Telogen effluvium is a form of nonscarring alopecia characterized by diffuse hair shedding, often with an acute onset. A chronic form with a more insidious onset and a longer duration also exists.[1, 2] Telogen effluvium is a reactive process caused by a metabolic or hormonal stress or by medications. Generally, recovery is spontaneous and occurs within 6 months, unless a background of pattern alopecia is present.
Telogen effluvium can affect hair on all parts of the body, but, generally, only loss of scalp hair is symptomatic.
Understanding the pathophysiology of telogen effluvium requires knowledge of the hair growth cycle. All hair has a growth phase, termed anagen, and a resting phase, telogen. On the scalp, anagen lasts approximately 3 years, while telogen lasts roughly 3 months, although there can be wide variation in these times between individuals. During telogen, the resting hair remains in the follicle until it is pushed out by growth of a new anagen hair.
In most people, 5-15% of the hair on the scalp is in telogen at any given time. Telogen effluvium is triggered when a physiologic stress or hormonal change causes a large number of hairs to enter telogen at one time. Shedding does not occur until the new anagen hairs begin to grow. The emerging hairs help to force the resting hairs out of the follicle. Evidence suggests that the mechanism of shedding of a telogen hair is an active process that may occur independent of the emerging anagen hair. The interval between the inciting event in telogen effluvium and the onset of shedding corresponds to the length of the telogen phase, between 1 and 6 months (average 3 mo).
Headington has described 5 functional subtypes of telogen effluvium, based on which portion of the hair cycle is abnormally shortened or lengthened. These subtypes represent variations on the principles discussed above. It is rarely possible to distinguish these subtypes clinically.
This condition is quite common, but exact prevalence is not recorded. A large percentage of adults have experienced an episode of telogen effluvium at some point in their lives.
No racial predilection is recognized.
Acute telogen effluvium can occur in either sex if the proper inciting conditions occur. Because hormonal changes in the postpartum period are a common cause of telogen effluvium, women may have a greater tendency to experience this condition. In addition, women tend to find the hair shedding more troublesome than men do; thus, more women seek medical attention for the condition. Chronic telogen effluvium has been reported mainly in women.
Telogen effluvium can occur at any age. It is not uncommon for infants in the first months of life to experience an episode of telogen effluvium.
Mortality has not been reported. Morbidity is limited to mild cosmetic changes. However, telogen effluvium can have substantial impact on those affected.[5, 6] Prognosis is good for recovery of normal hair density in acute telogen effluvium. A good cosmetic outcome can be expected in chronic telogen effluvium, even if hair shedding continues.
The symptom of both acute and chronic telogen effluvium is increased hair shedding. Patients usually only complain that their hair is falling out at an increased rate. Occasionally, they note that the remaining hair feels less dense. In both forms of telogen effluvium, hair is lost diffusely from the entire scalp. Complete alopecia is not seen.
Acute telogen effluvium is defined as hair shedding lasting less than 6 months. Patients with acute telogen effluvium usually complain of relatively sudden onset of hair loss. Careful questioning usually reveals a metabolic or physiologic stress 1-6 months before the start of the hair shedding. Physiologic stresses that can induce telogen effluvium include febrile illness, major injury, change in diet, pregnancy and delivery, and starting a new medication. Immunizations also have been reported to cause acute hair shedding. Papulosquamous diseases of the scalp, such as psoriasis and seborrheic dermatitis, can produce telogen effluvium.
Chronic telogen effluvium is hair shedding lasting longer than 6 months. The onset is often insidious, and it can be difficult to identify an inciting event. Because of the duration of the hair shedding, patients are more likely to complain of decreased scalp hair density, or they may note that their hair appears thin and lifeless.
The physical examination is the same in both acute and chronic telogen effluvium. Physical findings are sparse. Usually, the physician does not appreciate a decrease in hair density. However, if the patient's hair has been falling out for several months, the hair may appear thin when compared with old photographs.
Depending on the duration of hair loss, close examination of the scalp may reveal a higher than expected number of short new hairs growing. Because hair grows at a nearly constant rate of approximately 1 cm per month, the duration of the hair shedding can be estimated by measuring the length of the short hairs. Trichoscopy can be helpful in visualizing the hairs.
In active telogen effluvium, the gentle hair pull test will yield at least 4 hairs with each pull. If the patient's active shedding has ceased, the hair pull will be normal. Forced extraction of 10-20 hairs will yield a large percentage of telogen hairs. If greater than 25% of extracted hairs are in telogen, the diagnosis of telogen effluvium is confirmed.
There is one caveat to reliance on strict physical findings or numerical criteria in the diagnosis of telogen effluvium. Each patient's scalp hair has an individual characteristic growth cycle. There are patients who have a very long anagen phase and a small proportion of hair in telogen at any given time. These patients may experience an episode of telogen effluvium but have completely normal physical findings. History alone must guide the physician to the correct diagnosis in these cases.
There should be no areas of total alopecia in a patient with telogen effluvium. Scarring is not present. There also should be no sign of an inflammatory scalp dermatitis. Usually, there are no complaints of body hair loss.
