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Biomedical subjects

N M Fisk

Publications and source records attributed to N M Fisk.

At least 163 records · Page 9Linked to original sources

Prenatal determination of human platelet antigen type using DNA amplification following amniocentesis.

OBJECTIVES: To demonstrate that fetal human platelet antigen (HPA1) type can be determined, without the need for fetal blood sampling, by amplification of fetal DNA from amniotic fluid cells using polymerase chain reaction and allele specific oligonucleotide hybridisation. DESIGN: Oligonucleotide DNA primers were designed to amplify a portion of the platelet glycoprotein GpIIIa gene which spans the site of the single base change which differentiates HPA1a from HPA1b. Specific oligonucleotides were designed to hybridise either to the amplified HPA1a allele or to the HPA1b allele. Amniotic cells were used as the DNA template both directly and following formal isolation of DNA. Fetal HPA1 type, determined by this method in fifteen pregnancies not at risk of perinatal alloimmune thrombocytopaenia, was compared to typing of fetal blood obtained following cordocentesis. The methodology was then used to HPA type the fetus in two pregnancies at risk of the disease. SETTING: Department of Molecular Biology and Centre for Fetal Care, Queen Charlotte's Hospital. SUBJECTS: Fifteen women undergoing amniocentesis and fetal blood sampling for other indications and two women at risk of perinatal allo-immune thrombocytopaenia whose partners were heterozygotes. RESULTS: In the 15 control cases and the two clinical cases, determination of fetal HPA1 type from amniotic fluid cells agreed with typing of fetal blood. There was no difference in the efficiency of amplification from amniotic fluid cells directly or from isolated DNA. CONCLUSIONS: Fetal HPA type may be reliably determined by amplification of DNA from amniotic fluid cells, eliminating the need for fetal blood sampling or immunoglobulin administration when the fetus is HPA1a negative.

Amniocentesis↗

Clinical and echographic features of in utero cardiac dysfunction in the recipient twin in twin-twin transfusion syndrome.

OBJECTIVE: Fetal twin-twin transfusion syndrome (TTTS) presenting in the second trimester has been associated with almost no perinatal survival until recently, when serial drainage of amniotic fluid has improved the prognosis to 70%-80%. Most recipient twins now survive but develop cardiac dysfunction. The study was undertaken to evaluate the abnormal echocardiographic features and clinical complications of cardiac disease in the recipient twin of TTTS. DESIGN: Antenatal and postnatal echocardiographic and clinical observational study. SETTING: Antenatal studies in a tertiary referral centre. Postnatal management and follow up were performed by the same paediatric cardiologist, either at the obstetric hospital or at the regional referral centre. PATIENTS: Twin pregnancies complicated by TTTS with severe polyhydramnios diagnosed earlier than 25 weeks that proceeded until viability (n = 5). INTERVENTION: Serial fetal echocardiography with colour Doppler. Postnatal echocardiography in the first week and between two and seven months. Serial amnioreduction was performed in all pregnancies. Digoxin treatment, pericardiocentesis, paracentesis, or laser ablation of placental anastomoses was undertaken when there was hydrops. RESULTS: Increased cardiothoracic ratio and tricuspid regurgitation were seen in all recipient twins. High pulmonary artery velocities developed in three. One recipient twin died a week after delivery of endocardial fibroelastosis and infundibular pulmonary stenosis. Two other had balloon dilatation for pulmonary stenosis, one shortly after birth and one at four months. A further twin has apical thickening of the right ventricle at six months. The remaining recipient twin had normal echocardiographic findings at follow up. CONCLUSION: This report characterises for the first time a cardiac disease acquired in utero in the recipient twin in pregnancies complicated by TTTS. Clinical manifestations in utero range from mild to critical pulmonary stenosis or lethal cardiomyopathy. Although perinatal prognosis seems to be related to the severity of dysfunction when first diagnosed in utero, follow up in infancy is recommended in view of the possibility of progressive pulmonary stenosis.

Echocardiography, Doppler↗

Fetal intraluminal gastric masses after second trimester amniocentesis.

Eight instances of homogeneous, well-defined echoes within the fetal stomach were identified on routine second trimester detailed scan over a 7 month period, a prevalence of 1 in 287 or 0.35%. This finding was significantly more frequent in women who had cytogenetic amniocentesis than in those who had not had the procedure (4 in 266 [1.5%] versus 4 in 2031 [0.2%], respectively; P < 0.01). Indirect signs of intra-amniotic bleeding, such as particles in the amniotic fluid, chorioamniotic separation, or hyperechogenic bowel, were present in four cases. The association between echogenic material within the fetal stomach and cytogenetic material within the fetal stomach and cytogenetic amniocentesis is discussed.

Adult↗

Prenatal determination of fetal RhD type by DNA amplification.

BACKGROUND: An RhD-negative woman whose partner is heterozygous may have preexisting anti-RhD antibodies that may or may not affect a subsequent fetus, depending on whether it is heterozygous. A safe method of determining fetal RhD type early in pregnancy would eliminate the risks to an RhD-negative fetus of fetal-blood sampling or serial amniocenteses. METHODS: We determined the RhD type in 15 fetuses using the polymerase chain reaction in amniotic cells and serologic methods in fetal blood collected simultaneously. In another 15 fetuses, the RhD type determined from chorionic-villus samples was compared with that identified by typing of DNA from the fetus itself. RESULTS: RhD typing of DNA from amniotic cells correctly indicated the serologic type in every fetus. Of 10 fetuses with RhD-negative mothers, 4 were identified as RhD-negative and 6 as RhD-positive. Of five fetuses with RhD-positive mothers, four were identified as RhD-positive and one as RhD-negative. There was also complete agreement between the results of RhD typing of DNA from chorionic-villus samples and the results of typing of DNA from fetal tissue. Eleven fetuses were RhD-positive, and 4 were RhD-negative. Four RhD-positive fetuses had RhD-negative mothers. Three RhD-negative fetuses had RhD-positive mothers. There was no contamination by maternal RhD-positive DNA of the samples from RhD-negative fetuses. CONCLUSIONS: Determining fetal RhD type in amniotic cells without invading the fetomaternal circulation is a reliable method that will be valuable in the management of Rh alloimmunization.

