Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / @xirurgi_2025 / @xirurgi_2025 - 678 - файл
.pdf
16 Maxillofacial Trauma fortheGeneral Surgeon
https://t.me/medicina_free
Fig. 16.11 A patient with soft tissue trauma sustained
during an industrial accident. The injury would be
expected to damage the parotid duct and facial nerve
branches
229
skin. Wounds contaminated with gravel or
other foreign matter should be thoroughly
debrided. Tooth fragments are sometimesseen in adjacent soft tissues and need
to be removed. Plain radiographs and CT
scans can often show retained soft tissue foreign bodies, however they cannot be relied
upon completely.
(c) Tongue
The tongue is very vascular and muscular.
Lacerations may bleed signicantly. Repair
under local anaesthetic is possible; however,
it requires patient co-operation in order to
reduce movement of the tongue. Deep tissue
bites with 3/0 suture material are required.
Top Five Takeaways
1. Maxillofacial trauma is common.
2. Oral and maxillofacial trauma is often associ-
ated withhead and spinal injury.
3. Beware of the potential for acute or
delayed airway embarrassment in patients
with maxillofacial injuries.
4. Retrobulbar haemorrhage due to an orbital
injury is a surgical emergency.
5. Dental Practitioners are a good source of
advice and help with dental trauma.
Fig. 16.12 The intraoperative view of the patient in
Fig.16.11 showing lacrimal probes in the ends of the severed parotid duct prior to microsurgical anastomosis
non- specialist repair and referral should be
made to an oculoplastic or maxillofacial
surgeon.
(b) Lips
Care should be exercised in repairing lip lacerations, especially if the injury involves the
vermillion border. Accurate apposition of the
vermillion border is required, and this is
facilitated by the use of magnication.
Careful coaptation of the transected orbicularis muscles if involved is also required. A
full thickness laceration of the lip will necissitate closure of the mucosa, muscle and
References
1. Perry M. Advanced Trauma Life Support (ATLS):
can one size t all? Part 1: Dilemmas in the managment of the mulitply injured patient with coexisting
facial injuries. Int J Oral Maxillofac Surg. 2008;37(3):
209–14.
2. Perry M, Morris C. Advanced trauma life support
(ATLS) and facail trauma: cna one size t all? Part
2: ATLS, maxillofacial injuries and airway dilemmas.
Int J Oral Maxillofac Surg. 2008;37(4):309–20.
3. Tuckett J, Lynham A, Lee G, Perry M, Harrington
U. Maxillofacial trauma in the emergency department: A review. Surgeon. 2014;12(2):106–14.
4. Elledge RO, Elledge R, Aquilina P, Hodson J, Dover
S. The role of alcohol in maxillofacial trauma - a
comparative retrospective audit between two centres.
Alcohol. 2011;45(3):239–43.
5. Bahr W, Stoll P.Nasal intubation in the presence of
frontobasal fractures: A retrospective study. J Oral
Maxillofac Surg. 1992;50(5):445–7.
6. McLeod A, Calder I.Spinal cord injury and laryngoscopy - the legend lives on. Br J Anaesth.
2000;84(6):705–9.
230
https://t.me/medicina_free
P. Aquilina
7. Arrowsmith J, Robertshaw H, Boyd J.Nasotracheal
intubation in the presence of frontobasal skull fracture. Can J Anaesth. 1998;45(1):71–5.
8. Salvino C, Dries D, Gamelli R, Murphy-Macabobby
M, Marshall W. Emergency cricothyroidotomy in
trauma victims. J Trauma. 1993;34(4):503–5.
9. Ceallaigh P, Ekanaykaee K, Beirne C, Patton
D.Diagnosis and managment of common maxillofacial injuries in the emergency department.Part 5: dentoalveolar injuries. Emerg Med J. 2006;24(6):429–30.
10. Therapuetic Guidelines (digital). (2021, 11 23). Tooth
avulsion (knocked-out tooth). www.tg.org.au
Odontogenic Infections andDeep
https://t.me/medicina_free
Neck Collections
GaryR.Homan, AshimN.Adhikari,
andOliviaG.I.Homan
17
17.1 Introduction
The neurocranium, sub-cranial viscero-cranium
and cervical spine collectively provide a framework of structural support and protection for a
variety of complex anatomical structures that are
condensed into a small space.
