DISEASE PAGE

Ototoxicity Monitoring

Basal-first emission loss — DPOAEs catch cisplatin and aminoglycoside damage early.

The OAE signature

  • Progressive high-frequency emission loss advancing from the cochlear base toward the apex as cumulative drug exposure rises.[5]
  • High-frequency DPOAE monitoring detects cochlear injury earlier than the pure-tone audiogram, allowing dose review before functional loss.[3]
0 ms20 ms
— Normal ear— Ototoxicity Monitoring
Simulated TEOAE comparison. Educational signal model — not recorded patient data.

Audiogram companion

The pure-tone audiogram below accompanies the OAE signature. Reading the two together — what the threshold shows and what the emission shows — is the core diagnostic skill.

0204060801002505001k2k4k8kFrequency (Hz)
○ Right — PTA 17 dB (Normal)✕ Left — PTA 22 dB (Normal)
Pure-tone audiogram companion. dB HL increases downward, following clinical convention. Illustrative thresholds — not recorded patient data.

Why the emission looks this way

  • Aminoglycosides and platinum agents are selectively toxic to outer hair cells, with the basal turn affected first — so the highest-frequency emissions vanish earliest.[4]

TEACHING POINT

A baseline OAE before ototoxic therapy, followed by serial high-frequency DPOAEs, turns the emission into an early-warning system.[6]

Sources for this page are listed on the References page. Browse all condition patterns from the atlas home.