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Hyperventilation and Cerebrospinal Fluid Acidosis Caused by Topiramate

Resident, Department of Anesthesia and Intensive Care Unit, Military Teaching Hospital Sainte Anne, Toulon-Armees, France

Eric Meaudre, MD

Staff Anesthesiologist, Department of Anesthesia and Intensive Care Unit, Military Teaching Hospital Sainte Anne

Nadia Kenane, MD

Resident, Department of Anesthesia and Intensive Care Unit, Military Teaching Hospital Sainte Anne

Yves Asencio, MD

Resident, Department of Anesthesia and Intensive Care Unit, Military Teaching Hospital Sainte Anne

Julien Bordes, MD

Resident, Department of Anesthesia and Intensive Care Unit, Military Teaching Hospital Sainte Anne

Bruno Palmier, MD

Professor, Department Head, Department of Anesthesia and Intensive Care Unit, Military Teaching Hospital Sainte Anne

Reprints: Dr. Montcriol, Department of Anesthesia and Intensive Care Unit, Military Teaching Hospital Sainte Anne, BP 600, 83800 Toulon-Armees, France, fax 00 33 0494099698, ambroise.montcriol{at}free.fr

OBJECTIVE: To report a case of hyperventilation caused by topiramate therapy and propose a pathophysiologic mechanism for this disorder.

CASE SUMMARY: A 52-year-old woman with refractory seizure disorder was admitted to the burn care unit with burns over 10% of her body. Her seizure medications, unchanged and well tolerated for several months, included carbamazepine 1200 mg, lamotrigine 500 mg, phenobarbital 80 mg, and topiramate 150 mg per day. During hospitalization, despite a relatively normal arterial pH, the woman developed persistent hyperventilation, with respiratory rates up to 50 breaths/min. Alkalinization did not reduce the hyperventilation. Thoracic contrast-enhanced computed tomographic scan ruled out pulmonary embolism and persistent pneumonia. Salicylate and biguanide screening were negative; results of repeated thyroid and liver function tests were normal. Cerebral magnetic resonance imaging excluded a cerebral pathology. After cerebrospinal fluid (CSF) analysis showed acidosis (pH 7.14), topiramate was withdrawn and the patient's general condition rapidly improved. Forty-eight hours later, the CSF pH had increased to 7.26. The woman was discharged from the burn care unit on the 42nd hospital day.

DISCUSSION: Hyperchloremic normal anion gap metabolic acidosis, which can lead to hyperventilation, has been reported as an adverse effect of topiramate treatment. However, our patient had respiratory alkalosis. Concurrent etiologies of peripheral hyperventilation were excluded, leaving central neurogenic hyperventilation as the remaining etiology. Such central neurogenic hyperventilation associated with topiramate has previously been reported in intensive care. Our case report demonstrates CSF acidosis. Withdrawing topiramate reduced both CSF acidosis and hyperventilation. The mechanism of topiramate-induced CSF acidosis remains unclear. According to the Naranjo probability scale, the relationship of hyperventilation to administration of topiramate in our patient was probable.

CONCLUSIONS: Normal doses of topiramate may provoke central neurogenic hyperventilation, as a result of CSF acidosis. The acid-base status of critically ill patients receiving topiramate should be monitored carefully.

Key Words: central neurogenic hyperventilation, cerebrospinal fluid acidosis, topiramate

Published Online, March 18, 2008. www.theannals.com, DOI 10.1345/aph.1K508