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Neuroimaging
Original research
Imaging features and prognostic factors in fetal and postnatal torcular dural sinus malformations, part I: review of experience at Boston Children’s Hospital
  1. Edward Yang1,2,
  2. Armide Storey1,3,
  3. Heather E Olson2,4,
  4. Janet Soul2,4,
  5. Judy A Estroff1,2,
  6. Cameron C Trenor5,
  7. Benjamin K Cooper1,
  8. Edward R Smith3,6,
  9. Darren B Orbach1,2,3
  1. 1 Department of Radiology, Boston Children’s Hospital, Boston, Massachusetts, USA
  2. 2 Advanced Fetal Care Center, Boston Children’s Hospital, Boston, Massachusetts, USA
  3. 3 Cerebrovascular Surgery and Interventions Center, Boston Children’s Hospital, Boston, Massachusetts, USA
  4. 4 Department of Neurology, Boston Children’s Hospital, Boston, Massachusetts, USA
  5. 5 Stroke and Cerebrovascular Center and Division of Hematology/Oncology, Boston Children’s Hospital, Boston, Massachusetts, USA
  6. 6 Department of Neurosurgery, Boston Children’s Hospital, Boston, Massachusetts, USA
  1. Correspondence to Dr Darren B Orbach, Department of Radiology, Boston Children’s Hospital, Boston, MA 02115, USA; darren.orbach{at}childrens.harvard.edu

Abstract

Background Even for the most common dural sinus malformation (DSM), the torcular DSM (tDSM), generalizable statements about etiology and prognosis are difficult because neurosurgeons/neuroradiologists and obstetrical imagers have focused on different patient age groups, have reported different outcomes, and have offered differing pathophysiologic explanations.

Objective To examine the imaging features and outcomes of a local cohort of tDSMs across fetal–neonatal life for commonalities.

Methods Review of imaging and clinical outcome for a local cohort of 12 tDSM patients (9 fetal, 3 postnatal).

Results All 12 tDSMs had similar imaging characteristics, including enlargement of the torcular and intraluminal thrombus early on, later evolving to peripheral scar tissue after treatment or spontaneous regression. Spontaneous decrease in size of the tDSM was observed in 6 prenatal and 1 postnatal case, and this decrease appeared to be irreversible once it occurred. One of 9 prenatal tDSMs was demonstrated to have arteriovenous fistulae in utero, while 2 of 3 postnatal diagnoses had arteriovenous fisutlae. All 6 prenatal tDSM diagnoses followed to term and all 3 postnatal diagnoses had a grossly normal neurologic outcome after a median of 12 months of age.

Conclusions Prenatal and postnatal tDSMs have overlapping imaging features suggesting a common etiology, and involution of a tDSM is a key imaging biomarker for a favorable outcome. While there is reason for concern with postnatally diagnosed tDSMs, good outcomes may still be achieved across the fetal–neonatal age spectrum of presentations. These findings are generalized in part II of this article.

  • dural arteriovenous fistula
  • dural sinus malformation
  • fetal vascular malformation

https://doi.org/10.1136/neurintsurg-2017-013344

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    Introduction

    Dural sinus malformations (DSMs) were originally described in the neurointerventional literature as low flow dural arteriovenous fistulae (dAVF) in neonates and infants, featuring giant venous lakes at the affected dural sinus.1 2 DSMs were characterized by severe neurologic morbidity or death, seen in 41% of DSMs overall and in 71% of the more severely affected torcular DSM (tDSM) subgroup.1 This important observation has been a source of consternation when counseling parents of patients with tDSMs during pregnancy or early infancy.

