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BRIEF COMMUNICATIONS: M. J. Hasbani, L. H. Sansing, J. Perrone, A. K. Asbury, and S. J. Bird Encephalopathy and peripheral neuropathy following diethylene glycol ingestion Neurology 2005; 64: 1273-1275 [Abstract] [Full text] [PDF]

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M. Josh Hasbani, MD, PhD, Lauren Sansing-Hachmann, MD; Jeanmarie Perrone, MD; Arthur K. Asbury, MD; Shawn J. Bird, MD   (11 October 2005)

Encephalopathy and peripheral neuropathy following diethylene glycol ingestion

G. Patrick Daubert, MD, Abhishek Katiyar, MD; John Wilson, PhD; Lydia Baltarowich, MD   (11 October 2005)

Reply from the authors 11 October 2005
M. Josh Hasbani, MD, PhD, University of Pennsylvania, Department of Neurology 3 Gates, 34th and Spruce, Philadelphia, PA 19104, Lauren Sansing-Hachmann, MD; Jeanmarie Perrone, MD; Arthur K. Asbury, MD; Shawn J. Bird, MD Send Correspondence to journal: Re: Reply from the authors hasbani2001{at}yahoo.com M. Josh Hasbani, MD, PhD, et al.	We thank Daubert et al for their comments. Recent work by Alfred et al supports the concept that the delayed neurological injury following DEG intoxication is dose-dependent and may be predicted by the extent of renal impairment. [5] Early implementation of ethanol and dialysis could substantially alter a patient’s disease course. Such early treatment requires a high degree of clinical suspicion with timely recognition of the metabolic derangements seen in patients presenting following DEG ingestion. The diagnosis should be considered in patients presenting with nausea, vomiting, abdominal pain, gap acidosis, and evolving acute renal failure. The gap acidosis observed in DEG toxicity is milder than that seen in ethylene glycol intoxication. DEG and ethylene glycol toxicity share several delayed clinical neurological features including encephalopathy and cranial and peripheral neuropathy; however, the published electrophysiology suggests distinct mechanisms of injury to the peripheral nervous system. As pointed out in one patient with ethylene glycol intoxication, the pathology was felt to be a polyradiculopathy. [4] This conclusion was based on findings of preserved sensory potentials in the setting of absent F wave responses, similar to that seen early in demyelinating variants of GBS. These findings conflict with our patient in whom sensory responses were lost early along with decreased motor amplitudes and preserved conduction velocity. These results supported an acute axonal sensory motor polyneuropathy similar to that seen in the axonal variants of GBS. While it is sometimes surprising that mechanistically different injuries to the peripheral nervous system can result in similar clinical findings, we are reminded of this in the case of ethylene and diethylene glycol intoxication. Understanding the distinct mechanisms contributing to the pathogenesis of toxic neuropathies may provide a rational basis for drug development. References 5. Alfred S, Coleman P, Harris D, Wigmore T, Stachowski E, Graudins A. Delayed neurologic sequelae resulting from epidemic diethylene glycol poisoning. Clin Toxicol. 2205;43:155-9. Disclosure: The authors report no conflicts of interest.
Encephalopathy and peripheral neuropathy following diethylene glycol ingestion 11 October 2005
G. Patrick Daubert, MD, Wayne State University/Children's Hospital of Michigan Regional Poison Control Center 4160 John R, Suite 616, Detroit, MI 48201, Abhishek Katiyar, MD; John Wilson, PhD; Lydia Baltarowich, MD Send Correspondence to journal: Re: Encephalopathy and peripheral neuropathy following diethylene glycol ingestion gpat-md{at}sbcglobal.net G. Patrick Daubert, MD, et al.	We read with interest the article by Dr. Hasbani et al regarding diethylene glycol ingestion. [1] Diethylene glycol (DEG) has a rich history in the medical literature with several mass poisonings. We commonly group DEG with other alcohols and glycols but it deserves its own unique profile. DEG is an ether metabolized by alcohol dehydrogenase (ADH) to a corresponding aldehyde, which is subsequently metabolized by aldehyde dehydrogenase (ALDH) to an acetic acid compound. However, the current literature supports the notion that the ether bond in DEG remains intact with no resultant ethylene glycol formation. DEG is primarily excreted unchanged in the urine (61-85%) with the presence of varying amounts of hydroxyethoxy acetic acid (up to 30%). [2,3] Since the ether bond remains intact, it is currently believed that DEG is in and of itself toxic, unlike that of ethylene glycol. Furthermore, because ethylene glycol is not seen as a free molecule, the classic finding of oxalate crystaluria is absent. The other interesting perspective highlighted in this case is the pronounced neurologic features. This patient’s syndrome is nearly identical to the Stage IV delayed neurologic sequelae (DNS) seen following massive ethylene glycol intoxications. Facial diplegia is a classic finding in this syndrome in addition to multiple cranial nerve deficits, limb weakness, areflexia, and cerebral spinal fluid albuminocytologic dissociation. [4] Since its first description in 1978, all cases of DNS have been associated with renal failure and typically occur 6-12 days after ingestion. The etiology of the polyradiculopathy due to ethylene glycol is thought to be due to oxalate deposition in proximal nerve roots. However, considering the similarities between the syndromes caused by ethylene glycol and DEG (where no ethylene glycol is formed), another mechanism is probably involved. Due to the likelihood that the parent molecule of DEG is likely toxic and the metabolite is a potent acid, management of ingestions to DEG must take a more aggressive approach with a two-tiered response. First, inhibition of ADH by ethanol or fomepizole must take place. Second, early dialysis must also be implemented to remove the parent molecule. We commend Dr. Hasbani and his colleagues for their contribution to the toxicology literature on the clinical progression of human DEG poisoning. It is important for physicians to realize the often complex metabolic pathways of toxic molecules in order to provide effective treatment. References 1. Hasbani MJ, Sansing LH, Perrone J. Encephalopathy and peripheral neuropathy following diethylene glycol ingestion. Neurology 2005;64:1275-1275. 2. Wiener HL, Richardson KE. Metabolism of diethylene glycol in male rates. Biochem Pharmacol 1989;38:539. 3. Woolf AD. Diethylene glycol. Clin Toxicol Rev 1996;17:1. 4. Zhou L, Zabad R, Lewis RA. Ethylene glycol intoxication: Electrophysiological studies suggest polyradiculopathy. Neurology 2002;59:1809-1810. Disclosure: The authors report no conflicts of interest.