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Ординатура / Офтальмология / Английские материалы / Strabismus Surgery and Its Complications_Coats, Olitsky_2007

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23.7  Stretched Scar Syndrome

243

Fig. 23.20. Identification and retrieval of a lost muscle. a A lost rectus muscle will be found along the adjacent orbital wall. b A common mistake is to search for the muscle along the posterior aspect of the globe

treatment modalities should be considered. Assessment of postoperative motility may allow a more complete determination as to the best course of action for the specific patient and situation. Later retrieval of the lost muscle may be facilitated through the assistance of an oculoplastic surgeon skilled in surgery in the posterior orbit. Medial orbitotomy or trans-na- sal endoscopic retrieval of a lost medial rectus muscle has been reported [17, 18].

23.6.2Transposition Procedures when Attempted Retrieval

and Reattachment is Unsuccessful

If the detached or ruptured extraocular muscle cannot be retrieved and reattached to the globe without significant risk of complications, a backup surgical plan must be devised. Because partial disruption of the anterior ciliary circulation occurs as a result of loss of the anterior ciliary artery(ies) associated with the loss of the rectus muscle, the surgical plan must mitigate against the development of anterior segment ischemia, especially in susceptible patients (Chap. 20). A number of treatment options are available. The options in this setting include both transposition procedures and procedures to mechanically fixate the deviating eye in the primary position. The choices for transposition surgery include full tendon transposition,

partial tendon transposition, and muscle union procedures using nonabsorbable suture or other appropriate material [15] (chap. 13). Botulinum may be injected into the antagonist to further enhance the procedure (Chap.16).

While we once performed a full tendon transposition of the superior and inferior rectus muscles for the treatment of a lost medial rectus muscle in a young patient with a previous history of lateral rectus muscle surgery (thus disrupting the remaining anterior ciliary arteries), this should be done with extreme caution, and only in patients without systemic risk factors for anterior segment ischemia and after a long period of time has elapsed since the most recent strabismus surgery. Though timely repair is generally recommended, this is one situation where this rule does not apply. Repair with a transposition procedure usually involves techniques designed to spare some of the anterior ciliary circulation.

Choices include a modified Hummelsheim-type procedure with or without injection of botulinum toxin into the antagonist muscle and a modified Jensen-type procedure, also known as a string Jensen procedure [15] (Chap. 27). We reported the successful use of a modified Hummelsheim-type procedure in the management a patient who suffered traumatic disruption of the medial rectus muscle during endoscopic sinus surgery [19].

For a lost inferior rectus muscle, anterior transposition of the inferior oblique muscle has been successful [20]. Regardless of the surgical plan devised, it is important for the strabismus surgeon to consider the risk of anterior segment ischemia and minimize this risk whenever possible. In addition, the patient should have realistic goals regarding their potential outcome. In most cases, alignment in primary position can be achieved, but with a significant duction limitation. A compensatory head posture or the use of postoperative prism may also be necessary as an adjunct to surgery in some cases and the possible need for adjunct procedures should be reviewed with the patient prior to repair.

23.7 Stretched Scar Syndrome

Although it does not technically represent either a slipped or a lost extraocular muscle, patients who develop a stretched scar following strabismus surgery may have a similar presentation to patients who have a slipped muscle, but purportedly with some key differences. The stretched scar syndrome was first described by Ludwig [21], who examined a number of patients who had previously undergone recession of an extraocular muscle and presented with late-onset consecutive deviations, often many years following their initial procedure [22]. At the time of reoperation by Ludwig, patients were frequently found to have amorphous scar tissue separating the muscle tendon from the scleral attachment site (>Fig. 23.21). In several patients, initial repair of the overcorrection, which included removal of the scar, was followed by further recurrence. Ludwig postulated that scar lengthening after surgery was responsible for both the initial and secondary recurrent deviation. The rationale for this thought is substantial. Postoperative scar

244

Slipped and Lost Muscles

Chapter 23

Fig. 23.21. Stretched scar. Note the presence of amorphous material between the muscle tendon and the sclera. {Reprinted from Ludwig IH, Chow AY (2000) Scar remodeling after strabismus surgery. J AAPOS 4:326–333, with permission from American Association for Pediatric Ophthalmology and Strabismus [22]}

Fig. 23.22. Stretching of surgical scars is known to occur following surgical wound repair. (Courtesy of Mary Brandt, MD)

lengthening is seen after other nonophthalmologic surgical procedures, including skin closure, hernia surgery, and tendon and ligament repairs (>Fig. 23.22). Ludwig estimated that up to 50% of late overcorrections could be due to this condition, which she coined the stretched scar syndrome.

