It is estimated that 41 % of postmenopausal women will experience hair loss [2]. Female pattern hair loss (FPHL) is the most common form of hair loss in women of all ages. For the postmenopausal population, diffuse hair loss can be multifactorial [3, 4], with decreased follicular density with advancing age (so-called senescent alopecia), environmental factors, and medications all contributing. Our patient has a combination of telogen effluvium due to her hospitalization as well as underlying FPHL. When evaluating a woman with diffuse hair loss, it is therefore important to note the duration, precipitating events (if any), whether or not there is active shedding or just thinning, the patient’s hair care practices, her medical history including medications, systemic diseases, and the family history of hair loss.

The prevalence of FPHL increases with age, and the condition can begin or become more severe with the onset of menopause as the hair shaft diameter decreases [5]. In hair follicles on the crown of the scalp, testosterone is converted by the enzyme 5-alpha-reductase to dihydrotestosterone, which causes shortening of the hair cycle and a decrease in hair follicle size [6]. After menopause, it is theorized that the cessation of ovarian estrogen production contributes to a hormonal milieu dominated by increased androgen levels relative to estrogen, which contributes to worsening FPHL in genetically susceptible individuals [7]. Because estrogen has complex interactions with other biologically active molecules and different receptors, much is unknown about its effect on the hair shaft [7]. Differences in levels of the androgen receptor and the enzyme aromatase, as well as non-androgen causes, contribute to phenotypic heterogeneity in hair growth [8] (Fig. 11.2).

It is typical of FPHL to be insidious in onset. Some patients notice an increase in hair shedding, while others do not. The diagnosis of FPHL is made clinically, by observing hair density at different locations on the scalp. The density of the posterior or occipital scalp, an area typically spared by loss in this condition, is compared to the top of the head or crown. A visibly widened part on the crown in comparison to the occiput is diagnostic (Fig. 11.3). Some patients with FPHL have normal density on the crown and instead exhibit a decrease in length and thickness of hairs at both temples, sometimes causing recession of the hair line. When the diagnosis is in doubt, a scalp biopsy (read by a dermatopathologist) can be helpful. This will reveal a decrease in the ratio of large to small hairs, called follicular miniaturization [9].

Telogen effluvium is another common cause of hair loss in women. In contrast to the insidious onset of FPHL, telogen effluvium typically occurs acutely, and all patients notice hair shedding. It commonly follows a major stressful physical or emotional event that promotes synchronization of the hair cycle leading to excess hair shedding. Precipitating events include such things as acute illness, hospitalization, death of a family member, divorce, rapid weight loss, etc. The hair loss lasts for several months and is typically self-limited, with return to baseline volume in most patients. Sometimes the shedding can become chronic [10]. Telogen effluvium can coexist with the more common FPHL as it did in our patient, and sometimes a telogen effluvium can lead to the detection of underlying FPHL. Biopsies of telogen effluvium reveal normal follicular size and a variable increase in telogen hairs [9].

Medications play a potentially larger role in hair loss in postmenopausal women in comparison to their younger counterparts, because they are more likely to be on multiple medications. There are many drugs that can cause hair loss, although most do so in only a small percentage of patients [11]. The mechanism of medication-related hair loss is often, but not always, of telogen effluvium. Agents well known to cause hair loss include psychotropic agents such as lithium, fluoxetine and valproic acid, anticoagulants, antihypertensives such as beta blockers and angiotensin-converting enzyme inhibitors, retinoids, antibiotics such as isoniazid and antiretroviral agents, and exogenous androgens [11]. Stopping an oral contraceptive can also result in telogen hair loss, similar to postpartum loss. Chemotherapeutic agents can cause an anagen or severe telogen effluvium, due to their effects on the rapidly dividing hair matrix. Some of the newer, targeted cancer therapies such as human epidermal receptor, epidermal growth factor inhibitors, and vismodegib can cause alopecia, which can be scarring or non-scarring.

The differential diagnosis of postmenopausal hair loss includes two additional conditions which are encountered less frequently than the ones already discussed. Alopecia areata is a form of focal or rarely diffuse hair loss which is fortunately much less common in postmenopausal women [4]. It is an autoimmune disease that typically causes round areas of complete alopecia and, when severe, can progress to loss of all scalp hair (alopecia totalis) or even all scalp and body hair (alopecia universalis). A rare diffuse form exists that is difficult to distinguish clinically from telogen effluvium. A biopsy of alopecia areata may reveal an increase in catagen hair follicles, inflammation at the base of catagen hair follicles, and a decrease in follicular size [9].

