Telogen Effluvium
Published on May 19, 2026
Risk Factors
Postpartum women (2-5 months after delivery), recent high fever or severe illness, major surgery, crash dieting or nutritional deficiency (iron, zinc, biotin), hypothyroidism, discontinuation of oral contraceptives, emotional or physiological stress
Etiology
Premature shift of a large number of hair follicles from the anagen (growth) phase into the telogen (resting/shedding) phase, triggered by a physiological stressor occurring 2-3 months prior
Presentation
Diffuse, non-scarring hair thinning noticed over weeks to months; patient often reports increased hair on the pillow, in the shower drain, or on brushes; no focal bald patches
Classic Exam
Diffuse thinning without distinct bald spots, no scalp inflammation or scarring, positive hair pull test (more than 10% of pulled hairs come out easily, and the shed hairs have a club-shaped white bulb at the root)
Diagnostics
Clinical diagnosis in most cases; hair pull test yields telogen hairs (club hairs); labs to rule out underlying triggers: TSH, ferritin, CBC, zinc level; biopsy (rarely needed) shows increased telogen-to-anagen ratio
Management
Identify and remove the triggering stressor; reassurance that hair regrowth is expected within 3-6 months; correct any nutritional deficiency (iron supplementation if ferritin is low); no pharmacologic treatment is typically required
Keywords
"Diffuse hair loss," "2-3 months after stressor," "postpartum hair loss," "club-shaped bulb," "positive hair pull test," "non-scarring alopecia," "self-limited"
01Pathophysiology
The hair growth cycle consists of three phases: anagen (active growth, lasting 2-6 years), catagen (transition, lasting 2-3 weeks), and telogen (resting phase, lasting about 3 months, after which the hair falls out). Under normal conditions, roughly 85-90% of scalp hair is in anagen and only 10-15% is in telogen at any given time.
In telogen effluvium, a physiological or emotional stressor causes a synchronized premature transition of a disproportionately large percentage of anagen follicles into the telogen phase. Because the telogen phase lasts approximately 3 months, the clinical shedding becomes apparent 2-3 months after the inciting event, not at the time of the stressor itself. This temporal gap is the single most tested concept. Exam vignettes deliberately place the stressor in the patient's history to see if you can connect a remote event to the current complaint.
The shedding is diffuse because the shift affects follicles across the entire scalp rather than in a localized pattern. The follicles themselves are structurally normal and not destroyed, which is why this condition is classified as non-scarring alopecia and why full regrowth is expected once the trigger is removed.
The hallmark finding on microscopy or gross inspection of a shed hair is the club-shaped (bulb) root, indicating a telogen hair that has completed its resting phase and detached normally from the follicle. This distinguishes it from anagen effluvium, where the hair breaks off with a tapered or fractured shaft because the follicle was damaged mid-growth.
02Classification and Clinical Manifestation
Acute Telogen Effluvium
Timing
Onset 2-3 months after a single identifiable stressor; lasts less than 6 months
Trigger Examples
Childbirth, high fever, surgery, acute blood loss, crash diet, severe emotional stress, medication changes (stopping OCP, starting retinoids, heparin, beta-blockers)
Course
Self-limited; full recovery expected within 3-6 months after trigger removal
Chronic Telogen Effluvium
Timing
Shedding persists beyond 6 months, often fluctuates in intensity
Trigger Examples
Chronic iron deficiency, uncontrolled hypothyroidism, chronic illness, occult nutritional deficiency, persistent emotional stress; sometimes idiopathic (especially in middle-aged women)
Course
Hair density may remain reduced but rarely progresses to complete baldness; waxes and wanes
Type | Timing | Trigger Examples | Course |
|---|---|---|---|
Acute Telogen Effluvium | Onset 2-3 months after a single identifiable stressor; lasts less than 6 months | Childbirth, high fever, surgery, acute blood loss, crash diet, severe emotional stress, medication changes (stopping OCP, starting retinoids, heparin, beta-blockers) | Self-limited; full recovery expected within 3-6 months after trigger removal |
