ENT lecture for Intermediates

1. ENT

2. 1. Trauma to Ear and Upper aerodigestive tract
• Airway management is 1st priority
• Most penetrating pharyngeal and tracheal trauma can be managed conservatively
• Transections of less than 33% of tracheal lumen do not need operative repair
• Associated injuries must be sought – oesophageal and vascular

3. Trauma to Ear and Upper aerodigestive tract
• Ear Injuries
• May manifest as dizziness, deafness,otorrhoea/ rhinorrhea, meningitis
• LMN facial weakness may indicate temporal bone fracture

4. Trauma to Ear and Upper aerodigestive tract
• Auricular Hematoma
• Blunt trauma
• Hematoma between perichondrium and cartilage can cause fibrosis- cauliflower ear
• Infection can occur with cartilage resorption
• Complete evacuation of hematoma by repeated needle aspiration/ incision and drainage
• Pressure dressing, nylon suture to prevent hematoma re-accumulation

5. Trauma to Ear and Upper aerodigestive tract
• Auricular Laceration
• If simple, suture
• If skin defect, do full thickness post auricular skin graft
• Perichondrium intact- immediate graft
• Perichondrium denuded – delay skin graft until covered by granulation tissue
• Auricular Avulsion
• Partial avulsion small < 2cm - primary repair
• Large avulsion >2cm needs local/regional flap with or without cartilage graft
• Total avulsion – put auricle in sterile bag, transport in ice water, Reimplantation with
microvascular anastomosis
• Auricular Bites
• Antibiotics
• <12 hrs- primary repair , > 12 hours – allow healing by secondary intention with dressing

6. Trauma to Ear and Upper aerodigestive tract
• Ear Canal
• Outer half cartilaginous, medial half bony wall
• Objective is to avoid canal stenosis
• Hematoma and Laceration of canal
• Consider temporal bone fracture
• Drain hematoma
• Stent canal with antibiotic impregnated ribbon gauze for 1 week

7. Trauma to ear and upper aerodigestive tract
• Trauma to the pinna
• Lacerations can be simply sutured with approximation of cartilage without suturing
cartilage itself
• Avulsed segments of the ear can have attempted re-attachment if short duration of
injury and clean wounds
• Otherwise trimming cartilage so as to allow closure of skin over cartilage is alternative

8. Trauma to ear and upper aerodigestive tract
• Trauma to the middle ear
• Tympanic Membrane
• Most perforations heal spontaneously
• Ossicle disruptions can cause hearing loss and vertigo
• Tympanic membrane trauma may be secondary to blunt head trauma and is
associated with temporal bone basilar skull fractures
• May occur as a result of direct trauma, barotrauma or penetrating injury (Q-tip, match
stick)
• Clinically
• Ear pain, hearing loss, otorrhoea, imbalance, tinnitus

9. Trauma to ear and upper aerodigestive tract
• Trauma to the middle ear
• ATLS principles
• Ear examination is part of secondary survey
• Examine external ear, canal and tympanic membrane with otoscope
• Look for otorrhoea, obvious tympanic perforation, haemotympanum, ataxia,
nystagmus

10. Trauma to ear and upper aerodigestive tract
• Ear
• Hearing
• Weber’s Test
• Equal – non-lateralising
• If moving toward injured side – conductive hearing loss
• If moving away from injured side – sensorineural loss
• Rinne’s Test
• If air conduction better than bone conduction – normal
• If bone conduction better than air conduction – conductive hearing loss

11. Trauma to ear and upper aerodigestive tract
• Ear
• Management
• Leave FBs in place for ENTs to remove
• General measures – avoid water, AxBs ear drops, analgesia
• If minimal hearing loss, absence of vestibular findings and no signs of nerve injury – out patient
management
• If <25% disruption of eardrum – heals spontaneously.
• If >25%, require surgical repair
• Small perforation- keep ear dry, ENT in few days
• Large perforation – ENT surgeon to approximate free edges
• Vertigo/nystagmus- audiogram assessment

