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AIDS and ENTTuesday,

11th of August ‘15

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HIVRetrovirus – Viral RNA into DNATwo types – Type 1 and type 2Type 1 - more common and more pathogenicType 2 – less common and less pathogenicOnce entering the host, this attacks the T-lymphocytes and other CD4

surface markers.With the fall of the CD4 lymphocytes(<500/cu. mm) , the immunodeficiency

is seen and many other opportunistic and malignancy can appear.When the CD4 cell counts appear less than 200, death may appear in about

2-3 years.

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Epidemiology• First case came into medical attention as early as 1980’s. • These cases were detected by retrospective analysis to have occurred

in 1978 in USA and in late 1970’s in Equatorial Africa.• The first case was registered in 1986 in India.

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Current scenario

• Its magnitude has increased to over 100 folds since AIDS was first discovered.• India has over 5.2 million people who are HIV infected with only south Africa

ahead in terms.• 72000 new cases were reported in the year 2005.• Globally about 39.4 million people are infected• About 8 to 10% are from south-east Asia region.• The prevalence of HIV is about 0.91%.• There are focal epidemics in states like Tamil Nadu, Maharastra, Gujrat and

Andhra pradesh (NACO).

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Risk Groupsi. Homosexuals.ii. Heterosexually promiscuous individuals.iii. Prostitutes and truck drivers.iv. I. V. drug users.v. Recipients of blood and its products (haemophilia, thalassemia,

dialysis).vi. Children born to HIV mothers.

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Hazard to health workers is from blood and the body fluids such as• Amniotic • Pleura• Peritoneal• Pericardial

Risk of acquiring infections from specimen of Urine, sputum, stool saliva, tears, sweat and vomitus is negligible.

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Opportunistic infestations in AIDS• Pneumocystis carinii• Tuberculosis• Candida albicans• Cryptococcus neoformans• Mycobacterium species• Toxoplasma gonidii• CMV• Herpes zoster• Histoplasmosis• Herpes simplex

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Course of disease• Initial viraemia: mild C/F ( 1 - 2 weeks)

• Fever.• Headache.• Body ache.• Muscular rash.• Lymph node enlargement.

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• Latent period: • Asymptomatic up to 10 years.• No virus is detected in plasma• Virus replicates in lymphoid tissues such as LYMPH

NODES, TONSILS and ADENOIDS.• Infection can be detected by CD4 number and their

detonating function.• Antibody test becomes positive in 2-4 months of

infection.

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• Advanced disease: After several years.• CD4<200 cells/cu. mm• Patient’s immunity is compromised and is more susceptible

for opportunistic infections.

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ENT MANIFESTATIONS OF AIDS• Due to opportunistic infections of viruses, bacteria, fungi and

protozoa (or) due to activation of neoplastic processes.

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EAR

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External Ear:• Otitis externa

• Malignant otitis externa caused predominantly by Pseudomonas or by Aspergillus fumigatus.

• Treatment is by antibiotics for pseudomonas or IV amphotericin B followed by oral itraconazole for aspergillus.

• Kaposi’s sarcoma of ear• Most common • 300 times more common in people with AIDS• Kaposi’s sarcoma of auricle is more common

(others such as ext. auditory canal, middle ear)• Clinically it appears as RED PURPLE plaques or Nodules.• Treatment

• Medical: Bleomycin, vincristine, liposomal doxorubicin• Surgical: local cutaneous lesions - surgical extirpation.• ZIDOVUDINE should be included in treatment to reduce the extent of

immunosuppression and improve the prognosis.

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Middle Ear• Serous Otitis Media• Seen in both adults and paediatric cases up to 80% of population• Due to poor Eustachian tube functions• Secondary to viral infection, adenoid hypertrophy from HIV (or) due to viral

induced allergy or nasopharyngeal tumors• Treatment: Adnoidectomy to rule out B cell tumors and Kaposi’s sarcoma. An

early myringotomy or grommet insertion is recommended.

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• Acute Otitis Media• Seen in both adults and paediatric patients• Recurrent otitis media and chronic sinusitis are seen in paediatric cases.• Common pathogens include Str. Pneumoniae, H. influenza and Moraxella

catarrhalis.• Treatment:

• Medical: Ampicillin or amoxicillin, failure may be due to beta lactamase in such cases, clavulinic acid may be needed.