Ludwig and Chow [22] pointed out features which they believed helped to distinguish between a slipped muscle and a stretched scar. First, the overcorrection with a slipped muscle typically occurs shortly after surgery, generally within the first few weeks after surgery. In contrast, overcorrection in stretched scar syndrome usually occurs several months later. Second, a noticeable duction limitation is commonly associated with a slipped muscle, but is infrequently seen with a stretched scar.

They found that when a duction limitation was present, it was usually minimal. In rare cases, ocular rotations may be significantly limited as a result of pronounced lengthening of the scar.

Ludwig and Chow [22] described their experience in repairing 198 muscles during 134 operations in patients diagnosed with stretched scar syndrome. In this series, 73 procedures involved scar lengthening in 1 muscle and 59 procedures involved scar lengthening of 2 muscles [22]. In the majority of the 2­ -muscle cases, the scar lengthening was symmetric. The average lengthening of the scar was approximately 4 mm regardless of the muscle involved. Of the patients who could clearly date the onset of their consecutive deviation, approximately half noted onset beginning within 4 months of the original surgery. The remainder noted the onset an average of 18 months (range 4 months to 43 years) after the initial procedure. Those who could not clearly date the onset typically described it as a slow and gradual process.

Diagnosis of stretched scar syndrome can be suspected, but cannot be confirmed until the time of surgery to repair the deviation. During the surgical procedure, the distinction between the scar and the muscle tendon may be subtle. The scar can gradually blend into the tendon because the fibers of the scar often run parallel to the fibers of the tendon.

An important surgical tip that can assist the surgeon in making a diagnosis of stretched scar syndrome is that the distinction between stretched scar and muscle tendon can often be made more easily by visualizing the global surface of the muscle after the muscle has been detached from the globe (>Fig. 23.23). This is presumably because anterior Tenon’s capsule becomes adherent to the orbital surface of the scar, obscuring the true nature of the tissue.

The scar should be excised in its entirety after placing sutures in the muscle tissue posterior to the scar. Interestingly, once the scar tissue is removed, there tends to be a loss of the linear fiber arrangement and the scar takes on a more amorphous shape [22] (>Fig. 23.24) Histopathology of the excised stretched scar has demonstrated diffuse, dense connective tissue without the presence of skeletal muscle (>Fig. 23.25).

The argument could be made that the patients seen by Ludwig actually had a slipped muscle. As evidence against this criticism, recurrence was more commonly seen in those patients who underwent surgical repair of stretched scar using absorbable sutures to reattach the muscle to the sclera. Of the procedures performed using absorbable sutures, 42% developed recurrent stretching versus 6% of those where nonabsorbable sutures were used, prompting Ludwig and Chow [22] to recommend nonabsorbable suture use to reattach the muscle. The long-term impact of the use of nonabsorbable sutures on the recurrence of a stretched scar is unknown. Use of nonabsorbable sutures has been shown to reduce the stretching of scars in skin, scalp, and fascia repair [23, 24]. Use of a central locking suture placed after scleral tunnels are made, in order to support the center of the tendon, has also been suggested [22].

Treatment of patients suspected of having recurrent strabismus from stretched scar syndrome begins with a decision regarding the need to address the scar itself. For patients who have had a stable consecutive deviation for an extended pe-

23.7  Stretched Scar Syndrome

245

Fig. 23.23a,b. a Right lateral rectus muscle before disinsertion showing an indistinct scar-to-tendon junction (black arrow top). The insertion has been detached from the sclera and is suspended on 6-0 Polyglactin suture (white arrow bottom). Inspection of the inner surface of the lateral rectus demonstrates that the amorphous scar segment and transition to normal tendon (black arrow) become clear. White arrow indicates the scar insertion, suspended on a suture. {Reprinted from Ludwig IH, Chow AY (2000) Scar remodeling after strabismus surgery. J AAPOS 4:326–333, with permission from American Association for Pediatric Ophthalmology and Strabismus [22]}

Fig. 23.24a,b. Appearance of a stretched scar after removal. a Note the linear appearing fiber arrangement after normal extraocular muscle resection, and b loss of the linear arrangement of collagen when tension is eliminated following scar excision. {Reprinted from Ludwig IH, Chow AY (2000) Scar remodeling after strabismus surgery. J AAPOS 4:326–333, with permission from American Association for Pediatric Ophthalmology and Strabismus [22]}

Fig. 23.25. Histologic study of scar segment shows wavy bundles of dense connective tissue (left). Normal extraocular muscle tendon histologic study after resection. Collagen bundles are larger and more regularly oriented (right). {Reprinted from Ludwig IH, Chow AY (2000) Scar remodeling after strabismus surgery. J AAPOS 4:326–333, with permission from American Association for Pediatric Ophthalmology and Strabismus [22]}

246

Slipped and Lost Muscles

riod of time and without a duction deficit, exploration of the previously operated muscle(s) for a possible stretched scar is probably not required. However, in patients with a duction deficit, we would advise exploration of the previously operated muscle, with repair of identified pathology, if found, always being indicated.

