AUTHOR AND EDITOR INFORMATION

Section 1 of 11  

• Authors and Editors
• Introduction
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• Workup
• Treatment
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• Follow-up
• Miscellaneous
• Multimedia
• References

INTRODUCTION

Section 2 of 11  

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• Clinical
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• Medication
• Follow-up
• Miscellaneous
• Multimedia
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Background

In 1889, Doyne first to described angioid streaks in a patient with retinal hemorrhages secondary to trauma. Later in 1892, Knapp named them angioid streaks because of their resemblance to blood vessels. Angioid streaks result from pathological changes at the level of the Bruch membrane, which was confirmed histologically in the late 1930s.

Pathophysiology

Controversy about the pathophysiology of angioid streaks exists. In some diseases including pseudoxanthoma elasticum (PXE) and Paget disease, the Bruch membrane may become calcified and brittle with subsequent development of cracks. However, cytoimmunochemistry and x-ray analysis had shown that the earliest abnormality in PXE was abnormal accumulation and metabolism of polyanions (ie, glycosaminoglycans, glycoproteins) within the Bruch membrane.

The lines of force within the eye resulting from the pull of intrinsic and extrinsic ocular muscles on the relatively fixed site of the optic nerve have been studied. Those lines of forces had the same configuration as the peripapillary interlacement and radial extensions of angioid streaks. Such forces acting on the Bruch membrane undoubtedly account for the configuration of the breaks. However, in sickle cell disease, Bruch membrane calcification is not a common part of the pathology.

It is believed that the pathology may be a combination of diffuse elastic degeneration of the Bruch membrane, iron deposition in elastic fibers from hemolysis with secondary mineralization, and impairment of nutrition because of sickling, stasis, and small vessel occlusion. Klien proposed a dual mechanism as a cause of these cracks in general, as follows: a primary abnormality of fibers of the Bruch membrane, and an increase in availability of metal salts or a tendency for their deposition, resulting in a secondary brittleness of the membranes.

Frequency

United States

Not known

International

Not known

Mortality/Morbidity

Moderate to severe central visual loss is mainly related to foveal involvement with a dehiscence of underlying Bruch membrane or a neovascular membrane formation under the retina. Choroidal neovascularization (CNV) is the major cause of vision loss and affects 70-86% of patients with angioid streaks.

Race

No racial predilection is present.

Sex

No sexual predilection exists.

Age

The age of onset is variable with the underlying etiology. In one study, the age of onset of 50 patients with angioid streaks was reported as follows:

• Patients with PXE present in the third decade with a mean age of 51.7 years.
• Patients with sickle cell disease tend to be in their second and third decades with a mean age of 41.7 years.
• Patients with Paget disease tend to be older at the time of diagnosis with a mean age of 67 years. Angioid streaks in patients with no systemic disease or with rare etiologies tend to present late in life with a mean age of 65.7 years. Rare etiologies include patients with peptic ulcer, diabetes, hypertension, arthritis, breast cancer, metastatic cancer, rheumatoid spondylitis, and heart disease.

CLINICAL

Section 3 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

History

Visual acuity is normal unless a leakage, bleeding, or Bruch membrane dehiscence involves the central macula. Distorted central vision (metamorphopsia) and micropsia can be early signs of macular involvement.

Physical

Ophthalmoscopic findings are as follows:

