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Orbital defects1 Orbital defects1 Presentation Transcript

  • Dr. Ali RazaAssociate ProfessorRawalpindi Medical CollegeHoly Family HospitalRawalpindi
  •  F: Frontal bone with Bony Orbit associated suture and notch. <- Trochlea <- Optical Canal S: Superior orbital fissure I: Inferior orbital fissure L: Lacrimal bone E: Ethmoid bone.
  • Other Locations. The lacrimal gland and lacrimal sac as well as the potential for multiple compartment involvement.
  • Spaces of the Retrobulbar Orbit Intraconal space:  Contains CN II, ophthalmic artery, superior division of CN III, nasociliary nerve (V1), inferior division of CN III, and CN VI. Extraconal space:  Contains ophthalmic vein, lacrimal nerve (V1), CN IV and frontal nerve (V1).
  • Spaces of the Retrobulbar Orbit Cone:  Composed of the four rectus muscles and the thin intramuscular membrane which joins them and extends posteriorly to the insertion of the muscle tendons at the orbital apex.
  • THYROID OPHTHALMOPATHY PATHOLOGY HYPERTROPHY OF EXTRAOCULAR MUSCLES CELLULAR INFILTRATION PROLIFRATION OFORBITAL FAT
  • SOFT TISSUE INVOLVEMENT PERIORBITAL AND LID SWELLING CONJUNCTIVAL HYPERAEMIA CHEMOSIS SUPERIOR LIMBIC KERATOCONJUNCTIVITIS KERTOCONJUNCTIVITIS SICCA
  • Soft Tissue Involvement
  • Conjunctival Injection
  • Severe Chemosis
  • LID RETRACTION CONTRACTION OF LEVATOR OVER ACTION OF LEVATOR/SUPERIOR RECTUS OVER ACTION OF MULLER MUSCLE
  • LID RETRACTION DALRYMPLE SIGN IN PRIMARY GAZE VON GRAEFE SIGN(LID LAG) KOCHER SIGN
  • Lid Retraction
  • Lid Retraction
  • Dalrymple Sign
  • PROPTOSIS AXIAL BILATERAL/UNILATERAL COMPLICATIONS EXPOSURE  ULCER
  • Proptosis
  • Proptosis
  • Measurement
  • Exophthalmometer
  • Exophthalmometer
  • OPTIC NEUROPATHY VISUAL ACUITY DECREASED VISUAL FIELD DEFECTS CENTRAL/PARACENTRALSCOTOMA OPTIC ATROPHY
  • RESTRICTIVE MYOPATHY ELEVATION- INF RECTUS FIBROSIS ABDUCTION- MEDIAL RECTUS FIBROSIS DEPRESSION- SUPERIOR RECTUS FIBROSIS ADDUCTION- LATERAL RECTUS FIBROSIS
  • Restricted Eye MovementsRestricted Elevation LE Restricted Abduction LE
  • Thyroid Ophthalmopathy
  • Thyroid (Muscle Thickening)
  • Thyroid (Muscle Thickening)
  • THYROID EYE DISEASE Autoimmune disordercharacterised by infiltrative orbitopathy
  • THYROID EYE DISEASE Associated with normal to abnormal thyroid function which may coexist, precede or follow the orbitopathy. Related to but not the same as Graves Ophthalmopathy (GO) The natural history was described by Rundle and Wilson in 1945
  • Thyroid status- Of those patients with thyroid orbitopathy, approximately 80% are clinically hyperthyroid and 20% are clinically euthyroid.4 Most patients with euthyroid Graves orbitopathy, however, have some detectable laboratory evidence of subclinical hyperthyroidism. Both hyperthyroid and euthyroid patients can develop clinical signs and symptoms of thyroid orbitopathy. In general, patients with euthyroid Graves disease tend to have less severe orbitopathy
  • THYROID EYE DISEASE The goal is to identify and treat patients who are at particular risk of sight threatening complications. The disease has a finite period of activity until it becomes burnt out.The yellow region shows the early phase where there is the best response to treatment. Type 1 younger age group, whiter eyes with proptosis. Inflammation is mostly in orbital fat not muscles. Type 11 older patient with red eyes, severe sight threatening disease, tobacco addiction is frequent.
