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of omohyoid muscle

Thyroid gland

Cricothyroid

nerve (proximal stump)

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Fig. 6.17 The ansa cervicalis is found between the jugular vein and the omohyoid muscle (on the superior belly). The ansa cervicalis is cut just superior to the omohyoid branch

D. Costello et al.

Hyoid bone

Jugular vein

Superior belly

ANSA hypoglossi

Cricothyroid

muscle

Fig. 6.18 Recurrent laryngeal nerve exposed in the tracheo-oesophageal groove and anastomosed to the ansa cervicalis

Thyroid

cartilage

muscle

Inferior belly

of omohyoid muscle

ANSA cervicalis

Site of anastomosis

Recurrent laryngeal

6 Surgery forVocal Fold Immobility

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divided. Using a microscope, the stump of the ansa cervicalis is anastomosed to the distal stump of the RLN, using one or two microsutures 9-0 and brin glue (Fig. 6.18). A small drain is placed, and nal haemostasis is performed. The wound is closed in two or three layers.

6.2.3.3 Postoperative Care

During the rst week, movement of the head should be limited. The drain can be removed 1day after surgery.

No dietary limitations are required, but soft food may be preferred. In cases of aspiration, swallowing must be performed with the head turned towards the side of the operation. Swallowing usually improves within 2weeks.

The patient should be informed that the voice will rst be worse before it gets better. Improvement of the voice will take at least 6–9months, and it will gradually improve within 2years.

References

1. Nouraei SAR, Allen J, Kaddour H, Middleton SE, Aylin P, Darzi A, Tolley NS.Vocal palsy increases the risk of lower respiratory tract infection in low-risk, low-morbidity patients undergoing thyroidectomy for benign disease: a big data analysis. Clin Otolaryngol. 2017;42:1259–66.

2. Woo P, Pearl AW, Hsiung MW, Som P.Failed medialization laryngoplasty: management by revision surgery. Otolaryngol Head Neck Surg. 2001;124:615–21.

3. Green DC, Berke GS, Ward PH.Vocal fold medialization by surgical augmentation versus arytenoid adduction in the in-vivo canine model. Ann Otol Rhinol Laryngol. 1991;100:280–7.

4. Chang J, Schneider SL, Curtis J, Langenstein J, Courey MS, Yung KC. Outcomes of medialization laryngoplasty with and without arytenoid adduction. Laryngoscope. 2017;127:2591–5.

5. Alghonaim Y, Roskies M, Kost K, Young J.Evaluating the timing of injection laryngoplasty for vocal fold paralysis in an attempt to avoid future type 1 thyroplasty. J Otolaryngol Head Neck Surg. 2013;42:24.

6. Friedman AD, Burns JA, Heaton JT, Zeitels SM. Early versus late injection medialization for unilateral vocal cord paralysis. Laryngoscope. 2010;120:2042–6.

7. Vila PM, Bhatt NK, Paniello RC.Early-injection laryngoplasty may lower risk of thyroplasty: a systematic review and meta- analysis. Laryngoscope. 2018;128:935–40.

8. Snyder SK, Angelos P, Carty SE, Doherty GM, Howe JR, Lee JA, etal. Injection of bulking agents for laryngoplasty. Surgery. 2018;163:6–8.

9. Isshiki N, Okamura H, Ishikawa T.Thyroplasty type I (lateral compression) for dysphonia due to vocal cord paralysis or atrophy. Acta Otolaryngol. 1975;80:465–73.

10. Isshiki N, Morita H, Okamura H, Hiramoto M.Thyroplasty as a new phonosurgical technique. Acta Otolaryngol. 1974;78(5–6):451–7.

11. Hess MM, Fleischer S.Laryngeal framework surgery: current strategies. Curr Opin Otolaryngol Head Neck Surg. 2016;24(6):505–9.

12. Siu J, Tam S, Fung K. A comparison of outcomes in interventions for unilateral vocal fold paralysis: a systematic review. Laryngoscope. 2016;126(7):1616–24.

13. Desuter G, Zapater E, Van der Vorst S, Henrard S, van Lith-Bijl JT, van Benthem PP, Sjögren EV.Very long-term voice handicap index voice outcomes after Montgomery Thyroplasty: a cross-sectional

study. Clin Otolaryngol. 2018;43:1097. https://doi.org/10.1111/

coa.13113. [Epub ahead of print].

14. Ryu IS, Nam SY, Han MW, Choi SH, Kim SY, Roh JL.Long-term voice outcomes after thyroplasty for unilateral vocal fold paralysis. Arch Otolaryngol Head Neck Surg. 2012;138(4):347–51.

