Anoxic brain injury CT and MRI patterns - quick pictoral quide for junior radiologists.

Transcription

1 Anoxic brain injury CT and MRI patterns - quick pictoral quide for junior radiologists. Poster No.: C-1844 Congress: ECR 2017 Type: Educational Exhibit Authors: A. Kecler - Pietrzyk, W. Torreggiani ; Dublin/IE, Dublin 24/IE Keywords: Neuroradiology brain, Head and neck, CNS, CT, MR, CTAngiography, elearning, Diagnostic procedure, Education, Education and training, Ischemia / Infarction, Pathology DOI: /ecr2017/C Any information contained in this pdf file is automatically generated from digital material submitted to EPOS by third parties in the form of scientific presentations. References to any names, marks, products, or services of third parties or hypertext links to thirdparty sites or information are provided solely as a convenience to you and do not in any way constitute or imply ECR's endorsement, sponsorship or recommendation of the third party, information, product or service. ECR is not responsible for the content of these pages and does not make any representations regarding the content or accuracy of material in this file. As per copyright regulations, any unauthorised use of the material or parts thereof as well as commercial reproduction or multiple distribution by any traditional or electronically based reproduction/publication method ist strictly prohibited. You agree to defend, indemnify, and hold ECR harmless from and against any and all claims, damages, costs, and expenses, including attorneys' fees, arising from or related to your use of these pages. Please note: Links to movies, ppt slideshows and any other multimedia files are not available in the pdf version of presentations. Page 1 of 31

2 Learning objectives Anoxic Brain Injury is caused by prolonged and severe cerebral hypoperfusion. In adults it occurs most commonly in association with cardiac arrest, severe hypotension or less commonly protracted generalised seizures. The hypoperfusion and ischaemia is leading to diffuse brain injury/infarction, which have characteristic imaging patterns in adults and they differ from those seen in children. Imaging is often requested by physicians to establish extend of hypoxia/ ischemia related to brain damage especially in young adults or in cases of uncertain hypoxic/ ischaemic injury circumstances. There is also rising tendency of imaging use as a part of dead brain diagnosis in potential organs donors especially in ocular injury when brain stem can not be adequately assessed. Knowledge of anoxic brain injury imaging patterns is essential for every practicing radiologist and very important for trainees to avoid misinterpretation and subsequent repercusions. Images for this section: Page 2 of 31

3 Fig. 2: Axial images of non - contrast enhanced CT brain in patient admitted unconscious post cocaine overdose. Diffuse brain parenchyma hypo attenuation with loss of grey/ white matter differentiation and hypo density of basal ganglia. Page 3 of 31

4 Fig. 3: Axial and saggital views of non - contrast enhanced CT brain in elderly female with background ischemic heart disease post fall on ward and unconscious since. Reversal of grey/white matter differentiation is demostrated, most pronounced in occipital lobes (visual cortices) and cerebellum. Note also hypo attenuation of the caudate nucleus head on the right. Page 4 of 31

5 Fig. 4: Axial view of non - contrast enhanced CT brain (a) in patient admitted unconscious post cocaine overdose. Effacement of basal cisterns with resultant apparent increased attenuation giving rise to a pseudo subarachnoid sign. Axial view of non - contrast enhanced CT brain (b) in young female with background congenital cardiomyopathy admitted post cardiac arrest. Significant effacement of basal cisterns with resultant apparent increased attenuation giving rise to a pseudo subarachnoid sign. Page 5 of 31

6 Fig. 10: Axial MRI FLAIR (a), T2 (b), DWI B1000 (c), and ADC (d) images in patient found hanging from pylon demonstrating diffuse hypoxic/ischaemic changes throughout Page 6 of 31

7 the brain parenchyma with thickening of cortex especially well appreciated on FLAIR and T2 sequences and significant restricted diffusion on DWI and ADC MAP. Page 7 of 31