  • THYROID EYE DISEASE  LID RETRACTION1. sympathetic overactivity infiltration of levator / SR complex. hypotropia (retraction disappears on downgaze)  SIGNS:- Dalrymples (lid retraction), von Graefe (lid lag), Kocher´s (staring appearance)
  • THYROID EYE DISEASE INFILTRATION 1. soft tissue involvement :- chemosis, conjunctival injection over the recti insertions, puffy lids
  • THYROID EYE DISEASE  Superior limbic keratoconjunctivitis (SLK)
  • Optic neuropathy with visual loss The prevalence of optic neuropathy with visual loss in patients with thyroid orbitopathy is less than 5%. Optic neuropathy is, however, the most common cause of blindness secondary to thyroid orbitopathy. Its onset is often insidious and may be masked by other symptoms. These patients are usually older (age 50 to 70) are more frequently male, have a later onset of thyroid disease, and more often have diabetes. Optic neuropathy is usually bilateral, but up to one third of cases may be unilateral.
  • Optic neuropathy Although a history of decreased vision should be carefully sought, it is important to realize that optic neuropathy can occur in a significant number (18%) of patients with visual acuities in the range of 20/20 to 20/25 (6/6 to 6/7.5).*An afferent pupillary defect is present in 35%. An abnormal disc (either swollen or pale) is seen in only 52%. Visual field defects are present in 66%.Other tests that can be useful include color vision testing and visual evoked potentials (VEPs). The Farnsworth-Munsell 100-hue test is a sensitive indicator of optic nerve dysfunction, but pseudoisochromatic screening procedures (e.g.,Ishihara plates) rarely identify an acquired color defect unless optic neuropathy is severe.The pattern reversal VEP is very sensitive at detecting early optic neuropathy and may be a useful means of following patients after treatment.
  • Intraocular pressure The increased intraocular pressure measured during upgaze in patients with thyroid orbitopathy has been a controversial finding. When restriction of the inferior rectus muscle occurs, the intraocular pressure may increase by 6 mm Hg or more in upgaze as compared with primary gaze. The increased intraocular pressure in upgaze is a normal phenomenon exaggerated by thyroid orbitopathy In patients with severe infiltrative disease there is an increased pressure on upgaze as compared with normal controls and patients with mild disease. It is often not an indicator of early disease because it occurs infrequently in patients with minimal eye findings
  • INVESTIGATION SEROLOGICALT3 (hyperthyroid)T4 TSH (hypothyroid)TSI (thyroid stimulating immunoglobulin). RADIOLOGICAL TESTSOrbital CT (enlarged muscle belly, tendon normal). Coca-Cola bottle sign = muscle swelling deforming ethmoidal bones.MRI T2 showing oedema of muscles; repeating the scan in different positions of gaze can create a pseudo-video of eye movements (for assessment of muscle restriction). RADIOISOTOPE TESTS Octreoscan: quantitative uptake of radio-labelled octreotide (which is a somatostatin analogue).
  • VISUAL FIELD A visual field should be performed in all patients suspected to have optic neuropathy and is useful when following patients after initiation of treatment. Characteristically, a central scotoma or an inferior altitudinal defect is seen in cases of compressive optic neuropathy. Other visual field defects include an enlarged blind spot, paracentral scotoma, nerve fiber bundle defect, or generalized constriction.
  • CT findings in thyroid orbitopathy The most characteristic CT finding in thyroid orbitopathy is enlargement of the extraocular muscles with normal tendinous insertions onto the globe. Other findings include proptosis and anterior prolapse of the orbital septum due to excessive orbital fat and muscle swelling (see Fig. 4).Patients at risk for developing optic neuropathy may also have severe apical crowding, a dilated superior ophthalmic vein, and anterior displacement of the lacrimal gland. Of these, apical crowding is the most sensitive indicator for the presence of optic neuropathy The CT scan should be done in the coronal plane to assess the enlargement of the extraocular muscles at the apex because axial sections can sometimes be misleading.
  • THYROID EYE DISEASE  Orbital CT -(enlarged muscle belly, tendon normal)
  • SYSTEMIC THYROID DISEASE There are no good recent studies of the natural history of untreated hyperthyroidism, but based on older reports, Wilson56 determined that about one third of patients spontaneously improve, one third remain chronically hyperthyroid, and one third progress to thyroid storm and occasionally death. Because it is not possible to predict which patients will spontaneously improve, treatment of thyroid dysfunction is recommended.
