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645

FISET ET AL

mous cell carcinoma has been reported arising in cutaneous lesions of DLE, usually in association with
hypopigmentation, solar damage, and scarring.
References

1. Burge SM, Frith PA, Juniper RP, et al: Mucosal involvement in


systemic and chronic cutaneous lupus erythematosus. Br J
Dermatol 121:727, 1989
2. Lo JS, Berg RE, Tome&i KJ: Treatment of discoid lupus erythematosus. lnt J Dermatol 28:497, 1989
3. Lynch PJ: Dermatology for the House Officer (ed 2). Baltimore,
MD, Williams & Wilkins, 1987, p 205
4. Eisenberg E: Capsule dermatopathology: red, white, and ulcerated
oral lesions-Some considerations for the diagnostic approach.
J Dermatol Surg Oncol 13:2 1, 1987

.I Oral Maxillofac
50:645-649,

5. Hymes SR, Jordon RE: Chronic cutaneous lupus erythematosus.


Med Clin North Am 73: 1055. 1989
6. Tan EM: The 1982 revised criteha for the classification of lupus
erythematosus (SLE). Arthritis Rheum 25:1271, 1982
7. Sulica VI, Kao GF: Squamous cell carcinoma of the scalp arising
in lesions of discoid lupus erythematosus. Am J Dermatopath01 10:137, 1988
8. Habif TP: Clinical Dermatology (ed 2). St Louis, MO, Mosby,
1990, p 425
9. Kajalainene TK, Tomich CE: A histopathologic study of oral
mucosal lupus erythematosus. Oral Surg Oral Med Gral Path01
671547, 1989
10. Lever WF, Schaumburg-Lever G: Histopathology of the Skin
(ed 7). Philadelphia, PA, Lippincott, 1990, p 494
I 1. Green SG, Piette WW Successful treatment of hypertrophic lupus
erythematosus with isotretinoin. J Am Acad Dermatol 17:
364, 1987
12. Thivolet J, Nicolas JF, Kanitakis J, et al: Recombinant interferon
alphafa is effective in the treatment of discoid and subacute
cutaneous lupus erythematosus. Br J Dermatol 122405. 1990

Surg

1992

Disinhibition of Behaviors With Midazolam:


Report of a Case
LOUIS FISET, DDS,* PETER MILGROM, DDSJ 0. ROSS BEIRNE,
AND PETER ROY-BYRNE, MD5

Midazolam enjoys increasing favor among clinicians


for intravenous conscious sedation as a substitute for
diazepam because it is rapidly metabolized relative to
diazepam, has a rapid onset of action with excellent
amnestic properties, and is nonirritating. Nevertheless,
disinhibitory reactions to midazolam-5 (Table l), as
well as other benzodiazepineq6
have been reported.
Such paradoxical responses range from sexual
disinhibition15 to a group of behaviors that Dietch and

Received from the University of Washington, Seattle.


* Research Assistant Professor, Department of Dental Public
Health Sciences.
t Professor, Department of Dental Public Health Sciences and Director, Dental Fears Research Clinic.
$ Associate Professor and Director of Residency Training, Department of Oral and Maxillofacial Surgery.
$ Professor, Department of Psychiatry and Behavioral Sciences and
Director, Anxiety Disorders Program.
This work was partially supported by Contract no. NO1 DE 72569
from NIDR, NIH, and a small grant awarded bv the Alcohol and
Drug Abuseinstitute at the U&e&
of Washington.
Address correspondence and reprint requests to Dr Fiset: Department of Dental Public Health Sciences, Mail Stop SM-35, University
of Washington, Seattle. WA 98 195.
0 1992 American Association of Orat and Maxillofacial Surgeons
0278-2391/92/5006-0020$3.00/O

DMD, PHD,$

Jennings have termed aggressive dyscontrol, which


include hostility7-9 and rage reaction, 7 aggressiveness, paroxysmal excitement,* and assault.* These
untoward events are known to occur with both the
intravenour? as well as ora17-6routes of administration, and generally occur when larger doses are administered.2*4*6The highest incidence has been reported
among children and adolescents, but appears to be less
among the elderly.5,9 Although reactions following both
oral and intravenous dosing appear clinically similar,
reactions during intravenous use typically occur as a
result of failed anesthesia (ie, sedation). Whereas oral
usage never aims to sedate patients in this context, disinhibition may represent a different phenomenon.
Available reports suggest that some individuals may
be more susceptible to such reactions. One group at
greater risk may be people with alcohol dependency.
Chronic alcohol abuse has been implicated in alterations to the neuroregulatory mechanisms of the brain
and it interferes with synthesis and functioning of a
host of neurotransmitter systems in the central nervous system (CNS), including y-aminobutyric acid
(GABA). The long-term effects on these systems in
drinking and nondrinking alcoholics are not yet known,
but may indeed influence untoward responses to the
benzodiazepines.

