Management of Ocular Adnexal Trauma
Ginger Henson Rattan, Dwight R. Kulwin, Mark R. Levine,
Adham Al-Hariri, Jaime S. Schwartz, and Kara Couch
Introduction
The evaluation and management of patients who have
sustained ocular adnexal trauma can be challenging. Often
these patients have multiple injuries and are being cared for
by many different subspecialties. Evaluation of such patients
may seem daunting secondary to substantial bleeding and
edema. In addition, the emotional state of the patient and
family members often makes history taking and examination
especially difficult and time consuming. Despite these chal-
lenges, the examination and treatment of trauma patients can
be straightforward and efficient if undertaken in a systematic
fashion.
Before we can begin to discuss the treatment of periocular
trauma, it is first necessary to understand the reparative
process of wound healing on a cellular level.
G.H. Rattan, M.D. ()
Fellow in Ophthalmic Plastic and Reconstructive Surgery,
Cincinnati Eye Institute, Cincinnati, OH, USA
e-mail: ging516@yahoo.com
D.R. Kulwin, M.D.
Department of Ophthalmology, Cincinnati Eye Institute, Cincinnati,
OH, USA
M.R. Levine, M.D., F.A.C.S.
Department of Ophthalmology, University Hospitals of Cleveland,
Cleveland Clinic Foundation, Cleveland, OH, USA
A. Al-Hariri, M.D.
Department of Ophthalmology, Ochsner Clinic Foundation,
New Orleans, LA, USA
J.S. Schwartz, M.D.
Department of Plastic Surgery and Aesthetic Medicine,
Bright Health Physicians, Whittier, CA, USA
K. Couch, M.S., C.R.N.P., C.W.S.
Department of General Surgery, Walter Reed Army Medical Center,
Washington, DC, USA
E.H. Black et al. (eds.), Smith and Nesi’s Ophthalmic Plastic and Reconstructive Surgery,
DOI 10.1007/978-1-4614-0971-7_9, © Springer Science+Business Media, LLC 2012
9
Principles of Wound Healing
Epithelial wound healing is a complex cascade that begins
with tissue injury and ends with a goal of restoration of
architectural integrity. The repair process is regulated and
orchestrated by a myriad of cells, cytokines (signaling
factors), and growth factors.
Overall, the cascade of cutaneous repair is best described
as three overlapping stages known as inflammation, prolif-
eration, and remodeling. The initial inflammatory phase is
seen as hemostasis and inflammatory cellular infiltration.
The proliferative phase is characterized by granulation, fibro-
plasia, contraction, and epithelialization. The final phase of
remodeling allows for collagen synthesis and degradation to
improve and strengthen the repair process.
Underlying medical conditions such as malnutrition, dia-
betes mellitus, and exogenous corticosteroid administration
have been shown to impede the wound healing cascade.
Patients with these medical conditions may have difficulty
progressing through the normal stages of wound healing.
Phases of Wound Healing
Inflammation (Wounding Through Day 5)
Upon wounding, a series of hemostatic events begins the cas-
cade that eventually leads to reestablishment of epithelial
integrity. Chemical mediators are released by injured blood
vessels activating the intrinsic portion of the coagulation cas-
cade. This leads to vasoconstriction and platelet aggregation
and degranulation around damaged endothelium. These
released granules contain chemoattractant signaling factors.
Platelet adhesiveness is mediated by integrin receptors such
as GPIIb/IIIa. The clot initially made of collagen, platelets,
thrombin, and fibronectin forms, which further releases
cytokines and growth factors inciting the inflammatory
response. The clot serves as a chemo-modulator of the wound
healing response and also as scaffold that allows for further
207
208
regulatory cells and concentrated cytokines and growth
factors to work in a protected milieu [1].
Chemotaxis and Activation
The formation of a stabilizing clot results in cellular signaling
that attracts neutrophils, the initial cells in the wound-healing
cascade. Further accumulation of inflammatory mediators
leads to prostaglandin levels rising and vasodilatation as
local endothelial cells break cell-cell contact. This allows for
increased cellular traffic as neutrophils are attracted to the
injured zone by interleukin-1 (IL-1), tumor necrosis factor-
alpha (TNF-a), transforming growth factor-beta (TGF-b),
PF4, and bacterial products. Neutrophils are responsible for
clearing out invading bacteria and cellular debris by releas-
ing caustic proteolytic enzymes. There are a myriad of pro-
teases released targeting proteins, amino acids, or metal ions
within the enzymes. Serine proteases have broad specificity,
whereas metalloproteinases (which contain zinc ions) spe-
cifically digest collagen. Regardless of the protease, only the
extracellular matrix of wounded tissue will be destroyed.
This is due to the fact that protease inhibitors protect
unwounded tissue. However, this can be overwhelmed and
healthy tissue destroyed due to massive release or prolonged
protease concentration, which can be seen in chronic wounds.
Neutrophils also generate reactive oxygen free radicals
(through a myeloperoxidase pathway) that combine with
chlorine to help sterilize the wound from bacteria. These
oxygen free radicals may also play a part in chronic wounds
due prolonged or increase concentrations. Furthermore, acti-
vated complement fragments aid in bacterial killing through
opsonization.
The second cells attracted to the zone of injury and
probably the most important in orchestrating wound healing
are the macrophages. Around 48–96 h post-wounding,
monocytes are attracted to the area and transformed into
macrophages. Activated macrophages are responsible for
transitioning from the inflammatory to the proliferative phase
of wound healing. This is accomplished by mediating angio-
genesis through synthesis of vascular endothelial growth fac-
tor (VEGF), fibroblast growth factor (FGF), and tumor
necrosis factor-alpha (TNF-a), and fibroplasia by transform-
ing growth factor-beta (TGF-b), epidermal growth factor
(EGF), platelet derived growth factor (PDGF), IL-1 (inter-
leukin-1), and TNF-a [2]. Further, nitric oxide (NO) is
released by an inducible nitric oxide synthase activated IL-1
and TNF-a. Macrophages also play a role in pathogen kill-
ing and clearing of debris by synthesizing large quantities of
NO. TNF and IL-1 stimulates macrophage iNOS to produce
NO which will react with peroxide ion oxygen radicals to
yield an even more toxic peroxynitrite and hydroxyl radicals.
Debris clearing is accomplished by phagocytosis of
devitalized material, bacteria, and apoptotic neutrophils.
Further damaged extracellular matrix is cleared by matrix
G.H. Rattan et al.
metalloproteinases (MMP), which are expressed by
keratinocytes, fibroblasts, monocytes, and macrophages in
response to TNF-a. This also enhances migration of cells
through extracellular matrix [3].
Proliferation (Day 4–14)
This phase in characterized by epithelialization, angiogene-
sis, and provisional matrix formation. Epidermal growth
factor (EGF) and tumor growth factor-alpha (TGF-a) are
secreted by platelets and macrophages. This is the stimulus
for epithelial cells at the wounded edge to send out projec-
tions to try and reestablish a protective barrier against further
fluid loss and bacterial invasion. Reepithelialization begins
shortly after wounding and is stimulated by inflammatory
cytokines IL-1 and TNF-a. Further, fibroblasts synthesize
keratinocyte growth factors to stimulating epidermal thick-
ening and marginal basal cells to migrate into the wound,
proliferate, and differentiate into epidermis. When these
epithelial cells begin migrating, they do not divide until epi-
dermal continuity is restored. These cells flatten and migrate
as a sheet (epiboly) over the wound matrix. Cell adhesion
proteins glycoproteins such as tenascin and fibronectin pro-
vide the “railroad” tracks to facilitate epithelial migration.
After reestablishing the epithelial layer, keratinocytes and
fibroblasts secrete collagen type IV to form the basement
membrane. At this point the cells become more columnar
and divide to form the normal layers of epidermis.
Circulating bone marrow-derived cells are signaled to
migrate into the wound and develop into fibroblasts, which
along with endothelial cells are the predominant activated
cell types during this phase. Platelet-derived growth factor
(PDGF) and epidermal growth factor (EGF) derived from
macrophages and platelets stimulate fibroblasts to proliferate
and begin synthesizing collagen. Further differentiation takes
place among fibroblasts already present in the wound.
Stimulation by macrophage-secreted transforming growth
factor-beta-1 (TGF-b1) induces transformation into myofi-
broblasts for wound contraction. Transforming growth factor-
beta (TGF-b) is important in orchestrating many processes
during this phase. It peaks around day 7–14, which amplifies
extracellular matrix (ECM) production and decreases its
degradation. It also induces fibroblasts to begin synthesizing
collagen type I, increases production of cell adhesion pro-
teins, and decrease production of matrix metalloproteinases
(MMP) as well as increase production of inhibitors of metal-
loproteinase [4]. TGF-b also plays a large role in wounds
allowed to heal by secondary intention in which it stimulates
larger quantities of myofibroblasts for wound contracture.
