- •Ocular Blood Flow
- •Contents
- •1: Anatomy of the Ocular Vasculatures
- •Core Messages
- •1.1 Limbus and Conjunctiva
- •1.1.1 Cornea
- •1.1.2 Vasculature Distribution in the Anterior Segment
- •1.1.3 The Conjunctiva
- •1.1.3.1 The Conjunctival Arterial Supply
- •1.1.3.2 The Conjunctival Veins
- •1.2 Uveal Tract
- •1.2.1 The Iris
- •1.2.1.1 The Major Arterial Circle of the Iris
- •1.2.2 Ciliary Body and Processes
- •1.2.3 Choroid and Suprachoroid
- •1.2.3.1 Development of the Choroidal Vasculature
- •1.2.3.2 Arteries
- •1.2.3.3 Choroidal Veins (Vortex Veins)
- •1.2.3.4 Choriocapillaris
- •1.3 Optic Nerve Vasculature
- •1.4 Retina
- •1.4.1 Development of the Retinal Vasculature
- •1.4.2 Adult Retinal Vasculature
- •1.4.3 Nonprimate Adult Retinal Vasculatures
- •1.5 Conclusions
- •References
- •Core Messages
- •2.1 Introduction
- •2.3 Stochastic Error in the Entrapment of Microspheres
- •2.4 Methodological Errors and Practical Advice
- •2.4.1 Size of the Microspheres
- •2.4.2 Physical Characteristics of Microspheres
- •2.4.4 Dissection
- •2.4.5 Detection of RM and NAM
- •2.4.6 Detection of CM and FM
- •2.5 Biological Variation
- •2.5.1 Blood Pressure
- •2.5.3 Arterial Blood Gases
- •2.5.4 Other Possible Causes for Biological Variability
- •2.6 Summary for the Clinician
- •References
- •3: Laser Doppler Flowmetry in Animals
- •Core Messages
- •3.1 Introduction
- •3.2 History
- •3.3 Theory
- •3.4 Validation
- •3.5 Calibration
- •3.6 Zero Offset
- •3.7 Effects of Oxygen
- •3.9 Measurement Depth and Sampling Volume
- •3.10 Caveats
- •References
- •4: Oxygen Measurements in Animals
- •Core Messages
- •4.1 Introduction
- •4.2.1 Oxygen Electrodes
- •4.2.2 Hypoxyprobe
- •4.2.3 Magnetic Resonance Imaging
- •4.2.4 Phosphorescence Decay
- •4.2.5 Oximetry
- •4.3.1 Vitreal Oxygen
- •4.3.2 Intraretinal Oxygen
- •4.4 Oxygen in Avascular Retinas
- •4.5 Analysis of Retinal Oxygen Utilization
- •4.5.1 Fick Principle Analyses
- •4.5.4 Other Diffusion Models
- •4.6 Physiological Variations in Retinal Oxygen
- •4.6.1 Light
- •4.6.2 Hypoxia
- •4.6.3 Hyperoxia
- •4.6.4 Hypercapnia
- •4.7 Pathophysiology and Retinal Oxygen
- •4.7.1 Vascular Occlusion
- •4.7.2 Diabetes
- •4.7.3 Retinal Detachment
- •4.7.4 Retinal Degenerative Diseases
- •4.7.5 Retinopathy of Prematurity
- •4.8 Retinal Molecular Changes Related to Oxygen
- •4.9 Oxygen in the Optic Nerve Head
- •References
- •Core Messages
- •5.1 Measuring Technique
- •5.2 Normal Values
- •5.3 Retinal Pathologies
- •5.3.1 Diabetes Mellitus
- •5.3.2 Central Retinal Vein Occlusion
- •5.4 Summary
- •References
- •Core Messages
- •6.1 Introduction
- •6.1.1 Anatomy
- •6.3 Vessel Diameter Measurements Based on Photographic and Digitally Stored Images
- •6.3.1 Basics for Measurements on Stored Images
- •6.3.1.1 Measuring Principle
- •6.3.1.4 Problems and Measuring Errors
- •6.3.1.5 Physiological Variability of Vessel Diameter
- •6.3.2 Methods
- •6.3.2.2 Microdensitometry Based on Photographic Negatives
- •6.3.2.3 Measurements Based on Digital Images
- •6.4 Diameter Assessment for Blood Flow
- •6.4.1 Assessment of Flow by Use of Doppler Technique (CLBF)
- •6.5 Retinal Vessel Analysis
