Visual loss

The most feared complication of blepharoplasty surgery is visual loss. The most common cause is retrobulbar hemorrhage, although other etiologies have been reported (globe perforation, central retinal artery occlusion, retrobulbar optic neuritis, angle closure glaucoma).

Retrobulbar hemorrhage

The incidence of retrobulbar hemorrhage was reported in the plastic surgery literature at 0.04%.¹ More recently, an epidemiologic study of greater than 250 000 blepharoplasty cases performed by oculoplastic specialists found the incidence of retrobulbar hemorrhage to be 0.05%; associated permanent visual loss was diagnosed in 0.0045%.² This corresponds to a 1/2000 risk of significant hemorrhage and a 1/10 000 risk of permanent visual loss. Most often clinical presentation is within the first 24 hours after surgery, although bleeding has been reported as late as 9 days after surgery.³ Patients may complain of pain, pressure, diplopia and visual loss. Examination shows decreased visual acuity, lid edema, proptosis, subconjunctival hemorrhage, extraocular motility disturbance, increased intraorbital (resistance to retropulsion) and intraocular (tonometry) pressure and an afferent pupillary defect (Fig. 34.2).

Fig. 34.2 Retrobulbar hemorrhage producing ecchymosis after a frontal nerve block during transcutaneous blepharoplasty (A) and retrobulbar hemorrhage in a hypertensive patient demonstrating sudden proptosis and chemosis (B).

Many theories exist to explain the cause of retrobulbar hemorrhage, with vascular trauma being the most common. The final common pathway involves continued orbital bleeding leading to increased intraorbital and intraocular pressure with resultant ischemic damage to the retina and/or optic nerve.

Pearls

Pearls to avoiding retrobulbar hemorrhage include:

• Detailed preoperative evaluation with particular attention to medical problems such as diabetes, hypertension, coagulopathies and both prescription and over-the-counter anticoagulant medication use. Stopping all anticoagulants far enough in advance to allow normalization of bleeding parameters and platelet function is important.

• A past ocular history is necessary to rule out pre-existing causes of visual dysfunction, as rare reports of malpractice cases where patients have claimed pre-existing visual loss as a consequence of blepharoplasty do exist.

• Intraoperative control of hemostasis is critical. Koorneef’s description of the delicate connective tissue scaffold connecting the anterior orbital fat to deep orbital fat underscores the necessity to avoid excessive traction during fat excision. It is advantageous to delay wound closure by proceeding to another surgical site, returning later to reassess hemostasis prior to suturing.

• Postoperative prevention of hemorrhage involves all of the following:

– Elevation of the head of the bed decreases intravascular pressure.

– Avoidance of the Valsalva maneuver prevents a sudden rise in intraorbital pressure that may open a bleeding site. Consultation with the anesthesia team should include routine postoperative antiemetics, and when necessary, cough suppressants.

– Ascertain that the patient can at least count fingers. Decreased vision in the hand motions or light perception range is cause for concern. Recovery staff should be instructed to test the vision in each eye individually.

– Avoid “pressure dressings” as they delay diagnosis.

– Place ice compresses on each eye.

Once the diagnosis of retrobulbar hemorrhage is made, the treatment requires immediate attention. The first step should be to identify those hemorrhages that require medical or surgical care, based on the ophthalmic examination. If the intraocular pressure is elevated, as measured by tonometry or emergently by tactile evaluation, topical and systemic glaucoma medications can be used. Systemic corticosteroids are used for significant edema. When the bleeding threatens the visual system, or is worsening, surgical therapy is required. The first step is to open the incision widely through the orbital septum and explore the surgical site and orbit for signs of bleeding. Clots are evacuated and cautery is applied when bleeding sites are identified. If the condition remains unresponsive, a lateral canthotomy and cantholysis is performed. In severe cases, both the inferior and superior crus of the lateral canthal tendon can be released. When these measures fail, an emergent CT scan without contrast is warranted. If posteriorly organized hemorrhage is identified, bony decompression may be warranted to relieve orbital apex compression (Fig. 34.3). The treatment should be aggressive for the first 24–48 hours postoperatively, as vision has been reported to return in patients with “no light perception” that was present for 24 hours.