Healing by secondary intention and open wounds are
characterized by granulation tissue. Healthy granulation tis-
sue has a typical beefy-red appearance due to its dense popu-
lation of blood vessels, macrophages, and fibroblasts
embedded in a loose provisional matrix of fibronectin,
9 Management of Ocular Adnexal Trauma
hyaluronic acid, and collagen. Neo-angiogenesis induced by
VEGF is directed at vascular endothelial progenitor cells to
migrate and proliferate. This allows for the formation of the
rich bed of new capillary networks seen in these healing
wounds. Presence of granulation tissue is used as a clinical
indicator of the health of the wound and the even the overall
ability of a wound to heal.
Healing by secondary intention is also characterized by
wound contracture. Myofibroblasts are fibroblast-like cells
that also contain a-smooth muscle actin and microfilaments,
which confer the ability to generate contractile forces.
Clinically, wound contraction allows for a smaller wound
surface area needed to heal, which decreases time to heal and
also limits the amount of insensate scar that ensues. The
amount of contraction is related to the size and location. The
trunk and perineum allow for the greatest contracture in
which up to 80% of healing can occur by this process. More
importantly are the consequences of allowing wounds to heal
by secondary intention. Wound contractures on typically
mobile areas could lead to deformation and functional limi-
tations. This is pathologically seen in extremities, especially
across joints and eyelids.
Vascular endothelial growth factor (VEGF) secreted
mainly by keratinocytes at wound edges, but also mac-
rophages, fibroblasts, platelets, and other endothelial cells,
stimulate endothelial cells at venule edges to begin forma-
tion of new capillaries. VEGF production and release is also
stimulated in response to hypoxia from nitric oxide (NO)
released from endothelial cells [5]. This helps protect tissue
from ischemia and reperfusion injury and causes endothe-
lium to vasodilate.
Throughout this phase after activation and proliferation,
extracellular matrix (ECM) is laid down by fibroblasts. The
initial matrix is provisional and is composed of fibrin, gly-
cosaminoglycan (GAG), and hyaluronic acid (HA). Adhesion
glycoproteins, mainly fibronectin, laminin, and tenascin, are
present in the early matrix to facilitate cell attachment and
migration [6]. Integrin receptors on cell surfaces bind to
matrix glycosaminoglycans and glycoproteins. Fibroblasts
utilize hyaluronidase to digest the provisional hyaluronic
acid-rich matrix, which allows for larger sulfated gly-
cosaminoglycans to be deposited.
Concomitantly, while ECM is being laid down, disorga-
nized collagens are also being synthesized and secreted by
fibroblasts onto the fibronectin and GAG scaffold. Major
fibrillar ECM collagens are types I and III in wounded and
normal skin. The ratio of collagen type I:III is 4:1 in skin and
healed mature scar. Initially in wounded, healing skin, the
ratio is closer between types I and III (2:1), with type I col-
lagen always the predominant type.
Dermal collagen is a right-handed triple helix synthesized
and secreted by fibroblasts into the ECM. Here the N- and
C-terminal pro-peptides are cleaved and tropocollagen
209
molecules are formed. These molecules laterally aggregate
and are covalently cross-linked by the enzyme lysyl oxidase
to form collagen fibrils. These fibrils interact and aggregate
into fibers.
Remodeling Phase (14 Days to 1 Year)
This phase is characterized clinically by scar maturation.
Overall, in the previous phases the wound was internally
debrided to sterile environment and a structural extracellular
matrix (ECM) was deposited haphazardly to facilitate wound
closure and reestablishment of the internal milieu. A com-
plex balance of ECM degradation, synthesis, and deposition
of the initial disorganized repair characterizes remodeling.
This process also adds strength to wounded tissue and is seen
clinically as a raised, red scar becoming flatter and more
flesh-colored as the initially formed dense capillary network
regresses. This phase clinically is very important due to the
fact that wound strength and character are determined during
this time. A weaker wound may result if patients have matrix
deposition problems from diet or disease or may develop
hypertrophic or keloid scars if the balance between collagen
synthesis and degradation isn’t regulated well.
Initially, the ECM is composed mainly of fibrin and
fibronectin from the coagulation cascade of hemostasis and
macrophages. Fibroblasts begin to secrete proteins such as
glycosaminoglycans and proteoglycans as a preliminary and
disorganized framework for the matrix, which is replaced by
a stronger and more organized collagen matrix. Normal skin
collagen composition is 80–90% type I and 10–20% type III.
Type III collagen is 30% of granulation and 10% in mature
scar. Initial deposition of type III collagen, which does not
significantly contribute to wound strength, is not fully under-
stood. It does however coincide with the presence of fibronec-
tin, which has been thought to facilitate phagocytosis of
denatured collagen by coating it.
Despite the complex wound healing process ultimately
resulting in scar, healed skin morphologically has a lack of
connective tissue organization compared to pre-wounded
skin. Collagen fibers are secreted by fibroblasts as early as
3 days into the wound-healing cascade. Net collagen synthe-
sis continues for up to 6 weeks partly from an increase in the
number of fibroblasts and upregulated collagen synthesis per
cell. Initially laid collagen is thinner and oriented parallel to
the skin in a densely packed matrix. Granulation tissue col-
lagen has a greater hydroxylation and glycosylation of lysine
residues, which corresponds to thinner fibers [7]. The remod-
eling process degrades the initial collagen and replaces it
with thicker fibers that are oriented along stress lines. Overall,
this remains different than reticular pattern seen histologi-
cally in normal dermis. However, increased tensile strength
is positively correlated collagen thickness and orientation.
Most scars tend to be hypopigmented compared to
surrounding skin, but can be hyperpigmented especially in
210
darker skin types. Regardless, maturing scars should be kept
out of the sun and protective measures should be taken espe-
cially in sun-exposed areas such as the head, neck, and
extremities.
Wound tensile strength rapidly increases from weeks 1 to
8. This initially is due to the increased content of collagen
deposited. Further strengthening is accomplished by reorga-
nization and cross-linking of collagen. Wound strength never
returns to full strength. At week 1, it has 3% of final strength,
at 3 weeks 30%, and at full maturity, the wound will achieve
only 80% of pre-wounding strength [8]. This process utilizes
lysyl oxidase as the major intermolecular collagen cross-
linking enzyme. Further matrix metalloproteinases (MMP)
such as collagenases, gelatinases, and stromelysins degrade
ECM components. The balance of collagen deposition and
degradation is in part determined by regulation of MMP
activity. Changing concentrations of cytokines such as
TGF-b, PDGF, IL-1, and EGF influences activation. It is also
further suppressed by tissue inhibitors of metalloproteinase
(TIMP), secreted by fibroblasts and upregulated by TGF-b
and IL-6.
The final result of the wound-healing cascade is scar.
Even in its final matured state, it will be more fragile, inelas-
tic, and will not contain skin appendages such as hair folli-
cles and sweat glands compared to normal skin.
Clinical Factors Affecting Wound Healing
Wounding disturbs the delicate internal milieu and allows for
bacterial introduction. These organisms trigger a host
response resulting in inflammation. Acute and chronic
inflammatory infiltrates inhibit the wound healing cascade
by impairing fibroblast proliferation resulting in decreasing
ECM synthesis and deposition. More than 105 organisms/g
of tissue constitute clinical infection and will delay wound
healing.
Nutrition plays an important part in the anabolic wound
healing process. An adequate protein intake is necessary for
many internal processes, but imperative for ECM deposition.
Chronic protein depletion can result in poorly healed wounds
and, in severe cases, dehiscence.
Furthermore, vitamins and minerals play pivotal roles in
many aspects of the cascade. Vitamin C (ascorbic acid) is
necessary for hydroxylation of proline and lysine residues.
Hydroxyproline allows for newly synthesized collagen to be
transported out of cells. Hydroxylysine facilitates collagen
cross-linking. Vitamin A (retinoic acid) is involved in many
aspects of repair such as fibroplasia, collagen synthesis, and
cross-linking as well as epithelialization.
Vitamin A requirements are increased following injury
and supplementation may be required to maintain normal
serum levels. It has also been shown to reverse the impaired
G.H. Rattan et al.
healing that occurs with chronic corticosteroid treatment.
Being a fat-soluble vitamin, it can be given in toxic doses.
A typical oral dose is 25,000 every other day.
Vitamin B6 (pyroxidine) is utilized for collagen cross-
linking, and vitamin B1 (riboflavin) is associated with poor
wound healing if deficient. Minerals such as zinc and copper
have been implicated in poor wound healing due to the fact
that their divalent cations are cofactors in many important
enzymatic reactions. Zinc deficiency has been associated
with poor epithelialization and poor wound healing. This can
be easily corrected as a patient only needs to supplement
zinc for 10 days to improve the situation.