A number of surgical and medical specialties
lay claim to the diagnosis and management of a
wide range of diseases, deformities, defects and
disorders that afict the musculoskeletal and soft
tissue components of the head and neck.
While such subspecialties idiosyncratically
manage their respective pathologies, it is incumbent for all surgeons who operate in the head and
neck to have both a working knowledge of, as
well as a capacity to manage, both supercial and
deep neck space infections.
G. R. Hoffman (*)
Departments of Oral and Maxillofacial Surgery and
Head and Neck Surgery, John Hunter Hospital,
Newcastle, NSW, Australia
School of Medicine, University of Newcastle,
Newcastle, NSW, Australia
A. N. Adhikari
Department of Oral and Maxillofacial Surgery, John
Hunter Hospital, Newcastle, NSW, Australia
O. G. I. Hoffman
School of Medicine, University of Melbourne,
Melbourne, VIC, Australia
17.2 Infection
In its broadest sense, infection is arguably the
most common pathological denominator that can
affect any of the resident tissues and organs of the
head and neck. Infection can be dened as the
damage that results from the invasion by and
growth of pathogenic microorganisms within
host tissues. In doing so, they also have the capacity to both activate and overwhelm the host’s
innate and acquired immune defences.
The microorganisms that are responsible for
the damage can be classied as either bacterial,
viral, fungal or parasitic. For the purposes of this
dissertation, the infections that are discussed are
bacterial in origin.
Although a wide variety of pathogenic bacteria exist, they enlist remarkably common strategies to cause their local, regional and systemic
effects. These comprise an array of virulence
factors, which uphold their intrinsic ability to
adhere to (adhesins), invade into (invasins),
counter innate host immune defences (elaboration of coat proteins and superoxide dismutases),
multiply within and spread throughout, causing
primary cytotoxic damage (production of
destructive proteolytic enzymes) to host tissues
and organs.
These processes are modied by host anatomical factors and resistance capacity. The latter is
impaired by poorly or uncontrolled intercurrent
systemic disease.
© The Author(s), under exclusive license to Springer Nature Singapore Pte Ltd. 2023
B. Ashford (ed.), Head and Neck Surgery for General Surgeons,
https://doi.org/10.1007/978-981-19-7900-2_17
231
232
https://t.me/medicina_free
G. R. Homan et al.
17.3 Sepsis andSeptic Shock
The body’s ultimate response to the progression
of uncontrolled infection is sepsis. Sepsis is a
life-threatening condition that arises when the
physical, biochemical and pathological contributions to the host response become dysregulated
and result in injury to its own tissues and organs
(e.g., pulmonary injury/acute respiratory distress
syndrome, hypoperfusion and acute tubular
necrosis/acute renal failure, ischemia and gastrointestinal ulceration and disseminated intravascular coagulation).
Physiologist, Carl Wiggers, stated that “Shock
not only stops the machine, but it wrecks the
machinery.” For clinical operationalisation, the
organ dysfunction due to infection is qualied by
an increase in the sequential (sepsis related)
organ failure assessment (SOFA) score of two
points or more. At the bedside, a quick SOFA
(qSOFA) score can be used, where any two of
respiratory rate ≥22 breaths/minute, altered mental status or systolic blood pressure ≤100mm Hg
are suggestive of sepsis.
Septic shock is a subset of sepsis in which profound circulatory, cellular and metabolic abnormalities conspire to increase the risk of mortality
over sepsis alone. This is characterised by serum
lactate ≥2mmol/L and the requirement for vasopressor support in order to maintain a mean arterial pressure ≥65mmHg, despite adequate uid
resuscitation.
17.4 Aetiology andMicrobiology
Many contemporary authors have reiterated the
concepts espoused by renaissance philosopherdiplomat, Niccolò Machiavelli in his sixteenth
century treatise entitled Il Principe, where he
prophetically identied two fundamental tenets
of sepsis in annotating that, “Hectic fever, at its
inception, is difcult to recognise but easy to
treat; left unattended, it becomes easy to recognise and difcult to treat.” It is that philosophy
that underpins the subsequent discussion in this
chapter.