Fig. 34.3 CT scan after transcutaneous blepharoplasty showing aggregated clot and hemorrhage in the orbital apex. Posterior findings create the possibility for treatment with decompression rather than lateral canthotomy.

Globe perforation

Inadvertent globe penetration can result from any periocular procedure. Caution is necessary during local anesthetic injection, particularly in the thin upper eyelid of older patients. Prevention of this complication begins with the use of protective corneal shields during injection and surgery. Corneal shields should be lubricated with ophthalmic ointment prior to placement within the lids to avoid corneal abrasion. The range of potential ocular damage from penetration includes an open globe, corneal perforation, traumatic cataract, intraocular hemorrhage, a hypertensive or hypotensive globe, retinal tears and detachment (Fig. 34.4). Perforation of the globe is an ophthalmic emergency and necessitates emergent consultation with an ophthalmologist. A Fox shield should be placed over the eye in the interim and the patient should be instructed not to rub or press on the eye.

Fig. 34.4 A retinal flap tear with tractional retinal detachment is present after inadvertent corneal perforation during injection for an upper eyelid blepharoplasty. The patient also suffered from a traumatic cataract secondary to lenticular penetration.

How to place a corneal protective lens:

• Instill a tetracaine or proparacaine ophthalmic eye drop into the eye.

• Lubricate the protective shield with ophthalmic ointment.

• Insert the shell under the superior fornix from below.

• Evert the lower eyelid to allow the lower edge of the shell to move into the inferior fornix.

How to remove a corneal protective lens:

• Instill a tetracaine or proparacaine ophthalmic eye drop into the eye.

• Gently place an ocular muscle hook posterior to the lower edge of the shell.

• Guide the shell inferiorly over the lower lid.

Corneal abrasion

Corneal abrasion is generally a rapidly reversible cause of decreased vision postoperatively. The diagnosis is made by patient symptoms (pain, foreign body sensation, light sensitivity) and is usually apparent immediately after surgery. The diagnosis is confirmed by evaluating the cornea under a cobalt blue light after instillation of fluorescein (Fig. 34.5). Even though corneal abrasion is the leading cause of ocular pain and irritation following blepharoplasty, patients who complain of severe eye pain should be carefully examined under a slit-lamp to rule out globe perforation. Abrasions are often caused by drying of the corneal surface during surgery or inadvertent damage to the surface corneal epithelial layer. Sometimes, taping of the eyes during anesthetic induction causes an abrasion if the eyes are accidentally taped in an open position. Careful insertion and removal of well-lubricated corneal shields prevents this complication; as does the use of ophthalmic ointment into each eye at the completion of the procedure. Abrasions can be treated with ophthalmic antibiotic ointment four times daily, and should be resolved within 24 hours. Patching should be avoided, as it may mask a more serious complication, such as retrobulbar hemorrhage. Persistent signs and symptoms should prompt ophthalmologic evaluation.

Fig. 34.5 Pericentral corneal abrasion following blepharoplasty surgery. This is likely secondary to trauma, since exposure-related abrasions would be horizontal and linear.

Dry eye

Corneal irritation is somewhat common after blepharoplasty and symptoms are similar to, but less severe, than an abrasion. Patients may complain of foreign body sensation, dryness, irritation, blurry vision, photosensitivity and redness. These symptoms often arise from dried accumulation of clot or ointment in the eye and will respond to ocular lubrication with preservative-free tear drops and cool compresses. Alternatively, poor eyelid closure can cause exposure keratopathy, particularly inferiorly. This diagnosis is made by slit-lamp examination after the instillation of fluorescein. The examiner will see punctate corneal staining under blue light illumination in the affected region of the cornea. Treatment is with lubricating drops and ointment.

