A hordeolum is an acute focal inflammation of the eyelid, which develops due to microbial infection (usually Staphylococcus aureus) of the meibomian or Zeis glands.¹⁴ Pus forms within the lumen of the infected gland, and thus an acute hordeolum is formed. When an acute hordeolum involves the Zeis gland (external hordeolum), the abscess is centered in the pilosebaceous unit around an eyelash.¹⁰

The etiopathogenetic events leading to the development of a chalazion may be of infectious origin if it evolves from an unresolved hordeolum, or it may develop secondary to a sterile noninfectious obstruction of sebaceous gland ducts, which may or may not be complicated by a secondary infection on top.¹⁴,¹⁵ Either way, blockage of a meibomian gland duct results in rupture of the gland with the release of sebaceous contents into the tarsus and the surrounding tissues. This initiates an inflammatory, granulomatous, or foreign body reaction to the inspissated lipid secretions of the meibomian or Zeis glands.¹⁴,¹⁶,¹⁷ With time, the inflammatory process is then walled off, resulting in a cyst-like lesion.¹³,¹⁴

Predisposing factors for the development of single, multiple, or recurrent hordeola and chalazia are manifold. Poor lid hygiene as well as chronic staphylococcal blepharitis, demodicosis, meibomian gland dysfunction (MGD), and rosacea play a definite role.¹,³,¹⁴,¹⁸,¹⁹,²⁰,²¹ Other associated risk factors include young age, female sex, urban living, gastritis, anxiety, irritable bowel syndrome, chronic constipation, anemia, poor nutrition, IgM deficiency, viral conjunctivitis, and menstrual abnormalities or menstruation itself due to their impact on lipid metabolism.²¹,²²,²³,²⁴,²⁵,²⁶ Diabetes, hypothyroidism, and obesity are also possible risk factors due to the reduction of androgen levels.²⁴

Rosacea is common in patients with chalazia and is even twice as common as in patients with recurrent chalazia.²⁷ In a series of 51 patients scheduled for chalazion excision, 55% had rosacea, compared with only 12% in a control group without chalazia.²⁷ Two Demodex species (Demodex folliculorum and Demodex brevis) frequently inhabit the eyelids including the eyelash follicle (D. folliculorum) and the meibomian glands (D. brevis).¹⁸,¹⁹,²⁰ Both species frequently coexist and demodicosis should be ruled out in children as well as adults with recurrent chalazia.¹⁸,¹⁹,²⁰ A recent study demonstrated a high prevalence of D. brevis infestation in patients with recurrent chalazia.¹⁹ The same study also showed that the prevalence of demodicosis in patients with chalazia is far more common than the prevalence of chronic blepharitis
(69.2% vs 19.78%).¹⁹ It is not clear whether D. brevis causes chalazia by direct mechanical blockage of the meibomian gland orifices or indirectly by acting as a vector to bring in symbiotic bacteria like Bacillus oleronius or S. aureus.¹⁸,¹⁹ Although chalazia are not strictly considered within the context of MGD,²⁸,²⁹,³⁰ the presence of MGD predisposes to the development of chalazia, and chalazion is listed or labeled by the international workshop on MGD as a comorbidity, localized MGD, or plus disease.²⁸,²⁹,³⁰

The incidence and prevalence rates of hordeolum are largely unknown.¹,³,⁷ The condition is ubiquitous and most cases resolve on their own. In addition, people with hordeolum do not seek professional medical treatment often preferring to rely on home remedies, and even when they do, patients usually present to a general practitioner, so that hordeolum/chalazion cases are seldom reported. A recent study that sought to determine the epidemiology of eye-related emergency department visits on a national level in the United States between 2006 and 2011 showed that 3.8% of the visits were due to an acute hordeolum.³¹ Hordeola and chalazia are not limited to any age, race, or sex, although they may be more common in younger females. Chalazia also generally cluster around puberty, pregnancy, and menopause possibly due to hormonal influences on sebaceous secretion.¹,²⁴

The course of an acute hordeolum is relatively short and mostly self-limited but with an explosive onset.¹ Patients typically present with a variable degree of acute pain (slight to severe), irritation, and swelling. Cases with an acute external hordeolum typically experience a greater degree of pain and tenderness compared to an acute internal hordeolum.

