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Do we really need to panic in all acute vision loss in ICU Acute angle-closure glaucoma.

Byline: Ali Akal Ahmet Kucuk Funda Yalcin and Saban Yalcin

AbstractAcute angle closure glaucoma is a sight-threatening situation characterized by a sudden and marked rise in intraocular pressure (IOP) due to obstruction of aqueous humour outflow. Many local (ocular drops nasal and nebulized agents) and systemic drugs (e.g. atropine adrenaline ephedrine some psychoactive and antiepileptic drugs) that are widely used in intensive care units have the potential to precipitate such an acute attack. In this case report we describe progressive visual loss due to acute angle-closure glaucoma (AACG) in a 59 year old female patient followed in the ICU due to a massive pulmonary embolism.

Keywords: Acute angle closure glaucoma Intraocular pressure Intensive care unit Visual loss.

IntroductionVisual loss in critical care patients is a point of concern that warrants thorough assessment.1 Acute angle closure glaucoma (AACG) is a possible blinding situation represented by an unexpected and pronounced rise in intraocular pressure (IOP) due to obstruction of aqueous humour outflow. Numerous local (nasal and nebulized agents) and systemic drugs (e.g. atropine adrenaline ephedrine etc.) that are widely used in intensive care units have the capacity to provoke such an acute attack.2The risk is increased in predisposed subjects including certain ethnic groups such as Asians Canadians and Eskimos; elderly and female gender with a shorter eyeball larger crystalline lens shallower anterior chamber and a narrower drainage angle.3 In this case report we describe progressive visual loss due to acute angle-closure glaucoma (AACG) in a 59 year old female patient followed in the ICU due to a massive pulmonary embolism.

Case ReportA 59 year old female patient was admitted to our emergency department in May 2012 with chest pain and cyanosis. Her heart rate was 127 beats per minute (bpm) blood pressure was 78/46 mm/Hg and peripheral oxygen saturation was 89% with 10/L O2 via a nonrebreather mask. Her medical history revealed a urological operation due to renal stones three weeks previously. Bedside echocardiography showed an enlarged right ventricle and electrocardiography displayed a new right bundle branch block that was suspicious for a massive pulmonary embolus. Computerized tomography confirmed the diagnosis of bilateral massive pulmonary emboli (PE) and she was transferred to the ICU. Infusions of 0.01 g/kg/min epinephrine and with 10 g/kg/min dopamine were started due to haemodynamic instability. Twenty- four hours after the epinephrine and dopamine infusion visual loss in the right and left eyes with a bilateral frontal headache began and an ophthalmology consultation was requested. Intraocular pressure was measured as 44 mm Hg (right) and 53 mm Hg (left) with a Schiotz tonometer. Characteristics of AACG including diffuse epithelial corneal oedema shallow anterior chambers with iris convexity and fixed mid-dilated pupils were observed. The view of the retina was restricted due to corneal oedema. Gonioscopy was not tried in the critical care setting. Right and left eye acute angle closure glaucoma was diagnosed and all medications were rechecked dopamine and adrenaline infusions and nebulized agents were stopped. Oral acetazolamide (250 mg) four times daily topical pilocarpine (4%) four times a day and timolol (0.5%) twice daily were started. Two days after this acute attack the right and left eye intraocular pressures were in the normal range and visual acuity had completely recovered. She was discharged home one month after admission and right and left eye laser peripheral iridotomy was performed 3 weeks after ICU discharge (Figure).

A one year follow-up revealed no abnormalities.

DiscussionOphthalmologic complications are often encountered in intensive care unit (ICU) patients including metastatic endogenous endophthalmitis ischaemic optic neuropathy pupil abnormalities vascular occlusions rhino-orbital cerebral mucormycosis and acute angle closure glaucoma.4 Glaucoma is a potentially blinding disease caused by progressive and irreversible optic neuropathy.5 Studies have shown that a single AACG attack has been associated with permanent retinal nerve fiber layer loss visual field defects and optic disc pallor.6

Several classes of drugs including topical mydriatics anticolinergics antidepressants anticonvulsants antihistaminics sulphamate derivative adrenergics and sympathomimetic drugs have the capacity to actuate an acute attack of angle closure.7

