Pediatric head trauma occurs commonly with most being minor; however, seemingly low-risk presentations may have intracranial injuries, and thus it is important to maintain a high index of suspicion. The Glasgow Coma Scale (GCS) quantifies neurologic findings and allows uniformity in description and communication among team members involved in taking care of the patient. A GCS score of 14 to 15 is categorized as mild head injury; a GCS score of 9 to 13 as moderate head injury and GCS score less than 9 as severe head injury.
Figure 20.1 ▪ Penetrating Head Injury.
(A) This infant was stabbed in the head with a butter knife during a domestic dispute between his mother and angry father. He suffered no neurologic deficits after the knife was removed by neurosurgery in the operating room. (B) A lateral projection of the skull demonstrates the butter knife imbedded within the occipital-parietal region of the skull. (Photo/legend contributors: Mark Silverberg, MD/John Amodio, MD.)
Stabilize airway with cervical spine immobilization, breathing and circulation as indicated followed by evaluations for disability and exposure. Moderate hyperventilation, if signs of impending herniation, and fluid resuscitation, if evidence of hypotension, are critical.
Treat any seizures with a benzodiazepine or fosphenytoin, and consider using the latter prophylactically, if intracranial hemorrhage is present. Obtain laboratory tests including CBC type and cross-match, electrolytes, and coagulation profile in patients with serious head injuries. Consider obtaining ethanol level and toxicologic screen in adolescents. Order C-spine imaging in all patients with midline neck pain or neurologic deficits, and in all unconscious patients. Obtain a head CT scan (without contrast) if loss of consciousness, GCS score <13, penetrating injury, a high-risk mechanism of injury, clinical signs of basilar or depressed skull fracture, a posttraumatic seizure, a large scalp hematoma (especially parietal/temporal), repetitive vomiting, prolonged lethargy, amnesia, past history of bleeding diathesis (eg, hemophilia), significant past medical history (eg, shunts) or suspected abusive head injury. Leave any penetrating foreign bodies of the head in place for operative removal; consult neurosurgery emergently for such cases and for any abnormalities seen on the head CT scan.
Figure 20.2 ▪ Penetrating Head Injury.
An axial slice from a noncontrast head CT shows a penetrating gunshot wound with fracture of the frontal and parietal bones, and large hemorrhagic contusion along the tract of the bullet. High-density bullet fragments are also noted in the frontal region of the brain. (Photo/legend contributors: Mark Silverberg, MD/John Amodio, MD.)
Admit patients with abnormal CT findings, witnessed loss or change of consciousness, penetrating injuries, focal or abnormal neurologic examination, abusive injuries, evidence of depressed or basilar skull fracture, other significant associated injuries, persistent symptoms (even with a normal CT scan), amnesia, or an unreliable caretaker at home. Refer to the American Academy of Pediatrics guidelines for minor head injury for patients aged <2 years, and for patients aged 2 to 20 years. Discharge other patients with written instructions that are clear to the caretaker, including the directive to return to the emergency department (ED) immediately if the patient develops any of the following: (1) excessive sleepiness or difficulty in awakening; (2) confusion or abnormal behavior; (3) progressive headache; (4) progressive vomiting or nausea; (5) abnormal gait; (6) ataxia; (7) unequal pupils, double vision, or any visual disturbance; (8) convulsions; and (9) bleeding or watery drainage from the nose or ear.
Diffuse brain injury (concussion or diffuse axonal injury) is the most common type of head injury.
Prevent secondary brain injury in patients presenting with head trauma or multiple trauma.
Patients with epidural hematoma may present with the classic lucid interval and acutely deteriorate (“talk and die”).
Figure 20.3 ▪ Pneumocephalus.
(A) Lateral skull film of a 19-year-old male who sustained multiple stab wounds to the head, demonstrating extensive pneumocephalus. The bony matrix could not be conclusively evaluated because of the pneumocephalus. (B) A CT scan of the head of the same patient demonstrates numerous pockets of air in the sulci with marked subarachnoid pneumocephalus. (Photo/legend contributors: Binita R. Shah, MD/John Amodio, MD.)
The authors acknowledge the special contributions of Ayman Chritah, Karen L. Stavile, Kevin J. McSherry, David Listman, Binita R. Shah and Eileen C. Quintana, to prior edition.
Skull fractures occur as a result of a direct impact to the calvarium and are important to diagnose because of their association with intracranial injury. The parietal bone is involved most frequently. Linear fractures are most common (about 75%), followed by depressed and basilar fractures. Approximately 30% of children with depressed skull fractures have an associated intracranial injury. Typical head injury mechanisms include falls, sports injuries, and motor vehicle collisions. The morbidity and mortality from closed head injuries increase when there are associated extracranial injuries. Skull fractures are classified by appearance, location, degree of depression, and whether there is an associated scalp laceration. Comminuted skull fractures are multiple linear fractures. Open skull fractures are rare but increase the risk of central nervous system infection. Physical examination findings for skull fractures include hematoma, a palpable step-off or skull defect or crepitus. Most linear skull fractures heal without complications.
For a detailed approach to head trauma, see Head Trauma section. Order non contrast head CT scan for identification of skull fractures and any associated intracranial pathology (while radiographs may rule in a fracture, they cannot exclude intracranial injury). Clinical assessment is more difficult in children <2 years of age and especially those <3 months old while they are also more susceptible to injury from even minor trauma. Children of this age are also at greater risk of being victims of abuse, developing a growing fracture and having intracranial injuries. Maintain a higher index of suspicion and a lower threshold for obtaining a CT in this age group.
Consult neurosurgery for patients with depressed, basilar, or widely diastatic skull fractures, and admit them for observation with frequent neurologic checks. Admit all patients with persistent neurologic deficits, persistent vomiting, suspected nonaccidental injury or unreliable guardians.