12. Pharyngoesophageal injuries
• Uncommon, high morbidity and mortality.
• Difficult to detect clinically and appear to be the leading cause of delayed death from
neck trauma
• Aggressively search for pharyngoesophageal injuries in patients with any suggestive
signs using appropriate ancillary studies.
• There are no pathognomonic signs of esophageal injury
• Dysphagia, blood in the saliva, hematemesis, and subcutaneous air suggest the
diagnosis

13. Pharyngooesophageal Injuries
• Penetrating esophageal injuries are notoriously insidious, and delays in diagnosis
carry mortality rates as high as 20%.
• Delays over 24 hours further increase the mortality rate.
• If pharyngoesophageal trauma is suspected, MDCT alone is inadequate for
definitively ruling out injury, although it often identifies some sign of injury.
• Sensitivity of MDCT =low as 53 %.
• Direct esophageal studies (eg, contrast swallow and endoscopy) can provide a
diagnosis and sensitivity of nearly 100%

14. Pharyngooesophageal Injuries
• Given potential difficulties in diagnosis and the consequence of delays, many trauma
specialists obtain imaging studies to rule out esophageal injury in all cases of PNI
associated with soft signs of esophageal injury or wounds close to the pharynx or
esophagus (so-called "proximity wounds").
• MDCT is typically the initial study performed because it detects laryngotracheal,
vascular, and some esophageal injuries simultaneously and rapidly.
• In addition, if a pharyngoesophageal injury is not directly identified, proximity
wounds prompt the treating physician to order definitive studies to exclude violation
of the pharynx or esophagus.

15. Pharyngoesophageal Injuries
• A plain neck or CXR showing retropharyngeal air or pneumomediastinum, respectively,
suggests esophageal injury, non-specific.
• In such cases, immediate surgical consultation should be obtained to determine
management or the choice of subsequent imaging, should the patient not proceed
immediately to the operating suite.
• EAST suggest that either endoscopy of the esophagus/esophagography can be used to
rule out significant esophageal injury in stable patients with PNI .
• If the patient can cooperate, a Gastrografin or thin barium swallow can be performed
first, and if non-diagnostic, flexible esophagoscopy can be performed, increasing
sensitivity to nearly 100%

16. Management
• Early surgical consultation. Most PEIs are treated surgically, but few non-
operatively
• If not promptly diagnosed, PEI can cause mediastinitis and abscess or empyema
formation from the leakage of gastric contents.
• Start broad-spectrum antibiotics in all patients with possible PEI.
• Although some trauma specialists advocate decompressing the stomach with NG
tube, performing a blind procedure in a patient with PEI entails significant risk .We
do not believe this procedure should be performed blindly in the emergency
department (ED).
• Prophylactic antibiotics not indicated in penetrating trauma unless there is a
hollow viscous injury such as PEI, the wound is grossly contaminated, or surgical
exploration is performed.
• Tetanus prophylaxis should be administered as necessary

17. Laryngotracheal injuries
• Predominantly confined to the cervical trachea.
• Such injuries can result in respiratory distress, stridor, subcutaneous air,
hemoptysis, odynophagia, dysphonia, or anterior neck tenderness

18. Laryngotracheal injury
• (MDCT) is the imaging modality of choice in stable patients with PNI.
• Provides anatomic detail about laryngeal integrity, useful when cervical spine
immobilization is necessary
• Plain films should be inspected for signs of cartilaginous fracture and extra
luminal air if obtained.
• Most common complaint associated with cartilaginous fractures is hoarseness,
but dyspnea, hemoptysis, Globus sensation, ecchymosis, hematoma, crepitus,
and pain may be present.
• None of these signs and symptoms is predictive of injury severity.
• MDCT has some limitations.
• Degloving injury of the cartilage with denuded mucosa can be missed, as can certain types of
LT separation and mucosal perforation.
• Pediatric cartilaginous structures are poorly calcified and may be more difficult to visualize
than an adult larynx.

