4. Congenital, traumatic, inflammatory diseases of the neck region Flashcards

1
Q

Anatomy of Lymphatics of Head and Neck (2)

A

Waldeyer’s Lymphatic Ring (Inner): It consists of adenoids above, lingual tonsil below
and two palatine tonsils and tubal tonsils laterally one on each side.

Outer Circular Chain of Nodes (Outer Waldeyer’s Ring): Occipital, postauricular,
preauricular, parotid, facial, submandibular, submental, superficial cervical and anterior
cervical.

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2
Q

Rule of 7 - Function

A

The Rule of 7 provides a probable diagnosis of the neck mass based on the average
duration of the patient’s symptoms.

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3
Q

Rule of 7 in the neck

3 points

A

7 days—inflammation

7 months—neoplasm

7 years—congenital defect

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4
Q

Rule of 80 in the neck

5 points

A

80% of nonthyroid neck masses are neoplastic

80% of neoplastic neck masses are seen in males

80% of neoplastic neck masses are malignant

80% of malignant neck masses are metastatic

80% of metastatic neck masses are from primary sites above the clavicle.

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5
Q

Inflammatory Diseases of the Neck (1/8)

A

Pharyngeal and Adenotonsillar Disease

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6
Q

Inflammatory Diseases of the Neck :

Pharyngeal and Adenotonsillar Disease - Etiology

A

The four main sites of Waldeyer’s ring are connected by other minor lymphoid tissue
along the posterior and lateral pharyngeal wall completing the ring. These are all
considered mucosa-associated lymphoid tissue (MALT). These tissues react to
inflammatory disease, infection, trauma, acid reflux, and radiotherapy. Even the
vibratory effects of chronic snoring have been implicated in the development of
adenotonsillar disease.

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7
Q

Inflammatory Diseases of the Neck :

Pharyngeal and Adenotonsillar Disease - Complications.

9 points

A

Adenotonsillar infections present with three temporal patterns: acute, recurrent
acute, and chronic.

Acute infection is typically viral in origin but secondary bacterial invasion may
initiate chronic disease.

Viruses do not cause chronic infections; however, Epstein-Barr Virus (EBV) can cause significant hypertrophy.

Systemic EBV infection, also known as mononucleosis, can mimic bacterial
pharyngitis, but the progression of signs and symptoms demonstrates
lymphadenopathy, splenomegaly, and hepatitis. This can be diagnosed on
bloodwork (heterophile antibody or atypical lymphocytes).

The most common bacterial causes of acute tonsillitis are group A β-hemolytic
streptococcus species (GABHS) and S pneumoniae.

If GABHS is confirmed, then antibiotic therapy is warranted in the pediatric
population to decrease the risk (3%) of developing rheumatic fever.

Complications of GABHS pharyngitis, typically from S pyogenes, can be systematic and include poststreptococcal glomerulonephritis, scarlet fever, and rheumatic fever. Antibiotic therapy does not decrease the incidence of glomerulonephritis.

Scarlet fever, caused by blood-borne streptococcal toxins, causes a strawberry
tongue and a punctate rash on the trunk that spreads distally while sparing the
palms and soles. Peritonsillar abscess is also a common complication that is treated in an ambulatory setting through a transoral approach after appropriate topicalization and local anesthetic.

Deep neck space infections are rare from pharyngitis but can occur from odontogenic and salivary gland infections. These typically require a transcervical approach for incision and drainage.

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8
Q

Inflammatory Diseases of the Neck : Adenoids

Types (2)

A

Acute adenoiditis typically presents with purulent rhinorrhea, nasal obstruction,
and fever and can be associated with otitis media, particularly in the pediatric population. Recurrent acute adenoiditis is defined as four or more acute infections
in a 6-month period, but in an adult, this may be difficult to distinguish from
recurrent acute sinusitis, and endoscopy with or without imaging of the sinuses may be warranted to distinguish between the two diagnoses.

