Hand, Foot and Mouth Disease (Child)

1. Clinical Overview

Summary

Hand, Foot and Mouth Disease (HFMD) is a highly contagious viral illness predominantly affecting children under 5 years of age, characterised by the classical triad of painful oral ulcers, vesicular rash on hands and feet, and low-grade fever. The condition is caused by Enteroviruses, most commonly Coxsackievirus A16 (responsible for the majority of mild, self-limiting cases in the UK and Western countries) and Enterovirus 71 (EV71), which has been associated with severe neurological and cardiopulmonary complications, particularly in outbreaks across the Asia-Pacific region. [1,2]

The rash classically affects the palms, soles, and buttocks (the "hand, foot, mouth, bum" mnemonic), though in recent years Coxsackievirus A6 has emerged causing more widespread, atypical eruptions that can affect the trunk, limbs, and face, sometimes mimicking varicella or eczema herpeticum. [3] The oral lesions begin as vesicles on the tongue, buccal mucosa, and hard palate, progressing to painful shallow ulcers with erythematous halos, which are the primary cause of morbidity in uncomplicated cases due to feeding difficulties and dehydration risk. [4]

In the vast majority of cases (particularly Coxsackie A16), HFMD is a benign, self-limiting illness resolving within 7-10 days with supportive management alone (analgesia, hydration, infection control). [5] However, Enterovirus 71 carries a significant risk of severe complications including brainstem encephalitis, aseptic meningitis, acute flaccid paralysis, neurogenic pulmonary oedema, and myocarditis, with case fatality rates of 1-2% reported in major Asian outbreaks. [6,7] Recognition of red flag features prompting hospital admission is therefore critical.

A characteristic late sequela is onychomadesis (nail shedding) occurring 4-8 weeks post-infection, which is entirely benign and self-resolving. [8] There is currently no specific antiviral treatment for HFMD, and while EV71 vaccines have been developed and deployed in China and Taiwan with demonstrated efficacy, these are not yet available in the UK or Europe. [9] Prevention relies on rigorous hand hygiene and infection control measures, particularly in childcare settings where faecal-oral transmission is the predominant route. [10]

Clinical Pearls

"Hand, Foot, Mouth, Bum": The classical distribution includes the buttocks, which is often forgotten. Always examine the nappy area in suspected cases.

Palms and Soles - Rare Distribution: Most viral exanthems spare the palms and soles. If a rash prominently involves these areas in a febrile child, think HFMD, secondary syphilis, Rocky Mountain spotted fever, or infective endocarditis.

NOT Herpangina: Herpangina (also caused by Coxsackievirus) presents with posterior pharyngeal and soft palate ulcers ONLY, with no peripheral skin rash. HFMD includes the limb vesicular eruption.

EV71 is the Dangerous Serotype: While Coxsackie A16 causes mild disease, Enterovirus 71 is neurotropic and can cause devastating complications. EV71 outbreaks in Malaysia, Taiwan, China, and Vietnam have resulted in hundreds of childhood deaths from brainstem encephalitis and cardiopulmonary failure. [6,11]

Coxsackie A6 - The Great Mimicker: Increasingly common in Europe and the USA, Coxsackie A6 causes atypical HFMD with widespread eczema-like eruptions, bullous lesions, and prolonged desquamation. It can affect adults and cause delayed onychomadesis in up to 25% of cases. [3,12]

Nail Changes (Onychomadesis): Parents should be warned that nails may shed 4-8 weeks after the illness. This is benign, transient, and requires no treatment. Nails regrow normally over 3-4 months. [8]

Exclusion from Nursery is Controversial: UK Public Health England guidance states that exclusion from childcare is not necessary once the child is clinically well (afebrile, eating/drinking). However, many nurseries have their own policies requiring exclusion until vesicles are crusted. Viral shedding in stool continues for weeks regardless. [10,13]

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2. Epidemiology

Demographics and Incidence

Causative Organisms

HFMD is caused by a spectrum of Enteroviruses (genus Enterovirus, family Picornaviridae), which are small, non-enveloped, positive-sense single-stranded RNA viruses. [1]

Transmission Dynamics

HFMD is highly contagious with multiple routes of transmission: [10,13]

1. Faecal-Oral Route (Predominant):

   • Contaminated hands (nappy changing, inadequate handwashing).
   • Contaminated surfaces, toys, fomites (virus can survive on inanimate objects for days).
   • Faecal shedding continues for weeks to months after clinical recovery.

2. Respiratory Route:

   • Droplet transmission from oral secretions, vesicle fluid.
   • Coughing, sneezing, saliva.
   • Respiratory shedding peaks in the first week of illness.

3. Direct Contact:

   • Contact with vesicle fluid (hands, feet, mouth).

Incubation Period: 3-7 days (range 2-10 days). [5]

Infectious Period:

• Most contagious during the first week of illness (high viral loads in oral secretions).
• Viral shedding in stool continues for 2-8 weeks (occasionally months).
• Asymptomatic shedding is common (silent transmission). [10]

Immunity:

• Infection confers serotype-specific immunity (lifelong against that specific enterovirus).
• No cross-protection between serotypes (children can get HFMD multiple times from different viruses).
• Natural antibody levels wane over years (rare reinfections with same serotype possible).

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3. Aetiology and Pathophysiology

Viral Structure and Molecular Biology

Exam Detail: Picornavirus Family: Enteroviruses are small (30 nm), non-enveloped, positive-sense single-stranded RNA viruses. The lack of a lipid envelope makes them resistant to alcohol-based hand sanitizers and many disinfectants (requires soap and water handwashing or bleach-based surface cleaning). [1]

Genome Organisation: 7.4 kb RNA genome encoding a single polyprotein cleaved into structural proteins (VP1-VP4 forming the icosahedral capsid) and non-structural proteins (proteases, RNA polymerase). VP1 contains the major antigenic sites determining serotype.

Receptor Binding:

• Coxsackievirus A16: Binds to SCARB2 (Scavenger Receptor Class B Member 2) and PSGL-1 (P-selectin glycoprotein ligand-1).
• Enterovirus 71: Binds to SCARB2, PSGL-1, and annexin II. SCARB2 is highly expressed in the CNS, explaining EV71's neurotropism. [16]

Pathogenesis: From Infection to Rash

The pathogenesis of HFMD follows the classical enteroviral pattern of infection: [1,5]

Stage 1: Entry and Local Replication (Days 1-2)

• Virus enters via the oropharynx (swallowing contaminated saliva, food) or gastrointestinal tract.
• Initial replication in pharyngeal lymphoid tissue (tonsils, adenoids) and Peyer's patches (small intestine).
• Virus invades M cells (specialized epithelial cells overlying lymphoid follicles).

Stage 2: Primary Viraemia (Days 2-3)

• Virus spreads via lymphatics to regional lymph nodes.
• Enters the bloodstream → Primary viraemia.
• Dissemination to the reticuloendothelial system (liver, spleen, bone marrow, lymph nodes).
• Viral replication amplifies viral load.

Stage 3: Secondary Viraemia (Days 3-5)

• Massive viral release from reticuloendothelial sites → Secondary viraemia (higher viral load).
• Virus disseminates to target organs:
  • "Skin of hands, feet, buttocks: Viral replication in keratinocytes."
  • "Oral mucosa: Replication in epithelial cells (tongue, buccal mucosa, palate)."
  • CNS (in EV71): Crosses blood-brain barrier (mechanism unclear; potential routes include direct infection of endothelial cells, transcytosis, or "Trojan horse" entry via infected monocytes).

Stage 4: Immune Response and Vesicle Formation (Days 4-7)

• Innate Immunity: Type I interferons (IFN-α/β) provide early antiviral defense.
• Adaptive Immunity: Virus-specific CD8+ T cells and neutralizing IgM antibodies appear.
• Vesicle Formation:
  • Viral cytopathic effect + immune-mediated inflammation → ballooning degeneration of keratinocytes.
  • Intraepidermal vesicles form (clear fluid containing virus, inflammatory cells).
  • Oral vesicles rupture quickly → painful ulcers.
  • Skin vesicles on palms/soles evolve more slowly (thicker stratum corneum).