19. Laryngotracheal Injuries
• However, in most cases injuries missed by MDCT do not require operative repair,
including minor edema, hematoma, minor denuded cartilage, and non-displaced
fractures
• Further studies may be necessary in patients with clinical signs of injury or at high
risk for occult injury whose initial imaging, including MDCT, is non-diagnostic.
• Flexible nasopharyngoscopy and laryngoscopy = additional methods
• Endoscopy enables thorough evaluation when scatter artifact from metallic objects
obscures CT images.
• Flexible nasopharyngoscopy allows visualization of the hypopharynx and
supralaryngeal structures in an awake or sedated patient, while flexible laryngoscopy
allows evaluation of the larynx.
• Rigid endoscopy allows for evaluation of the distal airway but requires general
anesthesia.

20. Management Modalities
• Laryngotracheal injury
• A large proportion of patients with traumatic airway injuries require definitive
airways .
• Tracheal intubation using rapid sequence intubation (RSI) is safe in the majority
of patients exceptions exist.
• Timely repair of certain laryngotracheal injuries is important to prevent long-
term complications such as chronic pain, stenosis, or voice change.

21. 2. Acute upper airway obstruction – differential
diagnosis
• Intraluminal
• FB
• Luminal
• Papilloma
• Tumour
• Oedema (inhalational burns, anaphylaxis)
• Stenosis/stricture
• Trauma and collapse
• Low GCS and airway obstruction
• Extraluminal
• Haematoma
• Malignant compression

22. Caustic Ingestion
• Children - accidental
• Adults is usually intentional . Associated psychiatric illness. Suicidal intent often
ingest larger amounts of caustic agents than those who accidentally swallow these
agents - severe esophageal and gastric damage.
• Common causes is ingestion of strong alkali
• (sodium or potassium hydroxide) contained in drain cleaners, other household cleaning
products, or disc batteries
• "lye" implies substances that contain sodium or potassium hydroxide .
• Highly concentrated acids (hydrochloric, sulfuric, and phosphoric acid) contained in toilet bowl
or swimming pool cleaners, antirust compounds, or in battery fluid are less frequently ingested
• Liquid household bleach (5 percent sodium hypochlorite) ingestion is frequently reported but
rarely causes severe esophageal injury

23. Mechanism of injury
• Ingestion of alkali (eg, ammonia or sodium hydroxide) = liquefactive necrosis.
• Extends rapidly (within seconds) through the mucosa and wall of the esophagus
towards the mediastinum until tissue fluids buffer the alkali.
• Extensive transmural damage may result in esophageal perforation, mediastinitis, and
death .In the stomach, partial neutralization of the ingested alkali by gastric acid may
result in more limited injury
• Among patients with alkaline ingestions, gastric injury is most common in those who
ingest relatively large volumes (200 to 300 mL) .
• Duodenal injury is much less common as compared with the stomach and esophagus
• The process of liquefactive necrosis usually 3-4 days and is associated with vascular
thrombosis and mucosal inflammation, resulting in focal or extensive sloughing and
ulceration.
• Over 2 weeks, the esophageal wall becomes progressively thinner because of
sloughing and the development of granulation tissue and fibrosis. Re-epithelialization is
usually complete 1-3 months later. The likelihood of stricture formation depends upon
the depth of damage and degree of collagen deposition

24. Acid-induced injury
• Acid solutions cause pain upon contact with the oropharynx, therefore the amount of acid
ingested tends to be limited.
• Upper airway injuries are more common with ingestion of acid, perhaps related to their
bad taste, which tends to stimulate gagging, choking, and attempts to spit out the ingested
material .
• In contrast to alkaline solutions which are more viscous, acid preparations tend to pass
quickly into the stomach, causing less esophageal damage.
• As the acid flows along the lesser curvature of the stomach toward the pylorus,
pylorospasm impairs emptying into the duodenum, producing stagnation and injury that is
particularly prominent in the antrum.
• Food in the stomach tends to provide a protective effect.
• Acid ingestion typically produces a superficial coagulation necrosis that thromboses the
underlying mucosal blood vessels and consolidates the connective tissue, thereby forming
a protective eschar. Acid ingestion in sufficient concentration can cause esophageal and
gastric perforation with peritonitis

