Epidemiology
The United States Eye Injury Registry reports that 61% of eyelid/lacrimal trauma has coexisting globe injury, with 20% to 25% having an open globe. The median age is 27 years, and male patients outnumber females by almost 3 to 1. Most injuries occur at home (37%); other locations include industrial premises (16%), road (14%), recreational areas (11%), public buildings (3%), schools (3%), and farms (2%). Injury caused by blunt object is the most common etiology (30%), followed by those caused by sharp objects (19%), nail/hammer (11%), motor vehicle crashes (8%), gunshots (6%), BB/pellet gunshots (6%), fireworks (5%), and falls (4%).3
Lacrimal injury is found in more than one-third of eyelid lacerations, and two-thirds of cases involve young children. Although blunt trauma is the most common etiology in adolescents and adults, dog bites, falls, and collision with sharp objects while running are the most common etiologies in children. The lower canaliculus lacerations are the most frequent (54.1%–66.2%), followed by those of the upper canaliculus (27.5%–33.3%) and bicanalicular injury (6.3%–12.5%).4,5
Injury Types and Physiology
Eyelid and lacrimal injury occur when traumatic forces are greater than tissue elasticity strength. The type and extent of injury is related to the degree and direction of injurious force, speed of transfer, and contact surface area.6 The nature of the insult can be penetrating, cutting, or crushing.7 A good history is required to elicit the mechanism of trauma and the possibility of retained foreign body (Fig. 35.2).
Eyelid injuries range from contusion and abrasion to partial or full-thickness laceration. None of these categories is mutually exclusive, and they often occur in a continuum. The anatomic location of the injury will dictate the structures affected.
Contusion (bruising) results from blunt forces causing bleeding and effusion from blood vessels. The natural history consists of erythema and edema and evolves into a blue/black discoloration within 3 to 4 days. In general, color will change to yellow or green, depending on depth of injury and skin pigmentation, as resolution occurs over 2 weeks. When large vessels are affected, the ensuing hematoma may be sight threatening, especially when confined within the orbit (Fig. 35.3). Recognition and management of an orbital compartment syndrome was discussed in Chapter 34.
Abrasions range from small scratches to large areas of epidermal destruction. Scratches are typically caused by sharp objects being drawn across the skin, such as nails, claws, or rose thorns. Movement of the eyelid across a rough surface (e.g., road pavement) or significant pressure blow (e.g., airbag injury) can result in a larger area of injury (Fig. 35.4). Epithelialization begins a few hours after injury, and a scab forms within 24 to 48 hours. Superficial abrasion typically does not form a scar, but deep abrasion involving dermis and subcutaneous layer may form a scar. Management includes cleaning and debridement of foreign material, topical and systemic antibiotics, and avoidance of sun exposure.
Eyelid lacerations can be partial or full thickness. When these occur at the level of tarsus, the eyelid margin can be involved. Full-thickness laceration in the preseptal eyelid may affect the eyelid retractor muscles (levator, Müller muscle, and lower eyelid retractors). In the lateral canthal area, the lateral canthal tendon and lacrimal gland may be affected. In the medial canthal region, the medial canthal tendon and lacrimal canaliculi may be damaged.
Lacerations occur by tissue stretch, crush, avulsion, or tear.7 The laceration’s edges are typically irregular, and the depth and structures affected must be determined. Wounds must be thoroughly inspected for foreign material before repair, and topical antibiotic ointment should be used. Systemic antibiotics, especially in contaminated wounds, are recommended by some sources, but indications are determined by the nature of the injury.8
Fundamental Science of Wound Healing
Wound healing begins with or without surgical intervention. Debridement clears the affected area of infectious organisms, and surgical repair realigns tissue layers to restore structure and function. Wound healing is a complex process that is regulated by numerous cell types, cytokines, and growth factors. The healing cascade is classically described in three overlapping stages: inflammation, proliferation, and remodeling.9 Another conceptual construct divides wound healing into two major phases, known as the early phase and the cellular phase.10 The early phase (inflammation phase) commences immediately after injury, with hemostasis and formation of an early extracellular matrix (ECM) to provide structural staging for cellular attachment and proliferation. The second, “cellular” phase involves several types of cells working together to mount an inflammatory response, synthesize granulation tissue, and restore the epithelial layer. During days 1 and 2 of injury, macrophages mediate the inflammatory components of the wounds. Epithelial and mesenchymal cells interact to undergo phenotypic changes, allowing cellular migration for re-epithelization. Between days 4 and 14, fibroblasts and myofibroblasts coordinate to produce a collagen matrix bridging the wound, to align tissue layers, and to contract the wound. Also starting on day 4, endothelial cells begin angiogenesis. Last, the formation of dermal matrix also occurs at day 4, and alteration and remodeling of the wounds begins after the second week. The duration of wound alteration or remodeling can last weeks to months, depending on the wound size.
