Is there a causal relationship between the hypoxia-ischaemia associated with cardiorespiratory arrest and subdural haematomas? An observational study

Abstract

The aim of this study was to determine the frequency of subdural haematomas (SDHs) occurring in infants presenting following atraumatic cardiorespiratory collapse. This study was a review of retrospective case notes, brain imaging and post-mortem examinations carried out in the paediatric intensive care unit (PICU) and emergency department (ED) in a tertiary paediatric centre in the UK. The study included infants and children less than 4 years old dying in the ED or admitted to the PICU after atraumatic cardiorespiratory arrest. We identified macroscopic SDHs on brain imaging or post-mortem examination. Of those children who experienced a cardiorespiratory arrest from a non-traumatic cause and met inclusion criteria, 33 presented and died in the ED and 17 were admitted to the PICU. These children had a post-mortem examination, brain imaging or both. None of these infants had a significant SDH. One child had a small clot adherent to the dura found on post-mortem and two had microscopic intradural haemorrhage, but it is unclear in each case whether this was artefact, as each had otherwise normal brains. Subdural haematoma arising in infants or young children in the context of catastrophic cardiorespiratory compromise from a non-traumatic cause was not observed.

Figure 1

Case identification of children admitted to the paediatric intensive care unit. ICD, International Classification of Diseases; CNS, central nervous system; PM, post-mortem; DIC, disseminated intravascular coagulation.

Figure 2

Case identification of children dying in the emergency department. NAHI, non-accidental head injury; PM, post-mortem.

Figure 3

Diffuse hypoxic brain injury. 3-month-old infant scanned post mortem after presenting following a history of overlying. Unenhanced cranial CT at (a) the basal ganglia and (b) the bodies of the lateral ventricles showing a global reduction in cerebral density with loss of cortical visualisation and a “bright cerebellum” sign, with more pronounced hypodensity of the deep grey matter nuclei, the hippocampi, the midbrain and parts of the cortex.

Figure 4

Diffuse hypoxic brain injury in a 7-month-old infant admitted following a successful resuscitation of cardiac arrest with associated dilated cardiomyopathy. (a) Unenhanced cranial CT scan on the day of admission shows global reduction in cerebral density with reduced grey/white matter differentiation and a “bright cerebellum sign”. (b) Unenhanced axial T₂ and (c) T₁ weighted MRI scans 4 days following initial CT showing T₂ hyperintensity in the globi pallidi, with subtle T₂ hyperintensity in the putamen and thalami bilaterally. Note the absence of subdural haematoma on the T₁ weighted image. (d) Axial T₂ weighted MRI at 3 weeks following the acute presentation, demonstrating generalised atrophy, particularly affecting the basal ganglia.

Figure 5

Post-mortem cranial CT in a 3-month-old infant who presented to the emergency department in cardiorespiratory arrest after being found unresponsive in the parents' bed. Images (a) at the level of the basal ganglia and (b) through the centrum semiovale show generalised reduction in grey/white matter differentiation. Note the dense post-mortem appearances of the dural venous sinuses (white arrows).

Figure 6

Patchy hypoxic brain injury in a 1-month-old infant following an admission for apnoea. A cardiorespiratory arrest was witnessed on the ward. Unenhanced cranial CT scan shows focal loss of grey/white matter differentiation in the posterior temporal regions bilaterally (white arrows).

Figure 7

Focal hypoxic injury in a child aged 1 year and 11 months. MRI scan performed 3 days after a near-drowning incident. (a) Axial T₂ image shows subtle hyperintensity of the hippocampal tails (white arrows) and posterior putamen bilaterally (black arrows), with (b) corresponding high signal on the B = 1000 diffusion-weighted images.