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138
CHAP TER5 The front oftheneck
Types ofinjury that may occur following
penetratingtrauma
These are highly varied depending on the method of injur y (slash, stab,
clothesline, projectile), direction, and depth of wound. Transverse
wounds are especially wor rying as many of these may be simultaneously
involved. The following functional struc tures are all at var ying degrees
ofrisk:
• Airway
• Vascular
• Nerve(s) (hypoglossal, vagus, recurrent laryngeal, facial, brachial
plexus, spinalcord)
• Thorax (lungs, pleura, mediastinum)
• Lymphatic (thoracicduct)
• Oesophageal/ pharyngeal
• Cervicalspine
• Muscles (SCM and prevertebral).
Assessing injuries tothe front
oftheneck
Injuries to the front of the neck require careful assessment. Be methodical. Always star t using ATLS® guidelines, paying particular attention to
the airway. Consider the site and possible depth of injury (especially with
penetrating injuries). Think of the various anatomical structures that may
be injured and how these may be detec ted.
Remember that injuries to the root of neck can also involve the chest
andarm.
Overview ofsymptoms
• Vascular structures:active bleeding, hypovolaemia, haematoma
(expanding or pulsatile), peripheral pulses (compare with other
side— distal carotid, supercial temporal, brachial, or radial),bruit
• Larynx/ trachea, oesophagus:haemoptysis (ask patient to cough
and spit on paper), air bubbling through wound/ subcutaneous
emphysema, hoarseness, pain on swallowing, haematemesis
• Cr anial ner ves:facial, glossophar yngeal (check midline position of
soft palate), recurrent laryngeal (hoarseness, ineective cough),
accessory (shrug the shoulder), hypoglossal
• Spinal cord and brachial plexus, assess peripheral neurology
• Horner’s syndrome (miosis, ptosis, anhidrosis, enophthalmos).
Assessing direct injuries tothelar ynx
The main concern is sudden loss of the air way. Consider the following:
• Mechanisms of injury:assaults, ‘clothesline injury,’ strangulation,
penetrating injuries (gunshot wounds, knife).
• Development of oedema, and haematomas. This can occur even if
there are no obvious frac tures of the larynx.
• Obvious injur ies to the larynx have a high risk of airway
compromise— ask for immediatehelp.
ASSESSING INJ URI ES TO THE FRO NT OF TH ENECK
• Hyoid and thyroid fractures may lacerate phar yngeal mucosa, which
may be asymptomatic.
• Cr icotr acheal separation is highly unstable. B e careful during
examination.
• Pharyngoesophageal tears are often missed.
• Recurrent lar yngeal nerve injur y.
Investigations
These are tailored to the injuries suspected. CT (with contrast) is usually
a good st arting point and can rapidly assess both the neck and thorax.
Always follow local policy. Useful investigations include:
• Fibreoptic nasopharyngoscope:allows visualization of the endolarynx
with minimal risk to airway, evaluates mobility, lacerations, airway
patency, laryngeal oedema, and haematomas.
• CT of neck:diagnostic test of choice to evaluate laryngeal fractures
(hyoid bone, thyroid, and cricoid cartilage).
• Oesophagram with water- soluble contr ast (avoid barium as there is a
risk of mediastinitis if there is aleak).
• Direct laryngoscopy and oesophagoscopy.
Management principles
• Protect the airway and stabilize the cervical spine
(ABCs):endotracheal intubation may precipitate an air way crisis. In
some ca ses a surgical air way under local anaesthesia may be safer.
Get seniorhelp.
• Laryngeal/ tracheal injur y:seek senior anaesthetic help early as
swelling may result in delayed obstruction. These require urgent
referral.
• Pharyngoesophageal injur y:primar y closure if <24 hours, otherwise
consider drainage procedure, reconstruction, or oesophagectomy.
• Ver tebral ar tery injur y:emboliz ation is preferred due to dicult
exposure and control. If this fails, consider surgical repair.
• Carotid injur y:associated with high mortality (10 – 20%); primary
repair is the treatment of choice, otherwise consider patch grafting,
by- pass grafting, or ligation (avoid ligation if suspected stroke).
• Spinal/ brachial plexus injury:these require referr al to a specialist
unit. Protect the neck/ arm, to avoid movement. Document decits.
• Remember the chest, especially with penetrating injuries.
