THROAT DISORDERS

Throat is a common passage connected to nasal as well as oral cavity, consequently affected by variety of inhalant and ingestant insults. Three important protective lym­phoid structures—two lateral tonsils and one adenoids on posterior nasopharyngeal wall, collectively form the Waldeyer's ring.

Acute tonsillopharyngitis (sore throat): While tonsillo- pharyngeal involvement is common in many respiratory or systemic illnesses, the term acute tonsillopharyngitis usually refers to primary inflammation of the throat.

Etiologically ~80% cases are caused by viral infections (RSV, influenza, entero or adenoviruses) and anothe

15-20% by Group A #946; hemolytic streptococci (#946;HS). Sore throat due to other causes, e.g. Staph. aureus, S. pneumoniae is rare and usually represents superinfection. Epidemiology: Viral infections are perennial and more common in young children. Streptococcal sore throat (SST) is common in winter season and older children gt; 3 years.

Clinically, most cases present with acute onset of moderate fever, throat pain and dysphagia with consti­tutional features and a self-limiting course. Important clinical differences between viral and SST include:

• Presence of rhinitis, cough and hoarseness of voice is rare in SST and indicates viral etiology.

• Throat signs are generally minimal in viral illness while SST is associated with marked inflammation, follicular exudates and usually, tender cervical lymphadenopathy.

Centor criteria suggests score of 1 for each of the following five points: (a) absence of cough, (b) tender cervical lymphadenopathy, (c) fever gt;38°C, (d) tonsillar exudates/swelling and (e) age 3-14 years. Based on this score, risk of SST is stratified as low (1), moderate (2-3) and high (#8805; 4).

Complications include: (a) local extension of infection, e.g.

Diagnosis is clinical though throat culture is indicated in—(a) suspected cases of SST with centor score gt;1, (b) past history of rheumatic fever/heart disease, (c) persistent signs for gt;3 days, and (d) suspected diph­theria. Antibody tests, e.g. ASO titres are usually negative in early SST.

D/D mainly includes diphtheria (tough membrane that bleeds on separation), infectious mononucleosis (atypical lymphocytes), early measles (Koplik spots gt; rash), etc.

Treatment: Viral sore throat is self-limiting and treated symptomatically with rest (including voice rest), warm saline gargles, soft-diet and antipyretics, e.g. Paracetamol.

Antibiotics are indicated only in culture-proven or high-risk cases of SST (Centor score 4), with oral penicillin (250-500 mg BD) or amoxicillin (50 mg/kg OD) for 10 days. Oral azithromycin (10-15 mg/kg OD ? 3-5 days) or first-generation cephalosporins are equally effective and may be used, specially in Penicillin-allergic cases. Cotrimoxazole, sometimes used for prophylaxis, should not be used for treatment of SST.

Repeat throat cultures are not necessary after antibiotic therapy (except in rheumatic fever), as persistently positive cultures may be due to colonization/carrier state and need not be treated.

Prevention of SST is important, especially in cases with previous rheumatic fever, requiring long-term penicillin prophylaxis (Ch 17.6).

Chronic tonsillitis: Tonsils are normally enlarged in 4-8 years age-group due to normal lymphoid growth and all enlarged or hypertrophic tonsils should not be construed as chronic tonsillitis or indication for tonsillectomy.

Clinically, chronic tonsillitis is frequently associated with—(a) recurrent/persistent dry cough, (b) dysphagia, (c) growth failure, and (d) cervical lymphadenopathy.

Treatment: Most cases can be successfully treated with longer antibiotic therapy.

Tonsillectomy for recurrent tonsillitis is recommended only in cases with 7 documented episodes in the previous year or 5 episodes in each of the previous 2 years, or 3 episodes in each of the previous 3 years (paradise criteria).

Peritonsillar abscess (Quinsy) is the extension of pharyngotonsillitis into a potential space between superior constrictor muscle and tonsils, usually due to #946; hemolytic streptococci or oral anaerobes.

Clinically, apart from history of preceding sore throat, these cases present with high fever, severe throat pain, trismus (spasm of pterygoid muscles), dysphonia/ slurred speech and torticollis. On examination, affected tonsillar area is marked by displacement of tonsils and/ or pointing abscess over anterior faucial pillar, which may rupture spontaneously.

Treatment includes antibiotics and aspiration of pus with/without tonsillectomy.

Retropharyngeal abscess denotes extension of infection into the potential space between posterior pharyngeal wall and pre-vertebral fascia, as a complication of bacterial pharyngitis, vertebral osteomyelitis or penetrating injuries of pharynx.

Microbially, retropharyngeal abscesses are usually polymicrobial, with group A streptococci, Staph. aureus and oral anaerobes as predominant pathogens.

Clinically, these cases present with history of sore throat followed by high fever and severe dysphagia, dyspnea, throat pain. On examination, hyperextension of neck and a bulge in the posterior pharyngeal wall are strong indicators of retropharyngeal abscess.