Very rarely, ophthalmic lubricant may be inadvertently introduced into deeper eyelid tissues from a transconjunctival surgical wound. This can result in encapsulation of the ointment within the wounds, and subsequent cyst formation that responds to excision (Fig. 34.6). Although this complication is extremely rare, physicians should keep in mind that excessive amounts of ointment are unnecessary and may result in inoculation of the wound.

Fig. 34.6 This patient returned to her plastic surgeon after a lower eyelid blepharoplasty complaining of recurrent fullness of each lower eyelid (A). The lower eyelid masses appeared cystic and upon evacuation were firmly encapsulated (B,C). Opening of the capsule and chemical analysis of its contents revealed Lacri-Lube (Allergan, Irvine, CA) ophthalmic ointment encapsulated from a foreign body reaction (D).

Eyelid hematoma

Hematomas usually develop from bleeding of the orbicularis oculi muscle. Evaluation for symptoms consistent with retrobulbar hemorrhage should proceed first. Once ruled out, mild superficial hematomas can usually be treated conservatively with ice compresses. Larger, stable hematomas should be followed for 7–10 days, until adequate liquefaction has occurred. Rarely do they need to be drained by needle aspiration or reopening of the wound. In severe cases, they may result in tissue fibrosis and lid scarring. Expanding hematomas require immediate surgical exploration, evacuation and control of the bleeding source.

Infection

The development of cellulitis or abscess formation is exceedingly rare in the well-vascularized eyelid. Nonetheless, both complications have been reported and should be managed with appropriate oral or intravenous antibiotics. Abscesses require surgical drainage. Figure 34.7 shows a patient who developed pseudomonas cellulitis in three of four lids after blepharoplasty. She was treated with a combination of surgical drainage and intravenous antibiotics, but ultimately developed late cicatrization and skin dimpling.

Fig. 34.7 Three days postoperatively, a blepharoplasty patient developed pseudomonas cellulitis with associated abscess formation.

Eyelid sloughing

Eyelid necrosis has been reported sparingly in the literature and can follow inadvertent injection with formaldehyde or other substances (i.e. atropine, alcohol, boric acid) instead of local anesthetic. Complete eyelid sloughing can develop, necessitating multiple eyelid reconstructive procedures and setting the patient up for scarring, persistent lagophthalmos and chronic ocular irritation from dry eye (Fig. 34.8).

Fig. 34.8 Severe eyelid sloughing is seen in a patient after injection with formalin (A,B). The surgeon was inadvertently handed formalin instead of local anesthesia and the patient immediately complained of pain. Four stages of eyelid reconstruction were needed to provide sufficient corneal coverage (C).

Chemosis

Conjunctival edema can develop in the early or intermediate postoperative period as the result of incomplete eyelid closure, ocular allergy, sinusitis or surgical edema. Chemosis can be worsened by systemic conditions, such as renal failure (Fig. 34.9). Corneal drying may occur, as the edematous conjunctiva balloons around the cornea preventing adequate tear film dispersion. Additionally, the exposed conjunctival surface may keratinize, leading to worsening foreign body sensation and ocular irritation. Treatment is with preservative-free artificial tears and ointment. A mild topical steroid eye drop can be prescribed, but should only be given in conjunction with ophthalmic evaluation to assure normalcy of the intraocular pressure and to rule-out secondary infectious keratitis. Rarely, a temporary suture tarsorrhaphy may be needed.

Fig. 34.9 A patient with chronic renal failure who developed postoperative chemosis following lower eyelid blepharoplasty (A). Lubrication and time allowed significant resolution of the chemosis over 6 months. Note that mild persistent chemotic conjunctiva is present and can be a management problem in patients with underlying thyroid or renal disease (B).

Upper eyelid malposition

Ptosis

Postoperative ptosis can be seen frequently following upper eyelid blepharoplasty (Fig. 34.10). Often, this subtle levator attenuation seen in aponeurotic ptosis is present preoperatively, but goes undiagnosed.⁷

Fig. 34.10 Preoperative photo of a patient with concomitant dermatochalasis and aponeurotic ptosis (A) who underwent upper eyelid blepharoplasty without addressing the underlying ptotic eyelids (B). Note the residual blepharoptosis in the postoperative photo (B).

