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PEDIATRICS Vol. 111 No. 6 June 2003, pp. 1437-1442

EXPERIENCE AND REASON

Midaortic Syndrome in the Fetus and Premature Newborn: A New Etiology of Nonimmune Hydrops Fetalis and Reversible Fetal Cardiomyopathy

Ilana Zeltser, MD, Ira A. Parness, MD, Helen Ko, BS, RDCS, Ian R. Holzman, MD and Steven A. Kamenir, MD

Department of Pediatrics, Mount Sinai Medical Center, New York, NY 10029


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 CASE REPORT
 DISCUSSION
 CONCLUSIONS
 REFERENCES
 
Nonimmune hydrops fetalis is the final common pathway of many conditions that ultimately result in fetal anasarca. Even after extensive evaluation, the etiology of a small percentage of cases of hydrops remains unknown. We present a case of midaortic syndrome, also known as abdominal coarctation syndrome, in a fetus with hydrops and a severe cardiomyopathy. The clinical manifestations of midaortic syndrome in this fetus and premature newborn, including malignant hypertension and reversible cardiomyopathy, are detailed. The fetal pathophysiology of midaortic syndrome remains speculative, but likely includes fetal hypertension as the cause of cardiac dysfunction. To our knowledge, this is the first report of midaortic syndrome as an etiology for nonimmune hydrops fetalis.

Key Words: midaortic syndrome • abdominal coarctation • renal artery stenosis • hydrops fetalis • fetal cardiomyopathy

Abbreviations: NHF, nonimmune hydrops fetalis • RV, right ventricular • DA, ductus arteriosus • LV, left ventricular


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
CASE REPORT
 DISCUSSION
 CONCLUSIONS
 REFERENCES
 
Hydrops fetalis is a frequently lethal clinical syndrome manifesting as fetal anasarca that has multiple etiologies.1–3 Traditionally, it has been classified as either isoimmune hydrops fetalis or nonimmune hydrops fetalis (NHF) in origin. Among the various causes of NHF, primary cardiac etiologies account for ~25% of cases, including cardiomyopathies and structural anomalies with or without valvar regurgitation and arrhythmias.4 The etiology of NHF is considered idiopathic in 15% to 30% of cases.1,3 The following case report is the first description of midaortic syndrome, a rare anomaly of the aortic vasculature associated with abdominal coarctation and renal artery abnormalities,5–12 as an etiology of NHF. We also present for the first time the clinical manifestations of midaortic syndrome in the premature newborn, including malignant hypertension and reversible cardiomyopathy.


   CASE REPORT
TOP
 ABSTRACT
 INTRODUCTION
 CASE REPORT
DISCUSSION
 CONCLUSIONS
 REFERENCES
 
The patient was a premature newborn female delivered at 31 weeks’ gestation to a 34-year-old G6P1041 mother. Approximately 4 weeks before delivery, decreased fetal movement was suspected; a fetal sonogram revealed fetal anasarca. Serologic and infectious evaluations were normal, and, after serial follow-up showed continued hydrops, the mother was referred to our center. In addition to the hydrops, fetal echocardiography revealed severe right ventricular (RV) dysfunction and hypertrophy (Fig 1); the echocardiogram failed to demonstrate flow across the ductus arteriosus (DA). The left ventricle was dilated with only mildly depressed systolic function, the cardiac rhythm was normal at 136 beats per minute, and there was moderate tricuspid regurgitation with phasic flow reversal in the superior vena cava. A presumptive diagnosis of premature closure of the DA was made, and urgent delivery was recommended.


Figure 1
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  		Fig 1. Fetal hydrops: sagittal section of fetus demonstrating skin edema, marked ascites and biventricular cardiac hypertrophy. LV indicates, left ventricle; RV, right ventricle.

 
The neonate was delivered via urgent cesarean section without complication. After intubation, paracentesis of nonpurulent ascites was performed to allow for adequate lung expansion. The Apgar scores were 4 and 7 at 1 and 5 minutes, respectively. Birth weight immediately after drainage of ascites was 1750 g; nonhydropic weight was estimated at ~1500 g. Respiratory rate was 48 breaths per minute, preductal and postductal saturations were 100% on 21% fraction of inspired oxygen, heart rate was 157 beats per minute, and initial right upper extremity blood pressure was recorded at 86/46 mm Hg. There was a nonspecific grade II/VI systolic ejection murmur without a gallop rhythm. Liver size could not be determined secondary to abdominal distention, and femoral pulses were difficult to appreciate. There were no other abnormal physical features or focal neurologic deficits. Initial laboratory values revealed a hematocrit of 43%, total protein of 2.9 g/dL (29 g/L), and albumin of 1.5 g/dL (15 g/L).

