292
Surv Ophthalmol
35 (4) January-February
1991
48. Messinger A, Radkowski MA, Greenwald M, Pensler J: Orbital roof fractures in the pediatric population. Plust Reconstr Surg 84:213-218, 1989 49. Milauskas AT: Diagnosis and Management of Blowout Fractures of the Orbit. Springfield Ill, Charles C Thomas, 1969 50. Millman AL, Della Rota RC, Spector S, et al: Steroids and orbital blow-out fractures: A new systematic concept in medical management and surgical decision making: Adu Ophthal Plast Reconstr Sure 6:291-300. 1987 51. Nicholson DH, Guzak SVrLoss ofvision after repair oforbital floor fracture. Trans Am Acad Ophthalmol Otolaryngol 75: 1402, 1971 RW, Depeu RV: Blow-out fractures of the orbit in 52. Patterson the absence of diplopia and enophthalmos. Am J Ophthalmol 55:1253, 1963 of volumetric changes in 53. Pearl RM: Surgical management the bony orbit. Ann Plast Surg 19:349, 1987 54. Pearl RM, Vistnes LM: Orbital blow-out fractures: an approach to management. Am Plust Surg 1:267-270, 1978 . 55. Pfeiffer RL: Traumatic enoohthalmos. Am I Ophthalmol ?0:718, 1943 56. Putterman AM, Stevens T, Urist MJ: Non-surgical management of blow-out fractures of the orbital floor. Am J Ophthalmol 77:232, 1974 57. Putterman AM: Late management of blow-out fractures of the orbital floor. Trans Am Acad Ophthalmol Otolaryngol 83: 650-659, 1977 58. Schjelderup H: Some considerations concerning traumatic diplopia. Acta Ophthalmol28:337, 1950 59. Smith B: Early fractures of the orbit. Trans Am Acad Ophthalmol Otolaryngol 67:63, 1963 60. Smith B: The discovery of blow out fractures of the orbit. Adv Ophthal Plast Surg 6:193-195, 1987 L
_I
DUTTON, 61. 62. 63. 64. 65. 66.
67.
68.
1
69. 70. 71.
MANSON,
ILIFF, PUTTERMAN
Smith B: On the treatment ofblow-out fractures ofthe orbit. Plast Reconstr Surg 62: 100, 1978 Smith B, Converse JM: Early treatment of orbital floor fractures. Trans Am Acad Ophthulmol Otolaryngol 61:602, 1957 Smith B, Dyer JA, Bleeker GM: Discussion of lesions of the orbit affecting motility. Int Ophthalmol Clin 1:208, 1971 Smith B, Nightingale JH: Fractures of the orbit, blow-out and naso-orbital fractures. Int Ophthalmol Clin 18:137, 1978 Smith B, Regan WR: Blow-out fractures of the orbit. Am J Ophthalmol 44:733, 1957 Smith B, Lisman RD, Simonton J, et al: Vokmann’s contracture of the extraocular muscles following blow-out fracture. Plast Reconstr Surg 74:200, 1984 Stahlnecker M, Whitaker L, Herman G, Katowtiz J: Evaluation and secondary treatment of post-traumatic enophthalmos. Presented at the American Association of Plastic Surgeons, Coronado Beach, CA, April 29, 1985 .Tajima S, Sugimoto C, Tanino R, et al: Surgical treatment of malunited fractures of zygoma with diplopia and with comments on blow-out fractures. J Muxillofac Surg 2:201, 1974 Volkmann R: Die ischemischen muskella hmongen und frackturen. Centralbl Chir 8~80 1, 188 1 Whyte DK: Blow-out fractures of the orbit. Br J Ophthalmol 52:74, 1968 Wilkins R, Havins W: Current treatment of blow-out fractures. Ophthalmology 89:464-466, 1982
The illustrations in this article are copyright, Johns Hopkins Department of Art as Applied to Medicine. Reprint address: Paul N. Manson, M.D., Plastic Surgery, MIEMSS, 22 S. Greene Street, Baltimore, Maryland 21201.
III. The Conservative Approach. ALLEN M. PUTTERMAN, M.D., Department of Ophthalmology, Eye and Ear In irmury, Universit of Illinois at Chicago, and Machael Reese Hospital and Medical Center an d the University o? Chicago, Chicago, Illinois When the eye is struck by an object larger than the orbital entrance, such as a fist, a blow-out fracture of the orbital floor can occur. The force of the blow to the eye is transmitted to the orbital contents and then to the orbital walls. The weakest areas of the orbital walls - the medial wall and floor of the orbit - rupture, and the force of the blow is transmitted into the ethmoid and maxillary sinuses, which absorb the impact like a pressure valve. (This is most likely “nature’s way” of preventing an eye from rupturing.) When an orbital floor fracture occurs, there can be associated diplopia due to entrapment of orbital fat or the inferior ocular muscles into the fracture site and maxillary sinus. Enophthalmos and hypoophthalmos (downward sinking of the eye) can also occur due to displacement of the orbital contents into the maxillary and ethmoid sinuses. Infraorbital anesthesia is another symptom of the blow-out fracture; it is due to injury to the infraorbital nerve as it courses through the orbital fracture. The extraocular muscle motility and infraorbital anesthesia frequently improve, and the enophthalmos and hypoophthalmos either persist or worsen as the edema
and hemorrhage subside. When a blow-out fracture of the orbital floor is suspected, a thorough eye examination should be performed. The trauma that causes a blow-out fracture can also lead to a 5-10% incidence of injury to the eye, such as iritis, hyphema, retinal detachment, or glaucoma. When an orbital floor fracture is suspected, conventional orbital roentgenograms should be performed. If this does not demonstrate a fracture, orbital tomograms or computed tomographic (CT) scans of the orbit should be obtained. (I do not order CT scans routinely for all suspected orbital floor fractures. I do order them selectively to aid in differentiating an entrapped, inferior rectus muscle from a contused inferior rectus muscle or for evaluation of the size of the implant needed to treat late enophthalmos.)
