围产儿出生缺陷分析及干预措施

摘要目的：掌握围产儿出生缺陷的发生情况,探讨引起围产儿出生缺陷的相关因素,为制订及完善出生缺陷预防对策及干预措施提供科学依据。方法：按照全国出生缺陷监测中心制定的监测方案,对2010年10月1日～2011年9月30日在湘潭市县级及以上医疗保健机构住院分娩的围生儿出生缺陷监测资料进行分析。结果：5年出生缺陷的平均发生率为93．30／万,出生缺陷的发生率无明显趋势（x2=0．114,P=0．736）乡村的出生缺陷发生率明显高于城镇（X2=24．638,P〈O．001）,男性围产儿的出生缺陷发生率显著高于女性（XZ=6．693,P=0．010）,出生缺陷的发生率与季节无关（x2=3．852,P=0．278）,出生缺陷的围产儿死亡率大大高于非出生缺陷）L（X2=2904．583,P〈0．001）,先天性心脏病、肢体畸形（并指／趾、多指／趾、肢体短缩、马蹄内翻足）、唇裂及唇腭裂是高发的出生缺陷。结论：减少出生缺陷的发生是一项长期工程,需要采取综合措施,从各个环节入手,以预防为主,加强优生优育健康教育,落实婚前及围产期保健,推行新生儿疾病筛查,可有效降低出生缺陷的发病率,提高出生人口素质。     

Second-trimester diagnosis of limb-body wall complex with literature review of pathogenesis

Three fetuses having limb-body wall complex (LBWC) with craniofacial defects and 9 fetuses having LBWC without craniofacial defects were diagnosed and delivered in the second trimester at Mackay Memorial Hospital during the period January 1990 - May 2006. Cases of LBWC with craniofacial defects showed severe anomalies of the upper limbs, craniofacial defects, constrictive amniotic bands and cranioplacental attachment, whereas, cases of LBWC without craniofacial defects presented major anomalies of the lower limbs, abnormal genitalia, anal atresia, renal defects, abdominoplacental attachment and umbilical cord abnormalities. The perinatal findings of LBWC with or without craniofacial defects were compared and the pathogenesis was discussed.     

Teratogenicity and developmental toxicity of valproic acid in rats

The teratogenicity and developmental toxicity of valproic acid (VPA) was investigated in Sprague-Dawley CD rats at doses of 0, 150, 200, 300, 400, and 600 mg/kg administered by gavage on days 7-18 of gestation. The VPA-600 dose was maternally toxic, causing death in two of four dams. This dose produced 100% embryonic resorption. The VPA-400 dose was maternally toxic in as much as maternal weight gain was reduced, but no deaths occurred. At this dose five of fifteen litters were completely resorbed, and 52% of all embryos were resorbed. Among survivors, 49% were malformed (68% having skeletal defects and 41% visceral defects). Fetal weight was reduced by 43% in this group. Most of the defects were ectrodactyly, hydronephrosis, cardiovascular defects, hypoplastic bladder, rib and vertebral defects, and other defects of the limbs and tail. The VPA-300 dose (nine litters) produced fewer defects, larger fetuses, and no increase in resorptions. The defects at this dose were primarily cariovascular, rib, and vertebral. The VPA-200 dose (12 litters) produced no reduction in fetal weight, no increase in resorptions, and few defects. The defects noted were hydronephrosis, cardiovascular abnormalities, and rib defects, primarily wavy ribs. Additional litters were prepared using doses of 150 and 200 mg/kg and were allowed to deliver and grow until 70 days. These doses produced no reduction in maternal weight gain, no reduction in litter size, birth weight, or sex ratio of the offspring. These doses produced no reduction in offspring weight to day 70, no increase in mortality, and only rare cases (two offspring of each dose) of tail defects.(ABSTRACT TRUNCATED AT 250 WORDS)     

Evaluation of the General Practice Research Database congenital heart defects prevalence: comparison to United Kingdom national systems

