments: Neuroaxial analgesia is optimal for pain relief. There is also evidence supporting the effective use of #Trimeperidine** for pain relief without worsening obstetric and neonatal outcomes [68][69].
3.2. Surgical treatment
It is recommended in the active phase of labor (cervical dilation of 5–6 cm or more) to perform delivery by cesarean section if, in the absence of amniotic fluid, there is no progress in cervical dilation for more than 4 hours of adequate contractions (in strength, duration, and frequency) or 6 hours of labor augmentation due to insufficiently adequate contractions [70].
GCR BLEL 3Recommendation Grade B (Level of Evidence — 3).
It is recommended in secondary uterine inertia to evaluate the feasibility of operative vaginal delivery before performing a cesarean section [38].
LeveL of Recommendation BGrade of Evidence 2LeveL of Recommendation B (Grade of Evidence - 2).
Comments: less than 3% of patients in whom operative vaginal delivery was attempted are delivered by cesarean section [71].
It is recommended if there is no response to treatment for uterine dyscoordination within 4–6 hours, to resolve the issue of operative delivery via cesarean section [38].
LeveL of Recommendation BGrade of Evidence 2LeveL of Recommendation B (Grade of Evidence - 2).
3.3. Other treatment
Not applicable.
4. Medical Rehabilitation and Sanatorium-Resort Treatment
Not applicable.
5. Prevention and Dispensary Observation
Not applicable.
6. Organization of Medical Care
Medical care can be provided in obstetric medical organizations of the 1st, 2nd, and 3rd levels.
7. Additional Information
Not applicable.
Criteria for Evaluating the Quality of Medical Care
№ | Quality criteria | Grade of Recommendation | Level of evidence |
|---|---|---|---|
1. | Amniotomy was performed prior to initiating labor augmentation with #oxytocin**. | C | 2 |
2. | The first therapeutic step for uterine tachysystole during dinoprostone** or #oxytocin** administration was the removal of the dinoprostone** insert or reduction of the dose/cessation of #oxytocin** labor augmentation. | C | 2 |
3. | In the absence of contraindications, analgesia was used to treat the parturient woman with uterine dyscoordination. | C | 2 |
References
Show references
Sidorova I.S., Ishchenko A.I., N.A.N. Obstetrics and Gynecology. Textbook in 4 books. Book 2. Pathological Obstetrics. Moscow; 2019.
Cooper. D.A.R.D.B. Braxton Hicks Contractions. StatPearls Publ. 2024; .
LeFevre N.M., Krumm E., Cobb W.J. Labor Dystocia in Nulliparous Women. Am Fam Physician. 2021; 103(2):90–6. .
Cohen W.R., Friedman E.A. The second stage of labor. Am J Obstet Gynecol. 2024; 230(3):S865–75. https://dx.doi.org/10.1016/j.ajog.2022.06.014.
Suzuki S. Clinical Significance of Precipitous Labor. J Clin Med Res. 2015; 7(3):150–3. https://dx.doi.org/10.14740/jocmr2058w.
Vanessa A Barss M. Precipitous birth not occurring on a labor and delivery unit. 2024 p. https://www.uptodate.com/contents/precipitous-birt .
Karaçam Z., Walsh D., Bugg G.J. Evolving understanding and treatment of labour dystocia. Eur J Obstet Gynecol Reprod Biol. 2014; 182:123–7. https://dx.doi.org/10.1016/j.ejogrb.2014.09.011.
Gee S.E., Frey H.A. Contractions: Traditional concepts and their role in modern obstetrics. Semin Perinatol. 2020; 44(2):151218. https://dx.doi.org/10.1016/j.semperi.2019.151218.
Dencker A., Nilsson C., Begley C., Jangsten E., Mollberg M., Patel H., et al. Causes and outcomes in studies of fear of childbirth: A systematic review. Women and Birth. 2019; 32(2):99–111. https://dx.doi.org/10.1016/j.wombi.2018.07.004.