Consider admission with skull fracture if patient is <6 months of age, large scalp swelling over the fracture, known high-energy mechanism of injury, or concerning fracture location (eg, crossing a suture, extending into posterior fossa, or in a dural venous sinus or a vascular groove).
Normal variants such as vascular grooves, open metopic sutures, posterior fossa sutures, and accessory sutures may mimic skull fractures.
Basilar skull fractures (BSFs) are injuries that involve the base of the skull, typically involving the petrous portion of the temporal bone (but can involve any skull base). Patients present with distinct clinical findings (80% of cases) that include Battle sign (postauricular ecchymosis suggesting a mastoid fracture), raccoon eyes or periorbital ecchymosis (intraorbital bleeding from orbital roof fractures), hemotympanum, cerebrospinal fluid (CSF) rhinorrhea or otorrhea or cranial nerve palsies, tinnitus, hearing loss, anosmia, nausea, vomiting vertigo, or nystagmus. BSFs with underlying dural tears have an increased association with CSF leaks and thus an increased risk of intracranial infection (eg, Streptococcus pneumoniae, Streptococcus pyogenes, Haemophilus influenzae). Other complications include hearing loss (conductive or sensorineural in up to half of the children).
For a detailed approach to head trauma, see Head Trauma section. Obtain head CT scan, including imaging of the temporal bone (about 40% of BSFs are missed by CT scan). Admit children to ICU with BSF for monitoring and consult neurosurgery.
BSF usually results from a considerable force; always exclude brain injury.
Do not pass nasogastric tube (may lead to inadvertent passage through an injured cribriform plate).
Cranial nerve palsies (eg, I, VII, VIII, X) may be seen immediately or a few days after the injury.
Figure 20.7 ▪ Basilar Skull Fracture.
(A) “Raccoon eyes” are pictured here in this teenager with a 4-day-old basilar skull fracture. (B) Battle’s sign occurs when blood from a skull fracture tracks down to the neck and is visible there as a blue/purple discoloration seen under the skin. In this case, there are some green hues as well signifying that the blood has been around for a while and is starting to break down. (Photo contributor: Mark Silverberg, MD.)
Subdural hematoma (SDH) develops as a result of venous bleeding from bridging veins between the dura and the arachnoid membranes. SDHs are seen with significant mechanisms of injury and are often associated with underlying brain injury (eg, intracerebral hematomas, contusions). They may be bilateral and occur more commonly than epidural hematoma. Abusive head injury is a common etiology, especially when the child is <2 years of age. Presenting symptoms include irritability, vomiting, altered mental status, seizures, focal neurologic signs, and if young, a very full fontanelle. Predisposing factors for development of SDHs include osteogenesis imperfecta, glutaric aciduria type I, arachnoid cysts, cerebral atrophy, history of hydrocephalus, or bleeding disorders.
Figure 20.10 ▪ Subdural Hematoma.
An axial noncontrast head CT slice shows a large right subdural hematoma with a “hematocrit effect” indicating acute and chronic hemorrhage. There is significant mass effect present, with a midline shift. Also note effacement of the right cerebral gyri from cerebral edema. (Photo/legend contributors: Mark Silverberg, MD/John Amodio, MD.)
For a detailed approach to head trauma, see Head Trauma section. Obtain noncontrast head CT scan and neurosurgical consultation. Obtain baseline laboratory tests, including CBC, prothrombin time (PT)/partial thromboplastin time (PTT) with international normalized ratio (INR), a bleeding time, and type and cross. With suspicion of child abuse, obtain liver transaminase levels (occult abdominal trauma), and notify child protective services. Hospitalize patients to ICU for close monitoring. Even in the most critically injured children, surgical intervention may not be helpful. When necessary to operate, a craniotomy or craniectomy will effectively evacuate subdural hemorrhage in roughly 80% of patients.
Majority of SDHs in infants and children <2 years old are caused by inflicted head injuries, and children may present with very nonspecific clinical signs.
SDHs are seen as areas of increased density that appear concave (or crescent-shaped), covering and compressing the gyri and sulci over an entire hemisphere.
Epidural or extradural hematoma (EDH) is collection of blood between the dura and overlying calvarium. Common causes include low-velocity impact (falls) and nonaccidental injury, motor vehicle collisions (adolescents), and occasionally forceps delivery in neonates. Delayed EDH may occur in poly-trauma patient. EDHs may be of arterial or venous origin. Temporal EDHs are often due to injury to the middle meningeal artery (about 80%) or injury to the middle meningeal vein and dural sinus. In children, there are fewer temporal EDHs and the most common sites are frontal, parietooccipital, and posterior fossa. A patient with EDH may present with an asymptomatic period (lucid period) followed by headache, vomiting, and altered mental status that may progress to signs and symptoms of uncal herniation (fixed or dilated pupil on the same side as EDH and hemiparesis on the opposite side).
For a detailed approach to head trauma, see Head Trauma section. Rapid diagnosis is critical for successful management. Order a noncontrast head CT scan that will reveal typical biconvex or lenticular increased density of fresh blood. EDH is usually unilateral and localized and does not cross suture lines (as the outer layer of dura attaches to the skull there, preventing blood from expanding past it). Consult neurosurgery emergently; evacuation of EDH is necessary if there is any evidence of worsening mental status, an expanding bleed, or midline shift. Hospitalize patients to ICU if EDH is small and patient is asymptomatic for close monitoring and serial head CT scans.
Expanding EDHs are potentially life-threatening and often lead to herniation, if not recognized promptly.
Infants and young children have a higher frequency of venous EDHs.
Younger children with open sutures may not be symptomatic until their condition is critical.
