ARTICLE

Delayed Neurologic Sequelae Resulting from EpidemicDiethylene Glycol Poisoning

Sam Alfred, M.B.B.S., F.A.C.E.M.Division of Clinical Toxicology, Department of Emergency Medicine, Westmead Hospital,

Westmead, Australia

Patrick Coleman, M.B., M.R.C.P.I., F.R.C.A.P. and David Harris, M.B.B.S., F.R.A.C.P.Centre for Transplantation and Renal Research, Millenium Institute, Westmead, Australia

Tim Wigmore, B.A., M.A., B.M., B.Ch., F.R.C.A. andEdward Stachowski, M.B.B.S., F.A.N.Z.C.A., F.J.F.I.C.M.Department of Intensive Care Medicine, Westmead Hospital, Westmead, Australia

Andis Graudins, M.B.B.S., Ph.D., F.A.C.E.M. F.A.C.M.T.Clinical and Experimental Toxicology Unit, Department of Emergency Medicine,

Prince of Wales Hospital, Prince of Wales Clinical School, University of New South Wales,

Randwick, Australia

Background. Diethylene glycol (DEG) is a well-knownmetabolic and renal toxin usually ingested accidentally as anethanol substitute or as a contaminant in various medicinals. Todate, most poisonings have occurred in third-world countrieswhere early death from renal failure is very common. We reporta series of seven patients presenting with epidemic DEGpoisoning from a correctional facility with varying degrees ofmetabolic acidemia and acute renal impairment responding toemergent hemodialysis (HD). Significantly, three patients de-veloped delayed neurologic toxicity which has not been wellcharacterized in the past. Case Series. Seven male patients (agerange 19–55) presented over a 36 h period following ingestion ofvarying quantities of DEG. Initially three patients, ingesting thelargest quantities of DEG, presented more than 24 h postingestionwith severe metabolic acidemia (pH range 6.8–7.1) and anuricacute renal failure requiring HD. All three remained dialysis-dependent and developed significant cranial neuropathies withbulbar palsy in the second week postingestion. One patient diedwith cerebral oedema and a progressive encephalopathy. Twofurther patients presented within 24 h of ingestion with normalrenal function and a moderate metabolic acidemia (pH range7.2–7.28) requiring HD. They remained well. Finally, two furtherpatients presented with a history of trivial DEG ingestion and didnot require any therapy. Neurologic signs in the two survivinginitial presenters improved over 4–6 months although they

remained dialysis-dependent. Conclusion. Unrecognized DEGpoisoning may present with metabolic acidemia and anuric acuterenal failure. Established renal impairment may predict subse-quent delayed neurologic toxicity.

Keywords Diethylene glycol; Poisoning; Acute renal failure;

Bulbar palsy; Delayed toxicity

INTRODUCTION

Diethylene glycol (DEG) is an alcohol formed by the

condensation of two ethylene glycol molecules with an ether

bond. It was first isolated in 1869, and found its initial

commercial application as an industrial solvent in 1928. Since

then it has been increasingly employed as a cleaning and

softening agent in a variety of processes. Unfortunately, its

low cost of production has resulted in usage beyond the

industrial sphere. Despite documented toxicity in humans

(1–5), the pleasant smell and sweet taste of DEG have

resulted in its repeated use as an ethanol substitute and as a

vehicle for medical elixir preparations. Eight mass poisonings

involving DEG ingestion in humans have occurred within the

last 65 years with typical features of toxicity including

metabolic acidemia and acute renal failure (3,6–11).

Epidemic outbreaks of DEG poisoning have primarily

occurred in developing countries where the ability to diagnose

and adequately treat its toxicity is limited. Consequently, early

mortality and morbidity are high in cases of epidemic DEG

toxicity, with most deaths occurring within the first 2 weeks

Address correspondence to Dr. Sam Alfred, M.B.B.S., F.A.C.E.M.,Division of Clinical Toxicology, Department of Emergency Medicine,Westmead Hospital, Westmead, NSW, 2145, Australia; Fax: 61-2-9633-4296; E-mail: samalfred@bigpond.com

155

Clinical Toxicology, 43:155–159, 2005

Copyright D Taylor & Francis Inc.