Non- surgical management
This may be possible with small soft tissue injuries (haematomas), and
stable lar yngeal fr actures with an intact endolarynx. Patients are admitted for obser vation with a tracheostomy set at bedside. They should
be kept NBM, with the head of the bed elevated, voice rest , and given
humidied air. Prophylactic antibiotics, antireux medications, and systemic corticosteroids may also be required.
Indications forsurgical exploration include:
• Airway:compromise, hoarseness, progressive surgical emphysema
• Breathing:pneumothorax, pneumomediastinum
• Circulation:expanding haematoma, pulse decit, active bleeding,
haemoptysis, haematemesis
139
140
CHAP TER5 The front oftheneck
• Specic injuries:(bullet, knife, other); suspected foreignbody
• Specic laryngeal ndings:disrupted anterior commissure, exposed
cartilage, progressive subcutaneous emphysema, fractured/
dislocated laryngeal skeleton, dislocated arytenoids, vocal fold
immobility.
Urgent tracheostomy under local anaesthesia may rarely be required
to protect the air way. Ideally laryngeal injuries should be repaired
within 2– 3days to avoid infection and necrosis. Endoscopic repair may
be attempted for smaller mucosal disr uptions and repositioning of
arytenoids.
Beware of the patient who presents with surgical emphysema following
blunt neck trauma. If untreated, this can result in tension pneumothorax or
cardiac tamponade.
Diculty breathing, noisy breathing,
and upper airway obstruction
Not all noisy breathing is stridor. Moist sounds such as bubbling of secretions in the larynx or pharynx are common and not signicant.
fStridor
Stridor is an abnor mal, high- pitched, musical breathing sound caused by
a narrowing of upper airway. Children are at high r isk because they have
narrower airways. In young children, stridor should be regarded as an emer-
gency and treated immediately.
eStertor
Stertor is a low- pitched snoring or snuy sound produced by vibrations
of tissues in the nasopharynx, pharynx, or soft palate.
Stridor and ster tor are both due to turbulence of the air ow within a
partially obstruc ted respir ator y tract (Table 5.1). Bernoulli’s theorem—
if airpassesthrough a narrow tube, it s velocity increases at the narrowing and its pressure falls. This results in collapse of the airway.
Table5.1 Noisy breathing and thepos sible site ofa irw ay obstruc tion
Site of obstruction Characteristics of stridor
Nasopharyngeal
Oropharynx
Supraglottic
Glottic
Subglottic/ trachea
Tracheobronchial
Stertor with no gurgling
Gurgly stert or wit h hot pot atovoi ce
Inspiratory s tridor wit h hot pot atovoi ce
Inspiratory with hoarseness
Biph asic s tridor with barkingcough
Expiratory stridor with wheezing
DIFFI CULTY BREATHI NG, UPPER AI RWAY OBSTRUC TION
Assessment ofstridor
This is tailored according to the suspectedcause:
• Head and neck examination:or al cavity (macroglossia, tonsillar
hypertrophy, or infection), complete neurological exam (cranial
nerves), evaluate for external compression (trachea midline, goitre,
palpable laryngeal fractures).
• Nasal exam/ nasal endoscopy, for deformities/ masses.
• Fibreoptic laryngoscopy:assess patency, vocal fold mobility,
supraglottis, examine tracheal stoma (retroex to access subglottis).
• Cardiac and pulmonary examination (wheezing, chestpain).
• Direct laryngoscopy:evaluation of the glottis and supraglot tic.
• Bronchoscopy (rigid bronchoscopy for instrumentation).
• CXR and plain neck lms:screening lms for laryngotr acheal
structural defects, intrinsic lung and mediastinal disease.
• CT/ MRI of the neck/ chest.
• Arteriography:indicated if vascular abnormalities are suspected.
fUpper airway obstruction
Upper airway obstruction (UAO) is a life- threatening emergency that
requires prompt diagnosis and treatment . There are many causes,
see Table 5.2. Severe UAO can be surprisingly asymptomatic at rest
if it develops gradually. Sudden clinical deterioration is unpredictable.