Severe infections, as a cause of serious illness
or death, have been recorded in the spoken and
written word since antiquity.
As a subset, deep neck space infections are
usually polymicrobial and generally caused by
the resident bacteria that populate the oral cavity
and upper aerodigestive tract. These bacteria are
a mixture of aerobic, facultative or strict anaerobic organisms, with deeper infections more likely
to involve anaerobes.
Implicated bacteria from the oral cavity
include Streptococcus viridans and subsequent
colonisation with anaerobes such as
Septostreptococci, Fusobacteria, Prevotella,
Porphyromonas and Actinomyces species.
Aerodigestive bacteria include Streptococcus
pyogenes, Staphylococcus aureus and
Haemophilus inuenza, with Klebsiella and
Pseudomonas playing a role in immunocompro-
mised hosts. Many of these organisms are able to
produce beta-lactamase and, in turn, inhibit the
action of a broad range of conventional
antibiotics.
Although there are many causes of head and
neck infection, those of odontogenic origin continue to remain some of the most common, followed by those of the pharyngotonsillar origin [1,
2], and contribute to a signicant proportion of
those that present as deep neck space infections
encountered in clinical practice.
Odontogenic infections arise as a result of episodes of either dental pulp necrosis (and a resultant periapical abscess secondary and most
commonly to dental decay– but also any process
that exposes the dental pulp: attrition, erosion,
abrasion and trauma), periodontal disease
(chronic gingivo-periodontal pathos) or pericoronitis. A rising cause of related infections also
include osteonecrosis of the jaws resulting from
either therapeutic radiotherapy or pharmacotherapy (anti-resorptive or immune-modulation/
suppression).
Non-odontogenic causes include a variety of
acute conditions de novo or arising as exacerbations of chronic pathology such as otitis media,
mastoiditis, sinusitis, pharyngitis, tonsillitis, sialadenitis, thyroiditis, infected brachial cleft and
17 Odontogenic Infections andDeep Neck Collections
https://t.me/medicina_free
233
thyroglossal duct anomalies, suppurative cervical
lymphadenitis, post-surgical or traumatic head
and neck wounds.
They are typically diagnosed by thorough
history- taking and clinical examination.
17.5 Anatomy
Once odontogenic infection has spread beyond
the connes of the jaws, it is essentially anatomical factors that play a key role in the clinical presentation of disease.
In its simplistic presentation, if the suppurative exudate discharges above muscular attachments in the lower jaw or below muscular
attachments in the upper jaw, the resultant presentation is that of an acute alveolar or vestibular
abscess (parulis/gum boil). This may devolve
into a chronic state and present as an intra-oral
sinus tract, and for that matter, if the path of least
resistance is relatively short, it may present as an
extra-oral submental, submandibular or facial
sinus tract.
Infections can spread more broadly via
lympho- haematogenous dissemination and/or
direct extension via fascial layers, into the deep
recesses of the head and neck, with direct extension being the most common route of spread.
Retrograde ow through the veins that drain
the mid-face in association with the abundance of
anastomoses that exist between intra- and extracranial structures, may predispose to haematogenous spread, leading to serious complications
such as cavernous sinus thrombophlebitis and
cerebral abscess [3]. Haematogenous spread can
also cause bacterial endocarditis and infection of
distant sites, including prosthetic implants.
Lymphadenitis in the regional draining basin
often resolves with treatment of the primary
infection. Occasionally, this results in brosis or
suppuration and lymphadenopathy may be per-
sistent. Other causes of lymphadenopathy,
including neoplasia, need to be ruled out.