8 Fig. 13: Axial MRI T2 (a,c) and DWI B1000 (b,d) images in patient found hanging from pylon demonstrating involvement of medulla oblongata. Page 8 of 31

9 Background Extensive literature and on - line resources review was performed using search terms such as cerebral hypoxic/ischemic (anoxic) brain damage in adults, hypoxic /ischemic encephalopathy, diffuse anoxic brain damage, dead brain imaging patterns etc. Over 100 cases of anoxic brain injury from our institution were reviewed. From a selection of best cases we chose the most accurate CT and MR images to depict in systematic and clear way the imaging findings most commonly associated with the condition. Images for this section: Fig. 2: Axial images of non - contrast enhanced CT brain in patient admitted unconscious post cocaine overdose. Diffuse brain parenchyma hypo attenuation with loss of grey/ white matter differentiation and hypo density of basal ganglia. Page 9 of 31

10 Fig. 4: Axial view of non - contrast enhanced CT brain (a) in patient admitted unconscious post cocaine overdose. Effacement of basal cisterns with resultant apparent increased attenuation giving rise to a pseudo subarachnoid sign. Axial view of non - contrast enhanced CT brain (b) in young female with background congenital cardiomyopathy admitted post cardiac arrest. Significant effacement of basal cisterns with resultant apparent increased attenuation giving rise to a pseudo subarachnoid sign. Page 10 of 31

11 Fig. 13: Axial MRI T2 (a,c) and DWI B1000 (b,d) images in patient found hanging from pylon demonstrating involvement of medulla oblongata. Page 11 of 31

12 Findings and procedure details The brain consumes approximately 15% of the energy generated in the body and it has no energy stores of its own except for a small amount of glycogen in astrocytes. That is a main cause of its susceptibility to damage in settings of energetic crisis. Within the brain there is regional variation in susceptibility to energy depletion with grey matter (cortex and basal ganglia) being most sensitive followed by hipocampii, thalamus and brainstem. This selective vulnerability is caused by differences in morfology for example grey matter consists of neuronal cell bodies and uses approximately 3 times more energy then white matter to maintain resting potentials and restore ionic concentrations after synaptic transmission. Also production of glutamate (exitotoxin released excessively during energy depletion) is different in different areas of the brain. White matter is very rarely affected. Most commonly seen in setting of CO poisoning. Spine is spared in majority of the cases. CT patterns of hypoxic/ ischaemic (anoxic) brain injury: 1. Parenchymal cerebral and/or cerebellar edema with sulcal and other CSF containing spaces. (Fig 1.) 2. Decreased density of cortex with loss of grey/white matter differentiation. Subtle (Fig 1a,b.) or more extensive (Fig1 c,d). Subsequent blurring of the insular ribbons ( Fig 1 c.). 3. Reversal of grey/ white matter differentiation. ( Fig 3.) 4. Hypodensity of basal ganglia and/or caudate nuclei. (Fig 2.) 5. Hyperdensity of cerebellum due to effacement of cerebral parenchyma and relative increase in attenuation of cerebellar parenchyma (called sometimes reversal sign) (Fig 5.) 6. Pseudo - subarachnoid hemorrhage. (Fig 4.) 7. Herniation patterns. 8. Linear cortical enhancement (late sign, seen on CT only in very severe cases, not common) Page 12 of 31

