I. Clinical manifestations
Incubation period: mostly 2-10 days, average 3-5 days.
(A) Common case manifestation.
Acute onset, fever, scattered herpes on oral mucosa, maculopapular rash and herpes on hands, feet and buttocks, there may be inflammatory redness around the herpes and less fluid in the herpes. It may be accompanied by cough, runny nose, and loss of appetite. Some cases present only with a rash or herpetic pharyngitis. Most cases heal within a week and the prognosis is good. In some cases, the rash is atypical, e.g., a single site or only a maculopapular rash.
(ii) Severe cases manifest.
In a few cases (especially those younger than 3 years old), the disease progresses rapidly, with meningitis, encephalitis (brainstem encephalitis is the most dangerous), encephalomyelitis, pulmonary edema, circulatory disorders, etc. In a very few cases, the disease is critical and can lead to death, and surviving cases can have sequelae.
1, neurological manifestations: poor mental health, drowsiness, easily startled, headache, vomiting, delirium or even coma; limb tremors, myoclonus, nystagmus, ataxia, oculomotor disorders; weakness or acute flaccid paralysis; convulsions. On examination, meningeal stimulation signs, diminished or absent tendon reflexes, and positive pathological signs such as Bartholomew’s sign were seen.
2. Respiratory manifestations: shallow breathing, dyspnea or rhythm changes, lip cyanosis, coughing, coughing white, pink or bloody foam-like sputum; wet nymphal woven grass can be heard in the lungs
3, circulatory system performance: pale gray face, skin pattern, cold extremities, cyanosis of fingers (toes); cold sweating; capillary refill time is prolonged. Heart rate increases or decreases, pulse rate is shallow or weak or even disappears; blood pressure increases or decreases.
II. Laboratory tests
(A) Blood routine.
Leukocyte count is normal or reduced, and in critical cases, it may be significantly increased.
(B) Blood biochemical examination.
Some cases may have mildly elevated ALT, AST, CK-MB, and in critically ill patients, elevated cTnI and blood glucose; C-reactive protein (CRP) is generally not elevated. Lactate levels are elevated.
(iii) Blood gas analysis.
Respiratory system involvement may include decreased partial pressure of arterial oxygen, decreased oxygen saturation, increased partial pressure of carbon dioxide, and acidosis.
(iv) Cerebrospinal fluid examination.
Neurological involvement may show a clear appearance, increased pressure, increased white blood cell count, mostly mononuclear cells, normal or mildly increased protein, and normal sugar and chloride.
(E) Pathogenic examination.
CoxA16, EV71 and other enterovirus-specific nucleic acids are positive or enteroviruses are isolated. The rate of positive pharyngeal and airway secretions, herpes fluid, and feces is high.
(vi) Serological examination.
There is more than 4-fold increase in serum CoxA16, EV71 and other enterovirus neutralizing antibodies in the acute and recovery periods.
III. Physical examination
(i) Chest X-ray examination.
It may show increased texture of both lungs, grid-like and patchy shadows, and some cases are unilateral.
(B) Magnetic resonance.
There may be abnormal changes in neurological involvement, with brainstem and spinal cord gray matter damage predominant.
(C) EEG.
It may show diffuse slow waves, and a few may show spiky (sharp) slow waves.
(iv) Electrocardiogram.
No specific changes. Sinus tachycardia or bradycardia, prolonged Q-T interval, and ST-T changes are seen in a few cases.
IV. Diagnostic criteria
(A) Clinical diagnosis of cases.
1. Onset in the epidemic season, commonly seen in preschool children, infants and young children.
2. Fever with rash on hands, feet, mouth and buttocks, some cases may be feverless.
Very few severe cases have an atypical rash, which makes clinical diagnosis difficult and needs to be combined with etiological or serological examination to make a diagnosis.
In cases without rash, the clinical diagnosis of HFMD is not appropriate.
(B) Confirmation of the case.
Clinical diagnosis of cases with one of the following can confirm the diagnosis.
1. Positive specific nucleic acid test for enterovirus (CoxA16, EV71, etc.).
2.Enterovirus was isolated and identified as CoxA16, EV71 or other enterovirus that can cause HFMD.
3, There is a 4-fold or more elevated serum CoxA16, EV716 or other enterovirus neutralizing antibodies that can cause HFMD during the acute and recovery periods.
(C) Clinical classification.
1, ordinary cases: hand, foot, mouth and buttock rash with or without fever.
2. Severe cases.
(1) Heavy: manifestations of neurological involvement. Such as: poor mental health, drowsiness, easy to startle, delirium; headache, vomiting; limb tremors, myoclonus, nystagmus, ataxia, oculomotor disorders; weakness or acute flaccid paralysis; convulsions. Signs can be seen as meningeal irritation signs and diminished or absent tendon reflexes.
(2) Critical type: those with one of the following conditions
(1) Frequent convulsions, coma, brain herniation.
(②Respiratory distress, cyanosis, bloody foamy sputum, pulmonary rales, etc.
(3) Shock and other circulatory insufficiency manifestations.
V. Differential diagnosis
(a) Other childhood rash diseases.
Common cases of HFMD need to be differentiated from papular urticaria, chickenpox, atypical measles, early childhood emergency rash, herpes zoster and rubella. The differentiation can be based on epidemiological features, rash pattern, location, time of rash, presence of swollen lymph nodes, and concomitant symptoms, with the rash pattern and location being the most important. Eventually, the differentiation can be based on pathogenesis and serological tests.
(B) Encephalitis or meningitis caused by other viruses.
The clinical manifestations of encephalitis or meningitis caused by other viruses such as herpes simplex virus, cytomegalovirus (CMV), EBV, respiratory viruses, etc. are similar to those of severe cases of HFMD combined with CNS damage. For those with atypical rash, specimens should be retained as soon as possible for virological examination of enteroviruses, especially EV71, based on epidemiological history, and combined with etiological or serological examination to make (ii) Diagnosis.
(iii) Poliomyelitis.
Severe HFMD combined with acute flaccid paralysis (AFP) needs to be differentiated from poliomyelitis. The latter mainly presents with bimodal fever, flaccid paralysis before or during the fever remission in the 2nd week of the disease, and the disease mostly reaches its peak after the fever recedes without a rash.
(iv) Pneumonia.
Neurogenic pulmonary edema can occur in severe HFMD and should be differentiated from pneumonia. Pneumonia mainly manifests as fever, cough, shortness of breath and other respiratory symptoms, usually without rash, without pink or bloody foamy sputum; chest X-ray aggravation or reduction are in gradual evolution, visible solid lung lesions, pulmonary atelectasis and pleural effusion, etc.
(E) Fulminant myocarditis.
Severe cases of HFMD with circulatory disturbances as the main manifestation need to be differentiated from fulminant myocarditis. Fulminant myocarditis without rash, with severe arrhythmias, cardiogenic shock, As syndrome episodes manifest; myocardial enzyme profile is mostly significantly elevated; chest X-ray or cardiac ultrasound suggests heart enlargement and slower recovery from abnormal cardiac function. Eventually, the identification can be based on pathogenic and serological tests.