BACKGROUND: As part of an effort to validate the General Practice Research Database (GPRD) for future studies of medication use in pregnancy, this study examined whether the rates of all, and specific types of, congenital heart defects obtained from the GPRD are similar to those obtained from UK national systems. METHODS: The prevalence rates of heart defects for 2001-2003 were determined from the GPRD and compared with both the National Congenital Anomaly System (NCAS) and the European Concerted Action of Congenital Anomalies and Twins (EUROCAT). Rate ratios (RRs) and 95% CIs were calculated comparing the prevalence of all congenital heart defects as well as specific types of heart defects in the three data sources. In addition, the effect of the child's age on the frequency of heart defects in the GPRD was determined. RESULTS: The prevalence of heart defects in the GPRD was more than twice as high as in the NCAS and slightly higher than in the EUROCAT. All differences were statistically significant. The prevalence of specific heart defects varied across the GPRD, NCAS, and EUROCAT. The measured prevalence of congenital heart defects in the GPRD was higher if calculated including children up to age 6. CONCLUSIONS: The comparisons of the GPRD prevalence rates to national prevalence estimates demonstrate that the GPRD can serve as a more complete source of background prevalence for the most commonly occurring congenital heart defects, which is essential to properly assess possible associations between maternal exposures and congenital heart defects.     

Trends in rates of multiple vascular disruption defects, Atlanta, 1968-1989: is there evidence of a cocaine teratogenic epidemic?

Research suggests that, perhaps through mechanisms initiated by vasoconstriction and leading to vessel thrombosis or embolism, cocaine causes vascular disruption defects, and that frequent cocaine use during early pregnancy could disrupt multiple organ systems in the fetus. We hypothesized that if cocaine is an important cause of multiple vascular disruption defects, a rising prevalence of cocaine use by mothers during pregnancy should be accompanied by rising rates of these defects in their offspring. Using data from the Metropolitan Atlanta Congenital Defects Program, we identified all infants born in Atlanta from 1968 through 1989 who had nonsyndromic, provisional vascular disruption defects affecting more than one organ system: 61 infants (78%) had gastrointestinal and genitourinary defects, 7 (9%) had gastrointestinal and abdominal wall defects, 2 (3%) had gastrointestinal and limb reduction defects, 2 (3%) had limb reduction and abdominal wall defects, 2 (3%) had central nervous system and gastrointestinal defects, 2 (3%) had genitourinary and limb reduction defects, 1 (1%) had genitourinary and abdominal wall defects, and 1 (1%) had central nervous system and genitourinary defects. The prevalence of Atlanta infants with more than one vascular disruption defect is 0.13 per 1,000 live births. Chi-square analysis for trends showed no increase in prevalence during the study period. Our data are from one of the first population-based studies in which trends for defects potentially caused by maternal cocaine use are examined; the results of our study show no significant change in the prevalence of multiple vascular disruption defects over time.(ABSTRACT TRUNCATED AT 250 WORDS)     

Sex differences in the prevalence of human birth defects: a population-based study.

BACKGROUND: Sex differences in the prevalence of several human birth defects have often been reported in the literature, but the extent of sex differences for most birth defects is unknown. To determine the full extent of sex differences in birth defects in a population, we examined population-based data from the Metropolitan Atlanta Congenital Defects Program (MACDP). METHODS: MACDP records were analyzed for 1968 through 1995. We determined the sex-specific prevalence of all major birth defects, using the total number of live births by sex during these years as the denominator. For each specific defect, we calculated a relative risk with regard to sex on the basis of the ratio of prevalence among males to prevalence among females. Male-female relative risks were also determined for total major birth defects and for several broad categories of defects. RESULTS: The overall prevalence of major defects at birth was 3.9% among males and 2.8% among females. All but two of the major categories of birth defects (nervous system defects and endocrine system defects) had a higher prevalence among males. Defects of the sex organs were eight and one-half times more prevalent among males and accounted for about half of the increased risk of birth defects among males relative to females. Urinary tract defects were 62% more prevalent among males, and gastrointestinal tract defects were 55% more prevalent among males. Among specific defect types, twofold or greater differences in prevalence by sex were common. CONCLUSIONS: Our data indicate that sex differences in the prevalence of specific human birth defects are common, and male infants are at greater risk for birth defects than female infants. Several mechanisms have been proposed to account for these differences.     