Physiologic stress is the cause of telogen effluvium. These inciting factors can be organized into several categories, noted below. Evidence from mouse studies indicates that psychological stress can induce catagen, mainly by effects on neurotransmitters and hormones. In humans, however, the role these effects play in hair loss has not yet been determined. While substance P has been extensively studies in human hair follicles in vitro, in vivo studies have not been performed. In HIV disease, apoptosis may be related to HIV-1 viral protein R. Note the following causes:
Laboratory studies are of little use in the diagnosis of telogen effluvium if there is clear history of an inciting event. Scalp biopsy is the most useful test to confirm the diagnosis, although this is seldom necessary if the history is characteristic and a gentle hair pull produces numerous telogen hairs. Telogen hairs are identified by a white bulb and the lack of a gelatinous hair sheath.
If a biopsy is performed, some authors advocate taking three 4-mm punch biopsy specimens, all imbedded horizontally. This method provides a generous sample for determining anagen-to-telogen and terminal-to-vellus ratios and leads to greater diagnostic accuracy.
Chronic telogen effluvium may have a metabolic cause. Testing should be directed toward causes that are common and correctable. If any sign or symptom of hypothyroidism is present, a thyrotropin test is warranted. Iron deficiency is common in premenopausal women. Evaluation of CBC count, serum iron, iron saturation, and ferritin may be warranted. Note that CBC count results may be completely normal in women with mild iron deficiency and hair loss, particularly in women older than 40 years. Blood is more essential than hair, and the body will shed hair before red cell indices become microcytic. Also, note that ferritin behaves as an acute phase reactant. Inflammation can produce normal ferritin levels in an individual who is iron deficient. Although a low ferritin is proof of iron deficiency, a normal ferritin level does not exclude iron deficiency. Some experts in the field regard iron saturation as the most sensitive indicator of iron deficiency.
Occasionally, screening for renal and hepatic enzymes may detect a systemic cause of hair shedding. If syphilis is considered as a cause of hair loss, a rapid plasma reagin or Venereal Disease Research Laboratory test should be preformed.
If a patient is unwilling to undergo a scalp biopsy but would like confirmation of the diagnosis, serial hair collections may be obtained. This process can educate the patient in the normal hair cycle and can confirm the spontaneous resolution of the process.
The patient should be instructed to collect all hairs shed in a 24-hour period. The patient should not shampoo the hair during the day of collection. This process should be repeated every week or every other week, for a total of 3 or 4 collections.
Collections totaling 100 hairs or more in a given 24-hour period are indicative of ongoing telogen effluvium. If the collections are performed over several weeks while the telogen effluvium is resolving, the number of hairs collected each time should decrease. This finding can be very comforting to the patient.
An alternate method of hair collection has been proposed by Rebora et al. According to this method, the patient collects hair during shampooing and the physician both counts and measures the length of these hairs. This method has the advantage of being able to detect and differentiate between telogen effluvium and androgenetic alopecia, even when the 2 conditions occur in the same individual. The disadvantage to this method is that it cannot be used in patients who have short hair (< 3 cm). Additionally, the counting and measuring procedure is very labor intensive, which limits its practicality in normal clinical practice.
Ross et al report on the successful use of videodermoscopy in the diagnosis of hair and scalp disorders.
Histologic findings in telogen effluvium are subtle and are most easily seen on transverse sections of a punch biopsy. The number and density of hair follicles is normal, but an increased percentage of the hair follicles are in telogen or catagen phase. If more than 25% of the follicles are in telogen phase, the diagnosis is confirmed. The percentage of telogen hairs generally should not be higher than 50%.
Because acute telogen effluvium is a reactive process, which resolves spontaneously, treatment usually is limited to reassurance. Any reversible cause of hair shedding, such as poor diet, iron deficiency, hypothyroidism, or medication use, should be corrected.
While chronic telogen effluvium is less likely to resolve rapidly, reassurance is appropriate for these patients. Often, the knowledge that the hair loss will not progress to baldness is comforting to the patient. The patient should be encouraged to style the hair in a way that masks any perceived defects in hair density.
While topical minoxidil is not proven to promote recovery of hair in telogen effluvium, this medication has a theoretical benefit and is well tolerated. Patients who are eager to play an active role in their treatment may choose to use minoxidil.
Hair transplantation is not an effective treatment for telogen effluvium.
If an unbalanced diet is believed to be a contributing factor to telogen effluvium, especially in a case of chronic telogen effluvium, consultation with a dietitian may be extremely helpful. The dietary consultation should focus on adequate protein intake, replenishing low iron stores, and obtaining essential nutrients. If the patient takes large doses of vitamin A, this practice should be stopped.
In most cases, the patient is satisfied with an explanation of the cause and expected course of the condition. If a patient is distraught about hair loss, intermittent office visits for reassurance may be necessary.
The goals of pharmacotherapy are to reduce morbidity and to prevent complications.
Clinical Context: Minoxidil relaxes arteriolar smooth muscle, causing vasodilation; hair growth effects are secondary to vasodilation.
The mechanism of action in the treatment of telogen effluvium is unknown.