• At times, angioid streaks can be difficult to identify unless a careful examination of the posterior pole is performed.
• Angioid streaks usually present as linear gray or dark red lines with irregular serrated edges lying beneath normal retinal blood vessels. The streaks intercommunicate in a ringlike fashion around the optic disc in 27% of cases and radiate outward in a tapering fashion from the peripapillary area in 73% of patients. The streaks run a convoluted course and tend to terminate abruptly. Angioid streaks usually do not extend past the equator.
• Associated findings in patients with angioid streaks are as follows:
• • Peau d'orange or leopard skin spotting, consisting of speckled yellowish mottling of the posterior pole mostly apparent in the temporal macula. This finding occasionally may antedate the appearance of angioid streaks. It is seen more frequently in patients with PXE and is caused by alterations at the level of the Bruch membrane as demonstrated by the diffuse pattern of hyperfluorescence on indocyanine green angiography (ICGA).
  • Peripapillary chorioretinal atrophy, focal peripheral chorioretinal scars (salmon spots), and reticular pigment dystrophy of the macula may be present at time of diagnosis.
  • Optic nerve head drusen (hyaline bodies) may antedate the appearance of angioid streaks, and they may be the earliest clinical manifestations of PXE. As many as 25% of patients with angioid streaks have clinical or echographic evidence of disk drusen. These hyaline bodies were associated with neovascularization in the peripapillary area, and, in some patients, they were associated with acute visual loss due to pressure effect on the optic nerve head.
  • Crystalline bodies typically are seen in the midperipheral fundus or inferior to the optic nerve. These bodies are multiple, round, small, and subretinal lesions. Usually, these crystalline bodies cause some atrophy of the retinal pigment epithelium (RPE).
  • Optic atrophy may be seen in patients with Paget disease of the bone. It cannot be explained solely on the basis of bony compression.
• Severe visual impairment is caused by 1 of the following conditions in 70% of cases:
• • CNV with subsequent serous and hemorrhagic detachment of the fovea (most serious complication)
  • Choroidal rupture secondary to trivial trauma with secondary hemorrhage involving the fovea
  • Foveal involvement by a streak with damage to RPE and choriocapillaris (may result in permanent loss of central visual acuity)

Causes

• Idiopathic: In 50% of patients with angioid streaks, no associated systemic disease is present.
• Systemic association
• • PXE is an uncommon inherited disorder of connective tissue. It has generalized effects on the elastin fibrils in the dermis, arterial walls, heart, gastrointestinal (GI) tract, and Bruch membrane, resulting in mineralization and deposition of phosphorus. The 4 types of inheritance of PXE include 2 of which are autosomal dominant and 2 of which are autosomal recessive. It is the most common systemic disorder associated with angioid streaks. Diagnosing PXE is important because 85% of patients develop ocular involvement, usually after the second decade of life. The combination of PXE and ocular involvement is referred to as Grönblad-Strandberg syndrome.
  • Histologically, degenerative changes and calcifications of the elastic tissues in the skin and arteries are present. The following systemic findings may help the ophthalmologist to confirm the diagnosis of angioid streaks secondary to PXE, as well as to take care of complications.
  • Dermatologic findings include yellow papules "chicken skin" arranged in linear or reticulate pattern, in plaques, over the side of the neck, antecubital fossae, axillae, groin, and paraumbilical area.
  • Cardiovascular manifestations include accelerated hypertension at an earlier age due to atherosclerosis, which may be related to renovascular disease, premature coronary artery disease, peripheral vascular disease, and mitral incompetence.
  • Some patients develop genitourinary bleeding as part of PXE.
  • Neurologic findings may include cerebrovascular accidents, intracranial aneurysms, and cerebral ischemia.
• Paget disease is a chronic, progressive, and in some cases inherited disease, characterized by bone deformity. It may be confined to a few bones, or in some patients, it represents a generalized abnormality that gives rise to enlargement of the skull, kyphoscoliosis, deafness, and deformities of long bones. However, angioid streaks occur in fewer than 2% of patients. Osteoclastic activity with an osteoblastic reaction occurs. Although the etiology is unknown, some clinicians believe it is related to a slow virus infection, measles, or respiratory syncytial virus. Both males and females are affected equally.
• Ehlers-Danlos syndrome is a rare autosomal dominant disorder of collagen resulting from a deficiency of hydroxylysine. Ocular findings include epicanthal folds, keratoconus, high myopia, retinal detachment, blue sclera, ectopia lentis, and angioid streaks. Systemic associations include the following:
• • Skin and musculoskeletal - Thin hyperplastic skin that heals poorly, hyperextensible joints that may predispose to recurrent falls, hydrarthrosis, and pseudotumor formation over knees and elbows
  • Cardiovascular disease consists of bleeding diathesis, dissecting aneurysms, spontaneous rupture of large blood vessels, and mitral prolapse.
  • Others - Diaphragmatic hernias and diverticulum of the GI and respiratory tracts
• Hemoglobinopathies that occasionally are associated with angioid streaks include the following:
• Homozygous sickle cell disease (Hb-SS)
• Sickle cell trait (Hb-AS)
• Sickle cell thalassemia (Hb-thal)
• Sickle cell hemoglobin (Hb-SC)
• Hemoglobin H (Hb-H)
• Homozygous B-thalassemia major
• Intermedia
• Minor and hereditary spherocytosis
• The frequency of angioid streaks increases with age; it is about 1.5% in younger patients and increases to 22% in older patients. Complications such as macular degeneration and choroidal neovascular membranes are uncommon in this subgroup of patients with angioid streaks. In general, choroidal neovascular membranes (CNVM) and serous detachments of the macula are less common in black patients.
• Other systemic diseases associated with angioid streaks include the following:
• • Abetalipoproteinemia
  • Acromegaly
  • Dwarfism
  • Diabetes mellitus
  • Hemochromatosis
  • Facial angiomatosis
  • Idiopathic thrombocytic purpura
  • Chronic familial hyperphosphatemia
  • Hypercalcinosis
  • Diffuse lipomatosis
  • Acquired hemolytic anemia
  • Myopia
  • Neurofibromatosis
  • Epilepsy
  • Senile elastosis
  • Sturge-Weber syndrome
  • Trauma
  • Tuberous sclerosis