The relation between small size for gestational age and the sex ratio of children with birth defects

BACKGROUND: Infants with birth defects are more likely to be born small for gestational age (SGA) than are other infants. This study describes a relation noted between the percentage SGA and the percentage male among children with various defect types. The data source was case records collected by the Metropolitan Atlanta Congenital Defects Program, a population-based, active surveillance system, during 1968 through 1998. METHODS: The study calculated the correlation between the percentage male and the percentage SGA for isolated cases of 44 different defect types for male-dominant and female-dominant defects separately. RESULTS: The correlation coefficient was -0.47 (P < 0.01) for male-dominant defects and 0.20 (P > 0.05) for female-dominant defects. Male-dominant defects were more likely to show less than 15% SGA and more likely to show the strongest risk differences by sex. CONCLUSIONS: These results are consistent with genetic causation of strongly skewed sex ratios, at least among male-dominant defects. Review of the literature suggests that defects with sex ratios closer to 1 are likely to have lower recurrence risks and therefore are less likely to be inherited than are other defects with skewed sex ratios. Sex ratios closer to 1 and a high percentage SGA may be markers of acquired or environmental birth defects.     

Paternal age and the occurrence of birth defects

The association between paternal age and the occurrence of birth defects was studied using data collected in Metropolitan Atlanta. Paternal-age information for babies born with defects was obtained from birth certificates, hospital records, and interviews with mothers; for babies born without defects, the information was obtained from birth certificates. Several statistical techniques were used to evaluate the paternal-age-birth-defects associations for 86 groups of defects. Logistic regression analysis that controlled for maternal age and race indicated that older fathers had a somewhat higher risk for having babies with defects, when all types of defects were combined; an equivalent association for older mothers was not found. Logistic regression analyses also indicated modestly higher risks for older fathers for having babies with ventricular septal defects and atrial septal defects and substantially higher risks for having babies with defects classified in the category chondrodystrophy (largely sporadic achondroplasia) and babies with situs inversus. An association between elevated paternal age and situs inversus has not been reported before; the magnitude of the estimated increased risk for situs inversus was about the same as that found in this study for chondrodystrophy.     

Cavitation defects on the lingual ramus: a further expression of Stafne's defect.

Seven archaeological examples of 6,700 mandibles examined were found to have developmental cortical defects on the ramus. The defects, unusual in their position, were grossly and radiographically similar to developmental bone cavities (Stafne's) located in the sublingual region. Of the seven ramus defects, all of which were in adult males, six were in Alaskan Eskimos from Kodiak Island (N = 5) and Nelson Island (N = 1), and one was in a native American from Arkansas. Only five adult males from Finland have been reported with similar defects. A statistical examination of the metrics defining mandibular cavitation defects, along with prevalence data, suggest that the seemingly rare findings of ramus defects are an extreme manifestation of the continuum of severity of the Stafne's defect. Bilateral Stafne's defects also represent a severe manifestation.     