646
Table 1.

DISINHIBITION OF BEHAVIORS WiTH MIDAZOLAM

Disinhibitory Response to Intravenous Midazolam During Sedation for Surgical Procedures

Midazolam
Dosage (mg)

Other Drugs

Patient
Sex/Age (yr)

5
12
Unknown
2
0.5

Morphine (1 mg)
None
Unknown
Promethazine
None

M/3 I
F/49
Unknown
F/57
F/l4

Drug Response

Reversal Drug

Reference

Hostility, assault
Violent movement
Confusion, aggressiveness
Uncooperative, movement
Hostility, confusion,
hallucination

Amobarbital
Flumazenil
Flumazenil
Physostigmine
Haloperidol

Lobo, Miwa
RodrigoS
Ricou et al4
Knaack-Steineggar et al*
Bemakis et al3

Report of Case

In addition, clinical experience teaches that alcohol


dependent patients often require increased doses of
anesthesia, analgesic agents, and benzodiazepines during surgery7-21 to ensure comfort and cooperative behavior. This phenomenon is further complicated by
the threshold onset pattern of midazolam in contrast
to the typical linear dose-effect characteristic of diazepam sedation. Thus, the risk of adverse reactions to
midazolam may be increased in these individuals.
Another high-risk group may be patients with psychiatric histories of anger and aggressive behavior.*i4
Although this is an attribute common among alcoholics, it is also observed in nonalcoholic patients with
personality disorders. In such cases, disinhibitory effects
of benzodiazepines might just represent a normally occurring phenomenon triggered by the adverse aspects
of the dental surgical context rather than by a direct
pharmacologic effect of the benzodiazepines. This distinction is a subtle one, but the presence of such reactions following other sedative agents that act via different neurochemical mechanisms would suggest that
this is possible.
The following case report involves a nondrinking
alcoholic who received 18 mg of midazolam intravenously without demonstrating the desired signs of clinical sedation, but who exhibited disinhibitory behavior.

A 22-year-old 45-kg white woman classified by the American Society of Anesthesiology


(ASA) guidelines as a class I
risk reported for removal of her four impacted third molars

after receiving an explanation of the benefits and risks of


surgery and consenting to treatment, including intravenous
sedation. This case is noteworthy in that it was part of a
federally funded, multisite clinical trial to study the safety
and efficacy of intravenous sedative agents, in which drugs
were administered blindly. The protocol, which was approved
by the Universitys institutional review board, called for random assignment of subjects to one of five treatment groups.
Four syringescontaining normal saline placebo or active drug
for sedation were used to administer medications to the subjects. The active drugs, in order of administration, were fentanyl(O.1 mg/70 kg); midazolam, titrated to ptosis and slurred
speech end point (15 mg maximum); methohexital(l0
mg);
and an optional, follow-up dosage of either midazolam (10
mg maximum) or methohexital (200 mg maximum). The
treatment groups are shown in Table 2.
Data collected prior to clinical screening included a score
of 10 on the Corah Dental Anxiety Scale22 and 38 on the
Dental Fear Survey,23 both indicating low dental fear. Analysis
of the medical history and responses to the Marlowe-Crowne
Social Desirability Scale suggested possible repressed fears
and anger-related difficulties. 24In addition, the patient denied
having received treatment from a psychologist or psychiatrist
within the past 2 years, and estimated her emotional well
being as good (excellent, good, fair, poor, very poor scale).