Although it has been suggested that up to 50% of overcorrections may be due to stretched scar syndrome [22], the accuracy of this estimate is unclear. Several preventative techniques have been suggested to reduce the incidence of its occurrence. All involve attention to surgical details that are thought to enhance wound healing. The addition of a central locking bite to place a larger portion of the distal tendon in direct apposition to the sclera may have merit. Also, the surgeon should avoiding excessively tight sutures which could result in necrosis of the distal portion of tendon.

The use of postoperative corticosteroids could in theory inhibit collagen synthesis and repair which could result in the development of a weaker bond between the muscle tendon and the sclera, though there is no direct evidence that this occurs with administration of topical corticosteroids. Avoidance of the hang-back approach to recession surgery, opting instead for direct suturing of the muscle to the sclera, has also been suggested as possibly being protective in at-risk patients. These tips may or may not be valid, and at present there is little scientific evidence to suggest that these modifications in surgical technique will be successful in reducing the risk of developing a stretched scar.

While the role of scar stretching in strabismus requires further study, recognition that it may occur and that it may be associated with a large number of overcorrections is important. Fortunately, some of the tips recommended to theoretically reduce the occurrence of slipped scar syndrome are good general techniques that should be considered during strabismus surgery in all cases.

References

Chapter 23

7.Ward TP, Thach AB, Madigan WP Jr., Berland JE (1997) Magnetic resonance imaging in posttraumatic strabismus. J Pediatr Ophthalmol Strabismus 34:131–134

8.Raz J, Bernheim J, Pras E, Saar C, Assia EI (2002) Diagnosis and management of the surgical complication of postoperative “slipped” medial rectus muscle: a new “tendon step test” and outcome/results in 11 cases. Binocul Vis Strabismus Q 17:25–33

9.Mims JL 3rd (1992) Forming and teaching true knots for strabismus surgery. Ophthalmic Surg 23:477–481

10.Eitzen JP, Elsas FJ (1991) Strabismus following endoscopic intranasal sinus surgery. J Pediatr Ophthalmol Strabismus 28:168–170

11.Plager DA, Parks MM (1990) Recognition and repair of the “lost” rectus muscle. A report of 25 cases. Ophthalmology 97:131–136; discussion 136–137

12.Friendly DS, Parelhoff ES, McKeown CA (1993) Effect of severing the check ligaments and intermuscular membranes on medial rectus recessions in infantile esotropia. Ophthalmology 100:945–948

13.Greenwald M (1990) Intraoperative muscle loss due to muscletendon dehiscence. Proceedings of the 16th Annual Meeting of American Association of Pediatric Ophthalmology and Strabismus. Lake George, New York

14.Kowal L, Wutthiphan S, McKelvie P (1998) The snapped inferior rectus. Aust N Z J Ophthalmol 26:29–35

15.Paysse EA, Saunders RA, Coats DK (2000) Surgical management of strabismus after rupture of the inferior rectus muscle. J AAPOS 4:164–167

16.Miller JM (1989) Functional anatomy of normal human rectus muscles. Vision Res 29:223–240

17.Trotter WL, Kaw P, Meyer DR, Simon JW (2000) Treatment of subtotal medial rectus myectomy complicating functional endoscopic sinus surgery. J AAPOS 4:250–253

18.Lenart TD, Reichman OS, McMahon SJ, Lambert SR (2000) Retrieval of lost medial rectus muscles with a combined ophthalmologic and otolaryngologic surgical approach. Am J Ophthalmol 130:645–652

19.Brooks SE, Olitsky SE, de BRG (2000) Augmented Hummelsheim procedure for paralytic strabismus. J Pediatr Ophthalmol Strabismus 37:189–195; quiz 226–227

1.Parks MM, Bloom JN (1979) The “slipped” muscle. Ophthalmol20. Olitsky SE, Notaro S (2000) Anterior transposition of the inferior

ogy 86:1389–1396

2.Bloom JN, Parks MM (1981) The etiology, treatment and prevention of the “slipped muscle”. J Pediatr Ophthalmol Strabismus 18:6–11

3.Plager DA, Parks MM (1988) Recognition and repair of the slipped rectus muscle. J Pediatr Ophthalmol Strabismus 25:270–274

4.Murray AD (1998) Slipped and lost muscles and other tales of the unexpected. Philip Knapp Lecture. J AAPOS 2:133–143