Early Treatment The treatment of orbital floor fractures remains controversial. From 1950 to 1974, most of these fractures were considered a medical emergency and immediate surgery was advocated. Most sur-
ORBITAL FRACTURES geons believed that unless immediate surgery was performed, the patient would have permanent, visually handicapping double vision as well as cosmetically unacceptable enophthalmos. In 1974, Putterman et al” described 57 patients with pure blow-out fractures of the orbital floor who were followed up without surgery despite the severity of their symptoms and fractures. We found that this group of patients did surprisingly well. All had resolution of visually handicapping diplopia (although 20% had double vision in extreme upgaze, which was not bothersome), and none developed cosmetically unacceptable enophthalmos (although 20% had measurable enophthalmos less than 3 mm, which was cosmetically acceptable). Infraorbital anesthesia also decreased with time in these patients. Based on this study, we encouraged a conservative management approach to all blow-out fractures of the orbital floor and, in retrospect, I believe we were overexuberant in advocating that no blow-out fractures be operated on for four to six months. My philosophy of treating orbital fractures has become more clearly delineated after years of further study and experience.7,8,‘0 In the majority of cases the need for surgery versus observation is quite obvious. Early surgery (within one to three weeks after trauma) is indicated in patients with severe, visually handicapping, nonresolving diplopia with a positive forced duction test that does not allow upward movement of the eye, and with CT evidence of inferior rectus muscle entrapment, or in patients with severe cosmetically unacceptable enophthalmos or hypo-ophthalmos. In patients with minimal diplopia, good ocular motility, and no significant enophthalmos or hypo-ophthalmos, observation is in order. There is, I believe, no evidence to support that the size of the orbital fracture on CT scans or roentgenograms correlates with the amount of enophthalmos or hypo-ophthalmos. Therefore, I do not operate early on large orbital floor fractures that are not associated with significant enophthalmos or hypo-ophthalmos. There are exceptional cases in which immediate surgery (during the first few days after trauma) is indicated. One such patient, described by Berkowitz et al had complete prolapse of the eye into the maxillary sinus following an orbital floor fracture.’ The problem of whether to perform surgery exists in those marginal cases with slow but slight resolution of diplopia or with progression of a cosmetic deformity. In this group of patients, I closely examine the patient during the first one to three weeks after trauma. I monitor the changes in diplopia, extraocular muscle motility, enophthalmos, and hypo-ophthalmos. Diplopia is measured by charting areas of diplopia and simultaneous binocular vision in all positions of gaze on a drawn square the
“93
center of which is the primary position of gaze. Extraocular muscle motility is measured by the Urist light reflex technique.‘” Enophthalmos is measured by Hertel exophthalmometry, and hypo-ophthalmos is measured by aligning the top of a ruler through both medial canthi and noting where the ruler bisects each eye. Patients are placed on a regimen of systemic corticosteroids for five to seven days. For an adult weighing approximately 67.5kg, 60 mg of prednisone is given orally each day for 2 days, 40 mg for 2 days, and then 20 mg for 2 days. Millman et al demonstrated that steroids speed the resolution of diplopia in patients who do not need surgery and that these drugs cause no change in patients who require surgery.” If the motility restriction is secondary to orbital edema and hemorrhage, steroids lead to rapid resolution of these problems. However, if the motility restriction is secondary to true entrapment of the extraocular muscles or orbital tissues, steroids effect only a minimal improvement of diplopia. (This information should help in the decision and timing of surgery.) Troublesome diplopia is very common immediately after blow-out fractures of the orbital floor. I believe that most of the time this is due to entrapment of orbital fat within the fracture site and maxillary sinus, as well as edema and hemorrhage of the orbital fat.” Whitnall demonstrated vertical fibrous bands that traversed through the posterior-inferior orbital fat between the periosteum of the orbital floor and the inferior ocular muscles.” The posterior inferior orbital fat is very fibrotic compared to the looser, more pliable, anterior orbital fat that is encountered in blepharoplasty surgery. Tension on these bands, due to either entrapment or edema and hemorrhage of the orbital fat, can inhibit the motility of the eye (Fig. 1). (I have attempted to prove this theory by grasping the inferior orbital fat during blepharoplasty surgery, and I noted that patients had marked difficulty looking up and down. As soon as I released the orbital fat, the motility improved to normal.) The 1974 study by Putterman et al demonstrated that ocular tnotility disturbances following a blow-out fracture improved with time.” An explanation for this improvement is that resolution of orbital fat edema and hemorrhage leads to decreased tension on the orbital fat bands; a second explanation is that the orbital fat stretches. Another cause of motility problems following blowout fractures is due to actual entrapment of or injury to the inferior rectus muscle. A forced generation and duction test can aid in differentiating an entrapped muscle from a paretic one.” After application of a topical anesthetic to the eye, cotton-tipped applicators saturated with the solution are held over the 6 o’clock and 12 o’clock
294
Surv Ophthalmol
35 (4) January-February
DUTTON,
19 91
limbal position. A toothed forceps is then used to grasp conjunctiva and episcleral tissue at the 6 o’clock limbal position. An attempt is made to move the eye upward and downward, and the ease of these movements is judged. (If there is difficulty in elevating the eye with the forceps, this is measured as a positive forced duction test in upgaze and implies that the inferior rectus muscle or orbital contents are entrapped within the fracture site.) While still holding the forceps with tissue grasped at the 6 o’clock limbus, the examiner asks the patient to look downward. Normally a tug on the forceps is so strong that the instrument is almost pulled from the examiner’s hand. However, if there is minimal pull on the forceps when the patient attempts to look downward, this implies that there is injury to the extraocular muscle with secondary paresis, and this is known as a positive or abnormal generation test. Computed tomographic (CT) scans with reconstruction can also help differentiate entrapped extraocular muscles from swollen muscles.6*g One way of doing this is to obtain axial cuts at 3 mm intervals through the orbit. These axial views are then transmitted by satellite to a highly sophisticated computer which then relays this information back with views that are parallel with the inferior rectus muscle. This can accurately demonstrate entrapment or swelling of the muscle. If this instrumentation is not available, most CT scanners have a computer within them that can simulate this result. If reconstruction is not available, certainly the surgeon should obtain both axial and coronal views through the orbit in order to fully appreciate the inferior rectus muscle. These scans should greatly help in differentiating an inferior rectus muscle that is entrapped from a contused muscle (Figs. 2 8c 3). A contused muscle is usually not entrapped in the fracture site and can be differentiated from a normal muscle by its rounded appearance on the CT scan, compared to the normal appearance of the inferior rectus muscle, which is quite flat (Fig. 3). The decision to perform orbital surgery versus continued observation is thereby determined by closely examining the changes in diplopia, enophthalmis, extraocular muscle motility, and hypoophthalmos during the first two to three weeks after trauma. Again, systemic steroids should speed the improvement in those patients who do not have entrapped muscle and lead to minimal or no change in those who have entrapped muscle. A forced duction and a generation test as well as CT scans with reconstruction should help differentiate an entrapped muscle from a contused swollen muscle. Based on the above protocol, I usually recommend surgically exploring the orbital floor in those patients who have minimal improvement of or no
MANSON, ILIFF,
PUTTERMAN
Hemorrhage and edema of the inferoposterior orbital fat with or without fat entrapment restrict ocular motility after blow-out fracture.