• Surgical: tympanocentesis may be required if patient is not responding to antibiotics and also in toxic patients.• Myringotomy and drainage or with grommet insertion is necessary to treat

recurrent Otitis Media

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• Mastoiditis• Caused by Str. Pneumoniae, aspergillus (rare), Mycobacterium tuberculosis

• Chronic Otitis Media• Often by pneumocystis carinii.• Seen even in asymptomatic patients• Pateint presents with otalgia, otorrhoea, hearing loss.• Aural polyp is seen frequently in External auditory canal or middle ear.• Audiogram demonstrates conductive or mixed hearing loss.• The infection is spread through

a) Eustachian tube from nasopharynx.b) Haematogenousc) External auditory canal

• Treatment: trimethoprim-sulfamethoxazole for 3 weeks

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Inner Ear• SNHL• Frequent• 21 – 49%• Commonest by HIV itself• Exact site is uncertain but maybe cochlear or central lesion.• CMV is the most common secondary infection.• Toxoplasma causes abscess

“NEUROSYPHILIS, TB, MENINGITIS, side effects of HIV DRUG REGIMEN, RADIOTHERAPY can cause SNHL”

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• Cryptococcus Meningitis: • 30% patients• sub acute hearing loss• infiltration of cochlear and vestibular nerves and scarpa’s ganglion with Cryptococcus

and macrophages resulting in necrosis of nerve.• Diagnosis by India ink preparation. Should be tested for all HIV patients with H/O new

onset headache. • Treatment: Amphotericin B and 5-fluorocytosine.

• Syphilis• Otosyphilis and Neurosyphilis may accelerate the primary syphilis or reactivate the

latent syphilis.• Manifestations are shortened from 15-30 years to 2-3 years.• Diagnosis by history, unilateral or bilateral SNHL, VDRL, fluorescent treponemal antibody

absorption test which remains positive throughout life.• Treatment 24MU of penicillin IV for 3weeks.

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• Facial nerve paralysis• 30% get affected.• Due to direct HIV infections of CNS, opportunistic infections , primary or secondary

tumours or auto immunity.• Most common CNS pathology associated is toxoplasmosis.• Bell’s palsy is most common diagnosis for 7th nerve with HIV infection.

• HERPES ZOSTER is 7 times more common in HIV patients• They present with pain, herpetic vesicles of external auditory canal and concha along

the distribution of 7th nerve and peripheral facial palsy.• Treatment: High dose acyclovir. Role of steroids is controversial.

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NOSE

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• Cutaneous Lesions:• Kaposi’s, sarcoma: Pigmented irregular lesions (macular or nodular, black to dark brown

or red) on mucous membrane or skin of nose.• Herpes zoster: region of distribution of 5th cranial nerve. Due to reactivation of Varicella

zoster in trigeminal ganglion. Characteristic vesicles seen along sensory distribution. Giant ulcer of nose and face extending to surrounding facial skin.• Seborrhic dermatitis: seborrhea like rash involving nasolabial folds –red eruptions with

greasy scales. Can involve eyebrows, nasal and malar regions, post auricular regions, forehead and back. Treated by topical steroids and ketoconazole

• Nasal obstruction: adenoid hypertrophy, allergic rhinitis, polyposis, chronic sinusitis, neoplasms of nose or PNS.

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• Sinusitis:• 20-68%• Cases from acute to chronic with mucosal changes maybe seen.• Organisms involved are H. influenza, Staph. aureus, Pseudomonas aeruginosa cause

chronic sinusitis.• Fungal sinusitis by Pseudoallescheria boydii, Alterneria alternate, Aspergillus,

Cryptococcus and Candida.• Others include Legionella pneumoniae, Acanthamoeba castellani and CMV.

• C/F• Thick mucopurulent discharge with features of pneumonia and bronchospasm• Nasal congestion• Periorbital pain or pain over canine• Other constitutional symptoms such as fever, headache.

• Diagnosis by CT to know the extent

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• Treatment:• Amoxiclav or cephalosporins – minimum period of 3 weeks• In case of resistance, hospital admission is to be done and treated with IV

antibiotics or surgical drainage is done.• Mucolytics and decongestants for symptomatic relief and facilitate drainage.

• If medical therapy fail, repeated antral irrigation is helpful. Endoscopic sinus is often recommended to enhance drainage. Culture and sensitivity is a must to rule out opportunistic infections.

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Neoplasms• Kaposi’s sarcoma• Excessive proliferation of spindle cells of vascular origin• Non invasive• Mostly seen on palate, tongue or post. Pharyngeal wall• Purpulish should be differentiated from angioma or pyogenic granuloma• Can occur even when the CD4 counts are normal• Diagnosis by Biopsy which may show

• Proliferation of spindle cells• Endothelial cells• Extravasation of RBC• Hemosiderin laden macrophages

• Treatment includes radiation, intralesionoal vinblastine or cryotherapy.

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• NHL• 10-30%• Nose, PNS, nasopharynx and oral cavity are commonly involved• Tends to be more aggressive when the CD4 cells count drops less than 200• Both nodal and extra nodal symptoms may occur• CNS lymphoma are more common with patients of HIV• C/F – Bleeding, nasal obstruction, rhinorrhoea, mass effect on face, orbit or

surrounding structures• Diagnosis by Needle aspiration, tissue biopsy, Lumbar puncture if CNS and

bone marrow are involved

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Airway manifestations• Upper airway• Viral tracheitis• Fungal infections are rare• Neoplasms such as KS – stridor is an important symptom, fibroptic

bronchoscopy is important for diagnosis.

