Critical Care Medicine
Acute visual disturbance
1. Description of the problem
- Barriers to communication in critically ill patients
- Common visual disturbances in critically ill patients
- Corneal abrasion
- Vitreous hemorrhage
- Renal vascular occlusion
- Retinal tear and retinal detachment
- Cavernous sinus thrombosis
- Posterior reversible encephalopathy syndrome (PRES)
- Cortical blindness
- Pathogenesis of chemosis
- Mechanisms of corneal abrasions
- Mechanisms and risk factors for glaucoma
- Mechanisms and risk factors of vitreous hemorrhage
- Risk factors for retinal artery occlusion
- Risk factors for retinal tear and detachment
- Mechanisms for cavernous sinus thrombosis
- Mechanisms and risk factors for posterior reversible encephalopathy syndrome (PRES)
- Mechanisms and risk factors for cortical blindness
2. Emergency management
- 3. Diagnosis
- 4. Specific Treatment
5. Disease monitoring, follow-up and disposition
Special considerations for nursing and other allied health professionals
What's the evidence?
Acute Visual Disturbances in the Perioperative Setting
1. Description of the problem
Diagnosis of medical conditions in the ICU can be challenging. The focus often is on individual organ systems and the measurement of many different organ-specific indices. While many organ functions are easily measurable, this does not apply to the organs of the sensory system (e.g. the visual system). These organs require the presence of either symptoms or signs to indicate possible dysfunction. The presence of symptoms requires the ability of the patient to communicate, and critically ill patients have multiple barriers to effective communication, which contributes to fear, depersonalization and frustration.
Barriers to communication in critically ill patients
Many patients admitted to critical care units are mechanically ventilated and have an endotracheal tube in place. The endotracheal tube prevents them from speaking and often necessitates the administration of sedative medications to allow the patient to tolerate both the endotracheal tube and the ventilator.
Sedatives are an obvious immediate barrier to communication and have been shown to be causally associated with the development of ICU delirium, and can continue to impair communication, even after discontinuation of ventilation and sedatives. Delirium has been found in up to 80% of intensive care patient populations and could be the greatest barrier to effective patient communication, both in intubated and non-intubated patients. Patients who are nonverbal have to find other ways to communicate.
This could involve gestures, eye blinks, writing, touching or pointing. Gesture is the most common form of non-vocal communication used but unfortunately is often limited by the use of restraints. Many different forms of communication aids have been tried for critically ill patients, and there is evidence that an adequate means of communication can improve the patient’s well-being.
These alternative methods of communication have included pencil and paper, picture boards, keyboards and laser pointers attached to glasses. Unfortunately all of these devices require intact vision to work. For patients suspected to have visual problems, some thought is required as to how best to communicate with them, especially if they have been rendered nonverbal. At the most simple level it is important that any patient who normally wears spectacles is provided them in the hospital.
Common visual disturbances in critically ill patients
Normal vision is a complex neurophysiologic process. It requires a tear film to keep the cornea moist, which along with the lens helps focus, a retina, optic nerve and complex neuronal pathways to the cerebral cortex. All of these require oxygen, the delivery of which depends on adequate blood supply.
Visual disturbances can be caused by disruption at many places along the visual pathway. This can result in either monocular or binocular visual loss, which can be permanent or transient. Common causes of visual disturbance are chemosis, corneal abrasions, elevated intraocular pressure, vitreous hemorrhage, optic nerve trauma, posterior reversible encephalopathy syndrome and cortical blindness.
Chemosis is swelling of the conjunctiva and is a nonspecific sign. It can result from a disruption of the normal Starling forces that maintain fluid equilibrium within capillaries. Causes are venous obstruction, trauma, allergies, drugs, patient positioning and excessive crystalloid administration.
It can be symptomatic (some patients complain of a foreign body sensation) or asymptomatic, varying from being subtle to extremely pronounced, and can be unilateral or bilateral. The more pronounced the chemosis the more likely it is to cause some degree of visual disturbance and the greater the chance it will be noticed on physical examination.