Fig. 1.
change in visually handicapping diplopia during the first three weeks after trauma and for those who develop cosmetically unacceptable enophthalmos or hypo-ophthalmos during this period.” A positive forced duction test, a negative generation test, and evidence of extraocular muscle entrapment on CT scanning further supports performing early surgery in this group of patients. On the other hand, I advocate further observation, without surgery, of those patients with marked improvement or resolution of visually handicapping double vision or those without development of cosmetically unacceptable enophthalmos or hypo-ophthalmos during the first three weeks after trauma. This is supported by a negative forced duction test but by a positive or normal generation test and by contusion or rounding without entrapment of the extraocular muscles on CT scans. For patients requiring surgery within three weeks after trauma, I usually perform orbital floor surgery with the patient under general anesthesia. A lateral canthotomy and cantholysis and inferior fornix approach are used to isolate the fractured orbital floor.‘” Once the orbital contents are released from the fracture site and maxillary sinus, an orbital floor Silastic implant is placed over the orbital floor to prevent further prolapse of orbital contents back into the sinus. I place a thin, 0.5-10 mm
ORBITAL
FRACTURES
Fig. 2. CT scan of orbital floor fracture of the left eye with entrapment of inferior rectus in fracture site (ar-
row). (Reprinted
with permission
Ophthalmology 94:683-687,
from Putterman
AM:
1987.)
sheet of Silastic over the fractured floor. I then create an anterior tongue of the implant as previously described’” and place this within the fracture to prevent anterior migration of the implant. If this is not possible, I will drill holes in the inferior orbital rim and anchor the implant with 2-O Supramid sutures that pass through this hole and the implant.
Late Treatment The late treatment of visually troublesome diplopia and orbital floor fractures occurs in two clinical settings: patients who needed but refused early surgery and patients who were significantly improving during the initial weeks after trauma but did not have the expected complete resolution of bothersome diplopia. I perform extraocular muscle surgery once the motility and diplopia measurements stabilize. In my experience, orbital floor surgery has improved visually handicapping diplopia in a few patients when performed up to five weeks after trauma, but rarely does it improve extraocular muscle motility beyond that time. Therefore, I advocate muscle surgery rather than orbital floor surgery to treat late diplopia because, in my hands, it is more effective. The type of surgery selected is individualized, depending on the degree of extraocular muscle motility imbalance. Most patients will have difficulty looking downward and will notice diplopia in downgaze that interferes with reading. In these cases, if the eye moves upward normally and the results of a forced duction test are normal on upgaze, a reverse Knapp operation is performed in which the medial and lateral rectus muscles are placed at or several millimeters behind the original inferior rectus insertion. If, on the other hand, the forced duction test is positive and the eye does not
Fig. 3. Contusion of right inferior rectus muscle associated with an orbital floor fracture ofthe right eye (arrow). The muscle becomes rounded with edema and hemorrhage secondary to contusion as opposed to the normal inferior rectus seen on the left side, which is much flatter.
move upward normally, an inferior rectus recession must be performed initially to relieve the difficulty on upward movement. The inferior rectus is recessed to the position where the eye can be moved upward normally during surgery. Approximately three to six months later, a modified reverse Knapp procedure is performed. (The reason for not performing all of these procedures together is to avoid anterior segment ischemia and necrosis that can occur when three extraocular muscles are operated on simultaneously.) In the reverse Knapp procedure, the medial and lateral rectus muscles are attached to the inferior rectus muscle insertion site. Folk and I found that this procedure does not produce as good a result as the Knapp procedure, in which the medial and lateral rectus muscles are attached at the superior rectus insertion site. One possibility for the inferior results with the reverse Knapp procedure may be that the superior rectus inserts 8.8 mm from the limbus, whereas the inferior rectus inserts 6.6 mm from the limbus. We have therefore modified this surgery by attaching the medial and lateral rectus muscles approximately 2-3 mm behind the inferior rectus insertion to simulate the position it takes with the Knapp procedure (Fig. 4). We found that this gives much better downward motility. Our present philosophy is that if there is less than 10 prisms of hypertropia in primary position of gaze, we place the medial and lateral rectus muscles at the original inferior rectus muscle insertion site; if there is greater than IO
296
Surv Ophthalmol
\
35 (4) January-February
1991
I
Modified reverse Knapp procedure, in which the medial and lateral rectus muscles are attached to sclera several millimeters behind the insertion of the infe-
Fig. 4.
rior rectus muscle.
prisms of hypertropia in primary position, we place these muscles 2-3 mm behind the inferior rectus insertion. Another option to correct decreased eye movements on downgaze is to perform a Fadom operation in which the inferior rectus muscle is attached to the sclera on the opposite normal eye in order to restrict downward movement.* Although this leads to decrease in downward diplopia; it also inhibits downward movement and makes the patient tilt his or her head downward in order to read. This differs from the modified reverse Knapp procedure, which allows normal downward movement of the
DUTTON,
MANSON,
ILIFF, PUTTERMAN
eyes without having to tilt the head. For patients with pure blow-out fractures who develop late enophthalmos and hypo-ophthalmos, surgery can be performed to relieve the cosmetic disturbance. The Hertel measurements should stabilize before surgery is considered. If the enophthalmos is associated with significant downward sinking of the eye, I advocate treatment with a large Silastic orbital implant that is custom made (Fig. 5).4,5,‘o The technique used to isolate the orbital floor is similar to that used for early treatment of the fractures by a lateral canthotomy, cantholysis, and inferior fornix approach. The size and shape of the implants are determined by studying posterioranterior, and lateral tomograms and by considering their magnification, or if tomograms are not available, the size and shape of implants can be determined by studying CT scans. In addition, the depth that the eye sinks downward helps determine the thickness of the implant directly beneath the eye. Most of these implants are 2-3 mm thick anteriorly, are 4-6 mm thick behind the eye, and extend posteriorly 6-10 mm in thickness. The implant is secured with 2-O Supramid sutures to the inferior orbital rim through drill holes placed in the rim. If the enophthalmos is associated with a narrow palpebral fissure, with minimal downward displacement of the eye, I advocate a Mueller’s muscle-conjunctival resection ptosis procedure.‘~‘0~‘9~‘4 This technique widens the palpebral fissure and creates the illusion that the enophthalmos has resolved (Fig. 6). (This is the opposite of treating exophthalmos with upper lid retraction by excising Mueller muscle and recessing the levator to narrow the palpebral fissure.‘*) Suitable candidates are selected by applying 10% phenylephrine to the upper fornix. If the fissure widens enough that the patient finds the appearance acceptable, the Mueller’s muscle resection procedure can simulate this effect. For patients with enophthalmos and no narrow-
Fig. 5. Left: Patient has 3 mm of enophthalmos associated with a 4.5 mm downward depression of the right eye four months after a nonsurgically managed orbital floor fracture of the right eye. Right: After insertion of a Silastic orbital floor implant, eyes are aligned and the enophthalmos is relieved. (Reprinted with permission from Putterman AM: Trans Am Acad Ophthalmol Otolaryngol 83:650, 1977.)
Fig. 6. Left: Patient three years after a nonsurgically managed orbital fioor fracture of the left eye. Blepharoptosis ofthe left eye and 5 mm decreased palpebral fissure width occurred secondary to 5 mm of enophthalmos. Right: Six months after treatment of the left upper eyelid with Mueller’s muscle-conjunctival resection procedure. Elevation of the left has resolved. (Reprinted upper eyelid and increased palpebral fissure width create the illusion that the enophthalmos with permission from Putterman AM: Ophthalmic Surg 645, 1975.)
