CASE REPORT ethylene glycol, and adult respiratory distress syndrome; poisoning, ethylene glycol, adult respiratory distress syndrome

Adult Respiratory Distress Syndrome Secondary to Ethylene Glycol Ingestion

LCDR Timothy T Catchings, MD, USNR* Wilson C Beamer, MD*T

Larry Lundy* Donald S Prough, MD*

Winston-Salem, North Carolina

From the Section on Critical Care Medicine, Department of Anesthesia,* and

the Section on Emergency Medicine, Department of Surgery, t Bowman Gray

School of Medicine of Wake Forest University, Winston-Salem, North Carolina.

Received for publication September 7, 1984. Revision received November 6,

1984. Accepted for publication December 14, 1984.

Address for reprints: Wilson C Beamer, MD, Department of Anesthesia, Bowman

Gray School of Medicine, 300 South Hawthorne Road, Winston-Salem, North

Carolina 27103.

Presented is a case of ethylene glycol poisoning in a 24-year-old man who subsequently developed adult respiratory distress syndrome. The noncar- diogenic nature of the patient's pulmonary edema was documented udth hemodynamic monitoring, and a successful outcome was achieved with he- modialysis, ethanol, and intermittent mechanical ventilation with positive end-expiratory pressure. [Catchings TT, Beamer WC, Lundy L, Prough DS: Adult respiratory distress syndrome secondary to ethylene glycol ingestion. Ann Emerg Med June 1985;14:594-596.]

INTRODUCTION Ingestion of ethylene glycol is an uncommon cause of poisoning in the

United States. When it occurs, however, the consequences often are serious and can be fatal.l, 2 Although some cases of ethylene glycol poisoning may be accidental, others are the result of suicide attempts. The CNS, the cardiopul- monary system, and the renal system are primari ly affected, and their damage is the major cause of morbidity and mortality. Pulmonary edema has been described in a number of patients following poisoning with ethylene glycol, 3-7 but the mechanism of occurrence has not been elucidated.3,7

We present the case of a young man who, following the deliberate inges- tion of ethylene glycol, developed pulmonary edema, hypoxemia, and de- creasing pulmonary compliance that fit the criteria for the adult respiratory distress syndrome (ARDS). 8 Hemodynamic monitoring using a flow-directed, balloon-tipped (Swan-Ganz) catheter documented the noncardiogenic nature of the pulmonary edema with normal pulmonary capillary wedge pressures (PCWP).

CASE REPORT A previously healthy 24-year-old man was found comatose in his home

after having ingested an unknown liquid. He was evaluated at an emergency department, and he was given 0.8 mg naloxone and 25 g glucose intra- venously (IV) without effect. He was then transferred to the North Carolina Baptist Hospital where he was admitted to the intensive care unit 12 hours after being found. During those 12 hours his mental status showed pro- gressive deterioration in the emergency department and during transfer. On arrival at Baptist Hospital, he was comatose, with a blood pressure of 160/110 m m Hg, rectal temperature of 37 C, and pulse of 146. His respirations were 48 per minute and Kussmaul in character. There was no evidence of trauma, and no odor of alcohol was detected on his breath.

Funduscopic examination was normal, and his chest was clear to ausculta- tion. The abdomen was unremarkable~ there was no occult blood in the stool; and his skin was warm and dry. Heart sounds were normal. Neurologic examination revealed areflexia and semipurposeful movement to painful stimulation. His pupils were midposition and reacted briskly to light.

The hematocrit was 52.8%; the WBC count was 32,000, with 74% neu- trophils. Urinalysis revealed a specific gravity of 1.015; pH of 5; negative ketones; no cellular elements or casts; a trace of protein; numerous calcium phosphate crystals; and occasional oxalate crystals. Serum sodium con- centration was 143 mEq/L; potassium, 7.1 mEq/L; chloride, 108 mEq/L; and bicarbonate, 6.8 mEq/L.

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Urea nitrogen was 14 mg/dL; cre- atinine, 1.4 mg/dL; glucose, 176 rag/ dL; calcium , 10.0 mg/dL; and lactate, 1.2 mEq/L. Serum salicylate level was 5.1 mg/dL, and the serum ethanol level was zero. Urine drug screen was negative. Arterial blood gases (room air) revealed PaO2, 124 tort; PaCO2, 12 torr; and pH, 6.98.

The init ial chest radiograph was normal, and the ECG showed sinus tachycardia. Computed cranial tomog- raphy of the head was normal. Lumbar

puncture revealed an opening pressure of 26.0 cm H20. The cerebrospinal fluid contained 73 red blood cells w i thou t xan thoch romia ; 3 mono- nuclear WBCs; protein, 84 mg/dL; glucose, 145 mg/dL; and no organisms on Gram staining.