Stage 5: Resolution (Days 7-10)

• Neutralizing IgG antibodies appear.
• Viral clearance from blood and tissues.
• Vesicles crust over and heal without scarring.
• However: Virus continues to replicate in the GI tract and is shed in stool for weeks (faecal-oral transmission persists). [10]

Enterovirus 71: Neurotropism and Severe Disease

Why is EV71 More Dangerous?

EV71 has a unique ability to invade the central nervous system, particularly the brainstem, causing life-threatening complications: [6,7,11]

1. Brainstem Encephalitis (Rhombencephalitis)

• EV71 preferentially infects motor neurons in the pons and medulla.
• Pathology: Neuronal necrosis, microglial nodules, perivascular lymphocytic infiltrates.
• Clinical: Myoclonus (sudden jerking movements), tremor, ataxia, cranial nerve palsies (facial weakness, dysphagia, dysarthria), respiratory failure.
• Autonomic Dysregulation: Damage to medullary cardiovascular and respiratory centres → hypertension, tachycardia, hyperglycaemia, excessive sweating.

2. Acute Flaccid Paralysis (AFP)

• Anterior horn cell involvement (similar to poliomyelitis - EV71 is in the same genus).
• Asymmetric limb weakness, hypotonia, areflexia.
• Can progress to respiratory muscle paralysis requiring mechanical ventilation.
• Residual paralysis may persist (permanent disability in survivors). [17]

3. Neurogenic Pulmonary Oedema

• Pathogenesis: Autonomic storm from brainstem involvement → massive sympathetic discharge → systemic vasoconstriction + pulmonary vasoconstriction + increased capillary permeability → acute pulmonary oedema.
• Sudden onset of respiratory distress, pink frothy sputum, hypoxia.
• Can occur within hours of neurological signs.
• High mortality (up to 50% even with intensive care). [6,11]

4. Myocarditis

• Direct viral invasion of cardiac myocytes.
• Immune-mediated myocardial damage.
• Presents with tachycardia, arrhythmias, hypotension, cardiogenic shock.
• Can cause sudden cardiac death. [7]

Risk Factors for Severe EV71 Disease: [11]

• Age less than 3 years (especially less than 12 months).
• High fever (> 39°C) for > 3 days.
• Persistent vomiting.
• Hyperglycaemia (autonomic dysfunction marker).
• High viral load in blood/CSF.
• Specific EV71 genotypes (B and C more virulent).

Onychomadesis (Nail Shedding) Pathophysiology

Mechanism: Viral invasion of the nail matrix (at the base of the nail) → temporary arrest of nail growth (Beau's lines) → proximal nail plate detaches → nail sheds. [8]

Timing: 4-8 weeks post-infection (time for nail to grow out from matrix to free edge).

Affected Nails: Usually fingernails and toenails on extremities that had vesicles (though not always).

Outcome: Nails regrow normally from the matrix. No long-term sequelae. No treatment required. Reassure parents.

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4. Clinical Presentation

Typical Clinical Course (Timeline)

The classical presentation of HFMD follows a predictable pattern over 7-10 days: [4,5]

Oral Lesions: Characteristics and Distribution

Appearance:

• Early: Small vesicles (1-3 mm diameter), clear or yellowish fluid, on erythematous base.
• Late: Vesicles rupture quickly (within 24 hours) → shallow ulcers with grey-white base and red halo.
• Number: 5-30 lesions (average 10-15).

Distribution: [4]

• Tongue: Dorsal and lateral surfaces (most common site).
• Buccal Mucosa: Inside cheeks.
• Hard Palate: Anterior palate (contrast with herpangina which affects soft palate and posterior pharynx).
• Gingiva: Occasionally (less common than herpes gingivostomatitis).
• Lips: Inner surface (rare).

Clinical Impact:

• Pain: Main symptom. Interferes with feeding (especially acidic foods/drinks).
• Drooling: Child may drool excessively due to pain on swallowing saliva.
• Dehydration Risk: Refusal to drink → most common reason for hospital admission. [5]

Differential from Herpangina:

• Herpangina (also Coxsackievirus): Ulcers confined to soft palate, uvula, tonsillar pillars, posterior pharynx. NO limb rash. [15]

Skin Rash: Morphology and Distribution

Morphology: [3,4]

Distribution: [4]

• Hands:
  • Palms (classic site - most rashes spare palms).
  • Dorsum of hands.
  • Lateral aspects of fingers.
  • Web spaces.
• Feet:
  • Soles (classic site - most rashes spare soles).
  • Dorsum of feet.
  • Lateral aspects of toes.
• Buttocks:
  • Perianal area.
  • Gluteal region.
  • Often missed on examination - always check nappy area!
• Other (especially Coxsackie A6): Extensor surfaces of arms/legs, knees, elbows, trunk, face (atypical).

Number: 5-50 lesions (average 10-20). Some children have only a few vesicles; others have extensive eruptions.

Symptoms: Usually asymptomatic or mildly itchy. Not painful unless secondary infection.

Evolution: Vesicles evolve slowly compared to chickenpox (new lesions appear over 1-2 days, not continuously). All lesions tend to be at the same stage (contrast with chickenpox where all stages present simultaneously).

Atypical Presentations (Coxsackie A6)

Since 2008, Coxsackie A6 has caused increasingly atypical HFMD presentations: [3,12]

Clinical Pearl: If you see a child with "severe eczema herpeticum" but the child is systemically well and afebrile, consider eczema coxsackium (Coxsackie A6 superimposed on eczema). True eczema herpeticum (HSV) causes systemic illness, high fever, and requires IV aciclovir. [12]

Symptoms and Signs

Constitutional Symptoms:

• Fever: 38-39°C (low-grade). Duration 2-3 days in uncomplicated cases. Prolonged fever > 3 days or high fever > 39°C is a red flag (consider EV71).
• Malaise: Child is irritable, clingy, tired.
• Anorexia: Reduced appetite (due to oral pain).
• Abdominal Pain: Mild (viral replication in GI tract).
• Diarrhoea: Occasional (viral enteritis).

Local Symptoms:

• Oral Pain: Main complaint. Difficulty eating/drinking.
• Sore Throat: Pharyngitis (early symptom).
• Drooling: Painful swallowing.
• Itch: Mild (skin rash).

Red Flag Symptoms (Severe Disease - EV71): [6,11]

• Neurological:
  • Persistent headache/vomiting (raised ICP).
  • Altered consciousness, lethargy, drowsiness.
  • Myoclonus (sudden jerking movements of limbs or body - classic sign of brainstem involvement).
  • Tremor, ataxia (cerebellar signs).
  • Limb weakness, difficulty standing (acute flaccid paralysis).
  • Seizures.
• Cardiopulmonary:
  • Respiratory distress, tachypnoea, grunting (pulmonary oedema).
  • Tachycardia, hypotension (myocarditis, shock).
  • Cold extremities, prolonged capillary refill (circulatory failure).
• Autonomic Dysregulation:
  • Excessive sweating.
  • Mottled skin.
  • Hypertension (early sign of brainstem involvement).

Examination Findings

General Examination:

• Observations: Fever (38-39°C). Tachycardia (fever-related). Respiratory rate normal (unless complications).
• Hydration Status: Assess for dehydration (dry mucous membranes, reduced skin turgor, sunken fontanelle in infants, reduced urine output).
• Growth: Plot on centile chart (chronic illness unlikely in acute presentation).

Oral Cavity:

• Lips: May be dry/cracked (dehydration). Perioral vesicles (Coxsackie A6).
• Tongue: Vesicles/ulcers on dorsal and lateral surfaces. Red halos.
• Buccal Mucosa: Scattered ulcers.
• Palate: Hard palate involvement (spares soft palate - differentiates from herpangina).
• Gingiva: Usually spared (contrast with herpes gingivostomatitis which causes severe gingivitis).

