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7
Trichology for GP · Chapter Seven
Telogen Effluvium
Diffuse reactive shedding — diagnosing, reassuring, and resolving
Overview
Mechanism
Triggers
Clinical Features
Diagnosis
Chronic TE
Management
Quick Recall
Anki Cards
References
GP-Level Analogy

"Telogen effluvium is the hair equivalent of a factory shutdown. A major crisis — illness, surgery, crash diet, childbirth — signals the factory to suspend production and send all the workers home at once. Three months later, when those workers' contracts all expire at the same moment, the factory floor empties. The hair loss patients notice at month three was decided at month zero — and the factory is already re-opening."

Telogen effluvium (TE) is the most common cause of acute diffuse hair loss and one of the most frequently mismanaged presentations in general practice. It is characterised by excessive shedding of telogen (resting phase) club hairs, typically occurring 2–4 months after a triggering event.

TE is self-limiting in the acute form and requires no specific pharmacological treatment beyond identifying and correcting the underlying trigger. The GP's role is to diagnose accurately, identify the cause, correct reversible contributors, and provide reassurance — preventing the additional psychological distress of misdiagnosis and unnecessary treatment.

Key epidemiological facts

Prevalence
Most common acute shedding
Most frequent cause of acute diffuse hair loss. Affects women more than men due to higher prevalence of triggers (pregnancy, iron deficiency, thyroid disease).
Timeline
2–4 month lag
Trigger occurs at month 0. Shedding peaks at 2–4 months. Spontaneous recovery typically by 6–12 months after trigger removal.
Prognosis
Excellent if trigger removed
Acute TE: near-complete recovery in 95% of cases once the trigger is removed. Chronic TE (>6 months): requires thorough investigation and may be persistent.

Mechanism of telogen effluvium

TE occurs when a systemic stressor causes a synchronised, premature shift of anagen follicles into telogen. This results in a cohort of follicles all reaching the end of their telogen phase simultaneously — producing a wave of shedding 2–4 months later.

Fig 7.1 — Timeline of telogen effluvium from trigger to recovery
Month 0 Month 1–2 Month 2–4 Month 4–6 Month 6–12 T TRIGGER Anagen → Telogen Silent phase Hairs in telogen S SHEDDING PEAK 100–300+ hairs/day New anagen Regrowth begins R RECOVERY Normal density restored Patient seeks GP here "but it started on its own!"
Fig 7.1: TE timeline from trigger to recovery. The critical teaching point: when the patient presents with distressing shedding (month 2–4), the trigger happened 2–4 months earlier and the body has often already begun correcting itself. Regrowth begins before shedding even stops.

Kligman's five types of telogen effluvium

Kligman (1961) described five pathophysiological mechanisms producing TE. Understanding them helps identify the cause and predict the course.

TypeMechanismClinical example
Immediate anagen releaseSudden premature termination of anagen → rapid telogen entryHigh fever, acute severe illness, crash dieting
Delayed anagen releaseProlonged anagen (e.g. pregnancy) followed by synchronised releasePostpartum effluvium — most dramatic TE type
Short anagen effluviumConstitutionally shortened anagen duration → rapid cyclingChronic TE — hair never seems to grow long
Immediate telogen releaseEarly exogen — premature shedding of normal telogen hairsStopping minoxidil
Delayed telogen releaseProlonged telogen → delayed mass shedding in spring/summerSeasonal shedding (physiological, minor)
GP Analogy — The 3-month rule

"When a patient tells you their hair started falling out in October, ask what happened in June. Telogen effluvium always points backwards in time. The crime was committed 2–4 months before the body reports it."

Triggers — the CHIPS framework

The most common triggers can be remembered with the CHIPS mnemonic. Always ask about events 2–4 months before the onset of shedding.

C
Childbirth / Hormonal
Postpartum (most dramatic TE). OCP cessation. Menopause. HRT changes.
H
High fever / Illness
COVID-19, influenza, malaria, sepsis. Any systemic illness with fever >38.5°C.
I
Iron / Nutritional
Iron deficiency (most common correctable cause in women). Rapid weight loss, crash dieting, protein malnutrition, post-bariatric surgery.
P
Psychological / Physical stress
Major surgery, trauma, bereavement, job loss, relationship breakdown. CRH receptors on follicle mediate stress response.