13 9. CTA demostrates reduced or no contrast opacification of intracranial vessels ( especially lack of MCAs opacification and internal cerebral veins). (Fig 6 and 7.) 10. In severe cases of sudden flow cessation hyperdensity of venous sinuses is seen ( Fig 8.) Involvement is usually bilateral and often symmetrical. One or few from above listed features may be demostrated. CT patterns of poor clinical outcome include: reversal of grey/white matter differentiation, involvement of basal ganglia and/ or cerebellum and pseudo - subarachnoid haemorrage. MRI patterns of hypoxic/ ischaemic (anoxic) brain injury: 1. DWI is the earliest (within few hours) imaging modality to become positive (Due to cytotoxic oedema) Restricted diffusion is seen in most cases within cerebral cortex with predominance to sensory, visual and periolandic areas. It varies and may be very subtle (Fig 9.) or diffuse and extesive (Fig 10 c,d.) Early changes may also be seen within cerebellar cortex (Fig. 11), basal ganglia ( Fig 10.), thalami, hipocampii ( Fig 12) and at the level of brainstem (Fig 13 and 14.) 2. T1 and T2 weighted images demostrate no abnormalities in most of the cases in early stages. T2 weighted images typically become positive after 24 hours to 2 weeks and show oedema and increased intensity of the signal of grey matter structures (Fig 10 b.) 3. Hyperintensity of cortex on FLAIR can be seen within few days ( Fig 10 a) 4. T1 hyperintensities indicating cortical laminar necrosis become evident after approximately two weeks. This hyperintense signal does not represent haemorrhage, and it is believed to be caused by the accumulation of denatured proteins in dying cells. 5. In some instances, hypoxia/ ischemia causes bilateral, symmetric cerebral infarcts in the border zones between major arterial territories. It is usually associated with short hypoperfusion ( Fig 15.) Many sources describe it as a sepatate entity to anoxic brain injury as anoxia is not main cause of parenchymal changes, however we decided to demostrate one case of watershed changes as imaging findings oftern overlap. Page 13 of 31

14 MRI patterns of poor clinical outcome include: diffuse involvement of cortex (especially periolandic cortex), deep grey matter (basal ganglia, thalami) and cerebellar involvement. Additionally brainstem or hippocampal (Fig 13,14 and 12.) involvement is usually well demostrated on MRI DWI and is bad prognosis predictors. Dead brain diagnosis: CT Diffuse brain oedema with ventricular and sulcal effacement. Loss of grey/white matter differentiation or its reversal. Cereberral reversal sign. Pseudo - subarachnoid sign. Tonsilar herniation. Hyperdensity of venous system. Lack of MCAs opacification and internal cerebral veins on CTA. MRI Diffuse, extensive grey matter oedema. T1 Diffusely hypointense grey matter. T2 Diffusely hyperintense grey matter. DWI extensive restricted diffusion. Effacement of vetricular system. Brainstem involvement. Tonsillar herniation. Loss of normal flow voids. Images for this section: Page 14 of 31

15 Fig. 1: Axial (a) and coronal (b) views of non - contrast enhanced CT brain in patient admitted unconscious post cocaine overdose. Brain edema with very subtle loss of white/ grey matter differentiation is noted. Axial view of non - contrast enhanced CT brain in Page 15 of 31

16 patient admitted with multiorgan trauma (c) demonstrating brain edema and slightly more pronounced white/ grey matter differentiation. Axial view of non - contrast enhanced CT brain in patient post RTA (d). Extensive brain edema with loss of normal sulcal pattern and complete loss of white/ grey matter differentiation throughout both cerebral hemispheres Fig. 2: Axial images of non - contrast enhanced CT brain in patient admitted unconscious post cocaine overdose. Diffuse brain parenchyma hypo attenuation with loss of grey/ white matter differentiation and hypo density of basal ganglia. Page 16 of 31

17 Fig. 3: Axial and saggital views of non - contrast enhanced CT brain in elderly female with background ischemic heart disease post fall on ward and unconscious since. Reversal of grey/white matter differentiation is demostrated, most pronounced in occipital lobes (visual cortices) and cerebellum. Note also hypo attenuation of the caudate nucleus head on the right. Page 17 of 31

18 Fig. 4: Axial view of non - contrast enhanced CT brain (a) in patient admitted unconscious post cocaine overdose. Effacement of basal cisterns with resultant apparent increased attenuation giving rise to a pseudo subarachnoid sign. Axial view of non - contrast enhanced CT brain (b) in young female with background congenital cardiomyopathy admitted post cardiac arrest. Significant effacement of basal cisterns with resultant apparent increased attenuation giving rise to a pseudo subarachnoid sign. Page 18 of 31