Skin:

• Hands: Inspect palms (often missed). Vesicles with red halos. Dorsum of hands. Lateral fingers.
• Feet: Inspect soles. Vesicles on weight-bearing areas. Dorsum of feet.
• Buttocks: Always examine nappy area (perianal vesicles common).
• Trunk/Face: Examine for atypical distribution (Coxsackie A6).

Cardiovascular:

• Heart sounds: Regular, no murmurs (unless myocarditis - muffled heart sounds, gallop rhythm).
• Capillary refill: less than 2 seconds (unless shock).

Respiratory:

• Chest clear (unless pulmonary oedema - crepitations, wheeze).

Neurological:

• Conscious Level: Alert and responsive (GCS 15).
• Cranial Nerves: Normal (unless brainstem encephalitis - facial weakness, dysphagia, dysarthria).
• Limbs: Normal tone, power, reflexes (unless acute flaccid paralysis - hypotonia, weakness, areflexia).
• Gait: Normal (unless ataxia).
• Myoclonus: Observe for sudden jerking movements (EV71 red flag).

Examination Pearls for Exams: [4,5]

• Palms and Soles: Always examine - this is the diagnostic clue.
• Buttocks: Don't forget to look (ask permission, chaperone if appropriate).
• Hydration: Key assessment (admission decision depends on this).
• Myoclonus: If present, suspect EV71 and admit immediately.

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5. Differential Diagnosis

The key diagnostic challenge is distinguishing HFMD from other causes of oral ulcers and vesicular rashes in children.

Differential Diagnosis: Comparative Table

Clinical Reasoning: Key Diagnostic Questions

1. Are the oral ulcers anterior (tongue, buccal mucosa, hard palate) or posterior (soft palate, pharynx)?

• Anterior → HFMD, Herpes gingivostomatitis, Aphthous ulcers.
• Posterior → Herpangina.

2. Is there a rash on the palms and soles?

• Yes → HFMD (pathognomonic), Secondary syphilis (rare in children), Rocky Mountain spotted fever (rare in UK).
• No → Consider other viral exanthems, bacterial infections.

3. Is the rash generalised or localised?

• Localised (hands, feet, buttocks) → HFMD.
• Generalised → Chickenpox, Measles, Rubella, Scarlet fever.

4. Are all stages of the rash present simultaneously?

• Yes (macules, papules, vesicles, crusts together) → Chickenpox.
• No (uniform stage) → HFMD.

5. Is there severe gingivitis (bleeding gums)?

• Yes → Primary herpes gingivostomatitis.
• No → HFMD, Herpangina.

6. Is the child systemically unwell?

• Mild illness (low fever, eating reduced) → HFMD (uncomplicated).
• Severe illness (high fever, drowsy, shocked) → Consider EV71 complications, Stevens-Johnson syndrome, Kawasaki disease, sepsis.

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6. Investigations

Clinical Diagnosis

HFMD is a clinical diagnosis based on the characteristic triad of:

1. Oral ulcers (tongue, buccal mucosa, hard palate).
2. Vesicular rash (palms, soles, buttocks).
3. Low-grade fever (38-39°C).

No investigations are required for uncomplicated, typical cases. [5,13]

Indications for Investigation

Laboratory Findings

Viral Diagnosis:

• Enterovirus PCR (Throat swab, stool, vesicle fluid, CSF): Gold standard. Detects enteroviral RNA. Does not distinguish between serotypes (requires viral culture or sequencing).
• Viral Culture: Time-consuming (days to weeks). Rarely used clinically. Mainly for research/public health.
• Serotype-Specific PCR/Sequencing: EV71 vs. Coxsackie A16 vs. A6. Available in reference laboratories. Used in outbreaks or severe cases.

Blood Tests (Severe Cases):

• FBC: Usually normal WCC. Lymphocytosis (viral infection). Thrombocytopenia (rare, severe disease).
• CRP: Normal or mildly elevated (viral infection). Markedly raised CRP suggests bacterial superinfection.
• Glucose: Hyperglycaemia (stress response to brainstem encephalitis/autonomic dysfunction - poor prognostic marker). [11]
• Lactate: Elevated (shock, tissue hypoperfusion).
• Troponin: Elevated (myocarditis).

CSF Analysis (Neurological Involvement):

• Appearance: Clear.
• WCC: 10-500 cells/μL (lymphocytic pleocytosis). Occasionally polymorphs early.
• Protein: Normal or mildly elevated (0.4-1.0 g/L).
• Glucose: Normal (CSF:plasma ratio > 0.5).
• Enterovirus PCR: Positive (confirms CNS enteroviral infection).
• Pattern: Aseptic meningitis (lymphocytic CSF, negative bacterial culture). [6,17]

Imaging:

• MRI Brain (EV71 Encephalitis):
  • "T2-weighted: High signal intensity in brainstem (pons, medulla), posterior horns of spinal cord (anterior horn cell involvement in AFP)."
  • "Distribution: Dorsal pons/medulla (respiratory and cardiovascular centres)."
  • "Prognosis: Extent of brainstem involvement correlates with outcome. [6]"
• Chest X-ray (Pulmonary Oedema):
  • Bilateral alveolar infiltrates (bat-wing or diffuse).
  • Cardiomegaly (if myocarditis/heart failure).

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7. Management

Management Algorithm

┌─────────────────────────────────────────────────────────────┐
│                  SUSPECTED HFMD                             │
│    (Oral ulcers + Hand/Foot rash in child less than 5 years)        │
└────────────────────┬────────────────────────────────────────┘
                     │
         ┌───────────▼────────────┐
         │   CLINICAL ASSESSMENT   │
         │                         │
         │  1. Hydration status?   │
         │  2. Neurological signs? │
         │  3. Respiratory distress?│
         │  4. Fever duration/height?│
         └───────────┬────────────┘
                     │
        ┌────────────▼─────────────┐
        │   RED FLAGS PRESENT?     │
        │   (See list below)       │
        └──┬────────────────────┬──┘
           │ NO                 │ YES
           │                    │
┌──────────▼──────────┐  ┌──────▼────────────────────────────┐
│  UNCOMPLICATED HFMD │  │   HOSPITAL ADMISSION/REFERRAL     │
│   (Majority of cases)│  │                                   │
│                      │  │  RED FLAGS:                       │
│  SUPPORTIVE CARE:    │  │  • Severe dehydration (unable to  │
│                      │  │    drink, reduced urine output,   │
│  1. ANALGESIA:       │  │    dry mucous membranes, sunken   │
│     • Paracetamol    │  │    fontanelle, lethargy)          │
│       15 mg/kg QDS   │  │  • Neurological signs:            │
│     • Ibuprofen      │  │    - Altered consciousness        │
│       10 mg/kg TDS   │  │    - Myoclonus (jerking movements)│
│     • Topical:       │  │    - Tremor, ataxia               │
│       - Benzydamine  │  │    - Limb weakness                │
│         spray (> 6 yr)│  │    - Seizures                     │
│       - Lidocaine gel│  │  • Respiratory distress           │
│         (apply before│  │    (tachypnoea, grunting)         │
│         feeds)       │  │  • Prolonged high fever (> 3 days  │
│                      │  │    or > 39°C)                      │
│  2. HYDRATION:       │  │  • Age less than 12 months                 │
│     • Small frequent │  │  • Immunocompromised              │
│       sips of cool   │  │                                   │
│       fluids         │  │  MANAGEMENT:                      │
│     • Avoid acidic   │  │  • IV fluids (if dehydrated)      │
│       drinks (OJ, etc)│  │  • Enterovirus PCR (throat, CSF) │
│     • Ice lollies,   │  │  • LP if neurological signs       │
│       cold yogurt    │  │  • MRI brain (if encephalitis)    │
│       soothing       │  │  • ECG/Echo (if myocarditis)      │
│                      │  │  • CXR (if resp distress)         │
│  3. SKIN CARE:       │  │  • PICU referral if severe        │
│     • Keep lesions   │  │  • Supportive care (ventilation,  │
│       clean/dry      │  │    inotropes for shock)           │
│     • No specific    │  │  • NO SPECIFIC ANTIVIRAL          │
│       treatment for  │  │    (Ribavirin, IVIG, pleconaril   │
│       rash           │  │    investigational only)          │
│                      │  └───────────────────────────────────┘
│  4. SAFETY-NETTING:  │
│     • Warn parents re│
│       red flags      │
│     • Advise return  │
│       if unable to   │
│       drink, drowsy, │
│       or breathing   │
│       difficulties   │
│     • Nail shedding  │
│       4-8 weeks later│
│       (benign)       │
│                      │
│  5. INFECTION CONTROL:│
│     • Hand hygiene   │
│       (soap + water) │
│     • Disinfect toys │
│       /surfaces      │
│     • Exclude from   │
│       nursery until  │
│       well (afebrile,│
│       eating/drinking)│
│                      │
│  DURATION:           │
│  • Self-limiting     │
│  • Fever 2-3 days    │
│  • Ulcers heal 5-7 d │
│  • Rash fades 7-10 d │
└──────────────────────┘

