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Ptosis
Disease-a-Month ] (2016) ]]]–]]]
Contents lists available at ScienceDirect
Disease-a-Month journal homepage: www.elsevier.com/locate/disamonth
Ptosis Krishna Patel, MD, Sarah Carballo, MS, Lisa Thompson, MD
Blepharoptosis, also known as ptosis, is a common ophthalmologic condition defined by either unilateral or bilateral drooping of the eyelid. Ptosis can be caused by weakness of the levator palpebrae superioris and Muller's muscle, which are responsible for lifting the eyelid, or by pathology of the nerves innervating the muscles. Ptosis is prevalent in all age groups, and is important to identify, as it can lead to reversible loss of peripheral vision in adults and amblyopia in children. Occasionally, ptosis can also be a subtle clinical sign of disease elsewhere. Ptosis can be categorized by age: congenital vs acquired, as well as etiology: aponeurotic, neurological, mechanical, traumatic, and pseudoptosis.
Examination When examining a patient with ptosis, specific measurements should be taken in order to determine the severity of the ptosis. (1) The margin-reflex distance 1 (MRD1) is obtained by measuring the distance from the upper eyelid margin to the corneal light reflex. If the pupil is occluded due to severe ptosis, the MRD1 may be zero, or even a negative value. The normal MRD1 is 4–5 mm. MRD2 is a measure of scleral show, and is obtained by measuring the corneal light reflex to the lower eyelid margin. (2) The vertebral palpebral fissure can be measuring by finding the distance between the upper and lower eyelid. Normal measurement is 9–12 mm. (3) Upper eyelid crease position is the distance between the eyelid crease and the margin of the upper eyelid. The lid crease is formed by the insertion of muscle fibers from the levator into the skin. This measurement should be 8–9 mm in males and 9–11 mm in females. In patients with involutional ptosis, the lid crease may be elevated. (4) Levator function is measured by negating the action of the frontalis muscle, and then measuring upper eyelid excursion as a patient looks from downgaze to upgaze. Levator function can be classified as poor (0–5 mm lid elevation), fair (6–11 mm lid elevation), and good (4 12 mm lid elevation). (5) Lagophthalmos is the gap between the eyelids when the eyes are closed. Lagophthalmos can lead to dry eyes and exposure keratopathy. http://dx.doi.org/10.1016/j.disamonth.2016.10.004 0011-5029/& 2016 Elsevier Inc. All rights reserved.
2
K. Patel et al. / Disease-a-Month ] (2016) ]]]–]]]
In addition, extraocular muscle movements and pupillary exam should also be done to look for neurological abnormalities that may be causing the ptosis. Visual fields are done with lids in their ptotic state and then taped, to determine the degree of peripheral vision loss secondary to ptosis. External photographs are also taken as they can helpful in monitoring patients and obtaining measurements.
Congenital ptosis Congenital ptosis is the most common cause of ptosis in childhood, and is defined as ptosis present at birth or by 1 year of age. Also known as dysmyogenic ptosis, congenital ptosis is due to developmental dystrophy of the levator muscle. The most common cause of congenital ptosis is idiopathic, however, it can also be familial and transmitted in an autosomal dominant inheritance pattern. Approximately 75% of congenital ptosis is unilateral, and leads to amblyopia in 20% of cases either due to occlusion of the pupil or by causing amblyogenic astigmatism in the affected eye.1 Congenital ptosis can be mild (2 mm), moderate (3 mm), or severe (4 mm). In cases of mild ptosis, the eyelid may only partially cover the pupil, and so these patients may not have any abnormal positioning of the head. In cases of more severe ptosis, patients may present in a “chin-up” position with elevation of the eyebrow. The treatment for congenital ptosis is surgical. Ideally, surgery is delayed until patients are about 4–5 years of age, as eyelid tissue as larger and patients are more cooperative and amblyopia is treated by patching or other therapy. However, if the ptosis is severe or the clinical signs of early amblyopia are severe and are not treatable otherwise, surgery is considered sooner.