In the neonatal intensive care unit, the umbilical vein was readily catheterized but repeated attempts to achieve umbilical or radial arterial access were unsuccessful. There was cardiomegaly on a chest radiograph and a 12-lead electrocardiogram was normal for age. An immediate bedside echocardiogram was performed that revealed a moderate sized DA with nearly continuous nonrestrictive left-to-right flow. The aortic arch and proximal descending aorta appeared normal. Discrepant ventricular dysfunction was present, with severe RV and only mild left ventricular (LV) dysfunction noted in association with prominent biventricular hypertrophy. Given the apparent degree of right-sided heart failure, digoxin therapy was initiated; other inotropic agents were not administered.

Over the first several hours of life, the infant was noted to have persistent hypertension. Noninvasive blood pressure measures using a neonatal-size cuff were in the range of 130/50 mm Hg in the upper extremities, with lower extremity readings consistently in the range of 120/70 mm Hg. A sonogram of the head did not reveal any intraventricular hemorrhage.

Because of the severity of systemic hypertension, the upper-to-lower extremity blood pressure gradient and a normal appearing aortic arch by echocardiogram, a unifying diagnosis of midaortic syndrome was entertained. A bedside echocardiogram at 24 hours of age specifically directed at evaluating the abdominal aorta revealed: 1) moderate narrowing of the abdominal aorta extending distally from the renal arteries with a normal proximal abdomina1 aorta (Fig 2); 2) bilateral renal artery stenosis with a pressure gradient estimated at 50 mm Hg and 40 mm Hg across the left and right renal arteries, respectively; hypoplastic iliac arteries and hypoplasia of the superior mesenteric artery and celiac arteries (Figs 2 and 3); 3) a closed DA; and 4) reversal of the pattern of ventricular dysfunction previously seen: severe LV dysfunction had developed, whereas RV function had improved significantly. The echocardiographic findings of abdominal aortic coarctation and renal artery stenosis established the diagnosis of midaortic syndrome. Renal ultrasound showed morphologically normal kidneys. Random umbilical vein sampling for renin revealed a level of 132 ng/mL/h (132 2g/L/h), with normal for age <16.6 ng/ml/h (<16.6 6g/L/h). The clinical findings of improved cardiac output, a small upper-to-lower extremity systolic blood pressure difference (10–20 mm Hg) were consistent with the echocardiographic appearance of mild abdominal coarctation and suggested that renal artery stenosis was the dominant etiology for the systemic hypertension.


Figure 2
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  		Fig 2. A, Left flank window: coronal cut depicting the narrowed aorta extending from the level of the renal arteries to the iliac bifurcation. B, Same cut as in 2A more magnified to demonstrate the narrowest aortic segment immediately below the renal artery origins. Abd Ao indicates abdominal aorta; I, inferior; IVC, inferior vena cava; L, left; R, right; S, superior.

 

Figure 3
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  		Fig 3. A, Same cut as in Fig 2B: highly magnified color flow map of the renal artery origins demonstrating qualitatively, severe bilateral renal artery stenosis. B, Same cut as in Fig 2B: continuous wave Doppler interrogation of the left renal artery yields an estimated maximal instantaneous pressure gradient of ~52 mm Hg. CW indicates continuous wave; PG, peak instantaneous gradient; V, maximal velocity.

 
Management was directed at normalizing blood pressure to improve cardiac function, protect the cerebral vessels from potential hemorrhage, and ensure adequate renal blood flow in the setting of severe bilateral stenosis. Initial therapy using hydralazine and nitroprusside was ineffective, and a nicardipine drip was initiated, titrated to maintain a mean systemic blood pressure between 60 and 70 mm Hg. In addition to a maximum dose of continuous nicardipine infusion at a rate of 3 µg/kg/min, the infant received intermittent small doses of propranalol to counteract the tachyphylaxis to nicardipine. A follow-up echocardiogram at 6 days of life revealed significantly improved LV function and norma1 RV function. The infant maintained adequate renal function with creatinine levels ranging from 0.6 to 1.3 mg/dL (53–115 µmol/L).

