12-phase flow (12)

1. 1FRAME
   Frame SSNHL as an OTOLOGIC EMERGENCY (≥30 dB over ≥3 contiguous frequencies within ≤72 h) requiring the time-critical audiogram → MRI → steroid pathway. >90% is idiopathic (Chandrasekhar AAO-HNS 2019 PMID 31369359) but the engine first separates conductive loss and the can-not-miss vascular (AICA) cause. Stroke management is recognised then routed OUT, not authored here.
   advance: SSNHL scope confirmed; not-this-engine concerns (stroke management) routed by engine_id
2. 2ENTRY
   Recognise sudden (≤72 h) hearing loss — isolated vs with vertigo vs with focal neuro — and capture tempo + laterality up front (bilateral/recurrent reframes toward autoimmune/systemic) (AAO-HNS 2019 KAS 2 PMID 31369359)
   inputs: onset_tempo, laterality_unilateral_vs_bilateral
   advance: sudden onset within ≤72 h confirmed; laterality + accompanying-symptom pattern recorded
3. 3CONTEXT
   Bedside Weber/Rinne + otoscopy/tympanometry to separate SENSORINEURAL from CONDUCTIVE (cerumen, effusion, perforation) — the first hard fork (KAS 1); characterise vertigo/vestibular features; capture vascular-risk burden, ototoxic exposure, infection exposure. This phase builds the idiopathic-vs-retrocochlear-vs-vascular prior.
   inputs: weber_rinne_bedside, otoscopy_tympanometry, vertigo_and_vestibular_features, vascular_risk_burden, ototoxic_exposure, infection_exposure_lyme_syphilis_hiv
   actions: workup.ssnhl, workup.vertigo
   advance: SNHL vs conductive established; vestibular + vascular + exposure context captured; pretest prior assigned
4. 4RED_FLAGS
   Screen for the CAN-NOT-MISS posterior-circulation / AICA labyrinthine infarction: any focal neuro deficit, central HINTS (normal head-impulse with spontaneous nystagmus, direction-changing nystagmus, skew deviation), or sudden deafness on a high vascular-risk substrate → emergent stroke pathway, route OUT to neuro.posterior-circulation-stroke.core.v1 with carryover (KAS 2; Kim & Lee J Stroke 2016 PMID 28030893).
   inputs: focal_neuro_or_central_hints
   actions: calc.abcd2, workup.acute_stroke, protocol.stroke
   advance: central/vascular red flags screened; stroke pathway activated and routed by engine_id if positive
5. 5INITIAL_WORKUP
   Obtain formal pure-tone + speech audiometry ASAP (within 14 days) to CONFIRM SNHL, quantify severity and audiogram shape, and date the baseline curve (KAS 4). Do NOT order routine non-targeted head CT or indiscriminate blood panels (KAS 3/5 — strong recommendations AGAINST). Targeted labs (RPR/Lyme/HIV/ESR/ANA) + baseline glucose/creatinine only when bilateral/recurrent/young/systemic features warrant.
   inputs: pure_tone_speech_audiometry, autoimmune_infectious_panel, glucose_creatinine_baseline
   actions: workup.ssnhl, panel.cbc, panel.inflammation, panel.cmp
   advance: audiogram confirms SNHL ≥30 dB/≥3 contiguous freq; baseline curve dated; routine CT/labs withheld
6. 6BRANCHING_WORKUP
   Retrocochlear / central decision tree: MRI internal auditory canal (or ABR if MRI contraindicated) for vestibular schwannoma AND posterior fossa for infarction (KAS 6); vertigo-dominant continuous + central HINTS → AICA stroke route; episodic vertigo + fluctuating low-frequency loss + aural fullness → Ménière; bilateral/recurrent/young → autoimmune inner-ear / systemic workup; identified ototoxic/infectious cause → treat the cause, not the idiopathic pathway.
