Updated: Mar 6, 2008
Hippocrates described an array of facial injuries as long ago as 400 BCE. In 1823, von Graeffe described the use of an elastic tube placed in the nares to maintain an open airway. During the early 20th century, Sir Harold Gilles, father of plastic surgery, taught army personnel about breathing problems in patients with facial injuries. He recommended positioning them supine to maintain an airway. Frenchman René Le Fort studied cadavers in 1901 and described 3 basic types of facial fractures. Endotracheal anesthesia and radiography, developed during the First World War, led to a better understanding and treatment of facial fractures. During the Second World War, a multidisciplinary approach to treatment of facial fractures continued to improve outcomes of severely injured soldiers. Advent of CT-guided reconstruction, along with new surgical techniques, has improved the final appearance of patients with bony injuries immensely.
Maxillofacial fractures are the result of blunt or penetrating trauma. Most are blunt injuries caused by vehicular crashes, altercations, sporting-related trauma, occupational injuries, and falls. Penetrating injuries are mainly the result of gunshot wounds, stabbings, and explosions.
Determinants of type of injury (ie, soft tissue alone vs bony) are shape and velocity of the striking object.
The amount of force needed to fracture different bones of the face has been studied, and these bones have been divided into those that require high impact to fracture (greater than 50 times the force of gravity [g]) and those that require only low impact to fracture (less than 50 g).
Mandibular fractures usually occur in 2 or more locations because of the bone's U shape and articulations at the temporomandibular joints. Fractures also may occur at a site apart from the site of direct trauma. A large percentage of mandibular fractures are open, as they often fracture between teeth and communicate with the oral cavity.
Different mechanisms are associated with varying locations. Fractures from automobile crashes most frequently occur at the condyle and symphysis, those from motorcycle accidents at the symphysis and alveolus, and those from altercations mostly at the condyles, angles, and body.
For more information, see Medscape's Trauma Resource Center.
The mandible is the third most fractured bone of the face. Of these fractures, approximately 20-35% are at the condyle and ramus, 20-30% at the angle, 15-30% at the body, 8-20% at the symphysis, and 1-5% at the alveolar ridge.
One study placed the incidence of severe maxillofacial injury (fractures, lacerations) at 0.04-0.09% for motor vehicle crashes. Incidence of fractures due to motor vehicle injuries is higher in rural areas; altercation-related injuries are more frequent in inner cities.
Adult male-to-female ratio is 3:1. Suspect domestic violence or sexual assault in women as this may coexist in 30% of cases.
Male predominance is reduced to 3:2 in children. In nonmotor vehicle injury, the possibility of child abuse should be a concern.
Dislocations, Mandible
Foreign Bodies, Trachea
Fractures, Face
Neck Trauma
Pediatrics, Child Abuse
Airway obstruction
Aspiration of avulsed teeth
Other major traumatic injuries
Dentate, avulsed
Dentate, displaced
Dentate, fractures
When airway control is needed, rapid sequence induction often is the preferred method. Rapid sequence induction utilizes medications to induce unconsciousness and muscle paralysis to facilitate intubation. Cricothyroidotomy kit should be at the bedside in case problems arise.
Medication for pain control is appropriate, including NSAIDs, narcotics, and local anesthetics.
Patients with open fractures, which are the majority, should be given IV antibiotics. Current choices are penicillin or a cephalosporin. In penicillin-allergic patients, clindamycin is a good alternative. If the patient has an open wound, administer tetanus toxoid if the patient is not current.
These agents are used most commonly for relief of mild to moderately severe pain. Effects of NSAIDs in treatment of pain tend to be patient specific, yet ibuprofen is usually the DOC for initial therapy. Other options include flurbiprofen, ketoprofen, and naproxen.
Usually DOC for treatment of mild to moderately severe pain, if no contraindications. Inhibits inflammatory reactions and pain, probably by decreasing activity of enzyme cyclooxygenase, which inhibits prostaglandin synthesis.
