Fig. 7.1
Presumed non-infective endophthalmitis presented with corneal oedema, hypopyon and fibrin with normal ultrasonography and no adnexal inflammation. It needs close observation over the next 6–8 h with topical corticosteroids to look for early signs of resolution or worsening
Various approaches have been suggested. One approach, to be on the safer side, is to consider every postoperative ‘unusual’ inflammation as ‘infective unless proven otherwise’. In such an approach, a prompt vitreous biopsy/tap or AC tap with intraocular antibiotics in all such cases should be considered. This approach will cover all of the low-grade and the evolving fulminant infections. The downside is that for every infective case that receives appropriate treatment, nine of ten cases that did not need this treatment would also receive unnecessary treatment and associated risks. Potential risks, though very rare, include drug toxicity, surgical complications like retinal detachment or globe perforation from anaesthesia, false laboratory positives, economic burden, physical and mental pain not only to the patient but also to family and the surgeons and an unnecessary load on the infrastructure of the operating room and the microbiological laboratory.
An alternate approach is to consider all such ‘indeterminate’ cases as inflammatory and ‘presumed non-infective’ [11]. This approach needs a detailed evaluation of the patient and an individualised approach based on a sound protocol of management. Detailed evaluation to reach a clinical judgement of ‘presumed non-infection endophthalmitis’ requires careful attention to the following factors, pre-, intra-, and postoperative:
- 1.
Factors that could result in an inflammatory response need considerations. Detailed dialogue with the primary surgeon and patient along with a critical review of all previous documentation is needed to ascertain these factors:
- (a)
Preoperative factors that could result in increased inflammation: Hypermature cataract; phacolytic and phacomorphic glaucoma; pseudoexfoliation; post-traumatic cataract; post-uveitis cataract; cataract in eyes with chronic angle closure on long-term medication, especially with pilocarpine; post-rubella cataracts in children; eyes with pre-existing undetected new vessels iris (NVI); eyes treated for neovascular glaucoma; and eyes with underlying retinal detachment.
- (b)
Intraoperative factors that could result in increased inflammation: Poorly dilating pupils with or without posterior synechiae, floppy iris with frequent iris prolapse, retained viscoelastic, retained lens matter, prolonged surgical time, difficult lens removal, need for anterior vitrectomy, corneal pathology causing hazy view of lens, intraoperative increased bleeding including from globe perforation (peribulbar anaesthesia related)/angle vessels as in hypochromic cyclitis, pre-existing NVI, bleeding from surgical incision site or trauma to iris root, suprachoroidal/expulsive haemorrhage and uncooperative patient.
- (c)
Postoperative factors that could result in increased inflammation: Poor compliance to medication, rebound inflammation on tapering topical steroids or anti-inflammatory eye drops, development of de novo NVI in eyes with underlying ocular ischemic syndrome due to increased metabolic demand on the hypoxic tissues and diabetes mellitus (possible, but not definitively proven).
- (a)
- 2.
Investigation: Ultrasonography is essential when the posterior segment view is not clear. Vitreous pin point echoes and membranes (Fig. 7.2, top) are suggestive of infective aetiology, but a normal ultrasonography does not rule out early infection. Isolated echoes could also occur in vitreous haemorrhage and cannot be differentiated from echoes of infection in early stages. In old age, some vitreous debris gives vitreous echoes, and these could be differentiated from pathological echoes by careful comparison to the echoes in the non-infected fellow eye. Retained nucleus may be seen on ultrasonography (Fig. 7.2, bottom). Choroidal effusive detachment is more often seen in infective than non-infective cases. Pre-existing chronic retinal detachment could incite inflammation, but fresh choroidal and retinal detachment is more commonly seen in infective aetiology.
- 3.
The next step is a meticulous evaluation of signs and symptoms and investigations: Symptoms that favour an infective aetiology are severe pain, nausea and vomiting usually a few hours after surgery. Fever and other constitutional symptoms could follow. Signs that favour an infective aetiology include adnexal oedema, diffuse mild stromal corneal oedema with minimal cellular infiltration (on slit lamp), inferior retinal exudates (Fig. 7.3), few or more areas of retinal vasculitis or retinal haemorrhages (Fig. 7.4) [12], raised or low intraocular pressure, wound leak including positive Siedel test and ultrasonography features (vide supra).
