American Journal of Emergency Medicine xxx (2015) xxx–xxx

Contents lists available at ScienceDirect

American Journal of Emergency Medicine journal homepage: www.elsevier.com/locate/ajem

Case Reports

Severe neurologic impairment and uncommon magnetic resonance imaging findings after carbon monoxide poisoning☆ Abstract Carbon monoxide poisoning is the most common cause of fatal poisoning worldwide and can lead to severe brain damages. We report a delayed encephalopathy after a severe carbon monoxide poisoning with uncommon magnetic resonance imaging findings. A 41-year-old woman committed suicide by inhaling toxic fumes from a charcoal barbecue. When the first responders arrived on scene, she was unresponsive, with a Glasgow Coma Scale (GCS) score of 5/15 but still breathing. The patient's pupils were 3.0 mm, symmetric but slowly reactive. The blood carboxyhemoglobin concentration was 18.7%. She was intubated for airway protection and transferred to the hospital. A hyperbaric oxygen therapy was delivered. Sedative drugs were stopped a few days later, but she remained comatose (GCS 6/15: E1V1M4). A magnetic resonance imaging (MRI) was performed on day 7 and showed a bilateral hemorrhage in both globi pallidi (GP) (Fig. 1), most typical but uncommon manifestation of acute carbon monoxide poisoning (COP). Three weeks after her admission, she was completely weaned off the ventilator but was in a vegetative state with decorticated rigidity of the limbs (GCS 7/15: E3V1M3). A second MRI demonstrated diffuse demyelination lesions in the white matter (Fig. 2). The clinical picture and brain imaging findings were pathognomonic of Grinker myelinopathy, also known as delayed posthypoxic leukoencephalopathy (DPHL). Despite early and aggressive supportive care, she remained in a persistent vegetative state. The uptake of CO by hemoglobin with an affinity 200 times that oxygen leads to hypoxia in tissues, and a shift in the oxyhemoglobin dissociation curve to the left inhibits release of oxygen, further exacerbate tissue hypoxia. Brain damage can also be caused by other mechanisms, such as free radicals and inhibition of mitochondrial metabolism [1]. The type of lesions depends on the duration of CO exposure, its severity, the distance from the toxic source, and the age of the patient. In 1967, Lapresle and Fardeau [2] first reported these typical brain damage: diapedetic hemorrhages with hemosiderin-laden macrophages in the GP in cases with long-term survival after COP. Since then, several other patterns of brain injury have also been described, affecting other structures: the rest of the basal ganglia, thalamus, brainstem, cerebellum, white matter, and cerebral cortex [3]. Necrosis in the GP and diffuse homogeneous demyelination in the white matter are considered to be typical pathologic changes, whereas bilateral hemorrhage in both GP is an uncommon manifestation. Damage to the brain directly affects

the prognosis for patients who survive COP. The level of consciousness and the carboxyhemoglobin concentration have been found to be unhelpful in the prediction of chronic clinical behaviors [4]. Neuroimaging may better reflect clinical severity, help determine prognosis, and be an important diagnosis tool in ruling out other diagnosis. Magnetic resonance imaging is more sensitive than computer tomography for brain damage from COP [5]. The timing of MRI has a major effect on the results of imaging. Magnetic resonance imaging can demonstrate a diffuse white matter hyperintensity involving all lobes, injuries of gray matter structures such as the hippocampus or cerebral cortex, or also later demyelination of the white matter [1]. The combination of a clinical history of COP, neurologic symptoms, and delayed neuroimaging findings allows establishing the diagnosis of Grinker myelinopathy. After COP, initial treatment includes establishing a patent airway and administration of the highest available concentration and flow of oxygen. It remains controversial whether normobaric or hyperbaric oxygen therapy is the treatment of choice for acute COP [6]. Adequate treatment of acute COP; prevention of cerebral hypoxia and ischemia; and the prompt restitution of normal oxygenation, blood pressure, and acid-base balance after COP are the only possible measures in the prevention of DPHL. Bed rest and avoidance of stressful procedures for the first 10 days may also lower the risk [7]. Once DPHL has developed, the only option is to provide supportive care. Goal-oriented physical and cognitive rehabilitation is an important part of care process. Gradual recovery over a 3- to 12-month period is common; but impaired attention or executive function, parkinsonism, or corticospinal tract signs can persist [7]. As in this case, some episodes of DPHL that progress to coma have no known treatment to reverse the course. Because of the wide range of symptoms and the delay onset (several weeks), Grinker myelinopathy is often misdiagnosed. So, we suggest that patients with acute COP and coma should be monitored carefully for several weeks to detect early delayed neurologic dysfunctions and neuroimaging changes. Anticipation and recognition of Grinker myelinopathy should lead to earlier and more appropriate utilization of health care services [7]. Clément Hoffmann MD* Julien Bouix MD1 Burn Center, Percy Military Teaching Hospital, 101 avenue Henri Barbusse BP 406, 92141 Clamart cedex, France *Corresponding author. Burn Center, Percy Military Teaching Hospital 101 avenue Henri Barbusse, BP 406, 92141 Clamart cedex, France Tel.: +33 141466219, +33 141466731 E-mail addresses: [email protected] [email protected] (J. Bouix)

