fetal survival in idiopathic NIHF however appears worse than for other causes of NIHF such as tachyarrhythmia and haematologic disorders (Hansmann et al. 1989) with a mortality rate of 5O-IOO% (Etches & Lemon 1979; Schwartz et al. 1981). For recurrent idiopathic NIHF the reported mortality including the present series is 18/20 (90%) (Tables 1 and 2).
References Cumming D. C. (1979) Recurrent non immune hydrops fetalis. Obstet Gynecol54,124-126.
Etches P. E. & Lemon J. A. (1979) Report of 22 cases of non immune hydrops fetalis including 3 siblings. Pediatrics 64,326-332. Hansmann M., Gembruch U. & Bald R. (1989) New therapeutic aspects in non immune hydrops fetalis based on four hundred and two prenatally diagnosed cases. Fetal Ther 4,29-36. Potter E. L. (1943) Universal oedema of the fetus unassociated with erythroblastosis. Am J Obstet Gynecol46,13&134. Schwartz S. M., Viseskul C., Laxova R., McPherson E. W. & Gilbert E. F. (1981) Idiopathic hydrops fetalis: Report of 4 patients including 2 affected sibs. A m J Hum Genet 8,5946. Silverstein A. J. & Kanbour A. I. (1981) Repetitive idiopathic fetal hydrops. Ohstet Gynecol57,18S-21S.
British Journal of Obstetrics and Gynaecology October 1992, Vol. 99, pp. 856-857
Unreactive fetal heart rate pattern and atrial flutter J . S. S M O L E N I E C D. K . J A M E S Division of Fetal Medicine, University Department of Obstetrics, Bristol Maternity Hospital. Southwell Street, Bristol BS2 8EG. UK R. MARTIN Department of Child Health, Royal Hospital for Sick Children, St Michael’s Hill, Bristol BS2 8EG. UK
Case report A 34-year-old multiparous woman with an uneventful antenatal history presented in her third pregnancy at 37 weeks’ gestation to her local antenatal clinic for confirmation of the onset of labour as she had intended to have a home delivery. A prolonged (60 min) cardiotocograph (CTG) was unreactive; therefore she was referred to the maternity unit for assessment. Assessment at the maternity unit revealed a fetal heart rate on the CTG of 155 bpm with poor variability and with no reactivity to painful uterine contractions. Echocardiography (M-mode and 2-dimensional) was performed which revealed a structurally normal heart with an atrial rate of 440 beats per minute with variable conduction. Biophysical assessment, excluding CTG, was normal as was the umbilical artery Doppler (pulsatility index (PI) = 0.9). There was no evidence of cardiac enlargement or hydrops. Since she was in early labour she was transferred to the labour ward where amniotomy was performed. Throughout labour the CTG remained Correspondence: Dr J. S. Smoleniec, Bristol Maternity Hospital, Southwell Street, Bristol BS2 8EG.
unchanged. Fetal surveillance was maintained by performing regular fetal scalp blood samples for p H estimation which were normal. She had a normal vaginal delivery after 3 h of a 3340 g live infant male with good Apgar scores. The infant’s baseline fetal heart rate was 150 beats per minutes which increased to 230-240 bpm intermittently; examination of the infant was otherwise normal. A n electrocardiographic diagnosis of atrial flutter (rate > 400 bpm) was made with a variable atrioventricular block of 3-1:l. Echocardiography revealed no structural abnormality. The atrial flutter was treated with digoxin and sinus rhythm was established within three days. The infant was discharged six days after commencement of the digoxin (20 pg twice daily) in sinus rhythm which has been maintained during outpatient follow-up.
Discussion A diagnosis must always be made when confronted with an unreactive FHR pattern if unnecessary emergency caesarean section is to be avoided. By investigating as summarised in Table 1, the diagnosis can be made rapidly in most cases with the use of a CTG monitor and a ultrasound scan (USS) machine. The commonest cause for an unreactive FHR pattern is when the fetus is in behavioural state F1 (quiescent state), which o n average lasts 21 mintues (range 3-38 minutes) (Pillai & James 1990) with a maximum duration of 55 minutes (Nijhuis et al. 1982); therefore, the diagnosis can be made by prolonging the CTG for u p to 60 minutes. While this is being done a maternal history and examination to exclude maternal thyrotoxicosis or medication effect (benzodiazepines; pethidine) can be done. A drug induced unreactive FHR usually lasts 30-40 minutes without associated decelerations (Martin 1982). Cardiac arrhythmias can be diagnosed if the USS machine has an M-mode facility. If there is no arrhythmia but there is fetal movement with the F H R pattern remaining unreactive, this is suggestive of a neurodevelopmental abnormality in the fetus. However, if the fetus fails a
Table 1. Differential diagnosis and investigation of an unreactive fetal heart rate pattern.
