Conditions of Nose and Paranasal sinuses Choanal atresia Results from persistence of buccopharyngeal membrane Severity of presentation depends on whether unilateral or bilateral bilateral atresia: presents with immediate cyclical cyanosis (cyanosis interrupted by crying spells) unilateral: atresia can remain hidden for years and present with unilateral nasal obstruction and rhinorrhea. The average rate of choanal atresia is 0.82 cases per 10,000 individuals. F:M 2:1 Can be associated with other anomalies: CHARGE syndrome (coloboma, heart defects, atresia of
nasal choana, retardation of growth, genital or renal anomalies, ear anomalies) Unilateral atresia occurs more frequently on the right side. 30 % bony, 70 % mixed bony-membranous Treatment: airway management, surgical Choanal atresia McGovern nipple Epistaxis Bleeding usually arises from the nasal septum (littles area) Anterior Epistaxis.
Bleeding is less common from the lateral nasal wall, but is more difficult to control. Epistaxis Management: Direct digital pressure on the lower nose compresses the vessel on the septum and leaning forward, and will arrest the bleeding (Hippocratic method). Resuscitation ABC Blood tests: CBC, blood group, coagulation profile. Cauterize the bleeding point. This can be done with silver nitrate
(chemical) or electrical. If the site of bleeding is unidentified, use nasal packing. Anterior packing Posterior packing Surgical ligation Embolization The Nasal Septum Septal deviation In 80% of population Aetiology: trauma, developmental error
Symptoms: Nasal blockage: unilateral or bilateral Recurrent sinusitis Recurrent otitis media with effusion Recurrent epistaxis Signs:
Caudal dislocation S shaped C shaped Spurs Thickening
The Nasal Septum Treatment: Submucous resection (SMR) Septoplasty Complications of septal surgery
1 Post-operative haemorrhage, which may be severe. 2 Septal haematoma, which may require drainage. 3 Septal perforationsee below. 4 External deformityowing to excessive removal of septal cartilage 5 Anosmiafortunately rare, but untreatable when it occurs. The Nasal Septum Septal Perforation: Aetiology:
Post operative: septa; surgery Nose picking Trauma Wegeners granulomatosis cocaine addiction rodent ulcer (basal cell carcinoma)
lupus; Syphilis: perforation in bony septum The Nasal Septum Septal Perforation: Symptoms: epistaxis, crusting, obstruction, whistling on inspiration or expiration. Investigations: In any case where the cause is not clear, the following should be carried out:
1 full blood count and ESR to exclude Wegeners granuloma; 2 urinalysis, especially for haematuria; 3 chest X-ray; 4 serology for syphilis; 5 if doubt remains, a biopsy from the edge of the perforation is taken. Treatment: nasal douching, septal button, surgical closure Saddle Nose Deformity
Depressed nasal dorsum. Aetiolgies: Nasal trauma causing depressed fracture Excessive Removal of septum in submucous resection Destruction of septal cartilage by, haematoma or abscess, leprosy, tuberculosis, syphilis. Treatment: Surgery (augmentation rhinoplasty) MiscellaneousNasal Infections Acute coryza: common cold, viral, self limiting Nasal Vestibulitis:
VESTIBULE is apart of the dangerous area of the face because of the presence of the retrograde venous drainage through ophthalmic vein (without valves) which can lead to complications like cavernous sinus thrombosis Pyogenic staphylococci Topical and systemic antibiotics, flucloxacillin Furuculosis: staph aureus, management: warm compressors, topical and systemic antibiotics, drainage, analgesia. Never squeeze
Rhinitis Allergic Rhinitis Group of symptoms nasal congestion, rhinorrhea, sneezing, itching and/or postnasal drainage caused by IgE-mediated immunopathologic events pathophysiology o allergens contact nasal mucosa o expose of IgE receptor over mast cell o second exposure early-phase response (IgE mediated)
occurs within 5 minutes of allergen exposure with maximum effect at 15 minutes cross-linking of IgE receptors on mast cells causes degranulation: o histamine o leukotrienes (LTC4, LTD4, LTE4) o PGD2 o cytokines late phase response starts 5-7 h , cytokines recruit eosinophil, neutrophils and basophil History and Physical Exam
nasal o sneezing, congestion, rhinorrhea ocular o redness, itchiness, watery, conjunctivitis, burning laryngeal
o scratchiness, dry, irritated, cough other o seasonal pattern o food hypersensitivity o fatigue OE clear rhinorrhea congested or pale turbinates
periorbital puffiness , darking of skin under eyes allergic shinners due to venous congestion , fine crease in the eyelid dennies line , conjunctivitis allergic salute ; nasal tip transverse creases , congested turbinate open-mouthed breathing prominent pharyngeal lymphoid tissue Definitive Testing for Atopy In vivo test (Skin Testing) scratch test (not widely used) Skin prick test series of allergens inserted by needle into skin positive wheal-and-flare reactions compared to controls, risk of anaphylaxis