☆ No conflict of interest. http://dx.doi.org/10.1016/j.ajem.2015.05.034 0735-6757/© 2015 Elsevier Inc. All rights reserved.

Please cite this article as: Hoffmann C, et al, Severe neurologic impairment and uncommon magnetic resonance imaging findings after carbon monoxide poisoning, Am J Emerg Med (2015), http://dx.doi.org/10.1016/j.ajem.2015.05.034

2

C. Hoffmann et al. / American Journal of Emergency Medicine xxx (2015) xxx–xxx

Chrystelle Poyat MD2 Medical Department, Villacoublay Air Base 107, 78140 Villacoublay, France E-mail address: [email protected] Laure Alhanati MD2 Jean-Pierre Tourtier MD, PhD2 Emergency Medical Department, Fire Brigade of Paris 1 place Jules Renard, 75017 Paris, France E-mail addresseses: [email protected] (L. Alhanati) [email protected] (J. Tourtier) Elisabeth Falzone MD3 Department of Anesthesiology and Critical Care Medicine Percy Military Teaching Hospital, 101 avenue Henri Barbusse BP 406, 92141 Clamart cedex, France E-mail address: [email protected] 1

Tel.:+33 141466731

Fig. 1. T1 sequence of MRI demonstrating hyperintensities (hemorrhages) in both GP (large arrows).

2

Tel.:+33 141466219

3

Tel.:+33 141466224

http://dx.doi.org/10.1016/j.ajem.2015.05.034

References

Fig. 2. T2 fluid attenuated inversion recovery sequence of MRI showing diffuse white matter hyperintensity, involving all lobes (thin arrows).

[1] Beppu T. The role of MR imaging in assessment of brain damage from carbon monoxide poisoning: a review of the literature. Am J Neuroradiol 2014;35:625–31. [2] Lapresle J, Fardeau M. The central nervous system and carbon monoxide poisoning. II. Anatomical study of brain lesions following intoxication with carbon monoxide (22 cases). Prog Brain Res 1967;24:31–74. [3] Lo CP, Chen SY, Lee KW, Chen WL, Chen CY, Hsueh CJ, et al. Brain injury after acute carbon monoxide poisoning: early and late complications. Am J Roentgenol 2007;189:W205–11. [4] Hurley RA, Hopkins RO, Bigler ED, Taber KH. Applications of functional imaging to carbon monoxide poisoning. J Neuropsychiatry Clin Neurosci 2001;13:157–60. [5] Tuchman RF, Moser FG, Moshe SL. Carbon monoxide poisoning: bilateral lesions in the thalamus on MR imaging of the brain. Pediatr Radiol 1990;20:478–9. [6] Buckley NA, Juurlink DN, Isbister G, Bennett MH, Lavonas EJ. Hyperbaric oxygen for carbon monoxide poisoning. Cochrane Database Syst Rev 2011;13:Cd002041. http://dx.doi.org/10.1002/14651858.CD002041.pub3. [7] Shprecher D, Mehta L. The syndrome of delayed post-hypoxic leukoencephalopathy. NeuroRehabilitation 2010;26:65–72.

Please cite this article as: Hoffmann C, et al, Severe neurologic impairment and uncommon magnetic resonance imaging findings after carbon monoxide poisoning, Am J Emerg Med (2015), http://dx.doi.org/10.1016/j.ajem.2015.05.034

Severe neurologic impairment and uncommon magnetic resonance imaging findings after carbon monoxide poisoning.

Carbon monoxide poisoning is the most common cause of fatal poisoning worldwide and can lead to severe brain damages. We report a delayed encephalopat...
103KB Sizes 0 Downloads 9 Views