  • Treatment acute congestive ophthalmopathy, compressive optic neuropathy, motility disorders, eyelid abnormalities.
  • TREATMENT Acute Congestive Orbitopathy 1. SYMPTOMATIC:- elevate bedhead, lubricants, lid taping, diuretics 2. SYSTEMIC:- a) Normalise thyroid function with or without thyroxine. Patients rendered euthyroid do improve their GO score Tallstedt trial N Eng J Med 1992antithyroid drugs cause a 10% chance of new or worsening GObut radio-iodine causes a 30% chance of new or worsening GO.
  • Corticosteroids have been used successfully in the treatment of acute congestive orbitopathy Corticosteroids have been used successfully in the treatment of acute congestive orbitopathy. They are believed to work by altering cell-mediated immune response and diminishing the production of mucopolysaccharides by the orbital fibroblasts.Corticosteroids result in improvement of soft tissue involvement and compressive optic neuropathy (but do not have as much of an effect on diplopia Traditionally, a "short burst" of high-dose corticosteroids has been given, usually in the range of 60 to 120 mg/day of oral prednisone. Improvement in subjective symptoms such as pain and tearing usually occurs first, often as early as 24 to 48 hours, followed by improvement in soft tissue congestion and muscle function over a period of days to weeks.
  • Steroid Therapy Prednisone or prednisolone This is standard treatment but there are frequent side effects. No response in 35% of patients and anyway the response is only partial. High dose steroids given early in the disease when muscle swelling occurs does not necessarily limit the long term course of the disease. If there is no response to high dose steroids in the first three weeks they should be rapidly reduced. Prednisolone + orbital radiotherapy has slightly more effect than either alone.Use high dose pulsed methylprednisolone if urgent optic nerve decompression is required, This is more effective than oral treatment but it is expensive and not justified in most cases of TED.
  • Radiation therapy During the past few years, radiation therapy has reemerged as a useful form of treatment of severe orbitopathy. The rationale for the use of radiation therapy is reduction or elimination of the pathogenic orbital lymphocytes, which are markedly radiosensitive. It is also thought that the glycosaminoglycan production by fibroblasts is reduced, thereby reducing orbital edema, orbital tension, and conjunctival injection. Although congestive findings improve most consistently, significant improvement in proptosis and extraocular muscle function has been reported.Like corticosteroids, radiation therapy is most effective within the first year, when significant fibrotic changes have not yet occurred. Mourits and associates,135 however, suggest that periods of active orbital inflammation within the long natural history of thyroid orbitopathy would benefit from corticosteroids or radiation therapy.
  • Radiotherapy RETROBULBAR RADIOTHERAPY:- Trial of prednisone versus radiotherapy showed no difference in clinical improvement (about 50%).The patients all tolerated retrobulbar radiotherapy better than steroids Consider if steroid maintenance > 25mg/ day. Best effect in acute disease.Do not irradiate patients with diabetes mellitus as they are more susceptible to radiation retinopathy.2000rads/ 10days, effect starts at 4 weeks, maximal 4 months.
  • Compressive Optic Neuropathy Compressive optic neuropathy can cause permanent visual loss. The treatment possibilities include high doses of corticosteroids, irradiation, and orbital decompression. Some patients require only one of these modalities, while other patients need combined therapies.
  • Compressive Optic Neuropathy As in the treatment of acute congestive thyroid orbitopathy, radiation therapy is becoming increasingly popular. A retrospective series of 84 patients with compressive optic neuropathy treated with either corticosteroids or radiation therapy supports mounting evidence that radiation therapy may be safer and more effective than corticosteroids. Radiation therapy, however, must be administered in fractionated doses, which delays its beneficial effect. For this reason, if visual dysfunction progresses while the patient is on corticosteroids, surgical decompression is usually recommended if the patient is a surgical candidate.