Pearls

Pearls for avoiding overlooking preoperative ptosis include:

• Assure that the frontalis muscle is blocked when examining the upper eyelid position. Often patients with ptosis and/or excessive dermatochalasis compensate with involuntary frontalis recruitment.

• Carefully examine the margin reflex distance (MRD), palpebral fissure height (PF), levator function and upper eyelid crease height. Patients with excess upper eyelid tissue overhanging may mask a small MRD and PF distance. Aponeurotic ptosis is often accompanied by an increase in lid crease height, or a deep superior sulcus.

• When measuring MRD and PF, simultaneously block the frontalis muscle and mechanically lift the excess tissue.

• Plan a concomitant ptosis surgery along with blepharoplasty, if necessary.

Mechanical ptosis can result from postoperative edema or ecchymosis. This should resolve with conservative treatment, including cool compresses. If the ptosis remains persistent, it is possible that the edematous state led to levator attenuation; or, the patient may have developed a neurogenic ptosis. When persistent, the surgeon should consider ophthalmic evaluation.

Lagophthalmos

As mentioned previously, lagophthalmos occurs frequently in the postoperative period. Reasons for lagophthalmos include:

• Excessive skin removal.

• Surgical trauma to the orbicularis muscle.

• Tethering of the eyelids by sutures or Steri-Strips (3M, St. Paul, MN).

• Postoperative pain, leading to guarding and incomplete lid closure (Fig. 34.11).

Fig. 34.11 A transcutaneous blepharoplasty patient with postoperative guarding secondary to expected orbicularis paresis causing lagophthalmos. This is the finding that creates the need for ophthalmic lubricants in all postoperative patients.

Inadequate eyelid closure can lead to patient discomfort secondary to exposure keratopathy. The condition will be worsened in those with pre-existing dry eye disease or the absence of an adequate Bell’s phenomenon (Fig. 34.12). Preoperative evaluation should include an assessment of ocular sicca symptoms (foreign body sensation, tearing, irritation, photophobia and dryness), signs (abnormal tear film, punctate corneal staining and decrease in basal tear secretion) and adequacy of the Bell’s reflex. Lagophthalmos is usually temporary and conservative management in the intermediate postoperative period includes frequent lubrication, lid massage and lid taping.

Fig. 34.12 The difference between a good (A) and poor (B) Bell’s reflex is shown. Patients with a poor Bell’s phenomenon are at increased risk for corneal epitheliopathy.

Lower eyelid malposition

The most common reported complication after lower eyelid blepharoplasty is lower eyelid malposition, which may range from mild inferior scleral show (Fig. 34.13A) in up to 20% of patients to severe cicatricial ectropion (Fig. 34.13A,B) in 1%.^8,9 Lid malposition is the result of an imbalance in lower eyelid forces. Abnormal downward forces can result from excessive skin resection, scarring, imbrication of the orbital septum, edema and hematoma. Laxity of the tarsoligamentous sling causes a loss of normal upward traction and dynamic elasticity of the lower lid. Orbicularis oculi paralysis additionally destabilizes the lower eyelid position.

Fig. 34.13 Postoperative lower eyelid malposition after blepharoplasty can result in a range of deformities from mild inferior scleral show (A) to cicatricial ectropion (B).

Preoperative identification of patients at risk for lower eyelid retraction is of utmost importance in prevention of this complication. Predisposing factors include:

Additionally, horizontal eyelid laxity should be evaluated preoperatively. Evaluation of lower eyelid laxity hinges upon the snap-back and distraction tests. Eyelid snap-back is evaluated by inferiorly displacing the lower eyelid centrally. The lid should normally spring back into its position against the globe. An abnormal result can be quantified by counting the number of blinks required for the lower lid to regain its normal position. The distraction test is performed by manually distracting the central aspect of the lower lid perpendicularly away from the globe. Distraction of greater than 6–7 mm indicates lower eyelid laxity. If lower eyelid laxity is found, an appropriate tightening (i.e. lateral canthal tendon sling, horizontal shortening, medial canthopexy, lateral retinacular repair) should be performed at the time of blepharoplasty.