5.Knapp P (1978) Lost muscle. In: Symposium on strabismus. Transactions of the New Orleans Academy of Ophthalmology. CV Mosby, St. Louis, Mo., p 5

6.MacEwen CJ, Lee JP, Fells P (1992) Aetiology and management of the “detached” rectus muscle. Br J Ophthalmol 76:131–136

oblique for the treatment of a lost inferior rectus muscle. J Pediatr Ophthalmol Strabismus 37:50–51

21.Ludwig IH (1999) Scar remodeling after strabismus surgery. Trans Am Ophthalmol Soc 97:583–651

22.Ludwig IH, Chow AY (2000) Scar remodeling after strabismus surgery. J AAPOS 4:326–333

23.Nordstrom RE, Nordstrom RM (1986) Absorbable versus nonabsorbable sutures to prevent postoperative stretching of wound area. Plast Reconstr Surg 78:186–190

24.Elliot D, Mahaffey PJ (1989) The stretched scar: the benefit of prolonged dermal support. Br J Plast Surg 42:74–78

Hemorrhage

 

 

Chapter

 

 

 

 

24

 

 

 

 

 

 

24

24.1 Introduction

Hemostasis is important in any surgical procedure. Minor hemorrhage, easily controlled by cautery, occurs during many strabismus operations, while severe hemorrhage is uncommon. Severe hemorrhage can result in alteration of expected postoperative ocular alignment, retinal detachment, and even blindness. Awareness of potential causes of serious hemorrhage during strabismus surgery and of risk factors can reduce the occurrence of serious intraocular and periocular hemorrhage during and after surgery.

24.2 Risk Factors

Several subgroups of patients are at increased risk for significant hemorrhage during strabismus surgery. Patients with a bleeding diathesis and patients on anticoagulant medications are obvious risk groups. Despite this, hemorrhage is generally reasonably limited and easily controlled during strabismus surgery so that many surgeons do not ask patients to discontinue their anticoagulant medications prior to surgery. In a study of 108 adult patients undergoing strabismus surgery, hemorrhage significant enough to necessitate cautery to control bleeding to allow continuation of surgery occurred in 4 (14.8%) of 27 patients on anticoagulants compared to 1 (1.2%) of 81 patients who were not taking anticoagulants (unpublished data). Thus it is not unreasonable to recommend discontinuation of anticoagulants prior to strabismus surgery. The decision to discontinue anticoagulants prior to surgery depends on the complexity of the surgery, the health of the patient and the preference of the surgeon. The risk of health problems associated with temporary discontinuation of anticoagulant medications in patients with medical indications for these agents must be considered before making this recommendation.

Patients undergoing reoperations, especially if there is extensive scarring, are at increased risk of developing significant hemorrhage. Patients undergoing complex operations with limited exposure of the surgical site may also be at increased risk of intraoperative hemorrhage. Examples include large recession and posterior fixation suture surgery, both of which require surgical manipulation in the orbit well beyond the comfortable range of 10–12 mm from the limbus. Potential

causes of hemorrhage in these cases include scleral perforation causing vitreous and/or retinal hemorrhage and disruption of anterior ciliary vessels and/or vortex veins.

24.3 Eyelid Hemorrhages

Serious complications from eyelid hemorrhages are infrequent. Though not generally vision threatening, bruising of the eyelids following strabismus surgery can be alarming to patients because of both fear provoked by the appearance of the hemorrhage itself, and the potential negative social and vocational consequences associated with hemorrhage, which may prolong the time before a patient returns to work, or may lead to teasing at school in younger patients. The most common cause of eyelid hemorrhages following strabismus surgery is retrobulbar injection of anesthetic agents. Hemorrhages involving the eyelids can occur after both retrobulbar and peribulbar injection of anesthesia, but eyelid hemorrhages can also occur in patients who have not undergone retrobulbar or peribulbar injection. Patients may exhibit little or no bruising in the immediate perioperative period, developing mild to marked bruising of the lids during the first 24 h after surgery (>Fig. 24.1). Anticoagulant use may be associated with increased lid bruising. In addition to eyelid hemorrhages, buccal fat pad hemorrhage has been reported after retrobulbar injection in the absence of hemorrhage in the retrobulbar space [1].

Fig. 24.1. Eyelid hemorrhages following retrobulbar injection of anesthetic agent for strabismus surgery

248

Hemorrhage

The occurrence of eyelid (and subconjunctival) hemorrhages can be reduced by use of a sub-Tenon’s block. A small incision is made in the inferotemporal or inferonasal quadrant through conjunctiva and Tenon’s fascia. A blunt-tipped cannula is then used to administer anesthetic into the posterior sub-Tenon’s space. The technique is well accepted for use in eye surgery and is well tolerated by patients [2].