EDHs may occur without evidence of an overlying fracture making the diagnosis challenging.
Figure 20.12 ▪ Epidural Hematoma.
The head CT scan of a 12-month-old male who had a 27-inch television fall onto his head. (A) Multiple skull fractures of the right frontal, temporal, and occipital bones are seen in this bone window. (B) A large area of hyperdensity extending from the right frontal to the right parietal region, representing a large epidural hematoma is seen. Extensive hypodensity involving the right cerebral hemisphere and left frontal lobe, compatible with cerebral edema, and significant mass effect compressing the right lateral ventricles and causing a midline shift to the left is also seen. Diffuse soft tissue swelling and air overlying the right side of the skull is also seen. (Photo contributor: Binita R. Shah, MD.)
Brain contusions (intracerebral hematomas) result from direct external contact forces or from the brain striking the inner surface of the skull during an acceleration/deceleration type of trauma. A classic coup injury will occur at the site of impact, and a contrecoup injury will occur at a site remote to the impact site. Most contusions occur in the frontal and temporal lobes (may occur anywhere in the brain). These areas of bruising are associated with localized edema, ischemia, and mass effect.
For a detailed approach to head trauma, see Head Trauma section. Order a noncontrast head CT or MRI. The latter is more sensitive in discovering cerebral contusions since CT may not reveal nonhemorrhagic contusions or small petechial hemorrhages. Consult neurosurgery and admit patients to ICU with CT evidence of cerebral contusion or neurologic signs or symptoms or unreliable caretakers. Patients with simple concussions/nonhemorrhagic contusions with no neurologic symptoms can be sent home with good instructions explaining what to watch for in case of cerebral injury.
Patients with brain contusions may present with focal neurologic signs and/or confusion and an impaired level of consciousness.
MRI is the modality of choice to diagnose nonhemorrhagic cerebral contusions.
Brain contusions may delay the recovery process of a concussion.
Figure 20.13 ▪ Cerebral Contusion.
An axial noncontrast head CT slice shows blood within the gyri and brain parenchyma compatible with cerebral hemorrhagic contusion. A small subdural hematoma is also present (arrow). There is a slight shift of the midline from mass effect. (Photo/legend contributors: Mark Silverberg MD/John Amodio, MD.)
Figure 20.14 ▪ Coup and Contrecoup Injury.
The head CT scan of a young male who after becoming intoxicated fell to the ground, striking the left side of his head. Note the large left-sided scalp contusion (coup injury). Also note the right-sided cerebral contusion (contrecoup injury). (Photo contributor: Mark Silverberg MD.)
Mild traumatic brain injury (TBI) is a fairly common and important public health problem. It is usually benign but can have serious short and long-term sequelae. A concussion is defined as a complex pathophysiological process affecting the brain, induced by traumatic biomechanical forces. The hallmarks of concussion are headache and confusion with or without amnesia, often without a history of loss of consciousness. Frequently observed signs/symptoms of a concussion are vacant stare, unrelenting headache, memory deficits, incoordination, inability to focus, perseveration, slurred or incoherent speech, emotional extremes, and disorientation. Early posttraumatic seizures (within the first week after a head injury) occur in fewer than 5% of mild or moderate TBIs and are associated with a higher risk of posttraumatic epilepsy.
For a detailed approach to head trauma, see Head Trauma section. Not all patients with mild head injury need a CT scan. Observe these patients for at least 24 hours with attention to the increased risk of intracranial complications. Admit patients who have GCS score <15, any abnormality on CT scan, history of a seizure, any abnormal bleeding parameters or a home environment where the patient cannot be checked on regularly. If a patient is discharged, instruct the caregiver to seek medical care if there is difficulty waking the child, vomiting, a worsening headache, deteriorating vision, restlessness or confusion, weakness or numbness, or any evidence of urinary or bowel incontinence.
Recommend that the child not play full contact sports for at least 1 week after all symptoms have stopped. Consult neurology and/or sports medicine specialist for patient and caregiver counseling to help avoid the “second hit” phenomenon where patients develop permanent neurologic symptoms after a second concussion soon after the first event.
A mild TBI/concussion is an injury to the brain that results from acceleration/deceleration or a blunt force and generally does not show up on any radiologic imaging modality.
Patients who suffer a TBI need to be evaluated by a professional, and thoughtful advice needs to be given regarding return to play.
Nasal septal hematomas are collections of blood between the avascular septal cartilage and perichondrium and are almost always associated with facial trauma such as from motor vehicle collisions, sporting injuries, or assault. Intranasal surgery may also cause such an injury. Buckling forces result in tearing of the submucosal vessels underlying the perichondrium. Because the perichondrium is the sole blood supply to the cartilage, hematomas result in avascular necrosis of the cartilage if not drained promptly. Stagnant blood may promote bacterial proliferation and abscess formation as well. Accompanying fracture of the 2- to 4-mm-thick septal cartilage may lead to the formation of bilateral hematomas. Common complaints include nasal obstruction, pain, and epistaxis. Fever is less frequent in the acute phase, but may mark the progression of a hematoma to an abscess. Associated physical findings include external nasal deformity and significant tenderness to palpation. Early diagnosis and drainage is critical to prevent consequences of cartilaginous ischemia, including septal perforation and saddle-nose deformity. Failure to manage these collections may result in more serious complications, including intracranial abscesses, orbital cellulitis, meningitis, and cavernous sinus thrombosis.
Perform a physical examination with a nasal speculum and a headlight. An asymmetric septum with a blue or red hue confirms the diagnosis and direct palpation along the septum with a gloved finger or cotton-tipped applicator will reveal swelling or fluctuance. Use endoscopic nasal examination with a fiberoptic scope to better visualize the hematoma and better determine its extent.
