A 2-year-old boy presented with a gradually enlarging painless bump of 4 weeks’ duration on the left upper eyelid. The bump initially had been painful, and the eyelid surrounding it had been red. After 4 days, it ceased to be painful, but it increased in size over the following week. Since then, the bump had been stable, and the child had not been bothered by it. However, the boy’s mother was concerned that the eyelid had not been getting better and was covering his eye. The child was otherwise healthy, and he had reached his milestones appropriately.
Physical examination findings were normal other than a large, rounded, relatively well-defined nodule on the left upper eyelid measuring approximately 10 × 8 mm. The lesion had minimal overlying inflammation, and the remainder of the eyelid was not erythematous. The lesion had resulted in ptosis of the eyelid, which was covering approximately half of the pupil. There was no tenderness over the lesion and no preauricular adenopathy.
A chalazion is a lipogranulomatous inflammation of a meibomian gland, the modified sebaceous glands that secrete the lipid layer of the tear film to prevent evaporation between blinks. The gland ducts open on the lid margin, and each lid margin has 25 to 30 meibomian gland openings just posterior to the lashes. Inflammation of these glands is common in children, with adolescents more likely to develop chalazia during puberty.
Chalazia usually result from bacterial infection of the meibomian glands, causing internal hordeola. Internal hordeola are similar to external hordeola, which arise in the lash follicles (typical styes), but internal hordeola may be more painful, because the meibomian glands are located in the rigid tarsal plate in the eyelid. The infection typically resolves spontaneously or with antibiotics. Occasionally, however, the infectious process can spread and result in preseptal cellulitis. Chalazia also may result from blockage of the duct openings by debris or makeup.1
In cases of chalazion, the infectious process does not allow the lipid in the meibomian gland to drain. The retained lipid and its breakdown products in the gland cause a granulomatous inflammation consisting of lymphocytes and giant cells. This process further blocks the gland duct and results in a hard nodule that is typically nontender. Pressure on the nodule occasionally may express cheesy or toothpaste-like secretions from the lid margin. Eversion of the eyelid may demonstrate a yellowish streak corresponding to the occluded meibomian gland; however, everting the lid may be difficult in large lesions such as our patient’s.
Chalazia usually are only of cosmetic concern, since they rarely become reinfected. In children from birth to 10 years of age, large chalazia can compress the cornea, resulting in astigmatism and decreased vision, and very large chalazia can cause the lid to cover the pupil, resulting in no vision in that eye. In both cases, prompt treatment is required to prevent amblyopia.
Chalazia may remain stable for years but occasionally can rupture spontaneously. Rupture may occur internally or externally.
Nonsurgical treatment usually consists of warm compresses to attempt to liquefy the inspissated secretions in the gland, pressure on the lid to express the secretions, and a corticosteroid-antibiotic ointment to decrease inflammation of the lid margin. Intralesional corticosteroids (ie, triamcinolone acetonide) have been used in the treatment of chalazia. The injection can be given from the skin or from the conjunctival surface. Among the risks of injection are eyelid depigmentation and, rarely, vision loss from emboli caused by intravascular injection.
The gold standard therapy is incision and drainage of the involved meibomian gland. A special chalazion clamp is applied to the lid, everting it. A vertical incision is made overlying the most prominent part of the lesion on the conjunctival surface. The contents are drained, the clamp is removed, and the eye is patched. A corticosteroid-antibiotic ointment typically is prescribed postoperatively to treat the associated granulomatous inflammation.2
Some children may have multiple chalazia at the same time or have repeated recurrences. In these children, regular prophylactic lid hygiene is recommended. This consists of warm compresses twice a day to liquefy the thick meibomian secretions, followed by scrubs of the lid margin using diluted baby shampoo to remove debris that may block the meibomian gland openings. Short courses of systemic erythromycin may be used in patients who continue to have recurrences despite conservative management. In some children with particularly severe disease, these regimens may have to be continued long-term.3
Because our patient’s chalazion was large enough to present a significant risk of amblyopia, he was referred to ophthalmology for further management. He was prescribed warm compresses and a corticosteroid-antibiotic ointment twice a day for 4 weeks. If the chalazion did not respond to conservative treatment, he was to be sent to surgery for incision and drainage.
1. Lederman C, Miller M. Hordeola and chalazia. Pediatr Rev. 1999;20(8):283-284.
2. Gilchrist H, Lee G. Management of chalazia in general practice. Aust Fam Physician. 2009;38(5):311-314.
3. Çetinkaya A, Akova YA. Pediatric ocular acne rosacea: long-term treatment with systemic antibiotics. Am J Ophthalmol. 2006;142(5):816-821.