Inflammation Phase (Days 1–4)
Injury immediately triggers the coagulation cascade. Platelets aggregate at the wound to form a clot through adhesion of glycoproteins such as fibrin and fibronectin and secrete von Willebrand factor to strengthen adhesion.9 Activated platelets change shape from spherical to stellate and release stored granules containing adenosine diphosphate, serotonin, platelet-activating factor, platelet factor 4, and thromboxane A2 to activate additional platelets and to increase their affinity to bind fibrinogen.11 Secondary hemostasis involves tissue factor and contact activation that strengthens the clot with cross-linked fibrin. Blood vessel damage triggers a surge of thrombin through a series of reactions in which a zymogen (inactive enzyme precursor) of serine protease and its glycoprotein cofactors are activated. This contact activation pathway begins the formation of collagen complex with blood plasma proteins. These two pathways act to convert fibrinogen to fibrin, strengthening the clot. The clot traps proteins and particles and prevents further hemorrhage. Eventually, it leads to lysis and replacement with granulation tissue and collagen.12
Injured blood vessels release thromboxanes and prostaglandins, inducing vasoconstriction for 5 to 10 minutes. Histamine released from platelets then causes vasodilation and peaks at about 20 minutes after injury. The vessels become porous to allow protein extravasation into extravascular space, causing edema, and to admit leucocytes into the wound. Within an hour of injury, polymorphonuclear neutrophils (PMNs) are drawn by the chemoattractants fibronectin, transforming growth factor β, interleukin-1, tumor necrosis factor α, kinins, and bacterial products.9 As PMNs become the predominant cells in the first 48 hours, they phagocytize cellular debris and secrete proteases to break down damaged tissue. Bacteria obliteration is achieved with the release of free radicals and activation of the complement system via opsonization (making the foreign material more susceptible to phagocytosis).13
After 2 days, PMNs undergo apoptosis and are engulfed and degraded by macrophages, the second cells attracted to the zone of injury (Fig. 35.5). Monocyte concentration peaks at 24 to 36 hours. Besides releasing proteases and phagocytizing bacteria, macrophages function in regeneration and transition the inflammatory phase to the proliferative phase of wound healing. Hypoxia within the wound induces vascular endothelial growth factor, fibroblast growth factor, and tumor necrosis factor α. Macrophages stimulate fibroblasts to re-epithelialize the wound, to create granulation tissue, and to deposit new ECM. As inflammation subsides, PMNs and macrophages decline and the proliferative phase begins.14
Proliferation Phase (Days 4–14)
The proliferation phase is defined by angiogenesis, granulation tissue formation, epithelialization, and wound contraction.15 The presence of fibroblasts from days 2 to 5 marks the onset of proliferation even before the inflammatory phase has ended. In angiogenesis, chemical and cellular events overlap. The latent period comprises tissue swelling that aids angiogenesis by expanding and loosening the existing collagen ECM.9 As macrophages switch to the healing mode, they secrete endothelial chemotactic and growth factors that activate endothelial cells. Macrophages, mast cells, and activated endothelial cells degrade the clot to facilitate vascular sprouting. Activated endothelial cells retract and reduce cell junctions to loosen themselves from the endothelium, and they divide and migrate toward the wound to create new vessels. Hypoxia and acidosis in the wound activate angiogenic genes such as vascular endothelial growth factor and glucose transporter 1. Sprouted vessels give rise to capillaries. The endothelium of the new vessels matures by production of ECM followed by basal lamina formation. As reperfusion is established, the reduction of hypoxia and increased lactic acid cause macrophages to cease producing angiogenic factors.16
In fibroplasia and tissue granulation formation, fibroblasts, derived from bloodborne, circulating adult stem cells or precursors, migrate and proliferate to become the main cells at the wound.9 Fibroblasts initially deposit ground substance, part of granulation tissue and later collagen, critical to increase wound strength. Fibroblasts begin to produce type III collagen between 10 hours and 3 days, depending on wound size, and deposition peaks at 1 to 3 weeks. Granulation tissue is a rudimentary tissue consisting of new blood vessels, fibroblasts, inflammatory cells, endothelial cells, myofibroblasts, and provisional ECM (fibronectin, type III collagen, glycosaminoglycan, elastin, glycoprotein, proteoglycan). Type III collagen is later replaced by type I collagen, which is stronger and the main constituent of noninjured skin.17