Table 2. Treatment Groups for a Multisite Clinical Trial on the Safety and Efficacy
of Intravenous Sedative Agents
Group

First Syringe*

1
2
3
4
5

Saline
Saline
Saline
Fentanyl
Fentanyl

Second Syringe?
Saline
Midazolam
Midazolam
Midazolam
Midazolam

to
to
to
to

end
end
end
end

* Administered 0.1 mg/70 kg.


t Administered 1 mg/min to a maximum 15 mg.
z#Administered as a bolus immediately preceding local anesthesia.
$ Optional use at the discretion of the anesthesiologist.
11Administered 0.5 mg/min to a maximum 10 mg.
(I 200 mg maximum.

point
point
point
point

Third Syringe$

Fourth Syringeg

Saline
Saline
Saline
Saline
Methohexital

Saline
Saline
Midazolam
Saline
Methohexitalll

647

FISET ET AL

She further denied drinking alcohol or using illegal drugs


during the preceding 3 months.
Preoperative vital signs were recorded: blood pressure, 1301
62 mm Hg; heart rate, 60 beats per minute; respirations, 13/
min. Monitors were placed to measure end-tidal CO2 and
respiratory rate (Ohmeda 5200; Ohmeda, Englewood, CO);
oxygen saturation (Ohmeda Biox 3700); and intermittent
blood pressure (5-minute intervals) and pulse (Physio-Control
VSM2 electrocardiogram; Physio-Control, Redmond, WA).
Oxygen was administered by nasal mask at a flow rate of 5
L/min. A 20-gauge radiopaque Teflon (DuPont, Wilmington,
DE) indwelling catheter (Deseret Medical. Sandy. UT) was
placed in the right antecubital fossa without difficulty and a
continuous drip of 5% dextrose in water begun. At the Ominute interval (T = 0 minutes), 1.3 mL of a normal saline
placebo from the first syringe was administered over a lminute period. Beginning at the 2-minute interval, the entire
contents of the second syringe containing 15 mg of midazolam were titrated over a lo-minute period. At the 17-minute interval, 1 mL of a normal saline placebo from the third
syringe was administered as a bolus, followed immediately
by local anesthesia. At 19 minutes, during local anesthestic
administration,
and owing to the patients heightening
arousal, the anesthesiologist opted to administer partial contents of the fourth syringe, totaling 3 mg of midazolam. In
total, the subject received 18 mg of midazolam over an 18minute period followed by 90 mg (20 mg/mL) lidocaine, with
1:100,000epinephrine as a vasoconstrictor. However, because
of escalating disinhibitory behavior, the session was terminated following administration of the local anesthetic.
The entire session was videotaped, permitting a microanalysis of events. The recording revealed that at no time
during titration of the first 15 mg of midazolam was ptosis
or slurred speech observed. However, following administration of the first 4.5 mg of midazolam (T = 5 minutes) the
patient began to yawn and gradually became more talkative,
exhibiting frequent movement of her hands and arms. Her
speech, though always coherent, gradually slowed. During
administration of the local anesthetic, the subject became
increasingly disoriented and confused, and lost memory of
the oral surgeon despite his having reviewed the procedures
with her during the preoperative phase. She became belligerent and verbally abusive; further, she denied having received
any medications. This behavior, accompanied by her disruptive movements, caused the session to be terminated at 24
minutes without surgical intervention.
Postrecovery tests indicated the patient was not fully alert,
and she could not walk a prescribed 6 ft without support.
Moreover, she had no memory of receiving the intravenous
protocol. The subject was dismissed under the care of a companion 1 hour postoperatively after satisfactorily completing
tests for alertness and psychomotor recovery. During telephone contact later the same afternoon, she continued her
disinhibitory behavior.
The following morning the patient was again contacted by
telephone. Her disposition had returned to preoperative
pleasantness. She recalled the intravenous tube (IV) placement, but had memory of neither the local anesthetic procedure nor walking to the recovery room. She remembered
nothing of the ride home, nor anything else until late that
evening. On probing, she admitted to being an alcoholic, but
abstinent for 1 year. She further volunteered having entered
a rehabilitation center for alcohol abuse at age 14 years. She
denied a history of abuse of drugs other than alcohol.
The patient reported for third molar removal under local
anesthesia and nitrous oxide/oxygen analgesia 2 weeks later.