Mild eyelid retraction can often be managed with topical steroid ointment and massage. The patient is instructed to massage the lower eyelid superiorly in the medial or lateral one-third of the eyelid with a clean index finger. The lid should be molded against the globe (never distracted away from the globe) and stretched superiorly for 30–60 seconds. A total of 5 minutes of eyelid stretching 2–3 times daily is necessary. Additionally, if tolerated, the lower eyelid can be stretched mechanically with Steri-Strips placed in a superolateral direction from the lateral aspect of the lower eyelid. Steri-Strips usually are only helpful in mild cases, since they cannot overcome the forces of significant retraction. Most aesthetic patients prefer to use massage only.

While cases of over-resection of skin have become less common with the popularity of transconjunctival blepharoplasty, a role still exists for the transcutaneous blepharoplasty, making the potential for excess skin resection real. If over-resection is diagnosed early, skin sutures can be removed at 2–3 days postoperatively, and the wound gapped, allowing granulation of a portion of the eyelid. While not ideal, this option is better than the severe bowing or ectropion that is likely to result and will often necessitate skin grafting. Similar wound gapping can be performed with acceptable results in the upper eyelid. Massage is needed during granulation to stretch and counter the forces of contraction.

Corneal exposure

As in the early postoperative period, keratopathy may persist or become evident during the intermediate recovery period. Similar to patients with early corneal irritation, sutures or Steri-Strips may be tethering the eyelids since the orbicularis muscle may not have regained its protractor abilities. Additionally, over-resection of skin may become more apparent as initial postoperative edema resolves. First line treatment is generally expectant, with frequent ocular lubrication and taping, if necessary. One condition worth mentioning is the patient with undiagnosed thyroid ophthalmopathy who undergoes blepharoplasty and unmasks lid retraction and keratopathy (Fig. 34.14A&B). If necessary, the wound can be opened and allowed to granulate (Fig. 34.14C&D). Further treatment options are usually reserved for later in the postoperative course.

Fig. 34.14 A patient with undiagnosed thyroid ophthalmopathy with right upper eyelid retraction proceeds with upper lid blepharoplasty. Preoperative photograph (A) demonstrates mild asymmetry of the palpebral fissures with apparently minimal right upper eyelid retraction. One week postoperatively (B) the retraction is obvious and the wound is opened (C). After granulation, the appearance is reasonably symmetric at 3–4 weeks postoperatively (D).

Lacrimal system dysfunction

Epiphora can result from blepharoplasty surgery secondary to exacerbation of dry eye, exposure keratopathy or an impaired lacrimal pump apparatus. The lacrimal pump requires normal functioning of the superficial and deep heads of the medial canthal tendon, both extensions of the pretarsal and preseptal orbicularis oculi muscle. Dysfunction usually returns to normal with time, but lacrimal pump failure can produce long term epiphora.

Extended tearing requires further evaluation for punctal malposition or canalicular damage, and often requires the assistance of an ophthalmologist. Examination should focus on punctal eversion, as any rotation of the tear drain away from the tear lake will cause epiphora. If present, initial eyelid massage (described earlier) may be beneficial. Surgical correction usually involves a horizontal tightening procedure, medial spindle operation or medial or lateral canthopexy. While the eyelid and punctum can be positioned in better approximation to the globe, nothing strengthens a weakened lacrimal pump. Canalicular stenosis or obstruction is diagnosed by probing and irrigation of the tear drain system and requires lacrimal surgery for repair.

Strabismus and extraocular muscle disorder

Diplopia is a rare, but potentially disabling complication of upper or lower eyelid blepharoplasty. It is common for patients to complain of intermittent double vision following blepharoplasty, often secondary to an abnormal tear film, ophthalmic ointment, muscle contusion or temporary paresis, hematoma or edema. Signs that make diplopia less worrisome following surgery are:

Such patients should be treated with reassurance and preservative-free artificial tear drops.