Kissler K., Jones J., McFarland A.K., Luchsinger J. A qualitative meta-synthesis of women’s experiences of labor dystocia. Women and Birth. 2020; 33(4):e332–8. https://dx.doi.org/10.1016/j.wombi.2019.08.001.
Wray S. Insights from physiology into myometrial function and dysfunction. Exp Physiol. 2015; 100(12):1468–76. https://dx.doi.org/10.1113/EP085131.
Zackler A., Flood P., Dajao R., Maramara L., Goetzl L. Suspected Chorioamnionitis and Myometrial Contractility: Mechanisms for Increased Risk of Cesarean Delivery and Postpartum Hemorrhage. Reprod Sci. 2019; 26(2):178–83. https://dx.doi.org/10.1177/1933719118778819.
Pasquini L., Ponziani I., Pallottini M., Masini G., Seravalli V., Dani C., et al. Obstetric and Neonatal Outcomes in Mild Idiopathic Polyhydramnios. Children. 2022; 9(11):1624. https://dx.doi.org/10.3390/children9111624.
Algovik M., Nilsson E., Cnattingius S., Lichtenstein P., Nordenskjöld A., Westgren M. Genetic influence on dystocia. Acta Obstet Gynecol Scand. 2004; 83(9):832–7. https://dx.doi.org/10.1111/j.0001-6349.2004.00544.x.
Gao Y., Liu G., Kong P., Song Y., Zhang D., Yin Y., et al. Smooth muscle 22α deficiency impairs oxytocin-induced uterine contractility in mice at full-term pregnancy. Biochem Biophys Res Commun. 2020; 529(4):884–9. https://dx.doi.org/10.1016/j.bbrc.2020.05.220.
Kan N.E., Donnikov A.E., Tyutyunnik V.L., Kesova M.I., D.T.A. Molecular and genetic predictors of uterine inertia. Obstetrics and Gynecology. 2014; 8:27–32.
Jochumsen S., Hegaard H.K., Rode L., Jørgensen K.J., Nathan N.O. Maternal factors associated with labor dystocia in low-risk nulliparous women. A systematic review and meta-analysis. Sex Reprod Healthc. 2023; 36:100855. https://dx.doi.org/10.1016/j.srhc.2023.100855.
Waldenström U., Ekéus C. Risk of labor dystocia increases with maternal age irrespective of parity: a population-based register study. Acta Obstet Gynecol Scand. 2017; 96(9):1063–9. https://dx.doi.org/10.1111/aogs.13167.
Kissler K., Hurt K.J. The Pathophysiology of Labor Dystocia: Theme with Variations. Reprod Sci. 2023; 30(3):729–42. https://dx.doi.org/10.1007/s43032-022-01018-6.
Baev O.R., Kozlova O.A., Rubtsova S.V., Rumyantseva V.P., P.A.V. Effect of epidural analgesia on the duration of labor, incidence of uterine inertia, and cesarean section. Obstetrics and Gynecology. 2016; 6:41–6.
Arrowsmith S., Kendrick A., Wray S. Drugs acting on the pregnant uterus. Obstet Gynaecol Reprod Med. 2010; 20(8):241–7. https://dx.doi.org/10.1016/j.ogrm.2010.05.001.
Obstetrics: National Guidelines / ed. by G. M. Savelieva, G. T. Sukhikh, V. N. Serov, V. E. Radzinsky. - 2nd ed., revised and enlarged. Moscow: GEOTAR-Media; 2018. 1088 p.
Gifford D. Lack of progress in labor as a reason for cesarean. Obstet Gynecol. 2000; 95(4):589–95. https://dx.doi.org/10.1016/S0029-7844(99)00575-X.
KJÆRGAARD H., OLSEN J., OTTESEN B., DYKES A. Incidence and outcomes of dystocia in the active phase of labor in term nulliparous women with spontaneous labor onset. Acta Obstet Gynecol Scand. 2009; 88(4):402–7. https://dx.doi.org/10.1080/00016340902811001.