    Subsequent to the neurointerventional description in the postnatal population, a morphologically identical in utero lesion was described in the obstetric imaging literature, frequently seen with intraluminal thrombus.3 4 The vast majority of these fetal lesions had the same midline torcular location that had been associated with poor outcome in the neurointerventional literature. While labeled DSMs by some authors, these fetal cases could only be assessed for arterialization using Doppler ultrasound and lacked direct visualization of the angioarchitecture of the venous lakes. Additionally, some authors conceptualized these fetal dural sinus lesions as secondary manifestations of in utero dural sinus thrombosis, particularly in cases where the clot was a dominant morphological feature.3–14 Confusing matters further, fetopsy results from some of these fetal tDSMs suggested that the dilated pouch or area of thrombosis was actually extraluminal in some cases.15 16

    Better understanding of tDSMs and their natural history is critical, as a considerable number of tDSM pregnancies have been terminated electively based on a presumed poor prognosis. But in marked contrast to this expected clinical course, more recent literature has suggested a generally favorable prognosis for in utero tDSMs,4 11 17 among which reportedly 75–90% of pregnancies achieved survival with no neurocognitive sequelae. The pathophysiological basis of the improved outcome in this fetal subpopulation has been unclear and has been confused by questions as to whether tDSMs represent a single or multiple processes.

    To clarify the natural history, prognosis, and etiology of tDSMs, we undertook an analysis of patients with tDSMs encountered at our referral center to identify common features.

    Methods

    Definition of tDSM

    We focused on the tDSM because it comprises the single largest group of DSMs encountered in utero, and because of the poor outcome for this subgroup reported in the neurointerventional literature. We defined a tDSM as an intradural mass (fluid and/or clot) centered at the torcular, regardless of whether it was associated with demonstrable thrombus or arterialized flow. We included cases interpreted as intradural thrombus, dural sinus thrombus, or AVFs of varying flow rates, provided that there was evidence of enlargement and remodeling of the intradural space (eg, anteroposterior dimension greater than the brainstem). Only cases centered on the torcular were included for analysis; multifocal dAVFs or diffuse enlargement of the dural sinuses due to fistulae at the sigmoid sinuses were omitted.

    Patient population

    With institutional review board approval, we conducted a retrospective search of tDSM referrals to our Advanced Fetal Care Center in the past 10 years. Additionally, a database search of fetal MR studies performed since January 2001 in our institution’s Radiology Information System was conducted, using the search terms ‘torcular,’ ‘hematoma,’ ‘vascular malformation,’ ‘fistula,’ ‘thrombus,’ ‘arteriovenous malformation,’ and ‘dural sinus malformation’. These searches yielded a total of nine prenatally and three postnatally diagnosed tDSMs. Table 1 summarizes the details of these cases.

    View this table:
    Table 1

    Characteristics of the nine prenatally and three postnatally diagnosed cases of torcular dural sinus malformation

    Imaging technique

    Standard prenatal and postnatal imaging techniques were used. Details are provided in the online supplementary materials.

    Supplementary file 1

    Clinical outcome

    To allow comparison with the literature analysis in part II, we assessed outcome using a simplified three tiered outcome scale for cases seen at our institution (corresponding score from Barbosa et al 1 in parentheses):

    1. Favorable (minimal to no neurologic deficit) (Barbosa 3–5)

    2. Unfavorable/uncertain (moderate to severe deficit or unclear outcome, but certainly neither dead nor only minimally injured) (Barbosa 1, 2, or unspecified)

    3. Death (Barbosa 0)

    Results

    Referral center experience with tDSM

    Demographics

    A total of nine prenatally diagnosed tDSMs (mean presentation at 24 weeks' gestational age±5 weeks) and three postnatally diagnosed tDSMs (mean presentation at 67 weeks' postmenstrual age±24 weeks) were identified in our patient population (see table 1 and online supplementary table 1). Cases were evenly split between males and females. Of the nine prenatally diagnosed tDSMs, six were delivered live and have postnatal follow-up; three were electively terminated. One of the postnatally diagnosed cases (case No 10) was included in a prior case series.18

    Supplementary file 2

    Imaging characteristics

    At presentation, the mean anteroposterior dimension of the tDSMs was 2.7±0.8 cm and the mean craniocaudal dimension of the tDSMs was 4.0±1.3 cm for the fetal cases. For the three cases diagnosed during infancy, the mean anteroposterior dimension of the tDSMs was 3.5±1.0 cm and the mean craniocaudal  dimension of the tDSMs was 7.3±3.9 cm. Nine of the 12 cases had midline/symmetric tDSMs with 2 right side eccentric and 1 left side eccentric tDSMs (all 3 eccentric cases were fetal).

