Updated: Aug 13, 2009
Hand-foot-and-mouth (HFM) disease is a viral syndrome with a distinct exanthem-enanthem.
This clearly recognizable syndrome is characterized by vesicular lesions on the mouth and an exanthem on the hands and feet (and buttocks) in association with fever.
Hand-foot-and-mouth disease is caused by a group of RNA viruses called enteroviruses. The most commonly implicated enterovirus is coxsackievirus A16.1 However, coxsackieviruses A5, A9, A10, A16, B1, and B3; human enterovirus 71 (HEV71); as well as herpes simplex viruses (HSV) can cause the illness.
Cases are commonly spread via the fecal-oral or oral-oral route. Respiratory droplet transmission also may occur but is less likely. Typically, the virus seeds the GI tract via the buccal mucosa or the ileum. Over the next 72 hours (accounting for the incubation period), a viremia is established via spread through nearby lymph nodes.2
Distribution of this disease is worldwide, with a peak incidence in the summer and fall in temperate climates and with no seasonal pattern in the tropics.
This illness has, essentially, a full recovery rate. However, HEV71 has been recently implicated in several large outbreaks with severe complications and deaths. Complications are rare, but as with any pruritic rash, a secondary skin infection may occur.
Severe complications may occur when CNS or cardiopulmonary involvement is present. These sequelae include dysphagia, limb weakness, cardiopulmonary failure, and even death. Although death is very rare, it is most often due to pulmonary hemorrhage or edema.
Enteroviruses as a group are a cause of aseptic meningitis and encephalitis; however, Hand-foot-and-mouth disease is not usually associated with meningitis.
Males and females are affected with equal frequency. Males are more likely to become symptomatically ill.
Hand-foot-and-mouth disease, as well as severe disease complications, are more common among infants and children younger than 5 years.
Hand-foot-and-mouth disease is the most common cause of mouth sores in pediatric patients.
| Herpes Simplex | Pediatrics, Kawasaki Disease |
| Pediatrics, Bacteremia and Sepsis | Pediatrics, Measles |
| Pediatrics, Chicken Pox or Varicella | Pharyngitis |
| Pediatrics, Dehydration | Stevens-Johnson Syndrome |
| Pediatrics, Fever | |
| Pediatrics, Henoch-Schönlein
Purpura |
Mucocutaneous lymph node syndrome
Herpangina
Drug reaction
Aphthous stomatitis
No specific therapy for hand-foot-and-mouth (HFM) disease has been identified. Antibiotics are not indicated unless a complicating secondary skin infection is present.
Standard dosages of antipyretics (eg, acetaminophen, ibuprofen) are recommended on an as-needed basis for fever and analgesia.
Codeine can be used for significant pain that is not controlled with ibuprofen or acetaminophen. Topical treatments include diphenhydramine and lidocaine (or benzocaine). Lidocaine or benzocaine should only be applied with a cotton swab (and infrequently) to specific areas to avoid toxicity.
Pain control is essential for quality patient care. Some analgesics (eg, acetaminophen, ibuprofen) also are effective for treating fever.
Inhibits action of endogenous pyrogens on heat-regulating centers; reduces fever by a direct action on the hypothalamic heat-regulating centers, which, in turn, increase the dissipation of body heat via sweating and vasodilation. Effective for treating fever and relieving mild-to-moderate pain.
325-650 mg PO q4-6h or 1000 mg tid/qid; not to exceed 4 g/d
<12 years: 10-15 mg/kg/dose PO q4-6h prn; not to exceed 2.6 g/d
>12 years: 325-650 mg PO q4h; not to exceed 4 g/d
Rifampin can reduce analgesic effects of acetaminophen; coadministration with barbiturates, carbamazepine, hydantoins, and isoniazid may increase hepatotoxicity
Documented hypersensitivity; known G-6-PD deficiency
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Hepatotoxicity possible in chronic alcoholics following various dose levels; severe or recurrent pain or high or continued fever may indicate a serious illness; contained in many OTC products and combined use with these products may result in toxicity due to cumulative doses exceeding recommended maximum dose
Effective for treating fever or mild-to-moderate pain. Inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis.
400 mg PO q4-6h, 600 mg q6h, or 800 mg q8h while symptoms persist; not to exceed 3.2 g/d
20-70 mg/kg/d PO divided tid/qid; start at lower end of dosing range and titrate; not to exceed 2.4 g/d
Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently
Documented hypersensitivity; peptic ulcer disease; recent GI bleeding or perforation; renal insufficiency; high risk of bleeding
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Caution in congestive heart failure, hypertension, and decreased renal and hepatic function; caution in coagulation abnormalities or during anticoagulant therapy
Indicated for moderate to severe pain. Binds to opiate receptors in CNS, causing inhibition of ascending pain pathways, altering perception and response to pain.
10-60 mg/dose PO/IM/SC q4-6h prn; not to exceed 360 mg/d
0.5 mg/kg/dose PO/IM/SC q4-6h prn; not to exceed 60 mg/dose
Toxicity increases with concurrent administration of tricyclic antidepressants, MAO inhibitors, neuromuscular blockers, CNS depressants, phenothiazines, and narcotic analgesics
Documented hypersensitivity; HACE diagnosis or elevated ICP
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Use to treat cough in HACE diagnosed patients only if absolutely necessary; may depress hypoxic ventilatory rate and respiratory drive during sleep; caution when combined with acetaminophen to hepatotoxicity toxicity
Elicits antipruritic activity and weak local anesthetic action. Used topically for temporary relief of pruritus or pain.