The longer-term goal of medical therapy was to have the infant grow large enough to allow definitive surgical or catheter-based treatment of renal artery stenosis. However, over the course of several weeks, the patient’s blood pressure became increasingly refractory to aggressive medical management. Ultimately, the infant died at 3 months of age secondary to severe cardiac dysfunction and resultant heart failure. Neither postmortem nor placental pathology could be obtained.


   DISCUSSION
TOP
 ABSTRACT
 INTRODUCTION
 CASE REPORT
 DISCUSSION
CONCLUSIONS
 REFERENCES
 
Hydrops fetalis is a relatively rare but important cause of morbidity and mortality in the fetus and newborn. Despite improved understanding of specific etiologies associated with hydrops, combined in utero and postnatal mortality remains high, with about a 25% overall survival.2,3 To our knowledge, midaortic syndrome resulting in fetal cardiomyopathy as a cause for NHF has not been previously reported.

Midaortic syndrome, also known as abdominal coarctation syndrome, has been well-described in children and young adults.5–12 The syndrome manifests with variable narrowing of the abdominal aorta and its visceral branches. Stenosis of the renal arteries is common (90%), with less common involvement of the celiac and superior mesenteric arteries (20%–40%), and infrequent involvement of the inferior mesenteric arteries.11

Several possible etiologies, broadly classified as congenital or acquired, have been suggested for midaortic syndrome. Hypoplasia may occur during development of the abdominal aorta and its vascular branches, including the metanephric vasculature, which originate as successive branches from the abdominal aorta between the celiac axis and inferior mesenteric artery.11 The occurrence of midaortic syndrome in association with neurofibromatosis,11 Alagille syndrome,13 Williams syndrome,11 fibromuscular dysplasia,12 and mucopolysaccharidosis14 argues for a genetic etiology in some patients. As an acquired entity, this syndrome may occur from inflammation from such conditions as Takayasu’s arteritis,15 rubella,16 and various allergic or autoimmune conditions.7

Clinically, patients with midaortic syndrome typically present with significant hypertension, an abdominal bruit, diminished distal pulses, and, less commonly, with evidence for end-organ damage such as oliguric renal failure, claudication, or congestive heart failure.10.11 Diagnosis is usually made by angiography, but 1 report has described diagnosis by ultrasound.17 The earliest diagnosis previously reported in the literature has been a newborn male, product of a 38-week gestation, presenting with tachypnea and decreased femoral pulses,18 but most often midaortic syndrome is discovered in children, adolescents, or young adults.10,11 Untreated disease can result in progressive hypertension, renal failure, cerebral aneurysm, cardiac failure, and death in young adulthood.5,6

The choice of therapy for midaortic syndrome depends on patient age, size, and degree of renal artery stenosis and concomitant medical problems. Management strategies have included long-term medical therapy11 or for infants as a bridge to surgery,19 balloon aortic angioplasty with or without renal artery dilation,11,20 renal artery angioplasty with stent placement,21 nephrectomy,11,18 or surgical reconstruction of the diseased vascular segments.8–12 Results of angioplasty and stent placement have been variable, while mid- and long-term follow-up 1 to 18 years after surgical repair in children has shown most patients to be normotensive with minimal postoperative complications.10–12 Because of prematurity, small size, and bilateral renal involvement, only medical therapy was available for this patient. Standard antihypertensive therapy did not adequately control the hypertension. Despite concerns about use of calcium channel blockers in infants,22 the intravenous calcium channel blocker nicardipine initially worked effectively without apparent cardiac or other side effects.23 In our patient, though, tachyphylaxis developed after weeks of therapy.

Because midaortic syndrome has never been previously described as an etiology of NHF, its pathophysiology in this patient remains speculative. Mechanistically, hydrops fetalis may result from 1) increased capillary hydrostatic pressure from elevated central venous pressure; 2) decreased plasma colloid oncotic pressure from hypoalbuminemia; 3) increased capillary permeability; or 4) obstruction to lymphatic flow.3,24 Elevations in directly measured umbilical venous pressures in human fetuses with NHF have been documented when the etiology is secondary to cardiac failure (11–13 mm Hg in cardiac versus ~5 mm Hg in noncardiac NHF).25,26 Also, in a fetal lamb model, moderate elevation in venous pressure has been demonstrated to linearly decrease lymphatic flow,27 implicating poor lymphatic drainage as a contributing factor in NHF.