intradermal testing similar to prick test except allergen is placed intradermally more sensitive than prick test, risk of anaphylaxis In Vitro Testing radioallergosorbent test (RAST) RAST indications
equivocal skin tests results high risk of anaphylaxis skin disorders failed immunotherapy uncooperative patient advantages highly specific
no risk of anaphylaxis no effect from skin condition or medications disadvantages less sensitive requires up to 1-2 weeks for results more expensive Management of Allergic Rhinitis Level I: Avoidance, Symptomatic Relief
Prevention of Symptoms by Avoidance o o o First-line Pharmacotherapy o
lipid insoluble: do not cross BBB loratadine cetirizine fexofenadine Topical Glucocorticoids o antihistamines, decongestants, cromolyn
Second-generation and Third-generation Antihistamines o o o o clean for dust avoidance of smoke nasal saline to cleanse mucous membranes
reduce local inflammation Cromolyn Level II: Chronic Symptoms (Corticosteroids) adverse local effects: o candidiasis, nasal irritation, dryness, bleeding and crusting
adverse systemic effects: o increased gastric acid production, hypertension, masks signs of infection, sodium retention, hypokalemia, posterior subcapsular cataracts, menstrual irregularities, aseptic necrosis of femoral head Level III: Immunotherapy last resort treatment
criteria o pts with symptoms not easily controlled with pharmacotherapy o sensitive to allergens that cannot be avoided o symptoms that span two or more allergy seasons or are severe o are willing to cooperate in program of immunotherapy disadvantages o patient must be reliable for multiple injections
o requires a chronic regimen (3 years) o risk of worsening symptoms and anaphylactic shock contraindications o pregnancy o autoimmune disorders o immunological compromised patients o B-blockers (increases sensitivity to allergens) o easily avoidable allergens o noncompliant patients
Nonallergic Rhinitis Group of symptoms nasal congestion, rhinorrhea, sneezing, itching and/or postnasal drainage not caused by IgE-mediated immunopathologic events Classification Infectious Rhinitis Viral common cold Pathogens ( rhinoviruses (most common), respiratory syncytial virus, parainfluenza virus)
watery clear rhinorrhea, anosmia, congestion, lacrimation, low-grade fever Tx: antibiotics for suspected bacterial infections only, symptomatic therapy includes decongestants (topical and systemic), antihistamines, hydration, nasal saline irrigations, analgesics Bacterial Mainly; group A strep Tx: antibiotic regimen, symptomatic therapy similar to viral rhinitis Classification Hormonal Rhinitis (Hypothyroidism, pregnancy, OCP, menstrual cycle) Vasomotor Rhinitis
low nasal eosinophil counts and negative skin test results for allergy theory: abnormal functioning of parasympathetic input to turbinate and septal mucosa similar symptomatology to allergic rhinitis except with negative allergy evaluation Triggers (cold air, high humidity, anxiety, stress, exercise) Diagnosis of exclusion Tx; anticholinergic sprays , corticosteroid sprays Drug-induced Rhinitis caused by systemic drugs (antihypertensives most often implicated) Classification Gustatory Rhinitis (Alcohol, spicy foods)
Occupational Rhinitis nasal discharge or congestion due to exposure to airborne substance at work allergic or non-allergic Nonallergic Rhinitis with Eosinophilia Syndrome (NARES) lacks IgE-mediated immunopathologic events
nasal smears contain eosinophil symptoms of perennial rhinitis dx: allergic symptoms with negative allergic tests symptomatic relief similar to allergic rhinitis (nasal corticosteroids, antihistamines, decongestants) Classification Atrophic Rhinitis (Ozena)
atrophic mucosa on septum, turbinates wide nasal cavity may be associated with ozena (thick, foul smelling, dry crust) subjective nasal congestion and constant foul-smelling odour despite lack of objective evident of obstruction primary form; may be caused by infection with Klebsiella ozaenae secondary causes; over-aggressive nasal surgery Tx; saline irrigations Rhinitis medicamentosa from prolonged used of topical vasoconstricting agents (> 7 days) Tx; cessation of topical vasoconstrictors, replacement with nasal saline, oral antihistamines and/or steroid
sprays Acute RhinoSinusitis Aetiology: Common cold
Influenza Measles, whooping cough Dental Trauma Tumours Acute Rhinosinusitis Acute RhinoSinusitis Duration: Acute, < 12 weeks with complete resolution of symptoms. Chronic, 12 weeks symptoms without complete resolution of symptoms.
