Telogen effluvium — Viva

Q1: Definition and classification (2 min)

Question: Define telogen effluvium and outline its classification.

Model answer: Telogen effluvium (TE) is a non-scarring, diffuse hair loss caused by a premature shift of anagen (growth-phase) follicles into telogen (resting phase), producing synchronous shedding 2-3 months after a triggering event. The hallmark bedside signs are diffuse thinning, a positive hair pull test, and trichoscopic empty follicles with upright regrowing hairs; there is NO hair diameter diversity (>20 percent), NO exclamation-mark hairs and NO yellow dots. Headington classified five functional types: immediate anagen release (most common — febrile illness, drug, stress), delayed anagen release (postpartum TE), short anagen (children, idiopathic), immediate telogen release (drugs, faster onset) and delayed telogen release (seasonal, post-travel). The two clinical forms are acute TE (< 6 months) and chronic TE / CTE (> 6 months, Whiting) — a distinct middle-aged female phenotype that fluctuates for years and may overlap with early female pattern hair loss (FPHL).

Q2: Pathophysiology and the 2-3 month lag (3 min)

Question: Why is there a 2-3 month lag between trigger and shedding, and what molecular pathways drive TE?

Model answer: The hair follicle is a mini-organ that cycles through anagen (2-7 years, growth), catagen (2-3 weeks, regression), telogen (~3 months, rest) and exogen (release of the club hair). At any one time, 85-90 percent of scalp hairs are in anagen and 10-15 percent in telogen. In TE, a trigger synchronously terminates anagen in a large cohort of follicles (Headington's immediate anagen release) or releases prolonged anagen (delayed anagen release in postpartum). The molecular mediators include FGF5 and TGF-beta2 (catagen drivers), pro-inflammatory cytokines (IL-1, IL-6, TNF-alpha), hormonal changes (oestrogen withdrawal, cortisol surges, thyroid dysfunction) and iron- and zinc-dependent enzymes in the matrix. Once a critical mass of follicles enters telogen, the cluster of club hairs is shed at the end of telogen during exogen — 2-3 months later. Hence the diagnostic lag: the patient always presents AFTER the trigger. The corollary is to always ask "What happened 2-3 months ago?" — childbirth, fever, COVID-19, surgery, weight loss, drug change, severe stress, menstrual or iron losses.

Q3: Differential diagnosis and clinical examination (3 min)

Question: How do you distinguish telogen effluvium from its main mimics at the bedside?

Model answer: Use the three-step bedside algorithm: diffuse vs patterned vs patchy -> scarring vs non-scarring -> reversible vs irreversible. Trichoscopy discriminates:^[3]

• TE: diffuse, empty follicles, upright regrowing hairs, NO diameter diversity, NO exclamation-mark hairs, NO yellow dots, NO loss of follicular ostia.
• AGA / FPHL: patterned (bitemporal + vertex in men; central with preserved frontal in women), diameter diversity >20 percent, peri-pilar sign, vellus hairs.
• Alopecia areata: patchy (or diffuse AA), exclamation-mark hairs, yellow dots, sometimes black dots; positive pull test at the margin.
• Cicatricial alopecia: loss of follicular ostia (smooth, shiny, atrophic surface), perifollicular erythema/scale/pustules, scarring — biopsy the active margin.
• Anagen effluvium (chemotherapy): sheds within days to weeks, not 2-3 months; shed hairs are dystrophic anagen (broken, pigmented, tapered) not telogen club hairs (white bulb).
• Tinea capitis: predominantly children; scaling, broken hairs, occipital lymphadenopathy; KOH positive.
• Trichotillomania: irregular patches with hairs of varying lengths, history of pulling.

^[2][3]The hair pull test (>5-6 of 60 hairs) is positive in TE. The modified wash test (Rebora) counts hairs after a 5-day shampoo-free interval; >100 is abnormal.

Q4: Investigations (2 min)

Question: What is your first-line workup in suspected telogen effluvium?

Model answer: First-line: ferritin (target >70 microg/L in women with TE), TSH and free T4, CBC, vitamin D (25-OH), and zinc if deficiency is suspected. Ferritin is an acute phase reactant; check CRP if unexpectedly high. Trichoscopy is performed in the clinic to exclude AGA, AA and cicatricial alopecia. Second-line, if the diagnosis is uncertain: hair pluck trichogram (>25 percent telogen hairs suggests TE), wash test (Rebora, >100 hairs abnormal) and 4 mm punch biopsy from the active margin (only if there is diagnostic doubt or suspected scarring). In selected patients, add ANA (lupus), RPR/VDRL (syphilis), HIV, fasting glucose or HbA1c (PCOS, metabolic syndrome), and occult-blood / GI workup if iron deficiency without obvious cause. The ferritin threshold is debated (40 vs 70 vs 100 microg/L); most hair specialists now use 70 microg/L in symptomatic TE.

Q5: Management — trigger correction and reassurance (3 min)

Question: Outline the management of acute and chronic telogen effluvium.

Model answer: Acute TE: identify and treat the trigger; correct iron deficiency with oral iron until ferritin normalises per local cut-offs; replace vitamin D, zinc and other nutrients as needed; review and rationalise drugs (retinoids, anticoagulants, beta-blockers, lithium, valproate); address stress, sleep, postpartum factors and crash dieting; reassure with the 2-3 month lag explanation and the expected months-long regrowth timeline; advise gentle hair care (avoid traction, heat, chemical processing); arrange follow-up. Chronic TE / CTE is more challenging. Treatment is the same trigger hunt, but the threshold for adding topical minoxidil is lower because the condition is by definition persistent. Low-dose oral minoxidil is increasingly used off-label in chronic TE / FPHL overlap, with counselling about hypertrichosis, transient fluid retention, occasional hypotension and strict pregnancy prevention in women of childbearing age. Avoid in pure TE: finasteride, dutasteride, systemic steroids, PRP, microneedling and LLLT — these target AGA / FPHL, not TE.^[1][3]

Q6: Complications, prognosis and counselling (2 min)

Question: What is the prognosis of TE, and how do you counsel the patient?

Model answer: Acute TE has an excellent prognosis: full regrowth to pre-trigger density over months once the trigger is removed or corrected. Hair grows slowly, so visible recovery to the patient's previous length lags even after the trigger is gone. The patient will not go bald. Chronic TE is more variable: many patients fluctuate for years, with partial recovery and a tendency to overlap with FPHL over time. Predictors of poor prognosis include persistent unidentified trigger, concurrent early FPHL, uncorrected iron deficiency, polypharmacy and severe psychosocial comorbidity. The dominant "complication" is psychosocial impact — anxiety, depression, social withdrawal, secondary trichotillomania or traction from compensatory tight hairstyles; early psychology referral is part of good care. Red flags requiring re-referral: persistent shedding beyond a year, development of patterned loss, scarring on examination, systemic symptoms, or absence of an identifiable trigger despite a thorough history covering the preceding months.^[2][3]