Fig. 7. Left: Patient with 3 mm of enophthalmos associated with deep supratarsal sulcus two years after nonsurgical management of an orbital floor fracture of the left eye. Right: Same patient six months after excision of skin and orbital fat and elevation of a crease on the contralateral lid. (Reprinted with permission from Putterman AM: True ,4rn Acad Ophthalmol
Otolqngol
83:650,
1977.)
fissure or downward sinking of the eye who complain of a deep supratarsal sulcus, I excise skin and orbicularis and fat and reconstruct the crease at a higher level on the contralateral normal upper lid to camouflage this abnormality and create an acceptable cosmesis.‘.“’ The effect of this operation is to create symmetry of the upper eyelids (Fig. 7).
ing of the palpebral
Results of Early and Late Treatment The percentage of blow-out fractures that can be successfully followed without surgery versus those fractures that require surgery is difficult for me to calculate. The patients with blow-out fracture referred to me are usually already screened by physicians who are familiar with my approach to treatment; therefore, the majority of those patients with minimal or no diplopia or those patients with rapid improvement of diplopia are not examined by me. Instead, 1 tend to see patients with troublesome diplopia or cosmetically unacceptable enophthalmos or patients for whom the question of observa-
tion versus surgery is not clearly delineated. Despite this, 1 perform early surgery within three weeks after trauma on about 50% of patients and observe, without surgery, about 509% of patients. In the patients followed up without surgery, it usually takes one to three months for the residual diplopia to completely resolve or to stabilize. For those patients who have early surgery, handicapping diplopia usually worsens after surgery in about 75% of patients and takes one to five months to resolve. (It is therefore questionable whether early surgery creates a setting of diplopia similar to the one that occurs immediately after a blow-out fracture. The hemorrhage, edema, and extraocular muscle trauma lead to gradual resolution of diplopia following surgery similar to that following an untreated blowout fracture.) About 25%’ of these patients do not develop worsened diplopia after surgery. With the use of my present regimen of treating blow-out fractures, the need for late surgery in untreated blow-out fractures is rare. Less than 5% of surgically treated patients need secondary surgery..
298
Surv Ophthalmol
35 (4) January-February
1991
Summary In the majority of blow-out fractures it is usually quite clear whether to operate or to observe the patient. In the marginal cases in which there is slow but steady resolution of diplopia with slight change in enophthalmos or hypo-ophthalmos, the decision becomes more difficult. In this group of cases, frequent measurements of extraocular muscle motility, diplopia, enophthalmos, and hypo-ophthalmos are taken. Also, patients whose prognosis is favorable are placed on a regimen of systemic corticosteroids to speed resolution. Lastly, forced duction and generation tests combined with CT scanning and reconstruction can help differentiate an entrapped muscle from one that is contused and paretic. Based on these examinations, the decision for surgery versus observation can usually be made within three weeks after trauma. If patients have resolution of visually handicapping double vision and do not develop cosmetically unacceptable enophthalmos and if they have a negative forced duction test, a positive forced generation test, and contusion without entrapment of the extraocular muscle on CT scan, observation is continued. If, on the other hand, visually handicapping diplopia persists or cosmetically unacceptable enophthalmos or hypo-ophthalmos develops and if this is associated with a positive forced duction test, normal generation test, and evidence of entrapment without contusion on CT scans, orbital floor surgery is recommended within the first three weeks after trauma. Once this decision is made, treatment is performed as early as possible rather than waiting until 2 1 days have actually occurred. For most patients with visually handicapping diplopia that persists later than three weeks after trauma, extraocular muscle surgery is performed. This usually consists of initially recessing the inferior rectus muscle until the eye can move upward freely, and then three to six months later a modified reverse Knapp procedure is performed in which the medial and lateral rectus muscles are placed several millimeters behind the original inferior rectus muscle insertion. If cosmetically unacceptable enophthalmos and hypo-ophthalmos occur later than three weeks after trauma, they are treated surgically after the exophthalmometric measurements stabilize. If the enophthalmos is associated with hypo-ophthalmos, it is treated with a custom-fitting
DUTTON,
MANSON, ILIFF,
PUTTERMAN
Silastic orbital floor implant. If the enophthalmos is associated with a narrow palpebral fissure, it is treated with a Mueller’s muscle-conjunctiva resection procedure. If the enophthalmos is associated only with a deep supratarsal sulcus, it is treated by excising skin and orbicularis and fat and elevating the crease on the contralateral lid.
References RA, Putterman AM, Pate1 DB: Prolapse of the 1. Berkowitz globe into the maxillary sinus after orbital floor fracture. Am J Ophthalmol 91:253-257, 1981 for the manage2. Buckey EC, Meekins BB: Fadem operation ment of complicated incomitant verticle strabismus. Am J Ophthulmol 10k304, 1988 3. Millman AL, Della Rocca RC, Spector S, et al: Steroids and orbital blowout fractures. Adv Ophthalmol Plast Reconstr Surg 6:265-268, 1987 AM, Millman AL: Custom orbital implant in the 4. Putterman repair of late post-traumatic enophthalmos. Am J Ophthulmol 108:153-159, 1989 AM: Late management of blow-out fractures of 5. Putterman the orbital floor. Ophthalmology 83:650-659, 1977 AM: Orbital imaging, in Ernest JT (ed): Year Book 6. Putterman of Ophthalmology. Chicago, Year Book Medical Publishers, 1986, pp 15-18 AM: Blow-out fractures of orbital floor: surgery 7. Putterman or observation?, in Ernest JT (ed): Yearbook of Ophthalmology. Chicago, Year Book Medical Publishers, 1987, pp 13-16 AM: Management of orbital floor blow-out frac8. Putterman tures. Adv Ophthalmol Plast Reconstr Surg 6:281-285, 1987 9. Putterman AM: Discussion of Wojno T: The incidence of extraocular muscle and nerve palsy in orbital floor fractures. Ophthalmology 94:636-637, 1987 10. Putterman AM, Smith BC, Lissman RD: Blow-out fractures. Ophthulmol Plast Reconstr Surg 1:477-490, 1987 11. Putterman AM, Stevens T, Urist MJ: Nonsurgical management ofblow-out fractures of the orbital floor. AmJ Ophthalmol ?7:232-239, 1974 12. PuttermanAM, Urist MJ: Surgical treatment ofupper eyelid retraction. Arch Ophthalmol 87:401, 1972 13. Putterman AM, Urist MJ: Muller’s muscle conjunctival resection technique for treatment of blepharoptosis. Arch Ophthalmol 93:619-623, 1975 14. Putterman AM, Urist MJ: Treatment of enophthalmic narrow palpebral fissure after blow-out fractures. Ophthalmic Surg 6:45-49, 1977 15. Smith B, Putterman AM: Fixation of orbital floor implant: description of a simple technique. Arch Ophthalmol 88:598, 1970 16. Urist MJ: A lateral version light-reflex test. Am J Ophthalmol 63:808-815, 1967 17. Whitnall SC: The Anatomy of the Humun Orbit and Accessory Organs of Vision. London, Oxford University Press, 1932, ed 2, pp 300-316
Supported in part bv Core Grant EY 1792 from the National Eye institute, Bethesda, Maryland. Reprint address: Allen M. Putterman, M.D., 111 North Wabash Avenue, Suite 1714, Chicago, IL 60602.
