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Placenta praevia percreta with silent uterine incomplete rupture complicated with puerperal haemolytic-uremic syndrome

2006; Elsevier BV; Volume: 131; Issue: 1 Linguagem: Inglês

10.1016/j.ejogrb.2006.01.033

1872-7654

Dubravko Habek, Davor Petrović, Dražen Vidović, Goran Gudelj,

Electrolyte and hormonal disorders

Invasive malplacentation may occur in three forms, i.e. placenta accreta (78%), increta (17%) and percreta (5%), and is defined as invasive trophoblast penetration of deep uterine structures with possible invasion of other anatomical structures. It may occur as total (diffuse), partial, or focal invasive malplacentation. Placenta percreta is the most severe form of invasive malplacentation with trophoblast tissue penetration through the myometrium to the serosa [ [1] Morken N.H. Henriksen H. Placenta percreta—two cases and review of the literature. Eur J Obstet Gynecol Reprod Biol. 2001; 100: 112-115 Abstract Full Text Full Text PDF PubMed Scopus (47) Google Scholar ]. We report on a case of diffuse placenta previa percreta (PPP) with silent uterine rupture at the site of invasive malplacentation and development of puerperal hemolytic-uremic syndroma (HUS). A 37-year-old woman, gravida V, para V, of poor socioeconomic status, otherwise healthy, chronic smoker, was admitted to the emergency service for massive painless vaginal bleeding in the 35th week of uncontrolled pregnancy. Previous pregnancies and deliveries were normal. Obsolete prophylactic tocolysis with intravenous ritodrine (gestational age >34 weeks and the resulting vasodilation in the pelvic area may in fact have worsened bleeding) and volume replacement with Ringer's lactate 1000 mL were immediately performed in the prehospital emergency ward. Blood pressure 95/65, c.p. 100/min. Cardiotocography without uterine activity, narrowed undulating reactive curve (10–15 bpm), basal frequency 120/min, without decelerations. Speculum examination revealed an abundance of fresh and clotted blood in the vagina, soft uterus. Ultrasonography indicated total placenta previa with suspected invasive malplacentation, breech presentation of the fetus, normal fetal heart rate, normal amniotic fluid index and fetus biometrically for 34/35 weeks of pregnancy. Colour Doppler and magnetic resonance were not performed for technical reasons. Because of unceasing massive bleeding, urgent primary cesarean section was performed in endotracheal anesthesia. Laparotomy revealed a very thin lower uterine segment in the isthmus region, with bluish translucency through the peritoneum and incomplete, 4-cm rupture of the uterus. Upon removal of peritoneal tunica serosa, the rupture opening was expanded by fingers to provide access to fetal legs, whereby a live female newborn, 2800 g/44 cm, Apgar score 7/9, was successfully extracted. Upon placenta removal, placental growth up to the serosa was observed, allowing the lower uterine segment serosa to be palpated below and around the incomplete uterine rupture, and on the posterior uterine wall. There was abundant bleeding from the floor of the placenta, with atonic uterus. Uterotonics were prescribed, i.e. syntocinon 10 UI intramyometrically and 20 UI in infusion; methylergonovine 0.2 mg i.v. and 0.2 mg intramyometrically and Carboprost 2 × 250 μg into the myometrium. Uterine atony persisted, the lower uterine segment was soft, with abundant hemorrhage. Because of placenta percreta and uterine atony and multiparity, total hysterectomy was performed with preservation of the adnexa and drainage of the pelvic cavity. Intraoperative laboratory findings: erythrocytes 2.5 × 109, hemoglobin 71 g/L, haematocrit 0.21, platelets 198 × 106, fibrinogen 2.3 g/L. The patient was transfused with 1200 mL packed erythrocytes and fresh frozen plasma, and 2500 mL crystalloid and colloid solution. Early postoperative laboratory data (haemogram, coagulation, jonogram) were in reference value. On postoperative day 7, febrile state up to 38 °C and oliguria (<400 mL urine/24 h) occurred. On postoperative day 8, petechiae appeared on the skin, along with mild enterorrhagia and macrohematuria. Laboratory findings: thrombocytopenia (platelets 72 × 106), hemolytic anemia (erythrocytes 1.7 × 109, hemoglobin 61 g/L, bilirubin 80 mmol/L); acute renal insufficiency (urea 85 mmol/L, creatinine 420 μmol/L, potassium 5.4 mmol/L) and metabolic acidosis; fragmentocytes in peripheral blood smear. Blood culture, cervical swab and urinary culture were sterile. The diagnosis of HUS was made, and the puerpera was transferred to intensive care unit for further treatment. There she was treated with plasmapheresis, methylprednisolone, and low molecular heparin. Upon nephrologic management, the patient was discharged from the hospital in good general condition, 2 months after the cesarean section, free from HUS complications. The newborn showed normal psychomotor development. The histopathologic diagnosis indicated trophoblast invasion throughout the uterine layers and serosa (PPP).