15. Dastolfo C, Gartner-Schmidt J, Yu L, Carnes O, Gillespie AI.Aerodynamic outcomes of four common voice disorders: moving toward disorder-specic assessment. J Voice. 2016;30:301–7.

16. Gibbins N. The evolution of laryngeal reinnervation, the current state of science and thoughts for future treatments. J Voice. 2014;28:793–8.

17. Benninger MS, Chota RL, Bryson PC, Drake RL.Custom implants for medialization laryngoplasty: a model that considers tissue compression. J Voice. 2015;29:363–9.

18. Netterville JL, Fortune S, Stanziale S, Billante CR.Palatal adhesion: the treatment of unilateral palatal paralysis after high vagus nerve injury. Head Neck. 2002;24:721–30.

19. Montgomery WW, Blaugrund SM, Varvares MA. Thyroplasty: a new approach. Ann Otol Rhinol Laryngol. 1993;102:571–9.

20. Zeitels SM, Mauri M, Dailey SH. Medialization laryngoplasty with Gore-Tex for voice restoration secondary to glottal incompetence: indications and observations. Ann Otol Rhinol Laryngol. 2003;112:180–4.

21. Schneider B, Denk DM, Bigenzahn W. Functional results after external vocal fold medialization thyroplasty with the titanium vocal fold medialization implant. Laryngoscope. 2003;113:628–34.

22. Cummings CW, Purcell LL, Flint PW. Hydroxylapatite laryngeal implants for medialization. Preliminary report. Ann Otol Rhinol Laryngol. 1993;102:843–51.

23. Benninger MS, Manzoor N, Ruda JM. Short- and long-term outcomes after silastic medicalization laryngoplasty: are arytenoid procedures needed? J Voice. 2015;29:236–40.

24. Desuter G, Henrard S, Van Lith-Bijl JT, Amory A, Duprez T, van Benthem PP, Sjögren E. Shape of thyroid cartilage inuences outcome of Montgomery medialization thyroplasty: a gender issue. J Voice. 2017;31:245.e3–8.

25. Desuter G, Cartiaux O, Pierard J, Henrard S, van Lith-Bijl J, van Benthem PP, Sjögren E. Accuracy of thyroid cartilage fenestration during Montgomery medialization thyroplasty. J Voice. 2019;34:609. https://doi.org/10.1016/j.jvoice.2019.01.005. [Epub ahead of print].

26. Lekue A, García-López I, Santiago S, Del Palacio A, Gavilán J. Diagnosis and management with botulinum toxin in 11 cases of laryngeal synkinesis. Eur Arch Otorhinolaryngol. 2015;272:2397–402.

27. van Lith-Bijl JT, Mahieu HF, Stolk RJ, Tonnaer JA, Groenhout C, Konings PN. Laryngeal abductor function after recurrent laryngeal nerve injury in cats. Arch Otolaryngol Head Neck Surg. 1996;122:393–6.

28. Lin RJ, Smith LJ, Munin MC, Sridharan S, Rosen CA.Innervation status in chronic vocal fold paralysis and implications for laryngeal reinnervation. Laryngoscope. 2018;128:1628–33.

29. Smith ME, Houtz DR.Outcomes of laryngeal reinnervation for unilateral vocal fold paralysis in children: associations with age and time since injury. Ann Otol Rhinol Laryngol. 2016;125:433–8.

30. Zur KB, Carroll LM. Recurrent laryngeal nerve reinnervation in children: acoustic and endoscopic characteristics pre- intervention and post-intervention. A comparison of treatment options. Laryngoscope. 2015;125:S1–S15.

31. Marcum KK, Wright SC Jr, Kemp ES, Kitse DJ.A novel modication of the ansa to recurrent laryngeal nerve reinnervation procedure for young children. Int J Pediatr Otorhinolaryngol. 2010;74:1335–7.

32. Crumley RL.Update: ansa cervicalis to recurrent laryngeal nerve anastomosis for unilateral laryngeal paralysis. Laryngoscope. 1991;101:384–7; discussion 388.

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D. Costello et al.

33. van den Boer C, Wiersma AL, Marie JP, van Lith-Bijl JT.Treatment of unilateral vocal fold paralysis with ansa cervicalis to recurrent nerve anastomosis in a young adolescent: European case report. J Laryngol Otol. 2018;132:661–4.

