AJCN Tufts Nutrition Symposium, Boston Sept 24-26
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Purchase Article
Right arrow View Shopping Cart
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Konje, J. C
Right arrow Articles by Ladipo, O. A
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Konje, J. C
Right arrow Articles by Ladipo, O. A
Agricola
Right arrow Articles by Konje, J. C
Right arrow Articles by Ladipo, O. A
American Journal of Clinical Nutrition, Vol. 72, No. 1, 291S-297s, July 2000
© 2000 American Society for Clinical Nutrition

Articles

Nutrition and obstructed labor1,2,3

Justin C Konje and Oladapo A Ladipo

1 From the University Department of Obstetrics and Gynaecology, Leicester Royal Infirmary, Leicester, United Kingdom, and the Department of Obstetrics and Gynaecology, University of Wales College of Medicine, Heath Park, United Kingdom.

2 Presented at the meeting Iron and Maternal Mortality in the Developing World, held in Washington, DC, July 6–7, 1998.

3 Reprints not available. Address correspondence to JC Konje, University Department of Obstetrics and Gynaecology, Robert Kilpatrick Clinical Sciences Building, Leicester Royal Infirmary, Leicester LE2 7LX, United Kingdom. E-mail: justin.konje{at}gyn.obs.msmail.lri-tr.trent.nhs.uk.


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 ETIOLOGY
 CONSEQUENCES OF OBSTRUCTED LABOR
 PREVENTION
 CONCLUSIONS
 REFERENCES
 
Obstructed labor is one of the most common preventable causes of maternal and perinatal morbidity and mortality in developing countries. Among the common causes are cephalopelvic disproportion, malpresentation, and malposition. Recognizing the causes of obstructed labor is important if the complications are to be prevented. Adequate prevention, however, can be achieved only through a multidisciplinary approach aimed in the short term at identifying high-risk cases and in the long term at improving nutrition. Early motherhood should be discouraged, and efforts are needed to improve nutrition during infancy, childhood, early adulthood, and pregnancy. Improving the access to and promoting the use of reproductive and contraceptive services will help reduce the prevalence of this complication.

Key Words: Obstructed labor • cephalopelvic disproportion • supplementation • intergenerational effects


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
ETIOLOGY
 CONSEQUENCES OF OBSTRUCTED LABOR
 PREVENTION
 CONCLUSIONS
 REFERENCES
 
Nutrition is important in reproduction, including the safe delivery of infants. Philpott (1) and Moller and Lindmark (2) showed that failure to achieve a normal delivery was directly related to the height of the mother, which is influenced by nutritional status in childhood and adolescence. Flattening of the pelvis is generally associated with a height <152 cm (3). Other factors that can cause poor or distorted pelvic growth are rickets in infancy and childhood and osteomalacia in adolescence and adulthood (4). Early studies of the African pelvis showed that although the brim of the pelvis has a normal female shape, it is markedly smaller in all its diameters, and the resulting disproportion between the fetal head and the maternal pelvis (cephalopelvic disproportion) is a major indication for cesarean delivery due to obstructed labor (5).

Obstructed labor occurs when the passage of the fetus through the pelvis is mechanically obstructed. When it is not diagnosed quickly, or when it is improperly managed, obstructed labor is associated with significant complications. It is a major cause of maternal mortality, accounting for 1–5 deaths/1000 live births (6–9). In Bangladesh, for example, obstructed labor was found to be the third most common cause of maternal mortality in one study (10) and the most important cause of mortality in another (11). In addition to its effects on maternal mortality, obstructed labor can be a significant contributor to infant perinatal morbidity and mortality (6).

The prevalence of obstructed labor varies from one country to another, but it is more common in developing countries (12) because of the lack of adequate health care delivery facilities, poor nutrition, poverty (13), and socioeconomic and cultural factors that oppose orthodox antenatal care and delivery (14). In developing countries, the incidence of obstructed labor is difficult to estimate, primarily because of poor data collection procedures and secondarily because most of the reported studies are based on data from large, tertiary hospitals. Nevertheless, reported incidences vary from 1–2/100 deliveries in Nigeria (6, 15) to 3/100 deliveries in India (16). Estimates of these incidences are independent of cesarean delivery rates because most obstructed labors in developing countries were (4)—and are still—being treated by destructive operative deliveries (see below) rather than by cesarean delivery (JC Konje unpublished observation, 1998).

In cultures where child marriage is common and pregnancy occurs soon after menarche, obstructed labor can be common because young adolescent girls may not have achieved their maximal growth potential and thus start childbearing with an inadequate pelvis (17). Obstructed labor can also occur in subsequent pregnancies in which maternal nutrient deprivation may result in a distorted pelvis, or in women prone to pelvic fractures and other acquired pelvic deformities (4). Nutrient deficiencies such as calcium, vitamin D, folic acid, iron, and zinc deficiencies interact in combination with various biological and biosocial factors to determine the prevalence of obstructed labor (4). This article discusses the potential role of nutrition in the origins of obstructed labor and possible preventive nutritional measures.


   ETIOLOGY
TOP
 ABSTRACT
 INTRODUCTION
 ETIOLOGY
CONSEQUENCES OF OBSTRUCTED LABOR
 PREVENTION
 CONCLUSIONS
 REFERENCES
 
The most common cause of obstructed labor is disproportion between the fetus head and the mother's pelvis. Occasionally, however, obstruction is secondary to malpresentation, malposition, and fetal abnormalities, especially in women who deliver at home unattended, or with the help of an untrained midwife (6). The availability of ultrasound for detection of obstructed labor reduces the prevalence of malpresentation complications, but this is not often an option for most women in developing countries. Although there are many other causes of obstructed labor (18–23), their contribution is small compared with that secondary to disproportion, and they are nonnutritional in origin.