    Evidence of tDSM arterialization was present in one of the nine fetal cases and two of the three postnatal cases. In the fetal case (case No 1), there was direct arteriovenous communication between the middle meningeal arteries and the tDSM demonstrated on fetal MR (figure 1 and online supplementary figure 1), the first such imaging demonstration in utero, to our knowledge. Two other fetal cases had pulsatile blood flow on the margins of the tDSM by Doppler ultrasound (case Nos 6 and 8), although this could not be confidently ascribed to arterial flow.19 The two postnatally detected tDSMs with dAVFs (case Nos 10 and 11) had direct arteriovenous communication demonstrated using both MRI/MR angiography and conventional angiography (online supplementary figure 2). Postnatal case No 12 did not have identifiable arteriovenous communication at the tDSM even on catheter angiography (online supplementary figure 6).

    Supplementary file 3

    Figure 1
    Figure 1

    A torcular dural sinus malformation (tDSM) at 33 weeks (case No 1) demonstrates a dilated venous lake involving the torcular on HASTE imaging (A) and enlarged feeding arteries to the tDSM from the middle meningeal arteries on VIBE T1 (shown as a MIP in (B)).

    Evolution over time

    Serial imaging was obtained in eight of the nine fetal cases (two eventually terminated), and six had follow-up through at least the neonatal period, allowing for evaluation of their natural history. As seen in online supplementary table 1, all six cases followed to delivery underwent spontaneous tDSM regression, while two terminated cases were stable to increased in overall size at the time of termination (case Nos 2 and 3). It is particularly worth noting that three of the six cases with spontaneous involution initially increased in overall size before eventually decreasing (case Nos 1, 5, and 8), and tDSMs in our cohort never underwent an increase in size once a decrease was observed (ie, increase was an indeterminate finding but decrease appeared to be an irreversible process). These features of spontaneously resolving fetal tDSMs are illustrated in online supplementary figure 3. One postnatally diagnosed tDSM (case No 12) also demonstrated spontaneous regression with expectant management.

    tDSM thrombosis

    All 12 cases demonstrated the presence of thrombus at some point. Of the nine fetal tDSM cases, the thrombus was located posteriorly in four cases, anteriorly in four cases, and circumferentially in one case. The clots were lateralized to the right in three of nine cases and to the left in two cases; thrombus lateralization was not clearly attributable to eccentricity of the tDSM itself. In six of the nine prenatal cases (case Nos 3–5, 7–9), the thrombus demonstrated a two intensity pattern, with inner T2 hyperintense and outer T2 hypointense clot (figure 2), reminiscent of some fetopsy series demonstrating layering/concentric thrombus.12 17 20 In two of the three postnatal cases (case Nos 10, 12), the thrombus occupied nearly the entire volume of the tDSM, with the remaining postnatal case having only a small clot in the superior sagittal sinus adjacent to the tDSM. Of note, the fraction of the tDSM volume occupied by thrombus appeared to transiently increase in three of the six prenatal cases (case Nos 4, 5, 8), and the tDSM still went on to trend toward resolution.

    Figure 2
    Figure 2

    Spontaneous involution of a torcular dural sinus malformation (tDSM) (case No 4). Sagittal HASTE imaging at 28 weeks' gestation demonstrates an enlarged torcular complex with two intensity thrombus inferiorly (A). Sagittal T1 imaging at 35 weeks demonstrates contraction of the tDSM but an increased absolute size of the thrombus and percentage of the tDSM filled by clot (B). By 8 months of age, sagittal (C) and axial (D) T1 weighted imaging demonstrates resolution of the clot with apparent incorporation into the dural sinus wall.