34. Goding GS Jr. Nerve-muscle pedicle reinnervation of the paralyzed vocal cord. Otolaryngol Clin North Am. 1991;24:1239–52.

35. Hogikyan ND, Johns MM, Kileny PR, Urbanchek M, Carroll WR, Kuzon WM Jr. Motion-specic laryngeal reinnervation using muscle-nerve-muscle neurotization. Ann Otol Rhinol Laryngol. 2001;110:801–10.

36. Debnath I, Rich JT, Paniello RC.Intrinsic laryngeal muscle reinnervation using the muscle-nerve-muscle technique. Ann Otol Rhinol Laryngol. 2008;117:382–8.

37. Mendelsohn AH, Berke GS.Surgery or botulinum toxin for adductor spasmodic dysphonia: a comparative study. Ann Otol Rhinol Laryngol. 2012;121:231–8.

38. DeConde AS, Long JL, Armin BB, Berke GS. Functional reinnervation of vocal folds after selective laryngeal adductor denervation- reinnervation surgery for spasmodic dysphonia. J Voice. 2012;26:602–3.

Part III

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Benign and Diagnostic Neck Surgery

Incision andDrainage ofDeep Neck

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Space Infections

FrancisVaz, AleixRovira-Casa, andAndrewDias

7.1 Introduction

The incidence of deep neck space infections (DNSIs) has decreased since the discovery of antibiotics [1] and the improvement of dental hygiene. DNSI poses considerable challenges in diagnosis and treatment, and may potentially lead to life-threatening complications such as descending necrotizing mediastinitis, septic shock, pleural and pericardial effusion, cavernous sinus and internal jugular vein thrombosis, or carotid artery erosion [2]. DNSIs are categorized depending on the neck space involved. Those most frequently involved are the retropharyngeal, peritonsillar, masseteric, pterygopalatine, maxillary, parapharyngeal, submandibular, and parotid, and abscesses of the oor of the mouth [3]. The management of DNSI includes control of the airway, effective antibiotic therapy, and surgical intervention when indicated. When a signicant deep neck space abscess is diagnosed, incision and drainage (I+D) should be considered on an urgent basis in adults [4]. A different scenario is described for children, as conservative management may be effective for selected patients [5], but every case should be managed on its own clinical merits. The goals of surgery are to stop the progression of the infection, obtain a sample for microbiology and sensitivity, and create a drainage pathway.

7.2 Epidemiology

Before the antibiotic era, infections of the tonsillar and peritonsillar space were the most common cause of DNSI [1], but recent literature agrees that odontogenic infections are now the most common source of DNSI [6–9]. The incidence of DNSI has increased over the past few years [10]. It has been proposed that this phenomenon may be a consequence of reductions in the number of tonsillectomies and in antibiotic prescribing [11]. Paediatric DNSIs are more commonly attributed to lymphadenitis, presumably because of the low incidence of dental infection and the predominance of retropharyngeal abscess [12, 13]. DNSIs have been reported to be more frequent in adult men than in women [14–16], but no sex predilection has been proven among paediatric patients, possibly because of a lack of published data [10].

Risk factors for developing DNSI have been reported. Diabetes mellitus has been shown to have a 1.96 risk ratio for involvement of multiple deep neck spaces [17]. Immunosuppression from other sources, such as HIV infection, chemotherapy, chronic renal failure, hepatic disease, and chronic steroid therapy for autoimmune disease, also places a patient at increased risk for more severe and atypical infections [18].

Cultures of aspirates from deep neck abscesses are commonly polymicrobial and reect the oropharyngeal ora and the odontogenic nature of these infections.

F. Vaz (*) University College London Hospital (UCLH), London, UK

A. Rovira-Casa ENT Department, Guy’s and St Thomas’ NHS Foundation Trust, London, UK e-mail: aleix.rovira@nhs.net

A. Dias South Inrmary Victoria University Hospital, Cork, Ireland

https://doi.org/10.1007/978-3-031-36593-5_7

7.3 Clinical Investigation

DNSIs are a challenging problem, because the complex anatomy of the head and neck area makes them difcult to diagnose, easily spread to other structures, and potentially able to affect many cervical neurovascular and visceral structures. Clinical suspicion remains crucial for the important early diagnosis of this entity. Diagnosis of DNSI among children is even more challenging, as the presentation can be more

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F. Vaz et al.

subtle and the clinical examination can be more difcult [10]. Comprehensive history taking and clinical evaluation are keystones in the diagnosis of DNSI in both adults and children.

