Complications in Facial Trauma




This article reviews common complications encountered in the setting of facial trauma. Many complications are the result of the primary injury, and a facial plastic surgeon should be able to quickly identify these to prevent further morbidity. Common pitfalls and controversial topics are presented, as well as an overview of treatment for many complications.


Key points








  • Intracranial and ocular injuries are common with severe facial fractures, and must be quickly identified and appropriately treated.



  • Meticulous fracture reduction and implant placement are paramount in preventing postoperative complications.



  • Complications of rigid fixation are typically due to fixation of inadequately reduced fractures.



  • Close postoperative assessment allows for early recognition of complications, and provides the opportunity to intervene when necessary to achieve better long-term outcomes.






Introduction


Complications are common in the facial trauma setting, and there are several causes. All facial trauma surgeons should be knowledgable about potential associated intracranial and ocular injuries and how to prevent further morbidity. A multidisciplinary approach is often required, and early consultation with appropriate specialists is recommended. An understanding of common posttraumatic complications will guide surgical management. The most common complications of facial trauma are summarized in Tables 1 and 2 .



Table 1

Complications of facial trauma: soft tissue and viscera







































































































































Early Late/Postoperative
Soft tissue Infection/abscess Scar contracture
Loss of soft tissue Facial deformity
Unfavorable scarring Infection/abscess
Brain Dural laceration
Cerebrospinal fluid (CSF) leak
Hematoma (epidural, subdural, subarachnoid, intracerebral, intraventricular)
Diffuse axonal injury Recurrent CSF leak
Edema Meningitis
Traumatic brain injury Brain abscess
Edema
Concussion
Foreign body
Nasolacrimal apparatus Lacrimal injury Epiphora
Dacrocystitis
Parotid gland Hematoma Sialocele
Infection Salivary fistula
Sialocele Parotitis
Salivary fistula Chronic pain
Abscess Frey syndrome
Facial deformity
Eye Traumatic optic neuropathy Persistent diplopia
Retrobulbar hematoma Enophthalmos
Globe rupture Exopthalmos
Vision loss Lower-lid malposition
Diplopia Exposure keratitis
Muscle entrapment Blindness
Enophthalmos Sympathetic ophthalmia
Corneal abrasion
Superior orbital fissure syndrome
Orbital emphysema
Oculocardiac reflex (bradycardia)
Blindness
Sympathetic ophthalmia
Bone Delayed union
Fracture Nonunion
Bone loss Malunion
Infection/osteomyelitis
Dentition Malocclusion Malocclusion
Direct injury to tooth root Tooth loss
Avulsion Infection/abscess


Table 2

Complications of facial trauma: upper, middle, and lower face















































































































































































































Early Late/Postoperative
Skull fracture Traumatic brain injury Recurrent CSF
Meningitis/brain abscess Anosmia
CSF leak Meningitis/brain abscess
Pneumocephalus Seizure
Traumatic optic neuropathy Chronic sinusitis
Retrobulbar hematoma Cavernous sinus thrombosis
Cranial nerve injuries Blindness
Subdural hematoma
Frontal sinus fracture CSF leak Chronic sinusitis
Traumatic brain injury Alopecia
Meningitis Mucocele/mucopyocele
Pneumocephalus Meningitis/brain abscess
Osteomyelitis
Encephalocele
Frontal neuralgia
Forehead deformity
ZMC fracture Facial deformity Enophthalmos
Orbital injury Facial deformity
Malocclusion Diplopia
Enophthalmos Malar flattening
Canthal malposition
Ectropion
NOE fracture CSF leak Telecanthus
Telecanthus Persistent nasal deformity
Chronic sinusitis Pseudohypertelorism
Enophthalmos Scarring
Anosmia Forehead paresthesia
Ocular injury Enophthalmos
Traumatic brain injury Diplopia
Epiphora
Dacrocystitis
Anosmia
Midface retrusion
Orbital fracture Diplopia Scleral show/lower-lid retraction
Enophthalmos Persistent diplopia
Entrapment Ectropion/entropion
Cheek numbness (CN V2) Enophthalmos
Traumatic optic neuropathy Persistent entrapment
Globe rupture Prominent scar
Retrobulbar hematoma Lower-lid edema
Oculocardiac reflex (bradycardia) Cheek numbness (CN V2)
Corneal abrasion Canthal malposition
Exopthalmos Corneal abrasion
Lacrimal duct injury Ptosis
Epiphora
Exposure keratitis
Blindness
Telecanthus
Vertical dystopia
Nasal fracture Septal hematoma Deviated septum
Deviated nasal dorsum Nasal obstruction
Nasal obstruction Nasal deformity
Epistaxis Septal perforation
Mandible Malocclusion Malocclusion
Facial paresthesia (CN V2, 3) Facial paralysis (CN V2, V3)
Trismus Trismus
Facial deformity Facial deformity
Airway compromise Hardware exposure
Dental injury Dental injury
Delayed union
Nonunion
Infection/osteomyelitis
Malunion
TMJ ankylosis

