Lesson of the week: microbial keratitis in intensive careBMJ 1997; 314 doi: https://doi.org/10.1136/bmj.314.7078.433 (Published 08 February 1997) Cite this as: BMJ 1997;314:433
- J F Kirwan, ophthalmology registrara,
- T Potamitis, registrarb,
- H El-Kasaby, senior registrarb,
- M W Hope-Ross, consultantb,
- G A Sutton, consultantb
- a Royal Eye Unit Kingston Hospital Kingston upon Thames Surrey KT2 7QB
- b Birmingham and Midland Eye Hospital Birmingham B3 2NS
- Correspondence to: Mr J F Kirwan Department of Ophthalmology St George's Hospital London SW17 0QT
- Accepted 20 August 1996
Microbial keratitis is a severe complication of corneal exposure in unconscious patients. We report five cases of microbial keratitis in three patients who sustained visual loss as a result while unconscious in an intensive care unit. The devastating consequences of microbial keratitis continue to be seen despite preventive measures.
A 74 year old man underwent a coronary artery bypass graft. He subsequently had renal failure and the adult respiratory distress syndrome. He was admitted to intensive care, where he was artificially ventilated for two weeks. After a tracheostomy he contracted a respiratory tract infection with Pseudomonas aeruginosa for which no obvious source was found. Twelve days later he developed bilateral microbial keratitis secondary to corneal exposure. This rapidly deteriorated and he developed bilateral endophthalmitis and a corneal perforation in the left eye. He was treated with intravitreal and topical gentamicin, intravenous ceftazidime, and ciprofloxacin. The inflammation gradually resolved. The patient, however, was left with bilateral scarred, thinned, and vascularised corneas. Visual acuity was reduced to light perception only in each eye.
Over the following six months there was little improvement in vision. The main cause of visual loss in the right eye was thought to be the result of corneal opacity and cataract. He underwent a right combined corneal transplantation, cataract extraction, and insertion of an intraocular lens. The procedure was technically difficult because of the caseous nature of the recipient corneal tissue, which tended to disintegrate. Despite some persisting leakage, the graft remained clear with a visual acuity of 6/36.
A 31 year old man was involved in a road traffic accident, sustaining multiple trauma, including a right frontotemporal fracture extending into the orbit. He was transferred to a neurosurgical centre and remained unconscious throughout, requiring ventilatory support. After 12 days the opinion of an ophthalmologist was requested because of a right proptosis. He had microbial keratitis, with extensive corneal exposure, and was treated with topical cefuroxime and gentamicin. The following day a temporary tarsorrhaphy was performed. The causative agent was Acinetobacter calcoaceticus; this was also the cause of a lower respiratory tract infection that became evident two days later. This agent was resistant to the topical chloramphenicol that had been used for prophylaxis. The patient subsequently died of a pulmonary embolus.
A 7 year old girl was admitted to hospital with a head injury after a road traffic accident. She sustained a skull fracture and a left third cranial nerve palsy and required assisted ventilation. After four days periorbital swelling and chemosis occurred. The opinion of an ophthalmologist was sought: the patient had corneal exposure, with bilateral microbial keratitis, from which Pseudomonas aeruginosa was cultured. This organism was not cultured from any other site. The infection was treated with topical gentamicin, carbenicillin, and later chloramphenicol. Both eyes healed over the next four weeks, leaving bilateral corneal scarring. Two months later visual acuities measured 6/60 in each eye. Over eight months best corrected visual acuity improved to 6/24 in the right eye and 6/6 in the left eye.
The eyelids and the tear film are natural barriers to infection. The lids provide a physical barrier to trauma and desiccation, and they deter adherence of organisms to the ocular surface. Tears provide mechanical lubrication to wash away organisms, and they also contain antimicrobial substances. These include immunoglobulins and lysozyme, lactoferrin, ceruloplasmin, and complement components. The cornea is protected by an adherent glycocalyx and a mucin produced by goblet cells. The intact corneal epithelium also acts as a protective barrier.1
Most corneal infections require predisposing factors such as trauma or impaired host defences, to develop. Most bacteria are unable to penetrate the intact corneal epithelium. If lid closure is ineffective then the tear film is unable to provide coverage and the epithelium becomes susceptible to desiccation. The effect of paralysing and sedating agents means that these normal physiological mechanisms are impaired. Inadequate lid closure may occasionally lead to corneal exposure in otherwise normal patients during sleep.2 Normal lid closure is maintained during sleep by the tonic contraction of the orbicularis. Sedation leads to the loss of the blink response to corneal irritation, with impairment of tear film function. Orbital haemorrhage, lid trauma, conjunctival chemosis due to positive pressure ventilation, or a facial nerve palsy may lead to inadequate lid closure, exacerbated particularly by corneal anaesthesia with defective epithelial repair. A few case reports detail corneal complications developing in mechanically ventilated patients. The incidence of corneal exposure and secondary complications is probably low but remains unknown. A survey of patients in intensive care units, using fluorescein enhancement, indicated a very low incidence of corneal exposure (T Potamitis, unpublished data).
The organisms most commonly implicated in mild eye infections are Staphylococcus aureus, Haemophilus influenzae, and Streptococcus spp. An ocular infection rate of 7% has been reported in a paediatric intensive care unit.3 Several reports have described ocular infections from respiratory tract pathogens.4 5 In two of our cases the patient had a simultaneous infection of the same pathogen in the respiratory tract and eye. Infection may occur during routine bronchial toilet.5 Pathogens found in intensive care are often difficult to eradicate, and antibiotic drug resistance is a continuing problem. In two patients the initial antibiotic treatment had to be changed once microbiological data were available.
A survey of intensive care units showed that in most of them eye care was carried out every two hours on ventilated patients and, in other units, review was undertaken at least every six hours. Most units used some method of maintaining eye closure. The most common method was the application of a polyacrylamide gel (Geliperm).6 Simple use of this measure alone is not enough to provide corneal protection, and although convenient, this method has no confirmed efficacy. A recent report on patients with microbial keratitis in an intensive care unit showed a reduction in the microbial culture rate and number of cases of microbial keratitis on instigation of a complete programme of maintained eye closure, prophylactic gentamicin, and regular application of lubricating ointment, combined with regular observation. (B T Parkin, A Turner, E P Moore, S D Cook, Oxford ophthalmological congress, 1996.) Monitoring of eye closure needs to be carefully performed as incomplete eye closure may be unrecognised, particularly medially. This may well be most effectively achieved by use of taping. Closure by tarsorrhaphy makes examination difficult, with the risk of a silent infection. Prophylactic use of antibiotic ointment may have something to offer, both by avoiding drying due to exposure, and by preventing secondary infection. Alternatively, lubricating ointment may be combined with a separate topical antibiotic. Widespread antibiotic use, however, encourages the spread of bacterial resistance.
Without meticulous care, corneal exposure and its sequelae, sometimes with devastating consequences, is very likely. We emphasise the need for maintenance of lid closure in at risk patients. Early referral in suspicious circumstances is essential. Fluorescein aided examination may enhance the care of such patients by detecting an epithelial defect before the onset of superimposed corneal infection. In cases with an epithelial defect, particularly with exacerbating risk factors, early lid closure with a lower lid traction suture may be appropriate, as lid closure is maintained, but examination of the eye is still possible.