Short stature
Many studies that examined anthropometric measures as predictors of fetomaternal disproportion provided evidence that the shorter a woman is, the more likely is significant disproportion between the fetus and the maternal pelvis, which results in obstructed labor (24–31). Although maternal height can predict the risk of obstructed labor, it is also an index of a woman's general health and nutritional status from her childhood, in which genetic factors play a major role. Thus, the obstetric significance of a particular height needs to be related to the patient's own genetic background (2, 33). This is exemplified by the various cutoff points that have been identified in different studies as being associated with or predicting an increased risk of obstructed labor. For example, associations have been identified for heights <=150–153 cm in Ghana (27, 33), <155 cm in Burkina Faso (29), <156 cm in Denmark (34), <=150 cm in Kenya (35), <146 cm in Tanzania (36), and <140 cm in India (37); cesarean deliveries were predicted by a height <160 cm in Zimbabwe (38) and <=157 cm in the United States (39).

Calcium
Even after growth in height has stopped, there is a continuous need to lay down calcium in bone to maintain bone structure and, therefore, the shape of the pelvis. Calcium deficiency affects the bony pelvis. Severe deficiency causes rickets in children and causes osteomalacia in adults. Unlike rickets, which affects bones before the closure of the epiphyses, osteomalacia causes decalcification of fully formed bones. Osteomalacia is seldom seen in first pregnancies unless rickets in childhood has been followed by persistent vitamin D deficiency in puberty (4). Osteomalcia can develop after several pregnancies and worsens without treatment (4). Osteomalacia in women is more common in rural and economically deprived areas where lactation by the already nutritionally deprived women is prolonged and, additionally, the interval between pregnancies is not long enough to allow for replenishment of calcium stores (4). Although Brunvand et al (40) reported that vitamin D deficiency, which can cause osteomalacia and subsequent maternal pelvic deformities, is common in Karachi, it was not associated with obstructed labor. What is uncertain is the severity of vitamin D deficiency in these communities. Mild deficiencies alone are not enough to cause osteomalacia.

Defective calcium absorption or poor bioavailability are causes of vitamin D deficiency and, therefore, osteomalacia (41), which may cause pelvic deformities and subsequently obstructed labor. In fact, Chaim et al (42) observed a few cases of pelvic deformities of the osteomalacia type in Bedouin women who consumed large quantities of raghif, an unleavened bread with a high content of phytic acid. Insufficient dietary intake of vitamin D compounded by inadequate exposure to sunlight, which reduces the synthesis of vitamin D from cholecalciferol in the skin, are other factors that can cause osteomalacia. Vitamin D deficiency often occurs in situations in which calcium intake or bioavailability is also precarious because this enhances the metabolic inactivation of vitamin D (43).

Macronutrient intake and weight gain in pregnancy
The demand for both energy and nutrients is increased during pregnancy. For well-nourished women, only a small amount of additional energy is required because the body adapts to the increased energy demands and becomes more energy efficient by reducing physical activity and lowering the metabolic rate. It is only during the last trimester of pregnancy that average-sized, well-nourished women require an extra {approx}849 kJ/d (44). Research on pregnancy weight gain in women with normal prepregnancy weight showed that high gestational weight gain increases birth weight (45). Studies of white and Asian women, who are at a high nutritional risk in the West Midlands, England, and in Indonesia, showed that protein-energy supplementation during pregnancy did not significantly affect birth weight and length (46, 47). Similarly, Kramer (48) concluded that prenatal protein-energy supplementation proffered little benefit to either mothers or infants. Other studies, however, have shown that protein-energy supplementation of pregnant women at risk of delivering a low-birth-weight infant enhanced intrauterine growth (49–53).

Garner et al (54) suggested that interventions to increase birth weight could be hazardous to women because they could lead to more mechanical difficulties in labor in areas where access to the proper care might not be available. Few data are available to support this hypothesis. Prenatal supplementation (60 mg Fe and 250 µg folate, with or without 15 mg Zn) in Peru produced no effect on birth weight or head circumference (55). Goldenberg et al (56), however, found that daily supplementation with 25 mg Zn in early pregnancy for women with relatively low plasma zinc concentrations was associated with greater infant birth weights (126 g; P < 0.03) and head circumferences (0.4 cm; P < 0.02). This effect was greater in women with a body mass index <26 (expressed in kg/m2), in whom birth weight was 248 g higher (P = 0.005) and head circumference was 0.7 cm larger (P = 0.007). Ceesay et al (52) found a small (3.1 mm) but statistically significant (P < 0.01) increase in head circumference with daily high-energy supplementation (4.3 MJ), which translated into an increase of only 1.5 mm in diameter, which is unlikely to increase the prevalence of cephalopelvic disproportion.

Secular studies of birth weight showed an increase across generations with no reported adverse effects (57), presumably because other secular changes in maternal proportions also occur and this increase in fetal size does not create cephalopelvic disproportion. Li et al (58) found that mean birth weights of infants born to Southeast Asian parents who were born outside the United States increased annually by {approx}18 g (95% CI: 11, 25 g) between 1908–1981 and 1986. A similar secular change of birth weight during the same period was not observed for infants of US-born Asian mothers. This, the authors suggest, shows that migration from their native countries to the United States had a positive effect on the birth weight of infants born to these mothers. Secular changes in birth weight were also observed in Asians living in England (59). Infants of migrant Pakistanis were 139 g heavier and those of migrant Indians 25 g heavier in 1978 than they had been 10 y earlier, reinforcing the concept that environmental factors play an important role in intrauterine growth.

Despite the absence of any negative effect of supplementation on obstructed labor, the situation may be different for women whose skeletal—and, therefore, pelvic—growth was restricted during childhood and early adolescence but whose general food intake increased later. Abitbol et al (60) reported that mothers born and raised outside of the United States (with narrow pelvic dimensions) who eat a high-protein diet and receive adequate prenatal care after migrating as adults to the United States give birth to relatively large infants. This results in a marked cephalopelvic disproportion and severe dystocia, which frequently leads to cesarean delivery. Observations from the United Kingdom (JC Konje, unpublished observations, 1999) show that fetomaternal disproportion is more common in first-generation than in second-generation minority groups. These effects are more marked in women who are shorter and by inference more growth retarded.