Systemic factors are a known impediment to healing. For
example, a patient with arterial occlusions below the knee is
unlikely to heal a posterior heel ulcer without revasculariza-
tion. Similarly, diabetes mellitus is known to cause multiple
cellular changes which delay healing. Growth factor and
cytokine deficiencies have been found in both diabetic mouse
and diabetic human wounds. Specifically, there are deficien-
cies in PDGF, VEGF, IGF-1, IGF-II, TGF-b, aFGF, and IL-6.
Diabetics also have decreased angiogenesis, endothelial dys-
function, abnormalities in fibroblast function, extracellular
matrix, and decreased cellular infiltrate [9]. These factors, in
combination with the neuropathic changes and arterial occlu-
sive disease that occur with diabetes over time, lead to very
poor healing ability. Billions of healthcare dollars are spent
annually on diabetic foot ulcers and their treatment. Diabetic
wound healing proceeds far more effectively when tight gly-
cemic control is maintained. The hemoglobin A1C level is a
good indicator of blood glucose controls over the previous
3 months. Any discrepancies or problems maintaining nor-
mal blood glucose levels should be referred to an endocri-
nologist. Smoking has been shown to have deleterious effects
on wound healing, because one cigarette decreases local
blood supply by up to 30% for 2–4 h after each cigarette.
Insisting that the patient stop smoking during the wound-
healing period may play a crucial role in the outcome.
It is well established that wounds cannot heal without
adequate blood flow; so a careful assessment of perfusion
should be done for all wounds, particularly those on the dis-
tal extremities. Any patient with non-palpable distal pulses
should be referred for noninvasive testing or evaluation by a
vascular surgeon. In addition, in patients who have previ-
ously undergone revascularization procedures, re-occlusion
of the affected artery should be considered and evaluated in
the setting of wound deterioration without other factors, such
as infection, being present.
Excessive Healing
Many processes controlled at different times by signaling
cytokines’ upregulation and downregulation of target cells
characterize the normal wound-healing cascade. When stop-
gap signals are ineffective or absent, the synthesis of ECM,
9 Management of Ocular Adnexal Trauma
especially collagen, may continue and result in excessive
repair. The reasoning for this is not well understood, but cer-
tain aspects such as overexpression of profibrotic cytokines,
a lack of programmed cell death (apoptosis), and continued
presence of ECM secreting activated fibroblasts have been
implicated.
Further reasoning for excessive scarring may be attributed
to iatrogenic planning or traumatic wounds placement in
unfavorable areas. The least amount of tension on a wound
allows for the smallest and most cosmetic acceptable scar.
These areas are classically described as being within or par-
allel to natural skin creases (Langer’s lines). Tension along
the wound edge may cause separation and widening as well
as some healing by secondary intention.
Hypertrophic scars are defined as raised scars that have
not overgrown the boundaries of the original scar. Most
likely they form as the result of tension on wound edges and
are common across flexion surfaces of extremities, breasts,
sternum, and neck. They are usually self-limited and will
fade over time.
Keloid scars are characterized by overgrowth beyond
the original boundaries and behave like a benign skin
tumor. They are more commonly seen in darker-skinned
patients with African Americans having an incidence
between 6% and 16%. They have an autosomal dominant
genetic predisposition. However, simple primary excision
and closure usually results in recurrence. This may be due
to excessive wound healing stimuli and/or inappropriate
stopgap signals resulting in continued and unchecked
repair. They are relatively acellular and are composed
mainly of collagen. An appropriate number of fibroblasts
at the wound edge seem to overproduce collagen and dis-
turb the balance between synthesis and degradation. TGF-b
causes a greater degree of collagen gene expression, and
there is a greater degree of profibrotic growth factor expres-
sion in keloid compared to normal fibroblasts. Further
studies have also found that keloid keratinocytes are phe-
notypically different and induce a greater proliferation and
collagen expression in fibroblasts.
Eyelid Trauma
Systemic Considerations
Patients with ocular adnexal trauma often have other signifi-
cant injuries. This is especially true in patients injured by
motor vehicle accidents or falls. In general, the emergency
medical staff will have already addressed the life-threaten-
ing medical conditions prior to obtaining an ophthalmic
consultation. Nonetheless, it is important use an appropriate
treatment protocol for assessing patients with acute trauma
that is systematic in nature. This includes assuring the basic
211
ABCs of emergency care: establishing an adequate airway,
controlling excessive bleeding, and stabilization of the
patient’s circulatory status [10]. Ophthalmic evaluation and
treatment should be delayed until more serious systemic
problems have been addressed.
If respiratory obstruction is present, an adequate airway
should be immediately established. The facial region is
highly vascularized, and significant blood loss can rapidly
occur. Control of bleeding can usually be achieved by a com-
bination of pressure and ligation of large bleeding vessels.
Significant blood loss should be treated with volume
replacement.
Because injuries to the lids may be associated with trauma
to the head and neck region, it is mandatory to rule out a
cervical spinal injury. Until an appropriate evaluation can be
performed, the patient’s neck should be immobilized in a
cervical collar. The neurologic status should be evaluated,
especially for signs of a closed head injury. If there is a pos-
sibility of an intracranial injury, obtain a head computed
tomography (CT) scan and consultation with a neurosurgeon.
Occult chest and abdominal trauma should also be ruled out
in the severely traumatized patient.
General Principles
Once attention can be safely directed to the ocular adnexal
region, priority should be first given to the preservation of
vision. This entails evaluating the patient for any evidence of
ocular or optic nerve injuries (Fig. 9.1). This may be difficult
if the patient is uncooperative or unconscious. Furthermore,
a proper examination may be difficult secondary to swelling
of the eyelids or pain on opening of the lids. Bleeding may
also hamper attempts to evaluate the globe. Light pressure to
the lids usually controls generalized oozing. Care should be
taken not to create point pressure on the globe, because this
may further injure an already traumatized eye. Treatment of
eyelid injuries should be delayed until one can determine
that the globes are intact. If a ruptured eye is suspected, fur-
ther examination and treatment should be performed in an
operating room setting [11].
If the adnexal injury is significant or there has been con-
tamination, intravenous antibiotics should be administered.
Tetanus toxoid, 0.5 mL, should be administered if the patient
has not had a tetanus immunization within 5 years. If the
patient has never had a tetanus immunization, 250 units of
human tetanus immune globulin should be given [12].
Pain can be severe in traumatized patients, and pain relief
can facilitate the evaluation and treatment of injuries.
However, care should be used in regard to the type and
dosage of pain medication given, especially with regard to
the possibility of a head injury. Many of these patients are
intoxicated, adding a further degree of complexity.
212
Fig. 9.1 (a) Soft tissue injury to the eyelid. (b) CT scan of same patient with evidence of associated optic nerve injury
History
A carefully gathered history about the circumstances causing
an injury can be of great help in determining the type and
extent of the trauma. The mechanism of injury can indicate
the depth of a wound and if there may be a foreign body pres-
ent. A history of sharp trauma with a pencil or knife should
elicit suspicion of injury to deeper orbital structures like the
levator muscle, optic nerve, or extraocular muscles. Likewise,
a history of blunt injury to the periorbital tissues may raise
suspicion of an underlying orbital fracture or canthal
avulsion. Bite and claw injuries are notorious for causing
canalicular lacerations.
A patient’s specific reports of symptoms can also suggest
the type and extent of injury to be found. Decreased vision
suggests an injury to the optic nerve or globe. Diplopia, hyp-
esthesia, and pain on eye movement are indicative of an
orbital fracture. Pain with jaw movement or chewing may
indicate a zygomaticomaxillary complex fracture. Inquiry
should be made about loss of consciousness and neck or
trunk pain. If an animal bite is involved, it should be deter-
mined if the animal is up-to-date on its rabies immunizations
and if the animal has been quarantined (for 10 days) [13–16].
A history of previous ocular abnormality as well as other
medical problems should be elicited. Known allergies should
be documented, and a compilation of medications should be
noted. The most recent food or liquid ingestion should be
documented. There is a delay in gastric emptying after sig-
nificant trauma; so, if reasonable, surgery should be delayed
for at least 8 h if general anesthesia is required [17].
Patient Evaluation
The examination should be divided into four basic parts:
(1) the ocular examination, followed by (2) a periocular soft
G.H. Rattan et al.
tissue examination, (3) orbital evaluation, and (4) examination
of the face.
First an ocular examination must be performed first to
rule out an injury of the globe. In the conscious patient,
visual acuity, pupillary response, intraocular pressure, slit
lamp examination, and a dilated fundus examination should
be performed. Even in the unconscious patient, a complete
ocular examination is usually possible. For some cases an
evaluation under anesthesia is necessary, because trying to
manipulate the lids can cause further injury to the globe.
The periocular soft tissue examination should delineate
the extent and depth of lacerations. The eyelid margin should
be examined carefully first. A notch or abnormality in the
marginal contour should elicit suspicion for more extensive,
full-thickness injury. Any laceration medial to the punctum
should be inspected carefully for a canalicular laceration.