Persistent binocular diplopia requires additional consideration, especially if vertical. Transconjuctival and transcutaneous lower eyelid blepharoplasty can each result in iatrogenic strabismus.¹⁰ In both surgical approaches, the inferior oblique muscle is most commonly injured (Fig. 34.15). Damage may be direct, or secondary to aggressive cautery in the region between the nasal and central fat pockets. Some surgeons advocate identification of the inferior oblique muscle during fat resection under direct visualization, but realistically this is not likely, since most blepharoplasties are performed by non-ophthalmologists. Additionally, secondary blepharoplasty increases operative risk as anatomic identifiers may be ambiguous and fibrosis is often encountered.

Fig. 34.15 Example of a patient with inferior oblique paresis following transconjunctival blepharoplasty (A) with a close up view of the patient in downgaze (B).

Pearls

Pearls to avoid damage to the inferior oblique muscle:

• The most direct route to the extraocular musculature is through a deep forniceal incision. Avoiding this deep forniceal incision is crucial. The ideal location of an incision is approximately 5–6 mm inferior to the inferior tarsal border on the palpebral conjunctiva (Fig. 34.16).

• When in doubt, or as a routine, the inferior oblique muscle can be identified lying between the nasal and central fat pockets in the lower eyelid.

• Any clamping or traction on fat should not move the globe. If this occurs, suspect that an extraocular muscle is intertwined with the proposed resection and reevaluate.

Fig. 34.16 The ideal lower eyelid transconjunctival blepharoplasty incision is on the palpebral conjunctiva about 6 mm inferior to the inferior tarsal border. Note that a deep forniceal incision allows a more direct route to the inferior oblique muscle.

The superior oblique muscle can be injured during upper eyelid blepharoplasty, with mechanisms of injury similar to inferior oblique damage. Injuries to the inferior and lateral recti are exceedingly rare, but have been reported. The inferior oblique muscle rides over the inferior rectus muscle, making damage to the rectus less likely.

Initial treatment of diplopia is conservative, as it often resolves in the first few months as edema diminishes, even in the setting of iatrogenic trauma. Patients with concomitant misalignment may be temporized with prismatic spectacles. Expectant management is recommended until continued improvement ceases, at which point consideration for surgical repair may be advisable.

Upper eyelid malposition

Lower eyelid malposition

Late lower eyelid malposition is complex and requires careful consideration based on anatomic concepts. The lower eyelid is broken into three lamellae. The anterior lamella is comprised of skin and orbicularis muscle. The middle lamella contains tarsus and orbital septum. The posterior lamella is made up of the lower lid retractors and conjunctiva. Identification of the affected lamella, usually the result of deficient tissue, is the key to formulating a successful reconstructive plan. Additionally, horizontal laxity must be considered as a potential component of malposition.

An anterior lamellar deficiency is encountered after transcutaneous blepharoplasty and can best be diagnosed by noting lower eyelid movement with opening of the mouth (Fig. 34.17). Frank cicatricial ectropion can develop (Fig. 34.18A). Most disease states respond partially or completely to eyelid stretching (Fig. 34.18A&B). Placing the eyelid on stretch as early as possible is advisable. Surgical repair often involves placement of additional skin to replace the deficient lamella. A combined lateral tarsal suspension is appropriate if concomitant horizontal laxity is present. Tarsal suspension may be done alone as an indirect secondary procedure in those patients who are unhappy with the thought of skin grafting. These patients often require over-correction since gravity and midfacial movements will loosen the original position attained.

Fig. 34.17 Cicatricial lower eyelid retraction from excessive skin excision and anterior lamellar deficiency is best diagnosed by having the patient open their mouth and observing inferior excursion of the lower lids.

