Acute Tonsillitis in Children

I. Introduction & Definition

Acute inflammation of the palatine tonsils, often involving the pharynx (pharyngotonsillitis) and adenoids. It is a common pediatric condition peaking between 5–15 years of age.

II. Etiology

  • Viral (Most Common - 70%): Adenovirus, Rhinovirus, EBV (Infectious Mononucleosis), Enterovirus.
  • Bacterial (30%):
    • Group A Beta-Hemolytic Streptococcus (GABHS) – Most significant due to sequelae.
    • Staph. aureus, H. influenzae, Pneumococcus.
    • Anaerobes (Vincent’s angina).

III. Clinical Features

Symptoms:

  • Throat: Sudden onset of sore throat, odynophagia (pain on swallowing).
  • Systemic: High fever, malaise, headache, abdominal pain (mesenteric adenitis).
  • Voice: "Hot potato" voice (if peritonsillar involvement) or muffled.
  • Ears: Referred otalgia.

Signs:

  • Tonsils: Congested, enlarged, may meet in midline (Kissing tonsils).
  • Exudates:
    • Follicular: Yellow spots (pus in crypts).
    • Membranous: Coalesced exudate forming a membrane.
  • Lymph Nodes: Tender, enlarged jugulodigastric nodes.
  • Breath: Fetor oris.

IV. Grading of Tonsillar Hypertrophy (Brodsky Scale)

  1. Grade 1: Tonsils within tonsillar fossa (<25% of width).
  2. Grade 2: Tonsils beyond pillars (26–50%).
  3. Grade 3: Tonsils occupy 51–75% of oropharyngeal width.
  4. Grade 4: Tonsils occupy >75% (Kissing tonsils).

V. Differential Diagnosis (The "Membranous Tonsil")

  1. Acute Follicular Tonsillitis: Yellowish spots, confined to tonsil, easily wiped off.
  2. Diphtheria: Dirty grey membrane, adherent, bleeds on removal, extends to pillars/uvula.
  3. Infectious Mononucleosis (EBV): Membrane, generalized lymphadenopathy, hepatosplenomegaly.
  4. Vincent’s Angina: Ulcerative, dirty grey membrane, gram-negative fusiform bacilli.
  5. Candidiasis: White curd-like patches.

VI. Diagnosis & Investigations

  • Clinical Diagnosis: Based on history and examination.
  • Centor Criteria / McIsaac Score: To estimate probability of GABHS infection.
    • Score >3 indicates high likelihood of Strep (Empirical antibiotics or Rapid Antigen Test).
  • Throat Swab Culture: Gold standard for GABHS.
  • Rapid Antigen Detection Test (RADT): High specificity, lower sensitivity.
  • Blood Counts:
    • Bacterial: Neutrophilic leukocytosis.
    • Viral/EBV: Lymphocytosis with atypical cells.

VII. Complications

A. Suppurative (Local):

  1. Peritonsillar Abscess (Quinsy): Unilateral swelling, trismus, uvula deviation.
  2. Parapharyngeal/Retropharyngeal Abscess.
  3. Otitis Media.

B. Non-Suppurative (Systemic - Post-Streptococcal):

  1. Rheumatic Fever: Occurs 2–4 weeks later.
  2. Post-Streptococcal Glomerulonephritis (PSGN).
  3. PANDAS: Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal infections.

VIII. Management

1. General Measures

  • Bed rest and adequate hydration.
  • Analgesia/Antipyretics: Paracetamol (10-15 mg/kg) or Ibuprofen.
  • Saltwater gargles (for older children).

2. Antibiotic Therapy (Targeting GABHS)

  • Indication: Centor score >3, positive culture/RADT, or severe symptoms.
  • First Line:
    • Penicillin V: Oral for 10 days.
    • Amoxicillin: 50 mg/kg/day for 10 days.
  • Penicillin Allergy: Azithromycin or Clarithromycin.
  • Recurrent/Resistant: Co-amoxiclav or Clindamycin.

3. Surgical Management (Tonsillectomy)

Absolute Indications:

  • Airway obstruction causing Cor Pulmonale or severe Sleep Apnea (OSAS).
  • Suspected malignancy (unilateral hypertrophy).
  • Uncontrollable hemorrhage from tonsils.

Relative Indications (Paradise Criteria):

  • 7 episodes in the past 1 year.
  • 5 episodes/year for 2 consecutive years.
  • 3 episodes/year for 3 consecutive years.
  • History of Peritonsillar abscess (interval tonsillectomy).

IX. Prognosis

  • Excellent with treatment.
  • Most viral cases resolve in 3–5 days.
  • Untreated GABHS carries risk of Rheumatic Heart Disease.

Adenoid Hypertrophy in Children

I. Introduction

  • Definition: Hyperplasia of the nasopharyngeal tonsil (Luschka’s tonsil), a collection of lymphoid tissue at the junction of the roof and posterior wall of the nasopharynx.
  • Anatomy: Part of Waldeyer’s Ring (along with palatine, lingual, and tubal tonsils).
  • Physiological Course: Present at birth, hypertrophies during 3–7 years (period of peak immunological activity), and usually regresses by puberty.

