Pathogenesis
At baseline, about 10% to 15% of scalp hairs are in the telogen (shedding) phase (see Illus. 19.1).
A telogen effluvium occurs when, in response to a trigger, a large number of hairs (greater than 15%) enter the telogen phase at one time, which results in a sudden and increased number of shedding hairs.
The precipitating event usually precedes the hair loss by 6 to 16 weeks, which is the time required for a catagen hair to become a telogen hair.
Clinical Manifestations
In acute telogen effluvium, hair shedding is typically sudden, rather than a gradual thinning. The patient may state that the shedding hair may be seen on pillows, on combs and brushes, and in the bathtub, and she or he may bring in a plastic bag full of hair as proof of the dramatic alopecia (Fig. 19.11).
Possible triggers of acute telogen effluvium include medications, major illness, fever, physical trauma, surgery, general anesthesia, significant weight loss such as that caused by “crash” dieting, or severe emotional stress. The patient may describe a recent history of such an event that typically occurred 3 to 4 months before the onset of alopecia.
The medications that are most often implicated in acute telogen effluvium are anticoagulants, antimalarials, beta blockers, cholesterol-lowering medications, antidepressants, angiotensin-converting enzyme inhibitors, lithium, L dopa, propylthiouracil (which induces hypothyroidism), carbamazepine, oral retinoids, and immunizations.
When an acute telogen effluvium occurs in women during childbearing years, it may be associated with giving birth (postpartum effluvium and post-breastfeeding effluvium), aborted pregnancy, or the discontinuation of oral contraceptives.
The evidence of hair loss tends to be more subtle than in acute telogen effluvium.
The diffuse (nonpatterned) hair shedding involves the entire scalp and is usually not obvious to the clinician. Scarring and inflammation of the scalp are not seen.
It may be caused by the persistent presence of a trigger (such as medications) or by a rapid succession of several acute telogen effluviums. Chronic telogen effluvium may also have metabolic causes, such as iron or zinc deficiency, or result from low-protein diets, thyroid disease, or chronic systemic illnesses such as systemic lupus erythematosus or syphilis.
The patient may complain of both increased shedding, albeit less severe than in acute telogen effluvium, and hair thinning that ultimately manifests as more visible scalp.
Occasionally, patients state that the scalp hair simply feels less dense, that more of the scalp seems to be visible (Fig. 19.12), and that the hair has changed in texture. Complete alopecia is not seen.
If the precipitating event is removed, it usually takes about 1 year to completely return to the pre-effluvium hair volume, but hair may not grow back completely and rather a new baseline hair density is set.
Diagnosis
The diagnosis is often based on history with patients reporting the loss of 400 or more hairs per day (normal shedding is 40 to 100 hairs a day).
A gentle hair pull (of approximately 20 hairs) often yields more than four telogen hairs per pull. Telogen hairs can be identified by having a small white “bulb” at their proximal ends.
If the diagnosis is in doubt, a scalp biopsy will show an increased telogen-to-anagen ratio (>15%) and an absence of inflammation and/or scarring.
Laboratory Tests
When the cause of telogen effluvium is not clinically apparent, the following laboratory tests should be assessed when warranted by the history or physical examination:
A complete blood count, sexually transmitted disease testing, and antinuclear antibody tests
Serum ferritin and erythrocyte sedimentation rate (ESR) levels (a ferritin value >50 µg/L is optimal)
Serum dehydroepiandrosterone-sulfate (DHEA-S), free testosterone, prolactin, and morning cortisol levels (especially if virilization is evident)
Management 
Differential Diagnosis 
Helpful Hint 
Points to Remember Pathogenesis
Anagen effluvium is usually precipitated by a toxic event, such as a reaction to certain drugs. However, an acute and severe systemic illness such as systemic lupus erythematosus (SLE) may also result in an anagen effluvium. The dramatic hair loss usually starts 1 to 2 weeks after the precipitating event.
Among the agents that have been commonly associated with anagen hair loss are:
Clinical Manifestations
Anagen effluvium presents as a diffuse, nonscarring, noninflammatory type of hair loss (Fig. 19.13).
Diagnosis
The diagnosis tends to be straightforward because of an obvious triggering event, such as chemotherapy.
A hair pull test wherein a lock of hair is grasped to determine how many can be extracted with a firm pull will be positive with at least four anagen hairs (elongated or tapered end hairs) per pull.
Basics
Aging results in a gradual decrease of scalp hair density. Whereas a newborn has about 1,100 hairs per square centimeter, by age 30 this has decreased to about 600 hairs per square centimeter, and by age 50 this has further decreased to about 500 hairs per square centimeter.
This type of alopecia affects men and women equally and is seen in patients 50 years and older.
Clinical Manifestations
Patients generally complain of a thinning of scalp hair and do not report increased shedding.
Senescent alopecia is a diffuse, nonscarring, noninflammatory type of hair loss. It represents a diagnosis of exclusion.
Outline