The teeth were extracted without complications; the patient


cooperated without any of the disinhibitory behavior exhibited previously. However, on the following day the patient
complained of nausea and vomiting. Her pain medication
was changed from oxycodone and acetaminophen to hydrocodone with acetaminophen. She continued to experience
nausea, and was prescribed prochlorperazine suppositories,
which were partially effective. On the fifth day following the
extractions, the patient reported for a routine follow-up appointment and was upset because she had to drive herself to
the clinic and lost my car muffler on the way to the appointment. She complained of nausea, but was not orthostatic. She was therefore given more prochlorperazine and
pain medications. On the sixth day following the extractions,
the patient came to the emergency department complaining
of nausea. Treatment included intravenous fluids. Following
this, the patient had an uneventfully recovery.

Discussion
On the surface, this case appears to be a simple toxic
overdose with midazolam as a direct extension of drug

pharmacologic effects. 25 Established treatment guidelines were followed, but during titration the end-point
signs of ptosis and slurred speech were never observed,
although the patients speech pattern did slow. This
was confirmed following analysis of the videotape recording of the procedures. Thus, the desired sedative
effects of the drug never appeared, leaving only undesirable side effects.
The sedative effects of benzodiazepines are primarily
mediated by brainstem GABA-benzodiazepine neurons.26 These neurons inhibit a system of ascending
neurochemical pathways that normally exert a tonic
activating influence on cortical and subcortical stimuli.27 In contrast, effects of ataxia and memory impairment/confusion
are mediated via GABA-benzodiazepine receptors in the cerebeIlar and hippocampal/
forebrain areas.26 Thus, in this patient, brainstem receptors were either not sufficiently activated or the
arousal pathways they normally inhibit were too overactive to be suppressed. In contrast, those benzodiazepine receptors in other neuroanatomic regions were
sufficiently activated.
Because ethanol has potent acute effects on the
GABA-benzodiazepine complex,28 it is possible that
prolonged drinking could cause permanent alterations
in this receptor system and thereby alter a patients
responsivity to benzodiazepines. Evidence from animal
studies does show that the responsivity of ethanol-dependent mice to benzodiazepines may differ markedly
depending on the behavioral effect examined.29 Furthermore, molecular genetic studies showing regional
differences in the type of mRNA-coding for the benzodiazepine recepto? suggest that there may be different types of receptors in different brain regions, providing another possible mechanism for differential
behavioral susceptability.

648

Although the disinhibitory effects may have been


owing to the deleterious effects of alcohol on these brain
neuroregulatory mechanisms, they also may have resulted from a psychologic predisposition related to her
addiction. That is, the verbal hostility we observed may
be learned behavior associated with the life-style or
personality of some alcoholics. Our clinical experience
suggests that nondrinking alcoholics may exhibit the
same anxiety-related behaviors as drinking alcoholics.
Alcohol abuse may be used as a life-coping strategy;
patient expectations for intravenous anxiolytics may
be identical to experiences under the influence of alcohol. Similarly, the way in which the individual copes
with the stress of surgery (such as getting angry or moving around) may mimic a drunken episode. Whether
physiological or psychological factors are at play here
cannot be stated with certainty, but in 211 subjects
participating in the study, these events were a unique
experience.
In the study, we screened volunteers for alcohol consumption in excess of 20 drinks per week. This subject
stated she did not drink alcohol, but failed to divulge
her previous history of alcohol dependency. In 1988,
the National Council on Alcoholism estimated that
12.1 million true alcoholics reside in the US, while the
Office of Substance Abuse Prevention says that 36 to
43 million Americans will experience alcohol or other
chemical dependency in their lifetime.30 Given this high
prevalence, dental and medical practitioners undoubtedly treat alcoholics on a daily basis. As this case illustrates, often such individuals deny their condition
or underreport the amount of alcohol they consume.
Although relatively few dental patients receive intravenous benzodiazepines, increasing interest in the
use of oral benzodiazepines, such as diazepam, triazolam, and alprazolam, as premeditation the night before
treatment and as intraoperative sedation, continues to
grow. 3 Several reports8-2 suggest that these oral benzodiazepines may produce adverse reactions similar to
the ones described here. As previously noted, it is unclear whether these reactions occur via the same mechanism. They may represent an additional untoward
effect (ie, disinhibition) rather than the absence of a
desired effect (sedation), and magnify normally expected reactions such as memory impairment and
ataxia.
Because our understanding of these problems is incomplete, and because of the profound impact benzodiazepines and alcohol have on the neuroregulatory
systems in the CNS, we recommend that clinicians
prescribing sedative agents use caution when evaluating
patients for sedation in the dental environment. Alternate strategies may prove necessary for individual
patients with histories of alcohol dependency. Some
clinicians experienced in treating drinking and non-

