The presentation of carbon monoxide (CO) poisoning is non-specific and highly variable. The diagnosis is made when a compatible history and examination occur in a patient with elevated carboxyhaemoglobin levels. The severity of intoxication is difficult to assess accurately based on laboratory markers alone. Magnetic resonance imaging (MRI) has been shown to have superior sensitivity to computed tomography for the detection of abnormalities post CO poisoning. We report a novel imaging pattern on MRI undertaken in the acute setting in a patient with CO intoxication. We also discuss the management and follow up of patients with CO poisoning

Clarkson, Michael R.

Costello, Daniel J.

O'Neill, Siobhán B.

Ryan, Stephen A.

Sheehan, Donal W.

International Journal of Emergency Medicine

Cork Open Research Archive

Title Carbon monoxide poisoning: novel magnetic resonance imaging patternin the acute settingAuthor(s) Ryan, Stephen A.; Sheehan, Donal W.; O'Neill, Siobhán B.; Clarkson,Michael R.; Costello, Daniel J.Publication date 2012-06-28Original citation Ryan, S. A., Sheehan, D. W., O' Neill, S. B., Clarkson, M. R., andCostello, D. J. (2012) 'Carbon monoxide poisoning: Novel magneticresonance imaging pattern in the acute setting', International Journal ofEmergency Medicine, 5(1), 30 (3pp). doi:10.1186/1865-1380-5-30Type of publication Article (peer-reviewed)Link to publisher'sversionhttp://dx.doi.org/10.1186/1865-1380-5-30Access to the full text of the published version may require asubscription.Rights © 2012, Ryan et al. Licensee Springer. This is an Open Access articledistributed under the terms of the Creative Commons AttributionLicense (http://creativecommons.org/licenses/by/2.0), which permitsunrestricted use, distribution, and reproduction in any medium,provided the original work is properly cited.http://creativecommons.org/licenses/by/2.0Item downloadedfromhttp://hdl.handle.net/10468/5174Downloaded on 2018-08-23T20:25:45ZCASE REPORT Open AccessCarbon monoxide poisoning: Novel magneticresonance imaging pattern in the acute settingRyan A Stephen1*, Sheehan W Donal1, O’Neill B Siobhain2, Clarkson R Michael3 and Costello J Daniel1AbstractThe presentation of carbon monoxide (CO) poisoning is non-specific and highly variable. The diagnosis is madewhen a compatible history and examination occur in a patient with elevated carboxyhaemoglobin levels. Theseverity of intoxication is difficult to assess accurately based on laboratory markers alone. Magnetic resonanceimaging (MRI) has been shown to have superior sensitivity to computed tomography for the detection ofabnormalities post CO poisoning. We report a novel imaging pattern on MRI undertaken in the acute setting in apatient with CO intoxication. We also discuss the management and follow up of patients with CO poisoning.Keywords: Carbon monoxide, Poisoning, Magnetic resonance imaging, CerebellumBackgroundCarbon monoxide poisoning (CO) is common, potentiallyfatal, and probably under diagnosed because of its nonspe-cific clinical presentation. Given a typical history of COexposure it is readily diagnosed but recognizing the condi-tion in an unresponsive patient can be challenging. Theclinical findings of CO poisoning are highly variable andlargely nonspecific and laboratory markers alone offeran imperfect assessment of intoxication severity. Brainimaging is usually only undertaken if there are concernsabout alternate pathology to explain neurological decom-pensation. However, MRI can reveal abnormalities in thedeep white matter, cerebral cortex, globus pallidus, puta-men, thalamus, and hippocampus. Here we report a caseof carbon monoxide poisoning with an unusual pattern ofbilateral restricted diffusion in the cerebellar white matter,using MRI undertaken in the acute setting.Case presentationA 78-year-old lady was brought to the emergency depart-ment, having been found unconscious next to a runninglawnmower. The Glasgow Coma Scale score on arrival tothe emergency department was 3/15. Vital signs wererecorded as a pulse rate of 78 beats per minute, tem-perature of 35°C, blood pressure of 110/68 mmHg and arespiratory rate of 18 breaths per minute, with oxygensaturations as assessed by pulse oximetry of 98%.The duration of unconsciousness was unknown. Neuro-logical examination revealed equal and reactive pupils inthe midline with no focal abnormalities. The rest of theexamination was unremarkable. Co-oximetry of a bloodgas sample showed a carboxyhaemoglobin level of 26%.Electrocardiogram revealed no features of ischaemia andcardiac enzyme levels were normal.She was intubated and ventilated, and an emergent CTof the brain was reported as