Magnetic Resonance Neuroimaging Abnormalities in Heat Stroke

Transcription

1 Magnetic Resonance Neuroimaging Abnormalities in Heat Stroke Poster No.: R-0029 Congress: Type: Authors: Keywords: DOI: 2016 ASM Educational Exhibit E. Arnfield, Y.-T. T. Huang, F. Cominos, P. Cleland; QLD/AU CNS, Emergency, MR, MR-Diffusion/Perfusion, Imaging sequences, Ischemia / Infarction /ranzcr2016/R-0029 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 RANZCR's endorsement, sponsorship or recommendation of the third party, information, product or service. RANZCR 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 RANZCR 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,.doc documents and any other multimedia files are not available in the pdf version of presentations. Page 1 of 6

2 Learning objectives To examine a case report of heat stroke and discuss the pertinent neuro-radiological findings in the context of the pre-existing literature. Background Heat stroke is a critical illness characterised by hyperthermia (core body temperature greater than 40 degrees Celsius) with CNS dysfunction manifesting as delirium, convulsions, or coma 1. It is often accompanied by multi-organ failure and disseminated intravascular coagulation 2. Treatment primarily involves active cooling and support of organ function 3. CT brain in the acute setting is often unremarkable 4. Although heat stroke is not an uncommon illness and by definition involves CNS impairment, published magnetic resonance neuro-radiological findings are limited to case reports or series and are highly variable. We present a case study with findings on MRI in a patient who ultimately died from heat stroke encephalopathy. A previously well 53-year-old male was taken to hospital after collapsing while working as a labourer in a high temperature environment in Fiji. On arrival to hospital he was GCS 3-5 (M1-M3), hyperthermic (41 C), hypotensive (70/40), tachycardic (140bpm), and hypoxic (SpO2 80% on room air). He was resuscitated with IV fluids, given broad spectrum IV antibiotics, actively cooled, and intubated due to respiratory fatigue. He was transferred to a tertiary Australian intensive care unit the next day. Initial investigations revealed thrombocytopaenia, leukocytosis, an acute kidney injury, a transaminitis, and evidence of rhabdomyolysis. CT brain and C-spine were unremarkable. Although these biochemical abnormalities gradually improved, his neurological recovery remained slow off sedation. An EEG revealed diffuse cortical dysfunction with no evidence of seizure activity, and an MRI brain was performed on a 1.5-T scanner 5 days after the initial insult. Imaging findings OR Procedure details MRI brain revealed multiple foci of restricted diffusion on Diffusion Weighted Imaging (DWI) within the left centrum semiovale (see Figure 1), both caudate nuclei, both thalami (see Figure 2), and multiple cerebral gyri (bilateral frontal, left occipital- see Figure 3, and left parietal gyri) consistent with infarcts. Scattered supratentorial T1 and T2 hyperintense foci were also demonstrated, with no evidence of intracranial haemorrhage or mass Page 2 of 6

3 effect. The patient did not make any further neurological recovery and passed away following extubation 14 days after the event, with cause of death listed as encephalopathy secondary to heat stroke. The pathophysiology of heat stroke involves a complex interaction between the physiological response to hyperthermia, the systemic inflammatory response (including coagulation dysfunction), and the direct cytotoxic effects of heat 1. Similarly, CNS damage from heat stroke is multifaceted and is postulated to involve increased permeability of the blood brain barrier and subsequent vasogenic oedema causing elevated intracranial pressure 5, cerebral hypoperfusion due to shunting of blood to the peripheries in an attempt to dissipate heat 6, disseminated intravascular coagulation resulting in small vessel ischaemic change 7, and the directly toxic effects of heat itself on neuronal cells (which are especially pronounced in the purkinje cells of the cerebellum) 8. CT brain in the acute setting is often unremarkable 4. The most consistent magnetic resonance neuroimaging findings in the literature appear to be DWI abnormalities in the cerebellum (dentate nuclei, cerebellar hemispheres, and cerebellar peduncles) 2,9-14, although DWI abnormalities in the cerebral cortex 2,15, hippocampus 12, thalami 9,14, basal ganglia 12,13,16, and midbrain 14,17 are also reported. These abnormalities are usually symmetrical and bilateral 4, and late imaging often reveals diffuse cerebellar atrophy 16,18. This particular case is unusual in that all findings were supratentorial, and the cerebral findings were asymmetrical. Images for this section: Fig. 1: Hyperintense signal in the left centrum semiovale and left parietal gyri on T2 weighted FLAIR image (left), correlated with hyperintense signal on DWI (middle) and ADC restricted diffusion (right) in the same region. Page 3 of 6