Bite or claw injuries should raise suspicion for occult canali-
cular injury. Another sign of canalicular injury includes lat-
eral punctal displacement. The punctal position can be
compared with the contralateral punctum and the ipsilateral
opposing punctum. If there is any possibility of a canalicular
laceration, the involved canaliculus should be probed. A drop
of tetracaine placed in the eye before probing will make this
procedure more comfortable. Orbital fat prolapse through
the eyelid indicates penetration through the orbital septum
and potential deep orbital trauma and/or damage to the leva-
tor muscle. Lid position and levator function should be
assessed. Displacement or rounding of the canthal angles
should be noted.
The orbital evaluation begins with testing of extraocular
muscle function including range of motion and diplopia in
all fields of gaze. Test for hypesthesia of the cheek, side of
the nose, and upper lip and gum region. Palpation of the bony
orbital rims should be performed. Significant tightness of
the orbit on palpation should raise suspicion of compression
of the optic nerve. Proptosis or enophthalmos should be
9 Management of Ocular Adnexal Trauma
measured with a Hertel exophthalmometer. If a fracture or
foreign body is suspected, a CT scan of the orbits and/or face
is indicated. The CT scan is usually the study of choice in an
acute trauma setting. Direct axial and coronal views with
2-mm cuts should be obtained. The CT scan allows complete
evaluation of the bony orbit and may demonstrate the posi-
tion of foreign bodies. A magnetic resonance image (MRI)
scan may be useful in identifying optic nerve injury.
Because adnexal injury is often associated with facial
injuries, thorough examination of the head and neck should
be performed. It is wise to involve other specialists as needed.
It is important to photograph the injuries and to completely
document all findings.
Surgical Management
Surgical repair of adnexal trauma should preserve the eye
and vision, maintain function, and restore cosmesis [18].
The best way to accomplish these goals is through a well-
executed primary repair.
At surgery, the first priority is to establish the extent of
injury. A thorough exploration of all wounds should be per-
formed, looking for deep orbital penetration, foreign bodies,
or occult injury to the globe (Fig. 9.2). Debride only tissue
that is clearly devitalized, and minimize removal of tissue
when revising ragged wound margins. Eyelid skin is
extremely thin. Gentle manipulation of the wound edges will
minimize further trauma during the repair.
Care should be taken to remove all foreign bodies, because
retained foreign bodies can lead to chronic infection or
Fig. 9.2 (a) Small anterior lamellar eyelid injury. (b) Occult injury of the globe by full-thickness penetration through the eyelid
213
abscesses, especially if the foreign body is organic.
Preoperative radiographic mapping of foreign bodies can be
extremely helpful at the time of operation. Even with exten-
sive exploration and removal of foreign bodies, some small
fragments, especially glass, may spontaneously extrude for
months after the initial injury.
Wound decontamination should be carried out initially to
remove debris from the site of injury and reduce its bacterial
load. Sterile saline solution can be used for high-pressure
irrigation. Using a large syringe fitted with an 18–19-gauge
needle or short catheter will create a continuous stream under
pressure, which will reduce the bacterial counts by up to 1.5
log units and wound infection by 90% [19].
Once the wounds have been completely explored and
decontaminated, the goal of surgical treatment is to restore
the integrity of the five basic components of the eyelids: (1)
anterior lamellae – skin and orbicularis muscle, (2) posterior
lamellae – tarsus and conjunctiva, (3) canthal tendons, (4)
upper and lower canaliculi, and (5) levator complex. If
involved, the canthal tendons, lacrimal excretory system, and
levator complex should be repaired first, then attention can
be directed to the eyelid margin and skin. Often it appears
that there is loss of tissue when it merely is retraction of the
wound margins secondary to normal elasticity of the eyelid
structures or the thin tissue of the lids folding under itself. In
closing a wound, first pick identifying landmarks to reap-
proximate. These include points of acute angulation, hairline
of the brow, and the apices of traumatic flaps (Fig. 9.3). The
septum should not be incorporated in any repair of the trau-
matized lids. Some authors go as far as to recommend its
excision before closure of lid lacerations. Inadvertent or
214 G.H. Rattan et al.

Fig. 9.3 (a) Irregular laceration through the upper eyelid, eyebrow, and lateral canthal area. Arrows show significant landmarks. (b) Laceration is
closed first by approximating known landmarks and then closing the remaining wound

planned incorporation of the septum can lead to marked lid

retraction and lagophthalmos. These basic principles can be
applied to any injury of the adnexal area regardless of its
location or extent.

Operative Considerations

Most minor lacerations can be repaired in the emergency

room or intensive care unit. A small, specialized tray of
instruments simplifies these repairs. This tray should include
a Castroviejo needle-holder, iris scissors, and a small-toothed
pickup. A punctal dilator and 00 Bowman probe should be
included (Fig. 9.4). Useful sutures for such minor repairs
include 6–0 nylon, Vicryl, and mild chromic. Local anesthe-
sia can be obtained with 1% lidocaine with epinephrine
1:100,000.
In the operating room setting, most adnexal injuries can
be repaired with local anesthesia and monitored sedation.
General anesthesia should be used if there is a possibility of
an open globe, but no depolarizing agent should be given at
the time of induction. General anesthesia should be used for
extensive or complex injuries, canalicular lacerations, and in Fig. 9.4 Small ophthalmic plastic laceration tray consisting of
poorly cooperative individuals. If local anesthesia is used, Castroviejo needle-holder, Manhattan pickup, curved iris scissors,
the area of injury should be infiltrated with a solution of 1% punctal dilator, and Bowman probe
lidocaine with epinephrine 1:100,000 mixed equally with
0.5% bupivacaine (Marcaine) to provide a longer analgesic
effect. A regional nerve block can be used to augment the
local infiltration [14].
The entire face is prepped with a dilute solution of povi- Management of Blunt Trauma
done-iodine (Betadine) paint. Contaminated wounds can be
irrigated with a solution of 1 g of cefazolin (Kefzol) in Blunt trauma typically results in irregularly shaped lacera-
250 mL of normal saline. At the end of surgery, a broad- tions and avulsion injuries. This type of injury is commonly
spectrum antibiotic ointment can be applied over the wounds, seen in fist-related trauma or motor vehicle accidents when
and a patch may be used. the face comes into contact with the dashboard.
9 Management of Ocular Adnexal Trauma
Fig. 9.5 Repair of an avulsion of the medial canthal tendon. (a) Medial
canthal tendon has been avulsed from the periorbita, but the periorbita
is intact. (b) A 4–0 Polydek suture is passed in a crisscross fashion
through the cut end of the medial canthal tendon and then brought
through the periorbita in the area of the posterior lacrimal crest in a
posterior to anterior direction
Medial Canthal Injuries
Medial canthal tendon injuries are often associated with
canalicular injuries, and intubation of the canaliculus should
be performed before tendon repair. It is important to deter-
mine whether the posterior as well as the anterior horn of the
medial canthal tendon has been injured. If the posterior horn
has been transected, its repair is critical to proper lid apposi-
tion to the globe.
If both ends of the injured tendon can be found, it may be
repaired using nonabsorbable suture. The 4–0 double-armed
Polydek on a P-2 needle works well in this situation. Its small
semicircular needle is invaluable in reattaching the canthal
tendon in a posterior position. A horizontal mattress suture is
placed through the distal avulsed end of the tendon, and the
two needles are then brought from posterior to anterior
through the proximal portion of the tendon. If the proximal
portion of the tendon cannot be identified but there is intact
periorbita, the needles can be passed through this in the
region of the posterior lacrimal crest (Fig. 9.5). With
215
Fig. 9.6 When no periorbita remains, following a medial canthal ten-
don avulsion, a T-shaped microplate can be used to fixate the medial
canthal tendon in its normal anatomic position
complete avulsion of soft tissue from the bone, the authors
use a microplate to fixate the medial canthal tendon into its
normal position [20]. The microplate is attached to the
thicker bone of the anterior lacrimal crest, and the posterior
portion of the T-shaped plate is used to anchor the avulsed
medial canthal tendon (Fig. 9.6). Before repairing the medial
canthal tendon, this region must be evaluated for evidence of
bony fractures. Fractures must be stabilized before repair of
the tendon. If the bone cannot be stabilized, then transnasal
wiring of the medial canthal tendons should be used. The key
point to remember in repairing the medial canthal tendon is
that the repair must provide a posterior pull to keep the lid
well apposed to the globe and the lacrimal pump functioning
normally.
Lateral Canthal Injuries
When both sides of the transected lateral canthal tendon can
be identified, a 4–0 Polydek suture can be passed in a hori-
zontal mattress fashion across the cut ends of the tendon or
to the periorbita if needed. With periosteal fixation, the
216
transected tendon should be placed just above its normal
anatomic position because wound contracture will tend to
pull the canthal angle inferiorly [21]. If soft tissue has been
avulsed from the underlying lateral rim bone, small drill
holes can be made through the lateral orbital rim, just above
the lateral orbital tubercle and suture passed through these
holes and tied. Just as in medial canthal tendon repairs, the
lateral tendon should retain its posterior pull to keep the lid
in proper apposition with the globe.
