Ifosfamide is an antineoplastic agent that requires hepatic activation to t
he cytotoxic active metabolite ifosforamide mustard. During metabolism, the
byproduct, chloroacetaldehyde, which is structurally similar to both chlor
al hydrate and acetaldehyde, is produced. Secondary to its ability to cross
the blood-brain barrier, this metabolite may be responsible for the neurot
oxicity observed with ifosfamide. Any case of suspected ifosfamide-induced
neurotoxicity, together with a decision to treat, must be determined on an
individual patient basis. The differential diagnosis should include infecti
on, laboratory abnormalities, and concomitant drugs. At this time, literatu
re to support treatment modalities such as intravenous albumin and methylen
e blue is minimal.