- •6.5.1 Basics of Retinal Vessel Analysis
- •6.5.2 Static Vessel Analysis
- •6.5.3 Results and Limits of Static Vessel Analysis
- •6.5.4 Results and Limits of Dynamic Vessel Analysis
- •6.5.4.1 Stimulation with Flicker Light
- •6.5.4.2 Other Provocation Tests
- •6.5.5 Systems Available for Dynamic Vessel Analysis
- •6.6 Further Perspectives
- •References
- •Core Messages
- •7.1 Introduction
- •7.2 Retinal Laser Doppler Velocimetry
- •7.2.1 The Doppler Effect
- •7.2.2 Electric Field Scattered by Singly Scattering Particles Moving in a Capillary Tube
- •7.2.5 Experimental Test of the Bidirectional LDV Technique
- •7.2.7 The DSPS for RBCs Moving in a Retinal Vessel
- •7.2.7.1 Multiple Scattering of Blood
- •7.2.7.2 DSPS from RBCs Flowing in a Glass Capillary Tube
- •7.2.7.3 DSPS from Human Retinal Vessels
- •7.2.7.4 Exploring the Scattering Process
- •7.2.9 Instrumentation
- •7.2.10 Blood Flow in Retinal Vessels
- •7.2.12 Limitations, Safety, and Future Directions of the LDV Technique
- •7.2.13 Physiologic and Clinical Applications (Brief Overview)
- •7.3.1 The DSPS for RBCs Moving in the Microvascular Bed of a Tissue
- •7.3.2 Hemodynamic Parameters Derived from the DSPS
- •7.3.3 Detection Scheme for Optic Nerve and Subfoveal Choroidal Blood Flow
- •7.3.4 Critical Questions Regarding the Application of LDF to Ocular Blood Flow
- •7.3.4.1 LDF Sample Volume
- •7.3.4.2 Linearity of LDF
- •7.3.4.3 Scattering Scheme
- •7.3.5 Reproducibility of LDF
- •7.3.6 Applications of LDF
- •7.4 Summary for the Clinician
- •References
- •8: Color Doppler Imaging
- •Core Messages
- •8.1 Principles
- •8.2 Instrumentation
- •8.3 Procedure
- •8.4 Outcome Variables
- •8.5 Reproducibility
- •8.6 Physiological and Pharmacological Stimuli
- •8.7 Results in Patients with Disease
- •8.8 Advantages and Limitations
- •References
- •9: Other Approaches
- •Core Messages
- •9.1 Blue Field Entoptic Technique
- •9.1.1 Laser Speckle Technique
- •9.1.2 Pulsatile Ocular Blood Flow
- •9.1.2.1 Laser Interferometry
- •References
- •10: Systemic Determinants
- •Core Messages
- •10.1 Introduction
- •10.1.1 Ocular and Systemic Blood Flow
- •10.2 Local Skin Cooling Effect
- •10.2.1 Choroidal Blood Flow
- •10.2.2 Retinal Blood Flow
- •10.3 Aerobic Exercise
- •10.3.1 Choroidal Blood Flow
- •10.3.2 Macular Blood Flow
- •10.3.3 Retinal Blood Flow
- •10.4 Neural Activation
- •10.4.1 Valsalva Maneuver
- •10.4.2 Nicotine
- •10.5 Blood Pressure Versus Ocular Perfusion Pressure
- •10.5.1 Increased Ocular Perfusion Pressure
- •10.5.1.1 Choroidal Blood Flow
- •10.5.2 Decreased Ocular Perfusion Pressure
- •10.5.2.1 Choroidal Blood Flow
- •10.5.2.2 Optic Nerve Head Blood Flow
- •10.5.3 Neural Retinal Function
- •10.6 Blood Gases
- •10.6.1 Hyperoxia and Blood Flow
- •10.6.3 Hypoxia and Pulsatile Choroidal Blood Flow
- •10.6.4 Hyperoxia, Hypercapnia, and Retinal Function
- •10.6.5 Hypoxia, Hyperoxia, and Retinal Function
- •10.7 Regional Choroidal Perfusion
- •10.7.1 Cones Versus Rods: Structure and Function
- •10.7.2 Choroidal Angioarchitecture
- •10.7.3 Dark Adaptation
- •10.7.4 Protracted Blue Flicker
- •10.8 Aging
- •10.8.1 Structure