Acquired ptosis Aponeurotic ptosis, the most common cause of acquired ptosis in adults, results from disinsertion or dehiscence of the levator aponeurosis from the tarsal plate. Patients may present with elevated or absence of an upper lid crease or compensatory elevation of the affected eyebrow secondary to the devitalized attachments (Picture 1). The clinical picture may also include pseudoretraction of the unaffected lid due to Hering's law of equal innervation, which is the law of equal and simultaneous innervation to synergistic muscles. Levator function is usually normal (12–15 mm), as the muscle itself is unaffected. Aponeurotic ptosis may worsen in downgaze, and can limit the superior visual field and hinder the ability to read. A physiologic involutional change is commonly seen in the elderly, whereas repetitive traction on the eyelids, such as from rigid contact lenses, is more commonly seen in younger
Picture 1. Patient with aponeurotic ptosis with characteristic elevation of lid crease due to dehiscence of the levator aponeurosis from the tarsal plate.
K. Patel et al. / Disease-a-Month ] (2016) ]]]–]]]
3
patients.2 An eyelid speculum used in ocular surgery may also lead to the development of aponeurotic ptosis. Lid trauma may be caused by contraction of the orbicularis oculi against the rigid speculum, resulting in disinsertion of the levator aponeurosis. It has been noted to be a transient complication occurring in 6% of patients after cataract surgery3 and is also well documented in patients after radial keratotomy.4 Trauma or conditions which result in chronic eye rubbing (i.e., excessive crying, dry eyes, and foreign body sensation) can lead to ptosis as well.
Neurogenic ptosis Neurologic diseases affecting the neuromuscular junction, cranial nerves, brainstem, and sympathetic ganglia may also lead to specific forms of acquired ptosis. Myasthenia gravis (MG) is the first of the neurogenic forms of ptosis to be discussed here. It is an autoimmune disorder in which autoantibodies directed against postganglionic acetylcholine receptors damage the neuromuscular junction of skeletal muscle. The presence of these antibodies cause muscle fatigability and a variety of symptoms. Ocular symptoms of MG include fatigable unilateral or bilateral ptosis, ocular motor deficits causing diplopia, and orbicularis oculi weakness. Approximately 50% patients with MG initially present with isolated ocular findings. In patients with MG, symptoms resolve after several minutes of rest. The ice-pack test, in which an ice-pack is applied to an affected patient's eyelids for 3 min, will lead to improvement in ptosis. Edrophonium chloride typically causes a brief improvement in ptosis and ocular motility, and can be used as part of diagnosis as well. Acetylcholine receptor antibody (AChR-Ab) levels can be obtained, are detectable in about 70% of patients with ocular MG. Cranial nerve III (oculomotor nerve) palsy can also lead to neurological ptosis. Cranial nerve 3 (CN3) is split into an inferior and superior division. The inferior division innervates the ipsilateral inferior rectus, medial rectus, and inferior oblique muscles and pupil. The superior division innervates the ipsilateral superior rectus and levator palpebrae superioris muscles. Lesions affecting CN3 may occur anywhere along its path between the brainstem and the extraocular muscles, and can result in either partial or complete third nerve palsy. Patients with complete third nerve palsies will usually have significant ptosis and ophthalmoplegia, which may result in diplopia. In some cases, the ptosis may be so profound that patients are unaware of diplopia or pupillary involvement. Therefore, CN3 testing on physical exam is important. The affected eye will appear in the classic “down and out” position (Picture 2) with a mid-dilated and unreactive pupil. Partial third nerve palsies may affect only one of the divisions or only certain nerve fibers. Pupillary response may be intact, poor, or absent, depending on the lesion. In cases in which a mild anisocoria is present, it will be more apparent in brighter light than in the dark. Mild ptosis or subtle extraocular movement abnormalities may also be present in partial palsies (Picture 3).
Picture 2. Child with a cranial nerve 3 palsy with “down and out” position of the left eye.
4
K. Patel et al. / Disease-a-Month ] (2016) ]]]–]]]
Picture 3. Patient with a left cranial nerve 3 palsy. Note that the right eye is fixing in primary position (A), and only abduction is normal (B). He is limited in adduction (C), elevation (D), and depression (E).