Landmark papers by Grodinsky and Holyoke
[4], who used dyed gelatin injections to determine the path of least resistance between fascial
planes, Williams and Guralnick [5], who
described the anatomical basis of managing
Ludwig’s angina (a life-threatening cellulitis of
the submental and bilateral sublingual and submandibular spaces), and Granite [6], who summarised the literature on the potential interfascial
spaces of the head and neck, with periodic supplementation by a variety of sporadic anatomical studies [7] and case reports are fundamental
to an understanding of both the spread into and
occupancy of deep neck spaces. This work is
further supplemented by Flynn [8], who has
published extensively on odontogenic infections, and described the likely routes of spread,
based on causative teeth, and the approach for
draining their associated collections. This information is summarised in Table 17.1 [3, 8] and
depicted in anatomical drawings and imaging in
Fig.17.1.
These anatomical spaces are potential in
nature, until they are occupied by an inammatory exudate, and, in addition, are able to freely
communicate. The severity of an infection can be
linked to the anatomical location of the affected
spaces due to their effect on local structures,
including the airways and vital structures such as
the orbital contents, intracranial contents, carotid
sheath and mediastinum as well as their ability to
spread into these spaces.
As such, submandibular and masticator space
infections would be considered moderate risk, for
their ability to induce trismus and spread to highrisk spaces such as parapharyngeal, retropharyngeal and pretracheal. Infection spreading within
the so-called “danger space” (prevertebral space),
mediastinum or intracranially would be considered very high risk.
234
https://t.me/medicina_free
Surgical approaches
for incision and
drainage
Intraoral
Transcutaneous
Upper premolars and
molars, lower premolars
Intraoral
Transcervical
Intraoral
Transcervical
Lower third molars,
mandibular angle fracture
Lower third molars,
mandibular angle fracture
Intraoral
Lower molars Transcervical
Lower premolars and
Transcervical
molars, trauma
Transcervical
symphyseal fracture
Intraoral
Transcervical
Upper and lower molars,
tonsils, infection in
adjacent spaces
Transcervical
Intraoral
parapharyngeal
(especially lateral incisor)
G. R. Homan et al.
Transcervical
Transtemporal
Pterygomandibular, submas-
seteric, supercial temporal
pterygomandibular, buccal
Deep temporal, sublingual,
parapharyngeal, peritonsillar,
submandibular, submasseteric,
buccal
Buccal fat pad, parotid
duct, facial vessels
geal fascia and skin
Mandibular nerve and
vessels
pterygoid
Sublingual, submental, buccal,
parapharyngeal
Contralateral sublingual,
submental, submandibular,
parapharyngeal
Submandibular gland,
facial vessels
Submandibular gland and
duct, sublingual gland,
lingual and hypoglossal
nerves, lingual vessels
Anterior jugular veins Sublingual, submandibular Lower anterior teeth,
supercial layer of deep cervical
fascia posteriorly
and mylohyoid
supercial layer of deep cervical
fascia anteriorly
Retropharyngeal,
submandibular, sublingual,
pterygomandibular,
peritonsillar, along carotid
sheath
Divided by styloid process
Anterior: Styloid muscles
Posterior: Carotid sheath,
IX, XI, XII
and buccopharyngeal fascia
anteriorly and medial pterygoid
and parotid posteriorly
Buccal Upper anterior teeth
Loose connective tissue Parapharyngeal, mediastinum Spread from
Infraorbital nerves and
and prevertebral fascia
Pterygomandibular Upper molars Intraoral
vessels
Maxillary vessels,
mandibular nerve,
muscles of facial expression
temporalis
Submasseteric Upper and lower molars Intraoral
pterygoid plexus
Temporal fat pad, facial
nerve
Between temporalis and
temporoparietal fascia
Space Location Contents Communicating spaces Likely aetiology
Buccal Between buccinator/buccopharyn-
Table 17.1 Spaces involved in deep neck space infections, their contents, communications, likely causes and surgical approaches to draining them
Submasseteric Between mandible and masseter Masseteric vessels Supercial temporal,
Pterygomandibular Between mandible and medial
Submandibular Between mylohyoid and
Sublingual Between oor of mouth mucosa
Submental Between mylohyoid and
Parapharyngeal Between pharyngeal constrictors
Retropharyngeal Between pharyngeal constrictors
Infraorbital Between canine fossa and
Deep temporal Between temporal bone and
Supercial
temporal
Adapted from Bridgeman [3] and Flynn [8]
17 Odontogenic Infections andDeep Neck Collections
https://t.me/medicina_free
235
Fig. 17.1 Anatomy and computed tomography of deep
neck space infections. Anatomical drawings adapted from
Feigl [7], Granite [6], and Grodinsky and Holyoke [4].
