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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_4540_Библиотеки_им_академика_М_И_Перельмана.pdf
168
CHAP TER5 The front oftheneck
cVocal cord palsy and other
conditions
Unilateral vocal fold paralysis occurs from dysfunction of the recurrent
laryngeal (RLN) or vagus ner ve. Patients present with characteristic
breathy voice often accompanied by swallowing diculty, a weak cough,
and the sensation of shortness of breath. Causes include iatrogenic injury
to the vagus or recur rent laryngeal ner ve (histor y of head, neck, and
chest surgery). Recent URTI or recent intubation for any procedure can
also result in a vocal cord palsy. Blunt trauma and malignant invasion of
either the vagus or recurrent laryngeal ner ve (skull base, thyroid cancer,lung/ oesophageal cancer, and metastases to the mediastinum) are
rare causes.
Investigations
These include chest radiography (Pancoast tumour, mediastinal mass, or
massive cardiomegaly) and CT/ MRI to visualize the path of the vagus/
recur rent laryngeal ner ve. A left cord palsy requires imaging from the
base of skull to the mid chest (through the arch of the aort a) while a
right cord palsy evaluation should extend from the base of the skull
through the clavicle. EMG can be used to determine the prognosis of
RLN recovery.
Management
Indications for treatment are usually when there is signicant dysphonia
or an ineective cough in a patient at risk for aspir ation. Medical therapy
plays a very small role. When concomitant GORD and/ or sinonasal
allergic disease are present, medical therapy of these disorders may
help. Voice ther apy alone, or combined with surgical medialization of
the paralysed vocal fold may help. Multiple surgical options are available.
Temporary treatments involve endoscopic injection of a resorbable
material (autologous fat, collagen, absorbable gelatin sponge, hyaluronic
acid, etc.), into the aected vocal fold. The resultant medialization of
the paralysed vocal fold improves glottal competence and may improve
swallowing. Permanent treatment involves vocal fold injection or laryngeal framework surgery.
bReinke’soedema
This is swelling of thevocal foldswhich results in polypoidal degeneration and a chronic hoarse voice with occasional stridor. Patients present
with low- pitched, husky voices. Common causesinclude smoking,gastroesophageal reux, hypothyroidism,and chronic voice abuse. Biopsy
may be necessary to r ule out underlying malignancy.
Management
This includes removal of precipitating factors and speech therapy.
Surgery is usually ineective in completely restoring the voice; however,
stripping of the epithelium and let ting the uid to drain might help. CO2
laser plays a role in debulking excessive polypoidal mucosa .
VOCAL CORD PALS Y AND OTHER CONDITIONS
bVocal fold granulomas
Vocal cord granulomas are usually benign lesions found on the posterior third of the vocal fold corresponding to the vocal process of the
arytenoid cartilage. They occur unilaterally or bilaterally. Granulomas
of the larynx are classied under two groups: specic granulomas and
non- specic granulomas. Specic granulomas are rare and include granulomas caused by TB and syphilis. Non- specic granulomas are benign
and are histologically resemble pyogenic granulomas. Causes/ contributing factors include:
• Contact granulomas as a result of voice abuse ormisuse
• Granulomas of intubation
• Gastroesophagealreux
• Smoking, allergy, infections, postnasal drip, and chronic throat
clearing.
The dierential diagnoses include carcinoma, granular cell tumour of the
larynx, and sarcoid.
Presentation
Patients present with varying degrees of hoar seness and a low- pitched
voice; cough; throat clearing; and a rough foreign body sensation. There
may be a history of intubation, high- risk habits (smoking, caeine), pulmonary symptoms (chronic cough, use of inhalers), etc. Untreated, these
can result in airway obstruction, bleeding (usually minor), vocal fold xation, and posterior laryngeal stenosis.