Kyozuka H., Hiraiwa T., Murata T., Sugeno M., Jin T., Ito F., et al. Gestational weight gain as a risk factor for dystocia during first delivery: a multicenter retrospective cohort study in Japan. BMC Pregnancy Childbirth. 2022; 22(1):728. https://dx.doi.org/10.1186/s12884-022-05055-6.
Maaløe N., Kujabi M.L., Nathan N.O., Skovdal M., Dmello B.S., Wray S., et al. Inconsistent definitions of labour progress and over-medicalisation cause unnecessary harm during birth. BMJ. 2023; :e076515. https://dx.doi.org/10.1136/bmj-2023-076515.
Nystedt A., Hildingsson I. Diverse definitions of prolonged labour and its consequences with sometimes subsequent inappropriate treatment. BMC Pregnancy Childbirth. 2014; 14(1):233. https://dx.doi.org/10.1186/1471-2393-14-233.
Moscow, 2021, FSBI "TsNIIOIZ" of the Russian Ministry of Health, 171 pages. Main indicators of maternal and child health, activity of the child and maternity welfare services in the Russian Federation. 2022.
Rosenbloom J.I., Woolfolk C.L., Wan L., Stout M.J., Tuuli M.G., Macones G.A., et al. The transition from latent to active labor and adverse obstetrical outcomes. Am J Obstet Gynecol. 2019; 221(5):487.e1-487.e8. https://dx.doi.org/10.1016/j.ajog.2019.05.041.
Wang L., Wang H., Jia L., Qing W., Li F., Zhou J. The impact of stage of labor on adverse maternal and neonatal outcomes in multiparous women: a retrospective cohort study. BMC Pregnancy Childbirth. 2020; 20(1):596. https://dx.doi.org/10.1186/s12884-020-03286-z.
Young C., Bhattacharya S., Woolner A., Ingram A., Smith N., Raja E.-A., et al. Maternal and perinatal outcomes of prolonged second stage of labour: a historical cohort study of over 51,000 women. BMC Pregnancy Childbirth. 2023; 23(1):467. https://dx.doi.org/10.1186/s12884-023-05733-z.
Matta P., Turner J., Flatley C., Kumar S. Prolonged second stage of labour increases maternal morbidity but not neonatal morbidity. Aust New Zeal J Obstet Gynaecol. 2019; 59(4):555–60. https://dx.doi.org/10.1111/ajo.12935.
Sandström A., Altman M., Cnattingius S., Johansson S., Ahlberg M., Stephansson O. Durations of second stage of labor and pushing, and adverse neonatal outcomes: a population-based cohort study. J Perinatol. 2017; 37(3):236–42. https://dx.doi.org/10.1038/jp.2016.214.
Neal J.L., Ryan S.L., Lowe N.K., Schorn M.N., Buxton M., Holley S.L., et al. Labor Dystocia: Uses of Related Nomenclature. J Midwifery Womens Health. 2015; 60(5):485–98. https://dx.doi.org/10.1111/jmwh.12355.
Evan R. Myers, M.D., M.P.H., Gillian D. Sanders, Ph.D., Remy R. Coeytaux, M.D., Ph.D., Kara A. McElligott, M.D., M.P.H., Patricia G. Moorman, Ph.D., M.S.P.H., Karen Hicklin, Ph.D., Chad Grotegut, M.D., M.H.Sc., Margaret Villers, M.D., Adam Goode, D.P.T, P P.D. Labor Dystocia. 2020.
Hook. P.G.J.M.H.K.C.J.W. Van. Abnormal Labor. StatPearls Publ 2024 Jan-. 2024; Jan-.:https://www.ncbi.nlm.nih.gov/books/NBK459260/. .
Organization W.H. WHO Labour Care Guide. User’s Manual. 2020; .
First and Second Stage Labor Management. Obstet Gynecol. 2024; 143(1):144–62. https://dx.doi.org/10.1097/AOG.0000000000005447.
F. Gary Cunningham, Kenneth J. Leveno, Steven L. Bloom, Jodi S. Dashe B.L.H. Williams Obstetrics, 25th Edition. 2015.
Gill P., Henning J.M., Carlson K., Van Hook J.W. Abnormal Labor. StatPearls. 2024.