Untreated cases may rupture into pharynx or extend within fascial plains to produce neck swelling or mediastinal mass. Death may ensue due to aspiration, airway obstruction or erosion of major vessels.

Diagnosis rests on lateral X-ray of neck suggestive of increased retropharyngeal space with soft tissue mass and must be confirmed by CT scan.

Fig. 16.6A and B: Adenoids: (A) Adenoid facies; (B) Lateral X-ray showing obliteration of nasopharyngeal column.

Treatment includes intensive therapy with a semi­synthetic penicillin, e.g. clindamycin or ampicillin + sulbactum, to cover penicillinase-producing staphylo­cocci, along with surgical drainage of abscess.

Adenoidal hypertrophy is a common cause of chronic nasal obstruction, mouth-breathing and snoring in school children. Hypertrophy of nasopharyngeal adenoids may be developmental (normal lymphoid growth during 4-8 years) or post-infective, associated with faucial tonsillitis. Clinically, these cases present with:

• Persistent cough and rhinorrhea, due to post-nasal drip.

• Mouth-breathing and snoring with disturbed sleep, due to airway obstruction.

• Adenoid facies with open mouth, high-arched palate and maxillary prominence (Fig. 16.6A).

• Complications, e.g. (i) obstructive sleep apnea syndrome, (ii) failure to thrive due to chronic hypoxia, (iii) poor school performance due to disturbed night sleep, and (iv) chronic otitis media due to blocked eustachian tubes by hypertrophied tissue.

Diagnosis rests on lateral X-ray showing obliteration of nasopharyngeal air column (Fig. 16.6B), indirect pharyngoscopy or fiberoptic nasopharyngoscopy.

Management: As developmentally hypertrophic ade­noids often regress by 8-9 years, adenoidectomy is indicated only in—(a) persistent adenoids beyond gt;10 years, (b) recurrent nasopharyngitis or otitis media, (c) severe airway obstruction with growth failure or obstructive sleep apnea disorders.

Obstructive sleep apnea disorders (OSAD) is a common but under-diagnosed problem in childhood, characterized by—a combination of prolonged partial airway obstruction and intermittent complete obstruction (obstructive apnea), which may disrupt sleep or cause more serious complications, e.g.

Incidence: OSAD is estimated to affect ~1% of school children, though snoring-the milder variant, is more common in 8-10%. OSAD is most common during 5-7 years of age due to physiological adenoidal hypertrophy, with equal sex distribution in children (in adults, more common in males).

Predisposing factors include—(a) adenotonsillar hypertrophy, (b) recurrent respiratory infections, (c) cranio­facial abnormalities, e.g. cleft palate, micrognathia, macro- glossia, etc. (d) neuromuscular or brain-stem disorders,

(e) others, e.g. extreme obesity or sedative drug therapy.

Pathogenesis of OSAD involves a cyclic breathing irregularity due to failure in maintenance of normal airway tone during sleep. (sleep gt; decreased airway tone gt; airway narrowing gt; OSAD gt; hypoxia/hypercapnia gt; increased ventilatory efforts gt; arousal gt; increased airway tone gt; relieved airway obstruction gt; return to sleep).

Clinical spectrum varies from habitual snoring to severe sleep disturbances and consequences of prolonged hypoxia. Important problems include:

• Airway obstruction: Snoring, mouth-breathing, adenoid facies, pectus excavatum, stridor, etc.

• Disturbed sleep: Daytime sleepiness, behavioral problems, poor school performance.

• Chronic hypoxia: Growth failure, polycythemia and hemodynamic changes, e.g. pulmonary hypertension and right ventricular hypertrophy in severe cases.

Diagnosis rests on a clinical triad of—(a) snoring, (b) nocturnal breathing difficulties, (c) witnessed breathing pauses; which may confirmed on polysomnography in borderline cases.

Other findings, e.g. large adenoids, respiratory alkalosis with metabolic acidosis and unexplained polycythemia supports the diagnosis.

D/D of OSAD includes other causes of disturbed night sleep like nocturnal asthma, gastroesophageal reflux and behavioral problems, e.g. night terrors and narcolepsy. Treatment: As adenoidal hypertrophy is the commonest cause, adenotonsillectomy is the first step in treatment of significant OSAD. Non-responders may need night-time breathing support, e.g. CPAP to keep their airways open.

Pharmacotherapy is of limited value in children, while Medroxyprogesterone acetate (to stimulate ventilatory drive) and Protriptyline (to decrease REM sleep) have been found effective in adults. Extreme cases may require permanent tracheostomy or facial reconstructive surgery. Pharyngeal foreign bodies, e.g. fish-bones, present with dysphagia or prickly sensation in throat. Visible foreign bodies can be removed by Tongue-jaw lift maneuver (Ch 27.1.1), but blind finger-sweeps should never be attempted, which may push the body further back into airways or esophagus.

A neck and chest skiagram is advised in all cases to exclude deeper (airway/esophageal) foreign bodies or left-outs after removal.

16.5.4