25. Caustic Injuries
• Patients may complain of oropharyngeal, retrosternal or epigastric pain, dysphagia/odynophagia, or
hypersalivation.
• Other symptoms include vomiting and hematemesis. Caustic injury to the oropharynx causes pain
and inability to clear pharyngeal secretions with persistent drooling.
• Hoarseness, stridor, aphonia, and respiratory difficulties are less common and result from caustic
burns of the epiglottis and larynx.
• Fever, tachycardia, and shock generally imply the presence of more severe and extensive injury
• Persistent severe retrosternal or back pain may indicate an esophageal perforation with
mediastinitis.
• The presence of persistent, localized abdominal tenderness, rebound, and rigidity are suggestive of
an esophageal or gastric perforation with peritonitis.

26. Complications of Caustic Ingestion
• Bleeding
• UGIB in 3% usually occurs 2-4 weeks after ingestion
• Fistulization
• Fistulization into adjacent organs can occur at any time after massive ingestion of strong
corrosive agents.
• Patients with a chronic TOF usually present with frequent coughing following solid and
liquid intake, recurrent purulent bronchitis or pneumonia, recurrent aspiration, and
malnutrition.
• Aortoenteric fistulas are rare

27. Complications of Caustic Ingestion
Strictures
• Oesophageal stricture formation is the most common complication of caustic ingestion.
• 1/3rd develop esophageal strictures, primarily those with high-grade injuries .
• Stricture formation is directly related to the depth of injury .
• Develop within two months of corrosive ingestion, although it can occur as early as three weeks to
years after ingestion .
• Gastric strictures are uncommon because of the large diameter of the stomach and are mostly
caused by acids.
• Patients usually present with early satiety and postprandial vomiting months or years after
ingestion due to pyloric stenosis and gastric outlet obstruction.
• Barium swallow examination of the stomach demonstrates cicatrization, (predominantly involving
the antrum) and linitis plastica-type deformity with multiple pseudodiverticula.
• Esophageal squamous cell carcinoma
• 30% patients develop esophageal cancer
• Carcinoma at the site of previous lye stricture (scar carcinoma) has a better prognosis as
compared with other causes of esophageal squamous cell carcinoma

28. Imaging
• Radiographs -
• Patients with respiratory symptoms.
• CXR R/O other etiologies (eg, foreign body ingestion or pneumonia) and assess
for complications of the caustic ingestion (eg, esophageal or gastric perforation).
• Signs of perforation include :
• Pneumomediastinum
• Mediastinal widening
• Subcutaneous emphysema in the neck
• Pleural effusions
• Hydropneumothorax
• Subdiaphragmatic air.

29. Computed tomography
• All patients with caustic ingestion to determine the depth of necrosis, as signs and symptoms
alone are an unreliable guide to injury
• CT scan can reliably identify patients with transmural digestive necrosis which require
emergency surgery.
• Evidence of necrosis include esophageal wall blurring, peri-esophageal fat blurring, and the
absence of esophageal wall enhancement.
• CT examination is reliable and reproducible in some studies has outperformed endoscopy in
selecting patients for surgery or nonoperative management

30. Early upper endoscopy in patients who do not
require surgery
• Endoscopy can accurately predict the risks of stricture formation in patients with caustic
ingestion.
• Timing —
• Upper gastrointestinal endoscopy should be performed early (3 to 48 hours) and preferably during the
first 24 hours after ingestion in order to evaluate the extent of esophageal and gastric damage and guide
management.
• Contraindicated in patients who have evidence of gastrointestinal perforation
• If respiratory distress is present or there are signs of severe oropharyngeal or glottic edema and/or
necrosis, the patient should be intubated for airway protection prior to the upper endoscopy.
• In patients who are hemodynamically unstable, upper endoscopy should be postponed until the patient is
adequately resuscitated and is once again hemodynamically stable. However, if upper endoscopy is
delayed beyond 48 hours, endoscopic grading may be inaccurate due to the development of submucosal
hemorrhages and edema.
• Caution should be used when performing an upper endoscopy in such patients because of the increased
risk of esophageal perforation