The cornea forms one sixth of the outer coat of the eyeball, and is continuous with the conjunctiva. It is avascular, and the central portion gains its oxygen from that dissolved in the tear film. The tear film is regenerated by blinking and is a host defense mechanism due to dissolved immunoglobulins. Corneal abrasion is the most common surgical and general anesthesia complication and accounts for 3% to 8% of anesthesia-related malpractice claims. There are four main mechanisms associated with corneal abrasion: corneal exposure, globe pressure, chemical irritation and direct trauma.
Glaucoma is the world’s most common cause of blindness and is defined as a group of diseases that have a characteristic optic neuropathy with associated visual field loss for which elevated intraocular pressure is one of the primary risk factors. This disease is classified according to etiology (primary or secondary) and according to the status of the angle of the anterior chamber (open or closed). Closed angle glaucoma can be acute or chronic in onset and is responsible for 50% of the blindness worldwide related to glaucoma. The elevated intraocular pressure leads to degeneration of the axonal nerve fibers in the optic nerve with death of the cell bodies.
Visual problems can occur acutely as a consequence of pathology in any of the eye structures posterior to the lens. This includes the vitreous humor, the retina with its associated blood vessels and the optic disc. Given the concealed nature of these structures unless the patient is able to communicate or there is a very high index of suspicion, pathology here will be missed and unfortunately can lead to permanent visual disturbance.
Vitreous hemorrhage is a bleed into the vitreous cavity. It is painless and in the communicative patient will present as floaters or loss of vision in one eye.
Renal vascular occlusion
This is a common cause of painless sudden loss of vision. Perioperatively it can occur at a rate of 1.54 per 10,000 discharges. It can occur as a consequence of either retinal vein occlusion or central retinal artery occlusion.
Retinal tear and retinal detachment
There exists a potential space between the retina and retina pigment epithelium. A retinal tear can allow fluid from the vitreous cavity to move between these layers, and if left untreated 46% may progress to a retinal detachment. Communicative patients may complain of floaters or flashes of light that result from traction on the retina. Unfortunately the diagnosis is likely to be missed in non-communicative patients.
Cavernous sinus thrombosis
The cavernous sinuses are a pair of dural venous sinuses that lie on either side of the sella turcica. Cranial nerves III, IV, V and VI, along with the horizontal segment of the internal carotid artery, run either through the lumen or within the outside layers of the sinuses. This is an ophthalmological and neurological emergency with lethal consequences if not treated appropriately.
Posterior reversible encephalopathy syndrome (PRES)
PRES was first described in 1996. It is now a well-recognized clinical disease with specific neuroradiological findings. Symptoms are transitory neurological disturbances – altered mental status, seizures, headache and visual disturbances. The presentation can be acute or sub-acute.
Cortical blindness is blindness that results from bilateral lesions in the striate cortex of the occipital lobes. It is distinct from cerebral blindness, which is defined as a bilateral loss of vision due to disruption of the visual pathways posterior to the lateral geniculate nuclei.
Pathogenesis of chemosis
Patients operated on in the lateral position are more prone to developing edema of the dependent eye. The mechanism is thought to be increased venous pressure on the dependent side. A study of eye injuries and anesthesia found an association with the lateral position but did not discern a relationship between the dependent or non-dependent eye and consequent injury.
Prone positioning is associated with chemosis and can be more severe when the patient's head is below the level of the heart. The longer the amount of time spent in the prone position and the greater amount of fluid administered in this position, the greater the chance of developing chemosis.
Chemosis may also be caused by an allergic reaction to either a local or systemic substance. In the critical care unit, patients often have polypharmacy as part of their complex treatment plan and adverse drug reactions are not uncommon (19 per 1000 patient-days). Endotracheal tubes are often taped in place and local reaction may contribute to chemosis.