200-400 mg PO q4-6h prn; not to exceed 3.2 g/d
<6 years: Not established
6 months to 12 years: 20-40 mg/kg/d PO divided tid/qid
>12 years: Administer as in adults
Aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity; may decrease effects of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT in patients taking anticoagulants—monitor PT closely and instruct patients to watch for signs of bleeding; may increase risk of methotrexate toxicity; may increase phenytoin levels
Documented hypersensitivity; peptic ulcer disease; recent GI bleeding or perforation; renal insufficiency; high risk of bleeding
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in congestive heart failure, hypertension, and decreased renal and hepatic function; caution in coagulation abnormalities or during anticoagulant therapy
For relief of mild to moderately severe pain and inflammation.
Administer small dosages initially to patients with small bodies, older persons, and those with renal or liver disease.
Doses higher than 75 mg do not increase therapeutic effects. Administer high doses with caution and closely observe patient for response.
25-50 mg PO q6-8h prn; not to exceed 300 mg/d
<3 months: Not established
3 months to 12 years: 0.1–1 mg/kg PO q6-8h
>12 years: Administer as in adults
Aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity; may decrease effects of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT in patients taking anticoagulants—monitor PT closely and instruct patients to watch for signs of bleeding; may increase risk of methotrexate toxicity; may increase phenytoin levels
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in congestive heart failure, hypertension, and decreased renal and hepatic function; caution in coagulation abnormalities or during anticoagulant therapy
Used for relief of mild to moderately severe pain. Inhibits inflammatory reactions and pain by decreasing activity of enzyme cyclooxygenase, which decreases prostaglandin synthesis.
500 mg PO followed by 250 mg q6-8h; not to exceed 1.25 g/d
<2 years: Not established
>2 years: 2.5 mg/kg/dose PO; not to exceed 10 mg/kg/d
Aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity; may decrease effects of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT in patients taking anticoagulants—monitor PT closely and instruct patients to watch for signs of bleeding; may increase risk of methotrexate toxicity; may increase phenytoin levels
Documented hypersensitivity; peptic ulcer disease; recent GI bleeding or perforation; renal insufficiency
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Acute renal insufficiency, interstitial nephritis, hyperkalemia, hyponatremia, and renal papillary necrosis may occur; patients with preexisting renal disease or compromised renal perfusion risk acute renal failure; leukopenia occurs rarely, is transient, and usually returns to normal during therapy; persistent leukopenia, granulocytopenia, or thrombocytopenia warrants further evaluation and may require discontinuation of drug
Has analgesic, antipyretic, and anti-inflammatory effects. May inhibit cyclooxygenase enzyme, decreasing prostaglandin biosynthesis.
200-300 mg/d PO divided bid/qid
Not established
Aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity; may decrease effects of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT in patients taking anticoagulants—monitor PT closely and instruct patients to watch for signs of bleeding; may increase risk of methotrexate toxicity; may increase phenytoin levels
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Acute renal insufficiency, interstitial nephritis, hyperkalemia, hyponatremia, and renal papillary necrosis may occur; patients with preexisting renal disease or compromised renal perfusion risk acute renal failure; leukopenia occurs rarely, is transient, and usually returns to normal during therapy; persistent leukopenia, granulocytopenia, or thrombocytopenia warrants further evaluation and may require discontinuation of drug
Pain control is essential to quality patient care. It ensures patient comfort, promotes pulmonary toilet, and aids physical therapy regimens. Many analgesics have sedating properties that benefit patients who have sustained fractures.
DOC for treatment of pain in patients with documented hypersensitivity to aspirin or NSAIDs or in those with upper GI disease or taking oral anticoagulants.