Initial laboratory work should include a complete blood count with differential, serum glucose, and electrolytes; coagulation studies; HIV screening in adults; blood cultures; and appropriate cultures of aspirates obtained before antibiotics are instituted, if possible [18]. Cross-section imaging is crucial for characterizing the nature of a deep neck lesion, identifying the spaces involved, planning surgical drainage, evaluating the risk of airway obstruction, and aiding in the early recognition of complications. Ultrasound imaging is a useful tool to differentiate inammation from collection, and also can be used for guidance of percutaneous drainage.

Table 7.1 Neck spaces and infections

Space Limits Contents Masticator/

temporal space

Parapharyngeal space

Submandibular and sublingual space

• Lateral: Fascia over masseter muscle

• Medial: Fascia over pterygoid muscles

Inverted pyramid:

• Superior Base: Skull base (middle cranial fossa)

• Inferior Apex: Greater cornu of the hyoid bone

• Lateral: Medial pterygoid muscle, deep parotid, and mandible

• Medial: Superior constrictor and pharyngobasilar fascia

• Anterior: Pterygomandibular raphe

• Posterior: Prevertebral fascia

• Superior: Floor of mouth mucosa

• Inferior: Digastric

• Posterior:

Stylomandibular ligament and posterior belly of the digastric [27]

Partially divided by the mylohyoid muscle to create the sublingual space (above) and the submandibular space (underneath)

Mandible, mastication muscles (masseter, medial pterygoid, lateral pterygoid, and temporalis), third division of the trigeminal nerve (V3), internal maxillary artery, and buccal fat pad The styloid process divides this space:

• Prestyloid compartment: Styloid muscles, fat, lymph nodes, internal maxillary artery, inferior alveolar, auriculotemporal, and lingual nerves, and the deep lobe of the parotid

• Poststyloid compartment: Carotid artery, internal jugular vein, sympathetic chain, and cranial nerves IX, X, XI, and XII [21]

Sublingual and submandibular glands; hypoglossal, marginal and lingual nerves; Warton’s duct; and facial vessels

7.4 Airway Management

The rst action when dealing with a patient with suspected DNSI is to evaluate and secure the airway. Spaces that present more potential risk of airway impairment include the sublingual, parapharyngeal, and retropharyngeal spaces (see Table7.1 below). Upper airway bre-optic evaluation should be done during the rst clinical examination. If the patient is clinically short of breath or the examination shows airway obstruction, medical treatment should be administered. Oxygen, intravenous steroids, and epinephrine nebulizers should be the rst line of treatment. When surgical drainage is to be performed in a patient with airway obstruction, an expert anaesthetist is required, and an operating surgeon must be available to perform a surgical tracheostomy when necessary.

General considerations/ sources of infection Symptoms Surgical approach

Odontogenic infections are the commonest source of infection [19]

Related to multiple neck spaces, so pharyngitis, tonsillitis, parotitis, and cervical lymphadenitis are common sources of infection (as well as odontogenic infections through indirect spread from other DNSI) [22] Conservative treatment with antibiotics could be indicated [23, 24]

Due to its relation with the teeth, odontogenic origin is the most frequent source of infection. The mylohyoid muscle attachment becomes more superior as it runs posteriorly along the internal surface of the mandible, making the second and third molars the most common origin of infection

Trismus, sore throat, dysphagia, pain around the mandible, and preauricular area [20]

Prestyloid: Trismus (affects the masticator muscles) and medial displacement of the tonsil Poststyloid: Different symptoms according to the structures involved, such as Lemierre’s syndrome, Horner’s syndrome, or other cranial nerve palsies

Because of the location of this space, when the infection occurs bilaterally (Ludwig’s angina), the airway is compromised (a potential lifethreatening condition [28])

Medial to mandible: Intraoral Lateral to mandible: External approach

When the prestyloid compartment is affected, transoral approach has also been proven to be a valid option as an alternative to a transcervical approach [25, 26]

Intraoral or external approach

7 Incision andDrainage ofDeep Neck Space Infections

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Table 7.1 (continued)

Space Limits Contents Peritonsillar

space

Visceral space

Carotid sheath Conuence of each

Retropharyngeal space

Danger space

Prevertebral space

Between tonsil capsule and the superior constrictor muscle

• Superior: Hyoid bone

• Inferior: T4

• Anterior: Supercial

layer of deep cervical fascia

• Posterior: Prevertebral fascia

• Lateral: Parapharyngeal space and carotid sheath

layer of the deep cervical fascia (Lincoln’s Highway) from skull base to thorax

• Superior: Skull base

• Inferior: T4 (carina)