Conservative Management (Uncomplicated Cases)

The vast majority of HFMD cases are mild and self-limiting, requiring only symptomatic treatment and reassurance. [5,13]

1. Analgesia and Oral Pain Relief

Systemic Analgesia:

• Paracetamol: 15 mg/kg every 4-6 hours (maximum 4 doses in 24 hours). First-line.
• Ibuprofen: 10 mg/kg every 6-8 hours (maximum 3 doses in 24 hours). Alternative or addition if paracetamol insufficient.
• Avoid Aspirin (risk of Reye's syndrome in children).

Topical Anaesthetics (for oral ulcers):

• Benzydamine Hydrochloride (Difflam) Spray/Mouthwash:
  • "Mechanism: Local anaesthetic + anti-inflammatory."
  • "Dose: Spray 4-8 puffs onto oral ulcers before meals."
  • "Age: > 6 years (can sting in younger children)."
  • "Duration: Use for 3-7 days."
• Lidocaine Gel 2%:
  • Apply small amount to ulcers 15-20 minutes before feeds.
  • "Caution: Risk of aspiration if pharynx is numbed. Use sparingly."
• Choline Salicylate Gel (Bonjela):
  • AVOID in children less than 16 years (salicylate - Reye's syndrome risk).

Alternative Soothing Measures:

• Ice lollies: Numb oral mucosa, provide hydration.
• Cold milk, yogurt, ice cream: Soothing, easier to tolerate than hot foods.
• Avoid: Acidic (orange juice, tomatoes), spicy, salty, or rough foods (crisps, toast).

2. Hydration

Maintaining hydration is the most important aspect of management. Dehydration from oral pain is the commonest reason for hospital admission. [5]

Encourage Oral Fluids:

• Small frequent sips (every 10-15 minutes).
• Cool fluids (water, milk, diluted squash).
• Avoid acidic drinks (orange juice stings ulcers).
• Ice lollies, ice chips (dual benefit: hydration + analgesia).

Assess Hydration:

• Urine output: Aim for wet nappy every 4-6 hours (or 4-6 voids/day in older children).
• Mucous membranes: Moist (well-hydrated) vs. dry (dehydrated).
• Capillary refill: less than 2 seconds.
• Skin turgor: Pinch abdomen - should snap back immediately.
• Fontanelle: Flat (infants). Sunken = dehydration.

Admission for IV Fluids if:

• Child refuses oral fluids.
• Clinical dehydration (dry mucous membranes, reduced urine output, sunken fontanelle, lethargy).

3. Skin Care

The vesicular rash requires no specific treatment. [4,5]

• Keep lesions clean and dry: Gentle washing with soap and water.
• Avoid bursting vesicles: Let them resolve naturally.
• Calamine lotion: May soothe itch if present.
• No antibiotics unless secondary bacterial infection (cellulitis - spreading erythema, purulent discharge).

4. Infection Control and Exclusion Policy

HFMD is highly contagious. Infection control measures are essential to prevent spread: [10,13]

Hand Hygiene:

• Soap and water (not alcohol gel - enteroviruses are non-enveloped and alcohol-resistant).
• Wash hands after nappy changes, before food preparation, after touching lesions.
• Encourage older children to wash hands frequently.

Surface Disinfection:

• Clean and disinfect toys, door handles, surfaces with dilute bleach (1000 ppm sodium hypochlorite - standard household bleach diluted 1:50).
• Enteroviruses can survive on fomites for days.

Avoid Sharing:

• Utensils, cups, towels, dummies.

Exclusion from Childcare:

• UK Public Health England Guidance: Exclusion is not required once the child is clinically well (no fever, able to eat/drink). [13]
• Rationale: Viral shedding in stool continues for weeks (even in asymptomatic children), so exclusion does not prevent transmission.
• However: Many nurseries have their own policies (e.g., exclude until vesicles crusted). Check local policy.
• Pragmatic Approach: Child should stay home while unwell (fever, not eating/drinking), but can return once clinically well (usually day 5-7).

5. Safety-Netting and Parental Advice

Advise Parents to Return if:

• Child unable to drink (dehydration risk).
• Reduced urine output (dry nappies).
• Increased drowsiness, difficult to rouse (neurological concern).
• Breathing difficulties (pulmonary oedema).
• Severe headache, persistent vomiting (raised ICP).
• Jerking movements of limbs/body (myoclonus - EV71).
• Limb weakness, difficulty walking.

Expected Course:

• Fever settles in 2-3 days.
• Oral ulcers heal in 5-7 days.
• Rash fades in 7-10 days.
• Complete recovery in 7-10 days.

Nail Shedding (Onychomadesis):

• Warn parents that nails may shed 4-8 weeks after the illness.
• This is benign, temporary, and requires no treatment.
• Nails will regrow normally over 3-4 months. [8]

Hospital Admission: Indications and Management

Admit if:

• Severe dehydration (unable to drink, reduced urine output, clinical dehydration).
• Neurological signs (altered consciousness, myoclonus, tremor, ataxia, limb weakness, seizures).
• Respiratory distress (tachypnoea, grunting, hypoxia).
• Suspected myocarditis (tachycardia, arrhythmia, hypotension, gallop rhythm).
• Prolonged high fever (> 3 days or > 39°C - EV71 concern).
• Age less than 12 months (higher risk of severe disease).
• Immunocompromised.

Hospital Management:

Supportive Care:

• IV Fluids: 0.9% NaCl + 5% dextrose at maintenance rate (correct dehydration over 24-48 hours).
• Monitoring: Obs (HR, RR, BP, SpO2, temp) 4-hourly. Hourly neuro observations if CNS involvement.
• Nutrition: NG feeds if unable to take orally.

Investigations (Severe Cases):

• Blood: FBC, CRP, U&E, glucose, lactate, troponin.
• Throat/stool swab: Enterovirus PCR and typing (EV71 vs. Coxsackie).
• LP: If neurological signs (CSF enterovirus PCR, cell count, protein, glucose).
• MRI Brain: If encephalitis suspected (T2 high signal in brainstem).
• ECG/Echocardiogram: If myocarditis suspected.
• CXR: If respiratory distress (pulmonary oedema).

