**2. Mean headings**

38 Keratoplasties – Surgical Techniques and Complications

et al., 2009; Illingworth et al., 1995; Illingworth & Cook, 1998; McCellan et al., 2001; Seal,

*Diamidines.* Available diamidines include propamidine isethionate 0.1% (1000 g/ml) and hexamidine 0.1% (1000 g/ml); these are licensed as antibacterials in some European countries. The antimicrobial effects of the diamidines result from the cationic surface-active properties inducing structural membrane changes affecting cell permeability. When these molecules penetrate into the amoebic cytoplasm, denaturation of cytoplasmic proteins and enzymes occurs. Propamidine and hexamidine have been effective clinically against both the trophozoite and cyst forms of *Acanthamoeba*. Clinically, the diamidines are well tolerated by ocular tissues, although prolonged treatment with propamidine may lead to toxic keratopathy (Bacon et al., 1993; Dart et al., 2009; Illingworth et al., 1995; Illingworth & Cook,

Although neomycin has been widely used, it is ineffective against cysts in vitro. In addition, like all aminoglycosides it is toxic to the corneal epithelium and can often result in indolent corneal ulceration that may be incorrectly attributed to disease activity, nevertheless it is effective for the bacterial co-infection. Povidon-Iodine (Betadine) is amoebicid and cysticid generally, however it can be used in 0.5% concentrate as well (Bacon et al., 1993; Dart et al., 2009; Illingworth et al., 1995; Illingworth & Cook, 1998; McCellan et al., 2001; Seal, 2003). *Topical corticosteroids.* The role of steroids is controversial, but we believe that topical corticosteroids can have an important and beneficial role in the management of some cases of Acanthamoeba keratitis. The dead cysts persist in the corneal stroma and remain antigenic. This can give rise to a serious inflammatory reaction. Steroid treatment is unnecessary in most cases diagnosed early, which usually respond rapidly to antiamoebic drugs. However, persisting inflammation (anterior scleritis, severe pain, indolent ulcers, corneal inflammation, and anterior chamber inflammation) may respond dramatically to the addition of even low-potency topical steroid therapy, e.g. prednisolone 0.5%, or dexamethasone 0.1% 4 times daily. Clinicians should be careful to avoid use of corticosteroids if possible because they suppress the activity of the macrophage, which is the 'scavenger' phagocytic cell responsible for host immunity to Acanthamoeba. Use of nonsteroidal anti-inflammatory drugs, particularly flurbiprofen, is encouraged and also acts as both an analgesic and a mydriatic. When attendant to the inflammation secondary glaucoma appears, anti-glaucomatic drops are used. Pupil dilatators are also used for moving the pupil (Bacon et al., 1993; Dart et al., 2009; Illingworth et al., 1995; Illingworth &

With respect to the severity of the disease as well as the complications accompanying it there is

*Corneal abrasion* or debridement of the affected area of corneal epithelium may be successful if performed at an early stage. Repeated debridement is used in some centres to improve drug penetration (Dart et al., 2009; Illingworth & Cook, 1998; Reinhard & Sundmacher, 2000). *Cryosurgery* may be valuable in treating Acanthamoeba keratitis cases. Cryocoagulation to the ring infiltrate and central cornea breaks the infected cells and cyst walls (Amoils &

Deep lamellar keratectomy with a conjunctival flap is a suitable approach to help control the infection and to help relieve pain in patients with advanced Acanthamoeba keratitis

2003).

1998; McCellan et al., 2001; Seal, 2003).

Cook, 1998; McCellan et al., 2001; Seal, 2003).

a range of surgical methods to choose from.

Heney, 1999; Reinhard & Sundmacher, 2000).

(Cremon et al., 2002; Parthasarathy & Tan, 2007).

**1.6.2 Surgical treatment** 