    Delivery

    For the six prenatal cases with live births, one delivery was induced in response to pre-eclampsia (case No 4), three were delivered by cesarean section (case Nos 1, 8, 9), one underwent spontaneous vaginal delivery (case No 7), and one had an unknown mode of delivery (case No 5). Of the two pregnancies with induced or spontaneous vaginal delivery, only one had documented presence of the tDSM at the time of delivery (case 4). The postnatal tDSM cases were delivered by cesarean section in one case and vaginal delivery in two cases, but none of these postnatally diagnosed cases had documented presence of the tDSM at the time of delivery. Thus only one case in our cohort underwent vaginal delivery in the presence of a known tDSM. While no adverse effect was associated with vaginal delivery in this one case, conclusions about the overall safety of mode of delivery in the setting of a tDSM cannot be extrapolated from our data.

    Interventions and treatment

    Increasing ventricular caliber and mild congestive failure in the setting of arterialization prompted endovascular embolization of case No 1 at 3 months despite downward trending size of the tDSM. The only other therapeutic interventions were in two of the postnatally diagnosed cases. In case No 10, embolization was performed to address ongoing arterialization of the tDSM in the setting of signs of elevated intracranial pressure (distended scalp veins, macrocephaly, and vomiting). After embolization, clinical improvement rapidly ensued once anticoagulation was instituted to manage the postembolization increase of thrombosis (low molecular weight heparin titrated to anti-factor Xa levels of 0.5–1.0 units/mL) and venous drainage was redirected around the occluded superior sagittal sinus and torcular. In case No 11, staged embolization was performed to address signs of venous hypertension (distended facial veins and developmental delay) and was also well tolerated. In all three of these cases (case Nos 1, 10, 11), dAVF feeders arose primarily from the middle meningeal and occipital arteries, with minor contributions from other arteries. All three cases requiring intervention have had grade A (favorable) outcomes through follow-up, ranging from 18 months to 10 years.

    Clinical outcomes

    Serious complications from mass effect or venous congestion were uncommon in our cohort. In case No 2, an in utero left parietal infarct developed, presumably venous (online supplementary figure 4). The remaining prenatal and postnatal cases had mild or transient findings, with no lasting developmental delay or neurologic deficits at the time of the last follow-up. Case No 1 had mild congestive failure as well as prominence of the extra-axial spaces and ventricles by 3 months, resolved after endovascular embolization. Mild ventriculomegaly was also seen transiently with case No 8 in the setting of posterior fossa compression. Case Nos 7 and 9 had grade 1 germinal matrix hemorrhages, possibly unrelated to the tDSM. The three postnatally diagnosed tDSMs (case Nos 10–12) all presented with signs of venous congestion. One of these three patients had some pretreatment developmental delay, and two had mild to moderate ventriculomegaly (persistent moderate ventriculomegaly in case No 11). As seen in online supplementary table 1, all fetal cases who were carried to term and all postnatal cases had grade A outcomes through a median of 12 months of age, including those with ventriculomegaly or with an initial presentation of developmental delay. Additionally, complications of the tDSM were seen in only one of the three pregnancies ending in elective termination of pregnancy (case No 2 discussed above).