  • Orbital decompression Orbital decompression is indicated for compressive optic neuropathy when there has been failure of or contraindication for corticosteroids or radiation therapy or if corticosteroid dependence has developed with intolerable side effects. Other indications include excessive proptosis with exposure keratitis and corneal ulceration, pain relief, and cosmesis for disfiguring exophthalmos. Orbital decompression may also be indicated as a preliminary procedure to extraocular muscle surgery on a patient with sufficient proptosis to suggest that decompression might ultimately be required.
  • Orbital decompression A variety of approaches may be used, each with its own advantages and associated complications. The transorbital (via fornix or eyelid) approach to inferior and medial wall decompression is the most common approach used by ophthalmologists. The addition of a lateral wall advancement has the advantage of both further increasing the orbital volume and simultaneously improving upper eyelid retraction; this is the technique we prefer.
  • ORBITAL DECOMPRESSION Subciliary approach.Inferior & medial wall (6mm proptosis).Remove bone to posterior wall maxillary sinus (5mm more posterior on medial wall), Avoid IO neurovascular bundle, and the anterior and posterior ethmoidal arteries.Incise periosteum in A-P direction posteriorly and circumferentially anteriorly. Complications: visual loss, A pattern ET
  • Motility Disorders A major source of morbidity in thyroid orbitopathy, and the most frequent problem associated with orbital decompression surgery, has been strabismus. In patients with relatively minimal degrees of ocular misalignment, diplopia can be avoided with a compensatory head posture, Fresnel plastic press-on prisms, or temporary occlusion. Unfortunately there is significant image degradation as larger prisms are used, limiting their efficacy. If there is marked asymmetry in ocular deviation in different fields of gaze, prisms are also less effective. In some cases during the inflammatory period, use of intramuscular botulinum toxin has shown some efficacy. Extraocular muscle surgery should be postponed until the muscles are no longer inflamed and the deviation has remained stable for at least 6 months.
  • Eyelid Abnormalities As with other thyroid eye problems, eyelid retraction will often improve with time, and only an estimated 50% of patients with eyelid retraction have a significant eyelid abnormality 5 years later. Eyelid retraction can result from excessive autonomic discharge, levator fibrosis, or contraction of the inferior rectus muscle. Surgical correction of eyelid abnormalities should be performed only after orbital or extraocular muscle surgery because these operations may change eyelid position. For example, inferior rectus muscle restriction may cause upper eyelid retraction because of the superior rectus/levator palpebrae superioris overaction against the restriction. Specific techniques for repair of eyelid retraction are discussed in other chapters.
  • Steroid Therapy Prednisone or prednisolone This is standard treatment but there are frequent side effects. No response in 35% of patients and anyway the response is only partial. High dose steroids given early in the disease when muscle swelling occurs does not necessarily limit the long term course of the disease. If there is no response to high dose steroids in the first three weeks they should be rapidly reduced. Prednisolone + orbital radiotherapy has slightly more effect than either alone.Use high dose pulsed methylprednisolone if urgent optic nerve decompression is required, This is more effective than oral treatment but it is expensive and not justified in most cases of TED.
  • Radiation therapy During the past few years, radiation therapy has reemerged as a useful form of treatment of severe orbitopathy. The rationale for the use of radiation therapy is reduction or elimination of the pathogenic orbital lymphocytes, which are markedly radiosensitive. It is also thought that the glycosaminoglycan production by fibroblasts is reduced, thereby reducing orbital edema, orbital tension, and conjunctival injection. Although congestive findings improve most consistently, significant improvement in proptosis and extraocular muscle function has been reported.Like corticosteroids, radiation therapy is most effective within the first year, when significant fibrotic changes have not yet occurred. Mourits and associates,135 however, suggest that periods of active orbital inflammation within the long natural history of thyroid orbitopathy would benefit from corticosteroids or radiation therapy.
  • Radiotherapy RETROBULBAR RADIOTHERAPY:- Trial of prednisone versus radiotherapy showed no difference in clinical improvement (about 50%).The patients all tolerated retrobulbar radiotherapy better than steroids Consider if steroid maintenance > 25mg/ day. Best effect in acute disease.Do not irradiate patients with diabetes mellitus as they are more susceptible to radiation retinopathy.2000rads/ 10days, effect starts at 4 weeks, maximal 4 months.
