Complications
1. local
A. peritonsillar abscess (quinsy): is collection of pus between the tonsils
And its bed.
b. Retropharyngeal abscess.
c. Para pharyngeal abscess.
d. Acute otitis media: following extension of infection to the middle ear
Through the Eustachian tube.
2. General
a. Rheumatic fever and glomerulonephritis which follow group A Beta
haemolytic streptococcus,
b. Subacute bacterial endocarditis.
c. Septicemia: in untreated conditions.
tonsillectomy.
Indications for tonsillectomy
The indications for tonsillectomy are subject of some controversy.
1. Recurrent attacks of acute tonsillitis (5-6 attacks/year for at least two
successive years).
2. Peritonsillar abscess (quinsy) especially if occurred more than once.
3. Sleep apnea syndrome:
4. Tonsillectomy for biopsy purposes when the tonsil is thought to be the
site of neoplasm.
Others:
1. Diphtheria carriers.
2. Recurrent attacks of otitis media.
3. Acute rheumatic fever and acute nephritis if streptococcus tonsillitis
has been responsible for recurrence.
Contraindications
1. Bleeding disorders on clotting problems.
2. Acutely inflamed tonsil and recent upper respiratory tract infection.
Here it's safer to wait 3 weeks
3. Epidemic of poliomyelitis:
4. Cleft palate
Postoperative care
1. Nursing of patient in tonsillectomy position.( supine position, head slightly
elevated using a pillow. The head is turned to one side, and the mouth is held open with
a mouth gag
)
2. Careful monitoring of vital signs. So that any hemorrhage can be
detected.
3. Analgesia: paracetamol. NSAID should be avoided due to its effect on
the coagulation process.
4. Encourage the patient to move the muscles of the throat by
swallowing, talking and dinking.
5. Patients should be warned that referred otalgia may be a predominate
complaint following tonsillectomy.
Complications
1. Hemorrhage
 Primary Hemorrhage:
 Reactionary hemorrhage,
 Secondary: 2. Trauma:
3. Infection:
4. Otitis media:
5. Chest complications:
6. Pain:
1. Adenoid facies.
1. Open mouth.
2. Prominent upper incisor teeth.
3. Short upper lip.
4. Thin nose.
5. Hypo-plastic maxilla. • It leads to a small upper jaw,
6. High arched palate.
7. Dull expression due to hypoxia and deafness.
Adenoid Complications
1. Persistent snoring and sleep apnea syndrome.
2. Recurrent URTI.
3. Recurrent attacks of acute otitis media and otitis media with
effusion.
4. Orthodontic disturbances.
5. Speech problems (rhinolalia clausa).
6. Failure to thrive in infants.
Complications surgey
1. Hemorrhage (Primary, reactionary or secondary)
2. Trauma to the uvula, soft palate and Eustachian cushions.
3. Hyper-nasality (Rhinolalia aperta)
4. Incomplete removal and recurrence
Nasopharyngeal Carcinoma
Clinical Picture
Bi-modal age distribution with the first age peak at 2nd decade and the
other peak at 5th – 7th decade of life. It affects males more than
females.
1. Cervical lymphadenopathy: is often the presenting feature which may
be unilateral or bilateral.
2. Naso-respiratory symptoms: nasal obstruction, nasal speech and
epistaxis.
3. Tinnitus and aural symptoms due to Eustachian tube obstruction. This
may proceed to secretory otitis media.
4. Neurological symptoms: the most frequently involved nerves are V, VI,
IX and X. The latter 2 nerves paralysis leads to immobility of the soft
palate. Involvement of the sympathetic chain results in Horner’s
syndrome.
5. Pain and headache due to intracranial extension or sphenoidal
sinusitis.
Treatment
1. Radiotherapy is the treatment of choice
Treatment of ALLERGIC RHINITIS
I. Avoidance of the precipitating factors
II. Drugs
 Topical steroids: as nasal sprays like beclomethasone, budesonide
and mometasone. These are locally acting and not systemically
absorbed. A short course of oral steroids as prednisolone are
effective in severe seasonal symptoms.
 Antihistamines
o First generation (sedating antihistamines) as diphenhydramine
(Allermine) and chlorpheniramine (histidine).
o Second generation (non-sedating) antihistamines as loratadine
and fexofenadine.
o Topical nasal antihistamines as azelastine.
C. Sodium cromoglycate which is a mast cell stabilizer.
III. Immunotherapy (Hyposensitization): Involve injection of small
amounts of antigen to mop up‫ تخلص من‬the allergen specific
immunoglobulins in the patient. This may involve the production of
blocking antibodies that intercept the allergen before it can react with
IgE bound to mast cells.
2-VASOMOTOR RHINITIS (INTRINSIC RHINITIS)
Predisposing factors.
1. Hereditary.
2. Infection
3. Psychological and emotional upset.
4. Endocrine:
5. Drugs:
 Aspirin,
 antihypertensive drugs
 And over use of nasal drops which leads to rhinitis medicamentosa.
6. Atmospheric conditions as changes in humidity and temperature,
fumes and central heating.