In this fetus with midaortic syndrome and renal artery stenosis RV dysfunction was prominent. Given the significant postnatal hypertension, it may be that hypertension was also present prenatally. Fetal hypertension as a mechanism for cardiac dysfunction is supported by evidence in fetal lamb models showing that increases in afterload caused a decrease in fetal LV cardiac stroke volume.28 This same effect has also been documented in newborn lambs.29

Given the unique role of the placenta in augmenting homeostasis in the fetal circulation, can fetal hypertension even develop? Normally, the placenta is the major regulator of fetal volume status via transplacental transfer of fluid between the fetal and maternal circulations.3 The third trimester fetal kidneys typically receive only 2% to 4% of the combined ventricular output (versus 15%–18% of the postnatal cardiac output), suggesting a limited homeostatic role for the fetal renal system.30 However, despite a normally functioning placenta, chronic upper extremity hypertension has been created in a fetal lamb model of renal artery disease (via suprarenal aortic obstruction).31 In these experiments, plasma renin activity rose immediately after aortic obstruction with a concomitant rise in blood pressure. Subsequent investigation has shown that angiotensin mediates chronic hypertension, via vasoconstriction in the precapillary resistance vessels of the placenta.32 Others have shown that renin does not cross the placenta, implying that the fetal renin-angiotensin system can act autonomously.30 An elegant mathematical model developed by Faber and colleagues33 that accounts for much of the fetal experimental data in the literature suggests that hypertension in and of itself can lead to hydrops, but that cardiac failure is the strongest stimulus for the development of NHF. We could find only 1 report in the literature describing probable fetal hypertension.34 A 3-day-old boy presenting with systemic hypertension was found to have unilateral left intrarenal arterial abnormalities with an otherwise normal descending aorta; at the time of diagnosis, his heart showed severe biventricular dysfunction and hypertrophy. Together, these data suggest that there is a dynamic interplay between the fetal kidneys and placenta in response to hemodynamic disturbances and that chronic fetal hypertension leading to NHF is possible.

The cardiac findings of our case illustrate the sensitivity of the fetal and neonatal myocardium to increases in afterload. However, it also highlights that severe cardiomyopathy is reversible within days once loading conditions are normalized. Others have also noted this rapid reversibility of ventricular dysfunction.35 It is more difficult to explain the in utero discrepancy of RV versus LV dysfunction. This patient’s right ventricle became severely depressed while the left ventricle, despite working against the same afterload (because the DA was nonrestrictive and no aortic isthmus hypoplasia was present), developed only mild in utero dysfunction.

A final comment is merited regarding our incorrect initial fetal diagnosis of premature ductal closure. Although premature ductal closure is a well-known cause of fetal RV dysfunction and NHF,36 it is possible in this case, with poor RV cardiac output, that antegrade flow across the DA was lower velocity than normal. This, plus the technical limitations of imaging the DA in this hydropic fetus, mimicked premature closure of the DA. More persistent scanning attempting to image the DA in addition to optimizing Doppler settings to enhance demonstration of low velocity ductal flow may help to minimize this error in the future.


   CONCLUSIONS
TOP
 ABSTRACT
 INTRODUCTION
 CASE REPORT
 DISCUSSION
 CONCLUSIONS
REFERENCES
 
We report the first case of a premature infant with midaortic syndrome as the etiology of fetal hydrops, severe neonatal hypertension, and a reversible cardiomyopathy. The etiology and prenatal pathophysiology of this entity remain speculative, and the management of malignant hypertension in the premature neonate poses a particularly challenging therapeutic dilemma. Prenatal and neonatal diagnosis of this rare syndrome in the fetus with NHF and ventricular dysfunction requires a high index of suspicion as well as a detailed evaluation of the abdominal aortic vasculature.


   FOOTNOTES
 
Received for publication Oct 18, 2001; Accepted Dec 11, 2002.

Address for correspondence to Ira A. Parness, MD, Division of Pediatric Cardiology, Box 1201, Mount Sinai Medical Center, One Gustave L. Levy Place, New York, NY 10029. Email: ira.parness{at}mssm.edu


   REFERENCES
TOP
 ABSTRACT
 INTRODUCTION
 CASE REPORT
 DISCUSSION
 CONCLUSIONS
 REFERENCES
 

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PEDIATRICS (ISSN 1098-4275). ©2003 by the American Academy of Pediatrics

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