Chronic Telogen Effluvium | Shedding persists beyond 6 months, often fluctuates in intensity | Chronic iron deficiency, uncontrolled hypothyroidism, chronic illness, occult nutritional deficiency, persistent emotional stress; sometimes idiopathic (especially in middle-aged women) | Hair density may remain reduced but rarely progresses to complete baldness; waxes and wanes |
Clinical Manifestation
Clinical Feature | Detail |
|---|---|
Distribution | Diffuse, involves the entire scalp; sometimes the bitemporal region is more noticeable |
Scalp appearance | Normal scalp skin, no erythema, scaling, or scarring |
Hair pull test | Positive: gentle traction on a group of 40-60 hairs yields more than 6 hairs (>10%), and the extracted hairs have club-shaped white bulbs |
Hair density | Noticeably thinner overall but no focal patches of complete baldness |
Nails / Skin | Usually uninvolved; concurrent nail ridging (Beau's lines) can appear if the same systemic stressor also disrupted nail matrix growth |
03Diagnostic Workup
Hair pull test
Role
Best initial bedside test
Expected Finding
>10% of pulled hairs detach; all are telogen (club) hairs
Thorough history
Role
Identifies trigger
Expected Finding
Event occurring 2-3 months before onset of shedding
TSH
Role
Rule out hypothyroidism
Expected Finding
Elevated TSH suggests thyroid-related hair loss
Serum ferritin
Role
Assess iron stores
Expected Finding
Ferritin < 30-40 ng/mL is associated with hair shedding even before overt anemia develops
CBC
Role
Screen for anemia, chronic disease
Expected Finding
May reveal iron deficiency anemia or other hematologic abnormality
Zinc level
Role
Rule out zinc deficiency
Expected Finding
Low zinc can independently cause diffuse hair loss
Scalp biopsy
Role
Most accurate / confirmatory test (rarely needed)
Expected Finding
Increased telogen-to-anagen ratio (>25% of follicles in telogen); no inflammation, no scarring, no miniaturization
Test | Role | Expected Finding |
|---|---|---|
Hair pull test | Best initial bedside test | >10% of pulled hairs detach; all are telogen (club) hairs |
Thorough history | Identifies trigger | Event occurring 2-3 months before onset of shedding |
TSH | Rule out hypothyroidism | Elevated TSH suggests thyroid-related hair loss |
Serum ferritin | Assess iron stores | Ferritin < 30-40 ng/mL is associated with hair shedding even before overt anemia develops |
CBC | Screen for anemia, chronic disease | May reveal iron deficiency anemia or other hematologic abnormality |
Zinc level | Rule out zinc deficiency | Low zinc can independently cause diffuse hair loss |
Scalp biopsy | Most accurate / confirmatory test (rarely needed) | Increased telogen-to-anagen ratio (>25% of follicles in telogen); no inflammation, no scarring, no miniaturization |
Telogen effluvium is primarily a clinical diagnosis. The most important diagnostic tool is a careful history linking the onset of shedding to a stressor that occurred 2-3 months earlier. The hair pull test is the best initial bedside assessment: you grasp approximately 40-60 hairs between the thumb and forefinger, apply gentle traction, and count the hairs that come out. If more than 10% release easily and all have a club-shaped root, this is strongly consistent with telogen effluvium.
Laboratory testing is directed at identifying a correctable underlying cause rather than confirming the diagnosis itself. TSH and ferritin are the two highest-yield labs to order. Ferritin is worth special attention because a value below 30-40 ng/mL may drive hair shedding even when hemoglobin is still within normal range, meaning you cannot rely on CBC alone to rule out iron-related hair loss.
Scalp biopsy is reserved for cases where the diagnosis is unclear or chronic shedding does not improve despite trigger removal. Histopathology will show an increased proportion of telogen follicles (normal is approximately 10-15%; in telogen effluvium this rises above 25%) without inflammatory infiltrate, fibrosis, or follicular miniaturization. The absence of miniaturization is what separates this from androgenetic alopecia on biopsy.
