Geoffrey E. Rose
Geoffrey Rose graduated BSc Pharmacology, MBBS, and MRCP. His postgraduate ophthalmic training culminated in award of FRCS in 1985 and FRCOphth at its foundation in 1988. In 1990, the University of London granted an MS doctorate for corneal research and, in 2004, a Doctor of Science in Ophthalmology and Ophthalmic Surgery.
Professor Rose was appointed consultant to Moorfields Eye Hospital, London, in 1990 and is also a Senior Research Fellow of the NIHR Biomedical Research Centre of the Institute of Ophthalmology. He served as the British Council member of the European Society of Ophthalmic Plastic and Reconstructive, is a Past-President of the British Oculoplastic Surgical Society, and is President of the European Society of Oculoplastic and Reconstructive Surgeons.
David H. Verity
Dr. Verity is a Consultant Ophthalmic Surgeon, and Adnexal Service Director, Moorfields Eye Hospital, London.He is a Honorary Senior Clinical Lecturer, University College London.Trained in ophthalmology in the UK, Dr. Verity undertook two Fellowships in ophthalmic adnexal disease before joining the Consultant staff at Moorfields Eye Hospital in 2004.He is a Full Member of the British Oculoplastic Surgery Society (current Treasurer), Treasurer Elect for the European Society of Ophthalmic Plastic and Reconstructive Surgery, and Full Member of the International Society of Ocular Oncology.In 2009, he was elected to the Orbital Society, in 2010 became Editor-in Chief of the journal ORBIT, and in 2016 became Oculoplastic Section Editor for the Journal of Ophthalmic and Vision Research.His medical publications in peer-reviewed journals and books include 90(+) publications, and with a wide range of research interests, he is an active national and international teacher and surgical trainer.Dr. Verity also has a life-long interest in the charitable work of the St John Eye Hospital Group. In 2014, he was invested in the Order of St John, and in 2016 he joined the Board as Trustee of the Hospital Group.
Inflammation is the normal tissue response to any variety of noxious insults, and a mild degree of persistent inflammation is common in most tissues, especially those near the surface of the organism. With acute injury, there is typically vasodilatation and a protein-rich exudative inflammatory response, with rapid recruitment of neutrophils from the dilated neighbouring vasculature – this constituting the acute suppurative inflammation. Where the recruitment, degranulation and death of neutrophils occur in massive numbers, there is an excessive release of toxic cytokines and free radicals that will lead to destruction of neighbouring tissues and a spreading cytotoxic and ischaemic necrosis – as happens, for example, with the massive subcutaneous tissue death and purulence of necrotising fasciitis.
Where the neutrophil response is not overwhelming and the noxious inflammatory trigger(s) persists, the healing response starts almost simultaneously with the recruitment of cytotoxic inflammatory cells. This healing response includes the condensation of fibrin in and around the area of inflammation – the fibrin acting as a barrier to help limit spread of the inflammatory triggers, cytotoxic inflammatory cells and cytotoxic inflammatory mediators – and this fibrin “capsule” acts as a scaffold over which activated fibroblasts will migrate and secrete new collagen as a more permanent barrier (e.g. as in the “woody” wall of an abscess). Tissue debris accumulates rapidly during the acute inflammatory response, and part of the healing phase involves mechanisms to clear this undesirable debris that includes disabled invasive organisms, implanted foreign bodies and cellular debris due to the normal death of acute inflammatory cells (such as the neutrophil debris and proteins in pus) and from the unintentional death (necrosis) of “innocent-bystander” tissues in the vicinity of the inflammatory focus. Clearance of tissue debris occurs through the action of itinerant macrophages and starts a few days after inflammation is initiated. If the macrophages are unable to clear the debris – as, for example, with fine insoluble foreign bodies – then they may persist within coalescent macrophages, which are later manifest histologically as multinucleate foreign-body giant cells; very long-term persistence of this type of macrophage-predominant inflammation may lead to granulomas, with epithelioid macrophages – as seen with sarcoidosis or chronic tuberculosis.