19 Fig. 5: Saggital view of non - contrast CT brain of young patient admitted post prolonged cardiac arrest of unknown cause. Hyperintensity of cerebellar tissue is noted which is relative due to global hypo density of cerebral parenchyma. Note also low lying cerebrllar tonsils - sign of early herniation. Page 19 of 31

20 Fig. 6: Axial view of contrast enhanced brain angiography in patient admitted post RTA with multi organ trauma. No contrast opacification of cerebral vessels is noted. Page 20 of 31

21 Fig. 7: Saggital view of contrast enhanced brain angiography in patient admitted post RTA with multi organ trauma. No contrast opacification of cerebral vessels is noted. Page 21 of 31

22 Fig. 8: Non - contrast enhanced CT brain in patient with multi organ trauma. Diffuse loss of grey/ white matter differentiation. Hyper density of venous sinuses consistent with cessation of flow. Page 22 of 31

23 Fig. 9: Axial images from DWI in elderly patient with known poorly controlled arrythmia admitted to Intensive Care Unit post short duration cardiac arrest. Very poor response to trials of removal of endotracheal intubation tube. Other sequences showed no acute Page 23 of 31

24 abnormality. Symmetrical, subtle signal restriction involving temporal lobes, basal ganglia and hippocamp. Page 24 of 31

25 Fig. 10: Axial MRI FLAIR (a), T2 (b), DWI B1000 (c), and ADC (d) images in patient found hanging from pylon demonstrating diffuse hypoxic/ischaemic changes throughout Page 25 of 31

26 the brain parenchyma with thickening of cortex especially well appreciated on FLAIR and T2 sequences and significant restricted diffusion on DWI and ADC MAP. Page 26 of 31

27 Fig. 11: Axial MRI FLAIR (a), T2 (b), DWI B1000 (c), and coronal T2 (d) images in patient with prolonged seizure activity demonstrating T2/ FLAIR cortical hyper intensity and oedema involving in particular cerebellar hemispheres. Fig. 12: Axial MRI T2 (a) and DWI b1000 (b) images in patient admitted post unknown substance overdose with short duration cardiac arrest demonstrating diffuse hypoxic/ ischaemic changes with involvement of hippocampal areas bilaterally. Page 27 of 31

28 Fig. 13: Axial MRI T2 (a,c) and DWI B1000 (b,d) images in patient found hanging from pylon demonstrating involvement of medulla oblongata. Page 28 of 31

29 Fig. 14: Sagittal view of T2 weighted MRI on patient found hanging from pylon demonstrating high signal within brainstem. Page 29 of 31

30 Fig. 15: Axial views of T2 weighted (a), FLAIR (b), DWI B1000 (c) and ADC MAP (d) demonstrating extensive bilateral linear foci of high signal within the centrum semi - ovale. The abnormalities are at the borderzone of the ACA/MCA and MCA/PCA. Page 30 of 31

31 Conclusion Hypoxic / ischaemic injury patterns are in adults are different then those in children. They are highly variable and depend on severity and lenghth of insult but also modality and time of imaging. Personal information Contact: Dr Aneta Kecler - Pietrzyk anetakecler.pietrzyk@gmail.com Phone nr: AMNCH Hospital Dublin, Ireland References Muttikkal TJ, Wintermark M. MRI patterns of global hypoxic-ischemic injury in adults. J Neuroradiol Jul;40(3): Huang BY, Castillo M. Hypoxic-ischemic brain injury: imaging findings from birth to adulthood. Radiographics (2): BiagasK. Hypoxic-ischemic brain injury: advancements in understanding of mechanisms and potential avenues for therapy. Curr Opin Pediatr1999; 11: Page 31 of 31