Eyelid bruising can occasionally occur even after otherwise routine strabismus surgery under general anesthesia in patients who have not undergone a retrobulbar anesthetic block. We have seen this occur occasionally in patients following prolonged strabismus surgery, particular for complex reoperations associated with extensive scaring, such as repair of a slipped or lost muscles requiring extensive surgical manipulation. It is most likely to occur in our experience with surgery on the inferior rectus, inferior oblique or medial rectus muscles.

24.4 Orbital Hemorrhage

Orbital hemorrhages can occur during surgery due to disruption of muscular arteries or vortex veins (see below), and most orbital hemorrhages occur as a result of local anesthesia administration. Though most available data on hemorrhages associated with local ocular anesthesia involve cataract surgery, the information is valid for similar injections administered for strabismus surgery. Retrobulbar hemorrhage has been reported to occur in between 1% and 3% of cases performed under retrobulbar anesthesia [3]. Peribulbar anesthesia has also been associated with retrobulbar hemorrhage and permanent vision loss [4]. In patients who we feel are at particularly high risk for developing retrobulbar hemorrhage, we often achieve ocular anesthesia and akinesia through a sub-Tenon’s block using a blunt-tipped cannula to minimize this risk. Though the risk of retrobulbar hemorrhage is lower with a sub-Tenon’s infusion, we have experienced one case of retrobulbar hemorrhage despite the use of this technique [5] and retrobulbar hemorrhage has been reported following use of this technique for cataract surgery as well [6]. Our patient was a 62-year-old woman who

Chapter 24

underwent infusion of 3 ml lidocaine (2%) into the posterior sub-Tenon’s space. The agent was infused through a small conjunctival/Tenon’s fascia incision in the inferonasal quadrant using a 19-gauge blunt-tipped cannula. Upon withdrawal of the cannula, the patient complained of severe pain and acute proptosis developed. The conjunctiva became immediately edematous and hemorrhagic and eyelid ecchymosis was noted. Her intraocular pressure became acutely elevated to 68 mmHg and fundus examination revealed pulsations of the central retinal artery. A lateral canthotomy was performed resulting in reduction of her intraocular pressure. Strabismus surgery was abandoned and the patient did well, recovering without loss of vision. She underwent uneventful strabismus surgery 2 weeks later. While the mechanism for the hemorrhage following sub-Tenon’s anesthetic infusion was unclear in this case, we postulated that the volume of the fluid infused behind the globe may have displaced and ruptured a sclerotic vessel, with resulting hemorrhage. We recommend infusion of the minimum volume of anesthetic agent required to accomplish surgery and recommend slow infusion of the agent under low injection pressure.

Treatment of a retrobulbar hemorrhage is dependent on severity. If the intraocular pressure is not dangerously elevated and perfusion of the central retinal artery is not compromised, observation may be all that is warranted. Vision loss can occur due to both optic nerve compression and elevation of intraocular pressure. Simple measures that may be useful to control acute elevation of intraocular pressure include intermittent ocular massage, anterior chamber paracentesis, and administration of ocular hypotensive agents. Lateral canthotomy with or without inferior cantholysis may be required to control both intraocular and intraorbital pressure (>Fig. 24.2). Liu [7] described a simple technique for orbital decompression to treat severe retrobulbar hemorrhage not responsive to other measures such those described above. An inferonasal incision is made through the conjunctiva and Tenon’s capsule. A hemostat is then advanced 20 mm into the orbit along the medial orbital floor. Downward pressure is then applied on the hemostat to break the orbital floor and adjacent maxillary sinus mucosa, entering the maxillary sinus (>Fig. 24.3).

Fig. 24.2a,b. Lateral canthotomy for treatment of acute retrobulbar hemorrhage. a A hemostat is placed across the lateral canthus and removed after 30–60 s and the lateral canthus is then cut with scissors. b An inferior cantholysis can be performed if additional measures are needed

24.5  Muscle Hemorrhage

249

24.5 Muscle Hemorrhage

Hemorrhage from muscular arteries has been reported. We performed bilateral inferior oblique myectomy on a child several years ago. Two hemostats were placed across the inferior oblique muscle and the muscle segment between the clamps was removed in each eye. Cautery, which is typically applied to the cut edges of the muscle prior to removal of the hemostats, was inadvertently omitted on one eye. The proximal aspect the inferior oblique muscle was then tucked into Tenon’s capsule and the conjunctiva closed. Upon reemergence from anesthesia, the patient coughed and severe proptosis of the right eye developed without obvious external hemorrhage. The intraocular pressure was markedly elevated and pulsations of the central retinal artery were noted. A lateral canthotomy was performed and ocular hypotensive agents were administered. The surgical wound was opened and the proximal end of the hemorrhaging inferior oblique muscle was identified with some difficulty and cautery applied. Other than ocular adnexal bruising, the remainder of his recovery was routine and the patient did well without suffering loss of vision.