Management of Sharp Trauma
Extramarginal Lacerations
Simple Lacerations
These involve only skin and underlying muscle with little
tissue loss. It is important to examine the full extent of the
wounds. What may at first appear to be a relatively superfi-
cial wound or small puncture may have significant underly-
ing trauma.
The wound margins should be trimmed if there are ragged
edges or devitalized tissue. Slight undermining facilitates a
good closure with eversion of the wound margin. Care should
be taken so as not to have any significant tension on the
wound. Horizontal muscle lacerations will spontaneously
reapproximate themselves owing to the sphincter action of
the orbicularis oculi muscle. Vertical lacerations should be
closed deeply with 6–0 Vicryl sutures. The eyelid skin is
usually closed with 6–0 mild chromic sutures. Interrupted
sutures should be used for a curvilinear wound. Straight
portions of the wound can be closed with a running suture.
A 6–0 or 7–0 nonabsorbable suture, such as Prolene, can also
be used to close eyelid skin. Cutaneous lacerations that
extend past the eyelids should be closed with a 6–0 nonab-
sorbable suture; these sutures should be removed in
5–7 days.
Fig. 9.7 (a) Complex laceration
of the upper lid in a V-type
configuration with devitalized
apex. (b) Wound closure after
devitalized tissue and wound
edges are debrided with flap
advanced
G.H. Rattan et al.
Complex Lacerations
These include stellate lacerations and those with significant
loss of tissue or injury to submuscular structures. These
wounds should be irrigated with normal saline, and devital-
ized tissue should be debrided. Closure of these wounds is
individualized and depends on the location and extent of
injury. Lacerations of a V-type configuration in which the
apex is devitalized can be transformed into a Y configuration
after the devitalized tissue is removed (Fig. 9.7). Care must
be taken not to shorten the anterior lamella enough to cause
lid retraction. Wide undermining often facilitates wound clo-
sure. A valuable technique for tissue loss is the use of later-
ally or medially based advancement flaps (Fig. 9.8) [22]. The
incisions made to develop these flaps should be parallel with
the lid margin.
In general, it is advisable to minimize tissue rearrange-
ment and grafting at the time of initial closure. Frost-type
sutures may be used to prevent anterior lamella contraction
during the initial phases of wound healing.
Marginal Lacerations
Meticulous closure of lacerations that involve the eyelid
margin is crucial to achieve a correct anatomic repair and
minimize postoperative complications. Failure to achieve
these goals can lead to notching of the eyelid margin, poor
contour of the lid, and lagophthalmos with corneal exposure
(Fig. 9.9). What appears to be a small anterior eyelid lacera-
tion may have a more extensive posterior lamellar compo-
nent (Fig. 9.10). A laceration that appears to be only a few
millimeters in length anteriorly can completely disrupt the
tarsal plate posteriorly. Irregular or highly angulated mar-
ginal edges should be squared off in the anterior-posterior
plane of the lid. In other words, the margins of the wound
should be freshened to create straight and parallel edges.
In injuries with a small partial loss of tarsus, attempting
9 Management of Ocular Adnexal Trauma 217

Fig. 9.8 (a) Injury to the upper lid involving avulsion of central portion A temporally based advancement flap is developed. (c) A sliding flap is
of the anterior lamella. (b) Wound is debrided and margins freshened. then advanced and sutured into place with absorbable suture

Fig. 9.9 (a) Debridement of a lid wound in a V-type configuration can lead to notching and poor lid contour after wound closure. (b) Debriding
the wound in a line perpendicular to the lid margin gives a smooth lid margin without notching
218
primary closure without wound edge modification may lead
to wound dehiscence or notching [23, 24]. The entire vertical
portion of the tarsus needs to be removed corresponding to
the width of the defect. Care must be taken to be sure that the
tarsal excision is perpendicular to the margin. Vertical skin
removal should not cross the upper eyelid crease, because
incisions more superior can result in an unsightly scar with
contracture and lagophthalmos. If needed, a superior lid
crease incision can be made, anterior lamellae undermined,
and advanced in a line parallel with the lid crease (Fig. 9.11).
This gives a good cosmetic result and minimizes vertical
contracture.
Marginal lacerations are closed using a 6–0 double-arm
silk passed through the tarsal plate as a vertical mattress
suture, entering and exiting through the meibomian gland
orifices 1.5–2 mm from the wound edges in a far-far, near-
near fashion. Many surgeons now prefer to use a 7–0 Vicryl
for this marginal suture. This suture can be left long and used
as a traction suture during the repair of the tarsus. The tarsal
plate can be closed using 6–0 Vicryl sutures placed through
Fig. 9.10 Minimal eyelid laceration involving the margin
Fig. 9.11 Freshening of an upper eyelid injury with excision of tarsal
plate perpendicular to the lid margin to the superior border of the tarsal
plate. The anterior lamella dissection and freshening is stopped at the
G.H. Rattan et al.
an anterior approach at 90% depth, anterior to the conjunc-
tiva, so as not to rub on the cornea [7]. Additional sutures can
be placed at the anterior and posterior lash lines. Three to
four sutures are placed in the upper tarsus and two in the
lower tarsus. The long arms of the marginal sutures are tied
beneath 6–0 chromic skin sutures to keep them from abrad-
ing the cornea. The remainder of the skin can be closed using
6–0 mild chromic sutures (Fig. 9.12). The margin sutures
should be removed in 10–14 days. Earlier removal can lead
to separation of the wound and notching. In children, 7–0
Vicryl can be used as the marginal suture and left to come
out spontaneously.
Complex Marginal Lacerations
Undue tension should not be placed on a marginal laceration,
because this may lead to wound dehiscence and notching.
When tissue loss is too great to primarily close the wound,
horizontal relaxation of the lid is needed before wound clo-
sure. This can be achieved by means of a lateral canthotomy
and graded cantholysis of the superior or inferior crux of the
lateral canthal tendon (Fig. 9.13). The degree of cantholysis
can be fashioned to the need of the defect. The lateral canthal
site is closed with 6–0 chromic sutures. A 5–0 Vicryl can be
used to fixate orbicularis to lateral rim periosteum and to sup-
port the lateral canthal angle. If further anterior lamellar tissue
is needed for proper closure of the wound, a modified Tenzel-
type curvilinear flap can be raised as an extension of the
canthotomy (Fig. 9.14). For upper lid defects, the arc of the
circle should be below the lateral canthus, and for lower lid
defects, above the canthus [25, 26]. Additionally, when repair-
ing lid defects in this manner, a periosteal flap can be raised
from the lateral orbital rim and sutured to the severed end of
the lateral canthal tendon (Fig. 9.14b) to minimize the devel-
opment of late retraction and ectropion [13]. When lateral
superior lid crease, an incision along the lid crease with undermining
facilitates a cosmetically acceptable closure with minimal vertical scar-
ring and contracture
9 Management of Ocular Adnexal Trauma
Fig. 9.12 (a) Eyelid margin laceration has been freshened in a pen-
tagonal wedge configuration. First, silk suture is passed through the
tarsal plate and exits the meibomian gland orifices (A). This suture is
then tied, and the remaining tarsal plate is closed using partial-thickness
6–0 Vicryl sutures. Two more 6–0 silk sutures are placed behind the
Fig. 9.13 Full-thickness eyelid laceration with moderate loss of tissue.
(a) Wound is debrided and a lateral canthotomy performed. (b) Further
relaxation of the upper lid is achieved by a superior cantholysis.
canthal supportive procedures are used, the lateral canthal
angle should be placed 2–3 mm higher than its normal ana-
tomic position because gravity will bring the angle into proper
anatomic position in a few months. For those defects that have
even greater tissue loss, Mustarde-type flaps or lid-sharing
procedures can be used [27–29]. These techniques are cov-
ered in the chapters dedicated to eyelid reconstruction.
219
lash line (B) and in front of the lash line (C). (b) These marginal silk
sutures are left long and incorporated into the first skin suture, and the
remaining skin is closed using 6–0 mild chromic sutures. The inferior
portion of the wound has been modified in a hockey stick configuration
to reduce tissue puckering
(c) Wound is primarily closed and the lateral canthotomy is closed with
5–0 Vicryl suture
Traumatic Levator Dehiscence
If the septum of the upper lid is disrupted and orbital fat is
exposed, the wound should be thoroughly explored and the
levator complex identified (Fig. 9.15). Injury to the levator
aponeurosis or muscle should be repaired at the time of the
primary wound closure. The original wound may need to be
220
Fig. 9.14 Repair of lower eyelid defect with significant loss of tissue.
(a) Outline of Tenzel rotational flap needed for closure. (b) Tenzel flap
is elevated, and cantholysis is performed. Dotted line shows position of
Fig. 9.15 Patient suffered full-thickness laceration of the upper lid.