Another type of alopecia that typically occurs in postmenopausal women is frontal fibrosing alopecia. This is a variant of lichen planopilaris (LPP), a scarring (cicatricial), permanent alopecia of unknown etiology. LPP presents as small, discrete or confluent, patches of total hair loss with a smooth scalp surface and subtle perifollicular erythema and scale. It typically occurs in middle-aged women on the crown [12]. Frontal fibrosing alopecia causes similar scarring alopecia, but occurs in an older, typically postmenopausal age group and affects the frontal hairline and preauricular areas, as well as can result in loss of eyebrows and sometimes body hair (Fig. 11.4). Since its initial description in 1994 [13], it is increasing in frequency at a rapid pace [14]. The etiology of these disorders is unknown. Biopsy findings include lymphocytic inflammation around the superficial hair follicle, perifollicular fibrosis, and eventual replacement of hair follicles and sebaceous glands by fibrosis [9].

The management of diffuse scalp hair loss obviously depends on the underlying cause. Once recognized, a telogen effluvium requires no treatment beyond reassurance. Simple labs that are helpful to exclude systemic causes of hair loss include thyroid-stimulating hormone and measurement of iron levels and stores. Unlike the premenopausal patient where low iron is often due to heavy menstrual losses, iron deficiency in postmenopausal women may indicate more serious causes which need to be worked up, e.g., gastrointestinal ulcer, malignancy, or malabsorption. Low serum ferritin has been found in women with telogen effluvium and other types of non-scarring alopecia, although the role of iron supplementation in management of hair loss is controversial [15]. Some clinicians will supplement iron for a ferritin level below 70 ng/ml [16], even in the absence of anemia. Vitamin D is being increasingly ordered and supplemented, although there is little written about its association with hair loss [17, 18]. Medication lists should be scrutinized for possible offenders [11]. If the provider is uncertain of the mechanisms underlying loss of hair, a scalp biopsy can be helpful to detect miniaturization, but it requires specialized handling and interpretation by a dermatopathologist.

In cases of acute or severe and progressive hair loss, one should check for signs of androgen excess. In the postmenopausal population, these include, in addition to hair loss, hirsutism and signs of virilization. Women with evidence of this require workup, first, to search for excess androgen and, second, to find the source. Reported sources of androgen excess in women with postmenopausal hair loss include adrenal and ovarian tumors, hilar cell hyperplasia, ovarian hyperthecosis, and inadvertent contact with testosterone gel [19–23]. However, the majority of postmenopausal women with female pattern hair loss will not have elevated androgen levels [24].

The only medication approved by the Food and Drug Administration (FDA) for treatment of FPHL is topical minoxidil. This is available over the counter in two strengths, a 2 % solution that needs to be applied BID and a 5 % foam that can be applied once daily [25]. While it likely has several mechanisms of action, one is to cause vasodilation through its effect on potassium channels [26]. Its use lengthens the growing phase of the hair follicle and reduces miniaturization [26]. Common side effects include temporary shedding after onset of use, excess facial hair (sideburns and above the lateral brows), and irritation. Patients need to be counseled that treatment is best at stopping further loss, although some patients will experience some thickening of existing hair shafts [26]. It is important to note that minoxidil needs to be used continually for the results to be maintained and all hair gained from treatment will be lost upon discontinuation.

Patients who are intolerant of topical minoxidil or those with a limited response can be treated with oral antiandrogenic agents such as spironolactone or finasteride [27]. Note that these are used off-label for this indication and are not approved by the FDA. Spironolactone is a potassium-sparing diuretic approved for hyperaldosteronism and hypertension. It is used in FPHL for its antiandrogen properties, although there are few studies on its use for this indication. The response is dose related, with a high dose (200 mg split twice daily), resulting in maximum efficacy [28]. However, this dose is not appropriate in all patients. Spironolactone needs to be used cautiously in the elderly, especially those on other medications, because it is a diuretic and there is the potential for drug interactions and side effects, specifically hyperkalemia.