Chronic adenoiditis presents with persistent nasal discharge, halitosis, chronic
congestion, and postnasal drip.

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9
Q

Inflammatory Diseases of the Neck : Adenoids

Treatment (4)

A

In children, obstructive adenoid hyperplasia often requires surgical intervention to
help relieve obstructive symptoms such as snoring, obligate mouth breathing, and hyponasal voice.

The management of adenoid disease is slightly different than that for tonsillar
disease. Chronic infection can be treated with antibiotics, although this often does
not lead to a full resolution of symptoms.

Adenoidectomy is indicated for recurrent and chronic infections that have failed
conservative management.

Adenoidectomy is also the first line of surgical management for children with
chronic sinusitis because the adenoid can obstruct mucociliary clearance from the
sinonasal tract into the choana and ultimately into the pharynx.

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10
Q

Inflammatory Diseases of the Neck (3/8)

A

Tonsils

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11
Q

Inflammatory Diseases of the Neck : Tonsils

4 Points

A

Patients with acute tonsillitis present with sore throat, fever, dysphagia, and tender
cervical nodes with erythematous or exudative tonsils.

First-line treatment is with penicillin or a cephalosporin; however, in those with an allergy, a macrolide can be considered.

A peritonsillar abscess is an infection of the peritonsillar salivary gland (Weber’s gland), located between the tonsil capsule and the muscles of the tonsillar fossa.

In selected cases of active peritonsillar abscess, tonsillectomy is required in the
acute setting to treat systemic toxicity or impending airway compromise.

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12
Q

Inflammatory Diseases of the Neck (4/8)

A

Ludwig’s Angina

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13
Q

Ludwig’s Angina

3 Points

A

It is an inflammatory oedema of submandibular region and floor of the mouth, commonly due to streptococcal infection.

It causes diffuse swelling and brawny oedema of the submandibular region. It is common in severely ill and in advanced malignancy, causing trismus, laryngeal
oedema. Extension of infection into parapharyngeal space may lead to dreaded
internal jugular vein thrombosis.

As the infection is deep to the deep fascia in a closed fascial plane, it spreads very fast causing dangerous complications.

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14
Q

Ludwig’s Angina

Precipitating factors (6)

A

Caries teeth

Oral or other malignancy

Submandibular salivary infection/calculi

Chemotherapy

Chronic diseases like diabetes mellitus

Cachexia of any cause

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15
Q

Ludwig’s Angina

Clinical Features (4)

A

Fever, toxicity, diffuse swelling, dysphagia, dyspnoea, trismus.

Intraoral oedema is common.

Brawny swelling in submandibular region.

Putrid halitosis, drooling of saliva, earache.

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16
Q

Ludwig’s Angina

Treatment (3)

A

Antibiotics

IV fluids.

Decompression of the submandibular region is done, by making a deep incision extending into the deep fascia and also cutting both the mylohyoid muscles. Either it is left open and delayed suturing is done (better option) or it is loosely sutured.

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17
Q

Ludwig’s Angina

Complications (3)

A

Laryngeal oedema and respiratory distress, may require tracheostomy

Septicaemia

Extension of infection into parapharyngeal space

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18
Q

Inflammatory Diseases of the Neck (5/8)

A

Parapharyngeal Abscess

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19
Q

Parapharyngeal Abscess

3 points

A

It is infection of pharyngomaxillary space.

This is a cone-shaped space; base is formed by the base of skull; apex is formed by
the greater cornu of hyoid bone; medial wall by the superior constrictor; lateral
wall is formed by the lateral pterygoid, angle of mandible and below by submandibular salivary gland.

Usually, infection arises from the tonsils, after tonsillectomy and from the submandibular space.

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20
Q

Parapharyngeal Abscess

Clinical Features

2 points

A

It causes diffuse swelling in the upper neck, trismus, fever, toxicity.

Swelling lies behind the posterior pillar with oedema of soft palate.

21
Q

Parapharyngeal Abscess

Complications

3 points

A

Thrombosis of internal jugular vein.