- •10.8.2 Blood Flow
- •10.8.3 Retinal Function
- •References
- •11: Local Determinants
- •Core Messages
- •11.1 Introduction
- •11.2 Ocular Perfusion Pressure, IOP, and the Ocular Starling Resistor Effect
- •11.3 Types of Local Control
- •11.3.1 Myogenic Local Control
- •11.3.2 Metabolic Local Control
- •11.3.3 Flow-Mediated Vasodilation
- •11.3.4 Flow Control by Intercellular Conduction
- •11.4 Ocular Local Control
- •11.4.1 Optic Nerve Head (ONH)
- •11.4.2 Choroid
- •11.4.3 Retina
- •11.4.4 Ciliary Body
- •11.4.5 Iris
- •11.5 Caveats
- •11.6 Summary for the Clinician
- •References
- •12: Neural Control of Ocular Blood Flow
- •Core Messages
- •12.1 Overview of Ocular Blood Supplies and Their Neural Control
- •12.2 Neural Control of Optic Nerve and Retinal Blood Flow
- •12.3 Neural Control of Iridial and Ciliary Body Blood Flow
- •12.4 Neural Control of Blood Flow in Orbital Glands
- •12.5 Neural Control of Choroidal Blood Flow
- •12.5.1 Importance of the Choroid
- •12.5.2 Choroidal Innervation: Overview of Anatomy
- •12.5.3 Facial Nucleus Parasympathetic Input
- •12.5.3.4 Choroidal Autoregulation and the PPG Input to Choroid – Mammals
- •12.5.3.8 Choroidal Autoregulation and the PPG Input to Choroid – Birds
- •12.5.4 Oculomotor Nucleus Parasympathetic Input
- •12.5.4.1 Ciliary Ganglion Circuitry – Mammals
- •12.5.4.2 Function of the EW-Ciliary Ganglion Circuit – Mammals
- •12.5.4.3 Ciliary Ganglion Circuitry – Birds
- •12.5.4.4 Function of vSCN-EWM-Ciliary Ganglion Circuit – Birds
- •12.5.5 Sympathetic Superior Cervical Ganglion Input
- •12.5.6 Trigeminal Sensory Input
- •12.5.7 Intrinsic Choroidal Neurons
- •12.5.8 Disturbed Neural Control of Choroidal Blood Flow in Aging and Retinal Disease
- •12.5.8.1 Effect of Aging on Retina and Choroid
- •12.5.8.2 Effect of Disease on Retina and Choroid
- •References
- •13: Endothelial and Adrenergic Control
- •Core Messages
- •13.1 Nitric Oxide
- •13.2 Endothelins
- •13.3 Arachidonic Acid Metabolites
- •13.4 Adrenergic Control
- •13.5 Alpha Receptors
- •13.6 Topical Administration
- •13.6.1 Clonidine
- •13.6.2 Brimonidine
- •13.6.3 Beta Receptors
- •13.6.4 Timolol
- •13.6.5 Human Studies
- •13.6.6 Betaxolol
- •13.6.7 Human Studies
- •13.6.8 Levobunolol
- •13.6.9 Carteolol
- •13.6.10 Serotonin
- •13.7 Carbonic Anhydrase Inhibitors
- •13.8 Acetazolamide
- •13.9 Dorzolamide
- •13.10 Retrobulbar Blood Flow
- •13.11 Retinal Blood Flow
- •13.12 Choroidal and Optic Nerve Head Blood Flow
- •13.13 Brinzolamide
- •References
- •Core Messages
- •14.1 Introduction
- •14.2 Retinal Ischemia Basic Mechanisms
- •14.3 Oxidative Stress
- •14.6 Animal Studies Relating Ischemia, Glaucoma, and Neuroprotection
- •14.6.1 Retinal Ischemia
- •14.6.6 Role of Mitochondria (Fig. 14.6)
- •References
- •Core Messages
- •15.1 Introduction
- •15.2 Retinal Blood Flow in Diabetes
- •15.3 Retinal Hypoperfusion
- •15.3.1 Mechanisms of Hypoperfusion
- •15.3.1.1 Glycaemic Control
- •15.3.1.2 Protein Kinase C
- •15.3.1.3 Ion Channel Dysfunction
- •15.4 Retinal Hyperperfusion
- •15.4.1 Mechanisms of Hyperperfusion: A Link to Hypoperfusion, Tissue Hypoxia and Retinal Leukostasis?
