Obstetric Medicine最新文献

Maternal Graves' autoantibodies are well known to cause fetal and neonatal thyroid disturbances. Despite radioiodine therapy, Graves' autoantibodies are known to persist, which can cross the placenta and cause hyperthyroidism in the fetus. We present the case of a 26-year-old woman in her first pregnancy, clinically and biochemically euthyroid with history of treated Graves' disease, where the fetus showed signs of hyperthyroidism on antenatal scans. This was confirmed by amniotic fluid testing as fetal blood sampling was not feasible and successfully treated with maternal carbimazole whilst continuing thyroxine for the mother (block-replacement). We discuss the challenges in the diagnosis of fetal hyperthyroidism and treatment whilst maternal thyroid status is maintained on thyroxine.

Background: Unlike tachyarrhythmias, which are common in pregnancy, there is a paucity of data regarding maternal bradycardias. Our objective was to describe the characteristics, associated conditions, and prognosis of women who develop bradycardia post-partum.

Method: We conducted a retrospective chart review of patients referred to the Obstetrical Medicine service at British Columbia Women's Hospital from January 2012 to May 2020 for post-partum maternal bradycardia.

Results: Twenty-four patients with post-partum bradycardia were included (age 34.2  ±  4.8 years; heart rate 40.4  ±  8.1 beats per minute; blood pressure 131/72 mm Hg). Sinus bradycardia (79.2%) was the most common rhythm. Dyspnea (29.4%) and chest pain (23.5%) were common symptoms. Mean time to resolution of bradycardia was 3.6  ±  3.8 days. Associated conditions potentially explaining the bradycardia were preeclampsia (54.1%), underlying (16.7%), medications (8.3%), and neuraxial anesthesia (8.3%).

Conclusions: Maternal bradycardia is an uncommon condition complicating the post-partum period, that is generally self-limiting, with the majority only require clinical observation.

We report our experience of managing a massive haemothorax caused by a ruptured, previously unknown, pulmonary arteriovenous malformation (pAVM) at 34 + 5 weeks of gestation, which proved to be a manifestation of hereditary haemorrhagic telangiectasia (HHT), also known as Osler-Weber-Rendu syndrome. The patient underwent an emergency caesarean section under general anaesthesia after placement of a chest tube and gave birth to a healthy infant. A postoperative thoracic computed tomography angiography highlighted the presence of the large pAVM. Transcatheter embolization was performed right after the delivery. Subsequent patient's anamnesis, family history and genetic analysis finally revealed the presence of the syndrome. The aim of our report is to create awareness of this serious condition with potential life-threatening complications, especially in pregnancy. Simple criteria have been published and allow to easily consider HHT and the presence of potential AVM during anamnesis, ideally even before pregnancy.

Primary hypokalaemic periodic paralysis during pregnancy has been rarely reported. Four pregnant women with the acute onset of flaccid paralysis presented between January 2018 and December 2021. Focussed history and physical examination helped an appropriate radiological and laboratory investigation plan to be made. All women recovered within 4-7 days of potassium supplementation. Supplemental potassium continued until delivery. A pain management plan with continuous epidural infusion helped in avoiding stress-induced hypokalaemia. None of the women developed an episode of muscle weakness during the intervening period. In conclusion, a focussed history and targeted laboratory investigation are needed to diagnose primary hypokalaemic periodic paralysis. Early administration of oral or intravenous potassium is crucial in improving fetomaternal outcomes.

Hypercalcemia is rare in women of child-bearing age, and most cases are due to primary hyperparathyroidism. A 28-year-old woman, 14 weeks pregnant with dichorionic diamniotic twins, presented to hospital with vomiting, muscle cramps, and weakness. She had been taking calcium carbonate for gastric reflux and nausea from 5 weeks of gestation. Investigations revealed severe hypercalcemia, metabolic alkalosis, and renal injury. She was transferred to intensive care, receiving fluid resuscitation and subcutaneous calcitonin followed by dialysis. Investigations revealed suppressed PTH and PTH-related peptide, negative malignancy screening and low vitamin D level. Calcium and renal function quickly normalized and with cessation of calcium carbonate remained normal throughout the rest of pregnancy. Reports of calcium-alkali syndrome causing severe hypercalcemia are scarce, with most cases occurring later in gestation. This case represents a dramatic presentation requiring renal replacement therapy early in twin gestation.