Investigation and interpretation
Fetal behavioural state 1F Maternal drugs Cardiac tachyarrhythniia
Extend CTG recording to 60 min Extend CTG recording 40 min, no decelerations + history of pethidineidiazepam Echocardiography:B + M-mode Maternal historyiexaminationiblood tests for thyroid dysfunction Fetal behavioural study will show dissociation USS of CNS, e.g. anencephaly Biophysical assessment: (BPA) = no fetal movement;fetal blood sampling (FBS)* = normal fetal blood gases Abnormal BPA (decelerations with contractions): FBS* = abnormal fetal blood gas
Neurodevelopmental abnormality Congenital anomaly Brain death Fetal hypoxia
"Cordocentesisiscalp sample if in labour. biophysical assessment (BPA) after a 60 minute F H R unreactive pattern recording, this is suggestive of fetal brain death; this can be distinguished from fetal distress by there being no FHR decelerations and the presence of normal gases revealed by fetal blood sampling. The FHR in fetal brain death syndrome is always relatively high (Nijhuis et a/. 1990) in comparison to that of F1. Management of this case was simplified as the woman was multiparous, in early labour with a favourable cervical/ Bishop score, and there was no evidence of fetal hydrops. The problem of how to monitor for fetal distress in labour was overcome by performing regular fetal scalp sampling which was helped by a relatively short labour. Tachyarrhythmias are the commonest clinically important fetal arrhythmia. The majority (95%) of fetal tachyarrhythmias are due to reciprocating supraventricular tachycardia (RSVT) with atrial flutter (AF) being much less common . danger with atrial flutter is (Kleinman & Copel 1 9 9 1 ~ )The the development of cardiac failure (hydrops) and fetal death. In the presence of hydrops fetalis, atrial flutter is more difficult to treat as compared to RSVT (Kleinman & Copel 1991a), reflected by a 40-50% perinatal mortality and a high caesarean section rate (60-100%) (Maxwell et al. 1988; Hansmann et ul. 1991). Before considering treatment, it is important to exclude structural cardiac anomalies which can be present in up to 10% (Wladimiroff & Stewart 1985) of cases; these are considered to be more common with atrial flutter and are associated with an extremely poor prognosis with o r without vigorous in-utero and postnatal therapy (Moller e t a/. 1969; Kleinman & Copel 1 9 9 1 ~ )Other . causes to be considered are viral infections (coxsackie B and cytomegalovirus (Wladimiroff & Stewart 1985)) and maternal thyrotoxicosis. Accurate diagnosis of this type of arrhythmia is important before instituting antiarrhythmic therapy as all antiarrhythmic agents have a potential proarrhythmia effect on the fetus, and/or the mother, especially if given for the wrong arrhythmia. The long term prognosis is different depending on the type of arrhythmia. Whereas no or infrequent recurrences are found with atrial flutter after infancy (Moller et a/. 1969: Lundberg 1973), a 20% recurrence risk is reported with paroxysmal atrial tachycardia (Lundberg 1973). Digoxin is the
first line drug of choice in treating atrial flutter (Allan et al. 1991; Kleinman & Copel 1991b) with therapy continuing for up to 1 year post delivery. In the case of atrial flutter being diagnosed in the preterm fetus, then maternal administration of digoxin is the first drug of choice. Long term follow up of all atrial flutter cases is mandatory.
References Allan D. A,, Chita S. K., Sharland G. K. etal. (1991)Flecainidein the treatment of fetal tachycardias. B r Heart J 65,4648. Hansmann M., Gembruch U., Bald R. et al. (1991) Fetal tachyarrhythmias: transplacental and direct treatment of the fetus-a report of 60 cases. Ultrasound Ohstet Gynecol 1,162-170. Kleinman C. S. & Copel J. A. (1991~)Electrophysiological principles and fetal antiarrhythmic therapy. Ultrasound Obstet Gynecol 1, 286-297. Kleinman C. S. & Copel J. A. (1991b) Direct fetal therapy for cardiac arrhythmias:who, what, when, where, why and how? IJltrasound Ohstet Gynecol I, 158-159. Lundberg A. (1973) Paroxysmal tachycardia in infancy: follow-up study of 47 subjects ranging in age from 10 to 26 years. Pediatrics 51,26-35.
Martin C. B. (1902) Physiology and clinical use of fetal heart rate variability. In Clinics in Perinatology, Vo12 (Petrie R., ed) W. B. Saunders, London. pp 346-347. Maxwell D. J., Crawford D. C., Curry P. et al. (1988) Obstetric importance, diagnosis and management of fetal tachycardias. Br Med J 297,107-1 10. Moller J. H., Davachi F. & Anderson R. C. (1969) Atrial flutter in infancy. J Pediatr 75,643-651. Nijhuis J. G., Prechtl H. F. R., Martin Jr C. B. & Bots R. (1982) Are there behavioural states in the human fetus? Early Human Dev 6, 177. Nijhuis J. G., Crevels A. J. &Van Dongen P. W. J. (1990) Fetal brain death: the definition of a fetal heart rate pattern and its clinical consequences. Ohstet Gynecol Surv 45,229-232. Pillai M. & James D. K. (1990) Behavioural states in normal mature human fetuses.A r c h Dis Child (Fetal & Neonatal edn) 65,3943. Wladimiroff J. & Stewart P (1985) Treatment of fetal cardiac arrhythmias. B r J Hosp Med 34,134-140. Received 25 March 1992 Accepted I7 June I992