د. حسين جاسم
L5. Epistaxis, VMR, Nasal allergy, Nasal polyp

Epistaxis
     1.    Local causes:
a. Idiopathic:
spontaneous arterial bleeding from the septum in the Little's area  is the commonest, in young people venous bleeding from the retrocolumellar vein is also frequent, this may be initiated by slight trauma or by atmospheric drying leading to crusting.
b. Traumatic with abrasion of the nasal mucosa, as direct blow, foreign body and nose picking is also frequent cause.
c. Inflammatory: in acute, chronic rhinitis and atrophic rhinitis.
d. Neoplastic.
e. Environmental: high altitudes have a drying effect; air conditioned rooms, fumes, and dusts.     
       2.   General causes:
a. Hypertension does not cause epistaxis, but epistaxis in hypertensive people is more severe and prolonged.
b. Cardiac and pulmonary disorders which leads to increase venous pressure,
c. Blood diseases: on leukemia, hemophilia, purpura, sickle cell anemia, vitamin K & C deficiency, severe liver disease, Von-Will-brand disease, familial hemorrhagic telangictasia (Osler- Rendo disease).
      Sites of bleeding:                                                                                           
      1. Nasal septum:
Little's area (Kiesselbach"s plexus: sphenopalatine artery, anterior ethmoidal artery, posterior ethmoidal artery and superior labial artery) is the commonest site, 75-90% of cases, a bleeding polypus arises in this area, sometimes bleeding may come from behind a spur.
     2. Inferior turbinate and nasal floor.
   3. above the middle turbinate, from anterior ethmoidal vessels in case of hypertension.
     4. The middle meatus. 
     5. Sinuses. 
     Clinical features: 
The bleeding usually occur from the anterior nares, or flow back into  the  pharynx,  and  swallowing of blood  lead  sometimes  to haematemesis, malena, haemoptysis if inhalation of blood also occurs, familial multiple telangictasia often cause very sever bleeding. 
Treatment:
1. Immediate:
-   Pressure on the nostrils: from outside on the septum.
-   Ice or cold packs: applied to the bridge of the nose, or against the roof of the month.

-   Packing of the nose: By: a. Gauze or cotton wool impregnated with paraffin or BTPP (Bismuth iodoform paraffin paste), b. Inflatable bag or splint.
-   Sedatives: mild sedation will calm the patient, with bed rest.
-  Packing of the postnasal space: by inflatable (Foley's) catheter pass through nostrils and their balloons are expanded with 3-7 ml of air.
- Systemic antibiotic to prevent secondary infection when packing is retained for more than 24 hours.
2. Curative and preventive: when immediate treatment fails or repeated bleeding occurs.
-   Cauterization of the bleeding points: either by (silver nitrate) or (trichlor acetic acid) which is a useful chemical caustic in controlling bleeding or by electro galvanocautery, if these measures fail then:
-   Examination under general anesthesia to allows more effective cautery, or more effective anterior and posterior packing.
-   Arterial ligation is indicated rarely when the above measures fails, ligation of the external carotid artery, or ligation of the maxillary artery, or ethmoidal artery ligation.
-   Blood transfusion: when blood loss has been severe.
-   Embolization: by a fine catheter placed in the maxillary artery via the femoral artery with the aid of screening radiography, absorbable emboli. E.g. gel foam is injected.
            -  Vitamin C & K may be given.
            -  Injection of haemostatic like aminocarporic acid.
          - Treatment of the causative condition whether local or general.

 
Vasomotor Rhinitis (VMR)
   It is a combination of nasal obstruction .watery rhinorrhea and sneezing of unknown etiology, it may be due to a predominance of parasympathetic activity. Predisposing factors:
1. Hereditary factors.
2. Infection.
3. Psychological and emotional factors.
4. Endocrine influences: common at puberty, during menstruation and pregnancy.
5. Sensitive loci on septum and inferior turbinate (IT).
6. Drugs:  hypotensive drugs.
7. Overuse of local vasoconstrictors produces rhinitis medicamentosa.
Precipitating factors:
1. Change in humidity and temperature.
2.  Fumes, dust, and alcohol.
3. Reflex: sneezing on waking or getting out of bed onto cold floor and exercise. Pathology:
1. Hypertrophy of IT.
2. Polyps and hypertrophy of mucosa. 
Clinical features:
1. Sneezing which is paroxysmal.
2. Rhinorrhea which is profuse and watery.
3. Nasal obstruction which alternate from side to side.
4. Postnasal discharge and nasal tip dewdrop in elderly.     Differential diagnosis:
1. Allergy.
     2. Infection.
3. Foreign body.
Treatment:
1. Avoidance of precipitating factors and drugs.
2. Antihistamine: given by mouth.
3. Nasal steroids as drops, sprays (betamethasone, beclomethasone dipropionate), others like ipratropium bromide drops for watery rhinorrhea.
4. Cauterization and submucosal diathermy (SMD) and IT which lead to scarring and improve air way.
5. Trimming of the IT and correction of septal deformities.