Abbreviations: CN, cranial nerve; CSF, cerebrospinal fluid; NOE, nasoorbitoethmoid; TMJ, temporomandibular joint; ZMC, zygomaticomaxillary complex.




Surgical complications of soft tissue and viscera


Important overall tenets of facial trauma are to minimize scarring and prevent further injury to adjacent structures. The bony skeleton of the face protects multiple organs that are important to the functions of daily life. It is imperative that these organs are thoroughly evaluated at the initial presentation and the findings accurately documented. Scarring may be unavoidable, depending on the damage to soft tissue from the primary injury and/or location of the fractures and the access required for their repair. Lacerations should be copiously irrigated, minimally debrided, and closed primarily in a layered fashion. Local skin flaps may be used to cover defects, if necessary. Hypertrophic or cosmetically unfavorable scars can be treated with dermabrasion, serial excision, or scar revision.


Brain injuries occur in up to 89% of patients with complex facial trauma. All patients should be evaluated for potential involvement of the brain or cervical spine ( Table 3 ), and an urgent neurosurgical consultation should be obtained for any positive findings. Traumatic brain injuries can be classified as closed, penetrating, and explosive blast injuries, with the severity based on the Glasgow Coma Scale. Cerebrospinal fluid (CSF) leaks carry a 10% to 30% risk of developing meningitis, and can present acutely at the time of initial injury or in a delayed fashion. Symptoms include persistent clear rhinorrhea or otorrhea, description of a salty taste in the mouth by the patient, headaches, or recurrent meningitis, and can be confirmed with a positive β2-transferrin test of collected fluid. Most CSF leaks resulting from accidental and surgical trauma heal with conservative measures over the course of 7 to 10 days, although waiting for the leak to close spontaneously can increase the risk of meningitis, and close assessment to assure that complete resolution has occurred is necessary. Surgical management includes exposure of the leak with primary repair or patch placement. Meningitis is treated aggressively with parenteral broad-spectrum antibiotics. To prevent irreversible neurologic injury, spinal-cord injury should be suspected in all trauma patients until it is ruled out. Repair of facial fractures may initially be delayed while the patient is hemodynamically stabilized. If repair is performed before clearance of the cervical spine, it is imperative that the cervical spine remains in a neutral position. Closed reduction or external fixation techniques may be necessary to avoid injury to the spinal cord if access is inadequate.



Table 3

Intracranial complications
























Traumatic brain injury (TBI) Closed head TBI Typically a result of blunt impact. May result in a focal lesion in the brain (hematoma) or diffuse axonal injury (from shearing of axons against the skull base) Neurosurgical consultation necessary
Penetrating TBI Occurs with foreign body violation of the skull and dura, entering the brain parenchyma. The size, speed, and track of the projectile determine the extent of neurologic damage Neurosurgical consultation necessary
Explosive blast TBI More common in military combat and causes diffuse injury secondary to a pressure wave. Often results in rapidly developing cerebral edema, subarachnoid hemorrhage, and burst-pattern skull fractures Neurosurgical consultation necessary
Cerebrospinal fluid (CSF) leak Symptoms: persistent clear rhinorrhea or otorrhea, description of salty taste in mouth, headaches or recurrent meningitis Neurosurgical or otolaryngology consultation may be necessary. Conservative management: bed rest, head elevation, avoidance of nose blowing or straining, and stool softeners. Antibiotic prophylaxis and lumbar drain placement is controversial and often surgeon dependent. Current studies have found no benefit from prophylactic antibiotics, though remains controversial
Surgical management: transcranial, subcranial, or endoscopic approach with the placement of a mucosal, fascial, or bone graft. The endoscopic approach has become more prevalent and is shown to be safe and effective, with a 90% initial success rate that improves further with subsequent attempts, with lower morbidities than open procedures
Meningitis Symptoms: headache, nausea, photophobia, altered level of consciousness, fever, nuchal rigidity and pain with flexion of the neck Empiric first-line treatment in patients with postneurosurgical meningitis is intravenous vancomycin plus cefepime or ceftazidime


