The clinical indications for ocular ultrasound are as follows:
Trauma is one of the leading causes of unilateral loss of vision in the United States and accounts for an estimated cost of $200 million per year.11 Vision-threatening injuries include retrobulbar hematoma, retinal detachment, lens dislocation, traumatic optic neuropathy, and globe injuries.12 The most common presentation for a vision-threatening injury is blindness after the injury. However, vision loss may occur gradually because of unrecognized trauma or the patient may not be able to report vision loss due to lid swelling or alteration in mental status. As a consequence, ocular injuries are often missed in these patients. A retrospective review of trauma patients with potential ocular injury demonstrated that nonophthalmologists frequently missed or underestimated potential eye trauma, diagnosing only 72% of eye injuries and referring only 27% for ophthalmologic evaluation.13
Significant swelling of the periorbital tissues can be encountered with midface or craniofacial fractures, injuries that increase the risk of concomitant ocular injury. One study found that of 283 patients presenting with facial fractures, 71 had an ocular injury, with 32 (12%) suffering a serious ocular injury.14 While it is ideal for all facial trauma patients with suspected eye injury to have an examination performed immediately by an ophthalmologist, this is commonly not feasible. There are often more serious and life-threatening injuries that require emergent evaluation and treatment.
Ocular ultrasound can be performed at the bedside. It is noninvasive, so there is little risk for exacerbating an injury when it is performed correctly. Ocular ultrasound is useful even when medication, drugs, or hypoxia alter pupillary function. This is important in the initial clinical assessment of the eye, where pupil size, reaction to light, and the presence or absence of a relative afferent papillary defect are assessed.12
Retrobulbar hemorrhage can be diagnosed clinically when a significant hematoma is present.15 However, this vision-threatening emergency often goes unrecognized, especially in trauma victims with a decreased level of consciousness, and delayed diagnosis may result in irreversible damage to the optic nerve. CT typically reveals stretching of the optic nerve and a tented posterior sclera. Retrobulbar hematoma may cause damage to the optic nerve either through direct compression leading to ischemia or through traction by propelling the globe forward and stretching the nerve. The hematoma occurs as a result of bleeding within or around the cone formed by the extraocular muscles. This cone of muscles combined with the bony orbit forms a compartment in which ongoing hemorrhage leads to elevated intraorbital pressure. As the pressure rises, compression of the ophthalmic and retinal vessels can occur, resulting in ischemia and ultimately blindness.12 Any potential injury must be treated rapidly because irreversible damage may occur after only 60 minutes of ischemia.16
An open globe injury is defined as a full thickness wound involving the corneoscleral wall of the eye. This type of injury is typically caused either by blunt force, particularly to the anterolateral part of the orbit, or due to laceration by a foreign body.12,17 While some open globe injuries are obvious with vitreous extrusion, a significant proportion are not readily apparent. Clues to an open globe injury include bloodstained tears, lid lacerations, presence of a significant subconjunctival hemorrhage, or hyphema. However, none of these are pathognomonic for globe rupture. Furthermore, in cases involving small high-velocity projectiles, there may be no external signs of perforation.12 Standard CT evaluation for open globe injury has been shown to have a sensitivity and specificity of 75% and 93%, respectively.18 Ultrasound sensitivity is similar to a standard CT scan. The best test for identifying globe injury is thin slice CT (2-mm) with reconstructions, which can identify subtle findings such as scleral discontinuity.
Thin slice CT is also the test of choice for intraocular foreign body localization.9 Ultrasound has limitations when used for the detection of intraocular foreign bodies. In animal models, the sensitivity and specificity were 87.5% and 95.8%, respectively.10 One study compared CT with ultrasound in a prospective study of patients with opaque intraocular foreign bodies. Ultrasound had complete concurrence with surgical or clinical follow-up in 90% of 61 cases. The study concluded that ultrasound was useful, even though CT was more accurate in detecting the intraocular foreign bodies, because ultrasound was superior to CT in demonstrating intraocular damage associated with the foreign bodies.
Acute change in vision is a fairly common complaint in emergency and acute care settings. Symptoms may include floaters, flashing lights, double vision, and even complete blindness. Although these symptoms may be indicative of nonocular problems, they require rapid attention to exclude such processes as lens dislocation, vitreous hemorrhage, retinal detachment, and vitreous detachment.