normal. A diagnosis of en-cephalopathy secondary to CO poisoning was made. Shewas transferred to the intensive care unit and main-tained on 100% oxygen. She made a prompt recoveryand was extubated 8 h later. Subsequent collateral his-tory was suggestive of a complex partial seizure disorderas the cause of her initial collapse; family membersrecounted multiple episodes of behavioural arrest, alteredconsciousness and mutism in the past.An MRI was performed 17 h post admission andrevealed bilateral symmetrical restricted diffusion in thewhite matter of the cerebellar hemispheres (Figure 1).This pattern has only rarely been reported in CO poi-soning and usually MRI was not undertaken in the acutesetting [1,2]. Subsequent electroencephalogram (EEG)was unremarkable but importantly was undertaken 3 dayspost presentation.* Correspondence: stephenryan0@gmail.com1Department of Medicine, Neurology Service, Cork University Hospital, Cork,IrelandFull list of author information is available at the end of the article© 2012 Ryan et al.; licensee Springer. This is an Open Access article distributed under the terms of the Creative CommonsAttribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproductionin any medium, provided the original work is properly cited.Ryan et al. International Journal of Emergency Medicine 2012, 5:30http://www.intjem.com/content/5/1/30DiscussionCarbon monoxide (CO) is a colourless, odourless, tastelessand non-irritant gas. Sources of CO include inadequateventilation of appliances, faulty heating equipment andengine motors.Symptoms of poisoning are non-specific and vary frommild constitutional upset to coma, myocardial ischaemiaand death. Examination is usually unremarkable but mayshow subtle cognitive disturbance. Our patient presentedin an unconscious state with no focal signs on examina-tion. As the duration of unconsciousness was unknown,brain imaging was undertaken after arterial blood gasanalysis confirmed CO exposure. Initial CT brain imagingwas unremarkable. Magnetic resonance imaging (MRI)can reveal abnormal findings in CO-poisoned patients andis more sensitive than CT for their detection [3]. Therestricted diffusion seen in our patient’s cerebellum mayhave been caused by ischaemia. Anatomical studies under-taken on brains of CO poisoned patients have shown ab-normalities in the globus pallidus, other basal gangliastructures, hippocampus, cortex and cerebellum. Theselesions are microscopically necrotic and are foci of necro-sis or demyelination [4]. Cerebellar abnormalities in CO-poisoned patients are rare, and in one study that examinedvariables predictive of subsequent adverse outcomes, cere-bellar abnormalities on presentation were associated withan increased risk of cognitive sequelae at 6 weeks [5].Non-smokers may have up to 3% carboxyhaemoglobinwhilst smokers may have levels significantly higher at10% [6]. Standard pulse oximetry cannot differentiatebetween carboxyhaemoglobin and oxyhaemoglobin. Theabsolute level of carboxyhaemoglobin does not correlatewith presence of symptoms [7], ultimate outcome [6]or white matter hyperintensities on MRI [8], but doescorrelate with the initial level of consciousness [6].Carbon monoxide binds to the iron moiety of hemewith approximately 240 times the affinity of oxygen [9].Once this occurs an allosteric change results in greatlyreduced off load of oxygen to tissues.Treatment involves high flow oxygen (100% oxygen)via nonrebreathing reservoir facemask, or mechanicalventilation if indicated. This reduces the half-life of carb-oxyhaemoglobin from about 300 min to 90 min. Poisonedpatients should be evaluated for signs of cardiovascularischaemia and brain imaging performed if concernsof additional pathology are present. Hyperbaric oxygentherapy (HBO), which exposes patients to 100% oxygentherapy under supra-atmospheric conditions, has beenshown to elevate arterial and tissue oxygen tensions, andpromote CO elimination [9].Both physiological and randomized-controlled datasuggest a potential benefit [10], but uncertainty persistsin identifying patients who will benefit from HBO treat-ment. Most authorities would administer HBO if avai-lable and the following parameters were met: severemetabolic acidosis (pH<7.1), CO level >25, loss of cons-ciousness or signs of end organ ischaemia.ConclusionsThe addition of MR imaging to the diagnostic workupof CO-intoxicated patients offers additional informationto clinicians to better gauge patient outcome, especiallywhen other parameters are equivocal. Outpatient follow-up is required to assess for the development of DelayedNeuropsychiatric Syndrome (DNS), which can cause per-sonality changes, memory