Apply to affected area prn with cotton-tipped applicator or swish in mouth for 2 min, then expectorate
Administer as in adults
Potentiates effect of CNS depressants; because of alcohol content, do not give syrup dosage form to patient taking medications that can cause disulfiramlike reactions
Documented hypersensitivity; MAO inhibitors
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
May exacerbate angle-closure glaucoma, hyperthyroidism, peptic ulcer, or urinary tract obstruction; xerostomia may occur
Available as a gel or viscous oral solution. Decreases permeability of neuronal membranes to sodium ions, resulting in inhibition of depolarization and blocking transmission of nerve impulses. Initial treatment of choice for small sparse ulcers. Does not decrease healing time but may allow patient to better tolerate eating and drinking. Pain relief may be short lived, and frequent applications may be necessary.
Apply to affected area prn with cotton-tipped applicator
Administer as in adults
None reported
Documented hypersensitivity; avoid use in Adams-Stokes syndrome and Wolff-Parkinson-White syndrome
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
For external or mucous membrane use only; do not use in eyes
PABA derivative ester-type local anesthetic, minimally absorbed. Inhibits neuronal membrane depolarization, blocking nerve impulses. Used to control pain.
10-20% gel, apply to affected areas qid prn
Administer as in adults
None reported
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Not for use when infection is present; methemoglobinemia associated with overuse to mouth or throat
Numerous potential remedies for the pain associated with the oral lesions (which may cause the child to decrease oral intake) in hand-foot-and-mouth (HFM) disease have been reported. These remedies have not been studied in any comparative or validated methodology; however, anecdotally they have been successful. These include the following:
Suzuki Y, Taya K, Nakashima K, et al. Study on Risk Factors for Severe Hand-foot-and-mouth Disease. Pediatr Int. Aug 3 2009;[Medline].
Wolff K, Johnson RA, Suurmond D. Viral infections of skin and mucosa. In: Fitzpatrick's Color Atlas & Synopsis of Clinical Dermatology. 5th ed. New York, NY: McGraw-Hill; 2005:790-92.
Chang LY, Tsao KC, Hsia SH, et al. Transmission and clinical features of enterovirus 71 infections in household contacts in Taiwan. JAMA. Jan 14 2004;291(2):222-7. [Medline].
Chen KT, Chang HL, Wang ST, Cheng YT, Yang JY. Epidemiologic features of hand-foot-mouth disease and herpangina caused by enterovirus 71 in Taiwan, 1998-2005. Pediatrics. Aug 2007;120(2):e244-52. [Medline].
Cherry JD. Enteroviruses: polioviruses, coxsackieviruses, echoviruses and enteroviruses. In: Textbook of Pediatric Infectious Diseases. 5th ed. 2005:2007.
Cherry JD. Viral exanthems. Curr Probl Pediatr. Apr 1983;13(6):1-44. [Medline].
Davis H, Karasic R. Pediatric infectious disease. In: Atlas of Pediatric Physical Diagnosis. 3rd ed. 1997:347-8.
Marks M. Viral and presumably viral syndromes. In: Pediatric Infectious Diseases for the Practitioner. 1985:494-6.
Sasidharan CK, Sugathan P, Agarwal R, et al. Hand-foot-and-mouth disease in Calicut. Indian J Pediatr. Jan 2005;72(1):17-21. [Medline].
Wang CY, Li Lu F, Wu MH, et al. Fatal coxsackievirus A16 infection. Pediatr Infect Dis J. Mar 2004;23(3):275-6. [Medline].
HFM, enteroviruses, coxsackievirus A16, coxsackievirus A5, coxsackievirus A9, coxsackievirus A10, coxsackievirus A16, coxsackievirus B1, coxsackievirus B3, herpes simplex virus, yellow ulcers surrounded by red halos, hand-foot-mouth disease, hand-foot and mouth disease
Pamela L Dyne, MD, Professor of Clinical Medicine/Emergency Medicine, David Geffen School of Medicine at UCLA; Attending Physician, Department of Emergency Medicine, Olive View-UCLA Medical Center
Pamela L Dyne, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
Stacy Sawtelle, MD, Staff Physician, Department of Emergency Medicine, University of California at Los Angeles/Olive View
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Heather Kesler DeVore, MD, Clinical Attending Physician, Assistant Professor Physician, Department of Emergency Medicine, Washington Hospital Center/Georgetown University Hospital
Heather Kesler DeVore, MD is a member of the following medical societies: Emergency Medicine Residents Association and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
William G Gossman, MD, Associate Clinical Professor of Emergency Medicine, Creighton University School of Medicine; Consulting Staff, Department of Emergency Medicine, Creighton University Medical Center
William G Gossman, MD is a member of the following medical societies: American Academy of Emergency Medicine
Disclosure: Nothing to disclose.
Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
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Wayne Wolfram, MD, MPH, Clinical Associate Professor, Departments of Pediatrics, Children's Hospital and University of Cincinnati
Wayne Wolfram, MD, MPH is a member of the following medical societies: American Academy of Emergency Medicine, American Academy of Pediatrics, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
Richard G Bachur, MD, Associate Professor of Pediatrics, Harvard Medical School; Associate Chief and Fellowship Director, Attending Physician, Division of Emergency Medicine, Children's Hospital of Boston
Richard G Bachur, MD is a member of the following medical societies: American Academy of Pediatrics, Society for Academic Emergency Medicine, and Society for Pediatric Research
Disclosure: Nothing to disclose.
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