Sympathomimetic drugs including epinephrine norepinephrine dopamine phenylephrine and ephedrine are widely used in the ICU and are reported to cause AACG in several case reports. Phenylephrine drops that are used for ocular fundus examination might induce AACG in about 0.03% of nonselected patients.89 Systemic administration of ephedrine for flu and surgical anaesthesia or epinephrine to treat anaphylactic shock and ventricular fibrillation have been shown to cause AACG. Nasal ephedrine and naphazoline are reported to induce bilateral AACG in the acute management of epistaxis2 and AY2-adrenergic agents (salbutamol albuterol terbutaline) with anticholinergic drugs might also trigger transient angle closure.1 Medications with indirect sympathomimetic activity including amphetamines some antidepressant agents (imipramine monoamine oxidase inhibitors) and cocaine have been shown to induce AACG.210 In our case epinephrine dopamine and nebulized agents were used in the ICU due to haemodynamic instability and bronchoconstriction. All these drugs were stopped after the diagnosis and improvement in symptoms were resolved with the AACG treatment within the first 24 hours. Taking into consideration all the predisposed factors such as female gender age and ethnicity we think that medications might be the main factors that induced AACG in this patient. Symptoms including ocular or periocular pain nausea and/or vomiting and an antecedent history of intermittent vision and/or haloes might be seen and conjunctival injection corneal epithelial oedema mid- dilated unreactive pupil and shallow anterior chamber might be observed in ophthalmology consultation. IOP might also be elevated.11 However in ICU settings the characteristic signs and symptoms of AACG may be incorrectly ascribed to other causes resulting in improper pharmacologic treatment which may prolong the acute episode and postpone the exact diagnosis. Any patient presenting with signs or symptoms of AACG should be referred promptly to an ophthalmologist. Rapid diagnosis and appropriate treatment will facilitate prohibiting visual loss. In differential diagnosis acute orbital compartment syndrome conjunctivitis corneal abrasion laceration ulceration ulcerative keratitis endophthalmitis and vitreous haemorrhage should be kept in mind.

A standardized protocol of management involves intravenous acetazolamide (500mg) followed by oral acetazolamide (250mg) four times daily topical pilocarpine (4%) four times a day and timolol (0.5%) twice daily as well as betamethasone or prednisolone acetate every 3 hours applied to the affected eye. If the IOP is not reduced after 2 hours of this standard treatment other medications such as intravenous mannitol oral glycerol topical latanoprost or brimonidine can be added. Patients are reviewed at regular intervals for IOP control. Subjects are also examined for adverse effects of the medical therapy.11

After starting conventional treatment of AACG definitive surgical treatment including laser peripheral iridotomy or argon laser peripheral iridoplasty should be done immediately but these techniques must be delayed until haemodynamic stability of ICU patients is achieved. Also sufficient corneal clarity is crucial for surgery to be performed safely.12 In patients not suitable for immediate definitive surgery a delay in aborting an acute attack carries a significant risk of developing glaucomatous optic neuropathy.13 We believe that prompt medical treatment is essential in patients who are not appropriate for immediate definitive surgery especially those in the ICU with haemodynamic instability.

ConclusionWe believe that all individuals responsible for medication of patients in the ICU should be fully aware of the adverse effects of drugs. Nevertheless all patients should have initial ophthalmic evaluation and ICU staff should be aware of eye problems particularly in predisposed patients.

References1. Yalcin S Pampal K Erden A Oba S Bilgin S. Do we really need to panic in all anisocoria cases in critical care Indian J Anaesth 2010; 54: 365-6.2. Lachkar Y Bouassida W. Drug-induced acute angle closure glaucoma. Curr Opin Ophthalmol 2007; 18: 129-33.

3. Singer MS Salim S. Bilateral acute angle-closure glaucoma as a complication of facedown spine surgery. Spine J 2010; 10: e7-9.4. Grixti A Sadri M Datta AV. Uncommon ophthalmologic disorders in intensive care unit patients. J Crit Care 2012; 746: e9-22.

5. Prevention of blindness and visual impairment. Priority eye diseases. (Online) (Cited 2011 September 12). Available from URL: http://www.who.int/blindness/causes/priority/en/index7.html.6. Tsai JC Lin PW Teng MC Lai IC. Longitudinal changes in retinal nerve fiber layer thickness after acute primary angle closure measured with optical coherence tomography. Invest Ophthalmol Vis Sci 2007; 48: 1659-64.7. Lai JS Gangwani RA. Medication-induced acute angle closure attack. Hong Kong Med J 2012; 18: 139-45. 8. Wolfs RC Grobbee DE Hofman A de Jong PT. Risk of acute angle- closure glaucoma after diagnostic mydriasis in nonselected subjects: the Rotterdam Study. Invest Ophthalmol Vis Sci 1997; 38: 2683-7.9. Patel KH Javitt JC Tielsch JM Street DA Katz J Quigley HA et al. Incidence of acute angle-closure glaucoma after pharmacologic mydriasis. Am J Ophthalmol 1995; 120: 709-17.10. Wilcsek GA Vose MJ Francis IC Sharma S Coroneo MT. Acute angle closure glaucoma following the use of intranasal cocaine during dacryocystorhinostomy. Br J Ophthalmol 2002; 86: 1312.

11. Ramli N Chai SM Tan GS Husain R Hoh ST Ho CL et al. Efficacy of medical therapy in the initial management of acute primary angle closure in Asians. Eye (Lond) 2010; 24: 1599-60212. Saw SM Gazzard G Friedman DS. Interventions for angle-closure glaucoma: an evidence-based update. Ophthalmology 2003; 110: 1869-78.13. Lee JW Lee JH Lee KW. Prognostic factors for the success of laser iridotomy for acute primary angle closure glaucoma. Korean J Ophthalmol 2009; 23: 286-90
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Publication:Journal of Pakistan Medical Association
Date:Aug 31, 2014
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