HFMD is an acute infectious disease caused by enteroviruses (CoxA16 and EV71), mostly occurring in preschool children, with the highest incidence in the under-3 age group. The disease is mainly transmitted through the gastrointestinal tract, respiratory tract and close contact, with both patients and latent infections as the source of infection. The main symptoms are papular rash and herpes on the hands, feet and mouth. Meningitis, encephalitis, encephalomyelitis, pulmonary edema and circulatory disorders may occur in a few cases, mostly caused by EV71 infection, and the main cause of death is brainstem encephalitis and neurogenic pulmonary edema. I. Clinical manifestations.
Incubation period: mostly 2-10 days, average 3-5 days.
(A) Common case manifestations.
Acute onset, fever, scattered herpes on the oral mucosa, maculopapular rash and herpes on the hands, feet and buttocks, which may be surrounded by an inflammatory redness and less fluid in the herpes. It may be accompanied by cough, runny nose, and loss of appetite. Some cases present only as a rash or
Herpes pharyngitis
Some cases only present with a rash or herpes 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.
(b) Severe cases.
In a few cases (especially those less 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 foamy sputum; wet nymphal woven grass can be heard in the lungs.
3. Circulatory system manifestations: pale gray face, skin pattern, cold extremities, cyanosis of fingers (toes); cold sweating; prolonged capillary refill time. Heart rate increases or decreases, pulse is shallow and fast or weak or even disappears; blood pressure increases or decreases.
II. Laboratory tests
(A) Blood routine.
Leukocyte count is normal or reduced, and may be significantly increased in critically ill patients.
(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 acid positive or isolated to enterovirus. 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 during 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 those with 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, common in preschool children, infants and young children are more common.
32. 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 antibody that can cause HFMD during the acute and recovery periods.
(iii) Clinical classification.
1. Common cases: hand, foot, mouth, and buttock rash with or without fever.
2. Severe cases.
(1) Heavy: manifestations of neurological involvement. For example: 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 as bimodal fever, with flaccid paralysis occurring before or during the fever remission in the second week of the disease, and the disease mostly reaches its peak after the fever recedes without a rash.
(iv)
Pneumonia
.
Neurogenic pulmonary edema may occur in severe HFMD and should be associated with
pneumonia
differentiated.
Pneumonia
The main manifestations are fever, cough, shortness of breath and other respiratory symptoms, usually without rash and pink or bloody foamy sputum; chest radiographs show gradual evolution in terms of aggravation or reduction, and solid lung lesions, pulmonary atelectasis and pleural effusion are seen.
(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 manifested; myocardial enzyme profiles are mostly significantly elevated; chest X-ray or cardiac ultrasound suggests an enlarged heart and slower recovery from abnormal cardiac function. Eventually, the identification can be based on pathogenic and serological tests.
VI. Early identification of severe cases
Patients with the following characteristics, especially those under 3 years old, are likely to develop into critical cases within a short period of time, and should be closely observed for changes in condition, necessary ancillary examinations, and targeted rescue and treatment work.
(A) Persistent high fever that does not subside.
(B) Poor mental health, vomiting, easy to startle, shaking limbs and weakness.
(C) Increased respiration and heart rate.
(iv) Cold sweating, poor peripheral circulation.
(v)
Hypertension
.
(vi) Significant increase in peripheral blood leukocyte count.
(vii) Hyperglycemia.
VII. Disposition process
The outpatient physician should carefully inquire into the medical history during the consultation, focusing on the presence of similar cases in the vicinity and the history of exposure and treatment; pay attention to the rash, vital signs, neurological and pulmonary signs during the physical examination.
(a) Clinically diagnosed cases and confirmed cases are reported in accordance with the requirements of infectious disease category C in the Prevention and Control of Infectious Diseases Act.
(b) Common cases can be treated on an outpatient basis, and patients and families are advised to follow up when their condition changes.
Children under 3 years of age with persistent fever, poor mental health, vomiting, and disease duration within 5 days should be closely observed for changes in condition, especially the function of important organs such as heart, lungs and brain, and given targeted treatment according to their condition.
(c) Serious cases should be hospitalized. Critical cases are promptly admitted to the Intensive Care Medicine Unit (ICU) for treatment.
VIII. Treatment
(a) Ordinary cases.
1. General treatment: pay attention to isolation and avoid cross-infection. Proper rest, light diet, good oral and skin care.
2, symptomatic treatment: fever and other symptoms are treated with a combination of Chinese and Western medicine.
(II) Serious cases.
1.Treatment of neurological involvement.
(1) Control intracranial hypertension: limit the intake, actively give mannitol to lower cranial pressure treatment, 0,5-1,0g/kg each time, every 4-8 hours, 20-30 minutes rapid intravenous injection. Adjust the dosing interval and dose according to the condition. Add furosemide if necessary.
(2) Apply glucocorticoid therapy as appropriate, reference dose: methylprednisolone 1mg-2mg/kg?d; hydrocortisone 3mg-5mg/kg?d; dexamethasone 0,2mg-0,5mg/kg?d. After the condition is stabilized, reduce or stop the dose as soon as possible. Individual cases with rapid progression and dangerous conditions may consider increasing the dose, such as giving methylprednisolone 10mg-20mg/kg?d (the maximum single dose does not exceed 1g) or dexamethasone 0,5mg-1,0mg/kg?d within 2-3 days.
(3) Apply intravenous immunoglobulin as appropriate, total 2g/kg, given in 2-5 days.
(4) Other symptomatic treatment: hypothermia, sedation, anti-stunning.
(5) Closely observe changes in condition and monitor closely.
2. Treatment of respiratory and circulatory failure.
(1) Keep the airway open and administer oxygen.
(2) Ensure two intravenous channels are open, monitor respiration, heart rate, blood pressure and blood oxygen saturation.
(3) In case of respiratory dysfunction, promptly intubate the trachea using positive pressure mechanical ventilation. It is recommended that the initial adjustment parameters of the ventilator: inhaled oxygen concentration 80%-100%, PIP 20 -30cmH2O, PEEP 4-8cmH2O, f 20-40 times/min, tidal volume about 6-8ml/kg. Adjust ventilator parameters at any time according to blood gas and X-ray chest film results. Give sedation and analgesia as appropriate. If there are manifestations of pulmonary edema and pulmonary hemorrhage, PEEP should be increased, and nursing operations to reduce airway pressure such as frequent aspiration should not be performed.
(4) Limit fluid intake while maintaining stable blood pressure (adjust fluid volume according to central venous pressure, cardiac function, and invasive arterial pressure monitoring if available).
(5) Elevate head and shoulders 15-30 degrees and maintain neutral position; leave gastric tube and urinary catheter in place.
(6) Drug application: Milrinone, dobutamine, dobutamine and other drugs can be used according to the changes in blood pressure and circulation; diuretic drug therapy is applied as appropriate.
(7) Protect the function of important organs and maintain the stability of the internal environment.
(8) Monitor changes in blood glucose, and apply insulin in case of severe hyperglycemia.
(9) Inhibit gastric acid secretion: gastric mucosal protective agents and acid suppressants can be applied.
(10) Give antibiotic treatment when secondary infection occurs.
3.Treatment in recovery period.
(1)Promote the recovery of each organ function.
(2)Functional rehabilitation treatment
(3)Combination of Chinese and Western medicine treatment.