The natural history of an acute hordeolum generally spans 1 to 2 weeks, beginning with an initial phase whereby the eyelid is diffusely inflamed, with localized tenderness over the inflamed gland. Edema may be enormous and may spread to the other ipsilateral eyelid.¹⁴ In acute external hordeolum, the abscess is centered around an eyelash and usually points anteriorly onto the eyelid skin (Figure 55.1). In
a case of an acute internal hordeolum, dilation of the orifice of the involved meibomian gland can be observed, which on closer inspection will show that it is filled with inspissated secretion or purulent material that can be expressed with gentle pressure on the eyelid against the globe.¹,³,¹³ In some cases of acute hordeolum, the infection can progress to preseptal cellulitis, but rarely if ever does it penetrate the orbital septum resulting in orbital cellulitis.¹,³,³²,³³,³⁴

The acute phase ends with either complete resolution or the development of a chalazion. On rare occasions, residual inflammatory signs may persist for weeks simulating an acute lesion, although the pain and tenderness are absent.¹³ In cases of a nonresolving external hordeolum, a crust overlying the lesion may persist for weeks.¹³

If spontaneous resolution does not occur, an acute internal hordeolum can become chronic and develop into a chalazion forming a thin fibrous sac or a firm or even a hard nodule that may appear to bulge on the skin surface or form a fleshy mass on the tarsal conjunctiva (Figure 55.2). A chalazion may also protrude through the skin if it has originated from an external hordeolum or if an internal hordeolum ruptures anteriorly.³,³⁰,³⁵,³⁶ Large untreated chalazia can lead to destruction of the acini of the involved meibomian gland and may rupture through the tarsus leading to the development of a pyogenic granuloma. An alternative presentation of a chalazion is a more chronic onset where patients present insidiously with a firm, painless nodule beneath the skin without a history of acute onset. This form of presentation is not uncommon and both forms may be observed in the same patient at different times or even simultaneously.¹⁷

Eyelid comorbidities that may be observed in patients with hordeolum or chalazion include conjunctival scaring from a prior chalazion excision, diffuse meibomian gland disease, and a papillary reaction with hyperemia of the palpebral and tarsal conjunctiva.³⁵ Hordeola/chalazia rarely if ever threaten vision, although there have been occasional reports of large neglected chalazia resulting in amblyopia due to mechanical ptosis, hypermetropia, or induced astigmatism.¹⁵,³⁰

An acute hordeolum should be differentiated from preseptal or orbital cellulitis.¹⁴ The inflammatory process in acute hordeolum is caused by local lymphatic congestion and can be differentiated from more ominous infectious processes by the nature of the pain, which is localized in patients with acute hordeola but may be of a more diffuse and intense nature in preseptal/orbital cellulitis. The absence of tense erythema and leukocytosis may also help clinch the diagnosis.¹⁴

When associated with other nodules in the face, chalazia may be confused with a new entity of unknown etiology called idiopathic facial aseptic granuloma (IFAG).³⁷,³⁸,³⁹,⁴⁰ IFAG appears to be a granulomatous reaction circumscribed to the skin of the midface,³⁸ and, in contrast to chalazia, the inflammation does not involve the meibomian glands.³⁸,³⁹ These lesions usually present as asymptomatic erythematous subepidermal eyelid nodules in the cheek and/or the eyelid and should not be difficult to differentiate from chalazia. However, when they are confined to the eyelid without accompanying lesions in the midface, the distinction is difficult. It is imperative to differentiate both conditions because IFAG responds well to oral clarithromycin and surgical excision is unwarranted.³⁸,³⁹ Although some authorities consider IFAG to belong to the spectrum of rosacea,⁴¹ many differences exist, the details of which are beyond the scope of this chapter. Suffice to say that if clinical suspicion arises, referral to a dermatologist is indicated.³⁸,³⁹,⁴⁰,⁴¹ A zinc deficiency should be suspected in the pediatric population if hordeola are associated with a perioral rash. This condition typically occurs in children with food allergies with subsequent restrictions of the dietary intake of foods rich in zinc.⁷