Management
Medical therapy includes cough suppressants, anti- reux therapy, speech
therapy, and topical/ steroid injections (controversial). Surgical management has a high recur rence rate. Surgical is indicated for broepithelial
polyps, airway compromise, or suspicion of cancer.
bMuscle- tension disorders/ functional voice disorders
Functional voice disorders (muscle tension dysphonia) may account for
up to 40% of the cases of dysphonia. A recent URTI may precipitate
an already stressed lar yngeal system causing dysphonia. Other factors
include medications, neurological disorders, laryngeal trauma, hypothyroidism, and psychiatric. All patients must undergo a complete ENT
examination to rule out other causes.
bConversion dysphonia
The development of conversion dysphonia, also referred to as a psychogenic dysphonia, may result from a temporally psychologically or
emotionally traumatic event . The patient’s vocal qualit y is usually hypofunctional or aphonic. Fibreoptic laryngoscopy may demonstrate a lack
of vocal cord adduction during attempted phonation. However, coughing and throat clearing (vegetative phonation) demonstrate normal vocal
cord adduction. Treatment is voice therapy.
169
170
CHAP TER5 The front oftheneck
bCarotid artery disease
The common carotid artery divides into the internal carotid ar ter y and
the external carotid artery. The inter nal carotid artery supplies the
brain. Like any large vessel it is at risk of va scular disease. Risk factors are
similar to those for heart disease. They include:
• Age
• Smoking
• Hypertension
• Abnormal lipids or high cholesterol
• Diet high in saturatedfats
• Diabetes
• Obesity
• Sedentary lifestyle
• Family history of atherosclerosis, either coronary arter y disease or
carotid artery disease.
bCarotid stenosis
Atherosclerotic plaques can build up within the vessel wall, resulting in
stenosis. These are common in the elderly and may remain stable and
asymptomatic. However, they may also be a source of embolization.
Fragments can break o and obstruct smaller ar teries within the brain.
The resulting ischaemia can be either temporary (TIA), or permanent
(thromboembolic stroke).
Clinical features
TIAs by denition last <24 hours. They may presentwith:
• Weak ness or loss of sensation of a limb or the trunk on oneside
• Loss of sight (amaurosis fugax) in oneeye
• Vertigo
• Tinnitus
• Diculty speaking
• Confusion.
TIAs may be a warning sign, of ten followed by a stroke, a few days later.
Symptoms of a stroke are similar to a TIA, the main dierence being they
are usually more severe and are permanent, with little recovery.
Carotid stenosis is usually diagnosed by colour ow duplex ultrasound
of the neck. Occasionally CTA or MRA is required.
Management
This includes:
• Medication:antiplateletdrugs
• Carotid endar terectomy:surgical removal of the plaque and diseased
portions of the artery.
• Carotid stenting:this is a newer treatment and less invasive.
Acatheter is threaded into the area of stenosis and dilated with a
balloon. Astent is then placed to hold the vesselopen.
COUGHING UP BLOOD (HAEMOPTYSIS)
In asymptomatic severe carotid artery stenosis, carotid endarterectomy
reduces the risk of stroke in the next 5 years by around 50%. Patients
with carotid stenosis should be referred for medication (antihyper tensive drugs, anticlotting drugs, antiplatelet drugs, and statins). Clinical trials are still ongoing.
A TIA is a medical emergenc y because it is impossible to predict if it will
progress into a major stroke. Immediate treatment may increase the chance
of a full recovery.
eCarotid artery dissection
Carotid arter y dissection is separation of the layers of the artery wall.
It is a common cause of stroke in young adults. In addition to signs of a
stroke, patients may also experience headache or neck pain and develop
a Horner’s syndrome (decreased pupil size with drooping of the upper
eyelid). Spont aneous internal carotid ar tery dissection may have a history of stroke in their family or hereditary connective tissue disorders,
such as Marfan’s syndrome or Ehlers– Danlos syndrome.
Carotid arter y dissection may also occur following severe trauma to
the head or neck. This can also result in intimal dissections, pseudoaneurysms, thromboses, or stulas.