新型持续皮肤牵张器促进皮肤创面愈合的实验研究

目的：介绍自主研制的持续皮肤牵张器,探讨自主研制的持续皮肤牵张器治疗皮肤缺损的可行性和效果分析。方法：自主研制的持续皮肤牵张器8套;白色家猪6只,将每只猪的背部（两侧）切除矩形皮肤软组织缺损,形成12个创面,分为二组,实验组4只猪8个创面,对照组2只猪4个创面,创面均为10cm×6cm,实验组创面用自制持续皮肤牵张器行皮肤伸展术治疗,对照组创面自行愈合。结果：实验组与对照组每日创面缩小面积相差较多,差异有统计学意义,实验组皮肤缺损行5-6天皮肤伸展术治疗后,可直接行二期缝合关闭,对照组1周后仍存在较大皮肤缺损,无法缝合关闭。结论：应用自制持续皮肤牵张器行皮肤伸展术,可以早期快速闭合皮肤创面。自制持续皮肤牵张器克服了以往牵张器的不足,具有使用方便,效果可靠,并发症少等优点,有良好的应用前景。     

皮瓣移植结合骨牵张技术修复感染性胫骨复合皮肤组织缺损的临床效果观察

目的：观察皮瓣移植结合骨牵张技术修复感染性胫骨复合皮肤组织缺损的临床效果。方法：自2008年6月至2012年6月,共收治了胫骨感染性复合组织缺损16例,采用一期彻底去除病变坏死组织和病变的胫骨断端,切取同侧腓肠肌皮瓣、腓肠神经营养血管皮瓣转位、对侧小腿内侧皮瓣和游离皮瓣移植修复小腿皮肤缺损,二期行骨牵张延长术进行治疗。结果：所有16例胫骨复合组织缺损病例感染均得到了控制,移植的皮瓣顺利成活,胫骨截骨延长区成骨良好,断端骨愈合,其中2例出现针道感染,无血管神经并发症发生。骨延长2～9cm,平均延长5．5cm。外同定延长支架在停止骨延长8-20个月后拆除,双下肢等长,膝关节和踝关节功能良好。术后细菌培养＋药敏结果：金黄色葡萄球菌感染8例,表皮葡萄球菌感染4例,大肠杆菌感染1例,阴沟肠杆菌感染l例,肠球菌感染l例。结论：伤口彻底清创,胫骨断端坏死骨切除后一期行皮瓣移植,二期行骨牵张延长术是一种治疗感染性胫骨复合组织缺损的有效方法。     

Using birth defects registry data to evaluate infant and childhood mortality associated with birth defects: an alternative to traditional mortality assessment using underlying cause of death statistics

BACKGROUND: Although birth defects are a leading cause of death in infancy and early childhood, the proportion of all deaths to children with clinically diagnosed birth defects is not well documented. The study is intended to measure the proportion of all deaths to infants and children under age 10 occurring to children with birth defects and how and why this proportion differs from the proportion of deaths due to an underlying cause of congenital anomalies using standard mortality statistics. METHODS: A linked file of Michigan livebirths and deaths was combined with data from a comprehensive multisource birth defects registry of Michigan livebirths born during the years 1992 through 2000. The data were analyzed to determine the mortality rate for infants and children with birth defects and for children with no reported birth defect. Mortality risk ratios were calculated. The underlying causes of death for children with birth defects were also categorized and compared to cause- specific mortality rates for the general population. RESULTS: Congenital anomalies were the underlying cause of death for 17.8% of all infant deaths while infants with birth defects were 33.7% of all infant deaths in the study. Almost half of all Michigan deaths to children aged 1 to 2 were within the birth defects registry, though only 15.0% had an underlying cause of death of a congenital anomaly based upon standard mortality statistics. The mortality experience among children with birth defects was significantly higher than other children throughout the first 9 years of life, ranging from 4.6 for 5 year olds to 12.8 for children 1 to 2. Mortality risk ratios examined by cause of death for infants with birth defects were highest for other endocrine (28.1), other CNS (28.1), and heart (21.9) conditions. For children 1 through 9, the highest differential risk was seen for other perinatal conditions (39.0), other endocrine (29.7), other CNS (24.5), and heart (21.4). CONCLUSIONS: Childhood mortality analyses that incorporate birth defects registry data provide a more comprehensive picture of the full burden of birth defects on mortality in infant and children and can provide an effective mechanism for monitoring the survival and mortality risks of children with selected birth defects on a population basis.     