ISSN: 0731-3810 print / 1097-9875 online

DOI: 10.1081/CLT-200057875

Order reprints of this article at www.copyright.rightslink.com

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post exposure secondary to acute renal failure (3,6–11). A

small number of cases of neurologic impairment have been

reported following exposure to DEG (6,11–13). We report a

series of seven patients from a correctional facility who

presented to our health service 24 h after the recreational

ingestion of DEG. Despite rapid recognition and treatment of

systemic acidemia and acute renal failure, delayed neurologic

complications were observed in the second week post-

ingestion. These included cranial and peripheral neuropathies,

mental status changes, and recurrent seizures.

CASE SERIES

Over a 28 h period a total of seven correctional services

inmates presented to our tertiary referral center and an

associated district hospital following exposure to a cleaning

fluid which had been diluted with water and ingested for

recreational purposes. Situational constraints made formal

identification of the cleaning agent impossible; however DEG

was identified as the toxicological agent by gas chromatog-

raphy and mass spectrometry (GCMS) performed on samples

acquired from the drinking container used. Subsequent clinical

and biochemical progress was consistent with DEG exposure.

The initial two male patients aged 19 [P1] and 25 [P2]

years and previously well, presented to the affiliated district

hospital 28 h postingestion. Both complained of nausea and

vomiting and on examination exhibited Kussmaul respiration

at 30 breaths/min. They were alert, hemodynamically stable,

and anuric. Subsequent biochemical analysis revealed severe

metabolic acidosis with elevated anion and osmolar gaps, as

well as acute renal failure as evidenced by elevation of the

serum creatinine (Table 1). In view of the history of potential

toxic alcohol ingestion, intravenous ethanol therapy com-

menced. Patient-1 was transferred to our institution for urgent

hemodialysis while patient-2 initially remained at the

peripheral hospital where continuous veno-venous hemodial-

ysis (CVVHD) commenced prior to transfer to another tertiary

institution for intermittent hemodialysis.

Two hours later a 52-yr-old male patient [P3], with a

history of chronic obstructive pulmonary disease and epilepsy,

presented to our institution with an identical history of solvent

ingestion 30 h earlier. On arrival, he was agitated and

confused with a Glasgow coma score of 12. He suffered a

prolonged generalized tonic-clonic seizure requiring sedation,

intubation, and ventilation. Biochemical analysis revealed a

similar severe metabolic acidosis with elevated anion and

osmolar gaps (Table 1). He was also anuric with elevated

serum creatinine (Table 1). Ethanol therapy was initiated and

hemodialysis commenced.

The following day another two previously healthy male

patients, aged 27 [P4] and 20 [P5] years, presented to our

institution 21 h postingestion of the same liquid. Both

complained of nausea. They were alert and hemodynamically

stable with Kussmaul respiration. Both demonstrated a

metabolic acidosis with elevated anion and osmolar gaps.

Serum creatinine was normal in both cases. Ethanol and

haemodialysis were commenced.

Finally, two further previously well male patients aged 21

[P6] and 26 [P7] years presented to our facility stating that

they had ingested the same cleaning fluid, although in a dilute

form and smaller volumes. They were asymptomatic and

systemically well with normal acid base balance and no

osmolar gap. Serum creatinine levels were also normal. They

were observed for 6 h and were subsequently transferred back

to prison after repeat biochemical markers remained normal.

Patient-1 remained dialysis-dependent and anuric, but was

otherwise well until day 10 postingestion when he abruptly

developed hearing and visual impairment. These progressed

over the ensuing 24 h to complete hearing loss and blindness

and were associated with the development of a bulbar palsy

and a rapidly declining level of consciousness that required

endotracheal intubation and ventilatory support. Cranial CT

scan revealed no abnormality. Cerebral MRI showed high-

intensity signals suggestive of foci of oedema or infarction

within the left parietal and occipital lobes, and both cerebellar

hemispheres. His neurological state did not improve, and on

day 19 postingestion he developed severe cerebral oedema and

died. A limited autopsy found no evidence of central de-

myelination. Renal biopsy showed diffuse cortical necrosis

consistent with DEG toxicity (see Fig. 1).

Patient-2 was managed at a separate tertiary institution as

our acute hemodialysis capabilities had been overwhelmed.