Table5.2 Caus es ofupper airway o bstr uct ion ba sed onaetiology
Traumatic
causes
Laryngeal
stenosis
Air way
burn
Acute
laryngeal
injury
Facial
trauma
(mandibular or
maxillary
fr ac tures)
Haemorrhage
Infections Iatrogenic causes Tumours Angio- oedema
Suppurative
parotitis
Retropharyngeal
abscess
Tonsillar
hypertrophy
Ludwig’s
angina
Epiglottitis
Laryngitis
Laryngo -
tracheobronchitis
(cro up)
Diphtheria
Tracheal
sten osis po sttracheostomy
Tracheal stenosis
post- intubation
Mucou s ball f rom
transtracheal
catheter
Foreignbod ies
Vocal cor d
paralysis
Laryngeal
tumours
(benign or
malignant)
Laryngeal
papillo matosis
Tracheal
sten osis
(caused by
intrinsicor
extrinsic
tumours)
Anaphylactic
reactions
C1 inhibitor
deciency
ACE
inhibitors
141
142
CHAP TER5 The front oftheneck
Patients with possible UAO must never be sedated until the air way
is secured. Sedation may precipitate acute respiratory failure. Some
pharmacological interventions (adrenaline (epinephrine), steroids, and
heliox) provide temporary support but cannot signicantly improve
mechanical causes ofUAO.
fCroup (laryngotracheobronchitis)
This is an acute viral infection of the upper airway. There is swelling inside
the throat, which produces the classical symptoms of a ‘barking’ cough
(worse on crying), stridor, and hoarseness. It may produce mild, moder ate, or severe symptoms, of ten worse at night. Diagnosis is often clinical
but the causes previously listed must be carefully excluded. Management
includes keeping the child as calm as possible, steroids, and adrenaline
(epinephrine) in severe cases. Check oxygen saturation. Severe croup
may require admission. Inhalation of hot steam or humidied air may
soothe symptoms. Refer to paediatrics for advice.
eEpiglottitis (supraglottitis)
(See E Chapter 8, pp. 246–7.) This is a potentially life- threatening
disorder. It is typically caused by Haemophilus inuenzae type B. Noninfectious causes of epiglottitis may include tr auma, inhalation and chemical burns, or be associated with systemic disease.
(see http:// www.rch.org.au/ clinicalguide/ guideline_ index/ Acute_ Upper_
Airway_ Obstruction/ ; http:// www.das.uk.com/ guidelines/ guidelineshome.
html).
Initial management ofstridor
These patients can rapidly deteriorate, so call for senior help urgently.
• Evaluate the airway:quickly determine severity of obstruction and
stability of airway (acute vs chronic, progression of stridor, dyspnoea
at rest vs with exercise).
• Establish the air way:complete anoxia can result in death in
4– 5 minutes. Following injur y, secure the airway without moving
the cervical spine. Do not precipitate an airway crisis. Any attempt
at endotracheal intubation should also have a backup plan for an
emergent surgical airway. Initially suc tion blood clots and secretions
from the oropharynx (remove foreign bodies and teeth). Overcome
phar yngeal collapse with jaw thrust and chin lif t. Masked ventilation
may provide adequate oxygenation until able to secure.
• Administer ox ygen. Masked ventilation may adequately improve
oxygenation until help is available to secure airway. After establishing
a secure airway, ease of ventilation and maintenance of ox ygenation
should be reassessed.
• In some cases heliox (80% helium, 20% oxygen) may be used to
provide shor t- term oxygenation in stable airway obstructions. The
O2 concentration may be increased to 40%. Helium has a lower
molecular weight (decreased density) allowing easier passage past
narrow obstructions.
SUBGLOTTIC STENOSIS
• Consider humidication, corticosteroids, nebulized adrenaline
(epinephrine), and antibiotics.
• Once the airway is secure, further imaging may be required to
identify the precise cause of obstruction (if not apparent).
eSubglottic stenosis
The subglottic area is circumferentially bound by the cricoid cartilage and
is the narrowest part of the upper air way in infants (whereas the glottis is
the narrowest in adults). It is a complete non- pliable ring, unlike the trachea, which has a posterior membranous section, and the lar ynx, which
has a posterior muscular section. Narrowing of the subglottic area may
be congenital or acquired. Acquired stenosis (subglottic stenosis (SGS)) is
caused by either infection or tr auma. Iatrogenic injuries play a majorrole.
Congenital
Stenosis can be either membranous or cartilaginous. Membranous stenosis is usually circumferential and may extend upward to include the
true vocal folds. In cartilaginous stenosis, thickening of cricoid cartilage is
seen. This is less common than membranous stenosis.
Acquired
Historically, acquired SGS has been related to infections such as TB
and diphtheria which are very rare now. Stenosis today is more often
caused by endotracheal intubation or high tracheotomy tube placement.