Laterality patterns in infants with external birth defects.

The lateral distribution of external birth defects has not been reported in a comprehensive way, and patterns in this distribution have not been examined. This study presents the lateral distribution of 6,390 unilateral defects from among 102 defect categories in data collected by the Metropolitan Atlanta Congenital Defects Program. Among all defects, 49% (95% CI 48-51%) were right-sided. Among males and females, 51% (95% CI 50-53%) and 47% (95% CI 46-49%) of the defects, respectively, were right-sided. Of the 102 defect types, 57 had an excess of defects on the right side of the body; 39 had an excess of defects on the left side; and 6 were equally distributed. The excess on the right side was statistically significant for inguinal hernia, incarcerated inguinal hernia, microtia, preauricular sinus, talipes calcaneovalgus, and lambdoidal craniosynostosis. For the left side, the excess was statistically significant for preauricular tags, cleft lip, fused lip and cleft gum, cleft lip with cleft palate, congenital hip dysplasia, unstable hip, absent forearm or hand, anomaly of the knee, and skin tags. The percentage of right-sided defects among case subjects with unilateral defects was correlated with the percentage of males among all case subjects (r = 0.24, P < 0.05). Among male case subjects with unilateral defects, the correlation coefficient was 0.31 (P < 0. 01), and among females with unilateral defects, it was 0.11 (P > 0. 10). Differences in the lateral distribution of specific birth defects may be due to subtle differences in morphogenesis on the left and right sides of the embryo brought about by establishment of left-right asymmetry prior to organogenesis. The fact that more defect categories were right-sided than left-sided may be related to the observation that mitochondrial maturation in rat embryos is delayed on the right side. The right side, therefore, may be more susceptible than the left to defects caused by prenatal hypoxia. The significant correlation between the percentage right-sided and percentage male may then also be related to the observation that male sex hormones lower the mitochondrial respiration rate in rats and increase rat sensitivity to chemical hypoxia. Investigators should consider reporting the laterality of specific defects in both laboratory and epidemiological studies of birth defects. Right- and left-sided defects should perhaps be considered separately in etiologic studies of birth defects. Teratology 60:265-271, 1999. Published 1999 Wiley-Liss, Inc.     

Common congenital anomalies: Environmental causes and prevention with folic acid containing multivitamins

Congenital anomalies, congenital defects, or birth defects are significant causes of death in infants. The most common congenital defects are congenital heart defects (CHDs) and neural tube defects (NTDs). Defects induced by genetic mutations, environmental exposure to toxins, or a combination of these effects can result in congenital malformations, leading to infant death or long‐term disabilities. These defects produce significant mortality and morbidity in the affected individuals, and families are affected emotional and financially. Also, society is impacted on many levels. Congenital anomalies may be reduced by dietary supplements of folic acid and other vitamins. Here, we review the evidence for specific roles of toxins (alcohol, cigarette smoke) in causing common severe congenital anomalies like CHDs, NTDs, and ocular defects. We also review the evidence for beneficial effects for dietary supplementation, and highlight gaps in our knowledge, where research may contribute to additional benefits of intervention that can reduce birth defects. Extensive discussion of common severe congenital anomalies (CHDs, NTDs, and ocular defects) illustrates the effects of diet on the frequency and severity of these defects. Birth Defects Research (Part C) 108:274–286, 2016. © 2016 Wiley Periodicals, Inc.     