- •15.4.2 Retinal Autoregulation in Diabetes
- •15.5.1 Basement Membrane Thickening
- •15.5.3 Microaneurysms
- •15.5.4 Capillary Acellularity
- •15.6 Retinal Blood Flow and Vision Loss in Diabetic Retinopathy
- •15.6.1 Diabetic Macular Oedema
- •15.6.2 Proliferative Diabetic Retinopathy
- •15.7 Conclusions
- •15.8 Summary for the Clinician
- •References
- •Core Messages
- •16.1 Introduction
- •16.2 Choroidal Blood Flow
- •16.3 Systemic Vascular Factors and AMD
- •16.5 Choroidal Hemodynamic Changes in AMD
- •16.5.1 Choroidal Histopathological Vascular Changes in AMD
- •16.5.1.1 Choriocapillaris and Bruch’s Membrane in Aging and AMD
- •16.5.2 Choroidal Microcirculation in AMD
- •16.5.2.2 Choroidal Watershed Zones and Neovascularization
- •16.5.2.3 Laser Doppler Flowmetry Evaluation
- •References
- •Core Messages
- •17.1 Introduction
- •17.2 Potential Mechanisms of Ischaemic Damage in Glaucoma
- •17.2.2 Autoregulatory Disturbances
- •17.2.3 Mechanical Compression or Collapse of Vessels
- •17.2.4 Atherosclerosis
- •17.2.5 Vascular Endothelial Factors
- •17.2.6 Barriers to Nutrient Delivery
- •17.2.7 Circulating Vasoconstrictors
- •17.3 Evidence Base Supporting the Importance of Ischaemia in Glaucoma
- •17.3.1 Association and Causality
- •17.3.1.1 Reduction in Optic Nerve Head Blood Flow
- •17.3.1.2 Blood Pressure, Intraocular Pressure and Perfusion Pressure
- •17.3.1.3 Nocturnal Hypotension
- •17.3.1.4 Vasospasm
- •17.3.1.5 Endothelin and Other Circulating Peptides
- •17.3.2 Effects of Treatment
- •17.3.2.1 Calcium Channel Blockers
- •17.3.2.2 Topical Adrenergic Antagonists
- •17.3.2.4 Prostaglandin Analogues
- •17.4 Experimental Models of Ischaemia Relating to Glaucoma
- •17.4.1 Acute Ischaemia
- •17.4.2 Chronic Ischaemia
- •17.5 Summary
- •17.5.1 Diversity of Evidence
- •17.5.2 Evidence Base Compared to Intraocular Pressure
- •17.5.3 Requirements to Strengthen Evidence Base
- •References
- •Core Messages
- •18.1 Retinal Diseases
- •18.2 Uveitis
- •18.3 Optic Nerve Disorders
- •18.4 Systemic Diseases
- •References
- •Core Messages
- •19.1 Atherosclerosis
- •19.1.1 Pathogenesis of Atherosclerosis
- •19.1.2 Internal Carotid Artery Disease (ICA)
- •19.1.3 Effects on the Ocular Circulation
- •19.1.3.1 Retinal Artery Occlusion
- •Clinical Characteristics
- •Diagnosis
- •Mortality/Morbidity
- •19.1.3.2 Retinal Vein Occlusion (RVO)
- •Clinical Characteristics
- •Pathogenesis
- •Diagnosis
- •19.1.3.3 Ischemic Optic Neuropathy
- •Clinical Characteristics
- •Mortality/Morbidity
- •19.1.3.4 Asymptomatic Retinal Emboli
- •Background
- •Pathophysiology
- •19.2 Vasculitis
- •19.2.1 Takayasu’s Arteritis (Aortic Arch Syndrome)
- •19.2.1.1 Pathophysiology
- •19.2.1.2 Clinical Characteristics
- •19.2.1.3 Epidemiology
- •19.2.2 Behcet’s Disease
- •19.2.2.1 Clinical Characteristics
- •19.2.2.2 Pathogenesis
- •19.2.2.3 Diagnosis
- •19.2.2.4 Epidemiology
- •19.2.3 Thromboangiitis Obliterans
- •19.2.3.1 Diagnosis and Clinical Characteristics
- •19.2.3.2 Treatment
- •19.2.4 Temporal Arteritis
- •19.2.4.1 Epidemiology
- •19.2.4.2 Pathogenesis
- •19.2.4.3 Ocular Manifestations
- •19.2.5 Wegener’s Granulomatosis
- •19.2.5.1 Pathogenesis
- •19.2.5.2 Ocular Manifestation
- •19.2.5.3 Diagnosis
- •19.2.6 Kawasaki Disease
- •19.2.6.1 Clinical Characteristics
- •19.2.6.2 Diagnosis
- •19.3 Vascular Malformations
- •19.3.1.1 Diagnosis
- •19.3.1.2 Pathophysiology
- •19.4 Systemic Hypertension and Treatment