Intensive Care (Severe EV71 Complications):

• Brainstem Encephalitis:
  • PICU referral.
  • Mechanical Ventilation if respiratory failure (neurogenic pulmonary oedema, bulbar palsy).
  • "Blood Pressure Control: Avoid over-aggressive treatment of hypertension (autonomic dysregulation - can swing to hypotension)."
  • "Mannitol/Hypertonic Saline: If raised ICP."
  • "Seizure Control: Benzodiazepines, phenytoin, levetiracetam."
• Neurogenic Pulmonary Oedema:
  • "Intubation and Ventilation: Positive pressure ventilation."
  • "Diuretics: Furosemide (reduce pulmonary congestion)."
  • "Inotropes: Dobutamine, milrinone (if myocardial dysfunction)."
  • "Mortality: High (up to 50% even with aggressive treatment). [11]"
• Myocarditis:
  • "Inotropic Support: Dobutamine, adrenaline."
  • "Anti-arrhythmics: If ventricular arrhythmias."
  • "ECMO: Extracorporeal Membrane Oxygenation in refractory cardiogenic shock (case reports). [7]"

Experimental/Investigational Therapies (Not Standard Practice):

• IVIG (Intravenous Immunoglobulin): Used in some Asian centres for severe EV71 (case series suggest possible benefit, but no RCTs). Dose: 1-2 g/kg. [11]
• Milrinone: Phosphodiesterase inhibitor (inotrope + pulmonary vasodilator). Used in EV71 autonomic storm (reduces systemic and pulmonary vascular resistance). [11]
• Ribavirin: Broad-spectrum antiviral. In vitro activity against enteroviruses. No proven clinical benefit. Not recommended.
• Pleconaril: Capsid inhibitor (blocks viral uncoating). Development discontinued. Not available.

Prognosis in Severe Cases:

• EV71 Brainstem Encephalitis: Mortality 1-2% in outbreaks. Neurological sequelae in 10-30% of survivors (cognitive impairment, motor deficits, speech/swallowing problems). [6,11]
• Acute Flaccid Paralysis: Residual limb weakness in 50% at 1 year (similar to polio). [17]

Antiviral Therapy: Current Status

No Effective Antiviral Exists: There is currently no licensed antiviral treatment for enteroviral infections, including HFMD. [1,9]

Investigational Agents:

• Pleconaril: Capsid-binding inhibitor (prevents viral uncoating). Phase III trials showed modest benefit in enteroviral meningitis, but development was halted due to drug interactions (reduces oral contraceptive efficacy via CYP3A4 induction) and FDA concerns. Not available. [1]
• Pocapavir (V-073): Capsid inhibitor. In vitro activity. Clinical trials discontinued.
• Vapendavir (BTA798): Capsid inhibitor. Phase II trials for enteroviral infections. Development status unclear.

Ribavirin: Broad-spectrum antiviral with in vitro activity against enteroviruses. No proven clinical benefit in HFMD. Not recommended. [1]

Vaccines: EV71 Vaccines

EV71 Vaccines Available in China/Taiwan: [9]

Three inactivated EV71 vaccines have been licensed in China (Sinovac, Vigoo, Institute of Medical Biology) following large Phase III trials demonstrating:

• Efficacy: 90-97% protection against EV71-associated HFMD.
• Severe Disease Prevention: > 95% efficacy against EV71-associated hospitalisation and neurological complications.
• Safety: Well-tolerated. Mild local reactions (injection site pain, fever).
• Schedule: 2 doses (0 and 1 month) in children 6 months - 5 years.

Limitations:

• Serotype-Specific: Protect against EV71 only (no cross-protection against Coxsackie A16, A6, or other enteroviruses).
• Duration of Immunity: Uncertain (antibody levels wane over 2-3 years - booster doses may be required).
• Not Available Outside Asia: Not licensed in UK, Europe, USA, Australia. Unlikely to be introduced in low-EV71 burden regions.

Multivalent Vaccine Development: Bivalent (EV71 + CA16) and polyvalent vaccines are under development but not yet available. [9]

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8. Complications

Key Point: The vast majority of HFMD cases (Coxsackie A16) have no complications and resolve completely. Severe complications are almost exclusively associated with Enterovirus 71 in outbreaks (predominantly Asia-Pacific). [6,11]

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9. Prognosis and Outcomes

Uncomplicated HFMD (Coxsackie A16, A6)

• Prognosis: Excellent. Complete recovery in 7-10 days. [5]
• Fever: Resolves in 2-3 days.
• Oral Ulcers: Heal in 5-7 days without scarring.
• Rash: Vesicles crust and fade in 7-10 days. No scarring.
• Functional Recovery: Child returns to normal activity (eating, playing) by day 7-10.
• Recurrence: Child can get HFMD again (caused by different enterovirus serotype).
• Long-Term Sequelae: None. No chronic complications.

EV71-Associated Severe Disease

• Brainstem Encephalitis: [6,11]

  • "Mortality: 10-20% in severe cases (despite PICU care)."
  • "Survivors: 70-90% full recovery. 10-30% have neurological sequelae (cognitive impairment, motor deficits, speech/swallowing difficulties, epilepsy)."
  • "Prognosis: Worse if extensive brainstem involvement on MRI, prolonged unconsciousness, respiratory failure requiring prolonged ventilation."

• Acute Flaccid Paralysis: [17]

  • "Recovery: Gradual improvement over months. Physiotherapy essential."
  • "Residual Weakness: 50% have persistent limb weakness at 1 year (permanent disability in many)."
  • "Prognosis: Better in children less than 2 years (neuroplasticity). Upper limb involvement recovers better than lower limb."

• Neurogenic Pulmonary Oedema:

  • "Mortality: 30-50% (highest mortality complication). [11]"
  • "Survivors: May have chronic respiratory or neurological problems."

• Myocarditis: [7]

  • "Mortality: 20-30%."
  • "Survivors: Risk of chronic heart failure (dilated cardiomyopathy)."

Predictors of Severe Disease (EV71): [11]

• Age less than 3 years (especially less than 12 months).
• High fever (> 39°C) for > 3 days.
• Hyperglycaemia (> 8 mmol/L without diabetes - autonomic dysfunction).
• High viral load (qPCR).
• Specific EV71 genotypes (B5, C4 more virulent).
• Delayed presentation (> 3 days of illness before admission).

Case Fatality Rate:

• Uncomplicated HFMD (Coxsackie A16): less than 0.001% (virtually zero mortality).
• EV71 with CNS involvement: 1-2% (major Asian outbreaks). [6,11]

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10. Evidence and Guidelines

Key Guidelines

Evidence Summary

Clinical Features and Natural History:

• Ooi et al. (2010): Comprehensive review of EV71 clinical features, pathogenesis, and management. Brainstem encephalitis is the hallmark of severe disease. [6]
• Chang et al. (2004): Large cohort study (Taiwan 1998 outbreak) demonstrating EV71 case fatality 1.4%. Myoclonus is an early warning sign. [11]

Virology and Transmission:

• Xing et al. (2014): Systematic review of HFMD aetiology. Coxsackie A16 (49%) and EV71 (22%) most common. Coxsackie A6 emerging (12%). [1]
• Huang et al. (2019): Prolonged faecal shedding (median 28 days) explains difficulty in controlling transmission. Asymptomatic shedding common. [10]

Atypical Presentations (Coxsackie A6):

• Mathes et al. (2013): Coxsackie A6 causes atypical HFMD with widespread rash, eczema coxsackium, and high rate of onychomadesis (24%). [3]
• Lott et al. (2013): Onychomadesis following HFMD: benign, self-limiting, no treatment required. Nail regrowth complete in 3-4 months. [8]

Severe Disease and Complications:

• Chang et al. (2007): Neurogenic pulmonary oedema is the leading cause of death in EV71. Mechanism: autonomic storm from brainstem involvement. Mortality 50% despite ventilation. [11]
• Wang et al. (2003): MRI findings in EV71 encephalitis: T2 hyperintensity in dorsal pons/medulla. Extent of brainstem lesions correlates with prognosis. [6]
• Solomon et al. (2010): Acute flaccid paralysis due to EV71. 50% have residual weakness at 1 year. Similar to poliomyelitis. [17]

Vaccines:

• Zhu et al. (2014): Phase III trial of inactivated EV71 vaccine in China. Efficacy 97.4% against EV71-associated HFMD. Well-tolerated. [9]
• Li et al. (2014): Meta-analysis of EV71 vaccine trials. Pooled efficacy 94% (95% CI 89-97%). Reduces severe disease by > 95%. [9]

Management:

• UK PHE (2017): Exclusion from childcare not necessary once child is well. Faecal shedding continues for weeks regardless. Focus on hand hygiene. [13]
• McMinn (2002): No effective antiviral therapy available. Pleconaril development discontinued. Management remains supportive. [1]

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11. Prevention

Primary Prevention

1. Hand Hygiene (Most Important):

• Soap and water (not alcohol gel - enteroviruses are non-enveloped and alcohol-resistant).
• Wash hands:
  • After nappy changes.
  • After using the toilet.
  • Before food preparation and eating.
  • After contact with ill child.
• Teach children proper handwashing technique (20 seconds, all surfaces).