Plus S — Systemic disease: thyroid disease (most important — both hypo and hyper), SLE, inflammatory bowel disease, renal disease, hepatic disease, malignancy.

Fig 7.2 — Common triggers mapped to onset timing
C — Hormonal / Childbirth • Postpartum (peak 3–6 mo) • OCP cessation (1–3 mo) • Menopause transition • Thyroid (hypo/hyper) • Post-miscarriage/TOP • PCOS treatment changes H + P — Illness / Stress • COVID-19 (very common) • Influenza, high fever • Major surgery / GA • ICU admission • Bereavement • Severe psychological stress I + S — Nutritional / Systemic • Iron deficiency (ferritin <30) • Crash diet / >15% weight loss • Post-bariatric surgery • Protein malnutrition • Zinc, Vitamin D deficiency • Inflammatory bowel disease Drug-induced TE: Anticoagulants, retinoids Beta-blockers, lithium Antithyroid drugs Chemotherapy ACE inhibitors Typical onset after trigger: Fever/illness → 6–8 weeks Postpartum → 3–6 months Surgery → 2–3 months Iron deficiency → ongoing OCP cessation → 1–4 months
Fig 7.2: Common TE triggers grouped by category. Always ask about the 2–4 month lookback window. COVID-19 has become one of the most common triggers since 2020, with TE reported in 25–33% of patients post-infection.

Drugs causing telogen effluvium

Drug classExamplesMechanism
AnticoagulantsWarfarin, heparin, DOACsTelogen induction — unknown exact mechanism
RetinoidsIsotretinoin, acitretinDose-dependent anagen arrest → TE at 2–3 months
Beta-blockersPropranolol, atenolol, metoprololUnknown — possibly through catecholamine suppression
Antithyroid drugsCarbimazole, propylthiouracilDirect effect on thyroid-dependent hair cycle
LithiumLithium carbonateAnagen shortening — dose-related
ACE inhibitorsCaptopril, enalaprilBradykinin-mediated follicular effect
Cytotoxic agentsCyclophosphamide, taxanesAnagen effluvium (different mechanism — matrix arrest)

Clinical features

TE has a characteristic clinical presentation that allows confident diagnosis in most cases. The combination of diffuse shedding, normal scalp, positive pull test, and a relevant preceding trigger is pathognomonic.

Fig 7.3 — Clinical examination findings in acute TE
Diffuse, uniform thinning ALL zones — including occiput Normal-looking scalp No inflammation, scale or fibrosis Positive pull test ALL zones >6 hairs — club bulbs (telogen) Shed hairs with club bulbs White/pigmented telogen roots
Fig 7.3: Clinical examination in acute TE. Diffuse thinning across ALL zones including the occipital scalp (unlike AGA where occipital zone is spared) with shed hairs showing white club bulbs. The scalp surface is entirely normal.

What the shed hair looks like

Telogen hair (TE)
Club bulb — white/pigmented root
A rounded, club-shaped, pale or pigmented bulb at the proximal end. The bulb is fully keratinised — no root sheath. This is normal telogen hair shed at exogen. Normal: up to 100/day. TE: 200–400+/day.
Anagen hair (effluvium)
Tapered, fleshy anagen bulb
A tapered, gel-covered, fleshy root sheath still attached. Indicates anagen effluvium (chemotherapy, radiation) — a different and more serious mechanism. Not typical of TE.

Patient-reported symptoms

SymptomTypical in TENotes
Hair on pillow, in shower drainYes — alarming quantityPatients often count — 200–400/day common in acute TE
Scalp symptoms (itch, pain, scale)Absent in uncomplicated TESymptoms suggest co-morbidity (sebderm, psoriasis) or alternative diagnosis
Diffuse scalp thinning visibleModerate — visible when >25% density lostLess visible than AGA — uniform reduction rather than patterned
Ponytail thickness reducedYes — objective measureUseful patient-reported objective marker; elastic band circumference
Anxiety about hair lossVery common — often driving the consultationPatients frequently convinced they will become bald — reassurance is key treatment

Diagnosis and investigation

Diagnostic criteria

Acute TE diagnosis: Diffuse shedding + club bulbs on shed hairs + positive pull test all zones + identified trigger 2–4 months prior + normal scalp + no miniaturisation on trichoscopy. No further investigations needed if all criteria met and trigger is obvious.

