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Morbidity in a pediatric patient having alcohol ablation of an arteriovenous malformation

George Washington University Medical Center, Washington, USA, E-mail: djoffe{at}cnmc.org

To the Editor:

An otherwise healthy 25-month-old, 11.8 kg male child was scheduled for alcohol embolization of an arteriovenous malformation on the back of his skull. The procedure was performed under general anesthesia. The duration of the case was approximately three hours and 45 min, and the patient remained hemodynamically stable throughout. After obtaining a cerebral angiogram, the arteriovenous malformation and fistula were treated with 11.5 mL of anhydrous alcohol administered in 2–3 mL increments over approximately one hour. The procedure was stopped after a dose of 1 mL·kg^–1 of alcohol had been injected.

In order to monitor the metabolic effects of the injected alcohol, arterial blood gas chemistry and serum ethanol levels were obtained at the conclusion of the case. His arterial pH was 7.19, PaC0₂ 50 mmHg, Pa0₂ 121 mmHg, HC0₃^– 19 mmol·L^–1, BE –9, anion gap 31, Na⁺ 133 mmol·L^–1, K⁺ 4.6 mmol·L^–1, HCT 26% (preoperative 31.9%). The urine was serosanguinous at this time, and the serum alcohol level was 85.2 mg·dL^–1 (legal intoxication is defined as > 80 mg·dL^–1).

In response to the metabolic derangement, the patient received sodium bicarbonate 15 mEq iv. He was allowed to emerge from anesthesia, and his trachea was extubated in the catheterization laboratory. He was drowsy initially but arousable, and his breath smelled of ethanol. Shortly following admission to the pediatric intensive care unit (PICU), serum chemistry showed an improvement in his acid-base status. However, he was profoundly hypoglycemic, with a serum glucose of 14 mg·dL^–1. While dextrose 50% increased his serum glucose to 112 mg·dL¹, a peripheral blood smear showed "poc marks" on approximately 1% of erythrocytes. He was diagnosed with intravascular hemolysis secondary to the systemic absorption of anhydrous alcohol. The patient continued to be monitored in the PICU, where he was carefully hydrated and received a maintenance glucose infusion. His serum creatinine remained within the normal range, while serum alcohol concentration decreased to 7.5 mg·dL^–1 within two hours. The remainder of his postoperative course was uneventful, and the patient was discharged from hospital two days following the procedure, in good condition.

Doses of alcohol up to 1 mL·kg^–1 have been used for vascular ablation procedures. Multiple complications have been reported, including ethanol intoxication, intravascular hemolysis, hematuria, hyperthermia, elevated creatinine, hypoglycemia, pulmonary edema, pulmonary embolism, skin necrosis, and skin blistering.^1–3 The serum concentration of alcohol is proportional to the amount of alcohol injected.¹ This is the first reported case involving a young pediatric patient, and suggests that the effects of anhydrous alcohol are similar to those observed in older patients. However, our experience demonstrates several unique considerations in this population. Hypoglycemia in children is a non-dose dependent response to alcohol intoxication.^4,5 This patient had profound hypoglycemia which corrected quickly following dextrose administration.

The mechanism of metabolic acidosis in patients intoxicated with alcohol has not been clearly elucidated. In this setting, the base deficit and lactate levels do not correlate with serum alcohol levels.³ The etiology of the acidosis in this patient did not appear to indicate poor perfusion. The acidosis resolved quickly with a small dose of bicarbonate. Laboratory analysis suggested the etiology of the hematuria was hemolysis. Reports suggest that the incidence of hemoglobinuria is not related to the alcohol level.¹ Up to 28% of patients have been reported to have hemoglobinuria during alcohol ablation.

In summary, this report describes the systemic effects of anhydrous alcohol injected in a child for treatment of a cerebral arteriovenous malformation. Vigilance for complications, and a continuous infusion of glucose with frequent glucose monitoring, should be strongly considered in any young child undergoing these procedures.

Footnotes

Accepted for publication January 5, 2006.

References

1 Hammer FD, Boon LM, Mathurin P, Vanwijck RR. Ethanol sclerotherapy of venous malformations: evaluation of systemic ethanol contamination. J Vasc Interv Radiol 2001; 12: 595–600.[Medline]

2 Behnia R. Systemic effects of absolute alcohol embolization in a patient with a congenital arteriovenous malformation of the lower extremity. Anesth Analg 1995; 80: 415–7.[Medline]

3 Do YS, Yakes WF, Shin SW, et al. Ethanol embolization of arteriovenous malformations: interim results. Radiology 2005; 235: 674–82.[Abstract/Free Full Text]

4 Goldfrank LR, Flomenbaum NE, Lewin NA, Howland MA, Hoffman RS, Nelson LS. Goldfrank’s Toxicologic Emergencies, 7th ed. New York: McGraw Hill; 2002: 1635.

5 Ricci LR, Hoffman SA. Ethanol-induced hypoglycemic coma in a child. Ann Emerg Med 1982; 11: 202–4.[Medline]

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