Perform incision and drainage as soon as possible; this may require ENT consultation and may need to be done in an operating room, especially in young children. Incise the mucosa over the area of greatest fluctuance without involving the cartilage. If bilateral hematomas are present, stagger the incisions to avoid iatrogenic perforation. Suction clots and purulent fluid and collect cultures. Place a small passive drain, such as a cut penrose or large vessel loop, under the septal flap to prevent reaccumulation and suture it to the edge of the incision. Place small bilateral anterior packs in the nostrils to provide tamponading pressure and prevent recollection. The packs may be removed within 2 to 3 days. Initiate antibiotics that cover gram-positive and β-lactamase producing organisms. Obtain a CT scan of the brain and sinuses in any patient with signs of systemic infection to rule out septal abscess. Refer patients for follow-up with an otolaryngologist to remove packing and drains within 5 to 7 days. Patients will also need annual follow-up for monitoring of septal developmental abnormalities due to potential septal cartilage destruction.
Septal hematomas in children can occur with minor trauma, including simple falls or altercations. Younger children, including infants and toddlers, presenting with septal hematomas without concomitant injuries should raise the suspicion of child abuse.
Abscess formation is the most common complication of septal hematomas; failure to manage this collection may result in serious complications including intracranial abscesses, orbital cellulitis, meningitis, and cavernous sinus thrombosis.
Nasal fractures are the most common facial fractures in children and must not be confused with nasoorbitoethmoid (NOE)–type injuries, which are far less numerous. Typical etiologies of nasal trauma include falls, sports injuries, motor vehicle collisions, and physical confrontations. The nasal bones articulate with the nasal septum, which can also be fractured. Patients may complain of pain and nasal obstruction. Significant obstruction may result in mouth breathing and new-onset snoring. Fracture/dislocations of the nasal bones are typically associated with swelling and ecchymosis in the region and occasionally an overlying laceration. Many patients will also present with epistaxis.
Manage immediate life-threatening injuries first and stabilize airway, breathing, and circulation. Perform a complete physical examination, including a nasal speculum examination to exclude septal hematoma. Control epistaxis with cold packs and light pressure and consider use of topical decongestants to help control bleeding and aid visualization as well. If these methods do not stop the bleeding, use nasal packing. Document mucosal lacerations, septal deviation, or septal hematoma.
Order plain films or maxillofacial noncontrast CT when the history and physical findings suggest injuries more complex than a nondisplaced, isolated nasal fracture.
Refer patients with nasal pyramid deformity or obstruction to a facial trauma surgeon for closed nasal reduction under general anesthesia within 3 days. Because healing in children is faster than in adults, closed nasal reduction should be planned 4 to 7 days after the injury to be effective and avoid sequelae.
| Clinical Finding | Isolated Nasal Fracture | NOE Complex Fracture |
|---|---|---|
| Mucosal lacerations | +/− | +/− |
| Bony step-offs or deviations | +/− | + |
| Swelling or edema | ++ | +++ |
| Septal disruption | + | + |
| Septal hematoma | +/− | +/− |
| CSF rhinorrhea | − | +/− |
| Double vision or decreased visual acuity | − | +/− |
| Localized facial numbness | − | +/− |
| Telecanthus | − | ++ |
| Enophthalmos | − | +/- |
| Nasal telescoping | − | ++ |
| Flattened nasal dorsum | − | ++ |
| Periorbital ecchymosis | +/− | ++ |
Patients may be discharged with analgesics such as acetaminophen or narcotics and discharge instructions to avoid nose blowing and heavy lifting or physical exertion. Instruct patients to use cold packs to decrease swelling. Prescribe prophylactic antibiotics that cover gram-positive bacteria to prevent toxic shock syndrome to all patients with nasal packing.
Figure 20.19 ▪ Nasal Fracture.
An axial CT slice demonstrates bilateral comminuted nasal bone fractures (arrows) that were sustained when an unrestrained driver hit his face on the steering wheel in a MVA. There is also nasal septal deviation. (Photo/legend contributors: Mark Silverberg, MD/John Amodio, MD.)
The mandible is one of the most frequently fractured bones in children, and falls and motor vehicle collisions are the most common causes. In older children, mandible fractures may result from sports injuries and interpersonal violence. The condyle is the most common fracture site, representing up to 50% of all mandible fractures. In 20% of patients, both condyles will be fractured. Older children are potentially exposed to higher velocity/higher impact injuries, with resulting greater degrees of displacement and comminution. There is a significant rate of associated neurologic or other injuries among these patients.
Jaw pain and lip or tooth numbness may be present secondary to injury to the inferior alveolar nerve and there may be associated dental injuries or tooth avulsions that must be documented. Physical examination may reveal trismus and pain with jaw opening, floor of mouth swelling, or hematoma. Some fractures may result in retrognathia and tongue collapse with airway obstruction. Intraoral lacerations may also be seen. Deviation of the jaw with opening can suggest the presence of a condylar fracture with occlusion shifted as well. Ecchymosis over the chin or lacerations of the ear canal are external signs associated with some mandibular fractures.
Perform a complete physical and stabilize the patient as a first priority, including a facial trauma survey with palpation of the bony craniofacial skeleton for step-offs, mobile bony segments or crepitus, and a neurosensory assessment with attention to cranial nerve function, particularly the trigeminal nerve. Obtain panoramic radiograph or panorex if the patient is able to sit upright. If the patient cannot sit or c-spine immobilization is needed, a plain-film mandible series may be shot although maxillofacial CT scan (with axial and coronal reconstruction) is more commonly used. Multiplane protocols allow better visualization of fracture fragments or dislocations. If physical examination findings suggest a possible mandible fracture but plain radiographs are negative, consider obtaining a CT to rule out Greenstick or incomplete fractures. If other facial fractures are present, a CT scan is mandatory.