04Management and Treatment
Identify and address the trigger
Intervention
History-guided
Details
Correct nutritional deficiency, treat hypothyroidism, discontinue offending medication if possible
Iron supplementation
Intervention
Ferrous sulfate 325 mg PO daily (contains ~65 mg elemental iron)
Details
Indicated when ferritin < 30-40 ng/mL; take on an empty stomach with vitamin C to enhance absorption; recheck ferritin in 3 months
Thyroid correction
Intervention
Levothyroxine per standard dosing
Details
If TSH is elevated, normalize thyroid function
Zinc supplementation
Intervention
Zinc gluconate 50 mg PO daily
Details
If zinc level is low; supplement for 3-6 months
Reassurance
Intervention
Critical component of management
Details
Explain the self-limited nature and expected timeline for regrowth (3-6 months)
Minoxidil 5% topical
Intervention
Optional adjunctive therapy
Details
May accelerate regrowth in chronic cases or when patient is distressed; apply once daily to the scalp; not required in routine acute telogen effluvium
Step | Intervention | Details |
|---|---|---|
Identify and address the trigger | History-guided | Correct nutritional deficiency, treat hypothyroidism, discontinue offending medication if possible |
Iron supplementation | Ferrous sulfate 325 mg PO daily (contains ~65 mg elemental iron) | Indicated when ferritin < 30-40 ng/mL; take on an empty stomach with vitamin C to enhance absorption; recheck ferritin in 3 months |
Thyroid correction | Levothyroxine per standard dosing | If TSH is elevated, normalize thyroid function |
Zinc supplementation | Zinc gluconate 50 mg PO daily | If zinc level is low; supplement for 3-6 months |
Reassurance | Critical component of management | Explain the self-limited nature and expected timeline for regrowth (3-6 months) |
Minoxidil 5% topical | Optional adjunctive therapy | May accelerate regrowth in chronic cases or when patient is distressed; apply once daily to the scalp; not required in routine acute telogen effluvium |
The cornerstone of management is identifying and removing the inciting trigger. For acute telogen effluvium, no pharmacologic intervention is strictly necessary because the condition is self-limited. Once the triggering stressor has resolved, the shifted follicles re-enter anagen and new hair growth becomes visible within 3-6 months.
Reassurance is a testable management step. Vignettes may present a distressed postpartum patient with diffuse hair loss and normal labs, and the correct "next best step" is reassurance and observation, not medication.
When labs reveal a correctable deficiency, targeted supplementation is indicated. Iron replacement with ferrous sulfate 325 mg daily is the standard when ferritin is low. The goal is to bring ferritin above 40-70 ng/mL. Concurrent vitamin C (250-500 mg) improves absorption. Avoid taking iron with calcium, antacids, or tea, as these reduce absorption.
For chronic telogen effluvium that has persisted beyond 6 months without a clear remediable cause, topical minoxidil 5% may be offered to promote regrowth. Minoxidil shortens the telogen phase and stimulates follicles back into anagen. It is not a cure but can reduce the duration and severity of shedding. Patients should be counseled that an initial increase in shedding may occur during the first 2-4 weeks of minoxidil use (as miniaturized telogen hairs are pushed out by new anagen hairs), and this is expected, not a reason to discontinue.
There is no role for systemic corticosteroids, intralesional injections, or immunosuppressants in telogen effluvium.
05Differential Diagnosis and Distractors
Androgenetic alopecia (female pattern)
Why It Looks Similar
Also presents as diffuse thinning, non-scarring
Key Discriminator
Androgenetic alopecia shows a widened central part with preservation of the frontal hairline; biopsy reveals follicular miniaturization; no clear temporal link to a stressor; chronic and progressive
Alopecia areata
Why It Looks Similar
Can cause significant hair loss and a positive hair pull test
Key Discriminator
Alopecia areata produces well-defined circular patches of complete hair loss, not diffuse thinning; exclamation-point hairs (tapered proximal shaft) at patch borders; autoimmune association
Anagen effluvium
Why It Looks Similar
Also produces diffuse shedding
Key Discriminator
Anagen effluvium occurs during or shortly after exposure to the offending agent (chemotherapy, radiation, toxin), not 2-3 months later; shed hairs have tapered, fractured shafts (dystrophic anagen hairs), not club-shaped bulbs
Hypothyroidism-related hair loss
Why It Looks Similar
Can mimic telogen effluvium exactly
Key Discriminator
Check TSH; if elevated, the hair loss is driven by thyroid dysfunction; other features include fatigue, weight gain, constipation, dry skin, delayed relaxation of deep tendon reflexes