   CONSEQUENCES OF OBSTRUCTED LABOR
TOP
 ABSTRACT
 INTRODUCTION
 ETIOLOGY
 CONSEQUENCES OF OBSTRUCTED LABOR
PREVENTION
 CONCLUSIONS
 REFERENCES
 
Once obstructed labor has been diagnosed, the obstruction must be relieved. The method of relief will be determined by various factors, including the state of the mother, the state of the fetus, associated complications, and the environment. The initial steps should be adequate resuscitation of the mother by rehydration and intravenous provision of fluids and energy, and, when infections are thought to have supervened, antibiotics. Immediately thereafter, the fetus must be delivered. When the fetus is alive, a safe delivery for both the mother and the fetus must be the option. When the fetus is dead, most women in developed countries will be offered a cesarean delivery. In developing countries, management should aim to reduce complications and simultaneously ensure that the woman and her family maintain some confidence in the health care facility. Often, this may mean a destructive operation rather than a cesarean delivery. This is important because women with obstructed labor often avoid hospitals in the first instance because of fear of cesarean delivery (3). Moreover, performing a cesarean delivery that does not result in a live baby will further reinforce a woman's fears and result in her delivering at home in subsequent pregnancies, which increases the risk of uterine rupture and possibly maternal mortality (61).

If improperly managed, obstructed labor is associated with very severe complications. These are related to unrelieved pressure on the bladder, rectum, and lumbosacral trunk of the sacral plexus and to the method of delivery of the fetus. Some of the more common complications that can be considered nutritionally relevant are high perinatal morbidity and mortality (62), infections of the uterus and the urinary tract (6), maternal mortality (10, 11, 63–65), and secondary amenorrhea (66).


   PREVENTION
TOP
 ABSTRACT
 INTRODUCTION
 ETIOLOGY
 CONSEQUENCES OF OBSTRUCTED LABOR
 PREVENTION
CONCLUSIONS
 REFERENCES
 
Breaking the intergenerational cycle of growth failure
An intergenerational cycle of ill health and growth failure has been described in which undernutrition in childhood leads to small body size in adulthood. The critical periods are the intrauterine period, early childhood, and adolescence.

Intrauterine growth
Genetic and environmental influences affect maternal height and prepregnancy weight, both of which are important determinants of birth size (67). Malnourished women (ie, women who are short, underweight, do not gain sufficient weight during pregnancy, or are anemic) are more likely to deliver intrauterine-growth-restricted or low-birth-weight infants (68–70). Low birth weight and intrauterine growth restriction are not independent because birth weight is affected by intrauterine growth and gestation age; thus, both conditions need to be optimized to reduce the prevalence of low birth weight. Prentice (71) reviewed food-supplementation programs targeted at pregnant women and concluded that supplementation during late pregnancy can have a significant beneficial effect on birth weight in women who are genuinely at risk as a result of an inadequate home diet. The effect of food supplements will depend most likely on the nutritional status of the woman, which is multifactorial, and few good intervention studies have been conducted. Efforts to reverse intrauterine growth restriction have been disappointing and at times risky (72). Nevertheless, Strauss (72) agrees with Prentice (71) that energy supplementation in undernourished populations may be of significant benefit.

The concept of altering food and energy supplementation to influence intrauterine growth and therefore reduce fetal size and obstructed labor as proposed by Rush (73) is not justified. This is not only because of the multifactorial nature of fetal growth, but also because embarking on such a policy is not only unethical, it is also scientifically flawed. Having access to nutrition education during pregnancy is a fundamental human right and to not promote adequate food intake just because women are short, to theoretically reduce the risk of obstructed labor, is unacceptable in our contemporary world. There is epidemiologic evidence linking intrauterine growth and adult diseases such as diabetes mellitus, ischemic heart attack, and early death from stroke and hypertension (74). Deliberately withholding nutrition education or food supplementation during pregnancy may indirectly condemn offspring in future generations to these complications. There is insufficient justification on the basis of available evidence for such programmatic action.

Maternal micronutrient status may also affect the status of young offspring. A longitudinal study in Malawi among HIV-seropositive mothers showed that maternal vitamin A deficiency was related to linear growth of children after adjustment for confounding factors. At 1 y of age, children of vitamin A–deficient mothers were shorter than children of nondeficient mothers (75).

Ramakrishnan et al (76) examined the intergenerational effects of growth by using data from 14 studies of middle-class populations in developed countries. Overall, for every 100-g increase in maternal weight at the time of birth, child birth weight increased by 10–20 g. In a prospective analysis of data from Guatemala, Ramakrishnan et al (76) found that child birth weight increased by 29 g for every 100-g increase in maternal birth weight, which was almost double that reported for developed countries. Child birth weight increased by 53 g per 1-cm increase in maternal birth length, but this was reduced to 38 g/cm after maternal height and prepregnancy weight were controlled for, which the authors suggested was due to the intergenerational effects of maternal birth size. Child birth length also increased by 0.2 cm per 1-cm increase in mother's birth length and by 0.1 cm per 100-g increase in maternal birth weight, although the former was not significant after adult size was controlled for.

Growth in childhood
The most striking effects of the intrauterine environment on childhood growth are seen in children with intrauterine growth restriction, who remain significantly lighter and shorter than their peers (72). There is some tendency for catch-up growth in low-birth-weight children, but the deficits can persist even up to 12–14 y of age (77, 78); children at greatest risk of long-term stunting were low-birth-weight infants who were also severely stunted during infancy. The potential for catch-up growth in a cohort of Filipino children aged 2–12-y was greatest for children with greater growth potential, ie, those with taller mothers, longer length and lower ponderal index at birth, and less severe stunting during early infancy (78).