Nicholas M. LeFevre, MD; Ellisa Krumm, MD; and William Jacob Cobb M. Labor Dystocia in Nulliparous Patients. Am Fam Physician. 2021; 103.
Leathersich S.J., Vogel J.P., Tran T.S., Hofmeyr G.J. Acute tocolysis for uterine tachysystole or suspected fetal distress. Cochrane Database Syst Rev. 2018; 2018(7)https://dx.doi.org/10.1002/14651858.CD009770.pub2.
National Institute for Health and Clinical Excellence. Intrapartum care for healthy women and their babies. NICE Clinical Guideline CG 190. :https://www.nice.org.uk/cg190/history/. .
Harper L.M., Caughey A.B., Odibo A.O., Roehl K.A., Zhao Q., Cahill A.G. Normal Progress of Induced Labor. Obstet Gynecol. 2012; 119(6):1113–8. https://dx.doi.org/10.1097/AOG.0b013e318253d7aa.
Macones G.A., Cahill A., Stamilio D.M., Odibo A.O. The efficacy of early amniotomy in nulliparous labor induction: a randomized controlled trial. Am J Obstet Gynecol. 2012; 207(5):403.e1-403.e5. https://dx.doi.org/10.1016/j.ajog.2012.08.032.
Wei S., Wo B.L., Qi H.-P., Xu H., Luo Z.-C., Roy C., et al. Early amniotomy and early oxytocin for prevention of, or therapy for, delay in first stage spontaneous labour compared with routine care. Cochrane Database Syst Rev. 2013; https://dx.doi.org/10.1002/14651858.CD006794.pub4.
Upawi S.N., Ahmad M.F., Abu M.A., Ahmad S. Amniotomy and early oxytocin infusion vs amniotomy and delayed oxytocin infusion for labour augmentation amongst nulliparous women at term: A randomised controlled trial. Midwifery. 2022; 105:103238. https://dx.doi.org/10.1016/j.midw.2021.103238.
Wei S.-Q., Luo Z.-C., Xu H., Fraser W.D. The Effect of Early Oxytocin Augmentation in Labor. Obstet Gynecol. 2009; 114(3):641–9. https://dx.doi.org/10.1097/AOG.0b013e3181b11cb8.
Xenakis E.M.-J., Langer O., Piper J.M., Conway D., Berkus M.D. Low-dose versus high-dose oxytocin augmentation of labor — A randomized trial. Am J Obstet Gynecol. 1995; 173(6):1874–8. https://dx.doi.org/10.1016/0002-9378(95)90444-1.
Moraes F.C.A. de, Kelly F.A., Leite M.G.H.S.J., Dal Moro L., Morbach V., Burbano R.M.R. High-Dose versus Low-Dose Oxytocin for Labor Augmentation: A Meta-Analysis of Randomized Controlled Trials. J Pers Med. 2024; 14(7):724. https://dx.doi.org/10.3390/jpm14070724.
Selin L., Wennerholm U.-B., Jonsson M., Dencker A., Wallin G., Wiberg-Itzel E., et al. High-dose versus low-dose of oxytocin for labour augmentation: a randomised controlled trial. Women and Birth. 2019; 32(4):356–63. https://dx.doi.org/10.1016/j.wombi.2018.09.002.
Daly D., Minnie K.C.S., Blignaut A., Blix E., Vika Nilsen A.B., Dencker A., et al. How much synthetic oxytocin is infused during labour? A review and analysis of regimens used in 12 countries. Mastrolia SA, editor. PLoS One. 2020; 15(7):e0227941. https://dx.doi.org/10.1371/journal.pone.0227941.
Clinical Guidelines. "Failed induction of labor (cervical ripening and labor induction)." 2021. p. (https://roag-portal.ru/recommendations_obstetrics)
Boie S., Glavind J., Velu A. V, Mol B.W.J., Uldbjerg N., de Graaf I., et al. Discontinuation of intravenous oxytocin in the active phase of induced labour. Cochrane Database Syst Rev. 2018; 2018(8)https://dx.doi.org/10.1002/14651858.CD012274.pub2.
