Chapter 162. Lateral Canthotomy and Cantholysis or Acute Orbital Compartment Syndrome Management

Acute orbital compartment syndrome is defined as an acute elevation of intraorbital pressure with resultant rapid ocular dysfunction. Patients typically present with ocular pain, proptosis, and blurry vision. Clinical signs of an acute orbital compartment syndrome include decreased visual acuity, elevated intraocular pressure (>40 mmHg), an afferent papillary defect, chemosis, mydriasis, diminished retropulsion of the affected globe to direct manual pressure, ophthalmoplegia, and fundoscopic signs of retinal ischemia (rare).1–28

Orbital compartment syndromes have been described in multiple clinical settings. The presentation that Emergency Physicians will most likely encounter is an acute posttraumatic retrobulbar hemorrhage leading to an orbital compartment syndrome, with subsequent rapid loss of vision.1,2 Orbital compartment syndromes have been documented following blepharoplasty, retrobulbar anesthesia, orbital and sinus surgery, orbital fractures with intraorbital emphysema, spontaneous subperiosteal hemorrhages, and spontaneous retrobulbar hemorrhages.3–9 Orbital compartment syndromes may also occur as the result of chronic and progressive disease processes (e.g., neoplasms, infections, and inflammations).10

Acute orbital compartment syndromes demand prompt recognition because irreversible loss of vision and even permanent blindness occurs without rapid treatment.11 Once the diagnosis of an acute orbital compartment syndrome is made, emergent surgical intervention is indicated. An immediate lateral canthotomy and cantholysis are indicated within 1 hour of injury and ocular dysfunction. Medical interventions aimed at reducing intraocular pressure (e.g., mannitol, acetazolamide, topical beta-blockers, etc.) should be considered adjunctive therapy and not a substitute for surgical intervention.

The orbit of the eye is a closed space posterior to the orbital septum and contained within the bony orbit. The lateral wall of the orbit is formed by the zygomatic bone. The posterior wall is formed by the sphenoid bone. The medial wall is formed by the ethmoid bone. The roof is formed by the frontal bone. The floor is formed by the maxillary bone. The globe is enclosed in a fascial envelope within the bony orbit.

The medial and lateral canthal tendons provide structural fixation of the eyelids to the orbital rim. The lateral canthal tendon (LCT) is located posterior and inferior to the lateral canthal fold (Figure 162-1). The LCT originates from the superior and inferior lateral tarsal plates (Figure 162-1) and attaches to the lateral orbital tubercle of the zygoma (Figures 162-1 & 162-2). The LCT consists of a superior crus from the superior tarsal plate and a inferior crus from the inferior tarsal plate. The LCT measures 10.6 mm (SD ± 0.9 mm) in length from its attachment site to the lateral canthal angle. It is 10.2 mm (SD ± 0.8 mm) in width at its origin at the lateral ends of the tarsal plates. It attaches 1.5 mm (SD ± 0.3 mm) behind the orbital margin and approximately 9.7 mm (SD ± 0.8 mm) below the frontozygomatic suture at the lateral orbital tubercle.12 Immediately anterior to the LCT is Eisler's pocket, a collection of adipose tissue. Posterior to the LCT, at its attachment site to the lateral orbital tubercle is the check ligament of the lateral rectus muscle (Figure 162-2).

Any increase in intraorbital contents (e.g., retrobulbar hematoma, intraorbital emphysema, and retrobulbar abscess) will result in an elevation of intraorbital pressure because the orbit is a closed space. The globe itself may partially accommodate some of the elevation in intraorbital pressure by prolapsing forward (Figure 162-3). This will result in ocular pain and proptosis. The intraorbital pressure rises dramatically as the orbit approaches maximal distention. This rise in intraorbital pressure leads to a chemosis, elevated intraocular pressures, and compression of the intraorbital cranial nerves. If the compression is severe enough, the patient develops an ophthalmoplegia and an afferent papillary defect.