Surv Ophthalmol
35 (4) January-February
1991
48. Messinger A, Radkowski MA, Greenwald M, Pensler J: Orbital roof fractures in the pediatric population. Plust Reconstr Surg 84:213-218, 1989 49. Milauskas AT: Diagnosis and Management of Blowout Fractures of the Orbit. Springfield Ill, Charles C Thomas, 1969 50. Millman AL, Della Rota RC, Spector S, et al: Steroids and orbital blow-out fractures: A new systematic concept in medical management and surgical decision making: Adu Ophthal Plast Reconstr Sure 6:291-300. 1987 51. Nicholson DH, Guzak SVrLoss ofvision after repair oforbital floor fracture. Trans Am Acad Ophthalmol Otolaryngol 75: 1402, 1971 RW, Depeu RV: Blow-out fractures of the orbit in 52. Patterson the absence of diplopia and enophthalmos. Am J Ophthalmol 55:1253, 1963 of volumetric changes in 53. Pearl RM: Surgical management the bony orbit. Ann Plast Surg 19:349, 1987 54. Pearl RM, Vistnes LM: Orbital blow-out fractures: an approach to management. Am Plust Surg 1:267-270, 1978 . 55. Pfeiffer RL: Traumatic enoohthalmos. Am I Ophthalmol ?0:718, 1943 56. Putterman AM, Stevens T, Urist MJ: Non-surgical management of blow-out fractures of the orbital floor. Am J Ophthalmol 77:232, 1974 57. Putterman AM: Late management of blow-out fractures of the orbital floor. Trans Am Acad Ophthalmol Otolaryngol 83: 650-659, 1977 58. Schjelderup H: Some considerations concerning traumatic diplopia. Acta Ophthalmol28:337, 1950 59. Smith B: Early fractures of the orbit. Trans Am Acad Ophthalmol Otolaryngol 67:63, 1963 60. Smith B: The discovery of blow out fractures of the orbit. Adv Ophthal Plast Surg 6:193-195, 1987 L
_I
DUTTON, 61. 62. 63. 64. 65. 66.
67.
68.
1
69. 70. 71.
MANSON,
ILIFF, PUTTERMAN
Smith B: On the treatment ofblow-out fractures ofthe orbit. Plast Reconstr Surg 62: 100, 1978 Smith B, Converse JM: Early treatment of orbital floor fractures. Trans Am Acad Ophthulmol Otolaryngol 61:602, 1957 Smith B, Dyer JA, Bleeker GM: Discussion of lesions of the orbit affecting motility. Int Ophthalmol Clin 1:208, 1971 Smith B, Nightingale JH: Fractures of the orbit, blow-out and naso-orbital fractures. Int Ophthalmol Clin 18:137, 1978 Smith B, Regan WR: Blow-out fractures of the orbit. Am J Ophthalmol 44:733, 1957 Smith B, Lisman RD, Simonton J, et al: Vokmann’s contracture of the extraocular muscles following blow-out fracture. Plast Reconstr Surg 74:200, 1984 Stahlnecker M, Whitaker L, Herman G, Katowtiz J: Evaluation and secondary treatment of post-traumatic enophthalmos. Presented at the American Association of Plastic Surgeons, Coronado Beach, CA, April 29, 1985 .Tajima S, Sugimoto C, Tanino R, et al: Surgical treatment of malunited fractures of zygoma with diplopia and with comments on blow-out fractures. J Muxillofac Surg 2:201, 1974 Volkmann R: Die ischemischen muskella hmongen und frackturen. Centralbl Chir 8~80 1, 188 1 Whyte DK: Blow-out fractures of the orbit. Br J Ophthalmol 52:74, 1968 Wilkins R, Havins W: Current treatment of blow-out fractures. Ophthalmology 89:464-466, 1982
The illustrations in this article are copyright, Johns Hopkins Department of Art as Applied to Medicine. Reprint address: Paul N. Manson, M.D., Plastic Surgery, MIEMSS, 22 S. Greene Street, Baltimore, Maryland 21201.
III. The Conservative Approach. ALLEN M. PUTTERMAN, M.D., Department of Ophthalmology, Eye and Ear In irmury, Universit of Illinois at Chicago, and Machael Reese Hospital and Medical Center an d the University o? Chicago, Chicago, Illinois When the eye is struck by an object larger than the orbital entrance, such as a fist, a blow-out fracture of the orbital floor can occur. The force of the blow to the eye is transmitted to the orbital contents and then to the orbital walls. The weakest areas of the orbital walls - the medial wall and floor of the orbit - rupture, and the force of the blow is transmitted into the ethmoid and maxillary sinuses, which absorb the impact like a pressure valve. (This is most likely “nature’s way” of preventing an eye from rupturing.) When an orbital floor fracture occurs, there can be associated diplopia due to entrapment of orbital fat or the inferior ocular muscles into the fracture site and maxillary sinus. Enophthalmos and hypoophthalmos (downward sinking of the eye) can also occur due to displacement of the orbital contents into the maxillary and ethmoid sinuses. Infraorbital anesthesia is another symptom of the blow-out fracture; it is due to injury to the infraorbital nerve as it courses through the orbital fracture. The extraocular muscle motility and infraorbital anesthesia frequently improve, and the enophthalmos and hypoophthalmos either persist or worsen as the edema
and hemorrhage subside. When a blow-out fracture of the orbital floor is suspected, a thorough eye examination should be performed. The trauma that causes a blow-out fracture can also lead to a 5-10% incidence of injury to the eye, such as iritis, hyphema, retinal detachment, or glaucoma. When an orbital floor fracture is suspected, conventional orbital roentgenograms should be performed. If this does not demonstrate a fracture, orbital tomograms or computed tomographic (CT) scans of the orbit should be obtained. (I do not order CT scans routinely for all suspected orbital floor fractures. I do order them selectively to aid in differentiating an entrapped, inferior rectus muscle from a contused inferior rectus muscle or for evaluation of the size of the implant needed to treat late enophthalmos.)