With some inflammatory processes, there is a gradual shift from the neutrophil-predominant acute response to a lymphocyte-predominant chronic inflammation. Lymphocyte-predominant inflammation is often associated with the formation of characteristic follicles, with germinal centres and surrounding mantle zones, and these may rarely lead to the very late emergence of lymphomas.
When a patient presents with periocular inflammation, the most important caveat should be that this is not a specific diagnosis, but rather that is it a “normal” tissue response to some noxious stimulus [1]. The adage that “inflammation is a tissue response, and not a diagnosis” is extremely valuable as it should alert the clinician to remain ever vigilant for an emerging diagnosis in the patient with inflammation; this remains a key principle; otherwise, the cause of inflammation is easily missed, especially if anti-inflammatory drugs (particularly systemic corticosteroids) are used without establishing the underlying cause of inflammation. Anti-inflammatory drugs will not only mask the true state of the inflammatory process and lead to a delay in correct diagnosis, but also some of the unidentified causative agents will actually be worsened by use of these drugs.
The empirical use of anti-inflammatory drugs should be undertaken only if the clinical history, symptoms and signs are characteristic for a given disease. Such pathognomonic conditions include, for example, severe periocular eczema (Fig. 22.1a), an acute Meibomian abscess (Fig. 22.1b), acute orbital myositis (Fig. 22.1c, d) and the acute superior orbital fissure syndrome (Fig. 22.2). Although almost all of these characteristic inflammations will settle with treatment, if a “typical” condition does not respond as expected, the diagnosis should be reconsidered, and appropriate imaging and biopsy performed where appropriate.
Fig. 22.1
(a) Acute periocular eczema from allergy to neomycin eyedrops; the eczema is often most severe in the “spill-zone” of the lower eyelid. (b) Acute pretarsal abscess due to an infected Meibomian cyst erupting into the pretarsal space. (c) Left lateral rectus myositis presenting as pain, inflammation and localised redness developing over a few days. (d) Characteristic appearance of acute left medial rectus myositis, with marked swelling extending to the muscular insertion into the globe; the tendon is spared in most other causes of muscular enlargement
Fig. 22.2
Acute inflammation of the orbital apex at presentation, with a one-day history of left retrobulbar ache and overnight onset of slight eyelid swelling with some ptosis, diplopia due to a marked reduction in all left ocular ductions and some hypoaesthesia of the left forehead and scalp. There was a mild reduction in left visual acuity
Acute Inflammation of the Eyelid
Because of their external protective role and complexity, acute or subacute inflammation of the eyelids is most commonly due to infective causes – predominantly bacterial or viral – although trauma is another inflammatory cause. Localised and non-specific inflammation of the periocular skin often occurs due to collateral radiation damage during orbital radiotherapy or secondary to chemical or thermal injuries.
The location of an acute inflammation may be a guide as to the underlying infective cause: the inflamed tarsal nodule is almost always infection within a preceding Meibomian retention cyst, and this can erupt through the eyelid margin (Fig. 22.3a) or into the pretarsal space; rarely the tender eyelid nodule will be a harbinger of eyelid necrosis due to pyoderma gangrenosum [2]. Infection within the canaliculus is not uncommonly misinterpreted as an inflamed chalazion (Fig. 22.3b), but the defining feature is that canaliculitis occurs medially to the tarsus as defined by the presence of its lashes. Primary herpes simplex is the most common acute viral infection of the eyelid and usually has characteristic vesicles in an erythematous skin; recognition of this condition is important, as early treatment with topical antivirals may reduce the incidence of post-viral lacrimal canalicular obstruction. Low-grade infection within the frontal sinus tends, with time, to erupt into the preseptal tissues of the upper eyelid and present as erythematous swelling in the upper sulcus (Fig. 22.3c), and all such patients – in the absence of a tarsal inflammatory focus – should be imaged for underlying sinus disease, as it carries a risk of concomitant intracranial spread of infection [3].