2. Environmental Cleaning:

• Disinfect surfaces, toys, door handles with bleach-based cleaner (1000 ppm sodium hypochlorite - dilute household bleach 1:50).
• Enteroviruses can survive on fomites for days.
• Clean nappy changing areas thoroughly.

3. Avoid Close Contact:

• Isolate ill children (keep at home until well).
• Avoid sharing utensils, cups, towels, dummies.
• Avoid kissing/hugging ill children (saliva contains virus).

4. Food Safety:

• Wash fruits and vegetables thoroughly.
• Ensure safe water supply (risk in developing countries with contaminated water).

5. Exclusion from Childcare:

• UK Guidance: Exclusion not required once child is clinically well (afebrile, eating/drinking). [13]
• Rationale: Faecal shedding continues for weeks, even in asymptomatic children. Exclusion does not prevent spread.
• Pragmatic: Child should stay home while unwell (fever, not eating), but can return once recovered.

Secondary Prevention (Vaccination)

EV71 Vaccines (Available in China/Taiwan only): [9]

• Target Population: Children 6 months - 5 years.
• Schedule: 2 doses (0 and 1 month).
• Efficacy: 90-97% against EV71-associated HFMD. > 95% against severe disease.
• Limitation: Serotype-specific (no protection against Coxsackie A16, A6).
• Availability: Not licensed in UK, Europe, USA, Australia.
• Future: Multivalent vaccines under development.

No Universal Vaccine: Due to multiple enterovirus serotypes causing HFMD, a universal vaccine remains elusive. [1,9]

Public Health Measures

Surveillance and Outbreak Management:

• Enhanced surveillance in EV71 outbreaks (Asia-Pacific).
• Notification to Public Health if cluster of severe cases (neurological complications).
• Genotyping to identify circulating strains (EV71 genotypes B and C more virulent).
• Public education during outbreaks (hand hygiene, recognition of red flags).

Childcare/School Policies:

• Staff training on hand hygiene and infection control.
• Protocols for cleaning toys and surfaces.
• Information sheets for parents (symptoms, when to seek medical advice, exclusion policy).

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12. Examination Focus

High-Yield Facts for Postgraduate Exams (MRCPCH, MRCP, GP Registrar)

1. Classical Triad: Oral ulcers + Palmoplantar vesicular rash + Low-grade fever.

2. Causative Organisms:

• Coxsackievirus A16: Most common (UK/Europe). Mild, self-limiting.
• Enterovirus 71 (EV71): Neurotropic. Causes severe complications (encephalitis, pulmonary oedema, myocarditis). High mortality in Asian outbreaks.
• Coxsackievirus A6: Emerging. Atypical presentations (widespread rash, eczema coxsackium, onychomadesis).

3. Pathognomonic Features:

• Palms and Soles Involved: Rare - most rashes spare these areas. Think HFMD, secondary syphilis, Rocky Mountain spotted fever.
• Buttock Involvement: Often forgotten. "Hand, Foot, Mouth, Bum".

4. Differential Diagnosis:

• Herpangina: Posterior pharyngeal ulcers ONLY. No limb rash. Also Coxsackievirus.
• Primary Herpes Gingivostomatitis: Severe gingivitis (bleeding gums). High fever. HSV-1.
• Chickenpox: Generalised rash (centripetal). All stages present. "Dew drop on rose petal" vesicles.

5. Red Flags (EV71 Complications):

• Myoclonus (jerking movements) - pathognomonic of brainstem encephalitis.
• Prolonged fever (> 3 days) or high fever (> 39°C).
• Neurological signs (drowsiness, limb weakness, ataxia).
• Respiratory distress (pulmonary oedema).
• Tachycardia, hypotension (myocarditis).

6. Management:

• Supportive only: Analgesia (paracetamol, ibuprofen), hydration, topical anaesthetics (benzydamine).
• No specific antiviral (pleconaril not available).
• Admit if: Dehydration, neurological signs, respiratory distress.

7. Complications:

• Common: Dehydration (painful oral ulcers → refusal to drink).
• EV71: Brainstem encephalitis (myoclonus, respiratory failure), neurogenic pulmonary oedema (high mortality), acute flaccid paralysis (residual weakness in 50%), myocarditis.

8. Onychomadesis (Nail Shedding):

• Occurs 4-8 weeks post-infection.
• Benign, transient, no treatment required.
• Nails regrow normally.

9. Exclusion from Childcare:

• UK Guidance: Not required once child is well (afebrile, eating/drinking).
• Faecal shedding continues for weeks regardless.

10. Vaccines:

• EV71 vaccines available in China/Taiwan (90-97% efficacy).
• Not available in UK/Europe.

Viva Voce: Model Answers

Q1: A 2-year-old presents with fever, oral ulcers, and a rash on the hands and feet. What is your differential diagnosis?

Answer: "The key features are fever, oral ulcers, and a rash on the hands and feet. The most likely diagnosis is Hand, Foot and Mouth Disease, caused by Enteroviruses (Coxsackievirus A16 most commonly). The pathognomonic feature is the palmoplantar distribution of the rash - most viral exanthems spare the palms and soles.

However, I would consider differentials:

• Herpangina (also Coxsackievirus) presents with oral ulcers, but these are confined to the posterior pharynx and soft palate, with no limb rash.
• Primary Herpes Gingivostomatitis (HSV-1) causes oral ulcers, but the key differentiating feature is severe gingivitis with bleeding gums, and the rash is perioral, not on hands/feet.
• Chickenpox could present with fever and rash, but the rash is generalised (centripetal distribution, predominantly trunk), with all stages present simultaneously (macules, papules, vesicles, crusts), and oral lesions are less prominent.
• In very rare cases, secondary syphilis can cause palmoplantar rash, but this is extremely uncommon in children in the UK, and there would be other features (condylomata lata, generalised lymphadenopathy).

I would confirm the diagnosis clinically by examining the oral cavity (ulcers on tongue, buccal mucosa, hard palate), the palms and soles (oval vesicles with red halos), and the buttocks (often involved but frequently missed)."

Q2: What organism causes Hand, Foot and Mouth Disease, and which serotype is associated with severe complications?

Answer: "Hand, Foot and Mouth Disease is caused by Enteroviruses, which are small, non-enveloped, positive-sense single-stranded RNA viruses in the Picornavirus family.

The most common causative organism in the UK and Western countries is Coxsackievirus A16, which causes mild, self-limiting disease with an excellent prognosis.

However, Enterovirus 71 (EV71) is the serotype associated with severe complications. EV71 is neurotropic - it has a predilection for infecting the central nervous system, particularly the brainstem (pons and medulla). This can lead to life-threatening complications including:

• Brainstem encephalitis (rhombencephalitis) - characterised by myoclonus (sudden jerking movements), tremor, ataxia, and cranial nerve palsies.
• Neurogenic pulmonary oedema - resulting from autonomic dysregulation (massive sympathetic discharge causing pulmonary vasoconstriction and capillary leak). This is the leading cause of death in EV71, with mortality rates of 30-50% even with intensive care.
• Acute flaccid paralysis - similar to poliomyelitis (anterior horn cell involvement), with residual weakness in 50% of cases.
• Myocarditis - leading to cardiogenic shock.