He was managed in a manner identical to our patients. Initially

he showed improvement symptomatically with stabilization of

his acid-base status, but remained dialysis dependent. Renal

biopsy demonstrated near total cortical necrosis. During the

second week of his admission he also developed a bulbar

palsy with associated lower limb weakness suggestive of a

peripheral neuropathy. EMG and nerve conduction studies

confirmed a sensory-motor neuropathy involving the lower

limbs, which did not progress. His neurological signs im-

proved over time but did not resolve completely, He remains

dialysis-dependent.

Patient-3 had a turbulent clinical course, requiring re-

intubation on two occasions due to uncontrolled seizures. He

developed aspiration pneumonia with respiratory failure

complicated by significant pleural and pericardial effusions.

Fourteen days postingestion he developed a bulbar palsy and

unilateral facial nerve paresis. These deficits improved over

time, leaving residual mild facial nerve palsy. He also remains

dialysis-dependent.

In summary, patients 1, 2, and 3 presented in established

renal failure and remained dialysis-dependent long term. They

all developed significant neurologic sequelae 2 to 3 weeks

postingestion. Patient 1 died of neurological sequelae on day

19. Patients 4 and 5 presented with normal renal function, did

S. ALFRED ET AL.156

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not develop ongoing renal impairment, and were discharged

back to their correctional services facility where ongoing

medical review did not detect any evidence of evolving

neurological abnormalities over the ensuing weeks. Similarly,

patients 6 and 7 remained symptom free.

DISCUSSION

Diethylene glycol is a solvent with widespread industrial

usage; therefore its identification by GCMS within the

ingested fluid was consistent with the reported mode of

acquisition. Coupled with the lack of access to alternative

toxins within the prison system, a negative GCMS screen for

other toxins in the ingested fluid, and normal serological

parameters for alternative causes of elevated osmolar gaps

(glucose, lactate, ethanol, ethylene glycol, etc.) this presented

a strong case for DEG as a single agent exposure.

As evidenced in this case series DEG confers a significant

potential for the development of metabolic and renal toxicity if

ingested. Previous reports of epidemic DEG toxicity have

commonly occurred in third-world countries where access to

intensive care facilities and extracorporeal renal supportive

therapy is often nonexistent. Consequently patients com-

monly die rapidly as a result of metabolic acidemia and anuric

acute renal failure (3–11). There have been few long-term

survivors. However, delayed neurologic sequelae have been

observed in a small number of acute phase survivors with

ongoing renal impairment (12,13). We report significant and

delayed neurologic toxicity in three patients with established

renal failure at presentation following the ingestion of DEG

for recreational purposes.

Toxicological experience with DEG extends back to 1937

and the ‘‘Massengil Tragedy’’ in which 105 deaths resulted

following the release of a sulphanilamide elixir suspended in

DEG. Since then there have been mass casualties in South

Africa (1969), Spain (1985), India (1986 and 1998), Nigeria

(1990), Bangladesh (1990–1992), and Haiti (1996), with well

in excess of 500 documented deaths and many more un-

recorded. These epidemics can be attributed to the substitution

of DEG for more expensive, nontoxic glycols in medicinal

preparations. Typically acetaminophen elixirs have been

involved, explaining the preponderance of pediatric deaths.

Neurotoxicity following DEG poisoning was first reported

in South Africa, where three of seven DEG exposed children

with anuric acute renal failure developed optic neuritis (6).

Cerebrospinal fluid (CSF) from these three cases demonstrated

elevated protein levels which were thought to be indicative of

a demyelinating process (6). All seven children died despite

supportive therapy, which included peritoneal dialysis.

Autopsies demonstrated renal and hepatic changes consistent

with DEG poisoning without detectable CNS pathology (6).

Neurologic abnormalities were also reported in a number of

cases of pediatric DEG poisoning observed during the 1996

Haitian acetaminophen contamination episode. Facial nerve

paresis was seen in the acute acidemic phase of poisoning

(11). Unfortunately all children exhibiting this sign died of

renal failure, along with the vast majority of those exposed. Of

note, a 7-yr-old girl transferred to the United States for treat-

ment of established renal failure with hemodialysis devel-

oped optic neuritis, sixth cranial nerve and bulbar palsies on

day 10 postexposure (12), a delay similar to that observed in

our case series. Cerebrospinal fluid protein levels in this child

were found to be elevated, although myelin basic protein was

negative. An MRI demonstrated cerebral atrophy without evi-

dence of edema or demyelination. She was treated with high-

dose steroids and improved over time but was left with some

persisting neurologic abnormalities.