Etiologies of third nerve palsies are often specific to their location, and include, but are not limited to cerebrovascular conditions, structural damage, inflammatory or infectious processes, and trauma. Ischemic/diabetic third nerve palsy is the most common of these etiologies in the adult population. The pathogenesis of this condition is microvascular in nature and often peripheral.5 As such, hypertension and increased age also play a role. The past medical history and lab values, especially HbA1c, are important factors to obtain for this diagnosis. Perhaps the most dangerous etiology of third nerve palsy is compression from an intracranial aneurysm, most commonly at the posterior communicating artery. Especially in acute presentations, it is important to recognize this potential cause of a third nerve palsy, as it may represent an acutely enlarging aneurysm at risk of rupture. Imaging studies such as contrast-enhanced MRI with MRA
K. Patel et al. / Disease-a-Month ] (2016) ]]]–]]]
5
Picture 4. Ptosis of the right eyelid seen in a patient with Horner's syndrome.
or CTA have sensitivities of 95–98% for detecting aneurysm with associated third nerve palsy, though invasive cerebral angiography is the gold standard.6 Other etiologies include trauma and ophthalmoplegic migraine or “cranial neuralgia” in which the third cranial nerve is the one most commonly affected. Horner syndrome is the last of the neurogenic causes of ptosis to be discussed. The classic triad of Horner syndrome is ipsilateral ptosis, miosis, and anhidrosis secondary to interruption of the sympathetic neuron chain (Picture 4). In contrast to a third nerve palsy, the anisocoria of Horners is more prominent in dim light, as the affected pupil has delayed dilation. In Horner's syndrome, Muller's muscle is often affected, whereas in most other causes of ptosis, the levator superioris is often affected. This will result in a more mild ptosis. Other distinguishing symptoms of Horner syndrome include ipsilateral conjunctival injection, nasal congestion, and an increased near point of accommodation.7 The diagnosis can be confirmed with topical administration of apraclonidine. Careful observation will reveal that the affected pupil dilates more than the unaffected pupil, therefore changing the pattern of anisocoria. The ptotic lid will often reverse as well, showing a relative lid retraction. From here, associated symptoms can help determine the bigger picture and the underlying etiology of the Horner syndrome itself. Chronic Progressive External Ophthalmoplegia (CPEO) is a type of myopathic ptosis, due to defective mitochondrial function. Patients with CPEO may present with severe bilateral progressive ptosis, complete ophthalmoplegia with no restrictions on forced ductions, and orbicularis oculi weakness. Patients may have onset of this disease at any age. Kearns-Sayre syndrome is a variant of CPEO seen in the first or second decade of life. In this condition, patients have CPEO along with retinal pigmentary changes and cardiac conduction defects. In another variant, known as Refsum's disease, patients have elevated phytanic acid levels. Mechanical ptosis is secondary to an eyelid lesion which causes excess weight on the upper lid (Picture 5). This may be due to a number of causes including, but not limited to, infections, inflammation, and tumors which can be readily diagnosed from physical exam and history. Traumatic ptosis is oftentimes the result of increased swelling and inflammation secondary to orbital or facial trauma. It should always be evaluated properly to ensure more severe injury to the globe, extraocular muscles, or cranial nerves has not occurred.
Picture 5. Mechanical ptosis caused by excessive weight, or chalazion, on the upper eyelid.
K. Patel et al. / Disease-a-Month ] (2016) ]]]–]]]
6
Pseudoptosis is not true ptosis, as it is not caused by any pathology of the eyelids, but is rather the appearance of ptosis secondary to abnormalities of the globe or surrounding skin. An example of psuedoptosis is dermatochalasis, in which case upper eyelid skin hangs over the lid margin, giving the appearance of ptosis. Other examples are cases of microphthalmos, anophthalmos, and phthisis bulbi, in which a small or absent eye can give the appearance of ptosis.