31. 3. Foreign bodies in Ear, Nose, Upper
Aerodigestive Tract
• Nose
• Most commonly in young children
• 2 particularly problematic items – Button battery and paired magnets
• FBs usually on floor of nose below middle turbinate
• Clinical
• Asymptomatic
• Nasal discharge
• Epistaxis
• Nasal obstruction

32. Foreign bodies
• Nose
• Investigations not usually needed but if uncertain some FBs are radiopaque
• If non occlusive FB – remove under direct visualisation, if smooth and cannot
be grasped – pass foley or fogarty passed object and extract
• Blowing in mouth by parent may dislodge FB anteriorly

33. Foreign bodies
• Ear
• Also in children
• Clinically similar presentation to FB in nose
• Removal either by extraction or by ear irrigation

34. Foreign bodies
• Upper airway
• May present with clear history or delayed presentation and patient unsure
whether any foreign body was aspirated
• Clinical presentation varies from acute asphyxiation to chronic cough and
chronic lung pathology with bronchiectasis
• May mimic malignancy
• Clinical course depends on the nature of the FB – certain inorganic FBs illicit
minimal inflammatory reaction and may be incidental finding on imaging or
may cause sharp trauma to the airways – broken glass

35. Foreign bodies
• Airway
• Organic FBs may illicit severe inflammatory changes and chronic lung
problems if not diagnosed early
• Imaging may be helpful if uncertain diagnosis although not all objects are
radio opaque and will not neccesarily show, especially on plain films.
• CT may be more helpful

36. Foreign bodies
• Airway
• If upper airway
• Asphyxiating patient needs emergency airway maneouvers such as ACLS – Heimlich, back
slap, chest thrust
• If capable, attempts at intubation may be helpful
• Usually direct or indirect laryngoscopy is diagnostic and in case of direct may be
therapeutic to allow removal of FB with MacGills

37. Foreign bodies
• Airway
• If lower airways
• If asphyxiating – attempt may be taken at removal with direct laryngoscopy
• If failed, FB may be pushed downward by advancing ETT as far as possible and then
retracting tube – converts tracheal obstruction into bronchial FB
• Rigid or flexible bronchoscopy is gold standard for diagnosis and may be therapeutic
• Rigid requires patient to be placed under GA, flexible may be possible under local and
sedation

38. 4. ENT infections
• Peritonsillar abscess
• Collection of pus between the tonsillar capsule and the pharyngeal muscles
• Difficult to distinguish from peritonsillar cellulitis
• Generally arises from tonsillitis or pharyngitis
• Mostly in children and young adults, smoking is a risk factor
• Clinically
• Airway compromise
• Severe sore throat, muffled voice, drooling, trismus, unilateral neck swelling, ipsilateral ear pain
• Examination may be difficult due to trismus and drooling should alert to the possibility of
epiglotitis.
• Consider imaging or EUA

39. ENT infections
• Peritonsillar abscess
• Clinically
• Extremely swollen and fluctuant tonsil with deviation of uvula away from affected side
• Intraoral or submandibular ultrasound may demonstrate abscess
• CT may not be needed but can be helpful when there is a suspicion of
posterior or lateral pharyngeal wall abscesses.
• These patients will usually have neck stiffness

40. ENT infections
• Peritonsillar abscess
• Management
• Airway management
• In patients who have probable PTA – AxBs and drainage
• In patients who have probable peritonsillar cellulitis or possible abscess but
unclear – 24 hours of AxB therapy – if no response = drainage
• Methods of drainage
• Needle aspiration
• Incision & drainage
• Tonsillectomy, either in acute setting or interval