Chemosis can prevent adequate eyelid closure, causing exposure keratopathy. This can lead to an exposed cornea that then becomes dry and subsequently develops an abrasion. In fact, an exposed cornea is the primary risk factor for the development of bacterial keratitis, which can occur in nearly 1% of the critically ill population.
Mechanisms of corneal abrasions
Patients in the critical care unit, as mentioned previously, are often sedated and may even have neuromuscular paralytic drugs administered to facilitate ventilation. This can lead to lagophthalmos (failure of eyelids to close properly) and drying out of the cornea. These sedative drugs can also affect the tear film by decreasing the rate of tear production and decreasing blinking (which is a normal protective mechanism to restore the tear film).
The combined effect is to decrease the amount of oxygen available to the central cornea, leading to corneal edema, desquamation and ultimately an abrasion.
The avascular nature of the cornea makes it particularly susceptible to globe pressure. This can occur whenever there are procedures or care taking place around the head or neck. Classically pressure can be applied during mask ventilation with an ill-fitting mask or poor hand placement. Once a patient’s face is covered by drapes during procedures, then personnel present may be unaware of themselves or instruments placing direct pressure on the globe.
Irritation to the eye can result from cleansing materials used for surgical procedures. These can run into the eye during procedures in close proximity or from splashes. Any ointment or drug applied to the eye can also cause irritation. This could be from incorrect technique of administration, drug reaction or due to preservatives present in the drug, such as benzalkonium chloride.
The lagophthalmos present in patients in the ICU can predispose them to direct trauma. The typical ventilated ICU patient is often attached to multiple drips with associated tubing, ventilators with long circuits, oxygen tubing and monitors by multiple cables.
There is therefore a high possibility of some of these devices and their attachments directly striking an incompletely closed eye. These risks, combined with that of a delirious patient who may be thrashing about and directly touching the eye while wearing finger probes, etc., place the critically ill patient at high risk of developing a corneal abrasion.
Mechanisms and risk factors for glaucoma
Acute angle closure is sudden in onset and has an extremely high intraocular pressure. This can cause symptoms of pain, redness and reduced vision. Clinical signs may be that of a mid-dilated pupil, hazy cornea and hyperemia of scleral blood vessels. Risk factors for development are age >60, female sex, positive family history and hypermetropism.
In the critical care unit angle-closure glaucoma can be precipitated by the administration of drugs. The drugs cause pupillary dilation with consequent crowding of the anterior chamber, pupil block due to partial pupillary constriction of a previously dilated pupil and from an idiosyncratic reaction that changes the iridio-corneal angle by formation of cilo-choroidal effusions.
Drugs causing angle-closure glaucoma
Adrenergic agonists: These drugs can be administered systemically (e.g. epinephrine) or nebulized (e.g. albuterol). The route of absorption is not definitively known: it may be from delivery by the bloodstream or from absorption over the cornea and conjunctiva with nebulized medications. The resulting pupillary dilation can precipitate acute angle closure.
Anticholinergics: These can cause angle closure by a similar mechanism to the adrenergic agonists. It has been described with nebulized ipratropium and by the systemic administration of oxybutynin as part of the treatment of urge incontinence. There are also many commonly used drugs that have some anticholinergic activity. This applies to most antidepressants, and there are case descriptions of many different classes of these drugs precipitating angle-closure glaucoma.
Sulfa-based drugs: Topiramate and hydrochlorothiazide are both sulfa drugs that have been associated with the development of angle-closure glaucoma. This is considered to be an idiosyncratic reaction caused by suprachoroidal effusion and ciliary body edema leading to anterior rotation of the ciliary body and shallowing of the anterior chamber angle.
Mechanisms and risk factors of vitreous hemorrhage
It can be caused by rupture of an aneurysm, or a blood vessel in the eye, trauma to the eye, a retinal tear or detachment, or bleeding from neovascularization. Risk factors for its development are diabetes, hypertension, head trauma and carotid disease. Patients taking antiplatelet agents or anticoagulants have a four times higher odds of developing a hemorrhage compared to those not taking these medications. Nevertheless, antiplatelet agents or anticoagulants are rarely withheld due to vitreous hemorrhage.