Conclusion The treatment for ptosis will vary depending on the etiology, and in certain cases, such as myasthenia gravis, systemic therapy may correct the ptosis. However, in most cases, patients with ptosis require surgical correction with blepharoplasty. In mild cases, ptosis may be observed, and patients should be monitored every 3–12 months for progression. Primary care physicians can play an important role in the management of ptosis, as early diagnosis is crucial for optimal results. In children, early diagnosis can prevent amblyopia which may affect life-long vision. In adults, ptosis can be a harbinger for life threatening disease, or lead to significant vision loss. Measurements for evaluation of ptosis. Measurement
Method
Normal values
MRD 1
Upper lid margin to corneal light reflex
4–5 mm
Vertebral palpebral fissure
Distance between upper and lower eyelid
9–12 mm
Upper eyelid crease position
Distance between eyelid crease and margin of upper eyelid
8–9 males 9–11 females
Levator function
Negating frontalis, measuring eyelid exertion from downgaze to upgaze
0–5 mm (poor) 6–11 (fair) 4 12 mm (good)
References 1. Sudhakar P, Vu Q, Kosoko-Lasaki O, Palmer M. Upper eyelid ptosis revisited. Am J Clin Med. 2009;6:5–14. 2. Kersten RC, de Conciliis C, Kulwin DR. Acquired ptosis in the young and middle-aged adult population. Ophthalmology. 1995;102:924. 3. Bernardino CR, Rubin PA. Ptosis after cataract surgery. Semin Ophthalmol. 2002;17:144. 4. Linberg JV, McDonald MB, Safir A, Googe JM. Ptosis following radial keratotomy. Performed using arigid eyelid speculum. Ophthalmology. 1986;93:1509. 5. Keane JR, Ahmadi J. Most diabetic third nerve palsies are peripheral. Neurology. 1998;51:1510. 6. Jacobson DM, Trobe JD. The emerging role of magnetic resonance angiography in the management of patients with third cranial nerve palsy. Am J Ophthalmol. 1999;128:94. 7. Walton KA, Buono LM. Horner syndrome. Curr Opin Ophthalmol. 2003;14:357.
Picture references (1). (2). (3). (4). (5).
Chen, William PD. Published January 1, 2010. p. 193–210. ©2010. Kliegman RM, Stanton BMD, St. Geme J, et al. Nelson Textbook of Pediatrics. 19th ed. Philadelphia: Saunders; 2011. Rubin, Steven E; Shah, Raza M. Published January 2, 2014. p. 1225–1232.e2. ©2014. Liu, Grant T, MD; Volpe, Nicholas J, MD; Galetta, Steven L, MD. Published January 1, 2010. p. 415–447. ©2010. Bowling, Brad, FRCSEd(Ophth), FRCOphth, FRANZCO. Published January 1, 2016. p. 1–62. ©2016.
Contents lists available at ScienceDirect
Disease-a-Month journal homepage: www.elsevier.com/locate/disamonth
Ptosis Krishna Patel, MD, Sarah Carballo, MS, Lisa Thompson, MD
Blepharoptosis, also known as ptosis, is a common ophthalmologic condition defined by either unilateral or bilateral drooping of the eyelid. Ptosis can be caused by weakness of the levator palpebrae superioris and Muller's muscle, which are responsible for lifting the eyelid, or by pathology of the nerves innervating the muscles. Ptosis is prevalent in all age groups, and is important to identify, as it can lead to reversible loss of peripheral vision in adults and amblyopia in children. Occasionally, ptosis can also be a subtle clinical sign of disease elsewhere. Ptosis can be categorized by age: congenital vs acquired, as well as etiology: aponeurotic, neurological, mechanical, traumatic, and pseudoptosis.
Examination When examining a patient with ptosis, specific measurements should be taken in order to determine the severity of the ptosis. (1) The margin-reflex distance 1 (MRD1) is obtained by measuring the distance from the upper eyelid margin to the corneal light reflex. If the pupil is occluded due to severe ptosis, the MRD1 may be zero, or even a negative value. The normal MRD1 is 4–5 mm. MRD2 is a measure of scleral show, and is obtained by measuring the corneal light reflex to the lower eyelid margin. (2) The vertebral palpebral fissure can be measuring by finding the distance between the upper and lower eyelid. Normal measurement is 9–12 mm. (3) Upper eyelid crease position is the distance between the eyelid crease and the margin of the upper eyelid. The lid crease is formed by the insertion of muscle fibers from the levator into the skin. This measurement should be 8–9 mm in males and 9–11 mm in females. In patients with involutional ptosis, the lid crease may be elevated. (4) Levator function is measured by negating the action of the frontalis muscle, and then measuring upper eyelid excursion as a patient looks from downgaze to upgaze. Levator function can be classified as poor (0–5 mm lid elevation), fair (6–11 mm lid elevation), and good (4 12 mm lid elevation). (5) Lagophthalmos is the gap between the eyelids when the eyes are closed. Lagophthalmos can lead to dry eyes and exposure keratopathy. http://dx.doi.org/10.1016/j.disamonth.2016.10.004 0011-5029/& 2016 Elsevier Inc. All rights reserved.