Rollins et al. reported similar delayed neurologic deterio-

ration in a 55-yr-old man who ingested DEG in a suicide

attempt (13). Diagnosis of and treatment for his DEG exposure

were delayed for several days. By the time hemodialysis was

initiated the patient was in established renal failure. On day 5

he developed bilateral lower limb weakness, which progressed

over the course of the next 5 days to hyporeflexive quad-

raparesis and was associated with progressive mental obtun-

dation and coma requiring endotracheal intubation and

ventilation. CSF protein levels were elevated with a positive

myelin basic protein, and electromyography/nerve conduction

studies confirmed a severe neuropathy with demyelinating

features. MRI scanning again failed to demonstrate evidence

of demyelination. He died 18 days postingestion. Autopsy

revealed patchy meningeal and perivascular lymphocytic

infiltrates around the brainstem and occasional chromatolytic

motor neurons within the spinal cord. The cerebral white

matter did not show any evidence of demyelination. Periph-

eral nervous system changes included widespread severe

myelin loss in all the sampled sections. Similarly, dorsal and

ventral nerve roots immediately adjacent to the cord at all

FIG. 1. Renal biopsy showing DEG induced diffuse cortical necrosis.

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spinal levels demonstrated similar myelin losses, as did cranial

nerves 6, 7, and 8 (13).

The mechanism of DEG neurotoxicity has not been fully

elucidated. Initially, it was theorized that production of oxalic

acid and calcium oxalate was involved in the neurotoxicity

seen with DEG poisoning. Early studies of DEG metabolism

suggested that it was first metabolized to ethylene glycol and

subsequently oxalic acid (15–17). This was subsequently dis-

proved by examining the metabolism of radiolabelled DEG,

demonstrating that ethylene glycol and ethylene glycol–re-

lated byproducts are not produced during DEG metabolism

(18–22). The main metabolite of DEG has been identified as

2-hydroxyethoxyacetic acid (HEAA) (22). The metabolism of

DEG to HEAA in rats has been prevented by inhibition of both

alcohol and aldehyde dehydrogenases (22). Consequently,

HEAA and other yet-to-be identified metabolites of DEG may

be the mediators of DEG toxicity in humans. Transcellular

fluid shifts, membrane destabilization through phospholipid or

ion channel effects, metabolic acid-base derangements, and

osmotic metabolite accumulation within cells all present as

possible mechanisms for this cellular toxicity.

From a clinical perspective, DEG toxicity is capable of

producing both acute phase neurologic impairment, with optic

neuritis, facial nerve palsies and cerebral edema (6,9,11), and

a delayed neurotoxicity in the form of optic neuritis, central

and peripheral neuropathies that may be demyelinating in

nature (12–14). As evidenced in this case series and the

previous cases of DEG poisoning with delayed neurological

features, the presence of metabolic acidemia with established

renal failure on presentation to hospital may be predictive of

subsequent delayed neurologic toxicity. None of the patients

with normal renal function in our case series developed any

neurological signs on subsequent evaluation.

Diethylene glycol poisoning has the potential to produce

significant morbidity and mortality, particularly in patients

who have delayed presentations. As with all toxic alcohol

exposures, the aim of therapy is to recognize the poisoning

early in its course and to prevent the development of acidemia

and renal failure. Specific therapies to block alcohol de-

hydrogenase conversion of DEG to its toxic metabolites, such

as intravenous ethanol infusion or fomepizole, should be

employed (23,24). Hemodialysis should be instituted as soon

as possible to remove DEG, its metabolites, and to treat any

metabolic acidemia that is present. Clinicians must be aware

that patients presenting with or developing renal failure fol-

lowing DEG poisoning may go on to exhibit significant

central and peripheral neurologic complications several days

to weeks following the exposure. Currently, there are no spe-

cific therapies available to treat DEG-induced neurotoxicity.

The natural course of this condition is unpredictable. Patients

may have resolution of some or all of their neurologic signs

over a matter of weeks or months, or die with fulminant cen-

tral nervous system failure.

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159DIETHYLENE GLYCOL POISONING AND DELAYED NEUROTOXICITY

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