Risk factors for retinal artery occlusion
Risk factors for retinal artery occlusion are the same for any cardiovascular disease (e.g. age, hypertension, hypercholesterolemia, diabetes and smoking) or embolic disease phenomena and the work-up should be similar. There is literature to suggest that the rates of carotid disease are as high as 70% in those with central retinal artery occlusion.
Risk factors for retinal tear and detachment
Risk factors for retinal detachment are advancing age, previous cataract surgery, myopia, family history of retinal detachment, diabetic retinopathy and trauma. Retinal detachment presents as a spectrum from clouding of vision to loss of vision.
Mechanisms for cavernous sinus thrombosis
The most common cause of cavernous sinus vein thrombosis is extension of infections from other sites in its proximity. Sinusitis is the most prominent primary source, although any infection on the face has the ability to cause it. Other non-infectious conditions that may predispose to cavernous sinus thrombosis are malignancy (local or metastatic), trauma, dehydration and granulomatous diseases.
Mechanisms and risk factors for posterior reversible encephalopathy syndrome (PRES)
The mechanism of PRES is thought to be caused either by cytotoxic or vasogenic edema, with the current literature in favor of vasogenic. The increased systemic blood pressure may exceed the autoregulatory capacity of the cerebral vasculature, resulting in breakdown of the blood-brain barrier, with fluid extravasation and cerebral edema. The posterior circulation is affected more than the anterior circulation, which has a better sympathetic innervation that could protect it from the higher blood pressures.
The majority of cases of PRES are associated with hypertensive disorders (e.g. pre-eclampsia). PRES has been associated with many other conditions, including immunosuppression (HIV infection, immunosuppressive drugs such as cyclosporine), hemolytic-uremic syndrome, acute glomerulonephritis, blood transfusion and acute intermittent porphyria.
Mechanisms and risk factors for cortical blindness
The common causes of this condition are embolism or hypoperfusion of the visual cortex. Other causes of cortical blindness are hypoventilation, hypertension, trauma, meningitis and hypoglycemia. There is a lot of overlap between cortical blindness and PRES with regards to etiology, pathology and radiological findings.
Cortical blindness has a perioperative rate of 0.38 per 10,000 discharges, with a significantly higher prevalence in patients younger than 18 compared to those older than 18. Orthopedic, spinal and cardiac surgeries are all associated with cortical blindness.
There are various theories to the cause of this perioperative visual loss, with intraoperative anemia, prolonged operation and large blood loss all postulated. Cortical blindness has also been described with many angiographic procedures with no clear precipitant factor.
2. Emergency management
Diagnosis of chemosis
The diagnosis of chemosis is achieved by clinical examination of the patient with evidence of conjunctival swelling. Once chemosis is noted further symptoms should be elicited from the patient if possible. Specifically, foreign body sensation and pain should prompt evaluation by an ophthalmologist to examine for a possible corneal abrasion. Information from other members of the care team should be sought to identify when the chemosis began, along with careful review of the patient’s history and chart to look for precipitating causes.
Diagnosis of corneal abrasions
Detection of a corneal abrasion may be difficult in the ICU setting due to the impaired ability of many patients to communicate discomfort in their eye. Communicative patients may complain of blurred vision, pain or a foreign body sensation in the eye. A high index of suspicion is required by all staff involved with the care in appropriate recognition of risk factors. Increased tearing and conjunctival/scleral erythema should be a red flag for a possible abrasion.
These clinical signs may alternatively be cranial autonomic symptoms that are associated with trigeminal autonomic cephalgias. A careful history from the patient or family members should help identify those patients who previously suffered from these symptoms prior to hospital admission and thus guide care.
