In 1845, Buys Ballot verified Doppler's theory by borrowing a locomotive and having a trumpet player stand on the moving train, while an observer who had perfect pitch stood at the station. It was found that indeed the trumpet's pitch was half a note higher on approach to the stationary listener in comparison with when the trumpet player was stationary and half a note lower when moving away from the stationary observer.³

Doppler's equation is as follows:

V = (D_f × c)/(2F_o × cos A)

where V = velocity (blood flow velocity in this application), D_f = Doppler frequency shift or incidence frequency minus reflected frequency. In CDI, it is frequency of ultrasound emitted by transducer minus frequency returning to transducer after reflection off moving erythrocytes, c = speed of sound in tissue, F_o = frequency of the source (frequency of the ultrasound waves emitted from the transducer), and A = angle of incidence of ultrasound beam to the direction of blood flow. Maximum Doppler shift occurs when A = 0 degrees. This angle (A) is a source of significant error in measuring blood flow velocity if the angle used in measurement is greater than 45 degrees. Furthermore, as the angle (A) approaches 90 degrees, it becomes difficult to differentiate forward from reverse flow, and both may be detected and averaged. A also must be controlled to create reproducible results.

Scans are made through the eye and orbit in multiple planes to identify the desired structures and vessels. After the desired vessel is located and the angle of incidence selected, a few seconds of Doppler waveform are recorded. Several measurements are recorded for each vessel. The peak and trough of the frequency waveform are selected by the operator by visual inspection, and the instrument then calculates the flow velocities from these frequency shifts. The system analyzes a sample of pulsed Doppler signal from within a small sample volume (0.2 × 0.2 mm) to calculate blood flow velocities, correcting for the angle of incidence in the calculation. In each vessel examined, the peak systolic and end diastolic velocities can be determined, as well as the average velocity.

Another parameter calculated from CDI is pulsatility index, which is a measure of impedance or total resistance to flow from all factors. Arterial wall musculature is thought to account for most of the impedance. A number of different pulsatility indices have been developed. One commonly used with CDI is Gosling's pulsatility index, which is calculated using the equation:

pulsatility index = (peak systolic velocity - end diastolic velocity)/average velocity

Another is Resistive index or Pourcelot's ratio, which is calculated as follows:

resistive index = (peak systolic velocity - end diastolic velocity)/peak systolic velocity

These ratios are reported from 0 to 1 or from 0% to 100%, with 0 denoting no resistance and 1 or 100% meaning maximum resistance.

In addition to graphically displaying the frequency waveforms, CDI also displays a gray-scale 2D ultrasound image of the tissues and vessels. Normal orbital structures are well delineated ultrasonically with this equipment, including the globe, optic nerve, extraocular muscles, and orbital blood vessels. Intraocular structures also may be appreciated with this technique, including anterior chamber, lens, and vitreous cavity. Superimposed on this 2D display is the color-encoded Doppler shift. The color display allows for detection of blood flow below the resolution of the gray-scale image in the vessels. The color display and waveform distinguish and separately evaluate adjacent vessels, such as the central retinal artery and central retinal vein, which lie in close proximity within the optic nerve (Fig. 2). Colors may be arbitrarily assigned, but often red is used to designate flow toward the transducer and blue to designate flow away from the transducer. When the orbital vessels are examined through the closed lids, the ultrasound beam is nearly parallel to the vessels, and thus arterial flow is red and venous flow is blue. Arteries and veins also are differentiated ultrasonically by the pulsatile nature of flow in arteries in contrast to the more-continuous, less-dynamic flow in veins.

One of the limitations of CDI is that this technology measures blood velocity and not blood flow. The relationship between velocity and volumetric flow is described mathematically as follows:

Q = V × π(r²)

where Q = flow, V = velocity, r = radius, and π(r²) is the cross-sectional area of the vessel. It is difficult ultrasonically to reliably determine vessel cross-sectional area for small vessels; hence, we are interpreting velocity values and not blood flow values. For flow to remain constant at an area of vessel stenosis, the velocity of the blood cells must proportionally increase. Because imaging at an area of vessel stenosis may reveal an erroneously high velocity, one must interpret results of CDI with caution in regard to speculating on blood flow and ultimately tissue perfusion.

