HP is a life-threatening condition that is difficult to diagnose. As suggested by our case, the use of ovulation induction agents might increase the risk of HP16). However, establishing a diagnosis of HP is challenging. The main symptoms of HP are lower abdominal pain and vaginal bleeding. However, HP is sometimes asymptomatic17), resulting in misdiagnosis, late diagnosis, and life-threatening intra-abdominal hemorrhage18). Wang et al. reported factors in three categories that most commonly cause delayed diagnosis or misdiagnosis of ectopic pregnancy: (i) clinician-related factors include misunderstanding of patients' medical history, insufficient training in ultrasonography, and poor awareness of patient’s condition; (ii) patient-related factors include noncompliance with medical advice and lack of communication with clinicians and (iii) disease-related factors include complications of HP, atypical symptoms, delayed serum β-human chorionic gonadotropin level elevation, early rupture of cornual HP, asymptomatic ectopic pregnancy, and pregnancy of unknown location18). To rule out ectopic pregnancy, it is important to carefully evaluate the adnexa using ultrasonography despite confirmation of an intrauterine gestational sac and apparent lack of any risk factor.
Although our patient presented with severe shock, we performed laparoscopic surgery, which allows detailed examination of pelvic and abdominal conditions, to identify the cause of the shock. Consequently, we could confirm that the abdominal bleeding was due to tubal rupture and repeated laparotomy, which might have increased maternal abdominal adhesions from two previous cesarean sections.
Our patient also experienced life-threatening intra-abdominal hemorrhage. Although several studies have reported cases of HP, because of its rarity, they have mainly focused on diagnostic accuracy and maternal outcomes17). Little is known about neonatal outcomes. Maternal hypotension might cause fetal hypotension and hypoxemia, resulting in fetal cerebral hypoperfusion19). Fetal response to mild hypoxia is initially protective. In addition, fetal response to moderate hypoxia involves substantial compensations via the autonomic (parasympathetic [vagus] and sympathetic [beta-adrenergic]) nervous system20-23). However, these compensatory mechanisms break down in the presence of severe asphyxia, and fetal brain damage can occur because central blood flow is not sufficiently maintained24). Since fetal heart rate variability and fetal heart rate acceleration indicate parasympathetic and sympathetic activity, respectively, brain damage may affect the CTG pattern16,17). Here, fetal heart rate variability and acceleration were consistently observed, suggesting that maintaining normal fetal oxygenation could improve prognosis25). Severe fetal hypoxemia also causes local brain damage. Mallard et al. reported that severe umbilical occlusion for 10 min led to neuronal cell loss in the hippocampus in near-term fetal sheep26), potentially affecting fetal development. Our patient’s neonate showed no abnormalities in either antenatal fetal heart rate monitoring or fetal and placental growth, thus indicating a favorable neurological prognosis.
In conclusion, because HP is rare, little is known about its associated neonatal outcomes. This report highlights the successful laparoscopic management of severe hemorrhage in HP, followed by uneventful term gestation and a healthy singleton birth.