Iron deficiency alopecia
Why It Looks Similar
Diffuse thinning, non-scarring, common in menstruating women
Key Discriminator
Ferritin is low (< 30 ng/mL); may or may not have overt anemia; hair loss improves with iron repletion; technically a subset trigger of telogen effluvium
Tinea capitis
Why It Looks Similar
Hair loss on the scalp
Key Discriminator
Presents with scaling, erythema, broken-off hairs, and sometimes a kerion; KOH prep or fungal culture is positive; more common in children
Trichotillomania
Why It Looks Similar
Can cause diffuse-appearing thinning
Key Discriminator
Look for hairs of varying lengths in an irregular pattern, often unilateral or geometric; patient may deny pulling; biopsy shows traumatized follicles with trichomalacia
Differential | Why It Looks Similar | Key Discriminator |
|---|---|---|
Androgenetic alopecia (female pattern) | Also presents as diffuse thinning, non-scarring | Androgenetic alopecia shows a widened central part with preservation of the frontal hairline; biopsy reveals follicular miniaturization; no clear temporal link to a stressor; chronic and progressive |
Alopecia areata | Can cause significant hair loss and a positive hair pull test | Alopecia areata produces well-defined circular patches of complete hair loss, not diffuse thinning; exclamation-point hairs (tapered proximal shaft) at patch borders; autoimmune association |
Anagen effluvium | Also produces diffuse shedding | Anagen effluvium occurs during or shortly after exposure to the offending agent (chemotherapy, radiation, toxin), not 2-3 months later; shed hairs have tapered, fractured shafts (dystrophic anagen hairs), not club-shaped bulbs |
Hypothyroidism-related hair loss | Can mimic telogen effluvium exactly | Check TSH; if elevated, the hair loss is driven by thyroid dysfunction; other features include fatigue, weight gain, constipation, dry skin, delayed relaxation of deep tendon reflexes |
Iron deficiency alopecia | Diffuse thinning, non-scarring, common in menstruating women | Ferritin is low (< 30 ng/mL); may or may not have overt anemia; hair loss improves with iron repletion; technically a subset trigger of telogen effluvium |
Tinea capitis | Hair loss on the scalp | Presents with scaling, erythema, broken-off hairs, and sometimes a kerion; KOH prep or fungal culture is positive; more common in children |
Trichotillomania | Can cause diffuse-appearing thinning | Look for hairs of varying lengths in an irregular pattern, often unilateral or geometric; patient may deny pulling; biopsy shows traumatized follicles with trichomalacia |
06Traps and High-Yield Pearls
The most common way students miss telogen effluvium questions is by failing to connect the temporal gap between the stressor and the onset of shedding. The vignette will almost always bury the trigger 2-3 months back in the history (a delivery, a febrile illness, a surgery, a period of severe caloric restriction). If you are scanning only the present complaint, you will miss the diagnosis entirely and default to a wrong answer like androgenetic alopecia or alopecia areata.
A second frequent trap involves the postpartum patient. The vignette may describe a woman 3-4 months after an uncomplicated delivery who is alarmed by excessive hair shedding. Students may overthink this and consider postpartum thyroiditis or nutritional depletion from breastfeeding. While those should be screened for with TSH and ferritin, the answer in a straightforward vignette with normal labs is telogen effluvium with reassurance as the management.
The third trap is confusing telogen effluvium with anagen effluvium. Both cause diffuse hair loss, but the timing and hair morphology are different. Anagen effluvium begins within days to weeks of the insult (classically chemotherapy), and the hairs are broken and dystrophic. Telogen effluvium appears months later, and the hairs have intact club bulbs. If a vignette mentions chemotherapy and hair loss occurring within 1-2 weeks of treatment, that is anagen effluvium, not telogen.
Finally, remember that telogen effluvium never causes complete baldness and never causes scarring. If the vignette describes scarring, atrophy, or permanent follicular destruction, you are dealing with a scarring alopecia (lichen planopilaris, discoid lupus, central centrifugal cicatricial alopecia), and telogen effluvium should be eliminated immediately.
The core competency being tested is your ability to recognize a pattern of diffuse, non-scarring hair loss with a delayed onset relative to a physiological stressor, and to sequence your workup and management correctly: history and hair pull test first, targeted labs to exclude treatable triggers, and reassurance as the primary intervention.