Orbital vessels commonly imaged using CDI include the ophthalmic artery, central retinal artery and vein, superior ophthalmic vein, and short posterior ciliary arteries. Generally, the ultrasonographer starts by identifying the optic nerve. The ophthalmic artery, the largest artery in the orbit, can be found superomedial to the optic nerve in the anterior orbit in approximately 85% of individuals.^4,5 The velocity waveform of the ophthalmic artery shows a high and steep peak systolic value with a rapid decrease to a low-end diastolic velocity (Fig. 4). Often a dicrotic notch, which corresponds to aortic valve closure, is seen dividing the diastole waveform. Using the standard color-coding convention, the flow appears red as it is approaching the transducer. Normal velocities are compiled from several sources and are listed in Table 1.^6–11

TABLE ONE. Normal Orbital Color Doppler Parameters*

The central retinal artery can be found most easily within the optic nerve for approximately 12 mm behind the globe, where it runs a fairly straight course. It usually is located nasal to the adjacent central retinal vein. The transducer can be positioned so that central retinal artery flow is red and central retinal vein flow is blue. The velocity waveform of the central retinal artery is similar to but less steep than that of the ophthalmic artery (see Fig. 4). Blood flow through the central retinal artery can be affected by elevated intraocular pressure. Thus, it is important for the examiner to not exert excessive pressure on the globe with the transducer.

The central retinal vein, temporal to the central retinal artery within the optic nerve, has a much smoother waveform than that of the arteries; however, there is some pulsatility (see Fig. 4). A value called venous pulsatility index has been described¹² as follows:

venous pulsatility index = (Vmax - Vmin)/Vmax

where V = velocity (determined from the waveform). Unlike the pulsatility index and resistive index calculated for arteries, this venous pulsatility index does not provide a measure of vessel wall muscular resistance, since venous walls are not muscular. Instead, this value represents the increase in velocity of blood flow within the vein as a result of the pulsations of an artery in close proximity.

The posterior ciliary arteries often are more difficult to image. They can be found 10 to 20 mm behind the globe surrounding the optic nerve and are variable in number. The long posterior ciliary arteries may be seen entering the globe adjacent to the ciliary body with the aid of a gelatin standoff device placed between the globe and transducer. The waveforms are similar to that of the central retinal artery but may be less pulsatile (see Fig. 4). The reproducibility of velocity values for the posterior ciliary arteries is poorer than that for the previously discussed arteries because these are small vessels that can be difficult to locate and to determine how many are being imaged simultaneously. In addition, they may be tortuous, particularly in the posterior orbit, where they may be imaged as they bend back on themselves, thus changing the measured velocity values.

The superior ophthalmic vein lies above the optic nerve in the mid-orbit. The flow pattern and direction of flow are variable within this vessel. Usually there is a low-flow, continuous waveform that may show some fluctuation with the respiratory cycle. This vessel can be difficult to locate but is reported to be found in approximately 90% of normal orbits.^2,13 Asking the patient to perform a Valsalva maneuver may help to enlarge the vessel for easier location but also may reverse the flow in the vein to make it appear arterial (i.e., red color coming toward the transducer).

CENTRAL RETINAL ARTERY OCCLUSION AND AMAUROSIS FUGAX

One sight-threatening condition whose various etiologies have been better delineated by CDI is central retinal artery occlusion. Sergott and colleagues¹⁷ reported using CDI to assess orbital blood flow in patients with amaurosis fugax and central retinal artery occlusion. A number of ocular findings observed using CDI explained the visual changes in these patients, including ophthalmic artery stenosis, retrobulbar central retinal artery embolus (Fig. 5) and ocular ischemic syndrome, which is demonstrated by reversal of blood flow in the ophthalmic artery, and carotid ultrasonography showing a total occlusion of the ipsilateral internal carotid artery. Without the information gained from CDI, these patients would have been labeled with diagnoses of central retinal artery occlusion or amaurosis fugax without the exact mechanism of the visual loss being understood. This additional information allows physicians to tailor treatment specifically for these patients to prevent other morbidity.