Chandraharan E. Uterine Tachysystole, Hypertonus and Hyperstimulation: An Urgent Need to get the Definitions Right to Avoid Intrapartum Hypoxic-Ischemic Brain Injury. Glob J Reprod Med. 2021; 8(2)https://dx.doi.org/10.19080/GJORM.2021.08.555735.
Ahmed A.I., Zhu L., Aldhaheri S., Sakr S., Minkoff H., Haberman S. Uterine tachysystole in spontaneous labor at term. J Matern Neonatal Med. 2016; 29(20):3335–9. https://dx.doi.org/10.3109/14767058.2015.1125463.
Hobson S.R., Abdelmalek M.Z., Farine D. Update on uterine tachysystole. J Perinat Med. 2019; 47(2):152–60. https://dx.doi.org/10.1515/jpm-2018-0175.
Ayres-de-Campos D., Spong C.Y., Chandraharan E., FIGO Intrapartum Fetal Monitoring Expert Consensus Panel. FIGO consensus guidelines on intrapartum fetal monitoring: Cardiotocography. Int J Gynaecol Obstet. 2015; 131(1):13–24. https://dx.doi.org/10.1016/j.ijgo.2015.06.020.
Shirley M. Dinoprostone Vaginal Insert: A Review in Cervical Ripening. Drugs. 2018; 78(15):1615–24. https://dx.doi.org/10.1007/s40265-018-0995-2.
Chandraharan E., Ghi T., Fieni S., Jia Y.-J. Optimizing the management of acute, prolonged decelerations and fetal bradycardia based on the understanding of fetal pathophysiology. Am J Obstet Gynecol. 2023; 228(6):645–56. https://dx.doi.org/10.1016/j.ajog.2022.05.014.
Cheung K., Bonet M., Frank K., Oladapo O., Hofmeyr G. Clinical algorithms for management of fetal heart rate abnormalities during labour. BJOG An Int J Obstet Gynaecol. 2024; 131(S2):102–11. https://dx.doi.org/10.1111/1471-0528.16731.
Gülümser C., Yassa M. Clinical management of uterine contraction abnormalities; an evidence‐based intrapartum care algorithm. BJOG An Int J Obstet Gynaecol. 2024; 131(S2):49–57. https://dx.doi.org/10.1111/1471-0528.16727.
Caponas G. Glyceryl Trinitrate and Acute Uterine Relaxation: A Literature Review. Anaesth Intensive Care. 2001; 29(2):163–77. https://dx.doi.org/10.1177/0310057X0102900211.
Takakura S., Tanaka H., Enomoto N., Maki S., Ikeda T. The Successful Use of Nitroglycerin for Uterine Hyperstimulation with Fetal Heart Rate Abnormality Caused by a Controlled-Release Dinoprostone Vaginal Delivery System (PROPESS): A Case Report. Medicina (B Aires). 2021; 57(5):478. https://dx.doi.org/10.3390/medicina57050478.
OOO "Russian Society of Obstetricians and Gynecologists" RSOG. Clinical Guidelines. Fetal breech presentation. 2024.
Gummerus M. Tokolyse mit Hexoprenalin und Salbutamol im klinischen Vergleich*. Geburtshilfe Frauenheilkd. 1983; 43(03):151–5. https://dx.doi.org/10.1055/s-2008-1037077.
Woytoń J., Zimmer M., Fuchs T. [The use of Gynipral (hexoprenaline) in suppression of uterus contractions]. Ginekol Pol. 1999; 70(12):896–900. .
Zarubina E.N., Baklanov S.Yu., Zykova A.S., Semenova A.L., Teplyakova A.N., Ya.E.V. Normalization of dyscoordinated labor activity. Kremlin Medicine Clinical Bulletin. 2018; 4:107–9.
Yasaei R., Rosani A., Saadabadi A. Meperidine. StatPearls. 2024.