Irritation causes inammation which progress to ischaemia, ulceration,
and granulation tissue, resulting in stenosis and occlusion of the airway.
Additional factors include systemic illness, malnutrition, anaemia, and
hypoxia. Of ten, SGS has an insidious onset , and early manifestations are
mistaken for other disorders (asthma, COPD). Patients with mild stenosis
are usually asymptomatic, and only diagnosed following dicult intubation during anaesthesia. Symptoms otherwise include dyspnoea, stridor,
hoarseness, brassy cough, recurrent pneumonitis, and cyanosis. The
Cotton– Myers gr ading classies obstr uction into grade I(0 – 50%), grade
II (51– 70%), gr ade III (71– 99%), and grade IV (100% of the lumen, i.e. no
detectable lumen) (data from Annals of Otology, Rhinology & Laryngology,
103, 4, Charles M.Myer, David M.O’Connor, Robin T.Cotton, ‘Proposed
Grading System for Subglottic Stenosis Based on Endotracheal Tube
Sizes’, pp.319– 323. Copyright (1994) Sage Publications).
Management
Medical therapy is almost always unsuccessful. For mild or granular stenosis, serial endoscopic dilation with or without steroid injections may
be sucient. Carbon dioxide laser and topical mitomycin C are showing
promising results with endoscopic approaches. Reconstruction may be
necessary for mature and circumferential stenosis which is severe (>70%
luminal obstruction). The goals of open reconstruction are preser vation of the voice by expanding the subglottic air way and stabilizing the
expanded frame. Various procedures exist using grafts and stents.
143
144
CHAP TER5 The front oftheneck
eThe acutely swollenneck
Ludwig’sangina
This is a rapidly spreading, tense cellulitis of the submandibular, sublingual, and subment al spaces bilaterally. When advanced it is an obvious
diagnosis, with gross swelling both in the neck and the mouth. Earlier
infections still need to be treated seriously and need urgent referral.
Ludwig’s angina is a potential airway emergency which if not diagnosed and
treated quickly has a mortality rate of around 75% within the rst 12– 24
hours. With aggressive surgical intervention, good airway control, and
antibiotics this r ate has now droppedto5%.
Usually the cause is a submandibular space infection secondar y to an
infected wisdom tooth. Other causes include tonsillitis, infected mandibular fractures, and submandibular sialadenitis. From the submandibular space, the infection spreads to the ipsilateral sublingual space
around the deep lobe of the submandibular gland. It then pa sses to the
contralateral sublingual space and thence to the adjacent submandibular space. The submental space is also aected by lymphatic spread.
Infec tion can also originate in the sublingual space and spread laterally
to bothsides.
Left untreated, oedema and cellulitis spread backwards in the space
between the hypoglossus and genioglossus to the epiglot tis and lar ynx,
resulting eventually in respiratory obstruction.
Clinical features
• Systemicupset.
• Massive rm swelling bilaterally in theneck.
• Swelling in the oor of the mouth, forcing of the tongue up onto the
palate.
• A‘hot- potato’ voice. This term is used to describe the characteristic
pattern of speech, which has been likened to a person speaking
with a hot potato in the mouth. It has several causes in addition to
Ludwig’s angina.
• Diculty in swallowing and drooling.
• Inability to protrude the tongue.
• Eventually this leads to diculty breathing.
Indicators of severe infection in theneck
• Diculty breathing
• Shock
• Pyrexia
• Malaise
• Dysphagia/ drooling
• Tris m u s
• Dysphonia
• Inability to protrude thetongue
• HighWCC.
INFECTIONS DEEP IN THENECK
Management
The rst consider ation is the airway which can rapidly obstruct. Diculty
in breathing, swallowing, or talking, and gross swelling are all indications to
call for senior help (often anaesthetic) urgently. Refer to maxillofacial or
ENT team urgently. Further management includes IV uids (patients
often present af ter a few days, having not been able to drink), IV antibiotics (e.g. penicillin and metronidazole), together with surgical drainage
of the submandibular and sublingual spaces and removal of the underlying cause. If there is respiratory diculty, give ox ygen. These cases are
commonly associated with self- neglect (including alcohol and smoking)
and immunosuppression (e.g. diabetes).
eInfections deep intheneck
These can be easily overlooked. They usually arise following penetrating injuries, untreated tonsillitis or wisdom tooth infections. Once estab-
lished, the infection can rapidly spread throughout the neck into the chest and
become life- threatening. When this occurs mortality is high. In the early
stages diagnosis can be dicult.