A case report by Knapp and coworkers¹⁸ describes a patient with amaurosis fugax occurring only when the eye was abducted. Computed tomography revealed an intraconal mass, and CDI was used to confirm that the mass was the cause of the amaurosis by demonstrating a reduction of blood flow in the central retinal artery when the eye was abducted. This allowed the surgeon to feel confident that the mass was the cause of the visual obscurations and that the eye's vascular supply was likely not compromised in some other way.

CAROTID OCCLUSIVE DISEASE AND OCULAR ISCHEMIC SYNDROME

Hemodynamically significant carotid artery stenosis can lead to the ocular ischemic syndrome, amaurosis fugax, or central retinal artery occlusion.

Mawn and coworkers¹⁹ examined a group of 24 patients with greater than 75% carotid artery stenosis and found reduced mean central retinal artery and posterior ciliary artery systolic velocities as compared with normal patients. Half of these 24 patients had reversal of flow in the ophthalmic artery. Twelve patients underwent carotid endarterectomy, and their mean systolic flow velocities improved after surgery in the central retinal artery, posterior ciliary arteries, and ophthalmic artery. The patients with ocular ischemic syndrome had CDI parameters no different from patients with severe carotid artery stenosis without signs of ocular ischemic syndrome. These findings were consistent with those of Ho and associates²⁰ regarding patients with ocular ischemic syndrome.

Hu and associates²¹ went a step further and stated that there is a statistically significant difference in mean peak systolic and end diastolic velocities in the central retinal artery and ophthalmic artery among patients with varying degrees of carotid artery stenosis. These values, however, were not compared with those of normal patients.

Ho and coworkers²⁰ describe the use of CDI in the ocular ischemic syndrome. This series examines 16 eyes with ocular ischemic syndrome and shows reduced peak systolic velocities as well as increased vascular resistance in the central retinal artery and posterior ciliary arteries. Twelve of 16 eyes had reversal of ophthalmic artery blood flow (Fig. 6). This finding was thought to be quite specific for ocular ischemic syndrome by the authors, who had seen this phenomenon in multiple cases of ocular ischemic syndrome with associated internal carotid artery stenosis and only in one case of giant cell arteritis and once in an ophthalmic artery occlusion as a late development. It also was observed that the eyes in the study population with the worst visual acuity had no detectable posterior ciliary artery blood flow.

GIANT CELL ARTERITIS

Ho and coworkers²² present a consecutive series of 22 patients with biopsy-proven giant cell arteritis and appropriately matched control subjects. The patients with giant cell arteritis had reduced mean flow velocities in the central retinal artery and posterior ciliary arteries. Other findings included ophthalmic artery aliasing (turbulent high-velocity flow at focal areas of vessel stenosis) and, in one case, reversal of flow in the ophthalmic artery. Nine affected eyes demonstrated no detectable flow in the short posterior ciliary arteries. Williamson and colleagues²³ also render a case of giant cell arteritis in which the patient had anterior ischemic optic neuropathy. CDI demonstrated no flow in the posterior ciliary arteries and later, as the condition clinically worsened, no flow in the ophthalmic artery.

CAROTID-CAVERNOUS FISTULA

Another condition in which CDI has helped significantly in both diagnosis and monitoring is carotid-cavernous fistula. In this condition, there is a communication between the cavernous sinus and either the internal carotid artery or dural branches of the internal or external carotid artery. This can lead to arterialization of the orbital and conjunctival veins because of elevated pressure in the area of the cavernous sinus.

CDI in this condition frequently shows a dilated superior ophthalmic vein with a pulsatile, arterialized pattern of blood flow (Fig. 7). The flow velocity in the superior ophthalmic vein is increased, while the flow velocity in the ophthalmic artery may be decreased. The 2D ultrasound portion of this examination may highlight other features found in carotid-cavernous fistulas, such as enlargement of engorged extraocular muscles.

Flaharty and associates²⁴ reported the use of CDI in three patients with carotid-cavernous or dural-cavernous fistulas. All three patients had dilated superior ophthalmic veins with arterialized flow patterns. CDI was useful in the diagnosis of these patients, but more important, CDI provided a noninvasive means of following vascular parameters in both treated and untreated patients.