- •19.4.1 Etiology
- •19.4.1.1 Primary Hypertension
- •19.4.1.2 Secondary Hypertension
- •19.4.2 Pathophysiology
- •19.4.3 Pathology and Complications
- •19.4.4 Symptoms and Signs
- •19.4.5 Diagnosis of Hypertension
- •19.4.5.1 History
- •19.4.5.2 Physical Examination
- •19.4.5.3 Testing
- •19.4.6 Prognosis
- •19.4.7 General Treatment
- •19.4.7.2 Drugs
- •19.5 Hypertensive Retinopathy
- •19.5.2 Pathophysiology
- •19.5.3 Blood Pressure
- •19.5.3.1 The Risk of Stroke
- •19.5.3.2 The Risk of Coronary Heart Disease
- •19.5.4 Treatment
- •19.5.4.1 ACE Inhibitors and the Eye
- •References
- •Index
Color Doppler Imaging |
8 |
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Ingeborg Stalmans, Selim Orgül,
and Leopold Schmetterer
Core Messages
¥The CDI technique is used to measure blood velocities in the retrobulbar arteries: Ophthalmic artery, central retinal artery, nasal and temporal posterior ciliary arteries.
¥Widely used variables are peak-systolic, end-diastolic and mean ßow velocities, as well as resistance index.
¥The advantages of the CDI technique are: (1) not dependent on optic media,
(2) non-invasive, (3) good reproducibility with an experienced user.
¥It can be used in a number of vascularrelated ocular pathologies, from glaucoma to central vein occlusion.
I. Stalmans, M.D. Ph.D. (*)
Department of Ophthalmology, University Hospitals Leuven, Kapucijnenvoer 33, Leuven 3000, Belgium e-mail: ingeborg.stalmans@uz.kuleuven.ac.be
S. OrgŸl, M.D.
Department of ophthalmology, University of Basel Eye Clinic,
Mittlere-Strasse 91, Basel CH-4031, Switzerland e-mail: sorguel@uhbs.ch
L. Schmetterer, Ph.D.
Department of Clinical Pharmacology, Center of Medical Physics and Biomedical Engineering, Medical University of Vienna, Weahringer Guertel 18-20, Vienna
A-1090, Austria
e-mail: leopold.schmetterer@meduniwien.ac.at
¥Caution should be used when comparing results obtained with different ultrasound machines/probes, as data may not be interchangeable.
¥Velocity should not be read as ßow, as this correlation implies vessel diameter. Such variable has not been reproducible using the current technology.
8.1 Principles
Color Doppler imaging (CDI) is a technique that combines B-scan ultrasonography for the conventional imaging of tissue with velocity extraction based on the acoustic Doppler effect. In the eye, this technique can be employed for the visualization of blood velocities in the retrobulbar vessels including the ophthalmic artery (OA), the posterior ciliary arteries (PCAs), and the central retinal artery (CRA). With CDI, ultrasound waves with frequencies of several MHz are used. Analysing the time elapsed between emission and return can lead to a quantiÞcation of the reßecting structure depth. B-scan ultrasound can then be used to produce gray-scale images of the structures of the human eye. If a structure within the scattering volume of the ultrasound is moving, a Doppler shift is induced (Fig. 8.1). If the reßecting object is moving toward the transducer, the frequency of the returning sound wave is increased as compared to the emitted sound wave. If the reßecting object is, however, moving away from the ultrasound probe, the frequency of
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DOI 10.1007/978-3-540-69469-4_8, © Springer-Verlag Berlin Heidelberg 2012 |
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148 I. Stalmans et al.