325-650 mg PO q4-6h or 1000 mg tid/qid; not to exceed 4 g/d
<12 years: 10-15 mg/kg/dose PO q4-6h prn; not to exceed 2.6 g/d
>12 years: 325-650 mg PO q4h; not to exceed 5 doses q24h
Rifampin can reduce analgesic effects; barbiturates, carbamazepine, hydantoins, and isoniazid may increase hepatotoxicity
Documented hypersensitivity; known G-6-P deficiency
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Hepatotoxicity possible in chronic alcoholics following various dose levels; severe or recurrent pain or high or continued fever may indicate a serious illness; acetaminophen is contained in many OTC products and combined use with these products may result in cumulative acetaminophen doses exceeding recommended maximum dose
Drug combination indicated for treatment of mild to moderately severe pain.
30-60 mg/dose based on codeine content PO q4-6h or 1-2 tabs q4h; not to exceed 12 tab/d
0.5-1 mg/kg/dose based on codeine content PO q4-6h; 10-15 mg/kg/dose based on acetaminophen content; not to exceed 2.6 g/d of acetaminophen
CNS depressants or tricyclic antidepressants increase toxicity
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in patients dependent on opiates since this substitution may result in acute opiate-withdrawal symptoms; caution in severe renal or hepatic dysfunction
Drug combination indicated for relief of moderately severe to severe pain.
1-2 tab/cap PO q4-6h prn
<12 years: 10-15 mg/kg/dose acetaminophen PO q4-6h prn; not to exceed 2.6 g/d of acetaminophen
>12 years: 750 mg acetaminophen PO q4h; single dose not to exceed 10 mg of hydrocodone bitartrate; not to exceed 5 doses/d
Phenothiazines may decrease analgesic effects; CNS depressants or tricyclic antidepressants increase toxicity
Documented hypersensitivity; high-altitude cerebral edema; elevated intracranial pressure
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Tablets contain metabisulfite, which may cause hypersensitivity; caution in patients dependent on opiates since this substitution may result in acute opiate-withdrawal symptoms; caution in severe renal or hepatic dysfunction
Drug combination indicated for relief of moderately severe to severe pain. DOC for aspirin-hypersensitive patients.
1-2 tab/cap PO q4-6h prn
0.05-0.15 mg/kg/dose oxycodone PO q4-6h prn; not to exceed 5 mg/dose of oxycodone
Phenothiazines may decrease analgesic effects; CNS depressants or tricyclic antidepressants increase toxicity
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Duration of action may increase in elderly persons; be aware of total daily dose of acetaminophen patient is receiving; do not exceed 4000 mg/24 h of acetaminophen; higher doses may cause liver toxicity
DOC for narcotic analgesia because of its reliable and predictable effects, safety, and ease of reversibility with naloxone. Administered IV, may be dosed in a number of ways and commonly is titrated until desired effect obtained.
Starting dose: 0.1 mg/kg IV/IM/SC
Maintenance dose: 5-20 mg/70 kg IV/IM/SC q4h
Relatively hypovolemic patients: Start with 2 mg
IV/IM/SC and reassess hemodynamic effects of dose
Neonates: 0.05-0.2 mg/kg IV/IM/SC prn
Children: 0.1-0.2 mg/kg IV/IM/SC q2-4h prn
Phenothiazines may antagonize analgesic effects; tricyclic antidepressants, MAOIs, and other CNS depressants may potentiate adverse effects
Documented hypersensitivity; hypotension; potentially compromised airway in which establishing rapid airway control would be difficult
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Avoid in hypotension, respiratory depression, nausea, emesis, constipation, and urinary retention; caution in atrial flutter and other supraventricular tachycardias; has vagolytic action and may increase ventricular response rate
Prophylaxis is given to patients with open fractures. Therapy must cover all likely pathogens in the context of the clinical setting.
Interferes with synthesis of cell wall mucopeptide during active replication, resulting in bactericidal activity against susceptible microorganisms.