4 Fig. 2: Hyperintense signal in both thalami on T2 weighted FLAIR image (left), correlated with hyperintense signal on DWI (middle) and ADC restricted diffusion (right) in the same region. Fig. 3: Hyperintense signal in the left occipital pole on T2 weighted FLAIR image (left), correlated with hyperintense signal on DWI (middle) and ADC restricted diffusion (right) in the same region. Page 4 of 6

5 Conclusion Despite previously documented cases suggesting usual symmetrical and bilateral infratentorial involvement, this case illustrates that heat stroke can present with asymmetric and atypical distributions of DWI positive lesions on MRI brain. Personal information References 1. Bouchama A, Knochel JP. Heat Stroke. The New England Journal of Medicine. 2002;346(25): Fushimi Y, Taki H, Kawai H, Togashi K. Abnormal hyperintensity in cerebellar efferent pathways on diffusion-weighted imaging in a patient with heat stroke. Clinical Radiology. 2012;67(4): Chan YK, Mamat M. Management of heat stroke. Trends in Anaesthesia and Critical Care. 2015;5(2-3): Muccio CF, De Blasio E, Venditto M, Esposito G, Tassi R, Cerase A. Heat-stroke in an epileptic patient treated by topiramate: follow-up by magnetic resonance imaging including diffusion-weighted imaging with apparent diffusion coefficient measure. Clinical neurology and neurosurgery. 2013;115(8): Carlson RW, Sakha F. Unraveling the mysteries of heatstroke. Critical Care Medicine. 1996;24(7): Chen S-H, Niu K-C, Lin M-T. Cerebrovascular dysfunction is an attractive target for therapy in heat stroke. Clinical and Experimental Pharmacology and Physiology. 2006;33(8): Yaqub B, Al Deeb S. Heat strokes: aetiopathogenesis, neurological characteristics, treatment and outcome. Journal of the neurological sciences. 1998;156(2): Reynolds LP, Allen GV. A review of heat shock protein induction following cerebellar injury. Cerebellum (London, England). 2003;2(3): Kobayashi K, Tha KK, Terae S, Iijima Y, Katabami K, Minami Y, et al. Improved detection of heat stroke-induced brain injury by high b-value diffusion-weighted imaging. Journal of computer assisted tomography. 2011;35(4):498. Page 5 of 6

6 10. Lee JS, Choi JC, Kang SY, Kang JH, Park JK. Heat stroke: increased signal intensity in the bilateral cerebellar dentate nuclei and splenium on diffusion-weighted MR imaging. AJNR American journal of neuroradiology. 2009;30(4):E Li Jun XZ, Bin Wang, Junzu Geng. MRI findings in human brain after heat stroke. Journal of Nature and Science. 2015;1(2):e Mahajan S, Schucany WG. Symmetric bilateral caudate, hippocampal, cerebellar, and subcortical white matter MRI abnormalities in an adult patient with heat stroke. Proceedings (Baylor University Medical Center). 2008;21(4): McLaughlin CT, Kane AG, Auber AE. MR Imaging of Heat Stroke: External Capsule and Thalamic T1 Shortening and Cerebellar Injury. American Journal of Neuroradiology. 2003;24(7): Ookura R, Shiro Y, Takai T, Okamoto M, Ogata M. Diffusion-weighted Magnetic Resonance Imaging of a Severe Heat Stroke Patient Complicated with Severe Cerebellar Ataxia. Internal Medicine. 2009;48(12): Sudhakar PJ, Al-Hashimi H. Bilateral hippocampal hyperintensities: a new finding in MR imaging of heat stroke. Pediatric Radiology. 2007;37(12): Biary N, Monir Madkour M, Sharif H. Post-heatstroke parkinsonism and cerebellar dysfunction. Clinical Neurology and Neurosurgery. 1995;97(1): Bazille C, Megarbane B, Bensimhon D, Lavergne-Slove A, Baglin AC, Loirat P, et al. Brain Damage After Heat Stroke. Journal of Neuropathology and Experimental Neurology. 2005;64(11): Albukrek D, Bakon M, Moran DS, Faibel M, Epstein Y, Moran D. Heat-strokeinduced cerebellar atrophy: clinical course, CT and MRI findings. Neuroradiology. 1997;39(3): Page 6 of 6