2
K. Patel et al. / Disease-a-Month ] (2016) ]]]–]]]
In addition, extraocular muscle movements and pupillary exam should also be done to look for neurological abnormalities that may be causing the ptosis. Visual fields are done with lids in their ptotic state and then taped, to determine the degree of peripheral vision loss secondary to ptosis. External photographs are also taken as they can helpful in monitoring patients and obtaining measurements.
Congenital ptosis Congenital ptosis is the most common cause of ptosis in childhood, and is defined as ptosis present at birth or by 1 year of age. Also known as dysmyogenic ptosis, congenital ptosis is due to developmental dystrophy of the levator muscle. The most common cause of congenital ptosis is idiopathic, however, it can also be familial and transmitted in an autosomal dominant inheritance pattern. Approximately 75% of congenital ptosis is unilateral, and leads to amblyopia in 20% of cases either due to occlusion of the pupil or by causing amblyogenic astigmatism in the affected eye.1 Congenital ptosis can be mild (2 mm), moderate (3 mm), or severe (4 mm). In cases of mild ptosis, the eyelid may only partially cover the pupil, and so these patients may not have any abnormal positioning of the head. In cases of more severe ptosis, patients may present in a “chin-up” position with elevation of the eyebrow. The treatment for congenital ptosis is surgical. Ideally, surgery is delayed until patients are about 4–5 years of age, as eyelid tissue as larger and patients are more cooperative and amblyopia is treated by patching or other therapy. However, if the ptosis is severe or the clinical signs of early amblyopia are severe and are not treatable otherwise, surgery is considered sooner.
Acquired ptosis Aponeurotic ptosis, the most common cause of acquired ptosis in adults, results from disinsertion or dehiscence of the levator aponeurosis from the tarsal plate. Patients may present with elevated or absence of an upper lid crease or compensatory elevation of the affected eyebrow secondary to the devitalized attachments (Picture 1). The clinical picture may also include pseudoretraction of the unaffected lid due to Hering's law of equal innervation, which is the law of equal and simultaneous innervation to synergistic muscles. Levator function is usually normal (12–15 mm), as the muscle itself is unaffected. Aponeurotic ptosis may worsen in downgaze, and can limit the superior visual field and hinder the ability to read. A physiologic involutional change is commonly seen in the elderly, whereas repetitive traction on the eyelids, such as from rigid contact lenses, is more commonly seen in younger
Picture 1. Patient with aponeurotic ptosis with characteristic elevation of lid crease due to dehiscence of the levator aponeurosis from the tarsal plate.
K. Patel et al. / Disease-a-Month ] (2016) ]]]–]]]
3
patients.2 An eyelid speculum used in ocular surgery may also lead to the development of aponeurotic ptosis. Lid trauma may be caused by contraction of the orbicularis oculi against the rigid speculum, resulting in disinsertion of the levator aponeurosis. It has been noted to be a transient complication occurring in 6% of patients after cataract surgery3 and is also well documented in patients after radial keratotomy.4 Trauma or conditions which result in chronic eye rubbing (i.e., excessive crying, dry eyes, and foreign body sensation) can lead to ptosis as well.