Early Treatment The treatment of orbital floor fractures remains controversial. From 1950 to 1974, most of these fractures were considered a medical emergency and immediate surgery was advocated. Most sur-
ORBITAL FRACTURES geons believed that unless immediate surgery was performed, the patient would have permanent, visually handicapping double vision as well as cosmetically unacceptable enophthalmos. In 1974, Putterman et al” described 57 patients with pure blow-out fractures of the orbital floor who were followed up without surgery despite the severity of their symptoms and fractures. We found that this group of patients did surprisingly well. All had resolution of visually handicapping diplopia (although 20% had double vision in extreme upgaze, which was not bothersome), and none developed cosmetically unacceptable enophthalmos (although 20% had measurable enophthalmos less than 3 mm, which was cosmetically acceptable). Infraorbital anesthesia also decreased with time in these patients. Based on this study, we encouraged a conservative management approach to all blow-out fractures of the orbital floor and, in retrospect, I believe we were overexuberant in advocating that no blow-out fractures be operated on for four to six months. My philosophy of treating orbital fractures has become more clearly delineated after years of further study and experience.7,8,‘0 In the majority of cases the need for surgery versus observation is quite obvious. Early surgery (within one to three weeks after trauma) is indicated in patients with severe, visually handicapping, nonresolving diplopia with a positive forced duction test that does not allow upward movement of the eye, and with CT evidence of inferior rectus muscle entrapment, or in patients with severe cosmetically unacceptable enophthalmos or hypo-ophthalmos. In patients with minimal diplopia, good ocular motility, and no significant enophthalmos or hypo-ophthalmos, observation is in order. There is, I believe, no evidence to support that the size of the orbital fracture on CT scans or roentgenograms correlates with the amount of enophthalmos or hypo-ophthalmos. Therefore, I do not operate early on large orbital floor fractures that are not associated with significant enophthalmos or hypo-ophthalmos. There are exceptional cases in which immediate surgery (during the first few days after trauma) is indicated. One such patient, described by Berkowitz et al had complete prolapse of the eye into the maxillary sinus following an orbital floor fracture.’ The problem of whether to perform surgery exists in those marginal cases with slow but slight resolution of diplopia or with progression of a cosmetic deformity. In this group of patients, I closely examine the patient during the first one to three weeks after trauma. I monitor the changes in diplopia, extraocular muscle motility, enophthalmos, and hypo-ophthalmos. Diplopia is measured by charting areas of diplopia and simultaneous binocular vision in all positions of gaze on a drawn square the
“93
center of which is the primary position of gaze. Extraocular muscle motility is measured by the Urist light reflex technique.‘” Enophthalmos is measured by Hertel exophthalmometry, and hypo-ophthalmos is measured by aligning the top of a ruler through both medial canthi and noting where the ruler bisects each eye. Patients are placed on a regimen of systemic corticosteroids for five to seven days. For an adult weighing approximately 67.5kg, 60 mg of prednisone is given orally each day for 2 days, 40 mg for 2 days, and then 20 mg for 2 days. Millman et al demonstrated that steroids speed the resolution of diplopia in patients who do not need surgery and that these drugs cause no change in patients who require surgery.” If the motility restriction is secondary to orbital edema and hemorrhage, steroids lead to rapid resolution of these problems. However, if the motility restriction is secondary to true entrapment of the extraocular muscles or orbital tissues, steroids effect only a minimal improvement of diplopia. (This information should help in the decision and timing of surgery.) Troublesome diplopia is very common immediately after blow-out fractures of the orbital floor. I believe that most of the time this is due to entrapment of orbital fat within the fracture site and maxillary sinus, as well as edema and hemorrhage of the orbital fat.” Whitnall demonstrated vertical fibrous bands that traversed through the posterior-inferior orbital fat between the periosteum of the orbital floor and the inferior ocular muscles.” The posterior inferior orbital fat is very fibrotic compared to the looser, more pliable, anterior orbital fat that is encountered in blepharoplasty surgery. Tension on these bands, due to either entrapment or edema and hemorrhage of the orbital fat, can inhibit the motility of the eye (Fig. 1). (I have attempted to prove this theory by grasping the inferior orbital fat during blepharoplasty surgery, and I noted that patients had marked difficulty looking up and down. As soon as I released the orbital fat, the motility improved to normal.) The 1974 study by Putterman et al demonstrated that ocular tnotility disturbances following a blow-out fracture improved with time.” An explanation for this improvement is that resolution of orbital fat edema and hemorrhage leads to decreased tension on the orbital fat bands; a second explanation is that the orbital fat stretches. Another cause of motility problems following blowout fractures is due to actual entrapment of or injury to the inferior rectus muscle. A forced generation and duction test can aid in differentiating an entrapped muscle from a paretic one.” After application of a topical anesthetic to the eye, cotton-tipped applicators saturated with the solution are held over the 6 o’clock and 12 o’clock
294
Surv Ophthalmol
35 (4) January-February
DUTTON,
19 91
limbal position. A toothed forceps is then used to grasp conjunctiva and episcleral tissue at the 6 o’clock limbal position. An attempt is made to move the eye upward and downward, and the ease of these movements is judged. (If there is difficulty in elevating the eye with the forceps, this is measured as a positive forced duction test in upgaze and implies that the inferior rectus muscle or orbital contents are entrapped within the fracture site.) While still holding the forceps with tissue grasped at the 6 o’clock limbus, the examiner asks the patient to look downward. Normally a tug on the forceps is so strong that the instrument is almost pulled from the examiner’s hand. However, if there is minimal pull on the forceps when the patient attempts to look downward, this implies that there is injury to the extraocular muscle with secondary paresis, and this is known as a positive or abnormal generation test. Computed tomographic (CT) scans with reconstruction can also help differentiate entrapped extraocular muscles from swollen muscles.6*g One way of doing this is to obtain axial cuts at 3 mm intervals through the orbit. These axial views are then transmitted by satellite to a highly sophisticated computer which then relays this information back with views that are parallel with the inferior rectus muscle. This can accurately demonstrate entrapment or swelling of the muscle. If this instrumentation is not available, most CT scanners have a computer within them that can simulate this result. If reconstruction is not available, certainly the surgeon should obtain both axial and coronal views through the orbit in order to fully appreciate the inferior rectus muscle. These scans should greatly help in differentiating an inferior rectus muscle that is entrapped from a contused muscle (Figs. 2 8c 3). A contused muscle is usually not entrapped in the fracture site and can be differentiated from a normal muscle by its rounded appearance on the CT scan, compared to the normal appearance of the inferior rectus muscle, which is quite flat (Fig. 3). The decision to perform orbital surgery versus continued observation is thereby determined by closely examining the changes in diplopia, enophthalmis, extraocular muscle motility, and hypoophthalmos during the first two to three weeks after trauma. Again, systemic steroids should speed the improvement in those patients who do not have entrapped muscle and lead to minimal or no change in those who have entrapped muscle. A forced duction and a generation test as well as CT scans with reconstruction should help differentiate an entrapped muscle from a contused swollen muscle. Based on the above protocol, I usually recommend surgically exploring the orbital floor in those patients who have minimal improvement of or no
MANSON, ILIFF,
PUTTERMAN
Hemorrhage and edema of the inferoposterior orbital fat with or without fat entrapment restrict ocular motility after blow-out fracture.