Approximately 22% to 30% of orbital fractures have associated ocular injuries. It is imperative that all patients are evaluated for vision-threatening injuries and managed emergently to minimize loss of vision ( Table 4 ). The most common vision-threatening injuries include traumatic optic neuropathy, retrobulbar hemorrhage, and penetrating globe injury. Visual acuity, visual fields, color vision, extraocular movement, the pupil, and the fundus should be examined in all patients with periorbital injuries. Diplopia, caused by inflammation and/or edema, is common after both orbital injury and surgery. It may also be evidence of direct injury to the globe, entrapment of orbital soft tissue or extraocular muscles, and vascular or neural damage. Diplopia is usually temporary and should be closely monitored. If persistent after surgical repair, a computed tomography (CT) scan should be obtained to evaluate the implant and fracture repair for misplacement and/or incarceration of soft tissue. Unless entrapment or adherence has been identified, surgical exploration is rarely beneficial, and strabismus surgery may be required. The presence of a retinal injury may preclude immediate repair of periorbital bone injuries, and surgery should be delayed until approved by the consultant ophthalmologist.



Table 4

Ocular complications























Retrobulbar hematoma (RBH) Bleeding into the orbit causing increased intraocular pressure compromising the blood supply to the optic nerve and retina. Leads to progressive vision loss and eventual blindness
Venous: Slower progression. May not be evident until patient is in recovery or possibly after discharge
Arterial: Can progress within seconds, requiring frequent monitoring or palpation of the globe during surgery, especially if significant bleeding is encountered
Symptoms: proptosis, periorbital ecchymosis, increased intraocular pressure, tense globe, loss of direct pupillary light reflex, diplopia, ophthalmoplegia, and decreasing visual acuity/blindness First-line treatment: Immediate lateral canthotomy and inferior cantholysis
Adjunctive treatment: Head of bed elevation or reverse Trendelenburg (cervical-spine precautions), removal of intranasal packing, and immediate ophthalmology consultation with measurement of intraocular pressure. Administration of mannitol 20% (1–2 g/kg IV over 30–60 min), systemic corticosteroids (dexamethasone 8–10 mg IV every 8 h for 3–4 doses), acetazolamide (500 mg IV bolus) or topical antiglaucoma eye drops (Timolol ophthalmic drops 0.5%, 1–2 drops topically twice daily)
Second-line treatment: Orbital decompression and anterior/posterior ethmoid artery ligation
Traumatic optic neuropathy (TON) Clinical diagnosis referring to any insult to the optic nerve secondary to trauma
Direct TON: penetrating injuries severing the optic nerve. Permanent blindness results
Indirect TON: hematoma or secondary edema of the optic nerve within optic canal causing direct mechanical trauma or vascular ischemia, leading to further retinal ganglion cell injury and visual loss
Symptoms: relative afferent pupillary defect in the affected eye and varying loss of visual acuity from partial visual loss to blindness Ophthalmology consultation is necessary
Treatment: No standard of care. Options include observation, corticosteroids, and optic nerve decompression. Spontaneous visual recovery ranges from 0% to 60%. At present neither intervention has been found to be more effective than observation alone. Patients presenting with no perception of light to the injured eye have a poor prognosis for recovery with any course of action
Open globe injury/globe rupture Full-thickness defect of the cornea or sclera Findings: possible prolapsing uveal tissue, retina, or vitreous gel. Decreased intraocular pressure Do not manipulate the eye to prevent extrusion of contents. A protective eye shield is placed and emergent ophthalmology consultation is made. Early surgical repair, if possible. Enucleation or evisceration of the globe within 2 weeks with nonsalvageable injuries to avoid sympathetic ophthalmia
Sympathetic ophthalmia Rare, bilateral, granulomatous uveitis presenting after ocular trauma or surgical interventions, causing blindness in the noninjured (sympathetic) eye. Etiology thought to involve inflammatory and autoimmune response after ocular antigens exposed to the immune system. Presents weeks to years after injury Symptoms: insidious onset of blurry vision, pain, epiphora, and photophobia Ophthalmology consultation is necessary. Aggressive treatment with systemic corticosteroids or immunosuppressive therapy

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Aug 26, 2017 | Posted by in General Surgery | Comments Off on Complications in Facial Trauma

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