When suspected, an early ophthalmology consult should be obtained. Early treatment of corneal abrasions has been shown to have good outcomes with no long-term sequelae. The ophthalmologist may instill fluorescein dye using either drops or blotting paper that may cause a transient stinging sensation. The dye fluoresces a bright green color under a cobalt blue light and adheres to abrasions, allowing their localization.
Diagnosis of glaucoma
When glaucoma is suspected, an urgent ophthalmology opinion is required. The medication list should be reviewed and any unnecessary medication that may be implicated should be held until after ophthalmology consultation.
An ophthalmology exam may be done with a gonioscope at the slit lamp, allowing a view of the iridocorneal angle through a mirror or prism. Generally the more structures visualized, the wider the angle.
Diagnosis of vitreous hemorrhage
Funduscopic examination is required to make the diagnosis. There may be loss of the red reflex with large hemorrhages, but often the vitreous hemorrhage is visible with loss of fundus detail and visible floating debris.
Diagnosis of retinal vascular occlusions
Funduscopic examination is required for diagnosis. Vein occlusions may lead to multiple intraretinal hemorrhages or may present with vitreous hemorrhage. Retinal artery occlusions may show white retinal opacification with a cherry red spot in the macula.
Diagnosis of retinal tear and detachment
Diagnosis of both is done by funduscopic examination. Occasionally ultrasound is required when visualization of the retina is obscured by concomitant vitreous hemorrhage.
Diagnosis of cavernous sinus thrombosis
Clinical signs are bilateral chemosis, eyelid edema, ophthalmoplegia and proptosis. These signs result from damage to the nerves that pass through the sinus and impairment of venous drainage of the retinal and orbital vessels. Pupillary changes can vary as both parasympathetic nerves in the oculomotor nerve or the sympathetic nerves in the short ciliary nerves may be damaged.
Differential diagnosis includes orbital cellulitis (usually unilateral and does not cause papilledema), preseptal cellulitis (does not cause proptosis) or orbital apex syndrome (a complication of sinusitis that tends to have more posterior eye signs than anterior). The gold standard for diagnosis is either CT or MRI of the sinuses, orbit and brain.
Diagnosis of PRES
Seizures are usually present, and while they may start out focal, generalization is the norm. The altered mental status varies from lethargy to coma, but agitation may also be present. Visual disturbances can range from blurred vision to blindness and are bilateral due to involvement of the occipital cortex.
Neuroimaging shows edema mainly in the parieto-occipital lobes’ cortex and subcortical white matter. While this is the predominant area involved, changes can involve basal ganglia, frontal lobes, cerebellum and brainstem. MRI is the preferred imaging modality. FLAIR sequences give better characterization of lesions, especially those in a supratentorial location.
Diffusion-weighted MRI is more sensitive to changes in the distribution of water in the brain, is more sensitive for white matter edema and can distinguish vasogenic from cytotoxic edema.
Diagnosis of cortical blindness
The classic case is of a normal funduscopic exam and pupillary reactions to light with bilateral visual loss. Patients who are cortically blind will not react to threatening gestures or optokinetic stimulation.
4. Specific Treatment
While chemosis is usually not a risk factor for further serious visual problems, it has been noted to occur concurrently with other more serious visual problems. If the patient is suspected or at risk for any of these, then an urgent ophthalmological opinion should be sought to prevent permanent loss of vision.
Prevention is the better than treatment for corneal abrasion. In the operating room taping the eyes shut is routine practice. This practice is not recommended for care of the critically ill patient in the intensive care unit as it could cause distress both to the patient and the families, while it will remove the possibility of multiple methods of alternative communication by the patient.
Paraffin-based or methylcellulose ointments have also been administered to prevent corneal abrasion. However, these only prevent drying of the eye while not protecting against the other mechanisms of corneal abrasion. They themselves have been associated with significant morbidity, including blurred vision, which could cause more distress to the critically ill patient.
Completely preventing corneal abrasion in the ICU setting is difficult. Patient agitation should be appropriately controlled with sedatives and analgesics as indicated. Nursing staff should give proper attention to all cables, tubes, etc. that could possibly injure the eye and position them out of harm's way.
