Lateral Canthotomy - Clinical Tree

Introduction

The lateral canthotomy coupled with an inferior cantholysis is often the first step in many eyelid and orbital procedures. The detachment of the inferior crus of the lateral canthal tendon allows for greater horizontal laxity of the lower eyelid. It is commonly used in lower eyelid reconstruction techniques (i.e., semicircular advancement flap), inferior or lateral orbitotomies for greater exposure, or in eyelid tightening procedures such as a lateral tarsal strip. It is used as the sole procedure to emergently decompress the orbit in the setting of an “orbital compartment syndrome,” a condition characterized by multiple cranial neuropathies within the orbit due to an acute increase in intraorbital pressure.

Aside from airway compromise, an orbital compartment syndrome is one of the few true emergencies for the head and neck surgeon. Immediate intervention should be performed at the time of diagnosis to prevent permanent loss of vision.

Key Operative Learning Points

Recognition of the potential for an orbital compartment syndrome in the setting of trauma, the postoperative period, or secondary to acute orbital or sinus pathology is required for a prompt diagnosis.
Diagnosis of an orbital compartment syndrome is based on the clinical findings alone. Imaging is not sufficient to determine if a space-occupying lesion requires emergent treatment.
Clinical presentation of etiologies varies; it is the acute severity and loss of function that are the hallmarks of an orbital compartment syndrome.
Lateral canthotomy combined with an inferior cantholysis is essential to gain horizontal eyelid laxity and therefore greater orbital capacity.
Repeat intraocular pressure measurements are required to demonstrate adequate orbital decompression.
Adjunctive medical management should not delay necessary surgical intervention.

Preoperative Period

Orbital compartment syndrome is a rare condition which, if unrecognized or untreated, can lead to blindness. The most common causes are traumatic or iatrogenic etiologies and can range from a rapidly progressing space-occupying lesion to severe acute orbital vascular congestion. Several potential causes of an orbital compartment syndrome, such as mild retrobulbar hemorrhage, may be managed conservatively with serial ophthalmic examinations. It is the loss of function that is the hallmark of the development of an orbital compartment syndrome that requires immediate intervention.

Regardless of the etiology, the presenting symptoms of pain or pressure in the eye, decreasing vision, and diplopia should prompt further examination for objective signs of an orbital compartment syndrome. These include proptosis, afferent pupillary defect, increased intraocular pressure, and decreased eye movement. While there are no large published case series guiding when treatment should be initiated, the loss of vision when accompanied by the aforementioned signs and symptoms should prompt emergent intervention.

The orbit is enclosed by bone on all sides except anteriorly, and any forward displacement is limited by the eyelid apparatus and the tethering of the optic nerve to the globe. As intraorbital pressure rises, ocular perfusion decreases, leading to ischemia. Multiple cranial nerves within the orbit may be compromised, including the optic nerve and the nerves controlling eye movement.

Once the diagnosis is made, emergent orbital decompression is warranted by performing a lateral canthotomy and inferior cantholysis. The objective of the procedure is to allow for additional forward movement of the orbital contents, not actual drainage of the hematoma. Decreasing the intraorbital pressure restores normal circulation and prevents further loss of vision. Visual recovery is possible if this procedure is performed in a timely manner.

Orbital compartment syndrome after endoscopic sinus surgery is rare. If signs are present intraoperatively (sudden proptosis, afferent pupillary defect, globe firm to palpation compared to the contralateral side), a lateral canthotomy and inferior cantholysis is indicated, followed by conversion to an external approach. If diagnosed postoperatively, nasal packing is removed and the head is elevated to allow for drainage, followed immediately by lateral canthotomy and inferior cantholysis prior to re-exploration of the operative site in the operating room.

