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).