DIFFERENTIALS

Section 4 of 11  

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Other Problems to be Considered

Choroidal sclerosis
Myopic lacquer cracks-pseudoangioid streaks
Histoplasmosis
Retinal vasculitis and papillitis
Traumatic hemorrhage

WORKUP

Section 5 of 11  

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• Follow-up
• Miscellaneous
• Multimedia
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Lab Studies

• Only one half of patients with angioid streaks have systemic association. General workup is important to diagnose and treat other aspects of the disease that may be life threatening, such as GI hemorrhage, heart disease, anemia, and pathological fractures.
• Biochemical survey: Serum calcium, phosphorous, and alkaline phosphatase levels may be abnormal in untreated cases of Paget disease. Urinary excretion of pyridinoline crosslinks is a more specific and sensitive marker. In untreated patients, a close correlation between serum activity of alkaline phosphatase and urinary excretion of hydroxyproline exists. However, 10% of patients with Paget disease who are symptomatic have serum levels of alkaline phosphatase within the reference range.

Imaging Studies

• Fluorescein angiography
• • Red-free photographs show radiating irregular curvilinear lines of variable width and configurations.
  • Early fluorescein angiography (FA) reveals either hyperfluorescence due to window transmission defects of atrophic RPE or uncommonly hypofluorescence due to atrophy or separation of underlying choriocapillaries, which results in nonfilling window defects.
  • In late FA, some leakage at the margins of the streaks occurs from adjacent healthy choriocapillaries and from late staining of the sclera and deep choroidal vessels. The classic appearance of CNVM, RPE detachments, and serous or hemorrhagic detachments, also may be noted on FA.
• Indocyanine green angiography
• ICGA is superior to FA in defining occult choroidal neovascularizations. It shows angioid streaks in all eyes studies. Hyperfluorescent lines are visible in most cases. However, some patients exhibit hypofluorescence and tracklike fluorescence.
• Peau d'orange appearance of temporal macula can be seen on ICGA as a speckled pattern in the midperiphery. Hyperfluorescent lines look larger and more numerous than those seen on FA or red-free photographs.
• Radiology studies: X-rays of head, abdomen, and lower extremities are helpful to show bone involvement in Paget disease of the bone and premature calcification of arteries in PXE.

Other Tests

• Retinal function tests
• • Visual acuity is normal, as long as no damage to the foveal RPE and no leakage from the choroid through the Bruch membrane and RPE occur.
  • Visual fields are normal unless central macula is affected by the angioid cracks and RPE detachments.
  • Color vision is affected only when vision loss occurs and is similar to color vision in acquired macular diseases.
  • Electroretinography (ERG) findings are normal.
  • Electro-oculography (EOG) findings are normal in most cases. Findings may be subnormal in advanced cases.
  • Dark adaptation is normal.
• GI studies: GI hemorrhage is common in patients with PXE.

Procedures

• Dermatologic: Skin biopsy may provide important diagnostic clues in cases of PXE with angioid streaks.

TREATMENT

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Medical Care

Initially, patients are asymptomatic and no indication for prophylactic treatment is present. Angioid streaks are a generalized disorder of the Bruch membrane.