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associated with lower penetration depths. Given |
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Transducer |
that the retrobulbar vessels are located several |
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centimeters behind the front surface of the eye, |
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relatively high penetration depth is required, |
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Skin |
associated with limited resolution. |
US wave |
Doppler shift |
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Vessel |
Flow velocity
Fig. 8.1 Doppler principles
the returning sound wave is smaller than that of the emitted sound wave. In tissue, the main source of Doppler shifting is related to the movement of red blood cells within the tissue. Hence, blood ßow in retrobulbar vessels can be visualized, and blood velocity can be extracted. The Doppler shift Df depends on the velocity of the moving erythrocytes (v), the frequency of the incoming ultrasound waves f0, the velocity of the ultrasound wave within the tissue (C), and the Doppler angle. The velocity of the blood can be calculated as
v = f .C / (2 × f0.cosθ)
From this equation, it becomes clear that the highest Doppler shift is induced when the transducer is parallel to the vessel and the angle q = 0 because in this case cos q = 1. When the vessel is, however, perpendicular to the incoming sound wave, no Doppler shift is detected because cos q =0. In practice, measurement of Doppler frequencies are usually done at angles between 30¡ and 60¡ [36]. When the angle q is close to 0¡, problems arise from total reßection of the sound wave at the vessel wall. When the angle q is, however, close to 90¡, the frequency shift becomes largely dependent on the Doppler angle. In this situation, only small errors in measuring the Doppler angle may induce large errors in the frequency.
In ultrasound, there is an inverse relation between penetration depth and resolution. The higher the frequency of the ultrasound, the higher the resolution within the tissue. Since the amount of attenuation per unit distance is also increasing with tissue, higher frequencies are, however,
8.2Instrumentation
Nowadays, commercial CDI machines use pulsedwave Doppler. Pulsed-wave ultrasound probes emit series of pulses. These sound pulses are transmitted in the tissue, and the time until the reßected pulse wave is detected by the same ultrasound probe is measured. If a moving structure is present, there is not only a frequency shift in the returning ultrasound wave according to the Doppler effect but also a relative phase shift. Normally, the latter effect is used to extract the velocity data. The maximum velocity that can be detected with a pulsed Doppler probe depends on the pulse repetition rate, the vessel depth, the transmitter frequency, and the Doppler angle. If the velocity is too high, aliasing may occur, resulting in erroneous velocity extraction, but given that retrobulbar vessel is relatively small, this is not a limitation in ophthalmic use of CDI.
Since the delay of the incoming and the reßected wave is related to the depth of the reßecting interface, velocities can be measured at different depths within tissues. Combing pulsed-wave Doppler with B-scan imaging is called Duplex imaging. This technique of overlapping the Doppler signal with the gray-scale reßectance image allows for anatomical allocation of the velocity information. The direction of ßow is normally translated into a color scale on the ultrasound image (CDI). With this technique, the colored ßow information is visible in parallel to the gray-scale reßection image. Usually, ßow toward the probe is depicted in red and is arterial, while ßow away from the probe is depicted in blue and is venous. This means that blood ßowing from the heart shows up in red, whereas blood ßowing toward the heart shows up in blue.
Since CDI allows for relatively high time resolution [50], the blood velocity can be displayed as a function of time. Given the pulsatile nature of blood velocity in retrobulbar vessels, the systolic and the diastolic parts of the velocity signal can easily be identiÞed.
8 Color Doppler Imaging |
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CDI uses a linear array transducer consisting of linearly arranged, sequentially excited piezoelectric elements. As mentioned above, the frequency of the Doppler probe is chosen as a compromise between resolution and penetration depth. A typical transducer for retrobulbar CDI has a frequency of 7.5 MHz, but some investigators have used up to 12.5 MHz, thereby providing better resolution but also weaker Doppler signals.
8.3Procedure
When the patient is examined in a lying position, legs should be uncrossed to avoid inßuences on venous return. The patient is instructed to look straight while the eyelids are closed. The examiner is seated behind the head of the patient while the base of the examinerÕs hand rests on the patientÕs forehead, with a Þnger is placed on the patientÕs cheek (Fig. 8.2). The tip of the probe is covered with a sufÞcient amount of acoustic coupling gel to provide adequate contact between the probe and the skin. The probe needs to be gently positioned on the closed upper eyelid in order to avoid mechanical force on the eyeball. This may increase intraocular pressure and thereby perfusion pressure, leading to a change in perfusion pressure as discussed later in this chapter.