The anion gap was 28 (normal, 12 to 14), and Calculated serum osmola!ity was 315 m O s m wi th a measured serum osmolality of 369 mOsm. The "osmolar gap" was therefore 54 mOsm approximately 14 hours after inges-

Fig. Chest film shows diffuse alveolar infiltrates and pneurnomediastinum.

tion. The level of serum ethylene "glycol, drawn on admission, later re- turned 1,901 mg/L.

These findings led to the suspicion of ethylene glycol poisoning. Endo- tracheal intubation was performed for airway protection. Following gastric lavage wi th 2L normal saline, acti- va ted charcoa l was a d m i n i s t e r e d through the nasogastric tube and 100 mg thiamine and 500 mg pyridoxine -were given parenterally. Ethanol (5%} and 500 mL of 8.4% sodium bicarbo- nate was infused IV over the next 24 hours.

Arterial blood gases after intubation (on an FiO 2 of 0.21 and spontane- ous ventilation) were PaO2, 76 torr; PaCO2, 25 torr; and pH, 7.47. Hemo- dialysis against a bicarbonate bath was p e r f o r m e d us ing a f e m o r a l ve in catheter. The pat ient became pro- gressively oliguric and suffered two generalized tonic-clonic seizures.

On the second hospital day, arterial blood gases (on an FiO 2 of 0.21) deteri- orated to PaO2, 49 tort; PaCO2, 26 tort; and pH, 7.52. Increasing con- centrations of inspired oxygen were given (PaO 2 Of 101 tort on an FiO 2 of 1.0 with peak inspiratory pressures of 46 cm H20); subsequently requiring mechanical ventilation with positive end-expiratory pressure (PEEP).

On the morning of the third hospi- tal day, arterial blood gases (on an FiO 2 of 0.6, peak inspiratory pressure of 60 cm H20 , intermittent mechan- ical ventilation {IMV) of 10/minute, and 12.5 cm H20 of PEEP) were PaO2, 77 tort; PaCO2, 42 torr; and pH, 7.43. Anur ia developed, and a bal loon- tipped; f low-directed (Swan-Ganz) catheter was inserted through the right internal jugular vein. The central venous pressure was 8 tort; mean pul-

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ARDS Catchings et al

monary artery pressure {MPAP) was 20 tort; and PCWP was 10 torr with a cardiac index of 5.3 L/min/m 2.

A second chest radiograph (Figure) showed diffuse alveolar inf i l t ra tes wi th subsequen t de ve l opm e n t of a p n e u m o m e d i a s t i n u m , p r e s u m a b l y secondary to barotrauma. Nafci l l in 500 mg every four hou r s and to- bramycin 80 mg every other day were added, a l though subsequen t blood, urine, and sputum cultures were nega- tive for pathogens.

Over the next 24 hours, PEEP was adjusted to 15 cm H20 to keep the PaO 2 greater than 60 torr and the FiO 2 less than 0.6. Peak inspiratory pres- sures ranged from 64 to 78 cm I-I20. Subsequent PCWP remained between 10 and ll torr, with normal to slightly elevated cardiac outputs. Dialysis was cont inued every other day for azo- temia.

Ant ibiot ics were d iscont inued on the fourth hospital day. By the sixth hospital day, arterial blood gases had begun t O improve (PaO~, 93 torr ; PaCO2, 36 t0rr; pH, 7.48 on an FiO 2 of 0.4; and IMV of 2/minute). The pa- tient was extubated on the eighth day.

H e m o d i a l y s i s was d i scon t inued 15 days later after spontaneous urine out- put had resumed. After 22 days of hos- pitalization, the patient left the hospi- tal w i th a no rma l ches t f i lm a n d nearly normal renal function. Psychi- atric evaluat ion had conf i rmed that the ethylene glycol ingestion was a suicide attempt.

DISCUSSION E t h y l e n e g lyco l is a co lo r l e s s ,

odorless liquid tha t has a pleasant, somewhat bittersweet taste. It is most commonly encountered in antifreezes and deicers. Its p leasant taste and availability have led to its abuse as a substitute for ethanol and as an agent for suicide. The first case of poisoning was reported in 1930, 9 and as many as 60 dea ths per year have b e e n at- tributed to its ingestionjO, n In our Patient, the physical findings of coma, tachypnea and tachycardia, and the l a b o r a t o r y f i nd ings of a c i d e m i a , crystalluria, a large osmolar gap, and a large anion gap, were clues to the in- gestion of ethylene glycol.