Consult facial trauma surgery for all mandible fractures and dentistry if associated dental trauma is present. Obtain a chest radiograph in patients with avulsed teeth that cannot be accounted for to rule out tooth aspiration. Provide temporary stabilization of fractured mandibular segments with circumdental wires, such as a bridle wire, until definitive management is planned. In young children, this requires sedation and is most easily accomplished in a procedure suite or the operating room.
Admit patients with floor of mouth swelling, associated midfacial fractures, pain resulting in poor oral intake, severe associated soft tissue injury requiring operative repair or pain that is not well controlled with oral analgesia. All other patients may be discharged with appropriate follow-up and adequate analgesia. Acetaminophen with codeine or other opioid narcotics are appropriate choices. Mandibular fractures in children heal more quickly than in adults, so follow-up appointment should be scheduled within 24 to 72 hours if open reduction is being considered. Provide antibiotics that cover oral flora for a minimum of 7 days and instruct patients to adhere to a soft diet.
Mandible fractures can occur in predictable patterns (eg, combination of a symphyseal fracture with bilateral condylar fractures, a body fracture with a contralateral condylar fracture, parasymphyseal fractures with unilateral or bilateral condylar fractures). Exclude a possibility of a second fracture with appropriate imaging and clinical examination.
Exclude condylar fracture in a patient with chin ecchymosis, chin laceration, or a history of a blow to the chin from a punch, a fall, or the chin hitting the dashboard of an automobile.
Figure 20.23 ▪ Mandible Fractures.
(A) A coronal CT of a 12-year-old with bilateral condylar fractures that can result from forces directed at the chin. Greenstick (incomplete) fractures are common in the pediatric mandible as seen in the left condylar fracture (arrow). (B) A coronal CT in a different patient demonstrates comminuted fracture of the left parasymphyseal region of the mandible (arrow). Pediatric mandible fractures are often nondisplaced, and more amenable to conservative management. (Photo contributor: Sydney Butts, MD.)
Figure 20.24 ▪ Mandible Fracture.
(A, B) This 17-year-old patient was hit by a bus and sustained a comminuted mandible fracture and severe lower lip and cheek lacerations. Significant mandibular comminution can result from high-velocity injuries. The patient also had a maxillary dental alveolar fracture and multiple avulsed maxillary teeth. (Photo contributor: Sydney Butts, MD.)
Fractures of the midface and upper face with various degrees of bony disruption are usually caused by motor vehicle accidents, falls, and interpersonal violence. There are several important anatomical features of the pediatric craniofacial skeleton. The paranasal sinuses are not fully formed at birth. Before the development of the maxillary sinuses, pure Le Fort pattern fractures are rare. Similarly, frontal sinus fractures are rare until at least school age as postnatal development of the frontal sinus is not significant until the adult size is attained in adolescence. The lack of frontal sinuses and prominence of the calvaria in infants and toddlers results in a higher proportion of frontal skull and skull base fractures.
The Le Fort fracture patterns describe fracture lines that occur with some reproducibility after impact forces delivered to the maxilla. Varying degrees of midfacial retrusion and elongation are the hallmarks of these bony disruptions. The Le Fort I fracture line runs just above the maxillary alveolus from the rim of the pyriform aperture laterally ending at the pterygoid plates posteriorly. Patients will present with malocclusion—often an anterior open bite—and the alveolus will be mobile when manipulated. The Le Fort II fracture is also known as a pyramidal fracture. These fracture lines begin at the root of the nose where the nasal bones articulate with the frontal bones and run inferolaterally across the medial orbital walls to the lateral maxilla. The Le Fort III fracture is also referred to as craniofacial separation. This high fracture line results in maxillary separation from the cranial base. Step-offs and bony mobility will be palpable at the fracture sites. Hypesthesia of the second division of the trigeminal nerve (V2) is a common finding. Significant epistaxis may be a presenting feature in Le Fort II/III fractures, CSF rhinorrhea from a concomitant skull base injury may also be present. Many patients have marked midfacial edema and periorbital ecchymosis. Patients may also complain of visual acuity change, diplopia, or other ocular symptoms related to the fracture’s disruption of the bony orbit.
Several physical findings distinguish naso-orbital ethmoid (NOE) fractures from other midface fractures. The fractured segment of bone that results from an NOE fracture is demarcated medially by the nasal cavity, laterally by the orbit, and superiorly by the anterior skull base. This segment of bone is the site of attachment of the medial canthal tendon. The 3 types of fractures, as described by Markowitz, are defined by worsening severity of comminution of this central region, with the most severe resulting in marked comminution and avulsion of the medial canthal tendon from the bone. Physical findings include extraocular muscle restriction resulting in diplopia, nasal obstruction (lateral nasal wall impingement), epiphora, telecanthus (lateral displacement of the medial canthus) and loss of nasal dorsal support with telescoping. The proximity of the skull base and frontal sinus results in frequent simultaneous injuries of these regions.
Frontal sinus fractures are rare under the age of 6 years, as pneumatization of the frontal bone is not significant until then. Forehead lacerations, deformity, and hypesthesia of the first division of the trigeminal nerve (V) are physical findings associated with fractures of the anterior table of the frontal sinus. Fractures of the posterior table of the frontal sinus can result in dural lacerations and leakage of the CSF from the nose. CSF rhinorrhea is a presenting feature in 18% to 30% of frontal sinus fractures and should be actively sought by holding the patient’s head in a dependent position and looking for clear fluid leakage. A significant percentage of children with frontal sinus fractures will have an additional craniofacial fracture or intracranial injury.