Delayed retrobulbar hemorrhage has also been reported. Cates and coworkers [8] reported the case of a 4-year-old boy who developed a slipped medial rectus muscle in his right eye as a result of an orbital hemorrhage. The child had undergone medial rectus muscle recession in both eyes to a position 10.5 mm posterior to the limbus. The surgery was uncomplicated and good hemostasis was maintained throughout the procedure. The patient experienced rapid swelling, bruising of the eyelids, and periocular pain that began several hours after surgery. The surgeon was not contacted and when the patient was

Fig. 24.3. Simple technique of orbital decompression for retrobulbar hemorrhage not responsive to other measures. A hemostat is placed into an incision in the inferonasal quadrant and advanced 20 mm along the medial aspect of the orbital floor. The hemostat is then used to break the floor of the orbit to enter the maxillary sinus

seen 1 week later a large secondary exotropia was present and moderate limitation of adduction noted. Reoperation revealed a pseudo-tendon of the medial rectus muscle that remained partially attached 10.5 mm posterior to the limbus. The muscle itself was found 20 mm posterior to the limbus. It was advanced to a position 5.5 mm posterior to the limbus and the child ultimately did well. The authors postulated that inadequate cautery to muscular arteries in this active child may have resulted in the acute hemorrhage which occurred with sufficient force to detach the muscle from the globe. They suggested that if a hang-back suture had been used, the muscle position probably would not have been altered by the hemorrhage.

Todd and coworkers [9] reported a case of delayed orbital hemorrhage that did not develop until approximately 36 h after an otherwise routine horizontal recess and resect operation. During surgery, bleeding from the medial rectus muscle was noted, though hemostasis was achieved with cautery. The patient presented for follow-up with marked proptosis, count fingers vision, and a relative afferent pupillary defect. Computed tomography scan revealed a massively enlarged medial rectus muscle consistent with a muscle hematoma. A lateral canthotomy was performed and the muscle explored. A pulsatile bleeding artery was identified at the proximal muscle stump. The vessel was cauterized and the muscle sutured to the sclera. The patient was treated with oral steroids for 5 days and subsequently recovered visual acuity to the level of 20/20 and had good ocular alignment. The authors postulated that excessive coughing, which occurred on the first postoperative day, had stimulated the hemorrhage. In support of this theory, they noted that spontaneous orbital hemorrhage has occasionally been reported following straining [10]. Periorbital hemorrhages have also been reported following extensive coughing [11].

250

Hemorrhage

In a very unusual case, Carden and coworkers [12] reported the development of bilateral orbital hemorrhages during strabismus surgery which was being performed under general anesthesia. The patient had received no retrobulbar or peribulbar anesthesia. The procedure was uncomplicated until the surgeons noted that both ocular globes had become firm to palpation toward the end of the case. Proptosis and hemorrhaging from the conjunctival wounds developed. Intraocular pressure increased to 40 mmHg in both eyes. The patient’s blood pressure was well controlled throughout the procedure and there was no history of bleeding diathesis. The patient had previously undergone three other uncomplicated nonophthalmologic surgical procedures with no history of excessive bleeding.

She was managed with ocular hypotensive agents and her intraocular pressure decreased after 2 h of treatment. Bleeding from the surgical incisions ceased spontaneously. Investigation for a bleeding diathesis did not occur until approximately 2 weeks after surgery, at which time the evaluation was unremarkable. Unknown to her surgeons, she had been taking odorless garlic tablets prescribed by a naturopath and she had consumed five tablets (approximately 5 g of equivalent fresh bulb) the day before surgery. She had also consumed garlic regularly prior to surgery, but had not consumed any since surgery. The surgeons postulated that the garlic supplements were responsible for her bleeding diathesis. Garlic is known to have anticoagulant properties by inhibition of platelet aggregation. Because of potentially unpredictable hemostasis following garlic supplement ingestion, patients should cease ingestion of garlic tables at least 7 days prior to surgery. Bleeding has been reported in association with garlic ingestion during other surgical procedures as well, including transurethral resection of the prostate [13] and mammoplasty [14]. There is also a report of a spontaneous epidural hematoma in a patient taking garlic supplements [15]. Surgeons should be aware that patients may be taking naturopathic agents which could interact with other medications and/or be associated with intraoperative or perioperative hemorrhage. Both ginkgo balboa and ginseng, in addition to garlic supplements, have been associated with bleeding [16].