This injury extended through the septum, and there is exposed orbital
fat. On exploration of the wound, there was associated traumatic disin-
sertion of the central portion of the levator aponeurosis
extended or a separate superior lid crease incision made to
adequately explore the levator complex. Traumatic dehis-
cence of the levator muscle should be repaired with 5–0 non-
absorbable sutures such as Prolene. A detached levator
should be sutured to the tarsal plate at its normal attachment
level (Fig. 9.16). Care should be taken not to extend these
G.H. Rattan et al.
periosteal flap to be elevated. (c) Periosteal flap is sutured to lateral
border of tarsal plate after the wound has been closed. Tenzel flap is
rotated into position and closed
sutures in a full-thickness manner through the conjunctiva to
avoid rubbing against the cornea. The levator muscle may
also be dehisced in cases of blunt trauma. Patients with trau-
matic ptosis after blunt trauma should be observed for at
least 6 months before definitive repair is attempted (Fig. 9.17).
It is possible to see spontaneous improvement in levator
function and lid height up to that time.
Secondary Repair
A wound should be closed as soon as possible. However, a
delay in wound closure may be appropriate for a number of
reasons. If the patient is systemically unstable or has life-
threatening injuries, these should be addressed first. An
open globe should be treated before soft tissue is repaired.
If the patient is intoxicated or uncooperative, treatment
delay may be indicated. If immediate wound repair cannot
be performed, one can safely wait 24–48 h without an
increase in the complication rate or a poor long-term out-
come. Until surgery can be performed, tissues should be
repositioned into as near their normal anatomic position as
possible, topical antibiotic ointment applied, and a light
dressing placed. Use of oral antibiotics should also be con-
sidered. At the time of surgery, it may be necessary to trim
early granulation tissue from the edges of the wound prior
to repair.
9 Management of Ocular Adnexal Trauma
Fig. 9.16 (a) Injury of the upper
lid showing laceration
and disinsertion of the levator
aponeurosis. (b) Levator
aponeurosis is repositioned
in its normal anatomic position
and sutured to the anterior
tarsal plate
Fig. 9.17 Patient suffered a blunt trauma with resultant ptosis of the
upper lid and decreased lid excursion
Canalicular and Lacrimal System Trauma
Canalicular lacerations are a commonly missed adnexal
injury. These lacerations may be caused by direct trauma to
the canthal region, or indirectly by avulsive forces caused by
trauma elsewhere in the orbit (Fig. 9.18). They are common
with dog bites to the midface.
It is controversial as to whether monocanalicular lacera-
tions should be repaired. Some authors believe that upper
221
Fig. 9.18 Bowman probe placed through puncta and punctum, and tra-
versing the transected margins of the canaliculus
canalicular obstruction seldom leads to epiphora. In light of
the fact that the early repair of canalicular trauma is much
easier and more successful than late repairs or placement of
a Jones tube, it seems reasonable that all canalicular lacera-
tions should be primarily repaired. The diagnosis of a canali-
cular laceration is made by either direct visualization of the
cut canaliculus or by probing of the canaliculus.
Most canalicular repairs are performed under general
anesthesia. The nostril is packed with oxymetazoline-soaked
222
Fig. 9.19 Repair of transected canaliculus. The canaliculus is intu-
bated with a Silastic stent. Vicryl sutures (7–0) are placed both anteri-
orly and posteriorly, and tied after the first lid margin suture has been
placed and tied
cotton pledgets, and the face is prepped and draped. The
most important part of the canalicular repair is placement of
a stent across the transected portion of severed canaliculus
[30–32]. After the stent has been placed, two 7–0 Vicryl
sutures are placed anteriorly and posteriorly through the
adventitia of the severed canaliculus. These 7–0 sutures
should be tagged and not tied until the first lid margin suture
is placed (Fig. 9.19).
The marginal laceration is sutured with 6–0 silk sutures.
The first marginal suture is tied before the canalicular sutures
so that there is no traction on the wound when the 7–0 Vicryl
are tightened to approximate the canalicular edges. The
stents coming from the nostril may also be pulled tight while
the canalicular sutures are tied so as to take tension off the
repair.
If the canthal tendon has been severed, it should be
repaired before the canalicular sutures are tied. After the
wound has been approximated, the Silastic stent is tied with
three square knots in the nose. There should be no tension at
the puncta. A monocanalicular stent may be used in place of
a bicanalicular stent (Fig. 9.20) [33–35].
The stent is left in place for 6 months. If the lid laceration
involves the punctum, the canaliculus can merely be
marsupialized to prevent stenosis. Occasionally it is difficult
to locate the transected medial edge of the lacerated
G.H. Rattan et al.
Fig. 9.20 (a) Monocanalicular stent consisting of a punctal plug
inserted into a portion of a Silastic stent. (b) This monocanalicular stent
is introduced through the canalicular system while being fixated with a
Bowman probe through its lumen. The repair can then be performed
and the monocanalicular stent left in place
canaliculus. Fluorescein-dyed normal saline or viscoelastic
material can be injected into the intact canaliculus, with its
egress from the proximal cut canaliculus identifying the
canalicular opening. Methylene blue should be avoided
because it stains all the tissue and makes identification of the
canaliculus difficult. Another method to locate the hidden
transected end of a canaliculus is to pool normal saline in the
medial canthal area and then inject air through the intact
canaliculus. In ragged wounds, freshening of the margins
may be needed before identification of the canaliculus can be
made. Pigtail probes should be avoided [36].
Management of Dog and Human Bites
There are greater than one million reported animal and
human bites per year in the United States [37]. Animal bites
and human bites account for approximately 1% of all emer-
gency room visits, and dog bites account for 80–90% of
these cases. Children are particularly prone to dog bites
9 Management of Ocular Adnexal Trauma
because they tend to be on the same level as the animal and
often inadvertently provoke the animal. In addition, dog bites
in children tend to be more severe as the injury occurs most
commonly on the head, face, and neck [38, 39].
As with any other injury, it is important to elicit a com-
plete history regarding the attack including the animal
involved, the mechanism of the injury, and whether or not the
attack was provoked. It is especially important to document
the patient’s tetanus immunization status, drug allergies, and
any history of immunosuppression, splenectomy, or chronic
disease [37].
The first priority on examination is to assess the health of
the eye. It is important to ensure normal vision and rule out the
possibility of a ruptured globe or other serious injury to the
eye. Once it is established that the eye is healthy and unharmed,
the wound should be explored for depth as well as injury to
other structures like the canalicular system, levator muscle,
and canthal tendons [37]. As discussed previously, occult
injury to the canalicular system is common in animal bites and
scratches. It is important to inspect the defect and determine if
there is missing tissue or if the tissue has just been avulsed and
distorted secondary to the trauma and edema. Always have a
high suspicion for an occult foreign body and inspect the
depth of the would carefully [37]. If the patient is in signifi-
cant discomfort during the exploration, sometimes a mixture
of lidocaine with epinephrine and tetracaine gel (LET) can be
helpful if applied prior to the examination. Once foreign bod-
ies have been removed or ruled out, it is prudent to irrigate the
wound copiously with at least 150 mL of sterile saline through
a 19-gauge needle or catheter [40].
There is controversy regarding whether or not to close
bite wounds primarily or secondarily. Primary repair of facial
lacerations is almost universally recommended because it
gives a better cosmetic result and the incidence of infection
is less presumably related to the excellent blood supply of
the face [38]. Care should be taken to preserve as much tis-
sue as possible and minimize debridement [41].
The most common complication of bites is infection [33].
Two to five percent of dog bite wounds become infected [37].
Risk factors for bite infection include location on the face or
scalp of an infant, puncture wounds, crush injury, treatment
delay greater than 12 h, patient age greater than 50 years,
immunosuppression, diabetes mellitus, chronic alcoholism,
and vascular insufficiency [39].
Infections related to bite wounds are typically polymicro-
bial in nature, reflecting the abundant oral flora (aerobic and
anaerobic) of the animal as well as skin flora of the victim
[37]. The most common organisms cultured from infected
dog bite wounds include Pasteurella multicida, Pasteurella
canis, Streptococci sp., Staphylococci sp., and anaerobic
gram-negative rods [39, 42]. The most common isolates from
human bite wounds are Staphylococcus aureus, group A
beta-hemolytic Streptococcus and Eikenella corrodens [37].
223
The treatment of choice for all patients with a bite injury
is amoxicillin-clavulanate, 500 mg po q 8 h. It has excellent
coverage of skin flora as well as Pasteurella sp [39]. In
patients who are penicillin allergic, a combination of clin-
damycin and fluoroquinolone is recommended [42].
Indications for admission and IV antibiotics include fever,
severe cellulitis, immunocompromise, and patients who have
failed outpatient therapy [39].
Rarely, life-threatening sepsis may occur following dog
bites contaminated with Capnocytophaga canimorsus.