Provide hemodynamic resuscitation and secure the airway first. Order CT imaging of the head and facial bones (axial and coronal planes). Request ophthalmologic consultation for any midfacial fractures that involve the orbit, or in any patient with a change in visual acuity or positive findings on the initial ocular assessment. Document visual acuity, pupillary reflexes, and extraocular muscle motility.
Consult otolaryngology for all patients with unresolving epistaxis. Approach patients with skull base fractures who require intranasal packing to control bleeding with extreme caution to avoid worsening of the cranial base injury. Obtain otolaryngology and neurosurgery evaluations for all patients with CSF rhinorrhea. If possible, collect the fluid and send for glucose and β2-transferrin to confirm its origin.
Débride, clean, and repair minor facial lacerations in the emergency department. Repair more extensive lacerations in the operating room where better anesthesia and hemostasis can be achieved. It may be possible to use lacerations to access underlying fractures, obviating the need to make additional incisions. In these cases, irrigate the wounds and dress it with sterile gauze. Provide prophylactic antibiotics against gram-positive bacteria and anaerobes.
Figure 20.29 ▪ Nasoorbitoethmoid Fracture (NOE).
Single axial view at the level of the orbits in soft tissue algorithm demonstrates multiple fractures of the medial orbital walls and nasal septum. There is bilateral preseptal periorbital soft tissue edema. Hyperdensity in the right choroidal space of the right globe is compatible with choroidal hemorrhage. The left globe is deformed and not completely imaged; globe rupture and vitreous hemorrhage cannot be excluded. A characteristic V-shape of the posterior globe may represent an orbital hematocyst (tented globe). (Photo/legend contributors: Barry Hahn, MD/Steven Pulitzer, MD.)
Admit patients with midfacial trauma as there is a high incidence of associated neurologic injuries or other injuries distant to the head and neck. Discharge only those with the mildest injuries after evaluation by the facial trauma team with arrangements made for close follow-up.
NOE fractures can be misdiagnosed as simple nasal bone fractures. Overlying edema and inability to examine anxious or uncooperative patients are obstacles to diagnosis.
High impact forces, massive midfacial swelling, V2 sensory disturbance, and ocular signs and symptoms raise suspicion of a midfacial fracture rather than an isolated nasal fracture.
Involve the facial trauma surgeons early to avoid complications of facial growth restriction, subsequent procedures, and suboptimal function.
Orbital blowout fractures involve the thin bones of the floor and medial wall of the orbit while the orbital rim remains intact. These typically result from impact by a projectile larger than the orbit, such as a ball or fist. Because of the high incidence of concomitant intraocular injury, an ocular examination must always be performed on patients who have sustained orbital trauma. Common signs and symptoms include lid edema and ecchymosis, diplopia, enophthalmos, and infraorbital nerve hypesthesia. Air leakage from the sinuses may manifest as orbital emphysema, which will demonstrate crepitus on palpation of the lids or globe proptosis if severe. Binocular diplopia can occur if there is gaze restriction due to extraocular muscle swelling or entrapment.
Figure 20.30 ▪ Orbital Floor Blow-Out Fracture.
(A) An adolescent patient after blunt trauma to left orbit with an elbow. (B) Same patient with severe limitation on superior excursion. His dilated left pupil is due to eye drops to facilitate the posterior eye examination and not due to traumatic injury. (C) A coronal CT scan shows entrapment of the inferior rectus muscle and soft tissue attachments. Because the fracture size is small, and the tissue is minimally incarcerated, radiologic diagnosis can be missed. Urgent surgical repair is advised when signs of entrapment of the inferior rectus muscle or nearby attachments exist clinically and on the CT scan. (Photo contributor: Roman Shinder, MD.)
Figure 20.31 ▪ Orbital Floor Blow-Out Fracture.
(A) Left eye enophthalmos is appreciated 1 week after the injury in this patient. It is useful to determine the presence of enophthalmos by viewing the globe position after the periorbital edema subsides. The larger the fracture, the greater the likelihood of an enophthalmos. (B) A Coronal CT in a different patient demonstrates right orbital floor fracture with inferior displacement of fracture fragment into right maxillary sinus. (Photo contributors: Roman Shinder, MD. [A] and Mark Silverberg, MD. [B].)
Figure 20.32 ▪ Orbital Roof Fracture.
An axial CT slice shows a right orbital roof fracture (arrow) with a large orbital hematoma in a 3-year-old boy who had a television fall on his head. Such fractures are more common in young children and most do not require repair. (Photo contributor: Sydney Butts, MD.)
Obtain a CT scan of the orbits with axial and coronal reconstruction in all cases of suspected orbital fracture. Coronal sections offer the best view of the orbital floor. Examine the CT carefully for a “white eye” fracture, which is a trapdoor fracture with entrapment of the inferior rectus muscle. There is usually minimal loss of the floor integrity and a lack of blood in the maxillary sinus. However, on clinical examination there is significant limitation on vertical globe excursion associated with nausea, vomiting, bradycardia, or syncope. Immediate repair, usually within 24 hours, is indicated; consult a facial trauma surgeon urgently. If trapdoor fractures and entrapment are not present, discharge the patient with instructions not to blow his or her nose and to apply ice packs to the orbit for the first 24 to 48 hours. Nose blowing can cause intraorbital air entry from the paranasal sinuses that can lead to compressive optic neuropathy visual loss. Provide nasal decongestants and broad-spectrum antibiotics for 7 days.
Double vision is the most common complaint of patients with orbital blowout fractures.
Decreased motility due to entrapment is most commonly seen on superior excursion, though it may be seen in any direction.
As the swelling and hemorrhage within the orbit subside, eye movements will improve and the double vision will improve or resolve.
Consult surgery for open reduction of large fractures, nonresolving double vision, enophthalmos of 2 mm or more, or clinical entrapment.