Fig. 34.18 Postoperative view of a patient with cicatricial ectropion following trans-lid removal of an infected malar implant (A). Aggressive stretching and massage allowed some improvement and softening, making it possible to attain a good lid position with a lateral tarsal suspension (B). Starting the patient stretching early and often, even in seemingly useless situations, is important.

Middle lamellar deficiency is diagnosed by attempting to stretch the central aspect of the lower eyelid superiorly. A normal response is the ability to easily elevate the lower eyelid over the inferior corneal limbus. If the eyelid will not elevate, adhesions are present between the capsulopalpebral fascia and the orbital septum or the anterior tissue and the orbital septum. Successful repair in these instances requires lysis of these adhesions if conservative stretching has failed. A lateral fixation procedure or occasionally posterior lamellar lengthening may be necessary.

Posterior lamellar deficiency usually presents as entropion. While rare, the repair may involve addition of posterior lamella, such as hard palate grafting.

While repair of the malpositioned lower eyelid is complex, the most important factor is to understand that vertical eyelid deficiencies involve one or more the three lamellae; horizontal laxity may or may not be associated with the malposition and, if present, responds to tightening procedures.

Over- and under-resection of skin

Excessive skin resection has been addressed. The best preventative measure for excessive skin excision is a conservative surgical approach. If additional tissue requires attention after full resolution of postoperative edema, a second procedure can be undertaken.

Over and under-resection of orbital fat

Under-resection

Inadequate fat excision is easier to remedy. Patience is necessary to assure resolution of edema and ecchymosis prior to consideration of additional surgical resection.

Pearls

Pearls for avoiding inadequate fat resection:

• In the upper eyelid, the medial fat pocket is least accessible and may be inadequately addressed at the time of surgery. The medial fat pocket can be identified as a distinctly ‘whiter’ fat than the central pad. Identification of the medial fat is the first step towards its adequate resection.

• The lateral fat pocket is most commonly missed in lower lid blepharoplasty and is seen postoperatively as a lateral bulge (Fig. 34.19). There is a greater amount of connective tissue septae covering this pad. Excision of the superficial septae and fat allow additional prolapse of deeper fat with mild pressure on the globe. It is common to reherniate the lateral pocket if canthoplasty is performed concurrently. Attention should be directed to re-evaluate the lateral pocket if canthal tightening procedures are performed.

Fig. 34.19 A residual temporal fat pocket after transcutaneous blepharoplasty.

Eyelid crease abnormalities

Symmetry and reformation of the upper eyelid crease may be the single most important factor in a successful upper eyelid blepharoplasty outcome.¹³ The crease in women should be higher than in men, allowing adequate pre-tarsal show. Additionally, a women’s crease is more sharply demarcated. In men, some fullness should be left in the upper lid to allow the upper eyelid fold to cover the crease. When patients notice crease asymmetries, it is usually due to unilateral brow elevation with ptosis which elevates eyebrow skin superiorly.

Careful preoperative marking and placement of an incision is the first step to successful and natural crease retention. Eyelid crease formation techniques have been described, and can be useful in selected situations. While beyond the scope of this chapter, supratarsal suture techniques involve securing the skin to the fine threads of the levator aponeurosis to mimic natural formation of a crease. Early eyelid crease abnormalities should be followed. When persistent and cosmetically unacceptable, crease reformation can be performed surgically, or ptosis corrected to lower the eyebrow to secondarily redrape skin over the incision site.

Malar festoons

The best prevention of malar bags is to diagnose them preoperatively or to recognize patients who are at increased risk. Patients with mild malar festoons should be questioned about a history of thyroid disease, renal failure, chronic sinusitis, allergies and idiopathic edema. Patients who are predisposed to fluid accumulation should be advised of the risk of developing postoperative malar bags. Preoperative consultation with an internist is advised, as postoperative care often involves systemic steroids and/or diuretics. Patients who are at higher risk should be treated intra-operatively with intravenous steroids. Postoperative steroids (i.e. medrol dose packs) are useful. Furosemide (Lasix) 20 mg or 40 mg daily early in the postoperative course is helpful (Fig. 34.20). With time, this agent can be replaced with a milder diuretic, such as hydrochlorothiazide 50 mg per day. Medical treatment is continued for 7–10 days. While persistent malar festoons can be excised, the success rate is low, as patients are again at risk for retained fluid. If the underlying condition is systemic, eyelid surgery cannot locally correct the problem.