• Anterior: Pharynx/

oesophagus

• Posterior: Alar fascia

• Lateral: Carotid

sheaths

• Superior: Skull base

• Inferior: Diaphragm

• Anterior: Alar fascia

• Posterior:

Prevertebral fascia

• Superior: Skull base

• Inferior: Diaphragm

• Anterior:

Prevertebral fascia

• Posterior: Vertebral bodies

Loose connective tissue and branches from lingual, facial, and ascending pharyngeal vessels

Trachea, oesophagus, larynx, pharynx, and thyroid gland

• Common carotid artery

• Internal jugular vein

• Vagus nerve

Retropharyngeal lymph nodes and connective tissue

Loose areolar tissue Possibility of easy spread of

• Dense areolar tissue

• Prevertebral muscles

• Vertebral vessels

• Brachial plexus

• Phrenic nerve

General considerations/ sources of infection Symptoms Surgical approach

Although not a deep cervical space, the infection can easily pass through the superior constrictor muscle to the prestyloid parapharyngeal space, making it a potential source of deep cervical infection Uncommonly affected by DNSI; iatrogenic origin of infection has been described [29] Caudal extension to the superior mediastinum, potential source of mediastinitis [30]

Infections arise from direct inoculation or extension from the surrounding spaces [31]

Infections spread from the parapharyngeal space [32], or through lymphatic spread from nasal cavity or nasopharynx, (children) In adults, the most typical aetiology is trauma to the posterior pharynx resulting in retropharyngeal infection and eventual abscess formation [33, 34] Because of the location of this space and because it is not a common pathology, diagnosis can be delayed

the infection to the mediastinum, because its lower limit is at the level of the diaphragm. Infection in this space arises from the retropharyngeal space [29] Main pathway is by infection of the vertebral bodies and penetrating injuries. Tuberculosis may affect this space, creating the Pott’s abscess [37]

Children: Neck pain, neck swelling, fever, irritability, dysphagia, excessive drooling, and dyspnoea or noisy breathing suggestive of upper airway compromise [35, 36] Adults: Neck pain, fever, anorexia, nasal obstruction, snoring, dyspnoea [29]

Intraoral

External approach

Collection smaller than 2cm conservative management Airway compromise or no improvement after 24–48h of medical treatment: surgical drainage [33] Intraoral approach is the gold standard if the infection is contained medial to the great vessels [37]

Alar f

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7.5 Anatomy

7.5.1 Fascial Layers

The term fascia refers to a sheet or any other dissectible aggregations of connective tissue that forms beneath the skin to attach, enclose, and separate muscles and other internal organs [28]. Our necks are divided into spaces (Fig.7.1), and therefore, a comprehensive knowledge of the neck fascial framework is essential to plan surgical treatment and anticipate potential complications. The multiple layers of cervical fascia create the spaces through which DNSI arise and spread.

The supercial fascia of the neck is a layer of brofatty tissue connecting the overlying skin to the deeper fascial layers enveloping the platysma and the facial expression muscles [38]. Supercial space infections usually take the form of cellulitis. When an abscess arises in this space, I+D along Langer’s lines with appropriate antibiotic therapy is the treatment of choice.

The deep cervical fascia is divided into three layers. The supercial layer of deep cervical fascia (or investing fascia) originates from the posterior spinous processes of the vertebrae, nuchal line, and the mastoid process surrounding the neck to its anterior insertions into the sternum, hyoid, mandible, and zygomatic arches. On its way from posterior to

anterior, it envelops muscles (trapezius, sternocleidomastoid, anterior belly of the digastric, and masticatory muscles), two salivary glands (submandibular and parotid), and two fascial compartments (parotid and masticator spaces). This layer also forms the stylomandibular ligament, which separates the parotid from the submandibular gland [27]. This layer of fascia, medial and deep to the sternocleidomastoid muscle, contributes to the lateral aspect of the carotid sheath [30]. It has been reported that this layer is not present between the posterior edge of the sternocleidomastoid and the anterior surface of the trapezius [39].

The middle layer of deep cervical fascia (or visceral fas- cia) is divided into muscular and visceral divisions and encloses the anterior contents of the neck [30]. The muscular division surrounds the infrahyoid strap muscles (sternohyoid, sternothyroid, thyrohyoid, omohyoid). The visceral division surrounds the buccinator, pharyngeal constrictor muscles, larynx, trachea, oesophagus, thyroid, and parathyroid glands and extends down into the anterior mediastinum, overlying the brous pericardium and great vessels [30]. The visceral division contributes the buccopharyngeal fascia separating the oesophagus from the deep layer of the deep cervical fascia and forms the anterior border of the retropharyngeal space. The middle layer also contributes to the medial aspect of the carotid sheath.