EV71 has been responsible for major outbreaks in the Asia-Pacific region (Taiwan 1998, China, Malaysia, Vietnam) with case fatality rates of 1-2% in severe cases. It's much less common in the UK, but recognition of red flag signs (myoclonus, persistent high fever, neurological symptoms) is critical for early PICU referral."

Q3: What are the red flag features in a child with HFMD that would prompt hospital admission?

Answer: "The vast majority of HFMD cases are mild and managed with supportive care at home. However, I would admit if any of the following red flags are present:

1. Dehydration: This is the most common reason for admission. Signs include:

• Unable to drink due to painful oral ulcers.
• Reduced urine output (dry nappies, less than 4 voids/day).
• Dry mucous membranes, sunken fontanelle (infants), prolonged capillary refill, lethargy.

2. Neurological Signs (concern for EV71 brainstem encephalitis):

• Myoclonus - sudden jerking movements of limbs or body (highly suggestive of brainstem involvement).
• Altered consciousness, drowsiness, difficult to rouse.
• Tremor, ataxia (cerebellar signs).
• Limb weakness, difficulty standing (acute flaccid paralysis).
• Severe headache, persistent vomiting (raised ICP).
• Seizures.

3. Respiratory Distress (concern for neurogenic pulmonary oedema):

• Tachypnoea, grunting, use of accessory muscles.
• Hypoxia (SpO2 less than 92%).
• Pink frothy sputum (pulmonary oedema).

4. Cardiovascular Signs (concern for myocarditis):

• Tachycardia disproportionate to fever.
• Hypotension, cold extremities, prolonged capillary refill (shock).
• Gallop rhythm (S3 heart sound).

5. Prolonged or High Fever:

• Fever > 3 days or > 39°C (associated with increased risk of EV71 complications).

6. Other High-Risk Groups:

• Age less than 12 months (higher risk of severe disease).
• Immunocompromised child.

In hospital, I would initiate IV fluids for dehydration, perform investigations if severe (enterovirus PCR, LP if neurological signs, MRI brain, ECG/echo if cardiac signs), and refer to PICU if brainstem encephalitis or cardiopulmonary complications."

Q4: A child with HFMD develops nail shedding 6 weeks later. The parent is concerned. What would you advise?

Answer: "This is onychomadesis, which is a well-recognised, benign, late complication of Hand, Foot and Mouth Disease. It occurs in approximately 5-25% of cases (higher rates with Coxsackievirus A6).

Pathophysiology: The virus invades the nail matrix (the area at the base of the nail responsible for nail growth), causing a temporary arrest of nail production. This results in the formation of Beau's lines (horizontal ridges), and eventually the nail plate detaches proximally and sheds.

Timing: It typically occurs 4-8 weeks post-infection, which is the time taken for the nail to grow out from the matrix to the free edge.

Affected Nails: Usually the fingernails and toenails on the extremities that had vesicles, though not always.

Management: I would reassure the parent that this is:

• Entirely benign and self-limiting.
• Requires no treatment (no creams, antifungals, or vitamins needed).
• The nails will regrow normally from the nail matrix over the next 3-4 months.
• There are no long-term sequelae - the new nails will be completely normal.

I would advise keeping the nails clean and trimmed short to prevent snagging, and reassure that this is a well-documented phenomenon following HFMD with no cause for concern."

Q5: What is the exclusion policy for HFMD in childcare settings, and what is the rationale?

Answer: "The exclusion policy for Hand, Foot and Mouth Disease in the UK is based on Public Health England (PHE) guidance from 2017, which states that exclusion from childcare is not required once the child is clinically well (afebrile and able to eat and drink).

Rationale:

1. Prolonged Faecal Shedding: The virus is shed in stool for weeks to months after clinical recovery (median 28 days, sometimes longer). Excluding children until viral shedding stops would mean prolonged absence from childcare (impractical).

2. Asymptomatic Transmission: Many children (and adults) have asymptomatic or mild infections and continue to shed virus without knowing they're infected. These 'silent spreaders' mean that exclusion of symptomatic cases alone does not prevent transmission.

3. Faecal-Oral Transmission Route: The predominant route is faecal-oral (contaminated hands, surfaces, toys after nappy changes). Good hand hygiene (soap and water, not alcohol gel) and environmental cleaning (disinfecting toys and surfaces with bleach-based cleaner) are more effective at reducing transmission than exclusion.

However, I would advise that:

• The child should stay at home while unwell (febrile, not eating/drinking, miserable) for their own comfort and to reduce spread during the peak infectious period (first week of illness).
• They can return once clinically well (typically day 5-7 once fever has resolved and they're eating/drinking normally).

Nursery Policies: Some childcare settings have their own policies requiring exclusion until vesicles are crusted. While this is more restrictive than PHE guidance, it may be a pragmatic approach to reassure parents and reduce anxiety.

Key Message: The focus should be on hand hygiene (soap and water), cleaning toys and surfaces (bleach-based disinfectant), and educating parents about red flag symptoms requiring medical review."

OSCE Station: Clinical Examination

Scenario: You are the paediatric registrar in the Emergency Department. A 3-year-old child has been brought in by their parent with a 3-day history of fever, mouth sores, and a rash on the hands and feet. Examine the child and present your findings.

Approach:

1. Introduction and Consent:

• Introduce yourself to child and parent.
• Explain examination ("I'd like to examine [child's name], including looking in their mouth and at their skin").
• Gain consent. Chaperone if appropriate.

2. General Inspection:

• Observations: HR, RR, Temp, SpO2.
• Appearance: Alert and playful vs. lethargic/irritable.
• Hydration: Moist mucous membranes, skin turgor, fontanelle (if infant).

3. Oral Cavity Examination:

• Good light source (pen torch).
• Inspect:
  • "Lips: Dry/cracked? Perioral vesicles (CA6)?"
  • "Tongue: Dorsal and lateral surfaces - vesicles or shallow ulcers with red halos."
  • "Buccal Mucosa: Inside cheeks - scattered ulcers."
  • "Hard Palate: Anterior palate involvement (differentiates from herpangina)."
  • "Soft Palate/Posterior Pharynx: Should be relatively spared (cf. herpangina)."
  • "Gingiva: Should not have severe gingivitis (cf. herpes gingivostomatitis)."

4. Skin Examination:

• Hands:
  • "Palms: Inspect carefully - oval vesicles with grey/white centre and red halo (pathognomonic)."
  • Dorsum of hands, lateral fingers, web spaces.
• Feet:
  • "Soles: Weight-bearing areas - vesicles."
  • Dorsum of feet, lateral toes.
• Buttocks:
  • Always examine (ask permission, chaperone).
  • Perianal and gluteal vesicles (often missed).
• Other Areas (if atypical CA6):
  • Trunk, limbs, face (widespread distribution).
  • Eczematous areas (eczema coxsackium).

5. Cardiovascular and Respiratory Examination (Briefly):

• Auscultate heart (rule out myocarditis - gallop rhythm, arrhythmia).
• Auscultate chest (rule out pulmonary oedema - crepitations).
• Capillary refill (less than 2 seconds).

6. Neurological Examination (Red Flag Screen):

• Conscious level: Alert, GCS 15.
• Observe for myoclonus (jerking movements - EV71 red flag).
• Gait: If able, ask child to walk (ataxia?).
• Cranial nerves (if cooperative): Facial symmetry, swallow, gag (brainstem function).
• Limbs (if concerned): Tone, power, reflexes (acute flaccid paralysis?).

7. Presentation: "This is a 3-year-old child who is alert, well-perfused, with normal observations except for a temperature of 38.5°C. On examination of the oral cavity, there are multiple shallow ulcers with red halos on the tongue and buccal mucosa, sparing the soft palate and posterior pharynx. The gingiva is not inflamed. Examination of the skin reveals oval vesicles with erythematous halos on the palms of both hands and the soles of both feet. There are also vesicles on the buttocks in the perianal region. Cardiovascular, respiratory, and neurological examinations are unremarkable.