DISINHIBITION OF BEHAVIORS WITH MIDAZOLAM

drinking alcoholics advocate use of nitrous oxide/oxygen analgesia as the sole supplement to local anesthesia, citing the dissociative feelings induced by oral
and IV sedation as possible triggers for relapse and/or
untoward clinical behaviors.32 Despite the attractiveness of this recommendation, little clinical research has
been conducted to test its efficacy and provide a rationale for its use.
No conclusions, of course, should be drawn from a
single case report. However, this report, which was
broad in its documentation and included a history of
alcohol dependency, suggests that alcohol usage may
be an important contributing factor in disinhibitory
responses to benzodiazepines. Clinical trials of sedation
strategies with alcohol-dependent populations, though
desirable, may be unfeasible. Therefore, additional case
reports, including documentation of alcohol use histories, should be published to help provide a clearer
rationale for recommending treatment strategies using
sedative agents in such patients.
References
1. LoboBL, Miwa LI: Midazolam disinhibition reaction. Drug Intell
Clin Pharm 22:725, 1988
2. Knaack-Steinegger R, Schou J: Therapy for paradoxical reactions
to midazolam during regional anesthesia. Anaesthetist 36: 143,
1987
3. Bumakis TG, Berman DE: Hostility and hallucinations as a
consequence of midazolam administration. DICP 23:67 1,
1989
4. Ricou B, Forster A, Bruckner A, et al: Clinical evaluation of a
specific benzodiazepine antagonist (RO 15-1788). Br J Anaesth
58: 1005, 1986
5. Rodrigo CR: Flumazenil reverses paradoxical reaction with
midazolam. Anesth Prog 38:65, 1991
6. Litchfield NB: Complications of intravenous diazepam: adverse
psychological reactions (an assessment of 16,000 cases). Anesth
Prog 27:175, 1980
7. Dietch JT, Jennings RK: Aggressive dyscontrol in patients treated
with benzodiazepines. J&t Psychiatry 49: 184, 1988
8. Gardos G: D&inhibition of behavior bv antianxietv_ drugs.
_ Psv_
chosomatics 21:1025, 1980
.
9. Rosenbaum JF, Woods SW, Groves JE, et al: Emergence of hostility during alprazolam treatment. Am J Psychiatr 141:792,
1984
10. Lion A, Azcarate CL, Koepke HH: Paradoxical rage reactions
during nsvchotronic medication. Dis Nerv Svs 36:557, 1975
11. Zisook S, DeVaul l& Adverse behavioral effects of benzodiazepines. J Fam Pratt 5:963, 1977
12. Strahan A, Rosenthal J, Kaswan M, et al: Three case reports of
acute paroxysmal excitement associated with alprazolam
treatment. Am J Psychiatry 142:859, 1985
13. Gardner DL, Cowdry RW: Alprazolam-induced dyscontrol in
borderline personality disorder. Am J Psychiatry 14298, 1985
14. Binder RL: Three case reports of behavioral disinhibition with
clonazepam. Gen Hosp Psychiatry 9: 151, 1987
15. Fava M, Borofsky GF: Sexual disinhibition during treatment
with a benzodiazepine: A case report. Int J Psychiatry Med
21:99, 1991
16. Kales A, Bixler EO, Vela-Bueno A, et al: Comparison of short
and long half-life benzodiazepine hypnotics: Triazolam and
quazepam. Clin Pharmacol Ther 40:378, 1986
17. Edwards R, Mosher VB: Alcohol abuse, anaesthesia, and internal
care. Anaesthesia 35:474, 1980
18. Bruce DL: Alcoholism and anesthesia. Anestb Analg 62:84, 1983