Eighty percent of patients who develop this serious infection
have a predisposing risk factor, most commonly, asplenia. It
is important to think about this potentially fatal pathogen in
immunocompromised patients and those with asplenia. The
treatment for C. canimorsus is IV penicillin G.
There are a few special circumstances for which addi-
tional treatment is necessary. Rabies is responsible for 20,000
deaths/year worldwide. There is approximately one case per
year in the United States. An untreated person has a 20%
chance of contracting the virus. When rabies is suspected,
the wound should be irrigated with povidone-iodine as this is
associated with a decreased transmission rate. In addition,
the patient must receive passive immunization with the
human rabies immune globulin (HRIG) as well as active
immunization with the human diploid cell vaccine (HDCV)
or rabies vaccine adsorbed (RVA). HRIG is administered on
day 0 as a single 20 IU/kg dose half of which is injected
intramuscularly and the other half is injected around the site
of the exposure. One milliliter of the HDCV/RVA is injected
intramuscularly on days 0, 3, 7, 14, and 28. It is important
that the intramuscular injection be in the deltoid of adults or
the anterolateral thigh of infants. Injection in the gluteal
region has been associated with failure [39].
Human immunodeficiency virus (HIV) and hepatitis B are
of concern in cases of human bites wounds. The HIV status
of the biter should be obtained if possible. If HIV is sus-
pected, the wound should be irrigated with a virucidal agent
like 1% povidone-iodine. A baseline HIV test should be
obtained for the victim at the time of the injury with a follow-
up test 6 months later [39]. In general, HIV prophylaxis is
not recommended. Hepatitis B titers should be obtained from
the victim as well. If the victim does not have hepatitis B
antibodies, it is recommended to administer both the hepati-
tis B immunoglobulin as well as the HBV vaccination [37].
Gunshot Wounds of the Orbit
There are two types of firearm categories, non-powdered
(BB and pellet) guns and powdered guns (.38 Special, .357
Magnum).
A firearm is now estimated to exist in half of all US house-
holds. Two-thirds of these weapons are loaded and stored
224 G.H. Rattan et al.

within reach of children. This results in 150,000–500,000

missile injuries and 40,000–50,000 deaths annually [43].
The term ballistics refers to the science of the travel of an
object in flight. In the case of a gunshot wound, the energy
expended is kinetic energy or energy due to a motion of a
bullet penetrating tissue and/or bone. The kinetic energy of a
moving object is a function of its mass and its velocity so that
KE = 1/2 mv2 [43, 44]. Looking at the formula, it can be seen
that increasing a mass only results in a linear increase in
energy; however, increasing the velocity results in an expo-
nential increase in energy to the second power. Therefore,
the emphasis is on a lighter, spin-stabilized projectile at high
velocities rather than a large, slow projectile. In general,
powdered bullet wounds can be classified as either low-
velocity or high-velocity wounds with 2,000 ft/s being the Fig. 9.21 Entrance wound in anterior medial thigh from a Russian-
cutoff in the American literature. It takes a speed of about made AK-47 automatic rifle in Vietnam (approximate velocity:
3,000 ft/s)
125–230 ft/s to penetrate skin and bone. Entrance wounds
are typically oval to circular in shape and have a punched-
out, cleaned appearance with a surrounding zone of reddish
damaged skin. Exit wounds can appear stellate, slit-like,
crescentic, circular, or completely irregular. With greater
velocities, bullet deformation and tumbling within the body
can result in exit wounds becoming larger and more irregular
than entrance wounds (Figs. 9.21 and 9.22).
There are four components of missile and tissue
interaction:
1. Penetration
2. Missile fragmentation
3. Permanent cavity
4. Temporary cavity
The first three components are a result of the wounding
mechanism. Their extent depends on the kinetic energy of
the missile, which I have mentioned, is proportional to veloc-
ity squared. Higher missile velocities increase the rate of
Fig. 9.22 Exit wound posterior laterally showing the large exit wound
kinetic energy dissipation at impact causing greater damage. with hamstring muscles exposed
On impact, these high velocity bullets dissipate their kinetic
energy into other forms of energy, i.e., high, vibration, and
mechanic and vacuum forces, all of which can damage tissue.
At very high velocities, the bullet is more likely to fragment Table 9.1 Mass and velocity of some common missiles
leading to greater tissue destruction (Table 9.1) [45–47]. Velocity
There are some important considerations regarding non- Weapon Mass/grains Meters/feet/second
powdered guns. BB and pellet guns use compressed air or 12 Gauge Variable 412.7/1,354
gas to propel steel balls, lead, or plastic pellets. The air guns .22 49 323.1/1,150
are powered by a spring piston, pneumatic, or CO2. These .38 Special 158 257.6/755
methods are used in both air rifles and air pistols. BBs are .38 Sp.H.V. 110 345.6/1,020
made of steel with copper or zinc plating, measuring 4.5 mm .357 Magnum 158 395.6/1,235
in diameter. Pellets can be made of lead or steel-tipped plas- .45 225 259.1/900
tic and are generally 4.5 mm in diameter. Although most BB M-16 55 990.6/3,250
and pellet guns fire low-velocity missiles (muzzle velocity of .308 Winchester 150 859.5/2,820
less than 1,000 ft/s), they are still fast enough to penetrate Daisy Air Rifles
the cranium, abdomen, thorax, and paranasal sinuses Spring 5.4 gr steel 76.2–91.4/250–300
(Figs. 9.23–9.26). Approximately 80% of these weapons Pneumatic 5.4 gr steel 91.4–228.6/300–750
have muzzle velocities greater than 350 ft/s, and 50% have CO2 gun 7.7 gr lead 121.9/400
9 Management of Ocular Adnexal Trauma
Fig. 9.23 Patient with a double perforation of the left globe secondary
to a spring air rifle
Fig. 9.24 Plain film shows BB in the area of right parietal lobe after
traversing the left orbit and midface
velocities of 500–930 ft/s. A pellet velocity of only 150 ft/s
is necessary to penetrate human skin and 200 ft/s to penetrate
bone [46].
In general, ocular gunshot injuries can be classified as
either contusive or penetrating-perforating injuries. Contusive
injuries result from the cavitation effect from the shock
waves generated from high-velocity bullets. These injuries
include hemorrhage (hyphema, choroidal, vitreous, retina, and
225
Fig. 9.25 Lateral view plain film showing BB in right parietal lobe
Fig. 9.26 Following repair of the double perforation, the patient shows
an early ptosis and phthisis bulbi
retrobulbar hemorrhage), angle recession iridocyclodialysis,
concussive cataracts, lens dislocation, retinitis sclopetaria,
retinal edema, retinal detachment, and nerve avulsion.
Penetrating injuries can occur anywhere within the globe [48].
Late effects from severe orbitocranial trauma secondary to
gunshot wounds consist of orbital hematomas, orbital cellulitis
and abscess, meningitis, brain abscess, meningoencephaloce-
les, carotid cavernous fistula, cerebrospinal fluid rhinorrhea,
proptosis, endophthalmitis, diplopia, and blindness [48].
The management of gunshot wounds to the orbit requires
an interdisciplinary approach. Airway and cardiopulmonary
status is of prime consideration. Hemorrhage and shock
should be controlled, and complete neurologic examination
to rule out intracranial and spinal cord injuries should pre-
cede the ophthalmic examination. Every attempt should be
made to obtain an accurate history with emphasis on type
and mechanism of injury.
226
Fig. 9.27 Double perforations of the left globe from a shotgun at close
range
Fig. 9.28 Multiple facial fragments in soft tissue overlying bones
A complete orbital eyelid and ophthalmic examination is
essential. In general, blunt or penetrating injuries associated
with adnexal trauma presenting with decreased visual acuity,
the presence of a relative afferent pupillary defect, absence
of a red reflex, and presence of a retinal detachment are asso-
ciated with a significantly higher rate of very poor vision and
possible enucleation. The examination is complemented by
orbital ultrasound and CT and MRI scans of the head and
G.H. Rattan et al.
orbit (Figs. 9.27 and 9.28). Ultrasound can aid in detecting
posterior ocular lesions such as a foreign body and retinal
detachment that may have been obscured by anterior seg-
ment disruption and hyphema. Axial and coronal CT scan-
ning is crucial in evaluating gunshot wounds. It provides
visualization of soft tissue, bone structures, and foreign bod-
ies. A CT angiogram is valuable for suspected vascular inju-
ries such as carotid cavernous fistula or dural arteriovenous
malformations.
In the initial acute stages, MRI is not as useful as CT
because it does not show bony abnormalities and magnetic
foreign bodies may cause damage to the brain and intraocu-
lar structures. MRI does, however, provide better resolution
for low-density objects such as wood and vegetable matter,
and better resolution for detecting optic nerve lacerations
and avulsions.
