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Demanding clarification that venous thrombosis is representative of vascular trauma

We appreciate comments on our work; open debate is the forge in which science can be tested and refined. We agree absolutely with Donaruma et al that “Another point demanding clarification is interpreting venous thrombosis as representative of vascular trauma.”1 This clarification was the point of our article.2 Our article is based on data acquired by review of the literature concerning the validity of the hypothesis that thrombosis of bridging veins (BV) is a marker of rupture and abuse; an opinion would not require such a factual basis. We disagree that “hypoxia causes the SDH reported in cases of suspected AHT.” Instead, we suggested that dural based bleeding is the result of a complex cascade that includes hypoxia, oedema, and increased intracranial and central venous pressure. We agree that the duraarachnoid continuum is weakest in the deep dural border layers. We disagree that the bridging veins are weakest here; decades of repetition of a single study of four elderly patients do not constitute strong evidence; if we have missed these decades of literature, we would appreciate the citations. Anatomic evidence instead shows that the BV acquire a smooth muscle sphincter within the dura, a fact the authors ignore. We disagree that we misinterpret Rambaud. She, like Case, illustrated disrupted, thrombosed and inflamed vessels. We point out that there is nothing specific to trauma in venous inflammation in the presence of thrombosis. Thrombosis and inflammation are tightly interlinked, and thrombosis itself generates an inflammatory response. Neither illustrated correlation of their findings with the radiological observations in these cases. We agree that birth is an important contributor to intracranial haemorrhage. We considered it and specifically its potential effect on later findings and symptoms. Emerging data underline the importance of this consideration; SDH is an inflammatory condition and may precede and predispose to thrombosis, and the vast majority (81%) of SDH in infants thought to have been abused is old.3 We disagree that we overlooked the Rafaat study. We did not find it helpful. That study involved only 18 infants (0– 1 years) and did not provide sufficient data to know how long these babies may have been hypoxic, nor how long each was resuscitated. Rafaat compared his group with babies thought to have been abused, but his observations are infected by circularity. We are unaware of any autopsy verification of the assertion that the imaging appearance of “continuous intraand extraluminal thrombosis creates a lollipop/tadpole sign” or that this finding is unique to trauma. The authors do not explain how they exclude diapedesis of red cells from thrombosed vessels as contributing to this appearance. Diapedesis is not an indication of trauma; it simply reflects a damaged vein wall secondary to distention by thrombosis. We agree that nontraumatic causes are more common aetiologies of venous thromboses but are perplexed by the accusation we “should offer supporting evidence.” We provided this evidence in three comprehensive surveys of paediatric venous thrombosis.