The tale of global hypoxic ischaemic injury Poster No.: C-0400 Congress: ECR 2016 Type: Educational Exhibit Authors: L. M. Zammit, R. Grech ; Paola/MT, Dublin 9/IE Keywords: CNS, CT, MR, Education, Computer Applications-Detection, diagnosis, Imaging sequences, Acute, Ischaemia / Infarction DOI: 10.1594/ecr2016/C-0400 1 2 1 2 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. www.myesr.org Page 1 of 23
Learning objectives 1. 2. 3. To determine the timely radiological features of global hypoxic ischaemic injury To assess hypoxic-ischaemic brain injury in different radiological windows of Ct and MRI scanning To interpret changing radiological features in the light of clinical examination Page 2 of 23
Background Definition Global hypoxic ischaemia injury can affect the neonates, older children and adults. It is secondary to an underlying cause and typically presents with a deterioration in conscious level as scored on the Glasgow Coma Scale. It can be accompanied by clinical features related to its cause, typical biochemical derangements, often metabolic acidosis, and imaging. Pathophysiology HI-BI occurs when combined low oxygen tensions and limited blood supply are delivered to the brain. This results in cellular energy failure and neuronal death. Grey matter, basal ganglia and cerebellum are more susceptible to the ischaemic changes in view of their higher metabolic rate and there sensitivity to glutamate excitotoxicity. The pattern of involvement is characteristically symmetrical. Glutamate, an excitatory amino acid, is released in higher levels in global hypoxic ischaemic injury and its uptake is reduced. Intracellular calcium increases along with oxygen free- radicals. Lipid peroxidation follows and these changes cause a disturbance in the autoregulation of cerebral blood flow. Brain injury is often irreversible in global hypoxic ischaemic injury. The post- HI-BI sequelae include: 1. 2. 3. 4. seizures sensory deficits motor deficits e.g. dystonia, chorea cognitive ailments Clinical presentation Page 3 of 23
The main clinical feature in HI-BI is a deterioration in the conscious level or sudden death. This can occur secondary to a wide spectrum of causes. The main clinical feature in HI-BI is a deterioration in the conscious level or sudden death. This can occur secondary to a wide spectrum of causes. Hi-Bi has a trimodal presentation. Perinatal period: Birth asphyxia leading to hypoxic ischaemic encephalopathy Older children: Asphyxia Near-drowning Adults: Respiratory arrest e.g. fatal pulmonary embolism Cardiac arrest or dysrythmias Ischaemic or haemorrhagic CVA Metabolic derangements Toxicity e.g. CO Trauma +/- overt/covert bleeds Page 4 of 23
Findings and procedure details Fig. 1: DWI MR, at 24 hours: Cortical laminar necrosis. References: Medical Imaging Department, Mater Dei Hospital, Malta, EU Page 5 of 23
Fig. 2: DWI MR, at 48 hours: Cortical laminar necrosis. Gray matter and basal ganglia ischaemia with selective sparing of white matter. References: Medical Imaging Department, Mater Dei Hospital, Malta, EU Page 6 of 23
Fig. 3: Flair MR, at 24 hours: Cortical swelling. References: Medical Imaging Department, Mater Dei Hospital, Malta, EU Page 7 of 23
Fig. 4: FLAIR MR, at 48 hours: Cortical swelling. References: Medical Imaging Department, Mater Dei Hospital, Malta, EU Page 8 of 23
Fig. 5: FLAIR, at 12 hours: Face-of-panda sign. References: Medical Imaging Department, Mater Dei Hospital, Malta, EU Page 9 of 23
Fig. 6: DWI MR, at 12 hours: Face of Panda sign. References: Medical Imaging Department, Mater Dei Hospital, Malta, EU Page 10 of 23
Fig. 7: CT, at 6 hours: Global oedema with pseudo-subarachnoid sign. References: Medical Imaging Department, Mater Dei Hospital, Malta, EU Page 11 of 23
Fig. 8: TOF MRA, at 6 hours: Absence of flow within ICAs but preserved in ECA : red nose sign. (Cerebellar herniation post- meningitis) References: Medical Imaging Department, Mater Dei Hospital, Malta, EU Page 12 of 23
Images for this section: Fig. 1: DWI MR, at 24 hours: Cortical laminar necrosis. Medical Imaging Department, Mater Dei Hospital, Malta, EU Page 13 of 23
Fig. 2: DWI MR, at 48 hours: Cortical laminar necrosis. Gray matter and basal ganglia ischaemia with selective sparing of white matter. Medical Imaging Department, Mater Dei Hospital, Malta, EU Page 14 of 23
Fig. 3: Flair MR, at 24 hours: Cortical swelling. Medical Imaging Department, Mater Dei Hospital, Malta, EU Page 15 of 23
Fig. 4: FLAIR MR, at 48 hours: Cortical swelling. Medical Imaging Department, Mater Dei Hospital, Malta, EU Page 16 of 23
Fig. 5: FLAIR, at 12 hours: Face-of-panda sign. Medical Imaging Department, Mater Dei Hospital, Malta, EU Page 17 of 23
Fig. 6: DWI MR, at 12 hours: Face of Panda sign. Medical Imaging Department, Mater Dei Hospital, Malta, EU Page 18 of 23
Fig. 7: CT, at 6 hours: Global oedema with pseudo-subarachnoid sign. Medical Imaging Department, Mater Dei Hospital, Malta, EU Page 19 of 23
Fig. 8: TOF MRA, at 6 hours: Absence of flow within ICAs but preserved in ECA : red nose sign. (Cerebellar herniation post- meningitis) Medical Imaging Department, Mater Dei Hospital, Malta, EU Page 20 of 23
Conclusion There are characteristic radiological changes on CT and MRI in global hypoxic ischaemic injury. Magnetic resonance imaging provides better quality images of selective tissue injury in the brain. Changes can be followed through sequential scanning. They can potentially be used to assess response to pharmacological and interventional therapies. Page 21 of 23
Personal information L. M. Zammit, Foundation doctor, Year 2, Mater Dei Hospital, Malta, EU. R. Grech, Consultant Radiologist, Medical Imaging Department, Mater Dei Hospital, Malta, EU. Page 22 of 23
References Medical Imaging Department, Mater Dei Hospital, Malta. EU. Anderson, C. A. and D. B. Arciniegas (2010). "Cognitive sequelae of hypoxic-ischemic brain injury: a review." NeuroRehabilitation 26(1): 47-63. Lu-Emerson, C. and S. Khot (2010). "Neurological sequelae of hypoxicischemic brain injury."neurorehabilitation 26(1): 35-45. Calvert, J. W. and J. H. Zhang (2005). "Pathophysiology of an hypoxicischemic insult during the perinatal period." Neurological Research 27(3): 246-260. Busl, K. M. and D. M. Greer (2010). "Hypoxic-ischemic brain injury: pathophysiology, neuropathology and mechanisms." NeuroRehabilitation 26(1): 5-13. http://radiopaedia.org/articles/hypoxic-ischaemic-brain-injury-1 Page 23 of 23