Nasal Polyps
Aetiology
1. -Allergic and VMR (Vasomotor Rhinitis).
2. -Chronic rhinosinusitis.
3. -Mixed infection and allergy
4. -Cystic fibrosis.
5. - Bronchial asthma and aspirin intolerance.
fungal infection of sinuses are seen:
1. Fungal ball
2. Allergic fungal sinusitis
3. Non-allergic Eosinophilic Fungal Rhinosinusitis
4. Chronic invasive sinusitis.
5. Fulminant fungal sinusitis (acute invasive).
6. Saprophytic Fungal Infection
Epistaxis Is bleeding per nose.
Epistaxis from Little’s area
Aetiology
The two most common causes of epistaxis are idiopathy and trauma.
I. Local causes
1. Idiopathic.
2. Trauma:
3. Inflammatory: Acute rhinitis, sinusitis and allergy.
4. Anatomical and structural abnormalities: Septal deviation
5. Neoplastic as angioma and carcinoma.
6. Environmental: Air conditioners and industrial fumes.
II. Systemic causes




Cardiovascular as hypertension:
Hematologic: Haemophilia, leukaemia and ITP.
Drugs: Aspirin and anticoagulants as warfarin.
Diseases of blood vessel as Osler’s disease ( Hereditary
hemorrhagic telangiectasia).
Management ART
 A-Arrest of hemorrhage.
 R-Resuscitate the patient: If necessary plasma and blood
transfusion
 T-Treat the cause.
Arrest of the Bleeding by
1-Pressure on the nostrils in a sitting position, the mouth is kept open
and swallowing is forbidden.head leant forwards.
2-Ice packs on the nasal bridge.
3-Cauterization of the bleeding point: Either
 chemical cautery using silver nitrate or tri-chloroacetic acid
 Or electrical cautery.
Lubrication -- Vaseline or tetracycline
4. If epistaxis cannot be controlled do packing
a. Anterior packing:
Using one inch ribbon gauze impregnated with paraffin or Vaseline. The
pack may be left for 24-48 hours.
 Systemic antibiotics should be used
 Sedation
 Lubrication with creams such as Vaseline or genidin or tetracycline,
b. Postnasal packing:
 It is done under GA and prepared from a piece of gause soacked wit
paraffin or any antiseptic solution. The posterior pack stays in place
for 48 hours.
 urinary Foley’s catheter to fill the nasopharynx which can be done
without anesthesia.
 Lubrication
5. Surgical Treatment: If despite anterior and posterior packing, the
bleeding continues or recurs , surgical intervention is indicated.
 A-Submucosal resection of the nasal septum induce fibrosis at
Little’s area.
 B-Arterial ligation: The appropriate vessel is clipped under GA
depending on the area of bleeding.
 c- Embolization: unfit for surgery
Indications of tracheostomy
1. Upper airway obstruction:
 Congenital (subglottic stenosis, laryngeal web, laryngeal cysts).
 Trauma (foreign body, severe head and neck injury, swallowing
corrosive, inhalation of irritants).
 Infection (acute epiglottitis, laryngotracheobronchitis, diphtheria,
Ludwig’s angina).
 Tumor (tongue, larynx, pharynx, thyroid).
 Bilateral vocal cord paralysis (thyroidectomy complication, bulbar
palsy).
2. Protection of the trachea-bronchial tree:
 Neurological diseases (polyneuritis, myasthenia gravis, bulbar palsy,
Multiple sclerosis).
 Trauma (burns of the face and neck, multiple facial fractures).
 Coma (drug overdose, head injury, cerebrovascular accident).
 Head and neck surgery ( oro-pharyngeal resections, supraglottic
Laryngectomy).
3. Ventilatory insufficiency:
 Pulmonary diseases (advanced COPD, severe pneumonia).
 Neurological diseases (as above).
 Severe chest injury (flail chest).
Postoperative management
1. Close nursing observation is essential, especially in the first 24
hours. The patient should be positioned semi-sitting position.
2. Secure the tracheostomy tube properly to avoid accidental
dislodgement but not too tight to cause pressure necrosis.
3. If a cuffed tube was placed, regularly deflate the cuff to
prevent tracheal injury. Replace or clean inner cannula tubes as
needed.
4. Perform regular suctioning to remove tracheal secretions that
the patient cannot cough up. Use a sterile suction catheter to
reduce the risk of infection.
5. Provide humidification of inspired air, using a humidifier, wet
gauze, or saline instillation to keep the airway moist.
6. The patient will be unable to speak initially. Provide a
notebook or communication board until the larynx recovers
function and the patient can block the tube to speak while
exhaling.
7. Decannulate the tracheostomy tube as soon as feasible,
typically once the patient can tolerate it being "plugged" for 24
hours without issue.
Complications of tracheostomy
Hemorrhage:
Apnea: It is managed by allowing the patient to breathe a mixture of
95% O2 and 5% CO2.