Fig. 34.20 Pretreatment (A&C) and post-treatment (B&D) examples of malar bags responding to diuretic therapy. Each patient was treated with furosemide and potassium replacement. Time alone may have produced the same result, but Lasix treatment plays a role in minimizing the stretching and attenuation of malar and lower eyelid skin.

Suture tracks

Epithelial trapping can occur along suture tracks.

If present, suture tunnels can be unroofed with a fine needle or surgical blade. Light cautery may be applied.

Hypertrophic scarring

Keloid formation in the eyelid is exceedingly rare, but hypertrophic scars may result from wound gapping during healing. This usually responds well to massage and pressure with steroid ointment. Intralesional steroid injection can be attempted with caution. The thin eyelid skin can allow visualization of the steroid depot and hypopigmentation may occur. Any seepage of steroid deep to the levator can create ptosis.

Dermal pigmentation

Ecchymosis with prolonged resorption of blood contributes to dermal pigmentation. Blood staining of the dermis can take many months to fade. Expectant management is advisable. Trial and error treatment with hydroquinones can be attempted to lighten the pigmentation after months of expectant waiting.

Alopecia of lashes and chalazia

Localized loss of eyelashes is predisposed in patients with a history of blepharitis or chronic eyelid margin disease, such as chalazia. An incision site that is too close to the lash follicles may result in lash loss. Additionally, overzealous cautery in this region may damage follicles. If the follicle is not destroyed, eyelashes will generally re-grow in two months. Chronic edema in the setting of chronic inflammation (blepharitis) can produce lash loss.

Chalazion formation is stimulated after surgery in patients with a history of meibomian gland dysfunction or anterior blepharitis. Pretreatment with eyelid hygiene will minimize this risk. Patients should be advised to use warm compresses, lid scrubs and artificial tears. More severe cases may respond to flax seed oil supplementation or oral doxycycline. Surgical drainage can be performed if medical treatment fails.

Dry eye syndrome

True dry eye disease in a post-blepharoplasty patient can only be diagnosed after ample time has been allowed for resolution of common early and intermediate ocular sicca symptoms. Regardless of approach and degree of tissue conservation, upper and lower eyelid blepharoplasty widens the palpebral fissure. While generally well-tolerated, even a small amount of widening may “tip the scales” in the patient with unrecognized borderline tear production. For this reason, careful preoperative evaluation should include:

Although not contraindicated, the surgeon should proceed with caution when performing blepharoplasty on patients with dry eyes, especially in cases of severe keratoconjunctivitis sicca, where sight-threatening complications may arise.

Initial treatment of dry eye consists of ocular lubrication with preservative-free artificial tears and ophthalmic ointment. Failure of this treatment regimen should prompt ophthalmologic examination, with consideration of additional anti-inflammatory eye drops or punctal occlusion.

A small subgroup of preoperative patients with dry eye and very heavy upper eyelids are actually improved by removal of excess skin.¹⁴ In these cases, the eyelashes are pushed inferiorly due to fullness. Normal desquamation of the upper eyelid epithelium falls into the palpebral aperture producing the symptoms of dry eye without the physiologic findings of lacrimal, meibomian gland or goblet cell dysfunction.

Palpebral fissure asymmetries

Asymmetries of the eyelids, which can include the arch, height, curvature and width of the palpebral fissure, residual fat, dermatochalasis and eyelid crease position are the rule, not the exception. Patient expectations should include the fact that these asymmetries are always present preoperatively, as well as postoperatively. While gross disparities in surgical technique may result in iatrogenic asymmetry, adequate patient expectations must be addressed preoperatively to ensure that realistic expectations exist.