Does Intracranial Venous Thrombosis Cause Subdural Hemorrhage in the Pediatric Population?

Discussion

It has been proposed that spontaneous IVT may precipitate SDH in infants and children, resulting in SDHs that appear similar to traumatic SDHs seen in AHT.^12,13 The theory that dural venous sinus thrombosis leads to increased pressure or tension in cortical veins and thus results in subdural bleeding was not observed in any patient in this retrospective study.^{4⇓⇓–7,14} Our careful review of case reports that suggest IVT as an initiating event leading to SDH reveals that they barely satisfy the criteria for level III quality data, as established by the US Preventive Services Task Force. In fact, even in 1937, Bailey and Hass elegantly described 3 pediatric patients with IVT, 2 of whom had SDH at autopsy. In the authors' words, they could “establish no absolute interdependence of the original thrombus in the superior longitudinal sinus and the intracranial hemorrhage.”⁴ Bucy and Lesemann's report, in 1978, of a patient with idiopathic recurrent thrombophlebitis and SDH did not comment upon the use of therapeutic anticoagulation as a potential risk factor for SDH and presumed a causal relationship between IVT and SDH.⁵ More recently, in 1982, Matsuda et al reported the occurrence of IVT and SDH in a 33-year-old woman.⁶ Interestingly, the patient had received urokinase before the diagnosis of SDH; the patient's coagulation status at the time the SDH was diagnosed was not reported. Takamura et al reported on a 35-year-old man with multiple systemic hemangiomas, cerebral venous thrombosis, consumptive coagulopathy, and chronic left SDH.¹⁴ The authors postulated that collateral venous pathways caused hemodynamic stress and rupture of bridging veins, leading to SDH. In addition, the authors reported multiple areas of dural-based enhancement on MR imaging, leading to speculation that if the dura were involved with cavernous hemangiomata, the patient would reasonably be predisposed to develop SDH. In 2005, Singh et al reported on a 39-year-old man with IVT and bifrontal hygromas.⁷ No mention was made of antecedent trauma or whether the brain MR imaging evaluation included GRE imaging to assess for the presence of blood products.

None of the previous reports have substantiated the claim that increased intracranial pressure, either acute or chronic, resulting from IVT may play a role in causing SDH.¹⁵ Neither the previous mentioned case reports nor the autopsy series of Bailey and Hass described findings to support pre-existing elevated intracranial pressure.^{4⇓⇓–7,14} Other clinical and imaging observations observed in conjunction with IVT include brain herniation syndromes, cerebral ischemia, or strokes that one might observe with acute states of intracranial hypertension, secondary to acute IVT, were also not described.^{4⇓⇓–7,14,15} Therefore, in concordance with the literature, our study also does not support the correlation of IVT with SDH. It remains an untenable position that, in a child who presents with a traumatic SDH and then subsequently develops IVT, IVT is the cause and not the result of the injury. AHT can be a difficult diagnosis to make in an in infant or young child. There is rarely a history of trauma that correlates with the severity of the head injury, and other indicators of abusive injury are often present.

In our retrospective observational study of pediatric patients with isolated and extensive IVT, an association of IVT with SDH was not identified. We postulated that if venous backpressure in the setting of IVT had a causal relationship to SDH, we would expect to see SDH, particularly in our patients with extensive IVT. This was not the case in our study. In addition, 3 of our cases, which were excluded due to an absence of IVT, demonstrated a valuable point in the imaging of suspected IVT. In 2 cases excluded from our series, on noncontrast CT brain imaging, SDH—as well as epidural empyema—mimicked dural venous sinus thrombosis when, in fact, the venous sinus was compressed by the blood or empyema. In our excluded cases, the diagnosis of IVT was initially erroneously made on noncontrast CT. However, in each case where MRV was performed, IVT was not confirmed, and the diagnosis of SDH and/or epidural empyema was ultimately correctly established. These 3 cases reinforce an important point: When SDH, due to head trauma (abusive or accidental), is suspected, MR imaging and possibly enhanced MRV often have a critical role in accurately defining the character of hemorrhage and its location, assessing the adjacent brain parenchyma, and confirming venous patency.

The limitations of our study include the small subject group and retrospective design. Prospective studies to evaluate for the presence of IVT in the setting of documented AHT would be valuable to support our findings. In conclusion, in our study of pediatric patients, nontraumatic isolated and extensive IVT was not associated with subdural hemorrhage. Therefore, we conclude that IVT does not appear to be the initiating event for SDH. This study emphasizes the importance of having suspected head trauma cases read by a radiologist familiar with pediatric neuroimaging and the CT/MR imaging features of AHT. Collaboration with a clinician experienced in pediatric medicine and child abuse issues is also important for clinical corroboration.