Sensitivity, specificity, and positive predictive value of multiple malformations in isotretinoin embryopathy surveillance

Isotretinoin causes serious birth defects in about 25% of babies exposed in the first trimester of pregnancy. Despite warnings about the drug's teratogenicity, cases of isotretinoin embryopathy continue to occur; more than 80 such cases have been reported since 1982. The true magnitude of the problem is unknown, however, and case estimates range to more than 1,000. The need for isotretinoin embryopathy (IE) surveillance is therefore great. Sixty-one known cases were evaluated to determine the sensitivity (proportion of cases with a given defect pattern) of various defect combinations. Using data from the Metropolitan Atlanta Congenital Defects Program for the period before isotretinoin was available, we evaluated the specificity (proportion of malformed infants without exposure who do not have the pattern of defects) for the various defect combinations. Ear malformations (microtia, anotia, absence or stricture of auditory canal, missing pinnae) have an associated sensitivity of 70.5% and a specificity of 99.5%. Ear defects combined with central nervous system (CNS) defects (microcephalus, hydrocephalus, reduction deformities of the brain) and cardiovascular (CVS) defects (conotruncal defects, aortic arch abnormalities) have an associated sensitivity of 19.7% and a specificity of 100.0%. The case definition of ear defects combined with either CNS or CVS defects maximizes both specificity (99.9%) and sensitivity (45.9%). The investigators are now evaluating the feasibility of using this pattern of defects to monitor for IE within a national monitoring program.     

Behaviour of DNA-RNase A complex in the presence of formaldehyde]

A formaldehyde-produced fixation of defects caused by a despiralizing action of a protein was studied in the case of DNA-RNAase A complex. The concentration of the defects fixed was measured by kinetic formaldehyde method (KF-method). It was shown that following processes take place in the complex in the presence of formaldehyde: (a) fixation of defects; (b) unwinding of DNA; (c) inactivation of the protein. The rates of all these processes depend on the concentration of formaldehyde, phi. At formaldehyde concentrations above some critical value phic the protein is inactivated before the defects are fixed. At phi less than phic the protein inactivation proceeds more slowly than the fixation of defects; at sufficiently low formaldehyde concentration no inactivation of protein occurs practically during the fixation time (20 min). The number of new defects formed during the time of fixation is linear with the formaldehyde concentration in the region where no inactivation of the protein occurs. Therefore the initial concentration of defects can be determined through an extrapolation to zero concentration of formaldehyde. On the basis of the data obtained a method is proposed for the evaluation of the number of defects in DNA caused by the despiralizing action of proteins. A model is proposed describing the behaviour of the complexes of DNA with despiralizing proteins in the presence of formaldehyde.     

VEGF: a modifier of the del22q11 (DiGeorge) syndrome?

Hemizygous deletion of chromosome 22q11 (del22q11) causes thymic, parathyroid, craniofacial and life-threatening cardiovascular birth defects in 1 in 4,000 infants. The del22q11 syndrome is likely caused by haploinsufficiency of TBX1, but its variable expressivity indicates the involvement of additional modifiers. Here, we report that absence of the Vegf164 isoform caused birth defects in mice, reminiscent of those found in del22q11 patients. The close correlation of birth and vascular defects indicated that vascular dysgenesis may pathogenetically contribute to the birth defects. Vegf interacted with Tbx1, as Tbx1 expression was reduced in Vegf164-deficient embryos and knocked-down vegf levels enhanced the pharyngeal arch artery defects induced by tbx1 knockdown in zebrafish. Moreover, initial evidence suggested that a VEGF promoter haplotype was associated with an increased risk for cardiovascular birth defects in del22q11 individuals. These genetic data in mouse, fish and human indicate that VEGF is a modifier of cardiovascular birth defects in the del22q11 syndrome.     

Composite hyaluronate-type I collagen-fibrin scaffold in the therapy of osteochondral defects in miniature pigs

The potential of novel scaffold containing sodium hyaluronate, type I collagen, and fibrin was investigated in the regeneration of osteochondral defects in miniature pigs. Both autologous chondrocyte-seeded scaffolds and non-seeded scaffolds were implanted into two defects located in the non-weight-bearing zone of the femoral trochlea (defect A was located more distally and medially, defect B was located more proximally and laterally). Control defects were left untreated. Twelve weeks after the operation, the knees were evaluated in vivo using MRI. Six months after the implantation, the defects were analyzed using MRI, histological, and immunohistochemical analysis. In the A defects of chondrocyte-seeded scaffold group, hyaline cartilage and fibrocartilage was formed, containing type II collagen, acidic and neutral glycosaminoglycans while the non-seeded scaffold group was predominantly filled with fibrocartilage. Defects in the control group were predominantly filled with fibrous tissue. Histomorphometric analysis of photomicrographs revealed a significantly higher amount of hyaline cartilage in the cell-seeded scaffold group in A defects than in other groups. Both scaffold groups in A defects showed significantly less fibrous tissue than cell-seeded defects B and the control group. Both histological and MRI analysis proved that the novel composite scaffold has a potential to regenerate osteochondral defects within six months.     

Limb reduction defects in over one million consecutive livebirths

Limb reduction defects occurring among 1,213,913 consecutive livebirths in British Columbia during the period 1952-1984 inclusive were reviewed. A total of 659 cases of limb reduction defects were identified, 393 of them involving the long bones and 190 of them more than one limb. The time period 1966-1984, during which ascertainment was consistent, was evaluated, and an incidence of 5.97 per 10,000 livebirths (1 in 1,692 live births) was found. The data were evaluated for trends over time, sex ratio, and regional and ethnic distribution. Associated anomalies of other organ systems in these cases were analyzed, and overall about one-half of the cases have additional defects. The majority of these additional defects affect the musculoskeletal system and include such entities as clubfoot, hip dislocation, and congenital contractures. Defects are also frequent in other organ systems, such as the cardiovascular, gastrointestinal, and genitourinary systems. By far the most common limb defects are terminal longitudinal defects then terminal transverse defects. Of all cases of limb defects, 75% are upper limb and 25% lower limb. We found no evidence that one side is affected more frequently. About 6.5% of cases had another family member registered with a skeletal defect; 12.9% of cases died within the first year of life, the majority (85%) of those dying having additional defects. Etiological considerations are discussed for some subgroups.(ABSTRACT TRUNCATED AT 250 WORDS)     

A classification system and reconstructive algorithm for acquired vaginal defects

Although multiple flaps have been used for vaginal reconstruction, a logical approach to reconstruction of these often complex defects has not been described. The objective of this study was to establish a classification system for acquired vaginal defects and to develop a reconstructive algorithm derived from this system. This study is a retrospective review of a 7-year experience with 51 flaps in 37 consecutive vaginal reconstructions. Twenty-two partial defects and 15 circumferential defects were reconstructed in 35 patients. Average patient age was 48 years (range, 19 to 69 years). Of the 22 patients with partial vaginal defects, six involved primarily the anterior and lateral wall and 16 the posterior vaginal wall. Among the 15 patients with circumferential defects, four included only the upper two-thirds of the vagina and 11 encompassed the entire vagina. On the basis of these defects, a classification system was developed. Partial defects involving the anterior or lateral vaginal wall were classified as type IA defects and were reconstructed primarily with pedicled Singapore fasciocutaneous flaps. Partial defects involving the posterior wall were classified as type IB and were reconstructed with pedicled rectus abdominis myocutaneous flaps. Circumferential defects involving the upper two-thirds of the vagina were classified as type IIA defects and were reconstructed with a rolled rectus flap or, less commonly, sigmoid colon (one patient). Total circumferential defects, type IIB, were reconstructed largely with bilateral gracilis flaps. Six patients had major complications, including one perioperative death, one complete flap loss, one partial flap loss, and three pelvic abscesses. Three patients had minor complications that included delayed wound healing and donor-site infection. Vaginal defects can be categorized into one of four types on the basis of the location and extent of resection. Flap selection is determined on the basis of the type of defect. Using this algorithm, immediate vaginal reconstruction with pedicled regional flaps can be performed with minimal patient morbidity and few surgical complications.