Other authors depend on this classification: Acute sinusitis: 1 day to 4 weeks Subacute sinusitis: 4 weeks to 3 months Chronic sinusitis: > 3 months (sinusitis that is uncontrolled or inadequately managed and process irreversible without surgical intervention) Recurrent acute sinusitis: 4 or more episode of acute sinusitis that occur within 1 year and there is complete resolution of symptoms between the attacks
Acute exacerbation of chronic rhinosinusitis (when the symptoms of chronic rhinosinusitis exacerbate but return to base line after treatment ) Acute RhinoSinusitis Acute Bacterial RhinoSinusitis The causative organisms are usually streptococcus pneumoniae, Haemophilus influenzae or Staphylococcus pyogenes. In dental infections, anaerobes may bepresent. The mucous membrane of the sinuses
becomes inflamed and oedematous and pus forms. If the ostia are obstructed by oedema, the antrum becomes filled with pus under pressureempyema of the antrum. Acute Bacterial RhinoSinusitis Treatment:
CRS without nasal polyposis Microbiology: Mixed aerobes, anaerobes SYMPTOMS 1 Patients with chronic maxillary sinusitis usually have very few symptoms. 2 There is usually nasal obstruction and anosmia. 3 There is usually nasal or postnasal discharge of mucopus. 4 Cacosmia may occur in infections of dental origin.
Chronic Rhinosinusitis SIGNS 1 Mucopus in the middle meatus under the middle turbinate. 2 Nasal mucosa congested. 3 Imaging shows opacity, or mucosal thickening within the sinus. Treatment Medical FESS: functional endoscopic sinus surgery. Complications of Rhinosinusitis
Complications of Rhinosinusitis Ophthalmological Most common Intraorbital pathways: o o o o o direct extension (especially through thin walled lamina papyracea)
thrombophlebitis (valveless veins) congenital dehiscence trauma direct lymphatics Ophthalmological Chandler classification: Periorbital/Preseptal Cellulitis eyelid edema, erythema, tenderness No vision changes, chemosis, proptosis (exophthalmos), or restriction of ocular muscles Orbital Cellulitis
proptosis, chemosis may cause vision changes (afferent pupillary defect) children initially may lose the ability to distinguish green and/or red colors (colour vision) may limit extraocular muscles Periorbital/Preseptal Cellulitis
Chemosis is the swelling (or edema) of the conjunctiva. It is due to the oozing of exudate from abnormally permeable capillaries Ophthalmological Subperiosteal abscess collection of pus between periorbita and lamina papyracea ( under lamina papyracea) chemosis, proptosis
restricted extraocular motion , decreased vision most common strep.viridins Orbital Abscess collection of pus in orbital soft tissue proptosis, chemosis, restricted extraocular motion decreased vision Ophthalmological Cavernous sinus thrombosis pathogens o S. aureus (most common)
o hemolytic Streptococcus SSx o spiking fevers, toxaemia o Signs in cavernous sinus thrombosis Exophthalmos Paresis III/IV/VI Bilateral signs Reduced conscious level/cerebral irritation. Tx o IV ABx o may require ligation of IJV if septic emboli o anticoagulants (controversial)
o sinus surgery Neurologic meningitis (most common intracranial complication) epidural or subdural abscesses brain abscess, cavernous sinus thrombosis venous sinus thrombosis consider MRI when suspected intracranial or intraorbital complication Potts puffy tumour osteomyelitis or subperiosteal abscess of frontal bone with overlying soft tissue swelling by invasion of diplopic vein
most often seen in adolescents and young adults most common offending organism: S. aureu The infection erodes through the wall of the obstructed infected sinus to form a subperiosteal abscess. As expected it can be associated with extension intracranially with epidural abscess, subdural empyema, meningitis, and cerebral abscess formation. Dural sinus thrombosis is an other possible complication Tx: IV Abx, trephination, may require surgical debridement Potts puffy tumour Nasal polyposis
Bilateral Samters triad Symptoms Treatment: medical, surgical Olfactory disorders Anosmia is defined as loss or absence of the sense of smell. It is a common condition and affects approximately 1% of the population under age 60 years. Olfactory function also decreases with aging Abnormalities of olfaction include (i) anosmia (inability to detect odours) (ii) hyposmia (diminished olfactory sensitivity)
(iii) dysosmia (distorted identification of smell) (a) parosmia (altered perception of smell) (b) Phantosmia (smelling non-existent odours). Olfactory disorders The three most common causes of olfactory disorders are o sinonasal disease Most commonly polyp disease, chronic rhinosinusitis or allergic rhinitis. Sinonasal disease is the most treatable aetiology of anosmia. o postviral anosmia o head trauma
(Shearing force on olfactory filaments, olfactory bulb contusion and frontal lobe injury are proposed potential causative mechanisms. Olfactory disorders other causes o congenital o iatrogenic: Septoplasty, Rhinoplasty, turbinectomy, FESS o intranasal neoplasms o intracranial tumours (meningioma, frontal lobe glioma, pituitary adenoma, craniopharyngioma) o neurological disease ( epilepsy, MS, Alzheimer, Parkinson) o psychiatric disorders
o Systemic disease such as endocrine disturbances (e.g. hypothyroidism, diabetes mellitus) o aging o exposure to environmental chemicals Nasal trauma
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