Any patient with a metabolic acid- osis should have an anion gap calcu- l a t i on [(Na ++ - (HCO~ + C1-)] (normal, 12 to 14) to narrow the differ-

ential diagnosis. If the anion gap is el- evated, it limits the diagnosis to four categories: lactic acidosis, ketoacid- osis, renal failure, or toxins. 12 To cause a large osmolar gap (calculated osmolality - measured osmolality), a substance of small molecular weight must be present to account for these occult osmoles. 12 Such substances in- clude ethanol, isopropanol, methanol, ethylene glycol, mannitol, and glycer- ol. 2

Berman described three stages of toxici ty with ethylene glycol poison- ing: Stage I (occurring 20 minutes to 12 hours after ingestion), manifested by symptoms of intoxication, nausea, vomiting, seizures, and coma; Stage II (occurring 12 to 24 hours after inges- tion), manifested by tachypnea, tachy- cardia, p u l m o n a r y edema, and con- gest ive hear t failure; and Stage III (occurring 24 to 72 hours after inges- tion), manifested by flank pain, anuria, and azotemia. 3 Pulmonary congestion and edema are found f requent ly at pos tmor tem examination of patients dying f rom ethylene glycol poison- ing.3,s, 13 Other pulmonary findings in- c lude h e m o r r h a g i c l e s ions of the p leura l sur faces and lungs, in t ra- alveolar exudates, and occas ional ly bronchopneumonia, which raises the possibility of aspiration J4, I 5 0 x a l a t e crystals have been found within pul- monary vessels3 s Myocardial damage and congestive heart failure are found sometimes, but not all patients with ethylene glycol poisoning and pulmo- nary edema have evidence of cardiac failure.4,~s

The etiology of pulmonary edema occurr ing wi thou t cardiac failure is unclear ; Berman suggested a neu- rogenic origin. 3 It is possible ~:hat our pat ient aspirated, but there was no history suggestive of aspiration, and the chest radiograph was more com- patible wi th ARDS than aspirat ion Pneumonitis. Further, the rapid deteri- oration of chest radiograph findings and arterial blood oxygen levels, cou- pled with decreasing pulmonary com- pl iance, also was c o n s i s t e n t w i t h ARDS. 8 Hemodynamic monitoring of PCWP and cardiac output showed that the pulmonary edema was not second- ary to hydrostatic forces. Thus, while the exact mechanism of pulmonary e d e m a in the a b s e n c e of ca rd iac failure remains speculative, a direct toxic effect f rom the metabolites of ethylene glycol may be responsible.

SUMMARY Although m a n y deaths f rom eth-

ylene glycol have been attributed to cardiopulmonary dysfunction, most of the respiratory dysfunction in our pa- tient was manifest in the presence of normal cardiac function. Respiratory suppor t a i m e d at the nonca rd i ac nature of this disease with mechanical vent i la t ion and PEEP resulted in a successful outcome.

REFERENCES 1. Frommer JP, Ayus JC: Acute ethylene glycol intoxication. A m J Nephrol 1982; 2:1-5.

2. Moriarty RW, McDonald RH Jr: The spectrum of ethylene glycol poisoning. Clinical Toxicology 1974;7:583-596.

3. Berman LB, Schreiner GE, Feys J: The nephrotoxic lesion of ethylene glycol. A~n Intern Med 1957;46:611-619.

4. Pons CA, Custer RP: Acute ethylene glycol poisoning. A clinico-pathologic re- port of eighteen fatal cases. A m J Med Sci 1946;211:544-552.

5. Case records of the Massachusetts General Hospital, Case 38-1979. N Eng] J Med 1979;301:650-657. 6. Smith DE: Morphologic lesions due to acute and subacute poisoning with anti- freeze {ethylene glycol). Arch Pathol Lab Med 1951i51:423-433.

7. Walton EW: An epidemic of antifreeze poisoning. Med Sci Law 1978;18:231-237. 8. Asbaugh DG, Bigelow DB, Petty TL, et ah Acute respiratory distress in adults. Lancet 1967;2:319-323.

9. Anonymous: Possible death from drinking ethylene glycol ("Prestone'). Queries and minor notes. JAMA 1930;94: 1940.

10. Parry MF, Wallach R: Ethylene glycol poisoning. A m ] Med 1974;57:143-150.

11. Dreisbach RH: Handbook of Poison- ing, ed 11. Los Altos, California, Lange Medical Publishers, 1983, pp 191-192.

12. Narins RG, Gardner LB: Simple acid- base disturbances. Med Clin North A m 1981;65:321-346.

13. Friedman EA, Greenberg JB, Merrill JP, et ah Consequences of ethylene glycol poisoning. Report of four cases and review of the literature. A m / Med 1962;32: 891-902.

14. Hagemann PC), Chiffelle TR: Ethylene glycol poisoning. A clinical and patholog- ic study of three cases. J Lab Clin Med 1948;33:573-584.

15. Bowen DAL, Minty PAB, Sengupta A: Two fatal cases of ethylene glycol p0ison- ing. Med Sci Law 1978;18:102-107.

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