Poor food intake in early childhood is known to affect long-term physical growth (79, 80). The effects of single micronutrient supplementation on growth were also studied. Vitamin A supplementation had no effect on linear growth for preschool boys and girls in randomized supplementation trials in Indonesia (81), India (82), and the Sudan (83). The situation of linear growth with iron is equivocal. Among iron-deficient children (1.5–13 y of age), growth was improved after 8–15 wk of iron supplementation (84–87), although Gershoff et al (88) and Migasena et al (89) did not confirm these findings. Angeles et al (87) attributed the improvement in growth to reduced morbidity after iron supplementation. Allen (90) suggested that these mixed results may reflect the short duration of the interventions. Alternatively, the treatment effect may occur only if the child was initially anemic.

Brown et al (91) conducted a meta-analysis of 25 zinc intervention trials of children 0–13 y of age (mean: 3.6 y). Zinc supplementation had a significant effect on height (0.22 SD units), and the effects were greatest for the children who were the most zinc deficient or the most growth stunted. A randomized, controlled trial among rural Zimbabwean schoolchildren, however, found no effect of zinc supplementation on growth (92). Only one study was found that looked at the effect of multiple micronutrient (ie, vitamins A, C, D, E, K, B-12, B-6, niacin, thiamine, riboflavin, folic acid, pantothenic acid, iodine, iron, zinc, copper, manganese, and fluoride) supplementation on the growth of children aged 8–14 mo in a double-blind, community-based, randomized trial (93). Treatment was administered under supervision 6 d/wk over 12 mo. Final length in the supplemented group was 0.6 cm greater than in the placebo group after background variables were controlled for. Nevertheless, the effect was lower than expected for catch-up growth, which led the authors to suggest that supplementation with more than the apparently deficient nutrients is required. Allen (90), in her summary of a review of nutrient deficiencies and linear growth faltering, noted that single nutrient supplementation has not had the effect on growth that would be expected if that nutrient were limiting. She too suggested that multiple—rather than single—growth-limiting nutrient deficiencies coexist in children.

Adolescent growth
Brabin and Brabin (94) looked at adolescence, which is an intense anabolic period during which requirements for all nutrients increase. They suggested that the process of catch-up growth may increase nutritional risk because it reduces stores of critical micronutrients such as iron and vitamin A. On the basis of studies showing improved growth after iron supplementation, Brabin and Brabin also postulated that iron is an essential nutrient for skeletal growth and that deficiency may limit growth during adolescence. Similarly, on the basis of data from Swedish adolescents that showed an association between serum retinol and puberty stage, they suggested that vitamin A is important for sexual maturation and that deficiency can cause menstrual irregularities, such as menorrhagia, and thus contribute to anemia. Ilich-Ernst et al (95) performed a longitudinal study to look at, among other things, the simultaneous effect of growth and menarche on iron stores in adolescent girls. They found that the adolescent growth spurt and menstrual losses adversely affected iron stores in girls with low iron intakes (<9 mg/d). Delayed puberty has been reported in low-birth-weight children (96, 97), although Bhargava et al (98) documented an earlier onset of menarche in these children in a longitudinal study.

Pregnancy in adolescence imposes an even greater physiologic burden on girls, which is often worsened by poor dietary intakes and failure to use antenatal care optimally. Increased extraction from the adolescent parturient of nutrients (eg, iron, folic acid, and essential amino acids) when there are inadequate stores will result in deficiency and its consequent complications. Because adolescents are still growing, the implications of deficiency are restricted growth and fetopelvic disproportion that may result in obstructed labor.

Although a considerable amount of work has been invested in supplementing preschool children, few data are available to indicate whether food or micronutrient supplementation of girls during the rapid preadolescent growth phase can increase attained height, which could ultimately contribute to reducing maternal morbidity and mortality from obstructed labor.

Improved health
Growth in length is also compromised by common childhood infections, particularly diarrheal diseases in early childhood (99, 100). Infants with sustained Helicobacter pylori infection also grow less well than do children without the infection (101). Single and multiple helminthic infections have been shown to be associated with growth retardation (86) and catch-up growth has occurred in preschool-aged children after deworming (102, 103). Deworming school-aged children was also shown to improve physical growth (104). The adverse effects of chronic and acute infections on linear growth may result from micronutrient malnutrition or the induction of the acute phase response and production of proinflammatory cytokines that can affect long bone growth (99).

In some societies, a large number of adolescents are sexually active, resulting in a high prevalence of sexually transmitted diseases (105), such as HIV (106, 107), syphilis, and chlamydia (108). Some of these diseases are more prevalent in undernourished and immunocompromised individuals. Improved nutrition may, therefore, enhance growth not only directly but also indirectly by improving the immunologic status of adolescents.

To improve the health of women of reproductive age, health care providers need to be trained to identify women at high risk of obstructed labor (and other pregnancy complications) and the factors that can diminish this risk. Improving the utilization of health care facilities during pregnancy, especially in areas with early adolescent marriage, and the introduction of nutrition education and supplementation programs could reduce the prevalence of obstructed labor.


   CONCLUSIONS
TOP
 ABSTRACT
 INTRODUCTION
 ETIOLOGY
 CONSEQUENCES OF OBSTRUCTED LABOR
 PREVENTION
 CONCLUSIONS
REFERENCES
 
Obstructed labor remains a common cause of maternal morbidity and mortality in developing countries. However, the prevalence and incidence rates are unknown. Even in developed countries, intervention often occurs before labor becomes obstructed; thus, it is difficult to determine true incidence and prevalence rates. Eliminating obstructed labor will be difficult unless adequate data on prevalence become available; to this end, a better definition of an acceptable international standard for the diagnosis is needed, probably under the auspices of the World Health Organization. For example, a clear distinction has to be made between prolonged labor (resulting from inertia) and obstructed labor (which is mechanical). In this regard, there is the need to reeducate midwives, physicians, and all health care personnel. Population-based studies in different geographic zones will provide the necessary data on the prevalence rate of this complication of pregnancy. This can be achieved only through cooperation among governments; voluntary agencies; and primary, secondary, and tertiary care providers. A more effective means of assessing prevalence may be hospital cesarean delivery rates for failure to progress in labor due to disproportion. Such data, however, are likely to be biased toward urban areas and possibly the middle and upper classes. Nevertheless, these data can help to improve the standardization of data collection and provide a better understanding of the magnitude of the problem for programmatic action.