Displacement (dislodgment) of the tube
Obstruction of the tube
Surgical emphysema
Pneumothorax:
Subglottic stenosis: late complication
 Others:
1. Wound infection,
2. chest infection,
3. dysphagia and
4. Transient aspiration.
The characteristics of conductive hearing loss are:
1. Negative Rinne test, i.e. BC > AC.
2. Weber lateralized to poorer ear. (Affected)
3. Audiometry shows BC better than AC with air-bone gap.
4. The hearing Loss is not more than 60 dB.
5. Speech discrimination abilities are good since the cochlea is intact.
conductive hearing loss Etiology:
Congenital:
1. Meatal atresia
2. Fixation of stapes footplate
3. Fixation of malleus head
4. Ossicular discontinuity
5. Congenital cholesteatoma
Acquired:
External ear: Any obstruction in the ear canal, e.g.
1. wax,
2. foreign body,
3. furuncle,
4. acute inflammatory swelling,
5. benign or malignant tumor
6. Or atresia of canal.
Middle ear
1. Perforation of TM, traumatic or infective
2. Fluid in the middle ear, e.g. AOM, OME or haemo-tympanum
3. Mass in middle ear, e.g. benign or malignant tumors
4. Disruption of ossicles, e.g. trauma to ossicular chain, CSOM(Chronic
suppurative otitis media), cholesteatoma
5. Fixation of ossicles, e.g. otosclerosis, adhesive otitis media
6. Eustachian tube blockage e.g. retracted TM, serous OM.
The characteristics of sensorineural hearing loss are:
1. A positive Rinne test, i.e. air AC > BC.
2. Weber lateralised to better ear.
3. No air-bone gap on audiometry.
4. Hearing Loss may exceed 60 dB.
5. Speech discrimination is poor.
6. difficulty in hearing in the presence of noise.
7. Recruitment phenomenon. Quiet sounds are barely audible but loud
sounds seem abnormally loud. This is due to reduced functioning of
outer hair cells
8. Loss of frequency resolution
Types of Tinnitus
Non- pulsatile tinnitus
It is often described as a buzzing‫ أزيز‬, whistling, humming or ringing
tone.
It can be associated with
1. noise induced hearing loss,
2. presbycusis,
3. Meniere’s disease,
4. head injury,
5. otitis media,
6. wax impaction and other causes of hearing loss,
non-otologic causes can also be attributed to the conditions including :
1. CNS diseases ,
2. hypotension , hypertension,
3. hypocalcemia ,
4. epilepsy ,
5. migraine and
6. drugs(e.g. salicylates, nonsteroidal anti-inflammatory drugs, loop
diuretics)
Pulsatile Tinnitus
Causes of Pulsatile Tinnitus
Vascular and circulatory causes
1. Atherosclerosis of the internal carotid artery.
2. Vascular malformations.
3. Glomus tumours
4. Increased cardiac output (anemia, thyrotoxicosis, pregnancy)
Non-vascular causes
1. Otosclerosis
2. Paget’s Disease
3. Otitis media with effusion
4. Myoclonus. Myoclonus of the middle ear muscles or palatal
muscles
5. Idiopathic intracranial hypertension
6. Superior semicircular canal dehiscence syndrome
Treatment
1. reassurance
2. It tends to be worse at quiet times (e.g. at night when trying to
sleep) and worrying about it generally makes the tinnitus worse.
3. Address any underlying causes e.g. hypertension, carotid stenosis,
side effect of medications.
4. Sedation and tranquilizers (e.g. TCA) can be beneficial.
5. Behavioral therapy including coping strategies and tinnitus
retraining therapy (TRT).
6. A noise generator can mask tinnitus if interfering with sleep
7. A hearing aid may improve hearing loss
 Bone conduction hearing aids (BAHA):
 Indications for BAHA
1. Recurrent otitis externa or skin reactions associated with hearing aid
mould.
2. Congenital atresia and acquired stenosis of the external auditory
meatus.
3. Chronic otitis media with persistant otorrhea or large matoid cavities.
4. Conductive hearing loss: like otosclerosis as an alternative to surgery.
5. Unilateral sensorineural hearing loss.
Disorders of vestibular system
A. Peripheral
 Involve vestibular end organs and their first order neurons
(i.e. the vestibular nerve).
 The cause lies in the internal ear or the VIIIth nerve. They are
responsible for 85% of all cases of vertigo.
B. Central
Involve central nervous system after the entrance of vestibular nerve in
the brainstem and involve vestibulo-ocular, vestibulo-spinal and other
central nervous system pathways.
Peripheral (Lesions of end organs, vestibular nerve)
1. Meniere's disease
2. Benign paroxysmal positional vertigo
3. Vestibular neuronitis
4. Labyrinthitis
5. Vestibulo-toxic drugs
6. Head trauma
7. Perilymph fistula
8. Syphilis
9. Acoustic neuroma
Central (Lesions of brainstem and central connections)
1. Vertebro-basilar insufficiency
2. Posterior inferior cerebellar artery syndrome
3. Basilar migraine
4. Cerebellar disease
5. Multiple sclerosis
6. Tumors of brainstem and fourth ventricle
7. Epilepsy
8. Cervical vertigo