24.6 Vortex Vein Hemorrhage

Damage or disruption of the four vortex veins is uncommon during strabismus surgery despite the fact that vortex veins are encountered frequently during strabismus surgery. Damage to a vortex vein is unlikely to occur during routine surgery by a surgeon familiar with the relevant anatomy. Disruption of a vortex vein is most likely to occur during reoperations in which there is extensive scarring and tissue distortion, displacing one or more vortex veins to an unusual anatomic location. Vortex veins are generally quite elastic and forgiving, rarely rupturing if moderately stretched during surgery. Bleeding from a vortex vein can be pronounced, but easily controlled by pressure through temporary intraoperative packing of the operative site. Surgery can continue once bleeding has ceased, but if the adjacent tissues have become bloodstained and make delineation of tissue planes difficult, further surgery should be postponed

Chapter 24

until a later date. Data on complications associated with vortex vein damage following scleral buckling surgery are available, and may be similar to complications of vortex vein damage following strabismus surgery, though published data about this condition following strabismus surgery are not available. Doi and coworkers [17] reported an increased frequency of elevated­ intraocular pressure, vitreous hemorrhage, choroidal detachment, and vitreous opacification following scleral buckling surgery in which a vortex vein had been damaged.

24.7 Subconjunctival Hemorrhage

Subconjunctival hemorrhages occur following almost all strabismus operations. They can be particularly alarming to patients because they tend to progress in the first 24–48 h after surgery. The family who has been advised that increasing redness can be a sign of postoperative infection may call with concerns about an expanding subconjunctival hemorrhage. Careful postoperative explanation about the benign nature of subconjunctival hemorrhage can reduce patient and parent concerns after surgery. Warning patients about the potential for a subconjunctival hemorrhage to spread and about possible green and yellow discoloration of the hemorrhage that occurs during breakdown of hemoglobin as the hemorrhage resolves is important. The occurrence of subconjunctival hemorrhages can be reduced by use of cautery to the conjunctiva prior to sub-Tenon’s anesthesia infusion in patients undergoing cataract surgery [18], though it is likely that this technique would result in a reduction of subconjunctival hemorrhages in patients undergoing strabismus surgery.

24.8 Intraocular Hemorrhage

Intraocular hemorrhage can occur at several stages during strabismus surgery. Awad and coworkers [19] reported four patients who experienced anterior chamber collapse and hyphema following placement of traction sutures at the limbus during strabismus surgery. They abandoned surgery on these patients until the hyphema had cleared and later surgery was uneventful. None of the patients experienced loss of vision. Both localized [19] and severe [19–21] vitreous hemorrhage have been reported in association with eye wall perforation during strabismus surgery. Late-onset vitreous hemorrhage that was believed to be related to scleral perforation during previous strabismus surgery has also been reported [22].

References

1.Kuchtey R, Perry JD, Lerner L (2004) Buccal fat pad hemorrhage after retrobulbar injection. Am J Ophthalmol 137:1131–1132

2.Kumar CM, Williamson S, Manickam B (2005) A review of subTenon’s block: current practice and recent development. Eur J Anaesthesiol 22:567–477

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3.Morgan CM, Schatz H, Vine AK et al (1988) Ocular complica14. Burnham BE (1995) Garlic as a possible risk for postoperative

tions associated with retrobulbar injections. Ophthalmology 95:660–665

4.Puustjarvi T, Purhonen S (1992) Permanent blindness following retrobulbar hemorrhage after peribulbar anesthesia for cataract surgery. Ophthalmic Surg 23:450–452

bleeding. Plast Reconstr Surg 95:213

15.Rose KD, Croissant PD, Parliament CF, Levin MB (1990) Spontaneous spinal epidural hematoma with associated platelet dysfunction from excessive garlic ingestion: a case report. Neurosurgery 26:880–882

5.Olitsky SE, Juneja RG (1997) Orbital hemorrhage after the ad16. Ang-Lee MK, Moss J, Yuan CS (2001) Herbal medicines and

ministration of sub-Tenon’s infusion anesthesia. Ophthalmic Surg Lasers 28:145–146

6.Rahman I, Ataullah S (2004) Retrobulbar hemorrhage after subTenon’s anesthesia. J Cataract Refract Surg 30:2636–2637

7.Liu D (1993) A simplified technique of orbital decompression for severe retrobulbar hemorrhage. Am J Ophthalmol 116:34–37

8.Cates CA, Hodgkins PR, Morris RJ (2000) Slipped medial rectus muscle secondary to orbital hemorrhage following strabismus surgery. J Pediatr Ophthalmol Strabismus 37:361–362