The anatomy of the eye and the optic nerve head are identiÞed using the gray scale images in the B-scan mode (Fig 8.3a). Color Doppler is used to visualize the ßow within the vessels and allows
for identiÞcation of the appropriate vessels (Fig 8.3b). The sample volume is placed in the center of the vessel, and the angle is set parallel to the vessel to account for the Doppler angle (Fig 8.3c and d).
In order to obtain reliable and reproducible measurements using CDI, it is important to have a thorough knowledge of the retrobulbar vascular anatomy, as well as the characteristic waveforms of the different vessels, and the speciÞc locations that are conventionally chosen for measurement [51] (Fig. 8.4). The central retinal artery (CRA) and its corresponding vein lie close together in the middle of the optic nerve and cannot be measured separately by CDI. Therefore, a double waveform is obtained with a distinct pulsatile arterial waveform above the zero line and a gentle sinusoidal venous variation below the zero line (Fig 8.5a). The nasal and temporal short posterior ciliary arteries (NPCA and TPCA) are located on both sides of the optic nerve and should be measured at a position that is close to the optic nerve and as anterior as possible without receiving interference from the choroid. It is important to realize that individual short posterior ciliary vessels cannot be distinguished by CDI. Therefore, the obtained waveform represents the mass effect produced by a bundle of vessels rather than from individual ciliary vessels. These arteries produce a more uniform arterial pulse without a venous wave (Fig 8.5b). The ophthalmic artery (OA) is situated deeper in the orbit, and by convention should be measured on the nasal side of the optic nerve, immediately after it crosses the optic nerve (Fig 8.5c).
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8.4 |
Outcome Variables |
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Usually peak systolic and end diastolic velocities |
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(PSV, EDV) are extracted from the time slope of |
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the Doppler shift. Since the time course of the |
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velocity within a vessel may also carry informa- |
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tion on the vascular resistance distal to these vas- |
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cular beds, a resistance index (RI = (PSV − EDV)/ |
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PSV) is calculated to quantify vascular resistance |
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(Fig. 8.6). In addition, mean ßow velocity (MFV) |
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is often calculated as the time mean of the spec- |
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tral outline over a heart cycle. Data are measured |
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separately for the CRA, the nasal PCA, the tem- |
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poral PCA, and the OA. As mentioned above, |
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Fig. 8.2 Positioning |
individual short posterior ciliary vessels cannot |
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150 |
I. Stalmans et al. |
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a |
b |
c |
d |
Fig. 8.3 Imaging of retrobulbar structures and ßow
be distinguished by CDI because of their small size. Hence, bundles of vessels are examined, and the number of arteries contributing to the signal remains uncertain. Some authors also do not distinguish between nasal and temporal PCAs.
When measuring blood velocities using CDI, it needs to be considered that the Doppler angle inßuences the results. The direction of the sampling gate therefore has to be in good alignment with the angle of the measured vessel. If this is not the case, a measurement error is introduced, which is the more severe the larger the Doppler angle. In the CRA and the OA, the angle can usually be determined easily. In the PCA, however, the prob-
lem is more severe because of their smaller size, the more tortuous course, and the uncertain number of vessels within the probing volume.
The RI offers the advantage that it is independent of the Doppler angle. It is a dimensionless parameter that can take values between 0 and 1. The relation between RI and vascular resistance is, however, not entirely clear. Particularly, it seems that the value is largely dependent of the vascular compliance, which is deÞned as the ability of a vessel to distend and increase intravascular volume with increasing transmural pressure. In an in vitro model, where liquid was moved using a pulsatile pump, RI was independent of
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Fig. 8.4 Anatomy retrobulbar vessels
Arteria lacrimalis
Arteria ciliaris posterior longa 
Arteria ciliaris posterior brevis
Arteria ophthalmica 
Fig. 8.5 IdentiÞcation of retrobulbar vessels
Arteria dorsalis nasi
Arteria ethmoidalis anterior
Arteria ethmoidalis posterior
Arteria centralis retinae
Fig. 8.6 Measured parameters