Management
The aim of treatment is to prevent the onset or continuation of neurological decits. Treatments include observation, anticoagulation, stenting, and carotid artery ligation.
cCoughing upblood (haemoptysis)
Haemoptysis needs to be dierentiated from epistaxis and haematemesis. In children, lower respiratory tract infections and foreign body aspiration are common causes. In adults, bronchitis, bronchogenic carcinoma,
and pneumonia are the major causes. Determine if the patient is coughing up clots, fresh blood, blood- stained sputum, or sputum with streaks
of blood mixed in. Haemoptysis is classied as non- massive (<200 mL)
or massive, based on the volume of blood loss daily.Bleeding from a
high- pressure bronchial arter y can be profuse. Consider the following:
• Upper airway (nasopharyngeal) bleeding
• GI bleeding
• Neoplasm (bronchogenic carcinoma)
• Bronchitis, bronchiectasis
• Airway trauma, foreign body, pulmonary embolism
• Lung abscess, pneumonia, TB, mycetoma
• Systemic coagulopathy/ anticoagulants
• Goodpasture’s syndrome, idiopathic pulmonary haemosiderosis,
Wegener’s granulomatosis
• Arteriovenous malformation, elevated pulmonary venous pressure
(especially mitral stenosis),etc.
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CHAP TER5 The front oftheneck
In up to a third of patients, no cause can be found. Blood from the lower
bronchial tree typically induces cough, whereas a histor y of epistaxis or
expectorating without cough would be consistent with an upper respiratory source. Examining the expectoration may help localize the source
of bleeding.
Investigations
These include CXR , followed by breoptic bronchoscopy and highresolution CT in ca ses when malignancy is suspected.
Management
This includes stopping bleeding, aspiration prevention, and treatment of
the underlyingcause.
• Haemopt ysis >1000 mL per 24 hour s carries a mortality rate. Airway
maintenance is vital (death is more often due to asphy xiation). Give
oxygen and commence uid resuscitation. Call cardiothoracic/
general surgeons urgently (local protocol).
• Mild haemoptysis of ten is caused by an infection and can be managed
on an outpatient basis with close monitoring. If haemoptysis persists,
refer urgently to a respiratory specialist.
eForeign body ingestion
eForeign body inthe oesophagus
The most common foreign bodies in adults are sh bones, dentures, and
meat. The most common objects in children are coins. 95% of oesophageal foreign bodies obstruct at the cricopharyngeus (narrowest part of
adult GI tract). Patients present with dysphagia , drooling, chest pain, and
later with a fever. Left untreated, oesophageal perforation, mediastinitis,
pneumomediastinum, pneumothorax, and aspiration can alloccur.
Investigations
CXR to identify object. Always ask for soft tissue neck X- ray as well (both
anteroposterior and lateral views). CT may be required.
Management
• Obtain description of object (sharp objects like meat with bone or
dentures needs retrieval).
• Conser vative management— for food bolus without abone.
• Consider admission for IV uids, smooth muscle relaxants (hyoscine),
sedation (diazepam), and observation.
• Rigid oesophagoscopy. This is indicated for foreign bodies that
remain in the oesophagus for >2days. Large objects or batteries need
immediate retrieval.
eCaustic ingestion
• Alkaline ingestion (pH >12.5) causes liquefaction necrosis (and
perforation of oesophagus). Common alkali agents include alkali
batteries, bleaches, household ammonia, and hair straighteners.
• Acidic ingestion causes coagulation necrosis, rapid transit results in
skip areas and more severe damage to the stomach.
MISCELLANEOUS CONDITIONS
• Liquids burn more distal; solids (powder) burn more proximal.
• Severity of external and oropharyngeal injury does not correlate with
extent of oesophageal and gastric injury.
Patients present with drooling, mouth pain, str idor, dysphagia, chest or
abdominal pain, and oral injury. Left untreated, stricture, pneumonia,
tracheoesophageal stulas, laryngeal oedema, mediastinitis, and perforation mayoccur.
Investigations
CXR. Direct laryngoscopy with oesophagoscopy.
Management
• Evaluate airway (may require an emergent surgical airway).
• Identify agent, determine pH, amount, and concentration (call
toxicology information centre).
• Remove granules and powder with water, consider initial dose of
corticosteroids, IV antibiotics, NBM, IV hydration, do not induce
emesis, do not neutralize (this causes an exothermic reac tion).
• Evaluate for complications:CXR (mediastinitis), abdominal series
(gastric perforation),ABGs.
Miscellaneous conditions
bEagle syndrome (styloid– carotid artery syndrome)
This is a rare condition in which there is elongation of the st yloid process,
or calcication of the stylohyoid ligament . ‘Classic’ and ‘vascular’ forms
are described. Patient s are usually between 30 and 50years old and can
present with recurrent sore throat , dysphagia, neck pain, and otalgia.
Blackouts and sudden death due have also been repor ted and are due
to mechanical pressure on the carotid. Consider this when neurological
symptoms occurs upon head rotation. The tip of the st yloid process may
be palpable in the back of the throat. Plain lms and CT conrm the
diagnosis (the enlarged styloid may be visible on an OPT or a lateral soft
tissue X- ray). In both types, treatment is surgical (partial styloidectomy).
Tracheostomy
Ideally this should be carried out in theatre settings. Tracheostomy tubes
are placed through a small incision midway between the cricoid car tilage and suprasternal notch. Tissues are separ ated keeping to the midline of the neck. Meticulous haemostasis is essential at all times. Often
the thyroid isthmus obstructs access to the trachea and needs to be
retracted or securely ligated and divided. The thyroid is a highly vascular
organ and carelessness in manipulation can result in profound bleeding
postoperatively.
Once the anterior part of the tr achea is dened, it is opened, the
endotracheal tube withdrawn, and the tr acheostomy tube inser ted into
the lumen. Several dierent access openings in the trachea have been
described— a vertical slit, small hole, or the ‘Bjork ’ ap (which is a Ushaped ap at tached inferiorly). Each has it s own merits and which is
chosen is down to the operating sur geon. Once in place, the tube needs
173
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CHAP TER5 The front oftheneck
to be sutured to the skin and securely fastened around the neck with
tapes and the wound closed.
Tracheostomy indications
• Bypass upper airway obstruction (e.g. sleep apnoea, tumour).
• Prevention of aspiration and air way protection (cuedtube).
• Assist with tracheal- bronchial toileting (suctioning).
• Eliminate dead space and improve respiratory insuciency
(respiratory, cardiac, or neurological disease).
• Prevent complications from prolonged intubation (e.g. mucosal
ulceration, laryngeal stenosis, granulomas).
Tracheotomycare
• Maintain air way:especially for rst 48 hours to prevent accidental
dislodgement of tube. Ensure the tracheostomy tube is sutured to
the neck skin, clean the inner cannula daily. The rst tracheostomy
change may be considered after 3– 5days. This allows a tr act toform.
• Humidication:prevents tracheal cr usting and mucous plugs. Patients
with tracheostomies should never be without orid humidication.
• Pulmonary toileting:tracheostomy tubes disrupt ciliary function,
decrease subglot tic pressure (causing ineective cough), and increase
risk of micro- aspiration; they may require regular suctioning for the
rst fewdays.
• Skin care:cu dressings to prevent skin breakdown.
• Check cu pressure:cu pressure should be less than capillary
perfusion pressure (<25cmH2O) to prevent pressure necrosis
(and subsequent SGS, tracheal- innominate artery erosion,
tracheomalacia).
• Feeding:it can be dicult for solid food ingestion when cu is inated;
capping the tracheotomy tube facilitates swallowing.
• If patients are going to other depar tments in the hospital they should
be accompanied by appropriately trained personnel at all times and
should go with a mobile humidication system.
Although tracheostomy provides direct access to the lower respiratory
trac t for suctioning, many patients nd it dicult to produce an eective
‘explosive’ cough, useful in clearing secretions from the lungs. However,
they can be taught to expectorate, physiotherapists encouraging ‘hung’
using the diaphragm. With a cooperative and well- humidied patient,
very little suction is required; most patients can eectively clear their
lungs on theirown.
Decannulation
Tracheotomy tubes should be removed as soon as possible (especially in
children) to prevent long- term sequelae such a s tracheal ulceration, SGS,
tracheomalacia. Prior to decannulation, patients may undergo tracheostomy tube downsizing and a trial of capping, but this is not always necessary. Flexible nasopharyngoscopy can evaluate air way patency. Once
removed, place an air tight dressing to seal thestoma.
MISCELLANEOUS CONDITIONS
Tracheotomy complications
Tracheal stenosis, granulation tissue, tracheal- innominate artery erosion, SGS, vocal cord paralysis (the recurrent laryngeal ner ve runs alongside the trachea), chest infection, tracheo - oesophageal stula.
cSurgical (subcutaneous) emphysema
Subcutaneous emphysema occurs when air gets tr apped in the tissues
under the skin. It is usually seen in the chest wall or neck, but can occur
in other parts of the body and is typically seen in trauma situations with
penetrating injuries involving the airway. On palpation, a crackling sensation is felt under the skin as the gas is pushed through the tissue.
Aetiology
Air can enter the sof t tissues from rupture of any gas- lled struc ture, or
from the exterior. Causes therefore include:
• Ruptured lung (pneumothorax), often with rib fracture
• Ruptured bronchialtube
• Facial fractures
• Ruptured oesophagus
• Infection caused by gas- producing organisms (gas gangrene)
• Penetrating injuries
• Explosions.
This condition is rarely associated with breathing cocaine, corrosives
or chemical burns of the oesophagus, forceful vomiting’ (Boerhaave’s
syndrome), gunshot wounds, pertussis (whooping cough), and certain
medical procedures (central venous line, intubation, and bronchoscopy).
Massive emphysema has been reported following certain dental treatments (such as root canal treatment or surgical extraction of a tooth
using an air- powered rotary drill).
Management
Treat the underlying cause and emphysema will spontaneously resolve.
Rarely massive subcutaneous emphysema can cause signicant discomfort and cause air way compromise or venous compression. This may
require surgical drainage. When subcutaneous emphysema occurs due
to pneumothorax, a chest tube is frequently necessary.
bMediastinalmasses
Patients with mediastinal masses can present in dierent ways. It is often
an incidental diagnosis during evaluation for an unrelated condition.
Some patients present with complaints secondary to local mass eect
on adjacent structures, such as respiratory symptoms or swelling due
to compression of vascular structures or develop systemic symptoms
resulting from the mediastinal mass. Both benign and malignant mediastinal masses can develop from structures that normally are in the
mediastinum or present during development, as well as metastases of
malignancies from elsewhere in thebody.
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CHAP TER5 The front oftheneck
Investigations
CXR, CT scan of the chest (and C T- guided needle biopsy), MRI of the
chest, and mediastinoscopy with biopsy.
Management
The treatment used for mediastinal tumours depends on the t ype of
tumour and it s location. Thymic cancers require surgery, followed by
radiation or chemotherapy. Lymphomas are treated with chemotherapy
followed by radiation.
bGlobus
Globus is the feeling of a lump in the throat when actua lly there is no lump
present. Usually it is idiopathic in nature (globus phar yngeus or globus
hystericus), but occasionally may be secondary to identied pathology:
• Oesophagealspasm
• GORD
• Neuromuscular disorder s such asmyasthenia gravis, Parkinson’s
disea se,andstroke
• Rarely, cancers of the upper GItract.
Chapter6
177
Theear
Common presentations 178
Common problems and their causes 178
Useful questions and what to look for 181
Examination of the ear 185
Investigations 187
Injuries 188
Infec tions of the external auditory meatus and pinna 191
Infec tions of the middle ear 192
Infec tions of the adjacent bones 194
Otalgia (‘earache’) and otorrhoea 195
Otorrhoea 196
Deafness 196
Dizziness/ ‘vertigo’ 19 9
Tinnitus (ringing/ buzzing in the ear) 203
Eustachian tube problems 206
Miscellaneous conditions 207