   inputs: mri_iac_or_abr
   actions: workup.ssnhl, workup.vertigo, workup.acute_stroke
   advance: retrocochlear/central cause excluded or an identifiable (non-idiopathic) diagnosis assigned + routed
7. 7DIFFERENTIAL
   Terminal differential with named pivots: idiopathic SSNHL (isolated SNHL, normal MRI/neuro — the >90% default) vs conductive loss (Weber TOWARD affected ear + abnormal otoscopy/tympanogram pivot) vs vestibular schwannoma (asymmetric SNHL + MRI IAC enhancement + retrocochlear ABR pivot) vs Ménière (episodic vertigo + fluctuating low-frequency SNHL + aural fullness + tinnitus pivot) vs AICA / posterior-circulation infarction (other neuro signs / central-HINTS / vascular-risk pivot) vs autoimmune inner-ear (bilateral, rapidly progressive, steroid-responsive, recurrent pivot) vs ototoxic / infectious (identifiable exposure pivot)
   advance: single best diagnosis selected; idiopathic-SSNHL default vs identifiable cause flagged; central cause excluded or routed
8. 8RISK_STRATIFICATION
   Prognosis stratification driving urgency: presenting severity (severe/profound loss is the strongest independent poor-prognosis predictor — OR 6.6, Perez Ferreira Neto 2021 PMID 33557702), audiogram shape (flat/down-sloping/U-shaped worse), accompanying vertigo (worse — Bogaz 2015 PMID 26248967), older age, and time-to-treatment ≥14 days (independent poor predictor — OR 0.250). NEWS2/qSOFA only if the patient is systemically unwell or the stroke pathway is active.
   inputs: time_since_onset_days, vertigo_and_vestibular_features
   actions: calc.news2, calc.qsofa, calc.nihss
   advance: prognosis tier assigned; treatment urgency set by time-window + severity + vertigo
9. 9TREATMENT
   TIME-CRITICAL therapy for idiopathic SSNHL: (1) systemic high-dose corticosteroid as initial therapy within 2 weeks of onset — prednisone 60 mg/day (or methylprednisolone equivalent) ~10-14 days then taper (KAS 8); (2) intratympanic dexamethasone as PRIMARY therapy when systemic steroid is contraindicated/declined (diabetic, pregnant) — non-inferior to oral (Rauch JAMA 2011 PMID 21610239); (3) intratympanic steroid as SALVAGE for incomplete recovery at 2-6 weeks (KAS 10); (4) HBOT + steroid as combined initial (≤2 wk) or salvage (≤1 mo) option, greatest benefit in severe/profound loss (KAS 9a/9b; Rhee JAMA Oto 2018 PMID 30267033). Do NOT routinely give antivirals/thrombolytics/vasodilators/vasoactive agents (KAS 11, strong rec AGAINST) — antivirals only if a specific infection is identified. Counsel natural history + evidence limits (KAS 7).
   inputs: time_since_onset_days, diabetes, pregnancy
   advance: corticosteroid (systemic or intratympanic) started within window OR identifiable cause treated; salvage plan + audiometric follow-up booked
10. 10DISPOSITION
    Most idiopathic SSNHL is managed OUTPATIENT/urgent-ENT with rapid audiology + MRI + steroid initiation. Admit / route OUT when the AICA / posterior-circulation stroke pathway is active (neuro.posterior-circulation-stroke.core.v1) or a systemic emergency (sepsis, severe autoimmune) requires inpatient care. Conductive loss → treat the ear (cerumen removal, effusion, ENT) — exit the SSNHL steroid pathway.
    inputs: focal_neuro_or_central_hints
    advance: disposition documented; stroke/systemic cases routed OUT; conductive cases exited from steroid pathway
11. 11MONITORING
    Repeat audiometry at the conclusion of treatment and within 6 months of completion (KAS 12) to quantify recovery; assess for incomplete recovery at 2-6 weeks to trigger intratympanic SALVAGE (KAS 10); monitor steroid course (glucose, BP, mood, GI) and intratympanic-injection tolerance (otalgia, transient vertigo, TM perforation).
    inputs: pure_tone_speech_audiometry, glucose_creatinine_baseline
    actions: workup.ssnhl
    advance: post-treatment + ≤6-month audiogram obtained; salvage triggered if incomplete recovery; steroid toxicity surveilled
12. 12FOLLOWUP
    Counsel natural history and the limits of the evidence (KAS 7); for residual hearing loss and/or tinnitus, offer or refer for audiologic rehabilitation — hearing aids, CROS/BiCROS, cochlear implant for profound non-recovery, tinnitus management (KAS 13). Ensure the retrocochlear MRI/ABR result is closed-looped; recurrent/bilateral disease → autoimmune/systemic and neurotology follow-up. Headache/neuro re-presentation → re-screen for delayed posterior-circulation events.
    inputs: mri_iac_or_abr
    actions: workup.acute_headache
    advance: rehabilitation plan + tinnitus counselling documented; MRI/ABR result closed; recurrence and stroke-recurrence safety-net set