Primigesta, 22 years old, without morbid history, controlled since 7 weeks; normal physical examination, BP 110/70 mmHg; normal prenatal tests and ultrasound compatible with 7 weeks of pregnancy, according to the date of last menstrual period
Man/60 regular controls at 11, 15 and 19 weeks of pregnancy, maintaining BP range 100-110-70 mmHg.
She had 20 + 5 weeks of pregnancy due to bilateral deaf low back pain of 4 h duration associated with dysuria and fever.
On admission, BP 130/85 mmHg, heart rate 86 per min and temperature 37.8 °C normal physical appearance were detected, except for bilateral positive percussion.
Urine sediment showed leukocytes 15-20 and bacteria ++, hematocrit 35.8%, leukocytes 13800 mm3 without left shift, platelets 70,400 mm3; CRP 12 mg/dl, amylase, normal renal function.
She was hospitalized with a diagnosis of acute pyelonephritis and started intravenous antibiotic treatment with clindamycin and gentamicin.
The patient presented with malaise, normal blood pressure, mild pain in upper hemiabdomen, without physical examination findings.
After 24 h from admission, the tests showed hematocrit 32.9% with schistocytes smears, platelets 59,100 mm3, GPT 402 U/L, GOT 32 U/L alkaline pelvis, acid septa.
Obstetric ultrasound: single fetus, normal amniotic fluid, placenta normoinsesis, biometry concordant with 201⁄2 weeks; the anatomical evaluation highlights a cleft lip and palate and the rest normal.
Umbilical artery Doppler with fetal cardiac beats (FLC) at 140 per min, intermittent absent diastolic flow ( pulsatility index (PI) 1.62); venous duct showed increased resistance to bilateral artery (PI 1.49,t).
At 48 h after admission, the analyses were: negative urocultiva (antibiotic treatment was discontinued), proteinuria 440 mg/24 h, creatinine clearance 120 ml/min. With this background we postulate the persistence of severe preeclampsia PALPES).
The patient presented normotendinous remission, with abdominal pain, normal osteotendinous reflexes and laboratory tests with a paulatin decrease in hematocrit and platelets, associated with progressive increase of liver enzymes and elevation of serum creatinine.
Given the laboratory evolution, with a 21 + 2 week pregnancy, the diagnosis of HELLP syndrome was confirmed.
Conservative management with maternal surveillance was decided to try to achieve fetal viability and the initiation of dexamethasone was planned (which was finally not administered).
However, on the fifth day the absence of FCL (fetal death in uterus) was observed.
An abortion was induced with magnesium sulfate misoprostaxis under continuous infusion of magnesium sulfate (5 g load and 1 g/h administered subcutaneously 24 h after abortion).
A male dead fetus, 310 grams, left cleft lip and palate, without other evident malformations was obtained.
Placenta 260 g, normal appearance.
An instrumental review was performed in the operating room.
By platelet count 32600/mm3, 6U platelets were transfused with a control count of 53,500/mm3.
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The patient was placed in good general conditions, asymptomatic, always normotensive, with improvement of laboratory parameters.
She was discharged on the fourth day after abortion.
During outpatient follow-up at 11 days postpartum, the patient was normotensive (PA 108/74), 24-h proteinuria was negative.
Placental biopsy reported extensive zone of hemorrhagic infarction (30% of total mass).