Erosion into the internal carotid artery causing torrential bleeding.

Septicaemia.

22
Q

Parapharyngeal Abscess

Treatment

3 points

A

Under G/A, drainage is done by making incision (deep incision) between angle of
the mandible and hyoid bone. Early drainage is needed.

Antibiotics are given.

Causative pathology should be addressed.

23
Q

Inflammatory Diseases of the Neck (6/8)

A

Retropharyngeal Abscess

24
Q

Retropharyngeal Abscess - Types

A

Acute

Chronic

25
Q

Inflammatory Diseases of the Neck (7/8)

A

Acute Retropharyngeal Abscess

26
Q

Acute Retropharyngeal Abscess

3 points

A

It is infection and suppuration of retropharyngeal lymph nodes due to staphylococci
or streptococci organisms.

Commonly from tonsils or pharynx.

Common in infants and children.

27
Q

Acute Retropharyngeal Abscess

Clinical Features

2 points

A

It presents as lateral (paramedian, eccentric) smooth, tender swelling in the pharynx with dysphagia, dyspnoea, cough, toxic features and neck rigidity.

Diagnosis is obvious on proper clinical examination.

28
Q

Acute Retropharyngeal Abscess

Treatment

2 points

A

Antibiotics intravenously.

Drainage is done usually through per oral incision under careful general anaesthesia.
Only occasionally drainage may be done through a neck incision. Pus should be sent for culture.

29
Q

Inflammatory Diseases of the Neck (8/8)

A

Chronic Retropharyngeal Abscess

30
Q

Chronic Retropharyngeal Abscess

3 points

A

It is invariably due to tuberculosis of cervical spine.

Abscess is in the midline behind the prevertebral fascia.

There is destruction of the body of the vertebra due to tuberculosis.

31
Q

Chronic Retropharyngeal Abscess

Clinical Features

4 points

A

It is midline swelling in the posterior pharyngeal wall, which is smooth and
nontender.

Features of tuberculosis of cervical spine will be observed.

Often abscess may point in the neck in relation to sternomastoid.

Neurological manifestations may occur in severe disease.

32
Q

Chronic Retropharyngeal Abscess

Investigations

4 points

A

X-ray spine

Chest X-ray

ESR

MRI of cervical spine

; are essential investigations.

33
Q

Chronic Retropharyngeal Abscess

Treatment

3 points

A

Antitubercular drugs.

Drainage of the abscess should be done through neck approach (never intraoral approach).

Decompression of the vertebra and stabilisation is also often required

34
Q

Vascular/ Congenital Lesions - 2 groups

A

Vascular lesions can be broadly classified into two groups:

  1. hemangiomas
  2. vascular malformations.
35
Q

Vascular Lesions - Hemangiomas

5 points

A

Hemangiomas are the most common vascular lesion present in infancy and early childhood.

Infantile hemangiomas present largely within the first few weeks of life. Initially
they proliferate (2 weeks to 1 year), and then they begin to involute (1–7 years) until they have fully involuted, leaving the child with redundant skin, scar, or a fatty
lesion.

Early intervention can include medical management, such as systemic steroids,
intralesional steroids, intralesional interferon α-2a, or photocoagulation therapy, and surgical management, including excision with CO2 laser/microdebrider and
tracheotomy.

Systemic steroids assist with rapidly proliferating lesions until the child reaches approximately one year of age; however, it is associated with growth retardation
and immune suppression.

Congenital hemangiomas differ from infantile hemangiomas in that they reach their
maximal size at birth and do not have a proliferative phase.

36
Q

Vascular Malformations

7 points

A

Vascular malformations, in contrast to infantile hemangioma, are always present at
birth, although they may not be apparent for a few months.

Although they do not have a proliferative phase, they grow with the patient, have
hormonal growth spurts and do not involute.

Vascular malformations can be classified as low flow (capillary, venous, lymphatic, and mixed), which comprise approximately twothirds of all vascular malformations, or high flow (arteria and arteriovenous).