  • Compressive Optic Neuropathy Compressive optic neuropathy can cause permanent visual loss. The treatment possibilities include high doses of corticosteroids, irradiation, and orbital decompression. Some patients require only one of these modalities, while other patients need combined therapies.
  • Compressive Optic Neuropathy As in the treatment of acute congestive thyroid orbitopathy, radiation therapy is becoming increasingly popular. A retrospective series of 84 patients with compressive optic neuropathy treated with either corticosteroids or radiation therapy supports mounting evidence that radiation therapy may be safer and more effective than corticosteroids. Radiation therapy, however, must be administered in fractionated doses, which delays its beneficial effect. For this reason, if visual dysfunction progresses while the patient is on corticosteroids, surgical decompression is usually recommended if the patient is a surgical candidate.
  • Orbital decompression Orbital decompression is indicated for compressive optic neuropathy when there has been failure of or contraindication for corticosteroids or radiation therapy or if corticosteroid dependence has developed with intolerable side effects. Other indications include excessive proptosis with exposure keratitis and corneal ulceration, pain relief, and cosmesis for disfiguring exophthalmos. Orbital decompression may also be indicated as a preliminary procedure to extraocular muscle surgery on a patient with sufficient proptosis to suggest that decompression might ultimately be required.
  • Orbital decompression A variety of approaches may be used, each with its own advantages and associated complications. The transorbital (via fornix or eyelid) approach to inferior and medial wall decompression is the most common approach used by ophthalmologists. The addition of a lateral wall advancement has the advantage of both further increasing the orbital volume and simultaneously improving upper eyelid retraction; this is the technique we prefer.
  • ORBITAL DECOMPRESSION Subciliary approach.Inferior & medial wall (6mm proptosis).Remove bone to posterior wall maxillary sinus (5mm more posterior on medial wall), Avoid IO neurovascular bundle, and the anterior and posterior ethmoidal arteries.Incise periosteum in A-P direction posteriorly and circumferentially anteriorly. Complications: visual loss, A pattern ET
  • Motility Disorders A major source of morbidity in thyroid orbitopathy, and the most frequent problem associated with orbital decompression surgery, has been strabismus. In patients with relatively minimal degrees of ocular misalignment, diplopia can be avoided with a compensatory head posture, Fresnel plastic press-on prisms, or temporary occlusion. Unfortunately there is significant image degradation as larger prisms are used, limiting their efficacy. If there is marked asymmetry in ocular deviation in different fields of gaze, prisms are also less effective. In some cases during the inflammatory period, use of intramuscular botulinum toxin has shown some efficacy. Extraocular muscle surgery should be postponed until the muscles are no longer inflamed and the deviation has remained stable for at least 6 months.
  • Surgery STRABISMUS SURGERY:-Aim for maximal area of fusion without abnormal head posture.IR recession on adjustable +/- contra SR recessioniii) EYELID SURGERY:- Upper Lid retraction - Muller´s tenotomy (<2mm), levator Z myotomy or recession on hangback sutures, levator tenotomy +/- horns. Lower Lid retraction - Usually needs a spacer from donor sclera (lid retraction X 2 = amount of sclera required) iv) BLEPHAROPLASTY for excess skin and fat Ideally treatment combines a multidisciplinary coherent approach such as Combined radiotherapy and immunosuppression trial
  • INFLAMMATORY CONDITIONS
  • Orbital Cellulitis
  • Myositis
  • Orbital Scleritis
  • Inflammatory Lesion at the Apex of Orbit
  • Lymphoid Infiltration
  • ORBITAL TUMORS
  • Mucocoele
  • Pseudotumors
  • Dermoid Cyst
  • Dermoid Cyst
  • Capillary Haemangioma
  • Lymphangioma
  • Lymphangioma
  • Optic Nerve Glioma
  • Optic Nerve Glioma
  • Neurofibroma
  • Neurofibroma
  • Optic Nerve Meningioma (Rail Road Track Appearance RE)
  • Meningioma
  • Rhabdomyosarcoma
  • Rhabdomyosarcoma
  • Mucoid Tumor
  • Metastasis (CA Breast)
  • VASCULAR ANNOMALIES
  • Arterio-Venous Malformation
  • Varices
  • Venous Malformation (Valsalva’s Maneuver
  • Varices
  • Thank You
  • Thank You