Neurogenic ptosis Neurologic diseases affecting the neuromuscular junction, cranial nerves, brainstem, and sympathetic ganglia may also lead to specific forms of acquired ptosis. Myasthenia gravis (MG) is the first of the neurogenic forms of ptosis to be discussed here. It is an autoimmune disorder in which autoantibodies directed against postganglionic acetylcholine receptors damage the neuromuscular junction of skeletal muscle. The presence of these antibodies cause muscle fatigability and a variety of symptoms. Ocular symptoms of MG include fatigable unilateral or bilateral ptosis, ocular motor deficits causing diplopia, and orbicularis oculi weakness. Approximately 50% patients with MG initially present with isolated ocular findings. In patients with MG, symptoms resolve after several minutes of rest. The ice-pack test, in which an ice-pack is applied to an affected patient's eyelids for 3 min, will lead to improvement in ptosis. Edrophonium chloride typically causes a brief improvement in ptosis and ocular motility, and can be used as part of diagnosis as well. Acetylcholine receptor antibody (AChR-Ab) levels can be obtained, are detectable in about 70% of patients with ocular MG. Cranial nerve III (oculomotor nerve) palsy can also lead to neurological ptosis. Cranial nerve 3 (CN3) is split into an inferior and superior division. The inferior division innervates the ipsilateral inferior rectus, medial rectus, and inferior oblique muscles and pupil. The superior division innervates the ipsilateral superior rectus and levator palpebrae superioris muscles. Lesions affecting CN3 may occur anywhere along its path between the brainstem and the extraocular muscles, and can result in either partial or complete third nerve palsy. Patients with complete third nerve palsies will usually have significant ptosis and ophthalmoplegia, which may result in diplopia. In some cases, the ptosis may be so profound that patients are unaware of diplopia or pupillary involvement. Therefore, CN3 testing on physical exam is important. The affected eye will appear in the classic “down and out” position (Picture 2) with a mid-dilated and unreactive pupil. Partial third nerve palsies may affect only one of the divisions or only certain nerve fibers. Pupillary response may be intact, poor, or absent, depending on the lesion. In cases in which a mild anisocoria is present, it will be more apparent in brighter light than in the dark. Mild ptosis or subtle extraocular movement abnormalities may also be present in partial palsies (Picture 3).
Picture 2. Child with a cranial nerve 3 palsy with “down and out” position of the left eye.
4
K. Patel et al. / Disease-a-Month ] (2016) ]]]–]]]
Picture 3. Patient with a left cranial nerve 3 palsy. Note that the right eye is fixing in primary position (A), and only abduction is normal (B). He is limited in adduction (C), elevation (D), and depression (E).
Etiologies of third nerve palsies are often specific to their location, and include, but are not limited to cerebrovascular conditions, structural damage, inflammatory or infectious processes, and trauma. Ischemic/diabetic third nerve palsy is the most common of these etiologies in the adult population. The pathogenesis of this condition is microvascular in nature and often peripheral.5 As such, hypertension and increased age also play a role. The past medical history and lab values, especially HbA1c, are important factors to obtain for this diagnosis. Perhaps the most dangerous etiology of third nerve palsy is compression from an intracranial aneurysm, most commonly at the posterior communicating artery. Especially in acute presentations, it is important to recognize this potential cause of a third nerve palsy, as it may represent an acutely enlarging aneurysm at risk of rupture. Imaging studies such as contrast-enhanced MRI with MRA
K. Patel et al. / Disease-a-Month ] (2016) ]]]–]]]
5
Picture 4. Ptosis of the right eyelid seen in a patient with Horner's syndrome.
or CTA have sensitivities of 95–98% for detecting aneurysm with associated third nerve palsy, though invasive cerebral angiography is the gold standard.6 Other etiologies include trauma and ophthalmoplegic migraine or “cranial neuralgia” in which the third cranial nerve is the one most commonly affected. Horner syndrome is the last of the neurogenic causes of ptosis to be discussed. The classic triad of Horner syndrome is ipsilateral ptosis, miosis, and anhidrosis secondary to interruption of the sympathetic neuron chain (Picture 4). In contrast to a third nerve palsy, the anisocoria of Horners is more prominent in dim light, as the affected pupil has delayed dilation. In Horner's syndrome, Muller's muscle is often affected, whereas in most other causes of ptosis, the levator superioris is often affected. This will result in a more mild ptosis. Other distinguishing symptoms of Horner syndrome include ipsilateral conjunctival injection, nasal congestion, and an increased near point of accommodation.7 The diagnosis can be confirmed with topical administration of apraclonidine. Careful observation will reveal that the affected pupil dilates more than the unaffected pupil, therefore changing the pattern of anisocoria. The ptotic lid will often reverse as well, showing a relative lid retraction. From here, associated symptoms can help determine the bigger picture and the underlying etiology of the Horner syndrome itself. Chronic Progressive External Ophthalmoplegia (CPEO) is a type of myopathic ptosis, due to defective mitochondrial function. Patients with CPEO may present with severe bilateral progressive ptosis, complete ophthalmoplegia with no restrictions on forced ductions, and orbicularis oculi weakness. Patients may have onset of this disease at any age. Kearns-Sayre syndrome is a variant of CPEO seen in the first or second decade of life. In this condition, patients have CPEO along with retinal pigmentary changes and cardiac conduction defects. In another variant, known as Refsum's disease, patients have elevated phytanic acid levels. Mechanical ptosis is secondary to an eyelid lesion which causes excess weight on the upper lid (Picture 5). This may be due to a number of causes including, but not limited to, infections, inflammation, and tumors which can be readily diagnosed from physical exam and history. Traumatic ptosis is oftentimes the result of increased swelling and inflammation secondary to orbital or facial trauma. It should always be evaluated properly to ensure more severe injury to the globe, extraocular muscles, or cranial nerves has not occurred.