• Lower airway• Pneumocystii carnii pneumonia is very common (65%)• C/F – chest or sternal discomfort, cough, dyspnea on exertion and fever• X-ray shows diffuse bilateral alveolar or interstitial infiltrates• Diagnosis by hypertonic NaCl nebulization, staining with toluidine blue,

bronchoalveolar lavage can be done.

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ORAL MANIFESTATIONS

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• Oral candidiasis (30-90%)• Most common intraoral fungal infection• Oral candidiasis is an early sign of immunosuppression • Three forms

• Pseudomembranous – creamy plague which wipes off easily leaving a bleeding surface• Atrophic – red patches, tender.• Hyperplastic – thick heaped white plaques resembling leukoplakia cannot be wiped off

• Angular chelitis is another form with features such as fissuring, cracking, erythema, ulcerations at corner of mouth• Diagnosis by KOH preparation – mycelia, hyphae, spores; biopsy with PAS and culture

on SDA• Treatment: Topical and systemic antifungals ( Ketaconazole, fluconazole, Amphotericin

B in severe cases)

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• Hairy leukoplasia• White, hairy, slightly raised lesions of the lateral border of tongue, bilateral and does

not improve on therapy for oral candidiasis• Good indicator that that patient may progress to full blown immunodeficiency• Seen in floor of mouth, pharynx, buccal mucosa• Biopsy demonstrates ballooning in epithelium, hyperkeratosis, parakeratosis, acanthosis• Probably caused by EBV• Treatment by acyclovir, sulfa drugs

• Herpes simplex• 9%• Affects the palate, lips, perioral and gingival area.• Responds to acyclovir• CMV, herpes zoster, HPV also cause oral lesion

• Ginivitis and Periodontal disease• Acute necrotising ulcerative gingivitis by gram negative bacteria, anaerobic or candida

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ORAL NEOPLASMS• Kaposi’s Sarcoma – any mucosal surface, hard palate are common• Lymphoma - tonsils• Squamous cell carcinoma - tongue

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IDIOPATHIC ORAL LESIONS• Aphthous ulcers• 20%• <6mm minor, >6mm major• Well circumscribed erythematous border• Large lesion should be biopsied to rule out Carcinoma• Treated by steroids topically

• Xerostomia• Fairly frequent, unknown cause• Frequent oral salines, sugarless gum, salivary substitutes can be used for treatment

• Vocal cord edema• Previous radiation therapy or obstruction from KS• Recurrent laryngeal nerve paralysis due to CMV

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OTHER MASSES• HIV Lymphadenopathy• 2 or more sites for more than 3 months• LN are soft, symmetric 1-5cm• Sites – post. Triangle, Waldeyers ring, submental and sub clavicular.• ROUTINE BIOPSY “NOT HELPFUL”

• Parotid cyst and parotitis• Cyst is unique to HIV• Minimally tender, progressive, bilateral and generalised cervical lymphadenopathy• CT and MRI help in diagnosis• Surgery limited due to diagnostic difficulties and deforming lesions• Tetracyline is proved to be successful.

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Paediatric AIDS1. Cervical adenopathy2. Parotid gland enlargement3. Otitis media4. Sinusitis5. Recurrent adenotonsillitis6. Candidiasis7. URT8. thrombocytopenia

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Occupational risks• More risk is from cutaneous puncture than from contact with skin or

mucous membrane.• People such as surgeons, nurses, laboratory staff handling blood and

its products are at more risk.• On such incidents of injury, ELISA test is performed to establish

negative baseline.• Zidovudine therapy for 6weeks can be offered after exposure.

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Diagnosis of HIV• ELISA: sensitivity of 99.9%• Western blot• Blood tests: anaemia, leukopenia (lymphopenia & thrombocytopenia)• CD4 cell counts • P-24 antigen: core protein of AIDS. This is positive prior to seroconversion.• PCR: Quantitative test measuring virus load and relates the progression of

disease• ß2-macroglobulin levels – indicates macrophage-monocyte level. It rises at

seroconversion and rises with the progression of disease.

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Universal precautions• Wash hands before and after patient contact• Handle blood as potentially infections• Wear gloves for potential contact with blood and its products• Place used syringes in an impermeable container. DO NOT RECAP OR

MANIPULATE• Wear protective eyewear or mask during procedures such as bronchoscopy or

oral surgery• Wear gowns when blood splash is anticipated• Process all lab specimens as potentially infectious• Do not hold needle or tissue in your fingers while suturing

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ANTI RETROVIRAL DRUGS• NUCLEOSIDE ANALOGUES:

• Zidovudine• Stavudine

• PROTEASE INHIBITORS• Saquinavir• Ritonavir

• Combination of drugs

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THANK YOU!