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Year : 2006  |  Volume : 24  |  Issue : 4  |  Page : 283-285

The clinical and microbiological correlates of premature rupture of membranes

1 Department of Obstetrics and Gynecology, Holdsworth Memorial Hospital, Mysore - 570 021, Karnataka, India
2 Division of Epidemiology, University of California, Berkeley, USA
3 Division of Microbiology, Christian Medical College, Vellore - 632 014, India

Date of Submission18-Mar-2006
Date of Acceptance21-Jun-2006

Correspondence Address:
C Karat
Department of Obstetrics and Gynecology, Holdsworth Memorial Hospital, Mysore - 570 021, Karnataka
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0255-0857.29388

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 ~ Abstract 

Prematurity is the cause of 85% of neonatal morbidity and mortality. Premature rupture of the membranes (PROM) is associated with 30-40% of preterm deliveries. A case-control study conducted between July 2002 and 2003 examined the correlates and risk factors for PROM in Mysore, India. WBCs in vaginal fluid, leucocytes in urine, UTI and infection with E . coli , S . aureus , C. albicans and BV were significantly associated with PROM. BV, E. coli and WBCs in vaginal fluid were independent risk factors. Screening and treatment of BV and E. coli infection in pregnancy may reduce the risk of PROM.

Keywords: Case control study, prematurity, PROM

How to cite this article:
Karat C, Madhivanan P, Krupp K, Poornima S, Jayanthi N V, Suguna J S, Mathai E. The clinical and microbiological correlates of premature rupture of membranes. Indian J Med Microbiol 2006;24:283-5

How to cite this URL:
Karat C, Madhivanan P, Krupp K, Poornima S, Jayanthi N V, Suguna J S, Mathai E. The clinical and microbiological correlates of premature rupture of membranes. Indian J Med Microbiol [serial online] 2006 [cited 2020 Sep 25];24:283-5. Available from:

Preterm premature rupture of the fetal membranes (PROM) is associated with 30-40% of premature births and is an important cause of perinatal morbidity and mortality.[1] It has been estimated that 10% of perinatal deaths are directly or indirectly attributable to PROM.[2] Limited data are available for India,[3],[4] but studies from other parts of the world have shown the etiology of the condition to be multifactorial.[5],[6] Infection has been cited as a major cause of membrane damage.[7],[8]

There is growing evidence associating upper genital tract infections with PROM.[9],[10] One possible mechanism by which infections might act is through ascension from the cervical/vaginal area and replication in the placenta, the decidua and the membranes. Another hypothesis is that several organisms that are commonly present in the vaginal flora, including group B streptococci, S. aureus and microorganisms that cause BV, secrete proteases that degrade collagen and weaken the fetal membranes leading to PROM.[11],[12] Researchers have postulated that PROM may be the result of direct bacterial insults that necrotize tissue leading to host-mediated auto destruction.[13]

The purpose of this study was to evaluate the risk factors and correlates for PROM in women presenting with premature rupture of membranes at a tertiary care hospital in Mysore, South India.

 ~ Materials and Methods Top

A hospital-based case-control study of 150 patients presenting with PROM at greater than 31 weeks of gestation and 150 controls matched for age, gestational age and parity, was conducted between July 2002 and 2003 at Holdsworth Memorial Hospital, Mysore, South India.

The inclusion criteria were gestational age > 31 weeks; diagnosis of PROM confirmed by clinical finding of posterior vaginal pool, vaginal pH or ferning; cervical dilation of < 3 cms; singleton pregnancy; and clear liquor. Exclusion criteria included: woman in labour; mal-presentations; multiple gestation; medical disorders; and a history of cervical encirclage.

The Committee for Protection of Human Subjects at C.S.I. Holdsworth Memorial Hospital approved the study. Data were collected from all eligible participants who gave informed consent. A structured questionnaire collected data on sociodemographic and medical variables. Collected biological specimens included liquor from the posterior fornix of the vagina and midstream urine. Dipstick urinalysis was performed (Multistix 10SG, Bayer Diagnostics). If nitrites and leucocytes were found in the urine analysis, that patient's urine was also sent for culture.

Vaginal fluids were cultured on three primary culture media: blood, chocolate and McConkey agar. Cultures were incubated at 37oCelsius for 24 hours. Gram stain was done for diagnosis of BV using Nugent's score.

Data were entered in MS Excel and analyzed using Stata 8.0 (Stata Corporation, College Station, TX). The primary outcome was PROM, analyzed as a binomial variable. In univariate analysis, c 2sub test and Fischer's exact test were used to assess the associations between PROM and categorical variables and t -test and the Wilcoxon rank sum test were used for continuous variables. Likelihood-ratio tests were used to determine the statistical significance of each variable. Associations, measured as odds ratio (OR) and adjusted for relevant confounding factors, were estimated using multivariate conditional logistic regression analysis. In the first model, independent risk factors for PROM were identified. Variables significantly associated with PROM were tested and retained if they remained significantly associated with the outcome ( P 0.05) after inclusion of other potential predictors. All confidence intervals were calculated at the 95% level.