2.4 million U IM as single dose in 2 injection sites
50,000 U/kg IM
Probenecid can increase effects; tetracyclines can decrease effects
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Caution in impaired renal function
Third-generation cephalosporin that has broad-spectrum activity against gram-negative organisms, lower efficacy against gram-positive organisms, and higher efficacy against resistant organisms. By binding to one or more penicillin-binding proteins, arrests bacterial cell wall synthesis and inhibits bacterial growth.
1-2 g IV qd/bid for 5-7 d; not to exceed 4 g/d
>7 days: 25-50 mg/kg/d IV; not to exceed 125 mg/d
Infants and children: 50-75 mg/kg/d IV q12h; not to exceed 2 g/d
Probenecid may increase levels; ethacrynic acid, furosemide, and aminoglycosides may increase nephrotoxicity
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Adjust dose in renal impairment; caution in breastfeeding women and allergy to penicillin
Lincosamide useful as a treatment against serious skin and soft-tissue infections caused by most staphylococci strains. Also effective against aerobic and anaerobic streptococci, except enterococci. Inhibits bacterial protein synthesis by inhibiting peptide chain initiation at bacterial ribosome, where it preferentially binds to 50S ribosomal subunit, inhibiting bacterial replication.
600-1200 mg/d IV/IM q6-8h depending on degree of infection
20-40 mg/kg/d IV/IM tid/qid
Increases duration of neuromuscular blockade induced by tubocurarine and pancuronium; erythromycin may antagonize effects; antidiarrheals may delay absorption
Documented hypersensitivity; regional enteritis; ulcerative colitis; hepatic impairment; antibiotic-associated colitis
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Adjust dose in severe hepatic dysfunction; no adjustment necessary in renal insufficiency; associated with severe and possibly fatal colitis
This agent is used for tetanus immunization. Booster injection in previously immunized individuals is recommended to prevent this potentially lethal syndrome.
Used to induce active immunity against tetanus in selected patients. Tetanus and diphtheria toxoids are immunizing DOC for most adults and children >7 y. Necessary to administer booster doses to maintain tetanus immunity throughout life.
Pregnant patients should receive only tetanus toxoid, not diphtheria antigen-containing product.
In children and adults, may administer into deltoid or midlateral thigh muscles. In infants, preferred site of administration is midthigh laterally.
Primary immunization: 0.5 mL IM, give 2 injections 4-8 wk apart and third dose 6-12 mo after second injection
Booster dose: 0.5 mL q10y
Administer as in adults
Patients receiving immunosuppressants, including corticosteroids or radiation therapy, may remain susceptible despite immunization due to poor immune response; cimetidine may enhance or augment delayed-hypersensitivity responses to skin-test antigens; avoid concurrent use of medication with systemic chloramphenicol since it may impair amnestic response to tetanus toxoid; concurrent use of tetanus immune globulin may delay development of active immunity by several days (interaction is nevertheless clinically insignificant and does not preclude its concurrent use)
Documented hypersensitivity; history of any type of neurological symptoms or signs following administration of this product
FDA recommends that elective tetanus immunization be deferred during any outbreak of poliomyelitis because tetanus toxoid injections are an important cause of provocative poliomyelitis
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Do not use to treat actual tetanus infections, or for immediate prophylaxis of unimmunized individuals (use instead tetanus antitoxin, preferably human tetanus immune globulin) diminished antibody response to active immunization may be seen in patients receiving immunosuppressive therapy; better to defer primary diphtheria immunization until immunosuppressive therapy discontinued; routine immunization of symptomatic and asymptomatic HIV-infected persons recommended
Patients who may not have been immunized against Clostridium tetani products should receive tetanus immune globulin.
Used for passive immunization of any patient with a wound that may be contaminated with tetanus spores.