Fig. 1.
change in visually handicapping diplopia during the first three weeks after trauma and for those who develop cosmetically unacceptable enophthalmos or hypo-ophthalmos during this period.” A positive forced duction test, a negative generation test, and evidence of extraocular muscle entrapment on CT scanning further supports performing early surgery in this group of patients. On the other hand, I advocate further observation, without surgery, of those patients with marked improvement or resolution of visually handicapping double vision or those without development of cosmetically unacceptable enophthalmos or hypo-ophthalmos during the first three weeks after trauma. This is supported by a negative forced duction test but by a positive or normal generation test and by contusion or rounding without entrapment of the extraocular muscles on CT scans. For patients requiring surgery within three weeks after trauma, I usually perform orbital floor surgery with the patient under general anesthesia. A lateral canthotomy and cantholysis and inferior fornix approach are used to isolate the fractured orbital floor.‘” Once the orbital contents are released from the fracture site and maxillary sinus, an orbital floor Silastic implant is placed over the orbital floor to prevent further prolapse of orbital contents back into the sinus. I place a thin, 0.5-10 mm
ORBITAL
FRACTURES
Fig. 2. CT scan of orbital floor fracture of the left eye with entrapment of inferior rectus in fracture site (ar-
row). (Reprinted
with permission
Ophthalmology 94:683-687,
from Putterman
AM:
1987.)
sheet of Silastic over the fractured floor. I then create an anterior tongue of the implant as previously described’” and place this within the fracture to prevent anterior migration of the implant. If this is not possible, I will drill holes in the inferior orbital rim and anchor the implant with 2-O Supramid sutures that pass through this hole and the implant.
Late Treatment The late treatment of visually troublesome diplopia and orbital floor fractures occurs in two clinical settings: patients who needed but refused early surgery and patients who were significantly improving during the initial weeks after trauma but did not have the expected complete resolution of bothersome diplopia. I perform extraocular muscle surgery once the motility and diplopia measurements stabilize. In my experience, orbital floor surgery has improved visually handicapping diplopia in a few patients when performed up to five weeks after trauma, but rarely does it improve extraocular muscle motility beyond that time. Therefore, I advocate muscle surgery rather than orbital floor surgery to treat late diplopia because, in my hands, it is more effective. The type of surgery selected is individualized, depending on the degree of extraocular muscle motility imbalance. Most patients will have difficulty looking downward and will notice diplopia in downgaze that interferes with reading. In these cases, if the eye moves upward normally and the results of a forced duction test are normal on upgaze, a reverse Knapp operation is performed in which the medial and lateral rectus muscles are placed at or several millimeters behind the original inferior rectus insertion. If, on the other hand, the forced duction test is positive and the eye does not
Fig. 3. Contusion of right inferior rectus muscle associated with an orbital floor fracture ofthe right eye (arrow). The muscle becomes rounded with edema and hemorrhage secondary to contusion as opposed to the normal inferior rectus seen on the left side, which is much flatter.
move upward normally, an inferior rectus recession must be performed initially to relieve the difficulty on upward movement. The inferior rectus is recessed to the position where the eye can be moved upward normally during surgery. Approximately three to six months later, a modified reverse Knapp procedure is performed. (The reason for not performing all of these procedures together is to avoid anterior segment ischemia and necrosis that can occur when three extraocular muscles are operated on simultaneously.) In the reverse Knapp procedure, the medial and lateral rectus muscles are attached to the inferior rectus muscle insertion site. Folk and I found that this procedure does not produce as good a result as the Knapp procedure, in which the medial and lateral rectus muscles are attached at the superior rectus insertion site. One possibility for the inferior results with the reverse Knapp procedure may be that the superior rectus inserts 8.8 mm from the limbus, whereas the inferior rectus inserts 6.6 mm from the limbus. We have therefore modified this surgery by attaching the medial and lateral rectus muscles approximately 2-3 mm behind the inferior rectus insertion to simulate the position it takes with the Knapp procedure (Fig. 4). We found that this gives much better downward motility. Our present philosophy is that if there is less than 10 prisms of hypertropia in primary position of gaze, we place the medial and lateral rectus muscles at the original inferior rectus muscle insertion site; if there is greater than IO
296
Surv Ophthalmol
\
35 (4) January-February
1991
I
Modified reverse Knapp procedure, in which the medial and lateral rectus muscles are attached to sclera several millimeters behind the insertion of the infe-
Fig. 4.
rior rectus muscle.
prisms of hypertropia in primary position, we place these muscles 2-3 mm behind the inferior rectus insertion. Another option to correct decreased eye movements on downgaze is to perform a Fadom operation in which the inferior rectus muscle is attached to the sclera on the opposite normal eye in order to restrict downward movement.* Although this leads to decrease in downward diplopia; it also inhibits downward movement and makes the patient tilt his or her head downward in order to read. This differs from the modified reverse Knapp procedure, which allows normal downward movement of the
DUTTON,
MANSON,
ILIFF, PUTTERMAN
eyes without having to tilt the head. For patients with pure blow-out fractures who develop late enophthalmos and hypo-ophthalmos, surgery can be performed to relieve the cosmetic disturbance. The Hertel measurements should stabilize before surgery is considered. If the enophthalmos is associated with significant downward sinking of the eye, I advocate treatment with a large Silastic orbital implant that is custom made (Fig. 5).4,5,‘o The technique used to isolate the orbital floor is similar to that used for early treatment of the fractures by a lateral canthotomy, cantholysis, and inferior fornix approach. The size and shape of the implants are determined by studying posterioranterior, and lateral tomograms and by considering their magnification, or if tomograms are not available, the size and shape of implants can be determined by studying CT scans. In addition, the depth that the eye sinks downward helps determine the thickness of the implant directly beneath the eye. Most of these implants are 2-3 mm thick anteriorly, are 4-6 mm thick behind the eye, and extend posteriorly 6-10 mm in thickness. The implant is secured with 2-O Supramid sutures to the inferior orbital rim through drill holes placed in the rim. If the enophthalmos is associated with a narrow palpebral fissure, with minimal downward displacement of the eye, I advocate a Mueller’s muscle-conjunctival resection ptosis procedure.‘~‘0~‘9~‘4 This technique widens the palpebral fissure and creates the illusion that the enophthalmos has resolved (Fig. 6). (This is the opposite of treating exophthalmos with upper lid retraction by excising Mueller muscle and recessing the levator to narrow the palpebral fissure.‘*) Suitable candidates are selected by applying 10% phenylephrine to the upper fornix. If the fissure widens enough that the patient finds the appearance acceptable, the Mueller’s muscle resection procedure can simulate this effect. For patients with enophthalmos and no narrow-
Fig. 5. Left: Patient has 3 mm of enophthalmos associated with a 4.5 mm downward depression of the right eye four months after a nonsurgically managed orbital floor fracture of the right eye. Right: After insertion of a Silastic orbital floor implant, eyes are aligned and the enophthalmos is relieved. (Reprinted with permission from Putterman AM: Trans Am Acad Ophthalmol Otolaryngol 83:650, 1977.)
Fig. 6. Left: Patient three years after a nonsurgically managed orbital fioor fracture of the left eye. Blepharoptosis ofthe left eye and 5 mm decreased palpebral fissure width occurred secondary to 5 mm of enophthalmos. Right: Six months after treatment of the left upper eyelid with Mueller’s muscle-conjunctival resection procedure. Elevation of the left has resolved. (Reprinted upper eyelid and increased palpebral fissure width create the illusion that the enophthalmos with permission from Putterman AM: Ophthalmic Surg 645, 1975.)