II. Etiology

  1. Recurrent Infection: Viral (Rhino/Adenovirus) or Bacterial (Beta-hemolytic Streptococci, H. influenzae, M. catarrhalis).
  2. Allergy: Chronic allergic rhinitis leads to lymphoid hyperplasia.
  3. Environmental: Exposure to cigarette smoke (passive smoking).
  4. Gastroesophageal Reflux (GERD): Chronic irritation.

III. Clinical Features

Symptoms manifest due to obstruction of the nasopharynx, Eustachian tube dysfunction, or contiguous infection.

A. Nasal Symptoms

  • Nasal Obstruction: Bilateral, persistent.
  • Mouth Breathing: Especially during sleep.
  • Nasal Discharge: Chronic mucopurulent discharge (Adenoiditis).
  • Voice: Hyponasal speech (Rhinolalia clausa) – lack of nasal resonance.
  • Snoring & Sleep Disordered Breathing: Range from simple snoring to Obstructive Sleep Apnea (OSA).

B. Otologic Symptoms

  • Eustachian Tube Dysfunction: Blockage of the tubal orifice.
  • Recurrent Acute Otitis Media (AOM).
  • Otitis Media with Effusion (OME): "Glue ear" causing conductive hearing loss.

C. General/Systemic Features

  • Adenoid Facies: Classic appearance due to chronic mouth breathing.
    • Elongated face.
    • Open mouth / Prominent upper incisors ("Bunny teeth").
    • High arched palate.
    • Hypoplastic maxilla / Pinched nostrils.
    • Dull expression.
  • Sleep Disturbances: Restless sleep, night terrors, enuresis.
  • Pulmonary Hypertension: Rare complication of severe chronic OSA (Cor Pulmonale).

IV. Grading (Clemens Classification)

Based on Endoscopic view of Choanal obstruction:

  • Grade I: 0–25% obstruction.
  • Grade II: 26–50% obstruction.
  • Grade III: 51–75% obstruction.
  • Grade IV: 76–100% obstruction.

V. Investigations

  1. Diagnostic Nasal Endoscopy (Gold Standard): Directly visualizes size and choanal patency.
  2. X-Ray Nasopharynx (Lateral View): Soft tissue technique.
    • Fujioka’s Method (AN Ratio): Ratio of Adenoidal depth (A) to Nasopharyngeal space (N).
    • Interpretation: AN Ratio > 0.8 indicates significant hypertrophy.
  3. Tympanometry: To rule out Otitis Media with Effusion (Type B curve).
  4. Polysomnography (Sleep Study): If OSA is suspected (Gold standard for OSA).

VI. Differential Diagnosis

  1. Choanal Atresia: Unilateral or bilateral bony/membranous blockage.
  2. Antrochoanal Polyp: Solitary mass from maxillary sinus.
  3. Juvenile Nasopharyngeal Angiofibroma (JNA): Adolescent males, profuse bleeding.
  4. Allergic Rhinitis: Pale turbinates, sneezing.
  5. Foreign Body: Unilateral foul-smelling discharge.

VII. Management

A. Medical Management (First Line)

Indicated for mild-to-moderate symptoms without severe OSA.

  1. Intranasal Corticosteroids (INCS): Fluticasone/Mometasone for 6–12 weeks. Reduces adenoid size by decreasing lymphocyte infiltration.
  2. Antibiotics: For acute adenoiditis (Amoxicillin-Clavulanate).
  3. Saline Nasal Washes: To clear secretions.
  4. Control of Co-morbidities: Treat allergies and GERD.

B. Surgical Management: Adenoidectomy

Indications:

  1. Obstructive:
    • Severe nasal obstruction with mouth breathing/adenoid facies.
    • Obstructive Sleep Apnea (OSA).
  2. Infective:
    • Recurrent Rhinosinusitis (despite medical therapy).
  3. Otologic:
    • Chronic OME (>3 months) with hearing loss (usually with myringotomy).
    • Recurrent AOM.
  4. Dental: Severe malocclusion.

Surgical Techniques:

  • Conventional: Curettage (St. Clair Thomson curette) - "Blind" procedure.
  • Endoscopic Assisted:
    • Powered Microdebrider: Precision shaving (Shaver).
    • Coblation: Radiofrequency ablation (less bleeding, less pain).

VIII. Complications of Adenoidectomy

  1. Hemorrhage: Primary or reactive (rare compared to tonsillectomy).
  2. Grisel’s Syndrome: Atlanto-axial subluxation due to paraspinous inflammation.
  3. Velopharyngeal Insufficiency (VPI): Hypernasal speech (Rhinolalia aperta) if too much tissue is removed or if there is a submucous cleft palate.
  4. Regrowth: Possible, especially if done at a very young age.

IX. Prognosis

  • Excellent prognosis with appropriate treatment.
  • Untreated severe hypertrophy leads to permanent dental/facial deformities (Adenoid Facies) and cardiopulmonary sequelae (Pulmonary HTN).