The exact mechanisms by which orbital compartment syndromes result in blindness remain speculative.13–24 A common theory is that as the intraorbital pressure increases, orbital venous outflow is impeded and leads to diminished retinal and optic nerve arterial perfusion pressures. This results in an afferent pupillary defect, diminished visual acuity, and, rarely, fundoscopic signs of retinal ischemia. Over time, the elevated intraorbital pressure leads to irreversible optic nerve and/or retinal ischemia. Experimental studies have demonstrated that irreversible ischemic injury to the retina may occur within 90 minutes of vascular insufficiency.18–21 Additional theories suggest that direct mechanical compression or longitudinal traction on the optic nerve may contribute to the loss of vision in orbital compartment syndromes.22,24 Elevated intraorbital pressure may also occur from large volume fluid resuscitation in patients without ocular trauma.29

A history of progressive loss of vision following orbital trauma suggests a reversible disease process (e.g., retrobulbar hemorrhage). If loss of vision is immediate and complete following orbital trauma, the chance of recovery of vision is poor.25 This is because the loss of vision in the latter case is due to direct optic nerve, retinal, or vascular injury rather than an orbital compartment syndrome.

An acute orbital compartment syndrome is an indication for immediate orbital decompression.23 Multiple case series have documented the efficacy of immediate orbital decompression in restoring visual acuity to affected patients.24–28

There are no definite contraindications to performing this procedure, as permanent loss of vision may result from untreated acute orbital compartment syndromes. The patient's airway, breathing, circulation, and any life-threatening injuries must be addressed prior to performing this procedure. If the patient is very young, confused, or uncooperative, sedation and restraint or procedural sedation (Chapter 129) will be required to prevent iatrogenic injury to the globe.

• Povidone iodine or chlorhexidine solution
• Topical ocular anesthetic solution, proparacaine or tetracaine
• Lidocaine 2% with epinephrine
• 30 gauge 0.5 inch needle on a 3 cc Luer Lock syringe
• Ocular tonometer (applanation, Schiøtz, or Tono-Pen)
• Sterile saline or sterile water
• Straight mosquito hemostat
• Iris scissors
• Tissue forceps
• 2 × 2 gauze squares
• Topical ocular antibiotic ointment (e.g., bacitracin, ciprofloxacin, erythromycin, gentamicin, neosporin, polysporin, or sulfacetamide)
• #10 disposable scalpel (optional)
• Disposable hot tip cautery pen (optional)

Explain the procedure to the patient and/or their representative, including the risks, benefits, and outcome if it is not performed. This is a painful procedure for the awake and alert patient, so lucid patients will require parenteral medications for analgesia and sedation in addition to local anesthetics. Consider the use of procedural sedation (Chapter 129) if not contraindicated. Measure and record the visual acuity. Perform a brief ophthalmologic examination. Apply topical ocular anesthetic solution to the conjunctiva of the affected eye. Measure and record the intraocular pressure.

Place the patient supine. Clean the eyelids and surrounding skin of any blood, dirt, and debris. Apply povidone iodine or chlorhexidine solution to the eyelids and allow it to dry. Do not let these solutions drip into the eye. Irrigate the lateral canthal fold region with sterile saline or sterile water. Using aseptic technique, identify the lateral canthal fold (Figure 162-4). Inject 1 mL of local anesthetic solution with epinephrine subcutaneously using a 30 gauge, 0.5 inch needle on a 3 mL syringe along the lateral canthal fold. The goal is to anesthetize the tissue extending laterally from the canthal fold to the orbital rim. Caution must be exercised to avoid inadvertent needle puncture of the globe.

Insert a straight mosquito hemostat at the lateral canthal fold. Place one jaw of the hemostat anterior and one jaw posterior to the lateral canthal fold. Advance the tips of the hemostat laterally until the orbital rim is encountered. Clamp and compress the intervening tissue for approximately 1 minute. This will minimize any bleeding precipitated by the lateral canthotomy. Remove the hemostat. Cut all the tissue layers along the lateral canthal fold up to the orbital rim (lateral canthotomy) with an iris scissors (Figure 162-4). All tissue layers, from the skin to conjunctiva, must be incised down to the orbital rim. Use a #10 scalpel blade to cut the tissues in cases of severe distortion of the anatomy due to edema or if iris scissors are not readily available. A disposable hot cautery pen, if available, can be used to achieve hemostasis.