A major cause of obstructed labor is fetomaternal disproportion. Intergenerational cycles of chronic undernutrition, which may include calcium deficiency, are responsible for this in a large proportion of cases. Because of this, it may take more than one generation to overcome the effects of childhood disadvantage; the most effective way to reduce the incidence of obstructed labor is, therefore, to adopt measures to improve the health and nutrition of children during their rapid periods of growth, ie, infancy, early childhood, and adolescence. This means that an efficacious policy would be one that included effective interventions initiated from as early as infancy to beyond the conventional preschool years. Such programs must not only concentrate on nutrients that enhance skeletal growth but also aim to improve the general nutrition of the infant, child, and adolescent girl. Interventions should include infection control, the provision of hematinics, and, in some situations, calcium supplements.

Efforts must be made to increase the awareness of the importance of good health, especially during the adolescent period, including the need for a balanced diet and the elimination of infections in early childhood that commonly exist in malnourished children. Such infections potentiate the effects of nutrient deprivation on growth. Policies that encourage formal education of young women, delay the age of marriage, and promote family planning and contraceptive use may result in the age of first pregnancy being delayed and, therefore, increase the chance of girls completing adolescent growth.

For women who are undernourished and who have not achieved their full growth potential (ie, have a small pelvis), macro- and micronutrient supplementation may be important for fetal growth. Intrauterine growth can influence child and adolescent growth, and the effect is intergenerational. For this reason, it is likely to take a few generations to achieve secular changes in growth that will reduce and possibly even eliminate obstructed labor. There may be some justification in trading a transient increase in cesarean delivery for disproportion to future reduction in stunted growth and thus the eventual elimination of obstructed labor. However, the theoretical fear of increased obstruction can be obviated by the inclusion of an education program that encourages women in rural communities to accept orthodox health care and by a simultaneous increase in the number in health care centers and personnel in such communities.