Prophylaxis: 250-500 U IM in opposite extremity to tetanus toxoid
Clinical tetanus: 3,000-10,000 U IM
Prophylaxis: 250 U IM in opposite extremity to tetanus toxoid
Clinical tetanus: 3,000-10,000 U IM
None reported
Since antibodies in globulin preparation may interfere with immune response to vaccination, do not administer within 3 mo of live virus immune globulin administration; may be necessary to revaccinate persons who received immune globulin shortly after live virus vaccination
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Persons with isolated IgA deficiency have potential for developing antibodies to IgA and could have anaphylactic reactions to subsequent administration of blood products that contain IgA; do not perform skin testing since intradermal injection of concentrated gamma globulin may cause localized area of inflammation and can be misinterpreted, causing the medication to be withheld from a patient not allergic to this material; true allergic responses to human gamma globulin given in prescribed IM manner are extremely rare; do not admix with other medications since usually incompatible
Glynn SM, Asarnow JR, Asarnow R, et al. The development of acute post-traumatic stress disorder after orofacial injury: a prospective study in a large urban hospital. J Oral Maxillofac Surg. Jul 2003;61(7):785-92. [Medline].
Hendler B. Maxillofacial trauma. In: Rosen P, ed. Emergency Medicine: Concepts and Clinical Practice. Mosby-Year Book; 1998:1093-1103.
McGill J, Ling L, Taylor S. Facial trauma. In: Diagnostic Radiology in Emergency Medicine. Mosby-Year Book; 1992:51-76.
Smith R. Maxillofacial injuries. In: Harwood-Nuss A, ed. The Clinical Practice of Emergency Medicine. Lippincott, Williams & Wilkins Publishers; 1991:337-43.
Snell R, Smith M. The face, scalp, and mouth. In: Clinical Anatomy for Emergency Medicine. Mosby-Year Book; 1993:206-41.
Spoor T, Ramocki J, Kwito J. Ocular trauma. In: Wilson RF, Walt AJ, eds. Management of Trauma: Pitfalls and Practice. 2nd ed. Lippincott, Williams & Wilkins; 1996:225-41.
Sullivan W. Trauma to the face. In: Wilson RF, Walt AJ, eds. Management of Trauma: Pitfalls and Practice. 2nd ed. Lippincott, Williams & Wilkins; 1996:242-69.
McKay MP. Facial trauma. In: Marx JA, Hockberger RS, Walls RM, eds. Rosen's Emergency Medicine: Concepts and Clinical Practice. Vol 1. 6th ed. Philadelphia, PA: Mosby Elsevier; 2006:382-98/chap 39.
Hasan N, Colucciello SA. Maxillofacial trauma. In: Tintinalli JE, Gabor KD, Stapczynski SJ, eds. Emergency Medicine: A Comprehensive Study Guide. 6th ed. McGraw-Hill Co Inc; 2004:chap 257, p1583-1590.
mandible fracture, facial fracture, maxillofacial fractures, mandibular fractures, fractures of the mandible, high-impact mandibular fractures, low-impact mandibular fractures, maxillofacial injury, facial injury, jaw fracture
Thomas Widell, MD, Vice Chairman, Assistant Professor, Department of Emergency Medicine, Rosalind Franklin School of Medicine/The Chicago Medical School, North Chicago, Illinois; Associate Residency Director, University of Chicago Emergency Medicine Program, Chicago, Illinois; Program Director Emergency Medical Education, Attending Physician, Mount Sinai Hospital Medical Center, Chicago, Illinois
Disclosure: Nothing to disclose.
Michelle Ervin, MD, Chair, Department of Emergency Medicine, Howard University Hospital
Michelle Ervin, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, National Medical Association, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.
Eric Legome, MD, Residency Director, Assistant Professor of Emergency Medicine, Department of Emergency Medicine New York University, New York University Hospital, Bellevue Hospital Center, Manhattan VA
Eric Legome, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, Council of Emergency Medicine Residency Directors, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
Rick Kulkarni, MD, Medical Director, Assistant Professor of Surgery, Section of Emergency Medicine, Yale-New Haven Hospital
Rick Kulkarni, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: WebMD Salary Employment
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