Gently grasp the lower eyelid with a hemostat or forceps and retract it outward. Identify the LCT located just posterior and inferior to the lateral canthal fold (Figures 162-1 & 162-2). Dissect the conjunctiva and fascial tissues with a hemostat or iris scissors. A pocket of adipose tissue (Eisler's pocket) will be encountered beneath the superficial fascial planes (Figure 162-2). The LCT lies just posterior to this adipose tissue collection (Figure 162-2). Completely divide the LCT vertically at its midportion with an iris scissors or #10 scalpel (lateral cantholysis) to transect the inferior crus of the tendon.

A successful lateral canthotomy and cantholysis will cause an immediate decrease in intraocular pressure to less than 40 mmHg. Recheck the intraocular pressure. If the intraocular pressure remains elevated, reexplore the lateral canthal tendon region to make sure that the inferior crus has been completely transected. If transected, cut the superior crus of the tendon to transect it. Occasionally, the intraorbital and intraocular pressures will remain elevated despite successful cantholysis. These refractory cases necessitate emergent decompression of the deep orbital wall.7 Such decompressions call for operative techniques that are to be performed by Ophthalmologists and Otolaryngologists.

The resolution of proptosis, afferent pupillary defects, and restoration of visual acuity will usually not occur immediately. Patients who respond to surgical intervention will gradually regain their visual acuity over a period of hours to days.

Apply a topical antibiotic ointment along the canthotomy site. In orbital compartment syndromes, elevated intraocular pressures merely reflect elevated intraorbital pressures. Therefore, any attempts to decrease intraocular pressures will not reliably reduce retrobulbar optic nerve compression. Medical interventions decreasing intraocular pressure may be used following, or in conjunction with, a lateral canthotomy and cantholysis. These interventions are similar to those employed for the management of elevated intraocular pressures in patients with acute angle-closure glaucoma. This includes the use of topical beta-blockers, central acting alpha agonists, intravenous mannitol, and carbonic anhydrase inhibitors. These medications are not a substitute for surgical orbital decompression.

Many patients with an orbital compartment syndrome have other injuries requiring hospital admission following their Emergency Department evaluation and treatment. Ensure a timely Ophthalmologic consultation for a complete eye exam and possible repair of the canthotomy and cantholysis sites once the orbital compartment syndrome resolves. Repair of the lateral canthal fold and lateral canthal tendon is controversial. Many Ophthalmologists do not advocate suture repair, as a majority of wounds heal without complication by secondary intention. Patients with no other acute medical or surgical conditions, restored vision, a normal ophthalmologic examination, and normal postprocedural intraocular pressures may be discharged after evaluation by an Ophthalmologist.

Time constraints, abnormal anatomy (resulting from traumatized tissue), and lack of familiarity with the lateral canthotomy and cantholysis techniques can make this a challenging procedure. Hemorrhage is often minimal and can be controlled with direct pressure. The use of a disposable cautery pen can be helpful. Mechanical injuries can include globe perforation, injury of the lateral rectus muscle, scleral lacerations, and secondary ectropion. Most of these complications can be prevented by knowing and identifying the anatomic landmarks, reviewing the procedure before it is performed, and using extreme care in performing the canthotomy and cantholysis. Despite the use of aseptic technique, infections at the canthotomy and cantholysis sites can occur. They should be treated with parenteral antibiotics that cover typical skin flora.

Emergency Physicians must be able to promptly recognize and be prepared to manage an acute orbital compartment syndrome, defined by an acute elevation of intraorbital and intraocular pressure with resultant ocular dysfunction. Patients will present with ocular pain, proptosis, an afferent pupillary defect, and diminished visual acuity. An acute orbital compartment syndrome requires emergent treatment to preserve vision. An immediate lateral canthotomy and cantholysis are indicated, preferably within 1 hour of injury and ocular dysfunction. Medical management should be considered an adjunctive therapy. Many patients will regain their visual function if the procedure is performed soon after the injury and before permanent ischemic changes occur.