9.Todd B, Sullivan TJ, Gole GA (2001) Delayed orbital hemorrhage after routine strabismus surgery. Am J Ophthalmol 131:818–819

10.Sullivan TJ, Wright JE (2000) Non-traumatic orbital haemorrhage. Clin Exp Ophthalmol 28:26–31

11.Paysse EA, Coats DK (1998) Bilateral eyelid ecchymosis and subconjunctival hemorrhage associated with coughing paroxysms in pertussis infection. J AAPOS 2:116–119

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Adherence

 

 

Chapter

 

 

 

 

25

and Adhesion

 

Syndromes

 

 

 

 

 

25

Scar formation occurs following all strabismus procedures. The formation of an adequate scar, in fact, is required for normal postoperative healing. However, abnormal scar formation, or normal scar formation that occurs after unplanned intraoperative events, may lead to undesirable surgical outcomes. Adherence and adhesion syndromes occur following strabismus surgery and are due to fibrous scar formation that alters postoperative alignment and/or limits ocular rotations. This chapter will review these syndromes and discuss their prevention and treatment.

25.1 Fat Adherence Syndrome

The term fat adherence syndrome refers to a progressive restrictive strabismus associated with the intrusion of extraconal orbital fat into the sub-Tenon’s or episcleral space during surgery or following trauma. Exposed extraconal fat that enters the episcleral space can come into contact with the extraocular muscles, the sclera and/or other orbital connective tissue ­elements. A fibrous scar can develop which is attached to the orbital periosteum. This scar then contracts and leads to progressive strabismus with inhibition of ocular movement. The entrance of extraconal fat into the episcleral space occurs due to a disruption in posterior Tenon’s capsule, which normally acts as a barrier to fat entering this location (>Fig. 25.1). Fat adherence syndrome may occur following strabismus surgery, scleral buckling surgery, and other surgeries when violation of posterior Tenon’s capsule occurs. The condition may also occur as a result of orbital trauma. For the strabismus surgeon, the condition most commonly occurs following surgery on the inferior oblique muscle. As such, the typical motility disorder usually consists of a progressive hypotropia, an inability to fully elevate the involved eye and positive forced duction testing on attempted passive elevation of the globe.

The fat adherence syndrome was first described by Parks in 1972 [1]. Initially, he stated that the cause of the disorder was an adherence between the globe and orbital tissue to orbital fat which occurred following a violation of posterior Tenon’s capsule. Later, he suggested the cause was due to contracture of fibrous connective tissue found within the orbit secondary to inflammation. Parks felt that trauma to the orbital fat was necessary for the development of fat adherence syndrome but the orbital fat was not by itself the cause.

It has been difficult to explore the actual etiology of this syndrome. Attempts to produce an animal model of fat adherence syndrome have not been successful. Brooks and coworkers [2] could not reproduce fat adherence syndrome in a pig model in spite of severe surgical and thermal trauma to posterior Tenon’s capsule and orbital fat. Kerr [3] was able to produce a restrictive strabismus in a rabbit model by securing fat autographs between the inferior rectus muscle and the periosteum of the inferior orbital rim. However, there may be fundamental differences in the orbital anatomy and healing process that occurs in the pig orbit compared to humans. In addition, although the rabbit model can produce a restrictive strabismus that resembles that seen in fat adherence syndrome, the rabbit orbit does not contain a large amount of fat and therefore may not serve as an ideal model. Although the exact cause of fat adherence syndrome remains unknown, it seems clear from clinical and anecdotal evidence that violation of posterior Tenon’s capsule and trauma to the extraconal fat is necessary for the development of the syndrome. The rabbit model described above has suggested this as well. The amount of fat introduced in the experimental model correlated with the degree of restriction that later developed. Most ophthalmologists have interpreted the clinical evidence to suggest that poor surgical technique is a major cause of the development of fat adherence syndrome and provides the violation of Tenon’s capsule and trauma to extraconal fat needed for fat adherence syndrome to develop [4]. However, this view may be unfair, as violation of posterior Tenon’s capsule can occur even with well-performed surgery by expert surgeons.

25.2 Incidence

Parks [1] reported an incidence of fat adherence syndrome of 2% in patients undergoing inferior oblique muscle surgery in his original series. The incidence of fat adherence syndrome is unknown today. The number of cases appears to have decreased, most likely due to the recognition of the condition, and better understanding of the potential consequences of violating posterior Tenon’s capsule during surgery. Improvements in surgical techniques probably also contribute significantly to a reduction in the incidence of this complication. Some cases of restrictive strabismus following retinal surgical procedures occur due to fat adherence syndrome. Hwang and Wright [5]