Operative management depends on the type of injury and
its mechanism. Contrary to popular belief, bullets are not
sterilized on discharge. Furthermore, shotgun wadding has
been associated with a high degree of wound contamination
[43, 44]. In addition, with high-velocity wounds, temporary
cavity creates a vacuum which may pull foreign material into
the wound causing further wound contamination. Most low-
velocity gunshot wounds may be safely treated nonopera-
tively on an outpatient basis with simple local wound care
consisting of superficial irrigation and careful cleaning fol-
lowed by a dressing with or without systemic antibiotics.
Higher-velocity gunshot wounds may be managed by simple
debridement of the entrance and exit wound followed by
copious irrigation with antibiotics as well as intravenous and
systemic antibiotics with primary closure. It is important to
give tetanus prophylaxis or a reinforcing booster shot. In
contrast, high-velocity wounds not only cause severe soft tis-
sue and bone loss but also associated vascular injury requir-
ing more complex intervention [49]. Double perforations to
the globe may be treated as soon as the patient is neurologi-
cally stable, with every attempt to close both perforation
sites. This is followed by IV and intravitreal antibiotics with
vitrectomy to maximize a functioning globe. Careful follow-
up for potential complications such as endophthalmitis,
recurrence of hyphema, ocular siderosis, and sympathetic
ophthalmia is most important.
If the patient is neurologically unstable, delayed primary
closure is anticipated. The added delay may help the surgeon,
patient, and family decide, depending on the integrity of the
visual system, whether to repair the perforation site surgically
or to eviscerate or enucleate the globe. Evisceration is pre-
ferred over enucleation because it leaves the orbital anatomy
almost undisturbed. Sympathetic ophthalmia, although an
ever present threat, is uncommon. If sympathetic ophthalmia
is a concern, enucleation is the procedure of choice.
9 Management of Ocular Adnexal Trauma
References
1. Kurkinen MV. Sequential appearance of fibronectin and collagen in
experimental granulation tissue. Lab Invest. 1980;43:7.
2. Gk G. Wound healing. Facial Plast Surg Clin North Am.
2002;10(2):119–27.
3. Abraham DS. Tumor necrosis factor alpha suppresses the induction
of connective tissue growth factor by transforming growth factor-
beta in normal and scleroderma fibroblasts. J Biol Chem.
2000;275:15220.
4. Goldman R. Growth factors and chronic wound healing: past, pres-
ent and future. Adv Skin Wound Care. 2004;17:24.
5. Dulakk J, JĂłzkowicz A. Vascular endothelial growth factor
synthesis in vascular smooth muscle cells is enhanced by
7-ketocholesterol and lysophosphatidylcholine independently of
their effect on nitric oxide generation. Atherosclerosis. 2001;159:
325–32.
6. Pierce GM. Role of platelet-derived growth factor in wound heal-
ing. J Cell Biochem. 1991;45:319–27.
7. Forrest L. Current concepts in soft connective tissue wound heal-
ing. Br J Surg. 1983;70:133.
8. Sabiston D. Textbook of surgery: the biological basis of modern
surgical practice. 15th ed. St. Louis: Saunders; 1997.
9. Brem H. Surg Technol Int 2003;11:23–31.
10. Committee on Trauma of the American College of Surgeons.
Advanced trauma life support course. Chicago: American College
of Surgeons; 1984.
11. Goldberg MF, Tessler HH. Occult intraocular perforations from
brow and lid lacerations. Arch Ophthalmol. 1971;86:145.
12. Committee on Trauma of the American College of Surgeons: a
guide to prophylaxis against tetanus in wound management, 1979
revision. Reprinted from the Bulletin of the American College of
Surgeons; 1979.
13. Gonnering RS. Ocular adnexal injury and complications in orbital
dog bites. Ophthal Plast Reconstr Surg. 1987;3:231.
14. Herman DC, Bartley GB, Walker RC. The treatment of animal bite
injuries of the eye and ocular adnexa. Ophthal Plast Reconstr Surg.
1987;3:237.
15. Schultz RC, McMaster WD. The treatment of dog bite injuries,
especially those of the face. Plast Reconstr Surg. 1972;49:494.
16. Shannon GM. The treatment of dog bite injuries of the eyelids and
adnexa. Ophthalmic Surg. 1975;6:41.
17. Morris RE, Miller GW. Preoperative management of the patient
with a full stomach. In: Giesecke AM, editor. Clinical anesthesia:
anesthesia for the surgery of trauma. Philadelphia: FA Davis; 1976.
18. Garber PF, MacDonald D, Beyer-Machule CK. Management of
trauma to the eyelids. In: Della Roca RC, Nesi FA, Lisman RD,
editors. Ophthalmic plastic and reconstructive surgery, vol. I. St.
Louis: CV Mosby; 1987.
19. Hildreth HR, Silver B. Sensory block of the upper eyelid. Arch
Ophthalmol. 1967;77:230.
20. Shore JW, Rubin PA, Bilyk JR. Repair of telecanthus by anterior fix-
ation of cantilevered miniplates. Ophthalmology. 1992;99:1133.
21. Leone CR. Lateral canthal reconstruction. Ophthalmology. 1987;94:238.
22. Ramecki JM, Nesi FA, Spoor TC. Management of injuries to the
ocular adnexa. In: Spoor TC, Nesi FA, editors. Management of ocu-
lar, orbital, and adnexal trauma. New York: Raven; 1988.
227
23. Divine RD, Anderson RL. Techniques in eyelid wound closure.
Ophthalmic Surg. 1982;13:283.
24. Gassman DM, Berlin JA. Management of acute adnexal trauma. In:
Surgery of the eyelid, orbit, and lacrimal system. Am Acad
Ophthalmol; 1993.
25. Tenzel RR. Reconstruction of the central one-half of an eyelid.
Arch Ophthalmol. 1975;93:125.
26. Tenzel RR, Stewart WB. Eyelid reconstruction by the semicircle
flap technique. Ophthalmology. 1978;85:1164.
27. Hughes WL. New method for rebuilding lower lid. Arch Ophthalmol.
1937;17:1008.
28. Hughes WL. Reconstructive surgery of the eyelids. 2nd ed. St.
Louis: CV Mosby; 1954.
29. Mustarde JC. Repair and reconstruction in the orbital region.
Edinburgh: Churchill Livingstone; 1971, chaps. 7–8.
30. Hawes MJ, Segrest DR. Effectiveness of bicanalicular silicone
intubation in the repair of canalicular lacerations. Ophthal Plast
Reconstr Surg. 1985;1:85.
31. Crawford JS. Intubation of obstructions in the lacrimal system. Can
J Ophthalmol. 1977;12:289.
32. Crawford JS. Lacrimal intubation set with suture in the lumen.
Ophthal Plast Reconstr Surg. 1988;4:249.
33. Gonnering RS. Simplified monocanalicular silicone intubation.
Arch Ophthalmol. 1987;105:1024.
34. Long JA. A method of monocanalicular silicone intubation.
Ophthalmic Surg. 1988;19:204.
35. Patrinely JR, Anderson RL. Monocanalicular silicone intubation.
Arch Ophthalmol. 1988;106:579.
36. Saunders PH, Shannon CM, Flanagan J. The effectiveness of pigtail
probe method of repairing canalicular lacerations. Ophthalmic
Surg. 1978;9:33.
37. Brook I. Management of human and animal bite wound infection:
an overview. Curr Infect Dis Rep. 2009;11:389–95.
38. Javaid M, Feldberg L, Gipson M. Primary repair of dog bites to the
face: 40 cases. J R Soc Med. 1998;91:414–8.
39. Griego RD, Rosen T, Orengo IF, Wolf JE. Dog, cat, and human
bites: a review. J Am Acad Dermatol. 1995;33:1019–29.
40. Graham III WP, Calabretta AM, Miller SH. Dog bites. Am Fam
Physician. 1977;15:132–137.
41. Nerad JA. Techniques in ophthalmic plastic surgery. 1st ed.
Philadelphia: Saunders Elsevier; 2010.
42. Talan DA, Citron DM, Abrahamian FM, Moran GJ, Goldstein EJ.
Bacteriologic analysis of infected dog and cat bites. N Engl J Med.
1999;340(2):85–92.
43. Bartlett CS, Helfet DL, et al. Ballistics and gunshot wounds: effects
on musculoskeletal tissues. J Am Acad Orthop Surg. 2000;8(1):
21–36.
44. Evans MB. Gunshot wound ballistics. www.bcm.edu/oto/
grand/02_12_04,htm.
45. Scott RF, editor. The shooter’s bible. South Hackensack: Stoeger;
1983. p. 479–500.
46. Air Gun, From Wikipedia, en.wikipedia.org/wiki/Air_gun.
47. Great Lakes sports fishing council. www.great-lakes.org/reviews/
review-09–04–06.html.
48. Chu A, Levine MR. Gunshot wounds of the eye and orbit.
Ophthalmic Surg. 1989;20(10):729.
49. Bower GW, Rossiter ND. Management of gunshot wounds of the
limbs. Br Edit Soc Bone Joint Surg. 1997;79B(6):1031–6.