Obstetric Care Consensus No. 1. Obstet Gynecol. 2014; 123(3):693–711. https://dx.doi.org/10.1097/01.AOG.0000444441.04111.1d.
Verma G.L., Spalding J.J., Wilkinson M.D., Hofmeyr G.J., Vannevel V., O’Mahony F. Instruments for assisted vaginal birth. Cochrane Database Syst Rev. 2021; 2021(9)https://dx.doi.org/10.1002/14651858.CD005455.pub3.
Appendix A1. Working Group Composition
Oleg R. Baev – MD, Professor, Honored Physician of the Russian Federation, Head of the 1st Maternity Department at the National Medical Research Center for Obstetrics, Gynecology and Perinatology named after Academician V.I. Kulakov of the Russian Ministry of Health, Professor at the Department of Obstetrics, Gynecology, Perinatology and Reproductology of the Institute of Professional Education at the Sechenov First Moscow State Medical University of the Ministry of Health of Russia (Sechenov University) (Moscow). There is no conflict of interest.
Oleg V. Tysyachny – PhD, Researcher at the 1st Maternity Department of the National Medical Research Center for Obstetrics, Gynecology and Perinatology named after Academician V.I. Kulakov of the Russian Ministry of Health (Moscow). There is no conflict of interest.
Natalya V. Artymuk – D.Sc. (Medicine), Professor, Head of the Professor G.A. Ushakov Department of Obstetrics and Gynecology, Kemerovo State Medical University of the Russian Ministry of Health, Chief Freelancer Specialist in Obstetrics and Gynecology of the Russian Ministry of Health in the Siberian Federal District (Kemerovo). No conflict of interest.
Nadezhda V. Bashmakova – MD, Professor, Chief Researcher at the Ural Research Institute of Maternal and Infant Care of the Russian Ministry of Health, Chief Freelance Specialist in Obstetrics and Gynecology of the Russian Ministry of Health in the Ural Federal District (Yekaterinburg). There is no conflict of interest.
Tatyana E. Belokrinitskaya – D.Sc. (Medicine), Professor, Head of the Department of Obstetrics and Gynecology, Faculty of Advanced Training and Professional Retraining, Chita State Medical Academy of the Russian Ministry of Health, Honored Doctor of the Russian Federation, Chief Freelancer Specialist in Obstetrics and Gynecology of the Russian Ministry of Health in the Far Eastern Federal District (Chita). No conflict of interest.
Natalia V. Dolgushina – MD, PhD, Professor, Deputy Director for Research, National Medical Research Center for Obstetrics, Gynecology and Perinatology named after Academician V.I. Kulakov of the Russian Ministry of Health (Moscow). No conflict of interest.
Irina E. Zazerskaya – MD, PhD, Head of the Department of Obstetrics and Gynecology, Almazov National Medical Research Centre of the Russian Ministry of Health (Saint Petersburg). No conflict of interest.
Natalia E. Kan – MD, PhD, Professor, Deputy Director, National Medical Research Center for Obstetrics, Gynecology and Perinatology named after Academician V.I. Kulakov of the Russian Ministry of Health (Moscow). No conflict of interest.
Igor N. Kostin – MD, PhD, Professor, Professor of the Department of Obstetrics and Gynecology with a Course of Perinatology, Medical Institute of the Peoples' Friendship University of Russia (Moscow). No conflict of interest.
Lidia S. Logutova – MD, PhD, Professor, Leading Researcher at the Department of Research Coordination and Publishing, Moscow Regional Research Institute of Obstetrics and Gynecology (Moscow). No conflict of interest.
Anna I. Malyshkina – MD, PhD, Professor, Director of the Ivanovo Research Institute of Motherhood and Childhood named after V.N. Gorodkov of the Russian Ministry of Health, Chief freelance specialist in obstetrics of the Russian Ministry of Health, Chief freelance specialist in gynecology of the Russian Ministry of Health, Chief freelance specialist in women's reproductive health in the Central Federal District (Ivanovo). No conflict of interest.