In a report in the ultrasound literature of a traumatic carotid-cavernous fistula, CDI showed dilation of both the superior and inferior ophthalmic veins.²⁵

GLAUCOMA

Color Doppler imaging has been used in a number of studies to evaluate the optic nerve blood flow in patients with glaucoma.^7,26–29 Some theories regarding the etiology of glaucoma, in particular normal-tension glaucoma, propose a vascular abnormality, either as a result of vasospasm or otherwise altered hemodynamics. Harris and associates²⁹ showed that patients with normal-tension glaucoma had significantly lower end diastolic velocities and elevated resistive indices in a number of orbital vessels compared with those of control subjects. This result was shown to be responsive to vasodilation by inspiring carbon dioxide.

CDI also has been used to evaluate the effects of intraocular pressure-lowering agents on the blood flow in the surrounding vasculature.^27,28 In one such study, Mansberger and associates²⁸ examined the acute effect of apraclonidine on orbital hemodynamics and found no significant change except for a questionable difference in end diastolic velocity in the medial posterior ciliary artery. A similar evaluation tested the effects of timolol on orbital blood flow.²⁷ Although the study did not make any breakthroughs in the treatment of glaucoma, the authors did believe that this mechanism of evaluation using CDI was suitable for such a study.

In addition to using CDI to evaluate patients with normal-tension glaucoma and the drugs used to treat them, CDI has been used to look at glaucoma surgery outcomes. Trible and coworkers²⁶ used CDI to evaluate hemodynamics before and at several intervals after trabeculectomy. A significant increase in end diastolic velocity and a decrease in vascular resistance were found after surgery in the central retinal artery and posterior ciliary arteries, suggesting increased blood flow in those vessels.

With the mechanisms of glaucoma still so poorly understood, CDI may play a role in studying the possible hemodynamic etiology of the disease, as well as in evaluating the effects of various medical and surgical therapies.

ORBITAL LESIONS

Many types of orbital lesions have been evaluated using CDI, such as orbital varices, tumors, arteriovenous malformations, and capillary and cavernous hemangiomas.^13,30–32

Lieb and associates³¹ reported a case of a clinically suspected orbital varix that was examined with CDI. No vascular abnormalities were noted in the orbit until the patient performed a Valsalva maneuver. Then an area of vasculature expanded, showing flow toward the transducer. As the patient exhaled, the direction of flow reversed and the lesion became smaller. The optic nerve was displaced by the varix when it was at maximum dilation. Lesions of this type may be missed by computed tomography and magnetic resonance imaging unless the patient performs a Valsalva maneuver during the scan, which often is difficult because of the length of time required to complete the scan.

Another report in the literature using CDI shows a dilated and thrombosed superior ophthalmic vein in a patient with orbital cellulitis.³⁰ There was reversal of flow in the anterior orbital veins with shunting of blood to the contralateral superior ophthalmic vein. This level of detailed understanding of hemodynamics is not possible with static imaging techniques.

INTRAOCULAR TUMORS

A number of authors have described the use of CDI in evaluating intraocular tumors.^13,32–35 Lieb and associates³⁵ examined 44 intraocular masses with CDI and found that 92.8% of 28 untreated choroidal melanomas had detectable Doppler shifts. Patients whose melanomas had been treated with brachytherapy showed significantly lower maximum systolic Doppler shifts than did those with the untreated masses. Finally, in four choroidal hemangiomas, high systolic and diastolic Doppler shifts were observed, which is consistent with the histology of these lesions consisting of vascular networks. Three masses consisting of subretinal hemorrhage and simulating tumors showed no intrinsic Doppler shifts but were noted to have blood flow at their bases.

Guthoff and colleagues³⁴ found similar results. Forty-one of 42 choroidal melanomas produced detectable Doppler shifts. The one tumor that did not show detectable Doppler shift was very small. The peak and time-averaged velocities did not correlate statistically with tumor volume. Doppler shift also was determined in the 23 tumors that received brachytherapy. At 2 to 3 days after plaque removal, average velocities were increased compared with pretreatment values. However, at 2 to 10 months after treatment, there was a reduction in detectable Doppler shift in six of seven patients.