Lens dislocation is a condition frequently caused by blunt trauma. In a series of 71 consecutive patients presenting with ocular trauma, 12 were noted to have a lens dislocation.19 Lens dislocation can also occur without trauma and be idiopathic or hereditary (Marfan's syndrome). Ultrasound easily identifies the lens due to its anterior location. Using ultrasound, the clinician is able to evaluate the lens-supporting structures to determine whether the lens is subluxed or completely dislocated. Subtle lens subluxation can be a difficult diagnosis, even for experienced clinicians.
The incidence of spontaneous vitreous hemorrhage is about 7 cases per 100,000 people.20 Proliferative diabetic retinopathy, posterior vitreous detachment with or without a retinal tear, and retinal detachment are the most common causes. Symptoms of a spontaneous vitreous hemorrhage typically include floaters or clouded vision. Other symptoms such as flashes of light may be present, but these symptoms are usually due to the underlying cause of the hemorrhage, such as retinal detachment. As a vitreous hemorrhage ages, a membrane may form with attachments to the retina. When this membrane contracts, a retinal detachment may occur, usually weeks after the initial hemorrhage. Ultrasound allows for visualization of the hemorrhage as well as the potential cause. In fact, there is no other imaging modality that can reliably ascertain the anatomic position of the retina.20
Retinal detachments and retinal tears (Figure 19-1), which may be a precursor to detachment, are common causes of vitreous hemorrhage. Both represent a separation between the retinal sensory and the pigment layers. There are three types of retinal detachment: rhegmatogenous, tractional, and exudative. Most cases of rhegmatogenous retinal detachment are associated with a posterior vitreous separation; the detachment is caused by fluid seeping into a break in the sensory layer of the retina. Tractional retinal detachments occur when fibrous membranes in the vitreous pull the retina from the underlying retinal pigment epithelium, and they are typically seen with proliferative diabetic retinopathy or as a common sequela of aging. However, this condition is also associated with retinopathy of prematurity, sickle cell retinopathy, and prior vitreous hemorrhage. Exudative retinal detachment occurs with inflammatory, infectious, or neoplastic conditions that disturb the blood–retina barrier. This allows fluid to collect underneath the layers of the retina causing a separation. In most cases of retinal detachment, patients will complain of flashing lights, floaters, or a curtain-like vision loss.21 As the retinal tear progresses, retinal vessels may tear, producing a vitreous hemorrhage. This is a common association and is why patients with retinal detachments typically complain of floaters prior to the onset of peripheral or total vision loss.
Eye with retinal and posterior vitreous detachment.
Posterior vitreous detachment is a separation of the vitreous humor from the retina (Figure 19-1). The separation is painless and usually abrupt; patients complain of new floaters in conjunction with the onset of flashing lights. The clinical history can be similar to retinal detachment as patients with both problems complain of flashing lights at onset. This entity is a common presentation for acute visual change in the urgent care and emergency settings as it is a normal consequence of aging. The condition occurs often in older adults and over 75% of those greater than age 65 develop it.22 Vitreous detachment often has a benign clinical course that does not significantly threaten visual acuity; however, in approximately 15–30% of cases of vitreous detachment, a retinal hole is created that may lead to retinal detachment. Posterior vitreous detachment can also be associated with vitreous hemorrhage.23 Ultrasound is the modality of choice for evaluating the retina and vitreous. Ultrasound may be the only method for detecting posterior vitreous detachment and is also more accurate for identifying potential associated complications (retinal detachment or hemorrhage).
Headache, Head Trauma, or Altered Mental Status
Headache, head injury, and altered mental status are common presentations in the ED. These complaints may be associated with elevated intracranial pressure. While many modalities are available to evaluate potential elevated intracranial pressure, each has significant limitations. In the acute trauma patient, evaluating the presence of papilledema with an ophthalmoscope is difficult. Furthermore, papilledema can take hours to develop. CT is the most common initial diagnostic modality, but it may be unavailable or obtained early in the patients course before elevated intracranial pressure develops. When unstable patients are taken directly to the operating room for abdominal injuries, there may not be time for a head CT. In these patients, ocular ultrasound can provide a method for grossly assessing the intracranial pressure. In addition, multiple examinations can be readily performed on the same patient with an evolving clinical picture.
A direct communication between the subarachnoid space of the ventricles and the optic nerve sheath has been described in cadavers and an animal model. In an experimental model using rhesus monkeys, change in the optic nerve sheath diameter in response to changing intracranial pressure was demonstrated by varying the pressure in balloons placed in the subarachnoid space.24 Multiple clinical studies have demonstrated this effect in actual patients. One study comparing CT to ultrasound measurement of the optic nerve sheath diameter in patients with suspected intracranial hemorrhage showed a sensitivity and specificity of 100% and 95%, respectively.25 This procedure has also been described in pediatric patients.26