Sergey V. Martirosyan – PhD, Expert at the National Institute of Quality of Roszdravnadzor, Obstetrician-gynecologist, Associate Professor at the Department of Obstetrics and Gynecology, Faculty of Fundamental Medicine, Lomonosov Moscow State University (Moscow). No conflict of interest.
Anton V. Mikhailov – MD, PhD, Chief Physician of Maternity Hospital No. 17 of Saint Petersburg, Chief Obstetrician-Gynecologist of the Healthcare Committee of the Government of Saint Petersburg, Professor at the Departments of Obstetrics and Gynecology of the Mechnikov North-Western State Medical University and Obstetrics, Gynecology and Perinatology of the Pavlov First Saint Petersburg State Medical University (Saint Petersburg). No conflict of interest.
Stanislav V. Pavlovich – PhD, Associate Professor, Scientific Secretary, National Medical Research Center for Obstetrics, Gynecology and Perinatology named after Academician V.I. Kulakov of the Russian Ministry of Health (Moscow). No conflict of interest.
Oleg G. Pekarev – MD, PhD, Professor, Deputy Director of the Institute of Obstetrics, National Medical Research Center for Obstetrics, Gynecology and Perinatology named after Academician V.I. Kulakov of the Russian Ministry of Health (Moscow). No conflict of interest.
Vasily A. Petrukhin – MD, PhD, Professor, Honored Doctor of the Russian Federation, Honored Worker of Science and Technology of the Moscow Region (Moscow). No conflict of interest.
Viktor E. Radzinsky – Corresponding Member of the Russian Academy of Sciences, MD, PhD, Professor, Head of the Department of Obstetrics and Gynecology with a Course of Perinatology, Peoples' Friendship University of Russia, Honored Scientist of the RF (Moscow). No conflict of interest.
Vladimir N. Serov – Academician of the RAS, MD, PhD, Professor, Honored Scientist of the RF, President of the Russian Society of Obstetricians and Gynecologists, Chief Researcher at the National Medical Research Center for Obstetrics, Gynecology and Perinatology named after Academician V.I. Kulakov of the Russian Ministry of Health (Moscow). No conflict of interest.
Iraida S. Sidorova – MD, PhD, Professor, Academician of the Russian Academy of Sciences, Honored Scientist of the RF, Honored Doctor of the RF, Professor of the Department of Obstetrics and Gynecology No. 1, Faculty of General Medicine, I.M. Sechenov First Moscow State Medical University of the Ministry of Health of the Russian Federation (Sechenov University, Moscow). No conflict of interest.
Viktor L. Tyutyunnik – Professor, MD, PhD, Leading Researcher of the Center for Scientific and Clinical Research, National Medical Research Center for Obstetrics, Gynecology and Perinatology named after Academician V.I. Kulakov of the Russian Ministry of Health (Moscow). No conflict of interest.
Roman G. Shmakov – MD, PhD, Professor of the RAS, Director of the Moscow Regional Research Institute of Obstetrics and Gynecology named after Academician V.I. Krasnopolsky (Moscow). No conflict of interest.
Ildar F. Fatkullin – D.Sc. (Medicine), Professor, Head of the Prof. V.S. Gruздеv Department of Obstetrics and Gynecology, Kazan State Medical University, Chief freelance specialist of the Russian Ministry of Health in obstetrics and gynecology in the Volga Federal District (Kazan). No conflict of interest.
Larisa Fatkullina – Ph.D. in Medicine, Associate Professor at the Prof. V.S. Gruzdhev Department of Obstetrics and Gynecology, Kazan State Medical University, Head of the Obstetric and Gynecological Clinic, Republican Clinical Hospital of the Ministry of Health of the Republic of Tatarstan, Perinatal Center, Republican Clinical Hospital of the Ministry of Health of the Republic of Tatarstan (Kazan). No conflict of interest.