Angioid streaks are an uncommon entity to be studied and are treated as part of a controlled and randomized study. Treatment methods are based mainly on individual experience and extrapolation from the Macular Photocoagulation Study Group. Patients with angioid streaks are at higher risk of choroidal rupture and subretinal hemorrhage secondary to mild blunt trauma. They are advised to wear protective goggles and sports glasses when playing sports and during work. Treatment options include observation, laser photocoagulation, and surgical removal of CNVM under the fovea. Recently, the Food and Drug Administration (FDA) approved the use of photodynamic therapy (PDT) for CNVM secondary to age-related macular degeneration (ARMD).

• Observation
• • Initially, symptomatic patients complained of a decrease in their central visual acuity, and some developed distortion and metamorphopsia that was more disturbing than the associated central scotomas. Usually, central scotomas tend to increase in size if left untreated before subsequent scarring of the macula occurs.
  • Early at the time of diagnosis, more than 50% of patients had vision of 20/40 or better; one half of them became legally blind at average follow-up period of 3.5 years. Most eyes had vision 20/200 or worse after age 50 years.
  • In one study, 11 untreated eyes with subretinal neovascular membranes all had final visual acuity of counting fingers. Clarkson and Altman reported 29 patients seen on 2 occasions over a period of at least 6 months. Decreased vision of 2 lines or greater on the Snellen chart occurred in 13 of 29 patients.
  • Prophylactic laser treatment in clinically asymptomatic eyes without active choroidal neovascularization is not recommended. In one study, prophylactic treatment was associated with increased incidence of neovascularization at the site of treatment. However, patients who received laser photocoagulation noticed a decrease in the size of their central scotomas and early relief from visual distortion.
• Laser photocoagulation
• • Photocoagulation, including light (xenon) and argon, has been used since the early 1970s, although streaks themselves were treated to stop their progression toward the macula. Early treatment experiences with light and laser photocoagulation were disappointing and discouraging. Some investigators discouraged laser treatment for CNVM in angioid streaks.
  • Recent reports showed some success with argon laser for lesions that are located at least 100 µm from the center of foveal avascular zone (FAZ).
  • Laser therapy is believed to slow the progression of the CNV toward the fovea and stabilizes vision. Moreover, it improves the quality of vision (ie, size of central scotoma, decreases metamorphopsia). Successful treatment of CNV may not improve central vision in some patients since dehiscences in the Bruch membranes may involve and damage the foveal RPE.
  • Many investigators found that laser treatment, if administered early and adequately to CNV lesions, may have a favorable result on long-term visual outcome.
  • Many patients needed multiple treatments because of persistent leakage and recurrence that occurred during the first 3 months.
  • Patients need to be monitored closely with Amsler grids and FA.
  • In several series, the recurrence rate was reported as high as 77% of patients who underwent laser treatment. Most of recurrent CNVM were subfoveal. Incidence of recurrence was higher in angioid streaks than in other conditions, such as ARMD, degenerative myopia, and histoplasmosis.
  • Treating CNVM associated with angioid streaks is sometimes challenging. Both occult and classic CNV can occur in the same eye and usually are located very close to FAZ. RPE reaction is minimal around CNVM. Some of these membranes grow fast once they break through the Bruch membrane. Careful setup of laser power and spot size is important to prevent further damage to the brittle and mineralized Bruch membrane.
• Photodynamic therapy
• • PDT is a new modality that has been approved by FDA for treatment of CNV secondary to ARMD. It uses a light activated drug (eg, verteporfin [Visudyne]) and applying a nonthermal red light in the range of 689 nanometers. The total energy delivered is 50 J/cm² over a period of 83 seconds. The power of laser output can be adjusted according to size of CNV and ophthalmic lens magnification.
  • A recent study evaluated the short-term safety and visual effects after administering PDT in 13 patients with classic subfoveal CNV secondary to pathological myopia, ocular histoplasmosis syndrome, angioid streaks, and idiopathic causes. Most patients gained at least 1 line of vision. Reduction in the size of leakage area from classic CNV was noted in all patients as early as 1-week posttreatment, with complete absence of leakage in almost half of the patients. Up to 4 treatments were found to have short-term safety even with re-treatment intervals as short as 4 weeks.
  • Karacorlu et al evaluated the safety and efficacy of PDT with verteporfin for subfoveal CNV associated with angioid streaks in 8 eyes and showed that PDT generally achieved a short-term cessation of or a decrease of fluorescein leakage from subfoveal CNVM without loss of vision in patients with angioid steaks.
  • Long-term effects of PDT, especially in patients who may need multiple treatments are unknown. Patients with angioid streaks are at higher risk of recurrent CNV.