Mild pain, reduced vision even to level of light perception only, clear cornea, minimal hypopyon, normal intraocular pressure and poor view of retina with pupil closed by a fibrin membrane or few anterior vitreous cells can occur both in infective and non-infective cases and are non-specific with substantial overlap in infection versus non-infection cases [13].
- 4.
Once infection is not definitive and patient has ‘presumed non-infective endophthalmitis’, a definitive ‘ten-point protocol’-based approach is followed [11]:
- (a)
Document all the positive and negative findings, history and events as mentioned above.
- (b)
Discuss situation with patient and family, and keep them ready for any possible change in plan for surgical intervention.
- (c)
Start topical corticosteroids (prednisolone or betamethasone or dexamethasone) every half hour.
- (d)
Attempt to dilate the miosed pupil rapidly. Use a combination of 5% phenylephrine and 1% tropicamide, one drop every 10 min for 4–5 doses. Use 2.5% phenylephrine and 1% tropicamide if patient is hypertensive. Use 2% cyclopentolate and 1% tropicamide if patient is allergic to phenylephrine. Do not use atropine at this stage because it is a poor mydriatic and onset of action/peak action is slow and acts only after a couple of days.
- (e)
Use topical antibiotic, if desired, in routine dose of sixth hourly (options include tobramycin, moxifloxacin, ciprofloxacin, gentamicin, chloramphenicol) as per antibiotic policy of the treating centre.
- (f)
Do not use systemic antibiotics. A single dose of intravenous or intramuscular dexamethasone can be given if non-infective status could be ascertained.
- (g)
Admit the patient for above treatment, but do not delay the topical medications (as admission process takes its own time). If not admitting, keep the patient in the clinic area itself, and ensure topical instillation as per the protocol.
- (h)
Give antiglaucoma medication (oral acetazolamide, topical dorzolamide/timolol) as needed based on the intraocular pressure.
- (i)
Avoid or use only minimal oral or parenteral analgesic/anti-inflammatory drugs as they can camouflage the evolving pain severity, an important sign if it was not present earlier.
- (j)
Re-evaluate the patient in 4–6 h. This is the most critical step and has to be ensured. The symptoms and signs could be either same, worse or better. In each case a through and complete evaluation of patient is needed including detailed indirect ophthalmoscopy and slit-lamp retroillumination evaluation to look for presence and quality of the fundal red glow. Visual acuity and level of hypopyon are of less value in this evaluation. More important are retraction of fibrin and ability to dilate pupil well and get a peek into the posterior segment glow (Fig. 7.5).
At this stage one can decide to continue the same treatment and re-evaluate in the next 6 h or decide for surgical intervention. In our study, only 4 of 23 patients needed surgical intervention, and the remaining patients improved with medical therapy only. The patients who needed surgery often had low virulent and slow-growing organisms, and the delayed surgery still resulted in good outcomes [11].
- (a)
Fig. 7.2
Ultrasonography. Top left, moderately advanced endophthalmitis that shows fine dot-like echoes and normal choroidal thickening; top right, severely advanced endophthalmitis that shows membrane formation with dense echoes and choroidal thickening. Bottom—retained nuclear fragment with vitreous inflammation echoes causing an endophthalmitis-like appearance
Fig. 7.3
Post-cataract surgery 1 week—visual acuity 20/25; cells in AC were suspected to having non-infective inflammation. Dilated fundus examination showed yellow exudates in the inferior retina suggestive of infection that could have been easily missed. Ultrasonography at this early stage was normal
Fig. 7.4
Retinal vasculitis as the earliest sign of infection in post-traumatic infective endophthalmitis. Visual acuity was 20/25. Vitreous culture grew S. epidermidis [12]
Fig. 7.5
Clinical course of presumed non-infective endophthalmitis with topical corticosteroids. Top left—at presentation, fibrin in pupillary area, miotic pupil and hypopyon with clear cornea. Top right—after 8 h of frequent corticosteroids and four doses every 15 min of phenylephrine and tropicamide, the synechiae are broken and fibrin is retracting. Bottom left—72 h later, fibrin is mostly resolved, and there was no hypopyon. Bottom right—complete resolution at 1 week
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