649

OZAKl ET AL

19. St. Haxholdt 0, Krintel JJ, Johannson G: Pre-operative alcohol


infusion. Anaesthesia 39:240, 1984
20. Fox AW, Guzmen NJ, Friedman PA: The clinical pharmacology
of alcohol, in Barnes HN, Grossman MD, Delbanco (eds):
Alcoholism: A Guide for the Primary Care Physician. New
York, NY, Springer-Verlag, 1987, pp 29-43
2 1. Hoffman PL, Tatakoff B: Ethanols action on brain biochemistry,
in Tarter RE, Van Thiel DH: Alcohol and the Brain: Chronic
Effects. New York, NY, Plenum, 1985, pp 19-68
22. Corah NL: Assessment of a dental anxiety scale. J Dent Res 48:
496, 1969
23. Kleinknecht RA, McGlynn FD, Thomdike RM, et al: Factor
analysis of the Dental Fear Survey with cross validation. J
Am Dent Assoc 108:59, 1984
24. Crowne DP, Marlowe D: A new scale of social desirability independent of psychopathology. J Consult Psycho1 24:349, 1960
25. Pallasch TJ: Principles of pharmacotherapy: V. Toxicology and
adverse drug reactions. Anesth Prog 36:4 1, 1989
26. Roy-Byrne P. Nutt DJ: Benzodiazepines: Biological mechanisms,
in Roy-Byrne P. Cowley DS (eds): Benzodiazepines In Clinical

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Practice: Risks and Benefits. Washington, DC, American Psychiatric Press, 199 1
Hobson JA, Steriade M: Neuronal basis of behavioral state control, in Bloom FE (ed): Handbook of Physiology Section 1:
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the Brain. Bethesda, MD, American Physiological Society,
1986, pp 710-767
Ticky MK, Burch TP, Davis WC: The interaction of ethanol
and the benzodiazepine-GABA receptor ionophore complex.
Pharmacol Biochem Behav 18:15, 1983
Chan AWK, Lamgun M, Leong FW, et al: Does chronic ethanol
confer full cross-tolerance to chlordiazepoxide? Pharmacol
Biochem Behav 30:385, 1988
Royce JE: Alcohol Problems and Alcoholism: A Comprehensive
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Petersen JK, Milgrom P: Pain Relief In the Orofacial Regions.
Copenhagen, Munksgaard, 1989
American Dental Association: Treating the active or recovering
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Dental Association, 1989

Surg

1992

Cervicofacial Actinomycoses Following


Sagittal Split Ram& Osteotomy: A Case Report
GEORGE

WAYNE OZAKI, DDS,* A. OMAR ABUBAKER,


DMD, PHD,t
C. SOTEREANOS,
DMD, MS,* AND GARY T. PATTERSON,

The sagittal split ramus osteotomy (SSRO) has been


used for the treatment of various mandibular deformities, including mandibular retrognathia, prognathia,
apertognathia, and asymmetry. *2Because of anatomic
variations of the mandible, limited access to the surgical
site, and technical difficulty of the procedure, there is
a potential for many complications. The most common
complications associated with the SSRO are bleeding
and relapse.3 Other complications include fracture of
the mandible, unfavorable split, infection, airway obstruction, necrosis, neurosensory dysfunction, delayed
Received from the Department of Oral and Maxillofaciat Surgery,
School of Medicine, University of Pittsburgh, Pittsburgh, PA.
* Resident.
t Formerly, Research Fellow; currently, Assistant Professor, Department of Oral and Maxillofacial Surgery, Medical College of Virginia, Richmond.
$ Associate Professor.
5 Assistant Professor of Surgery.
Address correspondence and reprint requests to Dr Abubaker: Department of Oral and Maxillofacial Surgery, Medical College of Virginia, Box 566, Richmond, VA 23298.
0 1992 American Association of Oral and Maxillofacial Surgeons
0278-2391/92/5008-0021$3.00/0

DMD

wound healing, temporomandibular joint disorders,


trismus, malocclusion, and malunion or nonunion of
the osteotomized segments.3-6
Although infection has been reported as a complication of the SSRO, infection by actinomyces has not
been previously reported. This article will describe such
a case and its management.
Report of a Case
A 25year-old, healthy, white woman originally came for
treatment of her retrognathic mandible. Following presurgical
orthodontics, she was admitted and subsequently underwent
a bilateral SSRO with mandibular advancement. She encountered no intraoperative or early postoperative complications. However, 6 weeks postoperatively, the patient returned with a 2 X 3-cm swelling in the left submandibular
region (Fig 1). She denied any history of fever, chills, malaise,
intraoral or extraoral drainage, or ulcerations. The swelling
was indurated and slightly tender to palpation. Intraoral examination showed an entirely normal mucosa with complete
healing of the incision sites.
Her workup included a complete blood count with a differential count, urine analysis, electrolytes, blood urea nitrogen, serum creatinine, a facial radiographic series, and a

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