Computed tomography scans of deep neck space infec-
tions: (a and b) show a submandibular abscess from the
same patient, (c) buccal space abscess, (d) pterygomandibular abscess causing inammation of the medial pterygoid muscle and resulting in trismus
236
https://t.me/medicina_free
G. R. Homan et al.
17.6 Diagnosis—Management
17.6.1 Clinical Assessment
andWork-Up
Patients with deep neck space infections most
commonly present with odynophagia, dysphagia,
fever, neck pain, neck swelling, trismus and dysphonia. Additional symptomology may result
from their direct effect on adjacent structures and
is discussed later in this chapter. The signs and
symptoms of deep neck space infection are summarised in Table17.2.
The most sensitive clinical features to detect
moderate to high-risk infections are swelling,
lymphadenopathy and trismus [9] (Fig. 17.2).
The most specic features to differentiate
between moderate to high-risk and low-risk
infections are: dysphonia, oor of mouth elevation, dyspnoea, dysphagia or odynophagia, trismus, fever and tachypnoea [9].
The teeth most likely to cause moderate- to
high-risk infections are the mandibular second
and third molars as they drain directly to the submandibular and masticator spaces and can readily spread to the parapharyngeal space.
Miller etal. [10] showed that clinical assessment alone was only 63% accurate (55% sensitive and 73% specic) in identifying a drainable
collection of 2mL or more in deep neck space
infections. Contrast-enhanced computed tomography (CT) alone was only 77% accurate (95%
sensitive, 53% specic). Combining both of these
modalities lead to 89% accuracy with 95% sensitivity and 80% specicity. This highlights the
importance of CT as an adjunct to clinical assess-
Table 17.2 Signs and symptoms of deep neck space
infection
Signs Symptoms
Neck swelling
Fever
Trismus
Pharyngeal wall medialisation
Dysphonia facial swelling
Oral swelling
Tongue elevation
Floor of mouth swelling
Pharyngeal wall medialisation
Neck pain
Odynophagia
Dysphagia
Dyspnoea
Otalgia
Sialorrhea/drooling
ment as 40% of the purulent collections on CT
were not identied on clinical examination.
Ban etal. [11] developed a prediction tool for
the likelihood of nding purulent discharge at
incision and drainage and stated that any three of
the following was 81.4% accurate in predicting
pus (79.5% sensitive, 82.8% specic):
1. Peripheral rim enhancement on CT.
(a) Also a>2.45mL hypodense area on CT.
2. CRP>41.25mg/L.
3. ESR>56.5mm/h.
4. Neutrophil to lymphocyte ratio>8.02.
17.6.2 Treatment
In their work on Ludwig’s Angina, Williams and
Guralnick [5] stated that the fundamental tenets
of the management of deep neck space infections
are: “to establish an adequate airway, to relieve
tension, to secure drainage and to combat the
infection by supplementary measures.” Adoption
of these principles, lead to a drop in mortality of
54–10% in 3years. Notably, such improvement
occurred prior to the use of penicillin, the rst
true antibiotic, and highlights the role of securing
the airway and surgical egress in managing these
infections. Modern medical care has further
reduced the mortality from Ludwig’s Angina to
4%.
We expand on these tenets by outlining the
following additional steps:
1. Identify the presenting problem (i.e., infection
and spaces involved).
2. Attempt to identify the cause (e.g., odonto-
genic or pharyngotonsillar).
3. Determine the severity.
(a) Airway.
(b) Spaces involved.
(c) Duration and progression.
(d) Host factors.
(e) Determine setting of care (inpatient,
intensive care or outpatient).
4. Supportive medical care (including antibiot-
ics, uid resuscitation and nutrition).