Surgical Care

• Submacular surgery
• • Patients with classic subfoveal CNVM are not candidates for laser photocoagulation therapy. In the past, they were left without treatment. However, recent advances in instrumentation and vitreoretinal surgical techniques made it possible to remove CNVM without significant damage to RPE and neurosensory retina.
  • Eckstein et al reported encouraging short-term visual results in 31 consecutive patients with non–age-related subfoveal CNVM, including angioid streaks. Visual acuity improved or remained the same in 25 of 31 eyes. Moreover, visual acuity improved by more than 2 lines in 5 eyes (16%). Older patients and those with atrophic RPE had the worst outcome. Recurrent CNV occurred in 11 eyes (35%). Presence of subfoveal blood was associated with higher recurrence rate of membranes. No significant association between preoperative vision and length of symptoms was present prior to surgery to the final visual acuity.

Activity

Patients with angioid streaks have a high risk of choroidal rupture and subretinal hemorrhage secondary to mild blunt trauma. It is recommended that patients wear protective sports glasses whenever applicable.

MEDICATION

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The goals of pharmacotherapy are to reduce morbidity and to prevent complications.

Drug Category: Photosensitizers

Effects can induce vascular occlusion.

FOLLOW-UP

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Further Outpatient Care

• Screening and follow-up examination by means of Amsler grid and ophthalmoscopic examination, including FA, may be necessary to detect CNVM and treat recurrences.
• Patients who undergo laser treatment or surgery need close follow-up care during the first 3 months of treatment. If they stay asymptomatic and no FA leakage occurs, follow-up care every 6 months is recommended.

Complications

• Subretinal hemorrhage and serous detachment are common complications of angioid streaks. Incidence of subretinal hemorrhage and serous detachment caused by choroidal neovascularization is high, about 85% of all patients with PXE and 10-15% of patients with Paget disease of the bone. The disease is bilateral in all patients with an average age of onset older than 25 years.

Prognosis

• A high risk of serious complications such subretinal hemorrhage and serous detachment exists. Bilateral involvement is the rule, although it may not be symmetrical. Families with affected individuals need screening and regular eye examinations for early detection of any progression.

Patient Education

• Patients should be instructed to return if visual acuity decreases. Signs of decreased central visual acuity may include central blurred vision, difficulty in depth perception, and distortion of lines and objects.
• Families and patients will benefit from using an Amsler grid to detect early changes in asymptomatic but high-risk individuals.
• More emphasis should be placed on safety measures to avoid trauma even if trivial. Protective goggles are useful for young patients who participate in sports.

MISCELLANEOUS

Section 9 of 11  

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Medical/Legal Pitfalls

• Accurate diagnosis will help the doctor to educate the patient about vision-threatening complications.

MULTIMEDIA

Section 10 of 11  

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• Miscellaneous
• Multimedia
• References

Media file 1:  Red-free photograph of the optic nerve and posterior pole showing the cracks in the Bruch membrane. Notice the retinal arteries and veins crossing over the dark red streaks.
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Media file 2:  Early fluorescein angiography showing the early hyperfluorescence, window defect, of the angioid streaks.
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Media file 3:  Late fluorescein angiography of the same eye. Notice the staining of the streaks edges. Also, staining in the center of the macula is present due to extension of the Bruch membrane crack. When compared to pearly fluorescein angiography no active leakage is present.
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Media file 4:  Progression of angioid streaks. Large subretinal hemorrhage.
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Media file 5:  Same eye as in Image 4, 11 months later. Partial resolution of subretinal blood. Notice the old subretinal hemorrhage under the fovea and color change to white-yellow.
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Media file 6:  Late complication of choroidal neovascularization in angioid streaks. Same eye as in Image 5, 5 years later. Notice the extensive scarring and subretinal exudates and dehemoglobinized blood.
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Media type:  Photo

REFERENCES

Section 11 of 11

• Authors and Editors
• Introduction
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• Differentials
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• Follow-up
• Miscellaneous
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• References

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• Walker ER, Frederickson RG, Mayes MD. The mineralization of elastic fibers and alterations of extracellular matrix in pseudoxanthoma elasticum. Ultrastructure, immunocytochemistry, and X-ray analysis. Arch Dermatol. Jan 1989;125(1):70-6. [Medline].

Article Last Updated: Sep 30, 2005