These findings are consistent with Hand, Foot and Mouth Disease, most likely caused by Coxsackievirus A16. The child is clinically well with no red flag features. I would manage this with supportive care: analgesia (paracetamol and ibuprofen), hydration advice, and topical anaesthetics for oral pain (benzydamine spray). I would provide safety-netting advice to the parent regarding red flag symptoms (dehydration, neurological signs, respiratory distress) and advise they can return to childcare once the fever has settled and the child is eating and drinking normally."

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13. Patient and Layperson Explanation

What is Hand, Foot and Mouth Disease?

Hand, Foot and Mouth Disease (HFMD) is a very common viral infection that mainly affects young children, especially those under 5 years old. It's called "Hand, Foot and Mouth Disease" because it causes mouth ulcers (sores inside the mouth) and a spotty rash on the hands and feet. Sometimes the bottom (buttocks) is affected too.

It's caused by a group of viruses called Enteroviruses. The most common one in the UK is called Coxsackievirus A16, which causes a mild illness that gets better on its own in about a week.

Is it the same as Foot and Mouth Disease in animals?

No, this is a completely different illness. Foot and Mouth Disease in cattle and farm animals is caused by a different virus that does not affect humans. Your child has not caught anything from animals.

How did my child catch it?

Hand, Foot and Mouth Disease spreads very easily between children, especially in nurseries and childcare settings. It spreads through:

• Touching contaminated surfaces (toys, door handles) and then putting hands in the mouth.
• Coughing and sneezing (droplets in the air).
• Contact with the fluid from the blisters.
• Nappy changing (the virus is in the poo, and can spread if hands aren't washed properly).

The incubation period (time from catching the virus to becoming unwell) is about 3-7 days.

What are the symptoms?

Your child will typically have:

Day 1-2 (Start of illness):

• Low fever (38-39°C).
• Your child may be grumpy, tired, and not want to eat much.
• Sore throat.

Day 2-3 (Mouth sores appear):

• Small blisters appear inside the mouth (on the tongue, inside the cheeks, on the roof of the mouth).
• These blisters burst quickly and turn into painful ulcers (like mouth ulcers you might get yourself).
• Your child may drool, refuse to eat or drink, and cry because it hurts.

Day 3-4 (Rash appears):

• A rash appears on the palms of the hands, soles of the feet, and sometimes the bottom.
• The rash starts as small red spots, then turns into blisters (grey or white centre with a red ring around them).
• The rash is usually not itchy or painful.

Day 7-10 (Getting better):

• The fever goes away.
• The mouth ulcers heal.
• The rash dries up and fades away.
• Your child's appetite comes back and they feel much better.

Is it serious?

In the UK, Hand, Foot and Mouth Disease is usually mild and gets better on its own within a week. Your child will recover completely with no lasting problems.

However, very rarely (mainly in outbreaks in Asia), a specific type of the virus (called Enterovirus 71) can cause more serious complications affecting the brain, lungs, or heart. This is extremely rare in the UK, but it's important to know the warning signs (see below).

How can I help my child at home?

There is no specific medicine to treat Hand, Foot and Mouth Disease (it's a virus, so antibiotics won't help). The treatment is to keep your child comfortable while their body fights off the infection:

1. Pain Relief:

• Paracetamol (e.g., Calpol): Give the dose for your child's age/weight, every 4-6 hours if needed (maximum 4 doses in 24 hours).
• Ibuprofen (e.g., Nurofen): If paracetamol isn't enough, you can also give ibuprofen every 6-8 hours (maximum 3 doses in 24 hours).
• Mouth Spray (Difflam/Benzydamine): Your pharmacist can recommend a spray or mouthwash to numb the mouth ulcers (suitable for children over 6 years). Spray onto the ulcers before meals.

2. Fluids and Food:

• The most important thing is to keep your child hydrated (drinking enough).
• Offer small, frequent sips of cool fluids (water, milk, diluted squash).
• Cold foods are soothing: ice lollies, ice cream, yogurt, cold milk.
• Avoid acidic drinks (orange juice, lemonade) and spicy/salty/crunchy foods (crisps, toast) - these will sting the ulcers.
• Don't worry if your child doesn't want to eat solid food for a few days - as long as they're drinking, they'll be fine.

3. Comfort:

• Lots of cuddles and rest.
• Your child may be clingy and grumpy - this is normal.

When should I seek medical help?

You should take your child back to the doctor or to A&E urgently if you notice any of these warning signs:

• Your child is not drinking and you can't get fluids into them.
• Reduced wet nappies or not passing urine (sign of dehydration).
• Your child is very drowsy or difficult to wake up.
• Jerking movements of the arms, legs, or body (myoclonus - a sign of a more serious infection).
• Difficulty breathing, fast breathing, or grunting.
• Severe headache or persistent vomiting.
• Weakness in the arms or legs, difficulty walking or standing.
• Fever lasting more than 3 days.

These signs could indicate complications that need hospital treatment.

Can my child go to nursery?

According to UK government guidance, your child does not need to be excluded from nursery or school once they are feeling better (no fever, eating and drinking normally), even if they still have some spots.

However:

• Keep your child at home while they have a fever and are feeling unwell (for their comfort and to reduce spread).
• Once the fever has gone and they're eating/drinking normally (usually after about 5-7 days), they can go back to nursery.
• Some nurseries have their own rules (e.g., they may ask that the blisters have dried up). Check with your childcare setting.

How can I stop it spreading to other children?

Hand, Foot and Mouth Disease is very contagious, but you can reduce the risk of spread:

1. Wash hands frequently:

• Use soap and water (not hand sanitiser - the virus is resistant to alcohol-based gels).
• Wash hands after nappy changes, after touching the blisters, before preparing food, and before eating.
• Teach your child to wash their hands properly (sing "Happy Birthday" twice for 20 seconds).

2. Clean surfaces and toys:

• Wipe down toys, door handles, taps, and surfaces with a bleach-based cleaner (dilute household bleach).
• The virus can live on surfaces for several days.

3. Don't share:

• Don't share cups, utensils, towels, or dummies between children.

4. Good nappy hygiene:

• The virus is in the poo for weeks after the illness, so always wash hands thoroughly after nappy changes.

Will my child's nails fall off?

Sometimes (in about 1 in 20 children), the nails on the fingers or toes may shed about 4-8 weeks after the illness. This is called onychomadesis.

Don't panic - this is:

• Completely normal and harmless.
• Temporary - the nails will grow back normally over the next 3-4 months.
• No treatment needed - just keep the nails trimmed short to prevent snagging.

Can my child get Hand, Foot and Mouth Disease again?

Yes, unfortunately. There are many different viruses that can cause Hand, Foot and Mouth Disease. Once your child has had it from one virus, they're immune to that specific virus, but they can catch it again from a different virus. It's quite common for children to get HFMD more than once.

Key Takeaways for Parents

• Hand, Foot and Mouth Disease is a common, mild viral illness in young children.
• It causes mouth ulcers and a rash on the hands, feet, and bottom.
• It gets better on its own in about 7-10 days.
• Treatment is pain relief (paracetamol, ibuprofen, mouth spray) and plenty of fluids (ice lollies, cold milk).
• The most important thing is to keep your child hydrated (drinking).
• Watch out for warning signs (not drinking, very drowsy, difficulty breathing, jerky movements) and seek urgent medical help if these occur.
• Your child can return to nursery once they're feeling better (no fever, eating/drinking).
• Wash hands frequently (soap and water) to prevent spread.

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14. References

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Medical Disclaimer: MedVellum content is for educational purposes and clinical reference. Clinical decisions should account for individual patient circumstances. Always consult appropriate specialists and follow local guidelines. This content is intended for healthcare professionals and medical students preparing for postgraduate examinations (MRCPCH, MRCP, MRCS, FRACP, FRACS, FRANZCOG, USMLE, PLAB, AMC).