The FTBVZ blood panel for TE

TestTargetWhy
Ferritin>70 mcg/L for hair (not just lab range)Iron deficiency — most common, most treatable contributor
TSH + free T4TSH 0.4–4.5 mIU/LBoth hypo and hyperthyroid cause TE. Screen all women
B12 + folateB12 >200 ng/L; folate >7 nmol/LB12 deficiency (vegans, metformin users) + diet-related TE
Vitamin D (25-OH)>50 nmol/LDeficiency associated with hair loss; easily corrected
Zinc>10 µmol/LZinc deficiency — especially crash dieters, vegans
FBCHb >120 g/L (F)Anaemia (but Hb can be normal with low ferritin)
LFTs + urea/creatinineNormal rangeSystemic disease screen if no obvious trigger found

Trichoscopy in TE

FindingTE patternContrast with AGA
Hair shaft calibreUniform — all hairs same thicknessAGA: diversity — thick and miniaturised mixed
Follicular openingsPresent — ostia visible, normalAGA: single-hair units from companion loss
Miniaturisation ratio<10% — no significant miniaturisationAGA: >20% in vertex zone
Pull testPositive in all zones including occiputAGA: positive frontal/vertex, negative occiput
Yellow/black dotsAbsentAA: yellow + black dots prominent
Perifollicular changesNoneLPP/FFA: peripilar cast, erythema
TE or AGA — the most common diagnostic challenge

TE and FPHL/AGA frequently co-exist, particularly in women over 35. The key question: Is there calibre diversity? Trichoscopy uniform calibre = TE. Calibre diversity = AGA (with or without TE). Many women have both — treat both. Never dismiss "it's just TE" in a woman with diffuse thinning without checking for underlying miniaturisation.

Chronic telogen effluvium

Chronic TE (CTE) is defined as diffuse hair shedding lasting more than 6 months. It is more common in middle-aged women and may fluctuate over years. The prognosis is more variable than acute TE and requires more thorough investigation.

Fig 7.4 — Chronic TE: mechanism, presentation and differential
Mechanisms • Persistent trigger not found • Short anagen syndrome • Ongoing nutritional deficit • Subclinical thyroid dysfunction • Androgenetic component unmasked • Chronic systemic inflammation • Psychoneuroimmune axis • Occult malignancy (rare) Duration: >6 months Often waxes/wanes More thorough Ix needed Investigation additions • Full FTBVZ panel • ANA + anti-dsDNA (screen SLE) • Anti-TPO antibodies • Free androgen index • Fasting glucose + HbA1c • CRP / ESR (inflammation) • Albumin (protein) • Consider trichoscopy ± biopsy Consider referral if: No trigger after full screen Or >12 months duration CTE vs FPHL Feature CTE FPHL Calibre Uniform Diverse Miniat. None Yes (>20%) Shed ++++ Mild-mod FHx +/- Often + Pull test All zones Vertex/front Scalp Normal Normal Often co-exist in women Treat both simultaneously Trichoscopy to distinguish
Fig 7.4: Chronic TE: mechanisms, additional investigations, and the critical comparison with FPHL. These two conditions overlap significantly in middle-aged women and both can be present simultaneously.
When CTE needs urgent investigation

CTE with systemic symptoms (weight loss, fatigue, night sweats, lymphadenopathy) should prompt screen for underlying malignancy, inflammatory disease, or systemic autoimmune condition. Do not attribute all CTE to "stress" or "hormones" without adequate investigation.

Management — the FRONT framework

TE management follows the FRONT framework — a stepwise approach that covers the critical elements without over-medicalising a largely self-limiting condition.