Nasal Allergy

It's an abnormal reaction to certain substances.
Etiology: Mechanism:
1. IgE: is formed by lymphocytes.
2. IgE is bound to mast and basophile cells and interaction between them and the allergen lead to the secretion of active substances such as histamine and this lead to clinical manifestation.
  3. Capillaries become permeable and oedema occurs, eosinophiles: infiltrate the tissue; serous alveolar glands are stimulated, producing excess watery secretion.
Predisposing factors:
     1. Hereditary factors.
2. Physical factors like change in the humidity.
3. Infection: viruses and bacteria. Allergens may be grouped as:
1. Exogenous: comes from outside the body like:
a. Inhalants: dusts, pollens, feathers, fungal spores, house dust mites.
b. Ingestants: (foods) eggs, nuts, fish, milk, 
c. Contacts to skin and mucosa: face powders, hairs, nasal drops, 
d. Drugs: penicillin allergy, e. Infections: fungi and parasites.
     2. Endogenous: coming from within the body, like transudates and exudates.
Pathology: 
The reaction:
1. Local mucosal changes: oedema, infiltration with eosinophiles and plasma cells,      watery discharge, vascular dilatation which lead to purplish discoloration affecting the inferior turbinates and polyp formation.
2. Involvement of the sinuses: thickening of the lining mucosa and polypi formation and infection. 
Clinical types:
1. Seasonal (hay fever: pollinosis).
2. Perennial (non seasonal). 
Age incidence:
Nasal allergy often becomes manifest in children of school age which may be followed by asthma, nasal allergy is less common after fifty years of age.

Clinical features:

       1. Nasal obstruction usually bilateral.
2. Rhinorrhoea: clear watery discharge with post nasal drips.
3.  Sneezing which occurs in paroxysm.
4. Nasal irritation (tickling sensation).
5. Anosmia. Diagnosis:
1. Careful history.
 2. Clinical examination.
 3. Eosinophiles in nasal secretion or nasal mucosa in large numbers.
 4. Skin tests: especially in patients with seasonal symptoms.
Treatment:
1. Avoidance of precipitating factors.
2. Desensitization: if the allergens can not be avoided and medical treatment has failed, it is helpful in those patients, who are sensitive to only one or two allergens, (specific extracts: contain minute doses of known causal factors, they are applicable to inhalants chiefly, given as preseasonal injections).
3. Antihistamines: given by mouth have sedative side effects.
4. Endocrine therapy:
-   Topical steroids: sprays, drops & aerosols.
  5. Nasal provocation test: a drop test solution may produce rhinorrhea.     
  6. Elimination test: especially in food allergy.  
-   Depot steroids: triamcinolone acetonide 40 mg by I.M injection in seasonal rhinorrhea.
-   Systemic steroids: by mouth are dangerous.
5. Sodium cromoglycate: effective in controlling symptoms.
6. Surgical treatment: to relieve nasal obstruction, removal of polypi, reduction of inferior turbinate, antral washout.                                                    

Nasal Polyp
Pedunculated portion of edematous mucosa of the nose or paranasal sinuses.
Etiology:
1. Allergic factors: clue to sensitivity to one or more allergens.
2. Vasornotor factors: similar to allergic, but no allergens identifiable.
3. Inflammatory: the role of infection is unclear.
4. Aspirin intolerance: the mechanism is not known. 

Site of origin:
1.  Ethmoidal: the ethmoidal cells are the commonest sites, the middle      turbinate is the next in frequency, polyps from these sites tend to grow forwards towards the anterior nares, usually multiple and bilateral.
2.  Antral: the polyps from the antrum are single and emerge from the sinus   ostium   and   extend   backwards   to   posterior   choanae (antrochoanal polyp) they are commonly unilateral. 
Age incidence:
•-   simple ethmoidal polyps usually occur in adults, but children with cystic fibrosis can have them.
•-   Antrochoanal polyp occur more in children and young adults. 
Clinical features:
1. Nasal obstruction, anosmia; the onset is slow and insidious.
2. Epiphora, postnasal catarrh.
3. Headache, snoring, sneezing and clear rhinorrhea.
4. Men affected three times more than women.
5. Broadening of nasal bridge in long standing cases (frog face).
Diagnosis: 1. Radiography of the sinuses.
       2. Biopsy is essential when the polypus is unilateral and hemorrhagic.
Treatment:
1. Conservative

-  Anti histamine either locally or by mouth.
-  Local decongestants: as drops or sprays.
- Topical steroid therapy: beclomethasone spray will shrink existing polypi, and prevent recurrence of those removed surgically.
- Oral prednisolone: on reducing dose regimen is given for 1 5 days starting with 30 mg/day.
- Antibiotic is given for a week.
2. Surgical treatment and removal of polypi.

Best Wishes;
Saif AlDeen Adil