Capillary malformations arise from the cutaneous superficial plexus and are made
up of capillary and postcapillary venules with a pink, red, or purple macular-papular appearance.

Venous malformations arise from dilated vascular channels lined by normal endothelium; therefore, they are soft, compressible, and nonpulsatile. If they are
superficial, they will increase in size with Valsalva or dependent positioning. They can grow suddenly with trauma or in association with hormonal changes.

Lymphatic malformations typically present at birth with the majority (90%) being
identified by 2 years of age. They can be macrocystic (>2 cm), microcystic (≤2 cm),
or a combination. They are most commonly found in the head and neck, particularly
on the neck, and on physical examination they are soft and doughy with normal
overlying skin.

Treatment of vascular malformations is based on depth, size, and growth pattern.
Arteriovenous malformations are rare. but typically require surgical excision with
negative margins often after embolization. Lymphatic malformations are typically treated at least in part with surgical excision, although this is less successful for
microcystic lesions.

37
Q

Trauma Of the Head and Neck

Leads to :

A

Thoracic outlet syndrome (TOS)

38
Q

Thoracic outlet syndrome

Definition

A

It is syndrome complex due to neurovascular bundle compression in the thoracic outlet.

39
Q

Thoracic outlet syndrome two main spaces:

A
  1. Scalene triangle is bound by scalenus anterior, scalenus medius and first rib. It
    contains subclavian artery and brachial plexus.
  2. Costoclavicular space is bound by clavicle, first rib, costoclavicular ligament and
    scalenus medius. It contains subclavian artery and vein and brachial plexus.
40
Q

Thoracic outlet syndrome

Etiology

10 Points

A

Cervical rib.

Long C7 transverse process.

Anomalous insertion of scalene
muscles.

Scalene muscle hypertrophy.

Scalene minimus.

Abnormal bands and
ligaments.

Fracture clavicle or first rib.

Exostosis.

Tumours in the region.

Brachial plexus trauma and diseases

41
Q

Thoracic outlet syndrome

Clinical Features

Neurological Symptoms

4 points

A

Paraesthesia.

Pain in shoulder, arm, forearm and fingers.

Occipital headache as
referred pain from tight scalene muscles.

Weakness in forearm, hand.

42
Q

Thoracic outlet syndrome

Clinical Features

Vascular symptoms

3 points

A

Claudication

Ischaemic ulcers

Gangrene.

43
Q

Thoracic outlet syndrome

Signs

10 Points

A

Scalene muscle tenderness.

Pulsatile swelling in supraclavicular region with thrill and bruit (25%).

Bony mass above clavicle.

Adson’s test (+ve)

Roos test (+ve).

Elevated arm stress test (+ve).

Costoclavicular compression reveals
feeble/absence of radial pulse due to compression of the subclavian artery manoeuvre.

Hyperabduction manoeuvre.

Poor capillary refilling.

Absence or feeble pulse.

44
Q

Thoracic outlet syndrome

Investigations

7 points

A

X-ray neck and cervical spine.

Doppler.

Subclavian angiogram

CT angiogram

CT neck

Nerve conduction studies

Electromyography.

45
Q

Thoracic outlet syndrome

Conservative Treatment happens if :

A

Nerve velocity is > 60 m/second

46
Q

Thoracic outlet syndrome

Surgical Treatment happens if

A

Nerve velocity is < 60 m/second

47
Q

Thoracic outlet syndrome

Conservative Treatment

4 Points

A

Exercises—neck stretching, postural and breathing exercises

Drugs—analgesics, muscle relaxants, antidepressants

Avoid weight lifting

Physiotherapy

48
Q

Thoracic outlet syndrome

Surgical Treatment

3 Points

A

Transaxillary (ROOS)—mainly for first rib excision and also cervical rib

Supraclavicular approach for cervical rib and soft tissue excision, scalenotomy,
neurolysis, arterial reconstruction

Cervical sympathectomy may be needed.