   REFERENCES
TOP
 ABSTRACT
 INTRODUCTION
 ETIOLOGY
 CONSEQUENCES OF OBSTRUCTED LABOR
 PREVENTION
 CONCLUSIONS
 REFERENCES
 

  1. Philpott RH. Obstructed labor. Clin Obstet Gynaecol 1980;7:601–19.[Medline]
  2. Moller B, Lindmark G. Short stature: an obstetric risk factor? A comparison of two villages in Tanzania. Acta Obstet Gynecol Scand 1997;76:394–7.[Medline]
  3. Lawson JB. Obstructed labor. In: Lawson JB, Stewart DD, eds. Obstetrics and gynaecology in the tropics and developing countries. London: Edward Arnold Press, 1967:172–202.
  4. Cruickshank EK. Nutrition in pregnancy and lactation. In: Lawson JB, Stewart DD, eds. Obstetrics and gynaecology in the tropics and developing countries. London: Edward Arnold Press, 1967:11–28.
  5. Debbie DAM. The influence of maternal height on outcome: recent experience in maternity and child health in Ethiopia. J Trop Pediatr 1966;12:20–4.
  6. Konje JC, Obisesan KA, Ladipo OA. Obstructed labor in Ibadan. Int J Gynaecol Obstet 1992;39:17–21.[Medline]
  7. Hasan JT, Korejo R. Rupture of the uterus in full-term pregnancy. J Pakistan Med Assoc 1993;43:172–3.[Medline]
  8. Prual A, Huguet D, Garbin O, Rabe G. Severe obstetric morbidity of the third trimester, delivery and early puerperium in Niamey (Niger). Afr J Reprod Health 1998;2:10–9.[Medline]
  9. Antenatal screening for fetopelvic dystocia. A cost-effectiveness approach to the choice of simple indicators for use by auxiliary personnel. The Kasogo Project Team. J Trop Med Hyg 1984;87:173–83.[Medline]
  10. Khan AR, Jahan FA, Begum SF. Maternal mortality in rural Bangladesh: the Jamalpur District. Stud Fam Plann 1986;17:7–12.[Medline]
  11. Alauddin M. Maternal mortality in rural Bangladesh: the Tangail District. Stud Fam Plann 1986;17:13–21.[Medline]
  12. AbouZahr C, Wardlaw T, Stanton C, Hill K. Maternal mortality. World Health Stat Q 1996;49:77–87.[Medline]
  13. Stokoe U. Determinants of maternal mortality in the developing world. Aust N Z J Obstet Gynaecol 1991;31:8–16.[Medline]
  14. Wall LL. Dead mothers and injured wives: the social context of maternal morbidity and mortality among the Hausa of northern Nigeria. Stud Fam Plann 1998;29:341–59.[Medline]
  15. Oronsanye AU, Asuen MI. Obstructed labor—a four year survey at the University of Benin Teaching Hospital, Benin City, Nigeria. Trop Doct 1980;10:113–5.[Medline]
  16. Banerji B. Obstructed labor—analysis of 60 cases. J Indian Med Assoc 1966;47:379–81.[Medline]
  17. Harrison KA. Child-bearing, health and social priorities. A survey of 22,744 consecutive hospital births in Zaria, Northern Nigeria. Br J Obstet Gynaecol 1985;92(suppl 5):1–119.
  18. Heys RF, Murray CP, Kohler HG. Obstructed labor due to foetal tumors: cervical and coccygeal teratoma. Two case reports. Gynaecologia 1967:164:43–54.[Medline]
  19. Edwards WR. A fetal sacrococcygeal tumor obstructing labor after attempted home confinement. Obstet Gynecol 1983;61:19S–20S.
  20. Bluett D. Iniencephaly causing obstructed labor. Proc R Soc Med 1968;61:1281–2.
  21. Bowman PR. Obstructed labor due to locked twins. Ir J Med Sci 1983;152:134–44.[Medline]
  22. Turrentine MA, Andres RL. Recurrent Bandl's ring as an etiology for failed vaginal birth after cesarean section. Am J Perinatol 1994; 11:65–6.[Medline]
  23. Ogunbode O, Ajagba JA, Obisesan KA, Henderickse JP. Uterine fibroids and obstructed labor. Obstet Gynecol 1973;42:71–5.[Medline]
  24. Burgess HA. Anthropometric measures as a predictor of cephalopelvic disproportion. Trop Doct 1997;27:135–8.[Medline]
  25. Dujardin B, Van Cutsem R, Lambrechts T. The value of maternal height as a risk factor of dystocia: a meta-analysis. Trop Med Int Health 1996;1:510–21.[Medline]
  26. Hanzal E, Kainz C, Hoffmann G, Deutinger J. An analysis of the prediction of cephalopelvic disproportion. Arch Gynecol Obstet 1993;253:161–6.[Medline]
  27. Kwawukume EY, Ghosh TS, Wilson JB. Maternal height as a predictor of vaginal delivery. Int J Gynaecol Obstet 1993;41:27–30.[Medline]
  28. van Roosmalen J, Brand R. Maternal height and the outcome of labor in rural Tanzania. Int J Gynaecol Obstet 1992;37:169–77.[Medline]
  29. Sokal D, Sawadogo L, Adjibade A. Short stature and cephalopelvic disproportion in Burkina Faso, West Africa. Operations Research Team. Int J Gynaecol Obstet 1991;35:347–50.[Medline]
  30. Mahood TA. Maternal height, birthweight, obstetric conjugate and their influence on the management of parturients with a previous cesarean scar. Acta Obstet Gynecol Scand 1989;68:595–8.[Medline]
  31. Desai P, Hazra M, Trivedi LB. Pregnancy outcome in short statured women. J Indian Med Assoc 1989;87:32–4.[Medline]
  32. Camilleri AP. The obstetric significance of short stature. Eur J Obstet Gynecol Reprod Biol 1981;12:347–56.[Medline]
  33. Adadevoh SW, Hobbs C, Elkins TE. The relation of the true conjugate to maternal height and obstetric performance in Ghanaians. Int J Gynaecol Obstet 1989;28:243–51.[Medline]
  34. Kappel B, Eriksen G, Hansen KB, et al. Short stature in Scandinavian women. An obstetrical risk factor. Acta Obstet Gynecol Scand 1987;66:153–8.[Medline]
  35. Mati JK. The Nairobi birth survey III. Labor and delivery. J Obstet Gynaecol East Central Afr 1983;2:47–56.
  36. Essex BJ, Everett VJ. Use of an action-orientated record for antenatal screening. Trop Doct 1977;7:134–8.[Medline]
  37. Bhatt RV, Modi NS, Acharya PT. Height and reproductive performance. J Obstet Gynaecol India 1967;17:75–9.
  38. Tsu VD. Maternal height and age: risk factors for cephalopelvic disproportion in Zimbabwe. Int J Epidemiol 1992;21:941–6.[Abstract/Free Full Text]
  39. Witter FR, Caulfield LE, Stoltzfus RJ. Influence of maternal anthropometric status and birth weight on the risk of cesarean delivery. Obstet Gynecol 1995;85:947–51.[Abstract]
  40. Brunvand L, Shah SS, Bergstrom S, Haug E. Vitamin D deficiency in pregnancy is not associated with obstructed labor. A study among Pakistani women in Karachi. Acta Obstet Gynecol Scand 1998;77:303–6.[Medline]