 ~ Results Top

About 23% of the study cases were unbooked as compared to 17% of the controls. Rates of PROM positively correlated with women residing in rural areas, unbooked status and coming from a lower socio-economic background [Table - 1]. Fifty-eight cases (39%), as compared to 22 controls (14%), had WBCs in their vaginal fluid indicating presence of genital tract infection. Overall, 6% of cases had urinary tract infections at the time of admission, as compared to 2% of controls. Close to a third (n=56) of the cases reported having coitus in the past week as compared to 49 controls. The detection of BV and presence of E . coli or S. aureus were significantly associated with occurrence of PROM. Five women with PROM reported a previous history of PROM as compared to only one control. Although four cases of Group B streptococcus and four of P. mirabilis were detected, none of the controls had either infection.

Logistic regression analysis showed [Table - 2] a significant positive association between increased WBCs in the vaginal fluid (OR: 3.67; 95% CI: 2.09, 6.4), leucocytes in the urine (OR: 6.43; 95% CI: 1.4, 29.3), prior history of urinary tract infections (OR: 3.5; 95% CI: 1.05, 14.9), detection of BV (OR: 10.5, 95% CI: 3.5, 31.5), presence of E. coli (OR: 7.5; 95% CI: 2.8, 20.0), S. aureus (OR: 2.8; 95% CI: 1.24, 3.6) and subsequent occurrence of PROM.

In multivariate analysis, BV, E. coli or WBCs detected in vaginal fluid were all independent risk factors for being diagnosed with PROM. Interestingly, Candida infection was protective for PROM (a OR: 0.20; 95% CI: 0.07, 0.5).

 ~ Discussion Top

To the best of our knowledge, this is the first study exploring the risk factors and correlates for PROM in India. Interventions for prevention of PROM will have large public health implications here where less-than-optimal care and nutrition are observed during pregnancy. Studies have shown that malnourished women having decreased level of host defense factors regularly present in amniotic fluid so infectious agents such as E. coli and S. aureus may play a larger role.

Although it is widely agreed that PROM is multifactorial, findings from this study show that exogenous risk factors such as UTI, BV, E. coli and S. aureus are significantly associated with the condition. It remains to be seen whether these are a direct cause of PROM or are simply surrogate markers for another not yet identified pathogenic process.

Although the results of the study reinforce the notion that early detection and aggressive treatment of lower reproductive tract infections may lead to better outcomes in women at risk for PROM, there is still a great deal of research needed to fully explicate the biologic processes of the fetal membranes, especially with regards to exogenous risk factors such as nutritional deficiencies and infection.

 ~ References Top

1.Parry S, Strauss JF 3rd. Premature rupture of the fetal membranes. N Engl J Med 1998; 338 :663-70.  Back to cited text no. 1  [PUBMED]  [FULLTEXT]
2.Allen SR. Epidemiology of premature rupture of the fetal membranes. Clin Obstet Gynecol 1991; 34 :685-93.  Back to cited text no. 2  [PUBMED]  
3.Mathew R, Kalyani J, Bibi R, Mallika M. Prevalence of bacterial vaginosis in antenatal women. Indian J Pathol Microbiol 2001 ;44 :113-6.  Back to cited text no. 3    
4.Purwar M, Ughade S, Bhagat B, Agarwal V, Kulkarni H. Bacterial vaginosis in early pregnancy and adverse pregnancy outcome. J Obstet Gynaecol Res 2001; 27 :175-81.  Back to cited text no. 4  [PUBMED]  
5.Philip J. Etiology of pPROM. Obstet Gynecol Clin North Am 1992; 19 :251-63.  Back to cited text no. 5    
6.Spinillo A, Nicola S, Piazzi G, Ghazal K, Colonna L, Baltaro F. Epidemiological correlates of preterm premature rupture of membranes. Int J Gynaecol Obstet 1994; 47 :7-15.  Back to cited text no. 6  [PUBMED]  
7.Riedewald S, Kreutzmann IM, Heinze T, Saling E. Vaginal and cervical pH in normal pregnancy and pregnancy complicated by preterm labor. J Perinat Med 1990; 18 :181-6.  Back to cited text no. 7  [PUBMED]  
8.Duff P. Management of premature rupture of membranes in term patients. Clin Obstet Gynecol 1991; 34 :723-9.  Back to cited text no. 8  [PUBMED]  
9.Goldenberg RL, Hauth JC, Andrews WW. Intrauterine infection and preterm delivery. N Engl J Med 2000; 342 :1500-7.  Back to cited text no. 9  [PUBMED]  [FULLTEXT]
10.Gibbs RS, Romero R, Hillier SL, Eschenbach DA, Sweet RL. A review of premature birth and subclinical infection. Am J Obstet Gynecol 1992; 166 :1515-28.  Back to cited text no. 10  [PUBMED]  
11.McGregor JA, French JI, Lawellin D, Franco-Buff A, Smith C, Todd JK. Bacterial protease-induced reduction of chorioamniotic membrane strength and elasticity. Obstet Gynecol 1987; 69 :167-74.  Back to cited text no. 11  [PUBMED]  
12.Draper D, Jones W, Heine RP, Beutz M, French JI, McGregor JA. Trichomonas vaginalis weakens human amniochorion in an in vitro model of premature membrane rupture. Infect Dis Obstet Gynecol 1995; 2 :267-74.  Back to cited text no. 12    
13.Polzin WJ, Brady K. Mechanical factors in the etiology of premature rupture of the membranes. Clin Obstet Gynecol 1991; 34 :702-14.  Back to cited text no. 13  [PUBMED]  


[Table - 1], [Table - 2]

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