Fig. 7. Left: Patient with 3 mm of enophthalmos associated with deep supratarsal sulcus two years after nonsurgical management of an orbital floor fracture of the left eye. Right: Same patient six months after excision of skin and orbital fat and elevation of a crease on the contralateral lid. (Reprinted with permission from Putterman AM: True ,4rn Acad Ophthalmol
Otolqngol
83:650,
1977.)
fissure or downward sinking of the eye who complain of a deep supratarsal sulcus, I excise skin and orbicularis and fat and reconstruct the crease at a higher level on the contralateral normal upper lid to camouflage this abnormality and create an acceptable cosmesis.‘.“’ The effect of this operation is to create symmetry of the upper eyelids (Fig. 7).
ing of the palpebral
Results of Early and Late Treatment The percentage of blow-out fractures that can be successfully followed without surgery versus those fractures that require surgery is difficult for me to calculate. The patients with blow-out fracture referred to me are usually already screened by physicians who are familiar with my approach to treatment; therefore, the majority of those patients with minimal or no diplopia or those patients with rapid improvement of diplopia are not examined by me. Instead, 1 tend to see patients with troublesome diplopia or cosmetically unacceptable enophthalmos or patients for whom the question of observa-
tion versus surgery is not clearly delineated. Despite this, 1 perform early surgery within three weeks after trauma on about 50% of patients and observe, without surgery, about 509% of patients. In the patients followed up without surgery, it usually takes one to three months for the residual diplopia to completely resolve or to stabilize. For those patients who have early surgery, handicapping diplopia usually worsens after surgery in about 75% of patients and takes one to five months to resolve. (It is therefore questionable whether early surgery creates a setting of diplopia similar to the one that occurs immediately after a blow-out fracture. The hemorrhage, edema, and extraocular muscle trauma lead to gradual resolution of diplopia following surgery similar to that following an untreated blowout fracture.) About 25%’ of these patients do not develop worsened diplopia after surgery. With the use of my present regimen of treating blow-out fractures, the need for late surgery in untreated blow-out fractures is rare. Less than 5% of surgically treated patients need secondary surgery..
298
Surv Ophthalmol
35 (4) January-February
1991
Summary In the majority of blow-out fractures it is usually quite clear whether to operate or to observe the patient. In the marginal cases in which there is slow but steady resolution of diplopia with slight change in enophthalmos or hypo-ophthalmos, the decision becomes more difficult. In this group of cases, frequent measurements of extraocular muscle motility, diplopia, enophthalmos, and hypo-ophthalmos are taken. Also, patients whose prognosis is favorable are placed on a regimen of systemic corticosteroids to speed resolution. Lastly, forced duction and generation tests combined with CT scanning and reconstruction can help differentiate an entrapped muscle from one that is contused and paretic. Based on these examinations, the decision for surgery versus observation can usually be made within three weeks after trauma. If patients have resolution of visually handicapping double vision and do not develop cosmetically unacceptable enophthalmos and if they have a negative forced duction test, a positive forced generation test, and contusion without entrapment of the extraocular muscle on CT scan, observation is continued. If, on the other hand, visually handicapping diplopia persists or cosmetically unacceptable enophthalmos or hypo-ophthalmos develops and if this is associated with a positive forced duction test, normal generation test, and evidence of entrapment without contusion on CT scans, orbital floor surgery is recommended within the first three weeks after trauma. Once this decision is made, treatment is performed as early as possible rather than waiting until 2 1 days have actually occurred. For most patients with visually handicapping diplopia that persists later than three weeks after trauma, extraocular muscle surgery is performed. This usually consists of initially recessing the inferior rectus muscle until the eye can move upward freely, and then three to six months later a modified reverse Knapp procedure is performed in which the medial and lateral rectus muscles are placed several millimeters behind the original inferior rectus muscle insertion. If cosmetically unacceptable enophthalmos and hypo-ophthalmos occur later than three weeks after trauma, they are treated surgically after the exophthalmometric measurements stabilize. If the enophthalmos is associated with hypo-ophthalmos, it is treated with a custom-fitting
DUTTON,
MANSON, ILIFF,
PUTTERMAN
Silastic orbital floor implant. If the enophthalmos is associated with a narrow palpebral fissure, it is treated with a Mueller’s muscle-conjunctiva resection procedure. If the enophthalmos is associated only with a deep supratarsal sulcus, it is treated by excising skin and orbicularis and fat and elevating the crease on the contralateral lid.
References RA, Putterman AM, Pate1 DB: Prolapse of the 1. Berkowitz globe into the maxillary sinus after orbital floor fracture. Am J Ophthalmol 91:253-257, 1981 for the manage2. Buckey EC, Meekins BB: Fadem operation ment of complicated incomitant verticle strabismus. Am J Ophthulmol 10k304, 1988 3. Millman AL, Della Rocca RC, Spector S, et al: Steroids and orbital blowout fractures. Adv Ophthalmol Plast Reconstr Surg 6:265-268, 1987 AM, Millman AL: Custom orbital implant in the 4. Putterman repair of late post-traumatic enophthalmos. Am J Ophthulmol 108:153-159, 1989 AM: Late management of blow-out fractures of 5. Putterman the orbital floor. Ophthalmology 83:650-659, 1977 AM: Orbital imaging, in Ernest JT (ed): Year Book 6. Putterman of Ophthalmology. Chicago, Year Book Medical Publishers, 1986, pp 15-18 AM: Blow-out fractures of orbital floor: surgery 7. Putterman or observation?, in Ernest JT (ed): Yearbook of Ophthalmology. Chicago, Year Book Medical Publishers, 1987, pp 13-16 AM: Management of orbital floor blow-out frac8. Putterman tures. Adv Ophthalmol Plast Reconstr Surg 6:281-285, 1987 9. Putterman AM: Discussion of Wojno T: The incidence of extraocular muscle and nerve palsy in orbital floor fractures. Ophthalmology 94:636-637, 1987 10. Putterman AM, Smith BC, Lissman RD: Blow-out fractures. Ophthulmol Plast Reconstr Surg 1:477-490, 1987 11. Putterman AM, Stevens T, Urist MJ: Nonsurgical management ofblow-out fractures of the orbital floor. AmJ Ophthalmol ?7:232-239, 1974 12. PuttermanAM, Urist MJ: Surgical treatment ofupper eyelid retraction. Arch Ophthalmol 87:401, 1972 13. Putterman AM, Urist MJ: Muller’s muscle conjunctival resection technique for treatment of blepharoptosis. Arch Ophthalmol 93:619-623, 1975 14. Putterman AM, Urist MJ: Treatment of enophthalmic narrow palpebral fissure after blow-out fractures. Ophthalmic Surg 6:45-49, 1977 15. Smith B, Putterman AM: Fixation of orbital floor implant: description of a simple technique. Arch Ophthalmol 88:598, 1970 16. Urist MJ: A lateral version light-reflex test. Am J Ophthalmol 63:808-815, 1967 17. Whitnall SC: The Anatomy of the Humun Orbit and Accessory Organs of Vision. London, Oxford University Press, 1932, ed 2, pp 300-316
Supported in part bv Core Grant EY 1792 from the National Eye institute, Bethesda, Maryland. Reprint address: Allen M. Putterman, M.D., 111 North Wabash Avenue, Suite 1714, Chicago, IL 60602.