In cases of extraocular muscle entrapment, urgent surgical consultation is necessary to prevent muscle ischemia, chronic motility disturbance, and diplopia.
Facial fractures are less common in children than in adults, and are more likely to occur in children older than 6 years of age. Midface fractures, which include the zygomas, are rare in children because of the elastic properties of the pediatric skeleton. The midface is stationed between the mandible and cranium, which absorb the impact of most traumatic forces directed to this area. Paired zygomas provide midfacial width and cheek projection and with their 4 suture attachments comprise the zygomaticomaxillary complexes (ZMCs). The zygomaticomaxillary suture is part of the lateral buttress (zygomaticomaxillary), which along with the medial buttress (nasomaxillary) and posterior buttress (pterygomaxillary) forms the 3 vertical support columns that absorb the forces of mastication. The term tripod fracture is the result of fractures involving the zygomaticomaxillary, zygomaticofrontal, and zygomaticotemporal sutures. However, a ZMC fracture is in fact a quadripod fracture because the fourth suture, the zygomaticosphenoid suture, is also involved.
Patients with zygomatic fractures present with a loss of malar projection (which can be seen from a bird’s-eye or worm’s-eye view), and bony step-offs at the orbital rim, frontozygomatic suture, or temporozygomatic suture. Possible ocular findings include enophthalmos, exophthalmos, restricted gaze, and diplopia. Other associated findings include hypesthesia of maxillary division of the trigeminal nerve and trismus (difficulty opening the mouth because of impingement of the coronoid process from a posteriorly displaced ZMC fracture).
Stabilize airway, breathing, and circulation and the cervical spine, and perform a full head and neck examination. Plain radiographs are of limited value. Order a high resolution (at most 1.5 mm thickness) maxillofacial CT scan with axial and either true coronal or reconstructed coronal view as this is the best imaging modality to evaluate midfacial fractures. Three-dimensional reformats may also be helpful when available. If the patient has a mobile or displaced ZMC or zygomatic arch fracture with a cosmetic or functional deformity, consult a facial trauma surgeon. Manage patients with isolated nondisplaced or minimally displaced zygomatic arch or ZMC fractures with supportive care, observation, and instructions to follow up in 7–10 days.
Figure 20.34 ▪ Zygomatic Arch Fractures.
(A) This “jughandle” view of the skull shows a mildly displaced right zygomatic arch fracture (arrow). (B) An axial CT slice shows a comminuted fracture of the right zygomatic arch with severe medial displacement resulting in impingement on the coronoid process of the mandible. This is also known as a “W” fracture because of its shape (arrow). (Photo/legend contributors: Mark Silverberg MD/John Amodio, MD.)
Figure 20.35 ▪ Tripod Fracture.
(A) Drawing illustrating the quadripod nature of the zygoma. (B) A maxillofacial axial CT slice in an adolescent status post assault shows a displaced left ZMC fracture. The malar process has been pushed backwards, resulting in a typical ZMC fracture (long arrow). Also notice the subcutaneous air (short arrow) that probably escaped from the maxillary sinus at the time of the trauma. (Illustration by Kit Hefner, MS, CMI-Manager, Medical Illustration & Graphics, SUNY Upstate Medical University Syracuse, New York, [A] and Photo contributor: Sydney Butts, MD [B].)
The ZMC provides facial width and cheek bone shape.
The ZMC is a quadripod complex and not a tripod structure because of its articulation with the temporal, maxillary, frontal, and sphenoid bones.
ZMC or zygomatic arch fractures that cause cosmetic or functional deformities will likely require surgical intervention.
Facial injuries that involve the soft tissue can result from either blunt or penetrating trauma, and may occur in isolation or with associated facial skeletal fractures. Soft tissue injuries can range from simple lacerations to avulsion injuries with significant tissue loss. Animal bites can also be a cause of soft tissue injuries of the face in children. Interpersonal violence resulting in stabbing or human bites are additional causative factors in adolescents. Several specific subsites have unique presentations that must be recognized and managed appropriately.
Penetrating injury to the cheek can result in transsection of the parotid or Stensen’s duct that runs horizontally, just inferior to the zygomatic arch, and parallel to the buccal branch of the facial nerve, explaining the concurrence of facial nerve injuries in a significant number of duct injuries. Wound exploration may reveal pooling of saliva, especially on parotid massage, suggesting injury. Confirm the diagnosis by cannulating the duct from its intraoral opening with a lacrimal probe. The tip of the probe will be visualized within the wound.
Injuries of the lateral cheek/preauricular region, especially near the tragus of the ear, can result in the main trunk of the facial nerve being severed. The temporal branch of the facial nerve, which is responsible for forehead movement, is vulnerable along a path from the tragus to the lateral brow. The marginal mandibular branch may be transected when the injury occurs in the region of the lower border of the mandible. Paralysis of this branch results in elevation of the corner of the mouth. The zygomatic and buccal branches are vulnerable in the midcheek region. Inability to close the eye and drooping of the upper lip are the sequelae, respectively. It is imperative that all facial nerve branches are evaluated prior to any manipulation of the wound. Penetrating injuries of the lateral cheek may also result in trauma to the external carotid artery with acute hemorrhage.
Injury to the ear is complicated by the involvement of cartilage or soft tissue loss. Composite tissues losses (skin and cartilage for example) require special attention if successful reimplantation or partial salvage of the tissue is to be achieved.
Eyelid lacerations, periocular trauma, and injury to the nasal lacrimal system constitute several possible soft tissue injuries. Excessive tearing (epiphora) is one cardinal sign that the nasal lacrimal ductal system is not functioning.