    Imaging outcomes

    The last available follow-up imaging for the patients in this series demonstrate the evolution of treated and untreated tDSMs. In the six prenatally diagnosed cases followed to term, a peripheral small filling defect was present at or near the wall to which the thrombus was adherent in utero (online supplementary figures 1, 3, and 5). In one patient who is still being followed (case No 8), non-obstructive clot remains present, but the obtuse, smooth borders suggest evolving incorporation into the wall. Incorporation into the dural leaflets or wall of the sinus is also suggested by chronic clot which appeared extraluminal in some cases (case Nos 4, 5, 7). In some instances, calcification of the residual filling defect was identified on ultrasound (case No 8) or postnatal CT (case Nos 5, 7), a feature also noted in a few prior fetopsy and imaging series.21 22 Postnatal case Nos 10, 11, and 12 demonstrated chronic dural sinus obliteration and irregularity consistent with chronic thrombus or scarring, sometimes accompanied by sequestration of clot away from the scarred lumen (online supplementary figures 2 and 6).

    Discussion

    While sometimes differing pathophysiological explanations have been offered for tDSMs in the obstetric literature versus the neuroangiographic/neurosurgical literature,1 3–17 we found prenatal and postnatal tDSMs to have indistinguishable features in our local cohort. In addition to having identical giant venous lakes at the torcular, we found that tDSMs can have dAVFs detectable on imaging in utero, as was originally described in postnatal tDSMs. Conversely, we found that postnatal tDSMs can present without detectable arterialization despite having characteristic enlargement of the torcular. Likewise, there was a high frequency of thrombus in both prenatal and postnatal tDSM diagnoses, and spontaneous tDSM regression could be seen in both the prenatal and postnatal populations although this regression was less common in the postnatal cohort. Of particular interest, we found that tDSM regression was an irreversible event in our cohort even if it had been first preceded by tDSM enlargement. Finally, we found that the imaging appearance of tDSMs across the fetal–neonatal age group was similar after spontaneous regression or embolization, manifesting as seemingly sequestered thrombus and/or peripheral scar tissue.

    Although many of the tDSMs in our cohort could be managed expectantly, three of our subjects (one prenatal and two postnatal diagnoses) required intervention. Our approach has been to closely monitor neonates with tDSMs and to pursue early intervention when patient symptoms develop. These interventions were well tolerated, but it is worth emphasizing that abrupt changes in hemodynamics may necessitate anticoagulation, as shown in case No 10.

    In terms of outcome, our findings accord with other case series that suggest good (grade A) outcomes for prenatally diagnosed tDSMs. But contrary to the original reports of tDSMs, the outcomes of the postnatally diagnosed tDSMs were equally as good as prenatally diagnosed tDSMs in our cohort. While relatively small in number, these postnatal cases may indicate that there is room for optimism even for this subpopulation of tDSM patients. While the rudimentary nature of our outcome scale omits detailed neurodevelopmental assessments (eg, neuropsychological testing), the six subjects still followed by our center have disclosed no evidence of neurocognitive limitations, including the two followed into elementary school age. However, broader statements on the development outcomes of patients with treated or spontaneously regressed tDSMs will require longer term study of a larger patient population.

    Conclusion

    Although there was a greater propensity for arterialization and need for intervention in neonatal tDSM diagnoses, we found evidence for similar imaging characteristics and evolution in tDSMs across the fetal–neonatal range of age presentations, suggesting they have a common etiology. Therefore, the neonatal tDSM presentations may represent a subset of fetal tDSMs in which spontaneous regression does not occur. In part II of this article, we examine the literature for support of this interpretation. We also systematically review prognostic factors for tDSMs to inform a rational approach to managing fetal–neonatal tDSMs, with an emphasis on determining whether irreversible tDSM contraction seen in our cohort is a generalizable phenomenon.

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    Footnotes

    • Contributors EY and AS assembled the patient cohort, analyzed the patient data, and wrote the manuscript. EY, AS, and DBO reviewed the imaging data. HEO, JS, JAE, CCT, BC, ERS, and DBO identified the relevant patients and provided clinical information. DBO conceived of and supervised the study. All authors have contributed to the drafting of the manuscript and have approved the final version.

    • Competing interests None declared.

    • Ethics approval The study was approved by the Boston Children’s Hospital institutional review board.

    • Provenance and peer review Not commissioned; externally peer reviewed.

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