41. ENT infections
• Mucormycosis
• Aggressive fungal infection
• Primarily occurs in immunocompromised patients – HIV/ DM/chemotherapy
• Infiltrates vasculature and leads to rapidly developing necrosis
• Tissue blackens and usually presents with extension beyond sinuses
• Requires early diagnosis and aggressive early debridement and treatment
with Amphotericin B

42. 5. Causes and Management of Epistaxis
• Usually mild and self limiting but may be severe
• Presents in children < 10 and adults 45 – 65 mostly
• May have some seasonal variation
• Anterior bleeds
• Occur from Kiesselbach’s plexus
• Anastomosis of 3 vessels – septal branch of sup. Labial, septal branch of
anterior ethmoidal and lateral branch of the sphenopalatine
• Posterior bleeds
• Mostly from posterior lateral branches of sphenopalatine artery

43. Epistaxis
• Causes
• Anterior
• Most commonly nasal trauma – picking
• Low humidity causing dryness and irritation
• Allergic or viral rhinitis – increases vascularity
• FB
• Chronic excoriation or drug use

44. Epistaxis
• Causes
• Anterior & posterior
• Anticoagulation therapy
• Hereditary haemorrhagic telangiectasia – Osler-weber-rendu disease
• Familial bleeding diathesis – von Willebrand’s disease, haemophilia
• Carotid artery aneurysm
• Neoplastic lesions
• Hypertension – unclear link, may prolong bleeding more than cause it
• Intranasal steroid use

45. Epistaxis
• Evaluation
• ABCs – important to address airway and haemodynamic instability
• Important history – trauma, anticoagulation or bleeding disorders, recurrence or
1st episode
• INR only in anticoagulated patients
• Patient directed tamponade – blow nose to remove clots, spray oxymetazoline
and pinch alae to septum tightly for 10mins
• Otherwise, sit forward with plug in nose and cold compress on bridge of nose
• Do not attempt reduction in systemic blood pressure as this is poorly validated

46. Epistaxis
• Examination of the nose may be done after local anaesthetic is applied through
lignocaine soaked swab packing
• Nasal speculum should be used, and soft suction tip may help clear clots
• Sitting position to avoid aspiration or swallowing of blood which may induce
vomiting
• Anterior and posterior bleeding may be difficult to distinguish and most reliable is
probably proper anterior packing and persistent bleeding – suggestive of posterior
source

47. Epistaxis
• Treatment
• Anterior bleeding
• If bleeding stops with conservative measures mentioned before – do not pack, observe for
30 min and if no further bleeding, discharge with AxB ointment to be applied for 7 days
• Cautery
• Chemical with silver nitrate or electrical
• Effective but doesn’t work in overly bloody field and is extremely painful so needs adequate
anaethesia

48. Epistaxis
• Treatment
• Anterior bleeding
• Nasal packing
• with nasal tampons or ribbon gauze
• Nasal balloon catheters
• Thrombogenic foams/gels/pledgets
• Contralateral packing to compress

49. Epistaxis
• Treatment
• Anterior packing
• Toxic shock syndrome rarely occurs
• Signs are fever, hypotension, desquamination and mucosal hyperaemia
• Prophylactic antibiotics are not generally advised unless patients are at particularly high risk
for infection (DM, immunosuppression, etc.)
• Packing can be left in for 48 hours and then re-evaluated

50. Epistaxis
• Treatment
• Posterior packing
• Balloon catheters
• Foley catheters
• Cotton packing
• All the above are passed through the nose into the oropharynx and lodged after being pulled back
and placed on traction
• Anterior packing may then be done

51. Epistaxis
• Treatment
• Posterior bleeding
• Any patient with a posterior bleed should generally be admitted
• If still bleeding, consider coagulopathy or surgical intervention – endoscopically or
angiographically
• Embolization/Ligation of sphenopalatine or ethmoidal arteries

52. 6. Risk Factors, Presentation and Management
of Sinusitis
• Acute Infection < 4 weeks
• Most commonly viral, but may be challenging
• Definitions
• Symptomatic inflammation of the nasal cavity and paranasal sinuses
• Acute < 4 weeks
• Subacute 4 – 12 weeks
• Chronic > 12 weeks
• Recurrent 4 or more episodes per year