Scalp trauma includes simple lacerations to complex avulsions with exposed calvarial bone. Scalp avulsions often occur between the galea aponeurosis layer and the periosteum of the skull; however, the entire scalp layer may be missing, leaving exposed bare bone. Scalp injuries can be associated with massive hemorrhage (5 arterial branches that provide blood supply to the scalp emanate from both internal and external carotid arteries).
First stabilize airway, breathing, and circulation following Advanced Trauma Life Support (ATLS) protocols. Next begin evaluation of the facial trauma and provide tetanus and antibiotic prophylaxis with coverage of gram-positive organisms and anaerobes if the injury involves the nasal, pharyngeal, or oral cavities. Use simple pressure, gauze packing, hemostatic agents, or vessel ligation for hemostasis at the wound site. If there is massive hemorrhage from a significant arterial bleed, perform vessel exploration and ligation in the operating room. In some severe instances, obtain interventional radiology consultation for embolization.
Explore all wounds under sterile conditions after copious irrigation with sterile normal saline and close all wounds that can be safely repaired in the emergency department, optimally in a separate treatment area for privacy, minimization of patient/caregiver anxiety, and proper lighting and instrumentation. Facial wounds heal very well given their excellent blood supply; primary closure up to 24 hours after the injury is acceptable. Consider the use of conscious sedation to facilitate the repair. Otherwise, a low threshold for intraoperative repair should be adopted in the pediatric population.
If parotid duct injury is suspected, consult otolaryngology or plastic surgery. If a duct injury is confirmed, send the patient to the operating room for repair.
Diagnosis of a facial nerve injury is easiest when the patient is conscious and can follow commands. Consult the facial trauma team if there is a mechanism that may have resulted in facial nerve injury in an unconscious or unresponsive patient to coordinate the timing of wound exploration. It is possible for a seemingly minor penetrating trauma to be underestimated in the light of more serious injuries. Intraoperative exploration and repair of nerve transections should occur within 3 days of the injury.
Repair lacerations of the ear that extend through the skin to the cartilage without tissues loss by reapproximating the cartilage followed by soft tissue repair. If skin is absent and cartilage is exposed, use soft tissue advancement to avoid the need for daily wound care with antibiotic ointment and sterile dressing. If ear tissue is avulsed, reattach it primarily noting that avulsed ear tissue longer than 1.5 cm is not likely to survive. Other options include delayed reconstruction or banking the cartilage (removing the outer layer of skin) underneath the temporal scalp so that it can be used in the future secondary repair as a structural graft. For large, near total ear avulsion injuries, consult otolaryngology or surgery for microvascular techniques of reattachment.
Similar tenets of repair apply to the nose as to the ear, particularly if there is a composite injury. Use layered closure of wounds (nasal lining, cartilage, deep soft tissue, and skin).
Consult ophthalmology for all periocular trauma for a comprehensive examination of the globe. If possible, consult oculoplastic surgery for evaluation and management of patients with these delicate injuries to avoid secondary complications.
Repair extensive scalp injuries in the operating room and consult neurosurgery for concomitant skull or intracranial injury. Even seemingly minor degrees of tissue loss are challenging wounds to close as scalp tissue is quite inelastic. If repair can be accomplished in the ED, use layered closure with attention to repair of the galea aponeurosis and then the skin to prevent soft tissue depressions. Use pressure dressings or passive drains as needed.
Salivary duct injuries require surgical subspecialist consultation to repair.
Auricular avulsions are injuries where initial intervention makes a significant impact on outcome. If the avulsed ear can be salvaged, it should be put on ice immediately.
Figure 20.37 ▪ Auricular Trauma.
(A) Composite injuries to the ear involve multiple tissue types such as cartilage, connective tissue, and skin. Each must be approximated in the appropriate manner. (B) The same patient after his multiple layer closure. This wound should be examined by a physician in 24 to 48 hours to make sure the tissue is viable. (Photo contributor: Mark Silverberg, MD.)
Emergency physicians frequently care for children with lip lacerations. Common causes of lip trauma include falls, sports-related injuries, assaults, motor vehicle collisions, and animal or human bites. Patients may present with isolated lip lacerations or with lip wounds that occur in conjunction with other oral-maxillofacial injuries. It is important to appreciate the anatomic boundaries of the lip. The vermilion border marks the transition between the dry mucosa of the lip and the facial skin. Lip lacerations that extend beyond the vermilion border require meticulous evaluation and repair in order to achieve optimal cosmetic results.
Lip lacerations that result in disruption of the vermilion border require special care in order to avoid cosmetic deformity. Wound repairs with even small degrees of malalignment at the vermilion border will have an unacceptable cosmetic result. Thorough wound evaluation and preservation of the anatomic alignment of the vermilion border are the key elements in achieving optimal wound closure.
Carefully evaluate the laceration and the intraoral cavity for underlying alveolar fractures or loose, missing, or damaged teeth. Anesthetize the wound using a regional nerve block to prevent deformation of the wound edges and shape. Irrigate the wound and place the first suture to approximate the edges of the vermilion border. If the injury extends to the orbicularis oris muscle, repair the musculature with buried absorbable sutures, taking care to maintain good alignment. Use similar absorbable sutures to close the defect inside the vermilion border. Next, approximate the skin edges. In young children, use rapidly absorbable sutures on all tissues to avoid the additional anguish of suture removal. In older children, use monofilament nonabsorbable sutures on skin beyond the vermilion border, which should be removed in 3 to 5 days.
Coloring the wound edges with a surgical skin marker or methylene blue will aid with proper alignment of the vermilion border.
Injected local anesthesia may distort anatomy and interfere with wound margin approximation. An infraorbital nerve block can be used for the upper lip, and a mental nerve block will anesthetize the lower lip.
Gentle traction applied to the initial anchoring suture placed at the vermilion border can help approximate underlying tissue and facilitate wound closure.
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