Appendix A2. Methodology for Developing Clinical Guidelines
Target audience for these clinical guidelines:
Obstetricians-gynecologists
Midwives
Table 1. Level of Evidence (LoE) grading scale for diagnostic methods (diagnostic interventions)
LoE | Definition |
|---|---|
1 | Systematic reviews of studies with reference standard control or systematic reviews of randomized controlled trials with meta-analysis |
2 | Individual studies with reference standard control or individual randomized controlled trials and systematic reviews of studies of any design, except randomized controlled trials, with meta-analysis |
3 | Studies without consecutive reference standard control or studies with a reference standard not independent of the test method, or non-randomized comparative studies, including cohort studies |
4 | Non-comparative studies, case report |
5 | Only justification of mechanism of action or expert opinion is available |
Table 2. Scale for assessing levels of reliable evidence (LRE) for prevention, treatment, and rehabilitation methods (preventive, therapeutic, rehabilitation interventions)
LoE | Definitions |
|---|---|
1 | Systematic review of RCTs with meta-analysis |
2 | Individual RCTs and systematic reviews of studies of any design except RCTs, with meta-analysis |
3 | Non-randomized comparative studies, including cohort studies |
4 | Non-comparative studies, case reports or case series, case-control studies |
5 | Only justification of the mechanism of action of the intervention (preclinical studies) or expert opinion is available |
Table 3. Grade of Recommendation (GoR) scale for prevention, diagnostic, treatment, and rehabilitation methods (preventive, diagnostic, therapeutic, and rehabilitative interventions)
GoR | Definition |
|---|---|
A | Strong recommendation (all considered efficacy criteria (outcomes) are important, all studies are of high or acceptable methodological quality, and their conclusions on the outcomes of interest are consistent) |
B | Conditional recommendation (not all considered efficacy criteria (outcomes) are important, not all studies are of high or acceptable methodological quality, and/or their conclusions on the outcomes of interest are inconsistent) |
C | Weak recommendation (lack of adequate quality evidence (all considered efficacy criteria (outcomes) are unimportant, all studies are of low methodological quality, and their conclusions on the outcomes of interest are inconsistent) |
Appendix B. Physician Action Algorithms
Appendix C. Patient Information
What are labor abnormalities?
Labor abnormalities refer to disorders in the intensity, coordination, strength, rhythm, and duration of uterine contractile activity during childbirth. Labor abnormalities are a common pathological condition, observed in 20% of delivering women, and account for every third cesarean section. Due to the serious threat to the health of the mother and the fetus, labor abnormalities are considered one of the most important problems in modern obstetrics. Potential complications include fetal hypoxia, birth injuries, infections, massive hemorrhage, and fetal demise.
What are the main causes of labor abnormalities?
There are numerous predisposing factors for labor abnormalities, all of which can be classified into those that arose before or during pregnancy, as well as during childbirth.
How does labor progress in labor abnormalities?
Due to insufficient intensity, duration, and frequency of contractions, the cervix dilates slowly, which hinders the normal descent of the fetus.
What consequences can occur for the mother and child when labor abnormalities are diagnosed?
If measures aimed at correcting labor abnormalities are not taken, there is a high probability of injuries to the child or the mother. Sometimes there is a need for a cesarean section, the use of obstetric forceps, or vacuum extraction of the fetus. With timely initiated and effective therapeutic measures, the prognosis is favorable for both the mother and the child.
Can my partner be present during delivery?
The presence of a partner during delivery is encouraged, provided they have prepared to assist and are present at the birth.
Will pain relief be provided during labor?
Initially, it is recommended to use non-pharmacological methods of pain relief in labor, such as proper breathing techniques, the use of a birth ball, massage, warm compresses, cold applied to the back in case of lower back pain, and others, which prove effective in most cases. If non-pharmacological methods are ineffective, at your request, in the absence of contraindications, and if available at the medical facility, epidural analgesia can be performed. It should be noted that epidural analgesia is associated with an increased risk of prolonged labor duration.
How are labor abnormalities treated?
The prescription of medications is strictly individual and depends on the condition of the mother and fetus, the presence of obstetric or other pathology, and the type of labor abnormality.
Appendix G. Assessment Scales, Questionnaires, and Other Evaluation Tools
No