difficulties and gait disturbance[11].CO poisoning should be included in the differentialdiagnosis in patients found to have cerebellar white matterlesions on imaging.ConsentInformed consent was obtained from the patient forpublication and/or presentation of this case includingall medical data and accompanying images.Figure 1 a T2-weighted MRI of brain with abnormal signal in theleft medial temporal lobe (arrow). b Diffusion-weighted imaging(DWI) showing symmetrical bilateral restricted diffusion in cerebellarwhite matter (arrow) and in left medial temporal lobe (arrow).c Apparent diffusion co-efficient (ADC) map: corresponding areas aredark on ADC map, implying acute ischaemia. d Coronalreconstruction: Subtle signal abnormality in left hippocampus(arrow) possibly post-ictal in aetiology.Ryan et al. International Journal of Emergency Medicine 2012, 5:30 Page 2 of 3http://www.intjem.com/content/5/1/30Competing interestsThe authors declare that they have no competing interests.Authors’ contributionsSR was involved in patient care, concept, drafting and critically revising themanuscript. DS was involved in drafting the manuscript and reviewing thepertinent literature. SON was involved in patient care and the preparation ofthe radiological aspects of the manuscript. MC personally cared for thepatient and was involved in revising the manuscript. DC was involved inpatient care and critically revising the manuscript for important intellectualcontent. All authors read and approved the final manuscript.Open AccessThis article is distributed under the terms of the Creative CommonsAttribution License which permits any use, distribution and reproduction inany medium, provided the original author(s) and source are credited.Author details1Department of Medicine, Neurology Service, Cork University Hospital, Cork,Ireland. 2Department of Radiology, Cork University Hospital, Cork, Ireland.3Department of Medicine, Nephrology Service, Cork University Hospital, Cork,Ireland.Received: 3 March 2012 Accepted: 10 May 2012Published: 28 June 2012References1. Fan HC, Wang AC, Lo CP, et al: Damage to cerebellar white matter due tocarbon monoxide poisoning: a case report. Am J Emerg Med 2009, 27:757.2. Mascalchi M, Petruzzi P, Zampa V: MRI of cerebellar white matter damagedue to carbon monoxide poisoning:case report. Neuroradiology 1996,38:73–74.3. Tuchmann R, Moser F, Moshe S: Carbon monoxide poisoning: bilaterallesions in the thalamus on MR imaging of the brain. Pediatr Radiol 1990,20:478–479.4. Lapresle J, Fardeau M: The CNS and carbon monoxide poisoning.Anatomical study of brain lesions following intoxication with CO. Prog BrainRes 1967, 24:31–74.5. Weaver LK, Valentine KJ, Hopkins RO: Carbon monoxide poisoning: riskfactors for cognitive sequelae and the role of hyperbaric oxygen. Am JRespir Crit Care Med 2007, 176:491–497.6. Ernst A, Zibrak JD: Carbon monoxide poisoning. N Engl J Med 1998,339:1603.7. Hampson NB, Hauff NM: Carboxyhaemoglobin levels in carbon monoxidepoisoning: do they correlate with the clinical picture? Am J Emerg Med2008, 26:665–669.8. Parkinson RB, Hopkins RO, Cleavinge HB, et al: White matterhyperintensities and neuropsychological outcome followingcarbonmonoxide poisoning. Neurology May 2002 28, 58(10):1525–1532.9. Thom SR: Carbon monoxide pathophysiology and treatment, Physiology andmedicine of hyperbaric oxygen therapy. Philadelphia: Saunders Elsevier;2008:321–347.10. Weaver LK, Hopkins RO, Chan KJ, et al: Hyperbaric oxygen for acutecarbon monoxide poisoning. N Engl J Med 2002, 347:1057–1067.11. Thom SR, Taber RL, Mendiguren II, et al: Delayed neuropsychologicsequelae after carbon monoxide poisoning: prevention by treatmentwith hyperbaric oxygen. Ann Emerg Med 1995, 25(4):474.doi:10.1186/1865-1380-5-30Cite this article as: Ryan et al.: Carbon monoxide poisoning: Novelmagnetic resonance imaging pattern in the acute setting. InternationalJournal of Emergency Medicine 2012 5:30.Submit your manuscript to a journal and beneﬁ t from:7 Convenient online submission7 Rigorous peer review7 Immediate publication on acceptance7 Open access: articles freely available online7 High visibility within the ﬁ eld7 Retaining the copyright to your article    Submit your next manuscript at 7 springeropen.comRyan et al. International Journal of Emergency Medicine 2012, 5:30 Page 3 of 3http://www.intjem.com/content/5/1/30

Carbon monoxide poisoning: novel magnetic resonance imaging pattern in the acute setting

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Carbon monoxide poisoning: novel magnetic resonance imaging pattern in the acute setting

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