Amniotic Fluid↗

Disappearing lung echogenicity in fetal bronchopulmonary malformations: a reassuring sign?

Congenital bronchopulmonary malformations detectable on prenatal ultrasound include cystic adenomatoid malformation (CAM), lobar sequestration, and upper airway atresia. We describe three fetuses with prenatally detected intrathoracic lesions in which the associated pulmonary hyperechogenicity disappeared before delivery. In the first case of pulmonary sequestration, the infant was asymptomatic after birth. However, in a case of CAM and another with laryngeal atresia, respiratory distress developed after delivery, despite recent scans showing apparently normal lung fields. This experience suggests that ultrasonic resolution of hyperechogenic lung lesions in utero does not necessarily indicate resolution of the underlying pathology.

Abnormalities, Multiple↗

Transplacental transfer of cefuroxime in uncomplicated pregnancies and those complicated by hydrops or changes in amniotic fluid volume.

The transplacental transfer of cefuroxime was determined at antenatal fetal blood sampling in a cross sectional study of 78 patients between 15-35 weeks' gestation, 8-138 minutes after a maternal intravenous dose of 750 mg. Mean serum cefuroxime concentration, measured by high performance liquid chromatography, was 7.4 (95% confidence interval (CI) 6.8 to 8.1) mg/l in control fetuses; concentrations in hydropic fetuses were similar (6.2 mg/l, CI 4.7 to 7.7) but in fetuses with oligohydramnios they were significantly lower, (4.9 mg/l, CI 3.6 to 6.2). Antibiotic concentration did not correlate with gestational age and remained unchanged by transfusion of packed red cells. We conclude that (i) fetal serum concentrations of cefuroxime obtained after a maternal dose of 750 mg are only adequate for prophylaxis against organisms with a minimum inhibitory concentration of < 4 mg/l and (ii) transplacental passage of cefuroxime is significantly reduced in the presence of oligohydramnios.

Amniotic Fluid↗

Fetal blood sampling from intrahepatic vein versus cord insertion: effect on pH and blood gases.

OBJECTIVE: To determine whether venous pH, base excess, and blood gas values collected by antenatal ultrasound-guided sampling from the fetal intrahepatic vein (intra-abdominal umbilical vein, portal sinus, or portal vein) differ from those obtained from the placental cord insertion. METHODS: Retrospective analysis was done of 1053 clinically indicated fetal blood sampling procedures performed between 1988-1992. One hundred sixty-eight appropriate for gestational age (AGA) singleton fetuses were identified after exclusion of those with conditions believed likely to have impaired fetal blood gas status. Fetal venous pH, carbon dioxide pressure, oxygen pressure, and base excess from 52 samplings at the intrahepatic vein were compared cross-sectionally to those from 116 samplings at the placental cord insertion, using analysis of covariance to correct for gestational age. RESULTS: There was no systematic difference in the blood gas or acid-base values between the two sites of fetal venous blood sampling. CONCLUSIONS: Acid-base and blood gas status in AGA fetuses is not affected by the site of sampling. Values obtained at the intrahepatic vein may be interpreted using reference ranges derived from sampling at the placental cord insertion.

Acid-Base Imbalance↗

Amiodarone given by three routes to terminate fetal atrial flutter associated with severe hydrops.

BACKGROUND: We describe the concurrent administration of amiodarone using three different routes in order to provide: 1) rapid and adequate fetal loading without giving unduly high doses to the mother, and 2) a maintenance dose to the fetus without risking repeated invasive procedures. CASE: Rapid atrial flutter was seen on ultrasound in a fetus with severe hydrops at 27 weeks' gestation. Following failed transplacental therapy with sotalol and flecainide, amiodarone was administered to the fetus via the intravenous, intraperitoneal, and transplacental routes. Conversion to sinus rhythm and resolution of hydrops followed this treatment. CONCLUSION: Combined triple-route administration of amiodarone to the fetus can be effective in treating supraventricular tachycardia and may have a role in the management of life-threatening fetal arrhythmias refractory to transplacental therapy.

Adult↗

Intra-amniotic pressures following vaginal gemeprost prior to first and second trimester termination of pregnancy.

Intra-amniotic pressures were measured following 1 mg gemeprost for cervical preparation before first trimester vacuum aspiration (n = 10) and following 2 mg gemeprost before second trimester dilatation and evacuation (n = 15). Twenty-five women, matched for gestational age and parity, who did not receive gemeprost served as controls. Compared to control values (2-8 mmHg), basal intra-amniotic pressure (IAP) was significantly increased after 1 mg and 2 mg of gemeprost (median 20.0, range 4-45 mmHg, median 20.0, range 8-60 mmHg, respectively). Uterine contractions were recorded in 8 of 10 subjects after 1 mg (median delta IAP 28.0, 95% CI 10.0-42.6 mmHg) and 14 of 15 subjects after 2 mg (median delta IAP 52.5, 95% CI 26.7-60.3 mmHg). Gemeprost produces an increase in uterine contractility which may be additional to cervical softening properties and which may be responsible for the adverse effects of pain and bleeding experienced by some women prior to termination.

Abortion, Induced↗