All practitioners when performing procedures should take care to protect the eye from cleaning solutions and be cognizant of applying direct pressure either themselves or by instruments/drapes. Periodic checks for corneal exposure and prophylactic lubrication can be a very high-yield measure in sedated patients.
Superficial corneal abrasions are treated with antibiotic ointment (ointment is preferred over eye drops as it acts as a lubricant). This is commonly erythromycin ointment and is used for up to 5 days. Local anesthetic drops should not be used routinely as they may impair corneal re-epithelialization. Eye patches should be considered only for larger, more severe abrasions.
If done improperly, the eye could be prevented from closing under the patch, further worsening the abrasion. Follow-up with an ophthalmologist is recommended prior to discharge from the hospital as persistent abrasions can progress to a corneal ulcer or lead to long-term complications such as corneal thinning and perforation. ICU and burn patients are at a high risk of developing Pseudomonas corneal ulcer; this should be prevented at all costs.
Once diagnosed there are surgical and medical management options, with the latter being the more likely in the critically ill patient. Cholinergic agents (e.g. pilocarpine) can be administered as eye drops. The resulting pupillary constriction helps open the drainage angle.
Other options for treatment are beta-adrenergic antagonists (e.g. timolol), carbonic anhydrase inhibitors and prostaglandin analogs (e.g. latanoprost). Care must be taken when prescribing these medications, because if absorbed systemically they may have detrimental effects, especially given the fragile physiology of the typical critically ill patient.
Ophthalmology consultation is required and management varies depending on the etiology and duration of the hemorrhage. This could range from observation to urgent surgery.
Retinal vascular occlusion
The crucial difference between the vein and artery occlusion is that the artery occlusion is an ophthalmological emergency, with damage to the retina occurring in a few hours. The vein occlusion requires no acute intervention.
Retinal tears and detachment
Most retinal tears or detachments will require some form of surgery to repair them, so involvement of an ophthalmologist will be essential.
Cavernous sinus thrombosis
Treatment for infectious causes should include broad-spectrum empiric antibiotics that cover most of the common pathogens. Blood cultures should be sent. Treatment should continue for 3 to 4 weeks. Anticoagulation using heparin should be considered for non-infectious causes. Early (within 7 days) heparinization has been shown to reduce morbidity rates in survivors and possibly mortality rates. The optimal duration of warfarin therapy is unknown, but 4 to 6 weeks has been recommended.
PRES (Posterior Reversible Encephalopathy Syndrome)
It is important to recognize this condition early as it is reversible if treated promptly. Irreversible brain damage has been reported to occur with delayed and/or incorrect treatment. Blood pressure control is the mainstay of treatment. Goals for blood pressure are varied but should aim for at least a 20%-25% reduction initially, with more gradual control thereafter.
Parenteral antihypertensives should be the preferred initial choice (e.g. nicardipine, labetalol or sodium nitroprusside). The advantages of these drugs are that they can be titrated to effect and if hypotension occurs, they can be discontinued.
Seizures should always be treated. Standard seizure therapy and drug monitoring can be used (e.g. benzodiazepines, phenytoin). Magnesium can be considered for pregnant or peripartum women with PRES.
It is important to realize that regardless of the severity of the presenting symptoms (coma, status epilepticus and blindness), with appropriate management full recovery is possible.
There is no specific prophylaxis or treatment for cortical blindness. Removal of any precipitating cause and control of hypertension if present are the main management issues. Some authors recommend aggressive intravenous hydration and corticosteroids for cortical blindness post cerebral angiography.
Corticosteroids are hypothesized to stabilize the blood-brain barrier, thus decreasing the amount of vasogenic edema. Usually the blindness starts to resolve within a few days of the inciting events; however, there are case reports of persistent visual problems associated with cognitive deficits.
5. Disease monitoring, follow-up and disposition
Special considerations for nursing and other allied health professionals
What's the evidence?
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