Superﬁcial layer

Deep cervical fascia

Pretracheal

(visceral) fascia

Buccopharyngeal

(visceral) fascia

Carotid sheath

Prevertebral

layer deep cervical fascia

ascia (anterior layer of

prevertebral fascia)

Retropharyngeal

space

Danger space

Trachea

Infrahyoid fascia

Thyroid gland

Sternocleidomastoid muscle

Common carotid arte

Internal jugular vein

Oesophagus

Cervical vertebra (C7)

Fig. 7.1 The neck fascial framework

7 Incision andDrainage ofDeep Neck Space Infections

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The deep layer of deep cervical fascia (or prevertebral

fascia) contains the deep neck musculature, brachial plexus,

phrenic nerve, vertebral vessels, subclavian vessels inferiorly, and the vertebral column. It divides into two layers: the prevertebral and alar layers. Both layers contribute to the posterior aspect of the carotid sheath [40]. The carotid sheath is a conuence of each layer of deep fascia running from the skull base to the thorax.

7.5.2 Neck Spaces

The described fascial framework creates multiple real and potential deep neck spaces—understanding a space to be an anatomic region bounded by fascia. In this way, neck spaces are classied according to their location, for example suprahyoid, infrahyoid, or parapharyngeal. Table7.1 outlines the limits and contents of these spaces and lists considerations regarding infections in each space.

7.6 Most Relevant Complications

7.6.1 Necrotizing Fasciitis

Necrotizing fasciitis is a severe form of deep neck infection that occurs more often in older patients and those who are immunocompromised. Treatment requires critical care support, management of immunocompromising conditions, broad-spectrum intravenous antibiotics, and surgical exploration [41]. Debridement of dead tissue until a bleeding, viable edge or vital nerves or vessels are reached is recommended. Mortality may be as high as 20–30% in treated patients [42].

7.6.2 Mediastinitis

Mediastinitis is a rare complication of deep neck infection caused by the spread of infection along the retropharyngeal and prevertebral planes of the neck into the upper mediastinum [43]. Presentation includes diffuse neck oedema and pleuritic pain with deep breathing. Cross-section imaging with intravenous contrast often reveals the presence of uid collection, air-uid levels, or stranding or inltration of the mediastinal fat. Thoracotomy should be strongly considered in cases that extend beyond the upper mediastinum or that involve more than one mediastinal compartment.

7.6.3 Lemierre’s Syndrome

Lemierre’s syndrome is septic thrombophlebitis of the internal jugular vein following an oropharyngeal infection [44].

Up to 60% of cases are caused by a Fusobacterium necroph- orum infection [45]. Other pathogens that have been described include Streptococcus, Staphylococcus aureus, Klebsiella spp., and Pseudomonas [46]. The key to early diagnosis is awareness of the classic history and course of this illness. Diagnosis can be conrmed by showing thrombophlebitis of the internal jugular vein, culturing F. necroph- orum from normally sterile sites, or demonstrating metastatic lesions in this clinical setting. The cornerstone of management is draining of purulent collection where possible, with prolonged courses of appropriate antibiotics [47]. First-line therapy includes intravenous beta-lactamase-resistant antibiotics with or without heparin anticoagulation. Surgery to excise the jugular vein may be indicated in patients with a worsening clinical course despite appropriate medical therapy or in the event of neck abscess formation.

7.6.4 Ludwig’s Angina

Ludwig’s angina is a life-threatening cellulitis of the soft tissue involving the oor of the mouth and neck. Both the sublingual and submaxillary spaces are involved bilaterally. Infection in the lower molar is the most common cause of Ludwig’s angina. The infection is rapidly progressive, leading to aspiration pneumonia and airway obstruction [48].

7.7 Conclusion

DNSI can cause life-threatening emergency situations. Careful clinical, haematological, biochemical, and radiological assessments are required. Airway management should always be considered, with the airway secured if necessary. A clear understanding of the anatomy of the neck spaces and the approaches to them is required in order to tackle them surgically. Conservative approaches may be considered, but a careful, individualized management plan is needed for all patients.

References

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2. Hah YM, Jung AR, Lee YC, Eun YG.Risk factors for transcervical incision and drainage of pediatric deep neck infections. J Pediatr Surg. 2018;53:666–70.

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