Recent reports of hand, foot, and mouth disease (HFMD) in various cities have brought into focus another viral illness in India. Hence this article highlights the clinical management of HFMD and Herpangina caused by coxsackievirus.

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Understanding hand, foot and mouth disease

Hand, foot and mouth disease (HFMD) is a clinical illness caused by Picornaviridae family enteroviruses and is characterised by an oral enanthem and a macular, maculopapular, or vesicular rash of the hands and feet. Typically brought on by Coxsackievirus A16 and Enterovirus 71.

The number of kids contracting hand, foot, and mouth disease is making parents increasingly anxious at a time when COVID-19 and monkeypox infections are still a matter of worry. Chandigarh, Punjab, Maharashtra, Goa, Odisha, and West Bengal have reported many instances of the viral illness commonly known as HFMD.

Despite the fact that HFMD infections are frequent among youngsters at this time of year, the number of reported cases is much higher than usual. OPD visits by these patients are frequent.

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Standard treatment guidelines 2022 for hand, foot, and mouth disease in children have been issued by the Indian Academy of Pediatrics (IAP).

The following are the most important suggestions for the guidelines:

Transmission

1. Only humans are carriers.
2. The illness is transmitted by contact with faeces, saliva, and respiratory droplets.
3. The patient is most contagious during the first week of sickness, although an active virus may remain in the stool for 4–8 weeks.
4. Incubation is for 3 to 7 days.

Pathogenesis

1. Ingestion of virus shed from the gastrointestinal tract (GIT) or upper respiratory tract (URT) of infected people, or contact with vesicle fluid (oral or nasal secretions, saliva, blister fluid, and faeces of infected individuals). Once ingested, enteroviruses multiply in the submucosal lymphoid tissues of the colon and throat before migrating to regional lymph nodes.
2. Replication at these locations results in mild viremia infection of reticuloendothelial tissues and several organs [central nervous system (CNS), liver, and skin] which leads to clinical symptoms.
3. Additional replication at dispersed areas causes significant viremia with the production of type-specific antibodies. The death of infected cells is accompanied by inflammation and necrosis.

Clinical features

1. Low-grade fever, sore throat, malaise, maculopapular or papulovesicular rash on the hands and soles of the feet, and painful oral ulcerations are the clinical criteria for diagnosing HFMD.
2. Lesions on the skin are between 2 and 6 millimetres in diameter, with an erythematous halo, and progress into vesicles that burst and leave painless, shallow ulcers that do not scar.
3. Typically, painful oral exanthems affect the posterior oral cavity, including the soft palate. Tongue and buccal mucosa may also be affected by lesions, and discomfort may lead to dehydration.
4. Lesions resolve after 7 to 10 days.
5. Patients may have unusual skin lesions, such as hemorrhagic or purpuric lesions; bullae and pustules; trunk, cheek, or genital involvement; palm and sole of the foot desquamation; and accentuation in atopic dermatitis-affected regions (eczema coxsackium).
6. A small percentage of children with HFMD exhibited an arrest of the nail matrix. Beau lines (transverse ridging) or onychomadesis (nail shedding) occurred 3–8 weeks after HFMD.

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Herpangina

1. The symptoms of herpangina include a quick onset of fever, sore throat, dysphagia, and painful lesions in the posterior pharynx. Headaches and backaches may develop in older children, and 25% of cases include vomiting and stomach discomfort.
2. On the anterior tonsillar pillars, soft palate, uvula, tonsils, posterior pharyngeal wall, and sometimes the posterior buccal surfaces, there are lesions that are characteristic.
3. Lesions consist of isolated 1–2 mm vesicles and ulcers that grow to 3–4 mm over the course of 2–3 days and are encircled by erythematous rings of varying sizes up to 10 mm in diameter. The number of lesions may vary from one to more than fifteen but is often around five.
4. Generally, fever lasts 1–4 days, and symptoms resolve in 3–7 days.

Diagnosis

1. The majority of HFMD diagnoses are established clinically.
2. Approximately six weeks after infection, the virus may be found in the stool; however, shedding from the oropharynx often occurs within four weeks.
3. When etiologic confirmation is required, samples of the pharynx, stool, and vesicular fluid for cell culture or nucleic acid amplification [polymerase chain reaction (PCR)] should be acquired.
4. Light microscopy of vesicle biopsies or scrapings distinguishes HFMD from varicella-zoster virus and herpes simplex virus. Multinucleated and large cells are present in smears collected from the wet skin exposed after a vesicle is removed for both varicella and herpes (Tzanck smear). Lesions associated with HFMD lack giant cells.

Differential diagnosis

• Aphthous ulcers
• Herpetic gingivostomatitis
• Varicella
• Measles
• Erythema multiforme
• Rickettsial fever
• Rickettsial fever
• Scabies
• Stevens-Johnson syndrome

Management

Due to the self-limiting nature of HFMD, supportive treatment focuses on pain alleviation, fever reduction, and appropriate oral hydration. If the kid is unable to consume orally, is dehydrated, clinically sick, or if CNS or heart issues exist, admission and intravenous fluids may be necessary.

Children with dehydration should avoid using nonsteroidal anti-inflammatory medicines (NSAIDs) and acetaminophen to treat pain and fever.

Prognosis

The prognosis for HFMD is favourable. The majority of patients recover within a few weeks with no lasting effects. Acute sickness lasts ten to fourteen days. Some might develop severe consequences.

Complications

Persistent stomatitis with ulcers so painful as to induce dehydration. CNS complications (more common with Enterovirus 71 than Coxsackievirus):

• Rhombencephalitis (brainstem encephalitis)
• Acute flaccid paralysis
• Aseptic meningitis
• Guillain–Barré syndrome
• Acute cerebellar ataxia
• Intracranial hypertension
• Interstitial pneumonia
• Pulmonary oedema
• Pulmonary haemorrhage
• Myocarditis
• Pancreatitis
• Onychomadesis

Prevention

1. Proper hygiene-handwashing after contact with the patient and after diaper handling.
2. Disinfection of surfaces and toys.
3. Avoid close contact and sharing of utensils and cups with infected persons.
4. Proper disposal of wastes.

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Disclaimer- The views and opinions expressed in this article are those of the author and do not necessarily reflect the official policy or position of M3 India.

About the author of this article: Dr Monish Raut is a practising super specialist from New Delhi.