Picture 5. Mechanical ptosis caused by excessive weight, or chalazion, on the upper eyelid.
K. Patel et al. / Disease-a-Month ] (2016) ]]]–]]]
6
Pseudoptosis is not true ptosis, as it is not caused by any pathology of the eyelids, but is rather the appearance of ptosis secondary to abnormalities of the globe or surrounding skin. An example of psuedoptosis is dermatochalasis, in which case upper eyelid skin hangs over the lid margin, giving the appearance of ptosis. Other examples are cases of microphthalmos, anophthalmos, and phthisis bulbi, in which a small or absent eye can give the appearance of ptosis.
Conclusion The treatment for ptosis will vary depending on the etiology, and in certain cases, such as myasthenia gravis, systemic therapy may correct the ptosis. However, in most cases, patients with ptosis require surgical correction with blepharoplasty. In mild cases, ptosis may be observed, and patients should be monitored every 3–12 months for progression. Primary care physicians can play an important role in the management of ptosis, as early diagnosis is crucial for optimal results. In children, early diagnosis can prevent amblyopia which may affect life-long vision. In adults, ptosis can be a harbinger for life threatening disease, or lead to significant vision loss. Measurements for evaluation of ptosis. Measurement
Method
Normal values
MRD 1
Upper lid margin to corneal light reflex
4–5 mm
Vertebral palpebral fissure
Distance between upper and lower eyelid
9–12 mm
Upper eyelid crease position
Distance between eyelid crease and margin of upper eyelid
8–9 males 9–11 females
Levator function
Negating frontalis, measuring eyelid exertion from downgaze to upgaze
0–5 mm (poor) 6–11 (fair) 4 12 mm (good)
References 1. Sudhakar P, Vu Q, Kosoko-Lasaki O, Palmer M. Upper eyelid ptosis revisited. Am J Clin Med. 2009;6:5–14. 2. Kersten RC, de Conciliis C, Kulwin DR. Acquired ptosis in the young and middle-aged adult population. Ophthalmology. 1995;102:924. 3. Bernardino CR, Rubin PA. Ptosis after cataract surgery. Semin Ophthalmol. 2002;17:144. 4. Linberg JV, McDonald MB, Safir A, Googe JM. Ptosis following radial keratotomy. Performed using arigid eyelid speculum. Ophthalmology. 1986;93:1509. 5. Keane JR, Ahmadi J. Most diabetic third nerve palsies are peripheral. Neurology. 1998;51:1510. 6. Jacobson DM, Trobe JD. The emerging role of magnetic resonance angiography in the management of patients with third cranial nerve palsy. Am J Ophthalmol. 1999;128:94. 7. Walton KA, Buono LM. Horner syndrome. Curr Opin Ophthalmol. 2003;14:357.
Picture references (1). (2). (3). (4). (5).
Chen, William PD. Published January 1, 2010. p. 193–210. ©2010. Kliegman RM, Stanton BMD, St. Geme J, et al. Nelson Textbook of Pediatrics. 19th ed. Philadelphia: Saunders; 2011. Rubin, Steven E; Shah, Raza M. Published January 2, 2014. p. 1225–1232.e2. ©2014. Liu, Grant T, MD; Volpe, Nicholas J, MD; Galetta, Steven L, MD. Published January 1, 2010. p. 415–447. ©2010. Bowling, Brad, FRCSEd(Ophth), FRCOphth, FRANZCO. Published January 1, 2016. p. 1–62. ©2016.