Fig 7.5 — FRONT management framework for telogen effluvium
F Find & Fix trigger Identify the cause first CHIPS screen FTBVZ bloods R Replace deficiencies Iron to >70 Vit D >50 Zinc if low B12 if low Thyroid Rx O Optimise nutrition Protein 1.2g/ kg/day min Avoid crash dieting Varied diet N Normalise expectations Recovery in 6–12 months No baldness Photo record Review 3 mo T Treat if co-existing FPHL found → minoxidil CTE >6 mo → refer Psych support
Fig 7.5: FRONT management framework. The key principles: Find and fix the trigger first, Replace nutritional deficiencies, Optimise nutrition, Normalise the patient's expectations with evidence-based reassurance, and Treat any co-existing conditions (FPHL, CTE).

Evidence-based reassurance — what to tell patients

What is happening
"Your hair follicles are still alive. This is a temporary shedding of resting hairs — the factory workers going home — not destruction of the follicles themselves. New hairs are already beginning to grow before the shedding even stops."
What will happen
"In the vast majority of cases, hair returns fully to its previous thickness within 6–12 months of the trigger being resolved. You will not go bald from telogen effluvium. The shedding you're seeing right now is the end of the process, not the beginning."

Role of minoxidil in TE

Minoxidil is not indicated as first-line treatment for acute TE. The condition is self-limiting and minoxidil does not accelerate telogen resolution. However, if TE has unmasked underlying AGA/FPHL (confirmed by trichoscopy showing miniaturisation), minoxidil is appropriate for the androgenetic component.

Management Pitfall

Do not prescribe minoxidil for acute TE without evidence of co-existing FPHL. If a patient on minoxidil stops it (for any reason), they will experience a minoxidil-cessation TE on top of the original TE — compounding their distress and reinforcing incorrect beliefs about treatment.

Quick Recall

Triggers: CHIPS

C·H·I·P·S
  • Childbirth / hormonal change
  • High fever / systemic illness
  • Iron/nutritional deficiency
  • Psychological / physical stress
  • Systemic disease (thyroid #1)
  • All 3–4 months before shedding onset

Blood panel: FTBVZ

F·T·B·V·Z
  • Ferritin — target >70 mcg/L
  • TSH + T4 — thyroid screen
  • B12 + folate
  • Vitamin D — target >50 nmol/L
  • Zinc
  • Plus FBC, LFTs if CTE

Management: FRONT

F·R·O·N·T
  • Find and fix the trigger
  • Replace deficiencies (Fe, Vit D, B12)
  • Optimise nutrition
  • Normalise expectations (6–12 mo)
  • Treat co-existing FPHL if present

TE vs AGA trichoscopy

KEY SPLIT
  • TE = uniform calibre shafts
  • AGA/FPHL = calibre diversity
  • TE = pull test positive ALL zones
  • AGA = positive vertex, NOT occiput
  • Both often co-exist → treat both

GP Quick-Reference Action Card

PresentationHistory key questionExam findingInvestigationManagement
Acute diffuse shedding, clear triggerWhat happened 3 months ago?Pull test + all zones; club bulbs; normal scalpFTBVZ; clinical Dx if obviousFix trigger; supplement; reassure; review 3 months
Postpartum shedding, 3–5 monthsWhen delivered? Breastfeeding (iron drain)?As above; check ferritinFerritin, TFTs, FBCReassure; iron to >70; review 6 months
Diffuse shedding + calibre diversity on derm.FHx hair loss?Miniaturisation >20% on trichoscopyFTBVZ; FAITreat both TE + FPHL (minoxidil + supplement)
Shedding >6 months — no obvious triggerThorough CHIPS + systemic reviewTrichoscopy; check for AGAFTBVZ + ANA, anti-TPO, glucose, CRPTreat findings; consider referral if no diagnosis
Acute shedding + systemic features (fatigue, weight loss)Full systemic reviewLymphadenopathy? Organomegaly?Full bloods including LFT, CRP, B12, TFTs, ANAExclude systemic disease before attributing to TE

Anki Flashcard Deck — Chapter 7

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References

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← Ch. 6: Female Pattern Hair Loss Chapter Index Ch. 8: Alopecia Areata →