5. Treat surgically.
17 Odontogenic Infections andDeep Neck Collections
https://t.me/medicina_free
237
a
b
c d
Fig. 17.2 Clinical photographs of deep neck space infections. Clinical photographs of deep neck space infections:
(a) temporal space infection, (b) buccal space infection, (c)
submandibular space infection, (d) Ludwig’s Angina affecting the bilateral submandibular, sublingual and submental
spaces with elevation of the oor of mouth and tongue
238
https://t.me/medicina_free
G. R. Homan et al.
(a) Removal of the cause (tooth, tonsil or
other).
(b) Drain any suppurative exudate.
(c) Debride necrotic tissue.
6. Evaluate and re-evaluate.
(a) Identify causes of treatment failure and
adjust (i.e., changing antibiotics).
As is customary in all aspects of medical and
surgical care, the identication of the presenting
problem (and the spaces involved) can be
achieved by the undertaking of a thorough clinical history, selection of appropriate diagnostic
imaging (CT scan) and the requesting of relevant
blood tests. Orthopantomogram X-rays are also
helpful in the assessment of odontogenic infections as they are less susceptible to metal artefact
and show the teeth and potential causes of pulp
necrosis more clearly. Identication of the cause
follows from this but is not always obvious and,
in some instances, cannot be found.
Determining the severity of the infection
allows for appropriate determination of patient
disposition (outpatient, inpatient or intensive
care) and ideal delivery of care. The most important of these steps is to determine whether or not
the airway is at risk and this is a clinical decision.
Inability to lay at, tripoding and stridor are late
signs of impending airway obstruction. Patients
with impending airways should not be put in the
CT scanner until their airway has been secured.
Similarly, they should not be transferred to
another health facility for denitive management
until their airway has been secured. Thorough
clinical assessment includes exible nasopharyngolaryngoscopy to assess oedema and pharyngeal wall medialisation.
In the stable patient, the spaces involved on
CT and their proximity to the airway and muscles
of mastication can help predict potential airway
challenges. Often trismus will necessitate awake
bre-optic intubation with consideration given to
the establishment of a surgical airway being
required in more difcult cases. Although aspiration of purulent exudate is a potential consideration, safely securing the airway is paramount.
The anatomical spaces closest to the teeth are
considered low-risk spaces (i.e., vestibular, pala-
tal, buccal, infraorbital) as well as the subcutaneous space. These low-risk spaces can often be
treated in the outpatient setting under local anaesthetic, but host factors and the need for any supportive medical care should also be considered.
Moderate- and higher-risk infections should be
treated in an inpatient setting. The sublingual,
submental and masticator spaces are considered
moderate risk for their ability to spread to adjacent spaces and induce trismus. High-risk spaces
include those that affect the airway or other vital
structures including the parapharyngeal, retropharyngeal and pretracheal spaces. Once infection involves the prevertebral space, mediastinum,
or has gone intra-orbital or intra-cranial, the risk
of morbidity and mortality increases
signicantly.
Host factors such as diabetes mellitus, malnutrition, alcoholism, active malignancy and
immune compromise in its broadest sense
(including organ transplant, chemotherapy and
rheumatological patients) as well as the duration
and rate of progression of the infection can further affect the severity with more aggressive
treatment being required in immunecompromised patients and those with rapidly
progressing signs and symptoms.
Supportive medical therapy starts at assessment and includes uid resuscitation, nutritional
support and appropriate antibiotics. Most deep
neck space infections are sensitive to penicillins, but there is a growing trend to microbial
production of beta-lactamase. It is also important to note that whilst ampicillin and metronidazole cross the blood-brain barrier, clindamycin
does not. The use of steroids in pharyngotonsillar infections has been shown to help reduce
length of hospital stay, pain and trismus, but
their use in odontogenic infections is
controversial.
Fu etal. [12] showed that the most signicant
factors for requiring an admission to the Intensive
Care Unit (ICU) from odontogenic infections
were lower third molar involvement, dysphagia
and a CRP >150mg/L.All patients admitted to
ICU in their study were identied as having mandibular infections, submandibular swelling and
trismus.
Соседние файлы в папке @xirurgi_2025