History

1.
History of present illness
- a.
  Progressively decreased vision and pain in the eye on the affected side
- b.
  Binocular diplopia (double vision present with both eyes open, resolves with closure of either eye)
- c.
  Trauma
  - 1)
    Retrobulbar hemorrhage
  - 2)
    Orbital emphysema
- d.
  Recent surgery in the face
  - 1)
    Retrobulbar anesthesia for ocular surgery
  - 2)
    Periorbital surgery that violates the orbital septum (i.e., lower eyelid blepharoplasty)
  - 3)
    Endoscopic sinus surgery
- e.
  Severe orbital congestion
  - 1)
    Orbital cellulitis with or without abscess formation
  - 2)
    Idiopathic orbital inflammation (rare)
- f.
  Contributing maneuvers that increase intraorbital pressure (Valsalva, vomiting, coughing, sneezing)
2.
Past medical history
- a.
  Predisposing factors
  - 1)
    Orbital lesions that may spontaneously hemorrhage, such as vascular abnormalities (orbital varix, lymphangioma, arteriovenous malformations)
  - 2)
    Inherited or acquired coagulopathies
  - 3)
    Uncontrolled hypertension
  - 4)
    Rarely: connective tissue disorders (vitamin C deficiency, Elher-Danlos type IV)
3.
Medications
- a.
  Anticoagulants

Physical Examination

1.
Proptosis
- a.
  Forward displacement of the globe may be difficult to assess in the setting of periorbital edema. It may be helpful to compare one eye to the other.
2.
Decreased extraocular motility
- a.
  Usually diffuse
- b.
  Assessment may be made difficult secondary to periorbital edema. Make use of the corneal light reflex to check for any disconjugate eye movement.
3.
Elevated intraocular pressure
- a.
  In the acute setting, a handheld tonometer is preferred for its portability and ease of use.
- b.
  In the awake patient
  - 1)
    Use topical anesthesia with ophthalmic drops such as proparacaine or tetracaine.
  - 2)
    Have the patient focus on a distant target to facilitate cooperation (for sustained fixation and eyelid opening).
  - 3)
    If the patient is unable to keep his or her eyelids open, manually retract the upper eyelid to the superior orbital rim, with care not to place pressure upon the globe.
- c.
  Difficulty opening the eyelids secondary to eyelid edema
  - 1)
    Roll the eyelid margin tangentially away from the globe with a cotton-tip applicator, again with care not to place pressure upon the globe.
  - 2)
    To gain further access to the globe, a Desmarres retractor can be used to retract the lower eyelid inferiorly. This may further elevate the intraocular pressure transiently but can be helpful in attempting to examine extraocular motility and to check for an afferent pupillary defect.
- d.
  Check the contralateral intraocular pressure as an in vivo control.
- e.
  Note: Accurate assessment of intraocular pressure is ideal but may not be readily available in the emergent setting. In the setting of additional signs and symptoms of orbital compartment syndrome, in lieu of delays related to finding a tonometer, manual palpation of the globe may be sufficient. The affected eye will be firmer compared to the contralateral eye if the elevated intraocular pressure is severe enough. Increased resistance to retropulsion of the globe compared to the contralateral eye may also be elicited.
4.
Afferent pupillary defect
- a.
  Check in a darkened room.
- b.
  Have the patient fixate on a distant target.
- c.
  A bright, but concentrated, light source is repeatedly swung from the unaffected eye to the affected eye.
  - 1)
    An afferent pupillary defect is present if initial dilation, instead of constriction, is seen in the affected eye in response to a direct light stimulus.
  - 2)
    An absolute afferent pupillary defect is seen when direct light stimulus over the affected eye elicits no pupillary constriction in the affected eye, and there is no consensual constriction of the unaffected eye.
- d.
  Note: While an afferent pupillary defect is the most objective finding of optic nerve compromise, the finding alone does not diagnose an orbital compartment syndrome. It is this finding in conjunction with the additional findings that helps secure this diagnosis.

Imaging

1.
Computed tomography (CT) scan
- a.
  Is not required for diagnosis of orbital compartment syndrome, but it is helpful in discovering the definitive etiology.
- b.
  Concerning signs include the following:
  - 1)
    Proptosis—forward displacement of the equator of the globe beyond the orbital rim
  - 2)
    Straightening of the optic nerve
  - 3)
    Tenting of the posterior globe
  - 4)
    Lack of these features does not rule out an orbital compartment syndrome, as it is an evolving process that may not be captured on initial imaging.
- c.
  Large floor and medial wall defects do not preclude the development of an orbital compartment syndrome.

Indications

Emergent—orbital compartment syndrome
Initial steps for the following:
- Lateral or inferior orbitotomy
- Advancing tissue for reconstruction of the lower eyelid
- Horizontal eyelid tightening

Contraindications

None—This procedure is considered a low-risk intervention, especially in the setting of permanent loss of vision without surgical treatment. The onus on the surgeon is early suspicion, evaluation, and an urgent canthotomy and cantholysis.

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