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Special Feature
February 1998

Pathological Case of the Month

Author Affiliations

Copyright 1998 American Medical Association. All Rights Reserved. Applicable FARS/DFARS Restrictions Apply to Government Use.1998

Arch Pediatr Adolesc Med. 1998;152(2):200. doi:
Diagnosis and Discussion: Turquoise Discoloration of the Umbilical Cord and Membranes After Intra-amniotic Injection of Indigo Carmine Dye for Premature Rupture of Membranes

Figure 1. Turquoise discoloration of the umbilical cord.

Figure 2. Turquoise discoloration of the fetal surface of the placenta.

Figure 3. Histological appearance of the necrotizing acute chorioamnionitis (hematoxylin-eosin, original magnification ×100).

Figure 4. Clusters of polymorphonuclear leukocytes in the airspaces are suggestive of amniotic fluid infection syndrome (hematoxylin-eosin, original magnification ×100).

Diagnosis of premature rupture of membranes (PROM) must be considered in pregnant patients who complain of watery vaginal discharge. A vaginal pool or obvious leakage of fluid from the cervix is strong evidence supporting PROM. The fluid can be tested for "ferning" or its neutral or alkaline pH checked with phenaphthazine (Nitrazine Paper). The diagnosis is more complicated when amniotic fluid is absent. Some instances call for invasive techniques such as transabdominal injection of a dye (indigo carmine, Evans blue, fluorescein) into the amniotic cavity. A tampon in the vagina can be used to document subsequent leakage in cases of PROM. Methylene blue should not be used because it may cause fetal methemoglobinemia.1,2 Indigo carmine was used in this patient and produced the turquoise discoloration in the surface membranes of the umbilical cord and placenta. Inflammation may have enhanced the adsorption of the dye to these surfaces.

Spontaneous rupture of membranes often leads to the onset of labor. If labor begins shortly after PROM, management issues are simple. "Prolonged PROM" implies a latency period longer than 24 hours. The prevalence of PROM is about 2% to 3.5% before 37 weeks' gestation. Despite this apparently low prevalence in preterm gestation, 30% to 40% of preterm neonates are born to women who have PROM—making PROM the leading identifiable cause of preterm delivery.3

The overall prevalence of positive bacterial amniotic fluid cultures in women who have PROM is 28.5%.3 Patients with microbial invasion of the amniotic cavity are more likely to have chorioamnionitis, endometritis, and neonatal sepsis than patients who have a negative amniotic fluid culture on admission. Microorganisms isolated from the amniotic fluid of women with PROM are similar to those normally found in the lower genital tract. Mycoplasmas (Ureaplasma urealyticum and Mycoplasma hominis) are the most frequent isolates, followed by Streptococcus agalactiae (group B streptococcus), Fusobacterium, and Gardnerella vaginalis.3

Haemophilus influenzae organisms are uncommon in the female genital tract. An estimated 0.8% to 1% of all pregnant women harbor H influenzae. Serotyping has disclosed that from 6% to 20% of perinatal H influenzae infections are due to type b and rarely type c.4 The scarcity of fetal and neonatal infections due to H influenzae types b and c has been attributed to the protection provided by the mother's passively transferred anticapsular antibody. Most of the remaining H influenzae are nonencapsulated organisms and therefore "nontypable" by serologic tests. Various chemical reactions provide separation into biotypes. All the biotypes (1-8) are capable of producing maternal and perinatal infections.5 Among 45 cases of neonatal H influenzae sepsis reviewed by Friesen and Cho,6 the overall mortality rate was 5.5%; it was 90% for 20 infants of gestational age younger than 30 weeks. In most infants with H influenzae sepsis, acute chorioamnionitis is present but it may be mild even in the fatal cases. Funisitis and villitis are not consistently seen, but these lesions are associated with fulminant and fatal cases.5

Accepted for publication February 1, 1997.

Corresponding author: Halit Pinar, MD, Department of Pathology and Laboratory Medicine and Pediatrics, Women & Infants Hospital of Rhode Island, 101 Dudley St, Providence, RI 03905-2499.

Cowett  RMHakanson  DOKocon  RWOh  W Untoward neonatal effect of intra-amniotic administration of methylene blue.  Obstet Gynecol. 1976;48 ((suppl)) 74s- 75sGoogle Scholar
Troche  BI The methylene blue baby.  New Engl J Med. 1989;3201756- 1757Google Scholar
Romero  RQuintero  ROyarzun  E  et al.  Intra-amniotic infection and the onset of labor in preterm rupture of membranes.  Am J Obstet Gynecol. 1988;159661- 666Google ScholarCrossref
Wallace  RJBaker  CJQuinones  FJ  et al.  Non-typable H influenza (biotype 4) as a neonatal, maternal and genital pathogen.  Rev Infect Dis. 1983;5123- 136Google ScholarCrossref
Campognone  PSinger  DB Neonatal sepsis due to nontypable H influenza AJDC. 1986;140117- 121Google Scholar
Friesen  CACho  CT Characteristic features of neonatal sepsis due to H influenza Rev Infect Dis. 1986;8777- 781Google ScholarCrossref