  41. Strong JA, Truswell AS. Nutritional factors in disease. In: Macleod J, ed. Davidson's principles and practice of medicine. Philadelphia: Churchill Livingstone, 1974:142–7.
  42. Chaim W, Alroi A, Leiberman JR, Cohen A. Severe contracted pelvis appearing after normal deliveries. Acta Obstet Gynecol Scand 1981;60:131–4.[Medline]
  43. Fraser DR. Vitamin D. Lancet 1995;345:104–7.[Medline]
  44. Hytten FE. Nutritional physiology during pregnancy. In: Campbell DM, Gillmer MDG, eds. Nutrition in pregnancy. London: Royal College of Gynaecologists, 1983:1–18.
  45. Thorsdottir I, Birgisdottir BE. Different weight gain in women of normal weight before pregnancy: postpartum weight and birthweight. Obstet Gynaecol 1998;92:377–83.[Abstract]
  46. Watney PJM, Atton C. Dietary supplementation in pregnancy. Br Med J 1986;293:1102 (letter).
  47. Kusin JA, Kardjati S, Houtkooper J, Renquist UH. Energy supplementation during pregnancy and post-natal growth. Lancet 1992; 340:623–6.[Medline]
  48. Kramer MS. Effects of energy and protein intakes on pregnancy outcome: an overview of the research evidence from controlled clinical trials. Am J Clin Nutr 1993;58:627–35.[Abstract/Free Full Text]
  49. Prentice AM, Whitehead RG, Roberts SB, et al. Dietary supplementation of Gambian nursing mothers and lactational performance. Lancet 1980;2:886–8.[Medline]
  50. Brown MC. Protein energy supplements in primigravid women at risk of low birthweight. In: Campbell DM, Gillmer MDG, eds. Nutrition in pregnancy. Royal College of Gynaecologists, London: Springer-Verlag, 1983:85–98.
  51. Winkvist A, Habicht JP, Rasmussen KM. Linking maternal and infant benefits of a nutritional supplement during pregnancy and lactation. Am J Clin Nutr 1998;68:656–61.[Abstract]
  52. Ceesay SM, Prentice AM, Cole TJ, et al. Effects on birth weight and perinatal mortality of maternal dietary supplements in rural Gambia: 5 year randomised controlled trial. BMJ 1997;315:786–90.[Abstract/Free Full Text]
  53. Herrera MG, Mora JO, de Paredes B, Wagner M. Maternal weight/height and the effect of food supplementation during pregnancy and lactation. In: Aebi H, Whitehead R, eds. Maternal nutrition during pregnancy and lactation. Bern, Switzerland: Hans Huber, 1980:252–63.
  54. Garner P, Kramer MS, Chalmers I. Might efforts to increase birth weight in undernourished women do more harm than good? Lancet 1992;340:1021–2.[Medline]
  55. Caulfield LE, Zavaleta N, Figueroa A, Leon Z. Maternal zinc supplementation does not affect size at birth or pregnancy duration in Peru. J Nutr 1999;129:1563–8.[Abstract/Free Full Text]
  56. Goldenberg RL, Tamura T, Neggers Y, et al. The effect of zinc supplementation on pregnancy outcome. JAMA 1995;274:463–8.[Abstract]
  57. Alberman E, Filakti H, Williams S, Evans SJ, Emanuel I. Early influences on the secular change in adult height between the parents and children of the 1958 birth cohort. Ann Hum Biol 1991;18:127–36.[Medline]
  58. Li DK, Ni HY, Schwartz SM, Daling JR. Secular change in birthweight among southeast Asian immigrants to the United States. Am J Public Health 1990;80:685–8.[Abstract/Free Full Text]
  59. Clarson CL, Barker MJ, Marshall T, Wharton BA. Secular change in birthweight of Asian babies born in Birmingham. Arch Dis Child 1982;57:867–71.[Abstract]
  60. Abitbol MM, Taylor-Randall UB, Barton PT, Thompson E. Effect of modern obstetrics on mothers from Third-World countries. J Matern Fetal Med 1997;6:276–80.[Medline]
  61. Konje JC, Odukoya OA, Ladipo OA. Ruptured uterus in Ibadan: a 12 year review. Int J Gynaecol Obstet 1990;32:207–13.[Medline]
  62. Naeye RL, Dozor A, Tafari N, Ross SM. Epidemiological features of perinatal death due to obstructed labor in Addis Ababa. Br J Obstet Gynaecol 1977;84:747–50.[Medline]
  63. Adapter OF. Maternal mortality—a twelve year survey at the University of Aileron Teaching Hospital (UITH), Ilorin, Nigeria. Int J Gynaecol Obstet 1987;25:93–8.[Medline]
  64. Kwast BE. Obstructed labor: its contribution to maternal mortality. Midwifery 1992;8:3–7.[Medline]
  65. Martey JO, Djan JO, Twum S, Browne EN, Opoku SA. Maternal mortality and related factors in Ejisu District, Ghana. East Afr Med J 1994;71:656–60.[Medline]
  66. Bieler EU, Schnabel T. Pituitary and ovarian function in women with vesicovaginal fistula after obstructed and prolonged labor. S Afr Med J 1976;50:257–66.[Medline]
  67. Kramer MS. Determinants of low birth weight: methodological assessment and meta-analysis. Bull World Health Organ 1987;65:633–7.
  68. Adair LS. Nutrition in the reproductive years. In: Johnson FE, ed. Nutritional anthropology. New York: Alan R Liss, 1987:119–54.
  69. Scholl TO, Hediger ML. Anemia and iron-deficiency anemia: compilation of data on pregnancy outcome. Am J Clin Nutr 1994; 59(suppl):492S–501S.[Abstract/Free Full Text]
  70. Lechtig A Shrimpton R. Maternal nutrition: what relevance for children's survival and development? In: Kretchmer N, Quilligan EJ, Johnson JD, eds. Prenatal and perinatal biology and medicine. Chur, Switzerland: Harwood Academic Publishers, 1997:93–160.
  71. Prentice AM. Can maternal dietary supplements help in preventing infant malnutrition? Acta Paediatr Scand Suppl 1991;374:67–77.[Medline]
  72. Strauss RS. Effects of the intrauterine environment on childhood growth. Br Med Bull 1997;53:81–95.[Abstract/Free Full Text]
  73. Rush D. Nutrition and maternal mortality in the developing world. Am J Clin Nutr 2000;72(suppl):212S–40S.[Abstract/Free Full Text]
  74. Barker DJ. In utero programming of chronic disease. Clin Sci (Colch) 1998;95:115–28.
  75. Semba RD, Miotti P, Chiphangwi JD, et al. Maternal vitamin A deficiency and child growth failure during human immunodeficiency virus infection. J Acquir Immune Defic Syndr Hum Retrovirol 1997;14:219–22.[Medline]
  76. Ramakrishnan U, Martorell R, Schroeder DG, Flores R. Role of intergenerational effects on linear growth. J Nutr 1999;129(suppl): 544S–9S.
  77. Bhargava SK, Ramjii S, Srivastava U, et al. Growth and sexual maturation of low birth weight children: a 14-year follow-up. Indian J Pediatr 1995;32:963–70.