53. Sinusitis
• Definitions
• Acute viral
• Uncomplicated bacterial – no extension beyond sinuses
• Complicated bacterial – clinical evidence of extension

54. Sinusitis
• Pathophysiology
• Viral
• Rhinovirus , Influenza and parainfluenza viruses
• Direct inoculation and spreads across sinuses through nose blowing (increased pressure)
• Leads to inflammation, hypersecretion, decreased mucociliary clearance
• Bacterial
• Most commonly occurs secondary to viral sinusitis
• May be secondary to local or systemic factors predisposing to infection
• Strep pneumonia, H. influenza, Moraxella are most common pathogens but anaerobes may be
implicated if extension from dental root

55. Sinusitis
• Clinical
• May have nasal congestion and obstruction, purulent nasal discharge, facial pain,
tooth discomfort, pain on bending forward and ear symptoms
• In viral cases, symptoms usually peak after 4 – 6 days and subside by day 10.
Mostly don’t have fever
• Bacterial tend to last longer than 10 days, secondary worsening after starting to
improve

56. Sinusitis
• Complications
• Secondary to bacterial sinusitis
• Preseptal or orbital cellulitis
• Subperiosteal abscess
• Sinus bone osteomyelitis
• Meningitis
• Intracranial abscess
• Septic cavernous sinus thrombosis

57. Sinusitis
• Imaging
• Not indicated for uncomplicated sinusitis
• If CT is done – demonstrates air fluid levels in the sinuses, mucosal oedema and air
bubbles in sinuses. Non specific findings
• Indicated if spread beyond sinuses suspected

58. Sinusitis
• Treatment
• For viral and early uncomplicated bacterial, symptomatic management may be used
• Analgesia, decongestants, nasal saline irrigation, intranasal steroids
• Decision to defer antibiotics must be individualised – not for patients who can’t follow up and
careful consideration if immunocompromise
• If bacterial is unresponsive, oral antibiotics are used – 1st line is augmentin
• Surgery is reserved for maximal medical therapy unresponsive patients and patients
who have coexisting complications
• Involves drainage of sinus and specimens for bacterial cultures

59. 7. Indications, Procedure and Complications
of Tracheostomy
• Indications
• Acute airway obstruction
• Electively after major ENT resections
• Prolonged or anticipated prolonged intubation

60. Tracheostomy
• Advantages of tracheostomy
• Decreased work of breathing, improved ventilator synchrony and triggering
• Patient comfort and ease of secretion clearance
• Aspiration – risk is with ETT or trache
• Communication – improved with tracheostomy, manual occlusion may allow
phonation
• May have reduced rate of pneumonia
• May decrease ICO LOS, mortality unchanged

61. Tracheostomy
• Contraindications
• Relative
• Age < 15
• Bleeding disorders
• Neck distortion from haematoma/infection/previous surgery
• Obesity with obscure neck landmarks

62. Tracheostomy
• Techniques
• Percutaneous vs open
• Percutaneous is faster and doesn’t require theatre
• Some reports show less infection, bleeding, scarring but others are less clear on
these benefits
• Post insertion CXR adds little useful information after uncomplicated insertion

63. Tracheostomy
• Complications
• Acute
• Obstruction
• Tubes can obstruct by mucous plugs or the posterior membrane of the trachea
• Subcutaneous emphysema or pneumothorax
• Bleeding
• If thyroid is injured during procedure

64. Tracheostomy
• Complications
• Chronic
• Tracheal stenosis
• May occur secondary to formation of granulation tissue around tracheostomy insertion site
• Tracheoarterial fistula
• Most commonly innominate artery
• Usually if stoma performed too low
• Erosion of cuff into artery
• Herald bleed and thereafter a massive life threatening haemoptysis may develop
• Temporary control measures are overinflattion of cuff and passing and ETT to exclude
airway