Applied anatomy
The neck may be regarded as containing super cial and deep fascial
planes. These divide it into several specic compartments. Terminology
can be confusing.
Supercial cervicalfascia
This does not play a major role in deep neck infections. It encircles the
neck, blending with the fascia overlying the platysma muscle. Superiorly
it blends with the muscles of the face comprising par t of the ‘SMAS’
(super cial muscular aponeurotic system). This layer is important in certain t ypes of ‘face lif t’ procedures.
Deep cervicalfascia
This is subdivided into three additional layers:
• The most super cial layer of the deep cer vical fascia is also known
as the investing cervical fascia. This encircles the neck like a stock ing,
attaching to and enclosing the SCM, tr apezius, and omohyoid muscles
and the parotid and submandibular glands. Posteriorly it attaches to
the superior nuchal line. It can only distend a small amount.
• The middle layer of the deep cer vical fascia is also known as the
visceral layer. It encircles the strap muscles and the viscera of the
neck (larynx, pharynx, trachea, and thyroid gland). Part of this layer
covers the pharyngeal constrictors and the buccinator muscle— the
buccopharyngeal fascia.
• The deep layer of the deep cervical fascia is also called the
prevertebral fascia. It lies just anterior to the prever tebral muscles
of the spine allowing the pharynx to glide over them during neck
movements and swallowing.
145
146
CHAP TER5 The front oftheneck
These deep fascial planes divide the neck into several compartments,
called ‘fascial tissue spaces’. In the early stages of infection, the fascial
layers limit the spread of infection to within the associated compartment. However, untreated infection will eventually perforate the fascia
and spread more rapidly. Both the middle and deep layers pass into the
chest (Figures 5.2 and 5.3). One fascial space (the retropharyngeal) also
passes into the mediastinum. Deep neck infections can therefore result in
mediastinitis.
Figure5.2 CT sc an show ing la rge abscess d eep to t he SCM m uscle.
Figure5.3 Ope rative nd ing showing a h uge collect ion ofpus.
INFECTIONS DEEP IN THENECK
Commonly infected fascial tissue spaces intheneck
The mylohyoid muscle has been described as the ‘diaphragm’ of the
mouth, separating the oral cavity from the neck . It creates two large (and
two of the most commonly involved) spaces. These are the sublingual
space above the muscle and the submandibular and submental spaces
belowit.
Submandibularspace
This is triangular in shape, bounded superiorly by the mylohyoid muscle
medially and the mandible laterally, and the deep cervical fascia below. It
contains lymph nodes, the supercial lobe of the submandibular glands,
and blood vessels. It communicates with the sublingual space above, and
the deep pterygoid space posterior ly.
Surgical access can be made 2– 3cm below the lower border of the
mandible (to avoid injury to the mandibular branch of the facial nerve).
Skin and subcutaneous tissues are incised. Blunt forceps penetrate the
deep cervical fascia , aiming towards the mandibular border.
Submentalspace
This is contained by the two anter ior bellies of the digastric muscles.
Above is the mylohyoid muscle, and below the deep cervical fascia covered by platysma and skin. It contains submental lymph nodes and communicates posteriorly with the submandibularspace.
Surgical access is obtained behind the chin prominence in theneck.
Signs and symptoms indeep neck infections
These can be deceptive. Fever, malaise, dehydration, and lethargy are
common and patients rapidly become very ill. A very high WCC (>20) is an
ominous sign and often indicates tissue necrosis and a high risk of mortality.
Pain on swallowing should be taken seriously. It can be so severe that the
patient sits drooling, and unable to swallow their own saliva. There may
be cellulitis. Deep- seated abscesses do not uc tuate. Instead swelling
presents with a ‘dough- like’ consistency. Initially the fascia may direct
swelling medially, compromising the airway. Other important signs of
symptoms include dysphagia and trismus. Untreated (if air way obstruction or sepsis does not kill the patient), erosion into the carotid vessels
can result in septic emboli and stroke.
Management
Assess immediately for airway obstruction and when necessar y consider
urgent intubation or a surgical airway. Get senior help. Once the airway is
secure, assess the patient’s haemodynamic status and give uids. Often
they have sat at home for a few days unable to eat and drink so will probably be at least mildly dehydrated. These patients need to be admitted
urgently. Start IV antibiotics. Consider immunosuppression (diabetes,
alcoholics, long- term steroids, HIVetc.)
147