Wolff-Korman and associates³³ compared Doppler shift in 62 choroidal melanomas, 12 choroidal metastases, 18 choroidal nevi, two choroidal osteomas, and nine age-related macular degeneration lesions. All 62 melanomas showed Doppler shift. The 12 choroidal metastases showed significantly higher blood flow than did the melanomas. No Doppler shifts were found in the choroidal nevi, osteomas, or macular degeneration lesions.

Jain and associates³² made an attempt to characterize the blood flow patterns as seen by CDI in various choroidal lesions. Two choroidal melanomas showed no intratumoral Doppler shift but did have flow at the base of the tumor. One choroidal metastasis had blood flow demonstrated around but not within the lesion. This number of patients, however, is too small to make generalizations about the characteristic flow in the various types of lesions.

This Doppler information may be helpful in cases in which the mass cannot be observed directly because visibility through the ocular media is poor secondary to cataract, vitreous hemorrhage, or corneal opacity.

PSEUDOTUMOR CEREBRI

Mittra and associates³⁶ used CDI to evaluate blood flow parameters in 24 eyes with pseudotumor cerebri and chronic papilledema before and after optic nerve sheath decompression. Before surgery, blood flow velocities in the central retinal artery, posterior ciliary arteries, and ophthalmic artery were decreased compared with those of normal subjects. Patients with worse visual acuity had worse parameters. Thirteen eyes had improved visual acuity after surgery and showed improved CDI parameters for the posterior ciliary arteries and ophthalmic artery but no change in central retinal artery parameters. The eyes that worsened or remained stable after surgery showed no significant changes in CDI parameters.

CENTRAL RETINAL VEIN OCCLUSION

Williamson and coworkers³⁷ used CDI to evaluate 85 eyes with central retinal vein occlusion. Blood flow velocity was reduced in the central retinal vein and artery of eyes with central retinal vein occlusion. Eyes with ischemic vein occlusions had lower flow velocity in the central retinal vein than did nonischemic eyes. There was no correlation between degree of ischemia and central retinal artery parameters. More important, the risk of iris neovascularization was predictable from CDI evaluation within 3 months of onset of the vein occlusion. The minimum velocity in the central retinal vein was significantly lower in eyes that went on to develop iris neovascularization compared with eyes that did not develop neovascularization. The predictive values were high with a sensitivity of 75% and a specificity of 86%.

ACUTE RETINAL NECROSIS

Regillo and coworkers³⁸ used CDI to examine the orbital blood flow in 10 patients with unilateral acute retinal necrosis syndrome, with the unaffected eye used as a control. Flow velocity in the involved eye's central retinal artery was reduced significantly compared with the control eye, while flow velocities in the ophthalmic artery and posterior ciliary arteries were not reduced significantly. Fluorescein angiography and histopathologic analysis in this disease have demonstrated retinal capillary nonperfusion as well as patchy choroidal ischemia from vasculitis of the vessels supplying these areas, along with the vessels supplying the optic nerve. Many mechanisms are proposed to explain the decrease in central retinal artery blood flow velocity, including increased vascular resistance from the retinal necrosis or from destruction of small vessels by the infection or inflammatory response, or optic nerve head swelling mechanically compressing the central retinal artery. Patients with acute retinal necrosis may have a swollen optic disc that is then followed by optic atrophy, which is reminiscent of the disc appearance in the stages of anterior ischemic optic neuropathy. In fact, one patient in this series underwent optic nerve sheath decompression, which resulted in normalization of central retinal artery flow on CDI examination after surgery. The clinical significance of these findings is as yet unknown.

CDI AFTER SCLERAL BUCKLE

Regillo and associates³⁹ examined six patients using CDI both before and after a scleral buckling procedure for retinal detachment, using the fellow eye as a control. They found a significant decrease (53%) in mean central retinal artery blood flow velocity after surgery with no change in ophthalmic artery flow velocity. However, four of six patients returned many months after surgery for repeat CDI, and all demonstrated normalization of central retinal artery flow velocity in the operated eye. All six patients' visual acuities returned to within two lines of their predetachment acuities despite a transient decrease of as much as 53% of central retinal artery flow velocity. There was no clinical evidence of anterior or posterior segment ischemia in these patients.

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