Granulation tissue provides a base for epithelialization. Platelets and macrophages secrete epidermal growth factor and transforming growth factor α to stimulate keratinocytes at wound edge to project and to re-establish a protective barrier against fluid loss and further bacterial infiltration. Keratinocytes migrate within a few hours, whereas cellular proliferation occurs on the days 2 and 3 after injury. If the basement membrane is not breached, epithelial cells are replaced within 3 days by division and upward migration of cells in the stratum basale in the same fashion that occurs in uninjured skin. In deeper wounds, re-epithelialization proceeds from the wound margins and skin appendages such as hair follicles, sweat, and oil glands that enter the dermis lined by keratinocytes. Keratinocyte migration requires dissolution of desmosomes, is stimulated by lack of contact inhibition, and is enhanced by a moist environment (hence, the role of ointments and occlusive dressings). As epithelial cells climb over one another to migrate over granulation tissue, the first cells attach to the new basement membrane made by fibroblasts to form the stratum basale. They also secrete collagenase and matrix metalloproteinases to dissolve damaged ECM and plasminogen to dissolve the scab, and they phagocytize necrotic tissue. Keratinocytes also produce growth factors and basement membrane protein to aid epithelization and to assist in innate immune defense of the wound. Cellular proliferation occurs at a rate 17 times higher than in normal tissues, and rapid keratinocytes migration produces less prominent scar. As contact inhibition stops migration, keratinocytes re-establish desmosomes and hemidesmosomes. Further cellular division and differentiation occur to re-establish the normal skin strata.18
Contraction begins at 1 week when fibroblasts differentiate into myofibroblasts. This is a critical component of wound healing, as chronic wound contracture can lead to disfigurement and loss of function. In full-thickness wounds, contraction peaks at 5 to 15 days and can last for several weeks even after the wound is completely re-epithelialized.19 A large wound can become 40% to 80% smaller after contraction, at a speed of 0.75 mm per day, depending on the nature of tissues within the wound. Contraction is typically asymmetric and concentrates on an “axis of contraction” to allow for greater organization and alignment of cells with collagen.20
Myofibroblasts attach to each other and the wound edges by desmosomes and to fibronectin and collagen via many fibronexus connections to pull the ECM, thus reducing the wound size. Fibroblasts also produce additional collagen as myofibroblasts contract. The breakdown of the provisional matrix leads to a decrease of hyaluronic acid and an increase in chondroitin sulfate, which triggers the fibroblasts to stop migrating and proliferating, as this signals the onset of the maturation stage.21
Remodeling Phase (Day 14–1 Year)
Scar maturation occurs when collagen production and degradation reach equilibrium. Fibroblasts replace type III collagen with type I collagen. Disorganized collagen fibers are rearranged, cross-linked, and aligned along tension lines. The onset of the remodeling phase varies extensively, depending on wound size and whether it was surgically closed or not, ranging from 3 days to 3 weeks.22,23 The maturation phase can last for a year or longer, similarly depending on wound type.
Wound tensile strength increases rapidly from weeks 1 to 8 as a result of the deposition of collagen. At week 1, it has 3% of final strength, at 3 weeks 30%, at 3 months 50%, and at full maturity, the wound will achieve 80% of prewounding strength (Fig. 35.6). Clinically, the scar loses its erythematous appearance as blood vessels undergo apoptosis.24 The phases of wound healing typically progress in a predictable timely manner; however, many local, systemic, and environmental factors can affect the efficacy, speed, and manner of healing, leading to a chronic nonhealing wound or a keloid scar25,26 (Table 35.1).