  78. Adair LS. Filipino children exhibit catch-up growth from age 2 to 12 years. J Nutr 1999;129:1140–8.[Abstract/Free Full Text]
  79. Scholl TO, Hediger ML, Ances IG. Maternal growth during pregnancy and decreased infant birth weight. Am J Clin Nutr 1990;51: 790–3.[Abstract/Free Full Text]
  80. Martorell R, Ramakrishnan U, Schroeder DG, Melgar P, Neufeld L. Intrauterine growth retardation, body size, body composition and physical performance in adolescence. Eur J Clin Nutr 1998; 52(suppl):S43–S53.
  81. West KP, Djunaedi E, Pandji A, Kusdiono, Tarwotjo I, Sommer A. Vitamin A supplementation and growth: a randomized community trial. Am J Clin Nutr 1988;48:1257–64.[Abstract/Free Full Text]
  82. Rahmathullah L, Underwood BA, Thulasiraj RD, Milton RC. Diarrhea, respiratory infections, and growth are not affected by a weekly low-dose vitamin A supplement: a masked, controlled field trial in children in southern India. Am J Clin Nutr 1991;54:568–77.[Abstract/Free Full Text]
  83. Fawzi WW, Herrera MG, Willett WC, Nestel P, El Amin A, Mohamed KA. Dietary vitamin A intake in relation to child growth. Epidemiology 1997;8:402–7.[Medline]
  84. Aukett MA, Parks YA, Scott PH. Treatment with iron increases weight gain and psychomotor development. Arch Dis Child 1986;61:849–54.[Abstract]
  85. Chwang LC, Soemantri AG, Pollitt E. Iron supplementation and physical growth of rural Indonesian children. Am J Clin Nutr 1988; 47:496–501.[Abstract/Free Full Text]
  86. Latham MC, Stephenson LS, Kinoti SN, Zaman MS, Kurz KM. Improvements in growth following iron supplementation in young Kenyan school children. Nutrition 1990;6:159–65.[Medline]
  87. Angeles IT, Schultink WJ, Matulessi P, Gross R, Sastroamidjojo S. Decreased rate of stunting among anemic Indonesian preschool children through iron supplementation. Am J Clin Nutr 1993;58:339–42.[Abstract/Free Full Text]
  88. Gershoff SN, McGandy RB, Nondasuta A, Tantiwongse P. Nutrition studies in Thailand: effects of calories, nutrient supplements, and health interventions on growth of preschool Thai village children. Am J Clin Nutr 1988;48:1214–8.[Abstract/Free Full Text]
  89. Migasena P, Thurnham DI, Jintakanon K, Pongpaew P. Anemia in Thai children: the effect of iron supplementation on haemoglobin and growth. Southeast Asian J Trop Med Public Health 1972;3:255–61.[Medline]
  90. Allen LH. Nutritional influences on linear growth: a general review. Eur J Clin Nutr 1994;48(suppl):S75–89.
  91. Brown KH, Peerson JM, Allen LH. Effect of zinc supplementation on children's growth: a meta analysis of intervention trials. Bibl Nutr Dieta 1998;54:76–83.
  92. Friis H, Ndhlovu P, Mduluza T, et al. The impact of zinc supplementation on growth and body composition: a randomized, controlled trial among rural Zimbabwean schoolchildren. Eur J Clin Nutr 1997;51:38–45.[Medline]
  93. Rosado JL. Separate and joint effects of micronutrient deficiencies on linear growth. J Nutr 1999;129(suppl):531S–3S.
  94. Brabin L, Brabin BJ. The cost of successful adolescent growth and development in girls in relation to iron and vitamin A status. Am J Clin Nutr 1992;55:955–8.[Abstract/Free Full Text]
  95. Ilich-Ernst JZ, McKenna AA, Badenhop NE, et al. Iron status, menarche, and calcium supplementation in adolescent girls. Am J Clin Nutr 1998;68:880–7.[Abstract]
  96. Bhargava SK, Duggal S, Ramanujacharyulu TK, Choudhury P. Patterns of pubertal changes and their interrelationships in girls. Indian Pediatr 1980;17:657–65.[Medline]
  97. Sachdev HPS. Low birth weight in South Asia. In: Gillespie SR, ed. Malnutrition in South Asia: a regional profile. Kathmandu, Nepal: UNICEF Regional Office for South Asia, 1997;23–50. (Publication no. 5.)
  98. Bhargava SK, Ramjii S, Srivastava U, et al. Growth and sexual maturation of low birth weight children: a 14-year follow-up. Indian J Pediatr 1995;32:963–70.
  99. Stephensen CB. Burden of infection on growth. J Nutr 1999; 129(suppl):534S–8S.
  100. Martorell R, Habicht JP, Yarbrough C, Lechtig A, Klein AE, Western KA. Acute morbidity and physical growth in rural Guatemalan children. Am J Dis Child 1975;129:1296–301.[Abstract]
  101. Dale A, Thomas JE, Darboe MK, Coward WA, Harding M, Weaver LT. Helicobacter pylori infection, gastric acid secretion, and infant growth. J Pediatr Gastroenterol Nutr 1998;26:393–7.[Medline]
  102. Nabarro D. Nutritional problems in developing countries: priorities for the pediatrician. Monatsschr Kinderheilkd 1988;136:352–5.[Medline]
  103. Hlaing T. Ascariasis and childhood malnutrition. Parasitology 1993;107(suppl):S125–36.
  104. Bundy DAP, Guyatt HL. Schools for health: focus on health, education and the school-age child. Parasit Today 1996;12:1–16.
  105. WHO/Family Health/Adolescent Health. A picture of health. A review and annotated bibliography of the health of young people in developing countries. 1995;14:24–7.
  106. Mann J, Tarantola DJM, Netter TW. AIDS in the world. New York: United Nations, 1992.
  107. Shah IH. Sexual and reproductive health in sub-Saharan Africa—an overview. Afr J Reprod Health 1998;2:98–107.
  108. Brabin L, Kemp J, Obunge OK, et al. Reproductive tract infections and abortion amongst adolescent girls in rural Nigeria. Lancet 1995;334:300–4.



This article has been cited by other articles:


Home page
 Br Med BullHome page
J. Neilson, T Lavender, S Quenby, and S Wray
Obstructed labour: Reducing maternal death and disability during pregnancy
Br. Med. Bull., December 1, 2003; 67(1): 191 - 204.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Clin. Nutr.Home page
P. Nestel and F. Davidson
Introduction
Am. J. Clinical Nutrition, July 1, 2000; 72(1): 209S - 211.
[Full Text] [PDF]

This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Purchase Article
Right arrow View Shopping Cart
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Konje, J. C
Right arrow Articles by Ladipo, O. A
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Konje, J. C
Right arrow Articles by Ladipo, O. A
Agricola
Right arrow Articles by Konje, J. C
Right arrow Articles by Ladipo, O. A

HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS